Respiration – 2020

Caplan syndrome (also called rheumatoid pneumoconiosis) is a pulmonary manifestation of rheumatoid arthritis seen in individuals exposed to coal dust or other pneumoconiosis-causing particles (like silica).

It is characterized by:

• Multiple well-defined nodular opacities in the lungs (rheumatoid-like nodules)

• Association with occupational exposure (coal miners, silica workers, etc.)

• Histology: Central necrosis surrounded by fibrohistiocytic tissue

So, it’s essentially rheumatoid arthritis + pneumoconiosis, not tuberculosis or other infections.

Respiratory bronchioles mark the transition from the conducting portion to the respiratory portion of the airway — they are the first part of the respiratory zone where gas exchange begins.

They arise from terminal bronchioles and are characterized by:

• Walls interrupted by alveoli, which allows for limited gas exchange.

• Absence of cartilage and glands.

• Presence of Clara cells (now called Club cells) — non-ciliated, dome-shaped cells that secrete surfactant-like material, detoxify harmful substances, and regenerate bronchiolar epithelium.

Hence, it is incorrect to say that respiratory bronchioles lack Clara cells — they are, in fact, a defining feature of these airways.

❌ Why the Other Options Are Incorrect

• Have an interruption of alveoli in its walls:
  ✅ Correct — this is the hallmark of respiratory bronchioles; some portions of their wall open into alveoli.

• First part of the respiratory portion:
  ✅ Correct — they represent the beginning of the gas exchange zone.

• Lack glands in its walls:
  ✅ Correct — glands are absent beyond the larger bronchi.

• Lack goblet cells:
  ✅ Correct — goblet cells disappear beyond the terminal bronchioles; mucus would obstruct gas exchange here.

Pleuritis (inflammation of the pleura) is not exclusive to tuberculosis — it can result from various diseases involving infection, inflammation, or malignancy in adjacent structures:

• Mediastinal lymphadenitis: Enlarged, infected lymph nodes (like in TB or lymphoma) can spread inflammation to the pleura.

• Löffler’s pneumonia: A transient eosinophilic pneumonia (often due to parasitic migration) can irritate the pleura.

• Lung carcinoma: Tumors close to the pleural surface often invade or metastasize to the pleura, leading to pleuritic pain or effusion.

• Pericarditis: Inflammatory processes in the pericardium can spread to the pleura due to proximity.

Hence, all listed conditions can cause pleuritis through either direct extension or secondary inflammatory spread.

The rib described is the first rib, which has several atypical features compared to typical ribs:

• Single facet on head: articulates only with T1 vertebra

• No neck or only a rudimentary neck

• No prominent angle

• **Has a tuberosity on its superior surface for attachment of scalene muscles (serratus anterior tubercle is also present)

• Costal groove is shallow

Other options:

• Tubercle for serratus anterior → present but not unusual

• Single facet on head → normal for first rib

• Costal groove → present, though shallow

• Neck → present but rudimentary

The mediastinum is the central compartment of the thoracic cavity between the two pleural sacs. It is divided into superior and inferior parts by a plane passing through the sternal angle (T4–T5 level). The inferior mediastinum is further divided into anterior, middle, and posterior compartments.

The posterior mediastinum lies behind the pericardium and in front of the vertebral column (T5–T12). It contains several key structures:

• Esophagus

• Thoracic duct

• Descending thoracic aorta

• Azygos and hemiazygos veins

• Vagus nerves and sympathetic trunks

These structures are responsible for vital thoracic and abdominal communication pathways — for example, the thoracic duct drains lymph from most of the body into the left venous angle.

❌ Why the Other Options Are Incorrect

• Anterior mediastinum:
  Lies between the sternum and pericardium; contains fat, lymph nodes, and remnants of the thymus, but no esophagus or thoracic duct.

• Superior mediastinum:
  Contains thymus, great vessels (aortic arch and branches), trachea, esophagus (upper part), and thoracic duct, but the sympathetic chains are located posteriorly.

• Inferior mediastinum:
  A collective term — it includes anterior, middle, and posterior mediastina; not a specific compartment itself.

• Middle mediastinum:
  Contains the heart, pericardium, ascending aorta, pulmonary trunk, and phrenic nerves, but not the esophagus or sympathetic chains.

The twelfth rib (and also the 11th) is a “floating rib” with several distinctive features:

• Single facet on the head: articulates only with T12 vertebra

• No neck or tubercle: unlike typical ribs, which articulate with the transverse process

• No costal groove: unlike most other ribs, making neurovascular bundle less protected

• Floating: does not attach anteriorly to the sternum via costal cartilage

Other options:

• Angle, neck, costal groove, costal cartilage → either absent or underdeveloped in the 12th rib

Arterial partial pressure of oxygen (PaO₂) reflects the amount of oxygen dissolved in arterial blood.

• Normal PaO₂ in healthy adults: ~ 95 mmHg (range: 80–100 mmHg)

• Lower values: indicate hypoxemia

  • 70–75 mmHg → mild hypoxemia

  • 55 mmHg → moderate hypoxemia

  • 20 mmHg → severe, life-threatening hypoxemia

During quiet (normal) inspiration, only the diaphragm and external intercostals are primarily involved:

• Diaphragm contraction → increases vertical thoracic diameter

• External intercostals → elevate ribs 1–2 slightly

During forced inspiration, accessory muscles contribute:

• Scalenes, sternocleidomastoid, and external intercostals of 2–7 ribs

• This significantly increases the anterior-posterior and transverse thoracic diameter

Other options:

• Contraction of diaphragm / external intercostals → occur in quiet inspiration

• Elevation of first rib → occurs in both quiet and forced inspiration

• Relaxation of internal intercostals → mainly during passive expiration

Lung compliance measures the ease with which the lungs expand:

Compliance = (Change in lung volume) / (Change in transpulmonary pressure)

• Normal total lung compliance (both lungs): ~ 200 mL/cm H₂O

• High compliance: lungs expand too easily (e.g., emphysema)

• Low compliance: lungs stiff and resist expansion (e.g., fibrosis, ARDS)

Other options:

• 50–110 mL/cm H₂O → abnormally low

• 400–600 mL/cm H₂O → abnormally high

During inspiration, the diaphragm contracts and moves downward, and the external intercostal muscles elevate the ribs, expanding the thoracic cavity.

This expansion increases thoracic volume and thereby decreases intrapleural pressure (pressure within the pleural cavity) — making it more negative than its resting level.

• At rest (end of expiration): Intrapleural pressure ≈ –2 to –4 mm Hg relative to atmospheric pressure.

• During inspiration: It becomes even more negative (≈ –6 to –8 mm Hg), helping draw air into the lungs as alveolar pressure briefly falls below atmospheric pressure.

This negative pressure is essential for lung expansion and airflow into alveoli.

❌ Why the Other Options Are Incorrect

• More negative than +2 mm Hg:
  ❌ Incorrect — a positive intrapleural pressure never occurs during normal inspiration; it would indicate airway obstruction or forced expiration.

• More negative than 0.4 mm Hg:
  ❌ Incorrect — this value is far too small; intrapleural pressure is much lower (around –4 mm Hg) even at rest.

• More positive than +4 mm Hg:
  ❌ Incorrect — intrapleural pressure never becomes positive during inspiration; positive pressures appear only during forced expiration or Valsalva maneuver.

• More negative than –4 mm Hg:
  ❌ Incorrect — while this can occur in deep or forced inspiration, normal quiet inspiration typically reaches around –6 mm Hg, not beyond that physiologically in quiet breathing.

The posteroanterior (PA) view is the standard and most accurate X-ray orientation for evaluating chest lesions. In this view, X-rays pass from posterior (back) to anterior (front), with the patient standing and the chest pressed against the film or detector.

This position minimizes magnification of the heart and mediastinum and gives the most realistic view of thoracic structures. It also allows better visualization of lung fields, diaphragm, and costophrenic angles.

❌ Incorrect Options:

• Anteroposterior erect view: Used when the patient cannot stand, but it magnifies the heart and mediastinum.

• Anteroposterior view: Similar limitation as above; not preferred for accurate lesion assessment.

• Lateral view: Used as a supplementary view to localize lesions or assess the retrosternal and retrocardiac spaces, not as a primary diagnostic orientation.

• Supine view: Typically used in critically ill or bedridden patients; it distorts structures and makes lesion localization less accurate.

The oxygen-hemoglobin dissociation curve shows the relationship between PO₂ and hemoglobin saturation.

• Right shift → hemoglobin releases oxygen more easily to tissues

• Causes of right shift (factors that decrease Hb affinity for O₂):

  • Increased 2,3-DPG

  • High CO₂ (Bohr effect)

  • Low pH (acidosis)

  • High temperature → occurs during strenuous exercise

• Left shift → hemoglobin holds oxygen more tightly

  • Low 2,3-DPG, fetal hemoglobin, low temperature, high pH

Other options:

• Low 2,3-DPG / fetal Hb / low temperature / high pH → shift left, increasing oxygen affinity

Flail chest is a serious thoracic injury characterized by:

• Definition: A segment of the thoracic wall becomes detached from the rest of the chest wall

• Cause: Usually ≥3 consecutive ribs fractured in ≥2 places

• Clinical feature: Paradoxical movement of the flail segment during respiration:

  • Inward during inspiration

  • Outward during expiration

• Can lead to impaired ventilation and hypoxia

Other options:

• Single rib fracture / fracture at costal cartilage / first rib fracture → do not produce flail chest

• Multiple ribs fractured at one place → may cause pain but not flail segment

Persistent asthma refers to ongoing, chronic symptoms that occur daily or nightly, depending on severity:

• Key feature: Lower airway obstruction is reversible with bronchodilators or spontaneously

• Location: Affects lower airways (bronchi and bronchioles)

• Other features: Airway inflammation, hyperresponsiveness, mucus hypersecretion

Other options:

• Irreversible bronchoconstriction → characteristic of COPD, not asthma

• Upper airways → asthma primarily affects lower airways

• Permanent dilation → seen in bronchiectasis, not asthma

On the right lung, the arch of the azygos vein creates the most pronounced impression:

• Location: Posterior part of the superior lobe, near the hilum

• Other structures:

  • Right common carotid artery → does not leave a significant impression on the lung

  • Right phrenic nerve / right vagus nerve → minor grooves only

  • Thoracic aorta → impression is on the left lung, not right

This phenomenon is called hypoxic pulmonary vasoconstriction (HPV):

• Mechanism: When alveolar PO₂ falls below ~70 mmHg, pulmonary arterioles constrict.

• Purpose: Redirects blood flow from poorly ventilated alveoli to better-ventilated alveoli, improving ventilation-perfusion (V/Q) matching.

• Other options:

  • Decreased physiological shunt → actually V/Q mismatch can increase shunt

  • Damage to type-1 pneumocytes → not an immediate response to low PO₂

  • Nitrogen content increases → irrelevant to this mechanism

In the doctor-patient relationship, empathy is the ability to cognitively and emotionally understand the patient’s experiences and feelings without necessarily experiencing them oneself.

• Key aspects:

  • Active listening

  • Understanding the patient’s perspective

  • Responding appropriately to concerns

Other options:

• Feeling exactly what the patient feels → emotional contagion, not professional empathy

• Being ignorant / not listening / just careful → do not constitute empathy

• In the thorax, the esophagus changes its position relative to surrounding structures as it descends:

  • Upper thoracic esophagus: posterior to trachea, slightly right of midline

  • Middle thoracic esophagus: lies posterior to the trachea and left of the thoracic aorta

  • Lower thoracic esophagus (just before hiatus): lies medial to the aorta before entering the diaphragm

Other options:

• Anterior mediastinum / superior mediastinum / middle mediastinum / root of the neck → esophagus is posterior or lateral, not medial to the aorta

Atopic (allergic) asthma is the most common type of asthma, usually associated with IgE-mediated hypersensitivity to environmental allergens.

• Onset: Most frequently occurs in childhood, often before age 12

• Triggers: Dust mites, pollen, animal dander, mold

• Features: Recurrent wheezing, cough, and reversible airway obstruction

Other options:

• Adulthood / old age → more likely non-atopic or occupational asthma

• Neonatal / teenage → less common for initial development

Distinguishing features between bronchi and bronchioles include:

✅ Key point: Both bronchi and bronchioles contain smooth muscle, so this is not a distinguishing feature.

Elastic Fibers in the Distal Respiratory Tract

1. Alveolar ducts:

   • Surrounded by smooth muscle and elastic fibers, leading into alveolar sacs

   • Elastic fibers support recoil of ducts and adjacent alveoli

2. Alveolar sacs:

   • Composed of clusters of alveoli, with thin walls

   • Contain elastic fibers, but the density is less than in alveolar ducts, which serve as the main elastic “spring” for recoil

3. Interalveolar septa:

   • Contain capillaries and some elastic fibers

   • Main function is gas exchange, not elastic recoil

4. Respiratory bronchioles:

   • Mostly smooth muscle and epithelium, fewer elastic fibers

✅ Conclusion:

• The alveolar duct contains the greatest number of elastic fibers, more than the alveolar sac.

• Alveolar sacs rely on the fibers in alveolar ducts and septa but themselves have less dense elastic tissue.

In infants, the thoracic cage is highly compliant due to cartilaginous ribs and underdeveloped musculature:

• Increased elasticity of chest wall → thoracic movements contribute less to tidal volume

• Diaphragm becomes the primary muscle of respiration → abdominal (diaphragmatic) breathing is observed

• Ribs are more horizontal, limiting expansion, but the main reason is soft, elastic chest wall

Other options:

• Accessory cervical ribs → rare congenital anomaly, not normal

• Bucket handle / obliquity of ribs → relate to adult-type rib movement, not infant breathing

In asthma, repeated airway inflammation and hyperresponsiveness lead to structural remodeling of the bronchi:

• Smooth muscle hypertrophy and hyperplasia → makes airways more prone to bronchoconstriction

• Goblet cell hyperplasia and mucus hypersecretion → increases airway obstruction

• Subepithelial fibrosis → thickens airway walls

• These changes increase the likelihood of recurrent asthma attacks when exposed to triggers

Other options:

• Alveolar capillary constriction / alveolar wall degeneration → features of emphysema, not asthma

• Increased sensitivity followed by fainting / blue lips → not a structural change; possibly severe hypoxia

• Inflammation in bacterial infections → not specific to asthma airway remodeling

The vertebrae develop from the sclerotome portion of somites, which arise from paraxial mesoderm. During development, each sclerotome splits into a cranial (loosely packed) and caudal (densely packed) part.

The caudal half of one sclerotome fuses with the cranial half of the next — a process known as resegmentation, which allows spinal nerves to exit between vertebrae.
This migration of sclerotomal cells around the notochord and neural tube occurs around the 4th week of development, not the 6th week.

The notochord largely degenerates within the vertebral bodies but persists as the nucleus pulposus within the intervertebral discs. The mesenchymal cells remaining between vertebrae contribute to the annulus fibrosus portion of the intervertebral disc.

❌ Why the Other Options Are Incorrect

• Mesenchymal cells between sclerotomes form intervertebral discs:
  ✅ True — these form the annulus fibrosus, surrounding the nucleus pulposus.

• Notochord remnants are in the form of nucleus pulposus:
  ✅ True — the notochord persists in the center of the disc as the gelatinous core.

• Vertebrae develop from sclerotome portions of somites:
  ✅ True — sclerotomes give rise to vertebrae and ribs.

• Caudal and cranial ends of adjacent sclerotomes fuse:
  ✅ True — this resegmentation creates intersegmental vertebrae.

The hallmark feature of bronchial asthma is reversible bronchoconstriction due to airway hyperresponsiveness.

Key points:

• Symptoms: wheezing, chest tightness, cough, and sputum production

• Pathophysiology: airway inflammation, smooth muscle constriction, mucous hypersecretion

• Reversibility: obstruction can improve spontaneously or with bronchodilators

Other options:

• Irreversible constriction → characteristic of chronic bronchitis or emphysema (COPD), not asthma

• Destruction of smooth muscle → seen in emphysema, not asthma

• Persistent symptoms / same for every person → asthma is variable and episodic, not uniform

The defining pathology of chronic bronchitis is:

Mucous gland hypertrophy and hyperplasia

This causes:

• Excess mucus
• Thickened bronchial walls
• Narrowed airways
• Chronic productive cough

This is measured by the Reid index:

Normal value → less than 0.40
Chronic bronchitis → greater than 0.50

So when the question says increased mucosal gland depth relative to the bronchial wall, it is literally describing an increased Reid index, which is the hallmark of chronic bronchitis.

❌ Why the other statements are wrong

Slight increase in goblet cells only in small airways
Goblet cell hyperplasia occurs in both large and small airways, not just small ones.

Reid index of 0.4 is normal
0.4 is the upper limit of normal.
Chronic bronchitis is above 0.5.

Predominant lymphocyte infiltration
Inflammation is mixed — neutrophils, macrophages, and lymphocytes.

Smooth muscle hypertrophy
This is a feature of asthma, not chronic bronchitis.

Asthma is a chronic inflammatory disorder of the airways characterized by:

• Reversible bronchoconstriction

• Airway hyperresponsiveness

• Inflammatory cell infiltration (eosinophils, mast cells, T-helper cells)

Major risk factors include:

• Exposure to air-borne allergens (dust mites, pollen, mold, animal dander)

• Genetic predisposition / atopy

• Air pollution and tobacco smoke exposure

Other options:

• Exposure to radiation → not linked to asthma development

• High BMI → can worsen symptoms but is not a primary risk factor

• Alcohol exposure → not a direct risk factor

• High birth weight → no established association with asthma

The respiratory diverticulum (lung bud) arises as a ventral outgrowth from the foregut during the 4th week of embryonic development.

• This marks the beginning of the lower respiratory system.

• It later branches to form the trachea, bronchi, and lung buds.

Other options:

• 5th–8th weeks → period of branching morphogenesis and formation of bronchial tree and alveoli, not initial appearance.

• 6th–7th weeks → further airway branching and differentiation

Clara cells (Club cells) are non-ciliated, secretory epithelial cells found in the bronchioles. They:

• Secrete a component of surfactant (mainly phospholipids and proteins) that reduces surface tension in small airways, helping prevent their collapse during expiration

• Act as progenitor cells, replacing damaged bronchiolar epithelium

Other options:

• Engulfing microorganisms → function of alveolar macrophages

• Ciliary activity → ciliated epithelial cells, not Clara cells

• Producing mucus → goblet cells

The internal thoracic artery (ITA) is an important vessel that supplies the anterior chest wall, diaphragm, and breasts.

It begins in the root of the neck as a branch of the first part of the subclavian artery. From there, it descends posterior to the first six costal cartilages, about 1 cm lateral to the sternum, accompanied by paired veins.

It provides anterior intercostal arteries to the upper six intercostal spaces, pericardiophrenic and perforating branches, and then divides into its two terminal branches:

• Musculophrenic artery (to diaphragm and lower intercostal spaces)

• Superior epigastric artery (to anterior abdominal wall)

The ITA is often used in coronary artery bypass grafting because of its consistent structure and long-term patency.

❌ Why the Other Options Are Incorrect

• Musculophrenic artery arises from the internal thoracic artery as its terminal branch:
  ✅ True — one of the ITA’s terminal branches.

• It runs posterior to upper six costal cartilages:
  ✅ True — this protects it from trauma.

• It gives rise to anterior intercostal arteries:
  ✅ True — these supply the anterior thoracic wall.

• It runs superficial to the vagus nerve:
  ✅ True — the vagus nerve lies deeper in the mediastinum, not along the chest wall.

Bronchodilators work by relaxing bronchial smooth muscle, improving airflow.

• Levalbuterol → β₂-adrenergic agonist, causes bronchodilation

• Epinephrine → non-selective adrenergic agonist, bronchodilates via β₂ receptors

• Anti-adrenergic drugs → block α/β receptors in some contexts, leading to relaxation

• Anti-histamines → prevent histamine-induced bronchoconstriction

Acetylcholine, however, is a parasympathetic neurotransmitter:

• Acts on muscarinic receptors in bronchi → bronchoconstriction

• Not a bronchodilator; it’s actually the opposite.

According to Fick’s law of diffusion, the rate of gas diffusion across a membrane is:

Rate ∝ (A × ΔP × S) / (T × sqrt(MW))

Where:

• A = Surface area

• ΔP = Partial pressure difference

• S = Solubility

• T = Thickness

• MW = Molecular weight

• Increasing surface area (e.g., healthy alveoli) enhances diffusion, even if partial pressure is normal.

• Other factors: membrane thickness, solubility, and molecular weight also influence diffusion.

Other options:

• Decreased surface area → lowers diffusion (seen in emphysema)

• Decreased solubility / velocity → reduces diffusion

• Solubility of gas → affects diffusion, but “increased surface area” is the key factor in the question

Sympathetic ganglia include:

• Paravertebral (chain) ganglia

• Prevertebral (collateral) ganglia like celiac, superior mesenteric, inferior mesenteric

• Ganglion impar → the terminal ganglion of the sympathetic chain located anterior to the coccyx

Other options:

• Dorsal vagus nucleus → parasympathetic nucleus

• Dorsal root ganglion → sensory (afferent) neurons

• Ciliary ganglion / Otic ganglion → parasympathetic ganglia

In emphysema, alveolar walls are destroyed, reducing surface area for gas exchange. This leads to CO₂ retention (hypercapnia).

• Hypoventilation (respiratory rate 8/min) worsens CO₂ buildup.

• Increased PCO₂ → lowers blood pH, causing respiratory acidosis.

• The kidneys may compensate over time by retaining bicarbonate, but the primary disturbance is respiratory.

Other options:

• Respiratory alkalosis → caused by hyperventilation, not hypoventilation.

• Metabolic acidosis / alkalosis → disturbances in HCO₃⁻ or metabolic acids, not primarily due to emphysema.

The majority of CO₂ in the blood (~70%) is transported as bicarbonate (HCO₃⁻) in plasma. The rest is carried as:

• Carbaminohemoglobin (CO₂ bound to hemoglobin) → ~23%

• Dissolved CO₂ in plasma → ~7%

This conversion occurs via carbonic anhydrase in red blood cells and is critical for CO₂ transport from tissues to lungs.

During leukocyte recruitment, the adhesion-rolling phase is the first step in the leukocyte extravasation cascade.

• Selectins (L-, P-, and E-selectin) are expressed on endothelial cells and leukocytes.

• They mediate weak, transient binding to leukocytes, allowing them to roll along the vascular endothelium before firm adhesion.

Other options:

• Tumor necrosis factor (TNF) → activates endothelium, upregulates selectins and integrins, but doesn’t directly mediate rolling.

• C3b receptor → part of complement-mediated opsonization.

• Leukotrienes → mediate chemotaxis and increased vascular permeability.

• Histaminase → breaks down histamine, not involved in rolling.

On a chest X-ray, pleural effusion is most easily detected at the costophrenic angles — the acute angles formed between the diaphragm and the ribs.

• Normally, these angles are sharp.

• Fluid accumulation blunts the costophrenic angle, which is an early radiographic sign of effusion.

Other options:

• Cardiophrenic angle → can show effusion but less sensitive than costophrenic angle

• Infrasternal angle / Base of the lungs / Sternal angle → not the standard radiographic landmark for detecting pleural fluid

CO₂ Transport in Blood

1. Total CO₂ content in arterial blood:
   Normal total CO₂ in 100 ml of arterial blood is about 48 ml.

2. Forms of CO₂ in blood:

   • Bicarbonate (HCO₃⁻) → ~70% of total CO₂

   • Carbaminohemoglobin (CO₂ bound to Hb) → ~23%

   • Dissolved CO₂ in plasma → ~7%

3. Dissolved CO₂ alone:
   If someone quotes ~4 ml, they are probably referring only to the dissolved CO₂ fraction, not the total CO₂ content.

Conclusion:

• 48 ml/100 ml blood → total CO₂ content transferred from tissues to lungs

• 4 ml/100 ml → only dissolved CO₂, insufficient to represent the total transfer.

The trachea bifurcates at the level of the sternal angle (Angle of Louis), which corresponds to the T4–T5 intervertebral disc posteriorly.

• Right and left primary bronchi arise here.

• The carina (ridge inside the trachea at the bifurcation) is a key landmark in bronchoscopy.

Other options:

• T1/T2 → upper thoracic vertebrae, trachea still intact.

• T6/T7 → lower than the bifurcation, already within the lungs.

Nonsteroidal anti-inflammatory drugs (NSAIDs) exert their action by inhibiting cyclooxygenase (COX) enzymes, which catalyze the conversion of arachidonic acid → prostaglandins and thromboxanes.
By blocking this pathway, NSAIDs reduce:

• Inflammation

• Pain

• Fever

• Platelet aggregation (for some NSAIDs like aspirin)

Other options:

• Helps in formation of prostaglandins → opposite effect

• Helps metabolizing arachidonic acid → not the mechanism

• Formation of steroids → unrelated; corticosteroids act differently

• Inhibits lipoxygenase pathway → leukotriene pathway, target of specific drugs (e.g., zileuton)

Thromboxane A₂ (TXA₂) is a potent vasoconstrictor and platelet aggregator. It is synthesized primarily by activated platelets via the cyclooxygenase (COX) pathway from arachidonic acid.
It plays a crucial role in hemostasis and thrombosis.

Other options:

• Respiratory/olfactory epithelium → involved in lining and sensory functions, not TXA₂ production

• Neutrophils → produce leukotrienes, not TXA₂

• Mast cells → release histamine and leukotrienes, not TXA₂

The thoracic duct drains lymph from most of the body, including:

• Both lower limbs

• Left side of thorax and upper limb

• Left bronchomediastinal trunk

• Left intercostal nodes

The right intercostal nodes drain into the right lymphatic duct (or directly into the right venous angle), not the thoracic duct.

The olfactory epithelium is a specialized region responsible for smell, located in the roof of the nasal cavity. It also extends slightly onto:

• Upper part of the nasal septum (medial wall)

• Superior nasal concha (lateral wall)

It contains:

• Olfactory receptor cells

• Supporting (sustentacular) cells

• Basal cells (progenitors for new receptor cells)

Other options:

• Lateral walls / Medial walls / Floor → mainly lined by respiratory epithelium.

• Pharynx → not involved in olfaction.

The trachea and esophagus can be distinguished histologically by their epithelial lining:

• Trachea → ciliated pseudostratified columnar epithelium with goblet cells (respiratory epithelium)

• Esophagus → stratified squamous non-keratinized epithelium

Other layers (blood vessels, adventitia, submucosa, glands) are present in both organs and are not distinctive enough for differentiation.

Key features of the right main bronchus:

• More vertical than the left bronchus → why aspirated objects often enter the right lung

• About 6 cm in length

• Azygos vein arches superiorly and posteriorly to it

• Bifurcation (carina) at T4/T5 vertebral level

It does NOT lie posterior to the aortic arch — that is a feature of the left main bronchus, which passes under the aortic arch and anterior to the esophagus and thoracic aorta.

The interalveolar septum is the thin wall between adjacent alveoli, primarily designed for gas exchange. It contains:

• Blood capillaries – for oxygen and carbon dioxide exchange

• Reticular fibers – provide structural support

• Elastic fibers – allow recoil during expiration

• Dust cells (alveolar macrophages) – phagocytose inhaled particles

Neutrophils, however, are not normally present in the septum; they appear only during acute inflammation or infection.

✅ Correct Answer: Tobacco

Explanation:
Tobacco smoking is by far the most common cause of lung cancer, accounting for about 85–90% of all cases. Cigarette smoke contains numerous carcinogens, including polycyclic aromatic hydrocarbons, nitrosamines, benzopyrene, and heavy metals, which damage DNA in bronchial epithelial cells and lead to malignant transformation.

Prolonged exposure causes mutations in key genes such as TP53, KRAS, and EGFR, resulting in uncontrolled cell growth.
Both active and passive smoking increase the risk, and the risk correlates directly with the number of cigarettes smoked per day and duration of smoking.

Types of lung cancer most commonly associated with tobacco include:

• Squamous cell carcinoma (strongest correlation)

• Small cell carcinoma (neuroendocrine origin)

Cessation of smoking gradually reduces but never fully eliminates the risk.

❌ Aromatic fumes:
Contain carcinogens but are a minor occupational hazard, not the leading cause of lung cancer in the general population.

❌ Hydrocarbons:
Present in fuels and industrial emissions, they can be carcinogenic but are secondary contributors compared to tobacco.

❌ Radiation:
May increase risk (e.g., radon gas exposure), but contributes to a small fraction of cases.

❌ Sunlight:
Linked to skin cancers (e.g., basal cell carcinoma, melanoma), not lung cancer.

✅ Correct Answer: Asbestos

Explanation:
Asbestos exposure is the classic cause of malignant mesothelioma, a cancer of the pleural or peritoneal mesothelium. It typically develops decades after exposure and is most often seen in individuals who have worked in:

• Shipbuilding

• Construction and insulation

• Brake and roofing material industries

Pathogenesis: inhaled asbestos fibers lodge in the pleura, causing chronic inflammation, fibrosis (asbestosis), and DNA damage leading to malignant transformation of mesothelial cells.
Histologically, the tumor shows asbestos bodies (ferruginous bodies) — golden-brown, beaded rods coated with iron-containing protein.

Mesothelioma presents with:

• Progressive dyspnea

• Recurrent pleural effusions

• Chest pain

• Diffuse pleural thickening

While asbestos exposure also increases the risk of bronchogenic carcinoma, mesothelioma is its most specific malignancy.

❌ Coal dust:
Causes coal workers’ pneumoconiosis, a restrictive lung disease due to dust accumulation in alveoli, but not mesothelioma.

❌ Tin oxide:
Leads to stannosis, a benign pneumoconiosis with radiopaque deposits but no fibrosis or malignancy.

❌ Tobacco:
Strongly associated with lung carcinoma (especially squamous cell and small cell types) but not mesothelioma. However, smoking synergistically increases the risk of bronchogenic carcinoma in asbestos-exposed individuals.

❌ Silica:
Causes silicosis, characterized by nodular pulmonary fibrosis and increased susceptibility to tuberculosis — not mesothelioma.

✅ Correct Answer: Legionella pneumophila

Explanation:
Legionella pneumophila is a gram-negative intracellular bacterium that causes Legionnaires’ disease, a severe form of pneumonia — especially in immunocompromised patients, the elderly, and those with chronic lung disease.

It thrives in water sources such as air-conditioning systems, humidifiers, and hospital water tanks. Transmission occurs through inhalation of aerosolized contaminated water, not person-to-person spread.

In immunocompromised individuals, Legionella multiplies within alveolar macrophages, evading immune defenses, and leads to:

• Severe pneumonia with high fever, cough, and dyspnea

• Gastrointestinal symptoms (diarrhea, vomiting)

• Hyponatremia (low serum sodium)

• Elevated liver enzymes

Diagnosis is often made via urinary antigen testing or culture on buffered charcoal yeast extract (BCYE) agar.

❌ Haemophilus influenzae:
Common cause of pneumonia in children and adults with COPD, but not typically associated with immunocompromised states like Legionella is.

❌ Staphylococcus aureus:
Can cause post-influenza pneumonia or hospital-acquired pneumonia, but it’s not the most characteristic in immunocompromised hosts unless there is direct healthcare exposure.

❌ Klebsiella pneumoniae:
Causes lobar pneumonia in alcoholics, diabetics, or debilitated individuals, producing thick, mucoid “currant jelly” sputum — not specifically tied to immunosuppression.

❌ Mycoplasma pneumoniae:
Causes “walking pneumonia” in young, healthy adults (e.g., students, military recruits), not in immunocompromised patients.

✅ Correct Answer: Cyanide poisoning

Explanation:
In cyanide poisoning, oxygen delivery to tissues is normal, but cells are unable to utilize the oxygen because cyanide inhibits cytochrome c oxidase (Complex IV) in the mitochondrial electron transport chain.

This halts oxidative phosphorylation, preventing the production of ATP and causing cellular hypoxia despite normal oxygen levels in the blood — a condition called histotoxic hypoxia.
As a result, venous blood remains highly oxygenated (bright red), since tissues cannot extract or use the oxygen.

Clinical features include:

• Rapid loss of consciousness

• Hypotension and metabolic acidosis

• Bright red venous blood

• Smell of bitter almonds (in some cases)

Treatment involves amyl nitrite or sodium nitrite (to induce methemoglobinemia, which binds cyanide) and thiosulfate, which converts cyanide to a less toxic compound.

❌ Decreased hydrogen ion concentration (alkalosis):
This affects hemoglobin’s affinity for oxygen (Bohr effect) but does not block cellular oxygen utilization.

❌ Decreased 2,3-bisphosphoglycerate (2,3-BPG):
This shifts the oxygen dissociation curve to the left, meaning oxygen binds more tightly to hemoglobin, but cells can still use oxygen once released.

❌ Carbon monoxide poisoning:
This causes functional anemia by forming carboxyhemoglobin, reducing oxygen transport — not cellular utilization. Oxygen is not used because it’s not effectively delivered, not because enzymes are blocked.

❌ Increase in pH:
Alkalosis may affect oxygen binding but does not impair oxidative metabolism in cells.

✅ Correct Answer: Chylothorax

Explanation:
Chylothorax refers to the accumulation of lymphatic fluid (chyle) in the pleural cavity, giving the fluid a milky appearance due to the presence of emulsified fats (triglycerides) absorbed from the intestines.

The thoracic duct, which carries chyle from the gastrointestinal tract and lower body to the venous system, may be damaged or obstructed by:

• Malignant tumors (especially lymphomas, as in this case)

• Trauma or surgical injury to the thoracic duct

• Filariasis (less commonly)

The trapped lymph fluid leads to respiratory distress and must be distinguished from empyema or lipid effusions by its high triglyceride content and presence of chylomicrons.

❌ Suppurative pleuritis:
This refers to empyema, a pus-filled pleural effusion caused by bacterial infection (e.g., Streptococcus, Staphylococcus). The fluid here is purulent, not milky.

❌ Miliary tuberculosis:
A disseminated form of tuberculosis producing tiny granulomatous nodules in multiple organs, not a cause of milky pleural effusion.

❌ Pneumothorax:
Refers to air in the pleural cavity, not fluid. It causes sudden chest pain and dyspnea, but no fluid accumulation.

❌ Filariasis:
Can occasionally cause chylous effusion due to lymphatic obstruction by Wuchereria bancrofti, but in this case, the primary cause is the mediastinal lymphoma obstructing the thoracic duct.

✅ Correct Answer: Adenoma

Explanation:
An adenoma is a benign tumor arising from glandular epithelial tissue. The term “adeno” refers to glands, and “oma” denotes a benign neoplasm.
Adenomas may form in gland-forming organs (e.g., thyroid, adrenal, pituitary) or in non-glandular organs with secretory epithelium (e.g., colon, liver).

Histologically, adenomas maintain well-differentiated glandular architecture, do not invade surrounding tissues, and lack metastasis, distinguishing them from malignant adenocarcinomas.

Common examples include:

• Thyroid adenoma

• Hepatic adenoma

• Colonic tubular adenoma (precancerous but still benign)

❌ Choriocarcinoma:
A malignant tumor of trophoblastic (placental) origin, characterized by aggressive invasion and early blood-borne metastasis.

❌ Papilloma:
A benign epithelial tumor that grows on epithelial surfaces forming finger-like projections, not specifically glandular in nature.

❌ Sarcoma:
A malignant tumor derived from mesenchymal tissue (connective tissue, muscle, bone, etc.), not from epithelium.

❌ Polyp:
A macroscopic projection or growth from a mucosal surface. It describes a shape, not a tumor type. Polyps may be neoplastic (like adenomatous polyps) or non-neoplastic (inflammatory or hyperplastic).

✅ Correct Answer: Cyanosis

Explanation:
Cyanosis refers to the bluish or purplish discoloration of the skin and mucous membranes caused by an increased concentration of deoxygenated (reduced) hemoglobin in the blood — typically more than 5 g/dL.

It indicates inadequate oxygenation of the blood or impaired circulation, leading to visible changes especially in areas like the lips, fingertips, and nail beds.
There are two main types:

• Central cyanosis: due to systemic arterial desaturation (e.g., congenital heart disease, respiratory failure).

• Peripheral cyanosis: due to sluggish blood flow or local oxygen extraction (e.g., cold exposure, heart failure).

❌ Hypoxemia:
Refers to low oxygen tension (PaO₂) in arterial blood. It can cause cyanosis but is a biochemical finding, not a visible sign.

❌ Anorexia:
Means loss of appetite, unrelated to oxygenation or hemoglobin.

❌ Hypoxia:
Refers to reduced oxygen supply to tissues. Cyanosis can be a manifestation of hypoxia, but hypoxia itself is a physiologic state, not a color change.

❌ Anemia:
A reduction in total hemoglobin concentration. Paradoxically, cyanosis may not be seen in severe anemia because there’s not enough hemoglobin — even reduced — to impart a blue color.

✅ Correct Answer: Mycobacterium bovis

Explanation:
Mycobacterium bovis is a member of the Mycobacterium tuberculosis complex that primarily infects cattle but can transmit to humans through ingestion of unpasteurized milk or dairy products from infected animals.

In humans, it causes a disease clinically similar to tuberculosis, with symptoms such as anorexia, weight loss, lethargy, and abdominal pain — the latter often due to intestinal involvement (especially ileocecal region).
It can also spread to lymph nodes, bones, and other organs.

Pasteurization of milk has nearly eliminated M. bovis infections in developed regions, but it remains a concern in rural areas where unpasteurized milk consumption is common.

❌ Mycobacterium tuberculosis:
Causes pulmonary tuberculosis via airborne transmission, not through ingestion of contaminated milk.

❌ Mycobacterium ulcerans:
Responsible for Buruli ulcer, a necrotizing skin infection found in tropical regions, not systemic disease from dairy exposure.

❌ Mycobacterium leprae:
Causes leprosy (Hansen’s disease), affecting skin and peripheral nerves, and is not transmitted by milk or food products.

❌ Mycobacterium avium:
An opportunistic pathogen causing disseminated infections in immunocompromised individuals (e.g., AIDS patients), usually acquired from water or soil, not dairy.

✅ Correct Answer: Retention of dye due to the presence of mycolic acid

Explanation:
Mycobacterium tuberculosis appears red on Ziehl–Neelsen (acid-fast) staining because its cell wall contains mycolic acids — long-chain fatty acids that make the wall waxy, lipid-rich, and impermeable to most stains.

During the procedure, the bacterium takes up carbol fuchsin (red dye) when heated. The waxy mycolic acid prevents the dye from being removed even after treatment with acid-alcohol, which normally decolorizes other bacteria. Thus, Mycobacterium remains acid-fast — it retains the red dye, while the background and non–acid-fast organisms take up the blue counterstain (methylene blue).

❌ Transmembrane channels in its walls:
These channels help transport molecules but do not confer acid-fastness or dye retention. The key is the lipid-rich wall, not the presence of channels.

❌ Hydrophilic nature of its walls:
Mycobacteria have hydrophobic, not hydrophilic, cell walls due to high lipid content. This hydrophobicity actually hinders the penetration of ordinary stains.

❌ Discoloration by acid alcohol:
This describes non–acid-fast organisms, which lose the primary dye upon acid-alcohol washing. Mycobacteria resist this decolorization.

❌ Absorption of counter stain:
This occurs in non–acid-fast bacteria, which lose the red dye and then take up the blue counterstain. Mycobacteria, being acid-fast, do not absorb the counterstain significantly.

✅ Correct Answer: Usual interstitial pneumonia

Explanation:
Usual interstitial pneumonia (UIP) is the histopathologic pattern seen in idiopathic pulmonary fibrosis (IPF). It is a chronic, progressive interstitial lung disease that leads to irreversible scarring of lung tissue. The disease evolves through distinct stages:

1. Early interstitial fibrosis — patchy alveolar wall thickening with fibroblast foci.

2. Diffuse fibrosis — destruction of alveolar architecture and distortion of lung parenchyma.

3. End-stage “honeycomb lung” — cystic spaces lined by bronchiolar epithelium due to extensive fibrosis and alveolar collapse.

Grossly, the lung shows cobblestone pleural surfaces and firm, contracted parenchyma, especially in subpleural and basal regions.
Patients typically present with progressive dyspnea, dry cough, and fine “Velcro” crackles on auscultation.

❌ Non-specific interstitial pneumonia (NSIP):
Shows uniform interstitial inflammation and fibrosis without the patchy, temporally heterogeneous pattern of UIP. It generally has a better prognosis and no honeycomb lung formation.

❌ Cryptogenic organizing pneumonia (COP):
Characterized by intraluminal plugs of granulation tissue (Masson bodies) within alveoli and bronchioles, not interstitial fibrosis or honeycombing.

❌ Pneumoconiosis:
Caused by inhalation of inorganic dusts (e.g., silica, coal, asbestos). Though fibrosis may occur, honeycomb appearance is not the defining feature — lesions depend on the type of dust.

❌ Sarcoidosis:
A granulomatous disease with non-caseating granulomas, often involving hilar lymph nodes and lungs, but fibrosis, when present, is peribronchial — not the patchy subpleural honeycombing typical of UIP.

✅ Correct Answer: Small cell carcinoma

Explanation:
Small cell carcinoma (SCC) of the lung is a highly malignant neuroendocrine tumor that is strongly associated with smoking.
Molecularly, it is characterized by chromosomal deletions on the short arm of chromosome 3 (3p) and mutations in the tumor suppressor genes TP53 and RB1. These genetic alterations promote uncontrolled cell growth and resistance to apoptosis.

Pathologically, small cell carcinoma shows:

• Small, round to oval cells with scant cytoplasm and hyperchromatic nuclei

• High mitotic rate and necrosis

• Expression of neuroendocrine markers such as chromogranin A, synaptophysin, and CD56

It is centrally located and often causes paraneoplastic syndromes such as:

• SIADH (from ectopic ADH production)

• Cushing’s syndrome (from ectopic ACTH production)

• Lambert-Eaton myasthenic syndrome

❌ Squamous cell carcinoma:
Also linked to smoking, but it shows keratin pearls and intercellular bridges, and commonly involves mutations in the p53 gene without the characteristic Rb loss and 3p deletion combination.

❌ Large cell carcinoma:
A poorly differentiated non-small cell carcinoma that lacks glandular or squamous differentiation; it does not consistently show 3p deletions or Rb loss.

❌ Basal cell carcinoma:
Occurs in the skin, not the lung. It is associated with PTCH1 gene mutations, not with TP53 or 3p deletions.

❌ Adenocarcinoma:
Common in nonsmokers and peripheral lung regions, typically involving EGFR, KRAS, or ALK mutations, not 3p or Rb alterations.

✅ Correct Answer: Remodeling of airways with smooth muscle hyperplasia

Explanation:
The clinical picture — childhood onset, episodic wheezing, cough, dyspnea triggered by allergens (spring season), elevated IgE, and eosinophilia — is classic for bronchial asthma (a type I hypersensitivity reaction).

In asthma, repeated episodes of airway inflammation cause chronic structural changes known as airway remodeling, characterized by:

• Hypertrophy and hyperplasia of bronchial smooth muscle → narrowing of airways

• Thickened basement membrane due to subepithelial collagen deposition

• Goblet cell hyperplasia → increased mucus production

• Eosinophilic infiltration and presence of Curschmann spirals (mucus plugs) and Charcot-Leyden crystals in sputum

These changes contribute to airflow obstruction and hyperresponsiveness typical of asthma.

❌ Alveolar and interstitial edema with sheets of macrophages:
Seen in congestive heart failure and acute pulmonary edema, not in asthma. The fluid accumulation here is due to increased hydrostatic pressure, not airway inflammation.

❌ Dilatation of bronchi and loss of elastic tissue:
Characteristic of bronchiectasis, a condition involving chronic infection and destruction of bronchial walls, often with foul-smelling sputum — unlike the reversible obstruction in asthma.

❌ Inflammatory destruction of bronchiolar walls:
Seen in bronchiolitis obliterans, typically after viral infections or inhalation injury — not in allergic asthma.

❌ Patchy consolidation in lung parenchyma:
This finding suggests bronchopneumonia, where alveoli are filled with neutrophilic exudate — asthma involves airway, not alveolar, inflammation.

✅ Correct Answer: Acid-fast bacilli

Explanation:
The patient’s presentation — weight loss, low-grade fever, chronic productive cough, and blood-streaked sputum — strongly suggests pulmonary tuberculosis (TB). The acid-fast bacilli (AFB) seen as bright red rods against a blue background on Ziehl-Neelsen staining are characteristic of Mycobacterium tuberculosis.

These organisms have mycolic acids in their cell wall, which retain carbol fuchsin dye even after acid-alcohol decolorization — hence the term acid-fast.
Key findings include:

• Chronic cough with hemoptysis

• Upper lobe involvement (due to higher oxygen tension)

• Weight loss and low-grade fever (evening rise)

• AFB-positive sputum smear confirming infection

❌ Foreign body giant cells:
These are multinucleated macrophages formed in response to foreign materials (like sutures or splinters), not infection. In TB, Langhans giant cells may be found in granulomas on biopsy, but not in sputum.

❌ Branching septate hyphae:
These are seen in Aspergillus species infection, not TB. They appear as acute-angle (45°) branching filaments in sputum or tissue sections.

❌ Charcot-Leyden crystals:
These are bipyramidal crystals derived from eosinophil breakdown and are typically seen in bronchial asthma or parasitic infections, not TB.

❌ Gram-negative bacilli:
Commonly seen in bacterial pneumonias (like Klebsiella, Pseudomonas, or H. influenzae). Mycobacterium tuberculosis does not stain with the Gram method because of its waxy cell wall.

✅ Correct Answer: Nicotine

Explanation:
Nicotine is the primary addictive component of cigarette smoke and acts as a stimulant of the autonomic nervous system. It binds to nicotinic acetylcholine receptors (nAChRs) in both the central and peripheral nervous systems, leading to the release of catecholamines (epinephrine and norepinephrine) from the adrenal medulla.

This sympathetic activation results in:

• Increased heart rate

• Elevated blood pressure

• Heightened alertness and nervous activity

• Vasoconstriction, which reduces peripheral blood flow

Chronic nicotine exposure contributes to cardiovascular strain and increases the risk of hypertension and coronary artery disease.

❌ Aromatic hydrocarbons:
These include compounds like benzopyrene, which are potent carcinogens that damage DNA and lead to lung cancer, but they do not affect heart rate or the nervous system directly.

❌ Nitric oxide:
Although present in cigarette smoke, nitric oxide acts as a vasodilator and a free radical that contributes to oxidative damage — not stimulation of the nervous system.

❌ Asbestos:
This is an inorganic fiber, not a component of cigarette smoke. It causes asbestosis and mesothelioma when inhaled from occupational exposure, not increased heart rate.

❌ Silica:
Also an occupational dust hazard, silica causes silicosis but is not present in tobacco smoke and has no stimulatory effect on the nervous system.

✅ Correct Answer: Thromboxane A₂ causes platelet aggregation while prostaglandins decrease it

Explanation:
Both thromboxane A₂ (TXA₂) and prostaglandins (particularly prostacyclin, PGI₂) are derived from arachidonic acid through the cyclooxygenase (COX) pathway, but they have opposite physiological effects:

• Thromboxane A₂, produced mainly by platelets, causes vasoconstriction and promotes platelet aggregation — encouraging clot formation to stop bleeding.

• Prostacyclin (PGI₂), produced by vascular endothelial cells, causes vasodilation and inhibits platelet aggregation, preventing excessive clotting.

Together, they maintain a delicate balance between clot formation and blood flow — a perfect example of physiological antagonism.

❌ Thromboxane A₂ causes vasodilation while prostaglandins cause vasoconstriction:
The opposite is true — TXA₂ causes vasoconstriction, while prostaglandins (specifically PGI₂) cause vasodilation.

❌ Thromboxane A₂ decreases platelet aggregation while prostaglandins increase it:
This reverses their actual roles — TXA₂ promotes aggregation; prostacyclin inhibits it.

❌ Thromboxane A₂ mediates allergic reactions while prostaglandins do not:
Allergic reactions are primarily mediated by histamine and leukotrienes, not TXA₂.

❌ Thromboxane A₂ mediates pain while prostaglandins do not:
Pain and inflammation are mediated by prostaglandins (especially PGE₂), not thromboxane.

✅ Correct Answer: Slight increase in pulmonary pressure

Explanation:
During exercise, cardiac output increases significantly (up to 4–7 times the resting value) to meet the body’s higher oxygen demands. However, the pulmonary circulation accommodates this increased blood flow with only a slight rise in pulmonary arterial pressure.

This is because the lungs have several adaptive mechanisms:

• Recruitment: previously unused pulmonary capillaries open up.

• Distension: existing capillaries widen to allow more blood flow.
  These adjustments reduce pulmonary vascular resistance, allowing more blood to pass through without a large pressure rise.

As a result, despite the massive increase in flow, pulmonary pressure increases only slightly, maintaining efficient gas exchange and preventing pulmonary edema.

❌ Sometimes decreased, sometimes increased pulmonary pressure:
Pulmonary pressure follows a predictable physiological response — it slightly increases, not variably fluctuates, during exercise.

❌ Massive increase in pulmonary pressure:
This does not occur in healthy individuals; a massive rise would indicate pulmonary hypertension or left heart failure, not normal exercise physiology.

❌ No increase in pulmonary pressure:
Complete constancy is impossible because increased flow through any vascular system creates at least a minor rise in pressure, even with compensatory mechanisms.

❌ Decrease in pulmonary pressure:
This is physiologically impossible during exercise because both cardiac output and pulmonary blood flow increase.

✅ Correct Answer: Tidal volume + inspiratory reserve volume + expiratory reserve volume

Explanation:
Vital Capacity (VC) is the maximum amount of air a person can exhale after a maximal inspiration. It represents the total volume of air involved in active breathing (not including the residual volume that always remains in the lungs).
Mathematically:

VC=Tidal Volume (TV)+Inspiratory Reserve Volume (IRV)+Expiratory Reserve Volume (ERV)\text{VC} = \text{Tidal Volume (TV)} + \text{Inspiratory Reserve Volume (IRV)} + \text{Expiratory Reserve Volume (ERV)}VC=Tidal Volume (TV)+Inspiratory Reserve Volume (IRV)+Expiratory Reserve Volume (ERV)

• Tidal Volume (TV): air inhaled/exhaled in a normal breath (~500 mL)

• Inspiratory Reserve Volume (IRV): extra air that can be inhaled after a normal inspiration (~3000 mL)

• Expiratory Reserve Volume (ERV): extra air that can be exhaled after a normal expiration (~1100 mL)

Vital capacity reflects the functional strength of the respiratory muscles and the elasticity of the lungs and chest wall.

❌ Tidal volume + expiratory reserve volume + residual volume:
This combination excludes the inspiratory reserve volume and includes residual volume, which remains in the lungs after maximal expiration — it is not part of the vital capacity.

❌ Residual volume + tidal volume + expiratory reserve volume:
Again, this includes residual volume, which cannot be voluntarily exhaled, hence it does not contribute to vital capacity.

❌ Tidal volume + inspiratory reserve volume:
This equals Inspiratory Capacity (IC), not vital capacity.

❌ Tidal volume + expiratory reserve volume:
This equals Expiratory Capacity (EC), not vital capacity.

✅ Correct Answer: Pneumotaxic centre

Explanation:
The pneumotaxic centre, located in the upper pons, plays a critical role in regulating the pattern of breathing. It sends inhibitory signals to the inspiratory center (mainly the dorsal respiratory group in the medulla) to limit inspiration—that is, it stops the inspiratory ramp signal early.

By shortening the duration of inspiration, the pneumotaxic centre reduces tidal volume (the amount of air inspired per breath) but increases the respiratory rate. This allows for rapid, shallow breathing. Strong stimulation leads to faster breathing, while weak activity allows deeper, slower breaths.

❌ Ventral respiratory group of neurons:
Located in the medulla, this group mainly controls forced expiration and also contributes to increased inspiratory effort during exercise or distress, not to limiting tidal volume.

❌ Dorsal respiratory group of neurons:
Also in the medulla, this group generates the basic rhythm of inspiration. It is modulated by the pneumotaxic and apneustic centers but does not itself limit tidal volume.

❌ Central chemoreceptors:
These are located in the medulla near the respiratory center and respond to changes in CO₂ and hydrogen ion concentration in cerebrospinal fluid. They influence overall ventilation rate but do not directly limit inspiration duration or tidal volume.

❌ Apneustic centre:
Located in the lower pons, this center has the opposite effect — it prolongs inspiration by stimulating the inspiratory neurons and delaying the “off-switch” for inspiration.

✅ Correct Answer: Type 2 alveolar epithelial cells

Explanation:
Type II alveolar epithelial cells (also called Type II pneumocytes) are specialized cuboidal cells located in the alveolar walls, usually at the corners of the alveoli. Their main function is to secrete pulmonary surfactant, a lipoprotein substance that reduces surface tension within the alveoli and prevents their collapse (atelectasis) during exhalation.
Surfactant also helps maintain alveolar stability, improves lung compliance, and plays a role in host defense.

❌ Squamous epithelial cells of trachea:
These cells line the upper respiratory tract and serve a protective role. They do not participate in gas exchange or surfactant secretion.

❌ Type 1 alveolar epithelial cells:
These are flat squamous cells that cover about 95% of the alveolar surface area. Their function is gas exchange, not secretion. They form part of the blood-air barrier, allowing oxygen and carbon dioxide to diffuse efficiently.

❌ Endothelial cells:
These line the capillaries within the alveolar septa and are involved in gas exchange and fluid balance, not surfactant production.

❌ Secretory cells:
This is a nonspecific term; various secretory cells exist in the respiratory tract (like Clara cells in bronchioles), but not in the alveoli for surfactant secretion. The specific surfactant-producing cells are Type II pneumocytes.

✅ Correct Answer: Bicarbonate ion in plasma

Explanation:
The majority (about 70%) of carbon dioxide in the blood is transported as bicarbonate ions (HCO₃⁻) in the plasma. Inside red blood cells, carbon dioxide reacts with water under the action of carbonic anhydrase, forming carbonic acid (H₂CO₃), which quickly dissociates into H⁺ and HCO₃⁻ ions. The bicarbonate ions then diffuse out of the RBC into the plasma in exchange for chloride ions (the chloride shift). This mechanism allows efficient CO₂ transport from tissues to lungs for exhalation.

❌ Bicarbonate ion in red blood cells:
Although bicarbonate is produced in red blood cells, it does not remain there in significant amounts—it diffuses into the plasma almost immediately. Thus, the main storage form is in plasma, not within RBCs.

❌ Carbaminohemoglobin:
About 20–25% of CO₂ binds directly to hemoglobin (at globin’s amino groups) forming carbaminohemoglobin, but this represents a smaller fraction compared to bicarbonate transport.

❌ Dissolved in blood:
Only about 5–10% of CO₂ is simply dissolved in the plasma and carried as free gas. This form contributes minimally to total CO₂ transport.

❌ Carbonic acid:
Carbonic acid is a transient intermediate formed inside RBCs. It rapidly dissociates into bicarbonate and hydrogen ions, so its actual concentration in the blood is extremely low.

✅ Correct Answer: Inter-alveolar septum

Explanation:
The inter-alveolar septum is the thin wall that separates adjacent alveoli. It contains the capillary network through which gaseous exchange occurs between the air in the alveoli and the blood. Structurally, it consists of:

• Two layers of alveolar epithelium (simple squamous epithelium made of type I pneumocytes)

• A fused basement membrane between them

• Interstitial tissue containing elastic fibers, collagen fibers, and capillaries

This design provides maximum surface area with minimal diffusion distance, facilitating efficient gas exchange.

❌ Alveolar epithelium:
This refers to the lining of an individual alveolus, composed of type I and type II pneumocytes. It forms part of the septum but does not lie between two alveoli.

❌ Alveolar phagocytes:
Also called dust cells, these are macrophages that remove debris and microorganisms within the alveolar lumen. They do not form a structural barrier between alveoli.

❌ Alveolar ducts:
These are passages that connect the respiratory bronchioles to the alveolar sacs. They lead toward alveoli, not between them.

❌ Atrium:
The alveolar atrium is the central space into which multiple alveolar ducts open. It does not lie between alveoli; rather, it serves as a common opening area.

✅ Correct Answer:

Arachidonic acid

Prostaglandins are synthesized from arachidonic acid, a 20-carbon polyunsaturated fatty acid found in cell membrane phospholipids.
When cells are stimulated (e.g., by injury, inflammation, or hormones), phospholipase A₂ releases arachidonic acid from membrane phospholipids.
It is then converted into prostaglandin H₂ (PGH₂) through the cyclooxygenase (COX) pathway — the first step catalyzed by COX-1 and COX-2 enzymes.
PGH₂ serves as the common precursor for various prostaglandins, prostacyclins, and thromboxanes that regulate inflammation, vascular tone, and platelet function.

❌ Incorrect Options:

• Nitric oxide — ❌ A gaseous signaling molecule involved in vasodilation, not in prostaglandin synthesis.

• Arginine — ❌ Precursor for nitric oxide, not prostaglandins.

• Glucose — ❌ Used in energy metabolism, not in eicosanoid formation.

• Oxygen — ❌ Required as a reactant by the COX enzyme, but not the substrate from which prostaglandins are synthesized.

The correct amount of oxygen carried by 1 gram of hemoglobin is 1.34 ml.

This value, often called the Hüfner constant or oxygen-carrying capacity of hemoglobin, is a standard physiological measure.

❌ Why Other Options Are Incorrect:

• 20.1 ml: This is the total oxygen capacity per 100 ml of blood, not per gram of hemoglobin.

• 1.35 ml: Very close to the correct value, but the physiologically accepted constant is 1.34 ml O₂/g Hb (the slight difference comes from experimental rounding).

• 15 ml: Represents approximate O₂ content in venous blood per 100 ml, not per gram of Hb.

• 1 ml: Underestimates the O₂-carrying capacity of hemoglobin.

In glomus cells of the carotid and aortic bodies, the main mechanism of depolarization in response to hypoxia (low PO₂) is closure of oxygen-sensitive potassium (K⁺) channels.

Here’s how it happens step by step:

1. At normal PO₂, potassium channels remain open, allowing K⁺ efflux (movement out of the cell), which maintains a stable resting membrane potential.

2. When PO₂ drops below ~60 mmHg, these K⁺ channels close, reducing K⁺ efflux.

3. The inside of the cell becomes less negative (depolarized).

4. This depolarization opens voltage-gated calcium channels, allowing Ca²⁺ influx.

5. The increased intracellular calcium triggers release of neurotransmitters (like dopamine), which activate the afferent nerve endings of the glossopharyngeal and vagus nerves, leading to increased respiratory drive.

This mechanism is crucial in maintaining respiratory homeostasis. In chronic hypoxemia (e.g., COPD or high-altitude exposure), carotid bodies adapt, increasing their sensitivity to low oxygen and helping regulate ventilation.

❌ Why Other Options Are Incorrect:

• Opening of chloride channels: Would hyperpolarize the cell (more negative inside), inhibiting rather than stimulating activity.

• Opening of calcium channels: Occurs after depolarization; it’s a downstream effect, not the cause of depolarization.

• Opening of sodium channels: Not the main mechanism in these chemoreceptors — Na⁺ channels are important in neurons but not in glomus cell hypoxia sensing.

• Closure of sodium channels: Would reduce excitability and prevent depolarization.

Transpulmonary pressure (also called transmural pressure of the lung) is the difference between alveolar pressure (PA) and intrapleural pressure (Ppl):

​Ptp​=PA​−Ppl​

This pressure difference keeps the lungs expanded against the inward elastic recoil of lung tissue. When transpulmonary pressure increases (for example, during inspiration), the lungs distend as air flows in. Conversely, if it decreases (such as when the pleural cavity is breached in pneumothorax), the lungs collapse.

Thus, transpulmonary pressure is the main distending force that maintains lung inflation.

❌ Why Other Options Are Incorrect:

• Airway opening pressure: Refers to the pressure at the mouth or nose, not the pressure that keeps the lungs inflated.

• Airway closing pressure: The pressure below which small airways begin to collapse — important in pathology, not in lung distention.

• Transthoracic pressure: The difference between alveolar and body surface pressure; it reflects the overall pressure needed to expand both lung and chest wall, not just the lungs.

• Alveolar pressure: The pressure within the alveoli; it fluctuates during breathing but does not represent the distending force itself.

A buffer solution is a solution that maintains a nearly constant pH when small quantities of acid or base are added. It does so by containing a weak acid and its conjugate base (or a weak base and its conjugate acid). These components react with any added hydrogen ions (H⁺) or hydroxide ions (OH⁻), preventing large shifts in pH.

In biological systems, maintaining pH is critical — for example, blood is buffered by the carbonic acid–bicarbonate system (H₂CO₃/HCO₃⁻), keeping its pH around 7.4.

❌ Why Other Options Are Incorrect:

• Super-saturated solution: Contains more solute than normally possible at a given temperature; it relates to solubility, not pH stability.

• Strong acid solution: Completely ionizes and drastically changes pH with even small additions of acid or base.

• Unsaturated solution: Has not reached the limit of solute dissolution; again, unrelated to pH buffering.

• Saturated solution: Contains maximum solute at equilibrium, but it does not resist pH changes.

Breathing is controlled by several groups of neurons located in the medulla oblongata and pons, each responsible for different phases of respiration.

🔹 Ventral Respiratory Group (VRG)

• Located in the ventrolateral medulla.

• Inactive during quiet breathing.

• Activated during forceful breathing (active expiration)—for example, during exercise or labored breathing.

• Stimulates expiratory muscles, such as the internal intercostal and abdominal muscles, to contract and push air out of the lungs.

Thus, stimulation of the VRG leads to active (forced) expiration.

❌Why Other Options Are Incorrect:

• Dorsal Respiratory Group (DRG):
  Mainly controls inspiration, especially quiet inspiration, by stimulating the diaphragm via the phrenic nerve.

• Central Chemoreceptors:
  Respond to elevated CO₂ (via increased H⁺ concentration) in cerebrospinal fluid; they modulate respiration but don’t directly cause active expiration.

• Pneumotaxic Center (in Pons):
  Regulates the rate and pattern of breathing by inhibiting inspiration to prevent over-inflation of lungs, not directly involved in expiration.

• Apneustic Center (in Pons):
  Stimulates inspiration and is inhibited by the pneumotaxic center; does not initiate expiration.

🩺 Clinical Correlation:
In COPD or asthma, active expiration becomes a continuous process due to air trapping and increased work of breathing. The VRG is persistently stimulated, contributing to respiratory muscle fatigue over time.

Pulmonary surfactant is a phospholipid-protein complex secreted by type II pneumocytes (alveolar cells). Its key physiological role is to reduce, not increase, surface tension within the alveoli.

Mechanism:

• The alveolar surface is lined by a thin film of fluid that exerts surface tension due to cohesive forces between water molecules.

• This tension tends to make the alveoli collapse (atelectasis).

• Surfactant, mainly composed of dipalmitoylphosphatidylcholine, disrupts these cohesive forces, thereby lowering surface tension.

• This action stabilizes alveoli of different sizes and prevents collapse during expiration.

Therefore, the statement “Pulmonary surfactant → increases surface tension within alveoli” is incorrect

❌ Why Other Options Are Correct:

• Pneumocyte (alveolar cell) type I → cytoplasm through which gaseous exchange occurs:
  True. Type I pneumocytes are flat squamous cells covering ~95% of alveolar surface, facilitating rapid gas diffusion.

• Alveolar macrophage → removes inhaled particulates that reach the alveolus:
  True. These dust cells or alveolar macrophages phagocytose debris, microbes, and particles that escape mucociliary clearance.

• Pneumocyte type II → stem cell for more pneumocyte types I and II:
  True. Type II cells can divide and differentiate into both type I and type II pneumocytes, helping regenerate damaged alveoli.

• Pneumocyte type II → secretes pulmonary surfactant:
  True. Type II pneumocytes are cuboidal cells with lamellar bodies that store and release surfactant.