内科学教学课件：第十八章 肝性脑病

第十八章肝性脑病

HepaticEncephalopathy,HEHepaticcoma2023/3/232ConceptionAneuropsychiatricsyndromecausedbyseriousliverdiseasewith/orprotal-systemicshunt

2023/3/233EtiologyHepaticcirrhosis(chronicfailure)Protal-systemicshuntHepatomaAcutehepaticfailureAcutefattyliverofpregnancy,AFLPSeriousInfectionofbileduct2023/3/234ClassificationTypeA:acute(subacute)liverfaliureTypeB:porpal-systemicshuntTypeC:hepaticcirrhosis

2023/3/235pathogenesis

Hapeticfailure+porta-systemicshunt

toxicsubstanceintosystemiccirculationblood-brainbarrierdisfunction

biochemicaldisturbanceofbrainfunction

2023/3/236Pathogenesis

(hypothesis)AmmoniaFalseneurotransmitter&imbalanceofaminoacidgamma-aminobutyricacid(GABA)/BZMnAmmonia,mercaptans硫醇andshort-chainfattyacids

2023/3/237Pathogenesis

(hypothesis)Ammoniatoxicosisnitrogenoussubstancesproducedinthegut

bybacterialaction

2023/3/238氨中毒学说：1）氨的形成和代谢：产生：主要来自肠道尿素蛋白质

谷氨酰胺→

NH3+谷氨酸肠菌

NH3+CO22023/3/239局部pH对氨吸收的影响NH3＋H＋

NH4+OH-H+2023/3/2310发病机制

氨中毒学说：1）氨的形成和代谢：产生：

主要来自肠道其次来自肾脏：谷氨酰胺酶分解谷氨酰胺，pH调节

谷氨酰胺→

NH3+谷氨酸

少量来自横纹肌2023/3/2311发病机制

氨中毒学说：1）氨的形成和代谢：产生：

主要来自肠道其次来自肾脏：谷氨酰胺酶分解谷氨酰胺，pH调节

少量来自骨骼肌

清除：

转化：肝中：鸟氨酸循环合成尿素

脑肝肾中：

-酮戊二酸+NH3谷氨酸+NH3谷氨酰胺

2023/3/2312发病机制

氨中毒学说：1）氨的形成和代谢：产生：清除：排泄：肾：排出尿素，排出NH4+主排

肠：NH3，pH<6

肺：呼出NH3少量

2023/3/2313发病机制

氨中毒学说：1）氨的形成和代谢2）肝性脑病时血氨增高的原因氨的生成过多和代谢清除减少。肠道产氨增加：细菌，含氮物质肝合成尿素的能力减弱，门体分流的存在。肾脏排泄减少2023/3/2314发病机制

氨中毒学说：1）氨的形成和代谢2）肝性脑病时血氨增高的原因3）对中枢系统的毒性作用

a.干扰脑的能量代谢（干扰三羧酸循环，产

ATP减少；去氨代谢致ATP消耗增加。）

b.增加芳香族氨基酸的摄取

c.谷氨酸是大脑兴奋的递质

d.

谷氨酰胺是渗透剂诱发脑水肿-酮戊二酸+NH3谷氨酸+NH3谷氨酰胺2023/3/2315Pathogenesis

(hypothesis)AmmoniatoxicosisFalseneurotransmitter&imbalanceof

aminoacidOctopamine(鱆胺）aromaticaminoacids

（芳香族氨基酸）2023/3/2316Pathogenesis

(hypothesis)Ammoniafalseneurotransmitter&imbalanceof

aminoacid-aminobutyricacid/benzodiazepine(GABA/BZ)

BZBARBGABA2023/3/2317Pathogenesis

(hypothesis)Ammoniafalseneurotransmitter&imbalanceofaminoacidgamma-aminobutyricacid(GABA)/BZMn++Ammonia,mercaptans硫醇andshort-chainfattyacids

2023/3/2318Pathogenesis

(disterbanceofbrianfunction)neurotransmitter

EnergydisterbanceAstrocyte2023/3/2319Pathogenesis

(precipitatefactors)GastrointestinalbleedingExcessdietaryproteinHypokalaemiaHypovolemia,hyoxemiaUraemia

InfectionDrugs:Sedatives,antidepressants,hypnotics

Constipation2023/3/2320Clinicfeatures

intellect,personality,emotionsandconsciousness2023/3/2321Clinicfeatures0期MinorHE2023/3/2322Clinicfeatures

前驱期

stage1:mildabnormalofcharacter&behavior,asterixis(扑翼样震颤）2023/3/2323Clinicfeatures

Stage2:confusion,behavior,dyssomnia睡眠障碍Apathy淡漠,inabilitytoconcentrate,confusion,drowsiness困,hallucination幻觉slurringofspeech,mentalabnormal,hallucination,psychosis精神病-likedisorientation,inabilitytoperformsimplearithmetic,constructionalapraxia构造性失用症,Babinskisign,flappingtremor

2023/3/2324Clinicfeatures

Stage3:Lethargy昏睡,confusedstateofmind,Stage4:coma

2023/3/2325Investigations

Arterialammonia

Electroencephalogram(EEG)showsdiffuseslowingofthenormalalphawaveswitheventualdevelopmentofdeltawaves.evokedpotential(EP):VEP(visualEP);AEP(AuditoryEP);SEP(SomatosensoryEP)mentalarithmetictest心理智能检测

2023/3/2326156161412137918421110517181920212223242532023/3/2327diagnosis

①serioushepaticdisorders/portalsystemicshunting;②clinicalmentalconfusion,lethargy,coma③precipitatefactors;④hepaticfunctionorammonia

2023/3/2328DifferentiationPrimarypsychiatricdisorders

Coma2023/3/2329Management

ControltheprecipitatefactorsGastrointestinalbleedingDuretics,Paracentesis(volumes>3-5litres)HypokalaemiaInfectionConstipationDrugs(Sedatives,antidepressants,hypnotics)2023/3/2330Management

ControltheprecipitatefactorsNutritionGlucoseforenergyProtein:prohibitingforacutelimitingforchronicHEbranchaminoacidsvegetableproteinbetter2023/3/2331Management

ControltheprecipitatefactorsNutritionreducingtoxicproductsingutEnema灌肠&catharsis导泻:25~33%Mg2SO430~60ml;NS1000ml+vinegar50mlLactulose(30~60g/d)Lactitol(30~45g/d)Inhibitingintestinalbacteria:rifaximinMicroecologicagents2023/3/2332Management

ControltheprecipitatefactorsNutritionreducingtoxicproductsingut

re