9/26/25, 3:37 PM NBME 26 <span style="color:#000;font-weight:bold;">200+</span> (2025-2026 A+ Graded) Exam-Style Questions | Verified Solutio…
NBME 26 Exam Questions and Answers
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Question 1
1
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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 guanine to guanosine monophosphate and hypoxanthine to inosine
monophosphate. Patients with deficient activity of HGPRT are unable to salvage
guanine and
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
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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
Page 3 of 399
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Question 2
2
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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
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
Page 4 of 399
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NBME 26 Exam Questions and Answers
Latest
Page 1 of 399
1/399
,9/26/25, 3:37 PM NBME 26 <span style="color:#000;font-weight:bold;">200+</span> (2025-2026 A+ Graded) Exam-Style Questions | Verified Solutio…
Question 1
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 guanine to guanosine monophosphate and hypoxanthine to inosine
monophosphate. Patients with deficient activity of HGPRT are unable to salvage
guanine and
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
Page 2 of 399
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,9/26/25, 3:37 PM NBME 26 <span style="color:#000;font-weight:bold;">200+</span> (2025-2026 A+ Graded) Exam-Style Questions | Verified Solutio…
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
Page 3 of 399
3/399
, 9/26/25, 3:37 PM NBME 26 <span style="color:#000;font-weight:bold;">200+</span> (2025-2026 A+ Graded) Exam-Style Questions | Verified Solutio…
Question 2
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
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
Page 4 of 399
4/399
