Liver dystrophy symptoms and treatment. Fatty hepatosis of the liver: symptoms and treatment, diet, prevention. Fatty degeneration of pregnant women

Fatty liver disease is a chronic pathological condition characterized by the presence of excess fat in the liver. In another way, this condition is called The reasons for such obesity are many and almost every person is at risk for this disease.

The reasons:

• an abundance of fat in the diet;
• obesity;
• alcohol;
• high cholesterol;
• diabetes;
• protein deficiency;
• chemical poisoning;
• some medicines;
• hepatitis;
• unbalanced nutrition, and, as a result, lack or excess of vitamins and microelements;
• hereditary liver diseases and autoimmune processes.

This is the main list of causes of pathology, but fatty degeneration of the liver can overtake a person for other less obvious reasons. The difficulty is that before a strong progression of the disease, it may not show any symptoms. It depends on the stage of the disease.

Stages of fatty liver:

1. Steatosis. There are constant progressive changes in the work of the liver, dystrophy of fat cells occurs.
2. Steatohepatitis. Inflammation of the liver - hepatitis. There may be a violation and the occurrence of complications.
3. And as a result, oncology.

Symptoms:

As already mentioned, fatty liver disease is difficult to diagnose due to the lack of obvious symptoms. In the initial stages, there may be weakness, nausea, loose stools, flatulence, slight pain in the right hypochondrium. These symptoms may accompany other diseases, so it is very important not to wait for the manifestation of more dangerous body signals and consult a doctor in time to establish an accurate diagnosis. With a disease such as fatty degeneration of the liver, the symptoms in the later stages are most pronounced, the pain in the hypochondrium becomes stronger and more frequent, headache, fatigue, itching are added, and a sharp weight loss is possible.

Study:

When a person goes to a clinic for a preventive examination or while staying at home anxiety symptoms the doctor conducts the necessary research. A biochemical blood test is taken, including which reveal the presence or possibility of such a pathology as fatty degeneration of the liver. To clarify the diagnosis, it is necessary to

If, according to studies, the patient is diagnosed with fatty liver, treatment must be carried out comprehensively and comprehensively. Although the word "treatment" is not entirely appropriate for this disease. Rather, prevention and elimination of the causes of the development of the disease. As you know, the liver is a self-healing organ, but in order to restore and restore health, it needs support, support and protection.

The patient needs to make changes in his lifestyle, establish proper and rational nutrition, go in for sports and monitor his health. It is necessary to eliminate all the negative factors that led to the emergence of the diagnosis.

elimination negative factors:

• with a diagnosis of obesity - mandatory weight loss;
• food, according to the diet established by the attending physician. High amounts of fat should be avoided: fatty varieties meat, pastries, chocolate, smoked meats, cheeses, fatty cottage cheese, any fried foods, etc.;
• complete rejection of alcoholic beverages;
• physical exercises. For obese people, at least 30 minutes a day or walking at least 5,000 steps.
• lowering blood cholesterol levels.
• if possible, reduce the use of drugs;
• when working with poisons - a change of job or enhanced protection measures.
• in difficult cases and in the later stages, drugs are prescribed.

With timely access to a specialist and compliance with all recommendations, the prognosis for this disease is quite favorable.

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Normal life without fat is impossible. After intake with food, breakdown in the intestines, fatty acids are absorbed into the blood through the wall of the gastrointestinal tract and enter the liver for further processing.

The result of physiological restructuring is the formation of cholesterol, phospholipids necessary for the construction of cell membranes, the formation of hormones, participation in biochemical reactions.

Describing what is fatty liver symptoms and treatment, which have specificity, we note the violation of the process of natural lipid utilization by hepatocytes with high fat accumulation (over 50%). Cytoplasm, vacuoles and some other intracellular organelles are saturated with fats, therefore they cannot perform their functions. Physiologically, the concentration of fatty acids inside the liver cells does not exceed 5%. With fatty degeneration, depending on the degree, this level is exceeded. The condition is irreversible, since the lack of conversion of lipids into energy or the deposition of excess in the subcutaneous adipose tissue leads to the death and degeneration of the hepatic parenchyma. Morphologically, with this nosology, small clusters (small-droplet form) or large deposits (large-droplet variety) appear inside the lysosomes.

The etiological and pathogenetic mechanisms of the disease have not been established, so it cannot be completely cured. Scientists have identified provoking factors leading to lipid degeneration:

• Alcohol abuse in men disrupts the processes of intracellular fat metabolism. Blocking of biochemical reactions leads to difficulty in the physiological utilization of compounds, and excess cholesterol accumulates in lysosomes;
• Mechanisms of biochemical transformation of lipids are also violated in diabetes mellitus. The cause of the condition is the lack of glucose necessary for metabolic reactions;
• Obesity leads to excess deposits in the lipid depot of subcutaneous adipose tissue. Excessive accumulation leads to a lack of excretion pathways, so intracellular infiltration occurs;
• Metabolic diseases (protein deficiency) disrupt the transport processes between the liver and other tissues;
• Poisoning with hepatotoxic poisons, drugs.

The described provoking mechanisms are the result of practical observations, but the pathogenetic links of nosology have not been proven by scientific research. The need for early treatment is due to the development of cirrhosis, when degeneration leads to the growth of rough cirrhotic scars. The greater the destruction, the higher the degree of liver failure.

The main symptoms of fatty degeneration

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

Severe fatty degeneration symptoms, which can be traced clinically, has different morphological manifestations. When examining a biopsy specimen (a piece of tissue), several morphological varieties of dystrophic changes are observed.

In chronic viral and toxic hepatitis, not only lipids, but also proteins accumulate excessively in hepatocytes. Morphological examination reveals hyaline and hydropic granularity. The basis of its appearance is the destruction of the protein-lipid complex, which is part of the organelles.

The clinical symptoms of the form are due to the underlying disease:

• Soreness of the right hypochondrium;
• The appearance of linear expansion of blood vessels in the abdomen;
• Capillary asterisks (telangiectasias) all over the body.

grainy dystrophic changes appear against the background of oxidative phosphorylation, imbalance water-salt metabolism. The state is adaptive, compensatory aimed at restoring intracellular disorders that occur under the influence of viruses, bacteria, and the use of hepatotoxic drugs.

A classic sign of parenchymal fatty degeneration on histochemical examination is a single large vacuole filled with fatty inclusions, pushing the nucleus to the periphery.

On morphological examination, a yellowish, dull tissue is observed. With the degeneration of 50% of the cells, small oval-shaped vacuoles can be traced in some hepatocytes. Gradually, the clusters merge, and the cells die. The formation of fatty "cysts" leads to the formation of the following morphological conditions:

1. Segmental obesity lipid deposits are localized along the peripheral, central parts of the lobule;
2. Disseminated hepatosis fat droplets are located in separate hepatic cells;
3. Diffuse obesity is characterized by the defeat of the entire lobule, but the process is reversible.

In diabetes mellitus, the manifestations of hepatosis are not specific. Fatty degeneration appears due to a violation of glycogen metabolism. The absence of insulin leads to a significant decrease in the reserves of this substance. Compensatory hepatocytes increase in size due to the deposition of glycogen. Empty nuclei are observed in tissue biopsy specimens, the number of vacuoles increases.

In diabetes, ten different types of glycogenosis are distinguished, among which fatty degeneration is not a frequent option, but can be seen in patients with obesity. Histochemical examination of the cells shows the accumulation of specific eosinophilic granules.

The described changes cause symptoms depending on the degree of liver failure. Absence of a clinic upon death a small amount cells due to the high restorative functions of the liver tissue. Only with extensive damage does liver failure develop, leading to symptoms:

• Yellowing of the skin and sclera in violation of bile secretion;
• Encephalopathy in case of poisoning with toxins, ammonia;
• Skin rashes, itching, increased concentration of bilirubin;
• Pain syndrome under the ribs on the right, an increase in the size of the liver, cirrhosis.

The extreme degree of insufficiency is hepatic coma, the accumulation of fluid inside the abdomen (ascites). Lack of detoxification function leads to concomitant enlargement of the spleen, development kidney failure. Any liver symptom is life-threatening if accompanied by an accumulation of toxins in the blood.

Treatment of dystrophic conditions of the liver

Alcoholic steatosis is considered by doctors as a dangerous condition leading to death. Nosology provokes dangerous complications in medium degree degeneration (about 35% of the tissue).

The initial stages of the disease are stopped by the appointment of medications and the cessation of alcohol consumption, severe ones are characterized by high mortality. Approximately 5% of people die within a month when diagnosed with cirrhosis.

There are no specific drugs, so it is carried out symptomatic therapy essential phospholipids (Essentiale), choleretic agents (ursodeoxycholic acid), ademethionine, silibinin. The rationality of prescribing other hepatoprotectors is low.

In alcoholic hepatitis of viral or bacterial origin, the effectiveness of treatment with hepatoprotective drugs is reduced. Steroidal anti-inflammatory drugs are used to reduce progression. The most common representative of prednisolone.

The effectiveness of glucocorticoids in fatty degeneration has not been proven, but in practice the therapeutic effect is observed in the presence of 3 factors:

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

In practical literature, there are indications of the need for proper nutrition, which increases the survival of patients.

Principles of treatment of lipid degeneration of hepatocytes

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

The main risk factor for the disease is obesity. Scientific research proved that a decrease in body weight by 10% leads to a decrease in the concentration of cholestasis enzymes (AlAt, AsAt).

European experts point to the need for a gradual reduction in body weight. Optimal balance Weekly elimination of more than one and a half kilograms increases the risk of gallstone disease, so care must be taken when dieting.

Features of diet food:

• Calorie content of the diet is not more than 1200 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 exercise helps better assimilation fats, the accumulation of oxygen inside the muscle fibers, which increases the consumption of triglycerides.

In diabetes, obesity is caused by insulin resistance. The factor promotes the conversion of excess carbohydrates into fats. Correction of insulin tolerance is achieved by pharmacological agents thiazolidinediones, biguanides.

The elimination of elevated triglycerides is achieved by the regular use of medicines containing unsaturated fatty acids. Ursodeoxycholic acid agents have been used for a decade and have shown high efficiency. The mechanisms of therapeutic activity have not been proven, but the elimination activity of the drug on the elimination of congestive changes in the gallbladder and intrahepatic ducts has been revealed.

In severe liver failure, the protein content in the diet is limited. The daily content is not more than 50 grams. Laxatives are prescribed daily to cleanse the gastrointestinal tract, cleansing enemas. Dysbacteriosis is eliminated by the introduction of antibiotics through a probe (ampicillin, kanamycin, tetracycline).

To neutralize ammonia, arginine is administered at a dose of 50-75 grams per day.

Psychomotor agitation is stopped by haloperidol.

Therapy of steatohepatitis with folk remedies

The doctor prescribes herbal decoctions. Only a specialist will be able to correctly determine the type of therapy, combination and dose of each agent. If the pathology is detected in a timely manner, choleretic preparations immortelle, milk thistle, rose hips help at an early stage.

Herbal preparations reduce the activity of the chronic process, but only with certain nosologies. Therapeutic effect herbal decoctions and infusions, when compared with medicines, appears later, so the combination of medicines with plants is rational. With low process activity, you can use a pumpkin:

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

The second useful folk recipe for eliminating hepatosis is walnuts. To prepare it, you need to chop the nuts. Pour them into a jar, add honey and alcohol in equal proportions. Infuse the medicine for 1 month in a dark room. Use three times a day for a teaspoon.

Milk thistle is part of the popular hepatoprotectors Karsil, Silibinin. You can use the plant at home. The recipe is prepared by mixing dandelion, nettle, birch leaves and milk thistle. Pour boiling water over 2 teaspoons of the mixture, leave for 15 minutes. Take 2 glasses of medicine daily.

Herbal infusions and decoctions, when compared with tablets, have a mild, gradual effect. To increase efficiency, it is recommended to combine folk remedies with diet, exercise.

Features of the diet for dystrophic damage to hepatocytes:

• Avoid spicy, spicy foods;
• Give up fatty meat, fish, broths;
• Choose your products carefully in the store. They should not contain dyes, stabilizers, fragrances, anti-caking additives;
• Don't take too many medications unnecessarily;
• Useful oatmeal, buckwheat.

European scientists point to a fat-soluble effect apricot kernels. For steatohepatitis, eat 5 pieces daily (but no more). The central content of the fruit is saturated with vitamin B15, which is involved in the breakdown of lipids.

What actually is liver dystrophy?

Liver dystrophy, steatosis, lipodystrophy or hepatosis - all these terms refer to the same chronic disease in which liver cells are gradually replaced by fat.

It should be noted that this fatty liver is quite well known, as many common factors can trigger the development of this disease. Hepatosis of the liver - this is the very initial stage of development of the most popular ailment in modern world- cirrhosis.

Causes of liver dystrophy

Steatosis, as a rule, occurs due to such reasons:

• Intoxication with various hepatotropic poisons ( poisonous mushrooms, yellow phosphorus, etc.);
• Diabetes;
• Frequent drinking of alcoholic beverages;
• Abuse of foods that contain great amount preservatives and fats;
• Obesity or prolonged fasting;
• Parenchymal protein dystrophy;
• Uncontrolled use of certain drugs;
• Drug addict;
• Tumors of the pituitary gland.

Classification

First, based on changes in the structure of steatosis, several types of hepatic dystrophy are noted:

• Zonal diffusion. It is characterized by local fatty formations in specific areas of the liver. Clinical manifestations are quite strong.
• Disseminated widespread dystrophy. Fat formations are nearby and significantly compacted in the human liver. Symptoms: general weakness and discomfort in the right hypochondrium.
• Disseminated focal dystrophy. It is characterized by rare, dotted and inconsistently located fatty formations. Symptoms are not expressed.
• diffuse dystrophy. This type of liver dystrophy is characterized by copious amounts fatty inclusions, which may be in place of the entire liver or in one of its parts.

In addition, renal dystrophy can be divided into several stages depending on the period of development of the disease:

• Stage one - small fatty formations can be found in the liver cells, which have almost no effect on the functions of hepatocytes;
• Stage two - the beginning of destruction of the liver, that is, hepatocytes, is observed, and small inflammations or cysts can form near the dead cells.
• Stage three - liver changes can no longer be prevented, some parts of the liver die off, as a result, cirrhosis of the liver develops.

What is dangerous liver dystrophy?

Real liver dystrophy serious illness, which in no case can be missed or not paid due attention to specific symptoms.

Therefore, if a person with steatosis does not want to start treatment, then later he can expect:

• Increased risk of cardiovascular disease and diabetes;
• chronic hepatitis;
• Fibrosis;
• cirrhosis;
• Liver necrosis.

To avoid such horrific consequences, you need to listen to your body and be aware of the signs of liver dystrophy.

Symptoms and signs of fatty liver

Patients suffering from metabolic disorders in the liver cells often do not have complaints about their physical state, since in the initial stages hepatosis of the liver proceeds painlessly and outwardly imperceptibly.

The disease resolves within long period. Over time, the patient begins to experience discomfort in the form of:

• dull pain in the right hypochondrium;
• constant weakness of the body;
• headache;
• rapid exhaustion during activities requiring physical activity;
• dizziness.

The most rare case is liver dystrophy with clearly presented clinical symptoms. Of these, we can distinguish:

• sharp weight loss;
• sharp and unbearable pain;
• bloating.

Methods for diagnosing liver dystrophy

There are two ways to detect lipodystrophy:

• Blood chemistry. This analysis easily indicates an increase in the number special types proteins (alanine aminotransferase (ALT) and aspartate aminotransferase (AST)), which have the ability to increase in liver dystrophy.
• Abdominal ultrasound. It immediately detects the echo signs of hematosis and allows you to determine the exact diagnosis.
• liver tests.

Treatment of the disease

Before talking about drugs that help relieve symptoms and cure the disease, it should be noted that without following a certain diet, any medication will not work to its full potential and will not help as we would like. Often, one diet therapy is enough for recovery.

Only in the event that proper nutrition recommended by a doctor does not help get rid of liver dystrophy should medication methods of treatment be introduced. From a wide selection of medicines in getting rid of hepatosis of the liver, drugs can be used that contribute to:

• breakdown of fats
• removing it from the body.

It should be emphasized that it is necessary to repeat this course of treatment repeatedly, several times a year.

A sick person whose condition is stabilized with the use of drugs also needs:

• vitamin therapy,
• the use of hepatoprotectors and antioxidants that improve the functioning of the liver, perform a protective function in relation to cell membranes,
• immunomodulatory drugs that strengthen the body.

Also, if the patient suffers from this disease simultaneously with obesity, then it is recommended to him:

• gradually reduce weight (about 1-1.5 kilograms per week),
• do gymnastics,
• various exercises aimed at burning excess subcutaneous reserve reserves.

What specific physical activity worth doing, you should certainly find out from a specialist in the field of medicine.

Diet for sickness

Nutrition for fatty hepatosis must be carefully considered so that the daily diet includes the maximum amount of healthy rich foods:

The amount of fat should be reduced to a minimum.

The basic rules of the diet for lipodystrophy:

• Eat at least one hundred grams of protein per day;
• Completely abandon alcoholic beverages;
• 2/3 proteins must be of animal origin;
• Do not eat a large amount of food at a time, that is, eat fractionally;
• Do not consume more than twenty percent of fat from the total amount of food per day;
• Reduce consumption of preservatives and purine substances.

It is necessary to consider in more detail the diet and the necessary foods for hepatosis of the liver.

• boiled,
• steamed,
• baked in the oven (for example, fish or meat).

You also need to use, and quite often, cottage cheese and sour cream with a small content:

It is necessary to refuse saturated vegetables or meat broths. It is important to avoid:

• fatty meats and fish,
• mushrooms,
• tomatoes,
• bean products,
• raw onion and garlic
• various smoked and canned food.

It is important to drink at least a liter of fluid per day, for example:

• clean drinking water,
• herbal decoctions,
• milk, etc.

• vegetable salads with olive oil,
• vegetable or milk soups,
• boiled carrots,
• cabbage,
• various cereals (preferably oatmeal, buckwheat, semolina and rice).

Prevention

The most important fact in the prevention of the disease is the observance of proper nutrition, which includes the necessary components that are rich in vitamins and trace elements useful for the liver.

You also need to regularly undergo specific medical checks, which are carried out in the initial periods of the development of fatty hepatosis. This will certainly help prevent further development illness. Especially in the later stages, it is much more difficult to correct the situation, and sometimes it is already impossible.

The question of what liver dystrophy is is of interest to many patients who are faced with a similar diagnosis. As doctors explain, this is a coma that arose as a result of a deep inhibition of the functionality of the liver. Liver dystrophy (LP) is provoked by various diseases with a chronic course, in which the bile-forming gland is damaged.

The liver is a unique organ that plays an important role in lipid metabolism. Triglycerides from food enter the intestines, where they are broken down by enzymes, then they penetrate into bloodstream. Together with the blood, fats enter the liver, where they are converted into various substances necessary for the normal functioning of the body.

With excessive accumulation of lipids, fatty degeneration occurs, in which the concentration of fats in the organ increases 10 times. The content of triglycerides can reach more than 50% of the total volume of the gland, and normally this figure does not exceed 5%.

Causes of the disease

In most cases, DP occurs due to the fact that the response of hepatocytes (liver cells) to the effects of insulin decreases. Insulin is a hormone that transports glucose to the body's cells. Due to the fact that hepatocytes do not respond to the action of insulin, there is a lack of glucose in the liver. Glucose is very important for the normal functioning of liver cells, therefore, with a deficiency of the substance, they begin to die. Affected cells are replaced by adipose tissue over time. As a result, there are disorders of the functionality of the liver.

Hepatocytes become resistant to the effects of insulin due to genetic pathologies or metabolic disorders. Absence normal reaction liver cells can manifest itself due to immune aggression in relation to insulin.

Other causes of DP:

• The presence of bad habits (alcohol, smoking).
• Excessive consumption of fatty foods.
• Passive lifestyle.

All these factors negatively affect the state of the liver, provoking irreversible changes.

Take this test and find out if you have liver problems.

Symptoms of liver dystrophy are most often mild, and the patient may simply not pay attention to them. As a rule, patients do not complain of any disturbing phenomena. The pathological process develops slowly, and the clinical picture is not clear.

However, over time, the following symptoms appear:

• dull pain on the right under the ribs;
• hepatomegaly;
• nausea;
• eruption of vomit;
• stool disorders.

AT rare cases dystrophic changes in the gland are accompanied severe pain in the abdomen, a sharp decrease in weight, itching, staining of the skin and mucous membranes in a yellow tint.

Usually, the symptoms of DP are divided according to the type of pathology. With toxic liver dystrophy with widespread necrosis (tissue death) of the organ parenchyma, an increased growth of hepatocytes is observed, which are located next to the portal vein of the lymph nodes and spleen. DP is manifested by multiple bleeding in the skin, internal and serous membranes. In addition, there are necrotic and dystrophic changes in tissues that affect the heart muscle and pancreas.

Liver lipodystrophy

Fatty degeneration of the liver (fatty hepatosis) occurs due to the replacement of hepatocytes with fat cells. With hepatosis, fatty deposits accumulate, which look like drops on the liver.

The cause of fatty degeneration is the pathology of the gallbladder, its duct or intestinal tract. ZhDP (fatty liver) can provoke the following diseases:

• Severe obesity.
• Diabetes mellitus type 2 malabsorptive and maldigestive syndrome.
• Excessive consumption of alcoholic beverages.
• Taking corticosteroids, tetracyclines, estrogens, NSAIDs.

Lipodystrophy often occurs against the background of hepatitis with a chronic course (especially with type C hepatitis).

A macropreparation characteristic of IDP: hepatomegaly, the surface of the liver is smooth, the consistency is dense or flabby, the front edge of the organ is rounded, clayey, yellow or yellow-brown.

Toxic DP

Toxic liver dystrophy (TDP) is manifested by extensive rapidly developing necrotic processes that affect the structure of the liver. Usually, the pathology has an acute course, but sometimes it becomes chronic, provoking liver dysfunction.

Massive necrosis develops under the influence of toxins that are found in foods, such as mushrooms. Such poisoning occurs under the influence of external factors. Toxic degeneration of the liver may occur due to endotoxicosis. Such conditions include toxicosis in pregnant women, hyperthyroidism (an excess of thyroid hormones). Often TDP occurs against the background of hepatitis, then dystrophy is a symptom of its fulminant form.

Toxic liver dystrophy is accompanied by hepatomegaly, flabbiness or density of liver tissues, the organ turns yellow. If left untreated, the size of the gland decreases, the capsular membrane becomes wrinkled. Authority acquires grey colour and outwardly resembles a clay mass. For 3 weeks, the gland continues to decrease, its color changes to reddish. Over time, the reticular stroma of the liver begins to become exposed, in which dilated, blood-filled capillaries are visible. Liver cells are preserved only in certain areas of the lobules. This is how red dystrophy manifests itself.

Chronic TDP is a rare condition in which the patient is more likely to die due to rapidly progressive liver dysfunction.

Acute hepatic dystrophy

Acute liver dystrophy (ALP) is most often a complication of hepatitis A, which occurs in an unfavorable form. Separately, pathology develops quite rarely.

The disease is little studied, so doctors cannot accurately answer how it develops. It is also not clear whether there is a connection with the strength of the virus or if some other factors influence the pathological progress.

Aggravated parenchymal hepatitis is provoked by the following diseases: brucellosis, tick-borne relapsing fever, syphilis. In addition, the likelihood of complications of the disease during pregnancy or after an abortion increases. These factors adversely affect liver cells, provoking severe dystrophy.

Symptoms of ADP at an early stage resemble those of hepatitis A, so there is a risk of a significant deterioration in the patient's condition. The pathological process affects the nervous system, as a result, brain activity is disturbed. The disease is manifested by delirium, anxiety, convulsions, eruption of vomit. In this case, the patient must be urgently hospitalized in a psychiatric department.

The reverse reaction of the nervous system is also possible: indifference to everything that happens, depression, lowering of vitality, craving for sleep. Symptoms continue to grow, the patient loses consciousness, hepatic coma develops.

Alcoholic dystrophy

This type of dystrophy occurs due to excessive drinking for 10-12 years. Ethyl alcohol penetrates the body and poisons hepatocytes.

Alcoholic liver dystrophy (ALD) can occur against the background of hepatosis, cirrhosis, alcoholic hepatitis. Most often, it is hepatosis that causes gland dystrophy due to excessive drinking. If the patient refuses strong drinks at an early stage of hepatosis, then the condition of the liver improves after 2-4 weeks. In most cases, ADP does not show severe symptoms.

• Enlargement of the parotid salivary glands.
• Flexion contracture of fingers.
• Redness of the palms, and sometimes of the feet.

The easiest way to identify the disease is through laboratory tests and biopsy.

Diffuse dystrophy

Diffuse dystrophic changes in the liver parenchyma is a very dangerous condition. It occurs as a result of the fact that hepatocytes are not able to neutralize the toxins that enter the body. Liver cells cannot cope with large-scale poisoning, as a result, the parenchymal tissue begins to die, and fibrous tissue grows in the damaged areas. connective tissue. Diffuse changes are becoming more pronounced, and this threatens with liver failure. This is how diffuse DP manifests itself.

Degenerative dystrophic changes in the liver most often provoke a similar process in the pancreas. This is due to the fact that these organs are closely related to each other.

Focal dystrophy

Focal liver dystrophy (OLD) is difficult to detect using laboratory tests. This is quite difficult even despite the fact that there are functional disorders of the gland. Symptoms of the disease depend on the causes that provoked it.

With focal transformation, individual parts of the liver are affected

Focal DP, which arose as a result of excessive consumption of alcoholic beverages, is manifested by shortness of breath, loss of appetite, sometimes there is pain on the right side under the ribs. These signs become more pronounced when the patient moves.

The most effective methods for detecting pathology are magnetic resonance and computed tomography.

Granular dystrophy

This is the most common type of protein DP. Granular liver dystrophy (GLD) is characterized by a violation of the colloidal properties of the cytoplasm of the cell, in which a grain-like protein appears.

ZDP provoke the following factors:

• Inadequate feeding of the newborn.
• Intoxication.
• Infectious diseases.
• Violation of blood circulation and lymph circulation.
• Causes that provoke oxygen starvation of tissues.

Over time, with ZDP, protein metabolism in cells changes, the cytoplasm becomes cloudy, swells. Due to damage to the liver tissue, the bile-forming gland becomes flabby, its blood supply is disturbed.

It is important to distinguish the signs of RDD from the natural processes of protein synthesis in cells, in which granularity appears in the protein.

This pathology is reversible, but it has a severe course. Therefore, there is a possibility of degeneration of the ZDP into intracellular hyalinosis, dropsy or necrosis.

Protein DP

Protein degeneration of the liver (BDP) develops as a result of protein metabolism disorders and occurs against the background of amyloidosis, hyaline or granular degeneration.

In amyloidosis, amyloid (a protein-polysaccharide complex) is formed and deposited in the tissues.

With BDP, the liver acquires a granular structure, since drop-shaped and granular formations appear in the protoplasm of cells. They combine and fill the intracellular space. Protein structures become denser, the work of gland cells is disrupted, as a result, liver tissues die.

hydropic dystrophy

Hydropic degeneration of the liver (HDP, vacuole degeneration) is accompanied by the appearance of vacuoles (a cavity in the cell cytoplasm), which are filled with cytoplasmic fluid. In pathology, the cells of the parenchyma of the organ increase, which is accompanied by wrinkling or vacuolization of the nucleus.

As the disease progresses, the liver overflows with fluid, and its ultrastructures undergo decomposition. Affected cells look like containers filled with water and are a continuous cavity with a bubble-shaped nucleus. This is how GDP manifests itself.

Changes can only be detected using a microscope, since the liver does not change externally.

Yellow dystrophy of the liver

IDP is often a complication of pregnancy. The pathology is due to acute poisoning organism against the background of infectious diseases. Jaundice in a future mother can be provoked by DP, inflammation of the gallbladder, stones in the liver. In addition, the disease can occur independently due to autointoxication of the body (toxicosis).

IDP is a severe degree of toxicosis in expectant mothers. Pathology occurs due to severe poisoning by metabolites. The disease is manifested by staining of the skin and mucous membranes in yellow, profuse vomiting, clouding of consciousness, delirium and increased excitability. In addition, there is a possibility of a hemorrhagic rash (hemorrhage under the skin), the volume of urine decreases, it contains cyrosine and lecithin, and hepatic dullness decreases. If left untreated, the patient dies within a few days.

Diagnosis of the disease

Diagnosis of DP is difficult, since traditional laboratory tests are ineffective, despite the dysfunction of the gland.

The disease is usually asymptomatic, the only sign of pathology is hepatomegaly. The echogenicity of the liver during ultrasound remains within the normal range, and sometimes even increases, so it is quite difficult to distinguish DP from cirrhosis or fibrosis. Ultrasound procedure allows you to identify areas with increased echogenicity. Areas of low echogenicity can be identified using CT. Computed and magnetic resonance imaging are the most informative methods for recognizing DP. With their help, it is possible to determine focal hepatosis of the liver.

A biopsy is performed to detect pathology. With a pathomorphological examination of tissues, the doctor will determine the excess accumulation of fat.

Treatment Methods

Many patients wonder how to treat DP. Treatment consists in observing the following rules:

• Diet.
• Treatment of concomitant diseases.
• Restoration of the structure of the liver.
• Consolidation of results.

As a rule, doctors prescribe the following medications:

• hepatoprotectors,
• synthetic antioxidants,
• statins.

Hepatoprotectors stabilize cell membranes, restore their integrity. They improve the metabolism of bilirubin, fatty acids, proteins. For this purpose, Karsil, LIV-52, Hofitol, Essentiale, etc. are used.

Choleretic agents improve the secretion of bile, normalize its composition, and reduce congestion. With DP, Allohol, Holosas are prescribed.

Statins correct the lipid profile of the blood. With their help, the penetration of fats into the bloodstream is reduced, and excess cholesterol is excreted from the body.

If hepatic encephalopathy is observed with DP, then the patient is urgently hospitalized. The patient is administered drugs by the parenteral method, limit the amount of proteins. In addition, drugs are prescribed that correct the acid-base state. Acidosis is often manifested in DP; sodium bicarbonate is administered to prevent it. Antibacterial agents suppress the intestinal microflora.

With functional disorders of the liver, extracorporeal enterosorption is prescribed. Glucocorticoids are used to support metabolism.

To reduce the load on the liver and speed up recovery, it is necessary to revise the menu. The diet should include foods containing vitamins, fiber, pectins, carbohydrates. The daily norm of fat is 70 g. It is important to exclude foods that contain cholesterol and limit salt intake.

When treating DP, it is forbidden to drink coffee, tea, soda and alcohol.

Patients are allowed to eat soups with vegetables, cereals or based on skimmed milk. It is recommended to consume fresh, boiled, baked or steamed vegetables. Occasionally, you can enjoy low-fat ham, hard cheese (not spicy), egg white omelet or boiled eggs (no more than 1 egg per day). You can also include buckwheat, oatmeal, semolina and rice in your diet. In addition, sour-milk products with a low percentage of fat content are not prohibited.

Preventive measures and prognosis for DP

To prevent the disease, you should avoid the factors that provoke it. It is important to give up bad habits: alcohol, smoking, excessive consumption of food (especially fatty), passive lifestyle.

To maintain a high vitality and prevent the development of pathological processes, you should eat right, limit the use of hot, fried foods, smoked, canned products. In addition, the patient should constantly monitor the weight and maintain it within the normal range.

In order for the liver to function normally, you should do sports every day: walking, jogging, swimming, etc.

If DP is not accompanied by other diseases, then the prognosis is favorable. With dystrophy with pronounced complications, immunity decreases, the body becomes vulnerable to infectious diseases. Pathogenic microbes enter the body, as a result, the patient tolerates anesthesia, surgical procedures worse and recovers after them longer.

If the patient leads the wrong way of life and does not engage in treatment, then the pathology progresses. Then the probability of small-nodular cirrhosis, non-alcoholic steatohepatitis increases.

If during the treatment of DP the patient refused alcohol, follows a diet and the recommendations of a doctor, then most likely he will be able to maintain his working capacity and improve his general condition.

Based on the foregoing, liver dystrophy is a dangerous disease with a chronic course, which occurs as a result of deep inhibition of the functionality of the gland. In order to prevent dangerous complications, you must be attentive to your health and, if suspicious symptoms occur, contact a hepatologist or gastroenterologist. If necessary, the doctor will prescribe an ultrasound, MRI or CT scan, as well as a biopsy. The patient must strictly follow the recommendations of doctors and lead a healthy lifestyle.

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Fatty degeneration of the liver

Fatty degeneration of the liver is a syndrome that occurs due to the progression of fatty degeneration in the liver cells. The course of this disease is characterized by the occurrence of a process of pathological accumulation in the liver cells of fatty deposits in the form of fat drops. The cause of the development of this disease affecting the liver in many cases is the pathological processes occurring in the biliary and intestinal tracts. Risk factors for the development of fatty degeneration of the liver are also the presence of severe obesity in the patient, the second type of diabetes mellitus, malabsorption and maldigestive syndromes, and regular alcohol abuse. The consequences of using a number of drugs, such as: corticosteroids, tetracyclines, estrogens, as well as non-steroidal anti-inflammatory drugs, can lead to the development of fatty liver. Fatty degeneration of the liver, in addition, may accompany the course of various viral hepatitis taking place in chronic form especially hepatitis C.

Toxic dystrophy of the liver

Toxic dystrophy of the liver has as its manifestations massive progressive necrotic processes affecting the liver tissues. The disease, as a rule, is acute, and in some cases it can be present in the body in a chronic form, causing liver failure as the pathology progresses.

Massive necrosis of the liver is mainly caused by exposure to toxic substances contained in food products, including mushrooms, which cause poisoning with arsenic, phosphorus compounds, etc. These intoxications are exogenous in nature. Endogenous intoxications can also provoke toxic liver dystrophy. These include toxicosis that occurs in women during the period when they are carrying a child, thyrotoxicosis. The cause of toxic liver dystrophy is often a disease of viral hepatitis, in which this disease develops as one of the manifestations of its lightning-fast form.

Toxic degeneration of the liver causes changes in the body that are characteristic of each specific stage of the pathological progress of this disease. Initially, there is an increase in the size of the liver, this organ acquires either a flabby or dense consistency, it becomes characterized by an icteric tint. With the further course of the disease, the liver shrinks in size, and its capsular membrane becomes wrinkled. The liver tissue changes its color to grayish and takes on the appearance of a clay mass. In the later stages, after the third week of the disease, the process of reducing the size of the liver continues, it acquires a reddish tint. There is exposure of the hepatic reticular stroma, in which sinusoids are enlarged and overflowing with blood. Preserved hepatocytes remain only in the peripheral regions of the lobules. These phenomena indicate the transition of hepatic dystrophy to the stage of red dystrophy.

The presence of toxic dystrophy of the liver, which has passed into chronic stage is extremely rare clinical case, however, is associated with the probability lethal outcome patient due to progressive liver failure.

Acute liver dystrophy

Acute liver dystrophy predominantly appears as a complication that develops against the background of an unfavorable course of Botkin's disease. Cases of the appearance of this disease in an autonomous form, as evidenced by medical statistics, are extremely rare.

To date, medical research in the field of studying the mechanisms of development of dystrophic phenomena in the liver has not led to an unequivocal answer to the question of the cause of acute hepatic dystrophy. At present, the mechanisms of the pathological progress of this serious illness affecting the liver, and it remains unclear whether there is a correlation with the strength (virulence) of the virus, or whether there is an effect of some other factors.

The presence of brucellosis in a patient can lead to a aggravated course of hepatitis of a parenchymal nature, relapsing fever, syphilis, as well as the state of pregnancy and its artificial termination. All this causes high probability degeneration of hepatitis into a severe form of liver dystrophy.

Acute liver dystrophy at the initial stage recreates a clinical picture similar to the onset of the development of Botkin's disease, which is associated with a significant deterioration in the general condition of the patient. In this case, the nervous system is mainly affected, which is manifested in the appearance of various disorders of brain activity. Patients become delusional, tossing about in bed, convulsions and vomiting occur. In some cases, the appearance of such conditions became the justification for the need to hospitalize the patient in a psychiatric clinic. On the other hand, another, opposite reaction of the central nervous system to the development of the pathological process is possible. Apathy and a depressive state, a significant decrease in the vitality of the body, and increased drowsiness may appear. Up to the onset of unconsciousness and hepatic coma.

Alcoholic degeneration of the liver

Alcoholic dystrophy of the liver is a disease caused by excessive consumption of alcoholic beverages for a long period of time exceeding 10-12 years. Alcohol, in an immoderate amount entering the human body, has an extremely negative, hepatotoxic effect.

The appearance of alcoholic hepatic dystrophy can be a sign that fatty liver or steatosis, cirrhosis, alcoholic hepatitis. In the vast majority of cases, steatosis develops as the earliest stage in the progress of the pathological process in the liver due to alcohol abuse. After the cessation of the regular intake of alcohol in the patient's body, pathological changes due to steatosis developing in the liver return to normal state over a period of 2 to 4 weeks. Often, during the course of the disease, its at least some pronounced symptoms may be absent.

Alcoholic liver dystrophy has the same symptoms as chronic alcohol intoxication. It is diagnosed due to the detection of an enlarged size of the parotid glands, the presence of Dupuytren's contracture, palmar erythema. The presence of this disease in the patient's body is also evidenced by the results of laboratory tests and a liver biopsy.

Therapeutic measures for alcoholic liver dystrophy consist primarily in the absolute cessation of alcohol consumption by the patient. A course of treatment with corticosteroid drugs and essential phospholipids is prescribed. If the disease is in the terminal stage, a liver transplant may be indicated.

Diffuse dystrophy of the liver

Diffuse dystrophy of the liver is a pathological process that develops in the parenchyma, which is the main tissue from which this organ is formed. In specific liver cells, hepatocytes, there are processes aimed at detoxifying toxic substances entering the body. Hepatocytes take part in the processes of digestion, their role in this case is reduced to the secretion of bile, in which there are a number of enzymes that break down fats in the gastrointestinal tract. Liver cells ensure the neutralization of harmful substances by transforming them into those that do not pose a threat to the normal functioning of the body, and which are subsequently excreted along with bile.

Diffuse dystrophy of the liver occurs as a result of the fact that the liver cells are not always able to process the poison that enters 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 damage to the liver, the more it 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 the pancreas as well, since the functions of these two organs are in close connection with each other.

Focal dystrophy of the liver

Focal liver dystrophy presents certain difficulties in diagnosing this disease due to the fact that although there is a deterioration in the functioning of the liver, it is extremely difficult to fix these pathological changes through laboratory tests.

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

Focal liver dystrophy, which occurs, in particular, as a result of regular intoxication with large doses of alcohol, manifests itself in such phenomena as the appearance of shortness of breath, loss of appetite, etc. in some cases, patients note the occurrence of discomfort and heaviness in the right hypochondrium. Such symptoms are characterized by an increase in their intensity during movement.

Often, the detection of fatty infiltration of the liver becomes possible only when performing magnetic resonance imaging - MRI and computed tomography. Data diagnostic methods are the most effective way to detect focal liver dystrophy in a patient.

Granular dystrophy of the liver

Granular dystrophy of the liver is the most common type of protein degenerative pathology. With this disease, the colloidal properties of the cellular cytoplasm are violated, in which the appearance of a grain-like protein is observed.

The reasons for the appearance of this liver disease are: the lack of adequate feeding in infancy, and in later age periods- the consequences of intoxication, the presence of infections, disruption of the functioning of the circulatory and lymphatic systems, as well as the impact of factors that can provoke tissue hypoxia.

As granular degeneration of the liver develops, changes in protein cellular metabolism occur. With the progress of the pathological process of granular dystrophy, the cytoplasm acquires a swollen and cloudy appearance, as a result of which this liver lesion is also characterized as cloudy swelling. The liver affected by this disease acquires a flabby consistency, blood supply is disturbed in it.

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

Granular dystrophy of the liver is predominantly a reversible process, however, due to the severe course of the disease, there is the possibility of its degeneration into such forms as hyaline drop or gyro dystrophy, as well as necrosis.

Protein degeneration of the liver

Protein degeneration of the liver occurs as a result of a violation of protein metabolism and can be represented by amyloidosis, hyalinosis and granular degeneration.

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

Hyalinosis is a type of protein degeneration, which often occurs as a concomitant disease against the background of atherosclerosis. This pathology is characterized mainly by local localization, in particular, it can appear in the vessel wall during the formation of a blood clot. Hyalinosis tends to form translucent protein structures similar to cartilage hyaline tissue.

Protein dystrophy of the liver also acquires the form of granular dystrophy, which means the appearance of drop-shaped and granular protein formations in the cellular protoplasm. Combining into a single whole, these formations show a tendency to completely fill the entire internal cellular space. With granular dystrophy of the liver, protein cell structures are compacted, and the normal functioning of cells is disrupted. Granular dystrophy is fraught with pathological changes of a necrotic nature and leads to cell death.

Hydropic dystrophy of the liver

Hydropic degeneration of the liver, also known as hydropic degeneration, has such a feature that vacuoles containing cytoplasmic fluid appear in the cell. In the presence of this type of hepatic dystrophy, the parenchyma cells are enlarged, the nucleus in them acquires peripheral localization, in some cases its wrinkling or vacuolization is observed.

With the development of pathological changes, the cell overflows with fluid and its ultrastructures decompose. The cell becomes like a container filled with water, and is essentially one continuous vacuole with a bubble-like nucleus placed in it. A similar phenomenon, which is a sign that characterizes colliquational necrosis, is called balloon dystrophy.

Hydropic dystrophy of the liver can only be detected by examination using a microscope, since visual changes are not characteristic of the appearance of tissues and organs.

The prognosis in the presence of this disease seems unfavorable due to the fact that with hydropic degeneration of the liver, the functioning of this organ is significantly impaired. A negative prognostic factor is also that the outcome of this disease is focal or total cell necrosis.

Yellow dystrophy of the liver

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

Jaundice in a woman during the period in which she bears a child, as well as in the presence of other hepatic pathologies in addition to liver dystrophy, such as cholecystitis and the presence of stones in the liver, can also be present as an autonomous disease provoked by autointoxication of the body. This condition is known as concomitant pregnancy toxicosis.

Yellow liver dystrophy is one of the most serious toxicosis of pregnancy in terms of severity. The disease is caused by severe intoxication with the products of metabolic processes occurring during pregnancy, which differ in other features than the metabolism that occurs in the normal state 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 prolonged vomiting. Over time, the condition is aggravated by the fact that the skin and sclera acquire a pronounced icteric appearance, clouding of consciousness occurs, states of delirium and excessive excitation of the nervous system may occur. There is a possibility of multiple subcutaneous hemorrhages, in the composition of urine, the amount of which tends to be significantly reduced, the presence of cyrosine and lecithin is detected, and in addition there is a decrease in hepatic dullness. Due to the further deterioration of the general condition of the patient, there is a possibility of death after a few days.

Parenchymal dystrophy of the liver

Parenchymal dystrophy of the liver is based on the development of the pathological process associated with it, changes in the chemical-physical and morphological characteristics inherent in cellular proteins. The essence of such violations of the functioning of cells is the process of hydration, which the cytoplasm undergoes as a result of the fact that coagulation, denaturation takes place in the cell, or, on the contrary, the phenomenon of colliquation. In those cases in which there is a violation of protein-lipid bonds, membrane cell structures are characterized by the occurrence of destructive processes in them. The consequences of such changes are the development of necrotic processes of a coagulation - dry, or colliquat - wet nature.

Parenchymal dystrophy of the liver is classified according to its varieties as:

Hyaline-drop hydropic horn dystrophy.

Granular dystrophy, which is characterized by the appearance of protein grains in the cells of the parenchyma, can also be attributed to parenchymal dystrophy of the liver. This type of hepatic dystrophy is characterized by an increase in the volume of the organ affected by this disease, the acquisition of a flabby consistency and a dull appearance on the cut. The last given feature causes the fact that granular liver dystrophy is also called dull or cloudy swelling.

Liver dystrophy is a chronic or acute (depending on the form) liver disease that occurs with phenomena of fatty degeneration of hepatocytes (liver cells) or their massive necrosis. Diseases such as hepatosis and cirrhosis are consequences of the process of liver dystrophy.

It is accepted to allocate fatty and toxic dystrophy of the liver.

Toxic dystrophy of the liver

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

Etiology and pathogenesis of toxic liver dystrophy

Massive liver necrosis usually develops mainly with exogenous (poisoning food products, including mushrooms, compounds of phosphorus, arsenic, etc.) and endogenous (thyrotoxicosis, toxicosis of pregnant women) intoxications. It can occur with viral hepatitis as a manifestation of its fulminant form.

Pathological anatomy in toxic liver dystrophy

The changes that occur in toxic liver dystrophy are different in different periods of the disease. At the onset of the disease, there is some enlargement in the size of the liver, it becomes dense or flabby, with a yellowish tinge. With a further course, the liver decreases in size, becoming flabby, and its capsule acquires a wrinkled structure. Liver tissue becomes gray, clay-like.

Microscopically, the development of fatty degeneration of hepatocytes in the center of the liver lobules is observed, followed by their further necrosis and processes of autolytic decay with the formation of protein-fatty detritus with crystals of the amino acids leucine and tyrosine. With progression, these necrotic changes capture the remaining sections of the lobules. These changes in the liver characterize the onset of the stage of the so-called yellow dystrophy.

After 3 weeks of illness, the liver further decreases in size and becomes red. The reticular stroma of the liver is exposed with enlarged and sharply overflowing with blood sinusoids. Hepatocytes are preserved only along the periphery of the lobules. These changes characterize the onset of the stage of red dystrophy.

Symptoms of toxic liver dystrophy

With massive necrosis of the liver with toxic dystrophy of the liver, the development of jaundice, processes of hyperplasia of the lymph nodes and spleen located near the portal vein, the appearance of multiple hemorrhages in the skin, mucous membranes and serous membranes, necrosis of epithelial cells in the tubules of the kidneys, degenerative changes in the tissues of the pancreas and myocardium are noted hearts.

With the progression of this form of the disease, patients often die from the development of hepatorenal syndrome and liver failure.

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

Fatty degeneration of the liver

It is a disease or syndrome caused by the development of fatty degeneration in the liver cells in the form of a pathological deposition of fat drops in it. The liver cell accumulates fatty deposits.

Etiology of fatty liver

Fatty degeneration of the liver is a reaction of the liver to intoxication, sometimes associated with a number of diseases and pathological conditions. The most common causes of the fatty form of liver dystrophy are pathologies of the intestinal and biliary tracts, severe obesity, bypass intestinal anastomoses, long-term use parenteral nutrition, diabetes mellitus (type 2), maldigestion and malabsorption syndromes, celiac enteropathy, Wilson-Konovalov's disease and a number of genetically determined diseases, chronic alcohol intoxication, the use of certain drugs (corticosteroids, estrogens, tetracyclines, non-steroidal anti-inflammatory drugs, amiodarone). Almost all chronically occurring viral hepatitis, especially chronic hepatitis C, is accompanied by the development of fatty liver.

The pathogenesis of fatty liver

The basis of the pathogenesis of the described liver disorder is the process of accumulation of triglycerides and cholesterol in the liver tissues due to excessive absorption and formation of free fatty acids and excessive intake of fatty acids in the liver, a decrease in the rate of oxidation of fatty acids inside the mitochondria of hepatocytes, and difficulties in the processes of utilization of fats from the liver.

Pathological anatomy in fatty liver

The liver with fatty degeneration increases in size, becomes yellow or red-brown, its surface remains smooth. In liver cells, fat is determined from triglycerides. The process of accumulation of fats in hepatocytes can be dusty, large or small droplets. A drop of fat pushes the organelles inside the cells to the periphery. Infiltration with fats can cover both single hepatocytes and groups of hepatocytes and even the entire liver parenchyma. With fatty infiltration, hepatocytes die, and fat drops merge with each other and form fatty cysts with the growth of connective tissue.

Clinic of fatty degeneration of the liver

The course of fatty degeneration of the liver is usually asymptomatic and, mainly, the pathology is detected by chance during instrumental research methods. Pain is not a specific symptom of the disease.

Some patients complain of a feeling of heaviness and discomfort in the right hypochondrium, which are usually aggravated by movement. The liver in this disease is enlarged, but tenderness in the liver is quite rare on palpation. Fatty degeneration of the liver, which develops due to chronic alcohol intoxication, often occurs with anorexia, shortness of breath and a number of other symptoms.

Methods for diagnosing liver dystrophy

The use of traditional laboratory tests to confirm these violations is practically not informative. There is a moderate increase in the activities of the enzymes of serum transaminase and alkaline phosphatase. The level of total bilirubin, albumin and prothrombin are mostly within the normal range. There are no other abnormalities in the blood. When conducting an ultrasound, the doctor notes that the echogenicity of the liver tissues is mostly normal or increased. In some cases, only computed tomography and magnetic resonance imaging can reveal the presence of liver dystrophy. For the final confirmation of the diagnosis, a mandatory liver biopsy is required with histological examination obtained biopsies.

Treatment of liver dystrophy

An important measure in the treatment of liver dystrophy is the prevention of the development of necrosis and inflammation (steatohepatitis), the treatment of which is much more complicated. Treatment of liver dystrophy consists primarily in the elimination of the etiological causes that caused it, as well as in symptomatic treatment associated disease syndromes.

Among the drugs that improve functional states liver, one of the leading places is occupied complex drug heptral (ademetionine). The second leading drug in the treatment of liver dystrophy is the drug "ursodeoxycholic acid".

The information provided is not a recommendation for the treatment of liver dystrophy, but is a brief description of the disease for the purpose of familiarization. Do not forget that self-medication can harm your health. If signs of illness appear or are suspected, you should immediately consult a doctor. Be healthy.

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

Etiology

The change in metabolism, which develops under the influence of external and internal factors, leads to disruption of the structure of cells. This may be malnutrition, adverse living conditions, trauma, intoxication, poisoning, exposure to infection, endocrine disorders, circulatory pathology, hereditary defects. They affect organs directly or through changes in neurohumoral regulation. The severity of dystrophy is affected by the type of tissues, the strength and duration of exposure to the pathological factor, as well as the body's ability to respond to exposure.

These restructurings are companions of any disease. Sometimes they appear initially and cause a picture of the disease, and sometimes the disease itself disrupts cellular metabolism.

Dystrophic changes in the liver occur under the influence of the following factors:

inflammatory diseases - viral hepatitis, infections; toxic damage - the result of exposure to alcohol, drugs, poisons, industrial harmful substances; malnutrition - the predominance of fatty and carbohydrate foods; violation of the outflow of bile; systemic diseases; endocrine disorders; hereditary diseases.

Pathogenesis

A long study of the processes of dystrophy using the methods of biochemistry, histochemistry, electron microscopy showed that any of them is based on a violation of reactions involving enzymes and a change in the function of cellular structures. In the tissues, metabolites of the altered metabolism accumulate in large quantities, the ability to regenerate and the functions of the damaged organ are impaired. As an outcome - a violation of the vital activity of the body.

Dystrophic changes can proceed according to one of the mechanisms:

Decomposition - at the level of molecules, the structure of tissue systems, protein-fat and mineral compounds are restructured. The reason for this is the change in the ratio nutrients, accumulation of metabolic products, hypoxia, exposure to toxins, fever, shift in acid-base balance (often towards acidosis), disturbance of redox reactions and electrolyte balance. Under the influence of these factors, the components of cell organelles and large molecules can disintegrate or change. Proteins are hydrolyzed by lysosomal enzymes and denatured. More complex formations (amyloid, hyaline) are also formed along the same path. Infiltration is the impregnation of organ structures with metabolites of proteins, fats or carbohydrates that are freely found in the blood or lymph (accumulation diseases). Transformation is the reaction of the transformation of substances into each other - fats - into carbohydrates, carbohydrates into proteins, synthesis of glycogen from glucose. A large number of new substances are collected inside the cell. Modified synthesis is an increase or decrease in the formation of normal substances in tissues - proteins, fats, glycogen, which leads to their deficiency. Changes in synthesis can occur along the way of creating substances that are not usually inherent in this tissue. For example, glycogen is in the kidneys, keratin is in the lacrimal gland.

These pathological mechanisms may develop sequentially or simultaneously. Morphologically, dystrophies will manifest themselves as a violation of the structure of cells. Usually, after damage to various cellular structures, their regeneration begins. In pathology, it is violated even at the molecular level. Inside the cells, various grains, drops, crystals and other inclusions begin to be identified, which should not be there, or their number in healthy cells is insignificant. The process can also proceed in the opposite direction - inclusions or parts of organelles that are usual for them disappear in the cells.

At the organ level, dystrophy is manifested by a change in appearance. The color, size, shape changes, such processes are said to be “rebirth” or degeneration of the organ. The body changes its functioning - the synthesis of various substances, metabolism. If the etiology of dystrophy is removable and there is no deep damage, then there is the possibility of absolute restoration of the organ. In other cases, the processes are irreversible, necrosis develops.

Types of dystrophy

They are classified according to the level of damage they cause:

parenchymal - affect the parenchyma of the organ; stromal-vascular - rearrangements in microvessels and intercellular space; mixed.

If we consider the pathology of a certain metabolism:

protein; fat; carbohydrate; mineral.

By the extent of the process are:

local; general, or systemic.

There are also acquired and hereditary.

Parenchymal dysproteinoses

A change in the metabolism of cytoplasmic proteins, which are in a bound or free state, is called protein dystrophy. Bound proteins are various lipoprotein complexes, while free proteins are represented by cellular enzymes. Their physical and chemical structure changes, various peptide particles are formed in the cytoplasm. This entails a change in the exchange of water and electrolytes, osmotic pressure, and an increase in fluid saturation.

Morphologically, this is manifested by hyaline-droplet and hydropic dystrophy. The final phase in their existence can be cell necrosis. The final stage of the hyaline-drop metabolic disorder is coagulative necrosis, with hydropic at the end of colliquat cell necrosis. It is possible to consider these changes only with the use of microscopy of damaged areas. With hyaline-drop dysproteinosis, hyaline drops are collected in the cells. Cells affected by hydropic dystrophy increase in volume due to vacuoles with liquid transparent contents.

Granular dystrophy, or cloudy swelling - also parenchymal dystrophy, loss of protein in the form of grains. The causes are a variety of infections, circulatory pathology, malnutrition. Functionally, it does not impair the functioning of the organ and sometimes regresses without a trace.

Hydropic dystrophy, on the contrary, causes depression of liver function. It develops against the background of severe and moderate viral hepatitis, prolonged cholestasis, dystrophic form of cirrhosis. The most pronounced type is balloon dystrophy, which, with a prolonged increase, becomes irreversible and turns into colliquational necrosis. The cells are then melted to a liquid state. Immune cells come to the focus, which remove dead tissue. A scar forms in their place.

Hyaline droplet dystrophy in the liver is manifested by a decrease in cell size, thickening of protein formations. A special type is alcoholic hyaline, or Mallory bodies. This is a special protein, the result of the synthesis of hepatocytes. It is located in cells around the nucleus and has an acidophilic reaction (stains in Blue colour). It has leukotaxis - attracts leukocytes, is able to cause immune reactions, stimulates the formation of collagen. In the blood of patients with alcoholism, circulating immune complexes based on alcoholic hyaline are found, which can affect the kidneys with the formation of glomerulonephritis.

Parenchymal lipidosis

Fatty degeneration is the formation of a large amount of lipids in cells or deposition in areas where it was not previously present, as well as the synthesis of fats of an uncharacteristic structure.

The bulk of the accumulated fats in hepatocytes is neutral fat. It forms droplets that gradually merge into a large vacuole. Fat metabolism is disturbed in three cases:

Massive intake of fats into the body, which eventually leads to a lack of enzymes for their digestion. Toxic substances block the synthesis of fats. Lack of amino acids for the formation of lipoproteins and phospholipids.

The following factors provoke the development of lipidosis:

alcoholism; diabetes mellitus; general obesity; toxic damage; hereditary fermentopathy; diseases of the digestive system.

Fatty liver manifests itself in three forms:

disseminated - lipid droplets are located in separate cells; zonal - fats are collected in special areas of the hepatic lobule; diffuse - the distribution of fat throughout the lobule.

By the size of the inclusions, obesity can be large-drop and small-drop.

Long-term alcohol consumption in almost 50% ends with the formation of fatty hepatosis

Ethyl alcohol and its metabolic products increase the synthesis of fatty acids, but reduce their oxidation and the formation of lipoproteins. Cholesterol accumulates in large quantities, which reduces the permeability of cell membranes. Intracellular fat droplets push the nucleus to the periphery. But the synthetic work of the cell is not broken. With the refusal of alcohol, the reverse development of the process occurs. Functions are restored, accumulated lipids are gradually metabolized and excreted from the liver.

But if the patient prefers to drink alcohol further, then this threatens the transition of fatty degeneration into cirrhosis.

In patients with diabetes, fatty degeneration develops in 70% of cases. This is influenced by such factors:

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

As a result of the lack of insulin and the entry of glucose into the cells, lipolysis is activated - the metabolism of fats, aimed at satisfying energy hunger. The concentration of fatty acids in the blood increases, the liver tries to process them into lipoproteins. The excess goes to the resynthesis of triglycerides. But too a large number of lingers in hepatocytes, causing fatty hepatosis.

Fatty degeneration of the liver is a reversible process. The main role here is played by the cessation of the influence of the provoking factor - the exclusion of alcohol, the normalization of the composition of food, the reduction in the amount of fat, the controlled course of diabetes.

Fatty degeneration of pregnant women

Separately, it is worth considering the development of acute fatty hepatosis during pregnancy. This is a serious condition that often causes death of the mother or fetus. The causes of occurrence are not fully known. Assume the influence of heredity, a genetically determined defect in the mitochondrial enzyme system. This causes disruption of fatty acid oxidation.

Symptoms of pathology are varied. Some may not develop jaundice. But more often there is a classic course: weakness, lethargy, nausea, heartburn. Jaundice gradually increases, its significant severity is a danger to the mother and fetus. Against the background of heartburn, ulcers of the esophagus are formed, vomiting is possible. coffee grounds» with ongoing esophageal bleeding. Liver failure develops with a picture of clouding of consciousness. Often this is accompanied by a syndrome of disseminated intravascular coagulation, which causes death.

Suspicion of the development of acute fatty hepatosis in the 3rd trimester of pregnancy is an indication for emergency delivery to save the life of the mother and child.

carbohydrate degeneration

It is manifested by a violation of the structure or deposition of forms of carbohydrates in atypical places. Often this is the storage form - glycogen. In diabetes and glycogenosis, such processes become possible.

In diabetics, the content of glycogen in the cells is significantly reduced, but it accumulates in the nuclei, which is why they acquire an “empty” appearance, debugged along the vessels and 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 in anemia, leukemia, in places of inflammation. It accumulates in the muscles, heart, kidneys, vascular walls. Clinically, it can manifest as cardiac or respiratory failure with a fatal outcome.

Symptoms

The underlying disease that caused the dystrophy will give symptoms. Acute processes are accompanied by weakness, malaise, decreased performance. Stretching of the liver capsule or gallbladder disease will be accompanied by pain. Often it is a dull aching pain under the ribs on the right. Sometimes it radiates to the back, to the area of ​​the right kidney, to the neck, shoulder blade, shoulder on the right.

Patients are concerned about dyspeptic symptoms - nausea, heartburn, may be vomiting. The chair is broken, there are periods of constipation and diarrhea, often accompanied by bloating, flatulence.

A symptom of jaundice may appear after a few hours or days, as a manifestation of a violation of bilirubin metabolism. The first to react are feces and urine. The faeces become discolored and the urine becomes the color of beer. Parallel worries pruritus- irritation of skin receptors by circulating bile acids.

With advanced dystrophic processes, there are signs of a violation of protein metabolism. Immunity is reduced, infectious diseases occur more often. Lack of synthesis of protein coagulation factors is manifested by bleeding gums, hemorrhages in the skin, hemorrhoidal, gastrointestinal, uterine bleeding.

Protein deficiency 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, and neuromuscular reactions. It can develop acutely within 7 days, or longer, for 3 months.

The severity of violations depends on the speed of development and the causes that caused this condition. There are personality disorders, memory impairment and decreased intelligence.

Encephalopathy occurs in three stages:

Slight personality changes, complaints of sleep disturbance, decreased attention and memory. Severe personality disorders, often inappropriate behavior, mood swings, drowsiness, monotonous speech. Disorientation in time, stupor, mood swings, aggression, delusional states, pathological reflexes. Hepatic coma - a deep depression of consciousness, a decrease in tendon reflexes, the appearance of pathological ones.

In addition to neurological signs, there are other clinical symptoms - jaundice, liver odor, fever, tachycardia. With extensive necrosis, infection may join. Death often occurs from cerebral edema, renal failure, pulmonary edema, toxic or hypovolemic shock.

Diagnostics

The examination begins with the collection of anamnesis data:

patient complaints; time of onset of signs of the disease; their development over time; connection with various factors - alcohol consumption, nutrition, physical activity; indication of unprotected sexual contacts, injections, visits to the dentist, tattoos, blood transfusions in the last 6 months; the presence of gastrointestinal diseases intestinal tract, liver, diabetes, pregnancy.

General examination reveals excess weight, skin discoloration, scratching, bleeding in the skin, rash, pigmentation, swelling of the extremities, or accumulation of fluid in the abdominal cavity.

Liver dystrophy is morphological characteristic processes that are caused by the influence of various pathogenic factors. Therefore, the diagnosis aims to establish the disease that led to the development of organ dystrophy. For this, laboratory diagnostic methods are used. A complete blood count reflects the presence of inflammation in the body. A biochemical blood test makes it possible to judge the state of the synthetic function of the liver, the presence of cytolytic reactions, and cell damage.

A study is underway of markers of viral hepatitis, which also cause liver dystrophy.

The next step is an ultrasound. The method is non-invasive and allows you to identify diffuse or focal changes in fabric. The nature ultrasound image fatty infiltration of the liver, the development of fibrosis or cirrhosis can be assumed. On ultrasound, volumetric formations, cavities, cysts, calcifications are clearly visible, signs of portal hypertension are distinguishable.

The use of x-ray methods allows you to determine the presence of changes in the liver, an increase in its size. Contrasting of the biliary tract or vessels shows their condition, tortuosity, the presence of narrowing, obstruction to the outflow of bile. Methods such as CT and MRI are also used. There are no specific signs indicating the development of dystrophy. This can be guessed by detecting changes in the parenchyma characteristic of various diseases.

The morphological picture can be established only with the help of a biopsy. But this is a traumatic method that can lead to severe complications. Therefore, it is used only according to indications:

clarification of the etiology of liver disease; chronic viral hepatitis; storage diseases (hemochromatosis, Wilson's syndrome); biliary cirrhosis to determine the degree of inflammatory response and fibrotic changes; carcinoma; monitoring the effect of the treatment of these diseases.

There are conditions in which this method is absolutely contraindicated:

serious condition of the patient; menstrual bleeding in women; signs of a violation of blood clotting; a decrease in platelet levels; obstructive jaundice.

For the diagnosis of fatty degeneration, it is not advisable to use the method. This form has the ability to regress under the influence of treatment and diet. Therefore, the data obtained from the study will be irrelevant after 2-3 weeks.

Treatment

To effectively cope with the disease, therapy should go through the following steps:

rational nutrition; treatment of concomitant pathology; restoration of the liver; consolidation of results.

Conservative therapy

Treatment of concomitant diseases consists in adequate therapy of diabetes mellitus prescribed by an endocrinologist. Diseases of the gastrointestinal tract are treated by a gastroenterologist or a local internist. For treatment alcohol addiction If a person is not able to cope with the craving for alcohol himself, a narcologist is involved.

For treatment, drugs of various groups are used:

Hepatoprotectors. Antioxidants. Statins.

Hepatoprotectors can have various effects. They stabilize cell membranes, restore their integrity, and improve the synthetic abilities of cells. Contribute to the improvement of the metabolism of bilirubin, fatty acids, proteins. Representatives of the group are drugs Karsil, Liv-52, Hofitol, Essentiale, ursodeoxycholic acid and drugs based on it.

Also apply choleretic drugs Allohol, Holsas. They improve the synthesis of bile, its secretion, regulate the composition, reduce congestion in the liver.

Statins are used to correct lipid profile blood. They reduce the absorption of fats in the intestines, remove excess cholesterol, preventing it from getting back into the blood.

Treatment of a severe form of dystrophy, accompanied by hepatic encephalopathy, takes place in the intensive care unit. Treatment is symptomatic. The patient is transferred to parenteral nutrition and fluid administration, limit the amount of protein. Drugs are used to correct the acid-base state, often this condition develops acidosis, so the introduction of sodium bicarbonate is necessary. Antibiotics are prescribed to suppress intestinal flora.

Sometimes there is a need for extracorporeal detoxification, especially after the addition of kidney failure. To maintain the overall metabolism in large doses, glucocorticoids are used. This condition often ends in death.

Treatment with folk methods

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

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

Within a month, drink 2 glasses a day of an infusion made from milk thistle fruits, dandelion root, nettle, birch leaves. This mixture is poured with a glass of boiling water and infused for 15 minutes.

If you cut off the top from a ripe pumpkin and remove the seeds, you get a container into which you need to pour fresh honey and put it in a dark, cool place for half a month. After that, pour the resulting therapeutic composition into a jar and consume one spoonful before meals.

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

Grind milk thistle seeds to a powder. 3 tablespoons brew 0.5 liters of water, boil by half. Drink a tablespoon an hour before meals for 1 month.

Effectively helps decoction of dried pears and oatmeal. Take 4 tablespoons of oatmeal for a glass of fruit, boil in a liter of water. Eat the entire serving during the day.

St. John's wort, horsetail, rose hips, motherwort shoots mixed in equal parts. Boil a tablespoon of the mixture in a glass of water. Drink the resulting broth during the day, divided into 4 doses.

Mix a tablespoon of petals from wild rose flowers with half a spoon of honey. Eat this mixture after meals with tea.

Diet

Liver treatment does not imply a strict diet as for weight loss. Hunger will do even more harm. Nutrition should be balanced in lipid-protein composition. The fat content is limited due to animal origin - butter, cheeses, lard, meat of fatty breeds. This will reduce the saturation of food with fats, reduce their absorption, and hence negative impact on the liver.

The amount of protein, on the contrary, should be increased at the expense of animal products. It is their proteins that have a complete composition of amino acids, contain an indispensable group. Protein is needed for the synthetic processes of the liver - the construction of its own enzymes, the formation of lipoproteins from fats, the production of various proteins of the human body - the immune system, blood clotting.

The amount of carbohydrates is the largest, they are the energy substrate. But we must remember that preference is given to vegetable carbohydrates, fiber, dietary fiber. Simple sugars contained in sweets, rich pastries, are quickly processed, significantly raise the level of glucose, which will complicate the patient's situation.

Alcohol is absolutely forbidden, it is one of the reasons for the development of dystrophy, so it must be excluded in the first place.

The diet can be described as a dairy-vegetarian diet with the addition of lean meat and fish. Vegetables and fruits can be consumed in any form. The exceptions are sorrel, legumes, mushrooms.

The amount of salt is reduced to 15 g per day. In order not to be mistaken, food is cooked without salt, salted on your plate.

If the cause of dystrophy is diabetes mellitus, nutrition should be built on the system bread units. It calculates the amount of carbohydrates needed for a person per day. They are distributed according to meals and then, according to special tables, they determine how much one or another product can be eaten. This system helps control glucose levels in diabetics, reduces weight. It can also be used to feed overweight people. Excess weight will gradually go away.

If liver dystrophy has reached a severe state of hepatic encephalopathy, then nutrition is built differently. The amount of protein is limited to 50 g per day. This is necessary so that the liver can cope with the detoxification of protein metabolism products. If the condition worsens, it is generally canceled, parenteral nutrition is started.

Prevention and prognosis

Prevention is aimed at eliminating risk factors for conditions and diseases that lead to the development of dystrophic processes. Overweight it is necessary to take it under control, try to reduce it to acceptable numbers. To do this, you first need to determine the body mass index. If it is above 25, then it's time to think about weight loss.

Even if the weight is normal, but the diet is dominated by foods rich in fats, you should try to reduce their amount, this will reduce the load on the liver enzyme systems.

Starvation and rigid diets won't do any good. Protein deficiency will cause malnutrition and the development of fatty degeneration, because. there will be no substrate for the synthesis of protein-fat molecules.

Alcohol, even with a small but regular use, has a toxic effect on liver cells, damages them and causes pathological mechanisms for the synthesis of a non-typical hyaline protein or fat deposition. A complete refusal to drink alcohol in the early stages of fatty degeneration can lead to an improvement in the patient's condition. With advanced cirrhosis, this will hold back the onset of hepatic encephalopathy and the terminal stage.

Viral damage to the liver can be avoided if one is aware of the routes of transmission. To prevent hepatitis A, you need to observe personal hygiene, wash your hands, fruits, do not use drinking water from open sources. Viruses of types B and C are transmitted through blood, therefore, when performing invasive procedures, use disposable instruments, use only a personal manicure set, do not have unprotected sex, and after a blood transfusion, be examined for hepatitis after 6 months.

Women in the planning period of pregnancy should minimize the manifestations of existing chronic diseases gastrointestinal tract, pathology of the biliary tract. During pregnancy, as a result of hormonal changes, there is a risk of developing gestational diabetes mellitus, which can manifest fatty hepatosis as a latent hereditary disorder of estrogen metabolism. Therefore, following a diet low in fat and simple carbohydrates will prevent liver dysfunction.

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

Hydropic and its pronounced manifestation - balloon dystrophy - are varieties of parenchymal dysproteinosis. This term in pathological anatomy refers to dystrophic changes caused by disorders of predominantly protein metabolism in cells that make up the structure and ensure the functionality of any organ, that is, its parenchyma.

Dystrophy is a change caused by violations of protein metabolism in liver cells.

Classification of parenchymal dystrophies

Acute liver dystrophy has several different mechanisms of formation. These include:

• infiltration - at the same time, due to violations of the production of enzymes, an excess amount of metabolic products enters the cells;
• decomposition - consists in the disbanding of some structural elements of the cell, as a result of which metabolic processes occur incorrectly, and insufficiently oxidized metabolic products accumulate in the cells;
• cell production of abnormal chemical compounds;
• change in nutrients entering the cell organic compounds in such a way that as a result of metabolic processes only one type is formed (proteins, carbohydrates or fats).

Parenchymal dysproteinoses are classified depending on the time of occurrence, the prevalence of the pathological process, the ongoing morphological changes, as well as the type of substances accumulated in the parenchyma due to metabolic disorders.

According to the period of formation of dystrophy, they are divided into congenital and acquired. According to the prevalence of pathology, systemic and local disorders are distinguished. Morphological changes are classified depending on whether they affect only the parenchyma of the organ, or affect vascular system organ. Classification according to the type of substances predominantly accumulated by the body, protein, carbohydrate, fatty and mineral dystrophies are distinguished.

In addition to hydropic dystrophy, which refers to disorders of predominantly protein metabolism, dysproteinosis also includes hyaline-droplet and horn dystrophy, as well as primary aminoacidopathy.

Hydropic dystrophy is an edema of the cells that make up the parenchyma of an organ subject to pathological changes.

Hydropic dystrophy is also called vacuolar and is a swelling of the cells that make up the parenchyma of an organ subject to pathological changes. Mild cellular edema is reversible. If the process takes on a pronounced progression, such dystrophy is called ballooning and leads to the death of functional liver cells.

Vacuolar dystrophy is one of the most common disorders characterized by degenerative changes in the organ. Its difference from other types of dystrophies lies in the fact that new intracellular formations are formed - vacuoles - filled with a light liquid.

Symptoms

Hepatic hydropic dystrophy is most often provoked by hepatosis or viral and toxic hepatitis. In addition, the causes of pathological intracellular changes can be diabetes mellitus, glomerulonephritis, amyloidosis.

Most often, the degenerative process leads to a significant decrease or complete loss of organ functionality. With hepatic dystrophies, the patient quickly falls into a coma. Hepatic coma can occur in both acute and chronic pathological processes. Pathology develops with infectious diseases, significant intoxication with genototropic toxins, cirrhotic processes.

The clinical picture in the early stages of the disease is erased. Symptoms of the disease that provoked pathological metabolic disorders appear, but the pathology itself does not manifest itself. Symptoms of liver dysfunction may include:

A symptom of disorders in the liver is pain in the right hypochondrium

• pain in the right hypochondrium;
• nausea and vomiting;
• defecation disorders;
• jaundice;
• loss of appetite, weight loss.

In a pathological examination of micropreparations of the liver, heart or kidneys affected by hydropic dystrophy, external signs of pathology do not have a pronounced manifestation. Pathological changes are revealed under microscopic examination. Under a microscope, one can observe that the cells are enlarged and contain organelles filled with clear liquid. With a balloon type of pathology, the resulting vacuoles take the form of balloons, the nucleus shifts to the edges of the cell, and the structural elements are destroyed.

Diagnostics

To understand how to treat the disease, it is necessary to conduct a thorough diagnosis, to find out the causes of the pathological process. Held biochemical analyzes, the tissue of the affected organ, obtained by biopsy, is studied. If pathological changes become critical, patients are more likely to develop a coma. It is possible to determine the risk of coma by such signs as the characteristic "clapping" tremor of the limbs, as well as changes in the electroencephalogram.

To assess changes in the structure of an organ, clinical researches, allowing visual observation of the affected area: CT, MRI, ultrasound. But since hydropic degeneration practically does not change appearance of the affected organ, the most informative diagnostic method is microscopic examination of tissues.

Treatment

If parenchymal dysproteinoses are detected, treatment can be carried out with the help of antibiotics, potassium preparations, glucose solution. In order to cure any liver disease, a strict diet is essential. If dysproteinosis is suspected, doctors immediately limit the intake of proteins from food. The recommended dose of protein components is 50 g per day, but in severe cases, the protein is completely excluded.

Bowel movements are shown at least twice a day

Bowel movements are indicated at least twice a day. For additional cleaning, enemas are used. Antibiotics are prescribed to suppress the vital activity of the intestinal microflora. With a significant decrease or complete loss of liver functionality, a glucose solution is prescribed and glutamic acid to evacuate excess ammonia.

Anti-inflammatory drugs are prescribed nonsteroidal drugs in significant dosages. If the patient is in a coma, then the drugs are administered by diffuse methods. Blood transfusions and hemodialysis are also carried out.

The prognosis of the disease is extremely unfavorable. AT acute conditions death can occur within a few days. In other cases, a rapidly progressing cirrhotic process begins to develop in the affected organ.

Other types of liver dystrophy

In addition to hydropic, proteinaceous dystrophy can be granular and hyaline. Granular dystrophy is characterized by the fact that an uncharacteristic granularity formed by proteins appears in the cytoplasmic fluid of functional liver cells. Hepatocytes become swollen, increase in size, differ in cloudy contents. For hyaline-drop dystrophy, a decrease in functional cells in size is characteristic. This type of degenerative parenchymal change occurs as a result of increased cell wall permeability, excessive fluid loss, and consequent protein densification.

Fatty degeneration

Fatty degeneration of the myocardium - the pattern on the muscle fibers is smoothed out, and the organelles are split

Lipid degeneration is characterized by the accumulation of fat cells in areas where they should not be, and excessive accumulation in areas where they are normally present. Most often it occurs in the liver, myocardium and kidneys. Fatty degeneration of the myocardium begins with the so-called pulverized obesity. Minor inclusions of lipids appear in the functional cells of the heart muscle. While focal small droplet degeneration is proceeding, significant changes in the structure of the organ do not occur.

With the progression of the pathological process, these inclusions increase, connect with each other, and, in the end, displace the cytoplasm. Fatty degeneration of the myocardium is characterized by the fact that the pattern on the muscle fibers is smoothed out, and the organelles are split.

In the initial stages of pathology, it is very difficult to determine it macroscopically. It is possible to diagnose pathology only by examining a micropreparation obtained by biopsy, if fatty degeneration of the liver occurs, for example.

With the development of the transformation process, it can already be seen with the naked eye. If large-drop fatty degeneration of the liver progresses, then the structural elements of the organ increase in size, the walls become thinner. In a pathological examination on a section of the organ, fatty inclusions in the form of dirty yellow stripes can be observed.

carbohydrate degeneration

Most often, this condition is observed due to glycogen metabolism disorders, provoked by the progression of diabetes mellitus or glycogenosis. The body stores glycogen in case of unexpected hunger and stores it in the liver and muscle fibers, and releases the energy resource only in exceptional situations. Such situations include, for example, diabetes mellitus. With the progression of this disease, the pancreas does not produce insulin, as a result of which glucose ceases to accumulate in tissues and is excreted from the body. The body experiences a shortage of energy resources, and begins to use up the reserve. First of all, the glycogen contained in the liver is consumed, as a result of which the dystrophic process occurs. Peculiar vacuoles, empty spaces appear in the structure of hepatocytes, as a result of which they become light.

Glycogenoses are most often provoked by insufficient synthesis of enzymes necessary for the accumulation of glycogen. Diagnosis is carried out with the help of studies of micropreparations obtained by biopsy.

Mesenchymal dystrophy

This condition develops against the background of amyloidosis. As a result of violations of protein metabolism in cells, a protein-polysaccharide complex is formed, called amyloid. Such pathologies are detected by methods morphological studies, since the clinic is not expressed. With the progression of amyloidosis, functional liver cells atrophy, amyloid is deposited throughout the entire lobe of the organ, compresses the beams of the liver.

For any form of hepatic dystrophies, the prognosis is unfavorable. As a rule, with the rapid progression of the pathology, a lethal outcome occurs in the shortest possible time.

Video

Symptoms of fatty liver disease.

FATTY DYSTROPHY(syn. dystrophic obesity) - a violation of the metabolism of cytoplasmic fat, accompanied by damage to cellular structures; It is expressed in an increase in the amount of fat in cells that normally contain it, in the appearance of fat where it is not usually found, and in the formation of an unusual chemical in cells or in the extracellular substance of fat. composition.

Zh.'s development is usually connected with oxygen starvation(tissue hypoxia), so it is often found in diseases of the cardiovascular system, hron, lung diseases, anemia, hron, alcoholism, etc. Zh. occurs with many infections (diphtheria, tuberculosis, sepsis, etc.) and intoxications (phosphorus, arsenic, chloroform, dichloroethane, etc.), leading to metabolic disorders, sometimes with beriberi and one-sided low-protein nutrition, accompanied by a deficiency of enzymes and lipotropic factors. Zh.'s development can also be associated with a hereditary deficiency of enzymes that metabolize certain types fats (lipoids), which leads to the development of hereditary systemic lipoidosis (see Lipidoses).

The appearance of fat in a cell or intercellular substance during iron can be associated with its intake from the blood and lymph (fatty infiltration), the breakdown of fat-protein complexes of the ultrastructural components of the cell (fat decomposition, or phanerosis), with increased formation of fat from carbohydrates and proteins ( fat transformation), perverted synthesis. In some cases, these mechanisms are combined or replace each other. The predominance of one or another mechanism of development of Zh. simple obesity (see), connected with infiltration by fat of cytoplasm of a "healthy" cell.

Most often, iron is observed in parenchymal organs - the heart, liver, kidneys, in the cells of which fat is detected using a number of histochemical methods of investigation (see): Sudan III and scarlet stain it red, Sudan IV and osmium acid - black, Nile blue sulfate colors fatty acids dark blue, and neutral fats red. In the heart, dust-like or small-drop obesity of muscle cells is found, developing hl. arr. by lipofanerosis: most of the mitochondria disintegrate, the transverse striation of the fibers disappears, the nucleus becomes pyknotic or undergoes lysis. The process has a focal character and is observed in groups of muscle cells along the venous blood capillaries and venules. Accumulations of such fibers have the form of yellow-white stripes (printing. Fig. 5), which are clearly visible under the endocardium of the ventricles, especially in the region of the papillary muscles and trabeculae. The endocardium becomes striated and spotted ("tiger heart"). The heart with Zh. increases in size, its chambers are stretched, the myocardium is flabby, clay-like.

About Zh. (obesity) of a liver speak when the amount of the fat which is contained in hepatocytes in norm sharply increases and its qualitative structure changes. Obesity can be pulverized, small or large drops (Fig. 1 and 2). The fat drop pushes relatively intact organelles to the periphery of the hepatocyte, which becomes cricoid. The process involves single hepatocytes (the so-called disseminated obesity), groups of hepatocytes (zonal obesity) or the entire liver parenchyma (diffuse obesity). In cases of hypoxia and intoxication, obesity of hepatocytes occurs mainly centrolobular, in other cases (protein-vitamin deficiency, obesity, hyperlipidemia) - Ch. arr. periportally. With a sharp fatty infiltration, hepatocytes die, fat drops merge and form fatty cysts, around which a cellular reaction occurs, connective tissue develops. The liver at Zh. is increased, flabby, yellow or red-brown coloring.

Zh. of the kidneys often has a resorptive character (resorptive obesity), that is, it is associated with infiltration of the epithelium of the proximal and distal nephrons (printing. Fig. 6) and stroma with fat in hyperlipidemia, so characteristic of nephrotic syndrome of any etiology. Normally, fat is found in the epithelium of the thin segment (the loops of Henle), the intercalary sections of the tubules and collecting ducts. Usually it is neutral fat, cholesterol, phospholipids. Fatty infiltration leads to an increase in the size of the kidneys, expansion of the cortical substance, in which yellow blotches appear, visible on the surface and incision of the renal parenchyma.

Zh. of walls of vessels (arteries) is the cornerstone of atherosclerosis (see). At the same time, not only cholesterol and its esters, but also beta-lipoproteins and plasma proteins accumulate in the intima of the arteries. Accumulating macromolecular substances lead to the destruction of the intima, disintegrate and saponify. As a result, fat-protein detritus is formed in the intima, connective tissue grows, and a fibrous plaque is formed.

With hereditary lipoidosis, cerebrosides (see Gaucher disease), sphingomyelins (see Niemann-Pick disease), gangliosides (Tay-Sachs disease and generalized gangliosidosis), cholesterol and its esters (familial hypercholesterolemic xanthomatosis) can accumulate in tissues.

Railway leads to disruption or loss of the function of the organs in which dystrophy develops. Zh. d. myocardium, for example, very often is morphol, an expression of heart failure (see), and Zh. d. kidneys - morphol. expression of a nephrotic syndrome (see). In the liver against the background of Zh., cirrhosis develops. Fatty infiltration of the inner lining of the arteries may be one of the causes of impaired vascular patency.

The outcome Zh. depends on its expressiveness. If it is not accompanied by deep damage to cellular structures, then it is, as a rule, reversible. Deep breach The exchange of cellular fat leads to cell death.

Bibliography: Davydovsky I.V. General pathology person, s. 89, Moscow, 1969; Ivanovskaya T. E. and Tsinzerling L. V. Pathological anatomy, p. 26, M., 1976; Serov V. V. and Spiders V. S. Ultrastructural pathology, p. 142, M., 1975; Handbuch der allgemeinen Pathologie, hrsg. v. F. Biichner u. a., B. u. a., 1968; Molecular Biologie der Zelle, hrsg. v. H. Bielka and Jena, 1973.