Why does skin atrophy occur, types, symptoms of atrophy. Atrophy: definition, causes, types, morphological characteristics Treatment methods for atrophy


(atrophia) - pathological condition, accompanied by a decrease in the size, volume and weight of both the organ as a whole and its individual sections with a gradual decrease and cessation of functioning. In addition to organs, atrophy can affect certain tissues, nerves, mucous membranes, glands, and so on.

Atrophy is an acquired intravital process, that is, there is a drying out of elements that previously developed normally in accordance with age and physiological characteristics organism. This is its fundamental difference from hypoplasia, characterized by intrauterine underdevelopment of an organ, or another part of the body, for example, bones. Also, atrophy must be clearly distinguished from aplasia, in which the organ retains the appearance of early conception, or from agenesis - total absence some organ that occurred as a result of violations during ontogenesis.

A simple atrophic process is based on a decrease in tissue volume due to cell atrophy. Moreover, in most cases, a qualitative change in their structural elements is not observed at first, only later can their complete disappearance be observed. More precisely, the main constituent elements remain unchanged in the cell - the cytoplasm and the nucleus. Deep cellular metabolic disorders do not occur. In the future, atrophy can lead to a decrease in the number of cells.

degenerative atrophy is a combination of atrophy with degenerative degeneration of cells. A typical example is brown atrophy, characterized by the accumulation of lipofuscin in the tissue of the organ.

Classification

Atrophy is divided into many types, the main of which physiological And pathological.

physiological atrophy. This is a normal process that accompanies a person throughout life. As an example, obliteration and atrophy of the ductus arteriosus and umbilical arteries in newborn infants, thymus atrophy after adolescent puberty. For the elderly, atrophy of the gonads is characteristic, for old age- bones, intervertebral and articular cartilage, skin. To the advent senility and leads to dementia cortical atrophy with a characteristic lesion frontal lobes accompanied by destruction of the tissues of the cerebral cortex.

pathological atrophy. In turn, it is divided into general And local.

General pathological atrophy develops due to insufficient intake of nutrients into the body, or in case of violation or cessation of absorption of certain elements due to oncological, infectious diseases, diseases of the nervous system.
With the initial degree of cachexia, the accumulated fat from fat depots is consumed, then atrophy passes to the skeletal muscles, significantly reducing muscle mass. After a lack of nutrients affects the liver, heart, brain and other vital important organs disrupting their functioning. General muscular atrophy (cachexia) is manifested by such changes.

Local atrophy for reasons and mechanism of development is divided into the following types:

dysfunctional. This type of atrophy develops due to a decrease in the function of an organ or limb. Atrophy of the thigh and calf muscles in this case is caused by forced bed rest or hypodynamia. It is observed with bone fractures, when the patient is temporarily unable to give a full load on the broken limb. Loss of function from inactivity may include atrophy optic nerve arising after enucleation eyeball. Bone atrophy is manifested by osteoporosis with a decrease in the size of trabeculae.

compression(from pressure). Complete atrophy of an organ or some part of it can occur from prolonged squeezing him, for example, large sizes tumor. Atrophy of the kidney provokes compression of the ureter with a violation of the outflow of urine and the occurrence of hydronephrosis.

Discirculatory atrophy (ischemic). It begins after the narrowing of the lumen of the arteries that feed the organ, tissue or mucous membrane. Insufficient blood circulation in the tissue leads to nutritional deficiencies, oxygen starvation and metabolic disorders, ending with atrophic processes in cells with their gradual death. Hypoxia of the cells of the cerebral cortex contributes to the development of sclerosis and dementia. Generalized cerebral atrophy of the brain various degrees severity can be observed in newborns due to fetal hypoxia.

neurotic or neurogenic atrophy. It occurs due to a violation or blockage of nerve conduction (impulses) to the organ. This condition is caused by damage to neurons, destruction nerve fibers appearing after injuries, malignant neoplasms, hemorrhages. Damage to bone tissue, skeletal muscle or skin is most characteristic of this type of atrophy. It is the innervation that is common cause atrophy of the epithelium of the mucous membranes, one or both limbs. When defeated trigeminal nerve there is atrophy of the corresponding part of the face.

Atrophy provoked by various chemical, physical or toxic factors. Long-term infections with severe intoxication of the body, radiation exposure, chemical poisoning, long-term use of corticosteroids are the reasons for the development of this type of atrophy. Beam energy, related to physical factors, most often causes atrophy in the organs of hematopoiesis and reproductive organs. Sex glands, bone marrow cells, parts of the spleen atrophy. Long-term use of exogenous glucocorticoids can result in atrophy of the adrenal glands, and steroids - atrophy of the testicles.

dishormonal atrophy caused by a lack of trophic hormones. Hypofunction or functional deficiency thyroid gland, pituitary gland or ovaries leads to a decrease in the size of the uterus and mammary glands. Excess iodine results in atrophy of the thyroid gland, and a decrease in estrogen production leads to atrophy of the muscles of the vagina.

brown. With it, the organ acquires a brown hue due to the appearance in the protoplasm of cells of a brown pigment - lipofuscin. This type is characteristic of the heart, striated muscles or liver.

By external manifestations:

bumpy. The uneven distribution of the process is expressed in the unevenness and small tuberosity of the surface of the area with atrophy.

Smooth. With this form of atrophy, the physiological folds of the organ are smoothed out, its surface becomes smooth and glossy. Either the organ retains its original smoothness, which indicates a uniform distribution of the atrophic process. This mainly applies to the kidneys and liver.

By the nature of the damage:

Focal. It does not affect the entire surface of the mucosa or other tissue, but only its individual sections (foci). This type of atrophy is characteristic of the epithelium of the gastric and intestinal mucosa, manifested by multiple focal lesions.

diffuse. It spreads over the entire surface of the organ, often completely involving it in the process. The configuration of the organ does not change, but its complete drying (reduction in size) is observed.

Partial. An organ or tissue area is not completely affected. There is a reduction in the volume and size of a part of the organ.

Complete. characteristic of optic nerve atrophy. There is a complete destruction of the fibers and their replacement by cells connective tissue. There may be damage to the optic nerves of both eyes, or maybe only one.

IN separate category highlighted multisystem atrophy (ISA) is a neurodegenerative disease of a progressive nature with damage to the neural subcortical nodes white matter hemispheres, trunk, spinal cord and cerebellum.

Statistics:
According to statistics, multisystem atrophy is detected in 4.6 cases out of 100 thousand people, and 55% of them are in men of mature age (from 50 to 65 years).
Optic nerve atrophy in 21% of cases leads to irreversible blindness, and in 68% to partial, leading to disability.


Classification of MSA depending on the clinical picture:

1. Striatonigral degeneration. The symptoms of parkinsonism predominate.

olivopontocerebellar. Clinic cerebellar ataxia.

3. Shy-Drager Syndrome. Clinical picture orthostatic hypotension and other manifestations of progressive autonomic failure.

In children early age spinal cord can be identified Kugelberg-Welander amyotrophy. This hereditary disease, characterized by hyperplasia of the connective tissue, beam atrophy and hypertrophy of muscle fibers.

Causes

Factors provoking general cachexia:

1. Lack of nutrients;
2. Oncological diseases;
3. Lesions of the hypothalamus (cerebral cachexia);
4. Endocrine disorders(spinal cachexia);
5. Long-term infectious diseases.

The list of causes of local atrophy:

1. Pressure on an organ or part of it;
2. Limitation of motor activity and muscle load;
3. Violation of blood circulation due to ischemic lesions veins and arteries;
4. Innervation;
5. Severe intoxication of the body with serious infections;
6. Hereditary predisposition;
7. Radiation exposure;
8. Long-term use hormonal drugs;
9. Dishormonal disorders.

As an example, foci of atrophy of the left ventricle can be formed from blockage of the lumen of the artery that feeds this part of the heart, and the optic nerve - diseases of the retina, brain, its vessels, and so on. Loss of a tooth can lead to atrophy of the jaw bone.

Clinical manifestations

The symptoms of this pathology are diverse and depend on the nature of the lesion, localization, prevalence and severity.

With cachexia, the patient has a general loss muscle mass He is emaciated, thin. Progression leads to atrophy internal organs and brain cells.

Partial atrophy of the optic nerve is expressed in a decrease in vision, a sharp limitation or absence peripheral vision, the appearance of spots on objects when they are examined. The progression of the process may end total loss vision (complete atrophy of the optic nerves), not amenable to correction.

Symptoms of retinal atrophy - loss of clarity, the ability to distinguish colors. Gradual deterioration of vision leads to optical illusions. One of the outcomes of the disease is complete blindness.

Signs of skin atrophy - dryness, thinning, loss of elasticity. Foci of thickening of the skin may be observed due to the formation of connective tissue and dystrophy with colloidal skin degeneration, or idiopathic atrophy.

Patients with Kugelberg-Welander's disease first complain of difficulty walking, then atrophy passes to the hands, reducing muscle tone, disrupting their motor activity. Tendon reflexes fade away, various deformities are formed: feet, legs, chest and others.

Atrophy of the nasal mucosa leads to the shutdown of all its functions, and complete atrophy leads to a decrease in bones, the absence of cartilage and turbinates.

The process can affect the mucous membranes of the trachea, bronchi, which affects the lungs and the entire respiratory system generally. Thinning of the mucosa with the expansion of the lumen and scarring is an incomplete list of problems due to this pathology.
Decreased ovarian function with reduced estrogen secretion menopause threatens the atrophic process of the epithelium of the cervix.

Diagnostic methods

Each specific case of suspicion of a particular atrophy requires a specific set diagnostic measures.

The first and general step for any type of atrophy is a physical examination, consisting of history taking, visual examination, palpation, and so on. Laboratory research also required in all cases. Further diagnosis is different.

To detect atrophy of any organ, ultrasound diagnostics, computed or magnetic resonance imaging, scintigraphy, fibrogastroduodenoscopy, radiography, and so on.

For example, the main diagnostics for muscle atrophy is electromyography and muscle biopsy. laboratory method consists of defining certain indicators in general and biochemical analysis blood.

The diagnosis of optic nerve atrophy is made after analyzing the results of ophthalmoscopy, tonometry, fluorescein angiography and other studies.

Treatment

After establishing the cause that provoked the onset of the atrophic process, it is necessary to eliminate it, if possible. This will prevent further progression of the disease. Provided that atrophy and sclerotic lesions are not too advanced, it is possible to achieve partial or complete restoration of the structure and function of the damaged organ, or part of it. However, deep irreversible atrophic lesions are not amenable to any correction and treatment.

The choice of treatment is influenced by: the form, severity and duration of the disease, individual intolerance to medications, the age of the patient. If atrophy is the result of an underlying disease, then it is treated first. Other methods of treatment are selected strictly individually. Medical symptomatic and physiotherapeutic treatment, as a rule, is long-term. In some cases, they achieve positive effect, for example, stop the decrease in vision in retinal atrophy, and the treatment of another process may be ineffective.

Complications and consequences of atrophy

Atrophy leads to many consequences from the side different systems and organs: from a slight decrease in the volume of the structure, to complete drying of the organ. Clinically, this manifests itself in partial or complete blindness, a decrease in the functioning of the organ and related manifestations, immobilization, myxedema, infertility, dementia and other complications, up to death.

Atrophy is accompanied by the loss of some cells or their structural components, due to which they decrease in volume.

Causes of atrophy:

  • insufficient functional load,
  • pressure on the tissue by a growing tumor or organ contents,
  • loss of innervation
  • decreased blood supply,
  • inadequate nutrition,
  • cessation of endocrine stimulation,
  • aging.

Types of atrophy:

  1. dysfunctional (atrophy from inactivity) develops as a result of a lack of function (for example, atrophy of the muscles of a limb when its bone is fractured);
  2. pressure atrophy (atrophy of brain tissue due to pressure cerebrospinal fluid, accumulating in the ventricles of the brain with hydrocephalus, etc.);
  3. atrophy due to insufficient blood supply (kidney atrophy due to stenosis renal artery atherosclerotic plaque);
  4. neurotrophic atrophy that occurs when tissue innervation is disturbed (skeletal muscle atrophy as a result of the destruction of motor neurons in poliomyelitis);
  5. atrophy from the action of damaging (chemical or physical) factors (for example, atrophy of the bone marrow under the action of radiation energy).

Some of the above atrophic changes are physiological in nature (eg cessation of endocrine stimulation at menopause), others are pathological (eg loss of nerve trunks).

Basically, changes in cells are of a similar nature and are expressed by such a decrease in the volume of cells, in which their survival is still possible.

In many cases, atrophy is accompanied by a marked increase in the number of autophagic vacuoles or autolysosomes. These vacuoles are associated with membranes inside cells and contain fragments of cellular components: mitochondria, endoplasmic reticulum. These fragments are various stages destruction, and in them autolysosomes release their hydrolytic enzymes. Then the remains of cellular components are digested.

Cell fragments inside autolysosomes are not digestible and are stored as residual bodies. An example of such residual bodies are granules of lipofuscin. They give the fabric a brown color. With the so-called general atrophy, or cachexia, this process is called brown atrophy.

Atrophy can progress to the point at which damage to the cell leads to its death. If the blood supply is not adequate to the level that supports the life of even severely atrophied cells, damage occurs, then the destruction of the cell, and then the replacement of the vacated space with connective or adipose tissue.

Pathological atrophy can be local and general.

Local atrophy for reasons and mechanisms of development are distinguished:
1. Atrophy from inactivity (dysfunctional). It develops as a result of a decrease in organ function. For example, in the treatment of fractures, in immobilized skeletal muscles and bones. Prolonged bed rest, physical inactivity leads to rapid atrophy skeletal muscles. After the loss of muscle fibers, the restoration of the previous volume occurs due to the hypertrophy of the remaining cells. This is a long process. Bone atrophy is manifested in a decrease in the size of the trabeculae, which leads to osteoporosis from inactivity. Inactivity atrophy refers to atrophy of the optic nerve after enucleation of the eye.

2. Atrophy caused by ischemia. It develops as a result of narrowing of the lumen of the arteries that feed the organ. Hypoxia leads to a decrease in cell volume and to a decrease in organ function. In addition, hypoxia provokes the proliferation of fibroblasts and the development of sclerosis. As an example, the development of cardiosclerosis due to progressive atherosclerosis coronary arteries.

3. Atrophy from pressure. Large Encapsulated benign tumor can cause organ atrophy. When the pressure of the aneurysm is bone tissue patterns may form.

4. Atrophy during denervation (neurotic atrophy).

5. Atrophy as a result of a lack of trophic hormones, such as hormones of the pituitary gland, adrenal glands, gonads.

6. Atrophy under the influence of physical and chemical factors. Under the influence of radiation, pronounced atrophy occurs in bone marrow and genitals.

With local atrophy, the organ either decreases in size or is enlarged due to the accumulated fluid or the growth of the stromal component. With smooth atrophy, the folds of the organ are smoothed out, with a granular form, the organ takes on a bumpy appearance.

Allocate brown atrophy, in which the size of the cells decreases. This is due to a decrease in the intensity of cellular metabolism.

General atrophy (cachexia). Her reasons:
1. Lack of nutrients.
2. Cancer exhaustion.
3. Endocrine cachexia (for example, in Simmonds disease).
4. Cerebral cachexia (with damage to the hypothalamus).
5. Cachexia in chronic infectious diseases(for example, tuberculosis).

With general atrophy, fat first disappears from fat depots, then skeletal muscle atrophy occurs. The following suffer internal organs, then the heart and brain. In the liver and myocardium, there are processes of brown atrophy.

When the cause that caused the atrophy is eliminated, provided that the atrophic and sclerosing processes have not gone too far, it is possible to fully or partially restore the structure and function of the damaged organ. Deep atrophic changes are irreversible and non-curable.

Atrophy

Atrophy (Greek atrophia, lack of food, wilting) is a process characterized by a decrease in volume and size, as well as qualitative changes in cells, tissues and organs that are expressed to some extent. However, the phenomena of atrophy are not always pathological. Some organs at a certain age undergo atrophic changes due to age-related weakening of their functions. Such physiological atrophy (age-related involution) is observed, for example, in the thymus, ovaries and mammary glands. With senile atrophy as a physiological phenomenon, thinning and loss of elasticity of the skin, rarefaction of the spongy and thinning of the compact bone substance (osteoporosis), a decrease in the size of the internal organs and the brain, accompanied by a decrease in the thickness of the cerebral convolutions, are observed. Pathological atrophy differs from the physiological one both in the causes of occurrence and in some qualitative features. The basis of atrophy is the predominance of dissimilation processes over assimilation processes due to a decrease in the activity of cytoplasmic enzymes. Depending on the cause of atrophy, there are: 1) neurotic atrophy; 2) functional atrophy; 3) hormonal atrophy; 4) atrophy from malnutrition; 5) atrophy as a result of exposure to physical, chemical and mechanical factors.

Neurotic atrophy develops with traumatic or inflammatory destruction of the nerve conductors between the organ and nervous system, as well as in the destruction of nerve cells. It is observed in striated muscles (Fig. 1) with the death of motor nerve cells of the anterior horns of the spinal cord or with the disintegration of peripheral nerve trunks, for example, in acute poliomyelitis, progressing muscular atrophy. In this case, atrophy can also spread to the skin and bones.

Functional atrophy develops as a result of a decrease in the activity of the organ and is referred to as atrophy from inactivity. Due to insufficient cell function, there is a weakening or even absence of incentives necessary to maintain at a certain level the processes of assimilation and dissimilation in the cells of an inactive organ. Functional atrophy is observed in the muscles of the limbs with bone fractures and joint diseases that limit movement. This group includes: atrophy of the edges of the tooth socket, devoid of a tooth, atrophy of the entire alveolar process of the jaw in the absence of teeth, atrophy of the pancreatic parenchyma during ligation of its excretory duct, atrophy of the nerve trunks when specific excitation through them ceases, for example, atrophy of the optic nerve after removal of the eye apples.

Hormonal atrophy develops as a result of a violation of the activity of the endocrine glands. This group of atrophies includes: pituitary cachexia, which develops due to insufficiency of the pituitary gland, thyroid-induced cachexia, which occurs with a decrease in thyroid function. With the latter, they develop dystrophic changes in the skin in the form of mucous edema.

Atrophy from malnutrition can be general and local. General atrophy, or cachexia, develops with insufficient or malnutrition, as well as as a result of a profound metabolic disorder. Cachexia is observed in severe, debilitating diseases (tuberculosis, malignant neoplasms, diseases of the digestive system, starvation, chronic intoxication, diseases endocrine system) and is expressed by increasing general emaciation and atrophy of internal organs and muscles. There are cases of the development of severe forms of malnutrition due to damage diencephalon, the so-called cerebral cachexia. With cachexia of any origin, body weight gradually decreases, the volume of organs and cells decreases, some organs (liver, heart) take on a brown color. Atrophic changes in cachexia develop unevenly: some organs and tissues atrophy more strongly, others less. Later than in other organs, atrophic changes develop in the brain, first of all in subcutaneous tissue, in striated muscles. Local atrophy from lack of nutrition occurs due to narrowing of the lumen of the arteries. Yes, atherosclerosis. cerebral vessels leads to atrophy of the brain tissue, atherosclerosis of the vessels of the kidneys - to local atrophy, and wrinkling (Fig. 2). The atrophy is based on insufficient blood flow associated with local mechanical causes.

Atrophy due to action physical factors occurs when the body is exposed to radiant energy, which causes especially strong atrophic changes in the skin, lymph nodes, testicles and ovaries.

Atrophy as a result of the action of chemical factors includes atrophic changes in thyroid gland caused by the use of iodine. Atrophy from the impact of mechanical factors should include atrophy from pressure. It is observed in cases when any tissue is under the influence of a pressing force, for example, in the bone when it is compressed by a tumor node or an aneurysmal sac.

At the same time, the bones become thinner and deepenings, uzuras appear in them, which are formed in the areas of greatest pressure. Atrophy from pressure is observed in the kidney with difficulty in the outflow of urine (blockage of the lumen of the ureter with a stone). The urine accumulated in the pelvis puts pressure on the kidney parenchyma, the kidney tissue atrophies, the function gradually stops - hydronephrosis develops. Aatrophy from pressure develops in the brain with internal dropsy, when the outflow of cerebrospinal fluid from the ventricles of the brain becomes difficult. The fluid, accumulating to the cavities of the ventricles, puts pressure on the brain tissue, which leads to its thinning, as well as to the thinning of the bones of the skull.

The most sensitive to a lack of nutrition in the body is the parenchyma, that is, specific functioning elements. The interstitial tissue, the stroma, either does not participate in the process of atrophy, or even increases in volume. During atrophy, the parenchyma cells decrease (Fig. 3), primarily due to the compaction of the cytoplasm, and then the nucleus, and the death of cytoplasmic ultrastructures. With prolonged exposure to a damaging factor, the cell may completely disappear; this leads to the fact that along with a decrease in the volume of cells, their number also decreases. In the cells of certain organs, such as the liver, nerve cells, in muscle fibers, during atrophy, accumulation in the cytoplasm near the nuclei of a brown fat-protein pigment - lipofuscin. This gives the organ a brown color, and in such cases they speak of brown atrophy. During atrophy, cell nuclei retain their normal appearance for a long time and do not decrease in volume, but then they gradually wrinkle and disappear as a result of karyolysis when cells die. Sometimes in the muscles, in the liver, in the kidneys, atrophic multiplication of nuclei is observed as a manifestation of a kind of regenerative process.

In some organs (heart, lungs), with atrophy, the thickness of the walls decreases, while the cavities of the organ either decrease or expand. The latter is observed, for example, with emphysema, when, with atrophy and rupture of the alveolar septa, the lumen of the alveoli increases significantly, as does the volume of the entire lung. The consistency of the organ during atrophy is dense due to the relative predominance of the connective tissue stroma in it, which is not subject to atrophy. The edge of an atrophied organ, such as the liver, acquires a leathery character and is pointed (Fig. 4). The surface of the organ can be either smooth (smooth atrophy), or, due to the uneven distribution of the atrophic process, it becomes granular (granular atrophy), which is observed with arteriolosclerosis of the kidneys and cirrhosis of the liver. In muscles during atrophy, interstitial fatty tissue sometimes grows significantly (Fig. 1), which leads to a false impression of an increase in their volume (false hypertrophy).

Such a replacement, vacant, growth is sometimes observed around an atrophied organ, such as a kidney, pancreas.

Atrophy up to a certain phase is a reversible process. This can be observed, for example, in striated muscle atrophy that develops with trauma or poliomyelitis. In advanced cases of atrophy, when the structure of the organ is severely disturbed, full recovery it does not come.

With atrophy, the function of the organ decreases. So, atrophy of the glandular organs is accompanied by a decrease in secretion; with testicular atrophy, there is no spermatogenesis; atrophy of the pancreas leads to a violation of the metabolism of carbohydrates, fats and proteins and indigestion. With atrophy from pressure, for example, an aneurysmal sac on the spine, in the presence of a deep usury, the process may be complicated by compression of the spinal cord, and with pressure on the sternum, its complete destruction with protrusion of the aneurysm under the skin; chest.

Due to the fact that atrophy develops gradually, some of its types can be recognized and prevented at an early stage of development. With the timely elimination of the cause that caused the atrophy, a cure occurs with the restoration of the structure and function of the atrophied organ.

See also Hypoplasia, Degeneration of cells and tissues.

Are you categorically not satisfied with the prospect of irretrievably disappearing from this world? You don't want to end your life path in the form of a disgusting rotting organic mass devoured by grave worms swarming in it? Do you want to return to your youth to live another life? Start all over again? Fix the mistakes you've made? Fulfill unfulfilled dreams? Follow this link:

@ 2023 wowway.ru - Diets and nutrition. Diagnostics and analyses. Medicines. Cholesterol. Atherosclerosis