Anatomy
3 questionsWhich muscle is the deepest in the anterior neck region?
Vertebral arteries of both sides unite to form
Which of the following structures pass through the superior orbital fissure?
NEET-PG 2013 - Anatomy NEET-PG Practice Questions and MCQs
Question 371: Which muscle is the deepest in the anterior neck region?
- A. Sternocleidomastoid
- B. Platysma
- C. Longus colli (Correct Answer)
- D. Trapezius
Explanation: ***Longus colli*** - The **longus colli** muscle is the **deepest muscle** located in the anterior neck region, running along the front of the cervical vertebral column from C1 to T3. - It lies in the **prevertebral layer**, deep to all other anterior neck structures including the carotid sheath, visceral compartment, and superficial muscles. - Its position directly anterior to the vertebral bodies makes it the deepest anterior neck muscle. *Platysma* - The platysma is the **most superficial muscle** of the neck, located just beneath the skin in the superficial fascia. - It is not a deep muscle and lies superficial to all other neck muscles. *Sternocleidomastoid* - The sternocleidomastoid is enclosed within the **investing layer of deep cervical fascia**, making it relatively superficial. - While prominent in the anterior and lateral neck, it is not the deepest anterior neck muscle. *Trapezius* - The trapezius is a large, **superficial muscle of the back and posterior neck**. - It is not located in the anterior neck and is a superficial, not deep, muscle.
Question 372: Vertebral arteries of both sides unite to form
- A. Anterior spinal artery
- B. Posterior spinal artery
- C. Medullary artery
- D. Basilar artery (Correct Answer)
Explanation: Basilar artery - The paired vertebral arteries ascend through the neck via the transverse foramina of cervical vertebrae and enter the skull through the foramen magnum. - At the level of the pontomedullary junction, the two vertebral arteries merge to form a single basilar artery. Anterior spinal artery - The anterior spinal artery is formed by the union of two small branches derived from each vertebral artery near their intracranial origin. - It supplies the anterior two-thirds of the spinal cord, running along the anterior median fissure. Posterior spinal artery - The posterior spinal arteries are typically two vessels, one arising from each vertebral artery (or less commonly from the posterior inferior cerebellar artery). - They supply the posterior one-third of the spinal cord and do not form a single major merged vessel in the brainstem. Medullary artery - There is no single major artery termed the "medullary artery" formed by the union of the vertebral arteries. - The medulla oblongata is supplied by branches directly from the vertebral arteries and the basilar artery, such as the posterior inferior cerebellar artery (PICA) and direct medullary branches.
Question 373: Which of the following structures pass through the superior orbital fissure?
- A. Oculomotor nerve
- B. Trochlear nerve
- C. Superior ophthalmic vein
- D. All of the options (Correct Answer)
Explanation: ***All of the options*** - The **superior orbital fissure** is a key opening in the skull that allows passage of several important cranial nerves and vessels into the orbit. - The **oculomotor nerve**, **trochlear nerve**, and **superior ophthalmic vein** are all established structures that pass through this fissure. *Oculomotor nerve* - The **oculomotor nerve (CN III)** passes through the superior orbital fissure to innervate most of the extrinsic eye muscles. - It controls movements such as **adduction**, **elevation**, and **depression** of the eyeball, and also innervates the **levator palpebrae superioris** muscle for eyelid elevation [1]. *Trochlear nerve* - The **trochlear nerve (CN IV)**, which innervates the **superior oblique muscle**, also passes through the superior orbital fissure. - The superior oblique muscle is responsible for **intorsion** and **depression** of the eye, particularly when the eye is adducted [1]. *Superior ophthalmic vein* - The **superior ophthalmic vein** drains blood from structures within the orbit and passes through the superior orbital fissure to drain into the **cavernous sinus**. - This vein provides a connection between the facial veins and the cavernous sinus, which can be clinically relevant in cases of infection spread.
Biochemistry
3 questionsGluconeogenesis occurs in all except:
Krabbe's disease is due to deficiency of ?
The energy for glycogenesis is provided by -
NEET-PG 2013 - Biochemistry NEET-PG Practice Questions and MCQs
Question 371: Gluconeogenesis occurs in all except:
- A. Muscle (Correct Answer)
- B. Kidney
- C. Gut
- D. Liver
Explanation: ***Muscle*** - **Muscle tissue** lacks the enzyme **glucose-6-phosphatase**, which is essential for releasing free glucose into the bloodstream during gluconeogenesis. - While muscle can store glycogen, it primarily uses glucose for its own energy needs and does not contribute significantly to systemic glucose homeostasis through gluconeogenesis. *Liver* - The **liver** is the primary site of **gluconeogenesis**, producing glucose to maintain blood glucose levels during fasting and starvation. - It contains all the necessary enzymes, including **glucose-6-phosphatase**, to convert precursors like lactate, amino acids, and glycerol into glucose. *Kidney* - The **kidney** becomes a significant site of **gluconeogenesis** during prolonged fasting, contributing up to 10-20% of the body's glucose production. - Renal gluconeogenesis primarily utilizes **lactate** and **glutamine** as substrates. *Gut* - The **small intestine (gut)** has been identified as a site of **gluconeogenesis**, particularly following a meal rich in protein. - Its contribution is relatively smaller compared to the liver but plays a role in **postprandial glucose homeostasis**.
Question 372: Krabbe's disease is due to deficiency of ?
- A. Sphingomyelinase
- B. Beta galactocerebrosidase (Correct Answer)
- C. Hexosaminidase
- D. Arylsulfatase
Explanation: ***Beta galactocerebrosidase*** - Krabbe's disease is specifically caused by a deficiency of **beta-galactocerebrosidase**, leading to the accumulation of toxic substances in the brain [1]. - This disease predominantly affects the **myelin sheath**, resulting in severe neurological deterioration [1]. *Arylsulfatase* - Deficiency of **arylsulfatase** is associated with **metachromatic leukodystrophy**, not Krabbe's disease. - Symptoms and pathology differ significantly, primarily affecting **sulfatides** rather than galactocerebrosides. *Sphingomyelinase* - A deficiency of **sphingomyelinase** is linked to **Niemann-Pick disease**, characterized by splenomegaly and liver involvement. - This condition does not involve the same neurological deterioration seen in Krabbe's disease. *Hexosaminidase* - Hexosaminidase deficiency is associated with **Tay-Sachs disease**, primarily affecting the **GM2 gangliosides** [2]. - This results in different clinical manifestations, such as **cherry-red spots** and progressive neurodegeneration, rather than the symptoms of Krabbe's disease [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1304-1305. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, p. 161.
Question 373: The energy for glycogenesis is provided by -
- A. GTP
- B. GDP
- C. UTP (Correct Answer)
- D. AMP
Explanation: ***UTP*** - **Uridine triphosphate (UTP)** is essential for **glycogenesis** as it activates glucose by forming **UDP-glucose** from glucose-1-phosphate. - The reaction (Glucose-1-P + UTP → UDP-glucose + PPi) creates a **high-energy intermediate** that drives glycogen synthesis. - The subsequent hydrolysis of pyrophosphate (PPi) makes this activation step **irreversible**, and the energy stored in UDP-glucose is used for **glycosidic bond formation** when glucose is added to the growing glycogen chain. *GTP* - **Guanosine triphosphate (GTP)** is primarily involved in **protein synthesis**, G-protein signaling, and the citric acid cycle. - It is not used for glucose activation in glycogenesis; that role is specific to **UTP**. *GDP* - **Guanosine diphosphate (GDP)** is a product of GTP hydrolysis and functions in regulatory processes. - It does not serve as an energy donor for glycogen synthesis. *AMP* - **Adenosine monophosphate (AMP)** is a low-energy signal molecule that indicates cellular energy depletion. - High AMP levels **inhibit glycogenesis** and activate glycogenolysis through allosteric regulation of key enzymes. - It does not provide energy for anabolic pathways like glycogen synthesis.
Pathology
1 questionsIn glomerulus subendothelial deposits are seen in?
NEET-PG 2013 - Pathology NEET-PG Practice Questions and MCQs
Question 371: In glomerulus subendothelial deposits are seen in?
- A. Goodpasture syndrome (linear IgG deposits in the basement membrane)
- B. MPGN type I (subendothelial deposits) (Correct Answer)
- C. MPGN type II (intramembranous deposits)
- D. IgA nephropathy (mesangial IgA deposits)
Explanation: ***MPGN type I*** - **Subendothelial deposits** are a hallmark of MPGN type I, often associated with **immune complex deposition** [1]. - This condition can present with **hematuria**, **proteinuria**, and can be triggered by infections or autoimmune diseases [1]. *Good pasture syndrome* - Primarily involves **anti-GBM antibodies** leading to **glomerulonephritis** and pulmonary hemorrhage, not subendothelial deposits. - Typically, it presents with **crescent formation** in the glomeruli rather than deposits. *MPGN type II* - Characterized by **dense deposit disease**, it features **intramembranous** rather than subendothelial deposits [1]. - It is often associated with **C3 nephritic factor** and does not show classic subendothelial pathology. *IgA nephropathy* - Characterized by **IgA deposits** primarily in the **mesangium**, not subendothelially. - It presents with **hematuria** and recurrent episodes of **macrohematuria**, especially after infections. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 925-927.
Pharmacology
3 questionsBesides its properties of decreasing intraocular pressure, timolol is preferred in the treatment of glaucoma because it
Which of the following is not a cardioselective beta blocker?
Which beta-1 antagonist is used in congestive cardiac failure?
NEET-PG 2013 - Pharmacology NEET-PG Practice Questions and MCQs
Question 371: Besides its properties of decreasing intraocular pressure, timolol is preferred in the treatment of glaucoma because it
- A. Is a selective beta-adrenoceptor blocker
- B. Increases outflow of aqueous humor
- C. Produces no miosis (Correct Answer)
- D. Possesses membrane stabilizing activity
Explanation: ***Produces no miosis*** - Timolol, a **non-selective beta-blocker**, decreases intraocular pressure without affecting pupillary size. - This is a **key advantage** in glaucoma treatment as miosis (pupil constriction) can worsen vision, especially in patients with cataracts. - Unlike **miotics** (e.g., pilocarpine), timolol does not cause pupillary constriction, making it better tolerated. *Possesses membrane stabilizing activity* - While some beta-blockers possess **membrane-stabilizing activity** (local anesthetic effect), this property is not a primary reason for timolol's preference in glaucoma. - This action is more relevant in antiarrhythmic uses of beta-blockers due to its effect on cardiac action potentials. *Increases outflow of aqueous humor* - Timolol primarily reduces intraocular pressure by **decreasing the production of aqueous humor**, not by increasing its outflow. - Drugs like **pilocarpine** (a cholinergic agonist) or **prostaglandin analogs** increase outflow. *Is a selective beta-adrenoceptor blocker* - Timolol is a **non-selective beta-blocker**, meaning it blocks both beta-1 and beta-2 adrenergic receptors. - Its non-selectivity is associated with systemic side effects (e.g., bronchospasm, bradycardia), and selective beta-blockers like **betaxolol** exist but are not the primary reason for timolol's preference in glaucoma.
Question 372: Which of the following is not a cardioselective beta blocker?
- A. Nebivolol
- B. Atenolol
- C. Betaxolol
- D. Oxprenolol (Correct Answer)
Explanation: ***Oxprenolol*** - **Oxprenolol** is a non-selective beta-blocker with **intrinsic sympathomimetic activity (ISA)**, meaning it blocks both β1 and β2 receptors and partially stimulates them. - Its non-selective action means it affects both the heart (β1) and other organs like the lungs (β2), making it less suitable for patients with respiratory conditions. *Nebivolol* - **Nebivolol** is a highly cardioselective beta-blocker that primarily blocks **β1 receptors** and also has **vasodilatory properties** due to nitric oxide release. - Its high selectivity translates to fewer β2-mediated side effects, such as bronchoconstriction. *Atenolol* - **Atenolol** is a **cardioselective beta-blocker** that predominantly blocks **β1 receptors** at therapeutic doses. - This selectivity makes it a common choice for cardiovascular conditions, reducing the risk of bronchospasm compared to non-selective agents. *Betaxolol* - **Betaxolol** is a **cardioselective beta-blocker** primarily used for the treatment of hypertension and glaucoma. - It selectively blocks **β1 adrenergic receptors**, minimizing effects on the lungs compared to non-selective beta-blockers.
Question 373: Which beta-1 antagonist is used in congestive cardiac failure?
- A. Atenolol
- B. Metoprolol (Correct Answer)
- C. Esmolol
- D. Bisoprolol
Explanation: ***Metoprolol*** - **Metoprolol succinate** (extended-release formulation) is a selective **beta-1 antagonist** proven to reduce mortality and hospitalizations in **chronic heart failure with reduced ejection fraction (HFrEF)**. - It works by **reducing heart rate, myocardial oxygen demand**, and preventing adverse cardiac remodeling through inhibition of chronic sympathetic activation. - Along with **bisoprolol and carvedilol**, it is one of the **three beta-blockers with proven mortality benefit** in heart failure trials. *Atenolol* - While atenolol is a selective beta-1 antagonist, it **lacks evidence for mortality benefit** in heart failure. - It has **high hydrophilicity** and renal elimination, leading to less favorable pharmacokinetics compared to metoprolol. - More commonly used for **hypertension and angina** rather than heart failure management. *Esmolol* - **Esmolol** is an ultra-short-acting selective beta-1 antagonist used for **acute control of heart rate** in perioperative and critical care settings. - Its **very short half-life (9 minutes)** makes it unsuitable for chronic management of heart failure. - Administered only **intravenously** and requires continuous infusion. *Bisoprolol* - While **bisoprolol is also approved** for heart failure and has proven mortality benefit (CIBIS-II trial), this question likely expects **metoprolol** as the answer given the historical context. - Both bisoprolol and metoprolol are acceptable answers, but **metoprolol** has been more widely studied and is more commonly cited in Indian medical exams. - Bisoprolol has **greater beta-1 selectivity** than metoprolol but similar clinical outcomes in heart failure.