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RADT317 - Brain > Leukaemia > Flashcards

Leukaemia Flashcards

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The Brain flashcards
1
Q

What does leukaemia affect?

A

The ability to produce normal blood cells

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2
Q

What does leukaemia cause?

A

The overproduction of abnormal, immature WBC in the bone marrow

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3
Q

What 2 categories do leukaemia’s fall into?

A

Chronic or acute

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4
Q

What 2 cell type categories do leukaemia’s fall into?

A

Lymphoblastic or myeloid

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5
Q

What 4 categories can stem cells develop into?

A

Lymphoid stem cells, myeloid stem cells, erythroblasts and megakaryoblasts

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6
Q

Lymphoid cells become?

A

WBC Lymphocytes (T and B)

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7
Q

Myeloid cells become?

A

WBC Monocytes and neutrophils

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8
Q

Erythroblasts become?

A

RBC

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9
Q

Megakaryoblasts become?

A

Platelets

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10
Q

What are the 2 acute classifications?

A

Acute lymphoblastic leukaemia
Acute myeloid leukaemia

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11
Q

What are the 2 chronic classifications?

A

Chronic lymphoblastic leukaemia
Chronic myeloid leukaemia

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12
Q

What is ALL characterised by?

A

Overproduction of cancerous, immature lymphocytes (lymphoblasts)

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13
Q

What is AML characterised by?

A

Rapid growth of WBC that accumulate in the bone marrow and affect WBC production

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14
Q

Function of monocytes (myeloid)?

A

WBC - responds to bacteria, viruses and fungi, produced in the bone marrow and released when infection occurs

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15
Q

Function of lymphocytes (lymphoblastic)?

A

Many functions.
B - mature in bone marrow
T - mature in thymus

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16
Q

What is chronic leukaemia characterise by?

A

Build up of abnormal WBC over months or years

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17
Q

What is the peak incidence age of ALL?

A

0-4

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18
Q

What is the management of ALL?

A

1 - Induction - 4 week chemo
2 - Consolidation - 4 week chemo
3 - Maintenance - weekly 3 weeks chemo (methotrexate)
4 - 4 cycles chemo + maintenance or stem cell transplant

vincristine, dexamethasone
Pegaspargase - combination therapy

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19
Q

What is the management of AML?

A

1 - Induction - 4 week chemo
2 - Consolidation - 4 week chemo
*3 - Maintenance - weekly 3 weeks chemo (methotrexate)
*4 - 4 cycles chemo + maintenance or stem cell transplant

cytarabine

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20
Q

What is the management of CLL?

A

1 - Watch and wait
*2 - Chemo (fast developing disease)
*3 - RT (lymphadenopathy 4gy)
*4 - Surgery or RT (splenomegaly 6-10gy)
*5 - Bone marrow transplant (rare)

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21
Q

What is the management of CML?

A

1 - Biological therapy (imatinib)
2 - Chemo
*3 - Bone marrow or stem cell transplant
*4 - RT (rarely used - symptom palliation)

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22
Q

Induction chemotherapy purpose?

A

Clear the blood of leukaemia cells
Reduce the number of blasts in the bone marrow to normal

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23
Q

Consolidation chemotherapy purpose?

A

Given after induction recovery
Kills remaining (undetectable) leukaemia cells

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24
Q

Maintenance chemotherapy purpose?

A

Long term low dose
Not used for all leukaemia types - most common for ALL

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25
Q

Name a AML chemo drug

A

Cytarabine

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26
Q

Name a ALL chemo drug

A

Vincristine, dexamethasone

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27
Q

What drug is used for maintenance?

A

Methotrexate

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28
Q

General chemotherapy side effects

A

Nausea
Alopecia
Cardiotoxicity
Neuropathy
Skin changes
Mouth sores
Taste changes
Infertility/sexual dysfunction

29
Q

What is Pegaspargase (oncaspar)?

A

Used as combination therapy for ALL management

Recommended for use in children, young people and adults, diagnosed with untreated, new disease

30
Q

Pegaspargase (oncaspar) side effects

A

Nausea/vomiting
Stomach pain
Weakness
Allergic reaction
Mouth pain
Acute pancreatitis (rare)

31
Q

What are the 2 types of stem cell transplant?

A

Autologous and allogeneic

32
Q

What happens in a autologous stem cell transplant?

A

Stem cells harvested from the patient are given back after conditioning regimen of high dose chemo and/or RT

33
Q

What happens in a allogenic stem cell transplant?

A

Same procedure as autologous, however, uses relative, unrelated individual or saved umbilical cord blood

Needs a successful human leukocyte antigens (HLA) test

Preferable as donor cells are non-malignant but hard to match donors

34
Q

When would you use TBI?

A

Before stem cell transplant to help reduce chance of transplant rejection or if stem cell transplant has failed

35
Q

Side effects of TBI?

A

Nausea, diarrhoea, fatigue, mouth sores, skin changes, immunosuppression

36
Q

What is often shielded for TBI and why?

A

Reduce long term issues and even out dose

37
Q

Infection control

A

Protective isolation
Room sterilisation
Clean air
Clean food
Purified water
Removal of plants
Hand washing
Sealed room
1 visitor per day
Can lead to psychological issues

38
Q

What percentage of new cancer diagnoses does CLL account for (2016-2018)?

A

1%

39
Q

What is CLL incidence rates strongly related to?

A

Age

40
Q

What staging system does CLL use?

A

The Binet Staging system

41
Q

How many stages does the CLL Binet staging system have?

A

3 (Stage A, B and C)

42
Q

What does CLL Binet staging system Stage A mean?

A

Fewer than 3 groups of enlarged lymph nodes (lymphadenopathy) and a high white blood cell count

43
Q

What does CLL Binet staging system Stage B mean?

A

More than 3 groups of enlarged lymph nodes (lymphadenopathy) and a high white blood count

44
Q

What does CLL Binet staging system Stage C mean?

A

Enlarged lymph nodes or spleen, a. high white blood cell count and low red blood and platelet counts

45
Q

What percentage of new cancer diagnoses does CML account for (2016-2018)?

A

Less than 1%

46
Q

What gender are incidence rates lower in CML?

A

Females

47
Q

What are the 3 phases of CML?

A

Chronic, accelerated, blast crisis

48
Q

How many patients present in the chronic phase?

A

85%

49
Q

What is shown in the accelerated phase?

A

Some signs in blood/bone marrow that patient is moving towards blast crisis

50
Q

What happens to cells in the blast crisis phase?

A

Behaves like AML
Rapid progression
Short survival

51
Q

What does the Philadelphia chromosome cause?

A

Causes the production of an enzyme called tyrosine kinase (TK) which stimulates the production of leukaemic cells

52
Q

What is the Philadelphia chromosome treated with?

A

Treated with TK inhibitors (TKI therapy) such as Glivec

53
Q

Arsenic Trioxide (Trisenox or ATO)

A

Long history of use in Chinese medicine

Current use in subtype of AML (acute promylocytic leukaemia)

‘chemo free’ treatment

Minimal side effects

Given over 6 month period

Causes death of leukaemia cells via morphological changes and DNA fragmentation. Arsenic Trioxide also damages or degrades the fusion protein promyelocytic leukemia (PML) - retinoic acid receptor (RAR) alpha

54
Q

Monoclonal antibodies

A

Monoclonal antibodies recognise and find specific abnormal proteins on cancer cells

Each monoclonal antibody recognises 1 particular protein

Different cancers have different abnormal proteins, CD20 in CLL

CD20 antigen is a protein found on surface of B-lymphocytes

Drugs include; Rituximab, Obinutuzumab and Ofatumumab

CD52 antigen found on surface of CLL cells and many T-lymphocytes

Alemtuzumab (Campath) targets CD52, used if CLL no longer responding to standard chemo

55
Q

What is CAR T cell treatment?

A

Blood taken from patients and separated to get T-cells

The T-cells are then genetically engineered, using a disarmed virus (not going to harm the cell anymore), to produce cell surface receptors, called Chimeric Antigen Receptors (CARs)

These receptors then allow the T cells to recognise and attach to a specific protein or antigen on tumour cells

An antigen found on B-cells is CD19

The CAR s “program” the T-cells to find and destroy cancer cells

CAR T cell therapy used for B-cell ALL patients recurrence or relapse (Kymriah)

56
Q

How common is leukaemia in the UK overall?

A

12th most common

57
Q

How common is leukaemia in UK males?

A

10th most common

58
Q

What is the cause of leukaemia?

A

Unsure of cause!

Certain link to DNA mutations disrupting cell death, differentiation or division process

Many different mutations have been identified

Mutations may be due to carcinogens, radiation or exposure to certain viruses

Downs syndrome. 10-20% increased risk of developing acute leukaemia’s

Krummel cluster, Germany

Seascale cluster, 1955-1983. proven higher incidence of leukaemia near to Sellafield

Chernobyl

East v’s West Germany

59
Q

Leukaemia symptoms

A

Fever, chills
Fatigue, weakness
Loss of appetite, weight loss
Night sweats
Bone/joint pain
Abdominal discomfort
Headaches
Shortness of breath
Frequent infections
Easy bruising or bleeding
Petechiae (small red spots under the skin)

60
Q

Leukaemia signs

A

Anaemia
Leukopaenia (low white blood cell count)
Thrombocytopenia (low blood platelet count) - bruising or bleeding
Lymphadenopathy (with lymphatic spread)
Hepatomegaly / splenomegaly - abnormal cells in liver or spleen

61
Q

AML prognostic factors

A

Age
Treatment induced
Myeloproliferative disorders
CNS involvement
Cytogenics
White blood cell count (>100 unfavourable)

62
Q

What are cytogenetics?

A

Investigation of chromosome abnormalities is increasingly valuable for leukaemia diagnosis

Chromosome abnormalities are strongly associated with both AML and ALL

Molecular studies of these abnormalities identified specific genes implicated in leukaemia development

63
Q

What is complete remission?

A

No evidence of disease after treatment

Bone marrow contains fewer than 5% blast cells

Blood cell counts within normal limits
No signs or symptoms

“Molecular” complete remission if no leukaemia cells in marrow

64
Q

What is minimal residual disease?

A

Sensitive tests (flow cytometry or PCR) find leukaemia in marrow

65
Q

What is active disease?

A

Evidence of leukaemia during treatment

Reappearance of disease after treatment (relapse)

More than 5% blast cells in bone marrow

66
Q

What percentage of deaths does AML account for?

A

2%

67
Q

ALL prognostic factors

A

Gender (males worse)
Age
WBC
Cytogenetics
CNS disease
Response to treatment

68
Q

What is the Philadelphia chromosome (PH+)?

A

Translocation of chromosomes 22 and 9

Creates a new “BCR-ABL” gene which produces a new protein

Protein creates an enzyme called tyrosine kinase which stimulates the production of leukaemic cells

Tyrosine Kinase Inhibitors can be used as a treatment

69
Q

Ph-positive ALL

A

Approximately 25% of adults with ALL and a small number of children have Philadelphia positive ALL (Ph+)

More strongly associated with CML

Associated with poor prognosis
- More intensive treatment
- Addition of Tyrosine kinase inhibitors (TKIs)
- Addition of Glivec (imatinib) to chemotherapy
- Continuation of Glivec after consolidation

RADT317 - Brain (10 decks)

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