Pathophys Test 2

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Pathophys Test 2
2010-03-26 22:36:24

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  1. What is the anatomical disorder of achalasia? (p.9)
    • Incomplete relaxation of LES (lower esophageal sphincter) when swallowing and decrease in distal esophagus peristalsis
    • Esophagus enlarges over time
    • Stasis of food leads to putrefaction, infections, and ulcerations of mucosa
  2. What is esophageal reflux? (p.10)
    • Regurgitation of gastric juices into the esophagus that can lead to ulceration and erosion of mucosal lining
    • GERD commonly associated with transient relaxation of LES
    • NOT associated with swallowing
  3. When is GERD (esophageal reflux) most likely to occur?
    • After meals
    • When gastric emptying slowed due to digestion of fatty substances
    • Other causes include gastric intubation, radiation, alcohol intake, cigarette smoking, CNS-depressant drugs (morphine, valium), hiatal hernias, pregnancy
  4. What factors contribute to mucosal damage in GERD?
    • Length of time flux in contact with mucosa
    • Amount of HCl and pepsin in gastric juice (+ bile salts increases damage)
    • Ability of esophageal mucosa to repair itself
  5. What common measures are indicated for management of reflux? (p.12)
    • Elevate HOB
    • Avoid bedtime snacks and fatty foods
    • Stop smoking
    • Decrease alcohol intake
    • Medications: H2-receptor blockers; proton-pump inhibitors
    • Fundoplication
  6. How would you describe Barrett's Epithelium and its significance? (p.11)
    • Metaplastic cellular changes in esophagus secondary to GERD or other chemical or mechanical offenders
    • Pre-cancerous cells - must be watched closely
    • Outcome of long-standing esophageal reflux
    • Normal squamous mucosa replaced by columnar epithelium
    • Metaplasia --> dysplasia --> cancer
  7. A linear tear in the gastroesophageal wall associated with episodes of retching is referred to as what syndrome?
    • Mallory-Weiss syndrome
    • Characterized by linear tear in gastroesophageal junction
    • NOT disease
    • Mechanical tear
    • At risk: hiatal hernia, alcoholism, cigar smoking, tobacco chewing
  8. Acetylcholine effect on parietal cell:
    • Sight of smell of food --> secretion of ACh by vagus nerve
    • Bind M3 receptors on parietal cell
    • Activates Ca2+ channels
    • Movement of Ca2+ into parietal cells
    • Augments H+ - K+ ATPase pump (proton pump)
    • Reabsorbs K+ and secretes H+ ions; Cl- passively diffuses --> HCl secretion
  9. ECL cells effect on parietal cells
    • *Most significant*
    • ACh cells bind M1 receptors on ECL cells --> Histamine secretion
    • Histamine binds H2 receptors on parietal cells
    • Histamine H2 receptor binding activates enzyme adenylate cyclase
    • Activates ATP-driven H+-K+ pump
    • Secretes H+ and reabsorbs K+; Cl- diffuses passively into lumen combined with H+ forms HCl
  10. Gastrin effect on parietal cells
    • Food in stomach increases antral pH (pH >4)
    • Stimulates gastrin secretion
    • Circulates in bloodstream then acts on gastrin receptors (G receptors) on parietal cells and ECL cells
    • In parietal cells, gastrin mobilizes intracellular Ca2+, which like ACh, augments proton pump
    • On ECL cells, gastrin stimulates release of histamine --> increases HCl output
  11. At what pH will pepsin have maximal proteolytic activity? (p.15-16)
    pH < 3
  12. What is the goal for PPIs on gastric pH for healing of ulcers?
    • Increase gastric pH > 4
    • Inhibit proton-pump directly
  13. What are the most effective drugs for decreasing the secretion of HCl?
    Proton-pump inhibitors = 95% effective
  14. What are the potential adverse effects of proton-pump inhibitors?
    • Adverse effects have to do with increased pH >4.
    • Once pH>4, iron salts and B12 not well absorbed
    • Bacterial and viral infections also increase