Any disease that can cause hemolysis can cause hemolytic jaundice

Congenital hemolytic anemia

Acquired hemolytic anemia

On the one hand, due to the destruction of a large number of red blood cells, a large amount of unconjugated bilirubin is formed, which exceeds the uptake, conjugation and excretion functions of liver cells

On the other hand, anemia, hypoxia and the toxic effects of red blood cell destruction products caused by hemolysis weaken the metabolic function of bilirubin in liver cells, causing unconjugated bilirubin to remain in the blood, causing jaundice to exceed normal levels

Hemolytic jaundice generally causes the skin and mucous membranes to be light lemon in color, without skin itching

In acute hemolysis, there are also fever, chills, headache, vomiting, low back pain, varying degrees of anemia and hemoglobinuria, and the urine is soy sauce or tea-colored. Severe cases may have acute renal failure,

Chronic hemolysis is mostly congenital. In addition to anemia, there is also splenomegaly.

UCB mainly increases, CB is basically normal

As UCB in the blood increases, the formation of CB also increases compensatoryly, and the discharge from the biliary tract to the intestine also increases, leading to an increase in urobilinogen, a subsequent increase in fecal bilinogen, and a darker fecal color

Due to hypoxia and toxins, the ability of the liver to process increased urobilinogen is reduced, resulting in an increase in urobilinogen in the blood, which is excreted from the kidneys, so urobilinogen is increased in the urine, but there is no bilirubin

Due to various diseases that cause serious damage to liver cells, such as viral hepatitis, cirrhosis, toxic hepatitis, leptospirosis, sepsis, etc.

Due to severe damage to liver cells, the uptake and binding function of bilirubin by liver cells is reduced, so UCB in the blood increases.

Undamaged liver cells can still convert part of UCB into CB. Part of the CB is still excreted from the bile duct through the capillary bile ducts. The other part of CB is refluxed into the blood circulation due to the infiltration of swollen liver cells and inflammatory cells that compresses the capillary bile ducts and bile canaliculi or the obstruction of bile plugs, which blocks bile excretion. CB in the body increases and jaundice occurs

The skin and mucous membranes appear light to dark yellow, accompanied by mild skin itching, and other primary liver manifestations such as loss of appetite and abdominal effusion

Both CB and UCB in serum increase. In jaundice hepatitis, CB increases more than UCB, and the qualitative test of bilirubin in urine is positive

Intrahepatic cholestasis

Extrahepatic cholestasis

The skin and mucous membranes are dark yellow, and those with complete bile duct obstruction are dark yellow or even yellow-green, accompanied by skin itching and bradycardia, and the color of the feces becomes lighter and white clay.

Serum CB is mainly increased, and urine bilirubin test is positive. Because the enterohepatic circulation pathway is blocked, urobilinogen and fecal bibilogen are reduced or absent

Jaundice is caused by defects in the uptake, binding and excretion of bilirubin by liver cells

Gilbert syndrome

DJ syndrome

CN syndrome

Rotor syndrome