Fatty liver hepatosis: symptoms and treatment, diet, prevention. Fatty liver degeneration - what is it?

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Normal life without fats is impossible. After being consumed with food and broken down 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, and participation in biochemical reactions.

Describing what fatty liver disease is, symptoms and treatment, which have specificity, we note disruptions in the process of natural lipid utilization by hepatocytes with high fat accumulation (over 50%). The cytoplasm, vacuoles and some other intracellular organelles are saturated with fats and therefore cannot perform functions. Physiologically concentration fatty acids inside liver cells does not exceed 5%. In case of 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 fatty tissue leads to the death and degeneration of the liver parenchyma. Morphologically, with this nosology, small accumulations (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 fat intracellular metabolism. Blocking biochemical reactions makes it difficult to physiologically utilize compounds, and excess cholesterol accumulates in lysosomes;
• In diabetes mellitus, the mechanisms of biochemical transformation of lipids are also disrupted. 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 fat. Excessive accumulation leads to the absence of excretion pathways, so intracellular infiltration occurs;
• Metabolic diseases ( protein deficiency) disrupt transport processes between the liver and other tissues;
• Poisoning with hepatotoxic poisons and drugs.

The described provoking mechanisms are the result of practical observations, but the pathogenetic links of the 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 ethyl alcohol consumption has several synonyms: “hepatosteatosis”, “fatty liver”, “steatohepatitis”. Varieties reflect the diversity of pathogenetic mechanisms of the 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, have different morphological manifestations. When examining a biopsy sample (a section of tissue), several morphological types 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 granulation. The basis for its appearance is the destruction of the protein-lipid complex that is part of the organelles.

Clinical symptoms of the form are due to the underlying disease:

• Pain in the right hypochondrium;
• The appearance of linear dilations of blood vessels on the abdomen;
• Capillary stars (telangiectasias) throughout the body.

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

The classic sign of parenchymal fatty degeneration in a histochemical study is a single large vacuole filled with fatty inclusions, pushing the nucleus to the periphery.

A morphological examination reveals yellowish, dull tissue. When 50% of cells degenerate, 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 individual liver cells;
3. Diffuse obesity is characterized by damage to the entire lobule, but the process is reversible.

In diabetes mellitus, the manifestations of hepatosis are not specific. Fatty degeneration occurs due to impaired 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. In tissue biopsies, empty nuclei are observed, the number of vacuoles increases.

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

The described changes cause symptoms depending on the degree of liver failure. The absence of clinical symptoms when a small number of cells die is 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 due to impaired bile secretion;
• Encephalopathy due to poisoning with toxins, ammonia;
• Skin rashes, itching, increased bilirubin concentration;
• Pain syndrome under the ribs on the right; enlarged liver size, cirrhosis.

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

Treatment of dystrophic conditions of the liver

Alcoholic steatosis is considered by doctors as dangerous condition, leading to death. The nosology provokes dangerous complications with an average degree of degeneration (about 35% of the tissue).

The initial stages of the disease can be controlled by prescribing medications and stopping alcohol consumption; severe stages are characterized by high mortality. Approximately 5% of people die within a month when cirrhosis is diagnosed.

There are no specific drugs, so symptomatic therapy is carried out with essential phospholipids (Essentiale), choleretic agents(ursodeoxycholic acid), ademetionine, 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 is prednisolone.

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

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

In the practical literature there are indications of the need proper nutrition, increasing patient survival.

Principles of treatment of lipid degeneration of hepatocytes

• Elimination of risk factors;
• Drug management 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 to gradually reduce body weight. Optimal balance: weekly elimination of more than one and a half kilograms increases the risk cholelithiasis, so you need to be careful when following a diet.

Features of dietary nutrition:

• The calorie content of the diet is no more than 1200 kcal per day;
• Limiting saturated fatty acids in food;
• Carbohydrates are no more than 100 grams per day, but nutritionists can reduce this norm.

Daily physical exercise promote better absorption of fats, accumulation of oxygen inside muscle fibers, which increases triglyceride consumption.

In diabetes mellitus, the cause of obesity is insulin resistance. The factor helps convert excess carbohydrates into fats. Correction of insulin tolerance is achieved by pharmacological agents: thiazolidinediones and biguanides.

Elimination of high levels of triglycerides is achieved by regular use of medications containing unsaturated fatty acids. Ursodeoxycholic acid products have been used for ten years and have shown high effectiveness. The mechanisms of therapeutic activity have not been proven, but the elimination activity of the drug to eliminate congestive changes in the gallbladder and intrahepatic ducts has been identified.

In severe liver failure, the protein content in the diet is limited. The daily content is no more than 50 grams. To cleanse the gastrointestinal tract, laxatives are prescribed daily, cleansing enemas. Dysbacteriosis is eliminated by administering 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 treated with haloperidol.

Treatment 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 drug. If the pathology is detected in a timely manner, choleretic infusions of immortelle, milk thistle, and rose hips help at an early stage.

Herbal infusions reduce the activity of the chronic process, but only for certain nosologies. Therapeutic effect Herbal decoctions and infusions, when compared with medications, appear later, so the combination of drugs with plants is rational. If the process activity is low, you can use pumpkin:

• Select a ripe fruit and cut off the top edge in a circle. Remove the central part and add light honey to the resulting cavity. Cover the fruit and store in a dark place for 2 weeks. Pour 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. Take a teaspoon three times a day.

Milk thistle is part of the popular hepatoprotectors carsil and 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 and 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 effectiveness, it is recommended to combine folk remedies with diet and exercise.

Features of the diet for dystrophic damage to hepatocytes:

• Avoid hot, spicy foods;
• Avoid fatty meat, fish, broths;
• Choose products carefully in the store. They must not contain dyes, stabilizers, flavors, or anti-caking additives;
• Do not take a lot of medications unless necessary;
• Oatmeal and buckwheat porridge are healthy.

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

What exactly is liver dystrophy?

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

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

Causes of liver dystrophy

Steatosis usually occurs due to the following reasons:

• Intoxication with various hepatotropic poisons (poisonous mushrooms, yellow phosphorus, etc.);
• Diabetes;
• Frequent drinking of alcoholic beverages;
• Abuse of foods that contain huge amounts of preservatives and fats;
• Obesity or prolonged fasting;
• Parenchymatous protein dystrophy;
• Uncontrolled use of certain medications;
• Drug addict;
• Pituitary tumors.

Classification

Firstly, 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 strong enough.
• Disseminated widespread dystrophy. Fatty formations are nearby and significantly denser in the human liver. Symptoms: general weakness and discomfort in the right hypochondrium.
• Disseminated focal dystrophy. It is characterized by sparse, pinpoint and inconsistently located fat formations. Symptoms are not expressed.
• Diffuse dystrophy. This type of liver dystrophy is characterized by an abundant amount of fatty inclusions, which can be in place of the entire liver or on 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 may form near the dead cells.
• Stage three - liver changes can no longer be prevented, some areas of the liver die, and cirrhosis eventually develops.

Why is liver dystrophy dangerous?

Liver dystrophy is a truly serious disease that should never be overlooked or not paid due attention to specific symptoms.

Therefore, if a person with steatosis does not want to start treatment, then he can subsequently 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 liver cells often have no complaints about their physical state, since in the initial stages liver hepatosis is painless and outwardly imperceptible.

The disease goes away over a period of time long period. Over time, the patient begins to experience unpleasant sensations in the form of:

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

Most a rare case is liver dystrophy with clearly presented clinical symptoms. Among them we can highlight:

• sudden 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 amount special types proteins (alanine aminotransferase (ALT) and aspartate aminotransferase (AST)), which tend to increase due to liver dystrophy.
• Ultrasound of the abdominal cavity. It immediately detects echo signs of hematosis and allows an accurate diagnosis to be made.
• Liver tests.

Treatment of the disease

Before we talk about medications that help relieve symptoms and cure the disease, it should be noted that without following a certain diet, any medications will not work to their full potential and will not help as much as we would like. Often, diet therapy alone is enough for recovery.

Only if proper nutrition recommended by a doctor does not help get rid of liver dystrophy should you introduce medicinal methods treatment. From a wide selection of medications, drugs that help to get rid of liver hepatosis can be used:

• breakdown of fats,
• removing it from the body.

It should be emphasized that it is necessary to repeat this course of treatment 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 liver functioning and perform a protective function against cell membranes,
• immunomodulatory drugs that strengthen the body.

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

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

You should definitely find out from a medical specialist what specific physical activities you should do.

Diet for illness

Nutrition for fatty hepatosis must be carefully thought out so that the daily diet includes the maximum amount healthy products rich:

The amount of fat should be reduced to a minimum.

Basic rules of diet for lipodystrophy:

• Consume at least one hundred grams of protein per day;
• Completely abstain from alcoholic beverages;
• 2/3 of proteins should be of animal origin;
• Do not eat a large amount of food at a time, i.e. eat in small portions;
• Do not consume more than twenty percent fat from total number food for the day;
• Reduce consumption of preservatives and purine substances.

Diet should be looked at in more detail and necessary products nutrition for liver hepatosis.

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

You should also use, quite often, cottage cheese and sour cream with no high content:

It is necessary to avoid rich vegetable or meat broths. It is important to refuse:

• fatty meats and fish,
• mushrooms,
• tomatoes,
• legume products,
• raw onions and garlic,
• various smoked and canned foods.

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

• clean drinking water,
• decoctions of medicinal herbs,
• 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 preventing disease is maintaining proper nutrition, including necessary components, which are rich in vitamins and microelements beneficial for the liver.

You also need to regularly undergo specific medical checks, which are carried out in the initial periods of development. fatty liver disease. This will undoubtedly help prevent further development of the disease. Moreover, in the later stages it is much more difficult to correct the situation, and sometimes it is no longer possible.

The question of what liver dystrophy is is of interest to many patients who are faced with similar diagnosis. As doctors explain, this is a comatose state that arose as a result of deep depression of liver functionality. Liver dystrophy (LD) 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 important role in lipid metabolism. Triglycerides from food enter the intestines, where they are broken down by enzymes, and then enter the 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 is reduced. 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, a lack of glucose in the liver appears. Glucose is very important for the normal functioning of liver cells, so if there is a deficiency of the substance, they begin to die. The affected cells are eventually replaced by adipose tissue. As a result, liver function disorders appear.

Hepatocytes become resistant to the effects of insulin due to genetic pathologies or violations metabolic processes. The lack of a normal response of liver cells may be due to immune aggression towards insulin.

Other causes of DP:

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

All these factors negatively affect the condition of the liver, causing 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 clinical picture not explicit.

However, over time, the following signs appear:

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

IN in rare cases dystrophic changes in the gland are accompanied severe pain in the abdomen, sudden weight loss, itching, yellow discoloration of the skin and mucous membranes.

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

Liver lipodystrophy

Fatty liver degeneration (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 pathology of the gallbladder, its duct or intestinal tract. FLD (fatty liver) can cause the following diseases:

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

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

Macroscopic specimen characteristic of HDP: hepatomegaly, the surface of the liver is smooth, the consistency is dense or flabby, the anterior edge of the organ is round, clayey, yellow or yellow-brown.

Toxic DP

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

Massive necrosis develops under the influence of toxins found in foods, such as mushrooms. Such poisonings occur under the influence external factors. Toxic liver dystrophy can occur as a result of endotoxemia. Similar conditions include toxicosis in pregnant women and hyperthyroidism (excess 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 tissue, the organ is painted yellow. If left untreated, the size of the gland decreases and the capsular membrane becomes wrinkled. The organ becomes gray in color and resembles a clay mass in appearance. Over the course of 3 weeks, the iron 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 occurrence that increases the likelihood of patient death due to rapidly progressing liver dysfunction.

Acute hepatic dystrophy

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

The disease has been 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 whether 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 have a detrimental effect on liver cells, causing severe dystrophy.

Symptoms of ADP on early stage resemble signs of hepatitis A, so there is a risk of significant deterioration of the patient’s condition. The pathological process affects the nervous system and, as a result, is disrupted brain activity. The disease is manifested by delirium, anxiety, convulsions, and vomiting. In this case, the patient must be urgently hospitalized in a psychiatric department.

The opposite reaction is also possible nervous system: indifference to everything that happens, depression, decreased vitality, craving for sleep. Symptoms continue to increase, the patient loses consciousness, and hepatic coma develops.

Alcoholic dystrophy

This type of dystrophy occurs due to excessive consumption of alcoholic beverages for 10–12 years. Ethyl alcohol penetrates the body and poisons hepatocytes.

Alcoholic liver dystrophy (ALD) can occur against the background of hepatosis, cirrhosis, and alcoholic hepatitis. Most often, it is hepatosis that causes gland dystrophy due to excessive consumption of alcoholic beverages. If the patient gives up strong drinks at the early stage of hepatosis, the condition of the liver improves after 2–4 weeks. In most cases, ADP does not cause significant symptoms.

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

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

Diffuse dystrophy

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

Focal DP, which arose as a result of excessive consumption of alcoholic beverages, is manifested by shortness of breath, decreased appetite, and 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 cell cytoplasm, in which a grain-like protein appears.

ZDP is provoked by the following factors:

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

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

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

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

Protein DP

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

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

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

Hydropic dystrophy

Hydropic liver dystrophy (HDL, vacuolar dystrophy) is accompanied by the appearance of vacuoles (cavities in the cell cytoplasm), which are filled with cytoplasmic fluid. With pathology, the parenchyma cells of the organ increase, which is accompanied by shrinkage or vacuolization of the nucleus.

As the disease progresses, the liver becomes filled with fluid, and its ultrastructures undergo decomposition. The affected cells look like containers filled with water and are a solid cavity with a bubble-shaped core. This is how GDP manifests itself.

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

Yellow liver dystrophy

VDP is often a complication of pregnancy. The pathology occurs as a result of acute poisoning of the body against the background of infectious diseases. I have jaundice expectant mother can provoke DP, inflammation of the gallbladder, and stones in the liver. In addition, the disease can occur independently due to autointoxication of the body (toxicosis).

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

Diagnosis of the disease

Diagnosis of DP is difficult, since traditional laboratory research turn out to be 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 normal limits, and sometimes even increases, so it is quite difficult to distinguish DP from cirrhosis or fibrosis. Ultrasonography allows you to identify areas with increased echogenicity. Areas of low echogenicity can be identified using CT. Computed tomography 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 identify pathology. During a pathological examination of tissues, the doctor will determine excess accumulation of fat.

Treatment methods

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

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

Typically, doctors prescribe the following medications:

• hepatoprotectors,
• synthetic antioxidants,
• statins.

Hepatoprotectors stabilize cell membranes and restore their integrity. They improve the metabolism of bilirubin, fatty acids, and 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. For DP, Allochol and Holosas are prescribed.

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

If hepatic encephalopathy is observed during DP, the patient is urgently hospitalized. The patient is administered drugs parenterally, and the amount of proteins is limited. In addition, medications are prescribed that correct the acid-base state. Acidosis often occurs with DP; sodium bicarbonate is administered to prevent it. Antibacterial agents suppress intestinal microflora.

For functional liver disorders, extracorporeal enterosorption is prescribed. To support metabolism, glucocorticoids are used.

To reduce the load on the liver and speed up recovery, it is necessary to review the menu. The diet should include foods containing vitamins, fiber, pectins, and carbohydrates. Daily norm fat – 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 skim milk. It is recommended to eat 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, it is not prohibited dairy products with a low fat percentage.

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, overuse food (especially fatty), passive lifestyle.

To maintain high vitality and prevent the development of pathological processes, you should eat properly, limit the consumption of hot, fried foods, smoked and canned foods. In addition, the patient should constantly monitor his weight and maintain it within normal limits.

In order for the liver to function normally, you should exercise daily: race walking, jogging, swimming, etc.

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

If the patient leads an incorrect lifestyle and does not engage in treatment, then the pathology progresses. Then the likelihood of small-nodular cirrhosis and non-alcoholic steatohepatitis increases.

If during treatment for DP the patient abstains from alcohol and follows the diet and doctor’s recommendations, then most likely he will be able to maintain working capacity and improve his general condition.

Based on all of the above, liver dystrophy is dangerous disease with a chronic course, which occurs as a result of deep inhibition of the functionality of the gland. To prevent dangerous complications, you must be attentive to your health and, if suspicious symptoms occur, contact a hepatologist or gastroenetrologist. 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 conduct healthy image life.

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Description:

Liver dystrophy is a comatose state that is associated with profound depression of liver functionality. Hepatic coma occurs due to acute or chronic.

Symptoms:

There are several types of dystrophy syndrome.

Parenchymal protein dystrophy.
There are granular, hydropic and hyaline protein dystrophy.

With granular dystrophy, coarse protein grains appear in the cytoplasm of hepatocytes. Liver cells increase in volume, look swollen, cloudy (turbid swelling); in their cytoplasm the content of protein and water increases, which is in the form of grains and coagulates. Histochemical examination shows a decrease in the intensity of the reaction to total and basic protein, ribonucleoproteins. Dystrophy is based on the breakdown of the protein-lipid complex that is part of the membranes of organelles. With granular dystrophy, water-salt metabolism is disrupted, the intensity of redox processes, oxidative phosphorylation occurs, and accumulation occurs. acidic foods exchange. Granular dystrophy is of a compensatory-adaptive nature, as a rule, does not entail functional liver failure and is a reversible process. This is the most common type of damage to hepatocytes under various pathogenic (viral, bacterial, toxic) influences (mild form of chronic, inactive forms of cirrhosis, etc. )

Hydropic dystrophy is characterized by light swelling of cells (in contrast to the cloudy swelling in granular dystrophy). Hepatocytes are increased in volume, their cytoplasm appears optically empty, the content of protein and glycogen, the activity of oxidoreluctases are reduced, and the activity of hydrolases is increased. The most pronounced form of hydropic dystrophy is balloon dystrophy, which is irreversible at the height of development, which indicates the transition of the process to colliquation. In this case, the cytoplasm is optically empty and does not give histochemical reactions. Hydropic dystrophy occurs in patients with viral hepatitis (especially in severe and moderate forms), in the dystrophic form of cirrhosis, in long-term intra- and extrahepatic cholestasis, etc.

Hyaline droplet dystrophy is characterized by a decrease in the size of hepatocytes, homogeneous cytoplasm, intensely stained with acidic dyes (such as eosin), which served as the basis for calling this type of acidophilic dystrophy. An increase in the number of PAS-positive structures is observed. This type of dystrophy is associated with impaired permeability of cell membranes, loss of fluid and physicochemical changes in protein. As a result, protein substances become more dense and homogeneous. Hyaline dystrophy observed under various pathogenic influences, especially viral etiology.

Parenchymal fatty degeneration.
It is characterized by the accumulation of small fat droplets in the cytoplasm of hepatocytes, which then merge into larger ones or into one fat vacuole, which occupies the entire cytoplasm and displaces the nucleus to the periphery of the cell.

With severe obesity, the liver tissue on the section is dull and yellow in color. If more than 50% of the liver parenchyma is obese, they speak of fatty hepatosis. When stained with hematoxylin and eosin, light, unstained vacuoles (drops) of a round or oval shape are visible in the liver cells. Fat drops can merge and fill the entire cytoplasm of the hepatocyte. In severe obesity, hepatocytes overflowing with fat rupture, and fat droplets, merging with each other, form fatty “cysts.”

The following polymorphological forms of fatty liver are distinguished.

disseminated obesity, in which fat droplets are contained in individual hepatocytes (observed mainly under physiological conditions)
zonal obesity, when the central, intramural or peripheral zones of the hepatic lobule are affected by obesity;
diffuse obesity, i.e. obesity of the entire (or almost all) hepatic lobule. liver is reversible. It can be large-droplet or small-droplet:
Large-droplet (macroscopic) obesity is characterized by the presence of “empty” vacuoles in hepatocytes with a displacement of the nuclei to the periphery.
In small-droplet obesity, the fat droplets are small, while the nuclei with distinct nucleoli are located in the center, necrosis of the liver cells is expressed to varying degrees.
- Parenchymal carbohydrate dystrophy.
In clinical practice, glycogen metabolism disorders, which are more common in diabetes mellitus and glycogenosis, are of leading importance. In diabetes mellitus, the glycogen supply in the liver cells is significantly reduced, the content of which decreases by 30-50 times. At the same time, the accumulation of glycogen in the nuclei of hepatocytes is noted, which creates a picture of their peculiar vacuolization (“empty” nuclei). The most pronounced ones in the liver occur with glycogenosis - enzymopathies caused by a deficiency of enzymes involved in the breakdown of glycogen. Currently, there are more than 10 types of glycogenosis. With glycogenosis, the glycogen content in the liver tissue increases sharply, hepatocytes increase in size, are very weakly stained with eosin, due to this their cytoplasm looks “optically empty”, light, poorly sensitive to color, hyperplastic smooth ER, a few large lysosomes, cell membranes clearly contoured.

When stained with hemotoxylin and eosin, optically empty vacuoles of a round or irregular oval shape, 4-8 μm in diameter, are visible in the nuclei of hepatocytes, which are limited by a clear membrane that readily accepts basic dyes. Nuclear hyalinosis most often occurs in diabetes mellitus, diseases of the gallbladder and pancreas. Sometimes excessive glycogen deposition is observed in the nucleus - glycogenosis of hepatocyte nuclei. Due to the increase in cell size, the sinusoids are significantly reduced. In preparations stained with hematoxylin and eosin or by the Van Gieson method, “empty” cells are also revealed, reminiscent of the picture in balloon dystrophy, but the size of hepatocytes in glycogenosis is much larger than in balloon dystrophy. With glycogenosis, a sharply positive PAS reaction is observed in the cytoplasm of cells, which disappears after treatment of control sections with diastase or amylase. The outcome of glycogenosis types III and IV can be.

In case of chronic liver damage, a violation of the content of glycoproteins is observed. With fucoidosis, deposition of glycolipids containing MPS and fucose is observed in the liver tissue.

Antitrypsin deficiency often leads to hepatocyte dystrophy; antitrypsin is synthesized in the liver. With its deficiency, liver cirrhosis develops, and in 10% of patients. Antitrypsin deposition is associated with the absence of sialic acids and a defect in sialotransferases involved in the functioning of the Golgi complex. characteristic feature Antitrypsin deficiency is the deposition of round weakly acidophilic PAS-positive granules, resistant to diastase, in the cytoplasm of hepatocytes. The granule sizes range from 1 to 40 microns. In the absence of cirrhosis, granules are located predominantly in periportal hepatocytes; in cirrhotic livers, in hepatocytes adjacent to fibrous septa. A final diagnosis is possible only after immunomorphological detection of antitrypsin.

Mesenchymal dystrophy
These liver lesions occur in primary and secondary amyloidosis. Clinical manifestations of the liver are insignificant, so morphological research methods become of great importance. Microscopically, with amyloidosis, deposits of structureless homogeneous zosinophilic masses of amyloid are found between stellate reticulosindotheliocytes along the reticular stroma, in the walls of blood vessels and bile ducts and in the portal tracts. The intermedial part of the acini is predominantly affected. When the process is pronounced, the substance is deposited throughout the lobule, compresses the hepatic beams, and hepatocytes are exposed. Amyloid is stained with Congo red and in polarized light gives a picture of dichroism (brown-red color turns green). Amyloid deposits are similar in primary and secondary amyloidosis, but in primary amyloidosis the liver vessels are isolated, while there is no amyloid in the space of Disse.

Causes:

Hepatocellular coma, in most cases, is caused by acute viral hepatitis. Sometimes it occurs due to poisoning with genototropic poisons (poisonous mushrooms, towle nitrates, etc.), sometimes from the use of atophan, halothane, etc. Portocaval coma is a consequence of liver cirrhosis and occurs after infection. It happens that portacaval coma occurs due to irrational treatment with diuretics, as well as from improper use of sedatives and hypnotics.

Treatment:

For treatment the following is prescribed:

When signs of precoma appear, it is necessary to sharply limit the amount of protein in the daily diet to 50 g, and if further progression disease, stop introducing proteins by mouth.

The intestines are cleansed daily with an enema and laxatives; antibiotics that suppress the intestinal microflora are administered orally or through a tube (kanamycin 2-4 g per day, ampicillin 3-6 g per day, tetracycline 1 g per day). Vitamins, cocarboxylase, potassium preparations, glucose, and abundant parenteral fluid administration are used.

To neutralize blood ammonia, 1-arginine (25-75 g per day in a 5% glucose solution) and glutamic acid (30-50 g in a 10% solution) are administered. At psychomotor agitation haloperidol, GHB, chloral hydrate (1 g in enema) are prescribed. In case of development, a 4% solution of sodium bicarbonate is administered at a dose of 200-600 ml per day; in case of severe metabolic alkalosis, large amounts of potassium are administered (up to 10 g per day or more).

Glucocorticosteroid hormones are prescribed in large doses; prednisolone in precoma - 120 mg per day, of which 60 mg intravenously, in the coma stage - 200 mg per day intravenously; hydrocortisone up to 1000 mg per day intravenously. The use of diuretics is strictly contraindicated.

In recent years, for hepatic cell coma, exchange (5-6 liters daily), extracorporeal blood perfusion through the heteroliver or cadaveric liver, or cross-circulation have been used. The effectiveness of heterotopic liver transplantation is questionable.

When hepatic coma develops in patients, peritoneal or extracorporeal therapy is performed, which is very important to prescribe in a timely manner.

Forecast. In most cases, death occurs within a few days. With subacute liver dystrophy, a possible outcome is rapidly developing cirrhosis of the liver.

Hydropic and its pronounced manifestation - balloon dystrophy - are types of parenchymal dysproteinosis. This term in pathological anatomy refers to dystrophic changes caused by disturbances primarily in protein metabolism in the cells that make up the structure and provide the functionality of an organ, that is, its parenchyma.

Dystrophy is changes caused by disturbances in protein metabolism in liver cells

Classification of parenchymal dystrophies

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

• infiltration - in this case, due to disturbances in the production of enzymes, an excess amount of metabolic products enters the cells;
• decomposition - consists in the dissolution 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;
• production of abnormal chemical compounds by cells;
• changing the nutrient organic compounds entering the cell 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 appearance, the prevalence of the pathological process, the morphological changes that occur, as well as the type of substances accumulated in the parenchyma due to metabolic disorders.

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

In addition to hydropic dystrophy, which relates to disorders of predominantly protein metabolism, dysproteinoses also include hyaline-droplet and horny dystrophies, as well as primary aminoacidopathies.

Hydropic dystrophy is swelling of the cells that make up the parenchyma of an organ susceptible to pathological changes

Hydropic dystrophy is also called vacuolar dystrophy and is a swelling of the cells that make up the parenchyma of an organ susceptible to pathological changes. Mild cellular edema is reversible. If the process takes 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 is that new intracellular formations are formed - vacuoles - filled with light liquid.

Symptoms

Hepatic hydropic dystrophy is most often provoked by hepatosis or viral and toxic hepatitis. In addition, pathological intracellular changes can be caused by diabetes, 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 comatose state. Hepatic coma can occur in both acute and chronic pathological processes. Pathology develops in infectious diseases, significant intoxication with genototropic toxins, and 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 in any way. Symptoms of liver dysfunction may include the following:

A symptom of liver dysfunction is pain in the right hypochondrium

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

During pathological examination of microspecimens of the liver, heart or kidneys affected by hydropic dystrophy, external signs of pathology do not have a pronounced manifestation. Pathological changes are revealed by microscopic examination. Under a microscope, it can be observed that the cells are enlarged in size and contain organelles filled with clear liquid. With the balloon type of pathology, the formed vacuoles take on the appearance of balloons, the nucleus moves to the edges of the cell, structural elements destroyed.

Diagnostics

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

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

Treatment

If parenchymal dysproteinoses are detected, treatment can be carried out with antibiotics, potassium preparations, and glucose solution.

In order to cure any liver disease, it is imperative to follow a strict diet. If dysproteinosis is suspected, doctors immediately limit the intake of protein from food. The recommended dose of protein components is 50 g per day, but in severe cases protein is eliminated completely.

Indicated bowel movements at least twice a day It is recommended to have bowel movements at least twice a day. Enemas are used for additional cleaning. To suppress vital functions antibiotics are prescribed. If there is a significant decrease or complete loss of liver functionality, a glucose solution is prescribed and glutamic acid to evacuate excess ammonia.

Anti-inflammatory non-steroidal drugs are prescribed in significant dosages. If the patient is in a coma, then the drugs are administered by diffusion methods. Blood transfusions and hemodialysis are also performed.

The prognosis of the disease is extremely unfavorable. In 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, protein 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, and have cloudy contents. Hyaline droplet dystrophy is characterized by a decrease in functional cells in size. This type of degenerative parenchymal changes occurs as a result of increased permeability of cell walls, excessive fluid loss, and, as a result, compaction of proteins.

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 excess accumulation in areas where they are normally present.

Most often this occurs in the liver, myocardium and kidneys. Fatty degeneration of the myocardium begins with the so-called dust-like obesity. Minor lipid inclusions appear in the functional cells of the heart muscle. While focal small-droplet degeneration occurs, significant changes in the structure of the organ do not occur.

As the pathological process progresses, these inclusions increase in size, connect with each other, and ultimately 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.

As the transformation process develops, it can already be seen with the naked eye. If large-droplet fatty degeneration of the liver progresses, the structural elements of the organ increase in size and the walls become thinner. During a pathological examination, on a section of an organ, fatty inclusions in the form of dirty yellow stripes can be observed.

Carbohydrate dystrophy

Most often, this condition is observed due to disorders of glycogen metabolism, 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 uses the energy resource only in exceptional situations. Such situations include, for example, diabetes. As this disease progresses, the pancreas does not produce insulin, as a result of which glucose stops accumulating in the 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, glycogen contained in the liver is consumed, resulting in a degenerative process. In the structure of hepatocytes, peculiar vacuoles, empty spaces, appear, as a result of which they become light.

Glycogenosis is most often triggered by insufficient synthesis of enzymes necessary for the accumulation of glycogen. Diagnosis is carried out using microscopic examinations obtained by biopsy.

Mesenchymal dystrophy

This condition develops against the background of amyloidosis. Due to disturbances in protein metabolism, a protein-polysaccharide complex called amyloid is formed in cells. Such pathologies are identified using morphological research methods, since the clinical picture is not expressed. As amyloidosis progresses, functional liver cells atrophy, amyloid is deposited throughout the entire lobe of the organ, compressing the liver beams. For any form of hepatic dystrophy, the prognosis is unfavorable. As a rule, with rapid progression of pathology in as soon as possible

death occurs.

Video

Symptoms of fatty liver disease. Fatty liver degeneration is a rather dangerous disease of the digestive tract. It is characterized by the replacement of liver cells with fatty tissue, which causes the functionality of this organ to decrease. The danger of fatty degeneration is that the disease for a long time

Over time, a person begins to constantly feel nausea, vomiting, heaviness and pain in the right hypochondrium, and is faced with bowel problems and fatigue. Due to the formation of fat cells, the size of the liver begins to rapidly increase, while the organ loses its natural protective mechanisms.

Against the background of this disease, complications such as hepatitis often occur.

With fatty degeneration in the liver, various structural changes, which lead to disruption of the functioning of this organ.

Experts distinguish the following forms of this disease:

• Focal disseminated– a pathology in which numerous accumulations of fat cells are located on the liver. This form of the disease is asymptomatic for a long time.
• Severely disseminated– a liver disease in which fatty deposits are located throughout the entire area of ​​the liver. It quickly manifests itself with specific symptoms.
• Diffuse- liver disease in which adipose tissue fills all parts. With this form, the symptoms are obvious and well expressed.
• Zonal– damage to the liver tissue, in which fatty inclusions in the cells spread in certain lobes.
• Alcoholic– a rare form of the disease in which Ziewe syndrome manifests itself. Occurs as a result of alcohol, drug and other addictions.

Causes of the disease

Metabolic syndrome, or metabolic and hormonal disorders, is the most common cause of fatty liver. This disease is accompanied by an increase in blood lipid levels and the development of diabetes mellitus. This poses a serious risk of cardiovascular complications.

The following factors can provoke this disease::

Fatty liver occurs against the background of insulin resistance by cells, as well as due to disturbances in lipid and carbohydrate metabolism. Also, such a disease can develop due to excessive intake of fatty acids into the liver due to increased lipolysis or due to food consumed.

Symptoms of the disease

Symptoms of fatty degeneration depend on the degree of liver damage and the degree of development of this process. At the first stage, the disease does not show any signs; the pathology can be diagnosed only with a comprehensive examination.

Stage 2 of this disease is accompanied by the following symptoms:

At stage 3 of fatty degeneration, more serious manifestations occur, such as:

The thermal stage is characterized by the occurrence of complications such as renal failure and cirrhosis. Also added to this are shortness of breath, nosebleeds, bad smell from the mouth, loss of appetite, increased body temperature.

Fatty degeneration in pregnant women

Acute fatty degeneration in pregnant women is an extremely dangerous complication that can occur in any pregnant woman. Despite the fact that it occurs extremely rarely, the consequences of such a violation will be disastrous for both mother and child.

Can provoke liver degeneration in a pregnant woman following reasons :

• Constant attacks vomiting.
• Acute form of fatty hepatosis.
• Hepatosis with cholestasis.
• Inflammation of the liver with renal syndrome.

The first manifestations of this disorder can be detected as early as 30-38 weeks; earlier they occur in extremely rare cases.

The woman begins to complain of a feeling of lethargy, weakness, constant nausea and vomiting, and pain in the abdomen.

After some time, heartburn is added to everything, ulcers appear on the surface of the esophagus, which cause pain when swallowing. At the next stage of development, the disease is complemented by brown vomit, jaundice, ascites and anemia.

Diagnostics

The first stage of diagnostic measures is a detailed collection of anamnesis and visual inspection specialist. After this, palpation of the liver, abdomen, and tapping of the abdominal cavity are performed.

To determine the functioning of the body, it is prescribed general research and biochemical blood test, analysis for markers of liver diseases, general analysis of urine and feces.

All this is accompanied carrying out instrumental diagnostic methods:

Nutrition for liver dystrophy

In case of fatty liver degeneration, it is very important to observe special diet. It will help reduce the load on this organ, as well as restore all its basic functions. It is important to remember that you can consume no more than 50 grams of fat per day.

Also eliminate foods that are high in cholesterol from your diet. It is best to steam food, but you can stew and boil it.

Don't forget to follow following rules diets:

• Increase the amount of protein foods in your diet.
• Avoid drinking alcoholic beverages completely.
• Completely eliminate spicy, fried, salty foods.
• Drink at least 2 liters clean water in a day.
• Reduce the amount of animal fats.
• Eliminate simple carbohydrates.

Treatment of fatty liver

Unambiguous and unique correct scheme There is no cure for fatty liver. Therapy depends on the individual characteristics of the body and the degree of manifestation of the disorder. Usually therapeutic measures require the patient to exclude all provoking factors.

After this, drug therapy is carried out to restore liver tissue, stabilize metabolic processes, and eliminate toxic effects. The patient also needs to reconsider his lifestyle and start eating right.

You should not self-medicate - treatment of gastrointestinal tract should be carried out by a qualified specialist.

You should not ignore this disease or try to cure it yourself. Such a lesion requires the most complete and responsible approach, constant monitoring by a doctor. Treatment of fatty degeneration involves taking a number of medications. It usually consists of therapy with antioxidants and membrane stabilizers.

Drugs for the treatment of gastrointestinal tract can be divided into the following groups::

• Preparations based on essential phospholipids. This includes phosphatidylcholine products, thanks to which liver cells receive a protective layer. Among such drugs are Essliver, Essentiale, Hepabos and their analogues.
• Preparations from the group of sulfoamino acids - Dibikor, Heptral and others.
• Drugs plant origin, normalizing liver function - LIV 52, artichoke extract, Karsil and others.

To reduce the toxic effects on the liver and reduce intoxication, it is very important to drink vitamin complexes. For these purposes, it is permissible to use Niacin, ascorbic acid, vitamin B or E.

Consequences

Chronic fatty liver degeneration with the right approach to drug therapy has a very favorable prognosis. Of course, if such a problem is ignored for a long time, such a disease is complicated by cirrhosis of the liver - the organ begins to change its size, structure and shape.

This usually affects the elderly, as well as people who suffer from overweight body or diabetes. This disease poses a particular danger to pregnant women, since the risk of fetal mortality increases with relapse of cholestasis.

With a comprehensive approach to the treatment of gastric dysplasia, a person can live a long and fulfilling life.

Eating fatty junk food or alcoholic beverages will lead to a sharp development of the disease. Because of this, the quality and duration of life drops significantly and is shortened. In many cases, fatty degeneration flows into, which leads to the formation of stones in the ducts and the organ itself. Try to have regular check-ups with your doctor and follow all of your doctor's orders.

Prevention of fatty liver

To prevent the formation of prerequisites for fatty liver degeneration, it is enough to lead a healthy lifestyle. The most important thing is correct and good nutrition. Your diet should always include dishes high in useful elements and vitamins. You also need to eat often and in small portions so as not to overload your liver.

Proper nutrition is the best prevention of fatty liver.

TO preventive measures This also includes regular visits to your doctor for detailed medical examination. It will help to identify any abnormalities in the early stages and promptly prescribe appropriate treatment.

Lead an active lifestyle that normalizes the movement of food through the gastrointestinal tract and prevents stagnation. Don’t forget to take vitamin supplements regularly and treat any viral diseases in a timely manner.

death occurs.

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The liver is of great importance in the normal functioning of the human body, being a universal organ for cleansing and disinfecting all substances ingested from food.

The hepatocyte cells that make up the liver are capable of processing up to 1 million toxic substances within one minute. In the case of poor nutrition with a high content of spicy, fatty and canned foods, and alcohol abuse, the human body malfunctions. Micro and macro fats begin to be deposited on liver cells, eventually destroying hepatocytes and replacing them in the liver structure. Fatty liver hepatosis develops.

In this case, the enzymes of the destroyed cells enter the blood, which can be observed during the examination.

Non-alcoholic form of liver dystrophy

Based on epidemiological characteristics, a primary form is distinguished (metabolic disorders occur in the body) and a secondary form of dystrophy.

Diagnosis consists of blood biochemistry and ultrasound of the abdominal organs, which reveals an enlarged liver and its echogenicity. It is not recommended to do a biopsy, since fatty degeneration of this organ is capable of reversal in the absence of the factor that provoked it. It can be focal or diffuse in nature.

To perform a biopsy, a specific area of ​​tissue is taken, so the result of the study will not always be reliable.

Causes that can cause fatty liver

– alcohol abuse (according to research, this figure is for men – 350 ml of vodka per week, for women – 175 ml);

– foods high in fat;

– some medications have a side effect that causes the destruction of liver cells (for example, tetracycline antibiotics);

– among the diseases leading to fatty degeneration, it should be noted severe forms inflammation of the pancreas, anemia, obesity, diabetes, enteritis.

Symptoms for initial stage diseases are mostly not typical. Over time, dull pain develops in the right hypochondrium. Vomiting and bowel problems such as constipation or diarrhea may occur. Dizziness, weakness, apathy, and lack of strength appear. In rare cases, the symptoms are pronounced, accompanied by severe headaches, bloating, and itchy skin. A sick person can lose weight dramatically.

4 degrees of fatty liver are detected

0 degree. Some groups of liver cells are damaged by small drops of fat, which is located on the surface of hepatocytes.

1st degree characterized by the appearance of lesions of cells - hepatocytes with fat of medium and large droplet sizes.

2nd degree – fat droplets penetrate into the cells.

3rd degree occurs with large-scale damage to liver cells with cystic formations.

Factors that contribute to the development of the disease

• • long drinking bout;

• systematic consumption of alcohol at intervals of several days;
• poor diet low in protein;
• binge eating;
• fasting with rapid decline weight;
• poisoning with toxic substances (gasoline fumes, poisonous mushrooms, pesticides and others);
• some diseases are complicated by the development of fatty hepatosis;
• diverticula, gastritis, carriage of the human papillomavirus;
• adynamia (in other words, lack of movement, sedentary lifestyle life).

Alcoholic liver dystrophy

Alcohol consumption is the most dangerous for liver cells. . It is especially difficult for women. It develops gradually, without visible disturbances. Sometimes fatty degeneration is discovered when visiting a doctor with other complaints.

According to research, alcoholic liver dystrophy to varying degrees can be observed in 90-100% of cases of drinking alcohol.

As the effects of alcohol continue and liver cells continue to be destroyed, symptoms increase in frequency and severity.

Clinic for the development of alcoholic dystrophy

• • The appearance of characteristic stars on the skin.
  • Erythema of the skin on the feet and palms, nails are white in color.
  • Men become similar to women in certain ways:
  • enlargement of the mammary glands;

• • fat begins to accumulate on the hips and abdomen;
  • testicular atrophy occurs with subsequent development of impotence.
• Dilatation of capillaries on the face.
• Increased sensitivity of the skin to shock. The slightest injury causes bruises.
• The appearance of yellowness of the skin and sclera of the eyes.
• Digestive dysfunction (loss of appetite, irregular bowel movements, bloating).
• Pain on the right in the area where the liver is located is episodic and does not cause much concern.
• Fatigue, irritability, nervousness, and weakness appear.
• Skeletal muscle weakness is noted.

The longer the liver is destroyed, the more pronounced the symptoms become.

In order to help the body cope with the effects of toxic substances from alcoholic beverages, it is enough to stop drinking them. Liver function will recover over time if you take care of it and stop drinking alcohol.

Therapy

Proper treatment begins with stopping drinking alcohol.

1. Following a diet with fractional meals. Great content protein, microelements and vitamins. Exclusion from the diet of canned food and foods containing a large number of fructose. IN severe cases provide nutrition using a probe, intravenous infusion nutrient solutions.
2. Prescription of drugs to restore liver cells and their normal activity.
3. Vitamin therapy.
4. It is recommended to observe semi-bed rest for the first 10 days.
5. Limitation physical activity, exclusion of psychological unrest.

Alcoholic fatty degeneration does not require surgical interventions. All treatment consists of using a diet and giving up alcohol.
The most dangerous complications of severe forms of alcoholic dystrophy are cirrhosis and replacement of liver cells with fibrous tissue. The shape of the damaged organ does not change.

Herbs that are recommended for use for fatty liver

1. Turmeric, which is part of the drug "Holagol". Improves the permeability of the bile ducts, increases the amount of bile secreted, and reduces blood sugar.
2. Milk thistle. Helps restore hepatocytes, removes toxic substances from the liver, cleanses the bile ducts, relieves spasms of the gallbladder. It is one of the most effective herbs for the restoration of hepatocytes. Available in the form of oil.
3. Sorrel improves the flow of bile and helps reduce the amount of fat in liver cells. A decoction of the roots is used for medicinal purposes.
4. Cinnamon. When consumed regularly with food, the accumulation of fat in liver cells decreases and their number decreases. The good property of this spice is that it lowers sugar and cholesterol and reduces appetite.
5. Choleretic fees.

Treatment of alcoholic and non-alcoholic fatty degeneration requires a combination of diet and folk remedies. At an early stage it gives positive results.
From food, it is advisable to include in the diet sea ​​fish, low-fat cottage cheese, buckwheat, oatmeal. Avoid fatty, spicy, spicy foods.

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