Household Chemical Exposure — MCQs
Treatment of choice for acute arsenic poisoning is:
A farmer with pinpoint pupils, increased secretions and urination. What is the most likely diagnosis?
A patient comes to the casualty with organophosphate poisoning. He was started on atropine infusion and pralidoxime. After 2 hours, the patient had a sudden rise in temperature. What is the most likely cause of the fever?
Ochronosis is seen in poisoning with:
Which of these is the best for management of methanol poisoning?
Gastric lavage is contraindicated in?
Which of the following substances is a toxin but has also been historically used as a therapeutic emetic in poisoning management?
Miosis is caused by all EXCEPT -
Gastric lavage is contraindicated in the following:
Which of the following are true/false about clinical features of Fat embolism syndrome? 1. Tachypnea 2. Systemic hypoxia may occur 3. Fat globules in urine are diagnostic 4. Manifests after several days of trauma 5. Petechiae in anterior chest wall
Household Chemical Exposure Indian Medical PG Practice Questions and MCQs
Question 1: Treatment of choice for acute arsenic poisoning is:
- A. Ipecac
- B. Dimercaprol (Correct Answer)
- C. Penicillamine
- D. Activated charcoal
Explanation: ***Dimercaprol*** - **Dimercaprol** (also known as British Anti-Lewisite, BAL) is a chelating agent used for **acute arsenic poisoning**. [1] - It works by binding to arsenic, forming a stable, non-toxic complex that can be excreted from the body. - Among the given options, **dimercaprol is the correct choice** for treating acute arsenic poisoning. - **Note:** While dimercaprol is effective, newer chelators like **DMSA (succimer)** and **DMPS (unithiol)** are now preferred in modern practice due to better safety profiles and efficacy, though they are not listed in the options. [1] *Ipecac* - **Ipecac syrup** induces vomiting and is generally **contraindicated** in poisonings with corrosives, hydrocarbons, or substances that can cause rapid central nervous system depression. - It is **not effective** for systemic poisonings like arsenic, where absorption has already occurred, and can cause complications like aspiration. - Ipecac is largely obsolete in modern toxicology practice. *Penicillamine* - **Penicillamine** is another chelating agent, primarily used for **copper poisoning** (e.g., Wilson's disease) and sometimes for lead poisoning. - While it has some chelating properties, it is **less effective** than dimercaprol for acute arsenic toxicity and can have more significant side effects. - It is **not the first-line treatment** for arsenic poisoning. *Activated charcoal* - **Activated charcoal** is effective for adsorbing many toxins in the gastrointestinal tract, preventing their absorption. - However, it has **poor affinity for heavy metals** like arsenic and is therefore **not recommended** as the primary treatment for arsenic poisoning. - It may have limited benefit only if given very early after ingestion, but chelation therapy is the definitive treatment.
Question 2: A farmer with pinpoint pupils, increased secretions and urination. What is the most likely diagnosis?
- A. Alcohol poisoning
- B. Organophosphate poisoning (Correct Answer)
- C. Opioid poisoning
- D. Atropine poisoning
Explanation: ***Organophosphate poisoning*** - **Pinpoint pupils (miosis)**, **increased secretions** (salivation, lacrimation, bronchial secretions), and **urination** are classic signs of cholinergic crisis caused by organophosphate toxicity [1]. - The patient's profession as a **farmer** increases the likelihood of exposure to pesticides, which often contain organophosphates [1], [2]. *Alcohol poisoning* - While alcohol poisoning can cause CNS depression, it does not typically present with **pinpoint pupils** or **increased secretions** like salivation and urination. - Common signs include **ataxia**, **slurred speech**, **nausea**, and **vomiting**. *Opioid poisoning* - Opioid poisoning also causes **pinpoint pupils** and **CNS depression**, but it typically leads to **decreased secretions** and **urinary retention**, not increased urination [2]. - **Respiratory depression** is a hallmark feature, which is not highlighted here as a primary symptom. *Atropine poisoning* - Atropine is an anticholinergic agent, meaning it would cause the opposite effects of organophosphate poisoning [2]. - Symptoms would include **dilated pupils (mydriasis)**, **dry mouth**, **decreased secretions**, and **urinary retention**.
Question 3: A patient comes to the casualty with organophosphate poisoning. He was started on atropine infusion and pralidoxime. After 2 hours, the patient had a sudden rise in temperature. What is the most likely cause of the fever?
- A. Side effect of pralidoxime.
- B. Result of organophosphate poisoning.
- C. Unrelated or unknown cause.
- D. Fever due to atropine toxicity. (Correct Answer)
Explanation: ***Fever due to atropine toxicity.*** - **Atropine** blocks muscarinic receptors, leading to inhibition of **sweat glands** and subsequent rise in body temperature (hyperthermia), especially with high doses or prolonged infusion. - Given the patient is receiving an **atropine infusion** and developed fever, **atropine toxicity** is a primary concern. *Side effect of pralidoxime.* - While pralidoxime can cause side effects like dizziness, blurred vision, or tachycardia, **fever is not a typical side effect** of pralidoxime. - Pralidoxime works by **regenerating acetylcholinesterase** [2, 3] and does not directly interfere with thermoregulation in a way that would cause fever. *Result of organophosphate poisoning.* - **Organophosphate poisoning** typically causes **hypothermia** due to excessive cholinergic stimulation leading to peripheral vasodilation and increased sweating [1]. - **Fever** is not a direct result of the acute phase of organophosphate poisoning itself, but rather a complication of treatment or other factors. *Unrelated or unknown cause.* - While possible, it's less likely to be "unrelated or unknown" when a clear pharmacological explanation (**atropine toxicity**) exists for fever in the context of the patient's treatment. - It would be important to first rule out known causes related to the ongoing treatment before attributing it to an unknown cause.
Question 4: Ochronosis is seen in poisoning with:
- A. Boric acid
- B. HCl
- C. Carbolic acid (Correct Answer)
- D. Oxalic acid
Explanation: ***Carbolic acid (Phenol)*** - Carbolic acid causes **blackish-brown discoloration** of skin and tissues at the site of contact due to its **corrosive action and protein denaturation**. - This characteristic **dark staining of tissues** is a forensic marker of phenol poisoning and is sometimes referred to in forensic literature as "ochronosis-like" changes. - Phenol is absorbed through skin and mucous membranes and can cause **CNS depression, convulsions, and metabolic acidosis**. *Boric acid* - Boric acid poisoning manifests with **"boiled lobster" appearance** of skin (erythematous desquamation). - Causes **gastrointestinal symptoms** (vomiting, diarrhea) and **CNS effects** in severe cases. - Does not cause blackish tissue discoloration. *HCl (Hydrochloric acid)* - HCl is a **strong corrosive acid** causing severe chemical burns. - Produces **white or gray coagulated necrosis** of tissues on contact. - Does not produce the dark discoloration characteristic of phenol. *Oxalic acid* - Oxalic acid poisoning causes **hypocalcemia** by chelating calcium ions. - Leads to **cardiac arrhythmias, tetany, and renal toxicity** (calcium oxalate crystal deposition). - Does not cause tissue discoloration or ochronosis.
Question 5: Which of these is the best for management of methanol poisoning?
- A. Fomepizole (Correct Answer)
- B. Naltrexone
- C. Disulfiram
- D. Acamprosate
Explanation: ***Fomepizole*** - **Fomepizole** is a competitive inhibitor of **alcohol dehydrogenase**, the enzyme responsible for metabolizing methanol into toxic metabolites like formic acid. - By inhibiting this enzyme, it prevents the formation of these toxic metabolites, thereby reducing organ damage and metabolic acidosis in methanol poisoning. *Naltrexone* - **Naltrexone** is an **opioid receptor antagonist** used in the treatment of alcohol and opioid dependence. - It does not have any direct action on the metabolism of methanol or its toxic byproducts. *Disulfiram* - **Disulfiram** inhibits **aldehyde dehydrogenase**, leading to an unpleasant reaction when alcohol is consumed (flushing, nausea, vomiting). - It is used for alcohol cessation and has no role in the management of methanol poisoning. *Acamprosate* - **Acamprosate** is a medication used to reduce alcohol cravings in individuals recovering from alcohol dependence, possibly by modulating **glutamate neurotransmission**. - It does not directly affect the metabolism of methanol or mitigate its toxic effects.
Question 6: Gastric lavage is contraindicated in?
- A. Bicarbonate
- B. Hydrocarbons (Correct Answer)
- C. Organo-Phosphosphate poisoning
- D. PCM toxicity
Explanation: ***Hydrocarbons*** - Gastric lavage is contraindicated in **hydrocarbon poisoning** due to the high risk of **aspiration** [2]. - Aspiration of hydrocarbons can lead to severe **chemical pneumonitis**, which is often more life-threatening than the systemic toxicity from ingestion [2]. *Bicarbonate* - Ingesting a large amount of bicarbonate can cause **alkalosis** and electrolyte imbalances. - While gastric lavage is not typically the primary treatment for mild bicarbonate overdose, it is not absolutely contraindicated in cases of massive ingestion where there is a clear benefit to removing unabsorbed substance, especially if performed with proper airway protection [1], [3]. *Organo-Phosphosphate poisoning* - Gastric lavage is generally recommended for **organophosphate poisoning** if the patient presents within 1-2 hours of ingestion and is awake with an intact gag reflex, or with a protected airway [2]. - This helps remove unabsorbed poison and can reduce the systemic absorption of these highly toxic compounds. *PCM toxicity* - For **paracetamol (PCM) toxicity**, gastric lavage can be considered if the patient presents within 1-2 hours of ingestion and has ingested a potentially toxic dose, especially when activated charcoal is not immediately available or contraindicated [4]. - The primary treatment for PCM toxicity involves **N-acetylcysteine (NAC)**, but gastric emptying can play a role in reducing initial absorption [4].
Question 7: Which of the following substances is a toxin but has also been historically used as a therapeutic emetic in poisoning management?
- A. Thallium
- B. Copper sulphate (Correct Answer)
- C. Arsenic oxide
- D. Mercuric chloride
Explanation: ***Copper sulphate*** - **Copper sulphate** is a **potent toxin** that causes gastrointestinal irritation, hemolysis, hepatotoxicity, and acute renal failure upon ingestion. - It was **historically used as an emetic** to induce vomiting in certain poisoning cases for gastric decontamination, though this practice has been largely abandoned due to its own significant toxicity and the availability of safer alternatives. - This represents its dual nature: a poison itself, yet paradoxically used in poisoning management (not as an antidote, but as a gastric evacuant). *Thallium* - **Thallium** is a highly toxic heavy metal causing severe multi-organ failure, alopecia, peripheral neuropathy, and potentially fatal systemic toxicity. - It has **no therapeutic use** in poisoning management and is purely a toxicological concern. *Arsenic oxide* - **Arsenic oxide** (arsenic trioxide) is a well-known carcinogen and potent cellular poison that disrupts oxidative phosphorylation. - While it has modern therapeutic use in acute promyelocytic leukemia, it has **never been used in poisoning management** as an emetic or therapeutic agent. *Mercuric chloride* - **Mercuric chloride** is highly corrosive and causes severe gastrointestinal burns, acute tubular necrosis, and systemic mercury toxicity. - It is a **potent toxin with no therapeutic application** in poisoning management.
Question 8: Miosis is caused by all EXCEPT -
- A. Organophosphates
- B. Pontine hemorrhage
- C. Opiates
- D. Cyanide (Correct Answer)
Explanation: **Cyanide** - **Cyanide poisoning** primarily affects cellular respiration by inhibiting **cytochrome c oxidase**, leading to **anoxia** at the cellular level. - Its typical ocular manifestation is **mydriasis** (pupil dilation) due to **hypoxia-induced sympathetic overactivity**, not miosis. *Organophosphates* - **Organophosphates** inhibit **acetylcholinesterase**, causing an excess of **acetylcholine** at muscarinic receptors [2]. - This leads to **parasympathetic overstimulation**, including pinpoint pupils (miosis). *Pontine hemorrhage* - **Pontine hemorrhage** can disrupt the **sympathetic pathways** that run through the pons. - Loss of sympathetic input to the eye results in unopposed **parasympathetic tone**, causing **miosis**. *Opiates* - **Opiates**, such as morphine and heroin, centrally stimulate the **Edinger-Westphal nucleus**, increasing **parasympathetic outflow** to the eye [1]. - This increased parasympathetic activity leads to **constriction of the pupils**, commonly referred to as "pinpoint pupils" [1].
Question 9: Gastric lavage is contraindicated in the following:
- A. Barbiturate poisoning
- B. Paracetamol poisoning
- C. Kerosene poisoning (Correct Answer)
- D. Carbolic acid poisoning
Explanation: ***Kerosene poisoning*** - Gastric lavage is contraindicated in **hydrocarbon poisoning** like kerosene due to the high risk of **aspiration pneumonitis**. [1] - Aspiration of hydrocarbons can lead to severe **chemical pneumonitis**, acute respiratory distress syndrome (ARDS), and even death. *Barbiturate poisoning* - Gastric lavage can be useful in **barbiturate poisoning**, especially if presenting within 1-2 hours of ingestion, to remove unabsorbed drug. - It's part of the management strategy to reduce drug absorption and potentially speed up recovery. *Paracetamol poisoning* - **Gastric lavage** may be considered in paracetamol overdose, particularly if performed within 1-2 hours of ingestion, to remove unabsorbed drug. - However, **activated charcoal** is usually the preferred method for gastric decontamination in paracetamol overdose, followed by **N-acetylcysteine**. *Carbolic acid poisoning* - While typically considered a corrosive, gastric lavage might be cautiously used in **carbolic acid (phenol) poisoning** in specific circumstances, such as very early presentation or large ingestions, but it carries risks of esophageal injury. [2] - Dilution with milk or water is often preferred, but lavage should be avoided if there's evidence of significant caustic injury or perforation risk.
Question 10: Which of the following are true/false about clinical features of Fat embolism syndrome? 1. Tachypnea 2. Systemic hypoxia may occur 3. Fat globules in urine are diagnostic 4. Manifests after several days of trauma 5. Petechiae in anterior chest wall
- A. 1, 3, 4, 5 true & 2 false
- B. 1, 2, 3, 5 true & 4 false
- C. All are true (Correct Answer)
- D. 2, 4 false & 1, 3, 5 true
Explanation: ***All are true*** - **Tachypnea** (1), **systemic hypoxia** (2) [2], **fat globules in urine** (3) [2], **petechiae in the anterior chest wall** (5) [1], and manifestation **after several days of trauma** (4) [1] are all recognized clinical features or associated findings of **Fat Embolism Syndrome (FES)**. - The classic triad of FES includes **respiratory insufficiency**, **neurological symptoms**, and **petechial rash**, which frequently emerge 24-72 hours post-injury [1]. *1, 3, 4, 5 true & 2 false* - This option incorrectly states that systemic hypoxia is false. **Systemic hypoxia** is a common and serious manifestation of **Fat Embolism Syndrome**, often resulting from pulmonary microvascular obstruction [2]. - While other points are correct, the misidentification of hypoxia as false makes this option incorrect. *1, 2, 3, 5 true & 4 false* - This option incorrectly states that FES does not manifest after several days of trauma. **Fat Embolism Syndrome** typically has a delayed onset, occurring **12-72 hours (several days)** after the initial injury [1], [2]. - The delayed presentation is a key diagnostic characteristic distinguishing it from immediate post-traumatic complications. *2, 4 false & 1, 3, 5 true* - This option is extensively incorrect as it falsely identifies both **systemic hypoxia** and the **delayed manifestation** as false. - **Systemic hypoxia** is a hallmark of pulmonary involvement in FES [2], and **delayed onset** is a crucial diagnostic criterion.
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