Final Pharm: GI Drugs

Card Set Information

Author:
choward04
ID:
208273
Filename:
Final Pharm: GI Drugs
Updated:
2013-03-20 21:47:16
Tags:
Pharm
Folders:

Description:
Pharm
Show Answers:

Home > Flashcards > Print Preview

The flashcards below were created by user choward04 on FreezingBlue Flashcards. What would you like to do?


  1. What are the goals of GI drugs in the gut (2)?
    • 1. Decrease acidity
    • 2. Increase mucosal defense
  2. What are the 3 receptor sites for parietal cells?
    • 1. Histamine (H2)
    • 2. Gastrin (CCK-B)
    • 3. Acetycholine (M3)
  3. Which receptor is stimulated sight, smell, taste of food (CNS)?
    M3--> Acetylcholine
  4. Which receptor is stimulated by food, gastric distention?
    ACH+G cell--> Gastrin
  5. Which receptor is most stimulated during postprandial & nocturnal acid secretion?
    Histamine
  6. What are the acid secretion physiology steps? (4)
    • 1. Ca+ influx into parietal cell
    • 2. cAMP increases and activate protein phosphokinases
    • 3. Activation of H/K ATPase pump
    • 4. Hydrogen combines w/ CL- from the blood to form HCL
  7. What is the final common pathway for gastric acid secretion?
    Proton pump
  8. At the proton pump, H+ is transported out the cytoplasm and into _________________?
    secretory canalicus
  9. What are the 5 defensive factors of GI mucosa?
    • 1. Mucus secretion
    • 2. bicarb secretion
    • 3. prostaglandins
    • 4. blood flow
    • 5. regeneration after cellular injury
  10. What are 3 caustic agents that lead to GI erosion/ulceration?
    • 1. Gastric acid
    • 2. Bile
    • 3. Pepsin: breaks down protein
  11. What pH is pepsin irreversibly inactivated?
    >7
  12. What drugs have the action of reducing acidity? (3)
    • 1. Antacids
    • 2. H2 Receptor Antagonist
    • 3. PPI
  13. What GI drugs have the action of protecting the mucosa?
    • 1. Sulcralfate
    • 2. Prostaglandin Analogs
    • 3. Bismuth compounds
  14. Antacids function to increase or decrease gastric acidity?
    Increase pH
  15. Antacids react with HCL to form what?
    Na + H20 (for partial neutralization)
  16. T or F. Antacids are useful in heartburn prophylaxis?
    False
  17. Sodium bicarb reacts w/ HCL to form what?
    CO2 + NaCL
  18. What are the side effects of sodium bicarb (Alka Seltzer)? What patients should not take it? (3)
    • -S/E--> gastric distention, belching
    • -May exacerbate fluid retention in patients w/ HF, HTN, renal insufficiency
  19. Calcium Carbonate (TUMS) combines w/ HCL to form what?
    CO2 + CaCL2
  20. What are the S/E of Ca+ Carbonate and what risk does it have with dairy products?
    • S/E--> belching or metabolic alkalosis
    • Risk w/ diary--> hypercalcemia, renal insufficiency, & metabolic acidosis
  21. What is the S/E of each Aluminum & Magnesium Hydroxide?
    • AL salts--> constipation
    • Mg salts--> osmotic diarrhea
  22. What is the effect of taking antacids w/ other drugs?
    • -Reduce gastric hydrolysis of drugs
    • -Change gastric and/or urinary pH
  23. What is the MOA of H2RA?
    block histamine receptor--> decrease acid secretion
  24. T or F.  H2RA are highly effective o meal stimulated acid secretion?
    False: highly effective at inhibiting nocturnal acid secretion (histamine activity), modestly effective at meal stim (gastrin, acetyl, & histamine)
  25. H2RA inhibit 24hr acid secretion by what percent?
    60-70%
  26. What are the H2RA Dynamics? (5)
    • 1. Competitively inhibits H2 receptor
    • 2. Suppresses basal/meal stim acid secretion
    • 3 Highly selective to H2
    • 4. Decrease gastric secretion vol & pepsin concentration
    • 5. H2 blockade decreases gastrin/Acetyl. stimulation
  27. What are adverse effects of H2RA? (4)
    • 1. GI discomfort
    • 2 CNS effects (h/a, drowsiness, psychosis, hallucinations
    • 3. dermatologic (rash)
    • 4. hematologic (thrombocytopenia)
  28. What is the MOA of PPI?
    Irreversibly binds to H/K ATPase (proton pump)--> blocking final common acid secretion pathway
  29. PPI are best at inhibiting nocturnal secretion or basal/meal stim acid secretion?
    Inhibit basal & meal stimulated gastric acid secretion ~24hrs, some nocturnal activity w/ newly activating pumps
  30. Where in the GI are PPI absorbed?
    small intestine, transported in serum to acidic canaliculus of parietal cell for protonation to active form
  31. Converstion of PPI to active form requires what?
    actively secreting proton pump
  32. When should PPIs be taken to be most effective?
    30-60min prior to meal on an empty stomach
  33. What are some adverse effects of PPIs? (4)
    • 1. GI discomfort (N/D, pain)
    • 2. CNS (H/A, dizziness)
    • 3. Increased infection risk (c. diff, pneumonia)
    • 4. Rare: skin rash, increase liver enzymes
  34. How does sulcrafate work?
    Forms paste in water/acid soluntions that bind to ulcer or erosion for ~6hrs--> stimulating secretion of mucosal
  35. What are 4 effects of misoprostol?
    • 1. increase mucus & bicarb secretion
    • 2. Increase mucosal blood flow
    • 3. Bind parietal cells--> reducing histamine
    • 4. Stimulate cAMP production
  36. What are 3 effects of Bismuth compounds?
    • 1. Coats ulcers/erosions
    • 2. Stimulate prostaglandins, mucus, & bicarb
    • 3. Antimicrobial activity against H. Pylori
  37. What drugs are useful for GERD?
    antacids or intermittant H2RA
  38. What is 1st line therapy for Erosive Esophagitis?
    PPI (long term therapy often indicated)
  39. What med is the DOC for uncomplicated (no H. Pylori) PUD?
    PPI
  40. What is the treatment plan for H. Pylori?
    • -PPI is DOC
    • -H2RA if intractable infection
    • -1/2 dose at night to prevent recurrence
  41. What is the treatment plan for H. Pylori ulcers?
    • Triple therapy: 
    • -2 ABX + PPI x 14 days
    • -PPI x 4-6 weeks
  42. Why are PPIs effective for H Pylori?
    • 1. direct antimicrobial property
    • 2. increased pH
  43. Which GI med is best for NSAID-induced ulcers?
    PPI have better healing than H2RAs
  44. What are 5 clinical uses of GI stimulants?
    • 1. Selectively stim GI motor function
    • 2. ⇑ lower esophageal sphincter tone--> GERD

    3. ⇑ gastric emptying--> post-op

    4. ⇑ small intestine activity--> post-op ileus

    5.⇑ colonic transit--> constipation
  45. T or F. GI NS regulates motility & secretion autonomously.
    True
  46. What symptoms are caused by stimulation extrinsic afferent nerves?
    N/V, abdominal pain
  47. What symptoms are caused by stimulation of intrinsic primary afferent nerves?
    Perstalsis
  48. What is the effect of 5-HT3 stimulation?
    Vomiting
  49. What drug is good for inhibiting the 5-HT3 receptor and decreasing nausea?
    Ondansetron
  50. What is the effect of 5-HT4 stimulation?
    stimulate motility/peristalsis
  51. What drug is an agonist for 5-HT4 and promotes GI motility
    metoclopramide
  52. What is the effect of neostigmine?
    • Enhances gastric, small intestine, & colonic empyting
    • -good for acute colonic pseudo-obstruction
  53. What is the effect of Cholinomimetic agents? What are 2 drugs?
    • Increase GI function
    • -Bethanechol
    • -Neostigmine
  54. What are the side effects of cholimimetic agents?
    salivation, N/V/D, bradycardia
  55. What occurs with D2 stimulation?
    D2 dampens cholinergic smooth muscle stim
  56. What are the effects of D2 receptor antagonist?
    • -Increase esophageal perstalsis
    • -Increase lower esophageal sphincter pressure
    • -Increase gastric emptying.
  57. T or F. D2 receptor antagonists have NO effect on the stomach?
    False: only works on the stomach NOT the small intestine or colon
  58. What are the clinical uses of D2 Receptor Antagonist?
    • -GERD
    • -Surgery
    • -DM gastroparesis
    • -Advancing feeding tube
    • -chronic dyspepsia
    • -Emesis prophylaxis
  59. What are the adverse effects of D2 Receptor Antagonist? (CNS & EPS)
    • Metoclopramide
    • -CNS:--> restlessness, drowsiness, insomnia, anxiety, agitation
    • -EPS--> dystonia, akathesia, parkinsonian, tardive dyskinesia
  60. What is the effect metoclopramide & Domperidone on prolactin?
    Increases prolactin levels--> galactorrhea, gynecomastia, impotence, menstrual disorders
  61. What is the effect of Macrolides on GI activity?
    Directly stimulates motilin receptors on GI smooth muslce
  62. What are 4 indications for laxatives?
    • 1. Short term constipation relief
    • 2. Prevent straining
    • 3. Bowel prep
    • 4. Poison/Toxin elimination
  63. What are 2 contraindications and 3 adverse effects of laxatives?
    • Contraindications: Acute abdominal d/o, UC
    • Adverse effects: Diarrhea, abd cramping, fluid/electrolyte imbalance
  64. What are the effect of builk-forming?
    • -Water retained within stool
    • -Increased stool mass
    • -stimulate peristalsis
  65. How do stool softeners work?
    Reduce surface tension of liquid in stool (grease intestines)
  66. How do osmotics work?
    • -Increase stool liquidity
    • -Useful for acute/chronic constipation
  67. How do stimulants work in the GI tract?
    • -Act directly on the intestinal mucosa
    • -alter fluid secretion, stimulate peristalsis, increase fluid in stool
  68. What are 2 examples of GI stimulants?
    Senna & Bisacodyl
  69. What is an adverse effect of 5-HT4 receptor agonist?
    QT prolongation (not available in US)
  70. T or F.  Opioid agonists do NOT cross BBB?
    True
  71. What are the effects of opioid agonist? (3)
    • 1. Decrease motility
    • 2. slow stool passage
    • 3. increase time to absorb fluid
  72. What are 2 examples of opioid agonists?
    • 1. Loperamide
    • 2. Diphenoxylate & Atropine (lomotil)
  73. Name a 5-HT3 receptor antagonist that is approved for women w/ sever diarrheal IBS?
    Alosetron (lotronex)
  74. Which CL channel activator is approved for women with chronic constipation?
    Lubiprostone (Amitza)
  75. What is the primary use of 5-HT3 Antagonists?
    -Prevention of N/V associated with chemo (give 30min prior)
  76. What are adverse effects of 5-HT3 Antagonists? (5)
    Constipation, diarrhea, H/A, light-headedness, PROLONGED QT (Dolasetron-Anzemet)
  77. What drugs is best for delayed chemo induced N/V?
    Dexamethasone (enhances effectiveness of 5-HT3 antagonists
  78. What is the MOA of Phenothiazines? Name 2 drugs.
    Inhibit dopamine receptors in chemoreceptor zone (compazine, phenergan)
  79. What drug is considered first line therapy for mild-mod UC?
    Aminosalicylates (5ASA)

What would you like to do?

Home > Flashcards > Print Preview