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25 Cards in this Set
- Front
- Back
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What are the main symptoms of GERD? |
Heart burn and regurgitation. Acid reflux is the most common cause of GERD. |
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What are the two main types of reflux disease? |
1. 30% of patients have esophageal injuries - reflux esophagitis - reflux strictures - Barrett's esophagus - Esophageal adenocarcinoma
2. Non-erosive reflux disease |
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Explain how pain is activated in non-erosive reflux disease (NERD) patients. |
1. Low pH (even a pH of 6) activates chemoreceptors. 2. It is theorized that activation of trpV1 (capsaicin) receptor causes pain. 3. Erosion of mucosal barrier exposes nocireceptors |
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Why does Edrophonium reduce distension thresholds for pain in GERD patients? |
It increases cholinergic activity which stimulates pain receptors? *** |
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Why does atropine increase distension thresholds for pain in GERD patients? |
It decreases cholinergic activity. |
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T/F: Symptom severity correlates poorly with presence and severity of the disease. |
True, as symptoms can exist despite healing of lesions, while some patients with severely eroded esophaguses don't exhibit symptoms. |
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What is the occurence rate for duodenal and gastric ulcers? |
Duodenal ulcers are more common. Young adults are more susceptible to duodenal ulcers, while gastric ulcers are more common in older adults. Also more common in men for both types. |
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What are common symptoms of PUD? (6) |
1. Epigastric pain relieved by food intake or antacids 2. Pain between meals/ cause waking at night 3. Loss of appetite 4. Weight loss
If more severe: 5. Anemia 6. Blood in stool |
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What are the causes for PUD? |
PUD is caused by mucosal damage: - 50% by Helicobacter (H) pylori - 50% by NSAIDs - Critical illness, surgery, or hypervolemia may cause stress ulcers - Smoking exacerbates and slows healing |
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How do prostaglandins play a role in ulcers? |
PGE2 and PGI2 help with gastric mucosal protecion by: 1. Mucus production 2. Bicarbonate secretion (EP1 receptor) 3. Epithelial cell proliferation 4. Increased mucosal blood flow |
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How do H. pylori infections lead to ulceration? (3) |
1.The infection leads to chronic gastritis which disrupts acid homeostasis 2. Increased gastrin = increased H+ secretion and decreased mucus production 3. Decreased bicarbonate secretion
*Irradication of infection reduces ulcer recurrence |
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What are the treatment options for H. pylori-associated ulcers? |
10-14 day "triple therapy" consisting of PPI and clarithromycin + amoxicilling or metronidazole, then PPI for 4-6 weeks. |
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What are the treatment options for NSAID-associated PUD? |
1. Discontinue NSAIDs 2. PPI |
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What can be used to prevent stress ulcers? |
PPIs and H2RAs (similar efficacy) Sucralfate (mucosal protective agents) |
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What are some limitations to using baking soda (sodium bicarbonate) for PUD? |
React with HCl to form salt plus CO2. Belching and gastric distension High dose may cause alkalosis |
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What are some limitations to using Tums (calcium carbonate) for PUD? |
React with HCl to form salt plus CO2. Frequent consumption may result in hypercalcemia. May also cause belching and metabolic alkalosis. |
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How does magnesium hydroxide and/or aluminum hydroxide help with PUD? What are some limitations? |
Both elements react with HCl to form salts plus water, so no gas formed. Unabsorbed aluminum causes constipation, while magnesium causes diarrhea, so both cancel out the effects. Also both metals may be problematic with patients with renal failure. |
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MOA of PPIs? |
It is EC for delayed release into intestinal lumen. They become absorbed into acidified compartments (e.g. parietal cell canaliculus), where it reacts with the the H+ to form reactive thiophilic sulfonamide cations. This sulfonamide binds with H+/K+ pump as suicide inhibitor.
DOA is up to 24 hours until new pumps are made. |
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Adverse events of PPIs? |
Diarrhea, headache, abdominal pain similar to placebo.
Decrease B12 levels and decreased absorption for long term use.
Infection may also occur. |
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MOA of soraprazan/ revaprazan? |
Competes with K+ for binding site on proton pump, and may have greater acid suppression than PPI. |
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A H2RA can suppress acid release by: a. 25% b. 50% c. 80% d. >90% |
b. 50% |
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MOA of sucralfate? |
Mucosal protective agent. It is a sucrose-sulfated aluminum hydroxide complex, that breaks into sucrose sulfate (negative). It binds to positively charged proteins in the base of ulcers to prevent further erosion. |
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1. MOA and 2. Therapeutic use of metoclopramide/ domperidone? |
1. D2 receptor antagonists. Dopamine receptors inhibit GI motility, so D2 antagonists enhance release of ACh.
2. Used to stimulate gut motor function and improve gastric emptying for patients with impaired gastric emptying. (prokinetic agent) |
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What are adverse events of metaclopramide an domperidone? |
Metaclopramide: restlessness and drowsiness (enters CNS), insomnia, anxiety, extrapyramidal effects (shakiness and agitation)
Domperidone: well tolerated (does not pass CNS)
Both drugs elevate prolactin (possible spontaneous lactation) |
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How is erythromycin used in GI disorders? |
It is a macrolide antibiotic but it stimulates motilin receptors on GI SM for increased gastric emptying. |
