## Pathophysiology of Acute Pancreatitis **Key Point:** Pancreatic necrosis does NOT develop in all cases of acute pancreatitis. It occurs in only 20–30% of patients with acute pancreatitis and typically develops within 48–72 hours in those who do develop it. The majority of cases are mild (interstitial edematous pancreatitis) and resolve without necrosis. ### Why the Other Statements Are Correct | Statement | Accuracy | Explanation | | --- | --- | --- | | Acinar cell injury → premature zymogen activation | ✓ Correct | This is the central mechanism: bile reflux, alcohol, ischemia, or direct injury triggers intracellular activation of digestive enzymes, leading to autodigestion [cite:Harrison 21e Ch 347] | | Lipase > amylase specificity | ✓ Correct | Serum lipase has ~95% specificity for pancreatic disease; amylase can be elevated in salivary gland disease, renal failure, and other conditions | | Cytokine-mediated systemic inflammation | ✓ Correct | TNF-α, IL-6, IL-8, and other pro-inflammatory mediators drive SIRS and multi-organ dysfunction in severe pancreatitis | ### Severity Stratification **High-Yield:** Acute pancreatitis severity spectrum: - **Mild (80%):** Interstitial edematous pancreatitis, no organ failure, resolves in 1–2 weeks - **Moderately severe (10%):** Transient organ failure or local complications (fluid collections) without necrosis - **Severe (10%):** Persistent organ failure (>48 hours) and/or pancreatic necrosis **Clinical Pearl:** Pancreatic necrosis is identified on contrast-enhanced CT (CECT) as non-enhancing pancreatic parenchyma. It is NOT a feature of all acute pancreatitis cases and should not be assumed at presentation.
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