Anesthesiology
1 questionsWhich is the best confirmatory method to ensure the central line is in the jugular vein?
FMGE 2025 - Anesthesiology FMGE Practice Questions and MCQs
Question 331: Which is the best confirmatory method to ensure the central line is in the jugular vein?
- A. ETCO2
- B. Blood color
- C. Chest x-ray (Correct Answer)
- D. Blood pH
Explanation: ***Chest x-ray (Correct)*** - This is the **gold standard confirmatory method** to verify central venous catheter tip position, ensuring it rests appropriately in the **superior vena cava (SVC)** or at the cavoatrial junction - Post-procedure CXR is essential to screen for **mechanical complications** such as **pneumothorax** or hemothorax, which is paramount for patient safety - Provides anatomical confirmation of proper catheter placement *Blood pH (Incorrect)* - While blood gas analysis can differentiate an **arterial sample** from a venous sample (if accidental arterial puncture occurs), it does **not confirm the anatomical location** of the catheter tip within the venous system - Blood pH is a chemical test for systemic acid-base status, not an imaging technique for assessing catheter placement - Cannot verify the catheter tip is in the appropriate position (SVC/cavoatrial junction) *Blood color (Incorrect)* - Visual inspection of blood color (bright red for arterial, dark red for venous) is **unreliable and subjective** - Especially inaccurate in patients who are hypotensive, septic, or significantly hypoxic, as these conditions can darken arterial blood - Provides **no information** about the final resting location of the catheter tip, which is critical to avoid complications like cardiac perforation or malposition *ETCO2 (Incorrect)* - **End-tidal carbon dioxide (ETCO2)** measurement is used to monitor ventilatory status and efficiency of gas exchange - Primarily used for confirming **tracheal intubation** in airway management - This measurement is **completely unrelated** to the physical placement or confirmation of a central venous catheter
Internal Medicine
4 questionsA patient presents with fever and altered sensorium. Peripheral smear shows multiple ring stages. Best treatment is?
A patient presents with progressive shortness of breath for the last 6 months, accompanied by dry cough. Auscultation reveals bilateral basal end-inspiratory crepitations. There is no history of fever, joint pain, or occupational exposure. What is the diagnosis?
A patient has a long arm span, hypermobile joints and ectopia lentis. What is the defective protein?
A patient presents with contralateral face, arm, and leg weakness. NCCT shows intracerebral hemorrhage (ICH). What is the most likely location of the CNS bleed?
FMGE 2025 - Internal Medicine FMGE Practice Questions and MCQs
Question 331: A patient presents with fever and altered sensorium. Peripheral smear shows multiple ring stages. Best treatment is?
- A. Artesunate (Correct Answer)
- B. Chloroquine
- C. Primaquine
- D. Quinine
Explanation: Artesunate - The clinical presentation of fever and altered sensorium, along with a peripheral smear showing multiple ring stages (characteristic of P. falciparum), indicates severe malaria [1]. Intravenous artesunate is the recommended first-line treatment [1]. - Artesunate is a potent and rapidly acting artemisinin derivative that quickly reduces the parasite burden, leading to lower mortality rates compared to quinine in severe malaria cases [1]. Primaquine - Primaquine is primarily used to eradicate the dormant liver stages (hypnozoites) of P. vivax and P. ovale to prevent relapse, not for treating acute, severe falciparum malaria. - It is ineffective against the asexual erythrocytic stages of P. falciparum and can cause severe hemolysis in patients with G6PD deficiency. Quinine - Quinine is a second-line agent for severe malaria and is only used if artesunate is unavailable, due to its inferior efficacy and greater toxicity [1]. - Its use is associated with adverse effects known as cinchonism (tinnitus, headache, nausea) and can cause severe hypoglycemia and cardiac arrhythmias [1]. Chloroquine - Widespread resistance of P. falciparum to chloroquine makes it an ineffective choice for treating this infection in most malaria-endemic regions. - Chloroquine is typically reserved for the treatment of uncomplicated malaria caused by chloroquine-sensitive species like P. malariae, _P. ovale, or P. vivax (in areas without resistance).
Question 332: A patient presents with progressive shortness of breath for the last 6 months, accompanied by dry cough. Auscultation reveals bilateral basal end-inspiratory crepitations. There is no history of fever, joint pain, or occupational exposure. What is the diagnosis?
- A. Hypersensitivity pneumonitis
- B. Sarcoidosis
- C. Cor-pulmonale
- D. IPF (Correct Answer)
Explanation: ### IPF - The presentation of progressive **shortness of breath**, dry cough, and characteristic **bilateral basal end-inspiratory crepitations** (**Velcro crackles**) strongly suggests Idiopathic Pulmonary Fibrosis [1]. - IPF is a diagnosis of exclusion, supported here by the absence of fever, joint pain, or known occupational/environmental exposures (making it **idiopathic**) [1][2]. *Cor-pulmonale* - *Cor-pulmonale* is **right ventricular failure** secondary to pulmonary hypertension caused by underlying lung disease, and typically presents with signs of systemic venous congestion (e.g., peripheral edema, elevated JVP). - While advanced IPF can *cause* cor-pulmonale, it is not the primary process causing the initial restrictive pattern and bilateral basal **crepitations**. *Sarcoidosis* - Sarcoidosis often involves **bilateral hilar lymphadenopathy** and systemic features (e.g., skin or eye findings), which are absent in this presentation [4]. - Pulmonary fibrosis associated with sarcoidosis typically has an **upper lobe predominance**, unlike the basal findings described here [4]. *Hypersensitivity pneumonitis* - This diagnosis requires a history of exposure to an inhaled **antigen** (e.g., birds, molds) in the home or workplace, which is explicitly excluded in the patient history [3]. - Acute or subacute forms of HP often involve systemic symptoms like fever and chills, which are not mentioned in this slowly progressive presentation [3].
Question 333: A patient has a long arm span, hypermobile joints and ectopia lentis. What is the defective protein?
- A. Keratin
- B. Elastin
- C. Collagen
- D. Fibrillin-1 (Correct Answer)
Explanation: ***Fibrillin-1***- **Marfan syndrome**, characterized by a **long arm span (arachnodactyly)**, **joint hypermobility**, and superiorly displaced **ectopia lentis (hypermobile lens)**, results from mutations in the *FBN1* gene, which codes for **Fibrillin-1**.- **Fibrillin-1** is a critical component of connective tissue **microfibrils** found in the suspensory ligaments of the eye, periosteum, and aortic media, explaining the systemic clinical manifestations.*Collagen*- Defects in **Collagen** (e.g., Type I, III, or V) are associated with **Osteogenesis Imperfecta** (brittle bones) or **Ehlers-Danlos syndrome** (severe skin and joint hyperlaxity) [1].- While Ehlers-Danlos syndrome can cause joint hypermobility, the classic combination with **ectopia lentis** strongly differentiates Marfan syndrome from primary collagenopathies [1].*Elastin*- Mutations in the **Elastin** gene (ELN) are primarily linked to conditions like **Williams syndrome**, which typically presents with **supravalvular aortic stenosis** and characteristic facial features [2].- **Elastin** provides rubber-like properties to tissues, but its primary defect does not explain the specific loss of structural integrity leading to superiorly displaced **ectopia lentis** seen in Marfan syndrome [2].*Keratin*- **Keratin** proteins are intermediate filaments crucial for mechanical stability in **epithelial cells** (skin, hair, nails).- Defects in keratin primarily cause **epidermolysis bullosa** or various forms of **ichthyosis** (skin blistering/scaling), and do not lead to the systemic skeletal or ocular connective tissue anomalies observed here.
Question 334: A patient presents with contralateral face, arm, and leg weakness. NCCT shows intracerebral hemorrhage (ICH). What is the most likely location of the CNS bleed?
- A. Pons
- B. Midbrain
- C. Basal ganglia (Correct Answer)
- D. Medulla
Explanation: ***Basal ganglia*** - The **basal ganglia**, particularly the **putamen**, is the most common site for hypertensive intracerebral hemorrhage, which aligns perfectly with the deep parenchymal bleed seen on the provided NCCT scan. - A lesion in this location classically damages the adjacent **internal capsule**, where motor fibers for the face, arm, and leg are tightly packed, resulting in **contralateral hemiparesis**. *Midbrain* - A midbrain hemorrhage would present with distinct cranial nerve deficits, most notably **oculomotor nerve (CN III) palsy**, causing a "down and out" eye position, ptosis, and a dilated pupil. - Other characteristic signs include altered consciousness and **vertical gaze palsy** (Parinaud syndrome), which are absent in this patient's pure motor presentation. *Pons* - Pontine hemorrhages have a catastrophic presentation, typically causing a rapid descent into **coma**, **quadriplegia**, and classic **pinpoint pupils** due to disruption of descending sympathetic pathways. - The patient's presentation of contralateral hemiparesis without coma or pupillary changes is inconsistent with a pontine bleed. *Medulla* - Medullary hemorrhages are rare and cause specific brainstem syndromes like **Wallenberg syndrome**, characterized by vertigo, nystagmus, dysphagia, and ipsilateral facial numbness. - These syndromes involve complex crossed sensory and motor deficits, not the uniform contralateral motor weakness described in the question.
Pathology
2 questionsA patient had a road traffic accident (RTA). NCCT head was normal on admission. The patient later died after several days in the ICU due to coma. Brain biopsy revealed multiple punctate hemorrhages. What is the diagnosis?
What defect is seen in Bernard Soulier syndrome?
FMGE 2025 - Pathology FMGE Practice Questions and MCQs
Question 331: A patient had a road traffic accident (RTA). NCCT head was normal on admission. The patient later died after several days in the ICU due to coma. Brain biopsy revealed multiple punctate hemorrhages. What is the diagnosis?
- A. Subdural hemorrhage
- B. Intraventricular bleeding
- C. Ischemic injury
- D. Diffuse axonal injury (Correct Answer)
Explanation: ***Diffuse axonal injury*** - This condition is caused by **traumatic shearing forces** due to sudden acceleration-deceleration, as seen in RTAs, leading to widespread axonal damage [1][2]. - A key feature is a discrepancy between clinical severity (e.g., coma) and initial imaging, as non-contrast CT scans are often normal [2]. The presence of **multiple punctate hemorrhages** on biopsy or sensitive MRI sequences (like the one shown) is characteristic [2]. *Ischemic injury* - This results from reduced blood flow causing a stroke, not direct trauma, and presents with focal neurological deficits corresponding to an arterial territory [3]. - Pathologically, it leads to **liquefactive necrosis** in a specific vascular distribution, not diffuse punctate hemorrhages [3]. *Intraventricular bleeding* - This refers to hemorrhage within the ventricular system and would be clearly visible as a **hyperdensity** on an initial NCCT head scan [3]. - It is a distinct type of intracranial bleed and does not present as microscopic, diffuse parenchymal hemorrhages [3]. *Subdural hemorrhage* - This involves bleeding into the space between the dura and arachnoid mater, usually from torn bridging veins. - It appears as a **crescent-shaped** hyperdensity on a CT scan and is typically evident immediately after trauma. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 700-701. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 701-702. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 706-707.
Question 332: What defect is seen in Bernard Soulier syndrome?
- A. Deficiency of GpIIb/IIIa receptor
- B. Deficiency of ADP receptors
- C. Deficiency of GpIb receptors (Correct Answer)
- D. Deficiency of von Willebrand factor
Explanation: ***Deficiency of GpIb receptors***- **Bernard-Soulier syndrome (BSS)** is an autosomal recessive disorder caused by defective or deficient **Glycoprotein Ib (GpIb)** [1]; this receptor is necessary for platelet adhesion to the subendothelium via **von Willebrand factor (vWF)** [1], [2]. - This defect results in dysfunctional primary **hemostasis**, causing bleeding and characteristic findings like **giant platelets** (macrothrombocytopenia) and mild to severely prolonged **bleeding time**. *Deficiency of GpIIb/IIIa receptor*- Deficiency or dysfunction of the **GpIIb/IIIa receptor** (fibrinogen receptor) causes **Glanzmann thrombasthenia** [1], which impairs platelet aggregation, not initial adhesion. - In Glanzmann thrombasthenia, platelets fail to aggregate in response to most agonists (like ADP or thrombin), but the initial adhesion mediated by GpIb is preserved [1]. *Deficiency of von Willebrand factor*- Deficiency of **von Willebrand factor (vWF)** causes **von Willebrand disease (vWD)**, the most common inherited bleeding disorder. - vWF is the ligand that links GpIb on the platelet to the exposed collagen in the vessel wall [2]; its deficiency is distinct from the receptor deficiency seen in BSS. *Deficiency of ADP receptors*- Deficiency of **ADP receptors** (specifically the P2Y12 receptor) impairs the signal transduction critical for sustained platelet aggregation and granule release [2]. - While affecting primary hemostasis, this congenital receptor deficiency is separate from BSS and is rarely reported; the most common interference with this receptor is therapeutic (**clopidogrel**). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 668-669. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, p. 128.
Pediatrics
2 questionsA child presents with kawasaki disease with multiple small coronary artery aneurysms. Treatment is?
The infant is being evaluated for recurrent episodes of seizures. EEG shows Hypsarrhythmia. Which drug is preferred for management?
FMGE 2025 - Pediatrics FMGE Practice Questions and MCQs
Question 331: A child presents with kawasaki disease with multiple small coronary artery aneurysms. Treatment is?
- A. Aspirin for 6 weeks (Correct Answer)
- B. Aspirin for 4 weeks
- C. Aspirin lifelong
- D. Aspirin and clopidogrel for 6 weeks
Explanation: ***Aspirin for 6 weeks*** - After the acute phase is treated with **IVIG** and high-dose aspirin, the regimen is switched to low-dose aspirin for its **antiplatelet** effects to prevent thrombosis in the affected coronary arteries. - This low-dose therapy is typically continued for 6-8 weeks, at which point a follow-up **echocardiogram** is performed and inflammatory markers (like **ESR** and **CRP**) should have normalized. *Aspirin lifelong* - Lifelong antiplatelet therapy is generally reserved for patients with **large** or **giant** coronary artery aneurysms due to a high risk of **thrombosis** and stenosis. - For small aneurysms, which often resolve, therapy is guided by serial echocardiograms and is not typically lifelong from the outset. *Aspirin for 4 weeks* - A 4-week duration is insufficient, as it may not cover the entire period of coronary wall inflammation and thrombocytosis, which usually peaks in the subacute phase. - The standard follow-up interval for re-evaluation with an **echocardiogram** is at 6-8 weeks, making it logical to continue therapy at least until that point. *Aspirin and clopidogrel for 6 weeks* - **Dual antiplatelet therapy** with aspirin and clopidogrel is recommended for patients with **medium-sized** or **giant** coronary artery aneurysms, not for small aneurysms. - The flowchart provided indicates that for small aneurysms (Z score ≥2.5 to <5), **single antiplatelet therapy** with low-dose aspirin is the appropriate treatment.
Question 332: The infant is being evaluated for recurrent episodes of seizures. EEG shows Hypsarrhythmia. Which drug is preferred for management?
- A. Valproate
- B. Vigabatrin
- C. ACTH (Correct Answer)
- D. Carbamazepine
Explanation: ***ACTH*** - The EEG pattern shown is **hypsarrhythmia**, which is a disorganized, high-amplitude, and chaotic pattern characteristic of **West syndrome** (infantile spasms). - **Adrenocorticotropic hormone (ACTH)** is a first-line therapy for infantile spasms, particularly in cases not associated with tuberous sclerosis, and is effective in stopping spasms and resolving the hypsarrhythmia pattern. *Vigabatrin* - **Vigabatrin** is also a first-line treatment for infantile spasms but is specifically the drug of choice if the underlying cause is **Tuberous Sclerosis Complex (TSC)**. - It carries a risk of causing irreversible **peripheral visual field defects**, which requires careful ophthalmologic monitoring. *Valproate* - **Valproate** is a broad-spectrum antiepileptic drug but is not a first-line treatment for infantile spasms. - Its use is limited in infants due to the significant risk of fatal **hepatotoxicity**, especially in children younger than two years old. *Carbamazepine* - **Carbamazepine** is typically used for focal seizures and is known to be ineffective or may even **worsen** infantile spasms and other generalized epilepsies. - It is not indicated for the treatment of West syndrome due to its potential to exacerbate the seizures.
Radiology
1 questionsA patient presents with SOB and fatigue. CXR was done. What is the diagnosis? 
FMGE 2025 - Radiology FMGE Practice Questions and MCQs
Question 331: A patient presents with SOB and fatigue. CXR was done. What is the diagnosis? 
- A. Asbestosis (Correct Answer)
- B. Silicosis
- C. TB
- D. Byssinosis
Explanation: ***Asbestosis*** - The chest X-ray demonstrates classic features of asbestosis, including **pleural plaques** (calcifications on the pleura) and diffuse **interstitial fibrosis**, which is most prominent in the **lower lung zones**. - Asbestosis is a type of pneumoconiosis caused by the inhalation of **asbestos fibers**, and these radiographic findings are highly characteristic of long-term exposure. *TB* - Tuberculosis typically presents with findings in the **upper lobes** or apical segments of the lungs, such as **cavitations**, consolidation, or a **Ghon complex**. - The diffuse lower lobe interstitial pattern and pleural plaques seen in this image are not features of a typical TB infection. *Silicosis* - Silicosis is a pneumoconiosis that classically affects the **upper lung zones**, presenting as multiple small, rounded opacities that can coalesce into larger masses. - A characteristic finding, though not always present, is **"eggshell calcification"** of the hilar lymph nodes, which is absent here. Pleural plaques are not a typical feature. *Byssinosis* - Byssinosis, or "brown lung disease," is caused by exposure to cotton dust and often presents with a normal chest X-ray or non-specific findings of hyperinflation. - The diagnosis is primarily clinical, based on a history of chest tightness and dyspnea that improves over the work week. It does not cause the distinct pleural and parenchymal changes seen in asbestosis.