Respiratory System — MCQs

Respiratory System Indian Medical PG Practice Questions and MCQs

Question 801: Pulmonary vasoconstriction is caused by?

A. Thromboxane A2
B. Angiotensin-II
C. Hypoxia (Correct Answer)
D. Histamine

Explanation: ***Hypoxia*** - **Hypoxic pulmonary vasoconstriction** is a physiological response where the pulmonary arteries constrict in areas of low alveolar oxygen. - This shunts blood away from poorly ventilated areas of the lung to better-ventilated areas, optimizing **ventilation-perfusion matching**. *Thromboxane A2* - **Thromboxane A2** is a potent vasoconstrictor and platelet aggregator, primarily acting on systemic blood vessels and playing a role in hemostasis and thrombosis. - While it can cause some pulmonary vasoconstriction, it is not the primary physiological cause in response to low oxygen. *Histamine* - **Histamine** typically causes vasodilation in most systemic vascular beds but can cause **bronchoconstriction** in the airways and some degree of pulmonary vasoconstriction, mainly in allergic reactions. - It is not the primary physiological mediator for pulmonary vasoconstriction in response to hypoxia. *Angiotensin-II* - **Angiotensin-II** is a powerful systemic vasoconstrictor, involved in blood pressure regulation and fluid balance through the **renin-angiotensin-aldosterone system**. - Its primary role is in systemic circulation; it has a comparatively weaker effect on pulmonary vasculature compared to hypoxia.

Question 802: Which of the following groups of neurons are primarily responsible for forced breathing?

A. Pre-Botzinger complex
B. Dorsal group of neurons
C. Pneumotaxic center
D. Ventral group of neurons (Correct Answer)

Explanation: ***Ventral VRG group of neurons*** - The **Ventral Respiratory Group (VRG)** of neurons contains both inspiratory and expiratory neurons that are **inactive during quiet breathing** but become crucially active during **forced breathing**. - During **forced expiration**, the expiratory neurons within the VRG send signals to the **abdominal and internal intercostal muscles** to contract, actively expelling air. *Pre-Botzinger complex* - The Pre-Botzinger complex is widely recognized as the **pacemaker of respiration**, generating the **rhythm of breathing**. - Its primary role is in establishing the **basic respiratory rhythm**, not specifically in forced breathing. *Dorsal group of neurons* - The **Dorsal Respiratory Group (DRG)** of neurons mainly controls **inspiration** and is active during **quiet breathing**, sending impulses to the diaphragm and external intercostals. - While it initiates inspiration, it is not primarily responsible for the **active muscular contraction** seen in forced breathing. *Pneumotaxic center* - The **pneumotaxic center** (also known as the pontine respiratory group) helps to **fine-tune breathing rhythm** by inhibiting inspiration and promoting expiration. - Its main function is to prevent **over-inflation of the lungs** and ensure a smooth breathing pattern, rather than directly managing forced respiratory efforts.

Question 803: What is the primary process involved in the chloride shift?

A. Transport of bicarbonate ions out of RBCs (Correct Answer)
B. Formation of carbamino compounds in RBCs
C. Conversion of carbon dioxide to carbonic acid in RBCs
D. None of the options

Explanation: ***Transport of bicarbonate ions out of RBCs*** - The **chloride shift**, also known as the **Hamburger phenomenon**, is primarily the exchange of **bicarbonate (HCO3-) ions** out of the RBCs for **chloride (Cl-) ions** into the RBCs. - This transport occurs to maintain electrical neutrality as bicarbonate, produced from CO2, moves into the plasma for transport to the lungs. *Formation of carbamino compounds in RBCs* - The formation of **carbaminohemoglobin** occurs when CO2 binds directly to hemoglobin, which is a separate mechanism for CO2 transport. - This process does not directly involve the exchange of chloride and bicarbonate ions across the red blood cell membrane. *Conversion of carbon dioxide to carbonic acid in RBCs* - The conversion of CO2 to **carbonic acid (H2CO3)** by **carbonic anhydrase** is an initial step in CO2 transport within the RBC. - While this step precedes the chloride shift, it is not the primary process *involved* in the shift itself, which is the subsequent ion exchange. *None of the options* - This option is incorrect because the movement of bicarbonate ions out of RBCs is indeed the central event of the chloride shift.

Question 804: In which areas of the lungs can a mismatch of ventilation/perfusion ratio occur?

A. Apex only
B. Base only
C. Both apex and base (Correct Answer)
D. Neither apex nor base

Explanation: ***Both apex and base*** - Both areas have **physiological ventilation-perfusion mismatches** in normal healthy lungs due to gravitational effects on blood flow and ventilation. - In the **apex**, ventilation exceeds perfusion (V/Q ratio ~3.3, V/Q > 1), while in the **base**, perfusion exceeds ventilation (V/Q ratio ~0.6, V/Q < 1). - These regional differences are **normal findings** in upright position, not pathological conditions. *Apex only* - While the **apex** of the lung does have a V/Q mismatch (higher ventilation relative to perfusion), it is not the only area. - This option incorrectly excludes the **base** of the lung, which also experiences a physiological V/Q mismatch. *Base only* - The **base** of the lung does have a V/Q mismatch (higher perfusion relative to ventilation), but this option incorrectly excludes the **apex**. - This area receives more blood flow due to gravity, leading to a lower V/Q ratio compared to the apex. *Neither apex nor base* - This statement is incorrect as there are **physiological V/Q mismatches** present in both the apex and base of normal healthy lungs. - A perfectly matched V/Q ratio of 1.0 across the entire lung is an ideal that is not achieved in reality due to gravitational effects.

Question 805: What is the PRIMARY effect on partial pressures of gases in the alveoli with an increase in alveolar ventilation?

A. Increased partial pressure of O2 in alveoli
B. Decreased partial pressure of CO2 in alveoli (Correct Answer)
C. Increased CO2 diffusion from blood to alveoli
D. Increased O2 diffusion from alveoli to blood

Explanation: ***Decreased partial pressure of CO2 in alveoli*** - Increased alveolar ventilation leads to more frequent replacement of alveolar air, effectively "washing out" more **carbon dioxide**. - This results in a lower partial pressure of **CO2** in the alveoli, which is then reflected in arterial blood. *Increased partial pressure of O2 in alveoli* - While increased ventilation brings in more oxygen, the **partial pressure of O2** in the alveoli increases only slightly because hemoglobin is already nearly saturated with oxygen even at normal ventilation levels. - The primary impact of increased ventilation on oxygen exchange is improved diffusion into the blood rather than a significant rise in alveolar PO2. *Increased CO2 diffusion from blood to alveoli* - Increased alveolar ventilation causes a **decrease in alveolar PCO2**, which in turn enhances the **PCO2 gradient** between the blood and the alveoli. - This increased gradient drives **more CO2 diffusion** from the blood into the alveoli, allowing for greater excretion. *Increased O2 diffusion from alveoli to blood* - Increased alveolar ventilation *does* lead to **increased O2 diffusion from alveoli to blood**, as it maintains a higher partial pressure gradient for oxygen. - However, the most immediate and pronounced effect on *partial pressures within the alveoli* itself due to increased ventilation is the reduction in **PCO2**.

Question 806: When the value of V/Q is infinity, it means?

A. Dead space (Correct Answer)
B. The PO2 of alveolar air is 159mmHg and PCO2 is 0mmHg
C. Partial pressure of O2 and CO2 are equal
D. No O2 goes from alveoli to blood and no CO2 goes from blood to alveoli

Explanation: ***Dead space*** - A V/Q ratio of infinity indicates that there is **ventilation (V) without perfusion (Q)**. This represents alveolar dead space, where air enters the alveoli but no blood flow is available for gas exchange. - In this scenario, the ventilating air does not participate in gas exchange, essentially behaving like dead space in the respiratory system. *The PO2 of alveolar air is 159mmHg and PCO2 is 0mmHg* - When V/Q approaches infinity (dead space), alveolar gas composition approaches that of **inspired air**, with PO2 around 150-159 mmHg and PCO2 near 0 mmHg. - However, this describes the gas composition consequence rather than the fundamental physiological concept, which is "dead space." - Normal alveolar air (with normal V/Q) has PO2 around 100-104 mmHg and PCO2 around 40 mmHg. *Partial pressure of O2 and CO2 are equal* - The partial pressures of O2 and CO2 are **never normally equal** in the alveoli or blood; they always maintain a concentration gradient for efficient gas exchange. - When V/Q is infinite, alveolar gas tensions approach those of inspired air (high O2, very low CO2), not equal partial pressures. *No O2 goes from alveoli to blood and no CO2 goes from blood to alveoli* - While it is true that **no gas exchange occurs** (no O2 goes from alveoli to blood, and no CO2 goes from blood to alveoli) due to the absence of blood flow (Q=0), the primary physiological term for this condition is "dead space." - This option describes the consequence of an infinite V/Q ratio rather than the fundamental concept it represents.

Question 807: In forceful expiration, which of the following neurons gets fired?

A. VRG (Correct Answer)
B. DRG
C. Pneumotaxic centre
D. Chemoreceptors

Explanation: ***VRG*** - The **ventral respiratory group (VRG)** contains both inspiratory and expiratory neurons, and it is primarily involved in controlling the muscles necessary for **forceful breathing**. - During forceful expiration, the expiratory neurons in the VRG become active, stimulating accessory muscles of expiration like the **internal intercostals** and **abdominal muscles**. *DRG* - The **dorsal respiratory group (DRG)** primarily contains inspiratory neurons and is fundamental for **normal, quiet breathing**. - Its activity leads to contraction of the diaphragm and external intercostals, and it is largely inactive during quiet expiration, which is a passive process. *Pneumotaxic centre* - The **pneumotaxic center** (or pontine respiratory group) helps to fine-tune breathing patterns by **inhibiting inspiration**, thereby limiting the duration of inhalation. - It influences the rate and depth of breathing but does not directly activate muscles for forceful expiration. *Chemoreceptors* - **Chemoreceptors** (central and peripheral) monitor blood levels of **carbon dioxide (PCO2)**, **oxygen (PO2)**, and **pH**, and they send signals to the respiratory centers to adjust breathing accordingly. - While they regulate the overall respiratory drive, they do not directly fire to initiate forceful expiration; rather, they modulate the activity of the respiratory groups in the brainstem.

Question 808: What happens to gas exchange when the Va/Q ratio approaches infinity?

A. Partial pressure of O2 becomes negligible.
B. No exchange of O2 and CO2 occurs. (Correct Answer)
C. Partial pressure of CO2 becomes negligible.
D. Partial pressures of both CO2 and O2 remain normal.

Explanation: ***No exchange of O2 and CO2 occurs.*** - When the **Va/Q ratio approaches infinity**, it signifies a scenario of **ventilation without perfusion** (Q approaches zero). - This represents **alveolar dead space** - despite adequate ventilation, there is **no blood flow** to participate in gas exchange. - Therefore, **no O2 enters the blood** and **no CO2 leaves the blood**, making this the most accurate description of what happens to gas exchange. *Partial pressure of O2 becomes negligible.* - This statement is incorrect because with **no blood flow** (Q = 0), the alveolar air retains high O2 partial pressure. - O2 is being delivered via ventilation but not removed by blood, so **alveolar PO2** would approach that of **inspired air (~150 mmHg)**, not become negligible. *Partial pressure of CO2 becomes negligible.* - While this statement is technically true (alveolar PCO2 would approach zero/inspired air levels), it doesn't directly answer what happens to **gas exchange**. - With no blood flowing through the alveolus, no **CO2 from venous blood** can reach the alveolus to be excreted. - However, the question asks about **gas exchange** itself, not just partial pressures, making the first option more comprehensive. *Partial pressures of both CO2 and O2 remain normal.* - This statement is incorrect as the **Va/Q mismatch** significantly alters the partial pressures of both gases. - In infinite Va/Q scenario (dead space ventilation), **alveolar PO2 would be high** (approaching inspired air ~150 mmHg) and **alveolar PCO2 would be low** (approaching zero).

Question 809: Functional residual capacity (FRC) is defined as the volume of air remaining in the lungs at which specific moment in the respiratory cycle?

A. During active expiration
B. After normal expiration (Correct Answer)
C. At peak inspiration
D. During active inspiration

Explanation: ***After normal expiration*** - **Functional residual capacity (FRC)** is the volume of air remaining in the lungs at the end of a **normal, passive expiration**. - It represents the sum of the **expiratory reserve volume (ERV)** and the **residual volume (RV)**. *During active expiration* - **Active expiration** involves the use of accessory muscles to force more air out of the lungs than during normal expiration. - This process would result in a lung volume less than FRC, closer to the **residual volume**. *At peak inspiration* - **Peak inspiration** represents the total lung capacity (TLC), which is the maximum volume of air the lungs can hold after a maximal inspiratory effort. - This is the largest lung volume, significantly greater than FRC. *During active inspiration* - **Active inspiration** is the process of inhaling air, which increases lung volume. - FRC is a static volume measured at the end of expiration, not during the dynamic process of inhaling.

Question 810: With increase in age, which of the following statements about lung function is true?

A. Fibrosis of the interstitium decreases
B. Residual volume decreases
C. Mucociliary clearance increases
D. Pulmonary compliance increases (Correct Answer)

Explanation: ***Pulmonary compliance increases*** - With **increasing age**, there is a loss of **elastic recoil** in the lungs due to changes in elastin and collagen fibers, leading to an increase in **pulmonary compliance**. - This increased compliance means the lungs become less stiff and easier to inflate, but also less able to recoil and expel air effectively. - The **net effect** of aging is increased compliance, as the loss of elastic fibers is the predominant change in normal aging. *Residual volume decreases* - **Residual volume (RV)** actually **increases** with age. This is because the loss of elastic recoil makes it harder to fully exhale, causing more air to remain in the lungs after a maximal exhalation. - An increased residual volume contributes to an overall rise in **functional residual capacity** and total lung capacity in older adults. *Mucociliary clearance increases* - **Mucociliary clearance** generally **decreases** with age. This is due to a reduction in the number and function of cilia, as well as changes in mucus quality. - Impaired mucociliary clearance makes older individuals more susceptible to respiratory infections and difficulties in clearing secretions. *Fibrosis of the interstitium decreases* - The **fibrosis of the interstitium** can **increase** with age in some individuals. However, in normal aging (without pathological conditions), the predominant change is loss of elastic recoil rather than significant fibrotic changes. - When present, increased interstitial fibrosis would make the lungs stiffer, but this is not the primary age-related change in healthy individuals.

Practice by Chapter

Mechanics of Breathing

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Pulmonary Ventilation

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Pulmonary Circulation

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Gas Exchange in the Lungs

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Oxygen and Carbon Dioxide Transport

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Control of Breathing

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Respiratory Adjustments in Health and Disease

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High Altitude Physiology

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Diving Physiology

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Respiratory Function Tests

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