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12- Haematolgy > Malignancy > Flashcards

Malignancy Flashcards

1
Q

what is the best way to identify mature non-lymphoid cells?

A

morphology

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2
Q

malignant haemopoiesis is characterised by what?

A

inc numbers of abnorml and dysfunctional cells

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3
Q

what malignancy is characterised by proliferation of abnormal proegnitors with block in differentiation/maturation?

A

acute luekaemia

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4
Q

what malignancy is characterised by proliferation of abnormal progentiors but NO block in differentiation/maturation?

A

chronic myeloproliferative disorders

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5
Q

what is meant by ‘clone’ with regards to driver mutations?

A

population of cells dervied from one ‘parent cell’- the daughter cells share genetic marker of parent (they can diversify but will always share genetic backbone)

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6
Q

normal haemopoeisis is poly/monoclonal?

A

normal- polyclonal

malignant- usually monoclonal

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7
Q

what are the two types of haematological malignancy?

A

lineage (myeloid or lymphoid)

anatomical site (blood/lymph)

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8
Q

blood involvement is which kind of malignancy?

A

blood involvment = leukaemia

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9
Q

lymph node involvemnt is which kind of malignancy?

A

lymphoma

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10
Q

which malignancy involved the marrow?

A

myeloma → plasma cell malignancy in marrow

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11
Q

which malignancy can involve blood and lymph nodes?

A

Chronic Lymphocytic Leukaemia (CLL)

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12
Q

if somone presents with lymph nodes what should you always check?

A

bloods

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13
Q

define acute leukaemia

A

excess of ‘blasts’ >20% in either the peripheral blood or bone marrow → decrease of normal haemopoetic reserve i.e. low platelts, low neutrophils

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14
Q

who is acute myeloid leukaemia most common in?

A

more common in elderly

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15
Q

how is AML investigated?

A

blood count

coag screen

bone marrow aspirate

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16
Q

auer rods are typically seen in which malignancy?

A

Acute Myeloid Leukaemia (AML)

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17
Q

how is AML treated?

A

intensive chemo for multiple cycles

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18
Q

during chemo for AML risk of infection increases. if neutropenic fever suspected what should be done?

A

cover with broad spectrum antibiotic particulary gram -ve

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19
Q

what acute leukaemia tends to occur mainly in children?

A

acute lymphoblastic leukaemia ALL

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20
Q

ALL is a disease of which cells?

A

disease of primitive lymphoid cells (lymphoblasts)

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21
Q

ALL has a tendancy to involve which body system?

A

CNS

(in males can get into testes)

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22
Q

why is bone pain common in ALL?

A

rapid marrow expansion causes pain

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23
Q

how is ALL treated?

A

chemotherapy followed by maintainence therapy

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24
Q

what are the problems of marrow suppression?

A

anaemia

neutropenia

thrombocytopenia

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25
Q

which gram stain is higher risk in neutropenic patients?

A

gram -ve higher risk (can cause life threatening spesis within hours)

26
Q

which responds better to treatment- low or high grade Non-hodgkins lymphoma?

A

high grade

(grows more rapidly but repsonds better to treatment than slow growing low grade tumours)

27
Q

how is a diagnosis of Non-Hodgkins Lymphoma confirmed?

A

biopsy

28
Q

what protein is found on Hodgkins lymphoma?

A

CD30

29
Q

what is the treatment for Hodgkins?

A

brentuximab vedotin

30
Q

who tends to get hodgkins and who gets NHL?

A

young- Hodgkins

older- Non-Hodgkins

31
Q

which is more common Hodgkins or Non-Hodgkins?

A

Non-Hodgkins

32
Q

what is the abnormal cell found in Hodgkins Lymphoma?

A

Reed-sternberg cells (abnormal type of B lymphocytes)

33
Q

which has a better prognosis, hodgkins or non-hodgkins?

A

Hodgkins- generally easier to treat

34
Q

what is a malignancy of plasma cells?

A

myeloma

35
Q

what are the direct tumour cell effects of myeloma on the body?

A

bone lesions

bone pain

inc in calcium

marrwo failure

36
Q

what are the paraprotein mediated effects of myeloma on the body?

A

renal failure

immune suppression

amyloid

37
Q

how is myeloma classified?

A

type of antibody produced

38
Q

what is the benign form of myeloma?

A

MGUS (premalignant)

(monoclonal gammopathy of unknown significance)

39
Q

which steps in the cell cycle are involved in differentiation and in proliferation?

A

differentiate- G0 and G1

proliferate- S, G2, M

40
Q

what the two types of treatments for tumours with regards to the cell cycle?

A

cell cycle specific (tumour specific)

non-cell cycle specific (non-tumour specific)

41
Q

duration of dose rather than dose more important in specific or non-specific treamtent?

A

specific

In non-secific cumalitive dose more importnant rather than duration

42
Q

tyrosine kinase inhibitors can be used in the treatment of which malignancy?

A

chronic myeloid leukamia

43
Q

give an example of a tyrosine kinase inhibitor

A

imatinib

44
Q

in what disease is philadelphia chromosome seen?

A

Chronic myeloid leukaemia

45
Q

what are the two subtypes of Chronic Myeloproliferative DIsorders?

A

BRC-ABL1 positive

BRC-ABL1 negative

46
Q

what is seen in CML?

A

proliferation if myeloid cells- granulocytes

47
Q

other than myeloproliferative disorders what else can cause a high Hb?

A

chronic hypoxia i.e. COPD/sleep apnoea is a common reason for eleavted Hb

48
Q

bloods can look identical in myeloproliferative disorders vs reactive but what differentiates the two?

A

eoisinophilia and basophilia in MPD

reactive will have an explanation i.e. empyema

49
Q

what can be used to treat CML?

A

tyrosine kinase inhibitors i.e. imatinib

50
Q

what are the three forms of BRC-ABL1 negative myeloproliferative disorders?

A

Polycythameia Rubra Vera

Idiopathic myelofibrosis

essential Thrombocytopenia

51
Q

what are the two forms of Polycythaemia Rubra Vera?

A

primary or secondary

52
Q

what are some signs of polycythaemia?

A

headache, fatigue

itchy- especially when in bath/shower

plethroic (redness)

53
Q

what mutation is seen in >95% of people with Polycythaemia?

A

JKA2 mutation

54
Q

what is the treamtent for polycythaemia rubra vera?

A

venesect to Hc<0.45

aspirin

cytotoxic oral chemo i.e. hydroxycarbamide

55
Q

what is essential thrombocytopenia?

A

uncontrolled production of abnormal platelets?

56
Q

what does essential thrombocytopenia result in?

A

thrombosis

at very high levels can cause bleeding >1500 (platelts can bind to VWF so circulatory levels decrease)

57
Q

why is platelet count following surgery less realible in diagnosing throbocytopenia?

A

inc in platelets following surgery is normal- way of dealign with massive haemostatic challenge

58
Q

the JAK 2 gene is found in 50% patients with essential thrombovytopenia. in those that dont what other gene mutation will be present?

A

CALR- calreticulin

MPL mutation also

59
Q

how is essential thrombocytopenia treated?

A

aspirin

cytoreductive therapy to control proliferation i.e. hydroxycarbamide

60
Q

tear drop shaped RBC’s can be seen in which mhyeloproliferatve disorder?

A

myelofibrosis

61
Q

in additon to tear drop RBC’s what else is seen on blood film in myelofibrosis?

A

leucoerythroblastic

(nucelated red cells and myelocytes)

62
Q

how is myelofibrosis treated?

A

supportive: blood transfusion, platelets

allogenic stem cell transplantation in select few

JAK2 inhibitors

12- Haematolgy (9 decks)

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