Antiplatelet And Anticoagulant Flashcards

1
Q

Define thrombosis

A

Pathological formation of intravascular blood clot
In vein or artery
Characterised by lines of Zahn (if large vessel) and attachment to vessel wall

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2
Q

Describe Virchows triad

A

Things that cause thrombosis
1. Disruption of blood flow (stasis)
2. Endothelial cell damage
3. Hypercoaguable states

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3
Q

Example of
1. Disruption of blood flow

A

Immobilisation (bed rest)
Cardiac wall dysfunction
Aneurysm
Atrial fibrillation
Left atrial dilation due to mitral stenosis

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4
Q

Example of
2. Endothelial cell damage

A

Atherosclerosis - ruptured plaque
Vasculitis
Oxidised LDL
Cigarette smoke
Cytokines

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5
Q

Example of
3. Hypercoagulable states

A

Excessive procoagulant factors
Inherited (AT3 deficiency)
Classics presentation is recurrent DVTs or DVTs at young age

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6
Q

Drug to treat ischaemic stroke

A

Alteplase - administered 4.5 hours of symptom onset
Treatment with aspirin initiated 24 hours after thrombolysis

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7
Q

Describe venous thrombus

A

Most common cause is stasis of blood
Most common site of deep veins of lower limb
Red, swollen, painful leg
Can dislodge to the lungs causing a pulmonary embolism

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8
Q

Treatment of venous thrombus

A

Rivaroxaban
Warfarin or other anticoagulant

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9
Q

Describe arterial thrombosis

A

Due to endothelial damage related to turbulent blood flow at bifurcation or over atherosclerotic plaques in high velocity vessels

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10
Q

Treatment for arterial thrombosis

A

Inhibitors of platelet aggregation - aspirin

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11
Q

Describe pulmonary embolism and most likely cause

A

Intravascular mass that travels and occluded pulmonary blood vessels
- cause is a dislodged thrombus

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12
Q

3 stages of platelet activation

A

Adhesion
Release reaction
Aggregation

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13
Q

When platelets undergo shape changes they degranulate …

A

Release mediators ADP
Thromboxane A2 - from platelet cyclooxygenase
Calcium

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14
Q

What does ADP do

A

Induced expression of GP2b/3a (essential receptor for aggregation of platelets) and fibrinogen which acts as linker molecule in the developing clot

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15
Q

What is TXA2

A

A vasoconstrictor that also promotes platelet aggregation

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16
Q

Thrombin functions

A

Act on fibrinogen to produce fibrin monomers
Activates fibrin stabilising factor 13 (strengthens blood clot)

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17
Q

What switches off thrombin

A

Natural anticoagulant antithrombin3
- limits clot formation

18
Q

Functions of plasmin

A

Breaks down clot
Cleaves fibrin and fibrinogen into degradation products
Degrades some clotting factors
Blocks platelet aggregation

19
Q

3 main classes of thrombus treatments

A

Anticoagulants - factor Xa inhibitors
Antiplatelets - aspirin
Fibrinolytic agents - Alteplase

20
Q

4 classes of anticoagulant drug

A
  1. Selective factor Xa inhibitor - apixaban
  2. Direct thrombin inhibitors - dabigatran
  3. Heparin and low MW heparins
  4. Vitamin K antagonists - Warfarin
21
Q

Treatments for venous thromboembolism

A

Apixaban
If contraindicated - low MW heparin
Or
LMWH with vitamin K antagonist for at least 5 days until INR achieved

22
Q

DOACs: dabigatran etexilate mechanism of action

A

Reversible inhibitor of thrombin

23
Q

DOACs: apixaban mechanism of action

A

Reversible inhibitor of activated factor X
Prevents thrombin generation
Prevents thrombus development

24
Q

Indications of apixaban, dabigatran etexilate, edoxaban and rivaroxaban

A

Prevention of stroke
Secondary prevention of DVT

25
Q

Indications of apixaban, dabigatran etexilate and rivaroxaban

A

Preventions of venous thromboembolism following surgery

26
Q

Indications of rivaroxaban

A

Prevention of atherothrombotic events in patient with coronary or peripheral artery disease
Following an acute myocardial infarction

27
Q

Apixaban contraindications

A

Conditions with significant risk of bleeding
GI ulceration

28
Q

Is apixaban appropriate for elderly

A

Prescription potentially inappropriate
Risk of bleeding e.g sever hypertension

29
Q

Side effects of apixaban

A

Anaemia
Haemorrhage

30
Q

How does heparin inhibit coagulation

A

Activating anti thrombin III
- AT III is a naturally occurring inhibitor of thrombin and clotting factors IX, Xa, XI and XII
(ATIII becomes 1000x more active)

31
Q

What do LMWH do

A

Inactivate factor Xa and thrombin
- also via activation of anti thrombin III

32
Q

LMWH example

A

Dalteparin sodium

33
Q

Heparin and LMWH PK

A

Inactive given orally
Administered IV or SC
Heparin has shorter half life than LMWH
Renal excretion

34
Q

Heparin and LMWH adverse effects

A

Bleeding and hypersensitivity

35
Q

Heparin and LMWH overdose treatment

A

IV protamine

36
Q

Vitamin K antagonist example

A

Warfarin

37
Q

Warfarin mechanism of action

A

Inhibits activation of vitamin K1 dependent clotting factors II, VII, IX, X

38
Q

Side effects of warfarin

A

Haemorrhage and skin necrosis

39
Q

Aspirin mechanism of action

A

Inhibits COX-1 so inhibits synthesis of TXA2

40
Q

Clinical use of aspirin

A

Prevent thrombosis leading to transient ischaemic attack, stroke, myocardial infarction

41
Q

Alteplase and streptokinase function

A

Activate conversion of plasminogen to plasmin
- causes break down of fibrin

42
Q

Main hazard of Alteplase

A

Bleeding