Ivanovo Pharmaceutical College |
Coursework |
Means for the treatment of the liver and biliary tract. |
Discipline: Medicine. |
Completed by: Dimitrieva N. A. Student of group 31 - M Head: Rozhdestvensk 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 liver and biliary tract diseases ………………………… .............................. .................................................. ....................ten
Chapter 4: Medicinal plants used in 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 markedly. This is due to the fact that many biologically active substances of plant origin are successfully used in combination with other drugs.
The set goal of the course work is to study the principles of therapy of diseases of the liver and biliary tract with drugs and medicinal plants. During the course work, the following tasks were set:
1. to characterize the most common diseases of the liver and biliary tract;
2. to study the composition and action of medicinal products and plants used for the treatment of these diseases;
3. draw conclusions on the use of official drugs and plants in the treatment of liver and biliary tract diseases.
The material for writing this coursework was educational, reference literature, and also articles from modern medical journals and Internet resources were used.
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. In electronic sources, many aspects of the problem under study are disclosed.
The first chapter deals with the problems associated with the characteristics of the main liver diseases; in the second chapter, brief characteristics of diseases of the biliary tract are considered.
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 the conclusion, the conclusions drawn based on the analysis of the course material discussed in the course are presented.
Chapter 1: Brief description of the main liver diseases.
The role of the liver in the body is great. It performs a number of very important functions, one of which is bile formation, and bile takes part in digestion, especially in the processing and assimilation of fats. Bile enhances the contraction of the intestinal muscles (peristalsis), which contributes to the normal movement of food and residues of undigested food. Bile helps to reduce fermentation and putrefactive processes in the intestines. All nutrients absorbed in the intestines must necessarily 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. As the most common among them, experts identify an infectious factor (we are talking about hepatitis viruses), a sugar disease ...
Liver and biliary tract damage caused by the fluke Opisthorchis viverrini is a serious health problem in Asia, especially Thailand and Vietnam. In recent years, the flow of citizens of the Russian Federation to this tourist destination has sharply increased, and unclear cases of diffuse liver diseases have appeared in clinical practice in persons who were in these regions. It seems important to highlight the features of the development of liver and biliary tract lesions during infection with Opisthorchis viverrini for the timely recognition and treatment of this helminthiasis by specialists. The article describes in detail the clinical course of the disease: the acute stage can last up to 2 months, after which the clinical symptoms gradually subside and the disease passes into the chronic stage. Among the symptoms of the disease in some cases there may be only symptoms of cholangitis and cholecystitis, in others - a combination of them with signs of deficiency of digestive enzymes or allergic reactions. Treatment is carried out in 3 stages, the only drug for the treatment of any opisthorchiasis invasion is the anthelmintic praziquantel.
Keywords: Opisthorchis viverrini, trematode, liver disease, helminthiasis.
For citation: Akhmedov V.A., Gaus O.V. Modern views on the problem of liver and biliary tract damage associated with the helminth Opisthorchis viverrini // BC. Medical Review. 2016. No. 26. S. 1811-1814
Current views on liver and bile duct disorders caused by Оpisthorchis viverrini
Akhmedov V.A., Gaus O.V.
Omsk State Medical University
Liver and bile duct disorders caused by trematoda Opisthorchis viverrini (persists as metacercaria in the muscles of freshwater fish) is an important health care issue in Asian countries, in particular, in Thailand and Vietnam. In recent years, the number of Russian tourists who visit these countries is growing. Meanwhile, unclear diffuse liver disorders in patients who visited these areas are more common in clinical practice. It is of crucial importance to discuss clinical features of liver and bile duct disorders caused by Opisthorchis viverrini to provide early diagnosis and treatment of this helminthosis. The paper describes in detail clinical course of the disease. Acute phase lasts up to two months, then clinical symptoms gradually reduce, and the disease converts to chronic condition. The disease can manifest with the symptoms of cholangitis and cholecystitis only or in combination with digestive enzyme deficiency signs or allergic reactions. Three-step therapy with praziquantel is prescribed for Opisthorchis invasion.
Key words: Opisthorchis viverrini, trematoda, liver disorders, helminthosis.
For citation: Akhmedov V.A., Gaus O.V. Current views on liver and bile duct disorders caused by Оpisthorchis viverrini // RMJ. 2016. No. 26. P. 1811-1814.
The article is devoted to the problem of liver and biliary tract damage associated with the helminth Оpisthorchis viverrini
Literature
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5. Shin H.-R., Oh J.-K., Masuyer E. et al. Epidemiology of cholangiocarcinoma: An update focusing on risk factors // Cancer Sci. 2010. No. 101. P. 579–585.
6. Sithithaworn P., Yongvanit P., Duenngai K. at al. Roles of liver fluke infection as risk factor for cholangiocarcinoma // J Hepatobiliary Pancreat Sci. 2014. No. 21. P. 301–308.
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9. Songserm N., Promthet S., Wiangnon S., Sithithaworn P. Prevalence and co-infection of intestinal parasites among Thai rural residents at high risk of developing cholangiocarcinoma // Asian Pac J Cancer Prev. 2012. No. 13. P. 6175–6179.
10. Sripa B, Brindley PJ, Mulvenna J et al. The tumorigenic liver fluke Opisthorchis viverrini multiple pathways to cancer // Trends Parasitol. 2012. No. 28. R. 395-407.
11. Sripa B., Thinkhamrop B., Mairiang E. et al. Elevated plasma IL-6 associates with increased risk of advanced fibrosis and cholangiocarcinoma in individuals infected by Opisthorchis viverrini // PLoS Neglected Tropical Diseases 2012. No. 6. P. 1–9.
12. Wattanayingcharoenchai S, Nithikathkul C, Wongsaroj T. et al. Geographic information system of Opisthorchis viverrini in northeast Thailand // Asian Biomedicine. 2011. No. 5. P. 687–691.
13. Sripa B., Mairiang E., Thinkhamrop B. et al. Advanced periductal fibrosis from infection with the carcinogenic human liver fluke Opisthorchis viverrini correlates with elevated levels of interleukin-6 // Hepatology. 2009. No. 50. P. 1273-1281.
14. Yongvanit P., Pinlaor S., Loilome W. Risk biomarkers for assessment and chemoprevention of liver fluke-associated cholangiocarcinoma // J Hepatobiliary Pancreat. Sci. 2014. No. 21. P. 309–315.
15. Kusumaporn Chaiputcha, Supannee Promthet, Peter Bradshaw Prevalence and Risk Factors for Infection by Opisthorchis viverrini in an Urban Area of Mahasarakham Province, Northeast Thailand. 2015. Vol. 16.P. 4173-4176.
16. Ninlawan K., O "Hara SP, Splinter PL Et al. Opisthorchis viverrini excretory / secretory products induce toll-like receptor 4 upregulation and production of interleukin 6 and 8 in cholangiocyte // Parasitol Int. 2010. Vol. 59. No. 4. P. 616-621.
17. Yonglitthipagon P., Pairojkul C., Chamgramol Y. et al. Upregulation of annexin A2 in cholangiocarcinoma caused by Opisthorchis viverrini and its implication as aprognostic marker // Int J Parasitol. 2010. Vol. 40. No. 10. P. 1203–1212.
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Introduction
1. Diseases of the liver
1.1 Anatomy, structure, functions of the liver
2 Bile, bile formation
1.3 Major liver diseases
2. Diseases of the gallbladder
1 Anatomy, structure, function of the gallbladder
2 Major diseases of gallbladder
3. Modern diagnostics of liver and gallbladder diseases
1 Ultrasound examination (ultrasound)
2 Radioisotope scanning
3 Positron emission tomography
4 Computed tomography
5 Magnetic resonance imaging
6 Liver biopsy
4. Assessment of the availability of methods for diagnosing liver and gallbladder diseases
Conclusion
List of used literature
Introduction
In recent years, throughout the world, there has been a steady increase in liver and biliary tract diseases, of various etiologies, resulting in severe complications.
According to the prevalence of liver diseases in Russia, one can distinguish:
in the first place - toxic hepatitis - more than 50%,
in second place is viral hepatitis, 24% of patients.
the third most frequent cause is autoimmune hepatitis 10-13%,
The percentage of healthy and sick people on the territory of the Russian Federation:
Note to the diagram:
Liver disease affects 28% of people - and this is almost a third of all studied. Cholecystitis and gallstone disease are much more common than hepatitis
The topic under study is relevant due to the progressive growth of liver and gallbladder diseases, against the background of the latent course of the disease, the low frequency of patients seeking help from a doctor and not always correct diagnosis of diseases.
The aim of the course work is to prove the necessity of using modern methods of diagnosing diseases of the liver and gallbladder in the work of clinicians.
The object of the research is diseases of the liver and gallbladder.
The subject of the research is modern methods of diagnosing diseases of the liver and gallbladder.
To achieve this goal, you must:
To reveal the anatomical and physiological features of the structure of the liver and gallbladder, the functions of these organs and their diseases.
2. To consider the main complaints and syndromes in the pathology of the liver and gallbladder.
Determine the main methods for diagnosing diseases of the liver and gallbladder.
1. Diseases of the liver
1 Anatomy, structure, function of the liver
The liver is formed by a large right and 6 times smaller left lobes, which are separated by a sheet of the peritoneum. The liver weighs 1.5-2 kg - this is the largest glandular organ in the human body.
The blood supply to the liver is carried out simultaneously from two sources, which underlines the importance of the smooth functioning of the liver. The first source of fresh blood is the hepatic artery, which provides oxygenated arterial blood, and the second is the portal vein, which delivers venous blood from the spleen and intestines to the liver. Both blood vessels enter the liver through a depression located in the right lobe and symbolically called the gate of the liver.
On the inner hepatic surface, approximately in its middle part, there is a gate of the liver, through which the hepatic artery enters and the portal vein exits, as well as the common hepatic duct, which removes bile from the liver.
The structure of the hepatic lobule
The main structural unit of the liver is the hepatic lobule. It is formed by dividing the liver tissue by a connective tissue capsule that penetrates deep into the organ. The hepatic lobule is made up of liver cells called hepatocytes, which are interconnected in tiers, surrounding the bile ducts, venules and arterioles.
Liver functions:
) Participates in the process of digesting food, secreting bile.
) Takes part in all types of metabolism (in carbohydrate metabolism - the formation and accumulation of glycogen, in fat metabolism - by breaking down fats into fatty acids and ketone bodies with bile acids, also produces cholesterol and ensures the deposition of fat in the body).
) Regulates the balance of proteins, fats and carbohydrates. With a lack of carbohydrates from food, it synthesizes them from protein, with an excess of carbohydrates and proteins in food, it processes their excess into fats.
) Promotes the synthesis of hormones of the adrenal glands, pancreas and thyroid gland. It is involved in the synthesis of anticoagulants (substances that prevent blood clotting), the metabolism of trace elements by regulating the absorption and deposition of cobalt, iron, copper, zinc and manganese.
) Protective function (barrier for toxic substances, blood purification, neutralization of all poisons that enter the body from the outside).
) Control of the balance of homeostasis (constancy of the internal environment of the body) is ensured by biotransformation of foreign compounds into water-soluble non-toxic substances, which are excreted from the body by the intestines, kidneys and through the skin.
1.2 Bile, bile formation
Bile is a special fluid that is produced in the liver. Its main tasks are to improve absorption and to activate the movement of food through the intestines.
Bile is produced in the lobules of the liver.
Before bile enters the intestines, it goes through a difficult path along the biliary tract. First, from the liver, it enters the hepatic ducts, from there into the common bile duct, which connects to the gallbladder through the bladder duct. The place where the common bile duct flows into the duodenum is called the Vater papilla. It has its own muscle (sphincter of Oddi), which regulates the flow of bile into the intestines.
1.3 Liver diseases.
Congenital malformations.
Liver injury.
1. Open damage.
1.1. Stab and cut wounds.
1.2. Gunshot wounds.
2. Closed liver injuries (ruptures).
Focal diseases.
1. Inflammatory diseases.
1.1. Nonspecific (abscesses).
1.2. Specific (tuberculosis, syphilis, etc.).
2. Tumors of the liver.
2.2. Malignant tumors.
1. Echinococcosis.
2. Alveococcosis.
3. Opisthorchiasis.
4. Ascariasis.
Diffuse diseases (cirrhosis), the complications of which require surgical correction (portal hypertension).
Ø Chronic hepatitis
Chronic hepatitis is a chronic diffuse inflammatory process in the liver lasting more than 6 months.
Etiology
The disease is caused by acute viral hepatitis, alcohol abuse, dysfunction of the immune system (autoimmune reactions), exposure to certain drugs (salicylates, tetracycline, anabolic steroids, tranquilizers, anticonvulsants).
Depending on the etiological factor, there are: chronic viral hepatitis B, C, D, chronic autoimmune hepatitis, chronic toxic hepatitis.
Clinical manifestations
General weakness, fatigue, subfebrile body temperature, weight loss, impaired appetite, a feeling of heaviness and pain in the right hypochondrium, nausea, bitterness in the mouth, bloating, alternating constipation with diarrhea are noted, and nosebleeds sometimes occur. On examination, yellowness of the skin and sclera, skin itching, in some cases - hemorrhagic skin rashes are noted. Palpation of the abdomen reveals an enlarged liver (it is dense, painful). Sometimes there is an enlargement of the spleen, transient ascites.
There are millions of carriers of hepatitis B and C viruses. It should be noted that due to the lack of information on the ways of infection with viral hepatitis and measures of protection against them, the prevalence of drug addiction, compliance with hygiene rules, the incidence of viral hepatitis is steadily increasing.
Additional examination methods: detection of tissue and serum markers of hepatitis B, C and D viruses,
Ultrasound of the liver,
Puncture biopsy of the liver.
In the UAC - accelerated ESR.
Ø Cirrhosis of the liver
Liver cirrhosis is a chronic progressive liver disease that occurs with a significant decrease in the number of functioning hepatocytes, restructuring of the parenchyma and the vascular system of the liver, followed by the development of liver failure and portal hypertension. More often men are ill.
Etiology
The pathological condition is provoked by the transferred viral hepatitis, autoimmune hepatitis, chronic alcohol abuse, genetically determined metabolic disorders, obstruction of the biliary tract, the toxic effect of various chemicals (occupational hazards, medicinal substances, mushroom poisons).
Clinical manifestations
There are pains and a feeling of heaviness in the epigastrium and in the right hypochondrium, aggravated after eating and physical activity; nausea, vomiting, bitterness in the mouth, itchy skin, irritability, fatigue, bloating, fever, weight loss, impotence, menstrual irregularities, unpleasant liver odor from the mouth. On examination, attention is paid to a reduction in muscle mass, an icteric coloration of the skin, mucous membranes, fingers in the form of "drumsticks", expansion of the veins of the anterior abdominal wall, "spider veins", angiomas, "hepatic palms", bright red color of the lips and tongue, a decrease in the severity of secondary sexual characteristics, atrophy of the genital organs, ascites. With the course of the disease, symptoms associated with secondary damage to the heart, kidneys, pancreas, brain, and endocrine glands join. Characterized by an increase in the spleen with a decrease in the size of the liver. Damage to the nervous system is manifested by the development of hepatic encephalopathy (sleep disturbances, memory loss, headaches, dizziness, apathy, tremors of the fingers are noted, the extreme manifestation is the development of hepatic coma).
Hygiene The incidence of viral hepatitis is steadily increasing.
Additional examination methods:
Identification of tissue and serum markers of hepatitis B, C and D viruses,
Ultrasound of the liver,
Puncture biopsy of the liver.
In the UAC - accelerated ESR.
Biochemical blood test: an increase in transaminases, dysproteinemia, a change in FPP, an increase in direct and indirect bilirubin.
Radioisotope scanning is used.
The state of the liver largely determines the work of the whole organism.
A pathological violation of its functioning immediately affects the general well-being and can lead to a number of serious problems.
With insufficient attention to this vital organ, the emergence and development of liver failure, liver obesity, cirrhosis, and oncological disease can be missed. Timely diagnostics using modern methods will help identify such problems.
liver gallbladder disease
2. Diseases of the gallbladder
1 Anatomy of the gallbladder
The gallbladder is an elongated, hollow muscle sac that stores bile produced by the liver. Under the liver, the gallbladder controls the flow of bile into the duodenum. Bile and bile pigments play an important role in the breakdown and absorption of fats. It is not an irreplaceable organ and is often removed by a surgical procedure known as cholecystectomy in cases of gallbladder disease or gallstones.
Gallbladder anatomy
The gallbladder is a pear-shaped organ that is about 7 to 10 centimeters long and 2 to 3 centimeters wide. It has the ability to accumulate about 50 milliliters of bile inside itself, which can be released, if necessary, through the small bile duct (gallbladder canal) into the common bile duct. From here, bile enters the duodenal lumen. Usually this process is interconnected with the digestion process. The release of bile is carried out under the control of the autonomic nervous system in response to a signal about food intake. Therefore, often, when eating fatty foods, increased bile formation occurs and a person feels the movement of bile. This is just a response to a stimulus.
The wall of the gallbladder is made up of several layers, including the epithelium (inner layer), mucous membrane, muscular frame, and serous membrane (outer layer).
The structure of the gallbladder
The gallbladder consists of 3 parts - the fundus, body and neck. The bottom protrudes from under the liver and is the part visible from the front, which can be examined using ultrasound diagnostic methods. The body is the main dilated part that lies between the bottom and the cystic duct. The neck of the gallbladder is the narrow part that passes into the cystic duct.
The cystic duct is about 3 to 4 centimeters long and transports bile into the common bile duct.
Blood supply and lymphatic drainage
The arterial blood supply to the gallbladder is carried out through the portal artery, which departs from the right hepatic artery. Venous drainage occurs through the bile vein - this mainly accounts for the drainage of venous blood from the neck and cystic duct. Venous drainage of the body and the bottom of the gallbladder is carried out directly with the participation of the visceral surface of the liver and through the hepatic sinusoids. Lymphatic fluid drains into the cystic lymph nodes, which are located near the liver and exit into the abdominal lymph nodes.
The main functions of the gallbladder relate to the storage and secretion of bile.
Accumulation and storage of bile (concentrates the bile coming from the liver, increasing its volume (1 liter of bile can be concentrated in 50 ml).
Bile secretion (muscle contractions of the wall in response to nerve and hormonal factors that stimulate it in response to food intake)
2. Diseases of the gallbladder:
Developmental anomalies (atresia).
Injury to the gallbladder.
1. Injuries to the gallbladder and biliary tract.
2. Iatrogenic damage to the biliary tract.
Cholelithiasis.
Dyskinesia of the biliary tract.
dyskinesia of the gastrointestinal tract of hypertensive type
hypotensive dyskinesia
Acute cholecystitis.
Chronic cholecystitis.
Tumors of the gallbladder
1. Opisthorchiasis (surgical complications).
2. Ascariasis (surgical complications).
Ø Dyskinesia of the gastrointestinal tract of hypertensive type
It develops more often in young people with vegetative-vascular dystonia.
With this type of dyskinesia, the contraction of the walls of the gallbladder occurs with a simultaneous spasm of the sphincter of Oddi. There is a violation of the outflow of bile, the pressure inside the gastrointestinal tract rises, which is the cause of the appearance of sharp pain
Clinical symptoms
Pain syndrome is a consequence of a sudden increase in pressure in the gallbladder, usually after errors in the diet (the use of fatty, spicy, cold foods), psychoemotional stress. Pain occurs or worsens an hour or more after eating. Many patients note pain in the region of the heart, palpitations. Irradiation of pain in the right scapula and shoulder is noted. Sometimes attacks of pain are accompanied by dyspeptic syndrome: nausea, vomiting, constipation. Frequent manifestations of asthenic-vegetative syndrome: increased irritability, sleep disturbances, sweating, headaches.
On physical examination - pain on palpation in the projection of the gallbladder.
There are no signs of inflammation (rise in temperature, leukocytosis and accelerated ESR in the KLA).
With ultrasound, the gallbladder is rounded, its tone is increased, emptying, accelerated.
Duodenal intubation: after the introduction of magnesium sulfate, pain appears or intensifies; bile secretion, accelerated. In portions B and C, the amount of bile is reduced. There is no change in portion A.
Ø Hypotonic dyskinesia of the gastrointestinal tract
This type of dyskinesia develops against the background of a decrease in the tone of the smooth muscles of the walls of the gallbladder and the sphincters of Lutkens and Oddi.
As a result, the contractility of the gallbladder decreases, bile is poorly secreted in the duodenum during normal food stimulation. There is a stagnation of bile and an increase in its amount in the gallbladder. The gallbladder is enlarged, its contractions are sluggish. This can lead to infection of the gallbladder, that is, to the development of cholecystitis.
Clinical symptoms
Characterized by constant dull aching pain in the right hypochondrium without clear irradiation. There is a decrease in appetite, belching with air, nausea, bitterness in the mouth, flatulence, unstable stools.
On palpation, there is moderate pain in the gallbladder region.
Diagnostic data.
Ultrasound: the gallbladder is enlarged, emptying is slow and insufficient.
Cholecystography, cholangiography: the same data.
Duodenal intubation: after the introduction of magnesium sulfate, pain decreases; bile is secreted slowly, sometimes it is necessary to re-introduce a stimulant of bile secretion. Portion B is increased to 100-150 ml (normally 30-70 ml), there are no changes in portions A and C.
Ø Cholecystitis is an inflammation of the gallbladder.
Distinguish between acute and chronic cholecystitis.
Acute cholecystitis is a surgical disease.
Etiology of chronic cholecystitis:
Inflammation of the gallbladder is caused by a bacterial infection: E. coli, staphylococcus, enterococcus, streptococcus. A predisposing factor in the development of cholecystitis is a violation of the outflow of bile. The cause of bile stagnation can be a violation of the regimen and / or rhythm of nutrition, psychoemotional stress, physical inactivity, anatomical and constitutional features (bending of the gallbladder, obesity); constipation, pregnancy, changes in the chemical composition of bile in metabolic disorders, biliary dyskinesia, cholelithiasis.
Clinical symptoms: expressed during an exacerbation.
Pain syndrome is caused by stretching of the ducts (gallbladder) or spasm of the gallbladder (ducts). The pain is localized in the right hypochondrium, radiating to the right scapula, clavicle, shoulder. Pain is provoked by errors in diet (consumption of fatty and fried foods, wine, beer, spicy snacks), physical activity, stress, etc. The intensity of pain depends on the type of dyskinesia and the localization of inflammation. On palpation, pain in the projection of the gallbladder is determined. Dyspeptic syndrome is manifested by belching bitterness, a constant feeling of bitterness in the mouth, nausea, vomiting, flatulence, unstable stools. Intoxication syndrome: Weakness, malaise, subfebrile condition.
Objective examination: often obesity, bloating, occasionally enlargement of the liver (with cholecystocolangitis), pain on palpation of the abdomen in the projection of the gallbladder.
Additional research:
In the KLA - leukocytosis, accelerated ESR.
Duodenal intubation: inflammatory changes in portion B (with cholangitis, in portion C).
Ultrasound of the liver and gallbladder: signs of inflammation and impaired motility of the gallbladder.
Cholecystography: the data are the same.
Ø Chronic non-calculous cholecystitis (CCB) is a chronic inflammatory disease of the gallbladder, manifested by a violation of its motor and concentration functions.
Clinically manifested by nausea, pain in the right hypochondrium irradiating under the right scapula, right forearm 30-90 minutes after eating, subfebrile condition, chills, right-sided migraine.
Prolonged soreness in the classic bile points, deep palpation in the gallbladder area cause nausea.
By the nature of the course, chronic bile duct disease is often or rarely recurrent; in phase - in exacerbation or remission.
Ø Cholelithiasis (GSD)
Gallstone disease is a metabolic disease characterized by the formation of gallstones in the gallbladder and bile ducts.
Up to 10% of Europeans aged 21 to 30 suffer from this disease, every 26 resident of Russia. More often, people of mature age, mainly women, are ill.
Classification
There are three stages of ZhKB:
Stage of physical and chemical changes in bile
Stone-bearing stage
Calculous cholecystitis
Etiology and pathogenesis
The development of gallstone disease is associated with the combined effect of three factors:
metabolic disorders
stagnation of bile
inflammation
Metabolic disorders of an acquired or congenital nature lead to a change in the composition of bile, reduce its colloidal stability and cause the formation of an insoluble sediment, which later turns into stones.
A prerequisite for the formation of stones is stagnation of bile due to dyskinesia or anatomical changes in the IVS.
Inflammation of the gallbladder is also a predisposing factor for stone formation.
There are two main types of gallstones: cholesterol and pigmented (bilirubin).
Clinical symptoms
The symptomatology of gallstones depends on the number and size of stones, their location, and the activity of the inflammatory process.
Gallstones manifest clinically when they enter the gallbladder neck or bile duct, or when inflammation joins. In the first case, a clinic of biliary (hepatic) colic develops, in the second - chronic calculous cholecystitis.
Biliary (hepatic) colic
The development of an attack provokes the intake of fatty, fried, spicy, spicy, smoked food, physical and emotional stress, infection, work with a forward bend. The stone obstructs the bile duct, the outflow of bile is disturbed, as a result of which an increase in bile pressure occurs above the obstruction site.
Characterized by a sudden, against the background of complete well-being, the onset of pain in the right hypochondrium, radiating to the right scapula and subscapularis. Intense pain, cutting, accompanied by dyspeptic syndrome (vomiting that does not bring relief, flatulence), fever at the time of the attack. Sometimes the stone completely clogs the common bile duct, which is manifested by obstructive jaundice.
On palpation - tension of the muscles of the anterior abdominal wall,
Calculous cholecystitis.
Calculous cholecystitis is a form of chronic cholecystitis, characterized by the presence of stones in the gallbladder. The diagnosis is made in cases when signs of inflammation join stone-bearing and recurrent attacks of biliary colic: prolonged fever, chills, sweating, lingering of the tongue, inflammatory changes in the KLA, soreness in the gallbladder region.
Laboratory research:
KLA - leukocytosis, with a shift to the left, ESR.
OAM is a positive reaction to bilirubin.
LHC - an increase in the concentration of bilirubin, transaminases, alkaline phosphatase, alpha and gamma globulins, seromucoid, sialic acids, fibrin.
Study of gallbladder bile:
With calculous cholecystitis - an increase in the relative density of bile, microliths, sand, a decrease in the concentration of cholic and an increase in lithocholic bile acids, a decrease in the lipid complex, a large number of crystals of cholesterol, calcium bilirubinate, leukocytes, columnar and squamous epithelium.
With non-calculous cholecystitis - an acid reaction, a decrease in the relative density of bile, mucus flakes, a large number of leukocytes, columnar and squamous epithelium, crystals of fatty acids, an increase in the content of sialic acids and aminotransferases, a decrease in the concentration of the lipid complex, bilirubin, cholic acid.
Cholangiography
Oral cholecystography
Ultrasound - thickening of the gallbladder wall
CT (For detecting gallstones and diagnosing acute cholecystitis, it has no advantages over ultrasound)
Endoscopic retrograde cholangiopancreatography to assess the condition of the bile and pancreatic ducts
Percutaneous transhepatic cholangiography is an assessment of the state of the intrahepatic biliary system.
Diseases of the biliary tract are one of the most common diseases of civilization, and the attitude towards it should be civilized. The basis of this attitude is prevention and timely diagnosis. The choice of the correct diagnostic method largely determines the further treatment of the patient and the prevention of complications. This is not a disease in which one should agree to an operation only if complications develop.
3. Modern methods of diagnosing diseases of the liver and gallbladder
Among the instrumental methods for examining the liver, the most common are ultrasound (ultrasound), radioisotope scanning, computed tomography (CT), magnetic resonance imaging (MRI), biopsy.
1 Ultrasound examination (ultrasound)
Ultrasound examination of the liver is carried out on a special ultrasound machine, with the help of which in real time you can see the causes of pain in the liver: tumors, enlargement of the bile ducts, diffuse and other changes.
Many diseases can cause pain in the liver, and therefore ultrasound is an important step in diagnosing:
hepatitis A
cirrhosis of the liver
hemangiomas (benign neoplasms)
presence of metastases
cysts and cystic formations
liver malformations
hepatocellular carcinoma (cancer)
2 Radioisotope scanning
A radioisotope study of the liver, which consists in scanning the hepatobiliary system (liver, bile ducts and gallbladder), allows you to find out why the liver hurts. This diagnostic method can detect liver tumors, obstruction of blood vessels and bile ducts.
The main objectives of the study:
assessment of the degree of functioning of the liver and spleen
organ size determination
detection of neoplasms
Radioisotope scanning is one of the main stages in the diagnosis of liver diseases. This method was introduced in the 60s and has been found to be particularly effective in detecting liver tumors. In addition, with a reduced uneven absorption of isotopes and with an increased activity of the bone marrow, we can talk about the presence of chronic liver disease.
A gallium scan allows you to identify an inflammation (area of increased radioactivity) that leads to pain in the liver. As a rule, this diagnosis is especially effective in patients with chronic sepsis of unknown etiology.
This type of diagnosis is absolutely painless - radioactive material is injected into the blood (with the help of a dropper), the accumulation of which in the examined organs allows to identify the causes of the disease.
3 Positron emission tomography
Positron emission tomography is one of the most effective and informative diagnostic methods to identify the cause of liver pain. As a rule, this method is most often used to detect cancer and diagnose cancer metastases.
The method of positron emission tomography makes it possible to study the biochemical processes of the body with high accuracy, to identify tumor foci and to assess their activity. PET is also used to study hepatic blood flow.
In one study, it is possible not only to obtain a reliable diagnosis of malignant tumors, but also to determine the prevalence of the tumor process. Patients after treatment (surgical, conservative, chemotherapy) are also shown to carry out positron emission tomography - to track and timely determine the metastasis of the process, to assess the effectiveness of the treatment process.
Positron emission tomography is an absolutely safe and painless procedure.
4 Computed tomography
The essence of computed tomography is to obtain images of the liver in the form of horizontal slices (at least 10-12 images). The upper abdomen is exposed to X-rays, which are absorbed to varying degrees by different tissues. Information about this goes to the matrix, after which, in turn, to the computer, where you can see high-quality images of sections of the organ under study. With the help of computed tomography, you can see the localization, nature and length of the foci of the disease, their relationship with the surrounding tissues.
Computed tomography of the liver allows you to identify the cause of pain in the liver, to determine or clarify the type of disease. As a rule, CT is performed when diagnosing diseases such as:
obstructive jaundice
cysts and cystic formations
liver injury, bleeding, hematoma
cirrhosis of the liver
tumors and metastases
Today it is possible to conduct a spiral computed tomography, which has certain advantages over the traditional procedure - image quality and clarity (this is especially important when examining small vessels), the ability to register images at the right time (with the maximum concentration of contrast agent), reducing the time for conducting research. Before liver resection, computed tomography is always performed, since it can be used to study the anatomy of the organ and determine the localization of the pathological process.
5 Magnetic resonance imaging
Magnetic resonance imaging is a modern and effective diagnostic method that allows you to determine the cause of pain in the liver. The high accuracy and safety of the procedure (X-ray irradiation is not used in the study) made this method widespread and popular.
The essence of the operation of an MRI scanner is the interaction of magnetic fields and radio waves, with the help of which the entire human body or the area of interest (liver) is represented in the form of clear graphic images in three-dimensional dimensions. The advantage of this method is that not only the state of the tissue is assessed, but also their functions (temperature, blood flow velocity).
The magnetic resonance imaging procedure is absolutely safe and harmless. The only contraindication to this examination is the presence of metal bodies (implants, prostheses, pacemakers, pacemakers) in the human body.
The clarity of images obtained with magnetic resonance imaging is several times higher than with computed tomography, which allows you to see even the smallest blood vessels. In addition, depending on the task of the study, it is possible to obtain images in various projections (frontal, horizontal, sagittal).
Currently, the procedure of magnetic resonance therapy is becoming more widespread, as there is a constant improvement of this method, which allows obtaining more and more accurate results.
6 Liver biopsy
With a liver biopsy, a small piece of liver tissue is isolated and taken for a more thorough examination, which allows you to accurately determine the degree of inflammation and / or damage to the organ.
A biopsy can detect the following diseases that lead to pain in the liver area:
cirrhosis of the liver
infections (tuberculosis, brucellosis, herpes, syphilis, etc.)
focal lesions
malignant tumors
fever of unknown origin
A biopsy is also done to confirm a preliminary diagnosis and to evaluate treatment.
The main methods used to diagnose diseases:
Volumetric formation in the liver Liver metastases Ultrasound / CT, MRI Exclusion of HCC in cirrhosis Resectable tumor Hemangioma Echinococcal cyst Portal vein patency Ultrasound, CT, MRI Portal hypertension Budd-Chiari Syndrome Tung passability Trauma assessment Fatty liver CT, ultrasound, MRI Gallbladder stones Acute cholecystitis Dilation of the bile ducts Bile duct stones Biliary flow Pancreatic tumor If a patient has pain in the liver area, the choice of a test method depends on many factors. But in any case, the doctor who will carry out the diagnosis needs to know about all the symptoms (for example, pain in the liver when running and walking, nausea, bitterness in the mouth). There is no single algorithm for conducting diagnostic studies, but, as a rule, during the initial consultation, an ultrasound examination is mandatory, after which, on the basis of the data obtained, the doctor is determined with further actions. 4. Assessment of the availability of methods for diagnosing liver and gallbladder diseases In the table below, we will consider the availability of modern diagnostic methods in Sochi, depending on their availability, cost, the possibility of prescribing social services. population group. Table 1.
Research method Number of devices in the city Average research cost Possibility of free examination. Abdominal ultrasound be carried out Abdominal CT scan held Abdominal MRI Not carried out Scintigraphy Not carried out Liver biopsy Not carried out Thus, we found out that from the available examination methods in our city we can use ultrasound, CT, MRI. We also learned that ultrasound and CT can be performed on a referral from a doctor free of charge, therefore, for further research, we choose these particular diagnostic methods. Let's try to estimate the number of patients over the past three years who underwent these diagnostic methods for free and for a fee. Table 2. Past examinations of abdominal ultrasound and CT, free of charge.
Table 3. Past studies of abdominal ultrasound and CT scan, chargeable.
As can be seen from Tables 2 and 3, over the past 3 years, the ultrasound method has become more in demand both in terms of availability and price. Also, it is worth noting the possibility of conducting an ultrasound examination free of charge for a certain category of citizens, dispensary patients, UVOV and citizens equated to such, and within the framework of a general medical examination. The indicator of the demand for the CT method for free of course has grown, however, over the past 3 years, the number of CT scanners has increased 3 times, thereby reducing the number of studies for a fee. It is worth noting separately the high cost of the study, which is available only to 1/3 of patients, which undoubtedly speaks in favor of the ultrasound method. Now let's try to build diagrams based on the data in Tables 1 and 2, which allows us to assess the ratio of patients who underwent ultrasound and CT of the abdominal organs over the past 3 years. Table 4. Diagram showing the number of examined free of charge Table 5. Diagram showing the number of surveyed paid. Evaluating the results of the obtained data, we can conclude that the most accessible, widely used and acceptable in terms of price policy method for diagnosing diseases of the liver and gallbladder is ultrasound. In some cases (for example, in the screening diagnosis of jaundice), the ultrasound method is the most effective way to determine or clarify the diagnosis in diseases of the liver and gallbladder. In many medical institutions, in the presence of special equipment necessary for computed or magnetic resonance imaging, ultrasound is not performed, since CT and MRI are more informative. Conclusion In our time, technological progress has literally burst into medical practice. Computed tomography, nuclear magnetic resonance, sonography, fiber-optic technology made it possible to look into the most hidden corners of the human body, which made it possible to carry out the diagnostic procedure quickly and with a high degree of accuracy. Among the modern methods of examination, the advantages of which are difficult to overestimate, the method of ultrasound diagnostics stands out. Here are a number of qualities of this method: absolute painlessness of the procedure; harmlessness to the patient and the doctor; cheapness, and hence the availability for people of low material wealth; the speed of the study, which allows for express diagnostics, as well as conducting mass preventive examinations of the population; the compactness of the equipment, which makes it possible to use the ultrasound apparatus during the operation and in the conditions of mobile medical laboratories. As a result of my research, the effectiveness and economic and social need for the use of ultrasound machines in the presence of a half-click was proved, as well as the importance of CT, MRI, scintigraphy and biopsy methods as an additional study. New studies are being carried out to help clinicians solve problems of diagnosis and treatment of patients at the modern level, to determine the need for additional examination of a patient on an outpatient basis, which leads to a decrease in the number of patients referred to inpatient treatment, a decrease in the number of patients with complications, and also a decrease in the number of patients. , of working age. Bibliography 1. P.N. Zubarev, A.V. Kochetkov / Cholelithiasis, St. Petersburg, 2005. R.P. Samusev, N.N. Sentebrev / Atlas of Human Anatomy and Physiology, Moscow, 2010. S.V. Bound, N.N. Bezborodkina / Hepatoprotectors, Moscow, 2010. B.V. Petrovsky / Great Medical Encyclopedia, Moscow, 1982. Yu.A. Allakhverdov / Atlas of ultrasound diagnostics, Rostov-on-Don, 2011. E.V. Smoleva / Therapy, Rostov-on-Don, 2008. M.B. Ingerlabe / Analyzes. Complete reference book, Moscow, 2011. Ultrasound of the liver, gallbladder (Electronic resource).
Methods of examination of patients with liver and gallbladder disease
Introduction 3
1.Laboratory and instrumental methods of research of patients with diseases of the gallbladder 4
2.Diagnosis of patients with diseases of the gallbladder 7
3. Methods of diagnosis for liver disease 10
3.1 Hepatitis 10
3.2 Chronic hepatitis 12
3.2 Liver cirrhosis 15
3.3. Fatty liver disease 17
Conclusion 21
List of used literature 22
Introduction
The pathology of the biliary tract is an urgent problem for modern medicine. In the last decade, both in Russia and abroad, despite certain success in therapy associated with the appearance on the pharmacological market of new effective means for the correction of functional disorders of the digestive system, there has been a clear trend towards an increase in the incidence of the biliary system. Moreover, this trend is characterized by stability. So, 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, metabolic mechanisms. These tendencies are also typical for the pathology of the biliary system. According to the literature, the prevalence of diseases of the gallbladder and biliary tract 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 diseases of the biliary tract range from 26.6 to 45.5 per 1000 population.
The above facts allow us to speak about 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:
To consider laboratory and instrumental methods of research of patients with diseases of the gallbladder;
Describe diagnostic methods for liver disease.
Laboratory and instrumental methods for the study of patients with diseases of the gallbladder
With dyskinesia of the biliary tract, cholecystitis (without exacerbation), cholelithiasis in the interictal period, the general condition of the patient often remains satisfactory. With acute cholecystitis, exacerbation of chronic cholecystitis, a prolonged attack of hepatic colic with gallstone disease, the patient's condition may be moderate or severe.
The position of the patient with DVP and cholecystitis without exacerbation is, as a rule, active. The forced position of the patient is observed with an attack of hepatic colic (cholelithiasis, calculous cholecystitis). Patients are restless, rushing about in bed, trying (to no avail) to assume a position in which the pain is less noticeable.
The patient's appearance in most cases is not changed. Asthenic constitution and the associated connective tissue dysplasia are often the reason for the presence of hourglass-type gallbladder deformities in these patients, the presence of constrictions, membranes, kinks, diverticula in the gallbladder, which leads to the formation of biliary dyskinesia, and subsequently organic pathology - cholecystitis, cholelithiasis; hypersthenic constitution is often observed in persons suffering from cholelithiasis, mainly women, as well as in persons with hypokinetic biliary dyskinesia. 1
Skin integuments have the usual color in the case of DVT and chronic cholecystitis without exacerbation, as well as in case of cholelithiasis in the interictal period. During an attack of hepatic colic, patients may experience subicteric sclera, and with the development of obstructive jaundice, the skin becomes green-yellow. Deposition of cholesterol in violation of cholesterol metabolism in patients with cholelithiasis, calculous cholecystitis is accompanied by the appearance of xanthomas and xanthelasmas on the skin.
When carrying out abdominal percussion, it is necessary to pay attention to the size of the liver according to Kurlov, which in patients with DVP, cholelithiasis, cholecystitis without exacerbation, are not changed (along the right mid-clavicular 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. With the help of a very quiet percussion, it is possible to determine the size of the gallbladder with its significant increase (gallbladder dystonia with its hypokinesia, cholelithiasis).
With an exacerbation of cholecystitis, characteristic symptoms can be identified:
Zakharyin's symptom - sharp pain when tapping with a finger or pressing in the projection area of the gallbladder;
Vasilenko's symptom is a sharp pain when tapping a finger in the gallbladder at the height of inspiration;
Obraztsov-Murphy symptom - sharp pain when the hand is inserted into the right hypochondrium at the height of inspiration;
Ortner's symptom is pain when beating the edge of the hand along the right costal arch.
Superficial palpation of the abdomen reveals:
Severe local soreness in the projection area of the gallbladder with acute cholecystitis, biliary colic;
Mild, moderate pain at the point of the gallbladder with chronic cholecystitis, cholelithiasis during remission, with DGVP.
On palpation, the gallbladder is usually accessible when it is enlarged (hypokinetic type of gallbladder with gallbladder distress, cholelithiasis). 2
For the examination of 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 intubation;
Microscopic examination of bile;
Biochemical study of bile;
X-ray and radiological examinations;
Ultrasound examination of the hepatopancreatoduodenal zone;
Endoscopic examination, etc.
Diagnostics of patients with diseases of the gallbladder
The 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 alleged 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 have provided the path for therapeutic intervention,
Abdominal radiography. Plain abdominal radiographs are of limited value in diagnosing diseases associated with gallstones or jaundice. Only in 15-20% of patients it is possible to detect on simple radiographs contrasted stones localized in the right upper quadrant of the abdomen. Air within the biliary tree may indicate the presence of a fistula connecting the gallbladder to the intestines.
Oral cholecystography. Oral cholecystography was introduced in 1924. The function of the gallbladder is assessed based on its absorptive capacity. Radiopaque iodine dye, taken per os, is absorbed in the gastrointestinal tract and enters the liver, then it is excreted into the bile duct system and is concentrated in the gallbladder. Stones seen as filling defects in a visualized, contrasting gallbladder, or not visualized gallbladder, may not mean a "positive" result. False positive non-imaging can be noted in patients who, due to the prescribed examination, do not follow the instructions of the doctor, or in those who are unable to swallow tablets, as well as in cases where the tablets cannot be absorbed in the gastrointestinal tract or the dye is not excreted into the biliary 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 regarding the origin, size, and location of biliary dilatation, as well as the presence of tumors in and around the biliary tract and pancreas.
Biliary scintigraphy. Intravenous administration of a radioactive isotope, one of the iminodiacetic acid family, labeled with technetium-99t, provides specific information related to determining the patency of the cystic duct 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 for therapeutic correction as needed based on the clinical situation. It is used in patients with a complex of biliary problems, including strictures - * and tumors.
Endoscopic retrograde cholangiopancreatography (ERCP). Using an endoscope with a side view, 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 bile duct segment. The use of this method brings significant benefits to patients suffering from a disease of the common bile duct (benign and malignant nature).
Choledochoscopy. Despite the fact that the indirect imaging technique is fundamental in the diagnosis of patients with diseases of the extrahepatic biliary tract, direct examination and imaging of the biliary system is a worthwhile goal. Choledochoscopy performed during surgery can be effective in detecting 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 is carried out (for example, immunoglobulins responsible for the so-called humoral immunity of the whole organism, albumin, which retain 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 for the body. The liver metabolizes fats, detoxifies toxins (poisons), etc. The slightest violation of at least one of the functions of the liver leads to serious disturbances in the work of the whole organism. 4
Hepatitis
Acute hepatitis. Symptoms, course. In mild cases, acute hepatitis is practically asymptomatic, being detected only during random or targeted examination (for example, in the workplace among persons in contact with hepatotropic poisons, with household group poisoning with mushrooms, etc.). In more severe cases (for example, with toxic hepatitis), the clinical symptoms of the disease develop rapidly, often in combination with signs of general intoxication and toxic damage to other organs and systems. At the height of the disease, icteric coloration of the skin and mucous membranes, whitish-clay-colored stools, saturated dark-colored ("beer-colored") urine, hemorrhagic phenomena are characteristic. The color of the skin is orange or saffron. However, in mild cases, jaundice is visible only in daylight, the earliest is the icteric staining of the sclera and mucous membrane of the soft palate. There are frequent nosebleeds, petechiae; patients are worried about itching, 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 especially 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), an increase in the activity of a number of serum enzymes: aldolase, aspartate aminotransferase and especially alanine aminotransferase (much higher than 40 units), lactate dehydrogenase, hypoalbuminemia, hyperglobulinemia (predominantly, the content increases. indicators of protein-sedimentary samples (thymol, sublimate, etc.). The production of fibrinogen, prothrombin, VII, V coagulation factors by the liver is impaired, as a result of which hemorrhagic phenomena occur. taking into account the epidemiological situation in identifying the nature and cause of the disease.In unclear cases, first of all, one should think about viral hepatitis.Detection of the so-called Australian antigen is characteristic of serum hepatitis B (it is also detected in virus carriers, rarely in other diseases NS). Mechanical (subhepatic) jaundice usually occurs acutely only when the common bile duct is blocked by a stone in 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 determined in the blood, the stool is intensely colored, the osmotic resistance of erythrocytes is usually reduced. In the case of false jaundice (due to skin staining with carotene with prolonged and abundant consumption of oranges, carrots, pumpkin), the sclera are usually not colored, hyperbilirubinemia is absent.
With timely treatment, complete recovery is often achieved. 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 a clinical picture of acute hepatic or hepatic-renal failure, from which patients may die.
3.2 Chronic hepatitis
Polyethiological 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 an increase in the liver, pain or a feeling of heaviness, fullness in the right hypochondrium, dyspeptic symptoms; less often jaundice, skin itching, subfebrile condition are detected. Liver enlargement occurs in about 95% of patients, but in most cases it is moderate. The spleen is absent or slightly enlarged. Pain in the liver region of a dull character, constant. Frequent loss of appetite, belching, nausea, poor tolerance to fats, alcohol, flatulence, unstable stools, general weakness, decreased ability to work, hyperhidrosis. A third of patients have mild (subicteric sclera and palate) or moderate jaundice. Frequent, but nonspecific, an increase in ESR, dysproteinemia due to a decrease in the concentration of albumin and an increase in globulins, mainly alpha and gamma fractions. The results of protein-sedimentary tests - thymol, sublimate, etc. are positive. 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 content of bound (direct) bilirubin in the blood serum. The absorptive-excretory function of the liver is impaired (the half-life of bromsulfalein from the blood is lengthened).
With cholestatic hepatitis, more pronounced persistent jaundice and laboratory cholestasis syndrome are usually observed: the serum levels of alkaline phosphatase, cholesterol, bile acids, bound bilirubin, copper are increased.
Allocate inactive (inactive), benign, persistent and active, aggressive, progressive recurrent hepatitis.
Puncture liver 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.
Scanning the liver allows you to determine its size; with hepatitis, sometimes there is a reduced or uneven accumulation of a radioisotope drug in the liver tissue, in some cases its increased accumulation in the spleen occurs.
Differential diagnosis in cases with a vivid clinical picture of diffuse liver damage, first of all, should be carried out with cirrhosis of the liver. With cirrhosis, the symptoms of the disease are more pronounced, the liver is usually much denser than with hepatitis; it can be increased, but often decreased in size (atrophic phase of cirrhosis). As a rule, splenomegaly is observed, hepatic signs (vascular telangiectasias, hepatic tongue, hepatic palms) are often detected, symptoms of portal hypertension may occur. Laboratory studies show significant deviations from the norm in the results of the so-called liver tests; with 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 in the past of a disease that could cause liver fibrosis), long-term observation of the patient and 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 of decisive importance in the diagnosis.
Differential diagnosis with functional hyperbilirubinemia is based on the peculiarities of their clinical picture (mild jaundice with hyperbilirubinemia without vivid clinical symptoms and changes in laboratory liver tests 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. With focal lesions (tumor, cyst, tuberculoma, etc.), the liver is unevenly enlarged, and scanning determines the focus of destruction of the hepatic parenchyma.
Flow. Inactive (persistent) hepatitis is asymptomatic or with minor symptoms, changes in laboratory parameters are also insignificant. Aggravations of the process are uncharacteristic.
Chronic active recurrent (aggressive) hepatitis is characterized by severe complaints and vivid objective clinical and laboratory signs. Some patients have 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 (error 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 difficult.
Cirrhosis of the liver
About 2 million people die from cirrhosis of the liver every year. Cirrhosis and liver cancer are responsible for 90-95% of deaths in chronic liver disease.
What is cirrhosis of the liver?
Cirrhosis is the process of replacing the normal structure of the liver with scar tissue, which takes the form of nodes. These nodes not only do not perform any useful functions, but interfere with the normal functioning of the liver, squeezing blood vessels, bile ducts and normal liver tissue. At the same time, there is a violation of the production and accumulation of vital substances by the liver (proteins, fats, carbohydrates, hormones), the neutralization of poisonous and infectious agents worsens. The liver is the main outpost that takes over the entire flow of substances coming from the intestines. Among these substances, in addition to useful 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 poisoning the body penetrate into the blood.
The reasons for the development of cirrhosis.
The most common causes of cirrhosis are hepatitis B and C viruses and alcohol abuse. Alcoholism is the main reason. It is not precisely established how long and how much alcohol is needed for the development of cirrhosis. Most patients with this ailment, for at least 10 years, drank at least 0.5 liters of strong alcoholic drinks or several liters of wine or beer daily. The higher the daily dose of alcohol, the faster cirrhosis will develop. In women, less alcohol consumption leads to the development of alcohol. 10-20% of patients with chronic hepatitis B and C develop liver cirrhosis. Alcoholic-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's disease). In approximately 10-20% of patients, the cause cannot be established. 5
80% of cirrhosis proceeds imperceptibly, without attracting the attention of either the patient or the doctor. The rest of the patients complain of increased fatigue, pain in the right hypochondrium, bloating, periodic darkening of urine, weight loss, a tendency to "bruising", redness of the palms. In many patients, the disease is recognized only with the development of complications: the accumulation of fluid in the abdomen, impaired consciousness, bleeding from the esophagus and stomach, jaundice. A healthy liver protects the brain from toxins, and in cirrhosis, the blood, without being cleared of harmful substances by the liver, enters the brain. There is a violation of thinking, memory. 60-90% of liver cancer develops against the background of cirrhosis. Cancer in the early stages is difficult to recognize, its manifestations are mistaken for signs of progression of cirrhosis. Most often, the tumor manifests itself as abdominal pain. Sometimes you can feel a tumor-like volumetric formation in the right hypochondrium.
With cirrhosis of the liver, alcohol and any alcohol-containing drinks are categorically contraindicated, as this contributes to the progression of the disease. It is not recommended to consume carbonated drinks. If you do not have complications of cirrhosis, then special dietary restrictions are not required. In this disease, a low level of potassium in the blood is often found, so you need to include more fruits rich in potassium in the diet.
Fatty degeneration of the liver
Fatty liver disease (liver steatosis) is a fatty change in liver tissue when liver cells suffer from excess fat accumulation.
Causes of fatty degeneration.
The main causes of hepatosis are exposure to the liver of toxic substances, endocrine disorders, and unhealthy diet. Alcohol occupies a special place among toxic agents. However, in alcohol abusers, the development of the disease is associated both directly with the effect of alcohol on liver cells and with improper diet. The faster the development and the severity of the changes, the higher the amount of alcohol consumed. The role of other toxic factors (insecticides, organophosphorus compounds, etc.) is less significant. It is possible to develop medicinal hepatic steatosis, for example, in the treatment of tuberculosis, taking antibiotics, mainly of the tetracycline series, hormonal drugs. In the group of endocrine diseases, the leading place among the causes of hepatosis is diabetes mellitus, especially in the elderly. Perhaps the development of "fatty liver" in diseases of the thyroid gland. Steatosis also accompanies general obesity. The determining factor in the imbalance of food factors is the discrepancy between the total calorie content of food and the content of animal proteins in it, as well as the deficiency of vitamins and other substances. Malnutrition is the main reason for 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 reason for the development of hepatic steatosis in persons suffering from pulmonary diseases and cardiovascular insufficiency.
How do fatty hepatosis manifest?
Steatosis can be latent, manifesting itself with only a slight increase in the liver, or with pronounced manifestations. The most common sign is an enlarged liver. Palpation reveals soreness of the liver. Most patients also have independent pain in the right hypochondrium, and there may be nausea. Steatosis can take a long time, over many years. Periods of deterioration are followed by relative improvements in well-being. Exacerbations are more often associated with mental or physical stress, alcohol intake, infection.
The complications of steatosis, which are observed mainly in its severe forms, include the formation of cirrhosis of the liver. Due to impaired immunity in patients with steatosis, pneumonia is often observed, pulmonary tuberculosis may develop.
Treatment of hepatosis
Treatment of steatosis is a rather difficult, but solvable task for professionals and consists of several directions. Among them, a properly selected diet, a modification of a behavioral pattern (change in dietary habits, a change in the amount and composition of alcohol consumed, an increase in 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 hepatic metabolism. The prognosis, as a rule, is favorable and, with adequate treatment, it quickly reverses. However, supportive measures may be needed for quite a long time.
Prevention of hepatosis.
Prevention of hepatosis consists in eliminating the influence of toxic factors, adequate treatment of diabetes mellitus, full-fledged balanced nutrition, 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.
With an exacerbation of the disease for 3-4 weeks, you need to adhere to Diet No. 5 a, after improving the condition, you can switch to Diet No. 5. This diet is complete and basic, that is, the longer you adhere to it, the more guaranteed the improvement in health will be.
If it is necessary to enhance the choleretic properties of the diet, they resort to its lipotropic-fatty version, increase the amount of vegetables, fruits, bring the dose of vegetable oil to 50%, instead of the usual 30%. Both butter and vegetable oil are added to ready meals.
With cirrhosis of the liver, the recommendations remain the same: Diet No. 5 in case of deterioration and Diet No. 5 in remission. But if diarrhea appears, the fat is limited to 50-60 g. Laxative products are also excluded - pure milk, honey, jam, etc. etc.
If the appetite has completely disappeared or the taste is perverted, you should try to eat more fruits, berries, salads, and drink juices. Protein at this time is best obtained from dairy products, mild cheese, cottage cheese, eggs, boiled fish. For a while, you can include your favorite dishes in the diet, but without going overboard.
For portal hypertension, diets with a normal content of protein, carbohydrates, fats, but no salt are recommended. It's good if even the bread is salt-free. The amount of liquid is also limited, but prunes, figs, dried apricots are recommended. If hormone therapy is being carried out (prednisone, 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 also 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 has not waned. Currently, many researchers consider the pathology of the biliary system as a consequence of general neurosis, however, the possibility of the occurrence of gastrointestinal tract diseases based on pathological viscero-visceral interactions in the pathology of other abdominal organs (gastritis, peptic ulcer, colitis, diseases of the female genital area, etc.) ... The issues of targeted and adequate treatment of patients with biliary tract pathology remain controversial to this day.
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 was pointed out the need 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 the sphincter apparatus, depending on the type of disorders, including with the help of modern myotropic drugs. In recent years, sufficient experience has been accumulated in the use of enzyme preparations of the latest generations in the treatment of small intestinal digestion disorders, in dyskinetic disorders in the biliary system, in acute and chronic cholecystitis, reactive pancreatitis.
List of used literature
Propedeutics of internal diseases: Textbook for universities. / N.А. Mukhin, V.S. Moiseev. - M .: Geotar-Media, 2007.- 848p.
Propedeutics of internal diseases. Textbook for universities. / N.V. Ivashkin. - M .: MEDpress, 2005. - 240 p.
Propedeutics of internal diseases: Textbook for universities. / V.S. Moiseev.- M .: INFRA-M, 2004.- 768s.
Propedeutics of internal diseases: textbook. / A.S. Svistov.- M .: Medicine, 2005.- 536s.
Grebnev, A.L. Propedeutics of internal diseases: textbook. / A.L. Grebnev .- M .: Medicine, 2002.-592s.
1 Grebnev, A.L. Propedeutics of internal diseases: textbook. / A.L. Grebnev.- M .: Medicine, 2002.-P.254.
2 Propedeutics of internal diseases: Textbook for universities. / V.S. Moiseev .- M .: INFRA-M, 2004.- P. 369.
3 Propedeutics of internal diseases: textbook. / A.S. Svistov.- M .: Medicine, 2005.- P.299.
4 Propedeutics of internal diseases. Textbook for universities. / N.V. Ivashkin.- M .: MEDpress, 2005.- P.104.
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The symptomatic complex of liver tissue inflammation underlies many liver diseases and manifests itself in a number of stereotypical local and general pathophysiological changes.
The inflammatory reaction of the hepatic tissue can be conditionally divided into three main interrelated phases, which have a bright clinical, laboratory and morphological expression: 1) alteration with the release of inflammatory mediators, 2) a vascular reaction with exudation, and 3) proliferation.
Alteration (lat. - change) - the initial phase of the inflammatory response to pathogenic effects, 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 disintegration of cells and intercellular substance, biologically active substances (inflammatory mediators) histamine, serotonin, plasma kinins, prostaglandins, leukotrienes, RNA and DNA degradation products, hyaluronidase, lysosomal enzymes, etc. are formed.
Under the influence of inflammatory mediators, a second phase of the inflammatory reaction occurs, characterized by disorders of mainly microcirculatory blood flow, lymph circulation and bile secretion, - vascular reaction with exudation. As a result, there is an infiltration of liver tissue with leukocytes, exudation of plasma proteins, inflammatory hyperemia, changes in the rheological properties of blood, stasis, local hemorrhages, thrombosis of small vessels, etc. Lymphostasis and lymphothrombosis develop in the lymphatic microvessels, and cholestasis in the bile tubules and cholangioli. In this case, an excessive intake of protein in 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 hepatocyte necrosis. Extracellular protein dystrophy manifests itself at first mucoid, then fibrinoid swelling (fibrinoid), hyalinosis and amyloidosis. Mucoid swelling of fibrinoids and hyalinosis are successive stages of disorganization of connective tissue (liver stroma and vascular walls). A pronounced destruction of collagen fibers and the main substance of the connective tissue leads to fibrinoid necrosis.
In conditions of disorders of blood and lymph circulation and oxygen starvation (tissue hypoxia), along with protein dystrophy, usually develops fatty degeneration liver (dystrophic obesity), which is characterized by impaired metabolism of cytoplasmic fat.
The outcome of fatty degeneration of the liver depends on its severity. If it is not accompanied by deep damage to the cellular structures of the liver, then it turns out, as a rule, reversible. In acute fatty degeneration of the liver, 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, connective tissue develops (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 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 reactive readiness of the organism, the degree of its sensitization, is of particular importance. In some cases, with increased sensitivity, the inflammation is acute, 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 response most often it is serous (serous exudate permeates the liver stroma) or purulent (purulent exudate diffusely infiltrates the portal tracts or forms abscesses 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 from Kupffer's cells, endothelium, hematogenous elements, etc. are formed.
Chronic inflammation of the liver tissue is characterized by the 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.
The main role in the development of acute inflammation of the liver tissue is played by infectious agents (hepatitis A, B, C, D viruses, etc., enteroviruses, pathogens of acute intestinal infections, infectious mononucleosis virus, leptospira, etc.), toxic endogenous factors (infectious, burns, etc.) and exogenous origin (alcohol; industrial poisons - phosphorus, carbon tetrachloride; organophosphate insecticides; medicines - penicillin, sulfadimezin, PASK, etc.), ionizing radiation.
The course of acute inflammation of the liver tissue is usually cyclical, it lasts 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 mesenchymal cell reaction.
The main clinical signs of inflammation of the liver tissue are pain in the upper abdomen and right hypochondrium, enlarged liver and jaundice (see "Symptoms of hyperbilirubinemia").
Symptoms of liver dysfunctions are of some importance (see symptom complexes of liver failure).
Many patients have general clinical signs of the inflammatory process: fever (usually subfebrile) and the phenomena of intoxication of the body (weakness, sweating, etc.), leukocytosis, accelerated ESR, changes in protein, 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 that may be the first clinical manifestations of the disease: hepatic coma due to massive necrosis of the liver parenchyma (see "Symptoms of acute and chronic liver failure"), edematous-ascitic syndrome (see "Symptoms of portal circulation disorders caused by liver damage "), hemorrhagic syndrome (see" Diseases of the hemostatic system "), etc.
It should be noted that inflammation of the liver tissue (especially chronic focal) is often clinically asymptomatic or with minimal clinical symptoms, manifested mainly by an increase in the size of the liver. Therefore, a very important role in the timely diagnosis of inflammation of the liver tissue is played by serum-biochemical syndromes: 1) cytolytic, 2) mesenchymal-inflammatory; 3) regeneration and tumor growth.
Serum-biochemical cytalytic syndrome caused by damage to liver cells with a pronounced violation of membrane permeability.
Diagnosis of cytolytic syndrome is mainly carried out by blood serum enzymes: aspartate amine transferase (AST), alanine aminotransferase (ALT), gamma glutamine transferase (GGTP), lactate dehydrogenase (LDH).
AsAT in the blood serum of a healthy person is contained in an amount of 0.10 - 0.45 mol / (hl); AdAT - 0.10 - 0.68 mmol / hl). An increase in aminotransferases by 1.5 - 3 times is considered moderate, up to 5 - 10 times - medium, 10 times or more - high.
GGTP: the norm in blood serum is 0.6 - 3.96 mmol / (h.p.);
LDH: the norm is up to 3.2 μmol / (hl), inferior in sensitivity to ASAT 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 irritation syndrome of the hepatic reticuloendothelium) is caused by increased activity of the mesenchymal-stromal (non-epithelial) elements of the liver. For its diagnosis, thymol (timolveronal) and sublimate sediment samples, as well as indicators of gamma globulin and serum immunoglobulins, are used. Thymol test: norm 0 - 7 VD according to McLaghan, 3 - 30 IU according to Vincent. Sublimate test: the norm is 1.9 VD and higher. Serum gamma globulin: the norm is 8 - 17 g / l or 14 - 21.5% of the total amount of protein.
Serum Biochemical Regeneration and Tumor Growth Syndrome 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 determined 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 characteristic, and for regenerative processes in the liver - a 2 - 4-fold increase.
Morphological studies of biopsy material are of great importance in the diagnosis of inflammation of the hepatic tissue. The morphological substrate of inflammatory liver damage is dystrophic and necrobiotic changes in its parenchyma and stromal infiltration.
2.3 Symptom complex of impaired portal circulation caused by liver damage
Definition, causes and mechanisms of development
Symptonic complex of impaired portal circulation caused by liver damage, includes several syndromes, of which the most common is portal hypertension syndrome and associated hepatolienal syndrome, edematous ascitic syndrome, serum-biochemical liver bypass syndrome, and hepatargia syndrome, or portosystemic encephalopathy.
In clinical practice, the term portal circulation blood circulation in the portal vein system is indicated. The circulatory system of the liver includes two bringing blood vessels - portal vein through which 70 - 80% of the total volume of incoming blood flows, and its own hepatic artery (20 - 30% of the total volume of blood flowing to the liver) and one carrying vessel - the hepatic vein. Both bringing vessels branch out in the liver to a common capillary network, in which the capillaries formed as a result of arteriole branching are connected to the sinusoidal capillaries of the portal system. These capillaries open into the central lobular veins, through which blood flows further through the collecting veins to the main hepatic veins. The trunks of the hepatic veins open into the inferior vena cava.
Lymphatic drainage from the liver occurs through the superficial and deep lymphatic vessels. Superficial lymphatic vessels anastomose with deep, starting from around-lobular capillary networks. There are no lymphatic capillaries inside the lobules.
Violations of the outflow of blood from the portal vein vascular system usually lead to portal hypertension, sometimes reaching 600 mm of water column and 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 development of portocaval anastomoses and their varicose veins. The greatest amount of blood in portal hypertension flows through the veins of the esophagus and stomach, less - through the veins of the anterior abdominal wall, hepato-duodenal 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 sinusoidal zone. It very often develops with cirrhosis of the liver, in which the expanding connective tissue squeezes the intrahepatic venous vessels.
Suprahepatic form(2 - 3%) develops as a result of complete or partial blockade 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, phlebosperosis, 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 be in other liver diseases (for example, hepatitis, liver cancer, etc.), acute and chronic leukemia, etc. Such a 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 an intrahepatic block, it often develops edematous ascites 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, increased extravasation in the vessels of its microvasculature. As a result, extravasation of fluid from the vascular bed into the abdominal cavity is enhanced. The formation of ascites is facilitated 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 an increase in osmotic pressure in 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 neutralizing toxins is disrupted, angiotensin-11 and especially aldosterone are insufficiently inactivated. This leads to intoxication, a decrease and disruption of protein synthesis, fluid retention in the body. As a result of the predominance of globulins over albumin, persistent hypooncotic edema is formed most often in the lower extremities, since they are usually combined with venous congestion in the liver, portal hypertension and ascites.
It should not be forgotten 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 tuberculosis process, etc.
In the case of the development of powerful venous collaterals through portocaval anastomoses, a large amount of substances that are normally converted in the liver enters the general bloodstream through portocaval anastomoses: ammonia, urea, free phenols, amino acids, fatty acids, mercaptans, etc. These substances accumulate in the blood serum in high concentrations, are toxic and contribute to the development portosystemic encephalopatsh, which is often called hepatogy, or hepatocerebral syndrome. With the excessive flow into the blood of the above metabolic products of proteins, the concept of serum-biochemical liver bypass syndrome. The latter is found not only with the development of portocal 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 disease, chronic aggressive hepatitis, acute yellow atrophy of the liver, etc. ammonia in serum can be increased in 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, ascites, hepatolienal syndrome (splenomegaly and hypersplenism), esophageal-gastric bleeding from varicose veins of these organs, portopathic encephalic - biochemical liver bypass syndrome.
When examining a patient with portal hypertension, signs of collateral circulation - varicose veins on the anterior abdominal wall and hemorrhoids. In patients with suprahepatic portal hypertension, dilated veins are more often localized along the lateral walls of the abdomen, on the back and lower extremities. With intrahepatic portal hypertension, the dilated veins are localized on the anterior abdominal wall around the navel (Medusa's head) towards the chest or suprapubic region.
Development ascites preceded by bloating associated with flatulence, resulting from a deterioration in the resorption of gases from the intestines. In patients with significant ascites, the abdominal circumference is increased; in the standing position of the patient, the abdomen has a spherical shape with a protruding or drooping lower half. In the supine position, the abdomen spreads to the sides and resembles a frog. The navel may bulge, and white stripes appear on the skin of the abdominal wall from excessive stretching (striae). Percussion reveals a dull sound above the slope or lateral part of the abdomen. If the position of the body changes, then 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 noted with increased local arterial blood flow, caused, for example, by cirrhosis or 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 adhesions of the spleen with surrounding tissues, as well as spleen infarctions.
Hypersplenism is manifested by a decrease in the number of platelets to 80,000 - 30,000, the number of leukocytes - up to 3000 - 1,500 in 1 μl of blood. Moderate anemia is observed.
Patients with portal hypertension often experience hemorrhagic diathesis, due primarily to coagulopathy as a result of liver damage and thrombocytopenia due to hypersplenism. These are 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 ends with acute liver failure and the 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, delirium, etc.
Of the instrumental methods for diagnosing portal hypertension, the most informative are X-ray methods, eeophagogastroscopy, percutaneous splenomanometry.
Portal pressure is measured using percutaneous splenomanometry (the spleen is punctured and connected to the needle of the Waldmann apparatus for measuring venous pressure).
The level of blockade of the portal circulation and the state of the vessels can be obtained using splenoportography.
Dilated veins of the esophagus and stomach are usually detected during their X-ray and endoscopic examination.
Splenomegaly is detected by ultrasound, scintigraphy, and celiacography. Ascites (especially a small amount of fluid) - with ultrasound and computed tomography.
In portal hypertension, a test with an ammonia load is sometimes used, which makes it possible to determine the degree of portocaval shunting and indirectly assess the tolerance of food proteins. The patient is given 3 g of ammonium chloride inside, and then its content in the blood is determined. In a healthy person, after exercise, the concentration of ammonia in the blood does not change (the norm is 11 - 35 μmol / l). In the presence of serum-biochemical liver bypass syndrome, there is a clear increase in the concentration of ammonia in the blood serum by 2 - 3 times or more.
2.4 Snmptomocomplexes of acute and chronic liver failure
Definition, causes and mechanisms of development, classification
Symptom complex of liver failure - This is a pathological condition caused by profound disturbances of numerous liver functions that are important for the vital activity of the organism, accompanied by neuropsychic disorders of varying degrees of severity, up to the development of hepatic coma.
Liver failure by the nature of the course and dynamics of clinical and morphological manifestations is acute and chronic. Acute liver failure develops within a few hours or days and is characterized by clearly manifested and rapidly growing clinical symptoms. Chronic liver failure develops over several months or years, is characterized by a slow and gradual development of clinical manifestations.
Depending on the main pathogenetic mechanism of the 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 intake from the portal vein into the common bed through portocaval anastomoses of a significant part of the toxic products absorbed in the intestine (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 hepatic failure is usually observed with a predominance of the role of the underlying endogenous mechanisms.
The leading morphological substrate of hepatocellular failure is dystrophic and necrobiotic changes in hepatocytes. It is characterized by massive liver necrosis. Chronic hepatocellular failure is usually associated with both diffuse degenerative 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, acute and chronic hepatitis, cirrhosis, liver tumors, disorders of intrahepatic portal circulation, diseases complicated by subhepatic cholestasis (gallstone disease, etc.), poisoning with hepatotropic poisons, severe injuries, burns are most often noted. massive blood loss, etc.
Portal hepatic failure develops mainly due to liver bypass surgery. It is observed mainly in patients with liver cirrhosis with severe portal hypertension (see "Symptom complex of impaired portal circulation due to liver damage"). Portal hepatic failure is commonly associated with chronic liver failure.
The risk of developing liver failure due to the above reasons increases significantly under the action of the following risk factors alcohol abuse, drug intoxication (barbiturates), anesthesia and surgery, intercurrent infections, nervous shocks, gastrointestinal bleeding, food protein overload, 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.), the protective function of the liver, biliary and biliary functions, erythropoiesis and blood coagulation
In a healthy person, carbohydrates in the form of monosaccharides are absorbed in the small intestine and enter the liver through the portal vein system. A significant part of them is retained in the liver and turns into glycogen, some of the monosaccharides are converted into triglycerides and deposited in fat depots, some of them are spread throughout the body and used as the main energy material Violation of carbohydrate metabolism in liver damage consists in a decrease in glycogen synthesis, violation of its splitting and the formation of glucose from substances of a non-carbohydrate nature (glyconeogenesis), which causes the development of hepatogenic hypoglycemia. A decrease in the content of glycogen leads, in turn, to a decrease in its detoxifying function, in which glycogen is involved, turning into glucuronic acid.
Lipid absorption is most active in the duodenum and proximal part of the small intestine. The absorption rate 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 the thinnest lipoprotein membrane. A very small amount of fat in the form of triglycerides of fatty acids enters the bloodstream. The main amount of fat is deposited in fat depots
Violation of fat metabolism in liver damage manifests itself in a change 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 is significantly increased 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, protein starvation, fatty degeneration of the liver rapidly develops.
With pathological processes in the liver, prolonged 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. The amino acids absorbed into the blood enter the liver through the portal vein system, where a significant part of them is used for protein synthesis both in the liver and outside it, and a smaller part of them is deaminated with the formation of ammonia, which has a high toxicity. In the liver, non-toxic urea is synthesized from ammonia.
Violation of protein metabolism in liver pathology is manifested primarily by disorders of protein synthesis and the formation of urea.So, in 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, gamma globulins, which in a healthy person are synthesized in the lymphatic tissue and bone marrow, as well as paraproteins - qualitatively altered globulins, can begin to be produced in it.
Disruption of the synthesis of urea 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 inferiority of the liver can lead to the development of polyhypovitaminosis. Since the intermediate exchange of cyanocobalamin, nicotinic and pantothenic acids, retinol occurs in the liver, then if its parenchyma is damaged, the corresponding hypovitaminosis develops. Impaired absorption of fat-soluble vitamins due to a decrease in the biliary function of the liver also leads to a violation of the 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 effects in it, binding by proteins, metabolite of hormones are bound by various acids of the liver 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 the hyperfunction of the corresponding endocrine organs. The pathologically altered liver participates in a variety of ways in the pathogenesis of various endocrinopathies. So, in men with significant liver damage (for example, severe acute hepatitis, rapidly progressive cirrhosis of the liver), symptoms of androgen deficiency are often noted.
In a healthy person in the liver, 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 liver through the portal system, where they are converted into non-toxic substances. Violation of this antitoxic detoxifying 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 due to 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 digestion insufficiency", "Symptom complex of hyperbilirubinemia")
With liver damage, 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). Terminal liver failure ends hepatic coma and the death of the patient. In the development of hepatic coma, three stages are also distinguished, precom, threatening coma and actually(i.e. clinically significant) to whom.
In clinical practice, the initial (compensated) stage is often called small liver failure, and the second and third stages - large liver failure.
Clinic and diagnostics
Liver failure can manifest itself as a symptom complex of liver tissue inflammation, 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 the parameters of laboratory stress tests are revealed, indicating violations of the metabolic functions of the liver (serum-biochemical syndrome of hepatocellular insufficiency, or hepatodepression).
Detection of hepatodepressive syndrome is usually performed according to serum cholinosterase, serum albumin, serum prothrombin ivdex and proconvertin, as well as using stress tests (bromsulfaleic, indocyanic, etc.).
Cholinesterase: the norm in blood serum is 160 - 340 mmol / (hl); albumin - 35 - 50 g / l; prothrombin index - 80 - 110%, serum proconvertin - 80 - 120%. Bromsulfalein test(BSF) according to Rosenthal and White: normally 45 minutes after administration, no more than 5% paints. Indocyanic test: Normally, 20 minutes after administration, no more than 4% of the paint remains in the blood serum. The presence of hepatodepressive syndrome is evidenced by a decrease in hepatodepression indices and an increase in the amount of dye in the blood serum. Hepatodepression is considered insignificant with a decrease in indicators of hepatodepression 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 stunnedness of patients, their inadequacy, euphoricity 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 elbow bends, in the area of venipuncture, gingival and nosebleeds, 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 of fatty foods, dyspeptic symptoms, nausea and vomiting ...
Fever, often observed in liver failure, usually indicates a septic condition of the patient due to a reduced resistance to infection coming from the intestine. Fever with liver failure maybe be of non-infectious origin due to a violation of the liver inactivation of pyrogenic steroids and their accumulation in the blood.
Hyperbilirubinemia and jaundice are often a manifestation of functional insufficiency 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. So, in men with rapidly progressive cirrhosis of the liver, symptoms of androgen deficiency are often noted: along with a clear reverse development of hair growth, the penis, testicles decrease, sexual potency and libido are weakened. In many cases, gynecomastia appears, and the stroma of the prostate is often enlarged. Cirrhosis of the liver in childhood and adolescence leads to a strong slowdown in bone development, growth (Fanconi's "hepatic short stature"), puberty, which is associated with insufficient testosterone production. The weakening of the development of the reproductive apparatus determines the picture of eunuchoidism.
In women, the uterus, mammary glands atrophy, the menstrual cycle is disrupted. Violation of the inactivation of estrogens, and possibly some vasoactive substances, is caused by small skin 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 insufficiency. There are hypoproteinemia, hypergammaglobulinemia, hyperbilirubinemia, a decrease in the level of fibrinogen, cholesterol, dissociation of bile acids in the blood, high activity of indicator and organ-specific enzymes.
The third stage of liver failure is actually the stage of coma, in which, according to the severity of psychomotor disorders and changes in the electroencephalogram, 3 stages are distinguished in turn. V the first stage, precom, symptoms of encephalopathy progress; the feeling of anxiety, melancholy increases, fear of death appears, speech becomes difficult, neurological disorders increase.
The stage of precoma in patients with portocaval coma is characterized by the phenomena of portosystemic encephalopathy, i.e. transient disturbances of consciousness.
Electroencephalographic changes are insignificant. Patients at this stage are often depleted, or even cachectic. Profound metabolic disorders in the body are noted. Dystrophic changes are observed not only in the liver, but also in other organs.
The beginning of the impending catastrophe is evidenced by a decrease in the size of the liver with persisting or increasing jaundice, the appearance of a sweetish "liver" (methylmercaptan) odor from the mouth, an increase in hemorrhagic syndrome, tachycardia.
In the second stage, threatening coma, the consciousness of the patients is confused. They are disoriented in time and space, bouts of excitement are replaced by depression and drowsiness. Flapping tremors of the fingers and convulsions appear. Delta waves appear on the electroencephalogram against the background of a slowing down of the 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, there is clonus of the muscles of the foot, pathological reflexes (Babinsky, grasping, sucking), pathological breathing of Kussmaul and Cheyne-Stokes. Shortly before death, the pupils dilate, the reaction to light disappears, corneal reflexes fade away, sphincter paralysis and respiratory arrest occur on the electroencephalogram disappear a- and b-waves, hypersynchronous delta waves or irregular slow waves dominate
For hepatogenic encephalopathy, which is an integral part of hepatocellular (primary) failure, 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 indicators of hepatodepression
Portosystemic encephalopathy which occurs with portal-hepatic (secondary) insufficiency, is distinguished by the gradual development of coma without agitation and an obvious increase in jaundice. In functional terms, there is a distinct increase in liver bypass indicators (see "Symptom complex of impaired portal circulation caused by liver damage") with relatively stable (compared to the initial state) indicators of hepatodepression indicators.
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