A patient is taking aspirin to help prevent myocardial infarction and is experiencing moderate gastrointestinal upset. The nurse will contact the patient’s provider to discuss changing from aspirin to which drug?
Celecoxib (Celebrex)
Enteric-coated aspirin
Nabumetone (Relafen)
A COX-2 inhibitor
The Correct Answer is A
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.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is A
Explanation
A) Norepinephrine, dopamine, and serotonin:
Depression has been strongly linked to deficiencies in certain neurotransmitters in the brain, specifically norepinephrine, dopamine, and serotonin. These neurotransmitters play significant roles in regulating mood, emotions, and behavior. When their levels are low, individuals may experience symptoms of depression, such as sadness, low energy, anhedonia (inability to feel pleasure), and difficulty concentrating. Antidepressant medications often work by increasing the availability of these neurotransmitters in the brain.
B) Epinephrine, Norepinephrine, and Acetylcholine:
While norepinephrine plays a key role in depression, epinephrine and acetylcholine are not typically highlighted as the primary neurotransmitters involved in depression. Epinephrine (also known as adrenaline) is more associated with the body’s stress response and fight-or-flight reaction. Acetylcholine is involved in memory and learning processes, but it is not the primary neurotransmitter related to depression.
C) Acetylcholine, gamma-aminobutyric acid, and serotonin:
Acetylcholine and gamma-aminobutyric acid (GABA) are involved in many brain functions, but they are not the primary neurotransmitters linked to depression. While GABA may play a role in mood regulation, it is not typically associated with depression in the same way that serotonin, norepinephrine, and dopamine are. Serotonin is the exception in this answer
D) Gamma-aminobutyric acid, dopamine, and epinephrine:
Although dopamine is involved in depression, gamma-aminobutyric acid (GABA) and epinephrine are not the key neurotransmitters associated with the pathophysiology of depression. Epinephrine primarily affects the stress response, and while GABA does influence mood and anxiety, it is not the main neurotransmitter linked to depression itself.
Correct Answer is C
Explanation
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.
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