Body dystrophy, degrees of dystrophy. Dystrophy in infants

Dystrophy is a violation of metabolic processes, as a result of which the normal development of the body or individual organ slows down. The disorder can be detected at any age. However, it is most often diagnosed in children. Let us consider further the causes and symptoms of dystrophy of different types.

Muscle damage

Muscular dystrophy is a chronic hereditary pathology. It is expressed in the degeneration of the muscles that support the bone skeleton. Currently, 9 varieties of this pathology are known. They differ in the location of the disorder, characteristics, intensity of development, and age characteristics.

Predisposing factors

Modern medicine cannot identify all the mechanisms that trigger the degenerative process. However, it has been clearly established that muscular dystrophy is caused by mutations in the autosomal dominant genome responsible for the regeneration and synthesis of proteins involved in the formation of muscles. The location of the pathology varies, depending on the specific chromosome damaged during the changes.

Clinical picture

Muscular dystrophy is characterized by a set of main manifestations. However, depending on the location of the disorder, specific symptoms may be observed. The main manifestations include:

Gait disturbances. They arise due to a deficiency of muscle mass in the lower extremities.
Decreased muscle tone.
Skeletal muscle atrophy.
Loss of motor abilities acquired before the onset of pathology. In particular, the patient stops holding his head, sitting, and walking. Other skills may also be lost.
Dulling of pain sensitivity in the muscles.
Increased fatigue.
Frequent falls.
Replacement of muscle fibers with connective tissue. This leads to an increase in muscle volume, which is especially noticeable in the calf part.
Difficulties arise when jumping and running, getting up from lying and sitting positions.
Decrease in intelligence.

It must be said that muscle dystrophy cannot be completely cured. The therapeutic measures provided today are aimed at maximizing the relief of the clinical manifestations of the pathology and preventing complications.

Effect on weight

The main and most obvious symptom of dystrophy is loss of body weight. In this case, the pathology has several forms and degrees. In particular, there are:

Hypotrophy. It is characterized by insufficient weight relative to the patient's age and height.
Hypostatura. In this case, the lack of mass and insufficient growth are uniform.
Paratrophy. It is characterized by excess weight relative to body length.

The first form is considered the most common.

Degrees

There are also three of them. The main difference between the degrees is the intensity of the pathology. In addition, they differ in the level of body mass deficiency. To determine the degree of dystrophy, the patient’s actual weight is compared with the normal value typical for people of his age and gender. 1 tbsp. - weight deficit 10-20%, 2 - 20-30%, 3 - more than 30%.

Kinds

Classification of pathology can be carried out according to various criteria. One of them is the time of occurrence:

Prenatal dystrophy. This disorder occurs during fetal development. As a result, the child is born with the disease.
Postnatal dystrophy. This disorder develops after birth. This type of pathology is classified as an acquired disease.

In addition, there is a combined form. In this case, deviations in weight are the result of factors both in the prenatal period and after birth.

Additional classification

Dystrophy can be primary or secondary. The first arises and develops as an independent disease. At the same time, its course is influenced by a variety of factors. The secondary form is a consequence of past diseases, as a result of which food digestion slows down and metabolic processes are disrupted.

Congenital pathology

The main reason why intrauterine dystrophy occurs is toxicosis during pregnancy. It has also been found that conceiving a child before 20 or after 40 years also significantly increases the risk of developing the disease. Negative factors such as constant stress, unbalanced nutrition, lack of useful elements in food, smoking, and other bad habits are of no small importance. The occurrence of congenital dystrophy can also be caused by the work of a pregnant woman in hazardous production conditions, in enterprises that process chemical compounds. Of particular importance are the woman’s own pathologies.

Postnatal form

Its occurrence is associated with the influence of internal and external factors. The first include:

Deviations of physical development.
Disturbances of the endocrine system.
Disturbances in the central nervous system.
AIDS.

A separate group consists of factors such as food allergies and some hereditary diseases. Among the latter, in particular, cystic fibrosis, lactase deficiency, celiac disease, etc. Another very large group includes gastrointestinal pathologies. They are observed mainly in adult patients. These include:

Oncological diseases.
Polyps (multiple or single).
Gastritis.
Pancreatitis.
Cholecystitis.
Gallstone disease.

External factors

These include circumstances due to which the patient does not receive the required amount of nutritional compounds to form normal body weight. First of all, this is a nutritional factor. He is considered the most essential in the group. If we talk about children, dystrophy develops in them due to a lack of breast milk, an incorrectly selected formula for feeding, or the late introduction of complementary foods. In adults, the disorder begins as a result of a calorie deficit, an unbalanced diet, or a high or low content of carbohydrates or proteins. The second factor is toxic. It is associated with poor ecology, food poisoning and other forms of intoxication, and prolonged use of medications. Another factor is social. In children, frequent causes of dystrophy are constant quarrels with parents and lack of proper attention on their part. In adults, predisposing factors are frequent stress, problems at work or in personal life.

Features of manifestation

Dystrophy can be accompanied by minor symptoms or cause serious problems. Common symptoms include weight loss, loss of appetite, growth retardation (in children), fatigue, and sleep disturbances. The severity of the pathology will influence the intensity of the clinical picture.

Some stages of the disease have specific symptoms.

The first degree is characterized by anxiety, sleep disturbance, and loss of appetite. These symptoms are irregular and mild. In addition, the patient has a decrease in the elasticity of the skin and weak muscle tone. In some cases, minor problems with stool (diarrhea, constipation) are noted. If the disease occurs in a child, he will be more susceptible to infections than his peers. It should be said that weight loss (10-20%) is often difficult to distinguish from ordinary thinness.

At the second stage of the pathology, the signs become more pronounced. Patients begin to sleep poorly and move less. They often refuse to eat. There is a significant decrease in muscle tone. The skin becomes flabby, dry, and there is sagging of the integument. The thinness increases, the ribs become visible. In addition, wasting is observed in the arms and legs. There are obvious deviations in weight; children are 2-4 cm behind their peers in height. In addition, patients experience frequent vomiting, nausea, and regurgitation (in children). There may be undigested food in the stool. Vitamin deficiency develops intensively, manifested by dry skin, brittle hair and nails. Cracks appear in the corners of the mouth. There are also disturbances in thermoregulation. The body quickly cools down or overheats. The nervous system also suffers. The person becomes loud, nervous, restless.

At the third stage, external signs of pathology become very pronounced. The man looks like a mummy.

Liver

As you know, this organ performs the most important functions. In the presence of predisposing factors, fatty liver degeneration may develop. It is a chronic pathology of a non-inflammatory nature. The disease manifests itself as the accumulation of fatty inclusions in the organ, the degeneration of hepatocytes due to metabolic disorders. It has been established that pathology occurs in women 1.5 times more often than in men. As a rule, fatty liver is diagnosed after 45 years of age. In the absence of adequate therapy, the disease may progress. The consequences can be quite serious, including the death of the patient.

Therapy

Treatment of dystrophy is carried out with drugs such as:

"Essentiale", "Essliver", "Phosphogliv".
"Heptral", "Glutargin", "Methionine".
"Hofitol", "Gepabene", "Karsil".

Patients are also prescribed vitamins B2, PP, E and C. In addition, Ursosan, Ursofalk, etc. are prescribed. All medications are selected individually.

Retinal dystrophy

This is the name of a fairly large group of various pathologies. Regardless of the provoking factor, the nature and characteristics of the course of the disease, tissue death is the main symptom that characterizes eye dystrophy. Treatment of pathology should be carried out in a timely manner and adequate to the clinical picture. It is worth saying that the disease is accompanied by intense vision loss. Therefore, in the absence of timely and qualified assistance, complete blindness can occur. Retinal dystrophy is usually diagnosed in people suffering from diabetes, atherosclerosis, hypertension, and excess weight. The provoking factor is smoking. The development of pathology can be influenced by stress, viral infections, excessive exposure to sunlight, and lack of microelements and vitamins.

Retinal dystrophy: treatment

When treating pathology, an integrated approach is used. First of all, the patient is prescribed vasodilators. These, in particular, include drugs such as “No-shpa”. The patient is also prescribed:

Angioprotectors - Vazonit, Actovegin, Ascorutin, etc.
Antiplatelet agents - the drug "Thrombostop", for example.
Vitamins E, A and group B.

Regular use of medications can reduce or even completely stop the development of the disease. If the pathology has reached a more severe stage, physiotherapeutic methods are used. Among the main ones we can note laser stimulation of the retina, photo-, magnetic-electric stimulation.

Sometimes processes occur in the body that disrupt metabolic processes in the cells of the body. There are several reasons and factors contributing to this phenomenon. The result of this pathology is irreversible processes that lead either to an increase in the patient’s weight or to its rapid loss.

This phenomenon is called obesity or this is how dystrophic changes occur. The latter disease has many features.

A condition such as dystrophic changes in the body occurs in people with metabolic problems. Under the influence of certain factors, damage to cells and the space between them occurs in the human body, which leads to disruption of the functional characteristics of the organ in which such processes arose.

According to medical terms, dystrophic changes are a pathology leading to disruption of trophism, i.e., a certain set of mechanical processes responsible for the metabolism and integrity of cells of organs and tissues.

Based on the functions they perform, trophics are divided into cellular and extracellular. Depending on which trophism undergoes changes, the type of dystrophy acquired, as well as its symptoms, depends.

Children in the first three years of life are most susceptible to this disease. But the disease also occurs in adults under the influence of a number of factors. There is even such a type of pathology as chronic dystrophic changes - a disease whose symptoms appear in some people every 2-3 years. But the treatment of this disease gives good results and, if certain requirements are met, periods of exacerbation become less frequent.

This disease can easily spread to the entire body, then it falls under the “systemic” classification, i.e. general, or can be localized in one organ. In this case, the disease is called local. This separation is extremely important, because the treatment, as well as the symptoms, in this case, are completely different.

The etiology of the disease is also important. The causes and symptoms of acquired and congenital dystrophy have significant differences. The congenital disease begins to manifest itself from the very first months of the baby’s life.

This illness can be explained simply: the child has a genetic deficiency of certain substances involved in metabolic processes. The result is the accumulation of undigested proteins, fats or carbohydrates in the tissues of the body, which ultimately cause disruption in the functioning of one or another organ. Irreversible processes inevitably occur in the nervous system. Treatment of congenital dystrophy is impossible, and therefore death occurs in 100% of cases: most children with congenital dystrophy do not even live to see their first birthday.

Genetic varieties of dystrophy

In addition to general dystrophy, there is also local dystrophy, affecting one or another organ or a certain part of the body.

The most famous is Duchenne muscular dystrophy. This is a congenital genetic disease that is inherited. Duchenne muscular dystrophy is an exclusively male disease. It is characterized by symptoms such as decreased muscle tone and disruption of the central nervous system.

But the gene responsible for the development of such a disease as Duchenne muscular dystrophy is carried exclusively by girls. Representatives of the fairer sex also suffer from certain types of muscle dystrophy, but the symptoms of the disease are weaker, and therefore they are not diagnosed with Duchenne muscular dystrophy.

The disease is diagnosed in childhood. If a child does not begin to walk by the required age or falls frequently, the pediatrician may assume that the baby is developing a disease. After an examination by an orthopedist and certain examinations (blood test, muscle test, muscle biopsy), this diagnosis is either confirmed or refuted.

If the disease is present, over time, dystrophic changes will affect all parts of the child’s body: the muscles will weaken, then atrophy, the joints will become deformed and lose their shape.

Treatment for this disease is impossible, since the disease is a genetic disease. But psychological support and social adaptation are indicated for the baby and parents.

The next type of genetic disease is myotonic dystrophy. It is characterized by changes not only in muscles and bones, but also in the pancreas, thyroid gland, heart and brain. Myotonic dystrophy is equally common in both sexes, but women are also carriers. Myotonic dystrophy manifests itself as atrophy of the facial muscles, impaired vision and heartbeat, baldness, and in severe cases, mental retardation.

Dystrophies of internal organs

The most well-known dystrophy of internal organs is fatty liver. This is a condition in which islands of fat appear in the main filter of the human body, replacing the cells of the liver itself.

Often fatty liver disease does not manifest itself in any way, but if treatment is not carried out, the disease progresses to cirrhosis of the liver or acute liver failure. Fatty liver disease is treated quite simply - the patient is usually prescribed an enhanced, nutritious and balanced diet.

If metabolic processes are disrupted in the cells that form the patient’s heart muscle, myocardial dystrophy occurs. Myocardial dystrophy occurs for various reasons. Its appearance is promoted by a lack of certain vitamins, nutritional dystrophy, and poisoning by toxic substances.

Myocardial dystrophy is a consequence of certain ailments of the cardiovascular system, and therefore myocardial dystrophy does not have clear signs specific to it. Treatment in this case is aimed at restoring metabolic processes in the cells of the heart, its correct rhythm and nutrition of its cells. Myocardial dystrophy often leads to acute heart failure and death.

Dystrophic changes in the organs of vision

If processes are observed in the eyeball in which its tissues die, a diagnosis of retinal dystrophy is made. If it is not treated, it always leads first to deterioration and then to complete loss of vision. Eye dystrophy has two forms: acquired and hereditary, i.e. congenital. It is divided into two types: peripheral and central.

Peripheral eye dystrophy usually occurs in people who have suffered damage to the eyeballs, suffering from myopia or myopia. Central retinal dystrophy of the visual organs is an age-related phenomenon that affects older people who lead an unhealthy lifestyle or live in environmentally unfavorable areas.

It manifests itself as visual impairment: loss of its sharpness, brightness and clarity. If retinal dystrophy is not treated or the patient treats it independently, there is a high probability of complete atrophy of the eyes.

It is treated by an ophthalmologist using laser operations and medications. There are also folk recipes for this disease, but their use must be agreed with a specialist.

Another type of visual dystrophy is corneal dystrophy. This disease belongs to the category of hereditary, i.e. congenital. It manifests itself in various visual impairments in a child. It has several types, depending on the tissues in which it develops.

In addition to visual impairment, corneal dystrophy manifests itself as pain in the eyes, lacrimation, and aversion to bright light. Corneal dystrophy is treated depending on its type. This usually involves the use of medications, physical therapy, and surgery. Corneal dystrophy may not be passed on to the child if the mother received all the necessary nutrients during pregnancy and got enough sleep.

This disease affects not only internal organs, but also such parts of the body as fingers, or more precisely, nails. A condition in which the nail plate changes its shape is called nail dystrophy.

There is only one reason why nail plate dystrophy develops - violation of the rules for caring for it, mistakes in manicure, or simply failure to comply with hand hygiene. These factors can be complemented by weakened immunity, lack of vitamins, poor environment, infectious diseases and hand injuries.

Nail dystrophy has several varieties, differing in the location and degree of damage to the stratum corneum and nail bed. The symptoms of nail dystrophy are deformation and separation of the nail plate, and its thinning.

Treatment in this case involves eliminating the provoking factor and strengthening the nails using natural and medicinal means.

Weight loss due to poor diet

The most common type of this disease is nutritional dystrophy. It develops as a result of the patient’s proper nutrition. Nutritional dystrophy is the result of malnutrition, starvation, and exclusion of certain nutrients from the diet. The body simply does not have enough food and it uses up its existing reserves - subcutaneous fatty tissue.

When this supply runs out, the body begins to consume proteins, which are the mainstay of internal organs. Thus, nutritional dystrophy leads to atrophy of muscles, some organs and endocrine glands. The symptoms of the disease are indirect: nutritional dystrophy manifests itself as pain in the body, a constant feeling of hunger, and increased fatigue.

If treatment is not carried out, nutritional dystrophy leads to pathological changes in the heart muscle, stomach and intestines, muscles and bones, and the endocrine system. It has several degrees of severity. Treatment usually consists of increased nutrition and elimination of symptoms of the disease.

A practicing journalist, he tests recipes on himself.
Knows everything about men and traditional medicine.

A process as a result of which a particular tissue loses or accumulates substances that are not normally characteristic of it (for example, anthracosis - the accumulation of coal particles). Dystrophy is characterized by damage to cells and intercellular substance, as a result of which the function of the organ changes. Dystrophy is based on a violation of trophism, that is, a set of mechanisms that ensure metabolism and preservation of the structure of cells and tissues. Trophic mechanisms are divided into cellular and extracellular. Cellular mechanisms are provided by the very structure of the cell and its self-regulation, due to which each cell performs its characteristic function. Extracellular mechanisms include a system for transporting metabolic products (blood and lymphatic microvasculature), a system of intercellular structures of mesenchymal origin and a system of neuroendocrine regulation of metabolism. If there is a violation in any link of the trophic mechanisms, one or another type of dystrophy may occur.

Classification

By type of metabolic disorder

protein (dysproteinoses)
fat; (lipidoses)
carbohydrate;
mineral;

By localization of manifestations

cellular (parenchymal);
extracellular (stromal-vascular, mesenchymal);
mixed.

By prevalence

system(general);
local.

By etiology

acquired;
congenital:

Congenital dystrophies are always genetically determined diseases, hereditary disorders of protein, or carbohydrate, or fat metabolism. Here there is a genetic deficiency of one or another enzyme that takes part in the metabolism of proteins, fats or carbohydrates. This leads to the accumulation of incompletely broken down products of carbohydrate, protein, and fat metabolism in the tissues. It occurs in a wide variety of tissues, but the tissue of the central nervous system is always affected. Such diseases are called storage diseases. Sick children die during the first year of life. The greater the enzyme deficiency, the faster the disease develops and the earlier death occurs.

Morphogenesis

There are 4 mechanisms leading to the development of dystrophy:

Infiltration
Decomposition (phanerosis)
Perverted Synthesis
Transformation

Notes

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Synonyms:

See what “Dystrophy” is in other dictionaries:

Dystrophy... Spelling dictionary-reference book

Modern encyclopedia

Greek, from dys, and trephein, to nourish. Bad, insufficient nutrition. Explanation of 25,000 foreign words that have come into use in the Russian language, with the meaning of their roots. Mikhelson A.D., 1865. dystrophy (dys... gr. trophe nutrition) eating disorder... ... Dictionary of foreign words of the Russian language

Dystrophy- (from dis... and Greek trophe nutrition) (degeneration, degeneration), a pathological process consisting in the replacement of normal cell components with products of metabolic disorders or their deposition in the intercellular space. In the wide... ... Illustrated Encyclopedic Dictionary

- (from dis... and Greek trophe nutrition) the pathological process of replacing normal components of the cytoplasm with various ballast (or harmful) products of metabolic disorders or their deposition in the intercellular space. There are dystrophies... ... Big Encyclopedic Dictionary

Myopathy, hyalinosis Dictionary of Russian synonyms. dystrophy noun, number of synonyms: 7 amyloidosis (2) ... Synonym dictionary

dystrophy- and, f. dystrophie f., German Dystrophie dys.. times.., not..+ trophe nutrition. honey. A nutritional disorder of tissues, organs and the body as a whole, caused by metabolic disorders. Dystrophan a, m. Krysin 1998. Dystrophan a, m. jokel. About very bad... ... Historical Dictionary of Gallicisms of the Russian Language

DYSTROPHY, and, female. Violation of metabolism, nutrition of tissues, organs or the body as a whole. | adj. dystrophic, oh, oh. Ozhegov's explanatory dictionary. S.I. Ozhegov, N.Yu. Shvedova. 1949 1992 … Ozhegov's Explanatory Dictionary

I Dystrophy in children (dystrophia; Greek dys + trophē nutrition) chronic eating disorders in children. The following main types of dystrophy are distinguished: hypotrophy, hypostatura, paratrophy and hypertrophy (see Obesity). In addition, there is a special... Medical encyclopedia

AND; and. [from Greek dys not, times and trophē food, nutrition] Impaired nutrition of tissues and internal organs, the body as a whole, leading to their depletion. D. cardiac muscle. Alimentary disease (edematous disease as a consequence of exhaustion). ◁ Dystrophic, oh, oh... encyclopedic Dictionary

Books

Starvation disease (nutritional dystrophy), V.A. Svechnikov. Rarity! In this work, which aims to summarize our information and give a summary of our ideas about the disease, associated, first of all, with quantitatively insufficient and qualitative...
Facioscapulohumeral muscular dystrophy and its connection with facioscapulohumeral muscular dystrophy: history, clinical picture, genetics and differentials, Kazakov V.M.. ...

The fact is that I looked into the electron microscope and saw(shown in white in the image) between muscle fibers(Red color).

On the picture: muscle fiber biopsy for mild (A), moderate (B) and severe myopathy (C):

On the picture: normal muscle fibers of a healthy person:

Using the example of my patient who suffered. Emine's diagnosis: severe muscular dystrophy, confirmed by biopsy. Next, I will describe my approach to eliminating muscle weakness. I recommend watching a video on the topic of treatment of progressive Duchenne muscular dystrophy.

Muscular dystrophy is a disease of disruption of the creation of the protein that creates the framework of the muscle cell.

Holes form in the cell frame. Vital compounds and trace elements leak out of these holes. To patch up holes, the cell is forced to produce substances that are larger than these holes. The cell “swells” from the inside, i.e. swelling.
Increasing swelling puts pressure on muscle cells from the outside, pushing cell nuclei and mitochondria to the periphery.
The level of creatine phosphokinase in the cell increases and the muscle loses its ability to bind and retain creatine.
Creatine is needed by mitochondria to produce energy in the muscle cell.
Mitochondria reduce ATP production. ATP is the energy needed to operate the motor proteins actin and myosin. No energy - no movement.
Inside the muscle fiber, which is without movement, its own nutrition processes slow down.
The fiber membrane begins to secrete enzymes and amino acids that it does not need without the function of movement. Therefore, the theory of “defective membranes” arose.
During muscle movement, these enzymes and amino acids are needed. Their synthesis requires energy, which is not available. Therefore, muscle weakness occurs.
Muscle fiber atrophy begins.

Symptoms

The disease muscular dystrophy begins with the development of weakness and atrophy of a certain muscle group. Over the years, the dystrophic process captures more and more new muscle groups. This happens until complete immobility. The main symptom of myodystrophy is damage to the muscles of the pelvic, shoulder girdle and torso of the patient. The thigh muscles and shoulder muscles are affected in severe cases, which is what happened to the patient Emine: she could not stand up without support and walk, even short distances.

Muscular dystrophies bilateral

In the initial period, myodystrophy on one side may predominate, but as the disease develops, the degree of damage becomes the same in the patient’s symmetrical muscles. As the disease progresses, muscle strength decreases in almost all muscles. Areas of hypertrophic muscles appear on the body of a patient suffering from muscular dystrophy. This is pseudohypertrophy, which is not associated with an increase in muscle fibers. Pseudohypertrophy of muscles is associated with swelling in the muscles of the legs or arms. Such muscles are dense, but weak.

Forms of muscular dystrophy in adults

All figurative forms of the disease in question in adults differ:

types of inheritance;
the speed and nature of its flow;
the presence or absence of tendon retractions and pseudohypertrophies;
timing of the start of the process;
the unique topography of muscle pain;
other signs of progressive muscular dystrophy.

Issues of classification of myopathy (chronic and progressive hereditary muscle diseases) are being developed in different directions. Muscular dystrophy in adults is classified according to the type of inheritance:

Autosomal dominant.
Autosomal recessive.
Dominant and recessive.
Linked to the X chromosome.

Examination for myopathy

Clinical signs characteristic of muscular dystrophy are symptoms of flaccid paralysis in different muscle groups of a sick person without signs of damage to motor neurons and peripheral nerves. Neurologists the whole world cannot explain this.

Doctor Nikonov

My opinion: protein swelling between muscle fibers makes muscle movement impossible.

Not knowing this phenomenon bewilders doctors all over the world: “How is this possible? The muscle fiber is intact and undamaged. “Are motor neurons and peripheral nerves intact, in their proper places, and perfectly transmitting impulses from the brain to the muscles and from the muscles to the brain, but movements are difficult?”

Neurologists An electromyography is ordered. And again it’s a mystery to them: there are no changes in the structure of the muscle fiber. A decrease in the amplitude of the M-response, increased interference and polyphasic potential indicates difficulty in muscle movement without any pathology!

Pathological picture of the disease

Let's see what happens inside muscle cells in patients suffering from Duchenne muscular dystrophy. To do this, we will make an incision in the skin, expand it with an expander and take a small piece of muscle fiber.

A typical sign of muscular dystrophy is primarily a different diameter of muscle fibers. In a healthy person, the diameter of the muscle fibers is the same.

Characteristic signs of muscular dystrophy are atrophied and hypertrophied fibers, multiple internal nuclei and edema.

Examining stained sections of skeletal muscle, I observed denervation of myofibers, significant variation in myofibril size, and significant edema.

Explanation for the first photo:

The pale purple color is muscle fibers in cross-section.
Light spots both inside and outside the fibers are swelling.
Dark dots are nuclei that the edema has shifted to the periphery.

In the second photo normal muscle fiber of a healthy person is shown.

Severity of muscular dystrophy according to electron microscopy data, it is guided by the following indicators:

at mild degree the difference in the size of muscle fibers is moderate, initial signs of edema (white color).

On the picture: muscle fiber biopsy for mild (A), moderate (B) and severe dystrophy (C).

average degree severity corresponds to the movement of nuclei to the center of muscle fibers, expansion of the interfibrillar space due to increased edema between the cells.

On the picture: muscle fibers in progressive muscular dystrophy of moderate severity:

a) light purple muscle fibers;

b) light spots inside the muscle fibers - swelling, which has pushed the nuclei from the center of the cell to the periphery;

c) dark dots - muscle cell nuclei;

d) the arrow shows a muscle cell that cannot move due to a decrease in metabolic processes - darkens towards purple.

severe characterized by extensive foci of destruction of myofibrils, their fragmentation and disorganization, the appearance of hyaline-like substance and edema between muscle cells. Functionally, such tissue has weak strength, fatigue sets in quickly and signs of muscle fatigue develop. The photo will be presented a little lower.

This is the state of Emine’s muscles before contacting me:

Explanation of the photo“severe muscular dystrophy”:

Muscle fibers in section are colored blue.
The red dots are the nuclei of muscle cells.
The swelling is uncolored white.

Clinical picture of muscular dystrophy

Emine's first sign of Duchenne myopathy was weakness. She began to get tired with normal physical activity. Emine's earliest complaints were:

Fatigue when running, long walking.
Emine began to fall often.
Myalgia began to appear in the legs (pain in the muscle area), sometimes in combination with painful spasms.
Gradually walking began to become difficult.

Emine could not get up from the low chair without using her hands. When getting up, the woman resorted to using auxiliary techniques: “standing up with a ladder”, “climbing on one’s own” - Govers’ technique. A few years later, Emine could not get up from her haunches without help. The patient could not climb stairs.

After my influence on Emine’s muscles, she rises to the 17th floor without using her hands, immediately takes the elevator down and rises again to the 17th floor without getting tired!

Muscle atrophy develops mainly in the pelvic girdle and thighs (therefore, the emendic effect on Emine’s muscles was aimed at these areas).

The muscles of the upper limbs begin to atrophy later. Emine said that she could not pour herself tea or comb her hair. See the results of treatment for muscular dystrophy in the video below:

Dystrophy is a pathological process leading to structural changes in organs and tissues. Dystrophy is most often based on metabolic disorders, but dystrophy can also be a hereditary disease ( for example, retinal pigmentary dystrophy). During this process, cells and intercellular substance are damaged, which leads to loss of their function. Thus, the entire organ fails. For example, with corneal dystrophy, damage to its layers is noted, as a result of which it becomes cloudy and ceases to perform its main function.
There is a wide variety of dystrophies, classified according to systems, organs, causes, and so on.

Fatty liver

Fatty liver or fatty hepatosis is a syndrome manifested by various damage at the cellular level. Before we begin to describe fatty degeneration, you need to know that, depending on the cause, alcoholic and non-alcoholic fatty degeneration are divided. Both syndromes are characterized by the same morphological changes, namely fatty degeneration and an inflammatory response. The difference is that alcoholic liver dystrophy develops in people who abuse alcohol. With non-alcoholic dystrophy, the same changes are observed, but patients with this pathology are not characterized by systematic use of alcoholic beverages.

Characteristics of fatty degeneration at the cellular level
With this disease, pathological inclusions of fat are detected in liver cells. Fat droplets located in hepatocytes deform and disrupt cell function. As a result of this, they experience disturbances in cellular metabolism, leading to structural changes. Liver cells ( hepatocytes) and the intercellular substance die, which leads to a change in the function of the organ itself. The morphological diagnosis of fatty degeneration is made when the fat content in the liver exceeds 10 percent of the organ’s weight.

The liver is a vital organ that performs many functions. Thus, it is responsible for detoxification of the body, synthesis of hormones, and neutralization of various foreign substances. That is why the slightest disturbance in the structure of the liver leads to varied and numerous symptoms. The main cause of the development of fatty degeneration is considered to be an increased content of free fatty acids in the liver.

Non-alcoholic fatty liver

Synonyms for fatty liver are the terms fatty hepatosis, fatty steatosis, primary fatty degeneration. Non-alcoholic fatty degeneration, as a rule, is benign and asymptomatic. It is extremely rare to develop liver cirrhosis, hepatitis or liver failure. It was found that less than 10 percent of patients suffering from chronic hepatitis were previously diagnosed with fatty degeneration. This syndrome was first identified as an independent disease in 1980. Today, the detection rate of this pathology varies from 7 to 10 percent. For comparison, alcoholic fatty degeneration is diagnosed 15 times more often.

The causes of primary fatty degeneration are:

diabetes mellitus type 2;
hyperlipidemia ( increased levels of lipids in blood plasma).

Among the above reasons, the most significant are type 2 diabetes mellitus and hyperlipidemia. The first pathology includes metabolic syndrome and excess body weight. Hyperlipidemia is characterized by elevated levels of cholesterol or triglycerides in the blood plasma. Both lead to the accumulation of fat droplets in the liver cells and the development of fatty degeneration. Fatty liver degeneration can be provoked by certain medications with a hepatotoxic effect.

Medicines that cause fatty degeneration are:

amiodarone;
synthetic estrogens;
non-steroidal anti-inflammatory drugs.

Also, fatty liver can be a consequence of other diseases. Most often these are systemic diseases or metabolic pathologies.

The mechanism of formation of fatty degeneration
The basis for the formation of fatty liver is an increased concentration of free fatty acids in the blood. Normally, fatty acids accumulate in adipose tissue in the form of triglycerides. As needed, they enter the liver or muscles, where they are utilized. The need arises during times of severe stress, physical exertion or fasting. In these conditions, fats are broken down into free fatty acids and glycerol. After this, fatty acids are transported to the liver and oxidized. When too many acids enter the liver, the rate of their oxidation in the liver mitochondria decreases. Thus, the accumulation of fats occurs with their subsequent deposition in liver cells. When in a hepatocyte ( liver cell) too many drops of fat accumulate, the cell begins to deform and lose its function. This process is called fatty degeneration.

Next, a process called steatohepatitis occurs. It is characterized by inflammatory-necrotic changes in the liver parenchyma. The reason for this process is lipid peroxidation. As a result of peroxidation, free radicals are formed, which have a damaging effect on liver cells. Depending on the volume of fat droplets, as well as their quantity, several degrees of fatty degeneration are distinguished.

The degrees of fatty degeneration are:

zero degree– in certain groups of liver cells there are small droplets of fat;
first degree– moderately large droplets of fat are present in hepatocytes;
second degree– there is a phenomenon of intracellular obesity, which is characterized by diffuse ( common) large-droplet deposition of fat;
third degree– droplets of fat are deposited not only in the cell, but also outside it ( intracellular and extracellular fat deposition); The formation of fatty cysts is also typical.

Symptoms of fatty liver

Non-alcoholic fatty degeneration is observed mainly in women. According to the latest data, there are twice as many women with this disease as men. Most often, this pathology is registered in middle age ( 30 – 40 years). The main symptom of fatty hepatosis is a moderately enlarged liver. Further, the clinical picture is complemented by symptoms of liver dysfunction.

Symptoms of fatty degeneration are:

pain in the right hypochondrium;
asthenovegetative disorders;
increase in body weight.

Pain
Pain in the right side is one of the most common symptoms; it is observed in 60 percent of patients. The cause of pain is stretching of the fibrous capsule that covers the liver. There are no nerve endings in the liver itself, so any damage to it is not accompanied by pain symptoms. However, the top of the liver is covered with a membrane, which is abundantly supplied with nerve endings. When the liver is enlarged ( as in fatty degeneration), then the capsule covering it stretches, which provokes irritation of the nerve endings. Therefore, the more enlarged the liver is, the more pronounced the pain syndrome. With fatty liver, the pain is constant, dull and aching.

Dyspepsia
Dyspeptic symptoms with fatty liver are observed in more than 45 percent of patients. They are associated with stagnation of bile and deficiency of bile acids during digestion. Thus, bile acids break down fats into small particles, thereby ensuring their absorption. With a deficiency of bile, this does not happen, and therefore some patients develop intolerance to fatty foods. Also, dyspepsia with fatty hepatosis includes a feeling of heaviness in the abdomen, nausea and unstable stool.

Asthenovegetative disorders
This symptomatology occurs in one third of patients with fatty liver degeneration. It manifests itself with such symptoms as fatigue, weakness, headache. The cause of these symptoms may be a lack of vitamins or hypovitaminosis. Thus, some vitamins are synthesized in the liver. However, if its function is damaged, vitamin synthesis decreases and hypovitaminosis develops.

Weight gain
An increase in body mass index is observed in more than 45 percent of patients. This symptomatology is explained by metabolic disorders.

Alcoholic liver dystrophy

Alcoholic liver dystrophy is liver damage that develops as a result of systematic alcohol consumption. Ethanol has a toxic effect on liver cells, which leads to the development of alcoholic hepatitis. It is known that the main site of alcohol metabolism is the liver. A small part is metabolized in the lungs and kidneys. This explains such frequent liver damage during chronic alcohol intoxication.

Alcohol metabolism ( ethanol)
Under the influence of liver enzymes, ethanol breaks down into acetaldehyde. This releases a certain amount of calories ( There are 1,400 calories per 500 milliliters of ethanol.). But when ethanol is oxidized, the calories released have no nutritional value. This leads to the fact that the body’s existing reserves, namely proteins and fats, begin to disintegrate. The more ethanol is oxidized, the more fats are destroyed. Thus, fat becomes the main source of “fuel” for the body, which triggers the process of alcoholic fatty degeneration.
In addition to the above process, the liver is affected by the direct toxic effect of alcohol.

Stages of alcoholic liver dystrophy

Alcohol-induced liver damage often results in hepatitis or cirrhosis. How quickly the disease progresses depends on many factors, namely gender, age, and concomitant diseases. It is important to note that up to a certain stage, all changes in the liver are reversible. This means that with timely cessation of systematic alcohol consumption, the previous, normal structure of the liver is restored. This phenomenon is explained by high regenerative ( restorative) liver ability.

The stages of alcoholic liver dystrophy are:

first stage– actual fatty liver degeneration;
second stage– alcoholic liver hepatitis;
third stage– alcoholic cirrhosis of the liver.

First stage of alcoholic dystrophy
The first stage of alcoholic liver damage occurs in 60 percent of alcohol abusers. This stage is characterized by the same changes that occur with fatty liver degeneration. Fat deposition in hepatocytes occurs in the form of large large droplets. The main clinical sign is an enlarged liver, that is, hepatomegaly. The liver at this stage is moderately enlarged - by 3 - 4 centimeters. Therefore, the main complaint from the patient is pain. An enlarged liver stretches the capsule covering it and irritates the nerve endings, which causes pain. Also in the clinical picture at this stage there are symptoms such as nausea, bitterness in the mouth, unstable stool.

During a medical examination it is palpable ( palpable) moderately enlarged liver with smooth rounded edges. This characteristic of the liver is very important in the differential diagnosis. The first stage of alcoholic dystrophy is completely reversible.

Second stage of alcoholic liver dystrophy
Continued alcohol abuse leads to further damage to hepatocytes. Lipid peroxidation leads to damage to liver cell membranes and the development of an inflammatory reaction. A typical morphological feature at this stage is the presence of alcoholic hyaline in hepatocytes. In the second stage, the liver increases by 10–15 centimeters.

Alcoholic hepatitis in the second stage can be either acute or chronic. Acute alcoholic hepatitis develops suddenly, after prolonged drinking. Chronic alcoholic hepatitis develops gradually against the background of existing liver damage.

The clinical picture includes dull pain in the right hypochondrium, vomiting, diarrhea, and sudden weight loss. Jaundice often develops, which is characterized by icteric discoloration of the skin and mucous membranes, as well as skin itching. All liver enzymes are sharply elevated, the number of leukocytes rises, and the erythrocyte sedimentation rate reaches 50 millimeters per hour. As a rule, this stage progresses to cirrhosis.

The third stage of alcoholic liver dystrophy
The third stage or stage of cirrhosis is diagnosed in 10 to 15 percent of people who abuse alcohol. The main morphological characteristic of this stage is the formation of sclerotic nodes and restructuring of the liver architectonics. Destroyed hepatocytes are gradually replaced by connective tissue, which leads to deformation of the liver structure. The liver at this stage begins to decrease in size, which is an unfavorable sign. The clinical picture includes symptoms such as ascites ( popularly known as dropsy), gynecomastia ( breast enlargement in men), jaundice.

Treatment of fatty liver

Treatment of fatty liver is based on the complex use of vitamins, hepatoprotectors and other medications. In the first stages, regression of the disease and restoration of liver function are possible. In the later stages of fatty degeneration, symptomatic treatment is carried out. The goal of treatment is to slow down dystrophy and prevent the development of cirrhosis.

The groups of medications that are used in the treatment of fatty degeneration include:

vitamins;
hepatoprotectors;
corticosteroids.

Vitamin therapy
It is performed on all patients, regardless of the cause of the disease, since most have a vitamin deficiency. Vitamin therapy is especially important for alcoholic fatty degeneration. It is advisable to prescribe vitamins not in the form of tablets, but by parenteral administration ( intramuscularly or via intravenous drip). Vitamins B12, B1, B6, PP or combination drugs such as milgamma, demoton are prescribed. Milgamma is prescribed intramuscularly, one ampoule per day for a course of 10 days, Demoton - one ampoule every other day.

Hepatoprotectors
Hepatoprotectors are drugs that have a protective effect on the liver. This is a very large group of drugs that differ in origin and mechanism of action. Silymarin is widely used for prophylactic purposes. The mechanism of its action is due to the suppression of collagen synthesis by liver cells. Prescribed at a dose of 70–100 milligrams per day for 3 months. Ademethionine can be used instead of silymarin. The dose of ademetionine ranges from 800 to 1600 milligrams per day. Recently, essential phospholipids have proven themselves well. Studies have shown that they are most effective for alcoholic liver degeneration. An analogue of phospholipids is the drug Essliver Forte. In addition to essential phospholipids, it contains thiamine, riboflavin, pyridoxine hydrochloride, cyanocobalamin and tocopherol acetate. Thus, Essliver Forte not only prevents collagen synthesis, but also replenishes vitamin deficiency, which is observed in alcoholics. The drug is prescribed 2 capsules 3 times a day for six months.

Corticosteroids
Prescribed in exceptional cases, for example, with alcoholic hepatitis or in patients with hepatic encephalopathy. Recent studies have shown that the incidence of death in patients with alcoholic hepatitis is reduced when using 40 mg of prednisolone per day for 4 weeks. Less commonly recommended is pulse therapy, which is based on the use of high doses of steroids - from 300 milligrams per day for 2 to 3 days.

Muscular dystrophies

Muscular dystrophies are a group of hereditary diseases based on skeletal muscle dystrophy. Clinically, muscular dystrophies are manifested by muscle weakness, which limits the patient’s motor ability. Muscular dystrophies usually make their debut in infancy.

The mechanism of development of dystrophies is the dysfunction of voluntary muscles. Thus, in the human body there are three types of muscles - smooth and skeletal muscles, as well as myocardium ( heart muscle). Internal organs are composed of smooth muscle tissue ( stomach, intestines). The contraction of this type of tissue occurs involuntarily; a person cannot control it. Skeletal muscle is the muscle tissue that provides a person with movement. With muscular dystrophy, it is the skeletal muscles that are damaged, that is, the ones that provide a person with movement.

Types of muscular dystrophies include:

Duchenne dystrophy;
Becker muscular dystrophy;
myotonic dystrophy.

Duchenne muscular dystrophy

This is one of the most common forms of muscular dystrophy. The cause of Duchenne dystrophy is a genetic defect on chromosome X. This defect causes a deficiency of the protein dystrophin, which normally protects muscles from damage. With its deficiency, the muscles quickly break down and cease to function normally. Women with this defect do not develop the disease, but can pass the defective gene on to their children. If a male child receives this defective gene, he develops the disease. The onset of the disease occurs between the ages of 2 and 5 years.

Initially, dystrophy manifests itself in the muscles of the lower extremities and pelvic muscles. Further, “the disease rises higher” and affects the upper muscle groups. The morphological sign of Duchenne disease is degeneration ( destruction) muscle fibers. In their place, adipose and connective tissue begins to grow. A characteristic sign of this pathology is an increase in the calf muscles. This occurs due to the deposition of fat in them, as a result of which the muscles appear enlarged. This phenomenon is called pseudohypertrophy of the calf muscles and is characteristic mainly of Duchenne dystrophy.

Signs of Duchenne dystrophy include:

clumsy gait;
frequent falls;
difficulties when running, jumping;
constant weakness;
muscle contractures ( a condition when, due to involuntary muscle tension, the functions of the joint are limited).

Presymptomatic stage of Duchenne dystrophy
At this stage, symptoms of the disease have not yet appeared. However, there is often a delay
psychospeech and motor development in children. The diagnosis can only be made if there is a strong family history ( that is, if there were cases of Duchenne dystrophy in the family).

Early stage of Duchenne dystrophy
The main symptom of the early stage is increasing muscle weakness. A careful examination can reveal some positive symptoms of the disease. For example, when rising from the floor, a child rests his hands on his knees. This diagnostic symptom is called a positive Gowers test. A “duck walk” may also be observed - in this case, the child rests on the forefoot.

Late stage of Duchenne dystrophy
Independent walking at this stage is rarely observed. The child is unable to move or get up from the floor. Muscle weakness also affects the upper limbs. There is dystrophy of the respiratory muscles and damage to the heart.

Diagnosis of Duchenne dystrophy
Based on medical history, medical examination and specific laboratory tests. On examination, muscle weakness and enlargement are noted ( pseudohypertrophy) calf muscles. The child’s parents note that he began to crawl and walk much later. They may also experience delayed speech development.
Genetic analysis, muscle biopsy and laboratory tests are mandatory. A blood test reveals elevated levels of creatine phosphokinase and liver enzymes. A muscle biopsy reveals a deficiency of the protein dystrophin in muscle cells.

The prognosis for Duchenne dystrophy is unfavorable, as the disease progresses very quickly. Patients die at the age of 20 from respiratory failure or heart failure.

Becker's dystrophy

Becker's dystrophy is also a genetically determined disease, which is based on degenerative changes in muscle fibers. The cause is a defect in the gene encoding the dystrophin protein.
The onset of the disease occurs between the ages of 10 and 15 years. The first symptom is muscle weakness during intense physical activity. Further weakness is noted during moderate exertion, for example, when climbing stairs. The ability to move independently with Becker's dystrophy lasts up to 40 years.

Symptoms of Becker's dystrophy are:

muscle weakness – 100 percent;
pelvic muscle atrophy – 90 percent;
pseudohypertrophy of the calf muscles - 80 percent;
decrease in tendon reflexes – 70 percent.

Becker muscular dystrophy is also called benign dystrophy ( for comparison, Duchenne dystrophy is a malignant). The prognosis is relatively favorable.

Myotonic dystrophy

Myotonic dystrophy or Steinert's disease is relatively rare. Its development is caused by a genetic defect in the 19th chromosome. It affects both men and women equally. The onset of the disease often occurs between the ages of 30 and 40 years. The first manifestations of the disease are weakness of the facial muscles, delayed relaxation after contraction of the muscles of the limb. The peculiarity of this form is that in addition to the skeletal muscles, the smooth muscle tissue of the internal organs is damaged.

Treatment of muscular dystrophies

To date, there are no specific treatments for muscular dystrophy. Treatment is aimed at combating complications - frequent pneumonia, curvature of the spine, heart failure. Comprehensive treatment includes physical therapy, active and passive exercises, and rarely corticosteroids. Sometimes surgical treatment is recommended. It is performed to correct contractures or scoliosis. Mechanical means are widely used - braces, wheelchairs, canes.
For Duchenne dystrophy, corticosteroids such as prednisolone and deflazacort are prescribed. These drugs can slow the progression of muscle weakness and delay the loss of the ability to move independently by 2 to 3 years.

Myocardial dystrophy

Myocardial dystrophy is a degenerative lesion of the heart muscles, usually associated with metabolic disorders in them. Most often, cardiac dystrophy or myocardial dystrophy is an acquired disease. Myocardial dystrophies can be caused by a variety of reasons - malnutrition, taking certain medications, systemic diseases.

The causes of myocardial dystrophy are:

malnutrition;
toxic effects of alcohol;
systemic diseases.

Heart dystrophy due to diets and unbalanced nutrition

Myocardial damage can be caused by both excess and insufficient nutrition. Most often, the heart is affected by a protein-free diet, fasting, and insufficient intake of B vitamins and selenium.

Errors in nutrition that are accompanied by heart dystrophy include:

starvation;
protein deficiency ( kwashiorkor);
lack of B vitamins;
Selenium deficiency.

Myocardial dystrophy during fasting
As a rule, food refusal is observed in anorexia or other mental disorders. Fasting leads to degenerative changes in the myocardium. With prolonged fasting, basal metabolism decreases and heart function slows down. Morphological changes in the myocardium include fatty degeneration against the background of atrophy. Clinically, myocardial dystrophy in this case is manifested by a decrease in heart rate ( bradycardia), decreased blood pressure, edema. Long-term lack of vitamins and minerals leads to electrolyte disorders, namely a deficiency of potassium and other electrolytes. On the electrocardiogram ( ECG) there is a decrease in the voltage of the QRS complex, deviation of the electrical axis of the heart to the right. With further starvation, myocardial dystrophy can progress to heart failure.

Myocardial dystrophy in kwashiorkor
Kwashiorkor is a disease that occurs primarily in developing countries and is associated with insufficient protein intake. Since proteins are the main plastic substances of the body ( they are part of cells, enzymes), then when they are deficient, multiple organ failure occurs. The clinical picture of kwashiorkor includes growth retardation, malnutrition, and muscle dystrophy, including heart muscles. Symptoms are most pronounced between the ages of 5 and 6 years. Edema appears very early, the liver enlarges and the heart decreases. The electrocardiogram shows the same changes as during acute starvation - a decrease in voltage and a change in the T wave. With kwashiorkor, the nervous system also suffers - children become lethargic and apathetic.

Myocardial dystrophy due to deficiency of B vitamins
B vitamins are an integral part of many enzymes and participate in redox reactions. When they are deficient, carbohydrate metabolism is primarily disrupted. As a result, in tissues ( including in the heart muscle) pyruvic and lactic acid accumulate, and energy production decreases. Thus, tissue acidosis develops, which causes circulatory failure. With hypovitaminosis B, high cardiac output and low peripheral vascular resistance are observed. The clinical picture is characterized by symptoms such as palpitations, fatigue, and sometimes cardiac arrhythmias ( arrhythmias). Morphological signs of myocardial dystrophy due to hypovitaminosis include interstitial edema and degeneration of muscle fibers. Diagnosis consists of determining the concentration of vitamin B.

Selenium deficiency
Selenium is a trace element mainly found in the liver, kidneys, and spleen. In the human body, the concentration of selenium varies from 10 to 15 milligrams. It is part of the proteins of muscle tissue, including the heart. With selenium deficiency, the activity of certain enzymes decreases, which provokes the accumulation of free radicals and damage to cardiomyocytes ( heart cells). Insufficient intake of selenium into the body causes the development of congestive cardiomyopathy, which can be acute or chronic. In the acute form, cardiogenic shock, pulmonary edema and severe arrhythmias develop. The chronic form is manifested by bradycardia, decreased cardiac output and the development of heart failure.

Alcoholic myocardial dystrophy ( myocardial dystrophy)

Alcohol, heavy metals and some drugs have a toxic effect on the heart muscle.

Alcoholic myocardial dystrophy
Systematic consumption of alcoholic beverages is one of the risk factors for myocardial dystrophy. In more than 45 percent of cases, alcoholism causes dilated cardiomyopathy. Recent studies have shown that systematic alcohol abuse over 5 years leads to the development of myocardial dystrophy in every fifth woman and a similar disease in every fourth man.

Myocardial dystrophy is explained both by the direct toxic effect of ethanol on the heart muscle and by the indirect effect of intermediate metabolic products. Thus, in the body, alcohol is metabolized to acetaldehyde, which has vasodilating properties and also stimulates the secretion of catecholamines. The latter are involved in cellular metabolic reactions, including calcium transport, protein synthesis and tissue respiration. Alcohol metabolism products accumulate in the mitochondria of the heart muscle, disrupting cell function and changing the metabolism of the entire heart. Fats accumulate in myocardiocytes, and the phenomenon of fatty degeneration develops. Alcoholics also have multiple hypovitaminosis. Vitamin B deficiency has a major impact on the heart.

Alcoholic heart dystrophy most often develops after 10 years of systematic alcohol consumption, usually after 35–40 years. It manifests itself as shortness of breath ( first during physical activity, and then at rest), fatigue, weakness, arrhythmias. With alcoholic heart dystrophy, the risk of sudden cardiac death is high.

Toxic dystrophies also develop with the use of cocaine, heroin, and during treatment with antitumor drugs.

Cardiac dystrophy in systemic diseases

Systemic diseases are autoimmune connective tissue diseases. Since connective tissue is part of almost all organs and tissues, in these diseases there is a systemic ( multiorgan) damage to internal organs. Myocardial dystrophy is observed in systemic lupus erythematosus and scleroderma.

In patients with systemic lupus erythematosus, cardiac dysfunction is observed in 80 percent of cases ( damage to the heart is called lupus myocarditis). In this case, all structures of the heart are involved in the pathological process - the myocardium, pericardium, endocardium and cardiac vessels. But more inflammation affects the heart muscle ( myocardium) with the development of diffuse or focal myocarditis. In patients with lupus myocarditis, the electrocardiogram shows tachycardia, changes in the ST-T segment, and heart rhythm disturbances ( arrhythmias and blockades). Glucocorticoids, which are used in the treatment of systemic lupus erythematosus itself, also have a negative effect on the heart muscle. Long-term use of high doses of glucocorticoids leads to steroid dystrophy. Patients complain of frequent heartbeats, pain in the heart area, and shortness of breath.

With systemic scleroderma, heart damage appears 2 to 3 years after the onset of the disease. Morphological signs of myocardial dystrophy are diffuse fibrosis and necrosis of the heart muscle. This means that the myocardiocytes themselves die, and connective tissue develops in their place. Gradually, connective tissue replaces myocardial tissue. However, this tissue cannot contract as efficiently as the heart, which provokes the development of heart failure. Often, cardiac symptoms in this disease precede all other symptoms. Patients complain of pain in the heart, which occurs as angina pectoris. They are localized behind the sternum, have a pressing or squeezing nature, and also radiate to the left arm or shoulder blade.

Eye dystrophies ( retina and cornea)

Eye dystrophies are a group of diseases characterized by degenerative changes in various structures of the eye. Thus, with retinal dystrophy, changes affect various layers of the retina, and with corneal dystrophy, changes are observed in the layers of the cornea.

The retina is the inner layer of the eyeball, the structure of which consists of several layers. In the retina itself there is a central ( aka macula) and peripheral sections. Retinal dystrophy is a destructive ( destructive) process of the layers of the retina, most often due to their impaired nutrition. Dystrophic changes can be congenital ( family-hereditary) or purchased. In elderly people, senile retinal dystrophies are detected, in the development of which atherosclerosis plays an important role.

Types of retinal dystrophy are:

retinal pigmentary dystrophy;
macular degeneration;
ring-shaped retinal dystrophy.

Retinal pigmentary dystrophy

This pathology, which simultaneously affects both eyes and is accompanied by destruction of the pigment layer of the retina. The pigment epithelium is the tenth layer of the retina, which contains light-sensitive elements. That is why, when it is destroyed, patients complain of worsening vision in the dark. The causes of retinal pigmentary dystrophy are still unknown; family hereditary transmission of the disease is observed. The debut of pigmentary dystrophy occurs at a young age. The morphological sign is damage to the neuroepithelial layer of the retina with destruction of photosensitive elements ( rods and cones). At the same time, the pigment epithelium itself swells and moves into the inner layers of the retina, while fibrosis of the retinal vessels occurs in parallel. The disease lasts a long time with gradual loss of vision.

Symptoms of retinal pigmentary dystrophy are:

pigment deposition in the retina;
atrophy ( destruction) optic nerve;
narrowing of visual fields;
loss of vision at dusk.

Central vision in this disease is preserved for a long time, but over time it still decreases. Hereditary retinal dystrophies, including pigmentary retinal dystrophies, are difficult to treat. Drug therapy is aimed at improving retinal nutrition in order to slow down the destructive pathological process.

Macular degeneration ( central dystrophy)

The macula is the central part of the retina and is responsible for central vision. Macular degeneration ( macular degeneration) is most often age-related, that is, it develops in people of the older age group. Along with cataracts and glaucoma, this pathology is one of the most common causes of blindness in people over 60 years of age. In the Russian Federation, the frequency of this pathology is more than 15 people per thousand population, that is, every 20 Russians are susceptible to senile blindness due to macular degeneration.

The main symptom of macular degeneration is loss of central vision. Damage to the macula leads to visual illusions, such as distortion of lines, objects, or the appearance of spots in the field of vision. There are two forms of macular degeneration - “dry” and “wet”.

Dry form of macular degeneration
It is the most common and occurs in approximately 90 percent of cases. It is characterized by the accumulation of cellular waste products that reduce access for oxygen and nutrients to photoreceptors ( cones). Often this type of macular degeneration is asymptomatic. But as metabolic products accumulate in the retina, symptoms such as blurred vision and loss of areas from the field of vision appear. The prognosis for this form of dystrophy is relatively favorable, since high visual acuity is maintained for many years.

Wet form of macular degeneration
This form occurs much less frequently than the previous one, in approximately 10 percent of cases. However, it is more malignant with rapidly progressive vision loss. In the wet form, a process of “retinal neovascularization” is observed, which is characterized by the ingrowth of new vessels into the retina. Through these new and defective blood vessels, blood seeps into the thickness of the tissue. As a result, retinal edema develops and a sharp deterioration in vision. The wet form is characterized by a more rapid course and an unfavorable prognosis. Over several weeks or months, visual acuity decreases, leading to complete blindness.

Early signs of the disease
It is important to know that with macular degeneration, central and color vision suffers, therefore, first there is a loss of brightness and contrast of colors. This may manifest itself in distortion of the outlines; often the patient requires more illumination of the room than before. Further difficulties arise when reading - individual letters, syllables or even words may fall out. Later, visual acuity decreases, the patient has difficulties both at close range and when looking into the distance. If you do not consult a doctor at this stage, a translucent spot appears before your eyes, which sharply reduces your vision.

Ring-shaped retinal degeneration
In ring-shaped retinal degeneration, small, pinpoint white lesions appear around the macula. These lesions form clusters in the form of rings or semi-rings, hence the name dystrophy. In addition to the rings, small hemorrhages are visualized on the retina. The disease develops slowly, but visual acuity depends on the severity of the changes.

Corneal dystrophy

The cornea is the front part of the fibrous membrane of the eye. In a healthy person, the cornea is smooth, transparent, and does not contain blood vessels. The structure of the cornea is divided into five layers. Corneal dystrophy is a pathology in which the transparency of the cornea decreases, which causes a decrease in visual acuity.
There are primary ( congenital) and secondary ( acquired) corneal dystrophy. Primary dystrophies are characterized by earlier development of the disease, hereditary nature, and a slowly progressive course. As a rule, with congenital dystrophies, both eyes are affected simultaneously, which is why the pathological process is bilateral and symmetrical. The causes of these dystrophies are unknown, and the inflammatory element is not typical for them.
Depending on the location of the lesion, several types of dystrophies are distinguished.

Types of corneal dystrophy are:

epithelial dystrophies;
degeneration of Bowman's membrane;
stromal dystrophies;
endothelial dystrophies.

Epithelial dystrophy
This type of dystrophy is extremely rare. This is a hereditary pathology that manifests itself in the first years of life. Both eyes are affected at the same time. The main symptoms of dystrophy are the formation of many small bubbles in the central part of the cornea ( cyst). Over time, the bubbles turn into opacities, as a result of which the cornea ceases to be transparent. Decreased corneal transparency causes vision loss.

Bowman's membrane dystrophy
This is also a hereditarily caused dystrophy, which manifests itself in the first ten years of a child’s life. Early symptoms of dystrophy include photophobia and redness of the conjunctiva. The morphological feature is the formation of small erosions ( ulcers) in the cornea, causing the capsule to become cloudy and rough. As a result, the sensitivity of the cornea decreases and visual acuity decreases.

Stromal dystrophy
This type of dystrophy manifests itself at the age of 10–15 years. The course of the disease is slowly progressive; by the age of 40, visual acuity decreases significantly. Stromal dystrophy is characterized by the formation of small inclusions in the surface layers of the cornea. Under a microscope, these inclusions resemble “bread crumbs” or “snowflakes.” The more such inclusions, the cloudier the cornea becomes, and the more visual acuity decreases.

Endothelial dystrophy
This is a very rare type of dystrophy, which is characterized by extensive areas of “baldness” of the endothelium. The cornea swells and becomes gray-blue in color.

Treatment of retinal and corneal dystrophy

Treatment for retinal dystrophy includes vasodilators

Myocardial dystrophy (dishormonal, dysmetabolic, alcoholic, mixed origin, etc.) – causes, types and symptoms, diagnosis and treatment in children and adults