The liver dystrophy is a chronic pathological condition characterized by the presence of an excessive fat in the liver. In a different way, this condition is called the causes of such obesity. Many and almost every person is in the risk group for this disease.

The reasons:

• abundance of fats in the diet;
• obesity;
• alcohol;
• elevated cholesterol;
• diabetes;
• protein failure;
• poisoning chemical poisons;
• some drugs;
• hepatitis;
• unbalanced nutrition, and, as a result, lack or oversupply of vitamins and microelements;
• hereditary liver diseases and autoimmune processes.

This is the main list of causes of pathology, but the liver fatty can overtake human and for other less explicit reasons. The complexity is that to the strong progression of the disease, it may not show any symptoms. It depends on the stage of the disease.

Stages of obesity of the liver:

1. Steatosis. Permanent progressive changes in the liver work are noted, fat cell dystrophy occurs.
2. Steatogepatitis. The inflammation of the liver is revealed - hepatitis. Perhaps the violation and occurrence of complications.
3. And as a result, oncology.

Symptoms:

As already mentioned, the liver dystrophy is difficult to diagnose due to the lack of explicit symptoms. Weakness, nausea, liquid chair, flatulence, small pain in the right hypochondrium may be present at the initial stages. These symptoms may accompany other diseases, so it is very important not to wait for the manifestation of a more dangerous signals of the body and turn to the doctor in time to establish an accurate diagnosis. With such a disease, like a fatty dystrophy, symptoms in the later stages are most pronounced, pain in the hypochondrium becomes stronger and more often, headache is added, fast fatigue, itching, possibly a sharp weight loss.

Study:

When handling a person in a clinic for a prophylactic examination or, when you find an alarming symptoms, the doctor conducts the necessary research. Biochemical blood test is taken, including which they identify the presence or possibility of such pathology as a well-fat liver dystrophy. To clarify the diagnosis it is necessary to produce

If, according to research, the patient is diagnosed with liver dystrophy, treatment must be carried out comprehensively and comprehensively. Although the word "treatment" is not quite appropriate with a given disease. Rather, prevention and elimination of the causes of the development of the disease. As you know, the liver is a self-healing authority, but it requires support, support and protection for recovery and return health.

The patient needs to make changes to his lifestyle, to establish proper and rational food, play sports and follow their health. It is necessary to eliminate all the negative factors that led to the emergence of the diagnosis.

Elimination of negative factors:

• during the diagnosis of obesity - mandatory weight loss;
• food, according to a diet installed by the attending physician. It is necessary to avoid a large number of fats: fatty varieties of meat, baking, chocolate, smoked, cheeses, fatty cottage cheese, any fried food, etc.;
• full rejection of alcohol-containing drinks;
• physical exercises. For obese people for at least 30 minutes a day or walking at least 5,000 steps.
• reducing cholesterol levels in blood.
• if possible, reducing the use of drugs;
• when working with poisons - a change of work or reinforced protection measures.
• in difficult cases, drugs are prescribed in the later stages.

With a timely handling of a specialist and comply with all recommendations, the forecast for this disease is quite favorable.

Beep fatty dystrophy

Liver fatty dystrophy is a syndrome that occurs due to the progression of fatty dystrophy in liver cells. The course of this disease is characterized by the occurrence of the process of pathological accumulation in liver cells of fatty sediments with a kind of fat droplets. The cause of the development of this disease affecting the liver In many cases, pathological processes occurring in biliary and intestinal tracts are becoming the pathological processes. The risk factors for the development of liver dystrophy are also the presence of obesity in a pronounced form, a second type of diabetes mellitus Malaabsorption and majestic syndromes, regular abuse of alcoholic beverages. The consequences of the use of a number of drugs, such as: corticosteroids, tetracycles, estrogens, as well as medicines of a non-steroidal anti-inflammatory action group can lead to the development of fatty dystrophy. The liver fatty dystrophy besides this can accompany the flow of various viral hepatitis, which occur in chronic form, in particular - hepatitis C.

Toxic liver dystrophy

Toxic liver dystrophy has massive progressive necrotic processes that affect liver tissues as its manifestations. The disease, as a rule, is acute, as well as in some cases may be present in the body in chronic form, causing hepatic failure as the development of pathology progress.

The cause of massive liver necrosis is mainly becoming the effect of toxic substances contained in food products, including in mushrooms causing arsenic poisoning, phosphorus compounds, etc. These intoxication are an exogenous nature. Endogenous intoxication can also provoke toxic liver dystrophy. These include toxicosis arising from women at that time when they wear a child, thyrotoxicosis. The cause of toxic liver dystrophy is often the disease of viral hepatitis, in which this disease is developing as one of the manifestations of its lightning form.

Toxic liver dystrophy causes changes in the body, which are characteristic of this disease characteristic of each specific stage of the pathological progress. Initially, an increase in the size of the liver occurs, this body acquires either a decrepit or density consistency, it becomes characterized by a jaundice tint. With the further course of the disease, the liver is reduced in size, and its capsule shell becomes wrinkled. The hepatic fabric changes its color to grayish and acquires the appearance of a clay mass. At the later stages, after the third week of the disease, the process of reducing the liver in size continues, it acquires a reddish tint. Lighting the liver reticular stroma occurs, in which extended and over-blooded sinusoids are marked. The hepatocytes remained only in the peripheral areas of the lobes. These phenomena indicate the transition of hepatic dystrophy into the stage of red dystrophy.

The presence of toxic liver dystrophy we switched to the chronic stage is an extremely rare clinical case, but it is associated with the likelihood of a patient's death due to progressive liver failure.

Acute liver dystrophy

Acute liver dystrophy of the advantage appears as a complication, developing against the background of the unfavorable flow of Botkin's disease. Cases of this disease in autonomous form, as evidenced by medical statistics, are extremely rare.

To date, medical research in the field of studying the mechanisms for the development of dystrophic phenomena in the liver did not lead to a unambiguous response to the question of the cause of acute hepatic dystrophy. Currently, the mechanisms of the pathological progress of this heavy disease amazing the liver are still not fully understood, and whether the correlation with the force (virulence) of the virus remains unclear, or there is an impact of some other factors.

Consideration of a parenhimatous hepatitis of hepatitis can have a patient with brucellosis, returnful title, syphilis, as well as a state of pregnancy and artificial interruption. All this causes a high probability of rebirth of hepatitis into the heavy form of liver dystrophy.

Acute liver dystrophy at the initial stage recreates a clinical picture, similar to the beginning of the development of Botkin's disease, which is associated with a significant deterioration in the overall condition of the patient. At the same time, the damage is mainly the nervous system, which is manifested in the appearance of all sorts of brain disorders. Patients begin to wander, rushing on the bed, convulsions and vomiting happen. In some cases, the emergence of such states has become the rationale for the need to hospitalize the patient into a psychiatric clinic. On the other hand, it is possible other, the opposite reaction of the CNS to the development of the pathological process. There may be apathy and depressive state, a significant reduction in the life tone of the body, an increased drowsiness appear. Up to the onset of the unconscious state and hepatic coma.

Alcoholic liver dystrophy

Alcoholic liver dystrophy is a disease caused by the excessive use of alcoholic beverages over a long period of time exceeding 10-12 years. Alcohol, in an unlimited quantity, falling into the human body, has an extremely negative, hepatotoxic effect.

The appearance of alcoholic liver dystrophy can be a sign of the fact that there is a fatty dystrophy of the liver or steatosis, cirrhosis, alcohol hepatitis. In the overwhelming majority of cases, as the earliest stage of the progress of the pathological process in the liver due to alcohol abuse, steatosis develops. After stopping the regular flow of alcohol into the body of the patient, pathological changes due to the steatosis developing in the liver return to a normal state during from 2 to 4 weeks. Often, during the course of the disease, it may be missing at least as pronounced symptoms

Alcoholic liver dystrophy has the same symptomatic, which is characterized by chronic alcohol intoxication. Diagnosed as a result of the detection of increased size of the parotid glands, the presence of Dupuyretne Contracture, Palmar Erythema. The presence of this disease in the patient's body also testify the results of laboratory research and liver biopsy.

Therapeutic measures for alcohol liver dystrophy consist primarily in the absolute termination by the patient of alcohol consumption. The course of treatment with corticosteroid preparations and essential phospholipids is prescribed. If the disease is in the terminal stage, liver transplantation can be shown.

Diffuse dystrophy of the liver

The diffuse liver dystrophy is a pathological process that develops in a parenchym that is the main cloth from which this organ is formed. In specific hepatic cells, hepatocytes occur processes aimed at detoxifying poisonous substances entering the body. Hepatocytes take part in the processes of digestion, their role is reduced to the secretion of bile, in which a number of enzymes that break fats in the gastrointestinal tract are present. Liver cells provide neutralization of harmful substances by transformation into such that they do not pose a threat to the normal functioning of the body, and which are subsequently displayed along with bile.

Diffuse liver dystrophy arises as a result of the fact that the liver cells are not always able to recycle the poison entering the body. It happens that they cannot cope with the scale of intoxication, and as a result, poisoning leads to their death. Over time, the cells destroyed in this way are replaced by fibrous connective tissue. The more significant the degree of such a liver damage, the more it does, accordingly, negatively affects its ability to perform its functions.

As a rule, the development of diffuse pathological progress in the liver is accompanied by a similar process affecting also the pancreas, since the functions of the two organs are in close connection among themselves.

Heat focal dystrophy

The focal liver dystrophy represents certain difficulties in the diagnosis of this disease due to the fact that although there is a deterioration in the functioning of the liver to fix these pathological changes through laboratory studies seems extremely difficult.

Based on the reasons that caused the focal liver dystrophy, in each case, the presence of various objective and subjective symptoms and manifestations of this disease in each particular patient is characteristic.

The focal liver dystrophy, arising in particular as a result of regular intoxication by large doses of alcohol, is manifested in such phenomena as the appearance of the breath, deterioration of appetite, etc. In some cases, patients note the occurrence of unpleasant sensations and severity in the field of right hypochondrium. Such symptoms are characterized by an increase in their intensity while driving.

Often, the identification of adipose body infiltration becomes possible only when performing magnetic resonance - MRI and computed tomography. These diagnostic techniques are the most effective way to detect the patient with focal liver dystrophy.

Bench grainy dystrophy

The grainy liver dystrophy is the most common type of protein dystrophic pathology. With this disease, the colloidal properties of cell cytoplasm are broken, in which the appearance of grain-like protein is observed.

The reasons for the appearance of this hepatic illness become: no full-fledged feeding in infant age, and in later age periods - the consequences of intoxication, the presence of infections, the functioning of the functioning of blood circulation systems and the Lymph current, as well as the impact of factors that can provoke hypoxia tissues.

As the grainy liver dystrophy develops changes in protein cellular metabolism. The progress of the pathological process of the grainy dystrophy of the cytoplasm acquires the swollen and stupid appearance, as a result of which this lesion of the liver is also characterized as a muddy swelling. The liver affected by this disease acquires a decay consistency, blood supply is broken in it.

In the process of establishing a differentiated diagnosis, the grain dystrophy must be separated from the physiological processes of protein synthesis in cells in which graininess occurs in protein.

The grainy liver dystrophy is a reversible process, but due to the severe course of the disease, it is possible to rebirth into such forms as hyalin-drip or hyrophyra dystrophy, as well as in necrosis.

Stellic liver dystrophy

The protein liver dystrophy arises as a result of a violation of protein metabolic processes and can be represented by amyloidosis, hyaline and a grainy dystrophy.

A characteristic feature of amyloidosis is that in the presence of this disease in the tissues there is a special protein amyloid substance.

The hyaline is a variety of protein dystrophy, which often takes place as a concomitant disease against the background of atherosclerosis. This pathology is mostly distinguished by local localization, in particular, it can appear in the vessel wall in the formation of a thrombus. Hyalosu is typical forging translucent protein structures similar cartilage hyaline tissue.

The protein liver dystrophy also acquires the type of dystrophy, which means the occurrence in the cellular protoplasm of drop-shaped and grain-like protein formations. Combining into a single whole, these formations show a tendency to complete the entire internal cellular space. In the grainy liver dystrophy, protein cellular structures are compacted, and the normal functioning of the cells is disturbed. The grainy dystrophy is fraught with the occurrence of pathological changes in a necrotic nature and leads to the death of the cell.

Hydropic liver dystrophy

Hydropic liver dystrophy, also known as water dystrophy, has such a feature as the fact that vacuoles containing cytoplasmic fluid appear in the cell. In the presence of this type of hepatic dystrophy, the parenchyma cells differ in the increased size, the kernel in them acquires peripheral localization, in some cases it is observed or vacuolation.

With the development of pathological changes, the cell is overwhelmed with liquid and its ultrastructures decompose. The cell becomes similar to the water-filled container, and are essentially one solid vacuole with the core placed in it having a view of the bubble. A similar phenomenon, which is a sign that is characterized by the collicration necrosis, is called - a balloon dystrophy.

Hydropic liver dystrophy can only be detected in the study using a microscope, since visual changes are not peculiar to the appearance of tissues and organs.

The forecast in the presence of this disease seems unfavorable due to the fact that during the hydropic liver dystrophy is essentially violating the functioning of this body. The negative prognostic factor is that the outcome of this disease becomes the focal or total necrosis of cells.

Yellow liver dystrophy

Yellow liver dystrophy in acute shape can occur during pregnancy as one of the complications associated with it. The cause of it becomes the condition of acute intoxication, in which this disease is an aggravating factor in development in the body of infection development processes.

Jaundice in a woman in the period in which she triggers the child as well as in the presence of other liver pathologies in addition to the liver dystrophy, such as cholecystitis and the presence of stones in the liver, may also be present in the form of an autonomous disease provoked by autoinoxication of the body. Such a condition is known as accompanying pregnancy toxicosis.

Yellow liver dystrophy is one of the most serious gravity toxicosis of pregnancy. The disease is caused by severe intoxication by the products of metabolic processes occurring during pregnancy, which differ in other features than at the metabolism of the substances of the body with the usual condition of the body. Pathological progress at the beginning of its development is characterized by the appearance of jaundice, which is preceded by a period of severe, often very long vomiting. After time, the condition is aggravated by the fact that the skin and the sclera acquire a pronounced jaundice view, there is a cloud of consciousness, there may be a state of nonsense and excessive excitation of the nervous system. There is a possibility of multiple subcutaneous hemorrhages, as part of urine, the number of which shows a tendency towards a significant reduction, the presence of chyrosine and lecithin is found, and in addition, there is a decrease in liver stupidity. Due to the further deterioration of the general state of the patient, there is a likelihood of a fatal outcome after a few days.

Parenchimatous liver dystrophy

The parenchymal liver dystrophy is at the heart of the development of the associated pathological process of changing the chemical and physical and morphological characteristics of cell proteins inherent. The essence of such violations of the functioning of cells is a hydration process that is subjected to cytoplasm as a result of the fact that coagulation, denaturation, or by opposite, is the phenomenon of kolinkivation in the cell. In those cases in which the protein-lipid bonds violation occurs, membrane cellular structures are characterized by destructive processes in them. The consequences of such changes are to develop the necrotic processes of coagulative - dry, or a collible - wet nature.

Parenchimato liver dystrophy is classified by its varieties like:

Hyalin-drip hydropic horn dystrophy.

A grainy dystrophy, which is characterized by the appearance of protein grains in cells of protein grains in the cells of the liver can also be related to the liver parenchymatous liver dystrophy. This type of hepatic dystrophy is characterized by an increase in the amount of organ affected by this disease, the acquisition of a deryablial consistency and a dim outer look at the cut. The latter feature caused by the fact that the liver granular dystrophy is also called dim or muddy swelling.

The liver dystrophy is chronic or acute (depending on the form) of the liver disease, which proceeds with the phenomena of the fatty dystrophy of hepatocytes (hepatic cells) or their massive necrosis. Diseases such as hepatosis and cirrhosis are the consequences of the liver dystrophy.

It is customary to distinguish fat and toxic liver dystrophy.

Toxic liver dystrophy

It is manifested by the massive progressive necrosis of the liver tissue, is acute, less often a chronically occurring disease characterized by progressive liver necrosis and the development of associated liver failure.

Etiology and pathogenesis of toxic liver dystrophy

Massive liver necrosis are usually developing mainly in exogenous (food poisoning, including mushrooms, phosphorus, arsenic compounds, etc.) and endogenous (thyrotoxicosis, toxicosis of pregnant women) intoxication. It may occur in viral hepatitis as a manifestation of its lightning form.

Pathological anatomy with toxic liver dystrophy

Changes occurring in toxic liver dystrophy are different in different periods of the disease. At the beginning of the disease, there is some enlargence in the size of the liver, it becomes a dense or flabby, with a yellowish tinge. With a further flow, the liver decreases in size, becoming a flabby, and its capsule acquires a wrinkled structure. The liver fabric becomes gray, clay look.

Microscopically observed the development of hepatocyte fatty dystrophy in the center of the lobe of the liver, which replaces their further necrosis and the processes of the autolytic decay with the formation of protein-fatty detritus with the amino acid crystals of leucine and tyrosine. In progression, these necrotic changes capture the remaining departments of the poles. These changes in the liver are characterized by the offensive stage of the so-called yellow dystrophy.

After 3 weeks of the disease, the liver further decrease in its sizes and acquires red. The reticular sturge of the liver with extended and sharply crowded sinusoids is taken off. Hepatocytes are saved only along the periphery of the poles. These changes are characterized by the offensive of the red dystrophy stage.

Symptoms of toxic liver dystrophy

In case of massive liver necrosis with the toxic dystrophy of the liver, the development of jaundice, the processes of hyperplasia located near the portal veins of lymph nodes and spleen, the appearance of multiple hemorrhages in the skin, mucous membranes and serous shells, necrosis of epithelial cells in kidney channels, dystrophic changes in the tissues of the pancreas and myocardium Hearts.

When progressing this form of illness, patients are often dying from the development of hepatorenal syndrome and liver failure.

Toxic chronic liver dystrophy is extremely rare, when the disease recurrences, during which the postnurotic form of the liver cirrhosis develops.

Beep fatty dystrophy

It is a disease or syndrome due to the development of fatty dystrophy in hepatic cells in the form of pathological deposits in her fat droplets. The liver cell accumulates fat deposits.

Etiology liver fatty dystrophy

The liver fluid dystrophy is a liver reaction on intoxication, sometimes associated with a number of diseases and pathological conditions. Most commonly causes of fatty liver dystrophy are pathology of intestinal and biliary tracts, pronounced obesity, bypass intestinal anastomoses, long-term use of parenteral nutrition, diabetes mellitus (second type), Maldiage and Malabsorption syndromes, gluten-beanopathy, Wilson-Konovalov disease and a number of genetically determined diseases , chronic alcohol intoxication, the use of certain drugs (corticosteroids, estrogen, tetracycline, nonsteroidal anti-inflammatory drugs, amiodaron). Almost all chronically occupy viral hepatitis, especially chronic hepatitis C, are accompanied by the development of liver fatty dystrophy.

Pathogenesis of liver dystrophy

The pathogenesis of the described liver disorder is the process of accumulating triglycerides and cholesterols in the liver tissues due to excessive suction and formation of free fatty acids and excessive advent of fatty acids into the liver, reduce the oxidation rate of fatty acids inside the mitochondria of hepatocytes, the difficulties of the recycling processes from the liver.

Pathological anatomy at fatty liver dystrophy

The liver at fatty dystrophy is increased in size, it becomes yellow or red-brown, it remains smooth surface. In the liver cells, fats are determined from triglycerides. The process of accumulation of fats in hepatocytes can be dusty, large or fine-flowered. Fat droplets push organelles inside cells on the periphery. Infiltration of fats can cover both single hepatocytes and hepatocyte groups and even the entire liver parenchyma. For fatty infiltration, hepatocytes die, and fat drops merge among themselves and form fatty cysts with the growth of connective tissue.

Clinic of fatty liver dystrophy

The course of liver dystrophy is usually asymptomatic and, mostly, pathology is randomly detected when conducting instrumental research methods. Pain is not a specific symptom of the disease.

Some patients appear complaints about the feeling of gravity and unpleasant sensations in the field of right hypochondrium, which are usually amplified when driving. The liver with this disease is enlarged, but when palpation is painful in the liver, it is quite rare. The fatty dystrophy, which develops due to chronic alcohol intoxication, often flows with anorexia, shortness of breath and a number of other symptoms.

Methods for diagnosing liver dystrophy

The use of traditional laboratory studies to confirm the data of violations is practically not informative. There is a moderate increase in the activity of serum transaminase enzymes and alkaline phosphatase. The level of general bilirubin, albumin and prothrombin is preferably within the normal range. There are no other deviations from the norm in the blood. When conducting an ultrasound, the doctor notes that the echogenicity of the liver tissue is preferably normal or elevated. In some cases, only conducting computer tomography and magnetic resonance tomography allows you to identify the presence of liver dystrophy. For the final confirmation of the diagnosis, the mandatory implementation of the biopsy of the liver tissue with histological examination of the bioptats obtained is required.

Treatment of dystrophy cookies

An important event in the treatment of liver dystrophy is to prevent the development of necrosis and inflammation (steatohepatitis), the treatment of which is much more complicated. The treatment of liver dystrophy is primarily to eliminate the etiological, caused by its causes, as well as in the symptomatic treatment of concomitant disease syndromes.

Among the drugs causing the improvement of the functional states of the liver, one of the leading places is occupied by the complex drug heptral (adhemethionine). The second leading drug-based drug in the treatment of liver dystrophy is the drug "Ursodoxicole acid".

The information provided is not a recommendation for the treatment of liver dystrophy, and is a brief description of the disease in order to familiarize. Do not forget that self-medication can harm your health. When signs of illness or suspicion of it, it is necessary to immediately consult a doctor. Be healthy.

Any disease can be considered as damage to the organ with various pathogens or changing metabolic processes at the cellular level. In this case, they are talking about dystrophy - such a perversion of metabolism, which is accompanied by a violation of the structure. Often this is an adaptive response of the body to adverse effects of the external environment.

Etiology

Changes in metabolism, which develops under the influence of external and internal factors, leads to a violation of the structure of the cells. This may be defective nutrition, unfavorable living conditions, injury, intoxication, poisoning, infection, endocrine disorders, blood circulation pathology, hereditary defects. They affect organs directly or through a change in neuro-humoral regulation. The severity of dystrophy is influenced by the type of fabrics, the strength and duration of the impact of the pathological factor, as well as on the body's ability to respond to the impact.

These restructuring are satellites of any disease. Sometimes they appear primary and cause a picture of the disease, and sometimes the disease itself disrupts cellular metabolism.

Distrophic changes in the liver arise under the influence of the following factors:

inflammatory diseases - viral hepatitis, infection; toxic damage - the result of exposure to alcohol, drugs, poisons, industrial harmful substances; improper nutrition - the prevalence of oily and carbohydrous food; violation of bile outflow; systemic diseases; endocrine disorders; hereditary diseases.

Pathogenesis

A long study of dystrophy processes using biochemistry methods, histochemia, electron microscopy showed that any of them is based on violation of reactions involving enzymes and changing the function of cellular structures. In the tissues in large numbers, metabolites of a changed metabolism are accumulated, the ability to regenerate and the function of the damaged organ is disturbed. As an outcome - a violation of the life of the body.

Dystrophic changes can flow over one of the mechanisms:

Decomposition - at the level of molecules there is a restructuring of the structure of fabric systems, protein-fat and mineral connections. The reason for this is a change in the ratio of nutrients, the accumulation of metabolic products, hypoxia, the effects of toxins, fever, displacement of the acid-base balance (more often towards the acidosis), violation of redox reactions and the balance of electrolytes. Under the influence of these factors, the components of organomet cells and large molecules can disintegrate or modify. Proteins are subjected to hydrolysis of lysosomal enzymes and are denatured. The same ways are formed more complex formations (amyloid, hyalin). Theinfiltration - impregnation of organ structures with metabolites of proteins, fats or carbohydrates, which are freely in the blood or lymph (accumulation disease). Transformation - the reaction of the conversion of substances in each other - fats - In carbohydrates, carbohydrates - in proteins, glycogen synthesis of glucose. A large number of new substances are assembled inside the cell. A changered synthesis is the strengthening or weakening of the formation in the tissues of normal substances - proteins, fats, glycogen, which leads to their insufficiency. The synthesis changes can occur along the path of creating substances, usually not inherent in this tissue. For example, glycogen - in the kidneys, keratin - in the tear gland.

These pathological mechanisms can develop consistently or simultaneously. Morphologically dystrophy will manifest itself as a violation of the cell structure. Usually, after damage to various cellular structures, their regeneration begins. In pathology, it is disturbed even at the molecular level. Inside cells begin to determine a variety of grains, drops, crystals and other inclusions, which should not be there, or their number in healthy cells is insignificant. The process can flow in the opposite direction - in cells the usual inclusion or parts of the organell disappear in the cells.

At the dystrophy organ level manifests itself by changing the appearance. Color, size, form, about such processes say "rebirth" or degeneration of the organ. The authority changes its functioning - synthesis of various substances, metabolism. If the ethiology of dystrophy is eliminated and there are no deep damage, that is, the possibility of absolute recovery of the organ. In other options, the processes are irreversible, necrosis develops.

Distrophy types

Classify them in terms of damage caused by them:

parenchimatous - affect the parenchyma of the organ; Stromally-vascular - perestroika in microshogs and intercellular space; mixed.

If we consider the pathology of a certain metabolism:

protein; fat; carbohydrate; mineral.

By the extensity of the process there are:

local; common, or systemic.

Also allocate acquired and hereditary.

Parenchimatous disproteinosis

The change in the metabolism of cytoplasmic proteins, which are in the associated or free state, is called protein dystrophy. Related proteins are various lipoprotein complexes, and free by cellular enzymes. Their physico-chemical device changes, various peptide particles are formed in the cytoplasm. It entails the change in the exchange of water and electrolytes, osmotic pressure, increases the saturation of the liquid.

Morphologically, this is manifested by hyalin-drip and hydropic dystrophy. The terminating phase in their existence may become necrosis cells. The final stage of the hyalin-drip exchange disorder is coagulative necrosis, with hydropic, in the completion, the kolkivational cell death. Consider these changes are possible only with the use of microscopy of damaged areas. With hyalin-drip disproteinosis in cells, hyaline drops are collected. Cells affected by hydropic dystrophy are increasing in volume due to vacuoles with liquid transparent content.

Granular dystrophy, or muddy swelling - also parenchymal dystrophy, protein falling in the form of grains. The reasons are a variety of infections, blood circulation pathology, defective nutrition. It is functionally not incurred by a violation of the body and sometimes regresses without a trace.

Hydropic dystrophy, on the contrary, causes the oppression of the liver function. Develops against the background of severe and medium-free viral hepatitis, long cholestasis, dystrophic shape of the cirrhosis. The most pronounced view is a balloon dystrophy, which, with long-term increase, becomes irreversible and goes into collible necrosis. Cells are melted to a liquid state. Immune cells come to the focus, which remove dead cloths. The scar is formed in their place.

Hyalin-drip dystrophy in the liver is manifested by a decrease in cell size, sealing protein formations. Special type - alcohol hyaline, or Mallory Taurus. This is a special protein, the result of hepatocyte synthesis. It is located in the cells around the kernel and has an acidophilic reaction (painted in blue). It has leukothataxis - leukocytes attracts, is able to cause immune responses, stimulates the formation of collagen. In the blood of patients with alcoholism, circulating immune complexes based on alcohol hyaline, which are able to affect the kidney with the formation of glomerulonephritis.

Parenchimato lipidose

The fatty dystrophy is the formation of a large number of lipids in cells or deposition in areas, in which it was previously unprecedented, as well as the synthesis of fats of the uncharacteristic structure.

The main mass of accumulated fats in hepatocytes is neutral fat. It form drops that gradually merge into a large vacuole. Fatal exchange is violated in three cases:

The massive admission of fats in the body, which over time leads to a lack of enzymes for their digestion. The tank substances block the synthesis of firows. Amino acid substances for the formation of lipoproteins and phospholipids.

Provoke the development of lipidosis The following factors:

alcoholism; diabetes; general obesity; toxic damage; hereditary enzympathy; diseases of the digestion system.

The obesity of the liver is manifested in three forms:

disseminated - lipid drops are located in separate cells; zonal - fats are collected in special zones of hepatic lobes; diffuse - the distribution of fat throughout the salt.

In terms of inclusion, obesity can be large and fine-flowered.

Long-term alcohol consumption is almost 50% completed by the formation of fat hepatosis

Ethyl alcohol and its metabolic products enhance the synthesis of fatty acids, but reduce their oxidation and formation of lipoproteins. In large quantities, cholesterol accumulates, which reduces cell membranes permeability. Intracellular fat drops push the core to the periphery. But the synthetic work of the cell is not broken. If you refuse to alcohol, the reverse development of the process occurs. Functions are restored, the accumulated lipids are gradually metabolized and outlined from the liver.

But if the patient prefers to eat alcohol further, then it threatens the transition of fatty dystrophy into cirrhosis.

In patients with diabetes mellitus, fatty dystrophy is developing in 70% of cases. This is influenced by such factors:

age - more often occurs in the elderly; 2 type of diabetes is associated with obesity or violation of lipid metabolism; the severity of ketoacidosis.

As a result, the lack of insulin and glucose intake into the cells, lipolysis is activated - the metabolism of fats, aimed at thicing the energy hunger. The concentration of fatty acids in the blood increases, the liver is trying to recycle them into lipoproteins. The excess goes to triglyceride residence. But too much is delayed in hepatocytes, causing fatty hepatosis.

Liver fatty dystrophy is a reversible process. The main role here is the cessation of the influence of the provoking factor - the exclusion of alcohol, the normalization of food composition, reducing the number of fats, controlled by diabetes.

Fatty dystrophy pregnant women

Separately, it is worth considering the development of acute fat hepatosis against the background of pregnancy. It is a difficult condition that is often the cause of the death of a mother or fetus. The causes of the emergence are unknown. Inappropriate the effect of heredity, the genetically determined defect of the enzyme system of mitochondria. This causes a disruption of oxidation of fatty acids.

Symptoms of pathology are diverse. Some jaundice may not appear. But more often there is a classical current: weakness, lethargy, nausea, heartburn. Gradually increases jaundice, its significant severity is dangerous for mother and fetus. Against the background of the heartburn, the ulcers of the esophagus are formed, it is possible to vomiting the "coffee grounding" with the esophageal bleeding. The liver failure is developing with the picture of the cloud of consciousness. Often it is accompanied by a disseminated intravascular blood coagulation syndrome, which becomes the cause of death.

Suspicion of the development of acute fat hepatosis in 3 trimester pregnancy is an indication for emergency delivery to preserve the life of a mother and child.

Carbohydrate dystrophy

It is manifested by a disorder of the structure or deposition of forms of carbohydrates in atypical places. Often this is subject to a basin form - glycogen. In diabetes and glycogenases, such processes become possible.

In diabetics, the glycogen content in the cells is significantly reduced, but it accumulates in the nuclei, which they acquire the "empty" species, is debugged along the vessels, nerves, which damages them and leads to the development of diabetic angiopathy.

If the amount of glycogen in the tissues increases, this condition is called glycogenosis. This is observed with anemia, leukose, in places of inflammation. It accumulates in muscles, heart, kidneys, vessel walls. Clinically can manifest itself with heart or respiratory failure.

Symptoms

The main disease that caused dystrophy will give symptoms. Acute processes are accompanied by weakness, malaise, decrease in performance. Stretching the liver capsule or gallbladder disease will be accompanied by painful syndrome. Often it is a stupid pain under the ribs on the right. Sometimes she gives back to the area of \u200b\u200bthe right kidney, in the neck, shovel, shoulder on the right.

Patients bother dyspeptic phenomena - nausea, heartburn, may be vomiting. The chair is disturbed, there are periods of constipation and diarrhea, often accompanied by a bloating, meteorism.

The symptom of jaundice can manifest itself in a few hours or days, as a manifestation of the violation of the exchange of bilirubin. The first react to feces and urine. Feces are discolored, and urine becomes beer color. In parallel, the skin itching is irritating the skin receptors with circulating bile acids.

With far-fledged dystrophic processes, there are signs of disruption of protein metabolism. Immunity decreases, infectious diseases occur more often. The lack of synthesis of protein coagulation factors is manifested by the bleeding of gums, hemorrhages in the skin, hemorrhoidal, gastrointestinal, uterine bleeding.

Protein failure leads to insufficient water binding, which is manifested by multiple edema, the development of ascites.

The extreme degree of liver failure is hepatic encephalopathy. This is a syndrome that develops as a result of a metabolic disorder and is manifested by a change in consciousness, behavior, neuromuscular reactions. It can develop acute for 7 days, or longer, for 3 months.

The severity of violations depends on the rate of development and the reasons that caused this state. Personality disorders are observed, memory disorders and reduction of intelligence.

Encephalopathy flows into three stages:

Small personality changes, complaints about sleeping, decline in attention and memory. Exhaled personality violations, often inadequate behavior, mood swings, drowsiness, monotonous speech. Violation of the orientation orientation, copor, mood swings, aggression, delusional states, pathological reflexes. Entertainment Coma is a deep oppression of consciousness, a decrease in tendon reflexes, the appearance of pathological.

In addition to neurological signs, there are other clinical symptoms - jaundice, hepatic smell, fever, tachycardia. In case of extensive necrosis, infection can join. Death often comes from brain edema, renal failure, pulmonary edema, infectious-toxic or hypovolemic shock.

Diagnostics

The survey begins with the collection of abstract data:

patient complaints; the time of signs of signs of the disease; their development in time; communication with various factors - the use of alcohol, nutrition, physical exertion; indication of sex unprotected contacts, injections, visiting the dentist, tattoos, blood transfusion over the past 6 months; the presence of diseases gastrointestinal Intestinal tract, liver, diabetes, pregnancy.

With a general inspection, excessive weight, skin color, comb, hemorrhage in the skin, rash, pigmentation, swelling of the limbs or the accumulation of fluid in the abdominal cavity are detected.

The liver dystrophy is a morphological characteristic of the processes that are caused by the influence of various pathogenic factors. Therefore, the diagnosis is aimed at establishing a disease that led to the development of the organ dystrophy. This uses laboratory diagnostics methods. Common blood test reflects the presence of inflammation in the body. Biochemical blood test allows to judge the state of synthetic liver function, presence of cytolytic reactions, cell damage.

A study of markers of viral hepatitis, which also become the cause of liver dystrophy.

The next stage is to conduct an ultrasound. The method is non-invasive and allows you to identify diffuse or focal changes in the tissue. By the nature of the ultrasound image, you can assume fat infiltration of the liver, the development of fibrosis or cirrhosis. The ultrasound is well noticeable by volumetric, cavities, cysts, occasions, distinguishes the signs of portal hypertension.

The use of radiological methods allows you to determine the presence of changes in the liver, increasing its size. Contrasting the biliary tract or vessels shows their condition, apologies, presence of essences, obstacles to bile outflow. Methods such as CT and MRI are also used. There are no specific features indicating the development of dystrophy. This can be guessed by finding changes in the parenchyma characteristic of various diseases.

The morphological picture can only be installed using biopsy. But this is a traumatic method that can lead to severe complications. Therefore, it is used only by testimony:

clarification of the etiology of liver disease; chronic viral hepatitis; accumulation disease (hemochromatosis, Wilson syndrome); biliary cirrhosis to establish the degree of inflammatory reaction and fibrous changes; carcinoma; control effect from the treatment of listed diseases.

There are conditions in which this method is absolutely contraindicated:

heavy condition of the patient; menstrual bleeding in women; signs of blood clotting disorders; reduction of platelet levels; mechanical jaundice.

For the diagnosis of fatty dystrophy, use the method is inappropriate. This form has the ability to regress under the influence of the treatment and observance of the diet. Therefore, the data received from the study, in 2-3 weeks will be irrelevant.

Treatment

To effectively cope with the disease, therapy should be held at the following steps:

rational nutrition; treatment of related pathology; liver restoration; consolidation of results.

Conservative therapy

Treatment of concomitant diseases is adequate therapy of diabetes, appointed by an endocrinologist. Diseases of the gastrointestinal tract are treated by a gatroenterologist or precinct therapist. For the treatment of alcohol addiction, if a person is not able to cope with the alcohol, attract a narcologist.

For treatment, preparations of various groups are used:

Hepatoprotectors. Antioxidants.statin.

Hepatoprotectors can have different effects. They stabilize cell membranes, restore their integrity, improve the synthetic abilities of cells. Contribute to improving the metabolism of bilirubin, fatty acids, proteins. Representatives of the Group are Carsil, Liv-52, Hofitol, Essential, Ursodeoxycholic acid and medicines based on it.

Alcohol choleretic preparations are also used, Hollsas. They improve the synthesis of bile, its release, regulate the composition, reduce stagnant phenomena in the liver.

Statins are used to correct blood lipid profile. They reduce the absorption of fats in the intestine, remove excess cholesterol, not allowing him to get back into the blood.

Treatment of severe dystrophy, accompanied by hepatic encephalopathy, proceeds in the separation of intensive therapy. Treatment is symptomatic. The patient is transferred to parenteral nutrition and the introduction of the liquid, limit the amount of protein. Preparations are used to correct the acid-base state, and often as a state develops acidosis, so it is necessary to introduce sodium bicarbonate. Assign antibiotics to suppress the intestinal flora.

Sometimes there is a need for extracorporeal detoxification, especially after the attachment of renal failure. Glucocorticoids are used to maintain overall metabolicism in large doses. This state often ends with a fatal outcome.

Treatment by folk methods

As auxiliary treatment methods after consultation with the doctor, you can use phytotherapy and traditional medicine. They offer various recipes to get rid of dystrophy.

You can use 2 tablespoons of lemon juice daily, mixed with the same amount of water.

During the month, drink 2 glasses per day of infusion, cooked from fruits of fruits, dandelion root, nettle, birch leaves. This mixture is poured with a glass of boiling water and insist 15 minutes.

If we cut the top with ripe pumpkin, and the seeds are removed, then the container will be able to pour fresh honey and put on a subtyrer into a dark cool place. After that, the resulting therapeutic composition merge into the jar and consume before eating on one spoon.

On an empty stomach for a month they drink a mixture of freshly squeezed carrot juice and warm milk in an equal ratio.

Seeds of milk thistle to chop up the state of the powder. 3 spoons brew 0.5 liters of water, respect half. Drinking on a tablespoon an hour before meals 1 month.

Effectively helps the decoction of dried pears and oat groats. On a glass of fruits take 4 spoons of oatmeal, boil in a liter of water. Eat the whole portion during the day.

St. John's wort, Horseta, Rosehip Fruits, Entrunner shoots Mix in equal parts. Cutlery spoon mix on a glass of water to boil. Drink the resulting decoction during the day, dividing on 4 receptions.

A tablespoon of petals from rosehip flowers mix with half a spoon of honey. Eat such a mixture after eating, drinking tea.

Diet

The treatment of the liver does not imply a rigid diet as weight loss. Hunger will appline even greater harm. Power must be balanced in lipid-protein composition. Limited to the content of fats due to animal origin - butter, cheeses, fat, fatty meat. This will reduce saturation of food with fats, reduce their suction, and therefore the negative impact on the liver.

The amount of protein on the contrary should be increased due to animal products. It is their proteins that have a full-fledged composition on amino acids, contain an indispensable group. The protein is needed for synthetic liver processes - the construction of its own enzymes, the formation of fats of lipoproteins, the development of various human body proteins - the immune system, blood coagulation.

The amount of carbohydrates is the greatest, they are an energy substrate. But it must be remembered that preference is given to vegetable carbohydrates, fiber, food fibers. Simple sugars contained in sweets, baking, quickly recycled, significantly raise the level of glucose, which will complicate the position of the patient.

Alcohol is absolutely prohibited, it is one of the reasons for the development of dystrophy, so it needs to be excluded first.

The diet can be described as milky-vegetable with the addition of low-fat meat and fish. Vegetables and fruits can be used in any form. The exceptions are sorrel, legumes, mushrooms.

The amount of salt is reduced to 15 g per day. In order not to make a mistake, food is cooked without salt, they are hung in its plate.

If the cause of dystrophy is diabetes, nutrition should be built on the bread units. It calculates the amount of carbohydrates needed for a person for a day. They are distributed on food intakes and then on special tables are set as far as you can eat one or another product. This system helps to control the level of glucose in diabetics, reduces weight. It can also be used to power people with overweight. Excess weight will smoothly leave.

If the liver dystrophy reached the heavy state of hepatic encephalopathy, then the power is built differently. The amount of protein is limited to 50 g per day. It is necessary that the liver can cope with the detoxification of protein metabolism products. With a worsening of the state, it is generally canceled, parenteral nutrition begin.

Prevention and forecast

Prevention is aimed at eliminating the risk factors and diseases that lead to the development of dystrophic processes. Excess weight must be controlled, try to reduce it to acceptable numbers. To do this, first it is necessary to determine the body mass index. If it is above 25, then it's time to think about a decrease in weight.

Even if the weight is normal, but in the diet, food is prevailing rich in fats, it is worth trying to reduce their quantity, it will reduce the load on enzyme liver systems.

Fasting and hard diet will not be beneficial. Protein failure will cause the exhaustion and development of fatty dystrophy, because There will be no substrate for the synthesis of protein-fat molecules.

Alcohol even with a small but regular use has a toxic influence on liver cells, damages them and causes pathological mechanisms for the synthesis of not typical hyaline protein or fat deposition. A complete refusal to eat alcohol in the early stages of fatty dystrophy is capable of improving the condition of the patient. With a developing cirrhosis, this will hold back the offensive of hepatic encephalopathy and the terminal stage.

Viral liver damage can be avoided if you remember about the transmission paths. For the prevention of hepatitis, it is necessary to observe personal hygiene, wash your hands, fruit, do not use drinking water from open sources. Viruses of types B and C are indulge in blood, so when performing invasive procedures to use one-time tools, use only a personal set for manicure, not to enter into unprotected sexual bonds, and after transfusion of blood after 6 months to examine on hepatitis.

Women during pregnancy planning should be minimized by the manifestation of the existing chronic diseases of the gastrointestinal tract, the pathology of biliary tract. During pregnancy, the risk of developing gestational diabetes is created as a result of hormonal perestroika, can manifest the fatty hepatosis as a hidden hereditary violation of the metabolism of estrogen. Therefore, adherence to the diet with a low content of fat and simple carbohydrates will be preventing the violation of the liver.

Any diseases of the gastrointestinal tract must be diagnosed in a timely manner and treated.

Many people, encountered with the diagnosis of "liver dystrophy", fall into panic. Meanwhile, no case should be afraid, but, on the contrary, it is necessary to mobilize and make every effort to preserve your health and life. Indeed, the liver dystrophy is a very dangerous disease, so try to abide by all the appointments that the attending physician prescribes and will be healthy.

In the classical understanding of the liver dystrophy - this is a disease accompanied by a comatose state associated with a violation of the work of the main filtering organ of the person - the liver. The hepatic coma leads a wide variety of reasons, however, in most cases this phenomenon arises due to the necrosis of body tissues and substituting them with others, unable to function properly. However, there are several forms of the disease in which degradation occurs gradually at the cellular level.

Code of the ICD-10

International Classification of Diseases (ICD-10) is a large reference book that lists the most famous diseases to date. It is intended to simplify the procedure for transferring the patient from one hospital to another. At the same time, the patient does not need to re-undergo all surveys and pass tests. Do it only if there is a suspicion that the previously proved diagnosis is incorrect.

In the classification of the ICD-10, the liver dystrophy is described in Chapter K76 "The fat degeneration of liver, not classified in other categories", which, in turn, is also an integral part of the K70-K77 "liver disease" section. The largest subsection, which includes all the others, is called "diseases of the digestive system" and is denoted by the code K00-K93.

The reasons

The main cause of the liver dystrophy is to reduce the reaction of its cells on the effect of insulin - hormone, responsible for transporting glucose into the cells of our organism. The result of this glucose deficiency in hepatocytes (liver cells) becomes the result. Further development of events to predict is not difficult: experiencing a constant disadvantage of the substance they need, liver cells die, replacing a fatty tissue after a while, which causes the dysfunction of the patient organ.

Why can this failure occur? The cause of the pathological reaction of hepatocytes can be:

• Genetic pathology;
• Violation of metabolic processes.
• If the immune system begins to exercise aggression to insulin, it can manifest itself in the form of immunity of hepatocytes to this hormone.

Other reasons causing liver dystrophy can be:

• Incorrect meals - the predominance in the daily diet of fats and carbohydrates;
• Abuse of alcoholic beverages and cigarettes;
• Lack of sufficient physical activity.

These, at first glance, minor factors - the overwhelming majority of us to a greater or lesser degree sin it - adversely affect the liver state, launching pathological processes. If you continue to pass a passive existence and ignore the first SOS signals that the liver applies to us, the changes occurring in it can become irreversible.

Symptoms

In the early stages of development, the signs of pathological changes in the liver are expressed so insignificant that they may not notice them at all either, noticing, not to correlate with the beginning of a serious illness. Due to the very slow development of the process, the body gets used to changes and patients at first are not experiencing any noticeable discomfort.

Over time, the liver dystrophy begins to remind himself:

Occasionally, the pathological process may be accompanied by yellowing (to a greater or lesser extent) of skin cover, mucous membranes and eye proteins, sharp pain in the abdomen, rapid slimming. At the same time, a person can pursue a strong itching - so pronounced that the patient combers herself to blood.

If there is a toxic dystrophy of the organ at which necrosis of parenchyma occurs, liver cells that are raised veins of spleen and lymphatic nodes, begin to share hard. A number of dystrophic and necrotic changes occur in the tissues of the pancreas and the heart muscle, multiple bleeding occurs, affecting both internal and serous shells and skin covers. The chronic form of toxic liver dystrophy may lead to the development of large-sized cirrhosis and, due to the emergence of the patient due to the functional disorder of the patient or acute renal failure. To prolong your life at least for several years, you need to consult a doctor as soon as possible, go through a comprehensive treatment and start treatment.

Where does it hurt?

If someone complains of your pain in the liver or you yourself use a similar expression in private conversation, remember: it is impossible. The liver itself does not affect the organ itself there are no nerve endings. Significant painful sensations in the right half of the back, the epigastric area, under the blade or in the neck (also right), are not in the organ itself, but only in her shell, where the nerve endings are well developed.

If the liver is greatly increased (this may occur due to the inflammatory body of the inflammatory process), adjacent to the organs of pressure experiencing pressure, which can also cause pain in the right hypochondrium. In the early stages of the liver dystrophy, the patient has an unpleasant feeling in the right side, as if he interferes there, and sometimes reflexively trying to get rid of it, making characteristic television. At the very beginning of the disease, these sensations arise periodically, but over time they acquire the character of constant.

Paints may become stronger or almost to go. With intensive physical exertion and heavy sports workouts, pain in the right hypochondrium are intensified in the same way as the use of alcoholic beverages, reception of some drugs or too dense lunch.

If the pains on the right in the hypochondrium appear in the form of attacks or, in particular, they have become permanent, it is necessary to see the doctor as soon as possible: timely, the treatment will help prevent the transition of pathology into an irreversible process.

Forms

With toxic liver dystrophy, a necrotic process that destroys the normal structure of this organ is very rapidly developed. As a rule, doctors deal with the acute course of the disease, however, in some cases the process becomes chronic, as a result of which the liver gradually ceases to function normally.

Extensive necrosis can develop as a result of the impact on the body of patient of powerful toxins contained in some products - for example, mushrooms, - that is, the external factors affected its appearance.

Symptoms of toxic liver dystrophy may also appear due to internal factors - for example, toxicosis in women during pregnancy or excessive production hormones of the thyroid gland (hyperthyroidism). The liver dystrophy may appear against the background of the lightning form of hepatitis.

The characteristic signs of toxic liver dystrophy are:

• An increase in the sizes of the patient;
• Debrity or, on the contrary, excessive tissue density;
• Yellowish organic color.

If you do not start treatment in time, the size of the liver gradually decreases. Wrinkles are formed on the capsule shell. Iron itself from yellowish becomes gray and in appearance - like clay. The liver decrease continues for three weeks. By the end of this period, it acquires a shade, which can be characterized as a cross between gray and reddish.

Gradually takes place for the reticular stroma gland. Capillaries become well visible, which became wider because of overwhelming their blood. Hepatocytes are becoming less and less. They can be detected only in separate places. This pathological process is called red dystrophy.

The chronic form of hepatic dystrophy occurs quite rarely and in most cases ends with the death of the patient as a result of the rapid development of the dysfunction of the affected organ.

Acute liver dystrophy

As an independent pathology, the acute liver dystrophy is infrequent. As a rule, this complication of hard hepatitis A.

This pathology is not fully studied, therefore experts are still hampered with an exact answer, how its development occurs. In addition, it was still failed to find out which factors affect the development of the pathological process and how the hepatitis A. virus is associated with it.

Provoke the development of acute parenchymal hepatitis can:

• Syphilis;
• Brucellosis;
• Tick \u200b\u200breturn fever.

Much increases the possibility of developing complications in women during pregnancy or suffering an abortion - and in another case there is a weakening of the body's protective forces. All this negatively reflects in the state of hepatocytes and provokes the development of severe hepatic dystrophy.

The initial stage of acute liver dystrophy is very similar to the symptoms of hepatitis A. The patient's condition deteriorates sharply. A violation of brain activity develops due to the defeat of the nervous system. The patient becomes restless, ragged, he appears convulsions and severe vomiting. With such symptoms, it requires urgent treatment in the psychiatric department.

Worse, if instead of anxiety and excitement, the patient dwells in the opposite state: it becomes sluggish, apathetic, to all indifferent. Among other symptoms, the development of depression, constant drowsiness, reduction of life tone can be noted. Together with increasing symptom, the patient periodically fainting, during one of which he can go to the liver to whom.

Alcoholic liver dystrophy

The cause of the liver alcohol dystrophy is revealed in the title of this ailment: abuse of alcoholic beverages. Penetrating into the human body, ethanol destroys hepatocytes. If a person systematically uses alcohol (it is absolutely necessary to go into long-term ribs, there are enough two or three beer bottles every day), in ten years he is diagnosed with hepatic dystrophy. This may happen much earlier, if the acquaintance with alcohol occurred in adolescence, and a little later, if the elderly and earlier non-drinking man suddenly addicted to the alcohol.

The development of liver alcohol dystrophy is preceded by:

• Alcohol hepatitis;
• Hepatosis;
• Cirrhosis of the liver.

Hepatosis becomes the most common cause of dystrophic changes. The symptoms are expressed weakly and manifests itself in:

• A reddish shade of palms and stop;
• Contracts of fingers on hand;
• The increase in the salivary glands arranged near the oars.

Fortunately, in the early stages of the development of the disease, the process is reversible: enough for one or one and a half months to refrain from the use of alcoholic beverages, go to the diet and drink more water, as an improvement does not force yourself to wait. And with full failure to alcohol for a longer period, the patient iron is restored completely.

In more complex cases, it may be necessary in the reception of essential phospholipids and corticosteroid drugs. If the patient diagnosed the last stage of the disease, only liver transplantation can help.

Diffuse dystrophy of the liver

It is extremely dangerous to a condition that occurs with diffuse-dystrophic changes in the liver parenchyma. The reason for its appearance lies in the fact that hepatocytes cannot independently get rid of toxins entering the body. Liver cells, without cope with the load, begin to die. Instead, fibrous connecting tissue is formed. If the process does not stop on time, the disease will progress and, in the end, will lead to liver failure. This is the manifestation of diffuse dystrophy.

These changes may cause a similar phenomenon and in the pancreas. This is due to the fact that these two organs constantly interact with each other.

The main danger of focal liver dystrophy is that it is extremely difficult diagnosed in laboratory conditions. The most complete information can be obtained using computed tomography and magnetic resonance therapy, other methods are virtually useless.

The cause of focal liver dystrophy is excessive use of alcohol and alcohol-containing drinks. Signs of its manifestation:

• Reducing or complete absence of appetite;
• Dyspnea;
• In some cases, pain in the right hypochondrium.

Symptoms practically fade when the patient is immobile, and significantly enhanced while driving.

Bench grainy dystrophy

This pathology belongs to the most common types of protein liver dystrophy. In this case, colloidal properties of cell cytoplasm are broken, which leads to the appearance of grain-like protein.

The development of liver grainy dystrophy can be provoked:

• Defective feeding of a newborn;
• Poisoning drugs;
• Infection;
• Impaired blood and lymphorage;
• Oxygen starvation.

Grainy dystrophy develops gradually. In the late stages of the disease, pathological changes can begin. The change in the exchange of proteins, the cytoplasm is muttered and swells. The tissue of the bore-forming gland becomes flabby, swell. There is a lack of tide of blood.

When diagnosing, it should be borne in mind that the normal synthesis of proteins also has similarity with grainy signs.

Despite the reversibility of pathology, it can cause severe complications. So, in some patients, in the absence of proper treatment, intracellular hyaline, water dystrophy and necrosis were observed.

Stellic liver dystrophy

This form of hepatic dystrophy occurs due to the violation of protein metabolism. In itself, the disease cannot develop, however, may arise due to amyloidosis, as well as to paint from hyaline or liver dystrophy.

The amyloidosis is characterized by the fact that in the tissues of the liver, the protein-polysaccharide complex amyloid begins to be seen and postponed.

The hyaline is such a kind of protein dystrophy in which atherosclerosis develops. The disease is manifested in the formation of a vascular thrombus. In this case, protein deposits are formed, resembling the structure of cartilage.

With protein liver dystrophy, the organ structure becomes a grainy. This is due to the fact that in the protoplasm of cells, droplets or grainbursts are formed. However, unlike the grainy forms of dystrophy, they can be combined with each other, fill the space between the cells. The affected fabrics, as a rule, die away.

Hydropic liver dystrophy

With this form of the liver dystrophy in each cell, additional vacuoles filled with cytoplasm begin to form. As a result, the cells of the parenchyma organ increase in size. The affected surface is slightly wrinkled. As the disease progressing, the liver is increasingly filled with liquid and at a certain point can begin to decompose. The cell at the same time is a completely filled cavity in which the bubble-core is located.

Detect the disease, you can only exploring the liver particle under the microscope. All non-invasive examination techniques are not able to identify the disease.

Unfortunately, this form begins to manifest only when extensive cell necrosis begins. Treatment at this stage is not possible, only liver transplant can save the patient.

Yellow liver dystrophy

This form of hepatic dystrophy develops as a complication of pregnancy. There is diseases due to intoxication of the body, during the treatment of infection. Also, jaundice in pregnant women can cause a previously present liver dystrophy of any form or presence of concrections, as well as inflammation of the gallbladder.

For the yellow liver dystrophy, such symptoms are inherent:

• The skin and mucous membranes are yellow;
• Began abundant vomiting;
• Can periodically conscious consciousness;
• The body temperature increases (this phenomenon is often accompanied by nonsense and increased excitability);
• Hemorrhagic rash (subcutaneous diseases);
• Increases the volume of urine distinguished during the day.

During the examination in the urine of the patient, chyrosine and lecithin can identify. With external inspection, the reduction of hepatic stupidity can reveal. If within a few days not to start intensive treatment, the patient will die quickly.

Parenchimatous liver dystrophy

It looks like other forms of the disease and can combine their signs. Parenhim cells in this form begin to suffer the first, pouring into water. This can lead to various metabolic disorders and even to denaturation (destruction) of proteins.

The subspecies of parenchymal dystrophy are classified as follows:

• Hyalin-drip;
• Hydropic;
• Horny dystrophy.

The disease often passes into the granular shape of dystrophy.

Diagnostics

To identify the disease as such only during biopsy. All other examination techniques are ineffective. At the most important thing to find out during non-invasive checks, it is to know that the liver is increased in volume. The biopsy is resorted in the most extreme case, since for this checking it is necessary to make a patient incision under general anesthesia, introduce a special probe and pick up a piece of body tissues. In the future, the resulting micropreparation will be explored under a microscope, after which we can talk about the formulation of the final diagnosis.

What do you need to examine?

The sick body itself is subject to the survey. In addition, the patient gives some analyzes - urine and blood (and the last one is twice). Also, the patient must pass at least one non-invasive examination (for example, an ultrasound). If, according to the results of the survey, a suspicion will arise that the patient is sick of dystrophy of the liver, it will be offered to go to a biopsy surgeon.

How to examine?

Independent diagnosis of the disease is not possible, as it does not have pronounced symptomatic signs.

Tests cannot exactly indicate, from which disease is the patient suffers, they only indicate the defeat of the organ.

Treatment

Conservative therapy

The prevention of the disease is to change the lifestyle and reception of drugs that help the liver cope with the disease.

Treatment by folk methods

The liver dystrophy is a too dangerous disease to treat it yourself. Any means acting on the liver can cause a serious damage to it. If the patient has a desire to resort to traditional medicine, he should be consulted with a specialist.

Who to contact?

If the liver dystrophy is suspected, the patient can refer to the therapist to get a prescription to the continuation of treatment. Further examination and treatment produces a gastroenterologist.

Medicine

Most often for rehabilitation after such a disease and for the prevention of its occurrence, the Preparation of Lesfal is prescribed. This drug is a universal means that stimulates the rapid update of hepatic tissues.

A medicine in Ukraine is produced, in the Kiev region, however, it can be purchased in Russia and in Belarus.

The cost of the drug in Moscow is about 300 rubles.

Prevention

In order for the liver to a deep old age please you with a lack of reminders of yourself, fulfilling its functions, you need quite a bit:

Follow your weight and try to hold it within the norm;

Refrain from daily use of buns and buns, fatty fried meat, smoked sausages, canned food and fast food;

Do not assign medicines to yourself - if constant headaches are tormented, the joints do not go to the lower back, this is a respectful reason to consult a doctor, and not to buy half the pharmacy in the hope that "at least something will help";

Do not keep emotions in yourself - they say long suppressed anger, offense or anger beat on the liver. Apparently, without missed, since all these feelings in the literal sense of the word were written in a patient on his face, while he himself is invariably restrained and correct. Allow yourself from time to time to send the offender to the verbal knockout - or just do in boxing;

Play sports - for example, swimming or sports walking;

Resting actively - to spend the weekend lying on the sofa, attaching a favorite laptop on the stomach, perhaps, but completely unpleasant. Going out the whole family in the zoo, local history museum or to the exhibition of cats, build a dog for a dog or an aviary for the bats ... Are you alone? Make a list of Challenge and once a week, follow one point from the planned plan. So you will see, soon your life will play with new paints!

Forecast

Provided that the liver dystrophy does not accompany other diseases, the forecast is usually quite favorable. If there is a complication, as a result of which the resistance of pathogenic bacteria weakens, the latter, freely falling into the body, are applied to the already small forces of the patient. It is much heavier coming out of anesthesia, it does not tolerate surgery, the recovery period after which is significantly lengthened.

Cardinal lifestyle change, full of alcohol, strict adherence to the diet and adherence to all prescriptions of the attending physician are able to save not only health, but also the life of a person with liver dystrophy. On the contrary, continuing to lead a passive lifestyle, neglecting treatment, the patient risks "earn" steatohepatitis, or even cirrhosis of the liver.

Diet with disease

In the liver dystrophy, a significant role is given to the correct nutrition. In the daily diet should be present products containing the optimal quantity:

• Vitamins;
• Proteins;
• Fiber;
• Pectinov.

But with fats you need to be careful - the less they will be in the menu, the better.

With liver dystrophy, it is necessary:

• Exclude alcoholic beverages;
• Strictly monitor the amount of fats - they should be no more than 20% of daily food;
• Reduce the use of protein food - its number should not exceed 100-150 grams per day;
• Feed fractionally and drink at least 2 liters of non-carbonated water per day;
• Avoid using artificial food additives and other harmful substances.

As the basis of the daily menu, you can take the dietary table N5.

Do not forget about annual preventive medical examinations. The earlier the initial signs of the liver dystrophy will be revealed, the easier it is to heal.

At the same time, sinusoids are chosen by blood circulation in them; The death of individual hepatic cells is possible. The disease leads to the formation of the so-called star portal liver fibrosis.

Causes of liver dystrophy

Various reasons can be caused to fatty dystrophy of the liver: alcohol abuse, improper and defective nutrition and especially protein fasting; Endocrine disorders (lesions of the diancefral-pituitary system, pancreas islet), long-term infections (tuberculosis) and intoxication (phosphorus, chloroform, carbon tetrachloride, etc.), treatment with corticosteroids and antibiotics.

Symptoms and signs of liver dystrophy

At an early stage, the disease proceeds asymptomatic; Hepatomegaly is possible without noticeable functional deviations. The healthy liver is smooth and soft. In this even reversible period, the elimination of the cause leads to the normalization of the liver size. When progressing the disease, the liver becomes sensitive, dense. The high level of choline in the blood serum is determined, the activity of acetylcholineserase increases. The content of common serum fats is more frequently increased, and the first stage of the polarographic wave detects a tendency to rise. Emphasize increased sensitivity and liver vulnerability at fatty dystrophy, reduction of glycogen content in it.

In the terminal period of the disease, severe complications are possible: fat embolism, vessel thrombosis, hemorrhagic diathesis, hepatic coma. Convincing data indicating that stenosis can lead to a liver cirrhosis in a person, no.

Diagnosis. In cases of detection of an increased liver of soft consistency, in cases of discovery of an increased liver of a soft consistency, in the absence of noticeable functional disorders, especially when it concerns alcoholics, diabetes patients, ulcerative colitis, tuberculosis, or by alimentary disorders, etc. On the pathology of fat metabolism and the presence of fat The rebirth of the liver indicate a high level of choline in the serum, increased activity of acetylcholineserase, high content of common fats and an increased first stage of the polarographic wave. A reliable diagnosis can be supplied by a histological study of biopsy material from the liver.

Fat liver dystrophy is differentiated from the omission of the liver, chronic hepatitis and compensated inactive cirrhosis.

Treatment of fatty liver dystrophy

First of all, the reason for the obesity of the liver should be eliminated. The diet should be rich in animal proteins, vitamins, lipotropic substances with a limited amount of fats. Vitamin B6 can be prescribed due to the determinant dapotropic effect, as well as choline chloride, lipocaine, folic acid, empirically methionine and choline (the use of the latter in the clinic brought disappointment).

Non alcoholic etiology liver dystroy

Non alcoholic etiology liver dystrophy is called liver damage to various gravity, according to histological signs, resembling alcohol liver damage, but arising from those who do not abuse alcohol. It includes actually fatty dystrophy of the liver, damage to hepatocytes, necrosis and fibrosis; Cirrhosis of the liver with portal hypertension and other complications, including sepiecotted cancer. Lifespan with liver dystrophy lower than among the population as a whole.

In practice, the diagnosis of fatty dystrophy of non-alcohol etiology is put by an exception. It should be suspected of a patient with chronic liver damage, which does not abuse alcohol, with negative results of serological studies on viral hepatitis and the absence of innate or acquired liver diseases.

Related diseases and conditions

Non alcoholic etiology liver dystrophy is often found with type 2 diabetes, obesity and dlypoprotehememia, which, in turn, are closely related to the presence of metabolic syndrome.

Obesity. It is obesity that most often accompanies fatty dystrophy of the liver, not related to alcohol consumption. The presence of obesity is observed in 40-100% of cases of liver dystrophy with signs of hepatitis, and the liver fatty dystrophy with signs of hepatitis is detected in 9-36% of persons with obesity. In addition, the type of obesity is important.

Hyperlipoprotehemia (Hypertriglyceridemia, hypercholesterolemia or both) is detected in 20-80% of the liver dystrophy with signs of hepatitis.

As a rule, with adipose liver dystrophy with signs of hepatitis There are several risk factors at once.

In addition, risk factors Falls are feminine, fast weight loss, acute fasting, diverticulosis of the small intestine.

To the hereditary diseases in which the liver fatty dystrophy developsThese are Vilson's disease, homocystinuria, tyrosinemia, abetalipoprotehemia and hyoffetalipo-proteiding, as well as spontaneous Plnakelite Weber-Chrischene.

To liver dystrophy (especially with signs of hepatitis) can lead surgical interventions, for example, gastroplastoplasty, eynodileoanastomosis, biliopanecatic shunting.

Drugs and other substances. Fat liver dystrophy can cause a number of drugs and other chemical compounds. Among glucocorticoids, amiodarons, synthetic estrogens, tamoxifen, diethiphene (used in the past cardiovascular preparation), isoniazide, methotrexate, perghexylin, tetracycline, puromycin, bleomycin, dichloroethylene, etionine, hydrazine, hypoglycine, asparaginase, azacitidine, azauridine, azasherin . Permanent contact with petroleum products in production is also a risk of fatty liver dystrophy.

Symptoms and signs of dystrophy liver of non-alcoholic etiology

Symptoms. Most often, the fatty liver dystrophy flows asymptomatic; Sometimes patients complain of weakness, malaise, a non-timber pain.

Physical research. Almost three-quarters of patients are hepatomegaly, a quarter is splenomegaly.

Laboratory research. In the absence of signs of hepatitis, laboratory tests are uninformative. If they are presented, the basic change in the biochemical indicators of the liver function is to increase the activity of alosy and asat. Usually, these deviations are found at the next medical examination or when accessing a doctor on another occasion. There is no clear relationship between the activity of enzymes, on the one hand, and histological indicators and the severity of inflammation or fibrosis, on the other. Alat's activity is often higher than the activity of asat, which distinguishes fat liver dystrophy non-alcoholic etiology from liver damage during alcoholism when the ASAT activity is higher than the Alat, and the activity of the CFF can be somewhat raised; Bilirubin and albumin serum levels are usually normal. PV elongation indicates decompensated hepatic failure. In individual patients, a low titer of antinuclear antibodies is determined. However, antimitochondrial antibodies, antibodies to the hepatitis C and HBSAG blood virus in the blood, and serum levels of ceruloplasmin and α 1 -anttripsin do not go beyond the norm. Often there is an elevated serum ferritin level and increasing the saturation of transferin. In men, the excess iron in the body is expressed more than in women. In a third of the patients with adhesiveness of the liver with signs of hepatitis, homozygous or heterozygous mutation is detected in the HFE gene, leading to the replacement of cysteine \u200b\u200bin 282 positions on tyrosine (genetic hemochromatosis marker). Liver fibrosis in the presence of this mutation is usually stronger than.

Instrumental research. Various non-invasive methods of radiation diagnostics, including abdominal ultrasound, CT and MRI, apply to the diagnosis of liver dystrophy. None of them has sufficient sensitivity to identify inflammation and fibrosis of the liver. With CT and MRI, it is possible to detect only the extrahepatic manifestations of cirrhosis and portal hypertension. Thus, these methods lack no sensitivity or specificity to diagnose lively fatty dystrophy with signs of hepatitis and determine its severity.

Biopsy liver - A method that allows you to confirm the diagnosis of liver dystrophy, with signs of hepatitis or without them, evaluate the activity of hepatitis and the degree of fibrosis. It is still unclear whether the biopsy spend to all patients, since the results do not always affect the treatment. The biopsy is shown in the presence of patients with metabolic syndrome and with constantly increased, despite the proper treatment, activity of hepatic enzymes.

Histological picture With adhesive dystrophy of alcoholic and non-alcohol etiology is the same. Histologically distinguished 3 stages of liver dystrophy. The first stage is the fatty infiltration of hepatocytes without their inflammation and destruction. At the same time, in hepatocytes, fat accumulates fat. The second stage is fatty infiltration of hepatocytes with signs of necrosis and inflammation. The fatty dystrophy may be diffuse, and can be focused in the central zones of hepatic lobes. There is always inflammation of parenchyma to one degree or another; The cell infiltration consists of neutrophils, macrophages and lymphocytes. The necrosis of hepatocytes with sections of the emptying of parenchyma are possible; Mellary and Coonwoman can be found.

In 15-65% of patients, iron deposits in hepatocytes are detected. With adipose dystrophy with signs of hepatitis in 35-85% of cases, fibrosis is found around individual hepatocytes, around sinusoids and portal paths. The degree of fibrosis can vary greatly: from light fibrosis around small veins and cell groups to severe, extensive fibrosis. In 7-16% of patients with fatty dystrophy of the liver with signs of hepatitis at the first biopsy, cirrhosis of the liver is detected; Histologically, it is indistinguishable from the portal cirrhosis.

Causes of liver dystrophy of non-alcoholic etiology

The pathogenesis of fatty dystrophy of the liver of non-alcohol etiology is complicated; Apparently, not only liver, but also fat, muscular and other fabrics participate in it. The leading role in the pathogenesis of the disease is played by fatty tissue and insulin resistance. It is known that fats are poisoned in the fatty tissue of internal organs. With excess caloric content of food, the process of normal fats is violated, which affects the speed of both lipogenesis and lipolysis and leads to an increased flow from adipose tissue into the blood of free fatty acids. This, in turn, contributes to the accumulation of fats in the liver and transverse muscles. At the same time, cytokines are released, which disrupts the intracellular transmission of the signal when binding insulin with receptors and reduces the enhanced insuline glucose intake into the muscles. At the same time, disposal is suppressed and glucose products in the liver is stimulated. In addition, the availability of fatty acids in the liver stimulates their esterification and lipogenesis de Novo. At the same time, the level of apoprotein in 100 liters of LPONP increases. All this, combined, leads to the accumulation and oxidation of fats in the liver, stimulates its bode radical oxidation, the release of inflammatory cytokines and the activation of the ITO cells.

In general, although the specific mechanisms for the development of inflammation and necrosis of hepatocytes at fatty liver dystrophy are not quite understandable, at the base, most likely two processes lie at once: liver fluid infiltration, on the one hand, and free radical oxidation and release of pro-inflammatory cytokines that cause progressive defeat liver, - on the other. More and more data in favor of the fact that the second mechanism of the pathogenesis of fatty liver dystrophy is mediated by adipocities released from adipose tissue.

Adiponectin - Adipocin, which has anti-inflammatory properties. The network is a reliable connection between the low level of adiponectin and an increase in the amount of fatty fiber of internal organs, hyperlipoprotehemia and insulin resistance. Another adipocin, leptin, on the contrary, has a pro-inflammatory action. It promotes liver fibrosis, increasing the expression of a transforming factor of beta growth and stimulating the activation of the ITO cells. The pro-inflammatory cytokines produced by the fatty fiber of internal organs also includes FULL NAME and IL-6. They play a leading role in the development of insulin resistance, since the transmission of the intracellular signal is disturbed when binding insulin with receptors and contribute to inflammation. In addition, they have a negative impact on the immune system.

The course and forecast of the liver dystrophy of non-alcoholic etiology

The course of the disease depends on the histological picture. If there is no inflammation and destruction of hepatocytes, the disease usually does not progress, but if there are signs of hepatitis about 20% of patients with time, cirrhosis develops over time. If there are signs of hepatitis fatty dystrophy of the liver in most cases is considered a stable state, but in a number of patients it progresses and leads to severe liver cirrhosis. The risk factors are elderly age, the presence of metabolic syndrome, obesity, diabetes, a higher activity of asat than Alat.

Treatment of dystrophy liver of non-alcoholic etiology

The treatment of fatty dystrophy of the liver of non-alcohol etiology is not today; Available methods are aimed at eliminating the factors associated with the development of the disease. Patients are recommended to lose weight and refrain from alcohol, adjust hyperglycemia and hyperlipoprotehemia, cancel hepatotoxic drugs (glucocorticoids, estrogens, amiodar, perghexylin). With severe obesity, its surgical treatment is shown. In a number of small short-term studies of ursodeoxycholic acid, vitamin E, hemfibrosyl, betaine (choline metabolite), acetylcysteine \u200b\u200band metformin improved the biochemical indicators of the liver function and reduced the severity of its fat infiltration, but did not have a noticeable influence on the activity of inflammation or the severity of fibrosis.

Tiazolidindion derivatives (pioglitazone and roseglitone) increase the sensitivity of fat and muscle tissue to insulin and improve glucose absorption by their cells.

The result of physiological adjustment is cholesterol formation, phospholipids needed to construct cell membranes, hormone formation, participation in biochemical reactions.

Describing what kind of liver dystrophy symptoms and treatment, which have specificity, we note violations of the process of natural utilization of lipid hepatocytes with high accumulation of fats (over 50%). Cytoplasm, vacuoles and some other intracellular organelles are saturated with fats, so they cannot perform functions. Physiologically concentration of fatty acids inside the hepatic cells does not exceed 5%. With adequate dystrophy, depending on the extent, this level is exceeded. The state is irreversible, since the lack of transforming lipids into energy or deposit of excess in the subcutaneous fatty tissue leads to the death and rebirth of the hepatic parenchyma. Morphologically, with this nosology, small clusters (fine-closed form) or large sediments appear inside the lysosomes (the total variety).

Causes and provoking factors for fatty dystrophy

The etiological and pathogenetic mechanisms of the disease are not installed, so it cannot be fully cured. Scientists have allocated provoking factors leading to lipid reincarnation:

• The abuse of alcohol in men violates the processes of fat intracellular metabolism. Blocking biochemical reactions leads to the difficulty of physiological disposal of compounds, and the excess cholesterol is accumulated in lysosomes;
• In diabetes, the mechanisms of the biochemical transformation of lipids are also violated. The cause of the state is absence of glucose necessary for metabolic reactions;
• Obesity leads to excess deposits in the lipid depot of subcutaneous fatty tissue. Excessive accumulation leads to the absence of highlighting paths, therefore, intracellular infiltration occurs;
• Metabolic diseases (protein deficiency) violate transport processes between the liver and other tissues;
• Poisoning with hepatotoxic poisons, medicines.

The described provoking mechanisms are the result of practical observations, but scientific studies of the pathogenetic links of nosology have not been proven. The need for early treatment is due to the development of cirrhosis, when degeneration leads to the growing of coarse cryrrotic scars. The more degradation, the higher the degree of liver failure.

Basic symptoms of fatty dystrophy

Dystrophic syndrome with intrahepatic excess of fat inclusions against the background of ethyl alcohol use has several synonyms "hepatostatosis", "fatty liver", "steatohepatitis". Varieties reflect the diversity of pathogenetic process mechanisms. Long use of ethanol is accompanied by inflammation, common degenerative changes, blockade of metabolic reactions.

The pronounced fatty dystrophy symptoms that are traced clinically, has different morphological manifestations. In the study of the bioptate (tissue section) there are several morphological varieties of dystrophic changes.

With chronic viral and toxic hepatitis in hepatocytes, not only lipids are reduced, but also proteins. In a morphological study, hyaline and hydropic graininess are detected. The basis of its appearance is the destruction of the protein-lipid complex, which is part of the organhell.

Clinical symptoms of form are due to the main disease:

• Soreness of the right hypochondrium;
• The emergence of linear extensions of vessels on the stomach;
• Capillary asterisks (telegangectasy) throughout the body.

Grainy dystrophic changes appear on the background of oxidative phosphorylation, imbalance of water-salt metabolism. The condition is adaptive compensatoryly aimed at restoring intracellular disorders, occurring under the influence of viruses, bacteria, receiving hepatotoxic drugs.

A classic sign of parenchymal fatty dystrophy with a histochemical study is a single large vaccination filled with fat inclusions that repel the kernel to the periphery.

With a morphological examination, a yellowish, dull fabric is observed. When moving up 50% of cells in some hepatocytes, fine vacuoles of oval shape are traced. Gradually, the clusters merge, and the cells die. The formation of fat "cyst" leads to the formation of the following morphological conditions:

1. Segmental obesity Lipid deposits are localized along the peripheral, central divisions;
2. Disseminated hepatosis fat drops are in separate hepatic cells;
3. Diffuse obesity is characterized by the defeat of the whole slices, but the process is reversible.

In diabetes mellitus, the manifestations of hepatosis are not specific. Fat degeneration appears due to glycogen metabolism disorders. The absence of insulin leads to a significant reduction in the reserves of this substance. Compensatory hepatocytes increase in size due to glycogen deposit. In the bioptats of the fabric, empty kernels are observed, the number of vacuoles increases.

In diabetes, ten different types of glycogenesis are isolated, among which fatty dystrophy is not frequent option, but can be traced in patients with obesity. Histochemical study of cells shows the accumulation of specific eosinophilic granules.

The changes described determine the symptoms depending on the degree of liver failure. The absence of a clinic at the death of a small amount of cells is due to the high reducing functions of the hepatic tissue. Only with extensive lesion develops liver failure, leading to symptoms:

• The yellowing of the skin and the scool in the violation of biliary release;
• Encephalopathy in poisoning to toxins, ammonia;
• Skin rashes, itching is an increase in bilirubin concentration;
• Pain syndrome under the ribs on the right increase in the size of the liver, cirrhosis.

The extreme degree of insufficiency is the hepatic coma, the accumulation of fluid inside the abdomen (ascites). The absence of a detoxification function leads to a concomitant increase in the spleen, the development of renal failure. Any liver symptom is dangerous for life, if accompanied by the accumulation of toxins in the blood.

Treatment of dystrophic liver

Alcoholic steatosis doctors are considered as a dangerous state leading to death. Nonzology provokes hazardous complications at the average degree of rebirth (about 35% of the tissue).

The initial stages of the disease are stopped by the appointment of drugs and the cessation of alcohol consumption, heavy is characterized by high mortality. Approximately 5% of people per month in the diagnosis of cirrhosis.

Specific preparations do not exist, therefore, symptomatic therapy is carried out by essential phospholipids (essential), choleretic agents (ursodeoxycholic acid), admethionine, silibinin. The rationality of the appointment of other hepatoprotectors is low.

With alcohol hepatitis of viral or bacterial genesis, the effectiveness of treatment with hepatoprotective drugs is reduced. Steroid anti-inflammatory drugs are used to reduce progression. The most common representative of prednisolone.

The effectiveness of glucocorticoids at fatty dystrophy is not proven, but in practice, therapeutic action is observed if there are 3rd factors:

1. Increase portal pressure;
2. Lack of accumulation of nitrogen in the blood;
3. No gastric bleeding.

In practical literature, there are guidance on the need for proper nutrition that increases the survival rate of patients.

Principles of the treatment of lipid rebirth of hepatocytes

• Elimination of risk factors;
• Medical elimination of complications;
• Long use of hepatoprotectors.

The main risk factor is obesity. Scientific studies have proven that a decrease in body weight by 10% leads to a decrease in the concentration of cholestasis enzymes (Alat, ASAT).

European specialists indicate the need to gradually reduce body weight. Optimal balance Weekly elimination more than half a kilogram increases the risk of gallstone disease, so caution must be taken when the diet is observed.

Features of diet food:

• Calorie diet not more than 1,200 kcal per day;
• Restriction in food of saturated fatty acids;
• Carbohydrates are not more than 100 grams per day, but nutritionists can reduce this rate.

Daily physical exercises contribute to the better absorption of fats, accumulating oxygen inside the muscle fibers, which increases the flow rate of triglycerides.

In diabetes mellitus, insulin resistance is the cause of obesity. The factor contributes to the transformation of excess carbohydrates into fats. Correction of insulin-olelonce is achieved by pharmacological means of thiazolidindions, Biguenides.

The elimination of high triglyceride content is achieved by regular use of drugs containing unsaturated fatty acids. Ursodoxichetic acid agents are used ten years old and showed high efficiency. The mechanisms of therapeutic activity have not been proven, but the eliminating activity of the drug is revealed to eliminate stagnant changes in the bustling bubble and intrahepter ducts.

With severe liver failure, the protein content is limited in the diet. Daily content of no more than 50 grams. For the purification of the gastrointestinal tract, laxatives, cleansing enemas are prescribed daily. Dysbacteriosis is eliminated by the introduction of antibiotics through the probe (ampicillin, kanamycin, tetracycline).

Arginine in a dose of 50-75 grams per day is introduced for the neutralization of ammonia per day.

Psychomotor excitement is stopped by a haloperidol.

Therapy of steatohepatitis by folk remedies

Appoints plant decoctions doctor. Only a specialist will be able to correctly determine the type of therapy, a combination and dose of each means. If you reveal the pathology in a timely manner, in an early stage, the choleretic fees of the immortelle, a milk, rosehip, help.

Plant fees reduce the activity of the chronic process, but only with certain nosologies. The therapeutic effect of herbal decoctions and infusions when compared with medicines manifests itself later, therefore, a combination of drugs with plants is rational. With low activity of the process, you can use a pumpkin:

• Choose a ripe fruit, cut the top edge in a circle. Remove the central part, and add light honey to the resulting cavity. Close the fruit and store 2 weeks in a dark place. Drain the resulting solution in the jar. For treatment, take three times a day at 3 spoons of the drink in the morning, day and evening.

The second useful popular recipe for the elimination of hepatosis walnuts. For its cooking you need to grind nuts. Fall asleep them in a jar, add honey and alcohol in equal proportions. Insist medicine 1 month in a dark room. Use three times a day on a teaspoon.

The terminal is part of the popular hepatoprotectors of Carsil, Silibinin. Use the plant at home. The recipe is prepared by mixing dandelion, nettle, birch leaves and milk thistle. Pour 2 teaspoons of a mixture boiling water, insist 15 minutes. Eat daily for 2 glasses of medication.

Vegetable infusions and decoctions when compared with tablets have a soft, gradual effect. To improve efficiency, it is recommended to combine folk remedies with diets, exercise.

Features of diet with dystrophic damage to hepatocytes:

• Avoid sharp, spicy food;
• Refuse fat meat, fish, broths;
• Carefully choose products in the store. They should not contain dyes, stabilizers, flavors, anticipating additives;
• Do not take a lot of medicines without need;
• Useful porridge oatmeal, buckwheat.

European scientists point to the fat soluble effect of apricot bones. With steatohepatitis, eat 5 pieces (but no more). The central content of the fruit is saturated with vitamin B15 participating in the splitting of lipids.

vnormu.ru.

Why pathology develops

Most often, pathology is developing after 46-50 years.

The disturbed metabolism leads to the fact that the liver cannot allocate the desired amount of enzymes, for recycling.

As a result, they begin to accumulate in the cavity of the organ.

Such changes may occur when influencing the following factors:

1. Nutrition. Especially disadvantaged to liver sweets, semi-finished products and fast foods, preservatives, dyes and other toxins.
2. Long fasting or, on the contrary, permanent overeating. Hungry diets or improperly composed diet, vegetarianism - liver enemies. They lead to the obesity of the organ.
3. Hereditary factor. If there were relatives with liver diseases, then a person will develop dystrophic pathology in 89%.
4. The uncontrolled and long-term use of drug drugs.
5. Receiving an excessive amount of alcohol (liver alcohol fatty dystrophy).
6. Drug use.
7. Professional activities involving work at industrial enterprises where various types of chemicals produce.
8. Passive lifestyle.
9. Failure to work the hormonal system.
10. Low-formation affecting the pituitary.

The mechanism for the formation of fatty dystrophy is actually very simple. Fats come to the gastrointestinal tract (gastrointestinal tract) and amenable to the splitting process. If these components enroll in the liver a lot, and there are relaxing factors, the fats are exposed to synthesis and accumulate in liver cells. The same thing happens under the influence of carbohydrate substances that fall into the liver in large quantities.

Fat dystrophy can be classified as follows:

I View - fat inclusions are part of a single character, they are chaotic located in the liver. Clinical manifestations are missing.

II View - fat molecules are located tight. The person worsens well-being, there is pain in the field of liver.

III species - there is a local location of the fat capsules, they are located in certain areas of the organ. Symptomatics pronounced.

IV View - fat molecules are located almost throughout the liver or occupy one of the fractions. Symptomatomy - bright.

To classify another fatty dystrophy, depending on the stage:

I - in liver cells contain a small amount of fat molecules, but they do not affect the work of the organ, although the destructive mechanism is already running.

II - fat completely fills cells, they are destroyed, an inflammatory process can develop around each cell.

III - the processes are irreversible, necrosis develops, in most cases it is impossible to restore the liver functions at this stage.

How the disease is manifested

Signs of illness appear already in the second stage:

1. Drawing, still pain in the field of liver, which becomes stronger after the use of fatty foods, smoked, sharp dishes and alcoholic beverages. In this case, pain can be permanent or be periodically.
2. Bind in the mouth, belching with a bitter taste.
3. Nausea, ending almost always vomiting.
4. Flatulence.
5. Increase liver in size.
6. In the language there is a yellow raid, it is dense.
7. Diarrhea constipation constipation. Worried a permanent character.

Signs of the third stage of the defeat deliver very big discomfort and is expressed in:

• increased irritability;
• sleep violation;
• fatigue;
• worsening memory;
• tendency to depression;
• the accumulation of large quantities (up to 25 liters) of the free fluid (the stomach becomes very large);
• pain cannot be removed by analgesics;
• the jaggility of the skin;
• in rare cases, skin itching develops.

If the fatty dystrophy leads to necrosis of the liver tissues, such additional features and symptoms are observed:

• unpleasant smell of liver to bed and from the oral cavity;
• substantial increase in temperature;
• nose bleed;
• anorexia;
• violation of heart rhythms and respiratory gain.

It should be noted that as soon as the first symptoms appeared, immediately contact the hospital so that the doctor appoints a course of treatment. In no case cannot be treated for fatty dystrophy. This can lead to a fatal outcome. Another point - the disease develops rather quickly, so the treatment must be appointed in the shortest possible time.

Today, with timely handling of the hospital, treatment is effective, thanks to innovative techniques and new generation drugs.

It is not prohibited to apply folk treatment methods, but it is necessary to consult with the doctor before drinking brazers.

How is diagnostic examination and treatment

Diagnosis includes the following types of surveys:

• ultrasound procedure;
• cT scan;
• laparoscopic technique;
• biopsy to identify fat inclusions, their quantities, sizes and localization;
• blood tests.

When symptoms are studied, as well as on the basis of the diagnostic survey, treatment will be prescribed, the diagram of which will be developed in each individual case.

Treatment of fatty dystrophy is carried out in the complex. In this case, a prerequisite is a diet.

Only observing all the prescriptions of the doctors, you can get rid of fatty dystrophy. To treat dystrophy, doctors prescribe drugs to restore liver cells, funds normalizing metabolism, medication and vitamin complex to increase immunity. If an inflammatory drug is present, treatment provides for the reception of anti-inflammatory drugs.

Treatment with folk remedies

The treatment of liver dystrophy can be carried out pumpkin.

It is very rich in vitamins and minerals that help to restore cells in the shortest possible time and normalize exchange balance.

Cut the top of the pumpkin, clean from seeds, pour the cavity with honey and put in a cold place for 8-10 days. After that, honey merge into the container, and put in the refrigerator. Take 1 tbsp. l. 2 times a day. When allergic on beekeeping products, this method is prohibited.

Treat dystrophy is possible herbal harvest. In equal number, the following components are taken: a series, wormwood, sage, raspberry leaves, birch, chamomile, yarrow, linden. Ingredients crush and mix. Pour boiling water in a ratio of 1 part of the collection, 2 parts of the water. Insist 3 hours, strain and take during the day like tea.

You can treat dystrophy with the help of such a decoction: birch leaves, rosehip, hawthorn, red-faced rowan, spectal leaves, lingonberry, tolnaya, dandelion roots, Fennel fruits, St. John's wort. Components chop and pour water in a 1: 3 ratio. Boil on the steam bath mixture 20 min. Strain and drink like tea throughout the day.

Diet with liver dystrophy

The basic rules of the diet:

• increase the amount of food rich in protein (fermented milk products, meat of non-fat varieties);
• eliminate carbohydrates (white bread, sugar, rice, potatoes);
• reducing the number of animal fats (butter, oily fish and oil);
• be sure to include at least 2.5 liters of water per day;
• exclude alcohol;
• refuse fried, sharp, salted products.

How dystrophy will be treated directly on humans. If there is an extra weight, the person leads a sedentary lifestyle, one should completely get rid of such factors - to play sports, but without special physical exertion. On how to treat dystrophy with physical gymnastics can be obtained from a doctor.

The main tasks of dietary food during dystropy are the normalization of the basic functions of the organ and the resumption of cholesterol, fat metabolism; Stimulation of bile production.

The amount of fat consumed during the day should not exceed 50 g! This is a very important condition.

In addition, it is necessary to eliminate the products that are rich in cholesterol. In this case, it will be possible not only to help liver cells to recover, but also avoid thrombophlebitis.

Another important rule - dishes are better prepared for a couple or use in boiled, baked. In this case, they will not only be useful for the liver, but also retain all vitamins.

What is mandatory to include in the diet:

• soups on vegetable broth with croups, borsch;
• vegetables;
• vegetable salads;
• non-starny cheese, ham;
• boiled egg or steam oslet;
• oatmeal, buckwheat, semolina circuits;
• non-fat dairy products.

What to exclude:

• fatty products, mushroom broths and mushrooms;
• seafood;
• onions in fresh form, garlic, tomatoes, radish, legumes;

• pickles and marinades;
• dried products;
• preservation;
• coffee, cold or carbonated drinks.

It is very important not only to treat the disease, but also take all measures to prevent it.

Methods of prevention include: a healthy lifestyle, control of alcoholic beverages, improving immunity, care for health, sports. Only in this case will it be possible to prevent such a disease as the liver fatty dystrophy. It should be remembered that if you do not treat the disease, it will lead to a fatal outcome.

pechen1.ru.

What is liver dystrophy -

Dystrophy of the liver

What provokes / Causes liver dystrophy

Symptoms of liver dystrophy

Hyalin-drip dystrophy is characterized by a decrease in hepatocytes in sizes, homogeneous cytoplasm, intensely painted with acid dyes (such as Eosina), which served as the basis to name this type of acidophilic dystrophy. There is an increase in the number of chic-positive structures. This type of dystrophy is associated with violation of the permeability of cell membranes, loss of liquid and physicochemical changes in protein. As a result, protein substances become more dense and homogeneous. Hyalin dystrophy is observed in various pathogenic effects, especially viral etiology.

• disseminated obesity
• zonal obesity
• diffuse obesity

When painting hemotoxylin and eosin in hepatocyte kernels, optically empty vacuoles of round or incorrectly oval shape are visible, with a diameter of 4-8 microns, which are limited to a clear membrane, well perceiving the main dyes. Most often, the core hyaline occurs in diabetes mellitus, diseases of the gallbladder and pancreas. Sometimes excessive glycogen deposition is observed in the kernel - glycogenosis of hepatocyte nuclei. Due to the increase in sinusoid cells, significantly decrease. In preparations painted with hematoxylin and eosin or by the method of Van Gizon, "empty" cells resembling a picture of balloon dystrophy are also detected, but the size of hepatocytes during glycogenosis is much larger than with balloon dystrophy. In glycogenosis in the cytoplasm of cells, there is a sharply positive chic reaction, disappearing after processing control cuts with diastasses or amylase. The outcome of glycogenoses of III and IV types can be cirrhosis of the liver.

The deficiency of antitripsein often leads to the hepatocytes dystrophy, the antitripxin is synthesized in the liver. With its deficit, the lung emphysema is developing, and in 10% of patients - cirrhosis of the liver. The deposition of antitripxin is associated with the absence of sialic acids and the defect of sialotransferase involved in the functioning of the Golgji complex the most characteristic feature of the antitripsein deficiency is the deposition of round weakness-philic chic-positive granules resistant to diastasis in the cytoplasm of hepatocytes. The dimensions of the granules range from 1 to 40 microns. In the absence of cirrhosis, the granules are located mainly in the periportal hepatocytes, in the cirrotic liver - in hepatocytes adjacent to fibrous septam. The final diagnosis is possible only after the immunomorphological detection of antitripsein.

• Mesenchymal dystrophy

Diagnostics of liver dystrophy

medsait.ru.

What is liver dystrophy

Dystrophy of the liver - This is a comatose state that is associated with the deep oppression of the liver functionality. Koma hepatic arises due to acute or chronic liver diseases.

What provokes liver dystrophy

Hepatic cell coma, in most cases, is due to sharp viral hepatitis. Sometimes it arises due to poisoning with genototropic poisons (poisonous mushrooms, Toul Nitrates, etc.), sometimes - from the use of atofan, halotan, etc. A portional coma is a consequence of a liver cirrhosis, occurs after bleeding associated with infection. It happens that the portocawal coma occurs due to the irrational treatment with diuretics, as well as from the improper use of sedative and sleeping pills.

Symptoms of liver dystrophy

There are several varieties of dystrophy syndrome.

• Parenchimato protein dystrophy

Select grain, hydropic and hyalin protein dystrophy.

With a dystrophy of the hepatocyte cytoplasm, a rough protein grain appears. Liver cells increase in volume, look swearing, muddy (muddy swelling); The content of protein and water is increasing in their cytoplasm, which is in the form of grains, coagulites. With histochemical examination, there is a decrease in the intensity of the reaction to the general and main protein, ribonucleoprotein. Distrophy is based on the disintegration of the protein-lipid complex, which is part of the organizer membrane. With a sinth of dystrophy, the water-salt exchange, the intensity of redox processes, oxidative phosphorylation, is accumulated, and acid exchange is accumulated. The grainy dystrophy is compensatory and adaptive, as a rule, does not entail functional liver failure and is a reversible process. This is the most common type of hepatocyte damage at various pathogenic (viral, bacterial, toxic) effects (light shape of chronic hepatitis, inactive forms of cirrhosis, etc. .)

Hydropic dystrophy is characterized by light swelling of the cells (in contrast to muddy swelling at the grainy dystrophy). Hepatocytes are increased in the volume, their cytoplasm seems optically empty, the protein content, glycogen, oxidoretase activity, increased hydrolase activity. The most pronounced form of hydropic dystrophy is a balloon dystrophy, which at the height of the definiteness is irreversible, which indicates the transition of the process in the collevation necrosis. In this case, the cytoplasm is optically empty, does not give histochemical reactions. Hydropic dystrophy is found in patients with viral hepatitis (especially with severe and medium-free forms), with dystrophic form of cirrhosis, with long-term intra-and extrahepatic cholestasis, etc.

Hyalin-drip dystrophy is characterized by a decrease in hepatocytes in sizes, homogeneous cytoplasm, intensely painted with acid dyes (such as Eosina), which served as the basis to name this type of acidophilic dystrophy. There is an increase in the number of SIK-positive structures. This type of dystrophy is associated with violation of the permeability of cell membranes, loss of liquid and physicochemical changes in protein. As a result, protein substances become more dense and homogeneous. Hyalin dystrophy is observed in various pathogenic effects, especially viral etiology.

• Parenchimato fatty dystrophy

It is characterized by accumulating in the cytoplasm of hepatocytes of small drops of fat, then merging into a larger or one fat vacuol, which occupies the entire cytoplasm and displays the kernel on the periphery of the cell.

With pronounced obesity, the liver cloth on the cut dim, yellow. More than 50% of the liver parenchyma, more than 50% of the liver parenchyma, are talked about fatty hepatosis. When painting with hematoxylin and eosin in liver cells, light, unpainted vacuoles (drops) of round or oval molds can be merged and filling the entire cytoplasm of hepatocyte. With pronounced obesity, the hepatocytes overflowed with fat, and fat drops, merging with each other, form fat "cysts".

The following polymorphological forms of liver obesity are distinguished.

• disseminated obesityin which fat drops are contained in separate hepatocytes (observed primarily in physiological conditions)
• zonal obesitywhen the central, non-primary or peripheral zones of the hepatic lobby are exposed to obesity;
• diffuse obesity, i.e. obesity of the whole (or almost all) hepatic slices. The obesity of the liver is reversible. It can be large and fine-flowered:
  • Large (macroscopic) obesity is characterized by the presence of "empty" vacuoles in hepatocytes with nuclear displacement to the periphery.
  • In case of fine-closed obesity, the fat drops are small, while the kernels with distinct nucleists are located in the center, the necrosis of hepatic cells is expressed in varying degrees.

• Parenchimato carbohydrate dystrophy

In clinical practice, the leading importance is the violation of the metabolism of glycogen, which is more common in diabetes and glycogenases. In diabetes, glycogen stock in hepatic cells is significantly reduced, the content of which is reduced by 30-50 times. At the same time, the accumulation of glycogen in hepatocyte kernels is noted, which creates a picture of their peculiar vacuolasis ("empty" nuclei). The most pronounced violations of carbohydrate metabolism in the liver are occurring in glycogenoses - enzymes, due to the shortage of enzymes involved in glycogen splitting processes, currently has more than 10 types of glycogenosis. When glycogenoses, the glycogen content in the liver tissues increases sharply, hepatocytes are increased in size, it is very weakly colored by eosin, due to this, their cytoplasma looks "optically empty", a light, poorly perceive color, a hyperplazed smooth EPS, a few large lysosomes, cell membranes are clearly contoured.

When painting hemotoxylin and eosin in hepatocyte kernels, optically empty vacuoles of round or incorrectly oval shape are visible, with a diameter of 4-8 microns, which are limited to a clear membrane, well perceiving the main dyes. Most often, the core hyaline occurs in diabetes mellitus, diseases of the gallbladder and pancreas. Sometimes excessive glycogen deposition is observed in the kernel - glycogenosis of hepatocyte nuclei. Due to the increase in sinusoid cells, significantly decrease. In preparations painted with hematoxylin and eosin or by the method of Van Gizon, "empty" cells resembling a picture of balloon dystrophy are also detected, but the size of hepatocytes during glycogenosis is much larger than with balloon dystrophy. During glycogenosis in the cytoplasm of cells, a sharply positive SIC reaction is noted, disappearing after the processing of control cuts of diastasses or amylase. The outcome of glycogenoses of III and IV types can be cirrhosis of the liver.

With chronic lesions of the liver, there is a violation of the content of glycoproteins. In fucidososis in the liver tissue, there is a deposition of glycolipids containing MPS and fuchose.

The deficiency of antitripsein often leads to the hepatocytes dystrophy, the antitripxin is synthesized in the liver. With its deficit, the lung emphysema is developing, and in 10% of patients - cirrhosis of the liver. The deposition of antitripxin is associated with the absence of sialic acids and the defect of sialotransferase involved in the functioning of the Golgji complex the most characteristic feature of the antitripxin deficiency is the deposition of round weakness-philic sik-positive granules resistant to diastasis in the cytoplasm of hepatocytes. The dimensions of the granules range from 1 to 40 microns. In the absence of cirrhosis, the granules are located mainly in the periportal hepatocytes, in the cirrotic liver - in hepatocytes adjacent to fibrous septam. The final diagnosis is possible only after the immunomorphological detection of antitripsein.

• Mesenchymal dystrophy

These liver damage are found in primary and secondary amyloidosis. Clinical manifestations of liver amyloidosis are insignificant, so morphological research methods are of great importance. Microscopically, with amyloidosis, deposits of the structureless homogeneous zodine-spin masses of the amyloid between the stellate reticulose-ndoteliocytes along the reticular stroma, in the walls of the vessels and bile ducts and in the portal paths. The most accurate intermediate department of acinuses is affected. With a pronounced process, the substance is postponed throughout the salt, squeezes the hepatic beams, the hepatocytes are subjected to atrophy. The amyloid is painted Congo red and in polarized light gives a picture of dichroism (brown-red color becomes green). The sediments of the amyloid are similar in primary and secondary amyloidosis, however, during primary amyloidosis, the liver vessels are isolated, whereas there is no amyloid in the disse.

Diagnostics of liver dystrophy

The diagnosis is based on Anamnese data., clinical picture and described biochemical and encephalographic changes. An important feature of the threatening coma is cladder tremor and EEG changes. A special diagnostic value is similar to such a biochemical symptom of hepatic cell precance, as a decrease in blood coagulation factors - prothrombin, proactivity, proof, the total content of these factors is reduced by 3-4 times. For a portional coma, the most significant determination of ammonia in arterial blood and the spinal fluid.

Treatment of liver dystrophy

With the appearance of signs, the precance needs to sharply limit the amount of protein in the daily diet to 50 g, and with further progression of the disease, stop the introduction of proteins through the mouth.

The intestines are daily purified by enema and laxatives, orally or through the probe, antibiotics, suppressing intestinal microflora (Kanamycin 2-4 g per day, ampicillin 3-6 g per day, tetracycline 1 g per day). Used vitamins, cocarboxylase, potassium preparations, glucose, abundant parenteral fluid administration.

A 1-arginine (25-75 g per day in a 5% glucose solution), glutamic acid (30-50 g in the form of a 10% solution) is introduced to neutralize the ammonia of the blood), glutamic acid (30-50 g in the form of a 10% solution). In psychomotor excitation, haloperidol, GOM, chloralhydrate (1 g in the enema) are prescribed. In the case of the development of metabolic acidosis, a 4% sodium bicarbonate solution is introduced to 200-600 ml per day, with severe metabolic alkalosis, large quantities are introduced (up to 10 g per day or more).

Glucocorticosteroid hormones are prescribed in large doses; Premisolone in the precomme - 120 mg per day, of which 60 mg is intravenously drip, in the coma stage - 200 mg per day intravenously drip; Hydrocortisone up to 1000 mg per day intravenously drip. It is categorically contraindicated to the appointment of diuretic drugs.

In recent years, hepatic cell coma has been used in recent years (5-6 liters daily), elecorporal blood perfusion through a heterochine or a pipe liver, or cross-blood circulation. The effectiveness of heterotopic liver transplantability is questionable.

Under development, peritoneal or extracorporeal hemodialysis, which is very important to be prescribed in a timely manner, is carried out in patients with hepatic comewy renal failure.

Forecast. In most cases, the death occurs in a few days. When the liver dystrophy is possible, an outcome is possible in fast forming cirrhosis of the liver.

What doctors should contact if you have liver dystrophy

• Gastroenterologist
• Surgeon
• Hepatologist

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Causes of occurrence

The main causes of liver dystrophy:

The main mechanism for the development of liver lipidose is quite simple. Fats in the gastrointestinal tract are split into fatty acids and triglycerides. In the case when these substances come to the liver in large quantities and under the action of predisposing factors, there is a reverse reaction - fat synthesis (esterification). Another mechanism for the formation of fat in the tissues is its enhanced increase under the action of a large number of fast carbohydrates. With such a quantity of free fat, the liver does not cope and the lipid takes place within hepatocytes. Under the microscope it looks like drops of fat of different size throughout the liver.

Fat hepatosis from the obesity of the liver should be distinguished. In the first case, fat accumulates inside hepatocytes, and in the second - in the intercellular space, in the connective tissue between the cells.

Classification

Allocate the classification of fatty dystrophy, based on morphological changes (in the study of the liver bioptate under the microscope):

• Disseminated focal dystrophy - fat inclusion of single, rare, chaotically arranged in the liver. There are no clinical manifestations;
• Disseminated common dystrophy - fat inclusions are significantly densely located in the liver. The patient feels the overall deterioration of well-being, periodic discomfort in the right hypochondrium;
• Zonal dystrophy - fat inclusions are located locally, in certain liver zones. The clinic is expressed quite strongly;
• Duffuzny dystrophy - fat inclusions occupy all the liver or one of its poles. All the symptoms are pronounced, delivered a strong discomfort to the patient.

Also allocate classification in the development stages of the pathological process:

• Stage 1 - in hepatocytes contain small fat inclusions, which practically do not affect the function of cells, but the processes of destruction have already begun;
• Stage 2 - fat inclusions are completely filled with hepatocytes, their destruction occurs, and small areas of inflammation can develop around the affected cells;
• Stage 3 - the processes in the liver are irreversible, necrosis zones (liver cirrhosis) are developing.

Symptoms of liver dystrophy

Symptoms of liver disease depend on the stage of development of the process. The first stage of the process is completely asymptomatic, the patient still does not bother anything. Detect this period of the disease can only be accidentally, in the diagnosis of other disease, during bioptate microscopy.

Symptoms of 2 stages of liver dystrophy:

• Pain in the right hypochondrium - pulling, noving, average intensity, increase when taking oily, fried or acute food, alcohol. Periodically they are enhanced to grapple-shaped;
• Feeling of bitterness in the mouth;
• Nausea, originating most often simultaneously with pain in the hypochondrium;
• Meteorism (bloating);
• The language is covered with a white-yellow raid;
• Violation of the chair (constipation, diarrhea or their alternation).

The symptoms of the 3 stages of steatohepatosis are more serious complaints:

• Increased irritability;
• Sleep breakdown (sleepiness day and insomnia at night);
• Worsening memory;
• Tendency to depression;
• "Head of Medusa" (expanding the venous grid on the front abdominal wall);
• Ascites;
• Varicose veins in the esophagus;
• Jaundice;
• Amplification of pain in the right hypochondrium;
• Pronounced nausea after eating;
• Bitterness in the mouth;
• Rarely itching the skin.

In the terminal stage, when cirrhosis of the liver and hepatic insufficiency is expressed, additional symptoms are attached to the previous symptoms:

• Hepatic smell of mouth;
• Increasing body temperature;
• Nose bleeding;
• Deterioration or complete disappearance of appetite;
• Dyspnea.

Diagnostics

For the diagnosis of liver dystrophy, after examining a patient with a doctor, laboratory and instrumental diagnostic methods are prescribed:

Treatment of fatty liver dystrophy

Medical treatment of fat hepatosis

• Essential phospholipids - phosphoglie, essliver, essential;
• Amino acids - heptral, methionine, depth;
• Vegetable hepatoprotectors - Carsil, hepaben, Hofitol;
• Vitamins - vitamins E, C, PP and B2;
• Ursodoxicole acid preparations - URSOFALK, Ursosan.

All drugs are prescribed by individual courses, depending on the degree of liver damage and varies from minimal dosages to the maximum.

Diet facilitating the course of the disease

Treatment of any stage of liver dystrophy should begin with proper power:

• Increased protein food (dairy products, meat, eggs, fish caviar, etc.);
• Minimizing or even a complete refusal to receive "fast" carbohydrates (wheat products, sugar, white rice, potatoes). Porridge, products from rye, wholegrain wheat, corn and other types of flour, vegetables and fruits (except bananas and grapes);
• Some decrease in fat in the diet (the use of less fatty varieties of meat and fish, reducing cream and vegetable oils, etc.);
• Consumption of sufficient amount of clean water (at least 1.5 liters per day);
• Refusal to fried, sharp, saved for the whole period of treatment.

Also, such people should gradually reduce body weight (no more than 2-3 kg per month), increasing the load, reducing the amount of food used for one reception, increasing the multiplicity of food intake and decrease in calorie food.

Complications

Basic complications of liver fatty:

• Cirrhosis of the liver;
• Liver failure;
• Development of chronic hepatitis;
• Fatal outcome.

Prevention

The methods of preventing fatty hepatosis development include a number of rules and modifications of lifestyle:

• An increase in the amount of protein in the food diet, a slight decrease in fats and almost a complete refusal of "fast" carbohydrates (potatoes, white rice, sugar, wheat products);
• Reduction to a minimum or a complete refusal of alcoholic beverages;
• An increase in physical activity;
• Strict control over the reception of medicines, especially with hepatotoxic properties;
• Treatment of concomitant diseases that increase the risk of steatosis (diabetes mellitus, hormonal disorders, obesity, etc.).