Anticoagulation and NOACs Flashcards

1
Q

PT (INR) measures Extrinsic pathway (FVII and then combined pathway X + V -> II). Causes of prolonged PT?

A
Factor VII deficiency
Warfarin
Oral Xa inhibitors
LAC
Mild factor X, V or II def
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2
Q

aPTT measures intrinsic pathway (Factors XII, XI, IX and VIII and then combined X+V and II). Causes of prolonged aPTT?

A

Factors XII, XI, IX and VIII def
vWD
LAC
Mild X, V or II def

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3
Q

What is the best predictor of perioperative bleeding?

A

The bleeding history

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4
Q

How does Heparin affect the coag assay?

A

Prolong aPPT and TT

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5
Q

What test confirms the presence of Heparin?

A

Reptilase time

Activates prothrombin, not inhibited by heparin

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6
Q

What prolongs reptilase time?

A

Abnormal or reduced fibrinogen
Hypoalbuminaemia
Raised FDPs

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7
Q

What causes a prolonged PT and APTT?

A

Vit K def
Warfarin anticog
Liver failure
Combined V and VIII def

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8
Q

What causes a long PT, APTT, TT and normal or abnormal fibrinogen?

A

Heparin in large amounts
Liver disease
Finronogen def or disorder
Excess dabigatran and anticoagulation

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9
Q

What causes a long PT, APTT, Normal TT and Normal or abnormal Fibrinogen and low platelet count?

A

Massive transfusion

Liver disease

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10
Q

What causes a long PT, APTT, TT, low fibrinogen and low platelet count?

A

DIC

Acute liver disease

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11
Q

Antithrombin deficiency. What, associations?

A

AD
Prevalence of symptomatic disease 0.01%

Antithrombin inhibits XIIa, Xia, IXa and Xa

Acquired casues are DIC, cirrhosis, nephrotic syndrome and L- asparaginase therapy

Associated with VTE from puberty in 55%
Recurrence of 60%

Very high risk of VTE in pregnancy = 50%
prophylactic anti-coagulation and antithrombin concentrates at delivery

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12
Q

Protein C and S def.

What, prevalence, causes, associations?

A

AD
Prevalence of symptomatic disease is 0.1% or less

Acquired causes are liver disease, warfarin therapy, OCP and preg

Associations:
VTE from puberty, less risk than antithrombin. Spontaneous and associated with surgery, trauma, pregnancy etc.

Warfarin induced skin necrosis

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13
Q

Role of activated protein C?

A

Protein C inactivates Factor V and FVIII with protein S as a cofactor

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14
Q

What inherited clotting disorder is associated with venous, not arterial thrombosis?

A

Activated protein C resistance
- Mutation Factor V Leiden found

Moderate risk for venous thrombosis
Synergictic with OCP, preg, Sx

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15
Q

Elevated Factor VIII.
Cause
Main risk association

A

Elevtaed levels are related to ABO blood group - Group O have lower FVIII
Inherited in some

FVIII levels may rise with infection, inflammation etc
Rise with age, esp post menopause

Elevated FVIII >150% (1.5 IU/L) is associated with a 4.8 fold risk of VTE!!!
Greater than activated protein C resistance (Factor V Leiden) etc

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16
Q

Pregnancy associated VTE. Highest risk periods?

A

Highest risk post partum, 5 x higher
1st trimester higher risk than others.
Left LL more common = 85%

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17
Q

Coagulation Tx for unprovoked VTE?

A

3 months

With mild RF, 3 months then reassess

18
Q

Coagulation Tx period for Recurrent idiopathic VTE?

A

Long term warfarin

19
Q

First idiopathic VTE. Tx period?

When do you consider long term warfarin?

A
Tx for 3-6 months
Consider long term warfarin id
- life threatening 1st event
- unusual site esp if APLS
- incomplete recovery from primary event
- patient preference
- APLS
- high risk thrombophilia
20
Q

HITTS Mx?

A

Stop heparin
DO NOT GIVE PLATELETS
Start Danaparoid, argatroban or fondaprinux
Delay starting warfarin until platelet count recovers

21
Q

What are the long distance guidelines for VTE prevention in pts with no RF for VTE vs. patients with RF?

A
No RF:
Flight > 6 hrs
- avoid constrictive clothing around lower extrememties or waste
- avoid hydration
- do frequent calf muscle stretching

RF:
Above PLUS
- properly fitted below knee GCS providing 15-30 mmHg of pressure at the ankle (grade 2B) OR
Single dose LMWH injected prior to departure

No evidence for aspirin in VTE prevention associated with travel (grade 1B)

22
Q

Prasugel. MOA. Indications. CI?

A

Reversibly binds to P2Y12 receptor and inhibits platelet aggregation for the life of the platelet.

Indications:
ACS to be managed with PCI (with aspirin)

AE:
Common is bleeding
Rare - angioedema

CI:
Hx of stroke of TIA due to increased risk of bleeding

23
Q

Which factors initiate coagulation?

A

Factor VII and tissue factor (VIIa)

24
Q

Which bleeding disorder can have a severe phenotype but normal APTT and PT?

A

Factor XIII

Factor XIII crosslinks fibrin to stabilise the clot in the last step

25
Q

How is vWBD most commonly inherited?

Which factor is vWB a carrier for?

A

AD

Factor VIII therefore low in vWD and prolonged aPPT

26
Q

The antithrombotic effect of warfarin is due to its inhibition of?

A

Factor II (Prothrombin)
Antithrombotic effect is not present until the 5th day if therapy.
Depends on clearance of prothrombin which has a half life of 50 hrs.

27
Q

The anticoagulant activity of warfarin is dependent on?

A

The clearance of clotting factors from the systemic circulation after the 1st dose. The clearance is determined by the half lives.
the changes are noted 24-36 hrs and due to clearance of Factor VII which is the clotting factor with the shortest half life.

28
Q

What does prothrombinex contain?

A

Inactivated concentrate of II, IX and X with variable amounts of VII

Activated prothrombinex used when pt has an inhibitor

29
Q

Actions of antiphospholipid syndrome in vivo (inside living organism) vs. in vitro (test tube)?

A

In vivo = prothrombotic
In vitro = prolong APTT

If no AI features = primary APS

Tx: Lifelone anticoagulation

30
Q

Protein C activated by?

A

Thrombin

31
Q

Greater risk of recurrent DVT/PE. Antithrombin III deficiency or Protein C deficiency?

A

Antithrombin deficiency portends the highest risk of VTE but is not a common genetic thrombophilia

32
Q

What is the most common cause of acquired protein C resistance?

A

Factor V Leiden

33
Q

What is the difference between Factor V Leiden and Protein C deficiency?

A

Factor V Leiden is the congenital form of Protein C resistance.

Protein C def also affects the same pathway but does not cause resistance of FVL to APC - just less Activated protein C

34
Q

MOA protein C?

A

Inactivate FVa (cleaves Xa to thrombin) and inactivates VIIIa

35
Q

What is the better Tx for HITS in the prevention of thrombosis? LMWH or Direct thrombin inhibitor?

A

Direct thrombin inhibitor - danaparoid or fondaparinux.

Warfarin can be commenced once the PLTs >= 150, 000/microL

36
Q

How do you monitor Rivaroxiban?

A

Anti-Xa level specific for rivaroxiban

Also anti-Xa levels specific for Apixaban present

30% renal excretion
70% liver (CYP3A4)
Half life 9 hrs

37
Q

How do you measure for Dabigatran?

A

Dilute thrombin clotting time assay (HEMOCLOT assay)

Half life of dabigatran is 12-14h

38
Q

MOA of thrombolysis?

A

Activation of plasminogen

39
Q

What is the most common cause of bud chairi syndrome?

A

Polycythemia Rubra vera is themsot common cause overall.

Myeloproliferative disease cause 50%

Other causes:
PNH
Pregnancy and OCP
Drugs- azathioprine, adriamycin
Cancer esp HCC, renal
Hypercoagulable states e.g. FVL mutations, APLS, ATIII/PC/PS def 
Idiopathic 20%
40
Q

Myeloproliferative disorder BCR-ABL +ve. Dx?

A

CML

41
Q

Myelopriliferative disorder, BCR-ABL -ve, JAK-2 +ve. Dx?

A

PRV, > 90%

50% MF and ET

42
Q

Myelopriliferative disorder, BCR-ABL -ve, JAK-2 -ve. Dx?

A

50% ET and MF

Infrequent PRV