Curekuf W Cough Syrup Mechanism of Action

Pharmacology: Pharmacodynamics: Diphenhydramine suppresses the cough reflex by a direct effect on the cough centre in the medulla of the brain. Its antihistaminic action is by competing with histamine for H1-receptor sites on effector cells. The antimuscarinic actions of antihistamine provides a drying effect on the nasal mucosa. It diminishes vestibular stimulation and depress labyrinthine function. An action on the medullary chemoreceptive trigger zone may also be involved in the antiemetic effect.
Ammonium Chloride has irritant action on the gastric mucous membrane and may contribute expectorant action.
Pharmacokinetics: Diphenhydramine is readily absorbed from the GIT. It is metabolised in the liver and excreted mainly as metabolites in the urine. After an oral dose of 50 mg of Diphenhydramine HCl, plasma concentrations of 50 to 54 ng/ml are attained at 1 hour; at 2 hours, plasma concentration is 64 to 70 ng/ml. The plasma half-life after an oral dose is 13 to 21 hours. 98% is bound to plasma proteins. About 50% of an oral dose is metabolised in the liver before reaching the general circulation. Reactions include Ndeakylation and deamination. In the urine, up to 3% of a dose is excreted unchanged, up to 13% as basic amines and up to 65% as diphenylmethane metabolites. The major urinary metabolite appears to be diphenylmethoxyacetic acid in free or conjugated form.
Ammonium Chloride is rapidly absorbed from the GIT. The Ammonium is converted into urea in the liver. The anion thus is liberated into the blood stream and extracellular fluids causes a metabolic acidosis and decreases the pH of the urine. This is followed by transient diuresis.