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Third year pharmacology > ls6003 haemotology lecture 1 > Flashcards

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

A

VDLP

24
Q

what is CML

A

chronic myeloid leukaumia

25
Q

BCR-ABL

A

cancer causing gene (fusion gene) involed in pathogenesis of CML

26
Q

treatment of CML

A

TKI = imatinib = competitive inhibitor

27
Q

TKI resistance in CML

A

occurs in 30-40% of cases
mutations make up 50% of resistance
point mutations in ABL kinase domain reduce TKI sensitivity

28
Q

whats CLL

A

chronic lymphocytic leukaemia

29
Q

diagnosis of CLL

A

full blood count (CBC)

30
Q

why is treatment of CLL different to CML

A

there isnt a single mutation or abnormality, so more than one drug is needed. considered targeted therapy

31
Q

how is stage A or stage 1/II CLL treated

A

does not require therapy, therapy will do more harm

32
Q

what drug types are used to treat CLL

A

-corticosteroids
-purine analogues
-monoclonal antibodies
-novel therapies
-FCR

33
Q

what mAb in used to treat CLL

A

Rituximab (anti CD20)
less toxic compared to traditional chemo

34
Q

what 2 ways does Rituximab work by:

A

1) helping immune system destroyu the cancer cells
2)destroyin ghte cancer cells itself
-can harm healthy cells

35
Q

whats MM

A

multiple myeloma (MM) (not leukamia)
affects bone marrow, the cell in this cancer is plasma cells

36
Q

Treatment of MM, name the 5 types of drug

A

-anthracyclines e.g. doxorubicin
-alkylatin gagents: melphalan
-corticosteroids: dexamthasone
immunomodulatory agents (iMiDs): thalidomide
proteasome inhibitors: bortezomib

Third year pharmacology (7 decks)

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