General Physiology Practice Questions

Q: Fever increases the basal metabolic rate by approximately what percentage for each 1-degree Celsius rise in body temperature?

7%. **Explanation:** The correct answer is **7% (Option B)**. This relationship is based on the **Van’t Hoff’s Law**, which states that the velocity of chemical reactions increases as temperature rises. In human physiology, an increase in body temperature accelerates enzymatic activity and metabolic processes. For every **1°C rise** in body temperature, the Basal Metabolic Rate (BMR) increases by approximately **7%** (or roughly 13% for every 1°F rise). **Analysis of Options:** * **Option A (3%):** This value is too low. While some minor physiological fluctuations occur, a 1°C rise triggers a more significant metabolic demand than 3%. * **Option B (7%):** **Correct.** This is the standard physiological constant cited in major textbooks (like Guyton and Hall) regarding the thermogenic effect of fever on metabolism. * **Option C (10%):** While some older texts or specific clinical scenarios might approximate 10%, 7% is the precise "high-yield" figure required for competitive exams like NEET-PG. * **Option D (20%):** This is an overestimation. A 20% increase per degree would lead to rapid exhaustion of energy stores and severe metabolic acidosis during common febrile illnesses. **Clinical Pearls for NEET-PG:** * **Q10 Effect:** This refers to the temperature coefficient, representing the factor by which a biological process increases with a 10°C rise. * **Clinical Significance:** Fever-induced BMR increase explains why patients with infections experience rapid weight loss, increased heart rate (tachycardia), and increased respiratory rate (tachypnea). * **Thyroid Link:** BMR is primarily regulated by **Thyroxine (T4)**. While fever increases BMR acutely via temperature, T4 increases it by stimulating Na+-K+ ATPase activity across tissues.

Q: Which of the following is NOT a second messenger?

Protein kinase. **Explanation:** In cellular signaling, **second messengers** are small intracellular molecules or ions that relay signals received by cell-surface receptors (the first messenger) to target effector proteins. **Why Protein Kinase is the correct answer:** Protein kinases (e.g., PKA, PKC) are **enzymes**, not second messengers. They are typically the **effectors** activated by second messengers. For example, cAMP (second messenger) binds to and activates Protein Kinase A. The kinase then phosphorylates specific proteins to elicit a cellular response. Therefore, it is a downstream mediator in the signaling cascade rather than a messenger molecule itself. **Analysis of Incorrect Options:** * **cAMP (Cyclic Adenosine Monophosphate):** The most classic second messenger, produced by Adenylyl Cyclase. It mediates responses for hormones like Glucagon and PTH. * **NO (Nitric Oxide):** A unique gaseous second messenger that diffuses across membranes to activate soluble guanylyl cyclase, increasing cGMP levels. * **CO (Carbon Monoxide):** Similar to NO, CO acts as a gaseous signaling molecule (gasotransmitter) that can activate guanylyl cyclase and modulate ion channels. **High-Yield NEET-PG Pearls:** * **Common Second Messengers:** cAMP, cGMP, $IP_3$, DAG, $Ca^{2+}$, NO, and CO. * **Gaseous Messengers:** NO, CO, and $H_2S$ (Hydrogen Sulfide). * **IP3/DAG Pathway:** Phospholipase C cleaves $PIP_2$ into $IP_3$ (releases $Ca^{2+}$ from ER) and DAG (activates Protein Kinase C). * **Receptor Tyrosine Kinases (RTK):** Insulin and Growth Factors use this pathway, which often bypasses traditional second messengers by using direct protein-protein phosphorylation (e.g., JAK-STAT).

Q: Which one of the following molecules is used for cell signaling?

NO. **Explanation:** The correct answer is **NO (Nitric Oxide)**. **1. Why NO is the correct answer:** Nitric Oxide (NO) is a unique **gaseous signaling molecule** (gasotransmitter). In the cardiovascular system, it is synthesized from **L-arginine** by the enzyme **Nitric Oxide Synthase (NOS)** in endothelial cells. Being lipophilic, it diffuses across cell membranes into adjacent smooth muscle cells. There, it activates **soluble Guanylyl Cyclase (sGC)**, increasing intracellular **cGMP** levels. This leads to protein kinase G activation and calcium sequestration, resulting in **vasodilation**. **2. Why the other options are incorrect:** * **CO2 (Carbon Dioxide) & O2 (Oxygen):** These are metabolic gases involved in respiration and oxidative phosphorylation. While their concentrations can influence physiological processes (e.g., chemoreceptor activation or hypoxic vasoconstriction), they do not function as primary ligands or intracellular signaling molecules in the classical sense. * **N2 (Nitrogen):** This is an inert gas in the human body. It does not participate in biochemical signaling pathways. **3. High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of Nitroglycerin:** It acts as a prodrug that is converted into NO, causing rapid vasodilation in angina pectoris. * **Sildenafil (Viagra):** It inhibits **Phosphodiesterase-5 (PDE-5)**, the enzyme that breaks down cGMP. By prolonging cGMP levels initiated by NO, it maintains smooth muscle relaxation. * **NOS Isoforms:** * **eNOS** (Endothelial) and **nNOS** (Neuronal) are constitutive (calcium-dependent). * **iNOS** (Inducible) is found in macrophages and is involved in inflammation and septic shock. * **Other Gasotransmitters:** Besides NO, **Carbon Monoxide (CO)** and **Hydrogen Sulfide (H2S)** are also recognized as signaling molecules.

Q: Skeletal muscle contraction ends when?

Calcium is pumped back into the sarcoplasmic reticulum. **Explanation:** Skeletal muscle contraction is a calcium-dependent process. The correct answer is **D** because the relaxation phase begins when the stimulus from the motor neuron ceases, leading to the closure of Ryanodine receptors. The **SERCA pump (Sarcoplasmic/Endoplasmic Reticulum Calcium ATPase)** then actively transports $Ca^{2+}$ ions from the sarcoplasm back into the sarcoplasmic reticulum against a concentration gradient. As cytosolic calcium levels drop, calcium dissociates from **Troponin C**, allowing the Troponin-Tropomyosin complex to re-cover the active sites on actin, thereby preventing cross-bridge cycling. **Analysis of Incorrect Options:** * **Option A:** While ions (like $K^+$) move out of the cell during repolarization to reset the membrane potential, this does not directly terminate the mechanical contraction; the sequestration of calcium is the definitive "off switch." * **Option B:** Acetylcholine (ACh) is not "absorbed"; it is rapidly **hydrolyzed** by the enzyme Acetylcholinesterase (AChE) into choline and acetate. * **Option C:** Receptors do not "indraw" to end contraction. While prolonged exposure to ACh can lead to receptor desensitization, it is not the physiological mechanism for ending a single twitch. **High-Yield NEET-PG Pearls:** * **Calsequestrin:** A protein within the sarcoplasmic reticulum that binds to $Ca^{2+}$, allowing it to be stored at high concentrations. * **Malignant Hyperthermia:** Caused by a mutation in the **Ryanodine receptor (RyR1)**, leading to excessive calcium release and sustained muscle contraction/heat production. * **Rigor Mortis:** Occurs because **ATP is required for the relaxation phase** (to power the SERCA pump and to detach the myosin head from actin). Without ATP, the cross-bridges remain locked.

Q: Calcium is pumped back into the sarcoplasmic reticulum by which mechanism?

SERCA (Sarco/Endoplasmic Reticulum Calcium ATPase). **Explanation:** The correct answer is **SERCA (Sarco/Endoplasmic Reticulum Calcium ATPase)**. **1. Why SERCA is correct:** Muscle relaxation is an active process that requires the removal of calcium ions ($Ca^{2+}$) from the sarcoplasm back into the Sarcoplasmic Reticulum (SR). This occurs against a steep concentration gradient, necessitating **Primary Active Transport**. The SERCA pump utilizes ATP hydrolysis to transport two $Ca^{2+}$ ions into the SR for every ATP molecule consumed. This decrease in cytosolic calcium allows $Ca^{2+}$ to dissociate from Troponin C, leading to the cessation of cross-bridge cycling and subsequent muscle relaxation. **2. Why other options are incorrect:** * **Sodium-potassium pump ($Na^+/K^+$ ATPase):** This is a primary active transporter found in almost all cell membranes. It maintains the resting membrane potential by pumping 3 $Na^+$ out and 2 $K^+$ in; it does not directly transport calcium into the SR. * **Ryanodine receptor (RyR):** These are calcium-release channels located on the SR membrane. They are responsible for the efflux of calcium *out* of the SR into the cytoplasm during excitation-contraction coupling, not its reuptake. **3. High-Yield Clinical Pearls for NEET-PG:** * **Phospholamban:** In cardiac muscle, SERCA is regulated by a protein called phospholamban. When dephosphorylated, it inhibits SERCA; when phosphorylated (via $\beta$-adrenergic stimulation), inhibition is lifted, increasing the rate of relaxation (**Lusitropic effect**). * **Calsequestrin:** Inside the SR, calcium binds to this protein, which allows the SR to store high concentrations of $Ca^{2+}$ without significantly increasing the gradient against which SERCA must pump. * **Malignant Hyperthermia:** Caused by a mutation in the Ryanodine receptor (RyR1), leading to excessive calcium release.

Q: What is the primary function of the Golgi tendon organ?

Detecting reflex muscle tension. ### Explanation The **Golgi Tendon Organ (GTO)** is a specialized sensory receptor located at the junction of muscle fibers and tendons. It is arranged **in series** with the muscle fibers, making it exquisitely sensitive to changes in **muscle tension**. **1. Why Option B is Correct:** When a muscle undergoes forceful contraction, the GTO is stretched. It sends impulses via **Ib afferent nerve fibers** to the spinal cord. These fibers synapse on inhibitory interneurons, which then inhibit the alpha motor neurons of the same muscle. This mechanism, known as the **Inverse Stretch Reflex (Autogenic Inhibition)**, prevents muscle damage by causing the muscle to relax when tension becomes excessive. **2. Why Other Options are Incorrect:** * **Option A:** Detecting muscle length is the primary function of the **Muscle Spindle**. Muscle spindles are arranged **in parallel** with extrafusal fibers and mediate the stretch reflex (e.g., knee jerk). * **Option C & D:** Nutritional status and excretory functions are regulated by metabolic, endocrine, and autonomic systems (e.g., hypothalamus, kidneys), not by musculoskeletal mechanoreceptors. **3. High-Yield Clinical Pearls for NEET-PG:** * **Arrangement:** Muscle Spindle = Parallel; GTO = Series. * **Afferent Fibers:** Muscle Spindle = **Ia** (primary) and **II** (secondary); GTO = **Ib**. * **The "Clasp-Knife Response":** In upper motor neuron (UMN) lesions, exaggerated GTO activity contributes to the sudden "melting away" of resistance when a limb is passively stretched, a classic clinical sign of spasticity. * **Function:** While the muscle spindle is a feedback regulator of muscle **length**, the GTO is a feedback regulator of muscle **force/tension**.

Q: What is the term for the length of a muscle fiber at the start of contraction that is necessary to achieve maximum active tension?

Resting length. **Explanation:** The correct answer is **Resting length (Option B)**. This concept is fundamental to the **Length-Tension Relationship** in muscle physiology. **1. Why Resting Length is Correct:** The resting length ($L_0$) is defined as the optimal length of a muscle fiber at which it can develop the maximum active tension during contraction. At this specific length, there is **maximal overlap** between the actin (thin) and myosin (thick) filaments. This allows for the greatest number of cross-bridge formations. If the muscle is stretched beyond or shortened below this length, the number of potential cross-bridges decreases, thereby reducing the active tension produced. **2. Why the Other Options are Incorrect:** * **Equilibrium length (A):** This refers to the length of a relaxed muscle when it is not attached to the skeleton. At this length, the passive tension is zero, but it is typically shorter than the optimal resting length. * **Initial length (C):** While "initial length" refers to the length before contraction, it is a general term. It does not specifically denote the *optimal* length required for *maximum* tension. * **Overlapping length (D):** This is a descriptive term for the zone where filaments meet, but it is not the formal physiological term for the fiber length itself. **3. NEET-PG High-Yield Pearls:** * **Frank-Starling Law:** This is the cardiac application of the length-tension relationship; increased initial stretching of cardiac myocytes (preload) leads to increased force of contraction, up to a physiological limit. * **Sarcomere Length:** In mammalian skeletal muscle, the optimal sarcomere length for maximum tension is approximately **2.0 to 2.2 μm**. * **Total Tension:** Remember that Total Tension = Active Tension (from cross-bridges) + Passive Tension (from elastic elements like titin). Maximum *active* tension occurs specifically at $L_0$.

Question 1

Fever increases the basal metabolic rate by approximately what percentage for each 1-degree Celsius rise in body temperature?

Accepted Answer

7%

Answer

3%

Answer

10%

Answer

20%

Question 2

Which of the following is NOT a second messenger?

Accepted Answer

Protein kinase

Answer

cAMP

Answer

NO

Answer

CO

Question 3

Which one of the following molecules is used for cell signaling?

Accepted Answer

NO

Answer

CO2

Answer

O2

Answer

N2

Question 4

Which of the following statements regarding the homeostatic mechanism of the body is NOT true?

Accepted Answer

The body's homeostatic systems are primarily stabilized by positive feedback mechanisms.

Answer

Normal cell function depends on the constancy of extracellular fluid (ECF).

Answer

The actual environment of the cells of the body is the interstitial component of the ECF.

Answer

Renal and respiratory adjustments are constantly occurring to maintain homeostasis.

Question 5

Energy is required for which transport process across the cell membrane?

Accepted Answer

Active transport

Answer

Osmosis

Answer

Facilitated diffusion

Answer

Simple diffusion

Question 6

Skeletal muscle contraction ends when?

Accepted Answer

Calcium is pumped back into the sarcoplasmic reticulum

Answer

Ions move out of the cytoplasm

Answer

Acetylcholine is absorbed from the neuromuscular junction

Answer

Closure and indrawing of receptors

Question 7

Calcium is pumped back into the sarcoplasmic reticulum by which mechanism?

Accepted Answer

SERCA (Sarco/Endoplasmic Reticulum Calcium ATPase)

Answer

Sodium-potassium pump

Answer

Ryanodine receptor

Answer

None of the above

Question 8

What is the primary function of the Golgi tendon organ?

Accepted Answer

Detecting reflex muscle tension

Answer

Detecting muscle length

Answer

Monitoring nutritional status

Answer

Regulating excretory function

Question 9

Which of the following statements about ion composition in the body is true?

Accepted Answer

Sodium and chloride are the principal ions in extracellular fluid.

Answer

Intracellular and extracellular ion compositions are the same.

Answer

Phosphorus and magnesium are major ions intracellularly.

Answer

The kidney tightly regulates sodium, potassium, and chloride composition.

Question 10

What is the term for the length of a muscle fiber at the start of contraction that is necessary to achieve maximum active tension?

Accepted Answer

Resting length

Answer

Equilibrium length

Answer

Initial length

Answer

Overlapping length

General Physiology — MCQs

General Physiology — MCQs

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