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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
Os! N"# ECF
C$!%"r&!en&
ICF
C$!%"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.
5
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Os! N"# ECF ICF
Increased Increased 'x&anded Contracted
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*$? H 7 % 17 H %1? indicating concentration. The P4sm in this &atient is normal which would be
ex&ected in adult diarrhea since it is an isotonic loss o luid.
A. 4smotic diuresis secondary to diabetic ketoacidosis: no the P4sm would be higher due to
hy&erglycemia
C. Ina&&ro&riate AD* syndrome: no the P4sm would be lower due to the dilutional eect o adding
water to the 'C) com&artment. *owe(er ree water clearance is negati(e since AD* is constantlyconcentrating the urine
D. Central diabetes insi&idus: no P4sm would be higher and the ree water clearance &ositi(e in theabsence o AD*. These &atients are constantly diluting their urine.
'. 9enal ailure: no ree water clearance is /ero indicating a lack o both dilution and concentration.
17. A 1>%year%old man with ty&e I diabetes mellitus de(elo&s diabetic ketoacidosis. Physical examdemonstrates signs o (olume de&letion. The serum glucose is 1??? mg"d, and ketone bodies are
increased in the &lasma and urine. Ehich o the ollowing changes in electrolyte and (olume status
is most likely &resent in this &atientF
Os! N"# ECF
C$!%"r&!en&
ICF
C$!%"r&!en&
Increased Decreased Contracted ContractedIncreased Decreased 'x&anded Contracted
Increased Increased '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
C$!%"r&!en&
ICF
C$!%"r&!en&
ormal ormal Contracted ormalDecreased Decreased Contracted Contracted
Increased Increased 'x&anded Contracted
Decreased Decreased 'x&anded 'x&anded
Decreased Decreased Contracted 'x&anded
Answer: '. *y&ertonic loss o luid rom diuretic leading to hy&onatremia. Correlates with diagram B in
the study 2uestions -diagrams or 2uestions 87%;$0. The gradient a(ors mo(ement o water into the IC)
com&artment. ote the &ositi(e tilt test -BP dro&&ed and &ulse increased when sitting u&0 indicating
signiicant (olume de&letion.
Os! N"# ECF ICF
Decreased Decreased Contracted 'x&anded
1=. A 1>%year%old man with a recent head inury related to a motorcycle accident com&lains o
excessi(e thirst and ha(ing to urinate o(er 1? times a day. Physical exam is unremarkable. The
urine osmolality is 1?? m4sm"kg. ou sus&ect that the &ituitary stalk may ha(e been transected
rom the accident. Ehich o the ollowing changes in electrolyte and (olume status is most likely &resent in this &atientF
Os! N"# ECF
C$!%"r&!en&
ICF
C$!%"r&!en&
Decreased Decreased 'x&anded 'x&anded
Decreased Decreased Contracted 'x&anded
Increased Increased 'x&anded Contracted
Increased Increased Contracted Contracted
ormal ormal Contracted ormal
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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%;$0. 9emember that AD* is synthesi/ed in the hy&othalamus and
in the same ner(e tra(els through the &ituitary stalk into the &osterior &ituitary where it is stored. *eadtrauma is a common cause or se(erance o the stalk leading to diabetes insi&idus as well as
hy&o&ituitarism since all the releasing actors are &re(ented rom stimulating the &ituitary gland.
Os! N"# ECF ICF
Increased Increased Contracted Contracted
1>. A 85%year%old man with a 6= year history o smoking com&lains o headache and conusion.
Physical exam is unremarkable exce&t or scattered sibilant rhonchi in the lungs that clear with
coughing. A chest x%ray exhibits a &rominent right hilar mass. An 9I o the brain is negati(e or
s&ace occu&ying lesions. A s&utum cytology re&ort indicates the &resence o small hy&erchromatic
cells intermixed with necrotic debris consistent with a small cell carcinoma o the lung. Ehich o
the ollowing changes in electrolyte and (olume status is most likely &resent in this &atientF
Os! N"# ECF
C$!%"r&!en&
ICF
C$!%"r&!en&
Decreased Decreased 'x&anded ContractedDecreased Decreased 'x&anded 'x&anded
ormal ormal Contracted ormal
Increased Increased Contracted Contracted
Decreased Decreased Contracted '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%;$0.
Os! N"# ECF ICF
Decreased Decreased 'x&anded 'x&anded
8
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$?. 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
Os! N"# ECF
C$!%"r&!en&
ICF
C$!%"r&!en&
Increased *igh Contracted Contracted
Increased Increased 'x&anded 'x&anded ormal ormal Contracted ormal
Increased Increased 'x&anded Contracted
Decreased Decreased Contracted 'x&anded
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
Increased Increased Contracted Contracted
$1. A 8$%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
Os! N"# ECF
C$!%"r&!en&
ICF
C$!%"r&!en&Increased Increased 'x&anded Contracted
Decreased Decreased Contracted 'x&anded
Decreased Decreased 'x&anded 'x&anded
Increased Increased Contracted 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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Os! N"# ECF ICF
Decreased Decreased 'x&anded 'x&anded
$$. A 66%year%old woman has hy&otension increased skin and mucous membrane &igmentation and
&oor skin turgor. ,aboratory studies unco(er a low serum cortisol and electrolyte abnormalities. An
intra(enous ACT* stimulation test o(er the ensuing 5 days demonstrates no increase in serum
cortisol or its urinary metabolites. Plasma ACT* le(els are high. A random urine sodium is J 1??
m'2", - $? m'2",0. Ehich o the ollowing changes in electrolyte and (olume status is most
likely &resent in this &atientF
Os! N"#
ECFC$!%"r&!en&
ICFC$!%"r&!en&
Decreased Decreased 'x&anded 'x&anded
Decreased Decreased 'x&anded 'x&anded
Increased Increased Contracted ContractedIncreased Increased 'x&anded Contracted
Decreased Decreased Contracted 'x&anded
Answer: '. the &atient has Addisons disease with loss o aldosterone leading to a hy&ertonic loss o luid
in the urine and hy&onatremia. Correlates with diagram B in the study 2uestions -diagrams or 2uestions
87%;$0. *y&ocortisolism causes the increase in ACT* the latter ha(ing melanocyte stimulating
&ro&erties. @ince the adrenal cortex is destroyed -autoimmune0 IG ACT* stimulation will not cause any
increase in adrenal cortex metabolites -e.g. cortisol0. The electrolyte indings in Addisons disease are the
same as those seen in a &atient on an aldosterone blocker mainly hy&onatremia hy&erkalemia and anormal A+ metabolic acidosis.
Os! N"# ECF ICF
Decreased Decreased Contracted 'x&anded
=
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Items $5−$8%H CO2 ()*"r+$n"&e
A. Decrease
d
Increased Decreased
B. ormal ormal ormal C. ormal Increased Increased
$5. A 6$%year%old woman in *r$n)* ren"- .")-re is taking a -$$% )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
Os! N"# ECFC$!%"r&!en&
ICFC$!%"r&!en&
Decreased Decreased 'x&anded 'x&anded
Increased Increased 'x&anded 'x&anded
Increased Increased Contracted Contracted
Decreased Decreased Contracted 'x&anded
Increased Increased 'x&anded Contracted
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
Increased Increased 'x&anded Contracted
$=. 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. $$%yr%old woman with insensible water loss due to e(er
'. $7%yr%old construction worker with excessi(e sweating on a humid day
1?
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Answers A, (, E: A. $%yr%old child with a rota(irus inection: hy&otonic loss o salt
B. 6$%yr%old man with cirrhosis and ascites: decreased (enous return rom tra&&ing o luid in interstitial
s&ace -decreased oncotic &ressure0 and &eritoneal ca(ity -decreased oncotic &ressure and increased
hydrostatic &ressure0
'. $7%yr%old construction worker with excessi(e sweating on a humid day: sweat is a hy&otonic loss owater and salt
C. 8$%yr%old man with ina&&ro&riate AD* syndrome: no 'ABG is increased rom increased &lasma(olume related to excessi(e reabsor&tion o ree water
D. $$%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
11
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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=
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$ $.= 11? 55
5$. 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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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
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 &reå 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$!%"r&!en&
Increased Increased Contracted Contracted ormal ormal Contracted ormal
ormal ormal Contracted 'x&anded
Increased Increased 'x&anded Contracted
Decreased Decreased Contracted 'x&anded
Answer: B. isotonic loss o luid. o osmotic gradient. Correlates with diagram A in the study 2uestions.
17
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Os! N"# ECF ICF
ormal ormal Contracted ormal
6=. 9es&iratory alkalosis would be ex&ected as com&ensation in which o the ollowing &atient
conditionsF SELECT 2
A. *y&er(entilation
B. Chronic renal ailure
C. Pulmonary inarction
D. 'thylene glycol &oisoning
'. Gomiting secondary to gastritis
Answers: (, D. res&iratory alkalosis is com&ensation or a &rimary metabolic acidosis: B. Chronic renal
ailure: increased A+ metabolic acidosis
D. 'thylene glycol &oisoning: ethylene glycol is con(erted by alcohol dehydrogenase to glycolic and
oxalic acid the latter orming calcium oxalate crystals in the kidney tubules causing renal ailure
A. *y&er(entilation: no this &roduces a &rimary res&iratory alkalosis and metabolic acidosis is
com&ensation
C. Pulmonary inarction: no this &roduces a &rimary res&iratory alkalosis rom tachy&nea and metabolic
acidosis is com&ensation
'. Gomiting secondary to gastritis: no this &roduces a &rimary metabolic alkalosis and res&iratory
acidosis is com&ensation.
Items 6>−7=%H
58;'6
8;769
CO25''
76 !! H9
HCO'<
522
2> !E@/L9
;.?? 7$ 1$
;.$; 8? $8
;.$7 =? 56
;.$8 $8 11
;.5= ;? 6?
;.5= 6? $6
;.6$ $$ 16
;.78 $6 $1
;.7= 6> 5>
6>. A 57%year%old recently di(orced woman o(erdoses on +"r+)&r"&es.
Answer: B. Barbiturates de&ress the res&iratory center &roducing an acute res&iratory acidosis without
com&ensation.
%H
58;'6
8;769
CO25''
76 !! H9
HCO'<
522
2> !E@/L9
;.$; 8? $8
18
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Items 6>−7=%H
58;'6
8;769
CO25''
76 !! H9
HCO'<
522
2> !E@/L9
;.?? 7$ 1$
;.$; 8? $8
;.$7 =? 56
;.$8 $8 11
;.5= ;? 6?
;.5= 6? $6
;.6$ $$ 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 -$$% )re&)* &roduces
metabolic alkalosis. This is a mixed disorder: &* should be normal PC4$ markedly increased since both
disorders ha(e an increase in PC4$ and the bicarbonate should be markedly increased since both
disorders ha(e an increase in bicarbonate.
%H
58;'6 8;769
CO2
5''
76 !! H9
HCO'<
522
2> !E@/L9
;.5= ;? 6?
75. A se&tic ;$%yr%old man has urinary retention secondary to &rostatic hy&er&lasia. ou sus&ect the
&atient has en$&$)* s$*3 .
Answer: +. en$&$)* s$*3 &roduces a mixed disorder: res&iratory alkalosis− o(erstimulates theres&iratory center ! metabolic acidosis rom shock leading to lactic acidosis. This is a mixed disorder. The
1;
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&* changes neutrali/e each other. Both PC4$ and bicarbonate are decreased in both conditions &roducing
an additi(e eect.
%H
58;'6
8;769
CO25''
76 !! H9
HCO'<
522
2> !E@/L9
;.6$ $$ 16
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? $6 ;.6$ $$ 16
;.78 $6 $1
;.7= 6> 5>
76. A $1%year%old man with cystic ibrosis who has had recurrent &ulmonary inections almost all his
lie has e(er and a &roducti(e cough consistent with "*&e +r$n*)&)s $r %ne!$n)".
Answer: C. cystic ibrosis &roduces chronic obstructi(e lung disease and chronic res&iratory acidosis. An
"*&e +r$n*)&)s $r %ne!$n)" su&erim&oses an acute res&iratory acidosis on to& o a chronic
res&iratory acidosis. Chronic res&iratory acidosis is associated with metabolic alkalosis as com&ensation
unlike acute res&iratory acidosis -choice B0 which does not. The PC4$ is &robably higher than usual
owing to the su&erim&osed acute bronchitis or &neumonia. Beore the &atient got a su&erim&osedinection the &* was &robably around ;.55 and PC4$ around 8?. This is a ty&e o mixed disorder.
%H
58;'6
8;769
CO2
5'' 76 !! H9
HCO'<
522 2> !E@/L9
;.$7 =? 56
77. A 57%yr%old migrant worker inad(ertently drinks !e&4- "-*$$-. *e de(elo&s gastric u&set and
blurry (ision.
Answer: D. !e&4- "-*$$- &roduces an increased A+ metabolic acidosis because it is metaboli/ed by
alcohol dehydrogenase to ormic acid which &roduces o&tic neuritis and a &otential or blindness.
%H
58;'6
8;769
CO25''
76 !! H9
HCO'<
522
2> !E@/L9
;.$8 $8 11
78. A 78%year%old man is in *"r)$res%)r"&$r4 "rres&. ou arri(e on the scene N$ minutes ater the
&atient lost consciousness.
Answer: A. *"r)$res%)r"&$r4 "rres& is associated with a &rimary acute res&iratory acidosis -not
breathing0 ! metabolic acidosis rom lactic acidosis. 'x&ect a (ery low acid &*.
%H CO2 HCO'<
1=
8/18/2019 Acid Base F12
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58;'6
8;769
5''
76 !! H9 522
2> !E@/L9
;.?? 7$ 1$
7;. A $6%yr%old medical student de(elo&s an "n)e&4 "&&"*3 while taking a com&rehensi(e inal exam
Answer: *. an "n)e&4 "&&"*3 &roduces an acute res&iratory alkalosis owing to excessi(e blowing o o
C4$. ote the &artially com&ensated metabolic acidosis. on%renal mechanisms are able to lower the bicarbonate to 1= m'2",.
%H
58;'6
8;769
CO2
5'' 76 !! H9
HCO'<
522 2> !E@/L9
;.78 $6 $1
Items 6>−7=%H
58;'6
8;769
CO25''
76 !! H9
HCO'<
522
2> !E@/L9
;.?? 7$ 1$
;.$; 8? $8
;.$7 =? 56
;.$8 $8 11
;.5= ;? 6?
;.5= 6? $6
;.6$ $$ 16
;.78 $6 $1
;.7= 6> 5>
7=. A $ 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
58;'6
8;769
CO25''
76 !! H9
HCO'<
522
2> !E@/L9
;.7= 6> 5>
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 $5%yr%old marathon runner who is (olume de&leted ater running on a hot humid
day.
Answer: '. the &atient is losing sweat where there is a hy&otonic loss o more water than salt. This
causes hy&ernatremia with 'C) contraction and IC) contraction. The water that shits into the 'C) rom
the IC) is lost in the sweat.
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8;. The &atient is a 86%yr%old smoker with a small cell carcinoma o the lung and ina&&ro&riate AD*
syndrome.
Answer: D. *y&otonic gain o &ure water and no salt. *y&onatremia with 'C) ex&ansion and IC)
ex&ansion.
Items 87−;$
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
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;
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
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;
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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
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; (;
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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