Pseudoephedrine HCl, Triprolidine HCl, Codeine phosphate
Indications
Pseudoephedrine HCl, Triprolidine HCl, Codeine phosphate is used for:
PSEUDOEPHEDRINE
For the treatment of nasal congestion, sinus congestion, eustachian tube congestion, and vasomotor rhinitis, and as an adjunct to other agents in the optimum treatment of allergic rhinitis, croup, sinusitis, otitis media, and tracheobronchitis. Also used as first-line therapy of priapism
TRIPROLIDINE
For the symptomatic relief of seasonal or perennial allergic rhinitis or nonallergic rhinitis; allergic conjunctivitis; and mild, uncomplicated allergic skin manifestations of urticaria and angioedema. Also used in combination with other agents for the symptomatic relief of symptoms associated with the common cold
CODEINE
For treatment and management of pain (systemic). It is also used as an antidiarrheal and as a cough suppressant
For the treatment of nasal congestion, sinus congestion, eustachian tube congestion, and vasomotor rhinitis, and as an adjunct to other agents in the optimum treatment of allergic rhinitis, croup, sinusitis, otitis media, and tracheobronchitis. Also used as first-line therapy of priapism
TRIPROLIDINE
For the symptomatic relief of seasonal or perennial allergic rhinitis or nonallergic rhinitis; allergic conjunctivitis; and mild, uncomplicated allergic skin manifestations of urticaria and angioedema. Also used in combination with other agents for the symptomatic relief of symptoms associated with the common cold
CODEINE
For treatment and management of pain (systemic). It is also used as an antidiarrheal and as a cough suppressant
Adult Dose
Child Dose
Renal Dose
Administration
Contra Indications
Precautions
Pregnancy-Lactation
Interactions
Adverse Effects
Side effects of Pseudoephedrine HCl, Triprolidine HCl, Codeine phosphate :
Mechanism of Action
PSEUDOEPHEDRINE
Pseudoephedrine acts directly on both alpha- and, to a lesser degree, beta-adrenergic receptors. Through direct action on alpha-adrenergic receptors in the mucosa of the respiratory tract, pseudoephedrine produces vasoconstriction. Pseudoephedrine relaxes bronchial smooth muscle by stimulating beta2-adrenergic receptors. Like ephedrine, pseudoephedrine releasing norepinephrine from its storage sites, an indirect effect. This is its main and direct mechanism of action. The displaced noradrenaline is released into the neuronal synapse where it is free to activate the postsynaptic adrenergic receptors
TRIPROLIDINE
Triprolidine binds to the histamine h1 receptor. This blocks the action of endogenous histamine, which subsequently leads to temporary relief of the negative symptoms brought on by histamine
CODEINE
Opiate receptors are coupled with g-protein receptors and function as both positive and negative regulators of synaptic transmission via g-proteins that activate effector proteins. Binding of the opiate stimulates the exchange of gtp for gdp on the g-protein complex. As the effector system is adenylate cyclase and camp located at the inner surface of the plasma membrane, opioids decrease intracellular camp by inhibiting adenylate cyclase. Subsequently, the release of nociceptive neurotransmitters such as substance p, gaba, dopamine, acetylcholine and noradrenaline is inhibited. Opioids also inhibit the release of vasopressin, somatostatin, insulin and glucagon. Codeine's analgesic activity is, most likely, due to its conversion to morphine. Opioids close n-type voltage-operated calcium channels (op2-receptor agonist) and open calcium-dependent inwardly rectifying potassium channels (op3 and op1 receptor agonist). This results in hyperpolarization and reduced neuronal excitability
Pseudoephedrine acts directly on both alpha- and, to a lesser degree, beta-adrenergic receptors. Through direct action on alpha-adrenergic receptors in the mucosa of the respiratory tract, pseudoephedrine produces vasoconstriction. Pseudoephedrine relaxes bronchial smooth muscle by stimulating beta2-adrenergic receptors. Like ephedrine, pseudoephedrine releasing norepinephrine from its storage sites, an indirect effect. This is its main and direct mechanism of action. The displaced noradrenaline is released into the neuronal synapse where it is free to activate the postsynaptic adrenergic receptors
TRIPROLIDINE
Triprolidine binds to the histamine h1 receptor. This blocks the action of endogenous histamine, which subsequently leads to temporary relief of the negative symptoms brought on by histamine
CODEINE
Opiate receptors are coupled with g-protein receptors and function as both positive and negative regulators of synaptic transmission via g-proteins that activate effector proteins. Binding of the opiate stimulates the exchange of gtp for gdp on the g-protein complex. As the effector system is adenylate cyclase and camp located at the inner surface of the plasma membrane, opioids decrease intracellular camp by inhibiting adenylate cyclase. Subsequently, the release of nociceptive neurotransmitters such as substance p, gaba, dopamine, acetylcholine and noradrenaline is inhibited. Opioids also inhibit the release of vasopressin, somatostatin, insulin and glucagon. Codeine's analgesic activity is, most likely, due to its conversion to morphine. Opioids close n-type voltage-operated calcium channels (op2-receptor agonist) and open calcium-dependent inwardly rectifying potassium channels (op3 and op1 receptor agonist). This results in hyperpolarization and reduced neuronal excitability