NBME CBSE ACTUAL TEST QUESTIONS AND ANSWERS
2026/2027(Quiz bank with all the correct
answers)(usmle step 1)Medical examination
Section 1: General Principles & Cellular Pathology
Question 1
A 58-year-old man with a 30-pack-year smoking history presents with a
3-cm pulmonary mass. Biopsy reveals sheets of malignant cells with
scant cytoplasm, granular "salt-and-pepper" chromatin, and absent
nucleoli. Numerous mitotic figures and apoptotic bodies are present.
Which cellular process is most directly responsible for the apoptotic
bodies observed in this tumor?
A) Activation of BCL-2 with inhibition of caspase-9
B) Release of cytochrome c from mitochondria with activation of the
apoptosome
C) Activation of macrophage nitric oxide synthase causing oncotic
necrosis
D) Inhibition of p53 with failure of G1/S checkpoint arrest
Correct Answer: B
Rationale: Apoptotic bodies are the histologic hallmark of
programmed cell death, mediated by cytochrome c release from
,mitochondria, apoptosome (Apaf-1 + caspase-9) assembly, and
downstream executioner caspases (3, 6, 7). BCL-2 inhibits
apoptosis; p53 induces apoptosis via BAX, so its inhibition would
reduce apoptotic bodies; nitric oxide mediates oncotic rather than
apoptotic death.
Question 2
A 42-year-old woman presents with fatigue and pallor. Laboratory studies
show MCV 78 fL, serum iron low, ferritin low, and TIBC elevated. Which
molecular mechanism most directly accounts for the elevated transferrin
(TIBC) in this patient?
A) Hepcidin-mediated ferropontin degradation is increased
B) Liver transferrin synthesis is upregulated in response to low
intracellular iron stores
C) Defective DMT1 intestinal iron transport causes iron trapping in
enterocytes
D) Heme oxygenase-1 degrades heme in macrophages, releasing free iron
Correct Answer: B
Rationale: In iron-deficiency anemia, low body iron stores stimulate
hepatic transferrin synthesis (and thus TIBC rises), while ferritin is
depleted. Hepcidin is decreased (not increased) in iron deficiency,
allowing ferroportin-mediated iron export to continue. DMT1 defects
cause iron-refractory iron-deficiency anemia, not classic IDA.
,Question 3
A 67-year-old man undergoes an uncomplicated total hip replacement. On
postoperative day 4 he develops dyspnea, tachycardia, and hypoxia. A
ventilation-perfusion scan shows multiple segmental perfusion defects
with normal ventilation. Which inflammatory mediator is most directly
responsible for the systemic hemodynamic effects (hypotension,
tachycardia) seen in this patient within minutes of the embolic event?
A) Interleukin-6 release from activated T lymphocytes
B) Platelet-activating factor and thromboxane A2 from activated platelets
C) Tumor necrosis factor-alpha from alveolar macrophages
D) Complement C5a-mediated neutrophil chemotaxis
Correct Answer: B
Rationale: Acute pulmonary embolism produces rapid hemodynamic
compromise via platelet activation with release of thromboxane A2
and PAF, causing bronchoconstriction and pulmonary
vasoconstriction. IL-6 and TNF-α are later cytokine responses
(hours). C5a mediates neutrophil chemotaxis, not acute
hemodynamic compromise.
Question 4
, A 19-year-old college student is evaluated for recurrent sinopulmonary
infections with encapsulated organisms. Flow cytometry shows absent
CD19+ B cells. Which genetic defect is most likely responsible?
A) Bruton's tyrosine kinase (BTK) mutation
B) Adenosine deaminase (ADA) deficiency
C) Dihydrorhodamine oxidase defect
D) IL-2 receptor gamma chain mutation
Correct Answer: A
Rationale: X-linked agammaglobulinemia (Bruton's) is caused by BTK
mutation leading to absence of mature B cells (CD19+) and
immunoglobulins. ADA deficiency causes SCID with T-, B-, and NK-
cell deficiency. Dihydrorhodamine oxidase defect causes chronic
granulomatous disease (neutrophil defect).
Question 5
A 68-year-old male with long-standing hypertension dies of a myocardial
infarction. At autopsy, the left ventricular wall is markedly thickened.
Which cellular adaptation is most directly responsible for this finding?
A) Hyperplasia
B) Metaplasia
C) Hypertrophy
D) Atrophy
2026/2027(Quiz bank with all the correct
answers)(usmle step 1)Medical examination
Section 1: General Principles & Cellular Pathology
Question 1
A 58-year-old man with a 30-pack-year smoking history presents with a
3-cm pulmonary mass. Biopsy reveals sheets of malignant cells with
scant cytoplasm, granular "salt-and-pepper" chromatin, and absent
nucleoli. Numerous mitotic figures and apoptotic bodies are present.
Which cellular process is most directly responsible for the apoptotic
bodies observed in this tumor?
A) Activation of BCL-2 with inhibition of caspase-9
B) Release of cytochrome c from mitochondria with activation of the
apoptosome
C) Activation of macrophage nitric oxide synthase causing oncotic
necrosis
D) Inhibition of p53 with failure of G1/S checkpoint arrest
Correct Answer: B
Rationale: Apoptotic bodies are the histologic hallmark of
programmed cell death, mediated by cytochrome c release from
,mitochondria, apoptosome (Apaf-1 + caspase-9) assembly, and
downstream executioner caspases (3, 6, 7). BCL-2 inhibits
apoptosis; p53 induces apoptosis via BAX, so its inhibition would
reduce apoptotic bodies; nitric oxide mediates oncotic rather than
apoptotic death.
Question 2
A 42-year-old woman presents with fatigue and pallor. Laboratory studies
show MCV 78 fL, serum iron low, ferritin low, and TIBC elevated. Which
molecular mechanism most directly accounts for the elevated transferrin
(TIBC) in this patient?
A) Hepcidin-mediated ferropontin degradation is increased
B) Liver transferrin synthesis is upregulated in response to low
intracellular iron stores
C) Defective DMT1 intestinal iron transport causes iron trapping in
enterocytes
D) Heme oxygenase-1 degrades heme in macrophages, releasing free iron
Correct Answer: B
Rationale: In iron-deficiency anemia, low body iron stores stimulate
hepatic transferrin synthesis (and thus TIBC rises), while ferritin is
depleted. Hepcidin is decreased (not increased) in iron deficiency,
allowing ferroportin-mediated iron export to continue. DMT1 defects
cause iron-refractory iron-deficiency anemia, not classic IDA.
,Question 3
A 67-year-old man undergoes an uncomplicated total hip replacement. On
postoperative day 4 he develops dyspnea, tachycardia, and hypoxia. A
ventilation-perfusion scan shows multiple segmental perfusion defects
with normal ventilation. Which inflammatory mediator is most directly
responsible for the systemic hemodynamic effects (hypotension,
tachycardia) seen in this patient within minutes of the embolic event?
A) Interleukin-6 release from activated T lymphocytes
B) Platelet-activating factor and thromboxane A2 from activated platelets
C) Tumor necrosis factor-alpha from alveolar macrophages
D) Complement C5a-mediated neutrophil chemotaxis
Correct Answer: B
Rationale: Acute pulmonary embolism produces rapid hemodynamic
compromise via platelet activation with release of thromboxane A2
and PAF, causing bronchoconstriction and pulmonary
vasoconstriction. IL-6 and TNF-α are later cytokine responses
(hours). C5a mediates neutrophil chemotaxis, not acute
hemodynamic compromise.
Question 4
, A 19-year-old college student is evaluated for recurrent sinopulmonary
infections with encapsulated organisms. Flow cytometry shows absent
CD19+ B cells. Which genetic defect is most likely responsible?
A) Bruton's tyrosine kinase (BTK) mutation
B) Adenosine deaminase (ADA) deficiency
C) Dihydrorhodamine oxidase defect
D) IL-2 receptor gamma chain mutation
Correct Answer: A
Rationale: X-linked agammaglobulinemia (Bruton's) is caused by BTK
mutation leading to absence of mature B cells (CD19+) and
immunoglobulins. ADA deficiency causes SCID with T-, B-, and NK-
cell deficiency. Dihydrorhodamine oxidase defect causes chronic
granulomatous disease (neutrophil defect).
Question 5
A 68-year-old male with long-standing hypertension dies of a myocardial
infarction. At autopsy, the left ventricular wall is markedly thickened.
Which cellular adaptation is most directly responsible for this finding?
A) Hyperplasia
B) Metaplasia
C) Hypertrophy
D) Atrophy
