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Year 1: Cardiovascular System > 10. Clinical Haemostasis Thrombosis > Flashcards

10. Clinical Haemostasis Thrombosis Flashcards

1
Q

What is the state of normal haemostasis?

A

A state of equilibrium between fibrinolytic factors, anticoagulation proteins and coagulation factors, platelets

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2
Q

What are the characteristics of abnormal bleeding?

A

1) Spontaneous
2) Out of proportion to the trauma/injury
3) Prolonged bleeding from cuts = bleeding disorder
4) Restarts after appearing to stop
5) Prolonged nose bleeds

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3
Q

What is primary haemostasis?

A

Formation of an unstable platelet plug

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4
Q

What is secondary haemostasis?

A

Process of generating fibrin from fribinogen catalysed from thrombin

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5
Q

What makes up the primary haemostatic plug?

A

Platelet + Von Willebrand Factor + Collagen

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6
Q

What are possible defects of the primary haemostatic plug?

A

Collagen - Weakening of the collagen and vessel wall due to ageing and steroid therapy
Von Willebrand Factor - Genetic deficiency in this factor
Platelets - Drugs (aspirin) can affect platelet activity

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7
Q

Define thrombocytopenia

A

A relative decrease in the number of platelets in the blood

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8
Q

What is exposed when the endothelial wall is damaged?

A

Collagen and tissue factor

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9
Q

What causes failure of primary haemostasis?

A

No Von Willebrand Factor resulting in the platelets flying past the damaged endothelium

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10
Q

What are the defects of primary heamostasis - Pattern of bleeding?

A
  • Immediate
  • Easy Bruising
  • Nosebleeds (prolonged: >20 mins)
  • Gum bleeding (prolonged)
  • Menorrhagia (anaemia)
  • Bleeding after trauma/surgery
  • Petechiae (specific for thrombocytopenia)
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11
Q

What is petechiae?

A

Small blood spots which occur spontaneously in people who are thrombocytopenic

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12
Q

What can be used to measure the thrombin generation over time?

A

Thrombogram

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13
Q

In a thrombogram, after the TF trigger what happens?

A

There is a lag then a burst of thrombin. This lag phase is due to the cofactors and anticoagulant enzymes being generated

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14
Q

In haemophilia which coagulation factor is missing?

A

Factor VIII

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15
Q

How does haemophilia present itself on a thrombogram?

A

A slower increase in thrombin and not as much thrombin produced

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16
Q

What do defects of secondary haemostasis cause?

A

No fibrin mesh formation

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17
Q

What is the cause of defects of secondary haemostasis?

A

Deficiency or defect of coagulation factors running from 1-13

18
Q

List some common examples of secondary haemostasis defects?

A 
o Haemophilia: Factor 8 or Factor 9 (hereditary due to genetic defect) 
o Liver Disease (acquired - most coagulation factors are made in the liver)
o Drugs (warfarin - inhibits synthesis of coagulation factors)
o Dilution (results from volume replacement)
o Consumption (disseminated intravascular coagulation - acquired)
19
Q

What are two acquired coagulation disorders?

A

Disseminated Intravascular Coagulation

Consequences

20
Q

What is disseminated intravascular coagulation?

A

Generalised activation of coagulation - Tissue Factor. This consumes and depletes coagulation factors.

21
Q

What is disseminated intravascular coagulation commonly associated with?

A

Sepsis, major tissue damage and inflammation

22
Q

What is consequences?

A

Widespread bleeding, from IV lines, bruising. Deposition of fibrin in vessels causes organ failure

23
Q

Define haemophilia

A

The failure to generate fibrin to stabilise the platelet plug

24
Q

In haemophilia, because there is no fibrin…

A

There is no fibrin mesh stabilising the plug. The plug then falls apart easily

25
Q

What are the defects of secondary heamostasis - Pattern of bleeding?

A
  • Often delayed (after primary haemostasis)
  • Prolonged
  • Deeper: joints and muscles
  • Do not tend to get excessive bleeding from small cuts (because primary haemostasis is ok)
  • Small vessels are generally ok
  • Nosebleeds are rare
  • Bleeding after trauma/surgery
  • Bleeding after intramuscular injections
26
Q

What is a hallmark sign of haemophilia?

A

Haemarthrosis

27
Q

What is haemarthrosis?

A

Bleeding into joints resulting in an increase in pressure causing pain and swelling.

28
Q

What can affect clot stability?

A

Excess fibrinolysis

29
Q

Effects of thrombosis

A

Obstructed flow of blood

Embolism

30
Q

What are the effects of obstructed blood flow in the artery?

A

Myocardial infarction, stroke, limb ischaemia

31
Q

What are the effects of obstructed blood flow in the vein?

A

Pain and swelling

32
Q

What are the consequences of a thromboembolism?

A

Valve system might be damage leading to more blood stasis.
Thrombophlebitic syndrome
Pulmonary hypertension

33
Q

What is thrombophlebitic syndrome?

A

Swelling and ulcers in the leg due to damage to valves leading to stasis

34
Q

What factors can enhance the risk of a thrombosis?

A

Genetic factors, inflammatory disorder, pregnancy and combined contraceptive pill

35
Q

What are the three contributory factors of thrombosis?

A

Hypercoagulability, Stasis and Vessel wall injury

36
Q

Define thrombosis?

A

Abnormal formation of a blood clot in the circulatory system

37
Q

What will cause hypercoagulability in the blood?

A

Deficiency of anticoagulant proteins - Antithrombin, Protein C & S
Increased coagulant proteins/activity

38
Q

Vessel wall injury causes what effects?

A

Down regulation of thrombomodulin in an inflammatory state

39
Q

Why is there an increased risk of thrombosis in pregnancy?

A

There is reduced mobility and reduced flow due to the presence of the uterus and there are a number of blood coagulation changes that take place (rise in Factor 7 and Factor 8) and there is a decrease in protein S which will make the blood more procoagulant

40
Q

What is the treatment for thrombosis?

A

To lyse the clot e.g with tPA (although this carries a risk of bleeding)

Thrombolytic therapy is only used with stroke as there is an increased risk of bleeding - Cerebral haemorrhage

41
Q

How are clots prevented from happening?

A

Increase anticoagulant activity (heparin)

Decrease procoagulant activity

42
Q

What is the increased risk of thrombosis caused by combined oral contraception associated to?

A
  • Factor 5 Leiden
  • Reduced concentration of protein S
  • Reduced concentration of PAI-1
  • Reduced endothelial activation
  • Prolonged contact activation

Year 1: Cardiovascular System (21 decks)

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