Chemotherapy drugs

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  1. What are the aims of chemotherapy?
    To prolong survival and maintain good QOL
  2. What is chemotherapy?
    The use of cytotoxic drugs to kill tumour cells
  3. True or false: there are chemotherapy drugs licences for use in animals?
    False - only human chemotherapy drugs are used, none are licensed for animals
  4. What are chemosensitive tumours?
    Multicentric/disseminated tumours (lymphoma/leukaemia, high grade MCT)
  5. What makes these tumours chemosensitive?
    They are rapidly dividing and therefore sensitive to the drugs
  6. What are chemoresistant tumours?
    Solid, large, bulky tumours - poorly vasuclarised, necrotic centres, low cell division, low drug availability
  7. When might we use chemotherapy on chemoresistant tumours?
    Use surgery to remove the tissue bulk and stimulate division of any residual tumour cells.  Then use chemotherapy to kill off residual primary tumour cells as they are stimulated to divide post surgery.  Or use chemotherapy to delay the growth of subclinical metastases which are dividing rapidly at this phase of growth
  8. List the different steps of the cell cycle.
    G1, S phase, G2, M phase.  Also G0.
  9. In what stage of the cell cycle will cells not be affected by chemotherapy drugs?
    G0 - cells are not dividing
  10. List the different categories of chemotherapy drugs
    • Vinca alkaloids
    • Antimetabolites
    • Alkylating agents
    • Anti-tumour antibiotics
    • Miscellaneous (cisplatin, l-asparginase)
  11. What point of the cell cycle do vinca alkaloids affect?
    M phase
  12. What is the mechanism of action of vinca alkaloids?
    Inhibit the mitotic spindle and prevent chromosomes being pulled apart in cell division
  13. What is a rare side effect of vinca alkaloids?
    Neuropathy/neurotoxicity
  14. Give an example of a vinca aklaloid
    Vincristine, vinblastine
  15. How are vinca alkaloids administered?
    IV bolus
  16. What are vinca alkaloids used to treat?
    Lymphoma protocols, MCT protocols
  17. What stage of the cell cycle do antimetabolites work at?
    S phase
  18. What is the mechanism of action of antimetabolites?
    Analogues of the DNA nucleotides which target the synthesis of purines and pyrimidines and interfere with DNA synthesis
  19. What are cytosine arbinoside, mtheotrexate and hydroxyurea used to treat?
    Lymphoma/leukaemia protocols
  20. Why can 5-Fluorouracil not be used in cats?  What is it used to treat?
    • As it causes neurological side effects
    • Carcinomas
  21. What stage of the cell cycle do alkylating agents affect?
    non-specific
  22. What is the mechanism of action of the alkylating agents?
    Incorporate an alkyl group into DNA, forming covalent bonds that cause inter/intrastrand cross linking which inhibits RNA/protein synthesis, replication and transcription
  23. What is cyclophosphamide widely used for?
    Leukaemia/lymphoma due to its pronounced effect on lymphocytes
  24. What organs must be functional to administer cyclophosphamide to a patient?
    • Liver - metabolism is essential for cytotoxicity
    • Kidney - renal excretion
  25. What is a side effect of cyclophosphamide?
    Haemorrhagic cystitis
  26. What stage of the cycle do anti-tumour antibiotics affect?
    Non-specific
  27. What is the mechanism of action of anti-tumour antibiotics?
    • Intercalate in DNA to prevent RNA/protein synthesis.  
    • Inhibit topomerase II
    • Produce free radicals
  28. Doxorubicin, epirubicin and mitoxantrone are collectively known as?
    Anthracyclines
  29. What is a side effect of doxorubicin?
    Cardiotoxicity - must monitor heart function to ensure it is not impaired by cumulative dose
  30. What is cisplatin?
    A platinum compound with two chlorine atoms and two ammonia groups
  31. What is the mechanism of action of cisplatin?
    Similar to alkylating agents i.e. intrastrand crosslinking
  32. What are the side effects of cisplatin?
    • Nephrotoxicity - hydration and diuresis are essential
    • Vomiting and nausea - may require anti-emetics
  33. What compound is now used widely instead of cisplatin and why?
    Carboplatin - it is a derivative with less nephrotoxicity
  34. What is the mechanism of action of L-asparginase?
    It breaks down aspargine into aspartic acid and ammonia.  Tumour cells cannot make their own aspargine but normal cells cannot therefore it is selectively toxic to tumour cells.
  35. What are side effects of L-asparginase?
    • Anaphylatic reactions
    • Pancreatitis
  36. Give an example of a commonly used glucocorticoid for chemotherapy
    Dexamethasone or prednisolone
  37. What does an a) high b) low dose of glucocorticoid do?
    • a) inhibits lymphocyte proliferation 
    • b) reduced inflammation/stimulates appetite
  38. When might single drug protocols be used in chemotherapy?
    If the cell type is particularly sensitive or in combination with surgery and/or radiotherapy to prevent metastases in solid tumours
  39. What are the three types of combined drug protocols for chemotherapy?
    COP, CHOP and ALP
  40. What are advantages of using combined drug protocols?
    • Different drugs have different modes of action and act at different stages of the cell cycle
    • They have different modes of resistance
  41. What should be avoided in combined drug protocols?
    • Drug toxicities should not overlap
    • Drugs should not interfere with each other
  42. What is the fraction kill hypothesis?
    A given dose of chemotherapy drug kills a fixed percentage of the mass of cells in a tumour rather than a fixed number.  Therefore cancer drugs should be used at the highest possible dose to effect the highest possible fractional kill in conventional chemotherapy.
  43. List some side effects of chemotherapy drugs
    • Perivascular reaction ie pain, erythema, moist desquamation, necrosis
    • Alopecia
    • Vomiting, diarrhoea, anorexia, mucositis, colitis
    • Myelosuppresion - anaemia, thrombocytopenia, neutropenia
    • Haemorrhagic cystitis
    • Cardiotoxicity
  44. How do cells acquire drug resistance?
    • Decreased uptake
    • Increased target enzyme levels
    • Decreased drug activation
    • DNA repair
    • Drug cleavage
    • Increased efflux
  45. How does multi drug resistance occur?
    This is due to ATP binding cassette transporters that efflux drugs
  46. What is the most common ATP binding cassette transporter responsible for multi drug resistance?
    P-glycoprotein (p170)

Card Set Information

Author:
 Anonymous
ID:
 301017
Filename:
 Chemotherapy drugs
Updated:
2015-04-18 14:10:14
Tags:
Chemotherapy pharmacology
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Description:
Vet Med - Module 12
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