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SIXT NT I ION

MedSt ucy�

INTERNAL MEDIC NE REV EW

RECURRICULUM

B k 5 of

Topics n th s volume:

General Internal Medic ne

Neurology

Dermato ogy

R be A. Hannaman, MDEditor n Ch ef



Disclaimers

NOTICE: Medic ne and accepted standards of ca e a e constant y changing. We at MedStudy doou best to ev ew and nclude in th s publ cat on accu ate discuss ons of the standards of care andmethods of d agnos s Howeve , the edito in chief, the rev ewe s, the section edito s, the pub isherand all othe par ies nvolved w th the p epa at on and publ cation of this wo k do not guarantee thatthe nfo mation conta ned he e n is n every respect accurate o complete. MedStudy furthe d sc a msany and a l ab ty for damages and cla ms that may result from the use of info mat on o viewpo ntsp esented. We ecommend that yo con rm the mater a w th current sou ces of medical knowledgewheneve cons dering presentat ons or t eating patients.

ABIM Fo ove20 yea s, MedStudy has exce ed n dete min ng and teaching what a c nical y competentInterna Medicine physician should know. The American Board of Internal Med c ne (ABIM) tests thisexact same poo of knowledge. MedStudy's expe se, demonst ated by the supe b pass rate of thosewho use t in thei stud es, s n the actual "teaching of th s know edge in a c ear, earner-f iendly mannerthat resu ts n a stronger know edge base improved c n ca sk lls, and be er Board resu ts Altho gh whatwe teach s n sync w th what the Board tests MedStudy has no a iliation with the ABIM and ou authorsed tors, and reviewe s have no access to ABIM exam content. Ou material is deve oped as o g nal wo kby MedStudy phys cian authors w th additional input from exper contrib tors based on their extensivebackg o nds in professiona medica education. This content is designed to inc ude subject mattetyp ca y tested in certif cation and ecertification exams as out ned n the ABIM s pub c y ava lab e exambluep nts but makes no use of and d vu ges no details of ABIM's proprieta y exam content.

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General Internal Medic ne

PHAR ACOLOGY I0 - 1 M D CAL RECORDS 0 26

PHARMACOK ET CS .. l tADVA CED D RECTIV 26

Absorp ion 0 1 COMPETE CY OR DEC S O -MAK G CAPACITY 10 26

D s r bu on 0 1 S RROGACY 0 27

Excre on I0 1 E RG CY S T AT O S 0 27

chael s- en on Pharmacok ne cs 0 1 QUAL TY O E A D PA RE F Dr g n erac ons . 0 2 PALL AT VE CARE 0 27

STAT ST CS 0 3 PHYS C A RROR 0 27

SE S TIV TY A D SPEC F C TY 0 3 PHYS C A -ASS ST D S C DE A D E TH A AS A 0 2

The Bayes an4 Square I0 3 CPR A D D R 0 28

Sens v y and Spec c y I0 3 S C DE ATTEMPTS 0 28

Pos ve and Nega ve P ed c ve Value . I0-4 CULT RA D ERENCES . 10 28

Chang ng o mal L mi s. . 0 5 CO F DE T ALITY A D PUBLIC W LFAR 0 28

Li e hood Ra os I0 5 BRA DEATH 10 28

RESEARCH AND STUDY D S GN 10 6 PHYS C AN PHYS C A vs P B C WELFARS udy Des gns I0 6 OBL GAT O S 0 28P Val e 0 6 DR G R SEARCH 0 28

Type and Type 2 Errors 0 6 ANC A CO CTS 10 29

e a Analys s I0 7 SCE AR OS 10 29

Con dence n erval Char s I0-7 PREOPERAT VE CARD AC EVAL AT ON 0 30

umbe eeded o T ea 0 8 PR -OP SCR N G LABS 0 31 OSTEOPOROS S 10 8 PER OPERAT VE MED C E ANAGE ENT 0 31

OV RV W 0 8 PREVENT VE ED C N 0 32

R SK FACTORS 10 8 PAT E T D CAT O 10 32

SCR G .. . .. 0 9 Smoking Cessa on . 0 32

TREAT E T I -9 O her D sease R sks . 0 33

D g Therapy for Os eoporos s 0 10 SCR NG EXAMS 10 33

RACT RES I-Il Card ovascular D sease 0 33

GERIATRJCS 0 11 D abe es 0 34

DE OGRAPH CS 10 11 Abdom nal Aor c Aneurysm ...... 0 34

ASSESSME T l - l l Breas Cancer 0 34

TR T ON 0 12 Pros a e Cancer 0 34

MOB L TY A D GA T 0 2 Colorec al Cance l0 34

Fall ng 0 2 Cerv cal Cancer 0 34

mmo y 0 3 ng Cance . 0 34

Dec bi us Ulcers I0 13 Vacc na ons 0 35

UN TY 0 14 MA AGED CARE SS ES 0 35

PHAR ACOLOGY 10 14 ACCOUNTAB CAR ORGA ZAT O 0 35

DOCR NE l0 4 ACO " eve Even s l0 35

Bone 0 5 PO SO NGS 0 35

D abe es 0 15 OV RV W 0 35

Hyper hyroidism I0 16 O VERDOSE A AGE E T 10 36

Hormone Replacemen Therapy (HRT) 10 16 SPEC C TOX S 0 37

EUROLOG C 0- 6 Analges cs 0 37

Deli um 0 6 An chol nerg cs 0 3 8

Demen a 0 7 Ac d Alcohols I 0 38

Depress on 10 19 Prescr p on D ugs 0 39

S eep D s urbance I0 19 l ic Drugs 10 40

Res ess Leg Syndrome 0 20 M scellaneous . 0 40

Dizz ness 0 20 DR G W THDRAWAL 0 42

HEARI G 0 21 OPHTHAL O OGY 0 42 CAR OVASC LAR 0 21 GLA COMA 0 43

P O ARY .. ! 0 21 Ove v ew . 10 43

Geria c As hma 10 21 Pr mary Open-Angle G aucoma 0 43

Geria c Sleep Apnea 10 22 Angle-Closure G aucoma 10 43

ROLOGY 0 22 TH RET A 0 45

nary ncon nence 0 22 Re nal De achmen 10 45

ecal ncon inence 0 24 Re nal Vascular Occ us on 10 45

Ben gn Pros a c Hype plas a . 0 24 Macu ar Degene a on . 10 46

Erec le Dys nc on ( mpo ence) 0 24 OPT C RV 0 46

E TH CS 10 25 V TR O S H OR 10 46

PHYS CIAN'S D TY A D PAT ENT S R GHTS 0 25 CATARACTS 0 46

D SCONT N G PAT T RELAT O SH PS 0 26 CRAN AL NERVE DYSF C T ON l0 47



EYE JURY .. . . 0-47 Trauma ... ... . . .. ...... ... . ... . ............ 0 47 Alkali njury .. . . .... .... . . ....... 0-47

RED EY . 0 47 Assessment. .. . . . 0 47 Anter or Uve s I0-47 Ke atocon unct vi s S cca (Kerat tis) 0 48 V ral Conjunc v t s ..... . 0 48 Bacter a Conjunc v t s . .

I 0 48 nfec ous Kerat t s ................ .. .... ...... . . . . . ........ 0 8

OTH R Y NF CT ONS 10 48ndophthalm t s . ........... .... .. ..... . .. .... 0-48

Per o b tal and Orb ta Cellul t s . I0 49 Chalaz on 0 49 Stye 0 49

EYE M RG NC S R V EW . 0 49 H AR NG LOSS 0 49

CO DUCT VE HEAR NG LOSS . 0 49 S NSOR NEURAL HEAR NG LOSS . 0-49 ACUT H AR G LOSS . . . 0 50

R N AND W BER ES S . .. . .. . 0 50 OFF C PSYCH A RY... .. ........... ........ . .. ... . .. 0-50 PSYCHOSOC A SOR RS . ... 10 50

Eat ng so ders . 0 50 Anx ety D sorders . ...... . ... ... .... ........... 0 51 B polar Disorder.... .. ...... ...... ... .. ............. 0-52 Depress o . ..... . . ...... ..... ..... 0 52 Medicatio Co cat ons 0-52

GEN CS . . 0 53 WOME 'S H AL H 0-5

OF C OBS E R CS . . .. . . . 0 53 OFF C GY COLOGY 10-59

FOR URTH R R AD NG . 0 60



PHARMACOLOGY

PHARM COKINETICSbsorption

First-pass e ect: O al dr gs are absorbed f om the GIact, pass th ough e por al vein, and hen enter the

live . Dr gs me abolized by the iver then nde go " stpass metabolism T ese dr gs eq ire a muchhig eoral dose o be as e ective as a parente a dose of thesame medicine beca se of this rst-pass me abo ismCommon dr gs t a undergo rs -pass e ec :

Opia e-re a ed: mepe idine, mo phine, and naloxoneCa ci m an agonists nifedipine, ve apami , anddi iazemSome be a blockers labe alol, metoprolol, andp opranololT icyclic an idep essants

Ben odia epines (BDZs)Anticonv sants: valproic acid and phenytoin• NSAIDs ibuprofen, ketopro en, naproxen, and

indomethacin• Ot er cyclophosp amide, eop yl ine, wa fa in,

and me ronida o eSome dr gs eq i e anacidic envi onmen foabsorption specially heazole an i nga s(excep

cona o e and vo iconazo e ), i on, and thyroido mone. If used wiH2 blocke s or p oton p mp

in ibi ors (PP s), dose adj stment may be needed;giving the medica ion wit acid (e.g., vi amin C o

orange uice) may elp PP!s can also decrease calciumabsorption.Impo an T e inges ion oca ions(e g., ca cium andi on supplemen s o an acids containing magnesium anda minum) can inter e wi he absorp ion o thyroidhormoneorq inolones

DistributionVolume of distribution (V) [Kow] T is is e e ectivevo me for determining the total amount of d g in thebody and fo determining the loading dose The otaamoun o dr g in e body (D ) is eq a o the volumex concen a ionD =V (C )So the vol me o distribution isV D /CV = e vol me o dist ibution. T is is eapparentvolume in o which the dr g is dispe sedcp is t e concent ation o the dr g in the plasma If the tissues holdmore dr g t an t e plasma at eq i ib i m, "V is arge.Rule of umb: If he d ug is dosed at eac al - ife, he

o a amount o d ug (D ) is do b e e maintenancedose. No e that the loading dose does no depend onexcretion capabi i y T e oading dose in a patient wi

© 2014 MedStudy

P AR ACOLOGY

renal fail e is t esame as t at in a healthy pa ienbu if t e drug is c eared by e kidney, the subseq enmaintenance dose is very di e ent.

xcretion

D gs exc eted main y by theLiveinc de a o ose

mentioned above nde rst-pass e ectIn a person wi h ci r osis, the decreased s -pass e ecinc eases he e ec ive bioavailability o he above d gsC ea ance is also decreased, so he e ective dose of ad g may be very sma l.Mepe idineis metabo ized by t e iver o no meperidine,w ich is an ac ive me abolite ca sing CNS stim lation(incl dingseiz es) ere o e, in live disease, ere isless rst-pass e ect No mepe idine is cleared by ekidney So, ca e lly wa ch a patient with epatico

enal dys nction when on meperidine

ichael s enton harmacokinetics[Kow:] Michae is-Menton consis s of bot ze o-ordeand s o de in Michae is-Menton p armacokineticsAs a drug's p asma concen ration increases, t e rate ofd g elimina ion ass mes e amilia ype bo ic c r ewith a plateau eac ed w en al enzyme sys ems a esat ated ost medica ions a e metaboli ed in ineafas ion ( ate of d g me abo ism inc eases in p opo tion to dr g plasma concen ration) beca se d g p asmaconcen ration is we be ow avai ab e enzyme activesites Medications may assume ze o-order pharmacokinetics when t e d g concent ation far exceeds e

t erapeutic range, sa rating al enzyme systems ( ate od g me abolism no longe changes in propo tion o itsp asma concent ation) ese fac s are incorpo ated in t e Mic aelis-Men on eq a ion

First-Order K netics

First-order kine ics T e ra e at whic a d g is c ea edis dependen on (propor iona to) the d g concentrationTha is, the ra e o d g c earance increases as t e p asmaconcen ation of t e dr g increases w en you p ot ateo dr g metabo ism against dr g plasma concen ration(i is act a ly inea ) w en t e avai ab e enzymatic sites

fa exceed e s bstra e mo ec le. A er one half-life, ed ug leve in the body is on y ha o e initia level. Iis possible to de e mine t e ha - i e by c ecking2 bloodleve s a a certain in erval (between doses).As seen in ab e , 5 half-lives a e a patien iss ar ed on a rst-orde dr gwithou a loading dose, t edr g evel is97% o s eady sta e Also, i a rst-ordedr g is s opped, a p ot o p asma d ug concen rationagains time is a downward non linea c e. The dr gis 97% gone a e5 al -lives. So, when s ar ing patien son a medication wi no oading dose, s a y wait3 5ha - ives be o e echecking t e b ood leve o see ifyo need o ad us t e dosage.

10-1



10-2 PHARMACOLOGY

Table 10 1: H lf l v

#of Ha ives

2

3

4

5

Percent ofSt ady Stat

5

75

87 5

93 75

6.875

Zero-Order (Saturable) harmacokinetics

Zero-order c earance p ocesses are non- near andocc r when all the metabolizing enzyme system s tesare saturated and the max mum rate of metabo ism sach eved (Vmax) At this point, the rate o drug c earance s independent of (not propo t onal to) the drugplasma concentrat on (that s, t is non- near). That

means the d g concentrat on bui ds up and may ca setox c e ects because rate of d ug metabol sm s constant Steady-state d ug se m concentrat ons ncrease nd spropor on to dose changes. I you plot drug p asmaconcentrat on aga nst t me a er a zero-order drug sstopped, the curve s a downward l near c ve Beca seclearance s dose- or concentrat on-dependent, hal -l echanges as the concentration/dose of the dr g changes.

Because steady-state se um concentrat on is o enwell below the sat rab lity of enzyme systems l nearpha macokinet cs are the no m or most med cat ons

Drug nteractionsNote: There are thousands o drug nteract ons b tseveral are ve y ser ous and thus equently on examq est ons. We cover some o the most serio s andcommon ones here

Wa arin Interactions

abl 10-2 outlines the most impo ant wa ninteract ons that res t nincreased NR ( nte ationalno mal zed rat o). Espec ally know that methopris famethoxazole(TMP /SMX) can markedly ra se the

N w thin the rst few days o the apy. T /S X displaces warfa n om protein-bind ng s tes and decreases

Tab 10- W f ( d NR)

Most Severe

T P/SMX

E ythromycin

Am odarone

P opafenone

A ole ant nga s

Me ron dazo e

oss b

Qu nolones

Omeprazole

C ar thromyc n

Az omycin

P edn sone

Acetam nophen (> 5g/d)

warfa in metabo ism. However,any ant b ot c can a ectthe I w tho t a ect ng w n metabo ism bydecreasing v tam nproduc ng bacte a n the ntestine.

Two st dies show that ncreased R with warfa n+acetaminophen > 9, 00 mg/week eads to Ox risk ofhav ng I > 6.

Natural products w th the potent a to enhance theanticoag ant e ect of warfa n ncl de gl cosamine,g nkgo, gar ic, everfew and dong quai.

Drugs that Caus yperkalemia

ACE (angiotensin conver ing enzyme) inh bitors,A s, (angiotensin receptor b ockers), sp ronolactoneand other potassi m spar ng di retics, and heparincan ca se severe hyperkalemia The r sk is ar greaterwhen several o these d ugs are comb ned (as seen nthe treatment o hea ai ure) Trimethoprim can ca sehyperkalem a by block ng ami oride-sensitive channels

n the rena t bu e. The risk s greatest in the e der y andwith use of high-dose T P/SM

Statin Interactions

The most common stat n side e ect ismya gias Themost l e-th eaten ng reaction srhabdomyolys sCombin ng statins w th d ugs that slow the r metabo ismincreases the risk o d ug toxicity.

Stat ns are metabo ized by the iver's cytochrome P450system, except for pravastat n, which s metabo zed bythe k dney. Fibrates, e y hromyc n, cyc osporine a o eanti ngals, protease nh b tors, verapam , d t azem, and

amiodarone a ect stat n hepat c metabo sm.Grape uit j ice a so markedlyraises the b ood evels osome stat ns by inh b t ng in t al hepat c metabo ism.Lovastatin and simvastatin are most a ected; pravastatin

s least a ected (because it is metabo ized by the k dneys).

Other Int ractions I Side E ects to Know

[Know ]• os gl tazone and piog i zone cause edema worsen ng

congest ve hear a re (CHF), and we ght gain.• Dihyd opyrid nes (ni edip ne, am odip ne) cause

peripheral edema and const pat on.• SS s cause hyponatremia, sexua dys nction, and

may cause plate et dys nction• Top ramate causes non-an on gap acidos s and

kidney stones• Hydroch oroth a de ca ses owK , h gh Ca+ ow

a , and h gh uric ac d.• St John s wo t increases metabol sm of stat ns,

cyclosporin, some HIV/A DS dr gs, and oralcontraceptives ( >treatment ailure).

• SAIDs ncrease risk o symptomat c CH inpatients at risk for corona y ar ery disease (C D)

•

B sphosphonates can cause m scle and o nt pa n.

© 2014 MedStu y - Piease Report Copyr gh Infr geme ts o co y g t@ e st y.co





• Define irst-o de ki etics.

How lo g should you wa t be o e recheck nga b ood level for a drug t a fo lows irst orderk ne cs?

You ave nvented a tes t at is 90%se si veand 95%specif c o scree i g of b east canceI you ested 100 women wi h k own b eastcancer ow many wou d he es say havebreas cancer ( ue pos t ves)?Be able to ill n a squa e a d quicklydetermine sensi v ty specif c ty PPV, a d NP

Oral contracep ives increase r sk of DVT /PEand hyper ension

S A IS ICS

SE IV Y A D EC ICI Y

B Note: =true, F = a se P positive negative

[K ow statis cs per ec ly!]

o make sense of he 4 square used in answering sens vity and spec city q estions we go overFigure I -1. Let's assume we have a group o catt ebeing tested for a deadly disease hey go hro gh thetes ing station on he le and are d rected to either heupper co ral if heir est s pos ve or he ower corral if

DISEASED

STAT S CS

heir test is negative.A l cat e are then dr ven across thecorral to the r gh ; but th s disease s so deadly all thediseased catt e d e be ore they ge o he ar righ o hecorra So we are e withsets o ca ehe sq are

s very se in determin ng sensi vi y spec c y andposit ve and negat ve pred c ive values

d ensitiv y and speci city ry to account for hosewith

(sens ivity) the disease and hosew ho t(spec city)the disease.

ensitivity a es in o accoun on y those whohavethe disease Sens tivi y e pos ves(# o pa en swith disease who es pos tive) div ded by he total # ofpa ients with disease ( hose who test positiveplus he alsenegat ves)

Sens iv y /( P + F ) (Figure I

o e tha (1.0 - sens iv y) fa se-negative rate. hisimp ies that among pa ents wi h d sease here are somewho test nega ive. Hence the m emonic " OU( e s ive tests he p ru eOU disease because the fa senegative rate s ow).

A good screen ngtest sho d try o approach b ttyp cal y does not because there are some patients whohave the disease but do no test posi ve (fa se negat ves)

OU !!

pecificity akes n o account only hose who dono havehe d sease Spec ci ytr e nega ves (# o pa ien s

w thoutthe d sease who test negative) divided by he to a#o pa ients w thou the disease ( hose who test nega vep usthe false positives)

peci c y T /( F )

NOT SEASE. .... . . . .

Sensitivity= TP/(TP + FN)Specificity= TN/( P TN)PPV = TP/(TP FP)NPV = TN/( N TN)

note " ru s o top')

©2014 MedStu y

TP

®FP THIS ROW IS USED

FOR DETERMINING

@#WHOTEST POS POSI IVE PREDIC IVE

VALUE (PPV)

FN TN H S ROW IS USEFOR DE ERM N NG

@#WHOTEST NEG NEGA IVE PREDIC VE

VA UE (NPV

-.. .......

• #DISEASED :# NOT D SEASED : TOTAL#I J.

H S CO MN SED

OR DE ERMINING

SENS IV Y

HIS CO UMN USEDOR ETERMIN NG

SP ECI C Y

igur e 0- : he ay esia n 4 quar

S ROW IS SEDOR DE ERMIN NG

PREVA ENCE ( PRIORPRETES PROBABI I Y

3



10-4 ST ST CS

Note that ( .0 speci city)= false positive ra e. Th smp es that among pat en s wi hout disease the e are

some who tes posi ive Hence the mnemon c "SPI(SPeci c ests help leN disease beca se hefa se posi ve ate is lowe ).

A good con a o y es shou d y o approach 100% bu

o en does not succeed because some w thout the d sease test posi ve (fa se pos tives) N!!

To he p emembe : Note hatsens v tyakes ntoaccount only those who have the disease andspec ci y akes in o account on y hose whodo not have hed sease. This means tha sensit v y and spec city a e

ndependen of the p evalence(percentage) of the population w h the d sease! ens iv y and spec city arep operties of he es tse

Positive a d Nega ive Predictive Value

The positive predictive value (PPV) of a d agnos c

test s he probab l y of d sease n a pat en g ven apos ve test.

(disease positive est)

To gu e his yo ake into acco nt he numbe s of boththe t e posit ves and the false pos ves h s combna ondoes akep evalenc nto acco n . The pos vep edictive val e s gene ally h gher w th condit ons hata e mo e p evalen (common) than with condit ons hata e ess p evalen ( are) given the same sensitiv y andspeci city of a test. The fo m a s

= T I (T + F )

Th s makes sense ue pos ves div ded by all hosewho est posi ve! f a disease s rare even if he sens vi y and speci c y a e h gh he false pos ves mayg eat y outnumber he tr e positives making the chanceof having he disease with a positive est ( ) m chless Th s s one of the ma n fac o s sed to dete m newhethe a sc een ng p og am s feasible

The negative pred ct ve value (NPV) of a d agnos ctest is the p obab y of not having a d sease g ven anegative tes

N (no d sease negat ve est)

Us ng he4 sq a e the fo mula s

N = N I ( + FN)N ike takesnto acco nthe d sease p evalenceThe negative pred ctive va ue s gene ally higher w hcond ions hat a e ess p evalent (ra e) han with condt ons that a e more p eva ent (common) given he samesensitivity and spec city of a es

Tips• Note that n a the above (sens vity spec c y

N ) he "T ues go in the n me ato (on op)• deals w th no h ng b pos tives; N dea s

w th no h ng b t negatives ( n erms of test es ts)•

ensitivity deals w h positives; speci c ty dea swith negatives (in te ms of d sease sta s)

The p eva ence (or p o /p e tes p obab ity) s me e yhe fract on of the pop la ion who has the d sease

This s

evalence= (Total with disease) I Totaor

eva ence (T + FN) I [(T FN) + (F + )]

No a the da a may be g ven n a q estion asking yoo nd sensit vity spec c ty N ; t isvery se l

to use Tab e I0-3 n its st pped down fo m (Tab ).Yo nse he g ven va ues and hen calc late fo theblank spaces!

The "g vens in the following example are lled n Whenall he spaces a e l ed in he quest on is easi y answered.K ow this s u

Examp e The p evalence of cancer n a pop at on s /200 n a es nder conside at on f sens tiv y99%

and the f equency of abnorma es s in the pop la ion s

3% what s he a o of fa se pos ves o r e postives and s his a good screen ng es ? To solve std aw ab e and n he g ven n mbe s Thisgives sTab 5

f he popula on is not given assume m ll on/ 00 inc dence gives 5,000 o a pe sonsw hcancer

0 0 3 x m ll on g ves 3 000 o alabno mal es sThen j s sub ac to nd he n mbe without cance

able 10-3

D sease No D sease otal

Abn tests TPN tests N

ota TP+FN

FP

FP TN

able 10-

.Sketch this st

Abn tests

Nl tests

otal

W th W tho t

able 10 -5

Based on the g ven information:

W th W tho t

Abn tests

N tests 4

ota 99

P+FPFN+T

ota

ota

,

987

Note that the and 99 are the en minat sin

the sensitivity and speci city equations!

© 2014 MedStudy-Piease Repo C pyr gh Inf eme s oco y @ ed udy.co





• Whic of t e fo owing take o account diseaseprevale ce: sensitivi y, spec ficity PPV, PV?

•

Def e pos tive a d egative ke i ood atios terms of se si v ty a d specif ci y.

(995 000) and the number of no al tests (987 000) No e that he5 000and 995 000 are hedenominators n

he sens t v ty and speci c ty equa ions!

Then we nd he o her b anks in he order shown, 2,3and 4 Blank I s he on y one requir ng thought:

Sensi iv y= TP (TP + FN or 0 99= TP 5 000

So: P= 4 950

The o hers are found by subtract onTable I0-6)

Once you have the en re matr x l ed n you can solveany prob em provided there s enough nforma on In

h s examp e PPV= TP ( P+ FP = 38% - no a goodpercen age for a screen ng test If data given to solve theprob em are insu cien , becomes apparent when youare unable o ll n all the blanks

-6

. lcu t n

A n t sts

N t sts

ot

With

95

5

5

g g rm L m

W thout

8 5

98 95

995

ot

3

987

Wha happens f you change he cr eria for wha iscalled a normal tes ? If you ncrease the range for wha snormal you ge morenega vetes s bo h true negat vesand fa se nega ves. Th s decreases he sens tiv y whi e

ncreas ng the speci c ty.

Why is th s? Assume we d d th s for he previousexamp e. Because he numbers of people w th andw thout he disease (prevalence rema n the same hedenom nators in he sensitiv ty and spec c ty equationsrema n he same bu the numerators change In thesens v ty equat on thenumerator decreases (decreasedTP due to ncreased ) sosens v y decreases; efewer of those w th the d sease are found by the test.

n he speci c ty equa ion henumerator increases sospeci ci y ncreases i.e. those es ng negative are ess

ike y to have the d sease.

As disease preva ence and inc dence decrease henumber of fa se posi ives ncreases wh le he number of

false nega ives decreases so the ra o of fa se pos t ves

© 20 4MedStudy

STAT S CS 10 5

to false nega ves ncreases. This occurs because thereis no change n he sens t vi y or speci ci y of hed agnost c es .

Sens t v ty spec c y PPV and PY can also ben e preted om diagrams such as these:

No Disease D sease

A B C D E

Th s graph shows tes performance for a diagnost c tesin 2 popu a ions1 wi h he disease and wi hou

Remember ha sensi vi y= True posi ve (T ueposi ives + alse nega ves) Point A would have nofa se negatives since all of the group w th he diseasewou d have a va ue greater han A Thus Po n A has hebes sens t vi y Po n A a so has the bes false negat vevalue. Po n has no false pos t ves and would have thebes spec ci y and he bes posi ive predictive value

L k d R

The las h ng we' dea w th here s pos ive and nega vel kelihood ra os:

Positive l kelihood ra io Sens vity Speci city)

The pos ve ke hood ratio s used wi hposit ve esresul s .e. the probab of a pat ent who has the d sease

esting pos tive d v ded by he probab lity of a person nothav ng he d sease tes ing pos ive. or example if thepresence of periphera edema has a sens tiv ty of 80% anda spec c y of40% for the presence of ci hos s wha is

he likelihood ra io f a patien has edema? P ugging nthe numbers:

(.8 - 4)= ( 8 ( 6)= 1 33

S nce s he ra io of t ue pos ves to false pos ives t sessent ally he odds of disease given a pos ive tes result

(1 33for o aga nst . egat ve likelihood ra o( Sens vity)(Speci ci yUse h s when you have a nega ve tes result and you arelook ng o seehow much less ke ysometh ng s w h anegat ve es or example: If he absence of pe pheralpulses has a sensit v ty of90% for PAD and a speci c tyof 95% wha s the negat ve like hood ratio for PAD fa pa ien has pe phera pu ses? P ugging in he numbers:

( 9) ( 95)= ( 1) ( 95)=.105

h s s the ratio of fa se negat ves o true nega ves So tis essen ally he odds of d sease g ven a negative resul .



0-6 STA S CS

Pre-test p obabili y and post-test p obability may becalcu ated in te ms of odds us ng l kelihood at os. The

esu ts should be the same as the examp e above toarr ve at pos t ve and negative pred ct ve va uelf the p eva ence o cancer is 1/200, the odds of cancea e 1 fo to 199 against If the sens tivi y o a test is

99%, and the speci city is 99 2%, then the rue positiverate is 99% and the fa se posit ve rate s 8% Positiveike hood ratio (True positives to False pos t ves) s

99 to 8; the negative likelihood ratio ( alse negat ves toT ue negatives) is 1 to 99 2To a rive at the ost-test probab li y given a osit vetest esult, mu tiply the re test odds times theodds of disease g ven a positive test esult (Pos t velikelihood atio):

1/ 99 x 99/ 8 622 odds

To convert these post-test odds to a p obability, use theo mula odds/( +odds)

622 622= 384 o about 38%(wh ch s the positive p edict ve value)

The same calculation applies n the setting of a negat vetest resu t us ng a negat ve like hood ratio (ratio o alsenegatives to True negatives)

/ 99 x 1/99 2 00005 odds o disease o 0049%( 00005/1 00005) p obabi ty of d sease

This trans ates into a negat ve predictive va ue of99 995% (100% 0 0049%)Hence, post-test odds of disease p e-test odds ofdisease x odds of disease given a test esu t (the likehood atio)

The advantage o using like hood rat os and p e-testodds is that the e ect of p eva ence of d sease is easyto visualize and understand. With nc easing prevalenceof d sease, post test p obabil ty o d sease increaseswhethe you test positive o negat ve. Notice that positive p ed ct ve va ue ncreases w th pre test probabi ity(prevalence) of disease but the negative p edictive valuegoes down (and vice ve sa) This is simply due to thede nitions of positive and negative predictive valueNotice a so that ke ihood atios are una te ed by eva

ence of d sease since hey a e a unct on of sens tivand speci c ty This exp a ns why a negat ve HIV test

n a h gh p eva ence setting can have a vast y di erentnegative predictive va ue than n a ow prevalence setting t also helps explain why a negat ve stress test isunhelp l n the se ng of a pat ent with a high e-testprobab lity o co onary disease

R ARCH AN U Y IGNStudy DesignsThere are 2 primary categories of study designobservational and randomized

Observational trials co elate exposu es (such assmoking) w th outcomes (such as ung cancer), butdo not assign patients to one g oup o another Mostobservational tria s a e e the

• cohort t als, in wh ch a g oup of ndividuals arefollowed over time to see wh ch exposures cause

disease (e g , the am ngham Hear Study), orcase cont olt als, n which people w th d seasea e compa ed to those without, to identi elevantexposu es in the past

Randomized trials sp it a s ng e group o patientsandom y nto d e ent study g oups, usually an

intervention (e g , a drug) vs a control (e g., a acebo)The st ength o random assignment s that it reducesthe sk ofconfounding va ablesthat equently a isewhen pat ents choose t eatments themselves orexample, women who chose to take estrogen a ermenopause also presumably made othe hea thy esty e choices, ead ng to an apparent bene t or est ogen

n p event on o cardiovascular disease Randomi edtrials show that the e s no bene t to est ogen t sactua ly harm l.A though obse ational t a s have advantages theyare ess expens ve than random zed tr als and are ableto study exposures that we cannot ethically randomi e(smok ng, carcinogens, etc } the andomized trial is

ess susceptib e to er o and is usua ly conside ed the"gold standard study

PValue

The va ue s a way of exp essing a s udy'sstat st cals gni cance Sup ose a andom ed t ia compa es2 drugs and concludes that d ug A s bette than drug BThe smal e the value, the mo e con dent we can bethat drug A real y s be er than d ug B and that th sis not simp y a chance occu rence. Thus, if a study has a

va ue o 0 05, the like ihood that the esults a e due tochance s on yI in 20 ( 5% or = 0 05).P values o essthan 0 05 such as 0 01 o 0 001 mply evengreaterstatistical s gni cance Ap va ue : 0 05 s cons de edstat st cally signi cant th s is robably a they expectyou to know on an exam!

Type 1 and Type 2 ErrorsThese elate to statistical hypothes s testing. There s anull hy othesis, and then the e is analte ate hy othes s(The nul hypothesis s not t ue )

y e error = conc uding that the eis a d erence(rejecting nu hypothesis) when the e is no d erence

n othe words, it s thechance of a false pos t veesultThis chance s ypically exp essed by thevalue Th sre ects the wi ngness of the investigato to declare abene t when there is none You can th nk o this as s mila to the argument fo speci city of a study and how tcan be used to u e in a true e ect (Remembe SPIN.)

© 2014 MedStudy-Piease Repo t Copyr gh Inf geme s ocopy g @ eds dy.co





ui

• You read that a study shows a new treatmentfor lung cancer imp oves su v val by 6 % andthe p va ue o the study is .2 With theseres lts, wou d you recommend this treatment

ased on stat st ca s gnif cance?• What s the cutoff p va ue that s considered

stat st cal y sign cant

T e 2 error = concludi g tha there is o d erence(accepti g ull hypothesis or, more co ectly, fai ing

o reject he nu hypothesis) when one ex s s I othewords, his is hechance of a false-nega ve result. Th sis the kel hood hat the tria misses a rue di ere cebetwee he wo test groups

The ower of a study (I mi us the type 2 e ro va ue) issimi a to he a gume t forsens vityof a study. It e syou the ke ihood of ru ng ou a ue e ect. (RemembeSNOUT )

Suppose a study shows no d erence be weenexpe menta groups. If the powe is set at the typ ca80% evel, he cha ce of ype 2 er or is 20% I otherwo ds, you'II be wrong out of eve y 5 mes the sames udy is do e If you i crease the powe of he study to

95%, he fa se-negative rate is ow5% his gives you al le more co dence n he nega ive result because it isless like y to be fa sely egat ve, but equires he studyuse mo e pat en s, onger fo ow up, or (usua ly) both.

M ta Analys s

Meta ana ysis is he re ospective analysis of ma y studies(esse t a y a mathemat ca systema ic review) conce edw th he same op c It ge era y i vo ves the aggregatioof data to try o d a s t st cal y s gni ca "a swe ommultip e s dies tha have co ic g or onsigni can

esults By combining he resu ts of d erent st dies on thesame topic, we can bette unders a d he co lect ve e ec sof a er ent on.

There a e seve al methodo og cal aws a d biases involvedwith me a-ana yses, as we as seve a severe s atis icalco st a nts Comp g st dies wi h d e i g typeandtype 2 e rors is d cul . Other areas of d cu y include

A B

1 �

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0R m m

F1g e F1g e 3

© 4MedStudy

S S CS

ages of pa icipants and assump o s of the magnitudeof d erences expec ed amo g the expe men al groups.These fac ors, wh ch ead to me hodolog ca heteroge

e y, can esu n s atistically s gn ca t he erogeneityn he resul s fo unate y, he absence of statistica y

sig i ca hete oge e y is o ecessar y evide ce ofhe absence of he eroge e ty, because me hodo ogica

hete oge eity may ot be de ec ed using he su roga e ofstatistical hete oge e y test ng.

Conf d nc nt al Cha s

Con dence inte al (CI) char s a e eque t y used me a a a yses which are when resu s om a

availab e e eva stud es a e analyzed toge he for greaters a ist ca powe .A CI of95% is essentia ly the same as a = 0 .05A CI of99% is simi a o 0 .0 . the rst case, i re ects hespread of95% of the data po ts measu ed. In the seco d,

e ec s 99% of he spread of the da a po sA consisent resu tha fa s ou s de he con dence nter a of95%s s atisticallysign f cant A CI of 99% s even more

signi cant.

Look a the charts A- D) in Figure 0 2throughigure 0 5 . Pay a te ion to heve i al do ed i e,

wh ch a ways means o e ec . In cha tsA a d B thever ica dotted i e represe sno respo se otrea menIn C a dD, he ve tical dotted ine s equa o anodds

a ioof I (aga n, o e ec ). n other ep ese tat o s, hevertical li e may be g ve a spec c number that rep

esents he mea from the en ire popu at o or fromcont ols

Each plo ed so dhorizonta l ne on these chartsreprese s he 95% co dence i erva f om one s udy

The nu h o hesis (no di erence in reatme toutcomes) is being tested each char . If the d ee ce between rea me tx a d reatmenty is assumed tobe ze o, but 95% of the time he di ere ce s less tha(or g eater ha ) ze o, the there mus be a di e encein reatment outcomes that ca ot be gnored that is,s atist cal y signi can .

The null hypo hes s can a so be expressed as a a o, inwhich case, because t eatmen ou comes a e assumedto be he same, the ra o between ea me t g oupx andt ea me t groupy is I ( o di ere ce) In th s case, hevertica li e s show with a va ue ofI.

c D

�

. 1 1 1

Odd R Odd

F1g e 4 F1g e 5

10-7



10-8 OSTEOPOROSIS

So, if the "95% con dence inter al does not cross thever ica line ( ep esent ng no e ect), then the esu ts a econsidered s gni cant. Fo example, if you are eviewing a t al ooking at esponse to t eatment ( .e., ver caline = 0) and see that the 95% con dence nte val s0 5 to 9, you know the s udy shows a signi cant

esponse Howeve , f the 95% con de ce nter a s-0.7 to .6 then t is a nons gni cant esu t!Let's go over these cha s so you know at a g ance howto inte p et them:

• Cha A is a meta ana ys s w th each study show ng asign cant esponse to treatment.

• Cha B shows a s mila meta analysis in which noteven I of the studies shows a s gni cant esponse totreatment.

• Chart C shows a sign cant y d e ent odds atio nall studies reviewed. Odds atio is a way of compa

ng whethe the p obabi ty of an event is the same for2 groups usual y compa ing a cont ol group and thestudy g oup( = same odds).

• Cha D shows study w th non sign cant esu tsbut 4 others with s gni cant results; therefo e, themeta ana ysis shows an overall s gni cant esu t

Number Needed to reat

This helps us make the leap from stat stical signi canceto c inical s gni cance.

The number needed to treat (NNT) is the numbe ofpeople who need to be t eated fo a pe od of time top event I event. NNT is calcu ated by taking the nverse

of the abso ute isk reduction be ween inter ent on andcontrol g oups.

Example A new drug is stud ed to see f it can educehea t failure mo a ty. Mo a y n the t eatment a m(active d ug) was 10/I , wh le mor ality in the p aceboa m was 30/ 00 du ing a 4 yea fo ow up w th ap va ueof< 00 . So, this s statistical y sign cant Cl nically,you want to know how use l th s s go ng to be fopatients.

NNT /(30 /100 I0 /100) 1 /(0.3 0 ) 1 /0.2 5

h s means 5 patients must be treated for 4 yearsto p event death

Alte ative y, NNH means numbe needed to ha m. ts the number of pat ents who get a d g or inter ent on

fo each patient ha med.

Also note the d e ence betweenelat ve isk educt onand abso ute isk eduction. This d ug has a e at ve

isk reduct on of 66 7% (0.2/0 3) and an absolute iskeduct on of 20% Both re ect c nica sign cance,

but elat ve isk s somet mes used p eferentia y. f thet eatment and mo a ity numbers we e to be changed to

/ 00 and 3/ 00 respect ve y, the N T wou d changef om 5 to 50 because the abso ute isk eduction is now2% instead of 20%. But the e ative isk reduction s

still 66.7%

S m la log c s app ied to studies ooking at sc een ngtests (number needed to sc een)

OSTEOPOROS S

OVERV W

Osteopo os s s dec eased bone strength p ed sposingpatients to bone actu es. One ha f of all postmenopausawomen su e an osteopo osis related actu e dur ngtheir fetime. Most f ag ty f actu es occu in thosewithout a pr o rad og aph c diagnos s of osteopo osis.

Pr mary prevention of osteopo os s is controve s a . Asof 20 3, the USPSTF concluded that fo the pr ma yp eve t on of actures, the cur ent ev dence s nsu cientto assess the ba ance of the be e ts and ha ms of

• Combined v tamin D and ca cium supp ementation,in premenopausa women or nme

• Da y supp ementation w th greate than 400 U ofvitamin and g eater than 1,000 mg of ca c um,in noninst tut onal zed postmenopausal women

Fo postmenopausa women, the common p actice ofsupplementation with a comb nat o of I ,000 mg of calc um, and 400 U of vitamin D was found to havenoe ect on the incidence of fractures Supp ementation atth s leve was found toincrease a woman s isk of deveop ng kidney stones. Fo these easons, the SPS F

ecommends aga nst dai y use of ow dose ca cium( ,000 mg) and v tamin D (400 ) n postmenopausalwomen At present, ev dence s lacking fo suppor of

higher doses of supp emental calc um and vitamin Dsupplements in these women

n co t ast to the SPSTF the 20 I 0 Nat onaOsteopo os s Foundation gu deli es recommend vitaminD and calc um supplements to p event ac es inaladults 50 years of age The nst tute of Medicine epoissued n 20 0 a so cal s fo dual supplementation

Vitamin 0 does appea to p ay a ro e inp eventing fal sin the e de ly n a sepa ate statement, theSPSTF recommends use of v tamin D supp ementation (a ong w thexerc se or phys ca therapy) n community dwel ngadults 65 years of age

From a Boa d standpoint, it s easonable to accept thatvitami D supp ementation s recommended to preventfalls n the elderly and that ev dence s insu c entat present to ecommend fo or against vitamin Dand calc um supplementation fo p mary p eventionof osteoporos s.

R SK FAC ORSOsteopo os s s common n the e derly and s gene a ysuspected by c inical p esentation (F agility fracture s ac inical d agnosis i f postmenopausa )

© 2014 MedStudy - Piease Repo Copyr ght Infr g me s toco yr gh @medst dy. o





ui

A study shows a newer treatment for lungcance imp oves su v val by5%, and the95% conf dence interval o the study is

.6 to 4.9. Assum ng treatments have thesame s de e ects, wou d t be wo thwh le tocons de the new t eatment?

Be able to ca culate the NN

What a e the sk facto s fo os eopo os s?

How do you screen for osteoporosis?• How a e the Z sco e and T-sco e used n the

eva uat on of osteopo os s?• What a e the recommendations fo all pat ents

with osteoporos s?• Wh ch pat ents should be treated with drug

therapy for osteoporos s?

There are many r sk factors for pr mary osteoporosisbut these have the h ghest known r sk:

AgePersonal sto y of fragi i y fract re (no traumaor om fa ess than standing he g t)H story of ag ty acture nJS1degree re at veWe ght ess than 127 bs or BM I< 2A coho ntake of 2 or more dr nks/dayMenopause before age 40Current or prev ous use of g coco t co d therapy:> 3 months at a dose of> 5 mg/d of prednisoneC garette smoking

SCREENING

T e Nat ona Osteoporos s Fo ndation Guide ines of20 0 recommend screening a women age 65 or o deand a men 0 or o derwit DXA scans and se ect ve yscreening women and men > 50 years f they aveanyosteoporos s r sk factors particu ar y those sted above.T e USPSTF 20 I Guide nes are t e same for womenb t they do not promote screening n men stat ng thatt e ev dence s insu cient for assessing the balanceof r sks and bene ts n men Ev dence for the optima

nte va for repeat screening s lacking Recent datasuggest that the degree of osteopen a fo nd on t e n t ascan sho d d ctate appropriate screen ng nte va s

Cons der screen ng patients w t t e fo ow ngconditions regard ess of age and gender:

G d seases(UC Crohn's ce iac gastric bypassma absorption) Endocrine disorders ( yperparathyroid sm Cus ingsyndrome ypogonadism hyperthyro d sm)Medications (g cocor ico ds t yrox ne overrep acement t i m, p enobarb ta p enyto ncyc osporine)

© 2014 M d tudy

O EOPORO

Rhe matoid a thr t s SLEnorex a ner osa

Pro onged bed rest or w ee c air boundMu t p e vertebra compress on act res noted onx ray (2/3 of ve tebra fract res are pain ess)

Dua energy x ray absorpt omet y(DXA) s the prefer ed

met od for screen ng. t is q ck (abo t 5 minutes)inexpensive and quite acc rate

Bone minera dens ty (BMD) repo ts usua y have2 results the T-score and the Z-score:

he T score compares resu ts w th no ma youngea t y bone; aT score of 0 means the BMD is

I standard deviat on(S D) ess t an no ma about0% ow. AT score of 2 5 or ower s the de nit on

of osteoporos s (about 25% be ow norma ) whereasthose between - a d 2.5 suggest osteopen a.T e Z sco e compares the BMD resu t to age andsex-matched contro s and s now recommendedfor se n men and women< 50 years of age TheZ score s not used for treatment but rather to see

f there sacce eratedosteoporosis w ch wou dsuggest secondary factors s ch as drugs m ghtbe nvo ved

Bone minera densi y by DXA is an exce lent predictorof fracture risk but it does not take nto account ot err sk factors. In 2008 the Wor d Hea th Organization(WHO) deve oped a more comprehens ve r sk assessment too ca ed X . FR X is a we -va idated toothat ncorporates bot BMD and c in ca risk acturesand ca c ates one s 0 year risk of deve op ng a

ag ty acture These fracture probab t es req reca culat onsat www.s e ac k/ RAX

TREATMENT

Un ve sa recommendat onsfor a pat ents (regard essof age or risk factors) wit osteoporos s:

D eta y ca ci m of 1 200 500 mg/day(incl desupp ements if necessa y but g er amounts areno recommended d e to ncreased r sk of k dneystones and card ovascu ar disease)

o RDA for those w tho t osteoporos s ( p to age70 get 600 U v tam n D/day> 70 years of age:800 U v tamin D/day)

Reg ar weight bearing exercisea prevent on

Avo d tobaccoAvoid excess a co o se(< 2 drinks/day)

The 2010 Nat ona Osteoporosis o ndation guidel nesrecommend that ug the pys ou d be cons dered

n postmenopausal women and men > 50 ye rs of agepresent ng wit t ese ndings:

A h p or ve tebra act re(c n ca or radiograp c)T-score between 0 and 2.5 wit other pr or

fract res(not h p or ver ebra )

10-

http://www.shef.ac.uk/FRAX

http://www.shef.ac.uk/FRAX



10-10 OSTEOPOROS S

• -score< 2.5 (remember this means a score like3 0, 2.7, etc.; we are dealing with "less t an and

negative numbers)• T-score between 1.0 and 2 5and secondary causes

associated with hig sk of racture (steroid se ortotal immobilization)

• T-score between 1.0 and 2 5and a I0 year probability of ip racture> 3% or aI0 year probabi ityo any major osteoporosis related act re> 20%based on the U.S. adapted WHO a gorithmFRAXcalc lation

Dru Th r py f O p r

All drugs that increase bone density do so by their e ectson bone remode ing. hey can eitherincrease b i d p(stim late osteoblasts) or decrease breakdown (in ibitosteoclasts). A categori ation o the d gs whic isbased on t ese e ects on bone remodeling is anabo icvs. anticatabolic Anabolic agents stim ate bot osteob asts and osteoclasts but stim ate the osteoblasts moreleading to a net increase in bone b i ding and increasedbone density. Anticatabolic agents inhibit osteoc astst ereby decreasing the resorptive processAnabolic agents (stim late osteoblasts): e parathyroid

o mone teriparatide is currently t e only one availab e Teriparatide can be sed or only2 years beca seof cumu ative increased risk o osteosarcoma and onceit is discontin ed patients need to use a bisp osphonateAnticatabo ic agents (in ibit osteoc asts) incl de therest of t e osteoporosis d gs

• BisphosphonatesOral bisp osphonates a endronate (Fosamax®)ibandronate (Boniva® also avai able in IV ormsee below) risedronate (Actonel®)

o n ectable bisphosp onates ibandronate andzo edronate (Reclas )

• Denos mab (Pro ia )• HR ( ormone replacement t erapy)• Raloxi ene (Evista )• Calcitonin salmon

A ew notes on these treatments:

eriparatide is t e on y anabolic agent current yavailable. Parathyroid ormone causes both an increasein bone b ild p and an increase in bone resorption butt e net e ect is to b i d more bone than it breaks down.

HRT may prevent or reverse the development oosteoporosis b t its se in the peri and postmenopausalwoman is a two edged sword. Most recommend notusing HR as 51 ine therapy! See HR on age I 0 6.

Bisphosp onates are analogs o pyrophosp ate and likeestrogen and ot er anticatabo ic agents in ibit boneresorption. Bisp osp onates and HR appear to havean additive ef ect They e ectively act as antagonistso parat y oid mone whic ca ses resorption a

re ease of ca cium om the bone into the serum.

Bisphosphonates especia ly V have been associatedwit osteonec osis o t e aw Use caution i using thesed gs in patients who are aving extensive dental surgery.Another very important side e ect is severe m scle/ oint/bone pain. Atypical actures o the ong bones (mids aof the fem r) ave been repo ted in patients receivingbisphosphonates

Notes on the bisp osphonates• Alendronate is an option when a patient is uncom

ortab e wit HRT or H T is contraindicatedAlendronate is poorly absorbed and rarely causessevere esop agitis (altho gh this is ess of a prob emwit week y dosing). e patient must care lly

ollow the recommendations to take it with a g ass of water on an empty stomach and not eat or iedown for 30 min tes a er ingestion.

• Risedronate was FDA approved in April 2000 or theprevention and treatment of postmenopausal osteoporosis. t has t e same clinical e ect as alendronateb t may ave ewerG side e ects. Even so take thesame dosing precautions as wit alendronate.

• bandronate is the rst once mont y medicationapproved for postmenopausal osteoporosis.

• Zo edronic acidis given by V once a year. naddition to reducing fracture risk o edronic acidimproved surviva w en given wit in 90 days o ahip fracture.

• Denosumab is a monoclonal antibody that in ibitsthe RANK receptor, preventing pre osteoclasts ommaturing into osteoclasts decreasing bone resorption.

Calcitonin nasa spray at 200 mg/d increases bone mineradensity and decreases risk o vertebral act res. t is a sohelpfu forac te pain associated with ve tebra fracture. ere is no evidence t at it decreases ip ract re r sk.While ess potent than bisphosp onates for osteoporosiscalcitonin appears to be an e ective analgesic in thesetting of osteoporotic vertebral actures

Raloxifene: During t e development of anti estrogens itwas discovered that some s bstances that b ock the e ectof estrogen on some tiss es actual y mimic estrogenon ot ers! These are ca ed selective estrogen receptormodulators (SER s ) Examples are tamoxi en and raoxi ene. T e e ect o ra oxifene on bone and lipid evelsis similar to but ess than estrogen however it exertsestrogen antagonistic e ects on the breast and terusand may be ess like y to cause cancer than traditionalH . Ra oxifene is FDA approved for bot preventionand treatment o postmenopausa osteoporosis

ere is no consensus on the appropriate duration ofdr g t erapy for osteoporosis A endronate has s owne cacy or reducing fracture risk out to I0 years. Someexperts recommend a dr g o iday ofI to 2 years forlow risk patients w o have comp eted5 years of t erapy.

© 2014 MedStudy - Pi ase Repo Copyr ght Infr ng m ts o copy ght@ edstudy.co





2 GER ATR CS

Assessment (MoCA) est is more sensitive for mildcogn ve mpa rment than the MMSE or M ni-Cog.Assess ngde r um: The bes ool o assess del rium s

he Con sion Assessment Me hod CAM; 94- %sensitive; 9 -95%spec c). SeeTab e De ir um

s present when he patient has featuresI and 2 witheither 3 or .

More on del rium and dementia on page - 6 andpage

H ngand s onare assessed using traditional ins uments such as the whisper test and he Snellen eye charThe wh sper est s performed by covering he ear thais not being ested then wh spering a question whilestanding about 2 fee away. If he patient responds correct y, then no more tes ng s required. Give the pa ent6 tries. Refer for r her aud ome ric testing if he pa entanswers 3 or more questions (out of 6) ncorrec y.

and b ceis assessed by observ ng gai , and by

watch ng the pa en ge up om a cha r wa k across theroom tu around, walk back, and s down the "Upand o est ). The "t med e Up and Go tes s notpa icular y accurate in nc ional elders

Know tha elder y and teens) have more dr v ngv o a ons compared to he general popu a on. Usuallypat ent performance on the v s on, hearing, and gaiassessmen gives you an adequate assessment of apat ent's ab i y to operate a veh c e. Formal assessmenis o ered for he elder y th ough depar ments of motorvehicles

NUTR TION

We become ess ac ive as we age, and we lose muscleand body fat more muscle than fat) Nu r onalrequ remen s are reduced, so general y, older people ea

ess. Ma nu rition is still an issue though, because ofdec ining abi es and comorbid system c diseaseM ln i ion is diagnosed n any of the fo ow ngcircumstances

Unin en iona we ght oss of10 bs/6 months• BMI < 22

Albumin< 3.8 g/dLCho es ero < 160 mg/dAny vitamin de c ency

When malnu on s d agnosed, horough y assessfor mod ab e r sks e.g., decreased access tonutritious food den ure or teeth prob ems untrea edmed cal llness inabi ity to perform IADLs such asgroce y shopping

The age re a ed dec ine in appetite and energy needs isnatura y associated with d e a y rep acement of carbohydra es wi h fa s Counse ger a r c pa ents o ncrease

heir dai y u d and ber in ake and to eat heal hy fa s(monounsaturated and omega 3s) such as o ive oil, nu savocados and sh. Vitamin supp emen s are use n

hose w h poor oral n ake because h s age g oup isespecia y vulnerab e to de cienc es of vitamin D8 ,and ca c um

For those older than age 65, he Na onal Ins i u e onA coho Abuse and Alcohol sm and the Amer canGeriatrics Soc e y recommend no more han 2 3 dr nks/day and/or dr nks/week, with ower amounts for peopletaking meds w th alcohol po ent a ed side e ec s.

MOB LITY AND GA TFallingAge is associa ed with n re ed ns y and falls5 % of pat ents age 80 and o der fa l each year! Thee derly have a s i er, ess ag e ga t w h decreasedpos ion re exes5% of fa s resu t n fractures and

f the pat en canno get up possibly hypotherm a anddehydra ion.

Aging is assoc ated w h decreased propr ocep ion andbaroreceptor re exes, so o hos at c hypo ens on and

sway ng are common There s also an ncreased incidence of stpr d a ls n the elderly probably dueo hypo ension from inges ion of carbohydrates

The major pred ctorfor frac ure from a fall sos eo o os s

R skf ctorsfor falls:

Age• Fema e gender

Past h s ory of fallsRugs unt diness and dim ght ng in he homePoor vision

•

Or hosta c hypo ens onnsteady gaCognitive impa ment

bl -7: D m ss ssm f s ss ssm h d

Feature 1

Featu e 2

Featu e 3

Featu e 4

Acute onset and uctuating course: Is mental status acute y changed om baseline, and does t e c angeuctuate throug out t e day?

Inattention Is there a prob em focusing attention (e.g. easily distracted)?

Disorganized thinking: Is conversation ramb ing or irre evant? Are ideas il ogica in ow?

A tered level of consciousness Is the patient alert (normal state hyper-alert drowsy but easi y aroused

di cult to arouse or unarousable?

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What are he ajo fea ures o delir um, us ngthe Con usion Assessme t Me hod?

•

What are the criter a that d ag ose ma utr t o ?• Which ac o s assoc ated with ag g pred spose

pa ie ts to mbalance and alls?

What a e r sk acto s o fal s the e de ly?

How does i ob liza ion a ec serum calc umevels?

What facto s a e assoc ated w h deve op e t odecub us u cers?

Wha s the ole of wet-to-d y d ess gs decub us u cer t eatme t?

Musculoskeleta diseaseCard ovascular d sease (e.g., syncope)Psychot opic drug use

The drugs most common y mplicated a ebenzod azep nes, antidep essants, neu o ept c agents,and b ood pressu e med cat ons. Know that use ofphysica estra ntnc easesthe isk of serious fa s andinjur es, so avoid phys ca rest aints when poss ble

Fa l- sk assessmentn the elde ly inc udes 5 quicko ce tests:I) med Get Up and Go test

2) Gait speed (s ower= sk)3) andem (heel-to-toe walk4 V sual acuity5) Ca f c cumfe ence (sma e = sk)

Workup for the pat ent with fal s ncludes a good historyand physical exam, with emphas s on a multid sc plina yassessment and evaluat on for a cardiovascular cause.Do a syncope wo k p f the pat ent does not emembethe fal or if the h story is suggestive. A so think aboutweakness associated w th osteomalac a as a cause espec a y n nu s ng home pat ents who a e bedr ddenand neve get n the sunsh ne. Check 25 (0H D if

you suspect osteoma ac a, and t eat de ciency f foundbecause treatment decreases fa iskAnt cipatory gu dancefor falls may nclude estr ct onof ce a n act vities, impro ng the ghting at ho e (usen ght ghts , decreas ng haza ds ( emo e ugs and looseca pets , and p ac ng extra suppo s (ba s in the shower .Exercise (especially focused on balance and resistancet ain ng svery mpo tant n help ng patients ma ntainmobility and st ength, educe falls, and pro ong su v va .

Immobilit

Patients adapt to bedrest; and the onger a patient

is mmob zed the ha de t is to ambu ate again

© 201 MedStudy

GER ATR C

Immobi at on causes dec eased AD secret on-

diu es s dec eased b ood vo ume orthostatic symptoms. A so, mmob ization causes muscle atrophy. heheart cont nua y decondit ons a er 2 days of bedrest. heelderly a e mo e a ected by bedrest because they haveless rese e than young peop e eat withrehabi tation.

Know that prolonged immobility is associated withdevelopment of hyperca cemia (although th s s morecommon n teens and young adults a er traumat cimmob lization . he hyperca cem a improves w thmob zation.

Decubitus Ulcers

P essure u cers occu most commonly on the heels,trochanter, sacrum, and ac c est. he ma n et ology issusta ned pressu e ove a p om nent bone Shear ng and

iction tear the skin and cause necrosis with u ce ation.oist en i onments (notably, u ina y ncontinence and

malnutr tion(�I - b we ght oss in past6 months alsoncrease the risk for developing ulcers.

Know that decub ti nnursing home pat ents ncreasetheir mo ta ty (usua y om osteomyelit s andbacterem a/sepsis)

here a e4 stages of decubitus u cerations

Stage I s nonblanch ng e ythema (redd sh ma es).Stage 2 s partia th ckness sk n loss (smasuper c a ulceStage 3 s fu thickness sk n oss.Stage 4 s loss of tissue down to the muscle, tendon,or bone.

Bed bound patientsshou d be otated om side to side(3 degree ang e eve y 2 hours. h s prevents contactagainst bony p om nences ment oned above Specialmatt esses and hee e bow pads also he p, but t's cont ove s al whether most nte entions actua ly p e ent u cers

In estab shed u cers, keep p essure o the a ea; andif an escha exists, emove t for p oper staging hendetermine whether any arterial o venous insu ciencyex sts, t eat nfection f present, and mainta n a "c eanu ce .

E ect ve healing re u esdebridement of necrot c

t ssue back to healthy granulat on tissue, using eitherchem ca topica treatments or a scalpe

Next, the wound has to be cleaned and dressed properlyKnow that saline cleans ng s best because t s gent e ong owing tissue, and that od nes or perox des kill tissueif used epeated y. he choices for wound d ess ngsare wide and var able ollow the advice given by thewound ca e therap st. Know that as a means for deb ding wounds, wet-to-dry dressings ha e fa en out offavor because too o en they damage iable new t ssue.G e ant b ot cs, n add t on to loca wound care, f thepat ent s systemica ly l. Use deep wound cultu es togu de your choice.

10-13



- 4 GERIATRICS

Wounds do ot heal in ma ourished pa ien s so strict yfo ow t e reco e da io s of e u ritio ists toprovide adequa e increased utri io .

[Know:] Wou ds ha deve op in he setti g o a terial orvenous i su cie cy do o ea u less he ocal blood

ow is co rected - os o e via surgica i erventioSome imes his is easible so e i es o depending o

he patie t's comorbidi ies.

S age a d 2 u cers eal quick y bu s ages3 and 4usua y take o ths.

IMMUNITY

here is a age re ated decrease i immu i y. ota and B ce l u bers s ay e same but he number ofCD4 ce s i creaseswi age whi e the number oCD8 T ce s decreaseswit age. Also o lyha fo e

ce s remai co pete t which is w y e pes zos er a dreac iva io tubercu osis are o en seen in he elder y.

PHARMACOLOGY

he elder y are ve y sensi ive o drugs for he o lowi greasons:

Phar acoki etics change wi h agi g (a ec ingabsorption and e abo ism) causing i creased drugconcen rations.

he volu e o dis ribu io for a d ug increasesbecause of the propo io al increase of body faco pared o uscle.Excre ion decreases co sis e t wi age re a ed

decreases i renal and epa ic c ion.P armacody a ics of agi g i creased e ects ofd ugs especia yopioids and be zodia epi es.

General ru es or medications in he e derly:

S ar eds a aow dose- usua y about 1/2 e doserequired or he genera popu a io and gradua y

i ra e up o t e o mal herapeu ic dose. ("Star owand go s ow ) t e patie ge s in o troub e at hetherapeutic dose, try reduci g e dose gradua yma y e der y pa ie s ge sa isfac ory responseswi h sub herapeu ic doses.A y adverse eve should be assumed to be drug

re ated u til prove o herwise.Always ook to see i a prescribed drug is he causeof new symp oms be ore prescribing a ew drug osymptomatica ly trea he new symptoms.Look at a e der y patie t s edici e record for prescrip io of an a ypica a ipsychotic (see De i iuo age I 0-16 ) i e patie t is i stitu io a i ed and

alling ese are he os co mon causes of a sin nursi g o es

ors i se f ad inis ra io increase drama ica yonce a patien is prescribed3 or ore edica ions

der y pa ien s ge ve y con sed wi h pi ls a looka ike a d wi disti guis ing be wee ge eric a dbra d na es.

Some elder y pa ie s are depe dent o low dosebe odiazepi es (BDZs) or arco ics. For t ese patie tsat emp a s ow withdrawal o these medicatio s. hese

ave o e bee ispresc ibed as ea me for a xietyi somnia depressio c onic pain a d drug wi hdrawa.S ow y aper fo owi g these ge era pri cip es: aperBDZs over 3 o hs a er switc i g to a equiva edosage o a wa er so ub e BDZ suc as oxazepa (slowero set ess addictive po ential). Wi h narco ic depe de ce

rst de ermine e cause of pai (if a y) a d treat i wia o narcotic d ug (NSA D acetami ophen). Avoid o g

a ife arcotics in ea ing ge ia ic pai

K ow a up to5% o the e derly popula io i so estudies use erba supp e e s. Ma y do o div ge isi o ma ion u less you ask directly.

ENDOCRINE

e on y speci cho o al cha ge a occurs wi h

aging is ovaria fai ure: e average age of enopauseis 51. e ypo a a ic pitui a y go ada axis is alsodisturbed i e but ot as predictab y as i wo e .I bo sexes, e adre a o a g omeru osa dec inesin sy hesis o DH A and he pi ui a y secre io ofgrow ormo e wanes (a d subseque ly a so eve s o

GF 1 ). Ma y ot er or ones are or a i t e amou tproduced but do ot c io as well.

Many of hese ormone pe turba io s are e t o beassocia ed with e aging process buo e are co clusive y li ked Grow h o o e reduction appears o beassocia ed wit oss o usc e ass and strength; supp e e ta ion is not encouraged because i is associa ed

wi oo any side e ec s.he pinea gla d s e ato i production is disrup ed

wi agi g. his may cause poor s eep a d inso iaMe a o in supp emen a io ay elp some pa ients

Agi g pa ie s ave a reduction i e c eara ce oyroid o mo e, so hyroid replace e for hypo y

roidis can be star ed a a ower dose. SH i creaseswi h age especial y i wome (see docrino ogyBook 4) so a t is ti e a risi g SH wit out a accopa ied decrease i does ot meri rea e t forhypot yroidis

es ostero ep oduc ion decreases i e aging malebu e e ec is variab e. However t era eof speproductio is s ab e o ages 20 to70 years! FSH a dLH also dec i e but dispropor io a e y compared o t e

ore drastic decline in estos erone he low testostero e produc io is mos ike y due o dec i ing es icu ar

c io and ot o ypothala ic disease.

Low es ostero e is be ieved o be rela ed toe o lowi g a t ough direc causatio as no

been prove :• Decreased sexual fu c io

Decreased bo e mineral de sityDecreased usc e ass (a d increased fat)

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What should you do for an elder y woman whois on chron c low-dose benzodiazep nes for"ne ves ?

Wha s the ave age age of menopause?

Wha is andropause ?

What is the typ ca presentation of Pagetd sease?

What comp ications a e ger a ic pa entsspec fica ly at r sk o deve op ng as they a ebeing t ea ed o d abe es?

Me orm n shou d not be g ven o pat en s w thestima ed GFR be ow what calcu ation?

•

Decreased muscle strengthDecreased mentation

T e co ec ion of the above, in associa ion wi h red cedee tes osterone, as been ca ed"andropause. T e

Endocrine Society se o th g ide ines (2006) for treatmen of cer ain ma es with andropause who havesymp oms and a serum tes osterone< 200 ng/dL, witha trea ment goa of300 00 ng /d . In spite of this recommenda ion, there are no good st dies hat provea trea ment bene Donot screen elderly men and dono trea men wi h ow eve s if ey do not have symp

oms. Testosterone promotes red cel pro iferation andis trop ic o p ostate issue Men receiving testos erone

erapy need o have periodic moni oring of their bloodfor po ycy emia and rapid rises in PSAVi amin Dde ciency is common beca se of decreasedintake, decreased abso ion, red ced s n expos re,and poor conversion of the s orage to active form ofvitamin D As discussed n the sec ion on os eoporosisvitamin D supp ementation in t e e derly is controversia for preven ion of os eoporosis, but appears top ay an impor ant role in preven ion o fa s Ca ciums pplemen a ion in e der y withou osteoporosis is ikewise con roversial (seepa I0-8 and pa I 0-9 onOs eoporosis).

Bone

O p r

The majority of women > 80 years of age aveos eoporosis According to cu ent guide ines (seeOsteoporosis on p 1 -8), women 65 years of ageand older shou d be screened wi h a DXA scan a eastonce If e patien asany risk ac ors for vitamin Dde c ency (especially poor die or ack of s n exposure),check s ores by meas ring 25-( H) D

© 2014 MedStudy

E AT CS

P g

Page disease of bone occ rs in abouI% of peop e> age 40 in the U S It is us al y diagnosed a er discovering an iso a ed eleva ion of a ka ine phosp atase in anasymp omatic person T e disease res s om a misma ch o os eoc as and osteob as ac ivity (remodeling),

ca sing changes seen on x-ray bone scan, CT, or M inoca ized areas The bones are more brit le, vasc ar, andarger eading to ar itis, ig outpu ea t fai ure, and

ne ve compression, respectively

E io ogy: T ere is a clear genetic predisposi ion;some hypothesize a vira trigger, but tha remainscon roversial

Diagnosis is strongly s ggested by bone scan resu ts.Patients wit Paget disease have foca areas of markedincreased ptake.Treatmen is no req ired in t e majority o patien s andis not c rativeb t may be needed i ear ai re bone

pain, ne ve compression, or earing loss deve ops.Drugs used Bisphosp ona es (e idrona e, pamidrona e,and a endronate) given ora ly or IV are e ective in he

reatmen of Page disease SQ or IMcalci oninhas a sobeen shown to be e ec ive.

Diabetes

With aging, t ere is decreased carbo ydrate o erance,wi a s igh increase in as ing glucose. Both ins insensitivity and production decline E der y patients witdiabetes ge he same micro- and macrovascular complica ions as yo nger pa ien s, bu e elderly ave o bespeci cal y wa c edfor ife rea ening hypoglycemia,hypo ension, and dr g dr g interactions.

ypog ycemia more o en presen s as cogni iveimpairment in e elderly, ra her han rem lousnessand swea s T e most ike y ca ses o ypoglycemia areins linsand heinsu in secretagog es(sulfony reas andmeg i inides)G yb ride as about twice e incidenceof hypog ycemia in the elderly compared o g ipizide(27% vs. 14%!) and is no onger recommended foruse as a 15 ine su fony urea by e American Diabe esAssocia ion (ADA).Be cautious wit metfo in se in e e der y because of

e hig prevalence orena ins ciencyin is popu aion and the increased risk of lac ic acidosis. Assess the

es ima ed glomeru ar l ra e ra e (eGFR) prior o use ofme o min in pa ients> age 80, and donot give t e d gto any pa ien wi h an eG < 60, regardless of ageRosig i azone is no longer recommended by the ADAA so avoid piog itazone in the e derly, d e to he riskof edema and precipita ion o C The j ry is sti oon w e er ese dr gs are associa ed wi an increasedrisk of cardiac events and s roke

emember to adj st he ins lin doses downward asrenal nc ion declines with age, especia y as Gdrops be ow 50 cc/min

0-



0- 6 GER ATR CS

Hype hyroidism

Those > years of age with thyroid disease a e morelikely to have vague symptoms tha could indicate eit erhyper - or ypothyroidism. Fea ures of c assicyperthy

oidism, suc as ype e exia, eat in o e ance, emo ,nervo sness, po ydipsia, and inc eased appeti e, a e

o en absent in e derly persons Apathetic hyper yoidismcan be seen in e der y patien s and presents asapa hy, fatigue, anorexia/weigh oss, and achycardia.

Atrial b i ation and anorexia can occur in olde patientswi hypo yroidism; we are y see ese symptoms in

ypothy oid younger patien s

Hormone Replacement The apy (HRT)

Estrogen eplacement is he bes op ion for al eviatingvasomo o and other menopausa symptoms and can be

sed safe y fo sho periods

The mos s bs antia da a we ave on HRT a e om eWomen's Heal h Ini iative (WH ), p b ished in2 2.Prior to t is st dy, common p ac ice (based on observational data) ad been to presc ibe HRT to postmenopa salwomen to p otect their bones and p event co onary disease. The WH data, howeve , show that HRT (es ogenonly) is ine ective long erm for preventing ea disease, and that combination HRT is associated wi aslight yinc eased 1 skfo hea disease, s roke, venous

hrombosis, and b east cancer. Bot gro ps have anincreased incidence of ga lb adder disease Combinedtherapy red ces he risks of co on cance and os eopo o ic

ac res, b t no eno g to jus i these increased r sks.

o ow up ana ysis of t e WH da a el s us ha thewomen w o experience the ea disease and s okes aret e olde women in t e s dy

Conclusions om WH t a drive practice today:

Combination HRT is associa ed wit an increase inhear disease, s oke, veno s c o ting, breast cance ,and gal b adde disease Unopposed es ogen se is notassocia ed wi e eart disease o b east cancer is sYounger, perimenopa sa women do not appea tohave an increased r sk for hea disease and s oke withs or e m ( p o5 yea s) se of combination HRTBu o de women do

Est ogen alone causes endome ia hyperp asia andinc eases r sk of endometrial cancer Combina ionest ogen-p ogestin in women wi a uterus is noassociated wi h this r sk.

• P ema re ovarian fai re (menopa se before age4 )can be safely trea ed wi combination HRT nti t ewoman is5 years old en, stop and disc ss t e isks

T e impo an concept Donot give women > 5 yea so d combina ion HRT because it increases t ei is s forstroke, hea disease, b eas cance , veno s clo ing, andga lstones and the red ction in act res is inadeq a eto compensate for hese increased is s. Pe imenopa sa

use of est ogen replacemen is discussed late in O ceGyneco ogy on age I 59.

NEUROLOGIC

Del r umDeliriumis a t ansient al e a ion in conscio sness e atedto sys emic facto s t is a common p ob em in e e derlyPatients wi h unde ying demen ia and/o stro e are ahig est isk Main fea res are

abnorma attention span (easily distracted),disorganized inking (may ave allucinations), and

• a te edconscio sness (wi inc eased or decreasedmen a ac ivi y) thatc atesd ring the day and

ypica y wo sens a nig

Common precipitating causes of de irium inc udedr gs, poo n tri iona s at s, acute i lness (e g , infections, volume deple ion) Know tha physica res ain sand b adde cathe e s can incite de ir um as we l nthe post op pe iod, ncon olled pain is a ma o ca se,especia y in geria c pa ien s wi hip ac u es se of

opioids to manage pos ope ative pain isno associa edwith inc eased ates of de ir um1/3of cases are caused by dr gs. Be awareespecially ofmeperidine, NSA Ds, any new antimicrobia , diphen

ydramine, al ca diovascu ar dr gs and antidepressan s,an iemetics, bac ofen, H2 ecep o b oc ers, s eepinduce s, and e ba s (e g., S John s wo and va erian

oot) Acu e discontinuation of a cohol, benzodia epines(BDZs), SSR s, and pain medications may ca sewithdrawal de i ium.

Di e entiate deli i m om "sundowningSundowningis a distu bance in be avio at occ s predic ably in heevening among some pa ien s who ive in ch onic careenvi onments is no associa ed wi a p ecipita ingi lness and is no deli i m. Wit sundowning, usual y

e care faci ity can e l yo at e pa ien predic ab ydete ora es a nigh

ow that in the elderly, de i m may be t eon ymanifes ation of i ness. Any pa ien w o becomesde ir ous s ou d be t o o g y eval ated fo a se iousp ecipitating cause

va uate t e con sed patien wit an ob ective tool sucas t e MMSE or the C M (seepage I ) P ysicalexam sho d foc s on identi ing annder ying acuteillness t a may be associated wi con sion (e g , drugab se, epatic failure, emia, head in ries, st oke, andsei u es) Wor up e cen a nervous sys em imagingand LP) if no cause is fo nd a e a o o gh search

Trea ment of de i i m is suppor ive with focus ondiagnosis and trea ment of he nde lying ca seCa endars and o ien ing signs, nigh ig ts, newspapers,a radio, glasses, and ea ing aids he p stabi ize andprevent decompensation t is also necessary to minimizedai y s ess.

P a maco ogic t eatment of deliri m in t e elde y iso gh because he meds emselves can worsen he

conf sion Low-dose haloper do is an option, bu wa cfor prolonga ion of the QT inte va and donot use it

© 2014 MedStudy-Piease Repo t Copyr gh Infr ngemen s o copyr gh @me s y .com







What is apathet c hype hy o d sm?• What are he ma n featu es o del r um?

P ec p ta ng ac ors?• How is de um dif erent f om "sundowning ?• Wha is the ecommended n tia the apy for

e de ly pa en s wi h deli ium? What a e someopt ons fo d ug the apy, and wha are theirassociated sks?

How is demen a d f e ent rom del um?• What are he 3 mos common causes o

dement a in he U.S ?

When do patients der ve the grea es benefitf om A zhe me ea ment?

in patients with Parkinson's. Alte ative dr gs inc udethe a ypical antipsychotics: rispe done, o anzapine(Zyp exa®), and quetiapine (Seroque ) T ese dr gshave fewe sho -te m side e ects but ave beenassociated with increased mor ality wit ong term seDo not use BDZs in delirious patients because t eymake patients mo e con sed and drowsyUse of a "sitte and ot er nonpharmaco ogic inte ventions are a ways t e best15 choices Remember to avoidphysica est aint of geriat ic patients at a costs beca seit precipitates de i i m and ca ses fa s

Dementia

Patients wit dementia have a progressive dete iorationof cognition t at is insidious and ch onic b t withouta tered conscio sness, as with de i um T e dete ioration can be eit er very grad al o step-wise ( e ated tothe under ying ca se) T e cognitive impai mentp esents as

Di cu ty ea ing and emembe ing new informationDecreased problem-solving of bot simp e andcomp ex tasksDecline in spatia o ganization- t ey get ostT o ble wit imp lse cont o- nus al behavio

Some decline in cognition occurs with norma aging, butin cont astto dementia, memory oss is mild and s o dnot a ect t e patient s dai y living o be especia ynoticeable by familyMost patients in the U S wit dementia a e diagnosedwithA zheimerdisease(80%), followed by eithermu tiinfarct dementia or Lewy body dementia (a sou ce ofcu ent debate) Dementia is a common deve opment inpatients wit Pa kinson disease as wel See Neu ology,Book5, for a mo e thoro g disc ssion of dementia

© 2014 MedStudy

GERIATR CS

Depression can ook like dementia, especia y in thee de yA coup e of ways to te l t edi e ence: Dep essedpatients o en p esent comp aining of memo y oss, w i edemented patients a e b o g t in by fami y or iendsDepressed patients have a depressed a ect and slowing wit comp etion of t e MMSE or Mini-Cog, w i edemented patients have a mo e norma a ect and t y

ard. Assessment too s can elp identi the t e cognitive defects of dementia A sco e of<24 points on theMMS is consistent with dementia/de iri mAt t is time, t e position of t e U S Preventive ServicesTask Fo ce on sc eening for dementia is t at the e isinsu cient evidence to ecommend fo or against it

ine t eatment for A eimer s is the c olinesterasein ibito s (C s) donepezi (Aricept®), rivastigmine(Exe on®), and ga antamine (Ra adyne®) Best resu tswith C s are achieved in mi d-to-moderate Alzheimedementia, but ot e causes of dementia (e g., m ltiinfa ct and ewy bodies) sometimes a so imp ove C sdo not he p patients wit H ntington disease, oweveC s can be combined wit memantine (Namenda®),w ich is an N met y -d-aspar ate recepto antagonistC s provide a sma bene t and he p some patients car yo t t ei activities of dai y iving (ADLs) C s may bepa ic ar y se in controlling behaviora p ob emsin patients wit dementia T e e a e con icting data ontheir ong-te m e ects. Not eve y patient receives bene t he combination of cho inesterase inhibitor p usmemantine appea s to be better than CI alone.CI side e ects o en invo ve t e GI ract (na sea,vom1t g, diar ea, anorexia, and weight loss)Severe b adycardia due to AV block f om excessiveace y cho ine as been epor edIn Ma ch2008, t e ACP p b ished dementia t eatmentguide ines T e evidence-based eview fo nd i ebene t fo any of the c r ent c olinesterase in ibitorsor memantine T e a t ors conc ded t at individuapatient factors wo ld like y dete mine need to initiatethe apy because the data we e not very compe ing foinitiating t erapy in any patient Know t at the bene t

om eating Al heime s is greatestea yin the disease,and t e cho ineste ase in ibitors s ou d be stopped inpatients wit severe dementia.

Vit min Eis no onge ecommended as a supplementbeca se it may inc ease the isk of hear disease anddeat Gi go biloba ex ract andvitamins Aand D avenot been s own in clinical tria s to improve cognition ine der y patientsLewy body dementia LBD is marked by p og essivecognitive dec ine with concomi ant ha cinations, s eepdist bances, and park nsonian feat res Treatment ofLBD with neuro eptics may bring on a pa adoxicapsyc osis and worsening of pa kinsonism. The same mayoccu wit use of dopaminergic agents, making behavio athe apies p efe ab e to medications w en possib e

0- 7



10 8 GER A R CS

Table 10 -8: n tidepressant s , e lect ive eceptor Blockers

Drug T /2 Mech nism of Not s Drug of Cho ce C ution (!) n p ti nts . .(hrs) Act on B ocks ... for ..

Fluoxetine 72 SSRI May cause anxiety ... with insomnia(Prozac®, and insomnia

Serafem®)*Paroxetine 20 SSRI Most anticholinergic in whom anticho inergics(Paxil®, of the SSR s are to be avoidedPexeva®) Sedating in some withinsomnia

Sertra ine 25 SSRI G discomfort is . withinsomnia(Zo o ®)* common . with ir i able bowe

F uvoxamine 15 SSR Most sedating of the pts with agitation withir itab e bowel(Luvox®)* SSR s pts with insomnia

.. pts with obsessive-compu sive disorder

Cita opram 3 5 SSRI May cause anxiety with ong QT syndrome

(Ce exa®)* and insom ia, N ,headache, QT p olongation

Escitalopram 0 SSR S enantiomer of with ong QT sy drome(Lexapro®) cita opram;

may cause QTpro ongation

Nefazodone 3* SSRI and 5 HT2 Maintains s eep ... pts with insomnia on benzodiazepines or(Serzone®) and has anti a pha architec u e ... to main ain sexua antihis amines (interacts

adrenergic activity Sexua dys nction activity with cy ochrome P 450is un ike y system)*"

Ven afaxine 4 SSR and with insomnia

( exor®) norepinephrine withH N usua yreuptake and some increases b ooddopamine reuptake pressure, so not used in

these patients

Du oxetine 12 SSRI and norepi- A so indicated for pts with chronic(Cymba a®) nephrine reuptake bromya gia pain syndromes

and some dopamine reuptake

Bupropion 15 Reuptake of Sedation is unli ely withinsomnia(We lbutrin®) dopamine and some Sexua dys nction withH may

norepinephrine is un ike y increase b ood pressure

Mi azapine 20 Presynaptic a pha2 Agi ation is un ike y pts with insomnia Most anticho ine giof(Remeron®) receptor (increases Sexua dys nction to maintain sexua a these

seritonin and is un ike y activi y wi hN maynorepi re ease) Good for insomniacs i c ease b ood pressureAND 5 H 2 AND5 HT3

A l the SSR s have a tendency to cause agitation, sedation, and sexual dys nction Pure SSR s arenot ike y to increaseblood pressure.

May use oratadine (Claritin®) or orazepam (Ativan®) with nefa odone* T 2 is higher than this in e der y, especia y womenNote :Buspironeis a 5 HT A agonist that can be combined with an SSR to decrease the dose or improve e cacyNote 2 Any SSR may cause an increase of suicidal thought or actions inI of 50 age< 8 years

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• Wh t re c y pt f ger tr cdepre ? W t e c de e ect f

ed c t f depre ?• N e e ed c t typ c ly c ted

w t t e elde ly.• W t the le f be z d zep e

t e t e t f ?

Depression

Depression s themost common mental prob em in hee derly s par cu ar y ikely to occur n hose who l vein nstitu onal zed se ings and/or have chronic diseases,espec a ly j s a er a severe sickness or in states ofchronic pain. Know that he depressed elder y (espec a y

men) make up 1/4 of he s ccess l s ic de a temp sn he U S

Look for dysphor a, psychomo or s owing, anorexia,weight oss, and mu ple "aches and pa ns Know hainsom ais associa ed w h depress on, espec a ly n thee der y, although it s o known whether it is a symp omor a ca se. Depression-associa eddel sions are morecommon in he elderly than in the genera pop lation. Payspecial a en ion o he elderly man w h depressed mood,hope essness, chronic pain, and insomn a beca se h ss ic de risk is pa ic larly high

A hos of s bs ances and drugs can poten ia e depression,incl d ng alcoho , BDZs, opia es, and barbi ura es

ntreated hyroid disease, d abe es and pain are organicca ses Always check ha here is a recen assessmen ofthy oid nc on, pr or o nitia ing an idepressan herapy.

Trea men s sually psycho herapy comb ned w han depressan s; electroconv lsive herapy (ECT) may becons dered in severe cases. xerc sehe ps, oo Selec ivese oton n re p ake hibi ors(SSR s) are the I 51l ne drugsbeca se they have fewer side e ec s than o her cho cesThe mos common reason for s opp ng hese agents ssex a dys nct on! (SeeTab e I0-8.

When us ng antidepressan s in he elder y,a ways starwi h ow doses ( yp cal y 1/2 he normal dose) andincrease slowly w th he goal of even ua ly reaching thenormal herape ic dose. See patien s(or cal them) wi h n

weeks a er ini ia ing meds. Wa ch for he side e ec sof hyponatremia and tremor n elder y pat en s on SS s

t akes abo 8 weeks o see improvemen 6 1 mon hsis he s a d ra ion of trea ment Know ha rea ing apa en 's depression can he p heir comorbidit es improveas wel .

Sleep Disturbancensomnia

S eep dis urbance is a common problem in elder ypersons, and normal aging is associa ed wi h more

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GER ATR CS

freq ent awaken ngs. These d st rbances nclude dc lty fa ng as eep(> 30 m n es), eq en awakenings,wak ng oo early, and fee ing genera ly nres ored. Whenthe dis rbance a so causes problems for the pa en d r ng he day (e.g., poor concen ra ion, moodiness, s eep ness,fa ig e), i is c ass ed as " nsomnia.

Know wha sno nsomn a:

Some peop e can sleep well for only a few ho rsand have no p ob em nc oning the nex day.These patients simply have short-dura ion sleepPeop e who have chosen not o s eep at n gh(d e o work or o her reasons) and easi y fal asleepd ring he day are classi ed as hav ng " nsu c ents eep or "sleep depriva ion, no nsomn a

Insomnia, especia y in he elderly, s assoc a ed wi hworsening of hype tens on, hea t disease, ung disease,urinary incon inence, ch on c pain, and depression.

H story shou d focus on charac e zing he sleep

dis rbance(sleep logs help) and iden i ing any n reatedcomorb di es and or precipitan s(e.g , naps, s ress, newlys opped or star ed meds, a coho , ca eine, n co ne)

Med cations spec cally assoc ated w h nsom ia incl deco t cos ero ds, be a b ockers, be a agon sts, and stoppingsedatives or pain meds

Labs are recommended only to diagnose po en acomorb di ies (e.g., hyper hyroid sm, res less legs).Sleep s ud es are nnecessa y nti a pa ien has fai ed orespond o conser at ve managemen

Trea men shou d be d rec ed a improv ng any poor ymanaged comorb di es, and advise the pa ien ongoods eephygiene

Set a schedu e for s eep and s ick to itGet in he bed on y when yo re s eepy.

hen yo re rested, ge p.Minimi e excess light and so nd in he bedroomExercise d r ng the day, at leas 4 ho rs beforebedt me.S ay away om ca e ne, nico ine, alcoho , ande cess uids near bed ime.

at dinner or an evening snack to preven bed imeh nger.

Do not ght sleep f you can' sleep for > 0 mi u es,ge p and do some hing relaxing(read ng or music).No br ght ligh s or TV

The mos e cacio s reatmen in pa ents w thncomplica ed nsomnia isbehavioral no pha maco

log c. E der y pat ents are espec a ly suscep ib e to bado comes om s eep drugs.

Ben odia epines(BDZs) act al y do he p by decreasingthe freq ency of awaken ngs, red c ng time o faas eep, and increasing d ration of sleep B t hey havemany nega ve s de e ec s, incl ding addic ion, loss ofmemo y and accum ation of metabolites

0- 9



1 GERIATRICS

Non benzodiazep ne nsomn a d ugs, such as zolp de(Ambien®), zaleplon (Sonata ), and eszop clone(Lunes a ) have more selec ive e ec s han BDZsbecause hey a ec only a por ion of the ecep o subuni s ha BDZs a ec Because of his, non BDZs tendto have o e sedat ve han anx oly ic e ec s han BDZs.Addi iona y, they do not have as many side e ec s as

BDZs. Their cos can be prohib tive.Even so, both BDZs and non BDZs can cause con s on,wande ing mbalance, and dayt me grogginess in heelderly -hence bo h classes areavoided n ger atr cpa ien sMany s eep aid drugs in bo h he BDZ and non BDZclasses have rece ved FDA required label changes,ind ca ng ha the dr gs can cause a hypno ic s ate hatal ows pa ents to at e pt complex asks whi e s eeping� b zar e behaviors (e.g., having sexual n e coursewh le no appa en y awake, s eep ea ng, er at c dr v ng,

ak ng incoherent phone ca s). he DA equ ed

educed eco mended doses fo zolp dem produc s in3because of pe s s en pai men the nex mo ing.The mela onin agonist,ramelteon (Roze em ), doessee o imp ove sleep for so e patien s, and he d ug isno associa ed wi h any known un oward e ec s. I is agood choicefor he elder y, albeit wi h va iable e cacyS ay away from o der an depressan s (e g ,a i ripty ine), diphenhyd am ne, haloper do , andba bi u a es n ost pa ents (because of side e ec s),but especially in the e de y.

Restless Leg SyndromeRestless leg syndro e (R S) s a co mon sleep disorder n the elder y (p evalence= 20% in age> 8 yea s)The ha lma k of R S is eg disco for+/- pa esthesiasat es , e eved i med ate y w th move en . Usually,pain is "deep sea ed and ocalizes below the k ees.Sy p o s a e worse in the even ng and a nighR S can be p a y o caused by o he cond tions:iron de ciency (even wi hou ane ia), dia ys s,diabetic neuropa hy, mul p e sclerosis, Pa k nson's,pregnancy, and o hers. Make sure that he patien scompla n s a en t ac ual y aka hisia f o medica ons(pheno hiazines and SSR s).D agnos s s made based on c nical history, a nor alneuro exa , and absence of k dney disease Alwayscheck a fe in eve to ru e out iron de c ency even f

he pat ent does no have ane a.

The fo ow ng expe t panel t eat en reco mendat onsare based on whether the R S is in ermit en , daily, oref ac o y.

• In ermi en :T y non pharmaco og c he apy rsiron replace ent the apy; en a aler ing activi es(such as v deo games or c osswo ds); avo dance of

ca eine, n co ine, and alcoho Then, f needed, t yone of he fol ow ng:

o Dopa ne agonis s genera y are the d ugs ofchoice p amipexole, ropinirole

o Levodopa Be care - may cause aug en at on(wo sened sy p oms o rebound)Be zod azep nes (genera y avoided)

ow po ency opio ds (genera y avoided)• Dai y: y non pha acologic rst, then dopa ine

agon sts, gabapen n, and, ast y, ow po ency opio dsefractoryto dopa ine agonists T y gabapent n,

a d erent dopa ine agonist, co b na ion he apy,hen tramado and, las y, h gh potency opio ds

DizzinessD zziness s co mon in he elde y but sno a no alconsequence of aging. When any pa ien co p ains of"d zz ness, take a goodhis o y(more sens ive in akingthe d ag os s than PE, Jabs, o s udies) to dete ne wh chof the follow ng he pa ent is actua y describ ng:

Ver igo "sp nning, "whi ing, or " ov ng of eithehe pa ent or the env o en hat is worse w h head

movement and occurs n spells (days o weeks),then even ua ly esolvesPresyncope a os "faint ng or "black ng ouwhile e he s anding or sea ed (not supine),poss b y associated with sweat ng, a sensa ion ofwa m ng, visua b ur iness, and nauseaD sequi br u : balance with s and ng and wa king,especia ly w h tu ingNonspeci c dizziness: unable to charac e ize n o oneof he above ca egor es

A co p ete discussion about he workup of ve tigo isincluded in Neurology Book5. Mu isenso y de c tscausing d sequil br u and benign pos ional vert go areco on n ge atric pa ents, the cause is o e o enves ibula han in o her pa en g oupsThe com on causes of d zziness n the e de y usual ycan be discove ed byh s ory.P c p :D zz ness that sounds l ke p esyncope or"fa n ness should be aken se ous y and evalua ed w th aca diovascu ar workup, especially if he pa ien has known

hear d sease, pa pitat ons, or a h story of e syncope.Mu f cTh nk abou ult senso y de citsas a cause fo d sequil brium in the patient w h a x ofvisua , hea ng, or hopedic, and neu opa h c i pa ents(so e imes also called "benign dysequ lib u of aging )They co p ain of "fee ng unsteady and p ove w ha wa ker or when someone holds he ar T eat this by

axi izing support for each senso y pa rmen andprovid ng assistance devices (e.g , canes, walkers)B p a v (BPV) presen s as recur en(las s for weeks n spells), short ived(< inute)episodes of vert go ha p edo inantly occur when the

patien changes posit on. The ve tigo can be bad enough

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• What dangerous side e ects are somet messeen w th both benzod azep ne andnon-benzodiazepine sleep agents?

• W at is a common cond tion assoc ated w thest ess eg synd ome?

W at cause of dizz ness s associated witimprovement when the patient ho ds onto awa ker?

• Which mane ve he ps identify benign pos t onave go?

to cause na sea and vomit ng; b t, othe w se, the pat enthas no other symptoms (e.g , hear ng loss, headaches)Kow that BPV occu s more o en n ger atr c patientswho have g ant ce arter t s (See Rheumatology,Book 3 ) So, take a good h sto y in the dizzy elder ypatient to determine whether symptoms of vasculitis opolymyalg a rhe matica are a so p esent (e g , weightloss, eve s, muscu oskeletal pain)

In ncer ain cases, BPV can be diagnosed by theDix-Hallpike test This maneuver involves tu ing thepat ent's head, then rap dly tilting the pat ent backwardsfor 30 seconds, then up ight aga n, w th s bseq entobservation fo nystagm s Repeat the mane ver w ththe head tu ed in the oppos te d ect on A pos t vetest is visible nystagmus in e ther the rec mbent or theupright pos t on

In these cases, the di erent a diagnosis ncl descent alca ses o ve gosuch as ce ebella lesions (strokeso masses) so i the h sto y is suggestive, do u herwo k p w th mag ng and electronystagmog aphy(water ca ori s)

T eatment of BPV can be accomp shed th o gh one of2 o ce mane ve s, Ep ey and Semont, both eq ivalent

n e cacy and designed to eposition the m splacedotoliths thought to be responsible or the vertigo hemaneuvers are extens ons of the D x-Ha pike test,where you lean the patient backwa ds and o a dswith an associated neck tilt A te at vely, exerc ses can

be p esc ibed or home that aim to have the same res lt(b t a e ess e ective) No d gs a e used to treat BP

HEAR NG

Decreased hea ng is anage-re ated condition Abo t/3 of patients > 65 years of age have hea ing oss he

most common ca se sp esbyc sis, which is an agerelated sensor neural hear ng oss It is bilate al, and lossof highe f eq ency so nds is more common Be s reto check or cerumen impaction See othe ca ses ofdecreased hea ing on page I0- 49 Hea ing aids can helpthese pat ents.

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GER ATR

CARD OVASCULAR

Walk ng more than 4 ho s per week is assoc atedw th a d amat c decrease n ca d ovascu ar- e atedhospital ations n persons> 65 years of age

ola olic h p r n ions a common ndingin elde ly patients It inc eases the isk of myocard a

n a ction and stroke 2 x Severa stud es show thesepat ents bene t om eatment, so ong as the d asto cp essure does not a too ow(< 60 mmHg) Lowd astolic p essures have been associated w th increasedca diovasc ar events

n theelde ly, sta with abo t 1 2 the standa d dose ofany one o the o lowing: thiaz des (chlo ha done isnow be ng avo ed ove hyd ochlo othiaz de because oits superior e cacy n clin cal st dies), d hydropyr dineca cium channel blockers (e g , amlodipine), o ACE

nh bito s angiotensin II receptor b ocke sAvoidbeta blockers for treatment of systolic hype tension

n the elde ybecause they do not wo k as we asthe other treatments and have been assoc ated w thincreased mo a ity

he 6-month mor ality rate after an M inc eases withage rom 4% a o nd age 66 to 12% when older than80 years (Gro p = stMI, w th thrombo yt cs, discha ged om hospita ) Only abo t 75% o elig blepatients receive asp r n on discharge om the hospitalBe s e to p escr be an antplate et d g to these patients!CHF: The inc dence of congest ve hea t fa lu e (CHF)in the e der y s ncreas ng dramat cal y and s nowthe n mber I ca se o hosp ta izat ons n this gro p(N mber 2 s pneumonia )

T eat CHF itse pr ma ily w th diet, d uret cs,beta-blockers (speci ca y metop olol, car edilol, orb sop o o ) and AC nh b to s Sp rono actone can be a

sef adj nct that can also lower mor ality or systo chear fa ure D goxin s nd cated only o more seve eheart ail e and red ces hospital ations, b tnot ove allmo ality soso b de d n trate and hyd a azine has beenshown to lower mo al y in A rican-Ame cans w thsystolic hea ail e Use of NSA Ds is an impo antprec pitant o CH n olde patients who already have

isk facto s o CHF

Mo al ty bene t has been shown fo ACE inhibito s,beta-blockers, and low-dose spirono actone I yo

se sp onolactone, o lowK+ c osely Spirono actonebene t has been shown in patients with class 3 or 4heart fail e

PULMONARY

eriatric sthma

Elderly patients w th asthma may have ong stand ngd sease acq ired in ch ldhood yo ng adulthood, orthey may have deve oped it as an ag ng ad lt Aro nd8% of adults > age 65 a e diagnosed w th adu t-onset

asthma Be awa e that t iscommonly misd agnosedas

10-2



10-2 GERIATR CS

COPD because COPD is more l kely to occ r n th sage group.

R sks fo developmen o ad l -onse asthma a ethe same as fo younger pa ien s: al e gens andi tants (e.g., obacco smoke, occ pa ona vapors,a po on).

Como bid ies are mpo tan , espec a ly co ona y hea td sease, because t ea men of asthma w h be a-agonistscan cause myoca d a ischem a A so, beta-b ocke s

sed as antihype tens ve drugs can exace ba e ai wayobs ruc on, altho gh this is p ima i y the case w tho de , nonse ec ive be a-blocke s

As hma in he olde pa ien can present the same as inhe younger pa ien , a hough he e de ly tend to haveewer symptoms w h he same amo n of d sease

Speci cal y, hey complain ess of dyspnea assoc a edw th obs ct on and wheezing ike y due o theired ced ac vi y, hey a l to no ce hey are short ob ea h De ni ve d agnosis is made w hsp rometry,when he FEY 1 and FEY /FYC are educed.In the elde ly, the tradi ional cuto of 70% or a diagnos s o obst ct on, as ecommended by he GOLDg o p (see Asthma in Pulmona y Med cine, Book 2),

sno used. This s due to he fact hat this c i er ons no as spec c n h s age group andover d agnoses

as hma! Ins ead, fo diagnosis o asthma in he e de ly,mos expe s use an FEV/FYC< 89% o helower

imito normal for age. A response o b onchodi a orss st l expected, as pe he GOLD cri e ia, or d agno

s s:> 200 cc ncrease in FEV1 pos b onchodi ato and 2% of pred cted.

Separat ng COPD from as hma is important, especia lyn he e de y where rates o COPD are h gh. Know thatevers b e obs r ct on is consisten wi h asthma, and aow LCO s consis ent w th emphysema ous COPD

B onchoprovoca ion is used to d agnose as hma inpa ients wi h no ma sp ome y, he same way as t sused n younger peop e.

Management o ge a r c asthma is he same as oryounge pat en s, b theophyl ne snot ecommended,even as an al e at ve dr g, because o the signi cantpo en ial or toxicity.

eriat ic Sleep Apneah abo sleep apnea as a poten a cause of educed

cogn on n ge ia c pa ients. Know ha apnea hatesu s n poor sleep and excessive day me somno ence

ca r es a highe a e o mo b d y n patien s who a e ra land a eady prone o a s agnosis and management is

he same as in younge pa ents.

UROLOGYnary Incont nence

v v wNorma m c u t on s dependent on an in ac neuro og cpathway om he b a nstem o the b adde , which causes

elaxa on o he sphinc er muscle's tonic contractilestate jus mill seconds be o e con act on o he de r sor(bladder musc e) Add ona y, vol ntary con ro of m ct t on requ res comm nicat on between the cerebraco ex and the b ainstem.

U ina y ncont nence, altho gh a common ger a ricp ob em, isalways considered a pa ho og c condit on

hat s not a no ma consequence of ag ng Alwaysconsider the poss bil ty hat he patien has a ser ousunde y ng condition respons b e o he eakage

Norma , age-related changes o the ina y rac inc udedecreased ow a e, decreased b adder capacity, and

ncreased res dua vol me. As a nction of hesechanges, it s no mal for pat ents to ge p once d ing

he night o void

Ur nary ncont nence may be hought o as either a" sto ageproblem ("de so o b adde ove and undercon ac li y) o " out ow problem (o t e obs r c onor ncompe ence).

he e are 4 genera , symptom based ypes of urina yncon nence:

I) g = leakage (a lot o a l t le) associated wi hthe feel ng of u gency

2) ss = eakage associated w th increasedintra-abdom nal pressure (e g., co ghing, snee ng)

3) M x d= eakage assoc a ed w h both an urgency andncreased ntra-abdomina p ess re

4 m b dd m g("ove ow ) eakage(a o o a l t le) a e vo d ng

No e ha "ove act ve bladder s no necessar lyncon nence s a ro og c condi ion de ned byhe urgen need to void requen ly and du ng he

m ddle of he n ght. Occasional y, the rgency may beassoc ated w h leakage, in which case i is ca led " rge

ncon inence

g U ge incont nence ( I) s acommon cause of ge iat ic

ncon nence Wi h ge ncontinence, there s passage oe thersma lor large amo nts o u ne, assoc a ed w th asense o urgency o en set o by aprec pitating st m l s:hea ng r nn ng wa er, unlock ng the door o he ho se,enter ng co d environmen s.UI s related to overac ive b adder hey a e both causedby uncon o lab e bladder cont actions (" detr sor instability } usua y caused byCNS p oblems(te med "de rusorhyperre ex a ), b also somet mes a es t ofcyst t s

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• Wha a GOLD a fa f a h a ?

• u a a aqu a ?

Wha a 4 f ?

W a b a u?

• Wha h b a a f u a ?

• W a a au b a a ?

• Wha b a a h za a f a ?

Detr sor hype e exia s due to prog essive loss ofcomm nica ion be ween he on a obes and hem c ition cen er n the b a nstem. As the bladder osesthe modu a ng n uence om he b ain, ends to spasmmore o enT eatmen s bes accompl shed w h behav ora he apy,ca ed bladde a n ng. When an u ge o vo d becomesp ofound, the patient is nstructed to attemp e axat on

echniques that help he u ge subside and allows short ermvoiding de ay Once he ge is con ol ed, he pat encan wa k ca mly o the estroom and u ina e he goal

s to even al y delay vo d ng o eve yho s w h non e a leakage.

Bladde rain ngis mo e e ec ve than he more commonlypresc bed therapy of ant muscarinic agents (oxyb tyn n,to te od ne, feso erodine osp m, sol fenacin, da fenac n, hyoscyam ne, and cycl c an depressants), a lof which a e equiva ent in e cacy and relax he b addermusc e hey have othean cho ine gics de e ects (e g ,d y mouth, tachyca dia, constipation). Even so, theseantim sca n c agen s a e help when used as anadjunct

o bladde aining sho te m, as needed Remembeha an chol nergics can precipi a e ac e angle gla coma!

A so, donot use hem fo incontinence in pa ients who a e

aking cho neste ase nhibi o s for dement a because hecomb nationaccelerates cogn ve dec inePelv c m sc e exe cises (Kege 's) are also help for UI

Stress Incontinence

S ress na y ncon nence(SUI) is second n frequencyn ger a r cwomen. W th SU , he ure hra canno ma nain he p essure grad en eq ed fo ur nary con o

when here is an inc ease in intra abdomina press re(co gh mping, etc ) SUI is associa ed wi h mul iplevagina del veries, pe v c su gery, pos menopa sa hormona changes ( ow est ogen- a oph c e axat on of

the vag nal wa - ack of s pport for he u e h a) b

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ERIATR C

is some mes seen in ma es pos prosta ec omy. S essincont nence is in tial y bes ea ed wi h behav ora

herapy, espec al yKegel exerc ses (pe inea musc econ actions); efe ral o a pe v c oor physical he apyspecial s can be he p l in e ect ve teaching of Kegel'sNote tha some women w th ina y incontinence havea mixture of SUI and u ge ncont nence. S gery has

h gh cure a es b w th h gh isk of comp cationsPer ureth a co agen injections are an op ion fo hosewho canno have (o do no wan ) surgery and who dono mprove wi h exercises

he his o ygives yo the c ues to de erm ne whetherncontinence is d e to ge o stress ncon nence ook

fo he stim hat p ec pi a e eakage n a patien w hUI and ook for leakage associa ed wi h inc eased ntraabdomina press e wi h SUI

Mixed Incontinence

Mixed ncon nence, again, s a combina on of u geand s ress incon nence he ue etio ogy s nknown.Bladder ain ng and Kegel's he p hese pa ien s, oo.

ncomplete Emptying

Incomp ete b adder empty ng s sometimes s ca ed"ove ow ncontinence. s ca sed by e he anoveract ve b adde +/- an o t e obstr c ono by an

nde act ve b adder hat has roub e cont ac ng (e g ,d abe es Park nson's, MS, a coho ab se)

Al ho gh are n females, ncomp ete emptying in ma ess sual y ca sed by prostatic hype rophy.he ou le

obs r c ionca ses a dis ended bladder and high vo me,pos vo d e ent on An cho ine g c dr gs are he moscommon ca ses of d g nd ced ncomple e emp y ngPsychogen c reten on can also be a ca se.

Mos ypes of incomp ete emp y ng do ndeed causeurgency and may be seen as a ype of urge ncont nence

ea ment ncl des alpha b ocke s and/o 5 alphareduc ase nh b o s for men w th benign prostat chype trophy (BPH).

Review

B adder tra ning and Kege exerc ses: urge, st ess,and m xedDr gs fo ge and m xed (ant cho ne gics w han m sca inic effects) oxyb tyn n, tol e od ne,

osp um, so fenac n, dar fenac nD gs for stress None B adde t a ning andKege on ySu ge y ast esor for stress

ncomp ete emp y ng reat unde ying cause fpossible in ermi en ca he er za ion diaper ikega ments

Asymptomat c bac eriu ia, common in he e derly, isno a ca se of ncon nence. Also, ncon inence snevean nd cat on for a long e m b adder ca he e

10-23



10-24 G R ATR CS

Fecal Incontinence

Geriatric fecal incon inence is usua ly caused by fecalimpaction and secondary over ow incontinence. Theimpaction is norma y a result of ax musc es and neurona degeneration Typica presen ation is an elder yperson wi h comp aints of diarrhea and abdominaldiscomfo t and who has hard s oo in he rec a vauon physical exam Treatment is disimpac ion andsubsequent bu king agents

Benign Prostat c Hype p asiaThe prevalence of benign prostatic hyperplasia (BPH)increases from about I0% at age 30 o> 80% a age 85;abou 15% of these pa ien s have impaired urina ion.We sti do no unders and wha causes BP and haveye to iden i any speci c risk fac ors-excep ageBP does not increase he chance of prosta e cancer

Symptoms of BP are fairly speci c for urina y

retention: frequency, hesitancy di cul y sta ing ands opping he stream, urgency and noc uria Certain yo her diseases can cause these symptoms (e g bladder cancer cystitis) and shou d be considered beforemaking a diagnosis of BPH. Know tha serum pros atespeci c antigen (PSA) evels increase as he prostateincreases in size so PSA screening for prostate canceris less speci c in men with BP (more false positives).

The 2 de nitive tests tha shou d be done

I) a digi al rectal exam to palpa e he prostate and assessfor i regu ari ies and increased size and

2) a urina ysis to assess for hema uria (wi h a culture if

infec ion is suspec ed). BPH symptoms shou d noimmedia e y rigger PSA esting

reatment

BP is trea ed only if i signi can y a ects he pa ientadverse y and or if i is associated with out et obs uctioncausing hydronephrosis or acute kidney inj y

Trea men of symptoma ic pa ien s s a ts wi hehavioral therapy. Make sure patients know o reduce

in ake of ca eine and a coho (diure ics) s ay awayfrom uids before bed and a empt to urina e wice tocomp etely emp y he b adder

edica therapy:• General y sta wi ha pha blockers( era osin

doxazosin tamsu osin a fuzosin si odosin) a one• A 5 a phareductase inhibitor ( nasteride

du asteride) is then added ater if needed.

Note Of the a pha b ockers prazosin isnot used forBP because it requires frequen doses and has moreside effec s

os common side e ects of these meds areo thostasisand diz iness Be carefu wi h combining sildena l orva dena l wi h hese drugs because he combina ionworsens hypo ension.

The 5 a pha reductase inhibi ors which reducecircu ating estos erone ake at east6 months todecrease prostate size and re ieve symptoms Thesedrugs work be er for large pros a es and have a moredurab e effect. The ma or side e ec isimpairment ofsexual nction (decreased ibido and de ayed e acu a

ion) now that these drugsdecrease serum PSA even

in cancer patien s so recommendations are o mul ip yhe measured PSA by 2 2 5 depending on how longhe patien has been taking he drug

ransurethra resection of he prostate ( URP) isnow the reatmen of as resor used when drugs fai

o work

E ect le Dysfunct on (Impotence)Overview

The mos common type of ma e sexua dys nctionis erectile dysfunction (ED), which is de ned as

the inability to achieve or main ain an erection sufcien for sa isfac ory sexua intercourse t is notuncommon for men o experience brief episodes of ED." mpotence is he term rese ved forED tha occursin > 75% of sexual encoun ers.

The smooth musc e in he accid penis is in as a e of tonus or con raction due oa pha s imulation by norepinephrine cG P is made along withcA P made by he norepinephrine and vasoactiveintes inal peptide (VIP) pathways This cGMP causesthe re axa ion of the smooth musc e in the penis whichincreases he in ow through he helicine ar e y intothe erectile tissue The swe ing of his issue causescompression of he ou ow venules resu ting in asus ained erec ionED can be caused by organic or psycho ogicalprob emsor as a side e ect of medications (25% of cases!). Moscauses of ED are a least pa tia y organic The organiccauses are neurogenic vascu ar hormona and normaag g

lassic Presentations and auses of ED

There are many causes of ED. These can be grouped asfo lows

•

Organic causes: Usua lys owonse . Loss ofnoctu al and mo ing erections.Neurogenic Usua cause isdiabetes O her causesare surgica procedures (especia ly prostate) MSA S Parkinson's and other causes of peripheralneuropa hy Cyc is s who spend> 3 hours/weekon an upright bicycle can experience ED due opressure hat he sea p aces on the pudenda nerves(reducing b ood ow to cave osa artery)

o Vascu ar: Usua cause is diabetes and orcardiovascu ar disease O her causes are surgicaprocedures in amma o y conditions or pelvicfrac ure n e der y menED is caused by vascular

compromise in 50% (indica ed by a low penile

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How does prostatic hyperplas a af ect PSAleve s?

What s the n tia treatment for BP ? Whatmedicat ons a e common y used for t eatment?

• What s the most common cause of neurogen cED?

Which med cations most commonly cause ED?

If an exam presents a young ma e w th ED whos on no medications, what s the most likely

et o ogy?• What is the mechanism of action fo si denafil?

brachial press re index [PBPI]). ED due to vascu arcompromise indicates increased risk of presen and

re major vasc lar disease.o Hormonal: o en accompanied by a loss of libidoSymp oms may inc ude gradua onset of ontalheadaches or vis a dist rbances (space-occ pying tumor); hot ashes and decreased need for shaving(decreased androgens) fatig e+ weigh gain + dryskin constipation (hypothyroidism)

o No ma ag g: Sexua po encyd s decrease with ageMedications especially an idepressan s (SSR s),c onidine, spironolac one beta blockers, and thiazidediure ics. Many others a so cause ED but these aresome of the mos common y presc ibed meds in the

geria ric pop ationPsychogenic typica lyacu eonset. This is the us acause for ED in younger pa ients hey con in e ohave noc u a and mo ing erec ions, but ibidois lost ED is direc ly correla ed wi hd pressionUnfortunate y SSR s used or depression treatmenare also associa ed with a very high incidence ofsexua dys nction (generally de ayed ejac la ion)

Treatment Options for ED

st ine reatment for D Know]:Sildenafi citrate (Viagra®) inhibi s phosphodiesterase

type 5 (PD 5) an enzyme tha inac ivates cGMP. Iworks very we for many ca ses of ED, inc dingpsychogenic Side e ects are d e o itsasodila opro e ies headaches, shing dyspepsia b ish huein the vision Reports of hearing oss have a so beendoc men edVardenafil (Levi ra® S axyn®) is simi ar o sildena lin mechanism e ectiveness and side e ec sTadalafil (Cia is®) has the same mechanism of ac ionas si dena and vardena b with a longer ha f ife.Erecti e nc ion may be improved for up o 36 ho rs.This dr g is app oved for daily se One speci c side

e ec isbac pain Tada a l has recen ly gained FDA

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THIC

approva as treatment for BPH symptoms when sed ona daily basis a though he mechanism remains unc ear.Avanafil (Stendra™) is the newest agent (approved20 2) and is simi ar o he o hersPD 5 inhibitors are more likely to ca se hypo ensionwhen aken wi h nonse ec ive alpha blockers (pra osin,

doxazosin, and tera osin) roselec ive a pha b oc ers(tamsulosin and a osin) are ess likely o ca se hypo tension. There is a ris of hea ing loss wi hof hePD inhibitors Contraindications are any conc rrenni rates. Relative contraindications are C F, hypotension,

nstable angina HCM and severe aortic stenosisYohimbine is a naturally occur ing a pha b ocker. It hasminima e ect, but beca se it is inexpensive and hasminima side e ects i is o en tried on pa ients wi h amost y s oge i e iology Be er han p acebo b tm ch ess e ec ive han sildena l.Vacuum devices wor we but are clumsy to use hey

are indica ed on y when oral therapy is con raindica edor he patient prefers them o ora herapy2" line reatmen for ED:Alprostad (prostag andin E ) injec ed into he co poracave osa of the penis works we t is especially sein patien s wi h ED due to ne ro ogic dysfunction3 ine reatmen for ED:Pen le implants: Vario s types hydrau ic semirigidand exib e rods sua y sed on y for hose who havefailed al other therapy. Complica ions are associatedwith he surgery There is a risk of posts rgica infec tion Sca ring may ca se erections o c ve issueerosion may occur If there are no complications theyare e ec ive and pa ien sa isfaction ra es are high

THI S

OV RV WRead the ACP Ethics Manual, 61 Edi ion (re eased20 2) availab e online at:http://w annals org/con

en / 56/l Pa 2/73

Y N' DU Y ND N 'R GThe physician's duty o he pa ientIS basedon 4 princip es ha are he basis foral ethicalphysician patient interaction:

) Bene cence: the d ty to act in he best in erests andwelfare of the pa ien and the hea h of society

2) Nonma e cence: he d ty to do no ha m o he pa ient3) Respec for he pa ien s a tonomy: he ping the patien

ma e free non coerced choices4) Jus ice: he d y to trea al patien s (and by extension,

society) equitably and fairly

10-25

http://www.annals.org/con-






10-2 ETHICS

Let's ook at speci cs.The pat ent s r ght to accept o e se health ca e sbased on anothe 3 pr nc p es:

1) The phi os phical concept ofpersonal autonomy -a va ue held c ose to the hea in ou cultu e

2 Pe sona ibe y nte est under the Const tut on

3) Common law ight of se f dete m nat onPat ents shou d be ab e to choose and fo ow their ownideas and p ans for their ife. Const a nt of a person s eechoices s pe m ssibleonly when these cho ces nf ingeon anothe person's r ghts and we fare.ate a sm, thepractice of ove rid ng o gno ng p eferences of pat entsin o de to bene t them, used to be the standard of inteact on between the physician and patient. Today, exceptfor ce a n cases (mental illness and some eme gencies),pate a sm s considered eth ca ly imp ope at entsshou d be an active par of the dec s on ma ing processPat ents equ re info med consent, wh ch is de ned as

the willing acceptance of med ca ntervention - a eadequate d sclosureby the physician f the natu eof the intervent on and all of its ris s and bene ts.Patients a e entit ed to d sclosu e of the fol owing:

• he patient's cur ent med ca status with the p obab ecourse, whethe o not med ca ntervention is used

• The med ca nte vent ons that may he p and the r sksassociated w th themThe phys c an's opinion about other alte at ves

• The phys c an's own recommendat ons based on bestc in cal judgment

ow that phys c ans are esponsib e for car ng fopatients w th contagious infect ous diseases It s deemedunethical by AC for nte sts to re se care for patientswith HIVIAIDS, hepatitis viruses, mult d ug resistantTB, and in uenza because of a physic an's own fea ofbecoming infected. It is assumed that the phys c an ta esapp opr ate infect on cont ol precautions

now that phys c ans are esponsib e for p ovidinghonest nformation on d sab ty c a m fo ms and shou dnot a empt to assist a pat ent in obta ning d sabilitybene ts erroneous yGeneral y, physicians shou davo d caring for c osefam y members and f iendsUse of social media has added a new dimensionto nteractions with pat ents. The ACP wa s thatuse of soc al med a has the potential to b u sociaand p ofessiona bounda ies" and shou d be usedw th g eat caution.

It sa solu ely unethicalfor phys cians to have anysexua e at onship w th a cu rent pat ent, regard essof who initiates the relationship The eth cs document

om the Federation of State Medica Boards says thatphysicians cannot even have sexua e at onsh ps w ththe e ativesof ex sting pat ents.

Even fo me pat ents can cause ethical prob ems TheACP eth cs document says that phys c ans shou d

consu t with a col eague or other professiona befo ebecoming sexually nvo ved w th a forme patient "

D SCONT NU NG PAT ENTRELAT ONSH PS

Phys cians can sever e at onsh ps with pat ents so ongas care is ava able by another physician (anywheree se), and the pat ent's health s not sacr ced. Thephys cian must g ve the patient w t en not ce of intentand must request approval from the pat ent fo transferof medical eco ds to the accept ng physician. If th sp ocess is not fo lowed, ega action can be ta en fophys cian abandonment "

MED CAL RECORDS

The physica char be ongs to the hosp ta o phys c an,but the info mat on in the chart be ongs to the pat ent.If requested, you must re ease the ent e chart to thepatient, and you cannot ho d the cha hostage nexchange fo payment of serv ces. Howeve , t is legal tocharge a reasonable fee for copies.

ADVANCED D RECT VE

The advanced directive s the means pat ents have fostating which t eatments they would accept o dec neif they lost dec s on making capac ty he advancedd ective may a so speci genera goa s fo medical ca eand the pat ent's choice of a sur ogate - a pe son withdu able power of atto ey fo the patient's hea th ca e

A living will is a more focused fo m of advanceddirective, in which the patient, fo examp e, re ses lifesuppor when in a te mina condition. A lawye is notneeded to make a liv ng willThe patient has a ight to change his/her mind! Joe" hasa liv ng wil . If he comes into the emergency depar mentand requ es n ubation to su vive-and states that hehas changed his m nd and wants al possib e t ea mentsavai able - then you hono h s current dec s on.Know that u ds and nutr tion a e eth ca ly rega dedas the same as othe forms of t eatment, and patientscan address the desire for d scont nuation of uids and

nutrit on n the advanced directives.

COMPETENCY OR DEC S ON MAK NGCAPAC TY

The decision making capac y efers to the abil y tocomprehend, eva uate, and choose among realisticopt ons Decis on making capaci y is determ ned by thephysic an and at t mes may be di cu t to determine.Competency refe s to the ega determination of one'sdec s on mak ng capac y. Most decis ons on patient ca eare ca ed out without need for competency hearingsThe e are many ans tory or evers ble cond tions thatcan interfe e with th s capaci y. xamp es a e anx e

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• Name a scenario n whic a phys cia canethical y have a sexual ela ons p wit apa e t.

• What is t e dif e ence between a adva cedd ec ive a d a living wil ?

• 6 mo t s ago a ma wi h erm a ca cedecided o invoke a livi g w ll t at s ateshe refuses all ife suppo i case ofcardiopulmo a y a res Today, e presen s tot e eme gency departmen in seve e dist essand says e wa ts eve yth g do e i c ud gintubat on. H s fam y does o wa t anyt ingdo e; you ave t e sig ed livi g w at t ebedside W a should you do?

depression, drug-induced confusion, infection, and abnorma me abolic s ates. The waxing and waning associa edwi h cer ain condi ions, such as organic brain syndrome,is a manifestation of pa hology, and he pa ien shou d beconsidered o have impaired capaci y.

SURROGACY

A"surrogate or "proxy is a person who is authorizedo make decisions on beha f of an incapaci a ed person

Tradi iona y, the nex of kin has been considered hedefau surroga e. (In some s a es, here is a we -de ned

ist of the priori y for next of kin to assume surrogacy.) Ano her op ion is for the subjec to give someonedurab e power of a o ey. This means giving decision-making au horiza ion o a person who supersedesfami y members.Remember : The "con ract for heal hcare is between the physician and hepa ien , no hepa ient's family.The surrogate s decisions must promote he patien swishes and welfare If he pa ien has expressed cer ainwishes on a opic regarding medical in er en ion in

he pas , he surroga emus use tha knowledge in hedecision-making process This is known assubs edjudgment If he surroga e has no know edge of he

patien s wishes, then the surrogate should make decisionsbased on the pa ien s we fare. Welfare considerationsinc ude su er ng, preser a ion of life, res oration of nc

ion, and quality of ife; decisions should be based on whata reasonab e person would want in simi ar circumstancesThe surroga e s author y ends when the patien dies

i.e , they are not ab e to give consent for au opsy). Organdonation decisions should be broached a the appropriate

ime wi h decision makers by organ procurementspecia is s who are separa e om prospec ive donorshealth care providers in order o avoid con ic s of in erestor a perception of con icts of interes . Hea th careproviders of prospec ive recipients shou d no be providingcare to prospective donors for similar reasons.

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ETHIC

EMERGENCY SITUATIONS

For pa ien s unab e o express heir preferences, hephysician may perform ife sustaining emergencyprocedures under he presumption tha the alte ativewould be death or severe disabi ity. All sta es avesta utes empowering ealth care professiona s o ho d

certain pa ien s with psychiatric conditions agains theirwil for medica and/or psychia ric rea men , a hough hespeci c ogistics vary om s ate to s ate.

QUALITY OF LIFE AND PA N RELIEF INPALL AT VE CARE

The quali y of ife in termina y ill pa ients in pain isconsiderab y improved by proper pain re ie Terminalpatients in pain are in a special si ua ion and heirreques s for pain meds genera y shou d be honoredThe downside of pain medications is hat hey can causeconfusion and a decreased abi ity to communicate. You

have o strike a ba ance between maximum pain reliefand minimal decrease in consciousness The assis anceof hospice workers in his situation can be very he p .

PHYSICIAN ERROR

Physicians mus disc ose o he pa ienany errors inudgmen and procedure when the informa ion is deemed

"material to the patien s well-being n genera , youalways disclose errors isc osure isnot equiva ent toadmitting neglect.

PHYSICIAN-ASSISTED SU C DE ANDEUTHANASIA

y ed de ( S)is when hephysician supplies the means of dea h o a pa ien , suchas a prescrip ion for a lethal dose of medication alongwith instruc ions on i s use for ermina ing one s own

ife.is when he physician direct y administers

a e ha dose of a medication wi h the in en ion ofcausing dea h. As of 2013, 3 s ates have legalized PAS (Oregon,Washing on, and Vermon ) and s a e has a courcase se ting precedence for defense of he prac ice(Montana) Euthanasia is il egal in al50 states.

The test guidelines by he ACP and he AMA do notsupport any form of PAS or eu hanasiaKnow ha respec ing a pa ien s choice o refuse

ife-sustaining trea ment is di eren from eitherof heseGood end of ife care entai s trea men based on manyissues For ins ance, heACP Ethics Manual says hat,when providing comfort to a dying patient, " . . thephysician may appropriately increase medication orelieve pain, even if his ac ion inadver ent y shortens

ife This is known as he princip e < f"doub e e ec .

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1 28 ETHICS

CPR AND DNR

Cardiopulmonary esuscitation (CPR) is usua y astanding o der in a hospi a ; i.e , it is o be carried outwithout speci c order, on any pa ient who su e s cardiac o espiratory ar es Theonly ime CPR is not doneis when he e is an o de stating such - a "do no resus

cita e (DNR) o "do not a emp resuscitation (DNAR)or "no code o der The decision about non esuscitationhas 3 considerations that must be assessed:

1) Whe her or no CPR wou d be ile i e , tha heresuscitation wou d be unlike y to succeed or, if it didano he cardiac o respiratory arrest would soon fo low

2 he p eferences of he pa ien3 Expec ed qua ity of life of the pa ient if resuscita ion

succeeds

I is the responsibi ity of the physician to initiate codes a us discussions wi h he pa ient (or, if the pa ien isincompe en , with fami y members or a su oga e) who

is te mina y ill or has an incurable disease wi h an estima ed50% sur iva of less han3 yea s The a endingphysician should c early w ite he "do not resuscitateo der on he order shee in the pa ient's char if hatis the nal decision a er discussion with the patien(and/o fami y, surrogate) The prog ess notes shou ddetai he facts and opinions leading to ha decision

SUICIDE A EMPTS

Suicide a empts should a ways be reated despite thewishes of he patient hese patients are o en "cryingfor he p They are also o en in a pa ho ogica men a

s a e ha may be ansi ory o treatable This si ua ionis di erent from the patient who e ses ife sus ainingtreatmen . The di erence is tha with re sa of ca e,the patients are not ki ing themse ves-rathe , they'rerefusing he p that wou d keep them a ive

CUL URAL DIFFERENCES

A patien from anothe coun y/cul ure can present someethica dilemmas If fami y membe s of you e de lypatient state a wish that their grandmother not be o dabout a te minal il ness such as cancer, you can exp ainto you pa ient hat she is very sick and ask whether

she wishes to know he diagnosis t is up to he oexpress whe he she wishes o direc he own care odesignate her fami y members o make decisions egarding her ca e. This can then be considered anau ho izeddelega ion of decision making authority If the patientsays she wan s o k ow every hing and make her owndecisions you must side with he patien

CONFIDENTIALITY AND PUBLICWELFARE

he persona and medica information hat a physicianobtains f om a patient is (ethically and lega y)con den ialBu ! n gene al, if he condition o disease

of a patient can endanger o her persons, he physician islegally and ethic lly obl ga ed o repor the si uation o

he appropriate pa ties.

Many speci cs a e st aigh forward and are addressedwi h ega s a utes Common examples are sexual y ransmi ed diseases and condi ions ha could

a ect he ope ator of a mo or vehic e e.g , seizuresand seve e cardiac a hythmias O hers a e more dicu t A patient with a serious, highly infectious disease(e g., TB, meningococcemia) shou d not be a owed oinfec o he s. These patien s can be he d agains theirwill if thei behavior is considered a th ea o othe sSome infectious diseases may necessi ate info mingthe patien 's emp oyer (e g , heal h ca e worker foodwo ker).

Adolescents are a owed to consent for some serviceswi hou pa en al invo vemen in some s a es Know the

aws of you own s a e in his regard Ado escent consen fo con aception is p o ec ed unde fede a lawby language in he federal budge tha es icts individua states om passing een contraceptive aws, ifthat s a e eceives fede al subsidies for hea h care So,ado escent consent for bir h cont o is acceptable ina s a es Consen for abo tion services howeve , isstate dependent.

BRAIN DEATH

Physicians may s op treatmen if a person is "brain dead(loss of enti e brain function, including b ain stem). AnEEG is no requi ed for diagnosis Organs can hen bedona ed wi hou patien 's pr or consent if he nex of kin(o su oga e) gives permission, knowing hat the pa ienwou d wan ha .

PHYSICIAN-PHYSICIAN vs .PUBLIC E FARE OBLIGATIONS

The physician should no al ow y incompe ent orune hical conduc by othe physicians If you ow ofsuch conduc he evidence should be p esented to theapp op iate authori y This may be he division chief orethics committee of the hospita . Mos s ate and anycoun y medica societies now have con dentia treatmen of impaired physicians Physicians who stronglysuspec ano he physician is chemica y impai ed a eob iga ed o urge he physician o seek a en . Ifthis impairment may a ec medical competence, heob iga ion is to repo the "credible evidence to the

oca medica socie ote A physician canno ac on yon hearsay, bu must have credible evidence befo ereporting it.

DRUG RESEARCH

is une hical to use socioeconomic di erences in choosing pa ients for a drug s udy unless he socioeconomics a us is conside ed a variab e Fo examp e, you cannote hical y test a d ug only on hose who can pay for it

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u• You see a colleague drink ng shots in a bar

s ortly befo e is 12-hou s i t n t e eme gencydepa tment. Are you ob ga ed o in ormanyone?

• Know a l o he scenarios n e ethics op c!

Conversely, you cannot e hica ly o e a f ee drug foesea ch only o hose in a lowe socioeconomic status.

F NANC AL CONFL CTSThe ACP e h cs documen is ve y c ea ha ce tain

nancia re at onsh ps areunethical:Physic ansmust d sclose o pa ients f hey intend to

efe pat ents o a faci ty o esea ch study in whichhe physician has a nanc al s ake

A physic an shou d no refe pa ien s o a care facil ywhe e he physician ho ds a nancia in erest bu snot emp oyed.A physician may no pay ano he physic an fo

efe alsA phys c an may no rece ve payment o gi s(even "sma ones ) f om dev ce manufac u e s opha maceut cal compan es fo ecommending orusing hei p oduc s.Physic ans should no se p oducts ou of heio ces, unless hey a e mee ng an unme need of

he communi y (e g , selling c tches or wa ke s in asmall town) Phys cians should not sell supplemen sor cosme ics ou of he o cesPhys cians should not use unsubstan ated or falses a emen s in adve ising no shou d hey ominecessa y info ma ionPhysicians can and should ac as expe witnesses obene socie y, bu hey canno accep payment inexchange fo biased estimony Fees cha ged shou dbe fo easonable ime and expenses

SCENAR OS

Some scena iosI A pa ien ente s the hospi a unconscious and nea dea h

with a e m nal d sease What should he physician do if:The pat ent has a prope y execu ed liv ng will has ates no in ubation, CPR, etc.The pa ien has no liv ng wil , bu family memberssay hey s rong y p efe he pa en be a lowed odie with dign ty and w thou he oicsThe pa ien has a p ope ly execu ed iving will hatsta es no n uba on, CPR, e c ,bu family members(many of whom are awye s) say they want all possible heroic measu es o be done-and h ea en

d re consequences if he r wishes a e no fol owed!

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ETHICS

) A pa ien comes o he eme gency depa tmen wi h anex ensive acu e MI, is men ally compe ent, and refuses

o be adm ted despi e be ng fully informed of hepossible consequences Wha do you do?

3 A espi a o dependent pa ient eques s n writ ng o beex uba ed. Wha do you do?

4) A female health care worker who is found to have hepatis B an igen posit vi y eques s ha you not ell he

supe viso at the hospital whe e she wo ks.5 A man is diagnosed wi h inope able metas a c cance

He s a es o h s physician hat he does no wan hisw fe o know.

6) A newly ma ied man just nds ou ha he has a se iousautosomal dom nan gene c d sease; e g , Huntingtond sease. He equests hat he phys c an no te l his wife

7 A man nds out he s HIV pos tive and eques s hayou not ell his spouse

8 A woman with suspec ed meningococcal meningi isefuses o be adm t ed and wan s o go back to wo k

Answe s:I The phys cian shou d

Follow ins ructions in he liv ng wil .In this si ua ion he phys cian needs moreinforma ion; needs o know he w shes of thepatien , no the family!Fo low ins uct ons n he ving w ll; the cont acis be ween he physician and the pa ient. Bes des,so far, all ving wi s have uphe d in cour .

2) You mus show ca ing fo he pa ien 's s ua ion, yeta emp to dissuade he patien from eaving f the

pa ent s ill eaves, i is pruden o have he pa ient signout "AMA agains medica adv ce (the pat en is notega ly equi ed o do his) You canno s op patients om

leaving unless you hink hey a e men a y incompe eno a dange o o hers (e.g , they want to drive home)

3 You need more nfo mation (men al y competen ,fully info med, etc.). This is a problem wi h p obablefa eaching consequences-not jus fo you, bu fo hepa ient's other docto s, he hospi a , and the pa ient'sfamily The '1 s ep is o con act he hospi al's e hicscommit ee. You may also need assistance om hepa ient's o he docto s, family, psychia ry, and socialservices

4 Th s hea th ca e wo ke has a di ect ob ga ion no ocause ha m to the pat en s wi h whom she n e ac sIf she efuses o inform he hospi al nfection con ol

eam, hen you a e ob ga ed to do soAlthough the physic an can s ong y encou age he manof h s wife's mo a r ght to know the si uation, commun ca ing h s to the spouse is u ma ely he pa ient'sob iga ion and no the physician's.

6) In this case, he physician should s st ong y encouage he man o ell h s wife If hat fai s, he as esoris fo he physic an o ell he w fe because of he iskof harm o u e child en

7 In all V cases, he physician must make su e haanybody a sk (e g , h ough sexual con act odrugs)

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10 PREOPERAT VE CARD AC EVALUAT ON

is not ed. Whenever pat ents say they are go ng to dothe noti cat on, the phys c an must ensure it s doneUsua y, this obligat on is taken care of by the statehealth depa tment.

8) Th s pat ent may be he d aga nst her w or the goodo publ c we are.

PREOPERAT VE CARD AC EVALUAT ON

You must k ow how to preoperatively evaluate a pat entn order to determine the r sks o hav ng a cardiac event

in the per operative per od!

Several guidel nes have been produced by di erentmedica societies As of this wr ting, the AHNACCGu de nes for Per operative Card ovascular Eva uat onfor oncardiac Surge y is the most recent document,w th a focused update n 2009 regarding the use ofperioperat ve beta-b ockers to min mize intraoperativecard ac sk

These gu de nes recommend5 steps to be ollowed:Step 1: Does the pat ent need emergency noncardiacsurgery? If so, then the patient should proceed tosurge y; perioperative su veillance and postoperat ver sk strat cation and r sk-factor management shou dproceed as best as poss ble

f the answer is no, this snot emergent , proceed toStep 2.

Step Does the pat ent have anactive cardiac cond tion?•

Unstab e coronary syndrome(unstable or severeang na or recent M , de ned as more than 7 days but: I month)Decompensated hear fa ure

• S gni cant ar hythmias3'ddegree AV block,Mob tz 2 AV block, symptomat c ventricu ararrhy hm as, supraventricu ar arrhythmias(inc udesatrial b ) w th uncontrolled ventr cular rate

(> 00 bpm at rest), symptomatic bradycard a, newventricu ar tachycardia

• Severe va vular disease any symptomatic aort cstenosis asymptomatic aor c stenos s w th gradient > 40 mmHg, symptomat c m tral stenosis

I so, then the patient shou d undergo evaluat on andtreatment be ore noncard ac surge y.

f these are not present, proceed to Step3.Step 3 Is the pat ent undergoing low r sk surgery?Here, the guideline gets murky. It is de nite w th de n

ng ve y ow r sk as super cial, and the highest risk asmajor vascular procedures It sts endovascular abdominal ao ic aneu ysm repa r and carot d enda erectomy asintermed aterisk. A er l sting these speci ca ly, t goeson to state "The phys c an must exercise judgment toco rectly assess perioperat ve surgical risks and the needfor rther eva uat on. Wow, thanks guidel ne . In

general, though, any procedure that is "ambulato y innature and does not require "hospital adm ss on is usual y considered ow risk Other surgeries n th s category

nclude all breast s rgeries, ophthalmo ogic procedures,and endoscop c p ocedures.

So, you get to Step3 and the surge y s ow-risk,proceed w th surge y; if not, go to Step 4

Step 4 Does the patient have good nctional capacityithout symptoms If th s is t ue, proceed with

moderate to-high r sk surge y

What is a simp e, easy method to assess functionalcapac y? The gu deline recommends using a METlevel o 2 4. ow et's rev ew that "MET th ng aga n.Remember that nctional capac ty can be expressedas metabol c equiva ents (M Ts); I MET is the restingor basa oxygen consumption of a 70 kg, 40 year-oldman in a rest ng state. Funct onal capac s class edas exce ent(> 10 ETs), good (7 10 METs), moderate

(4 7 METs), poor (< 4 METs), or un own. Think o4 METs as equivalent to car y ng groceries upthe stairs.

xamp es assoc ated w th< 4 METs nclude slowballroom dancing, go ng w th a ca , and walk ng ata speed of 2 3 mph Activ ties that require > 4 METsinclude moderate cycling, c mbing hi s, skiing, singlestennis, and ogging There are several sca es (e.g., DukeAct v ty Status Index, Speci c Act v ty Scale) out there,but, n genera , this g de he ps you.

So if the pat ent can un up a hi or mow the awn w thout p ob ems then the pat ent l ke y can proceed withtheir p anned surge y. If they cannot, then we go to Step5.Step 5 Here, we have the patient who has gotten to Step5 because o e ther poor or unknown unctional capac ty,and we must use clin ca risk actors to help us dete m neif we can proceed with surge y.

The 5 c n cal r sk actors to ask aboutI H sto y of ischem c hea t d sease (h sto y o MI,

+ exerc se stress test, cu ent chest pa n, n trate use,ECG w th patho og c Qs)

2) Hea t fa ure history(pr or or compensated)3) Cerebrovascular disease histo y4) Diabetes requir ng insul n5 Rena nsu ciency(creat nine > 2 mg/dL)

If > 3 r sk factors are present, the surge y-speci crisk s impor ant ( able I 0 ) The guide nes say or" .. intermed ate r sk surgery, there are nsu cient datato dete mine the best strategy (proceed ng with p annedsurge y with t ght hear rate contro w th beta b ockadeor her card ovascu ar testing if t w changemanagement)

Bottom ne Ao ic, ma or vascular surge y orper pheral vasc ar surgery general y requ res thercard ac evaluat on. Low-risk procedures (endoscop c,supe cia , cataracts, breast surge y, o any ambu atorysurge y) do not. Intermediate .. t's up to your udgment.

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Q� uiKnow the 5 step process used in dete mining a patient equ res a p e-op cardiac evaluation.

W at type of p eoperative evaluat on is done i apatient requi es eme gent noncard ac su ge y?

Which patients a e sta ed on beta-blockersbefore su gery?

• Know t e preoperat ve sc eening abs and w ogets t em.

Scenarios you are l kely to encounter:

A low isk patient who can p oceed d rectly tosurgery of any ype without non nvasive test ngA moderate-risk patient w th good nct onal capac tywho can go directly to a non vascular surgeryA major r sk pat ent who needs u the workup asde ned n the charts prior to go ng to surge y

Beta blocke s: Know thath gh dose beta blockersusedper operat vely g ven w thout a h story of dose t t at onin beta blocker naive pat ents do educe pr ma ycard ac events but car y an inc eased r sk o mortaliand stroke hence they arenot ecommended.

Who gets beta blockers?

Vascular surgery pat ents w thpos tive preoperat vest esstestsCont nue these in pat entsalready receiv ngthemfor ang na arrhy hm as, or H NBeta blockers should be titrated when used n ordeto avo d sign cant bradycard a or hypotensionThe r use s not without r sk

PRE OP SCREENING LABS

Gene al gu del nes follow and are based on an amalgamof var ous soc et es' recommendat ons!

Hematocr t

> 65 years o age fo ma or surgeryAll su ger es that would/could result in majoblood loss

Table -9 : R s of Procedure ; AHA/ACC

Low Risk

Interm iateRis

M or Ris

© 2014 MedStudy

Endoscopies local biopsies breastbiopsies vasec omy, ca arac surgery

Surgeries: caro id end r erec omy:·intr peritone l ·i rathoracic, or hopedicprost te head nd nec

·

Surgeries aor ic and m jor vascu rc rdio hor cic, emergen major surgerylong procedures wi arge blood lossand or uid s if s

PREOPERA E CARD AC E ALUA ON

Not for mino su gery!CBC is not recommended unless cheaper thanhematocrit alone

Electrolytes: Not recommended unless h sto y suggestseason to check

C eat nine:

> 50 years of ageMajor su ge yHypotens on s likelyNeph otox c drugs to be used

Glucose l ve nction tests P /P U/A:notecommended unless clin cal signs/symptoms wa rant

ECG:

Yes for all vascular proceduresonvascula p ocedu es:

en> 45 years

Women > 55 yea so Known ca diac d sease

Cl n cal evaluat on suggests poss blecard ac diseaseD uret c use (electrolyte abno mal y possible)D hypertens on renal nsu c encyMa or su gical p ocedu e

CXR

> 50 yea s of age for ma or su gerySuspected ca d ac or pulmona y disease

F s:

Not recommended o healthy pat ents prior toany surgeryUse o dyspnea that is unexpla ned

Stents and such hold o on elect ve noncard acsurgery f:

W th n4 6 weeks of bare metal stent placementW th n12 months of drug-elut ng stent f pat entmust stop thienopy dine/aspir nWith n4 weeks o balloon ang oplas y

PER OPERATIVE MED C NEMANAGEMENT

Anticoagulant:

M nor su ge y ont nuea or su ge y:

o Stop IV hepa in6 hours before surgery.o Stop L W 2- 24 hours before su gery

Stop wa fa n3 5 days before su gery. (Use ahepar n bridge for those who need it )

Antiplatelet:

Aspi n ASA) ont nue for m nor surgery or in

those w th recent(6 months) I PC stroke; formajor surgery stop 5 0 days be o e su ge y

10-3



1( 2 PREVENT VE MED C NE

Clopidogre - stop 3 7 days before surgery.NSA Ds and COX 2 s op 1 3 days before surgery

Cardiovascula : Continue � b ocke s, calcium channeb ockers nit a es, ACE s, ARBs, and statins Diure icsand cho estyramine are usua y he dEst ogen Discontinue ho mone rep acement seve alweeks before su ge y (or continue oral cont acep ivesand inc ease eve of DVT p ophy axis).Diabe es agents

O al hypog ycemics stop 2 72 hou s befo esurge y depending upon ha f ife of d ug and riskof hypog ycemiaInte mediate ac ing insulin give / o /3 of usuaa.m dose.Basal insulin on inue o reduce dose.

Psychia ic medsMAO s op 0 14 days befo e su ge y.SSR s onside withho ding 3 weeksbefo e neurosu ge yAntipsycho ics con inueTricyc ic antidepressan s and i hium on inue,but some taper and discontinue seve al daysbefo e su gery.

eu ologicAnticonvu san s continue.An ipa kinsonian continue but somediscontinue the night befo e su ge y.Alzheime d gs iscon inue.

PREVENTIVE MEDI INE

PATIENT EDU ATIONow this en i e opic Conside all of Patien duca ion

highligh edThe most au ho i a ive single sou ce for p eventivemedicine in the United States is the U.S. Preven iveSer ices Task Fo ce ([ S ST ];http://www.uspreventiveservices askfo ce.o g/).Because pa ient education imp oves ou comes,periodica y reviewand counse pa ients on thefo owing

Tobaccoi ea ms

A cohol/Substance abusePhysical activity eveObesity

Check he e de y fo functional status gaitabno malities and for os eopo osis risk factors.Guide a pa ients abou self examination for skindisease gum disease STDs, and nutri ion.

Recommend sea be ts and good uid in ake.Go a hat?Teaching women to pe fo m ab east se f examdoesnot reduce thei morta i y om breast cancer so mosto gani a ions a eno onge recommendingi and someare ecommendingagainst i

Along simi a lines, the USPSTF now recommendsagains es icu ar se f examina ion fo ea y detectionof tes icu a cance because it is un ike y to changeoutcomes.Firearm rela ed inju y and dea h is amajo pub ic healthprob em. The physician's ethical ro e is o counsepatients abou earm safe y and to become invo vedin community e orts to p event earm in u ies Somestates have passed speci c laws p ohibiting physiciansf om inquiring about ownership of a earm

Smoking CessationTobacco smoke is esponsib e fo 90% of all lung cancedeaths and mo e hanI0% of ca diovascula dea hsThe SPSTF 200 recommendation sugges s using a"5 framework:

sk abou tobacco use.dvise to qui through clea pe sona ized messagesssess willingness to quit.ssis to qui

ange fo low up and suppo t

Know hat cessation of smoking canexacerbate

ulcerative coli is. stline medications fo smoking cessation:Bupropion SR

• icotine ep acement p oducts (gum, inhaler,o enges nasa spray, pa ch)

Yarenic ine (Chantix®)

Counse ing+ meds better than counseling alone.D ug the apy for smoking cessation is gene ally safe.Nicotine eplacement products do not inc ease cardiovascu ar isk even fo those who smoke while wea ingthe nico ine pa ch. Bup opion should be avoided in

patien s wi h sei ure diso de .Varenic ine is a par ia agonis of nico inic ace y cho ine

ecep ors. Both bupropion and va enic ine have beenassociated with serious neuropsychia r c side e ec s(behavior changes suicida ideation and behavio , anddep essed mood) n 008, the FDA issued a wa ing oclose y monito patients aking these dr gs fo mood orbehavio a changes.

ote tha ciga smoking inc eases the risk of corona yheart disease (relative risk= 1.27), COPD ( .45) andcancers of he mouth and throa (2.0 )

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http://www.uspreven-/



http://www.uspreven-/



UI

What patien educa ion top cs should you rev ewa d cou se pat e ts about per od ca ly?

Memor ze Tab e 0- 0!

Othe D sease sks The follow ng increase risk of d sease:

H gh ntake ofed meat nc eases isk of colorectalcance .Alcoho increases sk of co on, breas , esophagea ,and oropha yngeal cance s.Obes tyis assoc a ed w th ncreased sk of colon,b eas , endome ial, k dney and esophageal cance s and may increase r sk for p osta e, ovary andcer ix, ver and gall b adder, and pancrea c cancers,mye oma, and lymphoma! (Is here any h ng le ?)Bladde cancer s inve sely associa ed w th uidintake Inc dence n the high d intake g oup shalf that of those n thelow- d n akeg o p.Agen s ha ca se o increase he sk of cancerHPV ,HBV , HCV , HIV , EBV , andH pylori.

The following decrease r sk of d seaseHigh in ake of omatoesdecreases prostatecancer risk.F be educes heart d sease and d abe es. Not sureabo cancer, hough

Vi am n Dmay decrease co o ectal and prostatecance isk

Note ha supplemen a v tam ns and minera s donotdec ease cancer risk n pat en s wi hadeq atediets.Ce a n dr gs a e sed todecrease cance isks n spec apa ient popu ations:

Tamox fen and raloxifene dec ease breas canceNSAIDs and aspirin dec ease co on po yps andco on canceDutasteride and naste de decrease p os a e canceAspir n decreases sk of some co orec a cance s.

SCREENING EXMSOve v ewScreen ng pro ocols ab e I p ov des a oughs mmaryEvery o cia enti y de ai ing screening pro oco s has adi erent (b t usua y sim lar) s ggested p otocol fo eachdisease In the follow ng, hese abb eviations a e used

• ACP =Ame ican College of PhysiciansACS =Amer can Cance Soc etyNCI Na iona Cance Ins i e

USPSTF U.S. P even ve Ser ces Task Force

© 2014 MedStudy

PREVENT VE D C N

abl : Screen ng Exam Recommenda ions

Counseling aboutsmok ng

Counseling, other

Blood pressure

Cholesterol

Breast exams

Mammograms

D gital rec al exam

FOBT

Colonoscopy

Pap smear

PSA

Each visit

Init al visit and thenperiodically*

Each visit; at least every 2 years

Every 5 years is appropriate

Controvers al*

Yearly a er age 50*

Yearly a er age 50*

Yearly a er age 50 (notneeded a er colonoscopy)

See Gastroenterology Book 1

Every 3 years*

Inconclusive*

*See text:or more information

a d vascu a D seaseBloo r ss r an hol s rol

B ood p essure (BP): eve y 2 yea s andevery cl n calencoun e .Choles e ol: Screen men 35 65 years o d and women45 65 years o d every 5 ye rs. f he pa ient is placed on

ipid-lowering agents, then gene al y hey a e checked

eve y6

months o a year he ea er. If he sc een ng otalcho estero is nea the h esho d, it sho d be repeatedperiodica ly For treatment, see Endocrinology, Book 4 The Endocrino ogy sec ion a so disc sses herecommendat ons fo ip d screen ng con a ned n helatest document om the Na ional Cho estero EducationPane CEP), ent ed Ad l Trea men Pane III (w h

he relevant upda e om 2004). NCEP is an advisoryoup formed o of he Na iona Hea Lung and B ood

Insti ute (NH BI), which s a subset of NIH (as is NCI). The ATP I (and pdate) sc een ng recommenda onsvary s gh y om the ones is ed above b not by much The same s uation s tr e for BP recommendationscon ained n he la es doc men om he Jo n Na ionaCommit ee on P even ion, De ec on, Eval ation, and Treatmen of H gh B ood Press re (JNC, 2003)a so an NH BI adv so y g oup. We discuss JNC7 m

Neph o ogy, Book 2. Aga n, sl gh d e ences.

ar iovasc lar is as in Wom n

In 2008, the Amer can Co lege of Card o ogy w ote ag del ne spec cal y looking a ca d o ogy ss es in allwomen The main i ems o know

Hormone herapy shou dnot be sed as prima y o

seconda y p event on of ca d ac disease.

10-33



10 PREVENTIVE MEDIC NE

• Antiox dants shouldno be used as primary orsecondary prevent on of cardiac disease.

• olic ac d shou dno be used for prevention ofcardiac disease.Asp r n inhealthy women < 65 years o age snorecommended to prevent M (b is recommended for2 65 years to prevent stroke)

E R k

or pat en s who do not cu en y have ea disease buhave a east 2 r sk actors for hear disease (per NCEPATP cri eria - see Endocr no ogy, Book 4) know a5 year, I0 year, or i et me r sk or hea t disease can beest ma ed us ng one of he many esta ished r sk pred c ormodels (e g Framing am Risk Assessmen ). he resugives you good ins gh in o how aggressive yo needto be abo t red c ng their cardiovascu ar isk ac ors

Diabetes

The Amer can D a etes Association (ADA) recommendsannua screening w th a veno s as ing plasma g cose(no a ngers ick!) or peop e> 45 years of age i heyhave no sk actors Sta t earlier i they ave risk fac orss c as obes y and/or a am y history Hemoglob n AIC

s also accep ab e for screen ng

Retes n 3 years if norma

T e Ame ican Association o C nica ndocrino ogistsreco ends star ing screening at age 30 if any riskfac ors are present

Abdominal Aortic Aneu ysmOne imescreening or abdomina aor c ane rysms(AAAs) is recommended in men 65 75 years ofage they have a histo y o smoking (A /AHAand USPST ) or in men > 60 they had a s ling orparent wi AAA (A C/ AHA) Repea screen ng is norecommended No organiza ion recommends screeningm women

Breast Cancer

Breast cancer screening sing breast self exams c nica

breast exams, and mammography s now somewhatcon rovers al We d sc ss the op c in Onco ogy, Book 4

Prostate Cancer

Prostate speci c antigen (PSA) esting has con ributedo t e increased nding and reatment of early prostate

cancer A ho gh no trials have been concl ded ndcating s e ect veness as a screening test, consumerdemand has made a common y performed a test

The American ro ogical Association and ACSrecommend PSA and dig ta recta exam year y for men> 50 years o d

The A P recommends that ann a PSA bedisc ssed witmen etween the ages of 50 and 69 to determ ne heywan it based on bene s and harmsNo SA screening

s recommended for men> 0 years or hose wit a eexpectancy < I0 15 years In genera d scuss screeningat age 40 wit African Americans and n pat en s with afamily his ory of early pros a e cancer hedigital rectaexam, previo s y com ned w ser m PSA screen ng,

sno longer recommended by the A P

To add to the con sion, the 2012 SPST guide inesrecommend against PSA screen ng a oge her

A arge S s udy s owed no mor a y bene w hPSA screen ng. Add iona ly alse positive SA tests(80% ) result in more est ng and nega ve psyc o ogica e ects which have also een considered in t eserecommendat ons.

Co orecta Cance

This s discussed in depth n Gastroentero ogy Book 1

Ce vica Cancer

Pap smears have been proven e ective, but t erecommended in erva s bet een ese tests vary Mostrecommend star ng a age 2 . A er 3 nega ve res sw h ann a exams, con in e every 3 years unt 65 yearsold Women 30 65 years o age may opt or comb nedPap/HPV test ng every 5 years instead of ap a oneevery 3 years

previous Pap smears have een negative and hepa ent does not ave new sex a partners, pa ents> 65 years o d do no need r her smears. Youdo no need o ge a ap on women who have hadhys erectom es for en gn disease See Onco ogy Book 4for work p of a normal Pap smears

HPV esting is recommended f he Pap smear cyto ogyret s w t atypica squamous ce s o ndete minedsign cance (ASC S). sual y, t e HPV est is co lec edwi e Pap smear but i s saved un l cy ology resu tsare ava lab e AS S s d scovered, then he lab isinstructed to perform the HPV test ( ermed "re ex tesing ) Women wit AS S and he h gh risk H V ypes(e g 16 18 31) then go to co poscopy ( nstead of send

ng everyone w h AS US to co poscopy; cu s down onnnecessary proced res) O er abnormal ties on Papsmear a mos a ways go to co poscopy

Lung Cancer

About 85% o ng cancers are he res t o smok ngT e s at s o ng cancer screening is evo v ng basedLarge y on t e resul s of t e at ona ng Screen ng Tr al(N ST). The N ST randomi ed over 50,000 c rren and

o mer smokers age 55 4 to 3 ann a low dose T scans( D T) vs 3 annual chest x rays The study was ha tedear y at 6 5 years d e to a 20% reduct on in ung cancer

mor a i y in t e gro p screened w t DCT.

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• Should yo do PSA screening in a75-yea -o d man?

When s o d ap smea s be initia ed?

In July 2013, the USPSTF issued a dra recommendationn favo of low dose CT scan screen ng(G ade B) of

individua s who mee al of he fo lowing cr teria:

Men o women age 55 79Cur ent smoke s o have qu with n the pas 15 years

30 pack yea s of smoking his ory

Fa se-pos ive ates a e h gh n he Na iona LungSc eening T ia 24% of sc een ng CTs we e pos t ve andover 96% we e false pos t ves. Conce s abou he new

ung cance screening p oposal cen e around he po en ia

of overdiagnosis excess adia ion exposure and cosHoweve the evidence would sugges hatlung cancedeath s ave ed for every 450 500 scans done

Tobacco avo dance and cessat on con nue o be mpo ants eps n dec eas ng the bu den of disease. I s essentia haa smokers are adv sed n his ega d.

Vaccinations

Common adult vacc na ons a e d scussed n Infec ousDisease Book .

M G D R ISSU S

U T BL IZ T

Overv ew

The Accountab e Care O gan za ion (ACO) wasnt oduced in 2009 as a po en al new model of ca e fo

wh ch he Cen e s fo Medica e and Med ca d Studies(CMS) is encourag ng demonst a on p ojects I is ahea th ca e delivery and e mbu sement mode ha es

he eimbu sement to the qua y of heal h ca e de veredand he tota cos of care

Examp e 4 reg onal hosp a s combine he outpa ienserv ces to bette se ve he ocal popu ation. P imaryca e phys c ans and spec a s s f om each of he 4 hosptals pa cipate The costs of he se v ces a e bundled omee p ede e m ned budgets wh ch inc ude incen ivesto meet speci c pe mance imp ovement objectives

ACO "Never Even s

These a e events ha occur (in he npa ent se ngusual y) ha yp cal y shou d no occu f he pa ien

s receiving competent hea th care These events

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ANAGED CARE UE

commonly ca led "never even s a eno eimbu sedby C S

Fore gn ob ec retained a e su ge yA embo ismB ood ncompat bi yP essu e u ce stages II and IV

Fa s and auma (including f ac ure bu e ec icshock)Catheter-associa ed UTI or vascular-catheter nfectionManifes a ons of poo g ycemic con o (DKhype osmo a hypog ycemia)Su g cal s te nfect on nc uding med as in sfo ow ng CABGInfection, DVT/PE fo owing hip or knee ep acementDea h/D sabili y due o medication e o e ec ricshock burn fall use of es ain s or bed ai s ocon am nated d ugs ncu ed w thin a heal hca efac i y

nc den due o w ong oxygen o o her gasmpersonat ng a health care wo ker physic ano nurse!)Abduc on of patienSexua assau w th n o on fac y groundsSu ge y on w ong body pa o pat entImp antation of w ong eggInfan d scharged o w ong pe sonDeath/D sab lity due o pa ien e opementPa ent su c de or a empted su cide esu ng

n d sabil y

P S GS

W

Deaths from d ug ove dose have been stead yising ove he past 2 decades, w h aI 02% nc ease

f om 999 to 20 0! In 200 dr g overdose was thelead ng cause of "in u y death. In the age ange of25 to 64 years dea hs om ove dose exceeded hosecaused by moto veh cle acc den s! Abou 80% of fataloverdoses were unin ent ona and presc ip on drugsaccoun ed fo he majo ity of deaths!Opio dswe e hemost common dr gs nvolved o en found in comb nat onw h benzod a epinesMo e nformat on ega d ng d g ove doses n he Scan be found a he fo lowing s eh tp //www cdc gov/ homeand ec eat onalsafety/overdose/fac s html

Fi s we discuss an empiric app oach to overdoses;hen we focus on indiv dua ingestions. Inges ons

w h HAGMA (h gh-an on gap metabolic acidosis)and inc eased osmo a gaps a e covered exhaus ive yin Neph o ogy Book 2 CO po son ng is discussed nPu monary Medicine Book 2.

10-35

http://www.cdc.gov/

http://www.cdc.gov/



1 PO SON NGS

Tab e : hystcal Exam in Toxic nges ons

Physical Exam

"Excited : agitation,rest essness,hypertension,tachycardia,hyperventi ationhyperthermia, mydriasis(usua y)

Depressed : obt datio , ypote sion bradycardia hypove tilatio ,hypothermia miosis(usua ly)

Categor

Anticho i ergics

Sympathomimetics

Ha ucinogens

C olinergics

Sympatho ytics

Opiates

OV RDOS MANAG M N

Examples

Antihistami esNeuro eptiqs (ch orpromazine uetiapi e)Tr cyclic antidepressa ts i

Atropi eAntispasmodics (hyoscyamine)

• P ants nightshade (be ado na) a djimso weed

Ep ed neDextro et orphan (5-1 x t erapeutic dose)Cocai eA pheta i es

• Metha phetamine• MDMA ("ecstasy )

4 bromo 2 5 dimethoxyp e et ylamine ("2CB )2,5 dimethoxy ( ) propylt iop enet y amine ("blue mystic )

"

Lysergic acid diethy amide (LSD)Mesca i e (peyote)

• Phencyclidi e (PCP, ange d st )Psi ocybin (fo nd in certain mushrooms)

Orga ophosp ate and carbamate insecticides

C onidine

Oxycodone ( e ent y combined ith aceta i op en; asexte ded release fo ations E H Oxydose™, OxyContin®Oxy R® Roxicodo e®, Percocet®)

• Hydrocodone ( e ent y combined ith acetami op e ; hasextended re ease fo mu atio s; Lorcet®, Lo tab® Vicodi ®Zydone®, Co Gesic®, Hycet® Ma gesic®)

General ma agement of he ob unded or coma osepatie t is guided by h s o y, vi al s gns, and physicaexam. Assessment of airway s most impo ta , w h

mmed ate nt ba ion of the pat ent w th unstable vitasigns and/or inabil ty to p o ec he airway. Next, assess

hy hm wi h an ECG and con inuo s card ac moni o i gand assess blood oxyge a ion wi h pu se oximetry.

wi h "exci a io or dep ession a d know whichnges o s are assoc ated w th he presen ed scena ios( able I - ).

I cl ica p ac ice, many pa e s p ese w hco ges ons, a d the phys cal exam can be a m xed bagof signs symp oms.

p myd ias s= d lated pup s (big wo d, big pupi s);m os s= cons ic ed pup ls (sma word, small p p ls).

The fo ow ng nte ent ons a e usually empi ca ype fo med, except as no ed:

I 05 f b ood glucose low.Thiam ne mg IM o IV

• ABG +/- ca boxyhemog ob n leve , se m bas cchemistry, and general ox co ogy sc ee . Be sure oca cu a e he se m an on a d osmola gaps. Measu esal cy ate level f AG s i creasedSer m ace aminophe eve .

• Ser m CPK, f pa ien was immobil zed fo lo gper ods.

• CXR and supp emental oxygen p .Na oxo e f yo suspect op ate overdose, butbe care of dose (see Analges cs, nex page).

Be ab e o characterize the pa ien 's physica exam anddeterm ne whether he presen a ion is mos consis en

A e he pat en s stabi ized, cons dergas ic avagew th a la ge bo e o ogast ic tube this may be e ec veeven ho rs a e nges io f he dr g was ASA, ancho ine g cs, or narco ics. (These dr gs cause dec eased

gast ic moti i y.) Lavage wi h on y small amoun s oftap water (I cc) o p event fo cing he s omach coten s o he duode um. Fo ow w th activated cha coaland a catha ic (so b to o Mg c t ate). Know tha ac ivated cha coal snot e ec ve when the ove dose swi h heme a s ithi m and iron Con in ed dos gwi h o a cha coa is e ect ve in decreasing the evelsof a few dr gs byg dia ysis(abso t on via the ente icrec culation) espec al y d goxin, phenobarb a ,theophylline, tr cyc ics, and sal cy ates.Note There s a st ong re d towa do avagingpa ents wi h mos ove doses. The hough s hat lavage

s, n most cases, ne ec ive usi g activated charcoawi h cathart cs is a east as e ec ive, if no mo e so.

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• Wha ar h proc r s an s s ha osho l consi r for g n ral manag m n of anob n pa i n ?

• Ac va charcoa s no s for whaov r os s?

Shock is treated wit centra venous pressure (CVP)monitoring IV uids +/ dopamine.

A ka inization and acid cation of t e serum (andence t e ur ne) are based on t e pr nciple t at com

pounds n t eir ion zed form are ess t ssue-permeab eand more easi y e im natedby the kidneys. Weaklyacidic substances onize in an a kal ne environmentwhile weak y a kal ne substances on e in an acid cenv ronment. A ka in zat on of t e ur ne to a pH of> 7increases excret on o ASA tricyc cs and p enobarbta . Acid cat on of the urine wit ammonium chloride

ncreases excretion of amp etam ne and p encyc dine(PCP). Mix 2.75 mEq/kg in 60 cc NS and g ve througthe gastr c tube. Clamp for hour. Repeat q 6 ours unt lur ne pH< 5.0.

mpo tant Hemodia ysis may be necessa y in patientsw t severe overdose or renal fai ure. t is e ect ve nremoving drugs wit ow mo ecular we g tst at arenot ipid so uble protein bound or tissue bound i.e.drugs w t a sma l vo ume of distribut on. T ese inc ude

it ium chloral hydrate sa icy ates and a coho s (met

ano and ethy ene glyco ). D alys s is not e ect ve nremoving benzod a ep nes op ates or t cycl cs.

Also mpor ant C arcoa emoper sion (b oodpumped throug a charcoa ter) n contrast to dialysis removes drugs t at are ipid so ub e and proteinbound! t can also remove some o the same drugsas dialysis. A so like dia ysis it is most e ective nremov ng drugs wit alow vo ume of distribution (V).C arcoa emoperfus on s especial y good for d goxintheophyll ne and sa icylate overdoses.

SPECIFIC TOXINS

Refer to Tab e 0-11. A so see Tab e 0- 2 for asumma y of common poisoning agents and t e rusual antidotes.

An lg icOpiates

Op o d prescr ptions increased 700% rom t e years 997to 2007. Opioid overdoses ave l kewise dramatica y

ncreased. Of t e 22 000 deaths from prescription d ugsin 20 0, 75% nvo ved opio d ana gesics

Th nk opiate overdose (especia y on an exam) w enyou see t e fol ow ngcomb nation of s gns/symptoms:

obtundation ypoventi at on (decreased rate and t dal

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Table - : Tox s an An o s

oxin Antidote(s)

Acetaminophen N-acety cysteine

Digox n Ag bind ng agment

Opiates Naloxone

Benzod azep nes Flumazeni some scenarios)

N trates Methy ene b ue

Iron Deferoxamine

Carbon monox de Oxygen

Ethy ene glyco omep zo e

Methanol omepi o e

Organophosphates Atropine, Pralidoxime(2 PAM)

Cyanide Nitrates, Na thiosu ate

vo ume) decreased bowel sounds andconstricted pupi s.K ow that meperid ne propoxyphene and tramado areassociated wit seizures in intoxicated patients (especia ly t ose on dia ys s ); and methadone can increase theQT nterval caus ngtorsades.Naloxone is usua ly given V in doses o 2 mg up to amaximum of I0 mg. T e drug s ould be used toreverse

ypovent lat oninduced by opiates t shou d not beused in large doses as a d agnost c tool for op ate ntoxication because of t e risk o nducing w thdrawal in thec onic user T e dose of naloxone s ould be titrated

to resu t in normal vent lation ( 14 breaths/m nute)not consc ousness. Too great o a dose (enough to wakesomeone up complete y) can cause rap d reversal andwit drawal. Too sma o a dose can resu t in a need orintubation. Chronic users of opiates and those patientsw o n aled or ingested a arge dose of t e drug mayrequire an ntravenous drip of na oxone because tshal - ife s very sho t. Genera y 2/3 of the dose t atresults in adequate venti at on s given per our n a drip.

K ow t at acute lung injury s sometimes seen n op ateadd cts w o undergo rap d reversal o unconsc ousnessw t na oxone h gh ow oxygen via facemask. Patientsusua y recover w th suppo tive care.

A so recognize that naloxone is typ ca ynot t e co rectanswer f a scenar o presents a patient wit d lated pupi s.

Salicylates

Sa cy ates are metabolized in t e liver by con ugat onwith glyc ne or glucuron de. These pathways are

uickly saturated n a person who has overdosedresulting in acidem a. T e ncreased ASA level initia ly causes yperventilation t roug acentral e ect.This as a protect ve e ect since the ASA crosses theblood bra n ba ier ( e is more tissue permeable)w en the system is acidemic. Acidosis can worsen if

0-37



10 PO SON NGS

the HAGMA is compounded by actic ac dos s due topulmona y edema. If the patient stops hyperventi ating,

t s p obably due to espi atory m sc e fatig eThe class c presentat on of the pat ent w th an ASAoverdose is tachypnea and a m xed acid-base disorder(HAGMA + resp atory a ka os s) and a h sto yof having taken over-the co nte pa n medicineDepend ng on the dose, pat ents may add t ona lycomp a n of tinnitusTreatment of sa cy ate ove dose: decontaminat onwith activated cha coa with cathar ic andse m/u inealkalinizat on sing sod m b carbonate. Both hemodialys s and charcoa hemoperfus on have been sed insevere cases (salicylate evels>00 mg dL) The charcoal hemoperfusion removes the sa cylates better thanhemod a ys s b t does not correct any u d elect o yte

mbalance (Patients are o en hypokalem c )

am p90% of this drug s metabo ized n thel ve , byg ucuron dation or s lfation, to inactive metabo tes5% s exc eted nchanged through the k dneys The ast5% s metabo ized by way of the hepatic cytoch omeP-450 system to act ve metabol tes One of the act vemetabo ites s N-acetyl p benzoq none m ne(NAPQI),wh ch s highlyhepatotox c No a y, the sma amo ntof NAPQI s qu ck y detoxi ed by eacting w th thesul yd y g o p of glutathione fo m ng nontoxic mecapt ric ac d A arge overdose resu ts in depletion of thegl tath one and subsequent nc ease n these metabol tesA seve e overdose is o en fo owed by mi d N D. It s

on y a er 24 8 hours that ive tox c y ensues.Many ntentional ove dose pat ents present w thco- ngestionof mult p e s bstances. Always s spectacetaminophen as pa of the c inica pict e of anyove dose. It is standa d to check acetam nophen leve sregardless of the p esentation because unt eatedtox city is potent ally fatal

-a am p y m :Chronic mode ate-to-heavy se ofa coho has a 2 fo de ect Thecy och ome P 450 system is cranked up (so that moreNAPQI s produced), and the amo nt of glutath one

s decreased (so less is ava ab e for detox ng the

NAPQI) herefo e, long-t me use s of moderate-toheavy amo nts of alcoho who take acetam nophen nnor a o h ghe doses are at isk for seve e hepatictox city o iver fa lureT eatment of acetaminophen overdose: Activatedcha coal s bene cia , does not h nder use ofN-ace y cysteine (NAC), and s usually sed f pat entsp esent w thin 4 hou s of ngestion Altho gh the e

s great va iabi ity n the hepat c response to the overdose, a 4-ho r post- ngest on acetam nophen eve of

> 250 Jg mL ndicates a high probab l y of hepatotox cty if unt eated NAC s an e ect ve ant dote that wo ks

by increas ng the ava ab y of hepat c g utathione

AC is e ective when given w thin8 16 ho rsa erthe acetam nophen ove dose. Even when g ven late nthe co se to a pat ent w th signi cant ngestion andtoxicity, t red ces mo ta y and mp oves ive nction T eatment can be nit ated with e ther anIV or o alprotoco , which varies in their d ration IV is favo ed ifpat ents are vom t ng or p esent n ive fa lureBoth p otocols contin e dos ng unt the measuredacetam nophen leve s undetectab e o "clea ydec easing w th a min mum of dos ng over 20 hours(The spec c de nit on of "clea y decreas ngis controvers a )

AnticholinergicsDo not forget the presentation of anticholine gic

ntox cation (d scussed above and eiterated nab eI0-11). "Red as a beet; dry as a bone hot as a

ha e bl nd as a bat mad as a ha er; as a ask•

Red c taneous vasod lation• y: anhidros s• Hot hyper herm a• Blind mydriasis• Mad ha ucinat ons• F u na y etent on

The ant dote is physostigm ne

Acid AlcoholsI p py a (" ubb ng alcoho ) is a commosolvent and d s nfectant Like ethano , t hasNS

dep essante ects t is 2 to ethano in the ca ses ofalcohol ove dose. The main metabo ite is acetone, wh chca ses a prolonged CNS e ect The acetone causes keton ria b tno anion gap acidos s, and thesweet odorofacetone s ev dent on the pat ent's breath C S dep essionis the major e ect, a tho gh there may also be ca d acdepress on Abdom nal pain and vom ting a e s a yp esent Anosmo a gapof> 35 mOsm s pica ly seenw th toxic y Treatment G ve s ppo ve ca e, nc d

avage if< 2 hou s has passed s nce ingestion Make ea yse of hemo pe tonea d alys sn seve e cases.

M a (wood a coho ) tox ci y s sua y d e to

contaminated moonsh ne It is on y mildly inebriating, andmany signs of tox ci y a e delayed> 24 ho rs specia yv sua impa rment, om bl rr ng tob indness The toxicmetabo ites are for a dehyde and for c acid Ser mana ysis shows an nc eased an onand osmo a gap Treatw th fomepizo e, fo c ac d, and immediate d alys s Givefo ic acid to inc ease metabolism of the for c ac d

E y y (anti eeze) Alcohol dehydrogenasebreaks down ethy ene g yco to ts very toxic metabo ites,espec a ly oxalate P esence of oxa ate s ndicated byca c m oxa ate crys a sin the r ne andhypoca cem a(oxa ate che ates ca c um) Suspect if a patient appears

ntoxicated but witho t an a coho smell, and w th

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• What is he common ac d-base disordertyp cal y found when a pa ien presen swith ASAoverdose?

What drugs are used o rea acetam nophenoverdose?

Methanol causes what neuro og c defic ?• Does ethylene g yco cause an ncreased

osmo ar gap, anion gap or both?• Wha ECG finding correla es most c osely

w h he degree of n oxica on with a tricycl cantidepressant?

For tricyc ic overdose wha shou d you do o he rine?

a HAGMA and increased osmola gap. T eat wi hfomepizole, bica bonate for he ac dosis, calcium p , and

mmed a e d alysis

Prescript on DrugsTh oph llin : This dr g more o en presents asinadver e toxici y ather ha in e tio a overdose.Toxicity o e occ s in he contex of the pa ie thaving bee presc ibed another drug (or he bal prepa

at o ) ha inc eases theophy ine leve s Suspectoxic ty whe yo see a clin cal h story of obs ruc ivel ng disease and t emu o s ess achyca di ven r c laarrhythmias, vomi ing, +/- seiz res w th a theophyll elevel > 20 mcg/mL. This ox c ty can look like coca eo methamphe amine se. Be awa e of pat entsw th asthma who also use these i c t d ugs! K ow thed ugs tha commo ly i te act wi h heophy e a d

c ease evels: CYP3A4 inh bitors, ce ain macrolides,qui olones, and zi e o .

Treat w th s pport ve care (payi g atten ion ohypoka em a because i pred sposes o ven ic laar hythmia) and mul iple doses of ac ivated charcoalw th catha tic If vomiting is oo seve e to a low for charcoa , give ondanse ro /- a i id e. T ea seizures w h

diazepam T eat sup avent icular tachycardias (SVT)wi h adenos ne. tab e ven cular ar hythmias sua lyespo d to am oda o e; t eat hypote sio w th a pha

ago is s (phenylephrine or o ep nephr e) Odd y,beta blocke s ca reverse hypo ensio if the a pha agonis s don't wo k bu beta b ocke s shou d be given only

nder the g ida ce of a medical oxico ogist Cal po socon ro o get s ch advice. D alys s is ecommended inpa ients wi h sei res or ven ric la ar hy hmias

Li hi m: Men a status changes are the mos commomanifes a ion of overdose a ec g> 90%. O heCNS changes nc de seiz res a d symptoms d e toencepha opa hy (poor memory, incohere ce, d so ienta

io ) Patie ts may also get pa ki sonia symptoms a d

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POI ON NG

moveme t d so de s. Nausea, vom t g, a d d a hea a ea so commo . A ithi m level is obta ned for p poses ofdoc me t ng de t ve ove dose bu symptoms do otco relate w th levels

Do t forge about the compl catio s f om ch on cli h um use enal tubu ar ac dosis, ephroge c d abetes

s pid s, a d sicca symp oms

Trea me t Ac va ed charcoal iso e ect ve. Gastriclavage s recomme ded in h s se t g Restore uida d electroly e bala ce, and use hemodialys s i seve eli h um ove dose cases. Co s der seve e n oxicatiowhe the e a ea y symptoms cha acte s c of l th umpo soni g, when the li hi m levels are> 3 5 to mEq/L,o when he se um eve does o decrease app op ia e y

ric clic an i pr ssan s These d ugs are l poph lica d a e p otein bound, so they have a very la ge vol meof distribu ion and can o be emoved by d alysisCl ical prese a on of oxic ty ncludes seda io or

co fus on and a hy hm asTreatmen i c des gas ic decontamina on w thactivated cha coal w h ca har ic, f presentatio is w thin2 hou s of gest o G ve suppo t ve care and mon tofo ca diotox c s de e ec s. T icycl cs cause tachyca d aand PR, QT, a d QRS p o o gat o . TheQRS p o ogat o s the ECG change hat co relates most c ose yw h thedegree of intox ca io Ve ic lar achycardiaa d b illat on are also commo . The ca d ac problemso e espond to mai taini g analkalemic s a e ei herby hype ve tila on f he pat en s i t ba ed or w th Vbica bo a e Keep se m p 7.5 o 55 si g sodi mb carbona e ("alkal iz g the ur e ). Give lidocai e(JStchoice) or phenyto as eeded for ar hy hmias Usebenzodiazep nes for se zures

Digoxin Th s d ug is ot commo ly p esc bed buttox c ty is ot uncommo beca se he dr g has a very

ar ow he apeu ic ndex Levels donot co e a e withtox ci y, so yo have o pay close at e tio o s g s andsymptoms C i cal presen atio of tox c ty includesanorexia, N , bel y pa n, co sio , weakness cha ges

colo v s on, scotoma, a d bradyca d a w th hypotensio . The prese at o can appea as f he pa ien sbei g overt ea ed wi h an a ihype ens ve d ug h sis impo ant beca se pa ients who take d gox n o enalso ake an ihyper e sives. Labs may show po ass umd sturbances (hypo inac te tox c ty;hyper ch o ctox c ty) a d acute kid ey j y, wh ch s o e theca se of he inc ease i the serum level.

K ow the commo ly used d gs that can ncreasedigoxin evels when coadm is ered dil azem, ve apami , amiodarone Beca se d goxin s c ea ed by hekidney, decreases n GFR increase he se m leve .Treatmen inc udesco i ousca d ac mon ori g.P VCs are commo . O her co d ctio abno ma es

nc ude AV block w h j nc ional escapes and ser ousve tric lar arrhythm as. The ECG should be eval a ed

pe od cal y beca se digoxi ca at en or inve T

1 -3



1( PO SON NGS

waves, shorten the QT interval, and depress a era STsegments ( nd ngs often referred to as dig effect").

Treat with act vated cha coa f presen ed wi hin2 hours of nges ion Treat pa ien s who have serious ven ric lar a rhythm as (tachyca d a, bril at on,comp e e hear block, Mob z , and symp oma ic bradyca d a), se umK > 5 mEq/L, and ena fa ure ormenta s at s changes wi h Fab fragments (a d gox nant body). Be aware that presen ng hyperkalem a apid y everses w th ab an ibodies, so donot be over yaggressive in treatinghyperka emiaMuch con rove sy exis s abo t whether to g ve ca c m

o pa en s w th hype ka em a f om digoxin ox c y ( os abilize card ac memb anes) Conven ona eaching is

o w thho d he ca c um (and this is what we have wrien in Nephrology, Book 2), b t severa case eports

and ret ospect ve st dies show tha ca ci m does notharm hese pa ien s. The c ent standa d, howeve , snot to give calcium if you a e g v ng Fab an ibod es

because he hyperka em a s ap dly co ected, andar hy hm as are un sua

B z d z p :Overdose with ora benzodiazepinesa one rarely causes seve e toxicity, b i is a commondrug seen in co ngest on, espec ally with alcohol oopioids o e common scenarios of benzodiazep ne oxicity occu n the setting of opera ve anesthesia Pat entsw th benzod azep ne oxicity have CNS depression withotherw se norma v ta s and exam ( coma w h normav ta s"). eatmen s s a y s ppor ve Ac va ed chacoa s not ecommended Use of the ant dote mazenilis con oversia because i may prec pitate w hdrawa

seiz res n patients who are to eran o benzodiazepines

Illic t Drugs

C Ca dio oxicity can occu no ma er wha theo e of se Th s d g ca ses hythm d s bances

( nclud ng V b/tach), ischem a ( r espect ve of whe herthe pat ent has preex st ng athe osc ero c d sease),myocard s, and sys o ic dys nct on S spect use n ayoung pa ent p esenting w hM Seiz res and s rokea e a so common with coca ne; consider t in pat entswi h st time se zu e ow hat beta-b ocke s a enotused n th s group to treat angina o ve i ed myoca d al

schem a d e to conce s of nopposed alpha-recep ostimula on Ins ead, nitro, ca cium channe b ocke s,and BDZs a e 51 l ne ea men s

h mph m is a powe ful CNS st mu antha acute y ncreases he e ease of epinephr ne, no

ep nephrine, serotonin, and dopamine Cons demethamphe am ne toxic y in heswea y, severelyag tated o psycho c patient with achycard a and hyper

ension Seve e oo h decay occurs n chron c sersAcu e treatment of the seve ely ag tated pa en s w hIV ben od azep nes rst and hen antpsychotics, s ch asha oper do , if needed. M doses a e given f unab e to

give Watch forrhabdomyolysis n hese pat ents bymonito ing e ec oly es, B N, Cr, CPK, serum lac a e

iver enzymes, and c ot ng t mes

Ph y d (PCP) can cause ac te psycho icagita on, seizu es, dys on a (incl d ng aryngospasm),and hype ens ve c s s Seve e dyston a can ca se

habdomyolys s reat w h a ca m env onment and VBD s as needed, w th suppo tive care for compl ca ionssuch as rhabdomyolys s

H is an opiate Be care l w h the use of naloxonen ch on c use s because of he isk of p ecip a ing w h

d awa if yo ove shoot in dosage Hero n n ox ca ion ssome mes di c o d e en a e om alcohol intoxica on beca se bo h subs ances are CNS dep essan s, b talcohol us a y does no cons ric the pup ls or decreasethe bowe sounds

A 3,4-me hylened oxyme hamphe am ne a k a

cs asy ) s common y used by yo ng people in he setting of pa t es o aves The nges on of MD A res l sn feel ngs of e pho a, oss of nh b ons, cozy feelngs of in macy, and ncreased sex a a ousal due to anncreased release of sero on n The d ug s commonly

pe ceived as be ng ve y mild w h m nima risk andphysica e ects b t in actual ty, ecstasy possesses propert es hat esemble a combina on of amphe am nes andpeyo e (stim ant+ ha uc nogen) he d g s taken intab et fo m, and overdoses can resu t in dea hS de e ects of MDMA incl de b x sm awgrinding), anx e y, swea ng, hype ension, and tachyca dia Dangero s comp ca ions nc ude seve ehyponatrem a, mal gnan hype tens on, s oke, cardiacischemia, a hythm as, ao ic d ssection, and sero on nsynd ome Hyper he m a and rhabdomyo ysis are poss b it es, espec a y in pa ien s who dance a n ght anduse ecstasyAct vated cha coal is g ven f he pa ien p esen s w hinI hou of inges ion In ntox ca ed s ates, mos symptomsespond obenzodiazep nes(hyper ension, achyca diac,

ag ation) alope ido can poten ia y exace batehyper herm a A rhythmias espond to ca cium channeblockers. Beta blockers arenot recommended beca seof he poss bi ty of unopposed a pha ad ene g cs m lat on Hypona rem a sua y responds o wateres r c on hypona remic se z res sho d be t ea ed w hhyperton c sal ne

LS yserg c acid diethy amide s efer ed to as ac d"and ca ses hal cina ons Fa alities and mo b dityd r ng use a e un s a generally at b table to baddec s ons be ng made wh e in ox ca ed

Misce aneous

C b m x d Carbon monox de u ck y bindsw h hemog obin w th an a ni y of� 250x g ea erthan . This carboxyhemog ob n (COHb) dec easesa ter a oxygen conten , wh ch eads otiss e hypoxia

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Q� ui• A 30-year o d man presents with acute MI. What

i c t d ug should be ruled out as the cause?

Know ca bon monox de poison ng!• What are the 3 drugs used o eat cyan de

poiso g?

Symptoms are progressive and range omhe cheandlighthe e nessto et argy to unconsc o sness to comato e th.Be espec a y s sp c ous f the pat ent as been workingaround cars, gas/oil eat ng n ts, or generators Typ calrea fe scenarios:

C exhaust: garage mus c band sing a runn ng carto wa m up the garage on a coldwinter day-w t the

door c osed.E aust romg oline ere gener torsEspec a y s spect a er electr c ty as been ost,s c as a er a ood, r icane, or ice stormPoor combustion in he t ngunit Suspect when apatient cal s rom home inwinter (espec a ly nearsta o t e co d season) and says t e am ly iss ering from eadac e and l g theadednessT e pat ent may sound s ow to respond. Orthe patient ca s in t e winter and comp a ns o

eadac e and light eadedness, w ic improvesw en e goes outs de

W at to do? T e answer to any scenario n w ic thepatient ca ls you w t s spect symptoms, espec a lywit t e above environmenta factors, s to tel thepat ent to eave and get the fami y o t o t e o seimmed ately; then, you send an EMS unit there

O poisoning is respons b e for most deat s n patientswit s e inh ti n, so do not forget to c ec OHb

eve s w en manag ng smoke n alat on

T e bra n and ear areespecia ly sens t ve to O.Poison ng o en ca sesl ng ter t per nen NSimpairment w t cogn t ve de c encies ( e , memo yand ea ng) and personal ty and movement disorders

Feta emoglobin as especia ly g a n y or O,so treat pregnant pat ents aggress ve y

I yo s spect carbon mono de po soning, get ac xhe g in evel A hand eld breath analyzercan qu ck y ule t O po son ng, b t et anol causes

alse pos t ves:Mi d to moderate O to c ty occ rs at 15 30%

oderate to severe to ic ty occ rs f> 30%> 50% s o en atal

" er y red co orat on sr .

© 2014 edStudy

PO ON NG

Treat O po soning w th 00% 2 this decreasesthe alf l e o OHb rom about 5 hours too r.Hyperbar c 2 r er decreases the a fe to30 m n tes, but its ma n bene t s that it decreases t e

O nduced sc em c reperfus on inj ry to t e bra n

y erba ic o ygen s generally given formoder te tsevere O po soning. Ind cat ons or hyperbaric o ygen(g ve w t in6 ho rs)

oHb> 5 and> in pregn ntwomenLoss o consc o sness or any ocal ne ro de cit

cidos s pH< 7

End organ damage, especial y ac dosis

Smoke inhalation: Respiratory impa ment results romt e no ous c emica s n t e ungs or la yngea /air ayedema Suspect la yngea nvo vement f face or airways are b ed (e g., singed nasa airs). Do not forgetabout t e assoc ation be ween O po son ng and smo ein alat on.

Cyanide po soning cl es Patient s breath as ann r , and lab draw shows r ght re en s

l od yan de immediate y binds to theerricmoleculein the mitochondr al cytochrome o idase comple es,thereby b ocking cel ular aerobic metabo sm. Thesepat ents very q c y deve op eadac e, tachycardia,and tac ypnea. T is may uick y p ogress to coma andva ious card ac arrhyt mias Th n about cyanide poison ng n pat ents who ave been in a re or w o havereceived sod m nitropr sside or amygda n (c em cader ved from apricot and peac p ts that is used o enin erba compo nds) Laboratory eva uat on o t nelyshows signi cant l c c aci sis Diagnosis sclinical,a er e c ud ng other ca ses of actic ac dosis and carbonmono de po soning Assays e st to nd t e c em cain t e blood, but t ese are re erence tests that take a ongt me to ret

Tre tment or cyanide poison ng is the 3 step cyan deantidote package Goa is toind ce methe ogl inemiabeca se cyanide preferent a y b nds met emoglob nand produces a ess to c react on

Step 1: Hold amyl ni ite nder t e patient's nose for30 seconds.Step 2 Adm n ster 3%s i m nitrite T en tr tes conve t emog ob n to methemoglobin (t efe c fo m of hemog ob n), whic more e ective ycompetes with the cytoc rome o idases or t ecyanide Amy n trite inha ation ca ses a 3 5%methemoglobinemia whi e the sodi m nitriteca ses 0 methemoglobinem aStep 3 Administer s i thi s l teV w c actsas a s bstrate for t e enzyme rhodanese Th s enzymeconver s t e cyanide re eased om hemog obin toinact ve t ocyanate w ch s e creted renally

Signi cant to c ty can res t in a park nson an typesyndrome because cyanide s to c to t e basal ganglia

10-4



1(2 DRUG WITHDRAWAL

norganic lead:There are 3 scenarios to tes for leadexposure, depending on when he exposure occurred:

I) For ongo ngexposure, checkwhole bloodlead evel2) A er exposure has occurred, RBC pro oporphyr n

and z nc protoporphyrin levels rema n elevated orsevera mon hs.

3 or eva ua ng he e ec o exposure omyears be ore,he bes es s to measure ur ne lead 24 hours a erg v ngI gm o ED A

Organ c ead s l p d-so uble and rapidly excreted, andprev ous exposure snot detectab e!

nsectic de:Organophospha eand carbama e poisoningspresen identica y Symp oms inc ude ncreasedsalivation, m osis (smal pup s), N D, and abdominacramps A ected pa ients also compla n o chest t ghness and genera ed weakness Organophospha es aremore tox c than carbama es; hey b ndrrevers bly oace ylcho nes erase, whereas the carbamate bind ngis revers b e This is re ected by a decrease n he levelof RBC (no plasma!) ace y cho nesterase for severamon hs a er organophospha e poisoning, while re u s

o normal w hin hours a er carbama e po soning

reatmen or nsec cide po soning: The rou e o thepoison nto he body sderma absorpt on (especiallyorganophosphates), so decon am na e by removingclo hes and showering w th soap or modera e-to severesymptoms, g veatrop ne( 1 2 mg IV, repeat q5 minp ). Addi ional y, or organophospha es on y (nocarbamate), give 2 pro opam (2 PAM)

DRUG W T DRAWAL

So far, the d scussion has ocused on n ox ca on Youshould also know the fo lowing presenta ons o speci cd ug wi hdrawal

Heroin s the major opia e assoc a ed wi h phys ologicw thdrawa i a so has the mos add ctive potent alSymp oms usually s a t w thin6 hours to a day a er he

ast dose o dr g or can presen immedia e y n hese ng o opia e antagonists (e.g , na oxone, buprenorphine). arly symptoms include ag at on, rhinorrhea,

tearing, musc e aches, nausea, vom t ng, abdom napa n, and diarrhea De ni e y think abou this en ty inthe tear patien who s yawning hose two ac vi iestyp cally do no go toge her

xam shows d latedpup ls, yawning, hyperact ve bowelsounds, and piloerect on (from wh ch the erm "qu t ngco d urkey s der ved ) Tachycard a and hypertensionare seen n pa en s in severe dis ress (bu o en are notpresen in most pa ien s)Me hadone s g ven o pat en s who are ch on ca yaddicted to op ates and presen inacu ewi hdrawal the patien des res to stop op a e use entirely because

of addic on and re ses methadone, symp oms can beame iora ed w h c on dine and dia epam Promethazineis g ven or vom ting, and loperamide he ps the diar hea

Be zodiazepine (BDZ) w thdrawal can be ata tpresents wi h anx e y and tremu ousness, me ancho y, andsometimes psychos s/seizures Time o w thdrawal om

as dose depends on whe her he drug used has a shor orlong ha f e (up to3 weeks for d azepam). Ideally, thesedrugs would be tapered over a pro onged per od when apatien s d scon inu ng chron c use Withdrawal s rea edw th long-act ng benzod a epines

Ethanol Patients severely addic ed to ethano s arhav ng w hdrawals w hin abou6 hours om he lasdrin (This can happen even hough he pat en sthas a measurable blood alcohol eve If it's ower than

he patient is accus omed to having, hen they can w hdraw ) Symp oms ge more severe as t me passes A erabou 12 hours, pa ien s usua ly have an sola ed gener

al ed se zure. The next phase is halluc nos s, where thepat ent s senso ium s intact and BP/pu se are normalbu hey see, hear, and ee nonexis en phenomena Thelas withdrawa syndrome s de irium remens (DTs).DTs are marked by au onomic nstabi y and del riumUn rea ed, they last abou5 days Compl ca ons ncludevolume dep e ion, hypokalem a, hypomagnesem a, andhypophosphatem a or DTs, g ve good support ve care,rep ace th am ne w th g ucose, and give ong act ngBDZs. Replace e ec roly es p Watch out for re eedinghypophospha emia (discussed in Nephro ogy, Book 2)

or pa ien s who can be equen y observed, g ve repea

BDZ doses when symp oms recur The C n cal ns itu eWithdrawal Assessment (C WA) protocol s common yused to direc BDZ dos ng, and has been shown to resu t

n lower o a BDZ doses han uns ructured cl n cianassessmen . n s ua ons where obser ation s no as

easib e, xed dosing schedules are used Donot usehaloper dol for he de ir um because can precipi atese ures. Ch ord azepox de can be g ven ora ly to pa ien snot in DTs, if they desire o qu dr nk ng, to prevenalcoho w thdrawal.

OP ALMOLOGY

OV RV W Aqueous humor s produced by he ci iary body, owsthrough the pup l nto he anterior chamber, and hengoes through the trabecu ar ne work and in o heSchlemm canal The greater he resis ance to th s ow

n the trabecular network and he Schlemm canal, hegreater is he in raocular pressure Normal pressure is< 2 mmHg ( eI 0- ).

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ui

• How do you check for ongoing norganic leadexpos e? What about expos re 2 years ago?What i 0 yea s ago?

• What is the treatment or organophosphatepoison ng?

• What is the d erence between open ang e andang e-closure glaucoma? Wh ch s a medicaeme gency?

• What s the t eatment fo open-ang e g aucoma?Ang e c osu e g aucoma?

GLAUCOMAv v w

Glaucoma is an ns dious disease in wh ch a pro onged,e evated in raoc ar pressure causes progressivev s a e d oss d e o op ic nerve damage There are4 broad c assi ca ions: primary open-angle (POAG),closed ang e, congen tal, and secondar Know thespec cs abou POAG and angle-closure gla coma

m y p u mPr mary open ang e glaucoma (POAG) is the moscommon pe I is ca ed open-angle" beca se heorb has elevated pressure wi hno clos re of the in et of

he trabecular net ork These pa ients su ernnot cedgradua oss of per phera v sion ( unnel vision) ha canprogress to legal bl ndness before t s de ec ed

R sk fac ors include advanced age, fami y h s ory,A can Amer can race (5x increased r sk compared oo her races), and ncreased intraocular pressure

Posteriorchamber

gu r 10 6 : truct res of the ye

© 2014 MedStudy

OPHTHALMOLOGY

Be susp c ous and refer for oph halmologic eval a ionthose patien s w th risk fac ors and/or hose who have

c pp ng on fund scop c exam ( C pping"= cupocc pying > 50% of he op ic d sc; norma cupocc pies < 50% )Screen ng of POAG The American Academy ofOphtha mology (AAO) recommends a comprehens veeye exam by an ophthalmo og st or skilled optome r st a er the age of 40. A er he in t a screeningexam, repeat screen ng is usually recommended every3 5 years in pa en s wi hou risk factors and every1- 2years for those wi h one or more r sk fac ors (borderl ne in raocu ar press re, cupp ng, Afr can Americanrace, and fam y h stor ) Pat en s w th DM sho d beseen year y The AAO a so recommends hat AfricanAmericans have per od c exams be ween the ages of20 and 39 as we l For a indiv duals o der than 60, acomp e e exam should be done every- 2 years TheUSP T found ns c en evidence to recommend foror agains screen ng adu s for g aucoma

Trea men of POAG is w h med ca ions or laser surgeryThe follow ng meds are sed

Prostaglandins(topica ) areI 51 ine drugs becauseof he once-da ly dos ng and the few system cside effec s, especially compared to he opicalbeta-blockers These are expensive!Beta blockers( opica ) dramatically decreasein raocu ar pressure probably by decreasingprod ction of aqueo s humor I is hough aq eoushumor prod c ion is med a ed by onic sympathe ic(be a) stimulation

Nonse ect ve (timolo , carteo ol, evob nolo ,me iprano ol) may ca se e hargy, bradycardia,and exacerba ons of OPD

o Beta1-se ect ve (be axo o )

u u mPrimary angle c os re (c osed angle, narrow ang e)g aucoma, the most severe form of narrow-ang egla coma, s anoc ar emergencyk ow t we l R skfac ors nc de age> 40 years, female, hyperop a(farsigh edness), Asian race, and family his ory

ncont ast o primar open-ang e g aucoma, e eva edn raocular press re n ang e c osure gla coma is caused

by mechan cal obs r ct onof aq eous o ow thro ghthe trabec ar net ork, due o an anoma o s ir s con

g ra on or ris neovasc ariza ion he resu t ng rap dncrease in ntraocular pressure causes redness, severe

eye pain, nausea, and ha os aro nd igh s It can a so beassoc ated w th headache and present sim lar to m gra neLow igh cond t ons that prec p tate p pi lar di a a ion(e g , nigh ime or n he movie theater) are assoc a edwi h onsetPhysical exam shows decreased vision, increased

ntraoc ar pressure (o en> 30 mmHg), a narrowan er or chamber (di cult to assess), co eal edema,conj nc va hyperem a, and a xed, mid-d ated pupi

0 4



10 OPHTHALMO OGY

Ideal treatment includes immediate ophtha mologicrefer a fo alr my . f an ophtha mo og scannot see the pa en mmed ate y and the pa ien hasdec ne n vis on, ns te immed a e reatment:

g ve p ocarpineI drop, thengive predn sone I d op hen

• g ve ace azo am de

place pat ent sup ne, heng ve t moloI drop, wa I m nute, then

ns c ions w th ove - he-co n er med ca ions o ennclude admon ions to "avoid use in pat en s w h

g a coma ( ). These wa ngs apply n y•

give aprac onidineId op then

Image - : Co eal ulce1: Usually causedby improper use of contact lenses It isespecially seen with the extended-wearcontact lenses.

Image - Optic at phy has variouscauses, including prol erati e diabeticretinopathy and central retinal arte1occ usion In older patients also considerischemic optic neuropathy

Image 7 CMV tinitis Especially seenin people ith A DS

Image - : Branch retinal vein occlusion(BRVO) Main cause is hypertension but also seen with diabetes and with hyper iscosi syn mes Think of this as e aggerated AV

nicking ith the arte pinching o the ein.

Image I - P l e tive diabetic tinopath Rubeosis Blood essels grow onto the irisThis may cause intractable glaucoma Alsocaused by central tinal ein thrombosis

Image -5 oxoplasmosis

Image -8 A us senilis Common in older patients In patients< yrs it may be a sign of a lipid disorde

Image Heterochromia ocularmelanosis his is a norma/ nding in darkly pigmented persons Rarely caused by Fuchiridoc clitis

Image -3 ard date a seen in nondiabetic retinopathy is is caused by leaof p tein and lipids j m capil aries reatmentis photocoa ulation of the leaking capil aries

Image 6 Prol erative diabeticretinopat t ous hemorrhage

Image -9 Retinal detachment Thisusually occurs in ve1 myopic people Ito en occurs a er a it ous hemorrhage

Image - Central retinal veinocclusion (CRVO) Same causes as BRVO

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ui• D f d g w d• W f d ?•

w d d v d ?

to pa ients w th angle-closure gla coma not alreadyt eated w th r do omy.

THE RETINA

etina Detachment

Re inal detachment may occ r spon aneo sly It o enp esen s as as es or streaks of l gh (p otopsias),showers of black do s (hemo hage), or a "shade coming

down or "wav ng c r a n n a por on o he v s aleld V s al ac ity may be normal ni allyMyop a(nears ghtedness) is the bigges s fac or (Closed-anglegla coma ris s ars gh edness, or yperop a.)

P es mp ive diagnosis is based mainly on his o y, buoccas onally a por ion o e e na appears elevated or

olded on op halmoscop c exam

Trea ment: T s condi on req ires anemergent re eJ albeca se untreated pa al detachment can progressover o rs to otal re inal detac ment wi permanentblindness Small ret nal de achmen s are trea ed w thlase surgery o ack down the area Larger detacments eq rescleral buc l ng(a band aro nd he sclera

OPHTHALMOLOGY

o restore con act o retina wi h he wall of t e eye),ans-scle al d a nage of d, vi ectomy (removal of

vi reo s), o injec ion o gas or o e id in o e eye(to amponade he et na)

etinal Vascu ar Occlusion

Ret nal ery cclu onOccl s on of the central ret nalar e y s allyembol c a ses s dden, pa nless, n la e albl ndnessT s is atr e ocular eme gencyin which eve y min teco nts. Re nal edema (spar ng he rela vely h n fovea)c ea es pallor and e appea ance o a"che y ed spotin he mac laT eatment s directed towa d d slodging e embol sand incl des ocular massage and/or paracen esis oft e an er or chamber (to lower press e) Wh le wa ting or the oph halmolog st, have the patient get in o

heTrendelenburg posi on and brea he nto apaper

sack. Yo may massage the a ected globe wi h yo rndex nge s (5 sec press re, 5 sec no p essure, repeat)Un or unately, all hese temporary meas res are rarelye ect ve atients s bseq ently requ e a horo gsys emic evalua on for embolic and ca o id disease.

Ret na Ve n hrombo

Retinal vein th ombos s (RVT) ca ses s dden,painless, near to al loss of v s on Ca ses incl de

ype tens on, polycy hem a vera, and Waldenstr mmacroglobul nem a Re inal edema is accompa ied byhemoJ hage not a cher y ed spot.

Image 10-13:Papilledema. Seen with increasedintracranial pressure Think of tumor and pseudotumor ce bri Mimics opti neuritis/

papillitis, cept papilledema is bila eral

mage 10 14Allergic co juncti itis Usuall seasonal

mage 10 15Herpes eratitis of the corneaFrequently recurs

Image 10 16Pr l e tive diabeticretinopathy with disc neoplasia

© 2 MedStudy

mage I 0 17.·P ium ssociated withxpo ure to ultra iolet light and d in

Seen in farmers, p fessional go e etc

mage10 18S nechiae This is a possible sequela of iritis (iridocyclitis) 90%of iritisis idiopathic, but i is seen in i amma o

diseases such as iral infections andconnecti e tissue diseases

10-45



1� OPHT O OGY

Diagnosis is made with an ophthalmoscopic examshowing a "blood and thunder ndus with mu tip ehemor hages

Patients with RVT s ally are j st obse ved; however ifthey have macu a edema or neo-vasc larization, referimmediately to an ophthalmologist

acular DegenerationAge e ated macu a degene ation is the leading causeof ir eve sibleacq i ed egal b indness in developedco ntries The macu ar a ea of the retina consists of thefovea and the s rro nding area The fovea is esponsib e fo ne(20/ 20) vis al acuity A tho gh the mac lacomp ises only 2% of the visua eld, 25% of the conephotorecepto s are here, and it cor e ates with 50% ofthe primary visua area of the brain

There a e 2 types of age-re ated mac lar degeneration:• ph (o dry ). This is the most common type

It causes a g adual loss of central ac ity down to20 400 (pe iphera vision is spa ed)

v s (or wet ) This type is somewhatamenab e to t eatment with aser photocoag lation,photodynamic the apy, and/o int a-vit earanibizumab or bevaciz mab.

Risk factors fo both types inc udesmoking and owleve s of zinc and antioxidants in the diet However,most tria s have not shown any reduced isk withvitamin supplementation or antioxidants One recenttrial, howeve , did show reduced risk with vitam n8supplements This is being investigated rther

V , USC S, CR RV S

Medial r ctus ( l) S p io ec u ( ) Sup o ob iqu (IV

�ECLa al ct s (V nf io ectus ( ) nf io o li e ( )

@ ®L T R - MEDIAL

Noteh = i l v l

gur -7: ran al v s ss cia d w h

y m s

OPTIC NERVEp s

Optic neu itis (ON) is an in ammation of the optic ne veand is a f equent presentation ofmu tip e sclerosis(MS).

O presents with ocular pain, especial y with eyemovement On exam, he optic disc is usual y no alinitia ly("the doctor sees nothing, the patient sees nothing )and on y later develops pal or Refe the patient toaophthalmologist g coco icoids i prove vision moreq ick y, but these cont oversia beca se patientsnotgiven steroids timately regain vision as we l Typica ly, an

is done, ooking for evidence of MS

s h m p p hyIschemic optic ne ropathy is the feared complication ofgiant-cel (tempo al) ar e itis Othe signs and symptomsa e those of polymya gia heumatica malaise, feve ,weight oss, m scle aches, aw c a dication, e evatedESR (e yth ocy e sedimentation rate) Co icoste oidsa e started as p es mptive treatment even before thediagnostic tempora ar ery biopsy is done

V REOUS HUMOR Vit eo s degenerationoccu s in all elderly pe sons Theytend to get bothersome oate s, b ief unilateral ashinglights (f om the vitreo s traction on the retina), andvitreo s deta hment(with a s dden shower of oaters and

ashing lights) Vit eous detachment is not dange ousunless it damages the etina

s h m his a ca se of s dden, pain essoss of vision It is caused by either a vitreous

detachment tearing a retina vesse o as a resu t ofbreakage of the agile b ood vessels in diabetics withneovasc larization (p o iferative diabetic retinopathy)

Any patient with vitreo s detachment sho ld be refe redto an ophtha mologist, who looks for cur ent etinadetachment and also defects that, when epaired, mayforesta t re retinal detachment The eye with vitreo shemo rhage must be examined by u trasound to checkfor retina detachment

CA ARAC SThe c ys al ine ens of the eye is a clea biconvex structurebehind the iris and s ppo ted by the zon es he ens isinitial y pliable and reactive to accommodation As thelens ages, it gets less pliable and may get less c ear Any

ens opacity is called a cata act Cata acts cause a ve ygrad a , painless, p ogressive lossof vision Treatment iscata act surgery with eplacement of the ens

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ui

• What is the leading cause of acqu red egab indness in he U.S ?

Opt c neuri s may s gna the deve opmen owhat neu o og c d so der?

• What s vi reous hemor hage?

Know the eye movements assoc ated withthe , and 6thc an al nerves, and thesymptoms of the assoc a ed dys unctions.

CRAN AL NERVE DYSFUNCT ON

Suspect cranial nerve (CN) involvement in the pat entwho p esents with sudden onset of painless doublev sion(F g reI 0-7):

61hCN

(abd cens; CN V ) supplies the late al rect s.Paralysis: cannot move the eye late ally

1CN (trochlear, CN IV) paralysis Eye is deviatedpwa d and the head tilted towa d the ninvolved side

(B elschowsky s gn)

3'd CN(oc lomoto , CN II) Motor:2 branches,s per or and n e ior The s pe or b anch suppl es thes perio rect s and the levato palpebrae supe o s(eyel d m scle) The infer o branch nner ates the in erio ectus, nfe or oblique, and the medial ect s The e

s also a pa asympathetic component of CN III, wh ch syet anothe b anch t res lts n ton c const ct on o thep pil. Complete paralysis o CN I res lts in an eye thatis dev ated "down and o t (d e to nopposed activ tyo the supe or obliq e CN IV ] and late al rectus [CNV ]), a ptotic eyel d, and a d lated p pil f the eye snot dilated, the patient p obably has diabetic vasc ad sease a ect ng only the somat c b anches

EYE NJURY

TraumaCheck acui y nspect ante io chambe fo layeredblood (hyphema), co eal lace at on, subconj nct valhemorrhage, punct e wound, or p p l d sto t on; use

ophthalmoscopy to con rm clear v ew of ret na and noother s gns of hemor hage f there s pa n, inst ll oresce n to check o co eal abras on and ever , nspect,and swab the pper lid, look ng o afo e gn bodyAny abno mal nd ng, except perhaps a small co ealabrasion, req i es cons ltat on Neve patch co ealabrasions n contact lens wea ers

Alkali InjuryAlkali in y is a special fo m of t a ma whe e t eatmentdelay o m nutescan devas ate the eye Alkali apidlypenet ates the co ea and enters the anter or chamber,

where it wreaks havoc

© 0MedStudy

OPHTHALMO OGY

Treatment s immediate, consist ng ofpro se ir gat on,with l d eve s on to emove any alkali-conta ningpar cles Check pH o tea s to con m that it s no malbe ore d scont n ng i igat on Vessels may be blanchedby alkali solution in severe in u y, paradox cally creatingthe appearance o a wh te and qu et eye

RED EYE

AssessmentThe most common cause of a ed eye scon unct v tisConj nct v t s may be bacter a , viral (most commoncause), chem cal, or allergic A red eye also may ndicatemo e gent cond tions Wo k p sho ld incl de eval ation o ce ta n key di erent ating eatu es ac ty, pa n,and photophobia (l ght sens tiv ty) Other eatures toassess are p eauricula adenopathy, amount and type ofd scharge, and the locat on and amo nt of redness

Signi cant ndings:

1) Decreasedvis al ac ymay ind cate ase iousp oblemeq ring p ompt cons ltation Check o an a e

ent p pilla y defect (seen more o en in se io s eyeconditions)

2 Photophob ais a key feature of r docyclitis (and othermore serio s cond tions), wh ch should be eval atedp omptly (w th n24 ho s) fo poss ble ntensivetop cal steroid treatment.

3 Type of redness:B ight ed con uent blood is seen withs bcon unctival hemor hage.C l ary sh ( ed near co eal l mb s only n a s n

ray-l ke pat e ) s ggests docycl tis, kerat t s, oangle clos e gla coma and warrants efe ral to anophthalmologist.Di se con unctival hype emia is nonspeci c

4 Pa nis not common n typical nfectious ca ses of redeye In pat ents who have photophobia, ore gn bodysensat on, and/or v s on compla nts, cons de the mo eser o s condit ons o anter o uve tis, kerat t s, or ac teclosed-angle gla coma

5) Prea r cula adenopathy(may be tende ) s h ghlys ggestive of adenoviral con nctiv tis

6 Discharge, p r lent, s ggests bacte ial et ology

Clear ex date more l kely s ggests vi al Wh te, str ngyex date may be allerg c, espec a ly if associated w thpr itus the e is no p urit s, t is more l kely dry eye(keratocon unctivitis s cca, see next page)

Anterior UveitisThis s a to mmune n ammat on o the anterior eyestr ct es t occ s as a sol ta y problem b t s alsoseen with many d seases (e g , spondyloa th opath es,sa coidos s, l p s, and vascul tides)

Yo can make a p es mpt ve d agnosis with symptomso oc lar pa n, photophob a, and a c liary ush w th ano mal cornea and no mal nt aocula pressure Sl t

4



1 � OPHTHALMOLOGY

lamp exam reveals in ammato y cells oat ng in heaqueous humo o deposi ed on he co eal epi he um.Th s presentation equireseme gen efe a!Trea men : steroids ( o educe in amma on andscarr ng) and cyc oplegics ( o p event synechiae)

Keratoconjunctivitis Sicca (Keratitis)Th s s most common in the e de ly and n m dd e-agedwomen It may be an early sign of sys emic in amma orydisease, includ ng Graves disease, rheuma oid a h itis and sarco dosis Treat mos cases with a ti cial

ears (elec roly e solu ons methylcellu ose o o hermu at ons )

Viral ConjunctivitisVi uses are, by fa the most common cause of ed eyePatients have di se conjunctival hype em a and profuse wa e y discha ge (o en w h o her s gns/symp omsof a viral nfec ion) No speci c reatment us p ac icestrict hygiene Adenov us s one of he most commonetiologies, especially in the summe around swimmingpoo s It should eso ve n5-7 days

Bacterial ConjunctivitisBac e iacon unc iv s may be caused by staph, st ep

i uenzae Pseudom nas, M r ella o Neisse ia.Most cases of bacterial con unc ivi is resolve in5 dayseven w hout trea ment;bu we do treat and fo owclosely because the patient can deve op v sion lossRed eye wi h p o se puru en discharge s he ypicalp esentation.

T eat uncomplica ed cases wi h topical e ythromyc nsulfa o po ym in t methoprim (drops o ointmen ;drops are p efe ed fo adul s because v sion is blur fo� 20 m nutes a er inser on of ointmen s) Remembe :Some pat en s have su fa a e gy so wo sen ngconjunctivit s a e sulfa reatmen may be due o alle gyReserve qu no ones for the more serious casesIf complicated obtain cul u es init a e reatmentwi h gati oxacin o mox oxac nand efer to anophthalmo ogis Aminog ycos des a e no used muchanymore because they i tate he co ea and causein amma ion a er a few daysNeisse a conjunct v t s (can be gonococcal ormeningococcal) is a "hyperacu e (seve e co unct valdischa ge and redness) conjunct v t s hat e u res ea y

ecogn ion andagg essive opica t eatmento p evenp og ess on o co eal perforat on Systemic therapy isalso indicated

a en s who use ex ended-wearcon ac enseshave animpa ed ab y to ght conjunc vitis and are at highrisk fo develop ng v sion th eatening complications.A ways conside an ophtha mo ogy refe ral apresen at on if the patien wea s contact ensesPseud m nas conjunc ivit s can p og ess toco ea

pe fo a onove gh in hese patien s Any con act enswea er w h co unc vitis shou dimmed a e yd scon

inue use of he lenses S a hese pat en s on topicalga i oxac n o coverPseud m nas and g am pos ivesand efe o an ophtha molog s

Aca tham eba is a known cause of nfect on wi hcon ac lenswea ers, espec a y if the pa ent usestapwa e fo ens clean ng Usua ly, progresses apid y

o ke a s

Infectious Ke atitisThink about bacterial ke atitis in patien s who wearcontact lenses and who presen with a pa n eye ha

s d cu o keep open Non-lens wea e s can a so gebacte ial ke a it s especially if mmunocomprom sedOrganisms usually esponsible staph,Pseud m nasand pneumococcus

On exam he eye s red wi h amuco ddischa ge and

a v s blewh e spo(co eal opac ty) ha s eas y seenw h a penligh . F uo esce n stain ng shows the a eaas welTrea ment ncludes emergent referra o anophthalmolog stViral kerat tis can be caused by eac iva ionof atenthe es s mp ex may p esen sim a y o bacteriaconjunc ivitis (discussed above) F uo esce n s a n ngshows a cha ac e sticdend i ic b anch ng patte .Riskfacto s fo reac iva on inc ude aser eye trea men s and acomprom sed mmune sys em Diagnosis s pure y clinical because mos patien s have an bodies to HSV, and

v a cu u e takes days ea men s w h o a or opantivirals (but no bo h) Know ha top cal ste oids canse ious y exacerbate the infec on, so do no p esc ibeany opica s eroids for an eye unless you a e ce a n that

he unde ying diagnosis isno herpes kera i s Somepatients have prob ems with ecu ent disease (s milar tofeve b s e s om HSV); hese pa en s can be managedwith c onic o a antivirals

Aga n RememberAcantham eba in con act lens wearerswho use ap water for lens clean ng!

OTHER EYE INFECTIONS

EndophthalmitisEndoph ha mi is (infec ion inside the eye) can have anocular ( rauma ic) or sys emic (blood st eam seeding)source and can be bacterial o funga The mostcommon p esen a on s bac e a nfec ion a e cata

act su gery (w th in raocu ar lens [IOL] replacement)and the o ganism is usually a coagulase nega iveS aphyl c ccus emember If auma o the orb t isinvolved suspectBac llus ce eus!

at en s p esen wi h decreased v sua acui y hazyco ea pa n and hypopyon ( aye ing of whi e ce sv sib e in he an e io chamber)

© 2014 MedStu y - Piease Repo Copyr ght Inf ngeme t ocopy g t@ ed tu y. o





W v p fj v ?

A w p w vk p w f qf . W g m

?

Treatment Refer immediately. The ophthalmo ogistdoes vitrectomy and cu t res the vitreo s id; thenintraocular antibiotics are injected (vancomycin +ce azidime or amikacin). Systemic antibiotics areadded in severe cases, altho gh uti ity is controversia It is impo tant to choose antibiotics that cross theb ood-brain barrier; othe wise, the drugs donot reachthe vitreo s uid. A cataract IOL does not have to be

removed, nless the infecting organism is a fung s.Candida endophthalmitis is seen more common ybecause of the widespread se of prolonged intraveno s access and cases of fu gemia Candidacan reachthe eye via tra ma or bloodstream infection. Bacteriaand funga endophtha mitis present simi arly, which isthe reason why cu tures are of paramount impo tancein postsurgica patients. Risk factors for ca didemiainclude long-term venous access, ne tropenic immunocompromise, ong-term broad spectrum antibiotics,and corticosteroid treatme t. Know that injection d ugusers who di te d ugs (usua ly heroin) in contaminatedlemon ice are at increased risk Treatment incl desremova of the IOL and systemic azo e antif ngaltreatment (not ampho B beca se it does not achievehigh levels in the eye).

o t l O t l l tPeriorbital cell itis sually is a rapid y progressivece lulitis of the periorbital area, which may becomeorbita if not treated Patients present with warmth,redness, and swel ing aro nd the eye The key physicaexam nding is no mal extraoc lar m sc e movement,without associated diplopia or pain

If the patient has discon gate gaze, diplopia, orpain with eye movement, it is probably the res lt ofinfection that has moved into the orbital space. Thiswa rants a periorbita CT or MRI, and IV antibioticswith MRSA and strep coverage, such as vancomycinand ceftriaxone.

h z oCha a ion is caused by obst uctio of one of thetarsal (meibomian) g ands ming a smal nod lefo nd in the tarsus nder the eye id. Treat withwa m compresses Cha azion is not a problemunless

seconda y infection occ rs. S ch infectio s o enrequire ophtha mo ogic s rgery.

© 2014 Med tudy

HE RING LOSS

StS ye is an abscess at the base of an eyelid. Treat itwith warm compresses and a topica ophtha mologicantibiotic. Occasiona ly, it req ires drainage

EYE E ERGEN IE REVIEBrie y, here is how to approach ophtha mologicemergenc1es.

Treat emergently and immediately refer:

alkali b ,trauma,

• orbital cel itis,centra retina a te y occl sion,ang e clos re g aucoma, andoptic nerve infarction i giant-cel a teritis.

Refer immediately without o site treatment

penetrating oc ar inj ry,endophtha mitis,retinal detachment, a dkeratitis/keratoconj nctivitis.

Refer to be seen within 1- 2days:

retinal vein thrombosis,optic neuritis, and

• vitreous detachmen /hemorrhage.

HEARING L

NDU TIVE HEARING LHearing loss is conductive, sensorineural, or both.Cond ctive hearing oss occ rs because somethingb ocks so nd from entering the inner ear (e g , otitismedia, e stachian ube b ockage, otosclerosis, invasiveexternal otitis, TM perforation, and ceruminosis r anyother impaction of the exte al cana ).

Otosclerosis is an autosomal dominant trait with poorpenetrance. It is much more common i Caucasianstha in African-Americans. 0%of Caucasians developotosclerosis %become symptomatic

EN RINEURAL HEARING LSensorine ral hearing loss is ca sed by either cochleardamage or nerve damage (CN V II). It may be caused byviral infections, ototoxic drugs, meningitis, cochlear otosclerosis, M ni re disease, acoustic ne romas, or aging(presbycusis)Presbycus sis characterized by bilateral symmetricalsensorine ral heari g loss i the e uencies> 2,000H .

/3 of persons older than65years have some form.M e se seis an commo condition that stemsfrom excess p oduction or decreased drainage of endo

ymphatic id A ected patients have recurrent, severe

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1 OF CE P YCH A RY

attacks of vertigo that persist for several ours and o enare associated wit vomiting and prostration. Patientshave tinnitus llness in the ear and in more severecases progressive a ing loss(w ich is frequentlyone-sided) unti deaf, at hich time symptoms stop!

Diagnosis is made with the combination of ypicaclinica symptoms and demonstration of sensorineurahearing oss on audiomet yTreatment of acute episodes is benzodiazepines andantiemetics (no meclizine ). Chronic treatment incl desavoidanc of ca eine and salt with the addition ofdiuretics if symptoms contin e S rgery can p ay a rolebut sually comes at t e expense of hearing loss (A anShepard the rst American astrona t su ered omM ni re disease and was grounded from space ightfor 5 years. He even ua y made it to the moon a er acorrective surgery )

Ac u c u (vestibu ar schwannomas) are

benign ve y slow growing t mors of the8 cranial nervePatients sual y present wit tinnitus, ni ateralhearingoss and gait imbalance MR is the diagnostic test of

choice Treatment is radios rgery or surgical resection

U G Acute sensorineural hearing loss s ou d be eval atedand treated immediate y If the patient cannot be seenimmediately put them on prednisone(40 80mg/day)and eva ate as soon as possib e There is s ggestionthat earlier steroids may allow for a arger percentage to

ave hearing retu to them.

B Know how to perfo m t e Rinne and Weber tests todi erentiate between cond ctive and sensorine ralhearing loss

R test (Fig re I0 8 andable I0- 3) is based on t e

observation t at air-conductedsound is nor a y ouder t anbone conducted T e base oft e vibrating 256 Hz (best)

t ning fork is p aced over themastoid and the so nd of thisbone conducted hearing IS

: h

compared to t e air-cond cted sound the patient earswhen the t ning fork is placed next to the ear on t esame side

Wit no hearing loss theair conducted so ndis lo dest

• With onductivehearing oss t ebone cond ctionis louder

it sensorineu a earing ossbot air and bonecond ction are decreased but t e air cond ction isperceived as being o der

W b test consists of placing the base of a 56 or5 2Hz tuning fork on t e middle of the forehead Thepatient te s you whet er t e so nd ateralizes to oneside or stays in t e midd e.

f t e so nd is perceived as being in the middle t epatient either has no a hearing or t e earing ossis symmetrica

f t e so nd ateralizes there is either a conductive

hearing loss in the ipsilateral ear or sensorine ral lossin t e opposite ear

You can sim late t e Weber test by mming andsticking your nger in one ear (causing a conductive

earing oss) f yo r hearing is nor al t e so ndatera izes to t e p ugged-up ear

OFF C PSYC Y

E ting Di ord rA NAnorexia ne vosa syndrome s a ly begins postp be yand in early ad lt ood t a most a ways occ rs inmidd e to- pper class Caucasian women. Anorexia mayhave a genetic component (concordance in mono ygotictwins and increased risk in JS1 degree re atives)Cur ent y data donot suppor any increased incidenceof sex a abuse in anorexicsDiagnosis is clinica Typica ly diagnosis consists of acombination of the fo lowing:

Weig t osshas res ted in a weight at east5%

nder ideaPatients ave a preoccupation with food and have anintense fear of becoming fat

Table 0 - 3 : l \Ji OSII Co nd t I V<' vs lSO . f l qI ss W H' f l i . < Wt � Tes s

Ty f H Lexamples

None

Sensor neura ossin e ear)

Conduct ve loss n e ear)

Position A= Air ( .e , fork held nex o ear)Pos ion B Bone i e base on mas o d)

Sound > B

Le ear: Bo A& B decreased eq al y so s ilsound A> B

Le ear B > A

W bTun ng fork base e da midd e of fore ead

Sound doe not latera ize

a eralizes to he rig ear

Laterali e to he e ear

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What is the bes way to diagnose an acous icneuroma?

A R ne est is done The pat e ca ea theu i g fork more loud y w e i is on e bone.What does s mea ?

A Webe tes s do e on the same pa ient Hecan hear sou ds mo e oudly on t e e t s deW a does t is mean?

• young woma is b oug by e husba d orweight oss a d lack of menses or 6 mo sW a diagnosis s ou d you co sider?

ow does a orexia ne vosa d f e from bul mia?

There a e disturbances in the way body weight ands ze are exper enced. These pat ents have a d sto edself- mage and, desp te o en ext eme we ght oss,they not on y deny th nness but comp a n o fee ngfat. Th s is a "so cr te on beca se many youngindivid a s have a simi ar self-perception, althoughwithout the weight oss.Women have had bsenceof 3 or mo e consecutivemens a cyc es

In advanced cases, pat ents become emac ated,bradycard c, and hypotensive. Lab st dies showanem a hypoka em a, and hypoalbuminemia. Thesepat ents a e at sk fo sudden death romv nt lartachya rhythmi s, espec a y when efeeding.T eatment It s impor ant to establish a suppo iveadviso role with the patient Patients a e ve y res stantto psychothe apy, and outpat ent suppo t ve careo en wo ks j st as we as npat ent the apy. Explainthe dange s o sta va on, such as sudden death,and set rea st c, sho te m goa s or we ght gainAck ow edge the pat ent's pe ception and cont nual y

e nforce that yo do not et them get fat as they gainwe ght. T eatment s long-term w th equent ai resand setbacks. Ant dep essants may exacerbate seve eano exia because some are dieta y dep essants.

Cyproheptad ne, an appet te st mulant, may he pa litt e.Outcome s ve y poor n 3 %. Anorexics are more

ke y to ab se d ugs and have como bid anx ety,obsessive-comp ls ve, and/o pe sona ty diso de s.

Bulimia

B imia s the te m used or b nge eat ng o a geamounts of ood, ol owed by p rging eithe withvomit ng o w th laxatives t may be a va ant ofanorex a nervosa, and many bu m a patients havea h sto y of anorexia in thei past B mia pat entsare typ ca y 3 yea s o d (o der than ano ex a

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OFF CE P YCH TRY

pat ents). These pat ents a e us allynot < 8 % odeal we ght.

D agnosis of bu im a s c nica Typica symptoms ofb l m a inc de:

Recurrent ep sodes o binge eat ng at least peweek fo at east3 monthsSense of ack of control over eat ng behavioOver y conce ed with body we ght and shapeRegu a use o se f-ind ced vomit ng, axat ves,d et ng, fast ng, and v gorous exerc se to p eventwe ght ga n

Physica exam may show erosive skin esions on thengers where the teeth cause n y du ing attempts

to induce vom ting Denta e osionsand an ncreasein the s e of the sa iva y g and are a so seen Themost common lab abn m a e hypoka emia andmetabol c a ka osis om vom t ng and axat ve use.Th nk about b l m a ny ng pat ents p esent ng witha Ma lory Weis tear or seve e GERDT eatment s again suppor ve, w th the focus on slowlydecreasing the amo nt o ood eaten and dec eas ngthe equency o binge-eat ng episodes. T eatment, asw th anorexia, s long te m, with f equent fa ures andsetbacks. Antidep essants may he p.

Anxiet Disorders

Anx ety diso de s a e class ed nwaysI) Gene a zed anx ety diso de , wh ch is chron c and

ow g adePan c diso de , with b e and d amatic panic attacks

Generalized a xiet disorder: DSM- V d agnosticc iter a incl de anxiety worry abo t seve a activitieso events that s mo e than what is easonable for theevents for 2 6 months G ne li d anxiety disorde

s assoc ated w th substance ab se and other psych at icdiagnoses obsess ve compu s ve diso der, dep ess on,pan c diso de , and socia phob as. Somatic complaintsa e common (fatigue memo y p oblems, tens on, and

nab y to s eep).Treat w thbeh v orathe apy K ow that seve a br eencourag ng follow- p v s ts to a pr mary ca e physc an has the same e ect as p esc ib ng ben odia epines.Patients who req e mo e than behav ora therapycan be t eated withSS s as the 15 ne o the apy.B n d epines(BDZs can be conside ed SSR s a e

ne ect ve. Ab se o BDZs s very ow n this pat entpopu at on.B sp oneis se l as a BDZ s bst tute.Chronic treatment is s ally req i ed

Panic disorder is d agnosed when4 attacks haveoccur ed w thinI month, or 1 or mo e a acks are olowed by I month of ntense fea of anothe a ack.These pat ents o en have phob c avoidances of placesor sit at ons assoc ated w th attacks Secondary ma ordep ess on s a common comp icat on

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1�2 OFFICE PSYCH ATR

Treatment of panic disorder is usua y wi hSSR s andanxioly ics, such as benzodia epines or buspirone HC .The op mal trea ment is anSSRI , wi h on y sho t-termuse o ben od a ep ne. Psychotherapy may have somebene . Longer act ng ben od a epines (e.g., c onazepam) are pre erred over a pra o am, due to a pra o am'spotent a for abuse and higher oxici y in overdose

Bipolar D sorder

Bipo ar disorder is characterized as a major depressionwi h a leas episode o man a or hypomania. Bipolardisorder is rther ca egori ed based on severi y as ypel

(presence o psychosis, requent need for emergencydepa tment visi s and hospi aliza ions, poor overall

nctioning) or type II (m der leve o dys nct on).Most man c pat ents are euphoric and have in ated seles eem, decreased need or s eep, and pressured speechHyper-sexuali y and hyper-re igiosity are common, asis overspending. Some pa ents are just ri able, possibly also paranoid this is ermed dysphoric man a.

sychotic symp oms are common during manic episodes.

While manic episodes can be qui e dramatic, mosd sabili y assoc a ed with bipolar disorder s ems omdepression. B polar pat ents have high ra es of suic de,anx ety d sorders, and substance abuse.

Treatmen of bipolar disorder is usually accompl shedw th mood stab i ingmedica ions such as ant psycho ics (que iapine, olan apine), thium, andsei uremedications (divalproex sodium, amo r gine, carbama epine), ei her a one, or n combina ion An idepressantmedications are genera y not he p in pa ients w thbipolar disorder. An idepressants also carry he risk o"swi ch ng the pat ent into a manic phase of ness.

The a yp ca an ipsycho cs (e g., o an apine) do notappear to cause ard ve dysk nesia associa ed w th o deran ipsychot cs such as haloperido The a yp cal dr gsare associa ed wi h weigh gain, diabe es, and hyper pidemia. Know ha many of he antiepi ep c dr gs areassoc ated wi h increased risk o suicide. A so know thathia de d ure cs, ACE inh bi ors, and NSAI s ncreasethe ithium eve . Refrac o y b po ar d sorder s o en

reated with electroconvulsive therapy.

Depress onDepression s discussed brie y under Geria r cs (seepage 0 19). O course, h s does not mean i occurs onlyin the e derly, bu he genera population has the same

reatment options as he e derly.

For m d- o-moderate depress on the cu rent gu del nesrecommend psycho herapy and/or med ca ions for anini ial 2-week period I psychotherapy is ried a oneand there is no response, hen de n te y begin med ca

ions. A er you s ar meds, he guide nes say to moni orthe patien every 1 2 weeks by phone or o ce visi

or he ini ial 8 weeks. xpect a 56% response ra e at

2 weeks 8 % a 4 weeks, and 90% a 6 weeks. I here

s no response a 8 2 weeks on max mum doses ofhe chosen med cation, switch to a di eren d g or

augmen w th buprop on or busp rone. Thyroid augmen a ion is con roversial and no included in cu rentguidelines. Treat for 6 9 months for ini ial herapy, wi ha 2 week aper a er improvement. Ongoing reatmenw th an idepressant med cat ons s also very acceptab e

n pat ents w th recu ent depress on.

Med cat on Compl cationsN u g y (NMS) is an

diosyncra ic response o po ent neuro eptics, resu tingin au onom c dys nc ion, ex rapy am da symptoms,and high ever. The ever may reach I06° The neuro ept cs most common y invo ved areha oper dol,piperaz ne, pheno h az nes, and thioth xene MS is

hought o be due o a deple on of dopam ne t persis sor up o0 days a er the d g s stopped Treatmen s to

s op he causa ve d g and cool down he pat ent. G veoral dopam ne agonis s also to coun eract he dep et on.Bromocr p ine s he dr g o choice, but you may a so useamantadine and dan o ene.

S y (SS): One o the nct ons ofseroton n n the bra n is to modu ate body temperature.Sero onin d ugs can cause derangemen n thermoregula on a condi on e med seroton n syndrome.Think abou n pa ien s who are on a leastI seroton ndrug, bu t more o en occurs in pat en s on 2 or moreserotonerg c agen s Onset is genera ly wi h n 6 hours ostar ng the new or addit ona drug. Sero on n syndromecan have he presentation of SS I overdose.

Cl n ca presen a on s anx ety, d sor entat on, swea ng,tachycard a, hype tension, vomiting, and dia hea.Hype therm a can be marked. xam may show r gid ty,hyperre exia, and remors. This condi on ooks

ike neuro ep ic ma gnant synd ome, toxici y romanticho inerg cs, or overdose of sympathomime ics.Seroton n syndrome s a clinical d agnosis. o lab tescon ms it onspeci c ndings such as rhabdomyolysis and me abo ic ac dosis may be seen.

Treat by discont nu ng the serotonergic d g and g vingsupport ve care, ncluding cardiac moni oring. B Zsare he p or he anx ety and tachycard a The syn

drome usua y reso ves in 24 hours. The h pe therm ao en resul s om musc e rigidit ; so, very h pe therm c patients typ ca y require in uba on and para ys sCyproheptadine is a sero onin antagonis tha is g ven nsevere cases

erentia ing NMS and SS based on symptoms sd cu t because they present s m ar y w th au onomicchanges, hype the mia, and menta changes I s

mportan o know tha b ood tests easi y d stinguishbetween hem MS has increased CK, L H , AST(SGOT), and WBCs along w th a ow serum iron. No ma labs are o en seen with seroton n syndrome.

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ui

Des ribe a patient w th neu olepti malignantsynd ome

Def ne he Phi adelph a h omosomeR iscon n a on s n rom : It is very mpo an

to slowly titrate patien s o SSR!s. I is gene ally doneover seve a months, bu some pa en s requ e m ch

onge . f done too qu ckly, pa en s can develop ghheadedness, ve igo,shock-like pa esthesias, visualsymptoms, anxiety, nsomn a, and gastroin es nal symp

oms ( N/D). D agnos s s usua ly easy w h he his oryof recen SSRI dosage dec ease. T eatmen is o boost

he d g a e and, once s ab e, es a the ape ng a aslowe pace.

GENET S

His ocompa ibi ity an gens a e the ant gens involvedin gra ejection. hese are the ma kers that identi"se ' vs "non se ' fo the body s immune su ve ancesystem Many of the h stocompa bility genes a e c oselygro ped on chromosome 6, and th s a ea s ca ed themajo h stocompatib y comp ex (MHC). he h manMHC is e med HLAGene a ev ew of t ansc p ion and rans a ion The D Ahas coding sequences cal edexons, separa ed by ve y

sma noncod ng sequences ca edin ons. he fu gene( n ons+ exons) s t ansc bed by D A dependen R Apo yme ase into R A. he n ons a e then sp ced out ofthe R A before it leaves the n c e s, the eby forming themessenge R A (mR A). he mR A is then t ans atedinto protein: Each 3-base sequence compr ses acodon,wh ch de e m nes the am no acid ha at aches when

t is t ans a ed.Po n m tations are a change to a single base, and canres n eithe amissense o a nonsense m a ion.Missense m tat on s when a poin m at on causes adi e ent am no acid to be produced, as nSS (va neis subst t ed fo g utam c ac d). onsense mu at onproduces astop codon, wh ch stops he ranslation

ns on and deletion mutat ons: hesecause a "f amesh , which ca ses an abno ma p o e n f om hat poin

o he endpl c ng mu a ons resu om a poin m a on ahe area de ning the nct on between the intron andhe exon. h s es s in dysf nctiona pro eins.Beta

tha assemiaso en a e ca sed by sp icing m ta ons.C ues for autosoma dominan d sease:

Vertica transm ssion (invo ving seve a gene a ions).Risk o each child of a ected ndiv d a is50%.Ma e-male ansmission s obse ved

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GENETICS

o ma pa en s do no ransm he a ( nless a newmuta on occu s).

Cl es for X- nked nhe itance:nher ance of ai s fathe to da ghte all

daugh e s of a ected males are ca ers; no sonsof he fa he are a ected.

• If mo he s a "car ier, she has a50% iskoftransmitting the gene to her sons, and each son witha resu ing abnormal X ch omosome would hereforebe a ec ed. A "car ier mothe a so has a0% isk of

ansm ng he gene o he daugh e s who, n u ,become na ectedca r e s

Acq redchromosomal abno alit es A v al genehat can t ansfo m D A s cal ed a viraoncogene. he

h man ch omosomes a so conta n genes that a e assoc ated w h mal gnancy, cal ed cel u ar oncogenes oproto oncogenes. hese p o o-oncogenes p obably havesometh ng to do w h embryonal development and are

othe w se si ent, b t, w th ce ain ch omosoma earangement, hey become act ve. In bo h Ph ade ph ach omosome and B k s, he pro o oncogene becomesactive by anacq red rec procal t anslocation.

he hiladelph a ( hI) ch omosome t(9 22)was the51 chromosoma abnor a y found to be assoc ated

w h ma gnancy ( s fo nd n CML). he sw chca ses the c ABL"pro o-oncogene to be moved f omch omosome 9 o .Burkit lymphoma and its eukemic ana og, ALL (FABtype 3), have a ecip oca anslocation hat sw chesthe p oto-oncogene c C' on chromosome 8 o

ch omosome 14, , o : i e , t(8 1 ), t(8 ), o (8:2).Chromosome has the heavy cha n oc s he lambdagh chain oc s is on ch omosome , and the kappa

l ght cha n ocus is on ch omosome .Many e kemia and ymphoma pa ents have ach omosomal abno ma y. So id umo sa e yhaveabno mal ch omosomes.

WOMEN S HE TH

FF R

he fo ow ng is a compi a on of every hing w tenon p egnancy in hese Co e Cu ric lum books p usmo e h s compila ion makes easier to ev ewpregnancy as a spec c op c. Beca se his s a veryimpor an top c, cons de the en i e sect on h gh ghted

Dr gs n Pr gnanc

Dr g safe y in p egnancy s ca ego zed as fol owsA = We con ol ed human s d es have fa led o showrisk of a dr g o he fetus. Ve y few d ugs mee hiscategory. xamples include evothy ox ne, magnes ums lfate, and prenatal vitamins (of co rse )

1 - 3



10- WOM N S H AL

B = Animal reproduction s udies have not demonstrateda risk o the fe us, and t ere are no adequate rials inpregnan women. Examp es inc ude ace aminophen,rani idine, me for in, insulins, enoxapa n, andmany antibiotics.C = Some adverse effec in anima s dies but here areno control ed s dies in women Use on y if po entialbene outweig s poten ial risk to fet s Examplesincl de unfrac ionated heparin, oseltamivir, and manyan idepressants ( oxe ine, citalopram, b propion)D = Positive evidence of uman fe a risk, b maybe accep ab e despi e e risk (e.g. ife-t reateningil ness). Examp es incl de aspirin and NSA Ds, mostseizure medica ions (pheny oin carbama epine,p enobarbita , va proa e ) ACE inhibitors, t iazides,dia epam, li ium paroxetine, e racyc ine, andaminoglycosidesX = ca ses fetal abnormalities Do no se Examp esincl de iso re inoin, warfarin, halidomide DES,simvas a in and OCPsKeep in mind a pregnant women are genera lyexcl ded from mos ria s of medica ions, soinformation is o en unavai able regarding he safe yof a par ic lar agen . A 200I study no ed t a t ere isins cien information on 90% of drugs that wereapproved by t e FDA over he prior 20 years. Bo tom

ine: Yo must caref l y weigh t e risks and bene ts ofa medica ions during pregnancy from he s andpointof bo t e fe us and t e mo her.A so knowTab I -14 Mos Asked-Abo t Drugsin Pregnancy.

Table 0- 4: o ke bou D ug n egna cy

Do Not Use

ACE inhibito s ARBs, nitrop uss de

C pro oxac n doxycyc inetet acycline podophyl in metronidazole in sttrimeste

Most aminoglycosides

, meth ma o e

Most antihistam nes

Warfarin

Ok y to Use

C onid e, labeta o calcium ch n el b ke s

ials d goxinve apami procai amide

Su fasa az ne beta-lactams e yth omycazithromyc namphoter c n B

Gentamicin

PTU

Chlo pheniramine

Hepa n

Gastroente ology

Endosc pic W up

Esop agogastrod odenoscopy (EG ) is the option ofchoice for work p of many G diseases d ring pregnancyin order o imi or prec de t e use of radia ion.Endoscopic ultrasonograp y (EUS) is norma ly sedin eva ua ing pancreatic diseases is a so sed inbilia y duct disease when an ERCP wo ld no mal y beused b is contraindica ed (e g , ga lstone pancreatitisand pregnancy)

GE Ref ux i

LES pressure isdecreasedby progesterone (pregnancyincreases GE re x) as we l as chocolate, smoking, andsome medica ions, especia ly hose wit an icho inergicprope ties. Ranitidine, famotidine, and lansoprazoleare category B for refractory symptoms. Avoid bism hs bsa icylate d e to e sa icyla e exposure

C hn Di ease Me

FDA risk ca egory B (no evidence of risk in umans)• Me ronidazole (a t ough because of lack of da a, it

is contraindicated in1 rimes er)Prednisone

• Sulfasa a ineesalamine

Cons ipa i n

e a ered proges erone and estrogen levels are t eprobable cause of constipa ion inpregnancy

Panc ea i i

Cu len signis a so seen wi h intra peri oneal b eeding(especia ly r p red ec opic pregnancy), and er signis seen wi h o her ca ses of re roperi onea bleeding.

Liver Disea e

Un i e epati is A, epatitis E car es ave y high risforminan hepati is in t e3'd trimes er of pregnancy

wit a 20% fata ity ra e.1 rimes er Hyperemesis gravidar m can cause N/Vvo ume dep e ion, and mild increase in AS and AL2" rimes er bes ime for surgery for severelysymptomatic gallstone patients3rd rimes er

emember t a epatitis E can ca se f minanhepati is in t e3 d rimes er of pregnancy with a20% fa ality rate. e scenario presen ed may be apregnan woman rave ing o Sout eas Asia whocontracts hepa i is E (fecaloral transmission ike

epa i is A).

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ui• Know Table 10 -14 !

• Are ACE inh to s safe p egnancy?

• Du ng wha mes er s me on dazo econ aind ca ed?

• A pregnan woma has a DV . Wha common yused a ticoagu an s co traind cated?

• Is a S3 ga op o ma in pregnan wome ?• Is e ec ica cardioversio poss e du ng

p egna cy?• What do you have to ru e ou in a p egnan

pat ent who p esen s w th ew-onset a iafib atio and pu mona y edema?

Fatty iver of pregnancyis a very serious conditionin which the e ismic ovesicula fat deposition inthe ive (as in Reye synd ome), with only modeste evation of AST/ALT/Bi i. t occ s in the3'd

t imester and is associated with encephalopathy,hypog ycemia again like Reye synd ome),preec ampsia, panc eatitis, DIC and renafai u e. Ear y de ivery is requi ed.Intrahepatic cholestasis of pregnancy causes itchingand inc eased a k phos, bi i, AST, and A T.

Pulmona Medicine

Asthm Treatme t

Budesonide is p eferred in pregnancy, but a CS maybe used.

Tuberculosis reatme t

Do not se PZA in pregnancy because it causes birthdefects. St eptomycin is a so avoided.

ulmo ary Embolism and DVT Tre me t

The isk of venous th omboembo ism is e evated du ingpregnancy and postpa t m. P egnancy is gene ally

considered an abso ute cont aindication for wa fa in.Warfarin is a small molecule that crosses the p acentaand is a known te atogen. Unfractionated heparin is argeand does not cross the p acenta barrier, b t poses chalenges such as pa enteral dosing and need fo f eq entmonitoring. ow-mo ecu ar-weight heparins LMWH)can be se f-administe ed and eq i e ittle or no monito ing. Enoxaparin is genera ly conside ed to be safe forboth the mother and fetus in p egnancy category B).The 2012 American Co ege of Chest Physicians guide

ines ecommends the use of MWH du ing all phasesof pregnancy for prevention and treatment of veno sthromboembo ism in women with VTE or at e evated

isk e g , anti phospholipid antibody synd ome)

© 2014 MedStudy

WO EN ' HEALTH

Cardiology

Normal Fi di gs in Pregna t Wome

S3 AnS3 is no maand common y heard in chi dren andin pe sons with high cardiac o tput, s ch aspregnantwomen. S3 is virt a lya waysabno ma in nonp egnantpatients> 40 yea s o d.

Most p egnant women experience some pedal edemaow mu m rs and S3 gallops) a e also common, and

the jugu a venous pressu e inc eases

Abnorma C rdiac Issues in reg a cy

Abso ute cont aindications to p egnancy includep lmona y ar e ia hyper ensionand Eisenmengesyndrome. In secund m ASD ao tic stenosis, and di atedca diomyopathy the patient m st be close y watched. naor ic stenosis and di ated cardiomyopathy, patients areno ma y kept at bedrest. Sec nd m ASD patients areusua y not at isk for ca diac decompensation,un essthey deve opatria bri ation. Cyanotic hea t disease isthe worst isk.

rial fi rilla ion ike secundum ASD above, the initiapresentation of mitral stenosis MS) in a pregnant patientmay be new-onset atrial bril ation and pu mona yedema. The inc eased b ood vo ume in p egnancy cancause a p ecipitous exacerbation of MS so considert eating a pregnant S patients with digo in. E ect icaca diove sion is not cont aindicated in p egnancy.

Remember: n a p egnant patient p esenting withnew onset at ia b illation and p monary edema yoneed to r e out bothmitra stenosisand sec nd mASD.

o c dissec on: 3 trimeste of p egnancy, systemichype tension, cystic media nec osis, bic spid ao ticva ve, and coarctation of the ao a a e p edisposingfacto s.

alve surge y Po cine valves vs. mechanical valves)a e o en given to women of chi dbearing age toprec udethe use of anticoagu ants d ring p egnancy.

The e is recent controve sy abo t use of WH vs.warfarin fo anticoagulation with prosthetic valvesd ring pregnancy. Most now recommend discussionwith the woman abo t the isks and bene ts to he

and the unbo chi d of using wa fa in less risk ofth ombosis fo he ; inc eased risk of defects fo theinfant) vs MWH inc eased isk of th ombosis fothe mothe ; dec eased risk of defects for the infant).Long-te m use of heparin in p egnancy is associated withosteopo osis, and many ecommend increased RDAsfo calci m.

ate al ube ainfection d ring pregnancy is acommon cause of patent duct s ar erios s PDA),s p avalvu a aor ic stenosis, branch pulmonic stenosis

"periphe a PS ), and other congenita cardiac defects.

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10 WOM N'S H ALT

Infectious Disease

Bacterial nfec n

UTis: Streptococcus agalactiae and E. coli. Treat w thamp c ll n, cephalex n o n tro u anto n. C p o oxac n

snot g ven to p egnant women due to conce s of jo ntp oblems develop ng n the fet sListeria monocytogenes nfect ons occ most n thosew thdec easedcell lar mm n ty synd omes l ke AIDS,lymphoma, and le kem a but they also are seen nneonates the e derly andp egnantwomen The mostcommon p esentat on s n the 3' t meste and p esentsas a u-l ke llness and s p cked p by blood c lt reAlso s spect th s n a p egnant woman w th aUTI andnegat ve r ne cult eStreptococcus agalactiae (gro p B) s also a ca se ofpostpa t m endometr t s and bacte em a So suspect th s

n any woman who develops apostpartum ever!App ox mate y 5% of p egnant women haveChlamydiatrachoma/is n the r gen tal t acts; ant b ot c o ntment n

n ants eyes at b h doesnotp event th s co unct v t s(Th s o ntmentIS g ven only fo gonococcacon unct v t s )Gono hea s more l kely to d ssem nate n p egnantwomen The newborn s at sk for gonococcalconj nct v t s.Asymptomat c bacte r asho dbe t eated npregnantwomen (1/3 go on to pyelonephr t s!),neutropen cpat ents, andt ansp antpat ents

Paras c D seasToxoplasma gondii s se ous n the mmunocompetentonly facqu ed du ngpregnancy when t can ca secongen tal toxop asmos s (result ng n nte ectual d sab l ty and cho o et n t s) The fetus s more l kely tohave a congen tal nfect on f the d sease s acqu ed

ate n pregnancy ( 5% f tr mester 70% 3' trmeste ) P ev ous n ect on w th toxoplasmos s befo ep egnancy s gene a y not a conce n p egnancy

Vira Infec ons

ses w th the g eatest teratogen c potent al are CMva ce a zoste herpes s mplex, and bel a Th s sespec a ly e acq ed n theI st r mesterCMV s ub qu to sand the most common ca se ofcongen ta v ral n ect on 2% o all newbo shave the n ect onin utero, b t only a ew have anyabno mal t es These abnorma t es wh ch ange f omm d ne rolog c problems to m c ocephaly us allyocc r n mothe s w th a pr mary CMV n ect on.R be a s Ge an meas es(ssRNA v rus) I t sacqu red by a pregnant pat ent n theI tr mester there san 80% chance that the baby has congen tal defects usually seve e De ects ncl de cata acts, hea t p ob ems,

ntellectual d sab l and feta death It s d agnosed n

the mother by the hemagg t nat on nh b t on test Ith s test s negat ve n a new y exposed p egnant pat ent,

epeat t n 3 weeks (a er nc bat on per od) be o emak ng any dec s ons If t s then pos t ve, a the apeutabo t on sho d be cons dered You can d agnose ubel aprenata y by nd ng ube aIgM ant body n etalblood. mmune globul n doesnot p event the n ect onbut tmay g ve some fetal p otect on n the pat ent whodec nes the apeut c abo onVa ice a-zoste n ect on has as ghtr sk of ca s ngcongen tal defects The p egnant woman w th ch ckenpox has aI0% chance of develop ng severe pne mon aHIV: There s a mother to et s transm ss on sk o30% Th s s ed ced to< l% w th 3 dr g ant ret ov raltherapy (ART) So ens re that all pregnant women w thH V rece ve ART

F nga Infecti ns

H gh dose (400 800 mg/day) conazo e s nowcont a nd cated n p egnancy (catego y D) because oassoc ated abno mal t es o the cran um, ace bones,and hea t S ng e, ow dose uconazo e ( 50 mg to t eyeast n ect on rema ns catego y C

Neph o ogy

Du ngp egnancy, the e sncreasedcalc m abso pt onand excret on because theI ,25 ( H) D s> 2x no maEven so, frequency o rena stones s the same as nthe nonp egnant pat ent The ur nary tract o the pregnant pat ent s d lated and stones do deve op, mos

pass eas ly!There a e 4 catego es o HTN n p egnancyI) Chron c HTN: preex st ng HTN or HTN be o e

20 week o gestat on2) P eec amps a HTN+ prote nur a a e 20 week of

gestat on n woman w th no h story o HTN3) Preeclamps a that compl cates chron c hype ens on

wo sen ng HTNprote nu a a e 20 week o ges at onn a woman w th h sto y of controlled, ch on c HTN

4) Gestat ona HTN occurs a er 20 week and hasno p ote nur a

Pe the JNC epo t the stages of HTN do not apply np egnancy. HTN n pregnancy s de ned as m ld f BP s140 59 /90 09 and severe f BP: 160/II 0Ec ampsia s de ned as grand malse z res n a womanw th preeclamps a o gestat ona HTN

eec ampsia (o p egnancy nd ced hype ens on)more commonly occ rs n p m g av das us al y n the3 t mester, and esolves a er de very It s de ned aSBP> 40or DBP> 90 and prote n r a> 300 mg n24 hou s n a pregnant woman > 20 weeks gestat onThe e evated b ood p essure must be s sta ned w th atleast 2 ead ngs at east 6 ho rs apart.

© 2014 MedStu y - Piease Report Copyr ght Inf ngeme t o copyr g t@me y. om





• Should asympto a ic bacter u ia in a pregnant woman be t eated?

What s he problem w th ubella being acqu edin he 1st tr mes er?• Wha is the ma e na - o-fetal ransmiss on rate

of HIV withou ART? W th AR ?• How do you make the d agnosis o

p eec ampsia?• What a e he symptoms that may occu w h

preec ampsia?

Preec ampsia may be symptomatic o asymptoma ic(both have HTN and p oteinuria). Symptoms of preec ampsia can be mild (headache, vision changes) osevere (seizu es, low pla elets s oke or int acereb alhemo hage, pulmona y edema, hepa ic and/o enalfai u e, and p acen a ab uption)HEL P syndrome ispreeclampsia wi helevate live en ymes,low p a e e s,and microangiopa i hemo y ic anemia

Treat hypertension in n ( egardless of category) to preven stroke T eatment of he BP doesnot a ect the outcome of preeclampsia (weird . but t ue) ow

hat pregnant women wi h hype tension are a isk foadverse fetal ou comes if blood p essure is driven oolow This is one pa ient g oup in whom we ac ually have higher BP goals , no ower! EachI0 mmHg reduction in

SBP is associa ed with a reduc ion in feta bir hweighFo women with p eec ampsia, recommendations are to s ar reatmen if

1) symptoms are p esen or2) in asymptoma ic women when SBP 150 or DBP2

95 (al hough these speci c numbers are controversial),with a ta ge BP goal of< 130 150/80 100 mmHg

Bedrest is sti recommended for asymp omatic or mildpreec ampsia (especially if before 34 weeks ges a tion) although here are no clinica ria s o sugges ia ects ou come Fo severe, sy p omatic preec ampsiade ni ive t eatment is delivery U ima ely, ca e p oviders walk a ne ine be ween de ive ing a baby tooearly o relieve p eeclampsia and allowing fo ongegesta iona deve opmentWomen with controlled, chronic HTN (BP < 20/80)a e takenof BP meds, with frequent BP and symptommonito ing Meds are reinstitu ed for same BP asmentioned above for p eec ampsia (SBP 150 o BP

95), with targe of< 130 150/80 100 mmHgAny p egnancy complicated by ma ignant HTN oseve e, symptoma ic preeclampsia is rea ed wi h parenteral an ihyper ensives labetalo is the preferreddrug Hydralazine and CCBs a e also some imes used,but here are less data fo these dr gs Know tha he

© 20 4 MedS udy

WO EN' HEALTH

following an ihype ensives are : AC s/ARBs/ enin inhibito s (tera ogenic) and ni oprusside(cyanide poisoning in he baby)O al agents used o rea chronic, asymp omatic preeclampsia gestationa hyper ension and chronichype ension in pregnancy include abetalo (o he

beta-blockers have ess desi able e ec s, so labe a olis preferred) me hyldopa, extended re ease ifedipine,and hiazide diu etics (but wa ch for signs/symp oms ofvo ume contrac ion).

Be awa e tha ec ampsia can occur postpa um,a hough ra ely A woman who presen s hyper ensivewi h genera ized seizu es within 12 weeks a er delive yshou d be conside ed eclamp icS E with lupus nephritis: If he disease has beenin remission, here is a 90% chance of a successp egnancy If it up during p egnancy, however,25% of fe uses die, usually from he upus an icoagu ant

antibody causing h ombotic even sP egnancy andch onic renal failure: If the crea inineis < 2 and the pa ien with chronic kidney disease is nothyper ensive, there isnot an inc eased r sk of abo ionor ma fo mation, and here is inc ease in he a e ofprogression of the ena disease The eis an inc eased

isk of p egnancy induced hype ensionAs enalfailu ep ogresses chanceofp egnancyd .

ialysis patients become pregnan In stab erenal tr splant patien s, he outcome of p egnancy isusually great!

EndocrinologyThe S Osmostat

Pregnan women inc ease hei ci cula ing b ood vo umeby almost 50% This is accomp ished by resetting the osmotic set point causing A H o be released at a

owe osmo ality

P o act L vels

Es rogen di ectly h dopamine ou ow, soP L evels also can be seen in pregnancy and in pa ients

aking es ogen

P tu a A e o a

Abou 1/3 of pi ui ary mac oadenomas, some ofwhich cause inc eased pro actin evels,enlarge du ingp egnancy f the umor enlarges enough o causesymp oms bromo riptine can be restar ed (or surgery, ifvision is hrea ened) B omocrip ine is almost assured ysafe in pregnancy, and cabe goline is p obably also safe(less experience) Bu nei her drug is F A approved for

his use

10-57



1 WOMEN'S HEALTH

Thyroid Disease

One can usua y safely give 3treatment to hype thyroidpat ents, but t snot sa e to give t to eitherp gnantpat ents or patients withsevere hype thyroidism.

In pregnancy, surge y may be indicated to treat Gravesdisea e in pat ents with an assoc ated cold nodu e orrelapse a er rad at on, and in some young patients witha arge go ter

A ays treat pregnant hypothyroid patients and fol owtheir TSH levels dur ng pregnancy-because the rrequirements increase (The dose needs to be ncrea edto 50% more than the prepregnancy dose ) Failure totreat mate a hypothyroidism dur ng pregnancy canadversely a ect the baby

Pregnancy in Patients with Polycystic Ovaries

Treatment of PCOS rst ncludes educat on about

weight loss and then is dependent on the degree ohyperandrogenism and hether pregnancy is desired:• No hirsutis and no des re or pregnancy Prescr be

medroxyprogesterone every 1- 3 months to nducewithdrawal bleeding and to protect the endometr umf om hyperplasia.H rsuteand no desire for pregnancy: Prescribecombined es ogen progesterone ora contracept ves;h rsute symptoms a so can be ameliorated w thdepi ator es/shav ng. An insu n sensit zer, such asmetformin or a thia olid nedione, may also confer ave y modest additiona bene t on h rsutism

• Hirsute and desires pregnancy nduce ovulat on w thclom phene w th or ithout metformin

Pregnancy a so increases insulin res stance due toplacental hormones.

Diabetes in Pregnancy

With pregnancy, str ct diabetic control even be oreconception is impo ant Maintain PG< 00 mg/dL andA Ic 7%. Before concept on, contro of b ood g ucosereduces eta ma ormation and during pregnancy,it reduces m scarriages, etal anomalies/death, andnewbo prob ems Tight glycem c con o decreases

the risk of macrosom a (bi th we ght2

9 - 1 0 b) andshoulder dystocia in the newbo

During pregnancy, insul n requirements increase basedon gestationa age of the fetus Th s increased requirement s gone ediate y a er de very so antic patea reduct on in nsu n dosage o at east50% postpartum and obse ve the patient care lly the day a erdelive y Metform n and nsulins are the drugs ofchoice for managing DM n pregnancy [Kno ] Thesemed cat ons commonly employed in diabet c management are con n i ated n pregnancy

St t nsand A E s R s shou d be discontinuede o pregnancy

Many oral hypoglycem cs are catego y C

Hema o ogy I n o og

e de c ency is commonly seenm pregnant omenwho have had no prenata care

Breast cancer rates increase with early menarche, latemenopause, and ate stpregnancy

Neuro ogy

Migraine

Do not use trip tans n pregnancy, because of the r sk onduc ng schemia

Pseudot mor Cerebri

Pseudotumor cerebri usually occurs n premenopausalobese women (90%) and may occur during pregnancy

Seizures During Pregnancy

The background risk for b r h de ects s2 3% Thegoa of treatment during pregnancy is to contro theseizures-uncontro ed se ures can cause placentaabruption and early abor and premature delive y henthe risk of teratogenici y s compared to the prob emsthat seizures cause during pregnancy, the risk ofuncontrolled seizures s greater !

Maintain a pregnant woman on monotherapy andat the o est dose of medication possib e r sk omalformations ncreases as each drug s added.

There is no "safe ant epileptic dr g (AED), butvalproate s more like y to cause neural tube defects thanother common y used ant epilept cs.The teratogen c r sk o AEDs isdecreased by o c ac d,and a women of childbear ng age on ant epileptic d gsshou d take high dose folate dai y-some recommend4 mg/day for these high risk pat ents.

Phys cians genera ly give prophylact cvita in K dur ngthe last month of pregnancy n patients on AEDs Th s

s based on repo ts nd cating ncreased bleed ng inpatients on AEDs ost recent guide ines (A N AES2009 say there is not enough ev dence to recommend

or or aga nst use o prophy actic v tamin K

Carpal T nnel

now that pregnancy can cause an acute presentation ocarpal tunnel syndrome (CTS) that ypically imp ovesa er del ve y Splints are the best treatment for thispatient group

Rheumato ogy

ethotre ate use De n te contra nd cat ons ncludepree isting rena or iver disease (e g , HBV, HCV,a coho abuse) and pregnancy.

e uno ide use: contraind cated n pregnancy

© 2014 MedStudy-Piease Report Co yr gh Infr gement o co y g t@medstudy. om





ui

A pregnant woman has Graves disease. Whatcan you do to t eat he ?

o What s a common mine al def ciency npregnant women who have not had prenatacare?

o True or alse? DUB usua y does not requi e anyworkup

SLE and Pregnancy

SSA (Ro)/SSB (La) ant bod es are associated withneonatal lup s and congenita hea block Gene al

n e s sneed oknow abou h s r sk when co nse ngwomen wi h lup s about p egnancyLupus patients have ah gher inc dence of fa edpregnanc es R sk of pregnancy compl ca ons ( areor fetal problems) s much g eate f disease sact ve(espec a y rena man fes a ionsor if the mothe hasant -dsDNA o antiphospho ip d antibod es (APS)P egnant women w h APS and a histo y of rec r enm scarriages can be t eated w h hepa ns (low mo ecu

ar weight or nfrac onated) p us low dose aspi n todecrease nc dence of m scarriage Hear block s a ngin the 3' t imeste can be seen n bab es of mo he s withSLE who have SSA (Ro) SSB (La) ant bod es.If an SLE pat ent wishes to become pregnant and hashad a recent up s are,con nuehe g ucoco icoids.Measu e base ne complements, an dsDNA, SSASSB, and a 24-ho r rine protein before o ve y earlyin the pregnancy. F a es du ng pregnancy are managed with co cos ero ds.Refe p egnant women w hsystemic p s o a high isk obstet c an (and pediat iccard o ogist, f app opriate).

Avascu ar Necrosis of the Hip

Causes nc ude pregnancy, stero d use, s ck e celd sease, H VIAIDS, a coho ism, tra ma, Gaucherd sease, and hype coagu ab e states

De mat l yTreatment of Acne

Acne is mo e p ono nced in p egnancy due to nc easesn p oges erone. T ea men s foc sed on safer topical

agents (ery hromyc n, c ndamycin, and aze a c ac d) andavoidance of othe agents which a e known o be ha m

( sot etino n, azarotene, tetracyc ine, m nocycline). Top cal benzoy perox de is ca ego y C.

© 2014 MedStudy

WO EN ' H LT

e g and Imm n l gy

Pe sisten nasal conges ion may accompany pregnancy(rh nit s of p egnancy). It is gene a ly ea ed w hnon pha macologic measu es. Intranasa s e o ds havenot been shown o be e ec ive

OFF CE GYNECOLOGYO ce gyneco ogy has been partia y covered in p evio ssec ions Espec a y eview gynecologic nfec ons inInfec ous D sease, Book. Pap smear, ovar an cancer,and b east cancer are cove ed in Onco ogy, Book4. Os eopo osis s disc ssed earlier n this sect onAmenorrhea s d scussed n Endoc no ogy, Book 4

Postmenopausa B eeding

A woman shou d unde goendome ria assessment(biopsy or ansvagina u trasound) if she haspostmenopausal b eed ng:

In the absence of HRT herapyA e she has been on combined HRTcont nuous y fo1 yea witho bleedingAt an nexpec ed me d ring cyclic rep acement

Treatment Recommendations for MenopausaSymptoms

Vasomotor ns ab i y(ho ashes) shor erm est ogenhe apy ( f no h story of b east cancer or ca diovasc ar

disease) Mu t ple o her agen s have proven e cacyinc ud ng SSR s, SNRJs, and gabapen n.

Urogen a at ophy vag nal est ogen for moderate toseve e symp oms; mo s u ze s and l b cants fo mildsymptoms

Dysfunctiona Uterine Bleeding ( UB)

D B efers to excessive b eed ng due to pers stentanov a on n a ep od ct ve age woman w th ovar escapable of p oduc ng es rogen. The pat ent s per ods maybe oo equen , too ong, or wi h oo heavy of a ow.D B is a diagnos s of exc usion Therea many causes,

nc ud ng hypothy o d sm, ver d sease, rena d sease,coagulopath es pregnancy comp icat ons, anatomic

es ons, and dr gs, among o hers. T ea men foyoungwomen w h D B us a y cons stsof o a es ogen p ogestin p epa ations Oral cont acep

ives containing 35 50 g of ethiny est adiol a e o enused. 4 tablets a day a e given n t a ly h s nc easesbleed ng fo 1 2 days and genera y s ops the b eed ng

n 3 days. The pat ent s then given 2 pills per day fo20 mo e days W thd awa bleeding then occu s w hin2 5 days a e end ng eatment. This hormonal the apy

s given fo 2 3 mo e cyc es, usingI p ll pe day, andhen stopped

10-59



1� FOR URTHER RE D NG

Premenstrual Syndrome (PMS

PMS is a g oup of symptoms which most o en stardu ng the late utea phase and are gone within- dayso the onset of menses. The biochemistry o thisdys nction has not been estab ished.

No single trea ment has been proven e ective, but the

cause may be mu tifactor a so there are many avenueso treatment to explore with each patient You canachieve ovulato y suppression with ora contraceptivesThese patients may a so respond we l to the newermini-pi which contains on y progestin. Other simi

ar options include Depo P overa® and Norp ant . Oralnatura progesterone has been used with varying success

Various dietary changes he p some patients such asavoiding ca eine sa t sugar alcohol and/or choco ateVitamin supp ements such as vitamin B6 and vitaminE,have a so been e ective or some. Magnesium360 mg(as magnesium pyrro idone carboxy ic acid) orally tidgiven rom day 5o menstrual cyc e to the stday omenses may a so he p Note that no one o the abovetreatments is e ective for eve yone.

SSRs are s ine therapy or women with moderate tosevere symptoms Drugs such as uoxetine se tralineparoxetine and cita opram can be e cacious in up to2/3 of patients

FOR FURTH R R AD N

[Guide n s in b ]

C L YBauer A. hapter I. Clinical Pharmacokine ic and Phamacodynamic Concep s.In: Bauer , ed. App ed l n caPha macok net cs 2 ed ew York: cG aw- ll; 2008http //www.accesspharmacy com/content.aspx?a =3517000

us k ES tzgera d GA Molecular clocks in pharmacologyHandb Exp Pharmacol 20 3;(21 ):243 260

Yamash ta , Hash da M Pha acok net c cons derat onsor argeted drug del e y.Adv D ug Deliv Rev2013an;65(I):139 147

S S CSGuyatt G, Renn e D et alUse · Guides to the Medical Lit

eratu e: A Manual fo Evidence-Based Clinical Prac ice, 2"Ed t on Amer can edica Association, cGraw- ll; 2008http //www.jamae dence.com/resource/520

Hou W, arden D. Statist cs or the nonstatist c an: Pa t IIS h Med J2012 Mar; 05(3):131 35.

W ss ng DR, mm D. S a s cs or the nonstat st c an: Part I.South Med J 2012 Mar; I 05(3 ): 126 130

S S Sew ecki E n he cl n c. Osteopo os sAnn Inte Med

201 Jul 5; 55(l I I 15 qu I I 6

racture R sk Assessment Tool World Health Organizationol aborat ng entre or etabol c Bone D seases

www she ac k/ R X/tool jsp

Comm tt on Practic Bu l ins-Gyn cology he Am ricano l g of Obstetricians andGyn c l g sts. ACOG Prac

tic Bul t n N. 2Osteoporos s. b Gynecol 20 2S p 20 7 7 4

Guyatt GH orris SL t al M hodology for th D elopm nt of Ant thrombot cT h rapy and Pr nt on of hrombosis Gu d n s: ntithrombo c Th rapy and Preve on o

Thrombosis ' d American Colleg o Chest Physic ansE id nce-Bas d C n ca Practice G idelines. es/20 2 b 4(2 Supp 53S 70S

m S Ho s ma LJ et a . A PM Pr nt on Prac i Committ Scr ning or osteoporosis in h adu t U S pop lation:

PM posit on statemen on pr v n iv practiceAmJ Pd 2009 pr 36 4):366 375

M nagem nt o ost oporosis n postmenopausalw m n 0 0pos tion stat m nt of Th North Am rican M nopauseS ci

0 0 Jan- b 7):2 5 quiz 55 56

h Nat ona Os oporosis o nda onh tp// no .org pro fess ona nica1 guid lin s

Qas m SnowV,et al. Cl nical E cacy Assessm ntSubcomm t of the Am rican Coll g o Physic ansPharmaco ogic tr atment o o bond ns tyor ste p r i

o pr v n rac ur s: a c inica prac c guid in from thm rican Co l g of Physicians n

2008 S p 16 49 6 :404

Qas m Sno V t a . C inica E cacy Assessm ntSubcomm t of th Am rican College o Phys c ansScreen ng for osteoporos s in m n a clinical pract c guid n

om the merican ol eg o Phys ciansA n /e Me2008 May 6 4 6 0 684. Erratum in in/ rn2008 un 3 4 :888

S Pre n v Serv c s Task Forc Scr ening for

st p r s s:r comm ndat onstat m nt Am h c a20 May 5 83 0 7 200.

Wa tsNB, Adl r RA et a Endocrine Soci tyOst oporosis inmen: an Endocrin S c etyc inica practic guideine J l 1

cr o Mtab. 20 2 Jun 7 6 : 80 1 22

Wa ts NB Bi zikian JP t a AACE Osteoporosis Tas ForcAmer can Assoc ation o Clinical Endocrinolog sts edicalGu d lines for C nica Practic for th diagnosis and tr atm no p stmen pausal st p ros s o r P 20 0 NoD c 6 S pp 3: 37.

Watts B L wiecki EM t al Nationa Ost oporos so nda on 200 C inician ·s G de to Pr v ntion and r at

m n oOst p r sisand h Wor d H a h Organ zation

Fract R sk Assessmen Too FR X what they m an o thbone d nsitom trist and bon t chnologistJ C n e o2008 Oct Dec 4 :473 77.

CS

ayea D Eckstrom E et al pdate n ger atric med c ne.

J Gen nte n Med2012 Mar 27(3 371 375.

Lischka AR, ende sohn M, et al. A systematic re iew oscreen ng tools or pred c ng the de elopmen o dementiaCan J Aging 20 2 Sep 31(3 :295 311

Mc llan G Hubbard R . ra lty in older npatients: what

phys c ans need to owQJ 2012 o I 05(1 059 1065

© 014 u - p p g f g p g @

http://www.accesspharmacy.com/content.aspx?aID=3517000







http://www.jamaevidence.com/resource/520

http://www.shef.ac.uk/FRAX/tool.jsp

http://www.nof.org/professionals/clinical-guidelines











http://www.shef.ac.uk/FRAX/tool.jsp

http://www.jamaevidence.com/resource/520




Rengo F Parisi V, et al. Ins um nts for ge iat c ass ssm nt:new mul dimensional ass ssment app oaches. Nephrol.2012;25 Suppl 19:S73 - 8

Nutri ion

Johnson MA St at gi s to improve diet in olde adu sProc Nutr Soc 2013 Feb;72( I) 66 - 1 2

Mo ey JE Unde ut it on in o der adultsF m P ct 2012Ap ;29 Suppl I i89 - i93.

B st i M Mu 7 N Acad my or Nutr o andP s no ad my o Nut on n D s: foo andnu ition o o r adu s: p omot ngh a hand \ · l n ss

w 0 u g 2( ) 2

Mobili y and Gai

Mo : U Pr ven ve Sc Task F P v n onof n m uni dw ll ng ld r adults: S Pr t vSer sTas rc r o nda ion tat m ntAnn Intern

'e 2 0 1 A u g 1 (3 ):197 - 204.

P n< on Pre' nt onof Fall P r so m r cani r cs So c and Br h G r a r c o i y. Summar of

heUpdated Am n ria rics o yl � h r atri so n apra t gui ne ·pr , iono n

old r per J-1 C iu Soc 0 I an 148 5

Wound Os m and Con inen e ur nc L' (WOC ).Guidel ne forpr \' nt on nd m n em n or pr u reMou L u W un d. Os o y , and on in n N urs s

o y WO CN 0 0 un I OC \ l n p actic guidl n no 2).U . p men H alth a u an r ic s.

[OnI n ] http 11 \1 \\'.g uidel n g /c nt n ap� d =2 R6X&s ar h %22pr ur u c r 2

Pharmaco ogy

S tar DS Clinical pharmacology con ounders in o d r adu tsExp rt R v C/in Pharmac 20 2 Jul;5 4 397 402

Endocrine

Ralston SH Lay eld R Pa ogenesis o Page d s ase o boneCal fTissue Int. 20 2 Aug 91 2) 97 13

Wom n's H al Initiat v M nopausal Hormon Th apyn or at onNationa Institutes o H a th20 4ttp: /www nih.gov P index.htm

Bhas nS unn ngha G �t a Tas or E do r cie y T s o on rapy n m n" h androg n d fi n

y d o es an En l c n S ie y l al pra c guidel ne C n End i1 al. \f t b 20 Jun 95 :2 59

Brown AF Mangion \1 fo oun-on/ m n G oPan on I mp ingCar

orE ld r th D iabete ..m G S 00 a ;51 (5upp Guidel ): 6 - 80

y r VA U Pr \ n v \' Ta F rc M nop u aormon t ap >r primary pre on h n condi

t o s U. . Pr , n i S Ta F r rL · omm nda ions nn nt m 2013 Jan 1 XI : - 54

n A, v orlcy a D b em l u no peoplpo i ion ta nt n b alf o In a i na As oc aton

of Ger n ol ogy and ia ri s IAGG ) t urop an D bW rk ng P y f Older P op ED POP and h nte a

i nal a kF r of E\p <: in D b ·/ , d D o

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p c al cons ra ons or th edu at on and 'old r adult d b Am r can As ciat nof Diab t s

Di h v E d u . 00 an F b 26 (I ) 3 - 9

Ne ro ogic

o AX arada CN G iatr c dizzin ss vo ving diagnos icand t e apeutic approaches fo e emergency d partmen .

C/in eriatr Med 2013 F b;29I):

8 204Silber MH E enbe g B , t a Medica Adviso y Board of

he Res ess egs Synd om Founda ion An algorit m fo thmanagemen o restl ss l gs synd ome.Mayo C in Proc2004 Ju1 9 ) 916-922 Erratum inMa o C in Proc.2004 Oct 9I 0) 1341

Weisenbach S Boore LA et a Depression and cognitiveimpai ment n older adults Curr Ps chia Rep2012 Aug; 1 4):280-288

Hearing

Walk JJ C veland M e al. Audiom try scr n ng andnte p etationAm Fam Ph ician 20 3 Jan I ;87 :41 47

o e V U Pr nt , e S ic TaskF rc S r ening ng lo n ok u : SPr i S rvi

Task r c nda ion s a e t Ann m M e d

0 2 o \ 6 1 7 9 655- 61

Ca diovascu am r a Coll g of po M d h dz o Zaj o WJ al ric a l g Sports M dic n po i on stand

xer andph a a i i y r old r du s \ Sc px 009 ul 4 ): 510 0.

u mo ary

Gr gg Damberger M Ralls F Cogn tiv dysfunction and

obstruct ve s eep apn a om cradle to tombCurr Opin Pu mMe 20 2 Nov;18 6) 580- 8

de Nijs SB Vene amp N a Adul onset as ma s itreally di ent? ur R spir R v. 2013 Ma I ;22 12 ) 4 - 2Erra um in:Eur Respir R v 20 3 Jun I ;22 128) 93

Uro ogy

owther A, Gold , t al Managing incontin nc a 2 visiapp oach J Fam Pra t. 20 2 Sep;61 9) 544 551

Mazur J Helfand B t al In uences o neuro gu a oryfactors on t e developm n of low r u inary tract symptomsbenign prostatic hyperp as a and e ectil dysfunc on n ag ngm n Uro C in North Am20 2 b;39 77 88

S ah BJ Cho havatia S t a Fecal ncon inenc in t e eldely AQ Am astro nt .20 2 Nov; I07 II 1635 1646

A ra s P nd r onK M mb r f C mm tou n on n ul a onn ncn n n Four hn on Cons u a onon n on n n R omm n on

o th t a o al ce t f c C m t E alua ion and treatn o ur na ncont n ncp lv rgan prol ps and e ac t e ce\' umuml L' d 20 0 9 : - 0

M sce aneo s

m an b A s o c ia io andardsof m d ca arendi a b tc 1 D h C 20 3 J ;36 Supp I J - 6

10-61

http://v/v/v.guideline.gov/eontent.aspx?id=23868&se





















http://www.nih.gov/PHTindex.htm

http://www.nih.gov/PHTindex.htm




1�2 FOR FURTHER RE D NG

Hun SA Abraham W et al 2009 Focused update in orpoa ed nto th ACC/AHA 2005Guid lin s for the Diagnos s

and Manag ment of Hea t Fa lu nAdul sA Repo t o hAmerican Co lege o Card ology Founda ion/American H arA soc at on ask Fo ce on P act Guid l nes De e opedin Co labora ionw ththe Inte a ional Soc e y fo Hea tand ung TransplantationJAm C l C rdia/ 2009 Ap

4 53( 5 ee90 Erra um n:J m o / r dia/. 2009 D c5 54(25 2464

Nor h Am r an Menopause So iet . Es rogen and p ogestogen u e in po tmenopausal om n 200 posi on s at meno he No h Ame anM nopaus Soci ty Menopaus 20 0 Ma 7(2) 242 - 255

Qa eem A, Snow V t al Current pha macolog treatmenof demen ia: a in a pract ce gu d in rom the AmericanCol g of Phy icians and h Amer can Academy ofFami yPhy ician Ann Inte Med 2008 Mar 48(5 :370 - 378

Vandvik PO Lin o AM et a . Primary and Se ondarPre ent on of Cardio asculaD s ase An ithrombot c Therapyand Pre en on of Th mbos s 9' ed: American Co l ge o

Che Phy icians Eviden Bas d Cl n ca P ac e Guidel n sh sl 20 2 Feb; 4 (2 Supp ): 637S 8S

S

Dhai A Payne amesJ Prob em of capacity onsent andcon den ia tyBe t P Re /in Ob et Gy eco2013 Fe 27 1):59 75.

mehou e WE Fee e V e a A model o emergencydepar ment end o life communi ation a er a u e deva a ingeven pa : de on making capaci y urroga e andadvan e dire ve .A ca E g Med20 2 Sep 19(9):E 068-1072

imehou e WE Fee er V , e a A mode for emergen ydepa men end of i e ommunica ion a e a u e deva atingeven pa II moving f om re u ci a ve o end of e opal ia ive rea men .A d e Me2012 Nov 9 1 ):1300 1308

ACP Ethic Manua 6edi ion (r ased 012) a a labon ine a acponl neo g/ thic / hicman htm o n p nat Snyd L Ameri an Col eg o Phys ans Ethics, Pro ss onal m and Human R ghts Commi . Am r can Collegeof Phy ans Eth Manual s xth di onn er Me

2012 Jan 3; 56(1 Pt2) 73 - 0

P P V V L

S hieferm e le yer on S e a Preope a ve a e men

and perioperative managemen o cardiova cular kAngio o 20 3 eb 64 2):146 150

Fle he LA, B ckman JA et al 2009 ACCF/AHAfocusedupda e on pe iop at v be a b o k d nco po a d nto theACC/ AHA 2007 gu del nes on periop rati card o as u are alua on and car or nonca diac su geryi u lion2009 No 24;120(21): 169 2 6

S ening or A domin Ao i n e uJ TS I Dr f Re omm n- d lion Sl ment .S Pre en e S r ices Task Force 2005http /w uspre entiv se vicestask o e org/usps uspsan uhtm

P V V

20 3 ACC/AHA Guide ine on the Treatment of B ood Choleste ol o ReduceAth os l ot Cardiovascula Risk in Adultsh tp:// c ahajou a sorg/conten early/2013 / 1/0 .

ir 000043773 3853 7a c a on

Hande smanY, M hani k J et a Screeningand Mon tor ngof Prediabe s Am rican A sociat onof C ini a Endocrinologi s20 I.h p ou pa n .aac ompr diab sscr ningand-mon to ng pr d ab t s

Ame an Cance Society. Gu del nes the Ear y Dete tonof Can h p:1/www.cancer org/hea h y1 ind an e eay/ ancersc en i nggu ide i n s/american ance socie y gu deI n sfor th ear y dete on o � ance

American Co g of Phys c ans Cl n cal Prac i Gu del nesCurrent Guide ines.h p: ww a pon in .org cinica _ n rmation gu ide! n s gudeIine

Ame an Diab es A soc ationStanda ds o med cal ca ein d ab s 2013. i ete 2013 Jan;3 Suppl :S 1

Choban an AV, Bakr GL, et al H BI oint Na onalCommi ee on Prevention De ection,Evalua on, andT eatmento H gh Blood Pressu e h JNC7 report \

2003 May 21 28919 2560 - 2572

F o e MC,Ja nCR et a . ea ing o ac ose and Dependen : 2008 pdate Cl n cal Pra tice Gu d l nRo k lle,MD: U.S Depar m n o Hea th and Human S rv es. Publ cHealthS r ic . May 2008.http //www ahrq go/p ofess onas

n ans p o d rs/gu deI nes recom menda ions/tobac o/nd x htm

H ratzka LF Ba ri G e al 20 0 ACCF AHA AAT S ACRASA SCA CAI SIR STS SVM Guid in s fo thed agnosisand managem n of patients with thoracic ao ic d sease

m o / ia/ 20 0 Apr 55( 1 27 129

S een ng andT s ng o De ec Canc Nat onal Can eInsti u eht p//www an go/ anc op s/scr n ng

National Chol ste o Education P ogram (NCEP) E perPanel on Detection, Evaluat on, and T ea m nt of High B oodChole e o in Adul s Adult Treatmen Pan ).C cu/ n

2002 Dec 7 I 06(25)31 3 - 342h tp / www nhbi nihgov gu deI nes/cho st ol atp3ull pdr

ook TW H rsh A et a ACC/AHA ask o ce Managm nt o pa n sw thpe ph al ar ry d s ase (compi at on o2005 and 20 ACCF /AHA Guideline Recomm ndat onsJ m C / rdio 2013 Ap 9 61( 1 : 555 1570

comm ndations Adu s U S Pr n iveS vic s Task

Fo eh p: w uspre enti eser ices ask forc o g adue htm

Stone N B lek S Re ent Na onal ho t ol EducationP og am Adult r atmen Pan upda e ad us men s andopt ons m ia/ 2005 Aug22;9 (4A) 53E - 59E

U S Pr en e S r i es ask Fo c Counsel ng andin er en on o preven toba o u e and ba co causeddis as n adu s and pr gnan omenAnn te d

2009 Apr 2 ; 50(8):55 -555

P S S

Go dfrank o ico ogi Emergen ie . S. . M G aw Hil 20 4.Prin

© 20 4 MedStu y-Piease Report Co yr gh Infr geme s to co yr gh @meds dy. o

http://www.acponline.org/ethics/ethicman.htm











http://www.uspreventiveservicestaskforce.org/uspstf/uspsaneu
















http://www.circ.ahajournals.org/content/early/2013/l




















http://outpatient.aace.com/prediabetes/screening-








http://www.cancer.org/healthy/fmdcancerearly/can-












http://www.acponline.org/elinical_infor-







http://www.ahrq.gov/professionals/











http://www.cancer.gov/cancertopics/screening














http://www.nhlbi.nih.gov/guidelines/cholesterol/atp3full.pdf













http://www.uspreventiveservicestaskforce.org/adultrec
























Holstege CP, Borek HA. ToxidromesC it Car Clin 2012Oc ;28(4):479 498.

Shannon MWHaddad and Wincheste Clinical Manage-ment of Poisoning and D ug Ove do e, 4' ed 2007 Saunders

DR G W THDRAWAL

e raul JM O Co nor PG Subs ance abuse a d w hdrawaln he cr cal care se ngC it Ca e Clin 2008 Oc ;24(4)

767 -788

OPHTHALMOLOG

Amba A k nson JP e al Imm nology of age re a ed macular dege era oNat Re Jmmunol 2013 Jun;13(6):438 451.

Drugs for some commo eye d sordersT at Guide M d L20 2 Nov 0 123) 79 -86; qu z 2p follow g 86

Gadar a Ra hod N Fe andez KB e a New ns gh sn o nfec ous kera snt Ophtha/mol Clin 2013

W n er 53(): 63 -172

Graves JS Gale a S Acu e v sua loss and o her

neuro oph halmo og c emerge c es: ma agemeNew Clin 2012 eb;30(1) 75 99 v

Hahn P Fek a S Bes prac ces for rea men of re na veocclus onCu Opin Ophthalmol 2012 May;23(3)175 - 81

Kale N Managemen of op c neu s as a cl n cal y rseven of mul ple sc eros sCu Opin Ophthalmol2012 Nov;23 6) 472 476

K ng A AzuaraB a co A e al GlaucomaBM20 3 Jun 346 518

Schwa z SG Flynn HW e al. Upda e o re nal de achmensurge yCu Opin Ophthalmol 2013 May;24 3) 255-261

Sha ma S D agnos s of nfec o s d seases of he eyeE e (L nd).2012 eb;26(2) 177 -184.

Weyand CM aoYJ e a he mmunopa hology of g ancel a er s d agnos c a d herapeu c mpl ca ons Neu oophthalmol 2012 Sep 32 3):259 265

P ima y Open ngl laucoma Susp ct PP . Am i anc dmy of phthalmology T d P acti P Gu d l nec ob 20 0 http /on .a oo g pr dpract c -pat

pr m ryop n n g gIaucoma susp ct ppp octo r20

HEAR NG LO

Chau K, Cho JJ e al Ev dence based prac ce managemeno ad lt sensor eura hear g ossOt l01: ngol Clin No th

Am 20 2 Oc ;45(5) 94 -958Wall g AD D ckso GM Hear g loss older adul s.

Am Fam Phy ician 2012 J n 5;85(12) 150 - 156

Moy VA;U.S \ n ivS r i a k F Scr n ngo ea ing lo in o d adults: U ,· nt S r c s

kF comm nd onstatem nt. Ann lnr Me

2012No 6 157(9 ) 55

a l r J Chand a SSe l Am rican A d m oO o a ngo ogy-H dand Surg l n pra cg d n : sudd n h a ngos Ot l a g l H d ck S g20 2M ;I46 3Supp i :S 1 3

© 2014 MedStudy

OFF E P H ATR

be l MH D agnos s of an e y d sorders n pr ma y careAm Fam Ph ician. 2008 Aug 15 78 4):501 502.

Gale CK M ll champ J Amer can Academy of am lyPhys c a s Ge eral zed An e y D sorder [Cl ca Ev de ceHandbook]Ame ican Famil Ph ician 2013 Jan 87(2):122 -124

Geddes JR M k ow z DJ rea me of b polar d sorderL 2013 May;381(9878) 1672 1682

Perry PJ W bo CA Sero on syndrome vs ne rolep cma gnant syndrome a co ras of causes d agnoses, andmanagemen Ann Clin P chiat 20 2 May;24(2)155 162

Ph l ps M Kupfer DJ B polar d sorder d agnos s cha e gesand fu ure d rec onsancet 2013 May 381 9878)1663 -1671.

ren SA More ra M e a D manageme of pa e s w hea g d sordersAm me g Med 20 3 May;31(5) 859 865.

a ng D sorders Cr ca Po s for arly og oandM d al sk Ma ag me n he Care of I d v dualsw thEat n D sorders Academy o Ea ng D sorders. 20h p //

a ngd sordersucsd edu ed 0 1/ df s/A D%20Repo pdf

Prac c Gu d l es Am r ca Psycholog ca Assoca o200 h p psych a o l norg gu d s asp

N ma a ur yaK, Comp o M a Pr e o P ac ceComm ee of h Amer canColl ge P ent Med c eScr gdu ts or d p onpr mary are A pos ons a meo he m r can Col ege f Prev n v Med c Fa ct 2009 Oc ;58 I0 535 538

Oz e ADHe yBW; m anD c Asso a on Pos oof h Amer an D e e c Assoc a o nu oni t e ion

he r a m n o ea g d sorders A iet As so 20

Aug; 8 23 -1241U SPreve ti e Ser ces ask orc See g or dep ess on

adults U.S p e entive se v ces a k fo ce r comme da o Ann I t ed 2009 D c I 51( 784 792

GENET

OM M®O l ne Me de an Inher ance Man · An O eCa a og o Human Genes a d Gene c D sordersh p www.om m.org

Pago A, B rd TD e a ed ors Gene Rev ews™ In e e ]Seat le (WA) Un vers y o Wash gto Sea le 993h tp //www ncb lm n h gov/books/NBK 1116/h p //www cdcgov/genom cs/

WOMEN' HEAL H

r se CJ W ll amso C E docr ne d sease pregnancyClin ed 2013 Apr;13(2): 76 18

Melch orre K Sharma K e al Card ac s ruc ure andfu c o orma preg ancyCu Opin Obstet G necol2012 Dec;24 6) 413 421

Ha sch M Ha sch H e al Fam ly med c e obs e r csP im Ca e 20 2 Mar 39(1) 39 5

Odu ayo A Hladu ew ch M Obs e r c nephrology re alhemody am c and me abol c phys ology no mal pregna cy.Clin Am oc Neph ol 2012 Dec;7( 12) 2073 2080.

10-63

http://one.aao.org/preferred-practice-pattern/



















http://psychiatryonline.org/guidelines.aspx








http://www/

http://www.ncbi.nlm.nih.gov/books/NBKl

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http://www.ncbi.nlm.nih.gov/books/NBKl

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10 F R F RTHER READ NG

0stensen M, Vi ger PMet a In eraction of p egnancyand autoimmune rheuma ic d sease. Auloimmun Rev 2 12May; (6-7):A437 4 6

Ouzo nian JG ElkayamU. Physio ogic changes du ingnorma p egnancy and de ve yCardi / C in.2 2 Aug 3 3) 317 329

Pea ce CF Hansen W Headache and ne ro og ca disease inp egnancy C in Obslel Gy eco 2 2 Sep 55 3) 8 828

Rosene Mon e la Kommon Medica P b em inP egnanc n Go dman L and chafe A , ed Go dman'sCeci Medicine, 24 e 2 2, a nde s

Ty e H, Zi was MJ Pregnancy and de mato ogic the apyJ Am A ad De mato .2 13Apr;68 4):663-671 .

elix HM, Ce v nka D Dysfunc iona ute ine b eeding omhe prima y ca e pe spec i eJAAPA 2 2 Ap 25( 4) 4 7 49

N l DB, Wei and CM, et a Postmenopa sa b eeding ststeps in the wo upJ Fam P c 2 2 Oct 6(I ) 597 6 4

Rapk n AJ Akop ans AL Pathophysio ogy of p emenst al

synd ome and premenst al dyspho ic d so derMenopau eIn!. 2 2 J n 8(2) 52 59

F mu d bstetric ar e o n: n sus A i� n olleg ofOb tetricia nd Gy o gis sR c ndPub li a ions ht p:/ w\ .ac g r R u ce s_ nd Pub l ca tion

M sc B nj m n E t l. E ct nc s - B d uid l north Pr v n on dio a cu r D in W n- 201

Upd t Gu d line mth Am r ca H rt s oc t on.J m Co / d 20 I 57 121 ·1

m e n o lg " b tet rici n n Gyne c l gists R e s rc nd Publ c t n (C itt O n n ndG d in "Wom n H t C )hnp :/ www c g.or Re o rc nd P b ic i n

W Gull n c c nc c ning nd upd t dP p g de in sP m 2 9 36 ): 3

© 2014 MedStu y-Piease Repo t Copyr ght Infr ge ents to copy ght@me st y.co

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Neurology

COMA 1 FEC O S l- 8 OVERV EW - BACTER AL C S NFECT ONS 8WORKUP OF COMA - Acute Men ngitis ll- 8

Neuro ogic Exam F ndings - B a n A bscess ll- 8 Scans and Lab Work for Coma 2 V RAL CNS NFECT ONS - 9

Eva uat on o F nd ngs 2 CSF n Vira Encepha t s 9COND T ONS THA M M C COMA 11-3 Herpes S p ex Encepha s - 9 LOCKED- N SY DROME 3 Mosqu to Bo e A rbov ruses 9 VEGETAT VE STATE 3 D agnos s o Vira Encepha t s AK ET C M T SM -3 V ra Mye is CATATON A I 3 S ow V ruses and Prions BRA DEATH . . . 4 H V

HEADACHE 11-4 PARAS T C CNS FEC ONS 20M G E -4 Toxop asmosis

P esentat on 4 Neurocyst cercos s -20 Acute Treatment o Mig a ne 5 F NGAL CNS NFECT ONS -20Prophy ac c Treatmen o M gra ne 6 C yptococca Men ng tis

CL STER HEADACHE 6 STROKE and T A TENS ON HEA ACHE 11 7 T A -2 BEN GN SEX AL HEADACHE 1 COMPL CAT ONS OF T A

POST-TRA MAT C HEADACHE -7 CLASS F CA ON OF STROKES G ANT CELL ARTER T S PR MARY PREVE T O OF S ROKE 2

D OPATH C TRACRAN AL HYPERTENS ONI MAG G OF STROKES 2 2PSEUDOTUMOR CER BR SCHEM C STROKES 23

THALAM C PA N SYNDROME 8 Thr mbot c vs Embo c Strokes 23 DEL R M 11-8 Anter or C rcu at on 23 DEMENT A -8 Poster or C rcu at on -2

DEF N T ON 8 Lacunar n arcts 25WORKUP 8 Eva uat on o schem c Stro e 5

Eva uat ng Domains o Funct on -8 Acute Trea ment of schemic Str ke -26 Diagnos s o Dement a 8 Chr n c Trea ment o schem c Stro e -2 M d Cogn t ve mpa rment 1 9 N RACEREBRAL HEMORRHAGE Reve s b e Causes -9 S gns and Symptoms -28

CA SES OF DEMENT A 9 T eatment of nt ace ebra Hemorrhage 28 o ma P essu e Hydrocepha us 9 SUBARACHNO D HEMORRHAGE -2 8 A zhe mer D sease -0 D agnos s o SAH 9 Vascu ar Dement a Comp cations of SAH 9Fr ntotempo a Dement a 1 1 T eatment o S AH Creut e dt Jakob D sease - S BD RAL HEMATOMA Pa nson D sease Dementia (P D) EP DURAL HEMATOMA P ogress ve Supranuc ea Pa sy 2 TRANS ENT GLOBAL AM ES A -30Hunting on D sease l C S METAS ASES -30 A DS - 3 METABOL C A D TOX C SO ERS Depress on 3 WERN CKE'S KORSAKOFF S -3

D ZZ NESS 3 L TH M OX C TY 3S G S A D SYMPTOMS 3 ANT CHO NERG C TOX C TY -32 CA SES OF VERT GO 3D SEASES OF MUSCLE A D ERVE I -3

Ben gn Pos ona Vert go 3 MYELOPATH ES Vestibu a Neuritis 4 Me abo ic Mye opathy 32 Am nog ycos de Toxici y 4 n ect ous Mye opa h es - 3 M n e D sease 1 4n ammato y Mye opathy -33 Ve tebrobas ar T As Compress on nduced Mye opath es 33

YSTAGMUS M sce aneous Mye opath es -34 T NN TUS - 5 EUROPATH ES -35 SE ZURES 5 Mononeu opath es -35

GE ERAL ZED vs FOCAL 5 Po yneuropath es ll-38PSYCHOGEN C NONEP EPT C SE Z RES PNES 11-15 E ROM SC AR NC O SE Z R A RA 5 MYASTHE A GRAV S COMMON SE ZURE TYPES 6 LAMBERT EATO SYNDROME SE Z RE MA AGEMENT - MYOPATH ES

H story FLA MMATORY MYOPATH ES Scans and Lab E DOCR E MYOPATH ES Acute Treatment o Se z es 7 METABOL C MYOPATH ES Chron c Treatment o Se zu es M SC LAR DYSTROPH ES 1 Treatmen o Se zu es ur ng Pregnancy 8 A DS-RE ATE M OPA HY



NEUROMA . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . II-4 2DEMYE AT NG D SEASES ....... ......... ............... ........ - 2

MUL PLE SC EROS S ...... ... .... ...... ............... 1 - 2C n cal Manifestat ons of MS ... -4 D ag os s of MS . -4 3

Treatme t of MS .. . . ....... . . .. .. . . .. - PROGRESS VE M OCAL

E KOE CEPHA OPATHY (PM ) ... ... . ... ........ -44CE TRA PONT NE MYE INO YS S .. . .... . . -

MOVEMENT D SORDER S ..................... ............. ... .... 1 - PARK SON SM . .. . .. .... . .. ............... 44 PARK SON D SEASE .. . ........... . ... ................ . -45

D g os s .... . . ........ . .. . ......... 45Treatme t. .............. ....... . . .... . ... .. .. - 5

PROGRESS VE S PR NUCLEAR PA SY .. . ... . ......... 4 6TREMORS . . . ........ .. 47

Exaggera ed Phys o og c Tremor . . . -4 7 Esse t a emor . .... . ... . ...... -

TA D VE DYSK ES A ......... . . ... . ... ...... - OTHER MOVEMENT D SORDERS ...... ............ . ... 48

Neuro ept Ma g ant Syndrome . ............... 1 - 8 Hem fac a Spasm .. ............. .. ... .... 1 - 8 G es de a Tou ette Syndrome ..... . . . . .. ...... - 8

oca Dyston as .. . . . . ... .... ...... 48 M SCE ANEO S D SORDERS . ...... .. ... ....... -49

AC TE-ONSET UN ATERAL B INDNE SS ..... . .... . 9D P OP A . . . - 9 V S AL FIE D DE E CTS . ..... .. . 9

Scotomas .. ..... . .......... ...... .. .. . 1- 9B tempo a Hem a ops a .... . . . ..... 11-50

COMP EX REG ONA PA N SYNDROME . . . . .. 1 -50NARCO EPSY .. ...... . .... 50

OR RTHER READ NG ......... . ..... 50



COMA

OV RVI WLethargy, confusion, s upor, obtundation, and coma arete s that apply o dim nished eve s of consc ousness.Consciousness depends on the degree of a person'sa ertness and a ent onBo h the re icu ar ac ivat ngsys em (RAS)and the cerebral cor ex must be workinge ec ive y in order o sus ain no a consciousness

Thus, coma can be caused by e thera decrease n heac iv y of the ret cu ar act vat ng sys em (RAS)ora process that nvo ves he cerebra cor ex ofbothhem spheres. The RAS res des w thin he bra nstem, so

njury to the bra nstem, such as a hemorrhage in the ponsor m dbra n, can cause coma. Cer a n drugs (prescribedOTC, and i ici ) a so a ec he RAS direct y.

Me abo ic disorders are the most common cause ofcoma, fo owed by ntoxica ions and anoxic brain

damage.P um and Posner c assi the causes of coma n hefo owing ways:

Supratentor a• nfraten or a

Metabo cD use

u t factor a

WORKUP OF COMA

Neurologic Exam ind ngsOverview

A thorough history and neuro og ca exam are requiredto estab sh the diagnos s and he possible cause ofcoma Th s inc udes a rev ew of under y ng medicaland men a hea th i lnesses, medica ons ngestions,and ntoxicat ons TheG asgow Coma Scale was cons ruc ed to assess responsiveness of pa ien s wi hcerebra rauma. The components of the neurologicaexam na on must include observa ions aboutrespirat on(and resp rato y pa erns),pupi aryresponses, andmotor responses (or a lack thereo However the use ofth s sca e n he eva uat on of o her etio og es of acu ecoma prov des tt e ns ght nto the oca zat on of heanatom ca dysfunct on The prognostic va ue n non

raumat c coma depends sign cant y on the et ology.Vi a s gns nclud ng temperature pu se, resp ratory rate,and b ood pressure can provide clues to he diagnosis

Motor Responses

Motor responses such asdecerebrate and decort catepos ur ng, can help to oca ze the si e of njury

Decerebrate postur ng is a type of r gid ty hatoccurs when he on c abyr nth ne re ex tha res stsgrav tat ona force ac s w thou modu ation of thehigher brain, caus ng extens on of a extremi es

© 20 4 MedStudy

COMA

indicates an e ectivesever ngof the bra nfrom the sp na cord a he eve of them dbra nspec ca y below the eve of the red nucleusTh s postur ng can be seen dur ng unca(trans en orial; see next page) or onsi lar(cerebe um)bra nhern ation.

t s also seen n a var ety of condi ons such asmidbra n compress on by a mass, cerebe ar orother pos erior fossa esions and severe me abo icinsu s. I may occasiona y be seen n cerebrawhi e matter disease and basa gang ia esions

o Decerebrate pos uring is not seen much becauset occurs in less common s tuat ons and s rapid y

fo owed by dea hDecort cate postur ng is a type of r gid ty hat scharacteri ed by ex on of upper mbs withex ension of lower limbs t is caused by esions at a morerostra leve of inju y o both corticospina and r brospina racts resul ing from damage o bra n areas

hat can inc ude he cerebra wh te ma er, in e acapsu e and thalamus. These areupper mo or neuronles ons. Causes may inc ude anoxic or rauma ic bra n

n ury, s roke ntracran a hemor hage, bra n t mors,and encepha opa hy

n uncal he ation pat ents may progress fromdeco t cate o decerebra e postur ng.

Resp rat ons

Cheyne-Stokes respiration describes a pa icu arpa e of brea hing in wh ch the patient has per odsof hyperven ation a te at ng w th apnea. his

pattern occurs in b ateracerebra disease, impend nghe ation andbrainstem es ons t can a so be due tometabo ccauses.

Apneust c breath ng s charac er ed by a ser es ofs ow, deep nsp rat ons, each one he d for30 seconds or

onger, a er which the a r s expe ed by e as c recoiof he ungs, fol owed by an apneic pause The ra e ofapneus ic brea hing is common y a ound1.5 breaths perminu e. t s due to a les on of the ower pons

Atax c brea hing is very r egular and ypica y ind catesa es on of he medu la

Central neurogen c hypervent lat on: Les ons of theower m dbrain-upper pont ne tegmentum cause centra

neurogen c hyperven ation wh ch produces an increasen he rate and depth of resp rat on result ng in advanced

respiratory a ka os s

Pup ls

Remember tha in the comatose pa en , anyasymmet ybe ween the si es of the pup s must be consideredpa ho og c( ab eIl-l ). L ght reactiv ty a so needs to becarefully assessed.

1 -



1 -2 COMA

Table - : Pupil S ze nCo a

Size Descr ption C use Ex mples

fou d by EEG to bei onconvulsive st tusepi epticus.

One dilated Parasympathetic Oculomotor nerve compression from Fin ly, you y eedto do cerebrospi l u dex i tio ( nc uding

the usu b cter ndvir tests) you suspecte ng tis or e ceph tis

unreactive nerve problem uncal he iation, rupture o anpupil nte al carotid tery aneurysm

One pinpoint Sympathetic Lateral medullary syndrome• • pupil (miosis) nerve problem hypothalamus inj y

Ho er

Two midpoint Parasympathetic Midbrain disruption (can a ect one Evaluation of FindingsSup a e o al coma sdue to i ury of thehe sphere(s

nonreactive and sympathetic or both pupils anoxia hypothe m apupils nerve anticholinergics severe barbiturate

destruction overdose

• •Two dilatedunreactivepupils

Anoxia hypothermiaanticholinergics severe barbiturateoverdose

There re2 mech n s s

1) L ter (unc l) he i tion

Two pinpointreactive pupi s

Opiates pontine destructionA exp d g ss les on( u or, s roke, hemor h ge)

orces the uncus through the

Oculoves bula es g

Oculoceph lic (doll's eyes) nd ce-w ter c loric test g(eyes look tow rd the cold) test the s me vest bul rbr stem-ocu r muscle p thw y The co p ete bsenceof eye moveme t in response to oculovestibul r test gindic tes e ther severe d srupt on of br ste teg e t lsystems (m dbr inor po s) or pro ou d overdose osed t ve, nesthetic, or t co vu s t drugs.

Doll s eyes:•

De ition Whe the he d is tu ed, the eyes keep"looking the initi l d rection (eyes do not o owthe move ent o the he d) Doll s eyes n co toseperso dic tes th t the br stem s i t ctAbse tdo 's eyes s poorprognost c s g . Gener y, doll seyes re preserved e r y met bo c com heexceptio s re et bo c co s due to b rb tur tes

nd phe ytoi• Test g or doll s eyes, which requ res ov g the

he d, should be do eon y er -sp ne injury h sbee ruled out.

Reductio or bse ce of spo t eousblinking d losso co e l re exes re s g s of deepe ing com .

Scans and Lab Work fo ComaQuickly obt n T or MRI o the br i order to

r ow the d ere t l, especi lly when the c use su c e r

heck B , e ectro ytes, BUN, cre t e, g ucose,ABG, urin lysis, d tox co ogy screen for illic td ugsOther tests, such s n EEG, re helpful in dent ngno co vulsive st tus epi ept cus, espec lly whe there

s prior history of se zures I o e series of co tosep t ents i whom the c use w s unknow , 8% were

m dd e ope i g the tetor u . This puts pressure

o the br ste nd, there ore, the RAS. Bec useof the course o the 3 cr n e e, the he i t guncus compresses th s erve, c usi g ne l rged pupilipsil ter to the supr te tor l lesio

2) e tr l he i tion I jury to the th l us (such shemo h ge) results n dim nished co sciousness ve ye r y ts course ter, the pup s re d-pos t o

nd become xed As the he tio cont ues, thecourse beg ns to erge w th th t o unc l he i tion

n other words, ce t l d unc l he i t on sy dromesc n be d ere ti ted e rly on, but, l ter, the rcourses erge

Note, however, th t on T sc of the br in, tIS

hor o t sh o the p e body th t corre tes w thco sc ousness evel r ther th n tr nste tor l he tio :

P e l Shi o T0 33 46 88 13 m

o scious ess LevelAlertDrowsyStupor

om

f a e o al comais due to n n u y th t c usesdes ruct on or compressio o the br nstem. Sig sof in r te tori he i t on c ude bil ter l re ctivepinpoi t pup ls (due to po tine involve e t) drespir tory b or ties, i c ud g cluster bre th g,

pneus s (deep g sp g), nd t x c bre th ng There re3 possib e c uses

I) B s l r tery occ usio w th po ti e n rction2) erebe l r f rctio or hemo h ge3) osterior oss eopl s s

Exp sio o the contents of the poster or foss orces

the co te ts of th s comp r ment in1

of 2 direct o sup (upw rd he i t o) or down (dow w rd he i t on)

© 2014 MedStu y-Piease Repo t opyr ght Infr geme t to copyr gh @me t y.com





• What is the s gnificance o doll's eyes?• W at pupil nd ng is associated w th

uncal he niat on?• What is the presentation of locked n synd ome?• What is the defin tion o pe sistent

vegetat ve state?• What s a inet c mut sm vs. cataton a?

Upward he iation pushes the pos er or fossa conten sup under the ten orium, compressing he bra ns em.Downward he iation forces he cerebe ar ons ls down through he foramen magnum, compress ng the medu a

abolic coma has many causes, includ ng ischem a,hypoxia, hypog ycemia, hiamine de ciency (Wern cke's encephalopathy), organ d sease ( ung, l ver,kidney), and d ugs Early in metabo ic encepha opa thy, pa ents have changes in resp rato y pa e andmen ation Thepupils are typ ca lyreactive un i the

erminal stages. xceptions inc ude anticho inerg cox c ty, wh ch causes xed di a ed pupils, and severe

barbitura e intoxication In addit on, bo h hypothe miaand anoxia/ischem a can cause xed pup ls o va y ngsize Anoxic- xed pupi ary dila a ion las ng more hana few minutes mpl es severe and usua y rreversiblebra n damage

H IMIC

LO KED IN SYNDRO EThe locked- n syndrome is rare and mos o en causedby a esion of theventral pons as a result o basilar ar e yocclus on The es on pica y spares he soma osensorypathways and he ascend ng RAS respons b e or arousaand wake u ness, as we as midbra n s ruc ures hata ow the eyel ds o be raised hus, he lesion inter upts

he co icobu bar and corticospina pa hways, deprivinghe pa en o speech and the capacity o respond except

by ve tical gaze and b inking Persons with lockedin syndrome are awake and aware o he surround ngenvironment bu may have on y he ab l y to con roleye movemen s Typica y, they can communicate on yby using eye b inks andve icaeye movements. (Thee erent abducens nerve bers contro ng horizon aeye movements are common y destroyed.) Because

he cerebral cortex s spared, an EG is no mal. Somepa ien s can recover some unction, so rea ment shou dbe mu ti-d scip nary and shou d nclude physicaland speech therapy, pu monary rehab, and he pw th swal owing

© 2014 MedStudy

CONDIT ON THAT C CO A

VEGETATIVE Vege ative s ate resu ts rom severebi ateral cerebradys nct on, o en following a period o comaVegetat ve sta e is o en caused by anox c braindamage (e g , a er Ml) and may be the term na phaseof progressive cortical degenera ive processes such asAlzheimer and Creu z e d -Jakobdiseases

These patien s typical y have normal sleep-wakecycles bu no disce ib e cognitive nction. Respira t on can quicken n response to st mu a on, and youmay see certain automatisms such as swa owing,b xism, gr macing, grun ing, and moaning There is

oss o sph ncter contro G abno ma ities includeow amp itude delta fre uency background activ y,

burst suppression, widespread alpha and the a activ y,an a pha coma patte , and s eep sp ndles. S mulating

he pa ent causes m n mal f any change n backgroundEG ac ivi y

Neuropa hology shows co ical am nar necrosis, whichs o en extens ve, wi h a re a ve or comple e spar ng o

bra ns em s c ures (inc uding the R S)

Coma ose pa ien s who enter in o vege ative s a es mayrecover or progress to dea h no mally wi hin2 weeksVege ative sta e ha pers s s more than3 months is ca edpers s en vege a ive s ate Pa ien s who do not recovera er 3 mon hs are unl ke y o recover Genera y within5 years, demise occurs om pneumonia, urosepsis, orsudden dea h

AKINETI UTIS

Pa ients with akinetic mutism are profoundly apathe ic,a though they register mos o wha s happeningaround hem They may speak no ma y and re ateeven s rom the recent and d stant pas . This sta e scaused by b lateral les ons generally of the anteriorpar s o thef on al obes, leaving in act he motor andsenso y pathways.

ATATONIACatatonia is a s a e of stupor and of neu ogen c mo or

mmobil y associated wi h psych a r c s ates such asschizophrenia, depression, PTSD, and drug abuse.Pa ients with ca atonia are unresponsive, a though theyprese ve ocu ocepha ic responses (doll s eyes). Somepa ients d sp ay a waxy ex bi y of passive imbmovemen and hold seemingly uncomfortab e imbpostures for long periods (ca alepsy) Pecul ar motormannerisms or repe itive mot ons, seen in a number o

hese patien s, can g ve he impression of se ures Thereare no signs o s r c ra brain disease The EEG is typca ly no ma , al hough i shows di se s owing withma ignan cataton a

1 -



11-4 HEADAC E

BRA N DEATHThe cent al features of brain death are an irrevers b eabsence of al cereb a functions and absence of a b ainstem nctions, inc ud ng spontaneous resp at on. T s

egu a ly resu ts om catastrop c b a n damage (e.g ,trauma, cardiac a est, ce eb al emorr age), but you

need to exc ude reve s b e causes suc as d ug ove dose.Signs nd cating the absence ofce ebra nction a e thep esence of deep coma a ong w t the ack of spontaneousmovement and moto and voca esponses to a visual,auditory, and cutaneous st mu at on.

Diagnostic criteria for b ain deat :

I) Diagnos s of brain deat requires nowledge of thepreceding catast ophic event (cl n ca or maging)

esponsib e for the current status.2) A possib e metabo ic confounde s s ou d be exc uded

(e.g., elect o y es abno ma it es).

3 Toxins s ou d be exc uded.Co e tempe atu e s ou d be>97° F5 SBP s ould be> I00 mmHg (presso s a owed).

Absence of b ainstem function on exam, as ind catedby fol owing

• Loss of spontaneous eye movements• M d-position of the eyes

ack of ocu ocepha ic (do l's eyes) andocu ovestibu a (ca o c) responsesP esence of di ated or m d-pos t on xed pupi s(not sma e t an3 mm)

• Pa alys s of bulba muscula re (no facia movemento gag, cough, co ea , o suck ng e exes)

• Absence of moto and autonom c esponsesto noxious stimuli

• Absence of spontaneous espiratory movements

A e ng al the above c ter a an apnea test s ou dbe ca ed out

pnea test: Pre oxygenate t e pat ent w th100% 02;pC0 shou d be no ma . T en, d sconnect t e venti ato fo I0 m nutes and obser e for espiration. A posit vetest occu s when t e e s no resp at on even wit apC02 > 0mmHg o > 20 mmHg f om base ine. Repeatt is test6 hou s late .

Diagnos s of brain death can be madeonly by l lingt e above c in ca crite a.

Tests t at can support a d agnos s of b ain deat ( ut arenot mandatory except in c i d en) inc ude

Eva uat on of b a n b ood owAng og aphyTransc anial Dopp eM CT ang og ap ySPECT

• Electrop ys olog cal testsEEG

o Evoked potent a s

HEADACH

OVERV EWThe h story and exam nation a e crucial n d agnos ngthe type and etio ogy of eadac e, ncluding t equa tyof pa n (dull, s arp, t robb ng, and constant),ocat on,durat on, exacerbating o ame orat ngfactors, and associated symptoms Also mpo tant a e t e mode of onsetof pa n and var at on over t me. First, dete mine f the

eadac e is p imary or secondary.

Acco d ng to t e nte ational C ass cat on of HeadacheD so ders3'dedition (20 3 published by the nte at onaHeadache Society, headaches can be classi ed as pr maryo secondary. Fo a deta ed descript on, see tp //w .

hs-c assication.o g/ _down oads/m xe nte at onaHeadac e-C ass cat on-I I CHD20 3Beta.pdf

P mary headaches• ig aine• Tens on- ype headache• C uster eadac e and othe tr gemina a tonomic

cepha g asOther pr mary headachesPrima y headac es tend to be ch onic, recur ent, andw t out signs of neu ologic disease

Seconda y eadac es

Headac e due to ead and/o neck t a ma, c an ahype ens on, b ain tumo sHeadac e due to c ania o cervica vascular d sorde s(e g., ca otid dissect on, g ant ce l ar e it s)Temporal a ter tisHeadache due to nonvascu a ntrac ania d sorders(t mors, etc.)Headache due to a substance or ts w thd awa(EtOH, ca eine)Headache due to infection (men ng tis, encep a tis)Headac e due to diso ders of homeostasis(HTN, hype v scosity)

• Headac e of fac a pain (cran um, neck, eyes,s nuses, teeth)Headac e due to psyc iat c diso de s

M GRA NEPresentation[K ow.] M gra nes a e a common, a ge y fami iad so de c aracte ized by pe iod c, o en un ate a ,pu sat e (t robb ng) eadaches t at begin n ch d

ood, adolescence, or ea ly adu t life and dimin s nequency as patients get o de gra nes a e mo e

common n fema es90% of patients who present toeme gency departments w th recur ent headaches havemig aines. T ese eadac es a e typically uni ate al(� 0% but not cons stently on t e same side (unl kevascular headache secondary to ar eriovenous malformat on). ey last severa ou s, typ ca y4-72 ou s

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How is brain death diagnosed? Is an EEGrequ red?

What is an apnea test, and when should it berepea ed?

Name some gge s of m graine headaches.

What s he ma n d f erence between acompl ca ed m graine and a m graine wi h aura?

Which m gra ne pa ien s shou d no ece ve arip an d ug?

They are considered episodic if< 15 episodes per monthand chronic if> 15 episodes per month for 3 months.Less than 5% of episodic su erers progress to chronicsu erers per annum.Triggers include emotional stress, certain foods (e.g.,choco ate,aged cheese, and other foods that are richin ramine), alcohol ar icularly red wine or port),menst ation, exposure to glare or other strong senso ystimu i (inc uding per mes), and rapid changes inbarome ric pressure In women, they o en occur in thepremenstrua period and can be worsened by ora contraceptives. Migraines are frequent y associated withnausea, vomiting, sensitivi y to sme , photophobia, andphonophobia Movement of the head exacerbates thepain, while sleep and darkness may he p lessen the pain.

igrain wi h a ra (previous y called classic migraine)makes up 5% of a migraine headaches. It isprecededby an a u most common y visua symptoms, suchas spark ing ights (scinti ating scotomata) or jaggedzigzag ines (for i cation spectra) that move s ow yacross the visua elds for several minutes and mayleave scotomatous defects Migraine auras last for5 0 minutes and not longer!

igrain wi ho a ra (previously called co onmigraine), occurs without an aura and is� 5x morecommon than migraine with aura.

omplica migraine (rare) is associated withfocalneurologic symptoms, including numbness and ting ingof the lips, face, and hand (on one or both sides), armor eg weakness, s ight con sion, and/or dizziness.In any given patient, on y a few of these phenomenaare p esent, and they tend to be stereotyped with eacha ack If symptoms spread from one pa of the body toanother or evolve over time, they do so re ative y slow y,over severa minutes (not seconds, as in seizures).Such symptoms ast 5- 5 minutes on average and arefo owed by uni atera headache The neuro ogic de citscan be prolonged but are rarely permanent.Basilar mig aine a ects her instem.Patients are

ypica y young women or chi dren with a fami y histo yof mig aine

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HEADACHE

Patients with basilar migraines may expe ience:visua phenomena that occupyoth visua e ds(temporary cor ical blindness may occur),vertigo,dysarthria,staggering,

incoordi a oof the imbs,dip opia ("seeing doub e ), and

• tingling. (Ting ing may occur in both hands and feetand sometimes around both sides of the mouth.)

These sy ptoms ast 0-30 minutes and are usua yfo owed y an occipital headache. In exceptional cases,coma or transient quadrip egia may develop.

c phalic migraine (migraine without headache) canpresent with a norma transient neuro ogic dys nctionsuch as visua symptoms, foca sensory de cits, transientaphasia, or hemiparesis. This type frequent y occurs withadvancing age in patients who previous y experiencedmigraines with or without aura.

a s migrainos s is characterized by multip e orvirtua y continuous headaches with persistent scalptende ess, over 72 hours or onge

Acute Treatment of Migraine

Acute eat ent refers to any treatment that is givenwithin the 1 hou of the headache. Acetaminophen,aspiri , and NSAIDs are e ective in some patients,especia ly if the migraine is mi d and in equent. Next isthe "tr pt ns

Sumatriptan (Imitrex®) • A motriptan (Axert®)Zo mitriptan (Zomig®) • Eletriptan (Re pax®)Rizatriptan (Maxa t®) Frova riptan (Frova®)

• Naratriptan (Amerge®)

o head to head trials yet exist comparing the riptans;therefore, which to choose is based on a few features ofthe drugs

Rizatriptan works fastest. But k ow that concomitantuse of propranolo requires that you ad ust therizatriptan dose downward (proprano ol increasesthe eve s).

• Sumatriptan has 3 methods of de ivery (in ection,intranasa , and oral).Combinatio tablet of suma riptan+ naproxen workssynergistica y and better than taking either agent asmonotherapy

Because of risk of inducing ischemia, donot use triptansfor any of the fol owing conditions

Complicated or basilar migrainesCoronary heart disease (CHD) or P in meta angina

• History of strokeUncontrol ed b ood pressure

• Pregnancy

1 -5



HEADACHE

Also, do not combine triptans wi h monoamine ox daseinhib tors or use w thin24 hou s of e got drugsInstead of he riptans, IVprochlo perazine ometoc op amidea so s e ective for e minat on omig a ne n pa ients who present to the eme gencydepa men with vomiting D p enhyd amine,5mg V,

he ps p even he unusua dys onic eac on.Dihyd oe gotamine (DHE) can be e ective n somepatients, but also must be avoided n pa ents withC D, T , h story o per pheral ar e al d sease,and ver o k dney d sease. You can ry na cot cs, buthei use shou d be es icted o2 days pe week. Oralo IV corticos e o ds can be used to te mina e s atusmigra nosus.Inc eased use of any med ca ion, including ip ansand NSA Ds, o t eat equen headac es can inc ea ebound cal ed medication ove se headac es "Pa ents s ould be ns r cted not to take ana gesics mo ethan 10 days pe month hey need meds is o en,then p escribe prophylac c reatment.

Prophylactic reatment of Mig a neMig aine seems o be associated with an increased

isk ofischemic s roke, especia y n ce tain g oups ofwomen who have recu en eadaches w h au aThe American ear Assoc a on/Ame ican S rokeAssocia ion2014Guidel nes o the P even ion o Strokein Women recommendprophy axis o women w requent migraines wit au a f younger t an55 yea sandespecia y f ey a e akingo a cont acep ives(OCPs )

This guideline a so ecommends aggressive smokingcessat on e o ts in women with migraine w h au aGenera y avo d OCPs n women w o have m g a newith aura (increased r sk o s roke) For o e pa ents, e

equencyo headac e determines w e he p ophylaxisis needed; no ma ly, the es old is> - 3 headac esper month. There is usua y a lag ofweeks be ween

he sta t o prop y ax s and ts e ect.he major ca ego es o m graine prop y axis agen s:

• Be a-b ockers P op anolo and mo o a eDA-approved o mig a ne, but a enolo , metop o ol,

and nado ol a e a so used;no ecommended inpatien s> 0yearsand/o smoke s.

icyc ic antidepressants amit p y ine side e ec s= ove sedat on, d y mou , pa p a ons, o t os as s,b ur y v s on, we g ga n, const pa on, andshor -te m memo y impai men o con sion espec ally in t e elder y, or those w h base inecogn ive impai mentet acyclic an dep essan s, a so known

as norad energ c and speci c serotone gicantidep essants (NaSSA) (e g , mirtazapine), andm xed se o on n norepinep ine reup ake nh b to s(S R s) (e g , venlafaxine, du oxe ine )

• Anticonvu san s (valp oate, topirama e), wh c a esometimes used o a el. Top ama e can causekidney stones and thus is contraindicated in pa ien swith kidney s ones.

• Calcium c anne blockers (verapam l, nimodipine)may develop o erance.

• AC in ib ors and ARBs (l s nop l andcandesar an)

• SAIDs• SSR s There a e no enough da a o SSR s; ey

may even cause eadac es• Botu inum oxin nject on (Bo ox®) was app oved by

t e FDA n20 0 o ef actory chron c m g a ne ( e.,migraine occu ing5or mo e days pe month withheadaches lasting4 hou s per day o longe ) Thi yone n ec ons are del ve ed in o7 speci c ead andneck si es The reatment usua ly needs o e epeatedeve y1 weeks, on average.

De nite y use p op y actic agen s to ea comp ca eand basi a m g a nes Re axa on echn ues a so mabe he p l for pa ents to prevent eadac es

CLUSTER HEADACHEClus e headache s a distinc syndrome tha requent y

esponds o ea men with oxygen T e e m c usteis de ved rom he period city of t e eadac es: T eycan occu up to severa t mes/day for a few weeks be o eremitt ngC us er headache becomes c onic in10% opa ien s. Occas onally, is eadac e is e e ed to as the

su c de eadac e," because he assoc a ed pa n is so

in ense hat some pa ients have committed su c de whenthey were unable to ge e ef rom a clus e ep sodeC us er headaches a emo e common in men(5: I).

ey end o occur in e2 50 year age group70%opa ents nd haalcoholt ggers he r headacheThe da y a acks may occu at e same hou eacday ( n50% o pa ents) T e pain isuni atera , seve e(described as an ice-pick" o ot pok ") andperio ret o o bi al. t peaks quickly n5- 0 minu es andreso ves n an ou o twoAno her c a ac e istic feature s n ghtly ecu rence,abou to 2 hou s a e e onset of s eep o severa

t mes du ng t e nig t he clus e headache as beenca ed he ala m c ock headac e" because i ecu s egular y eac nig foto 2 weeks, fol owed therea erby comple e eedom for many mon hs or even yea s.Associated vasomo or phenomena nclude ipsila era

ocked nos l, ino ea, acr mat on, mios s, anush and edema of he c eek tha ast abou45 minu es

Clus e pa ien s tend to be res ess du ng attacks, asopposed o most migraine su ere s w o prefer a dark,quiet oom and st llnessTreatmen T e bes acu e t ea men isoxygen n a a iono oxygen at6 L m n x15 minutes is common yap d yabortive, act ng o inhibit neurona ac va ion n the

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• Which m gra ne prophy ac ic drug cau ekidney o e ?

• e c u e headache mo e common i meno women?

Wha a e he c ca fea u e o c u eheadache?

ow do you rea c u e headache?

Wha age i 1 e o p evenc u er headache ?

Wha he mo common varie y of headache?

igeminoce vical complex. However, th s s not a waysp ac ica or availab e. Subc aneous and n anasal ript ns are e ective and can be comb ned w oxygen; butremembe , e t p ans shou d no be sed in pa ien s witha is ory of or s ong risk fac ors fo CHD and s okeFo patien s w o don't get be e w t 02 and can' t ke

ptans, oc reotide and int anasa l docaine are options

Once a patient exper ences t eI sto what wi become ac s e ep sode,p ophylactict ea men can be ns tuted Ve apami is t e drug o c oice (o tpatient o a t a ionup to 480 mg), b monito he pa ien 's p lse and ECG

or bradycard a and heart b ock when i a ng h g er than240 mg Ot er d ugs sometimes sed nc ude l hium,me hy serg de, p edn sone, and top rama e The co ticosteroids a e used as ac e d gs w i e wa ng fo ve apam l

o work Taper o t e meds once e c s er is over.

TENS ON HEADACHETension eadac e, e mos common va iety o eadache,

s c arac erized by pain a is c ronic, b ate a , cons ant,non-th obb ng, "sq eezing, and devoid o m g ainous o c s e fea ures I can be intermi ten o c onicUn ike mos o e eadaches, i can be presen h oughout

e day o ong periods o t me. The onset s s ow withgrad a inc ement in n ensity typ ca y a the end o eday Sleep is normally ndis rbed, but headache re supon awaken ng It is more common n women A t d opa ents with c on c tension headac es have symptomso dep ession.

Treatment: Asp n, acetam nophen, o NSA Ds can besed fo ac e at acks.

P even ivemed ca on shou d be conside ed w en attacksocc r mo e t an2 days per week is should he pp event med ca ion over se, wh ch can p edispose toc onic eadac e. L m ing t eatment o9 days per month(2 doses of meds/day) e ps p even th s complica ion.E ect ve prop y act c d ugs include ami ripty neand other t cyc ics, et acycl cs (e g , se oton n ecepto blocke s[m azap ne ven afax ne see m g a ne

p op y ax s onpage 11 6]), and gabapentin. Not SSRJs

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HEADAC E

Re axat on, biofeedback, and behavio a therapy a ehe p n dea ng wi t e ens on tha br ngs abo theheadaches

BEN GN SEXUAL HEADACHEAlso ca led "coital eadac e, ben gn sexua eadac eoccu s mo e o en n men an women (4:l). The

eadac e occ s ei er as a ension ype headac e assex a exci emen nc eases o as a severe, obb ng

eadac e a e ime of orgasm T ese eadac es canpers st fo several minutes o o rs; they are benignI he eadac e does not esolve a e2 ho s o isaccompan ed by neck st ess, vomi ing, and/or neu ode c ts, u e ou an nderlying AV mal ormation wi h owi o s barac noid emo r age Eva ua e w th genne roimag ng. T ea en w th SA Ds befo e sex aact v y may prevent t e eadac e.

POST TRAUMAT C HEADACHEos ra ma c o post conc ss on headac e can occu

even a er a m nor head nj y I can be vasc la ,l ke migraine; howeve , some have proposed ha e

eadac e s d e o abnorma ne ro ransm ssion w thine brain Accompanying symptoms inc ude d zz ness

a ig e, insomnia, ne vousness, tability, and nabilto concen ra e Symp omatic rea men s s al ye ective, and e headac e o en spontaneo s y emi s

a ient reassu ance s mpo tan

G ANT CELL ARTER T S

G an ce ( emporal) ar e t s us ally occurs in pat en s> 55 years old H sto y is typ cally a recen onse ofheadache aw claud cation, at g e, we gh oss, and

ow g ade eve may be associated symptoms Up to50%o pa ients have a isto y of po ymya gia he ma icaDo no miss is d agnosis! f unt ea ed, schem c opticneu opa hy can cause i evers b e v sion loss Dip opiaoccu s in I0 5%of pa ients ys cal exam may show

empo a ar e y ende ess T e e ythrocyte sedimena on a e s common y very eleva ed, bu C reac ive

pro ein is a more sensit ve ma ker of n amma on Do atemporal ar e y b opsyf e d agnosis is s spec ed. Yieldof b ate al ar ery biopsy(- 2 nc es o issue) in expertcente s is abo 85% o t e Boa ds, i ESR and CR a eno al, it sno GCA Mo e n Rheuma ology, ook3.

D OPATH C NTRACRAN ALHYPERTENS ON I PSEUDOTUMORCEREBRIdiopa h c in racrania hype tension ([IIH] also ca ledpse do mor ce eb i) s a se of signs and symp omsheadaches, pap edema, and loss of vis on ausedby nc eased nt ac ania p ess e I o dinarily occ sin obese, p emenopa sa women 90%)and can occ r

d ng p egnancy I arely occ rs n c ild en o n men

1 -7



1 -8 DEL RIUM

O esi is strongly co related (90 95% of patients)and causal; with the increasing obesity o the U.S.pop lation, the incidence o IIH is a so inc easing.D that a e associated with I H inc de vitamin A(especia y in the orm of isotretinoin, sed for the t eatment of seve e acne), tetracyc ine, and cor icoste oids;b t the condition may also be p ecipitated by ste oidwithd awalSeve e, ir eversible vision oss is the major morbidityIt occ rs in> 6% o patients and is twice as common inmen as m women

The cardinal symptom o IH is am i g headachedescribed as dull o as a feeling o press re (90%) madeworse by h or st aining he e is a most always(90 1 00%) a h l visu l ld l ssaccompaniedby blind spots that may be noticeab e only with o mavis a eld testinP ls -s tinni us (60%)may be p esent

ther, less eq ent comp aints are b r ed vision,dizziness, minimal horizontal dip opia (8%) om6thner e paresis, transient vis al obscurations that o encoincide with the peak intensity of the headache, o mi dn mbness of the ace on one side

n exam, p p ll is a hallma nding6 hner epa sy may be obvio s either nilaterally or bilate ally.CT/M is typica ly al, with absence of de o mity,disp acement, o obst ction of the vent icu ar systemb t may show "slit ike vent ic es The CSF p essureis elevated, s a y in the range of 250 450 mm H(Normal CSF pressu e is generally< 200 mm H )

T eatment of H inc des a low-sodium weight reducingdiet, sy ptomatic t eatment fo headaches, ca b nicanhyd ase inhibito s (acetazo amide), and p evention ovision ossR lu s, with drainage of su cient

id to maintain C F pressure < 200 mm H , may behelp in 25%

rednisone wo s ac te y b t isn ecommended forc ronic cases of IIH beca se of side e ects, not the easto which is inc easing int ac anial pressu e nilate aoptic nerve sheath enestration may p ese e vision inthe acute setting.

n patients whose headaches a e nresponsive tomedications and weight reduction, mbar pe itoneash nt may have conside ab e success

H C P SY OThis synd ome causes re acto y ni ateral pain, whichcan a ect the n , as we as the a m and eg. Thalamipain synd ome can occ weeks to a er a thalamicin a ct (with hemisensory loss)

DELIRIUM

e i i m is an acute, and o en t ansient, onset of alte edmenta sta us, typical y within hours to days It is mostcommon y seen in hospitalized e de y patients in theIC The diagnosis is based on the c inica ha mar so dec eased at ention span and va ying stat s o consion T eatment is ai ed at identi ing any unde yingcause and suppo ive care elirium is a so disc ssed inGene a nte al Medicine, Book 5, Ge iat ics.

DEMENTIA

F Oementia is de ned as a c onic c gnitive declin with

o without behavio a impai ment that• Is p g ssiv• swith nor al dai y nctioning• s d e tod l uor an unde lying

s hi is d

Note how this de nition contrasts with encephalopathy,which causes alte ed states conscio sness omdeli ium to s po

WO K P

valua ing omains of unc ionAcco ding to m ltiple guide ines by the nsti ute oAging and the A zheime 's Association, dementia

is diagnosed l a er com l tion of the ol owing3 tasks, which eva ate s eci c domains f nction(disc ssed next):

) The health care professiona p r orms a tho o gh&Pthat inc udes obtaining histo y om the patientndan additiona informant (b ca se histo y from apotential y demented patient is not a ways e iab e).

2) u s hi testing (to excl de nder yingpsychiat ic diagnoses)

) b ective itivassessment using a validated tool(e g , the Mont ea Cognitive Assessment, the FolsteinMini Mental State Exam)

iagnosis of emen iaementia is diagnosed wh n abno malities exist in

2 o the following d a s , and when theabno malities also are ss v and i t ewithdaily ncti ning

) emor = acq iring and/or emembe ing newinfo mation o they as epetitive q estions, oseit ms, or get ost?

2) xecutive function reasoning and per ormingcomplex tasks o they understand app op iatedange ? Can they pe form thei A Ls, such as g oce ysh pping?

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ui

• Name some risk factors that are assoc atedw t IH.

• What is the clinical presentation o II ?• W at is delirium?• What is the c rrent de n t on o "dementia ?• Whic 5 doma ns may be mpa red n patients

with dementia?• W at s t e definition o "mi d cognitive

mpairment ?

W at percentage o patients w th MCI progressto dementia ann a ly?

• What is the clinical tr ad n norma pressureyd ocep alus?

) P rc ion = assessing visuospatial orientation:Do they recognize faces and objects? Can theydress themselves?

4) L n = comprehension and speaking appropriateang age Do they have prob ems reca ing common

words without hesitations?5 B h vior = behaving normal y and appropriate y

s there ndue agitation, apathy, loss o empathy,comp sive behavior?

Psychosis that is re ractory to treatment is a commonfeat re o advanced dementia

ild ognitive mpairmentWhen only 1 or more o the domains is in declineb t the impairment does not signi cantly impactdai y nctioning, the diagnosis is "mild cognitiveimpairment (MC )

MC can be either amnestic or non-amnesticA nesticMC is most common Not all patients with MC deteriorate into dementia. MC progresses to dementia at arate o abo t5- 10% per year Such progression is more

ikely in patients with a family history of Alzheimer

disease Patients with amnestic MC have memoryimpairment that does not signi cantly impact dai yliving, and general cognition is intact O those who dodeteriorate to Al heimer disease more o en they are thepatients with amnestic MC .

Patients with non amnestic MC have impairment in or more o the other domains (exec tive nction,

perception, words, or behavior), but daily living isnot impacted

©2014 M dStu y

DE NTIA

Revers ble ausesn eva ating dementia, exc de the fo owing treatable

causes o impaired cognition:

MedicationsVitamin 812 de ciency (may have associatedpo yneuropathy/myelopathy)Heav metal poisoning (arsenic, merc ry, and lead)HypothyroidismDiabetesChronic subdura hematomas (consider especial yin a coholics, in patients on anticoagu ants, and inelder y patients with a history o alls)

orma pressure hydrocepha sT mors, especia y involving the frontal lobes

n ection and in ammationAJDS Ne rosyphilis

o eurosarcoidosis Chronic meningitis Lup s cerebritisVascu itis

CAUSES OF DEMENT Aorma Pressure Hydrocepha us

Norma press re hydrocepha s (NPH) is a potentia ytreatable ca se o dementia t is characterizedradio ogica y by en argement o the ventric es without obstr ction o the aqueduct (i e , a comm nicatinghydrocepha us ) and no cerebral atrophy Signi cantcentra atrophy (with or without cortica atrophy) mayres lt in hydrocephal s ex vac o.

NPH o en occ rs a er head trauma, mening t s, ors barachnoid hemorrhage and a histo y o I o thesepremorbid conditions appears to be the best predictorof a bene cia response to sh nting (see be ow) Onetho ght abo t how this develops is that there is obstruction o the o t ow o cerebrospina uid at the leve ofthe arachnoid gran ations However, the intracraniapress re is norma , there is no papil edema, and theperson has no headache

NPH ca ses the c assic triado

1 a grad a y worseningdementia ,2 gait ataxia/apraxia (a magnet c gait, with the eet

apparently g ued to the oor) and3) urina y incontinence

O en, the gait problems and incontinence precede thedementia Patients may present with re ent a s d e togait instabi ity

Di erentiate NPH rom ventric lar di atation ca sedby di se white matter changes (Binswanger disease,see page I ), which is more common in patientswith hyper ension or diabetes me itus Note that it maypresent with the same clinical triad as PH

-9



- 0 DEMENT A

Treatmen : In most cases of NPH, the CSF open ngpressure is above mm H20, and the cell cou snormal. The treatme svent iculope onealor ve

iculoa ialshunt Cer a n es s may he p to ide ipat e ts who a e mos likely o respo d o shunting. These include c ca response to lumbar pu ctu e(LP), so ope cyste ography, a d dy am c MRI,wh ch measures the d rec io of CSF ow (but one ofhese ests s un versally re iab e) The most consis e timproveme t is a ained in pa ients wi h an den i edcause such as subarachno d hemo rhage, ch o cmen ng t s, o head trauma

lzh

AD Diagnosis

A zhe mer d sease (AD) is the most common causeof deme tiaa er age6 . I51deg ee e at ves have a4x orma creased r sk of deve op g .

Acco d g o2 guidelines, AD is diagnosed whehe ess isins dious, p og essive, and marked byimpa r en s 2 o mo edomains (memo y, execu vefunc ion g, pe cept on, wo ds, and behav o ), such hatthere issigni can impai me tin normal da ly c io

g. As w th MCI (p 11-9 ), the amnes ic prese a onof AD is he mos commo Pa ents w th A zheime 'shave ano alLP.I al sig s of AD commonly re ect hippocampadys nc ion, w th poo immed a e ecall and sho- ememo y Impai e of naming may a so be a earlys g As he d sease p og esses, mpa r e s emerge

v suospa ia and execut ve doma s, re ec gdys ct o i hepa ie aand o al obes, espect vely Changes e v ronment (such as vacatio s orhospi a stays) may be d sor e g, a d the pa e t maybecome los on wa ks or wh e d v g

o e the con as in he presen a io of AD wi hthe presenta o of Lewy body a d fro to emporaldemen ias a d spo ad c C eutzfeld Jakob disease,which a e seen i younger pat e s a d have amo e

ap da dvola ilecourse (more n he ex sect on)A so con as , mu t infarct deme t a presents w thstepw se de e io a oha is o e accompa ied bymotor or se sory mpai ent e ated o he areasof strokeDo no use any of the fo ow g for diag os s of AD:MR sca s tha show d spropor io ate a ophy, PETsca s demons a g amy o d depos t o o dec easedtrace up ake, and CS tau measureme s. hese b oma ke s a eno speci c enoughye , and ab o ali essomet mes are see pa ien s w th nor a cogn t on oMCI o yAdd t o a ly, dono d ag ose AD as a cause of deme t a

f he patienhas a h s ory of s g cant ce eb ovascular d sease

has c n ca featu es of Lewy body o ontotemporaldemen ia,

has ev dence of a othe psychia ic o neu olog clness, o

t kes a medicatio tha ca cause cogn t veimpa rment.

These must be ru ed ou as causes of the demen asymp oms. n an elderly pat e p ese ting w h demen

a w hou a movement d sorder, he mai d ag oseo co sider a e Al he me disease,vascula demen a,and mixed dement a wi h bo h neurodegene a ve andvascula componen s)

AD Treatment

The I 1line eatme for Alzheime s is cholines e asenh bi o s (C s)Do epez l (A cep ®)R vas igmi e ( xelon®)

• Galan amine (Ra adyne®)

No e: Tacrine (Cognex®) causes liver ox c y and is olo ger usedAdd ivedrug ea men cludes the N methyl-d aspa a erecepto a agon s mema i e Namenda ) Thecombina onof CI+ meman e appears o be be e

ha CI alone, espec ally for advanced AD. The C s produce a small mp ovemen n cogn t on a d,somet mes, in europsychia ric instab li y. Da a arecon ic ing o the r long- e e ects. No eve y pa e

eceives bene t. No e ha hese d ugs a e fo dementia o ly and shouldno be used o rea minor cogni ve

mpai me t (MCI). Bes resul s wi h C s a e achieved inmild o mode ate A heime d sease, bu othe types odeme tia (e.g , mul farc a d Lewy body deme tia)some imes also mp ove.Dose escala ons fo each of these med ca ons mus becar ed ou ove 4 weeks o mi imize s de e ects Thmai side e ec s are a o exia, ausea, a d occas onallyd a hea or b adyca dia (cholinerg c sy p oms) Rivas gm ne s ava lable as a patch ha has fewe GI s de ects and is use l demen ed pa ie s who will notswal ow med catio s The europsych at ic ins ab li y of late s age ADis commo a d d cu to treat. M ld o modera edepress on n he ea y stages may respo d to SSR s,trazodo e, or C s, but de i ely avo d ricycl ca tidep essa ts because of the a chol e gicsymptoms, pa icu arly sho e memo y mpai ea d con sion A ypical anpsycho ics olan ap eque apine, spe done, clozapine) have been used totrea he ag tatio , insom ia, de us o s, aggress on, andwande ing, bu in2 ,the FDA published an adv so y

hat hese d gs a e assoc ated wi hnc eased mo ali yin he elderly wi h deme ia (any cause) They should beused o ly n the mos ex reme cases of psychos s.

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• How is AD diagnosed?• ow are CSF tau measuremen s used i the

diag osis of AD?• What drug is used wi h a Cl fo the treatme

of adva ced AD?

Wha is a potentia complica ion from he useo a ypical a ipsychotics in e derly pa ientswith demen ia?

• Compa e and cont ast he eatu es o o malp essure hydrocephalus, A zheime disease,a d vascular dementia.

• How does he cli ica p ese ta ion ofro otempora deme ia dif er om that o

Alzheimer disease?

Is CJD insidious o rapid?

Vascular DementiaOv rvi w

Dementia associated with cereb ovascular disease can bedivided into2 gene a catego ies:multi-infa ctdementiaand di use white mattedisease (Binswange disease)

l i-infarc m n a

Mu ti-in a ct dementia is the term used o the chronic

cognitive de cits that can occu in patients who havehad seve al st okes The st okes may be large o sma lbut usually invo ve severa di erent b ain regions. Theoccu ence of dementia depends partly on the totavo ume of damaged cor ex but is a so mo e com onwith e hemisphe e lesionsMulti-infa ct dementi as gene ally have prominent motor,

e ex, visua , and gait abnorma ities, but they typica lydo not invo ve di cul y innamingof objects, as associated with A zheimer disease Another di e ence is theclinica course o symptoms. u ti-infarct dementia hasan abrupt onset withstepwise dete io ation o menta

nction, with more p ominent uc uations of cognition.By cont ast,Alzheime 'shas as ow, steady p og ession

ff s Whi a r is as

Ch onic hype tension is the most common cause ofdementia due to lacuna infarcts and di se white ma erchanges that a e visible on R . The changes esu t

om chronic ischemia mediated by occ usive diseaseo sma , penetrating cereb al ar e ies and a erio es.Diabetes is also a common cause o this conditionEa y symptoms inc ude mild con sion and impai mentsin memory, pe ception, and executive nctions. arkeddi culties in judgment and orientation develop late ,a ong with dependence on others for activities of daily

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DEMENTIA

living Neu opsychiat ic symptoms (apathy, anxie y,psychosis, euphoria, depression, agg ession) alsodeve op as the deep white matte changes and in a ctsaccumulate Pyramidal and ce ebellar signs may beseen With advanced disease, u inary incontinence anddysa h ia with or without othe pseudobu ba featu es(e.g., dysphagia, emotiona abi ity) are requent

Fronto empora Dementia

F ontotemporal dementia ([FTD]; p eviously Pickdisease) is uite similar in presentation and cou se toA heime disease, but it is character zed by amo e

apidand signi cant change in pe sona i y and behavior, o en withdisinhibition, language de cits, or both.The onset is in theyh to 6thdecades ( elatively young,compared to A heime 's), and the incidence in malesexceeds femalesCommon behavio a features include apathy,disinhibition, weight gain, food etishes, compulsions,and emotional distance or loss o empathy.Cognitive testing ypical y reveals spa ed memo y butimpaired planning, judgment, or language Patients o enshow an absence of insight into thei conditionThe naming of F D sub ypes is evolving based on theip imary manifestations e.g , behavio a va iant vs. prog essive non uent vs semantic atients with FTD havemo e focal atrophy of the frontal and tempo a lobes onCT o scan, compared with the di use atrophy ofAlzheimer s. Howeve , histology is the on y su e way todi e entiate the wo, pically at autopsy

Cur ently, there a eno primary pharmacologict eatments fo the ontotempo a dementias. azodone has been shown to result in some behavioralimprovement, main y in ir itabili y, agitation, dep essivesymptoms, and eating distu bances.

Creutzfe d Jakob Disease

C eut eldt Jakob disease (CJD) is one o the veryare(I pe million people)pr on diseases t s mainly

an in ectious il ness Based on obse vations o causes,CJD is divided intospo adic (sCJD, most common,95%) familial (about 5%) iatrogenic(iCJD), andvari

ant (vCJD). Usua ly, sC D p esents a ound ages55-65,and we have no idea what causes it When you see CJDin younge patients, think eithe iCJD o vCJD. vC Dis believed (but not de nitive y p oven) to be caused bythe p ion that causes "mad cow disease (bovine spongifo m encephalopathy) in ca e It appea s that thep ion jumped species and now in ects humans. iCJD iscaused by eceipt o in ected human tissues, hormones(growth hormone, gonadotropins, dural gra s, co ealor liver transp ants), or exposure to contaminated su gical inst uments. Fami ial CJD has genetic associations

ega dless o cause, CJD develops as arapidlyp og essivedementia (weeks as opposed to yea s) withcha acte isticstartle myoc onus(response to oud noises

11-11



2 DEMENTIA

or startle). The early stages of the neurologic diseaseare characterized by changes in behavior, emotionalresponse, and inte ectua nction, o en fo owed byataxia and vis al distortions, con sion, ha cinations,de sions, and agi ation. Dementia and m teness q icklyfo low the ear y symptoms. Younger pa ients with vCJDtend to have dementia with predominantly psychoticfeatures he disease invo ves the cerebra cortex, basaganglia, and spina cord.

The diagnostic go d standard is brainbiopsy. Suppor ivestudies include:

• Tl/T2 MR with di sion weighted images andFLAIR seq ences (he ps a so to di erentiate sCJDfrom vCJD)EEG (characteristic patte of "periodic sharp wavescomp exes on a di sely s owed background)

4-3 3protein in an otherwise bland CSFOn y the Nationa Prion Disease Pathologica

Survei ance ab does this test, at Case Weste , andsensitivity/speci city is<80%.)

Cre t feldt Jakob disease isfatal in< 1year in> 90%

Parkinson Disease Dementia (POD

Parkinson disease (PD) is ca sed by a oss of dopaminergicneurons in the s bstantia nigra. (See the ater discussion

nder Movement Disorders on page11-44.)Dementia in PD (P D) is common, event a y a ectingas many as 80% of patients Its freq ency increases withaging and, in contrast to A zheimer disease, primari ya ectsexec tive nctions and attention in its earlierstages, with re ative sparing of anguage, memory, andca cu ations unti ater in the disease course. Whendementia precedes or deve ops within I year a er theonset of motor dys nction, it is referred to as dementia with Lewy bodies DLB). Neuropatho ogy shows

ewy bodies mixed with amy oid p aques and neuro bri ary tang es characteristic of A zheimer disease( age ). Lewy bodies are spherica eosinophilicinc sions within the ne ron( mage1 -2)The ewy body e ements seem to corre ate most withthe degree of dementia, so Parkinson disease dementia isfreq ent y ca ed DLB. DLB sometimes occurswitho t

preceding Parkinson disease - b t is otherwise theidentica disease.

The core clinica feat res of PDD/DLB (besidesdementia) are spontaneo s motor feat res of parkinsonism; recurrent, vivid visual ha cinations andprominent uct ations of attention and cognition. Othersupportive clinica features inc de ha lucinations inother modalities e.g. tacti e o factory, or auditory),de sions, REM s eep behavior disorder (dream enactment), nexp ained fa s or oss of consc o sness,and depression.

Both the dementia and psychosis may be at least

par ia ly responsive to acetylcho inesterase inhibitors and memantine. Patients with DLB have poor

responses to the older antipsychotic drugs that block theD dopamine receptor, inc ding haloperido and ch orpromazine - and even to some of the newer atypicalne roleptics. They have a dramatic and severe worsening of symptoms with extreme sedation, increasedcon sion, and post ra instabi ity with fa s However,c o apine, which spares the D dopamine receptor, canbe helpf , with inconsistent bene t om q etiapine. Asmentioned in the section on Alzheimer's, antipsychoticdr gs are under anFDA safety advisory because they areassociated with an increased risk of death when used ine der y patients with dementia, and especia y so in thosewith DLB All antipsychotics other than clozapine andquetiapine sho ld be avoided in DLB.

P og ess ve Sup anuclea Palsy

Progressive supran clear palsy (PSP) has its onsettypically in the 6'h decade, with c inica feat res s chas di c lty in ba ance, abr pt fa s, vis a and ocu ardist rbances, s rred speech, dysphagia, and personali ychange, with prominent apathy. Di c ty in vo untavertica movement of the eyes, consistently downwardinitia ly but sometimes upward, and later paresis ofvoluntary saccades in a l directions are characteristic.Patients can also have apraxia of eye id opening (resemb ing b epharospasm) and eye id c osing. Cognitiveslowing and dementia are prominent feat res. Buzzwordfor PSP dementia withgaze pa syand fal s

Huntington Disease

H ntingt n disease HD) ca ses both adementia and amovement disorder. (More movement disorders are disc ssed star ing onpage 1 44. The gene responsible forHD is the HTT gene on chromosome 4p, which codesfor a mutant huntingt n protein that is probab y toxic.(Note: The protein is spelled with an , whi e the diseaseis spelled with an .) t is inherited in an a tosomal dominant fashion with complete penetrance Problems typica y begin in persons in theirate30s.HD ca ses dementia,chorea, and psychiatric dist rbances,inc ding persona ity changes, depression, andpsychosisMemory is relative y spared. Chorea is s a ly the hera ding symptom The emotional dis urbances and changes in

persona i y may be so severe as to ca se psychosis withpersecutory de usions or ha ucinations.

Disease is progressive with death (typica y ompne monia) within 30 years a er symptomsbegin. Diagnosis is made in the setting of positivefami y history, clinica fea ures, and genetic testingdemonstrating the TT gene.

Atrophy of the caudate n clei on CT or R ("boxcarventricles) is characteristic and corre ates withdeterioration in cognition. No c rative medicationexists, and the disease is invariablyfatal Tetrabenazinehas been approved and is e ective in contro ling mi dchorea. Side e ects are signi cant and include depression, sedation, and bradykinesia. Other symptoms can

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Q� uiHow do you diagnose Creutzfeldt-Jakobd sease?

Compa e and cont ast DLB and PSP w thPa k nson disease.

What is the problem w th us ng ant psychoticdrugs to treat pat ents with Park nson dement a?

What a e the c inical featu es of Hunt ngtondisease?

Name some featu es that distinguish dep ess onfrom dementia.

Name the maneuvers f equently emp oyed tot eat BPV.

be ame orated wi h ant psycho ics (neurolep ics), benzodiazepines (e g., c onazepam) and antidepressan s

Gene ic counse ing is ava lab e for fam y membersbut is perfor ed only � 15% of the ime. There areno gu de ines ha speci cally recommend screeningbecause of the gravi y of he diagnosis, f the test spos t ve.

A S is he mos common cause of demen ia in youngerpa en s Demen ia a ects half of al A DS patien s noon ant retroviral therapy (ART). The manifes a ons

can be mi d (minor cogni ive-motor d sorder) o severe(HIV associated demen a). Impairmen s re a ed o hedegree and d ra ion of mm nosuppress on. Con ro l ng he v s in a pat en who has had AIDS for a pro ongedperiod, w h a ow CD4 count, o en does no reversedemen a.

HIV associa ed demen ia (HAD) s charac erized bycogn ve impa en , movemen disorders, and depression. It sta ts wi h smal comprehens on problems andanhedon a, accompanied by tremor and gai abnormalit es. Over ime, pat en s deve op slower movemen s wi hsubs ant al cogn tive impairmen . Excl de oppor nis cinfect ons of the CNS as pa of he work p.

Image - :Seni e plaques withamy oid cor

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mage - Pa kin on di ea eith Lewy b die

D ZZ NE

Treatmen nc des reat ng the HIV with ART, focusingspeci ca y on designing a regimen of medicat ons thaen er the CNS at h gher leve s (al ho gh his has no beenshown o ca se neuro ogic mprovemen ) Assoc ateddepress on shou d also be rea ed. More on reatmen ofA DS in Infectious Disease, Boo I. A so, see more onHIV assoc a ed demen ia (HAD) on a 9

epressionSome pa ien s w thmajor depression presen wi hs gn can cogni ve dys nc ion, known as depressive"pseudo dementia. One d eren iat ng fea re s ha

ontal lobe re ease signs (e g., grasp, s ck, roo ing,and palmomental re exes) are common in patien swi h dement a, pa ic arly if modera e or advanced,bu hey arenot seen in isola ed depression. In addit on,

mmediate recall is common y poor n depress on, d e oat entiona dys nc ion, bu good in dementia.

Depression can be reac ive or endogenous Symptomsare he same for both In endogenous depression,patients, as expec ed, may have an abnorma response tothe dexamethasone suppression es in which he cortiso

s ni ially s ppressed, but the dura on of suppression ssho tened (normal is> 2 hours)

DIZZINESS

S G S A D SYMPTOMSWhen he e m "d zziness is used by a patien , i snecessary to d erent a e among he fo ow ng:

• Vertigo = a sense of sp nning or swaying.Ligh headedness presyncope (" feel ike 'm go ng o pass ou )Imba ance= uns eadiness.Vague= no one of the 3 above. It may be hard for hea ected person o describe

When we discuss dizziness here, we are consideringonly ve igo.

CAUSES OF VERTIGO

Ben gn osit onal ert goBenign posi ional ve tigo (BPV) describes rec rren ,brief ep sodes of ve igo ca sed by the motion ofchanging head pos t on I is hough o be d e o ooseo ocon a in he semic rcu ar cana . O ocon a are crysta sthat reside in he sacc e and u ric e. When they escapeth s region, hey can set up eddy cu en s in he endo

ymph, ca sing symp oms of ver go. BPV can a so becaused by head tra ma, abyrin hi is, or aging

Mos BPV resolves spontaneous y over a co p e ofweeks or can be reated s ccess y wi h variousrepos t on ng maneuvers hat move the o ocon a o

a pos tion of he nner ear hat s ess likely o nducevert go. These are the Epley and Semont maneuvers

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11 NYSTAGMUS

and the r var a ons. In some pa ients, ep sodes recurper od ca y om several days o many mon hs-rare yfor years.

Mec zine doesn' c re BPV, bu i s some mes sed ocon ro nausea BPV and non ve go causes of "dness are d scussed in Genera Inte a Medic ne Book5.

Ves ibular euri s Ves b lar ne 1s (ves ib ar neuron s, acu eper pheral vestib opathy) causes a sudden onset ofnon positiona ve t go that sself im edb t may

as weeks to months and occas ona y can recur Thisd sorder occ rs main y n yo ng o m dd e aged adu ts,w ho preference for e ther sex.

Vestibu ar neur s s caused by an n ammato yprocess a ect ng the vest b ar por on of hegthcranialne e and can be assoc a ed with v ra infec ons. ureves ibu ar ne rit s does no a ec hear ng. f hear ng isa ec ed, means i s no longer so e y he nerve beinga ec ed b also he labyr n hine canals and th s scalled ves bularabyr n his.

Us a y he onse of ver go s fair y abr p , a thoughsome pa en s descr be a prodromal period of severaho rs or days in wh ch hey fel o ba ance. ersis enceof he symp oms for a day or more d erentiates thed sorder from M n re d sease. he ver go s severe asa ru e and s associated with na sea and vomiting, t nn t s s common y absen , and hearing s not a ec ed

nlike M n re d sease (see below) he severe vert goand associa ed symp oms subs de n a matter of several

days, b t lesser degrees of these symptoms, made worseby rapid movements of the head, may pers st for severaweeks or mon hs

Cor cos e o ds probab y he p recovery More studiesare needed o con rm his e ect. If s ero ds are not used,

ea men ssymp oma con y. During he acute stage,an h stam ne d gs (e.g., p ome ha ne, c ona epam, andscopolamine) may be he p n reduc ng he symp oms.

mino lycos de ox ci yAm nog ycos de ox city can cause some nitiasensor ne ra hear ng oss and, a er, ntermit en mildve go

n re D seaseM n re d sease s charac er zed by rec ent a acks ofve tigo assoc a ed w h n erm ent nn t s ha beg nsbe ween 20 and 40 years of age. he character st c

r ad s ep sod cvert go (o en assoc a ed with na seaand vomit ng) and t nni us, w h deve opmentof

ow freq encyh ar ng ossa er recu ren ep sodes. Itequen y beg ns n atera y bu can become b a eran20-30% of pat en s.

he ma n pathologic changes cons st of an ncreasein he vo me of endolymph and disten on of heendolympha c sys em ( endo ymphat c hydrops), part yre a ed to sa in akeD agnos s s c nica A d ome ry can he p dete m ne fhear ng loss has occ red. If hearing oss is presen at

d agnos s, exc de neurosyph s as a ca se by check nga se m VORL or R

An ih s am nes, an iemetics, and seda ives are sed nac te ep sodes. Chronic reatment ncludes erad catingca eine and red cing the in ake of salt, alcohol, n cot ne,and monosodium glutama e. hiazide di re ics are sedwhen spe s con nue a er d e a y mod cat on.95%of pat ents get heir d sease nder contro and nc onno ma ly. For med ca y recalcitran M n re d seaseendo ympha c sac surge y, s rgica labyr n hectomyand ves bu ar ner e sec ons remain herape c op ons

Ve ebrobas lar I s Ver ebrobas ar IAs (transien schem c at acks) maycause n ermitten, re urr n ver go. h s poster or c rcu a on IA s us ally easy o diagnose because a socauses o her symp oms ofvertebrobasi ar nsu en y s ch asb la eralv s on loss, dip op a, dysar hria,atax a,and b ateral ex emity mo or or senso y dys nc onAnd, he pat ent regu arly has risk factors for s roke.Workup of the poster or c rcu a ion req res spec al

mag ng. [ now:] he standard work p of ook ng aonly he anter or circ lat on doesno ca ch s enoses n

he pos er orc rcu a ion. Current y, he recommended

testing for imag ng of the poster or c rcu a on isC orMR angiograph Know tha duplex Dopp er l raso ndsno recommended for these vessels because of a ack

of sensit vity

NYSTAGMUS

Nys agmus s an nvo n a y oscilla on of the eyes he movemen s may bependu ar( ike a pend lum) orjerk Jerk nys agmus has2 componen s: s ow and fast he eyes "dr (= slow component), and ry o qu ck yrecover (= fas component). The fas d rect on de nes

he d rec on of the nystagm s Nystagm s s some mes(b no always) assoc a ed w th ver goerk nys agmus s most common inv s ibu ardisorders

b t does no indicate whether the es on s wi h n thecen ra nervo s sys em, or f invo ves he cranianerve itsel Upbea ng jerk nys agmus sua y ndicatesa es on in the pons b t can be seen n es ons of hemed lla or cerebe m.Downbea ng jerk nys agmusind cates a es on a he cervicomedu ary j nc onGa ing n particu ar d rec ions precip tates he abnorma eye movements n ce tain types of nystagmus. or

ns ance, drugs (e g , an iep ept c med ca ons) may

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What are he clinical fea ures o M ni redisease?

Wh ch TIAs cause vertigo?

Wha bra n les on s suggested by upbea ng jerknystagmus? Downbea ng?

• What are some di erences between generalizedand foca sei ures?

Wha tes shou d you order f you suspectrecurrent pseudose zures (PNES)?

cause horizon al and ve ic g zeevoked nystagmus(occurr ng when he person looks r gh , le , or up) no her words, s p esent " n a d ect ons. Isolated ver

cal ga e-evoked nys agmus yp ca y nd cates d sease

n he pos e or fossa

TINNITUS

Know these causes of t nn tus:

Pulse synchronous t nn tus w th Hnterm en nn us w th M n re's

Asp r n overdoseH gh no se levelsHear ng loss

The t nn tus hat occurs w h hear ng loss s thought tobe a compensato y react on to the hea ng loss tsel Note tha no nn us occurs w th ves bu ar neur s.

SEIZURES

OVERVIEWConvulsion s an n ense pa oxysm of nvolunta yrepe i ive muscular contract ons, and t does not a wayshave to be presen dur ng se ureseizure s p efe ableas a gene c ter because t ncludes all paroxysmae ectr cal d scharges of he bra n tha cause loss of con

sc ousness; a e at on of pe cept on o mpa rmen ofpsych c nct on convuls ve movemen s; d stu banceof sensat on; or some combina on thereo pilepsy sde ned as a cond t on of recurren unp ovo ed se u es.The cond t on of p olonged o repe t ve convu s vese ures s termedstatus epilepticus and can bel fe threaten ng

t s cruc a o determ ne whethe the se u es arepr mary ( d opa h c) o secondary.

© 2014 MedStudy

T NN U

GENERA ZEDvs . FOCALSe ures arise from the cerebra cor ex

The 2010 n e at onal League Aga ns Ep epsy ( LAE)n e a ional C ass cat on of Ep ep c Se u es now

ca egor es se u e d sorde s ntogener izedand foc(p ev ous y pa a ):

Foca (o pa t a ) se ures nvo veI s de of the bra nThese a e noted for mo or act v y on1 s de of thebody (usually) and no mpa rment of consc ousnessGeneral ed se ures involve both hem sphe esof he bra n and resu t n d m n shed consc ousness.Any mo or ac vi y gene ally nvolves bo h s des ofthe body (but no necessar ly)

Fu her ( nte at ona ) class ca on of ep ept c se ures

Focal (par a ) sei uresSimple part a ; consc ousness ma n a nedComplex par ial consc ousness s mpa redPar a w h secondary general a on

Genera ed se ureso onconvuls ve: absence se re (typ ca and

atyp cal based on 3 second sp e on EEG)Convu s ve

yoclon c se u eClon c se reTon c se u eTon c-clon c se ureAton c se ure

Focal se u es a e mo e commonly due to focal bra nles ons wh e p ma y gene al ed se ures are mo ecommon y gene c (although the e a e many excep ions

o his ule of thumb)

PSYCHOGENIC NONEPILEPT CSE ZURES (PNES)PNES (pseudose ures) a e not due o abnor al bra nact v ty but are psychogen c Features tha suggestPNES nclude forced eye closure du ng even , pelv ct ust ng, vocal at on, absence of a post cta sta e

Order v deo EEG mon o ng f PNES s suspec ed. Note, however, ha 20% of pat ents w th PNES alsohave ep lepsy.

SE ZURE AURAA aura s a pe cep ua d s u bance that may precede afocal se re Auras dono occur w hp im ygenera

ed se u es No e hat a ras do occu w h m ra ne, bua l d scuss on here s n reference on y to se ures.

Auras have var ous man fes at ons a ect ng thens sThey can be soma osensory percep ons such as pa nnumbness, or t ngl ng or ela ed to o her senses They

- 5



- 6 SEIZURES

can be mos lymotor , ranging om remors or shak ng ogross mo or movemen They can also be:• Visua with ghts, pa te s, see ng objec s• Aud ory with vo ces, noises, ones, and o her sounds• O factory, p ca y wi h a bu rubber sme• Gus a ory wi h he percep on of s range as es

[K ow:] Auras, in the context of seizures, have been usedas a wa ng manifes ation of sei ure and have a owed

he pa ent to take precau ions. These auras are hough tobe produced byear yseizure ac iv y

A foca se zure can evo ve in o a focal seiz re w hdiminished consciousness, and either of hese can evolvesecondarily in o a generalized sei ure In any of thesesi ations, the preceding seizure s a so ca ed an auraby some

COMMON SEIZURE PESThe d scussion here addresses4 main types of se zures:

1) Generalized tonic clonic se zures are a so knownas a grand ma in o der ep lepsy i erat re Theseinvolve both hemispheres, w th resu t ng b lateramo or involvement Consciousness s impa red w tha pronounced pos ic al period These se zures can begenera zed om he start, or hey can be foca seiz reswi h secondary genera i at on

2) Absence se z res are a pe ofgenera edse zure thaused to be ca ed peti ma . These are nonconv s ve,general zed se ures w thno a a andno pos ctasymptoms The a acks occur w hou w ing and cons s ofa sudden inte p on of consc ousness during whichthe pat ent stares and brie y stops talking or ceases

o respond They can be induced by hypervent a ngAbsences have a charac er st c 3-per-second spike and

able 11-2: f p p (

DrugP enytoin

Carbamazepine

Valproic acid

thosuximideLamotr gine

Gabapentin

Clonazepam

P enobarbital

Topiramate

sed to Treat

Foca ()1Genera ized tonic c onic (a te ative)

Foca ()Genera ized tonic clonic (alte ative)

Genera ized tonic c onic (1)Absence (a te ative)Foca (a te ative esp if it gene a izes)

Absence (1) only:Foca (adjunctive use)

Focal (adjunctive use)

Absence (sho t te madjunctive use on y)Focal ( ast c oice)

Focal (monotherapy or adjunctive):General (monotherap� ,or adjunctive)

otable Advantages/Disadvanta ges

Good ong ha f fe so d e 2 /d,

Bad g h asia h utisa sening f feaymp adenopathyt malacia toxici may p nta

'nea no maconcen atio9s;:te atogenic <omp e pha aok netics si cant inte actions iver induce· % - , "

oo Toxicity is uncommonBad pona emiaeukopeniat romboc topen aaplastic anemiahepatotoxicityteratogeniciver nducer

� . 1

Q wide spec goode acy I fo n a a e

Bad GI side e ects ( ess \ ith D akote® fo lma a e y causeb ar ow s pp ession !datotox city/ iver fai1 e te atog cne

defects) ' , , ·� . i -

Bad may cause bone marrow suppression (rare)Good. wide s g d e cacye to e t& in

e de y pat ents·

Bad maycause seve e r d Stevens J hnson syndpid t at on ; qi

;Q i

oo the on y one withnosigni cant d ug interactionsrena c earance so it is use l in t ose wit liv

Bad ataxia amnesia imited e cacy

Bad sedation in adu ts hyperactivity in childrenother cognitive changes teratogenic

Levetiracetam Foca and generalized (monotherapy)oo we l toleratedin elder y patients; safe in Asian patients with HLA-B 1502 at increased risk for Jo nson syndrome

Bad depression fatigue ir itabi ityand increasedinfections

Note ( ) = primary drugNote Any of t e above AEDs can cause ataxia dizziness a soo ence..h it-" ; A i

© 20 4Med tudy - Piease Report Copyr gh Infr geme s tocopyr gh @me s y. om





• ame some enviro mental riggers for seizures suscep b e people

• What s he rea me of status ep lepticus?• Wh ch rug s use to ea a se ce seizures?

wave patte on EEG. 2/3 of a ected children outg wabsence seiz resFoca (a k a. simple pa ial) seizures or gina e in a smalarea of he co ex Co scio s ess is preserved Thesymp oms of a focal sei re depe d o he region ofcor ex om which he even is ge era ed For ins a ce, afoca sei re arisi g in the occipi al lobe(vis al cor ex)may be manifested by complex vis a hall ci a io s;e g., spi ing color l spheres Jackso ia sei res

are focal seizures hat i volve he mo or s rip. Thereca be ra sie , postic al paralysis of a ected limbs4 Focal iz r wi h imini h con c o n

(a.k a. comp ex partia sei res) have many ca sesA commo ype is hetemporal lobe sei ure. I his,

he preceding a ra may be a hall ci a io or percepal ill sion here is a period of al ered behavior a d

co sciousness, for which he pa ien is ater fo d obe am esic The mo or compo en s of he tempora lobe sei re take he form ofa omatisms(e g ,

ip-smac ing chewi g or swal owing movemen s, sa ivation, f mbling of the ha ds, or sh ing of he fee ).

a pi p ic is de ned as a seizure lasting> 30 minu es or a series of2 or more sei ures ithouregaini g consciousness i be ween I is co sidered amedical emergency A cause can be determi ed abo2 3 of he time. Us al causes in ad ts incl de s ro ealcohol or o her d gs, s oppi g or changing seiz remedica io s, hypoxia, CNS i fec io , metabo ic causes,

mor, and tra ma

Triggers for seiz res i s scep ible peop e i c udealcohol, cocai e, i e se emo ions, s robe lighti g, o dmusic, s ress, menst a io , and lack of sleep

SE ZURE MANAGEMENTH yWhe ob ai i g he his o y, check fora coholor d g se,head inj ry, sleep depr va io , diabe es, a d thyroid orpara hyroid s rgery

LLab tests shou d include g ucose, sodium, ca cium,magnesium, LFTs, a d B . If there are a y me i geasymptoms, do a mbar punc ure a d i c de a VOR o

he CSF st dies rder either an MR wi h gadolini m or aC wi h con rast a er the 51sei re o exc de a st c uralab o mali yMRI is almos always he bes euroimagi g

©2014 MedS udy

E ZUR

tes . euroimaging is no mal i classic childhood absencesei ures and ce ain gene ic epi epsy sy dromes AEEGshowi g epilep ifo m spi es( + / fol owing a slow wave)co ms he diagnosis of seizure a d may ocali e theo igi of he sei ures Ano ma EEG ever excl des thediag osis of epilepsy

A er a i itial seiz re, theris of rec r enceis increasedwhe here is a abno mal EEG, his ory of a prior

euro ogic inj ry, family history of sei ures, the stseiure is a focal seizure, a d or when he MRI revea s a

abno ality In approxima e y70% of a patients withepi epsy, he seizures are con rolled comple e y or almoscomple ely by medicatio s in a addi io a20 25%,theat ac s are sig i ca t y reduced i umber and severi .

c e treatment of seiz res: In ravenous be zodia epi es

(diazepam, lora epam, mida o am) are the dr gs of

choice Phe y oin a so is e ective, b it akes lo gero in se Alcohol withdrawal seizures are c stomar yreated acutely with I benzodia epi es or phenytoi

(agai , ben odia epi esI 1ypical rea me of sta s epilep icus in the ad l Give

thiamine and hen05 50 mL if the rapid gl cose es islow hen be zodiazepi e(l orazepam prefe ed x2 doses)followed by a loadi g dose ofphe y oinor equivale fosphe ytoi . Fospheny oi lac s he i ec io si e necrosisand cardiac rhythm complica io s of intravenous phenyoi i f sionbut is much more expe sive and may resui ower i i ial brai pheny oi levels, based on he timerequired for conversion om fosphe y oin to pheny oin

everthe ess, it is pop lar i he emerge cy depa me t.If the patie t is s i seizi g, give a'ddose of lorazepam,maximize the phe y oin dose, a d hen proceed to abarbi rate phenobarbi al or pentobarbital) IC set ingsare ge erally eeded if seizures are no co ol ed by he

rst2 doses of lora epam and a dose of phe y oi

C iepilep ic d gs(AEDs) are he mai s ay of rea ment,

with monotherapy he prefer ed goal (a le I -2). EDsin epi epsy are genera y s a ed a er2 or more p ovo ed seizures (Some say a er I focal unp ovo edseiz re if EEG is abno mal or head i u y his ory ) herisk of sei re rec r e ce a er2 seizures is - 60%a d is- 35% a er a sing e sei re. he choice of a iepi epticd ug depe ds primarily o he seizure type, wi h additio a considerations i c di g cos , side e ec pro e,a d patient prefere ce for a dosage sched e Commo ly,d ugs are o sta ed until a pa ie has su ered a leas2 seizuresFoca iz r : mos a lavai ab e AEDs are e ectivei the rea me of foca sei ures he o ab eexception ise hosuximide, an agent hat is used to rea on y abse ceseiz res Wi h few excep ions, the AEDs are considered

equally e ec ive he mai di ere ces are ha the older



11-18 INFECT ONS

AEDs are genera y cheaper; however, the ewer ones arege era y be er tolerated a d have fewer side e ects

Generalized seizures: The list of e ective agents forge eralized seizures is shorter, and inc udes

Va proate Lamotrigine

Topiramate LevetiracetaFe bamateRu amideZo isamide

Whe can you stop the medicatio ? This must bei dividualized sk factors i clude a seiz re withi thelast 2 years, epileptiform spikes on the EEG, abnormaMRI, and a late age of onset of the sei u es Patie ts whoare sei ure- ee for 2 4 years and have their AEDS gradual y withdrawn have a- 40% risk of recurrent sei res withi 2 years

K ow a so that cer ain A Ds r duce the e cacy of oracontraceptive pi s

Phe y oi• Phe obarbita

Carbama epineFe bamateTopiramateOxcarbazepi e

Wome taki g these A Ds shou d use a method of birthcontro other than ora contraceptives

Note: Ora co traceptives that co tai estrogen cadecrease the dr g co ce tration of the A Dla otrigine ,a d, th s, doses may eed to be increased empirica lyCo verse y, amotrigi e can decrease serum conce tratio s of progesti s (mini pi ) Thus, womeno progestin o y contraceptives are at risk of getting preg a t and should switch to a te ate methodsof co traception

Many of the drugs me tioned above are a soteratogens ;hence, the impor ance of knowi g their e ect opreg a cy The teratogens i clude: phe y oi , phenobarbital, carbama epine, topiramate, and va proic acid (SeeTreatme t of Seizures D ri g Preg ancy, ext )

Options for i tractab e epi epsy inc ude resectivesurgery (best for tempora obe epi epsy), vag s ervestimu atio (does 't work as wel as surgery), a d the ketogenic diet (works well in chi dre )

Drivi g restrictio s vary from state to state and co ti ueto evolve The pi epsy Foundation has updatedinformatio for your state: www epilepsyfoundation org

reatment of eizu es Du ing Pregnancy[K ow!]

The background risk for birth defects is 2 3%.Thegoa of treatment d ring pregna cy is to co tro theseizures uncontro ed sei res can ca se p ace taabr ptio a d early abor a d premature delivery Whe

the risk of teratoge icity is compared to the proble sthat sei ures cause duri g preg ancy, the risks of

contro ed seizures isgreater

Mai tain a preg a t woman on onotherapy atthe low st dose of medicatio possib e; risk ofma formatio s increases as each drug is added

There is o "safe AED, but valproate is more ike yto cause neura t bedefects than other common y sedantiepi eptics The teratogenic risk of AEDs isdecreasedby folic acid, a d th s, a wome of chi dbearing age ona tiepileptic drugs shou d take 2 g of fo ate daily

Physicians ge era y give prophylactic vita i K d ringthe ast onth of pregna cy in patients on AEDs, basedo reports indicati g increased bleeding i patients oA Ds However, most rece t guide ines say there is ote ough evide ce to recommend for or against se ofprophylactic vitami K.

INFECTIONS

BACTER AL CNS N CTIONScu e Men ngi s

Diagnose with a a ysis of the cerebrospina uid (CSF)If there are focal e rologic signs or papi ledema, do a CTbefore the lumbar pu c ure (LP) CSF latex aggl tinationtests are no lo ger recomme ded i theinitia eva uatioof me ingitis; they test forH injuenzae Streptococcus pneumoniae Neisseria meningitides coli, and Strep-tococcus agalactiae. With s spected me i gitis, s arantibiotics im ediate y a er the LP and b ood cu ures;do not wait for a y LP resu ts Also, if doing the LP isgoi g to be de ayed more tha 30 0 mi utes, go aheada d give antibiotics immediately (before the P) urtherdisc ssio a d treatme ts are feat red in I fectio sDisease, Book 1.

eurosyphi is a so is discussed i Infectious Disease,Book 1.

ra n bscessThe classic triad of symptoms is headache, fever, a dfocal ne rologica de cit(s) Most abscesses arise froi tracra ia extensio of cra ia i fections (si uses,teeth) or a er skull fract re or e ros rgica proced resMuch ess o e , they are d e to bacteremic seedingI ad ts, the most common organisms arestaph andstrep species (e g , epidermidis a er a penetratinghead i j ry), b t do t forget abo tNocardia In the

immu ocompromised, co sider toxop asmosis

© 2014 M t y-P R po t opy ght f g m t c py g t@m t y c m

http://www.epilepsyfoundation.org/






Which AEDs decrease the ef ec iveness of oralcon racep ives?

Wh ch AED serum concentra ion is reducedby estrogens?

• Which AED reduces he serum concen rat onof proges ins?

• Wha is he c ass c r ad o symp oms observedn pat en s with a bra n abscess?

How does rea men of a varice a infect on d f erfrom he rea ment o herpes simp ex?

What s he d agnos c est for Wes N e virusencephalit s?

VIRL CNS INFECTIONSCSF in V ral Encepha t sWith viral encephalitis, CSF has increasedlymphocy es,nor a to s ig tly increasedprotein, and nor al g ucose.EEG is a most a ways abno ma with di se s owing ofocal temporalchanges T e MR is more sensitive t anCT a d may s ow hemo rhagic c anges

Herpes S mplex Encephalit s

Herpes simp ex encep alitis is the most common ypeof non-epidemic vi al encepha itis In adults, it is usually due to a reactivation of t e HSV 1 vi s, although25% a e due to primary HSV 1 infection SV 2 issexual y transmitted and can cause aseptic me i gitisduring p ima y infection SV 2 less commonly causesencep alitis but can cause po y adicu itis and myelitisVarice a zoster vir s (VZV) ca a so cause encep alitis,especial y in the immunocompromised; and, it isassociated wit vesicu a esions that can be con sedfor e pes simp ex It's impo tant to think about VZVbecause t e dose of acyc ovi requi ed to reat is hig er Treat herpes encep a itis wit Vacyclovir and assumeit is caused by VZV until you can exclude. (So use

ig e i itia doses of acyc ovi .) Muc mo e o erpesis cove ed in nfectious Disease BookI.

Mosqu to-Borne Arbov rusesIf mos uitoes a e around, think about a bovir ses,especia yeaste weste equine and St Louis encepalitis viruses West Ni e virustends to cause encep alitison y in the olde patients wit como bidities and in theimmunocompromised. ( t causes "West Ni e feve inyounger and hea t y patients ) If a patie t has clinicalpicture of encep alitis and as accid pa alysis, thi k ofWest Ni e encephalitis.

© 2014 MedStudy

NFECT ONS

D agnosis of V ra Encephal t s

Polymerase chain reaction (PCR) DNA ampli catioof the erpes viruses now al ows for a easy, rapid, andaccurate diagnosis of e es simplex and osterAcute a d convalescent se um titers are d awn todiagnose mostarbovi ses. West Ni e diagnosis re uires

nding antibody in spina uid Vi alculture of spinaluid is use to identi most ot er causes of simp evi a me ingitis/encep alitis

V ral Myel t sMye itis is infection of t e spina co d a c assic viracause is o iomyelitis! Typica ly t is p esents as transverse myelitis, meani g it a ects a t ansverse segmentof the co d Common causes today a e otheente oviruses (coxsackie and e te ovi us) andavivi uses, suchas West Nile. Other for s of myelitis (less segme tal)ca be caused byhe pes simplex, varicella oster , and

Epstein Bar

Slow V ruses and Pr ons

Slow viruses:Subacute sclerosing panencepha itis (SSPE) is causedby t e measles vi s; most cases occur a ound age10,many yea s a e the initia infection.Progressive multifocal leukoence alopat y (PM )See be ow a d also unde Demyelinating Diseases on

age 42.

P io C eut fe dt Jakob disease (CJD) (Seeage )

HIV

Infection wit H V ca esult in dys nction ofany partof the nervous system. Patients get subacute encep alitis,pe ip era neu opat ies including mononeu itis mu tip ex, vacuo a mye opathy, and aseptic meni gitis

IV associated cog itive impai ment is common. tranges om asymptomatic to mild to what is ca edHIV associated dementia ( AD). n adu ts, it takes the foof a s owly o subacutely progressive dementia with lossof retentive memory, ina entiveness language disorde ,and apathyKnow t at t e di erentia diagnoses include p og essivemultifoca eukoencep alopathy, toxoplasmosis, andlymp omasSince the use of ART bega , the i cide ce ( ew casespe yea ) of HAD in t e U S has d opped by alPatients a e getting a di erent type of dementia postART t is dementia is associated mo e wit de cits incomplex reasoning and ess wit g obal impair ent Inaddition, even though the incidence is dropping, ADis occu ing in patients with ighe CD4 counts, even inpatients w o ave had ong te vira supp ession onantiret ovira agents

- 9



11- 0 NFEC O S

Poliomye itis is more ikely o occur in A DSpa ien s. Di erentiation be ween T myopathy andpo iomye i is may requi e a muscle biopsy

A DS has fo ms:

1 n chronic in a a ory demyelina ing po yneuropa hy(C OP), there is prog essive weakness of the egs

and oss of deep endon re exes. The e is a highpro ein eve and a high ce count in he pa ien sCSF T ea ments are co ticos eroids, IV G, andplasmapheresis - al equa y e ec ive

2) Dis a symmetric po yneu opathy is common in A DSpa ien s (1/3 ge i ). Symptoms are paresthesias of hefeet and dista weakness he egs T eatment co monlyinc udes t icyclic an idep essan s o gabapen in.

3) A painfu mononeuri is mul ip ex thought o be dueo focal vascu i is also occurs

v k ( ML)a ec swhite matte on y is typical y seen in pa ientswith T cell immune defec s (H V/A DS, chronics eroids, monoc ona antibodies) and chronicneop a s

icdiseases n addition, we are now seeing cases ofP in patients aking a number of immunosuppressants for reatment of rheuma o ogic, hemato ogic, andin amma o y bowe diseases (rituximab, uda abine,mycopheno a e, chronic co icos eroids), and wi h anewer drug to rea mu ip e sc erosis, na a izumabPM is caused by he humanJC polyomavirus, resultingin a progressive demyelination of he CNS whi e ma e .

Symptoms are varied and usua y sta wi h abno amenta ion (persona i y changes and in e lect aimpai ment) and hen s ur ed speech nitia symptomscan be followed by hemipa esis p og essing to quadriparesis, visual e d defec s, cortica b indness, aphasia,ataxia, dysar h ia, dementia, confusional s a es, and/orcoma Some patien s have a p edominan y cerebe arsyndrome.Diagnose wi hb ain biopsy Finding JC vi us in he CSFby PCR is suppor ive, a hough his occurs ess o en inpa ien s wi h PM being trea ed wi h ART.

Vacuola mye opathy (see nfec ious Myelopathies onpage -3 causes p ogressive weakness, incontinence,hyperre exia, and a axia The e is vacuo a ion and de eriora ion of he do sa and lateral spina columns isuncommon This mye opathy mus be di eren ia ed omB 2 de ciency and om spinal co d compression due tosome o her cause, such as ymphoma

P R C CN NFEC ONx

A DS ela ed b ain esions f you seemu ipler ng enhancing esions, hink oxoplasmosis (CNS

ymphoma, TB, and bacte ia infec ions are ess likely )Because oxo is areactiva ion infec ion, patien s ypicallyhave gG(but not g ) an ibody toT ondii But many

peop e have toxo antibodies, so a posi ive toxo gG is on ysuppo tive and not diagnostic Also know ha an absen

oxo gG doesno exc ude oxoplasmosis as he cause ofabrain esion in an A DS pa ien

Trea wi h sulfadiazine, pyrimethamine, and eucovorinAdd dexame hasone if he e is mid ine shi o apidde erioration

Do a brain biopsy if there is no improvement a eempi ic rea ment, if there is a mass e ect, or if he e ison y1 esion Some empi ica y rea sing e lesions if heCD4 coun is< 100 and the patient hasn't been on oxoprophy axis. Re apses occur o en

r cy t c rceurocys ice cosis is hemost common wor dwide

parasitic CNS infec ion. is caused by inges ing food orwate contaminated with T ni solium(a apewo m) fo ms cysts in the b ain, which initia y cause no sy p

·

toms Bu when he cyst wa s b eak down severa yea slater, it causes cerebral edema, common y wi hseizuresas the I stsymptom. n some patients, a la ge suba achnoid or in aven ricu ar cys may obs r c he ow ofCSF. n a mo e ma ignant fo m of he disease, he cys

icerci are loca ed in he basi a subarachnoid space,whe e they induce an in ense in amma o y eac ion

eading o hydrocephalus, vascu i is, and s oke as weas cranial nerve palsies.

R is he p efe red imaging moda i y - when wo msare viab e, R shows mul iple, non enhancinghypodense lesions As the worms die, they are surounded by edema and ai When dead, hey calci andshrink Support he diagnosis wi hT soliumantibody

esting on se m.

Treatmen of CNS infec ion is con roversia becauseof bo h he lack of andomized st dies and he propensi y of dying wo s to cause symp oms Most expe tsnow ea wi h high dose pra iquan e or a benda ole+/ co icos eroids. AEDs are given o patien s at highrisk for seizures o e about this infec ion in nfectiousDisease, Book I.

FUNG L CN NFEC ON

ry t c cc M tEspecia ly consider c yptococca meningi is whenwo king up a p og essive headache, cogni ive impairmen ,and/o meningeal signs in patients with A DS or onchronic cor icos e oids

CSF p ess re is usua lyve elevated S anda d CSFstudies can be en irely norma , so always check hecryp ococca antigen iterin the blood and CSF (in H Vpatients, sensitivi y/speci ci y is>95% . n H V nega ivepatien s, the CSF antigen is s il9 98% sensitive.

T ea with amphote icin B deoxycholate or liposomalampho B and ucy osine x2 weeks, hen change o oral

uconazo e x8 mo e weeks (minimum). ower doses

© 2014 Med udy-Plea e Repor opyrigh nfr ng m n ocopyrigh @med dy.com





• Aside from pat ents w th AIDS, PML can occurn wh ch pat ents? What are the symptoms

of PM ?• What s the treatment for CNS toxoplasmosis?

What is the cl n ca presentation ofneurocysticercosis?

• Character ze the CSF of a pat ent w thc yptococcal men ng tis.

• How useful s the CSF/serum cryptococcalantigen (sensit v ty/spec f city) in d agnos ngmen ng tis?

• Wh ch v ral nfect on recently has beenassociated with subsequent stroke?

of oral uconazo e a e used for secondary prophylaxisn mm nocompromised patients Manage e evatednt acran al p essu es w th da y taps o keep CSF pres

s re< 200 mm H , o pat ents can ose their v s onSh nts are approp ate f da ly taps are needed. Do no

se mann tol, ace azolam de, or co t cos eroidsore abou his nfect on in Infectious D sease, Book 1

STROKE and T A

V V W

S oke, a er hear d sease and cancer, s he 3' mostcommon cause of death n the U S. The terms o e isappl ed to a s dden focal neu olog c syndrome causedby ce eb ovasc lar diseaseCe e v sc dise se

efe s o an abnormal ty of the brain ca sed by pathologyof b ood vesse s s ch as:

Occ sio by embol s or thrombusVessel p eAlteredpe e yof the vesse wa

ncreasedv sc si yo other change in the qualityof the ood ow ng thro gh the ce ebral vesse s

he p mary vascular d sorder may be athe osc e os s,hyper ens ve arteriosc ero c change, arte it s, ane ysmald latat on, o a developmental malfo mation. The secondary parenchymal changes n the b a n es t ng om

he vasc a les on could be schemia, w h or w thoutinfarction, and hemo hageKnow hat varice a zoster infection has een denti ed asa sk factor fo schem c and hemo rhag c s okes and TIA( ncreases sk by 30%), especia ly if the p esentation sherpes zoste ophtha micus

© 2014 MedStudy

STROKE AND TIA

B a n schem awi out i rct o has een recen yde ned by the Ame can Stroke Associa on as a trans ent schem c a ackTIA). s h mic s okhas eende ned asi f rc io and may es lt in tempo ary orpe manent cogn tive, moto , and/o senso y de ci s.

Note that the la est g idel ne on IA om he Ame canSt oke Assoc ation hasremov a l refe ences tourtio of symptoms. The de nition was changed beca set ue nfarct on sometimes occu s even when symptomslast< 24 ho rs, making the p evious de nition of TIAoccas ona ly inco rect

C MPL C N F

TIA signa sImpending CVA

10% have schem c s roke w th n 3 months

50% do so w thin 48 hou sImpend ng card ac evento 3% have card ac events w th n 90 days.o AMI risk s nc easedo Mo tality n AMI a er TIA s inc eased.

R sk strati cat on of TIA, ABCD sco ege: : 60 I point,< 60 0P: 40/90 ,< 140/90 0

n ca : weakness= 2, sola ed speech= 1, o her = 0ration: 60 min 2, 0 59 m n1,< 0 m n 0

iabetes: present= , absen = 0

Score 2-day R sk of Stroke0 1 0%2�3 3% 4 5 4%

7 8%

2009 AH ASA guide ine recommends hospi al zat on w thin 72 ho rs of even f:

ABCD score 3

ABCD score 0 2 and unable to complete wo up w th n 48 hou sABCD score 0 2 and other ev dence tha even s were caused y ischem a

Patients w th T A shou d have imag ng w th n 24 ho rsor ASAP a er he symptoms to dete mine if anyinfa ction s presen Also order CT o MR ang ographyof intracran al and neck vessels, echo, and b ood wo kchem stries, BS, l p ds, CBC. Order an ECG to ru e o tatria rillation (AF) See mo e unde valuation ofIschemic St oke onag -2

1 -2



-2 STROKE AND TIA

L SS F ON OF S ROKESStrokes are c assi ed asischemic or hemo hagic .Ischemic strokes can be thrombotic or embolic

Ischemic strokes (87% of all strokes):

20% are due to large ar e y atherosclerosis.20% are due to cardiac emboli

• 25% are due to acunar/sma vesse infarcts5% are d e to vascular disorders (e.g., vascu itisor dissection)35% are c yptogenic

Hemo rhagic strokes are mainly ca sed by

Intracerebral hemor hage (ICH)Subarachnoid hemo rhage (SAH)

PR RY PREVEN ON OF S ROKEThe American ear Association (AHA) and theAmerican Stroke Association (ASA) p b ished the2010 guide ines for primary prevention of stroke, whichinc ude:

Treatment of blood pressure and ipidser guidelines)

Smoking cessationDiet and exercise

• Treatment of atria brillation with anticoagulationbased on nationa guide ines (See more on AF inCardiology, Book 3) using any of the fo owing

Aspirin

WarfarinAspirin + clopidogrel (in patients unableto to erate warfarin)

o Dabigatran, rivaroxaban, or apixaban (a te ativesto warfarin)

Carotid enda erectomy if>70% stenosis in se ectedpatients, if operative morbidi y and mor ali y is<3%Prophy axis for migraine (previously discussedon page I -6)Evaluation and treatment of obst uctive sleep apneaScreening for aneurysms with CTA or MRA for thefo owing:

Patients who have2

or more15

degree re ativeswith SAH/ane rysm (But screening is notrecommended in patients who have only 1a ected1 degree re ative )

o Patients who haveautosoma dominantpolycystic kidneydisease (ADPKD) and

or more re ativeswith ADP SAH/aneurysm

Image -3 CTofMCA str ke

G NG OF S ROKESIn 2009, the American Hear Association publishedrecommendations for how best to image patients withpossible stroke, based on an extensive iterat re reviewand specialty consensus publications The recommendations focus on the best se of CT and MRI A main

reason to do ne roimaging is to determine whether apatient is e igible for tiss e p asminogen activator (t-PA)but there are other ses:

Exclude intracerebra ( CH) or s barachnoidhemor hage (SAH)Detect ischemia

• xc de other i nesses that present as strokeImage the vesse s

• Assess possib e viability of infarcted tissue

Imaging with CT: A non-enhanced CT (N CT) scancan be per med as a basic fo m of stroke imaging(Image 1-3). The NECT can be enhanced by addingeither of the following

Angiography (CTA)Dynamic per sion studies (CTP)

When adding angiography evaluation of source images(SI) helps to inte ret the st dy (CTA S )

Imaging with M: M I can a so be enhanced usingadditiona imaging sequences

Di usion we ghted imaging (DWI)Per sion (MRP)Angiography (M A)

Gradient-reca led echo (G )l id-at enuated inversion recove y ( LAIR)

The CT and M enhancements he p to bet er accomp ishthe pu poses of imaging. Usual y most, if not a , of thesese uences are per o ed whenever yo order an MRIof the brain In the best circums ances, a CT scan withen ancements takes the same amo nt of time as an M Iwith enhancements or example, it akes10 min tes todo either NECT with CTA/CTA-SI and dynamic CTP orMR with LAIR, GR , MRP, and intracrania MRA!The major prob em today is that not al hospitals provideaccess to the scan er for t age situations In manyemergency depar ments, only CT is avai able

Now that you know the abbreviations and acronymswe'll go over which imaging to use in par ic larsituations

Intracerebra hemorrhage (ICH) MRI-GR ise iva entto N CT for nding blood. We used tobe ieve that CT was better, b t many st dies nowshow that it is not M is a so be er for detectinghemor hagic transformation of ischemic stroke

• Subarachnoid hemor hage (SAH): se N CT.There are some da a showing MRI with FLAIR is assensitive as N CT o ma er which test you choosea lumbar p ncture is sti l mandato y if the CT or MRIis negative

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a� ui• In addit on to exerc se, smoking cessat on, and

cont ol of d et, blood p essu e, and l p ds whatothe nterventions shou d be o ered to ce ta npatient g oups n orde to p event stro e?

• What maging study wou d you do or a pat entw th a suspected SAH?

• Wh ch imag ng study s best to evaluate theanter or carotid and posterio c culat ons npat ents w th T A or st oke?

• How does a pat ent w th an ACA st oketyp cally present?

• How does a pat ent w th an MCA stroketypica y p esent?

Ischemia: MRI-DWI is best. CTA SI is comparablebut it s not as good fo mag ng of the poste iofossa/brain stem and fo discover ng smal nfa cts.MR s also be ter than NECT to detect an occludedvesse

Because of the above n ess you pat ent has s gnsand symptoms of SAH M I+ OW and M I +seq ences (at minimum) are the best maging fo possible schem c st oke because they both exclude CH and

denti areas of nfarct on p ovided you can get thetest w tho t delay emember that t me from symptomonset> 4.5hours prec des se of t-PA(< 3 hou s best).

If you cannot get an MRI in a reasonable time frame,then get a CT w th CTA SI

CTA or MRA s recom ended to eva uate the ntra andextrac an a vasculature of patients withT A o st okesymptoms Both maging moda ties a e s gni cantlymo e sensit ve and speci c than carotid Dopp e

t aso nd for diagnos ng ext ac anial vasc ar stenos sCa ot d lt asound a so tends toover diagnose les onsand eads to nnecessa y su ge y n some patients C Ais better than M I at denti ing ntrac an a aneu ysms.

If performing C A or M doesn't extend the timepe iod f om symptom onset out past4 5ho rs max

mum (< 3 hou s best) e ther is ecommended as partof the initial eva at on of stroke because somet mesc otted vesse s can be treated w th rgent int aa er athe apy o stents. P at ents w th a a ge c otted vesseo en the m ddle cereb a ar e y (MCA) so ca ed "hardthromb s o not espond as we to t PA as to directintervention.

Altho gh assessing viab e brain t ssue a e nfa ction sone of the ma n p poses for maging a stroke pat entwe are still in the beginning stages of ea ing how toincorporate the data nto t eatment p ans. Dynam c CTPand MRP are the ead ng imaging techn q es.

© 2014 Med tudy

ISCHEMIC STROKEShrombotic vs mbol c trokes

STROKE AND IA

:Athe osc e ot c occl s on smost common in the inte al ca ot d m dd e cereb ave teb al and bas ar arte ies

The nitia neu o og c symptoms o en occ n a slowstepw se p og ession (te med "stroke n evo t on )

en patients have a history of TIAs n the same d st ibution as the p esent ng symptoms of the r st oke. If thepatient has not had IAs a clear di erentiation betweenthrombotic and embo ic may be di cult ther ra erca ses of th ombotic occ sion a e lupus anticoag lantpo ycythemia men ngovasc ar syphi is d ssect ngao ic ane rysm and th ombocy osis.

:Ne ro de c t s common yworst atonset Embo ic strokes typ ca y a enot p eceded by aTIA Embo i om the hea s al y go to the m ddle

> posterio > anter or ce ebra a er es. Embo i can alsobe mu tip e

Anter or rcula on y ( )

When the ACA is a ected d sta to the ante orcomm nicat ng ar ery the weakness and senso y ossa ect pr ma ily the contra ate a eg.

Ur nary ncontinence and ga t abnorma it es may a sobe present If theco p s cal osumis a ected patientsmay deve op "tactile agnos a wh ch is an nab ty to

ecogn ze objects by to ch

cclus on of the stem of the ACA proximal to theanter or communicat ng a te y s gene al y we to erated beca se co ate al ow is p ovided by the otheACA. When both arte ies ar se f om one stem the e s

esu t ng pa aplegia ncont nence ack of motivat on(te med "ab l a ) and fronta obe persona ty changes.

Bu phrase he patient w th theACA stroke typicallyp esents w thleg wea ness that soppos teto the s de ofthe st oke

dd y ( )

Most MCA stem occ sions a e omembo i MCAstrokes esu t ncontralatera weakness ("hem pleg a )which s denser f the inte a caps le is nvolved;sensory loss ("hemianesthesia ) and a homonymo shemianops a. If the dominant hemisphere s nvo ved(the le side n most peop e even e -handed indvid als) these pat ents exper enceaphasia A es onthat a ects the lowe part of the e onta lobe(Broca's a ea) causes expressive (a.k.a. Broca) aphasia. These patients understand language but they havet oubleforming words and sentences so their speech snon ent and e o t l A es on at the bounda y of thetempo al and par eta obes causes a "ent or "sen

sory aphas a ca ledWe icke aphas a hese patientscan t comp ehend wr tten o spoken lang age and have

1 -23



-24 STROKE AND TIA

er ors in the spontaneous speech o en speak ng ninvented wo ds termed "neologisms . An extens veinfa ct on may prod ce "g obal aphas a which is bothexpress ve and sensory If the nondominant hem sphereis invo ved, patients may experience changes n spat ape ception and may deve op hemineglect synd ome

With pa ietal les ons of either hemisphere "cor calsenso y signs are o en p esent: cont alatera loss of 2-po nt disc m nat on failu e to pe ce ve tact e stimuon the opposite side of the nvolved hemisphe e whenstimuli are presented to both sides simultaneously(termed "sensory nattention ) tacti e agnosia and aninabi i y to recognize le ers drawn on the pa m (te med''ag aphesthes a )If the les on invo ves the f onta obe patients may havea gaze p efe ence o gaze deviation they ook towa dthe s de of the esion fo 1 2 days a e the stroke

Buzz ph ases: The pat ent w th theMCA stroke typicallypresents with arm/ eg weaknessthat is opposite to theside of the stroke and a anguage de cit if the dominanthemisphere is nvo ved

Posterior Circulation b A y ( A) S k

PCA strokes typically ca se cont alatera homonymo shemianopsia s ally a s pe ior q ad antanops a withtempo al obe esions an inferior q ad antanopsia withparietal lobe les ons o a homonymo s hemianops awith medial occip ta es ons There may be mi d cont alate al sensory loss inab ity to name co ors (te med

"colo anom a ) fail e to see to and f o movementsinabi y to co nt objects inabili y to xate on points inper pheral visua elds (termed "ocular apraxia ) inab l tyto see more than 1 object at a time if the dominant occipi al

obe is involved (termed "sim anagnosia ) vis a ha lcinations and/or memo y lossIf the patient has color anom a the poste io aspect ofthe co pus callos m (splenium) may have been a ected

f d sruption of b ood ow occ rs b atera y thememo y loss s severe and pe s stent.B ateral co ical b ndness can es lt from s mu taneo so successive poster o cerebra ar ery occ us on butmay a so be d e to anox a elated to su gery especiallyca diac s rge y Occas onally pat ents with cor icalblindness deny the r vis al defect (Anton syndrome)Buzz ph ase The pat ent w thCA stroke typ callypresents with visual eld defects + color anomia +pa esthes aswitho t any moto ndings

S g H m p S k

Single hemisphere st okes ypica ly do not a ectpa as pinal muscles or musc es of the pharynx aw andfo ehead If these muscles are a ected think b laterahemispher c involvement o b ainstem stroke (below)Remember Upper moto ne ron es ons of cranial

ne ve 7 do not a ect eye c osu e or fo ehead wrink ng which helps yo to distingu sh cl nica y betweena central les on and Bell s palsy per phe al71hnerve

nvolvement)

V b / B A y O

Ve eb al and/o bas lar ar e y occ sion s the s alca se of brainstem st okes That the p oblem involvesthe posterior circulat onde ver ng b ood to bra nstem(poster or fossa) st c u es is suggested by the fo lowing

Bilate al extrem y motor and sensory dys nction(quadr plegia in seve e cases)

"C ossed senso y nd ngs (e.g r ght face le arm)• Ho er syndrome

Ce ebellar s gnsStupor and comaC an al nerve dys nction commonly not a ectedby s ngle hem sphere strokes (diplop a pha yngealweakness jaw weakness and dea ess)Crossed hem pleg as (e g ips ate a cran al nervede c t and contra ate a a m or leg weakness)

[Know ] Ave ebral strokmay ca se m d yy d m (also called Wallenberg syndrome) which

has a mixed bag of symptoms

psilatera ce ebe a signs and symptoms (d e tonvolvement of the nfe ior cerebella ped ncle and

cerebellum)Na sea vomiting nystagm s (vestibular n clei)

psilate al Ho e synd ome (due to invo vementof the descending sympathetic bers)I psilateral pa ate and voca cord weakness( nvolvement of the nuc e s ambig us)"Crossed sensory loss (ips ate a face andcontra late al body due to invo vement of thetr geminal nucleus and tract and sp nothalamictract espect vely)

B zz phrases: The pat ent with theposterio circulationst oke typical y presents with

Ver igo and diplop a if due to ver ebrobasi ar ar e y;sometimes w th antecedent TIA symptomsLatera medu lary synd ome (de ned above)Ve igo nystagm s na sea+ ataxia ( fcerebella )

(There are other bra nstem infarction syndromes b t wewon t d scuss them he e.)

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a� uiH w d p w PCA

yp y p ?• H w d y d g . p p

yth p y p y x ?W p

d y y d ? W yp ?

Lacunar nfarcts

Sma artery disease typica y due to chronichype te sion or diabetes, ca lead to small vesselocclusio with esulta t ec osis of small a eas of t ebrain Over time reso ption o these nec otic egionsca ses small in a cts o " acunae to develop.

Altho gh most are si ent ha lmarks ofsymptomaticacunar infarctsare:

Pu e hemip egia (with no sensory dys u ctio )P e hemise so y st oke (with o motor dys u ctio )Se sory moto st okeAtaxic hemipa esis (ataxia ipsi ateral to hemipa esis)Cl msy ha d-dysa t ia sy d ome

M ltiple bilate a f ontal obe lac nae ca es lt ipse dobu ba pa sy motio a labi ity with uninhibited c yi g o a ghte a d evidence o upper motor

e o sig s such as b isk jaw erk hype re exia and

Babi ski sig .

TROKE D

Evaluation of schemic Stroke

The patient with a ne ologic de cit should be assessedlike a y othe eme ge cy using the s rst stabi ize

i way reathi g a d i cu atio .

If the patient is stable take a good histo y The mostimpo tant eleme t is thetime o sy ptomonset beca se

that determines eligibi i y for anIV thrombo y ic. f thepatient awoke with de cits the the last time he/s eemembe s havi g o mal function is the time o symp

tom o set. Remembe that complicated migraines postictal states and s bd ral hemorrhages ca resemble ast oke; so ask about headaches sei ure activity a d falls

Physica exam ocuses o possib e so ces a d a te ativediagnoses. Look or evidence of sei u es (tongue biting)tra ma myoca dia ischemia ca otid and vertebral arteryb its ea t m mu s a d a hyt mias.

The National nstitutes o Health Stroke Sca e N HSS)score is a sta dardized instr ment inco porated as part o

a physical exam at most st oke cente s We've rep oducedthe ge e a co cepts o the scale inable 11-3, b t yourea ly shou d study and use the sca e.The N HSS helps to q a ti ne ro ogic de citscommunicate with euro ogists possib y identi t eocc ded vessel make a ea ly p ognosis a d identi apatie t s suitabi i y o thromboly ics Patie ts get pointsfor thei inabili y to comp ete the va ious parts of theassessment

Table -3: N H rok cal

ss ssm nConsc ousn ss L v

Consciousn ss Qu st ons

Consciousn ss: Comm nds

G z

V sion

F ci p sy

Motor: A nd L

t xi

S ns t on

L ngu g

Sp ch

Ext nct on n In tt nt on

ns i nsChoos r spons : rt, rous y minor st mu , r qu r s r p t d or p n s muunr spons v or r x s on y, or r x c

Ask onth n g . No p r i cr t. Aph sic nd st porous p ti nts scor2 In u tp ti nts scor I.Ask p t nt to op n nd c os y s, th n to p nd r s non p r t c h nd

st hor zon y mov m nts

st v su s y con ont on with ng r count n

Ask p ti nt to show t th or r s y rows nd c os y s

st for pron tor .

P rfo m n r-nos - g r nd h -shin t sts

Ass ss for s ns t on or gr m c to p npr ck or w thdr w l om nox ous st mu us

D scr wh t s h pp n ng n p ctur n m t ms pr nt d on p p r, nd r s nt nc .

R d words om ist.

Ass ss pr vious t sts to d t m n f p ti nt or nts only to on si

For th sc w th scor ng go tow n nds n h gov/doctors/ _Strok Sc p

© 014 MedS ud

25

http://www.ninds.nih.gov/doctors/NIH_Stroke_Scale.pdf





1 -26 TROKE AND TIA

A /ASA 013 Guideline for the Early Managementof Acute Isc emic Stroke recommends t e fol owingimmediate diagnostic tests at presen ation:

NECT or MRI of the brain (discussed onage -22) is done to rule out hemo rhage. If nega

tive for hemo age and the subsequent lumbar punc

ture is negative, then an RA can be done to evaluatevessels but this shou d not delay any necessaryreper sion therapyB ood glucoseOxygen sa uration measurementSerum e ectrol es and renal nction testsCBC wit plateletsP PTT INR

lead ECG ±telemetry monito ng for arr y hmiasOptiona tests in selected patients

o Thrombin time and/or ecarin clo ing time (ECT) ifon direct t ombin in ibitors

Hepatic nction testToxicology and alcohol screen.Pregnancy testAgain a lumbar punc ure wit CSF assessment shou dbe done if SAH is a conce and NEC(or RI withFLAIR) does not show b ood.EEG (if you suspect patient as seizures)

o CXR if ung disease is a conceo ABG if hypoxic

Acute Treatment of schemic troke

Crit cal imes

A ways refer via 911 to a Prima S oke Center (PSC) ora Compre ensive S roke Center (CSC)T e AH ASA 0 3 guide ine recommends t ese goals

Door to p ysicians ou d beS I 0 minutesDoor to stroke teams ou d beS 5 minutesDoor to CT initiationshou d beS 5 minutes.Door to CT interpretationshou d beS 45 minutesDoor to drug( 80% compliance)S 60 minutes.Door to st oke unitadmission s ould beS 3 ours

If the st oke occu red< 4 5 hoursago and t e NIH stroke

sca e rating is> 4 t P as been shown to bee ectivein decreasing severity or reversing neurologica de citsprovided t at the atient ts inc usion criteria ( 0 13stroke treatment guide ines om the American StrokeAssociation)

t-PA Criteria for < 3 Hours

Less than 3 hou s t PAinc usionc ite aDiagnosis of isc emic stroke causing measurab eneurologic de citOnset of symptoms< 3 hours before beginning

eatment• Age 8 years

Less than 3 ours t PAexc usioncriteriaMinor or rapid y im roving stroke symptomsSigni cant head trauma or p or stroke in ast 3 monthsSymptoms suggest SAHHisto y of prior in acrania emo hageIntracranial tumors or ar eriovenous ma fo mation(AVM) or aneu ysmArte a punc re at noncompressib e siteInfarct in ast7 daysRecent in acrania or intraspinal surgerySBP> 185 mmHg orDBP> 1 0 mmHgActive inte al b eedingP ate ets< /mmAnticoagulation with NR> I. 7 or PT> 5 secondsUsed direct thrombin inhibitors with abno malRaPTT/PT/EC /Xa activity assay (e.g i dinand derivatives [t e rudins] argatroban me aga andabigatran)B ood glucose< 50 or> 400 mg/dCT withmulti obar infarction(hypodensity> /3cerebral emisp ere)

Relative exc usionsSeizure wit osticta de citsMajor surge y or serious trauma in prior 4 daysGI or G hemo hage within ast 1 daysAMI within 3 months

Additional t PA criteria for .5 hours

Inc usion crite a (3 .5 ours):Diagnosis of isc emic stroke causing measurab eneuro de citOnset of symptoms within 3 5 ours beforebeginning eatment

Re ative exclusion criteria(3 .5 hours)Age> 80Severe st oke NIHSS> 5)On anticoagu ation regardless ofHisto y ofbot DM and prior isc emic stroke

ndovascular nterventions

Intra a terial brinolysis is bene cia for care l yse ected patients withmajor ischemic strokes < 6 hourscaused by occlusions of t eMCAwho are not candidatesfor IV b no yticsIntra a te al b inolysis or mechanical t rombectomy isreasonable in patients w o ave contraindications to useof IV brino yticsIntra a te al b nolysis or mechanica th ombectomis reasonable as rescue therapy in patients wit argeocclusions who have not responded to IV brinoly ics

© 2014 MedStudy-Piease Repo t Copyr gh Infr geme s to copyr gh @meds dy.com





What tests are recommended i the i it aleva uation of ischemic stroke?

I mag ng for SAH is egative a d suspicio ish gh, what is the next diagnostic test a d whatdoes t ook or?

What s the t me rame or prescr ption of t-PA inpat ents w th ischem c stroke?

Which patie ts w th a stroke between 3 a d4.5 hours are excluded rom t PA?

What are the recomme dat ons for lowering ob ood pressure i patie ts w th schemic strokewho do ot receive t PA?

Why should you keep a patie t w th an schemicstroke the posterior ossa under close

observat on?What are the recommended antip ate etreg mens post- schemic stroke?

What are the most common causes o ani tracerebra hemorrhage?

Note: No aspi in o a ticoagulatio (e g , fo DVTp ophy axis) within 24 hou s of t PA

I t ave ous st eptoki ase isnot ecomme ded fo acuteischemic st okes

h r sp c s of c sch mic rok CarManageme t that emphasizes supporti e ca e a dtreatme t of comp ications

• Give airway s pport to stroke patients with ed cedco scio sness or ai way compromise; oxyge p .

• Use ca diac monitor g fo the st 24 hours a e ast oke to assess fo a hy hmias.

• Treat hypertensio cautiously, so as not to exte di farct si e. If the patient meets c ite ia fo t PA exceptfo BP, go ahead a d eat to ed ce BP to 185/ 10then give t PA f not gi ing t PA, withho d meds forBP < 220/ 20 a d allow the patie t to gradua ly d opthei p essure o thei own fBP > 220/ 20, the eatwith the goa of reducing theBP 5% i the rst24 hours Recomme ded meds om g ideli es i cl deIV abeta ol, itrop usside, a d icardipi e i sio

• Resta t a tihypertensives fo patie ts witho g sta di g hypertensio a er 24 ho s if not

treated al eady fo BP > 220/ 20• Maintai ormoglycemia 140 80 mg dL• Look for a d t eat so ces of feve Give antipy etics to

reduce fever

© 201 MedStudy

TROKE AND TIA

n patients ineligib e fo treatment with t PA and whoare ot taking anticoag lation fo any othe u de i gdisease gi e 325 mg aspirin once, followed by dai aspi

i 50 325 mg/day whi e hospita ized Optima dose isot yet c ea The r sk of hemo hagic t a sfo mation of

a infarct is ot high eno gh to o set the bene ts of aspiri therapy, so treat al e igible patients even if asma lhematoma is present within the infa cted area The e is

o be e tto treating ischemic strokes with hepar orMWH , less the patient meets cr te a for anticoagula

tion with hepa i use otherwise (e g. atrial br ation o acardiac thromb s)

f the stroke occu s in theposte ior fossa admit thepatient fo close observatio . Expa sion of the contents ofthe poste ior fossa can ca se either pwa d or dow wardhe iation these patients then decompensate quick y andwitho t wa i g.

hronic eatment of schemic Stroke

Red ce the patient's r sk factors for st oke by treati ghyper ensio diabetes a d ipids accordi g to ationaguide i es, and add eithe aspi in 50 325 mg/dayextended- e ease dipyr damole o clopidog el

The combination of ASA + ER dip r damoleis bet ertha either agent a one se clopidog e i patients withaspiri alle gy. Know that aspirin c opidog el does oto e additio al bene t and does inc ease isk of b eeding

Headache is a common side e ect of dipyridamo e a dsometimes ca ses patients to self-discontinue the drugNo ma y the headaches ca be t eated s mptomatical

with acetami ophe Donot se ticlopidine it s expesive performs o better than the agents above, and cancause signi ca t eutropenia

Anticoag ate patie ts who have at ial bri latio if thepatient meets guide ines (See more on AF i Cardiolog , Book 3 Refe fo ca otid endarterectomy if thepatient has > 70% occlusion and a expected ifespanof> 5 yea s a d the anticipated operati e mo bidi y andmo ta i y is< 6%

INTRACEREBRAL HEMORRHAGE

verv ew

Hemo hagic stroke is genera y d e torupture of smala eries especia ly when the sma l a tery b anches o ata 90 deg ee a g e om the pa ent vessel a d the b oodpress e is ve y high The 2 most common ca ses a ehype ensiona d amyloid a giopathy Warfa i se is ar sk facto especially whe theIN is> 3

Some patie ts have preexisting evidence of i te mi ent,sma b eeds on MR of the brai It is possib e thatthese MRI-visib e "microbleeds are indicators of whichpatie ts are p o e to e i t ace ebra hemorrhage

Beca se the bleeding a ises om smal a e ies, thesymptoms of microb eeds ypically evo ve g ad a ly b tconti o sly

1 -27



11-28 S ROKE AND A

s d y p sHemor hagic s roke occu s in the fo owing areas of heb ain ( ommos common site to leas common):

1 Putamen and adjacent inte a capsule 50% :I hehema oma involves he inte a capsu e, he e iscont alate al hemiparesis and usua y senso y ossand hemianopsia. This type o hemor hage may bedi cu t o dis inguish f om a midd e cereb al ar e yin a ct (one of the easons to do the enhanced NECo MR looking fo b ood a presentation). Fo centralwhite mat e of he tempo a , pa ieta , o on a lobes,symptoms are based on he obe a ec ed

2) ha amus cont ala era hemianesthesia without"co ical senso y signs Some mo o signs may bepresen i he adjacent in e al capsu e is invo ved.

3 Pons: coma, pinpoint pupi s, and quad ip egia. he emay be dece eb ate posturing bi ate ally.

Ce ebe lum: acute dizziness, ataxia, and vomi ing withno change in men a ion and no loss o consciousness

Amy oid angiopathy is a common cause o hemo rhagicst oke a e the5 hdecade o life. The hemo hage tendsto be oba and subcor ical(I age and can bemultiple a e y invo ves he deep structures (as doesa hypertensive b eed). Hemo rhages may ecur withinmonths or yea s. Demen ia occurs in30%. O he clinical

ea ures inc ude acute eac ive hype ension, vomi ing,headache, and nucha igidity.

Remember he e a e o he causes o int acranialhemo rhage, including bleeding dia heses, auma, andbleeding into a tumo mass Know tha cocaine use cancause vascular malfo mations and aneu ysms, which canlead to major b eeding du ing episodes o seve e d uginduced hype tension So, a activecocaine use s witha ce ebral b eed shou d have an angiography (conventional, C or MRA) to eva uate or AV and aneu ysms

T Treatment inc udes the basic suppor ive care given toischemic s oke pa ien s. (Seepage 7Any anticoagu ant e ec s should be immediate y

eve sed with both vitamin K and eplacement o c ot ing

facto s, no mat er the reasons fo anticoagulation Givep otamine su fate fo any hemo hage associated with

mage 1-4: CTof acute intraerebral hematoma

un ractiona ed hepa in.A so, stop any an ipla eletagen s.

Con rol o in rac aniap essure (ICP) is impor

ant, andma nito is usua y used.

Cu en guide ines o manage blood p essure recommend continuous V antihype tensives (e.g., abe a ol,esmolo , nica dipine, and enalapri ) if systo ic bloodp essu e (SBP)> 220 mmHg o mean a te ia p essure(MAP) is> 50 mmHg. For hose with SBP180-220(MAP 130-150) and inc eased CP, conside in emit ent o continuous antihyper ensives, keeping theper sion pressu e 3 - 80 mm g Rapid eduction oBP is con aindica ed because it can lead o vascu acompromise and wo sening o neuro ogic de cits.

Depending on he si e of b eed, some c o s shouldbe su gically emoved Consider c ot emova oce ebel a hema omas >3 m. A so consider su ge yfor oba c o s> 30 mL wi hin I m of the su ace npatien s wi h minor de cits o deeply coma ose patientssurgery is gene ally not done. Neu osurgeons a ecus oma ily consul ed

SUBARACHNOID HEMORRHAGEv v w

Subarachnoid hemo rhage (SAH) usua y results rombleeding om an int acranial aneurysm. Aneurysms aremos common a the bi cation of vessels in theci cleof Willis o i s majo b anches. he age when this most

ikely occu s is be ween40 and 60, and it occurs inwomen more o en han in men

he majo ity occu in the an e io circu ation40% ofaneurysms a ec he inte a caro id a ery,35% involve

he an e io ce eb a arte y, and20% the midd e cerebraarte y.

Suba achnoid hemor hage can also occu a e apa enchymal b eed, when he e is uptu e into he ventricular system Non-aneu ysma causes o AH are a ebut inc ude AV ma o mations, sick e cell disease, b eeding diatheses, pi uitary apop exy, rauma, cocaine abuse,and intrac ania a e ia dissection. Among persons withsaccular aneurysms, there is an increased incidence ocongenita po ycystic kidneys, bromuscula dysplasiaof the ex racranial a teries, moyamoya disease, a eriovenous ma o ma ions o he b ain, and coa c a ion othe ao a

up u es commonly occu when the pa ient is ac ive

athe than at es More han/3of pa ien s epo t a history of" sen ine bleed symp oms days o weeks ear ier.

he cha ac e is ic symptoms of A a e the acute" thunderc ap o "wors headache of my i e sensa ionin combina ion withneck s i ess Co mon associatedsymp oms include oss of consciousness, nausea/vomiting, and photophobia Systemic mani es a ions of SAHmay include CG changes o a ge, peaked waveshyponat emia, and diabe es insipidus.

The most impo ant dete minan o outcome is heneu o ogica condi ion of the patient upon a iva a hehospital. I comatose, the p ognosis is poo .

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Wh u h v u u wh w h b b v hy v ?Wh h b u w h bh h ?Wh h u ?

• Wh u y u y ?Wh h u ub uh ?

iagno of SAHNon-enhanced CT ( ECT) is the best est o den

blood in e subarachnoid space. If h s s negative andthe ECT does not show a mass, hen do alumbar puncture The CT m ssesprogress ve y moresubarachnoidb eeds as me passes rom nitial rup ure p cking upon y abou 50%of bleeds a er 5 days n a SAH, CSF sb oody w xan hoch omic supe a ant (pink or yellow

n ); however, even clear CSF does no preclude thediagnosis because may take ours a er onse of thebleed before you nd red ce ls at e evel o the spinewhere you draw e CSF samp e

I a bleed is s l suspected in he set ing o a no maNECT and LP, then angiography s he procedure ofc oice CTA and M are al e at ves o invasive angiograp y, and e r sens vi y and spec c are close o

e s andard angiogramCTA s now ve y o eninc udedas an enhancemen o the bas c tr age ECT or patien swith s roke symp oms. The NECT in mag 5shows a massive subarachnoid hemorr age in w icha the w e in the bra n ssue is due to b ood n thesubarachno d space

Comp ca ion of SAHA er a sen nel bleed,rebleeding s common. The sk sh ghes n he rs4 ours, bu e risk rema ns g forat least 1mon .

Vasospasm may occur in

mage -5: Massive ubarachno d hemo ha e

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up to 70% o patients andbeg ns 3 5 days a er hehemor age It reachesa peak at 5 days andreso ves in weeks

The 3'd major comp cation is communicat nghydrocephalus, wh choccurs in 5 0% ofpa ients a er SAH T e

kelihood o ydrocephaus depends on the volume

of ntraven ricular andsubarachno d b ood

STROKE AND IA

Se zuresoccur n5 0%; /3beg n w in t eIstmonta er t e emorr age, while the remain ng occur with nthe year

rea en of SAHIf he patient s on an anticoagulant or antip a elet agent,stop he d ug be ore per o m ng any in erven ionsSurgical c ipp ngand endovascular co nser ionin o

he bleeding vessel are he major nterven ions used opreven he aneu ysm om bleed ng aga n Remaining

rea men focuses on preven ng e compl ca ons,such as calcium c an el blockers to prevent vasospasmCon rol of ICP and blood pressure is impo ant as well,a thoug recommenda ions are less clear cut t an wi hintracranial emor hages.

Know that 1 degree re atives o pa ents w o experienced a SAH ave a 2 5x ncreased risk o a SAH

0 0guide nes on he primary prevention o stroke do

recommend aneu ysma screen ng, as discussed previous y under Primary Prevention o Stroke onpage . o e on o er aneur sms:Myco ic aneur sms arecaused by sep c embol, most o en rom n ec edhearvalves. They are commonly sma l and occur n the distalvascu ature. Th s s n contrast to saccu ar aneurysmstha occur more p ox ma ly, a he branch po nts o thear er es (a he point w ere t e middle cerebra ar ebranc es o of t e in e al ca otid artery)

UBDURL EM TOMSubdural hema oma (SDH) s not always due to direc

rauma dece erat on forces can also cause ConsiderSDH in pa ents w a histo y o a s, b ows o thehead, and vehic e accidents Subdura bleeds are usuallyof venous origin.

SDH can be acu e or chronic, and each man fes sd erently Inacute SDH, l/ of t e pa ents immediate y become coma ose, but he ot erl/ remain lucid

or a per od o ours o days, a er wh c cogn ionbecomes gradua ly and progress vely mpaired untcoma deve ops

Symp oms may a so be uc ua ng O er s gns ofncreased ICP are o en present e g , headac e, nausea!

vom ing, neck s i ess, and gait abnormal esIn chronic S H, he trauma is o en forgotten Overa period of weeks, pa ien s may deve op headache,lightheadedness, s owness in th nk ng, apathy, d owsiness, unsteady ga , and occasionally se ure. n iallythey may be d agnosed as av ng a vascu ar lesionbra n umor, drug ntoxica ion, a depressive illness, orA eimer disease

NECT s used n tr age o ese pat ents, but MRIw t LAIR s e mos sensit ve es . ECT n

age 6shows a subdura ematoma w h a skullde ormity.

-29



1 -0 CNS TASTAS S

Treatment for SOH isypical y surgical

except for very smallb eeds without a y

euro ogic symptoms,which are observedclosely

EPIDURALHEMATOMA

11-6: Epidural hematomas,because of their a e

ria origin, evo ve more rapid y tha subdural hematomas hese are pically caused by temporal trauma thatdamages the middle meni geal ar e y in associationwith temporal bo e fractures. Symptoms of increasedICP are typica ly rapid a er the head trauma, but ashort period of lucidity may occur, followed by rapidobtundatio

As with SOH, diag osis ca be accomplished withNEC , but MRI with FLAIR is most sensitive

Treatment consists of early evacuation of the hematomavia a craniotomy. If untreated, he iation occurs, withmo a ity va ying om 15- 0%.

TRANSIEN GLOBAL AMNESIA

ransient globa amnesia ( GA) is characterized byabrupt onset of globa anterogradeamnesia, with a variable impai me t of retrograde memory not associatedwith any other major euro ogic signs or symptomsExcept for amnesia during and arou d the event, patientsrecover completely in 2/3 of cases within 2-12 hoursand in almost a cases within 24 hours TGA is considered benig , a d the condition recurs in eque tly

Patients are commonly betwee 50 and 80 years of ageand sudden y develop a inabi ity to make new memories They act disoriented, asking multiple questionsrepeatedly. The amnesia ca eve exte d back to years,although more common y just days to weeks. Somepatients have accompanying nausea and di iness. TIAca prese t simi ar y and shou d be considered.

Precipitati g eve ts are seen i many cases a d i c udestre uous exercise, intense emotio , sexua i tercourse, mild head trauma pai , temperature extremes(e.g , swimming in coldwater), cervical ma ipu ation, coughing spe s andother Va sa va like activities, and medical proceduresthat require a esthesia (e g ,colonoscopy) The etiology isunknown, a though migrainemay be a predisposi g factor.

NEC and brain RI with

DWI are ypically no ma .

B st

Parench a +

ur +

Epid l +

Men nge

PET a d SPEC studies have show hypoper sioa d hypome abolism i the hippocampi and associatedmesial temporal lobe structures during the attack, withresolution fo lowing the a ack The attacks se f resolve.No treatme t is necessary.

CN M A A

C S metastases typica y cause a s ow onset ofsymptoms (headaches, foca neuro de cits, impairedcog itio , sei ures, a d/or stroke symptoms), a thoughthey ca be abrupt if there is hemor hage into a tumor.

Know the fo owi g main mets to the brai (Table 11-4):ym brain metastases occur most commo ly

with lu g, re al, a d breast ancer, as we as witme a omaa d ymphoma

metastases occur with b easta d prostate cancer

metastases at the level of the spinal cord causba k pain, usua y worse whe lyi g dow New o setof b adderor bowel dys ctio (inco tinence, urge cyis ve y impor ant and shou d a er you to consider spi alepidura metastases, especia y in the set i g of ewback pai a patie t with a history of cancer specially p ostat , b east, and lu g cancer and with cordcompression symptoms (cauda equina), metastases mustbe ruled out!

ma igna cy is most freque t inlymphomas , carcinoma of the breast, a d me a oma.It is less common y see in cancers of the ung a d thgastrointesti a tract, chi dhood eukemia, and systemiclymphoma. MRI with co trast is the best imagi g studyTreatme t of CNS metastases depends o how ma ymetastases are present, the ca cer prog osis, a dthe nctio al status of the patient. A approachable, single metastasis i a nctional patient istreated with surge y a d radiatio Sma esions(< 3 m) a d/or surgica y inaccessible esio s canbe treated with stereotactic radiosurgery Less fu ctiona patie ts with numerous lesio s are usua ytreated with whole brai radiatio a d ch motherapy+ -co icosteroids

b 4

L ost t om Lym om R

+

+

+

+

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Q� uiDescribe the d erences between subdural andep dural hematomas.

A patient with h story of prostate cancer and newonset o ur nary ncontinence shou d make youcons der what d agnosis?

What is Wernicke encepha opathy?How is it treated?

How does the presentat o of the typ calWernicke patient di er from that o the typicaKorsako patient?

• What are the symptoms o lith um toxic ty?

What e ect does a hyponatremic state have onlithium resorpt on by the kidney?

B D D D

WERN CKE'S I KORSAKOFF'S

We icke encephalopathy and Korsako syndrome arecons dered di erent presentations of the same diseaseprocess. We icke's is mi der and revers b e wh e Korsako 's is more severe and on y pa ially revers b e. T ecause is t iam ne(B1)de c encyWernicke encephalopathy is most o en assoc ated w tha coho sm, but it can be seen n cases of prote n-energyma nutrition (extreme catabo ic states, kwas iorkor,

marasmus), malabsorpt on, and spec c oss of t iamineduring dia ys s.It is c aracterized by globa conf sion w th nattent on,apat y, disorientat on, and memo y oss t at worsensover days to weeks.Abnor a eye movements are typ a and nc ude

or ontal nys agmusand a d sordered conjugate ga ethat progresses to opht almop eg a (bilatera aterarect s weakness, e ther in iso ation or together w tpa s es of other extraoc ar musc es) The pup ls maybecome slugg sh yreactive to ght e person mayhave troub e standing or walking due tot ncal ata a.

Diagnosis is c in cal. f t e early s gns of t e disease arenot recognized and treated, a progressive depression ofconscio sness occurs with stupor, coma, and death n amat e of a week or two.Know t e typ cal We icke s presentation: con sed +wa ks d nk troub e mov ng eyesKorsakof synd ome s a chron c amnestic syndromeassociated wit alcohol sm, maln trit on, and v taminB1 de c ency o en co nc dent with We cke's and mayemerge as the symptoms of We icke s are eated. Theam es athat occurs with Korsako 's can bebo hretrograde and anterograde. A ent on and mentation appear

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MET BOL C ND TOX C D SORD RS

norma . Pat ents o enconfabu atebecause of the memoryprob ems. The stories are equent y appy-go-l ckyfantas es, so cal ed "g ee confabu ation.T e yp ca Korsako 's presentation anunde we ght,poo ynour s ed, but very attent ve alco o c who tellsfantastica stor est at co dn t poss b y be t e and t en

as no memory of t e d sc ss on.Other ne ro ogic man festat ons of t e ernicke/Korsako syndromes are perip era ne ropathy,retrobulbar optic neuropathy, mpa red o factoryd scrimination, and post ra hypotension.Treatment: Immed ate treatment w t t iam ne reso vest e problem of We icke's and prevents Korsakosyndrome Once Korsako syndrome develops, th am ne has on y par ia e ect. n fact, t e majority ofpat ents w o emerge om e icke s have reversib esymptoms of Korsako sTreatment for e icke encephalopathy is thiamine,

at a m n mum dose of 500 mg (in sa ine) by in sion3x/day for 2 3 days, fo owed by 500 mg t iamine IVor IM da y for anot er 5 days. Therea er, oral th am nesupp ementation shou d be cont n ed, ypica y at a doseof I00 mg/day. De ciency in ot er v tamins and m nera s, espec a y n ac n and magnes m, s o d a so becor ected. e icke's typ cal y improves w thin hoursof t am ne rep acement.In Nep ro ogy, Book 2, we d sc ss ow V glucosegiven to a c ron c a co o c causes a decrease in thea ready dep eted stores of p osp ate and can ca sehypophosphatem a A s m lar se uence can occurw th the th am ne stores V glucose can prec p tate

e cke encepha opathy in a co o cs.Remember Give IV th aminebefore IV glucose n anypatient wit a poss b e metabo ic ca se of coma

L TH UM TOX C TY

L thium eve s in t e upper therapeutic range equentlycause tremor and asterix s Remember:Hyponatremiacauses ncreased l thium r so ption om t e k dney.Above a eve of .5 2 mE / , t e pat ent deve opscon sion, de ir m, d zziness, nystagmus, atax a,stammer ng, d se myoclon s, neph ogen c d abetes

nsip dus, ver ica nystagm s, and opsoc on s. Toxiclith um eve s cause se zures and coma; treat withemod a ys s.

The symptoms of toxic y may resemb eCreut fe dt Jakob d seaseNote: Opsoclonus is rapid, invo untary, mu tivector al(hor onta and ve t cal), npred ctable, con ugate eyemovements

1 -3



11-2 DISEASES OF MUSCLE AND NERVE

ANTICHO INERG C TOX C TYClassically, symptoms are:

• red as a beet (cu aneo s vasodi at on),• dry as a bone (anhidros s),• mad as a hatte (hal ucina ons),• bl nd as a bat (my r as s)• ll as a ask (ur nary re en ion), and• hot as a ha e (hyper he mia).

See Genera In e al Medicine, Book5, for more detailon these and othe tox c es and t ea men s

D A OF MU CLE AND N RV

MYELOPATHIEMyelopa h es are d seases of he spina co d Typicalman estations are ga a axia, spasticity, an hyper

e ex a. Bowel and bladder incontinence arise as sease worsens There are many subcatego es

b i m d g d

Subacu e combined degene a ion o the sp nal cord ue oB12 e c encyis the proto ype for metabo c myelopa hy.Seve e B de c ency causes segmental oss o mye in,espec al y n hedorsal and atera columns C nicap esen a ion s g adual weakness assoc a ed wi h pares hes as an oss o p opr oception w th developmento atax a Severe cases end n ex ens ve b a era owerextremi weakness spas ic ty, and ur nary ncon inence+/ - cogni ve impai men . These cogn tive changes

nclude con sion, apa hy, elusions, parano a, andmen a dete iorationT p Think o B de c ency n a pa ient w th br sk kneejerks (d e to pyramida act ys nc ion) an absenank e jerks ( e o pe iphe a ne opa hy).Know hat the neurolog c changes can occur wi hout anyassociated macrocy osis o anem a! The CSF is typ cal ynorma an EMG shows s ow ng of sensory conduc on.D agnose by measuring se m B , methylma on c acid(M), an homocys e ne (HC) evels.M andHC are mo e sensitive es s ha are included o make ad agnosis in pa ients who have ow normal or normal Blevels In s a es of B de c ency, both MMA an HCare ncrease . Know ha copper de c ency n pat en s w h ma abso p ion or pos gastr c bypass can p esenl ke subacute comb ned egeneration of he cord d e toB de ciency.

nf

Advanced AIDS pa ients can getvacuo ar myelopathy

w h vac o ation and de e ioration o he do sal andla eral sp nal columns that presen s asascending pa esis

wi h a senso componen ( oss of v bration and propriocep on) an u inary ncon inence Clinical presentation

s very s mi ar o subacute comb ne egene a ion o theco I common y accompanies HIV assoc a ed dement abut occasional y occu s alone Many o he h ngs can oth s in a pat ent w th vir ua ly no immune system, b besure o exc u e a co d les on w h MR

d Sp na ep dural abscess is a medical emergency hatrequ res ap d diagnos s and treatmen o the bacteria

n ect on. The abscess can eve op ombac eremicseed ng om any sou ce orcontiguous in ect on a erspine su gery, b rarely om l mbar puncture R skfac o s include mmuno e ciency s a es (e g., abe es,HIV/AIDS), alcoho ism, an any conditions or behav

ors associated w h rans en bacteremia (e g , n ec ond g use and bo ls) The abscess may sta as a sp naos eomyeli is an progress o an abscess, causing cordcomp ession. aureus s he most common et o ogy ofep dura abscess.Remembe The main symp om o epidu al abscess sback pa n Suspec ep dural abscess in anyone who hasbeen bac e emic om any cause an presen s wi h backpain and fever Fo example, e out epidu al abscessin the postpa tum pa ent who ha an epidu al d ngde ivery he cause is a most a ways some pe onosocom aStaphyloc ccusspec es.Init al symptoms nc ude a ew days to2 weeks o feveran backache with ocalize ten e ess, ra cu a pa n,and neu o ogic de cits Not all pa ien s have all o the

symp oms, an he d agnos s can be eas ly missedAbscess s best diagnose with immed a e con astedMR withFLAIR (con asted CT s a ess sens iveal e a ive), B sk n est, an b oo c l es Pe fo mmye og aphy if he abscess is no c early seen by MR(or CT, if hat s he only op ion).T ea men immediate decomp ession w h aminec omyand rainagefo lowed by app opriatean ib o ics, excep

n cases o TB whe e treatmen s enti ely me cal (using4 r g antit berculous an m c obials)

d is berculo s os eomye it s of the spineand s somet mes associated with co d comp essionUsually, his fo m o TB s ue to react vation disease(rare y s prima y uberculosis) Less han 40% ofa ec ed pa ien s have cons i t ona symptoms ( ever,n gh swea s, and we ght loss) They a so have backpain and possible neurologic de ci s and/o rad c asymptoms.D agnosis req i es a high n ex o suspicion and iscon ed by b opsies fo pa ho ogy an cul e Aposit ve TB skin test o ser m inter ron gamma eleaseassay (IGRA) supports he diagnosis Treatment is withstanda d 4 d g TB herapy (See Pulmonary Medicine,Book 2, or spec c details.)

© 2014 MedStudy - Piease Repo t Copyr gh Infr eme tocopyr h @meds dy. o





Describe the f nd ngs in subacute combineddegenerat on due to 812 deficiency .

What other mineral deficiency can present kethe subacute comb ned degenerat on due tovitam n 8 2?

What are risk factors for an ep dural abscess?What s the most common cause?

What causes Pott disease?

Describe the c n ca presentationsof neurosyph lis.

What s the c n cal presentat on oftransverse myelit s?

What is Dev c d sease? Which auto-ant bodyis the culprit?

What are the symptoms of cerv ca myelopathy?

Syphi s

Neurosyphilis is a potential comp ication if syph is sunt eated a d as an earlier presentation in patients withH V/A DS.Both seco dary and ter ary syphi s cana ect the cord T eseconda yma ifestat on o me ingovascula syph s ca present as st oke o as nfa ctioo the spinal cord (ra e)Ter arysyp il s p esents ascog t ve mpairment, tabes do sa s, a d/or aort t s

T e cognitive impairment can be emembe ed by the

m emon cPARESIS: ersona y, ect, e exes, yes(A gyll-Robe so pup ), ensor um, ntellect, peechT e Argy Robe son pup is constr cted a d reacts toaccommodat on but does ot react to ig t

Tabes do sa s s syphil t c involvement o the poste ioco um s t at causes de c ts n p op oceptio ,ma i esting as ataxia a d paresthesias Tabes dorsal s isd agnosed us g the following:

• Screening tests or syphi is ( PR or VORL)• T -speci c testing (MHA-TP)• +/ Lumbar puncture and biopsies with outine path

and cu tures

Read mo e about d agnosis a d treatment of syphil s(including neu osyphi s) nfect ous Disease, ookl.

Inf ammatory Mye opathyTransverse Myelitis ( M)

T s a are p ob em caus ng ammat on of boths des of 1 o 2 segments of the cord (usua ly tho acic)T e exact cause s uncer a n, but it appea s to be aautoimmune reactio nset typical y follows a virainfection, but it s also assoc ated with mult ple sclerosis and severa auto mmune d so de s ( upus, mixed

connect ve t ssue disease, Sj g en's, scle ode ma, and

© 2014 MedStudy

DISEASES OF MUSCLE AND NERVE

r eumatoid a h it s) There are cases of it occurringeve more rarely a e some vaccinat ons

C ical presentatio is most o enacute a d p og essiveover a few days, wit ea ly paresthes as, bilate al legweak ess, a d numbness wit a se sory de cit belowt e evel o the es on Sph ncte ic d sturbances a dbackac e a e a so commo A sl ght asymmetry o thesymptoms and s gns, a senso y leve ove the trunk, or aBab nski s gn di ere tiate it from a rap dly progressivepolyneuropat y suc as Gui ain Barr synd ome

MR with co trast s ows the n ammat on o the cord CSF ana ysis shows nc eased protein, lymp ocy os s,a d normal g ucose

Neuromyelitis o tica ([NM ], a.k a Devic d sease):This variant of mye tis ma fests p ma i y by at ackingthe optic nerves a d sp nal cord The p esence of se m

IgG ant bod es, also k own as ant aquaporia tibod es, s associated with creased risk of recurrentmyelitis NM a t bod es also have a se sit vi of 73%a d spec ci of 91% for the d ag osis of Devic diseaseLes o s on b ain MR are also predict ve of p og ess onto S n d opat c cases of t ansverse myelit s

A 201 AAN guide ne ecomme ds emp c steroids andeven p asmap e es s if the e s no esponse to steroids,althoug the evel o evidence for t ese is weak

Compression nduced Mye opathiesCervica Spondylosis with Myelopathy

Ce v ca spo dy osis s age e ated wear a d tea ont e ce v ca spine t begins with cha ges in the inteverteb al d scs, whic occur g adually a d accumu atewith age Neck pai s commo f the disc he iates,

t w comp ess a ne ve oot, caus ng aradicu opathyat that leve Note Rad culopathy manifests by numbness, paresthesias, weakness, and hypore ex a in t ecor espo d g egio t at s supplied by the compressednerve root The a ea a ected is efe red to as dermatome(senso y) or myotome (muscle groups)

When t e spondy osis becomes mo e seve e, t mayresu t in comp essio o t e spi al co d tself (myelopathy), caus ng spastic y, ype re exia, a d ga t abnomalit es Ga t abnormal ties may be attr buted inco

rect y to nc eas ng age of the pat ent A quick test is tocheck re exes; i patients>65 yea s o age, ab sk ank ee excould be the sole clue to ce v cal mye opat y

f a heumatoid art it s pat ent prese ts w th a post opfocal eu o de c t, suspect C1 2 spi a cord trauma

nduced by i tubat on T s s ike y the patient hasc ronic asymptomat c C C2 subluxat on Anesthesiolog sts are general y wel awa e of th s susceptib l ty, a do de C-spine exion/extension views p eoperative y toassess for any signs of cervica sub uxatio f course,othe mecha isms ca cause simila i ury in thesepat ents.

1 -33



11 D EA E OF MU LE AND NER E

Thoracic Myelopathy

Tho acic sensory levels: T4/T5 at n pp e line and T 0at umb l cus. Thorac c spondylos s s d st nct yunusual

In thoracic myelopath es, th nk tumo , ver ebracompress on fractu e, or transverse myel t s�notcomp ess on om sp ne osteoar h tis

Lumbosac al Myelopathy

The cord ends at L - 2. umbosacral disease a ects thecauda equ naand ne veroots, and may cause , 5, orSl rad culopathy w th the follow ng presentationsA ected dermatomes

L =medial aspect of eg5 =antero ate a aspect of eg and dorsum of foot,ncluding great toe ( 5 = arge toe)

• SI late a s de of foot by the sma l toe(Sl Side of foot nearSma toe)

A ected myotomes5 = weakness of theg eat toe extenso and ankle

do s ex on (Pat ents have t ouble stand ng on theheel and present withfoot drop )S weakness of ankle planta exion (Pat ents havetroub e standing on the toes ) Ank e e ex is absent.

Lumba spinal stenosis s a congenital nar owing ofthe sp nal canal in the area of T Ll , the conus medular s. Pat ents a e more susceptible to mp ngement ofthe cauda equ na secondary to d sc d sease, l gamentousdegenerat on, and arthritis

Lumbar spinal stenos s may result n neurogenicc audication, character zed by a deep, progressive achein the egs, sometimes associated with lower ext em tynumbness, paresthesias, o weakness, wh ch is p ecipitated by stand ng or wa king for a few m nutes Thesesymptoms are aggravated by up ight posture, whichextends the sp ne, and el eved by s tting or squatting( ex ng h ps/sp ne)Buzz phrases that help d agnose spina stenosis nclude

gets be e whenbending over the shopp ng car " oimproves when walk ng uphi l " These act vities curve

the ver ebral bod es and open space n the canal.

D e ent al diagnosis for spinal stenosis includesvascular claudication, wh ch also causes symptomswhen wa k ng or exe cising eg muscles but not whenstand ng upr ght (ab e 11-)A p esumpt ve d agnosis of sp na stenos s is madecl n cal y. Neu o maging (usua ly MRI) before t eatment is not necessa y fo pat ents< SOyears old withno neuro og ca de cits n th s group of pat ents, MRI

s done only f the e is worsening of symptoms du ingthe stmonth of treatment o no mprovement by theend of this l stmonth n pat ents> 50 years old and

n those with neuro og ca de cits, mag ng s o endone mmediately to con m the d agnos s beforedetermin ng t eatment.

T eatment is conse ative physical therapy andanalgesics. Surgery s a ast eso fo patients who havedebi tating pa n not re ieved w th conse vative measu es. Su ge y s nd cated urgently, however, in patientsw th progressive neurologic de c ts o ncont nence

Mi cellaneou yelopa h e

Sy ingomyelia

Sy ngomyelia is a prog ess ve myelopathy caused bycav tat onof the central sp nal co d, typical y in thecerv ca eg on but may extend nto the tho ac c regionIt can be d opathic, deve opmenta , o acqu red About2/3 of cases a e associated w thArno d Ch armalformat on a congen tal malformation n wh ch the e sa downwa d shi of the cerebe ar tonsils and medul athrough the foramen magnum nto the cervical a ea ofthe spine, somet mes w th syr nx (cyst) format onSyr ngomyelia causes apa nless weaknessand wast ng

of the hands and arms (b ach a amyotrophy) andsegmental senso y lossof d ssociated type (i e , lossof the ma and pa nful sensat on with sparing of tactile, jo nt position, and vib ato y sense) Symptomsof syringomye a typ cally occu as a suspended" ocape l ke" sensory de c t ac oss the shou ders and

proximal upper mbs.The loss of pain and temperature, with nit a lypreserved ght touch and v brat on sensation, indicates

nvolvement of the crossing spinothalam c bers n thecent a par of the cord. When the anter or ho ce lsare affected, w th ate al expans on of the syrinx, weakness and at ophy of the upper limbs occur, startingin the hands and mov ng proximal y to include thearms and then shoulder muscles Occip ta and nuchalheadaches a e also very common

Diagnose syringomye a with MRI

Ante io Ho n Cell Diso de s

Anterior ho cell p ob ems causemotor de cits only.Amyot ophic late al scle osis ([ALS], a.k a. LouGehrig d sease) s the most common cause of anteriorho ce disorde . The ha lmark of A S is ma ked,simultaneous upper and lower motor neu on signs Men

are a ected mo e o en than women.

able 11-5: v .

mba SpinaS en i

Va cu a

C a d ca n

Change n Symp oms:Walking S n ing Si ing

Wor e W e Be er

W e Be e Be e

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Q� ui• What is lumbar spinal s enosis? W at are

t e c assic exacerbating and rel eving bodypos ions and movemen s?

• From t e pat ent's his o y, w at clues he pyou d erent ate lumbar spinal stenosis fromvascular c aud cation?

• What s he c n cal presentat on osyringomyel a?

• W a is the cl n ca presen a ion o ALS?• W a cond tions can cause UMN and LMN signs

n t e same pat ent?

A patient with ALS presents with some variation of:

d useh pe e ex aand spast c y(uppe moto neu on), along w hfasc cu a ons, wea ness, and at ophy( owe mo or neu on).

Consider A S n he patient wi h ower extremitywea ness (poss bly even falls), di cu ty w th nemotor sk s, and fasc culations and/or a ophy on examPatients epor seve e musc e c amp ng Cogn vedys nc on isnot a feature

A S is relent ess y prog essive, invo ving uppe andlower extrem ies, runca and bu bar muscu ature, andis e m natyp ca y within3- 5 years a er d agnos sManagement of these patients ncludes de ermin ng howto proceed with respi atory and nut itional suppo t asthe disease progresses Riluzole is commonly used, buextends fe by only about mon hs.

Polio used o be the most common cause of ante ioho ce d so der; now post-pol o synd ome mus alsobe conside ed. Pos -po io syndrome causesa e ex aand prog essive wea nessw thoutuppe motor neurons gns "Spinal muscular a ophy is a set of heredita ydiso de s of the an e ior ho lower motor neurons Apolio-like presentation today is more kely o be due toWest Nile virus encepha tis

Conditions that cause upper moto neu on (U N) andlower mo or neu on ( MN) ndings n he same patieninclude

A S (mo or)B12 de c ency with subacute combined degene ationof he cord (motor+ sensory)Cer cal myelopathy (moto sensory)Syr ngomyelia ( MN= arms, MN legs,motor sensory)Friedreich ataxia (ataxia mo or sensory)Syphilis (motor sensory)Hyperthy oidism (motor+ senso y)

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D EA E OF U CLE AND NERVE

NEUROPATHIES

verviewNeuropathies can be d vided nto several catego esbased on wh ch ner es are a ected

If the process nvolves only I nerve, t s calledm y.ononeuropath es are genera y due

oentrapmen (as with ca pal unnel syndrome) othecauses nc ude foca ischem a and auma

If o more ne es are a ec ed in a m ted d st ibution,the te mm m l l xs used Mononeurit smu plex results om system c diso de s l ked abeteso vascul t s.

Neu opathies hat symmetr cally and di se y nvolvethe pe phera ner es a e calledper pheral neuropa h es(o polyneu opathy). Per pheral neuropathies nvo ved sta segments mo e than proximal There a e manycauses of per phe al neu opathy (see be ow)

Invo vement of multiple ne ves w th n a plexus srefer ed to as plexopa hyhe workup for any neuropa hy includes glucose,

HbA c leve , ee T and TS leve s, vitam n B1 , ESR,c eatin ne, CBC, and a chest x ray lec omyographyand ne ve conduct on studies ( G/ CS) are done

ega dless of whe he the symp oms are mono orpo yneuropathy. EMG/ CS help o ident any d sease of musc e and ne ve conduc ion Se um prote nelectrophores s, mmunog obulin elect ophoresis, andquantitat ve immunoglobu n assays a e also done f thepat ent s> 40 yea s of age, part cula ly if the G/NCS sugges a demyelinating neuropathy

In ammato y and he ed ta yneuropath es are the mostfrequent y m ssed causes of po yneuropathy So, conside in ammato y causes and inc ude a care l familyh story in your evalua on of per phe al neu opath es!

Mononeuropath esF c l/ C m

oca mononeu opath es are caused by loca i ed per pheralne e damage, usual y om a comp ession injury(although ischem a can a so cause damage, especial y nauto mmune d seases assoc a ed w th vascu i is). Sing ener e involvement can be caused by ep osy, sarco d, andhe es zoster (in addition o the dermatoma ash)

he ma n sites of comp ess on or ent apment are theulna ne ve a hee bow, the median ne ve at thewr s,and the peronea ne ve at theknee (d sc ssed below)Because ad culopa hies and mononeu tis multip ex canhave presentat ons s m ar o iden ical to foca /compressive neuropathies, hey mus also be conside ed n thewo kup of pa ients presenting with foca neuropath csymptoms

d l y(acute wr st d op) s mostly omnerve compression but is occas onally seen as a esu t

of d abet cneu opathy (page 11 9) and may also occur



11- D SEASES OF MUSCL AND N RVE

with lead toxicity. t has been ca led "Saturday ig tpalsy in i ebriated patie ts because it occurs a erbouts of u consciousness w ereby the nerve becomescompressed in the radia groove o the umer s.This typica y resolves slow y over several weeks ormonths-provided the patient doesn't co inuallyrein jure t e nerve! Physica t erapy is the best treatment,

usi g wrist splintsLower brachial p exus i jury ( rom surgery/tumor/trauma) causes a c aw hand de ormi y, simi ar to thatwhic may be seen with sever ulnar europathy.

Carpal tunnel synd ome (CTS) is media er een rapme t at the wr st, typically om repetitive stress,causing se sory oss, paresthesias, and weakness involvi gthe rst or 4 digits of the hand, but patie ts can have paianyw ere in t e a or s ou der! T enar muscle a op ymay occur Median erve en rapme t at t e wr st almostinvar ably causes oc a awake ing due to hand paior paresthesias (Image 7. Prevale ce of hypot y

roidism is 0% in patients wit CTS, so most expertsrecomme d screening with TSH Don t orget about t eassociatio of CTS with acromega y, as we l

Initial treatme t of carpal tu nel syndrome is eutralalignment wrist splints a d modi ing the repetitivestress f t is is ine ective, steroid injectio may he p.Next step is median nerve re eas Cer ain exercises(yoga and some speci c physica t erapy exercises suchas "nerve g iding ) seem to he p Ultrasound he ps some

[Know:] Pregna cy can cause an acute presentation ofCTS that ypically improves a er de ivery Spli ts arethe best treatment for this patie t group

Ulnar neuropathy causes se sory loss and paresthesiasin t e little ger a d ulnar aspect o t e ri g nger, aswell as weakness of nger abductors a d adductors tis usually due to compression of the nerve at t e elbow(cubital unnel syndrome) but also may result rom a

esion at thewrist Rare y, trauma to the heel o the andcan resu t in an ulnar injury. E bow pads a d splintshelp Surgery is a so an option for re ractory cases

Sciatic ne ve compression causes pai andparesthesias that travel down the back or side of the eginto t e oot or ank e It ca , like S1 radiculopathy, causedi culty standi g on toes. U ike S1 radicu opathy, it

mage 7: Thumb muscle wasting due to carpal tunnel yndrome

does ot cause a decreased a kle jerk w en compared tothe opposite a k e ( able 6Peroneal ne e compression ypica ly occurs atthe proximal head of the bu a, causing foot dropRemember that L5 radicu opat y a so causes oot drop

To distinguis between pero eal erve compressio

and L5 radiculopathy Patie ts wit pero eal ervecompression cannot evert the foot well but can stilinvert it, w ile L5 radiculopathy prevents or hindersboth eversio a d inversio ( able II- 7 Also, it isuse u to test proximal 5 in ervated muscles such ast e ams ri gs and t ig abductors, whic wil not bea ected with peronea er e compression

[ now ] C arcot MarieTooth disease (page 1 -38) cancause symptoms similar to pero eal nerve compression

Mononeuritis Multiplex

Note that mo oneuritis multiplex can prese t ide tica yto t e focaVcompressive europathies above Rathertha bei g caused by ner e compression, mono euritismu tiplex is caused by asystemic disease ascu itis andvascu ar occ usion o the vasa ervor m (vesse s thatsupply t e nerves) are the mai causes

Consider a y o the followi g as a possib e cause omono europathy +/ multip ex

• Rheumatoid ar hritis•DM• Connective tissue diseases• ascu itis

• Polyarteritis• Lyme disease (Thi k o this in a hiker with new onsetoot drop )

• euralgic amyotrophy

Neura gic amyotrophy (ot er ames Parsonage Tu ersy drome, brachia p exus europathy, acute brachialradicu itis) is temporary in ammation of the brachialplexus that may ollow a vaccinatio or viral illnessInitia y, it causes extreme pain i the shoulder witradiation to the arm, neck, a d back Within hours todays a er the o set o pain, the s oulder musc es andproximal arm musculature become weak Bi atera

involvement may occur. Diagnosis is clinical, supported by EMG/NCS. It improves i years withconservative management

C S Lyme disease is discussed in In ectious DiseaseBook 1.

Bell's Palsy

Bell's pa sy is caused by dys nction of t e exte al7 hcrania erve It is regarded as idiopathic, butherpessimp ex(or its associated immu e response) is t e causeo most cases (de nitively supported by nding evidenceo the virus by PCR in t e a ected nerve roots)

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Where are t e main poi ts of compress o foulna , med an and pero ea ner es?

Nocturnal awaken ng with hand pa n sf equent y due to w at d ag osis? Wh c e e?

Mo o eur tis mu t plex s assoc ated w twh ch d seases?

What nfection s ou d you co sider in a kefrom Co necticut who p ese ts w th new o setof foot drop?

Name 3 d sease processes t at ca causefacia pa sy.

W at is t e c n cal p ese tation of Be l's pa sy?• D abetes s assoc ated wit w c neuropat ies?

Varice a zoster is also a cause and is the probablediagnosis when a clinical scenario includes vesiclesinvolving t e ympanic membrane and exte a audito ycanal (Ramsay Hunt syndrome).2 important systemic diseases can also cause a facialpa sy a presen s iden ically:

I) Lyme disease2) Acu eHIV

Some exper s call these pa sies "Bell's, but ot ersprefer to identi them as a sys emic manifestation of

yme orHIVOt er causes of facia pa sy neurosarcoidosis,Guillain-Bar syndrome, and paro id tumorsBel 's pa sy a ec s an entire a f of the face,inc uding t e forehead. It causes ipsi a eral facia muscleparalysis and occasionally results in no taste sensa ionon t e anterior 2/3 of ongue, oss of lacrimation, and

Table 11-6: S Ra iculopa hy vs Sc a ca

Sciatica

A toipto ?

No

No

D cr as dAnk J rk?

No

Tab e 11-7: LS Ra ic lopa hy vsP r al N v I J ry

Foot A to A toDrop? Inv rt Ev

Foot? Foot?

5 R4 culopa hy

Peroneal Nerve Yes Yes NoInjury

© 2014 Med tu y

DI EA E OF U C AND N RV

yperacusis Pregeniculate lesions are associated with the loss of tas e, sa iva ion, and acrima ion, w ile moredis al lesions spare ese nctionsTo elp di eren ia e Bell's pa sy om o er ne eda age, know t atc r ica esions spare t e musc esof t e forehead and upper eye id, whereas Be s pa sya ects emDiagnosis is clinica Imaging of the ead is rese edfor patients w o don' improve wit in6 mon hs or w ocontinue to progress wi facial weakness a er 3 weeks.

ow that if e pa sy is preceded by a period of facia t itc ing, he risk of tumor is ig er T ese patien ss ould have urgen imagingPatients w o begin to improve wi hin 3 weeks wi lcommon y recover complete y If complete ipsilateralpara ysis occurs, ll recovery is ess ike y.A week ofprednisonesho ens he course and improves

nc ion if s a ed within7 days of clinical onse S udiesassessing combined antivira drugs (acyclovir or valacyclovir) + prednisone s ow con icting results Someexpe s give bo h; others do not, unless obvious signsof erpes are present (i e , vesicles). Eye id surge y isreserved for patien s with severe pa sy, or where hereis co eal anes esia or xerop thalmia not amenable toeye ubricants

abeti Mo o europath s

[Know ] Diabe es is associated wi severa cranianeuropathies Neuropathies a ecting cranial ner es3, 4, and 6 present with eye pain, drooping eye ids,and doub e vision t ose a ecting cranial ner e7present with Bel 's Radial, ulnar, and peroneal iso atedneuropa hies are also more common in diabetics.Note that diabetic invo vement of t e 3 cranial ner e typica y presents wit double vision and weak eyemovemen s withou any c anges in the pupils Examquestions migh have t e pa ien presenting wi hdiplopiaand (pick one) c ronicsenso dys nction, r s drop, orfoo dropRemember: A diabetic 3 crania neuropa y spares

e pupi If a patien as a 3 crania neuropa hy wi hpupillary di a ation, think compression of the 3 cranialnerve by an aneu ysm of the posterior communicatinga te y T is war an s an urgent MRI and MRA!Diabetic lumbosacral p exopat y (amyotrop y) presen swi h leg pain (82%) fo lowed by proxima weaknessof he leg t ini ial y ends to be unila era (88%) buteven ually involves bot egs Au onomic dys nc ionoccurs in 50%; weight loss> 10 lbs occurs in abou 80%of patien s Sensory symptoms and signs can also occur.T e condi ion deve ops over mont s and so does pa ialor complete recove y No speci c treatment exis s, thougsteroids and cyc ophosp amide have been tr ed

1 -3



11- D SEASES OF MUSCLE AND NERVE

PolyneuropathiesDemyelinating vs. Axonal Polyneuropathies

Demyelinating polyneuropath es a ecmotor bers andpresent pr mar ly asweakness.Axona polyneuropat es are usua ly asensorimotorcomb na on, with sensory abnorma ities appearing rs(paresthes as progressing to numbness), then mo orweakness appear ng later

Guillain-Barr Syndrome

G illain-Barr syndrome (GBS) is the most commonauto mm ne, in ammatory polyne ropa hy We nowunders and that GBS is a syn rome withdemyelina ing(most common) an axona varian s.In e vast major y of cases, a mil gas roin es inaor respiratory infection prece es he polyne ropat y.GBS was repor ed a er in uenza vaccina on in e late

1970s an 990s and a er the meningococcal conjugatevacc ne n 2005 Ca sality as not been establishe forei er vaccine, and he subjec is gh y con roversial.T ere is no req irement with these vaccines o wapa ien s abo t poss ble GBS, bu pa en s wi h a s

ory of GBS are ca tione to avoi vacc nation for e1 year a er t e r illness.C ass c emyelina ngGBS (terme acu e in amma orydemyelinating po yra ic lone ropathy [A DP];90%of U.S cases) presen s as anascending paralysis ofm scles, inc ing respira ory muscles, withare exia.In practice, pa ients may ave some m ld sensoryabnormalities an paresthesias nitially, b t GBS s typically por raye as a pure mo or i ness w absentre exes Dis rbances in autonomic f nction and rinaryretention may also be seen.T e Miller F s eraxonal var an ( V]; 5% of cases)is a type of GBS that ncl es only are exia, atax a, andophthalmopleg a; e.g , pa ients nable to move he reyes or wa k pright.Two other rareaxonal var ants comprise the rema ning5% of cases.Paraparetic (par ial paralysis), a ax c, and purelymotor or p rely sensory forms of the illness ave alsobeen obse ved

n pa ien s with any type of GBS, e CSF has anormacell co nt an a ig pro e n("alb m nocytolog c dissociation ); s spec ano er d agnosis f e CSF has more than 0 W BC/mm3. EMG/NCS helps to c aracter e thevariant (axonal or demye nating).An GQI b gG is a n e serum protein meas rablein over 80% of MFV cases of GBS, and ass s s w h

iagnosis of th s var an .The acute axonal var ants are commonly assoc a ed w thpreced ngC m b c j jinfect ons an a so w thdevelopmen of many an ibod es agains e gang iosides

foundin perip eral nerves (espec a yanti GQlb).

C ose resp ratory monitoring an care are importantMeas rement of vital capac y (VC), maximal insp ra tory pressure (M P), and max mal expira ory pressure(MEP) are used for the beds de es imat on of diaphragma ic s rength and respira ory nc ion T e rend of

hese meas remen s is a g i e o he keli ood ofrespiratory fai re Use the 20 0 0 r le o e erminenee for ven lator s ppor VC< 20 mL!kg, M P essnega ve than 0 m H , an MEP< 40 m H .Plasmap eresis and V mmunoglob n herapy ( V G)are eq ally e ec ive Use 1 or e o er if pat en s present wit in 4 weeks of nit a symptomsDo not se steroids beca se they areno e ec iveComple e recovery is the norm for abou 80% however,I 0% of pa ien s have a very prolonge co rse with orwit ou signi cant resi ual weakness. Approxima ely5% of pat ents do no s rvive e il ness.

Chronic Inflammatory DemyelinatingPolyneuropathy (ClOP)

C DP beg ns nsid o slyand evo vess ow y, e er na steadily progressive or stepwise manner, attain ng itsmax m m severity a er several months n abou 5%of cases, C DP beg ns like a m or mo era e variant of GBS, b t i slowly worsens or has a chronicre aps ng courseChron c symme ric sensorimo or loss, EMG nd ngsof emyelina ion, and e evated CS protein de ne

he illness.C DP cases are s ally no traceab e to an nciting eventsuc as an infec ion. (St l, s usefu o t ink of C DPas "G il a n-Barr tha won' go away ) Consi er C DPin he pat en w h a emye nat ng po yne ropa hy (byEMG/NCS) ha extends beyon 8 weeks in d ra onLP an EMG res l s are dent ca o GBS (high prote n,no p eocy osis, and demyel nating po yne ropa y)Exc e systemic isor ers, spec ca y HIV, hepati tis vir ses, Lyme, thyro isease, diabetes, mye oma,sarco d, and connect ve tiss e sorders s ch as l pusUn ike in G i a n-Ba ,gl cocor coids astenrecovery and preven relapse n C DP Plasmapheres sor V G are also s an ar trea ments (Pick of the

) Several o her imm nomod lators ave been sechronica y.

Charcot-Marie-Tooth (CMT)

CMT sease s a ereditary motor and sensoryne ropa y and is by far (90%) e mos common n er

ed perip era polyneuropa hy There are 7 " ypescomposed of> 0 separa e sorders un er e general

eading of CMT, a l ca se by mu a ions in myelingenes t at are nherited variab y (au osomal dom nant,au osoma recessive, or X l nked).CMT seases are emyelina ngan are d erenate based on genet c markers. All have both motor an

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• What CSF findi gs are cha acte ist c ofGu ai Barr syndrome?

• How does the treatme t of ClOP d ffer from hetrea me t of Gui la -Ba r sy drome?

• Name he d ug used o eat diabetes ha alsoca i duce 812 de icie cy a d cause a severeperiphera neuropa hy.

• Wha are he cli ica p esenta ons omyasthe a g avis?

senso y impai ment and commonly present w h n herst2 decades of l fe. The neuropa hy s symmetrica and

progresses s owly The rea y rare ones end to clus er infam l es. D agnos s s very simp e with gene c tes ingEMG/ CS is rare y needed Treatmen is s ppo tive

Diabetic Peripheral Neuropathy (DPN)

Diabetes me it s s themost common ca se ofpo yneuropa hy in genera c n ca pract ce. DPN s anaxonalne ropathy ha mainly ca sessenso ychanges,

nc d ng pa n pares hes as andn mbness.M sc e weakness is generally m ld Some have loss ofre exes In ong-s anding cases trophic changes areno ed Some patients have predominan loss of jointposition and v bration sensations.Con ro of b ood s gars is the most mportant herapy.E ective treatments for pa n inc de the FDA approvedDPN drugs du oxe ne (Cymba ta®) and pregabal n (Lyrica } bo h are equa y e ec ve O herd gs that are sed includetr cyc ic antidepressantscarbamazep ne gabapen n amotr gine tramado andven afaxine op cal reatment with capsaic n cream andl doca ne a so he p.Be aware ha n30% of pa ientsmetfo m ntrea ment ofdiabe es mell us can resu t in ma abso ption of v tam n8 w th s bseq en peripheral neuropathy resemb ngDP Th s is a potent al y debi ating s de e ectof metform n

Alcoholic Peripheral Neuropathy

A cohol s direct y ox c o both nerves and musc esand causes many k nds of neuropa h es (per pheraau onom c compress ve). he po yne ropa hy s

ypically axona but is made worse f demye ina ion ss per mposed (ca sed by n tr ional de ciencies)Symptoms of alcoho c axonal ne opa hy s a wi h painand numbness n he fee n as ockingd s r b tion. Overtime pat ents lose re exes propriocept on and streng hPatien s s ow y recover w th m tiv amin therapy andabstinence from a cohol.

© 2014 MedStudy

NEURO U CULAR JUNCTION

Remember: Acute hiamine de ciency presents asWe icke's a po yne ropathy (weakness of ex raoc armusc es and atax a) associated w h de ir um

Other Causes of Axonal Neuropathies

Know other somewha common ca ses of axonal

po yneuropathy nc dingTox ns s ch as heav me a s (lead arsen c)Chemotherapy d gs (v ncr s ne)

sonia id86(pyr doxine) overdose om n t it ona supp ementsOrganophosphatesSystemic i nesses (myeloma po phy ias thy oidd sease hepa itis v ruses amy oidos s and HIV/A DS)

Time of Onset

D eren at ng among he polyneuropa h es is aided bythe time of onset:

Sho me of onset (days) is near y a ways dueto n ammato yim unologic toxic orvasc aretiology. Th nk po phyr a G illain-Barr and a few ofthe toxic po yneuropathies.Long onse (over severa years) s seen wi h he heredi

a y d sorders such as Charco Mar e-Too h or C PSubacute onset (several weeks to2 years) occurs inthe ma ority

o Toxicity ( ead and g e-sn ng cause main ymotor e ects while and vincr s ne causesensor mo or e ec s.)

o N tr ional de ciencies (espec a y B >86,and 8o Paraneop ast c (See ambe - atonpage11- 40.)o Rhe mato ogic disorders

NEUROMUSCULAR JUNCT ON

MY TH N GR VMyas henia gravis ( G) s anauto mm nedisorderMost patients have a toantibod es toe therthe postsynap c acety cho inereceptor or m sc e speci c tyros nek nase receptor (M SK)! An even sma er group of Gpatien s hasneither an i-ace y cho ne receptornor ant

M SK an bodies (te med "seronega ive MG )MG is assoc ated withthymomas(- 15%of pat ents)and thymic hype p asia (60%), al hough t is nounderstood exac y how the hymus is related o an bodyformat on Do a chest CT in patien s w th MG.There are2 forms of MG

I) Genera ized MG presents as episodic weakness withrepe it ve movemen s (weakness no t redness nosoreness). Symp oms are worse at he end of the dayCommon presenting complaints inc de weaknesswhi e br sh ng ha r p tting away dishes or c imbings a rs and d p op a af er a long day. Weaken ng w threpe ve muscle s mula on dur ng the phys cal exam

-39



11 NEUR USCULAR JUNCTI N

(muscle fatigabili y) s gges s the diagnosis. P osisis common Muscles of facial express on, mast ca

on, swa lowing and speech are a ec ed in80% ofpatien s a some me in he lness M sc e atrophy

s rare, and tendon re exes are normal.2) Ocular MG presents as weakness localized to he eyes

(lids and ex raocular m sc es)

Prac ce pear s: Demonstra ing fatigab e p os s ( .e ,worsen ng of ptos s on30 seconds of sus ained p ga e)is a good way o differen iate myasthenic ptosis omother forms of ptosis. Of course, the pupil s e w l benorma , n ke in Ho er syndrome In addi ion, thepat e of ex raocu ar m sc e weakness o en does not

t he dis rib on of a sing e ocu omo or nerve, andmay change from one exam nat on to he nex .D agnos s of myasthen a gravis s best con rmed bymeasuring ant bod es agains acetylcholine recep

or (AChR-A s) and aga nst muscle-speci c tyrosinek nase ([MuSK A s]; a receptor-associated prote n).AChR Abs are present n85- 90% of patients w hgenerali ed d sease b t on y in- 60% of those w hiso a ed ocu ar d sease O en, MuSK Abs are presenin pa ien s who are negative for AChR-Abs (50%).Antibody eve s are no necessarily prognostic, butthey do rise and fa l w th immuno herapy.The edrophonium (Tensi on®) tes s sua y notperformed because resu s are no as reliab e asan ibody meas remen s.The ice pack test can be used for pat en s w h p os s aspart of he r symp oms. ce in a glove is applied to theclosed eyelid for2 min es, which resul s in less ptos sSens iv ty of this est s80%.Rout ne electrod agnost c stud es, includ ng repet t venerve stimu at on s udies and sing e- ber MG, are

se n suppor ing the diagnosisDo thyro d f nct on s udies because0% of pat en swith myas hen a grav s havechron c a to e

h s. Look ou for symp oms that sugges upusor rheuma o d ar hri is, since here s considerableoverlap. mage the ches with CT or MR n alcon rmed diagnoses to ru e o t thymomaNote Deep tendon re exes are preserved in MG asopposed o ambe -Eaton synd omeTrea ments used for myasthenia gravis

An icho nes erase agen s (e g., pyridos gmineMes non® )mm nomod ators n pat en sncon rolleon

pyridos igmine (e.g. s ero ds, cyclospor ne,mycophenolate)

V G or plasmapheres s (for myas hen cc s sonlybeca se durat on of ac ion s very shor )Thymectomy ( akes years o see e ects, bu de ni elyperform n pa ien s wi hth mo a)

Myas henic cr s s s a rap d de er oration of myas hen athat can causeresp o a lureand qua pleg a. Arespiratory nfection or cer ain med cations can prec p

a e crises Bes des respiratory suppor , patien s respondto plasmapheresis and V G

now the few drugs that can precip ta e myasthen ccr sis in pa ients w th e ther known or und agnosed MG

• Aminoglycos des• �-b ockers• Procainam de• -interferon• Magnes um su fate• Penic llamine

Q nid ne

LAMBERT-EATON SYNDROMELamber aton myas henic syndrome is a paraneoplast c

syndrome Abo t60% of cases are seen nsmall celllung cancer o her assoc ated cancers include prosa e, breast, stomach, rec m, and ymphomas t s

a so seen rare y na o m uned seases. t s tself anau o mmune disease in which ant bod es are producedtha are speci c forcalc channels n presynap icper phera nerve erminals, causing decreased re ease oface cho ne from the nerve er nals.

ow he fol owing abou symptoms• p ca symp oms are gradually progress ve

prox ma m scle weakness aching h ghs, dry mouth(au onomic dys nct on), and hypore exia, especia yin he ower ex remi ies

• t looks l ke myas hen a grav s, excep trelinvolves the c larmuscles andrepe t eexerc semay prove he weakness for the rst fewcon rac ions

No e: Deep tendon re exes are depressed n L asopposed to MG where they are prese ved!D agnose Lamber -Eaton by measur ng voltage gatedcalc um channe antibodies (anti-VGCC) Anti-VGCCantibodies are no 100% speci c hey are some imesfound in pat en s who do not have Lambert- a onTherefore, measure hem on y in patien s who have a

h ghpre es probabi ity of tr e disease MG can helpd s ng ish between Lamber Ea on and myasthen aw th decremen a response (weaken ng) o rapidst mu a on n myas henia and incremental response(strengthen ng) o rapid s im lation in Lambert a onsyndrome.Look for ma ignancy n anybody d agnosed wi hLambert- a on spec a y small ce ung cancerTrea ment ncludes address ng any nderlyingma ignancy along wi h drugs that increase heamo nt of acety cho ine in he synapse (g anidine,3,4-diaminopyr dine, and pyr dost gmine). Refrac orycases can be treated w th V G or predn sone

© 2014 MedStu y-Pi ase Repo t C pyr ght Inf ng m nt t c py ght@m d tudy.c m





.

UI

How is MG d agnosed?

What other tests should be done n patientsw th myasthen a gravis?

What cancers are assoc ated w thLambert-Eaton synd ome?

• What happens to deep tendon ref exes in Gand ambe t-Eaton syndrome?

Where s the muscle weakness that occu swith inclusion body myos t s?

P og essive l mb gird e weakness in an adu tpatient who has a fami y histo y o the same s

nd cat ve of what d agnos s?

YO ATHIES

OTE

Myopathy simply means musc e disease. Myopathiesare typica ly classi ed under ne rom scu ar diseases(hence their discussion here). Symptoms can be musc eweakness sti ess cramps and spasms.

I FLA ATORY YO ATHIES

nflamma or myopathies are caused by chronic musclein ammation. Us al ca ses are:

DermatomyositisPolymyositisInc sion body myositis

Both dermatomyositis and po ymyositis common y cause

E evated CKProxima muscle weakness

Both respond to cor icosteroidsnc sion bo m osi is is a ess common type of

myositis in which patients present withA s ow y progressive painless m scle weaknesswith involvement o proxima (initial y) thendistal musc esE evated CKOc omotor m sc e sparing

Incl sion body myositis does not respond tocor icosteroids usc e biopsy in inc usion bodymyositis shows vac o ar inc sions.

More on dermato and po ymyositis in Rheumato ogyBook 3.

© 014 MedStudy

YOP TH E

O R E YO A H ES

Proximal m sc e weak ess of varying degrees may beseen in patients with hyper hyroidism acromega y,severe vitamin D de ciency and conditions o steroidexcess.

Hypothyroid patients have genera ized musc e

weakness mya gias s owness of contraction and re axation and may have increased CK. Muscle cramping isprominent in hypoparathyroidism.

ETA OLI YO ATH ES

Consider a metabolic ca se of m sc e dys nction m

patients with muscle atig e pain cramping and inmore severe cases contract res and myoglobinuria.These symptoms are precipitated by exercise in patientswith disorders o carbohydrate metabolism and byfasting in those with disorders of ipidmetabo ism. Themajor categories are

Disorders o carbohydrate metabo ism (e.g.myophosphorylase and phosphofr ctokinasede ciency)Disorders o lipid metabo ism (e.g. ca itinede ciency)Disorders of mitochondrial f nction (Mitochondrialmyopathies are distinguished by the presenceo ragged red bers on ight microscopy o amusc e biopsy.)

US ULAR YSTRO H ES

D ch nn musc ar dystrophy is anX-linked disorderthat causes progressive m sc e weakness star ing atabo t 2 years of age and progressing to death as a youngadu t. The weakness is more proximal than dista Lookfor an e evated CK

o onic dystrophy consists o 2 types o inheritedad t-onset ne romuscu ar disorders that havemultisystem e ects yotonic dystrophy typeI isca sed by m tations in theD K gene while type2resu ts from mutations in theCNBP gene. The geneticabnorma ities res t in weakened skeleta musc e myotonia (prolonged contraction on muscle percussion)cardiac cond ction defects cataracts hypogonadismand i s in resistance. Patients characteristically have

ronta ba ding and a "hatchet ace appearance as aresu t o jaw and tempora mus e wasting. ypica ypatients comp ain o ske etal m scle weak ess o enlimb girdle and have positive family history Considerthis disease in a patie t who presents as anadu twithsymptoms o m sc e dystrophy These patients shouldbe re erred to a neurologist who can make the diagnosis

sing genetic tests Treatment is s pportive only.

11-41



NEUROMA

A DS-RELATED MYOPATHYAlDS-related myopathy is uncommon and typ cally

hough to be due oz dovud ne(ZDV, AZT) bu someinves ga ors a r bu e h s o he d ect e ec s of hevirus (controvers a ). Patients presen w h a gene ali ed(proxima > d stal) wea ness and an elevated CKT eatmen :Stop he A T

N

Mor on neu oma (or orton me a arsalgia) s a air ycommon d sease o he oo in which he patien hasmetata sa pain. Gene a y it s d agnosed with MRI ou rasound, which shows a sma intr me a arsal ovoidmass e ential diagnosis inc udes a metata sa s ress

rac ure. T ea men s su g ca exc s on.

N NG

MULT PLE SCLEROS Sverview

[Know all the follow ng!] Mult p e scleros s ( S) s ademyelinating d sease o he cent al nervous system

ha usually begins be ween he ages o20 and 30 .Women a e a ec ed more o en than men (about : .The inc dence s h gher nnorthe la itudes, poss blybecause o reduced sun exposure. I has recen y been

ecogn ed thatv tam n may have an impo ant ro eas a mod able env onmental isk fac or. I s a ch on ccond ion with ep sodes o ocal disorde s of he opt cne ves sp na co d and brain, which remit and recurover a pe od of many yea s.

The d sease process s hought o be au o mmune,a hough no spec c an bod es have been found and hed sease may no a ways espond to immunomodula ors.Infect ons as an e iology haven' been exc uded omtheory One heory is tha there is an n t a nfectious insu tand an au o mmune eac on acts as a seconda y igge .Ano he s ha MS s a esu o T-ce sens a on

o myel n. A famil a aggregation o MS has alsobeen eported

The neuro ogical symptoms depend on he eg on obrain ha s a ected.There are 3 types of S:

I) Relapsing remitt ng (RLRM)Secondary progress ve

3) mary p og ess ve

The relapsing-rem ing type ( nitia y no mal but la eon with residua de cit between spe ls) can slow yt ans orm nto the p og ess ve ype (wh ch may bes owly p og ess ve f om onse ). ndeed, a hough8 %o cases a e in a y R RM, a e severa years moshave transformed to the p ogressive ype.

at ents with a I 51episode and with or more lesionson bra n MR have a90% r sk of developing MS in

0yea s as opposed to a 8% isk i no es ons a eound on b ain MRI.

l n cal an festat ons of

aroxysma symptomsmake up he usua course of earlydisease (except n chronic prog ess ve cases). Weaknesso numbness n or mo e mbs s the nitia symptom nabout /2of the pa ents T ng ng o the extremi ies and

ght band- ke sensat ons a ound he trunk or mbs a ecommonly associated symp oms.

Al hough st ict c er a a e used to diagnose MS (see"Diagnosis o S on nex page), p ace MS n the dif

erentia any me you encoun er he follow ng cha acters c syndromes (especia y i ecurren !).p u (ON) s he mos common presen a ion

of MS eye d sease and the 5man es ation n about

%of patients. It occurs at some time in 0%of al MSpa ents. I p esen s as arapid oss of v sion n one orbo h eyes, o en accompan ed by sl gh pain especia yon eye movemen . The vis on oss is usua ycen ral, buta var ety of eld e ects may beseen. W h un late ainvolvement, the Marcus nn pup l (a.k.a relativea erent pupi ary de ec ) s yp cally seen ( ght shined

n o the eyew th op ic neu it s producesslower andincomplete constr c ion o both pup s than gh sh ned

nto he healthy eye. On he sw ng ng ashlight test,when l gh s presented to the no mal eye, bo h pup sconst ct b isk y; but when he ash gh s swung to hea ec ed eye, bo h pup s pa adoxica y dilate.) The e is

swe ling of the op c disk, bu w th p ogress on, the diskbecomes pa e. ore han 90% o hese cases recovercomplete y.

ph h m p g(I O) s ano herabno a nding o en seen n MS cases O s causedby a esion n he "media ong tudinal ascicu us, and,although it presents as di culty in mov ng the eyes hori

on al y conve gence is normal. (Remember ha normalconvergence means he pa en can tu each eye nwardsl ghtly as he ol ows you nger o his nose so ha hecon nues to see a s ngle objec .) The e sadduction paresis ipsilatera o the lesion, with he de cit r ging omcomp ete med al rectus para ys s to sligh slow ng of anadduc ing saccade Ga e-evoked hori on al e k nystagmus is p esent in he abduc ng eye con ala e al o theeye w th adduc on weakness. (Remembe :Adduc ionmeans "toward he midline andabduc ionmeans "away

om he midl ne. ) When you hear of a ela ive y youngpa en being diagnosed w h n e uclear oph halmoplegia, th nk mult p e sc erosis. n o der pa en s, howeve ,i s mo e common y due to ce ebrovascula d sease hepresence o bilatera inte uc ear ophthalmoplegia n ayoung adul is v ual y d agnostic of MS.

my causes a rapid y evo v ng (several hou sor days) symmetr cal or asymme ical pa apa es s

or paraplegia ascending pares hesia oss of deep

© 2014 edStudy - Piease epo t Copyr gh Infr geme ts to copyr gh @ eds dy .com







W 2 ul p ?

W C F lp u ?

sensibility n the fee ; a sensory evel on he tr nksph ncter c dysfunct on and b ateral Bab nsk s gn(up ng b g oe w th m s rok ng of sole of foo ).

ther symptoms of MS may include genera zedf a igue, nebuloussenso yabno ma t es (pa n, paresthes as, tch g, feeling of co dness or swell ng, umbness[espec ally of he face]),ve tigo /diplopia, lower-extrem

ymo orweakness/para ys s,ataxic ga t, andbowel/b adderdys nct o . F e on of the neck may nducea ngling e ectr c l ke feel ng down the sho ders andback known as theLhermi e s gn.Young women w h bilatera tr gem nal neura g a and orb a eralIO have MS il p oven othe w se!Dement a isnot a yp ca feature of MS, espec ally n

he ear er stages, b t s bs ant al cogn ve mpa mentmay occ r in some patien s w thadvanced chron cprogressive d sease If yo r pa ent presen s w hdement a and ga t ab o ma es, a more ke y d agnos s

s Parkinson d sease, progressive s pranuclear palsy, orno mal press re hydrocephal s.Al symptoms of MS end toworsen n hehea , ca ed"Uhtho phenomeno Th s is beca se hea ncreasescond c on b ock demyelinated pa hways.

Diagnos s of MS

The d agnos s of MS is no longer based only on heh sto y and neuro og c exam. The rad t ona (Posner)cr eria nco pora ed signs and symp oms dicai g 2 CNS les ons separa ed intime and spacea d notcaused by o her CNS d sease. CSF nd ngs were a so

sed. The fact that MS es ons d ssem nate over t meand space has been, and still s, an essen a componen of making the diagnos s MS deve ops s ow y overtime w th new les ons occu ng n d eren parts of thebrain, hereby causing d erent neurological s gns andsymp oms. Newer cri er a nclude CNS mag ng.MR has become an essent a too n he workup ofMS. gado um MR shows the character s cenhancement or plaq es of pa chy myelin loss (wh tema er d sease) wi h90% sens t v y T2 weigh ed MRshows MS es ons as hyper ntense areas( a 8).Many non MS esions can show p as hyper ense,so hespeci c loca onwhere hese es ons are fo ndhas d agnos cweight Dawson's ngers refers toMS esions aro nd he ve ns hat rad a e ou om theventr c es.

© 2014 MedStudy

DE YEL NAT NG D EA E

The cu ent Mc onald cr ter a cons der more heav ythe MRI ndingsand have ess cons derat on of theCSF nd ngs han the prev o s (Posner) cri eria Thesenewer cr ter a pe m t acute les ons found o MRI to becons dered for the diagnos s hat s, use them o de nenew lesions dissemina ing over me and space:

• TimeT2 MRI show g anew hyper e se les on more

han30 days a er he in al eventorTl gadol ni m showinge hancementmore han3 mon hs a er the n a event

• Space (requires3 of he following) At leas TI gadol n um enhanc ng es on or9 2 hyper n ense les o sA leas l in aten or a lesionA eas j acort cal lesionAt east3 per ventr cu ar es ons

In add tion, cons der MRI of the cord, especially if

bra n imag ng doesn t reveal p aq es and the pa en spresentat on s ve y susp c ous for MS The d agnost ccr er a eq ate ce a n cord lesions to ce a n bra n

es ons MRI s a so esse tial oe o tcond tions hatcou d m m c MS Whi e matter d sease d e to schem a(e derly) and vasc l tis bo h have a very di eren patteof d stribu ion om tha seen w th MS.CSF ana ys s s pa t cu arly useful du ng acutee acerba ions.IgG mm oglobul nsto myel ncan befound n he cerebrosp nal id (When hese glob

ns are exam ned us ng electrophoresis, afew bandsappear hus the te mo goc ona bands.)90% of MSpa ien s have creased gG inde and o goc ona IgGbands n the CSF CSF prote n and ce l count s generallynorma n occasion, a small CSF ymphocytos s may bepresen , but shou d be no more than50 ce s/mm3Ev ked ct po en a s (visual, bra ns em audito y,and somatose sory evoked po en a s) can he p to es abl sh the d ag os s of MS by ident fy ng a cl nica lysi en 2 lesionSo, aga n, the workup for MS now inc udes aMRI,a l mbar p nctu e, and evoked po ent a s U timately,

he d agnos s s made us ng a comb a on of cl n cah sto y, phys ca exam,laborato y, and magingdata

mage l/ -8: ultip sc ro i J

1 -4



11 MOVEMENT D SORDER

Treatment of MS

There is no cure for MS. Treatment has now becomeve y spec al zed by ne rologists As a resu , genera

nte is s are expec ed to know tha he trea ment ofacute exacerba ons shigh-d s c ic s ids(as opposed o the myriad rea ment op ons for bo h

n ermitten and progress ve d sease). Gl cocor icoidsmay shor en he dura ion o exacerba ions bu do noalter the nat ral h sto y of MS. IV e hylpredniso one,I g/day for3 - 7 days, followed by a rap d predn soneaper, is o en o ered However, a recent(2012 sys

tema ic review (Cochrane Database) showed no diference in c inica , radio ogica , or pharmaco og caou comes when co paring ora vs IV steroids for MSrelapses. Parentera co costero ds are he trea men forop c neuri isOther drugs used to treat chronic MS are

u dul s (be a in erferons and onoc onaan ibod es), g a ira er ace ate (Copaxone®, a syn hetic

amino acid po ymer), and i p s ic d ugs.New d gs incl de ngol mod Be aware of heassoc a ion o progress ve m ifoca le koencepha opa

hy ([PML]; disc ssed nex ) wi h the dr gna a i umab,which is used o treat MS. For n er erons, on tor CBCand LFTS eve y6 on hs. In erferon causes -likesymptoms, fa g e, and depress onIn erferon and g atiramer red ce re apses by30%,wh lenatal zumab red ces relapses by- 60%. You wi l nobe expec ed to know de ai ed infor a ion abou hepharmacologica rea en o MS

PROGRESS VE MULT FOCALLEUKOENCEPHALOPATHY PML

ML (a ec swh te a ter only) s a progressivedemyel nat on seen in pa ents w th severe T ce i unode cienc es, espec al y IV/AIDS pat ents w th CD4co n s< 200 ce s/ 3 s caused by theJC vi sPML is also seen in patients rea ed w th chronic s eroidsor monoclona an ibodies.An exa p e of the monoc ona an bodies isnatal zu ab sed in the rea en of MS and odera eto-severe Crohn disease. Natalizu ab is an an bodyto the VLA 4 an gen expressed on ac iva ed T cellsand monocy es. Mos cases of ML o this ype haveocc rred wi h he co binat on of na al ab and other

m no odu ators.The c assic presentat on or ML s arap dcognitive

pa rmen assoc ated w th motor de c ts, aphasias,a axia, and visua eld de ects. (Man es a ions arevar able depend ng on what pa s of he bra n/cord area ected ) Dementia and foca co tica dys nction suchas he paresis, v sual de ci s, aphasia dysa hr a,and sensory mpa rment are pro inent The course

s s bac e and progressive, o en lead ng to death in3 6months.

Diagnose wi h brainbiopsy Find ng JC v rus by PCRin sp nal id is s ppor ve, altho gh sensi iv y of he

CR ana ysis decreases as he im une sys e is reconsti u ed on ART A T has improved mor a i y n pa ientsw th ML, bu many pa ients have pers sten neurologicde c s because the nerves are nab e o re yel na e.Antiv ral dr gs are ne ec ve.

CEN RAL PONT NE MYEL NOLYS SCen ra pon ne mye ino ysis (a k a. os oticdemye ination syndrome) occurs n pa ients wi h severehypona remia tha is correc ed oo q ckly wi h hyper

onic sa ne There s a progressively higher risk tha sd rec y corre ated wi h how ong he pa ient had beenhyponatre c before correc ion is s a ed, how low thesodiu concen ra ion was, and how rapid the n sion ofhype on c sa ine s.These pa ien s may presen wi h quadriparesis,

ut sm, pseudob bar palsy, chew ng and swa owing dys nct on, and/or ocked in syndrome. ara ys s

s nit al y accid, b spas c y develops wi h n a ewdays. See Hypona emia n Nephro ogy, Book2 for

ore discuss on.

MOVEMENT D SORDERS

PARK NSON SM[Know his opic we arkinsonism (secondaryParkinson's, ark nson syndrome) s a ne rolog calsyndrome w th he charac er stic set of 4 mo or fea ures

(the 4 s ).S gns and symp o s o parkinson s have4 majorcharac er s ics:

I) est ng tremor2 gid ty and exed pos ure3 e arded ovemen (bradyk nesia and hypok nesia)4) Loss o pos ura e exes

Res ng tre ors a a ra e o45 z (cyc es per second)occ r in the d sta ex rem ties. Tre or is s a y he15

symp om no iced. So e mes the tremor s present w thse, w h dra a c worsening a resa ien s wi h parkinsonism have di sencreased

m sc e one, which, combined w h he tre or, causeshe "cogwheeling seen wi h passive range of o ion

of the l bs The exed pos ure may nc ude he en rebody. The spine, elbows, hips, and knees ul ma e y maybecome exed. The classic hand posi on is exed MCP joints w th s raigh IP joints.Hypokines a/bradykines a s the prima y feature. Wi hhypok nesia, the pa ien has decreased a pl ude ovol n a y movemen s spec ally w th repe t ve tasks.This may manifest as micrograph a (progressive red ction in a p i ude o wr ng). Bradyk nesia s d c y

ni a ng move ent, slowness of ove ent, and

© 2014 MedStudy-Piease Repo t Copyr gh Infr ngemen s o copy gh @meds dy.com





•

U

What is the reatmen fo an acute exacerbat onofMS?

Wha disease s associa ed with he useof na al zumab?

What is he cause of cen ral pont nemye inolysis? What cl nical findings are seenin h s condi ion?

Wha are the 4 mo or featu es o parkinson sm?

Name some common drugs used to reatParkinson disease.

decrease or loss of spontaneous movement (maskedfacies, tendency to sit motion ess, decreased b inking)Loss of postura re exes contributes to the "festinatinggait and eventua y causes fa s and then the inabiity to stand or wa k without assistance Festinatinggait is when the patient walks progressively faster toremain under the fo ward center of gravity caused byt uncal exionThere are many causes of parkinsonism. Theserange from Parkinson disease to d ugs, toxins, metabo ic disease, infections, repeated head trauma, andcerebrovascular disease.The most common cause of parkinsonism is Parkinsondisease ([PD]; discussed next)

Many d ugs can cause secondary parkinsonism Theusual cu prits are:Dopamine-depleting d ugs (e.g , reserpine)Dopamine antagonists such as phenothiazines orbutyrophenonesAntiemetics such as metoclopramide

ug induced parkinsonism is ypically much moresymmetric than PDCommon toxins: carbon monoxide, manganese, andorganic so vents Repeated head trauma can alsocause parkinsonism (punch drunk syndrome). Parkinsonism a so occurs in some forms of Huntingtondisease (rigid form), frontotemporal dementia, andspinocerebellar ataxia

PARKINSON ISEASE

Diagnos sKnow! Parkinson disease ( D) is ac inicaldiagnosis

Diagnosis is especial y impor ant and o en missed in theear y stages.

© 201 M dStudy

VE ENT DI RD R

he core features of Parkinson disease are the tet ad o

I)hypo and bradykinesia,2 resting t emor,3 postura instabi i y, and4) rigidi

These are manifested as an expression ess face, pover yand slowness of vo unta y movement, resting tremor,stooped posture, axial instabili y, rigidity, and festinating gait or unknown reasons, symptoms always staon one side of the body and spread to the other side a era few yearsRule out causes of secondary Parkinson's. Rule outother neurodegenerative disorders such as pro essivesupranuc ear pa sy ( PS ; seepage 6 .The patho ogic ndings are loss of pigmented ce ls in thesubs antia nigra and other pigmented nuc ei (locus ce u

eus, raphe, and dorsal motor nucleus of the vagus). Many

of the remaining ce s con ain eosinophilic cy oplasmicinclusions, sur ounded by a faint ha o, ca ledLewybodiesThe motor features of Parkinson disease are caused bya dropout of dopamine producing cells in the substantia nigra of the midbrain In a norma ly nctioningbrain, the nigrostriata neurons produce dopamine Thisdopamine is released in the basal gang ia, where it has acomplex e ect on the motor system, faci itating volunta y movement When there is a decrease in dopamine

om deterioration of the substantia nigra, the motorsymptoms of P emerge 80% of patients with PD willeven ual y develop a dementia of the Lewy body type

TreatmentOverview

As with MS, treatment for P is ve y specializedFocus on diagnosis, major treatments, and sidee ects of treatment Staying active andexercising areimportant goa s that keep patients independent as ongas possib eDrugs that stimu atethe dopamine system are themainstay of therapy to treat symptoms:

Levodopa+ carbidopa with or without thecatecho -0 methy -transferase (COMT) inhibitorentacapone (Comtan®) or tolcapone (Tasmar®)Non ergot directdopamine receptor agonists:o Ropiniro e (Requipo Pramipexo e (Mirapex )o Rotigotine (Neupro® skin patch)

AmantadineAnticho inergicsMonoamine oxidase (MAO)-B inhibitors:

Selegi ineRasagiline

1 - 5



11- M VEM NT D S RD RS

Treatment of Mild PO

Anticholine gics such as amantadine, benztropine(Cogentin®), and trihexyphenidy a e sed to treat mi dsymptoms, especia y tremo .Anticholine gics can ca sealte ed mental stat s,inc ding psychosis, especia ly in patients>70 yea s o d

and in individ a s with cognitive impai mentTr cyclics, which have some anticho ine gic prope ties,may be conside ed in se ect patients fo initia the apy as ong as cognition is intact

Treatment of Mild-to-Moderate PO

Dopamine receptor agonists ( opinirole andp amipexo e) can be use as monotherapy formild-tomoderate PO,b t60% of patients will req ire adj nctiveL dopa a e4 yearsKnow that these dopa agonists, ropiniro e andpramipexo e, are associated with imp lse cont odisorders, s ch ashypersexuality omp lsive shoppin,andpathologi al ambling The MAO-B inhibitor sele i inedelays the need fo

dopa in patients with mild PO by app oximately9 months he e is now some evidence that asagi inemay a so slow decompensation in ea y Pa kinson disease o date, however, no treatment for PO has beenp oven to be "neu oprotective.Know that ombinin sel ilinewith t i y li sor SSR scan potential y ca se theserotonin syndrome. hisproblem is ca sed by excessive serotonergic activation of both CNS and per pheral eceptors. Signs andsymptoms inc de cognitive impai ment ranging omcon sions to hal cinations to coma; a tonomic e ectss ch as hype he mia, tachyca dia, shive ng, and sweating and somatic e ects s ch as hype re exia and c onus,

witching, and t emors Symptoms can be mi d to rapid yfata , depending on the amount of ove stim ation

Treatment of Severe PO

Mo seve symptoms a e commonly t eated withL-dopa + ca bidopa -dopa acts as a p ec so fodopamine synthesis in the basa gang ia. he carbidopab ocks conve sion of -dopa to dopamine in the periphery, a desirab e e ect beca sepe iphe aldopaminedoes not cross the blood brain ba e Additionally,periphera dopamine ca ses side e ects such as pos ralhypotension and nausea Ca bidopa does not he p withthe centra side e ects of L dopa that emerge a er seve al yea s Note that-dopa abso ption may be ed cedby dietary p oteinA tho gh dopa is the most e ective dr g fo PO, its

se iswithheld as longa possible, especially in yo ngepatients, to de ay the onset of comp ications that a ecommon with chronic use specia y dyskinesias andmotor uctuations

Di ect dopamine e epto a onists opini o e,p amipexole,and otigotine) and inhibito s(entacapone or tolcapone) are added to red ce the overall dai y dose of dopa, to even out the ser m leve sof this d ug, and to p ovide mo e contin o s dopamine

eceptor stim lationhe olde dopamine agonists (b omoc iptine

cabe goline, and per o ide) may have er ot elatedadverse e ects, inc uding a isk of valv a heart disease Cabe goline sho dnot be sed to reat patientswith Pa kinson's; it remains availab e for treatment ofp o actinomas.Neu a tiss e t ansp ants may res t in "r nawaydyskinesias and are c r entlynotrecommended for PDComp ications of PO therapy inc de the fo owing:

• End-of dose "wearing o ' e ects (due to sho tha f ife of-dopa)

• Unp edictable "on o ' uc ations that are

cha acte zed by np edic ab e loss ofdopa reatmente ect and dyskinesias(50% of patients a e3-5 yea s)• Psychiatric symptoms deve op in0%of patients

treated with dopa o dopamine receptor agonistshese symptoms inc ude agitation, conf sion, haucinations, and de sions de patients with cogni

tive impairment are especia y at risk. Approximate yI 7% of patients t eated with a dopamine a onistdeve op an imp se cont ol disorde

Know that patients who deve op psychosis with L dopatreatment sometimes require a red ction or a switch inthei meds to cont ol thei behavio hese patients a e

especiallys sceptib e to deve opment of ae oleptim li nant-like synd omewith the switch o dose ed ction This synd ome is sometimes termed "Parkinsonismhyperpyrexia and presents with hype the mia, delirium,m scu ar igidity, and a tonomic instabi i y "D ugho idays a e no longer used in Parkinson patients fothis same eason

PROGRESSIVE SUPRANUCLEAR PALSY

P og essive s p anuclea palsy (PSP) is simila toParkinson disease in that patients have bradykinesia,abnormal gait, inc eased m sc e tone, and later deve op

dementiaThe disease has its onset typically in the61hdecade(range 45- 5 yea s of age), with some combination ofdi culty in ba ance, ab upt fa s, visual and oc lar dist bances, s u ed speech, dysphagia, and changes inpe sonality. Ultimate y, the characteristic synd ome ofs pran c ea ophtha moplegia, pse dobulbar palsy, andaxia dystonia deve ops Patients typica y donot havea tremorWithin 2 yea s, these patients deve op the classicsymptom of ave al ophthamople ia, typica y withinitial impai ment of downga e, progressing to comp eteophthalmop e ia in a l directions S bseq ently, patients

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• What is a potential s de effect of anticholinerg cdrugs when used to treat Park nson's?

•

Ropinirole s associated w th what s de ef ects?• Seleg line can ca se serotonin syndrome when

combined with what ot er dr gs?• W at s t e cl n cal presentation of seroton n

syndrome?• What s a potent al compl cat on of an L-dopa

dose reduct on n a pat ent w th Parkinsonpsychosis?

• What s t e class c eye finding of progress vesup an clear palsy?

• What is t e cl n cal presentation of essent altremor? What mproves it?

What causes tardive dys nes a? How sTO treated?

have trouble reading, eating, and wa king down sta rs.There s a grad al sti ening and extens on of the neckWithin another2 -3 years, they may be nab e to wa kbeca se of marked mbalanceThe treatment is pa at ve, aimed to mprove the qua tyof li e These patients commonly d e of aspirat onpne mon a due to severe dysphag a

TREMORSverview

Based on when the tremor occ rs, t can be calledeither static or k netic:

Static tremors occur atrest, or when the head andextrem t es are held n a xed posit on (termedpostura tremor")

K net c tremors occur d r ng vo ntary movement.O these,action tremors persist unchanged throughout voluntary movement and genera y disappearat rest Intent ontremors occ r w th target d rected

movement and worsen as the movement un olds.Tremor syndromes o en include both static and kinetictremors; e g , the essent a tremor" nc des bothpostural and action tremors

xaggerate Phys ologic remorUsua y, normal patients have an unrecogni ab ephysio ogic tremor that has a freq ency of� 10 H .This norma tremor can be aggravated by anx ety,

right, hyper hyro dism, me abol c states such ashypoglycem a, drug w thdrawal states, and certaindr gs SSR s, cort costero ds, tricyc ics, theophyl ine,

© 2014 MedStudy

M VEMEN DIS R ERS

� agonists, nicot ne, and caf eine) Th s tremor can bepost ral or seen w thact on

ssential remorEssential tremor s the most common type onon phys o og c tremor and s o en fam a n famial cases, it seems to be transmitted as an autosomadominant tra t, w th variation in age at onset andsever ty t affects the hands as apost raland act ontremor w th a frequency of4- 8 H z It also can bea h gher requency and a ect the head and chin as a

yes, yes" or no, no" post ral tremor There may be anassoc ated voca tremor ssent a tremor is typ ca ybenign b t somet mes res ts in unctiona d sabilityNote that a post ral tremor of the head is very un ikelyto be d e to Parkinson's and is more o en essentiatremor Parkinson tremors that a ect the face usual yinvolve the ips or jaw onlyThe freq ency of essential tremor s typ ca lydecreased trans ent y by dr nk ng alcoho , and yo cano en d agnose an essential tremor when pat ents telyou that the r tremor mproves a er an a cohol c drinkPropranoo andpr m doneare e ect ve n red c ng the

imb tremorsGabapent n and topiramate reduce limb tremors a littlea so, b t both have many s de e ects In severe cases,botu in m tox n and deep bra n st mulation surgerycan be tried

TARDIVE DYSK NES A

Tardive dysk nes a T ) is mostly a resu t of long termant psychot c dr g use The on y way to be certa n toavoid s to keep patients o chronic antpsychotics,b t this cannot be accomplished in many patients w thchronic psychos s.Some atypical ant psychot cs(2"dgeneration drugs),par c lar y c o apine and quetiap ne marate Serq e!®), areless ke yto ca se T Clo ap ne can causebone marrow tox ci yTard ve dysk nesia cons sts o many invol ntarymovements ncl d ng dystonia, chorea, athetosis, and

remor The face, tongue, l ps, eyel d, and b lbar m s

cles are most o en invo ved, but neck, shoulder, andsp ne musc es with arch ng of the back may a so be seenC ona epam s a se ben od a ep ne for pat ents w thm d tard ve dysk nesias and anx ety xtract o g nkgobiloba has also recently been shown to be e ective orred cing tardive dyskines a n pat ents with sch ophren a Some pat ents may bene t from the presynapt cdopam ne dep et ng dr g, reserpine; however, s dee ects o th s dr g may inc de depression, orthostatichypotens on, and park nson sm Severe T cases canbe treated with bot l num toxin Deep brain stim at onsurgery can be used n the most severe cases that requirecont nued use of ant psychotic drugs.

1 47



MOVEMENT DISORD RS

O ER OVE OR ERNeuroleptic Mal gnant Syndrome Neuroleptic ma gnant synd ome is an n s alresponse to ant psychotics (both " ypica and "a ypcal ant psychotics), esu t ng in hypertherm a, gid y,diapho esis, autonomic instab ty, and a tered men astat s w th a sk of rhabdomyo ysis-induced enal fail

re. Occas onal y, other dr gs, s ch as metoclopram deand p omethaz ne can a so have the same e ect. Labso en show eukocy os s e ectroly e disturbances, andelevated CK evelsTh s syndrome may occur days, weeks o months a erneu o eptic treatment is begun t ca ries a mo a y

ate of 5- 30% if not recognized and t eated promptly[Know:] Pat ents w thPark nson'swho acutelyd scontinue the dopa the apy (or red ce dose) can deve opthis syndromeTreatment of ne roleptic ma ignant synd ome cons stsof immediate discontinuat on of any o ending drug;use of a directdopam ne agonistsuch as b omoc iptine, amantadine, o dant o ene; and s ppo t ve the apy,

ncluding adeq ate hydrat on and scrupu o s pulmonaryto let. If r gid y s su cient to a ect venti at on, thepatient shou d be sedated and pa alyzed. Patients who

equ e neu o ept cs may have ec r ence of ne olept cma gnant syndrome f the dr gs are restar ed

Hemifac a SpasmHem fac a spasm is a motor ana og to trigem nane ra gia (t c do oure x).80% of pat ents have a tor

uo s d lated bas lar a tery (basi ar do ichoectas a) thatoops around and i ritates the facial nerve! Other causesnclude aneurysm, aco st c ne roma, and, rarely, MS.

Botul n m tox n (Botox®) inject ons are customari ythe best treatment Some pat ents have bene ted fromsurge y to separate the facia ne ve f om direct contactw th the bas ar a tery (mic os rgica decompression).Occasionally, carbama ep ne, bac ofen, and gabapent nmay be e ective.

G lles de Ia Tourette SyndromeGi es de a Tou ette syndrome s a deve opmentaneu opsych atr c disorde cha acte i ed by ch onic

> 1 year d rat on) m ple moto tics and1 o mo evocal t cs. Moto tics may be s mp e nc ud ng eyeblink ng or oll ng, fac al gr macing and head or limb

jerking o comp ex, incl ding sem p rpose l movements s ch as tapping, mp ng and copying thegestu es of othe s (echop ax a) Vocal tics may a so bes mpe such as sn ng, sno ting, gr nt ng, and coughing, orcomplex nc uding tte ance of wo ds o phrases,obscen t es (cop o al a), o im tat ng the speech of others(echolal a) Onset s commonly be ween2 and 5yearsof age Many pat ents have comorb d attent on de cthype act v y d sorder (ADHD), obsess ve comp sived so der, lea ng disorders, o conduct disordersDiagnosis is c nica and req ires con rmat on of bothmotor and vocal t cs by a sk l ed obser erClon dine s ecommended as 51 l ne t eatment. If thetics are seve e eno gh to nterfere w th da ly nct oning, yp ca neu o eptics (e.g., uphenazine, pimo dehalope idol) a yp ca neuroleptics (e.g., isper done

ip as done, olanzap ne), or the part al dopam ne agonist arip prazole may be used. CNS side e ects s ch asmood ness and dep ess on are more common with the

yp ca ne oleptics wh le the newer atyp cal d ugsca se mo e we ght gain and metabol c synd omeM der t cs and/or associated ADHD may respondto clonid ne or g anfacine Mo e seve e ADHD canbe treated with stimu ants such as methy phenidate;newer data show that these d gs may not exace bate

tics as p ev ous y tho ght altho gh close mon to ingis necessa y Foca t cs have been treated withbot in m tox n

Focal Dyston asFocal o segmenta dystonias are inte mittent, b ief,o prolonged spasms o cont act ons of a gro p ofadjacent m scles that place the body pa n a forced and

nna ral pos tion

Table -8 : C A U B(A x)

Age Disease Etiology Cl n ca Cours Exam OutcomeO der Anter or ischem c < 60: atheroscleros s Nonprogress ve Opt c d sk From normal to(>50) opt c neuropathy > 60: g ant cell arter t s nfarct on complete �l ndness

Centra retina Vascu ar disease or N onprogressi e Hemorr ag c Usua y somevein occlusion venous t rombosis retinopat y v sual impairment

Central ret na Em ol c or throm ot c Nonprogressive Cher y red spot Only- 25% mainartery occ usion tain use l vision

Younger Optic neuritis Multip e sc erosis Progressive Marcus Gu pup l; 90% reco er(< 40) hours to days) optic disc pal or comp ete y

M graine Neurovascular Resolves rapid y Norma Normal ision

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What is t e c in cal presentation of neuro epticmal gnant syndrome?

•

W at como bid t es are associated w thTou ette synd ome?

W at antihypertens ve d ug is used to t eat t csin G l es de Ia Tourette synd ome?

What are causes of acute unilatera bl ndness(a.k.a. amauros s ugax) n olde pat ents?

W at do f ashes fol owed by dec easedv sion suggest?

What 4 symptoms a e associatedwith narco epsy?

3 focal dystonias are commonly asked about

I) B epharospasm is bi a eral force l invo u ary eyec osure a d may occur as a isolated sy drome or aspar of Meige syndrome

2) e ge syndrome s a comb a o of b epharospasma d oromand bu ar dyston a ( vo untary jaw open nga d jaw moveme ts).

3 Spasmod c o t col is occurs whe spasms of neck a dshoulder musc es tu he head o o e s de.

A few ora d ugs may o er m ld rel e be zod a epi esbac ofen a t choli ergics, a d sometimes a dopam

erg cs Howeverbotul um ox ns ow he reatmeof choice provid ng much more reliab e bu temporaryre ief when injected d rec ly in o the a ected muscles. trequ res repeat njections q -5 mo hs

MI CELLANEOU DI ORDER

ACUT O T U ATERAL B INDNE[Know a of he fol ow g ] SeeT a ble 1 - 8 for asumma y.

In older pa ents acu e o se ofunila eral bli d ess(a k a. amauros s fuga ) is usually due to a y of hefol owing:

Anter or ischem c op c europa hy (AI ON) whichmay be:

o A teritic (secondary to g a ce ar eri s)o Non-ar er c ( ess severe outcome)

Ret nal vei occ us on (secondary o d abetic ret navascular d sease)Re i al ar er occ us o (from hrombus or embolifrom he caro d a ery or heart)

In he you ger patie h nk optic neuri is butsomet mes can be from m graine. Migra ne induced

© 2014 M dStudy

MISCEL ANEOUS D SOR RS

bli d ess ypical y resolves rap dly whereas b dnessdue o a y of he other me oned causes s prolongedor permanent

schemic op c europathy op c neurit s and papiledema a ca prese wi hswolle d scs wi h ndalsp er hemorrhages. Remember: emporal (g a cell)

ar eri s a so causes d p op a and jaw c aud catio ." al nger ng as a cause of bl nd ess (mo o b ) ca be

u ed ou w th evoked action pote a s.

D PLOP A

Weak or para y ed eye muscles cause "ophtha mop eg aand manifest as d p op a. can be a resu t of d sease i

he muscle i self n the ne ve ha s mulates the muscleor i he euromuscular unctio (myasthe a gravis).

A rem nder of diseases ha may prese t w th d plop awe have covered most of hese separate y)

3rcand 61"cra al e ve palsiesMyas he ia gravisGraves d seaseWe cke e cephalopa hy

er F sher variant ofGBSBo ul smTick paralysis

nfec o s/Masses that a ec he cave ous s nus

If you see d plopia wi h pain:

hink d sease n he eyeball if pain is loca edi he eye.

h myopathy or orbi a processes f pa isprese w h moveme tof he eye uenza isa c assic cause of orbi a myopa hy.

Op ic neur tis may also cause pai o eye movemenbut i does ot cause dip op a!

V UA F D D F CTScotomas

Scotomas are a erations an iso a ed area of hevisual e d w h loss or dim ess of v s o Do a comple e oph halmolog c e am on a y pa en w th anytype of sco oma.Acephal c m gra e (m gra ne w hou headache) cacause "forti ca o scotomas hat co s a tly cha ge

s e a d may be bi ateral.

Moore's l gh n g streaks occur o der patie s uponenter ng a darkened area hey are caused by thevitreous pull g o the re ina; they are ben gn

Retinal detachme causes ashes fol owed bydecreased vision (from blood) or i creased oa ers.

h s is an oph halmolog cal emergency

49



11- FOR FURTHER READING

Bitemporal Hemianops aBitemporal hemianopsia is the te m for blindness in thela e a half o bo h visual e ds. It has several causes:

• Pi uitary adenomas (This is he one we allremembe )

• Craniopharyngioma• Meningioma• Aneurysm of the circle o Wi lis• Sarcoidosis (rare)

Me as atic ca cinoma ( a e)

COMPLEX REG ONAL PA N SYNDROMEThis syndrome causes ex reme enderness, pain,swelling, dysesthesias, and vasomoto instability in anextremi y a e a traumatic inju y.

NARCOLEPSYNarco epsy is caused by a selec ive loss ofhypoc e inin he hypo halamus the etiology of which is cu ren lyunknown More than 85% of Caucasian and Japanesepatients wi h na co epsy-catap exy syndrome have aspeci c HLA hap otype that includes H A DR1501( orme y ca led R 5 or DR2) and LADQB 0602( ormer y DQI or DQ6)

arcolepsy e rad

I) a colepsy2) Catap exy( /4 o pa ien s! With excitement, imbs

become accid, often resul ing in al s )

3 Hypnagogic ha lucinations (occu ring as pa iental s as eep)

4 S eep pa a ysis (on waking)

arcolepsy is eated wi h moda ni or armoda nil(non amphe amine drugs) stimu ants such as methyphenida e o methamphetamine (many side e ects andaddictive po ential) or sodium oxybate, especia y inmore severe cases with associated cataplexy Ca ap exymay a so be treated wi h icyc ics (e g , imip aminec omipramine, o pro riptyline) o the se ective se otonin

eup a e inhibitors (e g venla axine or uoxetine).

FOR FURT ER R NG

[Gu d inesin b ue]

COMBarlow P A pract cal eview of the Glasgow Coma Sca e andScore. Surgeon 2012 Apr; 0 2): 114 119.

Bruno MA, Van auden uyse A, e al From nresponsive wakeness to minimal y conscious PLUS and func onal locked-in

synd omes recen advances in o r unders anding o diso ders ofconscio sness J Neural 20 J l;258 7 :373 384

De Salvo S, Braman i P, e al Cl nica di eren ia ion andou come evalua ion in vege a ive and m n ma y consciouss a e pa ients he ne rophysiological approachFunct Neur l2012 u -Sep;27 3) 55 162

Hocker S, Rab ns e n AA Managemen o e pa ien wid minis ed respons venessNeur l C in.2012 Feb;30 1 : 9, vii

H S S evens RD e al. Emergency neuro ogica lifesuppor app oach to he pa ien wi comaNeurocri C re2012 Sep; 17 Supp :S54 59.

a es A o oz W, Serra Mes res Ca a onia n e emergencydepa men Eme MedJ 2012 Nov;29 11 863 867

Ko c oubey B, Lo e M Ins rumen al met ods in ed agnostics of oc ed in syndromeRestor Neural Neu sci20 3;31(I):25 40

Wijd ck EF, Var la P , t a Am i n A ad fN ol gy Evid n - d g id i upda : d t n ngb n dea h n du s r p t f Q t S nd dsSub mi o h m acad my u o g

Nturl g ' 20 Ju 7 (2 : 1 X

CO D T O S H M M C COMBoo CM Boone R , e al s t is pa en dead, vegeta ive, orseverely impaired? A 2004 291 :870 8 9

D CDe Luca GC Bartleson JD e al W en and how o nves iga e epa ien wi headacheSemin Neu l 20 0 Apr;30 2 : 13 44

vans RW. Diagnos c esting for migra ne and o her primaryeadac es Neur l Clin 2009 May;27 2 :393 15

e nde -de- as-Pe as C, Sc oenen J, e al Chronic ensionype headac e w a is newCurr Opin Neural

2009 J n;22 3 254 261

Galgano MA, Des aies M An upda e on e managemen ofpseu o umo ce e riClin Neu l Neu u20 3 Mar; 115 3):252 259.

G een MW Seconda y eadac esCon inuum (Minne p Minn) 2012 A g; 18 4):783 795

Na as S Headache and tempora ar eri is: when o s spectand ow o manageCurr P in He d che Rep2012 Aug; 6 4 :371 378

Nesb AD, Goadsby P.Cl s er headac e .2012 Apr 11;344 e2407

Will ams A. A concise discussion of headac e ypes ParIn! J Ph rm Compd 20 2 Mar Apr; 6 2): 125 132.

Williams LA A concise discussion of headache ypes, a t 2Migraine n/ Ph rm Compd 2012 May un; 16 3 182 188

Will ams A, Al en r A conc se d sc ssion of headac etypes, Par 3 M graine.n/J Ph rm Compd.2012 u Aug; 16 4 270 274

A i an ad m of g H ada u dl n . [On i http //www a G d n ho B T p ') pi d = 16

© 4MedStudy - Piease Repo t Co yr gh nfr geme toco yr gh @med dy.com

https://www.aan.com/Guidelines/home/



















Headache Classi ca ion Committee of he ln e ational Headache Soci ty (IHS) Th nte ational Classi cation of HeadacheDisorders 3d edit on (b a ersion)Cephalg ia 2013. http: /

ihs c lass cation.o g _ do n loads/mix d lnt a ona-H adach -C ass fca ion 1 CHD 20 13 Beta pdf

Holland S S lbe stein SD c al idence based gu del neupda e: NSAIDs and othe complemen ary t eatments for

episodic migraine p e ention in adults: epo t of the QualityStandards Subcomm ttee of h Am ican Academy ofNeurology and the Am can Headach Soci ty.Neu o o y.20 2 Apr 24 78( 17):346 1353

National Institut fo Health and Care Excellence Guidel ne:Diagnosis and managem n of headaches in young people andadults 202.http //ww . guid l n go cont nt.asp id 38444

Saper JR ake A et al. A pract ce gu de fo continuousopio d he apy for efrac o y daily headach :patient selection,phys cian eq i ements and ea men moni o ngHeadache20 I 0 ul 50(7 : 175- 93.

S lberstein SD Holland S e al.E idence based g idelinepdate: pharmacologic trea men episodic migra ne

pre ention in ad lts: repor of the Qualit StandardsSubcommitt e of the American Academy of N ur logy and theAmerican Headach Soc ety. eur lo 2012 Apr 24;78(17): 1337- 345. Erratum in: Veu ol .2013 Feb 26;80(9):871

DE ENT A

Boeve BF. Progress ve supran clear palsy.Pa kinsonism Relat Diso d 2012 Jan; 8 Suppl I :S 92- 194.

Ha AD, ng VS. Hun ngton s diseaseCu Opin e l2012 Aug;25(4 ):491-498

Jankovic J, Poe e W. Therap es n Parkinson s diseaseC Opin e l20 2 Aug;25(4) 433 447

K ssing L D pression and th risk for d m nt a.C Opin P hi t 20 2 Nov;25(6):457 461

Korczyn AD, Vakhapova V, t al. Vascular dementia.J e l S i2012 ov 5;322( 2):2 0

Mind E change Work ng Group Assessment diagnosisand t ea men of HIV associated neu ocognit ve disord r: aconsensus r por o the m nd e chang programClin Infe t Di 20 3 Apr;56 7)1004 1017.

Ra i MS. Update on Alzheime s Disease herapeutics.Rev Re ent Clin T ial 20 3 Jun;8(2) I I0- 1 8

Roohan P, Saha MK et al. Cr tzfeldt akob dis as n the

hospital sett ng: a cas eport and review.Minn Med2013 May;96(5):46 9.

Albe MSD Kosky ST e al. The diagnosis of m ldcogni ivimpa ment due o Alzhe me 's d s ase Recommendat ons

rom the National Instit te on Aging and Alzh me sAssociation \ rkgro pAlzheime m n ia.20 I.http: //www.al org documents c tom /Diagnos t c _ Recommendations MC due to Alz_proo pdf

Ame can Academy of eu ology Dement a Gu del nes[On ine]h tps / \ w aan.c m / uidelines home / ByTop c topicld= 15

Ame can Psychological A sociation. Guidelin s thevaluat on of dementia and age related cogniti e change.

m � hl. 201 Jan 67( I) 9

© 2014 Me Stu y

FOR FUR H R R G

Arms rong MJ Miyasak JM Ev dence based g idelinpharmacolog c t eatment of chor a in Hunting on disease:report of the g ideline developm nt subcommittee of theAmerican Academy of Neu ology eu l 20 2 Aug 7 79(6):597-603

Galvin J Sadowsky CH NI CDSADRDA. P acticalguidelines or he recogn tion and diagnosis of dementia.

J m B a d Fam ed 2012 May Jun;25(3) 367- 382.Jack CR Alber MS e al. Int oduction o th

ecommendat ons from the National nstitut on Aging and theAl h imer s Association o kgroup on d agnostic guidelinesfor Alzheimer s dis ase heime : Dementia 2011.http:1 / .alz.org/documents _custo ! nt o _Diagnostic_ Recomm ndations_A z proo pdf

McKhann GM Knopman DS, t al The diagnos s of dem n adue to Alzhe mer s d sease: Recommendations from theNa ional Inst tute on Aging and theAlzh imer' s Association

o kgro p, l heime Dementia20 l http / ww alz.org documents_custom Diagnost c R commendations _ Alz proof pd

Montine J, Ph lps CH al ational nstitute onAging; Alzh im r's Association. Nat onal Inst tu eon Aging A zhe mer s Association gu del n s fo then uropathologic assessmen of Alzheim r s disease: a prac icalapproach. ta eur path l 2012 Jan; 123( ) I-ll .

Qaseem A Snow V et al C ·ent pharmacolog c treatm ntof demen ia: a clinical practice g ideline f om he AmericanCollege of Physicians and he Ame ican Academy of amilyPhysicians nn Inte n ed 2008 Ma 4 148(5):370 378

Sado sky CH, Gal in Guidelines for the management ofcogn ti e andb ha ioral p oblems in dement aJ m Boa d Fam Me 2012 May Jun;25(3):350 366.

Sp rling RA, Ais n PS et al To ard de ning the p eclinicalstages of Alzhe mer s disease: R commendations om theNational nstit te on Aging and he Alzheime 's Associat on

orkgroup l heime s & Dementia20 l l.http / / w .alz org docum nts custom /Diagnostic _ Recommendat ons _ A z _ P eclinical.pdf

Zesiewicz TA Sulli an K e al. Pract ce Paramet treatmentof nonmoto symptoms of Park nsond s as : report of thQual y Standa ds S bcommittee of the Am rican Academy of

eu ology eu l 20 0 Mar 6;74( 1):924-93

DIZ NE

Kim HA, Lee H. R cent advanc s in c n ral acute vestib larsyndrome of a vascular caus J eu l S i2012 Oct 15;321(1 2) 7 22.

angguth B Elgoyhen AB. Current pharmacological tr atments fo tinnitus Expe t Opin Pha ma the1012 Dec;13 17):2495 2509

Syed I, Aldren C M ni re s dis ase: an evidence basedapproach o ass ssment and manag mentIn! J Clin P a t2012 Feb;66(2) 66-170.

usa RJ Gore R Dizziness and ver igo m rgenci s andmanagem nt. eur l Clin 20 2 eb;30 I ):61 74, vii v ii

Bhattacharyya , Ba gh K t al Ame ican Academy oOtola ngology Head and Neck Surge y oundation. Clinicalpractice guideline: benignpar xysmal positional er goOto/0 ngol ead e k Su g 2008 Nov; 39(5 Suppl 4):S47 8

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11-2 FOR FURTHER READING

SE ZURES

Berg A , Be kovic SF, et a Revised te mino ogy and concep sfor organiza ion of seiz res and epilepsies repor of he ILAECommission on Class cation and e mino ogy 2005-2009.Epi eps a20 0 Apr; 1 (4):676 68 .

p lepsy Fo nda ion.h p //ww .epilepsyfo nda ion org/

Kor CM, Sche e p lepsy classi ca ion a cyc e ofevol on and evol t onCurr Op n l2013 Apr 26(2):163-167

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p rt f h Th rap u i and T hnolog As m ntub mmi t and Qu l ty S ndardsubcommi eeo th

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r nch . A Kann r AM al E cac nd tol rab li f hn n pilep i drug :tr a m nt o r ra ry ep l psr po t f th h r p utics and T chnologyA s m tS b omm t andQu lity ndards b ommi o hAm ri anA d my ofN urology and th Am ri a Epi py

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Hard n C pp1, e l Pr c param r upd em n g ment s ue r om n ithepil p y focuson pr gnan y ( n d n ba d r \ obs r c lc mpl a ons and h ng inizu equ ncy r p r o

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re ie , : r p " h herap utic nd Techn logyAss m Sub ommi e of h Amer c n Academ oNe ur logVe r lo 2007 Oc 30 6 ( 1 1 77 2 1780

H rd n C M ad r K. al Pr c ic p ram t r updatm nagem n is u s l r om n ,i h.:pil psy-- cu on pr gnanc

n vid n ba d re ew ter og n sis and p rinat lut om rep t .th Quality S ndards ub mmi ee and Th r p u cs

nd hnol gy As e m n Subc mmi f h Ameri ncad m urol y and Am r can Epilep y o i y u _ 00 . ul1 73 2 - 1 1

Hard n C . P nn l PB l Pr c ic p r m r updam nag m n is ue r men ,· th pil p y f u on pr gn n y an ev d ncb s d re ie \· : it m n K l c id. bl dl ls and br st ding repor thQu li y S andards

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Krumholz A W ebeS, e P ct P r m ter: lu t ng anppar nt nprov k d r te z re n dult an d n e b s d

rcv \) r port o h Quality ndard Subcommi f thAm ric n Academy oN ur l gy and th Amer E p l psSoc ,\ l 007 o 20 69 21 :1 200

N ECT ON

Cen ner C Bateman et al. Manifes a ions of H Vin ec ion in he peripheral ne vous sys em.Lance/ New·o2013 Ma 2(3 :295 309

Del B o OH Ne rocys icercosisCont nu m( inneapM inn) 20 2 Dec 18(6 nfec ious Disease):392-1416.

Jackson A, van der ors C. New insigh s in he p even ion,diagnosis, and rea men of cryp ococca meningi is.C rr H VIA DS Rep2012 Sep 9(3)267- 2

Miha C ubelt B. nfec io s mye i is.Curr N r l Neuros iRep 2012 Dec; 12(6) 633-641.

ind xchange Wor ing Group Assessment, diagnos s,and ea men of H Y associa ed neurocognitive disordera consens s epor of he mind exchange p ogramC in nfe D s.2013 Apr 56( 1004 01

Rober GangneuxF, a M Epidemio ogy of anddiagnos ic s ra egies fo oxoplasmosisC n M robi Re2012 Apr;25(2 264 296 Rev ew. E atum nCl n Mi robiR v 20 2 u 25(3) 583

Spudich SS, Ances BM Neurologic compl ca ons of H Vinfec ion Top n i ir Med2012 un ul 20(2 :417.

Tan McArth r C H V associa ed ne o og ca disordersa g ide o pharmaco herapy.CNS rugs 2012 Feb 26(2123 134

Tan L, Smi h BR e a H Y associa ed oppor n s icinfec ons of the CNS.an e N ur 2012 l 1 (7) 605 617

P r 'c RDi muke WE t l Clinic l pr i e guid liner h m nagem ryp o ccal dis a 00 upd te b

h lnl ious Dis a S i Am r ca.inln i 20 0 b 1 0 3) 2 1 322

Tu k lAR G l rCA et l Th managemen o nc ph l tclinical practi e gu d li sby he ln 'ct us Dise s o

fAm r c lin 1 c t i 2008 Aug I 4 3 30 32

Tun l AR Ha m nB , t l Pr ct c gu delines f r thman g m nt f bact r alm gi . lin f t i

2004 Nov ;39(9 : 267 1284

S ROKE

Bar sch T Bu ler C T ansien amnesic syndromes.Nat Rev Ne r 2013 Feb 9(2) 86 97.

Miche S, Co eaF. Lac na versus non acunar synd omesFro Ne N ro c2012 30 94 98

Na onal ns u es of Hea h S o e Scale. [Online] h p //www.ninds nih gov/doc ors/ H_S rokeScale.pdf

© 2014 MedStudy-Piease Repo t Copyr gh Infr geme s to copyr gh @meds dy. om



















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u gery and Anesth s a Council onCardio ascular Radiologand Intervention Council onCa d o\'ascular Nur ing andth l terdiscipli a C uncil on Periphe al Vascula DiseaseThe American Academy of eu logya n sth v alue fthis statement as an educational tool r n ur gistsS ok .

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Schellinger PD B an RN et al E idence b sed guidelineThe r le f di usion and pe fus on MR r the diagno iof ac te ischemic str ke ep o the Th r peutic ndTech o og Assessme tSubc mmittee of the Americ nAcadem of eurol g N u l gy 010 Jul 13 75 )177 185 E um in. lo y 0 0 Sep 7 75( 10):9 8.

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Kop lm n MD Thomson AD t l Th Kor o ynd m :lini l p t psy ology, nd t tm ntAlc h l

200 M r Apr; 2 : 1 8-1 .

Lough ME. W i ' n ph l p thy: xp nding hdi gno ti toolb xNeur sych l Rev 20 2 Jun;22 2 81 -

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20 2 F b 2 37 817 :721 - 28S hiG S r A t l W n ph lop thy n

lini tt ng nd r nt d n in d gno ndm n g m ntLa cet New· / 2007 M y 6 2- .

Thom on Gu ini, t Th olution nd r m n Kor o ' yndrom : out o ight out o m nd

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Am to , G nn iL t l hor i pin l t nos ndmy op thy: r por o t o r r nd r i o thl t r tur .J Neur urg Sci 20 2 D 6 373-378.

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1 - FOR FURTHER READ NG

G eco A, Ga o A et a Be 's pa sy and auto mmun ty.Aut immun Re 2012 Dec 12(2):323-328

Knopp M Rajabal y YA Common and ess commonpe phe a ne e d so ders assoc a ed w h d abetesCurr Diabe es Rev. 2012 May;8(3) 229 236

cA th JC. Ne opath es.C ntinuum ( nneap M nn20 2 Feb 8(1) 06 25.

Pop ncha k SP Scha e AA Phys cal exam nation o pperext em ty comp essive ne opath esOrth p Clin N rth Am20 2 Oct 43(4):417 430

Schwend mann RN Metabo c n t t ona and o cmyelopath es.Neur l Clin 2013 eb 31(I ):207 218

Sm th GA (ed) Ne ropath esNe rom sc ar The apy f omBench to Beds de.Semin Neur / 2012 J 32(3) 1 1 2.

Wa ng AD D c son G G a n Ba synd omeAm Fam Physician 20 3 Feb 8 (3 : 9 -197

Ame can Academy of Ne ro ogy P act ce G de nesNe om sc ar [On! ne]h ps // .aan com /Guide ines/

Home / By op c? op c d= 9B V, Eng and J et a E dence based g del ne eatmentof pa n l d abe cneu opa hy epo o he Ame canAcademy o Ne ology he Ame can Assoc a on oNe om sc a and E ect od agnost c Med c ne and theAmer can Academy o Phys cal Med c ne and R hab l tat onN u lo 2011 May 17 76( 0)1 58 1 65. Errat m n

ur lo . 20 A g 9 6 603

Cho R Qaseem A et a . ACP Ame can Pa n Soc etyG de ne D agnos s and t eatment o o bac pa n. I teMe 2007 h p / w anna s.o g cgi/reprin /14 7/478 pd

Cho R Qaseem A et a . ACP G de ne D agnost c mag ngor lo back pa n Ad ce for h gh a e hea th ca e rom he

Ame can Co ege o Phys c ans.A te Me20 .h p // w .annals org/ content 5 / 3 18l l.pd +h m

Eng and JD G onse h GS et a . Pract ce Pa ame e e al at ono d sta symme c po yne opathy ole o a tonom c

est ngne ve b opsy and sk n b opsy (an e dence basedre e Repor o he Ame can Academy of Ne ro ogyAmer can Assoc a on o Ne om sc a and E ect od agnos c

ed c ne and Amer can Academy of Phys ca Med c ne andRehab tat on. e ol ogy 2009 Jan 13 72(2 177 84

England JD Gronseth GS e al P act ce Paramete e a a ono d s a symmet c po yne opa hy r e o abo a o y andgene c tes ng ane idence based re e . Repo t o heAme can Academy o Ne ology Ame can Assoc at on o

Ne om sc lar and E e trod agnost c Med c ne, and Ame canAcademy o Phys ca Med c ne and Rehab ta onNeur logv

2009 Jan 13 2(2 185 192

H ghes W d cks E et a . P ac ce pa ametemm no he apy for G la nBa syndrom epo t o he

Q al ty Standa ds S bcomm tee o he Ame can Academy oNeuro ogy r log 2003 Sep 3 61 (6 736 740.

M e RG Jackson CE et a . P ac ce pa amete pda e thecare of he pat ent w thamyo ophic a eral scle os s d gn r ona and esp rato y he ap es ane idence-based

e ie : repo o he Q a yStandards S bcomm ttee othe Ame can Academy o Ne o ogy. lo 2009 Oc

3 3 51218 226 Erra m n r l 2009 Dec

15 3 24 2134.N log ' 0 0 Ma 2 4(9 781.

M lle RG Jackson CE, e a . P act ce paramete pdatethe ca e o he pat en w thamyot ophic ate a sc e os sm t d sc p na y ca e symptom management and cogn·e /beha o al mpa en (ane idence based re ew epor o thQ al yStanda ds S bcomm t ee o theAme anAcademy oNe ology Neur logy. 2009 Oc 3 73 5 22 33

Sco ohman EM et aEvidence based g de ne

c n cal e a a on and treatment o t ans e se mye s epoo he herape t cs andTechn ology Assessment S bcomm eeof he Ame canAcademy o Ne o ogy ur log201 Dec 3 7 (24 2128 2134

Wa te s WC 3rd Ba sden J, et a . No h Ame canSp ne Soc e y. Degene at e l mbar sp na stenos s ane idence based clinical g de ne o the d agnos s andt a men o degene a e l mbar sp na stenos sS e2008 Ma - Apr 8 2 305 3 0

M SC L J C

Madd son P eatment n Lambe t aton myas hen csynd ome A n NY A ad S i2012 Dec 12 5: 8-84.

S vest NJ Wol e G . Myasthen a g av s.Semin Neu l2012 J 32(3):215-226

aph ades MS Bhatt M e a Oc la myasthen a g av s.Curr Opin Ophthalm l 20 2 Nov 23(6):537-542

Benata M Kam nsk HJ et al E dence rep he med cat ea men o oc a myasthen a an e dence based e e

epo t o he Q a y S anda ds S bcomm tee o the Ame canAcademy o Ne o ogy.N r logv 200 J n 2 68(242 44 2149.

MY P S

ste C Reed AM Id opath c n ammato y myopath esc ent ends n pathogene s, c n ca eat es and p to datet eatme t ecommendat ons a Clin Pr2013 Jan 88(I):83 05

Johnson NE Heatwo e CR. yoton c dyst ophy om benchto beds de.Semin Neur l 2012 J 32(3) 246 254

Pfe e G Ch nne y P D agnos s and ea ment om ochond a myopath esAnn e 2013 Feb 45(I 4-16.

B sh by K F nde R et al DMD Care Cons dera ons Wor ngG o p D agnos s and management o D chenne m sc ardys ophy part :d agnos s and pha maco og ca andpsychosoc a managemen L e eur l 20 0 Jan 9( 7 93

Bush y K F nde R e a . DMD Ca e Cons de a ons Wo k ngG o p D agnos s and managemen o D chenne m sc ladys rophy par 2 mp ementat on o m t d sc pl na y care

a r l 20 0 eb 9 2 1 89. E at m nLanc /New- f 20 0 Ma 9(3 23

MY L S S S

Aksam t AJ . P og essive m ti oca e koencep a opathyC ntinuum ( nneap M nn). 2012 Dec18 (6 nfec io sD sease 1374- 39 .

Coch ane S mma es On nehttp://s mmar es coch ane o g/CD006921 /a compa son o the e cacy o ora ve s s nt aveno s ste o ds n e aps ng em tt ng m t p e scle os sms

Zaj cek J. M t ple scle o sHandb k Clin Ne l20 3 110 461 470

© 2014 ed udy- tease epor opyrigh nfr gemen s ocopyrigh @meds dy com

https://www.aan.com/Guidelines/








http://www.annals.org/cgi/reprint/147/7/478.pdf










http://www.annals.org/content/T







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http://summaries.cochrane.org/






Ame c n Ac d myf eu ology P ctice G idelin s.Mu pl Sclerosis [On ne] https // .aan com G idelin s /

om / By op c? topic d= 1 8

Bo ter A, Edan G t a M l iple Sc ro i linical ResearchC n r, D partment o rology W yne St ate Univ s ySchool o M d c n en imm no ppr ion in a enw h rap dly wors n ng m p clero : r a ment guid n s

for h c n ci nLancet eu l. 2008 F : - 18 .F hman EM, Good n DS t al Th util ty of MR insusp ct d MS: report of th Th rapeu ics nd T chnologyAssessm n Subcommittee of th Americ n c demy of

e ology ! ro · 200 Sep 9;6 1 5 :60 61

MOVEMENT D SORD RS

A s MB, Ess ink RA t l. mpro i g th d agnos ccc r cy in Parkinsonism: thr e prong d ppro ch.

Pr ct Neural 201 2 Apr; 2 2) 77 87

Bi n en OJ N uf d KJ e . r atm nt of four psych tricmergenc es n th int nsive c re uni .Crit C re Med

20 1 2 S p;40(9 :2662-26 0

Bo B Progr ss supra uc r p syP rkinsonism Rel tDisor 20 1 2 Ja ; 18 Supp S 192 194

Chou K . In th clinic. P rkinson dis as Ann Inte Med2012 OV 6; 57(9) I C5 1 TC5 6

Gillma PK N ro eptic m ig a sy drome: m cha ismsinter ct o s, nd ca sal tyMov Disord20 0 S p 1 5;25( 1 2): 1 80- 90

Gr f M Lor nz B How to de l w th diplopiaRe Neural(P ris).201 2 Oct; 68(1 0) 720 728

J n ov c J, Po we W her p es in Parkinson's d s asCurr Op n 20 1 2 Aug;25 4 433-44

K t Chiu WZ t l R c n d c s in progr ssisupran cl ar pa sy a r iew.Curr Alzheimer Res201 1 M y;8(3 295 302

oo vanova SA. New insights i to th m cha ism od g induc d dyskin s aCNS Spe tr20 1 b; 8( 1 :5- 20

p S nd n J Men MA et l rug ind cedP rkinsonism in the e d rly inc d nc man g m ndpr v ntion Drugs Aging 20 2 b 1 ;29(2): 1 05- 18.

Migno EJ A prac ic l g ide to th th r py of n rco epsy ndhypersomnia sy drom s Neurother peuti s20 1 2 Oct;9(4 39 52

Roessn r V Scho ef d K l Pharm cologic l tr atm nt

of tic disord rs a d oure te Syndrom .Neuro h rm olo201 3 May;68 1 43 149.

Z u KE schl G An updat o tr morsCurr Opin20 1 2 Aug;25(4):4 5-482

Am r can Acad my o e ology P acti G id lin s.Mov m nt Di ord r nlinht p aan.com G d in / H me ByTop c?t p cld= 1

Bhidaya iri R, Fahn S, t al Ev d nc -ba d gu d l n : Tre me tof ard synd me : Repo of th Guid l eD v pmn Subcommit e of the Amer can Acad my o

ro ogy N e u g 0 Ju 8 (5): 63 69.

© 2 14 ed tudy

F FU H A G

Harden RN O kland r L, et . R ex Sympa het cDyst ophy Syndrom soc tion Compl x reg onal p nsyndrome pr ctic l diagnos ic nd r atment guide ines, 4th

dition. P in 201 eb; 1 4(2 1 80 229

Miyasa i JM Ma in W, e l Practic p ram te ni a on oea m nt for Par inson sd sease: an id nc b sed rev w:

epo o he Q ty S andard S bcommi tee of th me can

cad my of N rolog y eu o gy 2002 n 8 58 1 ): 1 17M y k JM, Shannon K, t a . Prac ic Param t r: luat on

nd tr tm of d press onpsychosis, nd dementia inParkinson dis s n idence bas d ie repo t of theQ ali y Standa ds S bcommi e of th meric n Acad my o

rology. eu ol 2006 pr 1 166 7):996- 1 002

Morg n hal r l KapuV K et St ndard o Pr ct commi tee of th Am r can Ac demy of Sl p M dicin .

Practic p am ters o th tre tm n of narco epsy nd oth rhyp r omn a of c n r l origin.S eep 2007 D c 0 2):1705- 1 R v .Err tum in S e p 2008 F b I 1 2): ableof conten

Pahw R F ctor SA, l P act c Par meter: rea ment ofParkins n dis s wi h motor uctua ions nd dys in s a ( n

idenc b s dr ie r por of the Quality St ndards Subcommit e of th Americ n Academy of Neuro ogy

eurolo y 2006 A r 1 66(7):98- 995.

Suchow rsky 0, Gronseth G t al P ctic P r m r:n uroprotecti e trat gi and lte ti th r pie forPark nson diseas ( n vid nc b d ie ) report of hQ al y S andard S bcommit e of the Am rican Acad my oNe rology e ur l 2006 p 1 166 7 :9 6 - 98 E a m

n: u rol 2006 J l 5;67 : 99

S chower ky 0, R ch S t al Pract c P r md gnos s nd prognosi of n w on e P kinson di e se ( n

id nc bas d r ie report of the Qu lity St nd rdsSubcomm te of th Am ican Acad my of eurology.

2006 A r 66(7):968- 975

Z si ic A Elbl R, l. Practice param t h r pi s forss ntial r mor: repor o theQu lity Standards Subcommitt

of he m r c n Acad my of N rologyN u o2005 un 28 64 12 :2008- 2020

Z s ew cz TA S l an KL a Pr ctice P ramet rrea ment of non motor ymptom o P k nson d ease por

of the Q al y S and rd S commi tee of the m ric nAc d my o N rology o 20 10 Mar 6 74 1 ):24 3 1.

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CONTACT D R ATIT S I2 2

ACN 2-2 Acne Vulgaris . . 2 2 Acne Rosacea l2 3 DRADENIT S 2 3

MO TH NDINGS 2 4 CUTAN OUS DR G REACT ONS 2-5 NFLAMMATORY SK N D SORD RS 2 5 NOT 2 5 PSOR AS S 12-5

Ove v ew . . 2 5 Types of Pso iasis 2 5 Nai Changes 2 6 D ugs sed to T ea Pso ias s l2 6 T ea men o Pso asis 2 7

LUPUS 2 7

SYST M C SCL ROS S SCLEROD A

2-8 SARCOIDOSIS l2 8

RYTHEMA NODOSUM l2 9 D RMATOMYOSIT S l2 9

ACT VE ARTHR T S 2 9 VASC L T S l2 9 PYOD RMA GANGR NOS M 2- 0 SWEET SYNDROM . . 2 0

VITAMIN D ICIENC S 2 O VITAMIN/M N RAL D C ENC S 2 0

SK N NF CT ONS l2 O BACT RIAL SK N NF CT ONS 2- O

Co nebac/erium 2 0 S aphy ococcus au us 2 10 S rep ococcus pyogenesG ou A St e 2 11

Go ococcus and Meningococcus 2 1 Pseudomonas 2 2 A i al B es 12 2

RJCK TS AL SKIN INFECT ONS 2 2 SP ROCHETAL SK N N CT ONS 2 12 VIRAL SKIN INFECT ONS 2 12 FUNGAL N CT ONS 2 13 PARASIT C S N INFECT ONS 2 1

SK N CANCER AND SK N ND NGS l2 BL ST R NG L S ONS l2 16 ROUND L S ONS . l2 18PIGMENT C ANG S 12 18PR R T S 2 19 A DS-R LATED SKIN LESIONS l2 20 D AB T C SKIN L S ONS 2-20 FOR FURTHER R AD NG 2-20



CO ON SKIN PROBLE S

ATOP C DER A S (ECZE AAtopic dermatitis ([AD]; I age 12-1) is a ch onic

n ammatory sk n condition w th a relapsin andem ttin cou se whic usua ly be ins in nfancy o

childhood and becomes less seve e with a e.85% of acases present at< 5 years of a e and the onset is area er a e30 t s cha acte zed by dry sk n and prurtus Subsequent scratchin leads to more n ammat onand l cheni cation (thicken n and ha den n of theskin, wit exa e ation of its normal ma kin s) as weas more itc in and sc atc n ("itch-sc atch cycle)

t s o en assoc ated wit a pe sona o fam ly h storyof eczema, alle c hinitis, o asthma E evated

evels and eos nop a a e common y seen n adults,the most common a eas nvo ved nclude the w sts, andantecub tal and popliteal fossas. They may also deve operythematous and edematous pr t c patches on the

head and neck hese may c ust and then weep, atleast art y f om scratc inFla es can be p ec p tated by cloth n ( a t cula ly wool

be s), emotiona stress, ae oaller ens (dust mites andpo len), and nfectionsS. aureus is o en p esent nsevere cases and ec ema he pet cum, caused by e essim ex v rus, can cause a severe d ssem nated nfect on. Occasionally, oral ant biotics are ven to dec easeco on at on of aureu and t us sho ten the course ofthe d seaseHydrat on, water tra pin a ents, and to ical cor icoste oids are t e mainstays of t eatment fo AD. Mid or

hi h potency top cal corticosteroids are used fo t etr nk and extrem t es, while low-potency top ca co ticoste oids a e ecommended fo t e face to lessen t e

isk of sk n atrop y and st iae Also, atients must beeducated to avo d r bbin or scratchin t e sk n lesionsTacro mus(P otopic®) andimecro mus( l de! ) a etop cal immunosup essants (calcineu in inhib to s) that

- : u lf w

© 2014 MedStudy

COMMON SKIN PROBLEMS

- are e ect ve alte at ves to top ca co ticostero ds. Sincet ese do not cause skin atrop y, t ey are espec a ly oodfor fac al les ons The e s a otent al r sk of sk n cancer

o T-cel ymphoma, so these a ents aren line fornte m ttenttreatment of ato ic dermat t s ese a entsshou d be avoided n H V+ patients or anyone with aweakened immune systemUse oral cyclosporine, a at oprine, mycophenolatemofet , or methot exate fo seve e AD t at does notres ond to conse vative t erapy. Ult aviolet t thea y may also be used n this sett n O a cor coste o dsare a ely nd cated for acute ares

SEBORRHEAeborrheic de mat tis a ects 5% of t e opulat on

and s a c on c cond t on that man fests as a ye ow,easy sca e ove yin e yt ematous atches or plaques

( age 12-2 . Prur tus s variab e t a ects a easwhe e sebaceous ands a e most act ve and espec a lyinvo ves t e scalp (dandru , eyeb ows, aranasal a ea,and exte al audito y canals, alt ou h t e chest, ax a,and o n areas may a so be nvo ved T ere s a stronassoc at on w thMalassezia f r, but t s unknown ft s fun us is a cause or esu t of the de mat tis.Seborrheic der at t s is common n at ents wit H VIA DS and Park nson disease.T eatment of sebor heic der atit s: f equent was inand an antidand u shampoo T e act ve n edientsn these s ampoos a e selen um su de, nc pyritone, salicylic acid, o tar. T e ant microb al shampoosinc ude ketocona ole o c c op ox

se low-potency top cal co t costeroids ncomb nationw th ketoconazo e cream fo sk n d sease Top ca ca cneurin inhib to s (tacrolimusand imecro mus) can beused asste o d spa in a ents

N ER GOtertrigois an tantde mat tis found in t e mace ated

sk n folds ( nframammary, ax a, roin) of obese

12-1



12-2 OMMON SK N ROBLEMS

patients. presen s w htender, br ghtly erythematous, mo st pa ches n hesk n fo ds d d cansecondar y infec heseareas. Suspec d dwhen sa e e papu esextend beyond the ma nles on. A so r le ou neacr r s and e y hrasma,Image -3: Contact d rmatitis

cau d by ing with nick lwh ch can m m c nonspe-ci c n er rigo. These can be ru ed out with a KOH testand Wood's lamp, respective y.Trea in er rigo w h op cal antifunga s and dryingagen s (ant nga powders, a um num sulfa e prod

c s, co s arch). Avoid he se of a c m powder in thegen tal area of women beca se of he poten a ncreasedrisk of ovar an cancer. We ght loss is cr cial to preventrec rrences.

CONT CT DERM T T S can be ca sed by a chem ca

tan (80% of cases), or t can be ofa lergicor gin (20%of cases; [Imag 12 3]). The mos common irr tants aresoapy wa er, rubb ng alcohol, and common househo dc eaners S c en expos re to these i r an s causes derma s ineve y ndiv d al For rri an con ac de mat is,p or sens iza on sno req red.The a lergic ype of contact dermati s s due to a T cell med a ed,delayed ype hypersensitivity reaction(Type

V hypersens t vi y) n he skin. Patients mus becomesensi ized o he an gen w th one or many exposures.A er sensit a ion and upon re exposure, he sk n deveops a pr i ic les on n 2 o 2 days The mos commona ergens are n cke , chrom um, neomyc n, and oleores nurush o (po son oak, poison ivy, and po son sumac)

ine trea men s den ing and remov ng heo end ng al ergen Symptoma c reatmen incl des coolcompresses, Bu ow s so ut on (al minum ace ate d ssolved n water,I 0), and top cal cor icosteroids. f thereact on is severe or nvo ves heface, g vesystemiccort cos eroids. Patch es ng s the go d s andard o dentcon act al ergens and can be used f the contac al ergen s

not obv o s. n patch est ng, m ip e s spec ed allergensare appl ed o the pa ent's back nder occlus ve dressngs. A er 48 ho rs, he dress ngs are removed and he

area s examined for ev dence of de ayed hypersens tiv yreact ons.

CNEAcne Vulgaris

he c n ca man fes a ons of acne vu gar s are:Open ("blackheads ) and c osed ( whiteheads )comedones

• Pap es

Pus ulesCystic esions

Comedonal acne s non n amma ory acne and developsin ear yado escence The pathogenes s invo ves occ s onof he follic es

n am atory acne occ rs as a reac on to several fac ors,nclud ngP op o b t m with n the fo c e,r ptured follicular epithe ium with leaking of sebum,

and he imm no og c response to hese factors. Acneseverity is genet c and hormona , w h an imbalancebe ween es rogens and androgens However, contraryto popu ar bel ef,mos pat en s w h acnedo no overproduce androgens The ike y e ology socallyhyper esponsivesebaceo s g ands o androgens (hence

he genetic predisposit on for many)However, in women with po ycyst c ovary syndrome(PCOS), acne is a common bu not spec c ex e amanifes ation of increased ser m androgens PCOSoccurs n 5 0% of a women, and abou /3 of womenwi h acne have PCOSFac ors tha may exacerbate acne inc ude cosme cs,o s, repe ive mechanical rauma (scrubbing), c o h ng(t rtlenecks, bra straps, and spor s he me s), hum dity,and heavy sweat ng. D e s a controvers a cause; somestudies have shown an associat on with m lk ntake(exacerbating) and low glycem c d e s (amel orating).S ress appears to worsen acne sever yAcne vulgaris di ers om rosacea by the presence ofcomedones (no seen in rosacea) and he ack of telangiectasia (seen n rosacea) Seea 12 4throughI a12 6

f ( f ) :Topical retinoids

are drugs of cho ce forcomedona acne. These includeadapalene, ret no n, and ta arotene These are generally applied a nigh because they can be deac iva ed bysun ight (adapalene is an exception). Note: Ta arotene(Ta orac®, Avage®)scontra nd cated in pregnancy!Side e ects are mainly sk n rr ation (s art a a owdose and apply 2 3 t mes per week) and photosens

iv y O her agen s for comedona acne inc ude topical

sa cylic acid, a e a c acid, and g ycolic acid; a 3 havean icomedonal act v tyf y (I a 1 4): Ben oyl perox de

n combinat on wi h op cae y h omycin or clindamyc nis used o treat heP of in amma o y acne. Thecombination herapydecreases deve opment of res stance,and commercial prepara ons are availab e ha haveboth products. Top cal re ino ds are also use l adjunc sTop ca dapsone, an e ec ive antim crob al agent, wasin ia ly approved by he FDA in 955; n 2009, i wasremarketed w h he rade name Ac one .

v f (I a e 12 5):Th s requ resoral antibio icssuch as tetracyc ne, doxycyc ine, and m nocycl ne in addi ion o the above

© 2014MedStu y - Piease Repo t Copyr ght Inf gements ocopy ght@ e stu y.





Q � .

·u i

W f b ?W f ?

•

C x f w f ?• W f ?

w f b w ?

top cal the apy. The high prevalence ofP acnes es s anceto erythromycin has led to decreased use of th s agent.TMP/SMX s ecommended in se ec ed re ac ory cases

so no n ®, C av s®, So ;1.0 m g/d)s h ghly e ect ve in seve e nod ocystic, sca ing,

or es stant cases b is also a powe lte a ogen. These of sotret noin is estr cted to physic ans who have

reg s e ed w th the e ec ronic FDA system (ca led he" PLEDGE™ p ogram ) and req res m l p e steps norder to prescr be (e.g.,2 p e ancy es s,2 forms of b r hcontrol) Se ious s de e ects nclude pse dot mor ce ebri(especia ly f used w he acyc nes), depress on and psychos s, pancreatit s, marked hype r g yceridemia, hea ingJoss, n ght v sion oss, and skeletal abnormal ies

- :M d

-5:M d v

© 014 MedStudy

CO ON KIN PROBLE

6 If ora so retinoin s sed, a o he acne reatmentsmus be stopped Again, conc rent use of o a sotretinoin and he fami y of e racycl ne an biotics can ca sepse dotumor cerebri.

O al cont acep ive herapy s sed in PCOS to dec easeandrogen excess and o regu ate menstr al cyc es.Sp ono actone, which has anti-androgen e ects, isalso used as hormona herapy n comb na ion with o alcon racept ves

Acne RosaceaAcne osacea( mage 12-6 s a l fe ong condi on thaprima ly a ects fa r skinned, m ddle aged patien s andpresents wi h erythema, e ang ectas as, and acne-l keles ons on he cent a face t is mo e common in women,but mo e severe in men I inc udes4 main s btypes:

I) ryth m t t l gi t ti(vasc ar) shing, faciaery hema, and elang ectasias

2 pu pu tu r fac al e ythema w h t ansientpapu es/p s es

3 hym t u hickened sk n, nodu es, h nophyma(bu bous nose)

4 O u r:wa e y/b oodshot appea ance, lid/per oc laery hema

Pa ients may have a ushing reac ionto var ous s mul(e g., alcohol, s ess, spicy foods) even before he les onsappear. Once he osacea man fests, the ush maybecomepe manen .T gger avoidance s ecommended.Treatment s topicalme on dazole, aze a c ac d, s l /s facetamide prepa a ons, or o al te racycl ne an ib otics. The lat e may be pa t cular y help for thepapulop st ar and oc ar s btypes.

hinophyma is mo e common n elderly men and mayreq i e surg ca therapy. Telang ectasias can be treatedwith ase he apy Know how to d s ng ish acne v lgar s f om rosacea Rosacea doesnot have comedonesand may have elangiec as as, n ke acne vulga s.

HID DENITIS

H dradenitis suppura va (acne inversa), wh ch a ec sapproxima e y1% of he popu a on, s a c ron c

1 -3



12- MOUTH FINDINGS

Image 12-7: Hidradenitis suppuraliva; mi d v . se ere

i ammato y scar ng process involv ng apocrine glandbear ng areas such as theax l aeand t e g o n/perianalregions ( mage 12 7). t typica ly deve ops a e p ber yand manifests as pain , deep-seated nod es, s nust acts and abscesses T e abscesses are usua y ste

le b t can become secondar y supe nfected. Whi et occ rs in both sexes (women> men 4: I) women

tend to have mo e ax llary and v var nvo vement wh e

per anal nvolvement s mo e common in men. Smokingand obes y corre ate w th severity of d sease.

he d sease p ocess begins w t d lated, occl dedfoll cles (comedones) that o en have m lt ple openingsSubsequently t e d sease can range f om mi d to seve e(indu ation sca ng pitting and draining abscesses)

T ea ment for draden t s should be guided by d seasesever ty and is o en challeng ng. If app cable smokingcessation and weight loss s o ld be recommended. Avoiddeodo ants (ant persp rants are okay), t g t synt et cc oth ng, and p o onged exposu e to ot hum d environments Ea ydisease sho ld be t eated w th % topical

cl ndamycin and intralesiona ste oids. Treatacute nfections w t nc sion d ainage and pack ng.Late diseaseshou d be t eated w t e t er o al tetracycl ne or o alc ndamyc n r fampinMo esevere disease may requi e

mmunos pp essants s ch as in x mab o etanercept,wh ch a e ant -TNF- - n b tors. Anti-androgens and zincg conate are controvers al with l m ted data to s pportthe r use. o seve e re actory lesions comp ete su gical excision s de n t ve therapy b t laser the apy s a so

ncreas ngly being sed.

MOUTH F ND NGS

[Know all of t ese!]

Hyperpigmented gingiva s seen in Addison d sease.

Koplik spots ( mage 12-8) are sma wh te pap es onan eryt ematous base, w ch a e fo nd on t e b ccalmucosa in pat ents w th meas es. ese sual y precedet e sk n es ons by severa days.Oral ha ry leukoplakia ( mage 12 9 ) most commonlyocc rs in patients w th HIV/AIDS. It man fests as asymptomat c wh te plaq es along the s des of the tong e. T is

s due to Epste n Bar v r s n the s pe c a laye s of thetongue's sq amous ep t eli m. In contrast toCandida, t

can t be sc aped o

mage -8: Kop ik po Image 1 -9 Ora hai a a

Erythroplakia consists of eryt emato s plaq es About90% of cases a e e ther dysplastic or carcinomato s, sod stinct on om le koplak a, w ich is gene ally ben gn,is cr c al

Peu -eghe s synd ome (mu tip e ntest na amatomato s po yps) s ould be u ed o t in patients withmelanot c pigmentat on( ent g nes) on t e l ps and buccalm cosa.

Beefy red tongue (gloss tis) s seen n pe icio sanemia and va ous B vitam n de c encies. It also canbe associated wit glucagonomas isc ssed nder Sk nCance and Skin Findings on page 12 14

Macroglossia (big tongue is assoc ated with mu t p emye oma p ima y amy oidosis lymphoma emangioma ac omega y ypothyroid sm angioedema, andDown syndrome

White lesions: c did as s, hairy eukoplakia (A DS)l c en planus L chen p an s also ca ses ce ationand ace- ike patches(W ck am striae).

pso ias s.

"Strawberry tongue sd e to n amed tongue

ongue

pap l ae and s associated w t scar et feve tox c s ocksyndrome and Kawasaki d sease (mucocutaneouslymp node syndrome commonly seen in ch ld en).

"Bald tongue s atrophy of t e l ng a pap ae assoc ated wit pellag a iron de ciency anemia, pe iciousanemia and xe ostomia (d y mout common y seen inSj gren synd ome, ymphoma mumps, and sarco dos s;may occasionally be diopat c).

© 2014 Med tudy-Piease Repo Copyr gh Inf gemen s ocopy ght@me st y .com







• Wh t nd ng n th bucc l muc c n b nth m ? c b nd n m th nd ng.

Wh t l n ct n c u h uk k ?• A b d t ngu n th h ch und ng

d t t ? c g ?Wh t d cut n u ct n

c t d th h n t n?

CU ANE US DRUG REAC NS

The following are the most frequent d g-assoc a edskin c anges. [ ow a of t em.]Penicillin (PCN):

Immed a eypersens v y react on anap y axis ( gE)De ayed ypersensitiv y reaction; imm ne comp exreac on, such as vasc lit s or morb ifo m e pt on

Tetracyclines p otosensitiv y (demeclocycline >doxycycl ne> te racyc ne> m nocycline). Other d gscommonly assoc ated w th p otosens iv y nclude:

oroq no ones, su fonam des, and am odaroneNSAIDs ur cari /angioedema n 1%, as hma n 0.5%,and may cause pho osens t v ty or toxic ep de mal necrolysis (TEN).Phenytoin

Hypersensitiv y syndrome ras , fac a edema,ymp adenopa y, and epa t s

Vario s sk n reactions, inc uding ery hemam ltfo meHype roph ed g ms (a so commonly ca sed bycyc ospor ne, nifed p ne, and amlod p ne a so seen inM3 and 4 s btypes of A L) and rs sm

Co icosteroids skin changes, nc d ng s r ae,atrop y, telang ectas a, p gmen ary changes, and acne

ke les ons.Wa arin necrot c pa c es (necros s) of skin appearing3 0 days a er star ing warfarin, yp ca ly occ r ngin pat en s w h unknownpro e n C de c ency. Les onsclass cal y a ect areas w h e h ghes fa deposit ons c as e breas s, bu ocks, g s, and abdomenRadiocontrast dye Th s can ca se car a/eryt ema(I: ncidence), and rarely ( ,000 nc dence) a severeanaphylac oid reac on (no gE media ed). There sa 30% chance of a repeat reac on n someone with a

sto y of prior react on o contrast dye, and o en thesecond presen a on is more severe. Prophylax s witan s amines (H+/ H2 b ockers) and cor cos ero ds(sta days pr or) decrease the incidence of th s reac

on 10 fold.Gadolinium a contrast material used for RI t asbeen assoc a ed w nephrogen c system c brosis

© 2014 MedStudy

CUT NEOUS DRUG RE C IO S

(NSF), a brot c d sease of the sk n and in e a organss m ar b t dist nct om sys em c sc e osis (sclerode ma) in at i yp ca y spares e face Pa ents witESRD or a G R< 30 m /min are at the h ghest r skThere is no good rea men , so prevent on s paramo ntDon' g ve gado in m o a pa en w s age 4 or worseC D!ACE inhibitors: Ang oedema occ rs in on y0 % of pat ents rea ed w h an A E inhibitor However,because s ch a arge number of pa ien s rece ve th sdr g, t s one of t e mos common ca ses of isolatedangioedema Ang oedema can occur at any t me d ingtrea ment w ACE in ib ors. Ang o ens n recep orb ockers (ARBs)rare ycause ang oedema However,t ey should be sed caut ously in pat ents who have aprev o s h s o y of ang oedema wit ACEI use aref lconsiderat on should be sed n his scenar o mak ngs re hat he bene o we ghs t e r sk (e g., systol c

ear fa lure, s gn can p o e n a)

DR SS syndrome r g reaction w h eos nop ilia andsystem c symp oms arr es a mor a y rate of aboutI 0%. Pa ents common y present w h a morb formras , fac a swe ng, fever, ymp adenopathy,j FTs,an epa omega y. The majority of cases have assoca ed eosinop il a. Ant convu san s and allopur no are

e mos common dr gs mp ca ed. Trea ment req resremoval of e o ending medica on. Sys emic steroidsare common y prescr bed, although data s ppo ng t eire ectiveness is controversia .

NFLAMMA RY SK N D S RDERS

Many of he d sorders described here are presen ed inmore detai n R e mato ogy, Book 3.

OverviewPsor as s s a response riggered byT ymphocy esn t esk n.The ep de m s becomeshyperpro fera ve, prod cing more sk n a a faster a e than normal. Traumaor r at on of norma sk n common y nduces esions ofpsor as sa the s e (Koebner p enomenon)A ypes of psor as s can be precip ated/exacerba edby stress, sunb , nfection (v s, s rep pharyng is),

ith m, andbe a-blockers) Obes ty is assoc a ed wi hpsor as s, and s gn cant weight Joss may lead to clinica

mprovement.

Types of Psorias sPlaque pso as s s t emost common type(Image 11) presents n yo ng adu s w h wellde ned, s able, s ow grow ng, e ythema o s skin les ons

wit d st nctivem ca ke(silve y) sca es P r s

12-5



12-6 NFLAMMATORY SK N D SORDERS

is variable (absent tosevere), w th pat entsusua y havi g mild

tchi g. It is yp ca lysymmetr cand occurs oextensor surfaces of theknees and e bows, thesacral area, a d the scalp(See Psoriatic Arthrit s nRheumatology, Book3.)

Guttate (e upt ve)psoriasis is an abrupt

mage Plaque psoriasis e upt o ofmult plesmalllesions (3- 10 mm

diameter), and usually occurs o thet unkof ch ldreor you g adults with no prev ous history of psoriasisStreptococca pha y g t s s a known t igger of guttatepso as1s.Flexural (i verse) psorias s a ectssk nfoldareas It isca led nverse because t soton the exte sor surfaces.There are 2 rare, espec allyseveretypes of psorias s:

) E ythrodermic psor as s2) Pustu ar psor asisErythrodermic psoriasis is a exfoliative reaction

which the e t re surface of the ski becomes red,wa m, a d scaly-and the pat e t sunable to cont olbody temperature. (Hypo/hyperthe mia is common )Dehydration, hypoalbum em a, a d anem a of chro cd sease are commo seque aePustular psoriasis has ma y sma pus ules, o e

coalesci g to form "psor at c akes of pus There are2 forms) Thelocal zedfo m a ects o ly the palms and soles

It is assoc ated with DIP jo t arthr t s2) The rare,general edform (von Zumbusch ype) is the

most severe fo mof psorias s a d may occur with thee ythrodermic type Sudden withdrawal of system ccorticostero ds is a well described i c ti g eve t

Nail ChangesThe most spec c na l d ng s an "oi spot o the

ails "Ice pickp t ngof the a ls is also common.These pits are usua y n sma groups on the a l.Thickened na ls a donycholys s(separat o of d stal

mage 2-12: Pi ed nai withonycho i

a l om the a l bed) arealso common psor as s( mag 2 2) Hav ngp tted na s i assoc at ow th onycholys s s fa rlyspec c for psor as s andmore stro g y assoc atedw th psor at c a thr tis.

Drugs Used to Treat Psorias s[K ow all of these ]Topica co icosteroids: P a ues are usual y treatedwith topical cort costero ds Long term use of h ghpotency stero ds may cause th nn ng of the sk n,stri

and steroid induced rosacea on the face. They are bestavo ded on the face a d tertrig nous areas To ncreasetheir e ectiveness, topical stero ds ca be occludedw th cel ophane or a p astic wrap.Oral cor costero dsmay actuallyworsen the d sease by caus ng a "rebound

are (See pus ular pso as s above )Tar is a t me ho ored treatment and is o en st l used i acompounded preparat o w th a co coste o d Tar preparat ons stain clothes but are we l toleratedCalcineurin inhibitors top ca acrol mus(Protop c®)a dtop cal pimecro mus(El de ®) These are o en usedfor fac al and inte rig nous areas where high pote cystero ds shou d ge era ly be avoided Be aware of the

FDA boxed wa i g for a pote tia i creased r sk oflymphoma and sk n ma igna cy.Retinoids (v tami A derivat ves):

azarotene gel ( azorac, Avage) decreasesthe hyperkeratosis or thick scales assoc atedw th psor as s Mai side e ect is sk n ir itationAc tret (Sor atane®), a 2 generatio oralreti oid, s used for the severe forms of all ypes.It is extremely tox c a d has a s mi ar side e ectpro le to sotret no n (See moderate to severe

n ammato y acne under Treatme t of Acne Vulgar so pag 22 )

Do ot use e ther drug in wome with ch ld beari gpote t al. Impo ta t The FDA has placed a 3 year postdosing morator um o pregna cy w th ac tretVitamin 03 analog: These age ts are ess e ect ve thanh gh pote cy topica stero ds, but do 't cause th n skinor striae

Ca cipotr e e (Dovonex®, a sy thetic v tami Da alog) is usually too i ritat g to app y to the faceand te ig nous areas

• Ca citriol (Vect caJ®, a sy thet c v tamin D ana ogn a o ntment base) is less itati g

Treatment of extensive psoriasis with vitami Da alogs may result n hypercalcemia, so the maximum doses for calcipotr ene and calc triol areI 00 gmand 200 gm per week, respect vely

Immunosuppressants Methotrexate (M X) a dcyc ospor e are both ve y e ective for extens ve severepsor as s

Methotrexate can cause severe iver and pulmo a ytoxicity, as we as bone mar ow suppression. Donotg ve M X to pat en s w th a h sto y of alcohol abuse,l ver d sease or severe k d ey impairment (the drugis excreted renally)

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ui

Nail p ing w th o yc olys s is a fa rly specif c ding o wha de ma o og c d so de ?

• Which drugs should be added to he reg men orpa en s with pso a ic arth s?

C aracter ze the ma ar rash o system c upus.

Cyclosporine is associated with rena oxici y andhyper ension and is recommended only forshor term"rescue use. Fair skinned Caucasians with a priorhistory of treatment wi h psora en and ultravio e A(PUVA should generallynot be trea ed with cyclosporine because they have a much greater risk fordeveloping squamous ce carcinoma.

Biologic immunomodulators: These arenewer, e ec

ive rea men s for psoriasisTNF alpha inhibitorse anercept(Enbre ®in iximab(Remicade® ada imumab(Humira®IL 12 and IL 23 b ockerustekinumab(Ste ara

Ultraviolet light may be added to the above reatmen sor used as monotherapy. UVB (290-320 nm therapy iso en used Narrow band (NB UVB (3 nm is possib y more e ec ive than the broader spec rum trea mentand is genera y he trea ment of choice. But, it requiresmore expensive equipmen and a onger dura ion oftherapy per session.PUVA (oral psora en+ VA light [320 400 nm] is

a so very e ective and is usual y given o hose who failUVB. UVA pene rates more deep y than VB and is esslikely to bu (hence he photosensitizing psora en ,butit is associated with acce erated pho oaging an increased

ike ihood of skin cancer (squamous ce carcinoma ,and possibly melanoma in fair skinned Caucasians.Future rea men with cyc osporine increases this risk.Any pa ien wi h psoriatic ar hri is is a risk forper anent join damage and should be reated with adisease modi ing oral/injectab e agen ( cyc osporine,me hotrexa e, or he biologics See R euma o ogy,Book 3.

Treatment of so iasisRecommended trea men for psoriasis depends on theseveri y of disease The severi y of psoriasis is de nednot on y by the extent of body surface area (BSAinvolvement (< 5 being considered mild 5-9 moderate, and�I 0% severe but also by invo vement of thehands, feet facia or genital regions. Involvemen ofthese ocations may in erfere signi can y with activi

ies of dai y living irrespective of the amount of BSAinvolved.Limited disease < 5%): Trea with hydration and

wa er rapping agen s. se high potency or u ra

© 2014 MedStudy

INFLAMMATORY SKIN DISORDERS

high potency opical cor icos eroids for no longer han4 weeks. aper o a mid po ency agen and add a vi aminD analog for main enance. For the sca p use a tar shampoo and/or opica s eroid lotions For more sensi iveareas ike the face, axi lae, and genita ia use

ow potency corticosteroids,topical tacro imus or pimecrolimus,ca ci riol or

opica retinoids (tazarotene .f he pa ien fai s to respond, UV based or shor erm

systemic herapy can be usedModerate disease (5 - 9 ): Treatment is he same as for

imi ed excep tha UV light therapy is rou ine y used,typical y NB UVB PUVA can be used for hose who failUVB herapy Depending on morbidity associated wi h

he disease, consider reatment with sys emic agents suchas me hotrexate acitre in (Soria ane , or a bio ogic.Widespread/severe disease (� I0% B VB is

recommended, wi h considera ion of P VA for fai ures.Treat with me hotrexate, cyclosporine, or a bio ogic.Combinations of hese herapies can a so be used.The combination of UVB or P VA with acitretin isespecial y e ective for pustular psoriasisGuttate psoriasis Treat with VB +/ topica s eroidsTrea any streptococca infection.Flexural psoriasis Treat with ow potency topicacor icosteroids or topical tacro imus/pimecro imus

LUPUS

Systemic lupus erythematosus (SLE) Ma ar (orbutter y rash occurs in about ha f ofacu eSL patientsand rarely occurs in patien swithou sys emic symptoms. Classical y, his rash invo ves bo h cheeks andex ends across the br dge of the nose, sparing he naso

abial fo d. The malar rash is ery hema ous and ei herat or s igh y edema ous and o en occurs a er sunlight

exposure (pho osensi ivity. N o scarring. Acne rosaceamay mimic a ma ar rash, but can bedis inguishedbyprominen e angiectasias, papu es/pus u es, and the lackof sys emic symp oms.Patien s can get a red, scaly rash on he backs of thehands, usua ly between he joint spaces of the ngers(spares he knuckles as opposed o dermatomyosi is,where the rash is over the knuck es (Got ron papu esand spares the spaces between Pa chy and di se nonscarring a opecia is common in S More on SL inRheuma o ogy, Book 3.Subacute cutaneous lupus erythematosus SC E)is a distinct subsetof upus characterized by erythematous macu es/papules tha evo ve in o papu osquamousplaques on sun exposed areas Like he acute rash ofS , bu in contrast o discoid upus these lesionsheal without scarring. any patien s are seroposi ivefor SSA/SSB antibodies Pa ients uncommon y have

signi can systemic manifesta ions.

12-7



1 -8 NFLAMMATORY K D ORDER

Chronic cutan ous lupus ryth ma osus (discoidlupus : Disco d les ons are e ythematous and raisedwit t g y adherent sca es T ey cause at ophicscarring. T ey usually occu onsun exposed a eas,

nc ud ng he face, sca p, neck, and ea canals. Only5% of discoid upus patien s develop SLE Howeve ,pa ents w th SL w o develop disco d lupus les onstend to have a very good p ognosis devo d of sign cant

enal man festa ons.

Int ales onal co cos ero ds are especial y e ect ve fod scoid lupus 1stline o a the apy includes ant ma a a s,suc as yd oxyc oroqu ne. More agg ess ve systemic

herapy wi mmunosupp essants (MTX, azathioprine)s used in seve e cases o for t ea ment of SLE w th sig

ni can system c invo vement

SYSTEMIC SCLEROSIS (SCLERODERMA)Scleroderma loca zed to the sk n on y= mo p ea.

orphea is cha ac e zed by plaques hat become sc eo c w th a ypop gmented cen e and ery ema ous

bo der. It usua y occu s n ch ld en o young adu tscan be just a few les ons ( oca zed mo ea) o w desp ead w h some con uence (gene a zed morphea).

Pat ents wi h system c sc erosis (SS ) a e classi edin o2 ma o sub ypes depending on t e ex en of sk nsc eros s:I) Lim ed scle os s2 D ffuse sc e os sLim d SSe(prev ous y C ST) is a grouping ofsymp oms t a as l m ted system c nvo vement, mos

common y man fes ing as skin t icken ng dista to theelbows and knees but some mes a ec ing the face andneck Pa ien s c ass ca y present w th seve a to a oft e CRE T fea ures: a c nosis cut s (sma tender nodules on the ngers), Raynaud syndrome, sophageadysmot li y, cle odacty y of he ngers, and elangectasias. An i cent ome e an body (ACA) s spec cfor l m ted SS and is seen n abou50% of pa en sPat ents w o a e ACA+ tend o develop mo e severed g ta ischem a andpulmona y hype ension.Difus SSe s the p ogress ve form of SS that eadsto di se sk n thicken ng and s more ke y o avemu organ invo vement (Ima e I 2-I3 ). T s subse scha ac e zed by ap d sk n nvo vement of trunk, face,uppe a ms, and ighs It

s equently assoc atedw th ant Sc70 (ant toposomerase-I) or ant NApo ymerase an bod

es and s mo e ke y todeve op in ers t a ungdisease and sc erode ma

enalcris s.

aynaud p enomenoneventua y deve ops n

almos a pa ents w thmage 3: Sy mic cl ro i

SS . In lim tedSS , aynaud's usually occurs seve alyears before other s gns and symp oms become apparent, w e indi se SS , e aynaud s typ ca ly occu ss mu taneously w t e ot er man festations.

Nailfold capilla y c anges (bu not in e ac ua na s)are commonly seen in bo h subtypes and co relate wi h

sever ty of d sease.here are no proven d sease mod ng treatmen s fo

SS

SARCO DOS SSa co dos s is an immune re atednoncasea ingg anu

omatous d sease tha o en a ec s the ungs, ymphnodes, eyes, and skin It s mos common n no he

uropean count es (e g , Sweden, Denmark) In heU S , owever, sa co dosis mos commonly a ectsA can Ame cans. Sk n nvo vemen is seen in abou25% of pa ien s Sa coidosis is a grea mimicke of o hed sorders, nc uding many dermato og c d seases.Les ons are div ded n o2 categories: spec c andnonspec c Spec c lesions have noncaseat ng g anu

omas on biopsy, whi e nonspeci c sk n les ons do nothave g anu omas and are cons dered eact ve

Speci c sarcoid skin es ons a e mos commonly foundon e ead, neck, and upper back Spec c es onsinc ude

Erythematous papules main y a ound t e face(t e mos common p esentation)

• Sca sarco dosis presenting as g anu omatouschanges in a healing skin wound o scar tissue(e.g , lace a on, ta oo)

• Plaque l ke lesionscropapu a es ons

Nonspeci c sk n les ons:E y hema nodosum (see nex ) is the most commonnonspec c sk n lesion seen in sarcoidos s and signalsa good p ognos s. Sa coidos s s one of e moscommon causes of nodosum Dono b opsyE nodosum in sa coidos s fo diagnosis e h stopathology w just s ow a panniculi is ( n ammat onof he fa ) and not g anu omas

fgren syndrome s an acu e fo m of sa coidos s hatpresen s wi h E nodosum, bilate a hila adenopa

hy, and a th tis, and is equen y accompanied byfeve s It is usua y self limi ing and equ res onlysuppor ive ca e

Lupus p rnio is a type of sarco dos s t a has skinchanges ang ng om vio aceous es ons on e tip oft e nose and ea lobes to arge pu ple nodules/ umo s ont e face and ngers I has a slow onset and almosnever

esolves! I s assoc a ed wi c onic d sease and ex rapu mona y invo vement.T eat cu aneous sa co d wi h opica cor icos eroids,

ntra esiona stero d injections, an mala a s, and me hotrexa e Lesions yp ca y respond o reatmen forpu monary sa coid

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W f ?

W k w?

W k ?

ERYTHEMA NODOSUME y hema nodosum( age -I4) consists of red, warm,ve y tende nodules that a e usually b late a symmetrica ,an classica ly located on the s ins. t s mo e common nwo en than en Causes of ery ema no osum [Know!]:

• Sarcoi osis (co on)• n ammatory bowel

d sease• nfection (TB, st epto

coccal deep ngal)• Drugs (especiallyoral

contraceptives, s fas,and pen c ins)

Wo l wi e streptococcainfect onis likely t emostcommon cause of erythema nodos m Treatmentincl des s ppo t ve t erapyand NSA Ds

D RMATOMYOSITIS

mag - : h mano os m

Buzzwords periorb talhe io rop cash ( +/ pe o b taledema; a g I2 I5 ) Th s is a v o aceous (purp e)sometimes scaly rash aro n the eyes.Pat ents also man fest photodistr bute e emato ssca y plaq es s i a to pso as s Go tron s gn is mac

a ery e a over the orsal aspects of the nterpha angeaVmetaca pop alangeal joints o over the elbows andknees

Go on papu es an extension of Go tron sign are at

toppe , eddish to vio et, so et mes sca ing pap lessomet mes they st ook like "c ga e e paper c nkl ng of the skin over theknuck es (MCP, P P, and/oD P). Go ron papu es a e the mostspec c nd ng w tde matomyos t s They may be descr bed only as a " asho "e uption over t e knuck es (age 2- 6) Aga n t iscont asts to t e nger as n SLEt atspares t eknuck es" echanic's hands are bi ate al symme c a eas ofhype keratotic sca e most commonly on the lateral nge sor on the pa m This nd ng s assoc ated w th ant synthe

ase syn ome ant Jo 1 antibo ies an interstitial lungd sease

Pat ents have symmet ic prox mal m scle weaknessbut may present solely w t cutaneo s d sease, te medamyopath c de matomyosit s

© 2014 MedStudy

INFLA ATORY KIN DI OR ER

mag - 5: P riorb al h l om g - 6: Go ron pap lrop c r sh

Treatment is cor icostero s T s s yp cally given fo year n a slowly taper ng dose A ste o d spar ng rug

(azathiop ine or met ot exate) is sometimes sta ed w tin tial t eatment othe clinicians sta it when the e sfa l re to espond to pre nisone

Ant mala as ( ydroxyc o oq ine) help wit theskin isease but onot ng fo the muscle d sease

gamma globu n may be e ect ve n patients who donot respond to the other med cations Tr als are examning t e e ectiveness of rit ximab n the treat ent of

de matomyos tis

Remember n older pat ents, dermatomyos t s may be aparaneop ast cphenomenon (GU/ovar an, G , ung, and

ymphoma a e most common.) A l patients sho d beo ered age-appropriate cancer screening Patients whotest positive fo anti pl /p 140 a e at par ic larly g

sk of cancer.

REACTIVE A THRITIS

Reactive a h tis s an mm nolog c eaction to annfect on e sewhe e in t e bo y and yp ca y occ rs

weeks a er a gen to rinary or gastrointest nal nfect on The c ass c t ad of urethr t s, con unct v tis, andasymmetric ar hr t s is seen n less than /3 of patientsCutaneo s manifestations a e common and inc u e kerato erma b ennorrhagicum and mucocutaneous genita

es ons and/or mouth cers

Keratode ma b enno r agic ( age 7) class ca ypresents as papu es/pus ules w t central eros on ancha acte ist c crust ng on the pa ms an so es and canbe ind st nguishab e om

p stula pso as sC rcinate balan t s p esentsas an ery hematous p s

ular or p aq e ke es onon the glans or sha of thepe s.

VASCULITISasculit s p esents most

classically as palpablepu pura, s ally startingon the egs Palpab e pupu a is t e ext avasation

mag - 7 r o rmbl nnorh g c m

12-9



1 VITAM N DEFICIENCI S

of RBCs into the ski and s commo ly caused by asma vesse vasculitis. Sk n biopsy typ ca y d sp ays"leukocytoc ast c vascu tis There are ma y causes ofcutaneous vascu itis nc ud ng nfec ion (vira bac eria e c ) co age vascular d sease and drug reac ionsUp o50% of self limited cuta eous cases may be id opa hic Always look for ex racutaneous ma ifes at o sespecially k d ey nvolveme . If a you g pa en presen s wi h ar hralg as, abdom na pai renal d seaseand palpab e purpura th nk gA vascu it s (former yHenoch-Sch n e n purpura).

PYOD RMA GANGR NO UMPyoderma ga gre osumis a in amma ory ulcer

p ca ly occurr ng on helegs ( mage 12- 8). ismost commo ly assoca ed with in ammatorybowel d sease, bu ca alsobe see wi h rheuma o dar hritis and hematolog cdyscrasias. Although ask b opsy is ot d agnos c it serves o exc udeo her causes for u cerationThe class c presen a io isa deep ulcera ion wi h an mage - 8: Pyoderma

n amed border that over gang e o um

ha gs the u cer Trea i g he colon zed bacte a usual ydoes no he p Pa ie s o en complai of pai ou of propor on o the cl nical appeara ce of he lesio . Pa hergy

he appearance of u cers or esions at sites of cu a eousauma is a common phe omeno .

I id opa h c cases 51line treatme s cor icosteroidsO herw se treat the under y g d sorder.

W T YNDROM

Sweet syndromeis a in amma ory d sorder tha is alsoreferred o as acu e febri e eutrophi ic dermatosis. t maybe d opathic or assoc ated with a under y ng disease(mos common y AML) or med catio (e g GCSF)Pa ien s haveh gh feverand pai red plaques� I chi d ame er ypical y o he upper extrem ties ru k eckand face. A sk biopsy shows a de se bu benignneu

rophi ic n lt a e ike in pyoderma ga grenosum a dBeh et's pathergy the les ons respond rama ica y o corticosteroids. Potassium iod de and colch c ne may a so beused as I st ine age ts

V AM N D F N

V AM N M N RAL D NDe cie cy of B12 fola e or ac n may cause d sehyperpigme a o as we l as ha r a d na l cha ges

N aci de c e cy resu ts in pellagra (remember the3 s:ermati is (pho ose s t ve areas) arrhea and emen

tia). son azid and carc o dcan also duce pe agrasymp oms. Iso az d is a compe it ve nhib tor of nico nam de-adeni e d uc eo ide ( aci precursor) anda so impa rs pyr dox ne fu c o ng wh ch is essentialfor niaci sy hesis om tryptophan

Tryptopha ca be metabo zed o ac n or sero o iby 2 separate pa hways. I carc no d mos of he

tryptopha s d verted o the product on of sero oninleav g the patie t at risk for niacin de cie cy.

Zi c de ciency causes an rr ta eczema oid redrash tha has a predilec o for per or cia (perioral,periocular anogeni al) a d acral areas (hands and fee ).Iro de ciency is commo y assoc ated wi h ha r ossand frag e ongi ud na na r dges

V tam n C de c ency can resu n fo licu ar hyperkeratosis espec a ly o he pos erolateral aspec of he

arms resemb g keratosis pi aris The hairs wi h n heseplugged fol cles become curled resul ng i "corkscrewha rs. Perifo cular purpura deve ops as the diseaseadvances

K N NF ON

BA T R AL K N NF T ONMuch of he fo ow ng and all treatmen s are coveredmore y in fec ious D sease Book.

Erythrasma is a well de ed red esio wi h someslight scali g It s usually found n he ax lla groinand toe webs. nobese women s seenunder thebreasts Gram posi veC b c u u uis eque t y sola ed from the esion (espec ally a eri has become scaly or macera ed).DDx: nea crurisC ,and er r go (a rr ta dermati is fou d i

he ski folds of obese pa ie ts) D ag os s Eryth asmauoresces br ght red(a tr bu ed to coproporphyr n III)

w th the Wood s amp (u trav olet l ght) Treat wi h benzoy perox de or top ca erythromyc n+/- a " azo ea fu gal cream severe cases oral er hromycin ortetracycli e may be used

l Impetigo: u us byfar the mos common causeof mpe igo which s a s asan e ythematous vesicu arlesion ha qu ck y becomespustu ar and crusty( honey co ored crust )Impe igo is high y contag ous a d pat en s ge era lydo appear system cally mage 9 B lo impe igo

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Q� uiPyoderma gangrenosum is associated w th w atsystemic il ness?

• How does zinc de c ency manifest on the sk n?

What 2 organisms can cause impetigo?

How does SSSS d f e om tox c epidermalnec olys s?

• C a acterize the es ons o d sseminatedgono rhea.

ill. The face and exposed areas a e most common ya ected. Methicil in- esistantt phyl c cc r( A ) is the cause of manyco muni y outbrea sofimpetigo. When impetigo, an infection of the epidermis,extends into the de mis, it is called ecthyma T eatmentis covered in Infectious Disease, BookI.

Bu ous impetigo usually occu s in young chi dren< 2 yea s old and p esents with the acute onset of la ge,

oose u lae (mage 12-19). n exotoxin/exfo iatin toxincauses c eavage of the epidermisStaphylococcal scalded skin syndrome (SSSS)p ma i y a ects new o s and child en <5 years of age;it rarely a ects immunocomp omised adults Patients with SSSS p esent withten er , red, peeling s in due toci cu ating toxins om oca ized staphin ection or colon z tion, gene a y occur ing at a non-skin site (sinuses;umbi icus in infants). Skin changes are simi a to those

seen in toxic epidermal nec olysis (noninfectious; athe ,a si e e ect o rugs), so consider it du ing the wo upThe skin in SSSS separates muchore su er ciallythan in toxic epidermal nec o ysis. he peeling skin iscaused y a similar exotoxin o exfo iatin toxin as seenin ullous i petigo ( oca ized fo m of SSSS) howeve ,it c rculates syste i lly in SSSS T eatment inc udesde idement of necrotic supe cia epidermis, topicalanti iotics fo bul ous impetigo esions, and o a anti iotics fo more severe/widespread disease.Toxic shock syndrome (TSS): r and pyag are the causes of TSS TSS presents with ab uptdevelopment of feve ,hypotension, and multio gansystem fai ure. Patients have a di se painless macu a e ythrode ma ("sunbu ) ash (acute·phase)followed y desquamation of the palms and so esduring the conva escent phase. atients a e commonly< 30 years of age, and mucosa invo vement is typicaIn contrast to st eptococca TSS, ood cu tures a eusually egati e. Treatment inc udes supportive ca e andsystemic antibioticsFolliculitis (in ammation of the fo icle) andfurun-cles (deep fo icu itis or " oi ) a e typica y caused y

r .Be aware that follicu itis associated withhotb is o en caused yPseudomon , notstaph.

© 2014 MedStudy

SK N NFECT ONS

(Group A Strep)Impetigo: Group A strep is a cause of impetigo a skininfection con ned to the epide mis so see ra ove.Ecthyma sta ts as an impetigo and then ecomesdeeper ,causing sha low ulce ations.Erys pelas is an explosi e su r cial infection(o encaused y group strep) that is co ned to the dermisand spre s uic lyt rough s n l mphatics( mage 12-20) The eis a clearly e rcatedarea of redness that iso en pa pable, indicatinginfection. It usual y starts

om a supe cia abrasion, ypica ly aroundthe cent a face withe thema and swe ing.L ph ngitic spre with ed st eaking is seen.Necrotizing fasciitis is ainvolving subcutaneous fat and fascia. Un ike erysipelas, it does not have a distinct border and can be di cultto diagnose ea y. he e are 2 typesype I, themostcommontype, is apoly icrobial infection(inclu inganaerobes) seen in immunocompromised patients, suchas diabetics.ypeli is genera y caused y g oup st epor MRS and most common ya ects ealthy in ividuals The RI EC score is a he p l too to use whenthe e is conce for nec oti ing fasciitis. This is asurgical e e ency, and there is ahigh or li r teeven with app opriate medical and surgica inte vention.Scarlet fever p mari y p esents in chi dren withpharyngitis andsc rlatina a ne, ed, sandpaper- ikerash that is mo e p ominent in skinfolds (Pastia's lines) andinvolves the and ex emities, ut spa es the pa msand so es. "S w rry " a so co only presents inthe acute phase. Du ng the conva escent stage, desquamation of the palms and soles occurs.Streptococcal toxic shock syndrome (TSS)causes symptoms simi ar to staphy ococca TSS(descri ed above) T eatment is with IV penicillin

(P )+ clindamycin +/ IVIG. In contrast to staphylococcal TSS, b ood cu tu es are usuallys ti eStrep throat PC is far and away the best treatment foa known group st ep throat infection. Give o al PC(x 0 days) or IM en athine PCN. Givee ycin forPC a le gic.Cli yc is o en adde to PC whenthe e is serious infection (to dec ease toxin p oduction),such as necroti ing fasciitis o toxic shock.

Gonococcus and MeningococcusDisseminated gonococca ect ocauses a few

(typically< 12) hemor hagic pustules on the ext emities,

12-11



12- 2 K N NFECT ON

Image 12-21 Ecthyma gangr nosum

Image 2 22Ro k Mountain spo ed feve (medial foo )

o en a ound the joi ts. Cult re of the sk n lesions istyp ca ynegative. Cult res sho d be taken from the

nitials te of nfection (o al m cosa, cerv x, u ethra, orect m), beca se t ey ave a m ch h g e y eldMeningococcemic sk n s gns star as macu a o petec iallesions and evolve to large purp ra P rp ra lminanscons sts of pu p a, ecc ymoses, a d con e t map-likeg ay-to-b ack ecrot c sk n les ons. It is assoc ated w t

severe infectio a d di se i avascula coagu at o .

Pseudomonas

causes a va iety of sk n i fect ons. t sthe ca se of"hot tub foll c itis No mal c lo ne evelsmay p event the poss b l ty o g owth of nfection w tht s organ sm T e p st les from ot t b foll c t sa e sua ly a ound t e b ocks and t ghs a d resolvew t o ttreatment n 1 week. 5% acet c acid compressesca be used fo symptomatic re e Pseudomo al sept cem a ca ses smal , dark-ce tered (nec ot c) pap es.In a ve y ll,e trope icpatie t, th s papule ca evolve

to ecthyma gangre osum a necrot c cer w th anerythematous rim(Image 2-2 )

A i l Bit r , E k ,a d r co e

cause nfect o f omdog and cat bites. Huma b tei fectio s a e caused bymult p ebacter a a d ca causeseve e i fect on.Treatment: C ean and lavage well and g ve AM/CL(amox cill n-c avulanate) asprophylaxis a dtreatment

Don't fo get tetan s vacc ne f due.

RICK TTSI L SKIN NF CTIONS

Rocky Mount in spotted fever is us ally eralded bysevera days of fever. he the patient gets sma es o s,w c p ogress dis b t o omperipheral to ce t a(centripetal) a d n pe ommacu atopetechialto pp ric. As yo can see ommage 222, the skin d ngscan be deceiv ng y nondescript See nfect ous sease,Book I, fo t eatment.

S ROCH T SKIN INF CTIONS

The st stage ofLyme dise se is o e associated w the hema m gra s(Image 2-23). Typically, t is is a slow y

(ove about week) e larg g, a nular e ythemato s raswith a c ear ce ter ( ooks ke ab seye. Occasio a y, thecente is not clearSyphil s: Acha cre(pai lessulce at site of oc lation)

nd catespr marysyph lis. D sesca i g papu esot epa ms and soes, tr nk, pe s, a d mucosal su facess ggest seco dary syp is, as does condy oma lata.Gummas occu nter arysyph l s, a d arepai ess,

d rated, od ar, or cerat ve les o s.

VIR SKIN INF CTIONS

Wa (ve cae) a e caused by a y o e of mo e t a6 pes of h ma pap lomavir ses( PV ), and theyoften reso ve spon a eous y. owever, beca se of theiu s ghtly appeara ce, pat e ts s ally equest treatme t,whic typ ca ly involves some fo m of t ss e dest uct o .

• Ve ruca vu gar s is the common wa ; t eat it w thl qu d troge , top cal acids, C0 lase , etc

•

Verruca p a a is the at war .• Ver ca p a ta is is the p a ta war(Image 2-24)

t a treatme t may cons st of a stro g acid(tr c o oacetic acid), concent ated ( %) sa icyl cac d p aste , l qu d t ogen, o aserCo dy omata acum nata a e a oge tal wa s. T eyare o en caused by HPV 6 a d 11. They are somet mes caused byPV 6, 18, a d31 the o coge c

PV types (assoc ated w t cancer of the ce x)Treat them with podop yll , ichloroacetic acid,

iqu d n trogen, or C0 ase . Podophy i s te atoge c, so dootg ve t topreg a tpat ents. A newet eatment for co dy oma ac mi at m is top cal

m qu mod (A dara®)[Know.] Mo l sc m co tagios m is ca sed by apoxv us It co s sts of smoot , umbi icated, pearlypap es (mage 2-2) It usua y occ rs c i d e(anywhere o the body except pa ms a d so es), b t youmay a so see it n the pe v c area of sex a y active you gadu ts a d it scommon i AI S pat e ts(can be sexa y t a smi ed) o lusc m con agiosum o e eso vessponta eo s y except n immunosupp essed patie ts(e.g., AIDS).

Image 2 23E1 hemamig ns

Image 12 24P anta wa /

© 2014 MedStu y - Piease Repo t C pyr gh Infr geme s tc pyr g @meds dy.c





What is the s gnif cance of inding a les on oecthyma gangrenosum on phys ca exam?

Which ant biot c s used to rea a cat bite?

Character ze the rash o erythema m grans.

Mo uscum con agiosum, if seen n anadu should ra se your susp c on or whaimmunode iciency?

How does he dose of acyclov r d er whenthe drug s used to treat var ce a and herpessimp ex in ec ons?

[K ow.] Measles ( ubeola) has several stages Theprodromal stage asts 3 4 days with feve , mala se, s nusd scharge, and a hacking co gh. Koplik spots (pathog

nomonic) o en appea on the palate f om I to severaldays befo e the onset of ash. As the Kopl k spots beginto disappea , a ed maculopapular ash starts on the faceand behind the ears and qu ck y spreads down a d andoutwa d with the densest concent at on of es ons f omthe face to the sho lde s. The palms/soles a e a ectedlast. Lesions g adua y fade in orde of appearance andmay have some desq amat onRubella ( German meas es, 3-day meas es) is ben gnexcept when it occurs in p egnant women. he ash

s s milar to meas es but lasts only 3 days Congenitalrube la results in a va ety of se io s bir h defects:

hea ma fo mations,oc a defects,

• m c ocepha y,intellectual disabil ty,

• deafness,TTP, andbone p oblems.

Varicella zoster virus (VZV) ca ses two d seasesch cken pox and herpes zoste (shing es).Both diseasespresent with vesic es on an e ythematous base. He pes

oste is reactivation of V V in a pe son ho has hadchicken pox.

hicken pox nc dence is decreased now d e tooutine vaccinat on of child en Rash is in t a ly mac

lopapula and rapid y prog esses to vesicles and then toscabbed les ons. These tend to come in "crops ove4daysHe pes zoster g o pedves cles along a de matome w th focal pa .O der age and mmunosuppress on are riskfactors f g ven with n7ho s of onset, antiv raltherapy w th acyc ovir,

© 2014 MedStudy

mage12-25:Molluscumontagiosum

SKIN NFECT ONS

famc c ovi , o valacyclovi dec eases the length of thed sease and the ke hood of p og ession to post hepetic neu a g a A herpes oste vacc ne is app oved aspr mary p event on for a pat ents> 50 years of age andthose who have a eady had an ep sode of her es zoste

n the mm nocomp omised, t eat both ch cken pox andherpes zoster with ntraveno sacyc ov athi e dosesthan what s used to t eat he pes simp ex nfect ons.

FUNGAL IN ECTIONSDermatophytes ,and ca se s pe c angal infections(o ter ayer of skin) and a e named accord ng to the siteinvolved

• T nea capitis (sca p ngworm)Tinea co po is (common ing o mI age 12-26)

inea c u is ock itch)T nea ng onychomycos s (nai s,mage 7)

inea ped s (athlete's foot,mage 8he diagnos s is o en madec n ca y, b t can be

con med ith potass um hydrox de (KOH) test on skinsc apings, which revealsbranch ng amento s hyphae

andidiasis s adeepe ngal infect on that ca ses edpatches in inte rigino s a eas Candidiasis of the mouth(thrush) ca ses white sem adhe ent plaques on thetongue and mucosa. Un ike hairy eukop akia, thesecanbe sc aped o . Vag nal candid as s has sim a plaquesw th cheesy d scha ge.Most f ngal skin nfections a e cont olled bytopicaant nga c e s. M con ole, c o imazo e, and topicaterb na ne ( amisiJ®) a e sed.T nea cap t sand ine

ng ium(onychomycosis) are except ons and m st be

mage12 26: inea corpo i mage2 27 i ea u guium oronychomyco i

mage2 28 inea pedis (athlete' foot

12-13



12- 4 K N C NCER ND K N F ND NG

Image 2- 9 Tinea versicolo

treated wi horal ant - gals. Ti ea cap t s requ res oralgriseo vin, erb a e, or i raconazo e. Trea ineau gu um wi h systemic terbina ne, tracona ole, or

ucona o e. (pi yr as s versico or) s caused by

Malassezia globosa or Malasseziafu r ( age 12-29).Sk fect o resu ts in hypopigme ted or hype igme ted (depe d g o he pat e 's ski o e/co or)spreadi g macu es usua y o the upper torso and upperarms. KOH sk scrap g:spaghetti a d m tballs.Treatme : m dazole creams, selenium sul de or ke oconazole shampoo, a /or ora itracona ole.

P T T O

L ce ou breaks occur schools, nursing home commut es, a d camps.

H (Pediculus humanus capitis) The recommended pes cide-based topical reatmen (app ied to hair

a d le on for 10 m nutes) is over- he coun errme ricream I% (Nix® cream ri se) because k lls both licea d eggs. It is approved forh d l ce o y. Other op calmedica io s that ca be used i clude % i dane shampoo (2" i e because of eurotoxic y) a d pyrethrin+p pero yl bu oxide (R D®, e c ) These do not kil the eggsand requ re another reatment a week ater I the U S ,

is e is owing agai st all commo pest c de-basedpreparatio s. Remova of nits (eggs) w h a e-toothedcomb fol owi g he appl ca io of a l trea me ts iscfor success l rea me t.A ewer reatmen ha is as e ec ve as RID bu co tai sno euro ox c pes c des isnzl al oho lotion(Ules a ). It kills by su ocat g he lice It s safe ich dre older tha6 mo hs.Treatment forr is nt head lice:Malathion s a h gh y e ective prescript onage ve e tin (yes, the drug tha k s hear wormsin dogs; S romecto ®) s he s rongest drug i is give

as 2 doses week apar . t s co sidered a 2 l eal e a ive o malathio

(Pediculus humanus corporis; [ mage 12-3])ve c othes and are o the body o ly whe feeding.

Treat ent s bath g a d care llaunderi g of clo hes

a d bed i ens.%

indane o on or pyrethrin+

p pero y

bu oxide are used if bodylice are found on heseams of c o hi g.P (Pthirus

pubis): The crab ouseis e ransm t

Image -30 Body lou e t and can also nfectthe eye ashes. Crab l ce

are ransmi ed by fomi es. Itch g s the moscommon man festa io of infec ion. Exam may revealb u sh macules (maculae ceruleae) he groin area.Treatme t is sim ar to tha of head l ce Use top capermethrin or pyret in+ p peronyl bu oxide. Washbedding and clothing in ho wa er a d use a ho dryer.

s caused by a m te(Sarcoptes scabiei) thau ne sinto he sk to lay eggs( mage 12 3) I is

spread byskin- to sk n on t s not live> 48 hourswi hou a host! shou d be considered a yo e wi hu exp a ed general ed tchi g, par icu arly hospi al

i ed or i sti tio alized pa ie s. D agnos s s made bym croscopic visua a io of the m te, feces, or eggsfrom skin scrapings.Treat w th5% permethr applied o all areas of

he body from he head down a d washed o a er8 4 hours.A seco d dose i 7 days is recomme dedUse oral vermec for severe or reca c ra t cases witha repea dose i 2 weeks. i dane has CNS oxici y, sodo ot use during preg a cy, in infants, or in you g ch ldre . Permethri (Category B) can be used preg ancy.Prec pi a ed su r s a so co s dered safe n preg ancy,but may be less e ec ive. Wash a l line s hot water.

Image 12-31: S abie tunne

SK N CANCER AND SK N F ND NGS

(BCC) arises om epidermabasal ce s and is the mos common form of skin ca cer,especia ly inCau asia s( mage 12-32). The usua ypeof CC is characteri ed by transluce t pearly papules,o en w th telangiecta c vesse s. spreads byl aexnsion and, when large e ough, gets a" ent aten appeara ce.

© 2014 M p p h f p @ .





ui

• What are the t eatments fo head lice? Whattopica treatme t is not pest c de-based?

• What is the metastatic potent a o basa cellcarci oma?

On wh ch areas of the body does squamous celcancer have the highest ate o metastas s?

• Fo me a oma, what measu ement is mostmpo ta t whe determi i g prog osis?

BCC is caused by ultraviolet (UV) rad at on fromsun exposure. t istyp cally ound onsun-exposed areassuch as the ead

and neck, but it mayappear e sew ere.

K ow t at t e metastat c potent a oBCC s < 0.1%BCCs are typ cal ysurgica ly removed. I m a ge 12 -3 2 : B as al ce ll carcinom a

q amo c ll carc oma (SCC): From kerat n z ngepidermal cells, s c occurs espec a ly infa r-sk nnedpersons and on sun-exposed areas, ike the dorsum o

ands, orearms, ears, and lower l p( ag e 2-33) Incontrast to t e ow metastat c potential o BCC, SCC hasa 0.3 5.0% metastat c potent a and even h g er when

t appears on theear ( %) and ower p( 3%)! T emetastatic rate o recu r ng tumors s 30%, and t e ratein SCC orig nat ng romscars approac es 40%. Ot err sk factors assoc ated w th a h gher rate of metastasesinc ude size > m, depth > 4 mm and Clark eveIVor Y, poorly d erent ated les ons, and immunocompromised hosts (transp ant pat ent).s are general yremoved surgica y

Act n c keratos s sprecancerous es ons t at candevelop into SCC. SCC in situ Bowen disease) s a non

nvas ve form of SCC. Both of these types of es ons canbe treated with c yot erapy, top ca 5- ourouracil, top

ca m quimod, and surgical excis on.

Image 12-33 Squamous cell carc noma of the ha d

© 2014 MedS y

KIN CANCER AN IN FIN NG

Image 2 34Mali an mela oma-s pe1 al p ad ng

la oma Th s a so tends to occur more common y nfair-skinned peop e, espec a ly t ose who had severe sunbu s n c ldhood ( age 2 34). There has been a 300%

ncrease in ncidence of me anoma in t e past 40 years.Ot er r sk actors are dysp ast c nev (descr bed be ow),a fam ly histo y o melanoma, a hig number o ord narynev , a congen ta nevus, and mmunosuppression. It sa most always comp etely curab e f caug t early enough.T i " DE w en assess ng a lesion t at m g t bemal gnant me anoma

symmetryorders are rregu arolor var ation

D ameter> 6 mm is susp c ousElevated or volv ng es ons are more suspicious

Prognost c factors inc ude age (< 50 years) of thepat ent, ocat ono the lesion (on t e t u ), and (mostimpo tant) the depth o the es on. Les ons < 0.76 mm n

depth have 99% ve-year su v va ; t ose> 3.6 mm have<50% ve-year su v val.

f the lesion is < 0 6 mm, you may sa e y exc se themelanoma w t a 1-cm, tumor ree marg n. (Previously,a 5-cm margin was recommended.) Lesions over0 76 mm n dept shou d be referred or evaluat on for asent ne ymp node procedure.

[K ow.] ark-sk nned nd v duals can a so get melanoma T e es ons tend to be n acral areas (pa ms, so es,and nail beds). Hutch nson na s gn s an impor ant cl nica c ue to subungua melanoma, wh c is typi ed byextension o brown or b ack pigment from the na l bed,

matr x, and na p ate to the adjo n ng cutic e and proxima or latera nai o ds.

D pla c v are "odd ooking mo es and mayeven look ikemelanomas(Image 2-35)

ey are markersor a propens ty

to deve op ma ignant melanoma.However, mostme anomas ar sede novo and notin a preexisting

Image 235: Dy pla i evus

12-15



1 -16 BL STER NG LES ONS

nevus. Removing all moles doesnot prevent me anomadevelopmen S andard of care is c ose ollow-up andmonitoring i izing photographic documentation Ia patient wit a dysp as ic nevus as2 re atives wi hma ignant me anoma e patien as a 300x chance oge ing ma ignan me anoma!Mycosis fungoides and S zary syndrome are t e mainforms of cutaneo s T ce ymp oma. Mycosis ngoides can be mis aken or psoriasis or ec ema S arysyndrome as per phera b ood invo vement in addi

ion o t e skin manifes a ions and is associated wit apoorer prognos sPaget disease of the breast is some ing o considerany ime there is apersisten (despi e reatment) uni atera oo ing ec emato s p aq e in hearea o e areo aIt is vi a ly a ways due o underlying in rad c al breastcancer and is due o re rograde ex ension o t e t morBy far t emos commoncauses of an ac e ec ema

ype ras on an areola arecon ac der atitisor skin

i i ation Especia ly consider Page disease if here isnoresponse to reatmen

Peutz-eghers syndrome consis s of mu tiple hamartoma ous po yps+ me anotic pigmen a ion ( entigines) ont e ips+ b cca mucosa Even thoug hese po yps arehamar omas t ere is s illsome risk o cancer becausean occasional adenoma occ rs. Note ha ealthy dark ypigmen ed peop e and hose wit Addison disease may

ave similar intraoral dark spo sGlucagonomas (secre ing pancrea ic alpha ce umors)secre e excessive amounts of g ucagon and can causea bee red ton e (t ink G ucagonoma= G ossitis)

ang lar c eili is and anecro y icmigratory erythematous ras Pa ients with glucagonomas may deve op the"4 Ds": iabetes DVT epression and ermatitisWeigh loss is charac eris icMetastases to the skin: T e 4 cancers a moscommon y avec taneous me astasesare n cancer

cancer me anoma and breas cancer in womenMacroglossia associa ed wit pinc p rpura ( u uraand ecchymosis deve op a er pressure or rubbing);s rong ys gges samy oidosis

Image 1 6 P phyria cutan a arda (PCT

BLISTERING LESIONS

Porphyria cu anea tarda (PCT) ( mage 12-36,mage 12-37) is hemost com on ype opo p y a PCT

ca ses yperp entation tense b iste sin s n-exposedareas milia skin agility and increasedacial hair PCTis ca sed by a congeni al or acquireddecreased activity ofuroporp yrinogen decarboxy ase ( RO ) w ich a owsa b i dup o p oto oxic porp yr ns in t e skin Symp omscan beinduced by ingestion o es o en or a co o anypa ien s ave associatedepatitis C Lab res s s a ys ow an increased serum Fe A T and AST To screencheck or increased ur narycop opo p yrinsand oporp y ns Patien s may avedark or pink neTrea ment is t e same as or hemochromatosis reg arph ebo omies ron may inhibi t e activi y of RO Bydecreasin iron stores wi phleboto y he ac ivi y oURO increases res ting in porp yr ns being me boli ed q ick y hus preven ing hem om bui ding p in

e skin An imalaria s (hydroxychloroquine) are alsoe ective by he pin to mobi i e por hyr ns T ey are ypical y used when p ebotomy is con raindica ed. PCT dueto HCV resolves wi h trea men o epa itisPorphyria variegata (variega e porphyria) is alsoknown as So t A can porp yr a is ca led var ega ebecause pa ien s can present in a var ety of ways T eycan have ac te episodes like acu e intermi en porp y a(A P) c ronic skin manifesta ions ike PCT or bo h

a ien s may get b is ers on sun-exposed areas and havemechanica agi i y of he skin T ese pa ien s may a sohave abdomina pain po yne opat ies and mentadist rbancesT e symp oms are d e o a de ciency o protoporphyrinogen oxidase whic leads to he b i d- p of excesspo yrins. Trea men of ac te a acks is he same as orA P l cose and ema in l cose and hema in t eoretica y work by in ibitin A A syn hase and preven ing t eacc m a ion of toxic precursors i eren ial diagnosis

o e hat A P presen s similar y to variegate porp yriaexcept wi ou the skin changes PCT (above) presen s wi h t e skin changes bu withou t e neuro/mentalc angesEpidermo ysis bullosa Patients ave b isterin a erminor skin rauma caused by congeni al s r ct radefec s o he skin e skin sp its at the junc ion of

mage I 2-37: P ph r a cutan a tarda (PC with bl st r

© 2014 MedStu y-Pieas R po Copyr ght Infr geme ts lo copy g @ e stu y.com





o What are he main fo ms of cu aneous T-cellymphoma? Which has the worse p og os s?

o W a are t e "4 Ds" hat pat en s wi hg ucagonomas deve op?

o Charac er ze he skin findings associa ed wipo p y ia cu anea a da.

o What ype o hepat tis s associa ed w hpo phyr a cu anea ta da?

o What s he pa hognomonic es on or eryt emamultiforme? Which virus s often he cause?

the epiderm s and he de s. There are many d ere tclass ca io s All class ca ons a e ge et cal y ansm t ed, a d each s due o a spec c gene mu a o hemajo c ass ca ions i clude ep dermolysis bullosa s mp ex (EBA), wh ch a ec s the kerati ge esKRT5 and

T 4; u ctio a ep de mo ysis bullosa (JEB), whicha ec s the lamin n a d co age ge es; and dystroph cepidermolys s bullosa (DEB), wh ch a ec s he co agenV gene

ikolsk sign Slight a eral pressu e on he ski causess oughi g of he ep dermis s posi ve i pemph gusvulga s, tox c epide mal ecrolys s ( N), a d staphylococca scalded sk n synd ome (SSSS). s nega ive inbu ous pemph goid

llo s p mphigoi causes ecur e crops oftense,

deep, i actbliste s (I 12-38). Older ndiv dualsa eusually a ected he d sease p ocess is c ass ed as aype hype sens t v eactionand ca appea s m lar

to u ca a whe t sta s has an au oimmu e etiologywith format o of a -basement memb a e an ibod

es Precipi a i g events include exposu e o UV light,ad a ion herapy, a d cer a n d gs includ g ose

mide, buprofen, captop l, and penicillam ne. he apyi cludes topical (m ld d sease) a d system c co ticostero ds and mmu osuppressants.

Image -38:Bu ous pemphig d

© 201 MedStudy

P mphig s v lgaris(I e 39) is aau oimmune d seasew th aep de maant bodies agai s desmosomes. h s causesacan ho ys s ( he separa ion of epidermacells f om each othedue to dec eased cohes on), wh ch esu s

the fo mation ofarge, super cia ,

loose bu ae hat peeo and eave denudeds O a mucosa

BLI TER NG ON

mage 39Pemph gu vulg r

involveme is common, and a y cuta eous a ea can bea ected reatme of pe phigus vu ga is is s m la otha of bul ous pemphigo d

r h ma m l iform co s s s of we -de ned es o svaryi g from a u ar to arge oid(I a e 2-40).Palms a d soles are eque tly i volved, and mucousmembranes may be a ected he " a get lesions arepathog omo c fo e y hema mult fo me t is caused byherpes s mplex virus,Mycoplasma, a d drugs ( SA Ds,pe c l i s, e c ). ea men involves an m c ob al therapy f a causa ive o ganism is found (e g.,Myco lasmaor removal of an o end ng med catio . He pes assoc a ed M s o e ecu rent, and pa ents may be e tf om suppressive a t v a he apy

v ns ohnson sy drome is a severe fo m ofery hema mu t fo me, a d some au hors co s der i paof the spec m of oxic ep derma necro ysis. s usua ly caused by a dr g and, by de n io , a ec s< 0% ofthe body su face a ea (BSA) eatment equi es emovalof the o end g drug and suppo t ve ca e. Co t costero dsa e controve sial and should be used fo o y a ve y shor

me, if a a .

oxic pi rmal n c o sis ( EN) s co s de ed a vara t o mo e seve e form of Stevens-Johnso syndrome

t s caused by a hyperse s t vity reac on to a d ug(e.g., al opu o , a t co vulsants, NSA Ds, sulfa,and an biot cs) L e SSSS, i esults i a pee i g

Image :E ythema mu t e

12- 7



ROUND LESIONS

Image - :Derma itis herpe ormis

or exfol at on of large areas of skin but it occurs at adeeper level than SSSS By de n ion i a ec s> 30%of the BSA. Treatment requires remova of the mplica ed drug aggress ve sk n care and suppo tive care inan ntensive care bu un t. Pa en s w h toxic ep dermal necro ysis do poorly, and mortal ty can be as h ghas 40%.

ermatitis he petifo mis (DH is a sk n d sease wherepruri ic ves cular les ons appear on theex ensorsur cesand m d- o lower back. Les ons are caused by gA deposi ion n he de mal papi ary t ps( ma 12 41). Giventhe extreme p ur tusin ac ves cles are o enno apparen I is associa ed w th celiac disease (g uten-sensi iveenteropathy) D and cel ac d sease can bo h be reatedw th a gluten ee d et. A e ativelydapsone can beused to treat D but s not e ective for cel ac disease.

R UN LESI NSG anuloma annu a e is an id opa h c annular r ngworm l ke les on wi hou scal ng which

ypically appears on thedis alpo tion of he ex remi es(Ima 1 -4 ). I o en occurs nch ldrenand youngwomen It usually sse f-l m ed d sappearing n mon hs

o a few years. O her trea men opt ons inc ude op cal orin ra es ona cor cos ero ds.

ummula eczema cons sts of small circular (nummular = coin shaped) prur ic lesions ha are morecommon on he extremities and are o en assoc ated w h d y skin and a opy. They are ve y

common in he elder y and have no patho ogics gni cance. Ru e ou funga infection. Trea w th mid tohigh po ency opical steroids.

mage Granuloma ann la e

Pity iasis osea isa rash common nch dren and youngadu s. Its e ologyis unknown bui may be infec

ous n or g n(poss b y humanherpesv rus6 or 7).The d sease isse fl mi ed yp cally

ast ng4-8 weeks

Image 3Herald patch of pi riasis rosea

mage Pi y iasis osea; gene al zed ash

A hera d pa chprecedes subsequen p tyr as s roseaes ons by1 2 weeks ( ma e 1 -43 ) This patch is

some mes con sed w h nea corpor s(Image 1 - 6on age 1 -13) Subsequently sma l p ur ic papu osquamous ova esions with the long axis parallel o skin fo dsand rib nes deve op in a "Christmas ee pa e usua yon he runk (ma e 12 44). All he les ons typica ly havea c l are e of sca e at the marg n Trea ment s symp

oma c No e: T nea vers color (p yrias s vers color) hasno re a ionship with pi yr as s rosea

ica ia (hives) are ra sed p uri ic we s on he skintha can be he man fes a on of an allergic reac ion. The

esions may have asmoo h or irregu ar border. Aspirin isa common cause of u ticaria They can be a manifesta onof a connec ve tissue d sease viral nfect on or may be

d opa h c. Trea men s pr mar y with an ih s am nes

PIG ENT C ANGES

Vitiligo is an auto mmune disease wh ch causesdes uc ion of melanocy es resu ing in depigmen a ion( ma e 2 45) usually occurs in healthy personsbu rarely t may a so be pa of apo yglandu ar au o

mmune(PGA) syndrome Wi h a PGA here may beany of he fo owing:OM, au o mmune hyro d d sease(hyper or hypo) Addison d sease/adrenal nsu ciency

© 2014MedStudy-Piease Report Copyr gh Inf geme s o copyr gh @meds dy.com





• With what Gl disorder s dermatitis herpet form sassociated?

• What s cha acter zed by a "Chr stmas t ee

pattern and a hera d patch?• What skin finding might you see with a

po yglandu ar autoimmune deficiencysyndrome?

• Hyperpigmented areas of the axilla a eassoc ated with what unde lying disease states?

• What diseases are on the short list of causes ofblack lesions?

• What is the signif cance of e uptive xanthomas?

hypoparathyroid sm, and pe CIOUS anemia. Anytime

you see a pat en w vi ligo, th n of t ese poss bil iesand screen appropr a ely!

uberous sclerosis s uncommon and au osomadom nant s associated wi h se zures, inte ec uadisabi ities periungual bromas, and hypopigmented(ash-lea macu es You can see hese macu es best witha Wood's amp Adenoma sebaceum manifests in thesepa ents as numerous mid-facial papules, w ich areac ually ang o bromas

Caf au laitspots are brown macules hat occurn assoc a on wi h neuro bromatosis ype (von

Reck nghausen disease) and Mc une Albr gh d sease

To a lesser degree, caf -au a spots occur n peop e w hno d sease( -2 spo s are nor a and common) n neuro broma osis,78%of patien s ave> 6 spo s and 95%

ave at least one spot> 1.5 m n Mc une Albright d sease, he spots ave a more rregu ar out ne.

Acanthosis nigricans is hyperpigmented sk n wa h ckened, ve ve y appearance, noticed most y in t es n fo ds( ma 4) nvo vemen of t e ax a

s common y shown as an examp e trare y s fam lal A t ough you typ ca y see s inobese pa ien s

mag 5 V iligo

© 2014 MedStudy

it is a so associa ed wG cancer, many endocr nopa h es and severaau oimmune problems

Malignan acant osisnigricans is severe and

progress ve and s usua yassoc a ed w h gastricadenocarc noma

PRURITU

Assoc ated endocr nopah es nc ude ush ng

d sease, hyper/ ypo yroid sm, acromega y, andd abetes mellitus veruseof niac n may a so cause

mag 12-46: Acan h sisnigricans

acanthosis n gr cans

Di use hyperpigmentation may occur in primarybil ary sc erosis, sc eroder a Addison d sease, emochromatos s (a grayish/bronze colora on), and with euse of e cancer drug busu fan her causes nc udeporphyr a cu anea tarda, ma absorp on and/or Wh pp esyndrome, pel agra (n ac n de c ency), B12 de c ency,and fola e de c ency heck for metastat c melanoma in"slate b ue pa en s!

Hyperp gmen a ion insun exposed areas can be causedby am odarone, porp yr a cutanea arda, and phenothiazines. Hyperp gmenta ion is di use bu darker insun-exposed areas in pellagra, b liary scleros s, andsc eroderma. Metho rexa e can cause react vation ofsunbu

B ack lesions: ons der he follow ng w en you seeblack es ons:

Rh nocerebral mucormycosisAn hraxEct yma gangrenosumEmboli to dista extremitiesMelanoma/Len igoWarfar n skin necros s

PRURITUS

The mos common cause of ch ng n e der y pa en s

is dry sk n her causes seen across he age spectruminc udeHyper or hypo hyro dismMalignancy ( h n ymphoma especia y Hodgkin s,bu a so breas cancer)

ron de ciency (even if pat ent is not anemic)Po ycy hem a rubra vera (aquagenic pruritus)

ron c (but not acute) renal fa ureho esta ic ver d sease

Diabe es me li us



12-20 A DS RELATE SK N ES O S

A D RELATED K N LE ON

Al skin cond tions become more common n HIV/AIDS.AIDS-related les ons nc ude he fo owing: xerosis (d yskin), sebor e c dermati s ( n v rtua y all pat ents!),telang ectas as, e es s mp ex, erpes zos er fo iculi

s Kapos sarcoma (S), and oral cand dias s. Patientsw h HIV/A DS can a so ge condy oma acuminatum(HPV),mollus u ont giosum ( oxv us), and baci aangiomatos s. Bac la y angioma os s resemb es KS bu scaused by a gram-negat ve baci lus,Bartonella henselae(same et o ogic agen of ca scra c d sease)

Trea e sebor he c derma s with opica low-potencystero ds +/ an ant ngal shampoo.

T e follicu t s is usual y due oun ontrol ed HIVinfection, but can also be due to a yeast,Pi rosporumorb culare,or Staphylococcus aureus.Genera ly, treamen w h an iretrovira herapy mproves t ese ras es

f no organism s found, considereos nop i i folli ul tis(eos no h s seen on b o sy) which can occur inH V/AIDS

Ora " ai y leuko lakia( a e 12-9 on pa e 12-4)s a o ugatedtongue w hw ite les ons along e

s decaused by heE ste n-B v us in immunocompromised HIV pa en s. reso ves w h an retroviral

herapy and on phys ca exam, it canno be scraped ohe tongue.

Kaposi sarcoma usually presen s as< 0.5 cm, purplered/v ole , macular/papu ar es ons, w ch are genera ly

on en atedon ehead neck and lowe extremities It

s common n pat en s w hadv n ed V .He es zoster s o en refrac o y to trea men in patientsw h HIVIAIDS. Trea w h acyc ov r or famc c ovir. Valacyc ov r a been assoc a ed wit t rombot c

hrombocytopen c pu ura n the immunocompromised,so s no recommended.

D ssem natedC ptococcusinfection may m a e molluscum contag osum.

Image I - 7: Eruptive xanthomas in a diabetic

Image I 8Ne robio i lipoidi a diabeti or m

D A ET K N LE ON

Eruptive xanthomas are due o severe hyper rig ycer dem a They are o en seen in d abetic ke oacidos s.T ey a ear abrup y as ye owish red papu es over heextensor su faces and but ocks. These les ons resolvewhen e yperg ycemia s controlled (mage 12-4 7

Necrobiosis lipoidica diabeticorum can be associated w th d abetes n approx ma elyI 20% of cases

(I a e 12-48). It s a n, a roph c yperp g entedp aque at appears on thes ins. I is subjec o trauma andu cerat on and s t ough o be due o m croang opat y.

Diabetic dermopathy (s n s ots) are dark a rophicmacules; they are common and o en appear on esh ns. ey ave no c in ca s gn cance.

FOR FURTHER READ NG

[Guide ines in b u )

C P B

Baldw n HE. Diagnosis and treatm nt of rosacea: stat of thart J Drug Derma to/.2012 Jun; (6 :725-730.

Co F, Smi h RC a agnos s and manageme t ofidrad nitis suppurativa.BMJ 2013 Apr 23;346 121

Gi t r K, Krueger G, et a Atopic d rmatitis esu ts n intrinsic barrier and immune abnorma ities: imp ications o contactd rmatitis JAlle C/in Imm nol 2013 b131(2 300 3 3.

mec GB C inica p actic Hidradenitis suppurativaN ng/ J Med 2012 a 12 366(2 58 164

Wi kin , ahM, et a Standard grading syst m fo rosaceaor of th Na iona Rosa a So ty xp Comm

on th c assi cat on and staging of rosacea. JAmA ad

Dermatol 2004 un 50(6 ttp://www.ncbi.n m.nih gov/ pubm d/ 15153893?dop =Abstract

© 2014MedStu y-Piease Repo t Copyr gh Infr gemen s to copyr g @meds dy.co

http://www.ncbi.nlm.nih.gov/



http://www.ncbi.nlm.nih.gov/



Sakuma H, Maibach H . O y skin: an overvie .SkinPharmac l Physiol 2012 25 5):227 235.

Titus S Hod J Dia nosis and treatment of acne.m FamPh ician2012 Oct 5 86(8):734 740

Usatine RP. n activ Derma o o y Atlas. Departm n ofFamily and Comm nity M d c n of th Univers ty of xasHea h Sc ence Center 20 3. h p // de a as n

Am c n Acad my o A l rgy As hm and Imm no o yAm ican ollege o All gy A hm and Imm nology.Con act d rm titis: prac ice par m t r.A llergy t mlmmu l 006 S p 97(3 S pp ):S l- 3 . E a m n:

llerg sthma /mmunol 2006 D c 7 6 819.

Am ric n Ac d m of D m ology. l nic l Guid lin .Acn Guid lin s h p/ www. do duc ion/cl n calg id lines

Am r c n Ac d my o D m ology l nic lG d li .Atopic Derma iti G id l n .h tp /www. d.or g/ d c ion/ clin c l g idel n

P I G idelin of c r h di gno i ande m

of atopic d rm t t sPart Gu deline o c re for h m n m nt nd r mentof atop c dermati i with topic l h r pi

P rt 3 Gu deli of c for h m n g m n and r tm ntof a op c d rm ti hsy mic gent

P rt 4 Guidel n of c r the man g m n nd eatm nt o atopicderma i r n ion o nd hof adjuncti h r .

B ld H D l Ros o Q Rosac m dic m n gm nt gu d in . Am ric n Acn& Ros c Soci yh tp /w acne nd o aca.o g uplo ds/AARS_ Ro c G dlin s pdf

Schn id r ill S l. Atop c d rmiti prac icp ram ter updat 012.J All g Cli lmm nol. 013

b 31 2 95 9 e1 7

S r u S,Krowchu DP t l. G d n of c fo cnv lgar manag ment Amer can Acad m o D rm tology.2007. h tp:// a d.o Fil Lib ry/Glob n g tion/Edcat on and al car G d in Acn lgari pdf

ch n ld LF Kr ow i A a d nc d ecomm ndation for th diagno i nd treatm n o p diatr c acnPedi tr cs 0 13 131(Suppl 3) h tp/ p diat c. ppublicat o og/co 131/Suppl me t_3 S 63 ll pd +h m

M S

Gibson AM, Somm amp S . va uation and mana m nof oral l sions in he mer ency depar m nt.Emer Med inN rth 2013 May 3 (2):455 463.

Mays JW Sarmadi M, et al Ora manif stations of systemica toimmun and in ammatory diseas s dia nosis and clinical mana ment.J Evid B ed Dent Pract2012 S p; 2(3Suppl):265-282.

C S C S

Ahmed AM Pritchard S t al. A review of cutaneo s drugruptions. lin Geriatr Med 20 3 May 9 2) 527 545

Ha n JW, Ma ro CM, et al. m ing adverse cutan ous

d u eactions.De m tolC/ n 2012 Oct 30 4):695- 730 v

© 20 4 MedStudy

FOR FURTHER READING

Cohan RH, Dav npo MS al ACR manual on contrastm d a. ACR Committe on Dru s and Contrast Media 20 3http // acr or / /med aAC R!Docum n s/PD/Quali

ySa y/Resourc s/Contrast Manual/2013_ Contrast_Media.pd

L MM Y SK S S

Ah ono itz Harp J et al. tio o y and managem n ofpyod rma an r nosum: a compr hensiv r v m J C/ nD rmatol 2012 un ; 3 3) 191-21 .

Cu ver DA. Sarco dosis.Imm nol lle lin No h m20 2 Nov;32(4) 487- 511.

Frech TM Shanmu am VK et al. Treatm nt o ea y di ussyst mic sclerosis skin disease lin xp Rhe matol2013Mar - Ap ;31 (2 Suppl 76) 166-171

Ha movic A, Sanchez M et a Sa coi osis: a comprehensivr vie and update for the de matolo st: part Cu aneo sd sease J m cad Derma/of 2012 May 66(5) 699 l- 18q z 717 7 8

Ha movic A, Sanchez M, et a Sarco dosis a comprehens vrevie and up ate or th dermatolo ist: pa . Extracutanous dis ase J m cad Derma to/ . 20 2 May;66(5) 7 9 e 0quiz 729- 730.

kit M Du du M t al. C taneous id r act ons a comprehensiv r vie of clinical mani estations, epid miolo y etiolo y,and management. ri Rev M crobi l2012 Au 38(3):191- 202.

Marzano AV Vezzoli P et al. Sk n involv m nt in c tan ousand systemic vasculitis. toimm n Re 2013 Feb 12(4)467-476

Morr s D, nman RD React ve arthritis: d v opments andchallen es in d a nosis and treatm nt.urr Rhe ma ol Rep

2012 Oc ; 14(5) 390 394.asquez R Send o C al. Mor hea and othe local zed

forms o scl od rma rr Opin Rheumatol 2012 ov24(6):685- 693

Zaba C F o nt no F. Skin disease in d rmatomyositis.rr Opin Rheumatol 2012 Nov;24(6):597 601.

M nt r A Korm nN J al. Gu d l n o c r for hmanag m nt o ori i ndp o ic thri ctio 1-6

Ame ican Ac d my ofD rm t logy Work Group. 0 I.hnp / w\\ \\ . cbi. lm ih go p m d 213067 5

Sec ion I. O · w ofp o as s nd guidelin of c r forh tm nt of p oria i ith biologic .JAm A Derma

. 008 M y

58(5

:826-850.Sect on 2 Psori cthrit o r i w ndguid li e ofca or tr tment with an mpha on th biolog c .J m

c d Derm t 008 M y 5 5 :85 864

S ction 3. G id lin of c r for he m nag m n ndtr tm n of p oria i th topical th r p . Am aDerm tol 009 Apr 60 4):6 3 659

S ct on 4 Gu d l n s of car r h m nag m n andtr atm n o p oriasi w h r d tion l t mic ag n .J m

c d De m 009 S p 61 3 51 5

S ct on5. G id lin s of c r r th r m nt of pso iaith phototh r pyand photoch moth r p. Am ad

D ma t ol 010 Jan 6 (1 :1 - 35.

12-21

http://www.dermatlas.net/

http://www.aad.org/education/clinical-













http://www.aad.org/education/














http://www.acneandrosacea.org/uploads/AARS_Rosacea_Guide-



















http://www.aad.org/File










http://pediatrics.aappublica-/









http://www.acr.org/~/media/ACR/Documents/PDF/Quali-




http://www.ncbi.nlm.nih.gov/pubmed/21306785






















http://www.dermatlas.net/



12- OR URTHER RE G

S on 6. Guid l n of car o th tr a m n of p oriasis and p oria ic a h : a a d p n a on and

v -b . JAmAcad . 20 1Ju ;65( I): 37 - 74

SK C S

Berk DR Bayliss SJ MRSA staphy ococca scalded skinsynd ome and o her cutaneo s bacteria emergencies

Pedi trnn 20 0 Oct;39 0) 627 33

Dawson A Dellaval e RP et a! In ec io s skin diseases: a rev ew and needs assessment Der tol Clin 2012Jan;30 1) 1 - 51 ix x Review

Elston DM Tick b tes and skin rashes Curr Opin Infect Dis20 0 Apr 23(2 : 132 138

mpinott J Uyeda H et a Pyode mitisn Br s Der tol2012 Mar Apr 87 2) 77 28

G nning K P ppittK et a Pedic los s and scabies treatmenupdate F Phy ici n 2012 Sep 15 86 6) 535 5

Lancerotto L Tocco et a Necrotizing asciit s class ca

tion diagnosis and managementJ Tr u cute C re Su g2012 Ma 72 3) 560 566

io P Wa ts mol uscum and things hatgo b mp on theskin a practical g ide rch Dis Child Educ Pr ct d 2007A g;92(4 :epl l 9 124

Rajan S Skin and so t tiss e n ections: c assi ing and treaing a spect um Cle e Clin J Med 2012 Jan; 9 ) 57 66

homas N Brook Anima bite assoc a ed in ect ons:mic obiology and trea ment xpert Re nti ect Ther20 Feb 9 2)2 5 - 226

Varade RS Burkempe NM taneous ngal in ect ons in thee derly C/in Geri tr Med 20 3 May 29 2) 46 478

C Bay rA a! n ctio a So y o Am icaClin calp a ti guid nby th nf ious Dis as society

o Am r ca o thtrea men of m thicil in-resistant tapho o cus aureu n ec ions in ad l s and chi drenC n Inf t

D . 011 F 1 5 (3 8 55 Errat min: Cl n nf s20 A gI 53 3 31

Ste ens D Bisno A et a . nfe t o s a So yoAm caPract ceg d n r h diagno andmanagmen o sk n and so t ss e nfectionsC n ln f e t Di 2005Nov 15;4 10 373 406 ·at m : C in nf t D 005

c 15 4( 1 830 n nf / s 2006 Ap 5;42(8) 1Dosage or n art t

SK C C SK S

o ncil ML ommon sk n cancers in older adults approachto diagnosis and management /in Geri tr Med 20 3May 9 ) 36 - 372

a ber MJ Heilman ER et a Dysplasticnev Der tol Clin2012 J l;30(3 :389- 0

Shen Z Ho man JD et a More than j st skin deep ac oc taneo s c ues to genet c syndromes wi h malignanciesOncolo ist 20 12 7 7) 930 - 936

alaudek I K e sch J et a How to diagnose nonpigmentedsk n t mors: a review o vasc lar str ct res seen with dermoscopy pa I Melanocyt c skin t morsJ c d Der to/20 0 S p 63 3) 361 - 374

ala dek I K e sch J et a How to diagnose nonpigmen edskin mors a rev ew o vasc lar st ct res seen with dermoscopy part I Nonmelanocytic skin morsJ c d Der o 2010 Sep;63(3) 3 386

Am rican Academy o mato ogy C n caguidelinesG de ines of ca e fo manag m nt and atm n o nonme anoma sk ncan r h tp://www aad.org/edu ation/cl n cal-

g idelinesB chakjian CKHalpe AC, e a Gu del nes of car ormanag m n and reatment o an ou m anoma Am canAcad my o rma o ogy n a G d n 20 1h tp:/ /www aad og/ du a on/inica guid nes

Del Rosso JQ C rr n reg mens and g ide inemp ications o he ea m nt ofa nk r at os s: Proceedings of aclinical o ndtable at h 0 Wint C in a ma o ogy

onfe ence C tan ou edi ine o 1h P a tion 200http //www c i om/leadmin/ qh _ar h /Article PDFI CT/0880 I000 I pd

B chak an CKHalpe n AC et a Am an A ad myofma o ogy uid in ocare o the managemento

p ma y cutan ou m anomaJ A ad D mato 201Nov;65(5): 032 047

Co G And backaR et a Nat ona Comp rehens veCancer N two k M anomaJ Nat/ Compr an e ' 0Mar 0(3):366- 00

M anoma NCCNg idelines pat n Nationa Comphe ns ive Can rN two k20 3 ht p / / www nc n og/ pat nt/ gu d in /m anoma/ ndhtm #2

B S L S S

ardones AR Ha l RP3' Management o derma itis herpe iormis unol ller Clin orth 0 2 May 32 2)

275-28 vi vii

h ng WH H ng Sl Recent advances in the genetics andimm nology o Stevens-Johnson syndrome and toxic ep dermal necrosis J Der ol Sci 2012 J n;66 3 190 -196.

j bojevic S ipozen J A toimm ne b llo s diseasesassoc ations Clin Der tol 20 2Jan eb;30 ) 733

Schmidt illikens D Pemphigoid diseases L nce 2013Jan 26 38 9863) 320 332

Sok mbi 0, Wetter DA inical ea res diagnosis andt eatment o e y hema m l i o me a review or the pract cingde matologist nt J Der to! 2012 A g;5 8) 889-902

St cherl ng M r rt-Berge A toimm ne blis e ng diseases

o the sk n utoi un Re 20 2 an; (3 :226 230 Ven gopal SS M rell D Diagnosis and clinical eat res opemphig s v lga is unol lle C/in orth 20 2May 32 ):233 - 243 v v

S SK S S

edeno a rent F, G me Flo esM et a ew insightsin o H V 1 prima y skin disordersJ In IDS Soc 20 an24 5

Mankah a A Mosam A ommon skin conditions in chi drenwith H V/AIDS J Clin Der tol 2012 n 13 3 :

53 66

© 2 14MedS udy - Piease Repo Copyr ght Inf ngeme t ocopy gh @meds dy.com












http://www.aad.org/education/clinical-guidelines









http://www.cutis.com/fileadmin/qhi_archive/ArticlePDF/















http://www.nccn.org/patients/



















Rodgers S, Leslie KS Skin nfectio s in HIV-i ectedi div dua s in he era ofHAARTC Opin I ect D s20 IA ; 4( ): 49

B K L

Be m B S re i S et a . S i signs d abe es me usJEur A ad De mato/ Ve er l.20 2 Oc ;26(I0): 203 2

evy Ze c erJA De ato og c a ifes a o o dia e es.J Diabete 2012 Mar 4( 8 7

© 2014 MedSt dy

FOR FURTH R R D NG 12-23