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FRACP Shuyu > Alfred Saturday course Haem 1 > Flashcards

Alfred Saturday course Haem 1 Flashcards

1
Q

biggest risk factor for a recurrent VTE

A

previous idiopathic DVT/PE

(20% of idiopathic VTE will have another event after stopping the anticoagulant)

continuation of anticoagulant longer does not reduce this risk

highest risk in the first 12 months, then 3-5%/year

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2
Q

what is the most common hereditary thrombophilia

A

factor 5 leiden/Activated protein C resistance (2-10%)

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3
Q

what hereditary thrombophilias would change management

A

deficiencies of natural anticoagulants:

  • Protein C, S and antithrombin
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4
Q

management of periop anticoagulation with surgery in antithrombin deficiency

A

replace antithrombin

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5
Q

which DOACs have been used for long term treatment of VTE

A

apixaban, rivaroxaban low dose (after the first 6 months of full dose anticoagulation)

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6
Q

duration of anticoagulation

A

provoked 3-6 mo

unprovoked at least 6 months

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7
Q

correlation between initial type of thrombotic event in APLS and the recurrence type

A

Arterial -> another arterial

Venous -> another venous

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8
Q

most common aetiology of antiphospholipid syndrome

A

primary antiphospholipid syndrome (>50%)

SLE next most common

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9
Q

lupus anticoagulant coagulation testing results

A

APTT prolonged that doesn’t correct w mixing

normal TVT

prolonged reptilase time

doesn’t correct with heparinase or protamine

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10
Q

what is the definition of “correction” of APTT with mixing

A

correction to 4-5 secs of the lab APTT normal range

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11
Q

how does TCT work

A

add thrombin and see how long it takes for blood to clot

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12
Q

which immunoglobulin for anticardiolipin is more associated with thrombosis

A

IgG > IgM

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13
Q

which test confers the lowest risk of APLS/thrombosis (e.g. LAC, aCL, beta2-GPI)

A

anti-cardiolipin

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14
Q

manageemnt of antiphospholipid antibody and no previous thrombosis or pregnancy complications (e.g. found incidentally)

A
  1. close clinical surveillance antepartum
  2. post-partum prophylaxis for 6/52
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15
Q

what postpartum risk factor confers the greated risk for the pregnancy associated VTE?

A

post-partum OR 4-21

placental abruption OR 2-16

post-partum haemorrhage OR 1.3-21

(but overall the greatest rist factor is a previous VTE OR 24.8)

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16
Q
A
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17
Q

what does anti-thrombin act on?

A

inhibits thrombin and anti-Xa

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18
Q

what is the clinical utilisation of fondaparinux

A

HIITS

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19
Q

which DOAC is a pro-drug

A

dabigatran

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20
Q

what DOAC is most dependent on renal function for excretion?

A

dabigatran (80% renal excretion)

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21
Q

dabigatran coagulation testing results

A
  • linear relationship with APTT
  • dilute TCT can be used to provide quantification (TCT exquisitely sensitive and normal result can almost disprove dabigatran in system)
  • INR/PT insensitive
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22
Q

what is the dilute TCT (or haemaclot) used for?

A

quantification of dabigatran

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23
Q

MOA of andexanet alfa

A

decoy Xa molecule that has no anticoagulating activity

can reverse all direct and indirect Xa inhibitors (including LMWH)

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24
Q

what is involved in the initiation of coagulation?

A

tissue damage and tissue factor activates VIIa

that activates Xa and Va

that creates a small amount of thrombin

which creates fibrin

25
Q

clinical epistaxis and recurrent GI bleeding - what kind of bleeding disorder is this most likely to indicate

A

platelet/vWF defect

26
Q

why does the INR not reflect the anticoagulation at the initiation of warfarin

A

factor VII drops first because of its shorter half life. Factor X and IX drops slower.

Moreover, there is a decrease of protein C and S and there is a theoretical prothrombic state at the initiation of warfarin

27
Q

a delayed failure to correct APTT - cause?

A

autoimmune inhibitor phenomenon (rather than haemophillia assoc inhibitor)

but haemophilia inhibitor can still be time dependent

28
Q

what does thrombin clottig time reflect and what are the causes

A

the action of thrombin on fibrinogen

causes:

  • abnormal fibrinogen/fibrinogen degradation product
  • heparin
  • paraprotein esp IgM
  • dabigatran
29
Q

haemophiia patient without family history (known family tree)

A

novel mutational events

1/3 of patients don’t have a family history

30
Q

severity classification of FVIII or FIX (factor levels)

A

severe <1%

mod 1-5%

mild >5%

31
Q

timing of post op bleeding (immediate vs delayed) and likely bleeding defect

A

platelets = immediate

coagulation factor def = delayed

32
Q

what HIV agents are assos with renal stones (significant especially in haemophilia)

A

protease inhibitors

33
Q

what does cryprecipitate contain?

A
  • fibrinogen
  • Factor VIII (the protein missing in patients with haemophilia A)
  • Factor XIII
  • von Willebrand factor (helps the platelets stick together)
34
Q

MOA tranexamic acid

A

blocks lysin residues and plasminogen cannot attach and break down fibrin

35
Q

route of liver biopsy for haemophilliacs

A

transjugular liver biopsy as bleeding is intravascular

36
Q

how to quantite factor inhibitors

A

bethesda assay

37
Q

Emicizumab MOA

A

factor VIII inhibitor bypassing fraction

monoclonal antibody overcomes the lack of factor VIII by bridging factors IX and X to restore haemostasis.

38
Q

what type of vWD can DDAVP be used in

A

only type I

should not be used in pregnancy

39
Q

what is bernard-soulier syndrome

A

abnormality of glycoprotein Ib-IX-V

actsl like vWFD

large platelets

40
Q

MOA romiplostin

A

genetically engineered protein which binds to the thrombopoietin receptor even though its structure differs from that of human thrombopoietin. Activation of the receptor increases platelet production

stimulates bone marrow production of platelets

only available in australia for patients who relapsed for splenectomy or cannot have one

41
Q

treatment of ITP platelets >30

A

observe

42
Q

treatment of ITP with platelets <30

A

steroids - 1st line

then IVIG, anti-D

43
Q

role of splenectomy in ITP

A

consider for:

-adults who have a relapse ot have not had a response to corticosteroids, IVIG, anti-D

44
Q

differences in ITP vs gestational thrombocytopenia

A
  • <70 more likely ITP
  • 1st trimester more likely ITP
  • history of ITP prior pregnancy
45
Q

when to treat ITP in pregnancy

A

plt <80, trial of steroids with gradual taper or IVIG

46
Q

what thrombotic microangiopathies are amendable to plasma exchange

A

TTP

catastrophic antiphospholipid syndrome

47
Q

pathogenesis of HITTS

A

formation of neoepitopes that occurs when heparin binds to PF4, resulting in conformational changes

the pathogenic HIT antibodies are directed against neoepitopes on a self protein

48
Q

what chromosome codes ABO blood group

A

9

49
Q

most common blood group in australia

A

O+

50
Q

what is the process of cross matching

A

donor red cells against patient serum/plasma

51
Q

what is the purpose of the direct antiglobulin test

A

looking for antibody bound/complement bound RBC in the circulation

(cf IAT where the antibody is in the serum/plasma and is added to reagent RBC and add AHG

52
Q

what is the commonest transfusion problem

A

TACO - transfusion associated circulatory overload

53
Q

what type of transfusion reaction is extravascular

A

delayed haemolytic transfusion reaction

due to an antibody stimulated by previous pregnancy or transfusions. IgG antidboy that bind to Fc receptors of splenic macrophages and gradually reduce them

54
Q

what antibody is involved in acute haemolytic transfusion reaction?

A

IgM antibodies which activates comlement and the membrane attack complex and rapidly destroys red cells

55
Q

definition of febrile non-haemolytic transfusion reactions

A

>1 degree increase in temperature and no other likely explanation

56
Q

most common cause of febrile non-haemolytic transfusion reactions

A

cytokine storm

(used to be antibodies against donor leukocytes before widespread leukophoresis)

57
Q

what blood product is most likely to cause TRALI

A

plasma

58
Q

most common cause of non-haemolytic transfusion reaction

A

interaction between donor granu

FRACP Shuyu (65 decks)

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