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Year 1- Principles of Disease (FOM) > Chemotherapy > Flashcards

Chemotherapy Flashcards

1
Q

What is chemotherapy?

A

Compound which targets DNA, RNA and proteins.

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2
Q

What is the aim of chemotherapy?

A

To force cells into apoptosis.

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3
Q

What cells are impacted by chemo?

A

It’s non-specific to target cells so all rapidly dividing cells are effected.

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4
Q

Name some of the cells which may be effected.

A

Oral mucosa, hair follicles and cells produced in the bone marrow.

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5
Q

How can chemo be given?

A

Orally or using an IV

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6
Q

How is the chemo prescribed?

A

Prescribed in cycles.

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7
Q

What is the purpose of the timing of the treatment?

A

Destroy cancer cells when they are at their most vulnerable while allowing other cells time to heal.

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8
Q

What are cycles of chemo determined by?

A

Pharmacokinetics such as half life and excretion of drugs involved.

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9
Q

Why is combination chemo given?

A

To increase efficacy (the ability to produce a desired or intended result)

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10
Q

Name the three settings in which chemo can be given.

A

Neoadjuvant, adjuvant, disease control/pallative.

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11
Q

Describe chemo given in an neoadjuvant setting

A

Given before surgery with the aim to reduce cancer signs.

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12
Q

Describe chemo given in an adjuvant setting

A

Used to reduce the risk of cancer returning,

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13
Q

Describe chemo given in an disease control/palliative setting

A

Given w the aim to control the disease for as long as possible.

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14
Q

Name the three main types of chemo.

A

-Alkylating agents and platinum drugs
-Antimetabolites
-Organic drugs

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15
Q

Describe how alkylating agents and platinum drugs work.

A

Form DNA adducts blocking DNA replication (all phases of cell cycle).

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16
Q

Describe how antimetabolites work.

A

Structurally mimic essential molecules required for cell division (S phase of cell cycle)

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17
Q

Give examples of organic drugs.

A

Vinca alkaloids / taxanes / anthracyclines

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18
Q

Describe how the organic drug Vinca alkaloids works.

A

Binds to tubulin and prevent microtubule assembly

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19
Q

Describe how the organic drug Taxanes work.

A

Binds to beta tubulin subunit inhibiting depolymerisation and disrupting mitotic spindle .

20
Q

Describe how the organic drug anthracyclines work.

A

Microbial antibiotic targets topoisomerase II.

21
Q

List some side effects of chemo.

A

-Nausea
-Vomiting
-Alopecia
-Renal failure
-Diahorrea

22
Q

Name three personalised systemic therapies.

A

Hormonal therapies, targeted therpaies, immunotheraies.

23
Q

Name three personalised systemic therapies.

A

Hormonal therapies, targeted therapies, immunotherapies.

24
Q

Name three personalised systemic therapies.

A

Hormonal therapies, targeted therpaies, immunotheraies.

25
Q

Name some hormonal therapies.

A

Anti - oestrogen, Aromatase inhibitors

26
Q

Name some immunotherapies.

A

PD 1, PD -L1, CTLA - 4

27
Q

List some hormone releasing cancers.

A

Breast, endometrium, ovarian, prostate, testes, and thyroid.

28
Q

Which hormones play a major role in breast cancer?

A

Oestrogens (estradiol/esterone)

29
Q

What do ostreogeans do?

A

Oestrogens promote cell proliferation within the breast tissue (higher rate of cell division = more chances for mutations).

30
Q

What does a prolonged exposure to oestrogen do?

A

Increases risk of breast cancer.

31
Q

Name two types of treatment against breast cancer and give examples.

A

Anti- oestrogen = Tamoxifen: Binds to the oestrogen receptor

Aromatase inhibitors = Letrozole: Block conversion to androgens to oestrogen

32
Q

What do tyrosine kinase inhibtors do?

A

Inhibit tumours which express the EGF receptor

33
Q

What are some of the side effects of tyrosine kinase inhibitors?

A

Diahorrea, dry skin, rash, hypertension, liver disfunction.

34
Q

Describe the EGF signalling pathway,

A
  1. EGF binds to the tyrosine kinase receptor on the cell membrane
  2. This leads to receptor dimerization and autophosphorylation.
  3. Following this, there is activation of intracellular transducers, including the RAS pathway
    and transcription, giving gene expression and growth.
35
Q

What do cyclins and cyclin dependant kinases do?

A

Control the passage of cells through each stage of the cell cycle.

36
Q

What cyclins/cyclin dependant kinases push cells out of G0->G1?

A

Cyclin D along with CDK 4/6

37
Q

What does the production of cyclin D do?

A

Regulates the level cyclin E.

38
Q

What does cyclin E do?

A

Pushes cells from G1. S phase

39
Q

What cells in the immune system composed of?

A

Derived from haematopoietic stem cells

40
Q

What do B cells do?

A

Produce tumour specific antibodies.

41
Q

What do T cells do?

A

Helper T- help other molecules in the body
Cytotoxic T- kill tumours and cells infected by viruses

42
Q

What do immune checkpoints ensure?

A

That self tolerance is maintained.

43
Q

What immune checkpoints activated by?

A

Ligand binding

For example, PD-1 to PD-L1
CTLA-4 to B7

44
Q

What do immune checkpoint inhibitors do?

A

Removal of the brakes of the immune system allowing increased T cell activity.

45
Q

What is pembrolizumab?

A

A selective humanised IgG4 monoclonal antibody targeted at the PD-1 checkpoint.

46
Q

What is the result of binding at the PD-1 checkpoint?

A

The T cell is not turned off to the cancer,

47
Q

List some side effects of immunology.

A

Everything ending in ‘itis; pretty much lol->

Colitis - most common
Pneumonitis
Hypophysitis/ Thyroid dysfunction/ Diabetes
Dermatitis
Hepatitis
Nephritis

Year 1- Principles of Disease (FOM) (40 decks)

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