A nurse in a community clinic is caring for a client who has systemic lupus erythematosus (SLE). Which of the following statements by the client should the nurse determine is the priority?

Rationale:
A. "I am aware that my diabetes is caused by an autoimmune disorder.": Type 1 diabetes mellitus results from the immune system attacking the insulin-producing beta cells in the pancreas. This autoimmune destruction leads to a complete deficiency of insulin, making lifelong replacement necessary.

B. "I know that my diabetes developed slowly over several years.": Type 1 diabetes often has a rapid onset, especially in younger individuals. Symptoms such as polyuria, polydipsia, weight loss, and fatigue can appear suddenly over days or weeks, rather than gradually over several years.

C. "If I lose weight, I may be able to stop taking insulin.": Weight loss does not eliminate the need for insulin in type 1 diabetes. Because the pancreas no longer produces insulin, insulin therapy remains necessary regardless of changes in body weight or physical condition.

D. "I have developed a resistance to insulin.": Insulin resistance is a feature of type 2 diabetes, where the body produces insulin but cannot use it effectively. In type 1 diabetes, the problem is a lack of insulin production due to the destruction of pancreatic beta cells.

Rationale:

• Hepatic encephalopathy: This is caused by the buildup of neurotoxins, particularly ammonia, due to impaired liver function. The client’s elevated ammonia level and history of chronic alcohol use and jaundice support this diagnosis. Early signs may include confusion and lethargy, progressing to coma if untreated.
• Uremic encephalopathy: This condition is caused by accumulation of urea and toxins due to kidney failure. There is no evidence in the case of renal impairment, such as elevated BUN or creatinine levels, making this diagnosis unlikely in the current context.
• Hypoglycemia: Low blood glucose can cause confusion or altered mental status, but this client’s symptoms and labs do not indicate hypoglycemia. There is no mention of a low glucose level, and the focus of concern is more aligned with liver failure than endocrine causes.

• Abdominal pain: Although abdominal pain is a relevant symptom in liver disease, it is nonspecific and not directly responsible for hepatic encephalopathy. It reflects general liver inflammation or ascites but does not cause neurologic symptoms on its own.
• Albumin 3.0 g/dL: Low albumin indicates reduced liver synthetic function and contributes to fluid shifts like ascites, but it is not neurotoxic. It does not directly cause hepatic encephalopathy or altered mental status.
• Ammonia 150 mcg/dL: This is a critically elevated value, more than double the normal upper limit. High ammonia levels are the most direct biochemical cause of hepatic encephalopathy and require immediate treatment to prevent worsening neurological decline.
• Total Bilirubin 2.0 mg/dL: While elevated bilirubin suggests cholestasis and impaired liver clearance, it leads to jaundice rather than mental status changes. It reflects liver dysfunction but is not the key factor in encephalopathy development.