Chemo Drugs Flashcards

(29 cards)

1
Q

What is cancer?

A

Uncontrolled proliferation of cells; neoplastic cells have abnormal, unregulated growth.

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2
Q

What are the 5 key characteristics of cancer cells?

A
  1. Persistent proliferation 2. Invasive 3. Metastatic 4. Immortal 5. Angiogenesis
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3
Q

What are the three primary treatment modalities for cancer?

A
  1. Surgery 2. Radiation 3. Chemotherapy
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4
Q

Why is understanding the cell cycle important in cancer therapy?

A

Chemotherapeutic drugs often target specific stages of cell proliferation.

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5
Q

Why is toxicity to normal cells a major issue in chemotherapy?

A

Cancer cells are similar to normal cells; drugs also affect normal cells with high growth fractions.

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6
Q

What is the significance of the growth fraction?

A

High growth fraction = more susceptible to chemotherapy; includes bone marrow, GI tract, hair follicles, testes.

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7
Q

What does ‘100% cell kill’ mean in cancer therapy?

A

All cancer cells must be eradicated to cure cancer; even a few remaining cells can cause recurrence.

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8
Q

How does first-order kinetics affect chemotherapy effectiveness?

A

A constant percentage of cancer cells are killed at each dose.

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9
Q

Why is early cancer detection challenging?

A

Tumors often aren’t detected until they reach ~10⁹ cells.

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10
Q

List Canada’s key cancer screening recommendations.

A

Breast: CBE every 2–3 yrs after 50; Cervical: Pap 1–3 yrs; Colorectal: FOBT every 2 yrs after 50; Prostate: DRE/PSA; Skin: Self-checks; Testicular: Self-exams from 15.

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11
Q

Why do solid tumors respond poorly to chemotherapy?

A

Many cells are in G₀ phase, where chemo is ineffective.

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12
Q

List five mechanisms of drug resistance in cancer cells.

A
  1. ↓ Uptake 2. ↑ Efflux 3. ↓ Activation (prodrug) 4. ↑ Repair/↓ Target sensitivity 5. ↓ Apoptosis
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13
Q

What is the benefit of intermittent chemotherapy?

A

Allows normal cells to recover faster than cancer cells.

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14
Q

Why is combination chemotherapy used?

A
  1. ↓ Resistance 2. ↑ Cell kill 3. ↓ Injury to normal cells
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15
Q

What are the three major toxicities from bone marrow suppression?

A
  1. Neutropenia 2. Thrombocytopenia 3. Anemia
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16
Q

What digestive tract injuries are common in chemotherapy?

A

Stomatitis (inflammation of Oral Mucosa) and diarrhea.

17
Q

Why are nausea and vomiting major concerns in chemotherapy?

A

They’re common, treatment-limiting, and require supportive care.

18
Q

What are the two major classes of anti-cancer drugs?

A
  1. Cytotoxic agents 2. Hormonal/other agents
19
Q

What is the difference between cell cycle phase-specific and non-specific drugs?

A

Specific: active phases only; Non-specific: any stage, more toxic to dividing cells.

20
Q

Describe alkylating agents and their mechanism.

A

Cross-link DNA by alkylating guanine; phase non-specific; example: Cyclophosphamide. (Memory Tip: alkyline cyclone) , prodrug, and need liver conversion. Delay onset. Most common indication Hodgkin (hog = ugly bumps)

21
Q

Describe platinum compounds and their mechanism.

A

Nonspecific, Cross-link DNA like alkylating agents and stop replication; example: Cisplatin; treat ovarian, testicular and advance bladder ca, side effects: nephro/ototoxicity + emetogenic (cisplatin NOE)

22
Q

Describe antimetabolites and their subclasses.

A

Inhibit Specific enzymes or prevent DNA replication; Cell Cycle S-phase specific; subclasses: folic acid, purine(adenine, guanine), pyrimidine (cytosine, thymine, uracil) analogs.

23
Q

How do antitumor antibiotics work?

A

Intercalate DNA to inhibit synthesis; nonspecific, IV only not oral, example: Anthracyclines; AE: cardiotoxic & Bone marrow impression

24
Q

How do mitotic inhibitors work and what are their types?

A

Cell cycle specific, Inhibit mitosis; types: Vinca alkaloids (block metaphase)- bind to tubulin protein and cause inappropriate distribution of chromosomes, Taxanes (stabilize microtubules): work in late G2 phase, freeze microtubules and cannot mitosis.

25
How do glucocorticoids help in cancer therapy?
Toxic to lymphoid tissue; Adjunct tx, reduce chemo side effects like nausea, pain and increase appetite. AE: osteoporosis, adrenal insufficiency, susceptibility to infection, GI ulcers, growth retardation.
26
How is androgen deprivation achieved in prostate cancer?
GnRH agonists (MOA: mimic GnRH and over time less testosterone) or castration; + androgen receptor antagonists (MOA: block androgen receptor in cancer cell itself, inhibit further GnRH release via negative feedback.
27
How is estrogen deprivation achieved in breast cancer?
Anti-estrogens (e.g., Tamoxifen), Aromatase inhibitors, Trastuzumab for HER2+ tumors.
28
What is the role of Trastuzumab in breast cancer?
Monoclonal antibody for HER2+ tumors; inhibits proliferation; IV only; cardiotoxic.
29
What are tyrosine kinase inhibitors and give an example.
Block phosphorylation → inhibit DNA synthesis; example: Imatinib (used for CML, GIST).