Forensic Medicine & Toxicology

Explore the basics of toxicology, defining toxicity, poison, and dose. Learn how dose determines whether a substance is therapeutic or toxic, and why higher dose implies greater risk.

Assess how toxicity manifests immediately as acute toxicity or after prolonged exposure as chronic toxicity, including unintentional overdose and accidental exposure, and classify poisons by symptoms and affected systems.

This lecture presents four steps in poisoning treatment—removal of poison, antidotes, elimination, and symptom management—plus protocols for inhaled, injected, skin or eye contact, and swallowed poisons.

This lecture discusses antidotes in forensic toxicology, contrasting non-specific and specific antidotes, highlights permanganate's oxidizing action, washing methods, alkaloid precipitation, and the neutralising role of milk of magnesia.

Identify specific antidotes that counteract poisons by receptor antagonism, such as atropine and naloxone, and explain chelating agents like calcium disodium EDTA for lead poisoning.

Doctors increase diuresis with intravenous fluids to boost kidney excretion of poisons; when kidneys fail, hemodialysis or peritoneal dialysis remove toxins, including amphetamine, aspirin, barbiturates, with exchange transfusion in children.

Classify poisons into irritants, systemic poisons, and miscellaneous, with corrosives further divided into mineral and organic acids, vegetable acids, and alcohol. Explain how corrosives cause tissue corrosion and protein precipitation.

Explore a forensic toxicology case of acute hydrochloric acid poisoning, detailing post-mortem findings of mucosal erosion, lip injuries, and stomach corrosion observed during autopsy.

Analyzes the microscopic gastric mucosa, revealing superficial involvement with deeper layers intact, and uses GC-MS to detect fluoride in blood and stomach contents, concluding death from acute hydrochloric acid poisoning.

Illustrates suicidal corrosive ingestion in developing countries causing gastric outlet obstruction from strictures, with endoscopy revealing mucosal damage, ulcers, and stenosis.

This case explains corrosive ingestion causing gastric outlet obstruction and a gastrojejunostomy to bypass the stomach–duodenum. It notes coagulative necrosis, ulcers, strictures, and symptoms of vomiting, dehydration, and weight loss.

Conservative management is the mainstay for corrosive injuries, with endoscopy to assess damage and supportive care including proton pump inhibitors, and, if strictures develop, surgical intervention for upper gastrointestinal obstruction.

This case study reports autopsy findings of an octogenarian who ingested sodium hydroxide, a corrosive alkali, causing liquefactive necrosis and disappearance of esophagus, trachea, and lungs, with gastric mucosa discoloration.

Explain how corrosive alkalis cause tissue injury through liquefaction necrosis, emulsification, and membrane disruption, destroying cells and extruding contents, with damage primarily in the upper GI tract squamous epithelium.