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Haematology > Thrombosis and haemostasis > Flashcards

Thrombosis and haemostasis Flashcards

1
Q

Primary haemostasis
Secondary haemostasis

A

formation of platelet plug
formation of clot to stabilise platelet plug

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2
Q

What does PT / INR test?

A

extrinsic pathway, factor 7 and common pathway

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3
Q

What does APTT test?

A

intrinsic pathway and common pathway
factor 8, 9, 11, 12 and common pathway

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4
Q

What factors are involved in the common pathway?

A

2, 5, 10 and fibrinogen

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5
Q

What are the natural anticoagulants?

A

protein S and protein C, antithrombin

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6
Q

Mixing studies
- how is it performed
- what do the results signify

A

mix patients plasma with pooled plasma
if APTT continues to be prolonged then this represents an inhibitor being present
if APTT corrects then this represents a factor deficiency

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7
Q

Causes of prolonged APTT

A

unfractionated heparin therapy
LMWH (only when over anticoagulated)
Deficiency of factors 8, 9, 11 or 12
Von Willebrand disease
Lupus anticoagulant

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8
Q

Causes of both APTT and PT prolongation

A

DIC
Liver disease
Common pathway deficiency: factor 2, 5, 10 or fibrinogen
Direct thrombin or factor Xa inhibitors: dabigatran, apix

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9
Q

Causes of prolonged thrombin clotting time

A

heparin
low fibrinogen
thrombin inhibitor

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10
Q

Cut offs for DOACs and CrCl

A

Dabigatran <30ml/min
Apixaban <25
Riva <15

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11
Q

Reversal agent for Dabigatran

A

idarucizumab

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12
Q

Apix / rivarox reversal agent
- is it available?

A

andexanet
- still undergoing trials

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13
Q

Idarucizumab dosing

A

2.5g infusions over 5-10 minutes x2

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14
Q

Management of bleeding in DOAC therapy
- mild bleeding
- significant bleeding
- life threatening bleeding

A
  • local haemostasis levels, delay next dose
  • administer charcoal if last NOAC ingestion <2 hours, transfusion support
  • administer one of the following: prothrombinex, TXA, FEIBA
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15
Q

Reversal for heparin

A

protamine

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16
Q

Reversal for warfarin

A

vitamin K, prothrombinex

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17
Q

What ratio of blood products should be used in massive transfusion protocol

A

4 PRBC : 2 FFP : 1 Platelets
Consider fibrinogen if <1 (or <2 in pregnancy related bleeding)

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18
Q

Tranexamic Acid MOA

A

antifibrinolytic, inhibits plasminogen activation and fibrinolysis
used in bleeding secondary to trauma or prevention of bleeding

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19
Q

Investigations for unprovoked VTE

A

lupus anticoagulant, anti B2glycoprotein, antithrombin
Age appropriate cancer screening
CXR, calcium

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20
Q

Indications for thrombophilia testing

A

recurrent VTE
VTE prior to age 50
VTE at unusual site (cerebral, mesenteric, portal, hepatic veins)
Combined arterial and venous thrombosis

21
Q

Components of thrombophilia screen

A

factor V leiden
prothrombin gene mutations
protein C and protein S
antithrombin deficiency
antiphospholipid antibodies

22
Q

Duration of treatment for VTE

A

strongly provoked - 3 months
minimally provoked - 3 months but consider longer
unprovoked - guidelines vary: indefinite vs. 3 months

23
Q

VTE: DOAC or warfarin superior?

A

DOAC non-inferior

24
Q

DOAC in obesity

A

consult haemataologist if BMI >40 or over Kg 120

25
Q

PE - when is thrombolysis indicated?

A

haemodynamic instability (bradycardia, hypotension, cardiac arrest)

26
Q

PEITHO study

A

thrombolysis not recommended in intermediate risk PE due to high risk of bleeding complications

27
Q

Predicting risk of VTE in cancer
- scoring system

A

Khorana risk score

28
Q

VTE treatment in cancer

A

LMWH, rivaroxaban, apixaban

29
Q

Haemophilia A
- gene involved
- mode of inheritance
- are females affected?

A

factor 8
x-linked
F can have bleeding phenotype in extreme lyonisation

30
Q

Haemophilia A bleeding sites

A

haemarthrosis, muscle, others, CNS
usually mild severity

31
Q

What is emicizumab?

A

bi-specific MAB binding factor 9a to factor 10 facilitating conversion to active 10a
used in haemophilia

32
Q

Von Willebrand disease
- inheritence mode
- patterns of bleeding

A

dominant
bruising, epistaxis
menorrhagia, bleeding after minor surgery

33
Q

vWD testing

A

APTT
Factor 8 activity
vWF antigen testing and function testing

34
Q

vWD types

A
  1. low levels of vWF
  2. poorly functioning
  3. absent vWF
35
Q

vWD treatment
type 1
type 2
type 3

A

1 - desmopressin, TXA
2. - desmopressin or vWF-Factor 8 concentrate
3. - TXA, vWF concentrate

36
Q

What is warfarin associated skin necrosis?

A

Occurring within first few days of initiation
Shortest half-lifes are factor 7 and protein C meaning the initial effect is procoagulant

37
Q

Which factors does Warfarin reduce?

A

Protein C, S
2, 7, 9, 10.

38
Q

Rate of CTEPH post PE
Rate of post thrombotic syndrome

A

5%
20-50%

39
Q

What antibodies are present in HITT

A

platelet factor 4 / heparin complex

40
Q

Diagnosis of HIT

A

4T score
Serotonin release assay (gold standard but slow ++)

41
Q

Management of HIT

A

cease heparin (and warfarin)
anticoagulate with argatroban, bivalirudin, fondaparinux

42
Q

Tests for unusual thromboses

A

JAK2 mutation
Paroxysmal nocturnal haemoglobulinaemia
APLS

43
Q

Haemophilia A severity grading

A

factor 8 level
<1 - severe
1-5 - moderate
>6 mild

44
Q

How do you calculate factor replacement dose?

A

Haemophilia A = desired factor level (eg 80) x weight x 0.5
For haemophilia A its just desired factor level x weight

45
Q

What is emicizumab?

A

bispecific MAB for haemophilia A - binds Xa and IXa

46
Q

PNH - what genes are mutated

A

CD 55 and CD 59
Involved in inhibition of complement

47
Q

Treatment for PNH

A

eculizumab - inhibits C5 convertase

48
Q

Treatment for aplastic anaemia

A

if young and matched sibling - allogenic stem cell transplant
otherwise; steroids then ciclosporin or cyclophosphamide

Haematology (5 decks)

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