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Phase 4 Haematology > Myeloid disorders and Leukaemia > Flashcards

Myeloid disorders and Leukaemia Flashcards

1
Q

What are two pre-leukaemic conditions?

A

Myelodysplastic syndrome,
Myeloproliferative disease

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2
Q

What is myelodysplastic syndrome?

A

Clonal stem cell disorders characterised by ineffective hamatopoiesis, peripheral blood cytopenia and risk of progression to AML.

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3
Q

What is the presentation of MDS?

A

Anaemia (fatigue, pallor and SOB),
Neutropenia (frequent or severe infections),
Thrombocytopenia (bleeding and purpura)

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4
Q

What is the diagnosis and treatment of MDS

A

Diagnosis - blood film which may show blasts and bone marrow biopsy.
Treatment - Watch and wait, supportive, erythropoiein, granulocyte colony-stimulating factor, chemotherapy and allogenic stem cell transplant (potentially curative)

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5
Q

What are myeloproliferative disorders and some examples and mutations.

A

Uncontrolled proliferation of a single type of stem cell. Examples include:
Primary myelofibrosis (low Hb, Low or high WCC and platelet count),
Polycytheaema vera,
Essential thrombocythaemia,
Mutations found: JAK2,

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6
Q

Describe features of myelofibrosis

A

It results in bone marrow fibrosis which affects the production of blood cells. Production of blood cells starts happening elsewhere in the liver, spleen and spine. Presents with constituitonal symptoms, marro failure, bone pain, splenomegaly, hepatomegaly

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7
Q

What is the presentation of myelofibrosis?

A

Non specific symptoms: Fatigue, weight loss, night sweats, fever.
Anaemia,
Splenomegaly,
Portal hypertension,
Low platelets and low WCC,
Raised Hb,
Gout

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8
Q

What is the blood film presentation of myelofibrosis?

A

Anisocytosis (varying sized cells)
Teardrop shaped RBCs,
Blasts

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9
Q

What are the clinical signs of polycythaemia?

A

Ruddy complexion,
Conjucnctival plethora (opposite of conjunctival pallor),
Splenomegaly,
Hypertension

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10
Q

How do you diagnose myeloproliferative disorders

A

Bone marrow biopsy. In myelofibrosis this can appear dry.
Testing for JAK2 mutations

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11
Q

What is the management of myelofibrosis?

A

Watch and wait if asymptomatic,
Supportive management of complications,
Chemotherapy,
JAK2 inhibitors (ruxolitinib)
Allogenic stem cell transplant

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12
Q

What is the presentation and management of polycythaemia?

A

Presentation - Pruritis, splenomegaly, hypertension, hyperviscosity, haemorrhage, low ESR.
Management - Venesection (keep Hb in normal), aspirin and chemotherapy

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13
Q

What is the management of essential thrombocytopenia?

A

Aspirin,
Chemotherapy eg, hydroxycarbamide,
Anagrelide

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14
Q

What are the four main types of leukaemia and their differentiating factors?

A

Acute myeloid leukaemia - Auer rods.
Acute lymphoblastic leukaemia - Most common in children, associated with downs.
Chronic myeloid leukaemia - three phases, associated with philadelphia chromosome.
Chronic lymphocytic leukaemia - warm haemolty

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15
Q

What is the presentation of acute lymphoblastic leukaemia?

A

Anaemia: Lethargy and pallor,
Neutropenia: frequent/severe infections,
Thrombocytopenia: easy bruising. petechiae
Bone pain (limping child),
Lymphadenopathy,

Splenomegaly,
Hepatomegaly,
Fever,
Testicular swelling.

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16
Q

What are the differentials of petechiae?

A

Leukaemia,
Meningococcal septicaemia,
Vasculitis,
Henoch schonlein purpura,
ITP/TTP

17
Q

Explain the diagnosis of acute lymphoblastic leukaemia

A

FBC: Anaemia, high WCC (in 50%), thrombocytopenia.
U&Es, LFTs, (importent for baseline) LDH (elevated)
Blood film: Blasts.
Bone marrow aspirate and trephine biopsy ALL diagnosed if >20% cells are lymphoblasts
CT/PET for staging.
Others: Immunphenotyping (CD10), cytogenetics, molecular (philadelphia chromosome)

18
Q

What is the management of ALL?

A

Steroids and aggressive chemotherapy. For relapsed patient’s, can use CAR T.
Supportive care: Blood transfusions, FFP, antibiotics granulocyte growth factor

19
Q

What are the indications for a stem cell transplant in acute leukaemia

A
  • Relapsed patients,
  • Those with high risk molecular profile,
  • Age less than 60 years,
  • Good performance (fit enough for the procedure)
20
Q

What are poor prognostic factors for ALL?

A

Age < 2 or >10.
WCC > 20
T or B cell surface markers,
Non-caucasian,
Male sex

21
Q

Describe features of acute myeloid leukaemia and its poor prognostic factors

A

Presentation: Anaemia, neutropenia (may have high (WCC), thrombocytopenia, bone pain, hepatosplenomegaly, gym swelling.
Poor prognostic factors: > 60 years, >20% blasts after first round of chemo, deletion of chromosome 5 or 7.
Can develop from MDS

22
Q

Describe features of acute promyelocytic leukaemia

A

It is associated with t(15:17) and presents in younger patients. It is important as there is a high risk of DIC, treat with all-trans-retinoic acid. However has good prognosis.
Blood film: Auer rods

23
Q

What is the presentation of chronic lymphocytic leukaemia?

A

Often none. Can present with:
Constitutional symptoms: anorexia, weight loss.
Bleeding,
Infections,
Lymphadenopathy

24
Q

What are the investigations for CLL?

A

FBC: lymphocytosis, anaemia (can be secondary to AIHA), thrombocytopenia.
Blood film: Smudge/smear cells.
Immunophenotyping via flow cytometry is key. Shows surface markers on malignant cells.

25
Q

What is the clinical staging of chronic leukaemia?

A

Stage A - Less than 3 involved nodes (survival 10yrs)
Stage B - More than 3 involved nodes, liver and spleen (survival 7yrs)
Stage C - Anaemia or thrombocytopenia (2 yrs)

26
Q

What are some complications that can arise with CLL?

A

Autoimmune haemolytic anaemia or Autoimmune thrombocytopenia, Treat with steroids.
Richter’s transformation - CLL into high-grade B cell lymphoma.

27
Q

What are symptoms of Richter’s transformation?

A

Patient’s become unwell very suddenly
Lymph node swelling,
Fever without infection,
Weight loss,
Night sweats,
Nausea,
Abdominal pain.

28
Q

What are the features of Chronic myeloid leukaemia?

A

Genetics: BCR-ABL defect on philadelphia chromosome t(9:22)
Presentation: anaemia, weight loss and sweating, massive splenomegaly, thombocytosis, neuro deficits due to hyperviscosity, gout and may undergo transformation

29
Q

What are the different phases of CML?

A

Chronic phase: asymptomatic, may have raised WCC.
Accelerated phase: More symptomatic, have anaemia, thrombocytopenia and immunedeficiency.
Blast phase: Blasts account for > 20%, severe symptoms and fatal

30
Q

What is the diagnosis and treatment of CML?

A

Diagnosis - Blood films and clinical features, Molecular testing (FISH) to identify BCR-ABL mutation which can occur on a Philadelphia chromosome (if BCR-ABL negative then not CML). Cytogenetic analysis (karyotyping)
Treatment - Imatinib (tyrosine kinase inhibitor) others: allogenic bone marrow transplant.

31
Q

What is tumour lysis syndrome?

A

Occurs when chemicals are released from dead cancer cells. It causes high uric acid, high potassium, high phosphate an low calcium

32
Q

What are the complications and treatment for tumour lysis syndrome?

A

Dysuria, abdo pain, weakness, nausea and vomiting, muscle cramps, seizures, cardiac arrhythmias, gout.
Treat - Allopurinol or rasburicase

33
Q

When is a bone marrow transplant indicated?

A

High cytogenetic risks,
Lack of remission after induction chemo,
High initial leukocyte count

Phase 4 Haematology (10 decks)

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