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322 GI meds

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