The mental health nursing instructor is talking with the class about depression. what deficiency does the instructor explain will result in depression?

A) Celecoxib (Celebrex):
Celecoxib is a selective COX-2 inhibitor that targets the cyclooxygenase-2 enzyme, which is primarily responsible for inflammation, pain, and fever. COX-2 inhibitors tend to cause less gastrointestinal irritation compared to nonselective NSAIDs like aspirin, which block both COX-1 and COX-2 enzymes. Because aspirin is causing gastrointestinal upset, switching to Celecoxib, which is less likely to irritate the stomach lining, may be an appropriate option to prevent myocardial infarction while minimizing gastrointestinal discomfort.

B) Enteric-coated aspirin:
Enteric-coated aspirin is designed to dissolve in the small intestine rather than the stomach, which may reduce some gastrointestinal irritation. However, it does not eliminate the risk entirely, and it still functions as a COX-1 inhibitor. If the patient is already experiencing gastrointestinal upset, simply switching to enteric-coated aspirin may not be sufficient to alleviate the discomfort, and other options should be considered.

C) Nabumetone (Relafen):
Nabumetone is a nonsteroidal anti-inflammatory drug (NSAID) with some COX-2 selectivity. While it may cause less gastrointestinal upset than non-selective NSAIDs like aspirin, it is still an NSAID and carries a risk of gastrointestinal side effects, especially with prolonged use.
D) A COX-2 inhibitor:
While COX-2 inhibitors, including Celecoxib, are typically effective in reducing inflammation and pain with fewer gastrointestinal side effects than traditional NSAIDs, the term "a COX-2 inhibitor" could refer to various drugs, and Celecoxib (Celebrex) is the most commonly used.

A) Acts directly on alpha-adrenergic receptor sites: Ephedrine does not act exclusively or directly on alpha-adrenergic receptors. While it can have some alpha-adrenergic effects, its primary mechanism is through the release of norepinephrine, which then activates both alpha and beta receptors. Therefore, this option is not entirely accurate for describing ephedrine's mode of action.

B) Stimulates the release of norepinephrine: Ephedrine primarily works by stimulating the release of norepinephrine from nerve terminals. The released norepinephrine then acts on both alpha and beta adrenergic receptors, leading to vasoconstriction (via alpha receptors) and increased heart rate and force of contraction (via beta receptors). This dual action helps raise blood pressure and improve cardiac output, making this the most accurate description of ephedrine's mechanism of action.

C) Acts directly on beta-adrenergic receptor sites: Although ephedrine does have beta-adrenergic effects (increasing heart rate and contractility), its primary mechanism is the indirect release of norepinephrine. It does not act directly on beta-receptors to the same extent as medications like isoproterenol. Therefore, while it does have beta-receptor activity, the main action is through norepinephrine release.

D) Stimulates the release of dopamine: Ephedrine does not primarily stimulate dopamine release. Dopamine release is more associated with drugs like levodopa or certain dopaminergic agents used in conditions like Parkinson’s disease. Ephedrine primarily affects norepinephrine and, to a lesser extent, acts on dopamine receptors, but it is not primarily a dopamine-releasing agent.