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STEPH BPT 2021 > Haematology > Flashcards

Haematology Flashcards

1
Q

Lab criteria APLS

A
  1. Lupus anticoagulant
    > Prolonged APTT that fails to correct with mixing with prolonged reptiliase time
  2. Anticardiolipin antibody >99th percentile
  3. Anti-B2 glycoprotein -1 antibody >99th percentile

Must be present on 2 occasions 12 weeks apart

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2
Q

Clinical criteria APLS

A

One or more arterial, venous thrombosis

One of more unexplained fetal deaths over 10 weeks gestation

One or more Premature birth before 34 weeks

Three or more unexplained miscarriages before 10 weeks

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3
Q

Anticoagulation for Antiphospholipid Ab and 1 foetal loss at ten weeks

A

Low dose aspirin/prophylactic LMWH during pregnancy

Post partum prophylaxis

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4
Q

Antiphospholipid Ab and no thrombosis or pregnancy complications

A

Post partum prophylaxis for 6/52

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5
Q

Pregnancy anticoagulation for Lab criteria + Clinical pregnancy criteria of 3 or more pregnancy losses

A

Antepartum prophylactic clexane + aspirin

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6
Q

Dabigatran benefit over warfarin in AF

A

Less ICH
Increased GI bleeding
Small increase in myocardial infarction

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7
Q

Dabigatran reversal agent

A

Idarucizumab 5g

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8
Q

Factors in Prothrombin X

A

IX, X, II

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9
Q

Tranexamic acid mechanism

A

inhibits the activation of plasminogen via binding at several distinct sites, the latter of which is a lysin residue involved in its binding to fibrin

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10
Q

FXa inhibitor antidote

A

Andexanet alpha

Antedote for apixaban, rivaroxaban

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11
Q

Factor 13

A

Coagulation factor XIII (FXIII) is converted by thrombin and Ca(2+) into an active transglutaminase (FXIIIa) in the final phase of coagulation cascade. Its main function is the mechanical stabilization of fibrin clot and its protection from fibrinolysis by cross-linking of fibrin chains and α(2)-plasmin inhibitor to fibrin

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12
Q

Haemophilia C

A

Factor 11 deficiency

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13
Q

FVIII/IX deficiency severity

A

<1 severe- spontaneous
1-5% mod - surgery/minor trauma
>5 mild - major trauma

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14
Q

Cryoprecipitate contents

A

Factor VIII, fibrinogen, Factor XIII, vWF and fibronectin from the FFP

Only used to replace fibrinogen nowdays

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15
Q

Biostate contents

A

FVIII + vWF

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16
Q

Factor IX replacements

A

MonoFIX - plasma derived

Benefix - recombinant

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17
Q

Desmopressin/ DDAVP (ADH)

A

Increases in FVIII and vWF

Treatment in mild T1 vWFD

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18
Q

Treatment of acquired inhibitors

A

Novoseven

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19
Q

Bernard-Soulier syndrome

A

Abnormality of platelet glycoprotein 1b-IX-V, a receptor for vWF

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20
Q

Glanzmann thrombasthenia

A

Defect in glycoprotein IIb/IIIa complex

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21
Q

Peak timing of thrombocytopaenia in gestational thrombocytopaenia

A

2 and 3rd trimester

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22
Q

Mechanism and treatment of idiopathic TTP

A

Autoimmune ADAMTS13 deficiency

Treated with PLEX

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23
Q

Treatent of HITTS

A

Fondaparinux

Bivalirudin - renal impaired

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24
Q

action of hepcidin in Anaemia CD

A

Increased hepcidin
Blocks ferroportin
Unable to absorb iron

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25
Q

HbH

A

Beta tetramers

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26
Q

Hb Barts

A

Gamma tetramers

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27
Q

HbA2

A

Alpha x2 Delta x 2

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28
Q

Intravascular haemolytic

A

Urine haemosiderin

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29
Q

Emicizumab

A

Treatment for haemophilia A

Bridges factor 9 and 10 in similar mechanism to factor 8

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30
Q

Smudge/smear cells

A

CLL

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31
Q

Lab/imaging reasons to treat MM

A

60% plasma cells
Serum free light chains >100
reater than one focal lesion on MRI

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32
Q

APML mutation

A

t(15;17)

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33
Q

APML RX

A

ATRA

Arsenic

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34
Q

Auer rods

A

AML

35
Q

Mode of inheritance vWD

A

Autosomal dominant

36
Q

CML cytogenetic abnormality

A

t(9;22)

37
Q

Antibody involved in haemolytic transfuion reactions

A

IgM

38
Q

Follicular lymphoma cytogenetic abnormality

A

t(14;18)

39
Q

Vincristine mechanism of action

A

Metaphase is the phase of the cell cycle when the chromosomes align at the middle of the cell and then begin to separate. Vincristine disrupts this process by binding to the tubulin protein, preventing the formation of microtubules and preventing the initiation of chromosome separation. The cell will then undergo apoptosis.

40
Q

The herpes virus Epstein-Barr establishes latent infection in which immune cell

A

B-Cells

41
Q

Pathogen associated with the development of adult T-cell leukaemia

A

HTLV-1

42
Q

CD classes associated with Reed-steinberg cells

A

CD-15 CD-30

43
Q

Marker that identifies peripheral stem cells

A

CD34

44
Q

Best method for reducing transfusion related GVHD

A

Irradiation

45
Q

Benefit of leukoreduction

A

Reduced TRALI
Reduced non-haemolytic transfusion reactions
Reduces CMV transmission
Reduces GVHD

46
Q

Most common gene mutation in hereditary haemochromatosis

A

H63D mutation of the HFE gene

47
Q

Absence of CD55 and CD 59 on RBC

A

Paroxysmal nocturna haemaglobinuria

48
Q

Triad of PNH

A
  1. Haemolytic anaemia
  2. Venous thrombosis (especially intraabdominal)
  3. Deficient haematopoesis (often pancytopaenia)

Signs occurring after infection

49
Q

PNH mechanism

A

Defective production of PIG-A which is essential for GPI anchor resulting in decreased CD55 and CD 59 on cells (protects from complement mediated lysis)

50
Q

Treatment of PNH

A

Anticoagulation if thrombosis

Eculizumab (anti-C5)

51
Q

Bites and blisters on film

X Linked

A

G6PD deficiency

52
Q

Thorny apple cells

Autosomal recessive

A

Pyruvate kinase deficiency

53
Q

Eliptocytes

A

Red cell membrane disorder

54
Q

Clinical outcomes iron overload

A
  • Cardiac failure
  • skin pigmentation
  • Endocrine failure: hypopituitary, hypogonadism, infertility, delyed puberty, failure to thrive, groath retardatin, diabetes, OP
55
Q

Clinical outcomes B thalassaemia

A

Severe anaemia - require transfuions
Hepatosplenomegaly
Iron overload - require chelation

56
Q

Good prognostic features AML

A 
NPM + 
CEBPA + 
t(15:17)
t(8:21)
Inversion q16
57
Q

Bad prognostic features AML

A

cKIT
FLT3 +
Del7q

58
Q

Treatment for AML that targets FLT-3

A

Midostaurin - kinase inhibitor

59
Q

APML genetics

A

t(15:17)

PML-RARa

60
Q

CML genetis

A

t(9:22) BCR-ABL

61
Q

MPD genetics

A

JAK-2 V617F mutation

62
Q

MDS genetics (good prognosis)

A

Deletion 5q

SPARC and RPS14 deficiency

63
Q

Treatment of CML

A

Tyrosine Kinase inhibitors

  • imatinib (effusion/oedema)
  • dasitinib (DM, long Qt, vascular events)
  • nilotinid (PAH)
64
Q

Good prognostic factor for ET/Primary myelofibrosis

A

CALR

65
Q

Treatment of PRV

A

Phlebotomy until haematocrit <45%

Low dose aspirin

66
Q

Cytogentic abnormality associated with response to lenolidamide in MDS

A

Deletion 5q

67
Q

HHV8 cancer-associated

A

Primary effusion lymphoma

68
Q

Hep C cancer association

A

Splenic marginal lymphoma

69
Q

Burkitt’s lymphomac cytogenetics

A

t (8:14) translocation

70
Q

Mantle cell lymphoma cytogenetics

A

t(11:14) translocation = cyclin D1

71
Q

Follicular lymphoma cytogenetics

A

t(14:18) translocation = BCL-2

72
Q

Treatment high-grade NH lymphoma

A

Radiotherapy
RCHOP
Rituximab if CD-20 positive
Transplant if relapse

73
Q

Treatment of low-grade NHL

A

RTx

Single agent chemo

74
Q

RCHOP

A 
Rituximab
Cyclophosphamide
Hydroxydaunrubacin
Vincristine
Prednisolone
75
Q

Hodgkin Lymphoma treatment

A

ABVD chemo
RTx
AutoSCT. ifrelapsed
AlloSCT if relapse post AUto

76
Q

ABVD agents

A

Doxorubicin
Bleomycin
Vinblastine
Dacarbazine

77
Q

CLL novel therapies

A

Obinutuzumab - mAB CD2-
Ibrutinib - B-TK inhibitor
Venetoclax - Inhibits Bcl-2 (TLS risk)
Idelalisib - PI3Kd inhibitor

78
Q

Ig subclassess involved in MM

A

IgG>IgA>IgM (waldenstroms)

79
Q

Bortezemib MOA/Indication / SE

A

MOA: Proteasome inhibitor
Indication: MM
SE: Peripheral neuropathy, diarrhoea, thrombocytopaenia

80
Q

CLL film

A

Smear cells

81
Q

When to consider treating CLL

A

Lymphocytes doubling in <6 months
Symptoms
Stage 3 - anaemia
Stage 4 - thrombocytopaenia

82
Q

Coeliac cancer association

A

T Cell lymphoma

83
Q

Treatment of ET

A

Aspirin

Consider cytoreduction if plt >1000

84
Q

Cells involved in haemophagocytic lymphohistiocytosis

A

cytotoxic T cells & Natural Killer (NK) cells.

STEPH BPT 2021 (16 decks)

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