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Haematology, Dermatology and GP learning > Haematological malignancies > Flashcards

Haematological malignancies Flashcards

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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
Q

how might rbc appear in DIC?

A

as schistocytes-fragmented rbc

26
Q

Support Tment in ALL?

A

Blood/platelet transfusion
Allopurinol to prevent tumour lysis syndrome
IV fluids

27
Q

Function of imatinib?

A

Tyrosine kinase inhibitor used in Philadelphia chromosome positive chronic myeloid leukaemia, and also in Ph positive ALL

28
Q

Name given to transformation of CLL to an aggressive lymphoma?

A

Richter’is syndrome

29
Q

2 peaks of incidence in Hodkin’s lymphoma?

A

Young adults and elderly

30
Q

RFs for Hodkin’s lymphoma?

A 
Male
Young adult or elderly
EBV
SLE
Post-transplantation
Affected sibling 
Obese
31
Q

What are B symptoms?

A

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
Q

why might a patient with essential thrombocythaemia present with an ischaemic foot?

A

increased platelets leading to blockage of arterial supply to foot.

33
Q

what cells are affected in polycythaemia vera?

A

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
Q

how can CML be cured?

A

stem cell transplantation

35
Q

most rapidly proliferating malignancy?

A

Burkitt’s lymphoma

36
Q

how does malaria predispose to Burkitt’s lymphoma?

A

causes abnormal proliferation of B cells

37
Q

why would you ausculatate the spleen?

A

bruit-splenic artery

splenic rub- occurs with infarct

38
Q

what might a patient with Hodkin’s lymphoma complain of if they drink alcohol?

A

pain in L side of upper abdomen-splenic pain due to splenomegaly

39
Q

define a lymphoma?

A

a malignant proliferation of lymphocytes which accumulates in LNs, causing lymphadenopathy, and can also be found in peripheral blood or infiltrate organs.

40
Q

likely diagnosis if a pink, opalescent lump is found?

A

lymphoma

41
Q

cause of Non-Hodkin’s lymphoma?

A

congenital immunodeficiency
acquired immunodeficiency- HIV, drugs
infection-EBV, H.pylori-GALT
environmental toxins

42
Q

signs and symptoms of Non-Hodkin’s lymphoma (malignant proliferation of lymphocytes excluding presence of Reed-Sternberg cells)?

A

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
Q

how is diagnosis of non-hodkins lymphoma confirmed?

A

LN biopsy

44
Q

what does raised LDH indicate in non-hodkin’s lymphoma?

A

a worse prognosis as released with cell turnover

45
Q

how are high grade non-hodkins lymphomas treated?

A 
R CHOP regimen: chemotherapy=
rituximab
cyclophosphamide
hydroxydanorubicin
vincristine
prednisolone

rituximab-kills CD20+ve cells by antibody directed cytotoxicity, and sensitises cells to CHOP.

46
Q

how does prognosis differ between low and high grade non-hodgkin’s lymphoma?

A

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
Q

causes of pancytopenia?

A

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
Q

characteristic appearance of rbc in myelofibrosis?

A

tear drop rbc

49
Q

appearance on X-ray of myeloma?

A

lytic ‘punched out’ lesions e.g. pepper pot skull, vertebral collapse, fractures, osteoporosis.

50
Q

symptoms of myeloma?

A

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
Q

how is myeloma screened for?

A

serum and urine electrophoresis

52
Q

common causes of death in myeloma?

A

infection

renal failure

53
Q

what test can be used to give an idea of prognosis in myeloma?

A

beta 2-microglobulin

if raised, assoc. with worse prognosis

54
Q

myeloma diagnostic criteria?

A

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
Q

complications of myeloma?

A

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

Haematology, Dermatology and GP learning (7 decks)

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