FMGE 2025 Practice Questions

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: Histological section is given below. Identify the marked cell.

Purkinje cell. ***Purkinje cell*** - The image displays a histological section of the **cerebellar cortex**. The arrow points to a large, flask-shaped neuron situated in a single layer between the outer molecular layer and the inner granular layer, which is characteristic of a **Purkinje cell**. - These cells are the primary output neurons of the cerebellar cortex, utilizing **GABA** as their neurotransmitter to exert an inhibitory effect on the deep cerebellar nuclei. *Stellate cell* - Stellate cells are small, star-shaped inhibitory interneurons located in the superficial part of the **molecular layer** of the cerebellar cortex. - They are significantly smaller than the cell indicated and are not organized into the distinct single-cell layer where the marked neuron is found. *Basket cell* - Basket cells are inhibitory interneurons found in the deeper part of the **molecular layer**, close to the Purkinje cell layer. - While they synapse on Purkinje cells, they are themselves much smaller and are not the large, flask-shaped cell bodies pointed to by the arrow. *Granular cell* - Granular cells are very small, densely packed excitatory neurons that constitute the **granular layer**, the innermost and most cellular layer of the cerebellar cortex (visible as the dark purple area at the bottom). - The marked cell is located in the layer just above the granular layer and is morphologically distinct, being much larger than a single granular cell.

Q: Which of the following amino acids primarily acts as a buffer in blood due to its ability to accept and donate protons at physiological pH?

Histidine. ***Histidine***- The side chain of **histidine**, the **imidazole group**, has a pKa of approximately 6.0, which is close to the physiological pH of **7.4**, making it an effective buffer.- This property is especially vital for the **buffering capacity of hemoglobin** in red blood cells, contributing significantly to pH homeostasis (Bohr effect).*Arginine*- Arginine possesses a **guanidinium group** in its side chain with a very high pKa (~12.5).- This high pKa means its side chain is almost always positively charged and protonated at physiological pH, rendering it ineffective as a physiological **acid-base buffer**.*Tryptophan*- Tryptophan has a large, non-polar **indole ring** side chain, which is chemically inert and lacks an ionizable group within the physiological pH range.- Since it cannot accept or donate protons near pH 7.4, it does not contribute to the **buffering system** of the blood.*Tyrosine*- Tyrosine contains a **phenolic hydroxyl group** with a pKa of approximately 10.5.- Because its pKa is significantly higher than physiological pH, it is largely neutral and incapable of mediating proton exchange effectively in the **blood plasma**.

Q: During starvation, which of the following hormones is primarily produced to maintain blood glucose levels?

Glucagon. ***Glucagon*** - Glucagon is the **primary counter-regulatory hormone** secreted by the pancreatic **alpha cells** in response to hypoglycemia during starvation. - It acts mainly on the liver to stimulate rapid glucose release through **glycogenolysis** and sustain long-term glucose production via **gluconeogenesis**. - Glucagon levels rise significantly within hours of fasting and remain elevated throughout prolonged starvation. *Insulin* - Insulin is an **anabolic hormone** secreted in response to high blood glucose (hyperglycemia) to promote storage and glucose uptake, thus lowering blood glucose levels. - During starvation, insulin secretion is characteristically **suppressed** to minimize glucose uptake by peripheral tissues and conserve it for the brain. *Cortisol* - Cortisol is a **glucocorticoid stress hormone** that does increase during prolonged starvation and contributes to gluconeogenesis and protein catabolism. - However, **glucagon is the primary and most rapid responder** to falling blood glucose levels, making it the correct answer to this question. *Somatostatin* - Somatostatin is a **paracrine inhibitor** secreted by pancreatic delta cells that locally suppresses the release of both insulin and glucagon. - While it modulates islet function, it is not the primary hormone responsible for mobilizing stored fuels and **raising blood glucose** during periods of fasting.

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 patient presents with a history of vomiting. Arterial blood gas analysis reveals the following: - pH: 7.5 - pCO₂: 48 mm Hg - HCO₃⁻: 30 mEq/L What is the most likely acid-base abnormality?

Metabolic alkalosis. ***Metabolic alkalosis***- The high pH (7.5) indicates **alkalemia**, while the elevated **bicarbonate (HCO₃⁻)** of 30 mEq/L identifies the primary metabolic cause [3].- The mild elevation in **pCO₂ (48 mm Hg)** shows appropriate respiratory compensation via **hypoventilation**, attempting to normalize the pH [1, 2]. *Metabolic acidosis*- Requires a low **HCO₃⁻** level (< 22 mEq/L) and a low pH (< 7.35), directly contradicting the observed **high pH** (7.5) and high HCO₃⁻.- This state often arises from conditions like **lactic acidosis** or **diabetic ketoacidosis**, which are not supported by these blood gas results [4]. *Respiratory acidosis*- While the **pCO₂ is elevated (48 mm Hg)**, if this were the primary disorder, it would drive the pH toward an **acidemic** state (< 7.35), which is inconsistent with the pH of 7.5 [3].- Elevated pCO₂ in the context of alkalemia indicates that the respiratory change is a secondary, **compensatory response** to the primary metabolic alkalosis [1]. *Respiratory alkalosis*- This condition is characterized by a low **pCO₂** (< 35 mm Hg) leading to alkalemia, typically due to **hyperventilation** [1].- This diagnosis is ruled out because the patient’s pCO₂ is significantly elevated (48 mm Hg), not low.

Q: What is the primary mechanism behind tissue damage in long-standing diabetes?

Hyperglycemia. ***Hyperglycemia*** - Chronic exposure to high glucose levels is the fundamental upstream trigger initiating all harmful biochemical pathways that lead to **microvascular** and **macrovascular** complications [4]. - It directly leads to the formation of **Advanced Glycation End products (AGEs)**, activation of the **protein kinase C** pathway, and increased **oxidative stress**, all contributing to irreversible tissue damage. *Insulin resistance* - This is a key defect in **Type 2 Diabetes** [4] that *causes* hyperglycemia, but the resulting high glucose level is the direct downstream mechanism causing structural organ damage. - Its primary immediate effect is impaired glucose uptake and utilization in peripheral tissues [1], rather than the intrinsic structural damage seen in **vascular endothelium** or nerves. *Sorbitol accumulation* - This is a specific downstream consequence of chronic **hyperglycemia** activating the **polyol pathway**; therefore, it is a mechanism of damage, not the primary inciting cause. - Accumulation of **sorbitol** and resultant depletion of **NADPH** primarily contributes to osmotic stress and oxidative damage in specific cells like pericytes and Schwann cells (neuropathy). *Decreased insulin secretion* - This is the core pathophysiological defect in **Type 1 Diabetes** and a feature of advanced Type 2 Diabetes (**beta-cell failure**) that *results* in hyperglycemia [3]. - The lack of insulin elevates blood glucose, making **hyperglycemia** the direct variable driving the damaging biochemical process in target tissues over time [2].

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: 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.

Q: In paracetamol poisoning, N-acetylcysteine is administered as an antidote. How does it act to prevent toxicity?

Restores glutathione levels. ***Restores glutathione levels*** - NAC acts as a **precursor** to the synthesis of **glutathione (GSH)**, which is essential for detoxifying the toxic metabolite of paracetamol, **NAPQI**. - By restoring GSH levels, NAC allows **NAPQI** to be conjugated and safely excreted, preventing **hepatocellular necrosis**. *Inhibits the toxin* - NAC does not directly inhibit the formation or activity of the toxic metabolite **NAPQI**, but rather boosts the body's capacity to detoxify it. - The primary mechanism is replenishment of the depleted endogenous antioxidant and detoxifying agent, **glutathione**. *Removes the toxin* - NAC does not increase the clearance or physical removal of paracetamol or its metabolites from the system (unlike measures such as **gastric lavage** or hemodialysis). - Its role is conversion: it helps convert the highly reactive **NAPQI** metabolite into a benign, excretable compound directly within the liver. *Neutralizes liver enzymes* - NAC's mechanism is not focused on neutralizing liver enzymes, but on preventing **NAPQI** from causing **covalent binding** and damage to these enzymes and other cellular macromolecules. - Paracetamol toxicity leads to damage due to **oxidative injury** and depletion of defenses, not primarily due to unwanted enzyme neutralization.

Question 1

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 2

Histological section is given below. Identify the marked cell.

Accepted Answer

Purkinje cell

Answer

Granular cell

Answer

Stellate cell

Answer

Basket cell

Question 3

Which of the following amino acids primarily acts as a buffer in blood due to its ability to accept and donate protons at physiological pH?

Accepted Answer

Histidine

Answer

Arginine

Answer

Tryptophan

Answer

Tyrosine

Question 4

During starvation, which of the following hormones is primarily produced to maintain blood glucose levels?

Accepted Answer

Glucagon

Answer

Insulin

Answer

Cortisol

Answer

Somatostatin

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 patient presents with a history of vomiting. Arterial blood gas analysis reveals the following: - pH: 7.5 - pCO₂: 48 mm Hg - HCO₃⁻: 30 mEq/L What is the most likely acid-base abnormality?

Accepted Answer

Metabolic alkalosis

Answer

Respiratory acidosis

Answer

Respiratory alkalosis

Answer

Metabolic acidosis

Question 7

What is the primary mechanism behind tissue damage in long-standing diabetes?

Accepted Answer

Hyperglycemia

Answer

Insulin resistance

Answer

Sorbitol accumulation

Answer

Decreased insulin secretion

Question 8

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 9

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

Question 10

In paracetamol poisoning, N-acetylcysteine is administered as an antidote. How does it act to prevent toxicity?

Accepted Answer

Restores glutathione levels

Answer

Removes the toxin

Answer

Neutralizes liver enzymes

Answer

Inhibits the toxin

FMGE 2025

Anatomy

Biochemistry

Internal Medicine

Pathology

Pediatrics

Pharmacology