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322 Exam 2

322 GI meds

TermDefinition
antiemetics correct or control vomiting; centrally or local acting
acute dystonia facial grimacing, involuntary upward eye movement, muscle spasm of tongue and face
akathisia restless, trouble standing still, feet in constant motion, rocking
serotonin antagonists (preferred drug) blocks serotonin receptors and afferent vagal nerve terminals in upper GI tract; ondansetron most effective in chemo
side effects of glucocorticoids fluid and sodium retention, fractures, osteoporosis
cannabinoids appetite stimulant; marinol
prokinetic agents increase tone and motility of GI tract; metocolopramide
metoclopramide, reglan suppresses emesis by blocking dopamine receptors in CTZ, increases peristalsis and gastric emptying
antidiarrheals inhibit gastric motility by decreasing intestinal motility and peristalsis
side effects of antidiarrheals constipation, CNS depression
adsorbents coat the wall of the GI tract absorbing bacteria or toxins that cause diarrhea
imodium slows motility by affecting water and electrolyte movement through the bowel; increases tone of anal sphincter reducing incontinence and urge
osmotic laxative hyperosmolar salts pull water into colon and increase water in feces to increase bulk, stimulating peristalsis and defecation
osmotic laxative produces semi formed and watery stool, lactulose and glycerin
stimulant laxative increases peristalsis by irritating sensory nerve endings in the intestinal mucosa
stimulant laxative bisacodyl and castor oil; harsh acts in 2 to 6 hours; can block absorption of fats and fat soluble vitamins
stimulant senns changes urine color; reddish brown
bulk forming laxative natural, fibrous substance that promotes large, soft stools by absorbing water into the intestine, increasing fecal bulk and peristalsis, promotes well formed, soft stools
emollient laxative stool softener, docusate given with full glass of water; may cause mild cramping
chloride channel activator laxatives activates chloride channels in small intestine leading to an increase in intestinal fluid secretion and motility
antiemetic assessment determine onset, frequency and amount of vomiting; risk for dehydration
red diarrhea lower GI tract, colon
black diarrhea upper GI tract
H2 blockers block receptors of parietal cells to reduce gastric acid secretion and concentration
H2 blockers treat gastric and duodenal ulcers, prevent acid reflux in the esophagus
PPI suppress secretion of hydrochloric acids into the lumen of the stomach by inhibiting hydrogen/ potassium ATPase enzyme system
PPI does not allow the body to produce HCl acid
adverse effects with long term use of PPI pneumonia, fractures and osteoporosis, rebound acid secretion, c diff
PPI prazole
peptic ulcer occur when there is a hyper secretion of HCl and pepsin which erode the mucosal lining
esophageal ulcer reflux of acidic gastric secretions into esophagus due to an incompetent cardiac sphincter
gastric ulcer breakdown of gastric mucosal barrier
gastric ulcer insufficient buffers to neutralize gastric acid in the stomach; pain 30 to 1.5 hours after eating
duodenal ulcer hyper secretion of acid from the stomach passing into the duodenum; pain occurs 2 to 3 hours after eating
GERD inflammation or erosion of the esophageal mucosa caused by reflux of gastric acid in the esophagus
antacids inorganic chemicals neutralize acids
nonsystemic antacids alkaline salts; milk of magnesia can cause diarrhea or constipation
systemically absorbed antacids calcium carbonate, sodium bicarbonate
H2 blockers prevent acid reflux, work quicker than PPI, reduce acid secretion
PPI suppress secretion of hydrochloric acid in lumen of the stomach
bulk forming laxative caution a decrease in fluid could cause an obstruction
drugs to treat PUD tranquilizers, anticholinergics, antacids, H2 blockers, PPI, prostaglandin E analog, pepsin inhbitors
Created by: ahommel
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