Hypoadrenocorticism, also known as Addison's disease, is an endocrine disease affecting both humans and animals alike, characterized by a decreased secretion of hormones by the adrenal gland. It is a rare, but a life-threatening disease in dogs that requires a lifelong therapy. The adrenal cortex is functionally and structurally separated from the marrow. It is divided into three different zones, each of which secretes a different group of hormones. The zona arcuata synthesizes mineralocorticoids, the zona fasciculata glucocorticoids, while the zona reticularis secrets androgen hormones. The function of the adrenal cortex is regulated by CRH and ACTH, originating from the hypothalamus and adenohypophysis. The hormones of the adrenal cortex have a number of functions that help maintain homeostasis. Glucocorticoids, i.e. cortisol, are involved in the metabolism of carbohydrates, proteins and fats, and are also involved in maintaining blood pressure. Alongside that, they also have immunosuppressive and anti-inflammatory effects. On the other hand, mineralocorticoids, i.e. aldosterone, play a major role in maintaining the physiological values of plasma electrolytes. At the same time, they contribute to the maintenance of normal blood volume and blood pressure associated with the RAAS system. Addison's disease is characterized by partial or complete loss of function of the adrenal cortex. The disease is divided into primary and secondary hypoadrenocorticism, having the primary one divided into the more common typical and the less common atypical form. Primary hypoadrenocorticism is most often of immune-mediated etiology, but at the same time, tumors, infections, inflammation, etc. can be the cause of damage to the adrenal cortex. The typical form is characterized by a deficiency of glucocorticoids and mineralocorticoids, while atypical Addison's disease is characterized only by a deficiency of glucocorticoids. Secondary hypoadrenocorticism occurs due to damage to the tissue of the hypothalamus or adenohypophysis, resulting in atrophy of the adrenal cortex. Certain breeds of dogs are predisposed to develop adrenal insufficiency due to hereditary traits of the disease, with the incidence being higher in females. 49 The clinical picture is markedly variable and nonspecific, and includes signs of almost all organ systems. It is divided into the acute form (addisonian crisis) and the more common chronic form. The most common symptoms include lethargy, diarrhea with or without blood, vomiting, muscle weakness, anorexia, weight loss, polyuria/polydipsia, bradycardia, and dehydration/hypovolemia. Laboratory findings may include anemia, absence of "stress leukogram", hyponatremia, hypochloremia, hypoglycemia, hypoproteinemia, acidosis, elevated urea and creatinine, elevated certain liver enzymes, etc. Objective diagnosis is made based on ACTH stimulation test. Other tests such as determining Na and K concentrations, Na: K ratios, basal cortisol, aldosterone concentrations, etc. may serve the clinician in raising the suspicion of hypoadrenocorticism. Patients in an addisonian crisis need to have their hypovolemia corrected, resolve their plasma electrolyte abnormalities, and they need a glucocorticoid replacement. Symptomatic therapy is also extremely important. Chronic hypoadrenocorticism is treated with lifelong glucocorticoid therapy and mineralocorticoids. The most important synthetic mineralocorticoids used in therapy are DOCP and fludrocortisone acetate, while the most common glucocorticoids are prednisone, prednisolone, hydrocortisone, and dexamethasone. The prognosis of patients with Addison's disease is excellent if the dose of medication is correctly determined for each dog individually, as well as if the owners continuously give therapy to the dog and bring them to regular examinations.