婦產(chǎn)科-7年制-化學(xué)物品

2020/11/251AcuteintoxicationCapital

university

of

medicalscience Xuan

wu

hospitalEmergency

DepartmentWang

jing2Case-1al

InformationMan，43

years

old，After

meals

2

hours（8pm)Dizzy（頭暈）,nausea,vomiting,weak,diarrheaVital

sign:

T:37°C,

P:48,

RR:17,BP:155/77mmHg202020/11/253Physical

ExaminationConscious:

clearConjunctiva（結(jié)膜）:not

pale,）Sclera（鞏膜）:not

icteric（Chest:

clear

breathing

sound;Heart:

no

murmurAbdomen:

soft

and

flat4prognosisAfter

6

hoursInstability

of

gait(步態(tài)不穩(wěn))Babbing（胡言亂語(yǔ)）Conscious

disturbance（意識(shí)）Deathafter

3

dayRespiratory

failureHeart

failureRenal

failure2020/1–1/25Bone

marrow

depressionImpression－intoxication八角蓮－江邊一碗水

Poisonous

site：rhizomeContent

:podophyllotoxin(鬼臼毒素)Toxic

symptom：abdominal

paindiarrheageneral

fatigueCNS

inhibition2020/11/25?evendeath。Whatispoison?2020/11/256What

is

poison?poisons

are

substances

that

cause

disturbancesto

organisms,

usually

by

chemical

reaction

orother

activity

on

the

molecular

scale,

when

aty

is

absorbed

by

an

organism.sufficientfour

states:solidliquidspraygas.2020/11/257For

example:poisonoussubstance?2020/11/258poisonoussubstancechemicalIndustry

mat.drugpesticideplantsanimals2020/11/259pharmaceutical

factorybromine(溴氣)divulge200people

intoxation2

12020/11/0globefish

poisoning味道鮮美，含有劇毒（神經(jīng)毒素），毒性比化鈉高一千倍我國(guó)2世紀(jì)就有關(guān)于河豚魚(yú)

的記載每年約50人1.

的明顯征兆：唇，舌和手指有輕微麻痹和刺感唇，舌和手指逐漸變得麻痹，隨即發(fā)生

，等癥狀，但存在知覺(jué)。說(shuō)話

，運(yùn)動(dòng)失調(diào)并肢端癱瘓。知覺(jué)喪失，呼吸麻痹導(dǎo)致

。2020/11/25112007江蘇金臺(tái)80

pupil

food-poisoning2020/11/25121994年冬和1995年春heavy

metal-Thallium

salt致死量鉈鹽后遺癥-全身癱瘓、雙目近乎失明、大腦萎縮、100公斤體重、基本語(yǔ)言能力喪失復(fù)旦

案---N-二甲基亞硝胺?，早上喝水，十點(diǎn)多，

、

、發(fā)。狀態(tài)，但病因仍不清楚燒。4月2日肝功能已經(jīng)出現(xiàn)損傷。4月3日血小板數(shù)量減少4月5日鼻4月8日陷入4月16日15時(shí)23分，

。2020/11/2514Poisoning

in

the

United

States2020/11/2515In

the

United

States

in

200532,691

poisoning

deathsdeath

<motor

vehicle

crashes35-54y>motor

vehicle

crashes.703,702

visits

EDCause ofpoisoning2020/11/2516Occupational

poisoningLife

poisoningAccidental

poisoningSuicidalAbuse

，addicthomicidesIntentionalandunintentionalIn

the

United

States

in

2005,32,691

poisoning

deaths23,618

(72%)

unintentional3,240

(10%)

undetermined

intent5,833

(18%)

intentional5,744

suicides89

homicides2020/11/25171.1-9.30

2005 Hang

Kong613

poisoned

Patients2020/11/25182020/11/25192020/11/2520AbsorptionIngest

by

mouthInhalation

（Powderdust、smoke、

）Skin

and

mucosa,muscle

orintravenous

injectionWound

(Insect stings

orbite)2020/11/2521metabolismspread

all

overbody

by

bloodliver

metabolismPoisonousnessPoisonousnessOxidationdeoxidize,hydrolyse,bonding2020/11/2522Elimination2020/11/2523breathe

out

by

respiratory

tract（gas，volatile

matter）Discharged

by

kidneyDischarged

by

alimentary

tractDischarged

by

skinDischarged

by

milkmechanismofaction2020/11/2524Local

effectPrevent

the

intake,

transportation

andutilization

of

oxygenInhibitory

enzyme

activityanesthetic

actionCompetition

receptorInterfere

physiologic

function

of

cell

ororganellesLocal

effectstrong

acid,strong

baseabsorptive

water

of

tissueProtein

and

fatdenaturationTissue

and

celldegeneration

and

necrosis2020/11/2525Prevent

the

intake,

transportationand

utilization

of

oxygencyanide

化物，hydrogen

sulfide硫化氫COcytochrome-oxydase2020/11/2526Cyanide---cytochrome-oxydasecompetitive

enzymeFluoride----Mg++2020/11/2527Inhibitory enzyme

activityInterfere

physiologic

functionofcell

or

organella2020/11/2528carbon

tetrachloride（CCl4）－－h(huán)epatocyte

(肝細(xì)胞)---deathPhenols(酚類(lèi))－－inhibiting

adenosinetriphosphate(三磷酸腺苷)The factor

of

influencetoxic

action2020/11/2529Physico-chemical

property

of

poisonfine

particle, solubility,

evaporabilitySusceptibility

of

individualsex,

age,nutrition

statushealth

statusliving

habitClinical

feature2020/11/2530Skin

and

mucosaeyeCentral

nervous

systemRespiratory

systemCirculatory

system

—arrhythmia

,cardiacarrest

,shockUrinary

systemBlood

systemDiagnosisHistorySign

and

symptomconscious

statebreathingheart

rateblood

pressurepupil,

skin

,

mucosa2020/11/253Laboratory

examination2020/11/2532Detection

ofpoison:blood,

gastric

juice

and

urineBlood

,urine

examinationManagement

principleRescueLifeGet

rid

of

the

environmentPrevent

absorptionElimination

poisonSpecific

antidotesHeteropathyPrevent

Complication2020/11/25decontaminationEmeticGastric

lavageActivated

carbon

adsorptionCatharsisWhole-bowel

irrigation2020/11/2534Specific

antidotesOrgnaophosphorus

-----Pralidoxime

，AtropineBenzodiazepines－－Flumazenil（氟

）Morphine－－NaloxoneIsoniazid－－vitamin

B62020/11/2535Eliminate

poisonForced

diuresis

強(qiáng)化利尿Blood

purification（血液凈化）hemodialysis

HD（血液透析）hemoperfusion,HP（血液灌流）plasmaexchange

PE（血漿置換）High

pressure

oxygen

高壓氧2020/11/256Case-2NameChart

No.AgeSexLin55676872Y/OMansent

by

AmbulancePR

68 RR

17 BP

95/552020/11/2538ChiefComplaint2020/11/2539Drink

Dimethoate(樂(lè)果):20-40mlAnd

some

unknown

drugPresentIllnessNausea/

vomitingGarlic-lik

rPast

/

Drugs

HistoryDrug

allergy

(-)deny

any

disease2020/11/2540Physical

Examination2020/11/2541ConsciousnessHead

&

NeckEyedrowsy(嗜睡)softpupil

1.5/1.5

L/RChestAbdomenExtremitycoarse

BS

and

moist

ralessoft,

no

tendermovable,

warmImpression2020/11/2542organophosphate

intoxicationAcuteOrganophosphateintoxicationPHARMACOLOGYAbsorption:

by

any

routestransdermaltransconjunctivalinhalationthrough

gastrointestinal

tractparenteralPHARMACOLOGYMetabolism:

vialiver

to

anactive form:

indirect

actingagent

ex:

Parathion

→

Paraoxonto aninactive

form:

most

agentsOnset

of

toxicology

depends

on:routedegree

of

exposurefat

solubilityaffinity

tothecholinesterase

activesitedirect

or

indirect

effectMECHANISMInhibition

of

cholinesteraseAccumulation

and

prolonged

effect

ofAcetylcholineMECHANISMSites:Parasympathetic（副交感神經(jīng)）:

ganglionic（神經(jīng)節(jié)）

nicotinicsitespostganglionic（節(jié)后）

muscarinic

sitesSympathetic:

ganglionic

nicotinic

sitesskeletal

muscle(N-M

junction):

nicotinicsitesCNS

sites2020/11/25482020/11/25CENTRAL

NERVOUS

SYSTEMACh

Skeletal

Muscle(nic)SomaticEfferentsystemACh(nic)ACh(nic)ACh(nic)NAACh(mus)ACh(nic)Blood

vesselsetcSweatGlandsAdrenalmedullaSympatheticsystemACh

Salivary

glands(mus)

etcPara-sympatheticsystem

492020/11/2550交感神經(jīng)副交感神經(jīng)循環(huán)

心跳加快大部血管縮心跳減慢部分血管舒呼吸支氣管平滑肌舒支氣管平滑肌縮粘液消化粘稠唾液，抑制胃腸運(yùn)動(dòng)抑制膽囊收縮促進(jìn)括約肌收縮泌尿尿肌舒，括約肌縮，稀薄唾液促進(jìn)胃腸運(yùn)動(dòng)促進(jìn)膽囊收縮使括約肌舒張

尿肌縮，括約肌舒眼瞳孔擴(kuò)大，睫狀肌松弛瞳孔縮小，睫狀肌縮皮膚

豎毛肌收縮，汗腺代謝

促進(jìn)糖元分解，促進(jìn)胰島素促進(jìn)腎上腺髓質(zhì)CLINICAL

FEATURESGeneral

considerations

:within

minutes

to12hourslow

dose:

muscarinic

symptoms

severe

intoxication:

nicotinic

and

CNSmaypredominantrancid

odor: clothing,

breath,

or

evenvomitussymptoms

to

appear

varywithroutesCLINICAL

FEATURESMuscarinic

effects:within

minutesSLUDGE:泥濘的S=Salivation(流涎)L=Lacrimation（流淚）U

=UrinationD

=DiarrheaG=GI

cramps（絞痛）E=EmesisCLINICAL

FEATURESMuscarinic

effects:Other

effects:Miosis:

in

the

early

stage→mydriais

may

occur

laterBradycardiac.Bronchorrhea（

物增多）d.Bronchonstriction（支氣管收縮）CLINICAL

FEATURESNicotinic

effects:appear

after

muscarinic

effectsmoderate

to

severeintoxicationMTWtHF:星期一到星期五M

=Muscle

cramps(肌痙攣)T

=TachycardiaW

=WeaknesstH

=HypertensionF

=Fasciculations（肌束震顫）CLINICAL

FEATURESS

effects:non

specificconfusionagitation（煩躁）lethargy（昏睡）seziure（驚厥）comaCLINICAL

FEATURESCauses

ofdeath:Muscarinic

effects:a.Excessive

pulmonary

secretionsb.Bronchoconstrictionc.Pulmonary

edemaNicotinic

effects:Respiratory

muscle

paralysis（麻痹）CNS

effects:Respiratory

center

depressionCLINICAL

FEATURES6.Delayed

organophosphate

toxicity(1)Intermediate

syndrome(IMS):a.Onset:1-4

daysb.Symptoms:→proximal,truncal

and

neck

flexormuscle

weakness→decreaseddeeptendonreflexes（腱反射）→cranial

nerve

palsies(顱神經(jīng)麻痹)→respiratory

depression→no

sensory

lossCLINICAL

FEATURES(1)

Intermediate

syndrome(IMS):c.Diagnosis:EMG→N-M

junctiondysfunctiond.Recovery:1-3

weekse.OPs

associated

with

IMS:Bidrin,

Demethoate,

Diazinon,Malathion,

Methamidophos,Monocrotophos,Parathionf.may

be

due

to

inadequate

oximetherapyCLINICAL

FEATURES6.Delayed

organophosphate

toxicity(2)Peripheral

neuropathy（周?chē)窠?jīng)病變）a.Onset:2-3

weeksb.Symptoms:distal

motor

polyneuropathy（遠(yuǎn)端多神經(jīng)?。ヽ.due

to

inhibition

of

neurotoxicesterase(NTE)→a protein

innervous

systemLABORATORYDonotwaitforcholinesterase

（膽堿酯酶）levels

to

startdetect

cholinesterase

levelsRBC:20-46

micromol/literPlasma:20-61

micromol/literPercentage

of

normalSymptoms>50%No

symptoms20-50%Mild10-20%Moderate<10%SevereLABORATORYRBCPlasmaAdvantageBetter

reflectionEasier

to

assay,decline

fasterSiteCNS,RBC,muscleCNS,plasma,liverRegeneration(untreated)1%

/

day25-30%

in

7-10

daysNormalization(untreated)35-49

days28-42daysUseUn ed

priorexposure

withelevated

plasmaAchEAcute

exposureFalse

depressionPernicious

anemiaHemoglobinopathyAntimalarial

txLiver

cirrhosisMalnutritionDrugs(succinylcholine,codeine)PregnancyDiagnosisHistorygarlic-likr（蒜臭味）typical

symptom：

Pupil

size

small,

mucussecretion，GI、

a。Laboratory

examination：serumcholinesterase,Organophosphatemetabolic

product。Atropine

test：1-2mg---atropinization2020/11/2562Differential

diagnosispoisonous

mushroomglobe

fish(河豚魚(yú))poisonacute

gastroenteritis-AGEHeatstrokeHypnotic

intoxicationPesticide

intoxication2020/11/2563TREATMENT1.Initial

management:(1)

Decontamination（排污）:a.Avoid

further

exposureb.Protection:

gowns

and

glovesc.Irrigation:

ocular

and

dermalexposured.Remove

and

discard

clothingTREATMENTInitial

management:Stabilization:ABC’s:

airway

protection

mostcommonly

neededOrogastric

lavage

or

NG

tube:

if

liquidingestion

and

pthas

not

vomited

yetIV

accessfor

antidotes

and

fluidsTREATMENT2.Antidotes(1)

Atropine:a.effect:→competitive

inhibition

of

Ach

atmuscarinic

receptors

in

smooth

musclesand

CNS→No

effect

on

nicotinic

receptor(N-M

junction):can’t

reverse

muscleweaknessb.bronchor

rhea→hypoxi

hycardia→more

atropinTREATMENTc.Dosage:

depends→initially:0.5-1.0

mg

IV

in

adults(0.01

mg/kg

in

children)→continous

infusions

to

maintain

adequatesecretion

control→atropinization:

mydriais

and

tachycardiad.end

point

of

therapy:

drying

of

secretione.observation

for

at

least

24hoursTREATMENT2.Antidotes:(2)

Pralidoxime

(2-PAM,Protopam)a.effect:

forma

complex

of

PAM-OP-AchE→PAM-OP

released

from

complex→AchE

reactivation→metabolize

Achb.decreases

atropine

effectc.treatmentas

early

as

possible→decreased

effect

after

36-48

hrsexposure→aging

effectTREATMENT(2)

Pralidoximed.dose:→adult:1-2

gms

IV

over

15-30

minutesthen

q6-12

hrs