Human Respiratory System: Solved MCQs, Short & Long Questions with Detailed Explanations | Chap 10 Guide

 

Multiple-Choice Questions (MCQs)

Below are the 10 MCQs from the provided text, with options, correct answers, and detailed explanations based on standard respiratory physiology.

1. During inhalation, diaphragm: (a) Contracts and moves upward (b) Contracts and moves downward (c) Relaxes and moves upward (d) Relaxes and moves downward

   Correct Answer: (b) Explanation: During inhalation, the diaphragm contracts and flattens, moving downward toward the abdomen. This increases the volume of the thoracic cavity, reducing intrathoracic pressure and allowing air to flow into the lungs.

2. Which part of the respiratory system acts as the respiratory surface? (a) Larynx (b) Trachea (c) Bronchi (d) Alveoli

   Correct Answer: (d) Explanation: The alveoli are thin-walled, sac-like structures lined with capillaries, serving as the primary site for gas exchange (oxygen diffusion into blood and carbon dioxide out) due to their large surface area and proximity to blood vessels.

3. How many oxygen molecules can attach with a haemoglobin molecule? (a) 1 (b) 2 (c) 3 (d) 4

   Correct Answer: (d) Explanation: A hemoglobin molecule consists of four polypeptide chains, each with a heme group that can bind one oxygen molecule, allowing up to four O₂ molecules to attach reversibly, facilitating efficient oxygen transport.

4. What is TRUE about respiratory pigments? (a) Transport oxygen from lungs to tissues (b) Transport oxygen and carbon dioxide in equal amounts (c) Transport less oxygen and more carbon dioxide (d) Regulate the pH of blood

   Correct Answer: (a) Explanation: Respiratory pigments like hemoglobin primarily bind and transport oxygen from the lungs to body tissues. While they also carry some CO₂, the main function is O₂ transport; pH regulation is more associated with bicarbonate buffering.

5. Which respiratory pigment is found in muscle tissue? (a) Haemoglobin (b) Melanin (c) Myoglobin (d) Chlorophyll

   Correct Answer: (c) Explanation: Myoglobin is a monomeric protein in muscle cells that stores oxygen, releasing it during muscle contraction for aerobic respiration. Hemoglobin is in red blood cells, melanin is for pigmentation, and chlorophyll is plant-specific.

6. What is the maximum amount of air that can be inhaled or exhaled during a respiratory cycle? (a) Tidal volume (b) Vital capacity (c) Inspiratory reserve volume (d) Expiratory reserve volume

   Correct Answer: (b) Explanation: Vital capacity is the maximum volume of air that can be exhaled after a maximum inhalation (typically 4.6-5.8 L in adults), including tidal volume plus reserve volumes. It represents the total usable lung capacity for a single breath.

7. In what form is carbon dioxide primarily transported in the bloodstream? (a) Dissolved in plasma (b) Bound to haemoglobin (c) Converted to bicarbonate ions (d) None of the above

   Correct Answer: (c) Explanation: About 70% of CO₂ is converted to bicarbonate ions (HCO₃⁻) via carbonic anhydrase in red blood cells, allowing efficient transport in plasma. Only 7% is dissolved, and 23% binds to hemoglobin as carbaminohemoglobin.

8. Which of the following treatments is commonly used to manage pulmonary TB? (a) Antibiotics (b) Cough syrup (c) Surgery (d) Chemotherapy

   Correct Answer: (d) Explanation: Pulmonary tuberculosis is treated with a regimen of multiple anti-TB drugs (e.g., isoniazid, rifampin) over 6-9 months, classified as chemotherapy. Antibiotics alone are insufficient; surgery is rare.

9. Which of the following is a common cause of pneumonia? (a) Bacterial infection (b) Viral infection (c) Fungal infection (d) All of these

   Correct Answer: (d) Explanation: Pneumonia can be caused by bacteria (e.g., Streptococcus pneumoniae), viruses (e.g., influenza), fungi (e.g., Pneumocystis), or aspiration, making all options common etiologies depending on the type.

10. Emphysema is characterized by: (a) Inflammation of airways (b) Narrowing of airways (c) Destruction of the alveoli in lungs (d) Fluid build-up in lungs

    Correct Answer: (c) Explanation: Emphysema, a form of COPD, involves irreversible destruction of alveolar walls, reducing surface area for gas exchange and causing air trapping. Inflammation/narrowing is more asthma/bronchitis; fluid is pulmonary edema.

Section 2: Short Questions

Below are concise answers to the short questions, based on respiratory system principles.

1. Define respiratory surface and list its properties. The respiratory surface is the thin membrane where gases (O₂ and CO₂) diffuse between air and blood. Properties: (i) Thin-walled for short diffusion distance; (ii) Moist to dissolve gases; (iii) Large surface area for efficient exchange; (iv) Richly supplied with blood capillaries for vascularization.
2. How nasal cavity functions in filtering the inhaled air? The nasal cavity filters air via coarse hairs (vibrissae) that trap large particles, sticky mucus that captures dust/microbes, and ciliated epithelium that sweeps debris toward the pharynx for swallowing/expulsion. It also warms (via blood vessels) and humidifies air.
3. Trace the path of air through different parts of the respiratory system. Air enters via nostrils/mouth → nasal cavity/pharynx (filtering/humidifying) → larynx (voice box) → trachea (windpipe) → primary bronchi → secondary/tertiary bronchi → bronchioles → terminal bronchioles → alveoli (gas exchange).
4. Describe the structure and function of alveoli. Structure: Tiny, thin-walled (simple squamous epithelium), balloon-like sacs clustered like grapes at bronchiolar ends, surrounded by pulmonary capillaries. Function: Site of external respiration—O₂ diffuses into blood, CO₂ out—due to large total surface area (~70 m²) and moist, vascular lining.
5. What is the role of diaphragm during inhalation and exhalation? Inhalation: Diaphragm contracts, flattens, and moves downward, expanding thoracic volume and lowering pressure to draw air in. Exhalation: Diaphragm relaxes, domes upward, reducing thoracic volume and expelling air (passive in quiet breathing, active in forced).
6. What are the three ways of the transport of carbon dioxide in blood? (i) Dissolved in plasma (~7%, as CO₂ gas); (ii) Bound to hemoglobin as carbaminohemoglobin (~23%); (iii) As bicarbonate ions (~70%, formed by CO₂ + H₂O → H₂CO₃ → H⁺ + HCO₃⁻ via carbonic anhydrase, then diffused into plasma).
7. What are the advantages of having millions of alveoli rather than a pair of simple balloon-like lungs? Millions of alveoli provide a vast surface area (~70 m² vs. ~1 m² for balloons) for rapid diffusion; thin walls ensure short diffusion paths; clustering allows efficient capillary networks; increases gas exchange efficiency, preventing hypoxia during activity.
8. Differentiate between:
• Internal and external respiration: External: Gas exchange in lungs (O₂ from air to blood, CO₂ from blood to air). Internal: Gas exchange in tissues (O₂ from blood to cells, CO₂ from cells to blood).
• Upper and lower respiratory tract: Upper: Conducting zone from nose/pharynx to larynx (filters/warms air, no gas exchange). Lower: From trachea to alveoli (conduction + gas exchange).
• Bronchi and bronchioles: Bronchi: Larger tubes with cartilage rings for support, lined with cilia/mucus. Bronchioles: Smaller, no cartilage, smooth muscle walls for airflow regulation, lead to alveoli.
• Haemoglobin and myoglobin: Haemoglobin: Tetrameric protein in RBCs, transports O₂ from lungs to tissues (binds 4 O₂). Myoglobin: Monomeric in muscles, stores O₂ for local use during contraction (higher affinity).

Long Questions

1. Describe the mechanism of inhalation and exhalation.

Inhalation (inspiration) and exhalation (expiration) are the mechanical processes of breathing, driven by changes in thoracic cavity volume and pressure, following Boyle's Law (pressure inversely proportional to volume).

• Inhalation Mechanism:
  • Diaphragm Role: The diaphragm contracts and flattens, moving downward (increasing vertical thoracic dimension).
  • External Intercostal Muscles: Contract, elevating the ribs upward and outward (increasing anterior-posterior and lateral dimensions).
  • Result: Thoracic volume expands, intrapulmonary pressure drops below atmospheric pressure (~759 mmHg vs. 760 mmHg), creating a pressure gradient that draws air into the lungs (passive flow).
  • Forced Inhalation: Internal intercostals and abdominal muscles assist for deeper breaths.
• Exhalation Mechanism:
  • Diaphragm Role: Relaxes and domes upward, reducing vertical dimension.
  • Internal Intercostal Muscles: Contract to depress ribs (in forced exhalation).
  • Result: Thoracic volume decreases, intrapulmonary pressure rises above atmospheric (~761 mmHg), expelling air. Quiet exhalation is mostly passive (elastic recoil of lungs); forced involves abdominal muscles compressing the abdomen.

This cycle maintains ~500 mL tidal volume at rest, ensuring efficient gas exchange.

2. Describe the transport of oxygen through blood.

Oxygen transport from lungs to tissues involves diffusion and binding, with ~98.5% bound to hemoglobin and ~1.5% dissolved in plasma.

• Uptake in Lungs (External Respiration):
  • O₂ diffuses from alveoli (PO₂ ~104 mmHg) across thin alveolar-capillary membrane into deoxygenated blood (PO₂ ~40 mmHg).
  • In red blood cells (RBCs), O₂ binds reversibly to hemoglobin (Hb), forming oxyhemoglobin (HbO₂): Hb + 4O₂ ⇌ Hb(O₂)₄. Binding is cooperative (sigmoid oxygen dissociation curve), favored by high PO₂, low PCO₂, low H⁺ (alkaline pH), and low temperature.
• Transport in Blood:
  • Arterial blood carries ~20 mL O₂/100 mL (15 mL bound to Hb, 0.3 mL dissolved).
  • Hb saturation reaches ~97% at lung PO₂.
• Delivery to Tissues (Internal Respiration):
  • At tissues, low PO₂ (~40 mmHg), high PCO₂, acidity (Bohr effect), and warmth shift the dissociation curve right, releasing O₂ from Hb.
  • Dissociated O₂ diffuses into cells for ATP production via aerobic respiration.
  • Myoglobin in muscles stores released O₂ for local use.

This ensures efficient O₂ delivery, with total cardiac output (~5 L/min) transporting ~1 L O₂/min at rest.

3. Describe the transport of carbon dioxide through blood.

CO₂, produced in tissues via cellular respiration, is transported back to lungs in three forms (~4.5 mL/100 mL blood at venous levels), with ~70% as bicarbonate for efficient buffering.

• Uptake in Tissues:
  • CO₂ diffuses from cells (PCO₂ ~46 mmHg) into blood capillaries (PCO₂ ~40 mmHg).
• Three Transport Forms:
  • Dissolved in Plasma (~7%): Directly as CO₂ gas, contributing to PCO₂.
  • Bound to Hemoglobin (~23%): Forms carbaminohemoglobin (HbCO₂) at amino groups: Hb-NH₂ + CO₂ ⇌ Hb-NH-COOH. Favored in deoxygenated blood (Haldane effect).
  • As Bicarbonate Ions (~70%): In RBCs, CO₂ + H₂O ⇌ H₂CO₃ (catalyzed by carbonic anhydrase) ⇌ H⁺ + HCO₃⁻. HCO₃⁻ exits RBCs via chloride shift (Cl⁻ enters for charge balance); H⁺ buffered by Hb.
• Release in Lungs:
  • Reverse processes: Low PCO₂ favors dissociation; oxygenated Hb releases CO₂ (Haldane effect). CO₂ diffuses into alveoli (PCO₂ ~40 mmHg) for exhalation.

This system prevents acidosis (CO₂ forms carbonic acid) and maintains blood pH ~7.4.

4. Describe the structure and function of haemoglobin.

Hemoglobin (Hb) is a tetrameric protein in RBCs responsible for O₂/CO₂ transport and pH buffering.

• Structure:
  • Composed of four polypeptide subunits: 2α and 2β chains (adult HbA), each with a heme prosthetic group (Fe²⁺-porphyrin ring).
  • Molecular weight ~64,500 Da; biconcave RBC shape maximizes surface for diffusion.
  • Allosteric: Binding at one site changes conformation (T to R state), enhancing cooperative binding (sigmoid curve).
• Functions:
  • O₂ Transport: Binds up to 4 O₂ reversibly (97% saturation in lungs); releases in tissues via Bohr/Haldane effects.
  • CO₂ Transport: ~23% as carbamino-Hb; buffers H⁺ from CO₂ hydration.
  • pH Regulation: Buffers via imidazole groups on histidine residues.
  • NO Signaling: Carries nitric oxide for vasodilation.

Defects (e.g., sickle cell) impair function; normal adult concentration: 15 g/dL blood.

5. Describe the causes, symptoms and treatment of sinusitis.

Sinusitis is inflammation of the paranasal sinuses, often following URIs.

• Causes:
  • Viral (most common, e.g., rhinovirus); bacterial (e.g., Streptococcus, ~2% cases); fungal (rare, immunocompromised); allergens/irritants blocking drainage.
• Symptoms:
  • Acute: Facial pain/pressure (worsens bending), nasal congestion/discharge (purulent if bacterial), headache, fever, postnasal drip, hyposmia (reduced smell).
  • Chronic (>12 weeks): Persistent congestion, fatigue, cough.
• Treatment:
  • Viral: Supportive—decongestants, saline irrigation, analgesics (ibuprofen); resolves 7-10 days.
  • Bacterial: Antibiotics (amoxicillin) + nebulization/steroids for inflammation.
  • Chronic: Endoscopic sinus surgery (FESS) to drain/remove obstructions; lifestyle (hydration, avoid allergens). Complications rare (e.g., orbital cellulitis).

6. Describe the causes, symptoms and treatment of pneumonia and pulmonary tuberculosis.

• Pneumonia:
  • Causes: Bacterial (Streptococcus pneumoniae), viral (influenza), fungal (Pneumocystis jirovecii); aspiration or hospital-acquired.
  • Symptoms: Fever, productive cough, chest pain, dyspnea, tachypnea, crackles on auscultation; severe: cyanosis, confusion.
  • Treatment: Antibiotics (e.g., macrolides for community-acquired); antivirals if viral; oxygen/supportive care; vaccination (pneumococcal). Hospitalization for severe cases.
• Pulmonary Tuberculosis (TB):
  • Causes: Mycobacterium tuberculosis (airborne droplets); latent (inactive) or active; risk factors: HIV, malnutrition.
  • Symptoms: Chronic cough (hemoptysis), night sweats, weight loss, low-grade fever, fatigue; cavitary lesions on X-ray.
  • Treatment: RIPE regimen (rifampin, isoniazid, pyrazinamide, ethambutol) for 6-9 months; directly observed therapy (DOT); isolation; surgery rare (lobectomy for drug-resistant).

7. Describe causes, symptoms and treatment of emphysema.

Emphysema is irreversible alveolar damage, a COPD component.

• Causes:
  • Smoking (main, via protease-antiprotease imbalance); alpha-1 antitrypsin deficiency; air pollution/long-term irritants; genetic predisposition.
• Symptoms:
  • Dyspnea (shortness of breath, progressive), chronic cough, wheezing, barrel chest (hyperinflation), pursed-lip breathing; late: weight loss, cor pulmonale.
• Treatment:
  • Smoking cessation (halts progression); bronchodilators (inhaled β-agonists), corticosteroids for exacerbations; oxygen therapy; pulmonary rehab. No cure—lung volume reduction surgery/transplant for severe; vaccinations (flu/pneumococcal) to prevent complications.

Inquisitive Questions

1. How does the structure of the alveoli optimize the exchange of gases like oxygen and carbon dioxide?

Alveoli (~300 million, 70 m² total area) are optimized for diffusion:

• Thin Walls: Simple squamous epithelium + basement membrane (~0.2 μm thick) minimizes diffusion distance (Fick's Law: rate ∝ 1/distance).
• Large Surface Area: Balloon-like clusters increase contact with capillaries.
• Moist Lining: Surfactant prevents collapse; fluid layer dissolves gases.
• Vascular Network: Dense pulmonary capillaries ensure countercurrent flow for efficient O₂ loading/CO₂ unloading. Type I cells for diffusion; Type II produce surfactant. This enables ~250 mL/min O₂ uptake at rest.

2. How do diseases like chronic obstructive pulmonary disease (COPD) affect gaseous exchange efficiency?

COPD (emphysema + chronic bronchitis) impairs exchange:

• Reduced Surface Area: Alveolar destruction (emphysema) lowers diffusion capacity (DLCO ↓30-50%).
• Airway Obstruction: Mucus/hyperplasia narrows bronchioles, causing V/Q mismatch (ventilation/perfusion imbalance)—high V/Q (dead space) wastes ventilation; low V/Q causes hypoxemia.
• Hyperinflation: Air trapping flattens diaphragm, reducing efficiency; chronic hypoxia/hypercapnia leads to cor pulmonale.
• Result: PaO₂ ↓, PaCO₂ ↑, fatigue; FEV1 <80% predicted. Treatment improves but doesn't restore full efficiency.

3. Can you explain the process of external respiration versus internal respiration in the context of gaseous exchange?

• External Respiration (Pulmonary): Occurs in alveoli—bulk flow brings air via ventilation; O₂ diffuses down gradient (alveolar PO₂ 104 mmHg → venous blood 40 mmHg) into capillaries; CO₂ diffuses out (blood 46 mmHg → alveolar 40 mmHg). Facilitated by thin membrane, large area, surfactant. Net: Arterializes blood (PO₂ ~100 mmHg, PCO₂ ~40 mmHg).
• Internal Respiration (Tissue): At systemic capillaries—O₂ unloads (arterial PO₂ 100 mmHg → tissue 40 mmHg or less) to cells; CO₂ loads (tissue 46 mmHg → blood 40 mmHg) from metabolism. Influenced by myoglobin, Bohr effect. Net: Supplies O₂ for ATP, removes CO₂ waste.

Difference: External = lung-blood interface (ventilation-driven); internal = blood-tissue (perfusion-driven); both diffusion-based but context-specific gradients.

4. How does the transport of like oxygen in the bloodstream support cellular respiration?

(Note: Assuming "like oxygen" means "oxygen"; if typo, clarify.) Oxygen transport sustains aerobic cellular respiration (Krebs cycle/ETC in mitochondria):

• Delivery: Hb carries 98% O₂, releasing via dissociation curve shifts (Bohr: low pH/PCO₂ unloads more) to capillaries, diffusing to cells (PO₂ gradient). Dissolved O₂ supplements.
• Utilization: In cytosol/mitochondria, O₂ accepts electrons in ETC, forming H₂O and driving ATP synthesis (~32 ATP/glucose vs. 2 anaerobic). Myoglobin buffers in muscles.
• Feedback: Low tissue O₂ increases ventilation/heart rate (hypoxic drive); prevents lactic acidosis. Without efficient transport, hypoxia impairs energy production, causing fatigue/organ failure.

5. What are the environmental factors that can influence gaseous exchange in humans?

• Altitude: Low atmospheric O₂ (hypobaric hypoxia) reduces alveolar PO₂, causing hyperventilation but diffusion limitation; chronic: polycythemia.
• Air Pollution: Particulates/O₃ irritate airways, increasing mucus/edema, reducing ventilation and V/Q matching.
• Temperature/Humidity: Cold/dry air thickens mucus, impairing clearance; heat increases metabolic demand, straining exchange.
• Smoking/Pollutants: CO binds Hb (carboxy-Hb), reducing O₂ capacity; irritants destroy alveoli (COPD).
• Exercise: ↑O₂ demand improves efficiency via capillary recruitment but extremes cause fatigue. Mitigation: Masks in polluted areas, acclimatization.