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47 Cards in this Set
- Front
- Back
Innervation of the GI tract |
The autonomic nervous system of the GI tract comprises both extrinsic and intrinsic nervous systems |
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Extrinsic innervation |
Parasympathetic; vagus and pelvic nerves, excitatory on the functions of the GI tract Sympathetic; inhibitory on the functions of the GI tract, |
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Intrinsic innervation |
Local reflexes to relay information within the GI tract Control most functions of the GI tract, - Myenteric plexus (motility) - Submucosal plexus (secretion and blood flow) |
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What are the official GI hormones? |
- Gastrin - Cholecystokinin (CCK) - Secretin - Glucose-dependent insulinotropic peptide (GIP) |
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Gastrin |
- G cells of stomach - Stimulated by; small peptides and amino acids, distention of stomach, vagus (GIP), - Inhibited by; H+ in stomach, somatostatin - Actions; increase gastric H+ secretion (parietal cells), stimulates growth of gastric mucosa |
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CCK |
- I cells of duodenum and jejunum - Stimulated by; small peptides and amino acids, fatty acids - Actions; contraction of gallbladder and relaxation of sphincter of Oddi, increased; pancreatic enzyme and bicarbonate secretion and growth of exocrine pancreas/gallbladder, inhibit gastric emptying |
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Secretin |
- S cells of duodenum - Stimulated by; H+ in duodenum, fatty acids in duodenum - Actions; increase pancreatic bicarbonate secretion and biliary bicarbonate secretion, decreased gastric H+ secretion |
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GIP |
- Duodenum and jejunum - Stimulated by; fatty acids, amino acids and oral glucose - Actions; increased insulin secretion, decreased gastric H+ secretion |
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Motilin |
Increases GI motility and is involved in interdigestive myoelectric complexes |
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Pancreatic polypeptide |
Inhibits pancreatic secretion |
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Glucagon-like peptide-1 (GLP-1) |
Binds to pancreatic beta cells and stimulates insulin secretion. Analogue of GLP-1 may be helpful in the treatment of type II diabetes mellitus |
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Paracrines |
- Diffuse short distances to act on target cells located in the GI tract - The GI paracrine are somatostatin and histamine |
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Somatostatin |
- Secreted in response to H+ in the lumen - Inhibited by vagal stimulation - Inhibits the release of all GI hormones and gastric H+ secretion |
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Histamine |
- Secreted by mast cells of the gastric mucosa - Increases gastric H+ secretion directly and by potentiating the effects of gastrin and vagal stimulation |
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Neurocrines |
- Synthesized in neurons of the GI tract, moved by axonal transport down the axons and released by action potentials in the nerves - GI neurons are; VIP, GRP and enkephalins |
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VIP |
- Released from neurons in the mucosa and smooth muscle of the GI tract - Produces relocation of GI smooth muscle, inkl. lower esophageal sphincter - Stimulates pancreatic HCO3- secretion - Inhibits gastric H+ secretion |
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GRP |
- Released from vagus nerves that innervate the G cells - Stimulates gastrin release from G cells |
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Enkephalins |
- Secreted from nerves in the mucosa and smooth muscle of GI tract - Stimulate contraction of GI smooth muscle - Inhibit intestinal secretion of fluid and electrolytes |
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Leptin |
- Secreted by fat cells - Decreases appetite |
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Ghrelin |
- Secreted by gastric cells - Increases appetite |
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Slow waves |
Are oscillating membrane potentials inherent to the smooth muscle cells of some parts of the GI tract (Cajal cells) |
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Gastric motility |
Gastric contractions are increased by vagal stimulation and decreased by sympathetic stimulation |
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Gastric emptying |
- Fastest when the stomach contents are isotonic - Fat inhibits gastric emptying (CCK) - H+ in the duodenum inhibits gastric emptying |
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Small intestinal motility |
Parasympathetic stimulation increases intestinal smooth muscle contraction and sympathetic stimulation decreases it |
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Segmentation contractions (small intestine) |
Mix the intestinal contents |
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Peristaltic contractions (small intestine) |
Propel the chyme through the small intestine toward the large intestine Coordinated by the enteric nervous system |
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Gastroileal reflex (small intestine) |
Mediated by the extrinsic ANS and possibly by gastrin. The presence of food in the stomach triggers increased peristalsis in the ileum and relaxation of the ileocecal sphincter. |
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Segmentation contractions (large intestine) |
In the proximal colon mic the contents and are responsible for the appearance of haustra |
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Gastrocolic reflex (large intestine) |
The presence of food in the stomach increases the motility of the colon and increases the frequency of mass movements.The reflex has a rapid parasympathetic component that is initiated when the stomach is stretched by food. A slower, hormonal component is mediated by CCK and gastrin. |
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Formation of saliva |
By the parotid, submandibular and sublingual glands. |
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Regulation of saliva production |
- Controlled by parasympathetic and sympathetic nervous systems (increased by both) |
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Parasympathetic regulation of saliva production |
- Cranial nerves VII and IX - By increasing transport processes in the acinar and ductal cells and by causing vasodilation |
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Sympathetic regulation of saliva production |
Increases the production of saliva and the growth of salivary glands, although the effects are smaller than those of parasympathetic stimulation |
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Which factors affect saliva production? |
Increased by; food, smells, conditioned reflexes and nausea Decreased by; sleep, dehydration, fear, anticholinergic drugs |
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What stimulates gastric H+ secretion? |
- Vagal stimulation - Gastrin - Histamine |
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What inhibits gastric H+ secretion? |
- Negative feedback of gastrin - Somatostatin; inhibit release of histamine and gastrin - Prostaglanding |
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Which drugs block gastric H+ secretion? |
- Antropine - Cimetidine - Omeprazole |
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Antropine |
A cholinergic muscarinic antagonist, inhibits H+ secretion by blocking the direct pathway, which uses ACh as a neurotransmitter. However, atropine does not block H+ secretion to completely because it does not inhibit the indirect pathway, which uses GRP as a neurotransmitter. |
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Pancreatic secretion |
Much higher bicarbonate concentration than plasma - to neutralize the acidic chyme. Contains enzymes essential for the digestion of protein, carbohydrate and fat. Isotonic |
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Stimulation of pancreatic secretion |
- Secretin - CCK - ACh |
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Composition of bile |
Bile contains; bile salts, phospholipids, cholesterol and bile pigments (bilirubin) |
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Production of bile |
- Produced continuously by hepatocytes - Stored in the gallbladder - The bile acids are conjugated with glycine or taurine to form bile salts |
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Carbohydrates |
Absorbed in the small intestine by Na+-dependent cotransport (glucose, galactose) and facilitated diffusion (fructose). |
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Proteins |
Absorbed in the small intestine by Na+-dependent cotransport (amino acids) and H+-dependent cotransport (di- and tripeptides) |
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Digestion of proteins |
- Endopeptidases; degrade proteins by hydrolyzing interior peptide bonds - Exopeptidases; hydrolyze one amino acid at a time from the C terminus of proteins and peptides - Pepsin; pepsinogen activated to pepsin when low pH - Pancreatic proteases; trypsinogen activated to trypsin by enterokinase |
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Lipids |
- Absorbed in the small intestine - Micelles form with bile salts in intestinal lumen - Diffusion of fatty acids, monoglycerides and cholesterol into cell - re-esterification in cell to triglycerides and phospholipids - Chylomicrons form in cell to and are transferred to lymph |
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Bilirubin production and excretion |
Hemoglobin is degraded to bilirubin by the reticuloendothelial system. Bilirubin binds to albumin in the circulation system. In the liver bilirubin is conjugated with glucuronic acid. A portion of conjugated bilirubin is excreted in the urine, and a portion into bile. In the intestine, it is converted to urobilinogen, which is returned to the liver and excreted as stercobilin and urobilin in feces. |