38 Acquired bleeding disorders

Question 1

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

Answer 1

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

If not significantly corrected: inhibitor.

Question 2

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

Answer 2

Heparin.

DIC (grossly prolonged).

Question 3

Which acquired bleeding disorder grossly prolongs the prothrombin time?

Answer 3

Oral anticoagulants.

Question 4

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

Answer 4

Liver disease.
Massive transfusion syndrome.
DIC.

Question 5

Which clotting factors does the liver synthesise? (4)

Which does the Kupffer cell synthesise?

Answer 5

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

Question 6

How does VKOR work?

Answer 6

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

Question 7

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

Answer 7

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

Question 8

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

Answer 8

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

Question 9

What is the definition of a massive transfusion?

Answer 9

Equal to patient blood volume in 24hrs. OR

50% blood loss in 3hrs.

Question 10

What are the haemostats abnormalities in massive transfusion due to?

Answer 10

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

Question 11

What is the pathophysiology of DIC? (4)

Answer 11

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

Question 12

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

Answer 12

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

Question 13

What are the causes of chronic DIC? (4)

Answer 13

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

Question 14

How is DIC managed?

Answer 14

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

Question 15

What is the site of action of rivaroxaban and apixaban?

Answer 15

FXa.

Question 16

What is the site of action of dabigatran?

Answer 16

Thrombin.

Question 17

Which coagulation tests are raised by dabigatran? (3)

Answer 17

APT.
APTT.
TPT.

Question 18

Which coagulation tests are raised by rivaroxaban? (3)

Answer 18

PT.
Possible APTT.
Specific antiXa.

Question 19

Which coagulation tests are raised by apixaban? (2)

Answer 19

Specific anitXa.

Possible PT.

Question 20

What is idarucizumab an antidote for?

Answer 20

Dabigatran.

Question 21

How is warfarin therapy controlled?

Answer 21

Titration around INR.

Question 22

Which drugs antagonise the effect of warfarin? (5)

Answer 22

Cholestyramine.
Spironolactone.
Rifampicin.
Carbamazepine.
Vitamin K.

Question 23

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

Answer 23

5-10mg IV vit K.

Four factor concentrate

Question 24

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

Answer 24

Withhold warfarin.

1-5mg IV vit K.

Question 25

How is heparin dosage monitored? (4).

Answer 25

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

Question 26

What his the management of a heparin overdose?

Answer 26

Stop infusion.

Protamine administration.

Question 27

Differentiate between the properties of LMWH and UFH:

Answer 27

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