Jaundice caused by the accumulation of bilirubin in the blood due to the impairment of liver cells and the obstruction of the uptake, binding and excretion of bilirubin
Hepatocellular jaundice refers to the damage to hepatocytesbilirubinJaundice caused by the accumulation of bilirubin in the blood.The pathogenesis of hepatocyte jaundice may have bothConjugated bilirubinRetention and bilirubin bindingReflow。
stayViral hepatitis、Leptospirosis、septicemia、Liver abscessOr phosphorus poisoning and other cases, the occurrence of jaundice are hepatocyte jaundice.Undamaged or slightly damaged hepatocytes can still formConjugated bilirubinHowever, some of the formed conjugated bilirubin can flow back into the blood, so there is also conjugated bilirubin in the blood.In addition, hepatocyte swelling, inflammatory exudates in the portal vein area, and the presence of bile emboli in the small bile ducts can all hinderbileExpel, and promote the combined bilirubin to flow back into the blood.Because there is both unconjugated bilirubin and conjugated bilirubin in the bloodQualitative determination of bilirubinDuring the testBiphaseReaction.The conjugated bilirubin can be discharged through the kidney, so bilirubin appears in urine.As the amount of conjugated bilirubin formed in the liver decreases, and some of the formed conjugated bilirubin flows back into the blood, the amount of bilirubin entering the intestine decreases.Absorbed from the intestinal tract into the bloodUrobilinogenAlthough not more than usual, due to poor liver function, the ability to ingest urobilinogen from blood is reduced, and the function to discharge it into the biliary tract is also reduced, so the amount of urobilinogen in blood is increased, and the amount of urobilinogen in urine is also increased.
2、 Pathogenesis
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Jaundice caused by damaged hepatocytes.When hepatocytes are damaged and the ability to deal with bilirubin is reduced, the normal metabolism ofIndirect bilirubinAll converted toDirect bilirubin, causing the increase of serum indirect bilirubin, and the uninjured hepatocytes can still convert indirect bilirubin into direct bilirubin input capillarybile duct。But becauseBile excretionWhen the pathway is blocked or flows through necrotic liver cells, it flows back into the blood, making the serum directlyIncreased bilirubinInfiltrate into tissues to form jaundice.
3、 Differential diagnosis
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The differential diagnosis of hepatocellular jaundice should pay attention to the clinical symptoms and signs, and ask whether there are accompanying symptoms, such asfever、rash、skin Itch, fatigue, abnormal appetite and urine and fecesBleeding tendencyAnd corresponding symptoms of various organ systems.The physical examination should be comprehensive and meticulous, without omission.Particular attentionSkin mucosaYellow dyeColor of(Hemolytic jaundiceOften presentLemonHepatocellular xanthosis is mostly golden or light yellow,Obstructive jaundiceMostly dark yellow or yellow green)lymph glandWhether the liver, gallbladder and spleen are swollen.The physical signs of different primary diseases are different,HepatomegalyMost patients with portal hypertensioncirrhosisIndemnity,liver cancerThe physical examination of patients with jaundice can detect hepatomegaly with nodular sensation,Spider nevusIs found inchronic hepatitisAnd cirrhosis.The course of hepatocellular jaundice can also be used as a reference for diagnosis, such as type AViral hepatitis EThe jaundice of type B, C and D chronic hepatitis can last for several months or become chronicIntrahepatic cholestasis。otherAcute jaundiceAfter the cause of disease is relieved or the disease is alleviated, it can subside in a short period of time, while jaundice caused by cancer is more progressive.
4、 Check
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1. The skin and mucosa are golden yellow, sometimesitch;
2. Both unconjugated and conjugated bilirubin in blood increased, and bilirubin (i.e. conjugated bilirubin) accounted forbilirubinMore than 35% of the total;
3. Urine bilirubin is positive,UrobilinogenThe content ofCholestasisDepends on the degree of liver damageIntestinal cavityReabsorptionThe urobilinogen in urine is increased because it cannot be oxidized into bilirubin in liver cells. However, when cholestasis occurs in liver at the peak of disease, although liver cells are severely damaged, the urobilinogen can be reduced or even absent;
4. The content of urinary bilinogen in feces can be normal, reduced or absent, and it also changes depending on the degree of cholestasis in the liver;
5. SerumtransaminaseIt is significantly higher, and the flocculating test result is positive;
In the compensatory period of liver disease and in the case of inactivity, patients can exercise a little, butliver functionIn case of damage or decompensation of liver disease and complicated infection, the patient needs to stay in bed to rest to ensure the liverblood flowAdequate.The diet of patients with hepatocellular jaundice should be high in calorieshigh protein, high sugar, low fat, low cholesterol and rich vitamins, easy to digest food is appropriate, liver function significantly decreases orhepatic encephalopathyStrictRestriction proteinQualitative intake, withascitesandEdemaTwenty five percent of patients need to strictly limit their sodium intake, avoid eating coarse and hard food, and prohibit drinking alcohol and taking drugs that damage the liver.Patients with severe liver disease are at risk of concurrent infection, which can be used appropriatelyBroad-spectrum antibioticPrevent infection.
The treatment of primary liver disease is more important for relieving hepatocellular jaundice, which should be carried out on the basis of clarifying the primary causeSymptomatic treatment。Alcoholic liver diseaseThe most important treatment for patients with viral hepatitis, such asChronic hepatitis B, generally requirednucleosides AnalogueAntiviral therapy,Hepatitis CYou need to apply directAntiviral drugsAntiviral therapy, regulating immunity, and appropriate combination of liver protection drugs.Other non hepatotropic viruses (e.gCytomegalovirus、EB virusCaused byIcteric hepatitisWe should focus on the treatment of primary disease plus liver protection, enzyme reduction, and jaundice abatement.Liver cirrhosis should first be treated for its etiology, and then attention should be paid tocomplicationTreatment, such as ascitesUpper gastrointestinal bleeding, hepatic encephalopathy andHepatorenal syndromeProcessing of.Primary liver cancerJaundice can be either hepatocyte jaundice or obstructive jaundice, and the latter is more common. For such patients, we should actively treat the primary disease in the liver if conditions permittumourIn progressSurgerycombined treatmentThis is the fundamental measure to control and eliminate jaundice.Artificial liverHepatocyte transplantation, liver transplantation andgene therapyIn recent years, it has gradually attracted public attention.Artificial liver support systemIt has become an ideal auxiliary support treatment for patients with severe jaundice, which can compensate or partially compensate for the detoxification andbiosynthesisFunction, provide time and opportunity for the recovery of hepatocytes, and gain time for patients waiting for donor liver transplantation.Hepatocyte transplantation refers to the transplantation of isolated and cultured hepatocytes in vitro into patients to replace or partially replace patientsHepatic insufficiency, applicable to acute and chronic diseasesLiver failureandgeneticLiver disease.orthotopic liver transplantation It is the best treatment choice for patients with terminal liver disease.Gene therapy has made remarkable achievements in recent yearsGene vectorThe role ofanimal modelSome achievements have been made, but its safety still needs to be studied due to potential side effects.