肝性脑病b

Hepatic encephalopathy肝性脑病,Overview Etiology and PathogenesisPathology Clinical manifestationLaboratory examinationDiagnosis and Differential diagnosisManagement,Contents of these classes:,Overview（概述）,Definition,a series of reversible neurological and psychopathic syndrome caused by severe liver disease and Portosystemic shunt, and metabolic disorder is underlying change.,Disturbance of consciousness /Coma,Relative terms （相关概念）,Minimal hepatic encephalopathy（MHE,轻微肝性脑病）The patient in this stage lack symptoms, which can be diagnosed by subtle Psychometric test .,Portosystemic encephalopathy(门体分流性脑病),Etiology and Pathogenesis,Etiology and Pathogenesis,Various kinds of liver cirrhosis , portosystemic shunting(TIPS) are most common. Severe hepatitis, acute hepatic failure, primary liver cancer, gestation related fatty liver and severe biliary tract infection are also the etiological factors.,Inducement,Upper gastrointestinal hemorrhage (上消化道出血）Potent diuresis （强利尿剂） Ascites exclusion（排放腹水） Protein meal （高蛋白饮食）,Inducement,Taking sedative or similar drug（服用镇静药） Constipation （便秘） Uremia（尿毒症）Infection,Pathogenesis （发病机制）,Common pathophysiologic change,Neurotoxin hypothesis Ammonia intoxication Change of neurotransmitter -Amino-butyric acid hypothesis False neurotransmitter hypothesis Tryptophan,Pathogenesis （发病机制）,Intestine,kidney,Muscle,NH3,NH4+,Liver,urine,Brain,liver,kidney,Glutamin,Ornithine cycle,ATP,Kidney and lung,Muscle,production and clearance of Ammonia,Neurotoxin hypothesis -Ammonia 氨中毒学说,How does ammonia cause neurologic dysfunction? Interfere with tricarboxylic acid cycle Increase concentration of aromatic amino acid Increase concentration of glutamine (Hypertonic ),Energy metabolism,Ammonia intoxication Hypothesis 氨中毒学说,-Amino-butyric acid hypothesis GABA/BZ复合体学说（三）,GABA/BZ co-receptor can bind to barbiturate and benzodiazepine, so enhance the inhibitory effect of GABA.GABA-receptor,False neurotransmitter Hypothesis 假性神经递质,Excitatory neurotransmitter in brain：noradrenaline(去甲肾）/dopamine（多巴胺）,Aromatic amino acid Tyrosine/phenylalanine,Tyramine(酪胺） and Benzol-Ethylamine （苯乙胺） in intestine,Be cleared,hydroxytyramine（羟酪胺）Phenolethanolamine（苯乙醇胺） In brain,Neuronaldysfunction,Tryptophan(色氨酸）,5-HT and 5-HITT，these two substances can inhibited the brain function.,Pathology,Pathology,Acute :no obvious change，just edemaChronic: astrocyte hypertrophy，neur decreased cortical necrosis,Clinical manifestation临床表现,Clinical manifestation,The clinical manifestation is various because of the different liver disease, or different degree of hepatic failure, or different inducement,Symptoms（症状）,Acute severe hepatitis :present coma in a short time .The portosystemic encephalopathy generally manifested as recurrence and chronic disturbance of consciousness /Coma Some patients absent symptom, and can be identified by psychometric test, which was called MHE,Typical symptoms,Prodrome stage（前驱期）: Higher cortical dysfunction: decrease in attention span, change in personality and behavior，sleep pattern change (wakefulness at night and drowsiness during a day). Maybe present flapping tremor. Electroencephalogram(EEG) is normal.Coma prophase（昏迷前期）:confusion，drowsiness and the ability of orientation and comprehension are decreased, flapping tremor and Babinski sign are positive, EEG is abnormal.,Lethargy stage（昏睡期）: lethargy ,mental confusion and neural signs become more abnormal. EEG is abnormal significantly.Coma stage（昏迷期） :light or deep coma flapping tremor and reflex are lose. abnormal EEG is more significant.,Typical Symptoms,LFTBlood ammonia testing(血氨）EEG: slower rhythms and triphasic waves Psychometric test（心理智能测验）Imaging examinationEvoked potentials（诱发电位）,Laboratory examination,1,2,4,3,5,6,8,7,10,9,11,13,12,15,14,17,16,18,19,21,20,22,24,23,25,Number connection test,Diagnosis & Differential diagnosis,Diagnosis,History: Severe liver disease and Portosystemic shuntingTypical manifestation: mental confusion, lethargy or coma.Inducement of HE Laboratory examination Significant liver injury and Blood ammonia increase. Flapping tremor Typical change in EEGEEG,Differential diagnosis,Diabetes mellitus (糖尿病）Hypoglycemia （低血糖）Uremia （尿毒症）Cerebrovascular accident（脑血管意外）,Management 治 疗,Removing the inducement（消除诱因）,The principle of management of HE is identifying and removing the inducementWithdraw the sedativeMaintain acid-alkali balance :Correct hypoxia, hypoglycemia and hypokalemiaHealing gastrointestinal bleeding and infectionPrevent the infection,Drug therapy （药物治疗）,Decreased the production and absorption of toxin Dietary therapy, Antibiotic, Lactulose, ProbioticsPromote the clearance of ammonia Ornithine-aspartate(鸟氨酸-门冬氨酸） Ornithine-Ketoglutarate （鸟氨酸-酮戊二酸） Glutamic sdium （谷氨酸） Arginine（精氨酸）Mediation neurotransmitter Branched chain amino acidGABA/BZ co-receptor antagonist Flumazenil （氟马西尼）,Therapeutic principle,Improvement of liver function.Cure the encephaledema（改善脑水肿）Artificial liver（人工肝）liver transplantation（肝移植）,Question,How to identified the minimal hepatic encephalopathy ?Which are common causes of HE?And how to treat ？,Analysis of the case,Male,55 years old,suffered from Hepatitis B for about 5 years. recently the patient present abdominal distention gradually. In local hospital he was diagnosed as liver cirrhosis ,and was given diuresis to relieve symptom for half a month. three days ago, the patient present hematochezia，once per day，about 100ml. Yesterday he presented mind confusion .PE:BP100