Alimentary dystrophy as a "side effect" of the pursuit of a slender body. Alimentary dystrophy Alimentary dystrophy manifests itself

Alimentary dystrophy is the depletion of the body due to insufficient intake of nutrients, in other words, a disease of malnutrition. In fact, this is a state when the body spends more resources on work (growth, development, physical and mental activity) than it receives with food.

The term was suggested by therapists who worked in Leningrad during the blockade of 1941-1942.

Causes of alimentary dystrophy

The main reasons that can lead to alimentary dystrophy are:

• prolonged fasting;
• inadequate nutrition, which does not provide the necessary amount of calories and nutrients, which does not cover the energy costs of the body.

In turn, the reasons for these factors can be a huge number.

Prolonged fasting can develop due to the following circumstances:

An obsessive fear (phobia) of eating a particular food is a separate group of reasons for prolonged starvation, which can lead to alimentary dystrophy. There are a number of food phobias. The most common of them are:

• amylophobia- fear of eating carbohydrates;
• carnophobia- fear of eating meat and offal;
• cybophobia- fear of eating any kind of food.

Food phobias leading to alimentary dystrophy (as well as phobias in general) have not yet been fully studied, they can appear suddenly in a person. AT most of the time they are preceded by:

• strong simultaneous (death of a loved one);
• not too pronounced, but constant stress (dissatisfaction with life situation, difficult work environment);
• a difficult experience in childhood, when the child was forced to take this or that food;
• obsessive stereotypes of society - for example, associated with the assertion that there is sweets - 100% harm without exception.

note

In the case of eating food that does not provide the necessary amount of calories and nutrients, alimentary dystrophy does not develop as quickly as during starvation, but its consequences are no less severe.

Contributing factors

A number of factors have been identified that do not directly lead to alimentary dystrophy, but in the presence of the above factors contribute to its development. First of all it is:

Development

The pathogenesis (development) of alimentary dystrophy is rather complicated. Before, figuratively speaking, giving up, the body in conditions of degraded or insufficient nutrition for a long time tries to maintain the energy supply of its physiological processes at the proper level. The mechanisms of such “self-help” are “multi-pass”, in the course of their implementation the body can be rebuilt more than once.

With inadequate intake of nutrients, the reaction of the body, first of all, is to consume reserves:

• fat (mainly involved subcutaneous adipose tissue and fatty tissue of the abdominal cavity);
• glycogen - a polysaccharide formed by glucose residues (its main strategic reserves are in the liver and muscles).

At first, protein reserves, as the main building reserve of the body, remain intact and are used to replenish energy expenditure when up to 30-50% of fat and glycogen reserves are consumed. . Since proteins, when broken down into amino acids, do not release the same amount of energy that is released when fats and carbohydrates are broken down, they are spent for energy purposes in greater quantities than fats and carbohydrates. Due to peptide (protein) losses, atrophy of all body structures develops - first of all, suffer:

• muscular system;
• internal organs;
• endocrine glands.

Moreover, protein is spent not only on muscle masses, but also on muscle fibers, which are part of:

• stomach;
• intestines;
• hearts;
• vascular wall

Sooner or later, energy stealing of organs and tissues occurs, which cease to fully perform the functions assigned to them by nature. . Structures for which a full amount of protein is important are especially affected - these are:

• motor muscles (equally upper and lower extremities, chest and abdominal cavity);
• heart;
• endocrine system;
• autonomic nervous system;
• central nervous system.

Gradually, functional failure of almost all organs and systems develops, at later stages of alimentary dystrophy, it results in more serious changes - multiple organ failure.

Symptoms of alimentary dystrophy

Clinical manifestations of alimentary dystrophy are very diverse, since all organs and tissues of the body suffer.

With alimentary insufficiency, patients complain of symptoms such as:

Complaints signaling that the central nervous system suffers are indicative. Patients report symptoms such as:

Also, in such patients, the psyche suffers.:

• the initial stage of alimentary dystrophy is characterized by nervousness, irritability and an aggressive type of behavior;
• with the development of pathology, lethargy and indifference to what is happening occur;
• acute psychoses with hallucinations are often observed .

The clinical course of the pathology can be:

• acute - more often in young people;
• chronic.

Complications

The most typical complications of alimentary dystrophy are:

• - the most common complication
• collapse - a sharp deterioration in cardiovascular activity;
• coma. A coma that develops as a result of alimentary dystrophy is characterized by a decrease in the frequency and depth of breathing, as well as a decrease in pulse rate. Often there is a specific type of breathing - the so-called Biot-type breathing (normal respiratory movements alternate with respiratory pauses lasting up to half a minute) and Cheyne-Stokes (the patient breathes shallowly and rarely, then breathing quickens and deepens, after 5-7 breaths / exhalations again becomes rare and superficial, then there is a respiratory pause - and so on with repetition);
• pustular diseases.

Physical examination

The data of a physical examination (examination, palpation of tissues, listening to individual organs) in alimentary dystrophy are characterized by high information content. Objective changes develop in almost all organs and systems.

General important changes are:

• progressive weight loss - up to 50%. The following pattern is observed: even after the start of treatment, the patient continues to lose weight for some time;
• lowering body temperature to 35-36 degrees Celsius.

When examining patients with alimentary dystrophy, the following signs are revealed:

• the tongue looks like a varnished surface due to smoothed (atrophied) papillae;
• the skin is pale (with severe alimentary dystrophy - earthy) with a yellowish tinge, cracked, wrinkled, flaky profusely. Often there is an increase in its pigmentation, which signals endocrine shifts;
• muscles are atrophic, unable to "keep" their usual shape, so it seems that they almost sag;
• with the development of pathology, the eyes seem to sink, dark circles are observed around the eyes (a consequence of increased pigmentation);
• at later stages, a number of patients may develop visible edema (due to protein breakdown).

On palpation (palpation), the following is noted:

• the skin is dry (like parchment), its turgor (elasticity) is reduced;
• at later stages, muscle tone is not determined at all, often the muscles are flabby, sometimes even similar to an amorphous mass. With the continued development of the pathology, muscle atrophy occurs, they are literally thinned, they make up half of the muscle volume normal for a person, or even less.

Auscultation (listening with a phonendoscope) is able to reveal inhibition of the activity of internal organs - in particular:

• hearts (tones are muffled or deaf);
• lungs (breathing is weakened);
• small and large intestines (peristalsis is weakened, in the later stages rare peristaltic noises are heard).

Of the additional signs, changes are observed:

• pulse;
• blood pressure.

At the initial stage, it is observed (the pulse is rarer than normal - less than 60 beats per minute), with the development of alimentary dystrophy, it is observed. The following specific sign is noted: even the slightest physical stress (for example, an elementary movement of an arm or leg) can cause an increase in heart rate.

Arterial and venous pressure is lowered.

According to the severity of the course, three degrees of alimentary dystrophy are distinguished:

According to clinical features, such forms of alimentary dystrophy are distinguished as:

• unedematous - it is also called dry or cachectic.
• edematous - the course is more benign than that of the non-edematous form.

Often, edema develops and increases early, while being combined with polyuria (increased amount of urine). With prolonged cachexia, edema is persistent and poorly amenable to drugs, while fluid can accumulate in the cavities (pleural and abdominal), this form of alimentary dystrophy is called ascitic.

Instrumental and laboratory diagnostic methods

The data of anamnesis, complaints and the results of a physical examination are sufficient to make a diagnosis of alimentary dystrophy. The data of instrumental and laboratory research methods complement the overall diagnostic picture.

Instrumental research methods reveal anatomical and physiological oppression from all organs and systems. Almost any method widely used in diagnostics will be informative - namely:

• chest organs - with it, a deterioration in the excursion (respiratory movements) of the lungs is detected;
• and - both methods allow to reveal the smoothness of the mucous membrane of both the stomach and intestines, the weakening of peristalsis;
• - during it, dystrophic changes are determined from the side of the heart, liver, pancreas, less often - kidneys;
• - demonstrates the weakening of the electrical potentials of the heart, fixes various kinds of arrhythmias

The data of laboratory research methods are indicative. In particular, in the diagnosis of alimentary dystrophy, methods such as:

• - it reveals (decrease in the number of erythrocytes and hemoglobin), leukopenia (decrease in the number of leukocytes), thrombocytopenia (decrease in the number of platelets);
• - a sharp decrease in the amount of blood serum proteins, as well as lipid fractions and cholesterol is determined;
• - the level of blood glucose is reduced;
• analysis of gastric juice - demonstrates a decrease in gastric secretion.

Treatment of alimentary dystrophy

With a mild degree, enhanced nutrition on an outpatient basis is sufficient as a therapeutic measure.

With moderate and severe severity, the patient must be hospitalized in a therapeutic hospital with well-heated wards.

Principles of nutrition in alimentary dystrophy:

Other appointments:

• strict bed rest with warming the body with heating pads;
• to improve gastric digestion, hydrochloric acid is prescribed, intestinal - enzyme preparations. For the same purpose, they practice the use of table wine 30-50 ml 1-3 times a day immediately before meals;
• the appointment of vitamins is also important - oral (through the mouth) and injection;
• in case of moderate and severe dystrophy, blood and its components are transfused - in the first case, whole blood is transfused, in the second, plasma is administered, as well as blood-substituting infusion preparations.

In the case of a severe form of alimentary dystrophy, apply:

• nutrition through a nasogastric (nasogastric) tube;
• sulfanilamide or.

If a coma occurs, then as an emergency, measures such as:

• general warming (the patient is covered with warm heating pads);
• the introduction of a glucose solution in small doses (40 ml) every 3 hours intravenously (with repetition until the patient wakes up from a coma);
• the introduction of a solution of calcium chloride intravenously in a stream (especially with convulsions);
• inside through a nasogastric tube - hot wine (preferably red), hot sweet tea or coffee;
• with shallow breathing - drugs that stimulate the respiratory center, hormonal agents (adrenaline).

Prevention

The only measure for the prevention of alimentary dystrophy is a good diet with the use of foods that ensure the normal intake of a sufficient amount of proteins (primarily), fats and carbohydrates into the body.

If a person is thin, and there are prerequisites for the occurrence of alimentary dystrophy, in addition to establishing nutrition, it is recommended:

• light work regime;
• increase in the period of rest and sleep;
• observation by the local therapist.

If a person finds himself in conditions of poor nutrition, which does not depend on him (war, natural disaster) and is fraught with poor nutrition, all efforts should be directed to consuming a normal amount of protein - for this purpose, the following is introduced into the diet:

• casein;
• soy products;
• gelatin;
• yeast.

Forecast

The prognosis of alimentary dystrophy is complex. Pathology may end:

• recovery;
• transition to a recurrent (repeating) or protracted form;
• death.

The prognosis depends on:

• degree of exhaustion;
• opportunities to improve nutrition.

The prognosis is poor in severe disease- a person slowly fades away, this process accelerates with an attached infectious lesion. Critical changes in the body leading to death can occur:

• slowly;
• accelerated (with the addition of another pathology);
• suddenly (instantaneous cardiac arrest is observed without any foreshadowing signs).

If complications have joined, then the disease takes a protracted form, which is difficult to treat, the prognosis worsens. If the therapy is successful, it should be borne in mind that the apparent recovery may not correspond to the biological one.

The prognosis is more favorable for:

• men;
• young people;
• patients with asthenic body type.

Kovtonyuk Oksana Vladimirovna, medical commentator, surgeon, medical consultant

A disease associated with protein deficiency. Nutritional dystrophy - energy deficiency. The most common cause of the disease is starvation.

Fasting can be forced or conscious. Often a person in pursuit of a beautiful figure suffers from this disease. Anorexia may develop.

In the modern century, many programs are devoted to this disease. Nutritional dystrophy is a social disease.

If the body does not receive the necessary substances, then the metabolism is disturbed. Or metabolism.

What are the possible causes of starvation? The most common causes of starvation include:

• war;
• ecological disaster;
• diet;
• narrowing of the esophagus

Narrowing of the esophagus can be a pathological process. It involves acquired pathologies rather than congenital ones.

However, this process is exacerbated by the following factors:

• heavy physical labor;
• hypothermia

What changes occur in the body. The body often starts the process of exhaustion. The body depletes glycogen and fat stores. To begin with, pathological processes concern the muscles and skin.

Then the internal organs suffer. Last but not least, the vital organs are already involved.

Even a full, adequate diet does not have a positive result. Since the heart and brain are damaged.

Vitamins and minerals are depleted. The immune system begins to function incorrectly. As a result, various infections join.

There are several stages in the development of the disease. In the first stage, emaciation is accompanied by a slight loss of body weight.

In the second stage, body weight is significantly reduced. There is a loss of performance. In the third stage, exhaustion is the most severe. To the point of being immobilized.

Symptoms

Alimentary dystrophy can manifest itself imperceptibly. The symptoms get worse later on. It depends on nutrition.

If the diet remains the same in the initial period, then the symptoms worsen. Become more pronounced.

What are the main symptoms of the disease? The main symptoms of the disease include:

• frequent urination;
• weakness;
• irritability;
• drowsiness;
• increased appetite;
• dyspepsia;
• bradycardia;
• decrease in body temperature;

The initial stage of the disease includes frequent urination. It often goes unnoticed by the patient.

Symptoms such as drowsiness and irritability are also predicted in the initial period of the disease.

Further complication of the disease is associated with the condition of the skin. The skin is flabby and dry. Dyspepsia is most noticeable.

The patient's performance deteriorates. He becomes lethargic and lethargic. The most severe deterioration of the patient's condition are mental disorders.

A complication of the disease is a hungry coma. It develops due to a decrease in glucose levels. The brain is not provided with the necessary energy reserves.

As a result of a hungry coma, heart failure can develop. Death comes from cardiac arrest.

Often associated with various infections. Tuberculosis may join. Or pneumonia, sepsis.

Diagnostics

A good method of diagnosing the disease is the collection of anamnesis. It allows you to determine the picture of the disease. It is only necessary to ask the patient about the methods of nutrition.

If we are talking about starvation, then the diagnosis can be made immediately. Laboratory diagnostic methods are also used.

Laboratory diagnostics includes a biochemical blood test. This allows you to detect a decrease in blood glucose. As well as a decrease in the level of all body cells.

It is known that the cells of the body are:

• erythrocytes;
• leukocytes;
• platelets

They are directly responsible for immunity. Therefore, a decrease in the level of these cells leads to suppression of the immune system.

Glucose nourishes all cells of the body. Responsible for energy metabolism. Therefore, a decrease in its level leads to energy starvation.

Additional methods for diagnosing alimentary dystrophy is ultrasound. Also MRI.

These studies allow you to determine the violation of the functioning of internal organs. Namely, dystrophy of organs.

It is also important to determine that these pathological disorders are the result of alimentary dystrophy.

Therefore, studies are carried out to exclude the following pathologies:

• oncology;
• diabetes

It is advisable to consult with specialists. For example, an endocrinologist and a gastroenterologist.

The endocrinologist will determine the hormonal imbalance in the body. If it is directly related to diabetes or other hormonal diseases.

The phthisiatrician will allow you to determine the tuberculous lesion of the body. Since it is with tuberculosis that exhaustion can be present.

Prevention

Alimentary dystrophy can be prevented. Prevention will be to establish proper nutrition.

In no case should a person exclude vital trace elements from the diet. Nutrition should be balanced, complex.

Proteins must be present in the consumed products. Glucose is also an important element in the diet.

If a person is on a diet. That requires a consultation with a nutritionist. It is this specialist who will correctly adjust the diet.

Self-flagellation and unauthorized refusal of products will not lead to good results.

A healthy lifestyle takes place in the prevention of alimentary dystrophy. Alcohol abuse and smoking leads to exhaustion of the body.

General intoxication of a person leading an unhealthy lifestyle contributes to metabolic disorders. Violated absorption of important trace elements and vitamins.

Severe stressful situations also lead to a pathological state of the body. Often fasting is the cause of stress.

Stress can be a cause of exhaustion. At first, a person does not feel much change in the body. Then the situation gets worse. The body stops eating.

Treatment

Treatment of alimentary dystrophy will be aimed at correcting a healthy lifestyle. The daily routine is normalized. As well as rest and sleep.

Inpatient treatment is indicated for this disease. Patients are placed in a well-ventilated ward. With enough light.

Including exclude contact of the patient with infectious patients. Since in this case there is a decrease in immunity. The patient is susceptible to various infections.

The first stage of the disease is treated with fractional nutrition. Food should be easily digestible.

In the second stage of the disease, nutrition is carried out as follows:

• enteral nutrition;
• parenteral nutrition

Parenteral nutrition may consist of administering solutions intravenously. What exactly is the patient's diet?

The diet includes animal proteins. They are indispensable in this case. It is also very necessary to supplement the diet with a certain amount of liquid.

Medical treatment is widely used. It is used to exclude all kinds of complications.

Antibiotics are administered immediately after sensitivity is established. If there is a hungry coma, then a 40% glucose solution is administered intravenously.

At a more severe stage of the disease, transfusion of blood products is widely used. For example, erythrocytes and plasma.

After treatment, the patient is rehabilitated. That is, rehabilitation consists in replenishing the physical and mental reactions of the body.

In adults

Alimentary dystrophy in adults is more often caused by conscious exhaustion of the body. This applies mainly to women.

The pursuit of a beautiful figure contributes to the development of various complications. In young women, exhaustion is the cause of self-starvation.

Unrequited love or unrequited feelings contribute to the development of starvation. Girls believe that a beautiful figure will help in love affairs.

But often the disease in this case ends in death. Since it is already becoming impossible to restore the normal functioning of organs and systems.

In adults, the disease is divided into the following forms:

• cachectic;
• edematous

The cachectic form of the disease is dangerous to health, as well as edematous. However, cachexia is the most serious disease.

The edematous form can be manifested by the development of edema. ascites develops. But in any case, this form is treatable than the edematous form.

The causes of the disease in men can also be conscious exhaustion. This may be due to bad habits.

An unhealthy lifestyle often provokes exhaustion. Due to this factor, various infections join. For example, tuberculosis.

In children

Alimentary dystrophy in children can be congenital. This is directly related to the pathology of internal organs. For example, the gastrointestinal tract and oral cavity.

Also, the reason for the development of alimentary dystrophy in children is often low socio-economic conditions in the family.

A child who grows up in poverty and takes the right ratio of proteins and other micronutrients is most susceptible to this disease.

If alimentary dystrophy develops at an early age, then the consequence of the disease is a fatal outcome.

The child's body develops, and the decrease in essential nutrients stops this development.

In this case, there are mental disorders. As well as weakness of the muscular system and certain outlines of a sick child.

Various infections often join a sick child. Tuberculosis, sepsis are concomitant factors of the disease.

Mental disorders in children can be pronounced. The child is whiny, irritated.

Failure at school. It is necessary to place the child in a hospital on time. Create the necessary conditions. Not only household, but also conditions for food.

Often parenteral nutrition. Since prolonged exhaustion leads to severe dystrophy of internal organs. The child's gastrointestinal tract atrophies. Stops functioning.

Forecast

In this case, the prognosis of the disease will depend on the stage. At the initial stage, the highest probability of establishing a favorable prognosis.

An unfavorable prognosis is appropriate for the second and third stages of the development of exhaustion. As various complications develop.

If nutrition is superimposed and the internal organs do not have time to atrophy, then the prognosis is good. However, the treatment is quite long. Recovery of the patient can take years.

Exodus

As mentioned above, the outcome of the disease depends on the presence of complications. And also from the stage of the disease. The most severe cachectic stage.

The edematous stage often ends favorably. But adjustment of a food, a mode of day and rest is required. Mostly at the initial stage.

If the treatment is not carried out on time, then there is a hungry coma. It leads to death.

The addition of various infections will also not lead to good results. The disease is exacerbated in this case.

Lifespan

Long-term physical and mental rehabilitation contributes to an increase in life expectancy. It is carried out not only after treatment, but also during.

However, there are sad statistics. The patient lives up to five years from the onset of the disease. Especially if the disease has passed into a severe stage.

If the disease can be stopped. The functions of organs are restored, then life expectancy increases.

But this fact depends on the timeliness of the treatment started. Namely - from the correction of lifestyle. Get treated on time and be healthy!

Absolute and complete starvation are catastrophic in their consequences for the body, if at a certain stage of this process the supply of food and water is not resumed. On the 5th-7th day of absolute and on the 60th-70th day of complete starvation, death inevitably occurs. Nowadays, these forms of fasting are relatively rare and, as a rule, are the result of extreme circumstances in which a person or group of people falls (during natural disasters, for example). Modern medicine has to deal with incomplete and partial starvation much more often. However, the full and absolute forms of this process will be considered in detail below, since they allow us to “in pure form” analyze the mechanisms of disturbances that occur in the body when nutrients (including, primarily, proteins) cease to enter it.

Complete starvation should be considered as a condition associated with the transition of the body to endogenous nutrition. In other words, in order to maintain the required level of energy metabolism, the body is forced to utilize its available reserves of nutrients, as well as products formed during tissue destruction. Complete starvation is also a long-term stress, as a result of which the enzyme systems responsible for the processes of hormone biosynthesis, which ensure the development of a general adaptation syndrome, are activated and rebuilt.

Utilization of fat reserves and tissue atrophy in the process of complete starvation lead to a gradual loss of body weight. At the same time, atrophy mainly affects the skin, adipose tissue, skeletal muscles, liver, kidneys, spleen, lungs, intestines and practically does not extend to the nervous system and heart muscle, whose mass remains unchanged until the death of the body, by the time of which it loses up to 50 % weight.

In the process of complete starvation, three periods are distinguished: initial (adaptive), stationary and terminal.

The duration of the first period is 2-4 days. During the first day of complete starvation, the energy needs of the body are mainly provided by the oxidation of carbohydrates, as evidenced by the fact that respiratory coefficient at this time is close to unity. However, starting from the second day, 84% of the body's energy expenditure is covered by fat oxidation and only 3% by carbohydrates. Protein synthesis is reduced, and their increasing breakdown leads to a negative nitrogen balance and an increase in the amount of ammonia in the urine.

In the second, the longest in time (55-60 days), period of complete starvation, the body adapts and totally rebuilds its enzyme systems to switch to endogenous nutrition. Almost throughout this period, 90% of energy costs are provided by the breakdown of fat and the oxidation of fatty acids. Respiratory coefficient-less than one and sometimes can even drop to 0.7. Slowly but steadily increasing ketonemia; noted creatinuria. Starting from the second half of the stationary period, there arises and gradually develops metabolic acidosis. However, in general, the basic vital functions of the body (body temperature, blood pressure, pulse rate, blood sugar) remain within normal limits, approaching its lower limit.

The motor and secretory functions of the gastrointestinal tract are characteristically changed. At the beginning of the period, his motor skills are sharply increased (the so-called hungry motility), then its intensity decreases. The secretion of digestive juices is slightly increased. In the gastric juice and pancreatic secretion, the content of proteins (albumins and globulins) increases, which, after splitting into amino acids, are absorbed by the body and used as a plastic material. As mentioned above, the main energy expenditure of the body is compensated due to the increased utilization of its own fats, however, the energy demand of the muscles is largely provided by the breakdown of carbohydrates. At the same time, glucose synthesis is based on the use of amino acids and fatty acids (one of the variants of gluconeogenesis).

In the third, terminal, period of complete starvation (it lasts 2-3 days), the avalanche-like growing violations of most body functions are based on deep disorders of enzyme systems. Increased breakdown and utilization of proteins do not allow the body to synthesize many enzymes in time and in sufficient quantities. Destruction of enzyme systems begins with enzymes involved in redox processes; further, other enzyme systems are also involved in it. Proteolytic enzymes retain their activity for the longest time. The disintegration and deactivation of enzyme systems is completed by the inevitable with complete starvation. beriberi(especially group B). As is known, vitamins of this group are actively used by the body as cofactors of many oxidative enzyme systems. By the end of the terminal period, pronounced changes in acid-base balance develop (metabolic acidosis increases), hypoproteinemia occurs, oncotic blood pressure decreases, which in turn can lead to hungry edema. The terminal period ends with agony and death as a result of uncompensated acidosis, intoxication of the body with metabolic products, complete destruction of enzyme systems, or the addition of any infectious disease that the body is no longer able to fight, since inhibition of protein synthesis affects both antibody production and phagocytosis .

Absolute starvation in its pathogenesis, it is very close to complete starvation, however, the intensity of the increase in disorders during absolute starvation is many times greater than during complete starvation. Dehydration of the body enhances the breakdown of proteins and autointoxication by metabolic products. The disruption of the colloidal structure of proteins, inevitable during absolute starvation, especially aggravates the condition of the starving and ultimately leads to their death on the 5-7th day of fasting.

Nutrition is one of the main factors determining health, well-being, life expectancy and active human activity.

Currently, according to UN estimates, only 25% of humanity eats normally, more than half of the world's population is undernourished or malnourished. Starvation as a social problem continues to exist in various countries of the world, and in this regard, diseases associated with malnutrition are widespread.

Starvation(substrate-energy deficiency) is a typical pathological process that occurs in the complete absence or insufficient intake of nutrients, as well as in a sharp violation of their composition or digestibility. During starvation, the body switches to endogenous nutrition, i.e. utilizes its own reserves of nutrients, as well as products formed during the destruction and atrophy of tissues. At the same time, a state of prolonged stress develops, as a result of which the enzyme systems responsible for the biosynthesis of hormones that ensure the development of a general adaptation syndrome are activated and rebuilt. Based on this, a number of pathologists consider starvation as a typical pathological process due to adaptation to a shortage of calories, food substrates and essential food components.

Starvation is physiological and pathological.

Physiological (temporary) starvation occurs in some animals as an adaptive reaction developed in the course of evolution, for example, during winter or summer hibernation of ground squirrels, marmots, badgers, hedgehogs, during cold stupor of amphibians, fish, reptiles, insects and is combined with deep inhibition of the central nervous system, a decrease in vital activity, which allows the animal to maintain vital activity for a long time in unfavorable periods of the year.

Pathological starvation is exogenous and endogenous. Exogenous starvation occurs when there is a lack or deficiency (as well as a violation of the composition) of food. Endogenous starvation is associated with pathological processes in the body itself (decrease or lack of appetite, eating disorders in the pathology of the oral cavity, esophagus, indigestion, absorption, vomiting, regurgitation in children, etc.).

There are the following forms of fasting: absolute starvation- in the complete absence of food and water; complete starvation- in the complete absence of food, but with the intake of water; incomplete starvation- insufficient in relation to the total energy consumption (under given conditions) nutrition.

Partial fasting(malnutrition, unilateral nutrition) - insufficient intake of one or more nutrients with food with its normal total calorie content. Partial fasting is protein, fat, carbohydrate, mineral, water, vitamin. Under natural conditions, the distinction between incomplete and partial starvation is difficult, because. malnutrition is usually combined with a violation of the composition of food.

imbalance- a condition caused by an incorrect ratio in the diet of essential nutrients with an absolute deficiency of any of them or without it.

The heaviest type of starvation is absolute starvation, without water intake, leading to the death of the body within 4-7 days with symptoms of dehydration and intoxication.

Complete starvation, in the development of which three periods are distinguished.

First period (2-4 days)- the period of initial adaptation (emergency adaptation) to new conditions of existence and uneconomical use of energy. Irritability, headache, weakness appear. In connection with the excitation of the food center, a strong feeling of hunger arises. The basal metabolic rate is increased. During the first day, the body's energy needs are mainly provided by the oxidation of reserve carbohydrates, the respiratory coefficient is close to 1.0. Starting from the second day, the energy consumption of the body is mainly covered by the oxidation of fats, the level of glucose in the blood is maintained due to the processes of gluconeogenesis. Despite the economical consumption of protein, due to plastic needs, it breaks down and synthesis decreases. A negative nitrogen balance develops.

Second period (40-50 days)- the period of maximum adaptation, "stationary" (the period of long-term stable adaptation). Energy resources are spent relatively evenly, energy costs are reduced, and basal metabolism is reduced. The rate of weight loss slows down, the feeling of hunger weakens.

Most of the energy comes from the oxidation of fats. The respiratory coefficient is reduced to 0.7. There is a mobilization of fat from the depot, develops lipemia, hypercholesterolemia, ketonemia, ketonuria, acidosis. There is an accumulation of intermediate metabolic products that have a toxic effect.

A number of adaptive mechanisms are activated, aimed at maintaining homeokinesis under conditions of nutrient deficiency, characterizing adaptation to starvation and indicating a transition to endogenous nutrition. Glycolytic and lipolytic enzyme systems are activated; increased activity of transamination enzymes in the liver. There is a selective activation of a number of lysosomal enzymes involved in the degradation of such cell components as proteins (cathepsins), nucleic acids (acid RNase and DNase), polysaccharides, mucopolysaccharides. This activation is adaptive in nature and is aimed at reutilization of macromolecules and subcellular structures that are less important for the life of the cell. The low molecular weight fragments formed in the process of intralysosomal digestion are included in the general metabolism and can be reused for the biosynthesis of macromolecules important for the life of the cell and partially to cover energy needs.

Protein consumption is reduced to a minimum, but in the end this causes an increase in the negative nitrogen balance. Since all enzymes are protein compounds, prolonged protein deficiency leads to a breakdown and weakening of their function, changes in metabolism. There is a sharp decrease in the secretion of digestive tract enzymes: suppression of the activity of pepsin, trypsin, amylase, lipase, etc., associated with the complete shutdown of the digestive function. Hypoproteinemia develops (weakening of the protein-forming function of the liver), oncotic blood pressure decreases. The exchange of water between blood and tissues, the ratio between intracellular and extracellular water is disturbed, edema may appear.

The main vital functions of the body during the first and second periods remain within the limits close to the physiological norm. Body temperature fluctuates at the lower limits of the norm, blood pressure may initially rise, then fall somewhat or fluctuate within normal limits. Myocardial contractility decreases, the risk of collaptoid conditions increases. A small initial tachycardia is replaced by bradycardia. The mass of circulating blood decreases in proportion to the loss of total weight. The motor activity of the stomach and intestines increases sharply at first (hungry contractions, sometimes of a spastic nature), later decreases. The amount of urine excreted decreases, the water balance becomes positive due to the accumulation of water in the body. Adynamia, apathy are growing, sometimes there are clouding of consciousness, mental disorders, anemia develops. Due to nutritional deficiency and under the influence of stress caused by hunger, secondary immunodeficiency occurs. The degree of atrophy and weight loss of different organs and tissues is uneven. The weight of the heart (3.6%) and brain (3.9%) decreases the least, and the adipose tissue decreases the most (97%).

Third period (3-5 days)- terminal (decompensation period), ending in coma and death. It begins after the reserves of fats are exhausted. It is characterized by a rapidly growing disorder of basic functions and metabolism due to disruption of the processes of energy supply to cells and the activity of enzyme systems. There is a deep depression of the central nervous system, weakness, apathy, the proposed food is rejected. The breakdown of protein, including vital organs, and the excretion of nitrogen in the urine increase. Protein is also used for energy purposes. The respiratory coefficient is 0.8. Ketonemia, acidosis and intoxication of the body with products of disturbed metabolism are increasing. Body temperature decreases, edema progresses (chloride retention and increased osmotic concentration in tissues, hypoproteinemia), weight loss increases. Death with complete starvation occurs with a loss of 40-50% of body weight. In persons who died from starvation, atrophic changes in organs and tissues are usually found. Life expectancy with complete starvation depends on body weight, age, sex, fatness before starvation, individual metabolic characteristics, and averages 60-75 days.

Conditions that increase metabolism, increase energy costs, shorten the life of a starving organism (the predominance of excitation processes in the nervous system, increased activity of a number of endocrine glands, muscle activity, overheating, dehydration, etc. Children endure starvation more severely than adults and die earlier; old people can fast longer than young people; women endure fasting more easily than men.

Even at the very beginning of the terminal period of starvation, properly carried out fattening can restore body functions. Initially, liquid food is introduced in a limited amount (in the absence of appetite, by force). After restoring the excitability of the food center, the volume of food is gradually increased, but without overload. Long-term consequences of starvation can be: fear of starvation, the desire to create food supplies, asthenic or apathetic states.

Partial starvation characterized by the possibility of long-term existence of the organism with insufficient intake of food and ongoing processes of digestion. In this case, the lack of protein plays the main role, and the body dies in the same way as during complete starvation, when 40-45% of the body's own proteins are used up. With prolonged incomplete starvation, a complex of disorders develops, characteristic of alimentary dystrophy.

Alimentary dystrophy(from Latin alimentarius - related to nutrition, synonyms: starvation disease, edematous disease, hungry edema, military edema). Alimentary dystrophy occurs as a result of prolonged malnutrition (lack of all food components).

The disease was widespread during the Great Patriotic War, during the blockade of Leningrad (1941-1943). Its duration ranged from 2-3 weeks with death to 2 years with gradual recovery. Contributing factors - neuro-emotional stress, cold, hard physical labor, infection, etc. It is manifested by general exhaustion, a progressive disorder of all types of metabolism, degeneration of tissues and organs with a violation of their functions. The main symptoms are general depression, anorexia, cachexia, diarrhea, splenomegaly, ascites, and edema. Edema is a consequence of the inhibition of the protein-forming function of the liver, leading to a decrease in the oncotic pressure of the blood plasma. The death of the organism is associated with extreme depletion of the neuroendocrine system, mainly the diencephalic-pituitary divisions, and overstrain of nerve cells.

Protein-calorie (protein-energy) insufficiency. The development of protein-calorie (protein-energy) insufficiency (BKN) is associated with the consumption of low-calorie foods containing insufficient amounts of protein.

MCI is one of the leading causes of child mortality in developing countries. It occurs mainly in children under the age of 5 years, sometimes in older children, less often in adults. Aggravating factors are: neuropsychic shocks, concomitant infections, adverse climatic conditions (strong insolation, high humidity and air temperature), hard physical labor, etc. MCI in children is always accompanied by a slowdown in growth and development. Its influence is most detrimental to the growth and development of the nervous tissue - cortical and subcortical structures of the brain (especially at the age of 6 months to 3 years), which leads to a violation of the mental and intellectual development of the child. Under some circumstances, BKN leads to nutritional dwarfism. In this case, children have reduced weight and height while maintaining normal body proportions. Severe forms of BKN include alimentary insanity.

Alimentary insanity(exhaustion, atrexia, cachexia, mummified or dry form of alimentary dystrophy) is a chronic disease that occurs in conditions of prolonged incomplete starvation, food intake low in protein and carbohydrates. It is distributed mainly in Africa. It usually occurs in children who develop CNF in the first year of life, often as a result of artificial feeding with highly diluted milk. It is characterized by general emaciation, metabolic disorders, dysfunction of most organs and systems. In the development of the disease, a long period of balanced fasting can be noted, during which the body maintains homeostasis due to a decrease in energy consumption and a decrease in metabolism by 15-30%. However, more often the body is not able to fully ensure the energy balance, and its own reserves begin to be spent on energy needs - fat depot lipids, tissue proteins. In the blood, the content of glucose, cholesterol and neutral fat decreases, the concentration of lactic acid increases; acetonuria appears, acidosis develops. The most serious changes occur on the part of protein metabolism - protein synthesis decreases, hypoproteinemia develops. The secretory and endocrine activity of the glands, especially the gastrointestinal tract, is disturbed; degeneration of all organs and tissues develops, hungry edema appears. From the side of the CCC - bradycardia, hypotension, slowing down of blood flow velocity. Disorders of the functions of the endocrine organs (pituitary, adrenal glands, thyroid and gonads), diencephalic-thalamic departments of the central nervous system are noted. There is a decrease in memory, lethargy, delayed physical development, wasting of muscles and subcutaneous fat layer (“monkey face”, face of a “little old man”), hair changes (thinning, lightening), vitamin deficiency may appear, body resistance decreases, susceptibility to infections increases . If the diet does not change, the body dies, more often from an attached infection.

Kwashiorkor(Proctor-Williams disease, "red child", "red Kvasha") - a disease that occurs mainly in young children as a result of a deficiency in the diet of proteins, especially animals, with sufficient or excess caloric content of food. A concomitant factor is a lack of vitamins, mainly of group B. A monotonous carbohydrate diet, typical of the poor in tropical countries, plays a role in the occurrence of the disease. The disease is distributed mainly in tropical Africa, Central and South America, India, Indochina. Kwashiorkor usually develops after weaning, especially with a sudden transition (without prior feeding) to adult feeding. It is characterized by a perversion of metabolic processes and a violation of the functions of most organs and systems. In the pathogenesis of the disease, the main role is played by the deficiency of essential amino acids, which leads to a disruption in the synthesis of vital proteins and, thus, to a delay in the growth and development of organs and tissues. Forced (due to lack of protein) excess consumption of carbohydrates leads to hyperproduction of insulin and exacerbates the pathology of protein metabolism. There is a delay in physical development, mental disorders, a decrease in the body's resistance, heart failure, dysproteinemia, widespread edema, anemia, diarrhea, lesions of the gastrointestinal tract, liver, pancreas, kidneys, skin (diffuse depigmentation of the skin, layered pigmented dermatosis - snake skin), hair (dispigmentation , redness, thinning, a symptom of the "flag" - multi-colored hair coloring on the head), etc. A lethal outcome occurs from acute renal failure or an associated infection.

vitamin deficiency. BKN is usually combined with vitamin metabolism disorders - beriberi and hypovitaminosis, which aggravate the course of any form of alimentary insufficiency. They can be primary (exogenous) and secondary (endogenous). Primary ones develop in the absence or deficiency of a vitamin in food, they are an independent form of partial nutritional insufficiency; secondary arise due to pathological changes in the body (impaired absorption or absorption of vitamins).

The main manifestations of hypovitaminosis are presented in table. eight.

Violations of mineral metabolism and microelement metabolism may be associated with a decrease, absence, excessive content of them in food and water; increased loss, retention in the body in violation of the excretion of these substances; inability of the body to absorb them. Data on the causes and consequences of violations of mineral metabolism and microelement metabolism are given in Table. 9.

Fasting treatment

The method of dosed starvation (unloading dietary therapy) consists in voluntary abstinence from food intake with unlimited (in case of complete starvation) water consumption and a number of detoxification hygiene procedures followed by restorative dietary nutrition according to a special scheme. Modern science recognizes fasting treatment for obesity, atherosclerosis, bronchial asthma, chronic gastritis, chronic non-calculous cholecystitis, pancreatitis, diseases of the musculoskeletal system, neurodermatitis, psoriasis, eczema. Absolute contraindications to its implementation are: pregnancy, malignant tumors, active tuberculosis, thyrotoxicosis, chronic hepatitis, liver cirrhosis, renal failure, IDDM, diseases of the blood system, decompensated heart failure, etc.

Table 8

Hypovitaminosis and its manifestations in humans

Dosed starvation enhances the processes of dissimilation, promotes the removal of "slags" from the body - pathological deposits of fat, salts, metabolic products. Switching to endogenous nutrition, the body consumes its own fats, carbohydrates, proteins, while the least active components of cells and tissues are first of all disintegrated, as a result of which, by starvation, the body manages to get rid of unnecessary, obsolete elements.

Table 9

Basic information about the causes and consequences of violations of mineral metabolism and microelement metabolism (according to V.A. Frolov)

Table 9 continued

At the same time, recovery processes are intensifying. After fasting, cells regenerate and their functions increase. In addition, the therapeutic effect of fasting is associated with adaptation to metabolic acidosis. In this regard, short periods of fasting can benefit the body. However, the use of this method does not always give a stable positive effect and requires medical supervision. Treatment and subsequent restoration of normal nutrition requires great care, careful monitoring of the patient in order to avoid complications and is carried out only in stationary conditions, self-medication is excluded. At the end of treatment, an achloride diet (fruit juices, kefir) with a sufficient content of vitamins and mineral salts is applied. Care should be taken with increasing the volume of food, given the hypofunction and atrophy of the gastrointestinal tract during therapeutic starvation. Repeated therapeutic fasting is possible only with full recovery from the previous fasting. The recommended duration, including the initial unloading and recovery periods, is 15 days in order to avoid the transformation of therapeutic starvation into stress.

A pathological condition that occurs as a result of prolonged complete starvation and is characterized by general exhaustion, metabolic disorders, disruption of the work of almost all organs and systems in medicine is called alimentary insanity. The disease belongs to the social, i.e. due to socio-economic conditions.

Etiopathogenesis of alimentary insanity

Pathology develops as a result of malnutrition. Despite the main factor, the disease affects people not only in countries with a difficult economic situation. Paying tribute to fashion, many starve consciously. In developed countries, people suffer from anorexia - a severe degree of alimentary insanity (alimentary dystrophy). And they do not stop even with noticeable changes in the body.

According to ICD-10, alimentary dystrophy has the code E41 and refers to severe malnutrition, with accompanying insanity.

The disease is characterized by protein-calorie deficiency. In the early stages of fasting, the body maintains hemostasis by reducing energy consumption. With a prolonged lack of nutrition, the body begins to consume fat reserves, tissue proteins, carbohydrates. Very quickly there is a decrease in glucose levels (25-40 mg%), as well as cholesterol and triglycerides. In parallel, the content of lactic acid increases. Acetone appears in the urine in large quantities. In the later stages, a decrease in blood acidity is observed.

There are changes in protein metabolism. This leads to a breakdown of those body functions that are realized with the participation of protein. Occurs which exacerbates dystrophy as a result of impaired absorption of nutrients and their absorption.

The structure of the disease is constantly changing under the influence of changing living conditions and nutrition of people.

Classification of pathology

In gastroenterology, the disease is classified according to the form and severity.

By form:

• Cachectic - extreme exhaustion. This form is extremely unfavorable. Weight loss can be up to 50%.
• Edematous, characterized by swelling, including internal. The form has a favorable therapeutic prognosis.

According to severity, 3 stages of alimentary dystrophy are distinguished:

• I. There is a slight weight loss, an increase in the frequency of deurination, with a constant volume of urine. Patients are thirsty and lacking in table salt - food is salted. There is an increase in appetite and at times puffiness appears.
• II. A sharp decrease in body weight. There is absolutely no fatty tissue in the chest, abdomen and buttocks. Deep folds and wrinkles appear on the face and neck. Patients suffer from constipation, chilliness develops. The general condition worsens, muscle weakness appears, working capacity is lost. There are changes in the psyche.
• III. Fat disappears completely. Severe weakness, a sharp decline in strength, against this background, atrophy of the skeletal muscles occurs. The skin is dry with many folds. With edematous form - accumulation of exudate in the abdominal cavity. There is a hungry coma, pronounced changes in the psyche.

Factors affecting the development of the disease

The causes of alimentary dystrophy are nutritional deficiencies, prolonged starvation. Also an energy crisis, when much more energy is consumed than comes from food.

There are not so few factors due to which a person eats poorly or practically does not eat at all. But most often, prolonged fasting is due to the following.

• Socio-economic disadvantage. Due to martial law, environmental disasters, forced imprisonment, a person cannot provide himself with a normal diet.
• Pathologies of the gastrointestinal tract, in which food intake causes unpleasant and sometimes painful sensations (heartburn, heaviness, bloating). Disease accompanied by nausea, vomiting (ulcer, gastritis).
• Refusal of balanced food in favor of some kind of diet (vegetarianism, the Kremlin diet, and others).
• Conscious refusal to eat in pursuit of an "ideal" appearance.
• Refusal of food in protest.
• Mental illness in which a person does not eat for no reason (schizophrenia) or because he is afraid of eating (sitophobia).

How does the disease manifest itself?

The main pathological process in alimentary dystrophy is exhaustion. It is accompanied by characteristic clinical manifestations:

• constant feeling of hunger;
• polydipsia: thirst is associated with violations of the water-salt balance;
• abnormal feeling of cold;
• pain in the muscles, starting from the lower extremities and gradually spreading to all groups;
• feeling of heaviness in the abdomen, bloating;
• violation of the stool: painful constipation is replaced by watery diarrhea;
• frequent urination;
• constant weakness, loss of strength;
• dizziness;
• lack of menstruation in women of childbearing age;
• mental disorder.

Complications

With alimentary dystrophy, the immune system is disturbed. The body cannot resist infections. The most common complication of dystrophy is tuberculosis, but, unfortunately, not the only one.

• A sharp drop in blood pressure and deterioration of the blood supply to organs (collapse).
• Hungry coma. At the initial stages, it is accompanied by a feeling of hunger, dilated pupils, fainting.
• Hypochromic anemia.
• Dysentery occurs against the background of a decrease in the secretory functions of the gastrointestinal tract.
• Pneumonia.

Alimentary insanity in children

Dystrophy can occur at any age. For a child, a lack of nutrients in the body, especially protein, is more dangerous than for an adult.

Protein deficiency occurs in two severe forms - alimentary insanity and kwashiorkor. The latter is characterized by a lack of protein in the diet with a sufficient amount of fats and carbohydrates. Kwashiorkor is commonly seen in children aged 1-4 years.

The word kwashiorkor, translated from the language of the indigenous inhabitants of West Africa, means "weaned from the mother's breast." The disease is most common in underdeveloped countries, where food is mainly fruits and vegetables and health care is practically not developed.

Due to the lack of protein in the child's menu, the work of the intestinal glands is disrupted, blood albumin and plasma colloid osmotic pressure decrease. As a result, cellular overhydration occurs, characterized by edema.

Due to damage to the intestinal mucosa, malabsorption develops. Frequent bowel movements promote increased excretion of lactic acid, acidosis develops. Formed fibrosis of the pancreas, fatty degeneration of the liver. In conditions of deficiency of protein and vitamins, anemia increases.

What is dangerous dystrophy in childhood?

The child is characterized by the immaturity of the immune system. In children with dystrophy, the protective functions of the body are practically inactive, complications in the disease are a frequent occurrence.

• Clerophthalmia. Insufficient hydration of the eyes develops against the background of deficiency or non-absorption of vitamin A.
• Hypothermia is characterized by pallor, lethargy, in severe cases, cyanosis of the skin and mucous membranes.
• Hypoglycemia. A critically low blood glucose level contributes to the development of disorders of the child's central nervous system and can cause death.
• Subcommittee.
• Heart failure. A decrease in myocardial contractility leads to inadequate blood supply to organs and, as a result, their atrophy.

How is the diagnosis carried out?

The basis for the diagnosis of alimentary dystrophy in adults and children is a thorough history taking and a careful examination of the patient. Physical examination consists in identifying and assessing the general condition:

• determining how much weight loss is progressing;
• temperature measurement allows you to determine the presence of hypothermia;
• assessment of the condition of the skin: color, moisture;
• examination of the eyes and the area around them: dark circles under the eyes indicate a lack of nutrients in the body.

To identify the degree of dystrophy and the presence of complications, laboratory tests are prescribed. According to the reduced indicators of erythrocytes and hemoglobin, the form of anemia is determined, according to the level of glucose - the stage of alimentary insanity.

Diagnostics includes instrumental examination:

• ultrasound scanning of internal organs;
• fluoroscopy;
• fibrogastroduodenoscopy - examination of the digestive tract using endoscopic equipment;
• colonoscopy.

Therapy Methods

Treatment of alimentary dystrophy at any stage begins with the normalization of nutrition, rest. In stationary conditions, patients are placed in a well-ventilated warm room. Patients with dystrophy should never come into contact with infectious patients.

At the I degree of pathology, fractional multiple meals are prescribed (light, quickly digestible food). At II and III degrees, patients are prescribed enpits and parenteral administration of glucose solutions (40%) every 2 hours, 50 ml each. Initially, the approximate daily calorie intake is 3,000 kcal, gradually increased to 4,500 kcal per day. The lack of liquid is replenished by drip injection of various solutions.

Therapy of infectious complications is carried out with antibacterial drugs. With the development of seizures, 10 ml of potassium chloride solution (10%) is injected into the vein.

Pathology monitoring

The prognosis of alimentary insanity depends entirely on the timeliness of seeking medical help. In the later stages, the disease is irreversible and fatal. Less often, when the conditions for the intake of nutrients into the body change, the pathology passes from stage III to stage II, and subsequently to clinical recovery.

Do not forget about the causes of starvation. If they are caused by fanaticism and phobias, the patient should visit a psychiatrist in parallel. If complications occur, the prognosis depends on the severity of comorbidities.

According to statistics, women are the most resistant to dystrophy. The most severely affected are the elderly and children.

Disease prevention

The main preventive measure is good nutrition with a sufficient balanced amount of proteins, vitamins and minerals. If hunger is a consequence of circumstances beyond the control of a person (war, environmental catastrophe), if possible, try to leave the place of disaster. If it doesn’t work out, try to be less nervous (this will not improve the situation), consume as much protein as possible, even if of non-animal origin. It is found in legumes, nuts and seeds.