Heavy Metals Toxicity PDF

Feature Arsenic Lead Mercury Sources Arsenous oxide (White Lead acetate (sugar of Elemental Hg, Mercuric arsenic), Paris Green, etc. lead), Tetraethyl lead chloride, Methyl mercury Routes of Oral, inhalati...

Feature Arsenic Lead Mercury Sources Arsenous oxide (White Lead acetate (sugar of Elemental Hg, Mercuric arsenic), Paris Green, etc. lead), Tetraethyl lead chloride, Methyl mercury Routes of Oral, inhalational, Inhalational, oral (dust, Inhalation (vapor), Exposure cutaneous contaminated food, ingestion, skin absorption etc.) Fatal Dose 200-300 mg (Arsenic 20 g (Lead acetate), 1-4 g (Mercuric chloride) trioxide) 100 mg/kg (Tetraethyl lead) Mechanism Binds to sulfhydryl groups, Inhibits heme Binds to mitochondrial of Action disrupts oxidative synthesis, binds to -SH enzymes (pyruvate phosphorylation groups dehydrogenase) Key Acute GIT: Severe abdominal GIT: Colic, constipation. Respiratory: Cough, Symptoms pain, vomiting, diarrhea dyspnea, pneumonitis. (bloody/rice-water). Neuro: Wrist drop, foot drop, convulsions, GIT: Abdominal pain, Neuro: Convulsions, coma, coma. vomiting, diarrhea. respiratory distress. Other: Facial pallor, Neuro: Tremor, ataxia, Other: Garlic breath odor, Burtonian lines (blue- seizures. hypotension black gum line), anemia Other: Metallic taste, renal failure Key Chronic Skin: Hyperpigmentation Neuro: Neuro: Erethism (emotional Symptoms (rain-drop pattern), Encephalopathy, instability, shyness), hyperkeratosis. cognitive decline. Danbury tremor, ataxia. Neuro: Peripheral GIT: Colic, constipation. Skin: Acrodynia (pink neuropathy (glove and Heme: Anemia, disease in children), stocking pattern), basophilic stippling, gingivitis, sialorrhea encephalopathy. Heme: Burtonian lines. Pancytopenia Other: Gout, sterility Diagnosis Urine arsenic >100 mcg in Blood lead levels >20 Urine/Blood mercury levels. 24 hours. Hair/Nail µg/dL, urinary lead Hair samples may indicate analysis for arsenic >150 µg/L. Peripheral chronic exposure to organic deposition. smear: Basophilic mercury. stippling of RBCs, microcytic hypochromic anemia. Manageme Decontamination: Gastric Chelation: BAL, Decontamination: Gastric nt (Acute) lavage, whole bowel CaNa2EDTA, DMSA lavage, activated charcoal. irrigation. (succimer). Supportive: Fluids, electrolytes. Chelation: BAL, DMSA. Chelation: BAL, D- penicillamine. Supportive: Fluid resuscitation, monitoring Supportive: IV fluids, renal/liver function monitoring of renal/liver function Manageme Chelation: BAL, Vitamin B1 Chelation: CaNa2EDTA, Chelation: BAL, DMSA, nt (Chronic) DMSA, folic acid, supportive therapy for thiamine neuro and renal symptoms Medicolega Homicidal, occupational Occupational disease, Criminal abortion, l hazard, delays cattle poisoning, Minamata disease (methyl Importance decomposition. abortion risk, mercury), Mad Hatter contaminant in drug syndrome abuse (e.g., cocaine). (elemental/inorganic mercury exposure). Unique Post-mortem imbibition: Lead line (Burtonian Mad Hatter syndrome Features Arsenic delays line) on gums, (emotional instability, decomposition. Fetal plumbism (painter's tremor), acrodynia (pink toxicity: Crosses placenta colic). Occupational disease) in children due to causing intrauterine death exposure common in chronic exposure. or newborn respiratory construction, battery, Minamata disease: distress. and paint industries. Environmental contamination. Detailed Clinical Features: Arsenic Acute Poisoning: o GIT: Severe abdominal pain, metallic taste, bloody or rice-water diarrhea, vomiting. o Neurological: Convulsions, coma, hyperpyrexia. o Cardiac: Hypotension, tachycardia. o Other: Garlic odor in breath, respiratory distress in severe cases. Chronic Poisoning: o Skin: Hyperpigmentation (rain-drop pattern), hyperkeratosis, Mees' lines on nails. o Neurological: Peripheral neuropathy (glove and stocking pattern), encephalopathy, polyneuritis. o Hematological: Pancytopenia, basophilic stippling. o Dermal: Melanosis, Bowen's disease, skin cancer. Lead Acute Poisoning: (Uncommon) o GIT: Abdominal colic, constipation. o Neurological: Encephalopathy, convulsions, coma, lead palsy (wrist/foot drop). o Other: Burtonian line on gums, facial pallor. Chronic Poisoning: o Neurological: Cognitive decline, peripheral neuropathy, wrist/foot drop. o Hematological: Microcytic hypochromic anemia, basophilic stippling, reticulocytosis. o Other: Lead line (Burtonian line), saturine gout, sterility, retinal stippling. Mercury Acute Poisoning: o Inhalation: Cough, dyspnea, fever with chills, headache, metallic taste, Kawasaki disease-like symptoms (red palms, fever, lymphadenopathy). o GIT: Abdominal pain, vomiting, diarrhea, shock, pulmonary edema. o Neurological: Tremors, convulsions, ataxia. Chronic Poisoning: o Neurological: Danbury tremor (coarse tremor of hands), erethism (emotional instability, shyness, depression), ataxia, reeling gait. o Skin: Acrodynia (pink disease in children), gingivitis, sialorrhea. o Other: Mercuria lentis (brown discoloration of lens capsule), renal damage, Minamata disease (organic mercury poisoning). A 45-year-old man presents with severe abdominal pain, vomiting, and bloody diarrhea. He has been using herbicides in his garden, and his breath smells of garlic. He also reports a metallic taste in his mouth. Problem-Based Questions: 1. What is the likely diagnosis, and what are the possible sources of exposure? 2. Describe the mechanism of action of this poison in the body. 3. What investigations would confirm poisoning, and how would you differentiate between acute and chronic exposure? 4. Discuss the management of acute poisoning, including the role of chelation therapy. 5. What are the medicolegal implications in cases of such poisoning, particularly concerning occupational exposure and homicidal poisoning? Diagnosis: Arsenic poisoning A 35-year-old male painter presents with fatigue, abdominal pain, and constipation. Physical examination reveals a blue-black line on his gums (Burtonian line) and weakness in his wrists (wrist drop). Blood tests show anemia and basophilic stippling. Problem-Based Questions: 1. What is the likely diagnosis, and what is the underlying mechanism of the toxicity in this case? 2. Explain the significance of the Burtonian line in the diagnosis of lead poisoning. 3. How would you approach the management of both the acute and chronic aspects of this poisoning? 4. What medicolegal issues arise when lead poisoning is linked to occupational exposure, and how can this affect liability for the employer? Diagnosis: Arsenic poisoning Significance of the Burtonian line in the diagnosis of lead poisoning:  When lead is ingested or inhaled, it enters the bloodstream and is distributed throughout the body. A portion of this lead binds to proteins and accumulates in various tissues, including bones, kidneys, and soft tissues like the gums. In individuals with chronic exposure to lead, hydrogen sulfide is produced by bacteria in the mouth, especially those involved in gum disease (gingivitis). This gas interacts with the lead ions that have accumulated in the gum tissues. The lead ions react with hydrogen sulfide to form lead sulfide (PbS), a compound that is blue-black in color. Lead sulfide is insoluble, so it remains deposited in the gum tissue, leading to the characteristic dark line. Employees' Compensation Act, 1923 Scope: This is one of the primary statutes that governs employer liability in cases of work-related injuries and illnesses. Employer's Obligation: The act mandates that employers provide compensation to workers for injuries suffered in the course of employment, regardless of fault. This includes: o Death or permanent disability due to workplace accidents. o Partial or temporary disability affecting the worker’s ability to earn. o Occupational diseases, such as lead poisoning, mercury exposure, or arsenic poisoning due to working with hazardous substances. Compensation Calculation: The compensation is based on the extent of injury, nature of the employment, and wages of the employee. Q1. Which of the following is a characteristic clinical feature of chronic arsenic poisoning? A) Basophilic stippling B) Burtonian line C) Mees' lines D) Acrodynia Answer: C) Mees' lines Q2. What is the mechanism of action of arsenic in the body? A) Inhibition of acetylcholinesterase B) Competitive inhibition of GABA C) Binding to sulfhydryl groups leading to disruption of oxidative phosphorylation D) Interference with calcium metabolism Answer: C) Binding to sulfhydryl groups leading to disruption of oxidative phosphorylation Q3. Which of the following is a common source of arsenic exposure? A) Lead-based paint B) Paris Green (insecticide) C) Battery manufacturing D) Thermometers Answer: B) Paris Green (insecticide) Q4. Burtonian line is a clinical sign of which type of poisoning? A) Arsenic poisoning B) Lead poisoning C) Mercury poisoning D) Cadmium poisoning Answer: B) Lead poisoning Q5. In lead poisoning, which of the following is commonly observed in the peripheral blood smear? A) Auer rods B) Heinz bodies C) Basophilic stippling D) Howell-Jolly bodies Answer: C) Basophilic stippling Q6. Which chelating agent is used in the management of lead poisoning? A) Dimercaprol (BAL) B) Atropine C) Naloxone D) Fomepizole Answer: A) Dimercaprol (BAL) Q7. Which of the following conditions is associated with chronic mercury poisoning? A) Peripheral neuropathy B) Wrist drop C) Danbury tremor (Hatter's shakes) D) Blue-black line on gums Answer: C) Danbury tremor (Hatter's shakes) Q8. Which form of mercury is primarily responsible for Minamata disease? A) Elemental mercury B) Inorganic mercury C) Methyl mercury D) Mercuric chloride Answer: C) Methyl mercury Q9. Which clinical feature is typically associated with acute mercury poisoning? A) Rice-water stools B) Garlic breath C) Colic and constipation D) Metallic taste and pneumonitis Answer: D) Metallic taste and pneumonitis Q10. Which of the following heavy metals can cross the placenta and lead to fetal toxicity? A) Lead B) Arsenic C) Mercury D) All of the above Answer: D) All of the above Q12. Which of the following is true regarding employer liability in cases of occupational heavy metal poisoning? A) Employers are always absolved of liability if they provide personal protective equipment (PPE). B) Employers can be held liable if they fail to comply with safety standards and occupational health regulations. C) Employees are solely responsible for avoiding heavy metal exposure. D) There is no legal framework for occupational exposure to heavy metals in India. Answer: B) Employers can be held liable if they fail to comply with safety standards and occupational health regulations.