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I need to learen > Disorders of Haemostasis COPY > Flashcards

Disorders of Haemostasis COPY Flashcards

1
Q

Give examples of minor bleeding symptoms

A 
Easy bruising
Gum bleeding
Frequent nosebleeds
Bleeding after tooth extraction 
Post-operative
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2
Q

Give examples of minor bleeding symptoms in women

A

Menorrhagia
Post-partum bleeding
Family history

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3
Q

What are the elements of a significant bleeding history

A

Epistaxis not stopped by 10 minutes compression pr requiring medical attention/transfusion
Cutaneous haemorrhage or bruising with no trauma
Prolonged (>15min) bleeding from trivial wounds
Menorrhagia requiring treatment that leads to anaemia
Heavy, prolonged or recurrent bleeding after surgery or dental extraction

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4
Q

Why might abnormal haemostasis occur

A

Lack of a specific factor
Failure of production (congenital and acquired) or increased consumption/clearance

Defective function of a specific factor
Genetic defect or acquire defect (drugs, synthetic defect, inhibition)

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5
Q

Give examples of disorders of primary haemostasis due to platelets

A

Low numbers - thrombocytopenia
Bone marrow failure e.g. leukaemia, B12 deficiency
Accelerated clearance e.g. immune (ITP), DIC

Impaired function
Hereditary absence of glycoproteins or storage granules
Acquired due to drugs

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6
Q

Describe auto-immune thrombocytopenic purpura

A
  1. Antiplatelet antibodies bind to a sensitised platelet
  2. Sensitised platelet binds to a macrophage via antibodies

Very common cause of thrombocytopenia

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7
Q

What are the mechanisms and causes of thrombocytopenia

A
  1. Failure of platelet production by megakaryocytes
  2. Shortened half life of platelets
  3. Increased pooling of platelets in an enlarged spleen
    (hypersplenism) + shortened half life
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8
Q

Give examples of hereditary platelet defects

A

Glanzmann’s thrombasthenia
Bernard Soulier syndrome
Storage Pool disease

No GPIIb/IIIa or GpIb or dense granules

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9
Q

Which drugs may cause one to acquire impaired function of platelets

A

Aspirin
NSAIDs
Clopidogrel

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10
Q

What are the functions of VWF in haemostasis

A

Binding to collagen and capturing platelets

Stabilising factor VIII (may be low if VWF is low)

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11
Q

Describe the cause of VWF disease

A

Hereditary - deficiency of VWF (Type 1 or 3) or VWF with abnormal function (type 2)

Acquired due to antibody (rare)

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12
Q

Give examples of primary haemostasis disorders involving the vessel wall

A

Inherited (rare) - Hereditary haemorrhagic telangiectasia Ehlers-Danlos syndrome and other connective tissue disorders

Acquired - Scurvy, steroid therapy, ageing (senile purpura), vasculitis

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13
Q

Describe the typical bleeding of primary haemostasis

A 
Immediate 
Prolonged bleeding from cuts
Epistaxes
Gum bleeding
Menorrhagia 
Easy bruising
Prolonged bleeding after trauma or surgery
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14
Q

What might be the typical bleeding specific to thrombocytopenia and severe VWD

A

thrombocytopenia - petechiae

Severe VWD - haemophilia-like bleeding

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15
Q

What are the tests done for disorders of primary haemostasis

A

Platelet count, platelet morphology
Bleeding time (PFA100 in lab)
Assays of von Willebrand Factor
Clinical observation

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16
Q

Which clotting factors are not serine proteases

A

V - co-factor
VIII - co-factor
XIII - transglutamidase

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17
Q

Which factors require post-transitional vit K dependent modification

A

II
VII
IX
X

18
Q

Describe the concentration-time graph for thrombin generation

A

After a TF trigger there is a surge in thrombin which then quickly decreases
Haemophilia - very small and slow peak (when thrombin is lowest)

19
Q

Describe haemophilia

A

Failure to generate fibrin to stabilise platelet plug
Deficiency in factor VIII/IX
Sex-linked recessive

20
Q

Describe the different bleeding in coagulation factor deficiencies (FVIII, IX, II, XI, XII)

A

VIII/IX - severe but compatible with life, spontaneous joint and muscle bleeding

Prothrombin - lethal

XI - bleed after trauma, not spontaneous

XII - no excess bleeding

21
Q

What are some acquired disorders of coagulation

A

Liver disease
Dilution
Anticoagulant drugs – warfarin

22
Q

How does liver failure lead to a coagulation disorder

A

Most coagulation factors are synthesised in the lvier

23
Q

Describe coagulation disorders due to dilution

A

Red cell transfusions no longer contain plasma

Major transfusions require plasma as well as rbc and platelets

24
Q

What are the causes of increased consumption

A

Acquired
Disseminated intravascular coagulation (DIC)
Immune - autoantibodies

25
Q

Describe disseminated intravascular coagulation

A

Generalised activation of coagulation – Tissue factor
Associated with sepsis, major tissue damage, inflammation
Consumes and depletes coagulation factors
Platelets consumed
Activation of fibrinolysis depletes fibrinogen
Deposition of fibrin in vessels causes organ failure

26
Q

Describe the typical bleeding in coagulation disorders (Secondary)

A

superficial cuts do not bleed (platelets)
bruising is common, nosebleeds are rare
spontaneous bleeding is deep, into muscles
and joints
bleeding after trauma may be delayed and is prolonged
frequently restarts after stopping

27
Q

How is bleeding due to platelet and coagulation defects clinically distinguished

A

Platelet - superficial bleeding into skin, mucosal membranes. Immediate after injury

Coagulation- bleeding into deep tissue, muscle and joints, delayed but severe and prolonged bleeding

28
Q

What are the tests for coagulation disorders

A

Screening tests (clotting screen)
Prothrombin time (PT)
Activated partial thromboplastin time (APTT)
Full blood count (platelets)

Factor assays (for Factor VIII etc)

Tests for inhibitors

29
Q

Which bleeding disorders are not detected by routine clotting tests

A 
Mild factor deficiencies
 von Willebrand disease
 Factor XIII deficiency (cross linking)
 Platelet disorders
 Excessive fibrinolysis
 Vessel wall disorders
 Metabolic disorders (e.g. uraemia)
 (Thrombotic disorders)
30
Q

What are some causes of fibrinolysis disorders

A

hereditary - antiplasmin deficiency

Acquired - drugs (tPA), disseminated intravascular coagulation

31
Q

Describe the genetics of von willebrand disease

A

Autosomal dominant
Type 2 = AD
type 3 = AR

32
Q

Describe the genetics of most bleeding disorders

A

Autosomal recessive

33
Q

What is the treatment for abnormal haemostasis from failure of production/function

A

Replace missing factor/platelets
- Prophylactic
- Therapeutic
Stop drugs

34
Q

What is the treatment for abnormal haemostasis from immune destruction

A

What is the treatment for abnormal haemostasis from failure of production/function

35
Q

What is the treatment for abnormal haemostasis from increased consumption

A

Treat cause

Replace as necessary

36
Q

What can be used in factor replacement therapy

A

Plasma
Cryoprecipitate
Factor concentrates
Recombinant forms of FVIII and FIX

37
Q

Describe plasma and cryoprecipitate for replacement therapy

A

Plasma = contains all coagulation factors

Cryoprecipitate = rich in fibrinogen, FVIII, VWF, FXIII

38
Q

Describe factor concentrates

A

Concentrates available for all factors except factor V.

Prothrombin complex concentrates (PCCs) Factors II, VII, IX, X

39
Q

What are the the principle treatments of Haemostatic

Disorders Causing Bleeding

A

Factor replacement therapy
Gene therapy (haemophilia)
Platelet replacement therapy

40
Q

What are some additional haemostat treatments

A

DDAVP
Tranexamic acid
Fibrin glue/spray

41
Q

Describe DDAVP

A

Desmopressin
Vasopressin derivative

2-5 fold rise in VWF-VIII (VIII>vWF)

Releases endogenous stores -
Hence only useful in mild disorders

42
Q

Describe transexamic acid

A

Inhibits fibrinolysis
Widely distributed – crosses placenta
Low concentration in breast milk

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