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Z YEAR 2 BRS CARDIO > Haemostasis > Flashcards

Haemostasis Flashcards

1
Q

What is haemostasis?

A

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

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2
Q

What is haemostasis for?

A
  1. Prevention of blood loss from intact vessels
  2. Arrest bleeding from injured vessels
  3. enable tissue repair
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3
Q

What is the immediate response to injury to endothelial cell lining? What happens?

A
  • Vessel constriction
    1. Vascular smooth muscle cells contract locally
    2. Limits blood flow to injured vessel
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4
Q

What happens in primary haemostasis?

A
  • Formation of an unstable platelet plug
    1. platelet adhesion
    2. platelet aggregation
    3. Limits blood loss + provides surface for coagulation
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5
Q

What happens in secondary haemostasis?

A
  • Stabilisation of the plug with fibrin
    1. blood coagulation
    2. Stops blood loss
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6
Q

What happens in fibrinolysis?

A
  • Vessel repair and dissolution of clot
    1. Cell migration/proliferation and fibrinolysis
    2. Restores vessel integrity
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7
Q

Why do we need to understand haemostatic mechanisms?

A
  1. Diagnose and treat bleeding disorders
  2. Control bleeding in individuals who do not have an underlying bleeding disorder
  3. Identify risk factors for thrombosis
  4. Treat thrombotic disorders
  5. Monitor the drugs that are used to treat bleeding and thrombotic
    disorders
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8
Q

What could be a reason for bone marrow failure?

A
  • leukaemia (infiltration by leukaemic cells)
  • B12 deficiency (due to infiltration by megablasts) which squeezes out normal haemopoesis including development of platelets from megakaroycties
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9
Q

What could be a reason for accelerated clearance?

A
  • immune (ITP): more than sufficient platelets made by bone barrow but are destroyed in peripheral circulation
  • Disseminated Intravascular Coagulation (DIC)
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10
Q

What are some reasons/name for low number of platelets?

A
  • thrombocytopenia
    1. Bone marrow failure
    2. Accelerated clearance
    3. Pooling and destruction in an enlarged spleen
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11
Q

What is a very common cause of theombocytopenia?

A

ITP

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12
Q

Why might there be hereditary impaired function of platelts?

A

Hereditary absence of glycoproteins or storage granules (rare)

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13
Q

Why might there be acquired impaired function of platelts ?

A

due to drugs: aspirin, NSAIDs, clopidogrel (common)

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14
Q

What is prostaglandin thomboxane A2 produced by?

A

platelets from arachidonic acid

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15
Q

What does aspirin bind to?

A
  1. Inhibits production of thromboxane a2
  2. Binds irreversibly blocking action of COX
  3. So reduced platelet aggregation
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16
Q

What does clopidorgel irreversibility block?

A

Irreversibly blocks ADP receptor P2Y12 (on platelet cell membrane)

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17
Q

What are the reasons for Von Willebrand disease?

A
  • Hereditary decrease of quantity +/ function (common)

- Acquired due to antibody (rare)

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18
Q

What is the effect of VWF on haemostasis?

A
  1. Binding to collagen and capturing platelets
  2. Stabilising Factor VIII
    - Factor VIII may be low if VWF is very low
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19
Q

What is VWD hereditary?

A
  1. VWD is usually hereditary (autosomal inheritance pattern)
  2. Deficiency of VWF (Type 1 or 3)
  3. WF with abnormal function (Type 2)
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20
Q

What are the hereditary reasons for vessel wall disorder?

A
  • Inherited (rare), abnormalities in collagen
    1. Hereditary haemorrhagic telangiectasia
    2. Ehlers-Danlos syndrome and other connective tissue disorders
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21
Q

What are the acquired reasons for vessel wall?

A
  1. Steroid therapy (LT can mean atrophy of collagen fibres supporting blood vessels in the skin)
  2. Ageing (‘senile’ purpura)
  3. Vasculitis
  4. Scurvy (Vitamin C deficiency) - defective collagen synthesis leading to weakening of capillary wall
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22
Q

What are typical primary haemostasis bleeding?

A
  1. Immediate
  2. Prolonged bleeding from cuts
  3. Nose bleeds (epistaxis):prolonged > 20 mins
  4. Gum bleeding: prolonged
  5. Heavy menstrual bleeding (menorrhagia)
  6. Bruising (ecchymosis), may be spontaneous/easy
  7. Prolonged bleeding after trauma or surgery
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23
Q

What are tests for disorders of primary haemostasis?

A
  1. Platelet count, platelet morphology
  2. Bleeding time (PFA100 in lab)
  3. Assays of von Willebrand Factor
  4. Clinical observation (look at connective tissue disorder)
  5. Note –coagulation screen (PT, APTT) is normal (except more severe VWD cases where FVIII is low)
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24
Q

How do you treat the failure of production/function for the treatment of abnormal haemostasis?

A
  1. Replace missing factor/platelets e.g. VWF containing concentrates
    i) Prophylactic
    ii) Therapeutic
  2. Stop drugs e.g. aspirin/NSAIDs
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25
Q

How do you treat the immune destruction for the treatment of abnormal haemostasis?

A
  1. Immunosuppression (e.g. prednisolone) (steroid)

2. Splenectomy for ITP

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26
Q

How do you treat the increased consumption e.g. in DIC for the treatment of abnormal haemostasis?

A
  • Treat cause

- Replace as necessary

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27
Q

Why do you use desmopressin (DDAVP) for haemostatic treatment?

A
  1. Vasopressin analogue
  2. 2-5 fold increase in VWF (and FVIII)
  3. releases endogenous stores of WVF (so only useful in mild disorders)
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28
Q

Why do you use tranexamic acid for haemostatic treatment?

A

Antifibrinolytic

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29
Q

What are some other haemostatic treatments?

A
  1. Fibrin glue/spray

2. Other approaches e.g hormonal (oral contraceptive pill for menorrhagia)

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30
Q

What are disorders of coagulation (secondary haemostasis)?

A
  1. The role of coagulation is to generate thrombin (IIa), which will convert fibrinogen to fibrin
  2. Deficiency of any coagulation factor results in a failure of thrombin generation and hence fibrin formation
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31
Q

What are the hereditary reasons for deficiency of coagulation factor production?

A
  • Factor VIII deficiency (haemophilia A)

- Factor IX deficiency (haemophilia B_

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32
Q

What are the acquired reasons for deficiency of coagulation factor production?

A
  1. Liver disease
  2. Anticoagulant drugs such as:
    - Warfarin
    - Direct Oral Anticoagulants (DOACs)
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33
Q

What are acquired reasons for dilution?

A

-Blood transfusion (inadequate replacement of plasma following massive haemorrhage)

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34
Q

What are acquired reasons for increased consumption?

A
  1. Disseminated intravascular coagulation (DIC) – common

2. Immune – autoantibodies – rare)

35
Q

What are some hereditary coagulation disorders?

A 
•Haemophilia A (Factor VIII deficiency) 
•Haemophilia B (Factor IX deficiency) 
-sex linked (X linked)
- in 104 births
•Others are very rare (autosomal recessive
36
Q

What is haemostasis?

A

Fibrin clot stabilising platelet plug

37
Q

What is haemophilia?

A

Failure to generate fibrin to stabilise platelet plug and will break away

38
Q

What is haemarthrosis?

A

Hallmark of haemophilia (in non developed countries) - spontaneous joint bleeding when factors 8 or 9 are very low

39
Q

What should be avoided for people with haemophilia?

A

Intramuscular injections

40
Q

What does absence of factor VIII and IX (haemophilia) lead to?

A
  • Severe but compatible with life

- Spontaneous joint and muscle bleeding

41
Q

What does absence of prothrombin (factor II) lead to?

42
Q

What does absence of factor XI lead to?

A

-Bleed after trauma but not spontaneously

43
Q

What does absence of factor XII lead to?

A

-No bleeding at all

44
Q

What are three main reasons for acquired coagulation disorders?

A
  1. Liver failure – decreased production in coagulation factors as most coagulation factors are synthesised in the liver
  2. Anticoagulant drugs
  3. Dilution
    •Red cell transfusions no longer contain plasma
    •Major haemorrhage requires transfusion of plasma as well as red cells and platelets
45
Q

What are the clinical features of coagulation disorders?

A
  1. superficial cuts do not bleed as platelets plugs is fine for small vessels but in large vessels falls apart so bleeding can restart after stopping
  2. bruising is common, nosebleeds are rare
  3. spontaneous bleeding is deep, into muscles and joints
  4. bleeding after trauma may be delayed and is prolonged
  5. Bleeding frequently restarts after stopping
46
Q

What is bleeding like due to platelet/vascular defect?

A
  1. Superficial bleeding into skin, mucosal membranes

2. Bleeding immediate after injury

47
Q

What is bleeding like in coagulation defect?

A
  1. Bleeding into deep tissues, muscles, joints

2. Delayed, but severe bleeding after injury and bleeding often prolonged

48
Q

What are some screening tests for coagulation disorders?

A
  1. Prothrombin time (PT)
  2. Activated partial thromboplastin time (APTT)
  3. Full blood count (platelets)
49
Q

What is normal haemostasis?

A

balance between bleeding and thrombosis, achieved by keeping coagulant factors and platelets in equilibrium with fibrinolytic factors and anticoagulant proteins

50
Q

What happens in bleeding?

A

more fibrinolytic factors and anticoagulant proteins than coagulant factors and platelets

51
Q

Why is there a reduction of coagulation factors and platelets?

A
  1. Lack of a specific factor

2. Defective function of specific factor

52
Q

Why would there be a lack of a specific factor?

A
  1. Failure of production: congenital and acquired

2. Increased consumption/clearance

53
Q

Why would there be a defective function of a specific factor?

A
  1. Genetic

2. Acquired: drugs, synthetic defect, inhibition

54
Q

What is involved in primary haemostasis?

A
  • Platelet
  • Endothelial wall
  • VWF
55
Q

What does damage to the endothelium result in?

A

exposure of collagen in vessel wall

56
Q

How do platelets adhere to the collagen in primary haemosatsis?

A
  1. directly through glycoprotein 1a receptor

2. by VWF via the gylcoprotein 1b receptor

57
Q

How are platelets activated?

A

release of their granular contents

with generation of thromboxane from arachnoic acid

58
Q

What does platelets activated lead to?

A

flip flopping and acitvation of GP2b/3a receptors on platelets

59
Q

What happens in ITP?

A
  1. Antiplatelet antibodies stick to the sensitised platelet

2. this will be cleared by the macrophages of the reticulo-endoethloial system in the spleen

60
Q

What is Glanzmann thrombothaenia?

A

absence of the GPII/bIIIa receptor on platelets

61
Q

What is Bernard Soullier syndrome?

A

absence of GPIb receptor

62
Q

What is storage pool disease?

A

group of disorders referring to reduction in the granular contents of platelets (dense granules)

63
Q

Is prostacyclin inihibited?

A

inihibited by cyclo-oxygenase unlike the non-nucelar plateletit can be further generated by endothelial cell

64
Q

How long is the effect of aspirin?

A

7 days where most of platelets present at time of ingestion of aspirin ingestion have been replaced by new platelets

65
Q

What happens in platelet plug formation?

A
  1. Site of vessel injury damage to the endothelial cell, exposing collagen
  2. Along comes VWF in its coiled forms and the shear stress result in this being unfolded and uncoiled and the platelets can adhere and the platelets become activated
  3. the same thing happens and platelet plug forms
    4, Plug cannot form in VWD
66
Q

What is petechia and purpura?

A

caused by bleeding under the skin

67
Q

What do purpura do when pressure is applied?

A

Not blanch

68
Q

What is a particular features of thrombocytopenia?

A

petechia (they are <3mm)

69
Q

What are the sizes of petechia, purpura and ecchymosis?

A
  • petechia (they are <3mm)
  • Purpa (3-10mm)
  • Ecchymosis (>10mm)
70
Q

When do you see purpura?

A

platelet (thrombocytopenic purpura) or vascular disorders

71
Q

What is wet purpura?

A

purpura over mucosal surfaces e.g, gum

72
Q

What happens in severe WVF?

A

haemophilia-like bleeding (due to low FVIII)

73
Q

What is normal platelet count?

A

150-200 x10^9 L

74
Q

What happens in platelet count fall below 100x10^9L?

A

No spontaneous bleeding but bleeding with trauma

75
Q

What happens in platelet count fall below 40x10^9L?

A

Spontaneous bleeding common

76
Q

What happens in platelet count fall below 10x10^9L?

A

Severe spontaneous bleeding

77
Q

Where is VWF synthesised?

A

in endothelial cells lining blood vessels

78
Q

Where is factor V synthesised?

A

synthesised in platelets

79
Q

How to avoid dilution effect with reduction in coagulation factor?

A

•Major haemorrhage requires transfusion of plasma as well as red cells and platelets

80
Q

What is disseminated intravascular coagulation?

A
  1. Generalised activation of coagulation – Tissue factor (normally does not come into contact with factor 7a leads to widespread and unregulated activation of coagulation
  2. Consumes and depletes coagulation factors
  3. Platelets consumed - thrombocytopenia
  4. Activation of fibrinolysis depletes fibrinogen – raised D-dimer
    (a breakdown product of fibrin)
  5. Deposition of fibrin in vessels causes organ failure and can result in sheering of rbc that flow through these vessles and red cell fragmentation
81
Q

What can disseminated intravascular coagulation be triggered by?

A
  1. sepsis
  2. major tissue damage (cancer)
  3. inflammation
  4. Obstetrics (severe preclampsyia)
82
Q

What is treatment of DIC?

A

Only way to switch this off is by treating underlying cause but in mean time replacement of missing coagulation factors (FFP / platelets)

83
Q

What are other tests for coagulation disorders?

A
  • Coagulation factor assays (for Factor VIII etc)

* Tests for inhibitors

Z YEAR 2 BRS CARDIO (18 decks)

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