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Pharmacology of The Blood

Pharmacology of The Blood

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Published by Sarah Ahmed
Last lecture for Dr. Rawan
Last lecture for Dr. Rawan

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Categories:Types, School Work
Published by: Sarah Ahmed on Dec 17, 2012
Copyright:Attribution Non-commercial


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Pharmacology of the blood
Last lecture we talked about thromboembolic disorders (pathologicdisorders).
Physiological thrombus: is important to stop bleeding.
Pathological thrombus: diseases like:
DVT (deep venous thrombosis).
PE (pulmonary embolism).
Ischemic stroke.
MI (myocardial Infarction).These are known as
thromboembolic disorders
in which we try toprevent thrombosis by different mechanisms:1.
Drugs that inhibit platelet aggregation and adhesiveness. Plateletsplay an important role for thrombus or clot formation.2.
Drugs that inhibit the action of the clotting factors.
Either drugs that are given parenterally (E.g., heparin), it will activate antithrombin III which is an endogenousprotease which activity is increased by heparin.)Antithrombin III will cause degradation of thrombin IIa andX.
Or drugs that are given orally (E.g., warfarin). Another typeof anticoagulants and it inhibits the synthesis of vitamin k dependent clotting factors. It has a delayed onset of actionbecause its site of action is in the liver, its effect is seen afterthe already synthesized clotting factors are depleted, and bythat it has a delayed onset of action. It is not used duringpregnancy because it can cross the placenta(teratogenicity).
At the end of the last lecture we talked about the differences betweenheparin and warfarin.
Heparin WarfarinOnset of actionRapid DelayedDuring pregnancySafe TeratogenicityRoot of administrationParenterally OrallyActive invivo and vitro vivoMonitored byLab test aptt PT prothrombin timeMOAActivates antithrombin III Inhibits synthesis of vitamin Site of action- Liver
 Antiplatelet drugs
drug (slide#30) will just remind you of aspirin”
Exam question: NSAIDs inhibit the synthesis of prostaglandins. How?
They inhibit the enzyme COX (cyclo-oxygenase). Most of them are non-selective, so they inhibit both COX1 and COX2.
 Aspirin has a major peculiar effect; it has anantiplatelet effect comparing with other NSAIDs, why?
Because it irreversibly inhibits COX1. Cox1 is important in theproduction of thromboxane A2, which is responsible to causevasoconstriction, and it will enhance platelet aggregation andadhesiveness. So once I block the synthesis of thromboxane A2 I caninhibit platelet aggregartion and platelet function.
Why does a low dose of aspirin have an antiplatelet effect?
We have COX1 and COX2, we have thromboxane A2 and prostaglandini2. The action of thromboxane A2 is opposite to the action of prostaglandin i2. Thromboxane A2 stimulates platelet activation andaggregation as well as vasoconstriction, while prostaglandin i2 or
prostacyclin inhibits platelet aggregation and induces vasodilatation.Low doses of aspirin will inhibit thromboxane A2, and prostacyclineffect is kept intact, and this is what we need; only inhibition of thromboxane A2 that is responsible for platelet aggregation. We do not want to inhibit prostacyclin because prostacyclin effect is important toinhibit platelet aggregation. Low doses inhibit thromboxane A2 morethan prostacyclin or prostaglandin i2. The higher doses of aspirin caninhibit both. We will use its inhibitory effect on thromboxane A2. So it ispreferred as an antiplatelet. Most boxes come in a dose between 80 and150 and some boxes say 80 to 180 mg. This is the dose that will have anantiplatelet effect. It was known in the past as baby aspirin (small doseof aspirin). It is important to be taken daily usually in the elderly people,especially males with a history of smoking, hypertension, diabetes,thromboembolic disorders including MI or stroke. So those individualshave higher chances to develop arterial thrombosis which can beinhibited by aspirin. They should take aspirin as a prophylactic daily(small dose) if aspirin is not contraindicated (peptic ulcer or bronchialasthma).Thromboxane A2 synthesis
doesn’t recover until the affected platelets
are replaced by new ones after 7 to 10 days. The affect of aspirin andother antiplatelets is prevention of arterial thrombosis, becauseplatelets play an important rule for thrombus formation in the arterialside.There are other types of antiplatelets that work with different mechanisms (E.g., ADP receptor antagonists, esterase inhibitors, etc...)The most important adverse effect of antiplatelets will be bleeding.We have another type of antiplatelets that are more expensive thanaspirin, and their adverse effects of bleeding are less than aspirin.Another example is tropix (Plavix, Ticlid).

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