FPGEE Pathophysiology 2 — Questions and Answers
Question 1: In cirrhosis, which mechanism is most responsible for the development of ascites?
- Increased lymphatic flow from the thoracic duct
- Portal hypertension combined with hypoalbuminemia reducing oncotic pressure (Correct answer)
- Excess aldosterone independent of portal hypertension
- Renal tubular acidosis causing sodium loss into the peritoneum
Correct answer: Portal hypertension combined with hypoalbuminemia reducing oncotic pressure
Portal hypertension increases hydrostatic pressure in the splanchnic bed while hypoalbuminemia (from hepatic synthetic failure) lowers colloid oncotic pressure, together driving fluid into the peritoneal cavity.
Question 2: A patient with an acute MI develops a new holosystolic murmur at the left sternal border 4 days post-infarct. Which complication is most likely?
- Mitral stenosis from papillary muscle scarring
- Ventricular septal rupture causing a left-to-right shunt (Correct answer)
- Aortic regurgitation from root dilation
- Pericarditis causing a friction rub misidentified as a murmur
Correct answer: Ventricular septal rupture causing a left-to-right shunt
Myocardial necrosis can cause rupture of the interventricular septum 3–5 days post-MI, creating an acute ventricular septal defect with a left-to-right shunt heard as a harsh holosystolic murmur.
Question 3: Which pathophysiological change is responsible for the elevated serum creatinine in pre-renal azotemia?
- Glomerular inflammation reducing filtration surface area
- Decreased renal perfusion reducing GFR without intrinsic tubular damage (Correct answer)
- Obstructive nephropathy increasing back-pressure on nephrons
- Tubular necrosis impairing creatinine secretion
Correct answer: Decreased renal perfusion reducing GFR without intrinsic tubular damage
Pre-renal azotemia results from reduced renal blood flow (e.g., dehydration, heart failure), which lowers GFR and creatinine clearance without structural kidney damage, making it rapidly reversible.
Question 4: In Graves' disease, the hyperthyroidism is caused by:
- Excessive TSH secretion by a pituitary adenoma
- IgG autoantibodies that stimulate the TSH receptor (Correct answer)
- Follicular destruction releasing stored thyroid hormone
- Dietary iodine excess triggering thyroid autonomy
Correct answer: IgG autoantibodies that stimulate the TSH receptor
Graves' disease involves thyroid-stimulating immunoglobulins (TSI/TRAb) that bind and continuously activate TSH receptors, driving unregulated thyroid hormone synthesis independent of pituitary TSH.
Question 5: A patient with COPD has a PaCO2 of 55 mmHg and HCO3- of 30 mEq/L. What pathophysiological adaptation is reflected by the elevated bicarbonate?
- Acute metabolic alkalosis from diuretic use
- Renal compensation for chronic respiratory acidosis by retaining bicarbonate (Correct answer)
- Respiratory compensation for metabolic alkalosis
- Acute respiratory alkalosis with secondary metabolic acidosis
Correct answer: Renal compensation for chronic respiratory acidosis by retaining bicarbonate
In chronic hypercapnia, the kidneys compensate by excreting more H+ and retaining HCO3-, raising serum bicarbonate to partially normalize arterial pH.
Question 6: Which mechanism underlies the thrombocytopenia in heparin-induced thrombocytopenia (HIT)?
- Heparin directly lysing platelets by complement activation
- IgG antibodies against heparin-PF4 complexes activating platelets and causing consumption (Correct answer)
- Heparin chelating calcium needed for platelet aggregation
- Antiplatelet antibodies cross-reacting with glycoprotein IIb/IIIa
Correct answer: IgG antibodies against heparin-PF4 complexes activating platelets and causing consumption
In HIT, IgG antibodies recognize heparin-PF4 complexes on platelet surfaces, triggering platelet activation, aggregation, and paradoxical thrombosis while depleting circulating platelets.
Question 7: In septic shock, the refractory hypotension is primarily due to:
- Cardiac tamponade from bacterial pericarditis
- Massive vasodilation driven by excess nitric oxide from bacterial endotoxins (Correct answer)
- Severe anemia reducing oxygen delivery capacity
- Adrenal insufficiency causing cortisol deficiency in all patients
Correct answer: Massive vasodilation driven by excess nitric oxide from bacterial endotoxins
Bacterial LPS and cytokines (TNF-α, IL-1) induce excess inducible nitric oxide synthase (iNOS) activity, leading to pathological systemic vasodilation and distributive shock.
FPGEE Pathophysiology 2
In cirrhosis, which mechanism is most responsible for the development of ascites?