A and E are acute and difficult to turn into cirrhosis.

Highest and most prominent

hepatolenticular degeneration

Hemochromatosis

alpha antitrypsin deficiency

pseudolobule formation

abdominal discomfort

gastrointestinal symptoms

Weakness

Mild hepatosplenomegaly

Decreased liver function

Portal hypertension (three edema)

rest

high protein high calories

Stifuvir

Lamivudine

Not too many <2 types

Nucleotide drugs (Treatment of hepatitis)

Reduced glutathione

polyene phosphatidylcholine

Limit water and sodium intake

diuretics

Increase plasma osmotic pressure

refractory ascites

bleeding period

Stop bleeding

prevention

Quinolones＞2W

early heparin

TIPS when necessary

The only way patients can survive long-term

Hypersplenism reduces the three lines

Jaundice→bilirubinurobilinogen↑

ALT,AST↑

Serum albumin↑globulin↓ A/G inversion

PT extension

Fibrosis index↑

Total bilirubin↑

Main trunk inner diameter＞13mm

The inner diameter of the splenic vein is greater than 8mm

Ascites serum protein gradient >11g

gold label Look for pseudolobule formation Diagnosis can be made if symptoms are not obvious during the compensatory period

Visible esophageal worm-like filling defect 👇 collateral circulation formation

Esophageal and gastric variceal bleeding

peptic ulcer

portal hypertensive gastroenteropathy

The most serious and common cause of death

Escherichia coli first, then Staphylococcus aureus as the resistance decreases

respiratory tract

Intestine

bile duct gallbladder

urinary tract

Spontaneous peritonitis (SBP)

Performance

diagnosis

severe liver disease

pulmonary vasodilation

arterial oxygenation disorder

Liver quickly↑ in short term

Persistent liver pain

Ascites is bloody

low sodium

Low chlorine

low potassium alkali

Sudden abdominal pain

Splenomegaly

bloody ascites within a short period of time

gastrointestinal bleeding