= Solution
\b[<Sulfuric acid> produces corrosive injury, <white phosphorus> can cause early gastrointestinal illness followed by delayed systemic poisoning, and <strychnine> produces painful, stimulus-sensitive <muscle spasms>.] The three patterns should be distinguished rather than treated as one syndrome. “Sulphuric acid” and “strychnia” are the historical spellings used in the examination.
With swallowed <sulfuric acid>, the principal symptoms are immediate burning pain in the mouth, throat and upper abdomen; excessive salivation; painful or difficult swallowing; and repeated <vomiting>, which may contain <blood>. Injury to the <larynx> can cause swelling, altered voice and obstruction of the <airway>. Severe gastrointestinal damage can lead to <hemorrhage>, perforation and circulatory <shock>. The extent of injury depends on concentration, quantity and contact, so no single appearance of the mouth measures the whole injury. Inhalation of acid mist principally causes irritation, coughing, chest tightness and difficulty breathing; severe exposure can damage the <lungs>. These are effects of a corrosive substance at its contact sites, not the symptoms of a selectively acting convulsant.<Sulphuric Acid: Toxicological Overview by the UK Health Security Agency>[“Health effects of acute or single exposure”, inhalation and ingestion: corrosive burns, dysphagia, vomiting, airway injury and systemic complications]{ref}
For <phosphorus poisoning>, the relevant toxic material is <white phosphorus>, also called yellow phosphorus. It should not be confused with ordinary dietary <phosphate> or assumed to have the same properties as <red phosphorus>. After ingestion there may be burning discomfort, thirst, nausea, <vomiting>, abdominal pain and <diarrhoea>. A garlic-like odour or luminescent vomit can be a clue, but their absence does not exclude exposure. Severe cases can collapse early. More deceptively, symptoms may improve for an interval before renewed illness, <jaundice>, tender enlargement of the <liver>, abnormal bleeding, <kidney> injury, confusion and <coma>. This sequence reflects delayed systemic injury, especially <liver failure>; apparent recovery from the first gastric symptoms is not proof that poisoning has ended.<White Phosphorus: Systemic Agent by the National Institute for Occupational Safety and Health>[“Signs/Symptoms”, ingestion and delayed effects: gastrointestinal phase, apparent improvement and subsequent multiorgan injury]{ref}
Exposure of the skin or eyes to burning <white phosphorus> can cause severe local burns and also systemic toxicity. Long-term industrial exposure with destructive jaw disease is a different presentation from the acute swallowed-poison pattern. Current institutional toxicology distinguishes these routes and time courses; an 1865 symptom description should not be stretched into a claim that all substances containing <phosphorus> behave alike.<White Phosphorus by the Agency for Toxic Substances and Disease Registry>[ToxFAQs, health effects: ingestion, local burns and chronic occupational jaw disease]{ref}
With <strychnine poisoning>, apprehension, restlessness and muscular stiffness are followed by repeated, intensely painful generalized <muscle spasms>. Slight touch, noise, light or movement can provoke an attack. The limbs become rigid and the trunk may arch backwards in <opisthotonus>; jaw closure and facial contraction can give <trismus> and <risus sardonicus>. The <respiratory muscles> may be fixed during an attack, causing difficulty breathing and <cyanosis>. Between attacks there may be substantial relaxation, while consciousness is initially preserved. The person can therefore be lucid and terrified of another attack. Exhaustion, overheating and ultimately <respiratory failure> can follow.<Strychnine by the Centers for Disease Control and Prevention>[“How it works” and “Signs and symptoms”: painful spasms, arching, initial consciousness and respiratory failure]{ref}
Repeated violent contractions may produce <hyperthermia>, <acidosis> and <rhabdomyolysis>, with dark urine and <acute kidney injury>. Initial awareness is characteristic, but advanced <hypoxia> can abolish it. The pattern differs from the immediate destructive pain of <sulfuric acid> and the often delayed organ injury of <white phosphorus>. The modern account of inhibitory <glycine receptor> blockade explains the stimulus-sensitive contractions, but that receptor mechanism is later knowledge, not something to attribute to an 1865 candidate.<Strychnine: Biotoxin by the National Institute for Occupational Safety and Health>[“Signs/Symptoms”, ingestion: complications of spasms]{ref}<Strychnine Poisoning by the California Poison Control System>[Discussion, glycine inhibition and clinical comparison]{ref}
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