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CardioRespiratory 2 > Haemostasis 2 > Flashcards

Haemostasis 2 Flashcards

1
Q

What is the balance between coagulation and fibrinolysis when bleeding?

A

Coagulation factors decrease and platelets decrease

Fibrinolytic factors and anti coagulants increase

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2
Q

Why may coagulation factors be low?

A

ailure of production: congenital and acquired

defective function of a specific factor:
genetic or acquired from drugs, synthetic defects, inhibition

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3
Q

How do platelets adhere to collagen?

A

Directly via GLpIa or GLpIb indirectly via VWF

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4
Q

What may be disorders of primary haemostsis?

A

Platelet disorders

Von Willebrand factor

The vessel wall

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5
Q

What is thombocytopenia?

A

Low numbers of platelets

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6
Q

What may cause thombocytopenia?

A

Bone marrow failure due to Leukaemia or B12 defiency

Accelerated clearance e.g. immune, disseminated intravascular coagulation

Pooling and destruction in an enlarged spleen

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7
Q

What may cause an impared function of platelets?

A

Hereditary absence of glycoproteins or storage granules - this is rare

Acquired due to drugs

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8
Q

What impairment is found with Glenzmann’s thrombasthenia?

A

Absence of GpIIb/IIIa

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9
Q

What impairment is found with bernal soulier syndrome?

A

Absence of GpIb receptors

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10
Q

What impairments are found with storage pool disease?

A

reduction of dense granules in platelet e/g/
ADP
ATP

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11
Q

Which drugs can cause impaired platelet function?

A

Aspirin
NSAIDs
Clopidogrel (common) - antiplatelet drug

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12
Q

What are the common anti platelet drugs?

A

Aspirin and clopidogrel

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13
Q

How does aspirin work?

A

irreversibly blocks COX to stop prostoglandin thromboxane A2 from being produced by the arachidonic acid in platelets

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14
Q

How does clopidogrel work?

A

irreversibly blocks ADP receptor on platelets

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15
Q

What is von willebrand disease?

A

Hereditary decrease of quantity which can +/- function

could also be acquired due to an antibody but this is rare

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16
Q

What are the two functions of VWF?

A

Binding to collagen and capturing platelets

Stabalising Factor VIII

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17
Q

If VWF is low then?

A

Factor VIII may be low

  • because they travel as a complex of glycoproteins and both are involved with hemophilia
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18
Q

What mutations can cause VWF disorder?

A

Deficiency of VWF - type 1 + 3

VWF with abnormal function - type 2

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19
Q

What can cause vessel wall disorders

A

inherited haemorrhagic telangiectasia Ehlers-Danlos and other connective tissue disorders - rare

Acquired is more common : steroid therpy, ageing, vasculitis, scurvy

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20
Q

What are the clinical features of disorders of primary haemostasis?

A

– imemdiate manifestation of bleeding
- prolonged bleeding from cuts
- nose and gum bleeding
- menorrhagia
- Eccyhmosis may be easy
prolonged bleeding after surgery

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21
Q

What is Ecchymosis?

A

Bruising

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22
Q

What can be seen on the skin due to bleeding under the skin due to thrombocytopenia

A

petechiae (<3mm) purpura 3-10mm) (these do not blanch when pressure is applied)

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23
Q

What can be seen on the skin due to bleeding under the skin due to vascula disorders?

A

Purpura

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24
Q

How does severe VWF disorder present?

A

Haemophilia like bleeding due to low FVIII

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25
Q

How do we test for disorders of primary haemostasis?

A
  • platelet count, morphology

bleeding time- PFA100

assays of VWF

clinical observation

*coagulation screen, PT, APTT are both normal in these patients (except for severe VWF due to low V8)

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26
Q

What platelet count would result in spontaneous bleeding?

A

less than 40x10^9 / L

if lower than 10x10^9/L then very severe spontaneous bleeding

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27
Q

How to treat failure of production / function that cayses primary haemotasis disorders?

A

replace : VWF, platelets

  • prophylactic
  • therapuetic

stop aspirin/NSAIDS

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28
Q

How to stop immune destruction based primary haemostasis disorder?

A

immunosuppression - prednisolone

splenectomy for ITP - Immune thrombocytopenic purpura

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29
Q

How to treat increased consumption causing primary disorders

A

treat cause

replace as necessary

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30
Q

What is Desmospressin used for?

A

Vasopressin analogue and can increase VWF from endogenous stores * only useful in mild disorders

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31
Q

What is tranexamic acid used for?

A

Antifibrinolytic

  • used in heavy periods
32
Q

What other (non conventional) haemostatic treatments are there for primary disorders?

A

fibrin glues and sprays in theatre

OCP - for menorrhagia

33
Q

What is secondary haemostasis?

A

coagulation

Platelet plug being stabilised by fibrin to stop blood loss

34
Q

What is the role of coagulation?

A

generate thrombin = 2a

converts fibrinogen to fibrin

Deficiency of any coagulation factor can cause failure of thrombin generation an hence the fibrin plug

35
Q

What can cause disorders of coagulation?

A

Coagulation factor production deficiency

dilution

increased consumption

36
Q

What can cause dificiency of coagulation factor production?

A

Hereditary: factor V8 / 9

haemophilia a/b

acquired: liver disease
anticoagulation drugs (warfarin and DOACs)
37
Q

What is dilution?

A

From blood transfusion

38
Q

what causes increased consumption disorders of coagulation?

A

Disseminated intravascular coagulation - common

immune antibodies - rare

39
Q

What is Haemophilia A and B?

A

a = factor 8 deficiency

b = factor 9

sex linked

40
Q

What is Haemarthrosis and what is this the hallmark of?

A

Spontaneous joint bleeding when factors 8/9 is low

  • can be avoided with propholaxis replacement therapy

if is it chronic haemarthrosis it can cause muscle wasting and joint deformity

41
Q

can you give a px with haemophilia intramuscular injection?

A

No

42
Q

What are some examples of lethal coagulation factor deficiencies?

A

Prothrombin

43
Q

What are the clinical bleeding signs of factor 11 deficiency?

A

bleed after trauma not spontaneously

44
Q

What are the bleeding signs of factor XII deficiency?

A

no bleeding

45
Q

Why does liver failure result in coagulation disorder?

A

Most factors are made in the liver

46
Q

How to avoid a dilutional effect after haemorrhage?

A

When giving blood transfusion do not just give red blood cells

require plasma and platelets to otherwise will lose coagulation factors

47
Q

What occurs in dissemniated intravascular coagulation?

A

general activation of coagulation - tissue factor

associated with SEPSIS or cancer, major tissue damage and inflammation

depletes factors

thrombocytopenia too

activation of fibrinolysis depletes fibrinogen == raised D dimer

48
Q

What is the D-dimer?

A

A breakdown product of fibrin

49
Q

What does the deposition of fibrin in vessels following increased consumption cause?

A

Organ failure

and sheering of red blood cells = fragmentation

50
Q

What are the clinical features of coagulation disorders?

A

Superficial cuts do not bleed as platelets are fine

bruising common

spontaneous bleeding is deep into muscles of joints

bleeding after trauma may be delayed and is prolonged

bleeding frequently restarts after stopping

51
Q

What tests are done for coagulation disorders?

A

Screening tests :
PT
APTT
full blood count

Coagulation factor assays for factor VIII

tests for inhibitors

52
Q

What could cause these results:

PT = 10.6s (normal)

APTT = 85s (high)

A
  • haemophilia A/B
  • factor XI, XII deficiency

intrinsic pathway

53
Q

What could cause these results:

PT = 26s (high)

APTT = 29s (normal)

A

Factor VII deficiency in extrinsic pathway

54
Q

What could cause these results:

both PT and APTT are high?

A
  • liver disease
  • anti coagulation drug
  • DIC
  • dilution
55
Q

How can we replace factors?

A

Factor replacement therapy

–> plasma FPP with all coagulation Factors

–> cryoprecipitate with fibrinogen, 8, 13, VWF

–> factor concentrates, available for all except factor 5

Prothrombin complex concentrates include factor 2, 7, 9, 10

Recombinant forms of Factor 8 and 9 are available on demand for bleed and on prophylaxis

56
Q

How was haemophilia first treated?

A

plasma derived clotting factors, however this was an issue to due to widespread viral contamination

then changes to recombinant clotting factors

recent developments to modify the half lives of the factors to less frequent injections

57
Q

What novel agents are being looked into for haemophilia treatment?

A

Bispecific antibody- Emicizumab binds to F8a and 10 to mimic function of F8 for Haem 8

Anti TFPI antibody

Antithrombin RNAi

58
Q

What novel treatments are being looked into for haemophilia?

A

Gene therapy

RNA silencing : targets natural anticoagulant antithrombin

59
Q

How do disorders of thrombosis present?

A

pulmonary embolism

Deep vein thrombosis

60
Q

How does pulmonary embolism present?

A

heart racing

palpitations

hypoxia

chest pain

haemoptysis

sudden death

61
Q

How may deep vein thrombosis - DVT present?

A

painful leg

swelling

red

warm

may embolise to lungs

post thrombotic syndrome

  • px may just say feels like pulled calf muscle
  • can cause post thrombotic syndrome
62
Q

what is thrombosis?

A

intravacular, inappropriate coagulation

venous or arterial

obstructs flow

may embolise to lung

63
Q

what is virchows triad?

A

3 factors contributing to thrombosis

  • blood
  • vessel wall
  • blood flow
64
Q

What is changes in blood a risk factor for?

A

venous thrombosis

65
Q

What is changes in vessel wall a risk factor for?

A

arterial thrombosis

66
Q

What is changes in blood flow a risk factor for?

A

both arterial and venous thrombosis

67
Q

What is thrombophilia?

A

increased risk of venous thrombosis

68
Q

How may thrombophilia present?

A

thrombosis at young

spontaneous thrombosis

multiple times

thrombosis whilst anticoagulated

69
Q

What happens to fibrinolytic factors and anticoagulant proteins during thrombosis?

A

decrease

antithrombin
protein C
protein S

70
Q

What happens to coagulation factors during thrombosis?

A

Increase

F 8, 2, 5 (due to activated protein C resistance)

myeloproliferative disorders can increase platelets

71
Q

what are the risk factors for venous thrombosis?

A
  • increasing age
  • inherited thrombophilic traits:

anticoagulant deficiency (antithrombin, protein C/S)

procoagulant excess (factor 5 Leiden
Factor 8, 2)
72
Q

How does the vessel wall changes cause arterial thrombosis?

A

Inflammatory endothelial cell changes can express coagulation proteins

73
Q

How does blood flow changes affect thrombosis?

A

travel e.g. flight
surgery
pregnancy

74
Q

How is venous thrombosis prevented?

A

assess and prevent

prophylactic anticoagulant therpay

75
Q

How to reduce risk of recurrence of venous thrombosis?

A

lower procoagulant factors e.g. warfarin, DOACs

increase anticoagulant activity e.g. heparin

CardioRespiratory 2 (12 decks)

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