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Path Processes* > Session 5 Haemostasis, Thrombosis And Emolism > Flashcards

Session 5 Haemostasis, Thrombosis And Emolism Flashcards

1
Q

How are blood clots formed?

A

Extrinsic pathway and intrinsic pathways both lead to…

  • factor Xa activates thrombin from prothrombin
  • thrombin converts fibrinogen to fibrin
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2
Q

How are platelets formed?

A
  • megakaryocytes produce platelets in the bone marrow
  • platelets bud from cytoplasm
  • normal life span = 7-10 days
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3
Q

When do adhesion and activation of platelets occur?

A

Adhesion

  • damage to vessel wall
  • exposure of underlying tissue
  • platelets adhere to collagen

Activation

  • secrete ADP, thromboxane and other substances to become activated
  • involved in activation of clotting cascade
  • provide some coagulation factors
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4
Q

What are the mediating factors of the clotting cascade?

A

1) fibrinogen
2) collage
3) ADP
4) thrombin
5) thromboxane

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5
Q

What is the role of the clotting cascade?

A

Enmeshed initial platelet plug to make stable clot

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6
Q

What is Von willebrand factor?

A

A coagulation factor. Involved in platelet adhesion to the vessel wall.

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7
Q

What is the role of the vessel wall in the clotting cascade?

A
  • vasoconstriction
  • production of Von willebrands factor, essential for platelet adhesion
  • exposure of collagen and tissue factor which initiates activation of clotting factors
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8
Q

What are some coagulation factor disorders?

A

Congenital

  • haemophilia A (factor 8)
  • haemophilia B (factor 9)

Acquired

  • liver disease
  • vit K deficiency
  • anticoagulant including warfarin (inhibits vit k)
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9
Q

What’s the difference between haemophilia A and haemophilia B?

A

A

  • x linked recessive
  • severity depends on amount of factor 8 present
  • bleeding into muscles and joints and post operative

B
- lack of factor 9

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10
Q

What is von willebrands disease?

A
  • autosomal dominant
  • abnormal platelet adhesion to vessel wall
  • lack of vWF production
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11
Q

What are the clinical presentation of VWD?

A
  • skin and muscle membranes bleeding e.g gum bleeding and bruising
  • prolonged bleeding after trauma e.g post surgery and dental extraction
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12
Q

What are some congenital and acquired problems with vessels?

A

Congenital

  • hereditary haemorrhaging
  • CT disorders e.g ehlers danlos

Acquired

  • senile purapura
  • steroid
  • infection
  • scurvy
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13
Q

What are thrombophilias?

A
  • acquired or congenital defects of haemostasis = increase patient risk of thrombosis
  • deficiency in natural anticoagulants

Relatively rare, don’t occur unless patient has additional risk factors

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14
Q

What’s is disseminated intravascular coagulopathy?

A
  • type of microangiopathic haemolytic anaemias
  • pathological activation of coagulation
  • numerous micro thrombi are formed in circulation
  • always a trigger e.g. malignancy, tissue injury, infections (gram neg sepsis), haemorrhage, ABO transfusion reactions, etc.
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15
Q

Why would a thrombosis occour?

A

Abnormalities in vessel wall
E.g atheroma, direct injury, inflammation

Abnormalities of blood components
E.g post partum , smoker, post op

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16
Q

How do arterial and venous thrombi differ in their appearance?

A

Arterial

  • pale
  • granular
  • lines of zahn
  • lower cell content

Venous

  • soft
  • gelatinous
  • deep red colour
  • higher cell content
17
Q

What is lysis?

A

Complete dissolution of thrombus, blood flow is reestablished, most likely when thrombi are small

18
Q

What is propagation?

A

Progressive spread of thrombi, distally in arteries, proximal in veins

19
Q

What is organisation?

A

Reparative process, ingrowth of fibroblasts and capillaries, similar to granulation tissue

20
Q

What is recanalisation?

A

Blood flow reset abolished and one or more canals form through original thrombus

21
Q

What’s an embolism?

A

Part of thrombus breaks off and travels through blood stream to lodge at a distant site

22
Q

What are the arterial and venous effects of thrombosis?

A

Arterial

  • ischaemia
  • infarction
  • depends on site and collateral circulation

Venous

  • congestion
  • oedema
  • ischaemia
  • infarction
23
Q

What are some predisposing factors to DVT?

A 
Immobility/bed rest 
Post operative
Pregnancy/post partum 
Oral contraceptives
Severe burns 
Cardiac failure
24
Q

What can treat dvt?

A

Intravenous heparin and oral warfarin

25
Q

What’s the difference between a major and minor PE?

A

Major pe - medium sized vessels blocked, patient short of breath and may cough blood and stained sputum

Minor - small peripheral pulmonary arteries blocked. Asymptomatic or mild shortness of breath.

26
Q

What does recurrent minor PE lead to?

A

Pulmonary hypertension

Path Processes* (10 decks)

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