NEET-PG 2013 Practice Questions

Q: The roof of the olfactory region is formed by?

Cribriform plate of ethmoid. ***Cribriform plate of ethmoid*** - The **cribriform plate** of the ethmoid bone forms the superior boundary, or roof, of the nasal cavity specifically in the olfactory region [1]. - It is perforated by numerous **olfactory foramina** through which the olfactory nerves pass from the nasal cavity to the olfactory bulb of the brain [2]. *Nasal bone* - The **nasal bones** form part of the bridge of the nose and contribute to the anterior part of the bony framework of the external nose. - They do not form the roof of the olfactory region within the nasal cavity. *Sphenoid* - The **sphenoid bone** is a complex bone at the base of the skull, contributing to the posterior wall of the nasal cavity and parts of the cranial floor. - It does not directly form the roof of the olfactory region. *Temporal bone* - The **temporal bones** are located on the sides and base of the skull, housing structures related to hearing and balance. - They are not involved in forming the roof of the nasal cavity or the olfactory region.

Q: Which muscle will be paralyzed when the radial nerve is injured just below the spiral groove?

Extensor Carpi Radialis Brevis. Extensor Carpi Radialis Brevis - The radial nerve travels in the spiral groove of the humerus and gives off branches in a specific sequence. - Proximal to the spiral groove: Branches to triceps and anconeus - Within/at the spiral groove: Branches to brachioradialis and extensor carpi radialis longus (ECRL) - Just distal to the spiral groove: Branch to extensor carpi radialis brevis (ECRB) [1] - this is the first branch after exiting the spiral groove - More distally: The nerve divides into superficial and deep branches (posterior interosseous nerve) [1] - An injury just below the spiral groove would paralyze ECRB while sparing muscles innervated proximal to or within the groove (triceps, anconeus, brachioradialis, ECRL). Supinator - The supinator is innervated by the deep branch of the radial nerve (posterior interosseous nerve), which branches off more distally in the proximal forearm. - This muscle would only be affected by injuries distal to the bifurcation of the radial nerve into superficial and deep branches, not by an injury just below the spiral groove. Extensor Digitorum - The extensor digitorum is supplied by the posterior interosseous nerve, which is a continuation of the deep branch [1]. - This innervation occurs significantly distal to the spiral groove in the posterior forearm compartment. - It would be affected by posterior interosseous nerve injuries, not by lesions just below the spiral groove. Abductor Pollicis Longus - The abductor pollicis longus is innervated by the posterior interosseous nerve in the distal forearm [1]. - This is the most distal of all the options and would only be affected by posterior interosseous nerve palsy, not by radial nerve injury at the spiral groove level [1].

Q: Vertebral arteries of both sides unite to form

Basilar artery. 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.

Q: Which of the following is a neutral amino acid?

Glycine. ***Glycine*** - **Glycine** has a hydrogen atom as its side chain, making it the **simplest amino acid** and electrically neutral at physiological pH. - Its **nonpolar side chain** contributes to its neutral charge and allows it to fit into various protein structures. *Aspartate* - **Aspartate** is an **acidic amino acid** with a carboxyl group in its side chain. - This **carboxyl group** can lose a proton, giving aspartate a net negative charge at physiological pH. *Arginine* - **Arginine** is a **basic amino acid** characterized by a guanidinium group in its side chain. - The **guanidinium group** contains multiple nitrogen atoms that can accept protons, making arginine positively charged at physiological pH. *Histidine* - **Histidine** is classified as a **basic amino acid** due to the imidazole ring in its side chain. - The **imidazole ring** has a pKa close to physiological pH, allowing it to be protonated and positively charged, but it is not neutral.

Q: What is the main enzyme involved in glycogen breakdown (glycogenolysis)?

Glycogen phosphorylase. ***Glycogen phosphorylase*** - This is the **rate-limiting and primary enzyme** for **glycogenolysis**, the breakdown of glycogen into glucose units. - It cleaves **α-1,4-glycosidic bonds** in glycogen, releasing **glucose-1-phosphate** units. - Regulated by both **allosteric mechanisms** and **hormonal control** (epinephrine, glucagon). - Works until it reaches 4 glucose residues from a branch point, where debranching enzyme takes over. *Glycogen synthase* - This is the main enzyme for **glycogenesis** (glycogen synthesis), not breakdown. - It catalyzes formation of α-1,4-glycosidic bonds to build glycogen chains. - This is the opposite direction of metabolism from what the question asks about. *Glucose-6-phosphatase* - This enzyme is involved in **gluconeogenesis** and the final step of converting **glucose-6-phosphate to free glucose**. - It is NOT directly involved in glycogen breakdown itself, but rather in the subsequent conversion pathway. - Found primarily in **liver and kidney** to release free glucose into blood. *Hexokinase* - This enzyme phosphorylates free glucose to **glucose-6-phosphate** (opposite direction). - It is involved in **glucose utilization**, not glycogen breakdown. - It traps glucose inside cells for metabolism or glycogen synthesis.

Q: Glucagon stimulates

Gluconeogenesis. ***Gluconeogenesis*** - **Glucagon** is a hormone that primarily acts to raise **blood glucose levels** by stimulating the production of glucose from non-carbohydrate sources. - This process, **gluconeogenesis**, occurs mainly in the liver and is initiated by glucagon to counteract hypoglycemia. *Glycogenesis* - **Glycogenesis** is the process of synthesizing **glycogen** from glucose and is primarily stimulated by insulin when blood glucose levels are high. - Glucagon's role is to *inhibit* glycogen synthesis and instead promote glycogen breakdown. *Fatty acid synthesis* - **Fatty acid synthesis** is an anabolic process that primarily occurs when there is an excess of energy and glucose, often stimulated by **insulin**. - Glucagon generally has an **inhibitory effect** on fatty acid synthesis, as its main goal is to mobilize energy stores, not create them. *Glycolysis* - **Glycolysis** is the breakdown of glucose to produce energy, and it is stimulated when glucose is abundant and energy is needed. - Glucagon primarily acts to *inhibit* glycolysis in the liver, thereby conserving glucose for use by other tissues and promoting its release into the bloodstream.

Q: What is the mechanism by which mercury causes damage?

Binds to -SH groups of enzymes. ***Binds to -SH groups of enzymes*** - Mercury, particularly its inorganic and organic forms, has a high affinity for **sulfhydryl (-SH) groups** found in **cysteine residues** of proteins and enzymes. - This binding disrupts the **tertiary structure** and **catalytic activity** of vital enzymes, leading to widespread cellular dysfunction and toxicity. *Causes toxicity through various mechanisms (not specific to -SH binding)* - While mercury can indeed cause toxicity through various mechanisms, the **most prominent and fundamental mechanism** underpins many of these downstream effects. - This option is too general and does not pinpoint the primary molecular interaction responsible for mercury's widespread cellular damage. *Indirectly inhibits the electron transport chain (ETC) by enzyme disruption* - This statement is partially true in that mercury's enzyme disruption can affect the ETC, but it's an **indirect consequence** rather than the primary mechanism itself. - The direct mechanism involves the initial binding to -SH groups, which then leads to the dysfunction of enzymes, including those involved in the ETC. *Indirectly inhibits protein synthesis by disrupting enzyme function* - Similar to ETC inhibition, mercury's disruption of enzyme function can ultimately impair protein synthesis, but this is an **effect down the causal chain**. - The initial and direct molecular interaction is the binding to sulfhydryl groups of key enzymes involved in various cellular processes, including protein synthesis.

Q: What is the mechanism of metabolism for alcohol, aspirin, and phenytoin at high doses?

Zero order kinetics. ***Zero order kinetics*** - This mechanism occurs when the **metabolic enzymes become saturated at high drug concentrations**, leading to a constant amount (not a constant percentage) of drug being eliminated per unit time. - Alcohol, aspirin, and phenytoin are examples of drugs that exhibit **saturable metabolism**, transitioning from first-order to zero-order kinetics at higher doses. *First pass kinetics* - This describes the **metabolism of a drug by the liver or gut wall enzymes before it reaches systemic circulation** after oral administration. - While relevant to the oral bioavailability of these drugs, it does not describe the specific mechanism of elimination at high doses. *First order kinetics* - In this mechanism, a **constant fraction or percentage of the drug is eliminated per unit of time**, meaning the rate of elimination is directly proportional to the drug concentration. - Most drugs follow first-order kinetics at therapeutic doses because metabolizing enzymes are not saturated. *Second order kinetics* - This is a **less common pharmacokinetic model** where the rate of elimination is proportional to the square of the drug concentration or involves two reactants. - It does not typically describe the common elimination patterns of most drugs, including alcohol, aspirin, and phenytoin.

Q: LH surge is associated with?

Increased estrogen & decreased progesterone. ***Increased estrogen & decreased progesterone*** - The **LH surge** is triggered by a significant rise in **estrogen** levels from the dominant follicle, indicating ovarian readiness. - At the time of the LH surge, **progesterone** levels remain low; they only begin to rise significantly after ovulation, when the corpus luteum forms. *Increased estrogen & increased progesterone* - While **estrogen** levels are high, **progesterone** only significantly increases *after* ovulation, as the corpus luteum develops. - High estrogen *and* high progesterone together are typically seen in the **luteal phase**, not at the peak of the LH surge. *Decreased estrogen & increased progesterone* - A decrease in **estrogen** would suppress LH, not trigger a surge. - Increased **progesterone** would also inhibit LH release via negative feedback in the follicular phase if it were to occur pre-ovulation. *Decreased estrogen & decreased progesterone* - Both **decreased estrogen** and **decreased progesterone** would lead to low FSH/LH levels and would not promote an LH surge or ovulation. - This hormonal profile is more characteristic of the very early follicular phase or menopause.

Q: Which of the following stimuli is primarily responsible for triggering the Bezold-Jarisch reflex?

Activation of cardiac C-fiber afferents. ***Activation of cardiac C-fiber afferents*** - The **Bezold-Jarisch reflex** is primarily triggered by stimulation of **cardiac mechanoreceptors and chemoreceptors** located in the ventricles, particularly the inferoposterior wall of the left ventricle. - These receptors have **unmyelinated vagal C-fiber afferents** that transmit signals to the medullary cardiovascular centers. - Activation of these afferents leads to the characteristic triad: **bradycardia, hypotension, and vasodilation** via increased parasympathetic activity and withdrawal of sympathetic tone. - Common triggers include vigorous ventricular contraction with decreased filling, certain drugs (veratridine), myocardial ischemia (especially inferior wall MI), and reperfusion. *Decreased venous return* - While **decreased venous return** creates the hemodynamic context (ventricular underfilling) that can lead to vigorous contraction of a relatively empty ventricle, it is not itself the *trigger* of the reflex. - The actual trigger is the activation of the ventricular receptors sensing this abnormal contraction pattern, which then signal via C-fiber afferents. - Decreased venous return alone, without receptor activation, would not produce the reflex. *Parasympathetic withdrawal* - **Parasympathetic withdrawal** would cause tachycardia and is opposite to the Bezold-Jarisch reflex, which involves **increased parasympathetic activity**. - This is a compensatory response seen in other reflexes like the baroreceptor reflex during hypotension. *Increased sympathetic stimulation* - **Increased sympathetic stimulation** produces tachycardia, increased contractility, and vasoconstriction—effects opposite to the Bezold-Jarisch reflex. - The reflex actually causes **sympathetic withdrawal** along with parasympathetic activation.

Question 1

The roof of the olfactory region is formed by?

Accepted Answer

Cribriform plate of ethmoid

Answer

Nasal bone

Answer

Sphenoid

Answer

Temporal bone

Question 2

Which muscle will be paralyzed when the radial nerve is injured just below the spiral groove?

Accepted Answer

Extensor Carpi Radialis Brevis

Answer

Extensor Digitorum

Answer

Supinator

Answer

Abductor Pollicis Longus

Question 3

Vertebral arteries of both sides unite to form

Accepted Answer

Basilar artery

Answer

Anterior spinal artery

Answer

Posterior spinal artery

Answer

Medullary artery

Question 4

Which of the following is a neutral amino acid?

Accepted Answer

Glycine

Answer

Aspartate

Answer

Arginine

Answer

Histidine

Question 5

What is the main enzyme involved in glycogen breakdown (glycogenolysis)?

Accepted Answer

Glycogen phosphorylase

Answer

Glycogen synthase

Answer

Glucose-6-phosphatase

Answer

Hexokinase

Question 6

Glucagon stimulates

Accepted Answer

Gluconeogenesis

Answer

Glycogenesis

Answer

Fatty acid synthesis

Answer

Glycolysis

Question 7

What is the mechanism by which mercury causes damage?

Accepted Answer

Binds to -SH groups of enzymes

Answer

Causes toxicity through various mechanisms

Answer

Inhibits electron transport chain

Answer

Inhibits protein synthesis

Question 8

What is the mechanism of metabolism for alcohol, aspirin, and phenytoin at high doses?

Accepted Answer

Zero order kinetics

Answer

First pass kinetics

Answer

First order kinetics

Answer

Second order kinetics

Question 9

LH surge is associated with?

Accepted Answer

Increased estrogen & decreased progesterone

Answer

Increased estrogen & increased progesterone

Answer

Decreased estrogen & increased progesterone

Answer

Decreased estrogen & decreased progesterone

Question 10

Which of the following stimuli is primarily responsible for triggering the Bezold-Jarisch reflex?

Accepted Answer

Activation of cardiac C-fiber afferents

Answer

Parasympathetic withdrawal

Answer

Decreased venous return

Answer

Increased sympathetic stimulation

NEET-PG 2013

Anatomy

Biochemistry

Pharmacology

Physiology