NEET-PG 2015 Practice Questions

Q: Intercalated disc is present in:

Cardiac muscle. ***Cardiac muscle*** - **Intercalated discs** are unique structures found only in cardiac muscle, forming specialized cell-cell junctions [1]. - These discs contain **gap junctions** for electrical coupling and **desmosomes** for strong adhesion, allowing the heart muscle to contract in a coordinated fashion. *Smooth muscle* - **Smooth muscle cells** are spindle-shaped and lack striations and organized sarcomeres. - They do not possess intercalated discs; instead, communication and coordination are often mediated by **gap junctions** scattered along the cell membranes [2]. *Skeletal muscle* - **Skeletal muscle cells** are long, multinucleated, and highly organized with prominent striations [3]. - They do not have intercalated discs as individual muscle fibers are innervated separately and generally do not directly communicate via specialized junctions for coordinated contraction. *All of the options* - As **intercalated discs** are characteristic features *only* of **cardiac muscle**, this option is incorrect. - Their presence in all three muscle types would contradict the specific cellular organization of smooth and skeletal muscle.

Q: What is the primary role of calnexin and calreticulin in the endoplasmic reticulum?

Act as chaperones. ***Act as chaperones*** - **Calnexin** and **calreticulin** are **chaperone proteins** located in the **endoplasmic reticulum (ER)**. - They bind to unfolded or misfolded glycoproteins to assist in their proper folding and assembly. - They are part of the **ER quality control system**, ensuring only properly folded proteins proceed to the Golgi apparatus. *Degrade misfolded proteins* - While misfolded proteins are eventually degraded through **ER-associated degradation (ERAD)**, this is not the primary function of calnexin and calreticulin. - These chaperones first attempt to **rescue and refold** proteins; degradation is a separate process involving other machinery. *Serve as tumor markers* - **Calnexin** and **calreticulin** are not typically used as **tumor markers** in clinical practice. - Their functions are related to protein quality control within the cell, not cancer detection. *Facilitate enzymatic reactions* - While some proteins in the ER are enzymes, **calnexin** and **calreticulin** themselves are not enzymes, nor do they primarily facilitate enzymatic reactions. - Their function is to ensure correct protein folding, distinct from direct catalytic activity.

Q: Which metabolic pathway is least active during 12 days of fasting?

Glycogenolysis. ***Correct: Glycogenolysis*** - **Glycogenolysis**, the breakdown of glycogen stores, is very active during the **initial hours of fasting** (first 24-48 hours) to maintain blood glucose levels. - However, after **12 days of fasting**, liver and muscle **glycogen stores are completely depleted**, making this pathway **essentially inactive** or the least active of all the metabolic pathways. - Once glycogen is exhausted, this pathway cannot contribute further to energy metabolism. *Incorrect: Gluconeogenesis* - This pathway becomes **increasingly active** during prolonged fasting to **synthesize new glucose** from non-carbohydrate precursors (amino acids, lactate, glycerol). - Essential for maintaining blood glucose for **glucose-dependent tissues** like red blood cells and parts of the brain that haven't fully adapted to ketones. - Remains a **crucial and active pathway** throughout prolonged fasting. *Incorrect: Ketogenesis* - **Ketogenesis** is **highly active** during prolonged fasting, producing **ketone bodies** (acetoacetate, β-hydroxybutyrate) from fatty acids in the liver. - Provides the **primary alternative fuel** for the brain (up to 70% of brain energy needs) and other tissues. - This is a **key metabolic adaptation** to preserve protein and glucose during starvation. *Incorrect: Lipolysis* - **Lipolysis** (breakdown of triglycerides into fatty acids and glycerol) is **highly active** during fasting to mobilize stored energy. - Provides **fatty acids** for direct oxidation by most tissues and **glycerol** as a gluconeogenic substrate. - A **fundamental process** for energy supply during nutrient deprivation.

Q: What is the time interval between somatic and molecular death?

1 - 2 hrs. ***1 - 2 hrs*** - The interval between **somatic death** (cessation of heart and respiration) and **molecular death** (death of individual cells) is typically 1 to 2 hours. - This time allows for the depletion of cellular energy reserves and the onset of irreversible cellular damage after the body's major systems have ceased functioning. *5-10 min* - This short interval is generally associated with the **depletion of oxygen** supply to the brain, leading to irreversible neurological damage, but not complete molecular death of all body cells. - Brain cells are highly sensitive to hypoxia and begin to die within minutes, but other body cells have varying tolerances. *10-30 min* - While some highly sensitive cells (like neurons) may experience **irreversible damage** or death within this timeframe, it is not long enough for the generalized molecular death of all body cells. - Organs like the heart or skeletal muscles can retain viability for longer periods post-somatic death due to anaerobic metabolism. *30 -1hr* - This is closer to the true interval for widespread molecular death but often still underestimates the time it takes for less metabolically active cells to fully succumb. - Some cellular processes can continue for up to an hour, but complete **irreversible cellular breakdown** across all tissues usually takes longer.

Q: Which of the following findings is diagnostic of iron deficiency anemia?

Increased TIBC, decreased serum ferritin. ***Increased TIBC, decreased serum ferritin*** - **Iron deficiency anemia** is characterized by depleted iron stores, leading to a **decreased serum ferritin** level, which is the most sensitive and specific marker for iron deficiency [4]. - In response to low iron stores, the body upregulates iron absorption and transport mechanisms, resulting in an **increased Total Iron Binding Capacity (TIBC)**, as there are more transferrin molecules available to bind iron [1]. *Decreased TIBC, decreased serum ferritin* - While a **decreased serum ferritin** is consistent with iron deficiency, a **decreased TIBC** is more indicative of **anemia of chronic disease** [1], where the body sequesters iron, leading to reduced iron availability for binding. - In **anemia of chronic disease**, both ferritin (an acute phase reactant) and TIBC can be reduced due to the inflammatory state [1], [2]. *Increased TIBC, increased serum ferritin* - An **increased TIBC** is seen in iron deficiency, but an **increased serum ferritin** indicates adequate or even **overloaded iron stores**, which contradicts the diagnosis of iron deficiency anemia. - High ferritin levels can be seen in conditions like **hemochromatosis** (iron overload) or **inflammation**, where ferritin acts as an acute phase reactant [5]. *Decreased TIBC, increased serum ferritin* - This combination is typical of **anemia of chronic disease**, where inflammation causes **increased serum ferritin** (as an acute phase reactant) and a **decreased TIBC** due to reduced production of transferrin [1]. - In this type of anemia, iron is often trapped within macrophages, making it unavailable for erythropoiesis despite seemingly normal or elevated stores [3].

Q: What effect does morphine have on muscle tone?

Increased muscle tone. ***Increased muscle tone*** - Morphine **increases skeletal muscle tone** and can cause muscle rigidity, particularly with rapid IV administration (truncal rigidity). - It significantly increases **smooth muscle tone** in various organs including the sphincter of Oddi (causing biliary colic), bladder sphincter (causing urinary retention), and GI tract (causing constipation). - This increased tone in sphincters and smooth muscle is a well-documented effect mediated through **opioid receptor activation**. *Bradycardia (not increased heart rate)* - Morphine typically causes **bradycardia** (decreased heart rate) due to vagal stimulation and central effects, not tachycardia. - Increased heart rate would be atypical and not a primary pharmacological effect of morphine. *Miosis (not mydriasis)* - Morphine characteristically causes **miosis** (pinpoint pupils) due to stimulation of the Edinger-Westphal nucleus of the oculomotor nerve. - Mydriasis (dilated pupils) is seen with anticholinergics or sympathomimetics, not opioids. *Respiratory depression (not stimulation)* - Morphine causes **respiratory depression**, not stimulation, by reducing the responsiveness of brainstem respiratory centers to CO2. - This is one of the most dangerous adverse effects and the primary cause of death in opioid overdose.

Q: Maximum cycloplegic action of atropine is seen at ?

1-3 hours. ***1-3 hours*** - Atropine, a **non-selective muscarinic antagonist**, reaches its **peak cycloplegic effect** approximately 1 to 3 hours after topical administration. - This peak activity is crucial for accurate retinoscopy and **refractive error measurement** in children, as it effectively paralyzes the ciliary muscle. *4-6 hours* - While atropine's cycloplegic effect is still present at 4-6 hours, it is generally **past its peak action** by this time. - Slower-acting cycloplegics might have their peak around this window, but not atropine. *1-2 weeks* - The **duration of action** for atropine's cycloplegic and mydriatic effects can last for 1-2 weeks, but this is the total duration, not when the maximum action is observed. - Patients are often instructed about the **prolonged effects** and potential for blurred vision and photophobia over this period. *30-60 minutes* - While some mydriatic effects might start within 30-60 minutes, the **full cycloplegic effect** of atropine, which requires maximum paralysis of the ciliary muscle, is not achieved in this short timeframe. - Shorter-acting cycloplegics like **cyclopentolate** or **tropicamide** would show peak action within this earlier interval.

Q: Tetany in muscle occurs in spite of normal serum Ca2+ level. Which ion is responsible?

Ionized Ca2+. ***Ionized Ca2+*** - While total serum calcium might be normal, **tetany** is specifically caused by a decrease in the concentration of **ionized (free) calcium** in the extracellular fluid. - Ionized calcium is the physiologically active form of calcium responsible for neuromuscular excitability. *Mg2+* - **Hypomagnesemia** can exacerbate hypocalcemia and contribute to tetany, but it is not the primary ion directly responsible for tetany when **total serum calcium is normal**. - A deficiency in Mg2+ can impair the release of **parathyroid hormone** and reduce target organ responsiveness to PTH. *K+* - Abnormalities in **potassium levels** (hypokalemia or hyperkalemia) primarily affect cardiac and muscular excitability, leading to arrhythmias or muscle weakness/paralysis. - While electrolyte imbalances are interconnected, changes in potassium are not the direct cause of tetany due to calcium's role. *Na+* - **Sodium ions** are crucial for nerve impulse transmission and muscle contraction by establishing the resting membrane potential and initiating action potentials. - However, direct changes in sodium concentration do not typically cause tetany; rather, they can lead to neurological symptoms like seizures (hyponatremia) or altered mental status (hypernatremia).

Q: Which of the following cell types is considered insulin-dependent?

Myocytes. ***Myocytes*** - **Myocytes** (skeletal muscle cells) are **insulin-dependent** and represent the **largest site of insulin-mediated glucose disposal** in the body - Insulin promotes translocation of **GLUT4 transporters** to the cell membrane, enabling glucose uptake - Skeletal muscle accounts for approximately **70-80% of postprandial glucose disposal**, making it the most quantitatively significant insulin-dependent tissue *Adipocytes* - **Adipocytes** (fat cells) are also **insulin-dependent** and utilize **GLUT4 transporters** for glucose uptake - Insulin stimulates glucose uptake and conversion to triglycerides for storage - However, adipose tissue accounts for only **10-15% of glucose disposal**, making it less quantitatively significant than skeletal muscle - Both myocytes and adipocytes are considered the two major insulin-dependent tissues in the body *Pituitocytes* - **Pituitocytes** are supporting cells in the pituitary gland - They use **insulin-independent glucose transporters** (GLUT1/GLUT3) - The pituitary gland requires constant glucose supply independent of insulin status *RBCs* - **Red blood cells** lack mitochondria and depend entirely on **anaerobic glycolysis** - Glucose uptake occurs via **insulin-independent GLUT1 transporters** - RBCs must maintain glucose uptake at all times, regardless of insulin levels

Q: During the sympathetic fight-or-flight response, what is the primary cardiovascular effect of epinephrine and norepinephrine on skeletal muscle vasculature?

Increased blood flow to muscles. ***Increased blood flow to muscles*** - **Epinephrine** and **norepinephrine** cause **vasodilation** in skeletal muscle arterioles, shunting blood toward tissues critical for immediate physical action. - This response ensures that muscles have adequate **oxygen** and **nutrients** to support intense activity, enabling a quick escape or confrontation. *Increased blood flow to the skin* - During fight-or-flight, the body prioritizes essential organs, causing **vasoconstriction** in the skin to redirect blood flow away from non-essential areas. - This redirection helps to conserve blood and reduce potential blood loss from surface injuries. *Bronchoconstriction* - **Epinephrine** and **norepinephrine** actually cause **bronchodilation**, leading to the relaxation of airway smooth muscles. - This effect increases the diameter of the airways, allowing more air to enter and exit the lungs, thereby enhancing **oxygen intake** and carbon dioxide expulsion. *Decreased heart rate* - The primary effect of **epinephrine** and **norepinephrine** is to **increase heart rate** and myocardial contractility. - This cardiac acceleration enhances **cardiac output**, ensuring rapid and efficient delivery of oxygenated blood throughout the body to meet the demands of stress.

Question 1

Intercalated disc is present in:

Accepted Answer

Cardiac muscle

Answer

Smooth muscle

Answer

Skeletal muscle

Answer

All of the options

Question 2

What is the primary role of calnexin and calreticulin in the endoplasmic reticulum?

Accepted Answer

Act as chaperones

Answer

Degrade misfolded proteins

Answer

Serve as tumor markers

Answer

Facilitate enzymatic reactions

Question 3

Which metabolic pathway is least active during 12 days of fasting?

Accepted Answer

Glycogenolysis

Answer

Gluconeogenesis

Answer

Ketogenesis

Answer

Lipolysis

Question 4

What is the time interval between somatic and molecular death?

Accepted Answer

1 - 2 hrs

Answer

5-10 min

Answer

10-30 min

Answer

30 - 1 hr

Question 5

Which of the following findings is diagnostic of iron deficiency anemia?

Accepted Answer

Increased TIBC, decreased serum ferritin

Answer

Decreased TIBC, decreased serum ferritin

Answer

Increased TIBC, increased serum ferritin

Answer

Decreased TIBC, increased serum ferritin

Question 6

What effect does morphine have on muscle tone?

Accepted Answer

Increased muscle tone

Answer

Respiratory stimulation

Answer

Decreased muscle tone

Answer

Mydriasis

Question 7

Maximum cycloplegic action of atropine is seen at ?

Accepted Answer

1-3 hours

Answer

1-2 weeks

Answer

4-6 hours

Answer

30-60 minutes

Question 8

Tetany in muscle occurs in spite of normal serum Ca2+ level. Which ion is responsible?

Accepted Answer

Ionized Ca2+

Answer

Mg2+

Answer

K+

Answer

Na+

Question 9

Which of the following cell types is considered insulin-dependent?

Accepted Answer

Myocytes

Answer

Pituitocytes

Answer

Adipocytes

Answer

RBCs

Question 10

During the sympathetic fight-or-flight response, what is the primary cardiovascular effect of epinephrine and norepinephrine on skeletal muscle vasculature?

Accepted Answer

Increased blood flow to muscles

Answer

Increased blood flow to the skin

Answer

Bronchoconstriction

Answer

Decreased heart rate

NEET-PG 2015

Anatomy

Biochemistry

Forensic Medicine

Pathology

Pharmacology

Physiology