hematology drugs Flashcards
heparin: mechanism, use, monitoring
mechanism: cofactor for antithrombin III. this decreases thrombin and factor Xa. short half-life.
use: immediate anticoagulation after PE, acute coronary syndrome, MI, DVT. used during pregnancy.
follow PTT
heparin: toxicity and antidote
toxicity: bleeding, thrombocytopenia, osteoporosis, HIT.
HIT: heparin induced thrombocytopenia. IgG abs against heparin bound to platelet factor 4 develop. Ab-heparin-PF4 complex activates platelets, causing thrombosis and thrombocytopenia.
antidote: protamine sulfate- positively charged molec that will bind negatively charged heparin.
What do we use to anticoagulate patients with HIT? How do these drugs work?
argatroban, bivalirudin.
these are derived from hirudin, the anticoagulant used by leeches. they inhibit thrombin directly.
Warfarin: mechanism, monitering, use, toxicity, antidote
mechanism: binds epoxide reductase, which is needed to convert oxidized vitamin K to reduced vitamin K. without vitamin K, patients can’t make factors 2, 7, 9, 10, or proteins C, S. (interferes with gamma-carboxylation of vitamin K-dependent factors).
monitor using PT/ INR.
use: chronic anticoagulation. not used in pregnant women.
toxicity: skin/tissue necrosis! also teratogenic (bone deformities, fetal hemorrhage, opthalmologic abnormalities, abortion). bleeds.
antidote: vitamin K; fresh frozen plasma
what are the direct factor Xa inhibitors? uses?
apixaban, rivaroxaban
they bind and directly inhibit factor Xa, obviously.
used for tx and prophylaxis of DVT and PE (rivaroxaban). stroke prophylaxis in pts with a fib.
heparin vs. warfarin: structure, route of administration, site of action, duration of action, treatment of overdose, monitoring
heparin: large anionic polymer, administered parenterally, acts on the blood, last for hours (not days), give protamine sulfate, monitered via PTT
warfarin: small lipid soluble molecule, given orally, acts on liver, lasts for days, give vitamin K or fresh frozen plasma for OD, monitor with PT.``
tPA: action, use, toxicity, antidote
mechanism: directly or indirectly aids conversion of plasminogen to plasmin. plasmin cleaves thrombin and fibrin clots. it increases the PT, PTT. no change in platelet count.
used for early MI, early ischemic stroke, PE.
toxicity: BLEEDS. contraindicated in pts with active bleeds, hx of intracranial bleed, recent surgery, known bleeding probs, severe HTN.
treat toxicity with aminocaproic acid, an inhibitor of fibrinolysis (also used for urokinase excess). fresh frozen plasma and crypoprecipitate can also be used to correct factor deficiencies.
clopidigrel
(also ticlopidine, prasugrel, ticagrelor).
inhibit platelet aggregation by irreversibly blocking ADP receptors (which incr. expression of GIIb/IIIa). inhibit fibrinogen binding by preventing glycoprotein IIb/IIIa from binding to fibrinogen.
used in acute coronary syndrome, stenting. decr. incidence or recurrence of thrombotic stroke
can cause TTP/HUS. (ticloplidine causes neutropenia)
Phosphodiesterase III inhibitors: names, use.
cilostazole, dipyridamole.
phosphodiesterase III inhibitors that incr. cAMP in platelets. this inhibits platelet aggregation. they are also vasodilators.
used for intermittent claudication, coronary vasodilation, prevention of a stroke or TIAs, angina prophylaxis.
Abciximab
(also eptifibatide, tirofiban)
GP IIb/IIIa inhibitors. they bind the IIb/IIIa receptor on activated platelets and prevent aggregation. Abciximab is made from monoclonal ab Fab fragments. used in unstable angina, percutaneous transluminal coronary angioplasty
can cause bleeding, thrombocytopenia
aspirin: mechanism, labs, overdose
irreversibly binds COX-1 and COX2 by covalent aceylation. platelets can’t synthesize new enzyme, so effect lasts until new platelets are produced. increases bleeding time, decreases TXA2, prostaglandins. no effect on PT and PTT.
overdose will cause an initial respiratory alkalosis, then an metabolic acidosis
