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STUDY GUIDE Q/A: FALL 2012

WATER AND ELECTROLYTE DISORDERS


HEMODYNAMIC DISORDERS
Items 111
A.
Proximal tubule
B.
Descending tubule
C.
Thick ascending limb: medullary segment with Na+/K+/2Cl- symporter
D.
Thick ascending limb: cortical segment with Na+/Cl- symporter
E.
Distal convoluted tubule/collecting tubule: Na +/K+ channels
F.
Collecting duct: H+/K+ ATPase pump
G.
Late distal/collecting duct
1.
A block at this site by a carbonic anhydrase inhibitor (e.g., acetazolamide) results in the loss of
sodium/potassium bicarbonate in the urine, hypokalemia, and production of a normal anion gap
metabolic acidosis.
Answer: A: proximal tubule: this is an example of an acquired type II proximal renal tubular acidosis.
Acetazolamide is a proximal tubule diuretic that blocks the reclaiming of bicarbonate. Bicarbonate is lost
in the urine as sodium bicarbonate. Loss of bicarbonate is matched by a gain in chloride (hyperchloremic
normal anion gap metabolic acidosis); hence the anion gap remains the same.
2.

In patients taking a loop diuretic or thiazides, an increased delivery of sodium to this site results in
hypokalemia and metabolic alkalosis if the patient is not taking oral potassium supplements.
Answer: E. Distal convoluted tubule/collecting tubule: Na+/K+ channels: potassium is lost in the urine
(causes hypokalemia) in exchange for sodium. Once potassium stores are depleted (patient is not taking
potassium supplements), sodium exchanges with protons and regenerated bicarbonate moves into the
blood producing metabolic alkalosis.
3.

A block at this site interferes with the generation of free water and non-parathyroid hormonerelated reabsorption of calcium.
Answer: C. Thick ascending limb: medullary segment with Na+/K+/2Cl- symporter: this is the primary
site for generation of free water and is also the site for non-PTH reabsorption of calcium. Obligated water
is removed from sodium, potassium, and chloride and remains in the tubule lumens as free water. Block
of chloride binding with loop diuretics not only results in loss of sodium, potassium, and chloride but also
calcium (useful in the treatment of hypercalcemia).
4.

A block at these sites by spironolactone results in sodium loss in the urine, hyperkalemia, and
normal anion gap metabolic acidosis. SELECT 2
Answers E, F: E. Distal convoluted tubule/collecting tubule: Na+/K+ channels
F. Collecting duct: H+/K+ ATPase pump: spironolactone is an aldosterone blocker and these 2 sites are
enhanced by aldosterone. Block of the first channel causes a loss of sodium and retention of potassium
(causes hyperkalemia), while a block of the second site causes a loss of potassium and retention of
protons (metabolic acidosis). Bicarbonate cannot be generated; therefore, protons combine with chloride
producing a normal AG metabolic acidosis. The hyperkalemia is somewhat offset by the loss of potassium
in the latter pump and may result in potassium moving into or close to the normal range.
5.

These sites are most susceptible to tissue hypoxia and invariably exhibit coagulation necrosis in
ischemic acute tubular necrosis. SELECT 2
Answers A, C: A. Proximal tubule

C. Thick ascending limb: medullary segment with Na+/K+/2Cl- symporter. There is a lot of oxidative
types of reactions in these areas; hence their susceptibility to hypoxia and coagulation necrosis,
particularly in ischemic acute tubular necrosis.
6.

This is the primary site for renal tubular acidosis secondary to a lowering of the renal threshold for
reclaiming bicarbonate.
Answer: A. Proximal tubule: this is type II RTA. The urine is initially alkaline due to the loss of filtered
bicarbonate that cannot be reclaimed. However, when the renal threshold and blood levels of bicarbonate
are the same (e.g., 15 mEq/L), the urine returns to an acid pH. Acetazolamide is the MCC of proximal
RTA. Heavy metal poisoning is another cause of proximal RTA. Rx of proximal RTA is to produce
volume depletion with thiazides which automatically raises the renal threshold for reclaiming bicarbonate.
7.

This is the primary site for renal tubular acidosis secondary to inability to secrete protons leading to
a defect in the acidification of urine.
Answer: F. Collecting duct: H+/K+ ATPase pump: protons combine with chloride leading to a normal AG
metabolic acidosis and bicarbonate cannot be regenerated (normal AG metabolic acidosis). Hypokalemia
is severe. Urine is alkaline because the protons are necessary to produce NaH 2PO4 and NH4Cl, which
acidify the urine. Rx is to give sodium bicarbonate.
8.

The presence or absence of antidiuretic hormone most affects the handling of free water at these
sites in the nephron.
Answer: G. Late distal/collecting duct: presence of ADH results in concentration and a negative free
water clearance, since free water is being reabsorbed back into the ECF. Absence of ADH, results in
dilution and a positive free water clearance, since free water is lost in the urine.
9.

In patients with calcium stones secondary to hypercalciuria, a thiazide diuretic acting at this site
allows for increased reabsorption of calcium out of the urine and less chance for calcium stone
formation.
Answer: D. Thick ascending limb: cortical segment with Na +/Cl- symporter: both sodium and calcium
share the same channel for reabsorption; therefore, blocking sodium reabsorption allows calcium total
access to the channel with the assistance of PTH. Note how loop diuretics are used to Rx hypercalcemia,
while thiazides are used to remove calcium from the urine (potential for hypercalcemia).
10.

Heavy metals like lead and mercury and drugs like the aminoglycosides primarily damage the renal
tubular cells at this site in the nephron.
Answer: A. Proximal tubule: heavy metals denature proteins leading to coagulation necrosis. The
proximal tubule is the first part of the nephron they encounter. Similar reasoning applies to the
aminoglycosides, which are nephrotoxic. Both of these drugs could produce Fanconi's syndrome, where
all the proximal tubule functions are impaired leading to proximal RTA and loss of uric acid, potassium,
glucose, phosphate, and amino acids in the urine.
11. The initial synthesis of ammonia occurs at this site of the nephron (FYI).
Answer: A. Proximal tubule: glutaminase in the proximal tubule converts glutamine (most abundant
amino acid and carrier of ammonia in a non-toxic form) to ammonia + glutamate. Ammonia is excreted
into the urine, reabsorbed, and then secreted again in the collecting tubule where it combines with protons
to form ammonium chloride, which acidifies the urine.

12.

A 78-year-old man post-transurethral resection for urinary retention secondary to prostate


hyperplasia receives an excessive amount of 0.9% normal saline. He develops dyspnea and
dependent pitting edema. He has a history of chronic ischemic heart disease. Physical exam
demonstrates jugular neck vein distention and bibasilar crackles. Which of the following changes
in electrolyte and volume status is most likely present in this patient?
POsm
PNa+
ECF
ICF
Compartment Compartment
A.
Increased
Increased
Contracted
Contracted
B.
Normal
Normal
Expanded
Normal
C.
Decreased Decreased
Contracted
Expanded
D.
Increased
Increased
Expanded
Contracted
E.
Normal
Normal
Expanded
Expanded
Answer: B. isotonic gain in fluid, with no gradient: would correlate with diagram C in the study
questions. The reason why he developed left sided heart failure (pulmonary edema) and right sided heart
failure (dependent pitting edema) is that he had preexisting ischemic heart disease and most likely had
increased renal retention of sodium related to a decreased cardiac output. In this setting, giving excess
isotonic fluid caused left-sided heart failure with an increase in hydrostatic pressure driving fluid into the
lungs and right-sided heart failure due to an increase in hydrostatic pressure driving fluid into the
interstitial space in the legs.

B.

POsm
Normal

PNa+
Normal

ECF
Expanded

13.

ICF
Normal

A 72-year-old man, with a history of ischemic heart disease, develops neck vein distention,
bibasilar crackles, and dependent pitting edema within 24 hrs after receiving multiple ampules of
intravenous sodium bicarbonate (hypertonic saline) during a cardiorespiratory arrest. Which of the
following changes in electrolyte and volume status is most likely present in this patient?
POsm
PNa+
ECF
ICF
Compartment Compartment
Increased
Increased
Expanded
Contracted
Decreased
Decreased
Expanded
Expanded
Decreased
Decreased
Contracted
Expanded
Increased
Increased
Expanded
Expanded
Normal
Normal
Contracted
Normal
Answer: A. hypertonic gain in fluid causing hypernatremia, correlates with diagram E in the study
questions. An osmotic gradient favors movement out of the ICF into the ECF. The ECF is expanded and
the ICF is contracted. The Rx is sodium restriction and diuretics.

POsm
Increased

PNa+
Increased

ECF
Expanded

ICF
Contracted

14.

A 58-year-old man has the following laboratory test abnormalities: urine volume 5 mL/min, plasma
osmolality 280 mOsm/kg (275295 mOsm/kg), and urine osmolality of 840 mOsm/kg. These
laboratory findings are most compatible with which of the following conditions?
A.
Osmotic diuresis secondary to diabetic ketoacidosis
B.
Volume depletion secondary to severe diarrhea
C.
Inappropriate ADH syndrome
D.
Central diabetes insipidus
E.
Renal failure
Answer: B. Volume depletion secondary to severe diarrhea. In order to answer the question, the free
water clearance must be calculated to see if he is concentrating or diluting the urine. COsm = 840 x 5/280
= 15, CH20 = 5 - 15 = -10, indicating concentration. The POsm in this patient is normal, which would be
expected in adult diarrhea, since it is an isotonic loss of fluid.
A. Osmotic diuresis secondary to diabetic ketoacidosis: no, the POsm would be higher due to
hyperglycemia
C. Inappropriate ADH syndrome: no, the POsm would be lower due to the dilutional effect of adding
water to the ECF compartment. However, free water clearance is negative, since ADH is constantly
concentrating the urine
D. Central diabetes insipidus: no, POsm would be higher and the free water clearance positive in the
absence of ADH. These patient's are constantly diluting their urine.
E. Renal failure: no, free water clearance is zero, indicating a lack of both dilution and concentration.
15.

A 19-year-old man with type I diabetes mellitus develops diabetic ketoacidosis. Physical exam
demonstrates signs of volume depletion. The serum glucose is 1000 mg/dL and ketone bodies are
increased in the plasma and urine. Which of the following changes in electrolyte and volume status
is most likely present in this patient?
POsm
PNa+
ECF
ICF
Compartment Compartment
Increased
Decreased
Contracted
Contracted
Increased
Decreased
Expanded
Contracted
Increased
Increased
Expanded
Contracted
Decreased
Decreased
Expanded
Expanded
Decreased
Decreased
Contracted
Expanded
Answer: A. the patient has type 1 diabetes mellitus and is in diabetic ketoacidosis with signs of volume
depletion. Glucose has surpassed sodium as the major osmotic force and increases POsm. Serum sodium
is low due to water shift out of the ICF into the ECF producing a dilutional hyponatremia. The ECF is
contracted owing to osmotic diuresis leading to volume depletion. ICF is contracted due to increased
POsm from glucose. Correlates with diagram E in the study questions (diagrams for questions 65-72).

POsm
Increased

PNa+
Decreased

ECF
Contracted

ICF
Contracted

16.

Which of the following characterize the findings in early endotoxic (septic) shock rather than either
hypovolemic or cardiogenic shock? SELECT 3
A.
Cold, clammy skin
B.
Increased cardiac output
C.
Increased venous return to the heart
D.
Decreased total peripheral resistance
E.
Decreased mixed venous oxygen content (MVO 2)
Answers B, C, D: B. Increased cardiac output: due to increased venous return to the heart owing to
arteriolar vasodilation
C. Increased venous return to the heart
D. Decreased total peripheral resistance: arteriolar vasodilation also drops the diastolic pressure
A. Cold, clammy skin: no, this is present in hypovolemic and cardiogenic shock due to catecholamine,
ATII, and ADH vasoconstriction of the vessels in the skin to redirect blood to more important areas
E. Decreased mixed venous oxygen content (MVO 2): no, it is increased in septic shock and decreased in
the other types of shock. It is increased owing to the increased blood flow through the microcirculation.
17. A 72-year-old woman is currently taking a thiazide diuretic for hypertension. She complains of
dizziness when standing up too quickly. Physical exam demonstrates a blood pressure of 130/88
mm Hg and a pulse of 100 bpm when lying down and a blood pressure of 110/80 mm Hg and a
pulse of 150 bpm when sitting up. The mucous membranes are dry and skin turgor is poor. Which
of the following changes in electrolyte and volume status is most likely present in this patient?
POsm
PNa+
ECF
ICF
Compartment
Compartment
Normal
Normal
Contracted
Normal
Decreased
Decreased Contracted
Contracted
Increased
Increased
Expanded
Contracted
Decreased
Decreased Expanded
Expanded
Decreased
Decreased Contracted
Expanded
Answer: E. Hypertonic loss of fluid from diuretic leading to hyponatremia. Correlates with diagram B in
the study questions (diagrams for questions 65-72). The gradient favors movement of water into the ICF
compartment. Note the positive tilt test (BP dropped and pulse increased when sitting up) indicating
significant volume depletion.

POsm
Decreased
18.

PNa+
Decreased

ECF
Contracted

ICF
Expanded

A 19-year-old man with a recent head injury related to a motorcycle accident complains of
excessive thirst and having to urinate over 10 times a day. Physical exam is unremarkable. The
urine osmolality is < 100 mOsm/kg. You suspect that the pituitary stalk may have been transected
from the accident. Which of the following changes in electrolyte and volume status is most likely
present in this patient?
POsm
PNa+
ECF
ICF
Compartment Compartment
Decreased Decreased
Expanded
Expanded
Decreased Decreased
Contracted
Expanded
Increased
Increased
Expanded
Contracted
Increased
Increased
Contracted
Contracted
Normal
Normal
Contracted
Normal
5

Answer: D. Central diabetes insipidus with loss of pure water and no salt from lack of ADH.
Hypernatremia occurs, however, there is a normal exam, because the loss of pure water does not result in
clinically significant volume depletion (produces dehydration). Correlates with diagram E in the study
questions (diagrams for questions 65-72). Remember that ADH is synthesized in the hypothalamus and
in the same nerve travels through the pituitary stalk into the posterior pituitary, where it is stored. Head
trauma is a common cause for severance of the stalk leading to diabetes insipidus as well as
hypopituitarism, since all the releasing factors are prevented from stimulating the pituitary gland.

POsm
Increased

PNa+
Increased

ECF
Contracted

ICF
Contracted

19.

A 63-year-old man with a 48 year history of smoking complains of headache and confusion.
Physical exam is unremarkable except for scattered sibilant rhonchi in the lungs that clear with
coughing. A chest x-ray exhibits a prominent right hilar mass. An MRI of the brain is negative for
space occupying lesions. A sputum cytology report indicates the presence of small, hyperchromatic
cells intermixed with necrotic debris consistent with a small cell carcinoma of the lung. Which of
the following changes in electrolyte and volume status is most likely present in this patient?
POsm
PNa+
ECF
ICF
Compartment Compartment
Decreased
Decreased Expanded
Contracted
Decreased
Decreased Expanded
Expanded
Normal
Normal
Contracted
Normal
Increased
Increased
Contracted
Contracted
Decreased
Decreased Contracted
Expanded
Answer: D. the patient has SiADH due to a small cell carcinoma of the lung. The MRI rules out
metastasis to the brain, so the mental status problems relate to cerebral edema from hyponatremia related
to water moving out of the ECF into the ICF. There is a hypotonic gain of pure water, therefore, the TBNa
is normal and the skin turgor is normal. This patient would be treated with demeclocycline (produces
nephrogenic diabetes insipidus) rather than water restriction, since he will die in a short period of time.
Correlates with diagram D in the study questions (diagrams for questions 65-72).

POsm
Decreased

PNa+
Decreased

ECF
Expanded

ICF
Expanded

20.

A 19-year-old hiker, who has been lost in the Sonoran desert for 3 days, has signs of volume
depletion. Which of the following changes in electrolyte and volume status is most likely present in
this patient?
POsm
PNa+
ECF
ICF
Compartment Compartment
Increased
High
Contracted
Contracted
Increased
Increased
Expanded
Expanded
Normal
Normal
Contracted
Normal
Increased
Increased
Expanded
Contracted
Decreased
Decreased
Contracted
Expanded
Answer: A. sweating will cause loss of a hypotonic salt solution leading to hypernatremia. Correlates
with diagram E in the study guide (diagrams for questions 65-72). The first step in managing this patient
is infusion of normal saline until the signs of volume depletion disappeared. Then he would be given 0.45
normal saline, which matches the tonicity of the sweat that he lost.

POsm
Increased

PNa+
Increased

ECF
Contracted

ICF
Contracted

21.

A 62-year-old woman has both left-sided and right-sided heart failure. Physical exam demonstrates
jugular vein distention, pitting edema, and bibasilar crepitant crackles. Which of the following
changes in electrolyte and volume status is most likely present in this patient?
POsm
PNa+
ECF
ICF
Compartment Compartment
Increased
Increased Expanded
Contracted
Decreased
Decreased Contracted
Expanded
Decreased
Decreased Expanded
Expanded
Increased
Increased Contracted
Contracted
Decreased
Decreased Contracted
Normal
Answer: C. Hypotonic gain of more water than salt leads to hyponatremia. Correlates with diagram D
(diagrams for questions 65-72). The hypotonic gain is from the fluid retained by the kidney when the
EABV is decreased. A hypotonic gain (greater increase in TBW than TBNa) translates into a
hyponatremia. The Starling's force abnormalities are related to an increase in hydrostatic pressure in the
pulmonary capillaries and in the venous system behind the right heart. The difference from SiADH is that
pitting edema is present in this case (increased TBNa +) but not SiADH (normal TBNa+). Rx is water and
salt restriction plus diuretics.

POsm
Decreased

PNa+
Decreased

ECF
Expanded

ICF
Expanded

22.

A 44-year-old woman has hypotension, increased skin and mucous membrane pigmentation, and
poor skin turgor. Laboratory studies uncover a low serum cortisol and electrolyte abnormalities. An
intravenous ACTH stimulation test over the ensuing 3 days demonstrates no increase in serum
cortisol or its urinary metabolites. Plasma ACTH levels are high. A random urine sodium is > 100
mEq/L (< 20 mEq/L). Which of the following changes in electrolyte and volume status is most
likely present in this patient?
POsm
PNa+
ECF
ICF
Compartment
Compartment
Decreased
Decreased Expanded
Expanded
Decreased
Decreased Expanded
Expanded
Increased
Increased
Contracted
Contracted
Increased
Increased
Expanded
Contracted
Decreased
Decreased Contracted
Expanded
Answer: E. the patient has Addison's disease with loss of aldosterone leading to a hypertonic loss of fluid
in the urine and hyponatremia. Correlates with diagram B in the study questions (diagrams for questions
65-72). Hypocortisolism causes the increase in ACTH, the latter having melanocyte stimulating
properties. Since the adrenal cortex is destroyed (autoimmune), IV ACTH stimulation will not cause any
increase in adrenal cortex metabolites (e.g., cortisol). The electrolyte findings in Addison's disease are the
same as those seen in a patient on an aldosterone blocker, mainly hyponatremia, hyperkalemia, and a
normal AG metabolic acidosis.

POsm
Decreased

PNa+
Decreased

ECF
Contracted

ICF
Expanded

Items 2326
pH
A.
Decrease
d
B.
Normal
C.
Normal

PCO2
Increased

Bicarbonate
Decreased

Normal
Increased

Normal
Increased

23. A 42-year-old woman in chronic renal failure is taking a loop diuretic because of retention of salt.
Answer: B. chronic renal failure (metabolic acidosis: pH, PCO2 [respiratory alkalosis],
bicarbonate [metabolic acidosis]) is taking loop diuretic (metabolic alkalosis: pH, PCO2 [respiratory
acidosis], bicarbonate [metabolic alkalosis]) for retention of salt. Both conditions neutralize each other.
pH
PCO2
Bicarbonate
B.
Normal Normal
Normal
24.

A 52-year-old smoker with chronic obstructive lung disease is currently taking a loop diuretic for
right sided heart failure. He has signs of volume depletion due to his diuretic.
Answer: C. chronic obstructive lung disease (chronic respiratory acidosis: pH, PCO2 [respiratory
acidosis], bicarbonate [metabolic alkalosis] ) is currently taking a loop diuretic (metabolic alkalosis:
pH, PCO2 [respiratory acidosis], bicarbonate [metabolic alkalosis]). pH is normalized, additive effect on
PCO2 and HCO3
pH
PCO2
Bicarbonate
C.
Normal
Increased
Increased
25. A 22-year-old man with type 1 diabetes mellitus has diabetic ketoacidosis and vomiting.
Answer: B. diabetic ketoacidosis (metabolic acidosis: pH, PCO2 [respiratory alkalosis],
bicarbonate [metabolic acidosis]) and vomiting (metabolic alkalosis: pH, PCO2 [respiratory
acidosis], bicarbonate [metabolic alkalosis]). They neutralize each other.
pH
PCO2
Bicarbonate
B.
Normal Normal
Normal
26. A 68-year-old man has a cardiorespiratory arrest and falls unconscious to the ground.
Answer: A. cardiorespiratory arrest: acute respiratory acidosis (not breathing) pH, PCO2
[respiratory acidosis], normal bicarbonate (no time for compensation) + metabolic acidosis from tissue
hypoxia leading to lactic acidosis: pH, PCO2 [respiratory alkalosis], bicarbonate [metabolic
acidosis]) ) Additive effect on lowering pH leading to a very low pH. Additive effect on PCO 2, since the
patient cannot breath and produce respiratory alkalosis as compensation for metabolic acidosis. There
would be no time for compensation for the acute respiratory acidosis, so bicarbonate would not be
increased and the bicarbonate would be decreased from the lactic acidosis, hence the additive effect is a
low bicarbonate.
pH
PCO2
Bicarbonate
A.
Decrease Increased
Decreased
d

27.

A 49-year-old woman has muscle weakness, polyuria, and circumoral paresthesias. Physical exam
demonstrates diastolic hypertension and flexion of the thumb into the palm on the side the blood
pressure is taken. A positive Chovstek sign is present. There is no evidence of pitting edema.
Laboratory studies show a mild hypernatremia, severe hypokalemia, and metabolic alkalosis. The
total serum calcium is normal. A random urine potassium is markedly elevated. Which of the
following changes in electrolyte and volume status is most likely present in this patient?
POsm
PNa+
ECF
ICF
Compartment
Compartment
Decreased Decreased
Expanded
Expanded
Increased
Increased
Expanded
Expanded
Increased
Increased
Contracted
Contracted
Decreased Decreased
Contracted
Expanded
Increased
Increased
Expanded
Contracted
Answer: E. This is classic primary aldosteronism. Gaining fluid in ECF. Hypernatremia establishes a
gradient favoring ICF contraction. Corresponds with diagram F. There is mild ECF expansion but not
enough increase in TBNa to produce signs of pitting edema due to the loss of sodium from the proximal
tubule related to the increase in peritubular capillary hydrostatic pressure from the increased plasma
volume. The tetany is due to the metabolic alkalosis and extra binding of calcium on the albumin (more
negative charges [COO-] in an alkaline pH) without altering the total calcium.
POsm
PNa+
ECF
ICF
Increased Increased
Expanded
Contracted
28.

An unconscious 26-year-old man, who is a roofer, is brought to an emergency room following a fall
from a 20 foot high roof. Physical exam demonstrates a weak pulse, cold, clammy skin, and a
blood pressure of 70/40 mm Hg. The ribs on the lower left side are fractured. A peritoneal lavage
demonstrates clotted blood. An intravenous line with 0.9% normal saline is currently in place while
blood is being crossmatched prior to surgery. Which of the following laboratory and
pathophysiologic events would you expect in this patient?
A.
Secondary aldosteronism
B.
Positive free water clearance
C.
Normal hemoglobin and hematocrit
D.
Decreased serum antidiuretic hormone
E.
Decreased effective arterial blood volume
Answers: A, E: the patient has hypovolemic shock from massive blood loss, most likely a ruptured
spleen, since the rib overlying the spleen is fractured. A. secondary aldosteronism: activation of RAA
system due to decreased renal blood flow and direct stimulation by catecholamines, E. decreased EABV:
B. Positive free water clearance: no, it should be negative, since there would be an increase in ADH and
concentration of urine
C. Normal hemoglobin and hematocrit: no, the hemoglobin and hematocrit would be decreased, because
the patient is receiving normal saline, which is replacing the volume deficit and uncovering the RBC
deficit. If the patient was not receiving isotonic saline, the Hb and Hct would very likely be normal.
D. Decreased serum antidiuretic hormone: no, it would be increased due to direct stimulation of ADH
release from the CNS
29.

You would expect a clinically significant decrease in effective arterial blood volume (EABV) in
which of the following clinical conditions? SELECT 3
A.
2-yr-old child with a rotavirus infection
B.
42-yr-old man with cirrhosis and ascites
C.
62-yr-old man with inappropriate ADH syndrome
D.
22-yr-old woman with insensible water loss due to fever
E.
25-yr-old construction worker with excessive sweating on a humid day
10

Answers A, B, E: A. 2-yr-old child with a rotavirus infection: hypotonic loss of salt


B. 42-yr-old man with cirrhosis and ascites: decreased venous return from trapping of fluid in interstitial
space (decreased oncotic pressure) and peritoneal cavity (decreased oncotic pressure and increased
hydrostatic pressure)
E. 25-yr-old construction worker with excessive sweating on a humid day: sweat is a hypotonic loss of
water and salt
C. 62-yr-old man with inappropriate ADH syndrome: no, EABV is increased from increased plasma
volume related to excessive reabsorption of free water
D. 22-yr-old woman with insensible water loss due to fever: no, water loss alone does not produce
clinically significant volume depletion (called dehydration). The EABV is normal.
30.

You would expect a patient with diabetic ketoacidosis and serum glucose of 1000 mg/dL to have...
SELECT 3
A.
hypertonicity with dilutional hyponatremia
B.
a decreased effective arterial blood volume
C.
random urine sodium < 20 mEq/L (< 20 mEq/L)
D.
expanded ECF compartment due to osmotic shifts
E.
positive tilt test when moved from a supine to sitting position
Answers A, B, E: A. hypertonicity with dilutional hyponatremia: glucose overrides sodium in the ECF
causing water to move out of the ICF into the ECF causing dilution of the serum sodium
B. a decreased effective arterial blood volume: yes, from osmotic diuresis related to glucose in the urine
producing a hypotonic loss of more water than salt (similar to sweat),
E. positive tilt test when moved from a supine to sitting position: excellent sign of volume depletion.
There is no effect of gravity when lying down so BP and pulse could be normal, but sitting up further
reduces venous return producing a drop in BP and increase in pulse
C. random urine sodium < 20 mEq/L (< 20 mEq/L): no, it is >20 mEq/L owing to a significant loss of
sodium in the urine from osmotic diuresis
D. expanded ECF compartment due to osmotic shifts: no, hyperglycemia favors a movement of water out
of the ICF into the ECF and then the osmotic diuresis causes the loss of that fluid in the urine. In other
words, the fluid in the ECF does not remain in that compartment very long owing to the loss of hypotonic
fluid in the urine.
Items 3137
Serum Na+
(135147)
A.
118
B.
130
C.
126
D.
130
E.
140
F.
140
G.
152

Serum K+
(3.55.0)
3.0
2.9
5.8
5.5
4.0
2.2
2.8

Serum Cl(95105)
88
80
96
88
100
114
110

31.

Serum HCO3(2228)
21
36
18
10
24
14
33

A 49-year-old man has fatigue and postural hypotension. Physical exam demonstrates dry mucous
membranes, an increase in heart rate and drop in blood pressure when moved from the supine to
sitting position, and increased pigmentation in the buccal mucosa. Laboratory studies reveal a low
serum cortisol and an increase in ACTH.
Answer: C: the patient has Addisons disease and no aldosterone activity: the aldosterone pumps that are
affected are the Na/K ATPase pump in the late distal and collecting tubules and the H/K ATPase pump in

11

the collecting tubules. Sodium is lost, potassium is retained, protons are retained and combine with
chloride resulting in a normal AG metabolic acidosis (note that the AG is 12 mEq/L: 126 - [96 + 18] = 12)
Serum Na+
Serum K+
Serum Cl- Serum HCO3(135147)
(3.55.0)
(95105)
(2228)
C.
126
5.8
96
18
Items 3137
Serum Na+
Serum K+
Serum Cl- Serum HCO3(135147)
(3.55.0)
(95105)
(2228)
A.
118
3.0
88
21
B.
130
2.9
80
36
C.
126
5.8
96
18
D.
130
5.5
88
10
E.
140
4.0
100
24
F.
140
2.2
114
14
G.
152
2.8
110
33
32. A 48-year-old man with left-sided heart failure has muscle weakness and clinical evidence of
volume depletion. He is currently taking a loop diuretic. An electrocardiogram shows prominent U
waves.
Answer: B. Classic hyponatremia, hypokalemia, and metabolic alkalosis from a loop diuretic.
Hyponatremia is due to a hypertonic loss of sodium in urine, hypokalemia from augmented Na/K
exchange, and metabolic alkalosis for exchange of Na with H ions leading to regeneration of bicarbonate.
This profile also fits vomiting. U waves indicate hypokalemia. Muscle weakness is the most common sign
of hypokalemia.
Serum Na+
Serum K+
Serum Cl- Serum HCO3(135147)
(3.55.0)
(95105)
(2228)
B.
130
2.9
80
36
33.

A 36-year-old woman in diabetic ketoacidosis has peaked T waves on an electrocardiogram. The


serum blood urea nitrogen (BUN) is 60 mg/dL (718) and serum creatinine is 6.0 mg/dL (0.61.2).
Answer: D. diabetic ketoacidosis, peaked T waves is not only due to a transcellular shift of potassium
out of cells but also retention of potassium from renal failure (BUN/creatinine ratio is 10/1). In renal
failure, both the serum BUN and creatinine rise proportionately due to the renal failure; hence, the ratio <
15/1 ratio. Expect dilutional hyponatremia, hyperkalemia, and increased AG metabolic acidosis. AG is 32
mEq/L (130 - [88 + 10])
Serum Na+
Serum K+
Serum Cl- Serum HCO3(135147)
(3.55.0)
(95105)
(2228)
D.
130
5.5
88
10
34.

A 34-year-old missionary in India develops cholera. Physical exam demonstrates severe volume
depletion.
Answer: F. cholera produces an isotonic loss of fluid owing to toxin stimulation of adenylate cyclase in
the small bowel. Diarrhea fluid has potassium and bicarbonate. Expect hypokalemia and normal AG
metabolic acidosis due to replacement of lost bicarbonate with chloride anions (hyperchloremia). There is
no hyperkalemia from a transcellular shift from acidosis because potassium is lost in the stool.
Serum Na+
Serum K+
Serum Cl- Serum HCO3(135147)
(3.55.0)
(95105)
(2228)
F.
140
2.2
114
14

12

Items 3137
Serum Na+
(135147)
A.
118
B.
130
C.
126
D.
130
E.
140
F.
140
G.
152

Serum K+
(3.55.0)
3.0
2.9
5.8
5.5
4.0
2.2
2.8

Serum Cl(95105)
88
80
96
88
100
114
110

Serum HCO3(2228)
21
36
18
10
24
14
33

35. A 48-year-old woman with Cushing's syndrome has severe diastolic hypertension.
Answer: G. Cushing's has mineralocorticoid excess just like primary aldosteronism. Lab findings are
similar.
Serum Na+
Serum K+
Serum Cl- Serum HCO3(135147)
(3.55.0)
(95105)
(2228)
G.
152
2.8
110
33
36. A 42-yr-old man has severe vomiting related to a viral gastritis. He has signs of volume depletion.
Answer: B. Vomiting leads to hyponatremia (loss of sodium in the vomitus) not hypernatremia.
Hypokalemia and metabolic alkalosis also occur. Best Rx is isotonic saline to replace the chloride and
volume depletion.
Serum Na+
Serum K+
Serum Cl- Serum HCO3(135147)
(3.55.0)
(95105)
(2228)
B.
130
2.9
80
36
37.

A 52-year-old type 2 diabetic on chlorpropamide has mental status abnormalities. Physical exam
is otherwise normal.
Answer: A. Classic SiADH from chlorpropamide, which enhances ADH release. Look for everything to
be decreased from dilution. Any serum sodium < 120 mEq/L is highly suspect for SiADH.
Serum Na+
Serum K+
Serum Cl- Serum HCO3(135147)
(3.55.0)
(95105)
(2228)
A.
118
3.0
88
21
38.

You would expect respiratory acidosis as compensation for which of the following patient
disorders? SELECT 2
A.
Barbiturate overdose
B.
Proximal renal tubular acidosis
C.
Chronic obstructive pulmonary disease
D.
Volume depleted patient taking a loop diuretic
E.
Volume depleted patient with protracted vomiting
Answers D, E. Respiratory acidosis is compensation for primary metabolic alkalosis: D. Volume depleted
patient taking a loop diuretic
E. Volume depleted patient with protracted vomiting
A. Barbiturate overdose: no, it produces acute respiratory acidosis and metabolic alkalosis is
compensation
B. Proximal renal tubular acidosis: no, it is an example of normal AG metabolic acidosis and respiratory
alkalosis is the compensation

13

C. Chronic obstructive pulmonary disease: no, it is an example of chronic respiratory acidosis and
metabolic alkalosis is its compensation
39.

You would expect an increase in effective arterial blood volume (EABV) in which of the following
clinical conditions? SELECT 3
A.
Right-sided heart failure
B.
Primary aldosteronism
C.
Acute myocardial infarction
D.
Overzealous infusion with 0.9% normal saline
E.
Infusion with excessive amounts of 3% hypertonic saline
Answers B, D, E: B. Primary aldosteronism: yes, due to excess sodium in the ECF, which increases the
plasma volume, D. Overzealous infusion with 0.9% normal saline, E. Infusion with excessive amounts of
3% hypertonic saline
A. Right-sided heart failure: no, EABV is decreased due to a decrease in cardiac output
C. Acute myocardial infarction: no, EABV is decreased due to a decrease in cardiac output
40.

Which of the following volume disorders represents a transudate secondary to a decrease in oncotic
pressure and increase in hydrostatic pressure?
A.
Patient with cirrhosis, dependent pitting edema, and ascites
B.
Patient with a pulmonary infarction who has a pleural effusion
C.
Patient with edema of the arm post-modified radical mastectomy
D.
Patient with congestive heart failure who has dependent pitting edema
E.
Patient with congestive heart failure who has bilateral pleural effusions
Answer: A. Patient with cirrhosis, dependent pitting edema, and ascites: portal hypertension increases
hydrostatic pressure leading to ascites and decreased albumin synthesis produces a decrease in oncotic
pressure leading to dependent pitting edema and ascites
B. Patient with a pulmonary infarction who has a pleural effusion: no, this is an exudate (protein and cell
rich fluid)
C. Patient with edema of the arm post-modified radical mastectomy: no, this is lymphedema
D. Patient with congestive heart failure who has dependent pitting edema: no, this is associated with an
increase in hydrostatic pressure from right-sided heart failure
E. Patient with congestive heart failure who has bilateral pleural effusions: no, this is due to an increase in
hydrostatic pressure
41.

Which of the following edema conditions represents a transudate secondary to an increase in


hydrostatic pressure? SELECT 2
A.
Patient with swelling of the arm after a bee sting
B.
Patient with cerebral edema secondary to hyponatremia
C.
Patient with congestive heart failure who has pulmonary edema
D.
Patient with congestive heart failure who has dependent pitting edema
E.
Patient with kwashiorkor who has ascites and dependent pitting edema
Answers C, D: C. Patient with congestive heart failure who has pulmonary edema: increase in
hydrostatic pressure from increased left ventricular end-diastolic volume and pressure. Pulmonary edema
occurs in left-sided heart failure.
D. Patient with congestive heart failure who has dependent pitting edema: in right-sided heart failure, the
blood accumulates in the venous system and raises the hydrostatic pressure leading to neck vein
distention, hepatomegaly, ascites, and dependent pitting edema.
A. Patient with swelling of the arm after a bee sting: no, this is an exudate from increased vessel
permeability related to histamine release in a type I hypersensitivity reaction.
B. Patient with cerebral edema secondary to hyponatremia: no, this is a water shift into the ICF from
hyponatremia (osmosis not a Starling's force abnormality)
14

E. Patient with kwashiorkor who has ascites and dependent pitting edema: no, this produces a transudate
due to decreased oncotic pressure related to a decreased protein intake
Items 4246
B

POsm

Serum ADH
The square represents normal values in a normally hydrated patient.
42. A 42-yr-old woman receives an intravenous infusion of 1 liter of 3% hypertonic saline.
Answer: C: hypertonic gain of fluid, increase POsm (hypernatremia), which is a stimulus for ADH
release
43.

A 62-yr-old smoker with a small cell carcinoma of the lung is diagnosed with inappropriate ADH
syndrome.
Answer: D: decrease POsm (hyponatremia) but increase in ADH. Normally, this should not occur. The
patient is concentrating urine when they should be diluting urine.
44.

A 63-yr-old instructor, who has been drinking a lot of water during an 8 hr lecture, has to make
frequent trips to the bathroom during every break.
Answer: A: instructor is drinking excess water and needs to dilute urine. Decreased POsm and inhibition
of ADH for dilution
45.

A 42-yr-old man, who is preparing for a marathon, forgot to bring replacement fluid during a 15
mile run on a hot, humid day.
Answer: C: patient is volume depleted and needs to concentrate urine. Increased POsm, which is a
stimulus for ADH release and concentration of urine.
46. A 22-yr-old man who suffered a head injury in a car accident now has increased thirst and polyuria.
Answer: B: central diabetes insipidus with no ADH. Loss of pure water leads to hypernatremia (increased
POsm). The patient is diluting urine when they should be concentrating urine. Opposite of SiADH.
47.

An afebrile 28-year-old medical student, who spent a weekend in Tijuana, Mexico, develops
traveler's diarrhea. Physical exam demonstrates signs of volume depletion. Which of the following
changes in electrolyte and volume status is most likely present in this patient?
POsm
PNa+
ECF
ICF
Compartment Compartment
Increased Increased Contracted
Contracted
Normal
Normal
Contracted
Normal
Normal
Normal
Contracted
Expanded
Increased Increased Expanded
Contracted
Decreased Decreased Contracted
Expanded
Answer: B. isotonic loss of fluid. No osmotic gradient. Correlates with diagram A in the study questions.

15

POsm
Normal

PNa+
Normal

ECF
Contracted

ICF
Normal

48.

Respiratory alkalosis would be expected as compensation in which of the following patient


conditions? SELECT 2
A.
Hyperventilation
B.
Chronic renal failure
C.
Pulmonary infarction
D.
Ethylene glycol poisoning
E.
Vomiting secondary to gastritis
Answers: B, D. respiratory alkalosis is compensation for a primary metabolic acidosis: B. Chronic renal
failure: increased AG metabolic acidosis
D. Ethylene glycol poisoning: ethylene glycol is converted by alcohol dehydrogenase to glycolic and
oxalic acid, the latter forming calcium oxalate crystals in the kidney tubules causing renal failure
A. Hyperventilation: no, this produces a primary respiratory alkalosis and metabolic acidosis is
compensation
C. Pulmonary infarction: no, this produces a primary respiratory alkalosis from tachypnea and metabolic
acidosis is compensation
E. Vomiting secondary to gastritis: no, this produces a primary metabolic alkalosis and respiratory
acidosis is compensation.
Items 4958
pH
(7.35
7.45)
7.00
7.27
7.25
7.26
7.38
7.38
7.42
7.56
7.58

PCO2
(3345 mm Hg)
52
60
80
26
70
40
22
24
49

HCO3(2228 mEq/L)
12
26
34
11
40
24
14
21
39

49. A 35-year-old recently divorced woman overdoses on barbiturates.


Answer: B. Barbiturates depress the respiratory center producing an acute respiratory acidosis without
compensation.
pH
PCO2
HCO3(7.35
(3345 mm Hg) (2228 mEq/L)
7.45)
7.27
60
26

16

Items 4958
pH
(7.35
7.45)
7.00
7.27
7.25
7.26
7.38
7.38
7.42
7.56
7.58

PCO2
(3345 mm Hg)
52
60
80
26
70
40
22
24
49

HCO3(2228 mEq/L)
12
26
34
11
40
24
14
21
39

50.

A 46-yr-old woman with rheumatoid arthritis develops tinnitus. You suspect the patient has
salicylate toxicity.
Answer: G. salicylate toxicity is a mixed disorder: respiratory alkalosis (respiratory center stimulation) +
metabolic acidosis (salicylic acid + lactic acid)
pH
PCO2
HCO3(7.35
(3345 mm Hg) (2228 mEq/L)
7.45)
7.42
22
14
51. A 19-year-old type 1 diabetic is in ketoacidosis and is vomiting.
Answer: F. ketoacidosis is an increased AG metabolic acidosis and vomiting produces metabolic
alkalosis. These 2 disorder neutralize each other. Note that the normal pH is on the acid side, so the
ketoacidosis is a little worse than the metabolic alkalosis.
pH
PCO2
HCO3(7.35
(3345 mm Hg) (2228 mEq/L)
7.45)
7.38
40
24
52.

A 49-year-old woman with chronic bronchitis secondary to smoking is taking a loop diuretic for
congestive heart failure.
Answer: E. chronic bronchitis produces chronic respiratory acidosis and a loop diuretic produces
metabolic alkalosis. This is a mixed disorder: pH should be normal, PCO 2 markedly increased, since both
disorders have an increase in PCO2, and the bicarbonate should be markedly increased, since both
disorders have an increase in bicarbonate.
pH
PCO2
HCO3(7.35
(3345 mm Hg) (2228 mEq/L)
7.45)
7.38
70
40
53.

A septic 72-yr-old man has urinary retention secondary to prostatic hyperplasia. You suspect the
patient has endotoxic shock.
Answer: G. endotoxic shock produces a mixed disorder: respiratory alkalosis overstimulates the
respiratory center + metabolic acidosis from shock leading to lactic acidosis. This is a mixed disorder. The

17

pH changes neutralize each other. Both PCO2 and bicarbonate are decreased in both conditions producing
an additive effect.
pH
PCO2
HCO3(7.35
(3345 mm Hg) (2228 mEq/L)
7.45)
7.42
22
14
Items 4958
pH
(7.35
7.45)
7.00
7.27
7.25
7.26
7.38
7.38
7.42
7.56
7.58

PCO2
(3345 mm Hg)
52
60
80
26
70
40
22
24
49

HCO3(2228 mEq/L)
12
26
34
11
40
24
14
21
39

54.

A 21-year-old man with cystic fibrosis who has had recurrent pulmonary infections almost all his
life has fever and a productive cough consistent with acute bronchitis or pneumonia.
Answer: C. cystic fibrosis produces chronic obstructive lung disease and chronic respiratory acidosis. An
acute bronchitis or pneumonia superimposes an acute respiratory acidosis on top of a chronic
respiratory acidosis. Chronic respiratory acidosis is associated with metabolic alkalosis as compensation,
unlike acute respiratory acidosis (choice B), which does not. The PCO 2 is probably higher than usual
owing to the superimposed acute bronchitis or pneumonia. Before the patient got a superimposed
infection, the pH was probably around 7.33 and PCO2 around 60. This is a type of mixed disorder.
pH
PCO2
HCO3(7.35
(3345 mm Hg) (2228 mEq/L)
7.45)
7.25
80
34
55.

A 35-yr-old migrant worker inadvertently drinks methyl alcohol. He develops gastric upset and
blurry vision.
Answer: D. methyl alcohol produces an increased AG metabolic acidosis, because it is metabolized by
alcohol dehydrogenase to formic acid, which produces optic neuritis and a potential for blindness.
pH
PCO2
HCO3(7.35
(3345 mm Hg) (2228 mEq/L)
7.45)
7.26
26
11
56.

A 56-year-old man is in cardiorespiratory arrest. You arrive on the scene ~2 minutes after the
patient lost consciousness.
Answer: A. cardiorespiratory arrest is associated with a primary acute respiratory acidosis (not
breathing) + metabolic acidosis from lactic acidosis. Expect a very low acid pH.
pH
PCO2
HCO3-

18

(7.35
7.45)
7.00

(3345 mm Hg)
52

(2228 mEq/L)
12

57. A 24-yr-old medical student develops an anxiety attack while taking a comprehensive final exam
Answer: H. an anxiety attack produces an acute respiratory alkalosis, owing to excessive blowing off of
CO2. Note the partially compensated metabolic acidosis. Non-renal mechanisms are able to lower the
bicarbonate to 18 mEq/L.
pH
PCO2
HCO3(7.35
(3345 mm Hg) (2228 mEq/L)
7.45)
7.56
24
21
Items 4958
pH
(7.35
7.45)
7.00
7.27
7.25
7.26
7.38
7.38
7.42
7.56
7.58

PCO2
(3345 mm Hg)
52
60
80
26
70
40
22
24
49

HCO3(2228 mEq/L)
12
26
34
11
40
24
14
21
39

58.

A 2 mth old child has repeated vomiting of non-bile stained fluid. You suspect congenital pyloric
stenosis.
Answer: I. vomiting produces metabolic alkalosis
pH
PCO2
HCO3(7.35
(3345 mm Hg) (2228 mEq/L)
7.45)
7.58
49
39
59.

Which of the following patients would most likely have clinical evidence of dependent pitting
edema if an alteration in Starling's forces is present plus a stimulus for renal retention of salt?
SELECT 2
A.
Patient with diabetes insipidus
B.
Patient with congestive heart failure
C.
Patient with inappropriate ADH syndrome
D.
Patient receiving excessive 0.9% normal saline
E.
Patient receiving excessive 5% dextrose and water
Answers: B, D. the patient must have an increase in TBNa+ and a preexisting Starling's force abnormality
+ renal retention of sodium in order to have pitting edema:
B. Patient with congestive heart failure: hypotonic gain of more water than salt
D. Patient receiving excessive 0.9% normal saline

19

A. Patient with diabetes insipidus: no, there is hypernatremia due to a loss of pure water. TBNa + is
normal. An osmotic gradient is established and water moves out of the ICF into the ECF and from the
ECF out into the urine as free water, so both compartments are contracted.
C. Patient with inappropriate ADH syndrome: no, the patient has a gain of pure water. TBNa + is normal.
An osmotic gradient is established causing water to move into the ICF. Both ECF and ICF compartments
are expanded.
E. Patient receiving excessive 5% dextrose and water: no, the patient is gaining a hypotonic solution with
no salt. TBNa+ is normal. An osmotic gradient is established (hyponatremia) and water shifts from the
expanded ECF compartment into the ICF compartment

20

Items 6062
MVO2

PCWP
SVR
Cardiac output
(LVEDP)
(TPR)
Decreased Decreased Increased
Decreased
Decreased Increased Increased
Decreased
Increased Decreased Decreased
Increased
Normal
Normal
Normal
Normal
LVEDP, left ventricular end-diastolic pressure; MVO 2, mixed venous oxygen content; PCWP, pulmonary
capillary wedge pressure; SVR, systemic vascular resistance; TPR, total peripheral resistance.
60.

A 72-year-old man with urinary retention from benign prostatic hyperplasia has a sudden onset of
fever and chills. His skin feels warm and his pulse is hyperdynamic.
Answer: C. This is septic (endotoxic shock). Remember vasodilation of arterioles decreases peripheral
vascular resistance (decrease in SVR, which is the same as total peripheral resistance). It drastically
lowers the diastolic blood pressure and causes blood to move quickly through the microcirculation (like a
dam with its flood gates wide open) making it impossible for tissue to extract oxygen (increased MVO 2).
Venous return to the heart increases (increased cardiac output). This is called high output cardiac failure.
The heart will not last too long with this increased load and eventually the patient will progress into
findings consistent with cardiogenic shock. Pulmonary capillaries become permeable owing to neutrophil
injury and an exudate leaks into the alveoli causing ARDS. PCWP (a measure of left-sided left ventricular
pressure) is decreased. This is an example of a non-cardiogenic pulmonary edema.
MVO2
PCWP
SVR
Cardiac output
Increased
Decreased
Decreased
Increased
61. A 75-year-old man with a known history of an abdominal aortic aneurysm experiences a sudden
onset of left flank pain and dizziness. He is brought to the emergency room and has a heart rate of
140 beats/minute, blood pressure of 60/40 mm Hg, and a pulsatile mass in his abdomen. You
suspect a ruptured abdominal aortic aneurysm.
Answer: A. the patient is in hypovolemic shock. The key difference from cardiogenic shock is the low
PCWP. MVO2 is low since the decreased cardiac output allows tissue to extract most of the oxygen out of
the blood. SVR is increased owing to vasoconstriction of the peripheral resistance arterioles, which
decreases the radius to the 4th power.
MVO2
PCWP
SVR
Cardiac output
Decreased Decreased Increased
Decreased
62.

A 60-year-old man has an acute myocardial infarction, which progressed into congestive heart
failure within 24 hrs of admission to the coronary care unit.
Answer: the patient has left-sided heart failure. Unlike hypovolemic shock, PCWP is increased from
backup of blood into the lungs from the overloaded left ventricle.
MVO2
PCWP
SVR
Cardiac output
Decreased Increased Increased
Decreased
63.

In treating a 65-year-old man with pulmonary edema patient, neck vein distention and dependent
pitting edema, which of the following is the MOST APPROPRIATE management of the patients
sodium and water intake?
Sodium intake
Water intake
A.
No change
No change
B.
Decrease
No change
C.
Decrease
Decrease
D.
No change
Decrease
E.
Increase
Increase

21

Answer: C. the patient has left-sided heart failure (pulmonary edema) and right-sided heart failure (neck
vein distention and dependent pitting edema). In either case, there is an alteration is Starling's forces
(increased hydrostatic pressure) and a decreased cardiac output leading to retention of a slightly
hypotonic salt-containing solution ( TBNa / TBW). Owing to the increase in hydrostatic pressure in the
venous system in right-sided heart failure, most of this hypotonic fluid will move into the interstitial space
and worsen the dependent pitting edema. Since both TBNa and TBW are increased, the best nonpharmacologic treatment for this patient and any other similar type of edema state (e.g., cirrhosis,
nephrotic syndrome) is to restrict both water and salt. Diuretics are the most useful pharmacologic
treatment.
Sodium intake
Water intake
C.
Decrease
Decrease
64.

In treating a patient with the inappropriate ADH syndrome, which of the following is the MOST
APPROPRIATE management of the patients sodium and water intake?
Sodium intake
Water intake
A.
Decrease
No change
B.
No change
No change
C.
Decrease
Decrease
D.
No change
Decrease
E.
Increase
Increase
Answer: D. patients with SiADH have a hypotonic gain of pure water without any salt. Therefore, only
water is restricted and not salt, since the TBNa + is normal.
Sodium intake
Water intake
D.
No change
Decrease

22

Items 6572

POsm

ICF

ECF

Volume
Note: the height of the squares represent plasma osmolality (POsm), while the width of the squares
represents volume in each compartment. ECF is the extracellular fluid compartment and ICF is the
intracellular fluid compartment. The dark lines represent the normal POsm and volume in each
compartment, while the hash marked lines represent the volume alteration.

A.

B.

C.

D.

E.

F.

65. The patient is a 45-yr-old man who is volume depleted secondary to the use of loop diuretics.
Answer: B. Hypertonic loss of fluid with hyponatremia with ECF contraction and ICF expansion
66.

The patient is a 23-yr-old marathon runner who is volume depleted after running on a hot, humid
day.
Answer: E. the patient is losing sweat, where there is a hypotonic loss of more water than salt. This
causes hypernatremia with ECF contraction and ICF contraction. The water that shifts into the ECF from
the ICF is lost in the sweat.
23

67.

The patient is a 64-yr-old smoker with a small cell carcinoma of the lung and inappropriate ADH
syndrome.
Answer: D. Hypotonic gain of pure water and no salt. Hyponatremia with ECF expansion and ICF
expansion.
Items 6572

POsm

ICF

ECF

Volume
Note: the height of the squares represent plasma osmolality (POsm), while the width of the squares
represents volume in each compartment. ECF is the extracellular fluid compartment and ICF is the
intracellular fluid compartment. The dark lines represent the normal POsm and volume in each
compartment, while the hash marked lines represent the volume alteration.

68.

A.

B.

C.

D.

E.

F.

The patient is a 68-yr-old man, with a known history of ischemic heart disease. He has pneumonia
due to Pseudomonas aeruginosa and is receiving an intravenous solution containing sodium

24

carbenicillin. He has physical findings consisting of bibasilar crackles, neck vein distention,
hepatomegaly, and pitting edema.
Answer: F. Hypertonic gain of sodium from the IV. Hypernatremia, ECF expansion, ICF contraction
69.

A 78-yr-old woman with a known history of ischemic heart disease has a bilateral hip replacement
for severe osteoarthritis involving the femoral heads. She has been overzealously infused with
0.9% normal saline and has pitting edema and bibasilar crepitant crackles.
Answer: C. Isotonic gain of fluid with normal serum sodium, expansion of ECF, normal ICF, since there
is no osmotic gradient
Items 6572

POsm

ICF

ECF

Volume
Note: the height of the squares represent plasma osmolality (POsm), while the width of the squares
represents volume in each compartment. ECF is the extracellular fluid compartment and ICF is the
intracellular fluid compartment. The dark lines represent the normal POsm and volume in each
compartment, while the hash marked lines represent the volume alteration.

A.

B.

C.

D.

E.

F.

25

70. The patient is a 42-yr-old medical missionary with cholera. He is volume depleted.
Answer: A. Isotonic loss of fluid. Serum sodium is normal, ECF is contracted, ICF is normal since there
is no osmotic gradient. Vibrio cholerae produces a toxin that stimulates adenylate cyclase, causing an
isotonic loss of fluid. There is no bowel inflammation.
71.

The patient is a 69-yr-old with ischemic heart disease and both left-sided and right-sided heart
failure.
Answer: D. Hypotonic gain of more water than salt from the kidneys leading to hyponatremia, ECF
expansion and ICF expansion. Note that the same schematic applies to both SiADH and heart failure,
since both are hypotonic gains of fluid. However, the physical exam is different, not to mention the
history. In SiADH, the TBNa is normal, hence skin turgor is normal, while in right-sided heart failure,
there is an increase in TBNa and dependent pitting edema.
Items 6572

POsm

ICF

ECF

Volume
Note: the height of the squares represent plasma osmolality (POsm), while the width of the squares
represents volume in each compartment. ECF is the extracellular fluid compartment and ICF is the
intracellular fluid compartment. The dark lines represent the normal POsm and volume in each
compartment, while the hash marked lines represent the volume alteration.

A.

B.

26

C.

D.

E.

F.

72. The patient is 82-years-old and has 105o F temperature from a lobar pneumonia.
Answer: E. Insensible water loss from fever. Hypotonic loss of pure water with hypernatremia, mild
ECF contraction (normal physical exam), and ICF contraction. Loss of pure water without any salt does
not alter skin turgor. This is called dehydration.

27

73.

Which of the following best explains the mechanism for hypokalemia in patient's with respiratory
or metabolic alkalosis?
A.
Potassium loss in the urine
B.
Potassium loss in the gastrointestinal tract
C.
Potassium shift into cells in exchange for protons
D.
Potassium shift into cells in exchange for chloride
E.
Potassium shift into cells in exchange for bicarbonate
Answer: C. Potassium shift into cells in exchange for protons (hydrogen ions).
A. Potassium loss in the urine: this would only be correct if the metabolic alkalosis was caused by loop or
thiazide diuretics or mineralocorticoid excess
B. Potassium loss in the gastrointestinal tract: this would only be correct for diarrhea, however, it
produces a normal AG metabolic acidosis. The expected hyperkalemia from a shift of potassium out of
the cell in exchange for protons does not override the greater loss of potassium in the stool
D. Potassium shift into cells in exchange for chloride: this exchange does not occur. The exchange of
chloride is with bicarbonate. When bicarbonate leaves a cell (e.g., the patient has respiratory acidosis and
a non-renal mechanism for increasing bicarbonate as compensation is required), chloride enters the cell in
order to maintain electroneutrality. When bicarbonate moves into a cell (e.g., the patient has respiratory
alkalosis and need a non-renal mechanism for removing bicarbonate from the blood to produce metabolic
acidosis as compensation), chloride moves out of the cell to maintain electroneutrality.
E. Potassium shift into cells in exchange for bicarbonate: this type of exchange does not occur in cells.
74.

Which of the following conditions are commonly associated with prominent U waves on an
electrocardiogram? SELECT 3
A.
Addison's disease
B.
Protracted vomiting
C.
Aldosterone blockers
D.
Distal renal tubular acidosis
E
Patient on high doses of albuterol
F.
Destruction of the juxtaglomerular apparatus
Answers B, D, E: a U wave indicates the presence of hypokalemia, B. Protracted vomiting: metabolic
alkalosis. Potassium is lost in the vomitus.
D. Distal renal tubular acidosis: block of proton/K + pump
E. Patient on high doses of albuterol: enhances the Na/K ATPase pump; hence increasing cellular uptake
of K+ and cellular loss of Na+
A. Addison's disease: no, loss of mineralocorticoids results in hyperkalemia, since the Na/K ATPase pump
in the distal and collecting tubule is dysfunctional. This is the primary pump for removing excess
potassium from the body.
C. Aldosterone blockers: no, same explanation as for A.
F. Destruction of the juxtaglomerular apparatus: no, destroying the JG apparatus lowers renin, which
lowers AT II and aldosterone. Decreased aldosterone results in hyponatremia, hyperkalemia, and normal
AG metabolic acidosis. This is called type IV RTA and is most often secondary to diabetic renal disease,
where the afferent arteriole is damaged by hyaline arteriolosclerosis.
75.

Which of the following conditions are commonly associated with peaked T waves on an
electrocardiogram? SELECT 3
A.
Patient with severe diarrhea
B.
Patient taking excess digitalis
C.
Patient with chronic renal failure
D.
Patient on high doses of a -blocker
E.
Patient with proximal renal tubular acidosis

28

Answers B, C, D: peaked T waves indicate hyperkalemia: B. Patient taking excess digitalis: blocks the
Na+/K+ ATPase symporter, so more K+ is pumped out of the cell
C. Patient with chronic renal failure: cannot excrete potassium (MCC), D. Patient on high doses of a blocker: inhibits the ATPase pump causing a loss of K + from cells and gain in Na+
A. Patient with severe diarrhea: no, it produces hypokalemia and a U wave
E. Patient with proximal renal tubular acidosis: no, it produces hypokalemia owing to loss of potassium
when it combines with bicarbonate in the urine and is excreted. Sodium is also lost in the urine when it
combine with bicarbonate to produce sodium bicarbonate.
76.

Which of the following is the initial step in the management of hyperkalemia?


A.
Loop diuretic
B.
Thiazide diuretic
C.
Calcium gluconate
D.
Cationic exchange resins
E.
Insulin with glucose infusion
Answer: C. Calcium gluconate: protect the heart with calcium gluconate. It does not lower potassium
levels. All the other choices deal with either shifting K + into cells (e.g., insulin, albuterol) or excreting K +
(e.g., diuretics)
A. Loop diuretic: yes, but not as the initial step, since it does not immediately protect the heart
B. Thiazide diuretic: same explanation as A
D. Cationic exchange resins: yes, they do bind to K+ in the bowel and aid in its excretion, however, it does
not work fast enough to protect the heart
E. Insulin with glucose infusion: yes, it shifts K+ into the cell by enhancing the Na/K ATPase pump,
however, it does not do it fast enough to protect the heart.
77.

The purpose for placing patient's at risk for thrombosis on low dose aspirin is to prevent
SELECT 3
A.
strokes
B.
platelet aggregation
C.
intravascular coagulation
D.
acute myocardial infarctions
E.
thrombosis in deep veins of the calf
F.
thrombosis in superficial varicose veins
Answers A, D, D: A. strokes
B. platelet aggregation
D. acute myocardial infarctions. The purpose of using aspirin is to prevent platelet aggregation and the
potential for forming a platelet thrombus overlying atherosclerotic plaques in the coronary artery or at the
branch of the carotid artery in the neck. Aspirin blocks platelet cyclooxygenase, which prevents the
synthesis of TXA2. TXA2 normally causes platelet aggregation.
C. intravascular coagulation: no, aspirin does not affect the coagulation factor pathway. Disseminated
intravascular coagulation is due to activation of the coagulation pathway (extrinsic, intrinsic, or both)
leading to the formation of fibrin clots in small vessels throughout the body. Coagulation factors that are
normally consumed in a fibrin clot are used up (e.g., fibrinogen, prothrombin, V, VIII); hence the patient
is also anticoagulated.
E. thrombosis in deep veins of the calf: no, venous clots resemble fibrin-clots that develop in a clot tube
(red top tube). They are due to activation of the coagulation system rather than activation of platelets to
aggregate.
F. thrombosis in superficial varicose veins: no, same explanation as in E

29

78.

Which of the following coagulation factors is an actual component of both venous and arterial
thrombi?
A.
Fibrin
B.
Factor XII
C.
Prothrombin (factor II)
D.
Factor V
E.
Factor VIII
Answer: A. fibrin: Fibrin is responsible for the stability of both venous and platelet thrombi. Fibrin has
cross-links that increase its tensile strength. Platelets normally have fibrinogen receptors. When platelet
initially aggregate, fibrinogen (carried by the platelet) attaches to the platelet receptors and loosely holds
them together. When thrombin is formed, the fibrinogen is converted into fibrin, which makes the platelet
thrombus stable. In venous clots, fibrin also holds the clot together and traps RBCs, platelets, and
leukocyte in its meshwork.
B. Factor XII: no, it is the primary coagulation factor, that when activated, initiates the clotting sequence
in the intrinsic system. It is not an actual component of the platelet and venous clot. Recall that platelet
thrombi generally occur in the setting of turbulence and endothelial cell damage in the arterial system,
while venous clots develop in the venous system in the setting of stasis and hypercoagulability. One
cannot expect a venous type fibrin clot, which traps RBCs, platelet, and leukocytes to develop in a rapid
blood flow situation. However, platelets become tightly adherent to areas of endothelial damage in high
flow situations, hence they are more likely to develop over atherosclerotic debris within the arterial
system, particularly when they begin to occlude the lumen and produce signs of ischemia. This is not to
say that the intrinsic or extrinsic system are not activated in the arterial system when endothelial injury
occurs, because it is activated and will produce thrombin, however, it will not be able to trap RBCs,
platelets, and leukocytes in it due to the rapid blood flow. The thrombin, however, will be able to convert
fibrinogen holding platelets together into fibrin to form a platelet thrombus.
C. Prothrombin (factor II): no, it is used up in the formation of a clot and is not an actual component of
the platelet and venous clot.
D. Factor V: no, it is used up in the formation of a clot and is not an actual component of the platelet and
venous clot.
E. Factor VIII: no, it is used up in the formation of a clot and is not an actual component of the platelet
and venous clot.
79.

A 23-yr-old man is placed in the intensive care unit after sustaining femoral bone fractures, multiple
pelvic fractures, and a laceration of the spleen from a motorcycle accident. Forty eight hours later,
he develops a sudden onset of dyspnea, petechial lesions on the thorax, and mental status
alterations. Laboratory studies reveal hypoxemia and thrombocytopenia. The prothrombin time and
partial thromboplastin time are both normal. The patient most likely has which of the following
disorders?
A.
Disseminated intravascular coagulation
B.
Pulmonary embolism
C.
Fat embolization
D.
Air embolization
E.
Pneumonia
Answer: C. Fat embolization: this is a classic case with all the clinical findings. Microglobules of fat
from the marrow and surrounding adipose enter the microcirculation and circulate throughout the body,
since they are small enough to move through capillaries. The fatty acids released from the fat damages the
endothelial cells in the microvasculature causing platelet adherence to the damaged endothelium, hence
they are used up and produce thrombocytopenia. Blockage of the microcirculation is therefore, due to the
microglobules of fat as well as tiny platelet thrombi. The endothelial cell damage does not occur
immediately and requires at least 24-48 hrs, hence the delay in symptoms in fat embolization. Dyspnea is
due to blockage of the pulmonary capillaries (perfusion defect leading to hypoxemia). Thrombocytopenia
30

is due to increased utilization in the formation of platelet thrombi in areas of endothelial damage and due
to adherence to the microglobules of fat. Thrombocytopenia is also the cause of the petechial lesions
(pinpoint areas of hemorrhage) in the patient. Mental status abnormalities are due to minute hemorrhages
into the brain from the blocked capillaries leading to cerebral edema.
A. Disseminated intravascular coagulation: this may occur in the setting of trauma, however, since the
coagulation system is activated in this disorder resulting in the formation of fibrin-clots, the prothrombin
time and partial thromboplastin time should be prolonged (fibrinogen, II, V, and VIII are consumed)
B. Pulmonary embolism: this may also occur in severely traumatized patients, however, there is no
history of calf tenderness (sign of deep venous thrombosis) or pleuritic chest pain, which invariably
accompanies a pulmonary embolus. In addition, a PE does not produce thrombocytopenia.
D. Air embolization: the clinical setting in this patient is not one for air embolism. This usually occurs in
head and neck types of surgery.
E. Pneumonia: the clinical setting is one of trauma, not infection. There is no mention of physical findings
in the lung that would lead one to suspect a pneumonia: e.g., signs of consolidation in the lung, crackles
in the lung with inspiration.
80.

A 23-yr-old scuba diver, who is diving in 100 feet of water, is forced to ascend to the surface owing
to mechanical difficulties with his diving gear. Within 1015 minutes after resurfacing, blood
begins to ooze out of both ear canals, his skin becomes mottled and pruritic, and he begins to lose
both bladder and bowel control. The pathogenesis of these findings most closely correlates with
which of the following factors? SELECT 2
A.
Fat embolization
B.
Carbon dioxide narcosis
C.
Nitrogen gas bubbles in tissue/vessels
D.
Movement from a high to lower atmospheric pressure
Answers C, D: C. Nitrogen gas bubbles in tissue/vessels: atmospheric pressure increase by 1 for every 33
feet descent into the water, which drives nitrogen into tissues. Rapid ascent causes the nitrogen to come
out of solution to form bubbles that block vessels and damage tissue,
D. Movement from a high to lower atmospheric pressure
A. Fat embolization: no, this usually occurs in the setting of trauma with fractures of the pelvic bones or
femur
B. Carbon dioxide narcosis: no, this is a feature of respiratory acidosis leading to retention of CO 2 and
severe hypoxemia.
81.

Which of the following are the most common sites predisposing for venous thrombosis and
embolization, respectively?
A.
Deep vein of calf / deep vein of calf
B.
Saphenous vein / deep vein of calf
C.
Deep vein of calf / saphenous vein
D.
Femoral vein / deep vein of calf
E.
Deep vein of calf / femoral vein
Answer: E. Deep vein of calf / femoral vein: most venous thrombi initially develop in the smaller caliber
vessel in the deep veins of the calf. In this location, they propagate towards the heart, hence extending
into the larger caliber femoral vein, where embolization is more likely to occur.
A. Deep vein of calf / deep vein of calf: no, it is not the MC site for embolization
B. Saphenous vein / deep vein of calf: thrombi in the saphenous commonly occur in the setting of
varicose veins, however the femoral vein is the MC site for embolization
C. Deep vein of calf / saphenous vein: thrombi in the saphenous vein, which is the superficial venous
system of the legs, cannot embolize since the thrombi could never get through the penetrating branches to
the deep venous system
D. Femoral vein / deep vein of calf: no, this is reversed
31

82.

Which of the following is the greatest risk factor for a venous clot in the lower extremity in a
patient who is 5 days post-operative for removal of a gangrenous gallbladder?
A.
Turbulent blood flow
B.
Stasis of blood flow
C.
Increased plasma viscosity
D.
Septicemia
Answer: B. Stasis of blood flow: lack of movement of the patient in bed predisposes to stasis and venous
thrombi that most commonly develop initially in the deep veins of the calf, hence the importance of
ambulation in the patient as soon as possible.
A. Turbulent blood flow: no, turbulent blood flow more often occurs in the arterial system at sites of
bifurcation and overlying atheromatous plaques. Platelet thrombi are more likely to develop in this setting
leading to a myocardial infarction or stroke.
C. Increased plasma viscosity: although this would predispose to venous clots, the clinical setting in this
patient would not lend towards a viscosity problem due to an increase in IgM (Waldenstrom's
macroglobulinemia, a malignant disorder of lymphoplasmacytoid cells) or a disorder involving globulins
that often congeal in cold temperatures (cryoglobulins)
D. Septicemia: although sepsis is a common finding in a gangrenous gallbladder, it would most likely
predispose to disseminated intravascular coagulation, with fibrin clots developing in capillaries
throughout the entire body
83.

A 65-year-old man with tachycardia associated with an irregularly irregular pulse develops a
sudden onset of pain in multiple digits in his foot. The digits are pale, swollen, and painful to
palpation. Which of the following is the most likely cause of the patient's clinical findings?
A.
Venous thrombosis
B.
Arterial embolization
C.
Atherosclerosis of digital vessels
D.
Paradoxical embolization
Answer: B. arterial embolization: the patient has atrial fibrillation (irregularly irregular pulse), which
predisposes to stasis in the left atrium and clot formation ("venous" type clot related to stasis even though
it is in the left heart). AF is the most dangerous arrhythmia predisposing to systemic embolization. Emboli
to the digital vessels has produced early signs of infarction of the digits related to ischemic coagulative
necrosis.
A. venous thrombosis: the clinical setting of atrial fibrillation favors arterial embolization than a venous
thrombosis of digital vein vessels. This would more likely occur in certain types of vasculitis (e.g.,
scleroderma, SLE).
C. atherosclerosis of digital vessels: the digital vessels rarely undergo atherosclerosis. Elastic and large to
medium-sized muscular arteries are more often predisposed to atherosclerosis.
D. paradoxical embolization: his refers to embolization of a venous clot to a site in the systemic
circulation. For this to occur, the patient would have to have a patent foramen ovale (atrial septal defect),
which would allow a venous clot to traverse the right atrium and enter the left atrium.
84.

In patients who are hypovolemic from massive blood loss or loss of salt-containing fluids (e.g.,
diarrhea fluid, sweat), which of the following is the first step in management of the patient?
A.
3% Hypertonic saline
B.
0.9% Normal saline
C.
0.45% Normal saline
D.
0.25% Normal saline
E.
5% Dextrose and water
Answer: B. 0.9% Normal saline: only fluid that is isotonic to plasma can raise the blood pressure in any
hypovolemic patient. 0.9% normal saline has the same tonicity as plasma and essentially acts like plasma
except for the absence of proteins. Even the hypovolemia associated with loss of whole blood can initially
32

be managed with normal saline until blood is available for transfusion. It is not possible to raise blood
pressure with a hypotonic salt solution (C. 0.45% Normal saline, D. 0.25% Normal saline, or E. 5%
Dextrose and water). Use of 3% hypertonic saline is rarely used, because it produces a chemical phlebitis
and damage to tissue if it should infiltrate into tissue. Some clinicians use it in treating SiADH or in
patients with hypertonic fluid loses (e.g., diuretics), however, this is not the norm.
85.

A 22-year-old woman develops abruptio placenta (placenta separates from the uterine wall owing to
a retroplacental clot). She suddenly develops cold, clammy skin, hypotension, dyspnea, and
cyanosis of her skin and mucus membranes. The baby is quickly delivered, while large amounts of
normal saline are infused as blood is being obtained for transfusion. Blood begins to ooze out of all
her venipuncture and IV infusion sites and the patient dies. Which of the following autopsy findings
would you expect in this patient? SELECT 2
A.
Large pulmonary embolus occluding the orifices of the pulmonary arteries
B.
Multiple pulmonary infarctions at the periphery of the lungs
C.
Fetal squamous cells and lanugo hair in her pulmonary vessels
D.
Fibrin clots in the small capillaries throughout the body
E.
Fat microglobules in the small capillaries throughout the body
Answers: C, D. the patient has amniotic fluid embolism and DIC. C. Fetal squamous cells and lanugo
hair in her pulmonary vessels: present in amniotic fluid and obtained entrance to the patient's circulation
via the uterine veins
D. Fibrin clots in the small capillaries throughout the body: amniotic fluid is rich in tissue thromboplastin,
which activates factor VII in the extrinsic coagulation system leading to disseminated small fibrin-clot
formation with consumption of clotting factors (fibrinogen, prothrombin, V, VIII). In addition to the
microthrombi, the patient is also anticoagulated, hence the oozing of blood from all the IV and
venipuncture sites.
A. large pulmonary embolus occluding the orifices of the pulmonary arteries: pulmonary emboli do not
develop this quickly, since the venous clot in the legs must develop first. Large thromboemboli that block
the orifices of the major pulmonary arteries are called saddle emboli and produce sudden death without
evidence of infarction (death occurs too quickly).
B. multiple pulmonary infarctions at the periphery of the lungs: see above discussion. Infarctions of the
lung arise when small thromboemboli occlude distal pulmonary vessels.
E. fat microglobules in the small capillaries throughout the body: this is not the proper clinical setting for
fat embolization.
86.

A 28-year-old scuba diver develops a sudden onset of severe pleuritic chest pain and dyspnea while
he exploring a coral reef in 70 feet of water. With the help of another diver, the patient is able to
safely swim to the surface. What is the most likely diagnosis in this patient?
A.
Pulmonary embolus
B.
Spontaneous pneumothorax
C.
Fat embolism
D.
Decompression sickness
Answer: A. pulmonary embolus: note that the patient does not have a history of rapid ascent (rules out
decompression sickness- choice D) but developed the chest pain while in 70 feet of water. The increased
pressure imposed on the body at this depth (over 2 atmospheres) causes venous thrombi to develop in the
deep veins of the legs which can embolize and produce a pulmonary infarction. If the chest pain and
dyspnea developed while coming to the surface, the answer would have been spontaneous pneumothorax
(choice B). In this case, a preexisting subpleural or intrapleural bleb (s) is likely to rupture as the
atmospheric pressure rapidly decreases, causing the bleb to expand and rupture. The lung or part of the
lung collapses with the loss of negative atmospheric pressure in the pleural cavity.
C. fat embolism: this is not the proper clinical setting for fat embolism

33

87.

A 39-year-old homeless man is brought into an emergency room by a friend. The man is stuporous
and is unable to answer questions. Laboratory tests are ordered and return with the following
values: serum sodium 137 mEq/L (135147), serum potassium 5.8 mEq/L (3.55.0), serum
chloride 97 mEq/L (95105), serum bicarbonate 12 mEq/L (2228), serum blood urea nitrogen 40
mg/dL (718), serum creatinine 4 mg/dL (0.61.2), and the urinalysis contains numerous crystals
that look like the back of an envelope. Which of the following statements apply to this patient?
A.
Normal anion gap metabolic acidosis
B.
Pre-renal azotemia
C.
Treatment with intravenous ethanol
D.
Patient drank methyl alcohol
E.
Hyperkalemia is most likely iatrogenic
Answer: the patient has ingested ethylene glycol (antifreeze) and has developed acute renal failure
(choice B-pre-renal azotemia is incorrect) due to obstruction of the renal tubules by calcium oxalate
crystals leading to an increased anion gap metabolic acidosis (choice A- normal anion gap metabolic
acidosis is incorrect) C. Treatment with intravenous ethanol: both ethylene glycol and ethanol are
metabolized by alcohol dehydrogenase and compete with each other for substrate binding to the enzyme
(example of a competitive inhibitor). By increasing ethanol (substrate), more ethanol is bound to the
active enzyme sites than ethylene glycol, leaving it unmetabolized (normally converted into oxalic and
glycolic acid). The unmetabolized ethylene glycol can then be removed by dialysis. The osmolal gap
would be > 10 mOsm (measured POsm - calculated POsm).
A. normal anion gap metabolic acidosis: no, the AG is 137 - (97 + 12) = 28 mEq/L ( 12 +/- 4). The
oxalate anions are replacing the buffered bicarbonate anions, hence electroneutrality is maintained.
B. pre-renal azotemia: no, the ratio of BUN to creatinine is 40 / 4 = 10 / 1, which is less than 15 /1 and
consistent with renal failure (see LM 18-19).
D. patient drank methyl alcohol: no, methyl alcohol is in window shield wiper fluid and is converted into
formic acid, which damages the optic nerve leading to blindness. Like ethylene glycol, however, it
produces and increased AG metabolic acidosis and is metabolized by alcohol dehydrogenase, hence the
treatment with IV infusion of ethanol is the same as well.
E. hyperkalemia is most likely iatrogenic: no, there are two reasons for the hypernatremia. One is renal
failure leading to dysfunction of the Na/K ATPase pump and retention of potassium and the other
transcellular shift of K into the blood as H ions enter cells for buffering.
88.

You would expect a patient with lead poisoning to have which of the following sets of electrolytes?
Serum Na+
Serum K+
Serum Cl- Serum HCO3(135147)
(3.55.0)
(95105)
(2228)

A.
118
3.0
88
21
B.
130
2.9
80
36
C.
130
3.0
108
10
D.
130
5.5
88
10
E.
140
4.0
100
24
F.
140
2.2
114
14
G.
152
2.8
110
33
Answer: C. lead poisoning produces proximal renal tubule damage often resulting in a proximal renal
tubular acidosis (normal AG metabolic acidosis) associated with Fanconi syndrome (loss of all the solutes
in the urine that are normally reabsorbed in the proximal tubules). A distal RTA could also have the same
set of electrolytes (e.g., due to amphotericin B or Bence Jones protein in multiple myeloma). See previous
electrolyte matching question.

34

C.

Serum Na+
(135147)
130

Serum K+
(3.55.0)
3.0

Serum Cl(95105)
108

Serum HCO3(2228)
10

Anion gap
12

89.

A 70-year-old man with urinary retention caused by prostate hyperplasia develops fever and warm
skin. A blood culture is positive for Escherichia coli. Which of the following chemical mediators is
most likely responsible for the warm skin in this patient?
A.
Complement C3b
B.
Leukotriene B4
C.
Leukotrienes C4, D4, and E4
D.
Nitric oxide
E.
Thromboxane A2
Answer: D (nitric oxide) is correct. The patient has septic shock due to E. coli as a complication of
urinary retention due to prostate hyperplasia. Endotoxins released from the cell wall of E. coli directly
damage endothelial cells, causing the release of nitric oxide (NO) and prostaglandin I2 (prostacyclin),
both of which vasodilate peripheral arterioles. Widespread arteriolar vasodilation causes warm skin.
Option A (complement C3b) is incorrect. Complement C3b is an opsonizing agent that facilitates
phagocytosis by leukocytes. It does not produce vasodilation of arterioles.
Option B (leukotriene B4) is incorrect. Leukotriene B4 activates neutrophil adhesion molecules and is a
chemotactic agent for leukocytes. It does not produce vasodilation of arterioles.
Option C (leukotrienes C4, D4, and E4) is incorrect. Leukotrienes C4, D4, and E4 cause vasoconstriction
of arterioles and bronchoconstriction.
Option E (thromboxane A2) is incorrect. Thromboxane A2 causes vasoconstriction of arterioles and
enhances platelet aggregation.
90.

A 50-year-old man with alcoholic cirrhosis has ascites and dependent pitting edema in the lower
legs. Fluid accumulation in the peritoneal cavity and legs occurs by which of the following
mechanisms?
A.
Decreased plasma oncotic pressure
B.
Increased plasma hydrostatic pressure
C.
Increased vessel permeability due to histamine
D.
Lymphatic obstruction with lymphedema
E.
Movement of water into the intracellular compartment
Answer: A (decreased plasma oncotic pressure) is correct. Edema is the accumulation of fluid in body
cavities (e.g., ascites) and in the interstitial space (e.g., peripheral edema). Edema caused by cirrhosis of
the liver involves alterations in vascular hydrostatic pressure and oncotic pressure. An increase in
hydrostatic pressure and/or a decrease in plasma oncotic pressure (hypoalbuminemia) causes outflow of a
protein-poor fluid (transudate) into body cavities and the interstitial spaces. In cirrhosis, the portal vein
encounters increased resistance to emptying blood into the liver sinusoids due to compression of the
sinusoids by regenerative nodules and fibrosis. This causes increased hydrostatic pressure (portal
hypertension) that contributes to ascites formation. The synthetic function of the liver is compromised in
cirrhosis, the synthesis of albumin is decreased. This decreases the plasma oncotic pressure, further
contributing to ascites. It is the primary mechanism for peripheral edema (dependent pitting edema) in
cirrhosis.
Option B (increased plasma hydrostatic pressure) is incorrect. In cirrhosis, increased hydrostatic pressure
only contributes to ascites formation and has no role in the development of peripheral edema.
Option C (increased vessel permeability due to histamine) is incorrect. Increased vessel permeability due
to histamine, causes a nonpitting type of peripheral edema. The edema fluid is a protein-rich exudate (> 3
g/dL) that contains polymorphonuclear leukocytes. The edema of a transudate is pitting and the protein
content is < 3 g/dL.

35

Option D (lymphatic obstruction with lymphedema) is incorrect. Obstruction of lymphatic channels


causes leakage of lymphatic fluid into the interstitial space (e.g., filariasis), producing lymphedema
(hyaluronic acid). Lymphedema is non-pitting in contrast to a transudate, which produces a pitting edema.
Option E (movement of water into the intracellular compartment) is incorrect. Movement of water
between the extracellular fluid compartment (ECF) and the intracellular fluid compartment (ICF) is called
osmosis. An alteration in the serum sodium concentration in the ECF compartment is the primary
mediator of water movements between the compartments. For example, in hyponatremia, water moves
from the ECF into the ICF compartment, while in hypernatremia, water moves from the ICF into the ECF
compartment. Although hyponatremia is commonly present in cirrhosis, water movement into the ICF
compartment does not produce pitting edema or contribute to ascites.
91.

A 70-year-old woman with severe osteoarthritis involving both femoral heads elects to have a total
hip replacement. Five days after surgery, she develops a sudden onset of chest pain and dyspnea.
The physician suspects that the patient has a pulmonary embolus with infarction. Which of the
following is the chief risk factor for pulmonary thromboembolic disease?
A.
Advanced age
B.
Decreased cardiac output
C.
Decreased hemoglobin concentration
D.
Immobilization
E.
Turbulent blood flow
Answer: D. (immobilization) is correct. The three main causes of intravascular thrombus formation are
endothelial cell injury (e.g., cigarette smoking), stasis of blood flow (e.g., post-surgery), and
hypercoagulability (e.g., use of oral contraceptives, hereditary factor deficiencies). Stasis of blood flow is
the most common cause of venous thrombus formation, which most often occurs in the deep veins below
the knee. Stasis of blood causes endothelial cell injury, which activates the coagulation system causing the
formation of an adherent, occlusive, dark red fibrin clot that entraps red blood cells, white blood cells, and
platelets. The clot propagates toward the heart and may break off once it reaches the femoral vein, which
is the most common site of pulmonary thromboembolic disease.
Option A (advanced age) is incorrect. The incidence of venous clots in the deep veins of the leg does not
increase with age.
Option B (decreased cardiac output) is incorrect. The cardiac output is normal in elderly patients,
therefore, there is no reason to suspect a decrease in cardiac output as a cause of the patient's
thromboembolic disease.
Option C (decreased hemoglobin concentration) is incorrect. Decreased hemoglobin concentration
decreases the viscosity of blood and reduces the risk of venous thrombosis.
Option E (turbulent blood flow) is incorrect. Turbulent blood flow contributes to endothelial damage
causing arterial thrombosis. Arterial thrombi usually overlie an atherosclerotic plaque in a muscular or
elastic artery. Arterial thrombi are composed of platelets held together by fibrin. Systemic
thromboembolism (emboli traveling within the arterial circulation), does not produce a pulmonary
infarction.
92.

Which of the following differentiates Bartter's syndrome from primary aldosteronism? SELECT 2
A.
Serum sodium
B.
Serum potassium
C.
Serum bicarbonate
D.
Plasma renin activity
E.
Serum aldosterone

Answers A, D: A. serum sodium, D. plasma renin activity.


Bartter's syndrome is due to a renal defect in Cl- reabsorption in the Na+-K+-2Cl- symporter in the thick
ascending limb (similar to a loop diuretic). There is a loss of Na+ (hyponatremia; hypernatremia in
primary aldosteronism), K+, and Cl- ions in the urine. Increased reabsorption of Na+ and secretion of K+
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in the late distal tubule and collecting tubule causes hypokalemia (also present in primary aldosteronism)
and increased secretion of H+ causes increased synthesis and reabsorption of HCO3- causing metabolic
alkalosis (both have an increase in bicarbonate). Hypokalemia stimulates increased prostaglandin
synthesis in the kidneys, which in turn stimulates hyperplasia of the juxtaglomerular apparatus with
increased renin leading to hyperaldosteronism (both have an increase in aldosterone). Unlike primary
aldosteronism, patient's are normotensive due to vasodilation of peripheral resistance arterioles by
prostaglandin. Increased PRA (decreased in primary aldosteronism).

Items 93-98

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93. Patient in hypovolemic shock.


Answer: D. metabolic acidosis: related to lactic acidosis from shock
94. Medical student who is anxious that develops tetany.
Answer: E. acute respiratory alkalosis: related to hyperventilation
95. Patient who is unconscious after overdosing on barbiturates
Answer: A. acute respiratory acidosis: due to hypoventilation
96. Patient living at high altitude for 10 years.
Answer: F. chronic respiratory alkalosis: time to compensate
97. Patient with chronic bronchitis and cyanosis
Answer: B. chronic respiratory acidosis: time for compensation
98. Patient who is on a loop diuretic and is not taking potassium supplements
Answer: C. metabolic alkalosis: related to increase sodium exchange for protons with an increase in
bicarbonate.

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