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?
What is the normal transpulmonary pressure during quiet breathing?
What is the partial pressure for oxygen in the inspired air?
Isocapnic buffering is?
Vital capacity is measured by:
In patients with emphysematous bullae, total lung volume is best determined by?
NEET-PG 2015 - Physiology NEET-PG Practice Questions and MCQs
Question 51: 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 52: 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 53: 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 54: 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 55: 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.
Question 56: What is the normal transpulmonary pressure during quiet breathing?
- A. 0 to + 1 cm H2O
- B. 0 to -1 cm H2O
- C. +5 to +8 cm H2O (Correct Answer)
- D. - 8 to - 5 cm H2O
Explanation: ***+5 to +8 cm H2O*** - Transpulmonary pressure (P_tp) is the **difference between alveolar pressure and pleural pressure** (P_alv - P_pl). - During quiet breathing at **functional residual capacity (FRC)**, alveolar pressure is **0 cm H2O** (atmospheric) while pleural pressure is approximately **-5 cm H2O**, giving P_tp = **+5 cm H2O**. - At end-inspiration during quiet breathing, pleural pressure becomes more negative (**-8 cm H2O**) while alveolar pressure remains near atmospheric, resulting in P_tp ≈ **+8 cm H2O**. - This positive transpulmonary pressure gradient is essential to **keep the lungs inflated** against elastic recoil and prevent **atelectasis**. *0 to +1 cm H2O* - This pressure is far too low to maintain lung inflation against elastic recoil forces. - Normal transpulmonary pressure must be several cm H2O positive to counterbalance the lung's tendency to collapse. - This value would result in **near-complete lung collapse**. *0 to -1 cm H2O* - A negative or zero transpulmonary pressure would mean pleural pressure equals or exceeds alveolar pressure. - This condition would cause **immediate lung collapse (pneumothorax)** as there would be no pressure gradient to keep the lungs expanded. *-8 to -5 cm H2O* - This range represents **pleural pressure**, not transpulmonary pressure. - Pleural pressure is indeed -5 to -8 cm H2O during quiet breathing, but transpulmonary pressure is calculated as the difference between alveolar and pleural pressures. - Confusing pleural pressure with transpulmonary pressure is a common error.
Question 57: What is the partial pressure for oxygen in the inspired air?
- A. 158 mm Hg (Correct Answer)
- B. 116 mm Hg
- C. 0.3 mm Hg
- D. 100 mm Hg
Explanation: ***158 mm Hg*** - The partial pressure of oxygen in inspired air (PIO2) is calculated by multiplying the **fraction of inspired oxygen (FiO2)** by the total atmospheric pressure. - At sea level, atmospheric pressure is approximately **760 mm Hg** and FiO2 is 21% (0.21), so 0.21 × 760 mm Hg = **159.6 mm Hg**, which rounds to 158 mm Hg. - This represents **dry atmospheric air** before it enters the respiratory tract. *116 mm Hg* - This value does not correspond to a standard physiological measurement in respiratory physiology. - It is lower than inspired air PO2 but higher than alveolar PO2, making it an intermediate value used as a distractor. - **Humidified tracheal air** has PO2 of approximately 150 mm Hg: (760-47) × 0.21 = 149.7 mm Hg, where 47 mm Hg is water vapor pressure. *0.3 mm Hg* - This value is extremely low and represents the approximate **partial pressure of oxygen in mixed venous blood**, not inspired air. - Such a low value in inspired air would indicate **severe hypoxia** incompatible with life. - This is used as an unrealistic distractor. *100 mm Hg* - This value represents the approximate **partial pressure of oxygen in alveolar air (PAO2) and arterial blood (PaO2)**. - It is lower than inspired air due to humidification, mixing with residual air, and continuous oxygen uptake by blood. - It does not represent the partial pressure of oxygen in the inspired atmospheric air.
Question 58: Isocapnic buffering is?
- A. None of the options
- B. Increased pCO2 with increased CO2
- C. Increased pCO2 with decreased CO2
- D. Normal pCO2 with increased CO2 (Correct Answer)
Explanation: ***Normal pCO2 with increased CO2*** - Isocapnic buffering refers to the process where the body buffers an **increase in lactic acid** or other metabolic acids without a significant change (maintaining it within a normal range) in **arterial partial pressure of carbon dioxide (pCO2)**. - This is achieved by an increase in **ventilation** stimulated by the acid, which expels more CO2 to compensate for the additional CO2 produced from the buffering reaction, thereby keeping pCO2 stable. *Increased pCO2 with increased CO2* - This scenario would indicate **hypoventilation** or a failure of the respiratory compensation mechanism to maintain pCO2 within normal limits during an increased metabolic CO2 load. - **Increased pCO2** would signify a state of **respiratory acidosis** or inadequate respiratory compensation, not isocapnic buffering. *Increased pCO2 with decreased CO2* - This statement is inherently contradictory; it is not possible to have an **increased pCO2** simultaneously with **decreased CO2** in the context of buffering. - **pCO2** is a measure of the partial pressure of carbon dioxide, directly related to the amount of CO2 present and dissolved in the blood. *None of the options* - This option is incorrect because "Normal pCO2 with increased CO2" accurately describes the physiological phenomenon of **isocapnic buffering**.
Question 59: Vital capacity is measured by:
- A. Plethysmography
- B. Nitrogen washout technique
- C. Spirometer (Correct Answer)
- D. Gas-dilution method
Explanation: ***Spirometer*** - A **spirometer** is a device used to measure lung volumes and capacities, including **vital capacity**. - It measures the volume of air inspired and expired by evaluating mechanical changes in the volume of air in the lungs. *Plethysmography* - **Plethysmography** is primarily used to measure **residual volume** and **total lung capacity**, not vital capacity directly. - This method measures changes in body volume to infer changes in lung volume. *Gas-dilution method* - The **gas-dilution method**, typically using helium, is used to measure the **functional residual capacity (FRC)** and subsequently calculate residual volume and total lung capacity. - It involves rebreathing a known concentration of gas to determine the volume of gas already in the lungs. *Nitrogen washout technique* - The **nitrogen washout technique** is also used to measure **functional residual capacity (FRC)** and detect uneven ventilation. - It involves breathing 100% oxygen to wash out all nitrogen from the lungs, allowing for calculation of lung volumes.
Question 60: In patients with emphysematous bullae, total lung volume is best determined by?
- A. Spirometry
- B. Any of the above
- C. Helium dilution method
- D. Plethysmography (Correct Answer)
Explanation: ***Plethysmography*** - This method accurately measures **total lung capacity (TLC)**, functional residual capacity (FRC), and residual volume (RV) by determining the **volume of gas in the thorax**. - It is particularly useful in conditions like **emphysema** with air trapping and bullae, as it accounts for **non-communicating air spaces** that other methods miss. *Spirometry* - Spirometry measures volumes of air that can be **exhaled or inhaled forcibly**, such as FVC and FEV1. - It cannot measure residual volume (RV) or total lung capacity (TLC) directly, especially in cases of **air trapping** where trapped air cannot be exhaled. *Helium dilution method* - The helium dilution method measures **communicating lung volumes**, like functional residual capacity (FRC), by assessing the dilution of a known concentration of helium after rebreathing. - In conditions with **emphysematous bullae** and air trapping, it **underestimates total lung volume** because it cannot measure air in non-communicating or poorly communicating spaces. *Any of the above* - Only plethysmography can accurately measure total lung volume in the presence of **emphysematous bullae** due to its ability to measure both communicating and non-communicating air spaces. - Spirometry and helium dilution methods would provide **inaccurate or incomplete measurements** in this clinical scenario.