References:

Brief introduction of symptoms:

Cirrhosis refers to the long-term or repeated damage to the liver due to one or more reasons, which leads to extensive liver parenchyma damage, hepatocyte necrosis, fibrous tissue proliferation, normal structure disorder of the liver and hardening of the texture. Can be complicated with splenomegaly, ascites, edema, jaundice, esophageal varices, bleeding, liver coma and so on.

Health guide:

1. Active prevention: Liver cirrhosis is the result of gradual degeneration of liver parenchyma caused by different reasons.

We should pay attention to the prevention and treatment of various primary diseases, actively prevent and treat chronic hepatitis, schistosomiasis and gastrointestinal infections, avoid contact with and application of substances toxic to the liver, and reduce pathogenic factors.

2. Emotional stability: The liver is closely related to spirit and emotion. Bad mood, depression and anger will all affect the function of the liver and accelerate the development of the disease. Establishing a strong will, cheerful mood, uplifting spirit and eliminating ideological burden will be beneficial to the improvement of the disease.

3. Dynamic and static combination: the compensatory function of liver cirrhosis is decreased, and patients with ascites or infection must stay in bed. During the period of fully compensatory function and stable illness, you can do some relaxing work or appropriate activities and carry out beneficial physical exercise, such as walking, doing exercises, Tai Ji Chuan, Qigong, etc. The amount of activity is that you don't feel tired.

4. Simple medication: blind abuse of general drugs will increase the burden on the liver, which is not conducive to liver recovery. Drugs harmful to the liver, such as isoniazid and barbiturates, should be used with caution or have contraindications.

5. Quit smoking and avoid alcohol: Alcohol can help fire and replenish blood, and long-term drinking, especially hard liquor, can lead to alcoholic cirrhosis. Therefore, drinking alcohol will aggravate the condition of patients with liver cirrhosis and easily cause bleeding. Long-term smoking is not conducive to the stability and recovery of liver disease, can accelerate the process of liver cirrhosis, and has the risk of promoting liver cancer.

6. Diet care: A diet with low fat, high protein, high vitamins and easy digestion is appropriate. Be regular, quantitative and temperate. In the early stage, you can eat more soy products, fruits and fresh vegetables, and eat sugar, eggs, fish and lean meat appropriately; When the liver function drops obviously and there are signs of hepatic coma, the intake of protein should be properly controlled, and a low-salt diet or a salt-free diet should be advocated. The daily intake of salt should not exceed 1 ~ 1.5g, and the drinking water should be within 2000ml. In severe ascites, the intake of salt should be controlled within 500mg, and the intake of water should be within 1000ml. Avoid spicy and irritating items and hard and cold food, and don't eat overheated food to prevent bleeding.

Cirrhosis is a chronic progressive liver disease, which is caused by many factors that damage the liver, such as chronic active hepatitis and long-term alcoholism. Mainly manifested as loss of appetite, fatigue, gingival bleeding, liver palm, spider nevus, jaundice, low albumin, splenomegaly, abdominal varicose veins, esophageal and gastric varices, ascites and so on. Serious complications such as gastrointestinal bleeding, hepatic coma and secondary infection often occur in the late stage. Patients with liver cirrhosis are also high-risk targets of primary liver cancer, and regular examination should be paid attention to.

Liver cirrhosis can be treated with Chinese and western medicine, which has a certain effect.

prescription

1. Patients with liver cirrhosis should pay attention to rest and avoid strenuous exercise; We should keep an optimistic mood and build up confidence in overcoming the disease.

2. The food used should be digestible and nutritious. High protein, high sugar, high vitamins and low fat are the principles of diet choice for patients with liver cirrhosis.

3. When there is ascites, stay in bed, increase nutrition and limit salt intake. It is best to adopt a salt-free or low-salt diet, with the salt content not exceeding 5g 1 yuan per day.

4. When ascites is obvious, water intake should be limited. Generally, the daily drinking water should be controlled at 1000 ml (equivalent to 2 bottles of salt water bottles used in hospitals). Severe hyponatremia should be limited to 500 ml.

5. Patients with esophageal varices should avoid irritating and hard food, so as not to damage esophageal varices and cause massive bleeding.

6. When hepatic coma is possible, the intake of protein should be limited, and vegetables should be the main food for three meals.

7. Quit smoking and drinking, and don't abuse "liver-protecting" drugs.

8. You should go to the hospital regularly for liver function, alpha-fetoprotein and ultrasound examination.

Zhang suffered from chronic hepatitis years ago. Since April last year, he has felt general malaise, obvious fatigue and swelling pain in his right upper abdomen. The doctor diagnosed it as "chronic hepatitis and cirrhosis" after examination. The doctor told him to take an appropriate amount of high-quality animal protein to ensure his nutritional needs. Due to the patients' insufficient understanding of the disease, they did not pay attention to it, and at the same time, they were overworked, which led to abnormal behavior, unclear answers, slow thinking and other early manifestations of liver coma. The patient's family is undecided about this. This doubt is also common sense that people should know, understand and master. Speaking of viral hepatitis B, you must be familiar with it. The patient-who once suffered from hepatitis, did not get a good rest and nutrition, which further damaged liver cells, degenerated cells, necrotized cells and proliferated fibrous tissue. Over time, the liver tissue structure is gradually destroyed and the texture becomes hard. The mild symptoms are loss of appetite, aversion to greasy food, abdominal distension, fatigue and discomfort in the liver area. In severe cases, liver function abnormalities such as ascites, digestion, detoxification, coagulation dysfunction and portal hypertension may occur. It should be pointed out that the early stage of liver cirrhosis should pay attention to rest and properly supplement high-quality protein, which is beneficial to the repair of liver cells. If the damage of liver cells is aggravated, the detoxification function of liver will decrease obviously. At this time, excessive intake of protein will not be worth the loss, resulting in excessive ammonia in the body and increased blood ammonia content, leading to hepatic coma. Therefore, patients with early hepatic coma must strictly control the intake of protein. In order to avoid negative nitrogen balance, protein, a leguminous plant with low ammonia production, can be supplemented. Although the blood ammonia decreased after treatment with antihyperglycemic drugs (the normal range was 37-8 1 mmol/L), protein should not be supplemented too quickly or too much. Fresh vegetables and fruits should be supplemented to ensure the supply of carbohydrates and appropriately limit the intake of fat. In addition, patients with liver cirrhosis should strictly abide by the following points: First, strictly ban alcohol, alcohol can aggravate liver cell damage, which is not conducive to liver cell repair. Second, you should avoid rough and hard foods, such as fractures, thorns and hard fruits, to prevent bleeding from esophageal and gastric varices. Third, patients with ascites edema should adopt a low-salt diet with a daily salt intake of less than 2 grams. Four, patients with liver cirrhosis should keep the stool unobstructed, such as constipation, edible sesame oil, honey and so on. To reduce the accumulation of ammonia and prevent hepatic coma. Fifth, eating less and eating more meals is conducive to liver rest and reducing the burden on the liver.

It can restore most liver functions, correct hypoproteinemia and improve internal circulation of liver. Renal filtration rate increased and ascites disappeared. However, the recurrence rate of ascites in liver cirrhosis is very high, and the treatment is becoming more and more difficult. Therefore, it is very important to prevent recurrence after discharge.

In terms of diet, patients with liver cirrhosis have increased secondary aldosterone, decreased urinary sodium excretion, increased sodium storage in renal distal convoluted tubules, and high-salt diet can further increase blood sodium level, which can induce ascites. At the same time, protein synthesis is impaired and albumin is decreased in patients with liver cirrhosis. If you eat a low-protein diet for a long time, it will aggravate hypoproteinemia and ascites will reappear. However, if you eat a high-protein and high-fat diet in large quantities, it will increase the burden on the liver and worsen the condition. Patients with liver cirrhosis often have esophageal varices, and eating rough food may puncture varicose veins. Upper gastrointestinal bleeding occurred. Therefore, we should vigorously reduce salt, moderate protein and low-fat diet; Eat foods rich in vitamins and choose soft foods that are easy to digest; Avoid overeating, hunger, smoking and drinking, pay attention to food hygiene and prevent diarrhea.

Rest to ensure more than 8 hours of sleep every day, avoid fatigue, and gradually increase the amount of activity, from rest to half-day work or even full-time work. Improve the immune function of the body, use Chinese and western medicine to promote the regeneration of liver cells, combine static and dynamic, and participate in physical exercise; Keep a happy mood, avoid sadness, and take part in more recreational activities to enhance physical fitness, improve the body's disease resistance, and promote liver function recovery and hepatocyte regeneration. Prevention of infection Patients with liver cirrhosis have low resistance and are prone to peritoneum and other infections. Moreover, patients with liver cirrhosis already have ascites infection or other infections. After treatment and control, if the control is not thorough, the infection will re-ignite or re-infect, ascites will appear. Therefore, patients with liver cirrhosis should avoid contact with infectious diseases and try not to go to public places during the epidemic of infectious diseases. Once an infection occurs, it should be treated thoroughly as soon as possible.

There are more than 200 kinds of drugs that can easily cause liver injury, such as tetracycline, cincofen, antimony, arsenic, chlorpromazine, barbiturates, urethane, azathioprine, isoniazid, p-aminosalicylic acid, chloral hydrate, chloramphenicol, erythromycin, etc., which should be banned or used with caution. Prevention and treatment of complications Patients with ascites due to liver cirrhosis are prone to complications such as upper gastrointestinal bleeding, hepatic encephalopathy, kidney disease, ulcer, hematological diseases, diarrhea and electrolyte disorder. And should be actively treated to minimize the damage to the liver.

How to Find and Treat Early Cirrhosis Medical Popular Science Magazine "Seeking medical advice-It is beneficial to open books" Author: Tang

China is a high incidence area of hepatitis B virus infection and hepatitis B, and cirrhosis caused by viral hepatitis is the most common, especially after hepatitis B, and alcoholic cirrhosis caused by alcoholism is the most common in foreign countries, especially in Europe and America.

The average adult suffers from hepatitis B. Through rest, proper nutrition strengthening and adjuvant treatment with Chinese and western drugs for protecting the liver, 90% of the patients can be cured, and only 65,438+00% of the patients turn into chronic hepatitis. Of the chronic hepatitis 10%, 20% may develop into cirrhosis, and about 1% may develop into liver cancer. So after suffering from hepatitis B, most of them can be cured. Therefore, there is no need to be nervous and panic.

The time from viral hepatitis to cirrhosis can be long or short. It takes 20 to 30 years for the long ones and only a few months for the short ones. Therefore, patients should do a good job of self-care, pay attention to conditioning and maintenance, which will not have much impact on life expectancy.

Chronic hepatitis must undergo liver fibrosis before it develops into cirrhosis.

How to find early cirrhosis?

The clinical manifestations of early liver cirrhosis are not obvious, and there may be no symptoms or only mild symptoms, such as fatigue, poor appetite, dyspepsia, nausea, vomiting, right upper abdominal pain, diarrhea and so on. These symptoms are not characteristic, and general gastrointestinal diseases can occur, not unique to early cirrhosis, and it is difficult to find them early simply by symptoms. In the physical examination of early cirrhosis, the liver is often enlarged, and some patients have enlarged spleen, and spider nevus and liver palm can be seen. Liver function tests are mostly in the normal range or slightly abnormal, especially protein changes, such as albumin decrease and globulin increase, and the ratio of albumin to globulin is close to or even inverted.

So, what other tests can find early cirrhosis?

1. The ideal gold indicator is to give the patient a liver biopsy. Using 1 s puncture method, a small amount of liver tissue was examined under microscope to find out whether there was fibrosis and connective tissue in the liver.

2. do a b-ultrasound examination. Hepatomegaly can be found in the early stage of liver cirrhosis, and the echo display of liver is enhanced and thickened. Once it develops to the late stage, the inner diameter of portal vein widens to more than 13mm, the width of splenic vein widens to more than 8mm, the spleen thickens, the liver shrinks, and the surface of the liver is not smooth and uneven, often accompanied by ascites.

3. Draw blood to check four serological indexes of fibrosis. Hyaluronic acid (HA), laminin (LN), procollagen Ⅲ (PⅢ P) and collagen Ⅳ (C Ⅳ). Among them, 2 ~ 3 items are obviously increased, so early cirrhosis can be considered.

Treatment of early cirrhosis

1. Pay attention to rest properly, don't be overworked, and you can take part in general light work.

2. The diet is mainly high in calories and protein. Eat foods rich in vitamins (fresh vegetables and fruits) and easily digestible foods. Don't eat hard and coarse food. Don't drink. Don't use drugs that damage the liver.

3. Drug therapy Under the guidance of experts, Chinese and western medicines that protect the liver are used to improve liver function. Anti-fibrosis therapies, such as Kangxian Pill, Compound Biejia Ruangan Tablet and γ -interferon have anti-fibrosis effects. If the patient's HBV replication index is positive (such as HBV-DNA positive and HBeAg positive), the nucleoside antiviral drug hepcidin (lamivudine) can be used. But don't take too much medicine, otherwise it will increase the burden on the liver and be unfavorable to the recovery of liver disease.

In short, efforts should be made to find and treat early cirrhosis. When the liver disease is still in the stage of fibrosis, through active treatment, the condition can be reversed and it is possible to fully recover. If the disease has progressed to cirrhosis, it can only be relieved by treatment. If the disease has developed to advanced cirrhosis, patients often have some complications, such as hepatic encephalopathy (hepatic coma), upper gastrointestinal bleeding, ascites, hepatorenal syndrome, infection and so on. And the prognosis is poor.

What is cirrhosis?

Cirrhosis is a chronic progressive diffuse change of the liver caused by various reasons. It is characterized by repeated and long-term damage to liver cells for one or more reasons, leading to degeneration and necrosis of liver cells. After extensive degeneration and necrosis of hepatocytes, connective tissue in the liver regenerated and diffuse proliferation of fibrous tissue appeared. At the same time, hepatocytes in the liver regenerate, forming regenerative nodules, and the normal hepatic lobule structure and blood vessel formation are destroyed, forming false lobules. After a long period of time (years or even decades), the liver gradually deforms and hardens, which is clinically called cirrhosis.

Cirrhosis is very common in China, most of which are posthepatitic cirrhosis, and a few are alcoholic cirrhosis and schistosomiasis cirrhosis. Because cirrhosis can be reversed or stopped after active prevention and treatment in the early stage, it will seriously affect the quality of life of patients and even endanger their lives in the later stage, so the prevention and treatment of cirrhosis is very important.

What are the causes of liver cirrhosis?

The etiology of liver cirrhosis can be divided into the following eight categories:

(1) Hepatitis virus: The most common infections are hepatitis B virus, hepatitis C virus and hepatitis D virus. Some hepatitis B virus-infected people develop chronic hepatitis, and a small number of chronic hepatitis B develop cirrhosis. About half of acute hepatitis C develops into chronic hepatitis, of which 10% ~ 30% will develop into cirrhosis. Hepatitis D virus depends on hepatitis B virus to produce hepatitis, and some patients develop cirrhosis.

(2) Alcohol factor: Long-term heavy drinking leads to liver cell damage, steatosis, necrosis, liver fibrosis, and severe cirrhosis.

(3) Cholestasis: Long-term chronic cholestasis leads to hepatocyte inflammation, bile duct reaction and even necrosis, leading to biliary cirrhosis.

(4) Congestion factors: Long-term repeated chronic cardiac insufficiency, constrictive pericarditis and hepatic vein occlusion can cause liver congestion, which will lead to necrosis and degeneration of liver cells due to hypoxia, and eventually lead to cirrhosis. Among them, cirrhosis caused by the heart is called cardiogenic cirrhosis.

(5) Drug-induced or chemical toxic factors: Long-term use of certain drugs, such as acetaminophen, cincofen and methyldopa, can lead to drug-induced hepatitis and eventually develop into cirrhosis. Long-term exposure to certain chemical poisons, such as carbon tetrachloride, arsenic and phosphorus, can cause toxic hepatitis and develop into cirrhosis.

(6) Metabolic disorder: copper metabolic disorder, seen in hepatolenticular degeneration. Iron metabolic disorders are found in hemophilia, galactosemia, fibrocystic diseases, α-antitrypsin deficiency, glycogen storage diseases, tyrosine metabolic disorders and hereditary hemorrhagic telangiectasia. These diseases are related to genetic metabolic defects and can all lead to cirrhosis.

(7) Parasitic infection: Schistosoma infection is common in southern China, which can lead to schistosomiasis and further lead to liver fibrosis and cirrhosis. If the human body is infected with Clonorchis sinensis and is not treated in time, cirrhosis will occur.

(8) Other factors: high malnutrition can lead to cirrhosis, and the cause of a few cirrhosis is unknown.

How to diagnose liver cirrhosis?

The typical symptoms of patients with liver cirrhosis are easy to diagnose, but some patients may have no typical clinical symptoms and are in the recessive compensatory period, which is difficult to diagnose at this time. So the diagnosis of liver cirrhosis is a comprehensive diagnosis.

(1) History of viral hepatitis, chronic alcoholism, chronic malnutrition, schistosomiasis or chemical drug poisoning.

(2) Symptoms: loss of appetite, ascites, nausea, diarrhea, mild hepatosplenomegaly and vascular nevus in the early stage (compensatory stage), ascites, bleeding tendency, jaundice, hepatosplenomegaly and liver volume reduction in the late stage (decompensated stage).

(3) Liver function examination: the liver function is normal or slightly abnormal in compensatory period, obviously abnormal in decompensated period, plasma albumin is decreased, globulin is increased, and the ratio is reversed, and γ globulin is obviously increased in protein electrophoresis.

(4) Blood test: leukopenia and thrombocytopenia in patients with hypersplenism, and pancytopenia in severe cases.

(5) Esophageal barium examination or endoscopic examination, esophageal or gastric varices.

(6)B-ultrasound examination: changes in the size, surface and morphology of the liver, echo, thickening of portal vein and splenic vein, ascites, visible fluid dark area, and increased spleen volume.

(7) Histological examination of liver: If there is fibrous septa formation, nodular hyperplasia or mixed nodular hyperplasia, diagnosis can be made.

What is the difference between chronic hepatitis and cirrhosis?

The main pathological change of chronic hepatitis is the collapse of reticular fibrous structure scaffold after hepatocyte necrosis, forming fibrous scar. The other is the regeneration of liver cells, forming concentric nodules of different sizes. In addition to 1 year medical history, the main points of clinical diagnosis of chronic hepatitis should also meet the following conditions: ① frequent or repeated symptoms, poor general health and obvious decline in work ability. (2) Hepatomegaly, with medium hardness or above, may have tenderness and some may be accompanied by splenomegaly. Spider nevus and liver palmar increase have certain significance in diagnosis. ③ Chronic liver function damage, especially the change of albumin/globulin ratio.

Clinically, it can be divided into: ① chronic active hepatitis: obvious symptoms of digestive tract (anorexia, abdominal distension, diarrhea) and general weakness. After the activity, the symptoms will get worse. Jaundice gradually aggravates, with pain in the liver area and occasional pain in the right upper abdomen. Hepatomegaly with tenderness. Liver function tests such as transaminase and musk turbidity showed positive changes in different degrees. ② Chronic inactive hepatitis: The symptoms are generally less, and the symptoms are not aggravated after the activity. Occasionally fatigue and poor appetite, but occasionally abdominal distension and fullness in the right upper abdomen. Hepatomegaly has no tenderness, and liver function is mostly in the normal range.

The main clinical manifestations of liver cirrhosis are hepatomegaly and splenomegaly, which are very common. However, diseases that may cause splenomegaly, such as malaria, kala-azar and schistosomiasis, should be excluded. Spleen enlargement has certain significance in diagnosis. X-ray examination of esophageal or gastric varices is of great value in the diagnosis of liver cirrhosis. Generally, it is not difficult to distinguish chronic hepatitis from medical history, signs and liver function examination. Sodium tetrabromophthalein sulfonate (BSP) test is very helpful, ultrasound examination can assist in diagnosis, and liver biopsy can diagnose chronic hepatitis or cirrhosis, but its indications should be strictly controlled.

What are the pathological characteristics and classification of liver cirrhosis?

Cirrhosis is a chronic liver disease caused by many reasons. It is characterized by repeated chronic degeneration and necrosis of liver cells, followed by fibrous tissue hyperplasia and nodular regeneration of liver cells, which destroys the normal lobular structure of the liver, changes the blood circulation path, makes the liver deform, shrink and harden, forms nodules, and leads to cirrhosis. There were no obvious symptoms in the early stage, but portal hypertension and abnormal liver function in different degrees in the later stage.

The classification of liver cirrhosis is complex and diverse, some according to the etiology, some according to the lesions, each with its own advantages and disadvantages. At present, according to the classification of International Research on Hepatology (IASL), it can be divided into viral hepatitis, alcoholic, biliary and occult cirrhosis according to the etiology. According to the focus, it can be divided into small nodules, large nodules, mixed nodules and incomplete interval cirrhosis. In China, it is often divided into portal vein type (equivalent to small nodules), necrotic type (equivalent to large nodules and mixed large and small nodules), biliary tract type, congestion type, parasitic and pigmented cirrhosis. Portal cirrhosis is the most common, followed by necrotizing cirrhosis and biliary cirrhosis.

What is the clinical stage of cirrhosis?

Cirrhosis is clinically divided into compensatory stage and decompensated stage. The compensatory period can also be called occult period, but it is asymptomatic and the routine examination of liver function is normal. When clinical symptoms appear, it has entered the decompensation period, mainly including burnout, fatigue, anorexia, abdominal distension, two? Pain, liver function decreased obviously, swollen liver often shrank, and ascites, edema, jaundice, fever and so on appeared. The clinical manifestations of decompensated cirrhosis can be summarized into two syndromes, namely abnormal liver function and portal hypertension.

What is early cirrhosis and what are its clinical manifestations?

Early cirrhosis refers to no specific symptoms or signs in clinic, no obvious abnormality in liver function examination, but obvious pathological changes in liver histology. Studies at home and abroad have confirmed that the content of various collagens in the liver of patients with early cirrhosis has increased, among which the deposition of type ⅰ and ⅲ collagen is mainly increased. Type ⅰ is the main type in the late stage of liver cirrhosis, and type ⅲ is the main type in the early stage of liver cirrhosis. With the development of liver fibrosis, the proportion of type ⅰ/ⅲ collagen increased from 1 to 1.59, and the type ⅰ collagen fibers increased, which participated in the formation of connective tissue and had strong reversibility, mainly in the late stage of liver cirrhosis.

Because early cirrhosis has no specific symptoms and signs in clinic, it is in the stage of subclinical lesions, but some patients may have the following manifestations.

(1) General symptoms: mainly fatigue, fatigue and physical decline. A few patients may have facial pigmentation.

(2) Symptoms of chronic dyspepsia: anorexia, abdominal distension or constipation, diarrhea or dull pain in the liver area, which is obvious after fatigue.

(3) Signs: Spider nevus can be seen in a few patients, and the liver is slightly to moderately swollen, which is more common in patients with alcoholic cirrhosis and generally has no tenderness. The spleen can be normal or slightly swollen.

The above clinical manifestations are often confused with primary chronic liver disease or do not attract the attention of patients.

Why are patients with liver cirrhosis prone to umbilical hernia and femoral hernia?

When liver cirrhosis is accompanied by ascites, it is easy to cause hernia due to the increase of intra-abdominal pressure, which is prominent in the weak points of abdominal wall, especially umbilical hernia, accompanied by varicose veins, so it is local cyanosis and there are also hernia addicts. When ascites disappears and intra-abdominal pressure decreases, hernia disappears. Hernia can also occur before the accumulation of ascites, which may be caused by the increase of intra-abdominal pressure caused by flatulence in the small intestine. The increase of gas in the small intestine is related to the overgrowth of bacteria in the intestine, indigestion absorption, decreased intestinal motility and peristalsis, anal exhaust disorder, increased portal vein pressure, intestinal wall edema and other factors.

What are the causes of peptic ulcer in liver cirrhosis?

The pathogenesis of peptic ulcer in liver cirrhosis may be related to the following factors.

(1) Mucosal microcirculation disorder: During portal hypertension, submucosal veins and capillaries of the upper digestive tract are blocked from expanding and stagnated, and microcirculation disorder and energy metabolism disorder make the mucosa lack nutrition, and cells die, resulting in erosion, ulcer and hemorrhagic lesions. Therefore, it is considered to be related to hypoxia caused by chronic venous congestion.

(2) The role of gastric acid: The gastric acid in patients with liver cirrhosis tends to increase. When portal vein shunt is formed, gastric acid-promoting substances (such as histamine, serotonin, etc. ) normally exists in the portal vein blood, and will not be inactivated by the liver, but will directly flow into the systemic circulation, leading to excessive secretion of gastric acid, causing mucosal erosion or ulcer.

(3) Endotoxemia: During portal hypertension, endotoxin absorbed by intestine directly enters systemic circulation through collateral circulation, causing endotoxemia and gastrointestinal bleeding.

(4) Liver function damage: especially in patients with hepatorenal syndrome, due to the retention of toxic substances in the body, it can directly destroy the mucosal barrier, leading to mucosal erosion, ulcer or bleeding in the upper digestive tract.

(5) Infection factors: Patients with liver cirrhosis have low immune function and are prone to infection. Infection can be used as a stress factor, which makes the body in a state of stress, increases the excitability of sympathetic nerve, secretes too much catecholamine, contracts visceral blood vessels, hinders the blood supply of mucosa and is prone to ulcer.

Why are patients with liver cirrhosis prone to fatigue?

Fatigue refers to the situation that the human body is prone to fatigue, feeling physically weak, mentally poor and physically and mentally difficult to persist. The degree of fatigue varies from mild to severe, and the degree of fatigue is consistent with the degree of liver disease activity. Causes of fatigue:

(1) Patients often lose their appetite for a long time and eat less, resulting in insufficient calories absorbed by the human body and unable to meet their own nutritional needs.

(2) Abnormal liver function, disorder of intermediate metabolism of carbohydrate, protein and fat, resulting in insufficient energy production.

(3) When liver injury or bile excretion is not smooth, cholinesterase in blood decreases, which affects the normal physiological functions of nerves and muscles.

(4) In liver cirrhosis, the process of transforming lactic acid into glycogen is blocked, and lactic acid accumulates too much after muscle activity, causing fatigue.

(5) Dysabsorption of vitamin E in liver cirrhosis leads to nutritional muscular atrophy and myasthenia.

What gastrointestinal symptoms do patients with liver cirrhosis have?

(1) Loss of appetite: it is the most common symptom, sometimes accompanied by nausea and vomiting, which is mostly caused by portal hypertension, gastrointestinal obstructive congestion and gastrointestinal secretion and absorption dysfunction caused by liver cirrhosis.

(2) Diarrhea: quite common, characterized by irregular or loose stools, no pus and no mucus. It is mostly caused by intestinal wall edema, fat malabsorption, niacin deficiency, parasitic infection and intestinal flora imbalance. A few other symptoms of liver cirrhosis are not obvious, but diarrhea is the main manifestation.

(3) Abdominal distension: it is common in clinic, and it is mostly caused by gastrointestinal peristalsis dysfunction, hypokalemia, flatulence, excessive ascites or hepatosplenomegaly during liver cirrhosis.

(4) Abdominal pain: The causes are perisplenitis, progressive necrosis of hepatocytes, perihepatitis, portal vein thrombosis and/or portal phlebitis. Peptic ulcer, biliary tract disease and intestinal infection can also cause abdominal pain.

What are the causes of anemia caused by liver cirrhosis?

Liver cirrhosis often has different degrees of anemia, 2/3 of which are mild to moderate, mainly normal cell anemia or small red cell anemia, and occasionally giant cell anemia. Causes of anemia:

(1) Hemolysis: A large number of red blood cells stay in the splenic sinus for a long time, leading to hemolysis.

(2) Hypersplenism: the destruction of red blood cells increases, causing anemia.

(3) Due to the disorder of fat metabolism, some abnormal lipids in plasma can cause hemolysis.

(4) Insufficient intake, poor absorption and utilization of nutrients such as vitamin B 12 and folic acid.

(5) In nonalcoholic cirrhosis, blood loss and iron deficiency may be the important causes of anemia.

(6) Erythropoiesis inhibition and iron utilization disorder are common in advanced cases.

What skin changes do patients with liver cirrhosis have?

The skin changes of patients with liver cirrhosis are characterized by gloomy or dull complexion, often pigmentation, which is often formed after a long course of disease, and is generally called "liver disease face". The reason for this is the following：

(1) Due to decompensated liver cirrhosis, liver function decreases, liver inactivation of estrogen in vivo decreases, and estrogen increases, which leads to the weakening of the inhibitory effect of thioamino on tyrosinase in vivo and the increase of the amount of tyrosine converted into melanin.

(2) Patients with liver cirrhosis have secondary hypoadrenocortical function, and the liver cannot metabolize melanocyte-stimulating hormone secreted by the anterior pituitary gland, which promotes the increase of melanin secretion.

In addition, patients with cholestatic cirrhosis show dark yellow and dull skin, and can also form chloasma and xanthoma, which is caused by the increase of lipid-like concentration in blood and deposition on the skin.

Why do patients with liver cirrhosis have bleeding tendency?

Patients with liver cirrhosis are prone to gum bleeding, nosebleed, petechiae, ecchymosis and hematoma. In skin friction, women often have excessive menstruation or prolonged menstruation, or bleeding after trauma is not easy to stop. The reason is:

(1) Coagulation factors synthesized by the liver, such as Ⅱ, ⅶ, ⅸ, ⅹ, etc., due to the decline of liver function. , decreased, leading to decreased coagulation function, and found that prothrombin time was prolonged and activity decreased.

(2) Patients with liver cirrhosis have more splenomegaly, hypersplenism, decreased platelet count and decreased platelet function, which weakens the hemostatic effect.

(3) In patients with liver cirrhosis, capillary fragility is increased, vitamin C is deficient, vitamin K utilization is blocked, and anticoagulants in blood are increased.

Generally speaking, with the progress of the disease, the degree of liver disease is aggravated and the bleeding tendency is more obvious.

What are the endocrine disorders in patients with liver cirrhosis?

In liver cirrhosis, due to the decline of liver function, the inactivation of estrogen decreases and the secretion of estrogen increases, which leads to the increase of estrogen in the blood and inhibits the production of androgen. Some patients have decreased secretion of adrenocortical hormone and gonadotropin, resulting in the following endocrine disorders:

(1) Male patients have enlarged breasts and less pubic hair;

(2) Female patients with scanty menstruation, amenorrhea and infertility;

(3) The skin capillaries dilate and hyperemia to form spider nevus and liver palm;

(4) Sexual desire and reproductive function decline; It can happen to men and women. Male testicular atrophy, sperm quantity and quality decreased; The incidence of anovulation cycle or infertility in women is increasing.

(5) Pigmentation can appear on the face, especially around the eyes, and there are also pigmentation on the palm texture and skin wrinkles.

How about pleural effusion in patients with liver cirrhosis?

It is not uncommon for patients with ascites due to liver cirrhosis to have pleural effusion, of which the right side is the most common, followed by the bilateral side, and only the left chest is the least. It is rare to have pleural effusion without ascites. Hepatic hydrothorax has no obvious symptoms, and severe restrictive dyspnea may occur when there is a large amount of hydrothorax, which may lead to pneumonia, atelectasis and pleural adhesion. The occurrence of pleural effusion is related to the following factors:

(1) hypoalbuminemia, low colloid permeability, leading to tissue fluid leakage.

(2) Due to portal hypertension, the pressure of azygos vein and semi-azygos vein system increases.

(3) The increase of hepatic lymphatic flow leads to the expansion, deposition and destruction of pleural lymphatic vessels, and lymph overflows to form pleural effusion.

(4) With the increase of abdominal pressure, the diaphragmatic tendon becomes thinner, forming diaphragmatic foramen, and ascites can leak into the chest cavity. Clinically, after diaphragm repair and pleurodesis, pleural effusion can disappear.

Why do patients with liver cirrhosis have jaundice?

Any obstacle of bilirubin uptake, transformation, movement in hepatocytes and excretion from the liver can cause hepatocellular jaundice. Some patients with liver cirrhosis will have jaundice for the following reasons:

(1) Hepatocyte damage: Fibroblasts proliferate and the structure of hepatic lobule is destroyed, which leads to the rupture of capillary bile duct, accompanied by inflammation, which increases the permeability of bile duct wall and decreases the excretion function. A large amount of bilirubin (conjugated bilirubin) cannot be discharged through intrahepatic bile duct, and then flows back to blood and lymph, and the concentration of bilirubin (mainly conjugated bilirubin) in blood increases.

(2) Inflammation and swelling of liver cells during liver cirrhosis: The ability of the liver to absorb, combine and excrete bilirubin decreases, resulting in part of bilirubin (unbound bilirubin) not being converted in the liver and staying in the blood, leading to an increase in unbound bilirubin.

The above factors increase the total bilirubin in patients' blood, and the increase of conjugated bilirubin and unconjugated bilirubin is the characteristic of hepatocellular jaundice. The possibility of obstructive jaundice complicated with biliary tract diseases must be ruled out clinically. Liver cirrhosis and jaundice suggest that liver cells are obviously damaged, which is of certain significance to judge the prognosis of the disease.