药理学基础知识点利尿药 糖皮质激素 化学治疗药物 抗恶性肿瘤药基础知识 化学治疗药物.docx
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药理学基础知识点利尿药 糖皮质激素 化学治疗药物 抗恶性肿瘤药基础知识 化学治疗药物.docx
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药理学基础知识点利尿药糖皮质激素化学治疗药物抗恶性肿瘤药基础知识化学治疗药物
药理学基础知识点:
利尿药糖皮质激素化学治疗药物抗恶性肿瘤药基础知识化学治疗药物
Givepeoplethepowertochangethefuture
Thebasicknowledgeofpharmacologyin2015:
thebasicknowledgeandchemicaltreatmentofantimalignantneoplasticdrugsinthedrugofdiureticglucocorticoid
diuretic
(1)effectivediuretics:
furthrice;Inhisacid;Bumetanide.
[actionmechanism]
ACTSonthepulploopsriseathicksection,specificitytocompetewithCl-,Na+-k+-2Cl-commonCl-combiningpartsofthetransportsystem,inhibitionofNaClreuptakeandactasapowerfuldiureticeffect.
[diuresis]rapid,powerful,transient,individualdifferences
【clinicalapplication】severeedema;Acutepulmonaryedema;Brainedema;Treatmentofacuterenalfailure(earlyurination);Topromotetheexcretionofpoisons.
(2)effectivediureticdrugs:
thiazinediuretics;
【】pharmacologicalactivitiesandmechanisms1.Diureticeffect:
features:
mild,lastingworkingpart:
pulploopsriseathicksectionofthecortexofdistalconvolutedtubules(start)effect:
inhibitionofK+,Na+-2cl-commontransportsystems;TopromoteNaplusminusKplusexchange;Effectofinhibitingcarbonicanhydrideenzyme.Thereductionofbloodpressurebydiuresisandbloodvolumeintheearlystage.Antidiuresis(antidiuresis)
A.clinicalapplication】【edema:
1.Themindedemapreferredmedicine2.Renaledema,renalfunctiondisorderdisabledorcarefulwith3.Livercirrhosisascites:
appropriateandspironolactoneshareb.hypertensionc.diabetesinsipidus
【poorresponse】1electrolytedisorder2hyperuria3metabolicchanges:
highbloodsugar,hyperlipemia.4anallergicreaction
(3)inefficientdiureticdrugs:
snails,aminophenylate,amilloli
[diuresisandmechanism]features:
sloweffect,weakeffect,lasting,notlosingpotassium.Site:
distalconvolutedtubuleandassembly-tubeintracellularaldosteronereceptor.Way:
thealdosteronereceptorforaldosterone.Result:
suppressNa+-k+exchange,rowNa+leaveK+
【clinicalapplication】thepersistentedemaofaldosteroneincreases.Itiscommonlyusedincombinationwithstrongeffectandmediumeffectdiureticmedicine,enhancesdiureticeffectandcancomplementK+
【adversereaction】1longusecausehighbloodpotassium:
kidneyfunctionbadpersontodisable.2sexhormoneresponse:
malebreastfemale,sexualdysfunction,women'spolytrichosis.
Pharmacologybasicknowledge:
glucocorticoid
glucocorticoids
Glucocorticoidhasapowerfulanti-inflammatoryeffectthatinhibitstheinflammatoryresponsefrommultiplecauses.Atthebeginningoftheinflammation,canheightenbloodvesselsoftension,relievecongestion,reduceMAOvascularpermeability,inhibitionofleukocyteinfiltrationanddevourreactionatthesametime,reduceinflammationfactors.Itcanrelievethesymptomsofredswellingandfever.Lateininflammation,glucocorticoidthroughinhibitionofcapillariesandfibroblastsproliferation,inhibitthesynthesisofcollagenandglycosaminoglycanandgranulationtissuehyperplasia,preventionandcontrolofadhesionandscarformation,reducesequelae.
[clinicalsignificance]
(1)severeacuteinfection:
adjuvanttherapywithglucocorticoidswhiletreatinginfectionwitheffectiveantimicrobialagents.Becauseofitsabilitytoincreasethetoleranceoftheharmfulstimulationofthebody,itisbeneficialtobuytimeandrescue.
(2)thesequelaeofanti-inflammatorytreatmentandthepreventionandcontrolofcertaininflammation:
ifinflammationoccursinvitalorgansofthehumanbody,itwillcauseseveredysfunction.Therefore,earlyapplicationofglucocorticoidtoreduceinflammatoryinfiltrationandreducetheexcessivehyperplasiaandadhesionofthefibersinthehealingprocess,preventthesequelaefromoccurring.
[pharmacologicalaction]
A,anti-inflammatoriesB,anti-immunefunction,especiallyincellimmune-c,anti-shockactionD,andanti-toxicity,canimprovethebody'stolerancetobacterialendotoxin.E,thestimulationofthebloodandhematopoieticsystem,G,caninducetheincreaseofgastricacidandpepsin
[clinicaluse]
A,alternativetreatmentB,andsevereinfectionareusedasadjuvanttherapyC,antishockD,autoimmunediseaseandallergicdiseaseE,hematopathyandtumortreatingF,anti-localinflammation
[adversereaction]
Hyperactivitysyndromeadrenocorticalfunction1,2,3induceandaggravatetheinfection,thedigestivesystemcomplication4,5,andothercomplicationscancausemovementsystemaberrations6,drugwithdrawalreaction:
(1),drug-inducedcorticaldysfunction
(2),thebouncephenomenon
Pharmacologybasicknowledgepoint:
chemicaltreatmentmedicine
chemothermy
Themechanismofantimicrobialaction:
(1)inhibitbacterialcellwallsynthesis
Thefunctionofthecellwallistomaintainthenormalformandosmoticpressureofthebacteriaandmaintainthenormalfunctionofthebacteria.Antimicrobialdrugscancausebacterialcellwalldefects,waterisinfiltratedbytheoutside,andthecellexpandsanddeforms,causingthecelltodissolveanddissolveanddie.
Appliedtothecytoplasm:
cycloserine,phosphodomycin
Appliedtocytoplasm:
vancomycin,bacillus
Appliedtothecytoplasm:
penicillin,cephalosporin
(2)thepermeabilityofthecellmembrane:
Thecytoplasmisincreased,protein,nucleotide,sugar,salt,andbacterialdeath
(3)inhibitthesynthesisofbacterialproteinsThecombinationofthetetracyclineandaminoglycosideantibiotics
Combinedwiththe50s:
erythromycin,chloramphenicol,andlincomycin
Affectthewholeprocessofproteinsynthesis:
aminoglycosideantibiotics
(4)affectfolateandnucleicacidmetabolism
?
Folicacidistheprecursorofsyntheticnucleicacid
?
Sulfamideandmethoxybenzine(TMP)caninhibittheenzymeanddihydrofolatereductase,whichinhibitsfolicacidmetabolismandinhibitsthegrowthandreproductionofbacteria.
Pharmacologybasics:
chemotherapydrugs
(2)
chemothermy
Bacterialresistancemechanism
(1)itproducesaninactivatedenzymethatcausestheantibiotictobeinactivated
Theseinactivatedenzymescanbeexpressedbyplasmidandchromosomalgenes
A)hydrolyzedenzymes-antibioticsforbeta-lactam
B)passivatingenzymes-aimedataminoglycosideantibiotics
C)other
(2)thetargetchangesofantimicrobialagents
A)changesthestructureofthetargetprotein,reducingtheaffinitywithantibiotics
RFPresistantbacteriachangethesubstructureoftheRNApolymerase
B)increasethenumberoftargetproteinsandmaintainnormalformandfunctionwhenthedrugispresent
Enterococcusisanantibioticforbeta-lactam
C)thenewsynthesisfunctionisnormalandthetargetproteinofantibioticaffinitylow
ThebacteriumproducespenicillinbindingproteinPBP2a,whichisextremelylowtomethoxillin
(3)reducingthepermeabilityoftheoutermembraneofthebacteria
Afterexposuretoantibiotics,bychangingthenatureofthechannelproteinsandtoreducethebacterianumberofmembranepermeabilitytopreventantibioticintothebacteriainthebodyandproduceacquireddrugresistance
(4)toenhanceactiveexternalsystemactivity
(5)bacteriachangetheirmetabolicpathways
Thereasonthatthebacteriumisresistanttosulfonamideis:
Therewasariseinaminobenzoicacid
Drug-resistantstrainsmakedirectuseofexogenousfolicacid
Thebasicknowledgeofpharmacology:
thebasicknowledgeofanti-malignanttumormedicine
【introduction】inpublicinstitutiontotestnetworktoprovidemedicalandhealthprofessionalknowledge,thefollowingbringeverycandidatesbasedonknowledgepoints-antitumormedicinepharmacologyfoundationknowledgerelatedcontent,foreverybodytostudyfor.
Therelationshipbetweentheproliferationcycleofthetumorandthedrugofchemotherapy
Tumorcellproliferationcycle:
1,theproliferativecellgroup2,thenon-proliferativecellgroup3,thenon-proliferativecellgroup(G1,S,G2,M)
Periodicnonspecificdrugs:
thecellsthatcaninhibitordestroythecycleoftheproliferationcycle,evenG0.Alkanes,antibiotics.
Cyclicallyspecificdrugs:
onlyoneissueofthecycleisstronger.
Themechanismandclassificationofanti-malignanttumordrugs:
Drugsthatinhibitthesynthesisofnucleicacids(DNA,RNA):
antimetabolitics
(1)thestericacidsynthaseinhibitor,preventingpyrimidinenucleotideformation:
5-fluorouracil
(2)DNApolymeraseinhibitors:
abglycoside
(3)nucleotidereductaseinhibitors:
hydroxylurea
(4)dehydrofolicacidreductaseinhibitor:
methylamine
DrugsthatdamageDNAdirectlyandstopitfrombeingcopied:
alkylation,certainanti-cancerantibiotics,andcisplatin.
ThedrugsthatinterferewiththetranscriptionprocesstoblockthesynthesisofRNA:
acidomycin,roerythromycin,andamycin.
4,thedrugsthataffectthesynthesisofproteins:
changchunalkaloids,taxol.
Drugsthataffectthehormonalbalanceofcancer:
corticosteroids,androgens,andestrogen.
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