Increased coechobiligen excretion in the feces

Introduction The increase in fecal gallbladder excreted in the feces is one of the characteristics of jaundice. Astragalus refers to the yellow stain caused by bilirubin deposition in the skin, sclera and diuretic membrane. The normal serum total bilirubin concentration is 1.7~1.71. When the minute bilirubin (both direct bilirubin) is lower than 3.4 umol/L, when the total bilirubin concentration is 34umol/L, the yellow value appears in the clinic. When the concentration of bilirubin in the serum exceeds the normal range and the jaundice is not visible to the naked eye, it is called recessive jaundice. Observation of jaundice should be carried out under natural light, and it must be distinguished from the yellowing of skin caused by taking a large amount of arsenic, carotene, etc., and it must be distinguished from the accumulation of fat under the bulbar conjunctiva.

Cause

May have unstable angina. Physical examination to prevent unstable angina: Physical examination is usually not helpful in affirming or excluding angina. Abnormal pulsation in the anterior region and short-term diastolic tone often suggest left ventricular dysfunction. During or after ischemia, there may also be manifestations of acute papillary muscle dysfunction, such as transient apical systolic murmurs, clicks, and so on.

an examination

Related inspection

Fecal bile

1. Rheumatoid factor (RF): The rheumatoid factor is an autoantibody against human denatured immunoglobulin present in the serum of patients with rheumatoid arthritis and other diseases.

2. Total protein (TP): Serum protein is the most abundant substance in serum solids.

3, albumin (A, Alb): synthesized by the liver, is the main protein component of normal human serum total protein. Albumin maintains blood colloid osmotic pressure and transports metabolites in the body.

4, protein electrophoresis: serum protein is a colloidal substance, under certain conditions with a charge and swimming in the electric field.

5. Blood ammonia: The ammonia in the human body is produced by the amino acid deamination in the process of protein metabolism, the decomposition of glutamine by the kidney and the action of bacteria in the intestine. Most of the ammonia synthesizes urea in the liver through the ornithine cycle. A part is used for the amination of keto acid, which synthesizes glutamine, and forms an ammonium salt in the kidney to be discharged from the urine. Blood ammonia plays an important role in the diagnosis and treatment of hepatic coma and hepatic encephalopathy. Urine ammonia determination is one of the indicators for assessing the imbalance of acid-base balance in the body. The methods for determination of blood ammonia include ion exchange resin method, direct method, electrode method and enzyme. The method, in which the enzymatic method is widely used, is widely used.

6. Total bilirubin (TBIL, STB): Total bilirubin includes direct bilirubin and indirect bilirubin.

7, combined with bilirubin (SDB, DBIL): unbound bilirubin in hepatocytes, combined with glucuronic acid to form a binding bilirubin, also known as direct bilirubin.

8. Unconjugated bilirubin (SIB, IBIL): Total bilirubin is composed of unconjugated bilirubin and bound bilirubin, and unconjugated bilirubin is bilirubin that does not bind to glucuronic acid.

9. Alanine aminotransferase (ALT): formerly known as alanine aminotransferase (GPT). ALT is contained in tissues and organs such as liver, kidney, heart and muscle.

10. Alkaline phosphatase (ALP, AKP): Alkaline phosphatase is a phosphomonoesterase widely distributed in human tissues and body fluids, in bone, liver, breast, intestinal mucosa, kidney, and placenta.

11, serous effusion glucose: serous effusion glucose quantitative refers to the detection of glucose content in the effusion to distinguish between leakage and exudate.

12, serous effusion: in the case of disease, the accumulation of excess fluid in the thoracic cavity, abdominal cavity or pericardial cavity (collectively referred to as the serosal cavity) is called serosal effusion.

Differential diagnosis

First, hemolytic jaundice

The skin of hemolytic jaundice and the yellow color of porcine membrane are often lightly pale lemon yellow, and often accompanied by anemia accompanied by pale skin. The causes of hemolytic jaundice are:

1 red blood cells themselves inherent defects;

2 red blood cells are damaged by external factors. Damaged red blood cells can be destroyed prematurely in the reticuloendothelial system or destroyed directly in the blood vessels.

The diagnosis of hemolytic jaundice mainly depends on the following laboratory tests:

1 The content of jejunal and urobilinogen increased;

2 serum bilirubin increased, Vanden's test showed an indirect reaction;

3 increased reticulocytes in the blood;

4 serum iron content increased;

5 bone marrow red system hyperplasia. See the hemolytic anemia section for details.

Second, hepatic jaundice

The diagnosis and identification of hepatic jaundice, in addition to medical history and clinical examination, often rely on experimental examination. Liver biopsy has important help in the differential diagnosis of some difficult cases, but it should be strictly controlled and carefully implemented.

(1) Huang Zeng type viral hepatitis

Since the turn of the century, viral hepatitis has been considered to be only type A and type B. Since the nature of hepatitis B virus was clarified after 1965, non-A, non-B hepatitis was also proposed in 1974 after transfusion and intestinal transmission. In 1977, hepatitis D virus (factor) was discovered in 1979 for hepatitis A virus. In vitro culture was successful. At the international conference held in Tokyo in 1989, according to current research findings, the pathogen of non-A, non-B hepatitis after transfusion was named hepatitis C virus, and the pathogen of non-A, non-B hepatitis transmitted in the intestine was named . Hepatitis virus. At present, viral hepatitis should include at least A, B, C, D, E type A, B, C, D, E)

1. Acute yellow viral hepatitis

Its jaundice is from a few days to a week. The most prominent symptoms are fatigue and loss of appetite. Nausea, liver pain or discomfort, with or without fever. Some cases are mainly misdiagnosed as gastrointestinal dyspepsia due to dyspepsia and diarrhea; some mainly show upper respiratory symptoms, often misdiagnosed as acute upper respiratory tract infection; a few cases can be misdiagnosed as fever and multiple joint pain Rheumatic fever. The clinical diagnosis of jaundice in the early stage is difficult, but at this time, the serum aminotransferase activity is often significantly increased. The positive rate of 100% is the most early diagnostic value. After the appearance of jaundice, the symptoms are relieved. At this time, the main signs are jaundice, hepatomegaly or hepatosplenomegaly, and the quality of the spleen is painful. The liver area often has sputum pain, and there is no obvious hepatomegaly. Liver function test brain blisters, turbidity, zinc turbidity are mostly positive, urinary urinary biliary discharge increased with bilirubin positive, helpful for diagnosis. Astragalus is usually 2-4 weeks, sometimes longer.

2, severe viral hepatitis

(1) Acute severe hepatitis (burst hepatitis) This type is rare. In the course of acute hepatitis, jaundice is rapidly progressive, or (and) the body temperature continues to rise, the disease should be considered first. Other signs of aura are persistent vomiting, psychotic symptoms, and liver odor. Psychiatric symptoms mainly manifest as irritability or ambiguity or personality change, pterygium during dynamism, catching clothes, lethargy, or lethargy. In some cases, diagnosis may occur, and deep coma (hepatic faint EEG often) Displaying abnormal waveforms is helpful for early diagnosis. Physical examination often finds deep yellow staining, liver turbidity and shrinkage, skin and membrane bleeding. Significantly reduced urine volume, proteinuria and casts. Liver function tests indicate severe liver Damage. If not treated early, the patient often dies within a short period of time. The pathological manifestation is acute hepatic necrosis.

(2) Subacute severe hepatitis (subacute hepatic necrosis is slower than fulminant hepatitis. Astragalus is progressively deepened, serum bilirubin is often >17umol/L, prothrombin time is prolonged, cholinesterase activity is prolonged Significantly reduced. And lack of energy. Digestive disorders, nausea and vomiting, physical decline, fever, hepatomegaly (or shrinkage) and tenderness. Gradually refractory tympanic and ascites, severe liver and kidney syndrome, or even Some people are comatose. Some patients can recover after active treatment, or develop into cirrhosis. If the infection is complicated or the liver function is severe, the prognosis is more dangerous.

(3) Chronic severe hepatitis: This type is subacute hepatic necrosis of chronic hepatitis. The clinical manifestations are as subacute severe hepatitis, but there are abnormalities in history, signs and tests of chronic hepatitis or post-hepatitis cirrhosis.

3, chronic jaundice virus hepatitis chronic jaundice hepatitis mainly based on:

1 The course of disease lasts for more than half a year;

2 The main symptoms are fatigue, loss of appetite, postprandial fullness, greasy irritability, nausea and vomiting, jaundice may be optional, and often mild and fluctuating, persistent liver enlargement and increased hardness, accompanied by tenderness With sputum pain, the diagnosis of splenomegaly is of great significance. In patients with acute hepatitis, the splenomegaly does not retract during the recovery period, which means that the course of disease is prolonged, or to chronic development; 3 abnormal liver function test, the more sensitive test is the urine urinary bilirubin test. Determination of serum aminotransferase activity and serum floc and turbidity reaction. The increase in serum electrophoresis of gamma globulin is a sign of chronic hepatitis. Acute hepatitis A does not develop chronic, while acute hepatitis B and non-A, non-B hepatitis have a chronic tendency. If it develops into cirrhosis, the liver shrinks and the hardness increases, the spleen enlarges, the serum albumin continues to decrease, and the gamma globulin continues to increase.

(B) Huang Heng type infectious mononucleosis

The disease is associated with jaundice about 5%-7%. Astragalus is generally mild. l% bed showed fever, hepatosplenomegaly, and lack of appetite. Abnormal liver function tests, atypical lymphocytes in flesh and blood, quite similar to acute jaundice-type viral hepatitis. Infectious mononucleosis is often epidemic, pharyngitis is more obvious, often there are obvious lymph nodes (especially cervical lymph nodes, gastrointestinal symptoms are mild, and there are typical blood cell morphology changes and heterophilic agglutination effect The price increases. In acute viral hepatitis, the absolute value of blood-type heterotypic lymphocytes is generally less than 900 per cubic millimeter, which lasts for only a few days (slowly after the fever period L; in the case of infectious mononucleosis, atypical lymphocytes The absolute value is usually more than 1000 per cubic millimeter and often lasts for more than two weeks.

(C) systemic giant cell inclusion disease

The disease mainly affects infants and young children, and there are also adult cases reported in the domestic literature. The pathogen is Cytomegalov-irus, which can infect the fetus through the placenta through asymptomatic pregnant women with viral infection. The newborn is born with a lack of energy, pertussis-like cough, hepatosplenomegaly, digestive disorder, growth within one month of birth. Stagnant, jaundice can also occur. Infants and young children mostly exhibit interstitial pneumonia or giant cell hepatitis. Brain damage can also occur. Adults can exhibit symptoms similar to infectious mononucleosis and blood, but negative heterophilic agglutination. Liver function test serum aminotransferase activity increased, some cases of turbidity reaction abnormal. Often occurs after losing a lot of fresh blood. Diagnosis should be based on a special serum complement binding test, cytomegalovirus is isolated from urine (or saliva), which is particularly diagnostic.

(4) Leptospirosis

The diagnosis of this disease needs to be based on:

1 epidemiological history, the disease is mainly infected by contact with infected water, and is more common in the rice harvesting season in rural areas;

2 acute fever, bulbar conjunctival hyperemia, intestinal muscle pain, bleeding tendency, jaundice, lymphadenopathy and liver and kidney dysfunction and other clinical manifestations;

3 Positive results can be obtained by early culture and animal vaccination. The serum agglutination lysis test and the complement fixation test can be positive for 1 week after onset. The onset of severe hepatitis is not as fast as leptospirosis, often with symptoms such as toxic jejunum and ascites, and no ball conjunctival hyperemia and intestinal irritations, no abnormal X-ray signs in the lungs, and early renal damage is not obvious. The differential diagnosis of special pathogens and serological tests is more significant.

(5) Yellow values caused by other acute systemic infections

Some acute systemic infections such as lobar pneumonia, return to heat. Malaria, typhus, typhoid fever, wavy fever, acute miliary tuberculosis, etc., can be complicated by jaundice. Astragalus is generally mild, due to liver parenchymal damage or hemolysis, or both. Acutely transmitted diseases complicated by jaundice, most of the lesions are located on the right side, especially in the lower right lobe.

(6) Primary acute pregnancy fatty liver

The disease is rare in clinical practice. The cause is unknown. Whether it is secondary to endocrine or nutritional disorders remains undetermined. It is a serious complication of obstetrics and is often misdiagnosed as fulminant hepatitis. Clinically, the following characteristics are distinguished from fulminant hepatitis:

1 more common first trimester within the 36th to 40th week;

2 have varying degrees of pregnancy edema, proteinuria or high blood pressure;

3 nausea, vomiting without incentives, followed by severe bleeding tendency, such as gums, skin, vaginal bleeding, morphine-like vomit or vomiting blood;

4 serum direct bilirubin quantification 171 umol / L%), while urinary bilirubin negative;

5 serum brain flocculent reaction is negative;

3 coma, jaundice depth, liver progressive reduction is generally less severe than fulminant hepatitis, acute renal insufficiency is earlier than;

1 Ultrasound or CT examination revealed typical signs of fatty liver. It is not difficult to identify the two in histopathological examination. The literature reports that a large number of intravenous tetracyclines (about 1.5 g / d) in pregnant women can also have the performance of acute fatty liver similar to pregnancy. The two can be compared with the history of drug treatment and the above characteristics.

(7) Toxic liver damage

Some drugs or poisons have hepatotoxic effects, which can cause hepatic steatosis and central necrosis of hepatic lobules. The clinical manifestations are hepatomegaly, yellow colonization and liver damage.

1. The following drugs have been reported to cause similar viral hepatitis, such as Xin Kefen, isoniazid, and Fushun, PAS. Halothane. Methyldopa and bisphenol are called to protect the pine. Alkali amines, sulfonamides. The general therapeutic dose of chlortetracycline, novobiocin, phenobarbital, thioxime, etc. / but antibiotics has few side effects unless the patient has allergies.

2, cotton seeds, Xanthium, some virulence rate contain cell virgin toxic, after taking it can cause severe liver damage and jaundice, and even hepatic coma.

3. The main chemical substances that can cause chemically toxic hepatitis are as follows:

1 metals, metalloids and their compounds such as lead. Mercury, manganese, arsenic, yellow phosphorus, chromium, antimony, key, hesitation, etc.;

2 organic compounds: amino and nitro compounds of benzene, phenols, gasoline, carbon disulfide, methane, methyl chloride, formaldehyde, ethanol, tea, carbon tetrachloride. Tetrachloroethylene, etc.

3 pesticides: organic phosphorus, organic chlorine, organic mercury, etc.

Acute chemical toxicity hepatitis has the following clinical features.

1 The incubation period is short, the fastest is 2-3d, such as yellow phosphorus, the longer one is about 1 week, such as DDT, M carbon sulfide, p-chloronitroaniline poisoning;

2 often have jaundice and hepatomegaly, but often no obvious fever, spleen is not swollen;

3 serum aminotransferase and bilirubin increased;

4 There is a clear history of toxic exposure.

Drugs that cause obstructive jaundice in the liver are discussed below in this chapter.

(8) Acute alcoholic hepatitis

There are many reports on foreign literature in this disease. People who have been drinking hard alcohol for many years have recently had alcoholism, and this disease must be considered when the following conditions occur:

1 new appetite loss, weakness, weight loss, nausea and vomiting, jaundice and abdominal pain;

2 hepatomegaly and tenderness, sometimes splenomegaly, accompanied by unexplained fever;

3 serum bilirubin increased, serum albumin decreased and globulin increased, serum flocculosis reaction, serum aminotransferase increased, many cases have serum alkaline phosphatase and elevated blood glucose, anemia, leukocytosis and mononuclear Increased cells; 4 liver biopsy revealed special inflammatory lesions.

(9) Cardiogenic Huang Zeng

The causes of cardiogenic jaundice are complicated, and the most important one is caused by hepatic cell congestion and hepatocyte hypoxia, resulting in poor function of hepatocytes to treat bilirubin. Mild jaundice can be seen in right heart failure caused by various causes, especially when accompanied by relative or organic tricuspid regurgitation. In cases of recurrent right heart failure, the incidence of cardiogenic jaundice is increased, but serum total bilirubin usually does not exceed 51 umol / L (3mg / L), occasionally a deep yellow value can occur, at this time the patient It can present green jaundice similar to biliary obstruction. Urinary urinary bilirubin excretion often increases in patients, and occasionally mild bilirubinuria can occur. The retention of sodium sulfonate is often increased, and the serum flocculation and turbidity tests are mostly normal, with a few positive. There was no significant increase in serum transaminase activity in simple hepatic congestion.

(10) Cirrhosis of the liver

All types of cirrhosis can be complicated by jaundice.

(11) Hyperthyroidism

Hyperthyroidism can be complicated by fatty liver and hepatocyte necrosis, and jaundice, but this is rare and occurs in heavier cases. This type of jaundice is not easily distinguished from concurrent acute viral hepatitis. If the patient has no history of hepatitis exposure, no pre-yellowing symptoms, no obvious loss of appetite, nausea, bloating and other symptoms of digestive disorders. The jaundice is likely to originate from hyperthyroidism. If there is no high serum aminotransferase activity, it is more supportive for the diagnosis of this type of jaundice.

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