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Semester 2 - Mechanisms of Disease > Session 5 - Haemostasis > Flashcards

Session 5 - Haemostasis Flashcards

1
Q

Why don’t you bleed to death from a minor injuet?

A

Haemostasis

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2
Q

What are the four factors upon which sucessful homeostasis depends?

A

vessel wall
platelets
coagulation system
fibrinolytic system

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3
Q

What are three types of blood vessels?

A

arteries, veins, capillaries

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4
Q

What do blood vessels do to prevent blood loss?

A

constrict to limit blood loss

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5
Q

What are the four roles of platelets?

A

adhere to damaged vessel wall
adhere to each other
form a platelet plug
platelet release reaction

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6
Q

Outline the platelet release reaction

A

Requires ATP
ADP, thromboxane A2 causes platelet aggregation. Serotonin and platelet factor 3 also released. PF3 important in coagulation.
Platelets coalesce after aggregation.

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7
Q

What kind of reaction is coagulation?

A

A cascade reaction, in which a series of inactive components are converted to active components.

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8
Q

What happens to prothrombin in the coagulation cascade, and what is its purpose?

A

Prothrombin –> Thrombin –> Fribrinogen –> Fibrin

Thrombin positively feeds forward on factors V, VIII and XI

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9
Q

Why is tight regulation of coagulation required?

A

1 ml of blood can generate enough thrombin to convert all the fibrinogen in the body to fibrin

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10
Q

Define haemostasis

A

The process which spontaneously arrests bleeding or haemorrhag

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11
Q

Why does there need to be a balance between coagulant and anti-coagulant factors?

A

To ensure clotting cascade initiates and terminates

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12
Q

What happens in the body if coagulant > anti-coagulant

A

Prolonged clotting, unstable clots

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13
Q

What happens in the body if coagulant levels < anti-coagulant

A

Brief coagulation and quick termination, excess bleeding

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14
Q

What is the extrinsic pathway in haemostasis?

A

endothelium is damaged causing the release of tissue factor

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15
Q

What is the intrinsic pathway in haemostasis?

A

activated by thrombin in a feedforward mechanism

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16
Q

What factor do both the extrinsic and intrinsic pathways meet?

A

At factor Xa

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17
Q

What are the 6 stages of fibrinolysis in haemostasis

A
  1. Thrombin binds to receptors on endothelium > protein C released
  2. Protein C degrades factors V and VIII in the liver
  3. Protein C causes urokinase-like plasminogen activator to be released
  4. ULPA converts plasminogen to plasmin
  5. Plasmin aids fibrinolysis
  6. tPG also aids fibrinolysis by the activation of plasminogen
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18
Q

Define thrombosis

A

The formation of a solid mass of blood within the circulatory system during life

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19
Q

Name two anti-thrombotic chemicals

A

prostacyclin

nitric oxide

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20
Q

Why does thrombosis occur ?

A

Abnormalities of vessel wall
Abnormalities of blood flow
Abnormalities of blood components

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21
Q

Give two possible abnormalities of blood flow

A

Stagnation
Venous stasis via the slow flowing blood in veins
Turbulence
Laminar flow disturbed > Cells hit vessel wall > damage can occur when vessels branch

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22
Q

Give three possible abnormalities of blood components

A

Smokers
Nicotine causes sticky platelets
Post partum
Liver compensates for blood loss by synthesizing more clotting factors
Post op
Liver compensates for blood loss by synthesizing more clotting factors

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23
Q

Give three possible abnormalities of vessel wall and how they could predispose someone to thrombosis

A

• Atheroma > cracks vessel wall > clotting cascade initiation
• Direct injury
• Inflammation (in vessel wall)
o E.g. primary vasculitis: thrombosis in temporal artery > blindess

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24
Q

What is the appearance of arterial

thrombi?

A
  • Pale
  • Granular – due to lots of platelets and fibrin
  • Lines of Zahn – ‘waves’ of thrombi
  • Lower cell content e.g. RBCs and WBCs
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25
Q

What is the appearance of venous thrombi?

A
  • Soft
  • Gelatinous
  • Deep red – lots of RBCs
  • Higher cell content – low fibrin & platelets
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26
Q

How can post mortem plots be distinguished from those that cause death?

A

Post mortem clots wash out easily, whereas DVT adher to vessel wall

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27
Q

What are the effects of arterial thrombosis?

A
  • Ischaemia
  • Infarction
  • Depends on site and collateral circulation
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28
Q

What are the effects of venous thrombosis?

A
  • Congestion
  • Oedema
  • Ischaemia
  • Infarction
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29
Q

Give four outcomes of a thrombosis

A 
Lysis
Propagation 
Organisation 
Recanalisation 
Embolism
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30
Q

Outline the process of lysis of a thrombosis

A
  • Complete dissolution of thrombus
  • Firbrinolytic system active
  • Bloodflow re-established
  • Most likely when thrombi are small
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31
Q

Outline propagation of a thrombosis

A
  • Progressive spread of thrombosis

- Goes distally in arteries, proximally in veins

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32
Q

Outline the process of organisation of a thrombosis

A
  • reparative process
  • Involves the ingrowth of fibroblasts and capillaries (similar to granulation tissue)
  • Lumen remains obstructed
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33
Q

Outline the process of recanalisation of a thombosis

A
  • Blood flow re-established but usually incompletely

- One or more channels formed through organising thrombus

34
Q

Outline the process of embolism of a thrombus

A
  • Part of thrombus breaks off
  • Travels through bloodstream
  • Lodges at distant site
35
Q

What are the effects of arterial thrombosis?

A
  • Ischaemia
  • Infarction
  • Effect depends on site and collateral circulation
36
Q

What are the effects of venous thrombosis?

A
  • Congestion
  • Oedema
  • Ischaemia
  • Infarction
37
Q

How could a DVT cause damage?

A

DVT dislodges, travels through right side of the heart to the lungs, causing a pulmonary embolism.

38
Q

What is the definition of an embolism?

A

Embolism is the blockage of a blood vessel solid, liquid or gas at a site distant from its origin

39
Q

What proportion of embolism are thrombo-emboli?

A

> 90%

40
Q

Give five factors which cause embolism, other than thrombi,

A
  • Air
  • Amniotic fluid
  • Nitrogen
  • Medical equipment
  • Tumour cells
41
Q

What arteries must a thrombosus travel through to reach the brain?

A

The carotid

42
Q

How can air infiltrate the vessels?

A

Small risk during head & neck surgery and venous injections

43
Q

Give some risk factors for DVT

A
  • Immobility/bed rest
  • Post-op
  • Pregnancy and post-partum
  • Oral contraceptives
  • Severe burns
  • Cardiac failure
  • Disseminated cancer
44
Q

How can bed rest cause DVT?

A

Muscles required to push blood back to the heart. Immobility means stasis ensues.

45
Q

How do oral contraceptives cause DVT?

A

Platelet aggregation

46
Q

How do severe burns cause DVT?

A
  • Bed rest/immobility ensues

- Dehydration > abnormalities of blood constituents > viscous blood

47
Q

How does cardiac failure cause DVT?

A

Stagnant blood

48
Q

How does disseminated cancer cause DVT?

A

Releases tissue thromboplastin - initiates clotting cascade

49
Q

What are two ways in which DVT can be treated?

A
  • intravenous heparin
  • oral warfarin
  • pulmonary embolectomy
50
Q

What is a massive PE?

A

Massive - >60% reduction in bloodflow, rapidly fatal.

51
Q

What is a major PE?

A

Major PE - Medium sized vessels blocked

52
Q

What is a minor PE?

A

Small peripheral pulmonary arteries blocked. Asymptomatic or minor shortness of breath

53
Q

What do recurrent minor PEs lead to?

A

Pulmonary hypertension

54
Q

Give four types of embolism

A

Cerebral embolism
Iatrogenic embolism
Nitrogen embolism
Fat embolism

55
Q

What is a cerebral embolism?

A
  • Atrial fibrillation -> Stasis -> Thrombus
  • Embolus in a cerebral vessel
  • Blocks blood supply > ischemia
  • Cerebral tissue will eventually undergo liquefactive necrosis
56
Q

What is an iatrogenic embolism?

A

An embolism caused by medical treatment (surgery, injection)

57
Q

What is a nitrogen embolism?

A
  • Results from rapid decompression resulting from quick ascent during a dive
  • Gaseous nitrogen forms in blood > blocks an airway
  • Pneumothorax; air cerebral embolism
58
Q

What is fat embolism?

A
  • Follows fractures of long bones and lacerations of adipose tissue
  • Fat globules enter circulation (marrow sinusoids and veins)
59
Q

Give three clinical features of a fat embolism (or more if you can)

A

o Rash

o SOB

o Dyspnoea

o Tachycardia

o Blood stained sputum

o Mental confusion

60
Q

How does heparin work?

A
  • Co-factor for anti-thrombin factor III
  • Prevent formation of new thrombi (do not lyse current ones)
  • Instantaneous response`
61
Q

How does warfarin work?

A
  • Delay between administration and effect > only acts of newly synthesized clotting factors in the liver
  • Competitive inhibitor for enzyme activating vitamin K
  • Can be taken orally - important as treatment can continue at home
62
Q

What is Haemophillia?

A

Hereditary x-linked recessive bleeding disorder affecting the clotting cascade

63
Q

What occurs in haemophillia A?

What occurs in haemophillia B?

A

A - Deficiency in factor VIII

B - deficient in factor IX

64
Q

What is the role of factor VIII in coagulation?

A

Serves as a cofactor for IX in the activation of factor X in the coagulation cascade

65
Q

What is Von Willebrand’s disease?

A

VWF is a protein synthesized by endothelium, and binds to factor VIII and acts to promot platelet adhesion to collagen. VWD involves reduced VWF activity

66
Q

What is disseminated intravascular coagulation?

A

Progressive activation of coagulation > failure of all components of haemostasis as a result of release of tissue factors. It results in clumps of fibrin mesh throughout circulation and uses up fibrinolytic factors resulting in bleeding risk.

67
Q

What is thrombocytopaenia?

A

Abnormally low platelet count, resulting in low platelet - usually accompanied by bone marrow dysfunction (leukaemia)

68
Q

What is there an abnormally low platelet count in thrombocytopaenia?

A
  1. Low production of platelets in the bone marrow
  2. Increased breakdown of platelets in the bloodstream (intravascular)
  3. Increased breakdown in the spleen or liver (extravascular)
  4. Sequestration of platelets (could be caused by DIC)
69
Q

What is thrombophillia?

A
  • Abnormality in blood clotting cascade (overactivity of clotting factors)> propensity to develop thromboses (clots)
  • Risk of DVT > PE
70
Q

How is thrombophillia acquired?

A
  • Can be congenital or acquired e.g. from oral contraceptive pills
71
Q

Give four thrombin inhibitors

A

Anti-thrombin III
Alpha 1 anti-trypsin
Alpha 2 macroglobulin
Protein C/S

72
Q

What is a key part of firbrinolytic therapy? When would it be used?

A

Streptokinase, which activates Plasminogen
Known as clot/thrombus busters

Would be used in coronary artery occlusion or thrombus cutting of circulation to limb

73
Q

What is DIC?

A

Disseminated Intravascular Coagulation
Pathological activation of clotting mechanisms in response to variety of diseases (infection, trauma, liver disease)
Small clots form throughout body, disrupting normal coagulation as use up all clotting factors.
Abnormal bleeding occurs from skin

74
Q

How does vitamin K work?

A

Vitamin K serves as an essential cofactor for a carboxylase that catalyzes carboxylation of glutamic acid residues on coagulation factors, such as prothrombin, VII, IX and X. This activates them, allowing them to bind to cell membranes and take part in clotting cascade

75
Q

Other than lack of blood coagulation on trauma, what are the effects of haemophillia?

A

Haemorrhage into major joints, causing synovial hypertrophy and pain
Muscle bleeding causes pain and necrosis of nerves

76
Q

Give two thrombin inhibitors and the disease they’re associated with if absent

A

Anti-thrombin III
Protein C/S

Thrombophillia and thrombosis

77
Q

What is a key part of firbrinolytic therapy? When would it be used?

A

Streptokinase, which activates Plasminogen
Known as clot/thrombus busters

Would be used in coronary artery occlusion or thrombus cutting of circulation to limb

78
Q

What is DIC?

A

Disseminated Intravascular Coagulation
Pathological activation of clotting mechanisms in response to variety of diseases (infection, trauma, liver disease)
Small clots form throughout body, disrupting normal coagulation as use up all clotting factors.
Abnormal bleeding occurs from skin

79
Q

How does vitamin K work?

A

Vitamin K serves as an essential cofactor for a carboxylase that catalyzes carboxylation of glutamic acid residues on coagulation factors, such as prothrombin, VII, IX and X. This activates them, allowing them to bind to cell membranes and take part in clotting cascade

80
Q

Other than lack of blood coagulation on trauma, what are the effects of haemophillia?

A

Haemorrhage into major joints, causing synovial hypertrophy and pain
Muscle bleeding causes pain and necrosis of nerves

Semester 2 - Mechanisms of Disease (16 decks)

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