Inflammation may be sparse in early disease
Edema and congestion seen in early disease
•
Inflammation dominated by neutrophils and variable necrosis in later stages of disease
•
Widespread fibroblastic proliferation can occur
•
Transmural fibrosis and Rokitansky-Aschoff (RA) sinuses, stigmata of chronic cholecystitis, may be present
•
Variant forms
Xanthogranulomatous: Foamy macrophages as a result of response to bile due from ruptured RA sinuses
Emphysematous: Necrotic wall with gas bubbles and often contains gram(+) bacilli
Eosinophilic: Eosinophils comprise > 90% of infiltrate; may be associated with parasites, hypereosinophilic syndrome
TERMINOLOGY
Definitions
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Acute inflammation of gallbladder
ETIOLOGY/PATHOGENESIS
Acute Calculous Cholecystitis
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Key elements are obstruction of cystic duct by stones and bile supersaturated with cholesterol
•
Trauma to mucosa releases phospholipase from lysosomes
Phospholipase converts lecithin in bile to lysolecithin, which damages gallbladder epithelium
•
Secondary bacterial infection with enteric organisms occurs in 20% of cases
•
Overgrowth by gas-producing organisms leads to emphysematous cholecystitis
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