Harmones Flashcards
Gastrin
Source: G cells of antrum and stomach
Action: increase gastric H+ secretion
increase growth of gastric mucosa
Increase gastric motility
Regulation: increased by stomach distenstion/alkalinization, amino acids, peptides, vagal stimulation
Decreased by stomach ph
Motilin
Source: small intestine
Action: produces migrating motor complex
Regulation: increases in fasting state
Motilin receptor agonists (erythromycin) stimulate intestinal peristalsis
GIP
Source: K cells of duodenum and jejunum
Action:
Exocrine: decrease gastric H+ secretion
Endocrine: increase insulin release
Regulation: increased by fatty acids, amino acids, oral glucose
Secretin
Source: S cells of duodenum
Action: increase pancreatic HCO3- secretion
Decrease gastric acid secretion
Increase bile secretion
Regulation: increased by acid, HCl most potent, fatty acids in lumen of duodenum
Begins at pH
Somatostatin
Source: D cells of pancreatic islets and GI mucosa
Action: decreased gastric acid and pepsinogen secretion
decreased pancreatic and small intestine fluid secretion
decreased gallbladder contraction
decreased insulin and glucagon, CCK and gastrin release
Regulation: increased by acid, decreased by vagal stimulation
antigrowth hormone effects
Nitric Oxide
Action: increased smooth muscle relaxation including lower esophageal sphincter
Loss is implicated in increased LES tone of achalasia
VIP
Source: parasympathetic ganglia in sphincters, gallbladder, small intestine, pancreatic islet cells
Action: increased intestinal water and electrolyte secretion
Increased relaxation of intestinal smooth muscle and sphincters
Inhibits gastric H+ secretion and stimulates pancreatic bicarbonate and Cl-
Regulation:
increased by distenstion and vagal stimulation
Decreased by adrenergic input
VIPoma: watery diarrhea, hypokalemia, and achlorhydria-inhibited by somatostatin
Intrinsic factor
Source: parietal cells of stomach
Action: viamin B12 binding protein required for B12 uptake in terminal ileum
Gastric Acid
Source: parietal cells of stomach (upper glandular layer)
Action: decrease stomach pH by secreting HCl
Regulation: increased by histamine (cAMP), ACh (Ca2+), gastrin (Ca2+) gastrin is trophic leading to hyperplasia
Decreased by somatostatin, GIP, prostaglandin, secretin
Gastrinoma: located in pancreas
gastrin secreting tumor that causes high level of acid secretion and ulcers refractory to medical therapy
Diarrhea and abdominal pain (MEN type 1)
Pepsin
Source: chief cells (stomach)
Action: protein digestion
Regulation: increased by vagal stimulation, local acid
pepsinogen activated to pepsin by H+
HCO3-
Source: mucosal cells (stomach, duodenum, salivary glands, pancreas) Brunner glands (duodenum)
Action: neutralizes acid
regulation: increased by pancreatic and biliary secretion with secretin
HCO3- trapped in mucus that covers the gastric epithelium
CCK
Source: I cells of duodenum and Jejunum
Action: increase pancreatic secretion
Increase gallbladder contraction
Decrease gastric emptying
Increase sphincter of Oddi relaxation
Regulation: increased by fatty acids and amino acids
Acts on muscarinic pathways to cause pancreatic secretion
a-amylase
Starch digestion
Secreted in active form from pancrease
Lipase, phospholiase A, colipase
Secreted from pancreas
Fat digestion
Proteases
Secreted from pancreas
Include trypsin, chymotrypsin, elastase, carboxypeptidases
Secreted as zymogens
Trypsinogen
From pancreas
converted to active enzyme trypsin leading to activation of other proenzymes and cleaving of additional trypsinogen molecules into active trypsin (postive feedback)
Converted to trypsin by enterokinase/enteropeptidase a brush border enzyme on duodenal and jejunal mucosa
Trypsin activated by serine peptidase inhibitor preventing pancretitis