Advanced Pathophysiology Flashcards

A patient with type 1 diabetes in diabetic ketoacidosis has deep, rapid respirations (Kussmaul breathing). What is the physiologic purpose of this breathing pattern?

Answer: To compensate for metabolic acidosis by blowing off CO2

Ketoacids lower serum pH and bicarbonate. Hyperventilation lowers PaCO2, which raises pH and partially compensates for the metabolic acidosis.

In heart failure with reduced ejection fraction, which compensatory mechanism contributes most to long-term adverse ventricular remodeling?

Answer: Chronic activation of the renin-angiotensin-aldosterone system and sympathetic nervous system

Neurohormonal activation helps short-term by maintaining perfusion pressure. Over time, angiotensin II, aldosterone, and catecholamines cause fibrosis, hypertrophy, and increased afterload, which is why ACE inhibitors, ARBs, ARNIs, beta-blockers, and MRAs are core therapy.

Which laboratory pattern is the hallmark of nephrotic syndrome?

Answer: Proteinuria above 3.5 g/day with hypoalbuminemia

Damage to the glomerular filtration barrier causes massive protein loss. This produces hypoalbuminemia, edema, hyperlipidemia, and lipiduria. Hematuria with RBC casts points to nephritic syndrome.

A positive tuberculin skin test and allergic contact dermatitis from nickel are examples of which type of hypersensitivity reaction?

Answer: Type IV (delayed, T-cell mediated)

Type IV reactions are mediated by sensitized T cells and appear 48 to 72 hours after exposure. They do not involve antibodies.

Which combination of factors makes up Virchow's triad for venous thrombosis?

Answer: Stasis, endothelial injury, and hypercoagulability

Venous thrombus formation results from venous stasis, vessel wall (endothelial) injury, and a hypercoagulable state. Examples are immobility, surgery or trauma, and malignancy or estrogen use.

Excess cortisol in Cushing syndrome most directly causes hyperglycemia through which mechanism?

Answer: Increased hepatic gluconeogenesis and peripheral insulin resistance

Glucocorticoids stimulate hepatic gluconeogenesis, promote protein breakdown to supply substrates, and reduce peripheral glucose uptake. The result is hyperglycemia and sometimes steroid-induced diabetes.