Endocrine disorders can be the result of
(See also Overview of the endocrine system.) Endocrine disorders can result from dysfunction due to peripheral endocrine gland itself (primary disorder) Under stimulation by the pituitary gland (comorbidities) overstimulation by the pituitary gland (comorbidities) The disorder may be (as hormone overproduction overactive ) or (as a lack of hormone production function) manifest. Very rarely will you find endocrine disorders (i. D. R. sub-functions) due to abnormal tissue responses to hormones. Clinical manifestations of sub dysfunctions are often insidious and non-specific. Endocrine overactivity An overactive endocrine glands may occur due to a pituitary overstimulation. but is much more common hyperplasia or neoplasia of endocrine gland itself. In some cases, degeneration of other tissues can produce hormones (ectopic hormone production). Excessive hormone levels can also result from exogenous hormone intake. In some cases, patients take a hormone without informing the attending physician (eg. As Hyperthyreosis factitia). A hypersensitivity of a tissue to hormones is also possible. Stimulation of peripheral endocrine glands by antibodies may occur. An example of this is the Graves’ disease. By disrupting a peripheral endocrine gland quickly large amounts of stored hormones can be released (eg. As thyroid hormone release in the context of subacute thyroiditis). Enzyme defects that occur in the synthesis of a peripheral endocrine hormone of the existing blockade may result in an overproduction of a hormone proximally. The overproduction of a hormone may be the organism an adequate response to a particular disease state. Endocrine function An underactive gland endocrine may be due to a pituitary under stimulation or failure of the peripheral gland. An underactive, which itself has its origins within the peripheral gland can be hereditary or acquired (autoimmune diseases, tumors, infections, vascular changes, toxins). Genetic diseases that cause a sub-function have, as a cause either a loss of the gene or the production of abnormal hormone. A decrease in hormone production a peripheral endocrine gland with a resultant increase in the production of pituitary hormone regulation can lead to hyperplasia of peripheral endocrine gland. For example, the lack of synthesis of thyroid hormone leads to excessive secretion of thyroid-stimulating hormone (TSH), and this in turn can lead to a goiter. Some hormones require conversion to an active form after being secreted from a peripheral endocrine gland. Some diseases may block this step (for. Example, a renal disease, the production of the active form of vitamin D inhibit). Antibodies against the circulating hormone or against its receptor can destroy the ability of the hormone to the receptor binding. Certain diseases or medications lead to increased degradation of hormones. Certain substances can interfere with the function of hormones. Abnormalities of the receptor or elsewhere in the peripheral endocrine tissues can also cause an underactive. Laboratory tests on Endocrine disorders The clinical manifestation of a sub-function is often insidious and non-specific. Therefore, the duration can be up to clinical diagnosis often months or years. Therefore, the biochemical diagnosis by determining the levels of peripheral hormones in the blood, pituitary hormones, or both in the blood often is crucial. Since most hormones are subject to a circadian rhythm, the determination at a set time should be. Hormones that vary over short periods (eg. As luteinizing hormone) make it necessary to determine or three or four values ??above 1 or 2 hours using a pooled blood sample. Hormones with a deviation from week to week (z. B., testosterone) make it necessary to determine separate values ??at an interval of one week. Messsungen of hormones in blood It is believed that free or bioavailable hormone (z. B. hormone that is not coupled to a specific binding protein) is the active form. Free or bioavailable hormone is determined using the Äquilibrierungsdialyse, ultrafiltration or liquid extraction method. Here, free and albumin-bound hormone is separated from binding globulin. These methods are expensive and time consuming. Analog and competing free hormone assays are today verfügbar.Bluthormonschätzungen with good sensitivity and specificity The values ??of the free hormone can be indirectly determined by determined the values ??of the binding protein and these are used for adjustment of the total serum hormone levels. However, the indirect methods are inaccurate if the binding capacity of the hormone-binding protein has been modified (eg., By a fault). In some cases, other indirect estimates are used. Because growth hormone (GH), for example, has a short half-life in serum and is difficult to detect in the serum, is insulin-like growth factor 1 (IGF-1) which is produced in response to GH often measured as an index of GH activity , Whether the measurement of circulating hormone metabolites can be used as an indicator of the amount of bioavailable hormone is currently the subject of research. Occasionally, instead of blood levels, and hormone levels in the urine (z. B. Free cortisol in the diagnosis of a Cushing’s disease) or in saliva bestimmt.Dynamische tests for safe assessment of pituitary dysfunction dynamic tests are necessary. In the case of sub-function, a stimulation test (z. B. ACTH stimulation) is used. Is an overactive suspected, a suppression test (eg. B.Dexamethason suppression) must be used. Therapy replacement of the deficient hormone suppression of excessive thyroid hormone production. A sub-function is usually treated by substituting the peripheral endocrine hormone, regardless of whether it is a primary or secondary defect (exceptions is the GH (a thyroid hormone) substitution with pituitary dwarfism. If resistance to a hormone prior to, drugs can be administered, decrease the resistance, (eg. as metformin or thiazolidinediones in diabetes mellitus type 2). Occasionally, a hormone stimulating medicine is used. irradiation, operative procedures and drugs which suppress the production of hormones, are used to an overactive to treat. In some cases, a receptor antagonist is given. aging and Endocrinology hormones change with the age of an individual. most hormone levels drop s from. Some hormone levels remain in the normal range such. B. TSH, ACTH (basal), thyroxine, cortisol (basal), 1,25-dihydroxycholecalciferol, insulin (increasing occasionally) and estradiol (in men). Some hormone levels increase. Hormones that increase as ACTH (as a response to corticotropin-releasing hormone), follicle stimulating hormone, sex hormone binding globulin, activin (for men), gonadotropin (in women), adrenaline (in very old people), parathyroid hormone, norepinephrine, cholecystokinin, vasoactive intestinal peptide, vasopressin (also loss of circadian rhythm), and atrial natriuretic factor are associated with either receptor or post-receptor defects which may result in a sub-function. Many age-related changes are similar to the changes in hormone deficiency. This leads to the hypothesis of “hormonal fountain of youth”, d. H. to the speculation that some age-related changes by the substitution of one or more hormones can be reversed. There is evidence for the hypothesis that replacement of certain hormones to improve the functionality of individual tissues (eg. B. muscle strength, bone density) leads, but there is little evidence in terms of mortality. In some cases, hormone replacement therapy can also be harmful, such as estrogen replacement in older women. A competing theory is that occurring at the age drop in hormone levels is a protective slowing of cellular metabolism. This concept is based on the so-called. Rate-of-living theory of aging, d. h., the higher the metabolic rate of an organism, the faster it dies. This concept is obviously supported by studies on the effects of a restricted food intake. The restriction of the food intake leads to the decrease of hormones that stimulate metabolism. Thereby, the metabolic rate is reduced; This restriction also results in rodents to a life extension. Specific age-related hormone decreases the levels of dehydroepiandrosterone (DHEA) and its sulfate increase with age dramatically. Despite the optimism regarding the role of DHEA substitution in the elderly, most clinical trials have shown no significant advantage. Pregnenolone is the precursor of all known steroid hormones. As well as the levels of DHEA decrease the hormone levels of pregnenolone with age. Studies in the 1940s showed the effectiveness of this hormone in the treatment of patients with arthritis. An effect on muscle strength and memory could not be demonstrated in additional studies. The levels of GH and its peripheral endocrine hormone (IGF-1) decrease with age. Sometimes do not show older people in which GH is substituted, an increase in muscle mass, but the muscle power. Side effects (eg. As carpal tunnel syndrome, arthralgia, water retention) are very common. GH may play a role in the short-term treatment of malnourished elderly patients, but in critically ill malnourished patients GH increased mortality. Substances that stimulate the production of GH in a more physiological patterns could improve the effectiveness and reduce the risk. The mirrors of melatonin, which is produced in the pineal gland, a hormone, taking also with age. This decrease could play an important role in the loss of the circadian rhythm with age. The estrogen replacement in older women is in menopause: hormone therapy. and testosterone replacement in older men is in discussion Male hypogonadism: testosterone replacement therapy (TRT) ..