38 Acquired bleeding disorders Flashcards Preview

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Flashcards in 38 Acquired bleeding disorders Deck (27)
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1
Q

How is the cause of a prolonged APTT determined: deficiency vs inhibitor?

A

Repeat test with 50:50 mix patient to normal plasma.

If not significantly corrected: inhibitor.

2
Q

Which acquired bleeding disorders prolong the thrombin time? (2)

A

Heparin.

DIC (grossly prolonged).

3
Q

Which acquired bleeding disorder grossly prolongs the prothrombin time?

A

Oral anticoagulants.

4
Q

Which acquired bleeding disorders typically show low platelets on a blood screen? (3)

A

Liver disease.
Massive transfusion syndrome.
DIC.

5
Q

Which clotting factors does the liver synthesise? (4)

Which does the Kupffer cell synthesise?

A

II.
VII (in Kupffer cells).
IX.
X.

6
Q

How does VKOR work?

A

Co-factor for gamma glutanyl carbonate. VKOR changes VitK epoxide back to VitK. Allows activation of clotting factors.

7
Q

What are the causes of vitamin K deficiency? (4).

A

Obstructive jaundice.
Prolonged nutritional deficiency.
Broad spectrum antibiotics.
Neonates (1-7 days).

8
Q

How is haemostasis impaired in liver disease? (6).

A

Thrombocytopenia.
Dysfunctional platelets (plasmin glycoprotein cleavage).
Reduced factor levels (except FVIII).
Delayed fibrin polymerisation (xs sialic acid).
Excessive plasmin activity.

9
Q

What is the definition of a massive transfusion?

A

Equal to patient blood volume in 24hrs. OR

50% blood loss in 3hrs.

10
Q

What are the haemostats abnormalities in massive transfusion due to?

A

Dilution effects: thrombocytopenia, clotting factor depletion (esp V, VIII, fibrinogen), citrate toxicity in neonates.
DIC.

11
Q

What is the pathophysiology of DIC? (4)

A

Consumption of clotting factors and platelets.
Microvascular thrombosis leading to ischaemia and organ damage.
Fibrinolysis activation.
Microangiopathic haemolysis.

12
Q

What are the causes of acute DIC? (5).

A
Sepsis.
Obstetric complications.
Trauma.
Acute intravascular haemolysis (ABO incom).
Fulminant liver disease.
13
Q

What are the causes of chronic DIC? (4)

A

Malignancy.
End stage liver disease.
Severe localised intravascular coagulation.
Retained dead foetus.

14
Q

How is DIC managed?

A

Treat underlying cause.
Supportive: maintain tissue perfusion, folic acid and vit K.
Possible platelet transfusion and fibrinogen concentrate.

15
Q

What is the site of action of rivaroxaban and apixaban?

A

FXa.

16
Q

What is the site of action of dabigatran?

A

Thrombin.

17
Q

Which coagulation tests are raised by dabigatran? (3)

A

APT.
APTT.
TPT.

18
Q

Which coagulation tests are raised by rivaroxaban? (3)

A

PT.
Possible APTT.
Specific antiXa.

19
Q

Which coagulation tests are raised by apixaban? (2)

A

Specific anitXa.

Possible PT.

20
Q

What is idarucizumab an antidote for?

A

Dabigatran.

21
Q

How is warfarin therapy controlled?

A

Titration around INR.

22
Q

Which drugs antagonise the effect of warfarin? (5)

A
Cholestyramine.
Spironolactone.
Rifampicin.
Carbamazepine.
Vitamin K.
23
Q

How should patients with overdose of warfarin with life threatening bleeding be managed?

A

5-10mg IV vit K.

Four factor concentrate

24
Q

How should patients with overdose of warfarin with no or non-life threatening bleeding be managed?

A

Withhold warfarin.

1-5mg IV vit K.

25
Q

How is heparin dosage monitored? (4).

A

APTT (not for LMWH).
Protamine titration.
Anti-Xa assay.
Calcium thrombin time.

26
Q

What his the management of a heparin overdose?

A

Stop infusion.

Protamine administration.

27
Q

Differentiate between the properties of LMWH and UFH:

A

LMWH: higher Xa:IIa action ration, improved bioavailability and longer half life. Monitoring not routinely required.

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