Increase in plasma viscosity is maximally caused by which plasma protein?
Which protein primarily contributes to oncotic pressure in the blood?
What is the composition of epithelial sodium channels?
What do motor evoked potentials primarily assess?
What does the transient response observed during the insertion of an electrode in electromyography (EMG) indicate?
Which of the following statements is true regarding smooth muscle contraction?
What physiological mechanism is responsible for the increase in the duration of expiration?
What is another name for the withdrawal reflex?
Tetany in muscle occurs in spite of normal serum Ca2+ level. Which ion is responsible?
Which transport process is mediated by carriers and occurs against the concentration gradient?
NEET-PG 2015 - Physiology NEET-PG Practice Questions and MCQs
Question 11: Increase in plasma viscosity is maximally caused by which plasma protein?
- A. Albumin
- B. All have equal effect
- C. Globulin
- D. Fibrinogen (Correct Answer)
Explanation: ***Globulin*** - Increased levels of **globulin** proteins, particularly in inflammatory or proliferative conditions, have a significant impact on plasma viscosity due to their **high molecular weight** [1]. - **Globulins** contribute to **hyperviscosity syndrome**, which can lead to clinical symptoms like fatigue and visual disturbances [1]. *Albumin* - While **albumin** is the most abundant plasma protein, its primary role is in maintaining **oncotic pressure**, not significantly affecting plasma viscosity. - An increase in albumin does not correlate with plasma viscosity increases to the extent seen with globulins. *All have equal effect* - Different plasma proteins do not have **equal effects** on viscosity; **globulins** and **fibrinogen** particularly influence it more than **albumin**. - The impact on viscosity varies significantly with protein concentration and type, making this statement inaccurate. *Fibrinogen* - **Fibrinogen** does contribute to plasma viscosity but is typically less than that caused by globulins, especially when globulin levels are markedly elevated. - Its effect is more pronounced during **coagulation**, rather than in the general increase of plasma viscosity associated with inflammatory states. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 141-142.
Question 12: Which protein primarily contributes to oncotic pressure in the blood?
- A. Albumin (Correct Answer)
- B. Globulins
- C. Fibrinogen
- D. Transferrin
Explanation: ***Albumin*** - **Albumin** is the most abundant plasma protein and its small size and high concentration make it the primary determinant of **oncotic pressure** in the blood. - Its presence in the capillaries draws water from the **interstitial space** back into the blood vessels, maintaining **fluid balance** and blood volume. *Fibrinogen* - **Fibrinogen** is a crucial protein involved in **blood clotting**, where it is converted into **fibrin** to form a clot. - While a plasma protein, its contribution to **oncotic pressure** is minor compared to albumin, as it's less abundant and larger in size. *Globulins* - **Globulins** are a diverse group of proteins involved in immune function (**immunoglobulins**), transport (e.g., **alpha** and **beta globulins**), and clotting. - While they contribute to total plasma protein concentration, their collective impact on **oncotic pressure** is secondary to that of albumin due to lower concentrations and varied molecular weights. *Transferrin* - **Transferrin** is a specific **beta-globulin** that plays a vital role in **iron transport** in the blood. - Its primary function is not related to **oncotic pressure**, and its concentration is significantly lower than albumin.
Question 13: What is the composition of epithelial sodium channels?
- A. 2α, 1β, 1γ
- B. 1α, 1β, 1γ (Correct Answer)
- C. 2α, 1β
- D. 2α, 1β, 2γ
Explanation: ***1α, 1β, 1γ*** - Epithelial sodium channels (**ENaCs**) are heterotrimeric complexes composed of one **alpha (α)**, one **beta (β)**, and one **gamma (γ) subunit**. - This specific subunit composition is essential for the channel's proper function in **sodium reabsorption** across epithelial tissues. *2α, 1β* - This composition is incomplete as it lacks the **gamma (γ) subunit**, which is a crucial component of the functional ENaC. - While alpha and beta subunits are present, the absence of the gamma subunit would impair the channel's ability to efficiently transport sodium. *2α, 1β, 2γ* - This composition is incorrect because a functional ENaC typically includes only **one gamma (γ) subunit**, not two. - An imbalance in subunit stoichiometry can lead to misfolding or improper assembly, affecting channel function. *2α, 1β, 1γ* - This combination correctly includes all three types of subunits (alpha, beta, gamma) but incorrectly states there are **two alpha (α) subunits**. - A functional ENaC has a single alpha subunit, making this option incorrect.
Question 14: What do motor evoked potentials primarily assess?
- A. Central motor pathways (Correct Answer)
- B. Both central and peripheral motor pathways
- C. Muscle regeneration
- D. Peripheral motor pathways
Explanation: ***Central motor pathways*** - **Motor evoked potentials (MEPs)** are generated by electrical or magnetic stimulation of the **motor cortex** and primarily assess the integrity of **central motor pathways**, specifically the **corticospinal tracts**. - MEPs are the **gold standard** for monitoring **upper motor neuron** function during neurosurgical and spinal procedures. - The technique is most sensitive to dysfunction in the **brain and spinal cord** (central nervous system), making this their primary clinical utility. *Peripheral motor pathways* - While MEPs do eventually activate peripheral motor neurons to produce muscle responses, they are **not the primary tool** for assessing peripheral pathways. - **Nerve conduction studies (NCS)** and **electromyography (EMG)** are direct and more specific measures for evaluating peripheral motor nerve function. *Both central and peripheral motor pathways* - Although MEPs provide information about the entire motor pathway from cortex to muscle, their **primary diagnostic strength and clinical application** is in detecting dysfunction within the **central nervous system**. - The latency and amplitude of MEPs are most sensitive to **conduction abnormalities along the corticospinal tract**, not peripheral nerves. *Muscle regeneration* - MEPs do **not assess muscle regeneration** or intrinsic muscle health. - **Electromyography (EMG)** with needle examination and **muscle biopsy** are the appropriate methods to evaluate muscle regeneration and myopathic processes.
Question 15: What does the transient response observed during the insertion of an electrode in electromyography (EMG) indicate?
- A. Spontaneous muscle activity
- B. Voluntary muscle contraction
- C. Cell membrane disruption (Correct Answer)
- D. Induced muscle contraction
Explanation: **Cell membrane disruption** - The **transient response** observed during electrode insertion in **EMG** is caused by the mechanical trauma of the needle disrupting the **muscle fiber cell membranes**. - This disruption leads to a brief depolarization and subsequent repolarization of the affected fibers, generating characteristic electrical activity. *Spontaneous muscle activity* - **Spontaneous muscle activity**, such as **fibrillation potentials** or **positive sharp waves**, occurs independently of electrode insertion. - While observed during EMG, these are indicative of **denervation** or **myopathy** and are not directly caused by the act of insertion itself. *Voluntary muscle contraction* - **Voluntary muscle contraction** is recorded when the patient actively contracts the muscle and results in **motor unit action potentials (MUAPs)**. - This is a distinct process from the transient activity produced by electrode insertion. *Induced muscle contraction* - **Induced muscle contraction** typically refers to activity caused by **nerve stimulation** (e.g., in nerve conduction studies) or direct electrical stimulation of the muscle. - This is not the mechanism for the transient response during simple electrode insertion.
Question 16: Which of the following statements is true regarding smooth muscle contraction?
- A. None of the options.
- B. Calmodulin plays no role in smooth muscle contraction.
- C. Phosphorylation of myosin is essential for contraction. (Correct Answer)
- D. Troponin plays a significant role in smooth muscle contraction.
Explanation: **Phosphorylation of myosin is essential for contraction.** - In **smooth muscle**, the **myosin light chain (MLC)** must be phosphorylated by **myosin light chain kinase (MLCK)** to enable interaction with actin and initiate contraction. - This phosphorylation causes a conformational change in the **myosin head**, increasing its ATPase activity and allowing cross-bridge cycling. *Calmodulin plays no role in smooth muscle contraction.* - **Calmodulin (CaM)** is crucial for smooth muscle contraction, as it binds **calcium ions (Ca²⁺)** forming a Ca²⁺-CaM complex. - This complex then activates **myosin light chain kinase (MLCK)**, which phosphorylates myosin, triggering contraction. *None of the options.* - This statement is incorrect because one of the provided options, "Phosphorylation of myosin is essential for contraction," is indeed true. *Troponin plays a significant role in smooth muscle contraction.* - Unlike **striated muscle (skeletal and cardiac)**, **smooth muscle** does not contain **troponin**. - Regulation of smooth muscle contraction is primarily **calcium-calmodulin-dependent**, with roles for **MLCK** and **MLCP**, rather than troponin.
Question 17: What physiological mechanism is responsible for the increase in the duration of expiration?
- A. J-reflex
- B. Head's paradoxical reflex
- C. Proprioceptors
- D. Hering-Breuer reflex (Correct Answer)
Explanation: ***Hering-Breuer reflex*** - The **Hering-Breuer reflex** is initiated by **stretch receptors in the bronchi and bronchioles** which are activated during lung inflation. - This reflex **inhibits inspiration** and **prolongs expiration**, preventing overinflation of the lungs. *J-reflex* - The **J-reflex** is stimulated by **juxtacapillary (J) receptors** in the alveolar walls, usually in response to pulmonary edema or congestion. - It typically causes **rapid, shallow breathing** and **bronchoconstriction**, not prolonged expiration. *Head's paradoxical reflex* - **Head's paradoxical reflex** (also known as the **inflation reflex** in newborns) involves an inspiratory effort triggered by lung inflation, often overcoming the Hering-Breuer reflex in specific conditions. - It tends to **increase respiratory rate** and depth, not prolong expiration. *Proprioceptors* - **Proprioceptors** are sensory receptors in muscles, tendons, and joints that provide information about body position and movement. - While they can influence respiration during exercise, they are not primarily responsible for directly **increasing the duration of expiration** as a reflex mechanism against overinflation.
Question 18: What is another name for the withdrawal reflex?
- A. Golgi tendon reflex
- B. Extension reflex
- C. Stretch reflex
- D. Flexor reflex (Correct Answer)
Explanation: ***Flexor reflex*** - The withdrawal reflex is also known as the **flexor reflex** because it causes the rapid flexion (bending) of a limb to withdraw it from a noxious stimulus. - This reflex is a **polysynaptic reflex** involving interneurons in the spinal cord. *Golgi tendon reflex* - The **Golgi tendon reflex** is a protective reflex that causes muscle relaxation in response to excessive muscle tension. - It involves activation of **Golgi tendon organs**, which are proprioceptors located in the tendons. *Extension reflex* - The **extension reflex** is typically observed in withdrawal reflexes of the opposing limb, known as the **crossed extensor reflex**, to maintain balance. - It involves the extension of the contralateral limb while the ipsilateral limb flexes. *Stretch reflex* - The **stretch reflex** (or myotatic reflex) causes muscle contraction in response to stretching of the muscle. - It is a **monosynaptic reflex** involving muscle spindles and maintaining muscle tone.
Question 19: Tetany in muscle occurs in spite of normal serum Ca2+ level. Which ion is responsible?
- A. Mg2+
- B. K+
- C. Na+
- D. Ionized Ca2+ (Correct Answer)
Explanation: ***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).
Question 20: Which transport process is mediated by carriers and occurs against the concentration gradient?
- A. Facilitated diffusion
- B. Osmosis
- C. Active transport (Correct Answer)
- D. Endocytosis
Explanation: ***Active transport*** - **Active transport** systems use carrier proteins to move molecules across a membrane **against their concentration gradient**, requiring **metabolic energy** (e.g., from ATP hydrolysis). - This process is crucial for maintaining cellular homeostasis, accumulating specific substances, and establishing ion gradients. *Facilitated diffusion* - **Facilitated diffusion** also uses **carrier proteins**, but it moves substances **down their concentration gradient**, thus **not requiring metabolic energy**. - It increases the rate of diffusion for molecules that cannot easily cross the lipid bilayer, like glucose. *Osmosis* - **Osmosis** is the movement of **water molecules** across a selectively permeable membrane **down their water potential gradient**, driven by solute concentration differences, and does **not involve carrier proteins**. - This process equalizes solute concentrations on both sides of the membrane. *Endocytosis* - **Endocytosis** is a bulk transport mechanism where cells **engulf substances** from outside by forming vesicles from the plasma membrane; it's a form of active transport but **does not typically involve specific carrier proteins** embedded in the membrane for individual molecules. - This process is used for taking in larger molecules, particles, or even other cells.