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Haematological malignancies Flashcards

1
Q

characteristics of acute haematological malignancies?

A

rapidly progressive, fatal within days-wks if not treated

immature (blast) cells predominate

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2
Q

how is distinction between myeloid or lymphoid classification of malignancy made?

A

analysis of proteins on cell surface (surface antigens)-immunophenotyping- can be done via flow cytometry.

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3
Q

population mainly affected by acute lymphoblastic leukaemia (ALL)?

A

children

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4
Q

population mainly affected by chronic lymphocytic leukaemia (CLL)?

A

elderly

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5
Q

RFs for leukaemia?

A

radiation
chemical and drugs e.g. benzene in industry, alkylating agents-AML, e.g. cytotoxic chemotherapy with cyclophosphamide, and topoisomerase II inhibitors
genetic e.g. Fanconi syndrome, ataxia telangiectasia, increased risk with trisomy 21. genes e.g. RUNX1 and CEBPA associations.
viruses e.g. human T cell lymphotropic retrovirus type 1 (HTLV-1)

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6
Q

which chromosomal abnormality is assoc. with 97% of chronic myeloid leukaemia cases?

A

philadelphia chromosome-an abnormal chromosome 22, reciprocal translocation between part of long arm of 22 and 9. so t (9;22) karyotype.
also found in ALL
results in formation of a fusion gene-translation produces fusion protein with TK activity and enhanced phosphorylating activity, causing altered cell growth, stromal attachment and reduced apoptosis.

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7
Q

commonest malignancy in childhood?

A

acute lymphoblastic leukaemia

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8
Q

symptoms suggestive of marrow failure in acute leukaemia?

A

breathlessness
fatigue
angina
claudication-anaemia
infections-neutropenia, common infections in ALL- CMV, zoster, meningitis, candidiasis, pneumocystis pneumonia.
bleeding and bruising-thrombocytopenia-petechiae, gum bleeding, fundal haemorrhage

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9
Q

symptoms suggestive of high WBC in acute leukaemia?

A

breathlessness
headache
confusion
visual problems

all result of leuostasis

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10
Q

symptoms suggestive of tissue infiltration in acute leukaemia?

A

bone pain

headache, cranial nerve palsies, meningism

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11
Q

symptoms suggestive of substance release from tumour cells in acute leukaemia?

A

bleeding and bruising-DIC

acute gout-hyperuricaemia

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12
Q

confirmation of acute leuakemia with blood count?

A

Hb low-anaemia
WBC usually raised
PLT low

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13
Q

confirmation of acute leukaemia with blood film?

A

blast cells

may be morphological identification of lineage e.g. Auer rods in blast cells in AML.

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14
Q

investigations for acute leukaemia diagnosis?

A

blood count
coagulation profile- to exclude DIC- low PLT (although can be raised in malignancy-chronic DIC), raised PT, APTT, reduced fibrinogen, increased fibrin degradation products e.g. D-dimers.
blood film
BM aspirate- increased cellularity, reduced erythropoieis and megakaryocytes (PLT precursor), replacement by blast cells, lineage confirmed with immunophenotyping.
CXR-mediastinal widening in T lymphoblastic leukaemia
CSF exam.-risk of CNS involvement in ALL HIGH.

therapy planning: US and Es, LFTs, serum urate
cardiac function-ECG and direct LV function tests e.g. echo.

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15
Q

principles of specific acute leukaemia tment?

A

induction chemotherapy

consolidation

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16
Q

additional tment to that used in AML for ALL?

A

need for CNS directed therapy- intrathecal chemotherapy
after intensive induction and consolidation, need 2 yr maintenance therapy to reduce risk of recurrence- MTX and mercaptopurine.

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17
Q

how can WCC be lowered in acute leukaemia to reduce leukostasis adverse consequences e.g. WBC thrombi in brain, heart and lungs?

A

hydroxycarbamide

leukopheresis

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18
Q

characteristic sign of Burkitt’s lymphoma?

A

jaw lymphadenopathy

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19
Q

characteristic cells with mirror-image nuclei found in Hodkin’s lymphoma?

A

Reed-Sternberg cells

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20
Q

staging of Hodkin’s lymphoma?

A 
Ann-Arbor staging:
1-LN
2-LNs on same side of diaphragm
3-LNs on both sides of diaphragm
4-extra-lymph nodal involvement
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21
Q

what can be given as supportive therapy to prevent tumour lysis syndrome in ALL?

A

allopurinol- inhibitor of xanthine oxidase

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22
Q

when is matched related allogeneic marrow transplantation considered in ALL patients?

A

once in 1st remission is best option in standard-risk younger adults

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23
Q

definition of haematological remission in ALL?

A

no evidence of leukaemia (raised WBC) in blood, a normal or recovering blood count and less than 5% blasts in a normal regenerating BM

24
Q

indicators of poor prognosis in ALL?

A 
male
adult
philadelphia chromosome:BCR-ABL gene fusion due to t(9;22)
CNS signs prese e.g. meningism
Hb reduced, or WCC >100 or B-cell ALL
25
how might rbc appear in DIC?
as schistocytes-fragmented rbc
26
Support Tment in ALL?
Blood/platelet transfusion Allopurinol to prevent tumour lysis syndrome IV fluids
27
Function of imatinib?
Tyrosine kinase inhibitor used in Philadelphia chromosome positive chronic myeloid leukaemia, and also in Ph positive ALL
28
Name given to transformation of CLL to an aggressive lymphoma?
Richter'is syndrome
29
2 peaks of incidence in Hodkin's lymphoma?
Young adults and elderly
30
RFs for Hodkin's lymphoma?
``` Male Young adult or elderly EBV SLE Post-transplantation Affected sibling Obese ```
31
What are B symptoms?
These indicate more extensive disease in hodkins lymphoma evaluation: Weight loss more than 10% in last 6 months Unexplained fever more than 38 degrees Or drenching night sweats
32
why might a patient with essential thrombocythaemia present with an ischaemic foot?
increased platelets leading to blockage of arterial supply to foot.
33
what cells are affected in polycythaemia vera?
all cells increased, although rbc are often only noted FBC: raised rbc, haematocrit and often raised PLT example of a type of myeloproliferative neoplasm which can sometimes lead to acute myeloid leukaemia. condition can cause myelofibrosis, resulting in significant splenomegaly. most people have a mutation in the JAK2 gene which controls proliferation of rbc.
34
how can CML be cured?
stem cell transplantation
35
most rapidly proliferating malignancy?
Burkitt's lymphoma
36
how does malaria predispose to Burkitt's lymphoma?
causes abnormal proliferation of B cells
37
why would you ausculatate the spleen?
bruit-splenic artery | splenic rub- occurs with infarct
38
what might a patient with Hodkin's lymphoma complain of if they drink alcohol?
pain in L side of upper abdomen-splenic pain due to splenomegaly
39
define a lymphoma?
a malignant proliferation of lymphocytes which accumulates in LNs, causing lymphadenopathy, and can also be found in peripheral blood or infiltrate organs.
40
likely diagnosis if a pink, opalescent lump is found?
lymphoma
41
cause of Non-Hodkin's lymphoma?
congenital immunodeficiency acquired immunodeficiency- HIV, drugs infection-EBV, H.pylori-GALT environmental toxins
42
signs and symptoms of Non-Hodkin's lymphoma (malignant proliferation of lymphocytes excluding presence of Reed-Sternberg cells)?
superficial lymphadenopathy extranodal disase: oropharynx e.g. sore throat, obstrcuted breathing due to involvment of Waldeyer's ring bone, CNS, gut, lung weight loss, fever, night sweats- less common than in Hodkins and indicate disseminated disease pancytopenia due to marrow involvement-anaemia, bleeding, infection.
43
how is diagnosis of non-hodkins lymphoma confirmed?
LN biopsy
44
what does raised LDH indicate in non-hodkin's lymphoma?
a worse prognosis as released with cell turnover
45
how are high grade non-hodkins lymphomas treated?
``` R CHOP regimen: chemotherapy= rituximab cyclophosphamide hydroxydanorubicin vincristine prednisolone ``` rituximab-kills CD20+ve cells by antibody directed cytotoxicity, and sensitises cells to CHOP.
46
how does prognosis differ between low and high grade non-hodgkin's lymphoma?
survival more for low grade, although low grade often incurable and widely disseminated at presentation, and disseminated disease at presentation indicates a worse prognosis.
47
causes of pancytopenia?
reduced BM production: aplastic anaemia (BM fails to develop), infiltration-(acute leukaemia, myelodysplasia, myeloma, lymphoma, solid tumours, TB), megaloblastic anemia, paroxysmal nocturnal haemoglobinuria, myelofibrosis, SLE. increases peripheral destruction: hypersplenism
48
characteristic appearance of rbc in myelofibrosis?
tear drop rbc
49
appearance on X-ray of myeloma?
lytic 'punched out' lesions e.g. pepper pot skull, vertebral collapse, fractures, osteoporosis.
50
symptoms of myeloma?
osteolytic bone lesions: backache, pathological fractures, vertebral collapse. hypercalcaemia- abdo pain, fatigue, dehydration, depression. signalling from myeloma cells increases osteoclast activation. marrow infiltration by plasma cells: anaemia, neutropenia, thrombocytopenia- infection and bleeding. renal impairment: light chain deposition in renal tubules e.g. distal LOH, changes induced in glomeruli by monoclonal Ig, light chains can be deposited as AL-amyloid causing nephrosis. recurrent bacterial infections as immunoparesis (reduction in 1 or 2 Igs), and due to neutropenia from disease and from chemotherapy tment.
51
how is myeloma screened for?
serum and urine electrophoresis
52
common causes of death in myeloma?
infection | renal failure
53
what test can be used to give an idea of prognosis in myeloma?
beta 2-microglobulin | if raised, assoc. with worse prognosis
54
myeloma diagnostic criteria?
monoclonal protein band in serum or urine electrophoresis increased plasma cells on BM biopsy evidence of end-organ damage from myeloma- hypercalcaemia, renal insufficiency, anemia.
55
complications of myeloma?
acute renal failure hyperviscocity- causes disturbed vision, reduced cognition and bleeding, treated with plasmapheresis to remove light chains. spinal cord compression-treat with dexamethasone and local radiotherapy hypercalcaemia-rehydrate

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