FMGE 2025 Practice Questions

Q: An RTA patient has received 4 units of packed RBCs within a few hours. Which of the following will be seen?

Hypocalcemia. ***Hypocalcemia***- The anticoagulant used in packed RBCs, **citrate**, chelates (binds strongly to) **ionized calcium** in the recipient's plasma. - Rapid infusion during massive transfusion overwhelms the liver's capacity to metabolize citrate, causing a rapid decrease in **serum calcium** levels, potentially leading to immediate complications like paresthesias or prolonged QT interval.*Hypernatremia*- Packed RBCs are suspended in solutions that are typically isotonic or slightly hypotonic in sodium, making **Hypernatremia** an unlikely direct complication of transfusion.- Resuscitation fluids (like Normal Saline) used alongside transfused blood are the more common cause of slight hypernatremia in trauma patients, not the blood components themselves.*Hyponatremia*- Although some older blood preservatives might contain less sodium, **Hyponatremia** is not a primary biochemical disturbance associated with massive blood product transfusion.- Dilutional effects or the use of specific hypotonic fluids would be required to induce significant **Hyponatremia**, which is rare with standard trauma protocols.*Hyperkalemia*- Stored RBCs leak **potassium** (K+) into the supernatant fluid during storage, making hyperkalemia a risk, especially with older units or in patients with impaired renal function.- However, **Hypocalcemia** due to immediate **citrate toxicity** is generally considered the most frequent and immediate metabolic derangement requiring intervention during massive transfusion.

Q: What is the name of the technical platform developed under India’s National Tele Mental Health Programme (NTMHP) to deliver mental healthcare services through a multi-tiered system via telephone, digital platforms, and online portals?

Tele-MANAS. ***Tele-MANAS*** - **Tele-MANAS** (Tele-Mental Health Assistance and Networking Across States) is the specific technical platform designated under the National Tele Mental Health Programme (NTMHP) of India. - It provides comprehensive, multi-tiered, 24/7 mental healthcare services through a national toll-free helpline number and digital platforms, aiming to strengthen **mental health support** accessibility. *NIKSHAY* - **NIKSHAY** is the web-enabled system used by the Government of India for surveillance, monitoring, and management of the **National Tuberculosis Elimination Programme (NTEP)**. - It is focused exclusively on **tuberculosis** management and tracking, not tele-mental health services. *Aarogya Setu* - **Aarogya Setu** is a mobile application developed by the Government of India for **COVID-19 contact tracing and health status tracking**. - While it is a digital health initiative, it is not the dedicated platform for the National Tele Mental Health Programme. *e-Sanjeevani* - **e-Sanjeevani** is India's national telemedicine service that provides general healthcare consultations (Doctor-to-Doctor and Patient-to-Doctor) across various medical specialties. - While it is a telemedicine platform, the dedicated platform for the NTMHP's specific mental health service delivery model is **Tele-MANAS**.

Q: A young female presents with ptosis showing diurnal variation. CT chest shows an anterior mediastinal mass identified as thymus gland cancer. Which receptor is affected in this patient?

Post-synaptic ACh Receptor. ***Post-synaptic ACh Receptor*** - The clinical presentation of **ptosis** with **diurnal variation** (worsening weakness throughout the day) and an associated **thymoma** are hallmark features of **Myasthenia Gravis** [1]. - Myasthenia Gravis is an autoimmune disorder characterized by antibodies that bind to and block or destroy **post-synaptic nicotinic acetylcholine (ACh) receptors** at the neuromuscular junction, leading to impaired muscle contraction [2]. *Presynaptic ACh Receptor* - Autoantibodies in common neuromuscular junction disorders do not target presynaptic ACh receptors. These receptors are typically involved in modulating neurotransmitter release via feedback mechanisms. - The primary presynaptic autoimmune disorder, **Lambert-Eaton Myasthenic Syndrome**, involves antibodies against voltage-gated calcium channels, not ACh receptors [3]. *Voltage-gated calcium channels at the NMJ* - This is the pathological target in **Lambert-Eaton Myasthenic Syndrome (LEMS)**, where antibodies inhibit presynaptic calcium influx, reducing acetylcholine release [3]. - LEMS is clinically distinct, often presenting with weakness that **improves with activity** (incremental response) and is strongly associated with **small cell lung cancer** [3]. *Acetylcholinesterase* - **Acetylcholinesterase (AChE)** is the enzyme responsible for degrading acetylcholine in the synaptic cleft; it is not the target of autoimmunity in Myasthenia Gravis. - In fact, **AChE inhibitors** (e.g., pyridostigmine) are a primary treatment for Myasthenia Gravis, as they increase the concentration and duration of ACh in the synapse to better activate the reduced number of receptors [2].

Q: A 35-year-old female with progressive limb weakness for the past 1 year. On examination, muscle fasciculations and hypertonia are noted, and the sensory system is intact. What is the diagnosis?

ALS. ***Correct: ALS (Amyotrophic Lateral Sclerosis)*** - This patient presents with the classic triad of ALS: **progressive limb weakness, fasciculations (LMN sign), and hypertonia/spasticity (UMN sign)** [1] - The combination of **both upper and lower motor neuron signs** is pathognomonic for ALS [1] - **Sensory sparing** is characteristic - ALS affects motor neurons only [1] - Age and progressive course over 1 year fits the typical presentation - El Escorial criteria require UMN + LMN signs in multiple regions *Incorrect: Multifocal motor neuropathy* - This is a **pure lower motor neuron disorder** with conduction block - Would present with fasciculations and weakness but **NO hypertonia** (no UMN involvement) [1] - Treatable with immunotherapy, making it an important differential to exclude [1] *Incorrect: Becker muscular dystrophy* - This is a **primary muscle disease**, not a motor neuron disorder - **No fasciculations** would be present (fasciculations indicate motor neuron pathology) [2] - Predominantly affects males (X-linked), presents with proximal weakness and calf pseudohypertrophy - Elevated CK levels would be expected *Incorrect: Spinal muscular atrophy* - This is a **pure lower motor neuron disorder** due to anterior horn cell degeneration - Would NOT present with **hypertonia or UMN signs** - Typically presents in childhood/early life with symmetric proximal weakness - Associated with SMN1 gene mutations

Q: A patient presents with symmetrical leg weakness and areflexia. He had developed diarrhoea 2 weeks ago. He was diagnosed as having GBS. What is the cause?

Demyelination of A, B-fibers. ***Demyelination of A, B-fibers***- GBS is an acute **demyelinating polyneuropathy** primarily affecting the myelin sheath of peripheral nerves and nerve roots (PNS involvement) [1].- Demyelination of large myelinated **A-fibers** (motor and sensory) explains the severe **symmetrical weakness** and **areflexia** [1]; demyelination of **B-fibers** contributes to common **autonomic dysfunction**.*Demyelination of B-fibers*- B-fibers are primarily **preganglionic autonomic fibers**; their demyelination causes autonomic instability (e.g., blood pressure fluctuation) but does not account for the profound motor weakness and areflexia that define GBS [2].- The cardinal features of GBS (weakness and areflexia) result from damage to the larger **A-fibers** (motor nerves) [1]. *Demyelination of the spinal cord*- GBS is a disease of the **Peripheral Nervous System (PNS)**, affecting nerve roots and peripheral nerves [2].- Demyelination confined to the spinal cord is characteristic of **Central Nervous System (CNS)** demyelinating diseases, such as **Transverse Myelitis** or **Multiple Sclerosis** [3]. *Cord inflammation*- **Spinal cord inflammation** or myelitis is a CNS process and typically results in upper motor neuron signs (spasticity, brisk reflexes) or distinct sensory levels, which are not seen in GBS.- GBS involves inflammation and attack on the **peripheral nerve myelin** or axons, specifically in the nerve roots and distal peripheral nerves [1].

Q: A patient has developed a cough and weight loss for the last 3 months. Biopsy of lung mass shows expression of chromogranin and synaptophysin. Which paraneoplastic syndrome will most likely occur in this patient?

SIADH. ***SIADH*** - The biopsy findings of positive **chromogranin** and **synaptophysin** are characteristic of a **neuroendocrine tumor**, with **Small Cell Lung Cancer (SCLC)** being the most likely diagnosis given the clinical presentation. - **SCLC** is well-known for causing paraneoplastic syndromes, the most common of which is the **Syndrome of Inappropriate Antidiuretic Hormone (SIADH)**, resulting from ectopic **ADH** production [1]. *Hypercalcemia* - Paraneoplastic hypercalcemia is most frequently associated with **Squamous Cell Carcinoma** of the lung [2]. - This occurs due to the tumor's production of **Parathyroid Hormone-related Peptide (PTHrP)**, which is not a typical feature of SCLC [2]. *Cushing syndrome* - Paraneoplastic Cushing syndrome results from the ectopic production of **Adrenocorticotropic Hormone (ACTH)**, which can also be seen in **SCLC** [1]. - However, **SIADH** is a more common paraneoplastic endocrine syndrome associated with SCLC compared to Cushing syndrome. *Gynaecomastia* - Gynaecomastia as a paraneoplastic syndrome is classically associated with **Large Cell Carcinoma** of the lung. - This is due to the ectopic secretion of **human chorionic gonadotropin (hCG)** by the tumor cells.

Q: A patient presents with palpitations, headache, and sweating. His BP is $180/100 \mathrm{mmHg}$ . 24-hour urinary metanephrine values are elevated. What is the diagnosis?

Pheochromocytoma. Pheochromocytoma - The constellation of symptoms—palpitations, episodic sweating, severe headache, and hypertension (the classic triad)—is highly suggestive of excessive catecholamine release. - The diagnosis is confirmed by the elevated 24-hour urinary metanephrines (metabolites of epinephrine and norepinephrine), which is the definitive biochemical hallmark of this adrenal medullary tumor. Carcinoid tumor - This tumor primarily secretes serotonin and other vasoactive substances, leading to symptoms like flushing, diarrhea, and bronchospasm (carcinoid syndrome) [1]. - The biochemical marker for this condition is elevated urinary 5-hydroxyindoleacetic acid (5-HIAA), not metanephrines. Carcinoid crisis - This represents a severe, life-threatening exacerbation of carcinoid syndrome involving severe flushing, profound hypotension, and cardiac arrhythmias. - It is typically an acute event triggered by stressors such as surgery or chemotherapy, unlike the chronic presentation described. Neuroblastoma - This malignant tumor of the neural crest primarily affects infants and young children (usually under 5 years old), making it unlikely in an adult patient. - Although it can secrete catecholamines, its primary presenting features usually include an abdominal mass, fever, and metastasis, and the key diagnostic marker is often high urinary VMA (Vanillylmandelic acid) and HVA (Homovanillic acid).

Q: In Myasthenia gravis, which of the following is the primary target of autoantibodies at the neuromuscular junction?

Post-synaptic ACh Receptor. ***Post-synaptic ACh Receptor*** - Myasthenia gravis is an autoimmune disorder where **IgG autoantibodies** are produced against the nicotinic **acetylcholine receptors (AChR)** on the post-synaptic muscle membrane [1], [2]. - These antibodies block acetylcholine from binding and also cause **complement-mediated destruction** and accelerated degradation of the receptors, leading to fatigable muscle weakness [1]. *Presynaptic ACh receptor* - Presynaptic acetylcholine receptors are involved in modulating the release of acetylcholine, but they are not the primary target of autoantibodies in Myasthenia Gravis. - Conditions targeting presynaptic components, like **Lambert-Eaton Myasthenic Syndrome**, involve a different pathophysiology. *Voltage-gated calcium channels at NMJ* - Autoantibodies against presynaptic **P/Q-type voltage-gated calcium channels (VGCCs)** are the hallmark of **Lambert-Eaton Myasthenic Syndrome (LEMS)**, not Myasthenia Gravis. - The blockade of these channels impairs the presynaptic release of acetylcholine, leading to a distinct clinical picture of weakness that often improves with activity. *Acetylcholinesterase* - **Acetylcholinesterase** is the enzyme that breaks down acetylcholine in the synaptic cleft; it is not the target of autoantibodies in this disease [3]. - **Acetylcholinesterase inhibitors**, such as pyridostigmine, are a primary treatment for Myasthenia Gravis because they increase the availability of acetylcholine at the neuromuscular junction [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 213-214. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1237-1238. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1238-1239.

Q: A patient with osteoarthritis, for the last 3 months, has been taking ibuprofen and has developed occult GI bleeding. Which is correct about the cause?

PGE-2 and prostacyclin production were reduced. ***PGE-2 and prostacyclin production were reduced***- NSAIDs like **ibuprofen** inhibit cyclooxygenase-1 (**COX-1**), which is responsible for synthesizing protective prostaglandins like **PGE2** and **prostacyclin (PGI2)** in the GI mucosa.- The loss of these protective factors impairs the mucosal barrier's ability to withstand acid, leading to ulceration, erosion, and subsequent **occult GI bleeding**. *Increased acid production*- NSAIDs primarily cause mucosal injury by reducing protective factors, not by significantly increasing **basal acid production**.- Although excess acid facilitates damage, the core mechanism of NSAID injury is the loss of **prostaglandin-mediated cytoprotection**. *PGE-1 and prostacyclin production were reduced*- While **prostacyclin (PGI2)** reduction is key, **PGE2** (not PGE1) is the major endogenous prostaglandin responsible for maintaining gastric mucosal integrity in humans.- Misrepresenting the primary protective prostaglandin (PGE2 vs PGE1) makes this option medically less precise than the former. *Mucosal injury due to inhibition of COX-2*- The severe gastrointestinal side effects, including bleeding and ulceration, are predominantly due to the inhibition of the constitutive **COX-1 isoenzyme**.- Selective **COX-2 inhibitors** (coxibs) were specifically designed to minimize GI toxicity by sparing the protective functions of COX-1.

Question 1

An RTA patient has received 4 units of packed RBCs within a few hours. Which of the following will be seen?

Accepted Answer

Hypocalcemia

Answer

Hyperkalemia

Answer

Hypernatremia

Answer

Hyponatremia

Question 2

What is the name of the technical platform developed under India’s National Tele Mental Health Programme (NTMHP) to deliver mental healthcare services through a multi-tiered system via telephone, digital platforms, and online portals?

Accepted Answer

Tele-MANAS

Answer

Aarogya Setu

Answer

e-Sanjeevani

Answer

NIKSHAY

Question 3

A young female presents with ptosis showing diurnal variation. CT chest shows an anterior mediastinal mass identified as thymus gland cancer. Which receptor is affected in this patient?

Accepted Answer

Post-synaptic ACh Receptor

Answer

Acetylcholinesterase

Answer

Voltage-gated calcium channels at the NMJ

Answer

Presynaptic ACh Receptor

Question 4

A 35-year-old female with progressive limb weakness for the past 1 year. On examination, muscle fasciculations and hypertonia are noted, and the sensory system is intact. What is the diagnosis?

Accepted Answer

ALS

Answer

Multifocal motor neuropathy

Answer

Becker muscular dystrophy

Answer

Spinal muscular atrophy

Question 5

A patient presents with symmetrical leg weakness and areflexia. He had developed diarrhoea 2 weeks ago. He was diagnosed as having GBS. What is the cause?

Accepted Answer

Demyelination of A, B-fibers

Answer

Cord inflammation

Answer

Demyelination of the spinal cord

Answer

Demyelination of B-fibers

Question 6

A patient has developed a cough and weight loss for the last 3 months. Biopsy of lung mass shows expression of chromogranin and synaptophysin. Which paraneoplastic syndrome will most likely occur in this patient?

Accepted Answer

SIADH

Answer

Gynaecomastia

Answer

Cushing syndrome

Answer

Hypercalcemia

Question 7

A patient presents with palpitations, headache, and sweating. His BP is $180/100 \mathrm{mmHg}$ . 24-hour urinary metanephrine values are elevated. What is the diagnosis?

Accepted Answer

Pheochromocytoma

Answer

Carcinoid crisis

Answer

Neuroblastoma

Answer

Carcinoid tumor

Question 8

A patient presents with weight gain, thinning of hair, and dry skin. Diagnosis is Hashimoto’s thyroiditis. Which antibody is seen in this case?

Accepted Answer

Anti-TPO antibody

Answer

Anti TBG

Answer

Long-acting thyroid-stimulating antibody

Answer

Anti-TSH receptor antibody

Question 9

In Myasthenia gravis, which of the following is the primary target of autoantibodies at the neuromuscular junction?

Accepted Answer

Post-synaptic ACh Receptor

Answer

Acetylcholinesterase

Answer

Voltage-gated calcium channels at NMJ

Answer

Presynaptic ACh receptor

Question 10

A patient with osteoarthritis, for the last 3 months, has been taking ibuprofen and has developed occult GI bleeding. Which is correct about the cause?

Accepted Answer

PGE-2 and prostacyclin production were reduced

Answer

PGE-1 and prostacyclin production were reduced

Answer

Increased acid production

Answer

Mucosal injury due to inhibition of COX-2

FMGE 2025

Anesthesiology

Community Medicine

Internal Medicine

Pathology

Pharmacology