Respiratory System — MCQs

Respiratory System Indian Medical PG Practice Questions and MCQs

Question 681: What is the primary function of the surfactant lining the alveoli?

A. Helps prevent alveolar collapse. (Correct Answer)
B. Is produced in alveolar type II cells and secreted into the alveolus.
C. Is decreased in the lungs of heavy smokers.
D. Is a phospholipid complex.

Explanation: **Explanation:** The **primary function** of pulmonary surfactant is to reduce surface tension at the air-liquid interface of the alveoli. According to the **Law of Laplace ($P = 2T/r$)**, smaller alveoli have a higher collapsing pressure. Surfactant reduces surface tension ($T$) more effectively in smaller alveoli, equalizing pressure across different-sized alveoli and **preventing alveolar collapse (atelectasis)** at the end of expiration. This increases lung compliance and decreases the work of breathing. **Analysis of Options:** * **Option A (Correct):** While all options are technically true statements regarding surfactant, the question asks for the **primary function**. Preventing collapse is the physiological purpose of its existence. * **Option B (Incorrect):** This describes the **site of synthesis**, not the function. Type II pneumocytes contain lamellar bodies that store surfactant. * **Option C (Incorrect):** This is a **clinical consequence**. Smoking decreases surfactant production/function, but it is not the primary role of the substance itself. * **Option D (Incorrect):** This describes the **biochemical composition**. Surfactant is 90% lipids (mainly Dipalmitoylphosphatidylcholine - DPPC) and 10% proteins (SP-A, B, C, D). **High-Yield NEET-PG Pearls:** 1. **Composition:** The most abundant component is **DPPC (Lecithin)**. 2. **Maturity:** Surfactant synthesis begins between **24–28 weeks** of gestation; adequate levels are reached by **35 weeks**. 3. **L/S Ratio:** A Lecithin/Sphingomyelin ratio **>2** in amniotic fluid indicates fetal lung maturity. 4. **Clinical Correlation:** Deficiency leads to **Infant Respiratory Distress Syndrome (IRDS)** or Hyaline Membrane Disease. Glucocorticoids (e.g., Betamethasone) are given to the mother to accelerate surfactant production in preterm labor.

Question 682: Which of the following ranges of hemoglobin O2 saturation from systemic venous to systemic arterial blood represents a normal resting condition?

A. 25 to 75%
B. 40 to 75%
C. 40 to 95%
D. 75 to 98% (Correct Answer)

Explanation: ### Explanation **1. Understanding the Correct Answer (D: 75 to 98%)** In a healthy resting individual, oxygen exchange occurs between the blood and tissues. * **Systemic Arterial Blood:** After passing through the lungs, hemoglobin is nearly fully saturated. Under normal physiological conditions (PaO₂ ≈ 95–100 mmHg), the saturation ($SaO_2$) is approximately **97–98%**. * **Systemic Venous Blood:** At rest, tissues extract only about 25% of the delivered oxygen. This leaves the remaining **75%** of hemoglobin saturated with oxygen ($SvO_2$) as it returns to the right heart (corresponding to a $PvO_2$ of approximately 40 mmHg). Therefore, the transition from venous to arterial blood represents a rise from **75% to 98%**. **2. Analysis of Incorrect Options** * **A & B (25% to 75%):** A venous saturation of 25–40% is seen during **strenuous exercise** or shock states where tissue oxygen extraction is significantly increased. It is not a "resting" value. * **C (40% to 95%):** While 95% is a plausible arterial saturation, 40% represents the partial pressure of oxygen ($PvO_2$) in venous blood, not the percentage saturation. Confusing $PO_2$ values with saturation percentages is a common distractor in NEET-PG. **3. NEET-PG High-Yield Pearls** * **P50 Value:** The $PO_2$ at which hemoglobin is 50% saturated is **26.7 mmHg**. * **Oxygen Extraction Ratio (OER):** At rest, OER is ~25%. During maximal exercise, it can rise to 75–85%. * **Sigmoid Shape:** The S-shape of the Oxyhemoglobin Dissociation Curve (ODC) ensures that even if arterial $PO_2$ drops from 100 to 60 mmHg, saturation remains relatively high (>90%). * **Venous Reserve:** The 75% saturation in venous blood acts as an "oxygen reservoir" that can be tapped into during periods of increased demand.

Question 683: Damage to the lower pons, leaving the upper pons intact, will result in what change to breathing pattern?

A. Apneusis
B. Rapid, shallow breathing (Correct Answer)
C. Irregular, gasping type of breathing
D. No change in breathing pattern

Explanation: ### Explanation The regulation of respiration is controlled by the respiratory centers in the brainstem. To understand the effect of lesions, we must look at the interaction between the **Pneumotaxic center** (upper pons) and the **Apneustic center** (lower pons). **Why "Rapid, shallow breathing" is correct:** The **Pneumotaxic center** (located in the Nucleus Parabrachialis of the upper pons) acts as an "off-switch" for inspiration. It limits the duration of inspiration, thereby increasing the respiratory rate. When the **lower pons is damaged** but the upper pons remains intact, the inhibitory influence of the Apneustic center is removed, and the Pneumotaxic center functions unopposed. This results in a shortened inspiratory phase, leading to a **rapid and shallow breathing pattern**. **Analysis of Incorrect Options:** * **A. Apneusis:** This is characterized by prolonged inspiratory gasps. It occurs only when the **upper pons (Pneumotaxic center) is damaged** while the lower pons (Apneustic center) and Vagus nerve are intact. * **C. Irregular, gasping breathing:** This (Ataxic breathing) typically occurs with lesions in the **Medulla**, where the rhythm-generating neurons (Pre-Bötzinger complex) are located. * **D. No change:** Any brainstem lesion between the pons and medulla significantly alters the automaticity and rhythm of respiration. **High-Yield Clinical Pearls for NEET-PG:** * **Pneumotaxic Center:** Limits inspiration (increases rate). * **Apneustic Center:** Prolongs inspiration (decreases rate). * **Vagus Nerve Interaction:** If both the Pneumotaxic center and the Vagus nerves are severed, the breath is held in the inspiratory position (**Apneustic breathing**). * **Pre-Bötzinger Complex:** The "Pacemaker" of respiration located in the medulla.

Question 684: Which of the following are true after 28 weeks of gestation?

A. Viable (Correct Answer)
B. > 1000 gm
C. Lecithin/Sphingomyelin ratio > 2
D. Type II pneumocytes present

Explanation: **Explanation:** The correct answer is **A (Viable)**. In clinical neonatology and forensic medicine, **28 weeks of gestation** is traditionally considered the threshold of **viability**. At this stage, the lungs have developed sufficiently (entering the saccular stage) to allow for gas exchange, and the central nervous system is mature enough to direct rhythmic breathing movements, giving the fetus a reasonable chance of survival outside the womb with neonatal intensive care. **Analysis of Options:** * **A. Viable:** Correct. While modern NICUs can save infants at 24 weeks, 28 weeks remains the standard benchmark for viability in many medical-legal contexts and textbooks. * **B. > 1000 gm:** Incorrect. While many 28-week fetuses approach this weight, the average weight at 28 weeks is approximately **1000 to 1100 grams**. However, weight is a variable growth parameter, whereas "viability" is a developmental milestone. * **C. L/S Ratio > 2:** Incorrect. An **L/S ratio > 2** typically indicates mature lungs and is usually achieved around **34–35 weeks** of gestation. At 28 weeks, the ratio is generally much lower, indicating a high risk of Respiratory Distress Syndrome (RDS). * **D. Type II Pneumocytes present:** Incorrect as a specific marker for 28 weeks. Type II pneumocytes (which produce surfactant) actually appear much earlier, around **20–24 weeks** of gestation. **Clinical Pearls for NEET-PG:** * **Surfactant production** begins at 20 weeks but reaches adequate levels for independent breathing only after 34 weeks. * **Glucocorticoids** (Betamethasone/Dexamethasone) are administered to the mother if preterm birth is expected before 34 weeks to accelerate surfactant production. * **Stages of Lung Development:** Embryonic → Pseudoglandular → Canalicular (16-26 wks) → Saccular (26 wks to birth) → Alveolar (Postnatal).

Question 685: What is the term for air forced or sucked into the connective tissue and facial spaces?

A. Empyema
B. Asphyxia
C. Emphysema (Correct Answer)
D. Aspiration

Explanation: ### Explanation **Correct Answer: C. Emphysema** The term **Emphysema** is derived from the Greek word *emphysan*, meaning "to inflate." In a general pathological sense, it refers to the abnormal presence of air within body tissues. While most commonly associated with **Pulmonary Emphysema** (permanent enlargement of air spaces distal to terminal bronchioles), the term also encompasses **Interstitial/Subcutaneous Emphysema**. This occurs when air is forced out of the airways (due to trauma, mechanical ventilation, or rupture of alveoli) and tracks into the connective tissue septa of the lungs, the mediastinum, and eventually the fascial planes of the neck and face. **Analysis of Incorrect Options:** * **A. Empyema:** This refers to a collection of **pus** within a naturally existing anatomical cavity, most commonly the pleural space (*Empyema thoracis*). It is an inflammatory exudate, not air. * **B. Asphyxia:** This is a condition of deficient supply of oxygen to the body which arises from abnormal breathing. It involves the combination of **hypoxia and hypercapnia** due to airway obstruction or lack of oxygen in the environment. * **C. Aspiration:** This is the accidental inhalation of foreign material (such as food, liquids, or gastric contents) into the subglottic airway or lungs. **High-Yield Clinical Pearls for NEET-PG:** * **Subcutaneous Emphysema:** Characterized clinically by **crepitus** (a crackling sensation like "Rice Krispies") upon palpation of the skin. * **Hamman’s Sign:** A crunching sound heard over the precordium synchronous with the heartbeat, indicative of **pneumomediastinum** (interstitial emphysema in the mediastinum). * **Radiological Sign:** On X-ray, interstitial emphysema appears as linear lucencies outlining tissue planes or major vessels (e.g., the "continuous diaphragm sign").

Question 686: Which of the following best describes the volume of air in the lung after normal expiration?

A. Maximal inspiration
B. Maximal expiration
C. Normal inspiration
D. Normal expiration (Correct Answer)

Explanation: ### Explanation The volume of air remaining in the lungs after a **normal (tidal) expiration** is known as the **Functional Residual Capacity (FRC)**. **1. Why the Correct Answer is Right:** The FRC represents the equilibrium point of the respiratory system. At the end of a normal breath out, the inward elastic recoil of the lungs is exactly balanced by the outward chest wall recoil. It is the sum of the **Expiratory Reserve Volume (ERV)** and the **Residual Volume (RV)**. This "buffer" volume is crucial because it prevents lung collapse and ensures continuous gas exchange between breaths, preventing large fluctuations in arterial blood gas levels. **2. Analysis of Incorrect Options:** * **A. Maximal Inspiration:** The volume of air in the lungs after a maximal inspiratory effort is the **Total Lung Capacity (TLC)**. * **B. Maximal Expiration:** The volume remaining after a forceful, maximal expiration is the **Residual Volume (RV)**. This volume cannot be measured by simple spirometry. * **C. Normal Inspiration:** The volume of air in the lungs after a normal breath in is the sum of FRC and Tidal Volume (TV). **3. High-Yield Facts for NEET-PG:** * **Measurement:** FRC cannot be measured by spirometry (because it includes RV). It is measured via **Helium Dilution**, **Nitrogen Washout**, or **Body Plethysmography** (the gold standard). * **Clinical Correlation:** FRC is **decreased** in restrictive lung diseases (e.g., pulmonary fibrosis) and obesity. It is **increased** in obstructive diseases (e.g., emphysema) due to air trapping. * **Anesthesia:** FRC decreases significantly in the supine position and under general anesthesia, which can lead to atelectasis.

Question 687: What is the mechanism of hypoxemia in asthma?

A. Hypoventilation
B. Decreased diffusion
C. Shunting
D. Ventilation-perfusion mismatch (Correct Answer)

Explanation: **Explanation:** In bronchial asthma, the primary mechanism of hypoxemia is **Ventilation-Perfusion (V/Q) Mismatch**. **1. Why V/Q Mismatch is Correct:** Asthma is characterized by widespread but uneven airway obstruction due to bronchospasm, mucosal edema, and mucus plugging. This leads to some alveoli being poorly ventilated while still being perfused (Low V/Q ratio). Blood flowing through these underventilated areas remains poorly oxygenated, which, when mixed with well-oxygenated blood from normal areas, results in a decreased arterial partial pressure of oxygen ($PaO_2$). **2. Why Other Options are Incorrect:** * **Hypoventilation:** While severe, life-threatening asthma can lead to respiratory muscle fatigue and hypercapnia (increased $CO_2$), the initial and most common cause of hypoxemia in an acute attack is V/Q mismatch, not a global failure of ventilation. * **Decreased Diffusion:** This is characteristic of interstitial lung diseases (e.g., pulmonary fibrosis) or emphysema (loss of surface area). In asthma, the alveolar-capillary membrane remains intact. * **Shunting:** True shunting (V/Q = 0) occurs in conditions like pneumonia, pulmonary edema, or anatomical shunts where alveoli are completely bypassed. In asthma, ventilation is reduced but rarely zero in the affected segments. **High-Yield Clinical Pearls for NEET-PG:** * **A-a Gradient:** In asthma, the Alveolar-arterial (A-a) oxygen gradient is **increased** (due to V/Q mismatch). * **Acid-Base Status:** Most patients with an acute asthma exacerbation present with **Respiratory Alkalosis** (due to hyperventilation triggered by hypoxia). * **The "Silent" Danger:** A **normalizing $PaCO_2$** in a worsening asthma patient is a "red flag" indicating impending respiratory failure and muscle fatigue.

Question 688: The normal value of P50 on the oxyhaemoglobin dissociation curve in an adult is:

A. 1.8 kPa
B. 2.7 kPa
C. 3.6 kPa (Correct Answer)
D. 4.5 kPa

Explanation: **Explanation:** The **$P_{50}$** is a standard physiological index used to describe the affinity of hemoglobin for oxygen. It represents the partial pressure of oxygen ($PO_2$) at which hemoglobin is **50% saturated**. **1. Why 3.6 kPa is correct:** In a healthy adult, the normal $P_{50}$ value is approximately **26.6 mmHg**. To convert this value into kilopascals (kPa), we use the conversion factor: $1\text{ kPa} \approx 7.5\text{ mmHg}$. Calculation: $26.6 / 7.5 \approx \mathbf{3.6\text{ kPa}}$. This value indicates a normal affinity of hemoglobin for oxygen under standard physiological conditions (pH 7.4, Temp 37°C, $PCO_2$ 40 mmHg). **2. Analysis of Incorrect Options:** * **1.8 kPa (~13.5 mmHg):** This represents an abnormally high affinity (Left shift). This is seen in fetal hemoglobin (HbF) or carbon monoxide poisoning. * **2.7 kPa (~20 mmHg):** This is lower than the adult average, often seen in conditions that shift the curve to the left (e.g., alkalosis, hypothermia). * **4.5 kPa (~34 mmHg):** This represents a decreased affinity (Right shift), seen in conditions like high altitude, fever, or increased 2,3-BPG. **3. High-Yield Clinical Pearls for NEET-PG:** * **Right Shift (Increased $P_{50}$):** Occurs when oxygen affinity decreases, facilitating "unloading" to tissues. Causes: **CADET**, face Right! (**C**O2 increase, **A**cidosis/H+, **D**PG increase, **E**xercise, **T**emperature increase). * **Left Shift (Decreased $P_{50}$):** Occurs when oxygen affinity increases, meaning Hb "clings" to oxygen. Causes: HbF, CO poisoning, Methemoglobinemia, and the opposite of the CADET factors. * **HbF vs. HbA:** Fetal hemoglobin has a lower $P_{50}$ (approx. 19–20 mmHg) than adult hemoglobin, allowing the fetus to extract oxygen from maternal blood.

Question 689: Carbon dioxide is transported in plasma as:

A. Dissolved form
B. Carbamino compounds
C. Bicarbonate
D. All of the above (Correct Answer)

Explanation: **Explanation:** Carbon dioxide ($CO_2$) is a metabolic waste product that must be transported from the tissues to the lungs. It is carried in the blood in three distinct forms, distributed between the plasma and the red blood cells (RBCs). 1. **Bicarbonate ($HCO_3^-$):** This is the **most significant** method, accounting for approximately **70%** of total $CO_2$ transport. While the conversion primarily occurs inside RBCs (catalyzed by Carbonic Anhydrase), the resulting bicarbonate is pumped out into the **plasma** via the Chloride shift (Hamburger phenomenon). 2. **Carbamino compounds:** About **23%** of $CO_2$ binds to the amino groups of proteins. While most of this binds to hemoglobin (Carbaminohemoglobin), a small fraction binds to **plasma proteins** (like albumin). 3. **Dissolved form:** $CO_2$ is 20 times more soluble than oxygen. Approximately **7%** of $CO_2$ is transported physically dissolved in the **plasma**. **Why "All of the above" is correct:** The question asks how $CO_2$ is transported in the **plasma**. Since $CO_2$ exists in the plasma as a dissolved gas, as part of carbamino-protein complexes, and predominantly as bicarbonate ions, all three options are physiologically accurate. **High-Yield Facts for NEET-PG:** * **Haldane Effect:** Deoxygenation of blood increases its ability to carry $CO_2$. (Occurs in lungs). * **Chloride Shift (Hamburger Phenomenon):** To maintain electrical neutrality, $Cl^-$ enters the RBC as $HCO_3^-$ leaves it. * **Solubility:** $CO_2$ is ~20-25 times more soluble than $O_2$. * **Enzyme:** Carbonic Anhydrase is absent in plasma; it is found in high concentrations within RBCs.

Question 690: Cyanosis is not seen in which of the following conditions?

A. Congestive Heart Failure (CHF)
B. Chronic Obstructive Pulmonary Disease (COPD)
C. Carbon Monoxide (CO) poisoning (Correct Answer)
D. High altitude

Explanation: **Explanation:** **The Core Concept:** Cyanosis is the bluish discoloration of the skin and mucous membranes caused by an absolute concentration of **reduced (deoxygenated) hemoglobin** exceeding **5 g/dL** in the capillary blood. It depends on the dark-blue color of deoxyhemoglobin. **Why Carbon Monoxide (CO) Poisoning is the Correct Answer:** In CO poisoning, carbon monoxide binds to hemoglobin with an affinity 200–250 times greater than oxygen, forming **Carboxyhemoglobin (COHb)**. Carboxyhemoglobin has a distinctive **cherry-red color**. Because the hemoglobin is "occupied" by CO rather than being "reduced" (deoxygenated), the blood remains bright red. Therefore, despite severe tissue hypoxia, the patient appears pink or cherry-red rather than cyanotic. **Analysis of Incorrect Options:** * **CHF (Congestive Heart Failure):** Causes **Stagnant Hypoxia**. Slowed circulation allows tissues more time to extract oxygen, leading to an accumulation of reduced hemoglobin (>5 g/dL), resulting in peripheral cyanosis. * **COPD:** Causes **Hypoxic Hypoxia** due to ventilation-perfusion mismatch and defective gas exchange. This leads to increased reduced hemoglobin in arterial blood, causing central cyanosis. * **High Altitude:** The low partial pressure of environmental oxygen ($FiO_2$) leads to inadequate oxygenation of hemoglobin in the lungs, resulting in hypoxic hypoxia and cyanosis. **NEET-PG High-Yield Pearls:** 1. **Anemia Rule:** Cyanosis is difficult to see in severe anemia because the total hemoglobin may be so low that reaching 5 g/dL of *reduced* hemoglobin is nearly impossible. 2. **Polycythemia:** Patients with polycythemia develop cyanosis more easily due to high total hemoglobin levels. 3. **Methemoglobinemia:** Characterized by **"Chocolate-cyanosis"** (brownish-blue skin) and blood that appears dark/muddy. 4. **Pulse Oximetry Pitfall:** In CO poisoning, standard pulse oximeters cannot distinguish between $O_2Hb$ and $COHb$, often giving a falsely normal $SpO_2$ reading.

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