Internal Medicine
5 questionsWhat is the management of undulant fever?
A patient has cheilosis with koilonychia and anemia. Diagnosis is?
Which classification is used for Barrett esophagus?
A female patient complains of chest pain while waking up in the morning. Pain is more in winter months. Which of the following best describes this patient?
CSF shows abundant PMNs with low sugar and elevated proteins. Diagnosis is?
FMGE 2025 - Internal Medicine FMGE Practice Questions and MCQs
Question 341: What is the management of undulant fever?
- A. Doxycycline
- B. Doxycycline plus ceftriaxone
- C. Doxycycline plus rifampicin (Correct Answer)
- D. Doxycycline with azithromycin
Explanation: ***Doxycycline plus rifampicin***- This is the **standard and preferred oral combination regimen** for treating **Brucellosis** (undulant fever), typically administered for 6 weeks [1].- The combination is crucial because it uses antibiotics that penetrate macrophages and have a **synergistic effect**, significantly reducing the risk of relapse compared to monotherapy.*Doxycycline*- **Doxycycline** is the cornerstone of treatment due to its excellent **intracellular penetration**, but **monotherapy** is associated with high rates of **relapse**.- It must be combined with a second agent (like **rifampicin** or **streptomycin**) to achieve adequate cure rates and prevent recurrence.*Doxycycline with azithromycin*- While macrolides like **azithromycin** show *in vitro* activity against *Brucella*, clinical data supporting this combination as a first-line treatment are generally lacking.- This combination is **less effective** and not recommended by major professional guidelines compared to regimens using **rifampicin** or aminoglycosides.*Doxycycline plus ceftriaxone*- **Ceftriaxone** (a third-generation cephalosporin) is used primarily for complicated brucellosis, especially **neurobrucellosis** (often added to the standard regimen).- It is **not recommended** as part of the standard initial **oral** regimen for uncomplicated brucellosis due to inferior efficacy compared to rifampicin.
Question 342: A patient has cheilosis with koilonychia and anemia. Diagnosis is?
- A. Esophageal cancer
- B. Achalasia cardia
- C. Plummer-Vinson syndrome (Correct Answer)
- D. Tylosis palmaris
Explanation: ***Plummer-Vinson syndrome***- This syndrome is defined by the classic triad of **dysphagia** (due to esophageal webs), **iron deficiency anemia**, and mucosal changes, which include **cheilosis** (angular stomatitis) and **koilonychia** (spoon nails) [1].- It is most common in middle-aged women and results from chronic, severe **iron deficiency**, which causes the epithelial atrophy leading to the observed symptoms [1].*Esophageal cancer*- While **Plummer-Vinson syndrome** is a pre-malignant condition that increases the risk of **esophageal squamous cell carcinoma**, the current presentation describes the syndrome's classic signs, not confirmed malignancy.- Malignancy typically causes progressive **dysphagia** and severe **weight loss**, and the specific triad of **cheilosis** and **koilonychia** is not the primary diagnostic feature.*Achalasia cardia*- This is a **primary esophageal motility disorder** characterized by the poor relaxation of the **lower esophageal sphincter (LES)** and aperistalsis of the esophageal body.- The main symptoms are **dysphagia** (to both solids and liquids) and **regurgitation**, but it is not associated with the systemic features of **iron deficiency anemia**, **cheilosis**, or **koilonychia**.*Tylosis palmaris*- **Tylosis palmaris** is a form of **palmoplantar keratoderma**, an inherited disorder causing marked hyperkeratosis (thickening) of the palms and soles.- Although it is strongly associated with an increased risk for **esophageal squamous cell carcinoma** (Howel-Evans syndrome), it does not cause the specific features of **iron deficiency anemia**, **cheilosis**, and **koilonychia**.
Question 343: Which classification is used for Barrett esophagus?
- A. Prague classification (Correct Answer)
- B. Johnson classification
- C. Forrest classification
- D. Savary-Miller classification
Explanation: ***Prague classification***- This classification is specifically designed for the standardized endoscopic assessment and documentation of **Barrett esophagus** (BE).- It uses two main parameters: the maximal extent (M) and the circumferential extent (C) of the columnar-lined esophagus, ensuring consistent reporting for surveillance.*Savary-Miller classification*- This classification system is used to grade the severity of **reflux esophagitis** (erosive esophagitis), not Barrett esophagus.- It categorizes esophageal mucosal injury based on the extent and depth of erosions.*Johnson classification*- This classification is generally not a recognized standard system for classifying key GI pathology like Barrett esophagus, unlike established systems such as the **Prague classification** or **Los Angeles classification** for reflux esophagitis.- *Note: A Johnson classification exists for pediatric hip dysplasia, but it is unrelated to GI endoscopy.* *Forrest classification*- This system is used exclusively to classify the appearance of **peptic ulcer bleeding** (or other upper GI bleed sources) seen during endoscopy.- It helps predict the risk of rebleeding and guides interventions, such as those performed for ulcers with adherent clots or active oozing.
Question 344: A female patient complains of chest pain while waking up in the morning. Pain is more in winter months. Which of the following best describes this patient?
- A. Ach-induced coronary vasoconstriction (Correct Answer)
- B. Fixed plaque obstruction
- C. Increased sympathomimetic drive in morning hours
- D. Subendocardial ischemia due to increased demand of myocardium
Explanation: ***Ach-induced coronary vasoconstriction***- This clinical presentation—chest pain at rest (especially in the morning hours) and exacerbation during winter months (due to cold exposure)—is the hallmark of **Variant (Prinzmetal's) angina**, which is caused by transient **coronary vasospasm**. [1]- The mechanism involves underlying endothelial dysfunction leading to hyperreactivity of coronary smooth muscle, which can be demonstrated via provoked spasm using agents like **Acetylcholine (ACh)** during diagnostic tests. [1]*Fixed plaque obstruction*- This pathology defines **Stable Angina**, where chest pain is typically predictable and primarily brought on by physical **exertion** when myocardial oxygen demand exceeds fixed supply. [1]- Stable angina rarely occurs exclusively at rest upon waking and does not typically exhibit marked seasonal variation associated with **vasospasm** triggers like cold.*Subendocardial ischemia due to increased demand of myocardium*- Demand ischemia results from factors that increase myocardial workload (e.g., high heart rate, exercise), leading to supply-demand mismatch, which is minimized during rest/sleep. [1]- Prinzmetal's angina is a *supply* problem (vasospasm) causing acute, severe **transmural ischemia**, often presenting with transient **ST elevation** on ECG, differentiating it from typical subendocardial demand ischemia.*Increased sympathomimetic drive in morning hours*- While the natural circadian rhythm involves an increase in sympathetic tone upon waking, potentially triggering cardiac events, this does not describe the specific mechanism of the chest pain.- The symptoms described are most diagnostic of **Prinzmetal's angina**, a distinct disorder defined by localized arterial hyperreactivity rather than general sympathetic increase.
Question 345: CSF shows abundant PMNs with low sugar and elevated proteins. Diagnosis is?
- A. Viral encephalitis
- B. Tubercular Meningitis
- C. Acute bacterial meningitis (Correct Answer)
- D. Viral meningitis
Explanation: ***Acute bacterial meningitis*** - The findings of abundant **Polymorphonuclear leukocytes (PMNs)**, **low CSF glucose** (due to bacterial consumption), and **elevated protein** are the classic triad for an acute bacterial infection of the meninges [1]. - A high PMN count indicates an acute inflammatory response, and the profound hypoglycemia and marked protein elevation distinguish it from most viral etiologies [1]. *Tubercular Meningitis* - While also associated with **low CSF glucose** and **elevated protein**, the predominant cell type is typically **lymphocytic** (mononuclear cells), not PMNs [3]. - The CSF often appears xanthochromic, and organisms like *M. tuberculosis* generally cause a subacute or chronic presentation rather than the acute presentation suggested by abundant PMN presence [3]. *Viral encephalitis* - CSF analysis usually reveals a **lymphocytic pleocytosis** (a higher proportion of lymphocytes), not a PMN predominance. - Glucose levels are typically **normal**, and protein elevation is usually mild to moderate, not markedly elevated. *Viral meningitis* - Similar to viral encephalitis, viral meningitis primarily causes a **lymphocytic pleocytosis** with a transient PMN phase early on, which quickly shifts to lymphocytes [2]. - The defining feature differentiating it from bacterial or tubercular meningitis is the **normal CSF glucose** level and milder protein elevation [2].
Ophthalmology
3 questionsThe finding seen in the image is:
A patient with pituitary adenoma compressing the optic chiasma now presents with loss of visual field. What visual field defect will be seen in the patient?
A patient presents with complaints of eye strain. The given image shows the focus of light rays in different meridians in the eye. Which refractive error is present in this patient?
FMGE 2025 - Ophthalmology FMGE Practice Questions and MCQs
Question 341: The finding seen in the image is:
- A. Arlt's line
- B. Pannus
- C. Horner-Trantas spots
- D. Herbert's pits (Correct Answer)
Explanation: ***Herbert's pits*** - These are pathognomonic signs of **cicatricial trachoma**, representing shallow, depressed scars located at the superior corneoscleral junction (limbus). - They are formed by the resolution and scarring of **limbal follicles**, which are characteristic of the active inflammatory stage of trachoma. *Horner-Trantas spots* - These are small, white, gelatinous nodules seen at the limbus, composed of degenerated eosinophils and epithelial cells. - They are a characteristic finding in **vernal keratoconjunctivitis (VKC)**, an allergic eye condition, and are not seen in trachoma. *Pannus* - Pannus refers to the growth of fibrovascular tissue from the limbus onto the peripheral cornea. - While a **superior pannus** is a common finding in trachoma, the specific depressions shown in the image are Herbert's pits, not the pannus itself. *Arlt's line* - This is a horizontal line of scar tissue found on the **tarsal conjunctiva** of the upper eyelid. - It is another sign of cicatricial trachoma but is located on the inner surface of the eyelid, not at the limbus as seen in the image.
Question 342: A patient with pituitary adenoma compressing the optic chiasma now presents with loss of visual field. What visual field defect will be seen in the patient?
- A. Superior quadrantanopia
- B. Homonymous hemianopia
- C. Bitemporal hemianopia (Correct Answer)
- D. Homonymous anopia
Explanation: ***Bitemporal hemianopia*** - A **pituitary adenoma** most commonly compresses the **optic chiasma**, where the nasal retinal fibers from both eyes decussate (cross over). - Damage to these crossing fibers specifically leads to the loss of the **temporal visual fields** in both eyes, which is the definition of bitemporal hemianopia. *Homonymous anopia* - This is a less specific term. **Homonymous** defects refer to the loss of the same side of the visual field in both eyes (e.g., the left side in both eyes). - These types of defects are caused by lesions located **posterior** (behind) the optic chiasma, not at the chiasma itself. *Homonymous hemianopia* - This defect describes the loss of the same half (either left or right) of the visual field in both eyes. - It results from a lesion in the visual pathway **posterior** to the optic chiasma, such as in the **optic tract**, **optic radiations**, or the **visual cortex**. *Superior quadrantanopia* - This refers to the loss of vision in the upper quadrant of the visual field, often described as a "pie in the sky" defect. - This is typically caused by a lesion affecting the contralateral **temporal lobe** (damaging **Meyer's loop** of the optic radiation), not the optic chiasma.
Question 343: A patient presents with complaints of eye strain. The given image shows the focus of light rays in different meridians in the eye. Which refractive error is present in this patient?
- A. Presbyopia
- B. Astigmatism (Correct Answer)
- C. Amblyopia
- D. Hypermetropia
Explanation: ***Astigmatism*** - The image illustrates that light rays passing through different meridians (vertical and horizontal) of the eye are focused at two separate points, which is the defining feature of **astigmatism**. - This refractive error, typically caused by an irregularly shaped **cornea** or lens, results in the formation of a **conoid of Sturm** (the interval between the two focal lines), causing blurred vision and symptoms like **eye strain**. *Amblyopia* - **Amblyopia**, or lazy eye, is a neurodevelopmental condition where vision is reduced in one eye because the eye and the brain are not working together properly; it is not a refractive error itself. - It can be caused by untreated refractive errors (like severe astigmatism) or **strabismus** during early childhood, but the diagram depicts an optical-physical phenomenon, not a neurological one. *Hypermetropia* - In **hypermetropia** (farsightedness), parallel light rays from all meridians would focus at a single point **behind the retina**, not at two different points as shown. - The image's depiction of two distinct focal lines for vertical and horizontal planes is inconsistent with the uniform focusing seen in simple hypermetropia. *Presbyopia* - **Presbyopia** is the age-related loss of **accommodation**, which is the eye's ability to change focus for near objects due to hardening of the **lens**. - It does not involve different refractive powers in different meridians and therefore is not represented by the optical diagram shown.
Pathology
1 questionsA skin graft was performed on an immunocompromised patient using tissue from another immunocompromised individual. Weeks later, the patient developed contractures and systemic symptoms. What is the most likely cause?
FMGE 2025 - Pathology FMGE Practice Questions and MCQs
Question 341: A skin graft was performed on an immunocompromised patient using tissue from another immunocompromised individual. Weeks later, the patient developed contractures and systemic symptoms. What is the most likely cause?
- A. Delayed wound healing
- B. Rejection due to recipient T8 cells
- C. Graft failure
- D. Graft-versus-host disease (Correct Answer)
Explanation: ***Correct: Graft-versus-host disease (GVHD)*** - GVHD occurs when **immunocompetent donor T lymphocytes** from the graft recognize recipient tissues as foreign and mount an immune attack [1] - Key scenario: **Immunocompromised recipient** receiving tissue from another person (even if donor is immunocompromised, donor T cells in the graft can still be functional) - The recipient's compromised immune system **cannot eliminate donor lymphocytes**, allowing them to engraft and attack host tissues [1] - **Contractures** are characteristic of chronic GVHD affecting skin and connective tissue - **Systemic symptoms** (fever, diarrhea, hepatitis) reflect multi-organ involvement typical of GVHD - Timeline of **weeks** fits both acute (2-100 days) and chronic (>100 days) GVHD *Incorrect: Delayed wound healing* - Would present as local wound complications, not systemic symptoms - Does not explain contractures or multi-organ involvement - Typically occurs within days, not weeks *Incorrect: Rejection due to recipient T8 cells* - This describes **host-versus-graft** (rejection), not graft-versus-host - Patient is **immunocompromised**, so recipient T cells are impaired and unlikely to mount effective rejection - Would cause graft loss, not systemic symptoms in the recipient *Incorrect: Graft failure* - Non-specific term that doesn't explain the clinical presentation - Would present as loss of graft function/wound dehiscence, not systemic symptoms - Does not account for contractures or multi-organ disease **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 244-245.
Pediatrics
1 questionsA 5 year old boy presented with hematemesis and was found to have splenomegaly, on examination. There was a past history of exchange transfusion in this child for neonatal jaundice. What is the probable diagnosis?
FMGE 2025 - Pediatrics FMGE Practice Questions and MCQs
Question 341: A 5 year old boy presented with hematemesis and was found to have splenomegaly, on examination. There was a past history of exchange transfusion in this child for neonatal jaundice. What is the probable diagnosis?
- A. Portal vein thrombosis (Correct Answer)
- B. Splenic vein thrombosis
- C. Liver cirrhosis
- D. Budd-Chiari syndrome
Explanation: ***Portal vein thrombosis***- This is the most probable diagnosis because **extrahepatic portal vein thrombosis (EHPVO)** is the most common cause of portal hypertension and variceal bleeding in pediatric patients.- A past history of **exchange transfusion** (which often utilizes umbilical vein catheterization) is a major risk factor for initiating ascending thrombophlebitis that leads to the development of a **portal vein thrombus**.- Manifestations include **splenomegaly** (due to portal hypertension) and **hematemesis** (due to bleeding from esophageal varices).*Splenic vein thrombosis*- **Isolated splenic vein thrombosis** causes *segmental portal hypertension*, typically resulting in localized high pressure leading mainly to **isolated gastric varices**.- While it causes **splenomegaly**, it is less likely to cause the severe, diffuse portal hypertension and extensive esophageal varices responsible for large-volume hematemesis seen in EHPVO.*Budd-Chiari syndrome*- This syndrome involves obstruction of the **hepatic veins** (or suprahepatic inferior vena cava), leading acutely to symptoms like tender **hepatomegaly**, intractable ascites, and often signs of **liver failure**.- The patient's presentation is characterized by isolated signs of *pre-hepatic portal hypertension* (splenomegaly and variceal bleeding), not the typical constellation of liver congestion seen in Budd-Chiari.*Liver cirrhosis*- Although cirrhosis causes portal hypertension, the history in a 5-year-old points toward a specific **pre-hepatic vascular etiology** (PVT) secondary to a neonatal event rather than a parenchymal disease.- Cirrhosis usually is accompanied by signs of chronic liver failure, such as **jaundice**, **synthetic dysfunction**, or **ascites**, which are absent in this typical EHPVO presentation.