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MS3 - Haematology > Haemato-oncology > Flashcards

Haemato-oncology Flashcards

1
Q

2 types of Acute leukaemia?

A
  1. acute myeloid leukaemia (AML)

2. acute lymphoblastic leukaemia (ALL)

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2
Q

How leukaemia leads to anaemia/immune suppression?

A

Uncontrolled expansion of hypofunctional cells in blood, bone marrow and other organs leads to suppression of normal haematopoiesis and immunity

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3
Q

Sx of leukaemia

A
  • anaemia,
  • bleeding
  • susceptibility to infection
  • hepatosplenomegaly
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4
Q

Endogenous RFs of leukaemia:

A
  • Chromosome fragility syndromes

- Downs syndrome

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5
Q

Exogenous RFs of leukaemia

A
  • Radiation
  • Chemotherapy
  • Benzene
  • Viral infection
  • Acquired immune deficiency
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6
Q

Epi of Acute Myeloblastic Leukaemia (AML)

A

Commoner in adults, Incidence 1:10,000 annually, Increased frequency with age (median >70 yr)

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7
Q

Bloods of of Acute Myeloblastic Leukaemia (AML)

A
  • low Hb and platelet count
  • WBC usually 20 – 100 x 109/L with blast cells visible on the peripheral blood film.
  • WBC >50 = high risk
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8
Q

Bone marrow results of Acute Myeloblastic Leukaemia (AML)

A
  • blasts > 20% of nucleated cells
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9
Q

Flow cytometry results of Acute Myeloblastic Leukaemia (AML)

A
  • CD13+, CD33+ helpful to confirm AML.
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10
Q

Good prognostics genetics of Acute Myeloblastic Leukaemia (AML)

A

t(15;17),
t(8;21),
inv16 .

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11
Q

Poor prognostics genetics of Acute Myeloblastic Leukaemia (AML)

A

Monosomy 7,

Abnormalities on chromosome 5, 1

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12
Q

Mx of Acute Myeloblastic Leukaemia (AML)

A
  1. combination therapy

2. supportive care

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13
Q

Combination therapy for AML?

A
  • cytosine arabinoside
  • daunorubicin.
  • Retinoic acid/arsenic trioxide
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14
Q

Duration of combination therapy for AML?

A

3-4 cycles of therapy given 4 – 6 weekly.

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15
Q

Complications of AML treatment?

A
  • Infection
  • Bleeding
  • Debility, profound weight loss
  • Social: inpatient for most of 6 months, loss of employment, stress on family
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16
Q

Success rate of AML treatment?

A
  • Overall complete remission rate: 85%

- Overall survival: 45-50% cured with chemotherapy alone

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17
Q

Acute Lymphoblastic Leukaemia (ALL) incident age?

A

peak age 2 – 10 years. Another peak >60 years

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18
Q

how to differentiate ALL from AML?

A

ALL commonly causes severe bone pain, sweats

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19
Q

Flow cytometry results for ALL?

A

may show blasts of B cell (CD10+, CD19+) or T cell lineage (20%)

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20
Q

Philadephila chromosome?

A

Philadelphia chromosome t(9;22) seen in 20-25 % of adults with ALL
- Poor prognostic marker but means specific therapy with tyrosine kinase inhibitors.

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21
Q

Poor prognostics genes of ALL

A
  • t(9;22)
  • t(4;11),
  • t(8;14)
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22
Q

Management of ALL?

A

Chemotherapy with complex combinations of cytotoxic drugs (eg steroids, vincristine, daunorubicin, asparaginase)

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23
Q

Course of chemotherapy for ALL?

A

a. Remission induction 2mo
b. Consolidation: 4 mo intense chemo
c. Maintenance: 2 yrs (less intense therapy; mainly oral cytotoxic drugs)

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24
Q

Success rate of ALL treatment?

A

> 85% cure in childhood ALL

>50% cure rate in adults who have intensive treatment on national trials

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25
Q

Minimum residual disease use?

A

used to decide treatment in children and adults after response after 2 cycles of therapy

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26
Q

Minimum residual disease method?

sensitivity?

A
  • Leukaemic clone can be identifed by DNA fingerprinting and accurately measured using Q PCR.
  • Sensitive (1 in 10,000 cells or better)
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27
Q

How does bone marrow transplant work? Effect on chemo?

A

Donor T cells kill leuakaemia via a graft versus leukaemia effect
- Allows use of higher doses of chemo

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28
Q

Immediate complications of bone transplant

A
  • Relapse
  • Graft versus host disease
  • Extramedullary toxicity
  • Infection
  • Rejection
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29
Q

Long term complications of bone transplant

A

infertility,

second cancers

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30
Q

Neutropenic sepsis cause?

A

results from the treatment of leukaemia and bone marrow transplantation

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31
Q

Sx of Neutropenic sepsis

A

• T >38C

or patient looks unwell

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32
Q

Mx of neutropenic sepsis?

A

culture and start broad spectrum antibiotics within 1 hour

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33
Q

Symptoms of myeloma?

A 
CRABI” acronym
C- Hypercalcaemia
R- Renal dysfunction
A- Anaemia
B- Bone – lytic lesions, fractures, osteoporosis
I- Infection
34
Q

Chronic Lymphocytic Leukaemia (CLL) def?

A
  • Clonal B cell lymphocytosis of >5 x 109/l persisting for more than 3 months
35
Q

Chronic Lymphocytic Leukaemia (CLL) peak age?

A

median age at diagnosis 72 years

36
Q

Chronic Lymphocytic Leukaemia (CLL) diagnosi?

A

Immunophenotyping:
Looking at antigens on WBC
- If score >3, CLL.
- If <3, likely other form of B cell malignancies (eg mantle cell lymphoma)

37
Q

Management of Chronic Lymphocytic Leukaemia (CLL)?

A
  1. chemo

2. BTK inhibition

38
Q

BTK inhibitors?

A
  • brutons tyrosine kinase inhibitor
  • ibrutinib
  • Tyrosine kinase: switches on cellular cycle
39
Q

Genetic prognostics of CLL?

A

17p depletion on cytogenetics (mutation), poor diagnosis

40
Q

Complications of CLL?

A
  • Infection
  • Auto-immune haemolytic anaemia
  • Secondary malignancy
41
Q

Causes of raised WCC

A
  1. infection
  2. proliferative
  3. inflammation
  4. steroids
42
Q

Chronic myeloid leukaemia (CML) sx?

A
  • Asymptomatic or
  • Hypermetabolic state (Weight loss, Sweats)
  • Leucostasis (due to high WBC: eg SOB, Priapism)
  • Symptoms from splenomegaly (eg Early satiety)
43
Q

Genetics of Chronic myeloid leukaemia (CML)

A
  • t(9,22); phaladelphia chromosome
44
Q

BCR-ABL gene?

A 
- philadelphia chromosome: 
Formation of Bcr-Abl
- Inhibition of apoptosis
- Up-regulates cell cycle progression and
differentiation
45
Q

Management of Chronic myeloid leukaemia (CML)?

A

Imatinib blocks formation of Bcr-Abl, improving the symptoms

46
Q

Monitoring of Chronic myeloid leukaemia (CML)?

A

monitor Bcr-Abl level

47
Q

Prognosis of Chronic myeloid leukaemia (CML)?

A

good nearly normal if treated

48
Q

Raised haemoglobin causes?

A
  1. EPO production
  2. COPD
  3. congenital heart disease in adults
49
Q

Causes of raised platelet count?

A
  1. splenectomy
  2. inflammation
  3. iron deficiency
  4. malignancy
50
Q

The Myeloproliferative neoplasms types?

A

I. Polycythaemia rubra vera

II. Essential Thrombocythaemia

III. Primary Myelofibrosis

51
Q

Genetics Myeloproliferative neoplasms?

A

JAK2 mutation

52
Q

JAK2 mutation significance?

A
  • wild type only causes proliferation when EPO binds

Mutation: doesnt need epo binding, causes proliferation without it

53
Q

Management of Polycythaemia Vera

A
  1. Venesection to maintain the Hct to <0.45
  2. Aspirin 75 mg/d unless contraindicated
  3. Cytoreduction should be considered
54
Q

Myelofibrosis Def?

A

Symptomatic anaemia

55
Q

Sx of Myelofibrosis

A
  • Discomfort from
    splenomegaly
  • Hypermetabolic symptoms (weight loss,
    sweats)
56
Q

Pathophysiology of Myelofibrosis

A

bone marrow becomes thickened (due to fibrin) so spleen starts producing RBC, and if spleen cant liver takes over

57
Q

Prognosis of Myelofibrosis

A

depends on the score, but in high risk survival 1/2 years

58
Q

Management of Myelofibrosis

A

ruxolotinib: JAK2 inhibitor

59
Q

Non hodgkin lymphoma (NHL) presentation

A
  • Enlarged Lymph nodes
  • B sx
  • Fatigue
    ◦ Itching
60
Q

B sx?

A

B Symptoms
◦ Drenching Night sweats
◦ Unexplained Fevers >38’C
◦ Weight loss >10% in last 6 months

61
Q

Diagnosis of Non hodgkin lymphoma (NHL)

A

Lymph node biopsy

62
Q

Staging of Non hodgkin lymphoma (NHL)

A

Ann arbor Staging scan:

  • CT Neck,Chest,Abdo,Pelvis or PET scan)
  • Bone marrow biopsy
63
Q

Ann arbor staging of NHL?

A

Stages 1-4 and tells you how many places you have lymphoma in:

  1. one place
  2. more than one on the same side of diaphragm
  3. both sides of diaphragm
  4. exta lymphatic ( eg lungs)

A (absence of B sx) or B (presence of B sx)

64
Q

Mx of Non hodgkin lymphoma (NHL)

A

Stage IA RCHOP x4 + Local Radiotherapy

  • Stage IIA – IV RCHOP x 6-8cycles

Given every 3 weeks
Risk of neutropenic sepsis day 7-10

65
Q

RCHOP chemotherapy

A
  • Rituximab (monoclonal antibody)
  • Cyclophosphamide
  • Hydroxydaunorubicin chemotherapy
  • Oncovin
  • Prednisolone
66
Q

Types of low grade lymphoma

A

◦ Follicular Lymphoma
◦ Marginal Zone Lymphoma
◦ Mantle Cell Lymphoma
◦ Small lymphocytic Lymphoma

67
Q

Hodgkin lymphoma mx?

A

Treat with

- ABVD +/- Radiotherapy

68
Q

hodgkin lymphoma RFs?

A

EBV
FH
HIV

69
Q

hodgkin lymphoma prognosis

A

> 85% 5 year survival*

70
Q

Myeloma def

A

Cancer of plasma cells with increased clonal plasma cells

71
Q

Bone marrow finding in myeloma

A

monoclonal paraprotein

72
Q

Monoclonal gammapathy of underterimined significance (MGUS) def?

A
  • have paraprotein of no significance
73
Q

Monoclonal gammapathy of underterimined significance (MGUS) Ix?

A
  • Serum monoclonal protein <30g/L
  • Clonal bone marrow plasma cells <10%
  • Absence of end-organ damage
74
Q

Monoclonal gammapathy of underterimined significance (MGUS) Mx?

A

Active monitoring

75
Q

smouldering myeloma

A
  • Serum monoclonal protein (IgG or IgA) ≥30g/L
  • or urinary monoclonal protein ≥500mg per 24h
  • and/or clonal bone marrow plasma cells 10-60%
  • Absence of myeloma defining events or
    amyloidosis
76
Q

General Mx of myeloma

A

I. Vigorously rehydrate with at least 3 litres of normal saline daily
II. Stop nephrotoxic drugs e.g. NSAIDs

77
Q

Main complications of myeloma?

A
  1. high calcium
  2. hyper viscosity syndrome
  3. spinal cord compression
78
Q

Hyper viscosity syndrome presentation?

A

◦ blurred vision
◦ headaches
◦ mucosal bleeding
◦ dyspnoea due to heart failure

79
Q

Hyper viscosity syndrome mx?

A
  • plasma exchange

- isovolaemic venesection (if cant plasma exchange)

80
Q

Spinal cord compression mangament?

A
  • Dexamethasone 40 mg daily for 4 days
  • Urgent MRI whole spine
  • Neurosurgical/spinal surgical review if bony lesion to decompress or stabilise spine
  • Local radiotherapy if non-bony lesions ASAP (within 24 hours)
81
Q

Myeloma medical mx?

A
  1. Traditional Chemo eg Cyclophosphamide,
  2. Dexamethasone
  3. Immune modulatory drugs e.g. thalidomide,
  4. Proteosome inhibitors (cause cell death)
    ◦ e.g. bortezomib

MS3 - Haematology (5 decks)

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