Murphy's Pharmacology

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Anonymous
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193811
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Murphy's Pharmacology
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2013-01-19 18:39:22
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Murphy Pharmacology
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Pharmacology for constipation, diarrhea, emesis, dyspepsia
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  1. Bulk forming laxatives
    MOA: aid in water retention and add bulk to feces

    • Metamucil (psyllium husk)
    • Cologel (methyl cellulose)

    • Bran, pectins, cellulose, lignin
    • Psyllium preparations
    • Methylcellulose
    • Calcium polycarbophil
  2. Osmotic laxatives
    MOA: alteration of the osmotic environment, increasing water retention in colon

    • Magnesium hydroxide (Milk of Magnesia)
    • Magnesium sulfate (Epsom salts)
    • Lactulose (Cephulac)

    • Sodium phosphates
    • Magnesium citrate
  3. Prokinetic agents
    • Metoclopramine (Reglan)
    •     MOA: complex, stimulation of 5-HT4 receptors on enteric neurons promoting the release of acetylcholine and act as a D2 antagonist which may potentiate acetylcholine release which stimulate gastric emptying and small intestinal motility via increased cholinergic stimulation

    • Bisacodyl (Dulculax)
    •     MOA: reduction of net absorption of water and electrolytes

    • Danthron
    •     MOA: enhance clonic motility

    Misoprostol
  4. Surfactant laxatives
    • Docusate salts (Colace and others)
    •    MOA: unknown

    • Poloxamers
    • Lactulose
  5. Stimulant laxatives
    • Metoclopramine (Reglan) 
    •    MOA: D2 agonist at low concentrations, 5-HT3 antagonist at high concentrations
    •    Prokinetic properties (stimulates gastric emptying and small intestinal motility)

    • Bisacodyl (Dulculax)
    •    MOA: reduction of net absorption of water and electrolytes

    • Danthron
    •    MOA: enhance clonic motility

    • Diphenylmethane derivatives
    • Anthraquinone derivatives
    • - Senna
    • - Cascara sagrada
  6. Fluorinated 4-quinolone antibiotics
    MOA: inhibit A subunit of DNA gyrase, an enzyme that prevents mechanical overwinding of the DNA following replication in bacteria

    • Ciprofloxacin (Cipro)
    • Ofloxacin (Floxin)
    • Norfloxacin

    • (Bismuth subsalicylate (Pepto-Bismol)
    •    MOA: coating of ulcerations and erosions and may also stimulate protective factor secretion, direct antimicrobial effect on H. pylori and by binding enterotoxins)
  7. Somatostatin analogs
    • Octreotide (Sandostatin)
    •    MOA: direct interaction with the somatostatic receptor, key regulatory hormone that acts at a number of sites including inhibition of endocrine secretions, decreased smooth muscle contractility, decreased fluid secretion, and decreased gastric acid secretion
  8. Piperidine opioid mu agonists
    MOA: stimulates reduction in GI motility via direct stimulation of the mu opioid receptor causing inhibition of presynaptic cholinergic nn in the submucosal and myenteric plexuses leading to increased colonic transient time and increased fecal water absorption

    • Diphenoxylate (Lomotil)
    • Difenoxin (Motofen)
    • Loperamide (Imodium)
    •    MOA: increases anal sphincter tone

    • (Oral rehydration (Pedialyte, Rehydralyte)
    •    MOA: stimulates water absorption by increased glucose and amino acid uptake)
  9. 5-HT3 antagonists
    MOA: block peripheral 5-HT3 receptors on intestinal vagal afferents, effectively blocking emesis regulated by vagal stimulation, and central 5-HT3 receptors in teh CNS vomiting center and in the CTZ

    • Ondansetron (Zofran)
    • Granisetron (Kytril)
  10. D2 antagonist prokinetic agents
    MOA: D2 antagonist activity in the CNS at the level of the chemoreceptor trigger zone (CTZ)

    • Metoclopramide (Reglan)
    •    MOA: complex, with stimulation of 5-HT4 receptors on enteric neurons promoting release of acetylcholine and act as a D2 antagonist which may potentiate acetylcholine release which stimulate gastric emptying and small intestinal mobility via increased cholinergic stimulation

    Trimethobenzamide (Tigan)
  11. Neuroleptics
    MOA: direct inhibition of muscarinic and dopamine (D2) receptors

    • Chlorpromazine (Thorazine)
    • Prochlorperazine (Compazine)
    • Haloperidol (Hladol)
  12. Glucocorticoids
    • Dexamethasone
    •    MOA: not fully understood in emesis and nausea, but alters gene expression via the steroid receptor thereby decreasing inflammation
  13. Cannabinoids
    • Dronabinol (Marinol, weed)
    •    MOA: delta9-tetrahydrocannabinol is active component which is an agonist for the cannabinoid receptor, direct mechanisms for effects on emesis not understood
  14. Antihistamines
    MOA: H1 receptor antagonists and act on vestibular effects and within brainstem

    • Promethazine
    • Diphenylhydramine
  15. Anticholinergics
    • Scopolamine
    •    MOA: M1 muscarinic receptor antagonist, most effective drug for motion sickness, admin 1 h prior to onset of motion

    • Ipecac
    •    MOA: effects chemoreceptor trigger zone (CTZ) of area postrema of the medulla

    • Apomorphine
    •    MOA: stimulates the CTZ
  16. H2 receptor antagonists
    MOA: competitive H2 receptor antagonists, blocking the H2 receptor resulting in a rapid, marked (90%) reduction in nocturnal acid release and 60-70% for 24 h acid release 

    • Cimetidine (Tagamet)
    •    MOA: binds to and blocks P450 metabolism that enhances the half-life of many drugs; inhibits binding of dehydrotestosterone to androgen receptors, inhibits estradiol metabolism, and increases prolactin levels all of which can lead to gynecomastia, impotance, and galactorrhea

    • Ranitidine (Zantac)
    •    MOA: binds 4-10 times less effectively to P450

    • Famotidine (Pepcid)
    •    MOA: does not interfere with liver P450 metabolism
  17. Proton pump inhibitor
    MOA: covalent modification of H+, K+ ATPase via formation of a disulfide linkage that irreversibly inactivates the pump

    • Omeprazole (Prilosec)
    • Lansoprazole (Prevacid)
  18. Nitroimidazol antibiotics/antiprotozoal
    Metronidazole
  19. Penicillin antibiotics
    Amoxicillin
  20. Macrolide antibiotics
    Clarithomycin
  21. Antacid salts
    • Al(OH)3 + Mg(OH)2 (mylanta, Maalox)
    •    MOA: buffers acid (HCl) thru formation of Al and Mg chlorides or Ca chlorides, thus reducing aggressive factor HCl and conversion of pepsinogen to pepsin

    • Calcium carbonate (Tums)
    • Sodium bicarbonate (Alka Seltzer)
  22. Mucosal protective agents
    • Sucralfate (Carafate)
    •    MOA: protect area of mucosal erosion and ulceration by producing a protective covering in the ulcerated area by the octasulfated form of sucrose polymerizing in the stomach under acidic conditions

    • Misoprostol (Cytotec)
    •    MOA: stimulation of mucosal secretions and HCO3- secretion via stimulation of the prostaglandin receptor by this PGE1 methy analog and a secondary action is the reduction of histamine-stimulated cAMP production leading to a reduction in acid release

    • Bismuth Subsalicylate (Pepto-Bismol)
    •    MOA: coating of ulcerations and erosions and may also stimulate protective factor secretion, direct antimicrobial effect on H. pylori and by binding enterotoxins

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