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STUDY GUIDE Q/A: FALL 2012

WATER AND ELECTROLYTE DISORDERS

HEMODYNAMIC DISORDERS

Items 1−11A. Proximal tubule

B. Descending tubule

C. Thick ascending limb: medullary segment with a!"# !"$Cl% sym&orter

D. Thick ascending limb: cortical segment with a!"Cl% sym&orter

'. Distal con(oluted tubule"collecting tubule: a!"# ! channels

). Collecting duct: *!"# ! ATPase &um&

+. ,ate distal"collecting duct1. A block at this site by a carbonic anhydrase inhibitor -e.g. aceta/olamide0 results in the loss o

sodium"&otassium bicarbonate in the urine hy&okalemia and &roduction o a normal anion ga&

metabolic acidosis.

Answer: A: &roximal tubule: this is an exam&le o an ac2uired ty&e II &roximal renal tubular acidosis.

Aceta/olamide is a &roximal tubule diuretic that blocks the reclaiming o bicarbonate. Bicarbonate is lostin the urine as sodium bicarbonate. ,oss o bicarbonate is matched by a gain in chloride -hy&erchloremic

normal anion ga& metabolic acidosis03 hence the anion ga& remains the same.

$. In &atients taking a loo& diuretic or thia/ides an increased deli(ery o sodium to this site results in

hy&okalemia and metabolic alkalosis i the &atient is not taking oral &otassium su&&lements.

Answer: '. Distal con(oluted tubule"collecting tubule: a!"# ! channels: &otassium is lost in the urine

-causes hy&okalemia0 in exchange or sodium. 4nce &otassium stores are de&leted -&atient is not taking

&otassium su&&lements0 sodium exchanges with &rotons and regenerated bicarbonate mo(es into the

blood &roducing metabolic alkalosis.

5. A block at this site intereres with the generation o ree water and non%&arathyroid hormone%

related reabsor&tion o calcium.Answer: C. Thick ascending limb: medullary segment with a!"# !"$Cl% sym&orter: this is the &rimarysite or generation o ree water and is also the site or non%PT* reabsor&tion o calcium. 4bligated water

is remo(ed rom sodium &otassium and chloride and remains in the tubule lumens as ree water. Block

o chloride binding with loo& diuretics not only results in loss o sodium &otassium and chloride but also

calcium -useul in the treatment o hy&ercalcemia0.

6. A block at these sites by s&ironolactone results in sodium loss in the urine hy&erkalemia and

normal anion ga& metabolic acidosis. SELECT 2

Answers E, F: '. Distal con(oluted tubule"collecting tubule: a!"# ! channels

). Collecting duct: *!"# ! ATPase &um&: s&ironolactone is an aldosterone blocker and these $ sites are

enhanced by aldosterone. Block o the irst channel causes a loss o sodium and retention o &otassium

-causes hy&erkalemia0 while a block o the second site causes a loss o &otassium and retention o &rotons -metabolic acidosis0. Bicarbonate cannot be generated3 thereore &rotons combine with chloride

&roducing a normal A+ metabolic acidosis. The hy&erkalemia is somewhat oset by the loss o &otassium

in the latter &um& and may result in &otassium mo(ing into or close to the normal range.

7. These sites are most susce&tible to tissue hy&oxia and in(ariably exhibit coagulation necrosis in

ischemic acute tubular necrosis. SELECT 2

Answers A, C: A. Proximal tubule

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C. Thick ascending limb: medullary segment with a!"# !"$Cl% sym&orter. There is a lot o oxidati(e

ty&es o reactions in these areas3 hence their susce&tibility to hy&oxia and coagulation necrosis

&articularly in ischemic acute tubular necrosis.

8. This is the &rimary site or renal tubular acidosis secondary to a lowering o the renal threshold orreclaiming bicarbonate.

Answer: A. Proximal tubule: this is ty&e II 9TA. The urine is initially alkaline due to the loss o iltered bicarbonate that cannot be reclaimed. *owe(er when the renal threshold and blood le(els o bicarbonate

are the same -e.g. 17 m'2",0 the urine returns to an acid &*. Aceta/olamide is the CC o &roximal

9TA. *ea(y metal &oisoning is another cause o &roximal 9TA. 9x o &roximal 9TA is to &roduce

(olume de&letion with thia/ides which automatically raises the renal threshold or reclaiming bicarbonate.

;. This is the &rimary site or renal tubular acidosis secondary to inability to secrete &rotons leading to

a deect in the acidiication o urine.

Answer: ). Collecting duct: *!"# ! ATPase &um&: &rotons combine with chloride leading to a normal A+

metabolic acidosis and bicarbonate cannot be regenerated -normal A+ metabolic acidosis0. *y&okalemia

is se(ere.

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1$. A ;=%year%old man &ost%transurethral resection or urinary retention secondary to &rostate

hy&er&lasia recei(es an excessi(e amount o ?.> normal saline. *e de(elo&s dys&nea and

de&endent &itting edema. *e has a history o chronic ischemic heart disease. Physical exam

demonstrates ugular neck (ein distention and bibasilar crackles. Ehich o the ollowing changes

in electrolyte and (olume status is most likely &resent in this &atientF

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ICF

C$!%"r&!en&A. Increased Increased Contracted Contracted

B. ormal ormal 'x&anded ormal

C. Decreased Decreased Contracted 'x&anded

D. Increased Increased 'x&anded Contracted

'. ormal ormal 'x&anded 'x&anded

Answer: B. isotonic gain in luid with no gradient: would correlate with diagram C in the study

2uestions. The reason why he de(elo&ed let sided heart ailure -&ulmonary edema0 and right sided heart

ailure -de&endent &itting edema0 is that he had &reexisting ischemic heart disease and most likely had

increased renal retention o sodium related to a decreased cardiac out&ut. In this setting gi(ing excess

isotonic luid caused let%sided heart ailure with an increase in hydrostatic &ressure dri(ing luid into the

lungs and right%sided heart ailure due to an increase in hydrostatic &ressure dri(ing luid into the

interstitial s&ace in the legs.

Os! N"# ECF ICF

B. ormal ormal 'x&anded ormal

15. A ;$%year%old man with a history o ischemic heart disease de(elo&s neck (ein distention

bibasilar crackles and de&endent &itting edema within $6 hrs ater recei(ing multi&le am&ules o

intra(enous sodium bicarbonate -hy&ertonic saline0 during a cardiores&iratory arrest. Ehich o theollowing changes in electrolyte and (olume status is most likely &resent in this &atientF

Os! N"# ECF

C$!%"r&!en&

ICF

C$!%"r&!en&

Increased Increased 'x&anded Contracted

Decreased Decreased 'x&anded 'x&andedDecreased Decreased Contracted 'x&anded

Increased Increased 'x&anded 'x&anded

ormal ormal Contracted ormal

Answer: A. hy&ertonic gain in luid causing hy&ernatremia correlates with diagram ' in the study

2uestions. An osmotic gradient a(ors mo(ement out o the IC) into the 'C). The 'C) is ex&anded and

the IC) is contracted. The 9x is sodium restriction and diuretics.

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16. A 7=%year%old man has the ollowing laboratory test abnormalities: urine (olume 7 m,"min &lasma

osmolality $=? m4sm"kg -$;7−$>7 m4sm"kg0 and urine osmolality o =6? m4sm"kg. Theselaboratory indings are most com&atible with which o the ollowing conditionsF

A. 4smotic diuresis secondary to diabetic ketoacidosisB. Golume de&letion secondary to se(ere diarrhea

C. Ina&&ro&riate AD* syndrome

D. Central diabetes insi&idus

'. 9enal ailure

Answer: B. Golume de&letion secondary to se(ere diarrhea. In order to answer the 2uestion the ree

water clearance must be calculated to see i he is concentrating or diluting the urine. C4sm H =6? x 7"$=?

H 17 C*$? H 7 % 17 H %1? indicating concentration. The P4sm in this &atient is normal which would be

ex&ected in adult diarrhea since it is an isotonic loss o luid.

A. 4smotic diuresis secondary to diabetic ketoacidosis: no the P4sm would be higher due to

hy&erglycemia

C. Ina&&ro&riate AD* syndrome: no the P4sm would be lower due to the dilutional eect o adding

water to the 'C) com&artment. *owe(er ree water clearance is negati(e since AD* is constantlyconcentrating the urine

D. Central diabetes insi&idus: no P4sm would be higher and the ree water clearance &ositi(e in theabsence o AD*. These &atients are constantly diluting their urine.

'. 9enal ailure: no ree water clearance is /ero indicating a lack o both dilution and concentration.

17. A 1>%year%old man with ty&e I diabetes mellitus de(elo&s diabetic ketoacidosis. Physical examdemonstrates signs o (olume de&letion. The serum glucose is 1??? mg"d, and ketone bodies are

increased in the &lasma and urine. Ehich o the ollowing changes in electrolyte and (olume status

is most likely &resent in this &atientF

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C$!%"r&!en&

ICF

C$!%"r&!en&

Increased Decreased Contracted ContractedIncreased Decreased 'x&anded Contracted


Decreased Decreased 'x&anded 'x&anded

Decreased Decreased Contracted 'x&anded

Answer: A. the &atient has ty&e 1 diabetes mellitus and is in diabetic ketoacidosis with signs o (olume

de&letion. +lucose has sur&assed sodium as the maor osmotic orce and increases P4sm. @erum sodium

is low due to water shit out o the IC) into the 'C) &roducing a dilutional hy&onatremia. The 'C) is

contracted owing to osmotic diuresis leading to (olume de&letion. IC) is contracted due to increasedP4sm rom glucose. Correlates with diagram ' in the study 2uestions -diagrams or 2uestions 87%;$0.

Os! N"# ECF ICF

Increased Decreased Contracted Contracted

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18. Ehich o the ollowing characteri/e the indings in early endotoxic -se&tic0 shock rather than either

hy&o(olemic or cardiogenic shockF SELECT '

A. Cold clammy skin

B. Increased cardiac out&ut

C. Increased (enous return to the heartD. Decreased total &eri&heral resistance

'. Decreased mixed (enous oxygen content -G4$0Answers (, C, D: B. Increased cardiac out&ut: due to increased (enous return to the heart owing to

arteriolar (asodilation

C. Increased (enous return to the heart

D. Decreased total &eri&heral resistance: arteriolar (asodilation also dro&s the diastolic &ressure

A. Cold clammy skin: no this is &resent in hy&o(olemic and cardiogenic shock due to catecholamine

ATII and AD* (asoconstriction o the (essels in the skin to redirect blood to more im&ortant areas

'. Decreased mixed (enous oxygen content -G4$0: no it is increased in se&tic shock and decreased in

the other ty&es o shock. It is increased owing to the increased blood low through the microcirculation.

1;. A ;$%year%old woman is currently taking a thia/ide diuretic or hy&ertension. @he com&lains o

di//iness when standing u& too 2uickly. Physical exam demonstrates a blood &ressure o 15?"==

mm *g and a &ulse o 1?? b&m when lying down and a blood &ressure o 11?"=? mm *g and a

&ulse o 17? b&m when sitting u&. The mucous membranes are dry and skin turgor is &oor. Ehicho the ollowing changes in electrolyte and (olume status is most likely &resent in this &atientF

Os! N"# ECF

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ICF

C$!%"r&!en&

ormal ormal Contracted ormalDecreased Decreased Contracted Contracted




Answer: '. *y&ertonic loss o luid rom diuretic leading to hy&onatremia. Correlates with diagram B in

the study 2uestions -diagrams or 2uestions 87%;$0. The gradient a(ors mo(ement o water into the IC)

com&artment. ote the &ositi(e tilt test -BP dro&&ed and &ulse increased when sitting u&0 indicating

signiicant (olume de&letion.

Os! N"# ECF ICF


1=. A 1>%year%old man with a recent head inury related to a motorcycle accident com&lains o

excessi(e thirst and ha(ing to urinate o(er 1? times a day. Physical exam is unremarkable. The

urine osmolality is 1?? m4sm"kg. ou sus&ect that the &ituitary stalk may ha(e been transected

rom the accident. Ehich o the ollowing changes in electrolyte and (olume status is most likely &resent in this &atientF

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C$!%"r&!en&

ICF

C$!%"r&!en&




Increased Increased Contracted Contracted


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Answer: D. Central diabetes insi&idus with loss o &ure water and no salt rom lack o AD*.

*y&ernatremia occurs howe(er there is a normal exam because the loss o &ure water does not result in

clinically signiicant (olume de&letion -&roduces dehydration0. Correlates with diagram ' in the study

2uestions -diagrams or 2uestions 87%;$0. 9emember that AD* is synthesi/ed in the hy&othalamus and

in the same ner(e tra(els through the &ituitary stalk into the &osterior &ituitary where it is stored. *eadtrauma is a common cause or se(erance o the stalk leading to diabetes insi&idus as well as

hy&o&ituitarism since all the releasing actors are &re(ented rom stimulating the &ituitary gland.

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1>. A 85%year%old man with a 6= year history o smoking com&lains o headache and conusion.

Physical exam is unremarkable exce&t or scattered sibilant rhonchi in the lungs that clear with

coughing. A chest x%ray exhibits a &rominent right hilar mass. An 9I o the brain is negati(e or

s&ace occu&ying lesions. A s&utum cytology re&ort indicates the &resence o small hy&erchromatic

cells intermixed with necrotic debris consistent with a small cell carcinoma o the lung. Ehich o

the ollowing changes in electrolyte and (olume status is most likely &resent in this &atientF

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C$!%"r&!en&

ICF

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Decreased Decreased 'x&anded ContractedDecreased Decreased 'x&anded 'x&anded




Answer: D. the &atient has @iAD* due to a small cell carcinoma o the lung. The 9I rules out

metastasis to the brain so the mental status &roblems relate to cerebral edema rom hy&onatremia related

to water mo(ing out o the 'C) into the IC). There is a hy&otonic gain o &ure water thereore the TBa

is normal and the skin turgor is normal. This &atient would be treated with demeclocycline -&roduces

ne&hrogenic diabetes insi&idus0 rather than water restriction since he will die in a short &eriod o time.

Correlates with diagram D in the study 2uestions -diagrams or 2uestions 87%;$0.

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$?. A 1>%year%old hiker who has been lost in the @onoran desert or 5 days has signs o (olume

de&letion. Ehich o the ollowing changes in electrolyte and (olume status is most likely &resent in

this &atientF

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C$!%"r&!en&

ICF

C$!%"r&!en&

Increased *igh Contracted Contracted

Increased Increased 'x&anded 'x&anded ormal ormal Contracted ormal



Answer: A. sweating will cause loss o a hy&otonic salt solution leading to hy&ernatremia. Correlates

with diagram ' in the study guide -diagrams or 2uestions 87%;$0. The irst ste& in managing this &atient

is inusion o normal saline until the signs o (olume de&letion disa&&eared. Then he would be gi(en ?.67

normal saline which matches the tonicity o the sweat that he lost.

Os! N"# ECF ICF


$1. A 8$%year%old woman has both let%sided and right%sided heart ailure. Physical exam demonstrates

ugular (ein distention &itting edema and bibasilar cre&itant crackles. Ehich o the ollowing

changes in electrolyte and (olume status is most likely &resent in this &atientF

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C$!%"r&!en&

ICF

C$!%"r&!en&Increased Increased 'x&anded Contracted




Decreased Decreased Contracted ormal

Answer: C. *y&otonic gain o more water than salt leads to hy&onatremia. Correlates with diagram D

-diagrams or 2uestions 87%;$0. The hy&otonic gain is rom the luid retained by the kidney when the

'ABG is decreased. A hy&otonic gain -greater increase in TBE than TBa0 translates into a

hy&onatremia. The @tarlings orce abnormalities are related to an increase in hydrostatic &ressure in the

&ulmonary ca&illaries and in the (enous system behind the right heart. The dierence rom @iAD* is that

&itting edema is &resent in this case -increased TBa!0 but not @iAD* -normal TBa!0. 9x is water and

salt restriction &lus diuretics.

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$$. A 66%year%old woman has hy&otension increased skin and mucous membrane &igmentation and

&oor skin turgor. ,aboratory studies unco(er a low serum cortisol and electrolyte abnormalities. An

intra(enous ACT* stimulation test o(er the ensuing 5 days demonstrates no increase in serum

cortisol or its urinary metabolites. Plasma ACT* le(els are high. A random urine sodium is J 1??

m'2", - $? m'2",0. Ehich o the ollowing changes in electrolyte and (olume status is most

likely &resent in this &atientF

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ICFC$!%"r&!en&



Increased Increased Contracted ContractedIncreased Increased 'x&anded Contracted


Answer: '. the &atient has Addisons disease with loss o aldosterone leading to a hy&ertonic loss o luid

in the urine and hy&onatremia. Correlates with diagram B in the study 2uestions -diagrams or 2uestions

87%;$0. *y&ocortisolism causes the increase in ACT* the latter ha(ing melanocyte stimulating

&ro&erties. @ince the adrenal cortex is destroyed -autoimmune0 IG ACT* stimulation will not cause any

increase in adrenal cortex metabolites -e.g. cortisol0. The electrolyte indings in Addisons disease are the

same as those seen in a &atient on an aldosterone blocker mainly hy&onatremia hy&erkalemia and anormal A+ metabolic acidosis.

Os! N"# ECF ICF


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Items $5−$8%H CO2 ()*"r+$n"&e

A. Decrease

d

Increased Decreased

B. ormal ormal ormal C. ormal Increased Increased

$5. A 6$%year%old woman in *r$n)* ren"- .")-re is taking a -$$% )re&)* because o retention o salt.

Answer: B. *r$n)* ren"- .")-re -metabolic acidosis: ↓ &* ↓ PC4$ Kres&iratory alkalosisL ↓↓ bicarbonate Kmetabolic acidosisL0 is taking -$$% )re&)* -metabolic alkalosis: &* PC4$ Kres&iratory

acidosisL bicarbonate Kmetabolic alkalosisL0 or retention o salt. Both conditions neutrali/e each other.

%H CO2 ()*"r+$n"&e

B. ormal ormal ormal

$6. A 7$%year%old smoker with *r$n)* $+s&r*&)e -n )se"se is currently taking a -$$% )re&)* or

right sided heart ailure. *e has signs o (olume de&letion due to his diuretic.

Answer: C. *r$n)* $+s&r*&)e -n )se"se -chronic res&iratory acidosis: ↓ &* PC4$ Kres&iratory

acidosisL bicarbonate Kmetabolic alkalosisL 0 is currently taking a -$$% )re&)* -metabolic alkalosis: &* PC4$ Kres&iratory acidosisL bicarbonate Kmetabolic alkalosisL0. &* is normali/ed additi(e eect on

PC4$ and *C45%H CO2 ()*"r+$n"&e

C. ormal Increased Increased

$7. A $$%year%old man with ty&e 1 diabetes mellitus has )"+e&)* 3e&$"*)$s)s and $!)&)n.

Answer: B. )"+e&)* 3e&$"*)$s)s -metabolic acidosis: ↓ &* ↓ PC4$ Kres&iratory alkalosisL↓↓ bicarbonate Kmetabolic acidosisL0 and $!)&)n -metabolic alkalosis: &* PC4$ Kres&iratoryacidosisL bicarbonate Kmetabolic alkalosisL0. They neutrali/e each other.

%H CO2 ()*"r+$n"&e

B. ormal ormal ormal

$8. A 8=%year%old man has a *"r)$res%)r"&$r4 "rres& and alls unconscious to the ground.

Answer: A. *"r)$res%)r"&$r4 "rres&: acute res&iratory acidosis -not breathing0− ↓ &* PC4$ Kres&iratory acidosisL normal bicarbonate -no time or com&ensation0 ! metabolic acidosis rom tissue

hy&oxia leading to lactic acidosis: ↓ &* ↔ PC4$ Kres&iratory alkalosisL ↓↓ bicarbonate KmetabolicacidosisL0 0 Additi(e eect on lowering &* leading to a (ery low &*. Additi(e eect on PC4$ since the &atient cannot breath and &roduce res&iratory alkalosis as com&ensation or metabolic acidosis. There

would be no time or com&ensation or the acute res&iratory acidosis so bicarbonate would not be

increased and the bicarbonate would be decreased rom the lactic acidosis hence the additi(e eect is a

low bicarbonate.

%H CO2 ()*"r+$n"&e

A. Decreased

Increased Decreased

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$;. A 6>%year%old woman has muscle weakness &olyuria and circumoral &aresthesias. Physical exam

demonstrates diastolic hy&ertension and lexion o the thumb into the &alm on the side the blood

&ressure is taken. A &ositi(e Cho(stek sign is &resent. There is no e(idence o &itting edema.

,aboratory studies show a mild hy&ernatremia se(ere hy&okalemia and metabolic alkalosis. The

total serum calcium is normal. A random urine &otassium is markedly ele(ated. Ehich o theollowing changes in electrolyte and (olume status is most likely &resent in this &atientF

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ICFC$!%"r&!en&


Increased Increased 'x&anded 'x&anded




Answer: '. This is classic &rimary aldosteronism. +aining luid in 'C). *y&ernatremia establishes a

gradient a(oring IC) contraction. Corres&onds with diagram ). There is mild 'C) ex&ansion but not

enough increase in TBa to &roduce signs o &itting edema due to the loss o sodium rom the &roximal

tubule related to the increase in &eritubular ca&illary hydrostatic &ressure rom the increased &lasma

(olume. The tetany is due to the metabolic alkalosis and extra binding o calcium on the albumin -more

negati(e charges KC44%L in an alkaline &*0 without altering the total calcium.Os! N"# ECF ICF


$=. An unconscious $8%year%old man who is a rooer is brought to an emergency room ollowing a allrom a $? oot high roo. Physical exam demonstrates a weak &ulse cold clammy skin and a

blood &ressure o ;?"6? mm *g. The ribs on the lower let side are ractured. A &eritoneal la(age

demonstrates clotted blood. An intra(enous line with ?.> normal saline is currently in &lace while

blood is being crossmatched &rior to surgery. Ehich o the ollowing laboratory and

&atho&hysiologic e(ents would you ex&ect in this &atientF

A. @econdary aldosteronism

B. Positi(e ree water clearance

C. ormal hemoglobin and hematocritD. Decreased serum antidiuretic hormone

'. Decreased eecti(e arterial blood (olume

Answers: A ': the &atient has hy&o(olemic shock rom massi(e blood loss most likely a ru&tured

s&leen since the rib o(erlying the s&leen is ractured. A. secondary aldosteronism: acti(ation o 9AA

system due to decreased renal blood low and direct stimulation by catecholamines '. decreased 'ABG:

B. Positi(e ree water clearance: no it should be negati(e since there would be an increase in AD* andconcentration o urine

C. ormal hemoglobin and hematocrit: no the hemoglobin and hematocrit would be decreased because

the &atient is recei(ing normal saline which is re&lacing the (olume deicit and unco(ering the 9BC

deicit. I the &atient was not recei(ing isotonic saline the *b and *ct would (ery likely be normal.D. Decreased serum antidiuretic hormone: no it would be increased due to direct stimulation o AD*

release rom the C@

$>. ou would ex&ect a clinically signiicant decrease in eecti(e arterial blood (olume -'ABG0 in

which o the ollowing clinical conditionsF SELECT '

A. $%yr%old child with a rota(irus inection

B. 6$%yr%old man with cirrhosis and ascites

C. 8$%yr%old man with ina&&ro&riate AD* syndrome

D. $$%yr%old woman with insensible water loss due to e(er

'. $7%yr%old construction worker with excessi(e sweating on a humid day

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Answers A, (, E: A. $%yr%old child with a rota(irus inection: hy&otonic loss o salt

B. 6$%yr%old man with cirrhosis and ascites: decreased (enous return rom tra&&ing o luid in interstitial

s&ace -decreased oncotic &ressure0 and &eritoneal ca(ity -decreased oncotic &ressure and increased

hydrostatic &ressure0

'. $7%yr%old construction worker with excessi(e sweating on a humid day: sweat is a hy&otonic loss owater and salt

C. 8$%yr%old man with ina&&ro&riate AD* syndrome: no 'ABG is increased rom increased &lasma(olume related to excessi(e reabsor&tion o ree water

D. $$%yr%old woman with insensible water loss due to e(er: no water loss alone does not &roduce

clinically signiicant (olume de&letion -called dehydration0. The 'ABG is normal.

5?. ou would ex&ect a &atient with diabetic ketoacidosis and serum glucose o 1??? mg"d, to ha(e...

SELECT '

A. hy&ertonicity with dilutional hy&onatremia

B. a decreased eecti(e arterial blood (olume

C. random urine sodium $? m'2", - $? m'2",0

D. ex&anded 'C) com&artment due to osmotic shits

'. &ositi(e tilt test when mo(ed rom a su&ine to sitting &osition

Answers A, (, E: A. hy&ertonicity with dilutional hy&onatremia: glucose o(errides sodium in the 'C)causing water to mo(e out o the IC) into the 'C) causing dilution o the serum sodium

B. a decreased eecti(e arterial blood (olume: yes rom osmotic diuresis related to glucose in the urine

&roducing a hy&otonic loss o more water than salt -similar to sweat0

'. &ositi(e tilt test when mo(ed rom a su&ine to sitting &osition: excellent sign o (olume de&letion.There is no eect o gra(ity when lying down so BP and &ulse could be normal but sitting u& urther

reduces (enous return &roducing a dro& in BP and increase in &ulse

C. random urine sodium $? m'2", - $? m'2",0: no it is J$? m'2", owing to a signiicant loss o

sodium in the urine rom osmotic diuresis

D. ex&anded 'C) com&artment due to osmotic shits: no hy&erglycemia a(ors a mo(ement o water out

o the IC) into the 'C) and then the osmotic diuresis causes the loss o that luid in the urine. In other

words the luid in the 'C) does not remain in that com&artment (ery long owing to the loss o hy&otonic

luid in the urine.

Items 51−5;Ser! N"#

51'6

1789

Ser! #

5';6

6;09

Ser! C-<

5=6

1069

Ser! HCO'<

522

2>9

A. 11= 5.? == $1

B. 15? $.> =? 58

C. 1$8 7.= >8 1=

D. 15? 7.7 == 1?

'. 16? 6.? 1?? $6

). 16? $.$ 116 16 +. 17$ $.= 11? 55

51. A 6>%year%old man has atigue and &ostural hy&otension. Physical exam demonstrates dry mucous

membranes an increase in heart rate and dro& in blood &ressure when mo(ed rom the su&ine to

sitting &osition and increased &igmentation in the buccal mucosa. ,aboratory studies re(eal a -$w

ser! *$r&)s$- "n "n )n*re"se )n ACTH.

Answer: C: the &atient has AddisonMs disease and no aldosterone acti(ity: the aldosterone &um&s that are

aected are the a"# ATPase &um& in the late distal and collecting tubules and the *"# ATPase &um& in

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the collecting tubules. @odium is lost &otassium is retained &rotons are retained and combine with

chloride resulting in a normal A+ metabolic acidosis -note that the A+ is 1$ m'2",: 1$8 % K>8 ! 1=L H 1$0

Ser! N"#

51'6

1789

Ser! #

5';6

6;09

Ser! C-<

5=6

1069

Ser! HCO'<

522

2>9

C. 1$8 7.= >8 1=


51'6

1789

Ser! #

5';6

6;09

Ser! C-<

5=6

1069

Ser! HCO'<

522

2>9

A. 11= 5.? == $1

B. 15? $.> =? 58

C. 1$8 7.= >8 1=

D. 15? 7.7 == 1?

'. 16? 6.? 1?? $6

). 16? $.$ 116 16

+. 17$ $.= 11? 55

5$. A 6=%year%old man with let%sided heart ailure has muscle weakness and clinical e(idence o

(olume de&letion. *e is currently taking a -$$% )re&)*. An electrocardiogram shows &rominent <

wa(es.

Answer: B. Classic hy&onatremia hy&okalemia and metabolic alkalosis rom a loo& diuretic.

*y&onatremia is due to a hy&ertonic loss o sodium in urine hy&okalemia rom augmented a"#

exchange and metabolic alkalosis or exchange o a with * ions leading to regeneration o bicarbonate.

This &roile also its (omiting. < wa(es indicate hy&okalemia. uscle weakness is the most common sign

o hy&okalemia.

Ser! N"#

51'6

1789

Ser! #

5';6

6;09

Ser! C-<

5=6

1069

Ser! HCO'<

522

2>9

B. 15? $.> =? 58

55. A 58%year%old woman in )"+e&)* 3e&$"*)$s)s "s %e"3e T w"es on an electrocardiogram. The

serum blood urea nitrogen -B9

). 16? $.$ 117 16

1$

8/18/2019 Acid Base F12

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51'6

1789

Ser! #

5';6

6;09

Ser! C-<

5=6

1069

Ser! HCO'<

522

2>9

A. 11= 5.? == $1

B. 15? $.> =? 58 C. 1$8 7.= >8 1=

D. 15? 7.7 == 1?

'. 16? 6.? 1?? $6

). 16? $.$ 116 16

+. 17$ $.= 11? 55

57. A 6=%year%old woman with Cs)n?s s4nr$!e has se(ere diastolic hy&ertension.

Answer: +. Cushings has mineralocorticoid excess ust like &rimary aldosteronism. ,ab indings are

similar.

Ser! N"#

51'6

1789

Ser! #

5';6

6;09

Ser! C-<

5=6

1069

Ser! HCO'<

522

2>9

+. 17$ $.= 11? 55

58. A 6$%yr%old man has seere $!)&)n related to a (iral gastritis. *e has signs o (olume de&letion.

Answer: B. Gomiting leads to hy&onatremia -loss o sodium in the (omitus0 not hy&ernatremia.

*y&okalemia and metabolic alkalosis also occur. Best 9x is isotonic saline to re&lace the chloride and

(olume de&letion.

Ser! N"#

51'6

1789

Ser! #

5';6

6;09

Ser! C-<

5=6

1069

Ser! HCO'<

522

2>9

B. 15? $.> =? 58

5;. A 7$%year%old ty&e $ diabetic on *-$r%r$%"!)e has mental status abnormalities. Physical exam

is otherwise normal.

Answer: A. Classic @iAD* rom chlor&ro&amide which enhances AD* release. ,ook or e(erything to

be decreased rom dilution. Any serum sodium 1$? m'2", is highly sus&ect or @iAD*.

Ser! N"#

51'6

1789

Ser! #

5';6

6;09

Ser! C-<

5=6

1069

Ser! HCO'<

522

2>9

A. 11= 5.? == $1

5=. ou would ex&ect res&iratory acidosis as com&ensation or which o the ollowing &atient

disordersF SELECT 2A. Barbiturate o(erdose

B. Proximal renal tubular acidosis

C. Chronic obstructi(e &ulmonary disease

D. Golume de&leted &atient taking a loo& diuretic

'. Golume de&leted &atient with &rotracted (omitingAnswers D '. 9es&iratory acidosis is com&ensation or &rimary metabolic alkalosis: D. Golume de&leted &atient taking a loo& diuretic

'. Golume de&leted &atient with &rotracted (omiting

A. Barbiturate o(erdose: no it &roduces acute res&iratory acidosis and metabolic alkalosis is

com&ensation

B. Proximal renal tubular acidosis: no it is an exam&le o normal A+ metabolic acidosis and res&iratory

alkalosis is the com&ensation

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C. Chronic obstructi(e &ulmonary disease: no it is an exam&le o chronic res&iratory acidosis and

metabolic alkalosis is its com&ensation

5>. ou would ex&ect an increase in eecti(e arterial blood (olume -'ABG0 in which o the ollowing

clinical conditionsF SELECT 'A. 9ight%sided heart ailure

B. Primary aldosteronismC. Acute myocardial inarction

D. 4(er/ealous inusion with ?.> normal saline

'. Inusion with excessi(e amounts o 5 hy&ertonic saline

Answers (, D, E: B. Primary aldosteronism: yes due to excess sodium in the 'C) which increases the

&lasma (olume D. 4(er/ealous inusion with ?.> normal saline '. Inusion with excessi(e amounts o

5 hy&ertonic saline

A. 9ight%sided heart ailure: no 'ABG is decreased due to a decrease in cardiac out&ut

C. Acute myocardial inarction: no 'ABG is decreased due to a decrease in cardiac out&ut

6?. Ehich o the ollowing (olume disorders re&resents a transudate secondary to a decrease in oncotic

&ressure and increase in hydrostatic &ressureF

A. Patient with cirrhosis de&endent &itting edema and ascitesB. Patient with a &ulmonary inarction who has a &leural eusion

C. Patient with edema o the arm &ost%modiied radical mastectomy

D. Patient with congesti(e heart ailure who has de&endent &itting edema

'. Patient with congesti(e heart ailure who has bilateral &leural eusions

Answer: A. Patient with cirrhosis de&endent &itting edema and ascites: &ortal hy&ertension increases

hydrostatic &ressure leading to ascites and decreased albumin synthesis &roduces a decrease in oncotic

&ressure leading to de&endent &itting edema and ascites

B. Patient with a &ulmonary inarction who has a &leural eusion: no this is an exudate -&rotein and cell

rich luid0

C. Patient with edema o the arm &ost%modiied radical mastectomy: no this is lym&hedema

D. Patient with congesti(e heart ailure who has de&endent &itting edema: no this is associated with an

increase in hydrostatic &ressure rom right%sided heart ailure'. Patient with congesti(e heart ailure who has bilateral &leural eusions: no this is due to an increase in

hydrostatic &ressure

61. Ehich o the ollowing edema conditions re&resents a transudate secondary to an increase in

hydrostatic &ressureF SELECT 2

A. Patient with swelling o the arm ater a bee stingB. Patient with cerebral edema secondary to hy&onatremia

C. Patient with congesti(e heart ailure who has &ulmonary edema

D. Patient with congesti(e heart ailure who has de&endent &itting edema

'. Patient with kwashiorkor who has ascites and de&endent &itting edema

Answers C, D: C. Patient with congesti(e heart ailure who has &ulmonary edema: increase in

hydrostatic &ressure rom increased let (entricular end%diastolic (olume and &ressure. Pulmonary edemaoccurs in let%sided heart ailure.

D. Patient with congesti(e heart ailure who has de&endent &itting edema: in right%sided heart ailure the

blood accumulates in the (enous system and raises the hydrostatic &ressure leading to neck (ein

distention he&atomegaly ascites and de&endent &itting edema.

A. Patient with swelling o the arm ater a bee sting: no this is an exudate rom increased (essel

&ermeability related to histamine release in a ty&e I hy&ersensiti(ity reaction.

B. Patient with cerebral edema secondary to hy&onatremia: no this is a water shit into the IC) rom

hy&onatremia -osmosis not a @tarlings orce abnormality0

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'. Patient with kwashiorkor who has ascites and de&endent &itting edema: no this &roduces a transudate

due to decreased oncotic &ressure related to a decreased &rotein intake

Items 6$−68

( C

Os!

A D

Ser! ADH

The s2uare re&resents normal (alues in a normally hydrated &atient.

6$. A 6$%yr%old woman recei(es an intra(enous inusion o 1 liter o 5 hy&ertonic saline.

Answer: C: hy&ertonic gain o luid increase P4sm -hy&ernatremia0 which is a stimulus or AD*

release

65. A 8$%yr%old smoker with a small cell carcinoma o the lung is diagnosed with ina&&ro&riate AD*syndrome.

Answer: D: decrease P4sm -hy&onatremia0 but increase in AD*. ormally this should not occur. The &atient is concentrating urine when they should be diluting urine.

66. A 85%yr%old instructor who has been drinking a lot o water during an = hr lecture has to make

re2uent tri&s to the bathroom during e(ery break.

Answer: A: instructor is drinking excess water and needs to dilute urine. Decreased P4sm and inhibition

o AD* or dilution

67. A 6$%yr%old man who is &re&aring or a marathon orgot to bring re&lacement luid during a 17

mile run on a hot humid day.

Answer: C: &atient is (olume de&leted and needs to concentrate urine. Increased P4sm which is astimulus or AD* release and concentration o urine.

68. A $$%yr%old man who suered a head inury in a car accident now has increased thirst and &olyuria.

Answer: B: central diabetes insi&idus with no AD*. ,oss o &ure water leads to hy&ernatremia -increased

P4sm0. The &atient is diluting urine when they should be concentrating urine. 4&&osite o @iAD*.

6;. An aebrile $=%year%old medical student who s&ent a weekend in Tiuana exico de(elo&s

tra(elers diarrhea. Physical exam demonstrates signs o (olume de&letion. Ehich o the ollowingchanges in electrolyte and (olume status is most likely &resent in this &atientF

Os! N"# ECF

C$!%"r&!en&

ICF

C$!%"r&!en&

Increased Increased Contracted Contracted ormal ormal Contracted ormal

ormal ormal Contracted 'x&anded



Answer: B. isotonic loss o luid. o osmotic gradient. Correlates with diagram A in the study 2uestions.

17

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Os! N"# ECF ICF


6=. 9es&iratory alkalosis would be ex&ected as com&ensation in which o the ollowing &atient

conditionsF SELECT 2

A. *y&er(entilation

B. Chronic renal ailure

C. Pulmonary inarction

D. 'thylene glycol &oisoning

'. Gomiting secondary to gastritis

Answers: (, D. res&iratory alkalosis is com&ensation or a &rimary metabolic acidosis: B. Chronic renal

ailure: increased A+ metabolic acidosis

D. 'thylene glycol &oisoning: ethylene glycol is con(erted by alcohol dehydrogenase to glycolic and

oxalic acid the latter orming calcium oxalate crystals in the kidney tubules causing renal ailure

A. *y&er(entilation: no this &roduces a &rimary res&iratory alkalosis and metabolic acidosis is

com&ensation

C. Pulmonary inarction: no this &roduces a &rimary res&iratory alkalosis rom tachy&nea and metabolic

acidosis is com&ensation

'. Gomiting secondary to gastritis: no this &roduces a &rimary metabolic alkalosis and res&iratory

acidosis is com&ensation.

Items 6>−7=%H

58;'6

8;769

CO25''

76 !! H9

HCO'<

522

2> !E@/L9

;.?? 7$ 1$

;.$; 8? $8

;.$7 =? 56

;.$8 $8 11

;.5= ;? 6?

;.5= 6? $6

;.6$ $$ 16

;.78 $6 $1

;.7= 6> 5>

6>. A 57%year%old recently di(orced woman o(erdoses on +"r+)&r"&es.

Answer: B. Barbiturates de&ress the res&iratory center &roducing an acute res&iratory acidosis without

com&ensation.

%H

58;'6

8;769

CO25''

76 !! H9

HCO'<

522

2> !E@/L9

;.$; 8? $8

18

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17/39

Items 6>−7=%H

58;'6

8;769

CO25''

76 !! H9

HCO'<

522

2> !E@/L9

;.?? 7$ 1$

;.$; 8? $8

;.$7 =? 56

;.$8 $8 11

;.5= ;? 6?

;.5= 6? $6

;.6$ $$ 16

;.78 $6 $1

;.7= 6> 5>

7?. A 68%yr%old woman with rheumatoid arthritis de(elo&s tinnitus. ou sus&ect the &atient has

s"-)*4-"&e &$)*)&4.

Answer: +. s"-)*4-"&e &$)*)&4 is a mixed disorder: res&iratory alkalosis -res&iratory center stimulation0 !

metabolic acidosis -salicylic acid ! lactic acid0

%H

58;'6

8;769

CO25''

76 !! H9

HCO'<

522

2> !E@/L9

;.6$ $$ 16

71. A 1>%year%old ty&e 1 diabetic is in 3e&$"*)$s)s and is $!)&)n.

Answer: ). 3e&$"*)$s)s is an increased A+ metabolic acidosis and $!)&)n &roduces metabolic

alkalosis. These $ disorder neutrali/e each other. ote that the normal &* is on the acid side so the

ketoacidosis is a little worse than the metabolic alkalosis.

%H58;'6

8;769

CO25''

76 !! H9 HCO'

<

522

2> !E@/L9

;.5= 6? $6

7$. A 6>%year%old woman with *r$n)* +r$n*)&)s secondary to smoking is taking a -$$% )re&)* or

congesti(e heart ailure.

Answer: '. *r$n)* +r$n*)&)s &roduces chronic res&iratory acidosis and a -$$% )re&)* &roduces

metabolic alkalosis. This is a mixed disorder: &* should be normal PC4$ markedly increased since both

disorders ha(e an increase in PC4$ and the bicarbonate should be markedly increased since both

disorders ha(e an increase in bicarbonate.

%H

58;'6 8;769

CO2

5''

76 !! H9

HCO'<

522

2> !E@/L9

;.5= ;? 6?

75. A se&tic ;$%yr%old man has urinary retention secondary to &rostatic hy&er&lasia. ou sus&ect the

&atient has en$&$)* s$*3 .

Answer: +. en$&$)* s$*3 &roduces a mixed disorder: res&iratory alkalosis− o(erstimulates theres&iratory center ! metabolic acidosis rom shock leading to lactic acidosis. This is a mixed disorder. The

1;

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&* changes neutrali/e each other. Both PC4$ and bicarbonate are decreased in both conditions &roducing

an additi(e eect.

%H

58;'6

8;769

CO25''

76 !! H9

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;.6$ $$ 16

Items 6>−7=%H

58;'6

8;769

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76 !! H9

HCO'<

522

2> !E@/L9

;.?? 7$ 1$

;.$; 8? $8

;.$7 =? 56

;.$8 $8 11

;.5= ;? 6?

;.5= 6? $6 ;.6$ $$ 16

;.78 $6 $1

;.7= 6> 5>

76. A $1%year%old man with cystic ibrosis who has had recurrent &ulmonary inections almost all his

lie has e(er and a &roducti(e cough consistent with "*&e +r$n*)&)s $r %ne!$n)".

Answer: C. cystic ibrosis &roduces chronic obstructi(e lung disease and chronic res&iratory acidosis. An

"*&e +r$n*)&)s $r %ne!$n)" su&erim&oses an acute res&iratory acidosis on to& o a chronic

res&iratory acidosis. Chronic res&iratory acidosis is associated with metabolic alkalosis as com&ensation

unlike acute res&iratory acidosis -choice B0 which does not. The PC4$ is &robably higher than usual

owing to the su&erim&osed acute bronchitis or &neumonia. Beore the &atient got a su&erim&osedinection the &* was &robably around ;.55 and PC4$ around 8?. This is a ty&e o mixed disorder.

%H

58;'6

8;769

CO2

5'' 76 !! H9

HCO'<

522 2> !E@/L9

;.$7 =? 56

77. A 57%yr%old migrant worker inad(ertently drinks !e&4- "-*$$-. *e de(elo&s gastric u&set and

blurry (ision.

Answer: D. !e&4- "-*$$- &roduces an increased A+ metabolic acidosis because it is metaboli/ed by

alcohol dehydrogenase to ormic acid which &roduces o&tic neuritis and a &otential or blindness.

%H

58;'6

8;769

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76 !! H9

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522

2> !E@/L9

;.$8 $8 11

78. A 78%year%old man is in *"r)$res%)r"&$r4 "rres&. ou arri(e on the scene N$ minutes ater the

&atient lost consciousness.

Answer: A. *"r)$res%)r"&$r4 "rres& is associated with a &rimary acute res&iratory acidosis -not

breathing0 ! metabolic acidosis rom lactic acidosis. 'x&ect a (ery low acid &*.

%H CO2 HCO'<

1=

8/18/2019 Acid Base F12

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58;'6

8;769

5''

76 !! H9 522

2> !E@/L9

;.?? 7$ 1$

7;. A $6%yr%old medical student de(elo&s an "n)e&4 "&&"*3 while taking a com&rehensi(e inal exam

Answer: *. an "n)e&4 "&&"*3 &roduces an acute res&iratory alkalosis owing to excessi(e blowing o o

C4$. ote the &artially com&ensated metabolic acidosis. on%renal mechanisms are able to lower the bicarbonate to 1= m'2",.

%H

58;'6

8;769

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5'' 76 !! H9

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Items 6>−7=%H

58;'6

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76 !! H9

HCO'<

522

2> !E@/L9

;.?? 7$ 1$

;.$; 8? $8

;.$7 =? 56

;.$8 $8 11

;.5= ;? 6?

;.5= 6? $6

;.6$ $$ 16

;.78 $6 $1

;.7= 6> 5>

7=. A $ mth old child has re&eated $!)&)n o non%bile stained luid. ou sus&ect congenital &yloric

stenosis.Answer: I. $!)&)n &roduces metabolic alkalosis

%H

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8;769

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7>. Ehich o the ollowing &atients would most likely ha(e clinical e(idence o de&endent &itting

edema i an alteration in @tarlings orces is &resent &lus a stimulus or renal retention o saltF

SELECT 2

A. Patient with diabetes insi&idus

B. Patient with congesti(e heart ailure

C. Patient with ina&&ro&riate AD* syndromeD. Patient recei(ing excessi(e ?.> normal saline

'. Patient recei(ing excessi(e 7 dextrose and water

Answers: (, D. the &atient must ha(e an increase in TBa! and a &reexisting @tarlings orce abnormality

! renal retention o sodium in order to ha(e &itting edema:

B. Patient with congesti(e heart ailure: hy&otonic gain o more water than salt

D. Patient recei(ing excessi(e ?.> normal saline

1>

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A. Patient with diabetes insi&idus: no there is hy&ernatremia due to a loss o &ure water. TBa! is

normal. An osmotic gradient is established and water mo(es out o the IC) into the 'C) and rom the

'C) out into the urine as ree water so both com&artments are contracted.

C. Patient with ina&&ro&riate AD* syndrome: no the &atient has a gain o &ure water. TBa! is normal.

An osmotic gradient is established causing water to mo(e into the IC). Both 'C) and IC) com&artmentsare ex&anded.

'. Patient recei(ing excessi(e 7 dextrose and water: no the &atient is gaining a hy&otonic solution withno salt. TBa! is normal. An osmotic gradient is established -hy&onatremia0 and water shits rom the

ex&anded 'C) com&artment into the IC) com&artment

$?

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Items 8?−8$MBO2 CW

5LBED9

SBR

5TR9

C"r)"* $&%&

Decreased Decreased Increased Decreased

Decreased Increased Increased Decreased

Increased Decreased Decreased Increased

ormal ormal ormal ormal,G'DP let (entricular end%diastolic &ressure3 G4$ mixed (enous oxygen content3 PCEP &ulmonary

ca&illary wedge &ressure3 @G9 systemic (ascular resistance3 TP9 total &eri&heral resistance.

8?. A ;$%year%old man with urinary retention rom benign &rostatic hy&er&lasia has a sudden onset o

e(er and chills. *is skin eels warm and his &ulse is hy&erdynamic.

Answer: C. This is se&tic -endotoxic shock0. 9emember (asodilation o arterioles decreases &eri&heral

(ascular resistance -decrease in @G9 which is the same as total &eri&heral resistance0. It drastically

lowers the diastolic blood &ressure and causes blood to mo(e 2uickly through the microcirculation -like a

dam with its lood gates wide o&en0 making it im&ossible or tissue to extract oxygen -increased G4$0.

Genous return to the heart increases -increased cardiac out&ut0. This is called high out&ut cardiac ailure.

The heart will not last too long with this increased load and e(entually the &atient will &rogress into

indings consistent with cardiogenic shock. Pulmonary ca&illaries become &ermeable owing to neutro&hilinury and an exudate leaks into the al(eoli causing A9D@. PCEP -a measure o let%sided let (entricular

&ressure0 is decreased. This is an exam&le o a non%cardiogenic &ulmonary edema.

MBO2 CW SBR C"r)"* $&%&

Increased Decreased Decreased Increased

81. A ;7%year%old man with a known history o an abdominal aortic aneurysm ex&eriences a sudden

onset o let lank &ain and di//iness. *e is brought to the emergency room and has a heart rate o16? beats"minute blood &ressure o 8?"6? mm *g and a &ulsatile mass in his abdomen. ou

sus&ect a ru&tured abdominal aortic aneurysm.

Answer: A. the &atient is in hy&o(olemic shock. The key dierence rom cardiogenic shock is the low

PCEP. G4$ is low since the decreased cardiac out&ut allows tissue to extract most o the oxygen out o

the blood. @G9 is increased owing to (asoconstriction o the &eri&heral resistance arterioles which

decreases the radius to the 6th &ower.MBO2 CW SBR C"r)"* $&%&

Decreased Decreased Increased Decreased

8$. A 8?%year%old man has an acute myocardial inarction which &rogressed into congesti(e heart

ailure within $6 hrs o admission to the coronary care unit.

Answer: the &atient has let%sided heart ailure.

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Answer: C. the &atient has let%sided heart ailure -&ulmonary edema0 and right%sided heart ailure -neck

(ein distention and de&endent &itting edema0. In either case there is an alteration is @tarlings orces

-increased hydrostatic &ressure0 and a decreased cardiac out&ut leading to retention o a slightly

hy&otonic salt%containing solution - TBa " TBE0. 4wing to the increase in hydrostatic &ressure in the

(enous system in right%sided heart ailure most o this hy&otonic luid will mo(e into the interstitial s&aceand worsen the de&endent &itting edema. @ince both TBa and TBE are increased the best non%

&harmacologic treatment or this &atient and any other similar ty&e o edema state -e.g. cirrhosisne&hrotic syndrome0 is to restrict both water and salt. Diuretics are the most useul &harmacologic

treatment.

S$)! )n&"3e W"&er )n&"3e

C. Decrease Decrease

86. In treating a &atient with the ina&&ro&riate AD* syndrome which o the ollowing is the MOST

ARORIATE management o the &atientMs sodium and water intakeF

S$)! )n&"3e W"&er )n&"3e

A. Decrease o change

B. o change o change

C. Decrease Decrease

D. o change Decrease'. Increase Increase

Answer: D. &atients with @iAD* ha(e a hy&otonic gain o &ure water without any salt. Thereore only

water is restricted and not salt since the TBa! is normal.

S$)! )n&"3e W"&er )n&"3e

D. o change Decrease

$$

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Items 87−;$

Os! ICF ECF

B$-!e

N$&e: the height o the s2uares re&resent &lasma osmolality -P4sm0 while the width o the s2uares

re&resents (olume in each com&artment. 'C) is the extracellular luid com&artment and IC) is the

intracellular luid com&artment. The dark lines re&resent the normal P4sm and (olume in each

com&artment while the hash marked lines re&resent the (olume alteration.

A; (;

C; D;

E; F;

87. The &atient is a 67%yr%old man who is (olume de&leted secondary to the use o loo& diuretics.

Answer: B. *y&ertonic loss o luid with hy&onatremia with 'C) contraction and IC) ex&ansion

88. The &atient is a $5%yr%old marathon runner who is (olume de&leted ater running on a hot humid

day.

Answer: '. the &atient is losing sweat where there is a hy&otonic loss o more water than salt. This

causes hy&ernatremia with 'C) contraction and IC) contraction. The water that shits into the 'C) rom

the IC) is lost in the sweat.

$5

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8;. The &atient is a 86%yr%old smoker with a small cell carcinoma o the lung and ina&&ro&riate AD*

syndrome.

Answer: D. *y&otonic gain o &ure water and no salt. *y&onatremia with 'C) ex&ansion and IC)

ex&ansion.

Items 87−;$

Os! ICF ECF

B$-!e

N$&e: the height o the s2uares re&resent &lasma osmolality -P4sm0 while the width o the s2uares

re&resents (olume in each com&artment. 'C) is the extracellular luid com&artment and IC) is the



A; (;

C; D;

E; F;

8=. The &atient is a 8=%yr%old man with a known history o ischemic heart disease. *e has &neumonia

due to Pseudomonas aeruginosa and is recei(ing an )n&r"en$s s$-&)$n *$n&")n)n s$)!

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*"r+en)*)--)n. *e has &hysical indings consisting o bibasilar crackles neck (ein distention

he&atomegaly and &itting edema.

Answer: ). *y&ertonic gain o sodium rom the IG. *y&ernatremia 'C) ex&ansion IC) contraction

8>. A ;=%yr%old woman with a known history o ischemic heart disease has a bilateral hi& re&lacementor se(ere osteoarthritis in(ol(ing the emoral heads. @he has been $ere"-$s-4 )n.se w)&

0;= n$r!"- s"-)ne and has &itting edema and bibasilar cre&itant crackles.Answer: C. Isotonic gain o luid with normal serum sodium ex&ansion o 'C) normal IC) since there

is no osmotic gradient

Items 87−;$

Os! ICF ECF

B$-!e

N$&e: the height o the s2uares re&resent &lasma osmolality -P4sm0 while the width o the s2uaresre&resents (olume in each com&artment. 'C) is the extracellular luid com&artment and IC) is the



A; (;

C; D;

E; F;

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;?. The &atient is a 6$%yr%old medical missionary with *$-er". *e is (olume de&leted.

Answer: A. Isotonic loss o luid. @erum sodium is normal 'C) is contracted IC) is normal since there

is no osmotic gradient. Vibrio cholerae &roduces a toxin that stimulates adenylate cyclase causing anisotonic loss o luid. There is no bowel inlammation.

;1. The &atient is a 8>%yr%old with ischemic heart disease and both let%sided and right%sided heart

ailure.

Answer: D. *y&otonic gain o more water than salt rom the kidneys leading to hy&onatremia 'C)

ex&ansion and IC) ex&ansion. ote that the same schematic a&&lies to both @iAD* and heart ailure

since both are hy&otonic gains o luid. *owe(er the &hysical exam is dierent not to mention the

history. In @iAD* the TBa is normal hence skin turgor is normal while in right%sided heart ailure

there is an increase in TBa and de&endent &itting edema.

Items 87−;$

Os! ICF ECF

B$-!e

N$&e: the height o the s2uares re&resent &lasma osmolality -P4sm0 while the width o the s2uaresre&resents (olume in each com&artment. 'C) is the extracellular luid com&artment and IC) is the



A; (;

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C; D;

E; F;

;$. The &atient is =$%years%old and has 106$ F &e!%er"&re rom a lobar &neumonia.

Answer: '. Insensible water loss rom e(er. *y&otonic loss o &ure water with hy&ernatremia mild

'C) contraction -normal &hysical exam0 and IC) contraction. ,oss o &ure water without any salt does

not alter skin turgor. This is called dehydration.

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;5. Ehich o the ollowing best ex&lains the mechanism or hy&okalemia in &atients with res&iratory

or metabolic alkalosisF

A. Potassium loss in the urine

B. Potassium loss in the gastrointestinal tract

C. Potassium shit into cells in exchange or &rotonsD. Potassium shit into cells in exchange or chloride

'. Potassium shit into cells in exchange or bicarbonateAnswer: C. Potassium shit into cells in exchange or &rotons -hydrogen ions0.

A. Potassium loss in the urine: this would only be correct i the metabolic alkalosis was caused by loo& or

thia/ide diuretics or mineralocorticoid excess

B. Potassium loss in the gastrointestinal tract: this would only be correct or diarrhea howe(er it

&roduces a normal A+ metabolic acidosis. The ex&ected hy&erkalemia rom a shit o &otassium out o

the cell in exchange or &rotons does not o(erride the greater loss o &otassium in the stool

D. Potassium shit into cells in exchange or chloride: this exchange does not occur. The exchange o

chloride is with bicarbonate. Ehen bicarbonate lea(es a cell -e.g. the &atient has res&iratory acidosis and

a non%renal mechanism or increasing bicarbonate as com&ensation is re2uired0 chloride enters the cell in

order to maintain electroneutrality. Ehen bicarbonate mo(es into a cell -e.g. the &atient has res&iratory

alkalosis and need a non%renal mechanism or remo(ing bicarbonate rom the blood to &roduce metabolic

acidosis as com&ensation0 chloride mo(es out o the cell to maintain electroneutrality.'. Potassium shit into cells in exchange or bicarbonate: this ty&e o exchange does not occur in cells.

;6. Ehich o the ollowing conditions are commonly associated with &rominent < wa(es on an

electrocardiogramF SELECT 'A. Addisons disease

B. Protracted (omiting

C. Aldosterone blockers

D. Distal renal tubular acidosis

' Patient on high doses o albuterol

). Destruction o the uxtaglomerular a&&aratus

Answers (, D, E: a < wa(e indicates the &resence o hy&okalemia B. Protracted (omiting: metabolic

alkalosis. Potassium is lost in the (omitus.D. Distal renal tubular acidosis: block o &roton"# ! &um&

'. Patient on high doses o albuterol: enhances the a"# ATPase &um&3 hence increasing cellular u&take

o # ! and cellular loss o a!

A. Addisons disease: no loss o mineralocorticoids results in hy&erkalemia since the a"# ATPase &um&

in the distal and collecting tubule is dysunctional. This is the &rimary &um& or remo(ing excess

&otassium rom the body.C. Aldosterone blockers: no same ex&lanation as or A.

). Destruction o the uxtaglomerular a&&aratus: no destroying the O+ a&&aratus lowers renin which

lowers AT II and aldosterone. Decreased aldosterone results in hy&onatremia 4%er3"-e!)" and normal

A+ metabolic acidosis. This is called ty&e IG 9TA and is most oten secondary to diabetic renal diseasewhere the aerent arteriole is damaged by hyaline arteriolosclerosis.

;7. Ehich o the ollowing conditions are commonly associated with &eaked T wa(es on an

electrocardiogramF SELECT 'A. Patient with se(ere diarrhea

B. Patient taking excess digitalis

C. Patient with chronic renal ailure

D. Patient on high doses o a β%blocker '. Patient with &roximal renal tubular acidosis

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Answers (, C, D: &eaked T wa(es indicate hy&erkalemia: B. Patient taking excess digitalis: blocks the

a!"# ! ATPase sym&orter so more # ! is &um&ed out o the cell

C. Patient with chronic renal ailure: cannot excrete &otassium -CC0 D. Patient on high doses o a β% blocker: inhibits the ATPase &um& causing a loss o # ! rom cells and gain in a!

A. Patient with se(ere diarrhea: no it &roduces hy&okalemia and a < wa(e

'. Patient with &roximal renal tubular acidosis: no it &roduces hy&okalemia owing to loss o &otassium

when it combines with bicarbonate in the urine and is excreted. @odium is also lost in the urine when itcombine with bicarbonate to &roduce sodium bicarbonate.

;8. Ehich o the ollowing is the initial ste& in the management o hy&erkalemiaF

A. ,oo& diuretic

B. Thia/ide diuretic

C. Calcium gluconate

D. Cationic exchange resins

'. Insulin with glucose inusion

Answer: C. Calcium gluconate: &rotect the heart with calcium gluconate. It does not lower &otassium

le(els. All the other choices deal with either shiting # ! into cells -e.g. insulin albuterol0 or excreting # !

-e.g. diuretics0

A. ,oo& diuretic: yes but not as the initial ste& since it does not immediately &rotect the heartB. Thia/ide diuretic: same ex&lanation as A

D. Cationic exchange resins: yes they do bind to # ! in the bowel and aid in its excretion howe(er it doesnot work ast enough to &rotect the heart

'. Insulin with glucose inusion: yes it shits # ! into the cell by enhancing the a"# ATPase &um&

howe(er it does not do it ast enough to &rotect the heart.

;;. The &ur&ose or &lacing &atients at risk or thrombosis on low dose as&irin is to &re(ent

SELECT '

A. strokes

B. &latelet aggregation

C. intra(ascular coagulation

D. acute myocardial inarctions'. thrombosis in dee& (eins o the cal

). thrombosis in su&ericial (aricose (eins

Answers A, D, D: A. strokes

B. &latelet aggregation

D. acute myocardial inarctions. The &ur&ose o using as&irin is to &re(ent &latelet aggregation and the

&otential or orming a &latelet thrombus o(erlying atherosclerotic &la2ues in the coronary artery or at the

branch o the carotid artery in the neck. As&irin blocks &latelet cyclooxygenase which &re(ents the

synthesis o TQA$. TQA$ normally causes &latelet aggregation.C. intra(ascular coagulation: no as&irin does not aect the coagulation actor &athway. Disseminated

intra(ascular coagulation is due to acti(ation o the coagulation &athway -extrinsic intrinsic or both0

leading to the ormation o ibrin clots in small (essels throughout the body. Coagulation actors that are

normally consumed in a ibrin clot are used u& -e.g. ibrinogen &rothrombin G GIII03 hence the &atientis also anticoagulated.

'. thrombosis in dee& (eins o the cal: no (enous clots resemble ibrin%clots that de(elo& in a clot tube

-red to& tube0. They are due to acti(ation o the coagulation system rather than acti(ation o &latelets to

aggregate.

). thrombosis in su&ericial (aricose (eins: no same ex&lanation as in '

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;=. Ehich o the ollowing coagulation actors is an actual com&onent o both (enous and arterial

thrombiF

A. )ibrin

B. )actor QII

C. Prothrombin -actor II0D. )actor G

'. )actor GIIIAnswer: A. .)+r)n: )ibrin is res&onsible or the stability o both (enous and &latelet thrombi. )ibrin has

cross%links that increase its tensile strength. Platelets normally ha(e ibrinogen rece&tors. Ehen &latelet

initially aggregate ibrinogen -carried by the &latelet0 attaches to the &latelet rece&tors and loosely holds

them together. Ehen thrombin is ormed the ibrinogen is con(erted into ibrin which makes the &latelet

thrombus stable. In (enous clots ibrin also holds the clot together and tra&s 9BCs &latelets and

leukocyte in its meshwork.

B. )actor QII: no it is the &rimary coagulation actor that when acti(ated initiates the clotting se2uence

in the intrinsic system. It is not an actual com&onent o the &latelet and (enous clot. 9ecall that &latelet

thrombi generally occur in the setting o turbulence and endothelial cell damage in the arterial system

while (enous clots de(elo& in the (enous system in the setting o stasis and hy&ercoagulability. 4ne

cannot ex&ect a (enous ty&e ibrin clot which tra&s 9BCs &latelet and leukocytes to de(elo& in a ra&id

blood low situation. *owe(er &latelets become tightly adherent to areas o endothelial damage in highlow situations hence they are more likely to de(elo& o(er atherosclerotic debris within the arterial

system &articularly when they begin to occlude the lumen and &roduce signs o ischemia. This is not to

say that the intrinsic or extrinsic system are not acti(ated in the arterial system when endothelial inury

occurs because it is acti(ated and will &roduce thrombin howe(er it will not be able to tra& 9BCs &latelets and leukocytes in it due to the ra&id blood low. The thrombin howe(er will be able to con(ert

ibrinogen holding &latelets together into ibrin to orm a &latelet thrombus.

C. Prothrombin -actor II0: no it is used u& in the ormation o a clot and is not an actual com&onent o

the &latelet and (enous clot.

D. )actor G: no it is used u& in the ormation o a clot and is not an actual com&onent o the &latelet and

(enous clot.

'. )actor GIII: no it is used u& in the ormation o a clot and is not an actual com&onent o the &latelet

and (enous clot.

;>. A $5%yr%old man is &laced in the intensi(e care unit ater sustaining emoral bone ractures multi&le

&el(ic ractures and a laceration o the s&leen rom a motorcycle accident. )orty eight hours later

he de(elo&s a sudden onset o dys&nea &etechial lesions on the thorax and mental status

alterations. ,aboratory studies re(eal hy&oxemia and thrombocyto&enia. The &rothrombin time and

&artial thrombo&lastin time are both normal. The &atient most likely has which o the ollowingdisordersF

A. Disseminated intra(ascular coagulation

B. Pulmonary embolism

C. )at emboli/ationD. Air emboli/ation

'. PneumoniaAnswer: C. )at emboli/ation: this is a classic case with all the clinical indings. icroglobules o at

rom the marrow and surrounding adi&ose enter the microcirculation and circulate throughout the body

since they are small enough to mo(e through ca&illaries. The atty acids released rom the at damages the

endothelial cells in the micro(asculature causing &latelet adherence to the damaged endothelium hence

they are used u& and &roduce thrombocyto&enia. Blockage o the microcirculation is thereore due to the

microglobules o at as well as tiny &latelet thrombi. The endothelial cell damage does not occur

immediately and re2uires at least $6%6= hrs hence the delay in sym&toms in at emboli/ation. Dys&nea is

due to blockage o the &ulmonary ca&illaries -&erusion deect leading to hy&oxemia0. Thrombocyto&enia

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is due to increased utili/ation in the ormation o &latelet thrombi in areas o endothelial damage and due

to adherence to the microglobules o at. Thrombocyto&enia is also the cause o the &etechial lesions

-&in&oint areas o hemorrhage0 in the &atient. ental status abnormalities are due to minute hemorrhages

into the brain rom the blocked ca&illaries leading to cerebral edema.

A. Disseminated intra(ascular coagulation: this may occur in the setting o trauma howe(er since thecoagulation system is acti(ated in this disorder resulting in the ormation o ibrin%clots the &rothrombin

time and &artial thrombo&lastin time should be &rolonged -ibrinogen II G and GIII are consumed0B. Pulmonary embolism: this may also occur in se(erely traumati/ed &atients howe(er there is no

history o cal tenderness -sign o dee& (enous thrombosis0 or &leuritic chest &ain which in(ariably

accom&anies a &ulmonary embolus. In addition a P' does not &roduce thrombocyto&enia.

D. Air emboli/ation: the clinical setting in this &atient is not one or air embolism. This usually occurs in

head and neck ty&es o surgery.

'. Pneumonia: the clinical setting is one o trauma not inection. There is no mention o &hysical indings

in the lung that would lead one to sus&ect a &neumonia: e.g. signs o consolidation in the lung crackles

in the lung with ins&iration.

=?. A $5%yr%old scuba di(er who is di(ing in 1?? eet o water is orced to ascend to the surace owing

to mechanical diiculties with his di(ing gear. Eithin 1?−17 minutes ater resuracing blood begins to oo/e out o both ear canals his skin becomes mottled and &ruritic and he begins to lose both bladder and bowel control. The &athogenesis o these indings most closely correlates with

which o the ollowing actorsF SELECT 2A. )at emboli/ation

B. Carbon dioxide narcosis

C. itrogen gas bubbles in tissue"(essels

D. o(ement rom a high to lower atmos&heric &ressure

Answers C, D: C. itrogen gas bubbles in tissue"(essels: atmos&heric &ressure increase by 1 or e(ery 55

eet descent into the water which dri(es nitrogen into tissues. 9a&id ascent causes the nitrogen to come

out o solution to orm bubbles that block (essels and damage tissue

D. o(ement rom a high to lower atmos&heric &ressure

A. )at emboli/ation: no this usually occurs in the setting o trauma with ractures o the &el(ic bones or

emur B. Carbon dioxide narcosis: no this is a eature o res&iratory acidosis leading to retention o C4$ and

se(ere hy&oxemia.

=1. Ehich o the ollowing are the most common sites &redis&osing or (enous thrombosis and

emboli/ation res&ecti(elyF

A. Dee& (ein o cal " dee& (ein o cal

B. @a&henous (ein " dee& (ein o cal

C. Dee& (ein o cal " sa&henous (einD. )emoral (ein " dee& (ein o cal

'. Dee& (ein o cal " emoral (ein

Answer: '. Dee& (ein o cal " emoral (ein: most (enous thrombi initially de(elo& in the smaller caliber

(essel in the dee& (eins o the cal. In this location they &ro&agate towards the heart hence extendinginto the larger caliber emoral (ein where emboli/ation is more likely to occur.

A. Dee& (ein o cal " dee& (ein o cal: no it is not the C site or emboli/ation

B. @a&henous (ein " dee& (ein o cal: thrombi in the sa&henous commonly occur in the setting o

(aricose (eins howe(er the emoral (ein is the C site or emboli/ation

C. Dee& (ein o cal " sa&henous (ein: thrombi in the sa&henous (ein which is the su&ericial (enous

system o the legs cannot emboli/e since the thrombi could ne(er get through the &enetrating branches to

the dee& (enous system

D. )emoral (ein " dee& (ein o cal: no this is re(ersed

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=$. Ehich o the ollowing is the greatest risk actor or a (enous clot in the lower extremity in a

&atient who is 7 days &ost%o&erati(e or remo(al o a gangrenous gallbladderF

A. Turbulent blood low

B. @tasis o blood low

C. Increased &lasma (iscosityD. @e&ticemia

Answer: B. @tasis o blood low: lack o mo(ement o the &atient in bed &redis&oses to stasis and (enousthrombi that most commonly de(elo& initially in the dee& (eins o the cal hence the im&ortance o

ambulation in the &atient as soon as &ossible.

A. Turbulent blood low: no turbulent blood low more oten occurs in the arterial system at sites o

biurcation and o(erlying atheromatous &la2ues. Platelet thrombi are more likely to de(elo& in this setting

leading to a myocardial inarction or stroke.

C. Increased &lasma (iscosity: although this would &redis&ose to (enous clots the clinical setting in this

&atient would not lend towards a (iscosity &roblem due to an increase in Ig -Ealdenstroms

macroglobulinemia a malignant disorder o lym&ho&lasmacytoid cells0 or a disorder in(ol(ing globulins

that oten congeal in cold tem&eratures -cryoglobulins0

D. @e&ticemia: although se&sis is a common inding in a gangrenous gallbladder it would most likely

&redis&ose to disseminated intra(ascular coagulation with ibrin clots de(elo&ing in ca&illaries

throughout the entire body

=5. A 87%year%old man with tachycardia associated with an irregularly irregular &ulse de(elo&s a

sudden onset o &ain in multi&le digits in his oot. The digits are &ale swollen and &ainul to

&al&ation. Ehich o the ollowing is the most likely cause o the &atients clinical indingsFA. Genous thrombosis

B. Arterial emboli/ation

C. Atherosclerosis o digital (essels

D. Paradoxical emboli/ation

Answer: B. arterial emboli/ation: the &atient has atrial ibrillation -irregularly irregular &ulse0 which

&redis&oses to stasis in the let atrium and clot ormation -R(enousR ty&e clot related to stasis e(en though

it is in the let heart0. A) is the most dangerous arrhythmia &redis&osing to systemic emboli/ation. 'mboli

to the digital (essels has &roduced early signs o inarction o the digits related to ischemic coagulati(enecrosis.

A. (enous thrombosis: the clinical setting o atrial ibrillation a(ors arterial emboli/ation than a (enous

thrombosis o digital (ein (essels. This would more likely occur in certain ty&es o (asculitis -e.g.

scleroderma @,'0.

C. atherosclerosis o digital (essels: the digital (essels rarely undergo atherosclerosis. 'lastic and large to

medium%si/ed muscular arteries are more oten &redis&osed to atherosclerosis.D. &aradoxical emboli/ation: his reers to emboli/ation o a (enous clot to a site in the systemic

circulation. )or this to occur the &atient would ha(e to ha(e a &atent oramen o(ale -atrial se&tal deect0

which would allow a (enous clot to tra(erse the right atrium and enter the let atrium.

=6. In &atients who are hy&o(olemic rom massi(e blood loss or loss o salt%containing luids -e.g.

diarrhea luid sweat0 which o the ollowing is the irst ste& in management o the &atientFA. 5 *y&ertonic saline

B. ?.> ormal saline

C. ?.67 ormal saline

D. ?.$7 ormal saline

'. 7 Dextrose and water

Answer: B. ?.> ormal saline: only luid that is isotonic to &lasma can raise the blood &ressure in any

hy&o(olemic &atient. ?.> normal saline has the same tonicity as &lasma and essentially acts like &lasma

exce&t or the absence o &roteins. '(en the hy&o(olemia associated with loss o whole blood can initially

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be managed with normal saline until blood is a(ailable or transusion. It is not &ossible to raise blood

&ressure with a hy&otonic salt solution -C. ?.67 ormal saline D. ?.$7 ormal saline or '. 7

Dextrose and water0.

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=;. A 5>%year%old homeless man is brought into an emergency room by a riend. The man is stu&orous

and is unable to answer 2uestions. ,aboratory tests are ordered and return with the ollowing

(alues: serum sodium 15; m'2", -157−16;0 serum &otassium 7.= m'2", -5.7−7.?0 serumchloride >; m'2", ->7−1?70 serum bicarbonate 1$ m'2", -$$−$=0 serum blood urea nitrogen 6?mg"d, -;−1=0 serum creatinine 6 mg"d, -?.8−1.$0 and the urinalysis contains numerous crystals

that look like the back o an en(elo&e. Ehich o the ollowing statements a&&ly to this &atientFA. ormal anion ga& metabolic acidosisB. Pre%renal a/otemia

C. Treatment with intra(enous ethanol

D. Patient drank methyl alcohol

'. *y&erkalemia is most likely iatrogenic

Answer: the &atient has ingested ethylene glycol -antiree/e0 and has de(elo&ed acute renal ailure

-choice B%&re%renal a/otemia is incorrect0 due to obstruction o the renal tubules by calcium oxalate

crystals leading to an increased anion ga& metabolic acidosis -choice A% normal anion ga& metabolic

acidosis is incorrect0 C. Treatment with intra(enous ethanol: both ethylene glycol and ethanol are

metaboli/ed by alcohol dehydrogenase and com&ete with each other or substrate binding to the en/yme

-exam&le o a com&etiti(e inhibitor0. By increasing ethanol -substrate0 more ethanol is bound to the

acti(e en/yme sites than ethylene glycol lea(ing it unmetaboli/ed -normally con(erted into oxalic and

glycolic acid0. The unmetaboli/ed ethylene glycol can then be remo(ed by dialysis. The osmolal ga&

would be J 1? m4sm -measured P4sm % calculated P4sm0.

A. normal anion ga& metabolic acidosis: no the A+ is 15; % ->; ! 1$0 H $= m'2", - 1$ !"% 60. The

oxalate anions are re&lacing the buered bicarbonate anions hence electroneutrality is maintained.

B. &re%renal a/otemia: no the ratio o B

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Ser! N"#

51'6 1789

Ser! #

5';6 6;09

Ser! C-<

5=6 1069

Ser! HCO'<

522 2>9

An)$n "%

C. 15? 5.? 1?= 1? 1$

=>. A ;?%year%old man with urinary retention caused by &rostate hy&er&lasia de(elo&s e(er and warm

skin. A blood culture is &ositi(e or Escherichia coli. Ehich o the ollowing chemical mediators is

most likely res&onsible or the warm skin in this &atientFA. Com&lement C5b

B. ,eukotriene B6

C. ,eukotrienes C6 D6 and '6

D. itric oxide

'. Thromboxane A$

Answer: D -nitric oxide0 is correct. The &atient has se&tic shock due to E. coli as a com&lication o

urinary retention due to &rostate hy&er&lasia. 'ndotoxins released rom the cell wall o E. coli directly

damage endothelial cells causing the release o nitric oxide -40 and &rostaglandin I$ -&rostacyclin0

both o which (asodilate &eri&heral arterioles. Eides&read arteriolar (asodilation causes warm skin.

4&tion A -com&lement C5b0 is incorrect. Com&lement C5b is an o&soni/ing agent that acilitates

&hagocytosis by leukocytes. It does not &roduce (asodilation o arterioles.

4&tion B -leukotriene B60 is incorrect. ,eukotriene B6 acti(ates neutro&hil adhesion molecules and is achemotactic agent or leukocytes. It does not &roduce (asodilation o arterioles.

4&tion C -leukotrienes C6 D6 and '60 is incorrect. ,eukotrienes C6 D6 and '6 cause (asoconstrictiono arterioles and bronchoconstriction.

4&tion ' -thromboxane A$0 is incorrect. Thromboxane A$ causes (asoconstriction o arterioles and

enhances &latelet aggregation.

>?. A 7?%year%old man with alcoholic cirrhosis has ascites and de&endent &itting edema in the lower

legs. )luid accumulation in the &eritoneal ca(ity and legs occurs by which o the ollowing

mechanismsF

A. Decreased &lasma oncotic &ressure

B. Increased &lasma hydrostatic &ressure

C. Increased (essel &ermeability due to histamineD. ,ym&hatic obstruction with lym&hedema

'. o(ement o water into the intracellular com&artment

Answer: A -decreased &lasma oncotic &ressure0 is correct. 'dema is the accumulation o luid in body

ca(ities -e.g. ascites0 and in the interstitial s&ace -e.g. &eri&heral edema0. 'dema caused by cirrhosis o

the li(er in(ol(es alterations in (ascular hydrostatic &ressure and oncotic &ressure. An increase in

hydrostatic &ressure and"or a decrease in &lasma oncotic &ressure -hy&oalbuminemia0 causes outlow o a

&rotein%&oor luid -transudate0 into body ca(ities and the interstitial s&aces. In cirrhosis the &ortal (ein

encounters increased resistance to em&tying blood into the li(er sinusoids due to com&ression o thesinusoids by regenerati(e nodules and ibrosis. This causes increased hydrostatic &ressure -&ortal

hy&ertension0 that contributes to ascites ormation. The synthetic unction o the li(er is com&romised in

cirrhosis the synthesis o albumin is decreased. This decreases the &lasma oncotic &ressure urther

contributing to ascites. It is the &rimary mechanism or &eri&heral edema -de&endent &itting edema0 incirrhosis.

4&tion B -increased &lasma hydrostatic &ressure0 is incorrect. In cirrhosis increased hydrostatic &ressure

only contributes to ascites ormation and has no role in the de(elo&ment o &eri&heral edema.

4&tion C -increased (essel &ermeability due to histamine0 is incorrect. Increased (essel &ermeability due

to histamine causes a non&itting ty&e o &eri&heral edema. The edema luid is a &rotein%rich exudate -J 5

g"d,0 that contains &olymor&honuclear leukocytes. The edema o a transudate is &itting and the &rotein

content is 5 g"d,.

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4&tion D -lym&a

acid base f12

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