(Chamberlain 2025)
1. A 60-y-o with history of long-term HTN has concentric LV hypertrophy. The
primary pathophysiologic process is:
a) Volume overload b) Pressure overload c) Myocarditis d) Infarction
Answer: b) Pressure overload. Rationale: Chronic high afterload (HTN) causes
concentric hypertrophy to reduce wall stress.
2. In acute myocardial ischemia, which cellular change appears earliest?
a) Fibrosis b) Coagulative necrosis c) Cellular swelling and loss of ATP d)
Calcification
Answer: c) Cellular swelling and loss of ATP. Rationale: Ischemia → ATP
depletion → ionic pump failure → cell swelling.
3. Graves disease causes hyperthyroidism primarily through:
a) TSH excess b) TSH receptor autoantibodies c) Pituitary tumor d) Iodine
deficiency
Answer: b) TSH receptor autoantibodies. Rationale: Autoantibodies stimulate
thyroid hormone production.
4. In type 1 DM, the pathogenesis is:
a) Insulin resistance b) Autoimmune β-cell destruction c) Excess glucagon d)
Pancreatitis
Answer: b) Autoimmune β-cell destruction. Rationale: T-cell–mediated loss of
insulin-producing cells.
5. A patient with nephrotic syndrome has hyperlipidemia because:
a) Increased LDL receptor activity b) Hepatic overproduction of lipoproteins c)
Decreased dietary intake d) Excess urinary cholesterol loss
Answer: b) Hepatic overproduction of lipoproteins. Rationale: Hypoalbuminemia
stimulates hepatic protein & lipoprotein synthesis.
6. Which acid-base disturbance is expected in aspirin (salicylate) overdose early?
a) Metabolic alkalosis b) Respiratory alkalosis c) Metabolic acidosis d)
Respiratory acidosis
Answer: b) Respiratory alkalosis. Rationale: Salicylates stimulate respirations
early → respiratory alkalosis, later mixed with metabolic acidosis.
7. Central diabetes insipidus results from:
a) ADH deficiency b) ADH resistance c) Excess ADH d) Excess aldosterone
Answer: a) ADH deficiency. Rationale: Pituitary/neurohypophysis failure reduces
, ADH → polyuria, dilute urine.
8. Primary hyperaldosteronism causes:
a) Hypokalemia and hypertension b) Hyperkalemia and hypotension c)
Hyponatremia only d) Metabolic acidosis
Answer: a) Hypokalemia and hypertension. Rationale: Aldosterone increases Na
retention and K excretion.
9. A shift of potassium out of cells into plasma occurs with:
a) Insulin administration b) β-agonists c) Acidosis d) Aldosterone excess
Answer: c) Acidosis. Rationale: H⁺ enters cells in exchange for K⁺ leaving →
hyperkalemia.
10.In ARDS, the primary pathological lesion is:
a) Alveolar consolidation by bacteria b) Diffuse alveolar damage with hyaline
membranes c) Bronchospasm d) Pleural effusion
Answer: b) Diffuse alveolar damage with hyaline membranes. Rationale:
Endothelial/epithelial injury → proteinaceous edema and hyaline membranes.
11.A transudative pleural effusion most likely results from:
a) Low oncotic pressure or high hydrostatic pressure b) Infection c) Malignancy
d) Pulmonary embolism
Answer: a) Low oncotic pressure or high hydrostatic pressure. Rationale: Starling
forces cause transudate (e.g., CHF, hypoalbuminemia).
12.COPD—emphysema phenotype—is characterized by:
a) Airway hyperresponsiveness b) Destruction of alveolar walls and reduced
elastic recoil c) Increased surfactant d) Pulmonary edema
Answer: b) Destruction of alveolar walls and reduced elastic recoil. Rationale:
Loss of alveolar septa leads to airspace enlargement and airflow limitation.
13.The most common cause of community-acquired pneumonia in adults is:
a) Mycoplasma b) Streptococcus pneumoniae c) Pseudomonas d) Viral only
Answer: b) Streptococcus pneumoniae. Rationale: Pneumococcus is the leading
bacterial cause.
14.Pathophysiology of systolic heart failure primarily involves:
a) Impaired ventricular filling b) Reduced contractility causing decreased EF c)
Valvular stenosis only d) Pericardial tamponade
Answer: b) Reduced contractility causing decreased EF. Rationale: Systolic HF =
impaired pump function → low EF.
15.Left heart failure commonly causes:
a) Systemic venous congestion b) Pulmonary congestion and edema c)
, Hepatomegaly primarily d) Peripheral edema only
Answer: b) Pulmonary congestion and edema. Rationale: Left pump failure backs
up into pulmonary circulation.
16.Right heart failure classically causes:
a) Pulmonary edema b) Pulmonary embolism c) Systemic venous congestion with
hepatomegaly, JVD, peripheral edema d) Hypertensive crisis
Answer: c) Systemic venous congestion... Rationale: RV failure → systemic
venous hypertension.
17.Stable angina arises from:
a) Coronary vasospasm b) Fixed atherosclerotic coronary obstruction provoked
by exertion c) Myocarditis d) Embolic occlusion
Answer: b) Fixed atherosclerotic obstruction. Rationale: Demand ischemia
secondary to obstructive plaques.
18.Atherosclerotic plaque rupture causing occlusion and chest pain is the
mechanism for:
a) Stable angina b) Unstable angina/MI c) Pericarditis d) Aortic dissection
Answer: b) Unstable angina/MI. Rationale: Plaque rupture + thrombosis → acute
coronary syndrome.
19.In DIC, consumptive coagulopathy results in:
a) Isolated thrombocytosis b) Widespread microthrombi and bleeding due to
consumption of clotting factors c) Hypercoagulable state only d) Hemophilia
Answer: b) Widespread microthrombi and bleeding. Rationale: Systemic
activation of clotting consumes platelets & factors.
20.Heparin-induced thrombocytopenia (HIT) is mediated by:
a) Direct platelet destruction b) Autoantibodies to platelet factor 4 causing platelet
activation and thrombosis c) Vitamin K deficiency d) Splenic sequestration
Answer: b) Autoantibodies to PF4. Rationale: Immune complex activates platelets
→ thrombosis with thrombocytopenia.
21.In iron deficiency anemia, typical lab findings include:
a) High ferritin b) Low MCV and low ferritin c) Macrocytosis d) Hemolysis markers
Answer: b) Low MCV and low ferritin. Rationale: Low iron stores → microcytic,
hypochromic anemia with low ferritin.
22.Pernicious anemia results from:
a) Iron deficiency b) Intrinsic factor deficiency from autoimmune gastritis causing
B12 malabsorption c) Folate deficiency d) Hemorrhage
Answer: b) Intrinsic factor deficiency. Rationale: Autoimmune destruction of