肝性脑病英文课件.pptVIP

Introduction and Conception Etiology Hepatic insufficiency Hepatic failure Hepatic encephalopathy (focal point) Hepatorenal syndrome PART I Introduction and Conception PART II Etiology PART III Hepatic insufficiency PART IV Hepatic encephalopathy Hepatic encephalopathy (HE) is a primary clinical manifestation of hepatic failure. Endogenous HE Have no apparent precipitating factors Often caused by extensive liver cell destruction Exogenous HE Precipitated by some known agents or abnormalities such as: gastrointestinal bleeding ingestion many proteins Often caused by portal-systemic shunts PART IV hepatorenal syndrome 3. Pathogenesis ◎ Ammonia Intoxication ◎ False Neurotransmitters ◎ Amino Acid imbalance ◎ The Gamma-Aminobutyric Acid hypothesis Several hypotheses ◎ Ammonia Intoxication Basis 1.Healthy dog Creating a portal-systemic shunting Fed by meat comatose 2. 80% patients with HE Blood ammonia levels 3. Cirrhosis patients ingestion of a large amounts of protein Hepatic coma 4. HE patients with cirrhosis Therapies to reduce ammonia absorption Ameliorations of HE Cause for elevated ammonia In normal conditions Urea Ammonia Kidney Ammonia Proteins, amines Urea, purines Ammonia is mainly produced in gastrointestinal tract Ammonia is detoxified in liver by conversion to urea through Krebs-Henseleit urea cycle. In Hepatic failure Krebs-Henseleit urea cycle function is impaired Blood ammonia level increased (endogenous) Ornithine Citrulline arginine arginase NH3 NH3 Urea In hepatic failure： substrates? enzyme? ATP? Portal-systemic shunting also reduces the urea production (exogenous) Ammonia production increased Blood ammonia level increased 1) Production of ammonia in intestine lumen increased 2) Production of ammonia in kidney increased Protein, urea, purine degraded Enzyme of bacteria ammonia glutamine glutaminase ammonia 3) Production of ammonia in skeletal muscle increased En