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CP - Haemostatasis > Acquired Disorders of Haemostasis > Flashcards

Acquired Disorders of Haemostasis Flashcards

1
Q

What does a mixing test indicate?

A

Whether an inhibitor is present - 50/50 mixture so prolonged APTT due to this & would otherwise be corrected

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2
Q

Liver disease - what would lab results be?

A

Low platelet count - portal hypertension and splenomegaly, prolonged PT, APTT and normal TT

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3
Q

DIC - what would lab results be?

A

Low platelet count, prolonged PT, APTT, grossly prolonged TT

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4
Q

Massive transfusion - what would lab results be?

A

Low platelet count, prolonged PT, APTT and normal TT

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5
Q

Oral anticoagulants - what would lab results be?

A

Normal platelet count, grossly prolonged PT, prolonged APTT and normal TT

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6
Q

Heparin - what would lab results be?

A

Normal platelet count, mildly prolonged PT, prolonged APTT, prolonged TT

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7
Q

Circulating anticoagulant - what would lab results be?

A

Normal platelet count, normal or prolonged PT, prolonged APTT, normal TT

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8
Q

Vit K deficiency - what would lab results be?

A

Normal platelet count, prolonged PT, prolonged APTT

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9
Q

Which clotting factors are vitamin K dependant?

A

2, 7, 9, 10

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10
Q

What is Vit K converted to and by which enzyme?

A

Vit K hydroquinone by quinone reductase

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11
Q

What is Vit K hydroquinone converted to and by which enzyme?

A

Vit K epoxide by glutamyl-carboylase

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12
Q

What is converted into Vit K?

A

Vit K epode by VKOR1

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13
Q

What is the target of warfarin?

A

VKOR1 and quinone reductase

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14
Q

What is a diagnostic test for Vit K deficiency/for warfarin

A

PIVKA - defective factor 2, 7, 9, 10 - proteins induced by vit K absence

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15
Q

What are the causes of Vit K deficiency

A

JDAN

J - jaundice
D - prolonged nutritional deficiency
A- broad spectrum antibiotics - affects gut flora synthesising Vit K
N - neonates ~ 1-7 days - no Vit K in

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16
Q

What is the site of coagulation factors

A

The hepatocytes EXCEPT F8 - synthesised by reticular epithelial cells/vascular endothelium

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17
Q

As liver disease progresses what happens to APTT,PT,TT

A

Prolonged APTT, PT, TT

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18
Q

What happens to platelet count with liver disease?

A

Thrombocytopenia - decreased platelet count due to hypersplenism from portal hypertension

19
Q

What is a major source or morbidity/mortality in px with liver disease?

A

Cirrhotic coagulinopathy - increased risk of sever bleeding from invasive procedures/surgery

Haemorrhage - local factors contribute to this e.g. portal hypertension > varicose veins in gullet, oesophageal varies and vatical bleeding worsened if also have coagulopathy/thrombocytopenia

20
Q

How does liver disease impair haemostasis?

A

TERPD

T - thrombocytopenia
E - excessive plasmin = activates fibrinolysis
R - reduced plasma/clotting factors
P - platelet dysfunction
D - delayed fibrin polymerisation - altered fibrinogen glucosylation (excess silica acid on fibrinogen molecules)

21
Q

What is considered to be a massive transfusion?

A

transfusion volume = px total blood overs in <24 hours if 50% blood volume within 1 hours

22
Q

Haemostats abnormalities in massive transfusion?

A

Dilution depletion of platelets and coagulation factors - due to standard pack transfusion (not clotting factors) - * must give FRESH FROZEN PLASMA

23
Q

What are the dilution effects of haemostasis?

A

Thrombocytopenia - at least 7-8L in adults usually transfused before problem is likely

Coagulation factor depletion - mainly F5, 8, fibrinogen

DIC common

Citrate toxicity - used as anticoagulant in red cells - uncommon BUT hyperthermia/neomates have increased susceptibility

Hypocalcaemia - from citrates/products transfused - no clinically significant effects on coagulation

24
Q

What is DIC?

A

Disseminated intravascular coagulation - a syndrome which occurs due to coagulation triggers - characterised by widespread fibrin deposition in small vessels and reduced platelets and clotting factors = bleeding

Thrombotic manifestation = end organ function, liver dysfunction, renal dysfunction, CNS dysfunction, necrotic skin lesions/ limb necrosis

25
Q

DIC - what are the main things?

A
  1. Consumption of clotting factors and platelets
  2. Microvascular thrombosis - tissue ischaemia end organ damage
  3. Activation of fibrinolysis - fibrin network damage RBC = microangiopathic haemolytic anaemia = microangiopathic haemolysis
26
Q

What are the ACUTE cause of DIC?

A

FATSO

Fulminan liver disease
Acute intravascular haemolysis e.g. ABO incompatible
Trauma/ tissue necrosis
Sepsis
Obstretic complications
27
Q

What are the CHRONIC causes of DIC?

A

MESO

Malignancy
End stage liver disease
Severe localised intravascular coagulation
Obstretic complication

28
Q

What lab tests would be done for DIC?

A

FBC, blood film
Coagulation screen - PT (70% prolonged), APTT (50% prolonged), TCT (usually prolonged)
[Fibrinogen]
FCP/D-Dimer - elevated in 85%

29
Q

Management of DIC?

A

Treat underlying cause - abs, obstetric intervention, chemo/ATRA/tumour resection

Supportive Treatment - maintain tissue perfusion and coordinate invasive procedures - FOLIC ACID & VIT K

30
Q

What product support would be in place for DIC?

A

Platelet transfusion if platelets <50
If PT/APTT ratio >1.5 = FFP 15ml/L
Fibrinogen <1g/l: Cryopreciptate/fibrinogen concentrate

31
Q

What would you use to reverse warfarin?

A

Vit K - required hours to work so give PCC prothrombin complex concentrate

32
Q

What enhances the effect of antithrombin?

A

Heparin

33
Q

What does antithrombin do?

A

Inhibitors thrombin and F10

34
Q

What is Dabigatran?

A

Direct Thrombin Inhibitor

35
Q

What are Rivoxaban/Apixaban?

A

F10a inhibitors

36
Q

What effects do Dabigran, Rivaroxaban and Apixaban have on coagulation tests?

A
  1. Dabigatran

Increases PT/INR, increases APTT, increases TCT, increases haemocri (TOC)

  1. Rivaroxaban

Increases PT/INR, APTT, specific antiXa

  1. Apixaban

Increased PT/INR, increase specific antiXa (TOC)

37
Q

VKA oral anticoagulants

A

Control of dosing by INR = (prothrombin ratio)ISI

Ratio of px prothrombin time/mean normal prothrombin time

ISI = correction factor to account for sensitivity of thromboplastin compared with the international reference preparation (IRP)

Normal range for INR = 2-3

38
Q

Which drugs interact with VKA Oral Anticoagulants?

A

CASE CAN CCCS

Corticosteroids
Ampicillin
Sulphonylureas
Erythromycin

Chlorpromazine
Amidarone
NSAIDs

Cimetidine
Cotrimoxazole
Cephalosporins
Sulphinpyrazone

39
Q

Which drug antagonise warfarin effect?

A

Carbamazepine, Cholestryramine, Rifampicin, Spironolactone, Vit K

40
Q

What are the recommendations for reversal of VKA Oral anticoagulant treatment?

A
  1. Lifethreatening haemorrhage - 5-10mg via k and IV 4 factor concentrate PCC e.g. octaplex/beriplex
  2. Non major bleeding - withhold war and give vit K 1-3mg IV
  3. INR > 8 - w/o haemorrhage - withhpld warfarin - give Vit K 1-5 mg orally
  4. INR 5-8 w/o haemorrhage - withhold warfarin - give Vit K orally if high risk for bleeding
  5. Unexpected bleeding at therapeutic levels - reverse warfarin and investigate underlying cause
41
Q

How can you monitor heparin?

A

UFH - APTT
Heparin level by protamine titration
Heparin level by anti-Xa assay
For LMWH - use anti-Xa assay as APTT not sensitive

42
Q

How can you manage bleeding?

A
  1. Stop infusion
  2. Consider protamine administration: 1mg neutralises 1000IU or heparin (max is 40mg)
    Effect of protamine on LMWH - less predictable and more complex
43
Q

LMWH vs UFH

A

LMWH - higher ratio of anti-Xa:anti-IIa activity
Improved bioavailability
Longer 1/2 life = OD administration
More predictable response

CP - Haemostatasis (5 decks)

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