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United States Medical Licensing Exam


Step 1

Sample CBT Section


Test Code: 8391

Teacher Version

Princeton Review Management, L.L.C.


All rights reserved

USMLE is a joint program of the Federation of State Medical Boards of the U.S. and the National Board of Medical Examiners, which are not affiliated with
The Princeton Review. The Princeton Review is not affiliated with Princeton University.

Time to complete this exam booklet....................................1 hour


Number of items ................................................................... 50
Todays date ................................................... _______________
General Directions
Read all the directions in this booklet very carefully. This practice test is intended to simulate
a portion of the actual test-taking experience. This booklet contains 50 items, which
represents the approximate number of items you will find in one of the actual USMLE CBT
timed sections.
This test is 1 hour long with no scheduled breaks. Locate Section 1 on the front of your
answer sheet. You should record all of your answers in Section 1.
If you need to leave the room, please leave your booklet over your answer sheet and inform the proctor
of your whereabouts. No time will be provided to make up for any absence from the testing
room after your proctor has indicated that the exam has begun. When time is called, no extra
time will be allowed to transfer answers from the booklet to the answer sheet. The top of
your answer sheet must be appropriately completed before any scoring will be done.

Good luck!

Sample CBT Section

SECTION 1 BEGINS HERE


DIRECTIONS (Items 150): Each of the numbered items is followed by a set of options. For each item, select
the BEST lettered option to answer the question or complete the statement. Locate the corresponding item
number in the appropriate section of your answer sheet and completely fill in the circle containing the lettered
option you have selected.
1. A 35-year-old male presents to his primary
care doctor with complaints of headache and
malaise. His blood pressure is elevated. He has
periorbital and pretibial edema. Urinalysis
reveals heavy proteinuria. Which of the following is the most likely principal component of
his proteinuria?
(A) Albumin
(B) Kappa light chains
(C) Lambda light chains
(D) Tamm-Horsfall protein
(E) Transthyretin

2. A 12-year-old boy is brought to his pediatrician by his mother with a two-day history of
tea-colored urine. He recently completed a
five-day course of penicillin for streptococcal
pharyngitis. His blood pressure is elevated. He
has periorbital edema. Which of the following
is the most likely microscopic renal lesion?
(A) Basement membrane immune complex
deposition
(B) Basement membrane thickening
(C) Foot process effacement
(D) Mesangial proliferation
(E) Subepithelial immune complex
deposition

(A) is correct. This patient has the nephrotic syndrome


that is characterized by hypoproteinemia, heavy
proteinuria, and edema. Most commonly, there is
glomerular injury resulting in the loss of the negative
charge of the glomerular basement membrane and
increased permeability. The major protein lost is
albumin, resulting is proteinuria and edema as plasma
oncotic pressure is decreased.

(E) is correct. Poststreptococcal glomerulonephritis most


commonly follows a Streptococcus pyogenes
pharyngitis by 914 days. Clinically, there is often
hypertension, edema, and hematuria (smoky or teacolored urine). The typical microscopic lesion is
subepithelial immune deposit.

Explanation B: No. Kappa light chains commonly


cause tubulointerstitial damage in patients with renal
involvement or multiple myeloma.

Explanation A: No. Membranous nephropathy is


characterized by immune complex deposition within
the glomerular basement membrane.

Explanation C: No. Lambda light chains are a less


common cause of tubulointerstitial damage in patients
with renal involvement or multiple myeloma.

Explanation B: No. Focal and segmental


glomerulosclerosis is characterized by basement
membrane thickening.

Explanation D: No. The Tamm-Horsfall protein is a


normal component of urine composed of proteins
secreted by the epithelial cells of the loop of Henle.
Tamm-Horsfall protein is the principal constituent of
hyaline casts that are formed in concentrated urine.

Explanation C: No. Foot process effacement is the


characteristic lesion of minimal change disease.

Explanation E: No. Transthyretin, or prealbumin, is a


protein carrier of thyroid hormone.

Princeton Review Management, L.L.C.


839-1298-3.0

Explanation D: No. Mesangial proliferation is a


nonspecific lesion, but is particularly prominent in
diabetic glomerulosclerosis.

3. A 30-year-old female presents to her primary


care physician with complaints of frequency,
urgency, and dysuria over the last twelve hours.
Urinalysis reveals many leukocytes. She is
treated with a three-day course of oral
ciprofloxacin. What is the primary target of the
antimicrobial action of ciprofloxacin?
(A) Binding of the 30S subunit
(B) Binding of the 50S subunit
(C) Competitive inhibition of dihydrofolate
reductase
(D) Inhibition of DNA dependent RNA
polymerase
(E) Inhibition of DNA gyrase

4. A 24-year-old female presents to her primary


care doctor with complaints of a pruritic rash
present for the last several days. The rash
began after a relaxing resort weekend that she
spent swimming, snorkeling, and sitting in the
hot tub. The rash is concentrated in areas
covered by her swimming suit. Which of the
following is the most likely etiologic agent?
(A) Pseudomonas aeruginosa
(B) Pseudomonas pseudomallei
(C) Streptococcus pyogenes
(D) Staphylococcus aureus
(E) Staphylococcus epidermidis

(E) is correct. DNA gyrase is the enzyme responsible


for supercoiling, nicking, and sealing bacterial DNA.
It is the target of the quinolone antibiotics, like
ciprofloxacin, which are bactericidal against a wide
variety of aerobes and facultative anaerobes.

(A) is correct. Pseudomonas aeruginosa is a cause of


folliculitis. In hot tubs and heated swimming pools that
are not frequently cleaned, large numbers of the
organism flourish and cause a folliculitis that is
concentrated in areas covered by swimming suits (as
these areas are persistently damp).

Explanation A: No. The 30S subunit is the target of a


number of antibiotics including the aminoglycosides
and tetracycline.

Explanation B: No. Pseudomonas pseudomallei is


endemic to Southeast Asia where it is a cause of
pulmonary infection.

Explanation B: No. The 50S subunit is the target of a


number of antibiotics including chloramphenicol,
clindamycin, and erythromycin.

Explanation C: No. Streptococcus pyogenes is most


commonly a cause of pharyngitis.

Explanation C: No. Trimethoprim is a competitive


inhibitor of dihydrofolate reductase.
Explanation D: No. Rifampin is an inhibitor of DNA
dependent RNA polymerase.

Explanation D: No. Staphylococcus aureus is an


uncommon cause of folliculitis in this setting.
Explanation E: No. Staphylococcus epidermidis may
cause cellulitis and occasionally folliculitis, but would
be an unusual pathogen in this setting.

Sample CBT Section

5. A 25-year-old female is brought to the Emergency Department with complaints of fever,


malaise, nausea, and diarrhea. She is hypotensive and has a prominent maculopapular rash.
She is currently in the middle of her menstrual
period. Which of the following toxin-producing
bacteria is most likely the cause of this
patients symptoms?
(A) Escherichia coli
(B) Pseudomonas aeruginosa
(C) Streptococcus pyogenes
(D) Staphylococcus aureus
(E) Staphylococcus epidermidis
(D) is correct. Toxic shock syndrome is most commonly
mediated by a pyrogenic exotoxin produced by
Staphylococcus aureus, toxic shock syndrome toxin 1
(TSST-1). The toxin is produced by a local
Staphylococcus aureus infection and is absorbed from
the site of infection to produce the systemic effects of
hypotension, rash, gastrointestinal symptoms, and
fever. The usual victim is a young female using superabsorbent tampons.
Explanation A: No. Escherichia coli is not a cause of
the toxic shock syndrome.
Explanation B: No. Pseudomonas aeruginosa is not a
cause of the toxic shock syndrome.
Explanation C: No. Streptococcus pyogenes is a
common cause of pharyngitis but not the toxic shock
syndrome.
Explanation E: No. Staphylococcus epidermidis is not
a cause of the toxic shock syndrome.

Princeton Review Management, L.L.C.


839-1298-3.0

6. A 67-year-old male is brought to the Emergency Department with complaints of crushing


substernal chest pressure. An electrocardiogram reveals changes consistent with an
anterolateral myocardial infarction. He is
administered streptokinase. Which of the
following best describes the thrombolytic
action of streptokinase?
(A) Activation of antithrombin III
(B) Activation of circulating plasminogen
(C) Activation of plasminogen bound to
fibrin
(D) Cleavage of fibrinogen to fibrin
(E) Competitive inhibition of fibrin
degradation
(B) is correct. Streptokinase is a naturally occurring
plasminogen activator that is obtained from hemolytic
streptococci. Streptokinase forms a complex with
circulating plasminogen, allowing activation of the
complex in place of tissue plasminogen activator (factor
XIIa). The fibrinolytic cascade then proceeds with
plasmin cleaving fibrinogen and fibrin into
degradation products.
Explanation A: No. Activation of antithrombin III is
the action of heparin.
Explanation C: No. Genetically engineered tissue
plasminogen activator works at the site of thrombus to
activate plasminogen bound to fibrin.
Explanation D: No. Plasmin cleaves fibrinogen and
fibrin to degradation products.
Explanation E: No. Inhibition of fibrin degradation is
an antifibrinolytic property.

7. A 28-year-old arborist is brought to the Emergency Department by his coworker. The patient
lost his balance while atop a tree and slipped,
barely avoiding a fall by grasping a limb with
his right arm. He is unable to flex his wrist or
move several of his fingers. There is numbness
of the medial arm, forearm, and hand. Which
of the following injuries is most likely?
(A) Axillary nerve
(B) Inferior trunk of the brachial plexus
(C) Long thoracic nerve
(D) Superior trunk of the brachial plexus
(E) Thoracodorsal nerve
(B) is correct. Injury to the inferior trunk (C8 and T1)
of the brachial plexus may occur when someone grasps
an object to break a fall. The resulting paralysis and
anesthesia are a reflection of the injury to the ulnar
nerve with paralysis of the wrist flexion and intrinsic
hand muscles and anesthesia of the medial portion of
the arm, forearm, and hand.
Explanation A: No. Injury of the axillary nerve results
is paralysis of the deltoid muscle and lateral arm
anesthesia.
Explanation C: No. Injury to the long thoracic nerve
results in paralysis of the serratus anterior muscle and
winging of the scapula.
Explanation D: No. Injury to the superior trunk of the
brachial plexus results in a waiters tip with the upper
limb hanging in medial rotation secondary to injury
to C5 and C6 nerve roots.
Explanation E: No. Injury of the thoracodorsal nerve
results is paralysis of the latissimus dorsi muscle.

8. A 45-year-old male is brought to the Emergency Department after an automobile accident. He is hypotensive and complaining of left
shoulder pain. Radiographs of his shoulder are
unremarkable. Injury to which of the following
organs most likely explains his symptoms?
(A) Gall bladder
(B) Large intestine
(C) Left lung
(D) Liver
(E) Small intestine
(F) Spleen
(G) Stomach
(F) is correct. Pain arising from an abdominal organ
is often poorly localized by the patient because pain
from an organ is referred to the spinal cord segment
that receives visceral sensory fibers from that organ.
Splenic pain is commonly referred to the left shoulder.
Hypotension is common after splenic injury secondary
to large volume blood loss from the injured spleen into
the abdominal cavity.
Explanation A: No. Biliary pain, such as from biliary
colic, often is referred to the right shoulder.
Explanation B: No. Colonic pain is poorly localized
and results in diffuse abdominal pain.
Explanation C: No. Pain from a pulmonary process
often is referred to the back.
Explanation D: No. Hepatic pain is generalized to the
right upper quadrant or epigastrium.
Explanation E: No. Small bowel pain is poorly
localized and results in diffuse abdominal pain.
Explanation G: No. Gastric pain, such as from a
gastric ulcer, often localizes to the epigastrium.

Sample CBT Section

9. A 2-month-old male is brought to the pediatrician by his mother who is concerned that he is
not gaining weight. She also notes that his
color is poor, especially when he tries to feed,
when he often grunts and turns dusky. Which
of the following cardiac lesions is most likely
to cause the patients symptoms?
(A) Atrial septal defect
(B) Patent ductus arteriosus
(C) Patent foramen ovale
(D) Tetralogy of Fallot
(E) Ventricular septal defect
(D) is correct. The Tetralogy of Fallot is the most
common cause of cyanotic heart disease in which
blood bypasses the lungs and mixes with oxygenated
blood. Four lesions comprise the Tetralogy of Fallot:
origin of the aorta is the right ventricle, pulmonary
arter y stenosis, ventricular septal defect, right
ventricular hypertrophy. As much as 75% of venous
return to the heart is passed, unoxygenated, from the
right ventricle to the aorta and the systemic circulation,
resulting in cyanosis.
Explanation A: No. An atrial septal defect results in a
left-to-right shunt of blood from the higher pressure
left side of the heart to the lower pressure right atrium.
There is no cyanosis as there is no mixing of venous
blood with oxygenated blood from the left side of the
heart.
Explanation B: No. The ductus ar teriosus is a
connection of the pulmonary artery with the aorta used
in fetal life to obviate blood flow through the lungs. If
this structure does not close soon after birth there is
persistent left-to-right shunt of blood from the higher
pressure aorta into the pulmonary veins, but no
cyanosis.
Explanation C: No. A patent foramen ovale functions
as an atrial septal defect with a small left-to-right shunt
of blood without cyanosis.

10. A 10-month-old male is brought to the pediatrician by his mother who is concerned about
his lack of interaction. He was previously
playful and happy but now hardly ever smiles.
On exam, he is found to have poor muscle tone
and a cherry-red macula. Deficiency of which
enzyme is most likely?
(A) Glucocerebrosidase
(B) Glucose-6-phosphatase
(C) Hexosaminidase A
(D) L-iduronidase
(E) Tyrosinase
(C) is correct. Tay-Sachs disease is an autosomal
recessive condition with deficiency of hexosaminidase
A. Symptoms begin between 6 to 10 months of age.
There is progressive motor and mental deterioration
with death by 4 years of age. The cherry red spot on
the macula reflects involvement of the retinal ganglion
cells.
Explanation A: No. Deficiency of glucocerebrosidase
results in Gauchers disease, the most common
lysosomal storage disease. There are several forms of
the disease, one of which is fatal in infancy with
prominent neurologic signs. Most commonly, patients
suffer the adult form with prominent splenomegaly and
bony complaints.
Explanation B: No. Deficiency of glucose-6phosphatase results in von Gierkes disease with
accumulation of glycogen in the liver. Growth may be
stunted but mentation is preserved.
Explanation D: No. Deficiency of L-iduronidase results
in Hurlers syndrome, a mucopolysaccharidosis, with
death in early childhood with skeletal abnormalities,
organomegaly, and characteristic facies. There is
corneal clouding.
Explanation E: No. Deficiency of tyrosinase results in
albinism as there no conversion of tyrosine to melanin.

Explanation E: No. In a ventricular septal defect, blood


flows from the higher pressure left ventricle to the lower
pressure right ventricle, a left-to-right shunt of blood
without cyanosis.

Princeton Review Management, L.L.C.


839-1298-3.0

11. A 4-month-old female is brought to her pediatrician by her mother who is concerned about
some photographs she recently had developed.
In the photographs, only the childs right eye
demonstrates a red reflex. Examination of the
left eye confirms absence of a red reflex.
Which of the following mechanisms is most
likely involved?
(A) Deletion in the long arm of chromosome 13
(B) Deletion in the short arm of chromosome 5
(C) Deletion of the short arm of chromosome 11
(D) Nondisjunction of chromosome 18
(E) Nondisjunction of chromosome 21
(A) is correct. Retinoblastoma is the result of inherited
or acquired deletions of the retinoblastoma tumor
suppressor gene on the long arm of chromosome 13.
The tumor arises most frequently in the first 2 years of
life with leukocoria, absence of the red reflex, poor
vision, or squint.
Explanation B: No. Deletion in the short arm of
chromosome 5 results in cri du chat syndrome.
Explanation C: No. Deletion in the short arm of
chromosome 11 results is aniridia (congential absence
of the iris) and is associated often with Wilms tumor.
Explanation D: No. Nondisjunction of chromosome 18
results in trisomy 18 (Edwards syndrome).
Explanation E: No. Nondisjunction of chromosome
21 during the first meiotic division results in Downs
syndrome.

12. A 62-year-old male complains to his primary


care doctor about a new tremor. Exam confirms
a new pill-rolling tremor. There is prominent
cog-wheeling rigidity and masked facies.
Which of the following most likely accounts
for this patients symptoms?
(A) Neuronal degeneration of anterior horn
cells
(B) Neuronal degeneration of the caudate
nuclei
(C) Neuronal degeneration of the corticospinal
tracts
(D) Neuronal degeneration of spinothalamic
tracts
(E) Neuronal degeneration of the substantia
nigra
(E) is corret. Parkinsons disease is characterized
pathologically by neuronal degeneration of the
substantia nigra. The clinical disease displays cogwheeling rigidity, masked facies, tremor, and difficulty
initiating and terminating gait.
Explanation A: No. Neuronal degeneration of the
anterior horn cells would result in a flaccid paralysis.
Explanation B: No. Neuronal degeneration of the
caudate nuclei is the pathologic change associated
with Huntingtons disease.
Explanation C: No. Neuronal degeneration of the
corticospinal tracts would result in spastic paralysis.
Explanation D: No. Neuronal degeneration of the
spinothalamic tracts would result in difficulty with
sensation.

Sample CBT Section

13. A 45-year-old male is brought to the Emergency Department by his family, who have
noted him to be behaving bizarrely. There is a
family history of early death. He is unable to
control pronounced choreiform movements of
his upper extremities and trunk. Which of the
following is the most likely neurotransmitter
disturbance?
(A) Depletion of acetylcholine
(B) Depletion of dopamine
(C) Depletion of -aminobutyric acid
(D) Excessive production of acetylcholine
(E) Excessive production of dopamine
(F) Excessive production of -aminobutyric
acid
(G) Excessive production of norepinephrine
(C) is correct. Huntingtons disease is an autosomal
dominant disorder characterized by involuntar y
choreiform movements, cognitive disturbance, and
emotional dysfunction. Onset is in the fifth decade.
There is atrophy of the caudate nucleus with depletion
of -aminobutyric acid.

14. A 24-year-old female presents to her primary


care physician with complaints of weakness
and fatigue, worse in the afternoons for the last
several months. The fatigue is relieved with a
short nap. She has prominent bilateral ptosis.
Which of the following is the target of the
autoantibodies in this disease?
(A) Acetylcholinesterase
(B) Muscle fiber acetylcholine-gated ion
channels
(C) Muscle fiber membrane
(D) Nerve fiber calcium channels
(E) Nerve fiber membrane
(B) is correct. Myasthenia gravis is an autoimmune
disease characterized by muscle weakness.
Autoantibodies block the binding of acetylcholine to
muscle fiber ion channels causing end-plate potentials
too weak to properly stimulate muscle fibers.
Explanation A: No. Diisopropyl fluorophosphate (a
nerve gas) as well as neostigmine and physostigmine
inactivate acetylcholinesterase, causing repetitive
stimulation of muscle fibers and spasm, not weakness.

Explanation A: No. There is a postulated role for


depletion of acetylcholine in the pathophysiology of
Alzheimers disease.

Explanation C: No. The target of the autoantibodies


in myasthenia gravis is not the muscle fiber membrane.

Explanation B: No. There is a postulated role for the


depletion of dopamine in the pathophysiology of
Parkinsons disease.

Explanation D: No. The target of the autoantibodies


in myasthenia gravis is not the nerve fiber calcium
channels.

Explanation D: No. Acetylcholine does not play a role


in the pathophysiology of Huntingtons disease.

Explanation E: No. The target of the autoantibodies in


myasthenia gravis is not the nerve fiber membrane.

Explanation E: No. Dopamine does not play a role in


the pathophysiology of Huntingtons disease. Excessive
amounts of dopamine are postulated to play a role in
schizophrenia.
Explanation F: No. Excess of -aminobutyric acid does
not play a role in the pathophysiology of Huntingtons
disease.
Explanation G: No. Norepinephrine does not play a
role in the pathophysiology of Huntingtons disease.

Princeton Review Management, L.L.C.


839-1298-3.0

15. A 19-year-old male presents to the student


health service after his roommate noted a
yellowish discoloration to his skin while up
late studying for an exam. After a meal and
several hours sleep the discoloration resolved.
Laboratory tests are obtained:
ALT = 25 U/dL
AST = 20 U/dL
Bilirubin (direct) = 0.8 mg/dL
Bilirubin (total) = 2.5 mg/dL
Which of the following is responsible for this
patients disease?
(A) Canalicular cholestasis
(B) Decreased activity of glucuronyl
transferase
(C) Impaired transport of bilirubin into the
bile canaliculus
(D) Impaired uptake of circulating bilirubin
(E) Immune hemolysis
(B) is correct. Gilberts disease is a result of decreased
activity of glucuronyl transferase. The condition is
benign with jaundice often occurring in times of
physiologic stress, especially fasting. In laboratory
tests, there is mild unconjugated (indirect)
hyperbilirubinemia.
Explanation A: No. Canalicular cholestasis is the cause
of jaundice during pregnancy or is a result of
extrahepatic biliary obstruction.
Explanation C: No. Impaired transport of bilirubin into
the bile canaliculus is the lesion in both Rotors
syndrome and Dubin-Johnson syndrome.
Explanation D: No. Impaired uptake of circulating
bilirubin is the lesion in neonatal jaundice.
Explanation E: No. Immune hemolysis may overwhelm
the ability of hepatocytes to take up bilirubin. This is
the case in erythroblastosis.

16. A 17-year-old female complains to her pediatrician of bilateral knee pain, worse on the left
side, for the last several months. She has also
felt fatigued for some time. She has marked
hepatosplenomegaly. Laboratory tests are
obtained:
Leukocytes = 3.4/mm3
Hematocrit = 20%
Hemoglobin = 7.6 g/dL
Platelets = 150,000/uL
Bone marrow biopsy reveals infiltration with
foamy macrophages. What is the most likely
accumulated storage product in this patient?
(A) Ganglioside GM2
(B) Glucosylceramide
(C) Glycosaminoglycans
(D) Glycogen
(E) Sphingomyelin
(B) is correct. Deficiency of glucocerebrosidase results in
Gauchers disease, the most common lysosomal storage
disease with accumulation of glucosylceramide in
macrophages, giving the macrophages a foamy
appearance. There are several forms of the disease, one
of which is fatal in infancy with prominent neurologic
signs. Most commonly, patients suffer the adult form with
prominent splenomegaly and bony complaints.
Explanation A: No. Tay-Sachs disease is an autosomal
recessive condition with deficiency of hexosaminidase A
which degrades ganglioside GM2. Symptoms begin
between 6 to 10 months of age. There is progressive motor
and mental deterioration with death by 4 years of age.
Explanation C: No. Deficiency of L-iduronidase results
in Hurlers syndrome, a mucopolysaccharidosis, with
death in early childhood with skeletal abnormalities,
organomegaly, and characteristic facies. There is
accumulation of glycoaminoglycans, extracellular matrix
components normally degraded by L-iduronidase, a
glycosidase.
Explanation D: No. Deficiency of glucose-6phosphatase results in von Gierkes disease with
accumulation of glycogen in the liver. Growth may be
stunted but mentation is preserved.
Explanation E: No. Deficiency of sphingomyelinase
results is Niemann-Pick disease with accumulation of
sphingomyelin. There is hepatosplenomegaly and
prominent neurologic involvement, often with death
in early childhood.

10

Sample CBT Section

17. A 14-year-old female complains to her pediatrician of fatigue and occasional yellowish
discoloration to her skin. She has marked
splenomegaly. Laboratory studies are obtained:
Leukocytes = 3.4/mm3
Hematocrit = 30%
Hemoglobin = 9.6 g/dL
MCV = 90 fL
MCHC = 45%
Platelets = 250,000/uL
Peripheral smear demonstrates spherocytes.
Which of the following abnormal proteins is
most likely the cause of this patients signs and
symptoms?
(A) -globin
(B) Ankyrin
(C) -globin
(D) Protein 4.2
(E) Spectrin
(E) is correct. Hereditary spherocytosis is an autosomal
dominant disease characterized by a deficiency of
spectrin. This defect in the erythrocyte cell membrane
results in instability and increased osmotic fragility.
Clinically, there is jaundice, anemia, and
splenomegaly. Laboratories confirm the anemia and
demonstrate an increased mean corpuscular
hemoglobin.
Explanation A: No. Defects in -globin result in the
-thalassemias.
Explanation B: No. Ankyrin is an er ythrocyte
membrane protein, but is not the etiology of hereditary
spherocytosis.
Explanation C: No. Defects in the -globin result in
the -thalassemias.
Explanation D: No. Protein 4.2 is an erythrocyte
membrane protein, but is not the etiology of hereditary
spherocytosis.

Princeton Review Management, L.L.C.


839-1298-3.0

18. A 35-day-old infant is brought to the pediatrician by her parents. Since discharge she has
not been feeding well and now seems lethargic.
The infant is dehydrated and hypotensive. She
has an enlarged clitoris. Serum electrolytes
demonstrate hyponatremia, hyperkalemia, and
hypoglycemia. Which of the following is the
most common cause of these findings?
(A) 3-hydroxysteroid dehydrogenase
deficiency
(B) 11-hydroxylase deficiency
(C) 17-hydroxylase deficiency
(D) 21-hydroxylase deficiency
(E) Cholesterol side chain cleavage enzyme
deficiency
(D) is correct. 21-hydroxylase deficiency is the most
common cause of congenital adrenal hyperplasia, a
group of autosomal recessive inherited diseases in
which deficiency of corticosteroid hormones results in
the unregulated secretion of ACTH and thus adrenal
hyperplasia. In 21-hydroxylase deficiency, there is
often severe adrenal insufficiency with hyponatremia
and hyperkalemia due to the lack of aldosterone.
Females are also virilized; males appear normal.
Explanation A: No. 3-hydroxysteroid dehydrogenase
deficiency is a rare cause of congential adrenal
hyperplasia, which also presents with adrenal
insufficiency and ambiguous genitalia in females.
Explanation B: No. 11-hydroxylase deficiency results
in the accumulation of 11-deoxycortisol, a weak
mineralocorticoid with resultant sodium retention and
hypertension.
Explanation C: No. 17-hydroxylase deficiency results
in hypokalemic alkalosis and hypertension.
Explanation E: No. Cholesterol side chain cleavage
enzyme deficiency results in almost no secretion of
cortisol, aldosterone, or sex steroids as this enzyme is
the rate-limiting step in generation of steroids. Infants
suffer severe adrenal insufficiency.

11

19. An 18-day-old infant is brought to the Emergency Department by her parents with a fever
of 39C (104F). The infant is lethargic. Blood
cultures are obtained and a subsequent culture
isolates a gram-positive cocci. Which of the
following is the most likely isolate?
(A) Haemophilus influenza
(B) Neisseria meningitidis
(C) Staphylococcus aureus
(D) Staphylococcus epidermidis
(E) Streptococcus agalactiae
(F) Streptococcus pneumoniae
(G) Streptococcus pyogenes
(E) is correct. Streptococcus agalactiae is the most
common cause of sepsis in the neonatal period.
Premature rupture of maternal membranes and
prematurity increase the risk. Exposure during birth is
common, as 1030% women have vaginal colonization
with the organism.
Explanation A: No. Haemophilus influenza is a gramnegative coccobacillus.
Explanation B: No. Neisseria meningitidis is a gramnegative rod.
Explanation C: No. Staphylococcus aureus is not a
common cause of neonatal sepsis.

20. A 6-year-old boy is brought to the pediatrician


for poor school performance. He is unable to
pay attention and often daydreams. Laboratory
studies are obtained:
Leukocytes = 5.5/mm3
Hemoglobin = 6.5 g/dL
Hematocrit = 20%
Platelets = 400/mm3
Smear = hypochromic, microcytic red
blood cells with basophilic stippling
Which of the following is the most likely
explanation?
(A) Attention deficit disorder
(B) Folate deficiency
(C) Lead intoxication
(D) Mercury intoxication
(E) Vitamin B12 deficiency
(C) is correct. Lead intoxication remains a problem
among children, especially in large urban areas where
lead paint is still prevalent. The target of lead toxicity
in children is the brain. Children may display altered
levels of consciousness or even have seizures.
Laboratories demonstrate anemia as lead disrupts
heme synthesis through inhibition of -aminolevulinic
acid dehydratase. Basophilic stippling is a classic
finding on blood smear and is due to ribosomal
clustering.

Explanation D: No. Staphylococcus epidermidis is not


a common cause of neonatal sepsis.

Explanation A: No. Attention deficit disorder should


be a diagnosis of exclusion after other serious diseases,
such as lead poisoning, are considered.

Explanation F: No. Streptococcus pneumoniae is not


a common cause of neonatal sepsis.

Explanation B: No. Folate deficiency results in a


macrocytic anemia.

Explanation G: No. Streptococcus pyogenes is not a


common cause of neonatal sepsis.

Explanation D: No. Mercur y intoxication is


characterized primarily by a proximal tubular necrosis.
Explanation E: No. Vitamin B12 deficiency results in a
macrocytic anemia.

12

Sample CBT Section

21. Which of the following represents an irreversible step in glycolysis?


(A) 1,3-bisphosphoglycerate 3-phosphoglycerate
(B) Fructose 6-phosphate fructose 1,6bisphosphate
(C) Fructose 1,6-bisphosphate glyceraldehyde 3-phosphate
(D) Glucose 6-phosphate fructose 6phosphate
(E) Glyceraldehyde 3-phosphate 1,3bisphosphoglycerate
(B) is correct. Phosphofructokinase catalyzes the
conversion of fructose 6-phosphate to fructose 1,6bisphosphate, an irreversible reaction. The pace of
glycolysis is critically dependent on the level of activity
of this enzyme.
Explanation A: No. Phosphoglycerate kinase catalyzes
the conversion of 1,3-bisphosphoglycerate to 3phosphoglycerate, a reversible reaction.
Explanation C: No. Aldolase catalyzes the conversion
of fructose 1,6-bisphosphate to glyceraldehyde 3phosphate, a reversible reaction.
Explanation D: No. Phosphoglucose isomerase
catalyzes the conversion of glucose 6-phosphate to
fructose 6-phosphate, a reversible reaction.
Explanation E: No. Glyceraldehyde 3-phosphate
dehydrogenase catalyzes the conversion of
glyceraldehyde 3-phosphate to 1,3-bisphosphoglycerate,
a reversible reaction.

Princeton Review Management, L.L.C.


839-1298-3.0

22. A 24-year-old male is brought to the Emergency Department by EMS. He was stung by a
bee several minutes ago and now is having
difficulty breathing. This reaction is mediated
by which of the following classes of immunoglobulins?
(A) IgA
(B) IgD
(C) IgE
(D) IgG
(E) IgM
(C) is correct. IgE is the class of immunoglobulins
responsible for anaphylactic reactions. Preformed IgE
stimulates the release of mast cell contents such as
histamine to mediate anaphylactic reactions.
Explanation A: No. IgA is the class of immunoglobulins
found in secretions such as tears, saliva, and intestinal
secretions, serving as a first line of defense against
many pathogens.
Explanation B: No. The function of the IgD class of
immunoglobulins is not known.
Explanation D: No. IgG is the principal class of
protective antibodies in serum capable of multiple
immune functions, including complement fixation.
Explanation E: No. IgM is the initial class of
immunoglobulin produced after antigenic challenge.

13

23. A 64-year-old male presents to his primary


care doctor with complaints of lower extremity
edema. He has a history of long-standing
congestive heart failure and has used diuretic
agents in the past to control his edema. He also
has a history of calcium oxalate kidney stones.
Which of the following agents is potentially
useful for the treatment of both these conditions?
(A) Bumetanide
(B) Ethacrynic acid
(C) Furosemide
(D) Hydrochlorothiazide
(E) Spironolactone

24. A 43-year-old male presents to his primary


care doctor with complaints of increasing
abdominal girth. He has a long history of
alcohol abuse and recently stopped drinking.
Spironolactone is prescribed to aid the control
of the patients increasing ascites. Which of the
following is the site of action of spironolactone?
(A) Ascending loop of Henle
(B) Collecting duct
(C) Descending loop of Henle
(D) Distal tubule
(E) Proximal tubule

(D) is correct. Thiazide diuretics, such as


hydrochlorothiazide, are hypocalciuric. These agents
decrease the amount of calcium excreted in the urine
and are therefore useful in patients who are prone to
the formation of calcium-containing kidney stones.
Additionally, these diuretics have a role in the treatment
of mild congestive heart failure and hypertension.

(D) is correct. Spironolactone is a competitive


aldosterone receptor antagonist. Its site of action is
the late distal tubule where it decreases sodium entry
into cells and increases potassium excretion, promoting
sodium and water loss with preservation of plasma
potassium. Spironolactone is especially useful for
patients with hepatic failure, as it counteracts the
chronic hyperaldosteronism in these patients.

Explanation A: No. Bumetanide is a loop diuretic.


These agents are hypercalciuric, increasing the amount
of calcium excreted in the urine.

Explanation A: No. The ascending loop of Henle is


the site of action of loop diuretics such as furosemide
and bumetanide.

Explanation B: No. Ethacrynic acid is a loop diuretic.


These agents are hypercalciuric, increasing the amount
of calcium excreted in the urine.

Explanation B: No. The collecting duct is not the usual


site of action of diuretics.

Explanation C: No. Furosemide is a loop diuretic.


These agents are hypercalciuric, increasing the amount
of calcium excreted in the urine.
Explanation E: No. Spironolactone is an aldosterone
antagonist. These agents have a neutral effect on the
urinary excretion of calcium.

14

Explanation C: No. The descending loop of Henle is


not the usual site of action of diuretics.
Explanation E: No. The proximal tubule is the site of
action of carbonic anhydrase inhibitors such as
acetazolamide.

Sample CBT Section

25. A 67-year-old male is diagnosed with colon


cancer. He is scheduled for a hemicolectomy
but does not keep his preoperative assessment
appointment for the surgery. When confronted
he says cheerfully, I couldnt miss such a
terrific day on the golf course, well have to
reschedule. Which of the following best
describes this patients reaction to his illness?
(A) Acceptance
(B) Anger
(C) Anxiety
(D) Denial
(E) Depression
(D) is correct. This patient is denying the seriousness
of his illness, an abnormal adaptive illness response.
Explanation A: No. The patient clearly has not
accepted his illness and need for potentially life-saving
intervention.
Explanation B: No. Anger is an abnormal adaptive
illness response when it begins to interfere with
interpersonal relations and leads to isolation of the
person.
Explanation C: No. Anxiety is an abnormal adaptive
illness response when it exceeds its usual protective
function and compromises the patients ability to make
necessary medical decisions.
Explanation E: No. Depression is an abnormal
adaptive illness response typified by sustained sadness.

26. A 54-year-old male presents to his primary


care physician complaining of pain in his left
eye for the last several hours. He did not
sustain any ocular trauma. The left eye is
inflamed. He has marked photophobia in his
left eye. His intraocular pressure is measured
and is markedly elevated in his left eye. Which
of the following lesions most likely accounts
for his symptoms?
(A) Corneal abrasion
(B) Inflammation of the iris
(C) Inflammation the uvea
(D) Obstruction at the canal of Schlemm
(E) Retinal detachment
(D) is correct. This patient has angle closure glaucoma
with increased intraocular pressure. This is a visionthreatening emergency. Aqueous humor is produced
by the ciliary body, passes through the posterior
chamber, and then into the anterior chamber where it
then drains into veins via the canal of Schlemm and
the trabecular meshwork. The most common site of
obstruction of the flow of aqueous humor is the canal
of Schlemm.
Explanation A: No. Corneal abrasion may be painful,
but does not cause increased intraocular pressure.
Explanation B: No. Inflammation of the iris is found in
some connective tissue diseases. It does not cause
increased intraocular pressure.
Explanation C: No. Inflammation of the uvea is found
in some connective tissue diseases. It does not cause
increased intraocular pressure.
Explanation E: No. Retinal detachment, usually
secondary to eye trauma, may cause blindness. It does
not cause increased intraocular pressure.

Princeton Review Management, L.L.C.


839-1298-3.0

15

27. A 6-year-old boy is brought to the pediatrician


by his mother who noticed swelling around his
eyes. The boy has prominent periorbital edema
as well as pretibial edema. He is hypertensive.
A 24-hour urine collection reveals 4.2 grams of
protein. Which of the following is the most
likely microscopic renal lesion?
(A) Basement membrane immune complex
deposition
(B) Basement membrane thickening
(C) Foot process effacement
(D) Mesangial proliferation
(E) Subepithelial immune complex
deposition
(C) is correct. Minimal change disease is primarily a
disease of children. Clinically, it is characterized by
the nephrotic syndrome with hypoproteinemia, heavy
proteinuria (> 3.5 grams/24 hours), and edema. Foot
process effacement is the characteristic pathologic
lesion of minimal change disease found by electron
microscopy. Light microscopic evaluation is usually
normal.

28. A 27-year-old female dislikes her boss immensely, yet wishes to succeed in her career at
her current place of employment. Today, she is
particularly upset with her boss and purposefully withholds pieces of a project her boss
needs for an important presentation. When
confronted, she is very apologetic about her
mistake, vowing to make up for it with her next
project. What defense mechanism is this
patient using?
(A) Acting out
(B) Displacement
(C) Passive-aggressive behavior
(D) Projection
(E) Suppression
(C) is correct. Passive-aggressive behavior is
aggression toward others expressed through passivity;
in this case, instead of confronting her boss about their
conflict, she passively withheld important information.
Explanation A: No. Acting out is a direct expression
of an unconscious wish.

Explanation A: No. Membranous nephropathy is


characterized by immune complex deposition within
the glomerular basement membrane.

Explanation B: No. Displacement is redirection of


conflicted feelings to a less important object than the
person or object arousing the feelings.

Explanation B: No. Focal and segmental


glomerulosclerosis is characterized by basement
membrane thickening.

Explanation D: No. Projection is attributing ones own


feelings to another person.

Explanation D: No. Mesangial proliferation is a


nonspecific lesion, but is particularly prominent in
diabetic glomerulosclerosis.

Explanation E: No. Suppression is the ability to contain


conflict and postpone action, worrying in response to
the conflict.

Explanation
E:
No.
Poststreptococcal
glomerulonephritis most commonly follows a
Streptococcus pyogenes pharyngitis. The typical
microscopic lesion is subepithelial immune deposition.

16

Sample CBT Section

29. A 40-year-old female presents to her primary


care physician with complaints of shortness of
breath and a chronic cough. She has suffered
idiopathic pulmonary fibrosis for several years,
but now her symptoms are more prominent.
She has coarse rales throughout both lung
fields and a prominent, widely-split second
heart sound. Which of the following is an
accurate description of the second heart sound?
(A) Aortic then pulmonic valve closure
(B) Aortic then pulmonic valve opening
(C) Mitral then tricuspid valve closure
(D) Mitral then tricuspid valve opening
(E) Pulmonic then aortic valve opening
(F) Tricuspid then mitral valve closure
(G) Tricuspid then mitral valve opening
(A) is correct. The second heart sound is composed of
closure of the semilunar valves, the aortic, and the
pulmonic valves. First, there is closure of the aortic
then the pulmonic valve. With long-standing
pulmonary hypertension, there is delayed closure of
the pulmonic valve secondary to volume and pressure
overload of the right ventricle, causing a prominent,
widely-split second heart sound.
Explanation B: No. The second heart sound reflects
aortic then pulmonic valve closure.
Explanation C: No. The first heart sound reflects mitral
then tricuspid valve closure.

30. What is the most powerful flexor of the thigh?


(A) Adductor magnus
(B) Iliopsoas
(C) Rectus femoris
(D) Sartorius
(E) Tensor fascia lata
(F) Vastus lateralis
(G) Vastus medialis
(B) is correct. The iliopsoas muscle is the most powerful
flexor of the thigh.
Explanation A: No. Adductor magnus adducts and
flexes the thigh; its hamstring portion also extends the
thigh.
Explanation C: No. Rectus femoris extends the leg at
the knee and aids the iliopsoas in thigh flexion.
Explanation D: No. Sartorius flexes, abducts, and
laterally rotates the thigh at the hip joint.
Explanation E: No. Tensor fascia lata abducts, medially
rotates, and flexes the thigh.
Explanation F: No. Vastus lateralis extends the leg at
the knee.
Explanation G: No. Vastus medialis extends the leg at
the knee.

Explanation D: No. The first heart sound reflects mitral


then tricuspid valve closure.
Explanation E: No. The second heart sound reflects
aortic then pulmonic valve closure.
Explanation F: No. The first heart sound reflects mitral
then tricuspid valve closure.
Explanation G: No. The first heart sound reflects mitral
then tricuspid valve closure.

Princeton Review Management, L.L.C.


839-1298-3.0

17

31. A 16-year-old male complains to his mother


that he is having difficulty on the swim team
that he recently joined at his high school. He is
able to sprint a few laps more quickly than
anyone on the team, but when asked to swim
longer distances, he is disabled by painful
muscle cramps. Which of the following is the
most likely enzyme deficiency?
(A) -1,4-glucosidase
(B) Branching enzyme
(C) Debranching enzyme
(D) Liver phosphorylase
(E) Muscle phosphorylase
(E) is correct. Deficiency of muscle phosphorylase
causes intolerance of exercise after preformed liver
glycogen stores are depleted. The result is painful
muscle cramping, as glycogen cannot be liberated as
an energy source from muscle.
Explanation A: No. -1,4-glucosidase deficiency, or
Pompes disease (type II of the glycogen storage
diseases), results in death before the age of 2 from
massive glycogen storage in the liver.
Explanation B: No. Branching enzyme deficiency, or
Andersens disease (type IV of the glycogen storage
diseases), results in death from liver cirrhosis at a
young age.
Explanation C: No. Debranching enzyme deficiency
(type III of the glycogen storage diseases) results in
death before the age of 2 from massive glycogen
storage in the liver.
Explanation D: No. Liver phosphorylase deficiency,
or Hers disease (type VI of the glycogen storage
diseases), results in death before the age of 2 from
massive glycogen storage in the liver.

18

32. A 64-year-old female is hospitalized for severe


pneumonia. She requires several days of mechanical ventilation in the intensive care unit.
After she is extubated and able to speak, she
appears to be speaking to people who are not
there. When asked to whom she is speaking, she
says she is speaking to her husband. There is no
one in the room except the patient during these
episodes. Which of the following is the best
description of this patients behavior?
(A) Delusion
(B) Hallucination
(C) Prevarication
(D) Projection
(E) Splitting
(B) is correct. This patient is hallucinating. After long
periods of intensive medical care, loss of day/night
cues and other external stimuli predispose patients to
hallucinations, false perceptions (voices, visions) that
do not exist.
Explanation A: No. Delusions are unreasonable,
usually paranoid thoughts based on some bit of reality.
Explanation C: No. Prevarication is lying, not a
psychiatric condition.
Explanation D: No. Projection is placement of personal
feelings onto another person or object as a defense
mechanism.
Explanation E: No. Splitting, a common ploy of
borderline personality disorder patients, involves
playing members of the staff against one another.

Sample CBT Section

33. A 43-year-old male presents to his primary


care physician with complaints of fever, chills,
night sweats, and a 4 kg (10 lb) weight loss in
the last 3 months. He also has a cough productive of yellow sputum. He has a history of HIV
infection (last CD4+ count = 500/mm3). Sputum
smear stained with the Ziehl-Neelsen method
demonstrates acid-fast bacilli. Pending culture
results, the patient is prescribed 4 medications.
Why is treatment with multiple medications
necessary?
(A) Anticipated noncompliance with
treatment
(B) Due to the patients HIV status
(C) Extreme virulence of the isolate
(D) High frequency of mutational resistance
(E) High rate of medication side effects
(D) is correct. This patient has Mycobacterium
tuberculosis infection. Mutational resistance to
antituberculous drugs occurs at a frequency of 10-7 to
10 -10 and mutants often come to predominate.
Resistance develops because organisms are sufficiently
numerous to include resistant mutants that can grow
during treatment and produce relapse. The use of
multiple medications reduces this problem because the
likelihood of a doubly or triply resistant mutant is very
low.
Explanation A: No. Noncompliance with the treatment
of Mycobacterium tuberculosis infection is a serious
problem, but is not the reason for the use of multiple
medications in its treatment.
Explanation B: No. Patients with HIV infection require
a longer period of treatment, but not additional
medications for the treatment of Mycobacterium
tuberculosis infection.

34. A 72-year-old female is admitted to the hospital with fever and hypotension. Several days
prior to admission, she began to have urinary
burning and frequency, but did not seek medical attention. Blood cultures are obtained on
admission and yield Escherichia coli. Despite
appropriate antibiotic treatment, she remains
hypotensive and develops disseminated intravascular coagulation. Endotoxin is implicated.
Which of the following is the most likely
component of endotoxin to be mediating these
effects?
(A) A subunit
(B) Lipid A
(C) O-polysaccharide side chain
(D) Peptidoglycan
(E) Polysaccharide core
(B) is correct. Lipid A is the component of endotoxin
responsible for the dramatic physiologic response that
includes fever, hypotension, leukopenia, and
disseminated intravascular coagulation.
Explanation A: No. A subunit is the pathogenic subunit
of the numerous A-B exotoxins, while B subunits
mediate cell-binding.
Explanation C: No. The variable O-polysaccharide
side chain of endotoxin is responsible for the antigenic
diversity of endotoxin.
Explanation D: No. Peptidoglycan is a component of
the gram-positive bacterial cell wall released as an
exotoxin.
Explanation E: No. The polysaccharide core of
endotoxin is responsible for the antigenic diversity of
endotoxin.

Explanation C: No. Mycobacterium tuberculosis is not


a particularly virulent organism, but without a multiple
medication regimen, is difficult to eradicate.
Explanation E: No. There is a high rate of medication
side effects from each anti-tubercular agent. However,
this is not the reason to prescribe multiple agents for
the treatment of Mycobacterium tuberculosis infection.

Princeton Review Management, L.L.C.


839-1298-3.0

19

35. A 72-year-old male presents to his primary


care physician with complaints of fatigue
worsening over the last several months. He has
splenomegaly. His peripheral blood smear
demonstrates typical cells of hairy-cell leukemia. Which of the following is a marker for
hairy-cell leukemia?
(A) Alpha-fetoprotein
(B) Beta2-microglobulin
(C) CA-125
(D) CD 25
(E) Carcinoembryonic antigen (CEA)
(F) Lactate dehydrogenase (LDH)
(G) Prostate specific antigen (PSA)
(D) is correct. Hairy-cell leukemia is an uncommon,
usually indolent hematologic malignancy. It is almost
unheard of in patients younger than 55 years old, and
is more prevalent in males. Malignant cells are CD 25
positive.
Explanation A: No. Alpha-fetoprotein is most
commonly elevated in hepatocellular carcinoma.
Explanation B: No. Beta2-microglobulin is elevated in
patients with multiple myeloma.
Explanation C: No. CA-125 is most commonly elevated
in patients with ovarian cancer.
Explanation E: No. Carcinoembryonic antigen is most
commonly elevated in patients with colon carcinoma.

36. A 19-year-old college student is seen less and


less by his friends. His appearance has become
disheveled and unkempt over the last several
months. He seems to have lost all interest in
his studies. Lately, he has been mumbling
about aliens and an invasion. His roommate has
found him talking to the television. Which of
the following neurotransmitter disturbances is
hypothesized to cause this psychiatric illness?
(A) Depletion of acetylcholine
(B) Depletion of dopamine
(C) Depletion of -aminobutyric acid
(D) Excessive production of acetylcholine
(E) Excessive production of dopamine
(F) Excessive production of -aminobutyric
acid
(G) Excessive production of norepinephrine
(E) is correct. Schizophrenia results in profound thought
disturbance with prominent withdrawal, paranoia,
auditor y hallucinations, and bizarre behavior.
Excessive amounts of dopamine are postulated to play
a role in schizophrenia.
Explanation A: No. There is a postulated role for the
depletion of acetylcholine in the pathophysiology of
Alzheimers disease.
Explanation B: No. There is a postulated role for the
depletion of dopamine in the pathophysiology of
Parkinsons disease.

Explanation F: No. LDH is a nonspecific marker that is


usually elevated in patients with lymphoma.

Explanation C: No. Depletion of -aminobutyric acid


is postulated to play a role in the pathophysiology of
Huntingtons disease.

Explanation G: No. Prostate specific antigen is a serum


tumor marker for prostate cancer.

Explanation D: No. Acteylcholine does not play a role


in the pathophysiology of schizophrenia.
Explanation F: No. Excess of -aminobutyric acid does
not play a role in the pathophysiology of
schizophrenia.
Explanation G: No. Norepinephrine does not play a
role in the pathophysiology of schizophrenia.

20

Sample CBT Section

37. Which of the following is the molecular defect


in globin that results in sickle cell anemia?
(A) Deletion of arginine at position 6 of the
beta chain
(B) Deletion of glutamate at position 6 of
the beta chain
(C) Deletion of valine at position 6 of the
alpha chain
(D) Substitution of glutamate for valine at
position 6 of the alpha chain
(E) Substitution of valine for glutamate at
position 6 of the beta chain
(E) is correct. Hemoglobin S is the abnormal
hemoglobin of sickle cell disease, secondary to a
substitution of valine for glutamate at the sixth position
of the beta chain. Patients are symptomatic from a
young age.
Explanation A: No. The defect is a substitution of a
valine for a glutamate at the sixth position of the beta
chain.
Explanation B: No. The defect is a substitution of a
valine for a glutamate at the sixth position of the beta
chain.
Explanation C: No. The defect is a substitution of a
valine for a glutamate at the sixth position of the beta
chain.
Explanation D: No. The defect is a substitution of a
valine for a glutamate at the sixth position of the beta
chain.

38. A 34-year-old male is visiting Venezuela on a


photography tour. After several days shooting
photos at the edge of a brackish swamp, he is
struck with massive watery diarrhea. He is airlifted to a hospital for intravenous hydration
and he recovers fully. Which of the following
enzymatic mechanisms does the toxin that
caused this patients diarrhea exploit?
(A) Activation of cGMP phosphodiesterase
(B) Irreversible deactivation of adenylate
cyclase
(C) Irreversible deactivation a phospholipase C
(D) Persistent activation of adenylate
cyclase
(E) Persistent activation of a phospholipase C
(D) is correct. Cholera toxin consists of A and B
subunits. The B subunits are used to gain entry into
the intestinal mucosal cells via recognition of
sphingolipids. Once in the cell, the A subunit
catalyzes the transfer of an ADP-ribose unit to the G
protein subunit. This impairs the ability of the G
proteins subunit to hydrolyze GTP to GDP, locking
the G protein in the activated form. Thus, adenylate
cyclase remains persistently activated, producing high
levels of intracellular cyclic AMP. High levels of cyclic
AMP stimulate activate transport of ions, including
sodium, resulting in massive secretory diarrhea.
Explanation A: No. Activation of cGMP
phosphodiesterase is involved in visual excitement.
Explanation B: No. Adenylate cyclase is persistently
activated by cholera toxin.
Explanation C: No. Phospholipase C is involved in
many cell functions, but not the action of cholera toxin.
Explanation E: No. Phospholipase C is involved in
many cell functions, but not the action of cholera toxin.

Princeton Review Management, L.L.C.


839-1298-3.0

21

39. A 45-year-old male presents to his primary


care physician with complaints of abdominal
pain, relieved with meals. He has been taking
ranitidine with some relief.
Esophagogastroduodenoscopy reveals a
duodenal ulcer. Tests for Helicobacter pylori
are negative. The patient is placed on
omeprazole. Which of the following is the
action of omeprazole?
(A) Antagonism of parietal cell histamine
H 2 receptor
(B) Enhancement of duodenal bicarbonate
secretion
(C) Inhibition of gastrin release
(D) Inhibition of parietal cell hydrogen/
potassium ATPase
(E) Stimulation of lower esophageal sphincter tone
(D) is correct. Acid secretion into the canaliculi of the
gastric parietal cell is accomplished by a membranebound ATPase that exchanges potassium and hydrogen
ions. The activity of the pump is controlled by gastrin,
histamine, and acetylcholine. Omeprazole is an
irreversible inhibitor of the hydrogen/potassium
ATPase.
Explanation A: No. Histamine H2 receptor antagonists
such as cimetidine and ranitidine are competitive
antagonists of the histamine H2 receptor on gastric
parietal cells. They reduce basal acid secretion, but
do not completely suppress acid secretion.
Explanation B: No. One of the postulated actions of
misoprostol, a prostaglandin E analogue, is
enhancement of duodenal bicarbonate secretion.

40. A 2-year-old male is brought to the pediatrician by his mother who is concerned about his
severe constipation. Her son frequently goes
without a bowel movement for a week to ten
days. Findings on barium enema suggest
Hirschsprungs disease. A rectal biopsy is
planned. Which of the following is the pathologic lesion of Hirschsprungs disease?
(A) Absence of ganglion cells
(B) Eosinophilic infiltration
(C) Mucosal inflammation
(D) Multiple colonic polyps
(E) Transmural inflammation
(A) is correct. Hirschsprungs disease, or congenital
megacolon, is characterized by congenital absence
of ganglion cells in the wall of the rectum. The
aganglionic segment is chronically contracted, making
passage of fecal contents difficult with resultant
constipation. Treatment is excision of the aganglionic
segment.
Explanation B: No. Eosinophilic infiltration of the rectal
wall is not the pathologic lesion in Hirschsprungs
disease.
Explanation C: No. Mucosal inflammation of the rectal
mucosa is most suggestive of ulcerative colitis.
Explanation D: No. There are several syndromes
associated with multiple colonic polyps developed at
an early age, the most common being familial
adenomatous polyposis, an autosomal dominant
inherited disease.
Explanation E: No. Transmural inflammation of the
rectal mucosa is most suggestive of Crohns disease.

Explanation C: No. Omeprazole does not inhibit


gastrin release.
Explanation E: No. Cisapride stimulates release of
acetylcholine from the esophageal myenteric plexus,
which increases lower esophageal sphincter tone.

22

Sample CBT Section

41. A 22-year-old female presents to her primary


care physician with complaints of headache
and visual changes. Visual field testing demonstrates a bitemporal hemianopia. Magnetic
resonance imaging of the brain reveals a tumor.
Which of the following is the most likely
location of the tumor?
(A) Left optic radiation
(B) Occipital lobe
(C) Optic chiasm
(D) Right parietal lobe optic tract
(E) Right temporal lobe optic tract
(C) is correct. A lesion that compresses the optic
chiasm, such as a large pituitary tumor, would destroy
the nasal half of the retinal information from both eyes.
As images are inverted on the retina, such a lesion
causes a bitemporal hemianopia.
Explanation A: No. A lesion of the left optic radiation
would result in a bilateral left hemianopia.
Explanation B: No. Total loss of the occipital lobe would
result in blindness.

42. Which of the following changes favor the


dissociation of oxygen from hemoglobin?
(A) Decreased carbon dioxide concentration
(B) Decreased hydrogen ion concentration
(C) Decreased temperature
(D) Increased 2,3-diphosphglycerate
(E) Increased pH
(D) is correct. An increase in the concentration of 2,3diphosphoglycerate favors the unloading of oxygen
from hemoglobin in tissues. Each of the other factors
is unfavorable and would shift the oxygen dissociation
curve to the left.
Explanation A: No. Increased carbon dioxide
concentration favors oxygen dissociation.
Explanation B: No. Increased hydrogen ion
concentration favors oxygen dissociation.
Explanation C: No. Increased temperature favors
oxygen dissociation.
Explanation E: No. Decreased pH favors oxygen
dissociation.

Explanation D: No. A lesion in the right parietal lobe


optic tract would result in a bilateral right inferior
quadrantinopia.
Explanation E: No. A lesion in the right temporal lobe
optic tract would result in a bilateral right superior
quadrantinopia.

Princeton Review Management, L.L.C.


839-1298-3.0

23

43. A 43-year-old runner presents to his primary


care doctor with questions about increasing his
athletic performance. He asks if a muscle
biopsy might give him information about how
to best train his particular muscle type. The
physician explains the difference between fast
and slow fibers while gently telling the patient
that muscle biopsy is an invasive and unnecessary test. Which of the following is characteristic of fast muscle fibers?

44. During which phase of the cell cycle do


chromatids line up on the equatorial plate?
(A) Anaphase
(B) Metaphase
(C) Prometaphase
(D) Prophase
(E) Telophase
(B) is correct. During metaphase of the cell cycle,
chromatids align on the equatorial plate.

(A) Fast fibers are designed for continuous,


prolonged activity
(B) Fast fibers have a high concentration of
myoglobin
(C) Fast fibers have an extensive capillary
network for oxygen delivery
(D) Fast fibers have large numbers of
mitochondria
(E) Fast fibers rely upon glycolytic metabolism for energy

Explanation A: No. During anaphase of the cell cycle,


the chromatids are pulled apart at the centromere.

(E) is correct. Slow fibers are designed for prolonged


continuous activity using oxidative metabolism. Fast
fibers are designed for rapid, powerful, but brief
muscle contractions using glycolytic pathways. In order
to optimize oxidative metabolism, slow fibers have a
more extensive capillary network for oxygen delivery,
more mitochondria, and a larger myoglobin content
than fast fibers. Slow fibers are also smaller in
diameter.

Explanation E: No. During telophase of the cell cycle,


the mitotic apparatus dissolves and new nuclear
membranes form in the two daughter cells.

Explanation C: No. During prometaphase of the cell


cycle, the nuclear membrane fragments and
microtubules begin to form from the kinetocore.
Explanation D: No. During prophase of the cell cycle,
the chromosomes condense.

Explanation A: No. Slow fibers are designed for


prolonged continuous activity.
Explanation B: No. Slow fibers have a high
concentration of myoglobin.
Explanation C: No. Slow fibers have an extensive
capillary network for oxygen delivery.
Explanation D: No. Slow fibers have large numbers
of mitochondria to support oxidative metabolism.

24

Sample CBT Section

45. A 35-year-old female presents to her primary


care physician with complaints of hot flashes,
night sweats, and irregular menstrual periods
over the last several months. Pelvic examination is normal. Laboratory studies are obtained.
Which of the following is most consistent with
premature ovarian failure?
(A) Decreased cortisol
(B) Decreased luteinizing hormone
(C) Increased estrogen
(D) Increased follicle stimulating hormone
(E) Increased progesterone
(D) is correct. This patient is experiencing classic
symptoms of menopause: hot flashes, sweats,
irritability, and irregular menstrual cycles. In such a
young patient, the most likely cause of these symptoms
is premature ovarian failure. As less and less estrogen
is produced by the failing ovaries, there is decreased
inhibition of the pituitary products with a resultant
increase in luteinizing hormone and a large increase
in circulating levels of follicle stimulating hormone.
Explanation A: No. Cortisol levels are not affected by
ovarian failure.
Explanation B: No. As less and less estrogen is
produced by the failing ovaries, there is decreased
inhibition of the pituitary products with a resultant
increase in luteinizing hormone and follicle stimulating
hormone.
Explanation C: No. As the ovaries fail, there is less
and less secretion of estrogen, which results in the
symptoms of menopause: hot flashes, sweats,
irritability, and irregular menstrual cycles.

46. Which of the following correctly identifies the


sequence of energy usage by contracting
muscle?
(A) Glycogen oxidative metabolism
phosphocreatine
(B) Lactate glycogen oxidative
metabolism
(C) Phosphocreatine glycogen oxidative metabolism
(D) Phosphocreatine oxidative metabolism glycogen
(E) Oxidative metabolism glycogen
lactate
(C) is correct. The muscle store of phosphocreatine is
depleted in 7 to 8 seconds after the initiation of muscle
contraction. The supply of glycogen is then used and
is depleted in approximately 1 minute. Finally,
oxidative metabolism is used as the primary source of
energy for muscle contraction. If the capacity of
oxidative metabolism is exceeded, lactate is generated.
Explanation A: No. Phosphocreatine is the first source
of energy used for muscle contraction.
Explanation B: No. Lactate is generated after the
capacity of oxidative metabolism is exceeded.
Explanation D: No. Glycogen is utilized prior to the
initiation of oxidative metabolism.
Explanation E: No. Glycogen is utilized prior to the
initiation of oxidative metabolism.

Explanation E: No. There is diminished production of


both estrogen and progesterone by the failing ovaries.

Princeton Review Management, L.L.C.


839-1298-3.0

25

47. A 54-year-old male is brought to the Emergency Department with crushing substernal
chest pain that began about 30 minutes ago. An
electrocardiogram demonstrates 3 millimeters
of ST segment elevation in the anterior leads
consistent with an acute myocardial infarction.
Sublingual nitroglycerin is administered with
amelioration of the pain. Which of the following best describes the intracellular action of
sublingual nitroglycerin?
(A) Activation of adenylate cyclase in
vascular smooth muscle
(B) Activation of guanylate cyclase in
vascular smooth muscle
(C) Activation of phospholipase C in
vascular smooth muscle
(D) Inhibition of adenylate cyclase in
vascular smooth muscle
(E) Inhibition of guanylate cyclase in
vascular smooth muscle
(B) is correct. Organic nitrates are vasodilators of
vascular smooth muscle that mimic the effects of
endogenous nitric oxide (or endothelium-derived
relaxing factor). The free nitric oxide radicals combine
with thiol groups in vascular endothelium to form
nitrosothiols. These nitrosothiols activate guanylate
cyclase, which raises the concentration of cyclic GMP.
Increased levels of cGMP act to reduce intracellular
calcium available to the contractile mechanism of
vascular smooth muscle, hence, there is vascular
smooth muscle dilatation.

48. Which of the following reactions depends upon


cobalamin (vitamin B12) as a cofactor?
(A) Acetyl CoA malonyl CoA
(B) Citrate isocitrate
(C) Pyruvate acetyl CoA
(D) Ribonucleoside diphosphate
deoxyribonucleoside diphosphate
(E) Ribose 5-phosphate 5phosphoribosyl-1-pyrophosphate
(D) is correct. The conversion of ribonucleoside
diphosphate to deoxyribonucleoside diphosphate by
ribonucleoside reductase is dependent on the transient
transfer of a tyrosyl radical. Vitamin B12 serves as the
source of this radical.
Explanation A: No. The conversion of acetyl CoA to
malonyl CoA by acetyl CoA carboxylase is the key
site of control for fatty acid synthesis, but does not
require vitamin B12 as a cofactor.
Explanation B: No. The conversion of citrate to
isocitrate by aconitase does not require vitamin B12 as
a cofactor.
Explanation C: No. The conversion of pyruvate to
acetyl CoA by pyruvate dehydrogenase requires
thiamine as a cofactor, not vitamin B12.
Explanation E: No. The conversion of ribose 5phosphate to 5-phosphoribosyl-1-pyrophosphate
(PRPP) by ribose phosphate pyrophosphokinase uses
ATP, but does not require vitamin B12 as a cofactor.

Explanation A: No. Activation of adenylate cyclase is


a commonly used intracellular messenger system, but
is not the mechanism of organic nitrates.
Explanation C: No. Phospholipase C is involved in
many cell actions, but is not the mechanism of organic
nitrates.
Explanation D: No. Inhibition of adenylate cyclase is
a commonly used intracellular messenger system, but
is not the mechanism of organic nitrates.
Explanation E: No. Organic nitrates act to activate
guanylate cyclase in vascular smooth muscle.

26

Sample CBT Section

49. Taste sensation to the anterior two-thirds of the


tongue is controlled by the afferent portion of
which cranial nerve?
(A) Cranial nerve V
(B) Cranial nerve VIII
(C) Cranial nerve IX
(D) Cranial nerve X
(E) Cranial nerve XII
(A) is correct. Taste sensations pass first through cranial
nerve V, then enter the chorda tympani, into the facial
nerve, then into the tractus solitarius of the brain stem.
Explanation B: No. Cranial nerve VIII is responsible
for the sensation of hearing.
Explanation C: No. Cranial nerve IX is responsible
for taste sensation of the posterior third of the tongue.
Explanation D: No. Cranial nerve X controls a few
taste buds on the base of the tongue and pharynx.
Explanation E: No. Cranial nerve XII controls motor
function of the tongue.

50. A 40-year-old male presents to his primary


care doctor with complaints of cough, fever,
and weight loss. He has a long history of
intravenous drug abuse. A bronchoalveolar
lavage reveals yeast forms consistent with
Pneumocystis carinii. He is confirmed to be
HIV positive. Prior to treating his HIV infection, a CD4 + count is obtained. What is the
most likely result?
(A) 100/mm3
(B) 300/mm3
(C) 400/mm3
(D) 600/mm3
(E) 800/mm3
(A) is correct. Pneumocystis carinii is a common
opportunistic infection in patients with HIV infection.
However, infection with Pneumocystis carinii is rare in
patients with CD4+ counts greater than 200/mm3.
Explanation B: No. Infection with Pneumocystis carinii
is rare in patients with CD4+ counts greater than 200/
mm3.
Explanation C: No. Infection with Pneumocystis carinii
is rare in patients with CD4+ counts greater than 200/
mm3.
Explanation D: No. Infection with Pneumocystis carinii
is rare in patients with CD4+ counts greater than 200/
mm3.
Explanation E: No. Infection with Pneumocystis carinii
is rare in patients with CD4+ counts greater than 200/
mm3.

END OF EXAMINATION

Princeton Review Management, L.L.C.


839-1298-3.0

27

LABORATORY VALUES
Reference Range

SI Reference Intervals

8-20 U/L
25-125 U/L
8-20 U/L
0.1-1.0 mg/dL // 0.0-0.3 mg/dL
8.4-10.2 mg/dL
140-250 mg/dL
0800 h: 5-23 g/dL // 1600 h: 3-15 g/dL
2000 h: 50% of 0800 h
Male: 25-90 U/L
Female: 10-70 U/L
0.6-1.2 mg/dL

8-20 U/L
25-125 U/L
8-20 U/L
2-17 mol/L // 0-5 mol/L
2.1-2.8 mmol/L
3.6-6.5 mmol/L
138-635 nmol/L // 82-413 mmol/L
Fraction of 0800 h: 0.50
25-90 U/L
10-70 U/L
53-106 mol/L

135-147 mEq/L
95-105 mEq/L
3.5-5.0 mEq/L
22-28 mEq/L
1.5-2.0 mEq/L

135-147 mmol/L
95-105 mmol/L
3.5-5.0 mmol/L
22-28 mmol/L
1.5-2.0 mmol/L

30-170 ng/mL // 60-280 ng/mL


40-220 ng/mL // 80-350 ng/mL
Male: 15-200 ng/mL
Female: 12-150 ng/mL
Male: 4-25 mIU/mL
Female: premenopause 4-30 mIU/mL
midcycle peak 10-90 mIU/mL
postmenopause 40-250 mIU/mL

104-590 // 208-970 nmol/L


140-760 // 280-1210 nmol/L
15-200 g/L
12-150 g/L
4-25 U/L
4-30 U/L
10-90 U/L
40-250 U/L

7.35-7.45
33-45 mm Hg
75-105 mm Hg
Fasting: 70-110 mg/dL
2-h postprandial: < 120 mg/dL
Fasting: < 5 ng/mL
provocative stimuli: > 7 ng/mL

[H+] 36-44 nmol/L


4.4-5.9 kPa
10.0-14.0 kPa
3.8-6.1 mmol/L
< 6.6 mmol/L
< 5 g/L
> 7 g/L

76-390 mg/dL
0-380 IU/mL
650-1500 mg/dL
40-345 mg/dL
50-170 g/dL
45-90 U/L
Male: 6-23 mIU/mL
Female: follicular phase 5-30 mIU/mL
midcycle 75-150 mIU/mL
postmenopause 30-200 mIU/mL
275-295 mOsmol/kg
230-630 pg/mL
20-70 U/L
3.0-4.5 mg/dL
< 20 ng/mL

0.76-3.90 g/L
0-380 kIU/L
6.5-15 g/L
0.4-3.45 g/L
9-30 mol/L
45-90 U/L
6-23 U/L
5-30 U/L
75-150 U/L
30-200 U/L
275-295 mOsmol/kg
230-630 ng/L
20-70 U/L
1.0-1.5 mmol/L
< 20 g/L

6.0-7.8 g/dL
3.5-5.5 g/dL
2.3-3.5 g/dL
0.5-5.0 U/mL
8-30% of administered dose/24 h
5-12 g/dL
35-160 mg/dL
115-190 ng/dL
25-35%

60-78 g/L
35-55 g/L
23-35 g/L
0.5-5.0 mU/L
0.08-0.30/24 h
64-155 nmol/L
0.4-1.81 mmol/L
1.8-2.9 nmol/L
0.25-0.35

BLOOD, PLASMA, SERUM


Alanine aminotransferase (ALT, GPT at 30C)
Amylase, serum
Aspartate aminotransferase (AST, GOT at 30C)
Bilirubin, serum (adult) Total // Direct
Calcium, serum (Ca2+)
Cholesterol, serum
Cortisol, serum
Creatine kinase, serum (at 30C) ambulatory
Creatinine, serum
Electrolytes, serum
Sodium (Na+)
Chloride (Cl)
Potassium (K+)
Bicarbonate (HCO3)
Magnesium (Mg2
(Mg +)
Estriol, total serum (in pregnancy)
24-28 wks // 32-36 wks
28-32 wks // 36-40 wks
Ferritin, serum
Follicle-stimulating hormone, serum/plasma

Gases, arterial blood (room air)


pH
PCO2
PO2
Glucose, serum
Growth hormone - arginine stimulation
Immunoglobulins, serum
IgA
IgE
IgG
IgM
Iron
Lactate dehydrogenase, (LP, 30C)
Luteinizing hormone, serum/plasma

Osmolality, serum
Parathyroid hormone, serum, N-terminal
Phosphatase (alkaline), serum (p-NPP at 30C)
Phosphorus (inorganic), serum
Prolactin, serum (hPRL)
Proteins, serum
Total (recumbent)
Albumin
Globulins
Thyroid-stimulating hormone, serum or plasma
Thyroidal iodine (123 I) uptake
Thyroxine (T4), serum
Triglycerides, serum
Triiodothyronine (T3), serum (RIA)
Triiodothyronine (T3) resin uptake

LABORATORY VALUES (cont'd)


Urea nitrogen, serum (BUN)
Uric acid, serum

Reference range

SI reference intervals

7-18 mg/dL
3.0-8.2 mg/dL

1.2-3.0 mmol urea/L


0.18-0.48 mmol/L

0-5 cells/mm 3

0-5 x 106/L
118-132 mmol/L
0.03-0.12
2.2-3.9 mmol/L
70-180 mm H2 O
< 0.40 g/L

CEREBROSPINAL FLUID
Cell count
Chloride
Gamma globulin
Glucose
Pressure
Proteins, total
HEMATOLOGIC
Bleeding time (template)
Erythrocyte count

118-132 mEq/L

3-12% total proteins


40-70 mg/dL
70-180 mm H 2O
< 40 mg/dL

2-7 minutes
Male: 4.3-5.9 million/mm 3
Female: 3.5-5.5 million/mm 3
Erythrocyte sedimentation rate (Westergren) Male: 0-15 mm/h
Female: 0-20 mm/h
Hematocrit
Male: 41-53%
Female: 36-46%
6%
Hemoglobin A1C
Hemoglobin, blood
Male: 13.5-17.5 g/dL
Female: 12.0-16.0 g/dL
Hemoglobin, plasma
1-4 mg/dL
Leukocyte count and differential
Leukocyte count
4,500-11,000/mm3
Segmented neutrophils
54-62%
Band forms
3-5%
Eosinophils
1-3%
Basophils
0-0.75%
Lymphocytes
25-33%
Monocytes
3-7%
Mean corpuscular hemoglobin
25.4-34.6 pg/cell
Mean corpuscular hemoglobin concentration 31-36% Hb/cell
Mean corpuscular volume
80-100 m3
Partial thromboplastin time (activated)
28-40 seconds
Platelet count
150,000-400,000/mm 3
Prothrombin time
11-15 seconds
Reticulocyte count
0.5-1.5% of red cells
Thrombin time
< 2 seconds deviation from control
Volume
Plasma
Male: 25-43 mL/kg
Female: 28-45 mL/kg
Red cell
Male: 20-36 mL/kg
Female: 19-31 mL/kg

SWEAT
Chloride
URINE
Calcium
Chloride
Creatinine clearance
Estriol, total (in pregnancy)
30 wks
35 wks
40 wks
17-Hydroxycorticosteroids
17-Ketosteroids, total
Osmolality
Oxalate
Potassium
Proteins, total
Sodium
Uric acid

2-7 minutes
4.3-5.9 x 1012/L
3.5-5.5 x 1012/L
0-15 mm/h
0-20 mm/h
0.41-0.53
0.36-0.46
0.06%
2.09-2.71 mmol/L
1.86-2.48 mmol/L
0.16-0.62 mmol/L
4.5-11.0 x 109/L
0.54-0.62
0.03-0.05
0.01-0.03
0-0.0075
0.25-0.33
0.03-0.07
0.39-0.54 fmol/cell
4.81-5.58 mmol Hb/L
80-100 fl
28-40 seconds
150-400 x 109/L
11-15 seconds
0.005-0.015
< 2 seconds deviation from control
0.025-0.043 L/kg
0.028-0.045 L/kg
0.020-0.036 L/kg
0.019-0.031 L/kg

0-35 mmol/L

0-35 mmol/L

100-300 mg/24 h
Varies with intake
Male: 97-137 mL/min
Female: 88-128 mL/min

2.5-7.5 mmol/24 h
Varies with intake

6-18 mg/24 h
9-28 mg/24 h
13-42 mg/24 h
Male: 3.0-10.0 mg/24 h
Female: 2.0-8.0 mg/24 h
Male: 8-20 mg/24 h
Female: 6-15 mg/24 h
50-1400 mOsmol/kg
8-40 g/mL
Varies with diet
< 150 mg/24 h
Varies with diet
Varies with diet

21-62 mol/24 h
31-97 mol/24 h
45-146 mol/24 h
8.2-27.6 mol/24 h
5.5-22.0 mol/24 h
28-70 mol/24 h
21-52 mol/24 h
50-1400 mOsmol/kg
90-445 mol/24 h
Varies with diet
< 0.15 g/24 h
Varies with diet
Varies with diet

IMPORTANT: The following codes should be copied onto your answer


sheet exactly as shown.
Copy this in
box 2 on your
answer sheet

2. TEST FORM

3. TEST CODE

MLE99

8 3 9

Copy this code in


box 3 on your
answer sheet; then
blacken the
corresponding
ovals, exactly as
shown

0
1
2
3
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8
9

0
1
2
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8
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0
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1
0
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Answer Sheet 10

General Directions
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