Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
48 Cards in this Set
- Front
- Back
|
What is the most common dose-limiting toxicity of chemotherapeutic agents?
|
Myelosuppression (bone marrow suppression)
|
|
|
What are the most common types of myelosuppression?
|
Neutropenia (decreased neutrophils)
Erythropenia (decreased RBCs) Thrombocytopenia (decreased platelets) |
|
|
What are a few common features of Biological Response Modifiers (BRMs)?
|
Usually human proteins.
Recombinantly produced. Unstable and cannot be administered orally. |
|
|
What is the FDA-Approved use for Aldesleukin (IL-2)?
|
Use against renal cell carcinoma.
|
|
|
What is the MOA for Aldesleukin? (IL-2)
|
IL-2 is a T cell growth factor.
|
|
|
How is Aldesleukin administered?
|
Given IV.
|
|
|
What are some adverse effects of IL-2 treatment (Aldesleukin)?
|
Capillary leak: a very severe, common side-effect of high dose IL-2 treatment.
Usually in the lung. Due to activated T cells that damage the endothelium. Also: myelosuppression |
|
|
What is the MOA of Interferon Alpha 2A (Intron A)? How is it administered?
|
Increases phagocytic activity of macrophages.
Increases cytoxicity of lymphocytes for target (cancer) cells. Given IV. |
|
|
What are some adverse effects of Interferon Alpha 2A? (Intron A)
|
Flu-like syndrome
Myelosuppression: can be life-threatening pancytopenia |
|
|
What is the MOA of Interferon Gamma?
|
Activates phagocytes
Generates toxic O2 metabolites within phagocytes |
|
|
What are some adverse side effects of IFN-g?
|
Flu-like symptoms.
|
|
|
Most terrifying animal?
|
() ()
( , ,) c(")(") |
|
|
What is the MOA of Erythropoietin (Epoetin-a)? How long will it take to see effects?
|
Stimulates stem cells to take the route of committed erythrocyte precursor to RBC.
Takes 2-6 weeks to see effects. |
|
|
What precautions should be taken before using Erythropoietin (Epotein-a)?
|
Measure plasma ertyrhopoietin levels to make sure chemotherapy is the cause of the anemia.
|
|
|
What are some adverse effects of Erythropoietin (Epoetin-a)? What are some contraindications?
|
CNS: Headaches
HEME: Iron deficiency (can exacerbate iron-deficiency anemia) Contraindication: Erythroid-based tumors |
|
|
What clinical use does granulocyte colony stimulating factor (G-CSF: Filgrastim) have?
|
Used as an adjunct to chemotherapy known to cause neutropenia.
|
|
|
What are some adverse reactions of G-CSF:Filgrastim?
|
Fever
Bone Pain |
|
|
What role does GM-CSF (Sargramostim) play in chemo?
|
Causes increase in monocyte and granulocyte precursors.
Increase in monocyte/macrophage killing of tumor cells. Higher doses stimulates RBC and platelet precursors. |
|
|
What are some adverse reactions of GM-CSF (Sargramostim)? When is it contraindicated?
|
Fever
Bone Pain Muscle Pain Rash Contraindicated: Leukemias |
|
|
What do differentiating agents do, and what effect might they have on cancer cells?
|
Trigger a cell to go from "undifferentiated" to a more "differentiated" state.
Slows down or stops growth, may kill cancer cells. |
|
|
What agents make up the Differentiating Agents?
|
Vitamin A Derivatives:
Tretinoin Bexarotene |
|
|
What is the MOA of the Vitamin A Derivatives? (Differentiating Agents)
|
Induce tumor cell differentiation to become mature, non-malignant cells. (by binding to RA receptors, RXR and RAR)
Bexarotene specifically binds to RXR >>>>>> RAR |
|
|
What are some Adverse Reactions to Differentiating Agents? (Vitamin A Derivatives)
|
Sensitivity to Sunlight
|
|
|
What is the MOA of Denileukin Diftitox (Ontak?)
|
Denileukin Diftitox is a conjugate of IL-2 and a toxin, Diphtheria Toxin.
IL-2 targets drug to T cells, and once attached, Diphtheria Toxin takes it out. |
|
|
What might Denileukin Diftitox (Ontak) be employed against?
|
T cell lymphoma.
|
|
|
What is trastuzumab?
|
An antibody against Her2/neu.
|
|
|
What is lapitnib?
|
Small molecule that blocks Her2/neu activity.
|
|
|
What is the half life of trastuzumab? How is lapitinib metabolized?
|
18-27 day half-life (trastuzumab)
Lapitinib is metabolized by CYP3A4. |
|
|
What is an adverse effect of trastuzumab? What type of anticancer agents should you not combine it with?
|
Cardiomyopathy.
Shouldn't combine with anthracyclines due to the stacking of cardiotoxic drugs. |
|
|
What two drugs are EGFR-1 Inhibitors?
|
Geftinib and Erlotinib.
|
|
|
How are Geftinib and Erlotinib administered?
|
Administered orally.
|
|
|
What type of cancer is Geftinib used against?
What type is Erlotinib used against? |
Geftinib : NSCLC
Erlotinib (with gemcitabine) : Pancreatic |
|
|
What are some adverse effects of EGFR-1 Inhibitors (Geftinib and Erlotinib?)
|
GI: Diarrhea
|
|
|
Mutations to which receptors cause resistance to Geftinib and Erlotinib?
|
EFGR, IGF-1, and K-Ras receptor mutations cause resistance.
|
|
|
What is the MOA of Cetuximab, and how is it administered?
|
MOA: Anti-EGFR monoclonal antibody.
Given IV. |
|
|
What cancers is Cetuximab effective against?
|
Colon Cancer
Head and Neck Cancer |
|
|
What is an ADR to Cetuximab? What can be done to prevent this?
|
Infusion sensitivity
Pre-treatment with H1 antagonist can help prevent. |
|
|
Why will Cetuximab only work on tumors with wild-type K-Ras?
|
Ras is downstream of EFGR in MAP kinase pathway.
Cetuximab prevents EGF ligands from binding to receptor. |
|
|
What is the MOA of Imatinib (Gleevec: STI571)?
|
Specific BCR-abl kinase inhibitor.
Inhibiting this kinase slows cell growth and can kill tumor cells. |
|
|
What are some ADRs of Imatinib (Gleevec: STI571)?
|
GI: common
EDEMA: common Heaptoxocity |
|
|
What is the MOA of Bevacizumab (Avastin)? What is its half-life?
|
Monoclonal antibody against VEGF
Prevents VEGF from binding to VEGFR. Half-life is 20 days. |
|
|
What cancers are susceptible to bevacizumab (Avastin)t?
|
Colon
NSCLC Breast Renal cell |
|
|
What are some ADRs of Bevacizumab (Avastin)?
|
GI: bleeding or perforation, intra-abdominal abscess formation
Epistaxis |
|
|
What is the MOA of Soafenib and Sunitinib?
|
Both are small molecule inhibitors of VEGFR-2 and PDGFRB kinase.
|
|
|
What cancer is most susceptible to Sorafenib and Sunitinib?
|
Renal Cancer
|
|
|
What is the (mostly minor) ADR of Sorafenib and Sunitinib?
|
Fatigue
|
|
|
If a drug ends in -mab, what kind of agent is it?
|
Antibody
|
|
|
If a drug ends in -nib, what kind of drug is it?
|
Kinase Inhibitor
|
