Addiction Medicine — MCQs

Addiction Medicine Indian Medical PG Practice Questions and MCQs

Question 31: Which organ is mainly affected in leukostasis?

A. Liver
B. Heart
C. Kidney
D. Lung (Correct Answer)

Explanation: **Explanation:** **Leukostasis** is a medical emergency most commonly seen in patients with Acute Myeloid Leukemia (AML) or Chronic Myeloid Leukemia (CML) in blast crisis. It occurs when the white blood cell (WBC) count exceeds 100,000/µL, leading to increased blood viscosity and the formation of "white cell thrombi" in the microvasculature. **Why the Lung is the Correct Answer:** The **lungs** and the **brain** are the two organs most frequently and severely affected by leukostasis. In the pulmonary vasculature, the large, non-deformable blasts adhere to the endothelium, causing local hypoxemia, vascular damage, and alveolar hemorrhage. This manifests clinically as **Acute Respiratory Distress Syndrome (ARDS)** or severe dyspnea. **Analysis of Incorrect Options:** * **A. Liver:** While hepatomegaly can occur due to leukemic infiltration, the liver is not a primary site for the microvascular occlusion characteristic of leukostasis. * **B. Heart:** Myocardial infarction due to leukostasis is rare. While the heart must pump more viscous blood, it is not the "mainly affected" organ compared to the lungs. * **C. Kidney:** Renal failure in leukemia is more commonly a result of **Tumor Lysis Syndrome** (hyperuricemia) rather than direct leukostasis. **Clinical Pearls for NEET-PG:** * **Definition:** Symptomatic hyperleukocytosis (usually WBC >100,000/µL). * **Most Common Symptoms:** Dyspnea (Lungs) and Altered Mental Status/Headache (CNS). * **Contraindication:** Avoid blood transfusions initially, as they further increase viscosity and worsen the stasis. * **Management:** Immediate **Leukapheresis** and aggressive hydration. Hydroxyurea is used for cytoreduction. * **Note:** Leukostasis is rare in Chronic Lymphocytic Leukemia (CLL) even with very high counts because lymphocytes are smaller and less "sticky" than blasts.

Question 32: In a patient with myasthenia gravis, a CT Chest reveals an anterior mediastinal mass. What is the most likely diagnosis?

A. Retrosternal goiter
B. Thymoma (Correct Answer)
C. Hilar lymphadenopathy
D. Aortic aneurysm

Explanation: **Explanation:** The clinical association between **Myasthenia Gravis (MG)** and **Thymoma** is a classic high-yield topic in Internal Medicine. Approximately **10–15%** of patients with MG have an underlying thymoma, while nearly **30–50%** of patients with a thymoma will develop MG. The thymus gland plays a central role in T-cell maturation; in thymoma, there is a breakdown in self-tolerance, leading to the production of autoantibodies against acetylcholine receptors (AChR) at the neuromuscular junction. Because the thymus is located in the **anterior mediastinum**, any patient diagnosed with MG must undergo a CT chest to screen for a thymic mass [1]. **Analysis of Incorrect Options:** * **A. Retrosternal Goiter:** While it can present as a superior/anterior mediastinal mass, it is not associated with Myasthenia Gravis. It usually presents with tracheal deviation or dysphagia. * **C. Hilar Lymphadenopathy:** This involves the **middle mediastinum** (e.g., Sarcoidosis, Tuberculosis, or Lymphoma) and does not have a direct pathophysiological link to MG. * **D. Aortic Aneurysm:** This is a vascular pathology of the middle or posterior mediastinum and is unrelated to autoimmune neuromuscular disorders. **NEET-PG Clinical Pearls:** * **Best initial screening test for MG:** Ice pack test or Edrophonium (Tensilon) test. * **Most specific antibody:** Anti-AChR antibodies (present in 85% of generalized MG). * **Management:** Thymectomy is indicated in all patients with thymoma and is often recommended in non-thymomatous generalized MG (ages 15–60) to improve clinical outcomes [1]. * **Differential for Anterior Mediastinal Mass (The 4 Ts):** **T**hymoma, **T**eratoma (Germ cell tumors), **T**errible Lymphoma, and **T**hyroid (Retrosternal goiter).

Question 33: What is the most common type of posterior mediastinal mass?

A. Neurogenic tumor (Correct Answer)
B. Lymph nodes
C. Neurogenic parasitic cyst
D. Teratoma

Explanation: The mediastinum is anatomically divided into anterior, middle, and posterior compartments. Understanding the characteristic masses of each compartment is a high-yield topic for NEET-PG. **Correct Answer: A. Neurogenic tumor** Neurogenic tumors are the most common cause of a posterior mediastinal mass, accounting for approximately **75-95%** of cases in this compartment. These tumors arise from the intercostal nerves, sympathetic chain, or paraganglia. In adults, they are typically benign (e.g., Schwannoma, Neurofibroma), whereas in children, they are more likely to be malignant (e.g., Neuroblastoma). **Explanation of Incorrect Options:** * **B. Lymph nodes:** While lymphadenopathy (due to sarcoidosis, lymphoma, or tuberculosis) is common in the mediastinum, it is most frequently associated with the **middle mediastinum**. * **C. Neurogenic parasitic cyst:** This is not a standard medical classification. While hydatid cysts can occur in the mediastinum, they are rare and not the most common finding. * **D. Teratoma:** Germ cell tumors, including teratomas, are classically found in the **anterior mediastinum** (one of the "4 Ts": Thymoma, Teratoma, Thyroid, and "Terrible" Lymphoma). **Clinical Pearls for NEET-PG:** * **Anatomic Boundaries:** The posterior mediastinum is located between the pericardium/trachea anteriorly and the vertebral column posteriorly. * **Radiology:** On a chest X-ray, neurogenic tumors often appear as a well-circumscribed, "dumbbell-shaped" mass if they extend into the spinal canal. * **Age Factor:** In the posterior mediastinum, a mass in an adult is likely a Schwannoma; in a child, consider Neuroblastoma or Ganglioneuroma. * **Extramedullary Hematopoiesis:** This is another rare but classic differential for a posterior mediastinal mass in patients with chronic hemolytic anemias (e.g., Thalassemia).

Question 34: Which vitamin should be supplemented first in an alcoholic patient?

A. Cyanocobalamine
B. Folic acid
C. Thiamine (Correct Answer)
D. Vitamin C

Explanation: The correct answer is **Thiamine (Vitamin B1)**. In chronic alcoholic patients, thiamine deficiency is common due to poor dietary intake, impaired gastrointestinal absorption, and reduced hepatic storage [1]. **Why Thiamine is first:** Thiamine is a critical cofactor for **pyruvate dehydrogenase**, an enzyme essential for glucose metabolism [3]. If a patient is given intravenous glucose (dextrose) before thiamine, the sudden glucose load consumes the remaining meager reserves of thiamine [2]. This can precipitously trigger **Wernicke’s Encephalopathy (WE)**, characterized by the triad of ophthalmoplegia, ataxia, and confusion [1]. Therefore, thiamine must always be administered **before or concurrently** with glucose to prevent permanent neurological damage (Korsakoff Syndrome) [5]. **Analysis of Incorrect Options:** * **Cyanocobalamin (B12) & Folic Acid:** While alcoholics are often deficient in these (leading to macrocytic anemia), their deficiency does not cause acute, life-threatening neurological crises upon glucose administration. They are supplemented later. * **Vitamin C:** Deficiency can lead to scurvy, but it is not the priority in the acute management of an alcoholic patient. **NEET-PG High-Yield Pearls:** * **Wernicke’s Triad:** Confusion, Ataxia, Ophthalmoplegia (most common sign: Abducens nerve palsy/Nystagmus) [5]. * **Korsakoff Psychosis:** Characterized by anterograde amnesia and **confabulation** (making up stories to fill memory gaps) [5]. * **Pathology:** Look for petechial hemorrhages in the **mammillary bodies** on MRI or autopsy [4]. * **Rule of Thumb:** "Thiamine before Glucose" is the gold standard in emergency departments for any patient with suspected malnutrition or alcoholism.

Question 35: A chronic alcoholic presents with altered sensorium. His random blood sugar (RBS) and urea nitrogen (UN) levels are normal. What is the most appropriate initial management?

A. Vitamin B1 injection intramuscularly (Correct Answer)
B. Dextrose 50%
C. Dextrose 10%
D. Normal saline

Explanation: **Explanation:** The clinical presentation of a chronic alcoholic with altered sensorium strongly suggests **Wernicke’s Encephalopathy (WE)** [1], a medical emergency caused by **Thiamine (Vitamin B1) deficiency**. **1. Why Vitamin B1 is the Correct Choice:** Chronic alcoholics are often malnourished and have impaired thiamine absorption. Thiamine is a critical cofactor for glucose metabolism (specifically the pyruvate dehydrogenase complex) [4]. In its absence, the brain cannot utilize glucose, leading to neuronal death. Administering Vitamin B1 immediately is the priority to prevent permanent neurological damage or progression to **Korsakoff Syndrome** [2]. **2. Why Other Options are Incorrect:** * **Dextrose 50% & 10% (B & C):** While altered sensorium often warrants checking for hypoglycemia, this patient’s RBS is **normal**. More importantly, administering glucose *before* thiamine in a thiamine-deficient patient can precipitate or worsen Wernicke’s Encephalopathy [2]. Glucose loading increases thiamine demand, rapidly depleting the remaining meager stores. * **Normal Saline (D):** While useful for hydration, it does not address the underlying metabolic emergency (thiamine deficiency) causing the altered sensorium. **NEET-PG High-Yield Pearls:** * **The Classic Triad of WE:** Encephalopathy (confusion), Ocular signs (nystagmus/ophthalmoplegia), and Ataxia [3]. (Note: The full triad is present in only ~16-38% of cases). * **Gold Standard Rule:** Always give Thiamine **before** or **concurrently** with Glucose in any patient with suspected malnutrition or alcoholism [2]. * **Diagnosis:** Primarily clinical. MRI may show bilateral symmetric hyperintensities in the **mamillary bodies** and periaqueductal gray matter [4]. * **Korsakoff Syndrome:** The chronic, irreversible stage characterized by anterograde amnesia and **confabulation** [3].

Question 36: On stopping alcohol, all the following changes are reversible EXCEPT:

A. Hepatitis
B. Cirrhosis (Correct Answer)
C. Microvesicular fatty change
D. Macrovesicular fatty change

Explanation: ### Explanation Alcoholic Liver Disease (ALD) follows a progressive spectrum of pathological changes. Understanding which stages are reversible is crucial for NEET-PG. **1. Why Cirrhosis is the Correct Answer:** Cirrhosis represents the **end-stage** of chronic liver injury. It is characterized by diffuse **bridging fibrosis** and the replacement of normal liver parenchyma with **regenerative nodules** [2]. Once the liver architecture is structurally distorted by dense collagen scarring (fibrosis), the process becomes **irreversible**, even if alcohol consumption ceases [3]. While abstinence can prevent further deterioration and complications, the existing architectural damage remains. **2. Why the Other Options are Incorrect:** * **Macrovesicular & Microvesicular Fatty Change (Steatosis):** This is the earliest response to alcohol. It involves the accumulation of lipid droplets within hepatocytes [1]. This stage is **completely reversible** within 2–4 weeks of total abstinence. * **Alcoholic Hepatitis:** This is an intermediate, inflammatory stage characterized by hepatocyte swelling (ballooning), Mallory-Denk bodies, and neutrophil infiltration. While it carries a high mortality rate in acute phases, the inflammatory changes and cellular damage are **potentially reversible** with aggressive treatment and long-term abstinence, provided it hasn't yet progressed to cirrhosis. **Clinical Pearls for NEET-PG:** * **Earliest change:** Fatty liver (Steatosis). * **Pathognomonic finding in Hepatitis:** Mallory-Denk bodies (ubiquitinated intermediate filaments) [1]. * **AST:ALT Ratio:** In alcoholic liver disease, the ratio is typically **>2:1** (due to pyridoxal phosphate deficiency affecting ALT more than AST). * **Reversibility Rule:** Steatosis (100% reversible) → Hepatitis (Potentially reversible) → Cirrhosis (Irreversible).

Question 37: A 9-year-old girl presents with a 6-month history of difficulty combing her hair and climbing stairs. She exhibits a positive Gower's sign and a maculopapular rash over her metacarpophalangeal joints. What is the most appropriate next investigation?

A. Erythrocyte Sedimentation Rate (ESR)
B. Rheumatoid Factor (RA factor)
C. Creatine Kinase (CK) (Correct Answer)
D. Electromyography (EMG)

Explanation: ### Explanation The clinical presentation of proximal muscle weakness (difficulty climbing stairs and combing hair), a positive **Gower’s sign**, and a characteristic **Gottron’s papules** (maculopapular rash over the MCP joints) in a child is diagnostic of **Juvenile Dermatomyositis (JDM)** [1]. **Why Creatine Kinase (CK) is the correct answer:** In inflammatory myopathies like JDM, the primary pathology is immune-mediated muscle fiber necrosis. **Creatine Kinase (CK)** is the most sensitive initial laboratory investigation to confirm muscle injury. It is typically elevated (often 10–50 times the normal limit) and serves as a crucial baseline marker to monitor disease activity and response to treatment [1]. **Analysis of Incorrect Options:** * **A. ESR:** While often elevated in systemic inflammatory conditions, ESR is non-specific and does not confirm muscle involvement. * **B. Rheumatoid Factor:** This is a marker for Rheumatoid Arthritis and other connective tissue diseases, but it has no diagnostic value for dermatomyositis. * **D. Electromyography (EMG):** While EMG can show characteristic features (myopathic potentials, irritability), it is invasive and painful. In the diagnostic algorithm, biochemical evidence of muscle enzyme elevation (CK) always precedes invasive testing. **High-Yield Clinical Pearls for NEET-PG:** * **Heliotrope Rash:** A violaceous discoloration of the upper eyelids (pathognomonic for Dermatomyositis). * **Gottron’s Papules:** Scaly, erythematous eruptions over the knuckles (MCP, PIP joints) [1]. * **Gold Standard Diagnosis:** Muscle Biopsy (shows perifascicular atrophy). * **Most Specific Autoantibody:** Anti-Mi-2 antibodies. * **Treatment:** Corticosteroids are the first-line treatment.

Question 38: Which of the following investigations is diagnostic of cystic fibrosis?

A. Deficiency of the enzyme mucinase
B. High sweat chloride content (Correct Answer)
C. Alpha-1 aldolase deficiency
D. Increased copper excretion in urine

Explanation: ### Explanation **Correct Answer: B. High sweat chloride content** Cystic Fibrosis (CF) is an autosomal recessive multisystem disorder caused by a mutation in the **CFTR (Cystic Fibrosis Transmembrane Conductance Regulator) gene** on chromosome 7 [1]. The CFTR protein functions as a chloride channel. In the sweat glands, its primary role is the **reabsorption** of chloride from the primary secretion. When CFTR is defective, chloride (and subsequently sodium) cannot be reabsorbed, leading to excessively salty sweat [1]. The **Pilocarpine Iontophoresis Sweat Test** remains the gold standard for diagnosis. A sweat chloride concentration **≥ 60 mmol/L** on two separate occasions is diagnostic of Cystic Fibrosis. **Analysis of Incorrect Options:** * **A. Deficiency of mucinase:** There is no recognized clinical condition involving mucinase deficiency related to CF. CF involves thick, inspissated mucus due to abnormal ion transport, not enzyme deficiency. * **C. Alpha-1 aldolase deficiency:** This is a distractor. **Alpha-1 antitrypsin deficiency** is a real condition leading to emphysema and cirrhosis, but "alpha-1 aldolase" is not a standard diagnostic marker for CF. * **D. Increased copper excretion in urine:** This is the diagnostic hallmark of **Wilson’s Disease**, a disorder of copper metabolism, not Cystic Fibrosis. **NEET-PG High-Yield Pearls:** * **Most common mutation:** ΔF508 (deletion of phenylalanine at position 508). * **Clinical Triad:** Chronic sinopulmonary disease, pancreatic insufficiency (steatorrhea), and male infertility (Congenital Bilateral Absence of Vas Deferens - CBAVD). * **Common Pathogens:** *Staphylococcus aureus* (early childhood) and *Pseudomonas aeruginosa* (most common in adults) [1]. * **Screening:** Immunoreactive Trypsinogen (IRT) levels in newborns.

Question 39: A patient who consumes alcohol daily seeks advice on the safe limit of alcohol intake to avoid liver damage. What is the approximate safe limit of alcohol consumption in this scenario?

A. 210 gm/week (Correct Answer)
B. 310 gm/week
C. 410 gm/week
D. 510 gm/week

Explanation: **Explanation:** The risk of developing alcoholic liver disease (ALD) is directly proportional to the duration and quantity of alcohol consumed. According to standard medical literature (Harrison’s Principles of Internal Medicine), the threshold for developing significant liver injury is generally considered to be **40–80 g/day for men** and **20–40 g/day for women** over a period of 10–12 years. **Why Option A is Correct:** To calculate the weekly limit based on the lower threshold for men (approx. 30g/day), the math follows: **30g/day × 7 days = 210 gm/week**. Consuming alcohol below this cumulative weekly dose is generally associated with a lower risk of developing cirrhosis or alcoholic hepatitis [1]. However, it is important to note that even lower amounts can cause damage in females due to lower gastric alcohol dehydrogenase levels and higher body fat percentages [2]. **Why Other Options are Incorrect:** * **Options B, C, and D (310, 410, 510 gm/week):** These values significantly exceed the established safety threshold. Consuming >300g per week (approx. >40g/day) puts an individual in the high-risk category for steatosis, alcoholic hepatitis, and eventual progression to cirrhosis. **High-Yield Clinical Pearls for NEET-PG:** * **Standard Drink:** In the US, one standard drink contains approximately **14 grams** of pure alcohol (e.g., 12 oz beer, 5 oz wine, or 1.5 oz spirits). * **AST:ALT Ratio:** A ratio of **>2:1** is highly suggestive of alcoholic liver disease (due to pyridoxal phosphate deficiency inhibiting ALT synthesis). * **GGT:** Gamma-glutamyl transferase is the most sensitive marker for chronic alcohol ingestion [1]. * **Maddrey Discriminant Function (DF):** Used to predict prognosis in alcoholic hepatitis; a score **>32** indicates severe disease and warrants corticosteroid therapy.

Question 40: All of the following are true of Henoch-Schönlein purpura, except:

A. Thrombocytopenia (Correct Answer)
B. Abdominal pain
C. Arthritis
D. Gastrointestinal bleed

Explanation: **Explanation:** Henoch-Schönlein Purpura (HSP), now commonly referred to as **IgA Vasculitis**, is a small-vessel leukocytoclastic vasculitis characterized by the deposition of IgA-dominant immune complexes [1]. **Why Option A is the Correct Answer:** The hallmark of HSP is **non-thrombocytopenic purpura**. In HSP, the platelet count is typically **normal or even elevated** (as an acute-phase reactant). The purpuric rash occurs due to inflammation of the blood vessel walls (vasculitis) leading to RBC extravasation, not due to a deficiency in platelets. If a patient presents with purpura and a low platelet count, alternative diagnoses like ITP or leukemia must be considered. **Why Other Options are Incorrect:** * **B & D (Abdominal Pain and GI Bleed):** Gastrointestinal involvement occurs in approximately 70% of cases [1]. It is caused by submucosal hemorrhage and edema. Symptoms range from colicky **abdominal pain** to life-threatening **gastrointestinal bleeding** or intussusception (typically ileo-ileal). * **C (Arthritis):** Migratory arthralgia or arthritis (usually involving the knees and ankles) is seen in about 75% of patients. It is typically transient and non-deforming. **High-Yield Clinical Pearls for NEET-PG:** * **Classic Tetrad:** Palpable purpura (without thrombocytopenia), arthritis/arthralgia, abdominal pain, and renal disease (IgA nephropathy) [1]. * **Demographics:** Most common vasculitis in children; often follows an Upper Respiratory Tract Infection (URTI). * **Diagnosis:** Primarily clinical. Biopsy of the skin shows **leukocytoclastic vasculitis** with **IgA deposition** on immunofluorescence [1]. * **Prognosis:** Generally excellent, but long-term prognosis depends on the severity of **renal involvement**.

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Behavioral Addictions

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Withdrawal Management

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