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Year 2 - LCRS - Pharmacology > Haemostasis and Thrombosis (22.01.2020) > Flashcards

Haemostasis and Thrombosis (22.01.2020) Flashcards

1
Q

3 stages

A
  1. initiation
  2. amplification
  3. propagation
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2
Q

What is the difference between haemostasis and thrombosis?

A
  • haemostasis is physiological
  • thrombosis is pathological
  • the underlying biological process is basically the same.
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3
Q

What are the types of drugs that are used in thrombotic conditions?

A
  • anticoagulants
  • antiplatelet drugs
  • fibrinolytics/clot busters/
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4
Q

Coagulation: explain the processes of coagulation, platelet activation and the actions of fibrin

A

Initiation - tissue Factor presentation ➡️ Prothrombinase-mediated formation of factor IIa (thrombin)

Amplification - thrombin (fIIa)-mediated platelet activation ➡️ ADP activates P2Y12 receptor ➡️ COX & GPIIb/IIa

Propagation - thrombin-mediated conversion of fibrinogen ➡️ fibrin strands

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5
Q

Atherosclerosis treatment: identify the drugs used in the prevention and treatment of atherosclerosis and the subsequent rupture of an atherosclerotic plaque

A
  • Treatment of atherosclerosis ➡️ antiplatelet drugs*
  • Antiplatelet drugs fall into 3 main categories:
    - COX inhibitors (aspirin)
    - P2Y12 receptor antagonists (clopidogrel)
    - GPIIb/IIIa receptor antagonists (abciximab)
  • Subsequent rupture of atherosclerotic plaque** thrombolytics
  • Thrombolytic drugs (alteplase) ➡️ tissue plasminogen activator
  • Antiplatelets used for prophylaxis, not specifically treatment of atherosclerosis
    • Thrombolytics can be used to treat ruptured plaques but mainly indicated for ischaemic stroke
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6
Q

Atherosclerosis treatment: identify the drugs used in the prevention and treatment of atherosclerosis and the subsequent rupture of an atherosclerotic plaque

A
  • Treatment of atherosclerosis ➡️ antiplatelet drugs*
  • Antiplatelet drugs fall into 3 main categories:
    - COX inhibitors (aspirin)
    - P2Y12 receptor antagonists (clopidogrel)
    - GPIIb/IIIa receptor antagonists (abciximab)
  • Subsequent rupture of atherosclerotic plaque** thrombolytics
  • Thrombolytic drugs (alteplase) ➡️ tissue plasminogen activator
  • Antiplatelets used for prophylaxis, not specifically treatment of atherosclerosis
    • Thrombolytics can be used to treat ruptured plaques but mainly indicated for ischaemic stroke
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7
Q

D-dimer test

A
  • detects fibrin degradation products

- used for DVT

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8
Q

Initial stages of thrombosis

A

Small-scale thrombin production

  1. Tissue factor (TF)
    TF bearing cells activate factors X & V forming ➡️ prothrombinase complex
  2. Prothrombinase complex
    This activates factor II (prothrombin) creating factor IIa (thrombin)
  3. Antithrombin (AT-III)
    AT-III ➡️ inactivates fIIa & fXa
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9
Q

Anticoagulants

A
  1. Inhibit factor IIa
    Dabigatran (oral) - factor IIa inhibitor
  2. Inhibit factor Xa
    Rivaroxaban (oral) - factor Xa inhibitor
  3. Increase activity of AT-III
    - Heparin (IV, SC) - activates AT-III (⬇️fIIa & ⬇️fXa)
    - Low-molecular weight heparins (LMWHs, e.g.Dalteparin) - activate AT-III (⬇️fXa)
  4. Reduce levels of other factors
    Warfarin (oral) - vitamin K antagonist
    Vitamin K - required for generation of factors II, VII, IX & X
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10
Q

What is the double meaning of the term anti-caogulatn?

A
  • can be used to describe all anti-thrombotic drugs (i.e. anticoagulants as well as anti-platelet drugs and fibrinolytic)
  • can be a subgroup of these i.e. the ones that have clotting factors as targets
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11
Q

What drugs would you give to someone with DVT? What about PE?

A

DVT:

  • parenteral dalteparin initially
  • maintenance treatment with warfarin/rivaroxaban

PE:

  • initially: dalteparin/heparin
  • maintenance treatment: RIVAROXABAN / WARFARIN
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12
Q

Dalteparin

A

= low molecular weight heparin

- has a fast onset of action

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13
Q

Virchows triad

A

= factors that increase the likelihood of thrombus formation

  1. Rate of blood flow
    Blood flow slow/stagnating ➡️ no replenishment of anticoagulant factors & balance adjusted in favour of coagulation
  2. Consistency of blood
    Imbalance between pro-coagulation & anticoagulation factors
  3. Blood vessel wall integrity
    Damaged endothelia blood exposed to pro-coagulation factors
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14
Q

What is more severe? A STEMI or an NSTEMI?

A
  • a STEMI is more severe because there is complete occlusion of a coronary artery
  • in an NSTEMI there is partial occlusion of an artery
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15
Q

STEMI vs NSTEMI

A

STEMI

  • ST elevated myocardial infarction
  • ‘White’ thrombus ➡️ fully occluded coronary artery
  • Treatment: antiplatelets & thrombolytics

NSTEMI

  • Non-ST elevated myocardial infarction (MI)
  • ‘White’ thrombus ➡️ partially occluded coronary artery
  • Treatment: antiplatelets

Caused by:

  • Damage to endothelium
  • Atheroma formation
  • Platelet aggregation
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16
Q

White vs. red thrombus

A

White thrombus

  • more likely in arteries
  • white because of foam cells
  • can cause an MI
  • tend to form INSIDE a BV wall

Red Thrombus:

  • more in veins
  • can occur in DVT (and cause a PE)
  • full of RBCs
  • forms in the BV lumen
  • better treated with anticoagulants
17
Q

White vs. red thrombus

A

White thrombus

  • more likely in arteries
  • white because of foam cells
  • can cause an MI
  • tend to form INSIDE a BV wall

Red Thrombus:

  • more in veins
  • can occur in DVT (and cause a PE)
  • full of RBCs
  • froms in the BV lumen
  • better treated with anticoagulants
18
Q

Amplification stage of thrombosis

A

Platelet activation & aggregation

  1. Thrombin
    Factor IIa ➡️ activates platelets
  2. Activated platelet
    - Changes shape (from disk to stellate)
    - Becomes ‘sticky’ and attaches other platelets
19
Q

Amplification - what platelet changes occur during its activation?

A
  • Thrombin - binds to protease-activated receptor (PAR) on platelet surface.
  • PAR activation ➡️ rise in intracellular Ca2+ (release from intracellular stores)
  • Ca2+ rise ➡️ exocytosis of adenosine diphosphate (ADP) from dense granules
  1. ADP receptors
    ADP activates P2Y12 receptors ➡️ platelet activation/ aggregation
  2. Cyclo-oxygenase
    PAR activation ➡️ liberates arachidonic acid (AA)
    Cyclo-oxygenase (COX) generates thromboxane A2 (TXA2) from AA
  3. Glycoprotein IIb/IIIa receptor (GPIIb/IIIa)
    TXA2 activation ➡️ expression of GPIIb/IIIa integrin receptor on platelet surface
    GPIIb/IIIa - involved in platelet aggregation
20
Q

Antiplatelet drugs

A
  1. Prevent platelet activation/ aggregation
    - Clopidogrel (oral) - ADP (P2Y12) receptor antagonist
  2. Inhibit production of TXA2
    - Aspirin (oral) - irreversible COX-1 Inhibitor
    (NB: High doses no more effective BUT more side-effects)
  3. Prevent platelet aggregation
    - Abciximab (IV, SC)
    - Limited use AND only by specialists

There is also a class if drugs that are PAR inhibitors

21
Q

How would you treat a stroke?

A
  • first do a CT to ensure that it is ischaemic and not haemorrhagic
  • then: Thrombolytic therapy ➡️ ALTEPLASE (tPA)

In emergencies you give clot busters. Other drugs will need more time to reduce the size of the clot but in strokes time is of the essence. There is a high risk of excessive bleeding with fibrinolytic which is why they are only used in emergencies.

22
Q

Propagation Stage

A

Generation of fibrin strands

  1. Activated platelets
    Large-scale thrombin production
  2. Thrombin
    Factor IIa ➡️ binds to fibrinogen and converts to fibrin strands
23
Q

Thrombolytics - mechanism

A
  • Anticoagulants & anti-platelets - DO NOT remove pre-formed clots

Thrombolytics

  • Convert plasminogen to plasmin
  • Plasmin is a protease that degrades fibrin
  • Alteplase (IV) - recombinant tissue type plasminogen activator (rt-PA)
24
Q

Where are clots that cause strokes generally formed?

A

In the atrium and embolisms to the brain so its not really a red or white thrombus

Year 2 - LCRS - Pharmacology (34 decks)

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