The nurse administers pseudoephedrine to a patient who is experiencing severe bronchospasm.
Which of these is an adverse reaction from the pseudoephedrine?

Choice A rationale

Pseudoephedrine is a sympathomimetic drug that acts primarily as an alpha and beta agonist, stimulating the central nervous system (CNS). This stimulation usually leads to wakefulness, nervousness, and insomnia, rather than excessive sleepiness, which is a CNS depressant effect. Drowsiness can occur but is less common than CNS stimulation effects, as the drug promotes adrenergic activity.

Choice B rationale

Pseudoephedrine stimulates beta-1 adrenergic receptors in the heart, leading to an increase in heart rate (tachycardia) and force of contraction. This enhanced cardiac activity can be perceived by the patient as palpitations (irregular or rapid heartbeat). The normal adult heart rate is 60 to 100 beats per minute, and this drug can push it toward the upper limit or beyond.

Choice C rationale

Pseudoephedrine acts as a vasoconstrictor by stimulating alpha-1 adrenergic receptors on blood vessels, leading to an increase in systemic vascular resistance. This increase in resistance and cardiac stimulation typically results in a rise in blood pressure (hypertension), not hypotension. The normal adult blood pressure is less than 120/80 mm Hg.

Choice D rationale

Pseudoephedrine is generally a bronchodilator due to its beta-2 adrenergic receptor stimulation, which relaxes bronchial smooth muscles and improves (not worsens) respiration. Shallow respirations are a sign of respiratory depression or distress, which is not a common adverse effect of this sympathomimetic, which tends to increase the respiratory drive.

Choice A rationale

Celecoxib is a highly selective inhibitor of the COX-2 enzyme, which is primarily induced at sites of inflammation and mediates the synthesis of pro-inflammatory prostaglandins. By specifically blocking COX-2, Celecoxib aims to reduce inflammation and pain with a lower risk of gastrointestinal adverse effects compared to non-selective nonsteroidal anti-inflammatory drugs (NSAIDs) that also inhibit constitutive COX-1.

Choice B rationale

COX-2 selective inhibitors, such as celecoxib, are considered second-generation NSAIDs, developed after the initial non-selective NSAIDs (like aspirin, ibuprofen), which are classified as first-generation. This newer class was designed to minimize the adverse effects, particularly gastrointestinal, associated with the non-selective inhibition of the constitutive COX-1 enzyme.

Choice C rationale

The primary advantage and design feature of COX-2 selective inhibitors are their reduced risk of gastrointestinal adverse effects, including peptic ulcers, compared to non-selective NSAIDs. Non-selective NSAIDs inhibit COX-1, which produces protective prostaglandins necessary for maintaining the gastric mucosal barrier, making their inhibition the main cause of ulcers.

Choice D rationale

COX-2 selective inhibitors work by reducing inflammation. The COX-2 enzyme catalyzes the conversion of arachidonic acid into pro-inflammatory prostaglandins. By inhibiting this enzyme, these drugs decrease the synthesis of these inflammatory mediators, thereby lessening the signs and symptoms of inflammation, pain, and fever.