Respiratory System — MCQs

Respiratory System Indian Medical PG Practice Questions and MCQs

Question 871: Damage to the pneumotaxic center will cause?

A. Apneusis (Correct Answer)
B. Apnea
C. Faster breathing with lesser tidal volume
D. Slower breathing with greater tidal volume

Explanation: ***Apneusis*** - The **pneumotaxic center** (located in the upper pons) functions to **limit and terminate inspiration** by inhibiting the apneustic center in the lower pons. - When the pneumotaxic center is damaged, the **apneustic center becomes unopposed**, resulting in prolonged, sustained inspiratory gasps with brief expiratory phases. - This characteristic breathing pattern is called **apneusis**, which is the classic result of pneumotaxic center damage. - Reference: **Guyton and Hall Textbook of Medical Physiology** - the pneumotaxic center provides the "off-switch" for inspiration; without it, apneusis develops. *Apnea* - **Apnea** refers to complete cessation of breathing. - This would require damage to the **medullary respiratory centers** (dorsal and ventral respiratory groups), not the pneumotaxic center. - Pneumotaxic center damage alters the breathing pattern but does not stop breathing entirely. *Faster breathing with lesser tidal volume* - This would occur if inspiration were shortened and respiration rate increased. - Pneumotaxic center damage has the **opposite effect** - it prolongs inspiration rather than shortening it. *Slower breathing with greater tidal volume* - While prolonged inspiration in apneusis may result in increased tidal volume, this description is **incomplete and imprecise**. - The hallmark finding is **apneusis** (prolonged inspiratory gasps), not simply "slower, deeper breathing." - This option misses the characteristic pathological breathing pattern that defines pneumotaxic center damage.

Question 872: Which of the following factors increases the resistance of the airways?

A. Inhaling cigarette smoke (Correct Answer)
B. Increasing lung volume
C. Increased sympathetic stimulation
D. Going to high altitude

Explanation: ***Inhaling cigarette smoke*** - **Cigarette smoke** causes irritation and inflammation of the airways, leading to **bronchoconstriction** and increased mucus production. These effects directly narrow the airway lumen, increasing resistance. - Exposure to irritants like cigarette smoke triggers reflex mechanisms that constrict **smooth muscle** in the bronchioles, reducing their diameter and thereby increasing the **resistance to airflow**. *Increasing lung volume* - As **lung volume** increases, the radial traction exerted on the airways by the surrounding parenchyma also increases. This traction tends to **widen the airways**, thereby decreasing resistance. - At higher lung volumes, the airways are stretched open, which reduces the **frictional forces** and improves airflow, leading to lower resistance. *Increased sympathetic stimulation* - **Sympathetic stimulation** (via beta-2 adrenergic receptors) causes **bronchodilation**, which involves the relaxation of smooth muscle in the airways. - This relaxation leads to a **widening of the airways**, thereby decreasing the resistance to airflow and facilitating easier breathing. *Going to high altitude* - Moving to **high altitude** primarily affects the **partial pressure of oxygen** and overall atmospheric pressure, but it does **not directly increase airway resistance**. - While high altitude can lead to changes in breathing patterns (e.g., hyperventilation), it does not directly cause narrowing of the airways or increased frictional forces within the respiratory tree.

Question 873: What is the primary cause of stridor?

A. Obstruction of the airway below the vocal cords
B. Obstruction of the airway above the vocal cords
C. Obstruction of the airway above the trachea
D. Obstruction of the airway at the level of the vocal cords (Correct Answer)

Explanation: ***Obstruction of the airway at the level of the vocal cords*** - Stridor is a **high-pitched** breath sound resulting from turbulent airflow through a **narrowed upper airway**. - **Glottic obstruction** (at the vocal cord level) is the **classic cause** of stridor, producing the characteristic inspiratory sound from conditions like **laryngospasm**, **vocal cord paralysis**, or **laryngeal foreign bodies**. - The **vocal cords** represent the narrowest point of the adult upper airway, making this level particularly prone to producing audible turbulent flow. *Obstruction of the airway below the vocal cords* - Obstruction in the **intrathoracic trachea** or **bronchi** typically causes **wheezing** rather than stridor. - However, **subglottic obstruction** (immediately below the vocal cords but still extrathoracic) can produce stridor, especially in conditions like **croup**. - The key distinction is whether the obstruction is in the extrathoracic (stridor) or intrathoracic (wheeze) airway. *Obstruction of the airway above the vocal cords* - **Supraglottic obstruction** (epiglottitis, retropharyngeal abscess) can also cause stridor, though the quality may differ slightly. - While this can produce stridor, the **most classic** presentation occurs at the glottic (vocal cord) level due to the critical narrowing at this point. - Severe pharyngeal obstruction may produce **stertor** (low-pitched snoring), but acute supraglottic pathology typically causes stridor. *Obstruction of the airway above the trachea* - This is a **non-specific term** encompassing both supraglottic and glottic regions. - While technically correct that stridor occurs "above the trachea," this lacks the anatomical precision needed to identify the **classic level** of obstruction at the vocal cords.

Question 874: Which of the following does NOT cause hyperventilation?

A. Decreased pH in CSF
B. CO poisoning (Correct Answer)
C. Increased adrenergic levels
D. Decreased plasma HCO3

Explanation: ***CO poisoning*** - **Carbon monoxide (CO)** binds to **hemoglobin** with a much higher affinity than oxygen, forming **carboxyhemoglobin**. This reduces the oxygen-carrying capacity of blood and shifts the **oxygen-hemoglobin dissociation curve to the left**, impairing oxygen release to tissues. - While it causes **tissue hypoxia**, CO poisoning does **not stimulate chemoreceptors** to induce hyperventilation because it does not significantly alter the **partial pressure of oxygen (PO2)** in the arterial blood, which is what peripheral chemoreceptors primarily respond to. Additionally, it does not directly increase **acidosis** that would stimulate central chemoreceptors. *Decreased pH in CSF* - A **decreased pH in the cerebrospinal fluid (CSF)** indicates an increase in **H+ ions**, which directly stimulates the **central chemoreceptors** located in the medulla oblongata. - This stimulation leads to an increased respiratory drive, resulting in **hyperventilation** to "blow off" more CO2 and thus normalize the CSF pH. *Increased adrenergic levels* - Elevated **adrenergic levels**, such as during stress, fear, or anxiety, stimulate the **respiratory center** in the brainstem. - This stimulation can lead to an increased rate and depth of breathing, causing **hyperventilation**. *Decreased plasma HCO3* - A **decrease in plasma bicarbonate (HCO3-)** is characteristic of **metabolic acidosis**. - To compensate for the metabolic acidosis, the body will **increase ventilation (hyperventilate)** to decrease the partial pressure of CO2 (PCO2), thereby raising the blood pH back towards normal.

Question 875: Which of the following stimulates peripheral chemoreceptors?

A. Acidosis
B. Low perfusion pressure
C. Hypoxia (Correct Answer)
D. Hypocapnia

Explanation: ***Hypoxia*** - Peripheral chemoreceptors, particularly the **carotid and aortic bodies**, are most sensitive to decreases in arterial **partial pressure of oxygen (PaO2)**. - **Hypoxia is the PRIMARY and MOST POTENT stimulus** for peripheral chemoreceptors, causing a dramatic increase in ventilation when PaO2 falls below 60 mmHg. - Among all stimuli, hypoxia produces the strongest response from peripheral chemoreceptors. *Acidosis* - **Acidosis does stimulate peripheral chemoreceptors**, but its effect is **much weaker** compared to hypoxia. - Peripheral chemoreceptors respond to decreased pH (H+ ions), but this is a **secondary stimulus**. - The effect of acidosis is **potentiated in the presence of hypoxia** (synergistic effect), but alone it produces a modest response. - When both options are present, **hypoxia is the correct answer** as the primary stimulus. *Hypocapnia* - **Hypocapnia** (low CO2 levels) **inhibits peripheral chemoreceptor activity** and reduces their sensitivity to other stimuli. - This acts as a respiratory depressant rather than a stimulant. - Note: **Hypercapnia** (elevated CO2) does stimulate peripheral chemoreceptors, but hypocapnia does not. *Low perfusion pressure* - **Low perfusion pressure** (hypotension) does not directly stimulate peripheral chemoreceptors. - Chemoreceptors respond to chemical stimuli (O2, CO2, pH), not mechanical pressure changes. - While severe hypotension can lead to tissue hypoxia, it is the resulting **hypoxia** that stimulates the chemoreceptors, not the pressure change itself.

Question 876: Which of the following lung volumes remains unchanged during pregnancy?

A. Total Lung Capacity (Correct Answer)
B. Tidal Volume
C. Functional Residual Capacity
D. Inspiratory Capacity

Explanation: ***Total Lung Capacity*** - The **total lung capacity (TLC)** represents the total volume of air the lungs can hold after a maximum inspiration and remains largely **unchanged** during pregnancy due to opposing physiological shifts. - While other lung volumes are affected by mechanical compression from the gravid uterus and hormonal changes, the **increase in inspiratory capacity** often balances the **decrease in functional residual capacity**, leading to a relatively stable TLC. *Functional Residual Capacity* - **Functional Residual Capacity (FRC)**, the volume of air remaining in the lungs after a normal expiration, **decreases significantly** during pregnancy due to the upward displacement of the diaphragm by the enlarging uterus. - This **reduction in FRC** makes pregnant individuals more susceptible to hypoxemia during periods of apnea or hypoventilation. *Inspiratory Capacity* - **Inspiratory Capacity (IC)**, the maximum volume of air that can be inhaled from the end-expiratory position, typically **increases during pregnancy**. - This increase is primarily due to a **higher tidal volume** and an enhanced ability to expand the chest wall. *Tidal Volume* - **Tidal Volume (TV)**, the amount of air inhaled or exhaled during normal breathing, **increases progressively** throughout pregnancy. - This increase is driven by **progesterone-mediated stimulation** of the respiratory center, leading to increased minute ventilation despite a relatively constant respiratory rate.

Question 877: The transport of CO2 in the blood is primarily influenced by which of the following factors?

A. Binding to hemoglobin as carbaminohemoglobin
B. Conversion to bicarbonate ions by carbonic anhydrase (Correct Answer)
C. Transport as carbonic acid in red blood cells
D. Direct dissolution in blood plasma

Explanation: ***Conversion to bicarbonate ions by carbonic anhydrase*** - This is the **primary mechanism** for CO2 transport, accounting for approximately **70%** of total CO2 transport in blood. - Inside red blood cells, CO2 combines with water to form carbonic acid (H2CO3), catalyzed by the enzyme **carbonic anhydrase**. - Carbonic acid **immediately dissociates** into hydrogen ions (H+) and **bicarbonate ions (HCO3-)**. - Bicarbonate ions then diffuse into plasma in exchange for chloride ions (chloride shift), making this the most quantitatively significant transport mechanism. - **Carbonic anhydrase** is the key enzyme that influences this process by accelerating the reaction by approximately **5000-fold**. *Binding to hemoglobin as carbaminohemoglobin* - Approximately **20-23%** of CO2 is transported by directly binding to amino groups on hemoglobin to form **carbaminohemoglobin**. - This is significant but less than bicarbonate transport. - Deoxygenated hemoglobin binds CO2 more readily than oxygenated hemoglobin (Haldane effect). *Transport as carbonic acid in red blood cells* - This is **not correct** because carbonic acid (H2CO3) is only a **transient intermediate** that exists momentarily. - It immediately dissociates into H+ and HCO3-, so CO2 is not actually transported "as carbonic acid" but rather as **bicarbonate ions**. - The carbonic acid step is part of the mechanism, but bicarbonate is the actual transport form. *Direct dissolution in blood plasma* - Only about **7-10%** of CO2 is transported dissolved directly in plasma. - CO2 has limited solubility in plasma, making this the least significant mechanism. - This dissolved CO2 contributes to the partial pressure of CO2 (PCO2) in blood.

Question 878: Which of the following statements about the Hering-Breuer inflation reflex is false?

A. Is mediated by vagal afferents from pulmonary stretch receptors.
B. Involves stimulation of the inspiratory center.
C. Protects against underinflation of the lungs. (Correct Answer)
D. Inhibits further inspiration when lung inflation is excessive.

Explanation: ***Protects against underinflation of the lungs.*** - The **Hering-Breuer inflation reflex** is activated by **stretch receptors** in the lungs during excessive inspiration, preventing overinflation. - Its primary role is to protect against **overinflation**, not underinflation, by terminating inspiration prematurely when lungs are excessively inflated. *Is mediated by vagal afferents from pulmonary stretch receptors.* - This statement is **true** and correctly describes the neural pathway of the reflex. - **Pulmonary stretch receptors** detect lung inflation and send signals via **vagal afferents** (vagus nerve) to the respiratory centers in the medulla oblongata. *Involves stimulation of the inspiratory center.* - The Hering-Breuer reflex is a **protective reflex** that is *inhibitory* to the inspiratory center, not stimulatory. - It works by sending signals via the **vagus nerve** to *inhibit* inspiratory neurons in the **medulla oblongata** when stretch receptors in the lungs are activated during excessive inflation. *Inhibits further inspiration when lung inflation is excessive.* - This statement is **true** and describes the key function of the reflex, which is to prevent overexpansion of the lungs. - When lung volume increases significantly, **stretch receptors** are activated, sending signals that *inhibit* the inspiratory effort and promote expiration.

Question 879: What is the definition of dry drowning?

A. Drowning in salt water
B. Drowning with minimal water aspiration
C. Drowning due to laryngospasm (Correct Answer)
D. Drowning in cold water with hypothermia

Explanation: ***Drowning due to laryngospasm*** - **Dry drowning** specifically refers to drowning events where there is little to no water found in the lungs, typically due to **laryngospasm**. - This reflex closure of the vocal cords prevents water from entering the trachea and lungs, leading to **asphyxia**. *Drowning in salt water* - This describes the **type of water** involved in the drowning, not a specific physiological mechanism like "dry drowning." - **Saltwater drowning** can cause acute respiratory distress syndrome (ARDS) and pulmonary edema due to osmotic shifts. *Drowning with minimal water aspiration* - While dry drowning involves minimal water aspiration, this choice is less precise as the **cause** of the minimal aspiration is the crucial factor. - The mechanism distinguishing dry drowning is the **laryngospasm**, not just the amount of aspirated water. *Drowning in cold water with hypothermia* - This scenario describes **cold-water immersion** complications, which can include hypothermia and a preserved diving reflex. - While it has distinct physiological effects, it is not the definition of **dry drowning** but rather a broader category of drowning incidents.

Question 880: In inspiration, the intrapleural pressure becomes:

A. More positive
B. Same as expiratory level
C. Initially positive then negative
D. More negative (Correct Answer)

Explanation: ***More negative*** - During inspiration, the **diaphragm contracts** and moves downwards, and the **external intercostal muscles contract**, pulling the rib cage upwards and outwards. - This increases the volume of the thoracic cavity, causing the intrapleural pressure to become **more negative** (i.e., further below atmospheric pressure), which in turn pulls the lungs outward and causes air to flow in. *More positive* - An increase in intrapleural pressure beyond atmospheric pressure (**positive**) would lead to lung collapse or prevent air from entering the lungs. - Positive intrapleural pressure is typically observed during **forced expiration** or in pathological conditions like **pneumothorax**. *Same as expiratory level* - Intrapleural pressure **changes dynamically** throughout the respiratory cycle, becoming more negative during inspiration and less negative (closer to atmospheric pressure) during expiration. - Maintaining the same pressure level would imply no change in lung volume, which is inconsistent with the process of breathing. *Initially positive then negative* - The intrapleural pressure is always **subatmospheric** (negative) during normal breathing due to the elastic recoil of the lungs pulling inward and the chest wall pulling outward. - A transient positive pressure followed by negative pressure is not characteristic of normal inspiration.

Practice by Chapter

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Pulmonary Circulation

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Control of Breathing

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High Altitude Physiology

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