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IMED2002 UWA > Leukaemia Part II > Flashcards

Leukaemia Part II Flashcards

1
Q

What is the incidence rate of Acute Myeloid Leukaemia?

A

4.1/100000 and is more common in adults

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2
Q

What causes Acute Myeloid Leukaemia? (Etiology)

A

Genotoxic exposures such as radiation and chemotherapy

History of other myeloid cancers

Genetic predisposition syndrome (Fanconi anaemia)

Idiopathic (Acquired genetic abnormalities)

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3
Q

What are the symptoms of acute myeloid leukaemia?

A

Anaemia,

lethargy,

leucopenia,

Thrombocytopaenia, infections, fevers and bleeding, (more common in AML than ALL)

bruising,

“blast” cells,

bone pain (more common in ALL than in AML),

weight loss, loss of appetite

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4
Q

What are the signs of acute myeloid leukaemia?

A

Leukaemic cutis (Skin lesion that is not tender and contains collection of blast cells) [not expected in ALL]

Gingival hyperplasia (Swelling of gums due to infiltration of blast cells here)

Conjunctival pallor (White under eyelids)

Bruises

Hepatosplenomegaly and lymphadenopathy are less common than in ALL

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5
Q

What is seen in FBC of acute myeloid leukaemia?

A

Pancytopaenia + blast cells

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6
Q

What is seen on blood film in acute myeloid leukaemia?

A

Pancytopaenia

Myeloblasts

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7
Q

What are the 4 types of myeloblastic leukaemia?

A

Acute myeloblastic leukaemia (know how this blood slide looks)

Acute promyelocytic leukaemia (know how this blood slide looks)

Acute monoblastic leukaemia

Acute erythroblastic leukaemia

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8
Q

What is the defining feature of acute myeloblastic leukaemia?

A

presence of granules and a large nucleolus

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9
Q

What is the defining feature of acute promyelocytic leukaemia?

A

Double lobed nucleus and denser granules and darker coloured nucleus and granules

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10
Q

What is the defining feature of acute monoblastic leukaemia?

A

Huge nucleus which is folded in an irregular manner and fine granules.

Grey coloured cytoplasm compared to more pink colour in normal blood slide

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11
Q

What is the defining feature of acute erythroblastic leukaemia?

A

Big nucleus big cell and lots of cytoplasm.

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12
Q

What does trephine look like for AML?

A

Hypercellular

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13
Q

What does bone marrow aspirate show in AML?

A

Myeloblasts (nucleoli, variable cytoplasm volume, numerous granules + Auer rods)

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14
Q

What are Auer rods?

A

Granules that line up

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15
Q

What is expected on Acute Myeloid Leukaemia cytometry?

A

CD13, CD14, CD117, HLA-DR, and CD34

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16
Q

Which karyotype images indicate a good prognosis for AML?

A

t (15, 17), t (8,21), t(16/16)

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17
Q

Which karyotype images indicate a good prognosis for AML?

A

t (15, 17), t (8,21), t(16/16)

t=translocation

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18
Q

Which karyotype is associated with a bad prognosis?

A

Monosomy 3, 5, and 7

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19
Q

What is the prognosis of a normal karyotype in AML?

A

Intermediate

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20
Q

What do molecular studies tell us about intermediate risk patients?

A

Whether their risk is more or less favourable

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21
Q

Does NPM1 have a good or bad prognosis?

A

Good

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22
Q

Does FLT3 have a good or bad prognosis?

A

Poor

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23
Q

How is AML treated?

A

Multiagent chemotherapy (induction and consolidation)

Allogeneic Stem Cell Transplant

Transfusion and Antimicrobial Support

24
Q

What is the 5-year survival rate of AML?

A

25%, however if acute promyelocytic leukaemia is treated it has a 90% 5-year survival rate

25
Q

Why is only consolidation and induction chemotherapy used in AML?

A

Because no evidence shows that maintenance chemo helps. (Induction 2 months, consolidation 4 months due to higher toxicity)

26
Q

How does Acute promyelocytic Leukaemia present?

A

Pancytopaenia and coagulopathy where patients blood excessively)

Blood film and Bone Marrow Analysis show excessive promyelocytes

27
Q

How is acute promyelocytic leukaemia treated?

A

Arsenic and ATRA (a vitamin A derivative)

28
Q

What does arsenic and ATRA do?

A

Forces promyelocytes to undergo maturation causing them to lyse

29
Q

What is the incidence rate of chronic myeloid leukaemia?

A

1 - 2/100000 in middle aged patients (slight male predominance)

30
Q

What are the symptoms of chronic myeloid leukaemia?

A

Often asymptomatic (incidental finding on blood tests) but sometimes presents as leucocytosis and thrombocytosis as well as fatigue, malaise, bleeding, and bruising.

31
Q

What are the signs of chronic myeloid leukaemia?

A

Enlarged liver and spleen

32
Q

What does full blood count show in CML?

A

Increase in number of most WBCs (neutrophils, eosinophils, monocytes, basophils, and myeloid cells at differnet stages of maturation)

33
Q

What does trephine show in CML?

A

Hypercellularity

34
Q

What translocation is characteristic in CML karyotype?

A

t (9,22) [philadelphia chromosome]

35
Q

What is labelled in FISH study to diagnose CML? How is the diagnosis confirmed?

A

ABL1 on chromosome 9

BCR on chromosome 22

Seeing a fusion between these 2 chromosomes indicates presence of a Philadelphia chromosome

36
Q

What happens when the Philadelphia chromosome expresses the gene in between both chromosomes?

A

A fusion protein Bcr-Abl is made which binds to ATP and can increase number of leukaemic cells indefinitely

37
Q

How is CML treated?

A

Tyrosine Kinase Inhibitor (Imatinib, Dasatinib, Nilotinib, and Ponatinib)

Allogenic Stem Cell Transplant

38
Q

What is the 5-year survival rate of CML before and after using tyrosine kinase inhibitor?

A

Pre-TKI 5 -year survival rate = 45%

Post-TKI 5-year survival rate = 90%

39
Q

How do the “-tinib” drugs treat CML?

A

They block ATP binding to Bcr-Abl protein which results in gene being switched off which switches off the entire leukaemia project. This drug must be used permanently.

40
Q

What is the incidence rate of Chronic Lymphocytic leukaemia?

A

6.75/100000 (most common in elderly that are >60 years old and slgihtly more predominant in males)

[occurs in 3% of elderly population]

41
Q

Which cells typically causes Chronic Lymphocytic Leukaemia?

A

B lymphocytes

42
Q

What are the symptoms of CLL?

A

Anaemia

Lymphocytosis (B symptoms)

Neutropenia

Thrombocytopaenia

Fevers, night sweats, and weight loss

Bleeding, bruising

Infections, fevers

Lethargy

43
Q

What are the signs of CLL?

A

Hepato+splenomegaly

Lymphadenopathy (large lymph nodes)

May affect tonsils and salivary glands

44
Q

What shows up on FBC of CLL?

A

Lymphocytosis with or without cytopaenia

45
Q

What shows up on blood film in CLL?

A

Lymphocytosis + smear cells

46
Q

What is a smear cell?

A

Cell in process of apoptosis

47
Q

What is seen in trephine of CLL?

A

Nodular infiltration

48
Q

What is seen in bone marrow aspirate of CLL?

A

a large number of mature lymphocytes

49
Q

How can ALL and CLL be told apart on a blood film?

A

ALL has granule

Nucleoli in ALL (immature formed cells)

Mature cells in CLL compared to immature in ALL

50
Q

How can ALL and CLL be told apart on a blood film?

A

ALL has granule

Nucleoli in ALL (immature formed cells)

Mature cells in CLL compared to immature in ALL

More closely packed in CLL compared to ALL

More pancytopaenia in ALL compared to CLL

51
Q

What is seen in flow cytometry of CLL?

A

Since mostly B cells we see B cell markers such as CD19, CD20, CD45. HLA-DR

Aberrant T-lymphocyte expresion: CD5

Special expressions: CD23, CD200

52
Q

What are cytogenetic studies used for in CLL?

A

For prognosis:

trisomy 12, del 13q = good prognosis

del 11q and del 17p = bad prognosis

53
Q

When is treatment used for CLL?

A

Treatment might not be needed at diagnosis unless there are symptoms and cytopaenia.

54
Q

How is CLL treated?

A

Multiagent chemo

Anti-CD20 antibodies (rituximab)

Small molecule inhibitors (venetoclax)

55
Q

What is the 5 year survival rate of CLL?

A

85%

56
Q

What does venetoclax act on?

A

Inhibits Bcl2 which is an antiapoptotic peptide

IMED2002 UWA (29 decks)

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