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Haem > haem oncology > Flashcards

haem oncology Flashcards

1
Q

types of myeloid cells

A

red cells
granulocytes/monocytes
platelets

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2
Q

types of lymphoid cells

A

B cells
T cells
natural killer cells
antigen presenting cells

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3
Q

which disease is defined by no bone marrow maturation

A

acute myeloid leukaemia

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4
Q

which disease is defined by dysfunctional bone marrow maturation

A

myelodysplasia

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5
Q

which disease is defined by overproduction of red cells

A

polycythaemia rubra vera

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6
Q

which disease is defined by overproduction of granulocytes

A

chronic myeloid leukaemia

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7
Q

which disease is defined by overproduction of platelets

A

essential thrombocytosis

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8
Q

which disease is defined by overproduction of megakaryocytes

A

primary myelofibrosis

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9
Q

link between myelodysplasia and acute myeloid leukaemia

A
  • myelodysplasia = dysfunctional bone marrow maturation
  • AML = NO bone marrow maturation
  • 25% of myelodysplasia progresses to AML
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10
Q

prognosis of ALL vs CLL

A 
ALL = rapidly progressive and survival only months without tx, however curable with chemo
CLL = slow progression and may never require tx, however not curable with chemo (managed not cured)
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11
Q

classification of lymphoid malignancies

A
  • high grade e.g. ALL

- low grade e.g. CLL

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12
Q

4 types of leukaemia and common ages affected

A
  • ALL = <5yo, >45yo
  • CLL = >55yo
  • CML = >65yo
  • AML = >75yo
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13
Q

general sx of leukaemia

A
  • fatigue
  • fever
  • failure to thrive in children
  • pallor (anaemia)
  • petechiae and abnormal bruising (thrombocytopaenia)
  • abnormal bleeding
  • lymphadenopathy
  • hepatosplenomegaly
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14
Q

differentials for petechiae

A
  • leukaemia
  • meningococcal septicaemia
  • vasculitis
  • HSP
  • ITP
  • non-accidental injury
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15
Q

ix in suspected leukaemia

A 
bloods:
- FBC
- LDH
- blood film
imaging:
- CXR
- CT, MRI, PET
special tests:
- bone marrow biopsy
- lymph node biopsy 
- LP
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16
Q

3 types of bone marrow investigation

A
  • bone marrow aspiration
  • bone marrow trephine (solid core sample, better assessment of cells)
  • bone marrow biopsy (iliac crest, under LA)
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17
Q

pathophysiology of ALL

A

acute proliferation of B lymphocytes

+ pancytopaenia (all other cell types are suppressed)

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18
Q

condition associated with ALL

A

downs syndrome

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19
Q

blood film finding in ALL

A

blast cells

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20
Q

genetics of ALL

A

associated with philadelphia chromosome (t(9:22) translocation)

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21
Q

pathophysiology of CLL

A

chronic proliferation of B lymphocytes

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22
Q

presentation of CLL

A

often asymptomatic

infections, anaemia, bleeding, weight loss

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23
Q

anaemia in CLL

A

warm autoimmune haemolytic anaemia

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24
Q

prognosis of CLL

A

can transform to high-grade lymphoma (Richter’s transformation)

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25
Q

blood film findings in CLL

A

smear or smudge cells

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26
Q

disease course in CML

A
  1. chronic phase -> can last ~5 years, often dx incidentally with raised WCC
  2. accelerated phase -> more symptomatic with anaemia, thrombocytopaenia and immunocompromise
  3. blast phase -> highest proportion of blast cells leading to severe sx and pancytopaenia (fatal)
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27
Q

genetics of CML

A

associated with philadelphia chromosome (t(9:22) translocation)

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28
Q

aetiology of AML

A

can be the result of a transformation from a myeloproliferative disorder such as PRV or myelofibrosis

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29
Q

blood film findings in AML

A

high proportion of blast cells

can have rods inside cytoplasm known as Auer rods

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30
Q

general mx in leukaemia

A
  • chemotherapy and steroids
  • radiotherapy
  • bone marrow transplant
  • surgery
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31
Q

complications of chemotherapy

A
  • failure
  • stunted growth and development in children
  • infections
  • neurotoxicity
  • infertility
  • secondary malignancy
  • cardiotoxicity
  • tumour lysis syndrome
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32
Q

what is tumour lysis syndrome

A
  • caused by release of uric acid from cells being destroyed by chemotherapy
  • uric acid forms crystals in interstitial tissue and tubules of kidneys causing AKI
  • can also release other chemicals such as potassium and phosphate
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33
Q

mx of tumour lysis syndrome

A

reduce uric acid levels with allopurinol or rasburicase

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34
Q

complication of tumour lysis syndrome

A
  • high uric acid levels
  • high phosphate levels (-> low calcium levels)
  • high potassium levels
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35
Q

definition of lymphoma

A

cancers affecting the lymphocytes in the lymphatic system

proliferation within lymph nodes leading to lymphadenopathy

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36
Q

epidemiology of Hodgkin’s lymphoma

A

~20% of all lymphomas

peaks at age 20 and age 75

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37
Q

risk factors for Hodgkin’s lymphoma

A
  • HIV
  • EBV
  • autoimmune conditions: RA, sarcoidosis
  • FHx
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38
Q

main presentation of Hodgkin’s lymphoma

A

lymphadenopathy (neck, axilla, groin) which is non-tender and rubbery
may get pain in lymph nodes when drinking alcohol
fever, weight loss, night sweats

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39
Q

general symptoms of lymphoma

A 
fatigue
itching
cough
SOB
abdo pain
recurrent infections
40
Q

ix in Hodgkin’s lymphoma

A 
bloods:
- LDH
imaging:
- CT, MRI, PET
special tests:
- lymph node biopsy
41
Q

findings on lymph node biopsy in Hodgkin’s lymphoma

A

Reed-Sternberg cells
-> abnormally large B cells with multiple nuclei with nucleoli inside them
appear like the face of an owl with large eyes

42
Q

what staging system is used for lymphoma

A

Ann Arbor

43
Q

Ann Arbor staging

A 
1 = confined to one region of lymph nodes
2 = >1 region but same side of diaphragm
3 = lymph nodes affected above and below diaphragm
4 = widespread involvement with non-lymphatic organs (lungs, liver)
44
Q

mx of Hodgkin’s lymphoma

A

chemotherapy + radiotherapy with aim to cure

45
Q

side effects of radiotherapy

A

risk of cancer
damage to tissues
hypothyroidism

46
Q

3 types of non-Hodgkin lymphoma and associations

A
  1. burkitt lymphoma (EBV, HIV, malaria)
  2. MALT lymphoma (H. pylori)
  3. diffuse large b cell lymphoma
47
Q

typical presentation of diffuse large b cell lymphoma

A

rapidly growing painless mass in >65yo

48
Q

risk factors for non-Hodgkin lymphoma

A
  • HIV
  • EBV
  • H. pylori
  • hepatitis B or C
  • exposure to pesticides (trichloroethylene)
  • FHx
49
Q

mx options in non-Hodgkin lymphoma

A
  • watchful waiting
  • chemotherapy
  • mab’s e.g. rituximab
  • radiotherapy
  • stem cell transplant
50
Q

definition of myeloma

A

cancer of plasma cells (antibody producing b cells)

51
Q

what is MGUS

A

monoclonal gammopathy of undetermined severity
excess of single type of antibody/ab components without other features of myeloma or cancer
often found incidentally, ?risk of progression to myeloma

52
Q

what is smouldering myeloma

A

progression of MGUS with higher levels of antibodies/ab components
pre-malignant, more likely to progress to myeloma

53
Q

most common antibody affected in multiple myeloma

A

IgG (~50% cases)

54
Q

urine findings in myeloma

A

Bence Jones protein
light chain component from monoclonal paraprotein (single type of antibody produced by all identical cancerous plasma cells)

55
Q

impact of myeloma on bone marrow

A

cancerous plasma cells invade bone marrow (bone marrow infiltration) leading to anaemia, neutropaenia and thrombocytopaenia

56
Q

what is myeloma bone disease

A

cytokines released from plasma cells leads to increased osteoclast activity and suppressed osteoblast activity
=> excess resorption of bone

57
Q

common sites of myeloma bone disease

A

skull
spine
long bones
ribs

58
Q

appearance of myeloma bone disease

A

patches of thin bone = osteolytic lesions

‘pepper pot’ or ‘rain drop’ skull

59
Q

complications of myeloma bone disease

A
  • pathological fractures

- excessive resorption of bone leads to hypercalcaemia

60
Q

what are plasmacytomas

A

individual tumours made from cancerous plasma cells as a result of myeloma

61
Q

what is myeloma renal disease

A

renal impairment in myeloma due to:

  • high antibody levels blocking flow through tubules
  • hypercalcaemia
  • dehydration
  • meds used to treat condition e.g. bisphosphonates
62
Q

main 4 features of myeloma and mnemonic

A

CRAB

  • calcium (elevated)
  • renal failure
  • anaemia (normocytic and normochromic)
  • bone lesions/pain
63
Q

risk factors for myeloma

A
  • older age
  • male
  • Black African ethnicity
  • FHx
  • obesity
64
Q

when to suspect myeloma

A

> 60yo with persistent bone pain (back pain++) or unexplained fracture

65
Q

initial bloods in suspected myeloma

A
  • FBC
  • calcium
  • ESR
  • PV
66
Q

ix in myeloma and mnemonic

A

BLIP

  • urine Bence jones protein
  • serum free Light chains
  • serum Immunoglobulins
  • serum Protein electrophoresis
67
Q

imaging in myeloma

A

assess for bone lesions - preference:

  1. whole body MRI
  2. whole body CT
  3. skeletal survey (XR)
68
Q

mx of myeloma

A
  • combination of chemotherapy with antineoplastic agent, thalidomide, dexamethasone
  • stem cell transplant
  • VTE prophylaxis while on chemo
69
Q

mx of myeloma bone disease

A
  • bisphosphonates
  • radiotherapy
  • orthopaedic surgery e.g. prophylactic IM rod or tx#
  • cement augmentation (injecting cement into vertebral# or lesions)
70
Q

complications of myeloma/tx

A
  • infection
  • pain
  • renal failure
  • anaemia
  • hypercalcaemia
  • peripheral neuropathy
  • spinal cord compression
  • hyperviscosity
71
Q

definition of myeloproliferative disorders

A

uncontrolled proliferation of a single type of stem cell

considered bone marrow cancers

72
Q

3 myeloproliferative disorders

A
  1. primary myelofibrosis
  2. polycythaemia rubra vera
  3. essential thrombocythaemia
73
Q

what is primary myelofibrosis

A

uncontrolled proliferation of haematopoietic stem cells

74
Q

what is polycythaemia rubra vera

A

uncontrolled proliferation of erythroid cell line

75
Q

what is essential thrombocythaemia

A

uncontrolled proliferation of megakaryocytic cell line

76
Q

prognosis of myeloproliferative disorders

A

have potential to progress to AML

77
Q

main gene association with myeloproliferative disorders

A

JAK2

78
Q

what is myelofibrosis

A

where uncontrolled proliferation (due to myeloproliferative disorders) leads to fibrosis of the bone marrow

79
Q

pathophysiology of myelofibrosis

A

proliferating cells release cytokines (important cytokine = fibroblast growth factor) which lead to fibrosis of the bone marrow. fibrosis affects production of blood cells leading to anaemia and leucopaenia

80
Q

what is extramedullary haematopoiesis and when does it occur

A

production of blood cells (haematopoiesis) occurring outside of the bone marrow (e.g. in liver and spleen) due to myelofibrosis (fibrosis of the bone marrow)
causes hepatosplenomegaly

81
Q

presentation of myeloproliferative disorders

A
  • may be asymptomatic
  • systemic sx: FLAWS
  • anaemia
  • splenomegaly
  • portal hypertension
  • low platelets (bleeding, petechiae)
  • thrombosis
  • red face (raised RBCs)
  • infections (low WCC)
82
Q

4 key signs on examination of polycythaemia

A
  1. conjunctival and facial plethora (excessive redness to conjunctiva)
  2. ‘ruddy’ complexion
  3. splenomegaly
  4. erythromelalgia (burning pain in hands)
83
Q

blood test findings in myelofibrosis

A
  • anaemia
  • leucocytosis or leucopaenia
  • thrombocytopaenia or thrombocytosis
84
Q

3 blood film findings in myelofibrosis

A
  1. teardrop-shaped RBCs
  2. varying sized RBCs (poikilocytosis)
  3. immature RBC and WC (blasts)
85
Q

when does myelofibrosis occur

A

in primary myelofibrosis or secondary to PV or essential thrombocythaemia

86
Q

how to diagnose myelofibrosis

A
  • bone marrow biopsy
  • bone marrow aspiration -> ‘dry’ as bone marrow has turned to scar tissue
  • genetic testing for JAK2 gene mutation
87
Q

mx of primary myelofibrosis

A
  • mild disease = monitoring
  • allogenic stem cell transplant
  • chemotherapy
  • supportive mx of anaemia, splenomegaly and portal hypertension
88
Q

mx of polycythaemia

A
  • regular venesection to keep Hb in range
  • aspirin to reduce risk of thrombosis
  • chemotherapy
89
Q

mx of essential thrombocythaemai

A
  • aspirin to reduce risk of thrombosis

- chemotherapy

90
Q

what is myelodysplastic syndrome

A

myeloid bone marrow cells don’t mature properly and don’t produce healthy blood cells

91
Q

epidemiology of myelodysplastic syndrome

A
  • more common in >60yo

- patients previously treated with chemo or radiotherapy

92
Q

prognosis of myelodysplastic syndrome

A

risk of transforming to AML

93
Q

presentation of myelodysplastic syndrome

A
  • asymptomatic and incidentally diagnosed on FBC
  • sx of anaemia
  • frequent/severe infection (neutropaenia)
  • purpura, bleeding (thrombocytopaenia)
94
Q

diagnosis of myelodysplastic syndrome

A

FBC -> anaemia, thrombocytopaenia, neutropaenia
blood film -> blasts
bone marrow aspiration and biopsy

95
Q

mx options for myelodysplastic syndrome

A
  • watchful waiting
  • supportive tx with blood transfusion
  • chemotherapy
  • stem cell transplant

Haem (3 decks)

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