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2013-02-05 23:29:28
DII Exam1c

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  1. Complications of untreated GERD:
    -How esophagus could be affected
    -How blood can be affected
    -How breathing could be affected
    • Esophagitis, esophageal bleeding/ulcers (hematemesis, melena), stricture, Barrett's esophagus, dysphagia
    • Anemia
    • Cough, asthma, throat/lung inflam/infection: sore throat, hoarseness; aspiration pneumonia
  2. what is melena and what is the test for it?
    • dark, tarry stools
    • guaiac test- to see if blood in stool (fecal occult blood test)
  3. disorder in which the esophageal cell type changes from squamous to columnar, and have increased risk for adenocarcinoma
    Barrett's esophagus
  4. esophageal inflammation caused by eosinophils, which are normally not present in esophagus, & this causes it to get stiff and narrowed with reduced motility; trigger is unknown
    -more common in males, and can occur at any age
    eosinophilic esophagitis
  5. what are symptoms of eosinophilic esophagitis? (6)
    • dysphagia (due to eosinophils stiffening the es)
    • food impaction (blockage)
    • other symptoms: pyrosis, N/V, chest pain, abdominal pain
  6. the elimination of allergens (food & air-borne) have shown improvement in histological and clinical symptoms. the pt should try an elemental feeding trial, and a 6-food elimination diet. the 6 foods are:
    • cow's milk protein
    • soy
    • peanuts
    • wheat
    • egg
    • seafood
  7. how is eosinophilic esophagitis diagnosed? (3)
    • by symptoms: GERD, dysphagia, food impaction, retrosternal chest pain
    • endoscopy: narrowing, exudates, rings/furrows (can see rings b/c of narrowing)
    • histology: lrg amt of eosinophils, bx after 6-8 wks on proton pump inhibitors or negative pH study (but this could be due to GERD), normal bx in rest of GI tract
  8. cellular debris- seeping w/in esophagus
  9. treatment for eosinophilic esophagitis
    no standardized protocol
    approaches used alone or in combination: (5)
    • acid suppression
    • systemic or topical steroids (effective stops when meds discontinued)
    • immunomodulators
    • diet modification (elimination diet)
    • endoscopic dilatation (must be careful not to puncture esophagus)
  10. long-term consequences of eosinophilic esophagitis (3)
    • wt loss (due to loss of appetite b/c of symptoms)
    • secondary malnutrition
    • acute esophageal perforations (es more susceptible to damage)
  11. possible causes (3) & treatments of esophageal stricture 
    • chronic inflammation (GERD)- due to buildup of scar tissue
    • ingestion of caustic chemicals
    • eosinophilic esophagitis

    *treatment depends on the cause
  12. how to manage esophageal stricture via nutrition
    • semisolid or liq foods, AT
    • small, freq meals, AT
    • eat slowly
    • avoid temp extremes
    • avoid acidic & highly spiced foods
    • lower fiber- may improve swallowing
    • protein & calorie-dense foods
    • TF may be indicated
  13. Barrett's Esophagus
    Pts have __ symptom for > 5 yrs
    Symptoms: (6)
    Diagnosis via: (2)
    Treatment: (3)
    • heartburn
    • waking at night due to pain; vomiting; hematemesis; melena; difficulty swallowing- strictures
    • endoscopy; tissue bx (chg in cell type is indicative)
    • H2 blockers, proton pump inhibitors, surgery
  14. Define PUD? Where do most peptic ulcers occur?
    • Erosion of mucosal lining of:
    • esophagus (rare)
    • stomach
    • duodenum
  15. What protective mechanisms are disturbed in the process of ulcer formation? (4)
    • reduced mucosal integrity: mucosal damage; reduced blood flow (can't get rid of excess acid)
    • increase in acid & pepsin secretion
    • renew and repair of epithelial cells
  16. What stimulates HCl production/secretion? What stimulates mucus production/secretion?
    • HCL: gastrin, acetylcholine, histamine (stimulate parietal cells to produce HCL)
    • mucus: prostaglandins
  17. Factors that affect mucosal integrity, and therefore can allow peptic ulcer to form (6)
    • H. pylori infection (damage)
    • NSAIDS, aspirin (damage)
    • steroids (damage)
    • excessive alc (damage + less mucosal blood flow)
    • smoking (less mucosal blood flow)
    • trauma (ischemia), brain injury (less mucosal blood flow)
  18. Factors that increase acid secretion, and therefore can allow peptic ulcer to form (4)
    • pepper, alc, caffeine, coffee
    • stress (inc amt of hydrocholine)
    • higher than normal maximal and basal acid production (genetics)
    • Zollinger Ellison syndrome
  19. condition in which a gastrinoma forms, and this tumor produces gastrin non-stop, which increases hcl levels (tumor can actually form in stomach, int or in pancreas)
    Zollinger Ellison syndrome
  20. most common cause of duodenal and gastric ulcers & PUD in general
    H. pylori
  21. What is the proposed role of H. pylori in the development of PUD?
    burrow in mucus layer of stomach or duodenum, then produce urease & toxins, and secrete proteins (cytokines) which interact w/epithelial cells & attract macrophages & neutrophils, resulting in inflammation & cell death. H. pylori can survive in low pH, and also urease production helps in survive more by neutralizing some of the HCL around where it burrows; also produces mucinase which destroys mucus
  22. What are the symptoms associated with PUD? (5)
    • ab pain
    • ingestion of food/antacids relieves pain for some, worsens pain for others
    • wt gain or loss
    • N/V
    • emergency symptoms: coffee ground hematemesis (acid brks down proteins, so blood looks like coffee grounds), melena
  23. How is PUD diagnosed? Differentiate among the methods used to diagnose PUD.
    • barium swallow w/x-rays
    • esophagogastroduodenoscopy (endoscopy)
    • --confirm contributions from other conditions: serum gastrin levels to find out if cause is ZE
  24. How is the H. pylori bacterium identified? (4)
    • endoscopy with tissue sample (sample + urea +pH indicator)
    • blood: antibody test
    • urea breath test: labeled carbon (breathe into a balloon-type and measure amt of labeled carbon)
    • stool antigen (HpSA) (H.pylori produces antigens (H. Pylori Stool Antigen)
  25. What are the aims of treatment of PUD? 
    • Relieve pain
    • Heal ulcer
    • Prevent recurrence
    • Maintain good nut status
  26. What is the primary mode of treatment for PUD due to H.pylori?
    Pt gets proton pump inhibitor (-azole) or H2 blocker (-tidine), 2 antibiotics, & bismuth salicylate
  27. What is the primary mode of treatment for PUD due to aspirin/NSAIDS and steroids?
    • stop using them
    • misoprostol (prostaglandin)
    • antisecretory agent (H2 blocker or PPI)
  28. What is the primary mode of treatment for PUD due to ZE?
    • PPI
    • remove tumor, or stomach (if needed)
  29. What is the primary mode of treatment for PUD due to stress ulcers? (3)
    • acid secretion suppressors
    • antacids
    • sucralfate
  30. What are nut management strategies for PUD? (6)
    • avoid alc (in symptomatic pts)
    • avoid blk & red/chili pepper
    • avoid low pH foods (only if oral or esophageal lesions present)
    • avoid caffeine, tea (reg), coffee
    • avoid other irritating foods
    • avoid eating 2 h before bed (causes nocturnal gastric acid hypersecretion)
  31. When is surgical management done for PUD? (4)
    • gastric rentention
    • severe, uncontrolled hemorrhage
    • perforation
    • ZE syndrome