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Advanced Pathophysiology
Q1: A 55-year-old man with chronic hypertension presents with left ventricular
hypertrophy on echocardiogram. This cellular adaptation is best described as:
A. Atrophy from decreased workload
B. Hypertrophy from increased mechanical demand [CORRECT]
C. Hyperplasia from hormonal stimulation
D. Metaplasia from chronic irritation
Correct Answer: B
Rationale: Hypertrophy is an increase in cell size resulting in enlarged tissue mass,
typically from increased mechanical demand (pressure overload in hypertension).
Atrophy (A) is decrease in cell size. Hyperplasia (C) is increase in cell number.
Metaplasia (D) is change from one differentiated cell type to another.
,Q2: In cellular injury, the "point of no return" is most closely associated with:
A. Depletion of ATP and cellular swelling
B. Massive calcium influx and activation of catabolic enzymes [CORRECT]
C. Accumulation of fat vacuoles in the cytoplasm
D. Formation of apoptotic bodies
Correct Answer: B
Rationale: Irreversible injury is marked by massive calcium influx, mitochondrial
dysfunction, and activation of phospholipases and proteases that destroy cellular
membranes and structures. While ATP depletion (A) occurs early, calcium dysregulation
marks irreversibility. Fat accumulation (C) is reversible. Apoptosis (D) is programmed
cell death, not the point of no return in accidental injury.
Q3: A patient with chronic bronchitis has hyperplasia of bronchial mucous glands. This
is an example of:
A. Compensatory hyperplasia to replace damaged cells
B. Hormonal hyperplasia stimulated by growth factors
,C. Pathologic hyperplasia due to chronic irritation [CORRECT]
D. Neoplastic proliferation of glandular tissue
Correct Answer: C
Rationale: Pathologic hyperplasia is proliferation in response to chronic irritation or
hormonal stimulation beyond normal limits, as seen in chronic bronchitis with mucous
gland hyperplasia. Compensatory hyperplasia (A) follows tissue loss. Hormonal
hyperplasia (B) is physiologic (e.g., breast development). Neoplasia (D) implies
autonomous growth, not reactive hyperplasia.
Q4: The primary difference between necrosis and apoptosis is that:
A. Necrosis is programmed cell death; apoptosis is accidental
B. Apoptosis is energy-dependent and maintains membrane integrity; necrosis is
accidental with membrane rupture [CORRECT]
C. Necrosis affects single cells; apoptosis affects groups of cells
D. Apoptosis causes inflammation; necrosis does not
Correct Answer: B
, Rationale: Apoptosis is programmed, energy-dependent cell death with intact
membranes and no inflammation. Necrosis is accidental cell death from injury, with
membrane rupture, cellular contents release, and inflammation. Option A reverses the
definitions. Option C reverses the pattern (necrosis affects groups). Option D is reversed
(necrosis causes inflammation).
Q5: During acute inflammation, the first response at the microcirculation level is:
A. Increased vascular permeability causing edema
B. Vasodilation and increased blood flow causing redness and heat [CORRECT]
C. Leukocyte adhesion and transmigration
D. Fibrin deposition and clot formation
Correct Answer: B
Rationale: The vascular phase of acute inflammation begins with transient
vasoconstriction followed by vasodilation (mediated by histamine, prostaglandins),
causing increased blood flow (rubor, calor). Increased permeability (A) follows.
Leukocyte adhesion (C) occurs later. Fibrin deposition (D) is part of repair, not initial
inflammation.