预防医学教学课件：Poisonous gases poisoning

1、Poisonous gases poisoning Irritant gases poisoning Asphyxiant gases poisoningDirect irritant and corrosive effects on eyes, mucous membrane of respiratory tract, and skin. Chlorine (Cl2): production of alkali, disinfectants, household cleaners Ammonia (NH3): fertilizer production, refrigeration phos

2、gene (COCl2): chlorinated hydrocarbon solvents decompose oxides of nitrogen (NOX): welding, auto exhausthydrogen fluoride (HF): microelectronicssulfur dioxide (SO2): paper manufacturing, oil refining sulfur trioxide (SO3)Irritant gasesThe most water-soluble substances are absorbed onto conjunctiva a

3、nd mucous membranes of the nose and upper respiratory tract (ammonia)The less water-soluble substances exert their harmful effects especially in the lower respiratory tract (oxides of nitrogen)Solubility of the gasToxicologyToxic pulmonary edemaToxicologyoverfull retention of water in the pulmonary

4、interstitial and alveolus space Mechanism of onset: (1)increased permeability of alveolar wall (2)increased permeability of blood capillary wall (3)obstructed return of lymph fluid Clinical effects Acute poisoning Chronic damages Clinical effects*Acute poisoning: 1. inflammation of eyes and upper re

5、spiratory tract reflex coughing, laryngeal spasm 2. toxic tracheitis, bronchitis and pneumonitis 3. toxic pulmonary edema (pneumochysis) Clinical stages: irritant stage latency period(2-6h) lung edema period convalescence period(3-4days) 4. adult respiratory distress syndrome (ARDS)Clinical effectsC

6、hronic damages: symptoms of conjunctivitis rhinitis pharyngitis bronchitisTreatment(1) On the spot treatment:(2) Keep respiratory tract unobstructed:(3) oxygen therapy: (4) Toxic pulmonary edema:Chlorine, Cl21. Physical and chemical properties greenish-yellow gas at room temperature and atmospheric

7、pressure choking smell Boiling point:-34.6 Gravity: 2.488 Soluble in water, alkali and organic solvents2. Opportunities of exposure salt electrolysis production of chloride paper-making, leather, printing and dyeing, sterilization 3. ToxicologyCl2Cl2+H2O HCl + HClOLow concentration: upper respirator

8、y tractHigh concentration: deep respiratory tract pulmonary alveoli 4. Clinical manifestationAcute poisoning: 1. irritation of eyes and upper respiratory tract: 2. toxic pulmonary edema: 3. skin lesions: ambustion, dermatitis 4. complication: infection, hemorrhage, pneumothoraxChronic damages: irrit

9、ation discoloration and incomplete of the teeth 5.Diagnosis & Prevention irritation reaction Mild poisoning Moderate poisoning Severe poisoningSimple asphyxiant gases: simply displace oxygen from the inspired air, causing asphyixa Carbon dioxide: fires Methane: mining Nitrogen: diving Chemical asphy

10、xiants gases: absorbed into the systemic circulation, interfering with the process of oxygen transport and utilization Carbon monoxide: fires Cyanide: gold extraction; electroplating and fires Hydrogen sulfide: oil refining; decaying organic matterAsphyxiating Gas Carbon monoxide is a colourless, od

11、ourless, tasteless, combustible, and explosive gas. lighter than airCarbon monoxide (CO) 1. Physical and chemical properties Produced by the incomplete combustion of carbonaceous substances. 2. Opportunities of exposureMechanism of action : In blood, CO binds with haemoglobin to form carboxyhaemoglo

12、bin (COHb) . CO competes with oxygen for binding sites on hemoglobin and decreases the oxygen hemoglobin saturation and oxygen delivery to tissues.3. ToxicologyO2+Hb HbO2COCOHbhypoxiaTissueO2cytochrome a3respiratory chain interception (1) acute poisoning 1. Consciousness may be lost with few symptom

13、s.2. COHb 10%: headache and subtle changes of mental function; COHb 20%: throbbing headache and loss of dexterity; COHb 30-40%: syncope; COHb 40-50%: coma and convulsions;3. The colour of skin and mucosa in patient is cherry, not cyanosis or in pale: COHb imparts a bright red color to blood.4. Sever

14、e acute CO poisoning may permanently damage the brain and heart.4. Clinical manifestation(2) delayed encephalopathy (2-60d) (3) chronic damage 5.Diagnosis Mild poisoning (10%) Moderate poisoning (30%) Severe poisoning (50%) delayed encephalopathyIndex: COHb In acute poisoning, immediately remove the

15、 patient from further exposure to CO and administer oxygen. Further treatment should be symptomatic. Patients with after-effects of acute poisoning should not be further employed in occupation involving exposure to CO. 6.Treatmenta flammable colourless gas with a typical rotten-egg odour.Olfactory f

16、atigue develops quickly, diminishing ones abilityto detect the odor. Hydrogen sulfide (H2S) 1. Physical and chemical properties 2. Opportunities of exposureoil refining decaying organic matterMechanism of actionInhibiting cellullar respiration in a similar fashion to HCN, blocking the utilization of

17、 oxygen, and anoxia develops in spite of normal quantities of oxygen in the blood.3. ToxicologyH2SInhalationH2S Na2SRespiratory tractNa+BloodH2S combine with Fe3+-S-S-Respiratory chain blockurineSO42-S2O32-Respiratory center Central nervous system Eyes Respiratory system In severe poisoning, coma, c

18、onvulsions, and death may occur, sometimes within a few seconds (a sudden death).4. Clinical manifestation acute poisoning chronic damage Treatment In acute poisoning immediately remove the patient from exposure and start symptomatic treatment. Artificial respiration may be necessary. 5.Diagnosis &

19、Treatment Mild poisoning Moderate poisoning Severe poisoningDiagnosisHydrogen cyanide (HCN)1. Physical and chemical properties 2. Opportunities of exposure colourless gas with atypical odour of bitter almonds one of the most rapidly lethal poisons electroplating metallurgy chemical engineering Mecha

20、nism of action HCN has a strong affinity for trivalent iron and binds firmly to cytochrome oxidase of the mitochondrial respiratory chain. Since cytochrome oxidase is present in all cells, all aerobic cellular respiration is impaired, and anoxia develops in spite of normal quantities of oxygen in th

21、e blood.3. ToxicologyHCN rapidly causes vertigo, convulsions, confusion, altered speech, coma, and death (sudden death).Initial symptoms of acute HCN poisoning include weakness, headache, confusion, and occasionally nausea and vomiting. Arterialization of venous blood, and the colour of skin and muc

22、osa in patient is cherry. 4. Clinical manifestation (1) acute poisoning (2) chronic damage prodromal perioddyspnea periodspasm periodparalysis period Acute HCN poisoning can be treated very efficiently. The patient should be immediately removed from further exposure, and contaminated skin should be

23、washed with warm water and soap. An effective treatment is sodium nitrite (NaNO2) given intravenously, forming methaemoglobin (MHb) which binds firmly with free cyanide ions to form cyanmethaemogolbin. Thereafter sodium thiosulfate (Na2S2O3) is given intravenously to increase the rate of conversion

24、of cyanide to thiocyanate. 5.Diagnosis & TreatmentNaNO2+Hb MHbCN-MHbCNNa2S2O3SCN-职业病案例分析患者张某，女，36岁，某皮鞋厂工人。因头痛、乏力、失眠、月经过多、牙龈出血而入院。入院查体：神志清楚，呈贫血貌，皮肤粘膜无淤点，体温37.2，脉搏74次/min，呼吸21次/min，血压110/65mmHG；心电图正常；胸部X线片未见异常改变。骨髓检查诊断为再生障碍性贫血；血象检查诊断为急性粒细胞型白血病。案例一该患者最有可能接触的是哪种有害物质 要确定其为职业性中毒，还需调查什么该种毒物慢性中毒的主要临床表现是什么问题讨论：皮鞋黏合剂主要成分中含有苯空气检测结果表明：空气中苯浓度最低为120mg/m3，最高达360m