严重肝病引起的以代谢紊乱为基础的神经ppt课件.pptVIP

Hepatic Encephalopathy福州白湖亭医院肝病科;Definition (1);Definition (2);Incidence/prevalence;Etiology ;Common precipitating factor;;Pathogenesis (1);Pathogenesis (2);Ammonia neurotoxicity;Ammonia neurotoxicity;Synergistic neurotoxins;Excitatory inhibitory neurotransmitter plasma amino acids imbalance ; Increased aromatic amino acids (AAAs) Tyrosine（酪氨酸）Phenylalanine（苯丙氨酸） Tryptophan（色氨酸〕 Due to the failure of hepatic deamination Decreased branched-chain amino acids (BCAAs) Valine（缬氨酸） Leucine（亮氨酸） Isoleucine（异亮氨酸） Due to increased metabolism by skeletal muscle and kidneys or increased insulin;Imbalance of plasma amino acid: More AAAs enter into blood-brain barrier and CNS Decreased synthesis of normal neurotransmitters Enhanced synthesis of false neurotransmitters Octopamine(苯乙醇胺) Tryptophan (?-羟酪胺) ;γ- Aminobutyric acid hypothesis;;Pathohistology;;Clinical manifestation;Clinical manifestation;;Clinical Grading of HE;Clinical Grading of HE;Laboratory and other tests; Reitan trail-making test;Writing chart;Diagnosis and differential diagnosis;Diagnosis;Diagnosis;Differential diagnosis;Treatment;The goals of therapy ;一、Identification and treatment of precipitating factors;二、Decreasing nitrogen load and ammonia productions and absorption of enteric toxins;Dietary protein restriction;Bowel cleaning;Nonabsorbable disaccharides;Antibiotics;Increasing ammonia metabolisms;三、Drugs that affect neurotransmission ;四、GABA/BZ receptor antagonists;Liver transplantation;Summary  Key issues of the HE topic