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notes to flashcards year 2 - LCRS1 > haemostasis and thrombosis > Flashcards

haemostasis and thrombosis Flashcards

1
Q

what are the different plasma clotting factors?

A
  • pro-coagulants: prothrombin, F5, F7-F13, fibrinogen

- anti-coagulants: plasminogen, TFPI, Protein C/S, antithrombin

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2
Q

what is the difference between haemostasis and thrombosis?

A

haemostasis - physiological process

thrombosis - pathophysiological process

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3
Q

what are venous thromboses and where do they form?

A
  • red thrombi
  • high fibrin
  • forms within blood vessel lumen
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4
Q

what are arterial thromboses? where do they form?

A
  • white thrombi
  • high platelets
  • thrombus forms within atherosclerotic plaque
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5
Q

what is Virchow’s triad?

A
  1. rate of blood flow (slow = no replenishment of anti-coagulant factors)
  2. consistency of blood (natural imbalance b/ pro and anticoagulation)
  3. blood vessel wall integrity (damage - exposure to collagen)
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6
Q

what is the cell based theory of coagulation?

A
  1. initiation - small scale production of thrombin
  2. amplification - large scale production of thrombin (on platelet surfaces)
  3. propagation - generation of fibrin strands by thrombin
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7
Q

what drugs target initiation?

A

anti-coagulants

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8
Q

what drugs target amplification?

A

anti-platelets

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9
Q

what drugs target propagation?

A

thrombolytics

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10
Q

what does tissue factor do?

A
  • TF bearing cells activate F10 and F5 forming prothrombinase complex
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11
Q

what is the prothrombinase complex?

A
  • activates F2 (pro-thrombin), forming thrombin
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12
Q

what does antithrombin do?

A

inactivates F10a and thrombin

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13
Q

name 4 anticoagulant drugs and what they do

A
  • dabigatran: inhibits thrombin (oral)
  • rivaroxaban: inhibits F10a (oral)
  • heparin: activates antithrombin (IV, SC)
  • warfarin: vit K antagonist, Vit K creates F2,7,9,10 (oral)
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14
Q

what are the indications for drug use?

A
  • DVT and PE
  • thrombosis during surgery
  • atrial fibrillation - prophylactic to strokes
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15
Q

what does thrombin do?

A

thrombin activates platelets in a +ve feedback effect

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16
Q

describe an activated platelet

A
  • changes shape

- platelets become sticky and attaches other platelets

17
Q

describe the steps to platelet activation

A
  1. thrombin binds to PAR (protease activated receptor)
  2. PAR activation –> rise in intraceullar Ca
  3. PAR activation also liberates arachidonic acid, turned into TXA2 by COX
  4. TXA2 induces expression of G1p2b/3a –> aids platelet activation
  5. raised Ca –> exocytosis of ADP dense granules
  6. ADP binds to another platelets P2Y12R –> activates platelets
18
Q

state the 3 antiplatelet drugs

A

Clopidogrel - ADP/ P2Y12R antagonist (oral)
Aspirin - irreversible COX1 inhibitor (oral)
Abciximab - GIp2b/3a antagonist (IV, SC)

19
Q

what are the indications for us of the antiplatelet drugs?

A

arterial thrombi

  • acute coronary syndromes (MI)
  • atrial fibrillation: prophylaxis of strokes
20
Q

what do activated platelets do in propagation?

A

large scale production of thrombin

21
Q

what does thrombin do in propagation?

A

thrombin binds to fibrinogen and converts it to fibrin strands

22
Q

name a thrombolytic drug and what it does

A

Alteplase - recombinant tissue-type plasminogen activator (rt-PA)

  • oral
  • plasminogen analogue
  • converts plasminogen to plasmin
  • this degrades fibrin and dissolves clot
23
Q

what are the indications for thrombolytic use?

A
  • stroke = 1st line

- ST elevated MI

24
Q

what is a DVT?

A

a red thrombus of deep veins of leg e.g. popliteal vein

25
Q

what is a DVT caused by?

A
  • stasis of blood

- damage to endothelium

26
Q

what is a PE?

A

thrombus detachment

27
Q

what is the management of DVT/PE?

A
  • reduce levels of anticoagulant factors
  • anticoagulants
  • e.g. Dabigatran, Rivaroxaban, Heparin, Warfarin
28
Q

what is a NSTEMI?

A

Non-ST-Elevated MI

29
Q

what is a NSTEMI caused by?

A 
caused by white thrombus
partially occluded coronary artery
- damage to endothelium
- platelet aggregation
- atheroma formation
30
Q

what is the management of a NSTEMI?

A
  • reduce lipid formation and platelet aggregation/activation
    = antiplatelets
    e.g. Clopidogrel, aspirin
31
Q

what is a STEMI?

A

ST elevated MI

32
Q

what is a STEMI caused by?

A
  • white thrombus
  • fully occluded coronary artery
  • damage to endothelium
  • atheroma formation
  • platelet aggregation
33
Q

what is the management of STEMIs?

A
  • reduce lipid formation, platelet aggregation/activation and dissolve thrombus
    = antiplatelets, thrombolytics
34
Q

what is the treatment if a clot is suspected?

A

thrombolytics

35
Q

what is the treatment if a clot is suspected to form in future in venous system?

A

anticoagulants

36
Q

what is the treatment if a clot if suspected to form in the future in arterial system?

A

antiplatelets

notes to flashcards year 2 - LCRS1 (58 decks)

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