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Pathology > Haematology part 2 (p22-34- leukaemia, lymphomas, myeloproliferative + transfusions) > Flashcards

Haematology part 2 (p22-34- leukaemia, lymphomas, myeloproliferative + transfusions) Flashcards

1
Q

Clinical features of acute leukaemia?

A

BM function failure- anaemia, thrombocytopenia (bleeding) + neuropenia (infection)
Organ infiltration- hepatomegaly, splenomegaly, lymphadenopathy, bone pain, CNS, skin, gum hypertrophy

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2
Q

What causes acute leukaemia?

A 
Most of the time unknown
Ionising radiation- radiotherapy
Cytotoxic drugs- chemo
Benzene
Pre-leukaemic disorders- MDS, MPD
Down's
Neonates
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3
Q

How is haematological malignancy diagnosed?

A 
Morphology +/- cytochemistry (stains)
Immunophenotyping using flow cytometry (lineage, differentiation)
Cytogenetics (chromsomal translocations)
Molecular genetics (PCR, point mutations etc)
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4
Q

Epidemiology of ALL?

A

Children (ALL children get cancer)

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5
Q

Epidemiology of AML?

A

Adulthood (risk increases with age) and under 2s (infant peak)

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6
Q

Clinical features of ALL?

A 
Anaemia
Thromobocytopenia
Neutropenia
Lymphadenopathy+++
CNS involvement+++
Testicular enlargement
Thymic enlargement
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7
Q

Clinical features of AML?

A

Anaemia
Thrombocytopenia
Neutropenia

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8
Q

Investigation findings for ALL?

A 
High WCC (blasts)
Lymphocytes+++

Flow cytometry:
CD34- Precursor/stem cells
CD3- T lymphocytes
CD19- B lymphocytes

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9
Q

Investigation findings for AML?

A 
High WCC (blasts)
Auer rods and granules

Flow cytometry:
CD34: precursor/stem cells
MPO: myeloid cells

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10
Q

What is the treatment for ALL?

A

Chemotherapy:
Remission induction- chemo agents with steroids
Consolidation- high dose multi drug chemo
CNS treatment
Maintenance- 2y in girls and adults, 3y in boys

Supportive:
Blood products, abx, allopurinol, fluid, electrolytes

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11
Q

What is the treatment for AML?

A

Chemo:
Similar to ALL but no CNS prophylaxis/maintenance therapy
(ATRA for M3 subtype)

Supportive:
Blood products, abx, allopurinol, fluid, electrolytes

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12
Q

Epidemiology of CML?

A

Middle aged typically 40-60

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13
Q

Investigation findings for CML?

A

Ph +ve (philadelphia chromosome) in 80%
PCR for BCR-ABL (philadelphia ch) fusion gene
WBC, Neutrophils 50-5000
Hypercellular BM with spectrum of immature and mature granulocytic cells in the blood
On examination- massive splenomegaly

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14
Q

Three different phases of CML?

A

Chronic phase
Accelerated phase
Blast phase

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15
Q

How is chronic phase CML treated?

A

Imatinib (BCR-ABL tyrosine kinase inhibitor)

Highly effective

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16
Q

Epidemiology of CLL?

A

M>F, elderly

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17
Q

Clinical features of CLL?

A

Asymptomatic and diagnosed on bloods in 80% of cases
Symmetrical painless lymphadenopathy
BM failure- anaemia, thrombocytopenia, neutropenia
Weight loss, fever, night sweats
Hepatomegaly and splenomegaly

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18
Q

Investigation findings for CLL?

A

High WBC with lymphocytosis >5
Low serum Ig
Smear cells (SMEAR CLLs)- blood film

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19
Q

What is the staging for CLL?

A

Binet:
Stage A- High WBC, <3 groups of enlarged lymph nodes and no treatment required
Stage B- >3 groups of enlarged lymph nodes
Stage C- Anaemia or thrombocytopenia

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20
Q

Treatment for CLL?

A

Many benefit from watchful waiting
Supportive treatment with transfusions, infection prophylaxis
1st line- if p53 deletion = alemtuzumab otherwise chlorambucil

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21
Q

What is a lymphoma?

A

Neoplastic tumour of lymphoid tissue (lymph nodes, spleen, MALT etc)

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22
Q

Epidemiology of Hodgkin’s lymphoma?

A

20% of lymphoma
M>F
Bimodal age incidence- 20-29 and >60
EBV associated

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23
Q

Clinical presentation of Hodgkin’s lymphoma?

A

Asymmetrical painless lymphadenopathy +/- obstructive/mass effect symptoms
B-symptoms (fever >38, drenching night sweats + weight loss >10% in 6m)
Pain in affected nodes after ALCOHOL

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24
Q

Investigations + findings for Hodgkin’s lymphoma?

A

CT/PET
Tissue diagnosis- LN or BM biopsy- cells stain with CD15+CD30
REED-STERNBERG cells- binucleate (owl eyed) cell

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25
Q

Staging of Hodgkin’s lymphoma?

A

Ann-Arbor Staging
Stage 1- one LN region
Stage 2- Two or more LN regions on same side of diaphragm
Stage 3- Two or more regions on opposite side of diaphragm
Stage 4- Extranodal sites (Liver, BM)
A: No constitutional symptoms
B: Constitutional symptoms

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26
Q

Hodgkin’s lymphoma treatment?

A

Excellent prognosis but intensive treatment-
1. Combo chemo (ABVD)
Adriamycin, bleomycin, vinblastine and dacarbazine
2. Radiotherapy (high risk of breast Ca)
3. Intensive chemo and autologous SCT (Relapsed pts)

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27
Q

What similar symptoms are there between the various subtypes of Non-Hodgkin’s lymphoma?

A

Painless lymphadenopathy
Constitutional symptoms
No pain after alcohol

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28
Q

What B cell subtypes of NHL are there?

A 
Burkitt's
Diffuse large B-cell
Mantle cell lymphoma
Follicular
Mucosal associated lymphoid tissue (MALT)
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29
Q

What T cell subtypes of NHL are there?

A 
Anaplastic large cell
Peripheral 
Adult T cell leukaemia/lymphoma
Enteropathy associated T cell lymphoma
Cutaneous T cell lymphoma
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30
Q

What are the three types of Burkitt’s lymphoma?

A

Endemic- Most common malignancy in equatorial africa, EBV associated, jaw involvement and abdo masses

Sporadic- Found outside africa, EBV associated

Immuno-deficiency- Non-EBV, HIV/post transplant patients

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31
Q

What is the histology of Burkitt’s described as?

A

Starry sky appearance

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32
Q

Treatment for Burkitt’s?

A

Chemotherapy (rituximab (anti-CD20 on B cells) + leukaemia protocol) or SCT

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33
Q

How does Diffuse Large B-Cell (DLBC) present?

A

Middle aged and elderly
Aggressive
Richter’s transformation
Other lymphomas occur secondary

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34
Q

Histology of DLBC?

A

Sheets of large lymphoid cells

35
Q

Treatment for DLBC and Mantle cell lymphoma?

A

Rituximab-CHOP

Auto-SCT for relapse

36
Q

How does Mantle cell lymphoma present?

A

Middle aged, M>F
Aggressive
Disseminated at presentation
Survival 3-5yrs

37
Q

Histology of mantle cell lymphoma?

A

Angular nuclei

38
Q

How does follicular B cell lymphoma present?

A

Indolent
Mostly incurable
12-15y survival

39
Q

Treatment for follicular B cell lymphoma?

A

Watch and wait

Rituximab CVP

40
Q

How does Mucosal associated lymphoid tissue present?

A 
Marginal zone NHL
Middle-aged
Chronic antigen stimulation:
H pylori -> gastric MALT lymphoma
Sjogren's -> parotid lymphoma
41
Q

Treatment for MALT?

A

Remove antigenic stimulus e.g. H pylori triple therapy

Chemotherapy

42
Q

How are T cell lymphomas treated?

A

Alemtuzumab (anti-CD52) can be used

43
Q

How does anaplastic large cell lymphoma present?

A

Children and young adults
Aggressive
Large epithelioid lymphocytes

44
Q

How does peripheral T-cell lymphoma present?

A

Middle aged and elderly
Aggressive
Large T cells

45
Q

When you hear adult T-cell leukaemia/lymphoma, what should you think?

A

Caribbean and Japanese

HTLV-1 infection, aggressive

46
Q

What is multiple myeloma?

A

Neoplasia of plasma cells of BM leading to production of monoclonal immunoglobulin

47
Q

Epidemiology of multiple myeloma?

A

Middle-Aged to Elderly

Increased incidence in Afro-Caribbeans

48
Q

Clinical features of MM?

A

CRAB
Calcium high- thirst, moans, grones, stones, bones
Renal failure (plus amyloidosis and nephrotic syndrome)
Anaemia (+ pancytopenia)
Bones- pain, osteoporosis, osteolytic lesions, fractures

49
Q

Investigation findings in MM?

A 
Dense narrow band on serum electrophoresis
Rouleaux on blood film
Bence Jones proteins in urine
ESR very high
>10% plasma cells in BM
50
Q

Staging of MM?

A

Durie-Salmon staging

51
Q

Treatment of MM?

A

Supportive for CRAB symptoms e.g. bisphosphonates
Aim- Induce remission for consideration of autologous SCT
First line- Bortezomib +/- dexamethasone, cyclophosphamide, lenalidomide
Auto-SCT- curative

52
Q

How does Waldenstrom’s Macroglobinaemia present?

A

Elderly men
Low grade NHL
Weight loss, fatigue, hyperviscosity syndrome (visual problems, confusion, CCF, muscle weakness)

53
Q

Treatment for Waldenstrom’s Macroglobinaemia?

A

Plasmapheresis for hyperviscosity, chlorambucil, cyclophosphamide

54
Q

How is amyloidosis diagnosed?

A

Congo-Red stain -> apple-green birefringence

55
Q

How is amyloidosis treated?

A

Velcade/chemo/auto-SCT

56
Q

What are myelodysplastic syndromes?

A

Heterogeneous group of progressive disorders featuring ineffective proliferation and differentiation of abnormally maturing myeloid stem cells

Characterised by:
Peripheral cytopenia
Qualitative abnormalities of cell maturation
Risk of AML transformation

57
Q

How do you differentiate myelodysplastic syndromes from acute leukaemia?

A

MDS <20% blasts

Acute leukaemia >20% blasts

58
Q

How do you treat MDS?

A

Supportive- transfusions, EPO, G-CSF + Abx
Biological modifiers- immunosuppressive drugs, lenalidomide, azacytidine
Chemotherapy
Allogenic SCT

59
Q

What is the prognosis of MDS like?

A 
Depends on International Prognostic Scoring System (IPSS)- BM blast %, karyotype
There is a mortality rule of 1/3:
1/3 die from infection
1/3 from bleeding
1/3 from acute leukaemia
60
Q

What is aplastic anaemia?

A

Inability of BM to produce adequate blood cells

61
Q

What is the management of aplastic anaemia?

A

Supportive- transfusions, Abx, iron chelation
Drugs- to promote marrow recovery- growth factors and oxymetholone (androgen)
Immunosuppressants- idiopathic AA
SCT

62
Q

What is Fanconi Anaemia?

A

Autosomal recessive pancytopenia
Presents at 5-10y
Skeletal abnormalities, renal malformations, microopthalmia, short stature, skin pigmentation

63
Q

What is dyskeratosis congenita?

A

X-linked with triad of skin pigmentation, nail dystrophy + oral leukoplakia
BM failure

64
Q

What are myeloproliferative disorders?

A

A group of conditions characterised by clonal proliferation of one or more haemopoietic component

65
Q

Which MPD is philadelphia chromosome positive?

A

CML

66
Q

What are Ph -ve MPDs associated with?

A

JAK2 mutations, especially polycythaemia vera

67
Q

What are the primary and secondary causes of polycythaemia?

A 
Primary:
Polycythaemia vera
Familial polycythaemia
Secondary (raised EPO):
Disease states, high altitude, chronic hypoxia e.g. COPD
68
Q

What causes relative polycythaemia?

A

Normal red cell mass but plasma volume reduced e.g. dehydration, burns, vomiting, diarrhoea, cigarette smoking

69
Q

What is polycythaemia rubra vera?

A

An MPD where erythroid precursors dominate the BM caused by JAK2 point mutations

70
Q

What are the clinical features of polycythaemia rubra vera?

A

Hyperviscosity
Blurred vision, headache
Plethoric, gout, thrombosis and stroke, retinal vein engorgement
Splenomegaly
Histamine release -> aquagenic pruritus (contact with water) and peptic ulcers

71
Q

Investigation findings in polycythaemia rubra vera?

A

Raised Hb, HCT, platelets + WCC

Low serum EPO

72
Q

How is polycythaemia rubra vera treated?

A

Venesection

Hydroxycarbamide + aspirin

73
Q

What is myelofibrosis?

A

A MPD where myeloproliferation leads to fibrosis of BM or replacement with collagenous tissue

74
Q

What are the clinical features of myelofibrosis?

A

Elderly
Pancytopenia symptoms
Extramedullary haematopoesis- hepatomegaly, massive splenomegaly, WL, fever
Can present with Budd-Chiari syndrome

75
Q

Investigation findings for myelofibrosis?

A

Blood film- tear drop poikilocytes, leukoerythroblasts

BM- fibrosis, ‘dry tap’

76
Q

How do you treat myelofibrosis?

A

Support with blood products, in some cases- splenectomy

Hydroxycarbamide, thalidomide, steroids and SCT

77
Q

What is essential thrombocythaemia?

A

An MPD where megakaryocytes dominate the BM

78
Q

What are the clinical features of essential thrombocythaemia?

A

Incidental finding in 50%
Venous and arterial thrombosis, gangrene and haemorrhage
Erythromelalgia
Splenomegaly, dizziness, headaches, visual disturbances

79
Q

Investigation findings in essential thrombocythaemia?

A

Platelet count >600x10^9
Blood film- large platelets and megakaryocyte fragments
Increased BM megakaryocytes

80
Q

Treatment for essential thrombocythaemia?

A

Aspirin
Anagrelide- reduces formation of plts from megakaryocytes
Hydroxycarbamide

81
Q

What causes haemolytic disease of the newborn?

A

Person may form red cell Ab through blood transfusion or if fetal cells enter woman’s circulation during pregnancy or delivery. If maternal Ab level is high, it can destroy fetal red cells if they have corresponding red cell Ag -> fetal anaemia + jaundice (HDN)

82
Q

How do you prevent anti-D formation in RhD negative women?

A

Give intramuscular anti-D Ig when she is at high risk of feto-maternal haemorrhage
Routine antenatal prophylaxis at 28 + 34w
Also give at delivery if baby is RhD positive

83
Q

Learn Transfusion flow chart on p34

A

Good job!

Pathology (13 decks)

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