Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Haematology > Introduction To Leukaemia > Flashcards

Introduction To Leukaemia Flashcards

1
Q
  1. Define Leukaemia?
A

Malignant disorders of haematopoietic stem cells associated with an increased number of white cells in bone marrow or/and peripheral blood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q
  1. What two lineages do WBC’s come from?
A
  1. Lymphoid (T/B lymphocytes) lineage

2. Myeloid (Macrophages,Neutrophils) lineage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q
  1. Leukaemia is a clonal disease- what does this mean?
A

o Clonal disease where all the malignant cells derive from a single mutant stem cell.
• 1st mutation is pre-leukaemia, 2nd mutation acquisition is full blown leukaemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q
  1. What are HSCs?
A

o Haematopoietic stem cells (HSCs) are self-maintaining (self-renew), pluripotent cells that can give rise to cells of every blood lineage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q
  1. What are progenitor cells?
A

o Progenitor cells can divide to produce many mature cells but have a finite lifespan (can’t divide indefinitely) and will eventually differentiate/mature.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q
  1. Can you tell the morphological difference between precursor cells and undifferentiated (multipotent) cells?
A

can’t tell the morphological differences between them and precursors because they don’t show the characteristics of mature cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q
  1. Can you tell the morphological difference between committed (unipotent) and precursor cells?
A

yes because they are committed to what they will become when they generate mature cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q
  1. How many new cases of leukaemia is there every day?
A

9900

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q
  1. What % of new daily cases are childhood?
A

31%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q
  1. Between what ages is there a peak rate of leukaemia cancers in?
A

85-89

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q
  1. What % has the incidence rate decreased by since early 1900s
A

18%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q
  1. How does leukaemia present itself?
A
  • Varies between diff leukaemia’s but;
  • 1st present with symptoms due to loss of normal blood cell production
  • Abnormal Bruising
  • Repeating abnormal infection
  • Anaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q
  1. What is the Aetiology of leukaemia?
A

Exact cause is unclear but there is a combination of predisposing factors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q
  1. Leukaemia is not usually hereditary except for some cases of *** ?
A

Chronic Lymphocytic Leukaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q
  1. In some cases, rare genetic diseases can predispose you to leukaemia , give examples of which diseases?
A
  • Fanconi’s anaemia

- Down’s syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q
  1. What 3 main types of genetic factors can cause leukaemia?
A
  1. Oncogenes/ Tumour Suppressor
  2. Chromosome Aberrations
  3. Inherited immune system issues
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q
  1. Explain how “Oncogenes/Tumour Suppressor genes” can play a genetic factor in leukaemia?
A

Activating mutations of oncogenes and inactivating mutations of tumour suppressor genes, this may involve genes specific to leukaemia or genes that are also common to other malignancies (TP53- Li-Fraumeni syndrome, NF1-Neurofibromatosis).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q
  1. Explain how “Chromosome aberrations” can play a genetic factor in increasing chances of leukaemia?
A

Translocations (e.g. BCR-ABL in CML) or numerical disorders (e.g. trisomy 21-Down syndrome).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q
  1. Give 2 examples of inherited immune system problems that might increase risk of leukaemia?-
A
  • Ataxia-telangiectasia

- Wiskott-Aldrich syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q
  1. What are some environmental and lifestyle related risk factors for leukaemia?
A
  • Radiation Exposure (radiation accidents or atomic bomb survivors)
  • Immunosuppression (after transplant)
  • Exposure to chemicals and chemotherapy
  • Lifestyle related risk factors (smoking,drinking, overexposure to sun, overweight)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q
  1. Why might a patient have exposure to chemicals and chemotheraphy?
A
  • Cancer chemotherapy with alkylating agents (e.g. Busulphan)
  • Industrial exposure to benzene
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q
  1. What are some controversial risk factors (uncertain/unproven) or leukaemia?
A

o Exposure to electromagnetic fields
o Foetal exposure to hormones and infections in early life.
o Mother’s age when child is born and parents’ smoking history.
o Nuclear power stations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q
  1. What is another name for acute lymphoid leukaemia?
A

Acute Lymphoblastic leukaemia (ALL)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q
  1. What is another name for chronic lymphoid leukaemia?
A

Chronic Lymphocytic Leukaemia (CLL)

25
Q
  1. What are the names given for acute and chronic myeloid leukaemia?
A

Acute Myeloid Leukaemia=
Acute myeloblastic leukaemia (AML)

Chronic Myeloid Leukaemia =
Chronic granulocytic leukaemia (CML)

26
Q
  1. Which age is mostly affected by acute leukaemia or chronic leukaemia?
A

Acute = Mainly Children

Chronic =Middle Age and Elderly

27
Q
  1. What is the difference between acute and chronic leukaemia for “Onset and Duration”
A

Acute = “Sudden onset, duration weeks-months”

Chronic = “Insidious (gradual) onset, duration years”

28
Q
  1. What is the difference between acute and chronic leukaemia for “WBC Count”
A

Acute = Variable WBC count

Chronic = High WBC Count

29
Q
  1. Define acute (rapid onset and short but severe course) leukaemia?
A

undifferentiated leukaemia characterised by uncontrolled clonal accumulation of immature white blood cells (myeloblasts and lymphoblasts).

30
Q
  1. Define chronic (persisting over a long time) leukaemia?
A

differentiated leukaemia that is characterised by uncontrolled clonal accumulation of mature white blood cells (cytes)

31
Q
  1. What percentage of leukaemia’s are ALL (acute lymphoblastic leukaemia) and what % are AML (acute myeloblastic leukaemia)
A

75% of leukaemia’s are ALL and 20% are AML.

32
Q
  1. What is meant by undifferentiated leukaemia’s? eg ALL and AML?
A

o large number of lymphoblasts (ALL) or myeloid blasts (AML) in bone marrow/blood.
oMaturation arrest: cells arrest in the blast cell pool so they cannot differentiate to become mature cells.

33
Q
  1. Typical symptoms of AML or ALL are due to the bone marrow suppression, what are some typical symptoms?
A
  1. Thrombocytopenia (platelet deficiency): purpura (bruising), epistaxis (nosebleed), bleeding from gums.
  2. Neutropenia (neutrophil deficiency): Recurrent infections, fever.
  3. Anaemia: lassitude (lack of energy), weakness, tiredness, shortness of breath.
34
Q
  1. To diagnose ALL or AML , a peripheral blood blast test (PB) could be done, how does this work?
A

check for presence of blasts and cytopenia (acute leukaemia >30% blasts).

35
Q

35.To diagnose ALL or AML , a bone marrow test/ biopsy (BM) could be done, how does this work?

A

taken from pelvic bone and results compared with PB.

36
Q
  1. What is the purpose of doing a lumbar puncture on a ALL /AML patient?
A

to determine if the leukaemia has spread to the cerebral spinal fluid (CSF).

37
Q
  1. What is more common: ALL or AML?
A

ALL is not very common but AML is very rare , so ALL out of the two

38
Q
  1. For both ALL and AML , state the PREVALENCE:
A

ALL:
Prevalence: commonest cancer of childhood.

AML:
Prevalence: most common in over 75 year old

39
Q
  1. For both ALL and AML , state the ORIGIN:
A

ALL:
Cancer of immature lymphocytes (lymphoblasts/blasts).

AML:
Cancer of immature myeloid white blood cells.

40
Q
  1. For both ALL and AML , state the CLASSIFICATION:
A

ALL:
B-cell & T-cell leukaemia

AML:
based on FAB system (French-American-British): M0-M7.

41
Q
  1. For both ALL and AML , state the TREATMENT:
A

ALL:
Chemotherapy (long term side effects are rare).

AML:
Chemotherapy, monoclonal antibodies (immunotherapy) +/- allogeneic bone marrow transplant.

42
Q
  1. For both ALL and AML , state the OUTCOME after treatment:
A

ALL:
• 5 year event-free survival (EFS) of 87% in 2010.
• 1 out of 10 ALL patients relapse- remission in 50% of these after 2nd chemotherapy treatment or bone marrow transplant.

AML:
5 year event-free survival (EFS) of 50-60%.

43
Q
  1. Why is there a poorer prognosis in Adult ALL?
A

poorer prognosis because disease presents different cell of origin and different oncogene mutations

44
Q
  1. What is chronic leukaemia characterised by?
A

Characterised by an increase number of differentiated cells -“differentiated leukaemia”.

45
Q
  1. What is more common out of the two:
    -Chronic Lymphocytic leukaemia (CLL)
    -Chronic Myeloid Leukaemia (CML)
    ???
A

CLL is more common

CML is rare

46
Q
  1. For both CLL and CML state the PREVALENCE?
A

CLL:
3,800 new cases diagnosed in the UK every year (average diagnosis age= 70).

CML:
742 new cases diagnosed in the UK every year (peak rate = 85-89y/o).

47
Q
  1. For both CLL and CML state the ORIGIN?
A

CLL:
Large numbers of mature (clonal) lymphocytes.

CML:
Large numbers of mature myeloid white blood cells

48
Q
  1. For both CLL and CML state the SYMPTOMS?
A

CLL:
Recurrent infections due to neutropenia, and suppression of normal lymphocyte function, anaemia, thrombocytopenia, lymph node enlargement, hepatosplenomegaly.

CML:
Often asymptomatic and discovered through routine blood tests.

49
Q

49.For both CLL and CML state the TREATMENT?

A

CLL:
Chemotherapy to reduce cell numbers

CML:
Targeted therapy: Imatinib.(cancer growth blocker- tyrosine kinase inhibitor)

50
Q

50 .For both CLL and CML state the OUTCOME after treatment?

A

CLL:
5 year event-free survival (EFS) of 83%. Many patients survive >12 years.

CML:
: 5 year event-free survival (EFS) of 90%.
o Eventually progresses to accelerated phase and then blast crisis (>30% of cells are blast).- allogeneic bone marrow transplant.

51
Q
  1. How do we diagnose CML?
A

very high white cells count (neutrophilia) and presence of Philadelphia chromosome.

52
Q
  1. What % of CML cases have a detectable Philadelphia chromosome?
A

95%

53
Q
  1. What translocation results in a philadelphia chromosome?
A

Balanced translocation between chromosomes 9 and 22 - t(9;22)(q34;q11).

Normal Chromosome 9 (with ABL gene)
Normal Chromsome 22 (With BCR gene)
Chromosomes break, chromosome 9 is unchanged, chromosome 22 has both ABL and BCR gene and therefore is now a Philadelphia chromosome

54
Q
  1. What does the BCR and ABL genes encode?
A

o BCR encodes a protein that needs to be continuously active and ABL encodes a protein tyrosine kinase whose activity is tightly regulated (auto-inhibition).

55
Q
  1. oBCR-ABL protein causes constitutive (unregulated) protein tyrosine kinase activity which causes what three things:
A
  1. Proliferation of progenitor cells in the absence of growth factors
  2. Decreased apoptosis
  3. Decreased adhesion to bone marrow stroma.
56
Q
  1. What are some clinical applications of the BCR-ABL oncogene?
A
  • 95% of cases of CML have a detectable Ph’ chromosome that allows diagnosis (by FISH which uses fluorescent probes).
  • Detection of minimal residual disease (small no of cancer cells remaining after treatment).
  • Therapy using drugs that specifically inhibit BCR-ABL. e.g. Imatinib (Glivec®, STI571). Cases negative for BCR-ABL require different therapy.
57
Q
  1. What is Imatinib and how does it work?
A
  • Imatinib is a small molecule inhibitor (competitor of ATP for the small pocket) that specifically targets ABL –CML treatment.
  • It inhibits BCR-ABL (but not other tyrosine kinases) which causes apoptosis of chronic myeloid leukaemia (CML) cells.
  • Remission induced in more patients, with greater durability and fewer side effects.
  • Some patients become drug resistant.
  • Also used for lung cancers and gastrointestinal tumours.
58
Q
  1. Compare Targeted therapies vs chemotherapy?
A

Targeted Therapies:

  • Design to interact with their targets
  • Act on specific molecular targets associated with cancer
  • Cytostatic (inhibit cell growth without directly killing cells).
  • Many are oral agents

Chemotherapy:

  • Identified because they kill cells
  • Act on all rapidly dividing cells (cancerous and normal)
  • Cytotoxic (kill cells)
  • Mainly intravenous, some oral agents

Haematology (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions