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237 Cards in this Set
- Front
- Back
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What are the 6 antiretroviral drug classes?
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Nucleoside Reverse Transcriptase Inhibitors, Non-Nucleoside Reverse Transcriptase Inhibitors, Protease Inhibitors, Fusion inhibitors, CCR5 Antagonist, and Integrase inhibitor
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What is the standard HIV therapy today?
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All patients receive at least 3 medications. 2 NRTIs and an additional medication. These can be taken as combination drugs in one pill, but will still receive minimum of 3 meds.
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Black Box WARNING for NRTIs?
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Lactic acidosis, hepatic steatosis (rare, life threatening)
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How are NRTIs eliminated?
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All renally eliminated except Abacavir
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What are the drugs in the NRTI drug class?
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Lamivudine (Epivir), emtricitabine (Emtriva), stavudine (Zerit), Zidovudine (AZT, retrovir), tenofovir (Viread), abacavir (Ziagen), didanosine (Videx)
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How is abacavir eliminated?
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Metabolized by alcohol dehydrogenase
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These two NRTIs are associated with minimal toxicity and at least one of them is usually included with every HIV pt therapy.
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Lamivudine and emtricitabine
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Which NRTI can cause nephrotoxicity?
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Tenofovir
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What are the AE of Abacavir?
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Hypersensitivity reaction, HLAB 5701 (need pharmacogenomic testing prior to starting this drug), poss increased risk of MI
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AE of Zidovudine?
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Anemia, neutropenia (bone marrow suppression)
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What HIV drug class can inhibit HIV but also inhibits mitochondrial DNA polymerase?
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NRTIs
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What 3 NRTIs in use today are more associated with inhibition of mitochondrial DNA?
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Ddl (didanosine), d4T (stavudine), and AZT (zidovudine)
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What NRTI is no longer in use today due to its high rate of toxicity and mitochondrial DNA inhibition?
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ddC (zalcitabine)
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General AEs of NRTIs
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Peripheral neuropathy, lipodystrophy (lipoatrophy), lactic acidosis, pancreatitis (didanosine >stavudine)
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Name the drugs used today in the NNRTI drug class
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Efavirenz (Sustiva), nevirapine (Viramune), Etravirine (Intelence)
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DI’s of the NNRTI drug class?
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CYP450 substrates (metabolized by CYP450), AND CYP3A4 inducers
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AE of NNRTI drug class?
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Rash, hepatotoxicity, increased transaminases
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NNRTIs have a short/long half life
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Long
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AE of efavarenz?
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Potentially teratogenic in 1st trimester, CNS side effects (dosed at bedtime), false-positive cannabinoid and benzodiazepine test
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AE of Nevirapine
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Hepatotoxicity secondary to HSR, Stevens-Johnson syndrome
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DI of Etravirine
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Induces CYP3A4 and inhibits 2C9 (bactrim & warfarin) &2C19 (clopidogrel (plavix))
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What is the 2nd generation NNRTI and is reserved for use if others are not effective or AEs are developed
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Etravirine
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Ritonavir used to be used as HIV treatment, it is now used as a pharmacokinetic protease inhibitor “booster”. How does this work?
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Inhibits CYP3A4 in GI tract and liver. CYP3A4 metabolizes PIs. Increases PI bioavailability and decreases PI elimination. Leads to higher PI drug levels=increased efficiency, decreased dose and/or longer dosing interval
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DIs of Ritonavir?
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Common with other CYP3A4 substrates, also inhibits CYP2D6
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What HIV drug class are substrates and inhibitors of CYP3A4?
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Protease inhibitors
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AE of protease inhibitors?
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Lipodystrophy, dyslipidemia, increased glucose, GI intolerance, increased transaminases
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Protease Inhibitor Contraindications due to DI’s
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Flecainide, propafenone, midazolam, triazolam, rifampin, simvastatin, lovastatin, fluticasone, st john’s wort. Atanzanavir & suppressing agents
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Which protease inhibitors are ALWAYS boosted?
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Lopinavir, saquinavir, darunavir, tipranavir
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Which protease inhibitors are never boosted?
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Nelfinavir
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What is the drug used as a boost to other protease inhibitors?
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Ritonavir
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MOA of Enfuvirite (Fuzeon, T20)?
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Binds to gp41 receptor to prevent fusion
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What drug should not be given with ritonavir due to increased risk of rhabdomyolysis?
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Sinvastatin, lovastatin
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What drug should not be given with ritonavir or other protease inhibitors due to the risk of Cushing’s Syndrome due to build up and inability to metabolize?
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Fluticasone – inhaled steroid. Some is ingested, CYP3A4 typically metabolizes, inhibited by protease inhibitors
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Fusion inhibitor Enfuviritide administration?
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Injectable only
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AE of fusion inhibitor enfuviritide?
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Injection site reactions – almost 100% of pts. But no drug interactions. Last line agent
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T/F fusion inhibitor enfuviritide is metabolized by CYP450 enzymes?
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FALSE. Metabolized by non-CYP450 pathways
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T/F CCR5 antagonist Maraviroc is metabolized by CYP450 enzymes?
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TRUE. Substrate of CYP3A4
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What is the only HIV drug that targets a HOST enzyme?
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CCR5 antagonist Maraviroc (Selzentry)
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MOA of integrase inhibitor Raltegravir?
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Prevents integration of viral DNA into host DNA
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AE of Integrase inhibitor Raltegravir?
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HA, dizziness, diarrhea
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Metabolism of Integrase inhibitor Raltegravir?
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Metabolized via glucoronidation UGT-1A1
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DI of integrase inhibitor Raltegravir?
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Rifampin induces UDP-GT (Raltegravir is metabolized by UGT1A1) increases metabolism of Raltegravir.
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What is the reason for the use of at least 3 HIV medications?
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Resistance can occur with less!
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What is the half-life of Efavirenz?
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36-100 hours (keep in mind so you do not unknowingly give the pt monotherapy and increase risk of resistance!)
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Which drugs have a low genetic barrier to resistance (if these drugs are given as monotherapy resistance is very likely)
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Lamivudine, emtricitabine, efavirenz, nevirapine, ripivirine, raltegravir
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Herpes virus are a(n) RNA/DNA virus
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DNA
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What agents can be used to treat herpes simplex, herpes zoster, and varicella zoster?
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Acyclovir (zovirax), Valacyclovir (Valtrex), Famciclovir (Famvir), Penciclovir (Denavir), Docosanol (Abreva)
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What are the 2 antiviral drugs that are prodrugs and what are the drugs they are metabolized to become?
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Valacyclovir prodrug for acyclovir. Famciclovir prodrug for penciclovir
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Which antiviral drug used for HSV/VZV/HZV is the only one available IV?
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Acyclovir
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MOA of antiviral medications acyclovir and penciclovir?
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Acyclovir/penciclovir are selectively activated by HSV and VZV enzymes and are triphosphorylated. 3 step process. Monophosphate is formed by thymidine kinase Triphosphorylated metabolites selectively inhibit HSV/VZVDNA synthesis.
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Thymidine kinase produced by ___ is more efficient compared to that produced by ____
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HSV/VZV
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HSV/VZV is easier to treat with antiviral medications?
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HSV
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MOA of Docosonol
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Docosonol prevents fusion of HSV to plasma membranes.
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When is the best time to use Docosonol?
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Prior to blister formation – use when tingling sensation is present – doesn’t get rid of blister but it can help it from becoming worse.
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When would acyclovir IV be used?
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HSV encephalitis, HZV in immunocompromised pts
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Admninistration of docosonol?
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Topical for herpes labialis
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AE of topical antiviral medications used for HSV/ VZV?
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Burning, stinging sensation (docosonal)
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AE of systemic antiviral medications?
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GI disturbances, HA, rash (valacyclovir, acyclovir), fatigue (Famciclovir)
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DIs for antivirals used to treat HSV/HZV/VZV?
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Probenecid blocks renal secretion of acyclovir and penciclovir
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Thiymidine kinase produced by the virus is essential for the first step of triphosphorylation of antiviral medications. How is this involved in drug resistance?
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Thymidine kinase deficiency or mutants
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Antiviral medications used for CMV?
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Ganciclovir (cytovene), Valganciclovir (Valcyte), Cidofovir (Vistide), Foscarnet (Foscavir)
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MOA of Ganciclovir?
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Triphosphorylated, inhibits viral DNA synthesis by inhibiting viral DNA polymerase
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AE of ganciclovir?
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Anemia, neutropenia, thrombocytopenia, GI disturbances
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Administration of ganciclovir?
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IV, intravitreal (CMV retinitis).
(very poor oral bioavailability) |
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If a pt has acyclovir resistance to HSV what drugs also used for CMV can be given?
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Foscarnet or cidofovir. Ganciclovir has acyclovir cross-resistance and should not be used.
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MOA of cidofovir
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Inhibits viral DNA synthesis by inhibitin DNA polyemerase. Activation not dependent on thymidine kinase.
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AE of cidofovir
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Nephrotoxicity
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DI of cidofovir?
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Probenecid blocks renal secretion
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Administration of cidofovir?
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IV
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Administration of foscarnet?
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IV
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MOA of foscarnet?
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Inhibits DNA polymerase and RT. Activation not dependent on thymidine kinse
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AE of foscarnet?
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Nephrotoxicity, fever, N/V/D, anemia
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What is the prodrug used for treatment of CMV that is given orally due to better oral bioavailability?
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Valganciclovir – metabolized to ganciclovir
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Indications/uses for ribavirin (Copegus, Rebetol)
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Symptomatic relief in young children with influenza A/B, RSV pneumonia, chronic Hep C infection
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MOA of ribavirin (Copegus, Rebetol)?
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Inhibits viral-specific RNA synthesis, inhibits formation of viral proteins/enzymes
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AE of Ribavirin (Copegus, Rebetol)
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Serious: cardiac arrest, apnea, bacterial pneumonia, pulmonary deterioration
Anemia, neutropenia, thrombocytopenia, rash, conjunctivitis |
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Can ribavirin be given during pregnancy?
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Teratogenic category X drug – use 2 forms of birth control during and for 6 mos after discontinuation of ribavirin!!!
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Administration of ribavirin
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PO (renal elimination), inhaled via specific product-based device
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Contraindication of ribavirin?
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Pts using ventilators. Pregnancy
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CDC advises against use of ______ and ______ for influenza treatment and prophylaxis due to resistance
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Amantadine and rimantadine
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MOA of amantadine and rimantidine?
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Interference with viral attachment and uncoating
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AE of amantadine?
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(causes release of dopamine) Ataxia, nightmares, insomnia
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What are the neuraminidase inhibitors?
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Oseltamivir (Tamiflu) and zanamivir (Relenza)
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What are the drugs used for treatment and prophylaxis of influenza A, influenza B, pandemic H1N1, and H5N1 (avian influenza)?
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Neuraminidase inhibitors – Tamiflu and Relenza
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MOA of neuraminidase inhibitors Tamiflu and Relenza?
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Inhibits neuraminidase, preventing budding from the host cell (essentially halts reproduction), prevents spread of infection.
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When should neuraminidase inhibitors be given to pts with influenza?
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Early in treatment (within 1st 48 hrs) or as prophylaxis
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Which neuraminidase inhibitor is a prodrug given PO?
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Oseltamivir (Tamiflu)
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Which neuraminidase inhibitor has poor bioavailability and is given as an orally inhaled product?
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Zanamavir (Relenza)
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AE of Oseltamivir (Tamiflu)
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N/V, serious skin and hypersensitivity reactions, neuropsychiatric side effects
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AE of Zanamavir (Relenza)
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Cough, bronchospasm (asthma, COPD) (remember this drug is orally inhaled!)
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What is the neuraminidase inhibitor that is administered IV only?
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Peramivir
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Why are systemic fungal infections and those of nails/hair difficult to treat?
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Poor vascularization of nails and hair difficult for drugs to penetrate these areas. Systemic infections require long term treatment
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What type of medication is Amphotericin B?
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Fungicidal
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Administration of Amphotericin B?
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Parenteral
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What types of fungal infection is Amphotericin B used to treat?
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Aspergillus, Cryptococcus, histoplasma
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AE of Amphotericin B?
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Infusion reaction, nephrotoxicity, electrolyte abnormalities – hypokalemia, hypomagnesemia
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What type of Amphotericin B causes less nephrotoxicity?
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Liposomal formulations: amphotericin B lipid complex (ABLC), liposomal amphotericin B (Ambisome)
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DI of Amphotericin B?
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Cumulative toxicity with other nephrotoxic agents
What medications are given for topical fungal infections? Ketoconazole (Nizoral), clotrimazole (Lotrimin), miconazole, econazole, tioconazole, butoconazole, terconazole |
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What is the medication used for yeast infection (candida, Cryptococcus)?
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Fluconazole
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What drug is used to treat endemic fungi (Histoplasma)?
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Itraconazole
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What are the medications Voriconazole (Vfend), and posaconazole (Noxafil) used to treat?
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Expanded yeasts, molds (aspergillus), serious systemic infections, and immunocompromised pts
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MOA of Triazoles?
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Inhibition of CYP450 – dependent enzyme that converts lanosterol to ergosterol (ergosterol = important component of fungal cellular membranes) increases cell membrane permeability. Results in cell lysis and death.
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Are triazoles fungistatic or fungicidal?
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Depends on the fungus it is targeting
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AE of triazoles?
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Generally well-tolerated, GI upset – n/v/d, hepatotoxicity
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Administration of fluconazole?
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PO, IV
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Fluconazole has a short/long half life
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Long
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Elimination of fluconazole?
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Renal excretion
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T/F Fluconazole is well absorbed and has no food or pH effect
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TRUE
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T/F Itraconazole is well absorbed and has no food or pH effect
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FALSE! Capsules – food and acidic pH requirement, lower bioavailability. Oral solution- empty stomach increases absorption, no pH effect, more GI upset
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T/F Fluconazole is well absorbed and has no food or pH effect
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FALSE! Empty stomach increases absorption
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T/F Posaconazole is well absorbed and has no food or pH effect
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FALSE! Optimal absorption with high-fat meal or liquid nutritional supplement
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Elimination of Itraconazole?
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Extensive hepatic metabolism
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Is Itraconazole hydrophilic/lipophilic?
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Highly lipophilic – high Vd
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AE of Itraconazole?
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HTN, hypokalemia, peripheral edema
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Administration of Itraconazole?
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Capsules, oral solution (not interchangeable!)
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AE of Voriconazole?
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Transient vision changes (flashes, color changes), visual hallucinations, photosensitivity, rash
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What antifungal medication has CSF penetration?
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Voriconazole
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Administration of Voriconazole?
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PO, IV
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Therapeutic drug monitoring of Itraconazole includes what drugs?
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Itraconazole + OH-itraconazole
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What is important to remember about Voriconazole and renal clearance?
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Use IV formulation only if CrCl>50mL/min.
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Elimination of Posaconazole?
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Hepatically metabolized
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Fluconazole DI?
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CYP 2C19 and 2C9 inhibitor
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Voriconazole DI?
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CYP450 2C19, 2C9, 3A4 inhibitor, CYP 2C19 and 3A4 substrate
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Ketoconazole/itraconazole DI?
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Cyp450 3A4 substrate and inhibitor
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Posaconazole DI?
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CYP 3A4 inhibitor, metabolized by glucoronidation
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Is terbinafine (Lamisil) fungistatic/fungicidal?
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Fungicidal
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Administration of terbinafine (Lamisil)
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PO treatment of onychomycosis 6wks for fingernails and 12 wks for toenails
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AE of terbinafine (Lamisil)?
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GI upset, HA, taste disturbances
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Terbinafine (Lamisil) DI?
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CYP450 2D6 inhibitor
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Is griseofulvin (Grifulvin) fungistatic/fungicidal?
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Fungistatic
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Why is terbinafine (Lamisil) a better choice for onychomycosis as opposed to itraconazole?
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Less toxicity and DI than azoles
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AE of Griseofulvin (Grifulvin)?
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Common: HA, fatigue, confusion, syncope, lethargy Less Common: hepatotoxicity, neutropenia, angioedema, urticaria
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What is the medication that is given ONLY for use incombination with amphotericin B?
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Flucytosine
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MOA of Flucytosine?
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Prodrug converted to 5-FU by fungal enzymes, causes formation of faulty fungal proteins and enzymes
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What is the indication for use of Flucytosine?
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Cryptococcal meningitis (ONLY for use in combination with amphotericin B)
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Administration of Echinocandins?
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Parenteral only (low bioavailability)
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MOA of Echinocandins?
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Inhibits fungal synthesis of Beta (1,3) D-glucan
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AE of Echinocandins?
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N/V, flushing, injection site reactions
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What CYP 450 enzyme interactions should you be aware of with Echinocandins?
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NONE – no CYP450 interactions
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What are the Echinocandin medications?
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Caspofungin, micafungin, anidulafungin
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DI of caspofungin?
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Rifampin can induce caspofungin
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Are echinocandins fungistatic/fungicidal?
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Candida (fungicidal), Aspergillus (fungistatic)
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What type of medication is Metronidazole (Flagyl)?
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Antiprotozoal
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Name the antiprotozoal agents
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Metronidazole (Flagyl), tinidazole (Tindamax, Fasigyn), Nitazoxanide (Alinia), Pentamidine (Nebupent, Pentam), Atovaquone, primaquine, chloroquine
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Indications for use of antiprotozoal agents metronidazole (Flagyl) and Tinidazole (Tindamax, Fasigyn)?
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Anaerobic bacteria, amebiasis, giardiasis, trichomoniasis, C. difficile colitis
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Warning or antiprotozoal agents metronidazole (Flagyl) and TInidazole (Tindamax, Fasigyn)?
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Concomitant alcohol (ethanol) use while taking the drug and for 48 hrs after (prevents adequate metabolism of alcohol – makes pts feel sick)
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Indications for use of Nitazoxanide (Alinia)?
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Giardiasis, Cryptosporidiosis
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Indications for use of Pentamidine (Nebupent, Pentam)?
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PCP Pneumocystis carinii pneumonia (opportunistic infection) – inhaled (prophylaxis) or parenteral (treatment)
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Indications for use of Atovaquone?
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PCP, toxoplasmosis – oral. Malaria (prophylaxis and tx when combined with proguanil)
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What levels should be checked prior to starting a pt on antimalarial medication primaquine?
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G6PD – if pts deficient, drug should not be given
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Name the antihelminthics
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Invermectin (Stromectal, Mectizan), Albendazole (Albenza), and Mebendazole (Vermox)
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MOA of Ivermectin (Stromectal, Mectizan)
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Binds selectively to glutamate-gated chloride channels, paralyzes worms by causing hyperpolarization of invertebrate nerve and muscle cells. Low affinity for human ligand-gated chloride channels. Poor CNS penetration
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MOA of antihelminthics Albensazole (Albenza) and mebendazole (Vermox)
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Inhibits formation of worm microtubules
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AE of antihelminthics Albensazole (Albenza) and mebendazole (Vermox)
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Bone marrow suppression, hepatotoxicity, acute renal failure
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3 medications that block GI muscle activity to decrease movement?
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Bismuth subsalicylate (Pepto-Bismol), Loperimide (Imodium), opium deriveratives (paregoric)
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MOA of Bismuth subsalicylate (Pepto-Bismol)
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Coats the lining of the GI tract and sooths irritation, preventing stimulation of local reflexes that cause excessive GI activity and diarrhea
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AE of Bismuth subsalycilate (Pepto Bismol)
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Black coating on tongue
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CI of Bismuth subsalycilate (Pepto Bismol)
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Avoid in pts with renal failure
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MOA of Loperimide (Imodium)
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Opoid agonist that does not cross BBB, but pts can develop physical dependence/withdrawal sxs with long-term use (rare). Slows peristalsis and allows increased time for absorption of fluid and electrolytes.
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AE of Loperimide (Imodium)
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Abdominal pain, N/V, bloating
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CI of Loperimide (Imodium)
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<2yo, fetal paralytic ileus, fever, E.coli/salmonella infections
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MOA of opium derivatives (paregoric)
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Inhibits peristalsis and diarrhea
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MOA of bulk forming laxatives
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Cause fecal matter to increase in bulk, increase GI motility by increasing fluid in the GI tract, stimulate stretch receptors
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Name some bulk forming laxatives
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Polycarbophyl (FiberCon), Methylcellulose psyllium (Metamucil), Methyl cellulose (Citrucel), Calcium polycabophil (Metrolan)
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MOA of stimulant laxatives
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Direct action on intestinal mucosa, stimulate myenteric plexus, alter water and electrolyte secretion
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Name some stimulant laxatives
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Senna (Senokot), Bisacodyl (Dulcolax), Castor Oil, Mineral oil
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How is the MOA of mineral oil slightly different than other stimulant laxatives?
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It lines the GI tract and prevents absorption of water and electrolytes
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Onset of action of mineral oil?
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6-8hrs
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Onset of action of Senna (Senokot)
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6-10hours
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Onset of action of Bisacodyl (Dulcolax)
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15-60minutes
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CI of castor oil?
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Avoid in pregnant women
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MOA of Saline and Osmotic Laxatives?
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Retain water in intestinal lumen, increasing intraluminal pressure; cholecysokinin release. Used to empty bowel before surgery or colonoscopic procedures.
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Onset of action of Saline and Osmotic Laxatives?
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EVACUATES bowel in 3 hrs
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Name some Saline and Osmotic Laxatives
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Magnesium salts (Epsom salt), MOM, Mag hydroxide, Mag citrate, Sodium Phosphate (enema), Lactulose, Glycerin, Sorbitol
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MOA of Surfactants/Stool Softeners
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Detergent activity, facilitates water to soften stool.
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Indications for use of surfactants/stool softeners?
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Useful for prevention of post-op and opioid induced constipation, often used in combination with senna (stimulant laxative)
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Name some surfactants/stool softeners
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Docusate sodium (Colace), Docusate calcium (Surfak)
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How is acetylcholine release into the gastric lumen triggered?
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Triggered by CNS response to food
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How is Gastrin release into the gastric lumen triggered?
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Triggered by acetylcholine stimulation of G cells in the antrum
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How is Histamine release into the gastric lumen triggered?
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Triggered by stimuli in the parietal cells
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3 mediators ____, ____, and ____ stimulate the potassium-hydrogen-adenosine triphosphate pump located on parietal cell surface
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Acetylcholine, gastrin, histamine
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Secretion of ____ occurs against a concentration gradient via active transport in response to acetylcholine, gastrin, and histamine release into the gastric lumen
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Acid
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Acid secretion into the gastric lumen is regulated through positive/negative feedback mechanism
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BOTH
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How is the gastric lining protected from the acid produced there?
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Mucus, prostaglandin, somatostatin, bicarbonate, blood flow
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What is the function of prostaglandin E2 in the stomach?
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Increases mucus production
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Peptic ulcers are _____ in the intestinal mucosa
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Breaks
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Three important factors for PUD development
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Bacterial infection with H. pylori, NSAID use, Cigarette smoking
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3 goals of therapy for PUD?
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Reduce gastric acidity, enhance mucosal defenses, eliminate H. pylori
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H. pylori is a gram +/- _____ bacterium
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negative, spiral
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How many pts with duodenal ulcers have a finding of H. pylori?
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90%
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How many pts with gastric ulcers have a finding of H. pylori?
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70%
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What is the mechanism of gastric injury due to H. pylori?
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Production of cytotoxin, breakdown of mucosal defenses
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What is the disorder in which the esophageal mucosa is damaged by the reflux of low pH material into the lower esophagus?
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Gastroesophageal Reflux Disease (GERD)
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Classic symptom of GERD?
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Heartburn which presents as pain in the center of the chest
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Is GERD caused by H. pylori?
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NO
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What is the cytotoxin that allows H. pylori to survive and also contributes to the development of PUD?
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Urease – converts to urea and creates an alkaline cloud around the H. pylori and is converted to ammonia which is damaging to gastric mucosal cells
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How do NSAIDS lead to gastric cell damage?
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Inhibition of COX enzymes decrease prostaglandins which increases gastric acid secretion, decrease blood flow and decrease mucus production as well as bicarb production. Can also cause damage by pH trapping when it is trapped inside the gastric cell.
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What types of drugs inhibit acid secretion (3 classes)
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H2 antagonists, PPIs, anticholinergic agents
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What types of drugs protect gastric mucosa (3 drug classes)
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Sucralfate, colloidal bismuth, prostaglandins
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Exmaples of H2 antagonists?
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Cimetidine, nizatidine, ranitidine, famotidine
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MOA of H2 antagonists?
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Competitive antagonism of H2 receptros to suppress gastric acid secretion
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Pharmacodynamics/kinetics of H2 antagonists?
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Peak concentration within 1-3hrs, renal excretion and hepatic metabolism
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AE of H2 antagonists?
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Diarrhea, HA, muscle pain, constipation, fatigue, confusion/hallucination (IV)
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DI of H2 antagonists
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Agents that require acidic mediums, cimetidine: inhibition of CYP3A4, 2D6, 1A2
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Site of action of H2 blockers?
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H2 receptor muscarinic antagonist (m3 receptor)
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Site of action of PPIs?
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Proton Pump – H+/K+/ATPase pump - decreases acid secretion from proton pumps
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MOA of proton pump inhibitors?
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Block k+/H+/ATPase (proton pump). Total shutdown of acid release because they work late in the acid production cycle
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Examples of PPIs?
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Lansoprazole, Pantoprazole, Esomeprazole, Omeprazole, Rabeprazole
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Where is the proton pump inhibitor prodrug converted to active drug?
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Parietal cell canaliculus (site of action)
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PPIs have a short/long half life?
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Short – but forms covalent bond to proton pump completely inactivating it until a new proton pump can be formed (approx 18 hours)
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DI of PPIs
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Hepatically metabolized by CYP2C19, 3A4 (exception rabprazole). Inhibits 2C19
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T/F PPIs do not cross the placenta
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FALSE
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AE of PPIs
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HA, Gi disturbance, nausea, enteric infections, long term unknown in humans (carcinoid tumors)(due to overstimulation and hyperplasia – has not been seen but it is possible)
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MOA of anticholinergic Dicyclomine?
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Muscarinic Ach receptor antagonist, decreases acid secretion
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AE of anticholinergic Dicyclomine?
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Dry mouth, constipation, blurred vision, cardiac arrhythmia, urinary retention
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PPIs are preferred treatment in what 3 conditions?
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PUD with H. pylori, Hemorrhagic ulcers, PUD in pt who requires NSAID use
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Indication for use of antacids?
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Acute pain relief – not the tx of choice for peptic ulcers.
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Anions used in antacids?
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Carbonate, bicarbonate, citrate, phosphate, hydroxide
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Examples of antacids?
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Aluminum hydroxide, magnesium hydroxide, sodium bicarb, calcium carbonate
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AE of antacids?
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Constipation (Al, Ca), Diarrhea (Mg), electrolyte abnormalities
MOA of Sucralfate? Complex salt of sucrose sulfate and aluminum hydroxide, forms a viscous gel that binds to positively charged proteins (albumin, fibrinogen) and sticks to areas of ulceration. Protects ulcerated tissue from aggressive factors such as pepsin, acid, and bile salts |
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Does Sucralfate alter gastric pH?
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NO
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What is the indication for Sucralfate?
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Symptomatic relief of ulcers
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AE of Sucralfate?
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Constipation (little systemic absorption)
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Why is Sucralfate difficult to use?
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Large tablets and frequent administration
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DI of Sucralfate?
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DI due to binding to drugs, impairing absorption.
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MOA of Colloidal Bismuth?
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Coating agent used in PUD – protects mucosa from acid and pepsin degradation. Barrier formation, stimulates mucosal bicarbonate and PGE2. Impedes growth of H. pylori
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Example of prostaglandin medication?
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Misoprostol (prostaglandin analog)
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MOA of Misoprostol?
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Prostaglandin analog,
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Indication for use of Misoprostol?
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Prevention of NSAID induced ulcers
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AE of Misoprostol?
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Abdominal discomfort, diarrhea
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CI of Misoprostol?
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Contraindicated in Pregnancy (has been used as an abortive agent)
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What is the preferred tx of H. pylori?
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Triple therapy – amoxicillin, clarithromycin, and PPI
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What is quadruple therapy for H. pylori?
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Tetracycline, metronidazole, PPI, bismuth
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Drug of choice for GERD?
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PPIs – aggressively raise gastric pH for long period
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Options for tx of GERD other than PPIs?
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H2 antagonists, antacids, sucralfate, metocopramide
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MOA of metoclopramide
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Enhances stomach emptying, increases lower esophageal tone
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What modifications to lifestyle/diet can be made that will impact risk factors for PUD and GERD?
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Avoid caffeine (increases acid secretion), avoid alcohol (direct toxic effect on mucosa), Quit cigarette smoking (decreases production of duodenal bicarb, decreases blood flow, decreases ulcer healing) AVOID NSAIDS
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