A patient presents with severe abdominal pain, vomiting, and distension, suspected of having a large bowel obstruction. Which nursing intervention is most appropriate to prioritize?

Rationale:

A. Weight fluctuations are not a common side effect of hydroxychloroquine. While chronic disease activity, dietary changes, or concurrent medications may influence a client’s weight, hydroxychloroquine itself is not known to cause significant weight gain or loss. Monitoring weight may still be part of overall health assessment in rheumatoid arthritis, but it is not a primary concern related to this medication.

B. High cholesterol is not directly associated with hydroxychloroquine use. Some disease-modifying anti-rheumatic drugs (DMARDs) or long-term corticosteroid therapy may affect lipid metabolism, but hydroxychloroquine generally does not alter cholesterol or lipid profiles. Cardiovascular risk assessment is important in rheumatoid arthritis, but hyperlipidemia is not a direct medication effect.

C. Eye problems are a well-recognized potential complication of hydroxychloroquine therapy. The drug can cause retinopathy, blurred vision, difficulty distinguishing colors, or changes in night vision, particularly with long-term use or higher cumulative doses. Retinal toxicity is irreversible if not detected early, so clients should undergo a baseline ophthalmologic examination before starting therapy and periodic follow-up exams (usually annually after 5 years of use, or sooner if risk factors are present). Nurses should educate clients to report any visual changes immediately, including blurred vision, difficulty reading, or changes in peripheral vision.

D. Development of ulcers is not a typical side effect of hydroxychloroquine. Gastrointestinal upset such as nausea, abdominal discomfort, or diarrhea may occur, but these are generally mild and manageable. Peptic or gastric ulcers are not directly related to hydroxychloroquine therapy.

Rationale:

A. Carafate (sucralfate) does not neutralize gastric acid. Unlike antacids, it does not chemically alter the pH of the stomach. While antacids temporarily reduce acid and provide symptomatic relief, sucralfate’s action is protective rather than neutralizing, focusing on shielding the ulcer from the harmful effects of acid, pepsin, and bile salts.

B. Carafate does not enhance gastric emptying or affect gastrointestinal motility. Prokinetic agents, such as metoclopramide, are used to increase gastric emptying and prevent reflux, but sucralfate’s mechanism is local mucosal protection, not altering the rate at which food or secretions move through the GI tract.

C. Carafate does not inhibit proton pumps or reduce gastric acid production systemically. Proton pump inhibitors (PPIs), like omeprazole, block the hydrogen-potassium ATPase enzyme in gastric parietal cells to suppress acid secretion. Sucralfate’s mechanism is mechanical and local, forming a protective barrier over the ulcer site rather than decreasing acid production.

D. Sucralfate forms a protective barrier over the ulcer site, binding to exposed proteins in the ulcer base to create a viscous, adhesive coating. This protective layer shields the ulcer from gastric acid, digestive enzymes, and bile salts, allowing the mucosal tissue to heal naturally while reducing pain and irritation. This barrier remains intact for several hours, making timing of administration important.