FMGE 2025 Practice Questions

Q: A corneal wisp test was performed, and the corneal reflex was elicited. Which of the following nerves is responsible for the afferent limb of this reflex?

Trigeminal Nerve. ***Trigeminal Nerve*** - The **afferent limb** (sensory input) of the corneal reflex is mediated by the **ophthalmic division (V1)** of the Trigeminal Nerve (CN V). - Sensory stimulation of the cornea sends impulses to the main sensory nucleus of CN V in the **pons**. *Facial Nerve* - The Facial Nerve (CN VII) constitutes the **efferent limb** of the corneal reflex, transmitting the motor signal. - This motor signal causes the eyelid closure reaction (blinking) by innervating the **orbicularis oculi** muscle. *Oculomotor Nerve* - The Oculomotor Nerve (CN III) is primarily responsible for most ocular movements and the **pupillary light reflex** (efferent limb), but not corneal sensation. [1] - It innervates the **levator palpebrae superioris** muscle, which controls eyelid opening, the opposite action of the reflex blink. *Abducens Nerve* - The Abducens Nerve (CN VI) is solely responsible for innervating the **lateral rectus** muscle, controlling lateral eye movement. - It plays no role in either the afferent (sensory) or efferent (motor) component of the corneal reflex pathway.

Q: A patient undergoing general anesthesia develops left lung collapse following intubation. On auscultation, breath sounds are heard only on the right side. What is the most likely cause of this condition?

Right endobronchial intubation. ***Right endobronchial intubation***- This is the most common cause of unilateral lung collapse *immediately* following intubation, as the endotracheal tube (ETT) is usually advanced too far into the **right main bronchus (RMB)**, which is wider and less acutely angled than the left.- When the ETT is solely in the RMB, air ventilates the right lung exclusively, resulting in **absent breath sounds** and subsequent **atelectasis** (collapse) of the non-ventilated left lung.*Mucus secretions obstructing the endotracheal tube*- Significant obstruction of the ETT by mucus would typically lead to **bilateral loss of breath sounds** or severely impaired ventilation (high peak inspiratory pressures), affecting both lungs equally.- The specific finding of unilateral breath sounds (only on the right) excludes a primary blockage of the ETT itself.*Pneumothorax on the left side due to positive pressure ventilation*- While a left **pneumothorax** can cause absent breath sounds on the left, it would involve air accumulation in the pleural space, often requiring significant barotrauma, and is a less frequent and less immediate cause than mainstem intubation following successful intubation.- The clinical picture of immediate unilateral absence of breath sounds following intubation is overwhelmingly attributed to ETT malposition, which causes obstructive **atelectasis** (collapse), not tension pneumothorax.*Bronchospasm*- **Bronchospasm** is characterized by diffuse airway narrowing, typically presenting with high **peak inspiratory pressures** and **wheezing** heard over both lung fields.- It impairs air entry bilaterally and would not result in the complete unilateral absence of breath sounds and lung collapse described, which is indicative of complete airway obstruction to the non-ventilated lung.

Q: A body brought for autopsy is cold and has developed rigor mortis in all 4 limbs and livor mortis at the back (fixed), but no signs of putrefaction. What will be the estimated time since death?

12-24 hrs. ***Correct Option: 12-24 hrs*** - At this stage, **rigor mortis** is typically fully established across all muscle groups (maximal development occurs around 12 hours) and has not yet started to resolve. - **Livor mortis** becomes **fixed** (non-blanching upon pressure) usually after 12 hours, placing the time since death beyond the initial 12-hour window. - **Putrefaction** has not yet begun, which is consistent with this timeframe as putrefactive changes typically start after 24 hours. *Incorrect Option: 6-12 hrs* - During this period, **rigor mortis** is still developing (maximal development is typically approached at 12 hours) and might not be present in all four limbs (starts in smaller joints/upper limbs). - **Livor mortis** is usually present but often still **unfixed** or only partially fixed, meaning it might shift or blanch with pressure. *Incorrect Option: 24-48 hrs* - Around 24 hours, **rigor mortis** generally begins to resolve (**passing off**) starting from the face and neck, contradicting the finding of full rigor in all four limbs. - This timeframe is when the first signs of **putrefaction** (e.g., green discoloration of the abdomen) usually become visible, which is stated to be absent in the body. *Incorrect Option: 36-48 hrs* - By 36 to 48 hours, **rigor mortis** is typically completely resolved (**secondary flaccidity**). - Putrefaction would likely be significantly advanced during this period, including potential signs like marked **marbling** or abdominal swelling.

Q: A child was brought to the casualty with complaints of vomiting and loose stools with a history of laxative use. On examination, arrhythmia is present. What will be the abnormality present?

Hypokalemia. ***Hypokalemia*** - **Laxative abuse** leads to significant gastrointestinal losses of fluid and electrolytes, particularly **potassium** - Combined with **vomiting and loose stools**, potassium depletion is further aggravated - **Hypokalemia causes cardiac arrhythmias** through altered myocardial excitability - **ECG changes** include: U waves, T wave flattening, ST segment depression, prolonged QT interval, and risk of ventricular arrhythmias - This is a classic presentation requiring **urgent potassium replacement** *Hypocalcemia* - Presents with **tetany, carpopedal spasm**, and perioral numbness - ECG shows **prolonged QT interval** but not typical arrhythmias seen here - Not primarily associated with laxative abuse *Hyperkalemia* - Causes **peaked T waves, widened QRS**, and bradyarrhythmias - Occurs with **renal failure or potassium retention**, not GI losses - Opposite of what occurs with laxative abuse and diarrhea *Hyponatremia* - Primarily causes **CNS symptoms**: confusion, seizures, altered sensorium - Cardiac arrhythmias are **not a typical feature** - Can occur with fluid losses but doesn't explain the arrhythmia

Q: Which electrolyte abnormality will lead to cardiac arrhythmia in patients with severe vomiting?

Hypokalemia. ***Hypokalemia*** - Severe vomiting leads to significant loss of gastric acid and subsequent volume depletion, often resulting in **metabolic alkalosis** and substantial **potassium** loss (due to renal compensation and direct GI loss) [1]. - **Hypokalemia** directly affects cardiac muscle repolarization, predisposing the patient to various arrhythmias, including **ventricular tachycardia** (e.g., *Torsades de pointes*) [2], [3]. *Hyponatremia* - While severe vomiting can cause hyponatremia (due to volume loss and inappropriate ADH release), symptomatic effects are primarily **neurological** (e.g., seizures, confusion), not typically cardiac arrhythmias [2]. - The effect on the heart tends to be mild unless the drop is very rapid and severe; it primarily influences **myocardial contractility** through fluid shifts [2]. *Hyperkalemia* - Hyperkalemia causes severe and characteristic ECG changes (tall, peaked T waves, broadened QRS, possible asystole), but it is **not associated** with severe vomiting, which typically causes **hypokalemia** [2]. - Hyperkalemia is more commonly seen in conditions like **renal failure** or acidosis [4]. *Hypocalcemia* - Hypocalcemia primarily affects the heart by causing **prolongation of the QT interval**, which can increase the risk of *Torsades de pointes*, similar to hypokalemia. - However, calcium losses from simple gastric vomiting are generally **not as dramatic** or primary as the potassium losses, making hypokalemia the most direct and common cause of arrhythmia in this specific clinical scenario [1].

Q: A 39-year-old patient with HIV and a CD4 count of 139 cells/μL presents with altered sensorium and impaired consciousness. CSF examination using an India ink preparation reveals a positive result. Which organism is most likely responsible?

Cryptococcus neoformans. ***Cryptococcus neoformans***- The classic finding of a positive **India ink preparation** upon CSF examination indicates the large polysaccharide **capsule** characteristic of this yeast.- In patients with advanced HIV (**CD4 <200** cells/μL), *C. neoformans* is the most common cause of **fungal meningoencephalitis** presenting with altered mental status.*Aspergillus fumigatus*- CNS infection with *Aspergillus* usually manifests as **focal cerebral lesions** (abscesses) or hemorrhagic infarction due to angioinvasion, not typically diffuse meningitis.- Diagnosis generally relies on culturing the fungus, **histopathology** showing septate hyphae, or detecting **galactomannan antigen** in the serum or CSF.*Histoplasma capsulatum*- While it can cause disseminated infection in patients with AIDS, CNS involvement is less frequent than *Cryptococcus* and the yeast is **intracellular** (within macrophages).- Detection typically utilizes **Histoplasma antigen testing** in urine or serum, as the small yeasts do not possess the large capsule highlighted by India ink.*Candida albicans*- *Candida* is a common cause of superficial or disseminated infection, but isolated **Candida meningitis** is rare, usually seen after neurosurgery or hematogenous seeding.- *Candida* **lacks the prominent capsule** that would produce a positive result on an India ink preparation.

Q: A patient is positive for HBsAg and anti-HBc IgM. What is the most likely diagnosis?

Acute hepatitis. ***Acute hepatitis***- The simultaneous presence of **HBsAg** (Hepatitis B surface antigen) indicates active infection [1], paired with **anti-HBc IgM** (Immunoglobulin M against the core antigen) [2].- **Anti-HBc IgM** is the serological hallmark of a recent or **acute** Hepatitis B infection, typically detectable for up to 6 months after symptom onset [1].*Chronic hepatitis*- Chronic infection is defined by the persistence of **HBsAg** for **more than six months** [1].- The predominant core antibody present in chronic infection is **anti-HBc IgG**, whereas Anti-HBc IgM becomes undetectable [1].*Recovery phase*- The recovery phase is marked by the presence of **anti-HBs** (Hepatitis B surface antibody), indicating clearance of the virus and protective immunity [1].- During recovery, **HBsAg** is negative, and **anti-HBc IgM** is absent, leaving only **anti-HBc IgG** and anti-HBs [1].*Vaccination*- Successful vaccination only produces immunity against the surface antigen, resulting solely in the presence of **anti-HBs** [1].- Both **HBsAg** and **anti-HBc** (IgM or IgG) are universally negative following vaccination [1].

Q: A patient presents with right-sided field defects in both eyes, but central vision remains unaffected. What is the most likely diagnosis?

Homonymous Hemianopia with Macular Sparing. ***Homonymous Hemianopia with Macular Sparing*** - **Homonymous hemianopia** refers to a visual field defect on the same side in both eyes (in this case, the right side), which precisely matches the patient's presentation. - **Macular sparing** occurs because the occipital pole, which processes central vision, often has a dual blood supply from both the **posterior cerebral artery (PCA)** and the **middle cerebral artery (MCA)**, protecting it during a stroke affecting one vessel. *Heteronymous Hemianopia with Central Sparing* - **Heteronymous hemianopia** involves defects on opposite sides of the visual field in each eye (e.g., loss of both temporal fields), which is inconsistent with the patient's right-sided defect in both eyes. - This type of defect is classically caused by a lesion at the **optic chiasm**, such as a pituitary adenoma, leading to **bitemporal hemianopia**. *Optic Chiasm Lesion* - A lesion compressing the optic chiasm, where the nasal retinal fibers cross, typically causes **bitemporal hemianopia** (loss of peripheral vision in both eyes). - This results in a **heteronymous** defect, not a **homonymous** one as described in the question. *Optic Tract Lesion* - A lesion in the optic tract (posterior to the chiasm) does cause a contralateral **homonymous hemianopia**. - However, lesions in the optic tract typically do not spare the macula, as the fibers from the macula are intermingled with other fibers at this point. Macular sparing points towards a more posterior lesion in the **visual cortex**.

Q: A neonate on examination has bilateral cataracts and, after investigations, is found to have a patent ductus arteriosus and salt and pepper retinopathy. What is the most likely congenital infection?

Rubella. ***Rubella***- The constellation of **bilateral cataracts**, **patent ductus arteriosus (PDA)**, and **salt and pepper retinopathy** is highly characteristic, if not pathognomonic, of **Congenital Rubella Syndrome (CRS)**.- Other common findings in CRS include **sensorineural hearing loss**, microcephaly, and **pulmonary artery stenosis**.*CMV*- Congenital Cytomegalovirus (CMV) infection is classically associated with **periventricular calcifications** on neuroimaging, microcephaly, and **sensorineural hearing loss**.- While CMV can cause chorioretinitis, it rarely causes the specific combination of **cataracts** and **PDA** found in this neonate, which strongly favors rubella.*Toxoplasma*- Congenital toxoplasmosis typically presents with the classic triad of **hydrocephalus**, **intracranial calcifications** (often random or diffuse), and focal **chorioretinitis**.- It is not typically associated with common cardiovascular defects like **PDA** or the specific appearance of **salt and pepper retinopathy**.*Varicella*- Congenital Varicella Syndrome is characterized by **skin scarring** (often a zigzag pattern), **limb hypoplasia**, and cortical atrophy.- Ocular findings usually involve **microphthalmia** and severe scarring rather than the specific combination of **cataracts** and **PDA**.

Q: A patient came to the hospital with muscle weakness, diarrhea, and bradycardia. He was diagnosed with organophosphate poisoning for which atropine was administered. After atropine administration, which of the following changes are not seen?

Muscle weakness. ***Muscle weakness*** - Muscle weakness in organophosphate poisoning is a **nicotinic effect** caused by excessive acetylcholine at the **neuromuscular junction (NMJ)** - This leads to initial fasciculations followed by depolarization blockade and paralysis - **Atropine is a muscarinic antagonist** and has **no effect on nicotinic receptors** - Therefore, atropine does **not reverse muscle weakness** - this requires **pralidoxime** (2-PAM) to reactivate acetylcholinesterase - Muscle weakness is the change that is **NOT SEEN** after atropine administration *Bradycardia* - Bradycardia is a **muscarinic effect** on the heart (M2 receptors on SA node) - Atropine effectively blocks cardiac muscarinic receptors, leading to **increased heart rate** - This change (reversal of bradycardia) **IS SEEN** with atropine administration *Diaphoresis* - Excessive sweating is mediated by **muscarinic receptors** on eccrine sweat glands - Atropine blocks these receptors, causing **dry skin** (anticholinergic effect) - This change (cessation of sweating) **IS SEEN** with atropine *Nasal discharge* - Rhinorrhea (nasal secretions) is a **muscarinic effect** - part of SLUDGE syndrome - Atropine blocks glandular muscarinic receptors, causing **drying of secretions** - This change (reduction in nasal discharge) **IS SEEN** with atropine **Key Concept**: Atropine reverses only **muscarinic** effects (SLUDGE, bradycardia, bronchospasm) but NOT **nicotinic** effects (muscle weakness, fasciculations). Pralidoxime is needed for nicotinic symptoms.

Question 1

A corneal wisp test was performed, and the corneal reflex was elicited. Which of the following nerves is responsible for the afferent limb of this reflex?

Accepted Answer

Trigeminal Nerve

Answer

Abducens Nerve

Answer

Oculomotor Nerve

Answer

Facial Nerve

Question 2

A patient undergoing general anesthesia develops left lung collapse following intubation. On auscultation, breath sounds are heard only on the right side. What is the most likely cause of this condition?

Accepted Answer

Right endobronchial intubation

Answer

Pneumothorax on the left side due to positive pressure ventilation

Answer

Bronchospasm

Answer

Mucus secretions obstructing the endotracheal tube

Question 3

A body brought for autopsy is cold and has developed rigor mortis in all 4 limbs and livor mortis at the back (fixed), but no signs of putrefaction. What will be the estimated time since death?

Accepted Answer

12-24 hrs

Answer

24-48 hrs

Answer

6-12 hrs

Answer

36-48 hrs

Question 4

A child was brought to the casualty with complaints of vomiting and loose stools with a history of laxative use. On examination, arrhythmia is present. What will be the abnormality present?

Accepted Answer

Hypokalemia

Answer

Hypocalcemia

Answer

Hyperkalemia

Answer

Hyponatremia

Question 5

Which electrolyte abnormality will lead to cardiac arrhythmia in patients with severe vomiting?

Accepted Answer

Hypokalemia

Answer

Hyponatremia

Answer

Hyperkalemia

Answer

Hypocalcemia

Question 6

A 39-year-old patient with HIV and a CD4 count of 139 cells/μL presents with altered sensorium and impaired consciousness. CSF examination using an India ink preparation reveals a positive result. Which organism is most likely responsible?

Accepted Answer

Cryptococcus neoformans

Answer

Candida albicans

Answer

Histoplasma capsulatum

Answer

Aspergillus fumigatus

Question 7

A patient is positive for HBsAg and anti-HBc IgM. What is the most likely diagnosis?

Accepted Answer

Acute hepatitis

Answer

Recovery phase

Answer

Vaccination

Answer

Chronic hepatitis

Question 8

A patient presents with right-sided field defects in both eyes, but central vision remains unaffected. What is the most likely diagnosis?

Accepted Answer

Homonymous Hemianopia with Macular Sparing

Answer

Optic Tract Lesion

Answer

Heteronymous Hemianopia with Central Sparing

Answer

Optic Chiasm Lesion

Question 9

A neonate on examination has bilateral cataracts and, after investigations, is found to have a patent ductus arteriosus and salt and pepper retinopathy. What is the most likely congenital infection?

Accepted Answer

Rubella

Answer

Varicella

Answer

CMV

Answer

Toxoplasma

Question 10

A patient came to the hospital with muscle weakness, diarrhea, and bradycardia. He was diagnosed with organophosphate poisoning for which atropine was administered. After atropine administration, which of the following changes are not seen?

Accepted Answer

Muscle weakness

Answer

Nasal discharge

Answer

Bradycardia

Answer

Diaphoresis

FMGE 2025

Anatomy

Anesthesiology

Forensic Medicine

General Medicine

Internal Medicine

Microbiology

Ophthalmology

Pediatrics

Pharmacology