藥理學(xué)名詞解釋(含英文)

藥物（drug）是指能夠影響機(jī)體（包括病原體）功能和（或）細(xì)胞代謝活動，用于疾病的治療、預(yù)防和診斷，以及計劃生育等方面的化學(xué)物質(zhì)。Drugsarechemicalsthatalterthefunctionoflivingsystemsbyinteractionsatthemolecularlevelandcanbeusedtoprevent,diagnoseandtreatdisease.不良反應(yīng)（adversedrugreactionADR）是指上市的合格藥品在常規(guī)用法、用量情況下出現(xiàn)的，與用藥目的無關(guān)，并給患者帶來痛苦或危害的反應(yīng)。副作用（ sideeffect）是由于藥物作用選擇性低，作用范圍廣，在治療劑量引起的，與用藥目的無關(guān)的作用。毒性反應(yīng)（toxiceffect）是由于用量過大或用藥時間過長引起的嚴(yán)重不良反應(yīng)。后遺效應(yīng)（residualeffect）是指在停藥后，血漿藥物濃度下降至閾濃度以下時殘存的藥理效應(yīng)。變態(tài)反應(yīng)（allergicreaction）是藥物引起的免疫反應(yīng)，反應(yīng)性質(zhì)與藥物原有效應(yīng)無關(guān)，其臨床表現(xiàn)包括免疫反應(yīng)的各種類型。致敏原可以是藥物本身或藥物代謝產(chǎn)物，亦可能是制劑中的雜質(zhì)或輔劑。繼發(fā)反應(yīng)（secondaryreaction）是繼發(fā)于藥物治療作用之后的不良反應(yīng)。停藥反應(yīng)（withdrawalreaction）是指患者長期應(yīng)用某種藥物，突然停藥后發(fā)生病情惡化的現(xiàn)象。特異質(zhì)反應(yīng)（idiosyncrasyreaction）是指少數(shù)患者由于遺傳因素對某些藥物的反應(yīng)性發(fā)生了變化。特異質(zhì)反應(yīng)表現(xiàn)為對藥物的反應(yīng)特別敏感，或出現(xiàn)與在常人不同性質(zhì)的反應(yīng)。依賴性（dependence）是藥物與機(jī)體相互作用所造成的一種狀態(tài)，表現(xiàn)出強(qiáng)迫要求連續(xù)或定期使用該藥的行為或其他反應(yīng)，其目的是感受藥物的精神效應(yīng)，或避免由于停藥造成身體不適應(yīng)。量效關(guān)系(does-effectrelationship)藥理效應(yīng)的強(qiáng)弱與其劑量大小或濃度高低呈一定關(guān)系，稱劑量-效應(yīng)關(guān)系，簡稱量效關(guān)系。最小有效量（minimaleffectivedoes）或最小有效濃度是指引起效應(yīng)的最小藥量或最低藥物濃度，亦稱閾劑量或閾濃度。最大效應(yīng)（maximaleffectEmax）在一定范圍內(nèi)增加藥物劑量或濃度，效應(yīng)強(qiáng)度隨之增加。但當(dāng)效應(yīng)增強(qiáng)打最大時，繼續(xù)增加劑量或濃度，效應(yīng)不再增強(qiáng)。這一藥理效應(yīng)的極限稱為最大效應(yīng)，又稱效能（efficacy）。效價強(qiáng)度（potency）用于作用性質(zhì)相同的藥物之間的等效劑量的比較，達(dá)到等效時所用藥量較小者效價強(qiáng)度大，所用藥量較大者效價強(qiáng)度小。構(gòu)效關(guān)系（structure-activityrelationship,SAR）藥物的結(jié)構(gòu)與藥理活性或毒性之間的關(guān)系稱為SAR。受體（receptor）是細(xì)胞在長期進(jìn)化過程中形成的，對生物活性物質(zhì)具有識別和結(jié)合的能力，并具有介導(dǎo)細(xì)胞信號轉(zhuǎn)導(dǎo)功能的蛋白質(zhì)。與受體特異性結(jié)合的生物活性物質(zhì)稱為配體（ligand）。激動藥（agonist）是指既有親和力又有內(nèi)在活性的藥物，它能與受體結(jié)合并激動受體而產(chǎn)生效應(yīng)。分為完全激動藥和部分激動藥。拮抗藥（antagonist）是指具有較強(qiáng)的親和力，而無內(nèi)在活性，拮抗藥與受體結(jié)合但不能激動受體。競爭性拮抗藥（competitiveantagonist）能與激動藥競爭相同受體，但其結(jié)合是可逆的，競爭性拮抗藥能使激動藥的量效曲線平行右移，但最大效應(yīng)不變。非競爭性拮抗藥指拮抗藥與受體的結(jié)合是相對不可逆的，或能引起受體構(gòu)象的改變，從而干擾激動藥與受體的正常結(jié)合，使激動藥不能競爭性對抗這種干擾。增大激動藥的劑量也不能使量效曲線的最大作用強(qiáng)度達(dá)到原來的水平。PA2：競爭性拮抗藥對相應(yīng)激動藥的拮抗作用強(qiáng)度，pA2=-log[A2],[A2]是指在拮抗藥這一濃度下，可使激動藥在2倍濃度使所產(chǎn)生的效應(yīng)恰好等于未加入拮抗藥時激動藥引起的效應(yīng)。PA2':非競爭性拮抗藥的親和力參數(shù)，又稱減活指數(shù)，是指使激動藥的最大效應(yīng)降低一半時，非競爭性拮抗藥摩爾濃度的負(fù)對數(shù)。pD2：藥物-受體復(fù)合物解離常數(shù)KD的負(fù)對數(shù)（-logKD）為pD2，其值與A和R的親和力成正比。意義是引起最大效應(yīng)的一半時（即50%受體被占領(lǐng)時）所需的藥物濃度。吸收（absorption）是指藥物從給藥部位進(jìn)入血液循環(huán)的過程。首關(guān)效應(yīng)（first-passeffect）是指某些藥物首次通過腸壁或經(jīng)門靜脈進(jìn)入肝臟時被其中的酶所代謝致使進(jìn)入體循環(huán)藥量減少的一種現(xiàn)象。分布（distribution）是指吸收入血的藥物隨血液轉(zhuǎn)運(yùn)至組織器官的過程。血腦屏障（blood-brainbarrier，BBB）指由腦毛細(xì)血管形成的血漿與腦細(xì)胞外液間的屏障以及由脈絡(luò)膜形成的血漿與腦脊液間的屏障。肝腸循環(huán)（hepatoenteralcirculation）由膽汁排入十二指腸的藥物有的直接隨糞便排出，但較多的藥物可由小腸上皮吸收，并經(jīng)肝臟重新進(jìn)入全身循環(huán)，這種肝臟、膽汁間、小腸的循環(huán)稱為肝腸循環(huán)。生物利用度（bioavailability,F）是指藥物從某制劑吸收進(jìn)入血液循環(huán)的相對數(shù)量和速度。是評價藥物制劑質(zhì)量的一個重要指標(biāo)。分為絕對生物利用度（absolutebioavailability）和相對生物利用度（relativebioavailability）。一般認(rèn)為，靜脈注射的生物利用度是100%，如果把靜脈注射與血管外途徑給藥時的AUC值進(jìn)行比較，并計算后者的生物利用度，即為絕對生物利用度。也可在同一給藥途徑下對不同制劑進(jìn)行比較，這就是相對生物利用度。半衰期（half-life,t1/2）指血漿消除半衰期，是藥物在體內(nèi)分布達(dá)到平衡狀態(tài)后血漿藥物濃度降低一半所需的時間，是表述藥物在體內(nèi)消除快慢的重要參數(shù)。一級消除動力學(xué)（firstordereliminationkinetics）是指血中藥物消除速率與血中藥物濃度的一次方成正比，即血藥濃度高，單位時間內(nèi)消除的藥量多；血藥濃度低，單位時間內(nèi)消除的藥量少。零級消除動力學(xué)（zeroordereliminationkinetics）是指血中藥物消除速率與濃度的零次方成正比，即血藥濃度按恒定消除速度進(jìn)行消除，與血藥濃度無關(guān)。穩(wěn)態(tài)血藥濃度（steady-stateconcentration，Css）在一級消除動力學(xué)藥物中，若按固定間隔時間給予固定藥物劑量，在每次給藥時體內(nèi)總有前次給藥的殘存量，多次給藥形成不斷蓄積，隨著給藥次數(shù)的增加，體內(nèi)總藥量的蓄積逐漸減慢，直至在劑量間隔內(nèi)藥物的消除量等于給藥劑量，從而達(dá)到平衡，這時的血藥濃度稱為穩(wěn)態(tài)濃度或坪濃度。調(diào)節(jié)痙攣（regulativespasm）：毛果蕓香堿激動睫狀肌環(huán)形纖維上M受體，使睫狀肌向虹膜中心方向收縮，懸韌帶松弛，晶狀體變凸，屈光度增加，使遠(yuǎn)物不能聚焦成像于視網(wǎng)膜上，因此模糊不清，此時，只適合于視特定近距離的物體，這種作用稱為調(diào)節(jié)痙攣。調(diào)節(jié)麻痹（regulativeparalysis）阿托品阻斷睫狀肌上的M受體，使睫狀肌松弛而退向外緣，懸韌帶拉緊，晶狀體變?yōu)楸馄?，其屈光度降低，故不能將近物清晰地成像于視網(wǎng)膜上，造成視近物模糊不清，只適于看遠(yuǎn)物，這一作用成為調(diào)節(jié)麻痹。膽堿能危象（cholinergicrisk）抗膽堿酯酶藥如新斯的明治療重癥肌無力，因應(yīng)用過量可使骨骼肌運(yùn)動終板處有過多乙酰膽堿堆積，導(dǎo)致持久去極化，加重神經(jīng)肌肉傳遞功能障礙，使肌無力癥狀加重，稱為膽堿能危象。腎上腺素升壓作用的翻轉(zhuǎn)（adrenalinereversal）a受體阻斷藥酚妥拉明等可取消去氧腎上腺素的升壓作用，可以部分阻斷去氧腎上腺素所致升高血壓作用，使腎上腺素的升壓carriersandtherequirementofenergyconsumption.Absorptionistheprocessinwhichdrugstransportfromthesiteofadministrationtothebloodcirculationafterextra-vascularadministration.Firstpasselimination:Somedrugsareinactivated/metabolizedintheGItractandliverbeforeenteringintothesystemiccirculationandresultinthereductionofactualdrugquantityenteringintosystemiccirculation.ThisprocessiscalledfirstpasseliminationDistribution:drugsabsorbedinthebloodtransportfromthebloodtotissues.Tissuepartitioncoefficient:whenthedistributionreacheshomeostasis,theratioofthedrugconcentrationbetweentissuesandplasmaremainsconstant,calledtissuepartitioncoefficientofdrugsExcretion:theprocessofparentdrugsortheirmetabolitesbeingdischargedfrombodybysecretoryorgansisknownasexcretionHepato-enteralcirculation:aportionofdrugsthosebeingcarriedtoduodenumviabilecanbereabsorbedviaepitheliaofsmallintestinesandentryintosystemiccirculationbywayofliver.Thiscyclealongliver,bile,smallintestineisknowashepato-enteralcirculationApparentvolumeofdistributionmeanstheratioofinvivodrugquantityversusconcentrationinplasmawhenthedrugreachesdynamicequilibriuminthebody.Halflife:meanstheperiodoftimewhenthedrugconcentrationinplasmareducestoone-half.AUC:areaunderthecurve,indicatestheareaundertheconcentration-timecurveBioavailability:indicatestherateandextentofabsorptionintothesystemiccirculationfollowingextravascularadministrationofdrugsClearance:mansthevolumeofbodyfluidcontainingadrugthatcanbeeliminatedbythebodyinunittime.Maintenancedose:inmostclinicalsituations,drugsareadministeredinsuchawayastomaintainasteadystateofdruginthebody,i.e,justenoughdrugisgivenineachdosetoreplacethedrugeliminatedsincetheprecedingdose.Loadingdose:whenthetimetoreachsteadystateisappreciable,asitisfordrugswithlonghalf-lives,itmaybedesirabletoadministeraloadingdosethatpromptlyraisestheconcentrationofdruginplasmatothetargetconcentration.PharmacodynamicsDrugactionreferredtotheinitialinteractionbetweendrugandbody.PharmacologicaleffectsisthephysiologicaleffectsinducedbydrugactionStimulation:enhancementofthebodyfunctionisStimulationInhibition:restraintordiminutionofthebodyfunctionisInhibitionEtiologicaltherapy:EliminationoftheetiologicalfactorstocurediseasesSymptomatictherapy:ImprovementofdiseasesymptomwithouteliminatingthecauseofthediseaseSidereaction:Intherangeoftherapeuticdosage,thedrugeffects,whicharenotrelatedtothecurrenttherapeuticpurpose,aredescribedassideeffects.Toxicreactioncanhappenedwhenthedoseofthedrugishighenoughordrugsarelongtermused.Allergicreactionisakindofresponseofthepatient’simmuno-systemtotheantigen.Itisnotdoserelatedandonlyoccurinafractionofthepopulation.IdiosyncraticreactionistheresultofabnormalreactivitytoadrugcausedbygeneticdifferencesSecondaryreactionresultsfromlong-termusingofdrug.NormalflorahasbeeninhibitedandtheinsensitiveflorabecomesprominentDrugtolerancemeanstheresponsetothesamedoseofadrugdecreaseswithrepeateduses.Physicaldependenceisanadaptivephysiologicalstateproducedbyrepeateduseofadrug.Oncedrugadministrationisstopped,abstinencesyndromeswilloccur.Psychologicaldependenceisthefeelingofsatisfactionandpsychicdrivethatrequireperiodicorcontinuousadministrationofthedrugtoproduceadesiredeffectortoavoiddiscomfort.Gradedresponse:Inacertainrangeofdoses,thepharmacologicalresponseincreaseswiththeincreasingofdoses,suchasbloodpressure,musclecontraction,urinaryexcretionofsodium.Thresholddoseindicatestheleastamountofdrugneededtoexerttherapeutic,alsoasknowasminimaleffectivedoseEfficacydescribesthemaximalbiologicalresponseproducedbyadrugConcentrationfor50%ofmaximaleffect(EC50):Theconcentrationthatgiveriseto50%ofmaximaleffectPotencyisatermdescribingthecomparativeexpressionofadrugactivitymeasuredintermsofdoserequiredtoproduceaparticulareffectofgivenintensityrelatedtoagivenstandardreference.Quantalresponse:Indicatethatagivendoseofadrughasorhasnotevokedacertaineffectinthevarioussubjectsunderinvestigation.LD50:Adosethatgivesrisetothedeathof50%ofsubjectsiscalledLD50TI:therapeuticindex.TI=LD50/ED50.Itisakindofindexevaluatedthesafetyofadrug.Receptor:AreceptorcanbedefinedasanybiologictargetmacromoleculeincellsthatinteractsspecificallywithextracellularsignalandconvertsitintointracellulareffectsLigand:Aligandisacompoundthatbindstoareceptorspeciallyandproducesthebiologicalresponse.ItwasalsocalledfirstmessengersDown-regulation/Desensitization:Chronicstimulationofreceptorscancausedecreasednumbersofreceptors.Up-regulation/Hypersensitization:Incontrary,chronicblockingreceptorsmayresultinreceptorup-regulationAgonistcanbindtoreceptors,thenactivatereceptorsandproducepharmacologicaleffect.Antagonist:Apureantagonist,whichcanbindtoreceptorswithoutintrinsicactivity,antagonizesthebiologiceffectsofthecorrespondingagonist.Toleranceissaidtodevelopwhentheresponsetothesamedoseofadrugdecreaseswithrepeateduses.Dependencemeansthebodyproducephysiologicalorpsychologicaldependenceandrequirementtosomedrugsafterlong-termuseofthedrugs.WithdrawalsyndromeTerminationofsomedrugsusingafterlong-termmedicationresultsinwithdrawalsymptomsorwithdrawalsyndromeCinchonism:Itisdescribedbythesymptomscausedbytoxicityofquinidineorquinineetal,thealkaloidsextractedfromcinchona,whichinclude3majorsymptoms:gastrointestinaldisturbancelikevomiting,nausea,diarrhea;visualandauraldisturbancesasdiplopia,photophobia,altered-color,hearingloss,tinnitus;andcentralnervoussystemeffectslikeheadache,confusion,psychosis.Mycardialremodeling:ItisthemostimportantintrinsiccompensatorymechanisminCHF.Itreferstotheslowdilationandstructuralchangesoccurredinthestressedmyocardium,includingmyocyteshypertrophy,proliferationofconnectivetissuecells(fibroblasts)andmyocardialfibrosis.Afteraninitialbeneficialeffect,mycardialremodelingcanleadtoischemicchanges,impairmentofdiastolicfilling,andmyocytesapoptosis.AngiotensinIIandaldosteronecancausemycardialremodelingduringCHF.Firstdosephenomenon:Itreferstoaprecipitousdropinstandingbloodpressure,palpitationandsyncopeshortlyafterthefirstdoseofsomeantihypertensivedrugs,especiallyprazosin.Thyroidstorm(thyroidcrisis):issuddenacuteexacerbationofallofthesymptomsofthyrotoxicosis,presentingasalife-threateningsyndrome.Insulinresistance:Adiabeticrequiringmorethan200units/dayisregardedasinsulinresistant.Acuteresistantmayresultfromtheincreaseofanti-insulinfactor-corticosteroids,growthhormonethyroxine,andestrogens.Chronicresistancemaybeduetoadeclineinnumberand/oraffinityofreceptorsortodefectsinpost-receptormechanisms.Hyperadrenalism-likesyndrome:Thisiscausedbylipidmetabolism,andredistributionorwater-electrolytemetabolismdisorders.Thesyndromeincludemoonfaces,buffalohump,centralobesity,skinatrophy,acne,crinosity,edema,hypokalemia,hypertension,diabetesmellitusetc.Reboundphenomena:Discontinuingorrepidextenuationofglucocorticosteriodscanleadoriginaldiseasesrecurringordeteriorating.Superinfections:Thereisacompletemicroecosysteminhealthadult.Afterlong-termusingbroad-spectrumantibiotics,sensitivebacteriagrowthisinhibited,non-sensitivebacteriatakesthechanceofbreeding,resultinginnewinfections.Chemotherapy：Itistousechemistrydrugstreatingorpreventingthediseasescausedbypathogenicmicrobe,helminthorcancercell.Antibacterialdrugs：substancestoinhibitorkillbacteriaandtopreventandcurethebacteroidalinflammation.Antibacterialspectrum：Antibacterialspectrumofadrugmeansthespeciesofmicroorganismsthatthedrugcaninhibitorkill.antibacterialactivity：Itmeanstheabilityofadrugthatthedrugcaninhibitorkillmicroorganisms.Minimalinhibitoryconcentration(MIC)：MICisthelowestconcentrationofantimicrobialagentsthatpreventsvisiblegrowthin18-24hoursincubation.Minimalbactericidalconcentration(MBC)：MBCisthelowestconcentrationofantimicrobialagentsthatkillsbacteriainculturemedium.Chemotherapeuticindex(CI)：CIisatermusedtoevaluatethesafetyofchemotherapeuticdrugs.ThevalueisLD50/ED50orLD5/ED95Post-antibioticeffect,PAE：PAEshowstheantimicrobialeffectaftertheconcentrationdecreasedbelowMIC.Chemotherapy：Itistousechemistrydrugstreatingorpreventingthediseasescausedbypathogenicmicrobe,helminthorcancercell.Chemotherapeuticindex(CI)：CIisatermusedtoevaluatethesafetyofchemotherapeuticdrugs.ThevalueisLD50/ED50orLD5/ED95Antibacterialdrugsaresubstancestoinhibitorkillbacteriaandtopreventandcurethebacteroidalinflammation.Antibacterialspectrumofadrugmeansthespeciesofmicroorganismsthatthedrugcaninhibitorkill.antibacterialactivity：Itmeanstheabilityofadrugthatthedrugcaninhibitorkillmicroorganisms.Minimalinhibitoryconcentration(MIC)：MICisthelowestconcentrationofantimicrobialagent