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GI Pharmacology

Byus-GI Pharmacology

QuestionAnswer
surface mucous and mucous neck cells secrete mucous
parietal cells secrete acid and IF
chief cells secrete digestive enzymes
enterochromaffin cells secrete histamine
G cells secrete gastrin
histamine stimulates secretion of acid and IF
gastrin stimulates secretion of acid, pepsin, and IF
regulation of gastric secretion-neural ACh release directly acts on target cells and indirectly acts via release of gastrin
regulation of gastric secretion-humoral release of gastrin which reaches gastric gland via blood circulation
regulation of gastric secretion-paracrine histamine present in gastric mucosa (mast cells) and stimulates gastric glands directly
stimulant of gastric secretion-ACh stimulates secretion of acid, pepsing, and IF by interacting with muscarinic receptors
stimulant of gastric secretion-gastrin a polypeptide present in antral mucosa that stimulates secretion of acid, pepsin, and IF
stimulant of gastric secretion-histamine stimulates secretion of acid and IF by interacting with H2 receptors
"other" stimulants of gastric secretion alcohol, caffeine, insulin-induced hypoglycemia and some barbiturates
Vitamin B12 deficiency/pernicious anemia impairment of IF secretion
anticholinergic agents hyposecretory agent: reduce amount/concentration, high doses needed side effects: dry mouth, increased HR blurred vision block ACh at postganglionic parasympathetic site ex) atropine
muscarinic cholinergic antagonist hyposecretory agent: reduce amount/concentration, high doses needed side effects: dry mouth, increased HR blurred vision reduce basal secretion of gastric acid
M1 antagonists hyposecretory agent: reduce amount/concentration, high doses needed side effects: dry mouth, increased HR blurred vision produce less side effects but are less efficacious than H2 antagonists ex) pirenzepine, telenzepine
histamine H2-receptor antagonists hyposecretory agent: reduce amount/concentration use: reduce basal and stimulated acid secretion cimetidine reduces pain, antacid taken, improves healing of peptic ulcer side effects: increased prolactin-->gynecomastia, mental confusion, inhibits
proton pump inhibitors hyposecretory agent: reduce amount/concentration prodrugs converted by acidic environment to covalently bond with proton pumps use: patients with hypergastrinemia if not controlled well with H2-antagonists side effects: nausea, diarrhea, inhibi
prostaglandins hyposecretory agent: reduce amount/concentration non-specific reduction of basal and stimulated acid output in patients with duodenal ulcers
acid neutralizing agents reduce acidity in stomach with minimal effects on secretory process contain weakly basic moiety-->raises stomach pH 1)systemic: can cause metabolic acidosis 2)non-systemic: neutralize acid but poorly absorbed-->minimal effect on electrolyte balance
sodium bicarbonate acid neutralizing agents rapid-acting with short duration of action excess leads to systemic alkalosis side effects: acid rebound due to gastrin release-->overproduction of acid, alkalinization of urine
calcium bicarbonate acid neutralizing agents rapid acting with prolonged duration of action may cause hypercalcemia and positive-phosphate balance side effects: acid rebound, nausea, frequent constipation
aluminum antacids acid neutralizing agents slow-acting side effects: can reduce bioavailability of other drugs, can cause constipation
magnesium antacids acid neutralizing agents poorly soluble, excess may elevate pH to 8 or 9 side effects: causes osmotic diarrhea, neurological/neuromuscular/cardiovascular impairments if not excreted by kidney fast enough
magnesium trisilicate acid neutralizing agents non-systemic, non-reversible, slow acting rarely elevates pH above 3 byproduct (SiO2) is adsorbent of other drugs
anti-inflammatory agents reduce secretion of mucin mucosal barrier "fortifying" agents: protect lining of gastric lumen from effects of acid and pepsin ex) ACTH, cortisone, aspirin
carbenoxolone sodium inhibits back diffusion of H+ protects mucosal barrier from bile acids and helps heal duodenal ulcers side effects: can cause water and salt retention and hypokalemia
prostaglandins PGE1 analogue used to prevent ulcers in patients taking NSAIDs; ex)misoprostol PGE2-cytoprotective effect; protects gastric mucosa from ulceration and erosion
antibiotics acts against H. pylori antifungals and antiparasitics: bismuth, metronidazole, tetracylcine, amoxicillin, clarithromycin use two antibiotics + bismuth side effects: black color to oral cavity or feces *also considered anti-diarrheal agent
cholestyramine, aluminum bind bile acids
metoclopramide stimulates gastric emptying
antacids raises pH increases LES pressure
cimetidine inhibits acid secretion
cholinergic drugs acts on smooth muscle of GI and urinary tracts, increasing LES pressure ex) bethanecol
metoclopramide-biochemistry structural antagonist of D2 and 5-HT3 receptors depresses vomiting center by acting on brain to block dopamine and 5-HT3 receptors and stimulates gut motility
metoclopramide-GI effects increases muscle tension of LES improves gastric emptying
metoclopramide-clinical use patients who have failed to intubate the duodenum in anesthesia for emergencies in patients with chronic GER superior to antimimetics in treating nausea and vomiting
metoclopramide-side effects CNS side effects (bound to dopamine receptors) nervousness, restlessness, drowsiness, blocks dopamine inhibition of aldosterone, stimulates prolactin secretion-->galactorrhea
maintenance of intestinal motility and peristalsis layers of smooth muscles intrinsic nerves: PANS stimulatory, SANS inhibitory
diarrhea excessive frequency or fluidity of bowel movements
constipation decrease in normal frequency of bowel movement accompanied by hard stool mostly caused by poor diet (lacking fiber)
opiates non-specific anti-diarrheal agents decrease acid secretion and motility
synthetic narcotics non-specific anti-diarrheal agents slow GI motility and insoluble ex) diphenoxylate, loperamide
anticholinergic agents non-specific anti-diarrheal agents decrease intestinal tone, decrease peristalsis side effects: dry mouth dizziness, tachycardia, urinary retention
adsorbents non-specific anti-diarrheal agents may absorb undesirable constituents from solution (toxins, bacteria, viruses) ex) bismuth salts, aluminum, activated charcoal
absorbants non-specific anti-diarrheal agents not absorbed by GI but they absorb water and bile salt ex) dietary fiber, bran, methyl cellulose
latobacillus cultures non-specific anti-diarrheal agents used to restore normal bowel flora
adrenal corticosteroids specific anti-diarrheal agent used to treat IBD but does not necessarily cure the infection ex) hydrocortisone, prednisone
anion exchange resins specific anti-diarrheal agent bind bile salts and remove them ex) cholestyramine, colestipol
bulk producers-hydrophilic laxative with water-absorbing capacity: increase volume of intestinal content, leading to reflex peristalsis and defecation ex) pectin, bran
bulk producers-saline laxative with non-absorbable salts which absorb water from intestine: increase volume of intestinal content, leading to reflex peristalsis and defecation ex) magnesium salts
fecal softener-anionic surfactants laxative that lower surface tension and allow water to penetrate fecal material: mix with fecal mass and act as emulsifying agents to soften fecal material ex) docusate
fecal softener-lubricant laxative that may interfere with absorption of fat soluble substances (vitamins): mix with fecal mass and act as emulsifying agents to soften fecal material ex) mineral oil, olive oil
stimulants-cathartics: diphenylmethane laxatives that act on colon to stimulate myenteric plexus: alter water and electrolyte fluxes by inducing changes in motility and net absorption of water in the intestine ex) phenolphthalein
stimulants-cathartics: anthaquinones laxatives that act on colon: alter water and electrolyte fluxes by inducing changes in motility and net absorption of water in the intestine ex) senna, danthron
stimulants-cathartics: castor oil axatives that act on small intestine to reduce water absorption and shorten intestinal transit time: alter water and electrolyte fluxes by inducing changes in motility and net absorption of water in the intestine
Created by: kphom001
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