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YR5 Haematology > Haemostasis and Thrombosis > Flashcards

Haemostasis and Thrombosis Flashcards

1
Q

What is the case mortality of VTE?

A

5%

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2
Q

What is thrombophlebitic syndrome?

A

Post-thrombotic syndrome resulting in recurrent pain, swelling, ulcers etc.

In 23% at 2-years (11% with TED stockings)

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3
Q

What can be a complication of PE?

A

Pulmonary HTN (heart failure with high mortality)

In 4% at 2 years

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4
Q

Why is thrombosis important?

A

Significant sequelae (death is rapid) but is preventable through thromboprophylaxis

May be indicator of underlying disease (cancer)

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5
Q

What is Virchow’s Triad?

A

3 contributory factors to thrombosis:

Blood viscosity
Blood flow
Vessel wall damage

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6
Q

What can cause high viscocity of blood?

A

Increased haematocrit + protein paraprotein or high platelet count

Net excess of procoagulant activity

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7
Q

List 4 anti-coagulant proteins in the coagulation cascade

A

TFPI (Blocks FXa + TF/FVIIa complex)

Protein C (Inactivates FVIIIa + FVa)

Protein S (Inhibits FIXa + co-factor to form activated protein C)

Antithrombin (inhibits FIIa, IXa + Xa)

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8
Q

What is the function of endothelial protein C receptors (EPCR) ?

A

Activation of Protein C
(anticoagulant)

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9
Q

What are 4 stimuli for increased haemostasis?

A

Infection

Vasculitis

Malignancy

Trauma

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10
Q

How do the stimuli result in increased haemostasis?

A

Anticoagulant molecules e.g. Thrombomodulin DOWNregulated

TF expressed

Prostacyclin (anti-platelet) production DECREASED

Adhesion molecules UPregulated

vWF release: platelet + neutrophil capture, neutrophil extracellular traps

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11
Q

What is netosis?

A

Neutrophils releasing DNA, vWF + histones

Activates XII to XIIa

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12
Q

In which phenomenon is netosis implicated?

A

Immunothrombosis

In many disorders, inflammation is sufficient to trigger + drive thrombus formation

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13
Q

How does a change in blood flow affect thrombosis?

A

Can result in accumulation of activated factors

Promotion of platelet adhesion + leukocyte adhesion + transmigration

Hypoxia produces inflammatory effect on endothelium

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14
Q

What are 4 types of causes of stasis? Give examples of each

A

Immobility: long haul flights, surgery

Compression: tumours, pregnancy

Viscosity: polycythaemia, paraprotein

Congenital: vascular abnormalities

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15
Q

What is the difference in high dose and low dose anticoagulation?

A

High dose: therapeutic

Low dose: prophylactic

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16
Q

What are 2 types of immediate anticoagulation treatments? What is the MOA?

A

Heparin: unfractionated + LMWH (Increase anticoagulant activity)

Direct acting anti-Xa + anti-IIa

(Reduce procoagulant activity)

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17
Q

What is a class of delayed anticoagulation medication? Give an example

A

Vitamin K antagonist: Warfarin

(Reduce pro-coagulant activity)

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18
Q

How do heparins work?

A

Immediate effect

Bind to + potentiate ANTI-THROMBIN

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19
Q

What is the long term disadvantage to heparins?

A

Osteoporosis

20
Q

How do DOACs work?

A

Bind directly to enzyme

Anti-Xa: Rivaroxaban, Apixaban, Edoxaban

Anti-IIa: Dabigatran

21
Q

What are the pharmacodynamics and pharmacokinetics of DOACs?

A

Oral
Immediate acting: peak in ~3-4 hours
Also useful in long term
Short half life, no monitoring required

22
Q

What are the pharmacodynamics and pharmacokinetics of warfarin?

A

Oral

Indirect effect: prevents recycling of Vit K
Onset of action is delayed
Levels of II, VII, IX + X fall
Protein C + protein S fall

23
Q

Can you give warfarin in an emergency?

A

No

Used long term only

Also no point in giving larger dose since it’s delayed regardless

24
Q

What is always important to consider when giving warfarin?

A

Need to measure INR (derived from prothombin time)

Narrow therapeutic window for each individual

25
Q

Why is dosing warfarin difficult?

A

Has numerous interactions

If high dietary VitK: need more Warfarin

Variable absorption

Interaction with other drugs: protein binding, competition/ induction of cytochromes

Teratogenic: can’t be used in pregnancy, must stop within 6w or risk fetal malformation

26
Q

What are 4 strategies for prophylaxis?

A

LMWH: Tinzaparin or Enoxaparin

TED stockings (surgical/ if heparin CI)

Intermittent pneumatic compression (increase flow)

DOAC +/- aspirin (orthopaedic pts)

27
Q

Why are DOACs preferred over other methods of anticoagulation?

A

Reduce risk of recurrence +

Reduce risk of intracranial bleeding by half compared to other drugs

28
Q

Broadly, what causes thrombophilia?

A

Increased coagulation factors + platelets

Decreased fibrinolytic factors + anticoagulant proteins

29
Q

Which 3 characteristics make the vessel wall antithrombotic?

A

Express anticoagulant molecules

Does NOT express tissue factor

Secretes antiplatelet factors

30
Q

Which anticoagulant molecules are expressed on the vessel wall?

A

Thrombomodulin: makes thrombin anticoagulant

Endothelial Protein C Receptor

Tissue factor pathway inhibitor

Heparans: protein C co-receptor

31
Q

Which anti platelet factors are secreted by the vessel wall?

A

Prostacyclin

NO

32
Q

Which 2 procoagulant molecules are kept out of the blood vessel? (in the sub endothelial tissue)

A

Collagen

Tissue factor

33
Q

What is immunothrombosis?

A

Active participation of innate immune system in forming a thrombus via distinct cellular + molecular interactions

Triggered by recognition of pathogens + damaged cells.

34
Q

How does stasis promote thrombosis?

A

Activation factors accumulate (rise above critical conc.)

Promote platelet adhesion

Promote leukocyte adhesion (NET) + transmigration

Endothelial cells become hypoxic- inflammatory stimulus, promotes adhesion + release of VWF

35
Q

How do thrombotic risk factors interact?

A

Genetic, acquired + circumstantial RFs often combine to produce thrombosis

May have powerful, unpredictable interactions

36
Q

Deficiency of which factor confers the highest risk of thrombosis?

A

Antithrombin deficiency

37
Q

How are different forms of Heparin administered?

A

Unfractionated: IV infusion, monitor APTT
LMWH: SC, No monitoring
Pentasaccharide: SC, No monitoring

38
Q

Why does renal function need to be considered before giving Heparin?

A

Don’t want anticoagulant effect to accumulate too much

39
Q

What can be given to reverse the effects of each class of anticoagulant?

A

Heparin: Protamine

DOAC: antibody to Dabigatran

Warfarin: Vit K/ Prothrombin complex concentrate

40
Q

Which anticoagulant is safe during pregnancy?

A

Heparin

41
Q

Give 6 groups of patients at increased risk of thrombosis

A

Medical inpatients: infection, inflammation, immobility

Cancer: procoag molecules, inflammation, flow obstruction

Surgical patients: inflammation, immobility, trauma

Previous VTE, FH, genetics

Obese

Age >60

42
Q

Which 6 patient factors must be considered as potential CIs to heparin prophylaxis? (ie increased risk of bleeding)

A

Bleeding diathesis: Haemophilia, VWD

Platelets <100

Acute CVA in previous month: haemorrhage/ thrombosis

SBP >200 / DBP >120

Severe liver/ renal disease

Active bleeding

43
Q

Which 3 procedural factors must be considered as potential CIs to heparin prophylaxis?

A

Neuro, spinal or eye surgery

Other surgeries with high risk bleeding

LP/ spinal/ epidural in previous 4h

44
Q

How are patients risk factors of recurrence classified from highest to lowest based on precipitant?

A

Idiopathic: HIGHEST- no identifiable cause to remove. Consider long term anticoagulation esp. DOAC

Non surgical: cOCP, flight, trauma. 3m +/- longer if high thrombotic RF

Surgery: LOWEST- only at risk in that circumstance. No need for long term anticoagulation.

44
Q

How are patients risk factors of recurrence classified from highest to lowest based on precipitant?

A

Idiopathic: HIGHEST- no identifiable cause to remove. Consider long term anticoagulation esp. DOAC

Non surgical: cOCP, flight, trauma. 3m +/- longer if high thrombotic RF

Surgery: LOWEST- only at risk in that circumstance. No need for long term anticoagulation.

YR5 Haematology (20 decks)

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