Cortical hypofunction

Introduction When most of the adrenal glands on both sides are destroyed, there is a manifestation of various corticosteroid deficiencies, called adrenal insufficiency. Can be divided into primary and secondary. Primary chronic adrenal insufficiency, also known as Addison disease, is relatively rare; secondary hypothalamic-pituitary dysfunction patients, due to insufficient secretion of CRF or ACTH, resulting in atrophy of the adrenal cortex.

Cause

It is caused by insufficient secretion of three steroid hormones (glucocorticoids, mineralocorticoids and androgens) in the adrenal glands.

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It is the most common to destroy the primary damage of the adrenal gland (such as autoimmune disease, sepsis and blood infarction, tuberculosis infection, metastases, etc.), but also secondary to hypofunction of the pituitary or hypothalamus. Acute adrenal insufficiency is often life-threatening and can develop into sputum, stupor or coma.

Symptoms of chronic adrenal insufficiency, similar to depression. Typical patients can be characterized by fatigue, muscle spasm, fatigue, weight loss, loss of appetite, apathy, irritability, and depression. Attention and memory can also be affected, and hallucinations and delusions are rare.

Differential diagnosis

Renal cortical necrosis is a rare form of death of kidney tissue that affects only the outer layer (cortex) of some or all of the kidneys without affecting the inner layer (medulla). Renal cortical necrosis can occur at any age. About 10% of cases occur in infants and children. More than half of neonates with renal cortical necrosis have a sudden placental separation (placental dissection) during childbirth; the other most common cause is blood flow bacterial infection (septicemia). In children, renal cortical necrosis can be followed by infection, dehydration, shock or hemolytic uremic syndrome. In adults, bacterial sepsis causes cortical necrosis to account for about one-third of all cases.

Renal cortical thinning: Chronic glomerulonephritis is the final stage of development of different types of glomerulonephritis. The lesion is characterized by a large number of glomerular glassy changes and sclerosis, also known as chronic sclerosing glomerulonephritis. From the naked eye, the kidneys are reduced in size and the surface is diffuse and fine-grained. The cut cortex is thinned and the boundary of the cortex is unclear. Increased fat around the renal pelvis. The gross lesion of chronic nephritis is called secondary granular pyknosis.

Adrenal hyperplasia, also known as adrenal genital syndrome or adrenal hypermutation: the birth defects of certain adrenal enzymes cause abnormal steroid production. Women cause false hermaphroditism and male genitals are huge. Enzyme defects are accompanied by excessive androgen products in the uterus of the fetus, which will develop normally in the female Müllerian catheter structure (ie, ovary, uterus, and vagina), while excess androgen exerts its male in the genitourinary and reproductive nodules. The effect of the vaginal and urethra is connected, and the enlarged clitoris is low and open. The labia are often hypertrophied, and severe cases have hypospadias and cryptorchidism. The adrenal cortex causes varying degrees of cortisol deficiency due to the majority of secreted anabolic male steroids.

It is the most common to destroy the primary damage of the adrenal gland (such as autoimmune disease, sepsis and blood infarction, tuberculosis infection, metastases, etc.), but also secondary to hypofunction of the pituitary or hypothalamus. Acute adrenal insufficiency is often life-threatening and can develop into sputum, stupor or coma.

Symptoms of chronic adrenal insufficiency, similar to depression. Typical patients can be characterized by fatigue, muscle spasm, fatigue, weight loss, loss of appetite, apathy, irritability, and depression. Attention and memory can also be affected, and hallucinations and delusions are rare.

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