A 25-year-old female with a previous history of rheumatic fever. Examination shows a loud S1 and mid-diastolic murmur. Which of the following valvular heart diseases does she have?
A patient with a history of rheumatic fever presents with a loud S1 and a low-pitched mid-diastolic murmur at the apex (best heard with the patient in the left lateral position). What is the most likely diagnosis?
A patient presents to the ER with central chest pain. He has a past medical history of heart disease. ECG is shown below. What is the diagnosis?
A patient after MI develops a broad QRS complex tachycardia. His BP is 120/85 mm Hg. ECG is given below. Best management?
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?
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?
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?
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?
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?
A 30-year-old male presents with deep-seated retro-orbital pain from cluster headache. What is the best management?
FMGE 2025 - Internal Medicine FMGE Practice Questions and MCQs
Question 41: A 25-year-old female with a previous history of rheumatic fever. Examination shows a loud S1 and mid-diastolic murmur. Which of the following valvular heart diseases does she have?
- A. MS (Correct Answer)
- B. TS
- C. MR
- D. AR
Explanation: ***MS*** - The combination of a history of **rheumatic fever** (the most common cause of MS globally) and the specific auscultatory findings are highly diagnostic of **mitral stenosis** [1]. - A **loud S1** results from the abrupt closure of the stiffened, high-pressure mitral valve, and a **mid-diastolic murmur** is caused by turbulent flow across the stenotic valve during rapid ventricular filling [2], [3]. *TS* - Tricuspid Stenosis (TS) is a rare sequelae of rheumatic fever and typically presents with a mid-diastolic murmur that *increases* with **inspiration** (**Carvallo's sign**) [2]. - The murmur of TS is best heard at the **left sternal border** (tricuspid area) and is usually accompanied by prominent signs of systemic congestion (e.g., ascites). *MR* - **Mitral Regurgitation** produces a high-pitched, blowing **holosystolic murmur** that typically radiates to the axilla, not a mid-diastolic murmur. - A loud S1 is often *absent* in significant MR as the valve leaflets do not coapt properly; S1 is usually normal or soft. *AR* - **Aortic Regurgitation** is characterized by a high-pitched **diastolic decrescendo murmur** best heard along the left sternal border [4]. - AR is frequently associated with signs of increased stroke volume and wide pulse pressure, such as the **Water-hammer pulse**, none of which are characteristic of this presentation.
Question 42: A patient with a history of rheumatic fever presents with a loud S1 and a low-pitched mid-diastolic murmur at the apex (best heard with the patient in the left lateral position). What is the most likely diagnosis?
- A. Mitral Stenosis (MS) (Correct Answer)
- B. Tricuspid Stenosis (TS)
- C. Mitral Regurgitation (MR)
- D. Aortic Regurgitation (AR)
Explanation: ***Mitral Stenosis (MS)*** - The classic auscultatory findings include a **loud S1** (due to forceful closure of the stiff mitral valve) and a low-pitched, rumbling **mid-diastolic murmur** at the apex, which are pathognomonic for MS [3]. - A history of **rheumatic fever** is the most common cause of mitral stenosis worldwide. The murmur is best heard in the **left lateral decubitus position**, and an **opening snap (OS)** may be heard after S2 [1], [3]. *Tricuspid Stenosis (TS)* - TS produces a mid-diastolic murmur, but it is best heard at the **left lower sternal border**, not the apex [2]. - The murmur of TS characteristically **intensifies with inspiration** (Carvallo's sign), a feature not described in this patient. *Mitral Regurgitation (MR)* - MR causes a **holosystolic (pansystolic) murmur**, meaning it occurs throughout systole, not diastole. - In chronic MR, the S1 sound is typically **soft or absent**, not loud, due to incomplete closure of the mitral valve leaflets. *Aortic Regurgitation (AR)* - AR is characterized by a high-pitched, blowing, **early diastolic decrescendo murmur** best heard along the left sternal border [4]. - It is associated with signs of a wide pulse pressure, such as **bounding peripheral pulses** (Corrigan's pulse), not a loud S1 or a mid-diastolic murmur at the apex.
Question 43: A patient presents to the ER with central chest pain. He has a past medical history of heart disease. ECG is shown below. What is the diagnosis?
- A. Inferolateral MI
- B. Anterolateral MI (Correct Answer)
- C. Constrictive pericarditis
- D. Acute pericarditis
Explanation: ***Anterolateral MI*** - The ECG shows significant **ST-segment elevation** in the anterior leads (**V1-V4**) and the lateral leads (**I, aVL, V5, V6**), which is characteristic of an extensive anterolateral myocardial infarction. - This pattern typically indicates an occlusion of the proximal **Left Anterior Descending (LAD) artery**. The ST depression in the inferior leads (II, III, aVF) represents **reciprocal changes**. *Inferolateral MI* - An inferolateral MI would present with ST elevation in the **inferior leads (II, III, aVF)** and lateral leads (I, aVL, V5, V6). - This ECG shows **ST depression** in the inferior leads, which argues against an inferior wall infarction and instead supports an anterior MI as reciprocal changes. *Acute pericarditis* - Acute pericarditis typically causes **diffuse, concave ST elevation** across multiple territories, not localized to the anterolateral leads as seen here. - It is also often associated with **PR segment depression**, which is not a prominent feature in this ECG. The ST segments here are **convex (coved)**, which is more typical for MI. *Constrictive pericarditis* - This is a chronic condition and does not cause acute ST-segment elevation. Its ECG findings are usually non-specific. - Typical findings for constrictive pericarditis include **low-voltage QRS complexes** and generalized T-wave flattening or inversion, which are not present on this ECG.
Question 44: A patient after MI develops a broad QRS complex tachycardia. His BP is 120/85 mm Hg. ECG is given below. Best management?
- A. Nitroglycerin iv
- B. Amiodarone iv (Correct Answer)
- C. Metoprolol iv
- D. Labetalol iv
Explanation: ***Amiodarone iv*** - The ECG shows a **monomorphic wide-complex tachycardia** in a patient with a history of myocardial infarction, which is presumed to be **ventricular tachycardia (VT)** until proven otherwise. - For a **hemodynamically stable** patient (BP 120/85 mm Hg), intravenous antiarrhythmics like **amiodarone** or procainamide are the first-line treatment for terminating the arrhythmia. *Labetalol iv* - Intravenous beta-blockers like labetalol are generally avoided in the acute management of VT, especially in patients with structural heart disease. - Their **negative inotropic** effects can precipitate **hemodynamic collapse** and cardiogenic shock in a heart already compromised by a recent MI. *Metoprolol iv* - Similar to labetalol, metoprolol is a beta-blocker that is not recommended for the acute termination of VT. - While crucial for long-term management post-MI, its administration during an active VT episode can lead to severe **hypotension** and cardiac decompensation. *Nitroglycerin iv* - Nitroglycerin is a vasodilator used for ischemic chest pain and has no **antiarrhythmic properties** to terminate VT. - Its use could cause significant **vasodilation** and hypotension, potentially destabilizing the patient and converting a stable VT into an unstable one requiring immediate cardioversion.
Question 45: 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?
- A. Acetylcholinesterase
- B. Voltage-gated calcium channels at the NMJ
- C. Presynaptic ACh Receptor
- D. Post-synaptic ACh Receptor (Correct Answer)
Explanation: ***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].
Question 46: 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?
- A. Multifocal motor neuropathy
- B. Becker muscular dystrophy
- C. Spinal muscular atrophy
- D. ALS (Correct Answer)
Explanation: ***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
Question 47: 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?
- A. Cord inflammation
- B. Demyelination of the spinal cord
- C. Demyelination of A, B-fibers (Correct Answer)
- D. Demyelination of B-fibers
Explanation: ***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].
Question 48: 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?
- A. SIADH (Correct Answer)
- B. Gynaecomastia
- C. Cushing syndrome
- D. Hypercalcemia
Explanation: ***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.
Question 49: 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?
- A. Carcinoid crisis
- B. Pheochromocytoma (Correct Answer)
- C. Neuroblastoma
- D. Carcinoid tumor
Explanation: 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).
Question 50: A 30-year-old male presents with deep-seated retro-orbital pain from cluster headache. What is the best management?
- A. Oxygen (Correct Answer)
- B. Verapamil
- C. Lithium
- D. Topiramate
Explanation: ***Oxygen*** - **High-flow oxygen** (100% at 7-15 L/min) is the safest and most effective **first-line abortive treatment** for an acute cluster headache attack [1] - It works rapidly to cause **vasoconstriction** and often terminates the severe retro-orbital pain within **15 to 20 minutes** - This is the preferred treatment for acute attacks due to its rapid onset and excellent safety profile *Verapamil* - Verapamil is a calcium channel blocker and is considered the **first-line prophylactic agent** for both episodic and chronic cluster headache, not acute treatment [1] - Its mechanism of action requires time, rendering it ineffective for terminating an ongoing acute pain episode - Used to prevent future attacks, not to abort current ones *Lithium* - Lithium is a prophylactic treatment reserved mainly for patients with **chronic cluster headache** or those who do not respond to Verapamil [1] - It has a slow onset of action and is not used to manage the acute pain of a cluster attack - Requires therapeutic monitoring due to narrow therapeutic window [1] *Topiramate* - Topiramate is an established prophylactic treatment primarily for **migraine**, and occasionally used as a second-line prophylactic agent for cluster headache - As a prophylactic medication, it plays **no role** in the acute termination or abortive management of a cluster headache episode