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Clinical Pathology > 38 - Acquired bleeding disorders > Flashcards

38 - Acquired bleeding disorders Flashcards

1
Q

What does APTT stand for?

A

Activated partial thromboplastin time

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2
Q

Heparin examples

A

UFH (unfractionated heparin)

Enoxaparin

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3
Q

Vit K antagonist e.g.s

A

Warfarin

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4
Q

Direct thrombin inhibitors

A

Hirudins

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5
Q

Problems with antithrombotics

A

High incidence of serious adverse effects (mainly bleeding-related)

Routine monitoring needed

Narrow therapeutic margin

Limited effectiveness in preventing VTE (venousthrombo embolism)

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6
Q

Vitamin K deficiency affects which factors

A

II, VII, IX, X

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7
Q

Causes of vit K deficiency

A

Obstructive jaundice

Prolonged nutritional deficiency

Broad spectrum antibiotics

Neonates (classical 1-7 days)

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8
Q

Liver disease - in relation to blood

A

Cirrhotic coagulopathy

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9
Q

Problems with cirrhotic coagulopathy

A

Increased risk of severe bleeding from invasive procedures or surgery

Conventional treatments don’t work

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10
Q

What is liver essential for in relation to blood

A

Making normal coagulation factors
Components of fibrinolytic system
Naturally occurring anticoagulants

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11
Q

Impaired haemostasis in liver disease leads to

A 
Thrombocytopenia
Platelet dysfunction
Reduced [plasma coagulation factors] except FVIII
Delayed fibrin polymerisation
Excessive plasmin activity
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12
Q

Massive transfusion definition

A

Volume equal patient’s blood volume in less than 24 hours

50% blood volume loss within 3 hours

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13
Q

Haemostatic abnormalities due to massive transfusion

A

Dilutional depletion of platelets and coagulation factors

Due to DIC - risk factors: trauma, head injury, prolonged hypotension

Underlying disease: liver or renal disease, drug treatment, surgery

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14
Q

When do effects of dilution set in and cause problems in haemostasis after how many litres?

A

> 7-8 litres

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15
Q

Dilution problems in haemostasis

A

Thrombocytopenia
Coagulation factor depletion, namely, Factor V and VIII and fibrinogen
DIC common
Citrate toxicity - uncommon
Hypocalcaemia - no clinically significant effect on coagulation

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16
Q

Citrate toxicity which groups are vulnerable

A

Hypothermic patients

Neonates

17
Q

Pathophysiology of DIC

A
  1. General disruption of physiological balance of procoagulant and anticoagulant mechanisms
  2. Consumption of clotting factors + platelets
  3. Microvascular thrombosis
  4. Activation of thrombolysis
  5. Microangiopathic haemolysis
18
Q

DIC - generally what is it?

A

Over active clotting proteins causing microclots

19
Q

Acute DIC - causes

A 
Acute DIC
Sepsis
Obstetric complications
Trauma/tissue necrosis
Acute intravascular haemolysis e.g. incompatible blood transfusion
Fulminant liver disease
20
Q

Chronic DIC - causes

A

Malignancy
End stage liver disease
Severe localised intravascular coagulation
Obstetric: retained dead foetus

21
Q

DIC - lab tests

A

FBC and Blood Film

Coagulation screen:
PT (70% prolonged)
APTT (50% prolonged)
TCT (usually prolonged)

[Fibrinogen]
FDP or D-dimer (elevated in 85%)
Not single diagnostic test - scoring systems used

22
Q

Management of DIC - underlying cause

A

Antibiotics
Obstetric intervention
Chemo/ATRA (all trans retinoic acid) /tumour resection

23
Q

ATRA

A

All trans retinoic acid

For acute myeloid leukaemia

24
Q

Management of DIC - supportive treatment

A

Maintain tissue perfusion
Co-ordinate invasive procedures
Folic acid and vitK supplements to support recovery period

25
Q

Oral anticoagulants

A

Control of dosing by INR

26
Q

What is INR?

A

Prothrombin ratio

Patient’s PT time / mean normal PT time

27
Q

Drugs which increase warfarin effect

A 
Cimetidine
Amiodarone
Sulphinpyrazone
Cotrimoxazole
Erythromycin
Cephlosporins
Ampicillin
NSAID's
Chlorpromazine
Sulphonylureas
Corticosteroids
28
Q

Drugs which antagonise warfarin effect

A 
Cholestyramine
Spironolactone
Rifampicin
Carbamazepine
VitK
29
Q

When to reverse oral anticoagulant treatment

A

Life threatening haemorrhage
Non-major bleeding
INR>8.0 w/o haemorrhage
INR>5

30
Q

Life threatening haemorrhage

A

5-10mg vit K via IV

Four factor concentrate

31
Q

Non-major bleeding

A

Withhold warfarin

Give vitK 1-3mg IV

32
Q

INR of >8.0 w/o haemorrhage

A

Withhold warfarin

Give vitK 1-5mg orally

33
Q

INR >5.0

A

Withhold warfarin.

Consider oral vitK if high risk for bleeding

34
Q

Unexpected bleeding at therapeutic levels

A

Reverse warfarin

Workout underlying cause

35
Q

What is tested for to monitor heparin?

A

Full anticoagulation assay

APTT most commonly used assay

36
Q

Alternative monitoring of heparin

A

Protamine titration
Anti-Xa assay
Calcium thrombin time
Anti-Xa (LMWH)

37
Q

Properties of LMWH vs UFH

A

LMWH: higher ratio of anti-Xa to anti-IIa activity

Higher bioavailability

Longer half-life allowing once daily administration

More predictable response not needing monitoring

Clinical Pathology (65 decks)

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