ls6003 haemotology lecture 1 Flashcards

1
Q

what is conventional chemotherapy

A

cytotoxic to most cells, meaning it can damage normal, healthy cells in addition to damaging and killing cancer cells.

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2
Q

what is targeted therapy

A

Targeted drugs often work by blocking cancer cells from copying themselves. This means they can help stop a cancer cell from dividing and making new cancer cells.

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3
Q

whats palliative treatment

A

prolongs survival, improves QoL, unlikely to cure

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4
Q

In leukaemia what is the next option after a patient fails cycles of chemo in response to diagnosis with leukaemia

A

bone marrow transplant

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5
Q

what is salvage chemotherapy

A

potentially curative combination chemo, given to patients who hav efailed or recurred after curative

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6
Q

what is adjuvant chemo

A

Adjuvant therapies are delivered after the primary treatment, to destroy remaining cancer cells.

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7
Q

what is neo-adjuvant

A

Neoadjuvant therapies are delivered before the main treatment, to help reduce the size of a tumor or kill cancer cells that have spread.

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8
Q

what factors are considered when designin gcombination therapy

A

-drugs with known efficacy against a particular tumour type
-non-overlapping toxicity profile
-possible synergistic killing effects
-action at different phases in cell cycle

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9
Q

define leukaemia

A

malignant clonal disorder of immature cells in haemopoietic system derived from a single ancestral transformed cell with genetic alteration

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10
Q

what is AML

A

acute myeloid leukaemia

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11
Q

can you have genetic predispostion to AML

A

chromosomal instability syndromes e.g. bloom syndrome (quite rare)

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12
Q

symptoms of AML

A

anaemia
neutropenia
thrombocytopenia (petechiae)
organomeglay
gum hypertrophy

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13
Q

whats the pathogenesis of AML

A

escape from apoptosis, loss of cell cycle control, genomic instability
activation of RTK->PI3K signalling ->AKT and mTOR
BCL2 over-expression = anti-apoptosis protein
TP53 mutations (stops cell cycle)

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14
Q

what is induction

A

high-dose combination therpay with intent to inudce complete remission (50->5% bone marrow leukaemia cell))

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15
Q

whats consolidation

A

aims to remove any residual leukaemia cells after induction

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16
Q

intensification

A

chemo after complete remission, often higher dose or altenate combination
intends to increase sure or remission duration

17
Q

whats the standard remission induction combination therapy

A

cytosine arabinoside (Ara-C) (purine antagonist), and anthracycline. 10 day cycle

18
Q

whats the standard consolidation therapy

A

high dose Ara-C, muliple cycles

19
Q

what are the 2 types of stem cell transplant

A

-allogeneic haematopoietic stem cell transplantation (Allo-HSCT) = uses donor cells, can result in GVHD, higher survival
-autologous HSCT (Auto-HSCT) = uses own cells, lower survival rate

20
Q

what is APL and what is its hallmark

A

acute promyelocytic leukaemia (APL)
hallmark= genetic alterations involving retinoic acid receptor alpha (RARA) gene

21
Q

what is ALL

A

acute lymphoblastic leukaemia
type of blood cancer that starts with lymphocytes in bone marrow. most common in children
increase in WBC
symptoms: reduced platelets

22
Q

what are the 2 types of ALL

A

B-ALL - effects ages 1-10, less severe
T-ALL - effects 10<, more severe, effects CNS

23
Q

induction of remission in ALL via what regimen

24
Q

what is CML

A

chronic myeloid leukaumia

25
BCR-ABL
cancer causing gene (fusion gene) involed in pathogenesis of CML
26
treatment of CML
TKI = imatinib = competitive inhibitor
27
TKI resistance in CML
occurs in 30-40% of cases mutations make up 50% of resistance point mutations in ABL kinase domain reduce TKI sensitivity
28
whats CLL
chronic lymphocytic leukaemia
29
diagnosis of CLL
full blood count (CBC)
30
why is treatment of CLL different to CML
there isnt a single mutation or abnormality, so more than one drug is needed. considered targeted therapy
31
how is stage A or stage 1/II CLL treated
does not require therapy, therapy will do more harm
32
what drug types are used to treat CLL
-corticosteroids -purine analogues -monoclonal antibodies -novel therapies -FCR
33
what mAb in used to treat CLL
Rituximab (anti CD20) less toxic compared to traditional chemo
34
what 2 ways does Rituximab work by:
1) helping immune system destroyu the cancer cells 2)destroyin ghte cancer cells itself -can harm healthy cells
35
whats MM
multiple myeloma (MM) (not leukamia) affects bone marrow, the cell in this cancer is plasma cells
36
Treatment of MM, name the 5 types of drug
-anthracyclines e.g. doxorubicin -alkylatin gagents: melphalan -corticosteroids: dexamthasone immunomodulatory agents (iMiDs): thalidomide proteasome inhibitors: bortezomib