NEET-PG 2024 Practice Questions

Q: A patient presents with symptoms of dermatitis, dementia, and cognitive decline. Which micronutrient deficiency is most likely responsible?

Niacin. ***Niacin*** - The classic triad of symptoms known as the "3 Ds"—**dermatitis, dementia, and diarrhea**—is characteristic of **pellagra**, a severe deficiency of **niacin (vitamin B3)**. - **Cognitive decline** is a common manifestation of the neurological symptoms associated with dementia in pellagra. *Thiamine* - **Thiamine (vitamin B1)** deficiency causes **beriberi**, leading to cardiovascular (wet beriberi) or neurological (dry beriberi/Wernicke-Korsakoff syndrome) symptoms. - While **fatigue and cognitive impairment** can occur, the constellation of prominent dermatitis and severe dementia is not typical of primary thiamine deficiency. *Tryptophan* - **Tryptophan** is an **essential amino acid** and a precursor to niacin. A deficiency in tryptophan could indirectly lead to niacin deficiency. - However, the direct deficiency of tryptophan as the primary cause of the "3 Ds" is less common than a direct niacin deficiency or impaired niacin synthesis. *Retinol* - **Retinol (vitamin A)** deficiency primarily affects **vision**, leading to **night blindness** and xerophthalmia. - It also plays a role in immune function and epithelial cell integrity, but it does not cause the specific triad of dermatitis, dementia, and cognitive decline seen here. *Riboflavin* - **Riboflavin (vitamin B2)** deficiency causes **angular stomatitis, cheilosis, and glossitis** along with seborrheic dermatitis. - While it can cause skin manifestations, it does not typically present with the severe dementia and cognitive decline characteristic of pellagra.

Q: Which transporter helps in the improvement of insulin resistance in type 2 diabetes mellitus (DM2) with regular exercise and physical activities?

GLUT 4. ***GLUT 4*** - **GLUT 4** is the **insulin-sensitive glucose transporter** predominantly found in **skeletal muscle** and **adipose tissue**. Regular exercise and physical activity increase the expression and translocation of GLUT 4 to the cell membrane, enhancing glucose uptake independent of insulin, thereby improving **insulin sensitivity** and reducing insulin resistance in DM2. - Exercise also stimulates **AMPK (AMP-activated protein kinase)**, which promotes GLUT 4 translocation to the cell surface, facilitating glucose uptake and utilization in active muscles. *GLUT 1* - **GLUT 1** is a basal glucose transporter found in nearly all cells, responsible for **basal glucose uptake** to meet basic metabolic needs, especially in **red blood cells** and the **blood-brain barrier**. - Its activity is largely **insulin-independent** and does not significantly contribute to the exercise-induced improvement in insulin sensitivity in skeletal muscle. *GLUT 2* - **GLUT 2** is primarily found in the **liver, pancreatic beta cells, kidneys, and small intestine**. It has a **low affinity** but **high capacity** for glucose transport, serving as a glucose sensor in beta cells and allowing efficient glucose uptake/release in the liver. - It plays a role in glucose homeostasis but is **not directly involved in the exercise-mediated improvement of insulin resistance** in peripheral tissues like muscle. *GLUT 3* - **GLUT 3** is a **high-affinity glucose transporter** primarily expressed in **neurons** and the **placenta**. It is crucial for providing a constant supply of glucose to the brain, even at low glucose concentrations. - Like GLUT 1 and GLUT 2, its activity is largely **insulin-independent** and does not play a significant role in improving insulin resistance through exercise in DM2.

Q: A 5-year-old girl was washing her doll with shampoo containing rotenone. Her mother noticed her in an unconscious state. Which enzyme is inhibited by the above chemical?

NADH dehydrogenase. ***NADH dehydrogenase*** - **Rotenone** is a potent **inhibitor of mitochondrial complex I (NADH dehydrogenase)**, preventing the transfer of electrons from NADH to ubiquinone. - This inhibition disrupts the **electron transport chain**, leading to a halt in ATP synthesis and cellular energy failure, causing symptoms like unconsciousness. *Succinate dehydrogenase* - **Succinate dehydrogenase** (Complex II) is involved in both the **Krebs cycle and electron transport chain**, but is not directly inhibited by rotenone. - Only severe compromise of the electron transport chain can cause a secondary effect, but not direct enzyme inhibition. *Cytochrome C* - **Cytochrome C** is a mobile electron carrier in the electron transport chain, but it is not directly inhibited by rotenone. - **Cytochrome C** transfers electrons from complex III to complex IV. *Cytochrome oxidase* - **Cytochrome oxidase** (Complex IV) is responsible for the final transfer of electrons to oxygen, which is not inhibited by rotenone. - Inhibitors like **cyanide and carbon monoxide** specifically target **cytochrome oxidase**. *Cytochrome b-c1 complex* - **Cytochrome b-c1 complex** (Complex III) catalyzes electron transfer from ubiquinol to cytochrome C, but is not inhibited by rotenone. - This complex is specifically inhibited by **antimycin A**, not rotenone.

Q: Caffeine impairs sleep by which of the following mechanisms?

Blocks adenosine action and promotes wakefulness. ***Blocks adenosine action and promotes wakefulness*** - Caffeine functions as a competitive **adenosine receptor antagonist**, primarily at A1 and A2A receptors in the brain. - By blocking adenosine, which is an endogenous sleep-promoting neurochemical, caffeine reduces its inhibitory effects on wakefulness centers, thus **promoting alertness** and delaying sleep onset. *Activates locus coeruleus & promotes wakefulness* - While caffeine indirectly influences brain regions that promote wakefulness, its primary mechanism is not direct activation of the **locus coeruleus**. - Its effects on wakefulness are mediated more broadly through antagonism of **adenosine receptors.** *No role in maintaining wakefulness* - This statement is incorrect; caffeine is well-known for its **psychoactive properties** and its ability to increase alertness and reduce fatigue. - Its widespread consumption is largely attributed to its role in **promoting wakefulness** and improving cognitive function. *Activates histamine release and prevents sleep* - Caffeine does not significantly activate **histamine release** as a primary mechanism for its wake-promoting effects. - The wake-promoting effects of histamine are mediated via H1 receptors, but this is a separate pathway not directly targeted by caffeine. *Inhibits phosphodiesterase and increases cAMP levels* - While caffeine does inhibit **phosphodiesterase enzymes** (particularly at higher concentrations), this is not the primary mechanism for its wake-promoting effects. - The concentrations required for significant phosphodiesterase inhibition are much higher than those achieved with typical caffeine consumption; **adenosine receptor antagonism** occurs at much lower doses and is the dominant mechanism for its effects on sleep and alertness.

Q: Phenobarbitone exerts its therapeutic effect primarily through which mechanism?

Enhancement of GABA-A receptor function. ***Enhancement of GABA-A receptor function*** - **Phenobarbitone** (phenobarbital) is a barbiturate that acts primarily by **enhancing GABA-A receptor activity** - It binds to a distinct **barbiturate binding site** on the GABA-A receptor complex - This binding **prolongs the duration of chloride channel opening** in response to GABA - Results in increased **chloride ion influx**, neuronal **hyperpolarization**, and **decreased neuronal excitability** - This mechanism underlies its **anticonvulsant** and **sedative-hypnotic** properties *NMDA receptor antagonism* - While some anticonvulsants work through NMDA receptor antagonism (e.g., ketamine, felbamate), this is **not the primary mechanism** of phenobarbitone *Voltage-gated sodium channel blockade* - Sodium channel blockade is the mechanism of action for drugs like **phenytoin, carbamazepine**, and **lamotrigine** - Phenobarbitone does not significantly block sodium channels at therapeutic concentrations *Voltage-gated calcium channel blockade* - Calcium channel blockers like **ethosuximide** (T-type) and **gabapentin** (α2δ subunit) work through this mechanism - This is not the primary mechanism for phenobarbitone *Potassium channel opening* - Potassium channel openers like **retigabine** increase potassium conductance - Phenobarbitone does not primarily work through this mechanism

Q: Sour taste is mediated by which of the following receptors?

OTOP1. ***OTOP1*** - The **OTOP1** receptor, an **otopetrin protein**, is responsible for detecting the **sour taste** sensation by mediating proton influx. - It functions as a **proton channel**, allowing hydrogen ions (H+) from acidic substances to enter taste receptor cells. *T1R1* - **T1R1** is a component of the **umami (savory) taste receptor**, forming a heterodimer with T1R3 to detect glutamate. - It does not directly detect sourness but is involved in the perception of amino acids. *T1R2* - **T1R2** is a component of the **sweet taste receptor**, forming a heterodimer with T1R3 to detect sugars. - This receptor is not involved in the transduction of sour taste. *T1R3* - **T1R3** is a common subunit that combines with **T1R1** for umami taste and with **T1R2** for sweet taste. - While essential for sweet and umami, it does not directly mediate the perception of sourness.

Q: Select the correct option regarding the function of receptors:

Pacinian corpuscle - fast vibration. ***Pacinian corpuscle - fast vibration*** - **Pacinian corpuscles** are rapidly adapting mechanoreceptors that are highly sensitive to **vibrations** and **deep pressure**. - Their layered structure allows them to detect even slight deformations and transmit information about **rapid changes** in mechanical stimuli. *Merkel cells - slow vibration* - **Merkel cells** are slow-adapting mechanoreceptors primarily responsible for sensing **light touch**, **texture**, and sustained pressure. - They are not associated with the detection of vibrations, whether slow or fast. *Meissner's corpuscle - stretch* - **Meissner's corpuscles** are rapidly adapting mechanoreceptors that detect **light touch**, **low-frequency vibration**, and discriminatory touch. - **Stretch sensation** is primarily mediated by Ruffini corpuscles and muscle spindle organs. *Ruffini corpuscle - light touch* - **Ruffini corpuscles** are slow-adapting mechanoreceptors that respond to **sustained pressure**, skin **stretch**, and joint position. - **Light touch** is primarily detected by Merkel cells and Meissner's corpuscles.

Q: Sequence the events in neuromuscular action potential conduction: 1. Sodium channels open in the end plate 2. Calcium enters at the nerve terminal 3. Release of acetylcholine

$2 \rightarrow 3 \rightarrow 1$ . ***Correct: $2 \rightarrow 3 \rightarrow 1$*** - **Calcium entry at the nerve terminal** is the initial trigger - when an action potential reaches the presynaptic nerve terminal, voltage-gated calcium channels open, allowing Ca²⁺ influx - **Acetylcholine release** follows - the increased intracellular calcium causes synaptic vesicles containing acetylcholine to fuse with the presynaptic membrane and release the neurotransmitter into the synaptic cleft - **Sodium channels open in the end plate** last - acetylcholine binds to nicotinic receptors on the motor end plate, opening ligand-gated sodium channels, which depolarizes the muscle membrane and triggers muscle contraction *Incorrect: $1 \rightarrow 2 \rightarrow 3$* - Places sodium channel opening first, which is physiologically impossible - Sodium channels at the motor end plate only open in response to acetylcholine binding - Cannot occur before acetylcholine is released from the nerve terminal *Incorrect: $1 \rightarrow 3 \rightarrow 2$* - Incorrectly sequences sodium channel opening before calcium entry - Violates the fundamental principle that calcium influx is required for neurotransmitter release - Acetylcholine cannot be released without prior calcium entry *Incorrect: $3 \rightarrow 2 \rightarrow 1$* - Places acetylcholine release before calcium entry, which is impossible - Calcium-triggered exocytosis is an absolute requirement for neurotransmitter release - Without calcium influx, vesicles cannot fuse with the presynaptic membrane

Q: A woman suffered a sunburn while enjoying a vacation on the beach. Now, while taking a shower, the lukewarm water (40° C) touching her back caused her to feel pain. What types of receptors were activated by the lukewarm water, and why did she experience pain?

Thermal nociceptors & allodynia. ***Thermal nociceptors & allodynia*** - Sunburn causes tissue damage, leading to the sensitization of **thermal nociceptors** (e.g., TRPV1 channels), making them responsive to normally innocuous thermal stimuli. - **Allodynia** is the perception of pain from a stimulus that does not ordinarily cause pain, such as lukewarm water after a sunburn, due to increased sensitivity of the pain pathways. *Thermal nociceptors & nociceptive pain* - While thermal nociceptors are involved, **nociceptive pain** typically refers to pain caused by direct tissue damage from a noxious (harmful) stimulus. Here, the lukewarm water itself is not noxious. - The pain experienced from the lukewarm water is not due to a *new* noxious stimulus but rather an exaggerated response to a *non-noxious* one. *Innocuous thermal receptors and hyperalgesia* - **Innocuous thermal receptors** (e.g., TRPM8 for cold, TRPV3/TRPV4 for warmth) normally detect non-painful temperature changes, not pain from sunburn. - **Hyperalgesia** is an increased response to a stimulus that *is* normally painful, but applied at a lower intensity. The lukewarm water is not normally painful. *Innocuous thermal receptors and allodynia* - As mentioned, **innocuous thermal receptors** are not primarily responsible for pain transmission, even in a sensitized state, as they are not nociceptors. - While **allodynia** is an accurate description of the pain type, the primary receptors activated for the pain sensation are sensitized nociceptors, not innocuous thermal receptors.

Question 1

A patient presents with symptoms of dermatitis, dementia, and cognitive decline. Which micronutrient deficiency is most likely responsible?

Accepted Answer

Niacin

Answer

Thiamine

Answer

Tryptophan

Answer

Retinol

Answer

Riboflavin

Question 2

Which transporter helps in the improvement of insulin resistance in type 2 diabetes mellitus (DM2) with regular exercise and physical activities?

Accepted Answer

GLUT 4

Answer

GLUT 1

Answer

GLUT 2

Answer

GLUT 3

Question 3

A 5-year-old girl was washing her doll with shampoo containing rotenone. Her mother noticed her in an unconscious state. Which enzyme is inhibited by the above chemical?

Accepted Answer

NADH dehydrogenase

Answer

Succinate dehydrogenase

Answer

Cytochrome C

Answer

Cytochrome oxidase

Answer

Cytochrome b-c1 complex

Question 4

Caffeine impairs sleep by which of the following mechanisms?

Accepted Answer

Blocks adenosine action and promotes wakefulness

Answer

Activates locus coeruleus & promotes wakefulness

Answer

No role in maintaining wakefulness

Answer

Activates histamine release and prevents sleep

Answer

Inhibits phosphodiesterase and increases cAMP levels

Question 5

Phenobarbitone exerts its therapeutic effect primarily through which mechanism?

Accepted Answer

Enhancement of GABA-A receptor function

Answer

Voltage-gated sodium channel blockade

Answer

Voltage-gated calcium channel blockade

Answer

Potassium channel opening

Answer

NMDA receptor antagonism

Question 6

Sour taste is mediated by which of the following receptors?

Accepted Answer

OTOP1

Answer

T1R1

Answer

T1R2

Answer

T1R3

Question 7

Select the correct option regarding the function of receptors:

Accepted Answer

Pacinian corpuscle - fast vibration

Answer

Merkel cells - slow vibration

Answer

Meissner's corpuscle - stretch

Answer

Ruffini corpuscle - light touch

Question 8

A patient is experiencing phantom limb pain after the amputation of the right limb. What is observed on a PET scan in a patient with phantom limb pain?

Accepted Answer

Neighboring cortical areas extending into the hand representation area

Answer

Expansion of right somatosensory cortex

Answer

Expansion of hand representation in the left somatosensory cortex into neighboring areas

Answer

General expansion of left somatosensory cortex

Question 9

Sequence the events in neuromuscular action potential conduction:
1. Sodium channels open in the end plate
2. Calcium enters at the nerve terminal
3. Release of acetylcholine

Accepted Answer

$2 \rightarrow 3 \rightarrow 1$

Answer

$1 \rightarrow 2 \rightarrow 3$

Answer

$1 \rightarrow 3 \rightarrow 2$

Answer

$3 \rightarrow 2 \rightarrow 1$

Question 10

A woman suffered a sunburn while enjoying a vacation on the beach. Now, while taking a shower, the lukewarm water (40° C) touching her back caused her to feel pain. What types of receptors were activated by the lukewarm water, and why did she experience pain?

Accepted Answer

Thermal nociceptors & allodynia

Answer

Thermal nociceptors & nociceptive pain

Answer

Innocuous thermal receptors and hyperalgesia

Answer

Innocuous thermal receptors and allodynia

NEET-PG 2024

Biochemistry

Pharmacology

Physiology