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The activator is recommended for transient ischemic attacks: Tissue plasminogen activator (tPA) is not indicated for TIAs because symptoms resolve without permanent infarction, and the risks of bleeding outweigh potential benefits.

The activator is recommended for patients with increased ICP: Increased intracranial pressure is a contraindication to tPA due to the high risk of cerebral bleeding and worsening neurologic injury.

The activator is not recommended if the stroke is less than 3 hours: This is incorrect, as tPA is most effective and safest when given as early as possible within the approved time window.

Fluid loss of 0.5 liters: This is inconsistent with the patient’s weight gain and declining urine output, which point toward fluid retention rather than loss.

Equal intake and output due to insensible losses: Equal intake and output would result in relatively stable weight, not a 1.5 kg increase within 24 hours.

40 kcal/kg/day: Caloric needs at this level are generally reserved for patients with severe stress, extensive trauma, burns, or hypermetabolic states. Providing excessive calories to a mildly stressed patient increases the risk of overfeeding, hyperglycemia, and increased carbon dioxide production.

25 kcal/kg/day: This level is often appropriate for unstressed or minimally stressed hospitalized adults. It may be insufficient to meet the increased metabolic demands associated with even mild physiologic stress in critical care settings. Inadequate intake can contribute to negative nitrogen balance and delayed recovery.

30–35 kcal/kg/day: This caloric range is more appropriate for patients experiencing moderate to severe stress, such as sepsis or major surgery. For a mildly stressed patient, this level may exceed metabolic needs. Higher caloric delivery can increase metabolic burden without added benefit.

Obstruction of urine flow: Obstruction to urine outflow causes postrenal acute kidney injury by increasing pressure within the urinary tract. This mechanism affects kidney function after urine is formed rather than blood flow to the kidneys. Examples include ureteral obstruction or prostatic enlargement.

Damage to kidney tissue: Direct injury to renal structures such as the tubules, glomeruli, or interstitium leads to intrinsic acute kidney injury. This pathology arises from ischemia, toxins, or inflammation affecting the kidney itself. It is not classified as prerenal.

Chronic kidney disease: Chronic kidney disease represents long-term, progressive loss of kidney function over months to years. It is not an acute process and does not describe a prerenal mechanism. Acute kidney injury involves a sudden decline in renal function.

Infuse 1 unit of platelet: Platelet transfusion is indicated for thrombocytopenia or active bleeding related to low platelet counts. Acute adrenal insufficiency does not involve platelet depletion or coagulation defects. This intervention does not address the underlying hormonal crisis.

Restrict daily fluid intake: Clients with acute adrenal insufficiency are at risk for hypovolemia and hypotension due to aldosterone deficiency. Fluid restriction would worsen dehydration and circulatory collapse. Fluid replacement is typically required rather than restriction.

Give oral spironolactone: Spironolactone is a potassium-sparing diuretic and aldosterone antagonist. In adrenal insufficiency, aldosterone levels are already low, making this medication inappropriate. Its use could worsen hyperkalemia and hypotension.

Cerebral hemispheric injury (decorticate): Decorticate posturing involves flexion of the upper extremities with extension of the lower extremities. This pattern suggests damage above the brainstem, typically involving the cerebral hemispheres or internal capsule. The fully extended posture described does not match this presentation.

Meningeal irritation: Meningeal irritation is associated with signs such as neck stiffness, photophobia, and headache. It does not produce abnormal posturing responses to pain. The described motor response reflects deeper neurologic injury rather than meningeal involvement.

Alcohol intoxication: Alcohol intoxication may cause altered mental status, impaired coordination, or decreased consciousness. It does not cause abnormal posturing such as rigid extension of all extremities. The neurologic findings described are not explained by alcohol use alone.

Increased protein diet: Increasing protein intake can raise ammonia levels because protein metabolism produces nitrogenous waste. In cirrhosis, impaired hepatic detoxification limits conversion of ammonia to urea. Excess protein may worsen hepatic encephalopathy symptoms.

Decreased sodium diet: Sodium restriction is commonly used to manage ascites and edema in cirrhosis. While important for fluid balance, it does not directly reduce ammonia production or levels. This intervention addresses volume status rather than encephalopathy risk.

Increased carbohydrate diet: Carbohydrates provide an alternative energy source and can help prevent protein catabolism. While beneficial as part of overall nutrition, increasing carbohydrates alone does not directly reduce ammonia production. It is supportive rather than primary management for hyperammonemia.