Heme/Onc Flashcards
Heparin
- mech
- clin use, follow what lab?
- tox
- reversal effects w/?
- big SE = ?
cofactor for act’n of ATIII -> decr’d thrombin and FXa, short t 1/2
- immediate anticoag, can use during preg bc doesn’t X placenta; follow PTT
- bl’ing, HIT, osteoporosis, drug interactions
- protamine sulfate (+ molec binds - hep)
- HIT = IgG Abs to hep:PF4 (on plts) -> thrombosis and thrombocytopenia
Lepirudin, bialirudin =
- used when?
direct thrombin inhib’s, deriv’s of hirudin
- alt to heparin for anticoag w/ HIT pt’s
Warfarin (Coumadin)
- mech
- metab’d by
- clin use, follow what lab?
- tox
- reverse effects w/?
interferes w/ gamma-carboxyl of VitK-dep CFs (2, 7, 9, 10, PrC/S), long t 1/2
- P450
- chronic anticoag, not used in preg women bc can X placenta follow PT
- bl’ing, teratogenic, skin/tissue necrosis (bc prC/S decr before others -> thrombosis), drug interactions
- VitK, for rapid effect give FFP
Heparin vs. Warfarin:
- size
- route of administration
- onset of action
- duration of action
- inhib’s coag in vitro
- lg anionic acidic polymer vs. sm lipid-soluble molec
- IV/SC vs. PO
- rapid (s) vs. slow (need CFs to end t 1/2)
- acute (hrs) vs. chronic (d’s)
- yes vs. no
Thrombolytics =
- MoA
- how do labs change?
- clin use
- tox
- C/I’d in?
- trt tox w/?
“-plase” Alteplase (tPA), reteplase (rPA), tenecteplase (TNK-tPA)
- convert plasminogen to plasmin
- incr’d PT/PTT, no plt ct change
- early MI, early stroke, severe PE
- bl’ing
- active bl’ing, hx of head bl, recent surgery, severe HTN
- aminocaproic acid (inhib’s fibrinolysis)
Aminocaproid acid =
inhib’s fibrinolysis; use for tPA tox
Protamine sulfate =
trt heparin overdose
ASA
- mech
- how do labs change?
- clin use
- tox
- don’t use in kids w/ viral infec, why?
- overdose causes?
irreversibly inhib’s plt COX-1/2 by covalent acetylation (lasts until new plts are made)
- no change in PT/PTT, incr’d BT, decr’d TXA2 and PGEs
- antipyretic, analgesic, anti-inflamm, anti-plt aggregation
- gastric ulcers, tinnitus (CNVIII), chronic use can cause ARF, interstitial nephritis and upper GI bl’ing
- risk of Reye’s synd
- resp alk and metab acidosis
ADP R inhib’s =
- mech
- clin use
- tox
Clopidogrel, ticlopidine, prasugrel, ticagrelor
- block ADP Rs -> inhib plt aggregation bc no GpIIb/IIIa R available for fibrinogen to bind
- ACS, coronary stenting, to decr chance of thrombotic stroke
- neutropenia (ticlopidine)
Clopidogrel =
ADP R inhib
Ticlopidine =
ADP R inhib
Prasugrel =
ADP R inhib
Ticagrelor =
ADP R inhib
PDE III inhib’s =
- mech
- clin use
- tox
cilostazol, dipyridamole
- incr cAMP in plts -> inhib aggregation; vasodilators too
- intermittent caudication, coronary vasodil, prevent stroke/TIA (w/ ASA), angina prophylaxis
- N, HA, facial flushing, hypotension, ab pain
Cilostazole =
PDE III inhib
Dipyridamole =
PDE III inhib
GP IIb/IIIa inhib’s =
- mech
- made from
- clin use
- tox
Abciximab, eptifibatide, tirofiban
- bind GP IIb/IIIa inhib on act’d plts, prevents aggregation
- mAB Fab fragments
- ACS, PCT coronary angioplasty
- bl’ing, thrombocytopenia
Abciximab =
GP IIb/IIIa inhib