Inorganic Irritants - Metallic and Non-metallic MCQs

The usual fatal dose of white phosphorous is 60-120 mg. Fulminating poisoning (death within 12 hours) may be seen when the patient takes a large dose. Early death is due to cardiac dysrhythmias, secondary to electrolyte abnormalities, such as hypocalcaemia and hyperkalaemia. Death after the first 24 h is due to hepatic failure. Fatal dose: 60-120 mg (1 mg/kg) of white phosphorus. Fatal period: Within 24 hours but may be delayed by 5-7 days. Diagnosis: Oral and skin burns, luminescent 'smoking' vomitus and stools with a garlic odour, and GIT and biliary damage characterize white phosphorus poisoning. Reference: Review of Forensic medicine and Toxicology, Gautam Biswas, 5th edition, Page No. 565

Ans. is 'a' i.e.,Lead [Ref Park 22"'Ile p. 752] More industrial workers are exposed to lead than any other toxic metal.

Cardiac arrythmias, myalgia and flaccid quadriplegia are characteristic of poisoning by Barium carbonate. Signs and symptoms of Barium carbonate poisoning: The most characteristic features are areflexia and paralysis. Barium induces hypokalaemia. (Ba 2+ ion is a muscle poison). GIT: Nausea, vomiting, salivation, abdominal pain and diarrhea. Muscular system: Tingling sensation, tremors, cramps, stiffness of the muscles, paralysis of the tongue and larynx, myoclonus, myalgia, flaccid quadriplegia. CVS: Hypertension, arrhythmia, ectopic beats, ventricular fibrillation, irregular pulse, shock, cardiac arrest. RS: Pulmonary edema, respiratory failure. CNS: Mydriasis, vertigo, headache, confusion, convulsions. Reference: Review of Forensic medicine and Toxicology, Gautam Biswas, 5th edition, Page No. 560

Arsenic can be detected even in conflagration of human bones. Hence, it is possible to detect poisoning by arsenic even in charred bones and ashes. Arsenic is volatile but much of the arsenic in bones is converted into arsenates, which are non-volatile. In suspected cases of poisoning by arsenic, all the available ashes and burnt bones should be preserved for chemical analysis. Reference: Textbook of Forensic Medicine and Toxicology, 2 nd Edition, P C Dixit, Page No. 184.

Explanation: Arsenic can be detected even in conflagration of human bones, so it is possible to detect arsenic poisoning, even in charred bones and ashes. Arsenic is volatile but much of the arsenic in bones is converted into arsenates, which are non-volatile. In India, cremation conditions often do not favour complete combustion. Even if arsenic is present as arsenic trioxide or another volatile form, not all arsenic is lost. Some volatilized arsenic may condense on cooler parts of the funeral pyre, preventing its complete loss. Arsenic is especially detectable in the spongy bones, such as the skull & vertebrae. Arsenic can persist here long after its disappearance from soft organs like the liver, spleen, kidneys, or brain. Thallium, cadmium and mercury are highly volatile and unlikely to be found in conflagrated remains.

:B Ans. is 'a > b' i.e., Lead > Mercury [Ref Reddy 306/e p.497-498] Burtonian line is blue line, which is seen on upper gums in lead poisoning. Similar blue line (but not called burtonian line in these cases) is also seen in poisoning with Mercury (Hg), Copper (Cu), Silver (Ag), bismuth (Bi), and Iron (Fe).

Postmortem findings in copper poisoning Skin may be yellow due to jaundice. Greenish-blue froth from the mouth and nostrils Mucous membrane of the mouth and tongue may have bluish or greenish-blue tinge. Internally, some discoloration is present in the mucous membrane of the esophagus and stomach. Stomach: Gastric mucosa is congested with desquamation and haemorrhages at places. Small intestine: Mucosa (upper part) may show necrosis. Liver: Soft and fatty. It shows centrilobular necrosis and biliary stasis. Kidneys: It may show acute proximal tubular necrosis. Haemoglobin casts may be seen in the tubules. Reference: Review of Forensic medicine and Toxicology, Gautam Biswas, 5th edition, Page No. 553, 554

Explanation: Minamata Bay disease was due to chronic organic mercury intoxication (Methyl mercury). Minamata disease: It is due to chronic organic mercury intoxication caused by eating contaminated fish and shellfish. In Minamata Bay (Japan), a factory discharged inorganic mercury into the water. The mercury was methylated by bacteria and subsequently ingested by fish. Local villagers ate the fish and began to exhibit signs of chronic mercury poisoning. Symptoms include disturbances in hand coordination, gait and speech, chewing and swallowing difficulties, visual blurring, tremors, rigidity, seizures and clouding of consciousness. Key Takeaway: Minamata disease is caused by chronic methylmercury poisoning from consumption of contaminated seafood.