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Cardio > Haematology Coagulation 2 > Flashcards

Haematology Coagulation 2 Flashcards

1
Q

Haemophilia: Description

A

Defect in Factors that affect clotting factors downstream

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2
Q

Haemophilia A

A

Defect in F8 gene causing reduced FVIII

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3
Q

Haemophilia B

A

Defect in F9 causing reduced FIX

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4
Q

Haemophilia: Inheritance

A

Sex Linked – FIND OUT MORE

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5
Q

Haemophilia: Clinical features of Haemophilia

A

Mild provoked bleeding if factor level >5%
Severe spontaneous bleeding if factor level <1%
• Soft tissue and joint bleedings (leads to synovitis) – chronic inflammatory changes
• Life-threatening CNS or GI bleeds
• Chronic arthropathy
• Treatment acquired HCV and HIV

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6
Q

Haemophilia: Treatment

A

Recombinant factor concentrate – personalised prophylaxis regimes to ensure factor levels never drop to ‘severe’ levels

→ Implant venous access device for easier infusions

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7
Q

Venous Thrombosis: VTE disease

A

Formation of fibrin-rich clots in low-pressure venous system

Includes DVT, PR, or thrombosis in axillary/ subclavian/portal. Mesenteric/cerebral veins

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8
Q

Venous Thrombosis: Thrombophilia

A

Increased propensity to VTE

Acquired + genetic risk factors

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9
Q

Venous Thrombosis: National burden of VTE

A

PE
DVT – 25K deaths per year in the UK

Elective Hip and Knee surgery % risk with no prophylaxis:
• 45% Hip
• 60% knee

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10
Q

Venous Thrombosis:DVT presentation common

A

Unilateral pain
Swelling
Tenderness
Discolouration

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11
Q

Venous Thrombosis: DVT presentation rare

A 
Dilated superficial veins
Venous gangrene (v. rare)
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12
Q

Venous Thrombosis:Note

A

Size of clot doesn’t relate to symptoms

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13
Q

Venous Thrombosis: DVT diagnosis

A 
Clinical history
Physical examination
Wells Score (screening) (2+) SEE MORE
D Dimer blood test (screening) – low good/
Confirmatory tests
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14
Q

Venous Thrombosis: Confirmatory tests

A

Doppler ultrasound
(Venography)
CTV/MRV for VTE at unusual

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15
Q

Venous Thrombosis: Doppler Ultrasound

A

Flow (red colour is not visible in the main vein (arrows), indicating lumen filled with thrombosis (SEE image)

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16
Q

Pulmonary Embolism: Symptoms

A 
SOB
Cough
(Pleuritic) chest pain
Haemoptysis
Syncope
Palpitations
Sweating
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17
Q

Pulmonary Embolism: Diagnosis and results

A 
Wells Score
ECG - Sinus tachycardia. R heart strain
ABG – Low O2/Co2
CXR – Usually normal potentially with wedge infarcts
V/Q scan – indeterminate in 50-70%
CT pulmonary angiogram - definitive
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18
Q

Pulmonary Embolism: DVT and PE sequelae

A 
PE →
•	Pulmonary Hypertension → Chronic PE
•	Death
Deep Vein insufficiency
•	Post-thrombotic syndrome
•	Venous ulcers
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19
Q

Pulmonary Embolism: Management of VTE

A

Fast acting anticoagulation minimum 3 moths (LMW Heparin or rivaroxaban)
• PE with haemodynamic effect may need thrombolysis or thrombectomy
• DVT graded compression stocking for PTS (minimum 6 months post DVT)
Long term anticoagulation?
Depends on individualised risk vs. benefit

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20
Q

Pulmonary Embolism: Who is at risk of VTE

A 
Genetic risk factors
Acquired risk factors:
•	Immobility
•	Trauma and surgery
•	Pregnancy and peurperium (post natal care)
•	Oestrogen therapy (e.g. COCP, HRT)
•	Inflammatory disorder (e.g. IBD)
•	Myeloproliferative disorders (e.g. Essential Thrombocythaemia)
•	Malignancy (e.g. Adenocarcinoma)
•	Antiphospholipid syndrome
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21
Q

Factor V Leiden: Definition

A

Sequence change in Factor V prevents inactivation by Protein C
5-10% Caucasians

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22
Q

Factor V Leiden: Epi

A 
5-10% Caucasians
Found in 20% of individuals with unexplained thrombosis
FVL – increased risk of VTE x 4
COCP – increased risk of VTE x4
COCP + FVL – increased risk of VTE x16
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23
Q

Anti-phospholipid syndrome: Clinical features

A 
CLOTs:
C: Arterial or Venous thrombosis
L:  Livedo reticularis
O: Obstetric complications - Recurrent miscarriage
T:  Thrombocytopaenia
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24
Q

Anti-phospholipid syndrome: Caused by

A

Antiphospholipid antibodies – bind to membrane phopspholipid glycoprotein complexes

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25
Q

Anti-phospholipid syndrome: Primary or Secondary to

A

Connective tissue disease (SLE)
Lympjoproliferative disorders (e.g. Lymphoma, CLL)
Infection
Drug induced

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26
Q

Anti-phospholipid syndrome: Antiphospholipid antibodies

A 
Anti-cardiolipin antibodies
Anti-beta2 glycoprotein antibodies
Lupus anticoagulants
•	Prolonged aPTT in the test tube
•	Is definitely not physiological anticoagulant – lab artefact
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27
Q

Antithrombotic drugs

A

Anti-platelet agents

Anti-coagulants

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28
Q

Anti-platelet act to

A

Arterial: Inhibit arterial thrombosis (ACS, PVD, CVD)

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29
Q

Anti-coagulant drugs

A

Veins and low pressure vessels:
Inhibit coagulation pathway
Inhibit venous/low pressure thrombosis (DVT, PE, CVA in AF and mechanilca heart valves, CBP, dialysis)

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30
Q

UK Licensed anticoagulants

A 
Inhibit production of thrombin:
•	UF Heparin
•	LMW heparin
•	Warfarin
•	Danaparoid
•	Fondaparinux
•	Bivalirudin
•	Argatoban
•	Apixiban
•	Dabigatran
•	Rivaroxaban
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31
Q

Heparin: Description

A

Paraentral antithrombotic
Naturally occurring glycosaminoglycan
Mixture of different wave lengths (UFH av. 50) (LMWH av. 15-20)

32
Q

Heparin: MOA

A

Increases activity of natural anticoagulant Antithrombin

Inhibits active clotting factors esp. Factors IIa and Xa

33
Q

UF Heparin Route

A

IV

34
Q

UF Heparin bioavailability

A

Variable poor

35
Q

UF Heparin Metabolism

A

Complex, renal

36
Q

UF Heparin half life

A

1-2

37
Q

UF Heparin adverse effects

A

Bleeding

Heparin induced thrombocytopenia

38
Q

LMW Heparin route

A

SC

39
Q

LMW Heparin bioavailability

A

Predictable, good

40
Q

LMW Heparin metabolism

A

Predictable, renal

41
Q

LMW Heparin half life

A

4-6

42
Q

LMW Heparin adverse effects

A

Bleeding

43
Q

LMWH used in

A
  1. Immediate management of VTE
  2. Thromboprophylaxis
  3. Acute coronary syndromes
  4. Warfarin unsuitable esp pregnancy
  5. Prophylaxis against venous thrombosis
44
Q

UFH

A
    1. Extra-corporeal circuits

7. High risk ‘bridging’ for surgery

45
Q

UHF Heparin: Absorption

A

Bolus Injection then IV infusion e.g. 5000 IU loading then 30,000 IU/24 hrs

46
Q

UHF Heparin: Measure of heparin

A
  • aPTT is best measure of heparin in ‘therapeutic’ activity range
  • Expressed as aPTT ratio (patient aPTT/ normal aPTT)
47
Q

UHF Heparin: Target aPTT range

A

1.5-2.5

48
Q

UHF Heparin: Monitor

A

PLT count

49
Q

LMW Heparin: Absorption

A

Four preparations – enoxaparin (Clexane)

50
Q

LMW Heparin: Dosing

A

‘Prophylaxis’ 40 mg sc od

‘Treatment’ 1.5 mg/kg od or 1mg/kg bd

51
Q

LMW Heparin:Monitoring

A

Not routine, won’t increased aPPt or PT at therapeutic levels
Anti-Xa test

52
Q

LMW Heparin: Over-anticoagulation with heparin: mild or moderate bleeding

A

Stop Heparin

53
Q

LMW Heparin: Over-anticoagulation with heparin: Severe

A

Stop Heparin
Protamine iv 1mg.100 IU heparin in lst hour max 40 mg)
Expect repeat treatment

54
Q

Warfarin: Action

A

Oral anticoagulant

A coumarin derivative

55
Q

Warfarin: MOA

A

Inhibits recycling of vit K

Vit K is needed for synthesis of clotting factors II, VII, IX and X

56
Q

Warfarin: When do we use warfarin

A

Long term management of VTE
Stroke prevention in atrial fibrillation
Sometimes, prevention of arterial thrombosis (plus antiplatelet agent)

57
Q

Warfarin: Absorption

A

Near 100% bio-availability

58
Q

Warfarin: Half life

A

36 hours

59
Q

Warfarin:Metabolism

A

Liver

60
Q

Warfarin: Causes

A

Increased PT and increased aPTT

61
Q

Warfarin: Monitoring

A

Longterm monitoring using INR (patient PT/ control PT)

62
Q

Warfarin:Typical dose

A

2-8mg od

63
Q

Warfarin: Interactions

A

Cranberry and grapefruit juice

64
Q

Warfarin:INR >5 and/or mild bleeding

A

STOP Warfarin

65
Q

Warfarin INR >8 and/or serious bleeding

A

STOP warfarin
Vitamin K 1-3 mg poor iv
Consider Vitamin K factor concentrate (eg Octaplex) plus Vit K1

66
Q

Rivaroxaban: MOA

A

Oral anticoagulant

Direct inhibitor of factor Xa

67
Q

Rivaroxaban: When do we use rivaroxaban

A
  • VTE after knee/hip replacement (10 md od)
  • Stroke prevention in non-valvular AF (20mg od)
  • Acute treatment of DVT (15 mg bd)
  • Long-term prevention of DVT and PE (20 mg od)
68
Q

Rivaroxaban: Peak plasma hours

A

• 3 hours

69
Q

Rivaroxaban:Half life

A

• 8 hours

70
Q

Rivaroxaban: Metabolism/excretion

A

• 75% liver metabolised/25% renal excreted

71
Q

Rivaroxaban: Interactions

A

Some drug interaction and unsuitable in renal impairment.

72
Q

Rivaroxaban: Monitoring

A

None

73
Q

Rivaroxaban: May cause

A
  • Increased PT and increased aPTT but doesn’t reflect anticoagulant effect.
  • Anti-Xa test
74
Q

Rivaroxaban: Accidental overdose or mild bleeding

A

• STOP rivaroxaban

75
Q

Rivaroxaban: Serious bleeding

A
  • STOP rivaroxaban
  • General measures
  • Specialist agents eg APCC
76
Q

Rivaroxaban:Safety of anticoagulation

A

Anticoagulant bleeding leads iatrogenic mortality
High bleeding risk:
• Renal impairment (heparins and RIV)
• Previous bleeding edp. CNS or GI
• Other coagulopathy eg anti-platelet drugs
• Age >75 years, frequent falls, bw <50 kg

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