What diseases can affect the adrenal gland??
Pheochromocytoma / Paraganglioma
Pheochromocytoma is a rare tumor of the adrenal medulla, but can also develop along the spinal cord from sympathetic and parasympathetic cells of the so-called pituitary gland. Border strands arise. These tumors are called paragangliomas.
Preparation of a large pheochromocytoma
The main hormones produced by the adrenal medulla are adrenaline and noradrenaline. Thus it is responsible for the acute stress reaction of the body. Pheochromocytomas and paragangliomas themselves are mostly benign tumors that rarely tend to generalize. The dangerous thing about these tumors is the uncontrolled production of adrenaline and noradrenaline. These and their degradation products are measured in the blood and urine as part of the diagnostic process and are elevated above normal levels.
Patients have general and rather non-specific symptoms, such as headache, subjectively felt palpitations and sweating. Typically these symptoms occur in attacks. The psyche can also be affected by the stress hormones and it is not uncommon for patients to report panic attacks, or conversely, a tendency to aggression. A tendency to high blood prere or elevated blood sugar levels may be detected by the family doctor. Rarely, however, a seizure-like release of the hormones is observed directly by the physician in the full picture, whereby here the patient becomes conspicuous with blood prere derailment and pallor with subsequent hot flushes. Examination and diagnosis of pheochromocytoma/paraganglioma is recommended for every newly diagnosed hypertension.
Primary hyperaldosteronism is the most common cause of secondary arterial hypertension and its cardiovascular sequelae. The cause of elevated blood prere is increased production of the hormone aldosterone, which is involved in salt and water balance regulation in the body. Aldosterone causes the body to retain too much salt and water, which increases blood prere. In the case of primary hyperaldosteronism, this increased production of aldosterone in the body can be caused either by a unilateral or bilateral enlargement of the adrenal glands or by a mostly benign tumor, a so-called "tumor of the adrenal gland". be caused by adrenal adenoma. However, benign non-aldosterone-producing adrenal adenomas also occur. These adrenal tumors can occur regardless of the actual presence of unilateral or bilateral adrenal enlargement. However, benign non-aldosterone-producing adrenal adenomas also occur. These adrenal tumors can occur independently of the actual presence of unilateral or bilateral adrenal enlargement. The only way to be sure whether an aldosterone-producing adrenal adenoma is really present is through a relatively complex invasive procedure, selective venous catheterization of the adrenal glands. However, this examination is only available at a few selected centers.
A number of antihypertensive drugs interfere with the aldosterone hormone system, resulting in decreased or reactively increased physiological concentrations. This complicates diagnosis, which is why a change in blood prere medication must usually be made before the hormone is measured. Ideally, the workup for hyperaldosteronism is done after a diagnosis of elevated blood prere and before blood prere medication is started.
With the exception of bilateral adrenal enlargement, therapy usually involves surgery and removal of the affected adrenal gland, although aldosterone action can also be inhibited with medication, but this is then associated with corresponding side effects.
Cushing's syndrome is characterized by an increased production of cortisol, the long-term stress hormone of the human body. There are different causes of a sog. Hypercortisolism. In ca. 15% is due to an adrenocortical tumor.
The adrenocortical tumor can also be malignant, which must be ruled out, especially in the case of a full-blown disease. This full-blown condition is characterized by a full moon face, brittle, parchment-like skin with a tendency to bruise, muscle weakness and pronounced stretch marks (wider>1cm) with possible weight gain. The therapy for a full-blown Cushing's syndrome caused by an adrenal tumor is surgery.
Difficulty in distinguishing the disease from subclinical Cushing's disease. Blemished skin with acne, poor wound healing, or a change in normal body hair may be present in this case. Subtle psychological symptoms may also occur, such as a tendency to depression, fatigue, changes in appetite, insomnia, nervousness, concentration problems or a decrease in libido. Patients are prone to conditions such as diabetes, hypertension and osteoporosis.
Diabetes, high blood prere and obesity can be grouped together to form the metabolic syndrome, which is also known as the fatal quartet if a lipometabolic disorder is also present. These diagnoses become more common with increasing patient age. Since the frequency of benign adrenal tumors is also increasing with age in the general population, it is currently not clear to what extent benign tumors of the adrenal gland do not produce hormones and also cortisol to some extent, which ultimately result in these clinical pictures. In contrast to the full-blown Cushing's syndrome, there is currently no uniform consensus on the benefit of surgical therapy in the case of subclinical Cushing's syndrome, as opposed to direct therapy of the secondary diseases. Ultimately, the diagnosis can only be made in selected. The following questions should be addressed by outpatient clinics specializing in hormone diagnostics.
Adrenocortical insufficiency / hypofunction of the adrenal glands
Adrenal hypofunction usually means that the adrenal gland is unable to produce sufficient cortisol to meet the body's needs. An underfunction of the adrenal glands can have many different causes. For a better understanding, it is important to know that the formation of cortisol in the adrenal glands is subject to a feedback control loop. In this process, the pituitary gland is stimulated by a higher-level control center in the brain, the hypothalamus. The pituitary gland releases adrenocorticotropic hormone (ACTH) in response to this stimulus, which then stimulates the adrenal gland to produce cortisol. Cortisol itself exerts an inhibitory function on the hypothalamus and pituitary gland, regulating blood cortisol levels.
This can lead to an underactivity of the adrenal gland and thus to a so-called "adrenal insufficiency". Hypocortisolism can occur at one of the three different levels of the described regulatory cycle. In case of a disturbance of the secretion capacity of the hypothalamus resp. of the pituitary gland is called tertiary or secondary adrenal insufficiency. These two disorders will not be discussed further here. Primary adrenal insufficiency occurs when the secretory capacity of the adrenal glands themselves is impaired. This can be caused by a process in which antibodies are formed against the patient's own adrenal tie, which is then recognized as foreign by the immune system and is therefore destroyed by it. Such a disease is called autoimmune disease. In the case of the adrenal gland, this is referred to as Addison's disease. Another cause of acquired adrenal insufficiency is tumor metastasis to the adrenal glands. Such depositions can originate, for example, from lung, kidney and breast tumors or from tumors of the digestive tract. Infections or hemorrhages can also lead to a loss of cortisol secretion function. After surgical removal of one adrenal gland, the remaining adrenal gland is usually able to completely take over the function of the other one. In case of bilateral adrenalectomy, permanent hormone replacement therapy is vital.
Adrenogenital syndrome / hyperandrogenemia (too much male hormones in the blood)
Adrenogenital syndrome is caused by an enzymatic disturbance of cortisol production in the adrenal gland. In most cases the so-called. 21-hydroxylase impaired in its function. 21-hydroxylase is an enzyme which synthesizes cortisol from the precursor substance 17-OH-progesterone. If 21-hydroxylase is not functional or only to a limited extent, the adrenal gland produces increased 17-OH-progesterone. However, 17-OH-progesterone is also the precursor substance of male hormones. This explains a masculinized hormone status depending on the activity of 21-hydroxylase. Depending on the extent of the remaining enzyme activity of 21-hydroxylase, a distinction is made between classic. The non-classical form of adrenogenital syndrome. The classic form can be further subdivided into the adrenogenital syndrome with salt loss. Subdivide into adrenogenital syndrome without salt loss. In classic adrenogenital syndrome with salt wasting, severe salt wasting occurs within the first months of life as a result of cortisol deficiency and, in female sufferers, pronounced general masculinization. Without substitution therapy with cortisol derivatives these children are not able to survive. In classic adrenogenital syndrome without salt wasting, residual activity of 21-hydroxylase makes the masculinization symptoms less pronounced. In contrast to the classical adrenogenital syndrome, the non-classical adrenogenital syndrome only becomes symptomatic in the course of the first decade of life. There is no cortisol deficiency in these patients. Therapeutically, the prevention of masculinization symptoms of female patients stand here. The prevention of premature puberty in male patients in the foreground. In very mild cases, the disease may remain undetected until adulthood. Only then become noticeable through fertility disorders or an increasing male pattern of hair growth.