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59 Cards in this Set

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Antineoplastics:
begin
Nucleotide synth inhibitors:
MTX, 5FU, 6MP, 6TG, Cytarabine
DNA inhibition: 1. TOPO Ø 2. X-linking 3. Intercalators
1. Etoposide, Doxorubicin 2. Cisplatin, alkylators 3. dactinomycin, doxorubicin, cyclophosphamide, Nitrosureas, Busulfan
Cellular division inhibition: 1. block MT synthesis 2. block MT depolymerization
1. Vinca alkaloids 2. Paclitaxel (Taxol)
MTX: 1. MOA 2. Uses
1. folate analog that inhibits DHF reductase, decreased dTMP hinder DNA/protein synthesis. S-phase specific. 2. leuk/lymphomas, breast cancer, termination of ectopic pregnancy, RA, psoriasis,
MTX: Toxicities
suppresses bone marrow REVERSIBLY, (give folinic acid LEUCOVORIN to 'rescue' myelosuppression. Stomatitis, hepatotoxic, CI: pregnancy
5-FU 1. MOA 2. Uses
1. Thymidine antimetabolite converted to dUMP which binds to folic acid and inhibits THYMIDYLATE SYNTHASE. Sphase 2. breast, ovarian, colon, HEENT cancers, basal cell carcinomas.
5-FU toxicities:
IRREVERSIBLE myelosuppression, photosensitivity, GI irritation.
6-MP 1. MOA 2. Uses (mini people)
activated by HGPRT and inhibits purine synthesis; Sphase specific. 2. acute leukemias, CML, non-Hodgkin
6-MP Toxicities: (tall grownups)
BMS, Hepatotoxic (coadmin with allopurinol increases toxicity). Azathioprine forms 6-MP
6-TG 1. MOA 2. Uses 3. TOX
same as 6MP. 2. uses: ALL 3. BMS, liver, CAN BE USED WITH ALLOPURINOL (unlike 6-MP)
Cytarabine 1. MOA 2. Uses 3. Tox
1. pyrimidine antimetabolite, Sphase, DNA pol inhibition. 2. Acute leukemias. 3. BMS, GI irritation, increase dose = neurotoxic
Dactinomycin: 1. MOA 2. Uses 3. Toxicities
1. intercalates DNA 2. Wilm's, Ewings, rhabdomyosarcoma, CHILDREN ACT OUT (Ped tumours) 3. MYELOSUPPRESION
Doxorubicin (adriamycin) 1. MOA 2. Uses 3. Tox
1. intercalator, creates DNA breaks, hinders replication/transcription. 2. Hodgkins (ABVD+), breast, endometrial, lung, ovarian, myeloma, sarcomas. 3. Cardiotoxic (dilation), BMS, GI distress
How to tx doxorubicin toxicity??
Dexrazoxane: inhibits free radical formation and may protect the heart in cardiomyopathy from doxorubicin.
Bleomycin?? 1. MOA 2. Uses 3. Tox
1. Generates free radicals, DNA strand scission, G2phase specific. 2. lymphomas, testicular skin CA 3. Pulm fibrosis, mucocutaneous reactions (blisters), HSN rcn
Etoposide 1. MOA 2. Uses 3. Tox:
1. Inhibits TOPO II, increase DNA degradation, Late S/early G2 phase reactant. 2. small cell carcinoma, prostate/testicular cancer. 3. BMS, GI irritation
Cyclophosphamide 1. MOA 2. Uses 3. Tox
1. alkylate DNA, attacks guanine N7, induces X-linking 2. nonHodgkin, ovarian/breast cancer/neuroblastoma, vasculitides. 3. BMS, hemorrhagic cystitis (mesna)
Nitrosureas (lomustine, carmustine) 1. MOA 2. Uses 3. Tox
1. Alkylates DNA, CROSSES BBB 2. Brain tumours 3. NEUROlogic
Busulfan 1. MOA 2. Uses 3. Tox
1. Alkylates DNA 2. CML 3. Pulm fibrosis, hyperpigmentation, adrenal insufficiency.
Cisplatin, Carboplatin, Oxiplatin. 1. MOA 2. Uses 3. Tox
1. alkylates DNA 2. testicular, bladdder, lung , ovarian 3. nephrotoxic, (add amifostine); deafness/tinnitis BMS (carbo>cis)
Vinblastine: 1. MOA 2. Uses 3. Tox
1. inhibit MT formation M-phase. 2. lymphoma, wilms, choriocarcinoma. 3. BMS
Vincristine 1. MOA 2. Uses 3. Tox
1. inhibit MT formation, M-phase 2. same uses as vinblastine (MOPP) 3. neurotoxic, GI distress
Paclitaxel 1. MOA 2. Uses 3. Tox
1. stabilizes MTs/NO DEPOLARIZES, M-phase 2. ovarian/breast carcinomas 3. BMS
Hydroxyurea (HU) 1. MOA 2. Uses 3. Tox
1. an antimetabolite that inhibits RIBONUCLEOTIDE REDUCTASE, reactivates HbF synthesis. 2. Sickle cell, PV, CML
Prednisone: 1. MOA 2. Uses 3. Tox
1. induces apoptosis of lymphoid cells, PLA2 blockage, IL2 suppression, COX2 block. 2. CLL, Hodgkin lympohma (MOPP), Autoimmune disease/suppression. 3. iatrogenic Cushing syndrome, GC excess (decrease Ca, K increased Na)
Tamoxifen/Raloxifene: 1. MOA 2. Uses 3. Tox
1. SERMs (selective estrogen receptor modulators). Prevents estrogen from binding estrogen receptor-positive breast CA cells leading to involution of estrogen-dependent tumours. 2. Breast Cancer. 3.hot flashes, increased risk of endometrial cancer. (RALOXIFENE IS RISK FREE OF EC)
Trastuzumab (Herceptin) MOA, Uses, Tox
monoclonal-Ab anti-HER2 (erb-B2); metastatic breat cancer, CARDIOTOXIC
Imantinib (Gleevac) MOA, Uses, TOX
small molecule anti-bcr/abl fusion; CML, GI stromal tumours; FLUID RETENTION
Rituximab MOA, Uses, Tox
mc-Ab against CD20, on most Bcell neoplasms; non-hodgkins lymphomas, RA (+ MTX)
Vemurafenib MOA, Uses, Tox
small molecule inhibitor of forms of B-Raf kinase with V600E mutation, Metastatic melanoma.
Bevacizumab MOA USES
mc-Ab against VEGF, inhibits angiogenesis; SOLID TUMOURS
AntiCOAGs
begin:
Heparin (IV, SC) MOA
activates ANTITHROMBIN III. INACTIVATES: Factors 2,7,9,10,11,12 (intrinsic). Slows PTT.
heparin MOA/USES
binds AT-III; complex inactivates THROMBIN/9a, 10a,12a. Acts in SECONDS, used ACUTELY (IV). Uses: acute MI, DVT, PE, Stroke, beginning therapy
LMWHs (ardeparin, dalteparin, enoxaparin)
inhibit Factor 10a, more nad thrombin less than heparin. USED IN LONGTERM use due to risk of heparin-Induced Thrombocytopenia (HIT).
Protamine sulfate?
reverses heparin and LMWH use
Direct thrombin inhibitors: Lepirudin/argatroban, hirudin, bivalirudin
bind directly to thrombin substrates/thrombin. (ATIII independent). Bind to soluble thrombin/clot-bound thrombin.
Warfin (PO), Coumadin
interferes with synthesis of vitamin K-dependent clotting factors (2, 7, 9, 10). Takes 2-5 days to work (chronic use). PT/INR used to monitor. Vit K reverses efx. CONTRAIND: Pregnancy. CYP450-Inducers DECREASE EFX, CYP450Ø incr. efx.
Thrombolytics: (streptokinase, alteplase, urokinase) MOA, Uses
convert plasminogen to plasmin to bust clots, uses: MI DVT PE ischemic stroke (tPA); CONTRAIND: active bleed, intracranial bleed (hemorrhagic stroke), recent surgery, severe HTN, OD: aminocaproic acid
Protein S MOA
activates protein C, this inactivates Factors 5a, 8a
tPA MOA
cleaves fibring mesh by activating plasminogen/plasmin
GpIIb/IIIa inhibitors:
reversible inhibitors. abciximab, eptifibatide, tirofiban.
Bernard Soulier disease
defective plug formation due to GPIb deficiency and platelets cannot bind to vWF
Glanzmann thrombasthenia:
defective plug formation from decreased GpIIb/IIIa which inhibits platelet-to-platelet aggregation (abcixumab MOA). Fibrinogen xlinking using these receptors. ADP induces these receptors to surface as well (so
Clopidogrel/Ticlopidine
BLOCK ADP receptor to inhibit aggregation
Aspirin
blocks Cox1/2 irreversibly, platelet aggregation inhibited through DECRE. PG synth (TXA2 stimulates platelet aggregation and vasoconstriction)
von Willebrand disease (AD)
defective platelet plug formation due to defect in quantity or quality of vWF which binds to exposed collagen in the SEC which facilitates platelet binding to wall via GpIb. vWF deficiency= increased bleeding time and PTT (vWF stabilizes Factor 8)
Tests for Coag system: PT/PTT
PT: extrinsic, 7, 10, 5, prothrombin, fibrinogen. PTT: intrinsic 12,11, 9, 8, 10, 5, prothrombin, fibrinogen
DX diseases of Platelets: Bernard-Soulier/Glanzmann
PTT, PT not affected, BLEEDING TIME INCREASED. Signs: gum bleeding, epistaxis, petechiae,
ITP (idiopathic thrombocytopenic purpura)
spleen makes Ab against platelet antigen (GPIIB/IIIA, GPIb/IX) Destoyed plates via splenic MØ, acute form: postviral/kids, selflimited. Chronic: adults, 1' or 2' (HIV, SLE). CS, Ig therapy, Splenectomy. Enlarged immature platelets, PT/PTT normal
TTP (thrombotic thrombocytopenic purpura)
pentad (Thrombocytopenic purpura, fever, renal failure, neuro changes, microangiopathic hemolytic anemia) usually in younger women, Smear= few plates, schistocytes. HUS looks similar (BUT DIARRHEA FOLLOWING E.COLI O157:H7 Infection)
vWF disease:
defective platelet plug due to defieint levels of vWF. AD. Increased BT, PTT (vWF stabilizes factor 8). Tx: Desmopressin??
DIC:
massive persistent activation of both coag/fibrinolytic system. Consumption deficiency. Etiology: amniotic fluid embolism, infection (gram neg, sepsis), malignancy, major traumas, head injury. DX: low plates, low fibrinogen, increased PTT/PT, INCR D DIMER, schistocytes
Excessive thrombosis: causes:
Protein C/S deficiency, Factor V Leiden deficiency, Prothrombin gene mutation, ATIII deficiency.
Protein C/S deficient:
lost ability to inactivate Factors 5/8, incr. DVT/PE, Cerebral V. thrombosis, Warfarin-induced skin necrosis
Prothrombin gene mutation:
3' untranslated region causes increased circulating thrombin and venous clots.
ATIII deficiency
potent inhibitor of clotting cascade and its deficiency leads to increased venous clots
Factor V Leiden deficiency (AD)
Mutation in factor 5 making it resistant to inactivation by Protein C. inherited disorder of blood clotting/hypercoagulability. PTT prolonged. DVT association and risk of clot in pregnancy.