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Pharm - Hem-Onc
Hem-Onc Pharmacology from First Aid 2013
| Question | Answer |
|---|---|
| What should you always give with chemotherapy to prevent gout from tumor lysis syndrome? | Allopurinol or febuxostat (xanthine oxidase inhibitors) |
| What is heparin's use/MOA? What genetic coagulopathy might dampen its effect? | MOA: AT3 up-regulator for ACUTE anticoagulation |
| What should you follow when dosing heparin? What is the antidote for its toxicity? | Follow PTT (although both are elevated) Antidote: protamine sulfate |
| How are LMWH's different from normal heparin? | Act more exclusively on factor X. Have better availability (can be injected). Longer half life. Not easily reversible. |
| What is a serious complication of heparin use? What can you use instead? | HIT: IgG to Hep/PF4 on platelet -> immune complex thrombosis/thrombocytopenia. Instead use "-rudins" e.g., bivalirudin |
| What is Coumadin's use/MOA? | MOA: Prevent Vit.K oxidation, preventing gamma-carboxylation of the following factors: II, VII, IX, X, C & S Use for CHRONIC (6mo) anticoagulation. |
| Out of heparin and coumadin/warfarin, which is safe for pregnancy? | Heparin. Warfarin wages "war" on the fetus. It is teratogenic. |
| What should you follow when dosing warfarin? What drugs affect its metabolism? | Follow PT/INR (although both are elevated) CYP450 met'd: Cipro and antifungals prolong its action. |
| What is the antidote for warfarin toxicity? | Acutely: Fresh frozen plasma, clotting factors Then: Vit. K injection (takes 6h to work) |
| What is a serious complication of warfarin use? | Warfarin skin necrosis: C&S are knocked out before the other coagulation factors, so patients are briefly hypercoagulable. |
| What are OCP's effect on coagulation? How does this affect heparin use? | OCP's inhibit AT3 and upregulate the synthesis of coagulation factors. OCP + smoking (endothelial damage) = thrombus risk!!! |
| Thombolytics: Naming, MOA, Use, Tox | Nom: end in "-plase", usually tPA MOA: convert pasminogen to plasmin, which cleaves thrombin/fibrin, inc PTT/PT Use: EARLY MI/stroke, severe PE Tox: causes bleeding, late administration may actually cause reperfusion injury (BAD) |
| How should you treat a tPA toxicity? | Aminocaproic acid |
| ASA (Aspirin): MOA, Uses by dose | MOA: irrev. inh. COX-1,2 on platelets, inc BT dec TXA2, no effect on PTT/PT Low dose- antiplatelet Med dose- antipyretic Hi dose- antiinflamm |
| What are the SFX and toxicities of aspirin? | Gastric ulcers, tinnitus (CN VIII), acute renal failure, respiratory alkalosis + metabolic acidosis. Also a mitochondrial un-coupler (hyperthermia). |
| Why shouldn't you give Aspirin to kids? When is it okay to do so? | Reye's syndrome: post-viral infection Must give in Kawasaki's CAD |
| ADP receptor inhibitors: names, MOA, Use, Tox | Clopidigrel, Ticlopidine, "clop" MOA: prevent exocytosis of GpIIb/IIIa Use: acute coronary syndrome Tox: Ticlopidine -> neutropenia |
| Similar to clopidigrel preventing GpIIb/IIIa exocytosis, what drugs bind and inhibit this receptor? | Abciximab: preventing aggregation. Same uses as ADP receptor inhibitors. |
| Clostazol, dipyridamole: MOA, Use, Tox | PDE III inhibitors: increasing cAMP in platelets, inhibiting platelet aggregation. Use: coronary vasodilation, TIA/angina prevention Tox: Nausea, headache, flushing, hypoTN |
| Anti-metabolite chemotherapeutics work in which part of the cell cycle? | S-phase |
| Name some antimetabolites and their targets. | MTX (folic acid analog) -> (T), DHFR 5-FU (pyrimidine analog) -> (T), thymid synth Cytarabine (pyrimidine) -> (T) 6-MP ("more purines") -> (A), (G) |
| How do you reverse myelosuppression in MTX toxicity? What about 5-FU? | MTX: Leucovorin - folic acid rescue 5-FU: have to give thymidine itself |
| Which antimetabolite chemo drug would become toxic with allopurinol? | 6-MP, as both it and allopurinol are metabolized by xanthine oxidase. (BTW, 6-MP is activated by HGPRT.) |
| What would you expect as a side effect of MTX? | Macrocytic anemia (DHFR inhibitor!). Also it causes mucositis and is teratogenic. |
| What antibiotics also serve as anti-tumor drugs? How/where do they work? | actinomycin-D: intercalates DNA (S-phase) Doxorubicin: intercalates + free radicals Bleomycin: free radical generation (Pulm sfx) |
| Which chemo drug famously has cardiotoxicity? How can you prevent it? | Doxorubicin (also causes alopecia and myelosupression). Give dexrazoxane to chelate iron and prevent this. |
| Alkylating agents work in which phase of the cell cycle? | All phases. They attack DNA regardless of its activity. |
| Name three major alkylating agents. | Cyclophosphamide/ifosfamide Nitrosureas - CNS tumors, cross BBB Busulfan |
| How does cyclophosphamide work? | It covalently inter-strand-links guanine at N7 after activation by the liver. |
| What are cyclophosphamide's toxic side effects and how are they prevented? | Hemorrhagic cystitis and bladder cancer. Prevent with Mesna. |
| What is a toxic side effect of Busulfan? | Pulmonary fibrosis, like Bleomycin. |
| What are two classes of chemo drugs that work during M-phase? What plants are they derived from? | Vinca alkaloids - periwinkle plant Taxols - yew tree |
| Vincristine, Vinblastine: MOA and Tox | MOA: bind tubulin and block polymerization of microtubules Vincristine Tox: neurotoxicity, peripheral np Vinblastine Tox: blast bone marrow (Bone) |
| Paclitaxel: MOA, Use, Tox | MOA: Prevent breakdown of tubulin MT's Greatest effect during anaphase Use: ovarian and breast tumors Tox: myelosuppression + H-S Rxn |
| Cisplatin, Carboplatin: MOA, Tox | MOA: cross-link DNA, made from platinum Nephrotoxicity - prev with amifostine/diuresis Ototoxicity - acoustic nerve damage |
| What chemo drug acts during G2 phase? What does it act on specifically? | Etoposide - inhibits Topo II |
| What are etoposide's toxic side effects? | GI irritation, alopecia, myelosup. |
| Hydroxyurea: Chemo MOA, alternative uses | RNT reductase inh: dec U/T synthesis (S-phase) Increases fetal Hb; use for CML, melanoma |
| When might corticosteroids be used in cancer chemotherapy? | To trigger apoptosis in CLL, NHL. |
| Tamoxifen, Raloxifene: MOA, Uses, Tox | MOA: SERM's, antagonists, agonists in bone Use: breast cancer, prevent osteoporosis Tox: tamoxifen is a partial agonist in the endometrium (risk), raloxifene prefered |
| Trastuzumab (Herceptin): MOA, Tox | Antibody against HER-2 (c-erb) tyrosine kinase in HER-2 positive breast cancers. Tox: cardiotoxicity |
| Imatinib (Gleevec): MOA, Tox | Antibody against bcr-abl (Philadelphia) tyrosine kinase. Use for CML. Tox: Fluid retention |
| Rituximab: MOA, Use | MOA: CD-20 Ab (most B-cell neoplasia) Use: NHL, RA with MTX |
| Vemurafenib: MOA, Use | MOA: inhibitor of B-Raf kinase V600E mutation Use: metastatic melanoma |
| Bevacizumab: MOA, Use | MOA: Ab against VEGF Use: many solid tumors |
Created by:
wmwebb89
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