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Week 3 - Female GU Pathology > Pharmacology VT: Cancer Chemotherapy > Flashcards

Pharmacology VT: Cancer Chemotherapy Flashcards

1
Q

Name the specialised characteristics of cancer cells [4]

A
  1. Uncontrolled proliferation
  2. Loss of original function (anaplasia)
  3. Invasiveness
  4. Metastasis (malignant cells)
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2
Q

How do normal cells become cancer cells? [4]

A
  1. Normal cells become cancer cells through a change in DNA
  2. Two main categories of genetic change:
    • Inactivation of tumour suppressor genes
    • Activation of proto-oncogenes to oncogenes
  3. Usually regulatory genes become mutated
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3
Q

What are the 3 types of cancer therapy and when are each used (generally)? [6]

A
  1. Surgical removal
    • only used for solid tumours
    • dependent on location
    • only if non-metastasised
  2. Irradiation
    • only if localised
  3. Chemotherapy with anticancer drugs
    • often only treatment available
    • selective toxicity required
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4
Q

What is selective toxicity? [1]

A

the ability of a drug to target sites that are relatively specific to the microorganism causing the infection

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5
Q

Cancer Chemotherapy

  1. What is the general mechanism of action of most anti-cancer drugs (and what do they not do)? [4]
  2. What are the general toxic effects of chemo? [13]
  3. What are the 2 categories of drugs? [4]
A
  1. general mechanism of action:
    • most anticancer drugs attack cell division
    • they do not reverse:
      • de-differentiation
      • invasiveness
      • metastasis
  2. general toxic effects:
    • bone marrow suppression (anaemia, immune depression, prone to infection, impaired wound healing)
    • loss of hair
    • damage of gastrointestinal epithelium
    • damage of liver, heart and kidneys
    • in children, depression of growth
    • sterility
    • teratogenicity (damage to embryo)
  3. categories of drugs:
    • cell-cycle specific drugs
      • drugs that are active only on dividing cells
    • cell-cycle non-specific drugs
      • drugs that are also active on resting (G phase) cells
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6
Q

What types of cells do solid tumours consist of and what types of drugs are these cells sensitive to? [4]

A

Solid tumours consist of:

  1. Dividing cells - progressing through cell cycle
    • sensitive to cell cycle specific drugs
  2. Resting cells - not dividing but could do so
    • insensitive to many drugs
    • cause many relapses
  3. Cells which can no longer divide but contribute to tumour size
    • not a problem
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7
Q

What is severe cumulative therapy? [1]

A

prolonged treatment required to reduce chance of relapse from resting cells

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8
Q

Name the 6 main classes of drug chemotherapy [6]

A
  1. Alkylating agents
  2. Antimetabolites
  3. Cytotoxic antibiotics
  4. Microtubule inhibitors
  5. Steroid hormones and antagonists
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9
Q

Alkylating Agents

  1. Describe the general mechanism of action of alkylating agents [3]
  2. Give examples of alkylating agents [9]
  3. What conditions does mechlorethamine treat? [2]
  4. What conditions does melphalan treat? [3]
  5. What is unique about cyclophosphamide and what is it used to treat? [2]
A
  1. general mechanism of action:
    • form covalent bonds with DNA, interfering with both transcription and replication
    • have 2 reactive groups which allows the drug to cross-link, with one strand of DNA or across the 2 strands of DNA
  2. examples of alkylating agents:
    • nitrogen mustards (melphalan, chlorambucil, cyclophosphamide, ifosfamide)
    • Cysplatin
    • Temozolomide
    • Lomustine
    • Busulphan
  3. mechlorethamine used to treat:
    • Hodgkin’s lymphoma
    • non-Hodgkin’s lymphoma
  4. melphalan used to treat:
    • multiple myeloma
    • ovarian cancer
    • breast cancer
  5. cyclophosphamide (a pro-drug) used to treat many cancers
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10
Q

Anti-metabolites

  1. Describe the general mechanism of action of anti-metabolites [1]
  2. What are the 2 types of anti-metabolites and give examples of each [10]
A
  1. antimetabolites interfere with nucleotide synthesis or DNA synthesis
  2. Nucleotide synthesis: antifolates
    • _​​_Methotrexate
    • Ralitrexed
    • Pernetrexed
  3. Nucleotide analoques
    • 5-fluorouracil
    • Cytarabine (Ara-C)
    • Gemcitabine
    • Fludarabine
    • Capecitabine
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11
Q

Describe the mechanism of action of:

  1. Methotrexate (folate antagonist)? [3]
  2. Fluoro-uracil (pyrimidine analogues)? [2]
  3. Mercaptopurines (purine analogues)? [3]
  4. Cytarabine (nucleotide analogues)? [3]
A
  1. Folate antagonists: Methotrexate
    • inhibition of dihydrofolate formation
    • inhibition of purine/pyrimidine nucleotide synthesis
    • ultimately, halt to DNA and RNA synthesis
  2. Pyrimidine analogues: Fluoro-uracil
    • prevents thymidine formation
    • stops DNA synthesis
  3. Purine analogues: Mercaptopurines
    • converted into false nucleotides
    • disrupts purine nucleotide synthesis
    • may be incorporated into DNA, disrupting helix
  4. Nucleotide analogues: Cytarabine
    • S-phase cell cycle specific
    • inhibits DNA polymerases
    • incorporation into DNA causes chain termination
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12
Q

Cytotoxic Antibodies

  1. Describe the general mechanism of action [1]
  2. Describe the mechanism of action of:
    • Dactinomycin [2]
    • Doxorubicin [3]
A
  1. Act mainly by a direct action on DNA as intercalators
  2. Dactinomycin:
    • inserts itself into the minor groove in the DNA helix
    • RNA polymerase function is disrupted
  3. Doxorubicin
    • inserts itself between base pairs
    • binds to the sugar-phosphate DNA backbone causing local uncoiling
    • impaired DNA and RNA synthesis
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13
Q

Microtubule Inhibitors

  1. Drug name? [1]
  2. Mechanism of action? [4]
A
  1. vincristine
  2. mechanism of action:
    • binds to microtubular protein
    • blocks tubulin polymerisation
    • blocks normal spindle formation
    • disrupts cell division
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14
Q

Describe the mechanism of action of the steroid hormone prednisone? [4]

A
  • Prednisone is a synthetic adrenocortical steroid hormone
    • it is converted in the body to active form:
      • prednisolone
        • suppresses lymphocyte growth
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15
Q

Hormone Antagonists

  1. Tamoxifen
    • Mechanism of action? [1]
    • Used to treat? [2]
  2. Flutamide/Bicalutamide
    • Mechanism of action? [1]
    • Used to treat? [1]
  3. Prostap
    • Mechanism of action [2]
    • Used to treat? [1]
A
  1. Tamoxifen
    • antagonist of oestrogen receptor
    • used to treat:
      • some breast cancers (that are oestrogen dependent)
      • it is also an ovulatory infertility treatment
  2. Flutamide/Bicalutamide
    • testosterone receptor antagonist
    • used to treat prostate cancer
  3. Prostap
    • pituitary downregulators → LHRH agonist
    • inhibits release of LH, which normally stimulates the testes to produce testosterone
    • used to treat prostate cancer
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Week 3 - Female GU Pathology (7 decks)

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