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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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At what pH will pepsin have maximal proteolytic activity? (p.15-16)
pH < 3
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What is the goal for PPIs on gastric pH for healing of ulcers?
- Increase gastric pH > 4
- Inhibit proton-pump directly
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What are the most effective drugs for decreasing the secretion of HCl?
Proton-pump inhibitors = 95% effective
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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
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