The nurse is performing a medication history on a patient who reports taking lorazepam (Ativan) for the past 6 months to treat an anxiety disorder. The patient states that the medication is not working as well as previously. The nurse will

A) Increased calcium: Sympathetic activation typically does not cause a direct increase in calcium levels. Calcium levels are more influenced by factors like parathyroid hormone (PTH) and vitamin D, or conditions such as bone disease or renal issues. Although some stress responses can lead to changes in calcium metabolism, an increase in calcium is not a typical response to sympathetic activation.

B) Decreased sodium: While sodium imbalances can occur in various conditions, the sympathetic nervous system does not directly cause a decrease in sodium. The body's handling of sodium is more influenced by factors like kidney function and the renin-angiotensin-aldosterone system. Stress-related changes in sodium levels are less likely to cause a significant decrease in sodium, making this an unlikely focus in monitoring.

C) Decreased potassium: During stress, the body releases catecholamines (like epinephrine) as part of the sympathetic nervous response, which stimulates the movement of potassium into cells. This can result in a transient decrease in serum potassium levels (hypokalemia). Monitoring for decreased potassium is important, as low potassium can lead to cardiac arrhythmias and muscle weakness, which are particularly concerning after surgery or trauma.

D) Increased chloride: Chloride is typically maintained in balance with sodium, and while it may shift in certain conditions, sympathetic activation does not directly lead to increased chloride levels. Most chloride imbalances are secondary to changes in sodium, acid-base disturbances, or kidney function. Therefore, an increase in chloride is less likely in this scenario.

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.