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Cardiovascular System > Clinical haemostasis and Thrombosis > Flashcards

Clinical haemostasis and Thrombosis Flashcards

1
Q

What is haemostasis a balance between?

A
  • fibrinolytic factors/anticoagulant proteins

- coagulation factors/platelets

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2
Q

What are the characteristics of abnormal bleeding?

A

Bleeding that is:

  • Spontaneous
  • Out of proportion to the trauma/injury
  • Prolonged
  • Restarts after appearing to stop
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3
Q

What are the main components of the primary haemostatic plug?

A

Platelet
Von Willebrand Factor
Collagen

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4
Q

Defects of Primary Haemostasis

A

Deficiency or Defective:

  1. Collagen - Vessel Wall
    - Steroid therapy makes the collagen and vessel wall weak
    - Ageing also weakens the vessel wall
  2. Von Willebrand Factor
    - VWF disease is a genetic deficiency in Von Willebrand Factor
  3. Platelets
    - Aspirin and other drugs can affect platelet activity
    - Thrombocytopenia is a relative decrease in the number of platelets in the blood
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5
Q

What happens if there is no von willebrand factor?

A
  • there is no primary haemostasis

- the platelets fly past the damaged endothelium and they can’t form a primary plug

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6
Q

Defects of primary haemostasis -bleeding patterns

A
  • Immediate
  • Easy Bruising
  • Nosebleeds (prolonged: >20 mins)
  • Prolonged gum bleeding
  • Menorrhagia
  • Bleeding after trauma/surgery
  • Petechiae (specific for thrombocytopenia)
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7
Q

What is petechiae?

A
  • Petechiae are small blood spots which occur in people who are thrombocytopenic
  • These appear spontaneously and are characteristic of thromobocytopenia
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8
Q

What is secondary haemostasis?

A

Process of generating fibrin

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9
Q

What does a thrombogram tell us?

A

It allows you to visually represent thrombin production over time

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10
Q

Is there a burst of thrombin immediately after the tissue factor trigger?

A

no there is a time lag

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11
Q

What happens in haemophilia?

A
  • failure to generate fibrin to stabilise the platelet plug
  • plug made falls apart
  • one of the coagulation factors (Factor 8) is missing causing failure of the thrombin burst
  • there is a much slower increase in thrombin and not as much thrombin is produced
  • this means that you do not get much of a fibrin mesh formed so the clot does not become stabilised
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12
Q

Defects of secondary haemostasis

A

Deficiency or defect of coagulation factor 1-13 e.g:

  • Haemophilia: Factor 8 or Factor 9
  • Liver Disease (acquired - most coagulation factors are made in the liver)
  • Drugs (warfarin - inhibits synthesis of coagulation factors)
  • Dilution (results from volume replacement)
  • Consumption (disseminated intravascular coagulation - acquired)
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13
Q

Acquired Coagulation Disorders :

Disseminated Intravascular Coagulation (also called consumptive coagulopathy)

A
  • Normally tissue factor is kept outside of the circulation
  • In pathology it might be found in the blood, expressed on WBCs
  • Associated with sepsis, major tissue damage, inflammation
  • Consumes and depletes coagulation factors and platelets
  • Activation of fibrinolysis depletes fibrinogen
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14
Q

What are the consequences of DIC?

A
  • Widespread bleeding, from IV lines, bruising, internal

- Deposition of fibrin in vessels causes organ failure

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15
Q

Defects of secondary haemostasis: pattern of bleeding

A
  • Often delayed (after primary haemostasis)
  • Prolonged
  • Deeper (joints and muscle)
  • Do not tend to get excessive bleeding from small cuts (because primary haemostasis is fine)
  • Small vessels are generally not badly affected
  • Nosebleeds are rare
  • Bleeding after trauma/surgery
  • Bleeding after intramuscular injections
  • Easy bruising
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16
Q

Haemoarthrosis and what is at a sign of?

A

HAEMOPHILIA

  • Haemarthrosis is bleeding into joints
  • They bleed into joints and the pressure builds up and the joint becomes swollen and painful
  • People with haemophilia are generally fine when dealing with small cuts
17
Q

Defects of Clot Stability: Excess Fibrinolysis causes

A
  • Excess Fibrinolytic (plasma, tPA)
    E.g. Therapeutic, some tumours
  • Deficient Antifibrinolytic (antiplasmin)
    E.g. Antiplasmin Deficiency (genetic)
18
Q

Unbalanced Haemostasis: Anticoagulant Excess causes

A

Usually due to therapeutic administration

E.g. heparin or thrombin and Xa inhibitors

19
Q

What are the effects of thrombosis?

A
  • Obstructed flow of blood
    Artery = myocardial infarction, stroke, limb ischaemia
    Vein = pain and swelling
  • Embolism
    Venous Emboli –> pulmonary embolism

Arterial Emboli –> usually from heart, may cause stroke or limb ischaemia

20
Q

Epidemiology of venous thrombo embolism

A
  • 1 in 1000-10,000 per annum
  • Incidence doubles with each decade
  • Cause of 10% of hospital deaths
21
Q

What are the consequences of thrombo embolisms?

A
  • After the first thrombosis the valve system might be damaged thus meaning that there is more stasis
  • Thrombophlebitic Syndrome = swelling and ulcers in the leg due to damage to valves leading to stasis
  • Pulmonary Hypertension
22
Q

What changes the risks of thrombosis?

A
  • Above the thrombotic threshold you will get a thrombosis
  • As you get older the risk of thrombosis increases
  • Various genetic factors can mean that you start at different points on the risk scale
  • Some things may enhance the risk e.g. inflammatory disorder, pregnancy, combined contraceptive pill

THROMBOSIS IS CAUSED BY INTERACTING GENETICS AND ENVRIONMENT

23
Q

What is virchow’s triad?

A

Blood - dominant in venous thrombosis

Vessel Wall - dominant in arterial thrombosis

Flow - complex, contributes to both

24
Q

Virchow’s triad in detail - blood

A

Deficiency of anticoagulant proteins - antithrombin, Protein C, Protein S

Increased coagulant proteins/activity - causes hypercoagulability e.g. Factor 8, Factor 5 Leiden

25
Q

Virchow’s triad in detail - vessel wall

A

Many proteins active in coagulation are expressed on the surface of endothelial cells:
Thrombomodulin
Tissue Factor
Tissue factor pathway inhibitor

Expression of these proteins can be altered in inflammation e.g. in the inflammatory state, thrombomodulin is downregulated

26
Q

Virchow’s triad in detail - flow

A

Reduced flow (stasis) increases the risk of venous thrombosis

This can be caused by surgery, fracture, long haul flights, bed rest etc.

27
Q

Increased risk of thrombosis (thrombophilia)

A

Pregnancy - 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

Malignancy

Surgery

Inflammatory Response

28
Q

Risk of post-operative venous thromboembolism

A

Thrombosis risk peaks after about 3 weeks and gradually decreases over the following 7 or 8 weeks

29
Q

What causes the increased risk of thrombosis associated with the combined oral contraceptive?

A
  • Factor 5 Leiden
  • Reduced concentration of protein S
  • Reduced concentration of PAI-1
  • Reduced endothelial activation
  • Prolonged contact activation
30
Q

Therapy for thrombosis

A

1) Treatment to lyse clot:
E.g. tPA (though this carries an increased risk of bleeding)

2) Treatment to limit recurrence/extension/emboli:

  • Increased anticoagulant activity e.g. heparin
  • Lower procoagulant factors
  • New anticoagulants (direct inhibitors)
31
Q

What is thrombosis?

A

intravascular coagulation, inappropriate coagulation, not preceded by bleeding and can be venous/arterial

32
Q

Why do some people get thrombosis?

A

due to:

  • age
  • genetics
  • illnesses
  • medication
  • acute stimulus
33
Q

Prothrombolytic therapy and its dangers

A
  • When a thrombosis has happened you may think it’s a good idea to give thrombolytic therapy but the only circumstance when this is done is with stroke
  • It isn’t done more often because there is an increased risk of bleeding (this could lead to cerebral haemorrhage so you need to make sure that the risk is worth taking)
34
Q

What is the main concern with acute clots?

A

stop embolisation

Cardiovascular System (19 decks)

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