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2a > Leukaemia > Flashcards

Leukaemia Flashcards

22.4.18 OHCM Lecture 18.1.18 Osmosis youtube ALL, AML, CLL, CML.

1
Q

What are the types of leukaemia and which is the most common?

A 
Acute lymphoblastic (ALL)
Acute myeloid (AML)
Chronic lymphoblastic (CLL) - commonest (25%)
Chronic myeloid (CML) (15%)
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2
Q

Why does acute myeloid leukaemia occur?

A

Myeloid progenitor cells are unable to differentiate so they proliferate in the bone marrow.
(osmosis)

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3
Q

Why might AML cause fatigue, infections and bleeding?

A

Proliferation of myeloid stem cells crowds out the normal cells in the bone marrow such as red blood cells, neutrophils and platelets. Decreased RBCs causes anaemia which causes fatigue. Neutropaenia causes infections and thrombocytopaenia causes bleeding.

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4
Q

What test differentiates between lymphoblastic and myeloid leukaemias? How does it work?

A

Nuclear staining for TdT, a type of DNA polymerase only present in lymphoblasts
Cystoplasmic staining for myeloperoxidase, an enzyme only present in myeloblasts.

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5
Q

What is the most common type of ALL?

A

B-ALL which affects B cells

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6
Q

What needs to be given to people with ALL as well as ‘normal’ chemotherapy and why?

A

Prophylactic injections into the scrotum and CSF because ALL passes the blood brain and blood testis barriers but chemotherapy drugs do not.
(osmosis)

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7
Q

What determines prognosis in ALL?

A

Cytogenetic abnormalities. t(12:21) infers good prognosis and is seen more in children.

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8
Q

What is acute lymphoblastic lymphoma?

A

The same thing as T-ALL. It causes a mass of malignant cells in the thymus (lymphoma) not just blood (leukaemia).

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9
Q

Which type of leukaemia is more common in 50-60 year olds?

A

AML.

osmosis

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10
Q

How can AML be further classified?

A
  1. Cytogenetic abnormalities, eg acute promyelocytic leukaemia - t(15;17).
  2. lineage - eg monocytic, megakaryoblastic
  3. Surface markers
    (osmosis)
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11
Q

Which subtype of AML would you consider in someone with gum deterioration?

A

Acute monocytic leukaemia. This infiltrates the gums.

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12
Q

Which subtype of AML would you consider in someone with Down’s syndrome?

A

Acute megakaryoblastic leukaemia.

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13
Q

What else can cause cytopaenia?

A

Myelodysplasia: only <20% buildup of myeloblasts in the bone marrow. Can still cause death via infections.
(osmosis)

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14
Q

Apart from fatigue, give 3 clinical features of leukaemia and what causes them.

A

Acute (2 weeks) onset of:
bone marrow failure: (fatigue), infections, bleeding
Infiltration: hepatosplenomegaly, lymphadenopathy, orchidomegaly, CNS involvement eg meningism.
Lecture 18.1.

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15
Q

What is the commonest cancer of childhood?

A

ALL.

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16
Q

What investigations would you do if you suspect leukaemia?

A

FBC - thrombocytopaenia, anaemia and low haemoglobin
Blood film: blast cells.
Chest and abdo X ray and CT scan to look for lymphadenopathy and any structures affected by compression.
Cytogenetic analysis to predict behaviour of disease

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17
Q

Describe supportive treatment needed for ALL.

A

Giving blood and platelets for bone marrow support
Infections: Prophylactic antifungals, antibiotics
Symptomatic
Holistic: help with psychological support

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18
Q

Describe definitive treatment for ALL.

A

Chemotherapy - 2/3 years, aim to destroy bone marrow cells.
Stem cell transplant
Palliative: low-dose treatment to control disease - depends what the patient wants.

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19
Q

Give 2 risk factors associated with ALL.

A

Down’s syndrome, ionising radiation eg X-rays during pregnancy.
(OHCM)

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20
Q

Give 2 risk factors associated with acute myeloid leukaemia.

A

Myelodysplasia
Radiation
Down’s syndrome

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21
Q

Give 3 clinical features of AML.

A

Acute onset
Marrow failure: anaemia, infection, bleeding. DIC in acute promyelocytic leukaemia.
Infiltration: hepatomegaly, splemomegaly, gum hypertrophy, skin involvement.

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22
Q

What is DIC and what can cause it?

A

Disseminated intravascular coagulation. A medical emergency that can be cause by acute promyelocytic leukaemia due to thromboplastin release.
(OHCM)

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23
Q

Is AML or ALL more likely to have CNS involvement?

A

ALL (*why?)

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24
Q

How is AML diagnosed and differentiated from ALL?

A

Bone marrow biopsy - Auer rods in AML but not ALL.
FBC: Possibly increased WCC but not always.
Blood film: few blast cells in peripheral blood.
(OHCM)

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25
Q

Give 2 complications of AML and how you would treat them.

A

Predisposition to infection by the disease and treatment - give prophylaxis and be alert to septicaemia and rare infections and presentations.
Chemo causes increased plasma urate so give allopurinol.

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26
Q

Describe the management of AML.

A

Walking exercises can relieve fatigue
Aim is to destroy leukaemic and immune cells then repopulate with transplant.
1. Chemo - very intensive, marrow suppression.
2. Marrow transplant
3. Older patients - low-dose/supportive care

27
Q

Give 2 infections commonly seen in acute leukaemia.

A

Candidiasis

Pneumocystis pneumonia

28
Q

Define chronic myeloid leukaemia.

A

Uncontrolled clonal proliferation of partially differentiated myeloid cells, usually caused by chromosomal translocation that affects granulocytes.

29
Q

Describe the epidemiology of CML

A

15% of leukaemias.
40-60 years old
Males slightly higher
80% have Philadelphia chromosome

30
Q

What is the location and significance of the philadelphia chromosome in CML?

A

t(9;22). It forms a fusion gene BCR/ABL on chromosome 22, which has tyrosine kinase activity. If present, prognosis is better than if absent.

31
Q

Describe the presentation of CML.

A

Chronic and insidious onset - slow-growing
Weight loss - tumour cells using up energy
Tiredness - anaemia
Fever - respiration from tumour cells?
Sweats *why?

32
Q

Why may you get gout in CML?

A

There is increased purine breakdown.

33
Q

Why may you get bleeding in CML?

A

Platelet dysfunction

34
Q

What causes abdominal discomfort in CML?

A

Splenic enlargement (in 75%) (OHCM)

35
Q

Give 3 signs of CML

A

Hepatosplenomegaly
Anaemia
Bruising

36
Q

What investigations would you do for suspected CML?

A

FBC - very increased WCC, myeloid cells eg neutrophils, monocytes, basophils, eosinophils; increase urate, B12
Biopsy: Hypercellular bone marrow
Cytogenetic analysis of blood or BM for philadephia (Ph)

37
Q

Describe the natural history of CML.

A

Variable, median survival 5-6 years.

  1. Chronic phase - few symptoms, lasts years
  2. Accelerated phase - increasing symptoms and spllen size
  3. Blast transformation - symptoms of acute leukaemia, possibly death.
38
Q

Describe the treatment of CML.

A
  1. BCR-ABL tyrosine kinase inhibitor: Imatinib
  2. More potent: dasatinib/ nilotinib.
  3. Chemotherapy with hydroxycarbamide
  4. Allogeneic stem cell transplantation - only cure, significant morbidity and mortality, used in younger patients.
39
Q

Give the class, brief mechanism and 3 side-effects of imatinib.

A

BCR-ABL tyrosine kinase inhibitor .Nausea, cramps, oedema, rash, headache, arthralgia. May cause myelosuppression.

40
Q

What uses the same mechanism as imatinib but is more potent causing a more rapid response?

A

Dasatinib, nilotinib.

41
Q

What is allogeneic transplantation?

A

From a HLA-matched donor.

42
Q

Apart from the rate of onset, give a difference between acute and chronic leukaemia.

A

In acute, the cells are not differentiated. In chronic, they are partly differentiated.

43
Q

What is a translocation?

A

Where two homologous chromosomes exchange parts.

44
Q

Define chronic lymphocytic leukaemia.

A

Progressive accumulation of a malignant clone of fully incompetent B cells, mainly caused by genetic abnormalities.

45
Q

Describe the epidemiology of CLL

A

Most common leukaemia (25%)

Females: males 2:1 (*why?)

46
Q

Give one genetic mutation which could increase risk of CLL.

A

Del17p13

OHCM

47
Q

What is Rai stage 0 CLL and what is median survival?

A

Lymphocytosis alone, >13 years

48
Q

What is Rai stage 1 CLL and what is median survival?

A

Lymphocytosis + lymphadenopathy, 8 yrs

49
Q

What is Rai stage 2 CLL and what is median survival?

A

Lymphocytosis + spleno/hepatomegaly, 5 yrs

50
Q

What is Rai stage 3 CLL and what is median survival?

A

Lymphocytosis + anaemia (Hb <110g/L) 2 years

51
Q

What is Rai stage 4 CLL and what is median survival?

A

Lymphocytosis + platelets <100x10^9/L 1 year

52
Q

Give 3 symptoms of CLL.

A

Often asymptomatic. Anaemic, infection-prome, weight loss, sweats, anorexia.

53
Q

Give 3 signs of CLL.

A

Enlarged, rubbery, non-tender nodes

Spleno/hepatomegaly.

54
Q

How is CLL diagnosed?

A 
Often incidental finding on routine FBC.
FBC: Increased lymphocytes
Autoimmune haemolysis
Marrow infiltration: low Hb, neutrophils and platelets.
(OHCM)
55
Q

Give 3 complications of CLL.

A

Autoimmune haemolysis
Infection due to hypogammaglobulinaemia (low IgG)
Marrow failure
(OHCM)

56
Q

What infection is common in CLL?

A

Herpes zoster

57
Q

Describe the first-line management of CLL.

A

If symptomatic:

1. Chemotherapy: Fludarabine + rituximab, +/- cyclophosphamide

58
Q

What could be used to treat CLL apart from fludarabine and rituximab?

A

Ibrutinib
Chlorambucil
Bendamustine
Ofatumumab

59
Q

What is used to treat autoimmune haemolysis in CLL?

A

Steroids

60
Q

What can be used to treat lymphadenopathy and splenomegaly in CLL?

A

Radiotherapy

61
Q

Why would you give IV human Ig in CLL?

A

Low IgG may cause recurrent infection, IV Ig helps with this.

62
Q

Describe the natural history of CLL.

A

1/3 never progress. 1/3 progress slowly, 1/3 progress actively. CD23 and beta-2 microglobulin correlate with bulk of disease and rates of progression.

63
Q

What causes death in CLL?

A

Infection

Transformation to aggressive lymphoma (Richter’s syndrome)

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