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Malignant haematology > Acute myeloid leukaemia > Flashcards

Acute myeloid leukaemia Flashcards

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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

Study These Flashcards
A

Hyperphosphatemia
Hyperkalemia
hyperuricaemia
Hypocalcemia

22
Q

What test confirms AML

Study These Flashcards
A

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

22
Q

Tests for AML

Study These Flashcards
A

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

23
Q

Immunophenotyping in AML

Study These Flashcards
A

CD13, CD33, CD34, CD117 + HLA-DR

24
How is cryogenetics carried out
conventional karyotypic analysis plus reverse transcriptase polymerase chain reaction (RT-PCR) or fluorescent in situ hybridization (FISH).
25
What can confirm AML on cryogenetics
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
What suggests AML in molecular studies
abnormalities in specific genes FLT3, NPM1, KIT, CEBPA, IDH1 and IDH2, p53, or RUNX1.
27
How differentiate from ALL
ALL is terminal deoxynucleotidyl transferase - TdT positive
28
What is considered complete remission from AML
<5% blast cells in bone marrow or peripheral blood
29
What type of AML is a medical emergency
Acute promyelocytic leukaemia
30
Treatment for acute promyelocytic leukaemia
Haematologicemergency -> 4U FFP correct DIC THEN All trans retinoic acid - ATRA and arsenic Induce maturaion of immature malignant cells
30
What determines the choice of chemotherapy
Cytogenetics
30
What are most commonly used chemotherapy drugs? Add ins for specific mutatinos?
Cytarabine and anthracyclines (daunorubicin) Midostaurin Ivosidenib Enasidenib
31
When use haematopoeitic cell transplantation in AML
Unfavourable prognostic factors eg cytogenetics OR remission not achieved through chemotherapy
32
Supportive treatment after HCT
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
What use to prevent PCP in neutropenic patients
Trimethoprim-sulfamethazole
34
Complications of AML
Tumour lysis syndrome Leukostasis DIC sev neutropenia Sev anaemia VTE
35
What is tumour lysis syndrome
After cytotoxi therapy Rapid destructiont umour cells -> massive release of IC componenets eg K+, PO4-, nucleic acids -> circulation
36
Lab featires of tumour lysis syndrome
Hyperkalaemia Hyperphosphatemia Hypoclacemia - phosphate bind Hyperuricaemai - nucleic acid -> uric acid
37
Clinical features of tumour lysis syndrome
N+V, diarrhoea Lethargy Haematuria Seizures, arrhtyhmoas Tetany, muscle cramps, paraesthesisa AKI - CaPo4 crystals and urate
38
What is leukostasis
Excessive leukaemic cellls >50 -> blood viscosity Resp or neuro distress
39
Clinical features of leukostasis
Chest pain Headahce Altered mental status Priapism
40
When is neutropenia svere
<500 eg<0.5
41
Sev thrombocytopenia
<10,000 u/L or active bleeding
42
When does VTE in AML most commonly occur
First 3 months of treatment
43
Clinical characteristics w favourable prognosis AML
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
Cytogenetic features favourabole AML
MDR 1-negative phenotype Translocations: t (8;21), inv (16), t (16;16), t (15;17) NPM1 mutation, CEBPA mutation
45
What is the five year survival with AML
24%
46
Who gets AML
Toward the elderly
47
What causes acute promyelocytic leukaemia
t15:17 mutation
48
Acute treatment APML
Infection broad antibiotics Transfus blood and plateltes Haematology- chemo, bone marrow transplant

Malignant haematology (16 decks)

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