Anti Platelet drugs Flashcards

1
Q

what causes artterial thrombosis

A

lipid deposits in endothelium
damage to endothelium of arteries recruits foamy macrophages rich in cholesterol
forms cholesterol rich plaque
high pressure system causes plaques to rupture
platelets recruited, adhere to expose endothelium and released VWf
platelets become activate - release granules that activate coagulation (more platelets come and form platelet plug)
causes acute thrombosis

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2
Q

how do platelets aggregate

A

via membrane glycoproteins (GPIIbIIIa) and fibrinogen

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3
Q

what type of thrombus in aterial disease

A

platelet rich

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4
Q

what is the treatment for arterial thrombosis

A

aspirin (+ other anti platelet drugs)

modification of risk factors (HPTx, diabetes, smoking)

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5
Q

what are atherosclerotic plaques rich in

A

cholesterol

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6
Q

what are stable atherosclerotic plaques like

A

hyalinised and calcified

cause stable angina (in coronary artery), intermittent claudication (leg artery)

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7
Q

what do unstable atherosclerotic plaques cause

A

when rupture cause: sudden onset of symptoms, unstable angina/ MI
stroke
=acute organ ischaemia and infarction

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8
Q

what are the risk factors for arterial thrombosis

A

(factors that cause damage to the endoethelium, increase in foamy macrophages and platelet activation)

  • hypertension (damage to endothelium, platelet activation)
  • smoking (endothelium (raises BP), platelets)
  • high cholesterol (accumulated in plaque)
  • diabetes (endothelium damage, platelets, cholesterol)
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9
Q

how do you prevent arterial thrombosis

A

stop smoking
treat hypertension and diabetes
lower cholesterol
anti platelet drugs

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10
Q

how are vessels damaged in Venous thrombosis

A

valves damaged (not atheromas like in arterial)

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11
Q

what do platelets do in arterial disease

A

adhere at site of injury to exposed collaged with help of VWf
activate and secrete chemicals (ADP, thromboxan A2) which causes aggregation at site of injury

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12
Q

how do platelets bind to subendothelial collagen

A

glycoprotein 1b and VWf

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13
Q

what happens in platelet activation

A

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

also release of granules (thrombin, thromboxane A2, ADP) which further stimuates platelet activation and recruitment (via ADP receptors on platelet surface)

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14
Q

how does aspirin work

A

inhibits cyclo-oxygenase which is needed to produce throboxane A2 (platelet agonist released from granules, attracts other to site of injury)

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15
Q

what are the side effects of aspirin

A

bleeding
blocks production of prostaglandins:
-GI ulceration (prostaglandins provide protective surface in the stomach, blockage of this more likely to get ulcer, and as on antiplatelet more likely to bleed from this)
-bronchospasm (having asthma a CI to aspirin)

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16
Q

what are the type of anti platelet drugs

A

aspirin (cyclo-oxygenase inhibitor)

clopidogrel and prasugrel (ADP receptor antagonists)

dipyridamole (phosphodiesterase inhibitor: reduces cAMP production which is a second messenger in platelet activation)

abciximab (GP IIb/IIIa inhibitors - inhibit aggregation)

17
Q

when is abciximab or other GP IIb/IIIa inhibitors used

A

as emergency medication e.g. if having MI surgery

18
Q

how long do anti platelet drugs have an effect for

A

the whole of affected platelets life span: 7-10 days

stop them 7 days prior to elective operations

19
Q

how can anti platelet drugs be reversed

A

platelet transfusions

20
Q

Causes organ ischaemia and is an inflammatory disorder instigated by damage to the endothelium
= arterial or venous?

A

arterial

21
Q

are platelets involved in venous thrombosis

A

no