Pathophysiology Flashcards

In cirrhosis, which mechanism is most responsible for the development of ascites?

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.

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?

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.

Which pathophysiological change is responsible for the elevated serum creatinine in pre-renal azotemia?

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.

In Graves' disease, the hyperthyroidism is caused by:

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.

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?

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.

Which mechanism underlies the thrombocytopenia in heparin-induced thrombocytopenia (HIT)?

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.

In septic shock, the refractory hypotension is primarily due to:

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.