NBME CBSE Final Exam Questions and
Correct Answers Already Graded A+ Brand
New Version 2025
1
Exam Section 1: Item 2 of 50
National, Board of Medical Examiners
Comprehensive Basic Science Self-Assessment
2. Free purine and pyrimidine bases are reutilized in normal metabolism. In children with Lesch-
Nyhan syndrome who have intellectual disability, poor muscle coordination, and self-mutilation
tendencies, there is a defect in the salvage of which of the following
pairs of bases?
A) Adenine and thymine
B) Guanine and hypoxanthine
C) Guanine and uric acid
D) Uracil and cytosine
E) Xanthine and hypoxanthine
- Correct Answer :B.
Lesch-Nyhan syndrome presents with intellectual disability, aggressive behavior, self-mutilation,
gout, and dystonia. The disorder is due to inactivating mutations of hypoxanthine-guanine
phosphoribosyltransferase (HGPRT), a key enzyme in the purine salvage
pathway, and is inherited in an X-linked recessive fashion. HGPRT catalyzes the conversion of
A+ TEST BANK 1
,guanine to guanosine monophosphate and hypoxanthine to inosine monophosphate. Patients
with deficient activity of HGPRT are unable to salvage guanine and
A+ TEST BANK 2
,hypoxanthine and develop resultant increased levels of xanthine and uric acid. Hyperuricemia in
Lesch-Nyhan syndrome is treated with xanthine oxidase inhibitors, such as allopurinol or
febuxostat, in order to reduce the synthesis of uric acid.
Incorrect Answers: A, C, D and E.
Adenine and thymine (Choice A) are purine and pyrimidine bases, respectively. Purine and
pyrimidine salvage are handled through two distinct pathways that are not commonly involved in
a single disease process.
Guanine and uric acid (Choice C) accumulation may occur as part of Lesch-Nyhan syndrome,
however, the accumulation of uric acid is also secondary to accumulation of hypoxanthine.
Choice B more accurately describes defective salvage of guanine and
hypoxanthine as the fundamental effect of HGPRT dysfunction. The accumulation of uric acid is
secondary.
Uracil and cytosine (Choice D) are pyrimidine nucleotides. Pyrimidine salvage is not affected by
mutations of HGPRT.
Defects of xanthine and hypoxanthine (Choice E) metabolism may result from defects in HGPRT.
However, HGPRT dysfunction results in impaired hypoxanthine salvage with resultant excessive
production of xanthine, rather than impaired xanthine salvage.
Educational Objective: Lesch-Nyhan syndrome presents with intellectual disability, aggressive
behavior, self-mutilation, gout, and dyst
2
Exam Section 1: Item 3 of 50
National Board of Medical Examiners
Comprehensive Basic Science Self-Assessment
3. A 42-year-old man is struck by a motor vehicle. His only injury is a closed fracture of the
proximal tibia. Initial neurovascular examination shows no deficits. Twenty-four hours later, he
has increased leg pain and paresthesias in the dorsal space between his
A+ TEST BANK 3
, first and second toes. The patient begins to pass dark red urine and becomes oliguric. Urinalysis
is positive for blood but no erythrocytes are seen on microscopic examination. Which of the
following acute disorders is the most likely cause of the renal
failure?
A) Glomerulonephritis
B) Hemolytic-uremic syndrome
C) Interstitial nephritis
D) Nephrotic syndrome
E) Tubular necrosis
- Correct Answer :E.
Tibial fractures present a high risk for compartment syndrome. The fracture results in blood
vessel injury and muscle injury, inflammation, and edema. Because the fascia containing the
anterior compartment of the leg does not stretch, bleeding and swelling can
cause increased pressure in the compartment. This increased pressure in turn inhibits venous
drainage, further increasing pressure in the compartment. Eventually the nerve supply and
associated arteries are compromised, leading to the classic signs and
symptoms of compartment syndrome. Signs and symptoms of compartment syndrome include
pain out of proportion to examination findings, pain with passive movement of the muscles,
paresthesia, pallor, pulselessness, and paralysis. Compromised blood supply
deprives muscle and tissue of oxygen and glucose, leading to tissue ischemia and necrosis.
Muscle necrosis leads to rhabdomyolysis, myoglobinuria, and acute renal failure. Evaluation of
rhabdomyolysis reveals red or brown urine and urinalysis is typically positive
for blood due to the presence of myoglobinuria without microscopic evidence of red blood cells.
A complication of rhabdomyolysis is acute kidney injury from acute tubular necrosis secondary to
the release of nephrotoxic myoglobin and nonprotein heme pigments.
Acute tubular necrosis typically occurs following an ischemic or nephrotoxic insult to the kidneys,
which results in loss of the tubular epithelium. Granular, muddy brown casts are common on
urinalysis. Compartment syndrome is treated by immediate fasciotomy to
A+ TEST BANK 4
Correct Answers Already Graded A+ Brand
New Version 2025
1
Exam Section 1: Item 2 of 50
National, Board of Medical Examiners
Comprehensive Basic Science Self-Assessment
2. Free purine and pyrimidine bases are reutilized in normal metabolism. In children with Lesch-
Nyhan syndrome who have intellectual disability, poor muscle coordination, and self-mutilation
tendencies, there is a defect in the salvage of which of the following
pairs of bases?
A) Adenine and thymine
B) Guanine and hypoxanthine
C) Guanine and uric acid
D) Uracil and cytosine
E) Xanthine and hypoxanthine
- Correct Answer :B.
Lesch-Nyhan syndrome presents with intellectual disability, aggressive behavior, self-mutilation,
gout, and dystonia. The disorder is due to inactivating mutations of hypoxanthine-guanine
phosphoribosyltransferase (HGPRT), a key enzyme in the purine salvage
pathway, and is inherited in an X-linked recessive fashion. HGPRT catalyzes the conversion of
A+ TEST BANK 1
,guanine to guanosine monophosphate and hypoxanthine to inosine monophosphate. Patients
with deficient activity of HGPRT are unable to salvage guanine and
A+ TEST BANK 2
,hypoxanthine and develop resultant increased levels of xanthine and uric acid. Hyperuricemia in
Lesch-Nyhan syndrome is treated with xanthine oxidase inhibitors, such as allopurinol or
febuxostat, in order to reduce the synthesis of uric acid.
Incorrect Answers: A, C, D and E.
Adenine and thymine (Choice A) are purine and pyrimidine bases, respectively. Purine and
pyrimidine salvage are handled through two distinct pathways that are not commonly involved in
a single disease process.
Guanine and uric acid (Choice C) accumulation may occur as part of Lesch-Nyhan syndrome,
however, the accumulation of uric acid is also secondary to accumulation of hypoxanthine.
Choice B more accurately describes defective salvage of guanine and
hypoxanthine as the fundamental effect of HGPRT dysfunction. The accumulation of uric acid is
secondary.
Uracil and cytosine (Choice D) are pyrimidine nucleotides. Pyrimidine salvage is not affected by
mutations of HGPRT.
Defects of xanthine and hypoxanthine (Choice E) metabolism may result from defects in HGPRT.
However, HGPRT dysfunction results in impaired hypoxanthine salvage with resultant excessive
production of xanthine, rather than impaired xanthine salvage.
Educational Objective: Lesch-Nyhan syndrome presents with intellectual disability, aggressive
behavior, self-mutilation, gout, and dyst
2
Exam Section 1: Item 3 of 50
National Board of Medical Examiners
Comprehensive Basic Science Self-Assessment
3. A 42-year-old man is struck by a motor vehicle. His only injury is a closed fracture of the
proximal tibia. Initial neurovascular examination shows no deficits. Twenty-four hours later, he
has increased leg pain and paresthesias in the dorsal space between his
A+ TEST BANK 3
, first and second toes. The patient begins to pass dark red urine and becomes oliguric. Urinalysis
is positive for blood but no erythrocytes are seen on microscopic examination. Which of the
following acute disorders is the most likely cause of the renal
failure?
A) Glomerulonephritis
B) Hemolytic-uremic syndrome
C) Interstitial nephritis
D) Nephrotic syndrome
E) Tubular necrosis
- Correct Answer :E.
Tibial fractures present a high risk for compartment syndrome. The fracture results in blood
vessel injury and muscle injury, inflammation, and edema. Because the fascia containing the
anterior compartment of the leg does not stretch, bleeding and swelling can
cause increased pressure in the compartment. This increased pressure in turn inhibits venous
drainage, further increasing pressure in the compartment. Eventually the nerve supply and
associated arteries are compromised, leading to the classic signs and
symptoms of compartment syndrome. Signs and symptoms of compartment syndrome include
pain out of proportion to examination findings, pain with passive movement of the muscles,
paresthesia, pallor, pulselessness, and paralysis. Compromised blood supply
deprives muscle and tissue of oxygen and glucose, leading to tissue ischemia and necrosis.
Muscle necrosis leads to rhabdomyolysis, myoglobinuria, and acute renal failure. Evaluation of
rhabdomyolysis reveals red or brown urine and urinalysis is typically positive
for blood due to the presence of myoglobinuria without microscopic evidence of red blood cells.
A complication of rhabdomyolysis is acute kidney injury from acute tubular necrosis secondary to
the release of nephrotoxic myoglobin and nonprotein heme pigments.
Acute tubular necrosis typically occurs following an ischemic or nephrotoxic insult to the kidneys,
which results in loss of the tubular epithelium. Granular, muddy brown casts are common on
urinalysis. Compartment syndrome is treated by immediate fasciotomy to
A+ TEST BANK 4
