Adrenal Insufficiency Symptoms
Adrenal insufficiency is a rare, gradually developing disease. It is caused either by destruction of the tissue in the adrenal gland, which is called the adrenal cortex and which secretes a corticosteroid hormone( Addison's disease), or in case of an adrenal cortex atrophy as a result of the cessation of its stimulation by the pituitary gland( secondary adrenal insufficiency).It is manifested by increasing weakness, pathological pigmentation of the skin and mucous membranes, hypotension, hypoglycemia. The manifestation of the disease depends on the lack of hormones in the adrenal cortex, like glucocorticoids and mineralocorticoids. The disease often develops due to atrophy of the adrenal cortex, and the development of clinical manifestations is often preceded by trauma, mental overstrain. It is also possible to defeat the adrenal glands in connection with tuberculosis, tumor, and apylyidosis. With Addison's disease, symptoms appear after about 90 percent of the adrenal cortex is destroyed. Insufficient corticosteroids can lead to health problems, such as an inability to recover even after a mild infectious disease. There may be complications such as prolonged weakness and shock, and death. Adrenal insufficiency occurs at any age in people of both sexes. Previously, this disease was not cured, but after the invention of corticosteroid-replacement therapy in the 1950s, the disease became curable. It is necessary, however, to take measures to avoid exacerbation of the disease - a sudden deficiency of steroids, which usually occurs after an infectious disease, trauma or stress, is a life threat and requires urgent treatment.
Causes of
Patients report gradually increasing weakness, fatigue. Most of them show violations of the gastrointestinal tract: loss of appetite, nausea, vomiting, abdominal pain, weight loss. Characteristic decrease in muscle strength, apathy, sometimes psychosis. Along with dehydration, hypotension and tachycardia are noted. In the blood - hypoglycemia, giperkaliemia, a slight increase in nitrogenous slags. Essential, but not necessarily, a sign of addison's disease is the hyperpigmentation of the skin and mucous membranes associated with the deposition of melanin, reminiscent of a dark tan. This pigmentation is most pronounced in the folds of the skin, in places subjected to friction and pressure. Manifestations of the disease are intensified during trauma, infection, when there may be so-called adrenal crises. At the same time, abdominal pain, adynamia, and collapse are possible.
Laboratory diagnosis of adrenal insufficiency is difficult. It requires the introduction of ACTH and subsequent determination in the urine of various steroid compounds, the amount of which in patients with addison disease varies little in comparison with the initial period.
AT to the adrenal glands are directed against the microsomal structures of cells of the adrenal cortex. They belong to IgG, they have organ-specificity and are more frequent in women. The determination of AT in the serum is used to establish the pathogenetic mechanisms of the development of primary adrenal atrophy. AT are detected in 38-60% of patients with idiopathic Addison's disease. Over time, the concentration of AT in Addison's disease may change, and they may disappear. AT to adrenal Ag can be detected in 7-18% of patients with tuberculous etiology of Addison's disease and 1% of elderly patients.
ADRENOGENITAL SYNDROME is associated with excessive secretion of the adrenal glands of male sex hormones. This can be associated with both a tumor of the adrenal cortex, and in some cases with increased pituitary hormones, stimulating the function of the adrenal glands. In this case, women develop violations of the menstrual cycle, there are signs of haemorrhage in the male type( grow beard, mustache, hair on the body), atrophy of the mammary glands. When examining such patients, an increased urinary excretion of 17-ketosteroids is detected. If a tumor is detected in such patients, surgical treatment is necessary.
Congenital adrenal cortex dysfunction is a group of autosomal recessive inheritance-related inheritance disorders of the hormones of the adrenal cortex, namely corticosteroids. Sometimes the term "adrenogenital syndrome" is used as a synonym for congenital dysfunction of the adrenal cortex. This statement is not entirely correct, since adrenogenital syndrome indicates a pathological change in the external genital organs due to a violation of adrenal hormone production, which can occur in other conditions, for example, in some tumors.
The essence of the term "dysfunction" with regard to the adrenal cortex is the inhibition of the production of only corticosteroids with simultaneous increase in the production of other hormones of this organ. In accordance with the defect of an enzyme involved in the formation of adrenal hormones( steroidogenesis), 5 main types of congenital adrenal cortex dysfunction are currently described. In addition, due to the presence or absence of an increase in the formation of male sex hormones( adrenal androgens), congenital dysfunction of the adrenal cortex is divided into: congenital dysfunction with increased androgen formation and congenital adrenal cortex dysfunction without increasing the formation of androgens( male sex hormones).
As a result of the influence of excess adrenal androgens, which begins already in the early stages of fetal development, neonatal girls have an intersex structure of the external genitalia. This condition is called female pseudohermaphroditism. The severity of the changes varies from simple clitoral hypertrophy to complete masculinization of the genitals, i.e., their male-type changes. In this case, the clitoris becomes penis, and the opening of the urethra moves to its head. The structure of internal genitalia in fetuses with female genotype with congenital dysfunction of the adrenal cortex is always normal. In genotypic boys with virile and salt-losing forms of the enzyme deficiency of steroidogenesis, penis enlargement and darkening of the scrotum are noted due to the deposition of a large amount of pigment.
In the absence of treatment after the birth of a child, there is a rapid appearance of male characteristics under the influence of male hormones. Bone growth zones are quickly closed, as a result, adults tend to have short stature.
These changes are designated as accelerated pseudo-puertata. In girls, in the absence of treatment, primary amenorrhea( absence of menstruation) is determined, which is also explained by the action of excessive amounts of male hormones( androgens).
There are two most common forms of congenital adrenal hyperplasia. They differ among themselves according to the type of enzyme that takes part in the formation of hormones by the adrenal glands. The first form is the deficiency of the enzyme called 21-hydroxylase, the second - the insufficiency of 11-hydroxylase.
In the case of idiopathic form of Addison's disease, it is very important to detect adrenal autoantibodies. The detection of autoantibodies even with normal concentrations of cortisol, aldosterone and increased concentration of ACTH in the blood indicates a latent adrenal insufficiency. Timely detection of adrenal autoantibodies promotes early diagnosis of adrenocortical dysfunction. With autoimmune genesis, Addison's disease is often combined with symptoms of other autoimmune diseases such as autoimmune hypothyroidism, hypoparathyroidism, diabetes mellitus, ovarian hypofunction, gastrointestinal diseases. There are cases of development of adrenal insufficiency in the presence of AT to ACTH receptors.