Alcoholic cirrhosis of the liver (K70.3). Differential diagnosis of liver cirrhosis Differential diagnosis of hepatitis and cirrhosis

Cirrhosis is a disease in which the parenchymal tissue of the liver is gradually replaced by connective tissue. The organ ceases to perform its functions, which leads to the death of the patient. The process develops over a long time; at the initial stages, the clinical picture is erased. With further development, symptoms appear that allow one to suspect pathology. But for a more precise diagnosis, differential diagnosis of liver cirrhosis is necessary.

The course of different types of cirrhosis is different, so several types of classifications are used to make a diagnosis.

According to the form of the processes, they are classified depending on the size of the formed nodes.

• Small nodular cirrhosis, sizes up to three millimeters in diameter.
• Large-knot, over three millimeters.
• Incomplete septal (septal) form.
• Mixed, with nodes of different diameters.

There are types of cirrhosis based on the causes and conditions of the disease.

• Viral – caused by viral hepatitis B and C.
• Alcoholic – caused by prolonged use of alcohol-containing substances.
• Medicinal – occurs after long-term use of medications that destroy the liver.
• Secondary biliary cirrhosis is associated with impaired functioning of the extrahepatic bile ducts.
• Congenital – caused by hereditary diseases.
• Stagnant - provoked by circulatory disorders.
• Budd-Chiari disease is endophlebitis of the hepatic veins with thrombosis, anomalies of vein development.
• Metabolic and nutritional – associated with metabolic disorders.
• Cirrhosis of unknown etiology - this group includes primary biliary, associated with pathology of immunoregulation, cryptogenic, presumably provoked by a nutritional factor, and Indian childhood, possibly caused by high copper content in drinking water.

The third type of classification is used to assess severity. It examines the functioning of liver cells in a patient. Known as Child-Pugh.

According to this table, three groups are determined, depending on the points scored. A – five or six points, B – up to nine, C – over ten.

The role of differential diagnostics in making a diagnosis

Differential diagnosis is a set of measures prescribed by the attending physician to clarify the diagnosis. Used to distinguish between diseases that have similar symptoms. The differential diagnosis of liver cirrhosis is established after the following studies:

• taking anamnesis;
• examination of the patient;
• clinical tests of blood, urine, feces;
• biochemical blood tests;
• coagulogram - study of the functioning of blood clotting factors;
• enzyme tests;
• examination for hepatitis markers;
• ultrasound examination;
• computed tomography or MRI;
• biopsy with histological examination of tissue;
• research using radioisotopes;
• laparoscopic examination.

Differential diagnosis of liver cirrhosis

Differential diagnosis is used in cases where it is necessary to exclude diseases with a similar clinical picture.

What diseases require differential diagnosis?

Primary cancer and cirrhosis-cancer. With similar symptoms, it is characterized by rapid development. Blood tests show leukocytosis, increased ESR, anemia. The patient quickly loses weight and complains of pain. Ascites develops quickly and is not treatable with diuretics. Differential diagnosis helps to determine this type of pathology during laparoscopy, MRI results, and when α-fetoprotein is detected.

Alveolar echinococcosis. An enlarged spleen and functional tests are misleading. Differential diagnosis – ultrasound, MRI, antibodies in the latex agglutination reaction.

Constrictive pericarditis. Symptoms of ascites and liver enlargement, as with cirrhosis. For differentiation, cardiac echography is performed. Accurate data is obtained from x-ray kymography.

Myelofibrosis. In the early stages, the enlargement of the spleen is pronounced. Trepanobiopsy, a bone marrow puncture, helps with differential diagnosis.

Amyloidosis, hemochromatosis. Differential diagnosis is based on biopsy results. Wilson-Konovalov disease is distinguished by low serum ceruloplasmin.

Comparative table of pathologies

The symptoms of all pathologies are similar, the differences lie in the details. Only through differential diagnosis is it possible to establish an accurate diagnosis.

Prognosis for cirrhosis

Estimated predictions can be made based on the Child-Pugh score. Patients who receive class A have a life expectancy of about twenty years, and the mortality rate after surgery is 10%. Class B has a shorter lifespan and postoperative mortality reaches 30%. The most severe is class C, 18% survive after surgery, and without surgery they live no more than three years.

Thanks to differential diagnosis, there is a chance to identify cirrhosis in the early stages of development. In such cases, the patient has the opportunity to extend his life for a long time, subject to the doctor’s recommendations.

Liver cirrhosis, which is similar in many clinical manifestations to chronic hepatitis, is characterized by:

signs of portal hypertension

· dilatation of the veins of the esophagus, hemorrhoidal, hepatic and splenic veins,

· pronounced and persistent ascites.

Signs of hepatic cellular failure (decrease in total serum proteins, albumin, transferrin, cholesterol, ChE, alpha-LP, II, V, VII factors of the coagulation system; increase in bilirubin (indirect);

· liver puncture biopsy data are sometimes crucial for differential diagnosis.

1. Cardiac asthma
2. Hypertensive crisis
3. Cardiogenic shock
4. Angina pectoris
5. Pulmonary edema
6. Myocardial infarction
7. Paroxysmal ventricular tachycardia
8. Anaphylactic shock
9. Complete transverse block with Morgagni-Adams-Stokes syndrome
10. Acute respiratory failure
11. Attack of bronchial asthma
12. Pulmonary hemorrhage
13. Spontaneous pneumothorax
14. Gastrointestinal bleeding
15. Hepatic colic
16. Hepatic coma
17. Acute renal failure
18. Renal eclampsia
19. Renal colic
20. Hemolytic crisis
21. Hemorrhagic vasculitis
22. Diabetic coma
23. Hypoglycemic coma
24. Thyrotoxic crisis
25. Acute adrenal insufficiency

1. Cardiac asthma: evacuation to hospital lying down, head elevated, accompanied by a doctor (emergency personnel). Acute left ventricular failure.

2. Hypertensive crisis type I: 6-8 ml of dibazole 0.5% with 2-4 ml of papaverine 0.5%; 40 mg Lasix IV (m); 5-10ml 25%MgSO4 (convulsive syndrome).

20 mg anaprilin p/i (tachycardia); seduxun, relanium (psychomotor); You can take 10 mg of nifedepine (0.075 mg of clonidine) - every 30 minutes until normalization (if there is nothing). A crisis without complications is treated on the spot, with complications - hospitalization, for the first time - in the hospital.

1. Acute large-focal myocardial infarction in the anterior, apical, lateral sections, complicated by cardiogenic shock (true, not arrhythmic). Lying down with the lower end elevated: 0.5-1 ml mezaton-0.5 ml intramuscularly (to increase blood pressure); 2ml cordiamine; 1 ml promedol 2% (blood pressure control); neuroleptanalgesia – 2 ml fentanyl, 1 ml droperidone, mezaton – 0.5 ml IV (med); 5-10ml 4% DOPA in saline solution or 1-2ml 0.2% NA; 90-180 mg prednisolone; KI. Evacuation to the hospital, accompanied by a doctor, IV 10,000 heparin.

Hospitalization: the same + rheopolyglucin, thrombolysis (up to 4 hours) - IV 1.5 ml streptase + 60 mg prednisone over 30 minutes (complications: bleeding, reperfusion arrhythmia - atrial fibrillation, gastric tachycardia - well stopped, short-lived) Fortal balloon counterpulsation .

1. Angina pectoris nitroglycerin p/i every 5 minutes blood pressure correction heating pads to the legs 2-4 ml 50% analgin intramuscularly 1 ml 2% promedol. Evacuation to the hospital with a paramedic.

Hospital: IV nitroglycerin, oxygen with N oxide.

5. Pulmonary edema complicating the course of concomitant heart disease (mitral stenosis predominates and combined insufficiency): evacuation to the hospital while lying down, head elevated, accompanied by a doctor (emergency personnel). Acute left ventricular failure.

Help: orthoptic position, nitroglycerin under the tongue (10 min) - until the condition improves (under blood pressure control) to blood pressure 90/60 - possible; oxygen inhalation through alcohol (KI-40); a dropper with saline solution; IV 1 ml of promedol-2% (slowly) – suppression of overstimulation of the respiratory center (until it stops); IV 20-60 mg of furosemide (1-3 amp) – combating congestion in the pulmonary circulation, preventing pulmonary edema; venous tourniquets on the lower extremities for 30-40 minutes; IV medl 0.5-1 ml korglykon 0.06%, strophanthin 0.05% - if ineffective (per 10 ml saline solution);

In the hospital: narcotics and diuretics if necessary; IV nitroglycerin 8-10 ml 1% in 200 ml saline solution (with increased blood pressure) - 5-10 drops/min, with alcohol n.g. – 4 ml per 400 ml saline solution, nitroprusside Na – drop; DOPA (for lowering blood pressure) – 5-10 ml 4% (200 ml saline solution) 60-90 mg prednisolone; Ventilation with increased pressure on exhalation and inhalation.

6. IHD, acute large-focal myocardial infarction in the area of ​​the lateral part of the left ventricle, the most acute stage.

PMP: nitroglycerin; promedol IR, rest i.v. 0.005% - 2 ml fentanyl, 2 ml - 0.25% droperidol i.v. 10,000 heparin.

Hospital: IV nitroglyceran 1000/hour heparin, thrombolysis. Complications: edema, cardiac asthma, ventricular extrasystole 60-80 mg lidocaine.

1. Paroxysmal ventricular tachycardia of the heart PMP: lidocaine or 5-10 ml novocainamide 10% + 0.3-0.5 mesatone - 1 ml/min; 1 ml 5% phenazepam (excitement).

Hospital: 4-8ml 2% lidocaine, electropulse therapy (external)

1. Anaphylactic shock: lying down, fixed tongue, cold to the injection site, subcutaneous injection of 0.1% adrenaline (0.5-1 ml of adrenaline - inject the injection site);

IM (IV) 100-150 hydrocortisol (60-120 prednisolone) + 2 ml diphenhydramine. Repeated s/c 0.5 ml of adrenaline, 2 ml of cordiamine; KI 10ml 2.4% - euphilin. Evacuation to hospital. Hospital + rheopolyglucin, prednisolone, mechanical ventilation.

Often people who feel pain in the right hypochondrium ask how to identify cirrhosis of the liver at the initial stage. But unfortunately, the disease initially occurs with almost no symptoms, and signs appear when the gland has already increased in size.

To protect the liver from chronic disease, you need to eat right, lead an active lifestyle and undergo preventive medical examinations that will help to detect liver dysfunction.

Liver cirrhosis (transformation of parenchymal tissue into pathological connective tissue) is a common disease that is the final stage of a number of chronic liver diseases. A diagnosis of liver cirrhosis is made, taking into account data from the medical history, physical examination, functional tests, laboratory and instrumental studies.

What indicates liver cirrhosis

If a person regularly drinks ethyl alcohol, then the probability of developing cirrhosis within 5–10 years is 35%

Therefore, when diagnosing liver cirrhosis, studying the patient’s medical history is of great importance. Symptoms of cirrhosis depend on the etiology of the disease, the rate of progression and the degree of organ damage. About 20% of patients at the early stage of the process do not notice any signs of the disease, while others only mention increased gas formation and decreased performance.

As the tissue degenerates, a temporary dull pain occurs in the right side, which occurs after drinking alcohol or heavy food, and does not go away after taking antispasmodics. Signs of bile stagnation are rapid saturation and itching of the skin.

In some cases, nosebleeds occur and fever begins. As the disease progresses, jaundice and signs of portal hypertension, varicose bleeding from hemorrhoidal and esophageal veins are detected, and the amount of fluid in the abdominal cavity increases (ascites).

The following symptoms are typical for patients with cirrhosis:

• “drumsticks” (the phalanges of the fingers are thickened);
• “watch glasses” (changes in the nail plate);
• palmar erythema (red palms);
• “Spider veins” (thin vessels are visible through the skin of the face and body).

Men sometimes experience decreased testicles and enlarged breasts (gynecomastia)

In most cases, severe cirrhosis leads to a decrease in body weight and dystrophy.

Thus, the doctor can assume cirrhosis of the liver during the first examination of the patient, after studying his medical history. In the later stages of cirrhosis, even the appearance of the patient changes, which can serve as an indirect sign of the development of pathology.

After interviewing the patient about his medical history, complaints and lifestyle, the doctor conducts a physical examination, which includes palpation and percussion of the abdominal cavity, and examination of the skin. Upon examination, the doctor notes yellowing of the skin and sclera, weight loss, capillaries on the body and face, dilated veins in the abdomen, enlarged abdomen, swelling of the legs, redness of the palms, and a red rash.

The severity of these signs depends on the degree of the disease and at an early stage they may be completely absent. When palpating and listening to the abdominal cavity, the doctor may notice:

• hepatosplenomegaly;
• decreased tone of the abdominal wall muscles;
• changes in the contour of the liver and spleen during percussion;
• dull sound when tapped.

When palpating the liver, the doctor receives a lot of information, since enlargement of the gland is typical even for the initial stages of the pathology. In the stage of decompensation, the organ is already significantly enlarged and protrudes beyond the edge of the costal arch by two centimeters. The doctor determines by touch that the gland is too dense and uneven due to the formation of nodules.

For the patient, palpation of the liver is painful

What do tests show?

Blood tests for liver cirrhosis show a lack of hemoglobin, leukocytopenia and thrombocytopenia, which indicates a pathological enlargement of the gland. The coagulogram notes a decrease in the prothrombin index, that is, the blood clots more slowly than normal.

Blood biochemistry reveals increased activity of liver enzymes (alkaline phosphatase, Alt, AST), increased total and direct bilirubin, potassium, sodium, as well as urea and creatinine, and decreased albumin. Additionally, in case of liver cirrhosis, tests are carried out for antibodies to viral hepatitis, and the content of alpha-fetoprotein is determined.

According to a blood test, a diagnosis can be made and the degree of compensation can be determined. To confirm primary biliary cirrhosis, the level of liver enzymes, cholesterol, and antimitochondrial antibodies is checked, and a gland biopsy is also required. Protein and red blood cells are found in the patient's urine.

Hardware research for diagnostics

It is impossible to diagnose cirrhosis only on the basis of the patient’s complaints, his medical history and laboratory blood tests, since the same data can be obtained for completely different pathologies of the biliary system, and the characteristic signs of cirrhosis develop with significant liver damage.

Hardware diagnostics also makes it possible to detect the cause of the disease, which is important for determining a treatment regimen

Differential diagnosis is carried out between liver cirrhosis and cancer. Verification and confirmation of diagnoses is carried out using ultrasound, laparoscopy and biopsy. If cirrhosis led to liver cancer, then pathologies can only be distinguished by laparoscopy.

During differential diagnosis, it is possible not only to make the only correct diagnosis, but also to determine the type of cirrhosis. During the research, the biliary system is thoroughly studied, which makes it possible to determine the cause of the development of the pathology and take measures to eliminate it.

Ultrasound

Diagnosis of liver cirrhosis includes an ultrasound examination of the gland. An ultrasound accurately determines the size of the organ and its shape, notes sound permeability, and looks for signs of portal hypertension and changes in the spleen. This study provides a low-resolution image, but it still allows one to recognize inflammatory processes and neoplasms in the gland.

At the initial stage of cirrhosis, the structure of the liver is still homogeneous, and at the stage of subcompensation and decompensation, fibrous tissue is already noticeable, replacing parenchymal tissue. With small-nodular cirrhosis, the echogenicity of the gland is increased evenly, and with large-nodular cirrhosis, individual nodes and a heterogeneous tissue structure are distinguished.

In the later stages of the disease, the right lobe of the liver is reduced, and in the latter the gland becomes smaller than normal. Thus, an ultrasound examination of the liver allows not only to make a diagnosis, but also to determine the stage of development of cirrhosis.

Tomography

Computed tomography of the abdominal cavity makes it possible to see the gland, its vessels and bile ducts in more detail. If necessary, an MRI of the liver is performed. Based on the study, a conclusion is made about the homogeneity and density of the gland tissue.

Using this method, you can examine the vessels and bile ducts and draw conclusions about their patency. Due to its high cost, the examination is carried out to clarify the results of other diagnostic studies.

The images show congenital anomalies of the hepatobiliary system, metastases of extrahepatic tumors, accumulation of iron in hepatocytes, and obstruction of the bile ducts. This information is useful in making a diagnosis and determining further treatment tactics, and can also shed light on the etiology of the disease.

Doppler

Doppler analysis of the vessels of the gland determines the course of the vessels, whether there are obstacles to blood flow, and also measures the diameter of the vessels and the speed of blood flow. It is determined whether there is a change in blood flow speed when holding your breath or straining.

Laparoscopic examination is an operation that is performed to confirm the diagnosis. The doctor visually evaluates the surface of the gland. In large-nodular cirrhosis, individual nodes larger than 3 mm are distinguishable, between which there are strands of fibrous tissue. With small nodules, there are small nodules on the liver, the space between which is filled with connective tissue.

All types of cirrhosis are characterized by thickening of the liver capsule and dilation of the veins.

During the operation, the doctor can take material for histological examination

Liver biopsy

The final diagnosis and treatment tactics can be determined after a liver biopsy. This procedure is not performed on all patients, since it has a number of contraindications and is somewhat painful, and in most cases the diagnosis can be made using non-invasive diagnostic methods.

The study of the material taken allows us to identify morphological changes in the liver tissue and suggest the cause of their degeneration. A biopsy is performed to clarify the diagnosis for diffuse liver damage (hepatitis, cirrhosis, hepatomegaly).

To collect the material, the skin is pierced with a puncture needle in the right hypochondrium between the 7-9 rib; the sample is taken using a special aspirator syringe. In cirrhosis, when examining a biopsy specimen under a microscope, nodules are found surrounded by fibrous tissue, and the hepatocytes differ in size, the vessels between them with uneven lumens.

With active cirrhosis, necrosis of parenchymal tissue, cell enlargement, and the absence of a boundary between normal and pathological tissue are detected. And with inactive cirrhosis, there is no necrosis, and the border between normal and pathological tissue is clear.

As additional methods for identifying the causes of cirrhosis, methods are used to detect enzyme deficiencies, indicators of iron metabolism and protein activity, which are markers of metabolic disorders, are checked.

Cirrhosis is an incurable disease, but if it is detected at an early stage, the provoking factor is identified and eliminated, then if dietary recommendations are followed, the prognosis for the patient’s life is relatively favorable.

Therefore, it is important to consult a doctor at the first sign of liver dysfunction. And since the pathology in most cases is the result of another chronic liver disease, cirrhosis can be completely avoided if you consult a doctor in a timely manner and undergo treatment for the primary disease.

When diagnosing liver cirrhosis, its differential diagnosis is of great importance. Cirrhosis today is the cause of death in about 90% of patients with chronic liver disease and occupies a leading place among other diseases of the digestive system.

The main reasons, more than 60%, causing cirrhosis are alcoholism and viral infections. According to statistics, 2-2.5 million people die every year in the world just from the viral form of this disease.

Etiology

As mentioned above, the main reasons why you can develop this disease are long-term alcohol abuse and viral infections, in particular viral hepatitis C, B and D.

Another fairly likely way to get sick may be a biliary tract disease already developed in the body: aggravated extra- or intrahepatic obstruction of the biliary tract; childhood cholangiopathy; obstructed outflow of blood from the venous tract from the liver; excessive or improper use of pharmacological drugs, leading to toxic poisoning and ultimately cirrhosis of the liver.

But, surprisingly, with the modern development of medicine, the causes of this disease still remain unknown.

For quite a long time, the disease may not cause any symptoms. Assessment of the stage of the disease can be traced through severe portal hypertension and hepatocellular insufficiency. An approximate assessment of these same parameters is given by the diagnostic table of the Child-Pugh criteria.

This table has the following 3 classes:

1. Compensated (class A);
2. Subcompensated (class B);
3. Decompensated (class C).

In class A, the course of the disease is marked by the absence of noticeable jaundice, nosebleeds and varicose veins, ascites and encephalopathy. Classes B and C are complicated compared to the first class, ascites is observed in a more severe degree, spontaneous peritonitis and pleural empyema, as well as a complication of encephalopathy of the liver tissue.

Types of disease and its complications

The liver, being a natural filter in the human body, is exposed to a high number of irritants. Although liver cells are characterized by regeneration, you should not think that because of this it can independently cope with most of these ailments.

Like all serious diseases, cirrhosis has its main types:

• Subacute: occurs with acute hepatitis and symptoms are present at the initial stage; transformation of viral hepatitis into cirrhosis occurs within 0.5-1 year, death is possible;
• Rapidly progressing or active: has specific biochemical and clinical symptoms of strong activity of poor liver function; life expectancy from the onset of the disease is about 5 years;
• Slowly progressive or passive: this disease is very invisible, but there are noticeable disturbances in the normal functioning of the liver; life expectancy within 10 years from the moment of illness;
• Sluggish (slow): symptoms of clinical activity are not expressed, and morphological activity is moderate, functional disruptions in the liver are not observed; a fatal outcome is unlikely, but possible, and the patient can live with this for more than 15 years;
• Latent: this type of disease does not burden the patient with obvious symptoms, the activity of liver cells is within normal limits; Almost all those who overcome such a disease will not affect their life expectancy.

1. Ascites;
2. Formation of blood clots in the venous tract;
3. Transformation into the so-called cirrhosis-cancer;
4. Complication of secondary infection;
5. Bleeding in the digestive tract from varicose veins;
6. Liver failure;
7. Hepatorenal and hepatopulmonary syndrome;
8. Formation of stones in the bile ducts.

In order to find out the general state of affairs in cirrhosis or directly identify it, the following studies are necessary:

1. Hemogram;
2. Immunogram;
3. Proteinogram;
4. Coagulogram;

These studies are the main ones for this problem; without their help, it is extremely difficult to make a correct diagnosis. There are also a number of other ways to collect more detailed information about the disease in the human body.

The functional performance of the liver can be changed, and markers of such syndromes as choleostasis, cytolysis, synentic inferiority syndrome and the development of tumor growth syndrome will help to monitor this.

Regardless of the type of this disease, the patient is required to undergo testing for the presence of viral hepatitis B, C, D, this makes it possible to determine the severity of the disease, its prognosis and makes it possible to further monitor the effectiveness of treatment.

In case of autoimmune cirrhosis of the liver, an analysis is performed to determine certain autoantibodies; their combinations make it clear what the doctor has to work with at the moment and draw up the most correct plan to combat the disease.

As has already become clear, for any type of this disease, the patient can be sent for additional examination, which will definitely give a better idea of ​​the situation and the stage of the disease in the patient’s body. Today, medicine has already advanced quite far and should not be neglected.

If you are dealing with a highly active form of cirrhosis, with active viral hepatitis, cholangitis or the so-called congestive liver, you need to carry out a differential diagnosis. This diagnosis is a method of exclusion, in which the attending physician does not try, based on the patient’s tests, to make the most appropriate diagnosis. And, based on the results, it excludes those forms of cirrhosis that are not suitable. First of all, the patient is examined for alcoholism and the presence of hepatitis B, C, D in the body.

This problem is also differentiated from other liver diseases, which can lead the liver to the same condition.

Differential diagnosis is also carried out for echinococcosis. With it, a gradual enlargement of the liver is observed, it becomes more dense and lumpy. This can be traced through a biopsy.

A more accurate and detailed diagnosis can be made taking into account the sections of etiology, morphology and morphogenesis, activity of cirrhosis, its functional characteristics, and the like.

Regarding the prognosis, for any type of illness it can be compiled based on the degree of morphological changes in the liver tissue and trends towards progressive development. The average life expectancy can be from 3 to 5 years, in rare cases more than 10 years.

Preventive methods can include vaccination against viral hepatitis or its timely treatment, giving up alcohol or reducing its consumption to 50 grams per day and, of course, examination. If you have the slightest symptoms or sufficient time has passed since the last examination, you should not waste time, but consult a doctor as soon as possible for an examination.

Chronic hepatitis is considered a liver disease in which clinical, laboratory and morphological changes persist for 6 months or more.

Etiology.

There are several groups of factors leading to the development of chronic hepatitis (CH):

1. Infectious factors.

Among them, viruses are of primary importance, and chronicity occurs only with hepatitis caused by viruses B (10-15% of cases), C (30-60%), D (90-100%).

Infectious factors also include leptospirosis (Weil-Vasiliev disease), infectious mononucleosis, protozoa (giardia, leishmania), chronic infections (syphilis, tuberculosis, brucellosis, malaria).

2. Toxic factors.

These can be industrial toxins: lead, arsenic, dyes, insecticides, organochlorine compounds, etc.

Many drugs have a toxic effect on the liver: sulfonamides with long-term use, NSAIDs, barbiturates, methyluracil, mercazolil, etc.

Alcohol has a toxic effect on the liver.

1. Toxic-allergic factors.

These include diffuse connective tissue diseases: SLE, SSD, UP, dermatomyositis.

4. Metabolic and endocrine disorders.

It is necessary to take into account vitamin and protein deficiency, both exo- and endogenous in nature, as well as endocrine diseases (diabetes mellitus, thyrotoxicosis, hypothyroidism).

1. Obstruction of the bile ducts.

It can be intrahepatic and extrahepatic.

It should be noted that the etiological factors are the same for chronic hepatitis and liver cirrhosis (LC).

Pathogenesis.

In the pathogenesis of CG and cirrhosis, two main points can be distinguished:

1. Persistence of the virus in hepatocytes, which leads to the death of liver cells and the growth of connective tissue in this place.

2. Immune and autoimmune disorders, in which any substance can serve as a trigger. These processes can predominate or fade into the background, which determines the severity of pathological changes in the liver.

Clinical picture.

In the clinical picture of chronic hepatitis there are 4 main syndromes:

1. Painful.

This is the most common syndrome in chronic hepatitis. The pain is localized in the right hypochondrium or upper part of the epigastric region, radiating to the right half of the lumbar region, right shoulder, right scapula. The pain is dull, intensifies with fast walking, running, shaking the body, with errors in diet (drinking alcohol, spicy and fatty foods).

P. Dyspeptic.

Patients may experience nausea, a feeling of bitterness in the mouth, belching, bloating, etc.

Sh. Cellular liver failure.

Clinically, this syndrome is manifested by jaundice of the skin and sclera, scratching, the appearance of spider veins (telangiectasia) on the upper half of the body, face and upper extremities, subcutaneous deposition of cholesterol (xanthelasma), liver palms (thenar and hypothenar hyperemia), and enlarged liver.

The liver with chronic hepatitis is enlarged in size, upon palpation it is rather dense, the edge is pointed or rounded, the edge is even, the surface is smooth, palpation is painful. The spleen, as a rule, is not enlarged. An enlarged spleen is more common with active hepatitis according to the clinical classification and with active hepatitis according to the new classification.

The full extent of liver dysfunction can be judged only after a thorough study of additional examination methods. Since the liver is involved in almost all types of metabolism, the list of additional examination methods is large.

This includes:

1. Study of pigment metabolism based on data on the content of serum bilirubin (total, direct and indirect), urine urobilin and stercobilin in feces. The complex of these tests makes it possible to identify the type of jaundice: parenchymal or mechanical.

2. Study of protein metabolism. With hCG in the blood serum, the synthesis of finely dispersed proteins decreases and the synthesis of coarsely dispersed proteins increases - dysproteinemia. Qualitative reactions confirming this are the thymol test and the Veltman reaction, a quantitative test is the analysis of protein fractions (decrease in albumin content and increase in the level of alpha-2 and gamma globulins).

The content of prothrombin and fibrinogen, proteins involved in blood clotting, is reduced in the blood serum, therefore, with hCG, the blood coagulation system is disrupted, which can lead to dangerous bleeding.

3. Carbohydrate metabolism also suffers. In patients, fasting blood glucose levels may increase and the sugar curve may change. However, in addition to the liver, the pancreas also participates in the utilization of glucose, so based on these tests alone it is difficult to say which of these organs suffers more. Therefore, it is preferable to load with carbohydrates, which would be absorbed only by the liver. Such a carbohydrate is galactose. The patient is given a load of 40 g. Galactose and monitor its excretion in the urine. Normally, no more than 3 grams should be released.

4. Fat metabolism. With hCG, cholesterol and beta-lipoprotein levels may increase or decrease.

5. Enzyme metabolism.

Damage to hepatocytes is indicated by an increase in the level of alanine transaminase (ALT), and the severity of hCG is judged by the degree of its increase. If the ALT level exceeds normal values ​​by no more than 5 times, the disease is said to be mild; if the ALT level increases by 5-10 times, the disease is of moderate severity; if it increases more than 10 times higher than normal, the disease is severe.

What is important is the increased level of lactate dehydrogenase (LDH), its fifth fraction, which indicates the death of liver cells, alkaline phosphatase (ALP), which increases during cholestasis.

6. To establish the etiology of chronic hepatitis, serum markers of hepatitis are determined by radioimmunological and enzyme immunoassay methods using test kits. Antigens and antibodies are determined.

7. The following instrumental diagnostic methods are used: radionuclide diagnostics, cholangiography, ultrasound, computed tomography.

8. To study the morphology of the liver, a percutaneous puncture biopsy of the liver can be prescribed; if it is impossible to perform it in complex differential diagnostic cases, laparoscopy or laparotomy with a liver biopsy is prescribed.

1U. Damage to other organs and systems.

Patients with chronic hepatitis often develop astheno-neurotic syndrome; the cardiovascular system may be involved in the process (brady- or tachycardia, arrhythmias appear), the urinary system (hepatorenal syndrome), the pancreas, intestines, etc.

Classifications

1. Clinical classification.

1. Chronic persistent hepatitis.

It is characterized by a benign course. It develops several years after acute hepatitis; exacerbations are rare and respond well to treatment. During the period of remission, the patients' ability to work was preserved.

2. Chronic active hepatitis:

A) with moderate activity

B) with pronounced activity (lupoid, necrotizing).

It is characterized by an active course. It develops immediately after acute hepatitis; other organs and systems are involved in the process. Liver functions are significantly affected. The ability to work of patients is often reduced even during remission.

3. Chronic cholestatic hepatitis:

A) with intrahepatic cholestasis

B) with extrahepatic cholestasis.

Signs of cholestasis are the appearance of jaundice, accompanied by itchy skin. Blood serum levels of cholesterol, bile acids, beta-lipoproteins, and alkaline phosphatase levels increase

P. In 1994, at the World Congress of Gastroenterology in Los Angeles, a new classification of CG was adopted, which is based on histological, serological and clinical criteria.

According to it they distinguish:

1. Autoimmune hepatitis.

2. Chronic hepatitis B, C, D.

3. Chronic hepatitis of unknown type.

4. Chronic hepatitis, which is not classified as viral or autoimmune.

5. Chronic drug-induced hepatitis.

6. Primary biliary cirrhosis of the liver.

7. Primary sclerosing cholangitis.

8. Wilson-Konovalov disease.

9. Alpha-1-antitrypsin deficiency of the liver.

The diagnosis according to this classification must include 3 components: etiology, degree of activity and stage of the disease.

The etiology is listed above.

The degree of activity is understood as a combination of clinical data, ALT level (see above) and the results of histological examination of liver biopsies.

When determining the stage of the disease, the presence of portal hypertension is assessed, and histologically, the severity of fibrosis.

Liver cirrhosis.

Liver cirrhosis (LC) is a chronic disease characterized by diffuse damage to the liver parenchyma and stroma with nodular regeneration of liver cells, diffuse development of connective tissue with disruption of the lobular structure and vascular system of the liver.

Etiology and pathogenesis.

As mentioned above, they are common with CG.

Classification according to morphological characteristics:

1. Micronodular cirrhosis, in which the size of regeneration nodes does not exceed 1.0 cm in diameter.
2. Macronodular cirrhosis, in which regeneration nodes are more than 1.0 cm in diameter.
3. Mixed, macromicronodular cirrhosis.
4. Septal cirrhosis, in which regeneration nodes are almost invisible.

The disadvantages of this classification are that a puncture biopsy of the liver must be performed, and the puncture biopsy does not always contain the necessary area of ​​parenchyma, from which changes in the entire liver can be judged.

Cuban (Havana) classification (1954)

1. Portal cirrhosis (corresponds to septal or micronodular).
2. Postnecrotic cirrhosis (corresponds to macronodular).
3. Biliary cirrhosis (corresponds to micronodular).
4. Mixed cirrhosis.

Clinical picture.

In the clinical picture of cirrhosis, several syndromes can be distinguished:

1. Painful (see in the CG clinic).

2. Dyspeptic (see CG clinic).

3. Cellular liver failure (see CG in the clinic, but with cirrhosis it is more pronounced). Upon objective examination, in contrast to hCG, the liver first increases in size and then decreases, its consistency is dense, the edge is sharp, palpation is painless. The surface of the liver is smooth, the edge is smooth in portal and biliary cirrhosis, the surface is lumpy, the edge is uneven in postnecrotic cirrhosis. In all types of cirrhosis, an enlarged spleen is detected.

4.Portal hypertension syndrome.

It is manifested by dilation of the veins of the esophagus, hemorrhoidal veins, saphenous veins on the anterior abdominal wall (“head of the jellyfish”), and the presence of ascites. The causes of ascites are: hypoalbuminemia, increased activity of the pituitary antidiuretic hormone, which is not inactivated in the liver, impaired inactivation of aldosterone in the liver.

5. Damage to other organs and systems (see CG clinic). In addition, with CP, the osteoarticular system is affected: the terminal phalanges of the fingers change like “drum sticks”, there may be “watch glass”, osteoporosis often develops, which leads to fractures.

The clinical picture of cirrhosis depends on the type of cirrhosis, and its severity depends on the stage of the disease. Features of the clinical picture depending on the type of cirrhosis are in the textbook.

Complications of cirrhosis:

1. Hepatic coma.

The mechanism of its development is associated with the accumulation of neurotoxic products (ammonia, phenol) in the body. Clinically, intoxication of the nervous system is manifested by the appearance of headaches, sleep disturbances (drowsiness during the day, insomnia at night), inhibition of reactions, and apathy. Then tremor of the fingers and pathological reflexes appear, and patients lose consciousness. Death occurs in 80% of cases.

1. Gastrointestinal bleeding.

They occupy second place in the structure of mortality after hepatic coma. They are dangerous because the dilation of the veins of the esophagus and hemorrhoidal veins is combined with a disorder in the blood coagulation system.

1. Portal vein thrombosis.
2. Development of various infectious complications.

Treatment of hCG and cirrhosis.

This is a complex and still unresolved problem. Treatment depends on the type of hCG or cirrhosis, the activity of the pathological process in the liver, concomitant diseases and other factors.

However, all patients without exception are first prescribed basic therapy, which includes:

1. Physically gentle regime. Hypothermia, overheating, insolation, hydrotherapy, sauna, and vaccinations are contraindicated for such patients.
2. Prescribing a diet within tables 5a and 5 according to Pevzner.
3. Detoxification measures, which include infusions of 5% glucose solution, saline, other saline solutions (disol, trisol, etc.), reambirin, etc.
4. Normalization of intestinal activity. For this purpose, patients are prescribed antibiotics (kanamycin, etc.) or sulfonamides (salazopyridazine, etc.) for 5-7 days, and then biologically active drugs such as lactobacterin, bifidumbacterin, bifiform and etc.
5. Prescription of enzyme preparations that do not contain bile acids.

Treatment of autoimmune chronic hepatitis and cirrhosis.

The leading role in their treatment is given to immunosuppressive therapy, that is, glucocorticoids and cytostatics. Currently, two treatment regimens are used:

1. Monotherapy with prednisone.

The initial daily dose of prednisolone is 30-40 mg, then the monthly dose of prednisolone is reduced by 5 mg, bringing to a maintenance dose of 10 mg.

1. A combination of prednisolone in an initial daily dose of 15-20 mg and azathioprine in an initial daily dose of 50 mg. The principle of treatment is the same as in the first regimen, the maintenance dose is 10 and 25 mg, respectively.

This regimen is more preferable, since the initial doses when combining drugs are smaller, therefore the course of treatment is shorter and there are fewer complications.

Long-term treatment with this kind of drugs requires the prescription of antibiotics due to the possible development of infectious complications.

Treatment of viral CG and CP.

The leading role in their treatment belongs to interferons, and alpha-interferon preparations are used. This is a natural drug - wellferon and recombinant forms (obtained using genetic engineering) - roferon, reaferon, intron-A, viferon, etc. They all have almost the same effectiveness, but patients tolerate natural wellferon better.

Interferons are administered intramuscularly, the administration interval is 3 times a week. Viferon is available in candles.

Doses of interferons depend on the type of virus that caused CG or cirrhosis.

For hCG caused by virus B, the dose of interferon is 5,000,000 IU three times a week for 6 months or 10,000,000 IU 3 times a week for 3 months.

For chronic hepatitis caused by the C virus, the dose of interferon is 3,000,000 IU 3 times a week for 2 months, and then depending on the effectiveness. If ALT levels normalize or decrease, continue interferon administration at the original or higher dose for another 6 months. If there is no positive dynamics, then further administration of interferons should be abandoned.

For chronic hepatitis caused by the D virus, the dose of interferon is 5,000,000 IU 3 times a week; if there is no effect, the dose is increased to 10,000,000 IU 3 times a week for up to 12 months.

Stable and long-term remission can be achieved with CG B in 30-50% of cases, with CG C in 25%, and with CG D in only 3% of patients.

The most common side effect of interferon therapy is flu-like syndrome (occurs in 75-90% of patients). It is manifested by the appearance of fever, myalgia and arthralgia. These symptoms are reduced if you take a paracetamol or aspirin tablet before the interferon injection, and administer the interferons before bed.

Other side effects less common: weight loss, hair loss, depression, leukopenia, thrombocytopenia.

In addition to interferons, interferon inducers can be used, which include roncoleukin, cycloferon, etc., as well as chemotherapy drugs - vidarabine, ribavirin, etc.

In the treatment of hCG and cirrhosis, vitamins (fat- and water-soluble), metabolites and coenzymes are used.

In case of alcoholic liver damage and/or the presence of cholestasis, Heptral is prescribed at a dose of 800-1600 mg per day orally or parenterally.

Symptomatic therapy for hCG and cirrhosis:

1. For jaundice - choleretic agents and antispastic agents.
2. For ascites - diuretics and pain medications.
3. For severe pain, analgesics.
4. For skin itching - desensitizing drugs, ion exchange resins (cholestyramine).
5. For bleeding - hemostatic therapy.