Respiratory System Practice Questions

Q: A patient with parotid gland cancer has damage to the glossopharyngeal nerve. As a result, which of the following respiratory reflexes will be impaired?

Carotid body chemoreceptor reflex. ### Explanation **Correct Option: D (Carotid body chemoreceptor reflex)** The **Glossopharyngeal nerve (CN IX)** serves as the afferent (sensory) pathway for the carotid body chemoreceptors and carotid sinus baroreceptors. Specifically, the **Hering’s nerve** (a branch of CN IX) carries impulses from the carotid body to the respiratory centers in the medulla. If the glossopharyngeal nerve is damaged, the body cannot sense or respond to changes in arterial $PO_2$, $PCO_2$, or pH via the peripheral chemoreceptors, thereby impairing this reflex. **Why other options are incorrect:** * **A, B, and C:** All three reflexes—the **Hering-Breuer inflation reflex** (triggered by stretch receptors), the **J-receptor reflex** (triggered by pulmonary capillary engorgement), and the **Irritant reflex** (triggered by noxious gases/dust)—rely on the **Vagus nerve (CN X)** as their afferent pathway. Since the question specifies damage only to the glossopharyngeal nerve, these Vagus-mediated reflexes remain intact. **High-Yield Clinical Pearls for NEET-PG:** * **Afferent Pathways:** Remember the "9-10 Rule": **Carotid** (Body/Sinus) = **CN IX**; **Aortic** (Body/Arch) = **CN X**. * **Peripheral vs. Central:** Peripheral chemoreceptors (Carotid/Aortic) are the primary responders to **Hypoxia** ($PO_2 < 60$ mmHg). Central chemoreceptors (Medulla) are primarily sensitive to changes in **$H^+$ and $PCO_2$**. * **J-Receptors:** Located in the alveolar walls near capillaries; their stimulation (e.g., in pulmonary edema) leads to rapid shallow breathing (tachypnea). * **Hering-Breuer Reflex:** In adults, this is a protective mechanism to prevent over-inflation and is typically active only when tidal volume exceeds 1.5 liters.

Q: What concentration of methemoglobin in the blood is typically required to cause cyanosis?

1.5 gm/dL. **Explanation:** Cyanosis is the bluish discoloration of the skin and mucous membranes, typically occurring when a specific threshold of deoxygenated or abnormal hemoglobin is reached in the capillary blood. **1. Why 1.5 gm/dL is Correct:** While central cyanosis traditionally requires **5 gm/dL of reduced (deoxygenated) hemoglobin**, methemoglobin has a much more profound effect on skin color. Because methemoglobin is dark, chocolate-colored, and has a high molar extinction coefficient, it produces visible cyanosis at much lower concentrations. Specifically, only **1.5 gm/dL of methemoglobin** is required to produce clinical cyanosis. This is why patients with methemoglobinemia often appear "cyanotic" despite having a normal PaO2 on arterial blood gas. **2. Analysis of Incorrect Options:** * **5 gm/dL (Option A):** This is the threshold for **reduced hemoglobin** (deoxy-Hb) to cause cyanosis. It is a classic "distractor" for students who confuse general cyanosis with methemoglobin-specific cyanosis. * **2 gm/dL (Option B):** This value is sometimes cited as the threshold for sulfhemoglobinemia to cause cyanosis, but it is not the standard for methemoglobin. * **12 gm/dL (Option D):** This is a dangerously high level associated with severe hypoxia and neurological symptoms, far exceeding the initial threshold for visible cyanosis. **High-Yield Clinical Pearls for NEET-PG:** * **The "Saturation Gap":** A hallmark of methemoglobinemia is a discrepancy between low SpO2 (pulse oximetry, often hovering around 85%) and a normal PaO2 (on ABG). * **Blood Appearance:** Blood in these patients appears **chocolate-brown** and does not change color when exposed to 100% oxygen. * **Treatment:** The drug of choice is **Intravenous Methylene Blue**, which acts as an exogenous electron acceptor to reduce Fe3+ back to Fe2+. * **Common Triggers:** Nitrites, benzocaine, dapsone, and sulfonamides.

Q: The normal intrapleural pressure at the start of inspiration is approximately cm of H2O?

-5.0. **Explanation:** The **intrapleural pressure (IPP)** is the pressure within the pleural cavity (the space between the visceral and parietal pleura). Under normal physiological conditions, this pressure is **subatmospheric (negative)** due to the opposing elastic recoil forces of the lungs (tending to collapse inward) and the chest wall (tending to expand outward). 1. **Why -5.0 cm H₂O is correct:** At the **start of inspiration** (which corresponds to the end of a normal expiration or Functional Residual Capacity), the inward recoil of the lungs and the outward recoil of the chest wall are in equilibrium. This creates a resting negative pressure of approximately **-5 cm H₂O**. This "suction" effect keeps the lungs inflated against the chest wall. 2. **Analysis of Incorrect Options:** * **-7.5 cm H₂O (Option A):** This is the approximate intrapleural pressure at the **end of inspiration**. As the chest wall expands during inspiration, the pleural space volume increases, making the pressure more negative (Boyle’s Law) to pull the lungs open. * **-2.0 cm H₂O (Option C):** This value is too high (less negative) for a healthy adult at rest. * **-0.5 cm H₂O (Option D):** This value typically represents the **intrapulmonary (alveolar) pressure** at the start of inspiration, not the intrapleural pressure. **High-Yield Pearls for NEET-PG:** * **Transpulmonary Pressure:** Defined as Alveolar Pressure minus Intrapleural Pressure ($P_{tp} = P_{alv} - P_{ip}$). It is always positive under normal conditions. * **Pneumothorax:** If the pleural cavity is breached, IPP becomes equal to atmospheric pressure (0 cm H₂O), leading to lung collapse. * **Basal vs. Apical IPP:** Due to gravity, IPP is **more negative at the apex** (~ -10 cm H₂O) and **less negative at the base** (~ -2.5 cm H₂O) in a standing position.

Q: What percentage of oxygen does mouth-to-mouth breathing deliver into the subject's respiratory system?

16%. ### Explanation **Correct Option: C (16%)** The correct answer is **16%** because mouth-to-mouth resuscitation utilizes the rescuer’s **expired air** to ventilate the victim. * **The Underlying Concept:** Atmospheric air contains approximately **21% oxygen**. During normal respiration, a healthy individual extracts only about 4–5% of that oxygen for cellular metabolism. Consequently, the air exhaled by the rescuer still contains a significant amount of oxygen—roughly **16% to 17%**. This concentration is sufficient to maintain tissue viability and oxygenate the victim’s hemoglobin (achieving an arterial oxygen saturation of about 80–90%) until advanced life support arrives. **Analysis of Incorrect Options:** * **A & B (8% and 10%):** These values are too low. If exhaled air contained only 8–10% oxygen, it would be insufficient to create a partial pressure gradient high enough to oxygenate the victim’s blood effectively, leading to rapid hypoxia. * **D (20%):** This value is nearly equivalent to atmospheric air (21%). It is incorrect because it fails to account for the oxygen consumed by the rescuer’s own body during the respiratory cycle. **High-Yield Clinical Pearls for NEET-PG:** * **CO2 Content:** Exhaled air contains approximately **4% Carbon Dioxide**. While this sounds counterintuitive, this CO2 can actually help stimulate the victim's respiratory center in certain clinical scenarios. * **Expired Air Composition:** O2 ≈ 16%, N2 ≈ 79%, CO2 ≈ 4%. * **Tidal Volume in CPR:** In mouth-to-mouth breathing, the rescuer should provide a breath over 1 second with enough volume to see a visible **chest rise**. * **FiO2 Comparison:** While mouth-to-mouth provides ~16% O2, a simple face mask at 6–10 L/min provides 35–50%, and a non-rebreather mask (NRBM) can provide up to 90–100%.

Q: Which of the following is NOT a feature of chronic mountain sickness?

Decreased mitochondria. **Explanation:** Chronic Mountain Sickness (Monge’s disease) occurs due to long-term exposure to high altitudes, leading to chronic alveolar hypoxia and subsequent physiological maladaptations. **Why "Decreased mitochondria" is the correct answer:** In response to chronic hypoxia, the body undergoes cellular adaptations to maximize energy efficiency. One such adaptation is an **increase in mitochondrial density** and myoglobin content in skeletal muscles. This enhances the cell's ability to utilize limited oxygen for oxidative phosphorylation. Therefore, "decreased mitochondria" is physiologically incorrect and is not a feature of the condition. **Analysis of Incorrect Options:** * **Hyperventilation:** Hypoxia stimulates peripheral chemoreceptors (carotid bodies), leading to a persistent increase in the rate and depth of breathing to improve arterial $PO_2$. * **Increased Erythropoietin:** Chronic hypoxia triggers the kidneys to release erythropoietin (EPO), stimulating the bone marrow to produce more RBCs (Polycythemia). This increases the oxygen-carrying capacity of the blood but also increases blood viscosity. * **Increased $HCO_3^-$ excretion:** Hyperventilation causes respiratory alkalosis (low $PCO_2$). To compensate and normalize pH, the kidneys increase the excretion of bicarbonate ($HCO_3^-$). **Clinical Pearls for NEET-PG:** * **Monge’s Disease:** Characterized by extreme polycythemia (Hematocrit >65%), cyanosis, and pulmonary hypertension leading to right heart failure. * **Acute Mountain Sickness (AMS):** Occurs within hours; primary symptom is headache. * **High Altitude Pulmonary Edema (HAPE):** Caused by uneven hypoxic pulmonary vasoconstriction. * **High Altitude Cerebral Edema (HACE):** Result of hypoxia-induced vasodilation and increased capillary permeability.

Q: Hypoxia due to slowing of circulation is termed as?

Stagnant hypoxia. **Explanation:** **Stagnant Hypoxia** (also known as ischemic or circulatory hypoxia) occurs when there is a **decrease in blood flow velocity** or a slowing of circulation. Even though the oxygen content of the arterial blood and the oxygen-carrying capacity are normal, the tissues do not receive oxygen at a sufficient rate because the blood is moving too slowly through the capillaries. This results in increased oxygen extraction at the tissue level, leading to a significantly widened arterio-venous (A-V) oxygen difference. Common causes include heart failure, shock, or local vascular obstruction (e.g., Raynaud’s disease). **Why other options are incorrect:** * **Anemic Hypoxia:** This occurs when the arterial $PO_2$ is normal, but the **oxygen-carrying capacity** of the blood is reduced. This is seen in conditions like anemia, hemorrhage, or carbon monoxide poisoning (where Hb is unavailable for $O_2$ binding). * **Histotoxic Hypoxia:** Here, the delivery of oxygen to the tissues is normal, but the **tissues cannot utilize it** due to the inhibition of cellular oxidative enzymes (e.g., Cyanide poisoning inhibiting Cytochrome Oxidase). **High-Yield Facts for NEET-PG:** * **Hypoxic Hypoxia:** Characterized by low arterial $PO_2$. It is the only type of hypoxia where **Cyanosis** is most prominent and oxygen therapy is highly effective. * **A-V Oxygen Difference:** It is **increased** in Stagnant Hypoxia (due to slow flow) and **decreased** in Histotoxic Hypoxia (as tissues fail to take up $O_2$). * **Cyanosis:** Is typically absent in Anemic hypoxia (not enough Hb to show blue color) and Histotoxic hypoxia (blood remains oxygenated).

Question 1

A patient with parotid gland cancer has damage to the glossopharyngeal nerve. As a result, which of the following respiratory reflexes will be impaired?

Accepted Answer

Carotid body chemoreceptor reflex

Answer

Hering-Breuer inflation reflex

Answer

Juxta pulmonary capillary receptor reflex

Answer

Irritant airway reflex

Question 2

What concentration of methemoglobin in the blood is typically required to cause cyanosis?

Accepted Answer

1.5 gm/dL

Answer

5 gm/dL

Answer

2 gm/dL

Answer

12 gm/dL

Question 3

The normal intrapleural pressure at the start of inspiration is 
                            approximately cm of H2O?

Accepted Answer

-5.0

Answer

-7.5

Answer

-2.0

Answer

-0.5

Question 4

The basal regions of the upright human lung are normally better ventilated than the upper regions because:

Accepted Answer

The lower regions have a small resting volume and a relatively large increase in volume

Answer

Airway resistance of the upper regions is higher than of the lower regions

Answer

There is less surfactant in the upper regions

Answer

The blood flow to the lower regions is higher

Question 5

What percentage of oxygen does mouth-to-mouth breathing deliver into the subject's respiratory system?

Accepted Answer

16%

Answer

8%

Answer

10%

Answer

20%

Question 6

Which of the following is NOT a feature of chronic mountain sickness?

Accepted Answer

Decreased mitochondria

Answer

Hyperventilation

Answer

Increased erythropoietin

Answer

Increased HCO3 excretion

Question 7

Hypoxia due to slowing of circulation is termed as?

Accepted Answer

Stagnant hypoxia

Answer

Anemic hypoxia

Answer

Histotoxic hypoxia

Answer

None of the above

Question 8

Excessive tidal volume load is prevented by activation of which of the following receptors?

Accepted Answer

Bronchial stretch receptors

Answer

J receptor

Answer

Thoracic muscle spindle

Answer

Aerial baroreceptor

Question 9

Decompression sickness, commonly known as 'the bends', is caused by what phenomenon?

Accepted Answer

Formation of nitrogen bubbles in muscles and joints

Answer

Escape of nitrogen bubbles from the myelin sheath of motor nerves

Answer

Blockage of pulmonary capillaries by nitrogen bubbles

Answer

Blockage of blood vessels in the brain and spinal cord by nitrogen bubbles

Question 10

Which of the following neurons predominantly fire during forceful expiration?

Accepted Answer

Ventral group of neurons

Answer

Dorsal group of neurons

Answer

Pneumotaxic center

Answer

Chemoreceptors

Respiratory System — MCQs

Respiratory System — MCQs

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