case 10.docx notes

7/23/2019 Case 10.Docx Notes

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Type 1Diabetes-

Session 1



Anatomy

Pancreas

THE PANCREAS

DEVELOPMENT:

• Starts out with a dorsal and ventral pancreatic bud on either side of theduodenum.

• The ventral bud rotates 180 and joins the dorsal bud.

• The stalk to the ventral bud becomes the major papilla

• The main pancreatic duct is formed from both dorsal and ventral buds.

• Annular Pancreas: The pancreatic lobes mirate around duodenum in thewron direction and fuse with each other! stranlin the duodenum.

o "an completel# block or at best result in stenosis of duodenum.



LOCATION: Retroperitoneal.

• $mbilical! %piastric! and left h#pochondriac reions.

• &t traverses diaonall# from the descendin 'second( duodenum all the

wa# over to the spleen.

EXTERNAL MORPHOLOGY:

• )ead ** snu up aainst the second and third parts of duodenum.

o +ower portion e,tendin inferiorl# from the head is the uncinate process.

• -eck ** directl# anterior to superior mesenteric arter# and veins! and the portal vein.

• od#

• Tail: The tail of the pancreas e,tends into the splenorenal liament!associated with the spleen.

INTERNAL MORPHOLOGY:

• There is a main pancreatic duct runnin down the center of the oran.

RELATIONSHIPS: Also see eternal !orp"olo#$

• The root of the transverse mesocolon runs alon the lonitudinal a,is ofthe pancreatic! directl# anterior to it. 'So the transverse colon lies on topof it(.

• +eft Adrenal /land and +eft idne# are just posterior to the bod# and tailof the pancras.

CLINICAL CONSIDERATIONS:

• eferred epiastric pain could be the pancreas or the allbladder. &f the

pain wraps around the the posterior! too! then the bile duct is probabl#compressed 'stenosis( which could be more serious than just allbladder.

• Pancreatitis: causes

o /allstones can block the major papilla in the duodenum. This wouldcause bile to back2ow into the pancreas.

o A stenosis in the pancreaticohepatic duct can cause acid ch#me toback2ow into the pancreas.

o The stones ma# block both common bile and pancreatic ductsabove! causin both to back2ow into pancreas.



VASC%LAR & LYMPH S%PPLY:

• Superior Pancreaticoduodenal Arteries 'Anterior and Posterior(: Thesecome o3 of the common hepatic! in turn o3 of the "eliac Trunk.

o The# also anastomose with the iht /astroepiploic.

o The# suppl# the head! enerall#.

• /reat Pancreatic Arter#! and &nferior Pancreatic Arter#! come o3 theSplenic Arter#! from the "eliac Trunk.

o Supplies bod# and tail.

K IDNEY



Suprarenal /lands:

• 4ultiple arterial branches suppl# it with blood! but onl# one vein emptiesit. 5%-6$S 7A&-A/%:

o iht Adrenal /land: &nferior 5ena "ava.

o +eft Adrenal /land: +eft enal 5ein.

• -%5% S$PP+: 6nl# s#mpathetic 'hence adrenaline(. The# are onl#innervated b# pre*anlionic 9bers! no post*anlions.

o The 9bers oriinate fro the s#mpathetic trunk ** /reater ThoracicSplanchnic -erves.

&7-%S:

• +ocation: etroperitoneum! T1*+;! in the perirenal space.

• )ilus: enal Arter#! enal 5ein! and enal Pelvis 'ureters( enter at thehilus.

• %+AT&6-S:

o iht idne# related to 4orrison<s Pouch.

o +eft idne# related to tail of the pancreas.

• etroperitoneal Spaces:



o Perirenal Space: The space containin the kidne#<s! bordered b#/erota<s =ascia.

o Anterior Pararenal Space: "ontains the other retroperitoneal orans** part of the duodenum! pancreas! ascendin and descendin

colon.

o Posterior Pararenal Space: 7oesn<t contain jack shit.

o ecause of the division of retroperitoneal spaces! patholo#escapes down into the pelvis! before it oes riht or left.

Histology Pancreas

Structures to &dentif#:

o intercalated duct

o intralo'(lar )(*t

o a&+&*apillaries

o Islets o, Lan#er"ans

o

Se*retor$ a*in(s



o A--D- *ells

o CT septa lo'(les

General In,or!ation

o Di#esti+e #lan) /it" "ea)- ne*0- 'o)$ - tail re#ions

o Mie) #lan) /it" en)o*rine an) eo*rine ,(n*tions

Eo*rine:

o T('(loa*inar #lan)s !anil$ *o!pose) o, sero(s se*retor$ (nits

o Se*retions proteol$ti* en1$!es

o Proteol$ti* En)o2pepti)ases: tr$psino#en- *"e!otr$psino#en

o Eopepti)ases: pro*ar'o$pepti)ases- proa!inopepti)ases- alp"a a!$lases- lipases

n(*leol$ti* en1$!es

o Has "or!onal& ne(ral *ontrol re#(lation: Se*retin 3 in*. ,l(i) se*retion- CC4 3 pro

en1$!e se*retion C"$!e o, sto!a*" an) )(o)en(! sti!(late enteroen)o*rine *ells to se*rete

CC0 an) Se*retin 5 *a(ses pan*reas to se*rete

o 6or!s !ost o, pan*reas- "as ti#"tl$ pa*0e) sero(s a*ini 3 *ir*(lar #lan)- s!all

*ir*(lar l(!en- )ar0l$ staine). 1$!o#en *ells arran#e) in lo'(le ,as"ion

o Lo'(les seperate) '$ t"in intralo'(lar- an) interlo'(lar CT septa 3 "a+e 'loo)

+essels- interlo'(lar )(*ts- pa*inian *orps(*les

o Pa*inian *orps(*le 2 *on*entri* *ir*les- li#"ter t"an s(rro(n)in# a*ini- is a sensor$

re*eptor



En)o*rine:

o Islets o, Lan#er"ans 7Pan*reati* Islets8 3 "i#"l$ +as*(lari1e) epit"eloi) tiss(e

o alp"a- 'eta- )elta- *ells in perip"er$- 'eta *ells also in *enter.

o li#"t stainin#- #lo'(lar- /it" t"in CT *aps(le s(rro(n)in# it.

o P$ra!i) s"ape) *ells ,a*in# *entral l(!en-



o Se*retions #o to lar#e +a*(lar net/or0 o, *apillaries 9(st o(tsi)e t"e islets-

o E*retes into inter*alate) )(*t- line) '$ lo/ *('oi)al epit"eli(!

Alp"a *ells 3 #l(*a#on 3 in* a!o(nt o, #l(*ose in 'loo)

eta *ells 3 ins(lin 3 )e* a!o(nt o, #l(*ose in 'loo)

Delta *ells 2So!atostatin 3 in"i'its t"e ot"er t/o

D(*t ,lo/:

it"in t"e islets- ,lo/ into pale stainin# *entro a*inar *ells /it"in l(!en

5inter*alate) 7sa!e as intralo'(lar8 )(*ts 5 interlo'(lar )(*ts 7si!ple *('oi)al epit"8 in

interlo'(lar CT septa 5 lar#er )(*ts 7 also interlo'(lar- '(t /it" strati,ie) *ol(!nar epit"8

The Eye



Part =unction

"ornea

A thin! transparent and curved membrane that covers the

front part of the e#e! protectin the inside of the e#e from

dust and other matter. &t also helps to focus the liht ontothe retina.

Pupil

The little black spot in the center of the iris that controls the

amount of liht reachin the retina b# e,pandin in the dark

to allow more liht in! and contractin in the liht to prevent

e,cess liht from enterin.

A>ueous humor

A 2uid produced b# the ciliar# bod# that circulates throuh

the front and rear of the e#e to maintain e#e pressure and

provide nourishment to the cornea and the lens.

&ris The colored part of the e#e that contains ver# 9ne musclesthat control the si?e of the pupil.

"onjunctiva A thin linin over the sclera that produces mucus to lubricate

the e#e.

"iliar# bod# "ontains a land that secretes a>ueous humor and a muscle

that contracts and e,pands to control the curvature of the

lens.

+ens =ocuses the liht onto the retina.

5itreous bod# A clear el that 9lls the e#e and provides it with a spherical



shape.

6ptic disk

The point where the retina meets the optic nerve! which is

often referred to as the blind spot because of its insensitivit#

to liht.

6ptic nerve 4ade up of a bundle of nerve 9bers! the optic nerve delivers

electrical impulses from the retina to the brain.

4acula A tin# part of the retina that focuses and produces color

vision.

etina A la#er of membrane linin the back of the e#e which

contains the liht*sensitive photoreceptor cells

"hloroid +ocated between the sclera and the retina! it is made up of

blood vessels that provide nourishment to the e#e.

Sclera The outer! white part of the e#e that ives protection to the

delicate inner structures.

• Abdominal Pain

• Shortness of reath

• &ncreasin Tiredness

• =atiue

• @eiht loss

• /ettin up in the middle of the niht to urinate

• lurrred vision

• +oss in muscle tone

•

4& 1kBm• $rine is positive for blood! protein! leucoc#tes! nitrites! lucose and

ketones

Abdominal Pain

Pre)o!inant s$!pto!s are na(sea an) +o!itin#- prono(n*e) t"irst-e*essi+e (rine

pro)(*tion an) a')o!inal pain t"at !a$ 'e se+ere.

http://en.wikipedia.org/wiki/Nausea

http://en.wikipedia.org/wiki/Polyuria



http://en.wikipedia.org/wiki/Abdominal_pain



http://en.wikipedia.org/wiki/Abdominal_pain

http://en.wikipedia.org/wiki/Nausea



So!eti!es- a')o!inal pain !a$ o**(r )(e to a pro'le! so!e/"ere else in $o(r 'o)$- s(*"

as $o(r *"est or pel+i* area. 6or ea!ple- $o( !a$ "a+e a')o!inal pain i, $o( "a+e:

• Severe menstrual cramps

• %ndometriosis

• 4uscle strain

• Pelvic in2ammator# disease 'P&7(

• Tubal 'ectopic( prenanc#

• $rinar# tract infections

As man# as CD of patients visitin diabetes clinics will report sini9cant /&s#mptoms. The entire /& tract can be a3ected b# diabetes from the oral cavit#and esophaus to the lare bowel and anorectal reion. Thus! the s#mptomcomple, that ma# be e,perienced can var# widel#. "ommon complaints ma#

include d#sphaia! earl# satiet#! re2u,! constipation! abdominal pain! nausea!vomitin! and diarrhea. 4an# patients o undianosed and under*treatedbecause the /& tract has not been traditionall# associated with diabetes and itscomplications.

oth acute and chronic h#perl#cemia can lead to speci9c /& complications.7iabetes is a s#stemic disease that ma# a3ect man# oran s#stems! and the /&tract is no e,ception. As with other complications of diabetes! the duration of thedisorder and poor l#cemic control seem to be associated with more severe /&

problems.

6or ot"er people- t"ese serio(s /arnin# s$!pto!s !a$ 'e t"e ,irst si#ns o, t$pe ; )ia'etes-

or t"e$ !a$ "appen /"en 'loo) s(#ar is +er$ "i#" 7 )ia'eti* 0etoa*i)osis 8:

• 7eep! rapid breathin

• 7r# skin and mouth

• =lushed face

• =ruit# breath odor

• -ausea or vomitinE inabilit# to keep down 2uids

• Stomach pain

Shortness of Breath

7iabetes can adversel# a3ect our breathin in a number of di3erent wa#s.

reathin diFculties don<t a3ect ever#one with diabetes and the risk of havin

http://www.ncbi.nlm.nih.gov/pubmedhealth/PMHT0022185




http://www.ncbi.nlm.nih.gov/pubmedhealth/n/pmh_adam/A003150/





http://www.nlm.nih.gov/medlineplus/ency/article/000320.htm








http://www.nlm.nih.gov/medlineplus/ency/article/000320.htm



diFcult# breathin can be reduced b# maintainin ood diabetes control and

a health# bod# weiht .

apid or laboured breathin! known as ussmaul breathin! can be a s#mptom

of diabetic ketoacidosis '7A(. etoacidosis is a short term complication of

diabetes caused b# ver# hih blood lucose levels accompanied b# a hih level

of ketones in the blood. etoacidosis will onl# usuall# a3ect people with diabetes

if the# haven<t taken suFcient insulin.

Increasing Tiredness

Hi#" 'loo) #l(*ose !a0es $o(r 'loo) <sl()#$-= slo/in# *ir*(lation so *ells *an>t #et t"e

o$#en an) n(trients t"e$ nee). Mar#aret *o!!ente)- <I *an tell i, !$ s(#ars are "i#" in t"e

!ornin#- 'e*a(se ?#ro##$> )oesn>t 'e#in to )es*ri'e it. ?Dr(##e)> is "o/ it ,eels.=

@ Lo/ s(#ars le+els also *a(se ,ati#(e- 'e*a(se /"en 'loo) s(#ar is lo/- t"ere is not eno(#"

,(el ,or t"e *ells to /or0 /ell.

@ In a))ition- "i#" 'loo) #l(*ose *an *a(se ,ati#(e t"ro(#" in,la!!ation. loo) +essels #et

in,la!e) '$ t"e s(#ar. "en t"is "appens- a**or)in# to ne/ resear*" - i!!(ne *ells *alle)

!ono*$tes *o!e into t"e 'rain- *a(sin# ,ati#(e.

Weight loss

&n addition to trierin the huner response! the brain also breaks down muscle

tissue and fat in an e3ort to provide ener# for the cells. &t is this process that

causes the sudden weiht loss associated with diabetes. &f the condition

continues! untreated! the bod# can o into ketoacidosis! accordin to GThePrinciples of Anatom# and Ph#siolo#.G &n ketoacidosis! the bod# produces

chemicals called ketones from breakin down fats too >uickl#. These ketones

enter the bloodstream and make the blood acidic! which can cause oran

damae and even death.

=atiue and weakness ma# be caused b# muscle wastin from the catabolic

state of insulin de9cienc#! h#povolemia! and h#pokalemia. 4uscle cramps are

caused b# electrol#te imbalance

Thirst

In*rease) t"irst in people /it" )ia'etes *an so!eti!es 'e- '(t *ertainl$ not al/a$s- an

in)i*ation o, "i#"er t"an nor!al 'loo) #l(*ose le+els.

People /it" )ia'etes /it" a**ess to 'loo) #l(*ose testin# e(ip!ent !a$ /is" to test t"eir

'loo) s(#ar le+els /"en t"e$ are t"irst$ to )eter!ine /"et"er t"eir 'loo) s(#ar le+els are

#oin# too "i#".

I, $o( )o not "a+e 'loo) #l(*ose testin# e(ip!ent an) are eperien*in# re#(lar t"irst /"i*"

$o( t"in0 !a$ 'e *onne*te) /it" $o(r )ia'etes- spea0 /it" $o(r "ealt" tea! /"o s"o(l) 'e

a'le to a)+ise $o(.

http://www.diabetes.co.uk/Diabetes-and-Weight-Loss.html

http://www.sciencedaily.com/releases/2009/02/090217173034.htm

http://www.diabetes.co.uk/diabetes_care/blood-sugar-level-ranges.html

http://www.diabetes.co.uk/blood-glucose/blood-glucose-testing.html


http://www.diabetes.co.uk/Diabetes-and-Weight-Loss.html

http://www.sciencedaily.com/releases/2009/02/090217173034.htm

http://www.diabetes.co.uk/diabetes_care/blood-sugar-level-ranges.html




Electrolyte e!lanation

H$per#l$*e!ia- os!oti* )i(resis- ser(! "$peros!olarit$- an) !eta'oli* a*i)osis res(lt in

se+ere ele*trol$te )ist(r'an*es. T"e !ost *"ara*teristi* )ist(r'an*e is total 'o)$ potassi(!

loss. Total 'o)$ potassi(! loss is (s(all$ present )espite nor!al or "i#" ser(! potassi(!

le+els. Potassi(! le+els !a$ appear to 'e "i#" )(e to t"e trans*ell(lar s"i,t o, potassi(! o(to, *ells. T"is is not )(e to 0etoa*i)osis )ire*tl$ '(t rat"er is )(e to ins(lin )e,i*ien*$ an)

"$peros!olalit$. A lar#e part o, t"e s"i,te) etra*ell(lar potassi(! is lost in (rine 'e*a(se o,

os!oti* )i(resis. Also- /"en 0etoa*i)s are e*rete)- t"e$ are (s(all$ e*rete) /it" Na or 4 in

t"e (rine- lea)in# to ,(rt"er 4 loss. Vo!itin# !a$ also *ontri'(te to potassi(! loss in t"ese

patients. Patients /it" initial "$po0ale!ia are *onsi)ere) to "a+e se+ere an) serio(s total

'o)$ potassi(! )epletion.

In a))ition- "$ponatre!ia is (s(all$ present- an) is (s(all$ )(e to t"e )il(tional e,,e*t o,

"$peros!olalit$ as /ater is s"i,te) ,ro! intra*ell(lar to etra*ell(lar *o!part!ents.

"etting #! in the night to #se the bathroom

$nder normal circumstances! 100D of the lucose that is 9ltered is reabsorbed.

/lucose reabsorption involves transport proteins that re>uire speci9c bindin. &n

a diabetic that has h#perl#cemia! the 9ltered load of lucose 'amount of

lucose 9ltered( can e,ceed the capacit# of the kidne# tubules to reabsorb

lucose! because the transport proteins become saturated. The result is lucose

in the urine. /lucose is a solute that draws water into the urine b# osmosis.

Thus! h#perl#cemia causes a diabetic to produce a hih volume of lucose*

containin urine.

These diseases and conditions ma# be more likel# causes of -octuria if the patient has diabetes! is at risk of diabetes! or has a famil# histor# of diabetes.

"hronic kidne# failure

7iabetes mellitus

)eart failure * 2uid retained in the les is reabsorbed when l#in down and must

be e,creted.

$rinar# incontinence

Breathing and P#lserapi)- )eep 'reat"in# is t"e respirator$ *o!pensation ,or "is !eta'oli* a*i)osis. T"is

"$per+entilation- t$pi*all$ seen in )ia'eti* 0etoa*i)osis- is *alle) 4(ss!a(l respiration.

T"e ,irst one is 'e*a(se in or)er to 'reat"e "ea+il$ $o( nee) to !o+e $o(r )iap"ra#! at a

(i*0er rate 7*a(sin# $o(r "eart to p(!p !ore 'loo) to t"e area8.

T"e Se*on) is 'e*a(se "$per+entilation re)(*es t"e *ar'on )ioi)e *on*entration o, t"e

'loo) to 'elo/ its nor!al le+el- t"ere'$ raisin# t"e 'loo)Bs pH +al(e- initiatin# *onstri*tion

o, t"e 'loo) +essels /"i*" s(ppl$ t"e 'rain. 7in or)er to #et !ore 'loo) into t"e 'rain $o(r

"eart p(!ps !ore in an) $o(r p(lse in*reases8.

http://www.rightdiagnosis.com/sym/nocturia.htm

http://www.rightdiagnosis.com/c/chronic_kidney_failure/intro.htm

http://www.rightdiagnosis.com/sym/numbness_of_both_elbows.htm

http://www.rightdiagnosis.com/sym/heart_failure.htm

http://www.rightdiagnosis.com/sym/urinary_incontinence.htm

http://www.rightdiagnosis.com/sym/nocturia.htm

http://www.rightdiagnosis.com/c/chronic_kidney_failure/intro.htm

http://www.rightdiagnosis.com/sym/numbness_of_both_elbows.htm

http://www.rightdiagnosis.com/sym/heart_failure.htm

http://www.rightdiagnosis.com/sym/urinary_incontinence.htm



Blurred Vision

l(rre) +ision res(lts ,ro! t"e e,,e*t o, t"e "$peros!olar state on t"e lens an) +itreo(s

"(!or. Gl(*ose an) its !eta'olites *a(se os!oti* s/ellin# o, t"e lens- alterin# its nor!al ,o*al len#t".

A$ID%BASE I&BA'AN$E and $(&PENSATI(N

Definitions

When pHa (arterial blood pH) differs from 7.4 +/- 0.02 (or the [H+] differs from 40

+/- 2 nE/!) there o""#rs acidemia (pHa $ 7.%&' [H+] 42 nE/!)

or alkalemia (pHa 7.42' [H+] $ %& nE/!).

f the pHa "han*e is d#e primaril to a "han*e in ,a2' there is respiratory

acidosis (,a2 42 mmH*) or respiratory alkalosis (,a2 $ %& mmH*).

When the pHa "han*e is d#e primaril to a "han*e in [H%-] from its normal

al#e of 24 m' there is metabolic acidosis ([H%-] $ 22 m) or metabolic

alkalosis ([H%-] 21 m).

Note -emia refers to "han*es in blood3 acidosis and alkalosis refer to

pathophsiolo*i" pro"esses that lead to pH "han*es in blood

(A) Metabolic acidosis: pH < 7.38; HCO3- < !M; ,a2 mmH* de"rease per

m de"rease in H%- (a"#te or "hroni")

Ca"ses:

etaboli" a"idosis is the most fre#ent a"id-base imbalan"e and ma be d#e to

() #$t%a%enal loss of bica%bonate' 5ith hper"hloremia and in"reased #rinar

e6"retion of H4

+

(eident as hi*h #rinar "ation *ap [l

-

] - [a

+

] - [8

+

] 0)

(2) &%ina%' loss of HCO3- (al9aline #rine' 5ith hi*h bi"arbonate' and little

H4+ and th#s no #rine "ation *ap)

(%) Acc"!"lation of o%anic anions (la"ta"idosis' 9etoa"idosis) 5ith lar*e plasma

anion *ap (d#e to or*ani" anions' [a+]+[8 +]-[l-]-[H%-]:)' ab#ndant

#rinar H4+ b#t no #rinar "ation *ap (H4

+ is e6"reted 5ith or*ani" anions so

that there is a lar*e #rinar osmolar *ap ; osm - 2([a+]+[8 +]) - [#rea] - [*l#"ose]

0. nl la"ta"idosis "an deelop in min#tes (as in sho"9).



(4) Dec%eased idne' p%od"ction of HCO3- (hper"hloremia' no plasma anion

*ap' and lo5 #rinar e6"retion of ammoni#m' (#rinar "ation *ap <0)3 seere

"hroni" renal fail#re ma res#lt in metaboli" a"idosis 5ith in"reased plasma anion

*ap (d#e to hi*h plasma [, i]) and lo5 #rinar H4+ e6"retion.

Co!pensations:

() *!!ediate b"ffe%in b rea"tion 5ith E= H%- represents >40? of rapid

(>2 hrs) b#fferin* of a"id. Hl + aH% < al+ H2% + 2 + H2

(2) +espi%ato%' co!pensation. @ lo5 pHa stim#lates A@' so ,a02 de"reases

minimiBin* the de"rease in pHa. =or ea"h m de"rease in [H%-] a mmH*

drop in ,a02 is e6pe"ted.

ote Ce"a#se of %espi%ato%' co!pensation for metaboli" a"idosis' ,a2 is

e6pe"ted to be belo5 its normal ran*e or (,aCO < 38 !!H). f ' be"a#se of

disease' there is no respirator "ompensation' then ,a2 5ill be normal or eleated'

and the respirator sstem is "ontrib#tin* to the a"idemia (see Despirator @"idosis

belo5)..

(%) iss"e pase. Entr of H+ into "ells a""o#nts for >10? of rapid (>2 h)

b#fferin* of poorl permeable a"ids (Hl or H24). Fhis phase is "apable of

b#fferin* 00? of the a"id b 24 h' and is d#e to the follo5in* ion e6"han*es and

b#fferin* of H+ b "ell proteins and H%-

(a) a+ in the = for H+ from the E=3 o""#rs in most tiss#es in"l#din* bone3

a""o#nts for 1:? of the entr of protons into the = (and bone).

(b) = 8 + for E= H+3 a""o#nts for 2:? of the entr of H+ into the =. a

res#lt in hper9alemia (1-7 mE/!) that affe"ts m#s"le and nere "ells and ind#"es

"ardia" arrthmias.

(") E= l- for = H0%-3 a""o#nts for 0? of the = b#fferin* of H+3 red#"es= H0%

- and intra"ell#lar pH3 o""#rs mostl in red "ells 5here Hb b#ffers

e6"ess H+.

(4) +enal pase. Generation of bi"arbonate thro#*h #rinar e6"retion of

ammoni#m and titratable a"ids' restores the depleted "ell H %- and b#ffer base

reseres oer 2-% das. anifest onl in "hroni" sta*e.

(/) Metabolic alalosis: pHa 0 7.1; 2HCO3- 0 4 !M; ,a2 0.7: mmH*

in"rease for ea"h m in"rease in [H%

-

] ("hroni" or a"#te)



Ca"ses:

() 5oss of ast%ic 6"ice (omitin*' s#"tion)

(2) ide effect of di"%etics and other forms of E=A "ontra"tion.

(%) H'pe%aldoste%onis! of ol#me depletion promotes renal H+ se"retion'

*eneration and retention of H%-.

(4) n hpo9alemia' 9 sifts o"t of cells in e$cane fo% H9' ind#"in*

e6tra"ell#lar al9alosis and intra"ell#lar a"idosis.

Co!pensations:

() +espi%ato%'. @s pHa in"reases' A@ is depressed and ,a2 in"reases (,aCO 0 1!!H). Fhis normaliBes blood pH b#t is limited b ens#in* hpo6ia. =or ea"h

m rise in H%-there is e6pe"ted a 0.7: mmH* rise in , a23 if this does not

o""#r' there is a respirator tenden" to al9alosis.

(2) Cell ionic e$canes. ome 2:? of the bi"arbonate load is ne#traliBed b

H+ deried from intra"ell#lar b#ffers that e6"han*e the H+ for e6tra"ell#lar a+. n

addition' >2? of e6tra"ell#lar H%- enters red "ells in e6"han*e for l-.

(%) Metabolic. n"reases in endo*eno#s or*ani" a"id prod#"tion ne#traliBe >: ? of an a"#te H%

- load. Hi*h pHa in"reases prod#"tion of la"ti" and "itri" a"ids 5hi"h

de"rease [H%-]. Hi*h blood pH stim#lates *l"olsis and inhibits the "itri" a"id

""le.

(4) +enal e$c%etion of HCO3- rises 5hen its "on"entration in plasma in"reases.

!o5erin* of [H%-] pl is limited b hi*h renal reabsorption rate stim#lated b hi*h

,a2' b E= ol#me "ontra"tion' b hperaldosteronism' b 8 + depletion' and b

hpo"hloremia. Fhese tend to perpet#ate the hi*h [H%-] pl. Ceta-inter"alated "ells

in se"rete bi"arbonate' in"reasin* its #rinar e6"retion.

(C) +espi%ato%' alalosis: pH 0 7.11; ,aCO < 38 !! H; [H%-] de"reases

($24 m) b 0.: m ("hroni") or 0. m (a"#te) per ea"h mmH* drop in , a02

Ca"se: Aleola% 'pe%entilation (altit#de' hsteria' aspirin e6"ess)

Co!pensations

() Cell b"ffe%s. n the ac"te state there is a 0. m de"rease in [H %-] for ea"h

mmH* de"rease in ,a2. Fhis de"rease is d#e to enhan"ed disso"iation of H + from



"ell b#ffers 5hen the [H+]i de"reases d#e to the lo5 ,a2. ell H+ e6"han*e for

E= a+ and 8 + and rea"t 5ith the E= H%-' red#"in* its "on"entration. ome

e6tra"ell#lar H%- enters "ells in e6"han*e for l- and is titrated b

H+ disso"iatin* from the "ell b#ffers.

n the c%onic state' there is a 0.: m de"rease in [H %-] for ea"h one mmH*

de"rease in ,a2. Fhis is d#e to

(2) +enal co!pensation d#e to in"reased H%- e6"retion asso"iated 5ith the lo5

,a2' 5hi"h de"reases H%- reabsorption. ;rinar e6"retion of H4

+ and

titratable a"id are transientl red#"ed' leadin* to a""#m#lation of metaboli" and

dietar a"ids 5hi"h help red#"e E= [H%-] (2HCO3

- < !M). Eent#all

#rinar H%- e6"retion "eases and e6"retion of H4+ and titratable a"id res#mes.

(%) Metabolic co!pensation b in"reased prod#"tion of la"ti" and "itri" a"ids that

rea"t 5ith and red#"e [H%-]e"f

(D) +espi%ato%' acidosis: pH < 7.38; ,aC 0 1 !! H; [H%-] in"reases (24

m) b 0.2: m ("hroni") or 0.0: m (a"#te) per ea"h mmH* rise in , a02

Ca"se: Aleola% 'poentilation

Co!pensations:

() ast cell ion e$canes. @n a"#te small rise in [H%-] pl is d#e to e6"han*e of

E= H+ for = (or bone) a+ (%7?) or for = 8 + (%?) and to e6"han*e of E=

l- for = (red "ells) H%- (%0?). Fhese rapid ioni" e6"han*es are asso"iated

5ith 2 b#fferin* b intra"ell#lar proteins. =or ea"h mmH* in"rement in

,a2 there is a small a"#te 0.01 m in"rement in H %-.

(2) Metabolic. Ded#"ed prod#"tion of la"ti" a"id "ontrib#tes abo#t :? to the

a"#te in"rease in [H%-] pl.

(%) +enal. n"reased H%- reabsorption stim#lated b hi*h ,a2 preents #rinar

loss of bi"arbonate.

n the transition to the "hroni" sta*e (-% das)' enhan"ed renal H4+' and titratable

a"id e6"retion "ontrib#te to f#rther in"rease [H%-] in E= and = aboe normal

(2HCO3- 0 4 !M)' ret#rnin* pH to5ards normal. @s the pH stim#l#s de"reases'

renal H4+ and titratable a"id e6"retion s#bside. Denal reabsorption of bi"arbonate

remains eleated as lon* as the ,a2 is hi*h.



ELECTROLYTES and ACID-BASE

OA5 /OD= >A#+

• TBW is normally 60 o! "ody #$i%&t' 60 o! (0 )% * +,L

o INTRACELLLAR. Intra/$lllar 1id is normally t#o

t&irds o! TBW' 6( o! +,L * ,2L

o E3TRACELLLAR. E4tra/$lllar 1id is normally on$

t&ird o! TBW' 55 o! +,L * +L

PLAS7A 8OL7E. Plasma is normally a"ot CD of

T@ ' 9 o! +,L * ,-5L

INTERSTITIAL 8OL7E. IS: is t&$ r$st o! t&$;olm$' +L - 5L * 0-L'

,OA*&M Deferen"e ran*e %.: - :.0 mE / !

• HYPOKALEMIA. D$/r$as$d < = in >lasma

o )#pokalemia is usuall# accompanied b# metabolic

alkalosis'

• HYPERKALEMIA. In/r$as$d < = in >lasma

o )#perkalemia is usuall# accompanied b# metabolic

acidosis.

OD*&M Deferen"e ran*e %: - 41 mE / !

• HYPONATREMIA.



o Pitting Edema :lid &as mo;$d !rom ;as/lar s>a/$

into int$rstitial s>a/$' T&$ intra/$lllar s>a/$s ar$ nota?$/t$d'

It o//rs "$/as$ o! an o?-"alan/$ o! Starlni%@s:or/$s.

Too m/& &ydrostati/ >r$ssr$. CH:

Too littl$ on/oti/ >r$ssr$. N$>&roti/

Syndrom$ Li;$r Cirr&osis

On$ sally nds h#ponatremia #it& t&$s$

/onditions "$/as$ t&$ >ati$nt &as %ain$d mor$

#at$r t&an sodim so t&$ sodim l$;$ls ar$dilt$d'

o !e"eb"a# Edema In &y>onatr$mia #at$r $nt$rs into

n$ron /$lls in "rain ------ /$r$"ral $d$ma' Pot$ntial!or &$rniation i! it is not /orr$/t$d'

Idiogeni$ Mo#e$%#es ar$ osmoti/ally a/ti;$

mol$/l$s /r$at$d "y t&$ /$r$"rm to try to

/om>$nsat$ !or t&$ /$r$"ral $d$ma' T&$y ar$$4/r$t$d into t&$ IS: to try to s/) t&$ #at$r oto! t&$ /$lls'

o Synd"ome o& Inapp"op"iate ADH 'SIADH( It is t&$

most /ommon /as$ o! &y>onatr$mia #it& a normal>&ysi/al $4am no $d$ma no lost s)in tr%or'

CASES. E/to>i/ >rod/tion "y a tmor s/& as

small-/$ll /ar/inoma o! t&$ ln%'

TREAT7ENT. R$stri/t inta)$ o! #at$r' El$/trolyt$

"alan/$ r$mains normalF no $l$/trolyt$adGstm$nts ar$ n$$d$d' Tr$at #it& ADHanta%onists'

• HYPERNATREMIA.

o De)yd"ation Pr$ #at$r loss in!antil$ diarr&$a'



TREAT7ENT. 7on<t ive the calculated amount of

2uid "a/) to t&$ >ati$nt' Al#ays %i;$ l$ss to>r$;$nt /$r$"ral &$rniation' T&$ "rain #ill ma)$osmoti/ally a/ti;$ idiogeni$ mo#e$%#es to try to

/om>$nsat$ !or t&$ d$&ydration' T&$n i! yo %i;$too m/& 1id t&$ "rain /an &$rniat$'

o Diabeti$ Ketoa$idosis 'DKA(

D$ to in/r$as$d osmoti/ !or/$ o! &y>$r%ly/$mia

1id #ill mo;$ !rom t&$ intra/$lllar s>a/$ intot&$ >lasma'

Sodi%m !on$ent"ation mst "$ adjusted !or t&$

>r$s$n/$ o! &y>$r%ly/$mia #&i/& isn@t normallyta)$n into a//ont' T&$ sodim /on/$ntration #ill"$ a/tally hiher t&an #&at is r$>ort$d' T&is istr$ #it& "lood s%ar 900'

• TOTAL *ODY SODI+M 'T*Na(.

o D$/r$as$d TBNa ------ d$/r$as$d 1id in int$rstitial

s>a/$ ------ de$"eased s,in t%"go"' Yo /an >ll on

s)in and it isn@t as $lasti/ or ti%&t'

o In/r$as$d TBNa ------ in/r$as$d 1id in int$rstitial

s>a/$ ------ pitting edema :lid a//mlat$d inint$rstitial s>a/$'

Pati$nt may still &a;$ )#ponatremia "$/as$ t&$

sodim /on/$ntration in "lood is d$/r$as$d' Btt&$ total "ody sodim #ill "$ in/r$as$d'

D#H=D+A*ON

• Ad%#t Dia"")ea is isotoni/ t&s adlt d$&ydration #ill s&o#

normal sodim l$;$ls'

o To r$&ydrat$ %i;$ t&$m #&at t&$y lost -- an isotoni/

salin$ soltion'

• In&anti#e Dia"")ea is &y>otoni/ t&s in!antil$ diarr&$a #ill

s&o# &y>$rnatr$mia'



o To r$&ydrat$ %i;$ t&$m #&at t&$y lost -- a pedia#yte

or &y>otoni/ salin$ soltion'

#D#MA

• !e##%#a" Edema Tiss%e Hypo.ia l$ads to /$lllar $d$ma'

Hy>o4ia ------ Na=< =-ATPas$ Pm> !ailr$ ------Na= /oll$/ts insid$ /$lls and "rin%s #at$r #it& it------ )yd"opi$ s/e##ing o! /$lls and /$lllar $d$ma'

• Pitting Edema CH: N$>&rosis Cirr&osis l$ad to >ittin%

$d$ma' Transdat$ /oll$/ts in int$rstitial s>a/$ $it&$r d$ toin/r$as$d &ydrostati/ >r$ssr$ CH: or d$/r$as$d on/oti/>r$ssr$ N$>&rosis /irr&osis malntrition'

• !e"eb"a# Edema In &y>onatr$mia #at$r $nt$rs into

n$ron /$lls in "rain ------ /$r$"ral $d$ma' Pot$ntial !or&$rniation i! it is not /orr$/t$d'

o Idiogeni$ Mo#e$%#es ar$ osmoti/ally a/ti;$ mol$/l$s

/r$at$d "y t&$ /$r$"rm to try to /om>$nsat$ !or t&$/$r$"ral $d$ma' T&$y ar$ $4/r$t$d into t&$ IS: to try tos/) t&$ #at$r ot o! t&$ /$lls'

OMO5A5*= ormal al#e is abo#t 2&I msm.

AC*D-/A#

• META*OLI! A!IDOSIS. D$/r$as$ t&$ HCO5- ------ t&$ >H

%o$s do#n' Com>$nsation. R$s>iratory Al)alosis #ill "rin%t&$ >H "a/) n$ar normal'

• META*OLI! ALKALOSIS. In/r$as$ t&$ HCO5- ------ t&$ >H

%o$s >' Com>$nsation. R$s>iratory A/idosis&y>o;$ntilation /an &$l> to "rin% t&$ >H "a/) n$ar normal'

o CASES.

0omiting Los$ $no%& stoma/& a/id to >rod/$

al)alosis'

Di%"eti$s Loo> dir$ti/s and t&iaid$s /an l$ad

to )ypo,a#emia ------ s$/ondary m$ta"oli/al)alosis'



• RESPIRATORY A!IDOSIS. In/r$as$ t&$ PCO, ------ t&$ >H

%o$s do#n' )#poventilation. Com>$nsation. 7$ta"oli/Al)alosis /an &$l> "rin% t&$ >H "a/) n$ar normal'

•

RESPIRATORY ALKALOSIS. D$/r$as$ t&$ PCO, ------ t&$>H %o$s >' )#perventilation. Com>$nsation. 7$ta"oli/A/idosis /an &$l> "rin% t&$ >H "a/) n$ar normal'

AN*ON ?A, Essentiall' the differen"e bet5een bet5een the "on"entrations of

"ations (a+ primaril) and anions (l-' H%-) in the blood.

• Hig) Anion ap Metabolic Acidosis. It indi/at$s t&at yo

&a;$ add$d a/ids to t&$ "lood. sali/yli/ a/id !ormi/ a/idla/ti/ a/id o4ali/ a/id sl!ri/ a/id'

• No"ma# Anion ap Respiratory Acidosis. It o//rs #&$n

yo ltimat$ly "$/om$ a/idoti/ "$/as$ o! losin% HCO5-'

NO+MA5 @A5&# of A+#+*A5 /5OOD-?A#

Item 0a#%e

>H ('+

JHCO5-K ,, - ,2 mE

L

PaCO, 55 - ++ mE

L

PaO, M0 - 00

mE L

case 10.docx notes

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