Relevance of liver and biliary tract diseases. The relevance of diseases of the gallbladder and biliary tract, their timely diagnosis and treatment in modern medicine. Definition, causes and mechanisms of development

Methods for examining patients with liver and gallbladder diseases

Introduction 3

1. Laboratory and instrumental methods for studying patients with gallbladder diseases 4

2. Diagnosis of patients with gallbladder diseases 7

3.Diagnostic methods for liver disease 10

3.1.Hepatitis 10

3.2.Chronic hepatitis 12

3.2.Liver cirrhosis 15

3.3. Fatty liver degeneration 17

Conclusion 21

References 22

Introduction

Pathology of the biliary tract is a topical problem for modern medicine. In the last decade, both in Russia and abroad, despite certain successes in therapy associated with the appearance on the pharmacological market of new effective drugs for the correction of functional disorders of the digestive system, there has been a clear tendency towards an increase in the incidence of the biliary system. Moreover, this trend is characterized by stability. Thus, according to scientific forecasting, the incidence of diseases of the digestive system in the next 15-20 years will increase in the world by at least 30-50% due to an increase in the number of diseases based on stress, dyskinetic, and metabolic mechanisms. These trends are also characteristic of the pathology of the biliary system. According to the literature, the prevalence of diseases of the gallbladder and bile ducts in Moscow among the adult population over the past 10 years has become almost 2 times higher than in Russia. Gallstone disease has become significantly “younger” and occurs not only in young, but also in early childhood. The disease began to appear quite often not only in women, but also in men. Currently, the prevalence rates of biliary tract diseases range from 26.6 to 45.5 per 1000 population.

The above facts suggest the relevance of the topic under consideration.

The purpose of this work is to study diagnostic methods for diseases of the liver and biliary tract.

To achieve this goal, the following tasks were set:

Consider laboratory and instrumental methods for studying patients with gallbladder diseases;

Describe diagnostic methods for liver disease.

Laboratory and instrumental methods for studying patients with gallbladder diseases

For biliary dyskinesias, cholecystitis (without exacerbation), cholelithiasis during the interictal period general state The patient most often remains satisfactory. At acute cholecystitis, exacerbation of chronic cholecystitis, prolonged attack of hepatic colic with cholelithiasis, the patient’s condition can be moderate or severe.

The patient's position with PVD and cholecystitis outside of exacerbation is usually active. The forced position of the patient is observed during an attack of hepatic colic (cholelithiasis, calculous cholecystitis). Patients are restless, tossing about in bed, trying (to no avail) to take a position in which the pain is less noticeable.

The appearance of the patient in most cases is not changed. The asthenic constitution and associated connective tissue dysplasia are often the cause of the presence in these patients of the gallbladder of the hourglass type, the presence of constrictions, membranes, kinks, diverticula in the gallbladder, which leads to the formation of biliary dyskinesia, and subsequently to organic pathology - cholecystitis, cholelithiasis; a hypersthenic constitution is often observed in persons suffering from cholelithiasis, mainly women, as well as in persons with biliary dyskinesia of the hypokinetic type. 1

The skin has a normal color in case of diarrhea and chronic cholecystitis without exacerbation, as well as in case of cholelithiasis during the interictal period. During an attack of hepatic colic, patients may develop subicteric sclera, and with the development of obstructive jaundice, the skin becomes green-yellow in color. Cholesterol deposition due to impaired cholesterol metabolism in patients with cholelithiasis and calculous cholecystitis is accompanied by the appearance of xanthoma and xanthelasma on the skin.

When performing percussion of the abdomen, it is necessary to pay attention to the size of the liver according to Kurlov, which is not changed in patients with ADHD, cholelithiasis, cholecystitis without exacerbation (along the right midclavicular line - 9 cm, along the anterior midline - 8 cm, along the left costal arch - 7 cm). An increase in the size of the liver can occur after hepatic colic in a patient with cholelithiasis, during an exacerbation of cholecystitis. Using very quiet percussion, you can determine the size of the gallbladder if it is significantly enlarged (distension of the gallbladder with its hypokinesia, cholelithiasis).

With exacerbation of cholecystitis, characteristic symptoms may be identified:

Zakharyin's symptom - sharp pain when tapping with a finger or pressing in the area of the gallbladder projection;

Vasilenko's symptom - sharp pain when tapping a finger in the area of the gallbladder at the height of inspiration;

Obraztsov-Murphy symptom - sharp pain when inserting the hand into the right hypochondrium at the height of inspiration;

Ortner's symptom is pain when tapping the edge of the hand on the right costal arch.

Superficial palpation of the abdomen reveals:

Severe local pain in the projection area of the gallbladder in acute cholecystitis, biliary colic;

Mild to moderate pain at the point of the gallbladder in chronic cholecystitis, cholelithiasis during remission, and in diarrhea.

The gallbladder is usually accessible by palpation when it is enlarged (hypokinetic type GIB with gallbladder distension, cholelithiasis). 2

To examine patients with diseases of the biliary tract, the following laboratory and instrumental research methods are used:

Clinical blood test;

Biochemical blood test;

Fractional chromatic duodenal sounding;

Microscopic examination of bile;

Biochemical study of bile;

X-ray and radiological studies;

Ultrasound examination of the hepatopancreatoduodenal zone;

Endoscopic examination, etc.

Diagnosis of patients with gallbladder diseases

A diagnostic approach to a patient in whom the doctor suspects the existence of problems associated with the extrahepatic biliary tract or gallbladder, should be based on clinical symptoms and the expected nature of the pathology. Advances in diagnostic radiology and corrective endoscopy have made it possible to accurately identify the nature and location of the pathological process and provide the way for therapeutic intervention,

Abdominal radiography. Plain radiographs abdominal cavity have limited value in the diagnosis of diseases associated with the presence of gallstones or jaundice. Only in 15-20% of patients can contrasted stones localized in the right upper quadrant of the abdomen be detected on plain radiographs. Air within the biliary tree may indicate the presence of a fistula connecting the gallbladder to the intestine.

Oral cholecystography. Oral cholecystography was introduced in 1924. The function of the gallbladder is assessed based on its absorptive capacity. X-ray contrast iodine dye, taken orally, is absorbed in the gastrointestinal tract and enters the liver, then excreted into the bile duct system and concentrated in the gallbladder. Stones seen as filling defects in a visualized, contrast-enhanced gallbladder or nonvisualization of the gallbladder may not indicate a “positive” result. False-positive non-imaging may occur in patients who do not follow the doctor's instructions for a prescribed test, or in those who are unable to swallow tablets, or in cases where tablets cannot be absorbed in the gastrointestinal tract or dye is not excreted into the biliary tract. tract due to liver dysfunction.

Abdominal ultrasonography. This method has replaced oral cholecystography as the method of choice when examining a patient for the presence of gallstones. The effectiveness of abdominal ultrasonography, or ultrasound, in the diagnosis of acute cholecystitis is not as significant as in the diagnosis of gallstones. Ultrasonography is used to identify intra- and extrahepatic biliary dilatation. 3

Computed tomography (CT). This test is not highly sensitive for detecting gallstones, but provides the surgeon with information related to the origin, size and location of biliary dilatation, as well as the presence of tumors located in and around the biliary tract and pancreas.

Biliary scintigraphy. Intravenous administration of a radioactive isotope, one of the iminodiacetic acid family, labeled technetium-99t, provides specific information relevant to the determination of cystic duct patency and serves as a sensitive method for the diagnosis of acute cholecystitis. In contrast to ultrasonography, which serves as an anatomical test, biliary scintigraphy is a functional test.

Percutaneous transhepatic cholangiography (PTC). Under fluoroscopic guidance and local anesthesia, a small needle is inserted through the abdominal wall into the bile duct. This method provides a cholangiogram and allows therapeutic adjustments if necessary based on the clinical situation. Used in patients with a complex of biliary problems, including strictures and tumors.

Endoscopic retrograde cholangiopancreatography (ERCP). Using a side-viewing endoscope, the biliary tract and pancreatic duct can be intubated and visualized. Advantages include direct visualization of the ampulla region and direct measurement of the distal segment of the bile duct. The use of this method brings significant benefits to patients suffering from common bile duct disease (benign and malignant).

Choledochoscopy. Although indirect imaging techniques are fundamental in the diagnosis of patients with diseases of the extrahepatic biliary tract, direct examination and visualization of the biliary system is a goal worth pursuing. Choledochoscopy performed during surgery can be effective in identifying bile duct strictures or tumors in patients.

Diagnostic methods for liver disease

The liver is the main laboratory of the human body. About 20 million chemical reactions per minute occur in this organ. Here the synthesis of blood proteins takes place (for example, immunoglobulins responsible for the so-called humoral immunity the whole body, albumins, which hold the required volume of fluid in the bloodstream and others), the synthesis of bile acids - substances necessary for the digestion of food in the small intestine, the accumulation and breakdown of glucose - the main source of energy of the body. The liver exchanges fats, neutralizes toxins (poisons), etc. The slightest violation of at least one of the functions of the liver leads to serious disturbances in the functioning of the entire body. 4

Hepatitis

Hepatitis is acute. Symptoms, course. In mild cases, acute hepatitis is practically asymptomatic, being detected only during random or targeted examination (for example, at work among people in contact with hepatotropic poisons, in case of household group poisoning with mushrooms, etc.). In more severe cases (for example, with toxic hepatitis), clinical symptoms of the disease develop quickly, often in combination with signs of general intoxication and toxic damage to other organs and systems. At the height of the disease, icteric discoloration of the skin and mucous membranes, whitish-clay-colored stools, deep dark-colored (“beer-colored”) urine, and hemorrhagic phenomena are characteristic. The color of the skin is orange or saffron. However, in mild cases, jaundice is visible only in daylight; icteric staining of the sclera and mucous membrane appears most early soft palate. Nosebleeds and petechiae are common; patients are worried itchy skin, bradycardia, depressed mental state, increased irritability of patients, insomnia and other signs of damage to the central nervous system are noted.

The liver and spleen are slightly enlarged and slightly painful. With particularly severe lesions and the predominance of necrotic changes in the liver (acute dystrophy), its size may decrease.

Laboratory studies reveal hyperbilirubinemia (100-300 µmol/l or more), increased activity of a number of serum enzymes: aldolase, aspartate aminotransferase and especially alanine aminotransferase (significantly above 40 units), lactate dehydrogenase, hypoalbuminemia, hyperglobulinemia (mainly increased content. Deviated from the norm indicators of protein-sedimentary samples (thymol, sublimate, etc.). The liver's production of fibrinogen, prothrombin, VII, V coagulation factors is impaired, resulting in hemorrhagic phenomena. Differential diagnosis. A carefully collected anamnesis is of great importance, establishing the possibility of professional or household intoxication, taking into account the epidemiological situation in identifying the nature and cause of the disease. In unclear cases, first of all you should think about viral hepatitis. Identification of the so-called Australian antigen is characteristic of serum hepatitis B (it is also detected in virus carriers, rarely in other diseases). Mechanical (subhepatic) jaundice usually occurs acutely only when the common bile duct is blocked by a stone due to cholelithiasis. But in this case, the appearance of jaundice is preceded by an attack of biliary colic; bilirubin in the blood is mostly straight, stool is discolored. With hemolytic adrenal jaundice, free (indirect) bilirubin is detected in the blood, the stool is intensely colored, and the osmotic resistance of red blood cells is usually reduced. In the case of false jaundice (due to staining of the skin with carotene during prolonged and abundant consumption of oranges, carrots, and pumpkins), the sclera is usually not colored, and there is no hyperbilirubinemia.

With timely treatment, complete recovery often occurs. In some cases, acute hepatitis turns into chronic, and then into cirrhosis of the liver. In some cases, acute liver dystrophy develops (see Hepatosis) with the clinical picture of acute liver or hepatorenal failure, from which patients can die.

3.2.Chronic hepatitis

Polyetiological chronic (lasting more than 6 months) liver lesions of an inflammatory-dystrophic nature with moderate fibrosis and predominantly preserved lobular structure of the liver. Among chronic liver diseases, chronic hepatitis is the most common.

Clinic. Characterized by enlarged liver, pain or a feeling of heaviness, fullness in the right hypochondrium, dyspeptic symptoms; Jaundice, skin itching, and low-grade fever are less common. Liver enlargement occurs in approximately 95% of patients, but in most cases it is moderate. There is no enlargement of the spleen or it is slightly enlarged. Pain in the liver area is dull, constant. Frequent loss of appetite, belching, nausea, poor tolerance to fats, alcohol, flatulence, unstable stools, general weakness, decreased ability to work, hyperhidrosis. In a third of patients, mild (subicteric sclera and palate) or moderate jaundice is detected. An increase in ESR and dysproteinemia due to a decrease in albumin concentration and an increase in globulins, mainly alpha and gamma fractions, are frequent, but nonspecific. The results of protein-sedimentary tests are positive - thymol, sublimate, etc. In the blood serum of patients, the content of aminotransferases is increased: ALT, AST and LDH, with difficulty in the outflow of bile - alkaline phosphatase. In approximately 50% of patients, slight or moderate hyperbilirubinemia is found, mainly due to an increase in the level of conjugated (direct) bilirubin in the blood serum. The absorptive-excretory function of the liver is impaired (the half-life of bromsulfalein from the blood is prolonged).

With cholestatic hepatitis, more pronounced persistent jaundice and laboratory cholestasis syndrome are usually observed: the blood serum contains increased levels of alkaline phosphatase, cholesterol, bile acids, conjugated bilirubin, and copper.

There are low-active (inactive), benign, persistent and active, aggressive, progressive recurrent hepatitis.

Liver puncture biopsy and laparoscopy make it possible to more accurately distinguish between these two forms of hepatitis, as well as to carry out differential diagnosis with other liver diseases.

A liver scan allows you to determine its size; with hepatitis, sometimes there is a reduced or uneven accumulation of the radioisotope drug in the liver tissue, in some cases there is an increased accumulation in the spleen.

Differential diagnosis in cases with a clear clinical picture of diffuse liver damage should first of all be carried out with liver cirrhosis. With cirrhosis, the symptoms of the disease are more pronounced, the liver is usually much denser than with hepatitis; it can be enlarged, but often reduced in size (atrophic phase of cirrhosis). As a rule, splenomegaly is observed, liver signs are often detected (vascular telangiectasia, hepatic tongue, hepatic palms), and symptoms of portal hypertension may occur. Laboratory tests show significant deviations from the norm in the results of the so-called liver tests; with a puncture biopsy - disorganization of the liver structure, significant proliferation of connective tissue.

Liver fibrosis, unlike hepatitis, is usually not accompanied by clinical symptoms and changes in liver function tests. Anamnesis (the presence of a disease in the past that could cause liver fibrosis), long-term observation of the patient and a puncture biopsy of the liver (if necessary) make it possible to differentiate it from chronic persistent hepatitis.

With fatty hepatosis, the liver is usually softer than with chronic hepatitis, the spleen is not enlarged, and a puncture biopsy of the liver is crucial in diagnosis.

Differential diagnosis with functional hyperbilirubinemia is based on the characteristics of their clinical picture (mild jaundice with hyperbilirubinemia without significant clinical symptoms and changes in laboratory liver test data and liver puncture biopsy). Amyloidosis with a predominant hepatic localization, in contrast to chronic hepatitis, is characterized by symptoms of other organ localizations of the process, a positive test with Congo red or methylene blue; the diagnosis is confirmed by a puncture biopsy of the liver. In case of focal lesions (tumor, cyst, tuberculoma, etc.), the liver is unevenly enlarged, and scanning determines the focus of destruction of the hepatic parenchyma.

Flow. Low-active (persistent) hepatitis is asymptomatic or with minor symptoms, changes in laboratory parameters are also insignificant. Exacerbations of the process are uncharacteristic.

Chronic active recurrent (aggressive) hepatitis is characterized by severe complaints and clear objective clinical and laboratory signs. Some patients experience systemic autoallergic manifestations of the disease (polyarthralgia, skin rashes, glomerulonephritis, etc.). Frequent relapses of the disease are characteristic, sometimes occurring under the influence of even minor factors (errors in diet, overwork, etc.). Frequent relapses lead to significant morphological changes in the liver and the development of cirrhosis. In this regard, the prognosis for active hepatitis is more severe.

Cirrhosis of the liver

About 2 million people die from liver cirrhosis every year. Cirrhosis and liver cancer are the cause of 90-95% of deaths from chronic liver diseases.

What is cirrhosis of the liver?

Cirrhosis is the process of replacing the normal structure of the liver with scar tissue that takes the form of nodes. These nodes not only do not perform any useful functions, but also interfere with the normal functioning of the liver by squeezing blood vessels, bile ducts and normal liver tissue. In this case, the production and accumulation of vital substances (proteins, fats, carbohydrates, hormones) by the liver is disrupted, and the neutralization of toxic and infectious agents worsens. The liver is the main outpost that receives the entire flow of substances coming from the intestines. Among these substances, in addition to the beneficial ones necessary for the body, there are harmful, toxic, and sometimes dangerous compounds for the body, which the liver neutralizes and returns to the intestines along with bile. And if the liver does not work well, then substances that poison the body penetrate into the blood.

Causes of cirrhosis development.

The most common causes of cirrhosis are hepatitis B and C viruses and alcohol abuse. Alcoholism is the main reason. It has not been established exactly how long and how much alcohol is needed for the development of cirrhosis. Most patients with this disease have been drinking at least 0.5 liters of strong alcoholic beverages or several liters of wine or beer every day for at least 10 years. The higher the daily dose of alcohol, the faster cirrhosis will develop. In women, less alcohol consumption leads to its development. 10-20% of patients with chronic hepatitis B and C develop cirrhosis of the liver. Alcohol-viral cirrhosis is especially difficult. They most often develop into liver cancer. There is a hereditary predisposition to the development of rare forms of cirrhosis (hemochromatosis, Wilson-Konovalov disease). In approximately 10-20% of patients, the cause cannot be determined. 5

80% of cirrhosis occurs unnoticed, without attracting the attention of either the patient or the doctor. The remaining patients complain of increased fatigue, pain in the right hypochondrium, bloating, periodic darkening of urine, weight loss, a tendency to bruise, and redness of the palms. In many patients, the disease is recognized only when complications develop: accumulation of fluid in the abdomen, impaired consciousness, bleeding from the esophagus and stomach, jaundice. A healthy liver protects the brain from toxins, and with cirrhosis, the blood, not cleared of harmful substances by the liver, enters the brain. There is a disturbance in thinking and memory. 60-90% of liver cancer develops against the background of cirrhosis. Cancer in the early stages is difficult to recognize; its manifestations are taken as signs of progression of cirrhosis. Most often, the tumor manifests itself as abdominal pain. Sometimes you can feel a tumor-like space-occupying formation in the right hypochondrium.

In case of liver cirrhosis, alcohol and any alcohol-containing drinks are strictly contraindicated, as this contributes to the progression of the disease. It is not recommended to drink carbonated drinks. If you do not have complications of cirrhosis, then no special dietary restrictions are required. With this disease, low potassium levels in the blood are often found, so you need to include more potassium-rich fruits in your diet.

Fatty liver

Fatty liver (liver steatosis) is a fatty transformation of liver tissue when liver cells suffer from excess fat accumulation.

Causes of fatty degeneration.

The main causes of hepatosis are exposure to toxic substances on the liver, endocrine disorders, and poor nutrition. Among toxic agents, alcohol occupies a special place. However, in people who abuse alcohol, the development of the disease is associated both directly with the effect of alcohol on liver cells and with poor nutrition. The speed of development and severity of changes is higher, the greater the amount of alcohol consumed. The role of other toxic factors (insecticides, organophosphorus compounds, etc.) is less significant. It is possible to develop drug-induced liver steatosis, for example, during the treatment of tuberculosis, taking antibiotics, mainly tetracyclines, and hormonal drugs. In the group of endocrine diseases, the leading cause of hepatosis is diabetes mellitus, especially in the elderly. It is possible to develop “fatty liver” in diseases of the thyroid gland. Steatosis also accompanies general obesity. The determining factor in the imbalance of nutritional factors is the discrepancy between the total calorie content of food and the content of animal proteins in it, as well as a deficiency of vitamins and other substances. Malnutrition is the main cause of the development of steatosis in chronic diseases of the digestive system (chronic pancreatitis). In chronic pancreatitis, it occurs in 25-30% of cases. Lack of oxygen is the main cause of the development of liver steatosis in people suffering from pulmonary diseases and cardiovascular failure.

How do fatty liver diseases manifest?

Steatosis can occur latently, manifesting itself only as a slight enlargement of the liver, or with pronounced manifestations. The most consistent symptom is an enlarged liver. Palpation reveals tenderness of the liver. Most patients also experience independent pain in the right hypochondrium, and there may be nausea. Steatosis can last a long time, over many years. Periods of deterioration are followed by relative improvements in well-being. Exacerbations are often associated with mental or physical stress, alcohol intake, and infection.

Complications of steatosis, which are observed mainly in its severe forms, include the formation of liver cirrhosis. Due to immune disorders, patients with steatosis often experience pneumonia, and pulmonary tuberculosis may develop.

Treatment of hepatosis

Treatment of steatosis is a rather complex, but solvable task for professionals and consists of several areas. Among them are a properly selected diet, modification of behavioral patterns (changes in eating habits, changes in the amount and composition of alcohol consumed, increased physical activity), a set of measures aimed at normalizing the energy metabolism of the liver, drug therapy with modern drugs, the action of which is aimed at stabilizing and protecting membranes liver cells, normalization of liver metabolism. The prognosis is usually favorable and, with adequate treatment, reverses itself quite quickly. However, supportive measures may be necessary for quite a long time.

Prevention of hepatosis.

Prevention of hepatosis consists of eliminating the influence of toxic factors, adequate treatment of diabetes mellitus, a nutritious balanced diet, and effective treatment of chronic diseases of the digestive system. Patients taking hormones for a long time should be prescribed drugs that improve liver function for prophylactic purposes.

Diets for liver diseases.

If the disease worsens, you need to adhere to Diet No. 5 for 3-4 weeks; after the condition improves, you can switch to Diet No. 5. This diet is complete and basic, that is, the longer you stick to it, the more guaranteed your health will improve.

If it is necessary to enhance the choleretic properties of the diet, resort to its lipotropic-fat version, increase the amount of vegetables and fruits, and increase the dose of vegetable oil to 50%, instead of the usual 30%. Both butter and vegetable oil are added to prepared dishes.

For liver cirrhosis, the recommendations remain the same: Diet No. 5 if the condition worsens and Diet No. 5 if the condition is in remission. But if diarrhea occurs, fat is limited to 50-60 g. Products that have a laxative effect are also excluded - milk in pure form, honey, jam, etc. If you are prone to constipation, add prunes, dried apricots, figs, raisins, beets, plums, etc.
If you have completely lost your appetite or have a perversion of taste, you should try to eat more fruits, berries, salads, and drink juices. At this time, it is better to get protein from dairy products, mild cheese, cottage cheese, eggs, and boiled fish. For some time, you can include your favorite dishes in your diet, but without going beyond what is permitted.

For portal hypertension, diets with a normal content of protein, carbohydrates, fats, but without salt are recommended. It’s good even if the bread is salt-free. The amount of liquid is also limited, but prunes, figs, and dried apricots are recommended. If hormonal therapy is carried out (prednisolone, triamcinolone, etc.), special attention should be paid to protein and potassium, their amount should be increased.

Conclusion

A close study of the pathology of the biliary system is determined by the complexity of many issues of the etiology and pathogenesis of diseases in this area, and, consequently, by the problem of prescribing rational etiopathogenetic therapy. These issues have been discussed in the literature for decades, but interest in them continues unabated. Currently, many researchers consider the pathology of the biliary system as a consequence of general neurosis, but the possibility of the occurrence of diseases of the gallbladder based on pathological viscero-visceral interactions in the pathology of other abdominal organs (gastritis, peptic ulcer, colitis, diseases of the female genital area, etc.) cannot be ruled out. . The issues of targeted and adequate treatment of patients with biliary tract pathology still remain controversial.

Many researchers and clinicians consider the stabilization of the function of the central nervous system and the elimination of general neurotic reactions to be the leading therapeutic measure. More than once on the pages of the medical press it has been pointed out that it is necessary to prescribe antidepressants and tranquilizers in the complex treatment of diseases of the gallbladder and the sphincter apparatus of the biliary system. Many drug therapy regimens are aimed at differentiated correction of the function of the gallbladder and sphincter apparatus, depending on the type of disorder, including with the help of modern myotropic drugs. In recent years, sufficient experience has been gained in the use of enzyme preparations of the latest generations in the treatment of disorders of small intestinal digestion, dyskinetic disorders in the biliary system, acute and chronic cholecystitis, reactive pancreatitis.

List of used literature

Propaedeutics of internal diseases: Textbook for universities./ N.A. Mukhin, V.S. Moiseev. - M.: Geotar-Media, 2007.- 848 p.

Propaedeutics of internal diseases. Textbook for universities./ N.V. Ivashkin.- M.: MEDpress, 2005.- 240 p.

Propaedeutics of internal diseases: Textbook for universities./ V.S. Moiseev.- M.: INFRA-M, 2004.- 768 p.

Propaedeutics of internal diseases: textbook./ A.S. Svistov.- M.: Medicine, 2005.- 536 p.

Grebnev, A.L. Propaedeutics of internal diseases: textbook./ A.L. Grebnev.- M.: Medicine, 2002.-592 p.

1 Grebnev, A.L. Propaedeutics of internal diseases: textbook./ A.L. Grebnev.- M.: Medicine, 2002.-P.254.

2 Propaedeutics of internal diseases: Textbook for universities./ V.S. Moiseev.- M.: INFRA-M, 2004.- P. 369.

3 Propaedeutics of internal diseases: textbook./ A.S. Svistov.- M.: Medicine, 2005.- P.299.

4 Propaedeutics of internal diseases. Textbook for universities./ N.V. Ivashkin.- M.: MEDpress, 2005.- P.104.

Surveys sick And methods intraoperative revision of extrahepatic gall ducts Increased interest...

Lecture Diseases liver, gall tract and peritoneum

Lecture >> Medicine, health

pancreatic cancer, liver, gall bubble, duodenum, ... careful examination sick, including laboratory and instrumental methods. Big...as one disease. Pathogenesis Inflammation gall bubble And gall ducts so...

Ultrasound and its applications (2)

Scientific work >> Physics

Angiography liver 205 3.3.2. Ultrasound angiography technique liver 207 3.3.3. Ultrasound picture liver...high information content and reliability of ultrasonic method diagnosis of many diseases and damage has risen to a qualitative level...

Objective methods abdominal examinations

Abstract >> Medicine, health

At diseases liver And gall ducts... Survey liver. The study begins with percussion liver. Like an airless organ liver ... method to a certain extent approaches direct percussion. If sick...share liver, gall bubble, right...

Ivanovo College of Pharmacy |
Coursework |
Means for the treatment of the liver and biliary tract. |
Discipline: Medicines. |
Completed by: Dimitrieva N. A. Student of group 31 – M. Supervisor: Rozhdestvenskaya N. V. Teacher of special disciplines |
Rating: _____Signature: ____________ |

2012 – 2013 academic year |

Contents:Introduction………………………………………………………………………………..1
Chapter 1: Brief description of the main liver diseases…………………………..2
1.1. Hepatitis………………………………………………………………………………..2
1.2. Cirrhosis……………………………………………………………………………….4
Chapter 2: Brief characteristics of the main diseases of the biliary tract………………………………………………………. ……………………………………...5
1.1. Cholecystitis………………………………………………………………………………………..6
1.2. Gallstone disease……………………………………………………………..8
Chapter 3: Drugs for the treatment of diseases of the liver and biliary tract.................................................................. ........................................................ ....................10
Chapter 4: Medicinal plants used for diseases of the liver and biliary tract………………………………………………………………………………………22
Conclusion…………………………………………………………………………………30
References………………………………………………………………………………………..31

Introduction.
Relevance of the chosen topic. In the last decade, the importance of treating diseases of the liver and biliary tract has increased significantly. This is due to the fact that many biologically active substances of plant origin are successfully used in combination with other drugs.
Goal course work- study the principles of treatment of diseases of the liver and biliary tract with drugs and medicinal plants. When completing the course work, the following tasks were set:
1. characterize the most common diseases of the liver and biliary tract;
2. study the composition and effect of drugs and plants used for the treatment of these diseases;
3. draw conclusions on the use of official medicines and plants in the treatment of diseases of the liver and biliary tract.
The material for writing this coursework was educational and reference literature, as well as articles from modern medical journals and Internet resources.
Reference literature was used to characterize drugs and medicinal plants. Educational literature and journal articles served as the basis for a brief description of diseases of the liver and biliary tract. Electronic sources reveal many aspects of the problem under study.
The first chapter addresses the problems associated with the characteristics of the main liver diseases; the second chapter discusses brief characteristics of biliary tract diseases.
The main part consists of chapters three and four, which are directly devoted to the description of drugs and medicinal plants used to treat diseases of the liver and biliary tract.
In conclusion, conclusions are drawn based on the analysis of the course material discussed in the course.

Chapter 1: Brief description of the main liver diseases.
The role of the liver in the body is great. She performs a number of very important functions one of which is bile formation, and bile takes part in digestion, especially in the processing and absorption of fats. Bile enhances the contraction of intestinal muscles (peristalsis), which contributes to the normal movement of food and undigested residues food products. Bile helps reduce fermentation and putrefactive processes in the intestines. All nutrients absorbed in the intestines must pass through the liver. Regulation of bile secretion, as well as other processes occurring in the liver, is carried out by the central nervous system and endocrine glands.
Diseases of this organ develop in humans for several reasons. Among the most common among them, experts identify an infectious factor (we are talking about hepatitis viruses), diabetes mellitus...

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The symptom complex of inflammation of the liver tissue underlies many liver diseases and is manifested by a number of stereotypical local and general pathophysiological changes.

The inflammatory reaction of the liver tissue can be conditionally divided into three main interconnected phases, which have a clear clinical, laboratory and morphological expression: 1) alteration with the release of inflammatory mediators, 2) vascular reaction with exudation and 3) proliferation.

Alteration (lat. -- change) -- the initial phase of the inflammatory response to pathogenic effect, and hepatocytes are more susceptible to it than the stroma and blood vessels of the liver. In some cases, it is limited to reversible changes, in others it leads to the death of tissue structures with the formation of areas of necrosis. During alteration, as a result of the breakdown of cells and intercellular substance, biologically active substances (inflammatory mediators) are formed: histamine, serotonin, plasma kinins, prostaglandins, leukotrienes, RNA and DNA breakdown products, hyaluronidase, lysosomal enzymes, etc.

Under the influence of inflammatory mediators, the second phase of the inflammatory reaction occurs, characterized by disorders of predominantly microcirculatory blood flow, lymph circulation and bile secretion - vascular reaction with exudation. As a result, infiltration of liver tissue with leukocytes, exudation of plasma proteins, inflammatory hyperemia occurs, the rheological properties of the blood change, stasis, local hemorrhages, thrombosis of small vessels, etc. occur. Lymphostasis and lymphothrombosis develop in lymphatic microvessels, and cholestasis develops in bile canaliculi and cholangioles. In this case, excessive protein intake into hepatocytes or intercellular substance, as well as a violation of protein synthesis causes the development of protein dystrophy (dysproteinosis). Cellular protein dystrophy in the case of rapid denaturation of the cytoplasmic protein, it can result in necrosis of the hepatocyte. Extracellular protein dystrophy manifests itself first as mucoid, then fibrinoid swelling (fibrinoid), hyalinosis and amyloidosis. Mucoid swelling of fibrinoid and hyalinosis are successive stages of disorganization of connective tissue (liver stroma and vascular walls). Severe destruction of collagen fibers and the main substance of connective tissue leads to fibrinoid necrosis.

In conditions of blood and lymph circulation disorders and oxygen starvation (tissue hypoxia), protein dystrophy usually develops along with fatty degeneration liver (dystrophic obesity), which is characterized by impaired metabolism of cytoplasmic fat.

The outcome of fatty liver disease depends on its severity. If it is not accompanied by deep damage cellular structures liver, it turns out to be, as a rule, reversible. With acute fatty liver degeneration, the amount of fat contained in hepatocytes increases sharply, and its qualitative composition changes. Hepatocytes die, fat droplets merge and form fatty cysts, around which a cellular reaction occurs and develops connective tissue(cirrhosis of the liver). The liver with fatty degeneration is enlarged, flabby, yellow or red-brown in color.

The third phase of the inflammatory response is proliferation, or proliferation of tissue elements of the liver. The outcomes of productive (proliferative) inflammation are different. Complete resorption of the cellular infiltrate may occur; however, more often, at the site of the infiltrate, as a result of the maturation of the mesenchymal cells included in it, connective tissue fibers are formed and scars appear, i.e. sclerosis or cirrhosis.

The inflammatory process in the liver can be diffuse and focal. The clinical course of inflammation of the liver tissue depends on many factors. Among them, the state of the body's reactive readiness and the degree of its sensitization are especially important. In some cases, when hypersensitivity, inflammation occurs acutely, in others it takes a protracted course, acquiring the character of subacute or chronic.

In acute inflammation, the phenomena of exudative and acute proliferative inflammatory reactions predominate. Exudative inflammatory reaction most often it is serous (serous exudate permeates the liver stroma) or purulent (purulent exudate diffusely infiltrates the portal tracts or forms ulcers in the liver).

Acute proliferative (productive) inflammatory response characterized by degeneration and necrosis of hepatocytes in various parts of the lobule and the reaction of the reticuloendothelial system. As a result, nested (focal) or diffuse (diffuse) cellular infiltrates are formed from Kupffer cells, endothelium, hematogenous elements, etc.

Chronic inflammation liver tissue is characterized by a predominance of cellular infiltration of the stroma of the portal and periportal fields; destruction (dystrophy and necrobiosis) of hepatocytes, sclerosis and regeneration of liver tissue. Alterative and exudative phenomena recede into the background.

Main role in development acute inflammation liver tissue is played by pathogens of infections (hepatitis A, B, C, D viruses, etc., enteroviruses, pathogens of acute intestinal infections, virus infectious mononucleosis, Leptospira, etc.), toxic factors of endogenous (infectious, burn, etc.) and exogenous origin (alcohol; industrial poisons - phosphorus, carbon tetrachloride; organophosphorus insecticides; medications - penicillin, sulfadimezin, PAS, etc.) , ionizing radiation.

The course of acute inflammation of the liver tissue is usually cyclical, lasting from several weeks to several months. Chronic inflammation of the liver tissue lasts for years.

Clinic in diagnostics

Clinical manifestations of inflammation of the liver tissue are determined by the prevalence of the process, the degree and ratio of damage to the liver parenchyma and the mesenchymal cellular reaction.

Main clinical signs inflammation of the liver tissue are pain in the upper abdomen and right hypochondrium, enlarged liver and jaundice (see “Symptom complexes of hyperbilirubinemia”).

Symptoms of liver dysfunction are of some importance (see symptom complexes of liver failure).

Many patients experience general clinical signs of the inflammatory process: fever (usually low-grade) and symptoms of intoxication of the body (weakness, sweating, etc.), leukocytosis, accelerated ESR, changes in protein and carbohydrate metabolism, etc.

The clinical symptoms of inflammation of the liver tissue are often obscured by the symptoms of the disease that caused it, for example, sepsis, systemic diseases with autoimmune pathogenesis (sarcoidosis, periarteritis nodosa, systemic lupus erythematosus, etc.).

Inflammatory damage to the liver tissue itself is the cause of severe complications, which may be the first clinical manifestations of the disease: hepatic coma due to massive necrosis of the liver parenchyma (see “Symptom complexes of acute and chronic liver failure”), edematous-ascitic syndrome (see “Symptom complex of impaired portal circulation , conditioned liver damage"), hemorrhagic syndrome (see "Diseases of the hemostatic system"), etc.

It should be noted that often inflammation of the liver tissue (especially chronic focal inflammation) is clinically asymptomatic or with minimal clinical symptoms, manifested mainly by an increase in the size of the liver. Therefore, serum-biochemical syndromes play a very important role in the timely diagnosis of inflammation of the liver tissue: 1) cytolytic, 2) mesenchymal-inflammatory; 3) regeneration and tumor growth.

Serum-biochemical cytalitis syndrome caused by damage to liver cells with a pronounced impairment of membrane permeability.

Diagnosis of cytolytic syndrome is mainly carried out using serum enzymes: aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamine transferase (GGTP), lactate dehydrogenase (LDH).

AST in blood serum in healthy person contained in an amount of 0.10 - 0.45 mol/(tsp); AdAT - 0.10 - 0.68 mmol/tsp). An increase in aminotransferases by 1.5 - 3 times is considered moderate, up to 5 - 10 times - medium degree, 10 times or more - high.

GGTP: norm in blood serum 0.6 - 3.96 mmol/(pp);

LDH: the norm is up to 3.2 µmol/(tsp), inferior in sensitivity to AST and ALT.

It should be remembered that hyperenzymemia develops not only with liver damage, but also with pathology of the heart and skeletal muscles, acute pancreatitis, nephritis, severe hemolytic conditions, radiation injuries, poisoning, etc.

Serum-biochemical mesenchymal-inflammatory syndrome(or hepatic reticuloendothelial irritation syndrome) is caused by increased activity of mesenchymal-stromal (non-epithelial) elements of the liver. To diagnose it, thymol (thymolveronal) and mercuric sediment samples are used, as well as indicators of gamma globulin and immunoglobulins in blood serum. Thymol test: norm 0 - 7 VD according to Maclagan, 3 - 30 IU according to Vincent. Sublimate test: norm 1.9 VD and higher. Serum gamma globulin: normal 8 - 17 g/l or 14 - 21.5% of the total protein.

Serum biochemical syndrome of regeneration and tumor growth caused by regenerative (acute viral hepatitis) and tumor (hepatocellular carcinoma) processes in the liver.

The main indicator of this syndrome is a2-feto-protein (normally it is either not detected or is detected in a very low concentration - less than 30 μg/l). For tumor processes, an 8-10-fold increase in the concentration of β1-fetoprotein is more typical, and for regenerative processes in the liver - a 2-4-fold increase.

Great importance in the diagnosis of inflammation of the liver tissue is given morphological studies biopsy material. The morphological substrate of inflammatory liver damage is dystrophic and necrobiotic changes in its parenchyma and stromal infiltration.

2.3 Symptom complex of portal circulation disorders caused by liver damage

Definition, causes and mechanisms of development

Symptocomplex of portal circulation disorders caused by liver damage, includes several syndromes, of which the most common are portal hypertension syndrome and associated hepatolienal syndrome, edematous ascitic syndrome, serum-biochemical liver shunt syndrome and hepatargia or portosystemic encephalopathy syndrome.

IN clinical practice term portal circulation indicates blood circulation in the portal vein system. The liver circulatory system includes two afferent blood vessels -- portal vein, through which 70 - 80% of the total volume of incoming blood enters, and the own hepatic artery (20 - 30% of the total volume of blood flowing to the liver) and one carrying vessel - the hepatic vein. Both afferent vessels branch in the liver to a common capillary network, in which the capillaries formed as a result of the branching of arterioles connect with the sinusoidal capillaries of the portal system. These capillaries open into the central lobular veins, through which the blood flows further through the collecting veins into the main hepatic veins. The trunks of the hepatic veins open into the inferior vena cava.

Lymphatic drainage from the liver occurs through superficial and deep lymphatic vessels. Superficial lymphatic vessels anastomose with deep capillary networks starting from the perilobular networks. There are no lymphatic capillaries inside the lobules.

Disturbances in the outflow of blood from the portal vein vascular system usually lead to portal hypertension, sometimes reaching 600 mm of water column or more. In healthy people, the pressure in the portal vein system ranges from 50 to 115 mm of water column. Portal hypertension contributes to the occurrence of portocaval anastomoses and their varicose veins. During portal hypertension, the largest amount of blood flows through the veins of the esophagus and stomach, the smaller amount flows through the veins of the anterior abdominal wall, hepatoduodenal ligament, rectum, etc. There are three forms of portal hypertension: intrahepatic, supra- and subhepatic.

Intrahepatic form(80 -- 87%) occurs as a result of damage to the venous bed in the liver, mainly in the sinusoid area. It very often develops with cirrhosis of the liver, in which the growing connective tissue compresses the intrahepatic venous vessels.

Suprahepatic form(2 -- 3%) develops as a result of complete or partial blockage of the hepatic veins. The causes of its occurrence are often obliterating endophlebitis or thrombophlebitis of the hepatic veins, thrombosis or stenosis of the inferior vena cava at the level of the hepatic veins.

Subhepatic form(10 -- 12%) occurs in the case of complete or partial blockade of the portal vein and its large branches (splenic vein, etc.).

The causes of subrenal portal hypertension are phlebitis, thrombosis, phleboscperosis, compression of the portal vein by tumors (for example, carcinoma or pancreatic cyst), enlarged lymph nodes, etc.

Stagnation of blood in the portal vein often leads to the development of splenomegaly and blood retention in the spleen, i.e. hepatolienal syndrome. It should be noted that this syndrome occurs not only in connection with portal hypertension, but can also occur with other liver diseases (for example, hepatitis, liver cancer, etc.), acute and chronic leukemia, etc. This combined damage to the liver and spleen with an increase in their volume is explained by the close connection of both organs with the portal vein system, the saturation of their parenchyma with elements of the reticulo-histiocytic system, as well as the commonality of their innervation and lymphatic drainage pathways.

A significant enlargement of the spleen is usually accompanied by an increase in its function (hypersplenism), which is manifested by anemia, leukopenia and thrombocytopenia.

Thrombocytopenia can lead to the development of hemorrhagic complications.

With severe portal hypertension, especially if it is a consequence of intrahepatic block, it often develops edematous-ascitic syndrome, those. ascites and characteristic hepatic edema occur.

In the formation of ascitic fluid, a significant role belongs to excessive lymph formation in the liver and increased extravasation in the vessels of its microvasculature. As a result, extravasation of fluid from the vascular bed into the abdominal cavity increases. The formation of ascites is promoted not only by increased hydrostatic pressure in the sinusoids and venules (portal hypertension), but also by a decrease in plasma oncotic pressure due to hypoproteinemia, as well as sodium retention and increased osmotic pressure in the liver tissue due to an increase in molar concentration as a result of metabolic disorders caused by hypoxia.

In the occurrence of edema, an important place is occupied by liver damage, in which the process of neutralization of toxins is disrupted, angiotensin-11 and especially aldosterone are insufficiently inactivated. This leads to intoxication, reduction and disruption of protein synthesis, and fluid retention in the body. As a result of the predominance of globulins over albumins, persistent hypooncotic edema is formed, most often in the lower extremities, as they are usually combined with venous stasis in the liver, portal hypertension and ascites.

We must not forget that a significant accumulation of fluid in the abdominal cavity can appear both as a result of portal hypertension and liver damage, and as a result of circulatory failure, damage to the peritoneum by a tumor and tuberculous process, etc.

In the case of the development of powerful venous collaterals, through portacaval anastomoses from the intestine enters the general bloodstream. a large number of substances that are normally subject to transformation in the liver: ammonia, urea, free phenols, amino acids, fatty acids, mercaptans, etc. These substances, accumulating in the blood serum in elevated concentrations, turn out to be toxic and contribute to the development portosystemic encephalopathy, which is often called hepatargy, or hepatocerebral syndrome. The concept of serum-biochemical liver shunt syndrome. The latter occurs not only with the development of portocoval anastomoses due to portal hypertension (for example, with cirrhosis of the liver), but also with severe parenchymal lesions of the liver, for example, with fatty liver degeneration, chronic aggressive hepatitis, acute yellow atrophy of the liver, etc. It should be remembered that the content ammonia in the blood serum can be increased with renal acidosis, chronic renal failure, hereditary defects in urea synthesis enzymes, etc.

Clinic and diagnostics

In clinical practice, the most common signs of portal hypertension are portocaval anastomoses in the form of dilated veins on the anterior abdominal wall and hemorrhoids accessible to inspection, ascites, hepatolienal syndrome (splenomegaly and hypersplenism), esophageal-gastric bleeding from varicose veins of these organs, portosystemic encephalopathy and serum -biochemical liver shunt syndrome.

When examining a patient with portal hypertension, signs can be detected collateral circulation -- dilation of veins on the anterior abdominal wall and hemorrhoids. In patients with suprahepatic portal hypertension, dilated veins are most often localized along the lateral walls of the abdomen, on the back and lower limbs. With intrahepatic portal hypertension, dilated veins are localized on the anterior abdominal wall around the navel (head of Medusa) towards the chest or suprapubic region.

Development ascites preceded by bloating associated with flatulence resulting from worsening resorption of gases from the intestines. In patients with significant ascites, the abdominal circumference is increased; when the patient is standing, the abdomen has a spherical shape with the lower half protruding forward or drooping. When lying on your back, your stomach spreads out to the sides and resembles that of a frog. The navel may protrude, and white stripes appear on the skin of the abdominal wall from excessive stretching (striae). Percussion reveals a dull sound over the sloping or lateral part of the abdomen. If the position of the body changes, the dullness also moves.

With pronounced portocaval anastomosis a constant noise is heard around the navel and in the epigastrium. Systolic murmur over the liver area can be observed with increased local arterial blood flow, caused, for example, by cirrhosis or a liver tumor.

Important symptoms of portal hypertension are splenomegaly And hypersplenism. With splenomegaly, patients complain of a feeling of heaviness or pain in the left hypochondrium, caused by extensive fusion of the spleen with surrounding tissues, as well as splenic infarctions.

Hypersplenism is manifested by a decrease in the number of platelets to 80,000 - 30,000, the number of leukocytes - to 3000 - 1500 in 1 μl of blood. Moderate anemia is observed.

Patients with portal hypertension often experience symptoms hemorrhagic diathesis, caused primarily by coagulopathy as a result of liver damage and thrombocytopenia due to hypersplenism. This is bleeding from varicose veins of the esophagus and stomach, nasal mucosa, gums, uterine bleeding, hemorrhoidal bleeding, etc. Bleeding from the veins of the esophagus and stomach sometimes occurs suddenly against the background of complete well-being. It is manifested by profuse bloody vomiting, often ending in acute liver failure and death of the patient.

Hepatoria, or portosystemic encephalopathy, manifests itself in various neuropsychiatric disorders. increased tendon reflexes, increasing muscle tone, muscle twitching, ataxia, etc., euphoria, irritability, psychosis, hallucinations, delusions, etc.

Of the instrumental methods for diagnosing portal hypertension, the most informative are x-ray methods, esophagogastroscopy, and percutaneous splenomanometry.

Portal pressure is measured using percutaneous splenomanometry (the spleen is punctured and attached to a Waldmann apparatus needle to measure venous pressure).

Information about the level of blockade of portal circulation and the condition of blood vessels can be obtained using splenoportography.

Dilated veins of the esophagus and stomach are usually detected by X-ray and endoscopic examination.

Splenomegaly is detected using ultrasound, scintigraphy and celiacography. Ascites (especially small amounts of fluid) - using ultrasound and computed tomography.

For portal hypertension, an ammonia load test is sometimes used, which makes it possible to determine the degree of portacaval shunting and indirectly assess the tolerance of food proteins. The patient is given 3 g of ammonium chloride orally, and then its content in the blood is determined. In a healthy person, after exercise, the concentration of blood ammonia does not change (the norm is 11 - 35 µmol/l). In the presence of serum-biochemical liver shunt syndrome, a clear increase in the concentration of ammonia in the blood serum by 2-3 times or more is observed.

2.4 Symptom complexes of acute and chronic liver failure

Definition, causes and mechanisms of development, classification

Symptom complex of liver failure -- This pathological condition, caused by profound violations of numerous and important liver functions for the life of the body, accompanied by neuropsychic disorders of varying severity, up to the development hepatic coma.

Liver failure, according to the nature of its course and the dynamics of clinical and morphological manifestations, can be acute or chronic. Acute liver failure develops over several hours or days and is characterized by clearly manifested and rapidly increasing clinical symptoms. Chronic liver failure develops over several months or years and is characterized by a slow and gradual development of clinical manifestations.

Depending on the main pathogenetic mechanism of development of liver failure, there are three main forms: 1) hepatocellular(true, primary or endogenous), which develops as a result of damage to the liver parenchyma; 2) portal-hepatic(portosystemic or exogenous), which is mainly due to the flow from the portal vein into the common bed through portocaval anastomoses a significant part of the toxic products absorbed in the intestines (ammonia, phenols, etc.); 3) mixed, in which the first and second pathogenetic forms of liver failure are simultaneously observed.

In clinical practice, a mixed form of liver failure is usually observed with a predominant role of underlying endogenous mechanisms.

The leading morphological substrate of hepatic cell failure is dystrophic and necrobiotic changes in hepatocytes. It is characterized by massive necrosis of the liver. Chronic hepatocellular failure is usually associated with both diffuse dystrophic changes in hepatocytes and progressive death of the parenchyma.

Hepatocellular failure can be a complication of any pathological process leading to damage to hepatocytes. Among the many causes of this disease, the most common are acute and chronic hepatitis, cirrhosis, liver tumors, disorders of the intrahepatic portal circulation, diseases complicated by subhepatic cholestasis (cholelithiasis, etc.), poisoning with hepatotropic poisons, severe injuries, burns, massive blood loss, etc.

Portal hepatic failure develops mainly due to liver shunting. It is observed mainly in patients with liver cirrhosis with severe portal hypertension (see “Symptomocomplex of impaired portal circulation due to liver damage”). Portal hepatic failure is usually associated with chronic forms of liver failure.

The risk of developing liver failure due to the above reasons increases significantly under the influence of the following risk factors: alcohol abuse, drug intoxication (barbiturates), anesthesia and surgery, intercurrent infections, nervous shock, gastrointestinal bleeding, overload of dietary protein, amino acids (methionine), paracentesis, use diuretic substances, acute cerebrovascular accident, etc.

Functional liver failure is expressed primarily in metabolic disorders (carbohydrates, fats, proteins, vitamins, hormones, etc.), protective function of the liver, bile-forming and bile-excretory functions, erythropoiesis and blood coagulation

In a healthy person, carbohydrates in the form of monosaccharides are absorbed in the small intestine and enter the bloodstream through the portal vein system to the liver. A significant part of them is retained in the liver and converted into glycogen, some of the monosaccharides are converted into triglycerides and deposited in fat depots, some of them are distributed throughout the body and are used as the main energy material. Impaired carbohydrate metabolism in case of liver damage is a decrease in the synthesis of glycogen, a violation of its breakdown and the formation of glucose from non-carbohydrate substances (glyconeogenesis), which causes the development of hepatogenic hypoglycemia. A decrease in glycogen content leads, in turn, to a decrease in its neutralizing function, in which glycogen participates, turning into glucuronic acid.

Absorption of lipids occurs most actively in the duodenum and the proximal part of the small intestine. The rate of absorption of fats depends on their emulsification and hydrolysis to monoglycerides and fatty acids. The main amount of fat is absorbed into the lymph in the form of chylomicrons - the smallest fat particles enclosed in a thin lipoprotein membrane. Very small amounts of fat enter the bloodstream in the form of fatty acid triglycerides. The main amount of fat is deposited in fat depots

Violation fat metabolism with liver damage, it manifests itself in changes in the synthesis and breakdown of fatty acids, neutral fats, phospholipids, cholesterol and its esters. As a result, the supply of endogenous fat to the liver significantly increases and the formation of protein-lipid complexes is disrupted, which leads to fatty infiltration of the liver. Therefore, for example, with alcohol intoxication, poisoning with hepatotropic poisons, and protein starvation, fatty liver degeneration quickly develops.

With pathological processes in the liver, long-term alimentary hypercholesterolemia may develop, associated with a violation of the liver’s ability to extract cholesterol from the blood.

Proteins are absorbed mainly in the intestine after their hydrolysis to amino acids. Amino acids absorbed into the blood enter the portal vein system into the liver, where a significant part of them is used for protein synthesis both in the liver and outside it, and a smaller part is deaminated to form ammonia, which is highly toxic. Non-toxic urea is synthesized in the liver from ammonia.

Disorders of protein metabolism in liver pathology are manifested primarily by disorders of protein synthesis and urea formation. Thus, with liver diseases, the formation of serum albumin decreases, A- and d-globudins, fibrinogen, prothrombin, etc. As a result, patients develop hypoproteinemia, hypooncotic edema and hemorrhagic syndrome. At the same time, if the liver is damaged, it can begin to produce gamma globulins, which in a healthy person are synthesized in the lymphatic tissue and bone marrow, as well as paraproteins - qualitatively changed globulins.

Violation of urea synthesis in the liver (the main pathway for neutralizing ammonia in the body) leads to hyperammonemia and associated toxic damage to the central nervous system.

Functional liver deficiency can lead to the development of polyhypovitaminosis. Since the intermediate exchange of cyanocobalamin, nicotinic and pantothenic acids, and retinol occurs in the liver, when its parenchyma is damaged, corresponding hypovitaminosis develops. Impaired absorption of fat-soluble vitamins due to a decrease in the biliary function of the liver also leads to impaired metabolism of these vitamins. In addition, when the liver is damaged, the conversion of certain vitamins into coenzymes (for example, thiamine) is reduced.

The liver is one of the most important organs, in which various hormones are inactivated. They are subjected to enzymatic influences, protein binding, hormone metabolites are bound by various liver acids and are excreted with bile into the intestines. The weakening of the liver’s ability to inactivate hormones leads to the accumulation of the latter in the blood and their excessive effect on the body, which is manifested by hyperfunction of the corresponding endocrine organs. A pathologically altered liver is involved in the pathogenesis of various endocrinopathies in many ways. Thus, in men with significant liver damage (for example, severe acute hepatitis, rapidly progressing cirrhosis of the liver), symptoms of androgen deficiency are often observed.

In the liver of a healthy person, many exogenous and endogenous toxic compounds become less toxic after appropriate chemical transformations.

Thus, the products of bacterial decarboxylation of amino acids and other transformations of proteins and fats in the intestine usually enter the portal system into the liver, where they are converted into non-toxic substances. Violation of this antitoxic neutralizing function leads to the accumulation of ammonia, phenols and other toxic products, which causes severe intoxication of the body.

In patients with significant liver damage, the body's resistance to infection decreases. This is explained by a decrease in the phagocytic activity of the mononuclear phagocyte system.

Liver cells secrete bile, which plays an important role in intestinal digestion (see “Symptom complex of intestinal digestive insufficiency”, “Symptom complex of hyperbilirubinemia”).

When the liver is damaged, anemia and hemorrhagic diathesis often develop. The former are caused by a violation of erythropoiesis due to a decrease in the deposition of many factors necessary for hematopoiesis - cyanocobalamin, folic acid, iron, etc. The latter are caused by a decrease in blood coagulation due to a decrease in the synthesis of prothrombin, coagulation factors (V, VII, IX, X) and fibrinogen, as well as hypovitaminosis TO.

Depending on the volume of the remaining unaffected liver mass (1000 - 1200 g or less) and the severity of the pathological process (the predominance of dystrophic or necrobiotic phenomena), three stages of liver failure are distinguished: initial(compensated), expressed(decompensated) and terminal(dystrophic). End-stage liver failure ends hepatic coma and the death of the patient. There are also three stages in the development of hepatic coma, someone threatening someone And actually(i.e. clinically pronounced) to whom.

In clinical practice, the initial (compensated) stage is often called minor liver failure, and the second and third stages - major liver failure.

Clinic and diagnostics

Liver failure can manifest itself as a symptom complex of inflammation of the liver tissue, parenchymal or cholestatic jaundice, edematous-ascitic and hemorrhagic syndromes, hepatogenic encephalopathy, endocrine disorders, etc.

Despite the variety of clinical manifestations of liver failure, the main criteria for assessing its severity are the severity of neuropsychiatric disorders and a decrease in indicators of hepatodepression. Hemorrhagic syndrome is also important for assessing the severity of liver failure.

Patients with minor liver failure complain of general weakness, emotional instability, and rapid mood swings. There is a decrease in the body's tolerance to alcohol and other toxic effects. Moderate changes in laboratory stress test parameters are detected, indicating disturbances in the metabolic functions of the liver (serum-biochemical syndrome of hepatocellular insufficiency, or hepatodepression).

Detection of hepatodepressive syndrome is usually carried out using serum cholinosterase, serum albumin, prothrombin index and serum proconvertin, as well as using stress tests (bromosulfalein, indocyanine, etc.).

Cholinesterase: the norm in blood serum is 160 -- 340 mmol/(tsp); albumin - 35 - 50 g/l; prothrombin index -- 80 -- 110%, blood serum proconvertin -- 80 -- 120%. Bromsulfalein test(BSF) according to Rosenthal and White: normally, 45 minutes after administration, no more than 5% paints. Indocyanine test: Normally, 20 minutes after administration, no more than 4% of the dye remains in the blood serum. The presence of hepatodepressive syndrome is indicated by a decrease in hepatodepression indicators and an increase in the amount of dye in the blood serum. Hepatosuppression is considered insignificant when indicators of hepatosuppression decrease by 10 - 20%, moderate - by 21 - 40%, significant - by more than 40%.

The main clinical signs of major liver failure are encephalopathy And hemorrhagic syndrome. In addition, patients may have signs of metabolic disorders, fever, jaundice, endocrine and skin changes, ascites, edema, etc.

The main symptoms of encephalopathy are stunned patients, their inadequacy, euphoria or, conversely, mental depression, insomnia at night and drowsiness during the day, sometimes severe headaches, dizziness, short-term disorientation and mild fainting.

Hemorrhagic syndrome is manifested by subcutaneous hemorrhages, especially on the elbows, in the area of venipuncture, gingival and nasal bleeding, a decrease in the prothrombin index and proconvertin. At this stage, there may be signs of metabolic disorders, including polyhypovitaminosis - weight loss, gray dry skin, glossitis, cheilosis, anemia, peripheral neuritis, etc. Patients complain of decreased appetite, poor tolerance fatty foods, dyspepsia, nausea and vomiting.

Fever, often observed in liver failure, usually indicates a septic condition of the patient due to reduced resistance to infection coming from the intestines. Fever due to liver failure Maybe be of non-infectious origin due to impaired inactivation of pyrogenic steroids by the liver and their accumulation in the blood.

Hyperbilirubinemia and jaundice are often a manifestation of functional failure of hepatocytes (see “Symptom complex of hyperbilirubinemia”).

An unfavorable prognostic sign of the development and progression of liver failure is edematous-ascitic syndrome (see “Symptom complex of impaired portal circulation due to liver damage”).

In chronic liver failure, endocrinopathies are possible. Thus, in men with rapidly progressing cirrhosis of the liver, symptoms of androgen deficiency are often noted: along with a clear reverse development of hair growth, the penis and testes are reduced, sexual potency and libido are weakened. In many cases, gynecomastia appears, the stroma often increases prostate gland. Liver cirrhosis in childhood and adolescence leads to a severe slowdown in bone development, growth (“hepatic short stature” by Fanconi), and puberty, which is associated with insufficient testosterone formation. The weakening of the development of the reproductive apparatus determines the picture of eunuchoidism.

In women, the uterus atrophies, mammary glands, will be violated menstrual cycle. Violation of the inactivation of estrogens, and possibly some vasoactive substances, is caused by small cutaneous telangiectasias - “spider veins”, palmar erythema, expansion of the cutaneous vasculature of the face.

The second stage of liver failure is characterized by pronounced manifestations of the serum-biochemical syndrome of hepatocellular failure. Hypoproteinemia, hypergammaglobulinemia, hyperbilirubinemia, decreased levels of fibrinogen, cholesterol, dissociation of bile acids in the blood, high activity of indicator and organ-specific enzymes are noted.

The third stage of liver failure is actually a coma stage, in which, according to the severity of psychomotor disorders and changes in the electroencephalogram, 3 stages are distinguished. IN first stage, precoma, symptoms of encephalopathy progress; the feeling of anxiety and melancholy intensifies, the fear of death appears, speech becomes difficult, and neurological disorders increase.

The precoma stage in patients with portacaval coma is characterized by the phenomena of portosystemic encephalopathy, i.e. transient disturbances consciousness.

Electroencephalographic changes are insignificant. Patients at this stage are often exhausted, or even cachectic. There are profound metabolic disorders in the body. Dystrophic changes are observed not only in the liver, but also in other organs.

The beginning of an impending catastrophe is indicated by a decrease in the size of the liver with persistent or increasing jaundice, the appearance of a sweetish “liver” (methyl mercaptan) odor from the mouth, an increase in hemorrhagic syndrome, and tachycardia.

In second stage, threatening coma, the patients' consciousness is confused. They are disoriented in time and space, attacks of excitement are replaced by depression and drowsiness. A flapping tremor of the fingers and convulsions appear. Delta waves appear on the electroencephalogram against a background of slowing alpha rhythm.

Stage three, complete coma, characterized by a lack of consciousness, rigidity of the muscles of the limbs and the back of the head. The face becomes mask-like, clonus of the foot muscles, pathological reflexes (Babinsky, grasping, sucking) are observed. pathological breathing Kussmaul and Cheyne - Stokes. Shortly before death, the pupils dilate, the reaction to light disappears, corneal reflexes fade, paralysis of the sphincters occurs and breathing stops. They disappear on the electroencephalogram A- and b-waves, hypersynchronous delta waves or irregular slow waves predominate

For hepatogenic encephalopathy, which is an integral part of hepatocellular (primary) failure, is characterized by the rapid development of deep coma, often occurring with a period of excitement, jaundice, hemorrhagic syndrome, and in functional terms, a rapid progressive decline in hepatodepression indicators

Portosystemic encephalopathy, which occurs with portal-hepatic (secondary) failure, is characterized by the gradual development of coma without excitement and a clear increase in jaundice. In functional terms, there is a clear increase in indicators of liver shunting (see “Symptomocomplex of impaired portal circulation caused by liver damage”) with relatively stable (compared to the initial state) indicators of hepatodepression.

Diseases of the liver and biliary tract

From this chapter you will learn why the liver does not hurt, and what bothers you on the right side; you'll think about whether it's worth eating dried fish and petting cats, you'll figure out how many stones your gall bladder can withstand...

They say that dreams are your clues for the future: what to do, what to watch out for. In this sense, the “dream book” did its best regarding the liver. Judge for yourself: “if you dream that you have a diseased liver, this means that a grumpy and dissatisfied woman will become your wife, filling your house with nagging and empty worries; hearing the smell of liver in a dream means running around on errands without results.” And I especially like “cutting the liver in a dream means winning the lottery.”

Let’s talk about this, since it’s unlikely that you treat your liver so badly that you are ready to turn your relationship with it into a lottery “if it gets sick, it doesn’t get sick.” Otherwise you would read in this moment a romance novel or detective story, and not a book from the “Natural drugs will help” series.

By the way, about natural drugs. It is thanks to the liver that many people turn their attention to natural remedies, realizing that chemical drugs, to one degree or another, do not affect it in the best way.

Why can the liver get sick?
and gallbladder

There is nothing superfluous in the body, and nature created the liver as the largest gland in our body for a reason. It has too many functions. Conventionally, they can be divided into digestive and all others. It’s impossible to say which are more important.
On the one hand, it is important that the liver stands in the way of hydrolysis products formed in the gastrointestinal tract entering the general bloodstream; they undergo enzymatic transformations in liver cells. Everything we eat and drink is absorbed in the stomach and intestines, enters the liver, and only after passing through this filter does it go to other organs. On the other hand, how could we live if the liver did not produce hemoglobin? What about blood clotting factors? They are also vital, not to mention the fact that a number of hormones “die” in the liver, having completed their function. If this process were disrupted, our body would simply become uncontrollable due to hormonal imbalances.

The liver not only stores blood “for every firefighter”, but also performs the function of a “stove” - it warms up the blood circulating through the vessels, maintaining a constant internal environment.

And finally, the liver is a very large digestive gland. Bile, produced by the liver, is a digestive juice. The main components of bile are bile salts. Bile acids are formed in the liver during the oxidation of cholesterol. During the day, about 1 liter of bile is formed. Between meals, bile accumulates in gallbladder. But it is released into the duodenum only in response to food intake. Bile salts emulsify fats, facilitating their contact with enzymes in digestive juices. They also activate pancreatic juice enzymes and promote fat absorption. As a result, bile creates optimal alkaline environment, necessary for the functioning of enzymes in pancreatic juice and intestinal glands.

Now that you understand how the liver and bile ducts work, it will be much easier to understand where you can expect a “blow”.

Let's start with the banal option. You don't bother choosing healthy eating, i.e. eat what you want and when you have to. In addition, you are the “happy owner” of vegetative-vascular dystonia, neurosis, spinal osteochondrosis, etc. Then, in addition, you will also receive discs
biliary tract nesia. In practice, this will mean that bile will be released not when it is required for normal digestion, but at its own discretion. The result is chronic stagnation of bile in the gallbladder, a tendency to form stones, decreased activity of liver cells and potentially even their degeneration into fibrosis.

Another situation is just as common, but more serious than just stagnation. Since the liver is a filter, it may not be able to cope with the load of filtering blood filled with toxins from the intestines affected by dysbiosis 24 hours a day (do not think that if you are not “abusing” it, then the liver is not subject to stress). And for those who are prone to alcoholic excesses, it is better to immediately learn by heart the section “The most effective natural remedies for liver diseases.” To the same section I also refer readers who take medications daily, work with paints, varnishes, adhesives, any types of fuel, etc. In these cases, there is a high risk of developing chronic hepatitis, and then cirrhosis of the liver.

It is extremely important that, as experienced drinkers say, “the liver is an unpaired organ.” It is impossible to completely remove it. And partial operations on the liver are difficult due to increased tissue bleeding. The gallbladder is also not a mistake of nature, and everyone should preserve it available means, since when you remove the bubble, you doom yourself to the risk of stone formation already in the intrahepatic bile ducts. Whether it is needed for the purpose of retaining bile can be easily understood by imagining that the kidneys, for example, would begin to excrete urine directly, bypassing the bladder...

The spread of laparoscopic surgeries to remove the gallbladder is a benefit for people, as it saves them from long hospital stays, complications, and blood loss. But this does not mean that everyone needs to remove stones along with the gallbladder. The composition of bile can and should be regulated by wisely using natural preparations.

Liver cells are very sensitive to both negative and positive influences. For most liver diseases, after 10-14 days of taking high-quality natural remedies, it is possible to reliably confirm (according to tests) an improvement in the function of the organ. Today, both chronic hepatitis and cirrhosis can be “kept in check” with a reasonable approach to diet and the use of natural remedies.

Before going on to describe the various diseases of this system and tell you what needs to be done, I simply must draw your attention to one very common misconception.

Visitors who come to us at the Health Recipes center with a desire to take care of their liver (“something is bothering the liver”), in most cases, do not suspect that the real cause of discomfort in the right side is problems with the gallbladder. The liver as such only hurts with hepatitis, cirrhosis and the like serious illnesses due to capsule stretching. Nature did not provide the liver itself with nerve endings.

Viral hepatitis

Viruses that cause hepatitis belong to different groups and have different biological properties. Hepatitis viruses include: hepatitis A virus, hepatitis B virus, hepatitis C virus, hepatitis D or delta hepatitis virus, hepatitis
titus E, hepatitis F virus and hepatitis G virus. Others are believed to exist. In addition, hepatitis can be caused by viruses such as yellow fever virus, herpes viruses, rubella virus, Coxsackie virus, Lassa fever virus, and Marburg-Ebola fever viruses. But we will focus on the most common ones. Moreover, I’ll tell you a secret, it would be possible not to continue the description at all. To help with natural remedies, the only thing that is of fundamental importance is that the disease is caused by viruses (which means we will activate antiviral immunity) and that they infect liver cells (hepatoprotectors, in any case, are the same).

Treatment of viral hepatitis is a very responsible process and should be carried out by a doctor. However, to be honest, no one knows whether you will come across a qualified doctor on your way who is not limited to recommendations like “rest, a positive attitude and vitamins” or not.
But the liver is yours, not the doctor’s. Here we will provide only those recommendations that will not be superfluous for any form of the disease, and even more so, only those that are known to be safe and effective. It is these additions that distinguish the standard approach to the treatment of hepatitis from the complex modern one.

You can become infected with hepatitis in a variety of ways.

Hepatitis A. The incubation period for hepatitis A (formerly known as infectious hepatitis) ranges from 15 to 45 days. The pathogen spreads mainly through food, through dirty hands, and is transmitted from person to person.

Hepatitis B. Typically spread through blood or blood fractions, but transmission can also occur through saliva, seminal fluid, vaginal secretions and other body fluids. In other words, during sexual intercourse, using other people’s personal hygiene items and medical procedures, as well as from mother to child during pregnancy. Relatively new method transmission - during acupuncture procedures, tattoos, piercings.

Hepatitis C. About 10% of cases are caused by blood transfusions (Alter, Sampliner, 1989).
Ordinary sexual contact plays a significant role in the spread of this form of hepatitis. Another important route of transmission is intravenous injection. It is known that this type of hepatitis occurs more often in drug addicts.

Delta hepatitis, also called hepatitis D, was first discovered in the late 1970s; fortunately, it is rare. The hepatitis D virus can only multiply in the presence of the hepatitis B virus, causing a more severe course of the disease.

The incubation period (from the moment of infection to the manifestation of the disease) for viral hepatitis can be very different: from 10 days for hepatitis A to 80 days (or even more) for hepatitis B.

In addition to acute hepatitis, there are also chronic forms, when the virus persists in liver cells, that is, it slowly engulfs one cell after another. It is even possible to introduce viral DNA into the chromosomes of the host cell. Oncogenic viruses are preserved in this form. This is the mechanism that explains why with hepatitis B the risk of developing liver cancer is several times higher.

It also happens that you carry the virus without any external manifestations diseases. A carriage is considered to be the detection of a special marker (HBsAg) in a person’s blood for more than six months in a row in the absence of other signs of hepatitis.

HBsAg carriage develops in more than 90% of newborns, 10-15% of children and young people and 1-10% of adults. In people with immunodeficiency conditions, carriage develops much more often. Knowing this, it is worth taking a closer look at the immunomodulators presented in this book. Finally, carrier status is slightly more common in men than in women. Carriers are one of the main distributors of the hepatitis B virus.

Currently, it is believed that there are more than 300,000,000 asymptomatic chronic carriers of hepatitis living on the globe, of which more than
3,000,000 - in our country. According to statistical research, the highest frequency of detection of HBsAg carriers (8.0-10.0%) was recorded in Uzbekistan, Turkmenistan, Kyrgyzstan and Moldova, which is useful to know when going on a trip or organizing, for example, the life of hired construction workers.

The HBsAg carrier state can last up to 10 years or more, in some cases for life. Nevertheless, there is a prospect of getting rid of the virus, and you need to take advantage of this, protecting the liver and increasing immunity.

How it manifests itself

Manifestations of hepatitis are different. That is why you can answer with confidence that you have not had hepatitis only after tests, and even then, if a carrier state (hepatitis B) has not formed, then the tests may not give an unambiguous answer. During bioresonance examinations at our center, we often see that the liver, for no obvious reason, looks as if it has been attacked by toxic substances. And the person does not drink, does not smoke, does not take medications and is not involved in any way with harmful substances at work. Often this indicates hepatitis suffered in an atypical form.

Symptoms of hepatitis A:

 body temperature rises to 38-39° (stays for 1-3 days);

 flu-like symptoms appear - headache, severe general weakness, feeling of weakness, muscle pain, chills, drowsiness, restlessness night sleep;

 loss of appetite, perversion of taste, feeling of bitterness in the mouth;

 nausea, sometimes vomiting;

 feeling of heaviness and discomfort in the right hypochondrium;

 change in color of urine (the color of strong tea) and feces ( White color);

 yellowing of the skin and whites of the eyes;

 with the onset of the icteric period, the temperature decreases and the condition improves, the symptoms of general intoxication disappear, but weakness, malaise and increased fatigue persist for a long time.

In the anicteric form, hepatitis A may well masquerade as severe form flu Complete recovery in most cases (90%) occurs within 3-4 weeks from the onset of the disease. In 10%, the recovery period lasts up to 3-4 months, but chronic hepatitis does not develop.

Symptoms of hepatitis B:

Joint pain is added to the symptoms of hepatitis A, and the severity of the condition and fever increase along with jaundice and reflect the degree of liver damage.

The acute phase of the disease occurs with symptoms of severe general intoxication. In acute hepatitis B, the recovery period is 1.5-3 months. But immunity is formed for life. Full recovery occurs in 70% of people. With weak immunity, the disease progresses to chronic form. The outcome of chronic hepatitis B is cirrhosis of the liver.

Symptoms of hepatitis C:

The same as for hepatitis B, but the increase in temperature is not so characteristic, and in general the symptoms are sluggish. Changes in the color of stool and urine are short-term, weight loss is typical; swelling of the legs, swelling of the anterior abdominal wall; redness of the palms.

Hepatitis C virus is the main cause of chronic hepatitis, cirrhosis and liver cancer. Immunity after hepatitis C is unstable, repeated infections are possible. Often the presence of the virus can only be determined by taking a blood test. Recovery from acute hepatitis C most often occurs with the icteric variant of the disease. The remaining majority of patients (80-85%) develop chronic carriage of the hepatitis C virus.

20-40% of patients with chronic hepatitis C develop cirrhosis of the liver, which may remain unrecognized for many years.

Chronic hepatitis

This disease develops either as a complication of viral hepatitis, or without infection - when liver cells are damaged by toxic substances (alcohol, drugs, industrial factors). The most common causes of toxic hepatitis are dichloroethane, carbon tetrachloride, chloroform, acetic acid, arsenic, copper sulfate. You probably yourself know that it is also not healthy to breathe exhaust fumes, vapors of adhesives, varnishes, paints, smoke from burning rubber, plastic, and polyethylene. Drug-induced toxic hepatitis can be caused by derivatives of phenathiosine, azathioprine, some contraceptive drugs, anabolic steroids, and tranquilizers.

How it manifests itself

The first and most common manifestation of toxic liver damage is pain syndrome. Pain in the right hypochondrium is observed even in initial stages influence of toxic substances. The pain intensifies after eating spicy or fatty foods. It is mostly dull in the right hypochondrium, but can also have a paroxysmal nature with irradiation to the right shoulder blade and arm.

The leading role in the origin of this syndrome is played by lesions of the biliary tract, namely dyskinesia. Over time, weakness, increased fatigue, and decreased performance develop. As it progresses, asthenoneurotic syndrome appears with symptoms of nervousness, hypochondria, and sudden weight loss. Moderate enlargement of the liver is observed in approximately 90% of patients, and slight enlargement is observed in 15-17%. Also of concern are indigestion and a feeling of bitterness in the mouth, decreased appetite, and unsteady stool. Jaundice (jaundice syndrome), usually mild, occurs relatively rarely - in approximately a quarter of patients. The appearance of spider veins and persistent redness of the palms is also rare.

Patients with chronic hepatitis should take into account what points may contribute to the deterioration of the condition. Few people think about many of them. In particular, the liver does not like vegetables and herbs with a strong taste (radish, radish, garlic, cilantro), as well as anything sour (cranberries, sorrel, vinegar) and bitter (mustard, horseradish), smoked foods and pickles.

Active sports lead to a redistribution of blood during exercise - it saturates the loaded muscles, and the liver tissue is drained of blood.

On the other hand, the body should receive approximately 100 grams of protein daily. The diet should include lean meat and fish, cottage cheese, egg whites, skim milk and sweets in reasonable quantities.

Cirrhosis of the liver

Cirrhosis in Greek means "red, lemon yellow." This is exactly the shade that the normally red liver takes on in sick people. Liver cirrhosis is a change in the structure of the liver in which normal liver cells are replaced by scar tissue.

Most often, cirrhosis is caused by hepatitis B or C, as well as alcohol or drug abuse. It is also not recommended to “eat” toadstools, which, unfortunately, is sometimes practiced by teenagers to obtain a hallucinogenic effect.

Severe disturbances in bile secretion for a long time are also not indifferent to the liver. Finally, there is an autoimmune mechanism for the development of cirrhosis, when the body digests its own cells.

There is one more factor you should be aware of. As a result of studying statistical data among people who do not drink alcohol, a significant connection was revealed between obesity or excess weight and hospitalization and death from cirrhosis of the liver. These are the people who did not expose their liver to toxic substances, but only “tortured” it increased loads related to digestion.

Changes in the structure of the organ and the loss of normal liver cells during cirrhosis lead to the fact that the liver is not able to synthesize proteins and other substances needed by the body, as well as neutralize toxins. Overgrown scar tissue compresses blood vessels, leading to poor circulation.

How it manifests itself

With cirrhosis, the liver increases in size or decreases in size. Over time, the belly increases. This is due to the accumulation of fluid in the abdominal cavity. Symptoms of dyspepsia occur:

 increased gas formation;

 nausea;

 feeling of bitterness in the mouth;

 belching;

 urinary retention.

The veins on the front wall of the abdomen expand, and a characteristic vascular pattern appears around the navel, reminiscent of the “head of a jellyfish.” Red spots that look like stars or small spiders appear on the chest, back and shoulders.

Symptoms of general intoxication in the form of headaches also appear. The person becomes weakened and loses weight. Jaundice and skin itching may develop.

Unfortunately, it is impossible to cure cirrhosis. But you can significantly slow down its course so that, if possible, fewer liver cells die.

Introduction

Laboratory and instrumental methods for studying patients with gallbladder diseases

Diagnosis of patients with gallbladder diseases

Diagnostic methods for liver disease

Hepatitis

3.2.Chronic hepatitis

Cirrhosis of the liver

Fatty liver

Conclusion

List of used literature

Lecture Diseases liver, gall tract and peritoneum

Ultrasound and its applications (2)

Objective methods abdominal examinations

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and gallbladder