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Antineoplastic Pharm

Intro to antineoplastic pharmacology

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