Substance Use Disorders — MCQs

A person becomes excited, restless, very talkative, and maniacal, followed by dullness and pallor. Examination reveals dilated pupils, elevated body temperature, ulceration of the nasal septum, and convulsions. Blood glucose is 150 mg/dl, and the patient experiences arrhythmia. Despite supportive measures, the patient dies. What is the most likely diagnosis?

Q260Easy

Which of the following is a cause for a suspected case of Delirium Tremens under investigation?

Substance Use Disorders Indian Medical PG Practice Questions and MCQs

Question 251: Which of the following is NOT true about naltrexone?

A. Acts on opioid receptors
B. Is used in the treatment of alcohol dependence
C. Is used to reduce craving in dependence
D. Is an opioid agonist (Correct Answer)

Explanation: **Explanation:** The correct answer is **D (Is an opioid agonist)** because Naltrexone is actually a long-acting **competitive opioid antagonist**. It binds to opioid receptors (primarily the mu-receptor) with high affinity, thereby blocking the effects of exogenous opioids and endogenous endorphins. **Analysis of Options:** * **Option A (Acts on opioid receptors):** This is true. Naltrexone has a high affinity for $\mu$ (mu) and $\kappa$ (kappa) opioid receptors. By blocking these receptors, it prevents the "high" or euphoria associated with opioid use. * **Option B (Used in alcohol dependence):** This is true. In alcohol use disorder, Naltrexone blocks the $\mu$-opioid receptors involved in the reward pathway. This prevents the release of dopamine in the nucleus accumbens that normally occurs when drinking alcohol. * **Option C (Used to reduce craving):** This is true. By modulating the reward circuitry and reducing the reinforcing effects of the substance (the "reward"), Naltrexone effectively reduces the psychological urge or craving to consume alcohol or opioids. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism in Alcoholism:** It reduces the "pleasure" of drinking and decreases the likelihood of a "slip" becoming a full-blown relapse. * **Prerequisite:** Patients must be **opioid-free for at least 7–10 days** before starting Naltrexone to avoid precipitating severe acute withdrawal. * **Contraindication:** It is contraindicated in patients with **acute hepatitis or liver failure** (hepatotoxicity risk). * **Naltrexone vs. Naloxone:** Naltrexone is orally active with a long half-life (used for maintenance), whereas Naloxone has poor oral bioavailability and a short half-life (used for acute overdose reversal).

Question 252: What is the drug of choice for managing alcohol withdrawal?

A. TEP
B. Chlormethazole
C. Chlordiazepoxide (Correct Answer)
D. Buspirone

Explanation: **Explanation** The management of alcohol withdrawal focuses on counteracting the CNS hyperexcitability caused by the sudden cessation of alcohol's GABAergic effects. **Why Chlordiazepoxide is Correct:** Benzodiazepines (BZDs) are the **gold standard** and drug of choice for alcohol withdrawal. They act as cross-tolerant agents with alcohol, enhancing GABA-A receptor activity to prevent seizures, delirium tremens, and autonomic instability. **Chlordiazepoxide** is preferred due to its long half-life and active metabolites, which provide a "built-in" tapering effect, ensuring a smoother withdrawal process with a lower risk of rebound symptoms. **Analysis of Incorrect Options:** * **TEP (Tetraethylthiuram disulfide / Disulfiram):** This is an alcohol deterrent used for **relapse prevention** (maintenance), not withdrawal. It inhibits aldehyde dehydrogenase; using it during active withdrawal can cause a life-threatening Disulfiram-Ethanol Reaction (DER). * **Chlormethiazole:** While historically used for withdrawal due to its sedative properties, it is rarely used today because of its high addictive potential and risk of fatal respiratory depression, especially if combined with alcohol. * **Buspirone:** An anxiolytic used for Generalised Anxiety Disorder. It has no cross-tolerance with alcohol and does not prevent withdrawal seizures or delirium. **High-Yield Clinical Pearls for NEET-PG:** 1. **Liver Disease Exception:** If a patient has significant liver cirrhosis, use **LOT** (Lorazepam, Oxazepam, Temazepam) as they undergo direct glucuronidation and do not have active metabolites. 2. **Wernicke’s Encephalopathy:** Always administer **Thiamine (B1)** before glucose to prevent precipitating Wernicke’s. 3. **Delirium Tremens:** Occurs 48–72 hours after the last drink; characterized by clouded consciousness and autonomic hyperactivity.

Question 253: The 'flash-back' phenomenon is most commonly associated with the use of which of the following substances?

A. Cannabis
B. Psilocybin
C. LSD
D. All of the above (Correct Answer)

Explanation: **Explanation:** The **'flash-back' phenomenon**, clinically known as **Hallucinogen Persisting Perception Disorder (HPPD)**, refers to the spontaneous recurrence of sensory distortions (visual trails, intensified colors, or geometric patterns) that were experienced during previous intoxication, occurring long after the substance has left the body. **Why "All of the above" is correct:** While **LSD (Lysergic acid diethylamide)** is the classic substance most frequently associated with flashbacks in medical literature, the phenomenon is not exclusive to it. Flashbacks are a characteristic feature of the entire class of hallucinogens. * **LSD (Option C):** The most potent hallucinogen; flashbacks can occur in up to 15-30% of chronic users. * **Psilocybin (Option B):** Found in "magic mushrooms," it acts on 5-HT2A receptors and can induce similar lingering perceptual disturbances. * **Cannabis (Option A):** Though classified as a cannabinoid, at high doses it possesses hallucinogenic properties and is a well-documented trigger for flashbacks, especially in heavy users or those who have previously used LSD. **Clinical Pearls for NEET-PG:** * **Mechanism:** Flashbacks are often triggered by stress, fatigue, or entering a dark environment. They are generally brief (seconds to minutes). * **Diagnostic Distinction:** Unlike a psychotic break, during a flashback, **reality testing remains intact** (the patient knows the sensations are not real). * **Treatment:** Most cases are self-limiting. If distressing, **Benzodiazepines** are the first-line pharmacological treatment to reduce anxiety and intensity. * **High-Yield Fact:** LSD does not cause physical dependence or withdrawal symptoms, but it produces rapid **tolerance** (tachyphylaxis).

Question 254: The primary site of lesion in Korsakoff's psychosis is?

A. Frontal lobe
B. Corpus striatum
C. Hippocampus (Correct Answer)
D. Cingulate gyrus

Explanation: **Explanation:** **Korsakoff’s Psychosis** is a chronic neuropsychiatric condition resulting from a severe deficiency of **Thiamine (Vitamin B1)**, usually following untreated Wernicke’s Encephalopathy in chronic alcoholics. **Why Hippocampus is the correct answer:** The hallmark of Korsakoff’s psychosis is **anterograde amnesia** (inability to form new memories) and **confabulation**. The **hippocampus**, along with the **mammillary bodies** and the **dorsomedial nucleus of the thalamus**, forms the core of the Papez circuit, which is essential for memory consolidation. While the mammillary bodies are the most classic site of atrophy, the **hippocampus** is a primary site of functional and structural lesions that explains the profound memory deficits seen in these patients. **Analysis of Incorrect Options:** * **A. Frontal lobe:** While frontal lobe atrophy can occur in chronic alcoholism (leading to executive dysfunction), it is not the primary site responsible for the amnestic syndrome of Korsakoff’s. * **B. Corpus striatum:** This area is primarily involved in motor control (Basal Ganglia). Lesions here lead to movement disorders (e.g., Parkinsonism or Chorea), not primary memory loss. * **D. Cingulate gyrus:** Although part of the limbic system, it is more involved in emotional processing and attention rather than the primary formation of new memories. **High-Yield Clinical Pearls for NEET-PG:** * **Wernicke’s Encephalopathy Triad:** Confusion, Ataxia, and Ophthalmoplegia (reversible). * **Korsakoff’s Psychosis Tetrad:** Anterograde amnesia, Retrograde amnesia, Confabulation, and Lack of insight (largely irreversible). * **Pathological Hallmark:** Hemorrhagic lesions in the **Mammillary bodies** (most specific) and Thalamus. * **Treatment Rule:** Always administer **Thiamine before Glucose** to prevent precipitating Wernicke’s crisis.

Question 255: Which of the following conditions is characterized by tolerance?

A. Alcohol dependence syndrome (Correct Answer)
B. Schizophrenia
C. Obsessive-compulsive disorder
D. All of the above

Explanation: **Explanation:** The correct answer is **Alcohol dependence syndrome**. **1. Why Alcohol Dependence Syndrome is correct:** Tolerance is a hallmark feature of **Substance Use Disorders**, specifically defined under the ICD and DSM criteria for dependence. It refers to a physiological state where either a markedly increased amount of the substance is required to achieve intoxication (or the desired effect), or there is a markedly diminished effect with continued use of the same amount of the substance. In Alcohol Dependence Syndrome, chronic consumption leads to neuroadaptation (downregulation of GABA receptors and upregulation of NMDA receptors), necessitating higher doses to achieve the same level of CNS depression. **2. Why the other options are incorrect:** * **Schizophrenia:** This is a psychotic disorder characterized by positive symptoms (hallucinations, delusions) and negative symptoms. While patients may have comorbid substance use, the disease process itself does not involve "tolerance" as a clinical feature. * **Obsessive-Compulsive Disorder (OCD):** This is an anxiety-related disorder characterized by intrusive thoughts (obsessions) and repetitive behaviors (compulsions). It does not involve the physiological neuroadaptation seen in substance tolerance. **High-Yield Clinical Pearls for NEET-PG:** * **ICD-10 Criteria for Dependence:** Requires 3 or more of the following within the last year: Strong desire (craving), impaired control, **tolerance**, withdrawal symptoms, neglect of alternative pleasures, and persistence despite harm. * **Reverse Tolerance:** Seen in advanced cirrhosis where the damaged liver cannot metabolize alcohol, leading to intoxication with very small amounts. * **Cross-Tolerance:** Occurs between alcohol and benzodiazepines/barbiturates because they act on the same GABA-A receptor complex; this is why benzodiazepines are the drug of choice for alcohol withdrawal.

Question 256: Which of the following is NOT an anti-craving agent used in the management of alcohol withdrawal symptoms?

A. Fluoxetine
B. Nitrafezole (Correct Answer)
C. Naltrexone
D. Acamprosate

Explanation: ### Explanation The management of Alcohol Use Disorder involves two distinct phases: management of acute withdrawal and prevention of relapse (anti-craving). **Why Nitrafezole is the correct answer:** **Nitrafezole** is an **aldehyde dehydrogenase inhibitor**, similar to Disulfiram. It is classified as an **Aversive Agent** (Deterrent therapy), not an anti-craving agent. It works by causing the accumulation of acetaldehyde if alcohol is consumed, leading to unpleasant symptoms (nausea, tachycardia, flushing). It does not reduce the physiological "urge" or craving to drink. **Analysis of Incorrect Options:** * **Naltrexone:** An opioid antagonist that blocks the mu-opioid receptors. It reduces the "reward" or euphoria associated with drinking and is a first-line **anti-craving** agent. * **Acamprosate:** A NMDA receptor antagonist and GABA-A agonist. It helps maintain abstinence by reducing the negative reinforcing effects (insomnia, anxiety) of protracted withdrawal. It is a gold-standard **anti-craving** agent. * **Fluoxetine:** While primarily an SSRI, it is used as an adjuvant anti-craving agent, particularly in patients with comorbid depression or Type B alcoholism (early onset, high impulsivity). **High-Yield Clinical Pearls for NEET-PG:** * **First-line anti-craving agents:** Naltrexone and Acamprosate. * **Acamprosate** is preferred in patients with liver disease (excreted renally). * **Naltrexone** is preferred in patients with renal failure (metabolized by the liver) but contraindicated in acute hepatitis or opioid users. * **Topiramate and Baclofen** are other emerging anti-craving agents. * **Disulfiram/Nitrafezole** require high motivation as they work on the principle of fear/punishment rather than craving reduction.

Question 257: Type B alcohol dependence is associated with all except?

A. Severe dependence
B. Late onset (Correct Answer)
C. Many childhood risk factors
D. Polysubstance abuse

Explanation: This question tests your knowledge of **Babor’s Classification of Alcoholism**, a high-yield topic for NEET-PG. Babor categorized alcoholics into two distinct groups (Type A and Type B) based on clinical characteristics and prognosis. ### **Explanation of the Correct Answer** **Option B (Late onset)** is the correct answer because it is a feature of **Type A**, not Type B alcoholism. * **Type B Alcoholism** is characterized by **early onset** (typically before age 25). These individuals often have a significant family history and a more severe clinical course. * **Type A Alcoholism** is characterized by **late onset** (after age 25), fewer childhood risk factors, and a better prognosis. ### **Analysis of Incorrect Options** * **A. Severe dependence:** Type B individuals show higher levels of alcohol dependence and more frequent physical consequences compared to Type A. * **C. Many childhood risk factors:** Type B is strongly associated with childhood conduct disorders, impulsivity, and a positive family history of alcoholism. * **D. Polysubstance abuse:** Type B alcoholics frequently use other substances (polysubstance abuse) and often have comorbid psychiatric conditions like Antisocial Personality Disorder. ### **High-Yield Clinical Pearls for NEET-PG** To differentiate between the two major classifications of alcoholism, remember this table: | Feature | Type A (Babor) / Type I (Cloninger) | Type B (Babor) / Type II (Cloninger) | | :--- | :--- | :--- | | **Onset** | Late (>25 years) | **Early (<25 years)** | | **Severity** | Mild/Moderate | **Severe** | | **Genetics** | Low genetic influence | **High genetic influence** | | **Personality** | Anxious/Harm-avoidant | **Impulsive/Novelty-seeking** | | **Gender** | Equal in Male/Female | **Predominantly Male** | | **Prognosis** | Good | Poor |

Question 258: A disulfiram-like reaction is seen with which of the following medications?

A. Metronidazole (Correct Answer)
B. Benzodiazepine
C. Fluoxetine
D. Acamprosate

Explanation: ### Explanation **Correct Option: A (Metronidazole)** The **disulfiram-like reaction** occurs when certain drugs inhibit the enzyme **aldehyde dehydrogenase (ALDH)**. Under normal circumstances, alcohol is metabolized into acetaldehyde, which ALDH then converts into harmless acetic acid. When ALDH is inhibited, **acetaldehyde accumulates** in the bloodstream, leading to symptoms such as flushing, tachycardia, palpitations, nausea, vomiting, and hypotension. **Metronidazole** is the classic antibiotic associated with this reaction; patients are strictly advised to avoid alcohol during treatment and for at least 48–72 hours after the last dose. **Analysis of Incorrect Options:** * **B. Benzodiazepines:** These are GABA-A receptor agonists used to treat alcohol withdrawal. They do not interfere with alcohol metabolism but have a synergistic CNS depressant effect if combined with alcohol. * **C. Fluoxetine:** An SSRI used for depression and OCD. While it may interact with other serotonergic drugs, it does not cause a disulfiram-like reaction. * **D. Acamprosate:** Used for maintaining abstinence in alcohol dependence by modulating glutamate/GABA systems. It does not affect alcohol metabolism and is safe to use even if a patient relapses. **High-Yield Clinical Pearls for NEET-PG:** * **Other drugs causing Disulfiram-like reactions:** Sulfonylureas (Chlorpropamide), Cephalosporins (Cefoperazone, Cefotetan), Griseofulvin, and Procarbazine. * **Disulfiram Mechanism:** Irreversible inhibition of Aldehyde Dehydrogenase. * **Management:** The reaction is usually self-limiting; management is supportive (IV fluids, antihistamines, and antiemetics). * **Contraindication:** Disulfiram should never be administered if the patient has consumed alcohol within the last 12 hours.

Question 259: A person becomes excited, restless, very talkative, and maniacal, followed by dullness and pallor. Examination reveals dilated pupils, elevated body temperature, ulceration of the nasal septum, and convulsions. Blood glucose is 150 mg/dl, and the patient experiences arrhythmia. Despite supportive measures, the patient dies. What is the most likely diagnosis?

A. Body stuffer syndrome (Correct Answer)
B. Acute dystonia
C. Delirium tremens
D. Meningitis

Explanation: ### Explanation The clinical presentation describes a classic case of **Acute Cocaine Toxicity**, specifically occurring in the context of **Body Stuffer Syndrome**. **1. Why Body Stuffer Syndrome is Correct:** Body stuffers are individuals who hurriedly swallow wraps of illicit drugs (usually cocaine or heroin) to avoid imminent detection by law enforcement. Unlike "body packers" (who use professional packaging), stuffers use poorly wrapped materials that are prone to leaking or bursting. * **Mechanism:** Cocaine is a potent sympathomimetic. Massive absorption leads to the "excited-maniacal" phase (tachycardia, hypertension, hyperthermia, and mydriasis). * **Clinical Clues:** The **ulceration of the nasal septum** is a pathognomonic sign of chronic cocaine use. The progression to **convulsions, arrhythmias, and death** despite supportive care is typical of a massive "leak" from swallowed packets. The elevated blood glucose (150 mg/dl) reflects a stress-induced catecholamine surge. **2. Why Other Options are Incorrect:** * **Acute Dystonia:** An extrapyramidal side effect of antipsychotics characterized by muscle spasms (torticollis, oculogyric crisis). It does not cause nasal septal ulceration, arrhythmias, or death. * **Delirium Tremens:** Occurs 48–96 hours after alcohol withdrawal. While it features autonomic hyperactivity (tachycardia, tremors), it is characterized by clouding of consciousness and visual hallucinations, not nasal ulceration or sudden cardiac death. * **Meningitis:** Presents with fever, headache, and neck stiffness. While it can cause convulsions, it does not explain the nasal septum ulceration or the specific sympathomimetic toxidrome described. **3. NEET-PG High-Yield Pearls:** * **Cocaine Toxidrome:** Mydriasis (dilated pupils), Hypertension, Tachycardia, Hyperthermia, and Psychosis. * **Nasal Septum Perforation:** Caused by chronic vasoconstriction (ischemic necrosis) from snorting cocaine. * **Management:** Benzodiazepines are the first-line treatment for cocaine toxicity. **Beta-blockers are contraindicated** due to the risk of "unopposed alpha-stimulation," which can worsen hypertension and coronary vasoconstriction.

Question 260: Which of the following is a cause for a suspected case of Delirium Tremens under investigation?

A. Chronic alcoholism
B. Alcohol withdrawal (Correct Answer)
C. Cocaine abuse
D. Cocaine withdrawal

Explanation: **Explanation:** **Delirium Tremens (DTs)** is the most severe manifestation of **alcohol withdrawal**, typically occurring 48 to 96 hours after the last drink in chronic heavy drinkers. **Why Option B is Correct:** The underlying pathophysiology involves a neurochemical imbalance. Chronic alcohol consumption enhances GABA (inhibitory) activity and inhibits NMDA/Glutamate (excitatory) receptors. When alcohol is abruptly stopped, the brain is left in a state of **GABA-ergic deficiency and NMDA overactivity**, leading to autonomic hyperactivity and the classic triad of DTs: **clouding of consciousness (delirium), vivid hallucinations (often visual), and autonomic instability** (tachycardia, hypertension, tremors). **Why Other Options are Incorrect:** * **A. Chronic Alcoholism:** While a prerequisite, the state of being intoxicated or chronically using alcohol does not cause DTs; it is the *cessation* of use that triggers the syndrome. * **C. Cocaine Abuse:** Cocaine is a sympathomimetic stimulant. Intoxication causes euphoria, pupillary dilation, and tachycardia, but not the specific delirium seen in DTs. * **D. Cocaine Withdrawal:** Withdrawal from stimulants typically results in "crashing"—characterized by dysphoria, hypersomnia, and increased appetite, rather than life-threatening delirium. **High-Yield Clinical Pearls for NEET-PG:** * **Timeline:** DTs occur 2–4 days after the last drink (unlike early withdrawal/tremors at 6–24 hours or withdrawal seizures at 12–48 hours). * **Mortality:** If untreated, DTs have a mortality rate of up to 5%–20%, usually due to arrhythmias or respiratory failure. * **Drug of Choice:** **Benzodiazepines** (e.g., Diazepam, Lorazepam) are the gold standard for management. * **Hallucinations:** In DTs, hallucinations occur in a state of clouded consciousness, whereas in **Alcoholic Hallucinosis**, the sensorium is clear.

Practice by Chapter

Neurobiology of Addiction

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Alcohol Use Disorder

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Opioid Use Disorder

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Cannabis Use Disorder

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Stimulant Use Disorders

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Sedative, Hypnotic, and Anxiolytic Use Disorders

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Tobacco Use Disorder

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Hallucinogen-Related Disorders

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Substance Withdrawal Syndromes

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Pharmacotherapy for Substance Use Disorders

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Psychosocial Interventions

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Dual Diagnosis Management

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