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MS3 - Haematology > Bleeding disorders > Flashcards

Bleeding disorders Flashcards

1
Q

Haemophilia types?

A

A and B

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2
Q

Haemophilia type A

A

Defect in F8 gene causing reduced FVIII (haemophilia A)

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3
Q

Haemophilia type B

A

Defect in F9 gene causing reduced FIX (haemophilia B)

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4
Q

Haemophilia genetics

A

Sex-linked recessive inheritance (on X chromosome)

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5
Q

Sx of Haemophilia

A

Coagulation pathway disorder

  • Mild or severe bleeding depending on factor level (Soft tissue and joint, CNS, GI bleeds)
  • Chronic arthropathy (bleeding in joint leads to inflammation)
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6
Q

Mx of haemophilia

A
  • Recombinant factor concentrate (synthetic factor 8 & 9)
  • prophylaxis every 2-3 weeks
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7
Q

normal roles of vwf?

A
  • VWF mediates PLT adhesion to collagen

- stabilises coagulation Factor VIII in the plasma

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8
Q

Mild Von Willebrand disease cause

A
  • Defective primary haemostasis
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9
Q

Mild Von Willebrand disease sx

A
  • Epistaxis
  • easy bruising
  • traumatic skin bleeding
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10
Q

Severe Von Willebrand disease cause

A
  • Additional coagulation pathway

- defect due to low FVIII

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11
Q

Von Willebrand disease tests?

A
  • Long aPTT in moderate or severe VWD (when FVIII level is low)
  • reduced plasma VWF activity
  • reduced plasma FVIII activity
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12
Q

Management of VWD?

A

I. Tranexamic acid
II. DDAVP/Desmopressin
III. VWF/FVIII concentrate

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13
Q

Tranexamic acid

A

Reduces clot break-down

antifibrinolytic

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14
Q

DDAVP/Desmopressin

A
  • Releases endogenous FVIII and VWF

- only works once, temporary release

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15
Q

Bleeding disorders acquired causes

A
  1. Abnormal synthesis
  2. Abnormal function
  3. Dilution
  4. Consumption
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16
Q

Potential causes of abnormal synthesis leading to acquired bleeding disorders?

A
  • Liver disease
  • Vitamin K deficiency (coagulation factors II, VII, IX, X)
  • Warfarin
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17
Q

Potential causes of abnormal function leading to acquired bleeding disorders?

A
  • Heparin and direct acting oral anticoagulants*
  • Renal failure (platelet dysfunction)
  • Anti-platelet drugs
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18
Q

Potential causes of dilution leading to acquired bleeding disorders?

A
  • Massive transfusion

* Cardiopulmonary bypass

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19
Q

Potential causes of consumption leading to acquired bleeding disorders?

A

(Thrombotic microangiopathies )
• Disseminated intravascular coagulation*
• Thrombocytopenia in sepsis

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20
Q

Liver damage and clotting?

A

I. ↓Synthesis of most clotting factors, fibrinogen and coagulation regulators
II. ↓PLT number
III. Biliary obstruction gives vit K malabsorption
IV. Hyperfibrinolysis

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21
Q

Vit K role?

A

needed for synthesis of Factors II, VII, IX and X

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22
Q

Disseminated intravascular coagulation (DIC) causes

A 
I. Sepsis
II. Major trauma
III. Obstetric emergencies (pre-eclampsia,
amniotic fluid embolism, retained POC)
IV. Advanced malignancy
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23
Q

Disseminated intravascular coagulation (DIC) pathophysiology

A

I. Pro-coagulant stimulus + loss of regulatory pathways –> Widespread activation of coagulation pathway

II. Fibrin/platelet rich
microvascular thrombi and Multiorgan failure

III. Platelet, fibrinogen and
coag factor consumption and bleeding

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24
Q

Management of DIC

A

• Fresh frozen plasma
• Platelet transfusion
• Fibrinogen concentrate or
cryoprecipitate

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25
Q

Thrombotic thrombocytopenic purpura (TTP) Sx?

A
  • onset fever, malaise, arthralgia
  • Bleeding
    • Variable neurological features
    • Chest pain
    • Jaundice + abdo pain
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26
Q

Thrombotic thrombocytopenic purpura (TTP) cause?

A

Caused by anti-ADAMTS13 antibodies

27
Q

Thrombotic thrombocytopenic purpura (TTP) pathology?

A

anti-ADAMTS13 antibodies-> Reduced proteolysis of VWF -> Circulating ultra-high molecular weight VWF multimers -> Platelet agglutination in ‘high shear’ vessels, microvascular, thrombosis, platelet consumption, mechanical haemolysis

28
Q

Diagnosis of TTP

A

Blood film is diagnostic: smashed in half

PLT reduced and Hb reduced

29
Q

Mx of TTP?

A 
PLASMA EXCHANGE or 
II. Supportive care
• RBC transfusion
• Aspirin and LMW heparin
• Iv corticosteroids
Rituximab
30
Q

DVT

  1. first investigation?
  2. secondary Ix?
A
  1. Wells score for DVT diagnosis
  2. I. Score >1=
    - DVT likely
    - Doppler USS
    II. Score 1 or less:
    - DVT unlikely
    - D dimer test
    - Doppler USS if high
31
Q

DVT complications?

A

Post-thrombotic syndrome:

  • Chronic swelling and aching
  • Venous eczema and ulcers
32
Q

PE complication?

A 
Chronic thromboembolic
pulmonary hypertension (CTPH)
  • 0.5-5% of treated clots replaced by fibrous tissue
  • Progressive Pulmonary HTN and RHF
33
Q

3 conditions that increase the risk of DVT?

A
  1. Antithrombin deficiency
  2. Factor V Leiden
  3. antiphospholipid syndrome
34
Q

Antithrombin deficiency mx

A
  • Long term anticoagulation
  • short term AT
    concentrate
35
Q

Factor V Leiden pathology?

A

Reduces inactivation of Factor V by activated protein C

36
Q

Management of anti phospholipid syndrome?

A
  • If thrombotic, long term anticoagulation (plus antiplatelet agent if arterial thrombosis)
37
Q

Immediate Management of DVT and PE?

A
  • Fast acting anticoagulant minimum 3 months

- (Rivaroxaban or LMW heparin)

38
Q

long term Management of DVT and PE?

A

anticoagulation:

  • Rivaroxaban,
  • warfarin.
  • LMWH in cancer or pregnancy
39
Q

2 types of Anti-thrombotic drugs

A
  1. Anti-platelet drugs

2. Anti-coagulant drugs

40
Q

Anti platelet drugs used for?

A

Treatment/prevention arterial thrombosis

eg ACS

41
Q

Anti coagulant drugs used for?

A

treatment/prevention venous thrombosis or low pressure vessel thrombosis
eg DVT, PE, CVA in AF

42
Q

NICE guidlines for VTE thromboprophylaxis

A

All patients at risk of VTE should:
• Mobilise early
• Receive pharmaceutical thromboprophylaxis (eg enoxaparin 40 mg once daily)

43
Q

mech of action of heparin

A

• Increases activity of natural anticoagulant
antithrombin

• Inhibits active clotting factors esp. Factors IIa
(thrombin) and Xa

44
Q

Route of UF heparin

45
Q

Route of LMW heparin

46
Q

Metabolism of UF heparin

47
Q

Metabolism of LMW heparin

48
Q

Half life of UF heparin

49
Q

Half life of LMW heparin

50
Q

Reversal of UF heparin

A

Protamine iv 1mg/100 IU heparin in last hr (max 40mg)

51
Q

Reversal of LMW heparin

A

Protamine iv 1mg/100 IU heparin in last hr (max 40mg)

52
Q

Direct oral anticoagulant (DOAC) example?

A

rivaroxaban

53
Q

Rivaroxaban mech of action

A
  • Factor Xa inhibitor

* Reduces thrombin generation

54
Q

Rivaroxaban use?

A

I. VTE prevention after knee/hip replacement

II. Stroke prevention in non-valvular AF

III. Acute and long term treatment of DVT

55
Q

Rivaroxaban half life?

56
Q

Rivaroxaban metabolised by

A

75% liver metabolised,

25% renal excreted

57
Q

Rivaroxaban reversal?

A

Specialist products (APCC, specific reversal agents) for severe bleeding

58
Q

Warfarin mech of action?

A

Inhibits vitamin K metabolism (factors 2,7,9,10)

59
Q

Warfarin uses?

A

I. when DOACs are unsafe
II. Long term VTE
III. Stroke prevention in AF
IV. With anti-platelet agent, to prevent arterial thrombosis

60
Q

when are DOACs unsafe

A
  • Mechanical heart valves,
  • Antiphosphoilipid syndrome,
  • CKD
61
Q

Warfarin half life

A

Plasma half life ~36 hours

62
Q

Warfarin metabolised by

63
Q

Warfarin reversal

A
  • Vitamin K if INR >8.0 for mild bleeding

- Vitamin K factor concentrate (eg Octaplex) plus Vit K for severe bleeding

MS3 - Haematology (5 decks)

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