Biochemistry
1 questionsWhich of the following is a mitochondrial inheritance disorder?
NEET-PG 2025 - Biochemistry NEET-PG Practice Questions and MCQs
Question 91: Which of the following is a mitochondrial inheritance disorder?
- A. Achondroplasia
- B. Cystic fibrosis
- C. Williams syndrome
- D. Kearns-Sayre syndrome (Correct Answer)
Explanation: ***Kearns-Sayre syndrome*** - It is a classic example of a **mitochondrial encephalomyopathy** resulting from large-scale deletions or duplications of mitochondrial DNA (**mtDNA**). - It is characterized clinically by the triad of **chronic progressive external ophthalmoplegia (CPEO)**, **retinitis pigmentosa**, and onset before age 20. - Follows **maternal inheritance** pattern typical of mitochondrial disorders. *Williams syndrome* - Williams syndrome is a disorder caused by a **microdeletion** of several genes on chromosome 7 (7q11.23). - It is inherited in an **autosomal dominant** fashion, though most cases arise spontaneously. *Achondroplasia* - This is the most common form of genetic dwarfism caused by a mutation in the **FGFR3 gene** (Fibroblast Growth Factor Receptor 3). - It exhibits an **autosomal dominant** inheritance pattern. *Cystic fibrosis* - Cystic fibrosis is caused by mutations in the **CFTR gene** (Cystic Fibrosis Transmembrane conductance Regulator) on chromosome 7. - It is transmitted via an **autosomal recessive** inheritance pattern.
ENT
2 questionsA patient presents to the clinic with a history of chronic ear drainage and hearing loss for several months. Otoscopic examination reveals a central perforation of the tympanic membrane. Pure tone audiometry confirms a conductive hearing loss. Based on these findings, what is the most appropriate next step in the definitive management of this patient's condition?
A 40-year-old patient presents with recurrent and severe nosebleeds from the anterior nasal septum. The bleeding has been refractory to nasal packing and chemical cautery. A decision is made to proceed with surgical ligation to control the bleeding. Which of the following arteries is the primary target for ligation in the management of this patient's anterior epistaxis?
NEET-PG 2025 - ENT NEET-PG Practice Questions and MCQs
Question 91: A patient presents to the clinic with a history of chronic ear drainage and hearing loss for several months. Otoscopic examination reveals a central perforation of the tympanic membrane. Pure tone audiometry confirms a conductive hearing loss. Based on these findings, what is the most appropriate next step in the definitive management of this patient's condition?
- A. Immediate commencement of broad-spectrum oral antibiotics
- B. Myringoplasty (Correct Answer)
- C. Modified radical mastoidectomy
- D. Exploratory tympanostomy
Explanation: ***Myringoplasty*** - This procedure involves the surgical repair of the **tympanic membrane (TM)** perforation (a central perforation in this case) and is the definitive treatment for chronic otitis media, tubotympanic type (safe CSOM). - Repairing the TM perforation eliminates the source of chronic drainage and optimally helps in resolving the **conductive hearing loss** by restoring the vibrating surface. *Modified radical mastoidectomy* - This procedure is primarily reserved for **unsafe chronic otitis media** (Atticoantral disease), typically involving **cholesteatoma** or extensive irreversible mucosal disease in the mastoid. - Since the patient has a **central perforation** (safe type) without mention of retraction pockets or cholesteatoma, this extensive surgery is overmanagement and not indicated. *Exploratory tympanostomy* - This term generally refers to making an incision in the TM (myringotomy) or placing a **ventilation tube (grommet)**, typically done for otitis media with effusion (serous otitis media). - It does not address the underlying **chronic irreversible perforation** of the TM causing the current symptoms; surgical repair is required. *Immediate commencement of broad-spectrum oral antibiotics* - Antibiotics are useful for managing acute exacerbations of CSOM (controlling active discharge or infection) but are not the **definitive treatment** for the underlying structural pathology (chronic perforation). - They cannot **repair the tympanic membrane** or permanently restore hearing; the structural defect requires surgical intervention (myringoplasty).
Question 92: A 40-year-old patient presents with recurrent and severe nosebleeds from the anterior nasal septum. The bleeding has been refractory to nasal packing and chemical cautery. A decision is made to proceed with surgical ligation to control the bleeding. Which of the following arteries is the primary target for ligation in the management of this patient's anterior epistaxis?
- A. Internal maxillary artery
- B. Sphenopalatine artery (Correct Answer)
- C. Anterior ethmoidal artery
- D. Facial artery
Explanation: ***Sphenopalatine artery*** - The **Sphenopalatine artery** (terminal branch of the internal maxillary artery) is the **dominant blood supply** to the nasal cavity, including the anterior nasal septum via its **septal branches**. - It is the **major contributor** to **Kiesselbach's plexus** (Little's area), which is located in the anteroinferior nasal septum and is the source of 90% of anterior epistaxis. - **Endoscopic sphenopalatine artery ligation (ESPAL)** is the **first-line surgical intervention** for refractory anterior epistaxis that has failed conservative management (packing, cautery). - This procedure has high success rates (85-95%) and is now the gold standard for surgical management of severe anterior and posterior epistaxis. *Anterior ethmoidal artery* - Branch of the **ophthalmic artery** (internal carotid system) that supplies the **superior anterior** nasal cavity and anterior ethmoid cells. - It contributes **minimally** to Kiesselbach's plexus; its main territory is the **roof and upper anterior nasal cavity**. - Anterior ethmoidal artery ligation (via external or endoscopic approach) is indicated for **superior anterior** or **roof bleeding**, NOT typical anteroinferior septal bleeding. *Facial artery* - The **superior labial artery** (branch of facial artery) contributes to the inferior aspect of Kiesselbach's plexus but is a **minor contributor**. - Facial artery ligation is **ineffective** for controlling severe nasal bleeding as it is too distal and doesn't address the main vascular supply. *Internal maxillary artery* - Parent vessel of the sphenopalatine artery; ligation is performed when **sphenopalatine artery ligation is technically difficult or has failed**. - Historically performed via **transantral (Caldwell-Luc) approach**, now rarely needed due to success of endoscopic sphenopalatine artery ligation. - Reserved for severe refractory cases or when endoscopic access is not feasible.
Obstetrics and Gynecology
2 questionsA 38-week pregnant woman in active labor with 5 cm cervical dilatation and regular contractions suddenly develops umbilical cord prolapse. What is the most appropriate immediate management?
A 32-year-old G2P1 woman with a previous cesarean section is undergoing a trial of vaginal delivery at 39 weeks. She is in active labor with 8 cm cervical dilation and fetal station at -1. Continuous fetal monitoring reveals fetal bradycardia, and maternal pulse is 110/min. What is the most appropriate next step in management?
NEET-PG 2025 - Obstetrics and Gynecology NEET-PG Practice Questions and MCQs
Question 91: A 38-week pregnant woman in active labor with 5 cm cervical dilatation and regular contractions suddenly develops umbilical cord prolapse. What is the most appropriate immediate management?
- A. Perform vaginal packing to protect the cord
- B. Administer oxytocin to expedite labor
- C. Manually elevate the presenting part, fill the bladder retrogradely, and prepare for emergency cesarean section (Correct Answer)
- D. Wait and observe
Explanation: ***Manually elevate the presenting part, fill the bladder retrogradely, and prepare for emergency cesarean section*** - The immediate priority in **umbilical cord prolapse** is to relieve pressure on the cord by manually elevating the **presenting fetal part** (e.g., the head) to prevent **fetal hypoxia**. - **Retrograde bladder filling** (500–750 mL saline) is a temporary measure, alongside administering **tocolytics** (like terbutaline) to stop contractions, while preparing urgently for an **emergency cesarean section**, which is the definitive management. *Wait and observe* - This approach is highly inappropriate and dangerous, as cord prolapse is an **obstetric emergency** requiring immediate intervention. - Observing or delaying action allows persistent compression, leading rapidly to **fetal circulatory compromise** and death. *Perform vaginal packing to protect the cord* - **Vaginal packing** is ineffective and may actually exacerbate compression on the exposed cord, worsening **fetal blood flow**. - The focus must be on elevating the presenting part away from the cervix and cord. *Administer oxytocin to expedite labor* - **Oxytocin** stimulates uterine contractions, which would significantly increase the compression forces on the **prolapsed cord**, thereby worsening **fetal distress** and ischemia. - Since the cervix is not fully dilated (5 cm), **emergency cesarean section** is necessary, not expedited vaginal delivery.
Question 92: A 32-year-old G2P1 woman with a previous cesarean section is undergoing a trial of vaginal delivery at 39 weeks. She is in active labor with 8 cm cervical dilation and fetal station at -1. Continuous fetal monitoring reveals fetal bradycardia, and maternal pulse is 110/min. What is the most appropriate next step in management?
- A. Administer oxytocin to augment labor
- B. Perform operative vaginal delivery
- C. Continue monitoring and wait
- D. Emergency cesarean section (Correct Answer)
Explanation: ***Emergency cesarean section*** - The combination of **fetal bradycardia** (acute distress) and maternal **tachycardia** (suggesting hemorrhage/shock) in a patient undergoing **trial of labor after C-section (TOLAC)** is highly indicative of **uterine rupture**. - Uterine rupture is a **Category I obstetric emergency** requiring immediate delivery to minimize fetal hypoxia/demise and manage maternal bleeding. *Continue monitoring and wait* - Waiting is dangerous and contraindicated in the presence of non-reassuring fetal tracing (bradycardia) combined with signs pathognomonic for **uterine rupture** (maternal tachycardia). - Any delay in delivery and surgical intervention significantly increases the risk of associated maternal and fetal **morbidity and mortality**. *Administer oxytocin to augment labor* - Oxytocin is absolutely contraindicated when **uterine rupture** is suspected, as increasing uterine contractility will exacerbate the tear, potentially worsening fetal compromise and maternal hemorrhage. - Augmentation would be appropriate only if labor was prolonged and vital signs were reassuring, which is not the case here. *Perform operative vaginal delivery* - The fetal station is still high at **-1**, making an immediate or easy operative vaginal delivery unlikely or risky. - The primary goal is immediate access to the uterus to control bleeding and deliver the fetus, which is best achieved via an **emergency laparotomy** (C-section).
Ophthalmology
2 questionsA 15-year-old female presents with a painless, gradually increasing mass located at the superotemporal orbital rim (upper outer quadrant of the orbit), present for the past 10 years. On examination, the mass is non-tender and slowly progressive. What is the most likely diagnosis?
A patient presents with guttate lesions in one eye and bullous keratopathy in the other eye. What is the most likely diagnosis?
NEET-PG 2025 - Ophthalmology NEET-PG Practice Questions and MCQs
Question 91: A 15-year-old female presents with a painless, gradually increasing mass located at the superotemporal orbital rim (upper outer quadrant of the orbit), present for the past 10 years. On examination, the mass is non-tender and slowly progressive. What is the most likely diagnosis?
- A. Epidermoid cyst
- B. Dermoid cyst (Correct Answer)
- C. Capillary hemangioma
- D. Lacrimal gland tumor
Explanation: ***Dermoid cyst*** - This diagnosis is strongly suggested by the classic presentation of a **painless**, **slowly progressive** mass in a young patient, located near the **superotemporal orbital rim** (lateral to the lateral canthus). - Dermoid cysts are **congenital choristomas** formed by sequestration of ectoderm along embryonic lines of closure, often presenting fixed to the periosteum. *Capillary hemangioma* - These tumors typically present in infancy and exhibit characteristic rapid growth followed by **spontaneous involution** (not slow progression over 10 years). - They are usually soft, compressible, and display color changes (red/blue), unlike the description of a firm, non-tender mass. *Lacrimal gland tumor* - Primary lacrimal gland epithelial tumors are rare in children and primarily occur in **adults** (40-60 years). - They typically cause axial proptosis and globe displacement (inferonasal) due to growth within the **lacrimal fossa**, usually presenting with symptoms related to pressure or pain if malignant. *Epidermoid cyst* - While also slow-growing and painless, epidermoid cysts are less likely than dermoid cysts to be found in the deep subcutaneous tissue fixed to the periosteum near the lateral canthus. - Epidermoid cysts contain only stratified squamous epithelium and keratin, while **dermoid cysts** also contain skin appendages (hair follicles, sebaceous glands).
Question 92: A patient presents with guttate lesions in one eye and bullous keratopathy in the other eye. What is the most likely diagnosis?
- A. Keratoconjunctivitis
- B. Fuchs' endothelial dystrophy (Correct Answer)
- C. Interstitial keratitis
- D. Viral corneal ulcer
Explanation: ***Fuchs' endothelial dystrophy*** - This condition involves progressive loss of corneal endothelial cells and deposition of abnormal basement membrane material (**guttae**). The presence of **guttate lesions** represents early disease. - As the disease progresses and the remaining endothelial cells fail to pump fluid effectively, the cornea swells, leading to epithelial and stromal edema, clinically described as **bullous keratopathy**. *Interstitial keratitis* - This is non-ulcerative inflammation predominantly affecting the **corneal stroma**, often associated with systemic infections like **congenital syphilis** or Cogan's syndrome. - It typically causes stromal clouding and deep **neovascularization** (ghost vessels) but does not primarily involve guttate lesions or asymmetric endothelial failure. *Viral corneal ulcer* - Viral ulcers (like those caused by **HSV**) present acutely with epithelial defects, often in a dendritic or geographic pattern, and cause significant inflammation. - They are acute processes characterized by surface epithelial involvement, not characterized by the slowly progressive, **endothelial-based changes** (guttae and bullae) seen in Fuchs' dystrophy. *Keratoconjunctivitis* - This is a general term for inflammation affecting both the cornea and conjunctiva, commonly seen in **adenoviral infections** or severe dry eye (**KCS**). - The primary findings are typically conjunctival injection and punctate epithelial erosions, not the specific endothelial deposits (**guttae**) or resulting severe edema (**bullous keratopathy**) characteristic of Fuchs' dystrophy.
Pathology
2 questionsA 45-year-old female presents with a 2-year history of progressive unilateral hearing loss, tinnitus, and unsteadiness. An MRI scan reveals a well-defined tumor located in the cerebellopontine angle (CPA). A surgical resection is performed, and subsequent histopathological examination of the tumor tissue is given below. Based on these histopathological findings, what is the most likely diagnosis?
A 15-year-old tall boy with long limbs presents to the OPD. On ocular examination, bilateral ectopia lentis is noted. Which gene is most likely affected in this inherited disorder?
NEET-PG 2025 - Pathology NEET-PG Practice Questions and MCQs
Question 91: A 45-year-old female presents with a 2-year history of progressive unilateral hearing loss, tinnitus, and unsteadiness. An MRI scan reveals a well-defined tumor located in the cerebellopontine angle (CPA). A surgical resection is performed, and subsequent histopathological examination of the tumor tissue is given below. Based on these histopathological findings, what is the most likely diagnosis?
- A. Meningioma
- B. Neurofibroma
- C. Ependymoma
- D. Schwannoma (Correct Answer)
Explanation: ***Schwannoma*** - The clinical presentation (unilateral hearing loss, tinnitus, CPA mass) is highly characteristic of a **Vestibular Schwannoma** (Acoustic Neuroma), which is the most common tumor of the CPA [2]. - The histopathology image shows the classic biphasic pattern of Schwannoma: cellular **Antoni A tissue** (with hyperchromatic nuclei arranged in palisades forming **Verocay bodies**) alternating with hypocellular, myxoid **Antoni B tissue** [1]. *Ependymoma* - Ependymomas typically arise from the ependymal lining of the **ventricular system** (e.g., fourth ventricle), making their primary location rarely the CPA outside the brainstem. - Histologically, they feature characteristic arrangements like **perivascular pseudorosettes** (tumor cells arranged around blood vessels) or true rosettes, which are absent in this image [3]. *Meningioma* - While meningioma is the second most common CPA tumor, its histology is defined by the formation of **concentric cellular whorls** and often includes laminated calcifications known as **psammoma bodies** [2]. - Meningiomas originate from arachnoidal cells and do not exhibit the distinct **Antoni A and B** tissue architecture seen in the provided slide. *Neurofibroma* - Neurofibromas are characterized by a diverse cellular population (Schwann cells, fibroblasts, mast cells) and lack the highly organized nuclear palisading and **Verocay bodies** seen in the image [1]. - They generally present as a looser, more haphazard proliferation of spindle cells within a prominent, often myxoid stroma, without clear distinction between **Antoni A and B** areas [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, p. 1250. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 727-728. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1312-1313.
Question 92: A 15-year-old tall boy with long limbs presents to the OPD. On ocular examination, bilateral ectopia lentis is noted. Which gene is most likely affected in this inherited disorder?
- A. FBN1 (Fibrillin-1) (Correct Answer)
- B. COL5A
- C. PAX6
- D. TGF-β R2
Explanation: ***FBN1 (Fibrillin-1)*** - The clinical triad of tall stature/long limbs (**Marfanoid habitus**) and **ectopia lentis** (lens dislocation) is characteristic of **Marfan syndrome** [1]. - Marfan syndrome is caused by an autosomal dominant mutation in the **FBN1 gene** on chromosome 15, which codes for the connective tissue protein **Fibrillin-1** [1]. *COL5A* - Mutations in **COL5A** (Type V collagen) are typically associated with the Classical type of **Ehlers-Danlos syndrome (EDS)**. - Clinical features of EDS primarily include **skin hyperextensibility** and **joint hypermobility**, which are not the most prominent features in this presentation. *PAX6* - The **PAX6 gene** is a master gene for eye development, and its mutation primarily causes **Aniridia** (absence of the iris) or other widespread ocular developmental defects. - Although ophthalmological findings are present, aniridia is not the key ocular finding, making PAX6 mutation an incorrect association. *TGF-β R2* - Mutations in **TGF-β R2** are linked to **Loeys-Dietz syndrome**, which involves severe **aortic root dilation** and craniocervical instability [1]. - While Loeys-Dietz syndrome presents with Marfanoid skeletal features, **ectopia lentis** is rare or absent, differentiating it from Marfan syndrome (FBN1) [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 153-154.
Pediatrics
1 questionsA 5-year-old child with chronic kidney disease (CKD) presents with bow legs. Laboratory investigations reveal: Serum Calcium: 9.1 mg/dL (normal) Serum Phosphate: 6.9 mg/dL (elevated) Alkaline Phosphatase: Elevated 25(OH) Vitamin D: Low What is the most appropriate next step in management?
NEET-PG 2025 - Pediatrics NEET-PG Practice Questions and MCQs
Question 91: A 5-year-old child with chronic kidney disease (CKD) presents with bow legs. Laboratory investigations reveal: Serum Calcium: 9.1 mg/dL (normal) Serum Phosphate: 6.9 mg/dL (elevated) Alkaline Phosphatase: Elevated 25(OH) Vitamin D: Low What is the most appropriate next step in management?
- A. Oral calcium + Vitamin D (Correct Answer)
- B. Growth hormone therapy
- C. Phosphate binder
- D. Calcium supplementation
Explanation: ***Oral calcium + Vitamin D*** - This child has **CKD-Mineral and Bone Disorder (CKD-MBD)** with renal osteodystrophy manifesting as bow legs (rickets). - Laboratory findings show **low 25(OH) Vitamin D** and **hyperphosphatemia** - both need to be addressed. - According to **KDIGO 2017 guidelines**, children with CKD and vitamin D deficiency should receive **vitamin D supplementation** (nutritional forms like cholecalciferol or ergocalciferol for 25(OH)D deficiency). - **Calcium supplementation** is added to maintain calcium homeostasis and suppress secondary hyperparathyroidism. - The combination addresses the **underlying rachitic changes** (bow legs) by correcting both calcium and vitamin D deficiency. - Activated vitamin D (calcitriol) may be added later if needed, but nutritional vitamin D replacement is the initial step for documented 25(OH)D deficiency. *Calcium supplementation alone* - While calcium is necessary, it does **not address the documented vitamin D deficiency**, which is a primary driver of the bone disease. - Vitamin D is essential for calcium absorption and bone mineralization - giving calcium alone will not correct the rickets or adequately suppress PTH. - Monotherapy with calcium is insufficient for managing CKD-MBD with documented vitamin D deficiency. *Phosphate binder* - Although phosphate is elevated (6.9 mg/dL), phosphate binders alone do not address the **severe vitamin D deficiency** or calcium homeostasis. - Phosphate control is important but is **part of comprehensive management**, not the sole initial step when vitamin D deficiency and rickets are present. - Current guidelines recommend addressing vitamin D deficiency concurrently with phosphate management. *Growth hormone therapy* - Growth hormone is indicated for **growth failure in CKD** after metabolic bone disease is optimized. - It does not correct the underlying **renal osteodystrophy** or vitamin D deficiency causing the bow legs. - GH therapy is considered only after stabilization of CKD-MBD parameters.