Proper nutrition for diseases of the nervous system. Muscular dystrophy

Weak and ineffective acting muscles often create problems that little is done to solve until they become serious. Although strength and normal muscle action give the figure grace and grace in movement, both are now rare.

Weak muscle tone impairs blood circulation, interferes with normal lymph circulation, and prevents efficient digestion, often causes constipation and sometimes makes it difficult to control urination or even have bowel movements bladder. Often, due to muscle weakness, the internal organs sag or lie on top of each other. Clumsiness of movements muscle tension and poor coordination, very commonly seen in malnourished children and usually unaddressed, are quite similar to symptoms seen in muscular dystrophy and multiple sclerosis.

Muscle weakness

Muscle is composed primarily of protein, but also contains essential fatty acids; therefore, the body's supply of these nutrients must be sufficient to maintain muscle strength. Chemical nature muscles and the nerves that control them are very complex. And since countless enzymes, coenzymes, activators and other compounds are involved in their contraction, relaxation and repair, every nutrient is necessary in one way or another. For example, calcium, magnesium, and vitamins B6 and D are needed to relax muscles, so muscle spasms, tics, and tremors usually improve with more of these substances in your diet.

Potassium is necessary for muscle contraction in the body. In just a week, healthy volunteers fed refined foods similar to what we eat every day developed muscle weakness, extreme fatigue, constipation, and depression. All this went away almost immediately when they were given 10 g of potassium chloride. Severe potassium deficiency, often due to stress, vomiting, diarrhea, kidney damage, diuretics or cortisone, causes slowness, lethargy and partial paralysis. Weakened intestinal muscles allow bacteria to release huge amounts of gases, causing colic, and spasms or displacement of the intestines can lead to intestinal obstruction. When death occurs due to potassium deficiency, autopsy reveals severe damage and muscle scarring.

Some people have such high potassium needs that they experience periodic paralysis. Examinations of these patients show that salty foods high in fat and carbohydrates, and especially sweet tooth, stress, as well as ACTH (a hormone produced by the pituitary gland) and cortisone reduce potassium levels in the blood. Even if muscles become weak, flaccid, or partially paralyzed, recovery occurs within minutes of taking potassium. Foods that are high in protein, low in salt, or rich in potassium can increase abnormally low potassium levels in the blood.

When muscle weakness leads to fatigue, gas, constipation, and inability to empty the bladder without the aid of a catheter, taking potassium chloride tablets is especially helpful. Most people, however, can get potassium by consuming fruits and vegetables, especially green leafy ones, and by avoiding refined foods.

Vitamin E deficiency appears to be a common, although rarely recognized, cause of muscle weakness. Just as red blood cells are destroyed by the action of oxygen on essential fatty acids, muscle cells throughout the body are destroyed in the absence of this vitamin. This process is especially active in adults who do not digest fat well. The nuclei of muscle cells and the enzymes necessary for muscle contraction cannot be formed without vitamin E. Its deficiency greatly increases the need for muscle tissue for oxygen, interferes with the use of certain amino acids, allows phosphorus to be excreted in the urine and leads to the destruction of a large number of B vitamins. All this impairs muscle function and recovery. Moreover, with an insufficient supply of vitamin E to the body, the number of enzymes that break down dead muscle cells increases by about 60 times. With a deficiency of vitamin E, calcium accumulates and may even be deposited in the muscles.

In pregnant women, muscle weakness due to vitamin E deficiency, often caused by iron supplements, in some cases makes labor difficult because the amount of enzymes needed to contract the muscles involved in labor is reduced. When patients with muscle weakness, pain, wrinkled skin and loss of muscle elasticity were given 400 mg of vitamin E per day, a noticeable improvement was observed in both old and young. Those who suffered from muscle disorders for years recovered almost as quickly as those who were ill short time.

Long-term stress and Addison's disease

Advanced adrenal fatigue, as in Addison's disease, is characterized by apathy, excruciating fatigue and extreme muscle weakness. Although at the beginning of stress it is mainly the protein of the lymph nodes that is broken down, with prolonged stress the muscle cells are also destroyed. Moreover, exhausted adrenal glands cannot produce the hormone that stores nitrogen from destroyed cells in the body; Normally, this nitrogen is reused to build amino acids and repair tissue. Under such circumstances, muscles quickly lose strength even with protein-rich foods.

Exhausted adrenal glands are also unable to produce sufficient amounts of the salt-retaining hormone aldosterone. So much salt is lost in the urine that potassium leaves the cells, which further slows contractions and weakens and partially or completely paralyzes the muscles. Taking potassium can increase the amount of this nutrient in cells, but in this case, salt is especially needed. People with exhausted adrenal glands usually have low blood pressure, meaning they don't have enough salt.

The adrenal glands quickly become exhausted when pantothenic acid is deficient, causing the same condition as prolonged stress.

Because stress plays a role in all muscle disorders, emphasis should be placed on restoring adrenal function in any diagnosis. An anti-stress program should be followed carefully, especially in the case of Addison's disease. Recovery occurs faster if the “anti-stress formula” is taken around the clock. No essential nutrient should be overlooked.

Fibrositis and myositis

Inflammation and swelling of the connective tissue of muscles, especially the membrane, is called fibrositis or synovitis, and inflammation of the muscle itself is called myositis. Both diseases are caused by mechanical injury or strain, and inflammation indicates that the body is not producing sufficient quantity cortisone. A diet with plenty of vitamin C, pantothenic acid and drinking milk around the clock usually brings immediate relief. In case of injury, it can quickly form scar tissue, so you should pay special attention to vitamin E.

Fibrositis and myositis often affect women during menopause, when the need for vitamin E is especially great, these diseases tend to cause significant discomfort before the cause is discovered. Daily intake Vitamin E for myositis brings a noticeable improvement.

Pseudoparalytic myasthenia

The term myasthenia gravis itself means severe loss of muscle strength. This disease is characterized by wasting and progressive paralysis that can affect any part of the body, but most often the muscles of the face and neck. Double vision, eyelids that don't lift, frequent choking, difficulty breathing, swallowing and speaking, poor articulation and stuttering are typical symptoms.

Isotope studies with radioactive manganese have shown that enzymes involved in muscle contractions contain this element, and when muscles are damaged, its amount in the blood increases. Manganese deficiency causes muscle and nerve dysfunction in experimental animals and muscle weakness and poor coordination in livestock. Although the amount of manganese required for humans has not yet been established, people suffering from muscle weakness may be advised to include wheat bran and whole grain bread in their diet (the richest natural springs).

In this disease, defects occur in the production of the compound that transmits nerve impulses to muscles, which is formed in nerve endings made from choline and acetic acid and is called acetylcholine. In a healthy body, it is constantly broken down and formed again. In pseudoparalytic myasthenia, this compound is either produced in negligible quantities or is not formed at all. The disease is usually treated with medications that slow down the breakdown of acetylcholine, but until nutrition is complete, this approach is another example of whipping up a driven horse.

It takes a whole battery to produce acetylcholine nutrients: vitamin B, pantothenic acid, potassium and many others. A lack of choline itself causes underproduction of acetylcholine and leads to muscle weakness, muscle fiber damage and extensive scar tissue growth. All this is accompanied by loss of a substance called creatine in the urine, which invariably indicates the destruction of muscle tissue. Although choline can be synthesized from the amino acid methionine if there is an abundance of protein in the diet, folic acid, vitamin B12 and other B vitamins are also required for the synthesis of this vitamin.

Vitamin E increases the release and utilization of acetylcholine, but if there is an insufficient supply of vitamin E, the enzyme needed to synthesize acetylcholine is destroyed by oxygen. This also causes muscle weakness, muscle breakdown, scarring and loss of creatine, but taking vitamin E will correct the situation.

Since pseudoparalytic myasthenia gravis is almost inevitably preceded by prolonged stress, enhanced by the use of medications that increase the body's needs, an anti-stress diet that is unusually rich in all nutrients is recommended. Lecithin, yeast, liver, wheat bran and eggs are excellent sources of choline. Daily diet should be divided into six small, protein-rich servings, generously supplemented with “anti-stress formula”, magnesium, B vitamin tablets with a high content of choline and inositol and possibly manganese. You should eat salty foods for a while and increase your potassium intake by eating plenty of fruits and vegetables. When swallowing is difficult, all foods can be crushed and supplements taken in liquid form.

Multiple sclerosis

This disease is characterized by calcareous plaques in the brain and spinal cord, muscle weakness, loss of coordination, jerky movements or spasms in the muscles of the arms, legs, and eyes, and poor bladder control. Autopsies show a marked decrease in the amount of lecithin in the brain and in the myelin sheath surrounding the nerves, where lecithin content is usually high. And even the remaining lecithin is abnormal because it contains saturated fatty acids. Additionally, multiple sclerosis is most common in countries where saturated fat intake is high, which is invariably associated with low blood lecithin levels. Perhaps due to the reduced need for lecithin, patients with multiple sclerosis are prescribed a low-fat diet less often and for a shorter duration. Significant improvement is achieved when three or more tablespoons of lecithin are added to food daily.

It is likely that a deficiency of any nutrient—magnesium, B vitamins, choline, inositol, essential fatty acids—can aggravate the course of the disease. Muscle spasms and weakness, involuntary shaking and inability to control the bladder quickly disappeared after taking magnesium. In addition, when patients suffering from multiple sclerosis were given vitamins E, B6 and other B vitamins, the progression of the disease slowed down: even in advanced cases, improvement was observed. Liming of soft tissues was prevented by vitamin E.

In most patients, multiple sclerosis occurred due to severe stress during a period when their diet lacked pantothenic acid. A lack of vitamins B1, B2, B6, E or pantothenic acid - the need for each of them increases many times under stress - leads to nerve degradation. Multiple sclerosis often treated with cortisone, which means that every effort should be made to stimulate normal hormone production.

Muscle dystrophy

Any experimental animals kept on a diet deficient in vitamin E developed muscle dystrophy after a certain period of time. Muscle dystrophy and atrophy in humans turn out to be completely identical to this artificially caused disease. Both in laboratory animals and in humans, with vitamin E deficiency, the need for oxygen increases many times, the amount of many enzymes and coenzymes necessary for normal operation muscles are noticeably reduced; muscles throughout the body are damaged and weakened when the essential fatty acids that make up the muscle cell structure are destroyed. Numerous nutrients are lost from the cells, and muscle tissue is eventually replaced by scar tissue. The muscles split lengthwise, which, by the way, makes you wonder whether a lack of vitamin E plays a major role in the formation of a hernia, especially in children, in whom its deficiency is simply terrifying.

For many months or even years before dystrophy is diagnosed, amino acids and creatine are lost in the urine, indicating muscle breakdown. If vitamin E is given early in the disease, the destruction of muscle tissue stops completely, as indicated by the disappearance of creatine in the urine. In animals, and possibly in humans, the disease develops faster if the food also lacks protein and/or vitamins A and B6, but even in this case, dystrophy is cured by vitamin E alone.

With prolonged vitamin E deficiency, human muscle dystrophy is irreversible. Attempts to use massive doses of vitamin E and many other nutrients have not been successful. The fact that the disease is “hereditary”—several children in the same family can be affected—and that chromosomal changes have been detected leads doctors to argue that it cannot be prevented. The hereditary factor can only be an unusually high genetic need for vitamin E, which is necessary for the formation of the nucleus, chromosomes and the entire cell.

The moment when muscle dystrophy or atrophy becomes irreversible has not been precisely established. On early stages these diseases can sometimes be treated with fresh wheat bran oil, pure vitamin E, or vitamin E plus other nutrients. When diagnosed early, some patients recovered after simply adding wheat bran to their food and homemade bread from freshly ground flour. In addition, the muscle strength of people suffering from this disease for many years improved markedly when they were given a variety of vitamins and mineral supplements.

Children with muscle dystrophy at the beginning of life began to sit up later, crawl and walk, ran slowly, had difficulty climbing stairs and getting up after falling. Often the child was ridiculed for many years as lazy and clumsy before seeing a doctor. Since huge masses of scar tissue are commonly mistaken for muscle, mothers of such children often took pride in how “muscular” their child was. Eventually the scar tissue shrinks, causing either excruciating back pain or shortening of the Achilles tendon, which is as disabling as the weakness of the muscles themselves. Often the Achilles tendon is lengthened surgically many years before the diagnosis of dystrophy is made, but vitamin E is not given as a preventative measure.

Every person with impaired muscle function should immediately undergo a urine test and, if creatine is found in it, significantly improve their diet and include large number vitamin E. Muscle dystrophy could be completely eradicated if all pregnant women and artificially-bred children were given vitamin E and refined foods that lack it were excluded from the diet.

Proper nutrition

Like most diseases, muscle dysfunction stems from a variety of deficiencies. Until the diet becomes adequate in all nutrients, one cannot expect either recovery or preservation of health.

Instructions

If dystrophy is of a nutritional nature, i.e. appeared as a result of prolonged diets, fasting or insufficient food intake, then the doctor, in addition to prescribing vitamins, enzymes, stimulants and dietary supplements, will recommend the patient to radically change his approach to nutrition.

To get rid of dystrophy, you need to eat at least 5 times a day. The diet must be complete and must include the required amount of proteins, fats and carbohydrates. It is important to eat more fruits and vegetables, drink more fluids and especially green tea. As food additives include powdered egg and brewer's yeast.

Suffering from dystrophy should take more frequent walks in the fresh air, walk, and gradually include it in your daily routine physical exercise. You can go to the gym twice a week for half an hour. After some time, the intensity of training and its duration should increase.

Since dystrophy can appear even in the mother, it is necessary to balance your diet and maintain correct image life - eliminate bad habits and stick to normal mode day. Afterwards, a woman should definitely consult a doctor about organizing proper feeding.

If dystrophy develops as a result of defects of the gastrointestinal tract, no half-measures, unfortunately, will help get rid of it. In this case, surgical intervention is necessary.

Muscular dystrophy (this term refers to a group of different muscle diseases) is hereditary. It is believed that there are still no drugs or medical devices that would slow down this progressive disease. All efforts of doctors in this case are aimed at combating possible complications. This is, first of all, a spinal deformity that develops due to weakness of the back muscles, as well as. Predisposition to pneumonia is due to weakness of the respiratory muscles. Such patients are observed by general practitioners and neurologists. In this case, good nutrition is also important. Eating boiled chicken meat is very beneficial.

In addition to medical treatment, massage is used. Some experts claim that rubbing butter into the muscles is effective for patients with muscular dystrophy. To do this, take the cream that is formed when milk settles, whip it, and rub the person with the resulting oil. For 20 minutes, rub the oil into the back and spine, then for 5 minutes into the back of the thigh and lower leg, then (movements from bottom to top). After this procedure, the patient is wrapped in a sheet and wrapped. He must rest for at least an hour. This massage is carried out every morning for 20 days. Then a 20-day break and repeat the entire course twice more.

Sometimes, ordinary people quite frivolously throw around the concept of dystrophy, calling every thin person “dystrophic” behind their backs or as a joke. However, few of them know that dystrophy is serious illness, which requires no less serious treatment.

What is dystrophy?

The concept itself dystrophy consists of two ancient Greek words - dystrophe, which means difficulty and trophe, i.e. nutrition. However, it is not connected with the fact that a person does not want or cannot eat well, but with the phenomenon when all the nutrients entering the body are simply not absorbed by it, which accordingly leads to a disruption of normal growth and development, which manifests itself not only externally , but also internally (dystrophy of organs and systems).

Thus, dystrophy is a pathology based on a disturbance (disorder) of cellular metabolism, which leads to characteristic structural changes.

The basis of the disease, according to pathological anatomy, there are processes that disrupt the normal trophism of the body - the ability of cells to self-regulate and transport metabolic products (metabolism).

Reasons for the development of dystrophy

Unfortunately, the reasons for the development of dystrophy can be different and there are many of them.

Congenital genetic disorders of metabolism.
Frequent infectious diseases.
Experienced stress or mental disorders.
Poor nutrition, both malnutrition and abuse of foods, especially those that contain large amounts of carbohydrates.
Digestive problems.
General weakening of the immune system.
Constant exposure to external unfavorable factors on the human body.
Chromosomal diseases.
Somatic diseases.

This disappointing list can be continued, since there are truly a great many reasons that can trigger the process of trophic disturbance at any moment.

But it would be a mistake to assume that they act on everyone in exactly the same way and are capable of triggering the development of dystrophy. By no means, due to the individuality of each human body, they either trigger the development of the disorder process or not.

Main symptoms of the disease

Signs of dystrophy directly depend on its form and severity of the disease. So experts distinguish between I, II and III degrees, the main symptoms of which will be:

I degree– reduction in body weight, tissue elasticity and muscle tone in the patient. In addition, there is a violation of stool and immunity.
II degree– subcutaneous tissue begins to thin out, or even disappears altogether. Acute vitamin deficiency develops. All this against the backdrop of further weight loss.
III degree– complete exhaustion of the body occurs and respiratory and cardiac dysfunction develop. Body temperature remains low, as do blood pressure readings.

However, there are basic symptoms that are characteristic of absolutely all forms and types of dystrophies, which can be observed in both adults and children.

State of excitement.
Decrease or complete absence appetite.
Sleep disturbance.
General weakness and fatigue.
Significant changes in body weight and height (the latter is observed in children).
Various disorders of the gastrointestinal tract.
Reduced overall body resistance.

At the same time, the patient himself, as a rule, refuses to acknowledge the impending threat, considering his condition to be the result of overwork or stress.

Classification of the disease

The problem is that dystrophy and dystrophy are different and in each individual case its manifestations may be different. It is for this reason that experts have determined the following classification of this disease.

According to their etiology they distinguish:

congenital dystrophy;
acquired dystrophy.

Depending on the type of metabolic disorder, it can be:

protein;
fatty;
carbohydrate;
mineral.

According to the localization of their manifestations, they are distinguished:

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

According to its prevalence, it can be:

systemic, i.e. general;
local.

In addition, one should take into account the fact that what stands apart from all types of dystrophies is congenital, which is caused by hereditary disorders of the metabolism of proteins, fats or carbohydrates. This happens due to a lack of any enzyme in the child’s body, which in turn leads to the fact that incompletely broken down substances (products) of metabolism begin to accumulate in the tissues or organs. And although the process can progress anywhere, nevertheless, the tissue of the central nervous system is always affected, which leads to death in the first years of life.

A striking example is hepatocerebral dystrophy, which is accompanied by dysfunction of the liver, central nervous system and brain.

Morphogenesis of other types of dystrophies can develop according to four mechanisms: infiltration, decomposition, perverted synthesis or transformation.

Features of types of dystrophy according to their localization and disruption of BZH metabolism

Cellular or parenchymal dystrophy is characterized by metabolic disorders in the parenchyma of the organ. The parenchyma of an organ (not to be confused with a parenchymal organ, i.e. non-cavitary) in this case refers to the set of cells that ensure its functioning.

Fatty liver degeneration – shining example a disease in which cells fail to cope with their function - the breakdown of fats - and they begin to accumulate in the liver, which can cause steatogapatitis (inflammation) and cirrhosis in the future.

Acute fatty degeneration of the liver can also be a dangerous complication, since it progresses quite quickly and leads to liver failure and toxic degeneration, which leads to necrosis of liver cells.

In addition, parenchymal fatty degenerations include cardiac degeneration, when the myocardium is affected, which becomes flabby, which leads to a weakening of its contraction function, ventricular degeneration and renal degeneration.

Protein parenchymal dystrophies are hyaline-droplet, hydropic, horny.

Hyaline droplet - characterized by the accumulation of protein droplets in the kidneys (less often the liver and heart), for example, with glomerulonephritis. It is characterized by a severe latent course, which results in an irreversible process of degeneration.

This type also includes granular dystrophy, characterized by the accumulation of swollen hypochondria cells in the cytoplasm.

Hydropic, in turn, is manifested by the accumulation of drops of protein liquid in the organs. The process can develop in epithelial cells, liver, adrenal glands and in the myocardium. If the number of such drops in a cell is large, then the nucleus is displaced to the periphery - the so-called balloon degeneration.

Horny dystrophy is characterized by the accumulation of horny substance where it should be normally, i.e. human epithelium and nails. Its manifestations are ichthyosis, hyperkeratosis, etc.

Parenchymal carbohydrate dystrophy is a disorder of the exchange of glycogen and glycoproteins in the human body, which is especially characteristic of diabetes mellitus or, for example, with cystic fibrosis - the so-called hereditary mucous dystrophy.

Extracellular dystrophy or mesenchymal can develop in the stroma (the base that consists of connective tissue) of organs, involving the entire tissue along with the vessels in the process. That is why it is also called stromal vascular dystrophy. It can be in the nature of a protein, fat or carbohydrate disorder.

A striking manifestation of this type of dystrophy is peripheral vitreochorioretinal dystrophy of the retina. It can be both congenital and acquired in nature and lead to decreased visual acuity (damage to the macula) and poor orientation at night, and ultimately to retinal detachment or pigmentary dystrophy. In addition, the cornea of ​​the eye may also be involved in the process.

Peripheral chorioretinal dystrophy is also characterized by serious disturbances in the nutrition of the fundus, which can lead to vision loss.

The most common phenomenon is muscular dystrophy, which is characterized by progressive weakness of human muscles and their degeneration - myotonic dystrophy, involving in the process not only human skeletal muscles, but also the pancreas, thyroid, myocardium and ultimately the brain.

Protein mesenchymal dystrophy can affect the human liver, kidneys, spleen and adrenal glands. In old age, the heart and brain are susceptible to it. As for the latter, the brain, this can lead to slowly progressive discirculatory encephalopathy - a disruption of the blood supply to the brain, as a result of which diffuse disorders increase and, as a consequence, a disorder of the basic functions of the patient’s brain.

As for stromal-vascular fatty degeneration, its striking manifestation can be the patient’s obesity and obesity or Dercum’s disease, when painful nodular deposits can be observed on the extremities (mainly legs) and torso.

It is noteworthy that the stromal vascular fatty degenerations can be both local and general in nature and lead to both the accumulation of substances and, conversely, to their catastrophic loss, for example, as in nutritional dystrophy, which can develop as a result of malnutrition and lack of nutrients, both in people and in animals.

Mesenchymal carbohydrate dystrophy is also called mucus degeneration of human tissue, which is associated with dysfunction of the endocrine glands, and which, in turn, can lead to edema, swelling or softening of the patient’s joints, bones and cartilage, for example, as in spinal dystrophy, which can often be found in postmenopausal women.

Mixed dystrophy (parenchymal-mesenchymal or parenchymal-stromal) is characterized by the development of dysmetabolic processes, both in the parenchyma of the organ and in its stroma.

This type characterized by metabolic disorders of such substances as:

Hemoglobin, which carries oxygen;
melanin, which protects against UV rays;
bilirubin, which is involved in digestion;
lipofuscin, which provides the cell with energy under hypoxic conditions.

Treatment and prevention of dystrophies

After making a final diagnosis and determining the type of dystrophy, it is necessary to immediately begin its treatment, which in this case directly depends on the severity of the disease and its nature. Only a doctor can correctly select the appropriate methods and drugs to eliminate such metabolic dysfunctions. However, there are a number of rules (measures) that must be observed for any type of dystrophy.

1. Organizing appropriate care for the patient and eliminating all factors that provoke complications (see causes of dystrophies).
2. Compliance with the daily routine, with the obligatory inclusion of walks in the fresh air, water procedures and physical exercises.
3. Compliance with a strict diet prescribed by a specialist.

As for preventing this complex disease, then it is necessary to maximally strengthen methods and measures for caring for oneself (or children) in order to completely eliminate, as far as possible, all negative factors that could cause this type of disorder.

It must be remembered that strengthening your own immunity and the immunity of your children from the very beginning early age, a rational and balanced diet, sufficient physical activity and lack of stress is the best prevention of all diseases, including dystrophy.

Dystrophy is a pathology that is caused by chronic nutritional disorders and is accompanied by tissue atrophy. Dystrophy can occur in people at any age, but this disease is most dangerous for children in the first years of life. The disease at an early age leads to delayed intellectual and physical development, decreased immunity, and metabolic disorders. Severe and moderate forms of dystrophy are rarely observed in socially prosperous regions.

Dystrophy is not always expressed by a person’s lack of weight relative to his height, as is typical for all hypotrophic patients. During another type - paratrophy, there is a predominance of a person’s weight over his height and the appearance of obesity. A uniform lag in both a person’s weight and height relative to age norms is another type of hypostatural type dystrophy. The most common and dangerous first type of disease – hypotrophic dystrophy.

Causes of dystrophy

In the prenatal period, primary nutritional dystrophy is caused by pathologies intrauterine hypoxia fetal and placental circulation. To the main risk factors during pregnancy include:

• infectious diseases in any trimester;
• woman's age under 18 and after 45 years;
• pathologies of the placenta;
• severe somatic diseases, including hereditary and chronic diseases, injuries;
• smoking;
• unfavorable social environment which leads to poor nutrition and nervous stress;
• toxicosis or gestosis in any trimester.

Acquired primary dystrophy may be a consequence of malnutrition in difficult social conditions or the result of poor-quality nutrition with protein deficiency. Also, recurrent infectious diseases, which are caused by recurrent otitis media, rotavirus and intestinal infections, lead to primary dystrophy.

Secondary dystrophy post- and prenatal period accompanies acquired and congenital:

The development of paratrophy is usually correlated with excessive calorie food and an increased amount of fats and carbohydrates in the daily menu. The appearance of paratrophy provokes diathesis of exudative-catarrhal and lymphatic-hypoplastic types with redness and inflammation of the mucous membranes and epithelium, as well as with the growth of lymphoid tissue. Dystrophy of the hypostatural type is accompanied by serious pathologies of the neuroendocrine system.

Today in medical practice there are several different classifications of dystrophic conditions. Taking into account what types of metabolic disorders predominate, allocate the following types dystrophy:

• carbohydrate;
• mineral;
• protein;
• fatty

Depending on the location of the pathology of metabolic processes, dystrophy can be cellular, extracellular and mixed.

According to etiology, dystrophy occurs:

• Acquired. Appears under the influence of external or internal factors and has a more favorable prognosis, in contrast to congenital forms.
• Congenital. The development of pathology is associated with genetic factors, that is, dysfunction of the metabolic processes of proteins, carbohydrates and fats is associated with hereditary pathology. Moreover, children’s bodies do not have one or more enzymes that are responsible for the metabolism of nutrients. As a result, incomplete breakdown of carbohydrates, fats or proteins occurs, and in the tissues there is an accumulation of metabolic products that have a detrimental effect on cell structures. The pathology affects a variety of tissues, but most often the nervous tissue is affected, which leads to a serious disruption of its functioning. Any types of congenital dystrophy are dangerous conditions that can lead to death.

Taking into account body weight deficiency dystrophy divided into the following groups:

• Hypostatrois. It is characterized not only by a lack of body weight, but also by a decrease in height, and these indicators do not correspond to age standards.
• Paratrophy. With this type of dystrophy, disturbances in tissue nutrition and metabolic processes lead to an increase in body weight.
• Hypotrophy. Today this is the most common type of disease. In this case, there is a decrease in weight relative to the person’s height. Taking into account the moment of appearance, congenital (prenatal), acquired (postnatal) and combined malnutrition are classified.

When dystrophy appears as a result of lack of proteins, carbohydrates(energy substances) or fats, then it is called primary. Secondary dystrophy is considered in cases where the pathology appears against the background of some other disease.

Hypotrophy at the first stage is expressed by a body weight deficit of approximately 15-22% relative to the physiological norm. The person’s condition is satisfactory, with a slight decrease in subcutaneous fat deposits, decreased skin turgor and appetite.

At the second stage of malnutrition with a person’s weight deficit of up to 30%, the patient’s motor activity and emotional tone are reduced. The patient is apathetic, tissue turgor and muscle tone are significantly reduced. A person has a greatly reduced amount of fatty tissue in the area of ​​the limbs and abdomen. Pathologies of thermoregulation are expressed in cold extremities and fluctuations in body temperature. Dystrophy at the second stage is accompanied by pathologies in the functioning of the cardiovascular system with arterial hypotension, tachycardia, and muffled heart sounds.

Hypotrophy at the third stage with a person’s weight deficit of more than 30% is also called nutritional insanity or atrophy. At this stage of the development of the disease, the general condition of the person is seriously disturbed, the patient is prone to indifference, drowsiness, anorexia, and irritability. With malnutrition at the third stage there is no subcutaneous fat. The muscles are completely atrophied, but muscle tone is increased due to disorders electrolyte balance and the presence of neurological disorders. Hypotrophy is accompanied by low body temperature, dehydration, weak and rare pulse, and arterial hypotension. Dyskinetic manifestations of dystrophy are expressed in vomiting, regurgitation, rare urination, and frequent loose stools.

Hypostature is a consequence of prenatal dystrophy of the neuroendocrine type. Congenital hypostatura is diagnosed during the birth of a child according to distinctive clinical symptoms:

Congenital persistent disorders of the nervous and endocrine regulation of processes are difficult to treat. In the absence of the above clinical symptoms and at the same time there is a lag in the physiological indicators of a person’s height and weight from age norms, hypostatura may be the result of constitutional short stature.

In children, paratrophy is most often provoked by excessive food intake or an unbalanced diet with insufficient protein and a large amount of carbohydrates. Inactive children on artificial feeding with various types of diathesis are more prone to paratrophy. Systematic physical inactivity and prolonged overfeeding often develop obesity, as one of the symptoms of paratrophic dystrophy. Also clinical symptoms of paratrophy are:

• lethargy;
• impaired emotional tone;
• fatigue;
• dyspnea;
• headaches.

Often appetite is reduced and is selective. Due to excess subcutaneous fat there is decreased muscle tone And lack of elasticity skin covers. Against the background of decreased immunity, functional and morphological transformations of internal organs are likely.

Diagnosis of dystrophy

The diagnosis of dystrophy is made on the basis of clinical characteristic symptoms, which include the ratio of a person’s weight to height, analysis of the body’s resistance to infectious diseases, the location and amount of subcutaneous fat, and assessment of tissue turgor. The stage of malnutrition is determined by laboratory tests of urine and blood.

Hypotrophy at the first stage - laboratory gastric secretion examinations and blood indicate dysproteinemia, which is expressed in decreased activity digestive enzymes and imbalance of blood protein fractions.

Hypotrophy at the second stage - according to laboratory examinations, a person with dystrophy at this stage has very pronounced hypochromic anemia with a low level of hemoglobin in the blood. Hypoproteinemia with low levels in the blood is also noted. total protein against the background of a strong decrease in enzyme activity.

Hypotrophy at the third stage - laboratory examinations indicate the presence in the urine of significant amounts of chlorides, phosphates, urea, in some cases ketone bodies and acetone, as well as blood thickening with slow sedimentation of erythrocytes.

The differential diagnosis of “hypostature” is determined by excluding diseases that are accompanied by a lag in physical development, for example, pituitary dwarfism, during which the human pituitary gland does not synthesize the required amount somatotropic hormones, or other mutational types of dwarfism with normal secretion of somatropin, but not the body’s sensitivity to it.

Dietary therapy is a fundamental aspect rational treatment dystrophy. Initially determined body tolerance to food, if necessary, enzymes are recommended: festal, abomin, pancreatin, panzinorm. At the next stage, a gradual adjustment of the energy value and volume of food consumed is made with constant monitoring of the loss or gain of body weight, diuresis and stool character. To do this, a food journal is created with the names and quantities of products recorded. Eating occurs in small portions up to 7-12 meals per day. Control is carried out until a person reaches physiological norms body weight.

As a stimulating treatment, courses of general tonic medications and multivitamin complexes are used: preparations with royal jelly, ginseng, oats, and lemongrass. Treatment of concomitant diseases and sanitation of foci of chronic infection. Increasing emotional status and eliminating physical inactivity is achieved through massage and complex physical therapeutic exercises.

Prenatal preventive measures, which are aimed at preventing the occurrence of intrauterine dystrophy, include: rest and work schedule, adequate sleep, feasible physical exercise, balanced nutrition, constant monitoring of the health of the fetus and the woman, control of the woman’s weight.

In a child, postnatal prevention of dystrophy is best carried out with natural feeding, regular monitoring of monthly weight and height gains during the first year and annual monitoring of subsequent dynamics of physical development.

In adult patients, prevention of dystrophy is possible with normal nutrition, treatment of major immunodeficiency diseases, as well as replacement therapy for malabsorption and enzymopathy.

You need to understand that strengthening your immunity, as well as the immunity of your children from birth, a balanced, rational and healthy diet, lack of stress and sufficient physical activity is best prevention any diseases, including dystrophy.

Therapeutic nutrition for dystrophy

Therapeutic nutrition for dystrophy

Vasily Filippovich Gladenin

V. F. Gladenin

Therapeutic nutrition for dystrophy

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Chapter 1. Dystrophies

Dystrophy– a pathological condition that characterizes various manifestations of chronic eating disorders. In this case, not only the digestive function is disrupted, but also the absorption of nutrients by the cells and tissues of the human body, the metabolism and vital functions of the body, its growth and development are disrupted.

Among the many causes of cell and tissue degeneration, nutritional dystrophy associated with nutrition occupies a special place. Synonyms for nutritional dystrophy are the following: starvation disease, edema disease, protein-free edema, starvation edema, military edema.

This is a disease of long-term malnutrition, manifested by general exhaustion, progressive disorder of all types of metabolism and degeneration of tissues and organs with disruption of their functions. This disease is not equivalent to a state of hunger or separate forms so-called partial nutritional deficiency, such as vitamin deficiency, one-sided feeding, etc.

In his writings, the writer Flavius ​​mentions hunger sickness. In Europe, it was first described in 1742 by the English doctor J. Pringel, who observed it in soldiers of besieged troops; outbreaks of starvation disease were observed in Napoleon's troops. More detailed information about the famine disease dates back to the First World War. From now on it begins research of this disease. R. A. Luria, V. A. Valdman, A. Belogolovy and others are participating in the work. Depending on the conditions that were the root cause of nutritional dystrophy (crop failure, flood, epidemics, wars, blockade, etc.), the form of the course of this disease develops .

The most complete form of nutritional dystrophy was observed by domestic scientists in besieged Leningrad during the Great Patriotic War. They published their observations in the monograph “Nutritional dystrophy in besieged Leningrad” edited by G. F. Lang. The monograph outlines all the variants of the course of this disease. The maximum increase in incidence occurred towards the end of the second month of the blockade. The mortality rate at this time reached 85%; men predominated among the sick. About 40% of the victims suffered from the edematous form of the disease. The duration of the illness ranged from 2–3 weeks followed by fatal up to two years with gradual recovery.

1. Etiology

The main etiological factor of nutritional dystrophy is prolonged (weeks, months) insufficiency of calories in food consumed. Depending on the degree of nutritional deficiency, the clinical picture of this disease develops.

The main etiological factor is joined by others, which stem from the poor state of the population (nervous-emotional stress, cold, heavy physical labor). Infectious diseases, especially intestinal ones, also increase the likelihood of developing nutritional dystrophy and aggravate its course.

In the development of nutritional dystrophy, not only quantitative, but also qualitative indicators of the diet, especially the lack of proteins, are important. With a lack of proteins and fats, there is a lack of essential amino acids, fatty acids and fat-soluble vitamins.

2. Pathogenesis

The disease of nutritional dystrophy can be considered as a clinical expression of impaired homeostasis due to the failure of many nutrients to enter the body in the required quantity and quality.

Clinical observations show that patients with nutritional dystrophy show signs of insufficient function of a number of endocrine glands - the pituitary gland, adrenal glands, gonads, thyroid gland, etc. (M. V. Chernorutsky).

With continued lack of nutrition, the body uses up its own reserves of fats, proteins and carbohydrates. There is a decrease in blood sugar levels down to the hypoglycemic level (25–40 mg%).

The level of lactic acid increases, acetone and acetoacetic acid appear in the urine increased quantity, later the blood pH decreases.

With nutritional dystrophy, general hypoproteinemia is observed, globulins predominate in the blood, and the function of the digestive glands changes. Arises enzyme deficiency, increasing the state of degeneration of tissues and organs due to impaired absorption of food products and their assimilation.

The production of hormones from the endocrine glands is disrupted, and hormonal deficiency develops.

Nutritional dystrophy may become more complicated infectious disease, which can cause death. In this case, extreme depletion of the neuroendocrine system occurs.

3. Pathological anatomy

IN different periods nutritional dystrophy may be associated various complications. The first period is characterized by small focal bronchopneumonia, especially in the cold season. In the next period of the disease, signs of acute and chronic dysentery are revealed, and pulmonary tuberculosis subsequently develops.

The corpse gives the impression of a skeleton covered in skin.

In the edematous form of nutritional dystrophy, pathological fullness is observed, the skin is pale, and an opalescent gray-white liquid is detected on the incision.

Internal organs are atrophic. The heart of an adult weighs no more than 90 g (the normal average is 174 g).

Blood clots are found in the veins of the extremities, which is associated with the low mobility of patients. All internal organs are reduced in size. There are no fat depots.

4. Clinical picture

In the clinical picture of nutritional dystrophy, three degrees (stages) of severity of the disease are observed (M. I. Khvilivitskaya).

First degree– distinct decrease in nutrition, pollakiuria, increased appetite, thirst, increased consumption table salt, as well as at times barely noticeable swelling. The patients are able to work.

Second degree– a sharp decrease in weight with the complete disappearance of fatty tissue on the neck, chest, abdomen and buttocks. The temporal fossae recede. General weakness, fatigue, and decreased ability to work appear. Increased chilliness is felt due to hypothermia (body temperature 34 ° C), and the psyche changes.

Third degree nutritional dystrophy - the disappearance of fat in all organs and tissues. Sharply expressed general weakness, adynamia, apathy are noted, and deep atrophy of skeletal muscles occurs. The skin is either dry and folded, or persistent swelling and ascites. Pronounced and persistent mental changes. Severe appetite disorders - from “ravenous hunger” to complete anorexia, from persistent constipation to fecal incontinence.

Changes occur in the central and peripheral nervous systems. Polyneuritis develops.

According to the clinical picture, the following forms of the disease are distinguished: cachectic, edematous and ascitic (observed in the edematous form). However, a transition from one form to another is possible. There are unpleasant sensations in the legs (paresthesia), dull pain in the soles, calf muscles, and thigh muscles.

Many patients with nutritional dystrophy show signs of parkinsonism.

At the beginning of the disease, patients are easily excitable and can be aggressive and rude. As the disease progresses, the victim's personality disintegrates. Memory loss is increasing. Feelings of shame and disgust disappear. Gradually, complete indifference and physical immobility sets in. At this time, food refusal is possible and death soon occurs.

Changes in the cardiovascular system are characterized by a decrease in heart size, bradycardia, arterial and venous hypotension. The number of heart contractions is reduced to 44–48 beats per minute, diffuse muscle changes are found: low voltage of the waves, flattening of T waves, slowing of intracardiac conduction.

Lung function is impaired.

Dyspeptic disorders are observed in many patients with nutritional dystrophy. Constipation is painful for several weeks. There are known cases of atonic intestinal obstruction requiring urgent surgery.

The protein-forming function of the liver is significantly impaired. There is a protein deficiency in the body.

5. Histochemical and luminescent studies of degenerative processes

For a long time, the concept of “dystrophy” did not have a clearly defined content. It was used both in a nosological sense to designate a disease (nutritional dystrophy, dystrophy of newborns), and in a biochemical sense to characterize metabolic disorders in organs and tissues, and in a morphological sense as a term equivalent to the terms “degeneration”, “degeneration”. Particular difficulties with this concept arose from the standpoint of biochemistry and morphology. Based on clinical and morphological comparisons, G. F. Lang argued that there is no morphological equivalent for a number of severe clinical disorders contractile function myocardium, having a purely biochemical basis. A “morphological dead end” has arisen in the problem of myocardial dystrophies. Ya. L. Rapoport puts morphological content into the concept of “myocardial dystrophy”.

The widespread development of histochemistry and electron microscopy resolved the contradiction between various interpretations the concept of “dystrophy”, allowing structural documentation of metabolic processes in cells and tissues and their disorders. Thus, the concept of “dystrophy” is concretized in certain morpho-chemical concepts. The time has come for visual observation of many metabolic processes occurring in cells, and thereby erasing the sharp line between morphology and biochemistry.

Dystrophy in children is a pathological condition that characterizes various manifestations of chronic nutritional disorders. In this case, not only the digestive function is disrupted, but also the absorption of nutrients by the cells and tissues of the human body, metabolism, the vital functions of the body, its growth and development.

Dystrophy in children is classified as a special group. According to the classification of G.N. Speransky and co-authors (1945), three types of dystrophy are distinguished: hypotrophy, hypostatura and paratrophy. In subsequent years (1969), G.I. Zaitseva and her co-authors made additions to this classification. They distinguish the type and degree (I, II, III) of the severity of dystrophy, the time of occurrence (dystrophy of prenatal, postnatal and mixed origin), the period of progression (initial, progression and convalescence), building it according to the etiological principle (exogenous, endogenous, exogenous-endogenous ). The attention of pediatricians is drawn to dystrophies of prenatal origin, which appear from the first days of a child’s life and are characterized by a delay in his physical development. This type of dystrophy is discussed in domestic and foreign literature under different names - neonatal dystrophy, dystrophy at birth, low birth weight, intrauterine malnutrition, etc. (1961, WHO). Severe forms intrauterine malnutrition is called neurodystrophy, emphasizing its origin in the central nervous system.

6. Etiology and pathogenesis of dystrophy in children

Exogenous and endogenous factors are important in the occurrence of dystrophies in children.

TO exogenous factors dystrophies include:

Nutritional (underfeeding, qualitative violation of the composition of food, the predominance of carbohydrates in it with a small amount of protein and fat, lack of vitamins);

Infections (dysentery, pneumonia, etc.);

Toxic factors;

Errors in child care.

TO endogenous reasons include the following:

Anomalies of the child's constitution;

Endocrine disorders;

Malformations of organs and systems (central nervous system, cardiovascular system, gastrointestinal tract, kidneys, lungs, etc.);

Hereditary metabolic disorders - amino acid, carbohydrate, fat, etc.

Pathogenesis dystrophy is complex. There is a decrease in the excitability of brain cells and the regulatory activity of the central nervous system is disrupted, which leads to dysfunction of all organs and systems, including dysfunction of the gastrointestinal tract. The absorption of proteins, fats and vitamins is impaired, the enzymatic energy of the blood is reduced, and the processes of absorption of nutrients by the cells and tissues of the body are disrupted. Eating and metabolic disorders develop. To maintain the vital functions of the body, proteins, fats and carbohydrates of its own tissues are used, which leads to cachexia (exhaustion).

In the formation of intrauterine dystrophies, maternal nutrition during pregnancy is of great importance, which may be sufficient in quantity, but insufficient in quality, i.e., in the content of individual foods. If the mother's diet contains insufficient protein and minerals a child may be born with stunted height and weight or overweight due to protein-free edema. Low child weight is associated with atrophy of organs and tissues.

Atrophy, which is observed with cachexia, is characterized by a decrease in the volume and size of organs as a result of qualitative changes in cells and tissues.

Depending on the cause of atrophy, the following types are distinguished:

1) neurotoxic;

2) functional;

3) hormonal;

4) from malnutrition;

5) as a result of exposure to physical, chemical and mechanical factors.

At the same time, dystrophic changes are observed in the organs.

With cachexia, fatty tissue in the epicardium, retroperitoneum, and perinephric region disappears, and diffuse decalcification of bones is noted, accompanied by pain.

Based on etiology, they distinguish exogenous cachexia And cachexia of endogenous origin.

The most common cause of exogenous cachexia is malnutrition in quantitative and qualitative terms. This leads to nutritional dystrophy and nutritional cachexia. Exogenous cachexia includes poisoning with arsenic, lead, mercury, fluorine, as well as vitamin deficiencies - beriberi, sprue, pellagra, rickets and developing in chronic stage radiation sickness.

In most cases, the patient has no subcutaneous fatty tissue, sagging and atrophy of the skeletal muscles are noted, the arms are hanging “like whips,” the stomach is retracted, the eyes are sunken, the hair is dry and falling out, the nails are brittle, the teeth become loose and fall out, the skin is dry, flabby, without signs. turgor, folded or stretched like a mummy, pale earthy in color. Skin pigmentation, hemorrhages, furunculosis, loose gums, stomatitis, clouding of the lens, etc. are often observed. Sometimes weight loss reaches such an extent that patients resemble a skeleton covered with skin; in some cases, swelling and dropsy of the cavities are observed. Cachexia is usually accompanied by general hypotension, hypotension of skeletal muscles, a sharp decrease in vascular tone, and arterial hypotension. Patients are indifferent to the environment and to themselves, are in a state of prostration, numbness, and their intelligence is sharply reduced. Usually they lie down, move with difficulty, and their movements are sluggish and slow. Sexual function drops sharply, and women experience amenorrhea. Oligouria is often observed, and in the edematous form, polyuria.

7. Mental disorders

The mental disorders of patients with cachexia are very diverse. In the initial stage, asthenia develops with a predominance of irritable weakness (see above), and with worsening general condition apathy (insensitivity, indifference) begins to predominate. Apathetic syndrome – mental disorder, in which there is complete mental emptiness, mental and physical adynamia, exceptional poverty of the affective sphere up to its complete blockade (“paralysis of emotions”).

Clinic of apathetic syndrome

Patients are indifferent to both their own personality and the surrounding phenomena of life. There are no desires, drives or aspirations. With the most pronounced depth of damage to emotional reactions, weakening of all mental manifestations a state of apathetic stupor develops. At the same time, there are no signs of mobilization of attention or intellectual tension. The patient lies on his back, all muscle groups are relaxed, the eyes are constantly open, the gaze is directed into space, not fixating on anything. Night wakefulness is characteristic - “waking coma” or “death with open eyes” (Jaspers (K. Jaspers)). With a less pronounced apathetic syndrome, patients are lethargic and, if at all, give monosyllabic answers. Consciousness is preserved, but attention is disoriented.

Etiopathogenesis apathetic syndrome is most typical for prolonged symptomatic somatic psychoses with tuberculosis, malaria, typhus, vitamin deficiencies, wound sepsis, endocrine disorders, with brain damage during injury, tumor, epidemic encephalitis, etc. Apathetic syndrome develops as a result of severe depletion of the body's reactive forces with the development cachexia and involvement of the interstitial brain in the process with disruption of the conduction of impulses between the cortex and subcortex during organic diseases brain. The pathological and anatomical picture shows the predominance of toxic-degenerative processes in the mesenchymal elements of the brain (M. E. Snesarev).

Diagnosis placed on the basis of the clinical picture.

Differential diagnosis includes stunning.

Stunning is a form of stupefaction, manifested by a decrease in consciousness and its devastation. Stunning occurs in various diseases that cause disorders of the central nervous system.

The main signs of deafness are difficulty in perceiving external influences due to an increase in the threshold of excitability of the analyzers, a narrowing of comprehension of the surrounding world due to a slowdown in thinking and weakening of analysis and synthesis, passivity of thinking due to a decrease in volitional activity, weakened memorization of current events with subsequent amnesia. Unlike other states of stupefaction, during stupor there are no productive psychopathological symptoms, such as hallucinations and delusions.

Based on the depth of disturbance of clarity of consciousness, the following degrees of stunning are distinguished:

1) nullification;

2) doubtfulness;

The boundaries between them are usually unclear.

Nullification- fog, confusion, - the mildest degree of stun. The patient's clear consciousness is periodically disrupted by a short-term, for several seconds or minutes, state of mild stupor: perception and comprehension of the environment becomes foggy and fragmentary, the activity of thinking and motor skills decreases. The patient becomes less talkative.

Doubtfulness– pathological drowsiness – deeper and more prolonged stupor. Perception external stimuli difficult: does not respond to weak stimuli; Only intense stimuli are perceived (loud conversation, intense light), but the reaction to them is slow and quickly exhausted.

Understanding of surrounding events is superficial, their comparison with past life experience is limited, orientation in place, time and space is disrupted. Speech is sluggish, laconic, movements are slow, fatigue sets in quickly; reacts inadequately or not at all to complex questions and tasks. The patient himself does not show interest in others, most of the time he lies passively with eyes closed, half asleep.

Sopor– unconsciousness, insensibility – pathological hibernation, deep stupor. The patient lies motionless, with his eyes closed, his face is amicable, and speech contact is impossible. Strong stimuli (strong sound, bright light, painful stimuli) cause undifferentiated, stereotypical defensive reactions.

Coma (deep sleep), comatose state– switching off consciousness. The patient has no reactions even to the strongest stimuli. In the initial stages, unconditional reflex reactions are possible (pupillary, corneal reflexes, reflexes from the mucous membranes), which disappear after some time.

There are also special forms of deep stunning in the form of apallic syndrome, or akinetic mutism.

Etiology and pathogenesis have not been fully studied. Stunning can be caused by exogenous and endogenous factors. Exogenous factors include alcohol, carbon monoxide and others, endogenous factors include uremia, intoxication, traumatic brain injury, intracranial tumors, inflammatory processes and circulatory disorders in the brain.

Stunning occurs when excitability decreases nerve cells cerebral cortex, when the activity of first the second and then the first signaling system is inhibited. A diffuse decrease in cortical activity occurs either due to damage to the cortical structures of the brain, or due to impaired stimulation of the cerebral cortex from the reticular formation.

Treatment is aimed at the underlying disease that causes dysfunction of the brain. Auxiliary therapeutic effect psychostimulants such as amphetamine, as well as metabolic drugs such as nootropics, glutamic acid.

Forecast depends on the nature of the disease during which stunning occurs. Most often the prognosis is poor.

Clinical picture

The main clinical symptoms of dystrophy in children: weight and height retardation; delayed psychomotor development; decreased body resistance; dyspeptic disorders.

In most observations, the body weight of a child with dystrophy is reduced, but it is also possible that it may increase. The degree of weight loss can vary, up to a sharp lag. Weight gain is possible due to water retention in the body. Children are lethargic, inactive, and their reaction to their surroundings is reduced. There is a tendency to various infections: purulent skin rashes, acute respiratory diseases, pneumonia, etc. With dystrophy, clinical signs of vitamin deficiency develop. Dysfunction of the gastrointestinal tract is manifested by frequent bowel movements and stool composition.

Severe intrauterine malnutrition is divided into four clinical forms:

1) neuropathic;

2) neurodystrophic;

3) neuroendocrine;

4) encephalopathic.

Neuropathic form characterized by increased excitability of the child, sleep disturbance, and a reduction in its duration. Manifestations of malnutrition are not pronounced, develop after birth, and are persistent. At neurodystrophic form the leading symptom is persistent weight loss, persistent anorexia (complete lack of appetite with an objective need for nutrition, caused by organic or functional dysfunction of the appetite center). Psychomotor development is somewhat delayed.

Neuroendocrine form characterized by persistent weight loss and significant stunting. At birth, physique abnormalities such as pituitary dwarfism and hemiasymmetry are detected. Sometimes symptoms associated with dysfunction of the endocrine glands appear.

8. Cachexia

Cachexia(Greek kachexia – “soreness, feeling unwell») – painful condition, associated with an insufficient supply of nutrients to the human body or a violation of their absorption. Cachexia occurs against the background of general exhaustion of a person, although in rare cases it is observed without exhaustion and even with noticeable obesity. It occurs in various chronic diseases, chronic intoxications, malnutrition and is accompanied by a sharp deterioration and disruption of homeostasis.

In this case, oligemia (hypovolemia) is observed, characterized by a decrease in total blood volume, and the ratio of plasma and red blood cells is disrupted. A decrease in the number of red blood cells is observed in anemia of various origins, the blood hemoglobin content decreases. A decrease in circulating plasma volume occurs as a result intensive care diuretics, plasma loss due to extensive burns, diarrhea, vomiting.

Severe physical weakness and symptoms of general asthenia appear.

Asthenia is known to be characterized increased fatigue and exhaustion, weakening, or even complete loss of ability for prolonged physical and mental work. Patients experience irritable weakness, expressed by increased excitability, easily changing mood, short temper, affective lability with features of capriciousness and displeasure, as well as tearfulness. Hyperesthesia is characteristic - intolerance to bright light, loud sounds, strong odors. Patients complain of headaches, sleep disturbances, and when barometric pressure drops, Pirogov's symptom is noted. Memory suffers, especially remembering current events.

Asthenic syndrome can develop after undergoing somatic diseases, traumatic brain injury, in the initial period of hypertension, with atherosclerosis, cerebral syphilis, progressive paralysis, endocrinopathies, schizophrenia, etc.

This condition most often occurs in people with a weak or unbalanced type of higher nervous activity.

The weight of the internal organs decreases (splanchnomicria), and dystrophic and atrophic changes are observed in them.

Dumping syndrome or dumping syndrome, characterized by a set of clinical, radiological and laboratory signs that develop after gastrectomy due to the rapid flow of gastric contents from the stomach stump into the small intestine, can also lead to cachexia.

Dumping syndrome refers to post-gastroresection complications, early and long-term complications after gastrectomy, vagotomy and anthrumectomy.

The frequency of these complications averages 10–15%, the size of the removed part of the stomach is 2/3-3/4. Therefore, in the surgical treatment of pyloroduodenal ulcers, preference is given to economical gastrectomy - anthrumectomy with vagotomy.

To complications early period after operations on the stomach, there are disturbances in evacuation from the gastric stump due to inhibition of the motor activity of the stomach due to surgical trauma, damage to the neuromuscular system, disturbances in electrolyte and protein metabolism and vagotomy, also observed acute obstruction afferent loop of the anastomosis.

Late complications - post-gastroresection syndrome - include dumping syndrome; adductor loop syndrome; hypoglycemic syndrome with sharp fluctuations in blood sugar levels followed by hypoglycemia; chronic post-resection pancreatitis due to surgical trauma; metabolic disorders that develop in connection with a violation of the functional synergy of the digestive system organs; Anemia is usually iron and vitamin deficiency.

The listed complications lead to disruption of the metabolism of proteins, fats, carbohydrates, vitamins, electrolytes, and ultimately cachectic nutritional dystrophy (cachexia), or edematous form, develops.

Dystrophy of cells and tissues– a pathological process that occurs in connection with metabolic disorders and is characterized by the appearance in cells and tissues of metabolic products that are changed quantitatively or qualitatively. Dystrophy of cells and tissues is considered as one of the types of damage.

The reasons leading to degeneration of cells and tissues are very diverse: disorders of blood and lymph circulation, innervation, hypoxia, infection. Intoxication, hormonal and enzyme disorders, hereditary factors, etc. The development of cell and tissue degeneration is based on a disorder of regulatory mechanisms (cell autoregulation, transport systems, integrative neuroendocrine trophic systems) providing trophism. Disorders of cell autoregulation mechanisms, which can be caused by various factors (hyperfunction, toxic substances, radiation, etc.) lead to energy deficiency and disruption of enzymatic processes. Enzymeopathy, acquired or hereditary, is the main pathogenetic link and expression of degeneration of organs and tissues. When the functioning of transport systems (microcirculatory blood and lymph) is disrupted, hypoxia develops, and it becomes leading in the pathogenesis of such discirculatory dystrophies of cells and tissues. A disorder of endocrine regulation of trophism (thyrotoxicosis, diabetes, hyperparathyroidism) is associated with the occurrence of endocrine, and with a violation of the nervous mechanisms of trophism (impaired innervation, brain tumor, etc.) – neurotoxic and cerebral dystrophy of cells and tissues.

Among the morphological mechanisms leading to the development of cell and tissue degeneration, there are:

Infiltration (for example, infiltration of the epithelial protein of the proximal tubules of the kidneys in nephrosis, infiltration of arterial intimal lipoids in atherosclerosis);

Perverted synthesis (synthesis of hemomelanin in malaria, synthesis of a pathological glycoprotein - amyloid in plasmacytoma);

Transformation;

Decomposition (decomposition of cell membrane lipoproteins, for example, a hepatocyte in fatty degeneration, or fibrous structures and the main substance of the vessel wall in fibrinoid swelling).

The study of the mechanisms of development of cell and tissue degeneration became possible thanks to the use of histochemistry, electron microscopy, autoradiography, histospectrography, etc.

Depending on the predominance of metabolic disorders, the following types of dystrophies are distinguished:

1) protein;

2) fat;

3) carbohydrates;

4) mineral degeneration of cells and tissues:

Parenchymatous;

Mesenchymatous;

Mixed.

Dystrophy of cells and tissues can be general (systemic) and local in nature.

Protein degeneration of cells and tissues, or dysproteinosis, is caused by excessive intake of proteins into cells or intercellular substance, perverted protein synthesis, or disintegration of tissue structures; physico-chemical and morphological properties proteins change. Parenchymal degeneration of cells and tissues:

Grainy;

Hyaline-drip;

Dropsy;

Balloon;

Acidophilic;

Horny.

Mesenchymal dystrophy:

Mucoid swelling.

Mixed dysproteinoses are a large group of dystrophic processes that occur when there is a metabolic disorder:

A) chromoproteins - hemosiderosis, melanosis, hemomelanosis, jaundice;

B) nucleoproteins – gout, uric acid infarction;

B) glycoproteins – mucous and colloid disproteinoses.

Fatty degeneration of cells and tissues, or lipidosis, is characterized by a change in the amount of fat in fat depots, the appearance of lipids where they are normally absent, and a change in the quality of lipids in cells and tissues. Disorders of neutral fat metabolism manifest themselves more often in a decrease, less often in an increase in its reserves; it may concern the entire body or a specific part of the body. A general decrease in the amount of adipose tissue is characteristic of cachexia, local - for regional lipodystrophy; overall increase fat reserves lead to obesity, local - observed with tissue or organ atrophy (fat replacement), with endocrine disorders. Disorders of lipid metabolism most often occur in cells parenchymal organs(myocardium, liver, kidneys) – parenchymal lipoidosis. Less commonly, it is characterized by the deposition of various types of lipoids in the reticuloendothelial system - systemic lipoidoses.

Chapter 2. Therapeutic nutrition for dystrophy

I. Dystrophy in children

1. Clinical picture of dystrophy in children

To the main clinical symptoms dystrophies in children include:

Changes in weight and height;

Delayed psychomotor development;

Decreased body resistance;

Dyspeptic disorders.

In most observations, the child’s body weight is reduced, but it is also possible that it may increase. The degree of weight loss can vary, up to a sharp lag. When water is retained in the body, weight gain is possible. With this pathology, children are lethargic, inactive, the reaction to what is happening is reduced, reduced protective forces body. They are prone to developing various infections: pustular diseases skin, acute respiratory diseases; pneumonia. There are signs of vitamin deficiency. The function of the gastrointestinal tract is impaired. The stool is delayed or increased in frequency, its color, reaction and consistency change.

Severe forms of intrauterine hypotrophy are divided into four clinical forms: neuropathic, non-dystrophic, neuroendocrine and encephalopathic. The neuropathic form is characterized by increased excitability of the child, sleep disturbance, and shortened sleep time. The manifestation of malnutrition is not pronounced, develops after birth, and is persistent. In the neurodystrophic form, the leading symptom is persistent weight loss. The neuroendocrine form is diagnosed by persistent retardation in weight and height. At birth, a type of pituitary dwarfism is noted. Sometimes symptoms associated with dysfunction are identified; the form is manifested by severe malnutrition of the third degree, anorexia, and a significant lag in psychomotor development.

Depending on the combination of signs of dystrophy, the nature of skin changes, its color, weight deficiency, three variants of intrauterine dystrophy of newborns (Clifford) are distinguished: Clifford I - maceration of the skin; Clifford II and III – maceration of the skin, its yellow color is combined with varying degrees of hypotrophy. The syndrome occurs during post-term pregnancy due to complex dysfunction of the placenta.

Diagnosis put on the basis clinical manifestations and height and weight indicators.

A. Gaucher disease

Fatty degeneration of the walls blood vessels(mesenchymal lipidosis) underlies atherosclerosis.

Carbohydrate dystrophy of cells and tissues concerns a violation of the metabolism of polysaccharides, mucopolysaccharides and glycoproteins. The most common disorder is glycogen polysaccharide metabolism. They are especially pronounced in diabetes mellitus, when tissue glycogen reserves sharply decrease, and in glycogenosis, characterized by excessive glycogen deposition (storage diseases) in the liver, heart, kidneys, and skeletal muscles.

Mineral dystrophies usually have a mixed nature: the metabolism of potassium, calcium, iron and copper is disrupted. An increase in the amount of potassium in the blood and tissues is observed with Addison's disease; potassium deficiency explains the occurrence of a hereditary disease - periodic paralysis. Disorders of calcium metabolism - calcinosis, calcareous degeneration, or tissue calcification, are characterized by the precipitation of lime in the tissues in the form of dense masses; There are metastatic (calcareous metastases), dystrophic (petrification) and metabolic (calcareous gout) tissue calcification. Iron is contained mainly in hemoglobin, and the morphology of disorders of its metabolism is associated with hemoglobinogenic pigments - chromoproteins. If copper metabolism is impaired, hepatocerebral dystrophy may occur, in which copper is deposited in the liver, kidneys, brain, and cornea.

B. Skin dystrophy– a pathological process that occurs in connection with metabolic disorders and is characterized by the appearance in cells or interstitial substance of metabolic products that are changed quantitatively and qualitatively. The term “skin degeneration” is often applied to these changes.

Reasons metabolic disorders, leading to the development of skin dystrophy, are varied: chronic inflammation, allergic and infectious factors, intoxication, circulatory disorders, malnutrition, hypovitaminosis, diseases of the endocrine glands, developmental defects, etc.

Skin dystrophies can be systemic or local in nature, congenital or acquired.

Skin dystrophy can be an independent nosological entity, as well as a symptom of a disease. With eczema, dermatitis and other diseases, vacuolization of the epithelium develops (vacuolar degeneration, or degeneration). For some viral diseases skin (chickenpox, herpes zoster) ballooning dystrophy is observed. Horny dystrophy is observed in squamous cell skin cancer and Darier's disease. In lichen planus, the epithelium undergoes colloid degeneration. In the connective tissue of the skin, mucous dystrophy may occur, in which collagen fibers turn into a semi-liquid substance, observed with skin myxedema, myxoma. Piamenian dystrophy occurs in skin cancer; a peculiar and progressive disorganization of connective tissue is observed in the skin during collagenosis (phases of mucoid swelling, fibrinoid and sclerosis). Calcareous skin degeneration occurs with injuries, scleroderma and tumors.

If dystrophic changes in the skin are not a consequence of previous pathological processes, but arise primarily, then such pathological processes are considered as independent nosological forms of skin diseases. They can be congenital or acquired.

There is hyperelastic skin of Unna (Ehlers-Danlos syndrome) - congenital disorder development of collagen structures, characterized by sharp extensibility of normal-looking skin. In this case, the pulled skin quickly returns to its original position. Hyperelastic skin is the main symptom of desmogenesis imperfecta. It should be differentiated from flabby skin - a congenital abnormality of connective tissue. In contrast to hyperelastic skin, flaccid skin is stretched and hyperplastic, hanging down in large, flabby and wrinkled folds. Sometimes this anomaly is combined with ligamentous weakness, growth retardation and mental retardation.

Senile skin dystrophy is a phenomenon of age-related involution that begins at the age of about 50 years.

Hyperkeratosis, parakeratosis, focal acanthosis, and hyperpigmentation develop in the epidermis. In the papillary layer of the dermis there is an accumulation of basophilic fibrous, granular and lumpy masses - a consequence of collagen destruction. Hyaline, colloid, and myloid dystrophies also occur.

Senile skin dystrophy manifests itself as keratosis in the form of raised yellowish-brown plaques with a rough surface or papillomatous growths with a warty brown surface. The skin becomes dry, rough, rough, yellow in color, sometimes with a slight sheen to the surface, with atrophic and pigmented spots and basal cell carcinomas. Unchanged areas of skin are also observed.

The skin of sailors and farmers has a reddish-brown color, thickened, rough, covered with pigment spots, with areas of keratosis and atrophy.

Diamond-shaped hypertrophic skin tendydystrophy of the back of the neck associated with prolonged exposure to sunlight. Microscopy of prepared preparations reveals foci of elastosis and hyamination of collagen fibers. The thickened skin is cut by deep grooves, forming a diamond-shaped pattern up to 5 cm in diameter, soft, yellowish-brown in color.

B. Diffuse elastomy of Drobrey– colloid skin dystrophy. The histological section shows elastorhexis, swollen elastic fibers that merge with collagen fibers; the resulting felt-like mass is painted black with acidic orsepn. Hair follicles are dystrophic, the epidermis is atrophic.

Diffuse elastoma is formed in older men, less often in young men. On the skin of the face, mainly in the cheek area and near the eyes, a sharply demarcated diffuse plaque of soft consistency appears, covered with wrinkled skin with papular rashes and multiple pinpoint depressions formed by dilated openings of the hair follicles (reminiscent of the surface of a lemon).

G. Gialoma– accumulation in the skin of a homogeneous colloidal mass with thickening of elastic fibers.

On open areas of the body, mainly on the face and neck, multiple nodules appear, resembling cysts of thickened skin containing a jelly-like mass. Skin elastoidosis is observed in older men: nodular, cystic, comedonal, colloidal dystrophy of the skin. At histological examination swelling, homogenization, interweaving of elastic fibers, comedones are noted, follicular cysts, inflammatory infiltrates around dilated vessels of the dermis.

This pathology is characterized by dense nodules (cysts) and comedones against the background of thickened, wrinkled, red skin. The pathology is localized on the back of the head, ears, and temporal region. It is observed in older, obese men.

Amyloid skin dystrophy develops in a small area (local amyloidosis) and can be a manifestation of general amyloidosis.

2. Treatment

As for the treatment of dystrophy in adults and the elderly, it is most often symptomatic. Particular attention is paid to the treatment of dystrophy in young children, and it is based on the type of dystrophy, etiological factor, severity, time of occurrence and period during the course of the disease. Treatment should be comprehensive, continuous (until recovery), and one of its mandatory components should be diet therapy. In mild cases of dystrophy associated with quantitative underfeeding, the administration of a sufficient amount of food in addition to supplementary feeding can solve the issue of curing the child. If a deficiency of proteins or fats is detected, the diet is adjusted accordingly.

Food for a young child is not only a source of energy necessary for heat generation and the functioning of organs and tissues, but also a plastic material necessary for the growing child’s body for metabolic processes, specific and nonspecific resistance child's body to environmental influences.

Rational nutrition of children is the most important factor in their lives, without which proper development child is impossible. The child’s food must satisfy the needs of his body and correspond to his physiological capabilities.

The amount of protein in food is special meaning for the development of an early child. A decrease in protein in the diet quickly leads to growth retardation and mental development. Protein is an essential substance! And you can’t limit yourself to a minimum of proteins in your diet. They must be administered with the child’s food in optimal quantities.

The need for proteins depends on the age of the child and his characteristics. When breastfed at the age of 3–4 months, children should receive 2–2.5 g of protein per 1 kg of body weight. This is usually satisfied by human milk protein. In this case, not only the absolute amount of amino acids matters, but also their ratio. The ratio of casein to albumin in human milk is 0.6:1, and in cow's milk it is 5.6:1.

End of introductory fragment.

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