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M104 Symposia > Leukaemia symposiu > Flashcards

Leukaemia symposiu Flashcards

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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
How is JAK2 activated?
by phosphorylation
26
What are the two different types of JAK2 V617F mutations?
homozygous and heterozygous
27
How does JAK2 result in cell survival and proliferation?
the activation of JAK2 results in the production of STAT, RAS and PI3K
28
What substance is produced by PI3K?
Akt
29
What occurs once RAS is produced?
the ERK/MAPK signalling pathway
30
What substance is produced from Akt and the ERK/MAPK signalling pathway?
transcription factors
31
What terms are associated with ERK?
a type of serine/threonine protein kinase | a signal transduction protein that transmits mitogen signals
32
Where is ERK located in cells?
generally located in the cytoplasm | on activation, it enters the nucleus
33
What role does ERK carry out in the nucleus?
it regulates transcription factor activity and gene expression
34
What is the role of the ERK/MAPK signalling pathway?
regulates cell growth, development and division
35
What is the role of the ERK/MAPK signalling pathway?
regulates cell growth, development and division
36
What are the roles of STATs?
to bind to DNA and allow the transcription of genes involved in immune cell division, survival, activation and recruitment
37
What are the roles of STATs?
to bind to DNA and allow the transcription of genes involved in immune cell division, survival, activation and recruitment
38
What is the Philadelphia chromosome (22) caused by?
translocation causing longer 9 and shorter 22
39
What is BCR-ABL formed by?
the combination of two genes BCR and ABL
40
What is BCR-ABL otherwise known as?
fusion gene
41
Which CMS is the BCR gene normally on?
CMS 22
42
Which CMS is the ABL gene normally on?
CMS 9
43
What is the role of Imatinib?
it binds to abl kinase and blocks its activity and normalises blood counts
44
What can CML sometimes transform into?
AML
45
What does acute myeloid leukaemia involve?
the uncontrolled proliferation of primitive cells in bone marrow
46
What is the effect of acute myeloid leukaemia?
bone marrow failure - anaemia, infections and excessive bleeding
47
What is the effect of acute myeloid leukaemia?
bone marrow failure - anaemia, infections and excessive bleeding
48
What are the clinical features of leukaemia?
anaemia, infections DIC, ulcers infiltration, bruises
49
What are the three different parts of bone?
marrow spongy bone cortical bone
50
How is AML treated?
``` Chemotherapy Combination regimes Myeloablative treatments Supportive Allogenic stem cell transplantation Transfusion of RBC, platelets and cryo/FFP ```
51
What is the effect of Chemotherapy?
it kills rapidly dividing cells
52
How does Myeloablative stem cell transplant destroy cancer cells?
it uses high doses of chemotherapy and may use radiation therapy
53
What is a side effect of Myeloablative stem cell transplant treatment?
healthy bone marrow / stem cells are destroyed
54
How is healthy bone damage from Myeloablative stem cell transplant treatment countered?
patients receive an infusion of new stem cells to rebuild blood and the immune system.
55
What does an allogenic stem cell transplantation involve?
transferring the stem cells from a healthy, matched donor's allograft to the patient’s body after high-intensity chemotherapy or radiation
56
What are examples of Supportive treatments for APL?
antibiotics and antifungals | blood transfusions to reduce infections
57
What is an allograft otherwise known as?
homograft
58
What are the chances that a sibling is a match for an allogenic transplantation?
1 in 4 chance but usually an unrelated donor
59
What are other terms for symptomatic treatment?
supportive care | supportive therapy
60
What are the features of Cd34+ hematopoietic progenitor cells?
they are multipotential - self-renewal | they can produce mature blood cells
61
What might occur as a result of allogenic stem cell transplantation?
Opportunistic infections | Neutrophinic sepsis
62
What are the features of Neutrophinic sepsis?
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
What is the maximum absolute neutrophil count in a patient with Neutrophinic sepsis?
0.5 x 109/L or lower
64
How is a patient managed when there is a high risk of death due to previous chemo in neutrophinic septic patients?
1st line – Tazocin +/- Gentamicin 2nd line – Switch to Meropenem +/- Teicoplanin 3rd line – Add anti-fungal, may need ITU
65
What type of bacterial infection makes for the most dangerous kind of Neutrophinic sepsis?
grM -VE
66
What is the first line of treatment for neutrophinic septic patients?
Tazocin +/- Gentamicin
67
What is the second line of treatment for neutrophinic septic patients?
Switch to Meropenem +/- Teicoplanin
68
What is the third line of treatment for neutrophinic septic patients?
add anti-fungal e.g. Ambisome (Amphotericin)
69
What are the two types of Tazocin drugs that can be taken for neutrophinic septic patients?
Piperacillin / Tazobactam
70
When is Teicoplanin used for second line neutrophinic septic patients?
when it is Gram +ve bacteria causing the sepsis
71
What is an example of an anti-fungal?
Ambisome (Amphotericin)
72
What is a fungal infection that can arise from allogenic stem cell transplantation?
Pneumocystis pneumonia
73
What are the effects if the graft rejects the host?
rashes, diarrhoea, depleted liver function
74
How is graft rejection treated?
immunosuppressants - ciclosporin
75
What causes AML?
multi gene mutations | Mainly DNMT3A methyltransferase mutation
76
How is leukaemia cured?
if all the leukemic stem cells are eradicated

M104 Symposia (11 decks)

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