FMGE 2025 Practice Questions

Q: Identify the marked area in the image given.

Pouch of Douglas. ***Pouch of Douglas*** - This is the **rectouterine pouch**, a peritoneal reflection between the posterior wall of the uterus and the anterior aspect of the rectum. - As the most dependent part of the female peritoneal cavity, it's a common site for fluid collection (blood, pus) and can be accessed for procedures like **culdocentesis**, as depicted by the needle. *Morrison's pouch* - Also known as the **hepatorenal pouch**, this is a potential space in the upper abdomen between the liver and the right kidney. - It is anatomically located far superior to the pelvic region shown in the image. *Vesicouterine pouch* - This is the peritoneal pouch located between the anterior surface of the uterus and the posterior surface of the urinary bladder. - The image clearly marks the space posterior to the uterus, not anterior. *Ischioanal Fossa* - This is a fat-filled space located lateral to the anal canal and inferior to the pelvic diaphragm within the perineum. - It is an extraperitoneal structure and not the intraperitoneal recess marked in the image.

Q: Histological section is given below. Identify the marked cell. ![img-34.jpeg](img-34.jpeg)

Purkinje cell. ***Purkinje cell*** - The marked cell is a **Purkinje cell**, identified by its large, **flask-shaped** (pyriform) body and its characteristic location in the cerebellar cortex. - These neurons form a distinct single layer, the **Purkinje cell layer**, situated between the outer, less cellular **molecular layer** and the inner, densely packed **granular layer**. *Stellate cell* - **Stellate cells** are small, star-shaped inhibitory interneurons located within the superficial part of the **molecular layer**; they are not the large, flask-shaped cells shown. - They are significantly smaller than Purkinje cells and do not form a distinct, single-cell-thick layer. *Basket cell* - **Basket cells** are inhibitory interneurons found in the deeper part of the **molecular layer**, close to the Purkinje cells. - Although they synapse on Purkinje cells by forming a 'basket' of fibers around the soma, the arrow is pointing to the large Purkinje cell body itself, not the smaller basket cell. *Granular cell* - **Granular cells** are the very small, densely packed neurons with dark-staining nuclei that form the **granular layer**, which is the dark purple layer at the bottom of the image. - The marked cell is clearly much larger than a granular cell and is located in the layer just above the granular layer.

Q: A Tzanck smear prepared from a vesicle shows multinucleated giant cells. What is the diagnosis?

HSV. ***HSV*** - The Tzanck smear is a rapid cytological test used to detect the viral cytopathic effects seen in vesicles caused by the *Herpesviridae* family, including **Herpes Simplex Virus (HSV)** and **Varicella-Zoster Virus (VZV)**. - The finding of **multinucleated giant cells** (also called **Tzanck cells**) formed by the fusion of infected keratinocytes is highly characteristic of herpetic infections. - **Important note**: The Tzanck smear **cannot distinguish between HSV and VZV** as both produce identical cytopathic effects. However, among the given options, **only HSV** is from the Herpesviridae family that causes vesicular lesions with this classic finding. - Clinical context (location, distribution, patient age) and confirmatory tests like **PCR** or **viral culture** are needed to differentiate HSV from VZV definitively. *HIV* - **HIV** (Human Immunodeficiency Virus) is diagnosed through blood tests, such as fourth-generation antigen/antibody screens or **PCR** for viral load. - The Tzanck smear is a test for vesicular dermatoses and **does not** play a role in the diagnosis of HIV infection. - HIV does not cause vesicles with multinucleated giant cells. *HPV* - **HPV** (Human Papillomavirus) causes warts and condylomas, which are diagnosed histologically showing characteristic **koilocytes** (squamous cells with perinuclear halos). - HPV lesions are **papular or verrucous**, not vesicular, and therefore would not yield multinucleated giant cells on Tzanck smear. - HPV does not belong to the Herpesviridae family. *EBV* - **EBV** (Epstein-Barr Virus) primarily causes Infectious Mononucleosis and is diagnosed using serological tests, such as the **Monospot test** (detecting heterophile antibodies) or EBV-specific antibodies. - EBV is **not associated with vesicular eruptions** and does not produce Tzanck-positive lesions. - EBV belongs to the Herpesviridae family but manifests systemically rather than with characteristic skin vesicles.

Q: A patient reports difficulty switching between movements and experiences uncontrollable hand movements. What is the most likely diagnosis?

Dysdiadochokinesis. ***Dysdiadochokinesis***- This term refers to the impairment in the ability to perform **rapid alternating movements**, directly matching the complaint of "difficulty switching between movements" [2].- It is a classic sign of **cerebellar dysfunction**, which also accounts for the associated **uncontrollable movements** (often reflecting associated **ataxia** or **dysmetria**) [3].*Intentional Tremor*- This tremor is absent at rest, but its amplitude increases significantly as the patient attempts to reach a **visual target** (e.g., during the finger-to-nose test).- While it is a sign of **cerebellar disease**, the primary complaint in the stem is difficulty *switching* movements, which is characteristic of **dysdiadochokinesis**.*Metamorphosis*- This neurological term typically refers to **perceptual distortion** (specifically, *metamorphopsia* is the distortion of visual size or shape), which is unrelated to motor control or coordination.- It is not the term used to describe the inability to perform **rapid alternating movements** or uncontrolled movements due to cerebellar pathology.*Resting Tremor*- A resting tremor is maximal when the limb is completely relaxed and **supported against gravity**, classically seen in **Parkinson's disease** [1].- This tremor usually **improves significantly** or disappears entirely when the patient performs voluntary action, distinguishing it from intentional tremors and general lack of coordination.

Q: A hypertensive patient’s lab results reveal hypernatremia, hypokalemia, and metabolic alkalosis. What is the most probable diagnosis?

Conn's Syndrome. ***Conn's Syndrome***- This condition, known as primary **hyperaldosteronism**, is defined by autonomous overproduction of aldosterone, leading to volume expansion and **hypertension** [1].- Aldosterone acts on the principal cells of the collecting duct to increase Na+ reabsorption (causing hypernatremia) while simultaneously promoting K+ and H+ excretion (causing **hypokalemia** and **metabolic alkalosis**) [2].*Addison’s Disease*- Addison’s disease is primary adrenal insufficiency, characterized by deficiency of mineralocorticoids and glucocorticoids [3].- This lack of aldosterone leads to impaired Na+ reabsorption and deficient K+ excretion, resulting in **hyponatremia** and **hyperkalemia** (the opposite of the clinical picture).*Diabetes Insipidus*- Diabetes Insipidus (DI) is a disorder of insufficient ADH action, resulting in polyuria and profound free water loss leading to **hypernatremia**.- DI does not arise from mineralocorticoid dysfunction, thus it would not typically cause **hypokalemia** or metabolic alkalosis.*Cushing's Disease*- Cushing's disease involves excess **cortisol** (a glucocorticoid), which can cause hypertension and occasionally hypokalemia.- However, the combination of **hypernatremia**, significant **hypokalemia**, and severe **metabolic alkalosis** strongly points toward primary **mineralocorticoid excess** rather than glucocorticoid excess [1].

Q: A neonate was born to a controlled gestational diabetes mother. At the time of birth, he was fine but 4 days later, he developed dyspnea with SpO2 80% at room air. What is the initial management?

Give 100% O2. ***Give 100% O2***- The infant is suffering from **severe hypoxemia** (SpO2 80%), which is a life-threatening emergency requiring immediate stabilization.- The initial step in managing severe, unexplained neonatal hypoxemia or respiratory distress is to administer **100% oxygen** (maximal FiO2) to quickly improve SpO2 above critical levels (typically targeting >90-95%) while investigations or ventilation preparations are made.*Give 21% to 30% O2*- This concentration range represents minimal supplementation and is insufficient for treating **severe hypoxemia** (SpO2 80%) in a neonate.- Such low levels of supplemental oxygen are typically reserved for patients with very **mild desaturations** or during the process of weaning oxygen support.*Give 50% O2*- While this is a higher concentration than room air, 50% O2 may still be inadequate for the initial stabilization of an infant with **SpO2 80%**.- In severe, life-threatening hypoxemia, the priority is maximum oxygen concentration (100% O2) delivery to ensure rapid correction of tissue hypoxia.*Observation*- An oxygen saturation of 80% signifies acute **respiratory failure** or severe compromise and must be treated as a medical emergency, not simply observed.- **Observation** without immediate intervention inevitably leads to worsening hypoxemia, potential end-organ damage, and cardiorespiratory arrest.

Q: While evaluating a 3-year-old with short stature, height is measured at 90cm and the lower segment is 45 cm. What is the likely diagnosis?

Spondyloepiphyseal dysplasia. ***Spondyloepiphyseal dysplasia*** - This child has an **upper:lower segment ratio of 1:1** (45 cm each), which indicates **adult body proportions at age 3** - Normal U:L ratio at 3 years should be approximately **1.3:1** (relatively longer trunk than legs) - Spondyloepiphyseal dysplasia causes **short trunk dwarfism** due to vertebral and epiphyseal involvement - The **limbs are relatively preserved**, leading to a **lower U:L ratio** than expected for age (approaching adult 1:1 ratio prematurely) - This creates **disproportionate short stature** with the trunk being the primary affected segment *Congenital hypothyroidism* - Causes **proportionate short stature** with generalized growth retardation - Would maintain normal U:L ratio for age (1.3:1 at 3 years) - Associated with delayed bone age, developmental delay, and other systemic features *Rickets* - Primarily affects the **lower limbs** with bowing deformities (genu varum/valgum) - Would cause a **higher U:L ratio** (relatively shorter legs) if severe - Does not typically present with this specific 1:1 ratio pattern *Achondroplasia* - Causes **short limb dwarfism** (rhizomelic shortening) - Would result in a **high U:L ratio** (relatively longer trunk than limbs) - Opposite pattern to what is seen in this case

Q: Mechanism of action of botulinum toxin is:

Inhibits the release of acetylcholine. ***Inhibits the release of Acetylcholine***- Botulinum toxin (BoNT) is a **zinc metalloprotease** that cleaves **SNARE proteins** (e.g., SNAP-25) essential for vesicular fusion and neurotransmitter release.- By preventing the exocytosis of **acetylcholine (ACh)** vesicles at the **neuromuscular junction**, BoNT causes irreversible chemical denervation and resulting **flaccid paralysis**.*Inhibits Elongation factor 2*- Inhibition of **Elongation factor 2 (EF-2)** targets the host cell's **protein synthesis** machinery, leading to cell death.- This mechanism is characteristic of toxins like **Diphtheria toxin** and *Pseudomonas aeruginosa* **Exotoxin A**, not botulinum toxin.*Inhibits the release of GABA*- While BoNT can inhibit the release of various neurotransmitters, its defining clinical effect of **flaccid paralysis** is primarily due to inhibition of **acetylcholine** at the peripheral neuromuscular junction.- Inhibition of **GABA** (an inhibitory neurotransmitter) in the CNS would typically lead to increased CNS excitability or spasms, which is contrary to the effects of botulism.*Increases cAMP*- Increasing intracellular **cAMP** levels, usually via activation of **adenylate cyclase**, is the mechanism used by toxins such as **cholera toxin** and **pertussis toxin**.- This mechanism primarily causes large fluid shifts (diarrhea) or cellular dysfunction (like impaired phagocytosis) and is unrelated to botulinum toxin's paralytic action.

Q: A 35-year-old male presents to the emergency department with complaints of blurred vision, dizziness, and severe headache after ingesting an unknown quantity of homemade alcohol earlier in the day. On examination, he is disoriented. Laboratory tests reveal severe metabolic acidosis with a high anion gap. Which metabolite is primarily responsible for the toxicity in this case?

Formic acid. ***Formic acid***- The severe clinical toxicity, including **high anion gap metabolic acidosis**, visual impairment (e.g., blurred vision, blindness), and central nervous system depression, is primarily due to the accumulation of **formic acid** (formate), which is the final toxic metabolite of methanol [1].**Formic acid** inhibits **cytochrome c oxidase** in the retina and brain, leading to cytotoxic hypoxia, specifically affecting the optic nerve and basal ganglia.*Methanol*- **Methanol** itself causes mild inebriation and CNS depression, but it is relatively non-toxic; the severe symptoms arise only after its metabolism begins [2].The signs and symptoms (blurred vision, severe acidosis) that lead to presentation typically occur after a latent period (12-24 hours) as the relatively slow conversion of methanol to **formate** occurs [2].*Formaldehyde*- **Formaldehyde** is the intermediate metabolite formed from methanol via **alcohol dehydrogenase (ADH)**; however, it is rapidly converted to formic acid by **aldehyde dehydrogenase (ALDH)** [1].Due to its rapid metabolism, **formaldehyde** does not accumulate significantly and is therefore not the major culprit responsible for the sustained **high anion gap acidosis** and end-organ damage seen clinically.*Acetic acid*- **Acetic acid** is the final, non-toxic metabolite of **ethanol** metabolism (ethanol -> acetaldehyde -> acetic acid).Ingestion of methanol does not result in the production of **acetic acid**, and this substance plays no role in the clinical picture of methanol poisoning.

Question 1

Identify the marked area in the image given.

Accepted Answer

Pouch of Douglas

Answer

Morrison's pouch

Answer

Vesicouterine pouch

Answer

Ischioanal Fossa

Question 2

Histological section is given below. Identify the marked cell. ![img-34.jpeg](img-34.jpeg)

Accepted Answer

Purkinje cell

Answer

Granular cell

Answer

Stellate cell

Answer

Basket cell

Question 3

A Tzanck smear prepared from a vesicle shows multinucleated giant cells. What is the diagnosis?

Accepted Answer

HSV

Answer

EBV

Answer

HIV

Answer

HPV

Question 4

A patient reports difficulty switching between movements and experiences uncontrollable hand movements. What is the most likely diagnosis?

Accepted Answer

Dysdiadochokinesis

Answer

Metamorphosis

Answer

Resting Tremor

Answer

Intentional Tremor

Question 5

A hypertensive patient’s lab results reveal hypernatremia, hypokalemia, and metabolic alkalosis. What is the most probable diagnosis?

Accepted Answer

Conn's Syndrome

Answer

Addison’s Disease

Answer

Cushing's Disease

Answer

Diabetes Insipidus

Question 6

A neonate was born to a controlled gestational diabetes mother. At the time of birth, he was fine but 4 days later, he developed dyspnea with SpO2 80% at room air. What is the initial management?

Accepted Answer

Give 100% O2

Answer

Observation

Answer

Give 50% O2

Answer

Give 21% to 30% O2

Question 7

While evaluating a 3-year-old with short stature, height is measured at 90cm and the lower segment is 45 cm. What is the likely diagnosis?

Accepted Answer

Spondyloepiphyseal dysplasia

Answer

Congenital hypothyroidism

Answer

Rickets

Answer

Achondroplasia

Question 8

What is the mechanism of action of botulinum toxin?

Accepted Answer

Inhibits acetylcholine release from the presynaptic terminal

Answer

Blocks the postsynaptic acetylcholine receptor

Answer

Inhibits acetylcholine reuptake

Answer

Inhibits acetylcholinesterase

Question 9

Mechanism of action of botulinum toxin is:

Accepted Answer

Inhibits the release of acetylcholine

Answer

Increases cAMP

Answer

Inhibits the release of GABA

Answer

Inhibits Elongation Factor 2

Question 10

A 35-year-old male presents to the emergency department with complaints of blurred vision, dizziness, and severe headache after ingesting an unknown quantity of homemade alcohol earlier in the day. On examination, he is disoriented. Laboratory tests reveal severe metabolic acidosis with a high anion gap. Which metabolite is primarily responsible for the toxicity in this case?

Accepted Answer

Formic acid

Answer

Formaldehyde

Answer

Acetic acid

Answer

Methanol

FMGE 2025

Anatomy

Dermatology

Internal Medicine

Pediatrics

Pharmacology