A serum potassium level of 3.2 mEq/L is reported for a patient with cirrhosis who has scheduled doses of spironolactone (Aldactone) and furosemide (Lasix) due. Choose the best nursing action.

Choice A reason: Increased serum chloride is not a typical finding associated with syndrome of inappropriate antidiuretic hormone (SIADH). In SIADH, the body's regulation of water is impaired, leading to water retention and dilutional hyponatremia. Serum chloride levels might not be significantly affected and are not the primary laboratory indicator for this condition.
Choice B reason: Elevated hematocrit is not directly related to SIADH. Hematocrit levels reflect the proportion of red blood cells in the blood. In SIADH, the main issue is water retention leading to dilutional hyponatremia, rather than changes in red blood cell concentration. Therefore, hematocrit levels are not a key laboratory finding in this disorder.
Choice C reason: Decreased serum sodium, or hyponatremia, is a hallmark finding in SIADH. The excessive release of antidiuretic hormone (ADH) leads to water retention, diluting the sodium in the blood and resulting in low serum sodium levels. This hyponatremia can cause symptoms such as disorientation, headache, and muscle cramps, as seen in the patient. Monitoring and correcting serum sodium levels is crucial in the management of SIADH.
Choice D reason: Low urine specific gravity is not expected in SIADH. In fact, patients with SIADH typically have a high urine specific gravity due to the excessive release of ADH, which causes the kidneys to reabsorb water and concentrate the urine. This concentrated urine reflects the body's attempt to reduce water excretion in response to elevated ADH levels. Therefore, low urine specific gravity would not be an initial laboratory finding in this condition.

Choice A reason: Increasing serum potassium levels would not indicate effective therapy for a patient with Addison's disease. In Addison's disease, the adrenal glands do not produce enough aldosterone, which is responsible for regulating sodium and potassium balance. As a result, patients with Addison’s disease often experience hyperkalemia (high potassium levels). Effective therapy typically aims to normalize potassium levels, so an increase would suggest inadequate treatment or worsening of the condition.
Choice B reason: Decreasing blood glucose levels would not typically be seen as a positive indicator in a patient with Addison's disease. The body’s ability to maintain normal blood glucose levels is compromised in Addison’s disease due to a deficiency in cortisol. Cortisol plays a key role in regulating glucose metabolism, and its deficiency can lead to hypoglycemia (low blood glucose levels). If blood glucose levels are decreasing, it may indicate inadequate glucocorticoid replacement therapy, suggesting the therapy is not fully effective.
Choice C reason: Decreasing serum chloride levels would not be expected in a patient with Addison’s disease who is receiving proper treatment. Chloride is regulated alongside sodium and is influenced by aldosterone. In Addison's disease, aldosterone deficiency leads to a decreased ability to retain sodium, which in turn can affect chloride levels. However, a decrease in chloride levels alone is not a clear sign of effective therapy. Normalization of serum sodium levels is a better indicator of treatment success.
Choice D reason: Increasing serum sodium levels is the correct finding that indicates effective therapy in a patient with Addison’s disease. In this condition, aldosterone deficiency results in sodium loss through the kidneys, leading to hyponatremia (low sodium levels). Effective therapy, which typically involves the administration of glucocorticoids and mineralocorticoids (such as fludrocortisone), helps to correct this imbalance by increasing sodium retention and normalizing serum sodium levels. This would demonstrate that the current therapies are working to restore the electrolyte balance.