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Vitamin intravenous

Vitamins may be affected adversely by changes in solution pEf, presence of other additives, storage time, solution temperature, and exposure to Ught. Because of variable stabilities of individual vitamins, intravenous vitamin solutions should be added to the PN solution as near to the time of administration as is clinically feasible, and should not be in the PN solution longer than 24 hours. [Pg.2607]

Thiamine (B ), a vitamin, intravenously to a client diagnosed with Wernicke-Korsakoff syndrome. [Pg.320]

Vitamins, intravenous solutions, and drugs used in nutrition Chapter 34... [Pg.533]

It is not always necessary to give every essential mineral and vitamin intravenously, since some of these nutrients may be provided in intramuscular or subcutaneous injections made at regular intervals. The present trend appears to be leading in the direction of giving greater mineral and vitamin supplementation than was done in the past... [Pg.590]

Manufacture of vitamin C starts with the conversion of sorbitol to L-sorbose. Sorbitol and xyHtol have been used for parenteral nutrition following severe injury, bums, or surgery (246). An iron—sorbitol—citric acid complex is an intramuscular bematinic (247). Mannitol administered intravenously (248) and isosorbide administered orally (249) are osmotic diuretics. Mannitol hexanitrate and isosorbide dinitrate are antianginal dmgs (see Cardiovascular agents). [Pg.54]

Alimentary biotin deficiency is rare. It may, however, occur in patients on long-term parenteral nutrition lacking biotin or in persons who frequently consume raw egg white. Raw egg white contains a biotin-binding glycoprotein, called avidin, which renders biotin biologically unavailable. Pharmacological doses of the vitamin (1-10 mg/d) are then used to treat deficiency symptoms. There are no reports of toxicity for daily oral doses up to 200 mg and daily intravenous doses of up to 20 mg [2]. [Pg.270]

Thiamin has a very low toxicity (oral LD5o of thiaminchloride hydrochloride in mice 3-15 g/kg body weight). The vitamin is used therapeutically to cure polyneuropathy, beri-beii (clinically manifest thiamin deficiency), and Wernicke-Korsakoff Syndrome ( Wernicke encephalopathy and Korsakoff psychosis). In mild polyneuropathy, 10-20 mg/d water-soluble or 5-10 mg/d lipid-soluble thiamin are given orally. In more severe cases, 20-50 mg/d water-soluble or 10-20 mg/d lipid-soluble thiamin are administered orally. Patients suffering from beri-beri or from early stages of Wernicke-Korsakoff Syndrome receive 50-100 mg of thiamin two times a day for several days subcutaneously or intravenously until symptoms are alleviated. Afterwards, the vitamin is administered orally for several weeks. [Pg.1288]

Immediate administration of 100 meg to 1 mg vitamin K subcutaneously or intravenously, followed by administration of FFP as necessary. Vitamin K administration via the intramuscular route may induce hematoma owing to coagulopathy, and intravenous administration should be slow because it has been associated with anaphylaxis. Prothrombin complex concentrate (PCC) at minimum dose of 50 units/kg should be given for life-threatening bleeding.27,28... [Pg.998]

For women whose breast cancer has metastasized to bone, bisphosphonates are recommended, in addition to chemotherapy or endocrine therapy, to reduce bone pain and fractures.28,64 Pamidronate (90 mg) and zoledronate (4 mg) can be given intravenously once each month. These bisphosphonates are given in combination with calcium and vitamin D. [Pg.1321]

O Parenteral nutrition (PN), also called total parenteral nutrition (TPN), is the intravenous administration of fluids, macronutrients, electrolytes, vitamins, and trace elements for the purpose of weight maintenance or gain, to preserve or replete lean body mass and visceral proteins, and to support anabolism and nitrogen balance when the oral/enteral route is not feasible or adequate. [Pg.1493]

PN should provide a balanced nutritional intake, including macronutrients, micronutrients, and fluid. Macronutrients, including amino acids, dextrose, and intravenous lipid emulsions, are important sources of structural and energy-yielding substrates. A balanced PN formulation includes 10% to 20% of total daily calories from amino acids, 50% to 60% of total daily calories from dextrose, and 20% to 30% of total daily calories from intravenous lipid emulsion. Micronutrients, including electrolytes, vitamins, and trace elements, are required to support essential biochemical reactions. Parenteral... [Pg.1494]

The water-soluble and fat-soluble vitamins in the parenteral multivitamin mix are essential cofactors for numerous biochemical reactions and metabolic processes. Parenteral multivitamins are added daily to the PN. Patients with chronic renal failure are at risk for vitamin A accumulation and potential toxicity. Serum vitamin A concentrations should be measured in patients with renal failure when vitamin A accumulation is a concern. Previously, vitamin K was administered either daily or once weekly because intravenous multivitamin formulations did not contain vitamin K. However, manufacturers have reformulated their parenteral multivitamin products to provide 150 meg of vitamin K in accordance with FDA recommendations. There is a parenteral multivitamin formulation available without vitamin K (e.g., for patients who require warfarin therapy), but standard compounding of PN formulations should include a parenteral multivitamin that contains vitamin K unless otherwise clinically indicated. [Pg.1498]

The efficiency of vitamin E in the suppression of free radical-mediated damage induced by iron overload has been studied in animals and humans. Galleano and Puntarulo [46] showed that iron overload increased lipid and protein peroxidation in rat liver. Vitamin E supplementation successfully suppressed these effects and led to an increase in a-tocopherol, ubiquinone-9, and ubiquinone-10 contents in liver. Important results were obtained by Roob et al. [47] who found that vitamin E supplementation attenuated lipid peroxidation (measured as plasma MDA and plasma lipid peroxides) in patients on hemodialysis after receiving iron hydroxide sucrose complex intravenously during hemodialysis session. These findings support the proposal that iron overload enhances free radical-mediated damage in humans. [Pg.853]

Ellis et al. [72] recently studied the effects of short- and long-term vitamin C therapy in the patients with chronic heart failure (CHF). It was found that oxygen radical production and TBAR product formation were higher in patients with CHF than in control subjects. Both short-term (intravenous) and long-term (oral) vitamin C therapy exhibited favorable effects on the parameters of oxidative stress in patients the treatments decreased oxygen radical formation and the level of lipid peroxidation and improved flow-mediated dilation in brachial artery. However, there was no correlation between changes in endothelial function and oxidative stress. [Pg.856]

Chelators of iron, which are now widely applied for the treatment of patients with thalassemia and other pathologies associated with iron overload, are the intravenous chelator desferal (desferrioxamine) and oral chelator deferiprone (LI) (Figure 19.23, see also Chapter 31). Desferrioxamine (DFO) belongs to a class of natural compounds called siderophores produced by microorganisms. The antioxidant activity of DFO has been studied and compared with that of synthetic hydroxypyrid-4-nones (LI) and classic antioxidants (vitamin E). It is known that chronic iron overload in humans is associated with hepatocellular damage. Therefore, Morel et al. [370] studied the antioxidant effects of DFO, another siderophore pyoverdin, and hydroxypyrid-4-ones on lipid peroxidation in primary hepatocyte culture. These authors found that the efficacy of chelators to inhibit iron-stimulated lipid peroxidation in hepatocytes decreased in the range of DFO > hydroxypyrid-4-ones > pyoverdin. It seems that other siderophores are also less effective inhibitors of lipid peroxidation than DFO [371],... [Pg.895]

The answer is c. (Hardman, p 15230 Administration of intravenous CaG would immediately correct the tetany that might occur in a patient in whom a thyroidectomy was recently performed. Parathyroid hormone would act more slowly but could be given for its future stabilizing effect. Long-term control of a patient after a thyroidectomy can be obtained with vitamin D and dietary therapy Calcitonin is a hypocalcemic antagonist of parathyroid hormone. Plicamycin (mithramycin) is used to treat Paget s disease and hypercalcemia. The dose employed is about one-tenth the amount used for plicamycin s cytotoxic action. [Pg.254]

Medical Management Immediate decontamination after exposure is the only way to prevent damage to victims, followed by symptomatic management of lesions. Hospital care tends to be supportive. It should be repeated that liquid arsenical vesicants produce more serious lesions on dermal surfaces than do liquid mustard. In toxic victims, liberal fluids by mouth or intravenous, and high-vitamin, high-protein, high-carbohydrate diets could be indicated. For those victims where shock is in evidence, provide the usual supportive measures such as intravenous administration, blood transfusions, or other vascular volume expanders should be indicated. [Pg.220]

The metabolism of cyanide has been studied in animals. The proposed metabolic pathways shown in Figure 2-3 are (1) the major pathway, conversion to thiocyanate by either rhodanese or 3-mercapto-pyruvate sulfur transferase (2) conversion to 2-aminothiazoline-4-carboxylic acid (Wood and Cooley 1956) (3) incorporation into a 1-carbon metabolic pool (Boxer and Richards 1952) or (4) combining with hydroxocobalamin to form cyanocobalamin (vitamin B12) (Ansell and Lewis 1970). Thiocyanate has been shown to account for 60-80% of an administered cyanide dose (Blakley and Coop 1949 Wood and Cooley 1956) while 2-aminothiazoline-4-carboxylic acid accounts for about 15% of the dose (Wood and Cooley 1956). The conversion of cyanide to thiocyanate was first demonstrated in 1894. Conversion of cyanide to thiocyanate is enhanced when cyanide poisoning is treated by intravenous administration of a sulfur donor (Smith 1996 Way 1984). The sulfur donor must have a sulfane sulfur, a sulfur bonded to another sulfur (e.g., sodium thiosulfate). During conversion by rhodanese, a sulfur atom is transferred from the donor to the enzyme, forming a persulfide intermediate. The persulfide sulfur is then transferred... [Pg.74]

Another application is the esterification of menahydroquinone-4, a water-insoluble vitamin K, with V,A-dimethylglycine [144], The 1-mono, 4-mono, and 1,4-bis esters were found to be water-soluble and rapidly hydrolyzable by liver and plasma esterases. A rapid pharmacodynamic response was seen after intravenous administration of the prodrugs. [Pg.488]

No specific antidote has been shown to be effective in treating 1,2-dibromoethane intoxication once absorption into the bloodstream has occurred (Ellenhorn and Barceloux 1988). Intravenous infusions of glucose may limit the hepatotoxicity of 1,2-dibromoethane (ERA 1989b). During the recovery phase, a diet rich in vitamin B and carbohydrates may limit liver damage (Dreisbach and Robertson 1987 Lawrence and Michaels 1984). Hemodialysis may be needed to regulate extracellular fluid and electrolyte balance and to remove metabolic waste products if renal failure occurs (ERA 1989b). [Pg.72]

When the alcoholic first presents for treatment, his/her nutritional status should be fully assessed. Vitamin supplementation should always be a component of this treatment. In the emergency room setting, the alcoholic patient usually receives intravenous fluids containing magnesium, thiamine, and multivitamin supplements. The yellow-colored fluid is commonly called a banana bag or rally pack. A daily... [Pg.196]


See other pages where Vitamin intravenous is mentioned: [Pg.46]    [Pg.1144]    [Pg.531]    [Pg.691]    [Pg.46]    [Pg.1144]    [Pg.531]    [Pg.691]    [Pg.156]    [Pg.293]    [Pg.97]    [Pg.231]    [Pg.54]    [Pg.532]    [Pg.1494]    [Pg.1508]    [Pg.852]    [Pg.670]    [Pg.1388]    [Pg.1609]    [Pg.39]    [Pg.220]    [Pg.225]    [Pg.348]   
See also in sourсe #XX -- [ Pg.269 ]

See also in sourсe #XX -- [ Pg.190 ]




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