Respiratory System Practice Questions

Q: If at the beginning of inspiration, pulmonary compliance is 0.2 L/cm H2O and the initial trans-pulmonary pressure is 5 cm H2O, what will be the transpulmonary pressure after inhaling 600 mL of air?

8 cm H2O. ### Explanation **1. Understanding the Correct Answer (C: 8 cm H2O)** The core concept here is the relationship between **Pulmonary Compliance ($C$)**, **Volume change ($\Delta V$)**, and **Pressure change ($\Delta P$)**. Compliance is defined as the change in lung volume per unit change in transpulmonary pressure: $$C = \frac{\Delta V}{\Delta P}$$ To find the new transpulmonary pressure, we first calculate the change in pressure ($\Delta P$) required to inhale 600 mL (0.6 L) of air: * **Given:** $C = 0.2 \text{ L/cm H}_2\text{O}$; $\Delta V = 0.6 \text{ L}$ * **Formula:** $\Delta P = \frac{\Delta V}{C}$ * **Calculation:** $\Delta P = \frac{0.6}{0.2} = 3 \text{ cm H}_2\text{O}$ The transpulmonary pressure ($P_{tp}$) must **increase** to expand the lungs. * **Final $P_{tp}$** = Initial $P_{tp}$ + $\Delta P$ * **Final $P_{tp}$** = $5 \text{ cm H}_2\text{O} + 3 \text{ cm H}_2\text{O} = \mathbf{8 \text{ cm H}_2\text{O}}$. **2. Why Other Options are Incorrect** * **Option A (4 cm H2O):** This suggests a decrease in pressure, which occurs during expiration, not inspiration. * **Option B (7 cm H2O):** This would be the result if the tidal volume was only 400 mL ($0.2 \times 2 = 0.4$). * **Option D (9 cm H2O):** This would imply a lower compliance (0.15 L/cm H2O) or a higher inhaled volume (800 mL). **3. Clinical Pearls & High-Yield Facts** * **Transpulmonary Pressure ($P_{tp}$):** It is the difference between Alveolar pressure ($P_{alv}$) and Intrapleural pressure ($P_{ip}$). It is always positive under normal physiological conditions to keep the lungs inflated. * **Compliance Trends:** * **Decreased Compliance:** Seen in Pulmonary Fibrosis, ARDS, and Pulmonary Edema (lungs are "stiff"). * **Increased Compliance:** Seen in Emphysema (loss of elastic recoil) and with aging. * **Specific Compliance:** Compliance divided by Functional Residual Capacity (FRC); used to compare lungs of different sizes.

Q: Diffusion capacity for carbon monoxide is decreased in all of the following conditions EXCEPT:

Chronic Bronchitis. **Explanation:** The **Diffusion Capacity of the Lung for Carbon Monoxide (DLCO)** measures the ability of the lungs to transfer gas from inhaled air to the red blood cells in pulmonary capillaries. It depends on three main factors: the surface area of the blood-gas barrier, the thickness of the alveolar-capillary membrane, and the pulmonary capillary blood volume. **Why Chronic Bronchitis is the Correct Answer:** In **Chronic Bronchitis**, the primary pathology involves inflammation of the airways and mucus hypersecretion. Crucially, the **alveolar-capillary unit remains intact**, and there is no significant destruction of the alveolar walls. Therefore, the DLCO remains **normal** (or occasionally slightly increased). This is a key physiological differentiator between Chronic Bronchitis ("Blue Bloaters") and Emphysema. **Why the other options are incorrect:** * **Emphysema:** Characterized by the destruction of alveolar walls, leading to a permanent increase in air space size. This significantly **reduces the surface area** available for gas exchange, thus decreasing DLCO. * **Interstitial Lung Disease (ILD):** Conditions like pulmonary fibrosis increase the **thickness** of the alveolar-capillary membrane, creating a barrier to diffusion and decreasing DLCO. * **Pulmonary Embolism:** This obstructs blood flow to the alveoli. Even if the alveoli are ventilated, the lack of perfusion (decreased **pulmonary capillary blood volume**) results in a drop in DLCO. **High-Yield Clinical Pearls for NEET-PG:** * **DLCO is Increased in:** Polycythemia, Alveolar hemorrhage (e.g., Goodpasture syndrome), Left-to-right shunts, and Exercise. * **DLCO is Decreased in:** Anemia, Emphysema, ILD, Pulmonary Hypertension, and Sarcoidosis. * **The "Gold Standard" Rule:** If a patient has obstructive lung disease (low FEV1/FVC), a **low DLCO points to Emphysema**, while a **normal DLCO points to Asthma or Chronic Bronchitis.**

Q: A person unacclimatized develops pulmonary edema in approximately how many days?

2-3 days. **Explanation:** The question refers to **High-Altitude Pulmonary Edema (HAPE)**, a life-threatening form of non-cardiogenic pulmonary edema that occurs in unacclimatized individuals who ascend rapidly to altitudes typically above 2,500 meters (8,000 feet). **1. Why 2-3 days is correct:** HAPE typically manifests **2 to 4 days** after arrival at high altitude. The underlying mechanism is **Hypoxic Pulmonary Vasoconstriction (HPV)**. In response to low alveolar oxygen, pulmonary arterioles constrict to divert blood to better-ventilated areas. However, at high altitudes, this constriction is global and uneven, leading to increased pulmonary capillary pressure, "stress failure" of the alveolar-capillary membrane, and subsequent leakage of fluid into the lungs. **2. Analysis of Incorrect Options:** * **6-7 days:** By this time, the initial acute phase of mountain sickness has usually either resolved through early acclimatization or progressed to severe illness. HAPE is an acute-onset condition. * **19-21 days:** This timeframe is associated with more advanced hematological adaptations, such as increased erythropoiesis (polycythemia), rather than acute edema. * **2nd-3rd month:** This duration is characteristic of **Chronic Mountain Sickness (Monge’s Disease)**, which involves pulmonary hypertension and right heart failure due to long-term exposure, not acute pulmonary edema. **Clinical Pearls for NEET-PG:** * **Early Sign:** The earliest sign of HAPE is often a **reduction in exercise tolerance** and prolonged recovery time. * **Treatment of Choice:** Immediate **descent** is the most definitive treatment. * **Pharmacotherapy:** **Nifedipine** (a calcium channel blocker) is used for prevention and treatment as it reduces pulmonary artery pressure. **Acetazolamide** helps in prevention by stimulating ventilation. * **Key Feature:** Unlike cardiogenic edema, the pulmonary capillary wedge pressure (PCWP) in HAPE remains **normal**.

Q: Which hormone stimulates respiration?

Progesterone. **Explanation:** **Progesterone** is a potent respiratory stimulant. It acts through two primary mechanisms: 1. **Central Stimulation:** It increases the sensitivity of the respiratory center in the medulla to Carbon Dioxide ($CO_2$). 2. **Direct Action:** It acts as a direct stimulant to the respiratory drive, increasing tidal volume and minute ventilation. This physiological effect is most evident during the **luteal phase** of the menstrual cycle and during **pregnancy**, where elevated progesterone levels lead to chronic hyperventilation. This results in a physiological decrease in arterial $PCO_2$ (hypocapnia), creating a favorable $CO_2$ gradient for the fetus to excrete waste. **Analysis of Incorrect Options:** * **A. Estrogen:** While estrogen can enhance the effect of progesterone by increasing progesterone receptor expression, it does not independently stimulate respiration to a significant degree. * **C. Corticosteroids:** These primarily influence metabolic and anti-inflammatory pathways. While they are used to treat respiratory distress (e.g., asthma or fetal lung maturity), they do not act as physiological stimulants of the respiratory center. * **D. Prolactin:** This hormone is primarily involved in lactation and reproductive suppression; it has no documented role in stimulating the respiratory drive. **High-Yield Clinical Pearls for NEET-PG:** * **Pregnancy Physiology:** Pregnant women often experience "physiological dyspnea" due to progesterone-induced hyperventilation, leading to a state of **compensated respiratory alkalosis**. * **Therapeutic Use:** Medroxyprogesterone (a synthetic progestin) has been used clinically to treat **Obstructive Sleep Apnea (OSA)** and **Pickwickian Syndrome** (Obesity Hypoventilation Syndrome) due to its ventilatory stimulatory effects. * **Acid-Base Balance:** In pregnancy, the normal $PaCO_2$ drops to approximately **30–32 mmHg** (Normal: 40 mmHg).

Q: What is the most potent vasoconstrictor of the pulmonary artery?

Hypoxia. **Explanation:** The correct answer is **Hypoxia**. In the pulmonary circulation, hypoxia triggers a unique physiological response known as **Hypoxic Pulmonary Vasoconstriction (HPV)**. Unlike systemic blood vessels, which dilate in response to low oxygen to increase blood flow, pulmonary arterioles constrict. This mechanism shunts blood away from poorly ventilated alveoli toward well-ventilated areas of the lung, optimizing ventilation-perfusion (V/Q) matching and preventing shunting. **Analysis of Options:** * **Hypoxia (Correct):** It is the most potent and physiologically significant stimulus for pulmonary vasoconstriction. It acts directly on pulmonary vascular smooth muscle cells by inhibiting voltage-gated potassium channels, leading to depolarization and calcium influx. * **Endothelin:** While Endothelin-1 is a powerful endogenous vasoconstrictor, it is not the primary physiological regulator of pulmonary vascular resistance compared to the immediate and potent effect of hypoxia. * **Angiotensin:** Angiotensin II is a potent systemic vasoconstrictor. While it can constrict pulmonary vessels, its effect is secondary and less potent than the localized response to hypoxia. * **TXA2 (Thromboxane A2):** This is a potent vasoconstrictor and platelet aggregator released during injury or inflammation, but it is not the "most potent" or primary regulator of pulmonary tone. **Clinical Pearls for NEET-PG:** * **V/Q Matching:** HPV is the lung's primary defense against hypoxemia. * **High Altitude:** Global hypoxia at high altitudes causes generalized pulmonary vasoconstriction, leading to **High-Altitude Pulmonary Edema (HAPE)**. * **Opposite Effects:** Remember: Hypoxia causes **vasodilation** in systemic circulation but **vasoconstriction** in pulmonary circulation. * **Nitric Oxide (NO):** The most potent pulmonary **vasodilator**.

Q: Which muscle is responsible for the change in pitch of sound?

Cricothyroid. **Explanation:** The pitch of the human voice is primarily determined by the **tension and length** of the vocal folds. **Why Cricothyroid is correct:** The **Cricothyroid muscle** is known as the "tensing muscle" of the larynx. When it contracts, it tilts the thyroid cartilage forward or pulls the cricoid cartilage upward. This action increases the distance between the thyroid and arytenoid cartilages, thereby **stretching and tensing** the vocal folds. Increased tension leads to a higher frequency of vibration, which results in a **higher pitch**. **Analysis of Incorrect Options:** * **Posterior cricoarytenoids:** These are the only **abductors** of the vocal folds (opening the glottis). Their primary role is respiratory, not pitch modulation. * **Lateral cricoarytenoids:** These are the primary **adductors** of the vocal folds, closing the glottis for phonation. * **Vocalis:** This muscle (the medial part of the thyroarytenoid) adjusts the local tension of the vocal folds. While it helps in fine-tuning the voice and "thickening" the folds to lower pitch, the primary muscle responsible for the gross change in pitch (especially high pitch) is the cricothyroid. **High-Yield Clinical Pearls for NEET-PG:** * **Nerve Supply:** All intrinsic muscles of the larynx are supplied by the **Recurrent Laryngeal Nerve (RLN)**, EXCEPT the **Cricothyroid**, which is supplied by the **External Laryngeal Nerve**. * **Safety Muscle:** The **Posterior Cricoarytenoid** is the "safety muscle of the larynx" because it is the only muscle that opens the airway. * **Injury:** Damage to the external laryngeal nerve (often during thyroid surgery) leads to an inability to tense the vocal folds, resulting in a **hoarse voice and loss of high-pitched notes** (important for singers).

Question 1

The vasodilatation produced by carbon dioxide is maximum in which of the following organs?

Accepted Answer

Brain

Answer

Kidney

Answer

Liver

Answer

Heart

Question 2

If at the beginning of inspiration, pulmonary compliance is 0.2 L/cm H2O and the initial trans-pulmonary pressure is 5 cm H2O, what will be the transpulmonary pressure after inhaling 600 mL of air?

Accepted Answer

8 cm H2O

Answer

4 cm H2O

Answer

7 cm H2O

Answer

9 cm H2O

Question 3

Diffusion capacity for carbon monoxide is decreased in all of the following conditions EXCEPT:

Accepted Answer

Chronic Bronchitis

Answer

Emphysema

Answer

Interstitial lung disease

Answer

Pulmonary embolism

Question 4

In a transection at the pontomedullary junction, respiration is maintained with slight irregularity. This is due to which structure?

Accepted Answer

Pre-Botzinger complex

Answer

Pneumotaxic centre

Answer

Apneustic Centre

Answer

Dorsal respiratory group

Question 5

An increase in which of the following increases the O2 affinity of hemoglobin?

Accepted Answer

Carbon monoxide added to the blood

Answer

Temperature

Answer

PCO2

Answer

H+ concentration

Question 6

A person unacclimatized develops pulmonary edema in approximately how many days?

Accepted Answer

2-3 days

Answer

6-7 days

Answer

19-21 days

Answer

2nd-3rd month

Question 7

Which hormone stimulates respiration?

Accepted Answer

Progesterone

Answer

Estrogen

Answer

Corticosteroids

Answer

Prolactin

Question 8

Which of the following factors is responsible for the pulmonary alveoli to be kept dry under normal circumstances?

Accepted Answer

Negative interstitial pressure

Answer

Macrophages

Answer

Tight junction between endothelium and alveolar surface

Answer

Pulmonary surfactant

Question 9

What is the most potent vasoconstrictor of the pulmonary artery?

Accepted Answer

Hypoxia

Answer

Endothelin

Answer

Angiotensin

Answer

TXA2

Question 10

Which muscle is responsible for the change in pitch of sound?

Accepted Answer

Cricothyroid

Answer

Posterior cricoarytenoids

Answer

Lateral cricoarytenoids

Answer

Vocalis

Respiratory System — MCQs

Respiratory System — MCQs

On this page

Practice by Chapter

Want unlimited practice?