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Semester 4 Revision > Leukaemia + Lymphoid Malignancies > Flashcards

Leukaemia + Lymphoid Malignancies Flashcards

1
Q

Define leukaemia (1)

A

Groups of diseases characterised by overproduction of WBCs or their precursors

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2
Q

What is the clinical presentation of leukaemia? (5)

A 
Varies b/w type
Symptoms due to loss of normal blood cell production
- abnormal bruising (platelet)
- repeated or abnormal infection (WBC)
- anaemia (RBC)
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3
Q

How do we classify leukaemias? (4)

A

Acute vs chronic

Lymphoid vs myeloid

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4
Q

What does lymphoid refer to? (2)

A

Involves cells of lymphocyte lineages

Mainly B-cell, more rarely T-cell

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5
Q

What does myeloid refer to? (3)

A

Involves cells of non-lymphocyte lineages
Common neutrophils/their precursors
(Can be erythroid, platelet, basophil lineages etc.)

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6
Q

What are acute leukaemias? (3)

A

Undifferentiated leukaemias
Characterised by immature WBCs (blast cells)
e.g. AML, ALL

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7
Q

What are chronic leukaemias? (2)

A

Differentiated leukaemias

Characterised by mature WBCs

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8
Q

4 types of leukaemia (4)

A

Acute lymphoblastic leukaemia (ALL)
Chronic lymphocytic leukaemia (CLL)
Acute myeloblastic leukaemia
Chronic granulocytic leukaemia

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9
Q

What genes are linked to leukaemia? (4)

A

Oncogene activation
Tumour suppressor gene inactivation
Some are specific to leukaemias
May involve genes similar to other malignancies e.g. RAS, MYC, P53

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10
Q

Chromosomal translocations + leukaemia (3)

A

To generate novel hybrid oncogenes
BCR-ABL (CML)
PML-RARA in AML type M4

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11
Q

What numerical chromosome changes can you get? (2)

A

Monosomy

Trisomy

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12
Q

How is leukaemia a clonal disease? (1)

A

All malignant cells are derived from a single mutant SC

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13
Q

What are the risk factors of leukaemia? (6)

A

RADIATION
- acute radiation accidents
- atomic bomb survivors
CHEMICALS
- industrial exposure to benzene
CHEMO
- alkylating agens e.g. Busulphan generates future risk of leukaemia
VIRUSES
- HTLV-1 predisposes to adult T-cell leukaemia
GENETIC (rare - some cases of CLL run in families, Down’s syndrome + Fanconi’s anaemia may predispose to leukaemia)
AGE

(Most not associated with any identifiable precipitating cause)

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14
Q

How do we treat leukaemia? (3)

A

Chemo with cytotoxic drugs
SC + BM transplant
Disease specific agents e.g. oncogene targeted drugs

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15
Q

What is chemotherapy? (3)

A

Combo of drugs used to kill leukaemic cells
Optimised for type + subtype of leukaemia
Cytotoxic drugs mostly target dividing cells

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16
Q

Examples of chemo drugs (7)

A 
Cytosine arabinoside
- cytosine analogue
- interferes with deoxynucleotide synthesis
- prevents successful DNA
replication

Vincristine

  • binds to tubulin dimers -> inhibits microtubule formation
  • so blocking mitotic spindle
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17
Q

Side effects of chemo (4)

A 
Kills normally dividing cells
GI epithelium - diarrhoea + nausea
Hair follicles - hair loss
Loss of fertility
Bone marrow suppression
18
Q

What is SCBMT? (4)

A

Stem cell + bone marrow transplant
Intense chemo + total body irradiation
Wipes out leukaemic cells + normal SCs
Reconstitute bone marrow by transplanted SCs

19
Q

What problems are there with SCBMT? (2)

A

Shortage of HLA matched donors

High mortality of procedure for old/v sick patients

20
Q

What are symptoms of acute leukaemias? (3)

A

Thrombocytopenia (purpura, epistaxis = nosebleed, bleeding from gums)
Neutopenia (recurrent infections e.g. oral thrush)
Anaemia (weakness, shortness of breath)

21
Q

How do we diagnose acute leukaemia? (2)

A

Presence of blasts or cytopenia in peripheral blood

Bone marrow aspirate >30% blasts = diagnostic

22
Q

Pathophysiology of acute leukaemia (3)

A

Maturation arrest - all immature, at exactly same stage
Auer rods
If cells are blocked from maturing the blast cell pool builds up

23
Q

What sorts of genes are involved in many chr translocations in acute leukaemias? (2)

A

Genes for TFs

Which control cell differentiation

24
Q

What can the type of chr abnormality help with acute leukaemia diagnosis? (2)

A

Determining prognosis + response to treatent

25
Q

How are acute leukaemias classified? (5)

A

FAB classification

  • based on stage of differentiation arrest
    • predominant cell type
  • also some rare ones that don’t fit main classifications

WHO
- acute leukaemias with specific chr translocations are classified separately

26
Q

How do we treat acute leukaemia? (4)

A

Chemo
Combo of drugs
Optimised for each type + sub-type of acute leukaemia
ALL (add chemo/radiotherapy to CNS)

27
Q

What are the two phases of chemo in acute leukaemia? (2)

A 
1 = remission induction
2 = consolidation therapy (to kill residual leukaemic SCs)
28
Q

What are the outcomes of ALL? (4)

A 
Kids > 90%  LT remission/cure
Adults have poorer prognosis:
- diff oncogens mutations
- diff cells of origin
- poorer tolerance to therapy
29
Q

What are the outcomes of AML? (2)

A

> 80% LT remission in young adults with aggressive treatment

Elderly unable to tolerate aggressive chemo/SCBMT

30
Q

What are CLLs called + why? (2)

A

Chronic lymphocytic leukaemia

As large number of mature (clonal) lymphocytes in BM/peripheral blood

31
Q

Symptoms of CLL (5)

A 
Recurrent infections (due to neutropenia + suppression of normal lymphocyte function)
Anaemia
Thrombocytopenia
Lymph node enlargement
Hepatosplenomegaly
32
Q

How do we treat CLL? (1)

A

Controlled by regular chemo to reduce cell numbers

33
Q

Prognosis of CLL? (2)

A

Some may die in

34
Q

What are the symptoms of CML? (3)

A

Anaemia
Night fever/night sweats
Splenomegaly
(Infection is not symptoms as lots of neutrophils)

35
Q

How do we diagnose CML? (4)

A

Neutrophilia (v high WBC count)
Left shit in blood + bone marrow
Presence of Philadelphia chr (95%)
BCR-ABL gene arrangment

36
Q

How do we treat CML? (3)

A

Controlled but not cured by chemo
Not cytotoxic drugs/interferon alpha
But imatinib

37
Q

Prognosis of CML? (3)

A

Survival on treatment usually measure in yrs

But eventually progresses to accelerated phase + then blast crisis (resembles acute leukaemia)

38
Q

How do we treat CML? (3)

A

Allogenic BM or SC transplant is curative
Autologous transplant sometimes tried
Most patients are >50yrs + do not tolerate transplant

39
Q

What is the Philadelphia chr?

A

come back to this

40
Q

What drugs specifically inhibits BCR-ABL? ()

A

Imatinib
Specific tyrosine kinase inhibitor
Inhibits BCR-ABL but notn most other tyrosine kinases
Causes apoptosis of CML cells

41
Q

How is Imatinib compared to previous treatments for CML? (4)

A

Induces remission in more patients
With greater durability
Less SEs
But some patients become drug resistant

Semester 4 Revision (15 decks)

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