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Malignant haematology > Acute myeloid leukaemia > Flashcards

Acute myeloid leukaemia Flashcards

1
Q

What is acute myeloid leukaemia

A

Bone marrow malignancy of myeloid cells causing immature cells arrested in development -> blood, impair haematopoiesis -> anaemia, bleeding, infections
Blast accumulation -> bone marrow failure

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2
Q

Genetic diseases ass w AML

A

Downs syndrome, Fanconi anaemia, Bloom syndrome

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3
Q

What genetics are ass w AML

A

FLT3, NPM1, CEBPA, RUNX1 mutations

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4
Q

Environemental factors ass w AML

A

Chemicals and radiation esp benzene and other petroleum products
Ionising radiation eg atomic bomb, therapeutic radiation

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5
Q

What lifestyle factor increases AML risk

A

Smoking
Dose dependent
Decreases after cessation

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6
Q

What treamtnet esp increases AML risk

A

Chemotherapy esp alkylating agents and topoisomerase II inhibtprs

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7
Q

WHat disroders increase risk of AML

A

Myedodysplastic sundrome or chronic myeloproliferative disorders

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8
Q

What is the first hit AML

A

First hit - mutation - proliferative advantage -> clonap expansion of haematopoietic stem cell in FLT3, NPM1, DNMT3A

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9
Q

What is second hit AML genes and how

A

Mutation in one of clonally expanded cells from first mutation affecting gene in haemtopoietic differntiation -> proliferation and blocking differntiation -> accumulation of immature blasts
RUNX1 or CEBPA

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10
Q

How do immature blasts cause bone marrow failure

A

Prevent normal haematopoiesis

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11
Q

WHO classification of AML tpyes

A

AML with recurrent genetic abnormalities
AML with myelodysplasia-related features
Therapy-related AML and MDS
AML, not otherwise specified
Myeloid sarcoma
Myeloid proliferations related to Down syndrome

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12
Q

AML subtypes in FAB classification

A

M0: Acute myeloblastic leukaemia without maturation
M1: Acute myeloblastic leukaemia with minimal granulocyte maturation
M2: Acute myeloblastic leukaemia with granulocyte maturation
M3: Acute promyelocytic leukaemia (APL)
M4: Acute myelomonocytic leukaemia
M5: Acute monocytic leukaemia
M6: Acute erythroid leukaemia
M7: Acute megakaryoblastic leukaemia

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13
Q

Clinical features of AML

A

Fever
Anaemia
Thrombocytopenia (ecchymoses, petechiae, musocal bleeds)
Coagulopathy
Bone pain
Leukaemia cutis
Gingival hypertrophy
CNS involvement
Organomegaly

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14
Q

Clinical history with AML

A

Frequent infections/fever
SOB, palpitations, weakness, fatigue, dizziness, pallor
TP - ecchymoses, petechiae, gingival bleed, epistacxis, menorrhagie
DIC - bleedng (only APML)
Bone pain - sternal discomfort, aching in extermitis
Nodular violaceous lesions on skin, gingival hypertrophy in Amonocytic or myelomonocytic
CNS involve - headahce, visual chnages, nerve palsies
Adenopathy, hepatomegaly, splenomegaly

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15
Q

What causes bone pain in AML

A

Expansion of medullary cavity by leukaemic process

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16
Q

FBC w AML

A

Normocytic, normochromic anaemia
Thrombocytopenia
Leucocyte count - low, normal or raised

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17
Q

What is seen on peripheral blood smear in AML

A

Raised myeloblasts
Auer rods

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18
Q

What do myeloblasts look like on blood smear

A

Immature cells w large nuclei, prominenet nucleoli pale bkue cytoplasm w Wright Giemsa stain

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19
Q

What are auer rods and how look on film and what mainly seen in

A

Pink/red rod shaped cytoplasmic granular inclusions
Myeloperoxidase positive
Pathogonimic of myeloblasts
Mostly seen in acute promyelocytic leukaemia

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20
Q

What is unique to acute promyelocytic leukaemia

A

Bleeding secondary to DIC much more common than other AMLs

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21
Q

What electrolyte abnormalities are seen with increasing cell lysis in AML

A

Hyperphosphatemia
Hyperkalemia
hyperuricaemia
Hypocalcemia

22
Q

What test confirms AML

A

Bone marrow aspiration and biospy
>20% myeblasts in bone marrow = confirmed

22
Q

Tests for AML

A

Bone marrow aspiration and biopsy
FBC, coag, U+Es, LFTs
Blood smear
Immunophenotyping
Cytogenic features
Molecular studies

23
Q

Immunophenotyping in AML

A

CD13, CD33, CD34, CD117 + HLA-DR

24
Q

How is cryogenetics carried out

A

conventional karyotypic analysis plus reverse transcriptase polymerase chain reaction (RT-PCR) or fluorescent in situ hybridization (FISH).

25
Q

What can confirm AML on cryogenetics

A

The abnormalities like: t (8;21)(q22;q22), inv (16)(p13;q22), t (16;16)(p13;q22), and t (15;17)(q22;q12), define AML irrespective of the blast count.

26
Q

What suggests AML in molecular studies

A

abnormalities in specific genes FLT3, NPM1, KIT, CEBPA, IDH1 and IDH2, p53, or RUNX1.

27
Q

How differentiate from ALL

A

ALL is terminal deoxynucleotidyl transferase - TdT positive

28
Q

What is considered complete remission from AML

A

<5% blast cells in bone marrow or peripheral blood

29
Q

What type of AML is a medical emergency

A

Acute promyelocytic leukaemia

30
Q

Treatment for acute promyelocytic leukaemia

A

Haematologicemergency -> 4U FFP correct DIC THEN
All trans retinoic acid - ATRA and arsenic
Induce maturaion of immature malignant cells

30
Q

What determines the choice of chemotherapy

A

Cytogenetics

30
Q

What are most commonly used chemotherapy drugs? Add ins for specific mutatinos?

A

Cytarabine and anthracyclines (daunorubicin)
Midostaurin
Ivosidenib
Enasidenib

31
Q

When use haematopoeitic cell transplantation in AML

A

Unfavourable prognostic factors eg cytogenetics
OR remission not achieved through chemotherapy

32
Q

Supportive treatment after HCT

A

Antibiotic prophylaxis - IV braod spec - febrile neutropenia
Trimethoprim-sulfamethoxazole for PCP if neutropenic
Imunisations
Hygeine
Surveillance
Nutritional support
Antiemetics - ondanestron
Transfusions for sev anaemia, thrombocytopenia

33
Q

What use to prevent PCP in neutropenic patients

A

Trimethoprim-sulfamethazole

34
Q

Complications of AML

A

Tumour lysis syndrome
Leukostasis
DIC
sev neutropenia
Sev anaemia
VTE

35
Q

What is tumour lysis syndrome

A

After cytotoxi therapy
Rapid destructiont umour cells -> massive release of IC componenets eg K+, PO4-, nucleic acids -> circulation

36
Q

Lab featires of tumour lysis syndrome

A

Hyperkalaemia
Hyperphosphatemia
Hypoclacemia - phosphate bind
Hyperuricaemai - nucleic acid -> uric acid

37
Q

Clinical features of tumour lysis syndrome

A

N+V, diarrhoea
Lethargy
Haematuria
Seizures, arrhtyhmoas
Tetany, muscle cramps, paraesthesisa
AKI - CaPo4 crystals and urate

38
Q

What is leukostasis

A

Excessive leukaemic cellls >50 -> blood viscosity
Resp or neuro distress

39
Q

Clinical features of leukostasis

A

Chest pain
Headahce
Altered mental status
Priapism

40
Q

When is neutropenia svere

A

<500
eg<0.5

41
Q

Sev thrombocytopenia

A

<10,000 u/L or active bleeding

42
Q

When does VTE in AML most commonly occur

A

First 3 months of treatment

43
Q

Clinical characteristics w favourable prognosis AML

A

Age < 50 years
ECOG performance status score < 3 or a Karnofsky score >60 %.
No comorbidities
No previous/causative myelodysplastic syndrome or myeloproliferative neoplasm
No history of exposure to cytotoxic agents and radiation therapy

44
Q

Cytogenetic features favourabole AML

A

MDR 1-negative phenotype
Translocations: t (8;21), inv (16), t (16;16), t (15;17)
NPM1 mutation, CEBPA mutation

45
Q

What is the five year survival with AML

A

24%

46
Q

Who gets AML

A

Toward the elderly

47
Q

What causes acute promyelocytic leukaemia

A

t15:17 mutation

48
Q

Acute treatment APML

A

Infection broad antibiotics
Transfus blood and plateltes
Haematology- chemo, bone marrow transplant

Malignant haematology (16 decks)

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