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My LSS- CVS > CVS 10: Thrombosis > Flashcards

CVS 10: Thrombosis Flashcards

1
Q

What needs to be in balance for haemostasis?

A
  1. Fibrinolytic factors, anticoagulant proteins
    vs
  2. Coagulation factors, platelets
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2
Q

What happens if fibrinolysis > coagulation?

  • Describe the features of this condition
A

Bleeding that is:

  • spontaneous
  • out of proportion to the trauma/ injury
  • unduly prolonged
  • restarts after appearing to stop
  • prolonged nose bleeds (epistaxis)
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3
Q

What forms the primary haemostatic plug?

A

Platelet- Von Willebrand Factor- Collagen

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4
Q

What are the defects of primary haemostats?

A
  1. Platelets- Aspirin can affect platelet activity, thrombocytopenia is a relative decrease in the number of platelets in the blood
  2. Von Willebrand Factor- VW disease= genetic deficiency of the factor
  3. Collagen- steroid therapy makes the collagen and vessel wall weak, raging weakens the vessel wall as well
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5
Q

What are the defects of primary haemostasis and its pattern of bleeding?

A
  • Immediate
  • Easy bruising
  • Nosebleeds (>20mins)
  • gum bleeding
  • menorrhagia
  • bleeding after trauma/ surgery
  • Petechiae (specifically for thrombocytopenia)
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6
Q

What are petechiae?

A
  • small blood spots which occur in people who are thrombocytopenic
  • Appear spontaneously
  • platelets are constantly busy plugging small holes in blood vessels= continuous process of repair
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7
Q

What is Secondary Haemostasis?

A
  • generation of thrombin from prothrombin
  • This converts fibrinogen to fibrin to form the insoluble mesh around platelets
    ==> blood coagulation, stops blood loss
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8
Q

How can you visualise the process of coagulation?

A
  • measure thrombin generation over time using a THROMBOGRAM
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9
Q

Why is there a lag in the thrombogram after the TF trigger?

A

During this time cofactors and anticoagulant enzymes are being generated and then you get the burst of thrombin

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10
Q

What happens during Haemophilia A on the thrombogram?

A

Factor 8 is missing

  • you don’t get the thrombin burst on the thrombogram
  • slower increase in thrombin
  • not much thrombin produced
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11
Q

What is the consequence of Haemophilia A?

A
  • Thrombin not produced
  • fibrinogen not converted to fibrin
  • fibrin mesh not formed
  • clot not stabilised
  • only left with primary platelet plug which falls apart easily
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12
Q

Name some causes of defects in secondary haemostasis

A

Genetic:
- Haemophilia A/B: F8/9
Acquired:
- Liver disease (most coagulation factors made in the liver)
- Drugs (warfarin- inhibits synthesis of coagulation factors)
- Dilution (results from volume replacement)
- Consumption (disseminated intravascular coagulation- DIC)

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13
Q

What is disseminated intravascular coagulation also known and what causes it?

A

CONSUMPTIVE COAGULOPATHY

  • generalised activation of coagulation- Tissue Factor
  • Consumes and depletes coagulation factors and platelets
  • activates fibrinolysis which depletes fibrinogen
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14
Q

What is DIC associated with?

A

Sepis, major tissue damage and inflammation

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15
Q

What are the consequences of DIC?

A
  • Widespread bleeding (from IV lines) bruising (internally)

- Deposition of fibrin in vessels causes organ failure

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16
Q

What is the pattern of bleeding when there is a defect in secondary haemostats?

A
  • often delayed
  • prolonged
  • deeper bleeding (in joints and muscle) because primary haemostasis insufficient in big vessels
  • small vessels are okay
  • nosebleeds are rare
  • bleeding after trauma/ surgery
  • bleeding after intramuscular injections
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17
Q

What is haemarthrosis and with which condition is it often associated?

A

associated with Haemophilia A/B

  • bleeding into the joints
  • pressure builds up and joint becomes stoles and painful
18
Q

Other than a decrease in coagulation, what could cause excessive bleeding?

A

Excess fibrinolysis

  • excess fibrinolytic (plasmin, tPa): therapeutic administration and some tumours
  • Deficient antifibrinolytic (antiplasmin): antiplasmin deficiency
19
Q

Give some examples of substances which are administered therapeutically and could cause an anticoagulant excess if administered at incorrect levels

A

Heparin
Thrombin
Factor Xa inhibitors

20
Q

What happens when coagulation factors> fibrinolytic factors?

A

Thrombosis

21
Q

What is thrombosis?

A
  • Inappropriate intravascular coagulation
22
Q

What are the effects of thrombosis?

A
  1. Obstructed Flow of blood
    - Artery: MI, stroke and limb ischaemia
    - Vein: pain and swelling
  2. Embolism
    - Venous emboli= pulmonary embolism
    - Arterial emboli= usually from the heart, may cause limb ischaemia or stroke
23
Q

What is deep vein thrombosis?

A

Thrombus in one of the deep veins mainly in the lower limbs where venous return of blood is obstructed

24
Q

What are the consequences of a thrombosis-embolism?

A
  • After the first thrombosis, the valve system might be damaged meaning, there is more stasis
  • THROMBOPHLEBITIC SYNDROME= swelling and ulcers in the leg due to damage to valve leading to stasis
  • Pulmonary hypertension
25
Q

What might be the risk factors for getting thrombosis?

A
  • genetic factors
  • effect of age
  • previous events (pregnancy), illnesses (inflammatory disorders) and medication (contraceptive pill)
26
Q

What is the name of the triad showing the three contributory factors of thrombosis? Name the three factors as well

A

Virchow’s Triad

  1. Blood- mainly venous thrombosis
  2. Vessel Wall- mainly arterial thrombosis
  3. Flow- complex, contributes to both
27
Q

The levels of which two types of substances in blood increases the risk of thrombosis?

A
  1. Deficiency of anticoagulant proteins

2. Increased coagulant protein

28
Q

Name some anticoagulant proteins that might be deficient in thrombosis

A

Antithrombin
Protein C
Protein S

29
Q

Name some coagulant proteins that could be in excess, causing thrombosis

A
  • factor 8
  • factor 2 and others
  • Factor 5 Leiden (increased activity because of Protein C resistance)
  • thrombocytosis (increase in platelets)
30
Q

Which molecules on the vessel wall increase the risk of thrombosis?

A

Protein expressed on the surface of endothelial cells:

  • thrombomodulin
  • tissue factor
  • tissue factor pathway inhibitor
31
Q

What causes the expression of these proteins to be altered and why?

A
  • Inflammation: malignancy, infection, immune disorders

- In the inflammatory state, thrombomodulin is down regulated

32
Q

How does flow increase the risk of thrombosis?

A
  • reduced flow (stasis) increases the risk of venous thrombosis
  • slower flow= coagulation factors closer together
  • more likely to be activated and for blood to clot
33
Q

When might flow of blood increase the risk of thrombosis?

A
  • during surgery
  • caused by a fracture (have to keep the bones still)
  • long haul flights
  • bed rest
34
Q

What is an increased risk of thrombosis called? what are the features of this condition?

A

Thrombophilia

  • thrombosis at a young age
  • idiopathic thrombosis
  • multiple thromboses
  • thrombosis whilst anti-coagulated
  • identifiable cause of the increased risk
35
Q

How does pregnancy cause an increased risk for thrombosis?

A
  • reduced mobility
  • reduced flow because of the uterus
  • blood coagulation changes (rise in F7 and F8) and decrease in Protein S which makes blood more coagulable
36
Q

What is the therapy for venous thrombosis?

A
  1. Treatment to lyse the clot: tPA (but increased chance of bleeding)
  2. Treatment to limit recurrence/ extension/ emboli
    • increased anticoagulant ability: heparin
    • lower procoagulant factors: warfarin, anti-platelets
    • Anti-coagulants
37
Q

Name three anti-coagulants

A

Rivaroxaban, Apixaban, Dabigatran

38
Q

Under which conditions is thrombolytic therapy offered and why?

A
  • only offered after a stroke
  • there is an increased risk of bleeding which could lead to cerebral haemorrhage
  • have to balance risk vs benefits
39
Q

What is offered instead of thrombolytic therapy and under which circumstances?

A
  • lowering procoagulant and increasing anticoagulant activity
  • when you have small clots and you want to stop it from growing/ embolising
40
Q

How does combined oral contraceptive increase the risk of thrombosis?

A
  • Factor V Leiden
  • Reduced concentration of Protein S
  • Reduced concentration of PAI-1
  • reduced endothelial activation
  • Prolonged contact activation

My LSS- CVS (21 decks)

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