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AntiNeoplastic Agents

AntiNeoplastic Agents

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Published by mers puno
a written report about antineoplastic medications for our pharmacology subject during our first semester in our junior year.
a written report about antineoplastic medications for our pharmacology subject during our first semester in our junior year.

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Published by: mers puno on Jun 08, 2009
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06/15/2013

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ANTINEOPLASTIC AGENTS
One branch of chemotherapy involves drugs developed to act on and kill or alter human cells – the
antineoplastic drugs
, which are designed to fight
neoplasms
, or cancers. When chemotherapy is mentioned, most people think of cancer treatment.Antineoplastic drugs alter human cells in a variety of ways, and they are intended to havea greater impact on the abnormal cells that make up the neoplasm or cancer than onnormal cells. This area of pharmacology which has grown tremendously in recent yearsnow includes many drugs that act on or are part of the immune system; these substancesfight the cancerous cells using components of the immune system instead of destroyingcells directly. This chapter discusses the classic antineoplastic approach and those drugsthat are used in cancer chemotherapy.
Neoplasms
All cancers start with a single cell that is generally different from the other cells inthe surrounding tissue. This cell divides, passing along its abnormalities to daughter cells,eventually producing a tumor or neoplasm that has characteristics quite different from theoriginal tissue. The cancerous cells exhibit
anaplasia
, a loss of cellular differentiationand organization, which leads to a loss of their ability to function normally. They alsoexhibit
autonomy
, growing without the usual homeostatic restrictions that regulate cellgrowth and control, which allows the cells to form a tumor.Over time, these neoplastic cells grow uncontrollably, invading and damaginghealthy tissue in the surrounding area and even undergoing
metastasis
, or traveling fromthe place of origin to develop new tumors in other areas of the body where conditions arefavorable for cell growth. The abnormal cells release enzymes that generate blood vessels(
angiogenesis
) in the area to supply both oxygen and nutrients to the cells, thuscontributing to their growth. Overall, the cancerous cells rob the host cells of energy andnutrients and block normal lymph and vascular vessels as the result of pressure andintrusion on normal cells, leading to a loss of normal cellular function.
Causes of Cancer
What causes the cells to mutate and become genetically different is not clearlyunderstood. In some cases, a genetic predisposition to such mutation can be found. Breastcancer, for example, seems to have a definite genetic link. In other cases, constantirritation and cell turnover, and even stress have been blamed for the ensuring cancer.Stress reactions suppress the activities of the immune system, so if a cell is mutatingwhile a person is under prolonged stress, research indicates that the cell has a better chance of growing into a neoplasm than when a person’s immune system is fully active.Pipe smokers are at increased risk for development of tongue and mouth cancers becausethe heat and chemicals in the pipe are constantly destroying normal cells, which must beincreased rapidly, increasing the chances for development of a mutant cell. People livingin areas with carcinogenic or cancer-causing chemicals in the air, water, or even theground are at increased risk of developing mutant cells as a reaction to those toxicchemicals. Cancer clusters are often identified in such high-risk areas. Most likely, a
 
mosaic of factors coming together in one person would eventually lead to thedevelopment of the neoplasm.
Cell-Cycle Nonspecific and Specific Drugs
Anticancer drugs cause cancer death by interfering with cell replication.
Cell-cycle nonspecific (CCNS) drugs
act during any phase of the cell cycle, and
cell-cyclespecific (CCS) drugs
exert their influence during a specific phase of the cell cycle.CCNS drugs (also called
cell-cycle independent 
) kill cells during the M and G
0
phases.CCS drugs (also called
cell-cycle dependent 
) are most effective against rapidly growingcancer cells. In general CCNS drugs include the alkylating drugs, antitumor antibiotics,and hormones. The CCS drugs include the antimetabolites and the mitotic inhibitors.
Growth fraction
and
doubling time
are two factors that play a major role in theresponse of cancer cells to anticancer drugs. Anticancer drugs are more effective againstneoplastic cells that have a high growth fraction. Leukemias and some lymphomas havehigh growth fractions and thus respond well to anticancer drug therapy. Small and earlyforming cancer cells and fast-growing tumors respond well to chemotherapy and have vahigher cure rate than slow-growing tumors in the advanced stages.
ALKYLATING AGENTS
One of the largest groups of anticancer drugs is the alkylating compounds.
Alkylating agents
cause cross-linking of DNA strands, abnormal base pairing, or DNAstrand breaks, thus preventing the cell from dividing. Drugs in this group belong to theCCNS category and kill cells in various and multiple phases of the cell cycle. However,they are most effective against cells in the G
0
phase. They are effective against manytypes of cancer, including acute and chronic leukemias, lymphomas, multiple myeloma,and solid tumors.I.
BUSULFAN (
 Busulfex 
,
 Myleran
)
ACTION:
Changes essential cellular ions to covalent bonding with resulting alkylation; thisinterferes with normal biologic function of DNA; activity is not phase specific; actionis due to myelosuppresion.
Used for treatment of chronic myelocytic leukemia (CML)
INDICATIONS AND DOSAGES:
Adults: PO (
 Induction
)
 – 1.8 mg/m
2
/day or 60mcg (0.06 mg)/kg/day until WBCs<15,000/mm
3
. Usual dose is 4-8 mg/day (range 1-12 mg/Day).
PO (
 Maintenance
)
– 1-3 mg/day
Adults: IV
– 0.8 mg/kg q6hr (dose based on IBW or actual weight, whichever is less;in obese patients, dosage should be based on adjusted IBW) for 4 days(total of 16 doses); given in combination with cyclophosphamide.
 
Children: PO
– 0.06-0.12 mg/kg/day or 1.8-4.6 mg/m
2
/day initially. Titrate dose toMaintain WBC of approximately 20,000/mm
3
.
ADVERSE REACTIONS:PO Route
CV:
Hypotension, thrombosis, chest pain, tachycardia, atrial fibrillation, heart block, pericardial effusion,
cardiac tamponade
(high dose with cyclophosphamide)
GI:
Anorexia, constipation, diarrhea, dry mouth, nausea, vomiting
RESP:
 Alveolar hemorrhage
, atelectasis, cough, hemoptysis, hypoxia, pleuraleffusion, pneumonia, sinusitis,
 pulmonary fibrosis
IV Route
CNS:
 
Cerebral Hemorrhage
,
coma
,
 seizures
, anxiety, depression, dizziness,headache, encephalopathy, weakness, mental changes
EENT:
Pharyngitis, epistaxis, cataracts
GI:
 Nausea, vomiting, diarrhea, weight loss
GU:
Impotence, sterility, amenorrhea, gynecomastia,
renal toxicity
, hypreuremia,adrenal insufficiency-like syndrome
HEMA:
 
Thrombocytopenia
,
leukopenia
,
pancytopenia
,
severe bone marrow depression
INTEG:
Dermatitis, hyperpigmentation, alopecia
OTHER:
 
Chromosomal aberrations
RESP:
 Irreversible pulmonary fibrosis
, pneumonitis
INTERACTION:
Concurrent or previous (within 72 hours) use of 
acetaminophen
may ↓ eliminationand ↑ toxicity. Concurrent use with high-dose
cyclophosphamide
in patients withthassalemia may result in cardiac tamponade. Concurrent use with
itraconazole
or 
phenytoin
blood levels effectiveness. Long-term continuous therapy with
thioguanine
may ↑ risk of hepatic toxicity. ↑ Bone marrow suppression with other 
antineoplastics
or 
radiation
 
therapy
. May ↓ the antibody response to and ↑ risk of adverse reactions from
live-virus vaccines
.
CONTRAINDICATIONS AND CAUTIONS:
Contraindications:
Hypersensitivity. Pregnancy or lactation (pregnancy D 3
rd
trimester). Failure to respond to previous courses (radiation and chemotherapy).
Precautions:
Active infections; decreased bone marrow reserve; obese patients (basedose on IBW); other chronic debilitating diseases (leukopenia, thrombocytopenia); patients with childbearing potential.
NURSING CONSIDERATIONS:
Assessment:
 High Alert:
Monitor for bone marrow depression. Assess for bleeding (bleedinggums, bruising, petechiae, guaiac stools, urine, and emesis) and avoid IMinjections and taking rectal temperatures. Apply pressure to venipuncture sites for at least 10min. Assess for signs infection (fever, chills, sore throat, etc.) duringneutropenia. Anemia may occur. Monitor for increased fatigue, dyspnea, andorthostatic hypotension. Notify physician if these symptoms occur.

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