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haemotology > cancers of the blood > Flashcards

cancers of the blood Flashcards

1
Q

what is multiple myeloma?

A

malignant disorder of plasma cells - b cells

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2
Q

what occurs within MM?

A

excessive secretion of monoclonal AB

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3
Q

what is the path of MM and the monoclonal AB?

A

excessive AB secretion
1. development of monoclonal gammopathy of undetermined significance MGUS
2. progression to MM

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4
Q

what is MGUS?

A

where most cases of MM arise from?
1. inciting event: initial cytogenic event abnormality - abnormal plasma cells clone secreting AB
2. progression to MGUS to MM: more cytogenic changes including change to bone marrow - bone cell infiltration

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5
Q

what are the clinical features of MM?

A

C: calcium - high
R: renal impairment
A: anaemia
B: bone disease

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6
Q

at what point is hypercalcaemia a medical emergency?

A

greater than or higher to 2.9mmol/L

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7
Q

why is anaemia seen in MM?

A

EPO deficiency

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8
Q

how is bone disease seen on imaging?

A

lytic lesions

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9
Q

what are the red flag symptoms seen in MM?

A

weight loss
anorexia
generalised weakness and excessive fatigue

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10
Q

apart from CRAB, what other features are seen in MM?

A

paraesthesia, splenomegaly, hepatomegaly, lymphadenopathy, neuro conditions: hyperviscosity conditions, spinal cord compression

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11
Q

what is hyperviscoisty syndrome?

A

headache, blurred vision, SoB, mucosal bleeding

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12
Q

how do you screen for MM?

A

investigate for monoclonal AB- protein electrophoresis and immunofixation

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13
Q

what immunoglobulins are assessed for?

A

igM - electrophoresis
immunofixation - higher ratio of heavier chains

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14
Q

how do you manage bony pain in MM?

A

bisphosphonates

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15
Q

what is ALL classically associated with?

A

most common in paeds
down syndrome

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16
Q

what is CLL most associated with?

A

warm haemolytic anaemia, Richter’s transformation and smudge cells

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17
Q

what is ritcher transformation?

A

CLL can transform into into aggressive lymphoma

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18
Q

what is CML linked to?

A

three phases - long chronic phase
philadelphia chromosome

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19
Q

what is AML linked to?

A

transformation from myeloproliferative
auer rods

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20
Q

what is burkitts lymphoma?

A

high grade B cell neoplasm

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21
Q

what are the two major forms of burkitts lymphoma?

A

endemic - african - maxilla/ mandible
sporadic- ileo caecal - usually HIV pts

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22
Q

what is burkitts associated with?

A

c-myc gene translocation t(8:14)
EBV linked to african form

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23
Q

what would microscopy show in burkitts?

A

starry sky
lymphocyte sheet interspaced with macrophages containing dead apoptic tumour cells

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24
Q

how is burkitts managed?

A

chemo - which can cause tumour lysis syndrome

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25
Q

what would indicate tumour lysis syndrome?

A

high k+
high phosphate
low ca2+
acute renal failure
hyperuricaema

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26
Q

what can help prevent tumour lysis syndrome in chemo for burkitts?

A

rasburicase

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27
Q

what is hodgkins lymphoma?

A

malignant proliferation of lymphocytes

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28
Q

what is seen on microscopy for hodgkins?

A

reed-sternberg cells

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29
Q

what age is hodgkins lymphoma most common

A

20s and 60s

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30
Q

what are RF for hodgkins lymphoma?

A

EBV
HIV

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31
Q

how does hodgkins lymphoma present?

A

lymphadenopathy - cervical/ supraclavicular - then axilla then inguinal
painless, non tender
B symptoms
mediastinal mass - cough, weird CXR

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32
Q

what is seen with alcohol and hodgkins lymphoma?

A

alcohol induced pain

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33
Q

what are B symptoms ?

A

weight loss
fever
night sweats
pruritic

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34
Q

what investigations are done for hodgkins lymphoma and what is seen?

A

FBC - normocytic anaemia
hypersplenism
coombs +ve
eosinophilia
high LDH
lymph node biopsy - reed sternberg cells

35
Q

why is there eosinphillia in hodgkins?

A

more cytokines eg IL- 5

36
Q

which hodgkins prognosis is worse?

A

lymphocyte depleted
B symptoms - usually poor prognosis

37
Q

which hodgkins prognosis is best?

A

lymphocyte predominant

38
Q

what are the different chemo combos in hodgkins lymphoma?

A

ABVD: standard
BEACOPP: more toxic but more likely to go into remission

39
Q

what are the management options of hodgkin lymphoma?

A

chemo
radiotherapy
combined chemo then RT
haemotopoietic cell transplantation - relapsed/ refractory hodgkins

40
Q

what is differenced between non hodgkins and hodgkins?

A

hodgkins - reed sternberg
non- hodgkins - everything else

41
Q

what is non-hodgkins lymphoma?

A

malignant proliferation of lymphocytes in lymph nodes or other organs
can affect B/T cells

42
Q

what is the 6th most common cancer in the UK?

A

non-hodgkins

43
Q

who is affected more in non-hodgkins?

A

men more then females

44
Q

what are RF for non-hodgkins?

A

elderly
cauasians
EBV
FamHx
chemical exposure - pesticides, solvents
previous chemo/ RT
immunodeficiency - transplant, HIV, DM
autoimmune conditions - sjogrens, SLE, coeliac

45
Q

how does non-hodgkins present?

A

non tender painless lymphadenopathy - rubbery, asymmetrical
B symptoms
other systems - gastric - abdo pain, dsyphagia,
bone marrow - bone pain, pancytopenia
testicular masses
fever

46
Q

what investigations are needed within non-hodgkins?

A

excisional biopsy
CT TAP
ESR - prognostic indicator
HIV test
LDH
FBC - normocytic anaemia
PET CT

47
Q

what is LDH?

A

lactate dehydrogenase
cell turnover - prognostic indicator

48
Q

how is non-hodgkns managed?

A

specific to sub type
rituximab in combo
neutropenia - prophylactic ABx
flu/ pneumococcal vax

49
Q

whoch grades have best prognosis in non-hodgkins?

A

low grade - better prog
high grade - worse prog but better cure rate

50
Q

what are complications of non-hodgkins?

A

bone marrow infilitration
spinal cord compression
Superior vena cava obstruction
side effects of chemo
mets

51
Q

what is ALL?

A

acute lymphoid leukaemia
neoplastic malignant proliferation of lymphoblasts - immature lymphoblasts accumulate in bone marrow
usually B cell

52
Q

what are RF for ALL?

A

young age
B cell - peaks at 3yrs
T cells - peak at 15-20
down syndrome
radiation exposure

53
Q

what are signs of ALL?

A

abrupt onset
anaemia - fatigue, SoB, pallor
neutropenia - fever, sepsis, pneumonia
bone pain
hepatosplenomegaly
lymphadenopathy

54
Q

how is ALL diagnosed?

A

FBC/ blood film: more lymphoblasts
high WCC
BM film: lymphoblast dominance - starry sky, mitotic figures
immunophenopathy- +ve nuclear staining

55
Q

how is ALL distinguised from ALL on the investigations?

A

ALL - immunophenotyping is +ve
AML: -ve

56
Q

how is ALL managed?

A

aggressive chemo
- more successful in kids
if brain mets: intrathecal chemo/ RT
tyrosine inhib: imatinib, dasatinib

57
Q

what is the ALL/ AML ABCDEF ?

A

A - acute
B- blast prodinate
C: children
D: drastic course
E; elderly
F: fair few WBC and fever

58
Q

what is AML?

A

neoplastic monoclonal prolif of myeloblasts in BM - accumulate of myeloblast

59
Q

what are RF of AML?

A

adults - peaks at 60yrs
radiation/ chemo
down syndrome - <5yrs
myeloproliferative disorders

60
Q

what are complications of AML?

A

DIC

61
Q

what are signs of AML?

A

abrupt onset
anaemia
thrombocytopenia
neutropenia
leukaemia cutis
gum swelling

62
Q

what is leukaemia cutis ?

A

skin infiltration of aml

63
Q

how is AML diagnosed?

A

FBC/ blood film - high leucocytes, anaemia
BM smear: high myeblasts. auer rods

64
Q

how is aml managed?

A

chemo
promyelotic - all trans retonic acid treatment
BM transplant

65
Q

what is CLL?

A

chronic lymphoid leukaemia
neoplastic monoclonal proliferation og fucntionally abnormal B cells

66
Q

what can cause CLL?

A

chromosome abnormalities
mutations in tyrosine kinase pathways

67
Q

what are RF of CLL?

A

fam history
agent orange exposure

68
Q

what are symptoms of CLL?

A

late onset
anaemia
thrombocytopenia
neutropenia
neoplastic infilitration

69
Q

what are complications of CLL?

A

abnormal iG secretion - hypogammaglobulinemia, autoimmunity
ritcher syndrome - progress to aggressive lymphoma

70
Q

how is CLL diagnosed?

A

FBC/ blood film - lymphocytosis, smudge cells
immunophenotyping - CD5, CD20, CD23
lymph node biopsy - small round lymphocyte infilitration

71
Q

what are smudge cells ?

A

disruption of fragile membranes of abnormal lymphocytes

72
Q

how is CLL managed?

A

chemo/ RT
BM transplant
immunotherapy

73
Q

what is CML?

A

chronic myeloid leukaemia
monoclonal proliferation of mature granulocytes/ precurosrs

74
Q

what are granulocytes?

A

eosinophils
basophils
neutrophils

75
Q

what Chr is linked to CML?

A

philadeplphia
cheese - C
milk - M

76
Q

what are RF for CML?

A

adult - above 40
radiation exposure
benzene exposure

77
Q

what are the three phases of CML?

A

chronic
accelerated
blast crisis

78
Q

what occurs within chronic phase of CML?

A

mainly neutophil dominance
B symptoms

79
Q

what occurs within accelerated phase of CML?

A

more basophils
anaemia
hepatosplenomegaly
lymphadenopathy
recurrent infections
bleeding
petechiae
ecchymose

80
Q

what is ecchymose?

A

bruises

81
Q

what occurs within blast crisis of CML?

A

rapid progression - poor prog
more myeblasts
bone pain
fever
significant splenomegaly

82
Q

how is CML diagnosed?

A

more granulocytes
BMM biopsy: hypercellularity of myeloid

83
Q

how do you manage CML?

A

tyrosine kinase inhib: imatinib, dasatinib nilotinib
BM transplant

84
Q
A

haemotology (4 decks)

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