â– PHYSIOLOGICAL CORE: Cholecystokinin (CCK) is a peptide hormone synthesized and released by enteroendocrine I-cells in the duodenum and jejunum in response to dietary lipids and amino acids.
â– SYSTEMIC FUNCTIONS:
1. Gallbladder Contraction: Stimulates contraction of the gallbladder to release stored bile into the duodenum.
2. Sphincter of Oddi: Stimulates relaxation of the sphincter of Oddi, allowing bile and pancreatic juice to enter the duodenum.
3. Pancreatic Enzyme Secretion: Acts on pancreatic acinar cells via CCK1 receptors, stimulating secretion of lipase, amylase, and proteases.
4. Gastric Emptying Delay: Delays gastric emptying, allowing sufficient time for lipid emulsification and digestion.
â– EMERGENCY MANAGEMENT:
Acute presentation requires rapid stabilization following standard clinical guidelines. Prioritize securing the airway, maintaining hemodynamic stability, and administering targeted antidotes.
â– SECONDARY PREVENTION METRICS:
Implementing long-term dietary adaptations, physical therapy, and compliance aids reduces the rate of recurring acute crises by more than half.
[HY-BOARD-1228]
🌟 Dynamic Clinical Key:
CCK-mediated contraction can precipitate acute pain (biliary colic) in patients with symptomatic gallstones. Fatty meals trigger CCK release, forcing the gallbladder to contract against an impacted stone in the cystic duct, causing epigastric or right upper quadrant pain. Do not delay emergency interventions for low-priority diagnostic tests. Patient education regarding warning signs and therapy adherence is the cornerstone of secondary prevention.