MindMap Gallery Cirrhosis
Cirrhosis is the hardening of the liver, which is mainly characterized by diffuse liver fibrosis, pseudolobule formation, and proliferation of extrahepatic and extrahepatic blood vessels. It is a chronic liver end state caused by different disease factors acting on the liver for a long time.
Edited at 2024-11-17 11:46:31Cirrhosis
diagnosis
Cirrhosis
Decreased liver function
Stem cell damage, bilirubin metabolism disorder, and reduced liver synthesis function
portal hypertension
Portal collateral circulation, splenomegaly, and peritoneal effusion
Liver biopsy shows the formation of pseudolobules to confirm the diagnosis
hepatic encephalopathy
Have severe liver disease and/or the basis for the formation of extensive portosystemic collateral circulation and the causes of hepatic encephalopathy
Clinical manifestations of hepatic encephalopathy
Obvious abnormalities in liver function biochemical indicators and/or increased blood ammonia
Head CT or MRI to rule out diseases such as cerebrovascular accidents and intracranial tumors
hepatorenal syndrome
Liver cirrhosis combined with peritoneal effusion
The rapidly progressive serum creatinine concentration rises to 2 times the baseline value within 2 weeks, or >226 μmol/L, and the slowly progressive serum creatinine concentration is >133 μmol/L.
After diuretics were stopped for >2 days and albumin volume expansion [1g/(kg·d), maximum amount (100g/d)] was performed, the serum creatinine value did not improve.
Rule out shock and renal parenchymal disease
No recent treatment with nephrotoxic drugs or vasodilator drugs
treat
Protect or improve liver function
Remove or reduce the cause of the disease
Anti-hepatitis virus treatment
Use drugs for liver damage with caution
Maintain enteral nutrition
protect liver cells
relieve cholestasis
Portal hypertension symptoms and treatment of complications
Ascites
Limit sodium and water intake
transjugular intrahepatic portacaval shunt
diuretic
Drain peritoneal fluid and add albumin
Antibiotic treatment of spontaneous bacterial peritonitis
EGVB
General first aid, active blood volume replenishment
Stop bleeding
Somatostatin, octreotide, pituitary vasopressin
Endoscopic ligation treatment
TIPS
Balloon compression to stop bleeding
hepatic encephalopathy
Remove triggers
Correct electrolyte and acid-base balance disorders
Prevention and control of infections
Reduce intestinal nitrogen source absorption
Use drugs for liver damage with caution
nutritional support
Promote ammonia metabolism in the body
Regulate neurotransmitters
block portosystemic shunt
Treatment of other complications
cholelithiasis
Conservative treatment
Anti-infection
portal vein thrombosis
anticoagulant therapy
hyponatremia
hepatorenal syndrome
TIPS
Hepatopulmonary syndrome
Oxygen, hyperbaric oxygen chamber
Hypersplenism
TIPS
Operation
TIPS
liver transplant
patient education
rest
Strictly prohibit alcohol
A low-protein, low-fat diet, mainly foods that are easy to digest and produce less gas
avoid infection
Take medication for the cause
Regular follow-up
complication
hepatic encephalopathy
liver cancer
hepatorenal syndrome
gastrointestinal bleeding
most common
cholelithiasis
Infect
Portal vein thrombosis or cavernous degeneration
Electrolyte and acid-base balance disorders
Hepatopulmonary syndrome
clinical manifestations
compensatory period
Symptoms are mild and may include abdominal discomfort, fatigue, loss of appetite, indigestion, and diarrhea.
Whether the liver is enlarged depends on the type of cirrhosis
The spleen is often mildly or moderately enlarged due to portal hypertension.
decompensation period
Decreased liver function
Malabsorption
Loss of appetite, nausea, anorexia, bloating, diarrhea
Malnutrition
Weight loss, fatigue, lack of energy
jaundice
Yellow staining of skin and sclera, dark urine
Bleeding and anemia
Nasal and gum bleeding, skin and mucous membrane petechiae, and ecchymosis
Endocrine disorders
Decreased androgens, increased estrogen
spider nevi, liver palms
Adrenocortical insufficiency, increased melanocyte-stimulating hormone
liver disease face
Increased antidiuretic hormone
Promote the formation of peritoneal effusion
thyroid hormone
Total T3 and free T3 decrease, and free T4 can increase or decrease.
Irregular low-grade fever
hypoalbuminemia
Lower limb edema and abdominal effusion
portal hypertension
Portal collateral circulation formation
Esophageal and gastric varices
High mortality rate due to rupture and bleeding
abdominal wall varicose veins
nevus varicose veins
Retroperitoneal anastomotic varicose veins
Splenorenal shunt
Hypersplenism and splenomegaly
Early signs of portal hypertension
Ascites
One of the most prominent manifestations of decompensated liver cirrhosis
pathology
Under the influence of various pathogenic factors, the liver experiences chronic inflammation, fatty degeneration, hepatocyte reduction, diffuse fibrosis, and intrahepatic and intrahepatic changes. The liver proliferates and gradually develops into cirrhosis.
Inflammation and other pathogenic factors activate hepatic stellate cells, causing them to proliferate and migrate. Collagen synthesis increases and degradation decreases. It is deposited in the Disse space and the space widens. The fiber bundles in the portal area and liver capsule extend toward the central vein of the hepatic lobule. These fiber intervals surround the regenerated nodules or resegment the residual liver lobules and transform them into pseudo lobules, forming the typical histopathological characteristics of liver cirrhosis.
Cause
circulatory disorder
Hepatic artery and/or inferior vena cava obstruction, chronic cardiac dysfunction, and constrictive pericarditis Can cause long-term liver congestion, hepatocyte degeneration and fibrosis, and eventually cirrhosis.
hepatitis virus
my country: Hepatitis B virus
European and American Countries: Hepatitis C Virus
parasitic infection
Schistosoma eggs are deposited near the hepatic portal vein, and fibrosis often causes portal vein perfusion impairment.
Clonorchis sinensis parasitizes in human extrahepatic bile ducts and causes biliary obstruction and inflammation
Inherited metabolic diseases
Copper metabolism disorder (hepatolenticular degeneration)
Hemochromatosis: Genetic abnormality on the sixth pair of chromosomes
alpha-antitrypsin deficiency
Unknown reason
cryptogenic cirrhosis
definition
Progression of chronic liver disease
Pathological features: chronic inflammation of the liver, diffuse fibrosis, pseudolobules, regenerative nodules, and intrahepatic and extrahepatic vascular proliferation
Clinical features: no obvious symptoms in the compensation phase, portal hypertension and decreased hepatic energy in the decompensation phase.
Patients often die due to chronic multi-organ failure such as esophageal and gastric variceal bleeding, hepatic encephalopathy, infection, hepatorenal syndrome, portal vein thrombosis, etc.