Hepatic Insufficiency (Liver Dysfunction) Student Notes PDF

(gān)(gōng)(néng)(bù)( Hepatic Insufficiency instructing teachers ： hu yejia 胡业佳 1 3.1 Hepatic Insufficienc ▲ Hepatic Encephalopat 3.2 Encephalopa 13.3 Hepatorenal Syndrom (gān)(xìng)(nǎo)(bìng) 2 unction o...

(gān)(gōng)(néng)(bù)( Hepatic Insufficiency instructing teachers ： hu yejia 胡业佳 1 3.1 Hepatic Insufficienc ▲ Hepatic Encephalopat 3.2 Encephalopa 13.3 Hepatorenal Syndrom (gān)(xìng)(nǎo)(bìng) 2 unction of liver Digestion Metabolis edema m jaund Excretion ice bleedi ng Synthesis infec Immunizatition renal dysfunction on hepatic 3 encephalopathy.1 Hepatic Insufficienc Due to various pathogenic factors on liver cells, liver morphological structure is destroyed in different degrees and the function is abnormal, then jaundice, bleeding, (gān)(gōng)(néng)(shu āi)(jié) infection, renal 肝功能衰竭 dysfunction and hepatic encephalopathy, this clinical syndrome is 4 Hepatic Failure Hepatic coma hepatic insufficiency..3 Hepatorenal Syndrome HRS refers to development of a reversible, functional renal failure in patients with severe disease (acute or 5.2 Hepatic Encephalopat liver encephalopathy Hepatic encephalopathy is a complex, potentially reversible disturbance of the central nervous system that occurs as a hepatic coma consequence of severe 6 liver disease..2 Etiology and Classificat A Acute liver failure Infection, drug, poisoning from B carbonte trichloride al-systemic bypass and phosphorus trinsic hepatocellular dis rrhosis C rtal hypertension, 7 rtal-systemic shunts 13.2.3 Grades Stage 0 ： Stage 1 ： Stage 2 ： Stage 3 ： Stage 4 ： 8 3.2.4 Pathogenesis onia intoxication hypothesi e neurotransmitter hypothe rmal plasma amino acid hypo BA hypothesis, mma-aminobutyric acid 9 onia intoxication hypothesi 学说 59μmol/L Hyperammone mia >59μmol/ Hepatic L Hepatic insuffici encephalo ency pacy product product 10 ion  aa oxidase NH3 25%urea urease NH3 urea urea Protei aa ornithine NH4+ n oxidase cycle urea cycle NH3 +NH3 NH3 glut glutam + α-ketoglutaric amic ine 11 glutami Causes of hyperammonemia (1) Insufficient ammonia (2) Increased elimination ammonia production 12 (1) Insufficient ammonia elimination ornithine cycle 13  carbamoyl phosphate synthet ornithine transcarbamoylase NH3 + 2ATP urea ornithine CO2 鸟氨酸 H2O - 瓜氨酸 arginase 精氨酸酶 citrulline H2O + H2O 精氨酸 - NH3 arginine + ATP Fumaric 富马酸 acid NH3+CO2+3ATP+Asp+2H2O → urea+2ADP+4Pi+AMP+fumaric 14  (2) Increased ammonia production bacteria in intestines, 1. protein, Gut, portal hypertension, urea digestive and absorption dysfunction, protein stays, intestinal 2. bacteria Hepatorenal is active syndrome, urea cannot Kidneysbe discharged produces NH3Muscles, 3. vasculature endothelium, and intestinal, mucosa produce NH3 16 Cerebral ammonia intoxication (1) Impairment of energy metabolism (2) Neurotransm itter (3) Inhibiting NH3 alteration nerve cells membrane action 17  (1) Impairment of energy metabolism ATP ATP Less productio More n consumed hypoglyce mia 18 (2) Neurotransmitter alteration 19 (3) Inhibiting nerve cells membrane action K ＋ Na+-K ＋ -ATP pump 20  3.2.4 Pathogenesis onia intoxication hypothesi e neurotransmitter hypothe 经递质学说 rmal plasma amino acid hypo BA hypothesis, mma-aminobutyric acid 21 In hepatic failure or portal systemic shunt formation, the normal neurotransmitter in reticular neurons reduces and / or false neurotransmitter (phenylethanolamine and octopamine) accumulates at the synapses that lead to disorder of transmission 22 reticular system a, Maintain the excitability of the cerebral cortex, so that b, Maintain the body is awake. muscle tension and circulation, respiratory Normal function. neurotransmitt noradrenaline, ers ： 23 dopamine  phenylethanolamin octopamine RCH2NH2+02+ H20→RCHO+NH β-hydroxylase 3+H2 Protein O2 monoami phenylalanine ne oxidase tyrosine (MAO)High decarboxylase er henylethylamine level tyromine in bloo d 24  β-hydroxylase henylethylamine phenylethanolamine tyromine octopamine HO CHOHCH2NH2 CHOHCH2NH2 HO noradren phenylethano aline CH CH NH lamine HO 2 2 2 CHOHCH NH 2 2 HO HO dopami octopam ne ine 25 se neurotransmitter hypoth henylethanolamine Excited octopamine impulses Cerebr Changes blocked of al consciousness, cortex coma extrapyramida asterixi l system s Basal Peripheral Vascular ganglia sympathetic dilatation, nerve 26 3.2.4 Pathogenesis onia intoxication hypothesi e neurotransmitter hypothe rmal plasma amino acid hypo BA hypothesis, mma-aminobutyric acid 27 mal plasma amino acid hypot Branched chain amino acid ： isoleucine and valine leucine, (BCAA) Aromatic amino acid (AAA) ： Phenylalanine, tryptophan and tyr Nomal: BCAA/AAA =3.0-3.5 ， Severe liver damage: BCAA/AAA < 2.4 28  Plasm amino acid imbalance and hepatic encephalopathy rmal aromatic amino acid metabol Tyrosine β- hydroxylase hydroxylase Phenylalanine dopa hydroxylase decarboxylase tyrosine dopa dopamine noradrena henylalanine henylalanine tyrosine 29  dopaminenoradrenaline henylalanine phenylethylamine phenylethanolami tyrosine tyromine octopamine AAA β-hydroxylase decarboxylase tryptophan 5-hydroxytryptamin 30 3.2.4 Pathogenesis onia intoxication hypothesi e neurotransmitter hypothe rmal plasma amino acid hypo BA hypothesis, mma-aminobutyric acid 31  aa Inoxidase the liver dysfunction, the octopamine liver may not clear enylethanolamine the enterogenous GABA NH3 GABA levels GABA, 25%urea are elevated in the urease blood. NH3 urea urea Protei + aa ornithine NH4 n oxidase cycle urea cycle NH3 +NH3 NH3 glut glutam + α-ketoglutaric amic ine 32 glutami  GABA combinated with receptor ， Cl internal flow into the synaptic neuron ， Neurons became hyperpolarization state ， these Cause the inhibition function of the nervous system. 33 others rotten apples 1. rotten eggs Mercaptan Methionine metabolites: 2. Fatty hepaticus fetor Acid 3. Phenol from tyrosine 4. Benzazole from tryptophan 34  Precipitating factors of HE 1, Gastrointestina Hypovole l bleeding mia, shock hypoxia 35  Precipitating factors of HE 1, Gastrointestinal bleeding Infusion of blood, eat meats, constipation 36 37  Precipitating factors of HE 2, disorders of electrolytes and acid-base alkalosis ： NH3+ H＋ + NH4 K＋ H＋ NH4+ H＋ NH3 38  Precipitating factors of HE 2, disorders of electrolytes and acid-base NH3 H+ Lactu lose bacter ia NH4+ Lactic acid + acetic acid dialysis acid 39  Precipitating factors of HE 3, infections Endotoxin Fever Hypovolemia Blood brain barrier Renal failure 4, abuse of sedative and 40 Treatment of HE 1, eliminating or correcting precipitating factors 2, reducing plasma ammonia and other toxins 3, correcting plasma amino acid imbalance and supplying normal neurotransmitters 4, artificial liver support 5, liver transplantation 41 The end. Thanks !