hema Flashcards
enoxaparin,
Low-molecular-weight heparin
act on factor Xa
better bioavailability and 2-4times longer half life
administered subcutaneously without monitering, not easily reversed
Heparin
cofactor for the activation of antithrombin, decrease thrombin, and decrease factor Xa.short half-life.
use for immediate anticoagulation for pulmonary embolism, acute coronary syndrome, MI, DVT. Used during pregnancy(does not cross placenta) follow PTT!!!!!!!!!!
TOX :HIT, reverse by protamine sulfate
dalteparin
Low-molecular-weight heparin
act on factor Xa
better bioavailability and 2-4times longer half life
administered subcutaneously without monitering, not easily reversed
heparin-induced thrombocytopenia
development of IgG antibodies against heparin bound to PLT factor 4 (PF4). Antibody-heparin-PF4 complex activates PLT–>thrombosis and thrombocytopenia
nonimmune: 1-2days, thrombocytopenia moderate to mild
immune: HITT, 4-14 days, thrombocytopenia
Lepirudin
derivatives of hirudin, anticoagulant used by leeches
inhibit thrombin
used as an alternative to heparin for anticoagulating pt with HIT
bivalirudin
derivatives of hirudin, anticoagulant used by leeches
inhibit thrombin
used as an alternative to heparin for anticoagulating pt with HIT
Warfarin
coumadin
involves synthesis and gamma-carboxylation of vit K-dependent factor II, VII, IX, X and protein C and S. FOLLOW PT/ INR
cytochrome P450. long half life.
use in chronic anticoagulation (after STEMI, venous thromboembolism prophylaxis, and prevention of stroke in atrial fibrillation)
NOT used in pregnancy!!!! tox: bleeding, teratogenic, skin/tissue necrosis,drug interaction. reversal use Vit K
streptokinase
causes thrombolysis through formation of plasmin by forming activator complex with plasminogen to cleave arginine-valine bond
argastroban
PT, PTT decrease
no antidote/ careful in patient with liver disease.
alteplase
tPA
thrombolytics: aid conversion of plasminogen to plasmin, which cleaves thrombin and fibrin clots.
increase PT and PTT, no change in PC
Use in early MI, early ischemic stroke, direst htombolysis of severe pulmonary embolism
TOX: bleeding, CI in pt with active bleeding and his of surgery, HTN
treat with aminocaproic acid
aminocaproic acid
inhibitor of fibrinolysis
antidote for thrombolytics
can also use tranexamic acid or fresh frozen plasma
aspirin
ASA
irreversibly inhibits COX-1 and COX-2 by acetylation,serine
PLT cannot synthesis new enzyme, effect lasts until new PLT produced
increase bleeding time & decrease TXA2 and PG. no effect on PT and PTT.
use: antipyretic, analgesic, antii-nflammatory, anti-PLT
TOX: GI, tinnitus, renal failure, reye’s, resp alka, meta acid
clopidogrel
inhibits PLT aggregation by irreversibly blocking ADP receptor. inhibit fibrinogen binding by preventing glycoprotein IIb/IIIa from binding to fibrinogen.
Use in prophylaxis acute coronary syndrome; prevention of AS following recent myocardial infarction.
ticlopidine
inhibits PLT aggregation by irreversibly blocking ADP receptor. inhibit fibrinogen binding by preventing glycoprotein IIb/IIIa from binding to fibrinogen.
Use in coronary stenting, decrease incidence or recurrence of thrombotic stroke.
TOX: Neutropenia, agranulocytosis, TTP, aplastic anemia
prasugrel
inhibits PLT aggregation by irreversibly blocking ADP receptor. inhibit fibrinogen binding by preventing glycoprotein IIb/IIIa from binding to fibrinogen.
Use in acute coronary syndrome; coronary stenting, decrease incidence or recurrence of thrombotic stroke.
ticagrelor
inhibits PLT aggregation by irreversibly blocking ADP receptor. inhibit fibrinogen binding by preventing glycoprotein IIb/IIIa from binding to fibrinogen.
Use in acute coronary syndrome; coronary stenting, decrease incidence or recurrence of thrombotic stroke
cilostazol
phosphodiesterase III inhibitor; increase cAMP in PLT, thus inhibiting PLT aggreagtion; vasodilator.
Use:intermittent claudication, coronary vasodilation, prevention of stroke or TIAs (with aspirin), angina prophylaxis
TOX: nausea, headache, facial flushing, hypotension, abdominal pain
dipyridamole
phosphodiesterase III inhibitor; increase cAMP in PLT, thus inhibiting PLT aggreagtion; vasodilator.
Use:intermittent claudication, coronary vasodilation, prevention of stroke or TIAs (with aspirin), angina prophylaxis
TOX: nausea, headache, facial flushing, hypotension, abdominal pain
abciximab
monoclonal antibody Fab fragment.
bind to the glycoprotein receptor IIb/IIIa on activated PLT, preventing aggregation.
use in acute coronary syndrome, percutaneous transluminal coronaryangioplasty, use with heparin sometimes
TOX: bleeding, thrombocytopenia
eptifibatide
bind to the glycoprotein receptor IIb/IIIa on activated PLT, preventing aggregation.
use in acute coronary syndrome, percutaneous transluminal coronaryangioplasty
TOX: bleeding, thrombocytopenia
tirofiban
bind to the glycoprotein receptor IIb/IIIa on activated PLT, preventing aggregation.
use in acute coronary syndrome, percutaneous transluminal coronaryangioplasty
TOX: bleeding, thrombocytopenia
methotrexate
folic acid analog that inhibits dihydrofolate reductase–> decrease dTMP–>decrease DNA and protein synthesis.
use: leukemias, lymphoma, choriocarcinoma, sarcoma
non-neoplastic: abortion, ectopic pregnancy, RA, psoriasis.
TOX: myelosuppression, which is reversible with leucovorin
macrovesicular fatty change to liver, mucositis, teratogenic
5-FU
pyrimidine analog bioactivated to 5-F-dUmp, which covalently complexes folic acid.
inhibits thymidylate synthase–>decrease dTMP->decrease DNA and protein synthesis
Use in colon cancer, basal cell carcinoma,
tox: photosensitivity, myesupression, not reversible by leucovorin, rescue with thymidine
cytarabine
arabinofuranosyl
pyrimidine analog–> inhibition of DNA polymerase
use in leukemias, lymphomas
tox: leukopenia, thrombocytopenia, megaloblastic anemia