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Medicine: Haematology > Leukaemia > Flashcards

Leukaemia Flashcards

1
Q

What is leukaemia?

A
  1. Clonal abnormality arising from the bone marrow.

2. Group of diseases characterised by malignant overproduction of WBCs or their immature precursors.

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2
Q

What are the 4 types of leukaemia?

A
  1. Acute myeloid leukaemia (AML)
  2. Acute lymphoid leukaemia (ALL)
  3. Chronic myeloid leukaemia (CML)
  4. Chronic lymphoid leukaemia (CLL)
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3
Q

How do you distinguish between AML and ALL?

A
  1. Clinically indistinguishable

2. Need bone marrow biopsy/peripheral blood smear/immunohistochemistry for diagnosis.

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4
Q

What type of leukaemia is increased in Down’s syndrome?

A
  1. Acute megakaroblastic leukaemia <5 years

2. ALL >5 years

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5
Q

What are the general signs and symptoms seen in leukaemia?

A
  1. Unexplained lumps in body/swollen glands.
  2. Unexplained fevers, tiredness, and weight loss.
  3. Unexplained bruising, blood in urine.
  4. Unexplained headaches and vomiting.
  5. Change in bowel and bladder habits.
  6. Persistent back pains
  7. Frequent infections
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6
Q

What are the risk factors for developing leukaemia?

A

EBV, radiation, family history

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7
Q

What do the cells look like in acute leukaemia and what is the clinical presentation?

A
  1. Undifferentiated immature, arrested early, all blastic cells.
  2. Anaemia, fever, infections, haemorrhagic tendencies.
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8
Q

What do the cells look like in acute leukaemia and what is the clinical presentation?

A
  1. Differentiated mature, arrested late, see range of cells.

2. Asymptomatic, insidious onset.

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9
Q

How is leukaemia generally investigated?

A
  1. FBC and blood smear
  2. Bone marrow and immunophenotyping for diagnosis
  3. CXR for mediastinal mass and LP for CNS infiltration
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10
Q

What are the signs/symptoms associated with bone marrow infiltration in leukaemia?

A

Anaemia, thrombocytopenia, neutropenia, bone pain.

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11
Q

What are the signs/symptoms associated with extra-medullary spread of leukaemia?

A

Lymphadenopathy, hepatosplenomegaly, orthopnoea (from mediastinal mass), testicular enlargement, gingival hypertrophy.

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12
Q

What is the difference between these conditions in cell types and location?

  1. AML
  2. ALL
  3. CML
  4. CLL
A
  1. Myeloid blasts in BM and blood
  2. Lymphoblasts in BM and blood
  3. Mature myeloid cells in BM and blood
  4. Mature lymphoid cells in BM and blood
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13
Q

What is the difference between these conditions in patient groups commonly affected?

  1. AML
  2. ALL
  3. CML
  4. CLL
A
  1. Adults (50-60) 4x more than children
  2. Commonest cancer in children
  3. Ages 20-50, rare in children
  4. Most common leukaemia in adults, never in children.
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14
Q

What is the difference between these conditions in blood results?

  1. AML
  2. ALL
  3. CML
  4. CLL
A
  1. Anaemia, thrombocytopenia, neutropenia
  2. Anaemia, thrombocytopenia, neutropenia
  3. Increased granulocytes of all types, WCC very high
  4. High lymphocytes, Hb and platelets normal/low
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15
Q

What is the difference between these conditions in unique cell features?

  1. AML
  2. ALL
  3. CML
  4. CLL
A
  1. Blast cells on blood film (big with a small cytoplasm), Auer rods differentiate from ALL.
  2. Blast cells on blood film
  3. -
  4. Abundant damaged B-cells - ‘smudge cells’
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16
Q

How can you distinguish between AML and ALL?

A

AML has Auer rods, ALL does not.

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17
Q

What is the difference between AML and ALL on bone marrow aspirate?

A
  1. AML - >30% myeloblasts

2. ALL - >30% lymphoblasts

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18
Q

What is the unique genetic aspect of CML?

A

Philadelphia chromosome (9, 22 - BCR-ABL fusion) present in >80% of cases.

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19
Q

What is the difference between these conditions in presentation and symptoms?

  1. AML
  2. ALL
  3. CML
  4. CLL
A
  1. Fever, fatigue, weight loss, loss of appetite, anaemia, infection, bleeding, DIC.
  2. Fever, fatigue, anaemia, infection, pallor, petechial rash, bleeding.
  3. Symptoms chronic and insidious, weight loss, fever, sweats, tiredness.
  4. Often no symptoms.
20
Q

What is the difference between these conditions in presence of hepatomegaly, splenomegaly, and lymphadenopathy?

  1. AML
  2. ALL
  3. CML
  4. CLL
A
  1. Hepatomegaly, splenomegaly, and gum hypertrophy.
  2. Hepatomegaly, splenomegaly, and lymphadenopathy.
  3. Splenomegaly (massive) and hepatomegaly.
  4. Lymphadenopathy (non-tender, could progress to lymphoma)
21
Q

How do you investigate suspected AML?

A
  1. FBC, U&Es, LFTs, clotting
  2. Blood smear for initial clues
  3. Bone marrow aspirate and trephine biopsy for confirmation.
  4. LP for blast spread to CSF
  5. Immunotyping
  6. Myeloperoxidase - Auer rods
  7. CD13, 33 surface markers
22
Q

How do you investigate suspected CML?

A
  1. FBC, U&Es, LFTs
  2. Blood smear
  3. Bone marrow biopsy
23
Q

How do you investigate suspected CLL?

A
  1. FBC, U&Es, LFTs
  2. Blood smear
  3. Flow cytometry
24
Q

How do you investigate suspected AML?

A
  1. FBC, U&Es, LFTs, clotting
  2. Blood smear for initial clues
  3. Bone marrow aspirate and trephine biopsy for confirmation.
  4. LP for blast spread to CSF
  5. Immunotyping
  6. Tdt nuclear staining (lymphoblasts only)
  7. B-ALL most common - CD10, 19, 20
  8. T-ALL - CD2-CD8
25
Q

What are the three phases of CML?

A
  1. Chronic phase
  2. Accelerated phase - will progress to crisis in 6-18 months
  3. Blast crisis - transformation to ALL/AML
26
Q

What is the treatment for AML?

A
  1. More aggressive initial treatment and over shorter period of time compared to ALL (4-6 months)
  2. Targeted therapy with Gemtuzumab
  3. Allogenic stem cell transplant if high risk cytogenetics
27
Q

What is the treatment for ALL (phases)?

A
  1. Induction phase (4-6 weeks) - destroy leukaemia cells - dexamethasone, vincristine, asparaginase.
  2. Consolidation phase (4-12 weeks) - intensify to get rid of leftover cells.
  3. Maintenance phase (2-3 years) - mercaptopurine (daily), methotrexate (weekly), vincristine and prednisolone (monthly)
  4. Prophylaxis methotrexate into CSF for every LP and scrotal fluid throughout each phase.
28
Q

What is the treatment for CML?

A
  1. Hydroxycarbamide (drop WCC)
  2. Then BCR-ABL tyrosine kinase inhibitors (imatinib, dasatinib)
  3. If blast crisis, treat for AML/ALL.
  4. Allogenic stem cell transplant
29
Q

How do you assess the risk in acute leukaemia?

A
  1. Low risk - age 1-9, WCC <50.

2. High risk - age <1 or >10, WCC >50, Ph chromosome = intensive treatment/consider bone marrow transplant.

30
Q

What is the Rai criteria used for?

A

Staging CLL

31
Q

What is the role of dexamethasone in leukaemia?

A

Direct chemotherapy agent in haematological malignancies. Give alongside ondansetron to increase anti-emetic effect.

32
Q

What is the role of vincristine in leukaemia?

A

Stops chromosomes separating in metaphase.

33
Q

What is the role of asparaginase in leukaemia?

A

Depletes tumour cells of asparagine as they cannot synthesise their own, leads to cell death.

34
Q

What is the role of methotrexate in leukaemia?

A

Anti-folate, folate needed for DNA base synthesis.

35
Q

What is the role of mercaptopurine in leukaemia?

A

Interferes with purine synthesis.

36
Q

What are the short term side effects of chemotherapy?

A

N&V, hair loss 2-3wks after, bone marrow suppression, febrile neutropenia and septic shock, constipation/diarrhoea.

37
Q

What are the long term side effects of chemotherapy?

A

Growth, fertility, endocrine, cardiac, cataracts, psychological, second cancers.

38
Q

In what type of tumour is tumour lysis syndrome common?

A

Common during chemotherapy for rapidly proliferating tumours (leukaemia, lymphoma, myeloma).

39
Q

What is there a risk of in tumour lysis syndrome?

A
  1. Cardiac arrhythmias and seizures

2. Acute renal failure

40
Q

What are the electrolyte abnormalities in tumour lysis syndrome?

A

Raised urate, potassium and phosphate. Lowered calcium.

41
Q

What is the treatment for tumour lysis syndrome?

A
  1. Prophylactic allopurinol inhibiting uric acid production (prevent renal issues)
  2. Hyperhydration to dilute and excrete excess uric acid.
42
Q

What is SVC syndrome, how does it present, and how is it treated?

A
  1. Reduced venous return from head, neck and upper limbs due to extrinsic compression (malignancy)
  2. Orthopnoea, SOB, stridor, hypoxia.
  3. Give steroids, balloon venoplasty and SVC stenting.
43
Q

What are the complications in hyperleukocytosis?

A

Tumour lysis syndrome, cerebrovascular and pulmonary stasis.

44
Q

What is the presentation of neutropenic sepsis and how is it managed?

A
  1. Raised temperature, neutrophilia, unwell patient within 6 weeks of receiving chemotherapy.
  2. Examine central line and catheter, treat empirically with piperacillin/tazobactam (tazocin).
45
Q

What is the most common metabolic abnormality in cancer patients and why does it occur?

A
  1. Malignancy associated hypercalcaemia.

2. PTHrP production, local osteolysis.

46
Q

What is the presentation of malignancy associated hypercalcaemia?

A

Weight loss, anorexia, nausea, polydipsia, polyuria, constipation, abdominal pain, confusion.

47
Q

What is the treatment for malignancy associated hypercalcaemia?

A

Aggressive rehydration, bisphosphonates if eGFR >30.

Medicine: Haematology (18 decks)

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