Practice Exam Questions with Answers &
Detailed Rationales
Question 1
A 68-year-old man with a 40-pack-year smoking history
presents with progressive dyspnea, chronic productive cough,
and worsening exercise intolerance. Pulmonary function
testing shows an FEV₁/FVC ratio of 0.55 with minimal
reversibility after administration of a bronchodilator. His
arterial blood gas on room air shows pH 7.37, PaCO₂ 52 mm
Hg, and PaO₂ 58 mm Hg. Which of the following best explains
the primary mechanism responsible for his chronic
hypercapnia?
A. Increased pulmonary capillary hydrostatic pressure
B. Decreased respiratory drive from medullary dysfunction
C. Increased physiologic dead space and ventilation-perfusion
mismatch
D. Reduced diffusion capacity caused by interstitial fibrosis
Answer: C. Increased physiologic dead space and
ventilation-perfusion mismatch
Rationale: Chronic obstructive pulmonary disease, particularly
emphysema, produces destruction of alveolar walls and
pulmonary capillary beds, increasing physiologic dead space.
Airway obstruction and uneven ventilation also produce
,significant ventilation-perfusion mismatch. These
abnormalities impair effective alveolar ventilation and
contribute to chronic CO₂ retention. Medullary respiratory
depression can cause hypercapnia but is not the primary
mechanism in this patient. Interstitial fibrosis primarily causes
restrictive disease and hypoxemia rather than the obstructive
pattern shown here.
Question 2
A 29-year-old woman presents with fatigue, weight loss,
diarrhea, and palpitations. Examination reveals a diffusely
enlarged thyroid, lid retraction, and a fine tremor. Laboratory
studies show suppressed TSH and markedly elevated free T₄.
Which of the following antibodies is most likely responsible
for her condition?
A. Anti-thyroid peroxidase antibodies
B. Anti-thyroglobulin antibodies
C. Thyroid-stimulating immunoglobulins
D. Anti-double-stranded DNA antibodies
Answer: C. Thyroid-stimulating immunoglobulins
Rationale: Graves disease is caused by IgG thyroid-stimulating
immunoglobulins that bind and activate the TSH receptor,
producing diffuse thyroid enlargement and increased
synthesis of thyroid hormones. Ophthalmopathy and pretibial
myxedema are additional characteristic findings. Anti-thyroid
peroxidase antibodies are associated with autoimmune
thyroid disease but are particularly prominent in Hashimoto
,thyroiditis. Anti-dsDNA antibodies are associated with
systemic lupus erythematosus.
Question 3
A 74-year-old woman develops sudden right-sided weakness
and aphasia. She was last known to be neurologically normal
90 minutes ago. CT of the head shows no hemorrhage. Blood
pressure is 176/102 mm Hg. Which of the following is the
most appropriate next step?
A. Administer intravenous alteplase immediately
B. Administer intravenous nicardipine and reassess for
thrombolysis eligibility
C. Begin intravenous heparin
D. Perform lumbar puncture before treatment
Answer: B. Administer intravenous nicardipine and reassess
for thrombolysis eligibility
Rationale: For acute ischemic stroke, intravenous
thrombolytic therapy generally requires blood pressure below
185/110 mm Hg before treatment. This patient's blood
pressure exceeds the threshold, so it should be carefully
lowered with an appropriate intravenous agent such as
nicardipine. Once blood pressure is controlled and other
contraindications are excluded, thrombolysis can be
considered within the appropriate therapeutic window.
Heparin is not routinely used as immediate treatment for
acute ischemic stroke. Lumbar puncture is contraindicated in
, this setting and is not part of routine evaluation for suspected
ischemic stroke.
Question 4
A 45-year-old woman presents with severe epigastric pain
radiating to the back and persistent vomiting. Serum lipase is
markedly elevated. She develops hypotension, tachycardia,
and oliguria despite aggressive intravenous fluid
administration. Which of the following is the most likely
cause of her worsening renal dysfunction?
A. Immune complex deposition in glomeruli
B. Renal artery thrombosis
C. Systemic inflammatory response causing renal
hypoperfusion
D. Direct pancreatic enzyme destruction of renal tubules
Answer: C. Systemic inflammatory response causing renal
hypoperfusion
Rationale: Severe acute pancreatitis can produce systemic
inflammatory response syndrome with widespread cytokine
release, increased vascular permeability, third-spacing, and
distributive and hypovolemic shock. The resulting reduction in
effective circulating volume and renal perfusion can cause
acute tubular injury and acute kidney injury. Pancreatic
enzymes do not directly digest the kidneys. Renal artery
thrombosis and immune complex disease would not explain
the acute systemic presentation.