Ammonium Chloride, Carbinoxamine maleate, Ephedrine HCl, Menthol
Indications
Ammonium Chloride, Carbinoxamine maleate, Ephedrine HCl, Menthol is used for:
AMMONIUM CHLORIDE
Ammonium chloride is primarily indicated in conditions like cough, metabolic alkalosis, urinary retention, urinary retention
CARBINOXAMINE
For symptomatic relief of seasonal and perennial allergic rhinitis and vasomotor rhinitis, as well as allergic conjunctivitis caused by foods and inhaled allergens. Also for the relief of allergic reactions to blood or plasma, and the symptomatic management of mild, uncomplicated allergic skin manifestations of urticaria and angioedema
EPHEDRINE
Ephedrine commonly used as a stimulant, appetite suppressant, concentration aid, decongestant, and to treat hypotension associated with anaesthesia
Ammonium chloride is primarily indicated in conditions like cough, metabolic alkalosis, urinary retention, urinary retention
CARBINOXAMINE
For symptomatic relief of seasonal and perennial allergic rhinitis and vasomotor rhinitis, as well as allergic conjunctivitis caused by foods and inhaled allergens. Also for the relief of allergic reactions to blood or plasma, and the symptomatic management of mild, uncomplicated allergic skin manifestations of urticaria and angioedema
EPHEDRINE
Ephedrine commonly used as a stimulant, appetite suppressant, concentration aid, decongestant, and to treat hypotension associated with anaesthesia
Adult Dose
Child Dose
Renal Dose
Administration
Contra Indications
Precautions
Pregnancy-Lactation
Interactions
Adverse Effects
Side effects of Ammonium Chloride, Carbinoxamine maleate, Ephedrine HCl, Menthol :
Mechanism of Action
AMMONIUM CHLORIDE
Its expectorant action is caused by irritative action on the bronchial mucosa, which causes the production of excess respiratory tract fluid, which presumably is easier to cough up
CARBINOXAMINE
Carbinoxamine competes with free histamine for binding at ha-receptor sites. This antagonizes the effects of histamine on ha-receptors, leading to a reduction of the negative symptoms brought on by histamine ha-receptor binding. Carbinoxamine's anticholinergic action appears to be due to a central antimuscarinic effect, which also may be responsible for its antiemetic effects, although the exact mechanism is unknown
EPHEDRINE
Ephedrine is a sympathomimetic amine - that is, its principal mechanism of action relies on its direct and indirect actions on the adrenergic receptor system, which is part of the sympathetic nervous system. Ephedrine increases post-synaptic noradrenergic receptor activity by (weakly) directly activating post-synaptic a-receptors and >-receptors, but the bulk of its effect comes from the pre-synaptic neuron being unable to distinguish between real adrenaline or noradrenaline from ephedrine. The ephedrine, mixed with noradrenaline, is transported through the noradrenaline reuptake complex and packaged (along with real noradrenaline) into vesicles that reside at the terminal button of a nerve cell. Ephedrine's action as an agonist at most major noradrenaline receptors and its ability to increase the release of both dopamine and to a lesser extent, serotonin by the same mechanism is presumed to have a major role in its mechanism of action
Its expectorant action is caused by irritative action on the bronchial mucosa, which causes the production of excess respiratory tract fluid, which presumably is easier to cough up
CARBINOXAMINE
Carbinoxamine competes with free histamine for binding at ha-receptor sites. This antagonizes the effects of histamine on ha-receptors, leading to a reduction of the negative symptoms brought on by histamine ha-receptor binding. Carbinoxamine's anticholinergic action appears to be due to a central antimuscarinic effect, which also may be responsible for its antiemetic effects, although the exact mechanism is unknown
EPHEDRINE
Ephedrine is a sympathomimetic amine - that is, its principal mechanism of action relies on its direct and indirect actions on the adrenergic receptor system, which is part of the sympathetic nervous system. Ephedrine increases post-synaptic noradrenergic receptor activity by (weakly) directly activating post-synaptic a-receptors and >-receptors, but the bulk of its effect comes from the pre-synaptic neuron being unable to distinguish between real adrenaline or noradrenaline from ephedrine. The ephedrine, mixed with noradrenaline, is transported through the noradrenaline reuptake complex and packaged (along with real noradrenaline) into vesicles that reside at the terminal button of a nerve cell. Ephedrine's action as an agonist at most major noradrenaline receptors and its ability to increase the release of both dopamine and to a lesser extent, serotonin by the same mechanism is presumed to have a major role in its mechanism of action