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M104 Symposia > Leukaemia symposiu > Flashcards

Leukaemia symposiu Flashcards

1
Q

What is the role of G-CSF?

A

it promotes neutrophils maturation

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2
Q

What are the genetic causes of cancer?

A

oncogenes and TSGs

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3
Q

What is the role of G-CSF?

A

it stimulates the bone marrow to produce more neutrophils

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4
Q

What are the epigenetic causes of cancer?

A

dysregulated gene expression and aberrant DNA methylation

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5
Q

What is the role of the proto-oncogene?

A

regulates normal cell division

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6
Q

What is the effect of mutations or recombination affecting a proto-oncogene?

A

can become a cancer-causing oncogene

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7
Q

What are the clinical features of Myeloproliferative disorders?

A

myelofibrosis (then splenomegaly)
polycythemia rubra vera
Essential thrombocythemia

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8
Q

What happens in Myeloproliferative disorders?

A

the over production of blood cells and platelets

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9
Q

What condition does myelofibrosis lead to?

A

splenomegaly

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10
Q

What are examples of processes that the JAK-STAT signaling pathway is involved in?

A

immunity, tumour formation

cell division, cell death

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11
Q

What are chronic myeloproliferative disorders otherwise known as?

A

myeloproliferative neoplasms

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12
Q

What do chronic myeloproliferative disorders have in common?

A

they are all part of a unique group of hematopoietic stem cell disorders
they share common mutations which continuously activate JAK2

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13
Q

What is the role of the JAK2 gene?

A

to provide instructions for making a protein that promotes cell proliferation

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14
Q

How does polycythemia rubra vera develop?

A

bone marrow stem cell undergoes an acquired abnormality
develop into RBC precursors
95% of which undergo a mutated JAK2

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15
Q

How does Essential thrombocythemia develop?

A

bone marrow stem cell undergoes an acquired abnormality
develop into megakaryocytes
50% of which undergo a mutated JAK2

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16
Q

How does primary myelofibrosis develop?

A

bone marrow stem cell undergoes an acquired abnormality
develop into megakaryocytes
reactive fibrosis occurs
there is a mutated JAK2 in 56%

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17
Q

What is the chance that polycythemia rubra vera will develop into Acute Myeloid Leukaemia?

A

5%

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18
Q

What is the chance that PVR will develop into primary myelofibrosis?

A

30%

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19
Q

What is the chance that Essential thrombocythemia will develop into primary myelofibrosis?

A

10 - 20%

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20
Q

What is the chance that primary myelofibrosis will develop into Acute Myeloid Leukaemia?

A

10%

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21
Q

What is the Jak-STAT signalling pathway important for?

A

erythropoietin to make more RBCs/ neutrophils

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22
Q

What is the effect of the JAK2 V617F mutation?

A

it causes the JAK-STAT signaling pathway to be switched on more
All able to develop to AML

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23
Q

What percentage of patients with PV will have the JAK2 V617F mutation?

A

nearly 100%

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24
Q

What percentage of patients with essential thrombocytosis and primary myelofibrosis will have the JAK2 V617F mutation?

A

about 50%

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25
Q

How is JAK2 activated?

A

by phosphorylation

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26
Q

What are the two different types of JAK2 V617F mutations?

A

homozygous and heterozygous

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27
Q

How does JAK2 result in cell survival and proliferation?

A

the activation of JAK2 results in the production of STAT, RAS and PI3K

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28
Q

What substance is produced by PI3K?

A

Akt

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29
Q

What occurs once RAS is produced?

A

the ERK/MAPK signalling pathway

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30
Q

What substance is produced from Akt and the ERK/MAPK signalling pathway?

A

transcription factors

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31
Q

What terms are associated with ERK?

A

a type of serine/threonine protein kinase

a signal transduction protein that transmits mitogen signals

32
Q

Where is ERK located in cells?

A

generally located in the cytoplasm

on activation, it enters the nucleus

33
Q

What role does ERK carry out in the nucleus?

A

it regulates transcription factor activity and gene expression

34
Q

What is the role of the ERK/MAPK signalling pathway?

A

regulates cell growth, development and division

35
Q

What is the role of the ERK/MAPK signalling pathway?

A

regulates cell growth, development and division

36
Q

What are the roles of STATs?

A

to bind to DNA and allow the transcription of genes involved in immune cell division, survival, activation and recruitment

37
Q

What are the roles of STATs?

A

to bind to DNA and allow the transcription of genes involved in immune cell division, survival, activation and recruitment

38
Q

What is the Philadelphia chromosome (22) caused by?

A

translocation causing longer 9 and shorter 22

39
Q

What is BCR-ABL formed by?

A

the combination of two genes BCR and ABL

40
Q

What is BCR-ABL otherwise known as?

A

fusion gene

41
Q

Which CMS is the BCR gene normally on?

A

CMS 22

42
Q

Which CMS is the ABL gene normally on?

A

CMS 9

43
Q

What is the role of Imatinib?

A

it binds to abl kinase and blocks its activity and normalises blood counts

44
Q

What can CML sometimes transform into?

A

AML

45
Q

What does acute myeloid leukaemia involve?

A

the uncontrolled proliferation of primitive cells in bone marrow

46
Q

What is the effect of acute myeloid leukaemia?

A

bone marrow failure - anaemia, infections and excessive bleeding

47
Q

What is the effect of acute myeloid leukaemia?

A

bone marrow failure - anaemia, infections and excessive bleeding

48
Q

What are the clinical features of leukaemia?

A

anaemia, infections
DIC, ulcers
infiltration, bruises

49
Q

What are the three different parts of bone?

A

marrow
spongy bone
cortical bone

50
Q

How is AML treated?

A 
Chemotherapy
Combination regimes
Myeloablative treatments
Supportive
Allogenic stem cell transplantation
Transfusion of RBC, platelets and cryo/FFP
51
Q

What is the effect of Chemotherapy?

A

it kills rapidly dividing cells

52
Q

How does Myeloablative stem cell transplant destroy cancer cells?

A

it uses high doses of chemotherapy and may use radiation therapy

53
Q

What is a side effect of Myeloablative stem cell transplant treatment?

A

healthy bone marrow / stem cells are destroyed

54
Q

How is healthy bone damage from Myeloablative stem cell transplant treatment countered?

A

patients receive an infusion of new stem cells to rebuild blood and the immune system.

55
Q

What does an allogenic stem cell transplantation involve?

A

transferring the stem cells from a healthy, matched donor’s allograft to the patient’s body after high-intensity chemotherapy or radiation

56
Q

What are examples of Supportive treatments for APL?

A

antibiotics and antifungals

blood transfusions to reduce infections

57
Q

What is an allograft otherwise known as?

A

homograft

58
Q

What are the chances that a sibling is a match for an allogenic transplantation?

A

1 in 4 chance but usually an unrelated donor

59
Q

What are other terms for symptomatic treatment?

A

supportive care

supportive therapy

60
Q

What are the features of Cd34+ hematopoietic progenitor cells?

A

they are multipotential - self-renewal

they can produce mature blood cells

61
Q

What might occur as a result of allogenic stem cell transplantation?

A

Opportunistic infections

Neutrophinic sepsis

62
Q

What are the features of Neutrophinic sepsis?

A

a temperature of 38°C +

any symptoms and/or signs of sepsis, in a person with an absolute neutrophil count of 0.5 x 109/L or lower

63
Q

What is the maximum absolute neutrophil count in a patient with Neutrophinic sepsis?

A

0.5 x 109/L or lower

64
Q

How is a patient managed when there is a high risk of death due to previous chemo in neutrophinic septic patients?

A

1st line – Tazocin +/- Gentamicin
2nd line – Switch to Meropenem +/- Teicoplanin
3rd line – Add anti-fungal, may need ITU

65
Q

What type of bacterial infection makes for the most dangerous kind of Neutrophinic sepsis?

A

grM -VE

66
Q

What is the first line of treatment for neutrophinic septic patients?

A

Tazocin +/- Gentamicin

67
Q

What is the second line of treatment for neutrophinic septic patients?

A

Switch to Meropenem +/- Teicoplanin

68
Q

What is the third line of treatment for neutrophinic septic patients?

A

add anti-fungal e.g. Ambisome (Amphotericin)

69
Q

What are the two types of Tazocin drugs that can be taken for neutrophinic septic patients?

A

Piperacillin / Tazobactam

70
Q

When is Teicoplanin used for second line neutrophinic septic patients?

A

when it is Gram +ve bacteria causing the sepsis

71
Q

What is an example of an anti-fungal?

A

Ambisome (Amphotericin)

72
Q

What is a fungal infection that can arise from allogenic stem cell transplantation?

A

Pneumocystis pneumonia

73
Q

What are the effects if the graft rejects the host?

A

rashes, diarrhoea, depleted liver function

74
Q

How is graft rejection treated?

A

immunosuppressants - ciclosporin

75
Q

What causes AML?

A

multi gene mutations

Mainly DNMT3A methyltransferase mutation

76
Q

How is leukaemia cured?

A

if all the leukemic stem cells are eradicated

M104 Symposia (11 decks)

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