anti- platelet/ coagulant and thrombolytic agents Flashcards
the mechanism of action for the antiplatelet drugs
and it plays an important role in
inhibit the platelet aggregation.
prevent atherosclerotic and thrombosis
the classification of antiplatelet depends on
mechanism of action :
1- thromboxane A2 synthesis inhibitor
2- phosphodiesterase inhibitor
3- adenosine diphosphate (ADP)antagonist
4-glycoprotein receptor antagonist
thromboxane A2 synthesis inhibitor works on
COX1
thromboxane A2 synthesis inhibitor ex.
aspirin
the inhibition of cox 1 caused by thromboxane A2 synthesis inhibitor does last until
7-10 days caused it is irreversible so new one need to be formed
the dose needed to produce the effect for thromboxane A2 synthesis inhibitor
75mg/day
thromboxane A2 synthesis inhibitors are used to reduce
the incidence of stroke and MI
phosphodiesterase inhibitor ex
dipyridamole
phosphodiesterase inhibitor mechanism
increase cAMP which in turn reduce the aggregation of platelet
which drug is used for transient ischemic and stroke attack
phosphodiesterase inhibitor (dipyridamole) low risk of bleeding than aspirin
adenosine diphosphate (ADP)antagonist ex.
ticlopidine , clopidogrel
the mechanism of adenosine diphosphate (ADP)antagonist
they inhibit GP IIb/IIIa receptor
the therapeutic use of adenosine diphosphate (ADP)antagonist
and for who
decrease the incident of thrombotic stroke
for who can not tolerate aspirin
the adverse effects of adenosine diphosphate (ADP)antagonist
ticlopidine -> neutropenia , thrombocytopenia , aplastic anemia
therefore the clopidogrel in main agent
glycoprotein receptor antagonist ex.
abciximab and eptifibatide
what is the abciximab
monoclonal antibody binds irreversibly to GP IIb IIIa receptor
the route of administration and the use of abciximab
IV
used after coronary artery procedure
what is the eptifibatide
synthetic inhibitor for GP IIb IIIa receptor
the main side effect for glycoprotein receptor antagonist
BLEEDING
thrombolytic drugs mechanism is
rapid lysis of already formed clots
what is the mechanism of thrombolytic drugs
activation of proenzyme plasminogen to PLASMINO which catalyze the degradation of fibrin
thrombolytic drugs ex.
alteplase (second generation)
streptokinase and urokinase (first generation)
alteplase (second generation) AKA:
plasminogen activator
streptokinase and urokinase (first generation) used to treat
MI, pulmonary embolism, acute ischemic stroke
the adverse effect of thrombolytic drugs
bleeding in the GIT and cerebral hemorrhage
Anticoagulant drugs reduce
Cutting ability of blood
What is the most common anticoagulant?
Heparin, warfarin
What is the drug of choice for rapid anticoagulant affect
Warfarin heparin
LMWHs ex.
Tinzaparin , enoxaparin, dalteparin , fondaparinux
What is the short fragments of heparin is called?
Low molecular weight heparin
What is the molecular weight for LMWH and heparin
LMWH -> 1k-10k
Heparin -> 15k
Hebron and all other LMWH call biologically drive from
Where as
Animal tissue
Whereas fundaparinux is synthesize
What is the administration of heparin? And what is the administration that contraindicated? And why? 
Parenterally
Intravenously or subcutaneous
IM is contradicted because it causes hematoma formation
What is the mechanism of action of heparin?
1- Find two antithrombin III -> induce conformational change that interact with coagulation factors
2- catalyze inhibition of thrombin
-> heparin -cofactor II and Xa
-> LMWH - cofactor Xa
Pharmacokinetics of a heparin
- Not absorbed from GIT
- Given intravenously or subcutaneously
- Produce immediate action if it’s given intravenously
- delay happened to 60 minutes if it’s given subcutaneously
Pharmacokinetics of warfarin
Absorbed rapidly, and completely from the G.I. system
Given oral or rectal administration
Anticoagulant test and antidote of heparin
APTT
Antidote, protamine sulfate
Anticoagulant test and antidote of warfarin
INR
Antidote, vitamin K
What is the adverse affect of heparin?
Bleeding
Thrombocytopenia
Hypersensitive reaction
Hyperaldosteronism
Hyperkalemia
Alopecia after 5 to 10 days
( Osteoporosis
Diminished renal function —> for longer than three months)
spontaneous fractions, if it’s used for more than six months
Advantage of LMWH
Better bioavailability
Longer duration
Predictable plasma level
Lower risk of bleeding
Lower incidence of thrombocytopenia
LMWH contraindication
Renal failure patient
Therapeutic uses for heparin and LMWH
Prevention and treatment of Venus thrombosis and pulmonary embolism
Prevention of thrombosis after myocardial infarction
Treatment of patient with unstable angina and MI
