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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

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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
Staging of Hodgkin's lymphoma?
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
26
Hodgkin's lymphoma treatment?
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)
27
What similar symptoms are there between the various subtypes of Non-Hodgkin's lymphoma?
Painless lymphadenopathy Constitutional symptoms No pain after alcohol
28
What B cell subtypes of NHL are there?
``` Burkitt's Diffuse large B-cell Mantle cell lymphoma Follicular Mucosal associated lymphoid tissue (MALT) ```
29
What T cell subtypes of NHL are there?
``` Anaplastic large cell Peripheral Adult T cell leukaemia/lymphoma Enteropathy associated T cell lymphoma Cutaneous T cell lymphoma ```
30
What are the three types of Burkitt's lymphoma?
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
31
What is the histology of Burkitt's described as?
Starry sky appearance
32
Treatment for Burkitt's?
Chemotherapy (rituximab (anti-CD20 on B cells) + leukaemia protocol) or SCT
33
How does Diffuse Large B-Cell (DLBC) present?
Middle aged and elderly Aggressive Richter's transformation Other lymphomas occur secondary
34
Histology of DLBC?
Sheets of large lymphoid cells
35
Treatment for DLBC and Mantle cell lymphoma?
Rituximab-CHOP | Auto-SCT for relapse
36
How does Mantle cell lymphoma present?
Middle aged, M>F Aggressive Disseminated at presentation Survival 3-5yrs
37
Histology of mantle cell lymphoma?
Angular nuclei
38
How does follicular B cell lymphoma present?
Indolent Mostly incurable 12-15y survival
39
Treatment for follicular B cell lymphoma?
Watch and wait | Rituximab CVP
40
How does Mucosal associated lymphoid tissue present?
``` Marginal zone NHL Middle-aged Chronic antigen stimulation: H pylori -> gastric MALT lymphoma Sjogren's -> parotid lymphoma ```
41
Treatment for MALT?
Remove antigenic stimulus e.g. H pylori triple therapy | Chemotherapy
42
How are T cell lymphomas treated?
Alemtuzumab (anti-CD52) can be used
43
How does anaplastic large cell lymphoma present?
Children and young adults Aggressive Large epithelioid lymphocytes
44
How does peripheral T-cell lymphoma present?
Middle aged and elderly Aggressive Large T cells
45
When you hear adult T-cell leukaemia/lymphoma, what should you think?
Caribbean and Japanese | HTLV-1 infection, aggressive
46
What is multiple myeloma?
Neoplasia of plasma cells of BM leading to production of monoclonal immunoglobulin
47
Epidemiology of multiple myeloma?
Middle-Aged to Elderly | Increased incidence in Afro-Caribbeans
48
Clinical features of MM?
CRAB Calcium high- thirst, moans, grones, stones, bones Renal failure (plus amyloidosis and nephrotic syndrome) Anaemia (+ pancytopenia) Bones- pain, osteoporosis, osteolytic lesions, fractures
49
Investigation findings in MM?
``` Dense narrow band on serum electrophoresis Rouleaux on blood film Bence Jones proteins in urine ESR very high >10% plasma cells in BM ```
50
Staging of MM?
Durie-Salmon staging
51
Treatment of MM?
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
How does Waldenstrom's Macroglobinaemia present?
Elderly men Low grade NHL Weight loss, fatigue, hyperviscosity syndrome (visual problems, confusion, CCF, muscle weakness)
53
Treatment for Waldenstrom's Macroglobinaemia?
Plasmapheresis for hyperviscosity, chlorambucil, cyclophosphamide
54
How is amyloidosis diagnosed?
Congo-Red stain -> apple-green birefringence
55
How is amyloidosis treated?
Velcade/chemo/auto-SCT
56
What are myelodysplastic syndromes?
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
How do you differentiate myelodysplastic syndromes from acute leukaemia?
MDS <20% blasts | Acute leukaemia >20% blasts
58
How do you treat MDS?
Supportive- transfusions, EPO, G-CSF + Abx Biological modifiers- immunosuppressive drugs, lenalidomide, azacytidine Chemotherapy Allogenic SCT
59
What is the prognosis of MDS like?
``` 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
What is aplastic anaemia?
Inability of BM to produce adequate blood cells
61
What is the management of aplastic anaemia?
Supportive- transfusions, Abx, iron chelation Drugs- to promote marrow recovery- growth factors and oxymetholone (androgen) Immunosuppressants- idiopathic AA SCT
62
What is Fanconi Anaemia?
Autosomal recessive pancytopenia Presents at 5-10y Skeletal abnormalities, renal malformations, microopthalmia, short stature, skin pigmentation
63
What is dyskeratosis congenita?
X-linked with triad of skin pigmentation, nail dystrophy + oral leukoplakia BM failure
64
What are myeloproliferative disorders?
A group of conditions characterised by clonal proliferation of one or more haemopoietic component
65
Which MPD is philadelphia chromosome positive?
CML
66
What are Ph -ve MPDs associated with?
JAK2 mutations, especially polycythaemia vera
67
What are the primary and secondary causes of polycythaemia?
``` Primary: Polycythaemia vera Familial polycythaemia Secondary (raised EPO): Disease states, high altitude, chronic hypoxia e.g. COPD ```
68
What causes relative polycythaemia?
Normal red cell mass but plasma volume reduced e.g. dehydration, burns, vomiting, diarrhoea, cigarette smoking
69
What is polycythaemia rubra vera?
An MPD where erythroid precursors dominate the BM caused by JAK2 point mutations
70
What are the clinical features of polycythaemia rubra vera?
Hyperviscosity Blurred vision, headache Plethoric, gout, thrombosis and stroke, retinal vein engorgement Splenomegaly Histamine release -> aquagenic pruritus (contact with water) and peptic ulcers
71
Investigation findings in polycythaemia rubra vera?
Raised Hb, HCT, platelets + WCC | Low serum EPO
72
How is polycythaemia rubra vera treated?
Venesection | Hydroxycarbamide + aspirin
73
What is myelofibrosis?
A MPD where myeloproliferation leads to fibrosis of BM or replacement with collagenous tissue
74
What are the clinical features of myelofibrosis?
Elderly Pancytopenia symptoms Extramedullary haematopoesis- hepatomegaly, massive splenomegaly, WL, fever Can present with Budd-Chiari syndrome
75
Investigation findings for myelofibrosis?
Blood film- tear drop poikilocytes, leukoerythroblasts | BM- fibrosis, 'dry tap'
76
How do you treat myelofibrosis?
Support with blood products, in some cases- splenectomy | Hydroxycarbamide, thalidomide, steroids and SCT
77
What is essential thrombocythaemia?
An MPD where megakaryocytes dominate the BM
78
What are the clinical features of essential thrombocythaemia?
Incidental finding in 50% Venous and arterial thrombosis, gangrene and haemorrhage Erythromelalgia Splenomegaly, dizziness, headaches, visual disturbances
79
Investigation findings in essential thrombocythaemia?
Platelet count >600x10^9 Blood film- large platelets and megakaryocyte fragments Increased BM megakaryocytes
80
Treatment for essential thrombocythaemia?
Aspirin Anagrelide- reduces formation of plts from megakaryocytes Hydroxycarbamide
81
What causes haemolytic disease of the newborn?
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
How do you prevent anti-D formation in RhD negative women?
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
Learn Transfusion flow chart on p34
Good job!

Pathology (13 decks)

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