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Flashcards in Antineoplastic Medications Deck (10)
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Describe the normal cell cycle



 Describe barriers to treatment with chemotherapy

Toxicity to normal cells-drugs lack selective toxicity
- Need for 100% kill for cure
- First Order Kinetics
- Lack of Immune Involvement
- Unknown Cure Interval


Lack of early detection:  Usually at least 1 million cells needed for symptoms, up to 1 billion cells for mass to be detected.  Consequences:  metastasis, decrease in drug responsiveness, worsening health of patient

The larger the tumor, the less responsive it is to cytotoxic medications-lower growth fraction, less blood supply to core
- debulking (Surgically taking out the visable tumor)

Drug Resistance:  Reduced drug uptake, increased drug efflux, reduced drug activation, increased repair of drug induced DNA damage.

Heterogeneous tumor cells

Location:  Especially CNS, large solid tumors



Describe methods to overcome chemotherapy barriers

Intermittent chemo is a great way, cause it allows normal cells some time to recover

Combination of cytotoxic medications
- Suppresses drug resistance-less likely to have multiple mutations
- Increased rate of tumor cells kill
- Decrease in injury to normal cells-use drugs with different toxicities

Specialized routes
 -Peritoneal cavity



 Understand common toxicities associated with chemotherapy

Bone Marrow related suppression!


Neutropenia - Nadir


Digestive tract



N & V

Hair loss (Alopecia)

Reproductive Toxicity 

Hyperuricemia (That’s why we give allopurinol)



Toxicity to heart lung and kidneys is unique.


Differentiate between cell-cycle phase specific and non-specific cytotoxic drugs

Cell-Cycle Phase Specificity
    - Cell-cycle phase nonspecific:  affects cells during any phase of cycle.
    - Cell-cycle phase specific:  because of mechanism of action, about ½ of  cytotoxic drugs work during specific phase.  



Discuss the utility of hormone modifiers

Least toxic of anticancer medications

Work at specific hormone receptors so highly selective

Most are used for breast, endometrial and prostate cancers

Glucocorticoids  also used in lymphomas and leukemias

Glucocorticoids:  Directly toxic to lymphoid tissues. 

Antiestrogens:  Blocks estrogen stimulation of cancer cells. 

Aromatase Inhibitors:  Postmenopausal women only-blocks production of estrogen from androgen precursors but not ovaries

GNRH Antagonists-for prostate CA, endometriosis.   “Chemical castration”. 



Discuss action and side effects of immunostimulants

Normally produced in response to viral infections and other stimuli, active against many solid tumors and hematologic malignancies

Enhance host immune response and also has direct antiproliferative effect on cancer cells

SE:  Flu-like symptoms, prolonged high dose can cause bone marrow suppression.



Describe the mechanism of action of imatanib (Gleevac)

Inhibits Philadelphia chromosome

Oral therapy for CML

Indefinite therapy, very expensive



Understand long term effects of chemotherapy and radiation


Deficits of language, memory, and attention

Atrophy of gray matter

Loss of hearing and vision

Peripheral neuropathies


Cardiomyopathy due to medications as well as radiation therapy




Xerostomia (facial radiation)

Hepatic fibrosis



Fibrosis secondary to medication

Pneumonitis due to radiation


Reproductive issues

Growth retardation



Understand tumor lysis syndrome.  When are patients most at risk?  What systems are most affected?

Patients most at risk 1-3 days after chemotherapy

Seen in rapidly growing cancers after administration of chemotherapy

Kidneys and Heart are most affected I’m not 100% about this 

- Heart for sure, tumor lysis syndrome causes lysis of cells which releases intercellular potassium causing cardiac dysrhythmias.