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1、acute toxicitycapital university of medical science xuan wu hospitalemergency departmentcontents background general introduction acute organophosphate poisoning acute carbon monoxide poisoning acute sedatives-hypnotics poisoning alcohol intoxication /withdrawalbackground there are about 9000000 kind

2、s of chemicla people have many opportunity to touch with poisonbackgroundthere are 1751476 poisoning pts in usa in 1993poison control center(pcc) is established in chicago 1953。major duty: 1. component of poison; 4.information2. dangerous 5. toxicology3. first aid 6. general knowledge of preservatio

3、nbackground countryside city。 countryside-pesticide intoxication。 city-food-poisoning, carbon monoxide poisoning ,hypnotic intoxication。 establish pcc in beijing,shanghai ,shenyang what is poison? a poison is anything someone eats ( ingestion), breathes (inhalation) , gets in the eyes (ocular exposu

4、re), or on the skin (dermal exposure) ,that can cause sickness or death if it gets into body or on the body. poison can be found in four forms: solid, liquid, spray and gas.general introduction toxic substance : drug ,chemical , bad food and so on. acute poisoning:short time, large dose chronic pois

5、oning :long time、 small doseetiopathogenisis and pathogenesy cause of a poisoning occupational poisoning life poisoningnaccidental poisoning , nsuicidalnabuse ,addication , homicdalpathogenesy-absorption by mouth; inhalation (powder dust、smoke、steam), skin mucosa, muscle or intravenous injection rec

6、tum 、 urinary canal、female sheath vagina、bladder、peritoneum、eye insect stings or bitepathogenesis - metabolism spread all over body by blood liver metabolismpoisonousnesspoisonousnessoxidation,deoxidize, hydrolyse, bondingpathogenesis - eliminate breathe out by respiratory tract(gas,volatile matter)

7、 discharge by kidney discharge by alimentary tract skin milk 1.local effect強酸、強堿強酸、強堿吸收組織水分吸收組織水分與蛋白質脂肪結合與蛋白質脂肪結合組織細胞變性壞死組織細胞變性壞死2.hypoxia 1)inhibition respiratory function:2)change blood constituent3)inhibition cells respiratory :cyanide,hydrogen sulfide4)destroy cardiovascular function1)1)破壞酶蛋白質部分

8、的金屬或活性中心破壞酶蛋白質部分的金屬或活性中心氰化物抑制細胞色素氧化酶氰化物抑制細胞色素氧化酶fefe+;一一氧化碳抑制細胞色素氧化酶氧化碳抑制細胞色素氧化酶fefe+從而破從而破壞酶蛋白質分子中的金屬,使細胞發(fā)生壞酶蛋白質分子中的金屬,使細胞發(fā)生窒息窒息2)2)毒物與基質競爭同一種酶而產生抑制作毒物與基質競爭同一種酶而產生抑制作用用, ,丙二酸結構與琥珀酸相似,抑制三丙二酸結構與琥珀酸相似,抑制三羥酸循環(huán)中琥珀酸脫氫酶羥酸循環(huán)中琥珀酸脫氫酶3.inhibitory enzyme activity3)3)與酶的活性劑作用:與酶的活性劑作用:氟化物與氟化物與mgmg+形成復合物,使形成復合物,

9、使mgmg+失去激活磷酸葡萄失去激活磷酸葡萄糖變?yōu)槊傅淖饔锰亲優(yōu)槊傅淖饔?)4)去除輔酶:去除輔酶:鉛中毒時,造成煙酸的鉛中毒時,造成煙酸的消耗增多,使輔酶消耗增多,使輔酶i i和輔酶和輔酶iiii減少,抑減少,抑制了脫氫酶的作用制了脫氫酶的作用5)5)與基質直接作用:與基質直接作用:氟乙酸直接與檸氟乙酸直接與檸檬酸相結合形成氟檸檬酸,阻止三羧酸檬酸相結合形成氟檸檬酸,阻止三羧酸循環(huán)的繼續(xù)進行循環(huán)的繼續(xù)進行 organophosphate poisoning,可抑制體內的,可抑制體內的膽堿酯酶,使組織中乙酰膽堿過量積蓄,引膽堿酯酶,使組織中乙酰膽堿過量積蓄,引起一系列以乙酰膽堿為傳導介質的神經

10、處于起一系列以乙酰膽堿為傳導介質的神經處于過度興奮狀態(tài),最后則轉為抑制過度興奮狀態(tài),最后則轉為抑制carbon tetrachloride poisoning,首先作用于,首先作用于cnscns,使之產生交感神經沖動,體內產生大量使之產生交感神經沖動,體內產生大量單胺類物質,使內臟血管收縮引起供血不足,單胺類物質,使內臟血管收縮引起供血不足,中毒數(shù)小時后可出現(xiàn)肝、腎損害中毒數(shù)小時后可出現(xiàn)肝、腎損害 4.dromotropism medium1. 一氧化碳與氧競爭血紅蛋白,而一氧化碳與氧競爭血紅蛋白,而形成碳氧血紅蛋白,破壞了正常的形成碳氧血紅蛋白,破壞了正常的輸氧功能輸氧功能2.2. 異煙肼與

11、維生素異煙肼與維生素b b及煙酸的結構相及煙酸的結構相似,因此,異煙肼在體內可與維生似,因此,異煙肼在體內可與維生素素b b競爭,而取代其作用,因而引競爭,而取代其作用,因而引起中毒起中毒5.competition receptor6.interfere cell or organella physiologic function carbon tetrachloride(ccl4)chcl3(trichlormethane)肝細胞膜中的肝細胞膜中的unsaturated fatty acidlipid peroxidationmitochondria(線粒體線粒體)、endoplasmic

12、reticulum(內質網內質網)變性變性hepatocyte(肝細胞肝細胞)death phenols(酚類酚類)線粒體內線粒體內oxidative phosphorylation(氧化磷酸化氧化磷酸化) uncoupling(解偶解偶聯(lián)聯(lián))inhibiting adenosine triphosphate(三磷三磷酸腺苷酸腺苷) synthesis(合成合成)、store(貯存貯存)。the factor of influence toxic action physico-chemical property of poison fine particle,solubility,evapor

13、ability susceptibility of individual sex,age, nutrition, health status, living habit diagnosis poisoning history sign and symptom conscious state breathing heart rate blood pressure pupil, skin , mucosalaboratory examination detection of poison: blood, gastric juice and urine blood ,urine examinatio

14、ntherapeutic principlecprget rid of the environmentdecrease absorptionspecific antidotes cleaning poison in gastrointestinal tractheteropathyprevent complicationemergent management breathing support circulation support treatment coma treatment convulsionspecific antidotesorgnaophosphorus -pralidoxim

15、e iodide,atropinebenzodiazepinesflumazenilpain -killernaloxoneisoniazidvitamin b6eliminate poison emetic gastric lavage activated carbon adsorption catharsis whole-bowel irrigationemetic壓舌板、刺激咽后壁壓舌板、刺激咽后壁飲溫水飲溫水200-300ml200-300ml吐根糖漿吐根糖漿+200ml+200ml水水休克、意識不清休克、意識不清禁用禁用攝入腐蝕性毒物攝入腐蝕性毒物-禁用禁用purpose of ga

16、stric lavageeliminate poison in gastric, prevent absorbpreparation for operation or some examinationindication and contraindication indication non-corrosive poison contraindication corrosive poisonstrong acid ,baseesophageal varix, aneurysm of aortasevere heart disease,upper gastrointestinal bleedin

17、g,gastric perforationprinciple of gastric lavage一般毒物的洗胃原則一般毒物的洗胃原則 一次性徹底洗胃一次性徹底洗胃(10000-20000ml)、)、停止洗胃標準為無色無味。停止洗胃標準為無色無味。有機磷中毒的洗胃原則有機磷中毒的洗胃原則 首次足量首次足量 20000-30000ml 持續(xù)胃腸減壓持續(xù)胃腸減壓 留置胃管接胃腸減壓器留置胃管接胃腸減壓器 反復少量洗胃反復少量洗胃 2000-5000ml/1-2h洗胃的操作步驟洗胃的操作步驟洗胃步驟:洗胃步驟: 1.先將胃內容物盡量抽盡先將胃內容物盡量抽盡 2. 灌入灌入300-500ml洗胃液洗胃液

18、 3. 再排出灌入液體再排出灌入液體 4. 反復灌洗直到洗胃液純清無味反復灌洗直到洗胃液純清無味 注意事項注意事項: 1. 洗胃液每次進入不宜過多,進出要平衡。洗胃液每次進入不宜過多,進出要平衡。 2. 洗胃液性質盡可能視毒物而定,液溫洗胃液性質盡可能視毒物而定,液溫37 3. 掌握適應癥與禁忌癥掌握適應癥與禁忌癥 洗胃要注意和觀察的幾個問題洗胃要注意和觀察的幾個問題 洗胃與胃出血的關系洗胃與胃出血的關系 少量可給保護胃少量可給保護胃粘膜藥,大量停止洗胃、持續(xù)胃腸減壓粘膜藥,大量停止洗胃、持續(xù)胃腸減壓觀察出血情況觀察出血情況 洗胃時要密切觀察生命體征、腹部情況、洗胃時要密切觀察生命體征、腹部情

19、況、洗出液的性質洗出液的性質catharsis and whole-bowel irrigation 硫酸鈉硫酸鈉-15-20+水水200口服口服 硫酸鎂硫酸鎂-15-20+水水200口服(引起高血鎂)口服(引起高血鎂) 20%甘露醇甘露醇250胃管內灌入胃管內灌入-1小時腹瀉、小時腹瀉、3小時排空。小時排空。 1%鹽水、肥皂水鹽水、肥皂水5000-高位連續(xù)灌腸清高位連續(xù)灌腸清洗洗 活性炭加入灌腸液,促進毒物吸附排出活性炭加入灌腸液,促進毒物吸附排出 eliminate poison forced diuresis 強化利尿強化利尿 blood purification(血液凈化)血液凈化)

20、hemodialysis hd(血液透析)血液透析) hemoperfusion,hp(血液灌流)血液灌流) plasma exchange pe(血漿置換(血漿置換) high pressure oxygen 高壓氧高壓氧hemodialysis hd血液透析血液透析 機理:血液經體外循環(huán)進入透析器,通過透析機理:血液經體外循環(huán)進入透析器,通過透析膜和透析液之間形成的膜和透析液之間形成的溶液濃度梯度溶液濃度梯度,促使血,促使血液內液內溶質彌散溶質彌散至透析液內。至透析液內。 可透析毒物的性質:可透析毒物的性質:water-solubility水溶性、水溶性、heavy metals, 生物性

21、毒物。生物性毒物。 種類:蛇毒、魚膽、利眠寧、種類:蛇毒、魚膽、利眠寧、diamorphine海海洛因洛因、撲熱息痛、撲熱息痛、isoniazid異煙肼異煙肼、aminoglycosides氨基糖甙類、氨基糖甙類、arsenic砷、砷、mercury汞等。汞等。hemoperfusion hp血液灌流血液灌流 機理:血液流經灌流器,血液中的毒物機理:血液流經灌流器,血液中的毒物被吸附到具有廣大表面積的吸附劑上。被吸附到具有廣大表面積的吸附劑上。 吸附劑:活性炭、合成樹脂吸附劑:活性炭、合成樹脂 毒物性質:脂溶性、大分子化合物、易毒物性質:脂溶性、大分子化合物、易與血漿蛋白結合的藥物、毒物。與血

22、漿蛋白結合的藥物、毒物。 種類:安定類、苯巴比妥類、抗抑郁類、種類:安定類、苯巴比妥類、抗抑郁類、有機磷類、伴有肝衰竭、腎衰竭者。有機磷類、伴有肝衰竭、腎衰竭者。plasma exchange pe血漿置換血漿置換 機理:將血液引入血漿分離器中,使血機理:將血液引入血漿分離器中,使血細胞與血漿分離,棄去全部血漿,注入細胞與血漿分離,棄去全部血漿,注入新鮮血漿和平衡液。新鮮血漿和平衡液。 毒物性質:與血漿蛋白結合率高(大于毒物性質:與血漿蛋白結合率高(大于60%)acute organophosphate poisoningacute organophosphate poisoning feat

23、ure :毒性大、起病快毒性大、起病快;發(fā)病迅速;發(fā)病迅速;中毒途徑多;診斷要快、準確;搶救及中毒途徑多;診斷要快、準確;搶救及時。時。 classify 分類:分類: 劇毒、高毒、中毒、低毒劇毒、高毒、中毒、低毒 acute organophosphate poisoning etiopathogenisis :accidental suicide pathogenesis : poison metabolism mechanism acute poisoning;chronic poisoningorganophosphate absorption: readily distributio

24、n: blood brain barrier metabolism: in the liver elimination: primarily in the urine half-life : 4 hoursmechanism 體內膽堿能神經的化學介質體內膽堿能神經的化學介質-乙酰膽堿乙酰膽堿 交感、副交感神經節(jié)前纖維交感、副交感神經節(jié)前纖維 副交感神經節(jié)后纖維副交感神經節(jié)后纖維 橫紋肌的運動神經橫紋肌的運動神經-肌肉接頭肌肉接頭 交感神經節(jié)后纖維(交感神經節(jié)后纖維(支配淚腺、血管平滑支配淚腺、血管平滑肌)?。?中樞神經系統(tǒng)中樞神經系統(tǒng)膽堿能神經末梢膽堿能神經末梢-膽堿酯酶膽堿酯酶central

25、 nervous systemach(nic)skeletal muscleach(nic)ach(nic)ach(nic)ach(nic)na ach(mus) ach(mus)blood vessels etcsweat glandsadrenal medullasalivary glandsetcpara-sympathetic systemcholine receptor muscarinic receptor(m-r)毒蕈堿 n heart : restrainnblood vessel:dilatationn smooth muscle:contractnsphincter pup

26、illae muscle: contractncontractglandular organ:secrete nicotinic receptor(n-r) 煙堿n1-r:gangliocyte;ganglioneureexcited n2-r:skeletal musclecontract急性有機磷中毒急性有機磷中毒-機理機理 有機磷毒物與有機磷毒物與膽堿酯酶膽堿酯酶acetylcholinesterase(ache)結合,形結合,形成磷?;憠A酯酶,失去水解活性,成磷酰化膽堿酯酶,失去水解活性,造成造成乙酰膽堿乙酰膽堿acetylcholine蓄積蓄積產生產生毒蕈堿毒蕈堿(m)樣、樣、煙堿

27、煙堿(n)樣癥狀樣癥狀和和中樞神經中樞神經系統(tǒng)的癥狀。系統(tǒng)的癥狀。the organophosphates are powerful inhibitors of carboxylic ester hydrolases, including acetylcholinesterase (found in nervous tissues and erythrocytes) and butyrylcholinesterase (plasma or pseudocholinesterase). as a result of this enzyme inhibition, the substrate ac

28、etylcholine accumulates急性有機磷中毒急性有機磷中毒-機理機理 中樞神經系統(tǒng):腦內中樞神經系統(tǒng):腦內ach含量增高含量增高-大腦大腦多部位先興奮后抑制。多部位先興奮后抑制。驚厥、呼吸中樞驚厥、呼吸中樞抑制。抑制。 神經神經-肌肉接頭:神經肌肉接頭:神經-肌肉接頭的傳遞肌肉接頭的傳遞阻斷,導致肌無力和肌麻痹。阻斷,導致肌無力和肌麻痹。 呼吸系統(tǒng):呼吸肌麻痹、氣道分泌物阻呼吸系統(tǒng):呼吸肌麻痹、氣道分泌物阻塞。塞。急性有機磷中毒急性有機磷中毒-機理機理 循環(huán)系統(tǒng):循環(huán)系統(tǒng): * 對心臟直接毒性對心臟直接毒性:心動過緩、心肌收縮力:心動過緩、心肌收縮力降低、各種心律失常降低、各種

29、心律失常 *抑制交感心血管中樞抑制交感心血管中樞:外周血管擴張、血:外周血管擴張、血壓下降。壓下降。 *興奮心血管迷走中樞:興奮心血管迷走中樞:心動過緩、心肌收心動過緩、心肌收縮力降低、血壓下降??s力降低、血壓下降。 神經節(jié)、腺體、平滑?。合袤w分泌增加、腸蠕神經節(jié)、腺體、平滑?。合袤w分泌增加、腸蠕動增加。動增加。中毒途徑及特點中毒途徑及特點 呼吸道吸收:呼吸道吸收:有機磷沸點低、易揮發(fā),有機磷沸點低、易揮發(fā),易從呼吸道吸收易從呼吸道吸收,30min發(fā)病。發(fā)病。 消化道吸收:消化道吸收:吸收快、吸收快、10min2h發(fā)病。發(fā)病。 皮膚黏膜吸收:皮膚黏膜吸收:有機磷是脂溶性,能透有機磷是脂溶性,能

30、透過皮膚黏膜入血,潛伏期長、過皮膚黏膜入血,潛伏期長、26h發(fā)病。發(fā)病。 主要致死因素:呼吸衰竭主要致死因素:呼吸衰竭symptoms and signs muscarinic: sludge, bronchorrhea, bradycardia and miosis. nicotinic: muscle weakness, fasciculation or paralysis tarchycardia, bronchodilation, mydriasis. cns: restless, drowsy, confusion, tremor, ataxia, delirium, seizure

31、, coma.muscarinic effects 毒蕈堿毒蕈堿(m)urinationmiosisbronchospasmemesislacrimationsalivationbradycardia hypotension尿頻、尿失禁尿頻、尿失禁縮瞳,視力模糊縮瞳,視力模糊氣管痙攣,分泌增加氣管痙攣,分泌增加嘔吐、腹瀉、腹痛嘔吐、腹瀉、腹痛流淚、流淚、流汗、流口水流汗、流口水肺水腫肺水腫心跳減慢,心跳減慢,血壓下降血壓下降nicotinic manifestations .muscular twitching, fasciculation , tachycardia, hypertensio

32、n central nervous system manifestations: headache頭痛頭痛, drowsiness 昏睡昏睡, confusion 意識混亂意識混亂, slurred speech言語不清言語不清, emotional lability 情感不穩(wěn)情感不穩(wěn), , ataxia 共濟失調共濟失調, tremor 震顫震顫, delirium 精神錯亂精神錯亂, seizure 癲癇癲癇. restrain center of breath and circulatedegree slight :che 50-70%。 muscarinic symptom and s

33、ign; midrange : che 30-50%, muscarinic symptom and sign, nicotinic effects heavy: che 30%, muscarinic, nicotinic ,central nervous system symptom and signdelayed neuropathy 急性中毒癥狀消失后急性中毒癥狀消失后2-3周周 motoriusthe lower limbs palsy麻痹麻痹, amyotrophy肌萎縮肌萎縮 nerve fibrofatty degeneration, nerve cell demyelinat

34、e脫髓鞘脫髓鞘 有機磷有機磷抑制抑制神經病靶酯酶(神經病靶酯酶(neuropathy target esterase ,nte)delayed neuropathy stages progression :sense neuropathy stable phase:sensory disability last 312 month :618 month motor function partly or complete recovery,spasm, motor nerve functional disturbance。intermediate syndrome 發(fā)生在急性中毒恢復后發(fā)生在急性

35、中毒恢復后14天天 癱瘓(頸屈肌、腦神經支配的肌肉、肢癱瘓(頸屈肌、腦神經支配的肌肉、肢體近側肌、呼吸?。w近側肌、呼吸?。?418天緩解天緩解 嚴重者呼吸衰竭嚴重者呼吸衰竭 神經肌肉接頭處突觸后功能障礙神經肌肉接頭處突觸后功能障礙laboratory examination serum cholinesterase organophosphate metabolic product othersdiagnosis history garlic-like odorgarlic-like odor蒜臭味蒜臭味 typical symptom: pupil sizepupil size small

36、, small, 胃胃腸道腸道 癥狀、癥狀、coma。 laboratory examination: serum cholinesterase, organophosphate metabolic product。 atropine test:1-2mg-atropinizationdifferential diagnosis muscarinic poison globe fish poison acute gastroenteritis;age heatstroke hypnotic intoxication pesticide intoxicationtherapeutic princ

37、ipleget rid of the environment cannot use the hot watereliminate the poison queasy、 gastric lavagespecific antidotes atropine、pamheteropathy oxygen therapy、diuresisemergency management airway breathing cardiopulmonary resuscitation;cpr cns:convulsion use valium and phenobarbital,forbid use succinylc

38、holine or morphine。 cerebral edema:mannitol、 glucocorticosteroid pneumonedema: atropine,aminophylline and morphine cant be usespecific antidotes cholinesterase resurrecter膽堿酯酶復活膽堿酯酶復活劑劑n樣癥狀效果好樣癥狀效果好 碘解磷定碘解磷定(pyraloxime methoiodide) 氯磷定(氯磷定(pyraldoxime methylchloride) atropine, block muscarinic recep

39、tors, causing inhibition of all muscarinic functions. early , enough, association, repetitions阿托品類生物堿阿托品類生物堿-莨 菪 堿顛茄曼佗羅the effect of atropine atropine poisoning1. blurred vision2. confusion3. restlessness4. coma;5. constipation6. urinary7. retention atropinization1. mydriasis2. tachycardia3. blushin

40、g4. skin and mucousdry 5. dry6. crackles disappearsymptomatic treatment keeping water-electrolyte and acid-base balance prevention and cure pulmonary infection make use of sedative plasmapheresis prevention and cure intermediate syndromeacute carbon monoxide poisoningacute carbon monoxide poisoning

41、無色、無臭、不溶于水的窒息性氣體無色、無臭、不溶于水的窒息性氣體 比重:比重:0.967 含碳物質不完全燃燒產生的氣體含碳物質不完全燃燒產生的氣體 空氣中最高允許濃度空氣中最高允許濃度0.05%或或30mg/m3 吸入過量可發(fā)生急性中毒吸入過量可發(fā)生急性中毒acute carbon monoxide poisoning濃度,濃度,暴露時間,暴露時間,min 癥狀癥狀0.0005 100 無明顯癥狀無明顯癥狀0.003 360 對中樞神經有害對中樞神經有害0.04-0.05短時間短時間 呼吸困難呼吸困難0.05-0.1短時間短時間 頭痛、暈眩頭痛、暈眩0.1-0.2 短時間短時間 短時間內死亡短

42、時間內死亡1 短時間短時間 立即死亡立即死亡acute carbon monoxide poisoning etiology livingpoisoning burn coalwater-heateroccupational poisoningmisoperationno protectionaccidental poisonincoal mineaccidentsuicidalhomicdalmechanismco+hb cohbco+fe+ restraint cell respirationcant carrying oxygenhypoxiaco+hbo2+hb=260co-hbo2-

43、hb=36001clinical manifestation slight: hbco10-20%,頭痛、眩暈、心悸、惡心、嘔吐、短暫暈厥。吸空氣可好轉。 midrange: hbco30-40%,昏迷、虛脫。皮膚櫻桃紅。吸空氣或高壓氧可很快清醒,數(shù)日恢復,不留后遺癥。 heavy:hbco50%,深昏迷、各種反射消失、瞳孔散大、血壓下降呼吸抑制。嚴重者昏迷數(shù)天出現(xiàn)臟器功能障礙。臨床表現(xiàn)-遲發(fā)腦病 意識障礙恢復后 經過2-60天的“假愈期” 3%-10%病人出現(xiàn)腦病: 神經意識障礙:癡呆、譫妄、去皮層狀態(tài)。 錐體外系神經障礙:震顫麻痹綜合征。 錐體系神經損害:偏癱、病理反射(+) 大腦皮層局灶

44、性功能障礙:失語、失明、繼發(fā)癲癇。laboratory examination 血血cohb測定:特異性、判斷嚴重程度測定:特異性、判斷嚴重程度 動脈血氣分析動脈血氣分析 腦電圖:彌漫性低波幅慢波腦電圖:彌漫性低波幅慢波 頭部頭部ct:具有鑒別診斷意義具有鑒別診斷意義診斷和鑒別診斷診斷和鑒別診斷 有吸入有吸入co病史病史 典型臨床表現(xiàn)典型臨床表現(xiàn) 實驗室檢查:定性或定量陽性、心肌酶實驗室檢查:定性或定量陽性、心肌酶增高增高 其他:心電圖、頭顱其他:心電圖、頭顱ct、腦電圖腦電圖 除外:安眠藥中毒,其他有毒氣體中毒、除外:安眠藥中毒,其他有毒氣體中毒、 腦血管意外、糖尿病酮癥酸中毒腦血管意外、糖

45、尿病酮癥酸中毒emergency treatmentget rid of the environmentoxygen therapy:hyperbaric oxygen treatment only after severe carbon monoxide poisoning in otherwise stable patients respiratory failure:mechanical ventilationexchange blood, blood transfusiondiuresis: prevention and cure brain edema promote recover

46、y of function:sugar、vitaminatp、coenzymea、cytochromec。acute sedatives-hypnotics poisoningbackground sedative-hypnotics are a group of drugs that cause cns depression. benzodiazepines (bzd) barbiturates nonbarbiturate nonbenzodiazepine sedative-hypnotics (nbnb)the most commonly used agents background

47、acute sedative-hypnotics poisoning withdrawal syndromeetiologybenzodiazepines (bzd) long acting (half life 30h):chlordiazepoxide (利眠寧利眠寧) diazepam(地西泮、安定)(地西泮、安定)flurazepam (氟安定)(氟安定) short acting (half life 6-30h):alprazolam(阿普唑侖阿普唑侖) ultrashort acting :triazolam(三唑侖三唑侖)etiology barbiturates ultras

48、hort acting methohexital (brevital甲己炔巴比妥甲己炔巴比妥) thiopental (pentothal硫噴妥那硫噴妥那) short acting pentobarbital (nembutal戊巴比妥戊巴比妥) secobarbital (seconal司可巴比妥司可巴比妥) intermediate acting amobarbital (amytal異戊巴比妥異戊巴比妥) butalbital (fioricet, fiorinal異丁巴比妥異丁巴比妥) long acting phenobarbital (luminal魯米那魯米那)nonbarbi

49、turate, nonbenzodiazepine sedative-hypnotics (nbnb)chloral hydrate (水合氯醛) ethchlorvynol (乙氯維諾)glutethimide (導眠能)methyprylon (甲乙哌酮)meprobamate (眠爾通)etiology一、pharmacokinetics :pharmacokinetics of the bzd most bzd are extensively metabolized by the liver. some are metabolized to products which are act

50、ive and may have a much longer half life than the parent drug. the major route of metabolism is n-demethylation. in the elderly cimetidine pathogenesispathogenesis2、pharmacokinetics of barbiturates barbiturates with low lipid solubility are excreted in the unchanged form by the kidneys. ie phenobarb

51、ital(苯巴比妥). barbiturates with high lipid solubility are metabolized to more polar compounds in the liver before being excreted via the kidneys. ie thiopental (硫噴妥). 3、pharmacokinetics of nbnb most nbnb are extensively metabolized by the liverpathogenesisw bzd in the cns, benzodiazepines exert their

52、clinical effect by enhancing the activity of the inhibitory neurotransmitter gaba. (the clinical effects of gaba release and gaba-gated chloride channels include sleep induction and excitement inhibition) w barbiturates in prolongation of the duration of opening of gaba-gated chloride channels, lead

53、ing to hyperpolarization of the membrane and suppression of neurotransmission. 。wnbnb similar to the action of barbiturates二、 the mechanism of actionpathogenesisbenzodiazepines- pathogenesisbzd受體受體+ gaba受體受體+ ci+通道通道感 覺 運 動 區(qū) ,有鎮(zhèn)靜催眠作用蛋白復合物bzd邊緣系統(tǒng),抗焦慮和抗驚厥不清123抑制中樞神經系統(tǒng)抑制中樞神經系統(tǒng)bzdgabachloride channelcl

54、-cl-hyperpolarizationclinical benzodiazepine blurred vision, dizziness, confusion, drowsiness, anxiety, agitation, and unresponsiveness or coma. bzd overdose in itself is remarkably safe. most patients with benzodiazepine overdose can be managed in the ed and released home after appropriate care. wh

55、en combined with other sedatives (most frequently alcohol), patients with benzodiazepine overdose can present with profoundly depressed levels of consciousness. . clinical barbiturates mild intoxication is characterized by ataxia, incoordination, nystagmus, slurred speech, and altered level of consc

56、iousness. moderate poisoning leads to respiratory depression and hyporeflexia. severe poisoning leads to flaccid areflexic coma, apnea, and hypotension. occasionally, hyperreflexia, rigidity, clonus, and babinski signs are present. miosis is common, but mydriasis may be present with certain agents.

57、generally, 10 times the hypnotic dose produces severe toxicity. chloral hydrate mild intoxication is characterized by ataxia, lethargy severe poisoning leads to stupor, coma, pinpoint pupils, hypotension, slow or rapid and shallow respiration, hypothermia, areflexia, and muscle flaccidity. arrhythmi

58、as clinicalclinical glutethimide (doriden) loss of brainstem reflexes flaccidity anticholinergic effects delayed gastric emptying may cause hyperthermia or heatstroke methaqualone (quaalude) resembles barbiturate poisoning has more pronounced motor problems (eg, ataxia) and is known as wallbanger be

59、cause of this phenomenon. can lead to severe muscular hypertonicity and seizuresclinicallab studies obtain a complete blood count (cbc), arterial blood gas (abg), glucose, chemistry, imaging studies: obtain an abdominal x-ray. chloral hydrate is radiopaque. other tests: obtain an electrocardiogram (

60、ecg); co-ingested drugs may have direct cardiac effects (eg, tricyclic antidepressants). quantitative serum drug concentrations are recommended for patients with serious toxicity barbiturates: for short-acting drugs, the lethal dose is 3 g or a serum concentration higher than 3.5 mg/dl. for long-act

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