FMGE 2025 Practice Questions

Q: Which of the following acts as a major intracellular antioxidant and helps in detoxifying reactive oxygen species?

Glutathione. ***Glutathione (Correct Answer)*** - **It is the most abundant non-enzymatic intracellular antioxidant**, found in high concentrations in nearly all cells. - It detoxifies **reactive oxygen species (ROS)**, particularly **hydrogen peroxide** and lipid hydroperoxides, through the **glutathione redox cycle**. - As a **tripeptide molecule** (not an enzyme), it directly acts as the major intracellular antioxidant. *Catalase (Incorrect)* - This is an **enzyme** responsible for the rapid decomposition of two molecules of **hydrogen peroxide (H₂O₂)** into water and oxygen. - While crucial for detoxification in peroxisomes, it is an enzyme, not the primary non-enzymatic antioxidant molecule like glutathione. *Superoxide dismutase (Incorrect)* - This is a **metalloenzyme** that catalyzes the dismutation of the highly reactive **superoxide radical (O₂⁻·)** into less reactive **hydrogen peroxide (H₂O₂)**. - It initiates the antioxidant defense but does not complete the neutralization of H₂O₂, which is handled by catalase or **glutathione peroxidase**. *Peroxidase (Incorrect)* - This is a general class of **enzymes** (e.g., **glutathione peroxidase**) that primarily use substrates like glutathione to reduce **hydrogen peroxide** or lipid peroxides to water or harmless alcohols. - It is an enzyme that works *with* antioxidants like glutathione, rather than being the major intracellular antioxidant molecule itself.

Q: A subject was brought to the Casualty with a history of RTA and head injury. On examination, he was conscious. When the doctor asked questions about the incident, his answers were irrelevant to the questions, but his speech was fluent. What could be the possible site of injury?

Superior temporal gyrus. ***Correct Answer: Superior temporal gyrus*** - The patient exhibits **fluent aphasia** (fluent speech) with severely **impaired comprehension** (irrelevant answers), which is the hallmark of **Wernicke's aphasia** [1]. - **Wernicke's area**, responsible for language comprehension, is located in the posterior aspect of the dominant hemisphere's **superior temporal gyrus** [1]. *Incorrect: Pre-central gyrus* - This area houses the primary **motor cortex**; damage typically results in contralateral **hemiparesis** or paralysis, not selective language comprehension deficits [1]. - Although cortical damage can cause speech articulation issues (**dysarthria**), it does not account for the specific fluent aphasia with catastrophic loss of understanding described. *Incorrect: Inferior frontal gyrus* - The dominant inferior frontal gyrus contains **Broca's area**, damage to which results in **non-fluent aphasia** (impaired speech production) with preserved comprehension [1]. - This presentation (fluent speech, poor comprehension) is diametrically opposite to the expected profile of **Broca's aphasia** [1]. *Incorrect: Brain stem* - Injury here often causes severe alterations in **consciousness**, cranial nerve palsies, or **dysarthria** due to involvement of motor pathways. - The brain stem is not primarily involved in complex, higher-order language functions like comprehension; pure Wernicke's aphasia is a **cortical syndrome** [1].

Q: A patient presents with fatigue, anemia, and hepatomegaly. Hemoglobin electrophoresis reveals the presence of HbS. What will be the appropriate treatment?

Hydroxyurea. Correct: Hydroxyurea - This is the primary disease-modifying therapy for Sickle Cell Disease (SCD), significantly reducing the frequency of vaso-occlusive crises and acute chest syndrome [1]. - It works by increasing the production of fetal hemoglobin (HbF), which interferes with HbS polymerization and subsequent sickling of red blood cells [1]. - Hydroxyurea is the first-line chronic management for symptomatic SCD patients [1]. *Incorrect: Blood transfusion* - Transfusions are reserved for acute, life-threatening complications of SCD, such as aplastic crisis, severe exacerbation of anemia, or prevention of stroke in high-risk patients [1]. - Chronic routine transfusions carry risks of iron overload (hemosiderosis) and alloimmunization, making them generally unsuitable for standard chronic management. *Incorrect: Iron supplementation* - Sickle cell anemia is a hemolytic anemia typically resulting in elevated iron stores due to chronic hemolysis, and if transfusions are given, iron overload (hemosiderosis) is a major concern. - Iron supplementation is contraindicated unless a specific, documented iron deficiency is present, as it can worsen iron deposition in vital organs. *Incorrect: Vitamin B12 supplementation* - Vitamin B12 is primarily used to treat megaloblastic anemia resulting from B12 deficiency (e.g., pernicious anemia). - SCD anemia is caused by chronic extravascular hemolysis, and while folic acid is often required due to high cell turnover, B12 is not the targeted treatment for HbS pathology.

Q: Which of the following genetic mutations is most commonly associated with familial cases of Amyotrophic Lateral Sclerosis (ALS)?

SOD1 gene mutation. ***SOD1 gene mutation***- Mutations in the **Superoxide Dismutase 1 (SOD1)** gene are historically significant and account for approximately 15–20% of all familial ALS cases.- The SOD1 protein is located in the cytoplasm and mitochondria, and mutations lead to toxic misfolding and aggregation, resulting in **motor neuron death**.*CFTR gene mutation*- The **CFTR (Cystic Fibrosis Transmembrane Conductance Regulator)** gene mutation is critically linked to the development of **Cystic Fibrosis**, a severe disorder of exocrine glands.- This mutation primarily affects chloride ion transport across epithelia, leading to highly viscous secretions, particularly in the airways and pancreas, not motor neuron disease.*HTT gene mutation*- Mutations involving the **HTT (Huntingtin)** gene, specifically expanded **CAG trinucleotide repeats**, cause **Huntington's disease**.- Huntington’s disease is characterized by progressive degeneration of the **striatum** and cortex, leading to movement abnormalities (*chorea*), cognitive decline, and psychiatric symptoms, distinct from ALS.*FMR1 gene mutation*- The **FMR1 (Fragile X Messenger Ribonucleoprotein 1)** gene is responsible for **Fragile X syndrome**, the most common inherited cause of intellectual disability.- The mutation involves expansion of the **CGG trinucleotide repeat**, typically leading to transcriptional silencing and symptoms like macroorchidism and behavioral issues, not primary motor neuron degeneration.

Q: Tau protein inclusions are involved in:

Alzheimer’s disease. ***Alzheimer's disease*** - **Tau protein** aggregation leads to the formation of **neurofibrillary tangles (NFTs)**, which are characteristic pathological hallmarks of Alzheimer's disease, particularly in the hippocampus and cortex [1]. - Hyperphosphorylation of Tau causes it to dissociate from microtubules, destabilizing the neuronal cytoskeleton and ultimately leading to **synaptic dysfunction** and cell death [2]. *Huntington's disease* - This disorder is caused by an expansion of a **CAG triplet repeat** in the *HTT* gene, leading to the accumulation of misfolded **Huntingtin protein**. - It is characterized by atrophy of the **caudate nucleus** and putamen (striatum) and is not primarily linked to Tauopathies. *Amyotrophic lateral sclerosis* - ALS is primarily characterized by the aggregation of **TDP-43** (Tar DNA-binding protein 43) in motor neurons, a distinct type of proteinopathy. - While some cases of ALS overlap with Frontotemporal Dementia (FTD) which can involve Tauopathies, classic ALS pathology is defined by **TDP-43 inclusions**. *CNS lymphoma* - CNS lymphoma is a **primary central nervous system (CNS) tumor**, usually a non-Hodgkin B-cell lymphoma. - Diagnosis relies on identifying atypical lymphoid cells and is not associated with misfolded Tau protein inclusions, which are features of **neurodegenerative diseases** [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1292-1295. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 721-722. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1288-1289.

Q: For testing blood clotting/coagulation parameters, blood is collected in which color-coded vacutainer tube?

Blue. ***Blue*** - The blue-coded vacutainer contains **Sodium Citrate** (3.2% or 3.8%), which is the required anticoagulant for performing coagulation studies, such as **PT** (Prothrombin Time) and **aPTT** (Activated Partial Thromboplastin Time) [1]. - **Sodium Citrate** works by binding and sequestering **calcium ions** (Factor IV), thereby reversibly preventing the coagulation cascade from proceeding until calcium is added back in the lab [1]. *Red* - The Red top tube typically contains **no anticoagulant** (or a clot activator) and is used to obtain **serum** after the blood clots naturally. - It is utilized for chemistry, serology, and blood bank tests, where the natural clotting process is required or coagulation factors are not needed. *Green* - The Green top tube contains **Heparin** (Lithium or Sodium Heparin), which inhibits clotting by augmenting the activity of **antithrombin III** [2]. - Although it provides plasma, it is unsuitable for routine coagulation assays because heparin itself significantly interferes with most coagulation factor tests. *Gray* - The Gray top tube contains **Potassium Oxalate** as an anticoagulant and **Sodium Fluoride** as a preservative. - It is specifically reserved for **glucose** and sometimes **lactate** measurements, as sodium fluoride inhibits enolase, thereby preventing glycolysis (glucose breakdown) by blood cells. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 128-130. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 583-584.

Q: Which of the following is pro-apoptotic?

Bax. ***Bax*** - Bax is a key **pro-apoptotic** effector protein from the Bcl-2 family [1]. Upon activation by stress signals, it translocates to the mitochondria and forms pores in the outer membrane [2]. - This pore formation, along with Bak, leads to **Mitochondrial Outer Membrane Permeabilization (MOMP)**, which releases **cytochrome c** and initiates the intrinsic caspase cascade of apoptosis [3]. *Bcl-2* - Bcl-2 is the prototypical **anti-apoptotic** protein that prevents apoptosis by binding to and inhibiting pro-apoptotic proteins like Bax and Bak [2]. - By preventing MOMP, it maintains mitochondrial integrity and is often overexpressed in cancers, such as follicular lymphoma, contributing to cell survival [2]. *Bcl-xL* - Bcl-xL is another major **anti-apoptotic** protein in the Bcl-2 family, with a function very similar to Bcl-2 [2]. - It promotes cell survival by sequestering pro-apoptotic BH3-only proteins and preventing the activation of Bax and Bak. *Mcl-1* - Mcl-1 (Myeloid cell leukemia-1) is a critical **anti-apoptotic** protein that is essential for the survival of various cell types [2]. - Its primary role is to inhibit apoptosis by neutralizing pro-apoptotic proteins, and its high levels are often associated with tumor progression and resistance to chemotherapy [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 65-67. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 310. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 64-65.

Q: A 7-year-old child is brought to the clinic with complaints of fatigue and poor concentration. The mother reports that the child has been eating non-food items such as chalk and soil for the past few months. A peripheral blood smear image shows microcytic, hypochromic red blood cells. Which of the following is the most likely diagnosis?

Iron deficiency anemia. ***Iron deficiency anemia*** - The patient's history of **pica** (craving and eating non-food items like chalk and soil) is a classic clinical sign of iron deficiency. - The peripheral blood smear confirms this diagnosis by showing **microcytic** (small) and **hypochromic** (pale) red blood cells, which result from impaired hemoglobin synthesis due to a lack of iron. *Vitamin B12 deficiency* - This condition causes **macrocytic anemia**, where red blood cells are larger than normal (high MCV), which is the opposite of the findings in this case. - Peripheral smear findings in B12 deficiency typically include **macro-ovalocytes** and **hypersegmented neutrophils**, neither of which is described or shown. *Thalassemia major* - Although thalassemia causes a **microcytic, hypochromic anemia**, it is a genetic disorder that typically presents in infancy with severe symptoms like failure to thrive and massive **hepatosplenomegaly**. - Pica is not a characteristic feature of thalassemia; it is strongly associated with iron deficiency anemia. *Lead poisoning* - Lead poisoning can cause microcytic anemia, but a key finding on the peripheral smear is **basophilic stippling**, which is not the prominent feature here. - While pica can be a risk factor for lead ingestion, pica itself is a more direct and classic symptom of underlying **iron deficiency**.

Q: A 5-year-old child is brought to the clinic with abdominal pain, irritability, and developmental delay. On examination, the child has pallor and a bluish line on the gums. Laboratory tests reveal microcytic anemia, and a peripheral blood smear shows red blood cells with basophilic stippling. Which of the following is the most likely diagnosis?

Lead poisoning. ***Lead poisoning***- All the symptoms—**abdominal pain** (colic), **irritability**, **developmental delay**, microcytic anemia, and the finding of a **bluish line on the gums** (Burton line)—are highly suggestive of chronic lead toxicity in a child. - The hallmark **basophilic stippling** on the blood smear is caused by lead inhibiting the enzyme **pyrimidine 5'-nucleotidase**, preventing RNA degradation.*Iron deficiency anemia*- While it causes **microcytic anemia** and pallor, it typically does not present with the severe neurodevelopmental regression or **abdominal colic** described.- Basophilic stippling is rare in iron deficiency anemia; the characteristic peripheral smear findings are severe **microcytosis** and **hypochromia**.*Sideroblastic anemia*- This condition is characterized by the presence of **ring sideroblasts** in the bone marrow and high iron levels, which requires specific testing for confirmation.- Although it can rarely present with basophilic stippling, it lacks the specific history of severe neurological and gastrointestinal symptoms (colic, developmental delay) associated with **lead exposure**.*Thalassemia minor*- This is a mild, often asymptomatic **microcytic, hypochromic anemia** caused by reduced globin chain synthesis, usually identified via routine screening or elevated **HbA2** on electrophoresis.- Thalassemia does not cause **basophilic stippling** (unless unstable Hb variants are present) and fundamentally lacks the systemic toxicity signs like **Burton lines** and **developmental delay**.

Q: As a neuron’s diameter increases, what effect manifests?

Conduction velocity increases. ***Conduction velocity increases*** - Increasing the diameter of an axon decreases the **internal (axial) resistance** ($R_i$) to passive current flow longitudinal to the axon. - Reduced internal resistance allows local current loops to spread further and faster, significantly increasing the **length constant**, thereby increasing conduction velocity. *Conduction velocity decreases* - This is incorrect, as larger diameter decreases internal resistance, leading directly to a **faster electrotonic spread** of depolarization and a higher conduction speed. - Decreased conduction velocity is typically observed in **small-diameter** or **demyelinated** axons where internal resistance is higher or membrane capacitance is altered. *Membrane resistance increases* - Membrane resistance ($R_m$) is determined by the density and activity of **leak ion channels** within the cell membrane, which is independent of the overall axon diameter. - While the total membrane area increases, the **specific membrane resistance** (resistance per unit area) does not change with diameter. *Action potential amplitude increases* - Action potential (AP) conduction is an **all-or-none** phenomenon, meaning the amplitude is fixed and determined by the electrochemical gradient of **voltage-gated sodium channels**. - Changes in axon diameter influence the **speed** of propagation (conduction velocity), but they do not alter the required peak voltage (amplitude) of the action potential.

Question 1

Which of the following acts as a major intracellular antioxidant and helps in detoxifying reactive oxygen species?

Accepted Answer

Glutathione

Answer

Superoxide dismutase

Answer

Peroxidase

Answer

Catalase

Question 2

A subject was brought to the Casualty with a history of RTA and head injury. On examination, he was conscious. When the doctor asked questions about the incident, his answers were irrelevant to the questions, but his speech was fluent. What could be the possible site of injury?

Accepted Answer

Superior temporal gyrus

Answer

Brain stem

Answer

Inferior frontal gyrus

Answer

Pre-central gyrus

Question 3

A patient presents with fatigue, anemia, and hepatomegaly. Hemoglobin electrophoresis reveals the presence of HbS. What will be the appropriate treatment?

Accepted Answer

Hydroxyurea

Answer

Blood transfusion

Answer

Iron supplementation

Answer

Vitamin B12 supplementation

Question 4

Which of the following genetic mutations is most commonly associated with familial cases of Amyotrophic Lateral Sclerosis (ALS)?

Accepted Answer

SOD1 gene mutation

Answer

HTT gene mutation

Answer

CFTR gene mutation

Answer

FMR1 gene mutation

Question 5

Tau protein inclusions are involved in:

Accepted Answer

Alzheimer’s disease

Answer

Amyotrophic lateral sclerosis

Answer

Huntington's disease

Answer

CNS lymphoma

Question 6

For testing blood clotting/coagulation parameters, blood is collected in which color-coded vacutainer tube?

Accepted Answer

Blue

Answer

Gray

Answer

Red

Answer

Green

Question 7

Which of the following is pro-apoptotic?

Accepted Answer

Bax

Answer

Bcl-2

Answer

Bcl-xL

Answer

Mcl-1

Question 8

A 7-year-old child is brought to the clinic with complaints of fatigue and poor concentration. The mother reports that the child has been eating non-food items such as chalk and soil for the past few months. A peripheral blood smear image shows microcytic, hypochromic red blood cells. Which of the following is the most likely diagnosis?

Accepted Answer

Iron deficiency anemia

Answer

Lead poisoning

Answer

Thalassemia major

Answer

Vitamin B12 deficiency

Question 9

A 5-year-old child is brought to the clinic with abdominal pain, irritability, and developmental delay. On examination, the child has pallor and a bluish line on the gums. Laboratory tests reveal microcytic anemia, and a peripheral blood smear shows red blood cells with basophilic stippling. Which of the following is the most likely diagnosis?

Accepted Answer

Lead poisoning

Answer

Thalassemia minor

Answer

Iron deficiency anemia

Answer

Sideroblastic anemia

Question 10

As a neuron’s diameter increases, what effect manifests?

Accepted Answer

Conduction velocity increases

Answer

Conduction velocity decreases

Answer

Membrane resistance increases

Answer

Action potential amplitude increases

FMGE 2025

Biochemistry

Internal Medicine

Pathology

Pediatrics

Physiology