A two-year-old female intact Jack Russell Terrier mix was presented to the Cornell University Hospital for Animals (CUHA) emergency service for evaluation of azotemia, lethargy, and inappetence of one week’s duration. She was treated by her primary veterinarian for a presumptive urinary tract infection with a non-steroidal anti-inflammatory medication (NSAID, carprofen). Abnormalities on bloodwork included hyponatremia, hyperkalemia, azotemia, hypercalcemia, hypoglycemia, and hypocholesterolemia. An ACTH stimulation test confirmed a diagnosis of hypoadrenocorticism (Addison’s disease). Because of her recent history of NSAID administration, special considerations had to be made for the initiation of her glucocorticoid treatment. Aggressive gastroprotectant therapy was initiated and the patient was started on a low anti-inflammatory dosage of a steroid (IV dexamethasone) as well as desoxycorticosterone for mineralocorticoid supplementation. She was monitored closely for renal changes and gastrointestinal signs. This paper will review the pathophysiology of Addison’s disease and provide insight into the thought process for the treatment strategy chosen in this case.