A 58-year-old woman with varicose veins of her legs asks you about the pathogenesis and complications of deep venous thrombosis (DVT). Which of the following is a potentially fatal complication of deep venous thrombosis?

A. Atherosclerosis:Intermittent claudication is caused by insufficient blood flow to the muscles during exertion, typically due to atherosclerotic narrowing of peripheral arteries. Plaque buildup reduces perfusion, leading to ischemic pain in the legs that resolves with rest. This patient’s symptoms of exercise-induced leg cramps are classic for peripheral arterial disease.

B. Congestive heart failure:Congestive heart failure leads to generalized fatigue and dyspnea due to impaired cardiac output, but it does not produce localized ischemic pain in the legs during walking. Claudication is a vascular, not cardiac, phenomenon.

C. Embolization of a mural thrombus:Acute arterial embolism from a mural thrombus can cause sudden limb ischemia and severe pain, pallor, and pulselessness. It does not produce the gradual, exertional pain pattern characteristic of intermittent claudication.

D. Systemic hypertension:Hypertension contributes to atherosclerosis over time but is not the direct cause of exercise-induced leg cramps. It may exacerbate vascular disease but does not directly produce intermittent claudication.

E. Valvular heart disease:Valvular heart disease can lead to heart failure or reduced cardiac output, potentially causing fatigue or exertional dyspnea. It does not selectively impair leg perfusion or cause ischemic leg pain with walking.

A. Caseous:A Ghon complex is characteristic of primary tuberculosis infection caused by Mycobacterium tuberculosis. The hallmark histologic feature is caseating granulomatous inflammation, with central caseous necrosis surrounded by epithelioid macrophages, Langhans giant cells, and lymphocytes. The necrotic center has a cheese-like appearance due to lipid-rich mycobacterial cell walls and immune-mediated tissue destruction.

B. Coagulative:Coagulative necrosis is typically seen in ischemic injury to solid organs such as the heart, kidneys, and spleen. Cellular architecture is preserved temporarily despite cell death, which differs from the amorphous, granular debris seen in caseous necrosis associated with tuberculosis.

C. Fat:Fat necrosis occurs in adipose tissue, commonly in acute pancreatitis or traumatic injury to fatty tissue. It involves enzymatic destruction of fat cells and formation of chalky calcium soaps, a process unrelated to granulomatous infections like tuberculosis.

D. Fibrinoid:Fibrinoid necrosis is associated with immune-mediated vascular damage, such as in vasculitis or malignant hypertension. It involves deposition of immune complexes and fibrin within vessel walls, not the granulomatous pattern typical of tuberculosis.

E. Liquefactive:Liquefactive necrosis is most commonly seen in brain infarctions and bacterial infections that produce pus. It results in complete digestion of dead cells into a liquid mass, which differs from the dry, cheese-like necrosis observed in tuberculosis.