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FRACP NOSH 2020 > Haematology > Flashcards

Haematology Flashcards

1
Q

What effect does DIC have on D-Dimer?

Why?

A

D-Dimer is elevated, as it reflects an increase in fibrin degradation products with the pathological and extensive fibrinolysis that occurs

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2
Q

What is the hallmark of DIC on coagulation profile?

A

Decreased fibrinogen

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3
Q

What will the blood film show in DIC?

A

Schistocytes / helmet cells due to microangiopathic haemolysis

Thrombocytopaenia

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4
Q

What do smudge cells on blood film indicate?

A

Chronic Lymphocytic Leukaemia

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5
Q

What is the difference between SLL and CLL?

A

SLL - primarily nodal, <5 lymphocytes in blood

CLL - primarily blood, >5 lymphocytes in blood

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6
Q

What haematological condition is venetoclax used for?

A

Refractory CLL

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7
Q

Which agent is used for MDS with del5q?

A

Lenalidomide

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8
Q

What are some side effects of imatinib?

A

Weight gain, nausea, diarrhoea, oedema, muscle cramps

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9
Q

What is the role of OCT-1?

A

It is the main transporter for imatinib.

High OCT-1 activity is associated with better response to imatinib

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10
Q

What is the most common finding on presentation of multiple myeloma?

A

Anaemia

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11
Q

What is daratumumab? What is its role in multiple myeloma?

A

Anti-38 monoclonal ab

Approved for use in relapsed MM

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12
Q

What is the main cause of hypercalcaemia in multiple myeloma?

A

Primarily due to increased osteoclastic bone resorption

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13
Q

What are the two main prognostic markers in multiple myeloma?

A

Beta 2 microglobulin + albumin

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14
Q

What do Dohle bodies in white cells indicate?

A

Toxic granulation

Seen in leukamoid reaction = immature cells in the blood due to

  • severe infection
  • severe sepsis
  • massive haemorrhage
  • bone marrow infiltration
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15
Q

What condition predisposes to warfarin-induced skin necrosis?

A

Protein C deficiency

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16
Q

Blood film = target cells + teardrop cells

A

Thalassaemia

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17
Q

Blood film = pencil cells

A

iron deficiency

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18
Q

Blood film = Bite cells

A

Caused by Heinz bodies, seen in oxidative haemolysis e.g. G6PD deficiency

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19
Q

Blood film = Spur cells (irregular projections)

A

Liver disease

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20
Q

Blood film = burr cells / echinocytes (regular projections_

A

Uraemia

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21
Q

Blood film = tear drop cells

A

Extramedullary haematopoiesis or thalassaemia

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22
Q

Blood film = nucleated RBCs

A

Severe haemolysis, hypoxia, stress or PMF

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23
Q

Blood film = Howell-Jolly bodies

A

Hyposplenism

They are nuclear remnants of RBCs usually removed by spleen

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24
Q

Blood film = any blasts

A

NEVER NORMAL on peripheral smear

Suggests haematological malignancy

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25
Q

Blood film = Auer rods

A

Acute myeloid leukaemia

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26
Q

Blood film = schistocytes

A

Microangiopathic haemolysis

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27
Q

What haem malignancy is HTLV-1 associated with?

A

Acute T-lymphoblastic Leukaemia / Lymphoma

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28
Q

What haem malignancy is EBV associated with?

A

Burkitt lymphoma
PTLD
Hodgkin lymphoma

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29
Q

What haem malignancy is HIV associated with?

A

DLBCL
Burkitt lymphoma
Hodgkin lymphoma
Primary CNS lymphoma

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30
Q

What haem malignancy is HHV-6 associated with?

A

Primary effusion lymphoma

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31
Q

What haem malignancy is benzene associated with?

A

Multiple myeloma

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32
Q

What haem malignancy is hair dye associated with?

A

Follicular lymphoma

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33
Q

What cytogenetic marker is associated with APML?

A

t(15,17)

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34
Q

What is the strongest adverse prognostic factor in AML?

A

Age >60

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35
Q

What is the biggest risk factor for recurrent DVT/PE?

A

Unprovoked VTE

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36
Q

What are the high risk inherited thrombophilias?

A
  • AT deficiency
  • Protein C / S deficiency
  • Factor V Leiden homozygote
  • Prothrombin gene mutation homozygote
  • Double heterozygotes for FVL and PGM
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37
Q

What kind of thrombosis are APLS at risk of?

A

Arterial AND venous

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38
Q

What are the APLS ab to test for?

A

Anti-Beta 2 glycoprotein 1
Anti-cardiolipin
Lupus anticoagulant

Must be repeated after 12 weeks to make diagnosis

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39
Q

What are the initial laboratory findings in lupus anticoagulant?

A

Prolonged APTT that does not correct with mixing.

Prolonged reptilase time, normal TCT

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40
Q

What are the 3 causes of prolonged APTT?

A

Factor deficiency
Inhibitor
Drugs

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41
Q

What are the 2 possible inhibitors that would prolong APTT?

A

Lupus anticoagulant

Specific factor inhibitor

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42
Q

Which of the APLS ab have the weakest correlation with thrombosis?

A

Anti-cardiolipin ab

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43
Q

What is the greatest risk factor for VTE in pregnancy?

A

Prior VTE

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44
Q

What are the direct thrombin inhibitors used in HITS?

A

Danaparoid
Argatroban
Bivalirudin

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45
Q

What is the main use of fondaparinux?

A

In patients with HITS + normal renal fx

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46
Q

Which DOAC is most reliant on renal function for excretion?

A

Dabigatran

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47
Q

What is the anticoagulant of choice in prosthetic heart valves?

A

Warfarin

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48
Q

What are 2 GpIIb/IIIa inhibitors?

What is their use?

A

Abciximab
Tirofiban

Coronary angiography

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49
Q

What type of bleeding is more characteristic of factor deficiencies?

A

Haemarthroses, deep muscle bleeds

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50
Q

What type of bleeding is more characteristic of platelet / vWF disorders?

A

Epistaxis + GI bleeding, skin, genito-urinary

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51
Q

Umbilical stump bleeding -> classic deficiency?

A

Factor 13

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52
Q

What are the factors involved in the common coagulation pathway?

A

Factor X, factor V, factor II (prothrombin), and factor I (fibrinogen)
**think of our currency, $1, $2, $5, $10

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53
Q

Which pathway does the APTT measure?

Which factors are involved?

A

Intrinsic pathway + common
Factor XII, XI, IX, VIII
Factor 1, 2, 5, 10

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54
Q

Which pathway does the PT measure?

Which factors are involved?

A

Extrinsic + common
Factor 7, TF
Factor 1, 2, 5, 10

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55
Q

Which factor drops first in warfarin administration?

A

Factor 7

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56
Q

Why is there a theoretical risk of pro-thrombotic state with warfarin initiation?

A

___

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57
Q

What level of Factor is present in ‘severe’ haemophilia?

A

<1%

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58
Q

Which type of haemophilia more commonly develop inhibitors?

A

Haemophilia A

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59
Q

What is the mechanism of tranexamic acid?

A

Forms a reversible complex that displaces plasminogen from fibrin -> inhibition of fibrinolysis

Also inhibits the proteolytic activity of plasmin

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60
Q

What is vWF’s role related to Factor VIII?

A

Acts as “chaperone” which binds Factor VIII to prevent its premature degradation

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61
Q

Which blood group has lower levels of vWF?

A

Group O blood group has lower vWF

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62
Q

What is the 1st line therapy for mild vWD?

A

DDAVP - releases vWF and FActor 8 from storage sites

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63
Q

What is the defect in Bernard-Soulier Disease?

What is it phenotypically similar to?

A

Glycoprotein 1b-IX-V

vWD

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64
Q

What is the defect in Glanzmann thrombasthenia?

What is the phenotype?

A

Glycoprotein 2b/3a complex

Severe bleeding diathesis

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65
Q

Which therapy raises platelets fastest (other than platelets) in ITP?

A

IVIG (faster than steroids)

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66
Q

What is the indication (in Australia) for TPO-mimetics in ITP?

A

For failed splenectomy or splenectomy contraindicated

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67
Q

What is the main treatment for TTP?

A

Plasma exchange

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68
Q

What is the main treatment for atypical HUS?

A

Eculizumab - C5 inhibitor

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69
Q

What is the pathogenesis of HITS?

A

Results from an auto-antibody against Platelet Factor 4 (PF4) in complex with heparin

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70
Q

What are the 4 Ts in the score for HITS?

A

Thrombocytopaenia severity
Thrombosis
Timing of onset after exposure
Other cause for thrombocytopaenia

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71
Q

Alternatives to heparin in HITS?

A

Direct thrombin inhibitors - bivalirudin, argatroban
Danaparoid
Fondaparinux

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72
Q

Which blood groups can AB people receive PRBC from?

A

ALL

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73
Q

Which ABO antibodies are in serum of O group?

A

Anti-A and Anti-B

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74
Q

Which ABO antibodies are in serum of AB group?

A

None

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75
Q

What are the VTE-prevention recommendations for a pregnant woman with no personal history of VTE, but a FHx and a Factor V Leiden mutation?

A

Observation antepartum

Only consider postpartum prophylaxis if other risk factors

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76
Q

What are the VTE-prevention recommendations for a pregnant woman with no personal Hx VTE who has antithrombin deficiency?

A

Therapeutic LMWH antepartum + 6/52 postpartum

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77
Q

What are the VTE-prevention recommendations for a pregnant woman with no personal Hx VTE who has a Protein C or S deficiency?

A

Prophylactic LMWH antepartum + 6/52 postpartum

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78
Q

What are the VTE-prevention recommendations for a pregnant woman with single prior provoked VTE (not during pregnancy)?

A

Observation antepartum, and prophylactic LMWH 6/52 postpartum

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79
Q

What are the VTE-prevention recommendations for a pregnant woman with single prior pregnancy-provoked VTE?

A

Prophylactic LMWH antepartum + 6/52 postpartum

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80
Q

What are the VTE-prevention recommendations for a pregnant woman with recurrent unprovoked VTE?

A

Therapeutic anticoagulation throughout

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81
Q

What is Andaxenet Alfa?

A

Recombinant FXa molecule

Works as FXa antidote by being a decoy for the drug to bind to

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82
Q

Where does Factor VII work in the coagulation cascade?

A

Initiation of clotting

Binds to Tissue Factor, which activates Factor X

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83
Q

What is the role of platelets in coagulation?

A

Platelets provide binding sites for coagulation factors and a phospholipid surface that promotes assembly of multicomponent complexes (i.e. X-ase, Prothrombinase)

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84
Q

What is contained in the prothrombinase complex?

A

Factor Xa + Factor Va

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85
Q

What is contained in the Extrinsic X-ase complex?

A

Factor VIIa + TF

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86
Q

What is contained in the Intrinsic X-ase complex?

A

Factor VIIIa + Factor IXa

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87
Q

What is the other name for Factor II and IIa?

A

Prothrombin -> Thrombin

88
Q

What is the other name for Factor I?

A

Fibrinogen

89
Q

What is the substance exposed at site of wound endothelium which initiates haemostasis?

A

Tissue factor

90
Q

What is Protein C’s role in coagulation?

A

Activated protein C binds to its co-factor protein S, which then inhibits factors Va and VIIIa -> slows the coagulation process

91
Q

How is Protein C activated?

A

Thrombomodulin binds to thrombin, changing its identity from procoagulant to anticoagulant. Thrombin then cleaves Protein C to activate it.

92
Q

What is the effect of Factor V Leiden mutation on coagulation?

A

Factor V Leiden is not as susceptible to cleavage by activated protein C and is therefore inactivated more slowly, resulting in a hypercoagulable state

93
Q

What does Reptilase Time measure?

A

Like TCT but uses reptilase instead of thrombin
Used in prolonged APTT that doesn’t correct.
Unaffected by heparin, thus if NORMAL -> prolonged APTT likely due to heparin

94
Q

What are the labelled uses of NovoSeven?

A

Factor 8 or 9 deficiency or inhibitor

95
Q

When should treatment for ITP be initiated?

A

PLts <30 or bleeding sx

96
Q

What is the classic pentad of TTP?

A 
Fever
MAHA
Thrombocytopaenia
Renal involvement
Neuro sx
97
Q

What is the role of ADAMTS13 in TTP?

A

ADAMTS13 cleaves vWF multimers. Severe deficiency of ADAMTS13 activity in TTP which results in large vWF multimers which cause endothelial injury

98
Q

What is the management of INR >10 with no bleeding?

A

Withhold warfarin

Give Vitamin K

99
Q

What is the management of INR 9 with no bleeding?

A

Withhold warfarin

100
Q

What does leukodepletion of PRBC help to avoid?

A

Febrile non-haemolytic reactions

101
Q

What does irradiation of blood products help to avoid?

A

Transfusion-associated GVHD

102
Q

What key substances does cryoprecipitate contain?

A

Fibrinogen
Factor 8
Factor 13
vWF

103
Q

What is the key treatment for low fibrinogen?

A

Cryoprecipitate

104
Q

What is the main use of Prothrombinex?

What does it contain?

A

Warfarin reversal

Factors 2, 7, 9, 10 (TV channels)

105
Q

What is the most common point of error resulting in ABO incompatibility?

A

Incorrect check at bedside of patient

106
Q

What is the cause of febrile non-haemolytic transfusion reaction?

A

Antibodies against donor leukocytes

107
Q

What is the most common blood product to cause sepsis?

A

Platelets (1/75,000)

108
Q

What is the presumed aetiology of TRALI?

A

Donor antibodies to recipient leukocytes, which are then primed and sequestered in the lungs.
Neutrophils are activated and release ++ cytokines, leading to capillary leakage

109
Q

What is the standard ratio of PRBC : FFP : Platelets in massive transfusion?

A

4 PRBC : 2 FFP : 1 platelets

110
Q

Where is iron absorbed from principally in the gut?

111
Q

Where is the largest pool of iron storage within body?

A

Red blood cells

112
Q

Where is hepcidin produced?

What is its role?

A

Liver.

Downregulates Ferroportin at BASOLATERAL membrane of enterocyte. Thus decreases uptake of iron by transferrin, reduced systemic absorption. In this setting, iron is trapped in enterocyte, and will be lost in enterocyte slouging

113
Q

What happens to iron at enterocyte brush border?

A

Reduced from Fe 3+ to Fe 2+, taken in by DMT1

114
Q

What is the effect of inflammation on hepcidin?

A

It is elevated. Acute phase reactant

Leads to functional iron deficiency

115
Q

What is the common iron state in polycythaemia vera?

A

Iron deficiency. DO NOT replace iron

116
Q

Is ferritin more specific or sensitive?

A

Specific, not sensitive

117
Q

Which element of iron studies will be most deranged in haemachromatosis?

A

Transferrin saturation -> will be very high

118
Q

What effect does liver disease have on transferrin?

A

Low -> liver produces transferrin

May lead to high TSat

119
Q

What is the favoured form of PO iron replacement?

How long will it generally take to replenish iron stores?

A

Ferrous sulphate

~6 months

120
Q

Which out of iron deficiency or thalassaemia will result in lower MCV compared to Hb level?

A

Thalassaemia lowers MCV out of proportion to Hb

121
Q

What is the key test to differentiate between iron deficiency and anaemia of chronic disease?

A

Soluble transferring receptor saturation

  • in IDA -> transferring receptors become upregulated due to cells being “hungry for iron”.
  • in ACD this level will be normal
122
Q

What is the key test finding in pure red cell aplasia?

A

Reticulocytes -> will be low

123
Q

3 causes of normocytic anaemia?

A

Acute blood loss
Anaemia of chronic disease
Pure red cell aplasia

124
Q

What is the role of Transcobalamin II ?

A

Binds functional B12 in ??__intestinal cell, transfers it to tissues and bone marrow

125
Q

What environment is required to liberate B12 from food?

A

Acidic environment

Affected by PPI

126
Q

What is role of IF in B12 metabolism?

A

Acts as chaperone for B12 to intestinal cell

127
Q

What is most specific test for pernicious anaemia?

A

Intrinsic factor Ab

128
Q

What is the best test to identify B12 deficiency?

A

Holo-transcobalamin II -> active form

129
Q

What is the best test to identify folate deficiency?

A

Red cell folate

130
Q

What are the elements of a haemolysis screen?

A 
Blood film (polychromasia, red cell morphology)
LDH
Haptoglobin (low)
LDH
Bilirubin
131
Q

What is role of haptoglobin?

Where is it produced?

A

Binds to free Hb in haemolysis

Made in liver, low in chronic liver disease

132
Q

What is the classic lab finding which distinguishes INTRAvascular haemolysis from EXTRAvascular?

A

Urinary haemosiderin will be positive in intravascular

133
Q

3 causes of INTRAvascular haemolysis?

A

Red cell fragmentation (MAHA, mechanical)
PNH
Paroxysmal cold haemoglobinuria

134
Q

What is the acquired genetic mutation in Paroxysmal nocturnal haemoglobinuria?

A

Mutation in PIG-A gene.

This is essential for complement activation

135
Q

What is a common vascular complication of PNH?

A

Highly thrombogenic condition

Large vessel thrombosis e.g. portal vein

136
Q

What does a lack of cell surface proteins CD55 and CD59 indicate?

137
Q

What is the gold standard diagnostic test for PNH?

A

Flow cytometry, looking for CD55 / CD59 cell surface markers

138
Q

What is the key medication for management of PNH?

A

Eculizumab - anti-C5 mab

139
Q

Classic finding on blood film of Warm AIHA?

A

Spherocytes (smaller without central pallor)

140
Q

What type of ab usually found in warm AIHA?

141
Q

What type of ab usually found in cold agglutinins?

142
Q

3 classic associations with Warm AIHA?

A

CLL
SLE + other autoimmune conditions
Drugs

143
Q

What is Evan’s Syndrome?

A

TTP + warm AIHA, associated with CLL

144
Q

Key management principles of warm AIHA?

A

Prednisolone + immunosuppression

Folate

145
Q

What does ‘thermal amplitude’ of cold agglutinins refer to?

A

The temperature threshold at which haemolysis occurs

146
Q

3 classic associations with cold AIHA?

A

Low grade lymphoma
Mycoplasma
EBV

147
Q

DAT finding in cold AIHA?

A

C3d. There will be no IgG (is usually IgM)

148
Q

What is the DAT finding in PNH?

A

Negative (complement mediated)

149
Q

What is the most common of the inherited RBC membrane defects?

Mode of inheritance?

A

Hereditary spherocytosis

Autosomal dominant

150
Q

What is gold standard diagnosis for Hereditary spherocytosis?

What is the finding of DAT?

A

Flow cytometry

Negative DAT

151
Q

Thorny apple cells on blood film?

A

Pyruvate kinase deficiency

152
Q

What is role of G6PD in

What is mode of inheritance of deficiency?

A

Involved in glutathione ?recycling

X-linked

153
Q

Classic finding on blood film in haemolytic crisis of G6PD deficiency?

A

Bite / blister cells

154
Q

What is HbA made up of?

A

Chains -> Alpha 2, Beta 2

155
Q

What is HbA2 made up of?

A

Chains -> Alpha 2, delta 2

156
Q

Which Hb lines are affected in beta thal?

A

HbA (only one with beta chains)

157
Q

Which Hb lines are affected in alpha thal?

A

HbA, HbA2, HbF

158
Q

What is phenotype of alpha thal trait?

A

Mildly low Hb
Low MCV
Normal iron studies

159
Q

How is alpha thal trait diagnosed?

A

Genetic studies

Will not be picked up on Hb electrophoresis

160
Q

HbH disease phenotype?

A

Significant anaemia
Chronic haemolysis with mild splenomegaly
Iron overload
May or may not be transfusion-dependant

161
Q

Hb Barts / Hydrops foetalis phenotype?

A

Fatal in utero

Increased maternal morbidity / mortality

162
Q

Beta thal findings on Hb electrophoresis?

A

Increased HbA2, and HbF

163
Q

What time of life does Beta Thal major manifest?

A

3-6 months of life, when body is switching from foetal Hb to adult forms

164
Q

Main cause of death in Beta thal major?

A

Cardiac failure, due to iron overload

165
Q

Genetic change leading to HbS (sickle cell)?

A

Point mutation in beta globin gene

166
Q

Most cause of death in sickle cell disease after puberty?

A

Acute chest syndrome

167
Q

What is a key benefit of hydroxyurea in sickle cell?

A

Increased HbF production, which directly inhibits sickling

168
Q

What is Crizanlizumab?

What is its potential role?

A

P-selectin mAb

Prevents pain crises in sickle cell disease

169
Q

What is significance of Flt3 mutation in AML?

What is the new therapeutic option for this?

A

Actiavtes TK activity, driving proliferation
Negative prognostic marker

Midostaurin -> targets Flt3 mutation

170
Q

What are 3 “good risk” cytogenetics in AML?

A

t(15, 17) - APML
t(8,21)
inv(16)

171
Q

Key management of APML?

Complication of this?

A

ATRA (all trans retinoic acid)
Helps promyelocytes to differentiate

ATRA syndrome - hyperleukocytosis, ARDS.
Mx - steroids, ventilatory support, may need to interrupt therapy

172
Q

What is significance of 5q deletion mutation in MDS?

What is key therapeutic used?

A

More favourable prognosis

Lenolidamide

173
Q

CML classic genetics?

A

Philadelphia chromosome -> t(9:22), BCR-ABL

174
Q

Key management of CML?

A

TKIs

1st gen - Imatinib
2nd gen - dasatinib, nilotinib

175
Q

Classic SEs of TKIs for CML?

A

Oedema, pleural effusions, GI SEs

176
Q

High WCC with basophilia/eosinophilia -> DDx?

177
Q

Choice of cytoreductive agent in pregnancy?

A

Interferon

178
Q

EPO level in PCV?

Differentiating feature from reactive polycythaemia?

A

Low EPO

Can also have thrombocytosis / leukocytosis

179
Q

Leukoerythroblastic blood film

180
Q

3 classic mutations in MPNs?

A

JAK2
CALR
MPL

181
Q

Implications of CALR mutation in essential thrombocythaemia

A

Better prognosis

Lower thrombosis risk

182
Q

Causes of polycythaemia with high EPO?

A

Cardio / lung disease
Testosterone use
High altitude

183
Q

What are high risk features of essential thrombocythaemia? (3)

A

Age >60
Plts >1000
Hx thrombosis

184
Q

What is the key treatment in high-risk MDS to decrease progression to AML?

A

Azacitidine - hypomethylating agent

185
Q

What would be a classic cause of bleeding tendency in essential thrombocythaemia?

A

Acquired vWD

186
Q

Classic flow cytometry finding in T cell lymphoma?

A

CD30 positive

187
Q

Match genetics with lymphoma

t(14;18):
t(8;14):
t(11;14):

Burkitt’s lymphoma
Mantle cell lymphoma
Follicular lymphoma

A

t(14, 18) -> follicular
t(8,14) -> Burkitt’s
t(11,14) -> mantle cell

188
Q

Name 3 high grade NHLs

A

DLBCL
Burkitts
Mantle cell lymphoma

189
Q

Name 3 low grade NHLs

A

Follicular
SLL/CLL
Marginal zone

190
Q

Match lymphomas to virus associations

Burkitts, Hodgkins, PTLD
T cell lymphoma / leukaemia
Primary effusion lymphoma
Splenic marginal zone lymphoma

EBV
HTLV-1
HCV
HHV-8

A

EBV - Burkitts, Hodgkins, PTLD

HTLV-1 - T cell lymphoma / leukaemia

HHV 8 - primary effusion lympoho

HCV - splenic marginal zone lymphoma

191
Q

Why is Rituximab not used in multiple myeloma?

A

Anti-CD20 -> b cell marker

Not expressed on plasma cells

192
Q

Usual chemo regime for DLBCL?

193
Q

What are Reed-Sternberg cells found in?

What are the cell surface markers typically expressed?

A

Hodgkin’s lymphoma

CD 15 / CD30

194
Q

What is usual chemo regime for Hodgkin’s ?

A

ABVD = doxorubicin, bleomycin, vinblastine, dacarbazine

195
Q

What is Brentuximab vedotin?

Role ?

A

Anti-CD30 ab

New option for relapsed Hodgkin’s

196
Q

What is the most common adult leukaemia?

197
Q

What are classic cell markers expressed in CLL?

198
Q

What is Richter’s transformation?

A

A low grade lymphoma transforming to high grade

199
Q

Indications for treating CLL?

A

Lymphocyte doubling time (NOT absolute count)
Symptomatic
Stage 3-4 disease

200
Q

What is prognostic implication of IVgH unmutated status in CLL?

A

Poor prognosis

201
Q

What is prognostic implication of Deletion 17p or tp53 mutation in CLL or multiple myeloma?

A

Poor prognosis

202
Q

What is obinutuzumab?

A

CD20 mAb, new version of rituximab with higher binding affinity

Used in CLL with del(17p) or tp53 mutant

203
Q

What is venetoclax?

A

BH3 mimetic -> inhibits function of BCL2 (which is anti-apoptotic)
Thus restores apoptosis

Associated with TLS

204
Q

What is treatment of choice in del(17p) or tp53 mutation CLL?

A

Ibrutinib OR Venetoclax + Obinutuzumab

205
Q

What parameters define a shift from MGUS to smouldering myeloma?

A

> 30g / L

Plasma cells in BM >10%

206
Q

What is the main benefit of lenalidomide compared to thalidomide re: SEs?

A

Less peripheral neuropathy

207
Q

Which agents increase risk of VTE in MM?

A

Thalidomide, lenalidomide (particularly in combo with dex)

208
Q

2 main purposes of conditioning for SCT?

A
  1. To provide adequate immunosuppression to prevent rejection of the transplanted graft
  2. To eradicate the disease for which the transplant is being performed
209
Q

Engraftment usually occurs when?

210
Q

Main indications for autologous hSCT?

A

MM

NH / Hodgkin’s Lymphoma

211
Q

Main cause of death following autologous hSCT?

A

Disease relapse

212
Q

Main indications for allogeneic hSCT?

213
Q

Most important factor determining GVHD post hSCT?

A

HLA matching

214
Q

What time frame defines ‘chronic’ GVHD?

A

Beyond day 100 post SCT

215
Q

DDx for new cytopaenias post SCT? (3)

A

Relapse
Drugs
Viruses (CMV, adenovirus)

FRACP NOSH 2020 (18 decks)

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