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FRACP Shuyu > RPA haem > Flashcards

RPA haem Flashcards

1
Q

AML vs CML on blood film

A

AML - large blasts, similar morphology CML - leukocytes in various stages of development; smaller sized

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2
Q

AML vs CML and bone marrow failure

A

AML is always assoc w BM failure where as CML is rarely assoc w BM failure Hence, AML presents w signs and symptoms of failures of the various lineages

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3
Q

Sweet’s syndrome

A

pruritic rash of the skin due to neutrophilic infiltration in skin could be caused by AML but also other immunological or iatrogenic causes

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4
Q

what type of AML is assoc w severe DIC

A

APML

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5
Q

4 tests at diagnosis for AML

A

morphology immunophenotype - good for distinguishing bw ALL and M chromosome analysis mutation analysis

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6
Q

proportion of AML w positive chromosome analysis

A

45%

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7
Q

AML vs ALL blood film

A

AML - fine granules/Auer rods - Auer rods are fine granules stuck together in a linear fashion - much cytoplasm ALL - no granules - slightly smaller blasts - scant cytoplasm

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8
Q

immunophenotyping characteristics of myeloid vs lymphoid

A

myeloid is generally higher number (aside from CD 13) myeloid CD 13, 33, 34, 117 lymphoid CD 3, 10, 19, blahblah

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9
Q

turnaround for FISH vs chromosome

A

6-8hr (FISH) vs a few days (chromosome)

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10
Q

AML w inferior prognosis

A

FLT3

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11
Q

APML blood film

A

promyelocytes very heavy granulation occasionally vaccuolated sometimes loaded with auer roads in bundles due to heavy granules

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12
Q

APML and DIC pathogenesis

A

85% of APML willdevelop DIC

APML membrane has a transmembrane glycoprotein that initiates coagulation causing DIC

release of tissue factor -> excessive release of thrombin plasminogen -> plasmin -> fibrinolysis -> clot formation can present w pancytopenia without blasts, with bruising +++

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13
Q

APML and DIC pathogenesis

A

85% of APML willdevelop DIC APML membrane has a transmembrane glycoprotein that initiates coagulation causing DIC release of tissue factor -> excessive release of thrombin plasminogen -> plasmin -> fibrinolysis -> clot formation can present w pancytopenia without blasts, with bruising +++

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14
Q

is d-dimer due to fibrin degredation or formation

A

formation as d-dimer is produced by plasmin lysis of cross-linked fibrin in thrombus

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15
Q

the most reliable index of DIC

A

D-dimer

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16
Q

APML cytogenetic abnormality

A

t(15,17)

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17
Q

how to detect APML cytogenetic abnormality

A

on FISH

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18
Q

what fusion gene is found in APML

A

PML/RAR alpha fusion protein

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19
Q

what does ATRA (all trans retinoic acid) target in APML

A

PML/RAR alpha fusion protein promotes differentiation

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20
Q

treatment of APML

A

ATRA + ATO (arsenic trioxide) +/- chemotherapy

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21
Q

ATRA syndrome

A

cell differentiation induced by ATRA leads to rising WCC and cytokine release –> leaky capillaries –> resp distress –> fluid overload Mx: steroids + chemotherapy

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22
Q

what chemotherapy agent is contained in all AML regimens

A

cytarabine (except APML where sometimes chemotherapy is not required)

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23
Q

what causes acute obstructive nephropathy in TLS

A

precipitation of UA, xanthine and phosphate in renal tubules

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24
Q

CML peripheral film

A

similar to a bone marrow can see full range of cell development stages

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25
Q

CML prognosis scoring

A

sokal score - spleen size, % blasts, age, platelet count

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26
Q

treatment targets of CML with TKI

A

0.1% leukaemic cells by 12 months

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27
Q

CML reasons for treatment failure

A

non compliance development of mutation T351I most common

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28
Q

secondary polycythemia

A

JAK2 negative EPO normal or high

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29
Q

Essential thrombocythemia and JAK2

A

only 60% of cases other genetic abnormalities CALR or MPL

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30
Q

what myelopropliferative disorder has the highest JAK2+ rate

A

polycythemia vera

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31
Q

non-JAK2 mutations in myeloproliferative disorders

A

CALR, JAK2

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32
Q

what allele is a risk factor for thrombosis in myeloproliferative diosorders

A

V617F mutated status and allele burdern

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33
Q

which myeloproliferative disorder always gets aspirin

A

PV ET is case by case

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34
Q

management of PV

A

low dose aspirin to all patients

venesect to Hct <0.45

anticoagulation if Hx of thrombosis

Hydrea if thormbosis/high risk

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35
Q

indications for cytotoxic therapy in MPN

A

extreme thrombosis risk rapid spleen enlargement

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36
Q

anagrelide

A

see slides

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37
Q

typical blood film for myelofibrosis

A

teardrop cells

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38
Q

Myelofibrosis treatment

A

allogenic transplant if debilitating symptoms and not suitable for alloSCT ruxolitinib (PBS for High risk and intermediate-2 risk myelofibrosis)

JAK2 inihibitors can lead to improved QoL but no improved survival shown yet

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39
Q

MDS prognosis

A

IPSS-R scoring: marrow blasts karyotype Hb Neutrophils Platelets

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40
Q

MDS management early/low risk

A

observation/supportive transfusions

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41
Q

MDS management intermediate/high risk

A

azacitidine - 30-50% response and overall survival benefit and decreased transformation to acute leukaemia alloSCT for <60 or 60-70 and fit

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42
Q

MOA of azacitidine

A

hypomethylating agent

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43
Q

MDS w 5q- abnormality treatment

A

lenalidomide

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44
Q

second gen TKIs for CML (2)

A

Dasatinib, Nilotinib

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45
Q

what are the AE of 2nd gen TKIs (cf 1st gen)

A

vascular issues so older people might use 1st gen

nilotinib - PAH, inhibition of plt function

dasatanib - diabetes, prolonged QTc, increased risk of vascular events

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46
Q

3rd gen TKI for CML

A

ponatinib effective for T315I mutations

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47
Q

CD20 and ALL

A

not in acute lymphoblastic leukaemia as more mature B cells

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48
Q

CD38 marker for?

A

plasma cells

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49
Q

CLL which cell lineage more common

A

B cell >95%

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50
Q

CDs in CLL

A

CD5, CD19, CD23

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51
Q

Mantle cell lymphoma vs CLL CD expression

A

both have CD5 + mantle has no CD23

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52
Q

smudge cells what malignancy

A

CLL (in vitro artefact)

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53
Q

Poor prognostic markers in CLL

A

beta 2 microglobulin LDH unmutated LgH (unreliable) FISH –> 17p deletion

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54
Q

when to do FISH in CLL

A

timepoint when patient is starting treatment (symptomatic patients)

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55
Q

indicaiton for treatment in CLL

A
  1. Evidence of progressive marrow failure as manifested by the development of, or worsening of, anemia and/or thrombocytopenia.*
  2. Massive (ie, ≥6 cm below the left costal margin) or progressive or symptomatic splenomegaly.
  3. Massive nodes (ie, ≥10 cm in longest diameter) or progressive or symptomatic lymphadenopathy.
  4. Progressive lymphocytosis with an increase of >50% over a 2-month period or LDT of <6 months. LDT can be obtained by linear regression extrapolation of absolute lymphocyte counts obtained at intervals of 2 weeks over an observation period of 2 to 3 months. Patients with initial blood lymphocyte counts of <30,000/microL, may require a longer observation period to determine the LDT. In addition, factors contributing to lymphocytosis or lymphadenopathy other than CLL (eg, infection) should be excluded.
  5. Autoimmune anemia and/or thrombocytopenia that is poorly responsive to corticosteroids.
  6. Symptomatic or functional extranodal involvement (eg, skin, kidney, lung, spine).
  7. Constitutional symptoms, defined as any one or more of the following disease-related symptoms or signs:
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56
Q

CLL treatment

A

Ritux, fludarabine, cyclophosphamide frail + elderly: Obinutuzumab anti-CD20 with enhanced ADCC + chlorambucil Oral enzyme inhibitors - ibrutinib - bruton’s tyrosine kinase inhibitor - venetoclax - bcl2 inhibitor - Idelalisib - PI3 kinase inhibitor

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57
Q

irbutinib

A

bruton’s tyrosine kinase inhibitor - blocks BCR signalling/activation. Induces apoptosis, blocks migration.adherence PBS listed for pts unsuitable for purine analogue - suitability based on age/fragility and also 17p del disease by FISH

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58
Q

venetoclax

A

mimics action for BH3 proteins restores the cell’s ability to undergo apoptotic death GRADUATED ORAL DOSING TO AVOID LIFE-THREATENING TUMOUR LYSIS

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59
Q

follicular lymphoma treatment - what grades determine treatment

A

grade 1-3 indolent lymphoma treatment 3b+ - treat as DLBCL

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60
Q

treatment options for follicular lymphoma

A

Ritux/obintuzumab + 1) CVP 2) benamustine 3) CHOP therapy at relapse chemo +rituximab add anthracyline if not used before obinutumab + bena CAR-T coming

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61
Q

obinutuzumab vs rituximab

A

obinu has enhanced ADCC but reduced complement activiation

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62
Q

Where does MALT most frequently occur?

A

primary gastric lymphoma

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63
Q

what preceeding infection is assoc w MALT

A

H. Pylori (eradication can be used as treatment)

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64
Q

mantle cell lymphoma cytogenetic markers

A

cyclin D t (11:14)

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65
Q

mantle lymphoma treatment

A

rituximab and chemotherapy cytarabine for the young R_bendamustine in >60 allog SCT relapsed disease can have ibrutinib

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66
Q

lymphoplasmacytic lymphoma (waldenstrom’s) genetic feature

A

aa change (L265P) in MYD88 –> ibruntinib minority has CXCR4 mutation - inferior prognosis

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67
Q

what antibody class does lymphoplasmacytic lymphoma produce

A

IgM –> hyperviscosity +++

68
Q

hairy cell leukaemia mutation

A

BRAF V600E which activates ME-ERK vemurafenib is not availbale in leukaemia however

69
Q

DLBCL pathology

A

large B cells w prominent nucleoi loss of follicular architecture ki-67 - proliferation marker (higher in DLBCL vs follicular)

70
Q

double hit DLBC

A

MYC and the gene for BCL2 on chromosomes 8 and 14 respectively

71
Q

R - CHOP

A

rituxcyclo vincristine doxorubicin pred

72
Q

which R-CHOP agent causes bad constipation

A

vincristine

73
Q

what EF is required to receive full dose anthracycline

A

EF>50%

74
Q

when does cardiotoxicity occur in anthracycline

A

6 months post

75
Q

what CD does peripheral T cell lymphoma express

A

not TdT or CD1 CD3+ because they are derived from post-thymic T cells (cf lymphoblastic lymphoma)

CD30+

76
Q

treatment for CD30+ Anaplastic large cell

A

bremtuximab anti CD 30 conjugated to tubulin toxim mono methyl auristatin E (MMAE) - causing cell arrest duration of response 13 months

77
Q

SE bremtuximab

A

peripheral neuropathy

78
Q

Burkitt’s lymphoma virus association

A

EBV HIV

79
Q

genetic BUrkitt’s lymphoma

A

myc oncogene (chrom 8) translocation to Ig promotors 8:14 (or 2:8 or 8:22)

80
Q

burkitt’s film

A

deep blue cytoplasma w vacuoles

81
Q

B-ALL relapsed refractory disease

A

inotuzumab ozogamicin

82
Q

Hodgkin lymphoma antigens

A

CD15, CD 30

83
Q

Hodgkin chemotherapy treatment

A

ABVD escalated BEACOPP <45 - sterility, premature menopause, long term risk MDS/AML

84
Q

Hodgkin treatment

A

PET adapted algorithms early stage favourable -> ABVD -> iPET escalation or deescalation and IFRT early stage unfavourable -> ABVD or escBEACOPP–>iPET escalation or deescalation advanced stage8 –> ABVD or escBEACOPP (see slides)

85
Q

what mAB is approved for Hodgkin’s Lymphoma

A

bremtuximab (anti CD30) for refractory of note pembrolizumab is also used (see slides)

86
Q

myeloma film appearance

A

basophilic cytoplasm with eccentric nucleus prominent golgi zones adjacent to the nucleus

87
Q

most common Ab in myeloma

A

IgG 60%

88
Q

MM criteria

A

plasma cell proliferating disorder + myeloma defining event CRAB or >60% plasma in BM >100 FLC ratio >1 focal lesion on MRI or skeletal surgery

89
Q

poor genetic prognostic marker in MM

A

see slides

90
Q

myeloma supportive therapies

A

bisphosphantes transfusion IVIG valtrex prophylaxis

91
Q

thalidomide SE

A

tiredness, constipation, sens neuropathy, DVT

92
Q

bortezomib SE

A

peripheral neuropathy a new proteasome inhibitor has recently been approved - carfilzomib has been approved recently w less peripheral neuropathy

93
Q

daratumumab MOA and SE

A

anti-CD38 refractory MM probably should be used in combination

SE: transfusion reactions (as CD 38 is also expressed on RBC)

94
Q

bortezomib MOA

A

proteasome inhibitor which inhibits NK-kappaB

95
Q

flutarabine MOA

A

purine analogue

96
Q

endotheliual function in haemostasis

A

release prostacyclin and nitric oxide –> prevents aggregation of platelets release t-PA - lyse fibrin above factors provide balance the following factors deal with things released by the platelets/clots ADPas from endothelial cell mops up ADP Thrombomudulin binds thrombin Heparan sulfate will activate antithrombin

97
Q

what does VWF adhere to at high sheer rate in platelets

A

GP ib-V-IX - reversible binding this slows down the platelets

98
Q

what factor does VWF carry

A

factor VIII

99
Q

what does VWF irreversibly bind to

A

GP IIb/IIIa cause platelet shape change and activation –> aggregation of VWF, fibrinogen, red cells, leukocytes

100
Q

platelet dense tubular system

A

calcium fux that trigger activation and PG synthesis

101
Q

platelet alpha granula

A

coagulation factors and adhesion receptors

102
Q

platelet shape change

A

microtubule system “pseudopodia” happens in activation

103
Q

platelet adhesion receptors

A

all result in calcium influx that results in microvesicle relsease and negatively charged phosphatidylserine exposure collagen –> GP VI thrombin –> PARs vWF –> GP Ib-V-IX Fibrin –> GP IIb/IIIa

104
Q

initiation of coagulation

A

tissue factor exposed on cell membrane/microparticle circulating factor VII binds TF and activates factor Xa trace thrombin is generated excress thrombin is cleared by antithrombin

105
Q

amplification of coagulation

A

thrombin activates IX and XI, cleaves factor VIII from vWF and activates factor VIII and V factor VIII and IX together activates factor X X -> Xa Xa and Va works togehter and generally thrombin from prothombin this creates a large thrombin burst this is assembled on the negatively charged thrombin surface

106
Q

propagation of coagulation

A

big thrombin burst changes fibrinogen into fibrin activates factor XIII which crosslinks fibrin

107
Q

lysis in coagulation

A

plasmin is the main molecule in lysis breaks down polymer into fibrin degradation products (d-dimer is a particular fibrin degradation product - only produced in fully formed clot)

108
Q

natural anticoagulants

A

antithrombin III switches off thrombin and X, IV, XI, XII protein C (cofactor is protein S) - switches off activates VIII and V tissue factor pathway inhibitor will switch off the initial tissue factor complex to localise the process

109
Q

fibrinolytic pathway

A

tPA and uPA changes plasminogen to plasmin plasmin degrades fibrin plasminogen activator inhibitor stops tPA and uPA (PAI-1 and PAI-2) respectively

110
Q

TAFI

A

TAFI when activated to TAFIa, functions to suppress fibrinolysis by the removal of lysine residues from the fibrin clot that are exposed as fibrin [in the fibrin clot] is degraded by plasmin. In this way tissue plasminogen activator binding is restricted and further activation of plasminogen to plasmin, prevented [remember - plasminogen binds to the lysine residues on the fibrin clot] and so the fibrin clot at the site of vascular injury is protected from fibrinolysis thrombin activatable fibrinolysis inhibitor cleaves off C-terminal lysine residue form fibrin and prevents binding to plasminogen. plasmin and tPA tranxemic acid competitively inhibits the same site also preventing fibrinolysis

111
Q

functions of thrombin

A

see slides

112
Q

PT testing

A

triggered by thromboplastin extrinsic pathway: TF, factor VIIa common pathway: Xa, Va, II, Thrombin, fibrin

113
Q

APTT testing

A

triggered by contact activation intrinsic pathway VIIIa, IXa, XIa, XIIa common pathway: Xa, Va, II, Thrombin, fibrin

114
Q

thrombin time testsing

A

add small amount of exogenous thrombin to convert fibrinogen to fibrin good assay for heparin (antithrombin III), dabigatran (direct thrombin inhibitor)

115
Q

anti Xa assay

A

measuring activity of factor Xa using chromophore (optical density)

116
Q

reptilase time

A

clots fibrinogen by a mechanism different from that of thrombin except it doesn’t respond to anti-thombin III like TT so can differentiate b/w heparin

117
Q

time dependent inhibitor - most common

A

factor VIII inhibitor initial mixing may show inhibitor but later it doesn’t correct

118
Q

severity of haemophilia

A

coag factor concentration % severe <1 - spontaneous bleeding moderate 1-5 - severe bleeding after minor trauma mild 5-25 - severe bleeding after surgery and slight bleeding after minor trauma

119
Q

acquired TTP pathogenesis

A

severe deficiency <10% in the activity of ADAMTS-13 excess of ultra large vWF

120
Q

TTP symptoms

A

Fever Anaemia Thrombocytopenia Renal failure Neurological dysfunction

121
Q

TTP lab findings

A

D-DIMER NEGATIVE (due to no cross linked fibrin) no activation/depletion of clotting proteins - APTT/PT normal fibrinogen normal activation and depletion of platelets BLOOD FILM - microangiopathic haemolytic anaemia

122
Q

TTP TREATMENT

A

plasma exchange, FFP, immunosuppression ritux avoid platelets

123
Q

where does vWF gets released from

A

Wiebel-palade body

124
Q

child pugh score for NOAC contraindication

A

contraindicated in B and C

125
Q

what DOAC interacts w amiodarine and verapamil (potential p-gp inhibitors)

A

dabigatran

126
Q

vitamin dependent factors

A

II, VII, IX, X, protein C and protein S

127
Q

which cancers to avoid DOAC

A

GI/GU/Brain cancer

128
Q

which DOAC will proong both APTT and TT

A

dabigatran the anti xas CAN also prolong APTT but not TT

129
Q

what does DOAC do to LA testing

A

potential false positive with dabigatran and rivaroxaban potential false negative with apixaban

130
Q

why might bone marrow SCT be collected instead of peripheral SCT (e.g. for genetic disease or aplastic anaemia)

A

t cell poor and stem cell rich decreased GVHD risk

131
Q

what CD marker to look for when collecting peripheral SCT

A

CD 34 - early haematopoietic stem cells

132
Q

most common non malignant cause for alloSCT

A

aplastic anaemia other indications are haemoglobinopathies and immunodeficiencies

133
Q

most common indication for autologousSCT

A

myeloma

134
Q

what tumours can get autoSCT

A

germ cell tumours

135
Q

most common autoimmune condition for autoSCT

A

scleroderma

136
Q

most common indication for alloSCT

A

AML all high risk get alloSCT when in remission

137
Q

when does engraftment occur

A

day 15

138
Q

what chemotherapy does haplo-related HSCT patients receive after HSCT?

A

day 3 cyclophosphamide because they have a preferential take up by self T cells and donor T cells are spared

139
Q

HSCT conditioning duration

A

10 days

140
Q

highest risk of CMV reactivation in HSCT

A

donor +ve receipient -ve

141
Q

venous occlusive disease clinical features

A

hepatomegaly w weight gain, fevers, bilirubin rise resembles Budd-Chiari syndrome

142
Q

histological findings of skin GVHD

A

lymphocyte infiltration of the dermis and basal vacuole changes

143
Q

treatment of GVHD

A

steroids cyclosporin (aim 200-300 levels) Acute GVHD: - steroids + calcineurin inhibitor + ATG triple therapy - if refractory: retux, alemtuzumab, ATG - anti IL2 - extracorporal chemotherapy Chronic GVHD add on therapies: methotrexate, mycophenolate - note they both inhibit the BM; methotrexate can cause mucositis and mycophenolate liver toxicity rituximab extracorporeal photochemotherapy SEE SLIDES

144
Q

GVHD prevention

A

donor selection ATG in unrelated donors

145
Q

when do HSCT patients get viral infection

A

late - post engraftment

146
Q

what is cytokine release syndrome driven by

A

IL-6 and TNF alpha

147
Q

anti IL-6 used in CRS

A

tocilizumab

148
Q

isolated APTT elevated incidental finding - correcting on mixing study; no prior bleeding hx

A

factor XII deficiency

149
Q

what antiepileptic will interact w rivaroxaban

A

phenytoin combined CYP3A4 and P-glycoprotein inducer reduces level of rivaroxaban

150
Q

what happens with solubte transferrin receptor in iron def anaemia

A

goes up

151
Q

what is assoc w pure cell aplasia

A

parovirus thymoma recombinant EPO CLL autoimmunoe

152
Q

what does cryoprecipitate contain

A

VIII, fibinogen, vWF, factor X, fibronectin

153
Q

what chemo mandates the requirement of irrad PRBC

A

fludarabine - lymphocyte depleting to avoid transfusion related GVHD

154
Q

what blood product is most assc w TRALI

A

FFP

155
Q

first line for non bleeding ITP

A

plt >30 no treatment steroids IVIG 2nd line or severe romiplastim after splenectomy rituximab in relapsed ITP as 2nd line no platelet transfusions unless critical bleeding requiring surgery

156
Q

emergency management of TTP in rural setting without PLEX

A

FFP

157
Q

gestational thrombocytopenia

A

diagnosis of exclusion - Most common at delivery, but can occur at any time during pregnancy. - Mild thrombocytopenia. (In 99 percent of women, the platelet count is ≥100,000 /microL.) - No increased bleeding or bruising. - No associated abnormalities on complete blood count (CBC). - No fetal or neonatal thrombocytopenia.

158
Q

paraprotein and clonal bone marrow cells cut off for MGUS vs smouldering/MM

A

paraprotei >30g/L bone marrow plasma >10% need both for smouldering/MM

159
Q

what bone lesion qualifies someone for multiple myeloma

A

One or more osteolytic lesions ≥5 mm in size on skeletal radiography, MRI, CT, or PET/CT. In the absence of osteolytic lesions, the following are not sufficient markers of bone lesions: increased FDG uptake on PET, osteoporosis, or vertebral compression fracture.

160
Q

burkitt’s lymphoma TLS prevention

A

RASBURICASE

161
Q

blinatumumab

A

cd3 and cd19 brings together T cell and B cell used in B-ALL

162
Q

alemtuzumab

A

CD52 mostly used in MS autoimmune side effects +++

163
Q

Howell Jolly bodies

A

hyposplenonism

164
Q

high risk thrombophillias

A

antithormbo III highest risk FVL/PTG homozygote/compount

165
Q

MOA of tranexamic acid

A

tranexamic bind to plasminogen (the site where fibrin normally binds) and stops the conversion of plasminogen to plasmin

FRACP Shuyu (65 decks)

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