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Molecular Basis Of Disease > Introduction To Luekaemia > Flashcards

Introduction To Luekaemia Flashcards

1
Q

Describe the presentation of leukaemia?

A
  • Varies between types of leukaemia
  • Typically first presents with symptoms due to loss of normal blood cell production
  • Abnormal bruising (commonest)
  • Repeating abnormal infection + Sometimes anaemia
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2
Q

State the methods used to diagnose leukaemia?

A
  • Peripheral blood blasts test (PB) - checks for presence of blasts + cytopenia -> >3% blasts = suspected acute leukaemia
  • Blast = precursor of mature RBCs
  • Cytopenia = V mature RBCs
  • Bone marrow test/biopsy -> taken from pelvic bone + results compared with PB
  • Lumbar puncture - Determine if leukaemia has spread to cerebral spinal fluid
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3
Q

State techniques used to investigate the molecular and pathophysiological characterisation of leukaemia?

A
  • Cytomorphology
  • immunophenotyping
  • next generation sequencing
  • flow cytometry
  • fluorescence in situ hybridisation
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4
Q

Describe the aetiology of leukaemia?

A
  • Exact cause is unclear
  • Combination of predisposing factors
  • Genetic, environmental
  • Lifestyle-related risk factors + uncertain factors
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5
Q

How does genetic risk factors contribute to leukaemia?

A
  • Not usually hereditary (sometimes in chronic lymphoctic Leukaemia)
  • Some rare genetic diseases (fanconi’s anaemia or Down’s syndrome) may develop to Leukaemia
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6
Q

State genetic risk factors for leukaemia and state examples of diseases for these

A
  • Gene mutations - oncogenes (activation) or/+ tumour suppressors (inactivation)
  • Common genes in other malignancies (TP53- li-fraumeni syndrome, NF1 neurofibromatosis)
  • Chromosome aberrations: Translocations + numerical disorders
  • Inherited immune system problems: Ataxia telangiectasia, Wiskott-Aldrich syndrome)
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7
Q

State environmental risk factors for leukaemia?

A
  • Radiation exposure (acute radiation accidents, atomic bomb survivors),
  • Exposure to chemicals and chemotherapy
  • Immune system suppression
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8
Q

State lifestyle risk factors for leukaemia?

A
  • Smoking
  • Drinking
  • Excessive exposure to sun
  • Overweight
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9
Q

State controversial risk factors for leukaemia?

A
  • Linked to childhood
  • Exposure to electromagnetic fields
  • Infections early in life
  • Mothers age when child is born
  • Parents smoking history
  • Nuclear power stations
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10
Q

Classifications of leukaemia
Complete the overall table pairing Lymphoid/Myeloid Cell lineage with Acute/Chronic degree of terminal differentiation

A
  • ALL -> Acute lympho-blastic L - Acute Lymphoid Leukamia
  • AML -> A myelo-blastic L - Acute myeloid Leukaemia
  • CLL -> C lympho-cystic L - Chronic Lymphoid Leukaemia
  • CML -> Granulocytic L - Chronic myeloid Leukaemia
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11
Q

Describe the difference between acute and chronic leukaemia

A
  • Acute: rapid onset and short but severe course - Undifferentiated L + Characterised by uncontrolled clonal and accumulation of immature white blood cells (-blast)
  • Chronic: persisting over a long time - Differentiated L + Characterised by uncontrolled clonal and accumulation of mature white blood cells (-cyte)
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12
Q

Describe the differences in age, onset, duration + WBC count between acute and chronic leukaemia

A
  • Acute vs Chronic
  • Age: Mainly children vs Middle age and elderly
  • Onset: Sudden vs insidious
  • Duration: Weeks to months vs years
  • White blood cells count: Variable vs High
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13
Q

Describe the characterisation of acute leukaemia and the incidence of the sub disease?

A
  • Increase lymphoblasts (ALL) or myeloid blasts (AML) in bone marrow (maturation arrest) and blood - “undifferentiated leukaemia”. >
  • ALL= 75% + AML = 25%
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14
Q

State the typical symptoms found in acute leukaemia?

A
  • Due to bone marrow suppression - Thrombocytopenia (platelet deficiency)
  • Purpura (bruising)
  • Epistaxis (nosebleed)
  • Bleeding from gums + Neutropenia
  • Recurrent infections
  • fever + Anaemia
  • lassitude
  • Weakness
  • Tiredness
  • Shortness of breath
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15
Q

Describe the difference in origin, classification + treatment of ALL compared to AML?

A
  • ALL: Cancer of immature Lymphocytes,
  • Classification: B-cell + T-cell Leukaemia
  • Treatment: chemotherapy
  • Adult ALL has poor prognosis as various presentation of disease
  • AML: Cancer of immature myeloid WBC
  • Classification: french-american-british system (MO-M7)
  • Treatment: chemotherapy, monoclonal AB (immunotherapy) +/-allogenic BM transplant
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16
Q

Describe the characterisation of chronic leukaemia?

A

Increase in differentiated cells

17
Q

Describe the difference in origin, classification + treatment of CLL compared to CML?

A
  • CLL: Increase in mature lymphocytes in BM + peripheral blood, Recurrent infections due to neutropenia, suppression of normal lymphocyte function, anaemia, thrombocytopenia, lymph node enlargement, hepatosplenomegaly
  • Treatment: Regular chemotherapy to decrease cell numbers
  • CML: Increase mature myeloid WBCs, asymptomatic + discovered via blood test
  • Treatment - imatinib
18
Q

State the diagnosis of CML?

A

Increase white cells (neutrophilia) in blood + BM + presence of philidelphia chromosome

19
Q

What type of leukaemia has detectable philadephilia chromosome and describe how its formed? VD

A

CML (95% of cases) -> BCR-ABL oncogene
- Formed via balanced translocation t(9;22)(g34;q11)

20
Q

Describe the role of genes in BCR-ABL oncogene and activity of the overall protein?

A
  • BCR: Encodes active protein continuously
  • ABL: Encodes protein tyrosine kinase -> activity is tightly regulated (auto-inhibition)
  • BCR-ABL protein -> Unregulated (constitutive) protein tyrosine kinase activity
21
Q

What are the effects of having BCR-ABL oncogene?

A
  • Proliferation of progenitor cells in the absence of growth factors
  • Decrease apoptosis
  • Adhesion to bone marrow stroma
22
Q

Describe 3 uses of the BCR-ABL oncogene?

A
  • Diagnosis: 95% of CML cases have a detectable Ph’ chromosome
  • Detection of minimal residual disease
  • Therapy: Drugs inhibit BCR-ABL Imatinib
  • Minimal residual disease shows that treatment isn’t fully effective or disease hasn’t been removed
23
Q

Describe the use of imatinib as a targeted therapy against Ph chromosome?

A
  • Small molecule inhibitor
  • targets specifically BCR-ABL gene (TK activity)
  • CML treatment: fusion gene can’t phosphorylate substrates - some patients become drug resistant
24
Q

What is imatinib also used for?

A
  • Gastrointestinal stromal tumour
  • Small cell lung cancer

Molecular Basis Of Disease (30 decks)

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