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Y6 Derm + Onco + Haem > Leukaemia 2 > Flashcards

Leukaemia 2 Flashcards

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1
Q

What is a leukaemia and what are the types

A

haemopoietic cells lose their ability to differentiate/mature into the end cells, remaining as precursor cells (blasts)

> 20% blast cells

Acute lymphoblastic = build up of lymphoid blast cells
Acute myeloid = build up of myeloid blast cells
Chronic leukaemia = the haemopoietic cells proliferate and differentiate but are non-functioning

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2
Q

What are the causes of ALL

A

proliferation of lymphoblasts (primitive lymphoid cells) → replacement of normal marrow → bone marrow failure and infiltration into other tissues

If build-up of B lymphoblasts → B-ALL (C10, C19, C20 surface markers)
If build-up of T lymphoblasts → T-ALL (CD2-CD8)

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3
Q

What is the most common leukaemia in children

A

Acute lymphoblastic leukaemia (ALL) (80%)
85% are B-lineage, 5% T cell lineage

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4
Q

What are the causes of AML

A

proliferation of myeloblasts (primitive WBCs) → Replacement of normal bone marrow elements → bone marrow failure

Monoblast AML
Megakaryoblast AML
Erythroblast AML

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5
Q

What are the risk factors for ALL

A

Radiation
Viruses
Down’s syndrome
NF1
Fanconi’s anaemia
Achondroplasia
Xeroderma pigmentosum
Siblings with ALL

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6
Q

What are the symptoms of leukaemia

A

Bone marrow failure
- Anaemia: pallor, lethargy, SOB
- Thrombocytopenia: bleeding gums, bruising, menorrhagia
- Neutropenia: opportunistic, recurrent infection

Local infiltration
- Lymphadenopathy
- Splenomegaly
- Testes, CNS (Sanctuary sites where chemotherapy cannot reach easily)
- Bone pain

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7
Q

What are the signs of ALL on examination

A

Testicular swelling
Thymic swelling
Hepatosplenomegaly
Lymphadenopathy
Tender bones
Mediastinal compression
Cranial nerve palsies
Retinal haemorrhage or papilloedema, leukaemic infiltration of the anterior chamber of the eye

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8
Q

What are the signs of AML on examination

A

Gum swelling/hypertrophy
CNS involvement (headaches, nausea, diplopia)
Skin rashes
Rare: deposits of leukaemic blasts in the eye, tongue and bone (fractures)

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9
Q

What investigations should be done for leukaemia

A

FBC: anaemia, neutropenia, thrombocytopenia
Clotting studies
Blood film
Cytochemistry (B or T lineage)
Immunohistochemistry

CXR: enlarge thymus, mediastinal lymphadenopathy, lytic bone lesions
Bone marrow biopsy: >20% blasts
Lumbar puncture
Bone radiograph: mottled appearance, “punched out” lesions

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10
Q

What is tumour lysis syndrome

A

↑ potassium, LDH, phosphate, uric acid

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11
Q

What are the diagnostic features specific to ALL

A

Blood film: positive TdT staining

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12
Q

What are the diagnostic features specific to AML

A

Blood film: Auer rods (myeloperoxidase crystalloid)
Immunohistochemistry: Myeloblast granules positive for Sudan Black staining

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13
Q

What is the management for leukaemia

A
  1. Reduce tumour lysis syndrome (WCC raised) → allopurinol, hyperhydration
  2. Cross match for blood tranfusion
  3. Transfer to specialist centre
  4. Platelet transfusion
  5. Bone marrow aspirate
  6. Chemotherapy (remission (pred) → maintenance (6-Mercaptopurine)

+ supportive care
- Blood products
- Antibiotics for any fever
- Prophylactic Abx to prevent PCP
- Anti-emetics
- Intrathecal methotrexate for CNS involvement

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14
Q

What is the prognosis for leukaemia

A

Children: 5-year disease-free survival of 80%
Adults: 5-year disease-free survival of 30-40%

Poor prognostic markers:
Age <2 or >10
Non-Caucasian
T/B-cell surface markers
Male sex

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15
Q

What are the causes of CLL

A

Accumulation of incompetent lymphocytes
Autoimmune disease:
- Haemolytic anaemia (10%)
- Thrombocytopenia
- Combination (Evan’s syndrome)

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16
Q

What are the symptoms of chronic leukaemia

A

May be asymptomatic

Systemic: weight loss, sweating
Bone marrow failure
- Anaemia → pallor, lethargy, SOB
- Thrombocytopenia → bleeding gums, bruising, menorrhagia
Abdominal discomfort, early satiety
Gout or hyperviscosity symptoms (headaches, visual disturbance, pruritus, worse after bath)
Blast crisis with symptoms of AML or ALL

17
Q

What are the signs of chronic leukaemia on examination

A

Splenomegaly (90%)
Bone marrow failure → cardiac flow murmur
Lymphadenopathy

18
Q

What would investigations show for chronic lymphocytic leukaemia

A

FBC: Anaemia | thrombocytopenia | raised lymphocytes | reduced serum immunoglobulins

Blood film:
- Smudge/smear cells
- Small lymphocytes

Bone Marrow aspirate/biopsy: lymphocytic replacement (25-95%) of normal marrow

19
Q

What is the management for chronic lymphocytic leukaemia

A

Stage via Rai and Binet systems

If asymptomatic → Watchful waiting

± chemotherapy, prednisolone, Abx prophylaxis, blood products, splenectomy, HSCT

20
Q

What are the complications of chronic lymphocytic leukaemia

A

15% transform into localised high-grade non-Hodgkin’s lymphoma (Richter’s transformation) or Prolymphocytic leukaemia
Chemotherapy complications (tumour lysis syndrome)

21
Q

What is the prognosis for chronic lymphocytic leukaemia

A

Best for early disease
11q and 17p deletions associated with poor survival
Gram –ve and encapsulated organisms are most frequent cause of morbidity and mortality in CLL

22
Q

What is the aetiology of chronic myeloid leukaemia

A

Chromosomal translation t(9,22): Philadelphia Chromosome (95%) - fusion of genes BCR and ABL → Increase tyrosine kinase activity → cell replication

23
Q

What are the phases of CML

A
  1. Relative stable chronic phase of variable duration (4-6 years)
  2. Accelerated phase (3-9 months)
  3. Acute leukaemia phase - blast formation
24
Q

What are the signs of CML on exam

A

Splenomegaly (90%)
Bone marrow failure → cardiac flow murmur

25
Q

What investigations should be done for CML

A

FBC - Raised WCC, basophils, eosinophils, neutrophils, platelets + Reduced Hb
Raised uric acid
Reduced neutrophil alkaline phosphatase
Raised vit B12 and trascobalamin

Blood Film
- Immature granulocytes
- Left shift

Bone Marrow trephine biopsy or aspirate:
- Hypercellular
- Raised myeloid-erythroid ratio

Cytogenetics: Philadelphia chromosome (t9:22)

26
Q

What is the management for CML

A

Specific treatment: Imatinib and Dasatinib (tyrosine kinase inhibitor) act as inhibitors of BCR-ABL
Chronic phase: Hydroxyurea or IFN-𝝰, with Allupurinol to prevent hyperuricaemia and gout
Stem cell transplant: allogeneic, autogenous
Acute phase: Treat as AML/ALL

27
Q

What are the complications and prognosis of CML

A

Transformation into acute leukaemia (80% AML, 20% ALL)
Depends on age, spleen size, % blasts in blood, platelet count
Mean survival 5 years
20% survive >10yr

Y6 Derm + Onco + Haem (49 decks)

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