Module 17 Cancer Flashcards
(60 cards)
1
Q
Cancer Definition
A
- Uncontrolled proliferation of cells
- Neoplastic cells
- Abnormal/uncontrollable cell growth
2
Q
Cancer Cell Characteristics
A
- Uncontrollable cell proliferation
- Invasive (adjacent tissue)
- Metastatic (travel to different sites)
3
Q
Treatment Options
A
- Surgery (tumour removal)
- Radiation (shrink tumours)
- Chemotherapy (drugs target cells)
4
Q
Radiation
A
- Shrink tumours
- Kill cancer cells
- DNA damage of ALL cells
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
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
7
Q
Growth Faction of Cells
A
- Ratio of proliferation cells to cells in resting (G0)
8
Q
Cell Types with High Growth Fraction
A
- Bone marrow
- GI epithelium
- Hair follicles
- Germinal epithelium of testes
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
10
Q
Breast Cancer
A
- Clinical examination every 2-3 years
- Women over 50
- Additional/earlier screening for high risk cases
11
Q
Cervical Cancer
A
- HPV risk factor
- Genital skin to skin contact spread
- Pap test 1-3 years for sexually active women
12
Q
Colorectal Cancer
A
- 50+ men & women
- Fecal blood test every 2 years
- Colonoscopy every 5 years for high risk
13
Q
Prostate Cancer
A
- 50+ men
- Digital rectal exam
- Prostate antigen blood test
14
Q
Skin Cancer
A
- Self-checks regularly
- Changes to birth marks/moles, skin growths, sores
15
Q
Testicular Cancer
A
- 15+ men
- Self testicular exam regularly
16
Q
Solid Tumours
A
- Large fraction of cells in resting (G0)
- Chemotherapeutic drugs target proliferating cells
- Poor response
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)
18
Q
Intermittent Chemotherapy
A
- Allows time for normal cells to recover
- Normal cells must grow back faster than cancer cells
19
Q
Combination Chemotherapy
A
- Multiple agents more effective
- Decrease resistance
- Increased cancer cells killed
- Decrease injury to normal cells
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
21
Q
Increasing Cancer Cells Killed
A
- Different mechanisms of action for each drug
- Attack cells in various ways
- Greater killed cells
22
Q
Decrease Injury to Normal Cells
A
- Drugs with no overlapping toxicities
- Greater anti-cancer effects
- Greater safety
23
Q
Bone Marrow Suppression
A
- Neutropenia
- Thrombocytopenia
- Anemia
24
Q
Neutropenia
A
- Decreased neutrophils in blood
- Type of white blood cells
- Help fight infection
25
Thrombocytopenia
- Decreased platelets in blood
- Clotting of blood
- Increase risk of bleeding
26
Anemia
- Decreased number of erythrocytes (RBC)
- Less of a concern
27
Digestive Tract Injury
- Stomatitis (oral mucosa inflammation)
- Progress to ulceration
- Diarrhea (secondary damage)
- Epithelial lining damage
28
Nausea/Vomit
- Common adverse effect
- Can be a limiting factor of treatment
- Anti-emetic drugs
- Prevention of dehydration/malnutrition
29
Cytotoxic Agent Types
- Alkylating agents
- Platinum compounds
- Antimetabolites
- Antitumour antibiotics
- Mitotic inhibitors
30
Cycle Phase Specific Drugs
- Effective to certain cell phase only
- Cell must be actively part of cycle
- Ineffective on G0 cells
31
Non-Specific Phase Drugs
- Act at any stage of cell cycle
- More toxic to proliferating cells
32
Alkylating Agents
- 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
Cyclophosphamide
- Most common alkylating agent
- Prodrug
- Converted to active form by liver
- Delayed onset of effect
34
Cyclophosphamide Uses
- Hodgkins disease
- Solid tumour
35
Platinum Compounds
- Platinum in chemical structure of drug
- Cross link DNA, inhibiting replication
- Bind to guanine nucleotides
- Cell cycle non-specific drug
36
Cisplatin
- Most common platinum compound
- Nephrotoxic
- Ototoxic (ear)
- Emetogenic (cause nausea/vomit)
37
Antimetabolites
- Inhibit enzymes/prevent DNA replication
- Similar to natural body compound
- Cell phase specific drug
- Act during S phase
38
Folic Acid Analogs
- Block conversion of folate to active form
39
Purine & Pyrimidine Analogs
- Inhibit DNA/RNA synthesis
40
Antitumour Antibiotics
- Kill cancer cells by intercalating DNA
- Move between DNA bases & bind
- Inhibit DNA synthesis by altering structure
- Poorly absorbed
- IV admin
41
Anthracyclines
- Antitumour antibiotic
- Bone marrow suppression
- Cardiotoxic
42
Mitotic Inhibitors
- Act during cell cycle
- Prevent mitosis (cell division)
43
Vina Alkaloids
- Derived from periwinkle plant
- Block mitosis during metaphase
- Bind to tubulin protein
- Interferes with microtubule organization
- Inappropriate chromosome distribution
44
Taxanes
- Act in G2 phase
- Stabilize microtubule bundles
- Prevent cell division
45
Glucocorticoids
- Adjunct to other chemotherapy agents
- Cancer derived from lymphoid tissue
- Directly toxic to lymphoid tissue
- Management of complication of other agents
46
Side Effects of Glucocorticoids
- Osteoporosis
- Adrenal insufficiency
- Infection susceptibility
- GI ulceration
- Electrolyte disturbance
- Growth retardation
47
Prostate Cancer Treatment
- Prostate tissue androgen dependant
- Androgen (testosterone) deprivation
48
GnRH Agonist/Surgical Castration
- Transient increase in testosterone at start of therapy
- Decrease GnRH activity
- Use desensitization & negative feedback
- Overtime testosterone synthesis & release is decreased
49
Androgen Receptor Antagonists
- Used in combination with GnRH agonist/castration
- Blocks androgen receptors in tumour cells
50
GnRH Function
- Causes release of testosterone from testes
51
Testosterone Function
- Feeds prostate cancer cells
- Negative feedback for GnRH release
52
Breast Cancer Treatment
- Estrogen causes proliferation of cancer cells
- Depriving breast cancer cells of estrogen
- Surgery
- Radiation therapy
53
Tamoxifen
- Common anti-estrogen drug
- Partial estrogen receptor agonist
- Block binding of endogenous estrogen to receptor
54
Aromatase Inhibitors
- Inhibit conversion of androgens to estrogens
- Decrease estrogen available to breast cancer cells
- Postmenopausal women only
- Doesn't block ovarian estrogen synthesis
55
HER2
- Transmembrane receptor
- Regulate cell growth
- Tumours with high HER2 have aggressive growth
56
Mechanisms of Trastuzumab
- Monoclonal antibody
- Binds to HER2
- Prevent cell proliferation
- IV admin
- Cardiotoxicity risk
57
Tyrasine Kinase Inhibitors
- Activate gene transcription/DNA synthesis
- Phosphorylate proteins on amino acid residues
- Increase tyrosine kinases activity in cancer
58
Imatinib
- Prototype tyrosine kinase inhibitor
- Inhibits cellular proliferation
- Cell death via apoptosis
59
Imatinib Uses
- Chronic myelogenous leukemia (CML)
- GI stromal tumours (GIST)
60
Imatinib Adverse Effects
- Nausea/vomit
- Edema
- Muscle cramps