Pathophysiology/Pharmacology
Final Exam Review
(Questions & Solutions)
2025
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,1. A 62-year-old man with acute ST-elevation myocardial infarction is
started on tissue plasminogen activator (tPA). Which pathophysiologic
effect of tPA underlies clot dissolution?
A. Direct inhibition of thrombin formation
B. Conversion of plasminogen to plasmin
C. Blockade of platelet GPIIb/IIIa receptors
D. Inhibition of factor Xa
Correct ANS: B
Rationale: tPA catalyzes plasminogen to plasmin, which degrades
fibrin and dissolves existing clots.
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2. A patient in septic shock demonstrates refractory hypotension despite
fluid resuscitation. Which endogenous mediator is chiefly responsible for
the vasodilation seen in this condition?
A. Endothelin-1
B. Nitric oxide
C. Thromboxane A₂
D. Angiotensin II
Correct ANS: B
Rationale: In sepsis, inducible nitric oxide synthase produces high
levels of nitric oxide, causing systemic vasodilation and hypotension.
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3. A 45-year-old woman with type 2 diabetes and a blood glucose of 480
mg/dL presents with confusion and dehydration. Arterial blood gas: pH
7.25, HCO₃⁻ 14 mEq/L, PaCO₂ 30 mmHg. Which acid-base disturbance is
present?
A. Metabolic acidosis with respiratory compensation
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, B. Respiratory acidosis with metabolic compensation
C. Mixed respiratory and metabolic alkalosis
D. Primary metabolic alkalosis
Correct ANS: A
Rationale: Low pH and HCO₃⁻ indicate metabolic acidosis; decreased
PaCO₂ reflects compensatory hyperventilation.
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4. A patient with acute respiratory distress syndrome (ARDS) is placed on
positive end-expiratory pressure (PEEP). What pathophysiologic change
does PEEP primarily counteract?
A. Alveolar overdistension
B. Surfactant overproduction
C. Atelectasis from alveolar collapse
D. Bronchial smooth muscle spasm
Correct ANS: C
Rationale: PEEP maintains alveolar patency at end expiration,
preventing collapse and improving oxygenation in ARDS.
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5. In chronic heart failure, activation of the renin–angiotensin–
aldosterone system (RAAS) leads to sodium retention. An ACE inhibitor
improves symptoms by:
A. Blocking angiotensin II formation
B. Stimulating aldosterone release
C. Inhibiting bradykinin degradation alone
D. Directly blocking AT₁ receptors
Correct ANS: A
Rationale: ACE inhibitors prevent conversion of angiotensin I to II,
reducing vasoconstriction and aldosterone-mediated volume overload.
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6. A patient receiving high-dose loop diuretics for volume overload
develops hypokalemia. Which segment of the nephron is responsible for
loop diuretic action?
A. Proximal tubule
B. Loop of Henle, thick ascending limb
C. Distal convoluted tubule
D. Collecting duct
Correct ANS: B
Rationale: Loop diuretics inhibit the NKCC2 cotransporter in the thick
ascending limb, leading to sodium, potassium, and chloride loss.
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7. A 30-year-old asthmatic in status asthmaticus fails albuterol therapy.
Which medication mechanism is next-line for bronchodilation?
A. Leukotriene receptor antagonism
B. β₂-agonism only
C. Muscarinic receptor blockade
D. Inhaled corticosteroids
Correct ANS: C
Rationale: Ipratropium bromide blocks M3 receptors, reducing vagal
bronchoconstriction when β₂-agonists alone are insufficient.
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8. In chronic obstructive pulmonary disease (COPD), loss of alveolar septa
reduces elastic recoil. Which inhaled agent improves airflow by reducing
airway smooth muscle tone?
A. Budesonide
B. Tiotropium
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