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Arsenic Toxicity

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Arsenic and many of its compounds are especially potent poisons. Arsenic disrupts ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress.
These metabolic interferences lead to death from multi-system organ failure
Arsenic poisoning is a medical condition caused by elevated levels of arsenic in the body. The dominant basis of arsenic poisoning is from ground water that naturally contains high concentrations of arsenic. A 2007 study found that over 137 million people in more than 70 countries are probably affected by arsenic poisoning from drinking water

Published in: Health & Medicine
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Arsenic Toxicity

  1. 1. ARSENIC TOXICITY toxicology
  2. 2. OUTLINES  Sources Moods of exposure Toxicokinetics Mechanisms of toxicity  Symptoms of acute and chronic toxicity Diagnosis Treatment Notable cases of arsenic poisoning References
  3. 3. SOURCES
  4. 4. MOODS OF EXPOSURE
  5. 5. 1- INGESTION:
  6. 6. ARSENIC CONTAINING FOODS:
  7. 7. 2- INHALATION:
  8. 8. 3- SKIN:
  9. 9. TOXICOKINETICS
  10. 10. . ABSORPTION
  11. 11. DISTRIBUTION
  12. 12. METABOLISM
  13. 13. EXCRETION
  14. 14. MECHANISMS OF TOXICITY
  15. 15. ARSENIC-INDUCED CARDIOVASCULAR DYSFUNCTION
  16. 16. ARSENIC-INDUCED DIABETES MELLITUS .
  17. 17. ARSENITE-INDUCED NEUROTOXICITY
  18. 18. ARSENIC-INDUCED NEPHROTOXICITY AND HEPATOTOXICITY
  19. 19. ARSENIC-INDUCED CARCINOGENICITY
  20. 20. SYMPTOMS OF ACUTE AND CHRONIC TOXICITY
  21. 21. SYMPTOMS OF CHRONIC ARSENIC POISONING Affected organ Features Skin  Excessive darkening of skin (hyperpigmentation) in areas that are not exposed to sunlight  Excessive formation of scaly skin on the palms and soles (arsenical keratosis)  Exfoliative dermatitis  Arsenic-induced skin cancers (especially Bowen disease , Squamous cell carcinoma) Nails  Transverse white bands of arsenic deposits across the bed of the fingernails (Mee's lines)
  22. 22. Hair  Arsenic deposits in hair Nervous system  Sensory changes, numbness and tingling in a “stocking-glove” distribution (sensory peripheral neuropathy)  Headache, drowsiness, confusion  Distal weakness of small muscles e.g. hands and feet Blood and urine  Haemolytic anaemia (moderate)  Leukopaenia (low white cell count)  Proteinuria (protein in urine)
  23. 23. Other  Inflammation of respiratory mucosa  Peripheral vascular insufficiency  Increased risk of cancer of lung, liver, bladder, kidney and colon
  24. 24. Features of acute arsenic poisoning Symptoms usually start within 30 minutes to 2 hours.  Acute arsenic ingestion is typically followed by a severe gastroenteritis, garlic odour and hypersalivation.  There is a characteristic sequence of multi-organ failure, with: neurological symptoms (within hours) and cardiac features, succeeded by adult respiratory distress syndrome and renal/liver dysfunction.  Marrow suppression develops after a few days to weeks in survivors, as does alopecia and an ascending motor neuropathy.
  25. 25. often present in breath and body tissues Hypersalivation, abdominal pain, vomiting, diarrhoea leading to hypovolaemic shock. Trivalent arsenic is corrosive - may cause oral burns, dysphagia and GI bleeding. Myocardial depression. Dehydration, hypovolaemia or shock. ECG changes including ST segment changes, prolonged QT interval, ventricular tachycardia, torsades de pointes and ventricular fibrillation. Gangrene of extremities.
  26. 26. Pulmonary oedema, adult respiratory distress syndrome and acute respiratory failure. Inhaled arsenic causes irritation, bronchospasm and pulmonary oedema Haematuria or haemoglobinuria (from acute haemolysis), proteinuria, acute tubular necrosis with acute renal failure. Jaundice, hepatomegaly, pancreatitis CNS depression, encephalopathy and coma. Seizures.
  27. 27. Acute haemolysis. Bone marrow suppression. Basophilic stippling and rouleaux formation may be seen on a blood film Rashes
  28. 28. DIAGNOSIS
  29. 29. TREATMENT
  30. 30. 1-TREATMENT OF ACUTE ARSENIC:
  31. 31. 2-TREATMENT OF CHRONIC ARSENIC
  32. 32. 1-Chelation 2-Nutrition 3-Removal Chemical and synthetic Supplemental methods are used to treat potassium decreases arsenic poisoning. the risk of Dimercaprol and experiencing a life-threatening dimercaptosuccinic acid are heart chelating agents that rhythm problem from sequester the arsenic away arsenic trioxide. from blood proteins and are used in treating acute arsenic poisoning. The most important side effect is hypertension. Dimercaprol is considerably more toxic than succimer.[citation needed]DMSA monoesters, e.g. MiADMSA, are promising antidotes for arsenic poisoning. Calcium sodium edetate is also used. Various techniques have been evolved for arsenic removal, most frequently using absorbents such as activated carbon, aluminium oxide, co-operative with iron oxide to form sludges, adsorption onto iron-oxide-coated polymeric materials, and electrocoagulation by nanoparticle. To remove the stress of heavy and toxic metals, an environment-friendly approach must be applied and the use of naturally occurring microbe must be emphasized. Bacteria, yeast, fungi, algae—all of them can be used for remediation processes and it is always recommended that microbe used for bioremediation must have natural decontamination process and the method should be cost-effective.
  33. 33. NOTABLE CASES OF ARSENIC POISONING
  34. 34. http://www.youtube.com/watch?v=W3Hvexu5SqM
  35. 35. STRAIN GFAJ-1 OF THE HALOMONADACEAE, ISOLATED FROM MONO LAKE, CALIFORNIA, THAT IS ABLE TO SUBSTITUTE ARSENIC FOR PHOSPHORUS TO SUSTAIN ITS GROWTH.
  36. 36. REFERENCE  http://www.atsdr.cdc.gov/csem/arsenic/docs/arsenic.pdf  http://toxsci.oxfordjournals.org/content/123/2/305.full  Agency for Toxic Substances and Disease Registry (2007)ToxGuide for Arsenic, USA: Centers for Disease Control and Prevention.  Agency for Toxic Substances and Disease Registry (2009) Case Studies in Environmental Medicine; Arsenic Toxicity, USA: Centers for Disease Control and Prevention.  WHO (2000) Air Quality Guidelines, 2 edn., Copenhagen, Denmark: WHO Regional Office for Europe.  American Conference of Governmental Industrial Hygienists (ACGIH). Documentation of the threshold limit values and Biological Exposure Indics. 5th ed. ACGIH, Cincinnati, OH, 1986.  Armstrong, C. W., Stroube, R. B., Rubio, T., and Beckett, W. S. Outbreaks of fatal arsenic poisoning caused by contaminated drinking water. Arch. Environ. Health 39, pp 274-279, 1984.  Axelson, O., Dahlgren, E., Jansson, C. D., and Rehnlund, S. O. Arsenic exposure and mortality. Acase reference study from a Swedish copper smelter. Br. J. Ind. Med. 35, pp 8-15, 1978.  Dr. D.n. Guha Mazumder, Chapter 4 : Diagnosis and treatment of chronic arsenic poisoning By. In editor. Diagnosis and treatment of chronic arsenic poisoning, : Institute of Post Graduate Medical; 2000. p.20  Steven Marcus. Medscape. Arsenic Toxicity treatment [serial on the Internet]. 2012 [cited 2014 Nov 23]. Available from: Copyright © 1994-2014 by WebMD LLC, MEDLINE database Web site: http://http://emedicine.medscape.com/article/812953-overview  Dr. D.n. Guha Mazumder, Chapter 4 : Diagnosis and treatment of chronic arsenic poisoning By. In editor. Diagnosis and treatment of chronic arsenic poisoning, : Institute of Post Graduate Medical; 2000. p.20  Steven Marcus. Medscape. Arsenic Toxicity treatment [serial on the Internet]. 2012 [cited 2014 Nov 23]. Available from: Copyright © 1994-2014 by WebMD LLC, MEDLINE database Web site: http://http://emedicine.medscape.com/article/812953-overview

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