Carbinoxamine, Dextromethorphan, Phenylephrine, Sodium Citrate
Indications
Carbinoxamine, Dextromethorphan, Phenylephrine, Sodium Citrate is used for:
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
DEXTROMETHORPHAN
For treatment and relief of dry cough
PHENYLEPHRINE
Phenylephrine is mainly used to treat nasal congestion, but may also be useful in treating hypotension and shock, hypotension during spinal anaesthesia, prolongation of spinal anaesthesia, paroxysmal supraventricular tachycardia, symptomatic relief of external or internal hemorrhoids, and to increase blood pressure as an aid in the diagnosis of heart murmurs
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
DEXTROMETHORPHAN
For treatment and relief of dry cough
PHENYLEPHRINE
Phenylephrine is mainly used to treat nasal congestion, but may also be useful in treating hypotension and shock, hypotension during spinal anaesthesia, prolongation of spinal anaesthesia, paroxysmal supraventricular tachycardia, symptomatic relief of external or internal hemorrhoids, and to increase blood pressure as an aid in the diagnosis of heart murmurs
Adult Dose
Child Dose
Renal Dose
Administration
Contra Indications
Precautions
Pregnancy-Lactation
Interactions
Adverse Effects
Side effects of Carbinoxamine, Dextromethorphan, Phenylephrine, Sodium Citrate :
Mechanism of Action
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
DEXTROMETHORPHAN
Dextromethorphan is an opioid-like drug that binds to and acts as antagonist to the nmda glutamatergic receptor, it is an agonist to the opioid sigma 1 and sigma 2 receptors, it is also an alpha3/beta4 nicotinic receptor antagonist and targets the serotonin reuptake pump. Dextromethorphan is rapidly absorbed from the gastrointestinal tract, where it enters the bloodstream and crosses the blood-brain barrier. The first-pass through the hepatic portal vein results in some of the drug being metabolized into an active metabolite of dextromethorphan, dextrorphan, the 3-hydroxy derivative of dextromethorphan
PHENYLEPHRINE
In general, α1-adrenergic receptors mediate contraction and hypertrophic growth of smooth muscle cells. α1-receptors are 7-transmembrane domain receptors coupled to g proteins, gq/11. Three α1-receptor subtypes, which share approximately 75% homology in their transmembrane domains, have been identified: α1a (chromosome 8), α1b (chromosome 5), and α1d (chromosome 20). Phenylephrine appears to act similarly on all three receptor subtypes. All three receptor subtypes appear to be involved in maintaining vascular tone. The α1a-receptor maintains basal vascular tone while the α1b-receptor mediates the vasocontrictory effects of exogenous α1-agonists. Activation of the α1-receptor activates gq-proteins, which results in intracellular stimulation of phospholipases c, a2, and d. This results in mobilization of ca2+ from intracellular stores, activation of mitogen-activated kinase and pi3 kinase pathways and subsequent vasoconstriction. Phenylephrine produces its local and systemic actions by acting on α1-adrenergic receptors peripheral vascular smooth muscle. Stimulation of the α1-adrenergic receptors results in contraction arteriolar smooth muscle in the periphery. Phenylephrine decreases nasal congestion by acting on α1-adrenergic receptors in the arterioles of the nasal mucosa to produce constriction; this leads to decreased edema and increased drainage of the sinus cavities
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
DEXTROMETHORPHAN
Dextromethorphan is an opioid-like drug that binds to and acts as antagonist to the nmda glutamatergic receptor, it is an agonist to the opioid sigma 1 and sigma 2 receptors, it is also an alpha3/beta4 nicotinic receptor antagonist and targets the serotonin reuptake pump. Dextromethorphan is rapidly absorbed from the gastrointestinal tract, where it enters the bloodstream and crosses the blood-brain barrier. The first-pass through the hepatic portal vein results in some of the drug being metabolized into an active metabolite of dextromethorphan, dextrorphan, the 3-hydroxy derivative of dextromethorphan
PHENYLEPHRINE
In general, α1-adrenergic receptors mediate contraction and hypertrophic growth of smooth muscle cells. α1-receptors are 7-transmembrane domain receptors coupled to g proteins, gq/11. Three α1-receptor subtypes, which share approximately 75% homology in their transmembrane domains, have been identified: α1a (chromosome 8), α1b (chromosome 5), and α1d (chromosome 20). Phenylephrine appears to act similarly on all three receptor subtypes. All three receptor subtypes appear to be involved in maintaining vascular tone. The α1a-receptor maintains basal vascular tone while the α1b-receptor mediates the vasocontrictory effects of exogenous α1-agonists. Activation of the α1-receptor activates gq-proteins, which results in intracellular stimulation of phospholipases c, a2, and d. This results in mobilization of ca2+ from intracellular stores, activation of mitogen-activated kinase and pi3 kinase pathways and subsequent vasoconstriction. Phenylephrine produces its local and systemic actions by acting on α1-adrenergic receptors peripheral vascular smooth muscle. Stimulation of the α1-adrenergic receptors results in contraction arteriolar smooth muscle in the periphery. Phenylephrine decreases nasal congestion by acting on α1-adrenergic receptors in the arterioles of the nasal mucosa to produce constriction; this leads to decreased edema and increased drainage of the sinus cavities