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Pathology 2060A > Lecture 17 > Flashcards

Lecture 17 Flashcards

Cancer chemotherapy (63 cards)

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1
Q

What are 5 characteristics of cancer cells?

A
  1. persistent uncontrollable cell proliferation
  2. invasive: cancer cells invade adjacent tissue, facilitating cancer growth in different areas of the body
  3. metastatic: the ability of cancer cells to travel to different sites in the body and invade to form new tumors
  4. immortal: cancer cells do not die, they continually divide
  5. angiogenesis: cancer cells develop their own blood vessels to supply nutrients
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2
Q

What are the 3 different treatment modalities for cancer?

A
  1. surgery
  2. radiation
  3. chemotherapy
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3
Q

What is radiation?

A
  • high energy radiation used to shrink and kill tumours & cancer cells
  • radiation damages DNA of cancerous and non-cancerous cells
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4
Q

What is chemotherapy?

A
  • drugs are used to treat cancer

- target rapidly dividing cells

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5
Q

What are the phases of the cell cycle?

A 
G0
G1
S
G2
M
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6
Q

What is G0?

A
  • cell is resting, no replication
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7
Q

What is G1?

A

cell prepares to synthesize (duplicate) its DNA

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8
Q

What is S?

A

cell synthesizes DNA

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9
Q

What is G2?

A

cell prepares for mitosis

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10
Q

What is M

A

-cell divides during mitosis

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11
Q

What are the obstacles to successful chemotherapy?

A
  1. toxicity to normal cells
  2. cure of cancer requires 100% cell kill
  3. Difficult early detection
  4. solid tumours respond poorly
  5. drug resistance
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12
Q

Why does chemotherapy cause toxicity to normal cells?

A
  • neoplastic (cancerous) cells v similar to normal cells so hard to specifically target
  • most toxicity to cells with high growth fraction (proliferating cells: cells in G0) like bone marrow, GI epithelium, hair follicles etc
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13
Q

What are the kinetics of cell death with chemotherapy?

A

first order = constant % of cancerous cells are killed at a given dose of drug

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14
Q

Why is cancer hard to detect early?

A
  • usually not detected until there at 10^9 tumour cells

- the early cancer is detected (usually before symptoms arise) the better the prognosis

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15
Q

What is the screening test for breast cancer?

A

-clinical breast examination

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16
Q

What is the screening test for prostate cancer?

A
  • digital rectal exam OR prostate specific antigen blood test
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17
Q

What is the screening test for skin cancer?

A
  • self checks performed regularly
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18
Q

What is the screening test for testicular cancer?

A
  • testicular self examination regularly
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19
Q

What are the mechanisms of resistance for chemotherapeutic drugs?

A
  1. decreased drug uptake
  2. increased drug efflux (ex. p-glycoprotein efflux transporter)
  3. decreased drug activation (in the case of prodrugs)
  4. reduced target sensitivity, increased cellular repair (mostly DNA)
  5. decreased apoptosis
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20
Q

What are some of the strategies for achieving max benefit from chemotherapy?

A
  1. intermittent chemotherapy

2. combination chemotherapy

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21
Q

What is intermittent chemotherapy?

A
  • administering drugs intermittently to allow for normal cells to recover
  • for success: normal cells must recover faster than the cancerous cells
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22
Q

What is combination chemotherapy?

A

using a number of chemotherapeutic agents together

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23
Q

Why is combo chemotherapy more effective?

A
  1. decreased resistance (unlikely canc. cells will undergo multiple different mutations)
  2. increased cancer cell kill (attack canc. cells in diff. ways so kill more than with a single agent)
  3. decreased injury to normal cells ( if they dont have overlapping toxicities = greater anti-cancer effects safely)
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24
Q

What are some of the chemotherapeutic associated toxicities?

A
  1. bone marrow suppression
  2. digestive tract injury
  3. nausea and vomiting
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25
What can bone marrow suppression lead to?
1. neutropenia: decreased neutrophils (white blood cell) in the blood 2. thrombocytopenia: decreased platelets in the blood, increased risk of severe bleeding 3. anemia: decreased # of erythrocytes (rbc's)
26
How can the digestive tract be injured by chemotherapy?
- stomatitis (inflammation of oral mucosa; may lead to ulceration) - diarrhea (secondary to the damage caused to the epithelial lining of the intestine)
27
What can prevent or lessen the effects of chemotherapeutic nausea and vomiting?
- anti-emetic drugs - prevention of dehydration - prevention of malnutrition
28
what are the two major classes of anti-cancer drugs?
1. cytotoxic agents | 2. hormonal and other agents
29
What are the 5 different types of cytotoxic agents?
1. alkylating agents 2. platinum compounds 3. antimetabolites 4. anti-tumour antibiotics 5. mitotic inhibitors
30
How else can cytotoxic agents be classified?
cell cycle phase specific or non-cell cycle phase specific
31
What are cell cycle phase specific cytotoxic drugs?
only effective if the cancer cell is in a specific phase of the cell cycle
32
What are non-cell cycle phase specific cytotoxic drugs?
- act during any stage of the cell cycle including G0 | - are more toxic to cells that are proliferating than cells in G0
33
What are alkylating agents and how do they work?
- highly reactive chemicals that transfer alkyl group to cell components (mostly DNA) - form cross-bridges btwen Nitrogen atoms on (dna) guanine nucelotides = miscoding, breaking of DNA, inhibition of DNA replicaiton - are cell-cycle non-specific
34
What is the most common alkylating agent?
- cyclophosphamide - prodrug that is activated in the liver (aka delayed onset of action) - mostly used for Hodgkins disease, solid tumours of head, neck, ovary, and breasts
35
What are platinum compounds?
- have platinum in chemical structure - cross-link DNA by binding to guanine nucleotides and inhibit DNA replication - are cell cycle phase non-specific
36
What is the most common platinum compound?
- CISPLATIN - used in metastatic ovarian and testicular cancer, advanced bladder cancer - is v nephrotoxic, ototoxic (toxic to ear, may cause deafness), and emetogenic
37
What are antimetabolites?
- similar to natural compounds our body uses to synthesize cellular constituents or incorporate into DNA - inhibit particular enzymes by preventing DNA replication - phase specific: S phase (most)
38
What are the 3 subclasses of antimetabolites?
1. folic acid analogs 2. purine analogs 3. pyrimidine analogs
39
What do folic acid analogs do?
block the conversion of folate to its active form
40
What do purine analogs do?
inhibit the synthesis of DNA and RNA
41
What do pyrimidine analogs do?
- inhibit the synthesis of DNA and RNA
42
What are anti-tumour antibiotics?
- kill cancer cells by intercalating DNA (move between the bases and bind = structural change that is unable to be used as replication template) - dna synthesis therefore inhibited - IV bc poorly absorbed
43
What is the most common anti-tumour antibiotic?
- anthracyclines - can cause severe bone marrow suppression - are cardiotoxic
44
What are mitotic inhibitors?
- inhibit mitosis (i.e prevent cell division)
45
What are the two subclasses of mitotic inhibitors?
- vinca alkaloids | - taxanes
46
What do vinca alkaloids do?
- derived from periwinkle plant - block process of mitosis during metaphase by binding tubulin and disrupting organization of microtubules - results in cell death
47
What do taxanes do?
- act in late G2 phase | - stabilize microtubule bundles to prevent cell division
48
What are the 3 different classes of hormonal agents?
1. glucocorticoids 2. drugs for prostate cancer 3. drugs for breast cancer
49
What are glucocorticoids?
- used as adjunct to other chemotherapeutic agents that are derived from lymphoid tissue - these are directly toxic to lymphoid tissue - can be helpful in managing complications of other drugs (less nausea & vomiting, less pain, better appetite)
50
What are the adverse effects of glucocorticoids?
- osteoporosis - adrenal insufficiency - susceptibility to infection - GI ulceration - electrolyte disturbance - growth retardation
51
What are drugs for prostate cancer?
- cancerous and normal prostate tissue is androgen dependent | - drug goal: androgen deprivation
52
How can androgen deprivation be achieved?
1. gonadotropin releasing hormone (GnRH) agonist or surgical castration (cancer sympt. initially increase due to transient increase in testosterone production) 2. androgen receptor antagonist (usually + GnRHa/castration; block androgen receptors in tumour cells)
53
How do GnRH and GnRH agonists work?
- GnRH = release of testosterone from testes = feeds cancer cells = negative feedback to inhibit further GnRH release - GnRH agonist = transient increase in testosterone = decreased GnRH activity through desensitization and negative feedback - net effect: decreased testosterone synth. and release
54
What are drugs for breast cancer?
- bc estrogen causes breast tumour cells to proliferate, main goal is it deprive c. cells from estrogen - estrogen receptor antagonism used adjunct to surgery/radiation
55
What are the 3 major classes of breast cancer treatment?
1. anti-estrogens 2. aromatase inhibitors 3. trastuzumab
56
What do anti-estrogens do?
- block estrogen receptors
57
What is the most common anti-estrogen?
- tamoxifen - partial estrogen receptor agonist = minimally activates the estrogen receptor & blocks endogenous estrogen from binding - net effect: blocking binding of estrogen to receptor
58
What are aromatase inhibitors?
- aromatization: process of converting androgens into estrogen - inhibit aromatization = decrease amnt of estrogen available - do not block ovarian estrogen synthesis = only useful in postmenopausal women
59
What is Trastuzumab?
- some patients with breast cancer have increased # of human epidermal growth factor receptor 2 (HER2) - HER2: transmembrane receptor that helps regulate cell growth - increased HER2 activity = aggressive tumour growth - this is a monoclonal antibody that binds HER2 and prevents cell proliferation - IV admin, may cause cardiotoxicity
60
What is another anti-cancer drugs?
1. tyrosine kinase inhibitors
61
What do tyrosine kinase inhibitors do?
- TK can activate gene transcription and/or DNA synthesis | - these inhibit this activity
62
What is imatinib
-prototype TKI - effective in treating leukemia and GI tumours -= complete inhibition of cell proliferation = cell death via apoptosis
63
What are the primary adverse effects of imatinib?
- nausea, vomiting, edema, muscle cramps

Pathology 2060A (18 decks)

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