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Product Name
:
ACT-SMART (tab)
Chemical Name
:
Triprolidine HCl Pseudoephedrine HCl
Therapeutic Category
:
Respiratory tract drugs
Pharmacologic Category
:
Alkylamine Derivative - Alpha/Beta Agonist • Decongestant • Histamine H1 Antagonist -Histamine H1 Antagonist, First Generation
Pharmaceutical Form
:
Tablets
Composition
:
Triprolidine HCl 2.5mg
Pseudoephedrine HCl 60mg
Pregnancy
Monitoring Parameters
Dosing
 
Dosing: Adult
Cold, allergy symptoms: Oral
Tablet : One tablet every 4-6 hours; do not exceed 4 doses in 24 hours
Dosing: Pediatric
Cold, allergy symptoms: Oral
Tablet :
Children 6-12 years:1/2 tablet every 4-6 hours; do not exceed 4 doses in 24 hours
Children >12 years: Refer to adult dosing.
Dosing: Geriatric
Refer to adult dosing.
Use
 
Temporary relief of nasal congestion, decongest sinus openings, running nose, sneezing, itching of nose or throat and itchy, watery eyes due to common cold, hay fever, or other upper respiratory allergies
Adverse Reactions
 
Frequency not defined.
Cardiovascular: Tachycardia
Central nervous system: Dizziness, drowsiness, fatigue, headache, insomnia, nervousness, transient stimulation
Gastrointestinal: Abdominal pain, appetite increase, diarrhea, nausea, weight gain, xerostomia
Genitourinary: Dysuria
Neuromuscular & skeletal: Arthralgia, weakness
Respiratory: Pharyngitis, thickening of bronchial secretions
Miscellaneous: Diaphoresis Adverse Reactions
Contraindications
 
Hypersensitivity to pseudoephedrine or any component of the formulation; MAO therapy, severe hypertension, severe coronary artery disease
Warnings / Precautions Drug
 
Concerns related to adverse effects:

CNS depression: May cause CNS depression, which may impair physical or mental abilities; patients must be cautioned about performing tasks which require mental alertness (eg, operating machinery or driving).

Disease-related concerns:

- Asthma: Use with caution in patients with a history of asthma.

- Cardiovascular disease: Use with caution in patients with cardiovascular disease (including hypertension and ischemic heart disease); contraindicated with severe disease.

- Diabetes: Use with caution in patients with diabetes mellitus.

- Increased intraocular pressure/glaucoma: Use with caution in patients with increased intraocular pressure or glaucoma.

- Prostatic hyperplasia/urinary obstruction: Use with caution in patients with prostatic hyperplasia and/or GU obstruction.

- Thyroid dysfunction: Use with caution in patients with thyroid dysfunction.

Concurrent drug therapy issues:

- Sedatives: Effects may be potentiated when used with other sedative drugs or ethanol.

Special populations:

- Elderly: Use with caution in the elderly; may be more sensitive to adverse effects.

- Pediatrics: Not for OTC use in children <6 years of age.

Other warnings/precautions:

- Self-medication (OTC use): When used for self medication (OTC), notify healthcare provider if symptoms do not improve within 7 days or are accompanied by fever. Discontinue and contact healthcare provider if nervousness, dizziness or sleeplessness occur.

Metabolism/Transport Effects

Triprolidine: Inhibits CYP2D6 (weak)
Interactions
 
Acetylcholinesterase Inhibitors (Central): Anticholinergics may diminish the therapeutic effect of Acetylcholinesterase Inhibitors (Central). Acetylcholinesterase Inhibitors (Central) may diminish the therapeutic effect of Anticholinergics. If the anticholinergic action is a side effect of the agent, the result may be beneficial. Risk C: Monitor therapy

Alcohol (Ethyl): CNS Depressants may enhance the CNS depressant effect of Alcohol (Ethyl). Risk C: Monitor therapy

Amphetamines: May diminish the sedative effect of Antihistamines. Risk C: Monitor therapy

Antacids: May decrease the excretion of Alpha-/Beta-Agonists. Exceptions: Aluminum Hydroxide. Risk C: Monitor therapy

Anticholinergics: May enhance the adverse/toxic effect of other Anticholinergics. Exceptions: Levocabastine (Nasal); Paliperidone. Risk C: Monitor therapy

Atomoxetine: May enhance the hypertensive effect of Sympathomimetics. Atomoxetine may enhance the tachycardic effect of Sympathomimetics. Risk C: Monitor therapy

Benzylpenicilloyl Polylysine: Antihistamines may diminish the diagnostic effect of Benzylpenicilloyl Polylysine. Management: Suspend systemic H1 antagonists for benzylpenicilloyl-polylysine skin testing and delay testing until systemic antihistaminic effects have dissipated. A histamine skin test may be used to assess persistent antihistaminic effects. Risk D: Consider therapy modification

Benzylpenicilloyl Polylysine: Alpha-/Beta-Agonists may diminish the diagnostic effect of Benzylpenicilloyl Polylysine. Management: Consider use of a histamine skin test as a positive control to assess a patient's ability to mount a wheal and flare response. Risk D: Consider therapy modification

Betahistine: Antihistamines may diminish the therapeutic effect of Betahistine. Risk C: Monitor therapy

Bromocriptine: Alpha-/Beta-Agonists may enhance the adverse/toxic effect of Bromocriptine. Including increased blood pressure, ventricular arrhythmias, and seizure. Risk C: Monitor therapy

Cannabinoids: May enhance the tachycardic effect of Sympathomimetics. Risk C: Monitor therapy

Carbonic Anhydrase Inhibitors: May decrease the excretion of Alpha-/Beta-Agonists. Exceptions: Brinzolamide; Dorzolamide. Risk C: Monitor therapy

CNS Depressants: May enhance the adverse/toxic effect of other CNS Depressants. Exceptions: Levocabastine (Nasal). Risk C: Monitor therapy

Droperidol: May enhance the CNS depressant effect of CNS Depressants. Management: Consider dose reductions of droperidol or of other CNS agents (e.g., opioids, barbiturates) with concomitant use. Risk D: Consider therapy modification

FentaNYL: Alpha-/Beta-Agonists (Indirect-Acting) may decrease the serum concentration of FentaNYL. Specifically, fentanyl nasal spray serum concentrations may decrease and onset of effect may be delayed. Risk C: Monitor therapy

HydrOXYzine: May enhance the CNS depressant effect of CNS Depressants. Risk C: Monitor therapy

Iobenguane I 123: Sympathomimetics may diminish the therapeutic effect of Iobenguane I 123. Risk X: Avoid combination

MAO Inhibitors: May enhance the hypertensive effect of Alpha-/Beta-Agonists (Indirect-Acting). Risk X: Avoid combination

Pramlintide: May enhance the anticholinergic effect of Anticholinergics. These effects are specific to the GI tract. Risk D: Consider therapy modification

Selective Serotonin Reuptake Inhibitors: CNS Depressants may enhance the adverse/toxic effect of Selective Serotonin Reuptake Inhibitors. Specifically, the risk of psychomotor impairment may be enhanced. Risk C: Monitor therapy

Serotonin/Norepinephrine Reuptake Inhibitors: May enhance the tachycardic effect of Alpha-/Beta-Agonists. Serotonin/Norepinephrine Reuptake Inhibitors may enhance the vasopressor effect of Alpha-/Beta-Agonists. Risk D: Consider therapy modification

Spironolactone: May diminish the vasoconstricting effect of Alpha-/Beta-Agonists. Risk C: Monitor therapy

Sympathomimetics: May enhance the adverse/toxic effect of other Sympathomimetics. Risk C: Monitor therapy
Lactation
 
C
Mechanism of Action
 
pseudoephedrine  : Directly stimulates alpha-adrenergic receptors of respiratory mucosa causing vasoconstriction; directly stimulates beta-adrenergic receptors causing bronchial relaxation, increased heart rate and contractility

Triprolidine is a member of the propylamine (alkylamine) chemical class of H1-antagonist antihistamines. As such, it is considered to be relatively less sedating than traditional antihistamines of the ethanolamine, phenothiazine, and ethylenediamine classes of antihistamines. Triprolidine has a shorter half-life and duration of action than most of the other alkylamine antihistamines. Like all H1-antagonist antihistamines, the Mechanism of Action of triprolidine is believed to involve competitive blockade of H1-receptor sites resulting in the inability of histamine to combine with its receptor sites and exert its usual effects on target cells. Antihistamines do not interrupt any effects of histamine which have already occurred. Therefore, these agents are used more successfully in the prevention rather than the treatment of histamine-induced reactions.
Pharmacodynamics / Kinetics
 
pseudoephedrine

Onset of action: Decongestant: Oral: 30 minutes (Chua 1989)

Peak effect: Decongestant: Oral: ~1-2 hours (Chua, 1989)

Duration: Immediate release tablet: 3-8 hours (Chua 1989)

Absorption: Rapid (Simons 1996)

Distribution: Children: ~2.5 L/kg (Simons 1996); Adults: 2.64-3.51 L/kg (Kanfer 1993)

Metabolism: Undergoes n-demethylation to norpseudoephedrine (active) (Chua 1989, Kanfer 1993); Hepatic (<1%) (Kanfer 1993)

Half-life elimination: Varies by urine pH and flow rate; alkaline urine decreases renal elimination of pseudoephedrine (Kanfer 1993)

Children: ~3 hours (urine pH ~6.5) (Simons 1996)

Adults: 9-16 hours (pH 8); 3-6 hours (pH 5) (Chua 1989)

Time to peak:

Children (immediate release) ~2 hours (Simons 1996)

Adults (immediate release): 1-3 hours (dose dependent) (Kanfer 1993)
Excretion: Urine (43% to 96% as unchanged drug, 1% to 6% as active norpseudoephedrine); dependent on urine pH and flow rate; alkaline urine decreases renal elimination of pseudoephedrine (Kanfer 1993)
 
   
 
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