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Pharmacology > Haemostasis and thrombosis > Flashcards

Haemostasis and thrombosis Flashcards

1
Q

What is haemostasis?

A

Essential physiological process.

Blood coagulation prevents excessive blood loss.

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2
Q

What is thrombosis?

A

Pathophysiological process.

Blood coagulates within blood vessels and obstructs blood flow.

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3
Q

What are the procoagulants (plasma clotting factors)?

A

Prothrombin
Factors V, VII-XIII
Fibrinogen

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4
Q

What are the anticoagulants (plasma clotting factors)?

A

Plasminogen
TFPI (tissue factor pathway inhibitor)
Proteins C and S
Antithrombin

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5
Q

What is atherosclerosis?

A

Pathophysiological process.

Thrombus forms within atherosclerotic plaque.

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6
Q

When may a clot become life-threatening?

A

If it dislodges from the vessel- embolism.

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7
Q

What is a feature of venous thromboses?

A

High fibrin components
High erythrocyte content
(Red thrombi)

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8
Q

What is a feature of arterial thromboses?

A

High platelet components
High lipid content
(White thrombi)

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9
Q

Why does a thrombus form?

A

Virchow’s triad.

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10
Q

What is Virchow’s triad?

A

Rate of blood flow.
Consistency of blood.
Blood vessel wall integrity.

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11
Q

What is the cell-based theory of coagulation?

A

Three stages: initiation, amplification, propagation.

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12
Q

What is involved in the initiation stage of the cell-based theory of coagulation?

A

Small scale production of thrombin.
Tissue factor bearing cells activate factors X and V, forming prothrombinase complex.
Prothrombinase complex activates factor II (prothrombin) creating factor IIa (thrombin).
Antithrombin (AT-III) inactivates factors IIa and Xa.
Anticoagulants work here.

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13
Q

What is involved in the amplification stage of the cell-based theory of coagulation?

A

Large scale thrombin production on the surface of platelets.
Factor IIa (thrombin) activates platelets.
Activated platelets change shape and become ‘sticky’, attaching other platelets.
Antiplatelets work here.

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14
Q

What is involved in the propagation stage of the cell-based theory of coagulation?

A

Thrombin mediated generation of fibrin strands from fibrinogen.
Activated platelets are involved in large-scale thrombin production.
Thrombolytics work here.

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15
Q

What are the constituents of blood?

A 
Blood cells (45%)- 99% erythrocytes.
Blood plasma (55%)- 90% water.
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16
Q

How does the rate of blood flow affect the risk of thrombus formation?

A

If blood flow is slow/stagnating, there is slow turnover of clotting factors- no replenishment of anticoagulant, balance adjusted in favour of coagulation.
e.g. long haul flight, DVT.
Increased likelihood of thrombus formation.

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17
Q

How does the consistency of blood affect the risk of thrombus formation?

A

Natural imbalance between pro-coagulation and anticoagulation factors, e.g. factor V leiden.
Increased likelihood of thrombus formation.

18
Q

How does the blood vessel wall integrity affect the risk of thrombus formation?

A

Damaged endothelia leads to blood being exposed to pro-coagulation factors. Increased likelihood of thrombus formation.

19
Q

What is dabigatran?

A

Factor IIa inhibitor
Oral
Inhibits initiation phase of cell-based theory of coagulation.

20
Q

What is rivaroxaban?

A

Factor Xa inhibitor
Oral
Inhibits initiation phase of cell-based theory of coagulation.

21
Q

What is heparin?

A

Activates AT-III (decreased factors IIa and Xa)
i.v., s.c.
Inhibits initiation phase of cell-based theory of coagulation.

22
Q

What are low molecular weight heparins?

A

Activate AT-III (decreased Xa)
e.g. dalteparin
Inhibits initiation phase of cell-based theory of coagulation.

23
Q

What is warfarin?

A

Vitamin K antagonist
Vitamin K is required for generation of factors II, VII, IX and X.
Oral
Inhibits initiation phase of cell-based theory of coagulation.

24
Q

List anticoagulant drugs.

A

Dabigatran
Rivaroxaban
Heparin
Low molecular weight heparins, e.g. dalteparin
Warfarin
These inhibit initiation phase of cell-based theory of coagulation.

25
Q

What are the indications for anticoagulant use?

A

Venous thrombosis
DVT and pulmonary embolism
Thrombosis during surgery
Atrial fibrillation- prophylaxis of stroke

26
Q

How does platelet activation occur?

A

Thrombin binds to protease-activated receptor (PAR) on platelet surface.
PAR activation leads to a rise in intracellular calcium.
Calcium rise leads to exocytosis of ADP from dense granules.
ADP activates P2Y receptors, leading to platelet activation/aggregation.
PAR activation liberates arachidonic acid.
COX generates thromboxane A2 from arachidonic acid.
Thromboxane A2 activation leads to expression of GPIIb/IIIa integrin receptor on platelet surface. GPIIb/IIIa is involved in platelet aggregation.

27
Q

What is clopidogrel?

A

ADP (P2Y) receptor antagonist.
Oral
Prevents platelet activation/aggregation.
Inhibits amplification phase of cell-based theory of coagulation.

28
Q

What is aspirin?

A

Irreversible COX-1 inhibitor.
Oral
Inhibits production of thromboxane A2.
Inhibits amplification phase of cell-based theory of coagulation.

29
Q

What is abciximab?

A

Prevents platelet aggregation.
i.v., s.c.
Limited use, only by specialists.
Inhibits amplification phase of cell-based theory of coagulation.

30
Q

List anti-platelet drugs.

A

Clopidogrel
Aspirin
Abciximab

31
Q

What are the indications for anti-platelet drug use?

A

Arterial thrombosis
Acute coronary syndromes- myocardial infarction
Atrial fibrillation- prophylaxis of stroke

32
Q

What is the mechanism of thrombolytic drug action?

A

Convert plasminogen to plasmin.
Anticoagulants and anti-platelets do not remove pre-formed clots.
Plasmin- protease degrades fibrin.

33
Q

Name a thrombolytic drug.

A

Alteplase
A recombinant tissue type plasminogen activator (rt-PA)
i.v.

34
Q

What are the indications for thrombolytic drug use?

A

Arterial and venous thrombosis
Stroke- first-line treatment
ST-elevated MI

35
Q

What causes DVT and pulmonary embolism?

A

Decreased rate of blood flow

Damage to endothelium

36
Q

How is DVT and PE managed?

A

Restore balance between coagulants and anticoagulants.
Decrease levels of anticoagulant factors
Use anticoagulant drugs.

37
Q

What is NSTEMI?

A

Non-ST elevated myocardial infarction.
Acute coronary syndrome.
White thrombus- partially occluded coronary artery.

38
Q

What causes NSTEMI?

A

Damage to endothelium
Atheroma formation
Platelet aggregation

39
Q

What is STEMI?

A

ST elevated myocardial infarction.
Acute coronary syndrome.
White thrombus- fully occluded coronary artery.

40
Q

What causes STEMI?

A

Damage to endothelium
Atheroma formation
Platelet aggregation

41
Q

How is NSTEMI managed?

A

Prevent further arterial occlusion.
Decrease platelet activation/aggregation.
Anti-platelets.

42
Q

How is STEMI managed?

A

Prevent death.
Decrease platelet activation/aggregation.
Dissolve clot.
Anti-platelets and thrombolytics.

Pharmacology (21 decks)

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