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Antiplatelets & Antithrombotics Flashcards

(19 cards)

1
Q

What causes atherosclerotic plaque?

A

an excess of cholesterol

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2
Q

What happens if a thrombus ruptures and breaks off?

A

The embolus could get lodged in the capillaries and block the blood flow.
Could cause damage to organs downstream

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3
Q

Damaged endothelial layers stimulate thrombus formation. What can cause this damage?

A
  • atherosclerosis of arteries

- physical damage caused by balloon angioplasty and stenting

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4
Q

What happens if a thrombus ruptures in an artery that peruses the brain?

A
  • embolus gets stuck in cerebral capillary

- acute ischemic stroke

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5
Q

What happens if a thrombus ruptures in an artery that perfuses the heart?

A
  • embolus gets stuck in the coronary artery

- acute MI

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6
Q

What happens if a venous thrombosis ruptures?

A
  • embolus gets stuck in the lung capillaries

- pulmonary embolism

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7
Q

Where are the 2 main sites that venous clots form?

A
  • lower leg veins

- right atria

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8
Q

Why don’t anti-platelet drugs work in the veins?

A

because clots in the veins involve RBCs, not platelets

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9
Q

What are the 3 parts of formation of a platelet plug?

A
  • platelet aggregation
  • platelet activation
  • platelet adhesion
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10
Q

What is the purpose of coagulation?

A
  • stabilize the platelet plug (clot)

- thrombin increases fibrin formation (reinforces plug)

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11
Q

What is fibrinolysis?

A
  • when the clot dissolves

- as the wound heals, it will destroy the clot

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12
Q

Name 3 platelet inhibitors and the mechanism.

A

Aspirin - COX inhibitor
Clopidogrel - ADP receptor blocker
Abciximab - GP IIb/IIIa blocker

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13
Q

Name 4 anticoagulants and their mechanism

A

Heparin - thrombin inhibitor
Warfarin - vitamin K antagonist
Dabigatran - thrombin antagonist
Rivaroxaban - factor Xa inhibitor

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14
Q

Name a thrombolytic agent.

A

tPA –> tissue plasminogen activator

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15
Q

What helps turn fibrinogen into fibrin?

A

thrombin

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16
Q

What helps fibrin break down?

17
Q

How can you prevent the formation of a platelet plug?

A
  1. selective change in PG levels
    - increase/maintain endothelial prostacyclin
    - decrease TXa2 levels in platelets
  2. block effects of released mediators
    - block ADP receptors–> blocks GPIIb/IIIa
  3. prevent GPIIb/IIIa receptor coupling
    - block receptor
18
Q

Aspirin blocks COX, how does this work to be a platelet inhibitor?

A
  • COX block PGI2 and TXa2
  • PGI2 inhibition –> platelets more stable, less aggregation
  • TXa2 inhibition –> platelets less sticky
19
Q

How do clots in the veins and arteries differ?

A

Arteries –> platelet-rich

Veins –> RBC-rich