B.6 Platelets and Thrombosis

Question 1

What are platelets?

Answer 1

Non-nuclear cellular fragments

Question 2

Pharmacologically describe the platelet adhesion process

Answer 2

1. Damage occurs exposing the subendothelial surface of the Vascular smooth muscle.
2. Platelets begin to stick which leads to aggregation reaction
3. This causes the release of mediators such as ADP, Thromboxane, and 5-HT.
4. Thromboxane stimulates other platelets to aggregate and stick together in the affected area
5. The release of serotonin causes vasoconstriction and reduces blood loss

Question 3

Continuation: Pharmacologically describe the platelet aggregation process

Answer 3

6. ADP binds to platelet receptors
7. this leads to the expression of glycoprotein IIb-IIIa
8. Glycoprotein IIb and IIIa binds to VWF and fibrinogen
9. This leads to the cross-linking of platelets

Question 4

What is venous thrombosis and what are the consequences?

Answer 4

Clots form in veins due to stasis of blood. may travel to the lungs and cause pulmonary embolism

Question 5

What is arterial thrombosis and what can it cause?

Answer 5

Thrombosis formed at the atherosclerotic site leads to arterial blockage causing a heart attack and stroke

Question 6

How can atherosclerosis associated disorders reverse/slow down

Answer 6

Using statins and lifestyle changes

Question 7

True/False
Venous thrombosis is more of a coagulation factor event leading to deep vein thrombosis

Arterial thrombosis is more of a platelet event causing MI and ischaemic strokes

And what are the key drugs?

Answer 7

True

Venous thrombosis- anticoagulation drug

Arterial thrombosis- antiplatelet drugs

Question 8

What is the role of PGI2 in cells?

Answer 8

Prevents platelet aggregation-acts on platelets to increase cAMP

Question 9

What is the role of thromboxane (TXA2) in cells?

Answer 9

Promotes aggregation, decreasing cAMP

Question 10

How does nitric oxide prevent platelet adhesion and aggregation?

Answer 10

The increased platelet cGMP

Question 11

How does aspirin work pharmacologically?

Answer 11

Prevents cyclo-oxygenase enzyme from converting Free AAEndoperoxides which then form PGI, prostaglandins, and thromboxane

This increases intern stops the production of thromboxane which causes platelets to stick

Question 12

When taking aspirin, why is PGI2 production favoured rather than thromboxane production?

Answer 12

Normal cells contain a nucleus meaning mRNA can resynthesis cox enzymes and therefore produce new PGI2

Platelets have no nuclei, therefore, cannot produce more COX until new platelets are synthesized

Question 13

What is the pharmacology of clopidogrel?

Answer 13

Inhibits ADP-induced expression of GP

therefore prevents the crosslinking of platelets

Question 14

How does Abciximab pharmacologically work

Answer 14

Monoclonal antibody against GPIIb/IIb

Therefore prevents the crosslinking of platelets