Clinical Skills/Critical care

Question 1

Increases cerebral blood ow (CBF) and cerebral metabolic rate of oxygen consumption (CRMO2)
A. Enfurane
B. Etomidate
C. Halothane
D. Isofurane
E. Ketamine
F. Thiopental

Answer 1

A. Enfurane
B. Etomidate
C. Halothane
D. Isofurane
E. Ketamine
F. Thiopental

Isoflurane, enflurane, and halothane are all inhalational (volatile) anesthetics. All inhalational anesthetics reduce the m etabolic rate of the brain, but also increase cerebral blood ow (CBF), which may lead to increases in intracranial pressure (ICP). At low doses all halogenated anesthetics have a similar efect on cerebral blood flow, but at higher doses enflurane and isoflurane increase CBF less than halothane. A combination of nitrous oxide and
halothane increases CBF more than halothane alone. Of the volatile anesthetics listed, isoflurane increases cerebral blood flow the least. Enflurane, at high doses, has cerebral irritant efects that can lead to spike-and-wave electroencephalogram (EEG) patterns. Etomidate is a carboxylated imidazole that is sometimes used for induction of anesthesia—its use is associated
with adrenal suppression, even after a single dose. Ketamine is a dissociative anesthetic that increases cerebral blood ow, cerebral oxygen consumption, and ICP. Thiopental is a short-acting barbiturate that is used for induction of general anesthesia—it rapidly crosses the blood–brain barrier and
causes reductions in both CMRO2 and CBF; the reduction in CMRO2 is greater
than the reduction in CBF, however. Thiopental is associated w ith a myocardial depressant e ect and increased venous pooling, which may lead to
decreased blood pressure, stroke volum e, and cardiac output

Question 2

Of the volatile anesthetics, it increases CBF the least.
A. Enfurane
B. Etomidate
C. Halothane
D. Isofurane
E. Ketamine
F. Thiopental

Answer 2

A. Enfurane
B. Etomidate
C. Halothane
D. Isofurane
E. Ketamine
F. Thiopental

Isoflurane, enflurane, and halothane are all inhalational (volatile) anesthetics. All inhalational anesthetics reduce the m etabolic rate of the brain, but also increase cerebral blood ow (CBF), which may lead to increases in intracranial pressure (ICP). At low doses all halogenated anesthetics have a similar efect on cerebral blood flow, but at higher doses enflurane and isoflurane increase CBF less than halothane. A combination of nitrous oxide and
halothane increases CBF more than halothane alone. Of the volatile anesthetics listed, isoflurane increases cerebral blood flow the least. Enflurane, at high doses, has cerebral irritant efects that can lead to spike-and-wave electroencephalogram (EEG) patterns. Etomidate is a carboxylated imidazole that is sometimes used for induction of anesthesia—its use is associated
with adrenal suppression, even after a single dose. Ketamine is a dissociative anesthetic that increases cerebral blood ow, cerebral oxygen consumption, and ICP. Thiopental is a short-acting barbiturate that is used for induction of general anesthesia—it rapidly crosses the blood–brain barrier and
causes reductions in both CMRO2 and CBF; the reduction in CMRO2 is greater
than the reduction in CBF, however. Thiopental is associated w ith a myocardial depressant e ect and increased venous pooling, which may lead to
decreased blood pressure, stroke volum e, and cardiac output

Question 3

Induces seizure discharges
A. Enfurane
B. Etomidate
C. Halothane
D. Isofurane
E. Ketamine
F. Thiopental

Answer 3

A. Enfurane
B. Etomidate
C. Halothane
D. Isofurane
E. Ketamine
F. Thiopental

Isoflurane, enflurane, and halothane are all inhalational (volatile) anesthetics. All inhalational anesthetics reduce the m etabolic rate of the brain, but also increase cerebral blood ow (CBF), which may lead to increases in intracranial pressure (ICP). At low doses all halogenated anesthetics have a similar efect on cerebral blood flow, but at higher doses enflurane and isoflurane increase CBF less than halothane. A combination of nitrous oxide and
halothane increases CBF more than halothane alone. Of the volatile anesthetics listed, isoflurane increases cerebral blood flow the least. Enflurane, at high doses, has cerebral irritant efects that can lead to spike-and-wave electroencephalogram (EEG) patterns. Etomidate is a carboxylated imidazole that is sometimes used for induction of anesthesia—its use is associated
with adrenal suppression, even after a single dose. Ketamine is a dissociative anesthetic that increases cerebral blood ow, cerebral oxygen consumption, and ICP. Thiopental is a short-acting barbiturate that is used for induction of general anesthesia—it rapidly crosses the blood–brain barrier and
causes reductions in both CMRO2 and CBF; the reduction in CMRO2 is greater
than the reduction in CBF, however. Thiopental is associated w ith a myocardial depressant e ect and increased venous pooling, which may lead to
decreased blood pressure, stroke volum e, and cardiac output

Question 4

Dissociative anesthetic
A. Enfurane
B. Etomidate
C. Halothane
D. Isofurane
E. Ketamine
F. Thiopental

Answer 4

A. Enfurane
B. Etomidate
C. Halothane
D. Isofurane
E. Ketamine
F. Thiopental

Isoflurane, enflurane, and halothane are all inhalational (volatile) anesthetics. All inhalational anesthetics reduce the m etabolic rate of the brain, but also increase cerebral blood ow (CBF), which may lead to increases in intracranial pressure (ICP). At low doses all halogenated anesthetics have a similar efect on cerebral blood flow, but at higher doses enflurane and isoflurane increase CBF less than halothane. A combination of nitrous oxide and
halothane increases CBF more than halothane alone. Of the volatile anesthetics listed, isoflurane increases cerebral blood flow the least. Enflurane, at high doses, has cerebral irritant efects that can lead to spike-and-wave electroencephalogram (EEG) patterns. Etomidate is a carboxylated imidazole that is sometimes used for induction of anesthesia—its use is associated
with adrenal suppression, even after a single dose. Ketamine is a dissociative anesthetic that increases cerebral blood ow, cerebral oxygen consumption, and ICP. Thiopental is a short-acting barbiturate that is used for induction of general anesthesia—it rapidly crosses the blood–brain barrier and
causes reductions in both CMRO2 and CBF; the reduction in CMRO2 is greater
than the reduction in CBF, however. Thiopental is associated w ith a myocardial depressant e ect and increased venous pooling, which may lead to
decreased blood pressure, stroke volum e, and cardiac output

Question 5

Decreases CBF and CRMO2 and produces cardiovascular depression
A. Enfurane
B. Etomidate
C. Halothane
D. Isofurane
E. Ketamine
F. Thiopental

Answer 5

A. Enfurane
B. Etomidate
C. Halothane
D. Isofurane
E. Ketamine
F. Thiopental

Isoflurane, enflurane, and halothane are all inhalational (volatile) anesthetics. All inhalational anesthetics reduce the m etabolic rate of the brain, but also increase cerebral blood ow (CBF), which may lead to increases in intracranial pressure (ICP). At low doses all halogenated anesthetics have a similar efect on cerebral blood flow, but at higher doses enflurane and isoflurane increase CBF less than halothane. A combination of nitrous oxide and
halothane increases CBF more than halothane alone. Of the volatile anesthetics listed, isoflurane increases cerebral blood flow the least. Enflurane, at high doses, has cerebral irritant efects that can lead to spike-and-wave electroencephalogram (EEG) patterns. Etomidate is a carboxylated imidazole that is sometimes used for induction of anesthesia—its use is associated
with adrenal suppression, even after a single dose. Ketamine is a dissociative anesthetic that increases cerebral blood ow, cerebral oxygen consumption, and ICP. Thiopental is a short-acting barbiturate that is used for induction of general anesthesia—it rapidly crosses the blood–brain barrier and
causes reductions in both CMRO2 and CBF; the reduction in CMRO2 is greater
than the reduction in CBF, however. Thiopental is associated w ith a myocardial depressant e ect and increased venous pooling, which may lead to
decreased blood pressure, stroke volum e, and cardiac output

Question 6

Decreases CBF and CRMO2 and suppresses adrenocortical response to stress
A. Enfurane
B. Etomidate
C. Halothane
D. Isofurane
E. Ketamine
F. Thiopental

Answer 6

A. Enfurane
B. Etomidate
C. Halothane
D. Isofurane
E. Ketamine
F. Thiopental

Isoflurane, enflurane, and halothane are all inhalational (volatile) anesthetics. All inhalational anesthetics reduce the m etabolic rate of the brain, but also increase cerebral blood ow (CBF), which may lead to increases in intracranial pressure (ICP). At low doses all halogenated anesthetics have a similar efect on cerebral blood flow, but at higher doses enflurane and isoflurane increase CBF less than halothane. A combination of nitrous oxide and
halothane increases CBF more than halothane alone. Of the volatile anesthetics listed, isoflurane increases cerebral blood flow the least. Enflurane, at high doses, has cerebral irritant efects that can lead to spike-and-wave electroencephalogram (EEG) patterns. Etomidate is a carboxylated imidazole that is sometimes used for induction of anesthesia—its use is associated
with adrenal suppression, even after a single dose. Ketamine is a dissociative anesthetic that increases cerebral blood ow, cerebral oxygen consumption, and ICP. Thiopental is a short-acting barbiturate that is used for induction of general anesthesia—it rapidly crosses the blood–brain barrier and
causes reductions in both CMRO2 and CBF; the reduction in CMRO2 is greater
than the reduction in CBF, however. Thiopental is associated w ith a myocardial depressant e ect and increased venous pooling, which may lead to
decreased blood pressure, stroke volum e, and cardiac output

Question 7

Which antiemetic medication lowers seizure threshold?
A. Phenergan
B. Droperidol
C. Tigan
D. Zofran
E. Reglan

Answer 7

A. Phenergan
B. Droperidol
C. Tigan
D. Zofran
E. Reglan

Phenergan (A), a phenothiazine antiem etic, has been show n to lower the seizure threshold

Question 8

The most appropriate drug to administer to a stable patient with a narrow complex supraventricular tachycardia (no serious signs or sym ptoms) after vagal
stimulation is
A. Adenosine
B. Digoxin
C. Procainamide
D. Quinidine
E. Verapamil

Answer 8

A. Adenosine
B. Digoxin
C. Procainamide
D. Quinidine
E. Verapamil

Adenosine (A) at an initial dose of 6 mg over 1 to 3 seconds, followed by a
repeat of 12 mg in 1 to 2 minutes as needed, is the initial drug of choice. If
lidocaine is ineffective, procainamide at a dose of 20 to 30 mg/m in for a maxim ]um of 17 mg/kg is given.

Question 9

Each is true of fat embolism except
A. Cerebral manifestations frequently occur in the absence of pulmonary manifestations.
B. Increased serum lipase occurs in up to half of all patients.
C. Petechia over the shoulders and chest is a classic nding.
D. Symptoms typically occur 12 to 48 hours after trauma.
E. Tachycardia and tachypnea are characteristic.

Answer 9

A. Cerebral manifestations frequently occur in the absence of pulmonary manifestations.
B. Increased serum lipase occurs in up to half of all patients.
C. Petechia over the shoulders and chest is a classic nding.
D. Symptoms typically occur 12 to 48 hours after trauma.
E. Tachycardia and tachypnea are characteristic.

Fat embolism syndrome may occur after long bone fractures or soft tissue
injury and burns. The syndrome is characterized by pulmonary insuffciency (E), neurologic symptoms, anemia, and thrombocytopenia. Onset of
symptoms typically occurs within the first 1–2 days following trauma (D).
A petechial rash (C) in nondependent areas is present in up to 50% of cases.
Neurologic involvement does not develop in the absence of pulmonary abnormalities unless there is the rare event of a paradoxical embolus through a
patent foramen ovale (A is false)

Question 10

Gamma irradiation of blood helps prevent
A. Graft-versus-host disease
B. Hemolytic transfusion reactions
C. Hepatitis B transmission
D. Nonhemolytic transfusion reactions
E. Transfusion siderosis

Answer 10

A. Graft-versus-host disease
B. Hemolytic transfusion reactions
C. Hepatitis B transmission
D. Nonhemolytic transfusion reactions
E. Transfusion siderosis

Graft-versus-host disease may occur when blood donor lymphocytes attack
the normal tissues of the transfusion recipient (particularly in immunocom -
promised patients). Transfusion-associated graft-versus-host disease m ay result if viable lymphocytes in blood are not irradiated

Question 11

Citrate toxicity from massive transfusions results from the
A. Binding of free ionized Ca21
B. Decrease of 2,3diphosphoglyceric acid (DPG) levels
C. Inactivation of factors 5 and 8
D. Interaction w ith platelets, rendering them dysfunctional
E. Precipitation of autoimm ]une hemolytic anemia

Answer 11

A. Binding of free ionized Ca21
B. Decrease of 2,3diphosphoglyceric acid (DPG) levels
C. Inactivation of factors 5 and 8
D. Interaction w ith platelets, rendering them dysfunctional
E. Precipitation of autoimm ]une hemolytic anemia

Anticoagulants such as heparin, citrate, and EDTA bind calcium (A). Banked
blood contains the anticoagulant citrate. Massive transfusions can lead to
acute hypocalcem ia in the critically ill patient

Question 12

Cortisol is suppressed with low-dose dexamethasone.
A. Cushing’s disease
B. Ectopic adrenocorticotropic hormone (ACTH) production
C. Both
D. Neither

Answer 12

A. Cushing’s disease
B. Ectopic adrenocorticotropic hormone (ACTH) production
C. Both
D. Neither

Cushing’s syndrome is the condition of overt glucocorticoid exposure regardless of the etiology. Cushing’s disease (A) is Cushing’s syndrome caused by an ACTH-producing pituitary adenoma. The dexamethasone suppression test is used to differentiate Cushing’s syndrom e of various etiologies. Generally, ACTH production and cortisol secretion are not suppressed by low - or highdose dexamethasone if the source of ACTH is an ectopic ACTH-producing
tum or (B). In Cushing’s disease (A), however (ACTH-producing pituitary
adenoma), the high-dose dexam ethasone suppression test is expected to
suppress ACTH and cortisol secretion. The metyrapone test is a test of ACTH
reserve and simulates 11-hydroxylase de ciency. Adm inistration of metyrapone inhibits cortisol synthesis, increasing ACTH secretion and increasing adrenal production, and thus urinary excretion, of 17-hydroxycorticosteroids.
An ACTH-producing pituitary adenoma is expected to respond to the metyrapone test, w hile an ectopic ACTH-producing tum or (B) is not

Question 13

Cortisol is suppressed with high-dose dexamethasone
A. Cushing’s disease
B. Ectopic adrenocorticotropic hormone (ACTH) production
C. Both
D. Neither

Answer 13

A. Cushing’s disease
B. Ectopic adrenocorticotropic hormone (ACTH) production
C. Both
D. Neither

Cushing’s syndrome is the condition of overt glucocorticoid exposure regardless of the etiology. Cushing’s disease (A) is Cushing’s syndrome caused by an ACTH-producing pituitary adenoma. The dexamethasone suppression test is used to differentiate Cushing’s syndrom e of various etiologies. Generally, ACTH production and cortisol secretion are not suppressed by low - or highdose dexamethasone if the source of ACTH is an ectopic ACTH-producing
tum or (B). In Cushing’s disease (A), however (ACTH-producing pituitary
adenoma), the high-dose dexam ethasone suppression test is expected to
suppress ACTH and cortisol secretion. The metyrapone test is a test of ACTH
reserve and simulates 11-hydroxylase de ciency. Adm inistration of metyrapone inhibits cortisol synthesis, increasing ACTH secretion and increasing adrenal production, and thus urinary excretion, of 17-hydroxycorticosteroids.
An ACTH-producing pituitary adenoma is expected to respond to the metyrapone test, w hile an ectopic ACTH-producing tum or (B) is not

Question 14

Increase in urinary 17-hydroxycorticosteroids after a metyrapone test
A. Cushing’s disease
B. Ectopic adrenocorticotropic hormone (ACTH) production
C. Both
D. Neither

Answer 14

A. Cushing’s disease
B. Ectopic adrenocorticotropic hormone (ACTH) production
C. Both
D. Neither

Cushing’s syndrome is the condition of overt glucocorticoid exposure regardless of the etiology. Cushing’s disease (A) is Cushing’s syndrome caused by an ACTH-producing pituitary adenoma. The dexamethasone suppression test is used to differentiate Cushing’s syndrom e of various etiologies. Generally, ACTH production and cortisol secretion are not suppressed by low - or highdose dexamethasone if the source of ACTH is an ectopic ACTH-producing
tum or (B). In Cushing’s disease (A), however (ACTH-producing pituitary
adenoma), the high-dose dexam ethasone suppression test is expected to
suppress ACTH and cortisol secretion. The metyrapone test is a test of ACTH
reserve and simulates 11-hydroxylase de ciency. Adm inistration of metyrapone inhibits cortisol synthesis, increasing ACTH secretion and increasing adrenal production, and thus urinary excretion, of 17-hydroxycorticosteroids.
An ACTH-producing pituitary adenoma is expected to respond to the metyrapone test, w hile an ectopic ACTH-producing tum or (B) is not

Question 15

Which of the following scenarios reflects an iron deffciency anemia?
A. Decreased mean corpuscular volume (MCV) and decreased total iron binding capacity (TIBC)
B. Decreased MCV and increased TIBC
C. Decreased MCV and normal TIBC
D. Increased MCV and decreased TIBC
E. Increased MCV and increased TIBC

Answer 15

A. Decreased mean corpuscular volume (MCV) and decreased total iron binding capacity (TIBC)
B. Decreased MCV and increased TIBC
C. Decreased MCV and normal TIBC
D. Increased MCV and decreased TIBC
E. Increased MCV and increased TIBC

Chronic iron deffciency results in a microcytic hypochromic anemia characterized by low mean corpuscular volume (MCV) values and decreased serum hemoglobin. The most common cause of a hypochromic, microcytic anemia is iron deffciency anemia, in which the serum iron concentration is decreased
and total iron binding capacity (TIBC) is increased. A normal or decreased
TIBC is not consistent w ith iron deffciency anemia (A, C). An increased MCV is
consistent w ith a macrocytic anemia as may be seen in B12 or folate deffciency
(D, E), but not iron deffciency anemia

Question 16

Prolongation of bleeding time usually occurs in
I. von Willebrand’s disease
II. Use of nonsteroidal anti-inflammatory agents
III. Uremia
IV Factor VII deficiency

Answer 16

A. I, II, III
B. I, III
C. II, IV
D. IV
E. All of the above

An abnormal bleeding time in a patient with a normal platelet count suggests
qualitative platelet dysfunction or abnormal platelet-vessel wall interactions.
Possible causes for an increased bleeding time include the use of aspirin or
NSAIDs (II), uremic platelet dysfunction (III), and von Willebrand’s disease (I). Although patients with von Willebrand’s disease usually have an abnormal bleeding time, the bleeding time may occasionally be normal due to cyclical variations in the von Willebrand factor. Factor VII deficiency (IV)
causes prolongation of the prothrombin time (PT), but elevations of the partial thromboplastin time (PTT) and bleeding tim e are not characteristic.

Question 17

Drugs that antagonize the anticoagulant effect of warfarin (Coumadin) include
I. Cholestyramine
II. Phenobarbital
III. Rifampin
IV Cimetidine

Answer 17

A. I, II, III
B. I, III
C. II, IV
D. IV
E. All of the above

Several drugs can antagonize the effects of warfarin through a variety of
mechanism s such as reduced absorption of warfarin in the GI tract caused by
cholestyramine (I); increased clearance of warfarin via induction of hepatic
enzymes (CYP2C9) by barbiturates (phenobarbital [II]), carbamazepine, or
rifampin (III); and by ingestion of large amounts of vitam in K. Cimetidine
(IV) promotes the effects of warfarin via inhibition of CYP2C9, decreasing the
m etabolism of warfarin. Other drugs that inhibit CYP2C9 are amiodarone,
azole antifungals, clopidogrel, cotrimoxazole, disulfiram , fluoxetine, isoniazid, metronidazole, sulfinpyrazone, tolcapone, and zafirlukast

Question 18

Side effects of thiazide diuretics include
I. Insulin resistance
II. Hyponatremia
III. Hypokalemia
IV. Flushing

Answer 18

A. I, II, III
B. I, III
C. II, IV
D. IV
E. All of the above

Metabolic side effects of thiazide diuretics include hyponatremia (I) and
hypokalemia (III) from renal loss, hyperuricemia from uric acid retention,
carbohydrate intolerance (I), and hyperlipidemia. Niacin is associated with
flushing (IV).

Question 19

Plasm a levels of phenytoin (Dilantin) are increased by all of the following except
A. Carbamazepine
B. Cimetidine
C. Coumadin
D. Isoniazid
E. Sulfonamides

Answer 19

A. Carbamazepine
B. Cimetidine
C. Coumadin
D. Isoniazid
E. Sulfonamides

Any drug metabolized by CYP2C9 or CYP2C10 can increase the plasma concentration of phenytoin by decreasing its metabolism . These drugs include,
but are not limited to, cimetidine (B), warfarin (C), isoniazid (D), and sulfonamides (E). Carbam azepine (Tegretol [A]) decreases plasma levels of phenytoin (Dilantin) by enhancing its metabolism . Conversely, phenytoin reduces serum levels of carbamazepine.

Question 21

The most common electrocardiogram (EKG) finding(s) in patients with pulmonary emboli is
A. A peaked T wave
B. An S1-Q3-T3 pattern
C. Rightward shift of the QRS axis
D. Sinus tachycardia (ST) and T wave changes
E. Bradycardia

Answer 21

A. A peaked T wave
B. An S1-Q3-T3 pattern
C. Rightward shift of the QRS axis
D. Sinus tachycardia (ST) and T wave changes
E. Bradycardia

Nonspecifc sinus tachycardia (ST) and T wave changes (D) occur in 66% of
patients. Only one-third of patients with massive emboli have the S1-Q3-T3
pattern (B) of acute cor pulmonale, right bundle branch block, and right axis
deviation (C). The utility of EKG in suspected pulmonary embolism (PE) is in establishing or excluding other diagnoses such as acute myocardial infarction.

Question 21

Which of the following disorders leads to hypernatremia?
A. Addison’s disease
B. Hyperaldosteronism
C. Hypothyroidism
D. Renal failure
E. Syndrome of inappropriate antidiuretic hormone (SIADH)

Answer 21

A. Addison’s disease
B. Hyperaldosteronism
C. Hypothyroidism
D. Renal failure
E. Syndrome of inappropriate antidiuretic hormone (SIADH)

Aldosterone (B) stimulates sodium reabsorption in the renal collecting duct,
leading to increased serum sodium concentration. SIADH (E) leads to hyponatremia because of inappropriate retention of free water despite low serum osm olality. Addison’s disease (A) and hypothyroidism (C) are associated with
SIADH. A severely compromised glomerular ltration rate, as in renal failure
(D), increases the fractional reabsorption of water in the renal proximal tubule, predisposing these patients to hyponatrem ia

Question 22

The most common acid–base disturbance in mild to moderately injured patients without severe renal, circulatory, or pulmonary decompensation is
A. Respiratory acidosis and metabolic alkalosis
B. Respiratory alkalosis and metabolic acidosis
C. Respiratory or metabolic acidosis
D. Respiratory or metabolic alkalosis

Answer 22

A. Respiratory acidosis and metabolic alkalosis
B. Respiratory alkalosis and metabolic acidosis
C. Respiratory or metabolic acidosis
D. Respiratory or metabolic alkalosis

Respiratory and metabolic alkalosis are the most common acid–base disturbances in mild to moderately injured patients without severe renal, circulatory, or pulmonary decompensation

Question 23

The reabsorption of Na 1 ions in the thin ascending Henle’s loop
A. Is by active transport
B. Is by a Na1 –K1 exchange pump
C. Passively follows the active transport of Cl 2 ions
D. Passively follows the active transport of water molecules

Answer 23

A. Is by active transport
B. Is by a Na1 –K1 exchange pump
C. Passively follows the active transport of Cl 2 ions
D. Passively follows the active transport of water molecules

Sodium transport by both the thin ascending and thin descending loop of Henle is almost entirely passive and follow s Cl2 ions (C). Sodium ions are actively transported in the early and distal convoluted tubule and in the thick ascending limb

Question 24

Of the two prodrugs that block the Gi-coupled platelet adenosine diphosphate (ADP) receptor, it has a slightly more favorable toxicity profile.
A. Abciximab (ReoPro)
B. Aspirin
C. Clopidogrel (Plavix)
D. Eptifilbatide (Integrilin)
E. Ticlopidine (Ticlid)

Answer 24

A. Abciximab (ReoPro)
B. Aspirin
C. Clopidogrel (Plavix)
D. Eptifilbatide (Integrilin)
E. Ticlopidine (Ticlid)

Aspirin (B) inactivates cyclooxygenase, the enzyme that produces the precursor of thromboxane A2. Ticlopidine (E) and clopidogrel (C) are thienopyridines that inhibit P2Y12, a G-protein-coupled receptor for adenosine diphosphate (ADP) on the platelet. They are both prodrugs requiring conversion to the active metabolite. Thrombocytopenia and leukopenia occur less commonly with clopidogrel than with ticlopidine. Abciximab (ReoPro [A]) and
eptifilbatide (Integrilin [D]) are the inhibitors of glycoprotein IIb/IIIa receptor, but the former is the Fab fragment of a humanized monoclonal antibody against the receptor, and the latter is a cyclic peptide inhibitor of the arginineglycine-aspartate (RGD) binding site on the receptor.

Question 25

Is the Fab fragment of a monoclonal antibody directed against the IIb/IIIa receptor
A. Abciximab (ReoPro)
B. Aspirin
C. Clopidogrel (Plavix)
D. Eptifilbatide (Integrilin)
E. Ticlopidine (Ticlid)

Answer 25

A. Abciximab (ReoPro)
B. Aspirin
C. Clopidogrel (Plavix)
D. Eptifilbatide (Integrilin)
E. Ticlopidine (Ticlid)

Aspirin (B) inactivates cyclooxygenase, the enzyme that produces the precursor of thromboxane A2. Ticlopidine (E) and clopidogrel (C) are thienopyridines that inhibit P2Y12, a G-protein-coupled receptor for adenosine diphosphate (ADP) on the platelet. They are both prodrugs requiring conversion to the active metabolite. Thrombocytopenia and leukopenia occur less commonly with clopidogrel than with ticlopidine. Abciximab (ReoPro [A]) and
eptifilbatide (Integrilin [D]) are the inhibitors of glycoprotein IIb/IIIa receptor, but the former is the Fab fragment of a humanized monoclonal antibody against the receptor, and the latter is a cyclic peptide inhibitor of the arginineglycine-aspartate (RGD) binding site on the receptor.

Question 26

Is a cyclic peptide inhibitor of the arginine-glycine-aspartate (RGD) binding site on the glycoprotein IIb/IIIa
A. Abciximab (ReoPro)
B. Aspirin
C. Clopidogrel (Plavix)
D. Eptifilbatide (Integrilin)
E. Ticlopidine (Ticlid)

Answer 26

A. Abciximab (ReoPro)
B. Aspirin
C. Clopidogrel (Plavix)
D. Eptifilbatide (Integrilin)
E. Ticlopidine (Ticlid)

Aspirin (B) inactivates cyclooxygenase, the enzyme that produces the precursor of thromboxane A2. Ticlopidine (E) and clopidogrel (C) are thienopyridines that inhibit P2Y12, a G-protein-coupled receptor for adenosine diphosphate (ADP) on the platelet. They are both prodrugs requiring conversion to the active metabolite. Thrombocytopenia and leukopenia occur less commonly with clopidogrel than with ticlopidine. Abciximab (ReoPro [A]) and
eptifilbatide (Integrilin [D]) are the inhibitors of glycoprotein IIb/IIIa receptor, but the former is the Fab fragment of a humanized monoclonal antibody against the receptor, and the latter is a cyclic peptide inhibitor of the arginineglycine-aspartate (RGD) binding site on the receptor.

Question 27

Blocks production of thromboxane A24
A. Abciximab (ReoPro)
B. Aspirin
C. Clopidogrel (Plavix)
D. Eptifilbatide (Integrilin)
E. Ticlopidine (Ticlid)

Answer 27

A. Abciximab (ReoPro)
B. Aspirin
C. Clopidogrel (Plavix)
D. Eptifilbatide (Integrilin)
E. Ticlopidine (Ticlid)

Aspirin (B) inactivates cyclooxygenase, the enzyme that produces the precursor of thromboxane A2. Ticlopidine (E) and clopidogrel (C) are thienopyridines that inhibit P2Y12, a G-protein-coupled receptor for adenosine diphosphate (ADP) on the platelet. They are both prodrugs requiring conversion to the active metabolite. Thrombocytopenia and leukopenia occur less commonly with clopidogrel than with ticlopidine. Abciximab (ReoPro [A]) and
eptifilbatide (Integrilin [D]) are the inhibitors of glycoprotein IIb/IIIa receptor, but the former is the Fab fragment of a humanized monoclonal antibody against the receptor, and the latter is a cyclic peptide inhibitor of the arginineglycine-aspartate (RGD) binding site on the receptor.

Question 28

Which laboratory finding in disseminated intravascular coagulation (DIC) correlates most closely with bleeding?
A. Decreased fibrinogen
B. Increased fibrin degradation products
C. Increased prothrombin time (PT)
D. Increased partial thromboplastin time (PTT)
E. Increased thrombin time (TT)

Answer 28

A. Decreased fibrinogen
B. Increased fibrin degradation products
C. Increased prothrombin time (PT)
D. Increased partial thromboplastin time (PTT)
E. Increased thrombin time (TT)

Disseminated intravascular coagulation (DIC) is a consumptive coagulopathy
characterized by widespread microvascular thrombosis, thrombocytopenia,
and depletion of circulating coagulation factors. Thrombocytopenia, reduced
fibrinogen levels, and prolongation of the prothrombin time (C) are the result of depletion, while the elevated D-dimer (B) is due to increased thrombolysis. While all of these abnormalities can be observed in DIC, decreased fibrinogen (A) correlates most closely with bleeding

Question 29

The definition of oxygen saturation is the
A. Amount of oxygen dissolved in plasma
B. Fractional concentration of inspired oxygen
C. Partial pressure of oxygen in the blood
D. Percentage of hemoglobin that is bound to oxygen
E. Ratio of unbound to bound hemoglobin

Answer 29

A. Amount of oxygen dissolved in plasma
B. Fractional concentration of inspired oxygen
C. Partial pressure of oxygen in the blood
D. Percentage of hemoglobin that is bound to oxygen
E. Ratio of unbound to bound hemoglobin

The oxygen saturation refers to the percentage of hemoglobin (Hb) that is bound to oxygen. In other words: Oxygen saturation 5 (Hb bound to oxygen / Total Hb).

Question 30

Metabolic responses to trauma include each of the following except
A. Hypoglycemia
B. Increased rate of lipolysis
C. Increased Na 1 reabsorption
D. Increased water reabsorption
E. Metabolic alkalosis

Answer 30

A. Hypoglycemia
B. Increased rate of lipolysis
C. Increased Na 1 reabsorption
D. Increased water reabsorption
E. Metabolic alkalosis

Hyperglycemia, not hypoglycemia (A), is one of the metabolic responses to trauma

Question 31

A normal PT, a prolonged PTT, and a bleeding disorder would result from a deficiency of factor
A. II
B. V
C. VIII
D. X
E. XII

Answer 31

A. II
B. V
C. VIII
D. X
E. XII

Deficiency of factors II (A), V (B), or X (D) causes prolonged PT and PTT. A
deficiency of factor XII (E) causes a prolonged PTT but no clinical bleeding.
Only a factor VIII deficiency (C, hemophilia A) would cause a prolonged PTT,
normal PT, and a bleeding disorder

Question 32

Shortest half-life
A. Factor II
B. Factor VII
C. Factor VIII
D. Factor IX
E. Factor X

Answer 32

A. Factor II
B. Factor VII
C. Factor VIII
D. Factor IX
E. Factor X

The prothrombin time (PT) measures the integrity of the extrinsic and common pathways (factors VII [B], X [E], V, prothrombin, and fibrinogen). The
activated partial thromboplastin time (aPTT) measures the integrity of the
intrinsic and common pathways of coagulation (factors XII, XI, IX [D], VIII [C],
X [E], and V). Hemophilia A is caused by a deficiency in factor VIII (C).
Hemophilia B (Christmas disease) is caused by a factor IX (D) deficiency. The
vitam in K–dependent factors are factors II (A), VII (B), IX (D), and X (E). A deficiency of factor II (A), V, or X (E) would result in prolongation of PT and PTT.
Factor VII (B) has the shortest half-life of the options listed

Question 33

Reflects the extrinsic pathway
A. Factor II
B. Factor VII
C. Factor VIII
D. Factor IX
E. Factor X

Answer 33

A. Factor II
B. Factor VII
C. Factor VIII
D. Factor IX
E. Factor X

The prothrombin time (PT) measures the integrity of the extrinsic and common pathways (factors VII [B], X [E], V, prothrombin, and fibrinogen). The
activated partial thromboplastin time (aPTT) measures the integrity of the
intrinsic and common pathways of coagulation (factors XII, XI, IX [D], VIII [C],
X [E], and V). Hemophilia A is caused by a deficiency in factor VIII (C).
Hemophilia B (Christmas disease) is caused by a factor IX (D) deficiency. The
vitam in K–dependent factors are factors II (A), VII (B), IX (D), and X (E). A deficiency of factor II (A), V, or X (E) would result in prolongation of PT and PTT.
Factor VII (B) has the shortest half-life of the options listed

Question 34

Deficient or abnormal in hemophilia A (classic)
A. Factor II
B. Factor VII
C. Factor VIII
D. Factor IX
E. Factor X

Answer 34

A. Factor II
B. Factor VII
C. Factor VIII
D. Factor IX
E. Factor X

The prothrombin time (PT) measures the integrity of the extrinsic and common pathways (factors VII [B], X [E], V, prothrombin, and fibrinogen). The
activated partial thromboplastin time (aPTT) measures the integrity of the
intrinsic and common pathways of coagulation (factors XII, XI, IX [D], VIII [C],
X [E], and V). Hemophilia A is caused by a deficiency in factor VIII (C).
Hemophilia B (Christmas disease) is caused by a factor IX (D) deficiency. The
vitam in K–dependent factors are factors II (A), VII (B), IX (D), and X (E). A deficiency of factor II (A), V, or X (E) would result in prolongation of PT and PTT.
Factor VII (B) has the shortest half-life of the options listed

Question 35

Deficient in hemophilia B (Christmas disease)
A. Factor II
B. Factor VII
C. Factor VIII
D. Factor IX
E. Factor X

Answer 35

A. Factor II
B. Factor VII
C. Factor VIII
D. Factor IX
E. Factor X

The prothrombin time (PT) measures the integrity of the extrinsic and common pathways (factors VII [B], X [E], V, prothrombin, and fibrinogen). The
activated partial thromboplastin time (aPTT) measures the integrity of the
intrinsic and common pathways of coagulation (factors XII, XI, IX [D], VIII [C],
X [E], and V). Hemophilia A is caused by a deficiency in factor VIII (C).
Hemophilia B (Christmas disease) is caused by a factor IX (D) deficiency. The
vitam in K–dependent factors are factors II (A), VII (B), IX (D), and X (E). A deficiency of factor II (A), V, or X (E) would result in prolongation of PT and PTT.
Factor VII (B) has the shortest half-life of the options listed

Question 36

All except this factor are vitamin K–dependent factors.
A. Factor II
B. Factor VII
C. Factor VIII
D. Factor IX
E. Factor X

Answer 36

A. Factor II
B. Factor VII
C. Factor VIII
D. Factor IX
E. Factor X

The prothrombin time (PT) measures the integrity of the extrinsic and common pathways (factors VII [B], X [E], V, prothrombin, and fibrinogen). The
activated partial thromboplastin time (aPTT) measures the integrity of the
intrinsic and common pathways of coagulation (factors XII, XI, IX [D], VIII [C],
X [E], and V). Hemophilia A is caused by a deficiency in factor VIII (C).
Hemophilia B (Christmas disease) is caused by a factor IX (D) deficiency. The
vitam in K–dependent factors are factors II (A), VII (B), IX (D), and X (E). A deficiency of factor II (A), V, or X (E) would result in prolongation of PT and PTT.
Factor VII (B) has the shortest half-life of the options listed

Question 37

Deficiency of factor II or this factor results in prolonged PT and PTT
A. Factor II
B. Factor VII
C. Factor VIII
D. Factor IX
E. Factor X

Answer 37

A. Factor II
B. Factor VII
C. Factor VIII
D. Factor IX
E. Factor X

The prothrombin time (PT) measures the integrity of the extrinsic and common pathways (factors VII [B], X [E], V, prothrombin, and fibrinogen). The
activated partial thromboplastin time (aPTT) measures the integrity of the
intrinsic and common pathways of coagulation (factors XII, XI, IX [D], VIII [C],
X [E], and V). Hemophilia A is caused by a deficiency in factor VIII (C).
Hemophilia B (Christmas disease) is caused by a factor IX (D) deficiency. The
vitam in K–dependent factors are factors II (A), VII (B), IX (D), and X (E). A deficiency of factor II (A), V, or X (E) would result in prolongation of PT and PTT.
Factor VII (B) has the shortest half-life of the options listed

Question 38

Antithrombin III deficiency
A. Abnormal PT, PTT, and bleeding time
B. Abnormal PT, normal PTT and bleeding time
C. Normal PT, PTT, and bleeding time
D. Normal PT, abnormal PTT and bleeding time
E. Hypercoagulable state
F. Normal PT, abnormal PTT, normal bleeding time

Answer 38

A. Abnormal PT, PTT, and bleeding time
B. Abnormal PT, normal PTT and bleeding time
C. Normal PT, PTT, and bleeding time
D. Normal PT, abnormal PTT and bleeding time
E. Hypercoagulable state
F. Normal PT, abnormal PTT, normal bleeding time

The two conditions listed that would cause prolongation of the PT, PTT, and
bleeding time (A) are disseminated intravascular coagulation and dysfibrinogenemia. Factor VII deficiencies and nutritional factor deficiencies result in
prolongation of the PT (vitam in K–dependent factors) without prolongation of the PTT or bleeding time (B). Factor XIII deficiency is not detected by routine laboratory screening and is characterized by normal PT, PTT, and
bleeding times (C). von Willebrandʼs disease (vWD) is a disorder of platelet–
vessel wall interaction, and the bleeding time is therefore prolonged. The PTT is also prolonged in vWD due to a concomitant factor XIII deficiency; the PT is normal (D). Antithrombin III is the major physiologic inhibitor of thrombin; its deficiency leads to unregulated thrombin formation, resulting
in a hypercoagulable state (E). A factor VIII deficiency (hemophilia A) results in a normal PT, abnormal PTT, and normal bleeding time (F)

Question 39

DIC
A. Abnormal PT, PTT, and bleeding time
B. Abnormal PT, normal PTT and bleeding time
C. Normal PT, PTT, and bleeding time
D. Normal PT, abnormal PTT and bleeding time
E. Hypercoagulable state
F. Normal PT, abnormal PTT, normal bleeding time

Answer 39

A. Abnormal PT, PTT, and bleeding time
B. Abnormal PT, normal PTT and bleeding time
C. Normal PT, PTT, and bleeding time
D. Normal PT, abnormal PTT and bleeding time
E. Hypercoagulable state
F. Normal PT, abnormal PTT, normal bleeding time

The two conditions listed that would cause prolongation of the PT, PTT, and
bleeding time (A) are disseminated intravascular coagulation and dysfibrinogenemia. Factor VII deficiencies and nutritional factor deficiencies result in
prolongation of the PT (vitam in K–dependent factors) without prolongation of the PTT or bleeding time (B). Factor XIII deficiency is not detected by routine laboratory screening and is characterized by normal PT, PTT, and
bleeding times (C). von Willebrandʼs disease (vWD) is a disorder of platelet–
vessel wall interaction, and the bleeding time is therefore prolonged. The PTT is also prolonged in vWD due to a concomitant factor XIII deficiency; the PT is normal (D). Antithrombin III is the major physiologic inhibitor of thrombin; its deficiency leads to unregulated thrombin formation, resulting
in a hypercoagulable state (E). A factor VIII deficiency (hemophilia A) results in a normal PT, abnormal PTT, and normal bleeding time (F)

Question 40

von Willebrand’s disease
A. Abnormal PT, PTT, and bleeding time
B. Abnormal PT, normal PTT and bleeding time
C. Normal PT, PTT, and bleeding time
D. Normal PT, abnormal PTT and bleeding time
E. Hypercoagulable state
F. Normal PT, abnormal PTT, normal bleeding time

Answer 40

A. Abnormal PT, PTT, and bleeding time
B. Abnormal PT, normal PTT and bleeding time
C. Normal PT, PTT, and bleeding time
D. Normal PT, abnormal PTT and bleeding time
E. Hypercoagulable state
F. Normal PT, abnormal PTT, normal bleeding time

The two conditions listed that would cause prolongation of the PT, PTT, and
bleeding time (A) are disseminated intravascular coagulation and dysfibrinogenemia. Factor VII deficiencies and nutritional factor deficiencies result in
prolongation of the PT (vitam in K–dependent factors) without prolongation of the PTT or bleeding time (B). Factor XIII deficiency is not detected by routine laboratory screening and is characterized by normal PT, PTT, and
bleeding times (C). von Willebrandʼs disease (vWD) is a disorder of platelet–
vessel wall interaction, and the bleeding time is therefore prolonged. The PTT is also prolonged in vWD due to a concomitant factor XIII deficiency; the PT is normal (D). Antithrombin III is the major physiologic inhibitor of thrombin; its deficiency leads to unregulated thrombin formation, resulting
in a hypercoagulable state (E). A factor VIII deficiency (hemophilia A) results in a normal PT, abnormal PTT, and normal bleeding time (F)

Question 41

Dysfibrinogenemia
A. Abnormal PT, PTT, and bleeding time
B. Abnormal PT, normal PTT and bleeding time
C. Normal PT, PTT, and bleeding time
D. Normal PT, abnormal PTT and bleeding time
E. Hypercoagulable state
F. Normal PT, abnormal PTT, normal bleeding time

Answer 41

A. Abnormal PT, PTT, and bleeding time
B. Abnormal PT, normal PTT and bleeding time
C. Normal PT, PTT, and bleeding time
D. Normal PT, abnormal PTT and bleeding time
E. Hypercoagulable state
F. Normal PT, abnormal PTT, normal bleeding time

The two conditions listed that would cause prolongation of the PT, PTT, and
bleeding time (A) are disseminated intravascular coagulation and dysfibrinogenemia. Factor VII deficiencies and nutritional factor deficiencies result in
prolongation of the PT (vitam in K–dependent factors) without prolongation of the PTT or bleeding time (B). Factor XIII deficiency is not detected by routine laboratory screening and is characterized by normal PT, PTT, and
bleeding times (C). von Willebrandʼs disease (vWD) is a disorder of platelet–
vessel wall interaction, and the bleeding time is therefore prolonged. The PTT is also prolonged in vWD due to a concomitant factor XIII deficiency; the PT is normal (D). Antithrombin III is the major physiologic inhibitor of thrombin; its deficiency leads to unregulated thrombin formation, resulting
in a hypercoagulable state (E). A factor VIII deficiency (hemophilia A) results in a normal PT, abnormal PTT, and normal bleeding time (F)

Question 42

Malnutrition
A. Abnormal PT, PTT, and bleeding time
B. Abnormal PT, normal PTT and bleeding time
C. Normal PT, PTT, and bleeding time
D. Normal PT, abnormal PTT and bleeding time
E. Hypercoagulable state
F. Normal PT, abnormal PTT, normal bleeding time

Answer 42

A. Abnormal PT, PTT, and bleeding time
B. Abnormal PT, normal PTT and bleeding time
C. Normal PT, PTT, and bleeding time
D. Normal PT, abnormal PTT and bleeding time
E. Hypercoagulable state
F. Normal PT, abnormal PTT, normal bleeding time

The two conditions listed that would cause prolongation of the PT, PTT, and
bleeding time (A) are disseminated intravascular coagulation and dysfibrinogenemia. Factor VII deficiencies and nutritional factor deficiencies result in
prolongation of the PT (vitam in K–dependent factors) without prolongation of the PTT or bleeding time (B). Factor XIII deficiency is not detected by routine laboratory screening and is characterized by normal PT, PTT, and
bleeding times (C). von Willebrandʼs disease (vWD) is a disorder of platelet–
vessel wall interaction, and the bleeding time is therefore prolonged. The PTT is also prolonged in vWD due to a concomitant factor XIII deficiency; the PT is normal (D). Antithrombin III is the major physiologic inhibitor of thrombin; its deficiency leads to unregulated thrombin formation, resulting
in a hypercoagulable state (E). A factor VIII deficiency (hemophilia A) results in a normal PT, abnormal PTT, and normal bleeding time (F)

Question 43

Factor VII deficiency
A. Abnormal PT, PTT, and bleeding time
B. Abnormal PT, normal PTT and bleeding time
C. Normal PT, PTT, and bleeding time
D. Normal PT, abnormal PTT and bleeding time
E. Hypercoagulable state
F. Normal PT, abnormal PTT, normal bleeding time

Answer 43

A. Abnormal PT, PTT, and bleeding time
B. Abnormal PT, normal PTT and bleeding time
C. Normal PT, PTT, and bleeding time
D. Normal PT, abnormal PTT and bleeding time
E. Hypercoagulable state
F. Normal PT, abnormal PTT, normal bleeding time

The two conditions listed that would cause prolongation of the PT, PTT, and
bleeding time (A) are disseminated intravascular coagulation and dysfibrinogenemia. Factor VII deficiencies and nutritional factor deficiencies result in
prolongation of the PT (vitam in K–dependent factors) without prolongation of the PTT or bleeding time (B). Factor XIII deficiency is not detected by routine laboratory screening and is characterized by normal PT, PTT, and
bleeding times (C). von Willebrandʼs disease (vWD) is a disorder of platelet–
vessel wall interaction, and the bleeding time is therefore prolonged. The PTT is also prolonged in vWD due to a concomitant factor XIII deficiency; the PT is normal (D). Antithrombin III is the major physiologic inhibitor of thrombin; its deficiency leads to unregulated thrombin formation, resulting
in a hypercoagulable state (E). A factor VIII deficiency (hemophilia A) results in a normal PT, abnormal PTT, and normal bleeding time (F)

Question 44

Factor XIII deficiency
A. Abnormal PT, PTT, and bleeding time
B. Abnormal PT, normal PTT and bleeding time
C. Normal PT, PTT, and bleeding time
D. Normal PT, abnormal PTT and bleeding time
E. Hypercoagulable state
F. Normal PT, abnormal PTT, normal bleeding time

Answer 44

A. Abnormal PT, PTT, and bleeding time
B. Abnormal PT, normal PTT and bleeding time
C. Normal PT, PTT, and bleeding time
D. Normal PT, abnormal PTT and bleeding time
E. Hypercoagulable state
F. Normal PT, abnormal PTT, normal bleeding time

The two conditions listed that would cause prolongation of the PT, PTT, and
bleeding time (A) are disseminated intravascular coagulation and dysfibrinogenemia. Factor VII deficiencies and nutritional factor deficiencies result in
prolongation of the PT (vitam in K–dependent factors) without prolongation of the PTT or bleeding time (B). Factor XIII deficiency is not detected by routine laboratory screening and is characterized by normal PT, PTT, and
bleeding times (C). von Willebrandʼs disease (vWD) is a disorder of platelet–
vessel wall interaction, and the bleeding time is therefore prolonged. The PTT is also prolonged in vWD due to a concomitant factor XIII deficiency; the PT is normal (D). Antithrombin III is the major physiologic inhibitor of thrombin; its deficiency leads to unregulated thrombin formation, resulting
in a hypercoagulable state (E). A factor VIII deficiency (hemophilia A) results in a normal PT, abnormal PTT, and normal bleeding time (F)

Question 45

Factor VIII deficiency
A. Abnormal PT, PTT, and bleeding time
B. Abnormal PT, normal PTT and bleeding time
C. Normal PT, PTT, and bleeding time
D. Normal PT, abnormal PTT and bleeding time
E. Hypercoagulable state
F. Normal PT, abnormal PTT, normal bleeding time

Answer 45

A. Abnormal PT, PTT, and bleeding time
B. Abnormal PT, normal PTT and bleeding time
C. Normal PT, PTT, and bleeding time
D. Normal PT, abnormal PTT and bleeding time
E. Hypercoagulable state
F. Normal PT, abnormal PTT, normal bleeding time

The two conditions listed that would cause prolongation of the PT, PTT, and
bleeding time (A) are disseminated intravascular coagulation and dysfibrinogenemia. Factor VII deficiencies and nutritional factor deficiencies result in
prolongation of the PT (vitam in K–dependent factors) without prolongation of the PTT or bleeding time (B). Factor XIII deficiency is not detected by routine laboratory screening and is characterized by normal PT, PTT, and
bleeding times (C). von Willebrandʼs disease (vWD) is a disorder of platelet–
vessel wall interaction, and the bleeding time is therefore prolonged. The PTT is also prolonged in vWD due to a concomitant factor XIII deficiency; the PT is normal (D). Antithrombin III is the major physiologic inhibitor of thrombin; its deficiency leads to unregulated thrombin formation, resulting
in a hypercoagulable state (E). A factor VIII deficiency (hemophilia A) results in a normal PT, abnormal PTT, and normal bleeding time (F)

Question 46

Often occurs with hypokalemia

Answer 46

A. Increased anion gap metabolic acidosis
B. Non-anion gap metabolic acidosis
C. Metabolic alkalosis
D. Respiratory acidosis
E. Respiratory alkalosis

An anion gap metabolic acidosis (A) is caused by fixed acids such as is seen in lactic acidosis, ketoacidosis, late salicylate toxicity, methanol poisoning, and ethylene glycol poisoning. A non-anion gap metabolic acidosis (B) is caused by decreased bicarbonate levels w ith a compensatory increase in chloride ions as is seen in diarrhea, early renal insufficiency, increased chloride load, and type II renal tubular acidosis. Addison’s disease is a form of primary adrenal insufficiency caused by the autoimmune-mediated destruction of the
adrenal gland. Addison’s disease is associated with a hyperkalemic non-anion
gap metabolic acidosis (B) and decreased extracellular uid volume due to
decreased mineralocorticoid activity in the kidney. Conversely, in situations
where there is increased mineralocorticoid activity, there is a tendency toward expansion of the extracellular fluid volume and hypokalemic metabolic alkalosis (C) as is seen in cases of Cushing’s disease and prim ary aldosteronism . Respiratory acidosis (D) is caused by hypoventilation and carbon dioxide retention as can be seen in myasthenia gravis. Respiratory alkalosis (E)
is the earliest abnormality and may be the only acid–base disorder in some
patients with salicylate overdose. Production of a mixture of endogenous acids, from a metabolic block, may later lead to metabolic acidosis.

Question 47

Addison’s disease
A. Increased anion gap metabolic acidosis
B. Non-anion gap metabolic acidosis
C. Metabolic alkalosis
D. Respiratory acidosis
E. Respiratory alkalosis

Answer 47

A. Increased anion gap metabolic acidosis
B. Non-anion gap metabolic acidosis
C. Metabolic alkalosis
D. Respiratory acidosis
E. Respiratory alkalosis

An anion gap metabolic acidosis (A) is caused by fixed acids such as is seen in lactic acidosis, ketoacidosis, late salicylate toxicity, methanol poisoning, and ethylene glycol poisoning. A non-anion gap metabolic acidosis (B) is caused by decreased bicarbonate levels w ith a compensatory increase in chloride ions as is seen in diarrhea, early renal insufficiency, increased chloride load, and type II renal tubular acidosis. Addison’s disease is a form of primary adrenal insufficiency caused by the autoimmune-mediated destruction of the
adrenal gland. Addison’s disease is associated with a hyperkalemic non-anion
gap metabolic acidosis (B) and decreased extracellular uid volume due to
decreased mineralocorticoid activity in the kidney. Conversely, in situations
where there is increased mineralocorticoid activity, there is a tendency toward expansion of the extracellular fluid volume and hypokalemic metabolic alkalosis (C) as is seen in cases of Cushing’s disease and prim ary aldosteronism . Respiratory acidosis (D) is caused by hypoventilation and carbon dioxide retention as can be seen in myasthenia gravis. Respiratory alkalosis (E)
is the earliest abnormality and may be the only acid–base disorder in some
patients with salicylate overdose. Production of a mixture of endogenous acids, from a metabolic block, may later lead to metabolic acidosis.

Question 48

Salicylate overdose (early stage)
A. Increased anion gap metabolic acidosis
B. Non-anion gap metabolic acidosis
C. Metabolic alkalosis
D. Respiratory acidosis
E. Respiratory alkalosis

Answer 48

A. Increased anion gap metabolic acidosis
B. Non-anion gap metabolic acidosis
C. Metabolic alkalosis
D. Respiratory acidosis
E. Respiratory alkalosis

An anion gap metabolic acidosis (A) is caused by fixed acids such as is seen in lactic acidosis, ketoacidosis, late salicylate toxicity, methanol poisoning, and ethylene glycol poisoning. A non-anion gap metabolic acidosis (B) is caused by decreased bicarbonate levels w ith a compensatory increase in chloride ions as is seen in diarrhea, early renal insufficiency, increased chloride load, and type II renal tubular acidosis. Addison’s disease is a form of primary adrenal insufficiency caused by the autoimmune-mediated destruction of the
adrenal gland. Addison’s disease is associated with a hyperkalemic non-anion
gap metabolic acidosis (B) and decreased extracellular uid volume due to
decreased mineralocorticoid activity in the kidney. Conversely, in situations
where there is increased mineralocorticoid activity, there is a tendency toward expansion of the extracellular fluid volume and hypokalemic metabolic alkalosis (C) as is seen in cases of Cushing’s disease and prim ary aldosteronism . Respiratory acidosis (D) is caused by hypoventilation and carbon dioxide retention as can be seen in myasthenia gravis. Respiratory alkalosis (E)
is the earliest abnormality and may be the only acid–base disorder in some
patients with salicylate overdose. Production of a mixture of endogenous acids, from a metabolic block, may later lead to metabolic acidosis.

Question 49

Myasthenia gravis
A. Increased anion gap metabolic acidosis
B. Non-anion gap metabolic acidosis
C. Metabolic alkalosis
D. Respiratory acidosis
E. Respiratory alkalosis

Answer 49

A. Increased anion gap metabolic acidosis
B. Non-anion gap metabolic acidosis
C. Metabolic alkalosis
D. Respiratory acidosis
E. Respiratory alkalosis

An anion gap metabolic acidosis (A) is caused by fixed acids such as is seen in lactic acidosis, ketoacidosis, late salicylate toxicity, methanol poisoning, and ethylene glycol poisoning. A non-anion gap metabolic acidosis (B) is caused by decreased bicarbonate levels w ith a compensatory increase in chloride ions as is seen in diarrhea, early renal insufficiency, increased chloride load, and type II renal tubular acidosis. Addison’s disease is a form of primary adrenal insufficiency caused by the autoimmune-mediated destruction of the
adrenal gland. Addison’s disease is associated with a hyperkalemic non-anion
gap metabolic acidosis (B) and decreased extracellular uid volume due to
decreased mineralocorticoid activity in the kidney. Conversely, in situations
where there is increased mineralocorticoid activity, there is a tendency toward expansion of the extracellular fluid volume and hypokalemic metabolic alkalosis (C) as is seen in cases of Cushing’s disease and prim ary aldosteronism . Respiratory acidosis (D) is caused by hypoventilation and carbon dioxide retention as can be seen in myasthenia gravis. Respiratory alkalosis (E)
is the earliest abnormality and may be the only acid–base disorder in some
patients with salicylate overdose. Production of a mixture of endogenous acids, from a metabolic block, may later lead to metabolic acidosis.

Question 50

Ethylene glycol overdose
A. Increased anion gap metabolic acidosis
B. Non-anion gap metabolic acidosis
C. Metabolic alkalosis
D. Respiratory acidosis
E. Respiratory alkalosis

Answer 50

A. Increased anion gap metabolic acidosis
B. Non-anion gap metabolic acidosis
C. Metabolic alkalosis
D. Respiratory acidosis
E. Respiratory alkalosis

An anion gap metabolic acidosis (A) is caused by fixed acids such as is seen in lactic acidosis, ketoacidosis, late salicylate toxicity, methanol poisoning, and ethylene glycol poisoning. A non-anion gap metabolic acidosis (B) is caused by decreased bicarbonate levels w ith a compensatory increase in chloride ions as is seen in diarrhea, early renal insufficiency, increased chloride load, and type II renal tubular acidosis. Addison’s disease is a form of primary adrenal insufficiency caused by the autoimmune-mediated destruction of the
adrenal gland. Addison’s disease is associated with a hyperkalemic non-anion
gap metabolic acidosis (B) and decreased extracellular uid volume due to
decreased mineralocorticoid activity in the kidney. Conversely, in situations
where there is increased mineralocorticoid activity, there is a tendency toward expansion of the extracellular fluid volume and hypokalemic metabolic alkalosis (C) as is seen in cases of Cushing’s disease and prim ary aldosteronism . Respiratory acidosis (D) is caused by hypoventilation and carbon dioxide retention as can be seen in myasthenia gravis. Respiratory alkalosis (E)
is the earliest abnormality and may be the only acid–base disorder in some
patients with salicylate overdose. Production of a mixture of endogenous acids, from a metabolic block, may later lead to metabolic acidosis.

Question 51

Cushing’s disease
A. Increased anion gap metabolic acidosis
B. Non-anion gap metabolic acidosis
C. Metabolic alkalosis
D. Respiratory acidosis
E. Respiratory alkalosis

Answer 51

A. Increased anion gap metabolic acidosis
B. Non-anion gap metabolic acidosis
C. Metabolic alkalosis
D. Respiratory acidosis
E. Respiratory alkalosis

An anion gap metabolic acidosis (A) is caused by fixed acids such as is seen in lactic acidosis, ketoacidosis, late salicylate toxicity, methanol poisoning, and ethylene glycol poisoning. A non-anion gap metabolic acidosis (B) is caused by decreased bicarbonate levels w ith a compensatory increase in chloride ions as is seen in diarrhea, early renal insufficiency, increased chloride load, and type II renal tubular acidosis. Addison’s disease is a form of primary adrenal insufficiency caused by the autoimmune-mediated destruction of the
adrenal gland. Addison’s disease is associated with a hyperkalemic non-anion
gap metabolic acidosis (B) and decreased extracellular uid volume due to
decreased mineralocorticoid activity in the kidney. Conversely, in situations
where there is increased mineralocorticoid activity, there is a tendency toward expansion of the extracellular fluid volume and hypokalemic metabolic alkalosis (C) as is seen in cases of Cushing’s disease and prim ary aldosteronism . Respiratory acidosis (D) is caused by hypoventilation and carbon dioxide retention as can be seen in myasthenia gravis. Respiratory alkalosis (E)
is the earliest abnormality and may be the only acid–base disorder in some
patients with salicylate overdose. Production of a mixture of endogenous acids, from a metabolic block, may later lead to metabolic acidosis.

Question 52

Primary aldosteronism
A. Increased anion gap metabolic acidosis
B. Non-anion gap metabolic acidosis
C. Metabolic alkalosis
D. Respiratory acidosis
E. Respiratory alkalosis

Answer 52

A. Increased anion gap metabolic acidosis
B. Non-anion gap metabolic acidosis
C. Metabolic alkalosis
D. Respiratory acidosis
E. Respiratory alkalosis

An anion gap metabolic acidosis (A) is caused by fixed acids such as is seen in lactic acidosis, ketoacidosis, late salicylate toxicity, methanol poisoning, and ethylene glycol poisoning. A non-anion gap metabolic acidosis (B) is caused by decreased bicarbonate levels w ith a compensatory increase in chloride ions as is seen in diarrhea, early renal insufficiency, increased chloride load, and type II renal tubular acidosis. Addison’s disease is a form of primary adrenal insufficiency caused by the autoimmune-mediated destruction of the
adrenal gland. Addison’s disease is associated with a hyperkalemic non-anion
gap metabolic acidosis (B) and decreased extracellular uid volume due to
decreased mineralocorticoid activity in the kidney. Conversely, in situations
where there is increased mineralocorticoid activity, there is a tendency toward expansion of the extracellular fluid volume and hypokalemic metabolic alkalosis (C) as is seen in cases of Cushing’s disease and prim ary aldosteronism . Respiratory acidosis (D) is caused by hypoventilation and carbon dioxide retention as can be seen in myasthenia gravis. Respiratory alkalosis (E)
is the earliest abnormality and may be the only acid–base disorder in some
patients with salicylate overdose. Production of a mixture of endogenous acids, from a metabolic block, may later lead to metabolic acidosis.

Question 53

The formula for mean arterial pressure is (DBP, diastolic blood pressure; SBP, systolic blood pressure)
A. (DBP 1 SBP)/2
B. DBP 1 (SBP 2 DBP)/2
C. DBP/2 1 SBP/3
D. DBP 1 (SBP 2 DBP)/3
E. DBP/2 1 (SBP 2 DBP)/3

Answer 53

A. (DBP 1 SBP)/2
B. DBP 1 (SBP 2 DBP)/2
C. DBP/2 1 SBP/3
D. DBP 1 (SBP 2 DBP)/3
E. DBP/2 1 (SBP 2 DBP)/3

The mean arterial pressure can be estimated by adding the diastolic pressure to one-third of the pulse pressure. This formula assumes that diastole makes up one-third of the cardiac cycle.

Question 54

Parathyroid hyperplasia or adenoma
A. Multiple endocrine neoplasia (MEN) type I (Werner’s syndrome)
B. MEN type IIA (Sipple’s syndrome)
C. Both
D. Neither

Answer 54

A. Multiple endocrine neoplasia (MEN) type I (Werner’s syndrome)
B. MEN type IIA (Sipple’s syndrome)
C. Both
D. Neither

MEN type I (Werner’s syndrome [A]) can be remembered as the “PPP” syndrome because it is characterized by parathyroid, pancreatic, and pituitary tumors. MEN type IIA (Sipple’s syndrom e [B]) is characterized by medullary thyroid carcinoma, pheochromocytoma, and tumors of the parathyroid glands. Rarely, pheochromocytomas may be seen in MEN type I (A). MEN type IIB (also know n as MEN type III) is associated w ith medullary thyroid carcinoma, pheochromocytoma, gastrointestinal and mucosal neuromas, and a marfanoid habitus

Question 55

Pancreatic islet cell hyperplasia, adenoma, or carcinoma
A. Multiple endocrine neoplasia (MEN) type I (Werner’s syndrome)
B. MEN type IIA (Sipple’s syndrome)
C. Both
D. Neither

Answer 55

A. Multiple endocrine neoplasia (MEN) type I (Werner’s syndrome)
B. MEN type IIA (Sipple’s syndrome)
C. Both
D. Neither

MEN type I (Werner’s syndrome [A]) can be remembered as the “PPP” syndrome because it is characterized by parathyroid, pancreatic, and pituitary tumors. MEN type IIA (Sipple’s syndrom e [B]) is characterized by medullary thyroid carcinoma, pheochromocytoma, and tumors of the parathyroid glands. Rarely, pheochromocytomas may be seen in MEN type I (A). MEN type IIB (also know n as MEN type III) is associated w ith medullary thyroid carcinoma, pheochromocytoma, gastrointestinal and mucosal neuromas, and a marfanoid habitus

Question 56

Pituitary hyperplasia or adenoma
A. Multiple endocrine neoplasia (MEN) type I (Werner’s syndrome)
B. MEN type IIA (Sipple’s syndrome)
C. Both
D. Neither

Answer 56

A. Multiple endocrine neoplasia (MEN) type I (Werner’s syndrome)
B. MEN type IIA (Sipple’s syndrome)
C. Both
D. Neither

MEN type I (Werner’s syndrome [A]) can be remembered as the “PPP” syndrome because it is characterized by parathyroid, pancreatic, and pituitary tumors. MEN type IIA (Sipple’s syndrom e [B]) is characterized by medullary thyroid carcinoma, pheochromocytoma, and tumors of the parathyroid glands. Rarely, pheochromocytomas may be seen in MEN type I (A). MEN type IIB (also know n as MEN type III) is associated w ith medullary thyroid carcinoma, pheochromocytoma, gastrointestinal and mucosal neuromas, and a marfanoid habitus

Question 57

Pheochromocytomas are common
A. Multiple endocrine neoplasia (MEN) type I (Werner’s syndrome)
B. MEN type IIA (Sipple’s syndrome)
C. Both
D. Neither

Answer 57

A. Multiple endocrine neoplasia (MEN) type I (Werner’s syndrome)
B. MEN type IIA (Sipple’s syndrome)
C. Both
D. Neither

MEN type I (Werner’s syndrome [A]) can be remembered as the “PPP” syndrome because it is characterized by parathyroid, pancreatic, and pituitary tumors. MEN type IIA (Sipple’s syndrom e [B]) is characterized by medullary thyroid carcinoma, pheochromocytoma, and tumors of the parathyroid glands. Rarely, pheochromocytomas may be seen in MEN type I (A). MEN type IIB (also know n as MEN type III) is associated w ith medullary thyroid carcinoma, pheochromocytoma, gastrointestinal and mucosal neuromas, and a marfanoid habitus

Question 58

Medullary thyroid carcinomas are common.
A. Multiple endocrine neoplasia (MEN) type I (Werner’s syndrome)
B. MEN type IIA (Sipple’s syndrome)
C. Both
D. Neither

Answer 58

A. Multiple endocrine neoplasia (MEN) type I (Werner’s syndrome)
B. MEN type IIA (Sipple’s syndrome)
C. Both
D. Neither

MEN type I (Werner’s syndrome [A]) can be remembered as the “PPP” syndrome because it is characterized by parathyroid, pancreatic, and pituitary tumors. MEN type IIA (Sipple’s syndrom e [B]) is characterized by medullary thyroid carcinoma, pheochromocytoma, and tumors of the parathyroid glands. Rarely, pheochromocytomas may be seen in MEN type I (A). MEN type IIB (also know n as MEN type III) is associated w ith medullary thyroid carcinoma, pheochromocytoma, gastrointestinal and mucosal neuromas, and a marfanoid habitus

Question 59

Mucosal and gastrointestinal neuromas
A. Multiple endocrine neoplasia (MEN) type I (Werner’s syndrome)
B. MEN type IIA (Sipple’s syndrome)
C. Both
D. Neither

Answer 59

A. Multiple endocrine neoplasia (MEN) type I (Werner’s syndrome)
B. MEN type IIA (Sipple’s syndrome)
C. Both
D. Neither

MEN type I (Werner’s syndrome [A]) can be remembered as the “PPP” syndrome because it is characterized by parathyroid, pancreatic, and pituitary tumors. MEN type IIA (Sipple’s syndrom e [B]) is characterized by medullary thyroid carcinoma, pheochromocytoma, and tumors of the parathyroid glands. Rarely, pheochromocytomas may be seen in MEN type I (A). MEN type IIB (also know n as MEN type III) is associated w ith medullary thyroid carcinoma, pheochromocytoma, gastrointestinal and mucosal neuromas, and a marfanoid habitus

Question 60

Marfanoid features
A. Multiple endocrine neoplasia (MEN) type I (Werner’s syndrome)
B. MEN type IIA (Sipple’s syndrome)
C. Both
D. Neither

Answer 60

A. Multiple endocrine neoplasia (MEN) type I (Werner’s syndrome)
B. MEN type IIA (Sipple’s syndrome)
C. Both
D. Neither

MEN type I (Werner’s syndrome [A]) can be remembered as the “PPP” syndrome because it is characterized by parathyroid, pancreatic, and pituitary tumors. MEN type IIA (Sipple’s syndrom e [B]) is characterized by medullary thyroid carcinoma, pheochromocytoma, and tumors of the parathyroid glands. Rarely, pheochromocytomas may be seen in MEN type I (A). MEN type IIB (also know n as MEN type III) is associated w ith medullary thyroid carcinoma, pheochromocytoma, gastrointestinal and mucosal neuromas, and a marfanoid habitus

Question 61

Characteristics of primary hyperaldosteronism include each of the following except
A. Edema
B. Hypokalemia
C. Increased diastolic blood pressure
D. Metabolic alkalosis
E. Suppression of plasma renin activity

Answer 61

A. Edema
B. Hypokalemia
C. Increased diastolic blood pressure
D. Metabolic alkalosis
E. Suppression of plasma renin activity

Hyperaldosteronism stimulates sodium reabsorption in the collecting ducts,
causing renal potassium wasting and leading to a hypokalemic (B), hypochloremic metabolic alkalosis (D). Both primary and secondary hyperaldosteronism present with hypertension (C). Primary hyperaldosteronism , or
Conn’s syndrome, is caused by autologous production of aldosterone either by
an adrenal adenoma or adrenal hyperplasia and causes feedback inhibition
of the renin-angiotensin system (E). Secondary hyperaldosteronism occurs
as a result of increased tone in the renin-angiotensin system , usually caused
by renal vascular disease. Secondary hyperaldosteronism usually responds to
angiotensin-converting enzym e (ACE) inhibitors. In the absence of associated
disorders, edema (A) is characteristically absent

Question 62

Adequacy of pulmonary ventilation is assessed by
A. FiO2
B. Oxygen saturation
C. PaCO2
D. Partial pressure of O2 in blood
E. Tidal volume

Answer 62

A. FiO2
B. Oxygen saturation
C. PaCO2
D. Partial pressure of O2 in blood
E. Tidal volume

The partial pressure of arterial CO2 is directly related to the rate of CO2 production by the body and inversely related to the rate of alveolar ventilation.
Of the choices listed, the adequacy of pulmonary ventilation is best assessed
by PaCO2 (C).

Question 63

Hypocalcemia
A. Atrial brillation
B. J-point elevation
C. Peaked T wave
D. Prolonged QT interval
E. U wave

Answer 63

A. Atrial brillation
B. J-point elevation
C. Peaked T wave
D. Prolonged QT interval
E. U wave

Hyperthyroidism is associated with atrial fibrillation (A). Hypothermia is associated with pronounced waves at the QRS-ST interval known as J-waves (B) or Osborn waves. Hyperkalemia is associated with
peaked T waves (C). A prolonged QT interval (D) can be seen with hypocalcemia and quinidine toxicity. Hypokalemia is associated with U waves (E)

Question 64

Hypokalemia
A. Atrial brillation
B. J-point elevation
C. Peaked T wave
D. Prolonged QT interval
E. U wave

Answer 64

A. Atrial brillation
B. J-point elevation
C. Peaked T wave
D. Prolonged QT interval
E. U wave

Hyperthyroidism is associated with atrial fibrillation (A). Hypothermia is associated with pronounced waves at the QRS-ST interval known as J-waves (B) or Osborn waves. Hyperkalemia is associated with
peaked T waves (C). A prolonged QT interval (D) can be seen with hypocalcemia and quinidine toxicity. Hypokalemia is associated with U waves (E)

Question 65

Hyperkalemia
A. Atrial brillation
B. J-point elevation
C. Peaked T wave
D. Prolonged QT interval
E. U wave

Answer 65

A. Atrial brillation
B. J-point elevation
C. Peaked T wave
D. Prolonged QT interval
E. U wave

Hyperthyroidism is associated with atrial fibrillation (A). Hypothermia is associated with pronounced waves at the QRS-ST interval known as J-waves (B) or Osborn waves. Hyperkalemia is associated with
peaked T waves (C). A prolonged QT interval (D) can be seen with hypocalcemia and quinidine toxicity. Hypokalemia is associated with U waves (E)

Question 66

Hypothermia
A. Atrial brillation
B. J-point elevation
C. Peaked T wave
D. Prolonged QT interval
E. U wave

Answer 66

A. Atrial brillation
B. J-point elevation
C. Peaked T wave
D. Prolonged QT interval
E. U wave

Hyperthyroidism is associated with atrial fibrillation (A). Hypothermia is associated with pronounced waves at the QRS-ST interval known as J-waves (B) or Osborn waves. Hyperkalemia is associated with
peaked T waves (C). A prolonged QT interval (D) can be seen with hypocalcemia and quinidine toxicity. Hypokalemia is associated with U waves (E)Hyperthyroidism is associated with atrial fibrillation (A). Hypothermia is associated with pronounced waves at the QRS-ST interval known as J-waves (B) or Osborn waves. Hyperkalemia is associated with

Question 67

Hyperthyroidism
A. Atrial brillation
B. J-point elevation
C. Peaked T wave
D. Prolonged QT interval
E. U wave

Answer 67

A. Atrial brillation
B. J-point elevation
C. Peaked T wave
D. Prolonged QT interval
E. U wave

Hyperthyroidism is associated with atrial fibrillation (A). Hypothermia is associated with pronounced waves at the QRS-ST interval known as J-waves (B) or Osborn waves. Hyperkalemia is associated with
peaked T waves (C). A prolonged QT interval (D) can be seen with hypocalcemia and quinidine toxicity. Hypokalemia is associated with U waves (E)

Question 68

Quinidine toxicity
A. Atrial brillation
B. J-point elevation
C. Peaked T wave
D. Prolonged QT interval
E. U wave

Answer 68

A. Atrial brillation
B. J-point elevation
C. Peaked T wave
D. Prolonged QT interval
E. U wave

Hyperthyroidism is associated with atrial fibrillation (A). Hypothermia is associated with pronounced waves at the QRS-ST interval known as J-waves (B) or Osborn waves. Hyperkalemia is associated with
peaked T waves (C). A prolonged QT interval (D) can be seen with hypocalcemia and quinidine toxicity. Hypokalemia is associated with U waves (E)

Question 69

Which of the follow ing is false of malignant hyperthermia?
A. Calcium is released from the muscle cell’s sarcoplasmic reticulum
B. End-tidal pCO2 increases
C. It is precipitated by the use of inhalational anesthetics.
D. Treatment is with dantrolene.
E. Use of succinylcholine can help prevent it.

Answer 69

A. Calcium is released from the muscle cell’s sarcoplasmic reticulum
B. End-tidal pCO2 increases
C. It is precipitated by the use of inhalational anesthetics.
D. Treatment is with dantrolene.
E. Use of succinylcholine can help prevent it.

Malignant hyperthermia is an inherited disorder characterized by fever
and rigidity that involves excessive release of calcium from the sarcoplasmic reticulum (A) of skeletal muscle precipitated by inhalational anesthetics (C) and depolarizing neuromuscular blocking agents such as
succinylcholine (E is false). Diagnosis can be made by an early rise in endtidal CO2 (B) followed by muscle rigidity and fever that may progress to rhabdomyolysis and renal failure. The administration of dantrolene (D) is critical in the treatment of this disorder.

Question 70

Of the following, the best choice for Clostridium difficile enterocolitis is
A. Clindamycin orally
B. Metronidazole (Flagyl) orally
C. Penicillin G orally
D. Penicillin VK intravenously
E. Vancomycin intravenously

Answer 70

A. Clindamycin orally
B. Metronidazole (Flagyl) orally
C. Penicillin G orally
D. Penicillin VK intravenously
E. Vancomycin intravenously

For the treatment of Clostridium difficile, a 10-day course of oral metronidazole (B) is the preferred treatment. Intravenous metronidazole can be used
in patients who cannot receive oral medications. Oral vancomycin is also effective in the treatment of this infection, but it is a second-line agent in an effort to limit vancomycin use. Oral vancomycin is the treatment of choice in pregnant or lactating females. Intravenous vancomycin (E) is not effective in this setting

Question 71

Pulsus paradoxus
A. Cardiac tamponade
B. Tension pneumothorax
C. Both
D. Neither

Answer 71

A. Cardiac tamponade
B. Tension pneumothorax
C. Both
D. Neither

Cardiac tamponade (A) occurs when pericardial flluid causes an increase in
pericardial pressure and resultant decrease in ventricular filling. Physical exam in cardiac tamponade reveals jugular venous distention from increased atrial (venous) pressures, narrowing of the pulse pressure, and pulsus paradoxus (inspiratory drop in systolic pressure is . 15 m m Hg). In tension pneumothorax (B), intrathoracic pressure is elevated, w hich impairs ventricular
filling, leading to increased atrial (venous) pressure.

Question 72

Increased venous pressure
A. Cardiac tamponade
B. Tension pneumothorax
C. Both
D. Neither

Answer 72

A. Cardiac tamponade
B. Tension pneumothorax
C. Both
D. Neither

Cardiac tamponade (A) occurs when pericardial flluid causes an increase in
pericardial pressure and resultant decrease in ventricular filling. Physical exam in cardiac tamponade reveals jugular venous distention from increased atrial (venous) pressures, narrowing of the pulse pressure, and pulsus paradoxus (inspiratory drop in systolic pressure is . 15 m m Hg). In tension pneumothorax (B), intrathoracic pressure is elevated, w hich impairs ventricular
filling, leading to increased atrial (venous) pressure.

Question 73

Increased pulse pressure
A. Cardiac tamponade
B. Tension pneumothorax
C. Both
D. Neither

Answer 73

A. Cardiac tamponade
B. Tension pneumothorax
C. Both
D. Neither

Cardiac tamponade (A) occurs when pericardial flluid causes an increase in
pericardial pressure and resultant decrease in ventricular filling. Physical exam in cardiac tamponade reveals jugular venous distention from increased atrial (venous) pressures, narrowing of the pulse pressure, and pulsus paradoxus (inspiratory drop in systolic pressure is . 15 m m Hg). In tension pneumothorax (B), intrathoracic pressure is elevated, w hich impairs ventricular
filling, leading to increased atrial (venous) pressure.

Question 74

Meningitis occurring within 72 hours after a basilar skull fracture is most commonly secondary to
A. Haemophilus influenzae
B. Neisseria meningitidis
C. Staphylococcus aureus
D. Staphylococcus epidermidis
E. Streptococcus pneumoniae

Answer 74

A. Haemophilus influenzae
B. Neisseria meningitidis
C. Staphylococcus aureus
D. Staphylococcus epidermidis
E. Streptococcus pneumoniae

Streptococcus pneumoniae (E) is the m ost common cause of meningitis in
the adult population

Question 75

Postoperative shunt infections are most commonly caused by
A. Coagulase-negative staphylococci
B. H. influenzae
C. Pseudomonas species
D. S. aureus
E. S. pneumoniae

Answer 75

A. Coagulase-negative staphylococci
B. H. influenzae
C. Pseudomonas species
D. S. aureus
E. S. pneumoniae

Coagulase-negative staphylococci (S. epider midis [A]) are the m ost common cause of postoperative shunt infections

Question 76

The most likely cause of a fever occurring in the rst 24 hours after surgery is
A. Atelectasis/postoperative inflammation
B. Deep vein thrombosis
C. Pneumonia
D. Urinary tract infection
E. Wound infection

Answer 76

A. Atelectasis/postoperative inflammation
B. Deep vein thrombosis
C. Pneumonia
D. Urinary tract infection
E. Wound infection

Fever is present in 15–40% of patients in the rst postoperative day, is
usually self-limited, and is attributed to atelectasis or postoperative
inflammation (A). Atelectasis as a cause of fever is somewhat controversial;
some authors argue that it is not atelectasis itself, but instead, postoperative
inflammation that is the cause of early postoperative fever. Deep vein thrombosis (B), urinary tract infection (D), pneum onia (C), and wound infection
(E) are less likely to cause fever on the first postoperative day

Question 77

A positive inotropic agent
A. Dobutamine
B. Dopamine
C. Both
D. Neither

Answer 77

A. Dobutamine
B. Dopamine
C. Both
D. Neither

Dobutamine (A) is a strong b1 receptor agonist and a weak b2 receptor agonist. b1 stimulation causes a positive chronotropic and ionotropic effect.
Dobutamine (A) is typically used in patients with decompensated systolic heart failure who also have a normal blood pressure. Dopamine (B) has dosedependent effects and, at a low dose, causes changes in renal and splanchnic blood flow as well as increased sodium excretion by the kidneys. At intermediate doses, dopamine (B) has a positive ionotropic and chronotropic effect via agonism of b1 receptors, although the ionotropic effect of dopamine
is much less than that of dobutamine. At high doses, dopamine stimulates
a receptors, causing systemic vasoconstriction and increased cardiac afterload, counteracting the increase in cardiac output. Both (C) dopamine and
dobutamine stimulate b2 receptors, w hich causes some degree of peripheral
vasodilatation (only at low doses for dopam ine). Norepinephrine is the firstline pressor of choice in septic shock.

Question 78

Has very little effect on a -adrenergic receptors
A. Dobutamine
B. Dopamine
C. Both
D. Neither

Answer 78

A. Dobutamine
B. Dopamine
C. Both
D. Neither

Dobutamine (A) is a strong b1 receptor agonist and a weak b2 receptor agonist. b1 stimulation causes a positive chronotropic and ionotropic effect.
Dobutamine (A) is typically used in patients with decompensated systolic heart failure who also have a normal blood pressure. Dopamine (B) has dosedependent effects and, at a low dose, causes changes in renal and splanchnic blood flow as well as increased sodium excretion by the kidneys. At intermediate doses, dopamine (B) has a positive ionotropic and chronotropic effect via agonism of b1 receptors, although the ionotropic effect of dopamine
is much less than that of dobutamine. At high doses, dopamine stimulates
a receptors, causing systemic vasoconstriction and increased cardiac afterload, counteracting the increase in cardiac output. Both (C) dopamine and
dobutamine stimulate b2 receptors, w hich causes some degree of peripheral
vasodilatation (only at low doses for dopam ine). Norepinephrine is the firstline pressor of choice in septic shock.

Question 79

Is the drug of choice in septic shock
A. Dobutamine
B. Dopamine
C. Both
D. Neither

Answer 79

A. Dobutamine
B. Dopamine
C. Both
D. Neither

Dobutamine (A) is a strong b1 receptor agonist and a weak b2 receptor agonist. b1 stimulation causes a positive chronotropic and ionotropic effect.
Dobutamine (A) is typically used in patients with decompensated systolic heart failure who also have a normal blood pressure. Dopamine (B) has dosedependent effects and, at a low dose, causes changes in renal and splanchnic blood flow as well as increased sodium excretion by the kidneys. At intermediate doses, dopamine (B) has a positive ionotropic and chronotropic effect via agonism of b1 receptors, although the ionotropic effect of dopamine
is much less than that of dobutamine. At high doses, dopamine stimulates
a receptors, causing systemic vasoconstriction and increased cardiac afterload, counteracting the increase in cardiac output. Both (C) dopamine and
dobutamine stimulate b2 receptors, w hich causes some degree of peripheral
vasodilatation (only at low doses for dopam ine). Norepinephrine is the firstline pressor of choice in septic shock.

Question 80

Has no effect on b2 receptors
A. Dobutamine
B. Dopamine
C. Both
D. Neither

Answer 80

A. Dobutamine
B. Dopamine
C. Both
D. Neither

Dobutamine (A) is a strong b1 receptor agonist and a weak b2 receptor agonist. b1 stimulation causes a positive chronotropic and ionotropic effect.
Dobutamine (A) is typically used in patients with decompensated systolic heart failure who also have a normal blood pressure. Dopamine (B) has dosedependent effects and, at a low dose, causes changes in renal and splanchnic blood flow as well as increased sodium excretion by the kidneys. At intermediate doses, dopamine (B) has a positive ionotropic and chronotropic effect via agonism of b1 receptors, although the ionotropic effect of dopamine
is much less than that of dobutamine. At high doses, dopamine stimulates
a receptors, causing systemic vasoconstriction and increased cardiac afterload, counteracting the increase in cardiac output. Both (C) dopamine and
dobutamine stimulate b2 receptors, w hich causes some degree of peripheral
vasodilatation (only at low doses for dopam ine). Norepinephrine is the firstline pressor of choice in septic shock.

Question 81

Has a dose-related effect
A. Dobutamine
B. Dopamine
C. Both
D. Neither

Answer 81

A. Dobutamine
B. Dopamine
C. Both
D. Neither

Dobutamine (A) is a strong b1 receptor agonist and a weak b2 receptor agonist. b1 stimulation causes a positive chronotropic and ionotropic effect.
Dobutamine (A) is typically used in patients with decompensated systolic heart failure who also have a normal blood pressure. Dopamine (B) has dosedependent effects and, at a low dose, causes changes in renal and splanchnic blood flow as well as increased sodium excretion by the kidneys. At intermediate doses, dopamine (B) has a positive ionotropic and chronotropic effect via agonism of b1 receptors, although the ionotropic effect of dopamine
is much less than that of dobutamine. At high doses, dopamine stimulates
a receptors, causing systemic vasoconstriction and increased cardiac afterload, counteracting the increase in cardiac output. Both (C) dopamine and
dobutamine stimulate b2 receptors, w hich causes some degree of peripheral
vasodilatation (only at low doses for dopam ine). Norepinephrine is the firstline pressor of choice in septic shock

Question 82

Of the following, the most common cause of neonatal meningitis is
A. H. influenzae
B. Listeria species
C. N. meningitidis
D. Staphylococci
E. Group B streptococci

Answer 82

A. H. influenzae
B. Listeria species
C. N. meningitidis
D. Staphylococci
E. Group B streptococci

Gram -negative bacilli (Escherichia coli) and group B streptococci (E) are
the most common causes of neonatal meningitis, followed by Listeria (B).
Streptococcus pneumoniae is the most common pathogen in the 4- to 12-week
age range. H. influenzae (A) is most common in the 3-m onth to 3-year
range. N. meningitidis (C) is the most common pathogen in children and
young adults.

Question 83

Each of the following is true of nitroprusside except’A. Cyanide accumulation may lead to metabolic acidosis
B. The cyanide is reduced to thiocyanate in the liver
C. The half-life of thiocyanate is 3 to 4 days
D. Thiocyanate is excreted in the gastrointestinal (GI) tract
E. With prolonged administration, accumulation of thiocyanate may cause an acute toxic psychosis

Answer 83

A. Cyanide accumulation may lead to metabolic acidosis
B. The cyanide is reduced to thiocyanate in the liver
C. The half-life of thiocyanate is 3 to 4 days
D. Thiocyanate is excreted in the gastrointestinal (GI) tract
E. With prolonged administration, accumulation of thiocyanate may cause an acute toxic psychosis

Nitroprusside is reduced by smooth muscle, and nitrous oxide and cyanide
are released. Cyanide is reduced to thiocyanate in the liver (B) by the action
of liver rhodanese, and the thiocyanate is then excreted in the urine (D is
false). The half-life of thiocyanate is 3 days (C) in patients w ith normal renal function. Prolonged adm inistration of nitroprusside or infusions at high doses may lead to accumulation of cyanide (causing lactic acidosis [A]) or
accumulation of thiocyanate (causing psychosis [E]).

Question 84

Isoproterenol
A. Acts almost exclusively on a -receptors
B. Decreases SBP
C. Increases DBP
D. Increases peripheral vascular resistance (PVR)
E. Relaxes smooth muscle

Answer 84

A. Acts almost exclusively on a -receptors
B. Decreases SBP
C. Increases DBP
D. Increases peripheral vascular resistance (PVR)
E. Relaxes smooth muscle

Isoproterenol is a nonselective b-receptor agonist, acting almost exclusively
on b receptors (A is false). It increases (or leaves unchanged) systolic blood
pressure (B is false) and decreases diastolic blood pressure (C is false), and
mean arterial pressure typically falls. It also decreases peripheral vascular
resistance (D is false) and relaxes smooth muscle (E)

Question 85

Splenectomy for hereditary spherocytosis
A. Corrects the anemia
B. Corrects the defects in red blood cells
C. Has no effect on red blood cell survival
D. Should not be preceded by vaccination
E. Should be perform ed before age 3

Answer 85

A. Corrects the anemia
B. Corrects the defects in red blood cells
C. Has no effect on red blood cell survival
D. Should not be preceded by vaccination
E. Should be perform ed before age 3

Splenectomy for hereditary spherocytosis leads to normal or near normal red blood cell (RBC) survival (B is false), correcting the anemia (A).
Splenectomy does not correct the underlying defect in red cell membrane
structure (B is false) and should be performed after age 4–5, when the risk
of severe infections is lower (E is false). Patients undergoing splenectomy
should be given a polyvalent pneumococcal vaccine several weeks before surgery to reduce the risk of bacterial sepsis (D is false).

Question 86

Epithelial migration occurs.
A. 12 hours
B. 5 days
C. 17 days
D. 42 days
E. 2 years

Answer 86

A. 12 hours
B. 5 days
C. 17 days
D. 42 days
E. 2 years

This question refers to the time line for wound healing associated with a
surgical incision w ith approximated edges (healing by primary intention).
In the first 12 hours of wound healing (A), epithelial cells migrate to the
wound edge laying down basement membrane as they travel, fusing in the
midline. Within 5 days (B) visible collagen synthesis has begun, the wound
begins to gain tensile strength, and wound contraction begins. Within
6 weeks (42 days [D]), the wound reaches its maximum amount of total collagen and collagen synthesis slows considerably. The wound may not reach its greatest tensile strength for a full 2 years (E).

Question 87

Increase in tensile strength occurs at least up to this point.
A. 12 hours
B. 5 days
C. 17 days
D. 42 days
E. 2 years

Answer 87

A. 12 hours
B. 5 days
C. 17 days
D. 42 days
E. 2 years

This question refers to the time line for wound healing associated with a
surgical incision w ith approximated edges (healing by primary intention).
In the first 12 hours of wound healing (A), epithelial cells migrate to the
wound edge laying down basement membrane as they travel, fusing in the
midline. Within 5 days (B) visible collagen synthesis has begun, the wound
begins to gain tensile strength, and wound contraction begins. Within
6 weeks (42 days [D]), the wound reaches its maximum amount of total collagen and collagen synthesis slows considerably. The wound may not reach its greatest tensile strength for a full 2 years (E).

Question 88

Wound contraction begins.

Answer 88

A. 12 hours
B. 5 days
C. 17 days
D. 42 days
E. 2 years

This question refers to the time line for wound healing associated with a
surgical incision w ith approximated edges (healing by primary intention).
In the first 12 hours of wound healing (A), epithelial cells migrate to the
wound edge laying down basement membrane as they travel, fusing in the
midline. Within 5 days (B) visible collagen synthesis has begun, the wound
begins to gain tensile strength, and wound contraction begins. Within
6 weeks (42 days [D]), the wound reaches its maximum amount of total collagen and collagen synthesis slows considerably. The wound may not reach its greatest tensile strength for a full 2 years (E).

Question 89

Maximum amount of total collagen occurs at this time.
A. 12 hours
B. 5 days
C. 17 days
D. 42 days
E. 2 years

Answer 89

A. 12 hours
B. 5 days
C. 17 days
D. 42 days
E. 2 years

This question refers to the time line for wound healing associated with a
surgical incision w ith approximated edges (healing by primary intention).
In the first 12 hours of wound healing (A), epithelial cells migrate to the
wound edge laying down basement membrane as they travel, fusing in the
midline. Within 5 days (B) visible collagen synthesis has begun, the wound
begins to gain tensile strength, and wound contraction begins. Within
6 weeks (42 days [D]), the wound reaches its maximum amount of total collagen and collagen synthesis slows considerably. The wound may not reach its greatest tensile strength for a full 2 years (E).

Question 90

Visible collagen synthesis begins.
A. 12 hours
B. 5 days
C. 17 days
D. 42 days
E. 2 years

Answer 90

A. 12 hours
B. 5 days
C. 17 days
D. 42 days
E. 2 years

This question refers to the time line for wound healing associated with a
surgical incision w ith approximated edges (healing by primary intention).
In the first 12 hours of wound healing (A), epithelial cells migrate to the
wound edge laying down basement membrane as they travel, fusing in the
midline. Within 5 days (B) visible collagen synthesis has begun, the wound
begins to gain tensile strength, and wound contraction begins. Within
6 weeks (42 days [D]), the wound reaches its maximum amount of total collagen and collagen synthesis slows considerably. The wound may not reach its greatest tensile strength for a full 2 years (E).

Question 91

Significant gain in tensile strength begins at this time.
A. 12 hours
B. 5 days
C. 17 days
D. 42 days
E. 2 years

Answer 91

A. 12 hours
B. 5 days
C. 17 days
D. 42 days
E. 2 years

This question refers to the time line for wound healing associated with a
surgical incision w ith approximated edges (healing by primary intention).
In the first 12 hours of wound healing (A), epithelial cells migrate to the
wound edge laying down basement membrane as they travel, fusing in the
midline. Within 5 days (B) visible collagen synthesis has begun, the wound
begins to gain tensile strength, and wound contraction begins. Within
6 weeks (42 days [D]), the wound reaches its maximum amount of total collagen and collagen synthesis slows considerably. The wound may not reach its greatest tensile strength for a full 2 years (E).

Question 92

The rapid increase in collagen content slows considerably at this point.
A. 12 hours
B. 5 days
C. 17 days
D. 42 days
E. 2 years

Answer 92

A. 12 hours
B. 5 days
C. 17 days
D. 42 days
E. 2 years

This question refers to the time line for wound healing associated with a
surgical incision w ith approximated edges (healing by primary intention).
In the first 12 hours of wound healing (A), epithelial cells migrate to the
wound edge laying down basement membrane as they travel, fusing in the
midline. Within 5 days (B) visible collagen synthesis has begun, the wound
begins to gain tensile strength, and wound contraction begins. Within
6 weeks (42 days [D]), the wound reaches its maximum amount of total collagen and collagen synthesis slows considerably. The wound may not reach its greatest tensile strength for a full 2 years (E).

Question 93

Each of the following is consistent with the Zollinger-Ellison syndrome except a(n)
A. Decrease in serum gastrin with secretin injection
B. Duodenal ulcer
C. Duodenal wall gastrinoma
D. Pancreatic gastrinoma
E. Increased serum gastrin level

Answer 93

A. Decrease in serum gastrin with secretin injection
B. Duodenal ulcer
C. Duodenal wall gastrinoma
D. Pancreatic gastrinoma
E. Increased serum gastrin level

Gastrinomas of the pancreas (D) or duodenal wall (C) cause an increase in the serum gastrin level (E). Peptic ulcer disease of the duodenum (B) caused by gastric acid production associated w ith a gastrinoma is known as the Zollinger-Ellison syndrome. Intravenous secretin increases serum gastrin
in patients w ith a gastrinoma (A is false)

Question 94

Non-anion gap acidosis
A. Type I (distal) renal tubular acidosis (RTA)
B. Type II (proximal) RTA
C. Both
D. Neither

Answer 94

A. Type I (distal) renal tubular acidosis (RTA)
B. Type II (proximal) RTA
C. Both
D. Neither

Type I (classic, or distal) renal tubular acidosis (RTA; A) is a hypokalemic, hyperchloremic metabolic acidosis caused by a selective defect in distal acidification (inability to lower urinary pH sufficiently in the distal nephron). The urinary pH is therefore inappropriately high in type I RTA (A) w ith a urine
pH . 5.5. Nephrocalcinosis and nephrolithiasis are common in type I RTA (A).
Type II (proximal) RTA (B) is a hyperchlorem ic, hypokalemic metabolic acidosis that is caused by a selective defect in proximal acidification—urine pH
is usually acidic in periods of acidosis. Proximal RTA (B) is rare and usually
found in patients with Fanconiʼs syndrome. The loss of 15% or more of filltered
bicarbonate at a normal serum bicarbonate level is pathognomonic of RTA
type II (B). Hyperkalemia is found in RTA type IV. Nephrocalcinosis is rare
in RTA type II (B), and the urine pH is less than 5.5 in this type. Both (C) RTA
type I and t ype II result in non-anion gap metabolic acidosis.

Question 95

Hyperkalemia
A. Type I (distal) renal tubular acidosis (RTA)
B. Type II (proximal) RTA
C. Both
D. Neither

Answer 95

A. Type I (distal) renal tubular acidosis (RTA)
B. Type II (proximal) RTA
C. Both
D. Neither

Type I (classic, or distal) renal tubular acidosis (RTA; A) is a hypokalemic, hyperchloremic metabolic acidosis caused by a selective defect in distal acidification (inability to lower urinary pH sufficiently in the distal nephron). The urinary pH is therefore inappropriately high in type I RTA (A) w ith a urine
pH . 5.5. Nephrocalcinosis and nephrolithiasis are common in type I RTA (A).
Type II (proximal) RTA (B) is a hyperchlorem ic, hypokalemic metabolic acidosis that is caused by a selective defect in proximal acidification—urine pH
is usually acidic in periods of acidosis. Proximal RTA (B) is rare and usually
found in patients with Fanconiʼs syndrome. The loss of 15% or more of filltered
bicarbonate at a normal serum bicarbonate level is pathognomonic of RTA
type II (B). Hyperkalemia is found in RTA type IV. Nephrocalcinosis is rare
in RTA type II (B), and the urine pH is less than 5.5 in this type. Both (C) RTA
type I and t ype II result in non-anion gap metabolic acidosis.

Question 96

Nephrocalcinosis commonly occurs.
A. Type I (distal) renal tubular acidosis (RTA)
B. Type II (proximal) RTA
C. Both
D. Neither

Answer 96

A. Type I (distal) renal tubular acidosis (RTA)
B. Type II (proximal) RTA
C. Both
D. Neither

Type I (classic, or distal) renal tubular acidosis (RTA; A) is a hypokalemic, hyperchloremic metabolic acidosis caused by a selective defect in distal acidification (inability to lower urinary pH sufficiently in the distal nephron). The urinary pH is therefore inappropriately high in type I RTA (A) w ith a urine
pH . 5.5. Nephrocalcinosis and nephrolithiasis are common in type I RTA (A).
Type II (proximal) RTA (B) is a hyperchlorem ic, hypokalemic metabolic acidosis that is caused by a selective defect in proximal acidification—urine pH
is usually acidic in periods of acidosis. Proximal RTA (B) is rare and usually
found in patients with Fanconiʼs syndrome. The loss of 15% or more of filltered
bicarbonate at a normal serum bicarbonate level is pathognomonic of RTA
type II (B). Hyperkalemia is found in RTA type IV. Nephrocalcinosis is rare
in RTA type II (B), and the urine pH is less than 5.5 in this type. Both (C) RTA
type I and t ype II result in non-anion gap metabolic acidosis.

Question 97

Urine pH . 5.5
A. Type I (distal) renal tubular acidosis (RTA)
B. Type II (proximal) RTA
C. Both
D. Neither

Answer 97

A. Type I (distal) renal tubular acidosis (RTA)
B. Type II (proximal) RTA
C. Both
D. Neither

Type I (classic, or distal) renal tubular acidosis (RTA; A) is a hypokalemic, hyperchloremic metabolic acidosis caused by a selective defect in distal acidification (inability to lower urinary pH sufficiently in the distal nephron). The urinary pH is therefore inappropriately high in type I RTA (A) w ith a urine
pH . 5.5. Nephrocalcinosis and nephrolithiasis are common in type I RTA (A).
Type II (proximal) RTA (B) is a hyperchlorem ic, hypokalemic metabolic acidosis that is caused by a selective defect in proximal acidification—urine pH
is usually acidic in periods of acidosis. Proximal RTA (B) is rare and usually
found in patients with Fanconiʼs syndrome. The loss of 15% or more of filltered
bicarbonate at a normal serum bicarbonate level is pathognomonic of RTA
type II (B). Hyperkalemia is found in RTA type IV. Nephrocalcinosis is rare
in RTA type II (B), and the urine pH is less than 5.5 in this type. Both (C) RTA
type I and t ype II result in non-anion gap metabolic acidosis.

Question 98

Defect in reabsorption of bicarbonate
A. Type I (distal) renal tubular acidosis (RTA)
B. Type II (proximal) RTA
C. Both
D. Neither

Answer 98

A. Type I (distal) renal tubular acidosis (RTA)
B. Type II (proximal) RTA
C. Both
D. Neither

Type I (classic, or distal) renal tubular acidosis (RTA; A) is a hypokalemic, hyperchloremic metabolic acidosis caused by a selective defect in distal acidification (inability to lower urinary pH sufficiently in the distal nephron). The urinary pH is therefore inappropriately high in type I RTA (A) w ith a urine
pH . 5.5. Nephrocalcinosis and nephrolithiasis are common in type I RTA (A).
Type II (proximal) RTA (B) is a hyperchlorem ic, hypokalemic metabolic acidosis that is caused by a selective defect in proximal acidification—urine pH
is usually acidic in periods of acidosis. Proximal RTA (B) is rare and usually
found in patients with Fanconiʼs syndrome. The loss of 15% or more of filltered
bicarbonate at a normal serum bicarbonate level is pathognomonic of RTA
type II (B). Hyperkalemia is found in RTA type IV. Nephrocalcinosis is rare
in RTA type II (B), and the urine pH is less than 5.5 in this type. Both (C) RTA
type I and t ype II result in non-anion gap metabolic acidosis.

Question 99

Hypokalemia
A. Type I (distal) renal tubular acidosis (RTA)
B. Type II (proximal) RTA
C. Both
D. Neither

Answer 99

A. Type I (distal) renal tubular acidosis (RTA)
B. Type II (proximal) RTA
C. Both
D. Neither

Type I (classic, or distal) renal tubular acidosis (RTA; A) is a hypokalemic, hyperchloremic metabolic acidosis caused by a selective defect in distal acidification (inability to lower urinary pH sufficiently in the distal nephron). The urinary pH is therefore inappropriately high in type I RTA (A) w ith a urine
pH . 5.5. Nephrocalcinosis and nephrolithiasis are common in type I RTA (A).
Type II (proximal) RTA (B) is a hyperchlorem ic, hypokalemic metabolic acidosis that is caused by a selective defect in proximal acidification—urine pH
is usually acidic in periods of acidosis. Proximal RTA (B) is rare and usually
found in patients with Fanconiʼs syndrome. The loss of 15% or more of filltered
bicarbonate at a normal serum bicarbonate level is pathognomonic of RTA
type II (B). Hyperkalemia is found in RTA type IV. Nephrocalcinosis is rare
in RTA type II (B), and the urine pH is less than 5.5 in this type. Both (C) RTA
type I and t ype II result in non-anion gap metabolic acidosis.

Question 100

The percentage of extracellularfluid represented by plasma volume is approximately
A. 5%
B. 15%
C. 20%
D. 40%
E. 60%

Answer 100

A. 5%
B. 15%
C. 20%
D. 40%
E. 60%

For the average adult male, total body water (TBW) makes up approximately 60% (E) of body weight. Intracellular fluid makes up 60% (E) of the TBW and extracellular fluid makes up 40% (D) of the TBW. Extracellular fluid is com prised of interstitial fluid (75%), transcellular fluid (5%), and
blood plasma (20% [C]).

Question 101

Each of the following occurs in venous air embolism except a(n)
A. Decrease in cardiac output
B. Increase in end-tidal pCO2
C. Increase in pulmonary artery pressure
D. Increase in pulmonary vascular resistance
E. Ventilation-perfusion mismatch

Answer 101

A. Decrease in cardiac output
B. Increase in end-tidal pCO2
C. Increase in pulmonary artery pressure
D. Increase in pulmonary vascular resistance
E. Ventilation-perfusion mismatch

Small air bubbles in the circulation can obstruct vascular flow. Venous air
embolism can travel to the pulmonary circulation obstructing small vessels, causing pulmonary vasoconstriction, increased pulmonary vascular resistance (D), and, therefore, increased pulmonary artery pressure (C).
Decreased pulmonary perfusion in areas of preserved ventilation results in a
ventilation–perfusion m ism atch (E) leading to decreased end-tidal pCO2
(B is false). Air in the right atrium may lead to im paired cardiac filling, and
therefore a reduction in cardiac output (A)

Question 102

The most sensitive noninvasive monitor of venous air embolism is
A. Auscultation of the chest w th a stethoscope
B. End-tidal pCO2
C. End-tidal pN2
D. Precordial Doppler
E. Pulm onary artery catheterization

Answer 102

A. Auscultation of the chest w th a stethoscope
B. End-tidal pCO2
C. End-tidal pN2
D. Precordial Doppler
E. Pulm onary artery catheterization

The most sensitive test for venous air embolism is transesophageal echocardiography. The most sensitive noninvasive monitor is the
precordial Doppler (D).

Question 103

Which EKG change in the anterior leads is the most characteristic finding in subendocardial ischemia?
A. Hyperacute T wave
B. Q wave
C. ST depression
D. ST elevation
E. T wave inversion

Answer 103

A. Hyperacute T wave
B. Q wave
C. ST depression
D. ST elevation
E. T wave inversion

Subendocardial ischemia is associated w ith ST depression (C) in the anterior leads. Transmural ischemia may lead to ST elevation (D) in the
electrocardiogram (EKG).

Question 104

Which set of laboratory values is most consistent with hypothyroidism of hypothalamic or pituitary origin?
A. Decreased thyroid-stimulating hormone (TSH) and decreased free thyroxine (T4)
B. Decreased TSH and increased free T4
C. Decreased TSH and normal free T4
D. Increased TSH and decreased free T4
E. Increased TSH and increased free T4

Answer 104

A. Decreased thyroid-stimulating hormone (TSH) and decreased free thyroxine (T4)
B. Decreased TSH and increased free T4
C. Decreased TSH and normal free T4
D. Increased TSH and decreased free T4
E. Increased TSH and increased free T4

Under normal conditions, thyrotropin-releasing hormone (TRH) is secreted
by the hypothalamus, driving TSH production by the anterior pituitary and
T4 production by the thyroid gland. Primary hypothyroidism is caused by
dysfunction of the thyroid gland itself, and would result in increased levels
of TSH and TRH w ith low T4 levels (D). In cases of secondary or tertiary hypothyroidism (pituitary or hypothalam ic dysfunction, respectively), there is a
reduction in T4 levels as well as a reduction in TSH levels (A). To distinguish
between secondary and tertiary hypothyroidism , a TRH challenge must be
administered, and the TSH response measured (as TRH is diffcult to measure
in vivo). In cases of tertiary hypothyroidism (hypothalam ic dysfunction), the
pituitary gland will appropriately produce TSH in response to a TRH challenge.
In secondary hypothyroidism (pituitary dysfunction), the pituitary gland will
not produce TSH in response to a TRH challenge test. Choices B and E are
hyperthyroid states (increased free T4). Choice C is a euthyroid state (norm al free T4). Note: Occasionally, in patients w ith hypothyroidism of pituitary
or hypothalamic origin, serum TSH concentrations may be slightly increased
rather than decreased if the form of TSH secreted is immunoactive but not
bioactive

Question 105

Of the following treatment options for hyperkalemia, which one does not alter serum potassium ?
A. Calcium
B. Cation-exchange resins
C. Hemodialysis
D. Insulin
E. Sodium bicarbonate

Answer 105

A. Calcium
B. Cation-exchange resins
C. Hemodialysis
D. Insulin
E. Sodium bicarbonate

Calcium gluconate (A) infusion is useful for cardiotoxicity (antagonizes the
membrane effects of potassium ), but it does not reduce serum potassium
concentrations. Cation-exchange resins (B) such as Kayexalate enhance potassium clearance across the intestinal mucosa reducing serum potassium .
Hemodialysis (C) is effective for reducing the serum potassium concentration
in patients with renal failure. The administration of insulin (D) and dextrose
causes a transient decrease in serum potassium levels by driving potassium
into muscle cells. The administration of sodium bicarbonate (E) also causes a
transient reduction in serum potassium levels via cellular shifts.

Question 106

pH= 7.5, pCO2= 30, HCO3= 19
A. Respiratory acidosis
B. Respiratory acidosis and metabolic acidosis
C. Metabolic acidosis
D. Metabolic acidosis and compensatory respiratory alkalosis
E. Respiratory alkalosis
F. Respiratory alkalosis and compensatory metabolic acidosis
G. Uninterpretable

Answer 106

A. Respiratory acidosis
B. Respiratory acidosis and metabolic acidosis
C. Metabolic acidosis
D. Metabolic acidosis and compensatory respiratory alkalosis
E. Respiratory alkalosis
F. Respiratory alkalosis and compensatory metabolic acidosis
G. Uninterpretable

The first step in the diagnosis of acid–base disorders is determining whether
the primary abnormality is an acidosis or an alkalosis, which can be determined by the pH. If the pH and pCO2 are both abnormal, a change in the same direction indicates a primary metabolic disorder; a change in opposite directions indicates a primary respiratory disorder. If either the pH or pCO2 is normal, there must be a mixed m etabolic and respiratory disorder; if the pH is
normal, the direction change in PaCO2 identifies the nature of the respiratory
disorder, and if the PaCO2 is normal, the change in pH identifies the nature of
the metabolic disorder. If there is a prim ary metabolic alkalosis or acidosis,
the measured serum bicarbonate should be used to calculate the expected pCO2. If the measured pCO2 is higher than predicted by the formula, a respiratory acidosis is also present. If the measured pCO2 is lower than predicted by the formula, a respiratory alkalosis is present. If a primary respiratory acidosis or alkalosis is present, the measured PaCO2 should be used to calculate an
expected pH value. If the pH is lower than expected, a metabolic acidosis is
also present. If the pH is higher than expected, a metabolic alkalosis is also
present. Formulas helpful in the calculation of simple acid–base disturbances are listed here

Question 107

pH= 7.3, pCO2= 52, HCO3= 29
A. Respiratory acidosis
B. Respiratory acidosis and metabolic acidosis
C. Metabolic acidosis
D. Metabolic acidosis and compensatory respiratory alkalosis
E. Respiratory alkalosis
F. Respiratory alkalosis and compensatory metabolic acidosis
G. Uninterpretable

Answer 107

A. Respiratory acidosis
B. Respiratory acidosis and metabolic acidosis
C. Metabolic acidosis
D. Metabolic acidosis and compensatory respiratory alkalosis
E. Respiratory alkalosis
F. Respiratory alkalosis and compensatory metabolic acidosis
G. Uninterpretable

The first step in the diagnosis of acid–base disorders is determining whether
the primary abnormality is an acidosis or an alkalosis, which can be determined by the pH. If the pH and pCO2 are both abnormal, a change in the same direction indicates a primary metabolic disorder; a change in opposite directions indicates a primary respiratory disorder. If either the pH or pCO2 is normal, there must be a mixed m etabolic and respiratory disorder; if the pH is
normal, the direction change in PaCO2 identifies the nature of the respiratory
disorder, and if the PaCO2 is normal, the change in pH identifies the nature of
the metabolic disorder. If there is a prim ary metabolic alkalosis or acidosis,
the measured serum bicarbonate should be used to calculate the expected pCO2. If the measured pCO2 is higher than predicted by the formula, a respiratory acidosis is also present. If the measured pCO2 is lower than predicted by the formula, a respiratory alkalosis is present. If a primary respiratory acidosis or alkalosis is present, the measured PaCO2 should be used to calculate an
expected pH value. If the pH is lower than expected, a metabolic acidosis is
also present. If the pH is higher than expected, a metabolic alkalosis is also
present. Formulas helpful in the calculation of simple acid–base disturbances are listed here

Question 108

pH= 7.35, pCO2= 17, HCO3= 9
A. Respiratory acidosis
B. Respiratory acidosis and metabolic acidosis
C. Metabolic acidosis
D. Metabolic acidosis and compensatory respiratory alkalosis
E. Respiratory alkalosis
F. Respiratory alkalosis and compensatory metabolic acidosis
G. Uninterpretable

Answer 108

A. Respiratory acidosis
B. Respiratory acidosis and metabolic acidosis
C. Metabolic acidosis
D. Metabolic acidosis and compensatory respiratory alkalosis
E. Respiratory alkalosis
F. Respiratory alkalosis and compensatory metabolic acidosis
G. Uninterpretable

The first step in the diagnosis of acid–base disorders is determining whether
the primary abnormality is an acidosis or an alkalosis, which can be determined by the pH. If the pH and pCO2 are both abnormal, a change in the same direction indicates a primary metabolic disorder; a change in opposite directions indicates a primary respiratory disorder. If either the pH or pCO2 is normal, there must be a mixed m etabolic and respiratory disorder; if the pH is
normal, the direction change in PaCO2 identifies the nature of the respiratory
disorder, and if the PaCO2 is normal, the change in pH identifies the nature of
the metabolic disorder. If there is a prim ary metabolic alkalosis or acidosis,
the measured serum bicarbonate should be used to calculate the expected pCO2. If the measured pCO2 is higher than predicted by the formula, a respiratory acidosis is also present. If the measured pCO2 is lower than predicted by the formula, a respiratory alkalosis is present. If a primary respiratory acidosis or alkalosis is present, the measured PaCO2 should be used to calculate an
expected pH value. If the pH is lower than expected, a metabolic acidosis is
also present. If the pH is higher than expected, a metabolic alkalosis is also
present. Formulas helpful in the calculation of simple acid–base disturbances are listed here

Question 109

pH= 7.55, pCO2= 32, HCO3= 12
A. Respiratory acidosis
B. Respiratory acidosis and metabolic acidosis
C. Metabolic acidosis
D. Metabolic acidosis and compensatory respiratory alkalosis
E. Respiratory alkalosis
F. Respiratory alkalosis and compensatory metabolic acidosis
G. Uninterpretable

Answer 109

A. Respiratory acidosis
B. Respiratory acidosis and metabolic acidosis
C. Metabolic acidosis
D. Metabolic acidosis and compensatory respiratory alkalosis
E. Respiratory alkalosis
F. Respiratory alkalosis and compensatory metabolic acidosis
G. Uninterpretable

The first step in the diagnosis of acid–base disorders is determining whether
the primary abnormality is an acidosis or an alkalosis, which can be determined by the pH. If the pH and pCO2 are both abnormal, a change in the same direction indicates a primary metabolic disorder; a change in opposite directions indicates a primary respiratory disorder. If either the pH or pCO2 is normal, there must be a mixed m etabolic and respiratory disorder; if the pH is
normal, the direction change in PaCO2 identifies the nature of the respiratory
disorder, and if the PaCO2 is normal, the change in pH identifies the nature of
the metabolic disorder. If there is a prim ary metabolic alkalosis or acidosis,
the measured serum bicarbonate should be used to calculate the expected pCO2. If the measured pCO2 is higher than predicted by the formula, a respiratory acidosis is also present. If the measured pCO2 is lower than predicted by the formula, a respiratory alkalosis is present. If a primary respiratory acidosis or alkalosis is present, the measured PaCO2 should be used to calculate an
expected pH value. If the pH is lower than expected, a metabolic acidosis is
also present. If the pH is higher than expected, a metabolic alkalosis is also
present. Formulas helpful in the calculation of simple acid–base disturbances are listed here

Question 110

pH= 7.22, pCO2= 55, HCO3= 22
A. Respiratory acidosis
B. Respiratory acidosis and metabolic acidosis
C. Metabolic acidosis
D. Metabolic acidosis and compensatory respiratory alkalosis
E. Respiratory alkalosis
F. Respiratory alkalosis and compensatory metabolic acidosis
G. Uninterpretable

Answer 110

A. Respiratory acidosis
B. Respiratory acidosis and metabolic acidosis
C. Metabolic acidosis
D. Metabolic acidosis and compensatory respiratory alkalosis
E. Respiratory alkalosis
F. Respiratory alkalosis and compensatory metabolic acidosis
G. Uninterpretable

The first step in the diagnosis of acid–base disorders is determining whether
the primary abnormality is an acidosis or an alkalosis, which can be determined by the pH. If the pH and pCO2 are both abnormal, a change in the same direction indicates a primary metabolic disorder; a change in opposite directions indicates a primary respiratory disorder. If either the pH or pCO2 is normal, there must be a mixed m etabolic and respiratory disorder; if the pH is
normal, the direction change in PaCO2 identifies the nature of the respiratory
disorder, and if the PaCO2 is normal, the change in pH identifies the nature of
the metabolic disorder. If there is a prim ary metabolic alkalosis or acidosis,
the measured serum bicarbonate should be used to calculate the expected pCO2. If the measured pCO2 is higher than predicted by the formula, a respiratory acidosis is also present. If the measured pCO2 is lower than predicted by the formula, a respiratory alkalosis is present. If a primary respiratory acidosis or alkalosis is present, the measured PaCO2 should be used to calculate an
expected pH value. If the pH is lower than expected, a metabolic acidosis is
also present. If the pH is higher than expected, a metabolic alkalosis is also
present. Formulas helpful in the calculation of simple acid–base disturbances are listed here

Question 111

pH= 7.25, pCO2= 28, HCO3= 12
A. Respiratory acidosis
B. Respiratory acidosis and metabolic acidosis
C. Metabolic acidosis
D. Metabolic acidosis and compensatory respiratory alkalosis
E. Respiratory alkalosis
F. Respiratory alkalosis and compensatory metabolic acidosis
G. Uninterpretable

Answer 111

A. Respiratory acidosis
B. Respiratory acidosis and metabolic acidosis
C. Metabolic acidosis
D. Metabolic acidosis and compensatory respiratory alkalosis
E. Respiratory alkalosis
F. Respiratory alkalosis and compensatory metabolic acidosis
G. Uninterpretable

The first step in the diagnosis of acid–base disorders is determining whether
the primary abnormality is an acidosis or an alkalosis, which can be determined by the pH. If the pH and pCO2 are both abnormal, a change in the same direction indicates a primary metabolic disorder; a change in opposite directions indicates a primary respiratory disorder. If either the pH or pCO2 is normal, there must be a mixed m etabolic and respiratory disorder; if the pH is
normal, the direction change in PaCO2 identifies the nature of the respiratory
disorder, and if the PaCO2 is normal, the change in pH identifies the nature of
the metabolic disorder. If there is a prim ary metabolic alkalosis or acidosis,
the measured serum bicarbonate should be used to calculate the expected pCO2. If the measured pCO2 is higher than predicted by the formula, a respiratory acidosis is also present. If the measured pCO2 is lower than predicted by the formula, a respiratory alkalosis is present. If a primary respiratory acidosis or alkalosis is present, the measured PaCO2 should be used to calculate an
expected pH value. If the pH is lower than expected, a metabolic acidosis is
also present. If the pH is higher than expected, a metabolic alkalosis is also
present. Formulas helpful in the calculation of simple acid–base disturbances are listed here

Question 112

If Qs and Qt are pulmonary shunt and total blood flow, respectively, and Cc, Ca, and Cv are the oxygen contents of end-capillary, arterial, and mixed venous blood, respectively, then the shunt fraction Qs/Qt =
A. Cc/(Cc 2 Cv)
B. (Ca 2 Cv)/Cv
C. (Cv 2 Ca)/Cc
D. (Cc 2 Ca)/(Cc 2 Cv)
E. (Ca 1 Cv)/(Ca 1 Cc 1 Cv)

Answer 112

A. Cc/(Cc 2 Cv)
B. (Ca 2 Cv)/Cv
C. (Cv 2 Ca)/Cc
D. (Cc 2 Ca)/(Cc 2 Cv)
E. (Ca 1 Cv)/(Ca 1 Cc 1 Cv)

The shunt fraction is the portion of the cardiac output that represents the
intrapulmonary shunt (Qs/Qt). The shunt fraction can be estimated from
measurements of the oxygen content of arterial blood, mixed venous
blood, and pulmonary capillary blood. The shunt fraction is expressed
as (Qs/Qt) 5 [(Cc 2 Ca )/(Cc 2 Cv)] (D). Since pulmonary capillary oxygen tension cannot be directly measured, it is estimated with the patient on 100% O2.

Question 113

Atropine toxicity produces each of the following except’A. Blurred vision
B. Decreased intestinal peristalsis
C. Dry mouth
D. Increased pulse
E. Increased sweating

Answer 113

A. Blurred vision
B. Decreased intestinal peristalsis
C. Dry mouth
D. Increased pulse
E. Increased sweating

High doses of atropine ( 10 mg) may cause a rapid, thready pulse (D); blurry vision (A); skin dryness and flushing; ataxia, hallucinations; dry mouth (C); delirium ; urinary retention; decreased intestinal peristalsis (B); dilated pupils; and com a. Decreased sweating is a manifestation of atropine toxicity (E is false).

Question 114

Each of the following is true of hyperosmolar coma exceptA. Free fatty acid concentration is lower than in ketoacidosis
B. Glucose concentration is higher than in ketoacidosis
C. It is more common in type 1 diabetes mellitus than in type 2 diabetes mellitus
D. Mortality is more than 50%
E. Volume depletion is usually severe

Answer 114

A. Free fatty acid concentration is lower than in ketoacidosis
B. Glucose concentration is higher than in ketoacidosis
C. It is more common in type 1 diabetes mellitus than in type 2 diabetes mellitus
D. Mortality is more than 50%
E. Volume depletion is usually severe

Hyperosmolar, nonketotic diabetic coma is usually a complication of type 2
diabetes mellitus (C is false). The other responses regarding hyperosmolar
nonketotic coma are true. The free fatty acid and glucose concentrations tend
to be higher than in ketoacidosis (A and B). Volume depletion is usually m ore
severe (E) than in ketoacidosis, and mortality is greater than 50% (D).

Question 115

b agonist

A. Clonidine
B. Isoproterenol
C. Phenoxybenzamine
D. Phentolamine
E. Prazosin

Answer 115

A. Clonidine
B. Isoproterenol
C. Phenoxybenzamine
D. Phentolamine
E. Prazosin

Clonidine (A) is a centrally acting a 2 receptor agonist that is used in the treatment of hypertension. Isoproterenol (B) is a nonselective b agonist. Phenoxybenzamine (C) is an irreversible a agonist that is somewhat selective for a 1 receptors. Phentolamine (D) is a competitive nonselective antagonist at a 1
and a 2 receptors. Prazosin (E) is a highly selective a 1 agonist

Question 116

Pure a 1 antagonist
A. Clonidine
B. Isoproterenol
C. Phenoxybenzamine
D. Phentolamine
E. Prazosin

Answer 116

A. Clonidine
B. Isoproterenol
C. Phenoxybenzamine
D. Phentolamine
E. Prazosin

Clonidine (A) is a centrally acting a 2 receptor agonist that is used in the treatment of hypertension. Isoproterenol (B) is a nonselective b agonist. Phenoxybenzamine (C) is an irreversible a agonist that is somewhat selective for a 1 receptors. Phentolamine (D) is a competitive nonselective antagonist at a 1
and a 2 receptors. Prazosin (E) is a highly selective a 1 agonist

Question 117

Noncompetitive a antagonist
A. Clonidine
B. Isoproterenol
C. Phenoxybenzamine
D. Phentolamine
E. Prazosin

Answer 117

A. Clonidine
B. Isoproterenol
C. Phenoxybenzamine
D. Phentolamine
E. Prazosin

Clonidine (A) is a centrally acting a 2 receptor agonist that is used in the treatment of hypertension. Isoproterenol (B) is a nonselective b agonist. Phenoxybenzamine (C) is an irreversible a agonist that is somewhat selective for a 1 receptors. Phentolamine (D) is a competitive nonselective antagonist at a 1
and a 2 receptors. Prazosin (E) is a highly selective a 1 agonist

Question 118

Competitive, nonselective a antagonist
A. Clonidine
B. Isoproterenol
C. Phenoxybenzamine
D. Phentolamine
E. Prazosin

Answer 118

A. Clonidine
B. Isoproterenol
C. Phenoxybenzamine
D. Phentolamine
E. Prazosin

Clonidine (A) is a centrally acting a 2 receptor agonist that is used in the treatment of hypertension. Isoproterenol (B) is a nonselective b agonist. Phenoxybenzamine (C) is an irreversible a agonist that is somewhat selective for a 1 receptors. Phentolamine (D) is a competitive nonselective antagonist at a 1
and a 2 receptors. Prazosin (E) is a highly selective a 1 agonist

Question 119

Central a 2 agonist
A. Clonidine
B. Isoproterenol
C. Phenoxybenzamine
D. Phentolamine
E. Prazosin

Answer 119

A. Clonidine
B. Isoproterenol
C. Phenoxybenzamine
D. Phentolamine
E. Prazosin

Clonidine (A) is a centrally acting a 2 receptor agonist that is used in the treatment of hypertension. Isoproterenol (B) is a nonselective b agonist. Phenoxybenzamine (C) is an irreversible a agonist that is somewhat selective for a 1 receptors. Phentolamine (D) is a competitive nonselective antagonist at a 1
and a 2 receptors. Prazosin (E) is a highly selective a 1 agonist

Question 120

The most appropriate cholinergic agent to be used in urinary retention is
A. Acetylcholine
B. Bethanechol
C. Carbachol
D. Choline
E. Methacholine

Answer 120

A. Acetylcholine
B. Bethanechol
C. Carbachol
D. Choline
E. Methacholine

Bethanechol (B) and carbachol (C) selectively stim ulate the urinary and gastrointestinal (GI) tract. Carbachol (C) is less desirable for urinary retention, however, because it has greater nicotinic action at autonom ic ganglia.

Question 121

Which of the following is false of polycythemia vera
A. Budd-Chiari syndrome is common.
B. Hyperuricemia can complicate the disorder.
C. It is the most common of the myeloproliferative disorders.
D. Massive splenomegaly is usually the presenting sign.
E. The use of alkylating agents should be avoided.

Answer 121

A. Budd-Chiari syndrome is common.
B. Hyperuricemia can complicate the disorder.
C. It is the most common of the myeloproliferative disorders.
D. Massive splenomegaly is usually the presenting sign.
E. The use of alkylating agents should be avoided.

Polycythemia vera is a chronic myeloproliferative disorder that results
in increased red cell mass. It is the most common of the myeloproliferative disorders (C). More than 20% of patients present w ith thrombosis; there is a 10% incidence of abdominal major vessel thrombosis such as the Budd-Chiari syndrome (A). The diagnosis is generally made by increased
hemoglobin and hematocrit on routine CBC (D is false). Hyperuricemia may complicate the disorder (B), and alkylating agents are generally avoided (E). Although massive splenomegaly can be the presenting sign, the
disorder is usually first recognized by a high hematocrit (D is false).

Question 122

The serum osmolarity of a patient with a sodium level of 130 m eq/L, K of 4.0 m eq/L, glucose of 126 mg/dL, and blood urea nitrogen (BUN) of 28 m g/dL is
A. 276
B. 285
C. 296
D. 304
E. 310

Answer 122

A. 276
B. 285
C. 296
D. 304
E. 310

Serum osmolarity can be calculated from the formula
Serum osmolarity = 2(Na 1 K) 1 Glucose/18 1 BUN/2.8
= 2(130 1 4) 1 126/18 1 28/2.8
= 2(134) 1 7 1 10 5 285,
where BUN = blood urea nitrogen

Question 123

Each of the following is a result of the use of positive end-expiratory pressure (PEEP) in the ventilated patient except
A. Decreased cerebral perfusion pressure
B. Decreased physiologic dead space
C. Decreased work of breathing
D. Improved lung compliance
E. Predisposition to barotraumas

Answer 123

A. Decreased cerebral perfusion pressure
B. Decreased physiologic dead space
C. Decreased work of breathing
D. Improved lung compliance
E. Predisposition to barotraumas

Positive end-expiratory pressure (PEEP) increases physiologic dead space
(B is false) by raising intra-alveolar pressure and lung perfusion, thereby impairing CO2 elimination

Question 124

The oxyhemoglobin dissociation curve is shifted to the right (decreased oxygen affinity) by
I. Acidosis
II. Decreased 2,3-diphosphoglyceric acid (2,3-DPG)
III. Fever
IV Banked blood

Answer 124

A. I, II, III
B. I, III
C. II, IV
D. IV
E. All of the above

The oxyhemoglobin dissociation curve is shifted to the right by acidosis (I),
fever (III), increased 2,3-diphosphoglyceric acid (DPG [II is false]), and hypoxemia, and to the left by alkalosis, hypothermia, banked blood (IV), and decreased 2,3-DPG (II).

Question 125

Gastrointestinal carcinoid tumors are most frequently found in the
A. Appendix
B. Colon
C. Ileum
D. Rectum
E. Stom ach

Answer 125

A. Appendix
B. Colon
C. Ileum
D. Rectum
E. Stom ach

Forty-six percent of carcinoid tumors of the GI tract are located in the appendix (A), the most common site for GI carcinoids. The ileum (28% [C]) and the rectum (17% [D]) are less frequently involved

Question 126

Alkalinization of the urine promotes excretion of
I. Salicylates
II. Tricyclic antidepressants
III. Phenobarbital
IV. Amphetamines

Answer 126

A. I, II, III
B. I, III
C. II, IV
D. IV
E. All of the above

The excretion of weak acids is facilitated by alkalinization of the urine and serum . Compounds such as phenobarbital (III), salicylates (I), chlorpropamide,
tricyclic antidepressants (II), 2,4-dichlorophenoxyacetic acid, diflunisal, fluoride, and methotrexate are weak acids. Amphetamines (IV) are weak bases,
the excretion of which is enhanced by acidification of the urine

Question 127

Reliably effective in von Willebrand’s disease
A. Cryoprecipitate
B. Fresh frozen plasm a
C. Both
D. Neither

Answer 127

A. Cryoprecipitate
B. Fresh frozen plasm a
C. Both
D. Neither

von Willebrandʼs disease is an autosomal dominant condition of altered hemostasis resulting from a deficiency of von Willebrand factor (vWF). vWF, under normal conditions, aids in platelet–platelet and platelet–subendothelial
interactions and stabilizes factor VIII. Treatment goals include replacing vWF
and factor VIII, w hich is best accom plished with the administration of cryoprecipitate (A). Hemophilia B is caused by a deficiency of factor IX that causes
inadequate generation of thrombin by the coagulation cascade. Historically,
fresh frozen plasm a (FFP [B]) was the treatm ent of choice for factor replacement in hemophilia. The use of FFP, however, has been supplanted by the use of recombinant factor IX, with a reduced risk of bloodborne diseases and transfusion reactions

Question 128

Used in the treatment of hemophilia B
A. Cryoprecipitate
B. Fresh frozen plasm a
C. Both
D. Neither

Answer 128

A. Cryoprecipitate
B. Fresh frozen plasm a
C. Both
D. Neither

von Willebrandʼs disease is an autosomal dominant condition of altered hemostasis resulting from a deficiency of von Willebrand factor (vWF). vWF, under normal conditions, aids in platelet–platelet and platelet–subendothelial
interactions and stabilizes factor VIII. Treatment goals include replacing vWF
and factor VIII, w hich is best accom plished with the administration of cryoprecipitate (A). Hemophilia B is caused by a deficiency of factor IX that causes
inadequate generation of thrombin by the coagulation cascade. Historically,
fresh frozen plasm a (FFP [B]) was the treatm ent of choice for factor replacement in hemophilia. The use of FFP, however, has been supplanted by the use of recombinant factor IX, with a reduced risk of bloodborne diseases and transfusion reactions

Question 129

The free water deficit in a dehydrated 70-kg man with an Na 1 of 160 is
A. 2 L
B. 4 L
C. 6 L
D. 7 L
E. 8 L

Answer 129

A. 2 L
B. 4 L
C. 6 L
D. 7 L
E. 8 L

Free water deficit can be calculated from the formula:
Free water deficit (L) = [(Na 2 140)/140] 3 body weight (kg) 3 0.6
= [(160 2 140)/140] 3 70 3 0.6
- 20 2 3 0.6 5 6 L

Question 130

Pure a agonist
A. Amrinone
B. Dopamine
C. Epinephrine
D. Neo-Synephrine
E. Norepinephrine

Answer 130

A. Amrinone
B. Dopamine
C. Epinephrine
D. Neo-Synephrine
E. Norepinephrine

Amrinone (A) and milrinone are phosphodiesterase inhibitors that prevent
the degradation of cAMP, resulting in positive cardiac inotropy and vascular
smooth muscle contraction. Dopamine (B) has dose-dependent pharmacologic and hemodynamic effects. At intermediate doses, dopamine increases cardiac output via stimulation of cardiac b receptors; at higher doses, peripheral
vasoconstriction occurs, w hich m ay cause undesirable increases in afterload
in patients with a tenuous cardiac status. Epinephrine (C) stimulates both
a and b adrenergic receptors. Neo-Synephrine (phenylephrine [D]) is a pure
a 1 receptor agonist. Norepinephrine (E) has similar activity as compared
with epinephrine at a and b1 receptors, but has relatively little action at b2
receptors

Question 131

Does not interact with a or b receptors
A. Amrinone
B. Dopamine
C. Epinephrine
D. Neo-Synephrine
E. Norepinephrine

Answer 131

A. Amrinone
B. Dopamine
C. Epinephrine
D. Neo-Synephrine
E. Norepinephrine

Amrinone (A) and milrinone are phosphodiesterase inhibitors that prevent
the degradation of cAMP, resulting in positive cardiac inotropy and vascular
smooth muscle contraction. Dopamine (B) has dose-dependent pharmacologic and hemodynamic effects. At intermediate doses, dopamine increases cardiac output via stimulation of cardiac b receptors; at higher doses, peripheral
vasoconstriction occurs, w hich m ay cause undesirable increases in afterload
in patients with a tenuous cardiac status. Epinephrine (C) stimulates both
a and b adrenergic receptors. Neo-Synephrine (phenylephrine [D]) is a pure
a 1 receptor agonist. Norepinephrine (E) has similar activity as compared
with epinephrine at a and b1 receptors, but has relatively little action at b2
receptors

Question 132

Effects vary significantly with dose administered
A. Amrinone
B. Dopamine
C. Epinephrine
D. Neo-Synephrine
E. Norepinephrine

Answer 132

A. Amrinone
B. Dopamine
C. Epinephrine
D. Neo-Synephrine
E. Norepinephrine

Amrinone (A) and milrinone are phosphodiesterase inhibitors that prevent
the degradation of cAMP, resulting in positive cardiac inotropy and vascular
smooth muscle contraction. Dopamine (B) has dose-dependent pharmacologic and hemodynamic effects. At intermediate doses, dopamine increases cardiac output via stimulation of cardiac b receptors; at higher doses, peripheral
vasoconstriction occurs, w hich m ay cause undesirable increases in afterload
in patients with a tenuous cardiac status. Epinephrine (C) stimulates both
a and b adrenergic receptors. Neo-Synephrine (phenylephrine [D]) is a pure
a 1 receptor agonist. Norepinephrine (E) has similar activity as compared
with epinephrine at a and b1 receptors, but has relatively little action at b2
receptors

Question 133

Primarily an a agonist with mild b1 activity
A. Amrinone
B. Dopamine
C. Epinephrine
D. Neo-Synephrine
E. Norepinephrine

Answer 133

A. Amrinone
B. Dopamine
C. Epinephrine
D. Neo-Synephrine
E. Norepinephrine

Amrinone (A) and milrinone are phosphodiesterase inhibitors that prevent
the degradation of cAMP, resulting in positive cardiac inotropy and vascular
smooth muscle contraction. Dopamine (B) has dose-dependent pharmacologic and hemodynamic effects. At intermediate doses, dopamine increases cardiac output via stimulation of cardiac b receptors; at higher doses, peripheral
vasoconstriction occurs, w hich m ay cause undesirable increases in afterload
in patients with a tenuous cardiac status. Epinephrine (C) stimulates both
a and b adrenergic receptors. Neo-Synephrine (phenylephrine [D]) is a pure
a 1 receptor agonist. Norepinephrine (E) has similar activity as compared
with epinephrine at a and b1 receptors, but has relatively little action at b2
receptors

Question 134

Balanced a and b agonist properties
A. Amrinone
B. Dopamine
C. Epinephrine
D. Neo-Synephrine
E. Norepinephrine

Answer 134

A. Amrinone
B. Dopamine
C. Epinephrine
D. Neo-Synephrine
E. Norepinephrine

Amrinone (A) and milrinone are phosphodiesterase inhibitors that prevent
the degradation of cAMP, resulting in positive cardiac inotropy and vascular
smooth muscle contraction. Dopamine (B) has dose-dependent pharmacologic and hemodynamic effects. At intermediate doses, dopamine increases cardiac output via stimulation of cardiac b receptors; at higher doses, peripheral
vasoconstriction occurs, w hich m ay cause undesirable increases in afterload
in patients with a tenuous cardiac status. Epinephrine (C) stimulates both
a and b adrenergic receptors. Neo-Synephrine (phenylephrine [D]) is a pure
a 1 receptor agonist. Norepinephrine (E) has similar activity as compared
with epinephrine at a and b1 receptors, but has relatively little action at b2
receptors

Question 135

Thallium intoxication causes each of the following except
A. Cardiac dysfunction
B. GI disturbance
C. Hirsutism
D. Lower extremity joint pain
E. Peripheral neuropathy

Answer 135

A. Cardiac dysfunction
B. GI disturbance
C. Hirsutism
D. Lower extremity joint pain
E. Peripheral neuropathy

Thallium intoxication is characterized by cardiac dysfunction (A), gastrointestinal disturbance (B), alopecia (C is false), lower limb joint pain (D),
and peripheral neuropathy (E). Thallium poisoning causes alopecia, not
hirsutism (C)

Question 136

Which of the following symptoms is least characteristic of acute intermittent porphyria?
A. Abdominal pain
B. Hypotension
C. Polyneuropathy
D. Psychosis
E. Tachycardia

Answer 136

A. Abdominal pain
B. Hypotension
C. Polyneuropathy
D. Psychosis
E. Tachycardia

Acute intermittent porphyria is characterized by colicky abdominal pain (A),
psychosis (D), (a predominantly motor) polyneuropathy (C), and tachycardia (E). Hypertension, not hypotension (B), typically occurs during an attack

Question 137

A patient on his third hospital day in the neuro intensive care unit abruptly develops bradycardia, hyperlipidemia, and rhabdomyolysis while on the ventilator.
The most appropriate next step is
A. Acquire cardiology consultation
B. Discontinue the offending agent
C. Initiate broad-spectrum antibiotics
D. Insulin administration
E. Renal dialysis

Answer 137

A. Acquire cardiology consultation
B. Discontinue the offending agent
C. Initiate broad-spectrum antibiotics
D. Insulin administration
E. Renal dialysis

The triad of bradycardia, hyperlipidemia, and rhabdomyolysis is consistent
with a propofol infusion syndrome in this ventilated neuro intensive care patient. This disorder involves the abrupt onset of heart failure, bradycardia,
lactic acidosis, hyperlipidem ia, and rhabdomyolysis. It typically occurs in the
setting of high-dose, prolonged propofol infusions. The most appropriate next
step after making the diagnosis is to discontinue the offending agent (B). A
cardiology consult (A) m ay be necessary if external pacing is needed, but the
propofol needs to be discontinued. Renal dialysis (E) may become necessary
depending on the severity of the rhabdomyolysis but is not the next best step.
Antibiotic therapy (C) would be appropriate for sepsis, but not for the propofol infusion syndrom e. Insulin adm inistration (D) is unlikely to be helpful.

Question 138

Which of the following descriptions best describes Cheyne-Stokes respiration?
A. Breathing is irregularly interrupted, and each breath varies in rate and depth
B. Few rapid deep breaths alternate w ith apneic cycles (2–3 second pause in full inspiration) in short cycles
C. Increase in rate and depth of respiration leading to respiratory alkalosis
D. Waxing and waning hyperpnea regularly alternates with shorter apneic periods
E. None of the above

Answer 138

A. Breathing is irregularly interrupted, and each breath varies in rate and depth
B. Few rapid deep breaths alternate w ith apneic cycles (2–3 second pause in full inspiration) in short cycles
C. Increase in rate and depth of respiration leading to respiratory alkalosis
D. Waxing and waning hyperpnea regularly alternates with shorter apneic periods
E. None of the above

Cheyne-Stokes respiration is characterized by waxing and waning hyperpnea regularly alternating w ith shorter apneic periods (D) and is thought to be related to isolation of the brainstem respiratory centers from the cerebrum rendering them more sensitive to carbon dioxide. Central neurogenic
hyperventilation is an increase in rate and depth of respiration leading to respiratory alkalosis (C) associated w ith lesions of the lower midbrain and upper pontine tegmentum . Apneustic breathing is caused by either basilar artery occlusion or low pontine lesions and is characterized by a few rapid deep breaths alternating w ith apneic cycles (2–3 second pause in full
inspiration [B]). With Biot breathing, or ataxic breathing, breathing is irregularly interrupted and each breath varies in rate and depth (A); Biot breathing is associated with lesions of the dorsomedial medulla

Question 139

Cushing’s reflex refers to
A. Increased heart rate in response to increased intracranial pressure
B. Increased systolic arterial pressure in response to increased intracranial pressure
C. Parasympathetic outflow in response to increased intracranial pressure
D. All of the above
E. None of the above

Answer 139

A. Increased heart rate in response to increased intracranial pressure
B. Increased systolic arterial pressure in response to increased intracranial pressure
C. Parasympathetic outflow in response to increased intracranial pressure
D. All of the above
E. None of the above

Cushing was the first neurosurgeon to recognize that increases in intracranial
pressure (ICP) com prom ise cerebral blood ow. Cushing’s reflex refers to the
rise in systemic arterial pressure (B) due to increased sym pathetic activity
(C is false) in response to rises in ICP. As the system ic arterial pressure rises,
bradycardia may also occur (A is false). The triad of hypertension, bradycardia, and abnormal breathing is known as Cushing’s triad.