This essay has been submitted by a student. This is not an example of the work written by our professional essay writers.
Hemodialysis works by removing blood from the body and having it flow across a special filter, along with solutions. The filter helps remove toxins. The blood is then return to the body. Hemodialysis requires special ways to access the blood in the blood vessels. Access may be needed on a short-term or long-term basis.
the kidneys, but instead mimics the toxin filtering job that normal functioning kidneys would normally perform. The two types of dialysis are hemodialysis and peritoneal dialysis.
Hemodialysis uses a special filter called a dialyzer that functions as an artificial kidney to clean a person's blood. The dialyzer is a canister connected to the hemodialysis machine. During treatment, the blood travels through tubes into the dialyzer, which filters out wastes, extra salt and water, then the cleaned blood flows through another set of tubes back into the body. The hemodialysis machine monitors blood flow and removes wastes from the dialyzer. This procedure is performed at a dialyzer center.
Carisoprodol is a centrally acting skeletal muscle relaxant that does not directly relax tense skeletal muscles in man. The mode of action of carisoprodol is relieving acute muscle spasm of local origin has not been clearly identified , but may be related to its sedative properties. In animals Carisoprodol has been shown to produce muscle relaxation by blocking interneuronal activity and depressing transmission of polysynaptic neurons in the spinal cord and in the descending reticular formation of the brain. The onset of action is rapid and last four (4) to six (6) hours .
Carisoprodol is metabolized in the liver and is excreted by the kidneys. One of the products of metabolism, meprobamate, is active as an auxiolytic. The degree to which it contributes to the efficacy of carisoprodol is unknown. Carisoprodol is dialyzabic by peritoneal and hemodialysis.
The pharmacokinetics of carisoprodol was determined in a small in vivo biostudy of five (5) men and five (5) women when the dose was normalized to 350mg, the mean peak plasma concentration (max2) achieved was 2.99 Â± 0.68 ug /ml. Women tended to reach peak plasma concentration earlier than men (1.45 Vs - 2.5 hrs) and had a faster apparent oral clearance (0.772 Vs 0.38 4 L/HOUR/Kg.). The clinical significance of these findings is unknown and they may in part be due to the small number of subjects present in the trial.
Carisoprodol is metabolized in the liver via cytochrome p450 enzyme, cyP2c19. This enzyme exhibits genetic polymorphism. For example, 15 to 20 percent of Asian populations may be expected to be poor metabolizers. For Caucasians and Blacks, the prevalence of poor metabolizers is 3 to 5 percent. Following a single 350 mg dose of carisoprodol, the corresponding normalized peak concentration of meprobamate, which is a metabolite of carisoprodol, was 2.08 + 0.48 ug/ml. These levels are approximately Â¼ of those seen following a single 400 mg dose of meprobamate.
Carisoprodol is eliminated by both renal and non-renal routes with a terminal elimination half - life of 2.44 + 0.93 hours. It is dialyzable by peritoneal and hemodialysis.
Xanax XR extended release tablets
Generic Name: Alprazolam
Alprazolam is a white crystalline powder which is souble in methanol or ethanol but which has no appreciable solubility in water at physiological pH
Following oral administration of Xanax (immediate release) tablets, alprazolam is readily absorbed. Peak concentrations in the plasma occur in one to two hours following administration. Plasma levels are proportional to the dose given, over the dose range of 0.5 to 3.0 mg, peak levels of 8.0 to 37 mg/ml were observed. Using a specific assay methodology, the mean plasma elimination half-life of alprazolam has been found to be about four (4) to two (2) hours range 6.3 - 26.9 hours) in healthy adults.
The mean absolute bioavailability of alprazolam from Xanax XR tablets is approximately 90 percent and the relative bioavailability compared to Xanax tablets is 100 percent. The bioavailability and pharmacokinetics of alprazolam following administration of Xanax tablet, are similar to that for xanax tablets. With the exception of a slower rate of absorption. The slower absorption rate results in a relatively constant concentration that is maintained between 5 and 11 hours after the dosing. The pharmacokinetics of alprazolam and two of its major active metabolites (4-hydroxy alprazolam and d-hydroxy alprazolum) are linear and concentrations are proportional up to the recommended maximum daily dose of 10mg given once daily.
Multiple dose studies indicate that the metabolism and elimination of alprozolam are similar for the immediate release and the extended - release products. Food has a significant influence on the bioavailability of Xanux XR tablets. A high-fat meal given up to two hours before dosing with Xanux XR tablets increased the mean Cmax by about 25 percent. The effect to this meal on Tmax depended on the timing of the meal, with a reduction in Tmax by about 1/3 for subjects eating immediately before dosing and an increase in Tmax by about 1/3 for subject eating one hour or more after dosing. The extent of exposure (AUC) and elimination half-life (t Â½) were not affected by eating.
The apparent volume of distribution of alprazolam is similar for Xanax XR and XANAX tablets. In vitro, alprazolam is bound (80%) to human serum protein. Serum albumin accounts for the majority to the binding.
Alprazolam is extensively metabolized in humans, primarily by cytochrome P 450 3A4 (cyP3A4) to two major metabolities in the plasma 4 - hydroxy alprozolam and a-hydroxyalprazolam. A benzophenone derived from alprazolam is also found in humans. Their half lives appear to be similar to that of alprazolam. The pharmacokinetics parameters at steady-state for the two hydroxylated metabolite of alprazolam (4-hydroxyalprazolam and a-hydrox yalprazolam) were similar for XANAX and Xanux XR tablets, indicating that the metabolism of alprazolam is not affected by absorption rate. The plasma concentrations of 4 - hydroxyalparozolam and a - hydroxyalprazolam relative to unchanged alprazolam concentration after both Xanux XR and XANUX tablets were always less than 10 percent and 4 percent respectively. The reported relative potencies in benzodiazepine receptor binding experiments and in animals models of induced seizure inhibition are 0.20 and 0.66, respectively, for 4 - hydroxyalprazolam and a - hydroxyalprazolam. Such low concentration and the lesser potencies of 4 - hydroxyalprazolam and a - hydroxyalprazolam suggest that they are unlikely to contribute much to the pharmacological effects of alprzolam - the benzophenone metabolite is essentially inactive.
Alprazolam and its metabolites are excreted primarily in the urine. The mean plasma elimination half-life of alprazolam following administration of XANAX XR tablets ranges from 10.7 - 15.8 hours in healthy adults.
Rifampicin is readily absorbed from the gastrointestinal tract (90%) . Peak plasma concentration occurs to 1.5 to 4 hours after an oral dose .After a 450mg oral dose, plasma levels reach 6 to 9ug/ml while a 600mg dose on an empty stomach yields 4 to 32 ug/ml/mean 7ug/ml. Food may reduce and delay absorption .Ellenhorn, 1988 Mandel,1985
Eighty nine (+/- ) percent of rifampicin in circulation is bound to plasma proteins. ( Goodman &Gilman, 1990) It is lipid soluble.
It is widely distributed in body tissues and fluids. When the meninges are inflamed, rifampicin enters the cerebrospinal fluid (4.0ug/ml after a 600 oral dose) . It reaches therapeutic levels in the lungs ,bronchial secretions, pleural fluid , other cavity fluid, liver , bile, and urine (Van Scoy, 1987) .
Rifampicin has a high degree of placental transfer with a foetal to maternal serum level ratio of 0.3 . It is distributed into breastmilk ( Chow & Jesesson , 1985).
Approximately 85% of rifampicin is metabolized by the liver microsomal enzymes to its main an active metabolite - deacetylrifampicin .Rifampicin undergoes enterohepatic recirculation but not the deacetylated form. Rifampicin increases its own rate of metabolism. Rifampicin may also be inactivated in other parts of the body .
Formylrifampicin isa urinary metabolite that spontaneously forms in the urine.
Rifampicin metabolite deacetylrifampicin is excreted in the bile and also in the urine .Approximately 50% of the rifampicin dose is eliminated within 24 hours and 6 to 30 of the drug is excreted unchanged in the urine, while 15 % is excreted as active metabolite. Approximately 43 to 60% of oral dose is excreted in the faeces . ( Van Scoy 1987, Drug Information 1990).Intrinsic total body clearance is 3.5 (+/- 1.6 ) ml/min/kg, reduced in kidney failure ( Goodman & Gilman 1990 ).
NEURON - GABAPENTIN
Pharmacokinetics and Drug Metabolism.
All Pharmacological actions following gabapentin administration are due to the activity of the parent compound; Gabapentin is not appreciably metabolized in humans.
ABSORPTION: - Food has only a slight effect on the rate and extent of absorption of gabapentin.
DISTRIBUTION: less than three percent of gabapentin circulates bound to plasma protein, the apparent volume of distribution of gabapentin after 150 mg intravenous administration is 58 + 6L (mean + SD): In patients with epilepsy steady state predose ( C min) concentration of gabapentin in cerebrospinal fluid were approximately twenty percent of the corresponding plasma concentration.
ELIMINATION: Gabapentin is eliminated from the systemic circulation by renal excretion as unchanged drug.
Gabapentin elimination half-life is 5 to 7 hours and is unaltered by dose or following multiple dosing. Gabapentin elimination rate constant plasma clearance, and renal clearance are directly proportional to creatinine clearance. In elderly patients and in patients with impaired renal function, gabapentin plasma clearance is reduced. Gabapentin can be removed from the plasma by haemodialysis.
Absorption: Following oral administration, peak serum concentrations of Digoxin occur at one to three hours. Absorption of Digoxin from Lanoxin tablets has been demonstrated to be sixty to eighty percent complete compared to an identical intravenous dose of Digoxin, when Lanoxin tablets are taken after meals, the rate of absorption is showed, but the total amount of Digoxin absorbed, is usually unchanged. When taken with meals high in bran fiber, however, the amount absorbed from an oral dose may be reduced. Comparisons of systemic availability and equivalent doses for oral preparations of Lanoxin.
Among dosage forms
60 - 80 percent
In some patients, orally administered digoxin is converted to inactive reduction products. It is suggested that one in ten patients treated with Digoxin tablets will degrade forty percent or more of the injested dose, certain antibiotics may increase the absorption of Digoxin.
Following drug administration, a six to eight hour tissue distribution phase is observed. This is followed by a much more gradual decline in the serum concentration of the drug, which is dependent on the elimination of Digoxin from the body. The peak height and slope of the early portion of the serum concentration time curve are dependent upon the route of administration and the absorption characteristics of the formulation - clinical evidence indicates that the early high serum concentration do not reffect the concentration of Digoxin at its site of action, but with chronic use, the steady state post distribution serum concentrations are in equilibrium, with tissue concentrations and correlate with pharmacologic effects.
Digoxin is concentrated in tissues and therefore has a large apparent volume of distribution. Digoxin crosses both the blood-brain barrier and the placenta. At delivery serum Digoxin concentration in the newborn is similar to the serum concentration in the mother. Twenty five percent of Digoxin in the plasma is bound to protein. Some serum Digoxin concentration are not significantly altered by large changes in fat tissue weight, the distribution space correlates best with lean body weight not total body weight.
Only a small percentage of a dose of Digoxin is metabolized. The end metabolites, which includes 3,4 - Digoxigenin, 3 - keto - digoxigenin, and their glucuronide and sulfate conjugates, are polar in nature and are postulated to be formed via hydrolysis, oxidation and conjugation. The metabolism of Digoxin is not dependent upon the cytochrome P - 450 system, and Digoxin is not known to induce or inhibit the cytochrome P - 450 system.
Elimination of Digoxin follows first order - kinetics (the quantity of Digoxin eliminated at any time is proportional to the total body content) Following introvenous administration fifty to seventy percent of a Digoxin dose is excreted unchanged in the urines. Renal excretion of Digoxin is proportional to glomuelar filtration rate and is largely independent of urine flow. In a healthy person with normal renal function, Digoxin has a half-life of 15 to 20 days. The half life in anuric patients is prolonged to three ( 3) to five (5) days. Digoxin is not effectively removed form the body by dialysis, exchange transfusion or during cardiopulmonary bypass because most of the drug is bound to tissue and does not circulate in the blood.