pharm GI.txt

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  1. ��Buffers drugs
    calcium carbonate (CaCO3), aluminum hydroxide (AlOH3), magnesium hydroxide (MgOH2)
  2. Buffers MOA
    buffers are bases that directly react with and neutralize stomach acid (increase pH)
  3. Buffers pharmacokinetics (absorption, formulation)
    Calcium, aluminum, and magnesium are typically poorly absorbed by the gut (unless given in very high doses). suspensions (dissolved in liquid) work better than powders.
  4. Buffers indications
    hyperacidity (including reflux), indigestion
  5. Buffers interactions x2
    cations may chelate other drugs, interfering with their absorption. Can also change gut pH, interfering with drugs that require a certian pH (true of all antacids! examples: decreased concentrations of tetracyclines, quinolones, biphosphonates). *both of these issues can be overcome by separating administration*
  6. should you combine magnesium and Kalexate?
  7. Buffers side effects x3
    CaCO3 = hypercalcemia, gas (carbon dioxide liberation from carbonate), constipation. Al = hypophosphatemia (binds to phosphate in gut, not absorbed), constipation. Mg = diarrhea (magnesium salt draws water into the gut).
  8. Buffer combinations x2
    Aluminum (slow reacting, constipation) often combined with magnesium (fast reacting, diarrhea). Simethicone is a surfactant often added to buffers to decrease bloating.
  9. Milk alkali syndrome?
    hypercalcemia and alkalosis caused by ingestion of large amounts of calcium antacids
  10. H2 (histamine) Antagonists drugs
    "idines" -- ranitidine, cimetidine, famotidine, nizatidine
  11. H2 Antagonists MOA
    binding of histamine to H2 receptors on parietal cells stimulates the secretion of H+ (sodium/potassium pump) via second messengers and cAMP. antagonists competitively block histamine binding, and therefore decrease acid secretion (particularly nocturnal acid secretion).
  12. H2 Antagonists indications
    too much acid (GERD, PUD, dyspepsia, gastritis), gastric protection in pts on life support
  13. H2 Antagonists interactions
    cimetidine inhibits CYP450 so numerous potential interactions (used less frequently because of this, also has to be prescription)
  14. H2 Antagonists side effects
    common diarrhea, HA, drowsiness, fatigue, muscle pain, constipation. rare confustion, delerium, slurred speech, thrombocytopenia.
  15. cimetidine additional side effects
    gynecomastia and galactorrhea
  16. Can H2 antagonist tolerence occur?
  17. Proton Pump Inhibitors (PPIs) (antisecratory agents) drugs
    "prazoles" -- omeprazole, pantoprazole, lansoprazole, esomeprazole, rabeprazole
  18. PPI MOA
    bind to active proton pumps, resulting in an irreversible inactivation of the pump and reducing the amount of H+ produced (increases pH). stomach has to make new pumps, which can take up to 48 hrs.
  19. PPI pharmacokinetics
    PPIs are prodrugs and access the proton pumps via the systemic circulation. Tablet is protected by an enteric coating until it reaches the small intestine, where it is absorbed and travels through the blood stream back to the stomach. Once it reaches the acidic stomach via this backdoor root, the prodrug PPI is activated by the acidic environment of the parietal cells. Take 30-60 mins ac for maximal activation and best results.
  20. PPI indications
    acid issues (GERD, ulcers, hypersecretory conditions like Zollinger-Ellison). also upper GI bleeding.
  21. PPI interactions
    omeprazole is an inducer of CYP1A2, but an inhibitor of CYP2C19 (effects of this include increased concentrations of warfarin, diazepam, phenytoin, digoxin, and carbamazepine).
  22. PPI side effects
    GI (N/D, constipation, pain, gas). Less common hypergastrinemia (gastrin hormone levels elevated because it is upstream of the acid suppression) -- can lead to rebound acidic hypersecretion with abrupt cessation of PPIs. Possible link between PPIs and C.diff.
  23. First-line H.pylori eradication combo therapy?
    PPI + clarithromycin (500mg) + amoxicillin (1000mg) BID
  24. Gastrointestinal Cycloprotectants -- prostaglandin analogues drugs
    misoprostol (prostaglandin E1 [PGE1])
  25. prostaglandin analogues MOA
    mimics endogenous prostaglandins, acting on prostaglandin E receptor 3 (EP3) on parietal cells that cause reduced activity of proton pumps. also stimulates the secretion of mucus and bicarbonate and enhancing mucosal blood flow, helping to enhance the mucous barrier that protects the lining of the stomach.
  26. prostaglandin analogues kinetics (T 1/2)
    short half-life, so must be administered frequently (3-4 times daily)
  27. prostaglandin analogues indications
    prevention of NSAID-induced ulcers (NSAIDS inhibit the production of endogenous prostaglandins via COX inhibition)
  28. prostaglandin analogues contraindications
    pregnancy (cat x -- prostaglandins stimulate uterine contractions)
  29. prostaglandin analogues side effects
    severe diarrhea and abdominal cramping (prostaglandins stimulate GI smooth muscle contraction)
  30. Gastrointestinal Cycloprotectants -- coating agents drugs
    sucralfate, bismuth
  31. coating agents MOA
    sucralfate is a complex of sucrose and aluminum hydroxide that forms a negatively-charged viscous paste in the acidic gut, which binds to positively charged proteins found in ulcers and forms a protective barrier for up to 6 hours. bismuth salts also form a protective barrier on ulcers, and additionally inhibit the growth and adherence of H.pylori to the mucosa. both also enhance secretion of prostaglandins, mucus, and bicarbonate.
  32. coating agents pharmacokinetics (T 1/2)
    sucralfate = has a short half-life and must be administered frequently (QID), take 1h ac because it is activated by acid (effectiveness can be decreased by antacids).
  33. coating agents indications
    sucralfate = ulcers. bismuth = H.pylori eradication, acute diarrhea, heartburn.
  34. coating agents contraindications
    bismuth = not used in children or teens with viral infections (because its combined with ASA, can lead to Reye's syndrome)
  35. coating agents interactions
    sucralfate = decreases concentrations of tetracycline, quinolone, levothyroxine, digoxin, and others by binding to them in the gut (separate dosing)
  36. coating agents side effects
    sucralfate = same as AlOH3. bismuth = black tarry stool, blackening of tongue, constipation, tinnitus.
  37. dopamine antagonists (prokinetics) drugs
    metoclopramide, doperidone
  38. dopamine antagonists MOA
    dopamine has an inhibitory effect on GI motility (D2 receptors inhibit ACh release), so antagonists will enhance motility. this includes increasing lower esophageal sphincter tone, and stimulating peristalsis. also act as antinauseants by central inhibition.
  39. dopamine antagonists pharmacokinetics (availability)
    domperidone = low oral bioavailability (extensively metabolized in first pass of liver), bioavailability increased with food, does not cross blood-brain barrier as easily as metoclopramide.
  40. dopamine antagonists indications
    disorders of GI motility (gastroparesis, nausea, vomiting), GERD, diagnostic procedures
  41. dopamine antagonists contraindications
    pts with obstruction or perforation
  42. dopamine antagonists interactions
    metaclopramide = increased concentrations of SSRI (serotonin storm, neuroletptic malignant syndrome)
  43. dopamine antagonists side effects
    hyperprolactinemia (dopamine inhibits prolactin release, so antagonism leads to increased prolactin which can result in gyynecomastia, galactorrhea, dysmenorrhea). metoclopramide = extrapyramidal issues (movement issues such as abnormal muscle tone, Parkinson-like sx, tardive dyskinesia), other CNS (drowsiness, restlessness, insomnia, anxiety, agitation), in infants rare methemoglobinemia.
  44. Fun fact #2!
    the antidote for metoclopramide toxicity is methylene blue :)
  45. Antidiarrheals categories
    opiates, bulk-forming agents
  46. Antidiarrheals -- opiates drugs
    loperamide, diphenoxylate, difenoxin
  47. opiates MOA
    stimulate mu opioid receptors in the gut, reducing/abolishing peristalsis in the colon (slows movement, increases opportunity for fluid absorption). Also enhances anal sphincter tone and rectal distension relaxation reflex.
  48. opiates pharmacokinetics (availability)
    Loperamide does not penetrate the blood-brain barrier (removed by P-glycoprotein transporters), so few euphoric effects. Loperamide/diphenoxylate have low solubility, so IV drug abuse risk is minimal.
  49. Antidiarrheals indications
  50. Antidiarrheals contraindications
    use with select severe, infectious diarrhea (interferes with the clearance of the bad bacteria). pts with preexisting GI motility reduction (severe inflammatory bowel disease)
  51. opiates side effects
    constipation. possible abuse potential (CNS effects).
  52. Antidiarrheals -- bulk-forming agents (hygroscopic/"water attracting" agents) drugs
    kaolin/pectin, attapulgite, bismuth
  53. bulk-forming antidiarrheals MOA
    not fully known -- may provide additional structural integrity to stool (they are essentially clay that is able to absorb a large amount of water), may bind enterotoxins that caused the diarrhea in the first place.
  54. bulk-forming antidiarrheals interactions
    doesn't selectively bind water, so can also bind drugs and nutrients (separate administration)
  55. Laxitives categories
    stimulants, bulk, osmotics, softeners, peripheral opioid antagonists
  56. Laxatives -- stimulants drugs
    sennosides, castor oil, bisacodyl
  57. stimulant laxatives MOA
    irritate the intestinal wall, leading to an accumulation of fluid and electrolytes as well as increased motility (mechanism unknown)
  58. stimulant laxatives pharmacokinetics
    designed to be released in the intestine but not before, or would cause irritation of the stomach (don't split/crush pills)
  59. Laxatives indications
  60. Laxatives side effects
  61. Fun fact #1
    castor oil contains ricin (poison!)
  62. Laxatives -- bulk (dietary fiber) drugs
  63. bulk laxatives MOA
    "ruffage" -- fiber cannot be broken down, so increased fiber causes increased bulk of stool which causes increased GI motility. fermentable fibers help increase bacterial content/bulk of stool, nonfermentable fibers draw water into the stool.
  64. bulk laxatives contraindications
    conditions where increasing bulk would be bad (obstruction, megacolon)
  65. bulk laxatives side effects
    diarrhea, abdominal distension
  66. Laxatives -- osmotics drugs
    lactulose (sugar), magnesium sulfate (salt), magnesium hydroxide (salt), magnesium citrate (salt), sodium phosphate (salt), polyethylene glycol (alcohol/sugar)
  67. osmotic laxatives MOA
    create an osmotic force in the lumen that draws water into the stool, resulting in more viscosity and more bulk. salts are more potent that sugars, but sugars are especially useful for opiate constipation and the elderly (or both!).
  68. osmotic laxatives side effects
    diarrhea. sugars = abdominal distension/flatulence. salts = electrolyte imbalances.
  69. Laxatives -- softeners drugs
  70. stool softeners MOA
    docusate salts are surfactants that allow mixing of aqueous and fatty substances in the stool. they also increases intestinal fluid secretion.
  71. mineral oil MOA
    slows absorption of water in the colon and softens the stool.
  72. mineral oil side effects
    N/V/D, perianal irritation, abdominal cramps, weakness, dizziness, syncope. messes with absorption of fat-soluble vitamins. do not administer hs due to danger of lipid pneumonitis.
  73. Laxatives -- peripheral opioid antagonists drugs
  74. peripheral opioid antagonists MOA
    activation of � opioid receptors in the gut slows things down. antagonization of these receptors increases peristalsis in the colon.
  75. Cannabinoid agonists drugs
    dronabinol (THC), nabilone, cannabidiol
  76. Cannabinoid antagonists drugs
  77. Cannabinoid receptors
    cannabinoid receptors are G-protein-coupled receptors found throughout the body, including in the mesolimbic dopamine pathway (reward pathway), and importantly here CB1 receptors in the hypothalamus are associated with feeding. These receptors are also found in adipocytes.
  78. Cannabinoid agonists pharmacokinetics
    oral bioavailability low to due first-pass metabolism. THC and its metabolites are both active.
  79. Cannabinoid antagonists pharmacokinetics
    lipophilic with very long half life (6-9 days, 16 days in obese pts due to fatty tissue deposits)
  80. Cannabinoid agonists indications
    emesis (chemo), anorexia (AIDS), neuropathic pain (MS)
  81. Cannabinoid antagonists indications
    smoking cessation, obesity
  82. Cannabinoid agonists contraindications
    CVD, hepatic/renal impairment, hx of psychosis, pregnancy
  83. Cannabinoid agonists side effects
    CNS (euphoria, drowsiness, impaired sensory perception), CV (tachy, hypotensive)
  84. Cannabinoid antagonists side effects
    nausea, severe depression
  85. Fun fact #3 --
    you are going to rock this pharm test.
  86. Pancreatic Enzymes drugs
    pancrelipase, pancreatin
  87. Pancreatic Enzymes MOA
    supplement pancreatic enzymes (amylase, lipase, proteases) when pancreas is not up to snuff
  88. Pancreatic Enzymes pharmacokinetics
    would be destroyed by gastric acids, so often are encapsulated or co-administered with acid suppressants. titrate dosing to patient, administer with meals or snacks, never crush or chew (mucosal/gastric irritation)
  89. Pancreatic Enzymes indications
    pancreatic enzyme deficiency (secondary to CF, chronic pancreatitis, pancreatectomy, GI bypass, duct obstruction)
  90. Pancreatic Enzymes contraindications
    pts hypersensitive to pork (they are enzymes from pigs)
  91. Pancreatic Enzymes side effects
    diarrhea, hyperuricosuria or renal stones (supplements have a high purine content, uric acid is the byproduct of the breakdown of purines)
  92. Serotonin Antagonists drugs
    "setrons" -- ondansetron, granisetron, alosetron, tropisetron, ramosetron, dolasetron, palonosetron
  93. Serotonin Antagonists MOA
    5-HT3 receptors in the gut mediate contraction of various segments of the GI tract, and their activation can signal nausea. antagonists decrease receptor stimulation on vagal sensory afferent neurons projecting to emetic center in the brainstem. central 5-HT3 receptors that also help mediate nausea are antagonized as well. other consequences include decreased small bowel motility, decreased colonic compliance.
  94. Serotonin Antagonists pharmacokinetics (T 1/2)
    prolonged biological half-life -- effect lasts well past the drug's elimination from the circulation.
  95. Serotonin Antagonists indications
    nausea, vomiting (especially useful with chemo)
  96. Serotonin Antagonists side effects
    constipation (more common) or diarrhea, HA, light-headedness. rare but serious effects include QT prolongation and other EKG changes, alosetron may also cause ischemic colitis.
  97. Antacids strength by class
    buffers weakest, H2 blockers middle, PPIs strongest.
  98. Antacids pharmacological approaches
    "step up" (start low, go high if no relief) or "step down" (start high, lower until sx return) approaches
  99. Trial off acute antaicid tx -- if sx return within __ months, pt should be put on maintenance therapy (of previously effective tx).
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pharm GI.txt
pharm GI.txt
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