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Cardio > Haematology Coagulation 1 > Flashcards

Haematology Coagulation 1 Flashcards

1
Q

Cell Based haemostasis: Model involves

A

Vessel wall
Platelet
Coagulation factors
Coagulation pathway

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2
Q

Enable regulated generation of

A

Thrombin

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3
Q

Thrombin polymerises

A

Fibrinogen to fibrin

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4
Q

Cell Based haemostasis: Model involves Stage 1

A

Collagen and TF exposed

Von Willebrand factor in plasma binds collagen

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5
Q

Cell Based haemostasis: Model involves Stage 2

A

Primary Haemostasis:
• Platelets adhere to vWF collagen
• Platelets activated

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6
Q

Cell Based haemostasis: Model involves Stage 3

A

Generation of Thrombin:
• TF initiates rapid thrombin generation on activated platelets
• Thrombin converts fibrinogen to fibrin clot
Serine proteases: (FVII, FX, FIX, FXI)
Co-factors: (FVIII and FV)

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7
Q

Cell Based haemostasis: Model involves Stage 4

A

Stable fibrin-platelet clot is formed

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8
Q

Regulation of haemostasis (3)

A

Thrombin is neutralised by antithrombin
Thrombin makes APC to stop new thrombin generation
Thrombin + tPA activated Plasmin which lyses fibrin

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9
Q

Clinical disorders of haemostasis →

A
  1. Primary haemostasis disorders:

2. Coagulation pathway disorders

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10
Q
  1. Primary haemostasis disorders:
A

a. Platelets
b. VWF
c. Vessel Wall

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11
Q
  1. Coagulation pathway disorders
A

a. Coagulation factors

b. Fibrinogen

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12
Q

Features of potential disorders of haemostasis

A

Abnormal bruising - primary haemostasis

Deep tissue bleeding – coagulation pathway

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13
Q

First line investigation

A
  1. Platelet count + blood film

2. Coagulation screen

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14
Q

Platelet count + blood film

A

Indicates platelet number (not function)

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15
Q

Coagulation screen

A

Indicates function of different parts of coagulation pathway:

  1. Prothrombin (PT)
  2. Activated partial thromboplastin time (aPTT)
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16
Q

Assay principle

A

Add coagulation ‘activator’ + Ca2+
Incubate at 37oC
Measure time to fibrin clot formation

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17
Q

Prothrombin information

A

‘Thromboplastin’ (tissue factor) activator added and measure clotting time
→ Detects abnormal FVII (extrinsic factor)
• FX, FV, FII, Fibrinogen
Long if there is a problem

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18
Q

aPPT information

A 
Kaolin or ‘contact activator’
Detects abnormal:
•	FVIII, FIX, FXI (intrinsic factors)
•	FX, FV, FII, Fibrinogen
Normal aPPT – can rule out certain things in conjunction with PT
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19
Q

Special coagulation tests

A

Used after clinical assessments and first line diagnosis:

  1. Coagulation factor activity assays
  2. Von Willebrand factor activity
  3. Fibrinogen level
  4. D-dimer level measures fibrinolysis)
  5. Platelet function tests
  6. Bone Marrow morphology
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20
Q

Platelets are made from

A

Megakaryocytes in marrow and are removed by spleen and liver (4 days life expectancy)
Low because:
• Reduced production
• Increased destruction

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21
Q

Reduced production seen in

A
  1. Chemo or radio therapy
  2. Leukaemia or other malignancy
  3. Aplastic anaemia
22
Q

Destruction seen in

A
  1. Autoimmune thrombocytopenia
  2. Hyperslenism – reduced platelets because the spleen is larger and so stimulated to work faster
  3. Consumptive coagulopathies (eg DIC)
  4. Sepsis
23
Q

Autoimmune Thrombocytopenia: Description

A

Abnormal auto-antibodies bind platelet glycoproteins causing rapid platelet destruction in spleen

24
Q

Autoimmune Thrombocytopenia: Causes

A

Idiopathic

2ary to infection, drugs, connective tissue disease, lymphoproliferative disorders (eg. CLL)

25
Q

Autoimmune Thrombocytopenia: Clinical features

A

Abnormal primary haemostasis

Cutaneous purpura

26
Q

Autoimmune Thrombocytopenia: Investigations

A

Reduced platelets count (FBC) and reduced Platelet count on film
Marrow shows increased megakaryocytes
No confirmatory test

27
Q

Autoimmune Thrombocytopenia: Treatment

A

Corticosteroids (immunosuppression)
Iv Immunoglobulin -
Splenectomy
TPO receptor agonists

28
Q

Von willebrand Disease: Description

A

Deficiency of VWF, commonest genetic haemostatic disorder

29
Q

Von willebrand Disease: VWF function

A

Mediates PT adhesion to collagen AND stabilises coagulation factor VII in the plasma

30
Q

Von willebrand Disease: MILD VWF

A

Defective primary haemostasis only causes with mild bleeding symptoms

31
Q

Von willebrand Disease: SEVER VWD

A

Additional coagulopathy pathway defect due to low FVIII

32
Q

Von willebrand Disease: Bleeding symptoms

A

Epitaxis
Easy bruising
Traumatic skin bleeding

33
Q

Von willebrand Disease: First line investigations

A

Platelet count normal

Long aPPT only in moderate or severe VWD (when FVIII level is low)

34
Q

Von willebrand Disease: Special coagulation tests

A

Reduced VWF activity

Reduced FVIII activity

35
Q

Von willebrand Disease: Treatment

A
  • Tranexamic acid – reduced clot breakdown (anti-fibrinolytic)
  • DDAVP/Desmopressin – release exogenous FVIII/VWF
  • VWF/FVIII concentrate
36
Q

Reduced platelet function: Definition

A

Abnormal platelet function can cause bleeding even with normal platelet number

37
Q

Reduced platelet function: Causes

A
  • Drugs: Aspirin, clopidogrel, NSAIDS
  • Renal or Liver failure
  • Cardiopulmonary bypass, haemofiltration
  • Genetic platelet function disorders
38
Q

Abnormal Blood Vessel Wall:

A
  • Senile Purpura – age related changes in blood vessels

* Scurvy – malnourishment (elderly) – Vit C

39
Q

Disorders of Coagulation Pathway:

A
  1. Acquired coagulation factor disorders

2. Heritable coagulation factor disorders (Coag 2)

40
Q
  1. Acquired coagulation factor disorders
A

a. Massive transfusion (dilution) – e.g. colloid, RBC’s w/o platelets
b. Liver disease (synthetic)
c. Disseminated intravascular coagulation (consumption)

41
Q

Liver disease affects

A

Primary Haemostasis and coagulation pathway

42
Q

How does liver disease effect this

A
  1. Reduces Synthesis of all clothing factors and fibrinogen
  2. Reduced Platelet number (Hypersplenism) and reduced PLT function
  3. Biliary obstruction gives vit K malaabsorption (reduced synthesis of Factors II, VII, IX and X)
43
Q

Presentation

A
  • Sub-conjunctival haemorrhage, jaundice and corneal arcus

* Oesophageal varices from portal hypertension

44
Q

Lab investigation in liver disease

A
  • Increased PT, increased aPPT and reduced PLT count
  • Fibrinogen and all clotting factors
  • Reduced anticoagulant proteins e.g. anti-thrombin
45
Q

Treatment of coagulopathy in liver disease

A
  • Stable abnormal clotting test results usually doesn’t need treatment
  • To treat or prevent surgical bleeding replace specific factors
46
Q

Treatment of bleeding liver disease

A
  • Vit K
  • Vit K dependent clotting factor concentrate
  • Fresh Frozen Plasma
47
Q

Disseminated intravascular coagulation (consumption): Description

A

Widespread activation of coagulation pathway (microvascular thrombosis) from excess thrombin generation – ischaemic tissue

  1. Activation of inflammation, complement, fibrinolysis - multisystem
  2. Consumption of platelets/coagulation factors- bleeding (because its widespread using up of clotting factors because of the excess thrombosis)
48
Q

Disseminated intravascular coagulation (consumption): Causes of DIC

A

Any sever illness:

  1. Sepsis
  2. Major Trauma
  3. Obstetric emergencies (pre-eclampsia, amniotic fluid embolism, retained POC)
  4. Advanced malignancy
49
Q

Disseminated intravascular coagulation (consumption): Diagnosis of DIC

A
  • Very high PT
  • Very high aPPT
  • Very low PLT count in sick patient
  • Very low fibrinogen
  • Very High D-dimer
50
Q

Disseminated intravascular coagulation (consumption): Treatment of DIC

A
  • Usually requires full supportive care and aggressive treatment of underlying causes
  • Support coagulation with FFP, cryoprecipitate and PLT transfusion

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