AANPCB Pathophysiology Flashcards
6 cards from real AANPCB practice questions. Tap to flip, then mark Knew It or Still Learning — missed cards come back until you master them.
Read the first 6 AANPCB Pathophysiology flashcards as text
Which pathophysiological change explains the increased risk of urinary tract infections in postmenopausal women?
Answer: Decreased estrogen reducing protective vaginal lactobacilli and thinning urethral tissue
Estrogen deficiency after menopause leads to vaginal atrophy, loss of lactobacilli, elevated vaginal pH, and urethral thinning, all of which increase susceptibility to UTI.
What is the primary pathophysiological mechanism of stable angina?
Answer: Fixed atherosclerotic plaque causing supply-demand mismatch during exertion
Stable angina results from a fixed coronary stenosis that limits myocardial oxygen supply during increased demand, causing predictable, exertion-related chest pain.
Which pathophysiological mechanism causes the hyponatremia seen in syndrome of inappropriate antidiuretic hormone (SIADH)?
Answer: Dilutional hyponatremia from water retention due to excess ADH
In SIADH, excess ADH causes inappropriate free water retention by the kidneys, diluting serum sodium and lowering its concentration.
In systemic lupus erythematosus (SLE), what pathophysiological mechanism causes the characteristic renal injury?
Answer: Immune complex deposition in the glomeruli triggering complement activation
SLE nephritis results from deposition of circulating immune complexes (antigen-antibody) in the glomerular basement membrane, activating complement and causing inflammatory damage.
Which mechanism explains why beta-blockers are beneficial in managing chronic heart failure?
Answer: They block chronic sympathetic overstimulation that causes maladaptive cardiac remodeling
Chronic sympathetic activation in heart failure causes tachycardia and ventricular remodeling; beta-blockers attenuate these harmful effects and improve long-term cardiac function.
What is the pathophysiological basis for the increased bleeding risk in patients with chronic liver disease?
Answer: Reduced hepatic synthesis of clotting factors and thrombocytopenia from splenic sequestration
The liver produces most clotting factors; cirrhosis impairs their synthesis, and splenomegaly from portal hypertension causes platelet sequestration, compounding the coagulopathy.