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;
44 Cards in this Set
- Front
- Back
What is the cell life cycle?
|
The period from the birth of a new cell to the time that cell divides
|
|
What happens prior to cell replication?
|
Duplication of all its constituents
|
|
What are the 5 phases of a normal cell cycle?
|
M, G1, S, G2, G0
|
|
What happens in the M phase of the normal cell cycle?
|
Mitosis – all cellular contents duplicated
|
|
What happens during the S phase of the normal cell cycle?
|
Each of the 46 chromosomes is duplicated by the cell
|
|
What happens during the G1 phase of the normal cell cycle?
|
Cellular contents excluding the chromosomes are duplicated
|
|
What happens during the G0 phase of the normal cell cycle?
|
Resting phase
|
|
How does cancer continue to replicate?
|
Tumor cells continue to divide under conditions that send normal cells to the G0 state
|
|
Is the cell cycle the same for tumor cells as it is for normal cells?
|
Yes, except the cell is not sent to the G0 state
|
|
How do cell cycle non-specific antineoplastics work?
|
They kill normal and malignant cells to the same extent. (radiation for example)
|
|
What are the cell cycle non-specific antineoplastics?
|
Nirosoureas (Carmustine, lomustine, semustine) and radiation
|
|
How do cell cycle phase specific antineoplastics work?
|
Cells in other phases are not affected – only those specifically targeted.
|
|
Name the M phase cell cycle phase-specific antineoplastics
|
Vinca alkaloids, paclitaxel, docetaxel
|
|
Name the S phase cell cycle phase-specific antineoplastics
|
Topoisomerase inhibitors, purine, pyrimidine, and folate antimetabolites
|
|
Name the G1 phase cell cycle phase-specific antineoplastics
|
Aspariginase, prednisone
|
|
Name the G2 phase cell cycle phase-specific antineoplastics
|
Bleomycin, etoposide
|
|
How do proliferating cell antineoplastics work?
|
Agents can preferentially kill proliferating cells as opposed to resting cells (not always phase specific – can still affect all phases)
|
|
Name the proliferating cell antineoplastics?
|
Alkylating agents –nitrogen mustards, ciplatin, carboplatin and Antibiotics – Anthracyclines, dactinomycin
|
|
Limitations of chemotherapy?
|
Difference between cancer cells & normal cells is minimal – proliferation rate may differ. Useful drugs without SE do not exist. Rapidly dividing cells are also destroyed by antineoplastics.
|
|
AE of chemotherapy antineoplastics?
|
Hair loss, increased susceptibility to infection, anemia, bleeding, n/v/d/c, stomatitis, anorexia, taste changes
|
|
Name the cytoprotective agents
|
Mesna (Uromitexan), Dexrazoxane (Zinecard), and amifostine (Ethyol)
|
|
How does Mesna (Uromitexan) work?
|
Prevents hemorrhagic cystitis caused by ifosfamide, cyclophosphamide. Reacts and detoxifies toxic compound released during bioactivation of ifosfamide and cyclophosphamide.
|
|
How does Dexrazoxane (Zinecard) work?
|
Protects against cardiotoxicity of anthracyclines. Chelates iron that acts as an oxidizing agent in heart.
|
|
How does Amifostine (Ethyol) work?
|
Used with cisplatin and cyclophophamide to reduce neutropenic fever and infection. Used with platinum agents to reduce cumulative renal toxicity. Free-radical scavenger.
|
|
AE of Amifostine (Ethyol)?
|
Causes decrease in BP in 50% of patients
|
|
What do biological response modifiers do?
|
Enhance patient’s immune system
|
|
What are the colony stimulated factors?
|
Erythropoietin, darbepoietin. Filgrastim, peg-filgrastim (G-CSF). Sargramostim (GM-CSF). Thrombopoietin.
|
|
What is erythropoietin?
|
Hormone produced by the kidney that regulates red blood cell production. Induces erythropoiesis by stimulating division & differentiation of erythroid progenitor cells. Induces release of reticulocytes from bone marrow into blood. Lineage specific.
|
|
What are the 2 erythropoietin products available?
|
Epoitin (Procrit, Epogen); T1W, Qweek. And Darbepoietin (Aranesp); Q1weeks
|
|
What are the uses for erythropoietin?
|
Anemia secondary to chemotherapy, CKD, surgery, HIV therapy, HCV therapy
|
|
What is the Black Box warning with erythropoietin?
|
Increased mortality, serious cardiovascular and thromboembolic events (heart failure, MI, stroke, blood clots) and tumor progression . When treated to a higher target Hgb (13-14).
|
|
What is important to remember in treatment with erythropoietin?
|
Treat to a target Hgb of 10-12 – BB warning in effect if treated to higher targets. Use lowest dose to prevent blood transfusions.
|
|
How is erythropoietin administered?
|
IV or SubQ
|
|
How do G-CSF and GM-CSF differ?
|
G-CSF is lineage specific – neutrophils specifically. GM-CSF is multi-lineage growth factor - stimulates neutrophils as well as monocytes and macrophages.
|
|
Why is G-CSF or GM-CSF used?
|
Increases production of neutrophils, decreases incidence of infection
|
|
AE of G-CSF and GM-CSF?
|
Main side effect – bone pain
|
|
How is G-CSF or GM-CSF administered?
|
SubQ or IV
|
|
Name of G-CSF medication?
|
Filgrastim (Neupogen, G-CSF)lineage specific, Pegfilgrastirim (Neulasta, G-CSF) pegylated form
|
|
Name of GM-CSF medication?
|
Sargramostim (leukine, GM-CSF) multi-lineage growth factor
|
|
How does thrombopoietin (TPO) work?
|
Increases platelet count by binding to and activating the human TPO receptor.
|
|
Uses for Thrombopoietin (TPO)?
|
Pts with ITP when other therapies (corticosteroids, immune globulin, splenectomy have been insufficient). Not commonly used – last line agent.
|
|
AE of Thrombopoietin (TPO)?
|
If response is inadequate, patient may have neutralizing antibodies to romiplostim or TPO or bone marrow fibrosis.
|
|
How is Thrombopoietin (TPO) administered?
|
SubQ once weekly (platelet half-life is 8-11 days)
|
|
Name of Thrombopoietin (TPO) medication?
|
Romiplostim (Nplate)
|