Day 3- Intro to oncology Flashcards
What are good genes? Protooncogenes or oncogenes?
What are tumor suppressor genes?
What happens in cancer cells?
Proto-oncogenes.
Regulate and inhibit inappropriate cell growth/proliferation, inactivate of these genes leads to cancer formation.
Angiogenesis, Self-proliferation, Resistance to antigrowth signals, limitless growth potential, metastasis, antiapoptotic effects.
What is the difference between hyperplasia and dysplasia?
Does a cancer grow faster or slower when it’s small?
When is a tumor detectable by palpation or radiography?
Hyperplasia–> increase in number of cells in a particular tissue or organ leading to increased size. Dysplasia–> abnormal change in size, shape, or organization of cells or tissues.
It grows faster.
10^9, If 10^12 it is lethal, if 10^4 it’s small enough for elimination by host immune system.
What are some warning signs for cancer?
What are cancer treatment modalities?
What is Curative treatment?
Change in bowel or bladder habits, a sore that does not heal, unusual bleeding or discharge, thickening or lump in the breast or somewhere else, indigestion or difficulty in swallowing, obvious change in wart or mole, nagging cough or hoarseness.
Surgery, Radiation, Traditional Chemotherapy, Targeted Drug Therapy.
Goal is to eliminate all cancer cells, Adjuvant therapy is administered after, Neoadjuvant is administered before surgical resection.
What is palliative treatment?
How can you dose chemotherapy?
Is cell cycle specific chemotherapy schedule or dose dependent?
Goal is to make patient more comfortable and alleviate symptoms.
BSA dosing(mg/m2), Weight based dosing(mg/kg), AUC.
Schedule dependent, Cell cycle non specific are dose dependent.
Are antimetabolites selective?
Does Antimetabolites cause myelosuppresion?
What are the Antimetabolites and do they work in the S phase?
NO!
YES!
Antifolates/ Folate antagonists, Antipyrimidines, Antipurines, Hydroxyurea. THESE ALL work in the S phase.
What are the Antifolates/Folate antagonists?
What is their MOA?
What are the Antifolates side effects?
Methotrexate, Pemetrexed.
Folates are essential factors in synthesis of DNA, needs to be reduced via DHFR and they attack this.
Myelosuppresion, Mucositis, N&V. MTX causes renal dysfunction at high doses, CNS toxicity, hepatoxicity.
What do you need to maintain urine ph>7 with MTX?
What are the clinical pearls to know about with Pemetrexed?
What special things to know about Leucovorin?
Leucovorin and Sodium bicarbonate.
Avoid NSAIDS, Supplement with folic Acid and Vitamin B12 to prevent myelosuppression. Predmicate with Dexamethasone day before, of, and after treatment to avoid rash.
Used in Folate rescue for high dose methotrexate, initiated 24 hours after and if you don’t your patient will die. Stabilizes fdUMP binding when using 5-FU.
What are your antipyrimidines?
What is 5-FU’s MOA?
What is 5-FU’s DLT?
Cytarabine(Cytosine), Gemcitabine(Cytosine), 5-fu(uracil), capectiabine(uracil).
Stabilizes fdUMP to inactivate thymidylate synthase and addition of leucovorin increased the stability(better as continuous infusion). Incorporates into DNA/RNA as a false nucleotide and intereferes with function(given as bolus).
Bolus= Myleosuppresion, Continuous infusion= diarrhea, hand-foot syndrome, mucositis.
What is 5-FU’s drug interaction to know?
What is Capectiabine?
What is Cytarabine’s MOA?
Strong inhibitor of CYP2C9(increased warfarin effect).
Prodrug to 5-FU, similar to continuous infusion of 5-FU. All similar stuff to 5-FU.
Analog of cytosine that inhibits DNA polymerase(involved in DNA elongation).
What is Cytarabine’s DLT and major effects?
What is Gemcitabine’s MOA and DLT?
What special things to know about Gemcitabine?
Myelosuppresion is DLT. Major effects are Cerebellar toxicity and conjunctivitis(steroid eye drops may help with this).
Similar to cytarabine and inhibits ribonucleotide reductase.
Achieves 20x more inctracellular concentration than cytarabine. rash responds to steroid, fever to tylenol.
What is 6-mercaptopurine’s MOA and DLT?
What is 6-MP’s drug interactions?
What is fludarabine’s MOA and DLT?
Incorporates into DNA as a false purine(guanine) and stops DNA synthesis, Myleosuppresion.
allopurinol, increases warfarin, causes hyperbilirubinemia.
Incorporates as false purine(adenine), inhibits DNA polymerase and ribonucleotide reductase. Myleosuppresion.
What special things to know about fludarabine?
What is Cladribine and Clofarabine MOA and DLT?
What special things to know about Cladribine and Clofarabine?
Prophylaxis required for PCP and HSV.
Same as Fludarabine.
Prophylaxis against PCP for Caldribine.
What is Hydroxyurea’s MOA and DLT?
What special A/E’s to know about Hydroxyurea?
What are the antimicrotubules and what phase do they affects?
Inhibits ribonucleotide diphosphate reductase. Myleosuppresion.
Can cause secondary leukemias, tumor lysis syndrome, skin hyperpigmentation, rash. Can be used to decrease white blood cell counts rapidly to prevent A/E of leukocytes.
Vinca alkaloids(destabilizes microtubule assembly), Taxanes(stabilizes microtubule assembly). M phase( vinas arrow down, taxanes arrow up).
What is Vincristines MOA and DLT?
What is Vincristine’s clinical pearls?
What is Vinblastine and Vinorelbine’s DLT?
Microtubule destabilizer, Peripheral neuropathies and constipation.
Doses are capped at 2 mg to minimize neurotoxicity, lethal if administered intrathecally. Substrate and weak inhibitor of CYP3A4.
Myelosuppresion. Similar to Vincristine. Watch for peripheral neuropathy.
What is Paclitaxel’s DLT?
What is Paclitaxel’s clinical pearls?
What is Docetaxel’s DLT?
Myelosuppresion, Causes a lot of hypersensitivity reactions.
Premed with dexamethasone, diphenhydramine, and ranitidine due to it containing Cremophor.
Myelosuppresion.
