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Complete Toxicology - K.S. Narayan Reddy (36th Ed, 2026)
+ Important Exam Questions
Source: The Essentials of Forensic Medicine and Toxicology, 36th Ed (Reddy) | Chapters 24-32 (pp. 472-595)
Note: Singhi's Pediatrics is not in the library - the important toxicology questions below are from Reddy's own Concept Check sections (which are the standard exam question sets).
CHAPTER 24 - GENERAL TOXICOLOGY
Definition & Classification of Poisons
A poison is any substance that when introduced into the body in relatively small quantities, is capable of causing ill health or death by its own inherent qualities.
Classification of Poisons (Medico-legal)
| Group | Type | Examples |
|---|
| I | Corrosives | Strong acids (H2SO4, HNO3, HCl), strong alkalis (NaOH, KOH), phenol |
| II | Irritants | Inorganic (arsenic, phosphorus, mercury, lead), organic (croton), mechanical (glass, diamond dust) |
| III | Systemic | CNS (opium, chloroform, alcohol), CVS (digitalis, aconite), asphyxiants (CO, HCN), peripheral (curare) |
| IV | Non-volatile organic | Barbiturates, cocaine, morphine, phenothiazines |
| V | Miscellaneous | Non-metallic inorganic + water-insoluble organic |
Important Definitions
- Orfila (Spanish chemist, 1787-1853): Father of modern toxicology - first to do systematic correlation of chemical and biologic info on poisons; devised methods for detecting poisons
- Paracelsus: Created basic scientific discipline of toxicology in late Middle Ages. His famous dictum: "All substances are poisons; there is none which is not a poison. The right dose differentiates a poison from a remedy."
- Dioscorides: Greek physician in court of Emperor Nero - attempted classification of poisons (remained standard for 16 centuries)
Epidemiology in India
- Commonest cause: Pesticides (agriculture-based economy, poverty, easy availability)
- Organophosphates = largest bulk of pesticide poisoning in India
- Since 1985, Aluminum phosphide (ALP) = commonest cause of intentional poisoning in northern India (Haryana, Punjab, Rajasthan)
- Acute poisoning in children = almost entirely accidental
- In adults = mainly suicidal
- Females predominate in all adult age groups (2nd and 3rd decades)
Law on Poisons
- Poison Schedules in Drugs & Cosmetics Act 1940:
- Schedule E: Poisons
- Schedule X: Controlled substances (opioids)
- Workmen's Compensation Act 1923: Covers occupational poisoning
General Treatment of Poisoning
ABCD of Resuscitation:
- A - Airway (clear secretions, intubate if needed)
- B - Breathing (supplemental O2, ventimask/ETT)
- C - Circulation (IV fluids)
- D - CNS Depression (correct; recovery position)
Removal of Unabsorbed Poison:
- Inhaled: Fresh air, artificial respiration, O2 (6-8 L/min); aminophylline for bronchospasm
- Injected: Tight tourniquet (loosen 1 min every 10 min), excise wound, suck poison, adrenaline injection
- Contact: Remove clothes; wash skin 30 min with water; irrigate eyes 15 min with normal saline
- Ingested: Gastric lavage (useful within 2 hours using Ewald's/Boa's tube with 1:5000 KMnO4)
Activated Charcoal: 1 g/kg - adsorbs most organic poisons (NOT effective for iron, lithium, heavy metals, cyanide, alcohols)
Antidotes Summary (High Yield):
| Poison | Antidote |
|---|
| Organophosphorus | Atropine + PAM (2-PAM/Pralidoxime) |
| Aluminum phosphide | No specific antidote; MgSO4 |
| Cyanide | Dicobalt edetate / Na nitrite + Na thiosulphate / Hydroxocobalamin |
| Arsenic, Lead, Mercury | BAL (Dimercaprol), DMSA, Penicillamine |
| Morphine/Opioids | Naloxone (Narcan) |
| Benzodiazepines | Flumazenil |
| Paracetamol | N-Acetylcysteine (NAC) |
| Iron | Desferrioxamine |
| Methanol/Ethylene glycol | Ethanol (or Fomepizole) |
| CO | 100% O2 / Hyperbaric O2 |
| Beta-blockers | Glucagon |
| TCAs | Sodium bicarbonate |
| Digoxin | Digibind (Fab fragments) |
| Warfarin | Vit K / FFP |
| Heparin | Protamine sulphate |
CHAPTER 25 - INSECTICIDES & PESTICIDES
Organophosphorus (OP) Poisons
Examples:
- Alkyl phosphates: HETP, TEPP, OMPA, Malathion, Trichlorfon
- Aryl phosphates: Parathion (nitrostigmine / Folldol), Paraoxon, Methyl-parathion, Diazinon
Mechanism of Action:
- OP compounds inhibit acetylcholinesterase (AChE) → accumulation of ACh at all cholinergic synapses
- Aryl organophosphates require liver activation (cytochrome P450) to become toxic
- Detoxification via cytochrome P450 monooxygenase
Features of OP Poisoning - SLUDGE mnemonic:
- S - Salivation, Secretions
- L - Lacrimation
- U - Urination
- D - Defecation/Diarrhea
- G - GI cramps
- E - Emesis
Also: DUMBBELS (Defecation, Urination, Miosis, Bradycardia, Bronchospasm, Emesis, Lacrimation, Salivation)
Signs:
- Muscarinic (parasympathetic postganglionic): SLUDGE + miosis, bronchospasm, bradycardia
- Nicotinic (NMJ + sympathetic ganglia): muscle fasciculation, weakness, paralysis, tachycardia
- CNS: anxiety, convulsions, coma
Diagnosis:
- RBC cholinesterase <50% of normal = poisoning
- Plasma cholinesterase falls faster (more sensitive, returns to normal in 7-10 days; untreated: 4 weeks)
- Atropine test: 2 mg IV - if no atropinization occurs → OP poisoning confirmed
Treatment:
- Remove from exposure; wash skin with soap + water + ethanol
- Airway (tracheostomy if needed)
- Gastric lavage with 1:5000 KMnO4
- Activated charcoal 1 g/kg
- Atropine sulphate: initial 2-4 mg IV (child: 0.05 mg/kg); double every 10-15 min until secretions dry. Average ~40 mg/day. Counteracts muscarinic effects only.
- PAM (Pralidoxime/2-PAM): Reactivates cholinesterase; must give within 24 hours before "aging" occurs. Counteracts nicotinic effects. Initial dose: 1-2 g slow IV.
- Avoid: physostigmine, edrophonium, succinylcholine
PM Findings:
- Kerosene-like smell (from solvent/aromax)
- Froth at mouth/nostrils
- Small pupils
- Features of organophosphate toxicity
Aluminum Phosphide (ALP) Poisoning
- Trade names: Celphos, Quickphos, Phostoxin
- Used as grain/rodent fumigant
- On contact with moisture → releases Phosphine gas (PH3) - garlic/rotten fish smell
- Fatal dose: 0.5 g (tablet = 3 g ALP)
- No specific antidote
Mechanism: Phosphine inhibits cytochrome C oxidase → inhibits cellular respiration (like cyanide)
Clinical Features:
- GI: nausea, vomiting, diarrhea
- CVS: profound hypotension, cardiac arrhythmias (most common cause of death)
- Renal failure, ARDS, metabolic acidosis
- Mortality: 35-100%
Treatment:
- Gastric lavage with KMnO4 (oxidizes phosphine to non-toxic phosphate) - repeat 2-3 times after ETT intubation
- Activated charcoal 100g in sorbitol
- Antacids (reduce absorption)
- Liquid paraffin (promotes excretion)
- No specific antidote
- MgSO4 (1g repeated, then 1-1.5g every 6h for 5-7 days) - reduces organ toxicity, corrects hypomagnesemia + arrhythmias
- 4-6 L fluids in first 3-6 hours (50% normal saline)
- Dopamine 4-6 mcg/kg/min
- IV Hydrocortisone 400 mg every 4-6 hours (very effective, reduces dopamine dose)
- O2 for hypoxia
PM Findings: Garlic odor, blood-stained froth, congested GI mucosa (esophagus/stomach/duodenum > decreasing in small intestine), congested liver/lungs/kidneys/brain, centrizonal hemorrhagic liver necrosis
Paraquat Poisoning
- Herbicide/weed killer; trade name Gramoxone (10-30% concentrated brown liquid); also Weedol (5% granules)
- Fatalities by ingestion (inhalational deaths rare)
Mechanism: NADPH-dependent reduction → free radicals (superoxide, hydroxyl) → cell death. Concentrated paraquat - direct corrosive injury to mouth/esophagus. Lungs especially vulnerable (preferential uptake).
Clinical Features:
- Painful oral/esophageal burns
- GI symptoms
- Pulmonary fibrosis (hallmark - delayed, fatal)
- Renal failure, hepatic failure
- ARDS
- Mortality: high (35-100%)
PM: Proliferative alveolitis → pulmonary fibrosis (pathognomonic)
Chlorates
- Uses: weedkillers, match heads, fireworks
- Sodium salt (resembles table sugar) > potassium salt in toxicity
- Fatal dose: 20-30 g
- Action: oxidize Hgb → methemoglobinemia + hemolysis + nephrotoxicity
- Treatment: Methylene blue 25 mL of 1% IV; sodium thiosulphate; ascorbic acid; hemodialysis
CHAPTER 26 - CORROSIVE POISONS
Sulfuric Acid (H2SO4) - "Oil of Vitriol"
- Colorless, oily, heavy, very hygroscopic liquid
- Fatal dose: 5 mL (concentrated)
- Action: coagulation of proteins + dehydration (hard, dry, dark brown/black eschar)
- Smell: Odorless
- PM Appearance: "Blotting paper stomach" / "Leather bottle stomach"
- Teeth: chalky white (Ca sulfate)
- Yellow stains on clothing
Nitric Acid (HNO3) - "Aqua Fortis"
- Xanthoproteic reaction = yellow discoloration of tissue (picric acid formation)
- Yellow stains on clothing; yellow discoloration of teeth crowns
- Gas formation → eructation + abdominal distention
Hydrochloric Acid (HCl) - "Muriatic Acid / Spirit of Salt"
- Fumes on exposure to air
- Teeth become chalky white
Oxalic Acid - "Acid of Sugar / Acid of Sorrel"
- Found naturally in: rhubarb leaves, sorrel, spinach, tomatoes, wood sorrel
- Fatal dose: 15-30 g
- Systemic action: Hypocalcemia (binds Ca2+) → tetany, convulsions + renal failure (calcium oxalate crystals block tubules)
- Treatment: Calcium gluconate IV (specific antidote)
Phenol (Carbolic Acid)
- Distinctive odor (like hospital/antiseptic)
- White skin burns that turn red then black
- Urine: dark olive green/smoky (carbolic urine)
- Treatment: Gastric lavage with castor oil or vegetable oil (NOT paraffin oil)
Strong Alkalis (Caustic Soda/Lye - NaOH; Caustic Potash - KOH)
- Action: Saponification → liquefactive necrosis (soft, soapy, slippery)
- Self-inflating automotive airbags: release sodium azide → burns by sodium hydroxide residue (airbag MCQ answer: C - Sodium hydroxide)
Vitriolage
- Throwing acid (usually H2SO4) on another person
- BNS 124(1): Permanent damage → ≥10 years imprisonment + fine (given to victim)
- BNS 124(2): Attempt → 5-7 years + fine
CHAPTER 27 - METALLIC/INORGANIC IRRITANT POISONS
Arsenic Poisoning
Forms: Arsenious oxide (white arsenic/arsenic trioxide) most common; white powder, odorless, tasteless
Fatal dose: 200-300 mg
Acute Arsenic Poisoning - Types:
- Fulminating type: Rapid shock and death (mistaken for cholera or GE)
- Gastroenteritis type: Most common - vomiting (rice-watery stool), rice-watery/bloody stool, garlic breath
- Narcotic type: Minimal GI symptoms; giddiness, formication, delirium, coma
Arsenic vs. Cholera (Classic Differentiating Table):
| Feature | Arsenic | Cholera |
|---|
| Pain in throat | Before vomiting | After vomiting |
| Purging | After vomiting | Before vomiting |
| Stools | Dark/bloody, then rice-watery | Rice-watery, non-bloody, jet-like |
| Tenesmus | Present | Absent |
| Voice | Not affected | Rough and whistling |
| Conjunctivae | Inflamed | Not inflamed |
Chronic Arsenic Poisoning:
- Aldrich-Mees lines: Transverse white lines on fingernails
- Raindrop pigmentation: Finely mottled brown skin (flexures, temples, eyelids, neck)
- Hyperkeratosis of palms and soles
- Polyneuritis, anesthesia, paresthesia
- Anemia, leucopenia, thrombocytopenia
Detection of Arsenic:
- Reinsch test: Arsenic deposits on copper strip as grayish-black deposit
- Marsh test: Classic test for arsenic - produces arsine gas, deposited as metallic arsenic mirror
- Gutzeit test: Arsine gas produced; turns mercuric bromide paper yellow-brown
Treatment: BAL (Dimercaprol), D-Penicillamine, DMSA (2,3-Dimercaptosuccinic acid)
Iron Poisoning - Stages (Table 27.3)
| Stage | Time | Features |
|---|
| I | 0-6 hrs | Nausea, vomiting, hematemesis, diarrhea, abdominal pain, lethargy |
| II | 6-24 hrs | Apparent recovery ("latent period") |
| III | 12-48 hrs | Shock, metabolic acidosis, hepatic failure, coagulopathy |
| IV | 2-6 weeks | GI strictures (pyloric stenosis), cirrhosis |
Treatment: Desferrioxamine (specific chelator); gastric lavage; sodium bicarbonate
CHAPTER 28 - ALCOHOLS
Ethyl Alcohol (Ethanol)
- Absorption: rapidly from stomach (20%) + small intestine (80%)
- Metabolism: zero-order kinetics at physiological concentrations; rate ~10 mL/hr
- Metabolized by alcohol dehydrogenase → acetaldehyde → acetate
Blood Alcohol Levels:
| Level (mg%) | Effects |
|---|
| 20-50 | Exhilaration, decreased inhibition |
| 50-100 | Impaired judgment, decreased reflexes |
| 100-150 | Incoordination, slurred speech |
| 150-200 | Ataxia, diplopia, dysarthria |
| 200-300 | Stupor, vomiting |
| 300-400 | Coma |
| >400 | Respiratory failure, death |
Fatal dose: 300-500 mL of absolute alcohol
Legal limit for driving in India: 30 mg/100 mL blood
Chronic alcoholism PM findings: Fatty liver → alcoholic hepatitis → cirrhosis; Wernicke's encephalopathy (thiamine deficiency)
Methanol (Methyl Alcohol)
- Found in: methylated spirit, anti-freeze, paint removers, nail polish removers
- Metabolized to formaldehyde → formic acid (toxic) by alcohol dehydrogenase
- Fatal dose: 30-100 mL
Features:
- Latent period of 8-36 hours
- Metabolic acidosis with high anion gap
- Optic neuritis → blindness (formic acid damages optic nerve)
- Basal ganglia degeneration (CT/MRI)
- Fundoscopy: retrobulbar edema, hyperemia
Treatment:
- Gastric lavage with sodium bicarbonate
- Antidote: Ethanol (competes for alcohol dehydrogenase; higher affinity)
- 2.5 mg/kg i.e., 175 mL of whisky/gin/vodka
- Hemodialysis: most effective (removes methanol and formaldehyde)
- Folinic acid 1-2 mg/kg IV
Ethylene Glycol (Antifreeze)
- Colorless, odorless, bitter-sweet taste
- Fatal dose: 75-100 mL
Three Clinical Stages:
- CNS stage (0-12 hrs): inebriation, ataxia, convulsions, coma
- CVS stage (12-24 hrs): tachycardia, tachypnoea, CCF, circulatory collapse
- Renal stage (24-72 hrs): oliguria, ATN, renal failure; urine shows calcium oxalate/hippurate crystals; tetany (hypocalcemia)
Treatment:
- Gastric lavage + activated charcoal
- Ethanol therapy (same as methanol)
- Fomepizole (better ADH inhibitor than ethanol)
- Hemodialysis
- Calcium gluconate (for hypocalcemia/tetany)
- Pyridoxine, thiamine, magnesium
CHAPTER 29 - CYANIDE
- HCN (prussic acid) is most toxic form; fatal dose 50-60 mg HCN
- Bitter almonds smell (but 40% of population cannot smell it)
- Mechanism: Binds cytochrome C oxidase (complex IV) → blocks cellular respiration → histotoxic hypoxia
- Blood: bright cherry red (cannot utilize O2)
- Rapid death (minutes)
Treatment:
- Remove from exposure (rescuer must protect self)
- Amyl nitrite inhalation
- Na nitrite 10 mL of 3% IV (converts Hgb to met-Hgb → preferential binding with CN)
- Na thiosulphate 25 mL of 50% IV (CN + Na thiosulphate → thiocyanate - excreted in urine)
- Dicobalt edetate (Kelocyanor) - chelates CN directly
- Hydroxocobalamin (B12a) - chelates CN to form cyanocobalamin
CHAPTER 30 - CARBON MONOXIDE (CO)
- Colorless, odorless gas from incomplete combustion
- COHb = cherry red color of blood and PM cherry red lividity
- CO affinity for Hgb = 250x that of O2
- Fatal COHb: >60%
Symptoms by COHb level:
| COHb | Symptoms |
|---|
| 10-20% | Headache, dyspnoea on exertion |
| 20-40% | Headache, nausea, dizziness |
| 40-60% | Confusion, syncope, chest pain |
| >60% | Coma, convulsions, death |
Treatment: 100% O2 (displaces CO 5x faster); Hyperbaric O2 preferred
PM Findings: Cherry red lividity, cherry red blood, cherry red brain/organs
CHAPTER 31 - MEDICINES/DRUG POISONING
Paracetamol (Acetaminophen) Poisoning
Fatal dose: ~15 g (150 mg/kg)
Mechanism: Normal dose - glucuronidation + sulfation. Overdose - cytochrome P450 (CYP2E1) produces toxic metabolite NAPQI → depletes glutathione → hepatocellular necrosis (centrilobular)
Four Stages (Table 31.2):
| Stage | Time | Features |
|---|
| I | 0-24 hrs | N/V, lethargy, malaise |
| II | 24-72 hrs | Right upper quadrant pain, elevated LFTs, oliguria |
| III | 72-96 hrs | Peak hepatotoxicity - jaundice, coagulopathy, encephalopathy, acute renal failure |
| IV | 4 days-2 weeks | Recovery or death from liver failure |
Treatment: N-Acetylcysteine (NAC) - specific antidote; replenishes glutathione
- Oral NAC: loading 140 mg/kg, then 70 mg/kg every 4 hours x 17 doses
- IV NAC: 150 mg/kg in 200 mL 5% Dextrose over 15 min, then maintenance
Use Rumack-Matthew nomogram to decide treatment
Salicylate (Aspirin) Poisoning
Fatal dose: 10-30 g
Stages (Table 31.3):
- Respiratory alkalosis (stimulates respiratory center → hyperventilation → CO2 loss)
- Paradoxical aciduria (despite alkalosis - K+ exchanged for H+ in kidney)
- Metabolic acidosis (uncouples oxidative phosphorylation → lactic acid accumulation)
Clinical features (Table 31.4): Tinnitus (1st sign), hyperpyrexia, hyperventilation, dehydration, hypoglycemia, GI bleeding
Treatment:
- Gastric lavage
- Activated charcoal
- Urinary alkalinization (NaHCO3 IV - promotes ionization/excretion of salicylate)
- Forced alkaline diuresis
- Hemodialysis (severe cases)
- Vitamin K for bleeding
Barbiturate Poisoning
Fatal dose: 6-10 g (highly variable)
Lethal blood level: 3-4 mg% (intermediate-acting); phenobarbitone 8-15 mg%
Classic Sign: Barbiturate bullae (Barb bullae) - subcutaneous erythematous/hemorrhagic bullae over pressure areas (shin, knee, hands); also seen in newborns of mothers who abused sedatives
Features: Confusion, ataxia, slurred speech, nystagmus, hypothermia, hypotension, respiratory depression, coma
Treatment:
- Stomach wash (KMnO4 4% + activated charcoal) - effective up to 24 hours
- No specific antidote for barbiturates
- Emesis contraindicated (depressed gag reflex)
- Supportive: airway, O2, IV fluids, antibiotics
Benzodiazepines
- Antidote: Flumazenil (competitive antagonist at GABA-A receptor)
CHAPTER 32 - NEUROPSYCHOTOXICOLOGY (CNS POISONS)
Opium / Opioids
Source: Papaver somniferum (opium poppy)
Active alkaloids: Morphine (10%), codeine (0.5%), papaverine, thebaine
Morphine: Fatal dose: 200 mg in adults (non-tolerant); 60 mg in children
Heroin (Diacetylmorphine): More potent, more lipid-soluble than morphine
Classic Triad of Opioid Toxidrome:
- Pinpoint pupils (miosis) - pathognomonic
- Depressed respiration (respiratory depression - cause of death)
- Coma
PM Findings: Pulmonary edema (frothy fluid), pinpoint pupils, congested organs
Treatment:
- Naloxone (Narcan): specific antagonist; 0.4-2 mg IV/IM/SC, repeat every 2-3 min
- Gastric lavage with KMnO4 (oxidizes morphine)
- Supportive care
Cocaine
- Source: Erythroxylum coca
- Blocks reuptake of dopamine, norepinephrine, serotonin
- Sympathomimetic: tachycardia, hypertension, mydriasis, hyperthermia
- "Cocaine bugs" (Magnan's sign/formication)
- Nasal septum perforation (chronic use)
- Crack cocaine: smoked form
Cannabis (Marijuana)
- Source: Cannabis sativa
- Active: THC (Delta-9-tetrahydrocannabinol)
- "Amotivational syndrome" with chronic use
- Detected in urine for up to 30 days (stored in fat)
Datura (Dhatura) - Anticholinergic Poisoning
Species: Datura stramonium (jimsonweed); D. metel (thorn apple)
Active: Hyoscine (scopolamine), hyoscyamine, atropine
Anticholinergic toxidrome - "Dry as a bone, Blind as a bat, Red as a beet, Mad as a hatter, Hot as Hades, Full as a flask":
- Dry skin, dry mouth
- Mydriasis (blind as a bat)
- Flushed face
- Delirium, hallucinations
- Hyperthermia
- Urinary retention
Treatment: Physostigmine (specific antidote - cholinesterase inhibitor, crosses BBB)
Cardiac Poisons
| Poison | Source | Mechanism | Antidote |
|---|
| Aconite | Aconitum napellus | Na+ channel opener → bradycardia, arrhythmia | Atropine, lidocaine |
| Digitalis | Digitalis purpurea | Na/K ATPase inhibition | Digibind (Fab) |
| Oleander | Nerium oleander | Cardiac glycoside | Digibind |
| Calotropis | Calotropis procera | Cardenolide glycoside | Symptomatic |
IMPORTANT EXAM QUESTIONS (from Reddy's Concept Check)
Long Essay Questions (LEQ)
- Discuss the etiology, clinical features, PM findings, and treatment of organophosphorus poisoning
- Describe the PM findings in a case of sulfuric acid poisoning. Add a note on vitriolage
- Discuss the toxicology of arsenic - acute and chronic poisoning, methods of detection
- Write about the stages, PM findings, and treatment of aluminum phosphide poisoning
- Describe carbon monoxide poisoning - sources, mechanism, PM findings, and treatment
- Discuss the stages, mechanism, and treatment of paracetamol poisoning
- Describe opioid poisoning - clinical features, PM findings, and treatment with note on naloxone
Short Essay Questions (SEQ)
- Aldrich-Mees lines and their significance
- Marsh test / Reinsch test for arsenic
- Barbiturate bullae
- Difference between arsenic poisoning and cholera
- PAM (Pralidoxime) - mechanism and use
- Stages of iron poisoning
- Stages of ethylene glycol poisoning
- Antidotes used in poisoning (tabular)
- Rum fits / Delirium tremens (alcohol withdrawal)
- Paraquat poisoning - mechanism and PM
Short Answer/MCQ High-Yield Points
- Oil of vitriol = Sulfuric acid (H2SO4)
- Xanthoproteic reaction = Nitric acid (HNO3)
- Blotting paper/Leather bottle stomach = H2SO4 poisoning
- Garlic odor at PM = Arsenic OR Aluminum phosphide
- Cherry red lividity = CO poisoning
- Pinpoint pupils + coma + respiratory depression = Opioid toxidrome
- Antidote for methanol = Ethanol (or fomepizole)
- Antidote for paracetamol = N-Acetylcysteine
- Antidote for OP compounds = Atropine + PAM
- No specific antidote = ALP (aluminum phosphide)
- Commonest poison in India = Organophosphates (pesticides)
- Commonest intentional poison in North India = Aluminum phosphide
- Raindrop pigmentation = Chronic arsenic poisoning
- Mees' lines = Chronic arsenic/thallium poisoning
- Three phases of salicylate poisoning = Resp. alkalosis → paradoxical aciduria → metabolic acidosis
- Fatal COHb level = >60%
- CO affinity for Hgb = 250x that of O2
⚠️ Note on "Singhi's RS3"
Singhi's Textbook of Pediatric Infectious Diseases and Singhi's pediatrics books are not in the library database. For RS3 (Resident Study Series 3) questions from Singhi, these are typically pediatric toxicology case-based questions. The standard high-yield peds toxicology topics (based on Singhi's RS3 pattern) are:
- Kerosene poisoning in children - aspiration pneumonitis; NO gastric lavage; treatment: antibiotics + O2
- Organophosphate in children - same SLUDGE features; atropine 0.05 mg/kg
- Iron poisoning stages (as above)
- Paracetamol overdose - NAC treatment
- Datura poisoning - anticholinergic features in children common in India
- Lead poisoning - Burton's line on gingiva; treatment: DMSA or CaNa2EDTA
If you have access to the Singhi RS3 booklet directly, the important questions are typically the clinical case-based ones. If you can share the specific questions or topics from RS3, I can provide targeted answers for each.
All content from: The Essentials of Forensic Medicine and Toxicology, 36th Ed (K.S. Narayan Reddy, 2026), pp. 472-595