Term
|
Definition
| Prevent the formation of spindle fibers in mitosis |
|
|
Term
| What category of Cancer Chemotherapy drugs is Vincristine under? |
|
Definition
|
|
Term
| Vincristine Acute Toxicity |
|
Definition
|
|
Term
| Vincristine Delayed Toxicity |
|
Definition
| Neurotoxicity with peripheral neuropathy, paralytic ileus, myelosuppression (occurs, but is generally milder and much less significant than with vinblastine), alopecia, SIADH |
|
|
Term
| Clinical Application of vincristine |
|
Definition
| ALL, Hodgkin’s and non-Hodgkin’s lymphoma, rhabdomyosarcoma, neuroblastoma, and Wilm’s tumor |
|
|
Term
|
Definition
| The delayed regrowth of bacteria following exposure to an antibiotic. |
|
|
Term
|
Definition
| Aminoglycosides effect can last several hours, therefore one larger does may be more effective than multiple small doses. |
|
|
Term
| Post Antibiotic Effect is affected by: |
|
Definition
| Duration of antibiotic exposure, bacterial species, culture medium and class of antibiotic. |
|
|
Term
| Mechanism of Resistance: Acyclovir, Famciclovir, Penciclovir, Valacyclovir |
|
Definition
| Can develop in HSV or VZV through alteration in viral thymidine kinase or DNA polymerase |
|
|
Term
| Mechanism of Resistance: Oseltamivir |
|
Definition
| Associated with mutation in viral hemagglutinin or neuraminidase (H275Y mutation) |
|
|
Term
| Mechanism of Resistance: Valgancyclovir |
|
Definition
| Resistance patterns same as those of ganciclovir (increases with duration of use - more common mutation in UL97, less common mutation in UL54) |
|
|
Term
|
Definition
| Increased resistance to this antiviral drug (up to 50%) resulted in markedly higher rates of seasonal H1N1 viral infection |
|
|
Term
| Mechanism of Resistance: Amphotericin B |
|
Definition
| occurs if ergosterol binding impaired by a) decreased membrane concentration of ergosterol or b) modification of sterol target molecule reduces affinity for drug |
|
|
Term
| Mechanism of Resistance: Flucytosine |
|
Definition
| Occurs through altered metabolism of flucytosine |
|
|
Term
| Mechanism of Resistance: Azoles |
|
Definition
| Occurs by multiple mechanisms. Increased number of resistant strains have been reported (may be due to prophylactic use of azoles) |
|
|
Term
| Primary resistance to cancer drugs |
|
Definition
| Also called "inherent drug resistance;" absence of response on the first exposure to a drug |
|
|
Term
| How does location of a tumor play a role in drug resistance? |
|
Definition
| 1) Drug must be able to penetrate the BBB that protects the CNS 2) Difficult for medication to reach large tumors with poor blood flow |
|
|
Term
| Acquired resistance to cancer drugs |
|
Definition
| Develops in response to exposure to a specific drug. A specific change in genetic makeup of a given tumor cell causes amplification or increased expression of one or more genes |
|
|
Term
| Systemic antifungal agents for systemic infections |
|
Definition
| Amphotericin B, Flucytosine, Azoles (Ketoconazole, Fluconazole) |
|
|
Term
|
Definition
| binds to ergosterol, a fungal cell membrane sterol, and alters the permeability of the cell by forming pores in the cell membrane |
|
|
Term
|
Definition
| PO poorly absorbed from GI tract - so effective only on fungi within the GI lumen and not for systemic infection; IV- >90% bound by serum proteins, widely distributed to tissues except CSF, mostly metabolized w/ some excreted slowly in urine over several days, T1/2=15 days. No adjustment in dose needed for renal function. May require intrathecal therapy for certain fungal meningitis infections. |
|
|
Term
|
Definition
| 2 broad categories of ADR: 1) immediate, infusion-related toxicity- fever, chills, muscle spasms, vomit, Headache, hypotension; decrease infusion rate, decrease daily dose, or premedicate to improve tolerance to infusion-related ADR, 2) slow, cummulative toxity: (a) prerenal renal failure or decreased perfussion, and (b) renal tubular injury & dysfunction- irreversible. Some level of renal impairment occurs in nearly every patient treated. |
|
|
Term
| Amphotericin B Spectrum of Action |
|
Definition
| Broadest spectrum of action of all antifungal agents- useful agent for nearly all life-threatening mycotic infections |
|
|
Term
| Amphotericin B Spectrum of Action list |
|
Definition
| Candida albicans, Cryptococcus neoformans, Histoplasma capsulatum, Blastomyces dermatiditis, Coccidiodie immitis, Aspergillus fumigatus |
|
|
Term
| Amphotericin B important use |
|
Definition
| Often used as initial induction regime to rapidly reduce fungal burden and then replaced by one of the azole drugs for chronic therapy or prevention of relapse |
|
|
Term
| Amphotericin B clinical uses |
|
Definition
| Mycotic corneal ulcers & keratitis, fungal arthritis, candiduria |
|
|
Term
| Amphotericin B resistance |
|
Definition
| If ergosterol binding is impaired by 1) decreased membrane concentration of ergosterol or 2) decreased affinity for drug by the sterol target molecule |
|
|
Term
|
Definition
| Drugs that exploit characteristics of cancer cells and inhibit metabolism in the proliferating cells: Antifolates, fluoropyrimidines, deoxycytidine analogs, purine antagonists |
|
|
Term
|
Definition
| An Antimetabolite; Antifolate MOA: folic acid analog that binds to DHFR, and inhibits synthesis of THF, preventing the formation of DNA, RNA and key cellular proteins synthesis |
|
|
Term
| Methotrexate (MTX) Toxicity and Adverse Effects |
|
Definition
| Mucositis. diarrhea, myelosuppression with neutropenia and thrombocytopenia. Renal Elimination: Dosage must be altered for those with renal insufficiency. |
|
|
Term
| Drug used to reverse MTX toxicity, or in high-dose MTX therapy to spare normal cells |
|
Definition
| Leucovorin or L-Leucovorin |
|
|
Term
| Pemetrexed Toxicity and Adverse Effects |
|
Definition
| Myelosuppression, skin rash, mucositis, diarrhea, fatigue, and hand-foot syndrome. Renal Elimination: Dosage must be altered for those with renal insufficiency. |
|
|
Term
|
Definition
| An Antimetabolite; Antifolate MOA: TS and DHFR inhibition and purine nucleotide synthesis |
|
|
Term
|
Definition
| An Antimetabolite; Antifolate MOA: inhibits TS, DHFR, and de novo purine nucleotide biosynthesis enzymes |
|
|
Term
| Pralarexate Toxicity and Adverse Effects |
|
Definition
| Myelosuppression, skin rash, mucositis, diarrhea, and fatigue. Renal Elimination: Dosage must be altered for those with renal insufficiency. |
|
|
Term
|
Definition
| An Antimetabolite; Fluoropyrimidine MOA: Forms bond with TS to effectively inhibit DNA synthesis |
|
|
Term
| 5-Fluorouracil (5-FU) Toxicity and Adverse Effects |
|
Definition
| Myelosuppression, diarrhea, nausea and vomiting, mucositis, hand-foot syndrome and neurotoxicity |
|
|
Term
|
Definition
| An Antimetabolite; Fluoropyrimidine MOA: metabolized in the liver by enzyme carboxylesterase to finally hydrolize and change into 5-FU in the tumor |
|
|
Term
|
Definition
| An Antimetabolite; Deoxycytidine Analog MOA: Blocks DNA synthesis and repair by competitive inhibition of polymerases |
|
|
Term
| Cytarabine (ara-C) Toxicity and Adverse Effects |
|
Definition
| Myelosuppression, mucositis, nausea and vomiting, and neurotoxicity with high-dose therapy |
|
|
Term
|
Definition
| An Antimetabolite; Deoxycytidine Analog MOA: inhibits DNA synthesis by binding to the DNA strand and inhibiting DNA polymerases |
|
|
Term
| Gemcitabine Toxicity and Adverse Effects |
|
Definition
| Myelosuppression by neutropenia, nausea and vomiting, flu-like syndrome, hemolytic-uremic syndrome and thrombotic thrombocytopenic purpura |
|
|
Term
|
Definition
| An Antimetabolite; Purine Antagonist MOA: Inhibits several enzymes of novo purine nucleotide synthesis |
|
|
Term
| 6-Thiopurines Toxicity and Adverse Effects |
|
Definition
| Increased risk of severe toxicities of myelosuppression, mucositis and diarrhea in those with pharmacogenetic syndrome involving loss of enzyme TPMT |
|
|
Term
|
Definition
| An Antimetabolite; Purine Antagonist MOA: inhibits DNA synthesis and repair by interfering with DNA polymerases and can also directly incorporate into the cell DNA, blocking DNA synthesis and function. It also causes apoptosis through unknown means. |
|
|
Term
|
Definition
| An Antimetabolite; Purine nucleoside analog MOA: inhibits DNA polymerases after metabolizing into its active form |
|
|
Term
| Fludarabine Toxicity and Adverse Effects |
|
Definition
| Myelosuppression and inhibitory effects on CD4 and CD8T cells leading to increased risk of opportunistic infections |
|
|
Term
| Cladribine Toxicity and Adverse Effects |
|
Definition
| Transient myelosuppression and decrease in CD4 and CD8T cells lasting over a year in some patients |
|
|
Term
|
Definition
| Requires 3 physphorylation steps for activation, which requires viral kinase therefore Acyclovir is selectively activated |
|
|
Term
| Acyclovir Mechanism of Action |
|
Definition
| Inhibits viral DNA synthesis by 2 mechanisms: The first mechanism the drug binds to the DNA template as an irreversible complex and the second is chain termination following incoroporation into viral DNA |
|
|
Term
|
Definition
| Genital herpes - helps reduce duration of symptoms, increases lesion healing and decreases duration of viral shedding as well as decreases time course of reocurring genital herpes. Also effective for treatment of shingles |
|
|
Term
| Acyclovir Adverse Effects and Toxicity |
|
Definition
| Minimal side effects - nausea/vomiting and headache. When given IV, chance of renal toxicity or neurologic effects |
|
|
Term
| Alkylating Agents: Mechanism of Action |
|
Definition
| Cytotoxic agents which transfer their alkyl group to various cellular components. Most common site of alkylation is the N7 position of guanine in DNA, however other DNA bases are alkylated as well. |
|
|
Term
| What happens when DNA bases are "Alkylated"? |
|
Definition
| Alkylation causes abnormal base pairing, which causes cross-linking between DNA strands or miscoding of DNA. Ultimately, it results in DNA strand breakage and cell death. |
|
|
Term
| Alkylating Agents: Adverse Effects |
|
Definition
Usually dose related and occur in rapidly growing tissues such as bone marrow (myelosuppression), GI tract and the reproductive system.
*Inhibition of GI mucosal cell division leads to anorexia, nausea and vomiting (usually within 30 min. of admin.).
*These agents are also powerful vesicants. |
|
|
Term
| Most Common Alkylating Agents |
|
Definition
| Cyclophosphamide, Chlorambucil, Cisplatin, Carboplatin, Oxaliplatin, Nitrosoureas (e.g., Lomustine) |
|
|
Term
| Nitrosoureas- Special considerations: |
|
Definition
| Highly lipid soluble and can cross the blood-brain barrier (effective in tx of brain tumors) |
|
|
Term
| Cell cycle-nonspecific (CCNS) agents |
|
Definition
Alkylating Agents:
(They damage DNA in any phase of the cell cycle, however they are most effective in late G1 and S phases of the cell cycle.) |
|
|
Term
| Oseltamivir (Tamiflu) Action |
|
Definition
| Interfere with release of progeny influenza virus from infeccted host cells, thus halting the spread of infection within the respiratory tract |
|
|
Term
| Oseltamivir (Tamiflu) Uses |
|
Definition
| Used in the treatment of the infection caused by the flu virus (influenza A and influenza B). May also be used to prevent and treat swine influenza A. |
|
|
Term
| Oseltamivir (Tamiflu) Uses |
|
Definition
| May reduce flu symptoms (weakness, headache, fever, cough, runny or stuffy nose, and sore throat) by 1 day. Is also used to prevent influenza infection if you have come into close contact with someone who has the flu. |
|
|
Term
| Oseltamivir (Tamiflu) Contraindications Precautions |
|
Definition
| Is not indicated to treat flu in children younger than 2 weeks of age nor to prevent flu in children younger than 1 year of age. Safety and efficacy have not been established. |
|
|
Term
| Oseltamivir (Tamiflu) Contraindications Precautions |
|
Definition
| There are no adequate studies in women for determining infant risk when using this medication during breastfeeding. Weigh the potential benefits against the potential risks before taking this medication while breastfeeding. |
|
|
Term
| Oseltamivir (Tamiflu) Contraindications Precautions |
|
Definition
| This medicine is not a substitute for an annual flu shot. . |
|
|
Term
| Oseltamivir (Tamiflu) Side effects |
|
Definition
| Nausea, vomiting, abdominal pain, headache, fatigue, diarrhea, transient neuropsychiatric events (self-injury or delirium) |
|
|
Term
| Oseltamivir (Tamiflu) Pharmocokinetics |
|
Definition
| Oral administration. Half life is 6-10 hours. Excretion is by glomerular filtration and tubular secretion in the urine, thus dosing should be adjusted in patients with declining renal function. |
|
|
Term
| Oseltamivir (Tamiflu) considerations |
|
Definition
| Early administration is crucial because replication of the influenza virus peaks at 24-72 hours after the onset of the illness. Duration of illness is decreased by 1-2 days with early administration. Prophylaxis is 70-90% effective in preventing disease after exposure. |
|
|
Term
|
Definition
| Binds to sterols in fungal cell plasma membranes, which changes membrane permeability and allows loss of potassium and small molecules from cells. This action reults in cell impairment or death. Usually inhibit fungal growth and multiplication, but if level is high enough, it can destroy fungi |
|
|
Term
| Amphotericin B (Pharmacokinetics) |
|
Definition
| Absorption: poorly absorbed from GI tract therefore oral dose only effective on fungi within the GI tract and cannot be used for systemic treatment; Excretion: slowly in urine over several of days': Half Life=15 days; no dose adjustment needed for patient with hepatic impairment, renal impairment and HD. Distribution: widely distributed in most tissues, 2-3% of blood level reached in CSF |
|
|
Term
| Amphotericin B (Clinical Indicators) |
|
Definition
| Broadest antifungal agent,Treatment of severe, invasive fungal infections including Aspergillum and Candida |
|
|
Term
| Amphotericin B (Adverse Reactions) |
|
Definition
| Infusion-Related Reactions: fever, chills, muscle spasms, vomiting, headache, hypotension; Cumulative Toxicity: renal damage/impairment and abnormalities in liver function tests |
|
|
Term
Mechanism of Resistance: Antivirals
(ie: Acyclovir) |
|
Definition
Two Mechanisms of Resistance:
1. Virus decreases or modifies viral enzyme (thymidine kinase) which is needed to convert drug to 'active' form (ie: drug can't turn 'on')
2.Virus modifies viral DNA enzyme(AKA polymerase) so that drug can't block the viral DNA enzyme (therefore, drug can't block viral DNA synthesis) |
|
|
Term
Mechanism of Resistance:
Chemotherapy |
|
Definition
1. Resistant due to location of tumor (can’t get drugs there to damage tumor)
2. Cancer involving CNS- drugs can’t get past the BBB (blood brain barrier)
3. Primary Resistance- absence of response on first exposure
4. Acquired Resistance- Increases genetic expression of one or more specific genes |
|
|
Term
|
Definition
| Antibacterial activity continues wihout any measurable level of the drug remaining. |
|
|
Term
| Oseltamivir (Tamiflu) MOA |
|
Definition
| Is a neuramindiase inhbitor that blocks the release of the influeza virus from the infected's cells. Used to decrease influenza A and/or B symptoms, duration or prophalatically if exposed to the virus. Must be given 24 to 72 hours of onset of symptoms. |
|
|
Term
| Oseltamivir (Tamiflu) pharmacokinetics |
|
Definition
Administered orally, absorbed in the GI tract
metabolized in the liver
Excreted via kidneys. Needs to be adjusted in renal impairment
80% bioavailability
1/2 life is 6-10 hours |
|
|
Term
| Oseltamivir (Tamiflu) ADR |
|
Definition
| rare rash and neuropsychotic events |
|
|
Term
| Oseltamivir (Tamiflu) resistance |
|
Definition
| Associated with point mutation within the virus or the enzyme neuraminidase |
|
|
Term
|
Definition
| Action on intermediary metabolism of proliferating cells to block nucleotide and nucleic acid synthesis. Sub groups: Folic Acid antagonist, pyrimidine antagonist, purine antagonist, and deoxycytidine analogs |
|
|
Term
| antimetabolites adverse effects |
|
Definition
| mucositis, myelosupression, diarrhea,nausea, fatigue. Renal adjustments for renal dsyfunction patients, especially for ASA, NAIDS, PCN, and cephalosporins with MTX. A/E related to dose and schedule for 5FU additionally include neurotoxicity and hand-foot syndrome. |
|
|
Term
| Methotrexate (MTX) Antimetabolites MOA |
|
Definition
| Binds with DHRF, interfering with the synthesis of DNA, RNA, and proteins. |
|
|
Term
| Pyrimidine Antagonist Antimetabolites: 5FU (MOA) |
|
Definition
| Inhibits thymidine synthase. Incorporates metabolites into both RNA and DNA therefore causing alternations in the RNA processing and inhibiting DNA synthesis and function. |
|
|
Term
|
Definition
| Competitive antagonist at androgen receptor. Potent antiandrogen. |
|
|
Term
| Flutamide (Eulexin) Clinical Indications |
|
Definition
| Used for the treatment of prostate cancer |
|
|
Term
| Flutamide (Eulexin) Adverse Drug reactions |
|
Definition
| Causes mild gynecomatica and mild reversible hepatic toxicity |
|
|
Term
|
Definition
| Inhibit DNA replication by the transfer of an alkyl group to nitrogen, most commonly to the N7 position of guanine. Cell death is caused by crosslinking between DNA strands or bases on the same strand, miscoding or DNA strand breakage. Damage of the DNA can occur in any phase of the cell cycle. Not cell cycle specific. |
|
|
Term
| Alkylating Agents (Adverse Effects) |
|
Definition
Adverse effects are generally dose-related and occur primarily in rapidly growing
tissues such as the bone marrow, GI tract and reproductive system. Nausea/vomiting, myelosuppression, potent vesicants, tissue damage at site of administration and systemic toxicity. Increased risk of secondary malignancies, especially leukemia. |
|
|
Term
| Alkylating Agents (Resistance) |
|
Definition
| Increased capability to repair DNA lesions, decreased transport of the alkylating drug into the cell and increased expression or activity of glutathione and glutathione-associated proteins. |
|
|
Term
|
Definition
| Cyclophosphamide – most widely used. Chlorambucil, Cisplatin, Nitrosoureas |
|
|
Term
|
Definition
Three steps of phosphorylation
--Step one is performed by Viral Enzymes
--Step two is performed by infected host cell enzymes (so you are assured it is specific to viral infected cells
Result: INHIBITION of VIRAL DNA synthesis |
|
|
Term
Acyclovir (Zovirax)
Clnical
Uses |
|
Definition
- HSV-1
- HSV-2
- VZV
But MORE potent agains HSV types 1 & 2
**Used to shorten the duration of viral infection esp. symptoms (pain, healing time) |
|
|
Term
Acyclovir (Zovirax)
Pharmacokinetics |
|
Definition
--Absorption/Bioavailability: LOW (15-20%), IV form available; Topical has high conc. in lesions without systemic evidence
--Distribution: diffuses readily into most tissues and body fluids with CSF conc at 20-50% of serum value
--Elimination: Kidney, Half life: 2.5 - 3 Hours with normal clearance, 20 hours in anuric patients |
|
|
Term
Acyclovir (Zovirax)
Adverse Reactions |
|
Definition
|
|
Term
|
Definition
| Inhibits mitosis. Derived from periwinkle plant, natural chemotherapy drug |
|
|
Term
| Vincristine mechanism of resistance |
|
Definition
| Increased expression of the MDRI gene in the patient leads to enhanced drug efflux and reduced intracellular accumulation of the drug. |
|
|
Term
| Vincristine indications/treatment |
|
Definition
| Hodgkins and non-Hodgkins lymphoma, myltiple myeloma, pediatric tumors such as Wilms tumor, neuroblastoma, Ewings sarcoma, rhabdomyosarcoma, combine with prednisone for remission induction in acute lymphoblastic leukemia in pediatrics |
|
|
Term
|
Definition
| Neuro: peripheral sensory neuropathy, autonomic nervous system dysfunction, myelosuppression, orthostatic hypotension, cranial nerve palsies, ataxia, SIADH |
|
|
Term
| Vincristine dosing considerations |
|
Definition
| Monitor patients for neurotoxicity, may need to decrease dosage. Also, dose must be adjusted in patients with liver impairment. |
|
|
Term
|
Definition
| Antibacterial activity persists beyond the time during which measurable drug is present. |
|
|
Term
|
Definition
| This antiandrogen slows tumor growth by acting as a competitive antagonist at the androgen receptor. Blocks hormones like testosterone from growing the tumor. |
|
|
Term
| Flutamide Pharmacokinetics |
|
Definition
| Rapidly metabolized and excreted in the urine. Must be taken three times daily. |
|
|
Term
|
Definition
| Treatment of prostatic carcinoma |
|
|
Term
| Flutamide Adverse Effects |
|
Definition
| Mild gynecomastia and mild reversible hepatic toxicity |
|
|
Term
|
Definition
| inhibits viral DNA synthesis once they penetrate the viral cells |
|
|
Term
| Acyclovir Pharmacokinetics |
|
Definition
| Can be given PO or by IV. Bioavailabity of oral acyclovir is low but is unaffected by food. Cleared primarily by glomerular filtration and tubular section of the kidneys and half life is 2.5-3 hours in patients with normal kidney fuction. |
|
|
Term
|
Definition
| Oral acyclovir has many uses: affective against first outbreaks of genital herpes, recurrent herpes labialis, varicella. IV acyclovir is effective against: herpes simplex encephalitis, neonatal HSV, and serious HSV or VZV infections. |
|
|
Term
| Acyclovir Adverse Effects |
|
Definition
| Generally well tolerated. Nausea, diarrhea and headache have been reported. IV has had reports of renal impairment and neurological effects. |
|
|
Term
|
Definition
| Structural Analogs. Certain substances that prevent or reduce the proliferation of cells especially cancer cells, by interferring in normal metabolic activity by competing, interferring, or substituting for an essential nutrient in the enzymatic process |
|
|
Term
| Antimetabolite Treatments |
|
Definition
| Used for different types of Cancers, re: Breast, colorectal, gastroesphageal, head and neck, CNS, lymphomas, non-hodgkens, bladder, small cell-lung, Mesothelioma, pancreatic, tissue cell sarcoma, hairy cell leukemia, AML, ALL, CML |
|
|
Term
|
Definition
| Reduction of ergosterol (primary sterol of the cell wall) synthesis by inhibition of fungal cytochrome P450 enzyme |
|
|
Term
| Fluconazole Pharmokinetics |
|
Definition
| High degree of water solubility and good CSF penetration. High oral bioavailability. Because of fewer hepatic enzyme interactions and better gastrointestinal tolerance, it has the widest therapeutic index of all the azoles, permitting more aggressive dosing in a variety of fungal infections. |
|
|
Term
| Fluconazole Adverse Drug Reactions |
|
Definition
| Relatively nontoxic; Fluconazole has less drug interactions than the other azoles; Fluconazole has the least effect of all the azoles on hepatic microsomal enzymes |
|
|
Term
| Fluconazole Clinical Uses |
|
Definition
| Azole of choice in the treatment and secondary prohylaxis of cryptococcal meningitis. Most common used for treatemetn of mucocutaneous candidiasis. Prophylatic use has been demonstrated to reduce fungal disease in bone marrow transplant recipients and AIDS patients. |
|
|
Term
|
Definition
| Transfer alkyl groups to any nitrogen they can find in the DNA. Can occur on single or both strands of DNA through cross-linking. Causes miscoding or DNA strand breakage and eventually cell death. Very non-specific but replicating cells at increased risk. Cells most susceptible late in G1 and S phases. |
|
|
Term
| Adverse Effects of Alkylating Agents |
|
Definition
| Generally dose related and occur in rapidly growing tissues (bone marrow, GI tract, reproductive tract). Nausea, vomiting. Strong vesicants and can produce systemic toxicity. Increased risk of secondary malignancies (acute myelogenous leukemia). |
|
|
Term
| Examples of Alkylating Agents |
|
Definition
| Cyclophosphamide, mechlorethamine, chlorambucil, bendamustine, melphalan, thiotepa, busulfan, carmustine, lomustine, altretamine, temozolomide, procarbazine, dacarbazine, cisplatin, carboplatin, and oxaliplatin |
|
|
Term
|
Definition
Alkaloid derivative of V rosea and is closely
related to vinblastine in structure |
|
|
Term
|
Definition
|
|
Term
| Vincristine Clinical Uses |
|
Definition
Hodgkin's and non-Hodgkin's lymphoma
rhabdomyosarcoma, neuroblastoma, Wilm's tumor, ALL (Acute lymphoblastic leukemia), Ewing's sarcoma |
|
|
Term
| Vincristine Delayed Toxicity |
|
Definition
| The main dose-limiting toxicity is neurotoxicity (peripheral sensory neuropathy, orthostatic hypotension, urinary retention, paralytic ileus or constipation, cranial nerve palsies, ataxia, seizures, and coma), myelosuppression, alopecia, and SIADH (syndrome of inappropriate secretion of antidiuretic hormone) |
|
|
Term
|
Definition
| antifungal agent with broadspectrum action, used for systemic infections |
|
|
Term
|
Definition
| binds to ergoterol (a sterol found in the cell membrane of fungi). This changes the permeability of the cell. Pores are formed in the cell membrane which causes leakage and cell death. |
|
|
Term
|
Definition
| 1)poorly absorbed from the gastrointestinal tract 2)widely distributed to tissues (but only 2-3% in the CSF) 3)serum half life is 15 days |
|
|
Term
|
Definition
| Adverse drug reaction can be related to the infusion-premedicate to reduce fever, chills, muscle spasms, vomiting, headache and hypotension. Cumulative toxicity can cause renal failure, and some degree of renal impairment usually occurs with all patients being treated with significant doses. Do not exceed >4 grams cumulative dose. |
|
|
Term
| Amphotericin B: Mechanism of Resistance |
|
Definition
| resistance occurs with impaired ergosterol binding |
|
|
Term
| Acyclovir: Mechanism of Resistance |
|
Definition
| resistance occurs through alteration in either the viral thymidine kinase or DNA polymerase |
|
|
Term
| Oseltamivir: Mechanism of Resistance |
|
Definition
| resistance may be associated with point mutations in the viral hemagglutinin or neuraminidase genes |
|
|
Term
|
Definition
| A neuraminidase inhibitor. An analog sialic acid that interferes with the release of progeny influenza virus from infected host cells. |
|
|
Term
|
Definition
| An orally administered prodrug that is activated by hepatic esterases and widely distributed throughout the body. Oral bioavailability is 80% and plasma binding is low. |
|
|
Term
|
Definition
| Active against influena A and B. A neuramididase inhibitor. Works by inhibiting neuraminidase which is essential for glycoprotein sysnthesis needed for viral replication and release. Thus inhibits step 8 in viral replication. Reduces symptoms by approx 1 day. Best results if used within 30 hours of the onset of symptoms. Renal elimination. Mild adverse effects: Nausea, anorexia, nervousness, insomnia, light-headedness, or difficulty concentrating. Side effects are dose related-may decrease after first week of administration. |
|
|
Term
|
Definition
| antibacterial activity persists beyond the time during which measurable drug is present. |
|
|
Term
| Mechanisms of Resistance: Antifungals |
|
Definition
| Impaired binding due to cell membrane changes, altered metabolism |
|
|
Term
| Mechanisms of Resistance: Antivirals |
|
Definition
| Alteration in viral thymidine kinase or DNA polymerase (nucleoside analogs), point mutations in viral hemagglutinin or neuraminidase (Oseltamivir) |
|
|
Term
| Mechanisms of Resistance: Chemotherapy |
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Definition
| Increased capability to repair DNA lesions, decreased transport of alkyl group, increased enzymes that catalyze conjugation (Alkylating agents); decreased folate carrier or receptors, altered proteins with decreased affinity, increased levels of target enzymes (Antimetabolites) |
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Term
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Definition
| MOA: Cytotoxic effects due to transfer of alkyl groups leading to eventual inhibition of DNA replication. ADR: Vesicant (severe skin, eye and mucosal pain and irritation), Systemic toxicity that is dose related-occuring in rapidly growing tissues (bone marrow, GI tract and reproductive system), N/V with in 30 minitues and Myleosuppresion. Alkylating agents are carcinogenic and there is an increased risk of secondary malignancies, esp. acute myelogenous leukemia. |
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Term
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Definition
| inhibits cytochrome P450- dependent synthesis of ergosterol and creates damage to cytoplasmic membrane. |
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Term
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Definition
| 90% absorbed, good tissue penetration including CSF. !/2 life of 30 hours, eliminated unchanged in urine. Good for once a day dosing. |
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Term
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Definition
| Few side effects- NVD in small amounts as well as HA. |
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Term
| fluconazole (Diflucan)Preganacy |
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Definition
| Low dose (150mg) for vaginal candida OK.High dose (400-800mg) causes birth defects in 1st Trimester. |
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Term
| fluconazole Intereactions |
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Definition
| Increases effects of other drugs- warfarin, phenytoin, cyclosorin and sulfonylurea oral hypoglycemics. |
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Term
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Definition
| Acyclic guanosine derivate with clinical activity against HSV-1, HSV-2 and VZV(10 times more potent aginst HSV-1 and HSV-2 than VZV) |
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Term
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Definition
| Acyclovir triphosphate inhibits viral DNS syntesis by:a) competition with deoxyGTP for viral DNA polymerase(irreversible binding) and chain termination by incorporation into viral DNA. |
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Term
| Acyclovir bioavailability |
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Definition
| Oral: poor (15-20%) unaffected by food.Iv form available.Topical formulation causes high concentrations in herpetic lessions, but is systemic undetectable. |
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Term
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Definition
| Cleared by glomerular filtration and tubular secretion.Half life is 2.5 -3 hrs in pts with normal renal functiona dn 20 hrs in pt with anuria. |
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Term
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Definition
| Generally well tolerated.Ocasionally nausea, vomitinf and headache.IV infussion may cause reversible renal toxicity. |
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Term
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Definition
*plant alkaloid
*MOA;prevents formation of mitotic spindle fibers in mitosis stopping cell division leading to cell death
*Toxicities; Myelosupression, rare neurotoxicity. |
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Term
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Definition
| A broad-spectrum antifungal used as initial treatment. May switch to a less toxic med further into treatment. MOA: Binds to ergosterol in the fungal cell membrane, creates pores in the membrane which lead to cell death. ADRs: infusion-related include fever, chills, nausea, vomiting. Cumulative ADRs include renal damage, liver damage and seizures. |
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Term
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Definition
| A drug that acts on the intermediary metabolism of proliferating cells. Drugs have unique clinical applications and toxicity. Examples-antifolates, fluropyrimidines, deoxycytidine analogs, purine antagonists |
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Term
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Definition
| An antimetabolite, folic acid antagonist that binds with DHFR and interferes with the formation of DNA, RNA, and cellular proteins. Excreted by the kidneys. Can be given oral, IV, or intrathecal. Toxicity results in mucositis, diarrhea, myelosupression with neutropenia and thrombocytopenia. |
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Term
| Methotrexate Clinical Application |
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Definition
| Breast cancer, head, neck cancer, osteogenic sarcoma, CNS lymphoma, non-Hodgkin’s lymphoma, bladder cancer, choriocarcinoma |
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Term
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Definition
| Antimetabolite, pro-drug, inactive until activated by a series of enzyme reactions. Once activated inhibits thymidylate synthetase. Responsible for thymidine synthesis, results in inhibition of DNA through a “thymineless death”. |
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Term
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Definition
| Related to dose and schedule. Given IV. Continuous infusion-mucosal damage, diarrhea, and stomatitis. Bolus infusion- myelosupression, decreased WBCs and platelets. Very short half life. |
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Term
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Definition
| Incorporates with RNA causing problems with processing and mRNA transcription. Substituted for uracil on mRNA and interferes with function. |
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Term
| 5FU Clinical Applications |
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Definition
| Colorectal cancer, anal cancer, breast cancer, gastroesophageal cancer, head/neck cancer, and hepatocellular cancer |
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Term
| clinical application of Flutamide |
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Definition
| treatment of Prostate Cancer |
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Term
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Definition
| competitive antagonist of androgen receptors |
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Term
| Flutamide adverse effects |
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Definition
| gynecomastia, liver damage |
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