First Aid Hematology and Oncology-Pharmacology – Flashcards
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Heparin MOA
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Cofactor for activation of antithrombin. Decreases thrombin and factor Xa.
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Clinical use, heparin
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Immediate anticoagulation for PE, acute coronary syndrome, MI, DVT. Used during pregnancy (doesn't cross placenta). Follow PTT.
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Toxicity, heparin
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Bleeding, thrombocytopenia (HIT), osteoporosis, drug-drug interactions.
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Antidote, heparin?
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Antidote=protamine sulfate (positively-charged, binds negatively-charged drug)
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Enoxaparin, dalteparin
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Low weight molecular heparins
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Low molecular weight heparins (enoxaparin, dalteparin)
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Heparins that act more on factor Xa, have better bioavailability and longer half life. Can be given subQ and no lab monitoring necessary. Not easily reversible.
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Heparin induced thrombocytopenia (HIT)
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Development of IgG abs against heparin bound to platelet factor 4 (PF4). Antibody-heparin PF4 complex activates platelets-->thrombosis and thrombocytopenia
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Lepirudin, bivalirudin
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Derivatives of hirudin, the anticoagulant used by leeches; inhibit thrombin. Alternative to heparin for anticoagulating patients with HIT.
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Warfarin MOA
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Interferes with normal synthesis and gamma carboxylation of vitamin K dependent clotting factors II, VII, IX and X and proteins C and S. Metabolized by cytochrome P-450 pathway. In lab, has effect on extrinsic pathway and increases PT (The EX-PresidenT went to war(farin)).
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Use, warfarin
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Used in chronic anticoagulation. Not used in pregnant women because can cross the placenta.
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PT/INR values, warfarin
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What labs should be followed during warfarin ttmt?
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Toxicity, warfarin
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Bleeding, teratogenic, skin/tissue necrosis, drug-drug interactions
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Reversal of warfarin
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Reversal: vitamin K Rapid reversal of severe overdose: fresh frozen plasma
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Alteplase
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A thrombolytic, tPA
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Reteplase
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A thrombolytic, rPA
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Tenecteplase
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Thrombolytic, TNK-tPA
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Alteplase, reteplase, tenecteplase
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Name the thrombolytics
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Thrombolytics
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Directly or indirectly aid conversion of plasminogen to plasmin, which cleaves thrombin and fibrin clots. Increased PT and PTT, no change in platelet count.
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Uses of thrombolytics?
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Uses: Early MI, early ischemic stroke, direct thrombolysis of severe PE
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Toxicity, thrombolytics?
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Toxicity=bleeding Contraindicated in pts with active bleeding, hx of intracranial bleeding, recent surgery, known bleeding diatheses, or severe hypertension.
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Ttmt of toxicity, thrombolytics?
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Ttmt of toxicity=aminocaproic acid (an inhibitor of fibrinolysis)
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Aspirin, MOA
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Irreversibly inhibits COX1 and 2 via covalent acetylation. Platelets can't make new enzyme, so effect lasts until new platelets are made. Increases bleeding time, decreases TXA2 and prostaglandins. No effect on PT or PTT.
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Clinical use, aspirin
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Use: antipyretic, analgesic, anti-inflammatory, antiplatelet (decreased aggregation).
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Toxicity, aspirin
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Toxicity: gastric ulceration, tinnitus (CN VIII). Chronic use can lead to acute renal failure, interstitial nephritis, and upper GI bleeding. Reye's syndrome in children with viral infection.
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What does OD on aspirin cause
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OD causes respiratory alkalosis and metabolic acidosis
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ADP receptor inhibitors?
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Clopidogrel, ticlopidine, prasugrel, ticagrelor
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MOA, ADP receptor inhibitors?
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Inhibit platelet aggregation by irreversibly blocking ADP receptors (ADP its receptor on surface of platelet causes GP IIb/IIIa insertion on the membrane, receptor for fibrinogen). Inhibits fibrinogen binding by preventing glycoprotein IIb/IIIa from binding to fibrinogen.
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Toxicity, ADP receptor inhibitors (ticlopidine)
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Toxicity: neutropenia
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Phosphodiesterase inhibitors
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Cilostazol is what type of drug?
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ADP receptor inhibitor
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Ticlopidine=?
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ADP receptor inhibitor
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Prasugrel=?
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ADP receptor inhibitor
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Clopidogrel=?
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ADP receptor inhibitor
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Ticagrelor=?
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Phosphodiesterase III inhibitor
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Dipyridamole=?
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Phosphodiesterase III inhibitors
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Cilostazol, dipyridamole are this type of drug
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GP IIb/IIIa inhibitor
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Abciximab is what type of drug?
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GP IIb/IIIa inhibitor
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Eptifibatide=?
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GP IIb/IIIa inhibitor
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Tirofiban=?
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GP IIb/IIIa inhibitors
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Abciximab, eptifibatide, tirofiban=what type of drugs?
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Cilostazol, dipyridamole MOA
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Phosphodiesterase III inhibitor, increase cAMP in platelets, thus inhibiting platelet aggregation; vasodilators.
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Clinical use, cilostazol, dipyridamole?
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Use: Intermittent claudification, coronary vasodilation, prevention of stroke or TIAs (combined with aspirin), angina prophylaxis
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Toxicity, cilostazol, dipyridamole?
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Tox: nausea, headache, facial flushing, hypotension, abdominal pain.
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MOA, abciximab, eptifibatide, tirofiban
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MOA: bind to glycoprotein receptor IIb/IIIa on activated platelets, preventing aggregation. Abciximab made from monoclonal Ab Fab fragments.
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Clinical use, abciximab, eptifibatide, tirofiban?
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Use: acute coronary syndromes, percutaneous transluminal coronary angioplasty.
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Toxicity, abciximab, eptifibatide, tirofiban?
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Toxicity: bleeding, thrombocytopenia
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Act on S phase, antimetabolites
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Antimetabolites act at what phase in the cell cycle?
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Act on S phase, G2 phase
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Etopiside acts on which phases on cell cycle?
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G2 phase
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Bleomycin acts on which phase of the cell cycle?
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M phase
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Vinca alkaloids and taxols work at which phase of the cell cycle?
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Methotrexate, MOA
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MOA:Folic acid analog that inhibits dihydrofolate reductase -v dTMP, v DNA, and v protein synthesis
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Methotrexate, clinical use
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Cancers: leukemias, lymphomas, choriocarcinoma, sarcomas Non-neoplastic: abortion, ectopic pregnancy, rheumatoid arthritis, psoriasis
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MTX, toxicity
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Toxicity: myelosuppression reversible with leucovorin (folinic acid) rescue) -Macrovesicular fatty change in liver -Mucositis -Teratogenic
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5-fluorouracil MOA
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Pyrimidine analog bioactivated to 5F-dUMP, which covalently complexes folic acid. This complex inhibits thymidylate synthase--> vdTMP-->v DNA and v protein synthesis
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5-fluorouracil uses
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Uses: Colon cancer, basal cell carcinoma
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5-fluorouracil toxicity
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Myelosuppresion which isn't reversible via leucovorin. Photosensitivity
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Antidote for 5-FU OD?
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Antidote=thymidine
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MOA, cytarabine (arabinogfuranosyl cytidine)
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MOA: pyrimidine analog-->inhibition of DNA polymerase
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Clinical use, cytarabine
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Clinical use: leukemias, lymphomas
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Tox, cytarabine
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Toxicity: leukopenia, thrombocytopenia, megaloblastic anemia
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MOA, azathioprine, 6-mercaptopurine (6-MP), and 6-thioguanine (6-TG)
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MOA: purine (thiol) analogs-->v de novo purine synthesis. Acitvated by HGPRT.
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Clinical use, azathioprine, 6-mercaptopurine (6-MP) and 6-thioguanine (6-TG)
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Use: Leukemias
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Azathioprine, 6-mercaptopurine, and 6-thioguanine toxicity
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Tox: bone marrow, GI, liver Metabolized by xanthine oxidase; thus increases toxicity with allopurinol
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Antitumor antibiotics
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What do dactinomycin (actinomycin D), doxorubicin, daunorubicin, and bleomycin have in common?
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Dactinomycin MOA
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Antitumor abx that intercalates in DNA
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Dactinomycin clinical use
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Use: wilm's tumor -Ewing's sarcoma -Rhabdomyosarcoma -Used for childhood tumors (children ACT out)
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Dactinomycin, toxicity
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Tox: myelosuppression
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Doxorubicin, daunorubicin MOA
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MOA: generate free radicals. Noncovalently intercalate in DNA-->breaks in DNA-->decrease replication
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Doxorubicin, daunorubicin use
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Use: solid tumors, leukemias, lymphomas
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Doxorubicin, daunorubicin tox
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Tox: cardiotoxicity (dilated cardiomyopathy) -Myelosuppression -Alopecia -Toxic to tissues following extravasation
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Doxorubicin, daunorubicin antidote
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Dexrazoxane (iron chelating agent), used to prevent cardiotoxicity
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Bleomycin MOA
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MOA: induces free radical formation, which causes breaks in DNA strands
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Bleomycin uses
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use: testicular cancer, lymphoma
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Bleomycin tox
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Tox: pulmonary fibrosis, skin changes. Minimal myelosuppression.
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Alkylating agents
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Cyclophosphamide Ifosfamide Nitrosureas (carmustine, lomustine, semustine, streptozocin) Busulfan
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Cyclophosphamide, ifosfamide MOA
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MOA: covalently X-link (interstrnad) DNA @ guanine N-7. Require bioactivation by liver.
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Uses, cyclophosphamide, ifosfamide
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Uses: solid tumors, leukemia, lymphomas, and some brain cancers.
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Tox, cyclophosphamide, ifosfamide
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Tox: myelosuppression -Hemorrhagic cystitis
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Mesna (thiol group binds toxic metabolite)
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Substance that can be used to prevent hemorrhagic cystitis caused by cyclophosphamide, ifosfamide
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Nitrousoureas
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Carmustine, lomustine, semustine, streptozocin are?
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MOA, nitrousureas
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MOA: require bioactivation, cross BBB-->CNS
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Uses, nitrousureas
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Uses: brain tumors (including glioblastoma multiforme)
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Toxicity, nitrousureas?
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Tox: CNS toxicity (dizziness, ataxia)
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MOA, busulfan
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MOA: alkylates DNA
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Uses, busulfan
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Uses: CML, also used to ablate pt's bone marrow before bone marrow transplantation.
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Toxicity, busulfan:
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Tox: pulmonary fibrosis, hyperpigmentation
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Microtubule inhibitors
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Vincristine, vinblastine Paclitaxel, other taxols
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MOA: vincristine, vinblastine
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MOA: alkaloids that bind to tubulin in M phase and block polymerization of microtubules so that mitotic spindle cannot form "Microtbules are the VINes of your cells
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Tox, vincristine
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Tox: neurotoxicity (areflexia, peripheral neuritis), paralytic ileus
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Tox, vinblastine
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Tox: bone marrow suppress Vinblastine BLASTS Bone marrow
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MOA, paclitaxel, other taxols
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MOA: hyperstabilize polymerized microtubules in M phase so that mitotic spindle cannot break down (anaphase cannot occur). "it is TAXing to stay polymerized"
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Toxicity, paclitaxel and other taxols
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Tox: myelosuppression and hypersensitivity
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MOA, cisplatin and carboplatin
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MOA: cross-link DNA
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Tox, cisplatin and carboplatin
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Tox: nephrotoxicity and acoustic nerve damage.
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Amifostine (free radical scavenger) and chloride diuresis
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How to prevent nephrotoxicity with cisplatin and carboplatin?
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MOA, etopiside, teniposide
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MOA: inhibit topoisomerase II-->increase DNA degradation
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Tox, etopiside, teniposide
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Tox: myelosuppression, GI irritation, alopecia
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MOA, hydroxyurea
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MOA: inhibits ribonucleotide reductase-->v DNA Synthesis (S phase specific)
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Tox, hydroxyurea
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TOx: bone marrow suppression, GI upset
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MOA, prednisone, prednisolone
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MOA: may trigger apoptosis, may even work on non-dividing cells
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Toxicity, prednisone, prednisolone
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Tox: Cushing-like sx, immunosuppression, cataracts, acne, osteoporosis, htn, peptic ulcers, hyperglycemia, psychosis
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MOA: tamoxifen, raloxifene
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MOA: SERMs, receptor antagonists in breast and agonists in bone. Block the binding of estrogen to estrogen receptor-positive cells.
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Toxicity, tamoxifen
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Tox: partial agonist in endometrium, which increases the risk of endometrial cancer; hot flashes
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Tox, raloxifene
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Tox: no increase in endometrial CA because it's an endometrial antagonist
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Trastuzumab (Herceptin) MOA
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MOA: monoclonal Ab vs HER-2 (c-erb B2), a tyrosine kinase. Helps kill breast cancer cells that overexpress HER-2, possibly through antibody-dependent cytotoxicity.
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Toxicity, trastuzumab
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Tox: cardiotoxicity
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MOA, Imatinib (gleevec)
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MOA: Philadelphia chromosome bcr-abl tyrosine kinase inhibitor
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Uses, imatinib
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Use: CML, GI stromal tumors
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Tox, imatinib
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Fluid retention=tox
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Rituximab MOA
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MOA: monoclonal Ab vs. CD20, which is found on most B cell neoplasms
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Vemurafenib MOA
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MOA: small molecule inhibitor of forms of the B-Rag kinase with the V600E mutation.
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Vemurafenib use
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Use: metastatic melanoma
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Bevacizumab MOA
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MOA: monoclonal ab vs VEGF. Inhibits angiogenesis.
