, Question 1
In a cell undergoing apoptosis via the intrinsic pathway, which molecular event
directly triggers the mitochondrial outer membrane permeabilization (MOMP)
that commits the cell to death?
A. Fas ligand binding to Fas receptor
B. Bax/Bak oligomerization and pore formation
C. Caspase-8 activation within the DISC
D. NF-B nuclear translocation
Correct Answer: B - Bax/Bak oligomerization and pore formation
RATIONALE
The intrinsic pathway is initiated by intracellular stress, leading to
Bax/Bak activation and MOMP, which releases cytochrome c.
Fas/FasL and caspase-8 are extrinsic pathway components, and NF-B
is pro-survival, not a trigger of MOMP.
Question 2
A patient with severe sepsis develops disseminated intravascular coagulation
(DIC). Which laboratory pattern best distinguishes DIC from primary
fibrinolysis?
A. Elevated D-dimer with normal platelet count
B. Prolonged PT/PTT with decreased fibrinogen and thrombocytopenia
C. Shortened bleeding time with elevated factor VIII
D. Isolated prolongation of thrombin time with normal fibrinogen
Correct Answer: B - Prolonged PT/PTT with decreased
fibrinogen and thrombocytopenia
Page 2
, RATIONALE
DIC is characterized by widespread activation of coagulation leading
to consumption of platelets and clotting factors (especially
fibrinogen), producing prolonged PT/PTT, thrombocytopenia, and low
fibrinogen. Primary fibrinolysis typically shows normal platelet count
and fibrinogen with elevated D-dimer; the other options do not reflect
the consumptive coagulopathy of DIC.
Question 3
Which genetic mechanism best explains the phenotypic variability observed in
individuals with the same pathogenic variant in a monogenic disorder such as
cystic fibrosis?
A. Anticipation due to trinucleotide repeat expansion
B. Modifier genes and environmental factors influencing disease severity
C. Genomic imprinting leading to parent-of-origin effects
D. Mitochondrial heteroplasmy
Correct Answer: B - Modifier genes and environmental factors
influencing disease severity
RATIONALE
Cystic fibrosis shows wide phenotypic variability largely due to
modifier genes (e.g., TGFB1, MBL2) and environmental exposures,
not anticipation or imprinting. Mitochondrial heteroplasmy and
imprinting are relevant to other disorders, but not the primary
explanation for CF variability.
Question 4
In a patient with chronic kidney disease, which compensatory mechanism
initially maintains glomerular filtration rate but ultimately contributes to
progressive nephron loss?
A. Decreased prostaglandin synthesis
B. Hyperfiltration in remaining nephrons via angiotensin II-mediated
Page 3
, efferent arteriolar constriction
C. Increased atrial natriuretic peptide (ANP) secretion
D. Reduced renal sympathetic nerve activity
Correct Answer: B - Hyperfiltration in remaining nephrons via
angiotensin II-mediated efferent arteriolar constriction
RATIONALE
Angiotensin II preferentially constricts the efferent arteriole, raising
intraglomerular pressure and causing hyperfiltration in remnant
nephrons, which initially preserves GFR but leads to
glomerulosclerosis. Reduced prostaglandins and ANP do not drive this
maladaptive hyperfiltration; reduced sympathetic activity would lower
renin release.
Question 5
Which statement best explains why a patient with a large right-sided
hemispheric stroke may exhibit ipsilateral gaze deviation and contralateral
hemiparesis?
A. Damage to the right frontal eye field impairs horizontal gaze toward
the left, while corticospinal fibers decussate in the medulla.
B. The stroke disrupts the right optic tract, causing contralateral
homonymous hemianopsia.
C. The stroke affects the right cerebellum, leading to intention tremor and
ataxia.
D. The stroke involves the right thalamus, causing contralateral sensory
loss.
Correct Answer: A - Damage to the right frontal eye field impairs
horizontal gaze toward the left, while corticospinal fibers
decussate in the medulla.
Page 4
In a cell undergoing apoptosis via the intrinsic pathway, which molecular event
directly triggers the mitochondrial outer membrane permeabilization (MOMP)
that commits the cell to death?
A. Fas ligand binding to Fas receptor
B. Bax/Bak oligomerization and pore formation
C. Caspase-8 activation within the DISC
D. NF-B nuclear translocation
Correct Answer: B - Bax/Bak oligomerization and pore formation
RATIONALE
The intrinsic pathway is initiated by intracellular stress, leading to
Bax/Bak activation and MOMP, which releases cytochrome c.
Fas/FasL and caspase-8 are extrinsic pathway components, and NF-B
is pro-survival, not a trigger of MOMP.
Question 2
A patient with severe sepsis develops disseminated intravascular coagulation
(DIC). Which laboratory pattern best distinguishes DIC from primary
fibrinolysis?
A. Elevated D-dimer with normal platelet count
B. Prolonged PT/PTT with decreased fibrinogen and thrombocytopenia
C. Shortened bleeding time with elevated factor VIII
D. Isolated prolongation of thrombin time with normal fibrinogen
Correct Answer: B - Prolonged PT/PTT with decreased
fibrinogen and thrombocytopenia
Page 2
, RATIONALE
DIC is characterized by widespread activation of coagulation leading
to consumption of platelets and clotting factors (especially
fibrinogen), producing prolonged PT/PTT, thrombocytopenia, and low
fibrinogen. Primary fibrinolysis typically shows normal platelet count
and fibrinogen with elevated D-dimer; the other options do not reflect
the consumptive coagulopathy of DIC.
Question 3
Which genetic mechanism best explains the phenotypic variability observed in
individuals with the same pathogenic variant in a monogenic disorder such as
cystic fibrosis?
A. Anticipation due to trinucleotide repeat expansion
B. Modifier genes and environmental factors influencing disease severity
C. Genomic imprinting leading to parent-of-origin effects
D. Mitochondrial heteroplasmy
Correct Answer: B - Modifier genes and environmental factors
influencing disease severity
RATIONALE
Cystic fibrosis shows wide phenotypic variability largely due to
modifier genes (e.g., TGFB1, MBL2) and environmental exposures,
not anticipation or imprinting. Mitochondrial heteroplasmy and
imprinting are relevant to other disorders, but not the primary
explanation for CF variability.
Question 4
In a patient with chronic kidney disease, which compensatory mechanism
initially maintains glomerular filtration rate but ultimately contributes to
progressive nephron loss?
A. Decreased prostaglandin synthesis
B. Hyperfiltration in remaining nephrons via angiotensin II-mediated
Page 3
, efferent arteriolar constriction
C. Increased atrial natriuretic peptide (ANP) secretion
D. Reduced renal sympathetic nerve activity
Correct Answer: B - Hyperfiltration in remaining nephrons via
angiotensin II-mediated efferent arteriolar constriction
RATIONALE
Angiotensin II preferentially constricts the efferent arteriole, raising
intraglomerular pressure and causing hyperfiltration in remnant
nephrons, which initially preserves GFR but leads to
glomerulosclerosis. Reduced prostaglandins and ANP do not drive this
maladaptive hyperfiltration; reduced sympathetic activity would lower
renin release.
Question 5
Which statement best explains why a patient with a large right-sided
hemispheric stroke may exhibit ipsilateral gaze deviation and contralateral
hemiparesis?
A. Damage to the right frontal eye field impairs horizontal gaze toward
the left, while corticospinal fibers decussate in the medulla.
B. The stroke disrupts the right optic tract, causing contralateral
homonymous hemianopsia.
C. The stroke affects the right cerebellum, leading to intention tremor and
ataxia.
D. The stroke involves the right thalamus, causing contralateral sensory
loss.
Correct Answer: A - Damage to the right frontal eye field impairs
horizontal gaze toward the left, while corticospinal fibers
decussate in the medulla.
Page 4
