38 Acquired bleeding disorders Flashcards Preview

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

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

Repeat test with 50:50 mix patient to normal plasma.
If not significantly corrected: inhibitor.

2

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

Heparin.
DIC (grossly prolonged).

3

Which acquired bleeding disorder grossly prolongs the prothrombin time?

Oral anticoagulants.

4

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

Liver disease.
Massive transfusion syndrome.
DIC.

5

Which clotting factors does the liver synthesise? (4)
Which does the Kupffer cell synthesise?

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

6

How does VKOR work?

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

7

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

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

8

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

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

9

What is the definition of a massive transfusion?

Equal to patient blood volume in 24hrs. OR
50% blood loss in 3hrs.

10

What are the haemostats abnormalities in massive transfusion due to?

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

11

What is the pathophysiology of DIC? (4)

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

12

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

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

13

What are the causes of chronic DIC? (4)

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

14

How is DIC managed?

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

15

What is the site of action of rivaroxaban and apixaban?

FXa.

16

What is the site of action of dabigatran?

Thrombin.

17

Which coagulation tests are raised by dabigatran? (3)

APT.
APTT.
TPT.

18

Which coagulation tests are raised by rivaroxaban? (3)

PT.
Possible APTT.
Specific antiXa.

19

Which coagulation tests are raised by apixaban? (2)

Specific anitXa.
Possible PT.

20

What is idarucizumab an antidote for?

Dabigatran.

21

How is warfarin therapy controlled?

Titration around INR.

22

Which drugs antagonise the effect of warfarin? (5)

Cholestyramine.
Spironolactone.
Rifampicin.
Carbamazepine.
Vitamin K.

23

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

5-10mg IV vit K.
Four factor concentrate

24

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

Withhold warfarin.
1-5mg IV vit K.

25

How is heparin dosage monitored? (4).

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

26

What his the management of a heparin overdose?

Stop infusion.
Protamine administration.

27

Differentiate between the properties of LMWH and UFH:

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

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