Arterial Thrombosis and Anti-platelet Drugs

Question 1

arterial thrombosis (3)

Answer 1

=high pressure system​
=atherosclerosis​
=platelet rich thrombus​

Question 2

arterial thrombosis- treatment

Answer 2

aspirin and other anti-platelet drugs​modify risk factors for atherosclerosis​

Question 3

atherosclerosis (4)

Answer 3

not the same as arterial thrombosis​

damage to endothelium​

recruitment of ‘foamy’ macrophages rich in cholesterol​

forms plaques rich in cholesterol​

Question 4

stable atherosclerotic plaques (2)

Answer 4

hyalinised and calcified​

stable plaques: stable angina (coronary artery), intermittent claudication (leg artery)

Question 5

unstable atherosclerotic plaques​ (4)

Answer 5

plaques rupture, platelets are recruited and cause acute thrombosis​

sudden onset of symptoms​

unstable angina or myocardial infarction (coronary arteries)​

stroke (cerebral arteries)

Question 6

platelets and arterial thrombosis​ (4)

Answer 6

Plaque ruptures – more likely high pressure environment of arteries​

Platelet adheres to it – exposed endothelium + release of Von Willebrand factor​

Platelets becomes activated - release granules that activate coagulation and recruit other platelets to developing platelet plug​

Platelet aggregation via membrane glycoproteins​

Question 7

risk factors for arterial thrombosis (4)

Answer 7

Hypertension= (damage to endothelium, platelet activation)​

Smoking= (endothelium, platelets)​

High cholesterol= (accumulated in plaque)​

Diabetes mellitus =(endothelium, platelets, cholesterol)​

Question 8

prevention of arterial thrombosis (5)

Answer 8

Stop smoking​

Treat hypertension​

Treat diabetes​

Lower cholesterol​

Anti-platelet drugs​

Question 9

platelet - adhesion

Answer 9

Platelets bind to subendothelial collagen via Glycoprotein 1b and Von Willebrand Factor

Question 10

platelet- aggregation

Answer 10

Platelets attach to each other via GPIIbIIIa and fibrinogen, at the same time…

Question 11

platelet- activation (3)

Answer 11

platelets alter shape to expose more phospholipid on the surface-provides a greater surface area for coagulation activation + fibrin production to stabilise the clot

process augmented by release of granules that stimulate platelet activation eg (thrombin ,thromboxane A2 and ADP)

occurs via receptors to ADP etc on the platelet surface

Question 12

aspirin- mech action

Answer 12

Inhibits cyclo-oxygenase which is necessary to produce Thromboxane A2 (a platelet agonist released from granules on activation)

Question 13

aspirin- side effects (4)

Answer 13

1. Bleeding​
2. Blocks production of prostaglandins=
   -GI ulceration​
   -Bronchospasm

Question 14

clopidogrel + prasugrel - mech of action

Answer 14

ADP receptor antagonists

Question 15

dipyridamole- mech of action

Answer 15

phosphodiesterase inhibitor - increases production of cAMP which inhibits platelet aggregation.​

Question 16

abciximab- mech of action

Answer 16

GP IIb/IIIa inhibitors - inhibit aggregation

Question 17

bleeding​ (3)

Answer 17

anti-platelet drugs affect platelet function for their 7-10 day life span​

stop anti-platelet agents 7 days prior to elective operations​

serious bleeding - reverse with platelet transfusion

Question 18

Arterial thrombosis - conclusion (3)

Answer 18

causes organ ischaemia and is an inflammatory disorder instigated by damage to the endothelium​

platelets are central and are recruited to ruptured plaques ​

antiplatelet drugs are useful in prevention

Question 19

Venous thrombosis- conclusion (3)

Answer 19

occurs in a low pressure system mainly by stasis​

platelets are not largely involved, and clots are rich in fibrin​

anticoagulants are useful in prevention​