Respiratory System Practice Questions

Q: The airway epithelial defect in cystic fibrosis is characterized by which of the following?

Defective chloride secretion. **Explanation:** Cystic Fibrosis (CF) is caused by a mutation in the **CFTR (Cystic Fibrosis Transmembrane Conductance Regulator) gene**, which codes for a cAMP-activated chloride channel. In the respiratory epithelium, the CFTR protein is responsible for the **secretion of chloride ions** from the intracellular space into the airway lumen. **Why Option A is correct:** In CF, the defective CFTR protein leads to a failure of chloride secretion. Under normal conditions, chloride secretion is followed by water to maintain airway surface liquid (ASL) hydration. When chloride secretion is defective, the ASL becomes dehydrated, leading to the formation of thick, viscid mucus that impairs mucociliary clearance and predisposes patients to recurrent infections. **Why other options are incorrect:** * **Option B:** In the lungs, CFTR normally exerts an inhibitory effect on the **ENaC (Epithelial Sodium Channel)**. In CF, the loss of this inhibition leads to **excessive sodium absorption** (not defective absorption). This further draws water out of the lumen, worsening mucus dehydration. * **Option C:** While CFTR is involved in chloride *reabsorption* in **sweat ducts** (leading to high salt content in sweat), the primary defect in the **airway epithelium** is a failure of chloride *secretion*. **High-Yield NEET-PG Pearls:** * **Inheritance:** Autosomal Recessive. * **Most Common Mutation:** ΔF508 (deletion of phenylalanine at position 508). * **Diagnostic Gold Standard:** Sweat Chloride Test (Chloride >60 mEq/L). * **Organ-Specific CFTR Function:** * *Lungs/Pancreas:* CFTR secretes Cl⁻ (Defect = thick secretions). * *Sweat Glands:* CFTR reabsorbs Cl⁻ (Defect = "Salty" sweat).

Q: The kind of hypoxia seen in the collapse of lungs and depression of the respiratory centre is:

Hypoxic hypoxia. **Explanation:** **1. Why Hypoxic Hypoxia is Correct:** Hypoxic hypoxia (also known as arterial hypoxia) is characterized by a **low partial pressure of oxygen ($PaO_2$)** in the arterial blood. In cases of **lung collapse (atelectasis)**, there is a reduction in the surface area available for gas exchange. In **depression of the respiratory center** (e.g., opioid overdose), hypoventilation occurs. Both conditions lead to inadequate oxygenation of the blood in the lungs, resulting in a decreased $PaO_2$ and low oxygen saturation ($SaO_2$), which is the hallmark of hypoxic hypoxia. **2. Why the Other Options are Incorrect:** * **Anemic Hypoxia:** Here, $PaO_2$ is normal, but the **oxygen-carrying capacity** of the blood is reduced due to low hemoglobin levels or dysfunctional hemoglobin (e.g., CO poisoning). * **Stagnant (Ischemic) Hypoxia:** $PaO_2$ and hemoglobin are normal, but **blood flow to the tissues is inadequate** (e.g., heart failure, shock, or local embolism). * **Histotoxic Hypoxia:** The blood delivers oxygen perfectly, but the **tissues cannot utilize it** because cellular enzymes (like cytochrome oxidase) are poisoned (e.g., Cyanide poisoning). **3. Clinical Pearls for NEET-PG:** * **Cyanosis:** Most commonly seen in Hypoxic and Stagnant hypoxia. It is **not** seen in Anemic hypoxia (Hb is too low to show blue color) or Histotoxic hypoxia (blood remains bright red). * **P50 Value:** A right shift in the oxygen-dissociation curve (increased P50) is a compensatory mechanism in most hypoxias except Histotoxic. * **High Altitude:** The most common physiological cause of Hypoxic hypoxia.

Q: The approximate amount of air left in the lungs after maximal forced expiration in a normal woman is:

1.1 L. ### Explanation The volume of air remaining in the lungs after a maximal forced expiration is defined as the **Residual Volume (RV)**. This volume cannot be exhaled because the small airways collapse at low lung volumes, trapping air, and the chest wall reaches its inward limit of compression. **Why 1.1 L is correct:** In a healthy adult, the average Residual Volume is approximately **1.2 L in males** and **1.1 L in females**. Since the question specifically asks for the value in a **normal woman**, 1.1 L is the most accurate physiological estimate. **Analysis of Incorrect Options:** * **0.5 L (Option A):** This value corresponds to the **Tidal Volume (TV)**, which is the volume of air inspired or expired during a single normal breath. * **2.0 L (Option B) & 1.8 L (Option D):** These values are too high for RV. However, a value around 2.2–2.4 L would represent the **Functional Residual Capacity (FRC)**—the air remaining after a *normal* (passive) expiration (FRC = RV + ERV). **High-Yield NEET-PG Pearls:** 1. **Measurement:** Residual Volume **cannot** be measured by simple spirometry because the air never leaves the lungs. It must be measured using indirect methods: **Helium Dilution**, **Nitrogen Washout**, or **Body Plethysmography**. 2. **Clinical Correlation:** RV is significantly **increased** in obstructive lung diseases (e.g., Emphysema, Asthma) due to air trapping, leading to hyperinflation. 3. **Formula:** $FRC - ERV = RV$ (where ERV is Expiratory Reserve Volume). 4. **Aging:** RV typically increases with age as the elastic recoil of the lungs decreases.

Q: What is the normal vital capacity of the lungs?

4700 ml. **Explanation:** **Vital Capacity (VC)** is the maximum volume of air a person can exhale from the lungs after a maximum inhalation. It is a key indicator of pulmonary function and reflects the total "usable" gas exchange surface. **Why Option D is Correct:** The normal Vital Capacity in a healthy adult male is approximately **4600–4700 ml**. It is calculated by the sum of three primary lung volumes: * **Tidal Volume (TV):** 500 ml * **Inspiratory Reserve Volume (IRV):** 3000 ml * **Expiratory Reserve Volume (ERV):** 1100–1200 ml * **Calculation:** $500 + 3000 + 1200 = 4700 \text{ ml}$. **Analysis of Incorrect Options:** * **Option A (500 ml):** This represents the **Tidal Volume (TV)**, which is the volume of air inspired or expired during a normal, quiet breath. * **Option B (1200 ml):** This represents the **Residual Volume (RV)**—the air remaining in the lungs after forceful expiration—or the **Expiratory Reserve Volume (ERV)**. * **Option C (3000 ml):** This represents the **Inspiratory Reserve Volume (IRV)**, the additional volume that can be inspired above the normal tidal volume. **High-Yield NEET-PG Pearls:** 1. **VC vs. TLC:** Vital Capacity does *not* include Residual Volume. Total Lung Capacity (TLC) = VC + RV (approx. 5800–6000 ml). 2. **Clinical Significance:** VC is decreased in **Restrictive Lung Diseases** (e.g., Pulmonary Fibrosis, Kyphoscoliosis) but remains relatively normal or is only slightly reduced in obstructive diseases. 3. **Timed VC:** The most clinically significant measurement is **FEV1** (Forced Expiratory Volume in 1 second), which is normally 80% of the FVC (Forced Vital Capacity). 4. **Factors:** VC is higher in males, taller individuals, and athletes; it decreases with age and in the supine position.

Q: Carbon dioxide retention is seen in all, except?

Carbon monoxide poisoning. **Explanation:** The core concept here is the difference between **Type I** and **Type II respiratory failure**. Carbon dioxide retention (Hypercapnia) occurs when there is an issue with **ventilation** (the movement of air in and out of the lungs), whereas oxygenation issues can occur even when ventilation is preserved. **Why Carbon Monoxide (CO) Poisoning is the correct answer:** In CO poisoning, the primary pathology is **impaired oxygen transport**, not a failure of ventilation. CO binds to hemoglobin with 210 times the affinity of oxygen, causing a leftward shift of the oxygen-dissociation curve. However, the lungs' ability to exhale $CO_2$ remains intact. In fact, patients often hyperventilate due to tissue hypoxia, which leads to **decreased** $PaCO_2$ (hypocapnia) rather than retention. **Analysis of Incorrect Options:** * **Respiratory Failure:** Specifically Type II respiratory failure (Ventilatory failure) is defined by the inability to eliminate $CO_2$, leading to hypercapnia. * **Ventilator Failure:** Any mechanical failure or setting mismatch that reduces alveolar ventilation will directly result in $CO_2$ accumulation. * **Pulmonary Edema:** While initially causing Type I failure (hypoxia with low $CO_2$), severe or end-stage pulmonary edema leads to respiratory muscle fatigue and increased dead space, eventually resulting in $CO_2$ retention. **High-Yield Clinical Pearls for NEET-PG:** * **CO Poisoning Triad:** Cherry-red skin (rarely seen clinically), headache, and normal $SpO_2$ (pulse oximeters cannot distinguish between carboxyhemoglobin and oxyhemoglobin). * **Type I Respiratory Failure:** Hypoxia with normal/low $PaCO_2$ (e.g., Pneumonia, early Pulmonary Edema). * **Type II Respiratory Failure:** Hypoxia with high $PaCO_2$ (e.g., COPD, Neuromuscular weakness, Opioid overdose).

Q: Carbon monoxide poisoning causes which of the following types of hypoxia?

Anemic hypoxia. **Explanation:** **Why Anemic Hypoxia is Correct:** Anemic hypoxia occurs when the oxygen-carrying capacity of the blood is reduced, even though the partial pressure of arterial oxygen ($PaO_2$) remains normal. In Carbon Monoxide (CO) poisoning, CO binds to hemoglobin with an affinity **200–250 times greater** than oxygen, forming **carboxyhemoglobin**. This effectively reduces the amount of hemoglobin available to transport oxygen. Furthermore, CO causes a **leftward shift** of the oxygen-hemoglobin dissociation curve, meaning the remaining oxygen binds more tightly to hemoglobin and is not easily released to the tissues. **Why Other Options are Incorrect:** * **Histotoxic Hypoxia:** Occurs when tissues cannot utilize oxygen despite adequate delivery (e.g., **Cyanide poisoning** inhibiting cytochrome oxidase). * **Anoxic (Hypoxic) Hypoxia:** Characterized by low arterial $PaO_2$ due to external factors like high altitude, airway obstruction, or alveolar hypoventilation. * **Stagnant (Ischemic) Hypoxia:** Occurs when blood flow to tissues is reduced despite normal oxygen content (e.g., heart failure, shock, or local embolism). **High-Yield Clinical Pearls for NEET-PG:** * **Pulse Oximetry:** Standard pulse oximeters cannot distinguish between oxyhemoglobin and carboxyhemoglobin, often giving **falsely normal** $SpO_2$ readings. * **Clinical Sign:** Patients may present with "cherry-red" skin discoloration (a classic but late sign). * **Treatment:** 100% Hyperbaric oxygen is the treatment of choice to displace CO from hemoglobin. * **Curve Shift:** CO poisoning is a classic cause of a **Left Shift** (along with Alkalosis, decreased 2,3-DPG, and Hypothermia).

Q: An increase in which of the following parameters will shift the oxygen dissociation curve to the left?

Oxygen affinity of hemoglobin. **Explanation:** The Oxygen Dissociation Curve (ODC) represents the relationship between the partial pressure of oxygen ($PO_2$) and the percentage saturation of hemoglobin ($SaO_2$). **Why the Correct Answer is Right:** A **Left Shift** indicates that hemoglobin has an **increased affinity for oxygen**. This means hemoglobin binds oxygen more tightly and is less willing to release it to the tissues. By definition, any factor that increases the oxygen affinity of hemoglobin will shift the curve to the left. At any given $PO_2$, the hemoglobin saturation will be higher than normal. **Why the Other Options are Wrong:** Options A, B, and C all cause a **Right Shift** (decreased affinity), which facilitates oxygen unloading to tissues (the Bohr Effect). * **A. Temperature:** Increased temperature (e.g., during fever or exercise) decreases affinity, shifting the curve to the right. * **B. Partial pressure of $CO_2$ ($PCO_2$):** Increased $CO_2$ leads to increased $H^+$ concentration (decreased pH). This stabilizes the "Tense" (T) state of hemoglobin, shifting the curve to the right. * **C. 2,3 DPG concentration:** This byproduct of glycolysis binds to the beta chains of hemoglobin, decreasing its affinity for $O_2$ and shifting the curve to the right. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Right Shift:** "**CADET**, face Right!" (**C**-$CO_2$, **A**-Acid/H+, **D**-2,3 DPG, **E**-Exercise, **T**-Temperature). * **Left Shift Causes:** Fetal Hemoglobin (HbF), Carbon Monoxide poisoning (COHb), Methemoglobinemia, and Alkalosis. * **$P_{50}$ Value:** The $PO_2$ at which hemoglobin is 50% saturated. A **Left Shift decreases $P_{50}$**, while a **Right Shift increases $P_{50}$**. Normal $P_{50}$ is approximately 26-27 mmHg.

Question 1

Increased alveolar O2 concentration is due to which of the following condition?

Accepted Answer

Ventilation-perfusion mismatch

Answer

Intracardiac right to left shunt

Answer

Asthma

Answer

Pulmonary hemorrhage

Question 2

The airway epithelial defect in cystic fibrosis is characterized by which of the following?

Accepted Answer

Defective chloride secretion

Answer

Defective sodium absorption

Answer

Defective chloride absorption

Answer

None of the above

Question 3

The kind of hypoxia seen in the collapse of lungs and depression of the respiratory centre is:

Accepted Answer

Hypoxic hypoxia

Answer

Anemic hypoxia

Answer

Stagnant hypoxia

Answer

Histotoxic hypoxia

Question 4

The approximate amount of air left in the lungs after maximal forced expiration in a normal woman is:

Accepted Answer

1.1 L

Answer

0.5 L

Answer

2.0 L

Answer

1.8 L

Question 5

What is the normal vital capacity of the lungs?

Accepted Answer

4700 ml

Answer

500 ml

Answer

1200 ml

Answer

3000 ml

Question 6

Respiration stops in the last stage of expiration, during forced expiration, because of:

Accepted Answer

Dynamic compression of airways

Answer

Respiratory muscle fatigue

Answer

Collapse of alveoli

Answer

Breaking effect of inspiratory muscles

Question 7

Carbon dioxide retention is seen in all, except?

Accepted Answer

Carbon monoxide poisoning

Answer

Respiratory failure

Answer

Ventilator failure

Answer

Pulmonary edema

Question 8

Carbon monoxide poisoning causes which of the following types of hypoxia?

Accepted Answer

Anemic hypoxia

Answer

Histotoxic hypoxia

Answer

Anoxic hypoxia

Answer

Stagnant hypoxia

Question 9

What is the effect on respiration when the pons is transected at its superior level?

Accepted Answer

Breathing becomes slower and deeper

Answer

Apneustic breathing

Answer

Breathing ceases

Answer

Irregular and gasping respirations

Question 10

An increase in which of the following parameters will shift the oxygen dissociation curve to the left?

Accepted Answer

Oxygen affinity of hemoglobin

Answer

Temperature

Answer

Partial pressure of CO2

Answer

2,3 DPG concentration

Respiratory System — MCQs

Respiratory System — MCQs

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