Opioid Use Disorders — MCQs
A patient presents to the emergency department with vomiting, diarrhea, lacrimation, abdominal cramps, and piloerection. The family members report a history of substance use for the past month. The clinical presentation is due to what?
Which drug is most commonly used worldwide in maintenance treatment for opioid dependence?
A patient presented with pain in the right lower quadrant of abdomen. He has history of renal stones in right kidney. He was prescribed an opioid which is agonist at kappa receptors and antagonist at mu receptors. The likely drug given was:
Which of the following is the most effective antagonist for morphine overdose?
What is the classification of Buprenorphine in terms of its action on opioid receptors?
A35 yr old lady with Normal PT and increased aPTT. 2 year back, she was operated for cholecystectomy & did not have any bleeding episode. What is next investigation for clinical diagnosis -
What are nitrergic neurons?
Punctate yellow exudates in the colon, found on endoscopic examination, are indicative of which of the following?
A person has a history of steatorrhea of long duration. D-xylose testing was performed. A 5-hour urine sample showed <4.5 g excretion after a 25g D-xylose load. What is/are the probable diagnosis?
A moderate increase in serum aminotransferases with AST/ALT > 3 is suggestive of which of the following?
Opioid Use Disorders Indian Medical PG Practice Questions and MCQs
Question 1: A patient presents to the emergency department with vomiting, diarrhea, lacrimation, abdominal cramps, and piloerection. The family members report a history of substance use for the past month. The clinical presentation is due to what?
- A. opioid withdrawal (Correct Answer)
- B. cocaine intoxication
- C. cocaine withdrawal
- D. opioid intoxication
Explanation: ***Opioid withdrawal*** - The constellation of **vomiting, diarrhea, lacrimation, abdominal cramps, and piloerection** (gooseflesh) are classic signs and symptoms of **opioid withdrawal**. - These symptoms reflect a **hyperactive sympathetic nervous system** as the body attempts to compensate for the absence of exogenous opioids. *Cocaine intoxication* - Cocaine intoxication typically presents with **euphoria, hyperactivity, tachycardia, hypertension, and paranoia**, which are not seen here. - It is characterized by **sympathomimetic effects**, leading to an agitated and stimulated state, rather than the distress seen in withdrawal. *Cocaine withdrawal* - Cocaine withdrawal typically manifests as **dysphoria, fatigue, increased appetite, psychomotor retardation or agitation, and vivid unpleasant dreams**, not the GI and autonomic symptoms described. - The primary symptoms are psychological and energetic, often described as a "crash" rather than the physical distress of opioid withdrawal. *Opioid intoxication* - Opioid intoxication primarily causes **CNS depression**, including **respiratory depression, meiosis (pinpoint pupils), sedation, and constipation**. - The patient's symptoms of vomiting, diarrhea, and lacrimation are contrary to the effects of opioid intoxication.
Question 2: Which drug is most commonly used worldwide in maintenance treatment for opioid dependence?
- A. Disulfiram
- B. Methadone (Correct Answer)
- C. Naltrexone
- D. Imipramine
Explanation: ***Methadone (Correct Answer)***- It is a **long-acting opioid agonist** that helps reduce cravings and withdrawal symptoms associated with opioid dependence, making it highly effective for maintenance treatment [2].- Its widespread availability and established efficacy in reducing illicit opioid use, crime, and disease transmission contribute to its global prevalence [1].- Methadone acts on **μ-opioid receptors** [2] and has a long half-life (24-36 hours), allowing once-daily dosing in maintenance therapy.*Disulfiram (Incorrect)*- This drug is primarily used in the management of **alcohol dependence** by causing unpleasant reactions when alcohol is consumed (inhibits aldehyde dehydrogenase) [3].- It has no role in the treatment of opioid dependence, as its mechanism of action is unrelated to opioid receptors.*Naltrexone (Incorrect)*- While used for opioid dependence, **naltrexone** is an **opioid antagonist** that blocks the effects of opioids [4].- Its use requires complete detoxification from opioids before initiation to avoid precipitated withdrawal, which can be a barrier to its common use in maintenance compared to methadone [1].- Less commonly used globally compared to methadone for maintenance treatment.*Imipramine (Incorrect)*- **Imipramine** is a **tricyclic antidepressant** primarily used to treat depression and some anxiety disorders.- It does not have any direct pharmacological action on opioid receptors and is not used in the treatment of opioid dependence.
Question 3: A patient presented with pain in the right lower quadrant of abdomen. He has history of renal stones in right kidney. He was prescribed an opioid which is agonist at kappa receptors and antagonist at mu receptors. The likely drug given was:
- A. Pentazocine (Correct Answer)
- B. Tramadol
- C. Buprenorphine
- D. Fentanyl
Explanation: ***Pentazocine*** - **Pentazocine** is a **mixed agonist-antagonist opioid analgesic** that acts as an **agonist at kappa opioid receptors** and a **weak antagonist or partial agonist at mu opioid receptors**. - This unique receptor profile makes it the drug described in the question. - It is effective for **moderate to severe pain** including **renal colic** (pain from renal stones), while having a **lower abuse potential** and **ceiling effect on respiratory depression** compared to pure mu agonists. *Tramadol* - **Tramadol** is a synthetic opioid that acts primarily as a **weak mu-opioid receptor agonist** and also inhibits the reuptake of **norepinephrine** and **serotonin**. - It does **not** have significant kappa receptor agonism or mu receptor antagonism. - Does not fit the description given in the question. *Buprenorphine* - **Buprenorphine** is a **partial agonist at mu opioid receptors** and an **antagonist at kappa opioid receptors**. - This receptor activity profile is the **opposite** of what is described in the question (which asks for kappa agonist, mu antagonist). *Fentanyl* - **Fentanyl** is a highly potent **pure mu-opioid receptor agonist**. - It has **no significant kappa receptor agonism** or mu receptor antagonism. - Does not match the pharmacological profile described in the question.
Question 4: Which of the following is the most effective antagonist for morphine overdose?
- A. Buprenorphine
- B. Nalorphine
- C. Naloxone (Correct Answer)
- D. Pentazocine
Explanation: ***Naloxone*** - **Naloxone** is a pure opioid antagonist that rapidly reverses the effects of opioid overdose by competing for and displacing opioids from the **mu-opioid receptors** - Its rapid onset of action (1-2 minutes IV) and high affinity for opioid receptors make it the drug of choice for treating **morphine overdose**, particularly in emergency settings - Has no intrinsic agonist activity, making it safe and effective for acute reversal *Buprenorphine* - **Buprenorphine** is a partial opioid agonist, meaning it produces some opioid effects but to a lesser degree than full agonists like morphine - While it can displace full agonists from receptors, it is primarily used in **opioid dependence treatment** rather than acute overdose reversal - Has a ceiling effect for respiratory depression and is not the first-line agent for emergency overdose management *Nalorphine* - **Nalorphine** is an older mixed agonist-antagonist that was historically used for opioid overdose - It has largely been replaced by **naloxone** due to its own opioid-like effects (agonist activity at kappa receptors) and less favorable side effect profile - Can cause respiratory depression itself, making it unsuitable for emergency use *Pentazocine* - **Pentazocine** is an opioid agonist-antagonist (kappa agonist, mu antagonist), meaning it acts as an agonist at some opioid receptors and an antagonist at others - This mixed action means it can precipitate **withdrawal symptoms** in opioid-dependent individuals and is not suitable for reversing a full opioid overdose - Used primarily for analgesia, not overdose reversal
Question 5: What is the classification of Buprenorphine in terms of its action on opioid receptors?
- A. Pure agonist
- B. Pure antagonist
- C. Partial agonist (Correct Answer)
- D. Mixed agonist-antagonist
Explanation: ***Partial agonist*** - **Buprenorphine** acts as a **partial agonist** at the **mu-opioid receptor**, meaning it binds to the receptor and produces some but not all of the effects of full opioid agonists. - This property contributes to its **ceiling effect** for respiratory depression and analgesic effects, making it safer in overdose compared to full agonists. - It has **high receptor affinity** but **lower intrinsic activity** compared to full agonists. *Pure agonist* - A **pure agonist** would fully activate opioid receptors, producing the maximum possible effect at the receptor. - Examples include **morphine** and **fentanyl**, which carry a higher risk of respiratory depression and overdose at higher doses. - These lack the ceiling effect seen with buprenorphine. *Pure antagonist* - A **pure antagonist** would block opioid receptors without activating them, reversing or preventing the effects of agonists. - An example is **naloxone**, which is used to treat opioid overdose by competitive inhibition. *Mixed agonist-antagonist* - **Mixed agonist-antagonists** (e.g., **pentazocine**, **nalbuphine**) act as agonists at some opioid receptors (kappa) and antagonists at others (mu). - Unlike buprenorphine, which is a partial agonist at mu receptors, mixed agonist-antagonists have different actions at different receptor subtypes. - They can precipitate withdrawal in opioid-dependent patients.
Question 6: A35 yr old lady with Normal PT and increased aPTT. 2 year back, she was operated for cholecystectomy & did not have any bleeding episode. What is next investigation for clinical diagnosis -
- A. Platelet aggregation test
- B. Anti viper venom assay
- C. Ristocetin cofactor assay
- D. Factor VIII assay (Correct Answer)
Explanation: ***Factor VIII assay*** - An isolated **increased aPTT** with a **normal PT** points to an abnormality in the **intrinsic pathway** of coagulation, which includes Factor VIII [1]. - The absence of bleeding episodes for a cholecystectomy suggests a **mild deficiency** or a defect that doesn't cause severe hemorrhage, making Factor VIII deficiency (Hemophilia A) a strong consideration [2]. *Platelet aggregation test* - This test evaluates **platelet function**, abnormalities of which typically present with mucocutaneous bleeding and a normal PT and aPTT. - The patient's presentation of an isolated prolonged aPTT does not primarily suggest a platelet function disorder. *Anti viper venom assay* - This test is primarily used to detect the presence of **lupus anticoagulant**, which can cause a prolonged aPTT but is often associated with thrombotic events, not bleeding. - While lupus anticoagulant can prolong aPTT without bleeding, a Factor VIII deficiency is a more common cause of an isolated prolonged aPTT that is compatible with no significant bleeding history. *Ristocetin cofactor assay* - This assay is used to evaluate **von Willebrand factor (vWF)** activity, which is involved in platelet adhesion and also stabilizes Factor VIII [3]. - While vWF deficiency can cause a prolonged aPTT, it typically presents with mucocutaneous bleeding, and the patient's history doesn't strongly suggest this [3].
Question 7: What are nitrergic neurons?
- A. Postganglionic neurons releasing nitric oxide.
- B. First-order neurons releasing nitric oxide. (Correct Answer)
- C. Postganglionic neurons releasing substance P.
- D. First-order neurons releasing calcitonin gene-related peptide.
Explanation: **Nitrergic neurons** are a specific class of neurons that utilize **Nitric Oxide (NO)** as their primary neurotransmitter. Unlike classical neurotransmitters stored in vesicles, NO is a gaseous molecule synthesized on demand by the enzyme **Neuronal Nitric Oxide Synthase (nNOS)** [1]. **Why Option B is Correct:** In the context of the autonomic and enteric nervous systems, nitrergic neurons are typically **first-order neurons** (primary neurons) that release NO to mediate physiological functions. In the gastrointestinal tract, they are the principal inhibitory neurons of the myenteric plexus, responsible for the relaxation of smooth muscles (e.g., the Lower Esophageal Sphincter and the Sphincter of Oddi) [2]. **Analysis of Incorrect Options:** * **Option A:** While some postganglionic parasympathetic fibers (like those in the corpora cavernosa) release NO, the term "nitrergic neuron" fundamentally refers to the primary/first-order signaling unit in the inhibitory pathways of the enteric nervous system. * **Option C & D:** Substance P and Calcitonin Gene-Related Peptide (CGRP) are neuropeptides associated with **peptidergic neurons**, primarily involved in pain transmission (nociception) and vasodilation, not nitrergic signaling [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Achalasia Cardia:** This condition results from the selective **loss of nitrergic neurons** in the myenteric (Auerbach's) plexus, leading to the failure of the Lower Esophageal Sphincter (LES) to relax. * **Erectile Dysfunction:** NO released from nitrergic nerves in the penis activates guanylyl cyclase, increasing cGMP and causing vasodilation [1]. Sildenafil works by preventing the breakdown of this cGMP. * **Infantile Hypertrophic Pyloric Stenosis:** Also associated with a deficiency of nNOS and nitrergic innervation at the pylorus.
Question 8: Punctate yellow exudates in the colon, found on endoscopic examination, are indicative of which of the following?
- A. Balantidium coli
- B. Ulcerative colitis
- C. Antibiotic-associated colitis (Correct Answer)
- D. Gluten-induced enteropathy
Explanation: ### **Explanation** The correct answer is **Antibiotic-associated colitis (Pseudomembranous colitis)**. **1. Why the Correct Answer is Right:** Antibiotic-associated colitis, most commonly caused by **_Clostridioides difficile_ (C. diff)** toxins, is characterized by the formation of **pseudomembranes**. On endoscopic examination (sigmoidoscopy or colonoscopy), these appear as classic **punctate yellow-white exudates** or plaques scattered over the colonic mucosa [1]. These plaques are composed of fibrin, inflammatory cells (neutrophils), and necrotic debris. As the disease progresses, these small punctate spots can coalesce to form larger membranes. **2. Why the Incorrect Options are Wrong:** * **Balantidium coli:** This parasitic infection typically causes **flask-shaped ulcers** (similar to Amoebiasis) rather than yellow exudative plaques. * **Ulcerative colitis:** Endoscopy typically reveals continuous mucosal inflammation starting from the rectum, characterized by **loss of vascular markings, friability, and "lead-pipe" appearance** in chronic cases [1]. It does not present with punctate yellow exudates. * **Gluten-induced enteropathy (Celiac Disease):** This primarily affects the **small intestine** (duodenum/jejunum). Endoscopic findings include scalloping of folds, fissuring, and a mosaic pattern, not colonic exudates. **3. High-Yield Clinical Pearls for NEET-PG:** * **Risk Factor:** Most common after the use of **Clindamycin**, Fluoroquinolones, or 3rd generation Cephalosporins [1]. * **Diagnosis:** The gold standard for diagnosis is the detection of **C. diff toxin A and B** in the stool via PCR or EIA [1]. * **Histology:** Look for the characteristic **"Volcano lesion"** (an eruption of fibrin and PMNs from an ulcerated crypt). * **Treatment:** First-line treatment is oral **Vancomycin** or **Fidaxomicin**. Metronidazole is now reserved for non-severe cases where other options are unavailable.
Question 9: A person has a history of steatorrhea of long duration. D-xylose testing was performed. A 5-hour urine sample showed <4.5 g excretion after a 25g D-xylose load. What is/are the probable diagnosis?
- A. Celiac disease (Correct Answer)
- B. Pancreatitis
- C. Blind loop syndrome
- D. Heal disease
Explanation: The **D-xylose absorption test** is a classic diagnostic tool used to differentiate between **malabsorption** (mucosal disease) and **maldigestion** (pancreatic insufficiency). D-xylose is a monosaccharide that is absorbed in the proximal small intestine by passive diffusion and does not require pancreatic enzymes for digestion [1]. 1. **Why Celiac Disease is Correct:** In Celiac disease, there is diffuse mucosal damage and blunting of the villi in the small intestine. This leads to impaired absorption of D-xylose [1]. A 5-hour urinary excretion of **<4.5 g** (after a 25g oral load) indicates intestinal mucosal dysfunction, confirming malabsorption. 2. **Why Pancreatitis is Incorrect:** In chronic pancreatitis, steatorrhea occurs due to a lack of lipase (maldigestion) [1]. However, the intestinal mucosa remains intact. Therefore, D-xylose is absorbed normally, and urinary excretion will be **>4.5 g** (Normal). 3. **Why Blind Loop Syndrome is Incorrect:** While Small Intestinal Bacterial Overgrowth (SIBO) can sometimes cause a false positive D-xylose test (as bacteria may metabolize the sugar), it is not the primary diagnosis associated with classic mucosal malabsorption in standard NEET-PG scenarios. 4. **Why Ileal Disease is Incorrect:** D-xylose is primarily absorbed in the **duodenum and jejunum**. Disease localized strictly to the terminal ileum (like Crohn’s) typically results in a normal D-xylose test but abnormal Vitamin B12 absorption (Schilling test). **High-Yield Clinical Pearls for NEET-PG:** * **Normal D-xylose test:** Points toward Pancreatic Insufficiency. * **Abnormal D-xylose test:** Points toward Mucosal Disease (Celiac, Tropical Sprue, Whipple’s) [1]. * **False Positives:** Can occur in patients with renal failure, ascites, or delayed gastric emptying. * **Gold Standard for Celiac:** Small bowel biopsy showing villous atrophy and crypt hyperplasia.
Question 10: A moderate increase in serum aminotransferases with AST/ALT > 3 is suggestive of which of the following?
- A. Acute viral hepatitis
- B. Prolonged hypotension
- C. Alcoholic liver disease (Correct Answer)
- D. Drug hepatotoxicity
Explanation: In alcoholic liver disease (ALD), the ratio of **AST to ALT is typically >2:1**, and a ratio **>3:1** is highly suggestive of the diagnosis. ### Why Alcoholic Liver Disease is Correct The biochemical basis for this ratio lies in two factors: 1. **Pyridoxal-5'-phosphate (Vitamin B6) Deficiency:** Chronic alcohol consumption leads to a deficiency of Vitamin B6, which is a required co-factor for ALT synthesis. Consequently, ALT levels remain relatively low even during liver injury. 2. **Mitochondrial Damage:** Alcohol is a mitochondrial toxin [1]. AST exists in both cytosolic and mitochondrial forms; alcohol-induced damage causes the preferential release of mitochondrial AST [1]. In ALD, the absolute values of transaminases are usually only **moderately elevated** (typically <300-500 IU/L). If AST exceeds 500 IU/L or ALT exceeds 300 IU/L, a co-existing cause (like acetaminophen toxicity) should be suspected [1]. ### Why Other Options are Incorrect * **Acute Viral Hepatitis:** Characterized by massive elevations in transaminases (often >1000 IU/L) with an **AST/ALT ratio <1** [2]. * **Prolonged Hypotension (Ischemic Hepatitis):** Causes "shock liver" with rapid, dramatic rises in transaminases (often >5000 IU/L) and LDH. * **Drug Hepatotoxicity:** Most drugs (except for specific toxins like acetaminophen in the late stage) typically present with an **AST/ALT ratio <1**. ### High-Yield Clinical Pearls for NEET-PG * **GGT (Gamma-Glutamyl Transferase):** The most sensitive marker for chronic alcohol ingestion, though less specific than the AST/ALT ratio [3]. * **Macrocytosis (High MCV):** Often seen in chronic alcoholics due to direct bone marrow toxicity or folate deficiency [3]. * **Rule of Thumb:** If AST/ALT >2, think Alcohol. If ALT > AST, think Viral or Fatty Liver (NAFLD).
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