Proper nutrition in diseases of the nervous system. muscular dystrophy

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

Weak muscle tone impairs blood circulation, interferes with normal lymph circulation, prevents efficient digestion, often causes constipation, and sometimes does not allow you to control urination or even void bladder. Often, due to muscle weakness, the internal organs descend or lie on top of each other. clumsiness of movements muscle tension and poor coordination, very often seen in malnourished children and usually left unattended, are quite similar to the symptoms seen in muscular dystrophy and multiple sclerosis.

Muscle weakness

Muscles are made up primarily of protein, but also contain 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 needed 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 are usually relieved by increasing the amount of these substances in food.

Potassium is necessary for the contraction of the body's muscles. In just a week, healthy volunteers who received refined food, similar to the one we eat every day, developed muscle weakness, extreme fatigue, constipation, and depression. All this almost immediately disappeared 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 bowel muscles allow bacteria to release large amounts of colic-causing gases, and spasm or displacement of the bowel can lead to blockage. When death occurs due to potassium deficiency, an autopsy reveals severe muscle damage and scarring.

In some people, the need for potassium is so high that they periodically experience paralysis. Studies of these patients show that salty foods high in fat and carbohydrates, and especially sweet cravings, stress, as well as ACTH (a hormone produced by the pituitary gland) and cortisone, reduce blood potassium levels. Even if the 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 levels of potassium in the blood.

When muscle weakness leads to fatigue, flatulence, constipation, and an inability to empty the bladder without the aid of a catheter, potassium chloride tablets are especially helpful. Most people, however, can get potassium by eating fruits and vegetables, especially leafy greens, and by avoiding refined foods.

Vitamin E deficiency is a common, though 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 poorly absorb fats. The nuclei of muscle cells and the enzymes necessary for muscle contraction cannot form without vitamin E. Its deficiency greatly increases the oxygen demand of muscle tissue, prevents 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 in the muscles and may even be deposited.

In pregnant women, muscle weakness due to vitamin E deficiency, often caused by iron supplements, sometimes 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 marked 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 a short time.

Prolonged stress and Addison's disease

Advanced adrenal exhaustion, as in Addison's disease, is characterized by lethargy, agonizing 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, muscle cells are also destroyed. Moreover, depleted adrenal glands cannot produce a hormone that stores the nitrogen of destroyed cells in the body; normally, this nitrogen is reused to build amino acids and repair tissues. Under such circumstances, muscles quickly lose strength even with protein-rich foods.

A depleted adrenal gland is also unable to produce enough of the salt-retaining hormone aldosterone. So much salt is lost in the urine that potassium leaves the cells, further slowing down contractions, weakening and partially or completely paralyzing the muscles. Potassium intake can increase the amount of this nutrient in the cells, but in this case, salt is especially needed. People with depleted adrenal glands usually have low blood pressure, which means they don't have enough salt.

The adrenal glands are quickly depleted in pantothenic acid deficiency, causing the same condition as prolonged stress.

Because stress plays a role in all muscle disorders, any diagnosis should emphasize restoration of adrenal function. An anti-stress program should be carefully followed, especially in the case of Addison's disease. Recovery is 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 damage or stretching, and inflammation indicates that the body is not producing enough cortisone. A diet high in vitamin C, pantothenic acid, and 24-hour milk intake usually provide 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 usually cause considerable discomfort before the cause is found. Daily intake vitamin E with myositis brings a noticeable improvement.

Pseudoparalytic myasthenia gravis

The term myasthenia gravis itself means a severe loss of muscle strength. This disease is characterized by emaciation and progressive paralysis that can affect any part of the body, but most often the muscles of the face and neck. Double vision, droopy eyelids, frequent choking, difficulty breathing, swallowing and speaking, poor articulation and stuttering are typical symptoms.

Isotopic studies with radioactive manganese have shown that the 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 a person has not yet been established, people suffering from muscle weakness can be recommended to include wheat bran and whole grain bread in the diet (the richest natural springs).

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

It takes a whole battery to make acetylcholine nutrients: vitamin B, pantothenic acid, potassium and many others. The lack of choline itself causes an underproduction of acetylcholine and leads to muscle weakness, damage to muscle fibers and extensive growth of scar tissue. All this is accompanied by the 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, provided 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 excretion and utilization of acetylcholine, but with insufficient supply of vitamin E, the enzyme necessary for the synthesis of acetylcholine is destroyed by oxygen. This also causes muscle weakness, muscle breakdown, scarring and loss of creatine, but vitamin E supplementation corrects the situation.

Since pseudoparalytic myasthenia gravis is almost inevitably preceded by prolonged stress, aggravated by medications that increase the body's needs, an anti-stress diet, unusually rich in all nutrients, is recommended. Lecithin, yeast, liver, wheat bran, and eggs are great sources of choline. Daily diet should be divided into six small, protein-rich servings, richly supplemented with "anti-stress formula", magnesium, B-vitamin tablets with a lot of choline and inositol, and possibly manganese. You should eat salty for a while and increase your potassium intake through an abundance 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, choppy movements or muscle spasm in 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 is normally high. And even the remaining lecithin is abnormal because it contains saturated fatty acids. In addition, multiple sclerosis is most prevalent in countries where high saturated fat intakes are invariably associated with low blood levels of lecithin. Perhaps because of the reduced need for lecithin, people with multiple sclerosis are less likely to be prescribed a low-fat diet, and it is shorter. Significant improvement achieved when three or more tablespoons of lecithin are added to food daily.

It is likely that a lack of any nutrient - magnesium, B vitamins, choline, inositol, essential fatty acids - can exacerbate the course of the disease. Muscle spasms and weakness, involuntary shuddering 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 development 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. 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 induced disease. Both in laboratory animals and in humans, with a deficiency of vitamin E, the need for oxygen increases many times over, the amount of many enzymes and coenzymes necessary for normal operation muscles, markedly 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 leave the cells, and muscle tissue is eventually replaced by scar tissue. Muscles split lengthwise, which, incidentally, makes one wonder if a lack of vitamin E plays a major role in the formation of a hernia, especially in children, whose deficiency is simply terrifying.

For many months or even years before a diagnosis of dystrophy is made, amino acids and creatine are lost in the urine, indicating muscle breakdown. If vitamin E is given at the onset of the disease, the destruction of muscle tissue is completely stopped, as indicated by the disappearance of creatine in the urine. In animals, and possibly in humans, the disease develops faster if the diet 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 suffer from it - and that chromosomal changes have been found 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 are sometimes treated with fresh wheat bran oil, pure vitamin E, or vitamin E in combination with other nutrients. When diagnosed early, some patients have recovered after simply adding wheat bran to their diet 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, crawl and walk later, ran slowly, climbed stairs with difficulty and got up after a fall. Often the child was ridiculed for years as being lazy and clumsy before going to the doctor. Since the huge masses of scar tissue are commonly mistaken for muscles, mothers of such children were often proud of how "muscular" their child was. Eventually, the scar tissue shrinks, causing either excruciating back pain or shortening of the Achilles tendon, resulting in as much disability as the weakness of the muscles themselves. It is not uncommon for the Achilles tendon to be surgically lengthened many years before a diagnosis of dystrophy is made, yet vitamin E is not given as a preventive measure.

Every person with impaired muscle function should immediately take a urine test and, if creatine is found in it, noticeably improve nutrition and include in it a large number of vitamin E. Muscle dystrophy could be completely eradicated if all pregnant women and artificial children were given vitamin E and refined foods devoid of it were excluded from the diet.

Proper nutrition

Like most diseases, muscle dysfunction stems from a variety of deficiencies. Until nutrition becomes adequate in all nutrients, neither recovery nor preservation of health can be expected.

Instruction

If dystrophy is alimentary in 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 the approach to nutrition.

In order to get rid of dystrophy You need to eat at least 5 times a day. The diet should 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 egg powder and brewer's yeast.

Suffering from dystrophy should walk more often in the fresh air, walk, and also gradually include in their daily routine physical exercise. You can work out in the gym twice a week for half an hour. After some time, the intensity of training and their duration should increase.

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

If dystrophy develops as a result of malformations of the gastrointestinal tract, no half-measures to get rid of it, unfortunately, will not help. In this case, surgical intervention is necessary.

Muscular dystrophy (this term is understood as a group of various muscle diseases) is hereditary. It is believed that such drugs or medical devices that would slow down this progressive disease still do not exist. All the efforts of doctors in this case are aimed at combating possible complications. This is, first of all, a deformity of the spine, which develops due to weakness of the back muscles, as well. The predisposition to inflammation of the lungs is due to the weakness of the respiratory muscles. Such patients are observed by general practitioners and neuropathologists. In this case, good nutrition is also important. It is very useful to eat boiled chicken meat.

In addition to medical treatment, massage is also used. Some experts argue that rubbing butter into the muscles is effective for patients with muscular dystrophy. To do this, take the cream, which is formed during the settling of milk, whipped, rub the person with the resulting oil. Within 20 minutes, oil should be rubbed into the back and spine, then for 5 minutes - into the thigh and lower leg from behind, then (movements from bottom to top). After this procedure, the patient is wrapped in a sheet and wrapped up. 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, the townsfolk rather frivolously scatter the concept of dystrophy, calling every thin person “dystrophic” behind their backs or jokingly. At the same time, 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 fully eat, but with such a phenomenon when all the nutrients entering the body are simply not absorbed by him, which accordingly leads to a violation of normal growth and development, which manifests itself not only externally. , but also internally (dystrophy of organs and systems).

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

At the heart of the disease, according to pathological anatomy, 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.
Postponed stresses or disorders of the human psyche.
Irrational nutrition, both malnutrition and the abuse of foods, especially those that contain a large amount of carbohydrates.
Problems from the digestive organs.
General weakening of the immune system.
Constant impact on the human body of external adverse factors.
Chromosomal diseases.
Somatic diseases.

This disappointing list can be continued, since there are really a great many reasons that can start the process of trophic disturbance at any time.

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

The 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 features of which will be:

I degree– decrease in body weight, tissue elasticity and muscle tone in the patient. In addition, there is a violation of the chair and immunity.
II degree- subcutaneous tissue begins to thin out, or even disappears altogether. Acute vitamin deficiency develops. All this against the background of further weight loss.
III degree- complete exhaustion of the body occurs and respiratory and cardiac disorders develop. The body temperature is kept at low rates, as well as blood pressure indicators.

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

A state of arousal.
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.
Decreased overall body resistance.

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

Disease classification

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

According to their etiology, they distinguish:

congenital dystrophy;
acquired dystrophy.

According to the types of metabolic disorders, it can be:

protein;
fatty;
carbohydrate;
mineral.

According to the localization of their manifestations, they distinguish:

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 apart from all types of dystrophies is congenital, which is caused by hereditary disorders in 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 split substances (products) of metabolism begin to accumulate in 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 impaired metabolism of BJU

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

Fatty degeneration of the liver - a prime example a disease in which cells fail to do their job - the breakdown of fats - and they begin to accumulate in the liver, which can cause steatohepatitis (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, when the myocardium is affected, which becomes flabby, which leads to a weakening of its contraction function, ventricular degeneration and kidney degeneration.

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

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

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 droplets of protein liquid in the organs. The process can develop in the cells of the epithelium, liver, adrenal glands and in the myocardium. If the number of such drops in the cell is large, then the nucleus is forced out to the periphery - the so-called balloon dystrophy.

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

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

Extracellular dystrophy or mesenchymal can develop in the stroma (the base, which 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 either congenital or acquired and can lead to reduced visual acuity (macula lesions) 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 severe disturbances in the nutrition of the fundus, which can lead to loss of vision.

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

Protein mesenchymal dystrophy can affect the liver, kidneys, spleen and adrenal glands of a person. In old age, the heart and brain are affected. As for the latter, the brain, this can lead to slowly progressive dyscirculatory encephalopathy - a violation of the blood supply to the brain, as a result of which diffuse disorders increase and, as a result, a disorder of the patient's basic functions of the brain.

As for stromal-vascular fatty degeneration, its vivid manifestation can be the patient's obesity and obesity or Derkum's disease, when painful nodular deposits can be observed on the limbs (mainly legs) and on the trunk.

Notable is the fact that stromal-vascular fatty degenerations can be both local and general in nature and lead both to the accumulation of substances, and, conversely, to their catastrophic loss, for example, as in alimentary dystrophy, which can develop as a result of malnutrition and nutritional deficiencies, both in humans and in animals.

Mesenchymal carbohydrate dystrophy is also called mucus of human tissues, 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 such as:

Hemoglobin, which transports oxygen;
melanin, which protects against UV rays;
bilirubin, which is involved in digestion;
lipofuscin, which provides the cell with energy in hypoxia.

Treatment and prevention of dystrophies

After making the 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), the observance of which is necessary for any type of dystrophy.

1. Organization of appropriate patient care and elimination of all factors provoking complication (see causes of dystrophies).
2. Compliance with the regime of the day, with the mandatory inclusion of outdoor walks, water procedures and physical exercises.
3. Compliance with a strict diet prescribed by a specialist.

As for prevention complex disease, then it is necessary to maximize the methods and measures for caring for oneself (or children), in order to completely eliminate, if possible, all negative factors that can cause this type of violation.

It must be remembered that strengthening your own immunity and the immunity of your children from the very early age, rational and balanced nutrition, sufficient physical activity and lack of stress - this is the best prevention of all diseases and dystrophy as well.

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

Dystrophy is not always expressed by a person's weight deficit 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 growth relative to age norms is another type of hypostatural dystrophy. The most common and dangerous first type of disease - hypotrophic dystrophy.

Causes of dystrophy

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

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

Acquired primary dystrophy may be the result of malnutrition in difficult social settings or the result of poor nutrition with protein deficiency. Also, recurring infectious diseases that 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, as a rule, correlates with too many calories and an increased amount in the daily menu of fats and carbohydrates. 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. Hypostatic type dystrophy 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 prevail, allocate the following types dystrophy:

• carbohydrate;
• mineral;
• protein;
• fat.

According to the place of localization of the process of pathology of metabolic processes, dystrophy can be cellular, extracellular and mixed.

According to the etiology, dystrophy happens:

• 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, the dysfunction of the metabolic processes of proteins, carbohydrates and fats is associated with hereditary pathology. Moreover, in the body of children there is no 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. Pathology affects a variety of tissues, but most often the nervous tissue is affected, which leads to a serious disruption of its functioning. Any kind of congenital dystrophy are dangerous conditions that can lead to death.

Subject to underweight dystrophy divided into the following groups:

• Hypostatruis. It is characterized not only by a lack of body weight, but also by a decrease in growth, inconsistency of these indicators with age norms.
• Paratrophy. With this type of dystrophy, malnutrition of tissues and metabolic processes leads to an increase in body weight.
• Hypotrophy. Today it is the most common form of the disease. At the same time, there is a decrease in weight relative to the height of a person. Considering from the moment of occurrence, congenital (prenatal), acquired (postnatal) and combined malnutrition are classified.

When does dystrophy appear? as a result of a 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 deficiency of human weight up to 30%, the patient has reduced motor activity and emotional tone. The patient is lethargic, tissue turgor and muscle tone are significantly reduced. A person has a greatly reduced amount of fatty tissue in the region of the limbs and abdomen. Pathologies of thermoregulation are expressed in cold extremities and fluctuations in body temperature. Dystrophy in the second stage is accompanied by pathologies in the work of the cardiovascular system with arterial hypotension, tachycardia, muffled heart tones.

Hypotrophy in 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 a person is seriously impaired, the patient is prone to indifference, drowsiness, anorexia, irritability. With malnutrition in the third stage, there is no fatty subcutaneous tissue. 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, arterial hypotension. Dyskinetic manifestations of dystrophy are expressed in vomiting, regurgitation, rare urination, frequent loose stools.

Hypostatura is a consequence of prenatal dystrophy of a neuroendocrine type. Diagnosis of congenital hypostatus at the time of birth according to the distinctive clinical symptoms:

Congenital stable 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 the physiological indicators of a person's height and weight lag behind 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 different 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;
• disturbed emotional tone;
• fast fatiguability;
• dyspnea;
• pain in the head.

Often the appetite is reduced and is selective. due to excess adipose tissue decreased muscle tone And insufficient elasticity covers of the skin. Against the background of a decrease in 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 relative to height, an analysis of the body's resistance to infectious diseases, the location and amount of subcutaneous fat, and an assessment of tissue turgor. The stage of malnutrition is determined according to laboratory examinations of urine and blood.

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

Hypotrophy in the second stage - according to laboratory examinations, a person with dystrophy at this stage has a pronounced hypochromic anemia with a low content of hemoglobin in the blood. There is also hypoproteinemia with a low amount in the blood total protein against the background of a strong decrease in enzymatic activity.

Hypotrophy in 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 thickening of the blood with slow erythrocyte sedimentation.

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 nanism with normal secretion of somatropin, but not the body's sensitivity to it.

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

As a stimulating treatment, courses of general tonic preparations and multivitamin complexes are used: preparations with royal jelly, ginseng, oats, lemongrass. It also treats comorbidities and sanitation of foci of chronic infection. Improving the emotional status and eliminating hypodynamia is achieved with the help of massage, the complex implementation of physical therapeutic exercises.

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

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

In adult patients, the prevention of dystrophy is possible with the condition of 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 function of digestion is disturbed, but also the absorption of nutrients by the cells and tissues of the human body, the metabolism and vital activity of the organism, its growth and development are disturbed.

Among the many causes of cell and tissue dystrophy, nutritional dystrophy occupies a special place. Synonyms of alimentary dystrophy are the following: starvation disease, edematous disease, protein-free edema, hungry edema, military edema.

This is a disease of prolonged malnutrition, manifested by general exhaustion, a progressive disorder of all types of metabolism and degeneration of tissues and organs with a violation of their functions. This disease is not equivalent to a state of hunger or individual forms so-called partial nutritional deficiencies, such as vitamin deficiency, unilateral feeding, etc.

In his writings, the writer Flavius ​​mentions the starvation disease. In Europe, it was described for the first time in 1742 by the English physician J. Pringel, who observed it among the soldiers of the besieged troops; outbreaks of starvation were observed in Napoleon's troops. More detailed information about the starvation disease refers to the period of the First World War. From this time begins Scientific research of this disease. R. A. Luria, V. A. Valdman, A. Belogolovy and others participate in the work. Depending on the conditions that were the root cause of alimentary dystrophy (crop failure, flood, epidemics, wars, blockade, etc.), the form of the course of this disease is formed .

The most complete form of alimentary 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 variants of the course of this disease. The maximum increase in the incidence occurred by the end of the second month of the blockade. Mortality at that time reached 85%, among the sick men predominated. About 40% of the victims suffered from the edematous form of the disease. The duration of illness ranged from 2–3 weeks, followed by lethal outcome up to two years with a gradual recovery.

1. Etiology

The main etiological factor of alimentary dystrophy is prolonged (weeks, months) insufficiency of calories of 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 come from the disastrous state of the population (nervous-emotional overstrain, cold, hard physical labor). Infectious diseases, especially intestinal ones, also increase the likelihood of developing alimentary dystrophy and aggravate its course.

In the development of alimentary 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 alimentary dystrophy can be considered as a clinical manifestation of disturbed homeostasis due to the failure to enter the body of many nutrients in the right quantity and quality.

Clinical observations show that patients with alimentary dystrophy showed 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 up to hypoglycemic levels (25–40 mg%).

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

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

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

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

3. Pathological anatomy

IN different periods alimentary dystrophy can join 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 found, and pulmonary tuberculosis develops in the future.

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

With the edematous form of alimentary dystrophy, pathological fullness is observed, the skin is pale, an opalescent gray-white liquid is determined on the incision.

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

Thrombi are found in the veins of the extremities, which is associated with low mobility of patients. All internal organs are reduced in size. Fat depots are absent.

4. Clinical picture

In the clinical picture of alimentary dystrophy, there are three degrees (stages) of the severity of the disease (MI Khvilivitskaya).

First degree– a distinct decrease in nutrition, pollakiuria, increased appetite, thirst, increased consumption table salt, as well as at times barely noticeable puffiness. 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. There are general weakness, fatigue, decreased ability to work. There is an increased chilliness due to hypothermia (body temperature 34 ° C), the psyche changes.

Third degree alimentary dystrophy - the disappearance of fat in all organs and tissues. Pronounced general weakness, adynamia, apathy are noted, deep atrophy of the skeletal muscles occurs. The skin is either dry and wrinkled, or persistent edema and ascites. Expressed and persistent changes in the psyche. Severe appetite disorders - from "wolf hunger" to complete anorexia, from persistent constipation to fecal incontinence.

There are changes in the central and peripheral nervous system. Polyneuritis develops.

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

Many patients with alimentary dystrophy show signs of parkinsonism.

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

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

Impaired lung function.

Dyspeptic disorders are observed in many patients with alimentary dystrophy. Painful constipation for several weeks. There are cases of atonic intestinal obstruction requiring urgent surgery.

The protein-forming function of the liver is significantly impaired. The body is deficient in protein.

5. Histochemical and luminescent studies of dystrophic processes

For a long time, the concept of "dystrophy" did not have a clearly defined content. It was used both in the nosological sense to refer to a disease (alimentary dystrophy, neonatal dystrophy), and in the biochemical sense to characterize metabolic disorders in organs and tissues, and in the morphological sense as a term equivalent to the terms "degeneration", "rebirth". Particular difficulties of this concept arose from the positions 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, which have a purely biochemical basis. There was a "morphological impasse" in the problem of myocardial dystrophies. Ya. L. Rapoport puts morphological content into the concept of "myocardial dystrophy".

The extensive development of histochemistry and electron microscopy has resolved the contradiction between various interpretations the concept of "dystrophy", allowing structural documentation of metabolic processes in cells and tissues and their violations. 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 thus the sharp line between morphology and biochemistry has been erased.

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

Dystrophy in children stands out in a special group. According to the classification of G. N. Speransky et al. (1945), three types of dystrophy are distinguished: malnutrition, hypostatura and paratrophy. In subsequent years (1969), G. I. Zaitseva and co-authors made an addition 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 the course (initial, progression and convalescence), building it according to the etiological principle (exogenous, endogenous, exogenous-endogenous ). The attention of pediatricians is attracted by dystrophies of prenatal origin, which manifest themselves from the first days of a child's life and are characterized by a lag in his physical development. This type of dystrophy is discussed in domestic and foreign literature under various names - neonatal dystrophy, dystrophy at birth, low birth weight, intrauterine malnutrition, etc. (1961, WHO). severe forms intrauterine malnutrition is called neurodystrophy, emphasizing their origin in the central nervous system.

6. Etiology and pathogenesis of dystrophy in children

In the occurrence of dystrophies in children, exogenous and endogenous factors are important.

TO exogenous factors dystrophies include:

Alimentary (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;

Mistakes in child care.

TO endogenous causes include the following:

Anomalies of the constitution of the child;

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 disruption of the regulatory activity of the central nervous system, which leads to dysfunction of all organs and systems, including dysfunction of the gastrointestinal tract. The absorption of proteins, fats and vitamins is disturbed, the enzymatic energy of the blood decreases, the processes of assimilation of nutrients by the cells and tissues of the body are disrupted. Eating disorders and metabolism develop. To maintain the vital activity 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. With insufficient content in the mother's diet of protein and minerals a child can be born with a lag in growth and weight or overweight due to protein-free edema. Reduced weight of the child is associated with atrophy of organs and tissues.

Atrophy, which is observed in 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 also observed in the organs.

With cachexia, fatty tissue in the epicardium, retroperitoneal space, in the perirenal region disappears, diffuse decalcification of the bones is noted, accompanied by pain.

On the basis of etiology, they are distinguished exogenous cachexia And cachexia of endogenous origin.

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

In most cases, the patient has no subcutaneous fatty tissue, flabbiness and atrophy of skeletal muscles are noted, hands hanging “like whips”, the stomach is drawn in, sunken eyes, dry hair, fall out, brittle nails, teeth become loose and fall out, skin is dry, flabby, without signs turgor, folded or taut like a mummy, of a pale earthy hue. Pigmentation of the skin, hemorrhages, furunculosis, friability of the gums, stomatitis phenomena, 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, arterial hypotension. Patients are indifferent to the environment and to themselves, are in a state of prostration, stupor, intelligence is sharply reduced. Usually they lie, move with difficulty, while the movements are sluggish, slow. Sexual function drops sharply, amenorrhea occurs in women. Often there is oliguria, and in the edematous form of polyuria.

7. Mental disorders

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 deterioration general condition apathy (insensitivity, indifference) begins to prevail. Apathetic Syndrome - mental disorder, in which there is complete mental emptiness, mental and physical weakness, exceptional poverty of the affective sphere up to its complete blockade (“paralysis of emotions”).

Clinic of apathetic syndrome

Patients are indifferent both to their own personality and to the surrounding phenomena of life. Desires, desires and aspirations are absent. With the most pronounced depth of damage to emotional reactions, the weakening of all mental manifestations a state of apathetic stupor develops. At the same time, there are no signs of mobilization of attention, intellectual tension. The patient lies on his back, all muscle groups are relaxed, his eyes are constantly open, his gaze is directed into space, without fixing on anything. Night wakefulness is characteristic - “awake coma” or “death with open eyes” (Jaspers (K. Jaspers)). With a less pronounced apathetic syndrome, patients are lethargic, if they give, then monosyllabic answers. Consciousness is preserved, but attention is disoriented.

Etiopathogenesis apathetic syndrome is most typical for protracted symptomatic somatic psychoses in tuberculosis, malaria, typhoid, beriberi, wound sepsis, endocrine disorders, brain damage during trauma, 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 in the process of the diencephalon with impaired conduction of impulses between the cortex and subcortex in organic diseases brain. In the pathological and anatomical picture, there is a predominance of toxic-degenerative processes in the mesenchymal elements of the brain (M. E. Snesarev).

Diagnosis put on the basis of the clinical picture.

The differential diagnosis is carried out with stunning.

Stunning is a form of obscuration of consciousness, 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 stunning are difficulty in perceiving external influences due to an increase in the excitability threshold of analyzers, narrowing of comprehension of the surrounding world due to slowing down of thinking and weakening of analysis and synthesis, passivity of thinking due to a decrease in volitional activity, weakening of the memorization of current events, followed by amnesia. Unlike other states of clouding of consciousness, there are no productive psychopathological symptoms during stunning, such as hallucinations, delirium.

According to the depth of violation of the clarity of consciousness, the following degrees of stunning are distinguished:

1) obnubilation;

2) doubtfulness;

The boundaries between them are usually indistinct.

Obnubilation- fogging, clouding of consciousness, - the mildest degree of stunning. The patient's clear consciousness is periodically disturbed by a short-term, within a few seconds or minutes, state of slight stupor: the 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 - a deeper and longer 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.

The comprehension of surrounding events is superficial, their comparison with past life experience is limited, orientation in place, time and space is upset. Speech is sluggish, laconic, movements are slow, fatigue sets in quickly; responds inadequately to difficult questions and tasks or does not respond at all. The patient himself does not show interest in others, most of the time 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 amimic, speech contact is impossible. Strong stimuli (strong sound, bright light, painful stimuli) cause undifferentiated, stereotyped defensive reactions.

Coma (deep sleep), coma- turning 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 a while.

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

Etiology and pathogenesis not fully explored. 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, inflammation, and circulatory disorders in the brain.

Stunning occurs with a decrease in excitability nerve cells the cerebral cortex, when the activity of the second and then the first signal system is inhibited. A diffuse decrease in cortical activity occurs either as a result of damage to the cortical structures of the brain, or in connection with a violation of stimulation of the cerebral cortex from the reticular formation.

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

Forecast depends on the nature of the disease during which the stunning occurs. An unfavorable prognosis is more often expected.

Clinical picture

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

In most cases, the body weight of a child with dystrophy is reduced, but its increase is also possible. The degree of weight loss can be different, up to a sharp lag. Weight gain is possible with water retention in the body. Children are lethargic, inactive, their reaction to the environment is reduced. There is a tendency to various infections: purulent rashes on the skin, acute respiratory diseases, pneumonia, etc. With dystrophy, clinical signs of vitamin deficiency develop. Dysfunction of the gastrointestinal tract is manifested by frequent stools and the composition of feces.

Severe intrauterine malnutrition is divided into four clinical forms:

1) neuropathic;

2) neurodystrophic;

3) neuroendocrine;

4) encephalopathic.

neuropathic form characterized by an increase in the excitability of the child, a sleep disorder, and a reduction in its duration. Manifestations of malnutrition are not pronounced, develop after birth, are persistent. At neurodystrophic form the leading symptom is a persistent lag in weight, persistent anorexia (complete lack of appetite with an objective need for nutrition, due to organic or functional disorders of the function of the center of appetite). Psychomotor development is somewhat delayed.

Neuroendocrine form characterized by persistent underweight and significant growth retardation. At birth, physique disorders such as pituitary dwarfism and hemiasymmetry are detected. Sometimes there are symptoms associated with impaired function of the endocrine glands.

8. Cachexia

cachexia(Greek kachexia - “soreness, bad feeling») – disease state associated with insufficient intake of nutrients in 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 fullness. 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 noted, characterized by a decrease in the total blood volume, the ratio of plasma and red blood cells is disturbed. A decrease in the number of red blood cells is noted with anemia various origins, the content of hemoglobin in the blood decreases. A decrease in the volume of circulating plasma occurs as a result of intensive care diuretics, plasma loss with extensive burns, diarrhea, vomiting.

There is a pronounced physical weakness and phenomena of general asthenia.

Asthenia is known to be characterized increased fatigue and exhaustibility, weakening, and even complete loss of the ability to prolonged physical and mental labor. Patients have irritable weakness, expressed by increased excitability, easily changing mood, irascibility, affective lability with features of capriciousness and displeasure, as well as tearfulness. Hyperesthesia is characteristic - intolerance to bright light, loud sounds, pungent odors. Patients complain of headaches, sleep disturbance, with a drop in barometric pressure, Pirogov's symptom is noted. Memory suffers, especially remembering current events.

Asthenic syndrome can develop after suffering somatic diseases, traumatic brain injury, in the initial period of hypertension, with atherosclerosis, syphilis of the brain, 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 (splanchnomycria), dystrophic and atrophic changes are observed in them.

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

Dumping syndrome refers to post-gastroresection complications, early and long-term complications after gastric resection, vagotomy and antrumectomy.

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 ulcer, preference is given to economical resection of the stomach - antrumectomy with vagotomy.

Complications early period after operations on the stomach, there are violations of evacuation from the stomach stump due to inhibition of the motor activity of the stomach due to surgical trauma, damage to the neuromuscular apparatus, electrolyte and protein metabolism disorders and vagotomy, it is also observed acute obstruction adductor loop of anastomosis.

Late complications - post-gastroresection syndrome - include dumping syndrome; afferent loop syndrome; hypoglycemic syndrome with a sharp fluctuation 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; anemia, usually iron deficiency and vitamin.

These complications lead to disruption of the metabolism of proteins, fats, carbohydrates, vitamins, electrolytes, and eventually alimentary cachectic dystrophy (cachexia), or edematous form, develops.

Degeneration of cells and tissues- a pathological process that occurs in connection with a metabolic disorder and is characterized by the appearance in cells and tissues of metabolic products that have been changed quantitatively or qualitatively. Degeneration of cells and tissues is considered as one of the types of damage.

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

Among the morphological mechanisms leading to the development of dystrophy of cells and tissues, there are:

Infiltration (for example, protein infiltration of the epithelium 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 pathological glycoprotein - amyloid in plasmacytoma);

Transformation;

Decomposition (decomposition of lipoproteins of cell membranes, for example, hepatocytes with fatty degeneration, or fibrous structures and the main substance of the vessel wall with fibrinoid swelling).

The study of the mechanisms of development of dystrophy of cells and tissues became possible due to the use of histochemistry, electron microscopy, autoradiography, histospectrography, etc.

Depending on the predominance of violations of the type of metabolism, the following types of dystrophies are distinguished:

1) protein;

2) fatty;

3) carbohydrate;

4) mineral degeneration of cells and tissues:

Parenchymal;

Mesenchymal;

Mixed.

Degeneration of cells and tissues can be of a general (systemic) and local character.

Protein degeneration of cells and tissues, or dysproteinosis, is caused by excessive intake of proteins into cells or intercellular substance, perverted protein synthesis or decay of tissue structures; physicochemical and morphological properties proteins are changed. Parenchymal dystrophy of cells and tissues:

grainy;

Hyaline drip;

dropsy;

Balloon;

acidophilic;

Horny.

Mesenchymal dystrophy:

Mucoid swelling.

Mixed dysproteinosis is 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;

C) glycoproteins - mucous and colloidal dysproteinoses.

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 not normally present, and a change in the quality of lipids in cells and tissues. Violation of the exchange of neutral fat is manifested more often in a decrease, less often in an increase in its reserves; it can affect the whole body or a specific part of the body. A general decrease in the amount of adipose tissue is characteristic of cachexia, a local decrease in the amount of adipose tissue is characteristic of regional lipodystrophy; overall increase fat reserves leads to obesity, local - observed with atrophy of a tissue or organ (fat replacement), with endocrine disorders. Lipid metabolism disorders are most common 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 lipoidosis.

Chapter 2

I. Dystrophy in children

1. Clinical picture of dystrophy in children

To the main clinical symptoms dystrophy in children include:

Change in weight and height;

Delayed psychomotor development;

Decreased body resistance;

Dyspeptic disorders.

In most observations, the child's body weight is reduced, but its increase is also possible. The degree of weight loss can be different up to a sharp lag. With water retention in the body, weight gain is possible. With this pathology, children are lethargic, inactive, the reaction to what is happening is reduced, defensive forces organism. 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 quickened, its color, reaction and consistency change.

Severe forms of intrauterine malnutrition are divided into four clinical forms: neuropathic, non-dystrophic, neuroendocrine and encephalopathic. The neuropathic form is characterized by an increase in the excitability of the child, a sleep disorder, and a shortening of sleep time. The manifestation of malnutrition is not pronounced, develops after birth, is persistent. In the neurodystrophic form, the leading symptom is a persistent lag in weight. The neuroendocrine form is diagnosed by a persistent lag in weight and height. At the birth of the physique, a type of pituitary dwarfism is noted. Sometimes symptoms associated with impaired function are determined, the form is manifested by severe malnutrition of the III degree, anorexia, a significant lag in psychomotor development.

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

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

A. Gaucher disease

Wall fatty degeneration blood vessels(mesenchymal lipidosis) underlies atherosclerosis.

Carbohydrate dystrophy of cells and tissues refers to a violation of the metabolism of polysaccharides, mucopolysaccharides and glycoproteins. The most common disorders of glycogen polysaccharide metabolism. They are especially pronounced in diabetes mellitus, when tissue glycogen stores are sharply reduced, and in glycogenoses, characterized by excessive deposition of glycogen (storage disease) in the liver, heart, kidneys, and skeletal muscles.

Mineral dystrophies usually have a mixed character: the metabolism of potassium, calcium, iron and copper is disturbed. An increase in the amount of potassium in the blood and tissues is observed in Addison's disease, potassium deficiency explains the occurrence of a hereditary disease - periodic paralysis. Calcium metabolism disorders - calcification, 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 found mainly in hemoglobin, and the morphology of its metabolic disorders is associated with hemoglobinogenic pigments - chromoproteins. In violation of copper metabolism, hepatocerebral dystrophy can occur, in which copper is deposited in the liver, kidneys, brain, and cornea.

B. Skin dystrophy- a pathological process that occurs in connection with a metabolic disorder and is characterized by the appearance in cells or an interstitial substance of metabolic products that have been changed quantitatively and qualitatively. These changes are often referred to as skin degeneration.

Causes metabolic disorders leading to the development of skin dystrophy are diverse: chronic inflammation, allergic and infectious factors, intoxication, circulatory disorders, malnutrition, hypovitaminosis, diseases of the endocrine glands, malformations, etc.

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

Skin dystrophy can be an independent nosological unit, as well as a symptom of any 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 degeneration is noted in squamous cell skin cancer, Darier's disease. With lichen planus, the epithelium undergoes colloidal degeneration. In the connective tissue of the skin, mucous degeneration can occur, in which collagen fibers turn into a semi-liquid substance, observed with skin myxedema, myxoma. Piamenic dystrophy occurs in skin cancer, a peculiar and progressive disorganization of the connective tissue is observed in the skin with collagenoses (phases of mucoid swelling, fibrinoid and sclerosis). Lime degeneration of the skin occurs with injuries, scleroderma and tumors.

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

Allocate hyperelastic skin of Unna (Ehlers-Danlos syndrome) - congenital disorder development of collagen structures, characterized by a sharp extensibility of normal-looking skin. In this case, the retracted skin quickly returns to its original position. Hyperelastic skin is the main symptom of desmogenesis imperfecta. It should be differentiated from flaccid skin - a congenital anomaly of the 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 weakness of the ligamentous apparatus, growth retardation and mental retardation.

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

Hyperkeratosis, parakeratosis, focal acanthosis, hyperpigmentation develop in the epidermis. In the papillary layer of the dermis - the accumulation of basophilic fibrous, granular and lumpy mass - a consequence of the destruction of collagen. There are also hyaline, colloid, myloid dystrophy.

Senile skin dystrophy is manifested by keratosis in the form of raised yellowish-brown plaques with a rough surface or papillomatous growths with a brown warty surface. The skin becomes dry, rough, rough, yellow, sometimes with a slight sheen of the surface, with atrophic and pigmented spots and basaliomas. Unaltered areas of the skin are also observed.

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

Rhomboid hypertrophic skin tendystrophy of the posterior surface of the skin 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 with deep furrows, forming a pattern in the form of rhombuses up to 5 cm in diameter, soft, yellowish-brown in color.

B. Diffuse elastoma of Drobrey- colloid dystrophy of the skin. On the histological section, elastorhexis is visible, elastic fibers, swollen, which merge with collagen fibers; the resulting felt-like mass is stained black with acid orsep. Hair follicles are dystrophic, the epidermis is atrophic.

Diffuse elastoma is formed in elderly men, less often in young men. On the skin of the face, mainly in the area of ​​the cheeks and near the eyes, a sharply delimited diffuse plaque of a soft consistency appears, covered with wrinkled skin with papular rashes and multiple punctate 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 a thickening of elastic fibers.

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

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

Amyloid degeneration of the skin develops in a small area (local amyloidosis) and may be a manifestation of general amyloidosis.

2. Treatment

As for the treatment of dystrophy in adults and the elderly, it is most often symptomatic. The treatment of dystrophy in young children is given especially close attention, and it is built taking into account the type of dystrophy, the etiological factor, the severity, the time of occurrence and the period during the course of the disease. Treatment should be complex, continuous (until recovery), and diet therapy should be one of its mandatory components. In mild cases of malnutrition associated with quantitative underfeeding, the appointment of a sufficient amount of food in addition to supplementary feeding can solve the problem of curing the child. If a deficiency of proteins or fats is detected, an appropriate correction of the diet is carried out.

Food for a young child is not only a source of energy necessary for the formation of heat and the functioning of organs and tissues, but also a plastic material necessary for a 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 life, without which proper development child is impossible. The food of the child must meet the needs of his body and correspond to the physiological capabilities.

The amount of protein in food is special meaning for early childhood development. A decrease in protein in the diet quickly leads to growth retardation and mental development. Protein is an essential ingredient! And the minimum of proteins in the diet can not be limited. They must be administered with the child's food in the optimal amount.

The need for proteins depends on the age of the child and his characteristics. With natural feeding 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 met by human milk protein. In this case, not only the absolute number 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 segment.

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