ALCOSED SYRUP

Indications

• Nasal congestion
• Sinusitis affecting the maxillary antrum

Dosage

Children: For children aged 6-11 years, the recommended dose is 30 mg 3-4 times a day. For children aged 12-17 years, the dose is 60 mg 3-4 times a day. Caution is advised in children under 6 years.

Adults: The typical adult dose is 60 mg every 4-6 hours, not exceeding 240 mg per day.

Mechanism of action

Pseudoephedrine acts primarily as a selective agonist of alpha-adrenergic receptors, which causes vasoconstriction of the nasal mucosa. This leads to a decrease in mucosal edema and congestion. It may also have some beta-adrenergic activity, contributing to bronchodilation.

Pharmacodynamics

The pharmacodynamic effects of pseudoephedrine include reduced nasal congestion and increased airflow through the nasal passages. Its action is dose-dependent, with higher doses leading to more pronounced effects. Side effects may include increased heart rate, hypertension, and CNS stimulation such as anxiety and insomnia.

Pharmacokinetics

Pseudoephedrine is well absorbed from the gastrointestinal tract, with peak plasma concentrations occurring within 1-2 hours after oral administration. It is metabolized primarily in the liver and has a half-life of approximately 5-8 hours. The drug is excreted mainly in the urine, with a portion being unchanged.

Contra-indications

• Severe hypertension
• Severe renal impairment
• Severe hepatic impairment
• Hyperthyroidism
• Angle closure glaucoma
• Use in children under 6 years of age is not recommended due to safety concerns

Adverse effects

• Anxiety
• Headache
• Insomnia
• Nausea
• Dizziness
• Dry mouth
• Increased heart rate (tachycardia)
• Hypertension
• Palpitations
• Rebound congestion
• Irritability
• Tremors
• Hallucinations
• Dermatitis
• Muscle weakness
• Vomiting
• Piloerection

Interactions

• Monoamine oxidase inhibitors (MAOIs) may enhance the hypertensive effects
• Other sympathomimetics may increase the risk of cardiovascular effects
• Caution with antihypertensive medications as pseudoephedrine may counteract their effectiveness

Precautions

• Use with caution in individuals with cardiovascular disease
• Caution in patients with diabetes due to potential hyperglycemia
• Monitor patients with a history of psychiatric disorders as it may exacerbate symptoms
• Use with caution in patients with a history of seizures

Pregnancy

Manufacturer advises avoidance due to potential risks such as defective closure of the abdominal wall in newborns after first trimester exposure.

Breast-feeding

Present in breast milk; manufacturer advises avoidance due to the potential for irritability and disturbed sleep in infants.

Storage

Store in a cool, dry place, away from direct sunlight. Keep out of reach of children.

Formulations

• Oral solution (e.g., Sudafed Decongestant 30mg/5ml liquid)
• Nasal drops (e.g., Galpseud 0.5% drops)

Indications

• Allergic rhinitis (hay fever)
• Urticaria (hives)
• Allergic conjunctivitis
• Common cold symptoms

Dosage

Children: For children aged 6-12 years, the dose is typically 2 mg every 4 to 6 hours, not exceeding 12 mg per day. For children under

Adults: The usual adult dose for chlorpheniramine is 4 mg every 4 to 6 hours, not to exceed 24 mg per day.

Mechanism of action

Chlorpheniramine binds to the histamine H1 receptor, preventing endogenous histamine from exerting its effects. This leads to temporary relief from symptoms such as sneezing, pruritus, and increased vascular permeability associated with allergic reactions. The drug competes with histamine for H1-receptor sites on effector cells, thus antagonizing most of the pharmacological effects of histamine, including its actions on smooth muscle and vascular permeability.

Pharmacodynamics

In allergic reactions, allergens trigger the degranulation of mast cells and basophils, leading to the release of histamine. Chlorpheniramine, as an H1 antagonist, competes for receptor binding, effectively blocking histamine-induced effects, such as itching, vasodilation, and bronchoconstriction. This results in relief from symptoms like sneezing, watery eyes, and nasal discharge.

Pharmacokinetics

Chlorpheniramine is well absorbed from the gastrointestinal tract. It undergoes hepatic metabolism and its effects can last for several hours. The onset of action is typically observed within 1 to 2 hours following oral administration, with peak effects occurring around 2 to 6 hours. The drug is eliminated primarily through urine, with a half-life ranging from 12 to 15 hours, though this can vary based on individual factors.

Contra-indications

• Hypersensitivity to chlorpheniramine or any component of the formulation
• Acute asthma attacks
• Severe hypertension
• Narrow-angle glaucoma
• Prostatic hypertrophy

Adverse effects

• Drowsiness
• Dizziness
• Dry mouth
• Blurred vision
• Constipation
• Urinary retention
• Confusion
• Headache

Interactions

• Alcohol
• CNS depressants
• MAO inhibitors
• Anticholinergic agents
• Beta-blockers

Precautions

• Use with caution in patients with cardiovascular disease
• Caution in patients with liver or kidney impairment
• Avoid in elderly patients due to increased risk of sedation and anticholinergic effects
• May impair the ability to drive or operate machinery

Pregnancy

Chlorpheniramine should be used in pregnancy only if clearly needed. Consult medical professionals for guidance.

Breast-feeding

Chlorpheniramine is excreted in breast milk. Caution is advised when administering to nursing mothers.

Storage

Store at room temperature, away from moisture and heat. Keep out of reach of children.

Formulations

• Tablets
• Syrup
• Oral suspension

Indications

• Nasal congestion due to cold
• Allergic rhinitis
• Sinusitis
• Eustachian tube dysfunction

Dosage

Children: For children aged 6 to 12 years, the recommended dose is 30 mg every 6 hours, not exceeding 120 mg per day. For children aged 2 to 6 years

Adults: The typical adult dose is 60 mg every 4 to 6 hours, not exceeding 240 mg per day.

Mechanism of action

Pseudoephedrine acts mainly as an agonist of alpha adrenergic receptors and less strongly as an agonist of beta adrenergic receptors. The agonism produces vasoconstriction in the mucosa of the respiratory tract, leading to decreased nasal congestion. It also inhibits norepinephrine, dopamine, and serotonin transporters, which may contribute to its sympathomimetic effects such as increased arterial pressure and heart rate. Additionally, pseudoephedrine has anti-inflammatory actions through the inhibition of NF-kappa-B and other transcription factors.

Pharmacodynamics

Pseudoephedrine causes vasoconstriction resulting in a decongestant effect. Its sympathomimetic properties can lead to increased heart rate and blood pressure. The duration of action is typically short unless formulated as an extended-release product. Patients may experience central nervous system stimulation, which should be considered when prescribing.

Pharmacokinetics

Pseudoephedrine is well absorbed from the gastrointestinal tract, with peak plasma concentrations occurring approximately 1 to 2 hours after oral administration. The drug is metabolized in the liver, primarily by the cytochrome P450 system, and has a half-life of about 6 hours. It is excreted mainly through the kidneys, with about 55-70% of the dose eliminated unchanged in the urine.

Adverse effects

• Increased blood pressure
• Centrally mediated side effects such as insomnia
• Nervousness
• Dizziness
• Headache
• Dry mouth

Interactions

• pseudoephedrine + linezolid: Severe (increases risk of elevated blood pressure)
• volatile halogenated anesthetics + pseudoephedrine: Unknown (additive effect)

Precautions

• Use with caution in patients with hypertension
• Use with caution in patients with cardiovascular disease
• May exacerbate conditions like hyperthyroidism or diabetes

Pregnancy

Use only if clearly needed, as safety in pregnancy has not been established.

Breast-feeding

Use with caution; small amounts may pass into breast milk.

Storage

Store at room temperature, away from moisture and heat.

Formulations

• Oral tablets
• Extended-release oral tablets
• Liquid formulations

Mechanism of action

Chlorpheniramine 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. Antihistamines used in the treatment of allergy act by competing with histamine for H1-receptor sites on effector cells. They thereby prevent, but do not reverse, responses mediated by histamine alone. Antihistamines antagonize, in varying degrees, most of the pharmacological effects of histamine, including urticaria and pruritus. Also, the anticholinergic actions of most antihistamines provide a drying effect on the nasal mucosa. /Antihistamines/ H1 antagonists inhibit most responses of smooth muscle to histamine. Antagonism of the constrictor action of histamine on respiratory smooth muscle is easily shown in vivo and in vitro. /Histamine Antagonists: H1 Antagonists/ H1 antagonists strongly block the action of histamine that results in increased permeability and formation of edema and wheal. /Histamine Antagonists: H1 Antagonists/ Within the vascular tree, the H1 antagonists inhibit both the vasoconstrictor effects of histamine and, to a degree, the more rapid vasodilator effects that are mediated by H1 receptors on endothelial cells. Residual vasodilatation reflects the involvement of H2 receptors on smooth muscle and can be suppressed only by the concurrent administration of an H2 antagonist. Effects of the histamine antagonists on histamine induced changes in systemic blood pressure parallel these vascular effects. /Histamine Antagonists: H1 Antagonists/ Many of the H1 antagonists tend to inhibit responses to acetylcholine that are mediated by muscarinic receptors. These atropine like actions are sufficiently prominent in some of the drugs to be manifest during clinical usage ... . /Histamine Antagonists: H1 Antagonists/

Pharmacodynamics

In allergic reactions an allergen interacts with and cross-links surface IgE antibodies on mast cells and basophils. Once the mast cell-antibody-antigen complex is formed, a complex series of events occurs that eventually leads to cell-degranulation and the release of histamine (and other chemical mediators) from the mast cell or basophil. Once released, histamine can react with local or widespread tissues through histamine receptors. Histamine, acting on H₁-receptors, produces pruritis, vasodilatation, hypotension, flushing, headache, tachycardia, and bronchoconstriction. Histamine also increases vascular permeability and potentiates pain. Chlorpheniramine, is a histamine H1 antagonist (or more correctly, an inverse histamine agonist) of the alkylamine class. It competes with histamine for the normal H₁-receptor sites on effector cells of the gastrointestinal tract, blood vessels and respiratory tract. It provides effective, temporary relief of sneezing, watery and itchy eyes, and runny nose due to hay fever and other upper respiratory allergies.

Mechanism of action

Pseudoephedrine acts mainly as an agonist of alpha adrenergic receptors and less strongly as an agonist of beta adrenergic receptors. This agonism of adrenergic receptors produces vasoconstriction which is used as a decongestant and as a treatment of priapism. Pseudoephedrine is also an inhibitor of norepinephrine, dopamine, and serotonin transporters. The sympathomimetic effects of pseudoephedrine include an increase in mean arterial pressure, heart rate, and chronotropic response of the right atria. Pseudoephedrine is also a partial agonist of the anococcygeal muscle. Pseudoephedrine also inhibits NF-kappa-B, NFAT, and AP-1. THESE AGENTS /BRONCHODILATORS/ ACT ON BETA-2 RECEPTORS TO RELAX BRONCHIAL SMOOTH MUSCLE & PERIPHERAL VASCULATURE, APPARENTLY BY STIMULATING PRODN OF CYCLIC ADENOSINE-3.5-MONOPHOSPHATE (CAMP)... Pseudoephedrine acts on alpha-adrenergic receptors in the mucosa of the respiratory tract, producing vasoconstriction. The medication shrinks swollen nasal mucous membranes; reduces tissue hyperemia, edema, and nasal congestion; and increases nasal airway patency. Also, drainage of sinus secretions may be increased and obstructed eustachian ostia may be opened. The pharmacological properties of the ephedrine derivative pseudoephedrine were investigated at the nuclear level. Following intraperitoneal injection of Sprague Dawley rats with pseudoephedrine, Fos induction was measured in various brain areas by Western blots and immunocytochemistry. Pseudoephedrine induced Fos-like immunoreactivity in the nucleus accumbens and striatum in a time and concentration-dependent manner with maximal effect at 60 mg/kg 2 hr after injection. Immunocytochemical studies confirmed that the majority of the signal was detectable in the nucleus accumbens and striatum. Pre-injection with the D1 dopamine receptor antagonist SCH23390 partially and completely blocked pseudoephedrine-induced Fos-like immunoreactivity in the striatum and nucleus accumbens, respectively, suggesting that the action of pseudoephedrine is mediated via dopamine release and results in the activation of D1 dopamine receptors. With the exception of the higher doses required, the actions of pseudoephedrine were similar to those previously described for the psychostimulant amphetamine.

Pharmacodynamics

Pseudoephedrine causes vasoconstriction which leads to a decongestant effect. It has a short duration of action unless formulated as an extended release product. Patients should be counselled regarding the risk of central nervous system stimulation.