ANSWER FOLLOWING QUESTIONS

Answer following questions

Answer following questions!

Q1- Distribution and metabolism of salicylate and paracetamol in the body, and the therapeutic and side effects?

Ans. Distribution of salicylate all through most body fluids and tissues proceeds at a fast rate after absorption. In addition from the plasma itself, fluids which have been found to comprise considerable allowances of salicylate after oral ingestion include spinal, peritoneal and synovial fluids, saliva and milk. Tissues containing high concentrations of the pharmaceutical are the kidney, liver, heart and lungs. Concentrations in the mind are generally reduced, and are minimal in feces, bile and sweat. (Harvey 2007)

The drug easily crosses the placental barrier. At clinical concentrations, from 50% to 90% of the salicylate is compelled to plasma proteins especially albumin, while ASA itself is compelled to only a very limited extent. However, ASA has the capability of acetylating diverse proteins, hormones, DNA, platelets and hemoglobin, which at smallest partly interprets its wide-ranging pharmacological actions. Excretion of salicylates happens principally by the kidney, through a blend of glomerular filtration and tubular excretion, in the form of salicylic quantities, as well as phenolic and glucuronides. Salicylate can be noticed in the urine soon after its ingestion but the full dose needs up to 48 hours for entire elimination. The rate of excretion of free salicylate is exceedingly variable, reported recovery rates in human urine extending from 10% to 85%, counting mostly on urinary pH. In general, it can be asserted that unpleasant urine facilitates reabsorption of salicylate by renal tubules, while alkaline urine promotes excretion of the drug.

Q2- The clinical management of salicylate and paracetamol overdose, and how the Clinical Chemistry laboratory can aid this process?

Ans. The majority of paracetamol overdose patients present early and are therefore attentive and respiring normally. Paracetamol is a common drug used for self-poisoning and is associated with potentially fatal liver damage. Patients accepted to clinic because of paracetamol overdoses were studied in alignment to determine their characteristics and components which might have discouraged them from taking paracetamol or decreased the dangers of the overdoseIf the patient is lifeless the airway must be defended and tracheal intubation may be required. There is a risk of aspiration of stomach contents if the persevering vomits. Salicylates in large doses are uricosuric agencies, lesser allowances may weigh down uric unpleasant clearance and therefore decrease the uricosuric effects of other drugs. Salicylates furthermore retard the renal elimination of methotrexate.

Q3-What is the difference between the toxic dose and the toxic level of a drug?

Ans. The difference is marginal however, the toxic effects of paracetamol are due to a minor alkylating metabolite (N-acetyl-p-benzo-quinone imine, abbreviated as NAPQI) that is produced through this enzyme, not paracetamol itself or any of the major metabolites. The metabolism of paracetamol is an very good demonstration of toxication, because the metabolite NAPQI is mainly to blame for toxicity rather than paracetamol itself. Another paracetamol-methionine combination tablet was withdrawn from the UK market after it was placed on the list of drugs not available for prescribing ...