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CVS > 11. Clinical Haemostasis and Thrombosis > Flashcards

11. Clinical Haemostasis and Thrombosis Flashcards

1
Q

What needs to be balanced for haemostasis?

A

• Fibrinolytic factors + anticoagulant proteins vs. coagulation factors + platelets

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2
Q

How does the balance in haemostasis change during bleeding?

A
  • More coagulation factors + platelets

* Less fibrinolytic factors + anticoagulant proteins

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3
Q

What are the characteristics of abnormal bleeding?

A
  • Spontaneous
  • Out of proportion to the injury
  • Unduly prolonged
  • Restarts after appearing to stop

(prolonged nose bleeds: >15min)

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4
Q

How does the endothelial cell lining respond to injury?

A
  • Vessel constriction (VSMCs contract locally to limit blood flow)
  • Primary haemostasis: formation of an unstable platelet plug to limit blood loss and provide a surface for coagulation
  • Secondary haemostasis: stabilisation of the plug with fibrin to stop blood loss
  • Vessel repair (cell migration/proliferation) and dissolution of the clot (fibrinolysis)
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5
Q

What 3 things can negatively impact the effects of collagen in haemostasis?

A
  • Steroid therapy
  • Ageing
  • Scurvy
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6
Q

What is thrombocytopenia?

A

A relative decrease in the number of platelets in the blood

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7
Q

What is Von Willebrand Factor disease?

A
  • Deficiency in Von Willebrand Factor
  • Less primary haemostasis
  • Platelets pass the damaged endothelium and can’t form a primary plug
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8
Q

What are the patterns of bleeding of a defect in primary haemostasis?

A
  • Immediate
  • Easy bruising
  • Prolonged nosebleeds
  • Prolonged gum bleeding
  • Menorrhagia (anaemia)
  • Bleeding after trauma/surgery
  • Petechiae (specific for thrombocytopenia)
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9
Q

What are petechiae?

A
  • Small spots in people who are thrombocytopenic
  • Appear spontaneously
  • Normally, platelets constantly plug small holes in blood vessels - continuous repair, but this is made difficult
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10
Q

Briefly outline secondary haemostasis

A
  • Prothrombin => thrombin
  • This converts fibrinogen => fibrin
  • Fibrin forms an insoluble mesh around the platelets
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11
Q

Why is there are lag in the thrombogram before the rise in thrombin?

A

Time needed for cofactors and anticoagulant enzymes to be generated

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12
Q

How is haemophilia visualised in a thrombogram and why does the condition lead to prolonged bleeding?

A
  • Factor VIII is missing
  • Failure of thrombin burst
  • Slower increase in thrombin
  • Not as much thrombin is produced
  • Failure to produce a fibrin mesh is formed - clot is not stabilised
  • Left with a primary platelet plug which can fall apart easily

(• Generally fine when dealing with small cuts - primary haemostasis still works)

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13
Q

Which coagulation factors does a defect of secondary haemostasis involve?

A

• I to XIII

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14
Q

What are common examples that lead to defects of secondary haemostasis?

A
  • Haemophilia (Factor VIII or IX)
  • Liver disease (most coagulation factors are made in the liver)
  • Drugs (warfarin inhibits the synthesis of coagulation factors)
  • Dilution (volume replacement)
  • Consumption (disseminated intravascular coagulation)
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15
Q

What is disseminated intravascular coagulation?

A
  • Acquired coagulation disorder (aka consumptive coagulopathy)
  • Generalised activation of coagulation (tissue factor is expressed in the blood when it doesn’t need to be)
  • Small clots develop throughout the bloodstream
  • Consumes and depletes coagulation factors and platelets
  • Activation of fibrinolysis depletes fibrinogen
  • Associated with sepsis, major tissue damage and inflammation
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16
Q

What are the patterns of bleeding of a defect in secondary haemostasis?

A
  • Often delayed
  • Prolonged
  • Deeper: joints and muscles
  • Don’t tend to bleed excessively from small cuts (primary haemostasis is usually enough)
  • Nosebleeds are rare
  • Bleeding after trauma/surgery
  • Bleeding after intramuscular injections
  • Easy brusing
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17
Q

What is the hallmark of haemophilia?

A
  • Haemarthrosis - bleeding into joints
  • Pressure builds up and joints become swollen and painful
  • Characteristic of severe haemophilia A and B
18
Q

What are 2 types of excess fibrinolysis?

A
  • Excess fibrinolytic (plasma, tPA) e.g. therapeutic administration, some tumours
  • Deficient antifibrinolytic (antiplasmin) e.g. antiplasmin deficiency (genetic)
19
Q

Give examples of anticoagulant excess

A

• Usually due to therapeutic administration:

  • Heparin
  • Thrombin inhibitor
  • Xa inhibitor
20
Q

What can a thrombosis in the artery and vein cause?

A

Artery
• Myocardial infarction
• Stroke
• Limb ischaemia

Vein
• Pain and swelling

21
Q

What can a venous and arterial embolism lead to?

A
  • Venous - pulmonary embolism
  • Arterial - usually from heart, may cause stroke or limb ischaemia

(right side of the heart goes to the lungs, left side of the heart goes to the brain)

22
Q

What is the prevalence of venous thromboemboli?

A
  • 1 in 1000-10,000 per annum
  • Incidence doubles with each decade
  • Pulmonary embolism is the cause of 10% of hospital deaths
  • Estimated 25,000 preventable deaths per annum
23
Q

What is the case mortality and recurrence of thrombo-embolism?

A
  • Mortality - 5%

* Reccurence - 20% in first 2 years, 4% per annum after

24
Q

Why is the recurrence high after an initial thrombosis?

A
  • Valve system might be damaged
  • More stasis
  • More likely to have another thrombosis
25
Q

Give 2 consequences of thromboembolism after the initial treatment

A
  • Thrombophlebitic syndrome

* Pulmonary hypertension

26
Q

What is thrombophlebitic syndrome?

A
  • Swelling and ulcers in the leg

* Due to damaged valves in the veins leading to stasis (lack of venous return)

27
Q

What is pulmonary hypertension?

A
  • Circulation in the lungs never return to normal
  • Shortness of breath
  • Damages the right side of the heart as it has to work harder
  • Can lead to heart failure
  • High mortality
28
Q

What factors can play a part in increasing the risk of thrombosis?

A
  • Genetic - doesn’t change
  • Ageing - gradual increase
  • Acquired risk - sharp, sudden increase
  • Other things e.g. inflammatory disorders, pregnancy, combined contraceptive pill etc. may enhance the risk
  • When this all passes the ‘thrombotic threshold’, you get a thrombosis
29
Q

What does Virchow’s Triad show?

A

Three contributory factors of thrombosis (inherited or acquired)
• Blood - dominant in venous thrombosis
• Vessel Wall - dominant in arterial thrombosis
• Flow - complex, contributes to both

30
Q

How does a faster blood flow affect thrombosis?

A
  • More activated coagulation factors get swept away

* Lower chance of a thrombus forming

31
Q

What is thrombocytosis?

A

Increased number of platelets

32
Q

Why is the vessel wall a contributory factor of thrombosis?

A

• Less is known about the vessel wall as it’s difficult to study
• Many proteins active in coagulation are expressed on the surface of endothelial cells:
- thrombomodulin
- tissue factor
- tissue factor pathway inhibitor
• These proteins can be altered in inflammation caused by malignancy, infection or immune disorders
• Thrombomodulin is down-regulated in the inflammatory state

33
Q

What is thrombophilia?

A
  • Abnormality of blood coagulation
  • Increases the risk of thrombosis
  • Thrombosis at a young age
  • Idiopathic thrombosis (immune system destroys platelets)
  • Multiple thromboses
  • Thrombosis whilst anticoagulated
34
Q

Why does pregnancy increase the risk of thrombosis?

A
  • Reduced mobility and flow due to the presence of the uterus
  • Rise in Factors VII and VIII
  • Decrease in Protein S
  • Blood becomes more procoagulant
35
Q

Why does malignancy increase the risk of thrombosis?

A
  • Increased inflammation
  • Tumour could secrete tissue factor
  • Tumour mass could restrict or block blood flow
36
Q

How does the risk of venous thromboembolism change after an operation?

A
  • Risk peaks after about 3 weeks

* Decreases over the following 7/8 weeks

37
Q

How can you lyse a clot (treatment)?

A

Use tPA (although this increases the risk of bleeding)

38
Q

Name 3 direct procoagulant inhibitors

A
  • Rivaroxaban (Xa)
  • Apixaban (Xa)
  • Dabigatran (IIa - thrombin)
39
Q

When is thrombolytic therapy given?

A
  • Only when a thrombosis leads to a stroke
  • Not done more often due to the increased risk of bleeding
  • Could lead to a cerebral haemorrhage so you need to balance the risks
40
Q

Which 2 main treatments can be used to increase anticoagulant and lower procoagulant factors?

A
  • Increase anticoagulant activity - heparin

* Lower procoagulant factors - Warfarin (blocks the production of vitamin K1 which is needed for some clotting factors)

41
Q

Why does combined oral contraceptive therapy increase the risk of thrombosis?

A

Reduced concentration of Protein S

CVS (21 decks)

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