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34 Cards in this Set
- Front
- Back
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What are the different diagnostic tests available for diagnosing gastric disease?
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Upper GI series/barium swallow. Esophageal pH monitoring. Endoscopy. Hemacult. Hgb/Hct; Bun/SCr. Empiric treatment. 13 or 14 C urea breath test (UBT), stool Ag, urease via endoscopic biopsy (H. pylori).
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What is GERD (gastro-esophageal reflux disease)?
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Reflex of stomach contents into the esophagus. It can be associated with laryngitis, cough, asthma, and dental erosions.
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What’s the pathogenesis of GERD?
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Altered motility (too fast or too slow), altered tone, decreased epithelial defense. Esophageal mucosa exposure to gastric acid contents, pepsin, bile acids. Could be prolonged esophageal transit time. Decreased resting pressure of the lower esophageal sphincter.
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In diabetic patients there’s usually altered tone in the lower esophageal sphincter. What does smoking - obesity - or pregnancy leave you vulnerable to?
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Altered sphincter tone.
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What are the complications of GERD?
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Irritation, wearing down, scarring, stricture (most common). Occult blood loss, anemia. Tooth discoloration (wearing on tooth enamel). Failure to thrive, anorexia (don’t want to eat if they always feel acid coming back up). Progressive obstruction. Hemorrhage. Barrett’s esophagitis.
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What is Barrett’s esophagitis?
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The cells themselves start to change and warp. The risk of esophageal cancer is really high.
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Non-pharmacologic treatment of GERD includes:
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Position (avoid recumbancy, slouching. Sleep with the HOB elevated - the actual mattress, not just propping one’s self up on pillows). Weight reduction. Smoking cessation. Diet restrictions (no snacks within 3 hours of lying down. Avoid large meals. No bedtime snacks. Avoid caffeine, chocolate, fatty & spicy foods, which may provoke symptoms)
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Remember that obesity increases the pressure on the sphincter. What about fatty foods or spicy foods? and caffeine
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The fatty foods slow down GI emptying, and spicy foods act as a local irritant. Caffeine stimulates acid secretion.
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Peptic Ulcer Disease (PUD) is an aggression/defense imbalance. Which is more common - duodenal or gastric ulcers?
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Duodenal
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Gastric acid causes ulceration ONLY in the presence of:
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Pepsin
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Why do stress ulcers occur?
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Usually because of decreased blood flow to the area. Think - peripheral vascular disease.
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“superficial gastritis”/mucosal erosion vs. craters. Where do stress ulcers usually occur - in the stomach or the duodenum?
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In the Stomach
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What are some unique risk factors that can lead to stress ulcers?
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Mechanical ventilation, coagulopathy = these patients are at the highest risk.
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There’s also NSAID-induced ulcers that occur with non-selective NSAIDS. The incidence is 0.8% unless there are risk factors. By inhibiting COX-1 activity NSAIDs lead to:
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Decrease in protective PG production
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The pathogenesis of peptic ulcers include alterations in the GI protective or aggressive factors. Protective factors include:
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Prostaglandins, Mucus, Bicarb, Mucosal blood flow.
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What are the aggressive factors?
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Acid, Pepsin, NSAIDs, H.pylori
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Risk factors for PUD include:
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NSAID use. Smoking cigarettes. Zollinger-Ellison syndrome (gastrinoma). Family history. H.pylori.
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What are the possibly-associated risk factors for PUD?
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Corticosteroids. Blood group O. HLA-B12, B5, Bw35 phenotypes. Stress. Poverty.
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There’s also other things that may lead to PUD:
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Delayed gastric emptying time. Regurge of duodenal contents. Overproduction of acid & pepsin. Impaired feedback mechanism. Increased incidence w/ cirrhosis, renal failure.
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What’s the clinical presentation of PUD?
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Epigastric pain (mild gnawing abdominal burning/pain/tenderness, chest pain). Dyspepsia, bloating, N/V, anorexia, weight loss. Blood streaked emesis/stool in 20% of patients. Hemorrhage.
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Regarding the epigastric pain in PUD - when does occur in DU (duodenal ulcers) and GU (gastric ulcers)?
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DU - about 3 hours post-prandial, feels better with food (sphincter closed). GU - worse with food, and worse at night
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What are the non-pharmacological treatments for PUD?
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Similar to those for GERD. Also, stress reduction, because stress leads to increased acid output.
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What are the treatment goals for PUD?
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Relieve symptoms. Promote ulcer healing. Prevent ulcer recurrence & complications. Cost-effective therapy.
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How can PUD be treated?
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By eliminating H.pylori. Reducing gastric acidity. Enhancing mucosal defenses.
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What are the 5 main types of pharmaceuticals we can use to treat PUD?
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Acid neutralizing agents. Inhibitors of acid production. Surface (protective) agents. Prokinetic agents. Antimicrobials.
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What’s an example of an acid neutralizing agent?
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Antacids
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What’s an example of an inhibitor of acid production?
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Proton pump inhibitors. H2-receptor antagonists.
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What’s an example of a surface (protective) agent?
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Sucralfate. Misoprostil. Colloidal Bismuth Compounds.
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Note: There’s no place for Sucralfate or prokinetic agents in treating PUD. What are these agents used for?
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for GERD and stress ulcers.
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Physiology of gastric acid secretion and sites of drug action. What are the 4 secretory products in the stomach?
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Mucus. Acid. Proteases. Hormones.
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What function does the mucus serve?
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It coats, lubricates, and protects from acid.
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Acid is secreted from the parietal cells. What’s its function?
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It activates pepsinogen, turning it into pepsin
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What are the proteases?
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Pepsinogen
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What hormone is released & function does it serve?
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Its important in controlling acid & gastric motility
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