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Week 4 - female GU/breast > Cancer chemotherapy > Flashcards

Cancer chemotherapy Flashcards

1
Q

What are the special characteristics of cancer cells?

A
  • Uncontrolled proliferation
  • Loss of original function (anaplasia)
  • Invasiveness
  • Metastasis (malignant cells)
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2
Q

When is surgical removal an option for cancer therapy?

A
  • Only for solid tumours
  • The location is suitable
  • If it has not metastasised
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3
Q

What are the two main categories of genetic change in the transformation of cancer cells?

A
  • Inactivation of tumour suppressor genes

* Activation of proto-oncogenes to oncogenes

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4
Q

What are the general toxic effects of chemotherapy?

A
  • Bone marrow suppression (blood cells) i.e. anaemia, immune depression, prone to infection, impaired wound healing
  • Loss of hair
  • Damage to GI epithelium
  • Liver, heart and kidney effects
  • In children, depression of growth
  • Sterility
  • Teratogenicity (damage to embryo)
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5
Q

What are the stages of the cell cycle?

A
  • G1 phase
  • S phase
  • G2 phase
  • Mitosis
  • G0
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6
Q

What happens in s phase?

A

DNA replication

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7
Q

What happens in the mitosis phase?

A

nuclear division and cytokinesis

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8
Q

What happens in the G1 phase?

A

There is a high rate of biosynthesis

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9
Q

What is the significance of the cell cycle with chemotherapy drugs?

A

Drugs that act on a cell cycle will only affect the cells in that stage of the cycle so the patient may need to be on the drugs for a long period of time

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10
Q

What happens if the restriction point after G1 phase is disabled?

A

The cell enters a cycle of uncontrolled proliferation

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11
Q

What is the name for the group of drugs that are active only on dividing cells?

A

Cell cycle specific drugs

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12
Q

What are cell cycle non specific drugs?

A

They are active on the resting (g phase) drugs

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13
Q

What cells do solid tumours consist of?

A
  • Dividing cells - progressing through cell cycle
  • Resting cells - not dividing but could do so
  • Cells which can no longer divide but contribute to the tumour size
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14
Q

Which cells in a solid tumour are most likely to cause relapse?

A

The resting cells as they are not sensitive to many drugs

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15
Q

Why must we aim for a total kill of all cancer cells?

A
  • The host immune system does not destroy the cells that will be left over as it hasn’t already
  • This would cause relapse
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16
Q

What are the main classes of chemotherapy drugs?

A
  • Alkylating agents
  • Antimetabolites
  • Cytotoxic antibodies
  • Microtubule inhibitors
  • Steroid hormones and antagonists
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17
Q

What is the mechanism of action of alkylating agents?

A
  • Form strong covalent bonds with the DNA
  • Interfering with both transcription and replication
  • Most alkylating agents have two reactive groups allowing the drug to cross link either within one strand of DNA or across the two strands of DNA
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18
Q

Where is lomustine active?

A

In the CNS

19
Q

What is special about Busulphan

A

It has a selective effect on bone marrow

20
Q

What is mechlorethamine?

A
  • Nitrogen mustard

* Was used as a blister agent

21
Q

What is mechlorethamine used to treat?

A
  • Hodgkins lymphoma

* Non Hodgkins lymphoma

22
Q

What is the route of administration of mechlorethamine and why?

A

IV, it kills the cells they encounter

23
Q

What is melphalan

A

Nitrogen mustard

24
Q

What is melphalan used to treat?

A
  • Multiple myeloma
  • Ovarian cancer
  • Breast cancer
25
Q

What is cyclophosphamide?

A

Nitrogen mustard, it is a prodrug that requires activation by phophoramidase

26
Q

Describe specific targeting with cyclophosphamide

A
  • Requires activation by phosphoramidase which has high activity in some tumours
  • However it is activated in the liver
  • But, it is less toxic and aldehyde dehydrogenase protects against the toxicity of the drug (and is in high concentrations in bone marrow cells, hepatocytes and intestinal epithelium
27
Q

What is the mechanism of action of cisplatin?

A
  • It stops DNA replication

* Targets N7 of purine nucleotides

28
Q

Where does resistance for cisplatin rise from?

A
  • Nucleotide excision repair mechanisms

* Efflux transporters for copper (heavy metals)

29
Q

How do any metabolites work?

A

They interfere with nucleotide synthesis or DNA synthesis

30
Q

Name 3 antifolates

A
  • Methotrexate
  • Ralitrexed
  • Pemetrexed
31
Q

Name 3 nucleotide analogues

A
  • 5-flurouracil
  • Cytarabine
  • Gemcitabine
  • Fludarabine
  • Capecitabine
32
Q

Mechanism of action of fluoro-uracil

A

Prevents thymidine formation

33
Q

Mechanism of action of mercaptopurines

A

Converted into false nucleotides, disrupts purine nucleotide synthesis and may be incorporated into DNA disrupting the helix

34
Q

What is the mechanism of action of cytarabine?

A
  • Nucleotide analogue
  • Sugar is arabinosine instead of ribose
  • undergoes cellular activation to ara-CTP
  • Inhibits DNA polymerases (so s phase specific)
  • Incorporation into the DNA causes chain termination)
35
Q

What is dactinomycin?

A

Cytotoxic antibiotic

36
Q

What is the mechanism of action of dactinomycin?

A
  • Inserts itself into the minor groove in the DNA helix

* Disrupts the RNA polymerase function

37
Q

What is doxorubicin?

A

cytotoxic antibody

38
Q

What is the mechanism of action of doxorubicin?

A
  • Inserts itself between base pairs

* Causes local uncorking impairing DNA and RNA synthesis

39
Q

What are vinca alkaloids?

A

Antibiotic - microtubule inhibitors

40
Q

What is the mechanism of action of vinca alkaloids?

A
  • Bind to micro tubular protein
  • Block tubules polymerisation
  • Block normal spindle
  • Disrupt the cell division
41
Q

What is prednisone and what does it do?

A

It is a steroid hormone with is converted to the active form prednisolone in the body which suppresses lymphocyte growth

42
Q

What is tamoxifen and what does it do?

A

It is an antagonist of the oestrogen receptor. As some breast cancers are oestrogen dependent, oestrogen stimulates their growth

43
Q

Prostate cancer hormonal treatment

A
  • Most prostate cancers are testosterone dependent
  • Testosterone receptor antagonists: flutamide or bicalutamide
  • Pituitary downregulators LHRH agonists inhibit LH release which stimulates the testes to produce testosterone

Week 4 - female GU/breast (7 decks)

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