Module 17 Cancer Flashcards

1
Q

Cancer Definition

A
  • Uncontrolled proliferation of cells
  • Neoplastic cells
  • Abnormal/uncontrollable cell growth
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2
Q

Cancer Cell Characteristics

A
  • Uncontrollable cell proliferation
  • Invasive (adjacent tissue)
  • Metastatic (travel to different sites)
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3
Q

Treatment Options

A
  • Surgery (tumour removal)
  • Radiation (shrink tumours)
  • Chemotherapy (drugs target cells)
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4
Q

Radiation

A
  • Shrink tumours
  • Kill cancer cells
  • DNA damage of ALL cells
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5
Q

Cell Cycle Phases

A
  • G0 resting, no cell replication
  • G1, duplication prep (DNA)
  • S, synthesizes DNA
  • G2, mitosis prep
  • M, division via mitosis
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6
Q

Toxicity of Normal Cells

A
  • Neoplastic cells similar to normal cells
  • Difficult to only target cancer cells
  • Occurs in cells with high growth fraction
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7
Q

Growth Faction of Cells

A
  • Ratio of proliferation cells to cells in resting (G0)
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8
Q

Cell Types with High Growth Fraction

A
  • Bone marrow
  • GI epithelium
  • Hair follicles
  • Germinal epithelium of testes
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9
Q

Curing Cancer

A
  • 100% of cancer cells killed
  • Difficult to test & determine
  • First order kinetics
  • Constant % of cells killed at dose of drug
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10
Q

Breast Cancer

A
  • Clinical examination every 2-3 years
  • Women over 50
  • Additional/earlier screening for high risk cases
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11
Q

Cervical Cancer

A
  • HPV risk factor
  • Genital skin to skin contact spread
  • Pap test 1-3 years for sexually active women
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12
Q

Colorectal Cancer

A
  • 50+ men & women
  • Fecal blood test every 2 years
  • Colonoscopy every 5 years for high risk
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13
Q

Prostate Cancer

A
  • 50+ men
  • Digital rectal exam
  • Prostate antigen blood test
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14
Q

Skin Cancer

A
  • Self-checks regularly
  • Changes to birth marks/moles, skin growths, sores
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15
Q

Testicular Cancer

A
  • 15+ men
  • Self testicular exam regularly
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16
Q

Solid Tumours

A
  • Large fraction of cells in resting (G0)
  • Chemotherapeutic drugs target proliferating cells
  • Poor response
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17
Q

Drug Resistance Types

A
  • Decreased drug uptake
  • Increased drug efflux
  • Decreased drug activation (prodrugs)
  • Reduced target sensitivity
  • Increased cellular repair (DNA)
  • Decreased apoptosis (cell death)
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18
Q

Intermittent Chemotherapy

A
  • Allows time for normal cells to recover
  • Normal cells must grow back faster than cancer cells
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19
Q

Combination Chemotherapy

A
  • Multiple agents more effective
  • Decrease resistance
  • Increased cancer cells killed
  • Decrease injury to normal cells
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20
Q

Decreasing Drug Resistance

A
  • Acquired due to random cell mutation
  • Unlikely cancer cells will undergo multiple mutation
  • Multiple drugs equal more effective therapy
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21
Q

Increasing Cancer Cells Killed

A
  • Different mechanisms of action for each drug
  • Attack cells in various ways
  • Greater killed cells
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22
Q

Decrease Injury to Normal Cells

A
  • Drugs with no overlapping toxicities
  • Greater anti-cancer effects
  • Greater safety
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23
Q

Bone Marrow Suppression

A
  • Neutropenia
  • Thrombocytopenia
  • Anemia
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24
Q

Neutropenia

A
  • Decreased neutrophils in blood
  • Type of white blood cells
  • Help fight infection
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25
Q

Thrombocytopenia

A
  • Decreased platelets in blood
  • Clotting of blood
  • Increase risk of bleeding
26
Q

Anemia

A
  • Decreased number of erythrocytes (RBC)
  • Less of a concern
27
Q

Digestive Tract Injury

A
  • Stomatitis (oral mucosa inflammation)
  • Progress to ulceration
  • Diarrhea (secondary damage)
  • Epithelial lining damage
28
Q

Nausea/Vomit

A
  • Common adverse effect
  • Can be a limiting factor of treatment
  • Anti-emetic drugs
  • Prevention of dehydration/malnutrition
29
Q

Cytotoxic Agent Types

A
  • Alkylating agents
  • Platinum compounds
  • Antimetabolites
  • Antitumour antibiotics
  • Mitotic inhibitors
30
Q

Cycle Phase Specific Drugs

A
  • Effective to certain cell phase only
  • Cell must be actively part of cycle
  • Ineffective on G0 cells
31
Q

Non-Specific Phase Drugs

A
  • Act at any stage of cell cycle
  • More toxic to proliferating cells
32
Q

Alkylating Agents

A
  • Transfer alkyl group to cell components (DNA)
  • Form cross bridge between nitrogen on guanine nucleotides
  • Results in miscoding DNA/inhibition of replication
  • Cell cycle non-specific drug
33
Q

Cyclophosphamide

A
  • Most common alkylating agent
  • Prodrug
  • Converted to active form by liver
  • Delayed onset of effect
34
Q

Cyclophosphamide Uses

A
  • Hodgkins disease
  • Solid tumour
35
Q

Platinum Compounds

A
  • Platinum in chemical structure of drug
  • Cross link DNA, inhibiting replication
  • Bind to guanine nucleotides
  • Cell cycle non-specific drug
36
Q

Cisplatin

A
  • Most common platinum compound
  • Nephrotoxic
  • Ototoxic (ear)
  • Emetogenic (cause nausea/vomit)
37
Q

Antimetabolites

A
  • Inhibit enzymes/prevent DNA replication
  • Similar to natural body compound
  • Cell phase specific drug
  • Act during S phase
38
Q

Folic Acid Analogs

A
  • Block conversion of folate to active form
39
Q

Purine & Pyrimidine Analogs

A
  • Inhibit DNA/RNA synthesis
40
Q

Antitumour Antibiotics

A
  • Kill cancer cells by intercalating DNA
  • Move between DNA bases & bind
  • Inhibit DNA synthesis by altering structure
  • Poorly absorbed
  • IV admin
41
Q

Anthracyclines

A
  • Antitumour antibiotic
  • Bone marrow suppression
  • Cardiotoxic
42
Q

Mitotic Inhibitors

A
  • Act during cell cycle
  • Prevent mitosis (cell division)
43
Q

Vina Alkaloids

A
  • Derived from periwinkle plant
  • Block mitosis during metaphase
  • Bind to tubulin protein
  • Interferes with microtubule organization
  • Inappropriate chromosome distribution
44
Q

Taxanes

A
  • Act in G2 phase
  • Stabilize microtubule bundles
  • Prevent cell division
45
Q

Glucocorticoids

A
  • Adjunct to other chemotherapy agents
  • Cancer derived from lymphoid tissue
  • Directly toxic to lymphoid tissue
  • Management of complication of other agents
46
Q

Side Effects of Glucocorticoids

A
  • Osteoporosis
  • Adrenal insufficiency
  • Infection susceptibility
  • GI ulceration
  • Electrolyte disturbance
  • Growth retardation
47
Q

Prostate Cancer Treatment

A
  • Prostate tissue androgen dependant
  • Androgen (testosterone) deprivation
48
Q

GnRH Agonist/Surgical Castration

A
  • Transient increase in testosterone at start of therapy
  • Decrease GnRH activity
  • Use desensitization & negative feedback
  • Overtime testosterone synthesis & release is decreased
49
Q

Androgen Receptor Antagonists

A
  • Used in combination with GnRH agonist/castration
  • Blocks androgen receptors in tumour cells
50
Q

GnRH Function

A
  • Causes release of testosterone from testes
51
Q

Testosterone Function

A
  • Feeds prostate cancer cells
  • Negative feedback for GnRH release
52
Q

Breast Cancer Treatment

A
  • Estrogen causes proliferation of cancer cells
  • Depriving breast cancer cells of estrogen
  • Surgery
  • Radiation therapy
53
Q

Tamoxifen

A
  • Common anti-estrogen drug
  • Partial estrogen receptor agonist
  • Block binding of endogenous estrogen to receptor
54
Q

Aromatase Inhibitors

A
  • Inhibit conversion of androgens to estrogens
  • Decrease estrogen available to breast cancer cells
  • Postmenopausal women only
  • Doesn’t block ovarian estrogen synthesis
55
Q

HER2

A
  • Transmembrane receptor
  • Regulate cell growth
  • Tumours with high HER2 have aggressive growth
56
Q

Mechanisms of Trastuzumab

A
  • Monoclonal antibody
  • Binds to HER2
  • Prevent cell proliferation
  • IV admin
  • Cardiotoxicity risk
57
Q

Tyrasine Kinase Inhibitors

A
  • Activate gene transcription/DNA synthesis
  • Phosphorylate proteins on amino acid residues
  • Increase tyrosine kinases activity in cancer
58
Q

Imatinib

A
  • Prototype tyrosine kinase inhibitor
  • Inhibits cellular proliferation
  • Cell death via apoptosis
59
Q

Imatinib Uses

A
  • Chronic myelogenous leukemia (CML)
  • GI stromal tumours (GIST)
60
Q

Imatinib Adverse Effects

A
  • Nausea/vomit
  • Edema
  • Muscle cramps