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262B Pharmacology > L9 - Antiplatelet and Anticoagulant > Flashcards

L9 - Antiplatelet and Anticoagulant Flashcards

1
Q

What is haemostasis?

A

process which causes bleeding to stop

- first stage of wound healing

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2
Q

What does haemostasis involve?

A

platelet activation and adhesion - forms clot

blood coagulation - fibrin formation which reinforces clot

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3
Q

What are the components of the coagulation cascade? What types of drugs have effect in each part?

A 
fast process
- platelet plug formation 
- antiplatelets
slow process
- fibrin clot formation 
- anticoagulants
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4
Q

What are the 3 stages in clot formation?

A

1 - platelet adhesion
2 - platelet shape change
3 - fibrin stabilises platelets

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5
Q

What is happens in the 1st step of clot formation?

A
  • decreased prostacyclin (PGI2) production from damaged endothelial cells (vessel damage)
  • platelets arrive at site + aggregate
  • aggregated platelets produce thrombin
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6
Q

What happens in the 2nd step of clot formation?

A
  • thrombin released from platelets in 1st step:
  • activates further platelets = reinforce platelet plug
  • binds to receptors causing increased intracellular Ca2+ in platelets = shape change + activate
  • activated platelets release platelet chemotactic agents (ADP + TXA2)
    = aggregation and reinforcement of clot
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7
Q

What happens in the 3rd step of clot formation?

A
  • thrombin (released from platelets in 1st step) conversion of fibrinogen to fibrin
  • fibrin fibres bind together to form fibrous clot = stabilises clot
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8
Q

What are the platelet chemotactic agents and where are they released from?

A
  • ADP and TXA2

- released from activated platelets

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9
Q

What effects does TXA2 (thromboxane A2) have?

A
  • platelet chemotactic agent

- causes vasoconstriction at the site of injury

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10
Q

Why is clot formation important?

A

it is involved in the pathology of cardiovascular disease

- causes thickening and narrowing of blood vessels + reduced blood flow to organs e.g. heart, brain

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11
Q

What are the uses of anticoagulants and antiplatelets?

A

they are used in preventative treatment of angina or TIA or as post-MI treatment

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12
Q

What are the three main causes of intravascular thrombi?

A
  • hyper-coagulation (genetic)
  • endothelial damage (hypertension)
  • stasis (atrial fibrillation)
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13
Q

What are the drugs that can prevent thrombosis and what part of the clotting cascade do they act?

A
  • antiplatelets: reduce platelet aggregation
  • anticoagulants: reduce blood coagulation (fibrin formation)
  • fibrinolytic drugs: increase fibrin breakdown
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14
Q

How do antiplatelets exert their effect?

A

inhibit platelet aggregation by:
- preventing the formation of chemotactic agents
- inhibiting the receptors the chemotactic agents act on
= reduces risk of thrombus formation

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15
Q

What is an antiplatelet drug?

A

low dose aspirin

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16
Q

What is a low dose of aspirin (range)?

A

75-150 mg/day

17
Q

What is the mechanism of action for aspirin?

A
  • irreversibly and non-selectively inhibits COX enzymes
  • inhibiting COX1 reduces TXA2 production
  • TXA2 is a chemotactic agent recruiting more platelets to endothelial injury site
18
Q

Why is it important to use low dose aspirin in antiplatelet treatment?

A

low dose only has effect on the platelets (COX1) in the portal circulation
high dose will be able to reach systemic circulation where it will effect platelets (COX1) AND vascular endothelium (COX2)

19
Q

What are the effects of COX1 in the clot formation?

A

COX1 produces TXA2 which promotes platelet aggregation and vasoconstriction
this initiates thrombus/clot formation
- good to inhibit with antiplatelet

20
Q

What are the effects of COX2 in clot formation?

A
  • COX2 produces PGI2 (prostacyclin)
  • PGI2 is an endogenous antiplatelet mediator as it reduces COX activity
  • PGI2 inhibits platelet aggregation and promotes vasodilation thus inhibits thrombus/clot formation
  • not good to inhibit with antiplatelet
21
Q

What are the side effects of aspirin?

A
  • well tolerated
  • not for people allergic to NSAIDs
  • can increase risk of gastric bleeding
  • not associated with significant oerative bleeding (dental procedures)
22
Q

What is an anticoagulant drug?

A

heparin and warfarin

23
Q

What is the mechanism of action for heparin?

A
  • increases the action of anti-thrombin III (AT-III)
  • increased AT-III binding to prothrombin and thrombin, and factor Xa
  • this prevents fibrin formation = prevents clot formation
24
Q

What is the antagonist for heparin? How does it work?

A

protamine sulphate

  • it binds with heparin to form an inactive complex
  • prevents binding to substrates
25
Q

What are the adverse effects of heparin?

A

haemorrhage

26
Q

What is the mechanism of action for warfarin?

A
  • inhibits vitamin K epoxide reductase
  • prevents reduction of vitamin K to active form
  • prevents vitamin K from activating clotting factors e.g. prothrombin
  • reduces fibrin formation
27
Q

How is warfarin administered and duration of action?

A
  • orally

- 2-5 days (given with heparin because it has instant effect while waiting for warfarin effect)

28
Q

How is the effect of warfarin able to be reversed? (4)

A
  • withdraw therapy (but has persistent action)
    reversal therapy:
  • vitamin K administration (slow acting)
  • fresh frozen plasma (fast acting, large volume required)
  • prothrombinex-VF (freeze dried factors, small volume required, expensive)
29
Q

What are the side effects of anticoagulants?

A 
- narrow TI
due to reduced clotting:
- haemorrhage
- GI bleeding
- bruising
- bleeding noses
metabolised via CYP450 drugs 
- many drug interactions (elderly)
30
Q

How is the development of adverse effects of anti-coagulants reduced?

A

INR - compare patient clotting time to normal healthy individual (~1)
- should be 2-4

31
Q

When are fibrinolytics used? How do they work?

A

when thrombus/clot already formed e.g.

  • MI: must give within 6 hours
  • stroke: must give within 4 hours
32
Q

What is an example of a fibrinolytic?

A

Recombinant Tissue Plasminogen Activator (rtPA)

e.g. alteplase

33
Q

What is the mechanism of action of alteplase?

A

it is a serine protease

  • converts plasminogen to plasmin
  • plasmin breaks down the clot (fibrin)
34
Q

How do fibrinolytics produce their effect?

A
  • increase thrombus/clot breakdown
35
Q

What is the adverse effect of fibrinolytics?

A

bleeding

262B Pharmacology (18 decks)

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