MindMap Gallery fatty liver disease cirrhosis
This is a mind map about fatty liver disease and cirrhosis, including causes, pathology, clinical manifestations, complications, auxiliary inspection, treat, prognostic indicators, etc.
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The ice hockey schedule for the Milano Cortina 2026 Winter Olympics, featuring preliminary rounds, quarterfinals, and medal matches for both men's and women's tournaments from February 5–22. All game times are listed in Eastern Standard Time (EST).
fatty liver disease cirrhosis
Cirrhosis (pseudolobules are a sign of formation)
Cause
Hepatitis B mainly HBV (viral hepatitis) → the main cause in my country
Most likely to cause hepatic encephalopathy
cholestasis
Parasitic infection (leading to significant portal hypertension)
Can easily lead to significant portal hypertension
★Fishermen are susceptible to parasites
circulatory disorder
genetic and metabolic diseases
pathology
portal cirrhosis
Pseudolobule formation (typical pathological manifestation of liver cirrhosis)
Congestive cirrhosis
Steatosis/betel nut liver
schistosomiasis cirrhosis
linear fibrosis
viral hepatitis
ballooning degeneration
clinical manifestations
Compensatory phase (the liver may become slightly enlarged during this phase)
Liver is slightly enlarged
Liver texture is hard
Mild abnormalities in liver function
★The spleen can also be slightly enlarged
Decompensation (shrinking of the liver)
Decreased liver function/insufficiency
Malabsorption
Malnutrition
Jaundice (hepatocellular jaundice)
Hemorrhagic anemia (reduced coagulation factors synthesized by the liver and related to hypersplenism)
Endocrine disorders
Sex hormone metabolism (increased estrogen/decreased androgen)
spider nevus liver palm
Gynecomastia
Portal hypertension (★splenomegaly but not hepatomegaly)
Portal collateral circulation formation
Esophageal and gastric varices
abdominal wall varicose veins
Retroperitoneal anastomotic varicose veins
Splenorenal shunt
hemorrhoids varicose veins
Hypersplenism and splenomegaly (earliest manifestation)
Peripheral blood shows varying degrees of platelet and leukopenia (pancytopenia)
Cause: Portal hypertension → Obstruction of splenic venous return → Passive congestion and enlargement of the spleen
Abdominal effusion/ascites (the most obvious manifestation) (one of the indicators to evaluate the severity of the condition)
Leakage is mainly caused by pressure (caused by pressure)
possible causes
Portal hypertension
hypoalbuminemia
★★Secondary aldosteronism (not primary aldosterone increase)
liver damage
★Biochemical tests increased by four and decreased by three
Estrogen ↑ Melanin ↑ Antidiuretic hormone ↑ (urine volume ↓) Aldosterone ↑ (protect Na and eliminate K)
Androgens↓ Glucocorticoids↓ Thyroid hormones↓
complication
gastrointestinal bleeding
Esophageal and gastric variceal bleeding (portal hypertension is the main cause)
sudden massive vomiting of blood
Tarry stool
Can induce hepatic encephalopathy (heavy gastrointestinal bleeding → decomposition of protein in blood → blood ammonia)
cholelithiasis
Infect
Spontaneous bacterial peritonitis (pantal abdominal pain/tenderness/rebound tenderness)
Hepatic encephalopathy (preferred test → blood ammonia) (asterixis is the characteristic manifestation)
Clinical stage
The first phase of personality change (prodromal phase)
Abnormal behavior in the second stage (early stage)
Stage three drowsiness (drowsiness) (drowsiness stage)
Stage 4 coma (coma stage)
Ammonia poisoning
The brain's sensitivity to ammonia becomes higher → Neurotoxic substances increase in the body of patients with liver disease → Under its influence → The brain becomes more sensitive to ammonia↑
The main place where the body produces ammonia gas
Digestive tract (neat acid rather than alkali)
ph>6→alkaline (ammonia easily diffuses into the blood)
ph<6→Acidic (ammonia is easily excreted with feces)
deal with
Enema with weak acid solution → makes the body more acidic
NH3 is the main source of poisoning and can pass through the blood-brain barrier/NH4 cannot pass through the blood-brain barrier
Cause
high protein diet
constipate
upper gastrointestinal bleeding
Diuretic/sedative use
A large amount of ascites
Electrolyte imbalance (alkalosis)
Hyposodium, hypokalemia, hypochloremic alkalosis
metabolic alkalosis
Liver cirrhosis → secondary elevation of aldosterone → water and sodium retention and K excretion → hypokalemia → alkalosis
mechanism
Ammonia poisoning, amino acid metabolism imbalance, false neurotransmitters
The energy metabolism of the brain is disturbed→Insufficient energy supply to cells
★Earliest symptoms
personality change
portal vein thrombosis
When hepatic blood flow is blocked
Moderate to severe abdominal pain
Ascites, intestinal necrosis → bloody ascites
No fever
Cirrhosis Abdominal Varicose Veins
Above the navel up/Down below the navel
Inferior vena cava obstruction → both upward
Superior vena cava obstruction → both downward
Hepatorenal syndrome
Mechanism performance
The patient’s kidneys have no substantial lesions
Because of portal hypertension→reduced systemic blood flow→insufficient renal cortical blood perfusion→renal failure
Oligo/anuria/azotemia
Kidney Failure Supplements
prerenal renal failure
Insufficient renal blood perfusion causes
postrenal renal failure
Caused by urinary tract obstruction
renal renal failure
ischemia and nephrotoxic substances
Auxiliary inspection
Liver function assessment
liver synthesis function
serum albumin
plasma coagulation factors
cholesterol
hepatic encephalopathy
electroencephalogram
blood ammonia
Asterixis
diagnosis
Liver biopsy → Pseudolobules are found (can confirm the diagnosis)
treat
Protect and improve liver function
Treatment of symptoms of portal hypertension
Ascites
Esophageal and gastric venous bleeding
Balloon compression and hemostasis (three-lumen two-bag tube)
medical treatement
Drugs that constrict visceral blood vessels
somatostatin
Hepatic encephalopathy treatment
dietary protein prohibition
Oral lactulose → acidifies the intestines and reduces ammonia absorption
prognostic indicator
hepatic encephalopathy
Bilirubin
albumin
ascites
thrombin
Replenish
Portal hypertension
Performance with the most characteristic diagnostic value
collateral circulation formation
Lower esophageal gastric varices
earliest
Splenomegaly
most dangerous
Esophageal varices
most outstanding performance
ascites
Cirrhosis
Most common complications
upper gastrointestinal bleeding
The most serious
hepatic encephalopathy
earliest
Splenomegaly
Splenomegaly
Cirrhosis can occur early
The reason is because of portal hypertension
Congestive swelling ≠ infiltrative swelling