A 52-year-old man from rural Maharashtra presents with fever, weight loss, and acute mononeuritis multiplex affecting the left ulnar and right peroneal nerves. Serum creatinine is 1.8 mg/dL with mild proteinuria and hematuria. CT angiography of the abdomen shows microaneurysms in the renal and mesenteric arteries. A skin biopsy of a tender subcutaneous nodule is performed. Histopathology reveals necrotizing arteritis of medium-sized arteries with fibrinoid necrosis, mixed inflammatory infiltrate, and destruction of the internal elastic lamina (**C**). ANCA testing is negative. HBsAg is positive. Which of the following best explains why the structure marked **C** is destroyed in this patient's vasculitis, and what is the pathophysiologic consequence?

Explanation

## Why option 3 is right In polyarteritis nodosa (PAN), particularly HBV-associated PAN, circulating immune complexes (HBV antigen–antibody complexes) deposit in the walls of medium and small arteries, triggering complement activation and fibrinoid necrosis. This transmural necrotizing process destroys the internal elastic lamina (**C**), which normally provides structural support and elasticity to the arterial wall. Loss of elastic lamina integrity is a hallmark histologic finding in PAN and directly predisposes to microaneurysm and saccular aneurysm formation (the characteristic "string-of-pearls" appearance on angiography). This patient's HBsAg positivity, mononeuritis multiplex, renovascular hypertension (from renal artery aneurysms), and angiographic microaneurysms are classic for HBV-associated PAN. The destruction of **C** (internal elastic lamina) is the pathologic basis for the segmental weakening that permits aneurysmal dilation. ## Why each distractor is wrong - **Option 1**: While immune complexes do cause transmural necrosis and aneurysm formation, this option does not specifically explain the mechanism of elastic lamina destruction or distinguish PAN from other vasculitides. It is less precise than option 3, which explicitly links HBV-related immune complexes to the pathology. - **Option 2**: ANCA-mediated pathology is the hallmark of ANCA-associated vasculitides (GPA, MPA, EGPA), not PAN. This patient's ANCA-negative status and HBsAg positivity rule out ANCA-mediated mechanisms. PAN is explicitly defined as ANCA-negative necrotizing arteritis. - **Option 4**: Complement-mediated lysis does occur in PAN, but this option incorrectly states that elastic lamina destruction leads to "exclusive arterial stenosis without aneurysm." In fact, elastic lamina destruction in PAN characteristically results in BOTH stenosis and aneurysm formation (segmental involvement), not stenosis alone. This is a critical distinction in PAN pathophysiology. **High-Yield:** PAN = immune complex–mediated (especially HBV-related) necrotizing arteritis of medium/small arteries → internal elastic lamina destruction → segmental aneurysms + stenosis ("string-of-pearls") + ANCA-negative + NO glomerulonephritis. [cite: Harrison 21e Ch 363; Chapel Hill Consensus Conference Classification 2012]