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BRS CARDIO & RESPIRATORY > 1b Haemostasis > Flashcards

1b Haemostasis Flashcards

1
Q

What is haemostasis?

A

the cellular and biological processes that enable both the specific and regulated cessation of bleeding in response to vascular insult

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2
Q

What is haemostasis for?

A

Prevention of blood loss from intact vessels
Arrest bleeding from injured vessels
Enable tissue repair

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3
Q

What is the response to injury to endothelial cell lining?

A

Vessel constriction - vascular smooth muscle cells contract locally which limits blood flow to the injured vessel

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4
Q

What does primary haemostasis involve?

A

Formation of an unstable platelet plug - platelet adhesion and platelet aggregation

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5
Q

What is the purpose of primary haemostasis?

A

Limits blood loss and provides a surface for coagulation

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6
Q

How do platelets bind directly to the exposed collagen?

A

The platelets bind to the GpIa receptor = binds directly to the exposed collage

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7
Q

How do platelets bind to Von Willebrand Factor?

A

Using the Gp1b receptor

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8
Q

What happens to the platelets after they bind and adhere to the endothelial lining?

A

Release of their granular contents = ADP and thromboxane

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9
Q

How do platelets aggregate with each other in primary haemostasis?

A

Using the GpIIb / IIIa receptor

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10
Q

What term is used to describe low platelet numbers?

A

Thrombocytopenia

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11
Q

What are some causes of thrombocytopenia?

A
  • Bone marrow failure
  • Accelerated clearance
  • Pooling and destruction in an enlarged spleen
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12
Q

What conditions might cause bone marrow failure

A

leukemia, B12 deficiency, BM infiltration

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13
Q

What conditions might cause accelerated clearance of platelets?

A

Immune (ITP), Disseminated Intravascular Coagulation (DIC)

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14
Q

What is ITP?

A

Immune Thrombocytopenic Purpura

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15
Q

Describe how ITP occurs?

A
  • Antiplatelet autoantibodies bind to the sensitized platelet
  • The sensitized platelets are then cleared by macrophages in the spleen
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16
Q

What is a very common cause of thrombocytopenia?

A

ITP

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17
Q

Describe how the function of platelets might be impaired?

A
  • Hereditary absence of glycoproteins or storage granules
  • Acquired due to drugs
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18
Q

What causes of Glanzmann’s syndrome?

A

Absence of GPIIb / IIIa

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19
Q

What causes Bernard Soulier Syndrome

A

Absence of GPIb

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20
Q

What causes storage pool disease?

A

reduction in the dense granules of platelets

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21
Q

Which drugs might cause an acquired impairment to the function of platelets?

A

Aspirin, NSAID’s, Clopidogrel

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22
Q

What are the two common antiplatelet drugs?

A

Aspirin and Clopidogrel

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23
Q

How does aspirin work?

A

irreversibly blocks cyclo-oxygenase meaning Thromboxane A2 cannot be produced

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24
Q

Why does aspirin not affect prostacyclin synthetase?

A

Because it can be further generated by the endothelial cells

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25
Q

How does clopidogrel work?

A

Ireversibly blocks the ADP receptor on platelets - P2Y12 on cell membrane

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26
Q

What are the two functions of Von Willebrand Factor in primary haemostasis?

A

Binding to collagen and capturing platelets
Stabilising factor VIII (8)

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27
Q

What is the usual inheritance pattern of VWD?

A

Hereditary = autosomal inheritance pattern
- Deficiency of VWF
- VWF with abnormal function

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28
Q

What are the inherited conditions of primary haemostasis related to the vessel wall?

A
  • Hereditary haemorrhagic telangiectasia
  • Ehlers-Danlos syndrome
  • Other connective tissue disorders
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29
Q

What are the acquired disorders of primary haemostasis related to the vessel wall?

A

Steroid therapy causes atrophy of the collage fibres which support the blood vessels

Ageing = senile purpure

Vasculitis

Scurvy

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30
Q

What is VWD a failure of?

A

Failure of primary haemostasis

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31
Q

What is a key sign of thrombocytopenia?

A

Petechiae - small red dots on the skin which are less than 3mm in size

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32
Q

What causes petechiae and purpura?

A

Bleeding underneath the skin

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33
Q

What is the difference between petechiae and purpura

A

Petechiae = < 3mm and Blanch when pressure is applied
Purpura = 3-10mm and do not blanch when pressure is applied

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34
Q

What conditions result in purpura on the skin?

A

Platelet (thrombocytopenic purpura) or vascular disorders

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35
Q

What are the typical bleeding features of primary haemostasis?

A

Immediate bleeding
Prolonged bleeding from cuts
Nose / gum / Heavy menstrual bleeding
Prolonged bleeding after trauma / surgery
Bruising

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36
Q

What is the medical term for nose bleeds?

A

Epistaxis

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37
Q

What is the medical term for heavy menstrual bleeding?

A

Menorrhagia

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38
Q

What type of bleeding is seen in Severe VWD?

A

Haemophillia like bleeding - around joints

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39
Q

What are the visible clinical features of primary haemostasis?

A

Petechiae
Purpura
Ecchymosis
Senile Purpura
Increased Skin Elasticity

40
Q

What would a coagulation screen (APPT and PT) show in a disorder of primary haemostasis?

A

Would be normal

41
Q

What tests are done for disorders of primary haemostasis?

A

Platelet count
Bleeding time
VWF assays
Clinical Observations

42
Q

What range of platelet count would result in no spontaneous bleeding but bleeding with trauma?

A

40-100 x 10^9 / L

43
Q

What range of platelet count would result in spontaneous bleeding?

A

10-40 x 10^9 / L

44
Q

What range of platelet count would result in severe spontaneous bleeding?

A

<10 x 10^9 / L

45
Q

What is the treatment principle for abnormal haemostasis due to immune destruction?

A

Immunosuppression
Splenectomy for ITP

46
Q

What is the treatment principle for abnormal haemostasis due to failure of production / function?

A

Replace the missing platelets / factors
Stop drugs like Aspirin

47
Q

What is the treatment principle for abnormal haemostasis due to Increased Consumption?

A

Treat the cause
Replace as necessary

48
Q

What is desmopressin and how can it help in disorders of primary haemostasis?

A

2-5 fold increase in VWF and Factor 8 - releases endogenous stores so only useful in mild disorders

49
Q

What is secondary haemostasis?

A

Coagulation

50
Q

What is the role of coagulation?

A

To generate THROMBIN (IIA) = converts fibrinogen into fibrin

51
Q

What are the three stages of secondary haemostasis?

A

Initiation
Amplification
Propagation

52
Q

What factor is deficient in patients with Haemophillia A?

A

Factor 8 deficiency

53
Q

What factor is deficient in patients with Haemophillia B?

A

Factor 9

54
Q

What are some causes of acquired deficiency of coagulation factor production?

A

Liver disease
Anti-coagulant drugs - Warfarin and direct oral anti-coagulants

55
Q

What is dilution and how does it cause a coagulation disorder?

A

Inadequate plasma replacement following blood transfusion, as only RBC’s are given, not plasma therefore more dilute

56
Q

What is the inheritance pattern of Haemophillia?

A

Sex (X) Linked

57
Q

What is haemophillia?

A

Lack of clotting factors results in a failure to generate fibrin to stabilise a platelet plug, therefore it becomes unstable, falls apart and bleeds

58
Q

What is the hallmark of haemophillia?

A

Haemarthrosis - spontaneous joint bleeding

59
Q

What specific method of treatment should be avoided in patients with haemophillia?

A

Intramuscular injections

60
Q

Which clotting factor deficiencies are compatible with life?

A

Haemophillia

61
Q

Which clotting factor deficiencies are not compatible with life?

A

prothrombin deficiency

62
Q

What does a factor 12 deficiency result in?

A

NO bleeding at all

63
Q

What does a factor 11 deficiency result in?

A

Bleeding after trauma but not spontaneously

64
Q

Why might liver failure case an acquired coagulation disorder?

A

Most of the clotting factors are synthesised in the liver - except VWF which is made in the endothelial cells of blood vessels

65
Q

What is disseminated intravascular coagulation?

A

Generalised activation of coagulation due to tissue factor which therefore consumes and depletes coagulation factors, resulting in thrombocytopenia

66
Q

What dimer is raised in DIC?

A

D dimer - breakdown product of fibrin due to increased fibrinolysis

67
Q

Why do superficial cuts not bleed in coagulation disorders?

A

The unstable platelet plug is sufficient to stop small vessel bleeds

68
Q

What are the clinical features of coagulation disorders?

A
  • Superficial cuts do not bleed
  • Bruising is common, nose bleeds are rare
  • Spontaneous bleeding into the muscles and joints
  • Bleeding after trauma may be delayed and is prolonged
  • Bleeding frequently restarts after stopping
69
Q

What are the two main clinical distinctions between bleeding due to platelet and coagulation defects?

A

Platelet = Bleeding is subcutaenous, mucosal membranes, and immediate after injury

Coagulation = bleeding is deeper (in muscle and joints) and is delayed after injury, but prolonged

70
Q

What does APTT measure?

A

The intrinsic pathway (12 11 9 8)

71
Q

What does PT measure?

A

The extrinsic pathway (3+7 - 10 5 2)

72
Q

What found conditions could cause a normal PT time but elevated APTT time?

A

Haemophillia A / B
factor 8 / 9 deficiency

73
Q

What condition could cause a normal APTT time but abnormal (elevated) PT time?

A

Factor 7 defiency

74
Q

What conditions could cause both APTT and PT to be raised?

A

Liver disease
Anticoagulant drugs
DIC
Dilution following RBC transfer

75
Q

What is used to replace all the coagulation factors?

A

Fresh Frozen Plasma

76
Q

What does cyroprecipitate contain?

A

Fibrinogen, Factor 8, VWF and factor 13

77
Q

What are recombinant forms of Factor 8 used for?

A

Used on demand to treat bleeds

78
Q

What are some of the novel treatments for haemophillia?

A

Gene therapy
Bispecific antibodies
RNA silencing

79
Q

Which drugs are increase fibrinolytic factors?

A

tPA and Heparin

80
Q

What are the signs of pulmonary embolism?

A

Tachycardia - palpitations
hypoxia
Shortness of breath
Chest Pain

81
Q

What are the signs of Deep vein Thrombosis/

A

Painful leg
Swelling
Redness
Warmth
May embolise to the lungs

82
Q

What do most people with disorders of thrombosis die of?

A

haemostatic end point

83
Q

What is a thrombosis?

A

It is an intravascular coagulation, can be venous or arterial (more commonly venous) which obstructs flow

84
Q

What are the three contributory factors to Virchow’s triad?

A

Blood
Vessel Wall
Blood Flow

85
Q

Which factor in Virchow’s triad is dominant in venous thrombosis?

A

Blood

86
Q

Which factor in Virchow’s triad is dominant in arterial thrombosis?

A

Vessel wall

87
Q

Which factor in Virchow’s triad contributes to both arterial and venous thrombosis?

A

Blood flow

88
Q

What is thrombophillia?

A

Increased risk of venous thrombosis

89
Q

What are anti-coagulant proteins?

A

Anti-thrombin
Protein C and Protein S

90
Q

What change to anti-coagulant proteins might lead to venous thrombosis?

A

Decreased anticoagulant proteins

91
Q

What might increase in order for a thrombosis to occur?

A

Coagulant factors
Platelets - in myeloproliferative disorders

92
Q

How does the risk of venous thrombosis change with age?

A

Increases with age

93
Q

How does inflammation relate to arterial thrombosis?

A

Many proteins active in coagulation are expressed on the surface of the endothelial cels and their expression is altered in inflammation

94
Q

What is stasis and what can cause it?

A

reduced blood flow

Surgery, long haul flights, surgery, pregnancy

95
Q

What is the cause of venous thrombosis?

A

Multi-causal = arises from interacting genetic and acquired risk factors, results in a cumulative risk which is over the thrombotic threshold

96
Q

What is the treatment of venous thrombosis?

A

Assess and prevent risks
Prophylactic anti-coagulation therapy
Reduce risk of recurrance - lower procoagulant factors, or increase anti-coagulant activity

BRS CARDIO & RESPIRATORY (26 decks)

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