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YR2 LCRS Pharmacology > 16. Haemostasis and thrombosis > Flashcards

16. Haemostasis and thrombosis Flashcards

1
Q

what does blood consist of?

A

blood cells (45%) and blood plasma (55%)

all coagulation factors/clotting factors reside in the plasma

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2
Q

which 2 categories do coagulation factors fall into?

A

PROCOAGULANTS
- promote clotting e.g. prothrombin, factors V, VII-XIII and fibrinogen

ANTICOAGULANTS
- prevent clotting e.g. plasminogen, TFPI, proteins C and S, antithrombin

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3
Q

what is haemostasis?

A

maintaining the balance between procoagulants and anticoagulants

prevents excessive blood loss by ensuring clot formation occurs at the site of injury

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4
Q

what is thrombosis?

A

a pathophysiological process where blood coagulates within a vessel leading to the obstruction of blood flow

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5
Q

where do thrombi form?

A

within the lumen of a vein or attach to the tunica intima of the vessel

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6
Q

what are venous thromboses referred to and why? what are they caused by?

A

red thrombi - they have a high erythrocyte content and high fibrin components

caused by decreased rate of blood flow and damage to the endothelium

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7
Q

what is atherosclerosis?

A

a pathophysiological process where a thrombus forms within an atherosclerotic plaque (between the tunica intima and the tunica media)

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8
Q

what are arterial thromboses referred to and why?

A

white thrombi - they have a high lipid content and high platelet components

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9
Q

what is virchow’s triad? outline it

A

reasons why a thrombus forms:

  1. rate of blood flow
  2. consistency of blood
  3. blood vessel wall integrity
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10
Q

why and when may a thrombus form due to rate of blood flow?

A

blood flow is slow –> no replenishment of anticoagulant factors so balance is tipped towards coagulation

may occur during long haul flights/when someone is immobile for a long time (e.g. injury)

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11
Q

why may a thrombus form due to consistency of blood?

A

there is a natural imbalance between procoagulation and anticoagulation factors (e.g. factor V leiden)

consistency of blood relates to the natural levels of clotting factors

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12
Q

why and when may a thrombus form due to blood vessel wall integrity?

A

damaged endothelia –> blood exposed to procoagulation factors

damage may occur during surgery/in individuals with consistent hypertension

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13
Q

what are the phases of coagulation?

A

INITIATION PHASE: small-scale production of thrombin. It occurs on the surface of tissue factor bearing cells

AMPLIFICATION PHASE: Large-scale production of thrombin, occurring on the surface of platelets

PROPAGATION PHASE: Thrombin mediated generation of fibrin strands. There is enough thrombin to convert fibrinogen to fibrin

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14
Q

what is involved in the initiation phase of coagulation?

A
  1. tissue factor bearing cells activate factors X and V to form the prothrombinase complex (FVa and FXa)
  2. the prothrombinase complex activates factor II (prothrombin) to produce factor IIa (thrombin)
  3. antithrombin (AT-III) comes and inactivates FIIa and FXa
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15
Q

describe some anticoagulant drugs

A

dabigatran - factor IIa inhibitor, taken orally

rivaroxaban - factor Xa inhibitor, taken orally

heparin - activates AT-III (decreasing FIIa and FXa)

low molecular weight heparins: activate AT-III (decrease FXa)

warfarin: vitamin K antagonist (vitamin K is needed to make clotting factors), taken orally

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16
Q

when are anticoagulants used?

A
  • mainly venous thrombosis
  • deep vein thrombosis and pulmonary embolism
  • thrombosis during surgery
  • atrial fibrillation
  • heparin is used in an emergency because it is fast acting
  • warfarin is used in the long term
17
Q

what is involved in the amplification phase of coagulation at a cellular level?

A

PLATELET ACTIVATION AND AGGREGATION

  1. factor IIa (thrombin) –> activates platelets
  2. activated platelet changes shape and becomes ‘sticky’ –> attached to other platelets –> aggregation
18
Q

what is involved in the amplification phase of coagulation at a molecular level?

A
  1. thrombin binds to protease-activated receptor (PAR) on the platelet surface
  2. PAR activation –> rise in intracellular Ca
  3. exocytosis of ADP from dense granules
  4. ATP activates P2Y12 receptors on platelet –> platelet activation/aggregation
  5. PAR activation also leads to liberation of arachidonic acid (AA) and activation of cyclo-oxygenase –> generates thromboxane A2 from AA
  6. thromboxane A2 activation –> expression of GPIIb/IIIa integrin receptor on the platelet surface which is involved in platelet aggregation
19
Q

describe some antiplatelet drugs

A

clopidogrel: ADP (P2Y12) receptor antagonist, taken orally
aspirin: irreversible COX-1 inhibitor that inhibits production of TXA2, taken orally
abciximab: inhibits GPIIb/IIIa

20
Q

when are antiplatelets used?

A
  • arterial thrombosis
  • acute coronary syndromes: MI
  • atrial fibrillation
21
Q

what is involved in the propagation stage of coagulation at a cellular level?

A
  1. large scale thrombin production
  2. thrombin binds to fibrinogen and converts fibrinogen to fibrin stands
    fibrin strands form a net which trap many things to form a solid core
22
Q

what do thrombolytics do? give an example

A
  • convert plasminogen –> plasmin (a protease that degrades fibrin) which dissolves a pre-formed clot

alteplase is a recombinant tissue type plasminogen activator

23
Q

when are thrombolytics used?

A
  • arterial and venous thrombosis
  • stroke (1st line treatment)
  • ST-elevated MI
24
Q

what is the main concern when using thrombolytics?

A

they can cause excessive bleeding

25
Q

what are the 2 types of acute coronary syndromes?

A
  1. non-ST elevated MI (NSTEMI)

2. ST elevated MI (STEMI)

26
Q

what causes NSTEMI?

A
  • ‘white’ thrombus –> partially occluded coronary artery

- caused by damage to the endothelium leading to atheroma formation and platelet aggregation

27
Q

how is NSTEMI managed?

A

prevent further arterial occlusion (decrease platelet activation/aggregation by using anti-platelets): aspirin, clopidogrel

28
Q

what causes STEMI?

A
  • ‘white’ thrombus –> fully occluded coronary artery
  • caused by damage to the endothelium leading to atheroma formation and platelet aggregation
  • more dangerous
29
Q

how is STEMI managed?

A

prevent death:

  • decrease platelet activation/aggregation
  • dissolve clot
  • anti-platelets and thrombolytics

YR2 LCRS Pharmacology (32 decks)

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