GI meds.txt

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tracey
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11500
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GI meds.txt
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2010-03-31 23:55:13
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Lecture # 1 Pharmacology Final
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GI MEDS
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  1. How do the basic cell functions protect the gut mucosa.
    The mucus and tight cellular junctions protect the stomach from pepsin and HCl acid and there is a rapid epithelial cell turnover cell turnover. Anything that interfere with the normal process will precipitate irritation/ulcers.
  2. How does PGE and NO
    • Increases mucus production
    • increase HCO3 production
    • Decreases HCl productions
    • Vasodilation causes rapid blood flow
  3. What are the defense mechanisms in GI tract
    • mucus
    • blood flow
    • PGE
    • HCO3
    • rapid cell turnover
  4. What factors irritate the GI tract
    • H. pylori
    • smoking, alcohol
    • stress --> HCl, pepsin, bile salts, pancreatic
  5. What is included in Peptic Ulcer Disease
    • Gastritis
    • Gastric ulcer from decreased protective factors and pyloric reflux
    • Duodenal Ulcer from increased HCl
  6. What causes stress ulcers
    • Hypoperfusion of the stomach
    • Increased HCl production
  7. What can cause hypoperfusion of the stomach
    • Hypovolemia
    • Shock
    • Burns and trauma
    • ischemia, anoxia/hypoxia
    • severe and/or prolonged stress
  8. What causes an increase in HCl production
    • Neuro injury
    • vagal nerve stimulation
  9. How is gastric acid secreted
    Gastric acid exhibits circadian rhythm and its peak is highest in the evening and lowest in the morning
  10. What are the basic management strategies for increased HCl
    Suppress nocturnal acid secretion which is unbuffered by food and causes prolonged duonenal acidification
  11. What the basic goals of managing HCl
    Keep the pH>4 because if it is >4 pepsinogen does not break down into pepsin, this prevents pepsin-acid complex which is proteolytic
  12. What is the side effect of low HCl?
    You don't absorb Vit B12 as well which results in anemia
  13. What are the overall goals of pharmacotherapy for ulcers
    • Relieve pain
    • Treat symptoms
    • Heal ulcer
    • Prevent complications
  14. What are the pharmacological options for ulcers
    • Antacids
    • H2 receptor antahonists
    • Sulcrafates
    • Prostaglandins
    • Proton pump inhibitors
  15. What are the heal times periods for the major medicines for ulcers
    • In general it takes 4-6 wks
    • Proton pump take 4 and the others take 4-6
  16. What is the MOA of antacids
    Neutralize
  17. Which antacid neutralizes more acid
    Liquid(150-180) compared to tablets (12meq)
  18. What is the goal of antacids
    Treat the symptoms they arent a cure
  19. What is the MOA of H2 blockers(H2 receptor antagonists)
    They competitively and reversibly bind H2 receptors on parietal cells decreasing cAMP production and secretion H2 stimulated gastric acid (which contains HCl)
  20. What is the strongest to weakest H2 blockers
    • "CRNF"
    • WEAK
    • cimetidine
    • ranitidine
    • nizatidine
    • famotidine
    • STRONG
  21. When treating duodenal ulcers with H2 blockers what is the best dosing schedule
    Nighttime dosing is more effective than bid dosing
  22. When treating refractory ulcers with H2 blockers what is the best dosing
    Use a high dose
  23. What is important to remember about drug interactions and H2 blockers
    Cimtidine, nizatidine, famotidine inhibit the cytochrome p450 system (remember that this will cause other drugs to accumulate in the body)
  24. What is the MOA of sucralfate
    • It is a sucrose sulfate aluminum salt complex that binds to the HCl and acts like a buffer and it binds to the inflamed tissue and creates a protective barrier for up to 6 hours
    • Inhibits pepsin activity
    • Stimulates PG synthesis in the mucus
    • Forms a physical barrier to prevent back diffusion of acid and pepsin
  25. What are the main side effects of sucralfate
    • Constipation
    • Aluminum tox in patients with renal failure
    • Hypophos because it binds to the gut and prevents absorption of phos
  26. What are the major drug interactions of sucralfates
    • May reduce absorption of other drugs that are typically absorbed in the stomach
    • Ex quinolones, dig, warfarin, phenytoin
  27. How should you administer multiple drugs when a pt is receiving sucralfates
    Administer 2 hours AFTER other drugs
  28. What is the MOA of action prostaglandins
    Inhibits histamine mediated cAMP production in parietel cells inhibiting HCl release
  29. What is cytotec(misoprostol)
    A prostaglandin analog used to treat gastric ulcers
  30. Why are GI problem are prostaglandins used for
    Prevention of NSAID induced gastric ulcers
  31. Who should NEVER use cytotec (misoprostol)
    Pregnant women bc it contains PG
  32. What should you avoid when taking cytotec (misoprostol)
    Mag containing antacids bc it may increase diarrhra and this is always a side effect
  33. What are the side effects of misoprostol
    • Abd cramping
    • Diarrhea
    • GYN issues
  34. What are the most commonly used proton pump inhibitors
    • Prilosec
    • Nexium
  35. The most powerful acid inhibiting and ulcer healing drugs available
    Proton pump inhibitors
  36. What is the MOA of proton pump inhibitors
    • Inhibits the last step in HCl secretiom by altering the activity of H+/K+ ATPase (proton pump) within the parietal cells
    • Result: reduced transport of H+ out of the cell
  37. What are side effects of proton pump inhibitors
    Sustained hypochlohydria results in chronic hypergastrinemia which leafs to gastric carcinoid tumors
  38. A side effect of proton pump inhibitors is carcinoid tumors what is the FDA recommendations
    Limit treatment to 4-6 weeks
  39. What is the most common cause of ulcers
    • h. pylori
    • It accounts for 80% of stomach ulcers and 90% of duodenal ulcers
  40. Do all people with h pylori have ulcers
    No most dont develop ulcers
  41. How does h pylori interfere with normal gastric function
    It survives in stomach bc it secretes enzymes that neutralize the acid This weakens the protective mucus coating of the stomach and duodenum
  42. How is h pylori spread
    • Food and water
    • It is in infected peoples saliva and can be spread from mouth the mouth cobtact
  43. What ate the goals of h pylori tx
    • Kill bact - antibs
    • Reduce stomach acid - H2 blockets or PPI
    • Protect stomach lining - bismuth subsalicylate
  44. What is the FDA approved tx regime for h pylori in patients with PUD
    • "Triple therapy"- administer each therapy for 10-14 days
    • OAC- omprazole amoxicillin chlarithomycin for 10 days
    • BMT - bismuth subsalicylate, metrodiazole and tetracycline for 14 days
    • LAC- lansoprazole, amoxicillin, chlarithromycin for 10 or 14 days
  45. What is GERD
    Gadtric contents back flow into the esophagus
  46. What are the symptoms of dysphagia
    • Dyapepsia
    • Regurgitation
    • Dysphagia
    • Odynophagia
  47. How does GERD effect the infant
    • Failure to thrive
    • Pulmonary aspiration
  48. How does GERD effect the child/adolescent
    • Esophagitis
    • Stricture formation
    • Barrets esophagus- adenocarcinoma
    • Esopghageal perforation
    • Asthma/wheezing
    • Bleeding/anemia
  49. What are the goals of GERD tx
    • Alleviate symptoms
    • Decrease frequency/duration of reflux
    • Promote healing
    • Prevent complications
  50. GERD therapy is directed at
    • Increasing LES tone- bethanechol,reglan
    • Increase esophageal clearance- bethanochol
    • Improve gastric emptying- reglan
    • Protect mucosa - sucralfate
    • Decrease acidity in reflux- antacids, H2antagonists,PPI
    • Decrease the volume available to reflux- reglan
  51. What are the phases of GERD therapy
    • I - lifestyle changes, antacids
    • IIa-H2, antagonists, prokinetic agents(reglan),bethanachol, sucralfate
    • IIb- high doses of H2 antagonists and PPI
    • III Nissen
  52. What is the MOA of Bethanochol (urecholine)
    Increases GI tone & motility and increases LES tone
  53. What type of medication is bethanechol
    Cholinergic - parasympathetic
  54. What the contraindications of bethanachol
    PUD or obstruction
  55. What are adverse effects of bethanechol
    Abdominal cramping & blurred vision
  56. What is the MOA of anticholinergics
    Inhibits gastric acid secretions by blocking acetylcholine receptors on the parietal cells
  57. When should anticholinergics be given
    1 hour after meals � it is not that effective
  58. What are the contraindications of anticholinergics
    • Remember it stops the cholinergics which is a parasympathetic (feed and breath)
    • Bleeding, tachycardia, glaucoma, achalsia, obstruction, or a suspected megacolon
  59. What are the adverse effects of anticholinergics
    Blurred vision, urinary hesitancy or retention, dry mouth, nose, throat, constipation
  60. Uneasiness of the stomach that often accompanies the urge to vomit
    Nausea
  61. contraction of the diaphragm & abdominal muscles with opening of the LES and forceful expulsion of gastric contents
    Vomitting
  62. Similar to vomiting but without gastric contents
    Retching
  63. Spontaneous vomiting without nausea and vomiting
    Projectile vomiting
  64. What triggers vomiting that is controlled by the brain
    • Chemoreceptor trigger zone (CTZ)-nerve fibers in the brainstem (medulla) sense changes in the chemical composition of the blood; this is an evolutionary protective mechanism
    • Increased ICP from trauma, infection, tumors, AVM, aneurysm
    • Cortex - unpleasant memory (anticipatory) sight, odor
    • Migraine HA
  65. What controls vomiting
    • Brain
    • Vesitubular nuclei in the brainstem
    • Sensors in the stomach and bowel
    • Protective mechanisms
    • Responses to inflammation or irritation of the gut
  66. What triggers vomiting that is controlled by the vestibular nuclei (brainstem)
    • The brainstem interprets signals from the inner ear or eye and uncoordinating signals cause N & V
    • Ex: Dizziness, motion sickness
  67. Why do protective mechanisms cause vomiting
    • Prevents the ingestion of harmful substances and irritating foods/drugs
    • Ex: opiods, dig, anesthetics, ETOH, Chemo
  68. What causes vomiting as a result of a response to inflammation or irritation
    • Ulcers, reflux, severe constipation, GI obstruction/gastric outlet obstruction
    • Infection: viral or bacterial
    • Tumor growth and invasion of the gut
    • Radiation
  69. What is the most common antiemetics
    Phenothiazines
  70. What is the MOA of the antiemetic drugs phenothiazines
    • Blocks dopamine receptors in the CTZ
    • Effective in most case of N & V
  71. When are phenothiazines NOT effective
    Motion sickness
  72. Compazine, Phenergen, Torecan, Tigan
    Phenothiazines
  73. What is the MOA of butyrophenones
    Block dopamine receptors in the CTZ
  74. What are the adverse effects of butyrophenomes
    • QT prolongation, torsades de pointes, EPS
    • They are generally less sedating than phenothiazines
  75. Droperidol and Haldol
    Butyrophenones
  76. What medication is usually used for motion sickness
    Antihistamines and anticholinergics
  77. meclizine, diphenhydramine, Dramamine
    antihistamines used to tx motion sickness
  78. This antiemetic for motion sickness is applied behind the ear
    Scopolamine
  79. What is the MOA of substituted bezamine
    Blocks dopamine receptors in the CTZ
  80. How does the dose of benzamine change the with different condition
    • 10-20 mg.kg po QID for gastroparesis, low dose chemo
    • 1-2 mg/kg for high dose chemo
  81. Reglan
    Substituted Reglan
  82. What is the MOA serotonin antagonists
    Selectively blocks serotonin (5HT3) receptors in the GI tract & CTZ
  83. Zofran, Kytril, Anzemet, Aloxi
    Serotonin antagonists
  84. Cortocosteroids are used for antiemetics, what are the adverse effects
    • Insomnia
    • Hyperglycemia
    • Inc appetite
    • Euphoria
    • Agitation
  85. What is the MOA of cannabinoids
    Unknown but likely causes depression of the higher cortical pathways leading to the emetic center
  86. What are some adverse effects of cannabinoids
    Sedation, euphoris, dysphoria, mood changes, hallucinations
  87. Marinol
    Cannabinoids
  88. What is the MOA of benzodiazopines
    Amnesic, anxiolytic and sedative properties
  89. What are common side effects of benzodiazopines
    Sedation, hypotension, disinhibition, motor incoordination
  90. Valium, versed, ativan
    • Benzodiazopines
    • Ativan is primarily used for nausea
  91. What are the cheapest benzodiazopines used for nausea and vomittting
    Dexamethasone, haldol, raglan
  92. What is large volume diarrhea
    Increased water content in stools, usually painless
  93. What causes large volume diarrhea
    • Osmotic problems r/t drugs
    • Malabsorption problems d/t pancreratic or bile defieciency, short gut, lactose disease, celiac disease
    • Deranged gut flora d/t antib�s, viruses,bacteria (salmonella, shingles, )- the bac�t attach to the bowel wall and make toxins, they invade and damage the brush border
    • Secretory problems from enteric organisms or laxatives- Ecoli secretes toxins that stimulates fluid secretions, S.aureus invades and destroys epithelial cells and alters fluid transport; parasites also cause secretory problems
    • Deranged motility � short gut, IBS
  94. What is the difference between opiods and opiates
    • Opiate � natural
    • opium � synthetic
  95. How doe opiods and opiates work to decrease diarrhea
    Inhibits intestinal motility
  96. Morphine, methylmorphine, camphorated tincture of opium
    Opium alkaloids (opiates) for diarrhea
  97. Lomotil and Imodium
    Synthetic opiums alkaloids for diarrhea
  98. How does kaopectate treat diarrhea
    Decreases the fluid in the stools
  99. How does pepto bismol decrease diarrhea
    Decreases intestinal secretions
  100. What other jobs do antidiarrheals do
    • May also absorb toxins and provide a protective coating for the mucosa
    • What are some negatives r/t antidiarrheals
    • May delay intestinal clearing of pathogens
  101. What are the contrindications of antidiarrheals
    • Not recommended for those with a fever, bloody diarrhea or < 2 years old
    • Not recommended for long term use
  102. What are causes of constipation?
    • Infrequent passage of stools and increased transit time
    • Failure to respond to the urge to defecate from pain, discomfort, hemorrhoids, sexual abuse, and toileting issues
    • Inadequate fiber, decreased fluid intake, abdominal wall weakness, inactivity and bedrest, pregnancy
  103. What occurs with chronic constipation
    • Dilation of the rectum or colon
    • Allows for large amounts of stool to build up with little or no sensation
  104. What is fecal impaction
    • Retention of hardened stool in rectum and colon
    • Can cause partial or complete bowel obstruction
  105. How does hyperosmotic colonic lavages work (preps)
    Increases intraluminal pressure and stimulates peristalsis
  106. Polyethylene glycol
    hyperosmotic colonic lavages
  107. What should you remember about hyperosmotic colonic lavages
    Has a lot of sodium and kids can become dehydrated
  108. When is miralax used
    Used for slow transit constipation and encopresis (leaking of stool) in children
  109. How do stimulants treat constipation
    Produces local irritation which increases intestinal motility
  110. When are bowel stimulants contraindicated
    Obstruction, peritonitis or recent abdominal surgery
  111. What type of drug is Dulcolax
    A stimulant for tx of constipation
  112. How do bulk forming cathartics work for constipation
    They are natural or synthetic polysaccharides/cellulose derivatives that aren�t absorbed therefore they
  113. Metamucil and citracel
    Bulk forming cathartics, used to treat constipation
  114. How do lubricant cathartics treat constipation
    Softens stool by acting as a wetting agent
  115. Mineral oil, glycerin chips
    Lubricant cathartics
  116. How do emollient laxatives work
    Act as surfactants that soften the fecal mass by facilitating the mixture of aqueous and fatty substances
  117. Colace
    Emollient laxative

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