Substance Use Disorders — MCQs

Substance Use Disorders Indian Medical PG Practice Questions and MCQs

Question 51: Which anticraving agent acts as an NMDA antagonist?

A. Naltrexone
B. Acamprosate (Correct Answer)
C. Baclofen
D. Topiramate

Explanation: ### Explanation **Correct Option: B. Acamprosate** Acamprosate is a structural analogue of GABA used for the maintenance of abstinence in alcohol dependence. Chronic alcohol consumption leads to a compensatory downregulation of GABA receptors and upregulation of NMDA (glutamate) receptors. When alcohol is withdrawn, this results in a hyper-excitable state. Acamprosate works by **antagonizing NMDA receptors** and potentially modulating GABA-A receptors, thereby restoring the neurochemical balance (homeostasis) between excitatory and inhibitory neurotransmission. **Incorrect Options:** * **A. Naltrexone:** This is an **opioid receptor antagonist** (primarily at the $\mu$ receptor). It reduces the "reward" or euphoria associated with alcohol consumption by blocking endogenous opioid pathways. * **C. Baclofen:** This is a **GABA-B receptor agonist**. While used off-label to reduce cravings and withdrawal symptoms in alcohol use disorder, its primary mechanism is not NMDA antagonism. * **D. Topiramate:** This is an antiepileptic that acts by facilitating GABA-A neurotransmission and antagonizing **AMPA/Kainate** glutamate receptors (not primarily NMDA). **High-Yield Clinical Pearls for NEET-PG:** * **Acamprosate** is the drug of choice for maintaining abstinence in patients with **liver disease** (as it is renally excreted) but is contraindicated in **renal failure** (CrCl < 30 mL/min). * **Naltrexone** is preferred for patients who want to reduce heavy drinking ("harm reduction") but is contraindicated in **acute hepatitis or liver failure**. * **Disulfiram** is an aversive agent (aldehyde dehydrogenase inhibitor) and does *not* reduce cravings; it works through fear of the Disulfiram-Ethanol Reaction (DER).

Question 52: Which of the following statements is FALSE regarding Naltrexone?

A. Parenterally administered (Correct Answer)
B. Used to prevent relapse of heavy drinking
C. Long acting
D. Causes hepatotoxicity

Explanation: **Explanation:** **Naltrexone** is a long-acting opioid antagonist used in the management of both Alcohol Use Disorder and Opioid Use Disorder. 1. **Why Option A is FALSE (Correct Answer):** Naltrexone is primarily administered **orally** (50 mg daily). While a long-acting injectable (depot) formulation exists (Vivitrol), the standard pharmacological profile taught for NEET-PG emphasizes its high oral bioavailability and effectiveness via the oral route. In contrast, **Naloxone** (a short-acting antagonist) must be given parenterally because it undergoes extensive first-pass metabolism. Therefore, stating Naltrexone is "parenterally administered" as its defining characteristic is incorrect in this comparative context. 2. **Analysis of Other Options:** * **Option B (Relapse Prevention):** Naltrexone reduces the "high" or craving associated with alcohol by blocking mu-opioid receptors. It is specifically indicated to reduce the frequency of heavy drinking days. * **Option C (Long Acting):** Naltrexone has a significantly longer half-life (approx. 4–13 hours for its active metabolite, 6-beta-naltrexol) compared to Naloxone (approx. 1 hour), making it suitable for maintenance therapy. * **Option D (Hepatotoxicity):** Naltrexone carries a dose-related warning for hepatotoxicity. Liver function tests (LFTs) should be monitored during treatment. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Competitive antagonist at $\mu$ (mu) receptors. * **Alcoholism:** First-line for reducing cravings (unlike Disulfiram, which is an aversive agent). * **Opioids:** Patients must be opioid-free for **7–10 days** before starting Naltrexone to avoid precipitating acute withdrawal. * **Contraindication:** Acute hepatitis or liver failure.

Question 53: The triad of Wernicke's encephalopathy includes all the following except?

A. Global confusion
B. Ataxia
C. Ophthalmoplegia
D. Visual hallucinations (Correct Answer)

Explanation: **Explanation:** Wernicke’s Encephalopathy (WE) is an acute, reversible neuropsychiatric emergency caused by a deficiency of **Thiamine (Vitamin B1)**, most commonly seen in chronic alcoholics. The diagnosis is primarily clinical and is defined by a classic **triad**: 1. **Ophthalmoplegia (Option C):** Characterized by ocular signs, most commonly horizontal nystagmus and bilateral abducens (6th nerve) palsy. 2. **Ataxia (Option B):** Primarily affecting gait and stance due to cerebellar involvement. 3. **Global Confusion (Option A):** An encephalopathy characterized by disorientation, apathy, and decreased consciousness. **Visual Hallucinations (Option D)** is the correct answer because it is **not** part of the Wernicke triad. Visual hallucinations are typically associated with **Alcohol Withdrawal Delirium (Delirium Tremens)** or Alcoholic Hallucinosis, rather than acute thiamine deficiency. **High-Yield Clinical Pearls for NEET-PG:** * **Pathology:** The most characteristic lesions are found in the **mammillary bodies**, periaqueductal gray matter, and the floor of the fourth ventricle. * **Korsakoff Psychosis:** If WE is untreated, it can progress to Korsakoff syndrome, characterized by **anterograde amnesia** and **confabulation** (filling memory gaps with fabricated stories). * **Management Rule:** Always administer **Thiamine before Glucose** in a malnourished or alcoholic patient. Giving glucose first can precipitate or worsen WE by consuming the remaining thiamine stores during carbohydrate metabolism. * **MRI Finding:** Increased T2/FLAIR signal intensity in the mammillary bodies is a highly specific finding.

Question 54: During alcohol withdrawal, which signs or symptoms typically appear last?

A. Cluster seizures
B. Hallucinations
C. Anterograde amnesia
D. Delirium tremens (Correct Answer)

Explanation: The timeline of alcohol withdrawal is a high-yield topic for NEET-PG, as symptoms follow a predictable chronological sequence based on the decline in blood alcohol levels. ### **Explanation of the Correct Answer** **Delirium Tremens (DT)** is the most severe and **last** manifestation of alcohol withdrawal. It typically occurs **48 to 96 hours** after the last drink. It is characterized by clouding of consciousness (delirium), autonomic hyperactivity (tachycardia, hypertension, fever), and vivid hallucinations. The underlying mechanism involves a profound rebound of the NMDA (glutamate) system and downregulation of GABA receptors after chronic suppression by alcohol. ### **Analysis of Incorrect Options** * **A. Cluster Seizures:** These are "rum fits" that typically occur **6 to 48 hours** after cessation. They are usually generalized tonic-clonic seizures and occur much earlier than DTs. * **B. Hallucinations:** Alcoholic hallucinosis occurs **12 to 48 hours** after the last drink. Unlike DTs, the patient’s sensorium is usually clear (they are conscious and oriented), and it precedes the onset of delirium. * **C. Anterograde Amnesia:** This is a hallmark of **Wernicke-Korsakoff Syndrome** (due to Thiamine deficiency), not a standard stage of the acute withdrawal timeline. ### **NEET-PG High-Yield Pearls** * **Chronology Summary:** 1. Insomnia/Tremors (6–12h) 2. Hallucinosis (12–48h) 3. Seizures (6–48h) 4. **Delirium Tremens (48–96h)**. * **Drug of Choice:** Benzodiazepines (e.g., Diazepam, Chlordiazepoxide). * **Liver Failure Patients:** Use **LOT** (Lorazepam, Oxazepam, Temazepam) as they undergo extrahepatic metabolism. * **Mortality:** DT is a medical emergency with a mortality rate of up to 5% if untreated, usually due to cardiovascular collapse or hyperthermia.

Question 55: A 'bad trip' is most commonly associated with the use of which substance?

A. Cocaine
B. Cannabis
C. LSD (Correct Answer)
D. Heroin

Explanation: **Explanation:** The term **'bad trip'** refers to a transient, acute adverse psychological reaction characterized by intense anxiety, panic, paranoia, and terrifying hallucinations. This phenomenon is most characteristically and commonly associated with **LSD (Lysergic Acid Diethylamide)**, a potent psychedelic. **Why LSD is the correct answer:** LSD acts primarily as a partial agonist at **5-HT2A receptors**. It causes profound alterations in perception (synesthesia), mood, and thought. A 'bad trip' occurs when these sensory distortions become overwhelming or nightmarish, often leading to a fear of "going crazy" or dying. Management typically involves a "talking down" approach in a quiet environment, or benzodiazepines if the patient is severely agitated. **Analysis of Incorrect Options:** * **Cocaine:** A stimulant that causes euphoria and increased energy. Toxicity leads to sympathetic overactivity (tachycardia, hypertension) and potentially "cocaine bugs" (formication), but not a 'bad trip' in the classic psychedelic sense. * **Cannabis:** While high doses can cause acute panic or "toxic psychosis," it is not the primary substance associated with the clinical definition of a 'bad trip.' * **Heroin:** An opioid that causes CNS depression, euphoria, and sedation ("nodding off"). Toxicity results in respiratory depression and miosis, rather than hallucinogenic crises. **High-Yield Clinical Pearls for NEET-PG:** * **Flashbacks (Hallucinogen Persisting Perception Disorder):** Recurrence of the 'trip' experience weeks or months after the last use of LSD. * **Tolerance:** LSD shows rapid tolerance (tachyphylaxis) but **no physical dependence** or withdrawal symptoms. * **Pupillary findings:** LSD causes **Mydriasis** (dilated pupils), whereas Heroin causes **Miosis** (pinpoint pupils).

Question 56: Which of the following drugs has no role in opioid detoxification?

A. Naloxone (Correct Answer)
B. Methadone
C. Buprenorphine
D. Clonidine

Explanation: ### Explanation The goal of **opioid detoxification** is to manage withdrawal symptoms safely while transitioning a patient off illicit opioids. This is achieved using either opioid agonists (to taper the dose) or non-opioid medications (to manage autonomic symptoms). **Why Naloxone is the Correct Answer:** Naloxone is a **pure opioid antagonist** with a very short half-life. It works by competitively displacing opioids from the mu-receptors. If administered to an opioid-dependent patient, it will **precipitate acute, severe withdrawal**. Therefore, it has no role in detoxification. Its primary clinical uses are the emergency reversal of opioid overdose and as an abuse-deterrent when combined with buprenorphine (Suboxone). **Analysis of Incorrect Options:** * **Methadone (Option B):** A long-acting **full mu-opioid agonist**. It prevents withdrawal symptoms and craving due to its long half-life, allowing for a controlled, gradual taper. * **Buprenorphine (Option C):** A **partial mu-opioid agonist**. It has a high affinity for the receptor but lower intrinsic activity, making it safer than methadone (less respiratory depression) for detoxification and maintenance. * **Clonidine (Option D):** An **alpha-2 adrenergic agonist**. It is a non-opioid medication used to treat the autonomic hyperactivity of withdrawal (tachycardia, hypertension, sweating, and restlessness). **NEET-PG High-Yield Pearls:** * **Drug of Choice for Opioid Overdose:** Naloxone (IV/Intranasal). * **Drug of Choice for Opioid Maintenance in Pregnancy:** Methadone. * **Naltrexone:** Unlike Naloxone, Naltrexone is long-acting and used for **relapse prevention** (post-detoxification), not for active detox. * **COWS Scale:** The Clinical Opiate Withdrawal Scale is used to monitor the severity of withdrawal during detoxification.

Question 57: Which drug is NOT used in the treatment of alcohol dependence?

A. Diazepam (Correct Answer)
B. Disulfiram
C. Acamprosate
D. Naltrexone

Explanation: The key to answering this question lies in distinguishing between drugs used for **Alcohol Withdrawal** versus those used for **Alcohol Dependence (Maintenance of Abstinence).** ### 1. Why Diazepam is the Correct Answer **Diazepam** is a benzodiazepine used primarily for the management of **acute alcohol withdrawal symptoms** and prevention of Delirium Tremens. While it is life-saving during the detoxification phase, it is **not** used for long-term treatment of dependence. In fact, benzodiazepines are generally avoided in long-term recovery because they have a high potential for abuse and cross-tolerance with alcohol. ### 2. Analysis of Other Options (Drugs for Dependence) The following drugs are FDA-approved for maintaining abstinence and reducing craving in alcohol dependence: * **Disulfiram (Option B):** An **Aversion Therapy** agent. It inhibits the enzyme *aldehyde dehydrogenase*, leading to the accumulation of acetaldehyde if alcohol is consumed. This causes the unpleasant "Disulfiram-Ethanol Reaction" (flushing, tachycardia, nausea). * **Acamprosate (Option C):** A NMDA receptor antagonist and GABA-A agonist. It helps maintain abstinence by restoring the chemical balance in the brain ("calming the glutamate storm") and is particularly useful in patients with liver disease. * **Naltrexone (Option D):** An **Opioid receptor antagonist**. It reduces the "reward" or euphoria associated with drinking and decreases cravings. It is the drug of choice for patients who want to reduce heavy drinking. ### 3. NEET-PG High-Yield Pearls * **Drug of Choice (DOC) for Alcohol Withdrawal:** Benzodiazepines (e.g., Chlordiazepoxide, Diazepam). * **DOC for Withdrawal in Liver Failure:** **L**orazepam, **O**xazepam, **T**emazepam (The "**LOT**" drugs, as they lack active metabolites). * **Acamprosate** is preferred in patients with **renal impairment** (contraindicated) but safe in liver disease. * **Naltrexone** is contraindicated in acute hepatitis or liver failure.

Question 58: The drug Antabuse acts by which of the following mechanisms?

A. Decreasing ethanol absorption
B. Enhancing urinary excretion of ethanol
C. Increasing pulmonary excretion of ethanol
D. Blocking the metabolism of ethanol (Correct Answer)

Explanation: **Explanation:** **Antabuse (Disulfiram)** is a classic pharmacological intervention used in the treatment of alcohol dependence. It acts as an **irreversible inhibitor of the enzyme Aldehyde Dehydrogenase (ALDH).** 1. **Why the correct answer is right:** Normally, ethanol is metabolized in the liver: Ethanol → Acetaldehyde (via Alcohol Dehydrogenase) → Acetic Acid (via Aldehyde Dehydrogenase). By blocking ALDH, Disulfiram prevents the conversion of acetaldehyde into acetic acid. This leads to a **5–10 fold increase in blood acetaldehyde levels** if alcohol is consumed, resulting in the **Disulfiram-Ethanol Reaction (DER)**. Symptoms include flushing, tachycardia, nausea, vomiting, and hypotension, which serve as an aversive deterrent. 2. **Why the incorrect options are wrong:** * **A:** Antabuse does not interfere with the gastrointestinal absorption of ethanol. * **B & C:** Ethanol is primarily eliminated via hepatic metabolism (90-95%). Only a small fraction is excreted unchanged via urine, sweat, or breath. Antabuse does not enhance these minor excretory pathways. **Clinical Pearls for NEET-PG:** * **Aversive Therapy:** Disulfiram is a form of "Aversion Therapy" (Classical Conditioning). * **Timing:** It should never be administered until the patient has abstained from alcohol for at least **12 hours**. * **Duration of Action:** Because it inhibits the enzyme irreversibly, its effects can last for **1–2 weeks** after the last dose (until new enzymes are synthesized). * **Contraindications:** Severe cardiac disease, psychosis, and pregnancy. * **Other drugs with Disulfiram-like reactions:** Metronidazole, Griseofulvin, Cefotetan, and Sulfonylureas.

Question 59: Which of the following symptoms is MOST characteristic of polyuria?

A. Excessive thirst and fluid intake (Correct Answer)
B. Frequent urination, especially at night
C. Sudden onset of severe headache
D. Unexplained weight loss

Explanation: **Explanation:** In the context of Psychiatry and Substance Use Disorders, **Polyuria** (excessive urination) is most characteristically associated with **Polydipsia** (excessive thirst and fluid intake). This relationship is frequently tested in the context of **Lithium therapy**, a mainstay for Bipolar Disorder. Lithium inhibits the action of Antidiuretic Hormone (ADH) on the distal renal tubules, leading to Nephrogenic Diabetes Insipidus. This results in the inability to concentrate urine, causing polyuria and a compensatory increase in thirst (polydipsia) to maintain fluid balance. **Analysis of Options:** * **A (Correct):** Polyuria and polydipsia are physiologically linked. In psychiatry, "Psychogenic Polydipsia" (compulsive water drinking) is also seen in patients with schizophrenia, leading to dilutional hyponatremia. * **B (Incorrect):** While frequent urination at night (nocturia) can occur with polyuria, it is a non-specific symptom often associated with prostatic hypertrophy or urinary tract infections rather than the primary physiological definition of polyuria. * **C (Incorrect):** Sudden severe headache ("thunderclap headache") is characteristic of Subarachnoid Hemorrhage or a Hypertensive Crisis (e.g., MAOI interaction with tyramine), not polyuria. * **D (Incorrect):** Weight loss is a feature of uncontrolled Diabetes Mellitus (which causes polyuria), but it is a systemic consequence rather than a characteristic symptom of the polyuria itself. **High-Yield Clinical Pearls for NEET-PG:** * **Lithium Side Effects:** Polyuria and polydipsia occur in up to 70% of patients. If a patient on Lithium develops sudden polyuria, check renal function and serum lithium levels (Therapeutic range: 0.6–1.2 mEq/L). * **Psychogenic Polydipsia:** Look for "water intoxication" symptoms like seizures and hyponatremia in chronic psychiatric inpatients. * **Management:** Amiloride is the drug of choice for Lithium-induced polyuria as it blocks the epithelial sodium channels (ENaC) through which lithium enters the collecting duct cells.

Question 60: Which of the following is considered a 'rave drug'?

A. Cocaine
B. Methamphetamine (Correct Answer)
C. Heroin
D. Cannabis

Explanation: **Explanation:** **Methamphetamine (Option B)** is the correct answer. In the context of psychiatry and substance abuse, "rave drugs" (or club drugs) are a group of psychoactive substances used by young adults at all-night dance parties (raves), clubs, or concerts. Methamphetamine, a potent central nervous system stimulant, is frequently used in these settings to increase energy, alertness, and euphoria, allowing users to dance for extended periods. Other classic rave drugs include MDMA (Ecstasy), Ketamine, GHB, and Rohypnol. **Analysis of Incorrect Options:** * **Cocaine (Option A):** While a powerful stimulant, it is traditionally classified as a major drug of abuse rather than a specific "rave drug." Its short half-life and high cost distinguish its typical use pattern from the sustained endurance sought at raves. * **Heroin (Option C):** An opioid and CNS depressant. It induces sedation and respiratory depression ("nodding off"), which is the functional opposite of the high-energy environment of a rave. * **Cannabis (Option D):** Primarily a hallucinogen/depressant. While widely used, it is not categorized under the specific "rave drug" umbrella, which focuses on stimulants and dissociative anesthetics. **Clinical Pearls for NEET-PG:** * **Mechanism:** Methamphetamine increases the release and blocks the reuptake of dopamine, norepinephrine, and serotonin. * **Clinical Sign:** Look for "Meth Mouth" (severe tooth decay) and "crank sores" (skin picking) in chronic users. * **Management:** There is no specific antidote for methamphetamine toxicity; management is supportive, primarily using benzodiazepines for agitation and seizures. * **MDMA (Ecstasy):** Often tested alongside Meth; it is known for causing hyperthermia and hyponatremia (due to excessive water intake and SIADH).

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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