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91 Cards in this Set

  • Front
  • Back
receptor on platelets that binds fibrinogen and other macromolecules?
antiplatelet factor released from endothelium
aggregating substances released from degranulating platelet?
what is drotrecogin alpha and how is it used clinically?
activated protein C
to treat septic shock
UFH (unfractionated heparin)?
glycosaminoglycan from animal source
high density of (-) charges
1/3 have necessary sequence for activity
necessary part of heparain for activity?
pentasaccharide sequence
LMWH (low molecular weight heparins)?
digest unfractionated heparin
only 15-25% contain necessary sequence
synthetic pentasaccharide binding sequence for heparin
actions of heparins?
effective anticoagulant in vivo and in vitro;
arrests thrombosis and prevents embolization especially on the venous side of circulation;
prolonged whole blood clotting time, thrombin time, prothrombin time, partial thromboplatin time;
bleeding times may be unaltered
heparin mechanism?
antithrombin catalyst to inhibit proteolytic activity of most of the proteolytic enzymes (IIa and Xa are most important);
enhance activity of the Tissue Factor Pathway Inhibitor
most important enzymes inhibited by heparin?
which enzyme are LMWH and fondaparinux unable inhibit and why?
complex can formed only by chains at least 18 saccharides long;
so these are more Xa selective
major disadvantage of heparins?
must be administered parenterally
which route of administration is avoided with heparins and why?
IM, possible hematoma
UFH elimination?
half life is dose dependent and nonlinear due to rapid but saturable mechanism and slower, non-saturable, dose-independent renal clearance
LMWH and fondaparinux elimination?
by renal clearance;
more predictable anticoagulant response with better bioavailability, longer half-life, and dose-independent clearance
toxicity associated with heparins?
major bleeding
major bleeding as toxicity with heparins?
osteoporosis as toxicity with heparins?
seen only on prolonged use of 10-15000 UFH/day for more than one month
HIT (heparin induced thrombocytopenia)?
due to IgG against complexes of UFH and platelet factor 4 that form on the surface of platelets and activate their Fc-gamma-RIIa receptors;
platelets count begins to decline 5-10 days after starging UFH;
less likely SC;
associated with thromboembolic disorders
patients at highest risk of HIT?
postoperative orthopedic
cardiac surgery
vascular surgery
thromboembolic disorders associated with HIT?
pulmonary embolism
cerebral thrombosis
ischemic injury to legs or arms
recombinant derivative of hirudin
direct irreversible thrombin inhibitor
approved for patients with HIT
heparin substitute
no antidote
direct reversible thrombin inhibitor
approved for patients with HIT
heparin substitute
no antidote
why do lepirudin and argatroban make the transition to warfarin complicated?
can increase INR
why is warfarin not substituted for UFH in HIT?
has been associated with venous limb gangrene or multicentric skin necrosis;
should not be used until thrombocytopenia has been resolved
treatment of heparin overdose?
withdrawal of UFH
basic protein that combines with UFH to form a stable salt;
can only neutralized anti-IIa activity of LMWH;
does not reverse fondaparinux
most common test for UFH effect?
activated partial thromboplastin time (aPTT)
most accurate and reliable test for UFH effect?
factor Xa titration
coumarins action?
suppress formation, by the liver, of some of the factors involved in blood coagulation
coumarins mechanism?
antagonize action of vitamin K;
block generation of gamma-carboxyglutamic acid residues;
required for factors II, VII, IX, X and proteins C and S
major disadvantage of coumarins?
long latent period - must wait for clotting factors to be catabolized or resynthesized at conclusion of therapy
which isomer of warfarin is most potent and how is it metabolized?
less potent warfarin isomer and how is it metabolized?
R-warfarin CYP1A2
major advantage of warfarin?
can be given orally
challenges of warfarin therapy?
narrow therapeutic window;
variability in dose response;
interactions with drugs and diet;
lab control is difficult to standardize;
understanding of pharmacokinetics and pharmacodynamics;
need good patient communication
factors involved in patient's response to warfarin?
vitamin K
liver disease
congestive heart failure (hepatic congestion)
presence of infection
following surgery
presence of other drugs/herbals
what factors increase patient's sensitivity to warfarin?
genetic variations that have consequence to warfarin therapy?
may need to lower warfarin doses in these individuals
which drugs potentiate warfarin's effects?
fluconazole + warfarin interaction?
inhibition of CYP2C9
increased S-warfarin
amiodarone + warfarin interaction?
increased S and R warfarin
omeprazole + warfarin interaction?
increased R-warfarin
drugs that inhibit actions of warfarin?
vitamin K
cholestyramine + warfarin interaction?
binding in gut to decrease absorption
decreased plasma levels
barbiturates + warfarin interaction?
increased metabolism due to induction of CYP;
decreased warfarin plasma levels
vitamin K + warfarin interaction?
decreased effect of warfarin
toxicity associated with warfarin?
recurrent skin necrosis
most consistent risk factor for bleeding with warfarin therapy?
history of bleeding (especially GI)
warfarin and pregnancy?
warfarin can cross the placenta so should be avoided
when should patients wear a 'medic alert' bracelet?
if on anticoagulant
treatment of warfarin overdose?
prothrombin complex concentrates
oral vit K (phytonadione)
oral vit K
may complicate reestablishment of warfarin therapy since has long duration of action
recommendations on antithrombic and thrombolytic therapy?
heparins are used immediately (rapid onset);
warfarin administered at same time as heparin;
heparin is not discontinued until INR indicates that warfarin is effective
purpose of INR?
absolute prothrombin time can vary and this allows a way for it to be standardized
for which condition is recommended range of INR higher than the usual 2-3?
2.5-3.5 for mechanical prosthetic heart valves
binds to plasminogen thereby converting plasminogen into a plasmin like molecule capable of converting plasminogen to plasmin
requires fibrin for activity - less random proteolytic dstruction of blood clotting factors
nonglycosylated deletion mutation of wild type tPA
derivative of alteplase
advantage of single bolus administration
which fibrinolytics have specificity for fibrin?
which fibrinolytic is antigenic?
which fibrinolytic can be administered as single bolus?
therapeutic use of fibrinolytics?
treat acute MI as an alternative to PCI
importance of time in administering fibrinolytics?
recently formed thrombi are easier to lyse than aged thrombi
which fibrinolytic is approved for acute ischemic stroke?
adverse effects of fibrinolytics?
arrhythmias (on reperfusion)
fever and allergic reactions (streptokinase)
aminocaproic acid?
binds reversibly to plasminogen to block binding of plasminogen to fibrin and its activation and transformation to plasmin
treatment of bleeding episodes in hemophilia patients with inhibitors to factor VIII or IX;
off label to stop other instances of uncontrolled bleeding
why low doses of aspirin?
COX1 in platelets are inhibited more selectively because lower doses are required;
higher doses would inhibit formation of prostacyclin that is actually an antiplatelet agent
vascular disorders for which aspirin has been shown to be effective and lowest effective dose?
TIA and ischemic stroke (50 mg)
unstable angina (75 mg)
acute MI (160 mg)
acute ischemic stroke (160 mg)
irreversible blocking of P2Y12 purinergic receptor for adenosine diphosphate which indirectly inhibits the binding of fibrinogen to its platelet receptor (GIIb/IIIa)
clopidogrel pharmacokinetics and consequences?
prodrug converted to active form by two CYP-dependent oxidation steps;
function polymorphisms may interfere in as many as 30% of patients
prasugrel pharmacokinetics?
prodrug that undergoes hydrolysis by intestinal esterases and only one CYP-dependent oxidation step to convert to active form
indications for clopidogrel and prasugrel?
prophylaxis before and after PCI in combination with aspirin;
acute coronary syndrome;
post MI porpylaxis;
stroke prevention in TIA or previous thrombotic stroke
percutaneous coronary intervention
(ie angioplasty)
adverse effects of ADP pathway inhibitors?
bleeding (prasugrel > clopidogrel)
clopidogrel interactions?
CYP2C19 inhibitors (proton pump inhibitors: omeprazole, esomeprazole);
caution with other drugs that may cause bleeding
Fab fragment of monoclonal antibody
GIIb/IIIa antagonist
most efficacious platelet agents?
GIIb/IIIa antagonists
GIIb/IIIa antagonist
GIIb/IIIa antagonist
GIIb/IIIa antagonists administration?
IV in the hospital
direct reversible thrombin inhibitor (derived from hirudin);
inactivates platelet bound Xa and clot bound thrombin;
no known antidote
indications for bivalirudin?
used (with aspirine, clopidogrel and provisional GPI) instead of heparin in patients with unstable angina undergoing PCI
inhibition of phosphodiesterase
blockade of uptake of adenosin
combo with low dose aspirin for stoke prevention