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12 Cards in this Set

  • Front
  • Back
Produced by G cells in antrum
Target cells - parietal cells and chief cells
GASTRIN
Response -increase in HCI, intrinsic factor, and pepsinogen secretion
inhibited by :


  • pH <3.0,
  • somatostatin,
  • secretin,
  • CCK,
  • vasoactive-intestinal peptide
  • gastric inhibitory peptide
GASTRIN
produced by D cell in the antrum
stimulated by acid in the duodenum
somatostatin
produced by K cell in the duodenum
Target cells - parietal cell of the stomach, and beta cells of the pancreas,
Response- decrease in HCL and pepsin, increase in insulin release
gastric inhibitory peptide
produced by I cells of the duodenum and jejunum
Response - gallbladder contraction , relaxation of the sphincter of Oddi, increases pancreatic enzyme secretion , some increase in intestinal motility
CCK
produced by S cells of duodenum
secreation stimulated by fat, bile, pH <4, inhibited by gastrin
Secretin
produced by cells in gut and pancreas
Secretion stimulated by fat and acetylcholine,
Response - increased intestinal secretion (water and electrolytes) and motility
Inhibits gastrin release
vasoactive intestinal peptide
Secretion stimulated by: glucose,glucagon, CCK
Secretion inhibited by somatostatin and pancreatostatin
Response - cellular glucose uptake; promotes protein synthesis
insulin
• Response – ↑ pancreatic HCO3− release, inhibits gastrin release (this is reversed in patients withgastrinoma), and inhibits HCl release

• High pancreatic duct output – ↑ HCO3−, ↓ Cl−


• Slow pancreatic duct output – ↑ Cl−, ↓ HCO3− (carbonic anhydrase in duct exchanges HCO3− forCl−)

Secretin

(gastrin-releasing peptide) – ↑ intestinal motor activity, ↑ pancreatic enzyme secretion, ↑gastric acid secretion
Bombesin
released from terminal ileum following a fatty meal → inhibits acid secretion andstomach contraction; inhibits gallbladder contraction and pancreatic secretion
Peptide YY
Bowel recovery
• Small bowel 24 hours

• Stomach 48 hours


• Large bowel 3–5 days