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357 Cards in this Set
- Front
- Back
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Prophylaxis MAC
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azithromycin
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Treatment of MAC
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azithromycin, rifampin, ethambutol, streptomycin
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Treatment of M. leprae
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dapsone, rifampin, clofazimine
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Side effect of ethambutol
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optic neuropathy (red-green color blindness)
(RIPE) |
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Isoniazid Mechanism
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decrease synthesis of mycolic acids
(only drug used as solo prophylaxis of TB) |
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Toxicity of Isoniazid
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INH injures NEURONS and HEPATOCYTES
hemolysis if G6PD deficient, neurotoxicity, hepatotoxicity, SLE-like syndrome pyridoxine (vitamin B6) can prevent neurotoxicity Different INH half lives in fast vs. slow acetylators |
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Mechanism of Rifampin
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inhibits DNA-dependent RNA polymerase
binds to beta subunit of DNA directed RNA polymerase; inhibits further RNA production |
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Clinical use of Rifampin
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TB!!
delays resistance to dapsone when used for leprosy meningococcal prophylaxis and chemoprophylaxis in contacts with children with H. flu type B |
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Toxicity of Rifampin
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minor hepatotoxicity and drug interactions (increases p450); orange body fluids (nonhazardous side effect)
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Rifampin's 4 R's
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RNA polymerase inhibitor
Revs up microsomal p450 Red/orange body fluids Rapid resistance if used alone |
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Resistance mechanism for aminoglycosides
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modification via acetylation, adenylation, or phosphorylation
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Chloramphenicol resistance mechanism
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modification via acetylation
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Resistance mechanism for macrolides
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remember, macrolides inhibit protein synthesis by blocking translocation; bind to the 23S rRNA of the 50S ribosomal subunit
resistance: methylation of rRNA near erythromycin's ribosome-binding site |
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Resistance of tetracycline
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due to decreased uptake or increased transport out of the cell
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Prophylaxis of recurrent UTI's
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TMP-SMX
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Prophylaxis of PCP
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TMP-SMX and aerosolized pentamidine
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Prophylaxis of Syphilis
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benzathine penicillin G
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Treatment of MRSA
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vanco
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Treatment of VRE (vancomycin resistant enterococcus)
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linezolid and streptogramins (quinupristin/dalfopristin)
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Toxicity of amphotericin
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fever/chills (shake and bake), hypotension, nephrotoxicity, arrhythmias, anemia, IV phlebitis (amphoterrible)
hydration reduces nephrotoxicity liposomal amphotericin reduces toxicity |
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Nystatin
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Binds to ergosterol and disrupts fungal membranes (too toxic for systemic use)
use for 'swish and swallow' for oral candidiasis (thrush) and topically for diaper rash or vaginal candidiasis |
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Azoles
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Inhibit fungal steroid (ergosterol) synthesis
for systemic mycoses |
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Fluconazole
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use for cryptococcal meningitis in AIDs patients because it can cross the BBB and also use for candidal infections of all types (yeast infections)
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Ketoconazole
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use for Blasto, coccidioides, histoplasma, candida
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Toxicity of azoles
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hormone synthesis inhibition (gynecomastia), liver dysfunction (inhibits p450), fever, chills
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Flucytosine
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Action: inhibits DNA synthesis by conversion to fluorouracil, which competes with uracil
used in systemic fungal infections in combo with amphotericin B Toxicity: N/V, diarrhea, bone marrow suppression |
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Caspofungin
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inhibits cell wall synthesis (fungus)
use for invasive aspergillous Toxicity: GI upset, flushing |
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Terbinafine
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inhibits fungal enzyme squalene epoxidase
used to treat dermatophytoses (especially onychomycosis) |
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Griseofulvin
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Mechanism: interferes with microtubule function; disrupts mitosis, deposits in keratin-containing tissues (like nails)
Use: oral treatment of superficial infections; inhibits growth of dermatophytes (tinea, ringworm) Toxicity: teratogenic, carcinogenic, confusion, headaches, increases p450 and warfarin metabolism |
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Amantadine
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Blocks viral penetration/uncoating (M2 protein); also causes release of dopamine from intact nerve terminals
Used for prophylaxis of Influenza A and Rubella (also use for parkinsons) Toxicity: ataxia, dizziness and slurred speech |
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Zanamivir, oseltamivir
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inhibits influenza neuraminidase, decreasing the release of progeny virus
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Ribavirin
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inhibits synthesis of guanine nucleotides by competitively inhibiting IMP dehydrogenase
USE: RSV, chronic Hep C Toxicity: hemolytic anemia; severe teratogen |
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Acyclovir
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Mech: monophosphorylated by HSV/VZV thymidine kinase; triphosphate formed by cellular enzymes; preferentially inhibits viral DNA polymerase by chain termination
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Use of Acyclovir
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HSV, VZV, EBV
used for herpes induced mucocutaneous and genital lesions as well as for encephalitis prophylaxis in immunocompromised patients; for herpes zoster, use a related agent, famciclovir no effect on latent forms of HSV and VZV |
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Ganciclovir
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Mechanism: 5'-monophosphate formed by a CMV viral kinase or HSV/VZV thymidine kinase...preferentially inhibits viral DNA polymerase
USE: CMV, especially in immunocompromised patients Toxicity: leukopenia, neutropenia, thrombocytopenia, renal toxicity; more toxic to host enzymes than acyclovir |
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Foscarnet
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Mechanism: viral DNA polymerase inhibitor that binds to the pyrophosphate-binding site of the enzyme; NO required activation by viral kinase
USE: CMV retinitis in immunocompromised patients when ganciclovir fails; acyclovir-resistant HSV Toxicity: nephrotoxicity |
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Saquinavir, ritonavir, indinavir, nelfinavir, amprenavir
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protease inhibitors
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Protease inhibitor mechanism and toxicity
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(ends with -navir)
Mech: inhibits asembly of new virus by blocking protease in progeny virions Toxicity: GI intolerance (nausea, diarrhea), hyperglycemia, lipodystrophy, thrombocytopenia (indinavir) |
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Nucleoside reverse transcriptase inhibitors
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Zidovudine (ZDV...before AZT), didanosine, zalcitabine, stavudine, lamivudine (3TC) and abacavir
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Non-nucleoside reverse transcriptase inhibitors
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nevirapine, efavirenz, delavirdine
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Toxicity of reverse transcriptase inhibitors
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bone marrow suppression (neutropenia, anemia), peripheral neuropathy, lactic acidosis (nucleosides), rash (non-nucleosides), megaloblastic anemia (ZDV)
can use GM-CSF and erythropoietin can be used to reduce bone marrow suppression |
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ZDV
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a reverse transcriptase inhibitor that can be used for general prophylaxis and during pregnancy to reduce risk of fetal transmission
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Enfuvirtide
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fusion inhibitor (HIV)
Mech: binds viral gp41 subunit; inhibits conformational change required for fusion with CD4 cells blocks entry and subsequent replication |
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Toxicity of enfuvirtide (fusion inhibitors)
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hypersensitivity reactions, reactions at subcutaneous site, increased risk of bacterial pneumonia
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Mechanism of interferons
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glycoproteins from human leukocytes that block various stages of viral RNA and DNA synthesis; induce ribonuclease that degrades viral RNA
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IFN-alpha
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used for chronic hepatitis B and C, Kaposi's sarcoma
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IFN-beta
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used for multiple sclerosis
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IFN-gamma
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used for NADPH oxidase deficiency
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Toxicity of interferons
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neutropenia!
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do NOT use in pregnancy
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Sulfonamides (kernicterus)
Aminoglycosides (ototoxicity) Fluoroquinolones (cartilage damage) Erythromycin (acute cholestatic hepatits in mom...clarithryomycin is embryotoxic) Metronidazole (mutagenesis) Tetracyclines (discolored teeth, inhibition of bone growth) Ribavirin (teratogenic) Griseofulvin (teratogenic) Chloromphenicol (gray baby) |
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Cyclosporine
Mechanism |
binds to cyclophilins
complex blocks the differentiation and activation of T cells by inhibiting calcineurin, thus preventing the production of IL-2 and its receptor Used to suppress organ rejection |
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Toxicity of cyclosporine
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Nephrotoxic (preventable with mannitol diuresis)
predisposes patients to viral infections and lymphomas |
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Tacrolimus
Mechanism |
binds to FK-binding protein; inhibiting secretion of IL-2 and other cytokines
Used in organ transplants |
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Toxicity of tacrolimus
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SIGNIFICANT: nephrotoxicity, peripheral neuropathy, hypertension, pleural effusion, hyperglycemia
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Azathioprine
Mechanism |
antimetabolite precursor of 6-mercaptopurine that interferes with the metabolism and synthesis of nucleic acids; toxic to proliferating lymphocytes
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Clinical use of Azathioprine
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kidney transplantation, autoimmune disorders (including glomerulonephritis and hemolytic anemia)
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Toxicity of Azathioprine
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bone marrow suppression; active metabolite mercaptopurine is metabolized by xanthine oxidase; thus, toxic effects may be increased by allopurinol
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Muromonab-CD3
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monoclonal antibody that binds to CD3 on the surface of T cells; blocks cellular interaction with CD3 protein responsible for T-cell signal transduction
can cause cytokine release syndrome, hypersensitivity reaction |
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Sirolimus (rapamycin)
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Binds to mTOR; inhibits T-cell proliferation in response to IL-2
used with cyclosporine and corticosteroids in kidney transplants Toxicity: hyperlipidemia, thrombocytopenia and leukopenia |
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Mycophenolate mofetil
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inhibits de novo guanine synthesis and blocks lymphocyte production
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Daclizumab
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monoclonal antibody with high affinity for the IL-2 receptor on activated T cells
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Etanercept
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Mechanism: recombinant form of human TNF receptor that binds TNF
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Clinical use of etanercept
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RA, psoriasis, ankylosing spondylitis
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Infliximab
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Mech: anti-TNF antibody
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Use and toxicity of Infliximab
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use: crohn's disease, RA, ankylosing spondylitis
toxicity: predisposes to infections (reactivation of latent TB) |
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Mechanism of heparin
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catalyzes the activation of antithrombin III, decreases thrombin and Xa; short half life
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Use of heparin
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immediate anticoagulation for pulmonary embolism, stroke, angina, MI, DVT
used during pregnancy, DOES NOT CROSS THE PLACENTA FOLLOW PTT given parenteral (IV, SC) rapid onset of action |
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Toxicity of heparin
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bleeding, thrombocytopenia (HIT), osteoporosis, drug-drug interactions; for rapid reversal of heparinization, use PROTAMINE SULFATE (positively charged molecule that acts by binding negatively charged heparin)
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Heparin induced thrombocytopenia
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heparin binds platelets, causing autoantibody production that destroys platelets and overactivates the remaining ones, resulting in a thrombocytopenic, hypercoagulable state
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Lepirudin, bivalirudin
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hirudin derivatives
directly inhibit thrombin used as an alternative to heparin for anticoagulating patients with HIT |
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Warfarin (coumadin!!!)
Mechanism |
interferes with normal synthesis and gamma-carboxylation of vitamin-K dependent clotting factors (II, VII, IX, and X, and protein C and S)
metabolized by p450 affects EXtrinsic pathway and increases PT!!! long half life |
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Clinical use of warfarin
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chronic anticoagulation
NOT used in pregnant women (because warfarin, unlike heparin, can cross the placenta) follow PT/NR values can be given orally slower onset of action, but longer half-life |
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Toxicity of warfarin
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bleeding, teratogenic, skin/tissue necrosis, drug-drug interactions
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Streptokinase, urokinase, tPA (alteplase), APSAC (antistreplase)
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thrombolytics
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Mechanism of thrombolytics
(streptokinase, urokinase, tPA, APSAC) |
directly or indirectly aid conversion of plasminogen to plasmin, the major fibrinolytic enzyme, which cleaves thrombin and fibrin clots
increases PT and PTT, no change in platelet count |
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Aspirin
Mechanism |
acetylates and irreversibly inhibits cyclooxygenase (both COX-1 and COX-2) to prevent conversion of arachidonic acid to thromboxane A2
increases bleeding time no effect on PT or PTT |
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Toxicity of aspirin
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gastric ulceration, bleeding, hyperventilation, Reye's syndrome, tinnitus (CN VIII)
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Mechanism of Clopidogrel and ticlopidine
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inhibits platelet aggregation by irreversibly blocking ADP receptors
inhits fibrinogen binding by preventing glycoprotein IIb/IIIa expression |
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Clinical use of Clopidogrel and ticlopidine
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acute coronary syndrome; coronary stenting; decrease incidence or recurrence of thrombotic stroke
(toxicity...can cause neutropenia...at least ticlopidine can) |
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Abciximab
Mechanism |
monoclonal antibody that binds to glycoprotein receptor IIb/IIIa on activated platelets, preventing aggregation
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Use of abciximab
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acute coronary syndromes, percutaneous transluminal coronary angioplasty
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Methotrexate
Mechanism |
S-phase specific antimetabolite
Folic acid analog that inhibits dihydrofolate reductase, resulting in decreased dTMP and therefore decreased DNA and protein synthesis |
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Use of methotrexate
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leukemias, lymphomas, choriocarcinoma, sarcoma, abortion, ectopic pregnancy, RA and psoriasis
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Toxicity of methotrexate
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myelosuppression, which is reversible with LEUCOVORIN (folinic acid) 'rescue'
macrovesicular fatty change in liver mucositis |
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5-Flurouracil
Mechanism |
S-phase specific antimetabolite
pyrimidine analog bioactivated by 5F-dUMP, which covalently complexes folic acid...this complex inhibits thymidylate synthase, resulting in decreased dTMP and same effects as MTX |
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Clinical use of 5-FU
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colon cancer and other solid tumors, basal cell carcinoma (topical)
synergy with MTX |
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Toxicity of 5-FU
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myelosuppression, which is NOT reversible with leucovorin
photosensitivity can 'rescue' with thymidine |
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Mechanism of 6-mercaptopurine
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blocks de novo purine synthesis
activated by HGPRTase |
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Use for 6-mercaptopurine
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leukemias, lymphomas (not CLL or Hodgkin's)
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Toxicity of 6-mercaptopurine
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bone marrow, GI, liver
metabolized by xanthine oxidase; thus toxicity is increased with allopurinol |
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Cytarabine (ara-C)
mechanism, use and toxicity |
Inhibits DNA polymerase
use for AML Toxicity: can CAUSE leukemia, thrombocytopenia, megaloblastic anemia |
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Cyclphosphamide, ifosfamide
Mechanism |
alkylating agents; covalently x-link (interstrand) DNA at guanine N-7
requires bioactivation by liver |
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Clinical use of cyclophosphamide, ifosfamide
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Non-Hodgkin's lymphoma, breast and ovarian carcinomas
also immunosuppressants |
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Toxicity of cyclophosphamide, ifosfamide
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myelosuppression, hemorrhagic cystitis, which can be partially prevented using MESNA
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Nitrosureas
(Carmustine, lomustine, semustine and streptozocin) Mechanism |
alkylate DNA; requires bioactivation; crosses BBB into the CNS
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Use of nitrosureas (carmustine, etc)
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brain tumors (including glioblastoma multiforme)
because nitrosureas cross the BBB (toxicity, however, is CNS toxicity...dizziness and ataxia) |
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Cisplatin, carboplatin
Mechanism |
act like alkylating agents
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Clinical use of cisplatin and carboplatin
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testicular, bladder, ovary and lung carcinomas
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Toxicty of cisplatin and carboplatin
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nephrotoxicity and acoustic nerve damage
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Bulsulfan
mechanism, use and toxicity |
alkylates DNA
CML toxicity: pulmonary fibrosis, hyperpigmentation |
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Doxorubicin (adriamycin) and daunorubicin
Mechanism |
generates free radicals and noncovalently intercalates in DNA (creating breaks in DNA strand to decrease replication)
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Clinical use of doxorubicin (adriamycin) and daunorubicin
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part of ABCD combination regimen for Hodgkin's and for myelomas, sarcomas and solid tumors (breast, ovary, lung)
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Toxicity of Doxorubicin (adriamycin) and daunorubicin
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cardiotoxicity!!
myelosuppression and marked alopecia toxic extravasation |
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Dactinomycin (actinomycin D)
Mechanism |
intercalates DNA
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Clinical use of Dactinomycin
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Wilm's tumor, Ewing's sarcoma and rhabdomyosarcoma
Toxicity: myelosuppression (Think, ACTinomycin D used for childhood tumors...children ACT out) |
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Bleomycin
Mechanism |
induces formation of free radicals, which cause breaks in DNA strands
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Clinical use of Bleomycin
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testicular cancer, lymphoma (part of aBcd regimen for Hodgkin's)
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Toxicity of Bleomycin
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pulmonary fibrosis, skin changes, but minimal myelosuppression
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Hydroxyurea
Mechanism |
inhibits Ribonucleotide Reductase (which will then decrease DNA synthesis...this is therefore S phase specific)
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Clinical use of hydroxyurea
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melanoma, CML, sickle cell disease
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Toxicity of hydroxyurea
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bone marrow suppression, GI upset
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Etoposide (VP-16)
Mechanism |
G2 phase specific agent that inhibits topoisomerase II and increases DNA degradation
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use of etoposide
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(remember...topo inhibitor)
small cell carcinoma of the lung and prostate, testicular carcinoma |
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Toxicity of etoposide
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myelosuppression, GI irritation, alopecia
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Prednisone
Mechanism Use |
Mech: may trigger apoptosis, may even work on non-dividing cells
Use: most commonly used glucocorticoid in cancer chemotherapy used in CLL, Hodgkin's lymphomas (part of the MOPP regimen); also as immunosuppressant used in autoimmune disease |
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Toxicity of prednisone
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cushing-like symptoms, immunosuppression, cataracts, acne, osteoporosis, hypertension, peptic ulcers, hyperglycemia, psychosis
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Tamoxifen, raloxifene
Mechanism |
receptor antagonists in breast, agonist in bone
blocks the binding of estrogen to estrogen receptor positive cells used in breast cancer and also useful to prevent osteoporosis |
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Toxicity of tamoxifen
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may increase the risk of endometrial carcinoma via partial agonist effects
'hot flashes' raloxifene does NOT cause endometrial carcinoma because it is an endometrial antagonist |
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Trastuzamab (herceptin)
Mechanism Use Toxicity |
Mech: monoclonal antibody against HER-2 (erb-B2); helps kill breast cancer cells that overexpress HER-2, possibly through antibody-dependent cytotoxicity
Use: metastatic breast cancer Toxicity: cardiotoxicity |
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Imatinib (Gleevac)
Mech, use and toxicity |
Mech: philadelphia chromosome bcr-abl tyrosine kinase inhibitor
use: CML, GI stromal tumors Toxicity: fluid retention |
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Vincristine, vinblastine
Mechanism |
M-phase specific alkaloids that bind to tubulin and block polymerization of microtubules so that mitotic spindle cannot form (microtubules are the VINES of your cell)
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Clinical use of vincristine, vinblastine
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part of MOPP (Oncovin is vincristine) regimen for lymphoma, Wilm's tumor, choriocarcinoma
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Toxicity of Vincristine
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neurotoxicity (areflexia, peripheral neuritis), paralytic ileus
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Toxicity of vinblastine
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vinBLASTine BLASTs Bone marrow (suppression)
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Paclitaxel, other taxols
Mechanism |
M-phase specific agents that bind to tubulin and hyperstabilize polymerized microtubules so that mitotic spindle cannot break down (anaphase cannot occur)
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Use of Paclitaxel
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ovarian and breast carcinomas
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Toxicity of paclitaxel
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myelosuppression and hypersensitivity
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Hydrochlorothiazide
Adverse effects |
hypokalemia, mild hyperlipidemia, hyperuricemia, lassitude, hypercalcemia, hyperglycemia
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Loop diuretics
Adverse effects |
Potassium wasting, metabolic alkalosis, hypotension, ototoxicity
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Clonidine
Adverse effects |
dry mouth, sedation, severe rebound hypertension
(alpha 2 agonist) |
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Methyldopa
Adverse effects |
sedation
POSITIVE COOMBS TEST (alpha 2 agonist) |
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Hexamethonium
Adverse effects |
(nicotinic antagonist...used to prevent vagal reflex responses in BP)
can cause severe orthostatic hypotension, blurred vision, constipation, sexual dysfunction |
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Reserpine
Adverse effects |
sedation, depression, nasal stuffiness, diarrhea
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Guanethidine
Adverse effects |
(decreases the release of catecholamines)
orthostatic and exercise hypotension, sexual dysfunction, diarrhea |
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Prazosin
Adverse effects |
(alpha 1 selective blocker)
1st dose orthostatic hypotension, dizziness, headache |
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Beta-blockers
Adverse effects |
impotence, asthma, cardiovascular effects (bradycardia, CHF, AV block), CNS effects (sedation, sleep alterations)
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Hydralazine
Adverse effects |
nausea, HA, lupus-like syndrome, reflex tachycardia (compensatory tachycardia...contraindicated in angina/CAD), angina, salt retention, fluid retention
(use hydralazine with beta blockers to prevent reflex tachycardia and a diuretic to block salt retention) |
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Minoxidil
Adverse effects |
hypertrichosis (were-wolf syndrome...excessive body hair), pericardial effusion, reflex tachycardia, angina, salt retention
use with beta blockers to prevent reflex tachycardia and use with a diuretic to block salt retention |
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Nifedipine, verapamil
Adverse effects |
dizziness, flushing, constipation (verapamil), AV block (verapamil), nausea
(cardiac depression, peripheral edema, flushing, dizziness, and constipation) |
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Nitroprusside
Adverse effects |
cyanide toxicity (release CN)
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Diazoxide
Adverse effects |
(this is a K+ channel opener that hyperpolarizes and relaxes vascular SM)
hypoglycemia (reduces insulin release, hypotension) |
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Captopril, enalapril and fosinopril
Adverse effects |
hyperkalemia, cough, angioedema, taste changes, hypotension, pregnancy problems (fetal renal damage), rash, increase renin
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Hydralazine
Mechanism |
increases cGMP which causes smooth muscle relaxation
vasodilates arterioles > veins and thus causes an afterload reduction |
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Clinical use of hydralazine
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severe hypertension, CHF
first line therapy for hypertension in pregnancy, with methyldopa |
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Minoxidil
Mechanism |
Rogaine!! vasodilator!!
K+ channel opener - hyperpolarizes and relaxes vascular smooth muscle |
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Minoxidil
Clinical use |
severe hypertension
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Nifedipine, verapamil, diltiazem
Mechanism |
Calcium channel blockers!!
blocks voltage-dependent L-type calcium channels of cardiac and SM and thereby reduces muscle contractility |
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Best calcium channel blocker for vascular smooth muscle
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Nifedipine (thus do NOT use for arrhythmias)
nifedipine > diltiazem > verapamil |
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Best calcium channel blocker to use for heart problems
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Verapamil > diltiazem > nifedipine
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Clinical use of calcium channel blockers
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hypertension, angina, arrhythmias (not nifedipine), Prinzmetal's angina, Raynaud's
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Nitroglycerin, isosorbide dinitrate
Mechanism |
vasodilate by releasing NO in smooth muscle, causing an increase in cGMP and smooth muscle relaxation
Dilate veins >>> arteries and therefore decreases preload (NO crosses SM cells and activates cGMP...relaxes SM) |
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Nitroglycerin, isosorbide dinitrate
Clinical use |
angina, pulmonary edema
also used as an aphrodisiac and erection enhancer |
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Nitroglycerin, isosorbide dinitrate
Toxicity! |
tachycardia, hypotension, flushing, HA, 'Monday disease' in industrial exposure, development of tolerance for the vasodilating action during the work week and loss of tolerance over the weekend, resulting in tachycardia, dizziness and HA on reexposure
(severe hypotension if taken with Viagra...sildenifil...also, remove transdermal patch BEFORE defibrillation) |
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Nitroprusside
mechanism |
short acting
increases cGMP via direct release of NO |
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Fenoldopam
Mechanism |
dopamine D1 receptor agonist - relaxes renal vascular SM
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diazoxide
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potassium channel opener - hyperpolarizes and relaxes vascular smooth muscle
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Goal of antianginal therapy
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to reduce myocardial O2 consumption (MVO2) by decreasing 1 or more of the determinants of MVO2:
end diastolic volume, BP, heart rate, contractility, ejection time |
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Beta blockers that should NOT be used for angina
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labetalol, pinodolol and acebutolol
because these are partial agonists |
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Lovastatin, pravastatin, simvastatin, atorvastatin
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HMG-CoA reductase inhibitors!!
big decrease in LDL, mild increase in HDL, mild decrease in TGs Inhibits cholesterol precursor, mevalonate (leads to upregulation of LDL receptors on liver) Side effects: expensive, reversible increase in LFTs, myositis!!! do NOT use in pregnancy (if have hepatitis, probably should not take this drug) |
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Niacin
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decreases LDL, increases HDL, and mildly decreases TGs
inhibits lipolysis in adipose tissue; reduces hepatic VLDL secretion into circulation Side effects: red, flushed face, which is decreased by aspirin or long-term use |
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Cholestyramine, colestipol
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bile acid resins
decreases LDL (slightly increases HDL and slightly increases TGs) prevents intestinal reabsorption of bile acids; liver must use cholesterol to make more TOXICITY: patients HATE this drug because it tastes bad and causes GI discomfort; decreases absorption of fat-soluble vitamins (inhibits enterohepatic reuptake of intestinal bile salts...increases fecal loss of bile acids...increases bile acid synthesis...increases cholesterol synthesis and eventually increases expression of LDL receptors on cell surface of hepatocytes) |
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|
Cholesterol absorption blockers
|
Ezetimibe
only decreases LDL decently blocks intestinal absorption of cholesterol, acting at the level of the small bowel brush border...reduction in hepatic cholesterol stores and an increase in the blood clearance of cholesterol Side effects: rare increase in LFTs |
|
|
Fibrates!!
|
gemfibrozil, clofibrate, bezafibrate, fenofibrate
main effect is decreasing TGs upregulates lipoprotein lipase which will increase TG clearance Side effects: myositis and increase of LFTs |
|
|
Mechanism of digoxin
|
direct inhibition of Na/K ATPase leads to indirect inhibition of Na/Ca exchanger/antiporter
this ultimately leads to an increase in intracellular calcium which leads to positive inotropy (digoxin has 75% bioavailability, 20-40% is protein bound, half life is about 40 hours, urinary excretion!!!) |
|
|
Clinical use of digoxin
|
CHF (increases contractility)
atrial fibrillation (decreases conduction at AV node and depression of SA node) |
|
|
Toxicity of Digoxin!!
|
may cause increase PR, decrease QT, scooping of ST segment, T-wave inversion of ECG
increases parasympathetic activity: nausea, vomiting, diarrhea, blurry yellow vision Arrhythmia Toxicities of digoxin are increased by renal failure (decreased excretion), hypokalemia (potentiates drug's effects), and quinidine (decreases digoxin clearance; displaces digoxin from tissue-binding sites) |
|
|
Digoxin (lippincott book)
|
increases force of contraction which decreases EDV
leads to decreases of sympathetics...decrease PVR decrease HR which increases vagal tone HR decreases and myocardial demand decreases |
|
|
Quinidine, verapamil and amiodarone with regards to digoxin
|
can cause digoxin intoxication by displacing digoxin from protein binding sites...and competing with digoxin for renal excretion
|
|
|
Antidote for digoxin toxicity
|
slowly normalize K+, lidocaine, cardiac pacer, anti-dig Fab fragments, Mg++
|
|
|
Class I antiarrhythmics
|
Na+ channel blockers
local anesthetics slow or block (decrease) conduction (especially depolarized cells) decreases slope of phase 4 depolarization and increases threshold for firing in abnormal pacemaker cells are state/use dependent (selectively depress tissue that is frequently depolarized...like fast tachycardia) |
|
|
Class IA
|
sodium channel blockers
quinidine, amiodarone, procainamide, disopyramide |
|
|
Actions of Class IA
|
increases AP duration, increases effective refractory period (ERP), increases QT interval
affects both atrial and ventricular arrhythmias, especially reentrant and ectoptic supraventricular and ventricular tachycardia |
|
|
Toxicity of Class IA
|
quinidine, amiodarone, procainamide, disopyramide
quinidine causes cinchonism (HA, tinnitus; thrombocytopenia; torsades de pointes due to increase in QT interval) procainamide: reversible SLE-like syndrome |
|
|
Class IB
|
lidocaine, mexiletine, tocainide
(phenytoin as well) |
|
|
Mechanism of Class IB
|
affects ischemic or depolarized Purkinje and ventricular tissue
useful in acute ventricular arrhthymias (especially post-MI) and in digitalis-induced arrhythmias |
|
|
Toxicity of class IB
|
lidocaine, mexiletine, tocainide
local anesthetic; CNS stimulation/depression, cardiovascular depression |
|
|
Class IC
Mechanism |
flecainide, encainide, propafenone
no effect on AP duration useful in V-tachs that progress to VF and in intractable SVT usually used only as a last resort in refractory tacharrhythmias |
|
|
Toxicity of Class IC
|
flecainide, encainide, propafenone
proarrhythmic, especially post-MI (contraindicated) significantly prolongs refractory period in AV node |
|
|
Toxicity for ALL class I drugs
|
hyperkalemia
|
|
|
Class IIA
|
Beta blockers!!
propranolol, esmolol (very short acting), metoprolol, atenolol, timolol |
|
|
Mechanism of Class IIA drugs
|
beta blockers!!
decrease cAMP, decrease calcium currents; suppress abnormal pacemakers by decreasing slope of phase 4 AV node is particularly sensitive - increase PR interval Esmolol is very short acting |
|
|
Clinical use of Class IIA drugs
|
v-tach, SVT, slowing ventricular rate during atrial fibrillation and atrial flutter
(useful in tachycardia cause by increased sympathetic activity) |
|
|
Toxicity of Class IIA drugs
|
Beta blockers!!
impotence, exacerbation of asthma, cardiovascular effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alterations) May mask the signs of hypoglycemia metoprolol can cause dyslipidemia!!! |
|
|
Class IIIA
|
potassium channel blockers
Sotalol, ibutilide, bretylium, amiodarone |
|
|
Mechanism of IIIA
|
increase AP duration, increase ERP
used when other antiarrhythmics fail increase QT interval (decrease outward potassium current during repolarization of cardiac cells) prolong duration of action potential WITHOUT altering phase 0 of depolarization of resting membrane potential |
|
|
Toxicity of amiodarone
|
PULMONARY FIBROSIS, corneal deposits, HEPATOTOXICITY, skin deposits, resulting in photodermatitis, neurologic effects, constipation, cardiovascular effects (bradycardia, heart block, CHF), HYPOTHYROIDISM/HYPERTHYROIDISM
(always check PFTs, LFTs and TFTs with amiodarone) class IIIA potassium channel blocker used for refractory supraventricular and ventricular tachycardias |
|
|
Toxicity of other IIIA other than amiodarone
|
Sotalol: torsades de pointes, excessive beta block
Ibutilide: torsades Bretylium: new arrhythmias, hypotension |
|
|
Class IV antiarrhythmics
|
Calcium channel blockers!!
Verapamil, diltiazem |
|
|
Mechanism of Class IVA
|
calcium channel blockers!!
primarily affect AV nodal cells decrease conduction velocity, increase ERP, increase PR interval used in prevention of nodal arrhythmias (like SVT) |
|
|
Toxicity of Class IVA
|
constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression); torsades de pointes (bepridil)
|
|
|
Adenosine
|
pushes potassium out of cells...this hyperpolarizes the cells
this is the drug of choice in diagnosing/abolishing AV nodal arrhythmias very short acting (about 15 seconds) toxicity includes flushing, hypotension, chest pain |
|
|
K+
|
depresses ectopic pacemakers in hypokalemia
(like digoxin toxicity) |
|
|
Mg++
|
effective in torsades de pointes and digoxin toxicity
|
|
|
Diphenhydramine, dimenhydrinate, chlorpheniramine
|
1st generation H1 blockers
Clinical uses: allergy, motion sickness, sleep aid Toxicity: sedation, anti-muscarinic, anti-alpha adrenergic Remember: H1 receptors activate phospholipase C |
|
|
Loratadine, fexofenadine, desloratadine, cetirizine
|
2nd generation H1 blockers
Use: allergy Toxicity: far less sedating than 1st generation because of decrease entery into CNS |
|
|
Isoproterenol
|
nonspecific beta-agonist
relaxes bronchial smooth muscle (beta 2) adverse effect is tachycardia (beta 1) |
|
|
Albuterol
|
beta 2 agonist
relaxes bronchial SM use during acute exacerbation beta agonists increase adenylate cyclase, increase cAMP and thus increase bronchodilation |
|
|
Salmeterol
|
beta 2 agonist
long-acting agent for prophylaxis adverse effects are tremor and arrhythmia |
|
|
Theophylline
|
methylxanthine!
inhibits phosphodiesterase, decreases cAMP hydrolysis...increases bronchodilation also is an adenosine receptor antagonist that prevents bronchoconstriction usage is limited because of narrow therapeutic index (cardiotoxicity, neurotoxicity) metabolized by cytochrome p450 |
|
|
Ipratropium
|
muscarinic antagonist (similar structure to atropine)
competitive blocker of muscarinic receptors, preventing bronchoconstriction also used for COPD slower onset of action, compliance is an issue (bitter taste) |
|
|
Cromolyn
|
PROPHYLAXIS of asthma
prevents release of mediators from mast cells effective ONLY for prophylaxis of asthma NOT effective during an acute asthmatic attack...toxicity is rare |
|
|
Beclomethasone, prednisone
|
corticosteroids used in asthma
inhibits the synthesis of virtually all cytokines inactivates NF-kB, the transcription factor that induces the production of TNF-alpha, among other inflammatory agents 1st line therapy for chronic asthma! |
|
|
Zileuton
|
antileukotriene
5-lipoxygenase pathway inhibitor blocks conversion of arachidonic acid to leukotrienes (blocks converstion to 5-HPETE) |
|
|
Zafirlukast, Montelukast
|
blocks leukotriene receptors
especially good for aspirin-induced asthma |
|
|
Guaifenesin
(Robitussin) |
expectorant, mucolytic
removes excess sputum but large doses necessary; does not suppress cough reflex |
|
|
N-acetylcysteine
|
mucolytic --> can loosen mucous plugs in CF patients
also used as an antidote for acetaminophen overdose |
|
|
Lispro
|
short acting insulin
|
|
|
Aspart
|
short acting insulin
|
|
|
NPH
|
intermediate acting insulin
|
|
|
Lente
|
long acting insulin
|
|
|
Ultralente
|
long acting insulin
|
|
|
Action of insulin in diabetes
|
binds insulin receptor (tyrosine kinase action)
Liver: increase glucose stored in glycogen Muscle: increase glycogen and protein synthesis, potassium uptake Fat: aids TG storage |
|
|
Clinical use of insulin
|
Type 1 DM
also, life threatening hyperkalemia and stress-induced hyperglycemia |
|
|
Toxicities of insulin
|
hypoglycemia, hypersensitivity reaction (very rare)
|
|
|
Action of sulfonylureas
|
close K+ channels in beta-cell membrane, so cell depolarizes --> triggering of insulin release via increase in calcium influx
|
|
|
Tolbutamide and chlorpropamide
|
1st generation sulfonylureas
(used for type 2 DM...increase insulin release) |
|
|
Glyburide, glimepiride, glipizide
|
2nd generation sulfonylureas
(used for type 2 DM...increases insulin release) |
|
|
Clinical use of sulfonylureas
|
stimulates release of endogenous insulin in type 2 DM
requires some islet function, so useless in type 1 DM |
|
|
Toxicities of type 1 sulfonylureas
|
(tolbutamide, chloropropamide)
disulfiram-like reactions |
|
|
Toxicities of type 2 sulfonylureas
|
(glyburide, glimepiride, glipizide)
hypoglycemia |
|
|
Action of metformin
(a biguanide) |
exact mechanism is unknown
possibly decrease gluconeogenesis, increases glycolysis, decrease serum glucose levels |
|
|
Clinical use of metformin
|
used as oral hypoglycemic
can be used in patients without insulin function |
|
|
Toxicity of metformin
|
lactic acidosis!!
|
|
|
Glitazones: pioglitazone and rosiglitazone
Action |
increases target cell response to insulin
|
|
|
Clinical use of glitazones
|
monotherapy in type 2 DM or combined with other diabetes agents
|
|
|
Toxicity of glitazone
|
weight gain, edema, hepatotoxicity and CV toxicity
|
|
|
alpha-glucosidase inhibitors
|
acarbose and miglitol
|
|
|
action of acarbose and miglitol
|
(alpha-glucosidase inhibitors)
inhibits intestinal brush-border alpha-glucosidases delayed sugar hydrolysis and glucose absorption lead to decreased postprandial hyperglycemia |
|
|
Clinical use of acarbose and miglitol
|
used as monotherapy for type 2 DM or in combo with other diabetic drugs
(inhibits intestinal brush border alpha-glucosidases) |
|
|
toxicity of acarbose and miglitol
|
GI disturbances
|
|
|
Orlistat
Mechanism |
alters fat metabolism by inhibiting pancreatic lipases
|
|
|
Orlistat
Clinical use |
long term obesity management (in conjunction with modified diet)
|
|
|
Orlistat
toxicity |
steatorrhea, GI discomfort, reduced absorption of fat-soluble vitamins, headache
|
|
|
Sibutramine
Mechanism |
sympathomimetic serotonin and norepinephrine reuptake inhibitor
|
|
|
Sibutramine
Clinical use |
short-term and long-term obesity management
|
|
|
Sibutramine
Toxicity |
hypertension and tachycardia
(used for obesity...sympathomimetic serotonin and norepinephrine reuptake inhibitor) |
|
|
Propylthiouracil, methimazole
Mechanism |
inhibits organification and coupling of thyroid hormone synthesis
Propylthiouracil also decreases peripheral conversion of T4 to T3 |
|
|
Clinical use of propylthiouracil, methimazole
|
hyperthyroidism
(inhibits organification and coupling of thyroid hormone synthesis...propylthiouracil also decreases peripheral conversion of T4 to T3) |
|
|
Toxicity of propylthiouracil, methimazole
|
skin rash, agranulocytosis (rare), aplastic anemia
|
|
|
GH is used for...
|
GH deficiency and Turner's syndrome
|
|
|
Somatostatin (octreotide) is used for...
|
acromegaly, carcinoid, gastrinoma, glucagonoma
|
|
|
Oxytocin is used for...
|
stimulates labor, uterine contractions, milk let-down; controls uterine hemorrhage
|
|
|
ADH (desmopressin) is used for...
|
pituitary (central, NOT nephrogenic) DI
|
|
|
Levothyroxine, triiodothyronine
Mech and use |
thyroxine replacement
used for hypothyroidism and myxedema |
|
|
Toxicity of levothyroxine, triiodothyronine
|
tachycardia, heat intolerance, tremors, arrhythmias
|
|
|
Glucocorticoid mechanism
(hydrocortisone, prednisone, triamcinolone, dexamethasone, beclomethasone) |
decreases the production of leukotrienes and prostaglandins by inhibiting phospholipase A2 and expression of COX-2
|
|
|
Clinical use of glucocorticoids
|
Addison's disease, inflammation, immune suppression, asthma
|
|
|
Toxicity of glucocorticoids
|
iatrogenic Cushing's syndrome - buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, easy bruisability, osteoporosis, adrenocortical atrophy, peptic ulcers, diabetes (if chronic)
|
|
|
Opioid analgesics
|
morphine, fentanyl, codeine, heroin, methadone, meperidine, dextromethorphan
|
|
|
Clinical use of opioid analgesics (like morphine, fentanyl, codeine, heroin, methadone, meperidine, dextromethorphan)
|
pain, cough suppression (dextromorphan), diarrhea (loperamide and diphenoxylate), acute pulmonary edema, maintenance programs for addicts (methadone)
|
|
|
Toxicity of opioid analgesics!!
|
addiction, respiratory depression, constipation, miosis (PINPOINT PUPILS), additive CNS DEPRESSION with other drugs
tolerance does NOT develop to mioisis and constipation; toxicity treated with naloxone or naltrexone (opioid receptor antagonist) |
|
|
Toxicity of benzodiazepines
|
sedation, tolerance, dependence
|
|
|
Toxicity of carbamazepine
|
diplopia, ataxia, blood dyscrasias (agranulocytosis, aplastic anemia), liver toxicity, teratogenesis, induction of cytochrome p450
|
|
|
Toxicity of Ethosuximide
|
GI distress, fatigue, headache, urticaria, Stevens-Johnson syndrome
(ethosuximide: EFGH: ethosuximide, fatigue, GI, and headache) |
|
|
Toxicity of phenobarbital
|
sedation, tolerance, dependence, induction of cytochrome p450
|
|
|
Steven Johnson syndrome
|
prodrome of malaise and fever followed by rapid onset of erythematous/purpuric macules (oral, ocular, genital)
skin lesions progress to epidermal necrosis and sloughing |
|
|
Nystagmus, diplopia, ataxia, sedation, gingival hyperplasia, hirsutism, megaloblastic anemia, teratogenesis, SLE-like syndrome, induction of cytochrome p450
|
toxicity of phenytoin
|
|
|
GI distress, rare but fatal hepatotoxicity (measure LFTs), neural tube defects in fetus (spina bifida), tremor, weight gain
contraindicated in pregnancy |
valproic acid
|
|
|
Toxicity of Lamotrigine
|
Steven Johnson syndrome
|
|
|
Toxicity of gabapentin
|
sedation, ataxia
|
|
|
Toxicity of topiramate
|
sedation, mental dulling, kidney stones, weight loss
|
|
|
Mechanism of phenytoin
|
use-dependent blockade of sodium channels; inhibition of glutamate release from excitatory presynaptic neuron
|
|
|
Clinical use of phenytoin
|
tonic-clonic seizures
class IB antiarrythmic |
|
|
Location of synthesis of NE
|
locus ceruleus
|
|
|
Location of synthesis of dopamine
|
ventral tegmentum and substantia nigra pars compacta
|
|
|
Location of synthesis of serotonin (5-HT)
|
raphe nucleus
|
|
|
Location of synthesis of ACh
|
basal nucleus of Meynert
|
|
|
Toxicity of phenytoin
|
nystagmus, ataxia, diplopia, sedation, SLE-like syndrome, induction of cytochrome p450
chronic use produces gingival hyperplasia in children, peripheral neuropathy, hirsutism, megaloblastic anemia (decrease folate absorption), and malignant hyperthermia (rare); teratogenic (fetal hydantoin syndrome) |
|
|
LTB4
|
neutrophil chemotactic agent
|
|
|
LTC4, LTD4, and LTE4
|
function in bronchoconstriction, vasoconstriction, contraction of smooth muscle and increase in vascular permeability
|
|
|
PGI2
|
inhibits platelet aggregation and promotes vasodilation
|
|
|
NSAIDs mechanism
|
Ibuprofen, naproxen, indomethacin, ketorolac
reversibly inhibits both COX-1 and COX-2 blocks prostglandin synthesis |
|
|
Toxicity of NSAIDs
|
renal damage, aplastic anemia, GI distress, ulcers
|
|
|
PGI
|
prostcyclin
decrease platelet aggregation, decrease vascular tone, decrease bronchial tone, decrease uterine tone |
|
|
PGE and PGF
|
prostaglandins
decrease vascular tone, decrease bronchial tone and increase uterine tone |
|
|
Thromboxane
|
increase platelet aggregation, increase vascular tone and increase bronchial tone
|
|
|
Celecoxib
|
reversibly inhibits specifically the COX 2 which is found in inflammatory cells and mediates inflammation and pain
spares COX 1, which helps maintain the gastric mucosa and thus should NOT have the corrosive effects of other NSAIDs on the GI lining |
|
|
Toxicity of celecoxib
|
increase risk of thrombosis, sulfa allergy, less toxicity to GI mucosa (lower incidence of ulcers, bleeding)
|
|
|
Acetaminophen mechanism
|
reversibly inhibits COX, mostly in the CNS
|
|
|
Toxicity of acetaminophen
|
overdose produces hepatic necrosis, acetaminophen metabolites deplete glutathione and forms toxic tissue adducts in liver; N-acetylcysteine is antidote...regenerates glutathione
|
|
|
Colchicine
|
ACUTE GOUT!!!
depolymerizes microtubules, impairing leukocyte chemotaxis and degranulation |
|
|
side effects of Colchicine
|
GI effects, especially if given orally!!
(again, use colchicine in ACUTE GOUT!!) |
|
|
Indomethacin is...
|
less toxic than colchicine and is more commonly used in acute gout
|
|
|
Probenicid
|
chronic gout!!
inhibits reabsorption of uric acid in PCT (also inhibits secretion of penicillin) |
|
|
Allopurinol
|
chronic gout!!
inhibits xanthine oxidase, decreases conversion of xanthine to uric acid also used in lymphoma and leukemia to prevent tumor lysis-associated urate nephropathy |
|
|
Allopurinol interacts with...
|
azathioprine and 6-MP
|
|
|
What should probenicid and allopurinol NOT be used for...
|
acute gout!!
(do NOT give salicylates for gout) |
|
|
Etanercept
|
recombinant form of human TNF receptor that binds TNF
|
|
|
Use of Etanercept
|
RA, psoriasis and ankylosing spondylitis
(recombinant form of human TNF receptor that binds TNF) |
|
|
Infliximab
|
anti-TNF antibody
|
|
|
Use of Infliximab
|
Crohn's disease, RA, ankylosing spondylitis
(but can predispose to infections...reactivation of TB) |
|
|
Zileuton
|
blocks lipoxygenase
|
|
|
Zafirlukast and montelukast
|
block receptors of leukotrienes
|
|
|
Cimetidine, ranitidine, famotidine and nizatidine
|
H2 blockers!! reversible block of histamine H2 receptors...leads to decrease in H+ secretion by parietal cells
|
|
|
Clinical use of H2 blockers like cimetidine, ranitidine, famotidine and nizatidine
|
peptic ulcer, gastritis, mild esophageal reflux
|
|
|
Toxicity of cimetidine!
|
potent inhibitor of p450
also has antiandrogenic effects (prolactin release, gynecomastia, impotence, decrease libido in males) can cross BBB (confusion), dizziness, headaches...and placenta |
|
|
Toxicity of both cimetidine and ramitidine
|
decrease renal excretion of creatinine
|
|
|
Omeprazole and lansoprazole
|
proton pump inhibitors!!
irreversibly inhibit H+/K+-ATPase in stomach parietal cells |
|
|
Clinical use of PPIs like omeprazole and lansoprazole
|
peptic ulcer, gastritis, esophageal reflux, Zollinger-Ellison syndrome
|
|
|
Bismuth, sucralfate mechanism
|
bind to ulcer base, providing physical protection, and allows HCO3- secretion to reestablish pH gradient in the mucous layer
|
|
|
Use of bismuth and sucralfate
|
increase ulcer healing, traveler's diarrhea
|
|
|
Triple therapy of H. pylori ulcers
|
Metronidazole, Amoxicillin (or Tetracycline) and Bismuth
|
|
|
Misoprostol
|
A PGE1 analog
increases production and secretion of gastric mucosa barrier, decreases acid production |
|
|
Clinical use of Misoprostol
|
prevention of NSAID-induced peptic ulcers; maintenance of a PDA
also used to induce labor |
|
|
Toxicity of Misoprostol
|
diarrhea, contraindicated in women of childbearing potential (abortifacient)
|
|
|
Pirenzepine, propantheline
|
Muscarinic antagonists
blocks M1 receptors on ECL cells (so you decrease histamine secretion) and M3 receptors on parietal cells (decrease H+ secretion) |
|
|
Toxicity of pirenzepine and propantheline
|
tachycardia, dry mouth, difficulty focusing eyes
(these are muscarinic antagonists used in peptic ulcers...blocks M1 on ECL cells to decrease histamine secretion and blocks M3 receptors on parietal cells to decrease H+ secretion) |
|
|
Antacid use
|
can affect absorption, bioavailability, or urinary excretion of other drugs by altering gastric and urinary pH or by delaying gastric emptying
|
|
|
Overuse of aluminum hydroxide
|
an antacid
causes constipation and hypophosphatemia; proximal muscle weakness, osteodystrophy, seizures, hypokalemia (AluMINIMUM amount of feces) |
|
|
Overuse of magnesium hydroxide
|
diarrhea, hyporeflexia, hypotension, hypokalemia and cardiac arrest
(Mg = Must Go to the bathroom) |
|
|
Overuse of calcium carbonate
|
hypercalcemia and rebound increase in acid (and hypokalemia)
can chelate and decrease effectiveness of other drugs (like tetracycline) |
|
|
Sulfasalazine
|
a combo of sulfapyridine (antibacterial) and mesalamine (anti-inflammatory)
activated by colonic bacteria used in UC and Crohn's |
|
|
Toxicity of sulfasalazine
|
malaise, nausea, sulfonamide toxicity, reversible oligospermia
|
|
|
Ondansetron
|
5-HT3 antagonist
powerful central-acting antiemetic used to control vomiting postoperatively and in patients undergoing cancer chemotherapy |
|
|
Toxicity of ondansetron
|
HA and constipation
(5-HT3 antagonist...central-acting antiemetic) you will not vomit with ONDANsetron, so you can go ON DANCing |
|
|
Cisapride
|
prokinetic agent
acts through serotonin receptors to increase ACh release at the myenteric plexus increases esophageal tone; increases gastric and duodenal contractility, improving transit time (including through the colon) NO LONGER USED BECAUSE: serious interactions (torsades des pointes) with erythromycin, ketoconazole, nefazodone, fluconazole |
|
|
METOCLOPRAMIDE
MECHANISM |
PROKINETIC!!!
D2 receptor antagonist; increases resting tone, contractility, LES tone, motility...does NOT influence colon transport time |
|
|
Clinical use of metoclopramide
|
diabetic and post-surgery gastroparesis!!!
(D2 receptor antagonist...) |
|
|
Toxicity of metoclopramide
|
increase parkinsonian effects
restlessness, drowsiness, fatigue, depression, nausea, diarrhea drug interaction with digoxin and diabetic agents; contraindicated in patients with small bowel obstructiona |
|
|
Tx alcohol withdrawal with
|
benzodiazepines
|
|
|
Tx anorexia/bulimia with
|
SSRIs
|
|
|
Tx anxiety with
|
barbiturates, benzos, buspirone, MAO inhibitors
|
|
|
Tx ADHD with
|
methylphenidate (ritalin) and amphetamine
|
|
|
Tx atypical depression with...
|
MAO inhibitors
|
|
|
Tx bipolar disorder with
|
Mood stabilizers: lithium, valproic acid and carbamazepine
|
|
|
Tx depression with
|
SSRIs and TCAs
|
|
|
Tx depression with insomnia
|
trazodone and mirtazapine
|
|
|
Tx OCD with
|
SSRIs
|
|
|
Finasteride (propecia)
|
5 alpha-reductase inhibitor
decreases conversion of testosterone to DHT useful in BPH promotes hair growth, used to treat male-pattern baldness |
|
|
to prevent male pattern hair growth...
|
give a drug that will encourage female breast growth
|
|
|
Flutamide
|
a nonsteroidal competitive inhibitor of androgens at the testosterone receptor
used in prostate carcinoma |
|
|
What are ketoconazole and spironolactone used for?
|
in the treatment of polycystic ovarian syndrome to prevent hirsutism
both have side effects of gynecomastia and amenorrhea |
|
|
Ketoconazole...
|
inhibits steroid synthesis
used in treating hirsutism and PCOS |
|
|
Spironolactone
|
inhibits steroid binding
used in treating PCOS and to prevent hirsutism |
|
|
Mechanisn of Leuprolide
|
GnRH analog with agonist properties when used in a pulsatile fashion
antagonist properties when used continuosly (Leuprolide can be used in LIEU of GnRH) |
|
|
Clinical use of leuprolide
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infertility (pulsatile)
prostate cancer (continuous - use with flutamide), uterine fibroids |
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Toxicity of leuprolide
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remember, leuprolide is a GnRH analog
antiandrogen, nausea, vomiting |
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Sildenafil, vardenafil
Mechanism |
inhibits cGMP phosphodiesterase, causing increase in cGMP, SM relaxation in the corpus cavernosum, increase blood flow and penile erection
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Toxicity of sildenafil, vardenafil
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headache, flushing, dyspepsia, impaired blue green color vision
risk of life-threatening hypotension in patients taking nitrates |
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Mechanism of Mifepristone (RU-486)
Toxicity of Mifepristone |
competitive inhibitor of progestins at progesterone receptors
Toxicity: heavy bleeding, GI effects (nausea, vomiting, anorexia), abdominal pain |
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Clinical use of Mifepristone
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(remember, this is a competitive inhibitor of progestins at progesterone receptors)
termination of pregnancy...administered with misoprostol (PGE1) |
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Kill this...
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sh*t.
: ) |
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Advantages of oral contraception (synthetic progestins, estrogen)
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reliable, < 1% failure
decrease risk of endometrial and ovarian cancer; decrease incidence of ectopic pregnancy, decreased risk of pelvic infections, regulation of menses |
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Disadvantages of oral contraception
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taken daily, no protection against STDs, increase TGs, depression, weight gain, nausea, hypertension, hypercoagulable states
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Hormone replacement therapy
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used for relief or prevention of menopausal symptoms (like hot flashes, vaginal atrophy) and osteoporosis (due to diminished estrogen levels)
unopposed estrogen replacement therapy (ERT) increases risk of endometrial cancer, so progesterone is added...possibel increase CV risk |
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Dinoprostone
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PGE2 analog causing cervical dilation and uterine contraction, inducing labor
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Ritodrine/terbutaline
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beta-2 agonist that relaxes the uterus
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Anastrozole
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aromatase inhibitor used in postmenopausal women with breast cancer
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Exemestane
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testosterone...used to treat ER positive breast cancer
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Testosterone causes...(toxicity)
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masculinization in females; reduces intratesticular testosterone in males by inhibiting Leydig cells...leads to gonadal atrophy; premature closure of epiphyseal plates
increases LDL and decreases HDL |
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Estrogen can be used in men for...
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androgen-dependent prostate cancer
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Toxicity of estrogen
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increase risk of endometrial cancer, bleeding in postmenopausal women, clear cell adenocarcinoma of vagina in females exposed to DES in utero; increase risk of thrombi
contraindicated in ER positive breast cancer |
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Ethinyl estradiol, DES and mestranol
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estrogens
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Progestins
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bind progesterone receptors, reduce growth and increase vascularization of endometrium
used in oral contraceptives and in the treatment of endometrial cancer and abnormal uterine bleeding |
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Clomiphene
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estrogen partial agonist (SERMs)
partial agonist at estrogen receptors in pituitary gland prevents normal feedback inhibition and release of LH and FSH from pituitary, which stimulates ovulation used to treat infertility and PCOS may cause hot flashes, ovarian enlargement, multiple simultaneous pregnancies and visual disturbances |
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Tamoxifen
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antagonist on breast tissue
used to treat and prevent recurrence of ER-positive breast cancer SERM (estrogen partial agonist) |
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Raloxifene
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agonist on bone
reduces reabsorption of bone used to treat osteoporosis SERM (estrogen partial agonist) |
