A patient with diabetes is starting on insulin therapy.
Which type of insulin will the nurse discuss using for mealtime coverage?

Choice A rationale

Biologic response modifiers are primarily used for autoimmune diseases like rheumatoid arthritis due to their ability to target specific components of the immune system. They are not standard for osteoarthritis, as OA is a degenerative joint disease without a significant autoimmune component. These treatments do not address the inflammation or pain related to OA effectively.

Choice B rationale

Opiates are used for severe, short-term pain management but carry risks such as addiction and tolerance. They do not address the underlying inflammation in osteoarthritis. Long-term use is generally avoided for OA as safer options like NSAIDs are more effective for managing chronic symptoms without these risks.

Choice C rationale

Disease-Modifying Antirheumatic Drugs (DMARDs) are more effective for autoimmune conditions like rheumatoid arthritis, not osteoarthritis. OA lacks the autoimmune pathology targeted by DMARDs, making them unsuitable for managing OA symptoms like pain or stiffness.

Choice D rationale

NSAIDs are the first-line therapy for OA as they effectively reduce both inflammation and pain associated with the condition. By inhibiting cyclooxygenase enzymes, NSAIDs decrease prostaglandin production, leading to improved joint function and symptom control, making them the most common choice for OA symptom management.

Choice A rationale

While alcohol is a known irritant to the gastric lining, it is not the primary cause of peptic ulcer disease. Excessive alcohol consumption contributes to mucosal damage but lacks the direct causative action of Helicobacter pylori, which colonizes the stomach lining and interferes with protective mechanisms, leading to ulcer formation. Alcohol merely exacerbates existing risk factors rather than initiating disease.

Choice B rationale

Helicobacter pylori is the most common cause of peptic ulcer disease globally. Its mechanism involves producing urease, neutralizing stomach acid and enabling bacterial survival. It induces inflammation and mucosal damage, compromising the stomach's protective lining. Persistent infection leads to ulcer formation. This bacterial colonization is implicated in up to 90% of duodenal ulcers, making it the key pathogenic factor in PUD.

Choice C rationale

Smoking is a risk factor for peptic ulcer disease but functions more as an aggravating agent than the primary cause. Tobacco use increases gastric acid secretion and decreases bicarbonate production, weakening mucosal defenses. It also reduces the efficacy of Helicobacter pylori eradication therapy, prolonging ulcer disease. However, it does not directly induce the condition independently, highlighting its secondary role in PUD pathology.

Choice D rationale

Stress is associated with peptic ulcer disease but is not a primary causative factor. Psychological stress can lead to hypersecretion of gastric acid, aggravating mucosal vulnerability in susceptible individuals. However, its role is predominantly indirect, amplifying existing risk factors like Helicobacter pylori infection. Stress-induced ulcers are typically seen in critical illnesses or severe physiological stress conditions, differing from PUD pathogenesis.