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Pharmacology > Module 17 > Flashcards

Module 17 Flashcards

1
Q

Cancer

A
  • uncontrolled proliferation of cells
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2
Q

Neoplastic cells

A

cancer cells

abnormal and uncontrollable cell growth

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3
Q

Characteristics of Cancer Cells (5)

A

1) persistant uncontrollable cell proliferation
2) invasive
3) metastatic
4) immortal
5) angiogenesis

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4
Q

Cancer - invasive

A

invade adjacent tissue facilitating cancer growth in different areas of the body

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5
Q

Cancer - is metastatic

A

ability of cancer cells to travel to different sites in the body and invade to form new tumours

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6
Q

Cancer - imortal

A
  • cancer cells do not die they continually divide
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7
Q

cancer + angiogenisis

A
  • cancer cells develop their own blood vessels to supply nutrients –> crucial for proliferation
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8
Q

Treatment for cancer

A

1) surgery
2) radiation
3) chemotherapy

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9
Q

Treatment for cancer - radiation

A

high energy radiation used to shrink tumours and kill cancer cells
- damage DNA of both cancerous and non-cancerous cells

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10
Q

Treatment for cancer - chemotherapy

A
  • chemotherapeutic drugs target rapidly dividing cells
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11
Q

The cell cycle

A 
- process of proliferation.
5 phases
     1) G0
     2) G1
     3) S
     4) G2
     5) M
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12
Q

G0

A

phase of cell cycle

cell is resting, does not replicate

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13
Q

G1

A

phase of cell cycle

cell prepares to synthesize (duplicate) its DNA

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14
Q

S

A

The cell synthesizes DNA

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15
Q

G2

A

The cell prepares for mitosis

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16
Q

M (cell cycle)

A

The cell divides in a process called mitosis

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17
Q

Obstacles to sucessful chemotherapy - toxicity to normal cells

A

Neoplastic cells are similar to normal cells … difficult to target only cancer cells during chemotherapy

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18
Q

Which cells does chemotherapy kill?

A

cells with a high growth fraction (Cancer cells and other normal cells)

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19
Q

What is a growth fraction

A

ratio of proliferating cells to cells in the resting G0 state

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20
Q

What cells in the body have high growth fraction? (4)

A
  • bone marrow
  • GI epithelium
  • hair follicles
  • germinal epithelium of testes (that gives rise to sperm)
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21
Q

what percent of cancer removed is considered ‘cured’

A
  • 100% cell kill
  • difficult, no good tests to determine whether cancerous cells are present in the body in low numbers
  • kinetics of cell death is first order (constant percentage of cancerous cells are killed at a given dose of drug)
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22
Q

Why is early detection of cancer important?

A
  • cancer is almost significantly progressed by the time it is diagnosed
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23
Q

ideal treatment of cancer

A

surgical exision followed by chemotherapy

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24
Q

Screening for cancer - breast cancer

A
  • clinical breast examination every 2-3 years for women over 50
  • high risk patients should be screened more often and maybe earlier than 50
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25
Q

Screening for cancer - cervical cancer

A
  • sexually active women should have a pap test every 1-3 years
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26
Q

Risk factors for cervical cancer

A
  • Human Papillomavirus (HPV)

- spread by sexual contact…75% of women and men will have 1 HPV infection in their lifetime

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27
Q

Screening for cancer - colorectal cancer (2)

A
  • men and women 50+ who are not at high risk should have fecal occult blood test every 2 years
  • colonoscopy every 5 years in high risk patients
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28
Q

Screening for cancer - prostate cancer

A
  • men over 50 should have digital rectal exam

- and/or Prostate Specific Antigen blood test

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29
Q

Screening for cancer - skin cancer

A
  • self checks performed regularly

- look for changes to birthmarks and/or moles, new skin growths, sores that don’t heal properly

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30
Q

Screening for cancer - testicular cancer

A
  • men over age 15 should regularly perform the testicular self examination
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31
Q

Solid Tumours and Chemotherapy

A

solid tumours have a large fraction of cells int he resting G0 state

most chemo drugs target proliferating cells, solid tumours dont respond as well

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32
Q

Drug resistance - chemotherapy (5)

A

1) decreased drug uptake
2) increased drug efflux
3) decreased drug activation (ie. prodrugs)
4) reduced target sensitivity, increased cellular (DNA) repair
5) decreased apoptosis

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33
Q

Drug Resistance to Chemotherapy - P-glycoprotein

A
  • P-glycoprotein is an efflux drug pump.
  • by not allowing cellular accumulation of chemo drugs, P-Gp can cause multiple drug resistance
  • resistant cells are not killed by chemo agents –>therapeutic failure
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34
Q

Strategies to achieve maximum benefit from chemotherapy

A
  • intermittent chemotherapy

- combination chemotherapy

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35
Q

Intermittent chemotherapy

A
  • kill cancer cells by administering chemo drugs intermittenly, giving time for normal cells to recover
  • for this strategy to be successful, normal cells must grow back faster than cancerous cells
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36
Q

Combination chemotherapy - why is it more effective? (3)

A

1) decreased resistance (multiple drugs with multipl actions make therapy less likely to be affected by mutations)
2) increased cancer cell kill (killing them by different mechanisms of action)
3) decreased injury to normal cells (less overlapping toxicities)

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37
Q

Chemotherapeutic associated toxicities

A
  • bone marrow suppression
  • digestive tract injury
  • nausea and vomiting
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38
Q

Chemotherapy + bone marrow suppression (3 effects)

A

1) neutropenia (decreased neutrophils)
2) thrombycytopenia (decreased platelets)
3) anemia (decreased red blood cells)

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39
Q

Neutropenia - what, dangers

A

decreased neutrophils in the blood

neutrophils = a WBC that helps fight infection

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40
Q

Thrombocytopenia - what, dangers

A

Decreased platelets in the blood

  • platelets involved in coagulation of blood
  • decreased platelets = increased risk of serious bleeding
41
Q

Chemotherapy - digestive tract injury

A
  • stomatitis (inflammation of oral mucosa) can lead to ulceration
  • diarrhea (secondary to damage of epithelial lining of intestine)
42
Q

stomatitis

A

inflammation of oral mucosa

43
Q

Chemotherapy - nausea and vomiting (treatment)

A
  • common and serious adverse effect (may lead patients to refuse further treatment)
  • treat with anti-emetics, prevent dehydration, prevent malnutriotion
44
Q

Drugs to treat cancer - classifications (2)

A
  • Cytotoxic agents

- hormonal and other agents

45
Q

Cytotoxic agents - categories (5)

A
  • alkylating agents
  • platinum compounds
  • antimetabolites
  • antitumour antibiotics
  • mitotic inhibitors
46
Q

Cytotoxic agents - classification based on cell cycle phase

A

1) cell cycle phase specific drugs

2) cell cycle phase non-specific drugs

47
Q

Cytotoxic drugs - cell cycle phase specific drugs (when are they effective)

A
  • only effective if the cancer cell is in a specific phase of the cell cycle (G1-M)
  • EX: mitotic inhibitors are only effective when cancer cells are undergoing mitosis
  • must include cells actively part of the cell cycle (not effective for cells in G0)
48
Q

Cytotoxic drugs - cell cycle phase non-specific drugs (when effective)

A
  • act during any stage of the cell cycle including G0

- they are still more toxic to cells that are proliferating than cells in G0

49
Q

Alkylating Agents - mechanism of action

A
  • highly reactive chemical that transfers an alkyl group to cell components (primarily DNA)
  • they act by forming cross-bridges between nitrogen atoms on guanine nucleotides that make up our DNA
  • result = miscoding, breaking of DNA, and posible inhibition of DNA replication
50
Q

Alkylating agents - cell cycle classification

A

cell cycle phase non-specific = effective during any phase of the cell cycle

51
Q

Alkylating agent common name

A

cyclophosphamide

52
Q

Cyclophophamide - mechanism of action

A
  • is a pro-drug - must be converted to active form by the liver
53
Q

cyclophosphamide - time of onset

A

delayed (is a pro-drug and needs to be metabolized by liver)

54
Q

cyclophosphamide - indications for use

A
  • Hodgkins disease

- solid tumours of the head, neck, ovary, breast

55
Q

Platinum compounds - structure

A
  • drugs with platinum in their chemical structure
56
Q

Platinum compounds - mechanism of action

A
  • Act by cross-linking DNA and therefore inhibiting DNA replication
  • cross-link DNA by binding to guanine nucleotides
57
Q

Platinum compounds - cell cycle classification

A

cell cycle phase non-specific

58
Q

Platinum compounds - common drug

A

Cisplatin

59
Q

Cisplatin - indications for use

A
  • platinum compound

- metastatic ovarian and testicular cancers, and advanced bladder cancer

60
Q

Cisplatin - adverse effects (3)

A
  • nephrotoxic
  • ototoxic (toxic to ear –> deafness)
  • emetogenic (causes nausea and vomiting)
61
Q

Antimetabolites - what

A

Similar to natural compounds the body uses to

  • synthesize cellular constituents
  • incorporate into DNA
62
Q

Antimetabolites - mechanism of action

A
  • inhibiting particular enzymes or by preventing DNA replication
63
Q

Antimetabolites - cell cycle based classification

A

phase-specific –> S-phase

64
Q

Antimetabolites - classification based on function (3)

A

1) Folic acid analogs
2) purine analogs
3) pyrimidine analogs

65
Q

Folic acid analogs

A

block conversion of folate to its active form (= no DNA replication)

66
Q

Purine analogs

A

(purines [adenine, guanine] used to make DNA and RNA)

Purine analogs inhibit synthesis of DNA and RNA

67
Q

Pyramidine analogs

A

(pyrimidines = cytosine, thymine, uracil)

Pyramidine analogs inhibit synthesis of DNA

68
Q

Antitumour antibiotics - mechanism of action

A
  • kill cancer cells by intercalating DNA (move between bases of DNA, bind to DNA, cause change in structure of DNA = altered DNA is unable to be used as a template for synthesis = DNA synthesis is inhibited
69
Q

Antitumour antibiotics - route of administration

A

very poorly absorbed and therefore are given intravenously

70
Q

Anthracyclines - drug class

A
  • a type ot Antitumour antibiotic
71
Q

Antitumour antibiotics - adverse effects (2)

A
  • can cause severe bone marrow suppression and are cardiotoxic
72
Q

Mitotic Inhibitors - mechanism of action

A

Act during cell cycle to inhibit mitosis and prevent cell division

73
Q

Vinca alkaloid (what, mechanism of action)

A
  • mitotic inhibitor
  • block metaphase by binding to protein tubulin (microtubule) disrupting organization of microtubules –>disruption of chromosomes + cell death
74
Q

Taxanes (what, mechanism of action)

A
  • a mitotic inhibitor
  • acts in late stage of G2 (just prior to mitosis)
  • Taxanes stabilize microtubule bundles –> prevent cell division
75
Q

Hormonal agents to treat cancer (6)

A

1) glucocorticoids
2) gonadotropin releasing hormone agonist
3) androgen receptor antagonist
4) anti-estrogens
5) aromatase inhibitors
6) Trastuzumab

76
Q

Glucocorticoids - when used

A
  • used as adjunct to other chemo agents in cancers derived from lymphoid tissue
77
Q

Glucocorticoids - mechanism of action

A
  • directly toxic to lymphoid tissue
78
Q

Glucocorticoids - adverse effects (LT use) (6)

A
  • osteoporosis
  • adrenal insufficiency
  • susceptibility to infection
  • GI ulceration
  • electrolyte disturbane
  • growth retardation
79
Q

Glucocorticoids - other effects (not just cancer killing) = 3

A
  • management of complications of other chemo
    1) reduction in nausea and vomitting
    2) reduction of pain
    3) improved appetite
80
Q

Drugs for prostate cancer

A
  • Gonadotropin Releasing Hormone (GnRH agonist)

- Androgen Receptor Antagonists

81
Q

Goal of drugs treating prostate caner

A

androgen deprivation

82
Q

Gonadotropin Releasing Hormone (GnRh) agonist - mechanism of action

A
  • GnRH agonists - cause transient increase in testosterone production (cancer symptoms may increase at start of therapy)
  • over time, testosterone synthesis release is decreased

1) GnRH cause release of testosterone from testes
2) testosterone ‘feeds’ prostate cancer cells, but also acts by negative feedback to inhibit further GnRH release
3) GnRH agonists cause transient increase in testosterone, but then cause decreased GnRJ activity through desensitization and negative feedback
4) net effect is decreased testosterone synthesis and release

83
Q

Androgen Receptor Antagonists - use

A

Used in combo with a Gonadotropin Releasing hormone agonist or castration

84
Q

Androgen Receptor Antagonists - mechanism of action

A

block androgen receptors in tumour cells

85
Q

Drugs for breast cancer

A

1) anti-estrogens
2) aromatase inhibitors
3) Trastuzumab

86
Q

Treatment of breast cancer

A
  • Primary treatment = estrogen deprivation (estrogen feeds tumour)
  • combine with surgery and radiation therapy
87
Q

Anti-estrogens - mechanism of action

A
  • block estrogen receptors
88
Q

Tamoxifen - mechanism of action

A
  • an anti-estrogen drug
  • a partial estrogen receptor agonist (minimally activates estrogen receptor but also blocks endogenous estrogen from binding to its receptor)
89
Q

Aromatase inhibitors - mechanism of action

A
  • inhibits aromatization (process of converting androgens ino estrogen)
  • decrease amount of estrogen available to breast cancer cells
90
Q

Aromatase inhibitors - considerations of population

A
  • does not stop ovarian estrogen synthesis

- therefore, only useful in post-menopausal women

91
Q

Trastuzumab - mechanism of action

A
  • breast cancer patients with increased number of Human Epidermal Growth Factor Receptor 2 (a transmembrane receptor that helps regulate cell growth) will have especially aggressive tumour growth
  • Trastuzumab is a monoclonal antibody that binds to HER2 and prevents cell proliferation
92
Q

Trastuzumab - route of administration

A

IV (antibodies are degraded in stomach and poorly absorbed)

93
Q

Trastuzumab - Adverse event

A
  • cardiotoxicity
94
Q

Tyrosine Kinase Inhibitors - mechanism of action

A

Stops Tyrosine Kinases’ natural function

  • protein kinases are enzymes that phosphorylate proteins on specific amino acids (tyrosine)
  • activity of tyrosine kinase can activate gene transcription and/or DNA synthesis, making them an attractive option for the treatment of cancer
  • increased activity of tyrosine kinases have been observed in many cancers
95
Q

Imatinib - drug class

A
  • prototype tyrosine kinase inhibitor
96
Q

Imatinib - mechanism of action

A
  • causes complete inhibition of cellular proliferation and cell death via apoptosis (programed cell death)
97
Q

Imatinib - target disorders

A
  • chronic myelogenous leukemia (CML)

- gastrointestinal stromal tumours (GIST)

98
Q

Imatinib - adverse effects (4)

A
  • nausea
  • vomiting
  • edema
  • muscle cramps

Pharmacology (6 decks)

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