內(nèi)容講稿課件-chapter30.drugs for digestive disorders

DrugsforDigestiveYECaseAmaledriver,30yrsIntermittentupperabdominalpainfor3yrs,worseathunger,betteraftermeal,hadhypnalgia（夜間痛）Withsourregurgitation（反酸）andbelching（噯氣）Tarry（柏油樣便）4days.Gastroscope(胃鏡)foundanulceratduodenalbulbarHp(+)Diagnosis:duodenalbulbarulcerwithEffectsofDrugsontheDigestiveDigestivesystemanddrugtherapyhaveareciprocal互惠)relationship.SomemedicationscauseGIsymptoms;conversely,someGIdisordersaltertheabsorptionandmetabolismofdrugs(liverfailure)DrugsaffectingtheGItractdrugsusedinacid-pepticdisorders(DigestantsAntiemeticsLaxatives(瀉藥Cholagogue(利膽Othersincludecholinergics,anticholinergicscorticosteroidsandanti-§1DrugsforPepticThegastrointestinaltracthaveitsownprotectivemechanismsandthisisgenerallyinabalancewithdestructivefactorsCellprotectivemechanismsinSecretionofmucusandDilutionofgastricacidbyfoodandPreventionofdiffusionofHCLfromthestomachlumenbackintothegastricmucosalPresenceofprostaglandinAlkalinizationofgastricsecretionsbypancreaticjuicesandbileCellDestructiveEffectsinGastricacid,secretedbyparietalParietalcells（壁細(xì)胞）containreceptorsforacetylcholineandhistamine,allofwhichstimulategastricacidAcetylcholineisreleasedbyvagusnerveendingsinresponsestimuli,suchasthinkingaboutGastrin(胃泌素)isahormonereleasedbythestomachandduodenuminresponsetofoodingestionAffectsparietalcellswhichinturncausesgastricacidtobereleasedinstomach.HistamineisreleasedfromcellsinthegastricmucosaandintonearbyparietalFactorsaffectinggastricacidCelldestructiveeffectsH.pylori(helicobacterpylori，HP，幽門螺旋桿菌)isagramnegativebacteriumfoundinthegastricmucosaofmostptswithchronicgastritis,affectmucosalfunction.1983年，WarrenandMarshallseparateHelicobacterPylorifromhumangastricmucosalIn75%ofthosewithgastriculcersandin90%ofclientswith（十二指腸）Spreadbyoralfecalroute（糞口途徑）orbyiatrogenic（醫(yī)源性Pepsin（胃蛋白酶）isaproteolyticenzymethathelpsdigestproteinfoodsandalsocandigestthestomachwallDrugs,alcohol,DrugtacticsfordigestiveInhibitdestructiveEnhanceprotectiveneutralizesmorethan90%ofgastricthepHto yinhibitsconversionofpepsinogentopepsin,theactivityofFormadrugmembraneovertheulcercalciumcarbonate(碳酸鈣aluminumhydroxide(氫氧化鋁magnesiumsodiumbicarbonate(碳酸氫鈉,小蘇打Drugsinhibitgastricacid1.H2receptorcimetidine（西咪替丁,(法莫替丁),Nizatiding(尼扎替丁)Vagal(迷走）stimulationcausesreleaseofhistaminefromcellsinstomach,actsonreceptorsinparietalcells>>>>increasesHCLproduction.S.E:CimetidineaffectstheProtonPumpinhibitorsAlsocalledH+-K+-ATPaseStronginhibitorsofgastricacidBindirreversiblytothegastricprotonpumppreventthereleaseofgastricacidfromparietalSuppressesacidsecretioninresponsetoallstimuliincludinghistamine,gastric,andantiH.Arethedrugsoffirstchoiceinerosive（腐蝕性食管炎）erosivegastritisandZollinger-MoreeffectivethanH2RA;FastersymptomreliefandfasterhealingSideeffectsarenausea,omeprazole（losec,奧美拉唑）1st 2nd 3rdAnticholinegics&GastrinRMcholinoceptorPirenzepine(哌侖西平GastrinreceptorProglumide(丙谷胺InhibitHClIncreasemucousMucosalprotectiveGastricmucosalCellMucus－HCO3-misoprostol（米索前列醇thederivativeofInhibitHClIncreasemucusandHCO3-IncreasebloodflowandmucosalContraindicatedinwomenofchildbearingageandduringpregnancy.MayinduceabortionSucralfate硫糖鋁possiblebindtotheulcerandformaprotectivebarrierbetweenthemucosaandgastricacid,pepsinandbilesalts;andstimulatingprostaglandinsynthesisbismuthpotassiumcitrate(枸櫞酸鉍鉀Bindwithpepsinanddecreaseitsbindtotheulcerandformaprotectivebarrierbetweenthemucosaandgastricacid,pepsinAntihelicobacterContraindication:renalAgentsAgainstH.pylori(抗幽門H.Pyloriaresensitivetomanyantibacterialdrugs,butit’sdifficulttoeradicate(根除)ifnotusethemcombinedRequirescombinationoftwoantimicrobialsandaPPIoranH2RAUseamoxicillin,clarithromycin,metronidazoleortetracyclineforantibioticportionMorethanantimicrobialisindicatedtoBismuthcompoundisaddedforitsantibacterialeffectsaswellasincreasingtheHCO3-andmucouscontentsofthestomachAddinganH2RAorPPIdecreasesS/EandhastenshealingGeneralusedcombination阿莫替林鉍制劑（bismuth§2ModulatorsofDigestivesystemfunctionI.Digestants（助消化藥DilutedAntiemeticDrugs(止吐藥Thevomitingcenter,chemoreceptortriggerzone(CTZ,催吐化學(xué)感受區(qū))andGItractcontainbenzodiazepine,cholinergic,dopamine,histamine,opiateandserotoninreceptorsthatarestimulatedbyemetogenic（催吐drugsandtoxinsForexample:chemotherapymaystimulatetheCTZwhichthenthevomitingMotionsickness（舟車暈浪）—changesinbodyreceptorsininnerear>>transmittedtotheCTZandthevomiting1.H1receptorDiphenhydramine(苯海拉明Dimenhydrinare(茶苯海明,乘暈寧2.Mcholinoceptor3.D2receptorThiethylperazine硫乙拉嗪Domperidone(多潘立酮,嗎丁啉4.5-HT3receptorDrugspromotegastrointestinal 利）:5-HT4receptoragonist,enhanceAchreleaseBethanechol:MceptorNeostigmine:AchEMetoclopramide甲氧氯普胺GIdopamineRantagonistAntidiarrheals&Diarrheaisasymptomofnumerousconditionsthatincreasebowelmotility;causesecretionorretentionoffluidsintheintestinallumenandcauseinflammationorirritationoftheGItract.Endresult:bowelcontentsarerapidlypropelledandabsorptionoffluidsandelectrolytesislimitedCausesofAbuseof Intestinalinfections—E.Coli0157:H7Traveller’sdiarrhea(E.coli),Campylobacter（彎曲桿菌）SalmonellaShigella（志賀氏菌）,rotatInflammatorybowelDruginduced—pseudomembranous（假膜Opiaterelateddrugs:opiumtincture（阿片酊）tincturecamphorcompound（復(fù)方樟腦酊Defenoxinwithatropine—Diphenoxylatewithatropine—Bismuthsubsulicylate（次水楊酸鉍Medicinalcharcoal（活性炭Whenstomachandduodenumare（膨脹）withfood,gastrocolic（胃結(jié)腸）andduodenocolic（十二指腸結(jié)腸）reflexesareinitiatedThecerebralcortexcontrolsthedefecationreflex（排便反射）sothatdefecationcan ceptabletimesandplacesInpeoplewhoinhibitthedefecationreflexorfailtorespondtotheurgetodefecate,constipationdevelopscontactcathartics（刺激性瀉藥，接觸性瀉藥osmoticlaxatives（滲透性瀉藥，容積性瀉藥surface-activeagents（潤滑性瀉藥LaxativesarechemicalsubstancesthatacttofacilitatepassageofbowelCathartics—apurgative（凈化的）actionofthebowelsactionisstrongerandgenerallyproduceseliminationofliquidstoolsIndicationsforObtainstoolAccelerateexcretionofparasitesafteranthelminthics（驅(qū)腸蟲藥）startedAccelerateeliminationofpotentiallytoxicPreventstrainingat（延時）stool,Relieveconstipati