Pharmacology Module 2 - Anticancer & Vaccines

Front 1

Cancer cells:
Characteristics

Back 1

Persistant growth & division
Invasion of surrounding tissues
Ability to metastasize
Do not undergo apoptosis

Front 2

Cell Cycle:
Phases

Back 2

G1, S, G2, M, G0

Front 3

Cell Cycle:
G1 Phase

Back 3

Synthesis of components for DNA synthesis

Front 4

Cell Cycle:
S Phase

Back 4

DNA synthesis

Front 5

Cell Cycle:
G2 Phase

Back 5

Synthesis of components for mitosis

Front 6

Cell Cycle:
M Phase

Back 6

Mitosis

Front 7

Cell Cycle:
G0 Phase

Back 7

"Resting" phase

Front 8

Relationship between chemotherapeutic
drugs and growth fraction

Back 8

Chemotherapeutic drugs are much
more toxic to tissues that have
a high growth fraction.

Growth fraction: The ratio of
proliferating cells to G0 cells.

Front 9

Chemotherapy treatment:
Obstacles

Back 9

Chemotherapy drugs are toxic to normal cells
"Cure" requires 100% kill
Early detection is rare
Solid tumors respond poorly
Drug resistance
Cancer has many different cell types
Limited drug access to cancer (distribution)

Front 10

Chemotherapy treatment:
Intermitent therapy

Back 10

Gives normal cells a chance to recover between sessions.
Over time the population of cancer cells is reduced, ideally to zero.

Front 11

Chemotherapy treatment:
Combination therapy

Back 11

Utilizes more than one drug, and is therefore more effective.
Reduces the chance of drug resistance.
Reduced injury to normal cells

Front 12

Chemotherapy treatment:
Major toxicities

Back 12

Bone marrow suppression,
Digestive tract injury,
Nausea/Vomiting,
Alopecia,
Reproductive toxicity,
Carcinogenic

Front 13

Bone marrow suppression:
What is it/Examples

Back 13

Major toxicity of chemotherapy

Neutropenia (leading to ↑ risk of infection),
Anemia,
Thrombocytopenia (leading to abnormal bleeding)

Front 14

Digestive tract injury
What is it/Why

Back 14

Major toxicity of chemotherapy

epithelial cells have a high growth fraction and are therefore sensitive to chemotherapy drugs

Front 15

Chemotherapy agents:
Groups

Back 15

Alkylating agents,
Platinum compounds,
Antimetabolites,
Antitumor antibiotics,
Mitotic inhibitors

Front 16

Chemotherapy agents:
Cell-cycle specificity

Back 16

50% are cell-cycle phase specific,
50% are cell-cycle phase nonspecific

Front 17

Alkylating agents:
Mechanism of action

Back 17

Adds an alkyl group to cell DNA, therby disrupting the DNA and killing cancer cells

Front 18

Alkylating agents:
Cell-cycle specificity

Back 18

Cell-cycle phase nonspecific

Front 19

Alkylating agents:
Resistance

Back 19

Common

Front 20

Alkylating agents:
Toxicity

Back 20

Toxic to tissues with high growth fraction

Front 21

Alkylating agents:
Example

Back 21

Cyclophosphamide (Cytoxan)

Front 22

Platinum compounds:
Mechanism of action

Back 22

Form cross-links between DNA strands, thereby disrupting DNA and killing cancer cells

Front 23

Platinum compounds:
Cell-cycle specificity

Back 23

Cell-cycle phase nonspecific

Front 24

Platinum compounds:
Toxicity

Back 24

Toxic to tissues with high growth fraction

Front 25

Platinum compounds:
Example

Back 25

Cisplatin (Platinol-AQ)

Front 26

Cisplatin (Platinol-AQ):
Unique ADR's

Back 26

Kidney damage

Front 27

Antimetabolites:
Mechanism of action

Back 27

Resemble natural metabolites (folic acid, pyrimidines, purines)
Cancer cells uptake these agents instead of the natural ones
These agents disrupt the metabolic processes of cancer cells

Front 28

Antimetabolites:
Cell-cycle specificity

Back 28

Most are S-phase specific

Front 29

Antimetabolites:
Toxicity

Back 29

Toxic to tissues with high growth fraction

Front 30

Antimetabolites:
Folic acid analog

Back 30

Methotrexate (Rheumatrex, Trexall)

Front 31

Antimetabolites:
Pyrimidine (cytosine) analog

Back 31

Cytarabine, AKA: "Ara C"

Front 32

Antimetabolites:
Pyrimidine (uracil) analog

Back 32

Fluorouracil

Front 33

Antimetabolites:
Purine analog

Back 33

Mercaptopurine (Purinethol)

Front 34

Antitumor antibiotics:
Mechanism of action

Back 34

Derived from Streptomyces
Binds to tumor DNA, distorting it, thereby disrupting RNA and protein synthesis

Front 35

Antitumor antibiotics:
Cell-cycle specificity

Back 35

Cell-cycle phase nonspecific

Front 36

Antitumor antibiotics:
Examples

Back 36

Doxorubicin (Adriamycin, Doxil)
Bleomycin (Blenoxane)

Front 37

Doxorubicin (Adriamycin, Doxil):
Unique ADR's

Back 37

Cardiotoxicity

Front 38

Bleomycin (Blenoxane):
Unique ADR's

Back 38

Lung injury

Front 39

Mitotic inhibitors:
Mechanism of action

Back 39

Inhibit mitosis of tumor cells

Front 40

Mitotic inhibitors:
Cell-cycle specificity

Back 40

M-phase specific

Front 41

Mitotic inhibitors:
Examples

Back 41

Vincristine (Oncovin)
Paclitaxel (Taxol)

Front 42

Vincristine (Oncovin):
Group
Unique ADR's

Back 42

Vinca alkaloids
Peripheral neuropathy

Front 43

Paclitaxel (Taxol):
Group
Unique ADR's

Back 43

Taxanes
Severe hypersensitivity reactions (hypotension, dyspnea, angioedema, uticaria)

Front 44

Glucocorticoids:
Use to treat cancer

Back 44

Lymphoid cancers (leukemias, lymphomas), typically with other agents
Treatment of CINV
Reduction of brain swelling r/t radiation
Appetite promotion

Front 45

Glucocorticoids:
Mechanism of action

Back 45

Suppression of mitosis, causing regression of lymphoid tissue

Front 46

Glucocorticoids:
Toxicity

Back 46

Few short-term affects
Adrenal suppression seen with long-term use

Front 47

Glucocorticoids:
Examples

Back 47

Prednisone (Deltasone)
Dexamethasone (Decadron)

Front 48

Hormonal agents & Biologic response modifiers:
General characteristics

Back 48

All are cell-cycle phase nonspecific
Lack serious toxicities of cytotoxic agents
Mainly used for breast and prostate cancers

Front 49

Prostate cancer:
Hormonal agent examples

Back 49

Leuprolide (Lupron)
Flutamide (Eulexin)
Estrogens

Front 50

Leuprolide (Lupron):
Uses

Back 50

Prostate cancer
Endometriosis

Front 51

Leuprolide (Lupron):
Mechanism of action

Back 51

Suppresses production of androgens (testosterone)
Chemical castration
A gonadotropin-releasing hormone agonist

Front 52

Leuprolide (Lupron):
ADR's

Back 52

Hot flashes (most common)
Impotence, Decreased libido

Front 53

Flutamide (Eulexin):
Uses

Back 53

Prostate cancer (in combination with Leuprolide)

Front 54

Flutamide (Eulexin):
Mechanism of action

Back 54

Blocks androgen receptors in tumor cells
An androgen receptor blocker

Front 55

Flutamide (Eulexin):
ADR's

Back 55

Gynecomastia (most common)
Possible liver damage (Monitor LFT's)

Front 56

Estrogens:
Uses

Back 56

Prostate cancer (second-line drug)

Front 57

Estrogens:
Mechanism of action

Back 57

Suppresses production of androgens (which prostate tumor cells are dependent upon)

Front 58

Estrogens:
ADR's

Back 58

Thrombolitic disorders, gynecomastia, fluid retention, depression

Front 59

Estrogens:
Examples

Back 59

Diethylstilbestrol diphosphate (Stilphostrol)

Front 60

Breast cancer drugs:
Groups

Back 60

Antiestrogens
Aromatase inhibitors
Trastuzumab (Herceptin)
Cytotoxic drugs

Front 61

Antiestrogens:
Uses

Back 61

ER positive breast cancer
Prevention of breast cancer in women considered high-risk

Front 62

Antiestrogens:
Mechanism of action

Back 62

Blocks estrogen receptors

Front 63

Antiestrogens:
Examples

Back 63

Tamoxifen (Nolvadex)
Raloxifene (Evista)

Front 64

Tamoxifen (Nolvadex):
Use

Back 64

Most widely presribed drug for breast cancer
"gold standard"

Front 65

Tamoxifen (Nolvadex):
ADR's

Back 65

Hot flashes (most common)
Blood clots & increased risk for uterine cancer (most significant)

Front 66

Raloxifene (Evista):
ADR's

Back 66

Does NOT increase risk for uterine cancer

Front 67

Aromatase inhibitors:
Uses

Back 67

ER positive breast cancer in post-menopausal women

Front 68

Aromatase inhibitors:
Mechanism of action

Back 68

Blocks the production of estrogen from the adrenal glands
"Aromatase" is the enzyme that converts adrenal androgens to estrogen

Front 69

Aromatase inhibitors:
Effectiveness

Back 69

More effective than Tamoxifen with few ADR's
May be the new "gold standard"

Front 70

Aromatase inhibitors:
ADR's

Back 70

Generally well tolerated
May increase risk for osteoporosis & bone fractures

Front 71

Aromatase inhibitors:
Examples

Back 71

Anasrozole (Arimidex)

Front 72

Trastuzumab (Herceptin):
Uses

Back 72

HER2-positive breast cancer

Front 73

Trastuzumab (Herceptin):
Mechanism of action

Back 73

A monoclonal antibody that binds to "human epidermal growth factor receptor 2 (HER2)"
Inhibits cell proliferation and promotes cell death

Front 74

Trastuzumab (Herceptin):
ADR's

Back 74

Cardiotoxicity
Hypersensitivity reactions

Front 75

Biologic response modifiers:
Mechanism of action

Back 75

(1) Boost host immune response
(2) Cause cancer cells to become non-malignant
(3) Interfere with proliferation of cancer cells

Front 76

Biologic response modifiers:
Example

Back 76

Interferons

Front 77

Interferons:
What are they?

Back 77

Naturally occuring proteins with antiviral, anticancer, and immune actions
AKA: Immunostimulants

Front 78

Interferons:
Uses

Back 78

Cancers, Viral hepatitis, Multiple Sclerosis

Front 79

Interferons:
ADR's

Back 79

Flu-like syndrome (common)

Front 80

Live vaccine:
Definition

Back 80

Contains live microorganisms that have been made weak or avirulent

Front 81

Live vaccine:
Contraindications

Back 81

Contraindicated in the immunosuppressed

Front 82

Live vaccine:
Examples

Back 82

MMR
Varicella

Front 83

Killed vaccine:
Definition

Back 83

Contains killed whole or partial microbes

Front 84

Killed vaccine:
Examples

Back 84

Pertussis
H. influenzae type b
Hepatitis A, B
Polio
Influenza, Pneumonia

Front 85

Toxoid:
Definition

Back 85

A bacterial toxin made non-toxic
Used to force creation of antibodies against the toxoid

Front 86

Toxoid:
Examples

Back 86

Tetanus toxoid
Diphtheria toxioid

Front 87

Active immunity:
Definition

Back 87

Production of antibodies by an individual in response to infection or administration of vaccines or toxoids

Front 88

Active immunity:
Time to develop/duration

Back 88

Protection takes weeks to months to develop, but is long-lasting

Front 89

Passive immunity:
Definition

Back 89

Obtained through administration of preformed antibodies after expose for a pathogen

Front 90

Passive immunity:
Time to develop/duration

Back 90

Protection is immediate, but is short in duration

Front 91

Passive immunity:
Example

Back 91

Administration of immunoglobulin after tetanus or Hepatitis B exposure

Front 92

Vaccines:
ADR's

Back 92

Generally very safe
Some mild reactions are common (local pain, redness, swelling, fever)
Serious reactions are rare

Front 93

Vaccines:
Contraindications

Back 93

Anaphylactic reaction to a particular vaccine
Anaphylactic reaction to vaccine component (egg), Moderate - severe illness (vaccinate after illness resolution)

Front 94

Influenza vaccine:
Special populations

Back 94

All children 6 - 23 months
Children <6 months with chronic illness
Elderly
Adults with chronic illness
Health care workers

Front 95

Meningococcus vaccine:
Special populations

Back 95

Dense populations
(colleges, Military)

Front 96

MMR vaccine:
Special populations

Back 96

Colleges, Military

Front 97

Td vaccine:
Special populations

Back 97

Elderly
Adults with chronic illness
Asplenic individuals

Front 98

Hepatitis B vaccine:
Special populations

Back 98

Health care workers
Sexually active individuals
Individuals with Hx of STD
Injection drug use

Front 99

HPV vaccine:
Special populations

Back 99

Teenage girls