Veracold VT Mechanism of Action

Pharmacology: Pharmacodynamics: Paracetamol: ATC code: N02BE01.
Analgesic: The mechanism of analgesic action has not been fully determined. Paracetamol may act predominantly by inhibiting prostaglandin synthesis in the central nervous system (CNS) and to a lesser extent, through a peripheral action by blocking pain-impulse generation. The peripheral action may also be due to inhibition of prostaglandin synthesis or to inhibition of the synthesis or actions of other substances that sensitise pain receptors to mechanical or chemical stimulation.
Antipyretic: Paracetamol probably produces antipyresis by acting centrally on the hypothalamic heat regulation centre to produce peripheral vasodilation resulting in increased blood flow through the skin, sweating and heat loss. The central action probably involves inhibition of prostaglandin synthesis in the hypothalamus.
Chlorpheniramine maleate: ATC code: R06AB02.
Chlorpheniramine is a potent antihistamine (H1-antagonist). Antihistamines diminish or abolish the actions of histamine in the body by competitive reversible blockade of histamine H1-receptor sites on tissues. Chlorpheniramine also has anticholinergic activity. Antihistamines act to prevent the release of histamine, prostaglandins and leukotrienes and have been shown to prevent the migration of inflammatory mediators. The actions of chlorpheniramine include inhibition of histamine on smooth muscle, capillary permeability and hence reduction of edema and wheal in hypersensitivity reactions such as allergy and anaphylaxis.
Phenylephrine hydrochloride: ATC code: C01CA06.
Phenylephrine hydrochloride is a sympathomimetic agent with mainly direct effects on adrenergic receptors (predominantly alpha-adrenergic activity) producing nasal decongestion.
Pharmacokinetics: Paracetamol: Paracetamol is readily absorbed from the gastrointestinal tract with peak plasma concentrations occurring about 10 to 60 minutes after oral doses. The absorption of paracetamol was slow and incomplete in vegetarian subjects compared with non-vegetarian subjects. Paracetamol is distributed into most body tissues. It crosses the placenta and is present in breast milk. Plasma protein binding is negligible at usual therapeutic concentrations but increases with increasing concentrations.
The elimination half-life of paracetamol varies from about 1 to 3 hours.
Paracetamol is metabolised mainly in the liver and excreted in the urine mainly as the glucuronide and sulfate conjugates. Less than 5% is excreted as unchanged paracetamol. A minor hydroxylated metabolite (N-acetyl-p-benzoquinone imine), is usually produced in very small amounts by cytochrome P450 isoenzymes (mainly CYP2E1 and CYP3A4) in the liver and kidney. It is usually detoxified by conjugation with glutathione but may accumulate after paracetamol overdosage and cause tissue damage.
Chlorpheniramine maleate: Chlorphenamine maleate is absorbed relatively slowly from the gastrointestinal tract, peak plasma concentrations occurring about 2.5 to 6 hours after oral doses. Bioavailability is low, values of 25 to 50% having been reported. Chlorphenamine appears to undergo considerable first-pass metabolism. About 70% of chlorphenamine in the circulation is bound to plasma proteins. There is wide interindividual variation in the pharmacokinetics of chlorphenamine; values ranging from 2 to 43 hours have been reported for the half-life. Chlorphenamine is widely distributed in the body, and enters the CNS.
Chlorphenamine maleate is extensively metabolised. Metabolites include desmethyl- and didesmethyl chlorphenamine. Unchanged drug and metabolites are excreted primarily in the urine; excretion is dependent on urinary pH and flow rate. Only trace amounts have been found in the faeces.
A duration of action of 4 to 6 hours has been reported this is shorter than may be predicted from pharmacokinetic parameters.
More rapid and extensive absorption, faster clearance, and a shorter half-life have been reported in children.
Phenylephrine hydrochloride: Phenylephrine has low oral bioavailability owing to irregular absorption and first-pass metabolism by monoamine oxidase in the gut and liver.