MERCURY POISONING.ppt

1、NEUROTOXICOSIS Bodnar R.Ya.,PLANNEUROTOXICOSIS,Mercury poisoning Industrial uses. Pathogenesis of Mercury poisoning. Clinical picture. Diagnosis. Treatment. Tetraethyllead poisoning Industrial uses. Pathogenesis of Tetraethyllead poisoning. Clinical picture. Diagnosis. Treatment.,Manganese poisoning

2、 Industrial uses. Pathogenesis of Manganese poisoning. Clinical picture. Diagnosis. Treatment.,MERCURY POISONING,MERCURY POISONING,Mercury has been used commercially and medically for centuries. In the past it was a common constituent of many medications. It is still used in hospitals in thermometer

3、s and blood-pressure cuffs and commercially in batteries, switches, and fluorescent light bulbs. Large quantities of metallic mercury are employed as electrodes in the electrolytic production of chlorine and sodium hydroxide from saline. These uses still give rise to accidental and occupational expo

4、sures.,MERCURY POISONING,Today, however, exposure of the general population comes from three major sources: fish consumption, dental amalgams, and vaccines. Each has its own characteristic form of mercury and distinctive toxicologic profile and clinical symptoms. Dental amalgams emit mercury vapor t

5、hat is inhaled and absorbed into the bloodstream. Dentists and anyone with an amalgam filling are exposed to this form of mercury. Liquid metallic mercury (quicksilver) still finds its way into homes, causing a risk of poisoning from the vapor and creating major cleanup costs. Humans are also expose

6、d to two distinct but related organic forms, methyl mercury (CH3Hg+) and ethyl mercury (CH3CH2Hg+).,MERCURY POISONING,Fish are the main if not the only source of methyl mercury, since it is no longer used as a fungicide. In many countries, babies are exposed to ethyl mercury through vaccination, sin

7、ce this form is the active ingredient of the preservative thimerosal used in vaccines. Whereas removal of certain forms of mercury, such as that in blood-pressure cuffs, will not cause increased health risks, removal of each of the three major sources described in this article entails health risks a

8、nd thus poses a dilemma to the health professional.,MERCURY POISONING,Exposure to mercury from dental amalgams and fish consumption has been a concern for decades, but the possible risk associated with thimerosal is a much newer concern. These fears have been heightened by a recent recommendation by

9、 the Environmental Protection Agency (EPA) that the allowable or safe daily intake of methyl mercury be reduced from 0.5 g of mercury per kilogram of body weight per day, the threshold established by the World Health Organization in 1978, to 0.1 g of mercury per kilogram per day.,The Global Cycle of

10、 Mercury,In nature, mercury vapor (Hg0), a stable monatomic gas, evaporates from the earths surface (both soil and water) and is emitted by volcanoes Anthropogenic sources include emissions from coal-burning power stations and municipal incinerators. After approximately one year, mercury vapor is co

11、nverted to a soluble form (Hg2+) and returned to the earth in rainwater. It may be converted back to the vapor form both in soil and in water by microorganisms and reemitted into the atmosphere. Thus, mercury may recirculate for long periods. Mercury attached to aquatic sediments is subject to micro

12、bial conversion to methyl mercury (MeHg), whereupon it enters the aquatic food chain. It reaches its highest concentrations in long-lived predatory fish, such as sharks.,The Global Cycle of Mercury,Panel indicates the routes of transfor-mation to methyl mercury as originally,The Global Cycle of Merc

13、ury,Panel depicts the increase in mercury concentrations in feathers of fish-eating birds in Sweden. The period covered by these data corresponds approximately to the growth of industrialization in Sweden.,Acute MERCURY poisoning,Acute mercury poisoning occurs rarely. It arises up after contact with

14、 large quantities of mercury.,Acute MERCURY poisoning,The main symptoms of the acute poisoning are hypersalivation, inflammation and formation of ulcers of mucous of the mouth, swelling of salivary glands, increase of submandibular lymph nodes, inflammation of gums, nausea, vomiting, diarrhea, tenes

15、mus, intestinal colic.,Acute MERCURY poisoning,Necrotizing nephrosis with acute renal failure often develops. acute bronchitis, pneumonia. Very often liver, nervous system are affected. In blood: hemolysis, leukocytosis, increase of ESR (to 30-50 mm/h), increase of blood protein, nitrogen.,Mercury p

16、oisoningNecrotizing nephrosis,Acute MERCURY poisoning,After the acute poisoning: a chronic diseases of kidneys, chronic colitis, hepatitis astheni syndrome. After the treatment may be complete recovery.,Chronis MERCURY poisoning,Occurs after contact with mercury during 8-10 years. Clinical symptoms

17、develop gradually and are characterized by affection of the NERVOUS SYSTEM. According to the degree of expressiveness of pathological process chronic poisoning is divided into 3 stages: INITIAL (FUNCTIONAL), MODERATE AND SEVERE.,MERCURY POISONING DIAGNOSIS,Early typical symptoms: irritability, weakn

18、ess, Gingivitis stomatitis. Confirmation of diagnosis is mercury determination in urine and feces. Presence of mercury in urine without proper clinical symptoms indicates a “mercury carriage”.,MERCURY POISONING Treatment,-To destroy mercury and excrete it from organism antidotes are recommend: Uniti

19、ol, Sucsimer, sodium thiosulphate. - Most effective is Unitiol (sodium 2,3-dymercaptopropansulfonat) - 5% 5-10 ml (0,05 g or 5% 1 ml per 10 kg of patients weight). 1 day - 2-4 injections, next 6-7 days 1 injection/ day. - Its sulfhydryl groups form untoxic complexes with poison and are excreted with

20、 urine.,MERCURY POISONING Treatment,Sodium thiosulphate 30% 5-10 ml i/v slowly. Drugs which improve metabolism and blood supply of brain (Pyracetam, Stugeron). Glucose 40% 20 ml + Vit. C, Vit.B 1, B 12, B 6. Tranquilizers. Symptomatic therapy.,TETRAETHYLLEAD POISONING,TETRAETHYLLEAD POISONING,TEL is

21、 an oily transparent liquid which contains a 64,07 % of lead, well dissolves in organic solvents (ether, alcohol, benzol, petrol and other) and in fats.,TETRAETHYLLEAD POISONING,L is applied as antidetonate. A dangerous contact with TEL may occur -at its producing, - mixing with a fuel, - at cleanin

22、g of petrol cisterns. Tetraethyllead is a strong neurotrop poison.,TETRAETHYLLEAD POISONING,TETRAETHYLLEAD POISONING,TETRAETHYLLEAD POISONING,Tetraethyllead Poisoningis characterized by neurological symptoms.,Toxic affection of cerebral neurocytes,ACUTE TETRAETHYLLEAD POISONING,in 1-3 hours after a

23、contact with L the first symptoms of the acute poisoning appear. According to the degree of expressiveness of clinical manifestations there are three STAGES of the acute poisoning by L: - INITIAL, - PRECULMINATION, - CULMINATION.,CHRONIC TETRAETHYLLEAD POISONING,is observed in workers who worked in

24、contact with L during long period. A clinic develops gradually and can be poorly expressed. According to thedegree of expressiveness of clinical manifestations there are three STAGES of the chronic poisoning: I-st (initial), II-nd III-rd.,ACUTE TEL POISONING Treatment,To wash up skin (with warm wate

25、r and soap), to make gastric washing, to use absorbents. Patients with acute TEL poisoning need complete rest, hypnotic medicines from the group of barbituratus (phenobarbital, barbital sodium or etaminal sodium). At hyperexcitability barbamil (i/m or i/v) or hexenal are prescribed. hypertensive sol

26、ution of glucose i/v, Vitamine therapy. Warm baths are recommended before sleep.,CHRONIC TEL POISONING Treatment,Treatment of patients with the chronic form of TEL poisoning is appointed taking into account expressiveness of clinical manifestations. For such patients - drugs which influence on a tis

27、sue metabolism (glutamine acid, glucose, vitamins C, B1, B2, ATF, riboxin), - tranquilizers (Diasepam, Tazepam) are recommended.,MANGANESE POISONING,Manganese poisoning,The occupational manganese poisoning occurs among workers who work - on the manganese mines, - in metallurgical industry at steel m

28、aking , -special alloys producing (ferromanganese to 80 % of manganese, mirror cast-iron to 15 % of manganese), - at making of electrodes and gumboils which are used for the electric welding, - in chemical and lacquer-paint industry, - in agriculture (stain of seed for stimulation of plant growth),

29、- in rubber industry. - Most dangerous is ground and sifting of pound ore, because a lot of small disperse dust of manganese appear.,VARIANTS OF CLINICAL COURSE,Manganese poisoning,- The oxides of manganese are quickly absorbed. - In blood manganese circulates as an unsteady complex with plasma prot

30、eins. - Manganese is deposited in bones, cerebrum, parenchyma organs. - It is excreted from the organism with feces and urine. - Manganese may cause bronchial asthma and eczema because of its allergic influence.,Manganese poisoning Pathogenesis,Manganese, as a microelement, takes part in biological

31、processes of organism. It influences on metabolic processes, depresses cholinesterase activity, affects metabolism of serotonin. At the protracted and systematic getting into the organism it has a direct influence on nervous tissue, and causes vascular violations, increase capillary permeability. It

32、 changes activity of enzymes of nervous cells, depresses the biosynthesis of catecholamines, intensifies protein metabolism.,Manganese poisoning Pathogenesis,The action of manganese is divided into two phases. I phase cholinergic is characterized by predominance of cholinergic influence. II phase ph

33、ase of areactivity injury of acetylcholinoreactive structures. A manganese influences on the function of thyroid, cardiovascular system, gastrointestinal tract, liver and other.,Acute Manganese poisoning,In industry acute manganese poisoning occurs rarely. It arises up at breathing in large quantiti

34、es of dust which contains manganese. Manganese poisoning causes severe disorders of blood circulation, dyspnea, frequent syncopes. In easy cases of poisoning irritation of the mucous of respiratory tracts, cough, and headache are observed.,CHRONIC MANGANESE POISONING,Clinical picture of the chronic

35、manganese poisoning is characterized by three stages. ! The special feature of clinical course of chronic manganese poisoning is inclination to its progress after stopping contact with a metal.,MANGANESE POISONINGDIAGNOSIS,Special attention is paid to early diagnosis of chronic manganese poisoning. Its necessary to find out a professional route, sanitary description of labor conditions (manganes