How is Addison disease treated and clinically managed?

Choice A reason: Reassessing vital signs in 1 hour is not an immediate action and does not address the patient’s current symptoms of dizziness and unsteady gait, which indicate a potential problem that requires immediate attention. Waiting an hour to reassess may delay necessary interventions that could prevent harm.
Choice B reason: Assisting the patient into a sitting position and notifying the healthcare provider is the most appropriate action. The symptoms of dizziness and unsteady gait, along with a BP of 98/60 mmHg, suggest that the patient may be experiencing orthostatic hypotension or a side effect of Carbidopa-Levodopa. Elevating the patient's position can help prevent falls, and notifying the healthcare provider ensures that the situation is assessed and managed promptly. This action addresses the immediate safety of the patient and facilitates appropriate medical intervention.
Choice C reason: Administering the next dose of Carbidopa-Levodopa early is not recommended without specific orders from the healthcare provider. It could potentially lead to overmedication and worsen the patient’s symptoms or cause adverse effects. Medication administration should always follow the prescribed schedule unless otherwise directed by the healthcare provider.
Choice D reason: Educating the patient about increasing his exercise is important for overall health and mobility but is not an immediate intervention for the acute symptoms of dizziness and unsteady gait. The patient’s current condition requires prompt assessment and intervention rather than education on exercise, which can be addressed later once the immediate issue is managed.

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.