| Term 
 | Definition 
 
        | treatment for hemochromatosis |  | 
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        | Term 
 | Definition 
 
        | Chelator (treatment for hemochromatosis) |  | 
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        | Term 
 | Definition 
 
        | combo of sulfapyridine (antibacterial) and 5- aminosalicylic acid (anti- inflammatory). activated by colonic bacteria used for Chrons, UC  Tox: malaise, nausea, sulfonamid tox, reversible oligospermia  |  | 
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        | Term 
 | Definition 
 
        | 5-HT3 antagonist.  decreases vagal stimulation. Central acting anti-emetic. controls vomiting  Tox: headache, constipation |  | 
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        | Term 
 | Definition 
 
        | D2 receptor antagonist increases LES resting tone  increases contractility, and motility doesn't influence transport time  Use: diabetic and gastroporesis (post sx), antiemetic  Tox: Increases parkinson like effects, restlnessness, drowsiness, fatigue, depression, nausea, diarrhea  contraindications: Bowel Obstruction, parkinson diease  |  | 
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        | Term 
 | Definition 
 
        | PGE1 analong - increases production/ secretion of gastric mucous barrier
 - decreases acid production
 USES: prevention of NSAID induced gastric ulcers (NSAIDS block PGE1) ;
 also used to prevent abortions and induce labor (ripens cervix)
 Tox: diarrhea
 Contraind: in women with child bearing potential (abortifacient)
 |  | 
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        | Term 
 | Definition 
 
        | Use: ulcer healing, traveler's diarrhea MOA: bind to ulcer base, allowing bicarb secretion--> increase pH in mucous layer
 Tox: constipation
 Sucralfate Tox: can decrease absorption of other drugs, generally given on empty stomach
 |  | 
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        | Term 
 | Definition 
 
        | azoles (Omeprazole, Lansoprazole, esomeprazole, pantoprazole, dexlansoprazole) USE: peptic ulcer, gastritis, reflux, ZE syndrome
 MOA; irreversibly inhibits H+/ ATPase in stomach parietal cells
 Tox: increased risk C. diff, pneumonia (b/c decreased aciditiy to fight bacteria),
 hip fractures (interefere with Calcium absorption)
 decreased Mg 2+ with long term use
 |  | 
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        | Term 
 
        | H2 blockers (ines: cimetifdine, famotidine, ranitidine, nizatidine)
 |  | Definition 
 
        | reversibly blocks histamine h2 receptors. USE: peptic ulcer, gastritis, reflux
 TOX: cimetidine inhibits CYP-P450, antiandrogenic effects (prolactin release, gynecomastia, impotence, decreased libido in males)
 ranitidine decreases renal excretion of creatinine; inhibits tubular transport in kidney
 |  | 
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        | Term 
 | Definition 
 
        | Long acting somatostatin analog USE: acute variceal bleeds, acromegaly, VIPoma, carcinoid tumors
 TOX: nausea, cramps, steatorrhea
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | azoles (Omeprazole, Lansoprazole, esomeprazole, pantoprazole, dexlansoprazole) USE: peptic ulcer, gastritis, reflux, ZE syndrome
 MOA; irreversibly inhibits H+/ ATPase in stomach parietal cells
 Tox: increased risk C. diff, pneumonia (b/c decreased aciditiy to fight bacteria),
 hip fractures (interefere with Calcium absorption)
 decreased Mg 2+ with long term use
 |  | 
        |  | 
        
        | Term 
 
        | H2 blockers (ines: cimetifdine, famotidine, ranitidine, nizatidine)
 |  | Definition 
 
        | reversibly blocks histamine h2 receptors. USE: peptic ulcer, gastritis, reflux
 Tox: cimetidine= inhibts CYP450; antiandrogenic effects (prolactin release, gynecomastia, impotence, decreased libido in males); crosses BBB (confusion, dizziness, headaches), and crosses placenta
 both cimetidine and ranitidine decrease renal excretion of creatinine/ inhibit tubular transport in kidney
 |  | 
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        | Term 
 | Definition 
 
        | small molecular weight organic compounds that inhibit activity of HmG coA reductase; share HMG like structure and bind competitively to active site of enzyme 
 Pathway of cholesterol synthesis: ( HMG synthase= acetyl coA + acetyl acetyl CoA ---> HMG CoA)
 HMG CoA reductase: HMG coA--> malevalonate) -----> cholesterol
 |  | 
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        | Term 
 | Definition 
 
        | third line tx HBV HBV drug ; lower dose required for HBV than HIV
 MOA: comp. inhibits HBV DNA POL (rev. transcriptase)
 causes DNA chain termination
 TOX: headache, insomnia, GI discomfort
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | 2nd line treatment for HBV NRTI (also initially used for HIV tx)
 effective against Lamivdine res. strains of HBV
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | 1st line hBV tx more effective than lamuvidine and Entecavir (> viral load reduction)
 not suggested in those with untreated HIV
 |  | 
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        | Term 
 | Definition 
 
        | 1st line tx for chronic hBV nucleotide analog
 Tox: renal impairment, decreased bone mineral density,
 |  | 
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        | Term 
 | Definition 
 
        | tx for chronic and acute hBV MOA: anti-viral, immunomodulatory, anti-proliferative
 - signal anti-viral protein synthesis to inhibit viral replication, transcription, translation, protein processing, and viral maturation
 TOX: fevers, chills, headache, thrombocytopenia, neurotox, CV effects (hypotension, tachycardia)
 Pegylated interferons- polyethylene glycol group attached to IFN, which increases t1/2 and slows clearance--> allows for less frequent admin.
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | HCV tx - used in conjunction with other drugs; doesn't work on its own ; guanosine analog
 MOA: unknown, but somehow inhibits viral replication
 TOX: hemolytic anemia, fatigue, rash, insomnia, depression
 |  | 
        |  | 
        
        | Term 
 
        | Simepravir, Paritaprevir, Grazoprevir |  | Definition 
 
        | NS3/4A protease inhibitors direct acting antivirals for HCV
 - block proteolytic cleavage of viral protein precursors
 |  | 
        |  | 
        
        | Term 
 
        | Ledipasvir, Ombitasvir , elbasvir, Declatasvir |  | Definition 
 
        | NS5A phosphoprotien inhibitors - block viral replication
 HCV Tx!
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | NS5B POL inhibitors - block POL required for transcribing HCV- RNA  genome and RNA transcription
 |  | 
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        | Term 
 | Definition 
 
        | Corticosteroid USE: Chrons
 MOA: controls rate of protein synthesis ; reverses capillary permeability and lysosomal stabilization at cellular level to control/ prevent inflammation ; depresses migration of polymorphonuclear leukocytes and fibroblasts
 TOX: headache, resp infection, dyspepsia, dizziness
 |  | 
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        | Term 
 | Definition 
 
        | 5-aminosalicylic acid deriv. USE: chrons
 MOA: diminshes inflammation by blocking arach. acid metabolite production
 TOX: headache, diarrhea, upper abd pain, nausea , sinusistis
 AVOID  TAKING  WITH ANTACIDS
 |  | 
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        | Term 
 | Definition 
 
        | USE: Chrons MOA: purine synthesis inhibitor ; blocks activation of inflamm. T cells
 |  | 
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        | Term 
 | Definition 
 
        | binds bile acids in intestine and prevents their reabsorption. Increases incorporation of chol --> bile acids.  USE: may be used in Chrons, when terminal ileum resected and bile acids not absorbed, so have cAMP dependent Cl- secretion in colonic epithelial cells --> Na and water follow CL- into lumen causing secretory diarrhea and steattorhea. Used as treatment for bile acid diarrhea.    |  | 
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