外科學(xué)復(fù)習(xí)大綱（Eternal science review outline）

外科學(xué)復(fù)習(xí)大綱(Externalsciencereviewoutline)

Surgeongeneral

1.Asepsisisaseriesofpreventivemeasuresadoptedbythe

needleonmicrobiologicalandinfectionpathways,including

sterilization,sterilization,operationrulesandmanagement

systems.

Sterilizationmeanskillingall1ivingmicroorganisms.Common

sterilizationisincluded

Highpressuresteamsterilizationmethod:thisisthemost

commonandreliablemethodforsterilizationofsurgical

supplies.High-pressuresteamsterilizercanbedividedinto

lowerexhaustandpre-vacuumtype.Highpressuresteam

sterilizationmethodisusedforthegeneralabilityofhigh

temperatureobjects,suchasmetalinstruments,glass,enamel,

dressing,rubber,medicineandothersterilization;

Boilingsterilization:commonlyusedboilingsterilizers.But

thegeneralaluminumpotwashtheoil,alsocanboil

sterilization.Thislawshallbeapplicabletometal,glassand

rubbergoodssuchasinstrument,theinthewater,afterboiling

for1000csupremefor15~20minutes,generalbacteriacan

bedestroy,butneedtoboilforatleastonehourwithspores

ofbacteriatokill;

Firemethodforuseinanemergency.Thesterilizationmethod

includestheinfusionofliquidmedicineandtheformaldehyde

steamfumigationmethod.

Sterilizationreferstothedestructionofpathogenic

microorganismsandotherharmfulmicroorganisms,butdoesnot

requiretheremovaloreliminationofallmicroorganisms.

Commonlyuseddisinfectionmethod:

Sterilizationofliquidmedicine:sharpinstruments,

endoscopesandotherunsuitableinstrumentsforthermal

sterilization.

1.Thesolutionofthenewgerminalsolutionis30minutes,

oftenusedforthedisinfectionofblades,scissorsand

stitches.

70%alcohol,soakfor30minutesandusethesamepurposeas

thenewjuresolution.

10%formaldehydesolutionfor30minutes,suitablefor

sterilizationofureteralcatheter,plasticandplexiglass.

2.2%glutaraldehydeaqueoussolution,soakingfor10?30

minutes,isthesameasthenewjersolution,butthe

sterilizationeffectisbetter.

1.Thesolutionofbaptistery,whichismoreantibacterial,is

betterthanthenewone.

Formaldehydevaporfumigationmethod

2.Electrolytebalance,diagnosisandtreatment

Theelectrolytebalanceisregulatedbytheneuro-endocrine

system.Thetwosystemsworktogetherinthekidney,regulate

theabsorptionandexcretionofwaterandelectrolyte,thus

achievingtheelectrolytebalance.Divideintowaterandsodium

metabolicdisorder,potassiumabnormality,?

Diagnosisandtreatment

Metabolicdisorderofsodiumandwaterpermeability,suchas

lackofwaterWaterisproportionaltothelossofsodium,serum

sodiuminthenormalrange,extracellularfluidosmotic

pressureinthenormalrangeForreducedthevolumeof

extracellularfluid,withabalancedsaltsolutionorisotonic

salineaddedbloodvolumeassoonaspossible,eliminatethe

primarycause

Lowpermeabilityandwaterandsodiumareabsentatthesame

time,butlackofwaterislessthansodium.Therefore,the

serumsodiumislow,andtheextracellularfluidislowand

positivetodealwiththecauseofthedisease,andusesaline

solutionorhypertonicsalinedrip

Highpermeabilityofwaterwaterandsodiumlossatthesame

time,butlackofwatermorethansodiumdeficiency,sothehigh

serumsodium,extracellularfluidhashighpermeabilityassoon

aspossibletoremovethecause,notoralstatic5%glucose

injectionand5%sodiumchloride,supplementlostfluids.

WaterintoxicationCollectiveintowaterthandisplacement,

waterretentioninthebody,causebloodosmoticpressuredrop

andincreasebloodcirculationImmediatelystopwaterintake,

expelexcessmoisture,severedegreeofuseofdiuretics

Potassiumunusuallylowpotassium

Thenormalvalueofbloodpotassiumofbloodserumis3.5-5.5

mmol/Lbelowthisvalueindicatingthattheearlytreatment

ofhypokalemiaisthecauseoflowpotassiumblood,soasto

reduceandsuspendthepotassiumloss.Theamountofpotassium

inpotassiumwasreducedbypotassium,40to80mmol(KC13-6g).

Highinpotassium

Whenserumpotassiumwasmorethan5.5mmol/L,itwassaidthat

potassiumhyperkalemiawasusedtodeactivateallpotassium

drugsorsolutionstoreduceserumpotassiumconcentration.

Usingcationexchangeresin;hemodialysis

Calciumisunusuallylowincalcium

Serumcalciuminserumwasdeterminedtobelessthan2mmol/L

tocorrecttheprimarydisease,while10%calciumgluconateor

5%calciumchloridewasused

Highcalcium

Theserumcalciumintheserumishigherthan45mmol/L,mainly

duetohyperthyroidism,followedbybonemetastaticcarcinoma

3.Shock:(thecontentsofthetablearehelpfuland

understandable.)

Conceptisthebodyafterstrongpathogenicfactorsattack,due

totheeffectivecirculatingbloodvolumedecline,thebody

reservoirs,tissueischemiahypoxia,nerve-aclinical

syndromeofhumoralfactorsindisorder.Itsmain

characteristicsare:themicrocirculationirrigationinthe

importantorgantissue,themetabolicdisordersandthe

systemicdysfunction.Inshort,shockisaresponsetothe

decreaseofeffectivecirculatingbloodvolume,whichisthe

pathologicalprocessofmetabolicandcellulardamagecaused

byinsufficienttissueirrigation.Variousneuro-humoral

factorsareinvolvedintheoccurrenceanddevelopmentof

shock.

Hemorrhagicshockwascausedbyseverehemorrhage(suchas

uppergastrointestinalbleeding,ruptureofliverandspleen,

externalpregnancyandtraumatichemorrhage,etc.).Alarge

amountofplasmaloss(suchassevereburns)wascausedby

severeburnshock,mainlyduetothelossofalargeamountof

plasmasamplefluid.Dehydration(e.g.,acuteintestinal

obstruction,highlevelsofjejunalfistula,etc.).Dueto

severevomiting,alargeamountoffluidwaslost.(4)severe

trauma(suchasfracture,crushinjury,majorsurgery,etc.),

oftencalledtraumaticshock,inadditiontothemainreason

forthebleeding,tissueinjuryafteralargenumberoffluid

buildup,breakdownthereleaseoftoxinsandbacteria

pollution,nervousfactors,etc.,arethecauseofthedisease.

Septicshock(alsocalledtoxicshock)becauseoftheserious

bacterialinfections(suchassepsis,obstructivecholangitis

andperitonitis,etc.),seemoreatseveregram-negative

bacilli,alsovisibleYuGelanpositiveofbacteria,andmold,

virusesandrickettsialinfection.Accordingtoitsclinical

hemodynamicchangeintolowexhausttypehighresistance,low

power,decreaseincardiacoutputandperipheralvascular

contraction)andhighlowresistancetype(highpowertype,

increasedcardiacoutput,peripheralvascularexpansion)two

types.Lowerrowtypehighresistanceofshockinhemodynamic

changes,similartonormallowbloodvolumeshock,themain

characteristicsofhighranklowresistancetypeshockwas

closetonormalorslightlylowbloodpressure,cardiacoutput

closetonormalorslightlytall,reducedthetotalperipheral

resistance,centralvenouspressureclosetonormalorhigher,

arteriovenousdifferenceofoxygenpartialpressuretoreduce,

etc.(thefirsttwoaremostcommon)

CardiacshockDuetoacutemyocardialinfarction,severe

arrhythmia,cardiactamponade,pulmonaryembolism,decreased

leftventricularsystolicfunction,ordiastolicfillingisnot

enough,tohavedecreasedcardiacoutput.

Neurogenicshockiscausedbyintensestimulation(suchaspain,

trauma,etc.),whichcausesastrongneuroreflexivevascular

dilation,andthesurroundingresistanceisreducedandthe

effectivecirculationisrelativelyinsufficient.

Anaphylacticshockofcertainsubstancesanddrugs,foreign

bodyproteinandsoon,cancausethehumanbodytodevelop

allergicreactiontocausesystemicbloodvesselstoexpand

sharply,causingshock

Surgicalcommonshockislowbloodvolumemoreshock,traumatic

shock,inparticular,followedbysepticshock,insurgical

patientswithsuppurativecholangitis,diffuseperitonitis,

strangulationobstructionandburnsepsis

Microcirculationofpathophysiologicalchanges

1)microcirculationsystolic:whenasharpdropincirculating

bloodvolume,intravascularpressuredrop,themainarchand

thecarotidsinusbaroreceptorreflexthatmedullaoblongata

theheartcenter,vasomotorcenterandsympatheticnervous

excitement,ACTSontheheart,smallbloodvesselsandthe

adrenalglandandsoon,makestheheartbeatfasterincrease

cardiacoutput,adrenalmedullaandthesympathetic

postganglionicfibrereleasealargenumberofcatecholamine,

makethesurroundingskin,skeletalmuscle)andinternalorgans

(liver,spleen,etc.)ofsmal1bloodvesselsandcapillaries

smoothmuscle(includingcapillaryforwardaboutmuscle)

strongcontraction,arteriovenousshuntanddirectchannels

open.Theresultisthattheresistanceofthemicroarterial

isincreased,thebloodflowofthecapillaryisdecreased,the

bloodflowoftheveinismaintained,andthebloodpressure

remainsthesame.Themicrovascularareceptorinthebrainand

heartisless,sothecerebralarteriesandcoronaryarteries

arenotcontractingobviously,andthevitalorgansstillget

adequatebloodflow.Duetothedecreaseofbloodflowinthe

capillaryvessels,theinternalpressureofthebloodvessels

isdecreased,andtheexternalfluidofthebloodvesselscan

enterthebloodvesselsandthebloodvolumeispartially

compensated.Microcirculationsystoleistheperiodof

compensationforshock.

Microcirculationexpansionperiod:whenthemicrocirculation

bloodvolumecontinuestodecrease,

Changesinmicrocirculationwillfurtherdevelop.Prolonged,

extensivemicroarterialcontractions,arteriovenous

short-circuitanddirectaccesstothebloodflowof

capillariescontinuedtodecrease.Causedbyalackoftissue

perfusion,oxygenandnutrientscannotbebroughtintothe

organization,theorganizationofmetabolicdisorder,

resultingfromlackofoxygenmetabolismacidicsubstances

(suchaslacticacid,pyruvicacid,etc.),andisnotremoved

intime,makethecapillariessphincterbeforelosingto

catecholamineresponseability.Microarterialandcapillary-

anteriorsphincter.However,thesmallveinsofthecapillaries

havealargetolerancetoacidosisandarestillina

contractionstate,sothatalargeamountofbloodisstuckin

thecapillarynetwork,andthecirculationofbloodisfurther

reduced.Thehydrostaticpressureinthecapillarynetwork

increases,waterandsmallmoleculeplasmaproteinpermeates

bloodvessels,bloodconcentration,bloodviscosityincreases.

Atthesametime,whenthetissueisdeprivedofoxygen,the

mastcellsaroundthecapillariesarestimulatedbyhypoxiato

producealotofhistamine.Thecapillariesthatareinthe

stateofclosureareexpandedandevenallthecapillariesare

opensimultaneously.Inthisway,thevolumeofcapillarytube

increases,thebloodisdelayed,thebloodvolumeisdecreased,

thecardiacoutputisdecreasedfurther,andthebloodpressure

drops.

Microcirculationfailureperiod:stayintheblood

microcirculation,bloodviscosityincreasesduetotheforce

andacidicbloodhighcondensationcharacteristics,makethe

redbloodcellsandplateletsarepronetoaggregation,

capillariesinmicrothrombusformation,adiffuse

intravascularcoagulation,bloodperfusiontostop,increase

tissuehypoxia,makeintracellularlysosomaldisruption,

releasethesolubleenzyme.Dissolveproteinenzymeexcept

directlydigestproteins,alsocanbecatalyticproteinsto

formvariousexcitationpeptide,causecellautolysis,and

damageothercells,functionalandorganicdamageofdifferent

organs.Whenthecapillarytubeisblockedformorethanone

hour,themetabolismoftheinjuredcellstopsandthecell

itselfdies.

Insevereshock,multipleinternalorganfailurecanoccur,

whichiscalledmulti-organfailure.Thecauseofthe

occurrenceismicrocirculationdisorder.Theoccurrenceof

secondaryinjuryofinternalorgansandshockisclosely

relatedtothedurationofshock

Thebloodclottingofthelungiscausedbythemicrocirculation

ofthelungs,andthelackofoxygencausesthecellsinthe

capillariesandthealveolitobedamaged.Thepermeabilityof

bloodvesselwallincreased,andtheplasmainternal

macromoleculeexudedfromthebloodvessels,resultingin

pulmonaryinterstitialedemaandsubsequentalveolaredema.

Withredbloodcellscanentertheinterstitiallungalveoli,

alveolarepitheliumdamaged,alveolarsurfaceactive

substancesgenerateddecreases,thealveoliincreases,the

surfacetensionoftheliquidininterfacetoalveolaratrophy,

atelectasis,pulmonaryalveolusistransparentmembrane

formation.

Intheearlystageofrenalshock,theinsufficientcirculation

ofbloodandtheincreaseinthesecretionofantidiureticand

aldosteronecanproducerenalinsufficiency.Ifshocktimeis

short,aftertreatmentofbloodpressurerecovery,therenal

functioncanberestored.Iftheshocklastslonger,therenal

ischemiacantakemorethan3hours,andtherenalparenchymal

damagecanoccur,andacuterenalfailurecanoccurinsevere

cases.Shockcomplicatedwithacuterenalfunctionfailure,

besidesismainlycausedbyalackoftissuebloodperfusion,

andcertainsubstances(suchashemoglobin,myoglobin

depositioninrenaltubuleformationoftubetypemechanical

blockage,andtoxicsubstancesonthedamageofrenaltubular

epithelialcellsalso

Thediastolicperiodoccurredin80%ofcoronaryirrigation.

Thesmoothmuscleofthecoronaryarteryissuperiortobeta

-receptors.Duringtheperiodofshock,althoughtherewasa

largeamountofcatecholamineinthebody,thenarrowingofthe

coronaryarterieswasnotobvious,sotherewasnosignificant

decreaseinthebloodsupplyoftheheart.Duringtheperiod

ofshocksuppression,thecardiacoutputandaorticpressure

decreased,andthediastolicbloodpressuredecreased,sothat

thecoronaryarteryirrigationdecreasedandthemyocardial

hypoxiawasdamaged,causingthecardiacdysfunction.In

addition,hypoxemia,metabolicacidosisandhighblood

potassiumcanalsodamagetheheartmuscle.Cardiac

microcirculationthrombosiscancausethefocalnecrosisof

myocardiumandfurtherdevelopintoheartfailure.

Inliverandgastrointestinalshock,visceralvasospasmand

decreasedhepaticbloodflow,

Itcauseshepaticischemia,hypoxia,bloodstagnation,hepatic

sinusandmicrothrombosisinthecentralvein,causingnecrosis

ofhepaticlobulesandevenlargenecrosis,whichcandamage

the1iver.Livermetabolismanddetoxificationarenotcomplete,

leadingtoliverfailure.Gastrointestinalischemia,hypoxia,

causesmucousmucosahemorrhage,theintestinalmucosabarrier

functionisimpaired

Inthecaseofbrainshock,thearterialpressurewaslowand

thebloodflowdecreased.Thecontractionofthesmoothmuscle

ofthesmallarteriesinthebrainisaffectedbythechange

ofbloodcarbondioxidepartialpressureandph.Theincrease

inbloodflowtothebrainisincreasedwhenthecarbondioxide

partialpressureincreasesorthephdecreases.However,this

regulatingfunctionshouldhaveacertaincardiacoutputand

meanarterialpressure.Therefore,persistenthypotension

causedbycerebralbloodperfusionisinsufficient,makeglial

cellsaroundthecapillariesswelling,duetothecapillary

permeabilityincreaseatthesametime,theplasma

extravasationclearancetobraincells,causecerebraledema

andincreasedintracranialpressure.

Theclinicalperformanceoftheshockcompensatoryperiodwas

duetoacorrespondingcompensatoryabilityintheearlystage

ofthebody*sreductionintheeffectivecirculationofblood

volume,andthepatients，centralnervoussystemwaselevated

withexcitabilityandsympatheticadrenalaxisexcitability.

Itcanbeexpressedasnervous,excitedoragitated,paleskin,

coldlimbs,rapidheartrate,lowpulsepressure,fast

breathing,andreducedurinevolume.

Theshocksuppressionperiodischaracterizedbyapathy,

insensitivity,andevenconfusionorfainting.Cyanosisofcold

sweatandlip;Pulserate,bloodpressureprogressivedecline.

Whenserious,thewholebodyskin,themucousmucosais

obviouslyinthecyanosis,thelimbiscold,thepulseis

confused,thebloodpressureisnotmeasured,theurineisnot

evenurine,(seeP47table6-1)

4.Classificationofnarcoticmethods,thelimitedamountof

anesthetics,theperformanceandtreatmentprinciplesof

intoxicationandallergicreactions:

Clinicalanesthesiaclassification:generalgeneral

anesthesia(inhalationgeneralanesthesia,intravenous

anesthesia);Localanesthesia(surfaceanesthesia,local

infiltrationanesthesia,regionalblockandnerveblock);

Intrapleuralanesthesia(subarachnoidblock),epiduralblock

(epiduralanesthesia),andsacralobstruction;Compound

anesthesia;Basicanesthesia.Inadditiontoclinical

anesthesia,intensivetestingandtreatment,firstaidand

resuscitation,paintreatmentareallunderanesthesia.

Generaladministrationofanestheticsandtheir1imits:(P93

table8-6)

Procaine:suitableforinfiltratinganesthesia,concentration

of0.5%,adultlimitofIg/time

Tetracaine:suitableforsurfaceanaesthesia,common

concentrationof1%-2%,eyedrops0.5%to1%,adulttime1imit

surfaceanesthesia40mg,nerveblock80mg

Lidocaine:usedinvariousanesthesiamethods,commonlyused

inconcentrationsof0.25-0.5%,surface-anesthetic2%to4%,

nerveblock1%to2%,adultlimitedsurfaceanaesthesiaoflOOmg,

nerveblock,andinfiltrationanesthesia400mg

Bupivacaine:thenerveblockconcentrationis0.25-0.5%,which

issuitableforlaborandanalgesia.Theusualconcentration

is0.125%andtheadultlimitis150mg

Toxicreaction:

Performance:thepatientoftenexperiencedsymptomsof

narcolepsy,vertigo,multilingual,coldwar,panicand

disorientationduringmildtoxicity.Ifyoucontinuetodevelop,

youloseconsciousness,andthemusclesandlimbstremble,and

theseareoftentheprecursorsofconvulsions.Onceconvulsions

orconvulsionsoccur,itcanbefataltorespiratoryand

circulatoryfailureduetolackofrespiration.

Treatmentprinciple:thetreatmentshoulddeactivatethe

administrationofanestheticsimmediately,andsupport

breathingandcirculationfunctions,suchassupply,

artificialrespirationanduseofboostermedicine;

Anticonvulsioncanbestaticallystableorthiopentalsodium,

alsofeasibletrachealintubation.

Allergicreactions:

Performance:allergicreaction,abnormalreaction,rare.It

referstotheuseofasmallnumberofanestheticstodevelop

hives,laryngealedema,bronchospasm,hypotensionandvascular

neuroedema,orevenlife-threatening.

Treatmentprinciple:discontinuethemedicationfirst,keep

theairwayopenandtreatwithoxygen.Themaintenanceof

circulationstabilitydependsmainlyontheproper

replenishmentofbloodvolume.Incaseofemergency,theblood

vesselboostershouldbeselectedandthecorticosteroidsand

antihistaminesareused

5.Depthofburn,degreeofseverity,clinicalmanifestations,

prognosisandtreatmentprinciplesofdifferentdepths,

Calculationoftheareaofburnandtheamountofreplenishment:

Burndepthidentificationanditsclinicalmanifestationsand

prognosis:three-degreequartile

Theprincipleofclinicalperformanceprognosistreatment

Idegreesonlyhurtskinstratumcorneum,germinallayeralive,

regenerationability.SurfaceHongGongporphyritic,dryness,

burningsensationinthe3to7daysdesquamationheal,

short-termpigmentationIdegreeburnsjustkeepcleanand

smallareaofshallowdegreeburnscanbindupafterdebridement

ShallowIIdegreeofinjuryandmalpighianlayer,dermal

papillarylayer.Localrednessandswellingisobvious,with

differentsizesofblisters.Itcontainspaleyellowclarifying

fluid.Th