GI Physiology Secretory Flashcards
Gastrin
Source: G cells (antrum of stomach)
Action: increase: H+ secretion, growth of gastric mucosa, gastric motility.
Regulation: increased by stomach distention/alkalinization, AA & peptides, vagal stimulation; decreased by stomach pH <1.5.
Clinical Notes: Increased a lot in Zollinger-Ellison Syndrome. Increased by chronic PPI use. *Phenylalanine & Tryptophan are potent stimulators.
Cholecystokinin (CCK)
Source: I cells (duodenum, jejunum).
Action: Increase: pancreatic secretion, gallbladder contraction, sphincter of Oddi relaxation; Decrease: gastric emptying.
Regulation: Increased by fatty acids, AA.
Notes: Acts on neural muscarinic pathways to cause pancreatic secretion….
Secretin
S cells (duodenum - further down than CCK’s I cells).
Action: Increases: pancreatic HCO3- secretion, bile secretion; Decreases: gastric acid secretion.
Regulation: Increased by acid, fatty acids.
Note: Increased HCO3- neutralizes gastric acid in duodenum, allowing pancreatic enzymes to function.
Somatostatin
Source: D cells (pancreatic islets, GI mucosa - Antrum).
Action: Decreases: gastric acid and pepsinogen secretion, pancreatic and small intestine fluid secretion, gallbladder contraction, insulin and glucagon release.
Regulation: increased by acid; decreased by vagal stimulation.
Notes: “Antigrowth hormone”: inhibits digestion and absorption of substances needed for growth.
Glucose-dependent Insulinotropic Peptide (GIP aka “Gastric Inhibitory Peptide”)
K cells (Duodenum, Jejunum). Action: Exocrine - decreases H+ secretion; Endocrine - Increases insulin release. Regulation: increased by fatty acids, AA, oral glucose.
Vasoactive Intestinal Popypeptide (VIP)
Source: parasympathetic ganglia i sphincters, gallbladder, small intestine.
Action: Increase: intestinal water & electrolyte secretion, relaxation of intestinal smooth muscle and sphincters.
Regulation: Increased by distention and vagal stimulation; Decreased by adrenergic input.
Clinical Notes: VIPoma=non-alpha, non-beta islet cell pancreatic tumor that secretes VIP; WDHA Syndrome=copious Watery Diarrhea, Hypokalemia, Achlorydia.
Nitric Oxide role in GI system
Action: increases smooth muscle relaxation, including LES.
Clinical Notes: Loss of NO secretion –>Achalasia.
Motilin
Source: Small Intestine.
Acion: produces MMCs (Migrating Motor Complexes).
Regulation: Increase in fasting state.
Clinicalnotes: Motilin R agonists (ERYTHROMYCIN) used to stimulate intestinal peristalsis.
Intrinsic Factor (IF)
Source: parietal cells (body of stomach).
Action: Vitamin B12-binding protein (uptake in terminal ileum).
Clinical notes: autoimmune destruction of parietal cells –> chronic gastritis & pernicious anemia.
Gastric Acid
Source: Parietal cells (Body of stomach).
Action: Decrease stomach pH.
Regulation: Increased by: histamine (main pathway - from ECL cells first stimulated by gastrin), ACh, Gastrin; Decreased by: somatostatin, GIP, PG, Secretin.
Pepsin
Source: Chief cells (Body of stomach - further than parietal cells).
Action: protein digestion.
Regulation: Increased by vagal stimulation, local acid (H+: inactive pepsinogen–>pepsin).
HCO3- in the GI system
Source: Mucosal cells (stomach, duodenum, salivary glands, pancreas) & Brunner’s Glands (duodenum).
Action: neutralizes acid.
Regulation: increased by pancreatic & biliary secretion with SECRETIN).
Notes: HCO3- is trapped in mucus that covers the gastric epithelium.
alpha-amylase
Source: pancreas.
Action: starch digestion.
Notes: Secreted in active form.
Lipase, phospholipase A, colipase
Source: pancreas.
Action: Fat digestion.
Proteases
Source: pancreas.
Action: protein digestion.
Notes: Trypsin*, chymotrypsin, elastase, carboxypeptidases - proenzymes (zymogens).
