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Antineoplastic Pharm
Intro to antineoplastic pharmacology
| Question | Answer |
|---|---|
| Induction | Given to induce a remission Common usage: acute leukemia |
| Adjuvant | Used after initial surgery or radiation to prevent recurrence |
| Neoadjuvant | given prior to surgery or radiation therapy to reduce tumor size |
| Salvage | Used after recurrence of refractory tumor following chemo |
| Chemosensitive | Used concurrently with radiation to increase radiosensitivity |
| Palliative | Given specifically to address symptom management without expecting to significantly reduce the cancer |
| What are the four responses to chemotherapy? | (CR): complete disappearance of tumor (PR): >50% decresase in tumor/lesions (SD): no new lesions; PR>SD>PD (PD) >50% increase in product of measured lesion |
| What normal tissue is also susceptible to anticancer drug? (divide rapidly) | Bone marrow, hair follicles, GI tract |
| What two cancers are difficult to treat due to slow growth? | Colon and lung carcinoma |
| Tumor Determinants | Growth Fraction, Total tumor burden, Cell cycle phase, Drug resistance |
| Host Determinants | General Health Status, Tumor Site, Immunocompetence |
| What are some complications to effective cancer treatment? | Number of dividing vs resting cells change Biochemical/biological character change By the time detectable, tumors are subclones of different cells Genetic instability--drug resistance mutation rate= 1/10,000 there's a 50/50 chance of res. cell 100 cel |
| Tumor Perfusion | Uneven distribution of oxygen, nutrients cause uneven cell growth. Tumor doubling time decreases as tumor mass increases. Uneven drug distribution: cells may survive initial treatment |
| Clinically detectable tumor | 1x10^9 cells (1 cm) |
| Lethal tumor | 1x10^12 |
| Larger tumors are harder to kill. Why? | -more difficult for drug to reach (poor blood flow) -slower growth=less sensitive to drug therapy -increased metastasis -more therapy needed, higher toxicity |
| Palliative Chemotherapy | Transient remission, extended survival, eventual death |
| Curative Chemotherapy | -Tumor initially reduced by surgery or radiation (debulking) -Continued drug treatment after clinical evidence disappears to prevent recurrence |
| Mitotoxicity Hypothesis | Drugs need to interfere with process of division and growth of cells. -Poison S phase, keep from progressing to M phase. No division=cell death!! |
| Cell Cycle Specific (CCS) | Cells must be mitotically active for drug to produce its effects Drug target only available at particular phase Effective: high growth fraction |
| Cell Cyce Non-Specific (CCNS) | Drug effect may be enhanced but not dependent on mitotic activity Effective: low and high growth fraction |
| Major Mechanisms of Tumor Resistance | -decrease drug uptake/increase drug efflux -decrease drug activation/increase drug inactivation -overexpression or mutation of drug target -increased repair of drug damage to DNA -increased intracellular nucleophile concentrations of substances (glut) |
| Adverse Effects | Most IV admin. -catastrophic tissue damage -requires professional to administer Toxicities Widely Variable -transient: nausea, vomitting -reversible: bone marrow depression, alopecia -irreversible: cardiac, pulmonary, and bladder toxicities |
| Adverse Effects (continued) | Chemotherapy related tumor many drugs are mutagens. neoplasms arise 10+ years later |
| Vital Organ Systems & Cancer Treatment | Blood cells: anemia, fatigue Digestive tract: mouth ulcers, loss of taste, diarrhea, consitpation Reproductive system: infertility Hair loss Vomiting/Nausea |
| Alkylating Agents (Chemo drugs) | largest class highly reactive alkyl groups alkylation of DNA: N7 position of guanine Cause: excessive cross linkings (can't divide) and DNA strand breakage (deprivation) |
| Antimetabolites (Chemo drugs) | Interfere with DNA synthesis *most are prodrugs activated through incorporation normal biosynthetic pathways Drug Classes: Antifolates Nucleoside analogs |
| Antibiotics (Chemo drugs) | General Classes: cyclic petapeptides anthracyclines complex glycopeptides Bind to DNA to inhibit RNA synthesis (transcription) -break DNA strands or inhibit topoisomerase |
| Antimitotic Agents (Chemo drugs) | disrupt chromosome disrupt DNA replication and mitosis Genteral types: microtubule inhibitors: hyperstablize and destabilize |
Created by:
lhumm07
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