Phenytoin Sodium - FDA prescribing information, side effects and uses. Dosage Form: injection, solution. WARNING: CARDIOVASCULAR RISK ASSOCIATED WITH RAPID INFUSIONWARNING: CARDIOVASCULAR RISK ASSOCIATED WITH RAPID INFUSIONThe rate of intravenous Phenytoin Sodium Injection administration should not exceed 5. Interracial Irish Dating. Careful cardiac monitoring is needed during and after administering intravenous Phenytoin Sodium Injection. Although the risk of cardiovascular toxicity increases with infusion rates above the recommended infusion rate, these events have also been reported at or below the recommended infusion rate. Reduction in rate of administration or discontinuation of dosing may be needed (see WARNINGS and DOSAGE AND ADMINISTRATION). Indications and Usage for Phenytoin Sodium.
Parenteral Phenytoing Sodium Injection is indicated for the treatment of generalized tonic- clonic status epilepticus, and prevention and treatment of seizures occurring during neurosurgery. Parenteral phenytoind should be used only when oral phenytoin administration is not possible [see DOSAGE AND ADMINISTRATIONand WARNINGS AND PRECAUTIONS.
Phenytoin Sodium Dosage and Administration. General Dosing Information. Because of the increased risk of adverse cardio. Phenytoin clearance is decreased slightly in elderly patients and lower or less frequent dosing may be required [see CLINICAL PHARMACOLOGY]. Because of the risks of cardiac and local toxicity associated with intravenous phenytoin, oral phenytoin should be used whenever possible. In adults, a loading dose of 1.
Original Article. Early Identification of Refractory Epilepsy. Patrick Kwan, M.D., and Martin J. Brodie, M.D. N Engl J Med 2000; 342:314-319 February 3, 2000 DOI: 10. Dating Ariane Boat on this page. Number: 0202. Policy. Aetna considers magnetic resonance spectroscopy (MRS) (also known as NMR spectroscopy) medically necessary for distinguishing recurrent brain. Ataxia — Comprehensive overview covers causes and treatments for this lack of muscle coordination. The cerebellum (Latin for "little brain") is a major feature of the hindbrain of all vertebrates. Although usually smaller than the cerebrum, in some animals such as.
The rate of intravenous administration should not exceed 5. Slower administration rates are recommended to minimize the cardiovascular adverse reactions. Continuous monitoring of the electrocardiogram, blood pressure, and respiratory function is essential. The loading dose should be followed by maintenance doses of oral or intravenous phenytoin every 6- 8 hours. Ordinarily, Phenytoin Sodium Injection should not be given intramuscularly because of the risk of necrosis, abscess formation, and erratic absorption. If intramuscular administration is required, compensating dosage adjustments are necessary to maintain therapeutic serum levels.
An intramuscular dose 5. When returned to oral administration, the dose should be reduced by 5. Monitoring serum levels would help prevent a fall into the subtherapeutic range. Serum blood level determinations are especially helpful when possible drug interactions are suspected.
INTRODUCTION. Malignant blood diseases may be classified: According to the clinical course: Chronic leukemias; Acute leukemias. According to the lineage. Primary intracranial tumors of the brain structures, including meninges, are rare with an overall five-year survival rate of 33.4%; they are collectively called. Disorders. All Disorders. NINDS Binswanger's Disease Information Page; NINDS Brachial Plexus Injuries Information Page; NINDS Brown-Sequard Syndrome Information Page.
In pediatric patients, the drug should be administered at a rate not exceeding 1- 3 mg/kg/min or 5. As non- emergency therapy, Phenytoin Sodium Injection should be administered more slowly as either a loading dose or by intermittent infusion. Because of the risks of cardiac and local toxicity associated with intravenous phenytoin, oral phenytoin should be used whenever possible. Because adverse cardiovascular reactions have occurred during and after infusions, careful cardiac monitoring is needed during and after the administration of intravenous Phenytoin Sodium Injection.
Reduction in rate of administration or discontinuation of dosing may be needed. Because of the risk of local toxicity, intravenous Phenytoin Sodium Injection should be administered directly into a large peripheral or central vein through a large- gauge catheter. Prior to the administration, the patency of the IV catheter should be tested with a flush of sterile saline.
Each injection of parenteral Phenytoin Sodium Injection should then be followed by a flush of sterile saline through the same catheter to avoid local venous irritation due to the alkalinity of the solution. Phenytoin Sodium Injection can be given diluted with normal saline.
The addition of parenteral Phenytoin Sodium Injection to dextrose and dextrose- containing solutions should be avoided due to lack of solubility and resultant precipitation. Treatment with Phenytoin Sodium Injection can be initiated either with a loading dose or an infusion: Loading Dose: A loading dose of parenteral Phenytoin Sodium Injection should be injected slowly, not exceeding 5. Infusion: For infusion administration, parenteral Phenytoin Sodium Injection should be diluted in normal saline with the final concentration of Phenytoin Sodium in the solution no less than 5 mg/m. L. Administration should commence immediately after the mixture has been prepared and must be completed within 1 to 4 hours (the infusion mixture should not be refrigerated). An in- line filter (0. Parenteral drug products should be inspected visually for particulate matter and discoloration prior to administration, whenever solution or container permit. The diluted infusion mixture (Phenytoin Sodium Injection plus normal saline) should not be refrigerated.
If the undiluted parenteral Phenytoin Sodium Injection is refrigerated or frozen, a precipitate might form: this will dissolve again after the solution is allowed to stand at room temperature. The product is still suitable for use.
Acute cerebellar ataxia in children. INTRODUCTIONAcute cerebellar ataxia is a syndrome that occurs in previously well children, often presenting as a postinfectious disorder [1- 5]. The pathogenesis, clinical presentation, evaluation, and prognosis of acute cerebellar ataxia will be reviewed here.
The differential diagnosis and evaluation of the child presenting with acute ataxia is discussed separately. See "Approach to the child with acute ataxia".)In adults, a wide variety of processes can cause cerebellar ataxia, and these can present with acute or chronic disease courses. The diagnostic considerations in an adult with ataxia are discussed separately.
See "Overview of cerebellar ataxia in adults".)EPIDEMIOLOGYAcute cerebellar ataxia accounts for 3. The incidence of this disorder in the pediatric age group is at least 1 in 1.
PATHOGENESISAcute cerebellar ataxia may occur unheralded or, more commonly, after an acute febrile illness [1- 3,5]. Varicella infection- induced cases, once the most common single postinfectious cause, has diminished due to vaccination [7,9]. See "Clinical features of varicella- zoster virus infection: Chickenpox", section on 'Neurologic complications'.)Numerous other infectious agents have been implicated in the pathogenesis of acute cerebellar ataxia, including coxsackievirus, echovirus, enteroviruses, Epstein- Barr virus, hepatitis A, herpes simplex virus I, human herpesvirus 6, measles, mumps, parvovirus B1. Borrelia burgdorferi (Lyme disease), malaria, Mycoplasma pneumoniae, and typhoid fever [2,1. The syndrome has been anecdotally reported following vaccination for varicella, hepatitis B, rabies, meningococcal group C, and human papilloma virus, all without evidence of systemic infection [1,2,1. However, rates after vaccination are much lower than in association with infection: For example, the association of acute cerebellar ataxia with varicella infection is at least 3. Literature review current through.
This topic last updated. Jan 1. 0, 2. 01. 8.
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CAUSES OF CANCER - -EFFECTS OF CANCERMy home page. More of my notes. My medical students. Especially if you're looking for. Medline, which will.
You owe it to yourself to learn to. Not only will you find some information. Alternative (complementary) medicine has made real progress since my.
If you are. interested in complementary medicine, then I would urge you. Alternative Medicine page.
If you are looking for something on complementary. Association of Naturopathic Physicians. And for your enjoyment.. I cannot examine every claim that my correspondents. Sometimes the independent thinkers. You also know that extraordinary claims require.
When a discovery proves to. When a. decades- old claim by a "persecuted genius".
If you ask me about. I will simply invite you to. Who knows? Perhaps. Our world is full of people who have found peace, fulfillment, and friendship. I've learned that they leave the movements when, and only when, they. In the meantime, nothing that I can say or do will.
I am a decent human being. I no longer. answer my crank mail. This site is my hobby, and I do not accept donations, though I appreciate those who have offered to help. During the eighteen years my site has been online, it's proved to be.
It is so well- known. I'm not worried about borrowers. I never refuse requests from colleagues for permission to. So, fellow- teachers.
Don't sell it for a profit, don't use it for a bad purpose. William Carey as my institution. Drop me a note about. And special. thanks to everyone who's helped and encouraged me, and especially the. William Carey. for making it still possible, and my teaching assistants over the years.
Whatever you're looking for on the web, I hope you find it. Health and friendship! BIBLIOGRAPHY / FURTHER READINGMore of Ed's Notes: LEARNING OBJECTIVESDefine the following terms and use them appropriately. Knudson two- hit model. Recognize the ways in which the growth properties of cancer cells differ from normal. Explain the. Nowell multi- step clonal evolution model.
Briefly describe how the classic transforming viruses caused cancer. Explain why cancers produced by a particular transforming virus.
Tell the features common to most or all genuine. Explain why cancers produced by a particular chemical carcinogen in a particular. Give. the evidence for radiation carcinogenesis in humans, and the resulting tumors.
Explain how we believe certain mutations make ras oncogenic. Explain the importance of myc oncogenes in certain cancers, and the two ways myc is activated. Describe tumor- suppressor genes (anti- oncogenes) in considerable detail, and explain why tumors. Explain the Knudson two- hit.
Recognize the important tumor viruses for humans. Tell how they differ from the transforming. Tell how they effect their damage. Describe the Delaney Clause and its repeal. Evaluate media and government claims about "things that cause cancer" intelligently and honestly. Critique the following statement, overheard in a supermarket check- out line: "Cancers are.
The natural way to cure. Give the overall cure rate for newly- diagnosed cancers in the US today. Identify cancers that are increasing and decreasing in the U. S., and suggest reasons why. Identify. cancers that are common in some countries and rare in others. Suggest reasons why. Distinguish "benign" and "malignant".
Explain how certain benign tumors cause serious disease. Explain the various mechanisms by which cancer causes pain, disability, and death. Explain how paraneoplastic syndromes happen (tumor products. Given the name of a paraneoplastic syndrome, tell its effect on the patient. Explain the concept of "tumor markers", substances produced by the tumor. Explain what is meant by an "oncofetal antigen".
Describe the common tumor- suppressor gene deletion syndromes ("autosomal dominant tumor. Recognize each of the following tumor- family syndromes by physical signs. Hippel- Lindauataxia- telangiectasia. Recognize cancer quackery and its methods. Recognize why a scientific. Appreciate the devastating impact of a cancer diagnosis to a patient, and the need for intelligent.
RECOMMENDED READING: The "Neoplasia" chapters in Big or Pocket Robbins. R& F. All. are pretty good. I've followed the sequence in Big Robbins. KCUMB Students"Big Robbins" - - Neoplasia. Lectures follow Textbookbr>. QUIZBANKCell growth #'s 1- 2.
If you have gotten this far, you should already know how to recognize benign and malignant tumors. Please ask for help if this is still a problem.
Tumors are overgrowths, clones within clones, of cells bearing cumulative genetic injuries. NOWELL'S LAW" is my term). Tumor cells typically have failure of division control. At least some of these. Among the many hundreds of known kinds of tumors.
Risk factors are known for various. Oncogenes are slightly altered (ACTIVATED) versions of normal genes involved in cell division.
Activation may. occur by point mutation, translocation, or increased copy number. Oncogenes tell the cell to divide when it shouldn't. This message overrides normal instructions.