During the sympathetic fight-or-flight response, what is the primary cardiovascular effect of epinephrine and norepinephrine on skeletal muscle vasculature?
EPSP is due to?
Which of the following neurons in the cerebellar cortex is primarily excitatory?
What is one of the specific functions of the primary motor cortex located on the anterior edge of the pre-central gyrus?
Which part of the sympathetic nervous system is responsible for secreting catecholamines?
What is the typical resting membrane potential (RMP) of smooth muscle cells?
Which of the following statements is TRUE regarding the Bohr effect?
What is the Haldane Effect?
What is the total surface area of the respiratory membrane in a healthy adult human?
Damage to pneumotaxic center along with vagus nerve causes which type of respiration?
NEET-PG 2015 - Physiology NEET-PG Practice Questions and MCQs
Question 31: During the sympathetic fight-or-flight response, what is the primary cardiovascular effect of epinephrine and norepinephrine on skeletal muscle vasculature?
- A. Increased blood flow to muscles (Correct Answer)
- B. Increased blood flow to the skin
- C. Bronchoconstriction
- D. Decreased heart rate
Explanation: ***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 32: EPSP is due to?
- A. Sodium ion influx (Correct Answer)
- B. Potassium ion influx
- C. Sodium ion efflux
- D. Calcium ion influx
Explanation: ***Sodium ion influx*** - An **Excitatory Postsynaptic Potential (EPSP)** is caused primarily by the binding of an **excitatory neurotransmitter** to its receptor, leading to the opening of **ligand-gated ion channels** permeable to sodium (Na+) ions. - The **influx of positively charged sodium ions** into the postsynaptic neuron causes a **depolarization** of the membrane potential, making it more likely to reach the threshold for an action potential. *Potassium ion influx* - **Potassium (K+) influx** is not the primary mechanism for generating an EPSP; instead, **potassium efflux** (movement out of the cell) is typically involved in **repolarization** after an action potential or in generating **Inhibitory Postsynaptic Potentials (IPSPs)**. - The movement of K+ into the cell would make the membrane potential more negative, leading to **hyperpolarization** or preventing depolarization. *Sodium ion efflux* - **Sodium (Na+) efflux** is mediated by the **Na+/K+ pump** and is crucial for maintaining the resting membrane potential, but it does **not directly cause an EPSP**. - Pumping Na+ out of the cell would **hyperpolarize** the cell or oppose depolarization, making an action potential less likely. *Calcium ion influx* - While **calcium (Ca2+) influx** is vital for many neuronal processes, including **neurotransmitter release** from the presynaptic terminal, it is **not the primary ionic basis** for generating an EPSP in the postsynaptic neuron itself. - Significant Ca2+ influx can occur during an **action potential** or lead to intracellular signaling, but it's not the main depolarizing current responsible for an EPSP.
Question 33: Which of the following neurons in the cerebellar cortex is primarily excitatory?
- A. Purkinje
- B. Basket
- C. Golgi
- D. Granule cells (Correct Answer)
Explanation: ***Granule cells*** - **Granule cells** are the only neurons in the cerebellar cortex that are **excitatory**, utilizing glutamate as their neurotransmitter. - They receive input from **mossy fibers** and project their parallel fibers to Purkinje cells and other interneurons. *Purkinje* - **Purkinje cells** are the primary output neurons of the cerebellar cortex and are **inhibitory**, releasing GABA. - They integrate vast amounts of information and project to the **deep cerebellar nuclei**. *Basket* - **Basket cells** are **inhibitory interneurons** located in the molecular layer of the cerebellum. - They synapse on the somata of **Purkinje cells**, providing potent inhibition. *Golgi* - **Golgi cells** are **inhibitory interneurons** found in the granular layer of the cerebellum. - They receive excitatory input from **parallel fibers** and inhibit granule cells, forming an important feedback loop.
Question 34: What is one of the specific functions of the primary motor cortex located on the anterior edge of the pre-central gyrus?
- A. Control of voluntary movement (Correct Answer)
- B. Increase extensor muscle tone
- C. Perception of pain
- D. Inhibition of stretch reflex
Explanation: ***Control of voluntary movement*** - The **primary motor cortex (M1)**, located in the **precentral gyrus**, is critically involved in generating neural impulses that control the execution of **voluntary movements**. - It plays a key role in **planning and executing complex, skilled movements**, especially of the distal musculature. *Increase extensor muscle tone* - While motor pathways influence muscle tone, the primary motor cortex's most specific role is not simply increasing extensor tone; rather, it coordinates a wide range of movements involving both flexors and extensors. - **Spasticity** or increased muscle tone (often extensor) is more commonly associated with damage to the **corticospinal tracts (upper motor neuron lesions)**, which *prevents* the fine-tuning inhibitory control from the cortex. *Perception of pain* - **Pain perception** is primarily processed in the **somatosensory cortex** (postcentral gyrus), limbic system, and insula, not the primary motor cortex. - The primary motor cortex is responsible for **motor output**, not sensory interpretation. *Inhibition of stretch reflex* - While descending motor pathways can modulate spinal reflexes, the direct and primary function of the primary motor cortex is not the specific inhibition of the stretch reflex. - The **gamma motor system** and other spinal interneurons are more directly involved in modulating the sensitivity of the stretch reflex.
Question 35: Which part of the sympathetic nervous system is responsible for secreting catecholamines?
- A. Cardiac ganglion
- B. Cervical sympathetic chain
- C. Adrenal medulla (Correct Answer)
- D. Thoracic sympathetic chain
Explanation: ***Adrenal medulla*** - The adrenal medulla acts as a modified **sympathetic ganglion**, directly innervated by **preganglionic sympathetic fibers**. - Upon stimulation, it releases a high concentration of **epinephrine** (adrenaline) and a smaller amount of **norepinephrine** (noradrenaline) into the bloodstream, acting as hormones. *Cardiac ganglion* - **Cardiac ganglia** are parasympathetic ganglia located in the heart, involved in regulating heart rate and contractility via acetylcholine release. - They do not secrete **catecholamines** but rather act as relay stations for parasympathetic innervation. *Cervical sympathetic chain* - The **cervical sympathetic chain** primarily innervates structures in the head, neck, and upper limbs, influencing functions like pupils, salivary glands, and sweat glands. - While it contains sympathetic neurons, its primary role is not the systemic release of **catecholamines** into the bloodstream. *Thoracic sympathetic chain* - The **thoracic sympathetic chain** provides sympathetic innervation to organs in the thoracic and abdominal cavities, influencing heart rate, bronchodilation, and visceral blood flow. - Like other sympathetic ganglia, it releases norepinephrine at target organ synapses, but it does not serve as a major endocrine gland for systemic catecholamine release.
Question 36: What is the typical resting membrane potential (RMP) of smooth muscle cells?
- A. -90 mV
- B. -70 mV
- C. -60 mV (Correct Answer)
- D. -40 mV
Explanation: ***-60 mV*** - Smooth muscle cells typically have a **resting membrane potential of -55 to -60 mV**, which is **less negative** compared to skeletal muscle (-90 mV) or neurons (-70 mV). - This relatively depolarized RMP allows them to be **more easily excited** and enables **spontaneous slow wave depolarizations** and pacemaker activity in some smooth muscle types. - The less negative potential is due to higher resting permeability to Na+ and Ca2+ compared to skeletal muscle. *-90 mV* - This is the typical resting membrane potential for **skeletal muscle cells** and **large myelinated nerve fibers**. - Such a highly negative RMP provides a **larger buffer against accidental excitation** and ensures precise voluntary control. - This value is maintained by high K+ permeability and active Na+/K+ ATPase activity. *-70 mV* - This is the characteristic resting membrane potential of **most neurons**, allowing for efficient generation and propagation of action potentials. - It represents a balance between depolarizing and hyperpolarizing influences, optimal for neuronal signaling. - This is more negative than smooth muscle but less negative than skeletal muscle. *-40 mV* - This value is **too depolarized** to be a stable resting potential for smooth muscle and would be **near threshold potential**. - At -40 mV, voltage-gated calcium channels would be significantly activated, causing sustained contraction rather than a resting state. - This might represent a **partially depolarized state** or the RMP of specialized pacemaker cells like cardiac SA node cells, but **not typical smooth muscle**.
Question 37: Which of the following statements is TRUE regarding the Bohr effect?
- A. Decreased affinity of Hb to O2 is associated with increased pH & decreased CO2
- B. Decreased affinity of Hb to O2 is associated with increased pH & CO2
- C. Decreased affinity of Hb to O2 is associated with decreased pH & increased CO2 (Correct Answer)
- D. Decreased affinity of Hb to O2 is associated with decreased pH & decreased CO2
Explanation: ***Decreased affinity of Hb to O2 is associated with decreased pH & increased CO2*** - The **Bohr effect** describes how **hemoglobin's (Hb) affinity for oxygen (O2) decreases** in the presence of increased **acidity (decreased pH)** and higher **carbon dioxide (CO2)** concentrations. - This physiological adaptation ensures that O2 is **released more readily** to tissues that are actively metabolizing (e.g., muscle during exercise), as these tissues produce more CO2 and lactic acid, leading to a drop in pH. *Decreased affinity of Hb to O2 is associated with increased pH & decreased CO2* - An **increased pH** (more alkaline) and **decreased CO2** actually **increase Hb's affinity for O2**, shifting the oxygen dissociation curve to the left. - This scenario promotes **oxygen loading** onto hemoglobin, typically occurring in the lungs rather than O2 release in the tissues. *Decreased affinity of Hb to O2 is associated with increased pH & CO2* - This statement combines an **increased pH** (which increases Hb-O2 affinity) with **increased CO2** (which decreases Hb-O2 affinity), leading to a contradictory and incorrect physiological effect based on the Bohr principle. - The net effect of an increased pH would typically dominate in terms of O2 binding. *Decreased affinity of Hb to O2 is associated with decreased pH & decreased CO2* - While **decreased pH** does reduce Hb's affinity for O2, **decreased CO2** would tend to increase it. - Therefore, this combination does not accurately represent the primary conditions that lead to a significant decrease in Hb-O2 affinity as described by the Bohr effect in active tissues.
Question 38: What is the Haldane Effect?
- A. O2 delivery by increased CO2
- B. CO2 delivery by increased CO2
- C. CO2 delivery by increased O2 (Correct Answer)
- D. O2 delivery by increased CO
Explanation: ***CO2 delivery by increased O2*** - The **Haldane effect** describes how **oxygenation of hemoglobin** decreases its affinity for **carbon dioxide (CO2)**, leading to the release of CO2 from the blood. - This is crucial in the lungs, where high oxygen levels promote CO2 unloading for exhalation. *O2 delivery by increased CO2* - This describes the **Bohr effect**, where an increase in **carbon dioxide (CO2)** or acidity in the tissues causes hemoglobin to release **oxygen (O2)**. - The Haldane effect is the converse, relating oxygen binding to CO2 release, not the other way around. *CO2 delivery by increased CO2* - This statement is inherently circular and does not describe a physiological effect. - It confuses the mechanism with the substance being transported. *O2 delivery by increased CO* - **Carbon monoxide (CO)** has a much higher affinity for hemoglobin than oxygen, forming **carboxyhemoglobin** and impairing oxygen delivery. - This is related to **carbon monoxide poisoning**, not a physiological regulatory effect like the Haldane or Bohr effects.
Question 39: What is the total surface area of the respiratory membrane in a healthy adult human?
- A. 30 m2
- B. 50 m2
- C. 75 m2 (Correct Answer)
- D. 100 m2
Explanation: ***75 m²*** - The **total surface area** of the respiratory membrane in a healthy adult human is approximately **70-80 m²**, with 75 m² being the most accurate estimate among the given options. - This large surface area is primarily attributed to the presence of approximately **300-500 million alveoli**, which are crucial for efficient gas exchange. - Modern measurements using **stereological techniques** have refined earlier estimates and established this range as the current standard. *100 m²* - This value represents an **older estimate** that has been revised downward with more accurate measurement techniques. - While historically cited in older textbooks, current physiological data supports a **smaller surface area** of approximately 70-80 m². *30 m²* - This value is significantly **underestimated** for the total respiratory membrane surface area. - Such a small surface area would result in highly **inefficient gas exchange**, leading to severe respiratory compromise and inability to meet metabolic demands. *50 m²* - While larger than 30 m², this is still an **underestimation** of the full respiratory membrane surface area. - It does not adequately account for the extensive and intricate branching of the **respiratory bronchioles** and the vast number of alveolar sacs.
Question 40: Damage to pneumotaxic center along with vagus nerve causes which type of respiration?
- A. Cheyne-Stokes breathing
- B. Deep and slow breathing
- C. Shallow and rapid breathing
- D. Apneustic breathing (Correct Answer)
Explanation: ***Apneustic breathing*** - Damage to the **pneumotaxic center** prevents the normal inhibition of inspiration, leading to **prolonged inspiratory gasps**. - **Vagal nerve damage** further removes the inhibitory feedback from the lungs, exacerbating the inspiratory "holds" characteristic of apneustic breathing. *Cheyne-Stokes breathing* - This pattern is characterized by a **crescendo-decrescendo pattern** of breathing, interspersed with periods of **apnea**. - It is often associated with conditions like **heart failure**, stroke, or severe neurological damage, not specifically the pneumotaxic center and vagus nerve. *Deep and slow breathing* - This pattern can be seen in conditions like **Kussmaul breathing** (due to metabolic acidosis) or as a compensatory mechanism. - It does not directly result from the combined damage of the **pneumotaxic center** and the **vagus nerve**. *Shallow and rapid breathing* - This pattern is commonly seen in restrictive lung diseases, anxiety, or pain, where tidal volume is decreased and respiratory rate increased. - It does not reflect the **prolonged inspiration** that would result from a compromised pneumotaxic center and vagal input.