Respiration – 2019

The radial artery is the most common site for arterial puncture when obtaining arterial blood gases (ABG) — especially in conditions like respiratory distress syndrome (RDS).
It’s preferred because:

• It’s superficial and easily palpable.

• Has good collateral circulation via the ulnar artery and palmar arches.

• Minimizes complications if thrombosis occurs.

Other options:

• Ulnar artery → not preferred; used only if radial access is unavailable.

• Carotid artery → risky; close to vital structures.

• Popliteal artery → deep, difficult, and uncomfortable.

• Tibial artery → small and not ideal for ABG.

Gas diffusion follows a pressure gradient — from higher to lower partial pressure.
In the lungs, PCO₂ in pulmonary capillary blood (~45 mmHg) is higher than that of alveolar air (~40 mmHg) and much higher than that of inspired air (~0.3 mmHg).
Therefore, CO₂ diffuses from the capillary blood → alveoli → out with expiration, because the alveolar (and inspired) PCO₂ is lower.

Other options:

• Pulmonary capillaries → have higher PCO₂, so CO₂ moves out of them.

• Pulmonary vein → carries oxygenated blood, already low in CO₂.

• Bronchial artery → systemic blood supply, not part of gas exchange.

Type II pneumocytes (septal cells) are cuboidal epithelial cells found in the alveoli.
They produce pulmonary surfactant, a lipoprotein substance (mainly dipalmitoyl phosphatidylcholine) that reduces surface tension, thereby preventing alveolar collapse (atelectasis) during expiration.

Other options:

• Type I pneumocytes → form the thin gas-exchange surface, not surfactant.

• Alveolar macrophages → clear debris and microbes, not surfactant producers.

• Clara (Club) cells → secrete components of surfactant in bronchioles, not alveoli.

• Epithelial cells → too general; specifically Type II cells are responsible.

Type I pneumocytes (flat, squamous cells covering ~95% of alveolar surface) are derived from Type II pneumocytes, which act as progenitor (stem-like) cells.
After alveolar injury, Type II cells divide and differentiate into Type I cells to restore the epithelium.

Other options:

• Capillary endothelium → forms capillary lining, not alveolar epithelium.

• Alveolar macrophages → derived from monocytes, not epithelial origin.

• Brush border cells → found in bronchioles, not alveoli.

• Epithelial cells → too general; both pneumocytes are epithelial, but specifically Type II gives rise to Type I.

The M3 (muscarinic) receptors mediate parasympathetic stimulation of the detrusor muscle in the urinary bladder, causing its contraction during urination (micturition).
They act via Gq protein, which increases intracellular calcium in smooth muscle cells.

Other options:

• α₁ (A1) → causes contraction of the internal urethral sphincter, promoting urine retention.

• α₂ (A2) → mainly presynaptic inhibition; not involved in bladder contraction.

• β₂ (B2) → causes relaxation of smooth muscle (opposite effect).

• Nᵥ (nicotinic) → present at autonomic ganglia, not at the bladder muscle itself.

The posterior mediastinum lies behind the pericardium and in front of the vertebral column. It contains several vital structures, including:

• Thoracic duct

• Esophagus

• Sympathetic trunks

• Descending thoracic aorta

• Azygos and hemiazygos veins

Other options:

• Superior mediastinum → contains great vessels, trachea, thymus, and vagus/phrenic nerves.

• Middle mediastinum → contains heart, pericardium, and roots of great vessels.

• Anterior mediastinum → mostly fat, lymph nodes, and thymic remnants.

• Inferior mediastinum → divided into anterior, middle, and posterior parts; “posterior” is the one with these structures.

Mycobacterium tuberculosis has a waxy cell wall rich in mycolic acid, a long-chain fatty acid that makes the bacterium acid-fast.
During Ziehl–Neelsen staining, this lipid layer retains the primary stain (carbol fuchsin) even after treatment with acid-alcohol — hence they appear bright red against a blue background.

Other options:

• Formation of transmembrane channel → unrelated to staining.

• Causes it to take counter stain → acid-fast bacilli resist counterstaining.

• Gives it hydrophilic properties → mycolic acid is hydrophobic.

• Decolorization by acid → acid-fast bacilli resist decolorization.

The olfactory epithelium is located in the roof of the nasal cavity, extending slightly onto the upper part of the nasal septum (medial wall) and superior nasal concha (lateral wall).
It contains olfactory receptor cells, supporting (sustentacular) cells, and basal cells responsible for smell perception.

Other options:

• Lateral wall / Medial wall / Floor → may contain respiratory epithelium, not olfactory.

• Vibrissae → coarse hairs in the vestibule, not part of olfaction.

Epinephrine (and other β₂-adrenergic agonists) causes bronchodilation by acting on β₂ receptors in the smooth muscle of the bronchi and bronchioles.
This increases the diameter of the respiratory passages, reducing airway resistance and improving airflow.

Other options:

• Adrenergic antagonist → causes bronchoconstriction.

• More air entry → result of dilation, not a cause.

• Water intake → no direct effect on airway diameter.

• Steroids → reduce inflammation over time, not immediate dilation.

The angle of the rib is the most common site of rib fracture because it’s the most curved and weakest part, located a few centimeters lateral to the tubercle.
This area bears the brunt of bending stress during trauma.

Other options:

• Costal groove – protects intercostal vessels and nerves (rarely fractures here).

• Facet of head – articulates with vertebral bodies, less exposed.

• Tubercle – articulates with transverse process, protected by muscles.

• Neck – stronger, near vertebra.

Rifampin acts by blocking bacterial DNA-dependent RNA polymerase, preventing transcription and thereby halting RNA and protein synthesis.
It’s bactericidal and especially important in tuberculosis, leprosy, and prophylaxis for meningococcal exposure.

Other options:

• RNA-dependent DNA polymerase → inhibited by reverse transcriptase inhibitors (antivirals, not anti-TB).

• Arabinogalactan synthesis → target of Ethambutol.

• Mycolic acid synthesis → inhibited by Isoniazid.

• Glycosylation → not a target of anti-TB drugs.

The thin film of pleural fluid between the visceral and parietal pleura creates a slight negative pressure known as pleural pressure (or intrapleural pressure).
This pressure helps the lungs adhere to the chest wall and expand during inspiration.

Other options:

• Transpulmonary pressure → difference between alveolar and pleural pressure.

• Pericardial pressure → within pericardial sac, around the heart.

• Atmospheric pressure → pressure of air around the body.

• Alveolar pressure → pressure inside alveoli.

Transpulmonary pressure = Alveolar pressure − Intrapleural pressure.
It represents the distending (recoil-opposing) pressure that keeps alveoli open. The greater this pressure, the more the lungs expand.

Other options:

• Interpulmonary pressure = Alveolar pressure itself.

• Intrapleural pressure = Pressure in pleural cavity (normally negative).

• Interpleural pressure and atmospheric pressure are unrelated to this difference.

❌ Inappropriately Matched

Pyrazinamide – Hypoglycemia → ❌ incorrect

It should be Pyrazinamide – Hyperuricemia, not hypoglycemia.

1. Immobilization → venous stasis → thrombus formation in deep veins (usually femoral or popliteal).

2. Thrombus dislodges → travels via IVC → right atrium → right ventricle → pulmonary arteries.

3. Occlusion → ↓ perfusion, ↑ dead space, V/Q mismatch → hypoxemia and dyspnea.

4. In large emboli → acute right heart strain → hypotension and possible sudden death.

📋 Why the other options are incorrect

In adults, obesity is now recognized as the most common and strongest predisposing factor for asthma — both for developing the disease and for poor control once it appears.

🔬 Pathophysiological Link Between Obesity and Asthma:

1. Mechanical factors:

   • Increased abdominal and thoracic fat reduces lung volumes → decreased functional residual capacity (FRC) and expiratory reserve volume (ERV) → airway narrowing.

2. Inflammatory factors:

   • Adipose tissue releases proinflammatory cytokines (TNF-α, IL-6, leptin) that promote airway inflammation.

   • Decreased adiponectin (an anti-inflammatory adipokine) worsens this imbalance.

3. Immune modulation:

   • Leads to a non-allergic phenotype of asthma (Th1-dominant rather than Th2), common in adults.

4. Reduced response to therapy:

   • Obese asthmatics often show less improvement with corticosteroids.

⚖️ Why Other Options Are Incorrect:

The description — fever, chest pain, blood-stained (rusty) sputum, and gram-positive lancet-shaped diplococci — perfectly fits Streptococcus pneumoniae, the most common cause of community-acquired pneumonia.

🔬 Key Microbiological Features of Streptococcus pneumoniae:

⚕️ Clinical Correlation:

Typical pneumococcal pneumonia presents as:

• Sudden onset of high fever and pleuritic chest pain

• Rusty sputum due to RBC lysis

• Consolidation seen on chest X-ray (often one lobe)

Common in elderly, alcoholics, splenectomized, or immunocompromised patients.

⚖️ Why Other Options Are Incorrect:

Immotile Cilia Syndrome, also known as Kartagener’s syndrome (a type of Primary Ciliary Dyskinesia), is caused by a defect in the dynein arms of cilia and flagella.

🔬 Normal Ciliary Structure (Axoneme):

Cilia and flagella share a common internal structure called the axoneme, with the “9 + 2” arrangement:

• 9 peripheral doublets of microtubules

• 2 central single microtubules

• Connected by nexin links and powered by dynein arms

🧩 Dynein arms (both inner and outer) are ATPase motor proteins that generate sliding forces between adjacent microtubule doublets → this sliding is converted into bending motion of the cilium.

⚕️ Defect in Dynein Arms → Immotile Cilia:

When dynein arms are absent or dysfunctional:

• Cilia cannot beat properly → impaired mucus clearance → chronic respiratory infections, sinusitis, bronchiectasis

• Sperm flagella become immotile → male infertility

• Random organ rotation during development → situs inversus in about 50% of cases

⚖️ Why Other Options Are Incorrect:

The respiratory epithelium (lining the nasal cavity, trachea, and bronchi) is a pseudostratified ciliated columnar epithelium with goblet cells — a classic structure for mucociliary clearance.

🔬 Cell Types in Respiratory Epithelium:

🚦 Mechanism:

The beating cilia on columnar cells move the mucus blanket upward toward the pharynx — this is the mucociliary escalator, a key defense mechanism of the respiratory tract.

Damage to these cilia (e.g. in smokers or primary ciliary dyskinesia) impairs mucus clearance, predisposing to infections.

The respiratory membrane (also called the alveolar–capillary membrane) is an ultra-thin barrier where the exchange of O₂ and CO₂ occurs between alveolar air and pulmonary capillary blood.

🔬 Structure of the Respiratory Membrane:

It consists of six microscopic layers (from air to blood):

1. Thin layer of alveolar fluid with surfactant

2. Alveolar epithelium (type I pneumocytes)

3. Epithelial basement membrane

4. Interstitial space (very thin)

5. Capillary basement membrane (fused with epithelial one in most places)

6. Capillary endothelium

📏 Thickness:

• Average thickness = 0.5 µm (i.e. less than 1 µm)

• Surface area ≈ 70 m² (roughly half a tennis court!)

This extreme thinness allows rapid diffusion of gases according to Fick’s law, which states that diffusion rate is inversely proportional to membrane thickness.

⚕️ Clinical Insight:

In conditions like:

• Pulmonary edema (fluid accumulation)

• Fibrosis (thickened membrane)
  → membrane thickness increases → gas exchange becomes impaired, leading to hypoxia.

Each somite (derived from paraxial mesoderm) differentiates into three parts:

1. Dermatome → forms dermis of skin

2. Myotome → forms skeletal muscles

3. Sclerotome → forms vertebrae and ribs

🦴 Formation of Vertebrae:

• Sclerotomal mesenchyme migrates around two central structures:

  1. Notochord — central rod

  2. Neural tube — dorsal hollow structure

These migrating sclerotomal cells surround both structures in different directions:

• Around the notochord → vertebral body

• Around the neural tube → vertebral arch

• Into the body wall → ribs (in thoracic region)

🩻 Therefore:

➡️ The mesenchyme surrounding the neural tube forms the vertebral arch (including the pedicles, laminae, and spinous process).
Meanwhile, the mesenchyme surrounding the notochord forms the vertebral body.

⚖️ Why Other Options Are Incorrect:

During embryonic development, the notochord appears in the 3rd week as a midline rod of mesodermal cells that serves as a primitive axial skeleton and a signaling center for the surrounding tissues.
It plays a critical role in:

• Inducing the formation of the neural tube (future CNS).

• Defining the vertebral axis.

• Organizing somite differentiation.

🦴 Fate of the Notochord:

• Most of the notochord degenerates as the vertebral column forms around it.

• However, a small remnant persists in the center of each intervertebral disc as the nucleus pulposus — the gelatinous, shock-absorbing core that helps maintain flexibility of the spine.

❌ Why Other Options Are Incorrect:

Henderson–Hasselbalch Equation
pH = pKa + log([A-] / [HA])

When acid and base are in equal concentrations:

If
[A-] = [HA]

then
[A-] / [HA] = 1

and since
log(1) = 0

→ pH = pKa

This is the buffer’s point of maximum buffering capacity, where the solution resists pH changes most effectively.

Why the Other Options Are Incorrect:

The lipid membrane (cell membrane or plasma membrane) is primarily made up of a phospholipid bilayer, which forms the basic structural framework of all biological membranes.

🧩 Main components of the membrane:

1. Phospholipids → most abundant

   • Amphipathic molecules (hydrophilic head + hydrophobic tail)

   • Arrange as a bilayer, forming a semi-permeable barrier

2. Cholesterol → stabilizes membrane fluidity and integrity

3. Glycolipids and sphingolipids → present in smaller amounts, important for cell recognition and signaling

4. Proteins → embedded within or attached to the lipid bilayer

⚖️ Relative Abundance:

The trachea is a fibro-cartilaginous, mucous-membrane-lined tube connecting the larynx to the bronchi.
Histologically, it has four main layers (from inside outward):

1. Mucosa – pseudostratified ciliated columnar epithelium with goblet cells

2. Submucosa – contains seromucous glands

3. Cartilaginous layer – C-shaped hyaline cartilage rings joined posteriorly by trachealis muscle

4. Adventitia – outer connective tissue that blends with surrounding structures

⚙️ Key Structural Facts:

So, the odd statement is that the cartilage is “in the adventitia” — it is not.
The C-shaped cartilage lies deep to the submucosa and superficial to the adventitia.

⚖️ Why Others Are Correct:

• Fibroelastic membrane in lamina propria: ✅ True.

• Epithelium columnar ciliated: ✅ True (pseudostratified).

• Thick basement membrane: ✅ Characteristic of trachea.

• Seromucous glands in submucosa: ✅ True.

Histotoxic hypoxia occurs when the cells are unable to utilize oxygen, even though:

• The blood oxygen content and saturation are normal, and

• Blood flow to tissues is adequate.

This happens because a toxic substance blocks cellular oxidative enzymes, especially cytochrome oxidase in the electron transport chain of mitochondria — preventing oxygen use for ATP production.

The most classic example is cyanide poisoning.

⚙️ Mechanism Summary:

👉 So, the blood remains bright red and oxygen-rich, but tissues cannot extract or use that oxygen.

⚖️ Why the Other Options Are Incorrect:

During quiet inspiration, only the diaphragm and external intercostal muscles are actively involved.
Accessory muscles—like the scalenes, sternocleidomastoid, and pectoralis minor—are not used unless inspiration becomes forced or labored.

The 1st rib is elevated primarily by the scalene muscles (especially scalenus anterior and medius), which act only during forced inspiration to further enlarge the thoracic cavity.

Thus, elevation of the 1st rib occurs during forced inspiration, not during quiet inspiration.

⚙️ Summary of Muscle Actions:

⚖️ Reasoning Against Other Options:

The descending thoracic aorta gives off several visceral and parietal branches, but coronary arteries are not among them.
Instead, the coronary arteries arise directly from the ascending aorta, just above the aortic valve at the aortic sinuses.

⚙️ Branches of the Descending Thoracic Aorta:

🔹 Visceral branches (to organs):

• Bronchial arteries

• Esophageal arteries

• Pericardial arteries

• Mediastinal arteries

🔹 Parietal branches (to body wall):

• Posterior intercostal arteries (3rd–11th)

• Subcostal arteries

• Superior phrenic arteries

⚖️ Why the Other Options Are Correct Branches:

In asthma management, drugs are classified as:

1. Relievers (short-term control) → relieve acute bronchoconstriction

   • e.g. Salbutamol (short-acting β₂ agonist)

2. Controllers (long-term control) → reduce airway inflammation and hyperresponsiveness

   • e.g. Inhaled corticosteroids (ICS) such as Beclomethasone, Budesonide, Fluticasone

Beclomethasone is a glucocorticoid that works by:

• Decreasing airway inflammation

• Reducing eosinophil and mast cell infiltration

• Enhancing β₂-receptor sensitivity

• Decreasing mucus secretion

It is not for acute attacks, but for long-term prophylactic therapy to prevent exacerbations.

⚖️ Why the Other Options Are Incorrect:

In congestive heart failure (CHF), blood backs up into the lungs → pulmonary congestion and increased pulmonary venous pressure.
As a result:

• Red blood cells leak into the alveoli.

• Alveolar macrophages phagocytose these extravasated RBCs and degrade hemoglobin into hemosiderin (an iron-storage pigment).

• These macrophages appear brown or golden due to hemosiderin granules → called “heart failure cells.”

So, the “phagocytosing cells having dark centers” are alveolar macrophages laden with hemosiderin.

🔬 Key Features on Histology:

• Large, irregular cells in alveolar spaces

• Brown pigment (hemosiderin) in cytoplasm (Perl’s Prussian blue stain positive)

• Found in chronic pulmonary congestion secondary to left-sided heart failure

⚖️ Why the Other Options Are Incorrect:

This 62-year-old patient with chest tightness, breathlessness, cough, and suffocation is showing classic signs of respiratory failure — often seen in conditions like COPD exacerbation, severe asthma, or acute bronchitis.

In such cases:

• Ventilation is impaired (↓ alveolar ventilation)

• CO₂ retention occurs (↑ PaCO₂)

• Blood becomes acidic due to accumulation of carbonic acid

Hence → Respiratory acidosis (↑ pCO₂, ↓ pH).

⚙️ Mechanism Summary:

CO2 + H2O <-> H2CO3 <-> H+ + HCO3-

When CO₂ builds up, more H⁺ ions are produced → acidosis.
The kidneys later retain HCO₃⁻ as a compensatory response, but acidosis persists acutely.

⚖️ Why the Other Options Are Incorrect:

The thoracic duct is the main lymphatic channel of the body. It drains all lymph except from the right upper quadrant, which includes:

• Right side of head and neck

• Right upper limb

• Right side of thorax

These regions instead drain into the right lymphatic duct, not the thoracic duct.

⚙️ Thoracic Duct Drainage Summary:

Thus, if the thoracic duct is ligated, lymph from the right upper quadrant — including the right intercostal nodes — remains unaffected, since it never drained into the thoracic duct in the first place.

⚖️ Reasoning for Incorrect Options:

• Left brachiomediastinal trunk: ✔️ Drains into thoracic duct → affected

• Left parasternal nodes: ✔️ Drain via thoracic duct → affected

• Diaphragmatic nodes: ✔️ Inferior ones drain into cisterna chyli → affected

• Left jugular trunk: ✔️ Drains into thoracic duct → affected

The pressure generated by surface tension in the alveoli is governed by Laplace’s Law, which states:

P = 2T / r

Where:

• P = pressure inside the alveolus (due to surface tension)

• T = surface tension

• r = radius of the alveolus

👉 According to this law:

• Pressure is directly proportional to surface tension (T)

• Pressure is inversely proportional to the radius (r)

This means smaller alveoli (with smaller radius) generate higher pressure — which tends to make them collapse more easily.

That’s exactly why pulmonary surfactant is crucial: it reduces surface tension, especially in smaller alveoli, preventing alveolar collapse (atelectasis) and maintaining uniform inflation.

⚖️ Reasoning for Incorrect Options:

• Directly/Inverse on blood flow through lungs: ❌
  Surface tension pressure is independent of pulmonary blood flow.

• Directly on radius of alveoli: ❌
  The relation is inverse, not direct.

• Directly on surface area: ❌
  Surface tension acts along the interface, not total surface area.

Let’s clarify carefully —

Ischemic (or stagnant) hypoxia is defined as:

“Reduced tissue oxygenation due to decreased blood flow (perfusion) despite normal arterial oxygen tension (pO₂) and hemoglobin concentration.”

So while thrombosis is indeed a common cause, the definition (as asked here) is:
👉 Decreased blood flow to tissues with normal Hb and pO₂.

This phrase directly describes ischemic hypoxia, where the circulation — not the oxygen content — is the problem.

⚖️ Clinical reasoning:

The mediastinum is divided into four parts for descriptive anatomy:

1. Superior mediastinum – above the sternal angle (contains great vessels, trachea, esophagus, etc.)

2. Inferior mediastinum, which is subdivided into:

   • Anterior mediastinum – between sternum and pericardium

   • Middle mediastinum – contains the heart, pericardium, roots of great vessels, and phrenic nerves

   • Posterior mediastinum – behind the pericardium (contains thoracic aorta, azygos vein, esophagus, etc.)

Thus, the heart and pericardial sac are located in the middle mediastinum, a part of the inferior mediastinum.

The respiratory tract is divided into two main parts for both anatomical and clinical reasons:

• Upper respiratory tract: Includes structures from the nose down to the larynx.

• Lower respiratory tract: Begins below the larynx and includes the trachea, bronchi, and lungs.

The cricoid cartilage serves as the boundary between these two regions. It is the only complete ring of cartilage in the airway and lies at the level of C6 vertebra. Below it, the trachea begins — marking the start of the lower respiratory tract.

❌ Why the Other Options Are Incorrect:

• Thyroid cartilage:
  Located above the cricoid cartilage; it forms the prominent “Adam’s apple.” It is part of the larynx but not the boundary between upper and lower respiratory tracts.

• Soft palate:
  Separates the nasopharynx from the oropharynx — this division is within the upper respiratory tract, not between upper and lower tracts.

• Hyoid bone:
  Lies above the larynx and serves as an attachment for muscles of the tongue and pharynx. It does not separate the respiratory tract divisions.

• Epiglottis:
  Acts as a valve to prevent food from entering the trachea during swallowing. It lies within the larynx but does not demarcate upper and lower respiratory parts.

As the vertebral column forms, most of the notochord degenerates in the regions where vertebral bodies develop. However, in the regions between vertebrae — where intervertebral discs form — the notochord persists as the nucleus pulposus.

The nucleus pulposus is a soft, gelatinous central portion of the intervertebral disc that allows flexibility and acts as a cushion between vertebrae.

❌ Why the Other Options Are Incorrect:

• Notochordal plate:
  This is a transient embryonic structure formed during gastrulation before the definitive notochord develops. It does not persist in adults.

• Annulus fibrosus:
  This is the tough, fibrous outer ring of the intervertebral disc, derived from sclerotome (mesoderm), not the notochord.

• Prechordal plate:
  A separate structure located anterior to the notochord; it contributes to the development of the forebrain and midface, not the spine.

• Blastula:
  Refers to an early stage of the embryo (a hollow ball of cells) before gastrulation — unrelated to the notochord’s fate.

Sclerotomes are the ventromedial portions of somites, which arise from the paraxial mesoderm on either side of the neural tube. They give rise to vertebrae and ribs and play a key role in forming the axial skeleton that supports the thoracic cavity and, indirectly, the respiratory system (since ribs and vertebrae form the framework protecting the lungs).

The somites begin forming by the third week, but sclerotome migration and vertebral development occur later, around the fourth week.

Therefore, the statement claiming that sclerotome moves around the spinal cord during the 3rd week is inaccurate, as this movement actually occurs in the 4th week.

❌ Why the Other Options Are Correct:

• Notochord is completely regressed in the vertebral region: True. The notochord disappears where vertebral bodies form, persisting only as the nucleus pulposus of intervertebral discs.

• Somites are derived from the paraxial mesoderm: True. Somites form from paraxial mesoderm and segment along the neural tube.

• They undergo process of resegmentation: True. Each vertebra forms from the fusion of the caudal half of one sclerotome and the cranial half of the next.

• Somites form the vertebrae: True. Sclerotome components of somites give rise to vertebrae and ribs.

🩺Clinical Correlation:

Improper resegmentation or migration of sclerotomes can lead to congenital vertebral anomalies such as hemivertebrae or spina bifida, which can distort the thoracic cage and compromise respiratory function in severe cases.

During inspiration, ribs 7 to 10 undergo the bucket handle movement, where the ribs move upward and outward, increasing the transverse diameter of the thoracic cavity.
This motion helps expand the lungs laterally, contributing to efficient air entry.

• Pump handle movement: Ribs 2–6, increasing anteroposterior diameter.

• Bucket handle movement: Ribs 7–10, increasing transverse diameter.

• Floating ribs (11–12): Do not participate; they move minimally or not at all.

❌ Why the Other Options Are Incorrect:

• Floating ribs: Not attached anteriorly, so they don’t move like handles.

• Attached ribs: Too vague — most ribs are attached posteriorly.

• Ribs 1 to 9: Overincludes upper ribs that show pump handle movement.

• Ribs 1–2: Involved in pump handle movement, not bucket handle.

Asthma is fundamentally a chronic inflammatory disease of the airways.
This inflammation makes the bronchial smooth muscle hyperreactive to various stimuli (like allergens, infections, or irritants), resulting in recurrent episodes of wheezing, breathlessness, and cough.

Even when symptoms subside, the underlying inflammation persists, causing structural changes over time known as airway remodeling.

❌ Why the Other Options Are Incorrect:

• Periodic spasm of bronchial muscle:
  This explains acute bronchoconstriction, not the chronic recurrence of asthma.
  It’s a symptom, not the cause.

• Fibrous scarring on lungs:
  Seen in fibrotic lung diseases, not asthma.

• Bacterial / Viral infection:
  These can trigger asthma attacks but are not the root cause of chronic asthma.

✅ Correct Answer:

Summarizing

When a doctor listens carefully to a patient’s statements and then repeats and concludes the main points at the end, the communication technique used is called summarizing.

It helps the doctor:

• Confirm understanding of the patient’s story,

• Show that they were actively listening, and

• Clarify or correct any misunderstandings before proceeding.

Summarizing is often used at the end of a consultation segment or before moving to a new topic to ensure shared understanding between doctor and patient.

❌ Incorrect Options:

• Selective reflection — ❌ Involves focusing on and echoing specific emotional or meaningful parts of what the patient said, not the full summary.

• Paraphrasing — ❌ Means rewording the patient’s message briefly to show understanding, usually mid-conversation, not concluding it.

• Funneling — ❌ A questioning technique that moves from broad, open-ended questions to specific, focused ones.

• Empathy — ❌ The emotional understanding of a patient’s feelings; it can accompany summarizing but is not the same communication skill.

✅ Correct Answer:

Acquired immunodeficiency syndrome (AIDS)

Patients with AIDS (caused by HIV infection) have a very high risk of developing tuberculosis, both primary infection and reactivation of latent TB.
This happens because HIV destroys CD4⁺ T lymphocytes, which are essential for cell-mediated immunity — the body’s main defense mechanism against Mycobacterium tuberculosis.

As a result, TB progresses more rapidly in HIV-positive patients and often presents atypically, with extrapulmonary involvement or negative chest X-rays, making diagnosis more difficult.

❌ Incorrect Options:

• Chronic obstructive pulmonary disease (COPD) — ❌ May affect lung function but does not cause immunosuppression; risk of TB is not significantly increased.

• Chronic sinusitis — ❌ A localized infection of the sinuses; unrelated to TB susceptibility.

• Diabetes — ❌ Increases TB risk moderately, but not as dramatically as AIDS.

• Leprosy — ❌ Also caused by a Mycobacterium species (M. leprae), but co-infection with TB is uncommon.

✅ Correct Answer:

95 mm Hg

The partial pressure of oxygen (pO₂) in arterial blood (PaO₂) under normal conditions at sea level is approximately 95 mm Hg.
This reflects the amount of oxygen dissolved in the plasma and corresponds to a hemoglobin saturation of about 97–98%.

It slightly decreases with age or at higher altitudes but remains around this value in healthy adults.

❌ Incorrect Options:

• 120 mm Hg — ❌ Higher than normal; may occur only with supplemental oxygen, not in normal arterial blood.

• 60 mm Hg — ❌ Represents hypoxemia; seen in respiratory disorders like COPD or high altitude.

• 75 mm Hg — ❌ Approximate value for mixed venous blood, not arterial blood.

• 45 mm Hg — ❌ Typical pCO₂ (carbon dioxide) level in venous blood, not oxygen pressure.

✅ Correct Answer:

Nadolol

Nadolol is a non-selective β-blocker, meaning it blocks both β₁ receptors (in the heart) and β₂ receptors (in the bronchi, blood vessels, and other tissues).
Because of this, it reduces heart rate and contractility but can also cause bronchoconstriction, so it is contraindicated in asthma and COPD.

❌ Incorrect Options:

• Salbutamol — ❌ A β₂ agonist, not an antagonist; it dilates bronchi, used in asthma.

• Metoprolol — ❌ A β₁-selective blocker (cardioselective), safer in airway disease.

• Bisoprolol — ❌ Also β₁-selective, mainly acts on the heart.

• Atenolol — ❌ Another β₁-selective blocker with little to no effect on β₂ receptors.

✅ Correct Answer:

Right ventricle

During systole, the right ventricle contracts and ejects blood into the pulmonary artery through the pulmonary valve.
At this moment, the pressure in the pulmonary artery equals the pressure in the right ventricle, because the valve is open and there is free flow of blood between the two chambers.

• Normal right ventricular systolic pressure ≈ 25 mmHg

• Normal pulmonary artery systolic pressure ≈ 25 mmHg

This equality lasts until the end of systole, when the ventricular pressure falls and the pulmonary valve closes to prevent backflow.

❌ Incorrect Options:

• Superior vena cava — ❌ Carries venous blood at very low pressure (≈0–5 mmHg); unrelated to systolic pulmonary pressure.

• Left ventricle — ❌ Generates much higher pressure (≈120 mmHg) to pump blood into the systemic circulation, not the pulmonary artery.

• Right atrium — ❌ Has low pressure (≈2–6 mmHg), filling the right ventricle passively during diastole.

• Left atrium — ❌ Receives oxygenated blood from pulmonary veins; pressure is ≈8–10 mmHg, not equal to pulmonary artery pressure during systole.

✅ Correct Answer:

Endoderm of foregut

The epithelium of the lower respiratory system — including the larynx, trachea, bronchi, and alveoli — arises from the endoderm of the foregut during embryonic development.

Around the 4th week, a respiratory diverticulum (lung bud) forms as an outpouching from the ventral wall of the foregut.

• The endoderm gives rise to the epithelial lining and glands of the lower respiratory tract.

• The surrounding splanchnic mesoderm forms the cartilage, smooth muscle, and connective tissue.

❌ Incorrect Options:

• Endoderm of neural crest cells — ❌ Neural crest cells contribute to nerves and connective tissues, not respiratory epithelium.

• Endoderm of nasopharynx — ❌ This gives rise to upper respiratory structures, not the lower respiratory tract.

• Endoderm of midgut — ❌ Forms structures like the small intestine and part of the large intestine, not the lungs or trachea.

• Ectoderm — ❌ Forms the epidermis and nervous system, not the respiratory epithelium.

✅ Correct Answer:

Pericardiophrenic artery

The phrenic nerve descends through the thorax alongside the pericardiophrenic artery, which is a branch of the internal thoracic artery.
Both structures run between the pleura and pericardium, supplying the diaphragm and pericardium as they descend anterior to the root of the lung.

This close association is clinically important because injury to either structure (for example, during pericardial procedures) can affect diaphragmatic movement or phrenic nerve function.

❌ Incorrect Options:

• Superior epigastric artery — ❌ A terminal branch of the internal thoracic artery, but it supplies the anterior abdominal wall, not the diaphragm or phrenic nerve.

• Inferior epigastric artery — ❌ Arises from the external iliac artery and supplies the lower abdominal wall; unrelated to the phrenic nerve.

• Internal thoracic artery — ❌ The parent vessel of the pericardiophrenic artery; it runs vertically along the chest wall, not directly with the phrenic nerve.

• Musculophrenic artery — ❌ Another branch of the internal thoracic artery, but it runs more laterally along the costal margin, not accompanying the phrenic nerve.

✅ Correct Answer:

Groove for heart

The left lung has a prominent cardiac impression (groove for the heart) on its mediastinal surface, created by the position of the heart and pericardium lying adjacent to it.
This impression is much deeper on the left than on the right lung because most of the heart, particularly the left ventricle, lies to the left of the midline.

Other distinctive features of the left lung include:

• Cardiac notch (near the anterior border)

• Lingula (a tongue-like projection of the superior lobe)

❌ Incorrect Options:

• Groove for arch of azygos vein — ❌ Found on the right lung, where the azygos vein arches over the right lung root to enter the superior vena cava.

• Groove for subclavian artery — ❌ Present on the apex of the left lung, but also found on the right lung apex (for the right subclavian artery); thus, not unique to the left lung.

• Groove for ascending aorta — ❌ Seen on the right lung, not the left.

• Groove for phrenic nerve — ❌ Present on both lungs, as the phrenic nerve descends anterior to each lung root.

✅ Correct Answer:

Transpulmonary pressure

The difference between alveolar pressure (Pₐ) and pleural pressure (Pₚₗ) is known as the transpulmonary pressure (Pₜₚ).

Ptp=Pa−PplPₜₚ = Pₐ – PₚₗPtp​=Pa​−Ppl​

This pressure represents the distending force that keeps the lungs inflated — it is the pressure across the lung wall. A higher transpulmonary pressure means greater lung expansion during inspiration.

• Alveolar pressure (Pₐ): Pressure inside the alveoli.

• Pleural pressure (Pₚₗ): Pressure in the pleural cavity (normally negative).

The difference between these two determines how much the lungs expand or recoil.

❌ Incorrect Options:

• Thoracic cage pressure — ❌ Not a defined physiological pressure; refers generally to pressure in the chest cavity.

• Negative pressure — ❌ Describes the nature of pleural pressure, not the difference between alveolar and pleural pressures.

• Pleural pressure — ❌ One of the components of the equation, not the resulting difference.

• Elastic recoil — ❌ A property influenced by transpulmonary pressure, but not the pressure itself.

✅ Correct Answer:

T10

The lungs end inferiorly at approximately the level of the 10th thoracic vertebra (T10) posteriorly during normal expiration.
The lower border of the lung follows this pattern:

• Midclavicular line: 6th rib

• Midaxillary line: 8th rib

• Paravertebral line (posteriorly): T10

These landmarks are important for safe thoracentesis, ensuring the needle is inserted below the lung margin (usually around the 8th or 9th intercostal space posteriorly) to avoid puncturing the lung.

❌ Incorrect Options:

• T12 — ❌ Too low; corresponds more closely to the lower border of the pleura, not the lung itself.

• T8 — ❌ Too high; this level corresponds to the midaxillary line, not posteriorly.

• T6 — ❌ Represents the anterior border (midclavicular line) of the lung, not the posterior end.

• T7 — ❌ Lies between anterior and lateral levels; not the inferior posterior limit.

✅ Correct Answer:

Hemothorax

A hemothorax is the accumulation of blood in the pleural cavity, often resulting from rupture of an aortic aneurysm, chest trauma, or rupture of intercostal vessels.

In this case, the X-ray shows fluid in the pleural cavity following aortic aneurysm rupture, which causes massive internal bleeding into the pleural space. This leads to sudden circulatory collapse with undetectable pulse and blood pressure, consistent with hypovolemic shock due to internal hemorrhage.

❌ Incorrect Options:

• Tension pneumothorax — ❌ Involves air, not blood, in the pleural cavity; causes lung collapse and mediastinal shift but no fluid on X-ray.

• Hydropneumothorax — ❌ A mixture of air and fluid in the pleural cavity; occurs due to lung rupture or trauma, not aneurysm rupture.

• Hydrothorax — ❌ Accumulation of serous (clear) fluid, usually from heart failure or nephrotic syndrome, not blood.

• Chylothorax — ❌ Accumulation of lymph (chyle) due to thoracic duct injury, giving a milky appearance, not hemorrhagic.

✅ Correct Answer:

50 g/L

A pleural fluid protein concentration above 30 g/L (or 3 g/dL) typically indicates an exudative effusion, but when the serum protein level is normal, a value around 50 g/L confirms an exudate beyond doubt.

Exudative pleural effusions occur due to increased capillary permeability caused by inflammation, infection, malignancy, or pulmonary embolism. They are protein-rich and often contain inflammatory cells.

In contrast, transudative effusions (e.g., in heart failure, cirrhosis, nephrotic syndrome) are protein-poor, with pleural fluid protein levels below 25 g/L.

❌ Incorrect Options:

• 10 g/L — ❌ Too low; typical of transudative effusion.

• 30 g/L — ❌ Borderline; may suggest a weak exudate, but 50 g/L more clearly fits an exudative profile.

• 3 g/L — ❌ Far below exudate levels; strongly suggests transudate.

• 5 g/L — ❌ Still within transudative range; protein content too low.

✅ Correct Answer:

Carbonic anhydrase

Carbonic anhydrase is the enzyme that catalyzes the reversible reaction between carbon dioxide (CO₂) and water (H₂O) to form carbonic acid (H₂CO₃), which then dissociates into bicarbonate (HCO₃⁻) and hydrogen ions (H⁺):

CO₂ + H₂O ⇌ H₂CO₃ ⇌ H⁺ + HCO₃⁻\text{CO₂ + H₂O ⇌ H₂CO₃ ⇌ H⁺ + HCO₃⁻}CO₂ + H₂O ⇌ H₂CO₃ ⇌ H⁺ + HCO₃⁻

This enzyme is found in red blood cells, renal tubular cells, and alveolar cells.
It is crucial for CO₂ transport in blood, acid–base balance, and regulation of pH in tissues and plasma.

❌ Incorrect Options:

• Alkaline phosphatase — ❌ Catalyzes the removal of phosphate groups, not CO₂ hydration.

• Acetylcholinesterase — ❌ Breaks down the neurotransmitter acetylcholine at synapses.

• Adenylate cyclase — ❌ Converts ATP to cyclic AMP (cAMP) in signal transduction pathways.

• Protein kinase — ❌ Adds phosphate groups to proteins to regulate their activity, unrelated to CO₂ or bicarbonate.

✅ Correct Answer:

VI (Sixth cranial nerve)

Compression between the 5th and 6th cervical vertebrae (C5–C6) most commonly affects the sixth cervical spinal nerve (C6 nerve root) — not the cranial nerve VI.
This nerve root exits above the C6 vertebra, and compression at this level (for example, due to a herniated intervertebral disc or spondylosis) can produce C6 radiculopathy.

C6 nerve root involvement typically causes:

• Pain radiating from the neck to the lateral forearm, thumb, and index finger

• Weakness in biceps and wrist extensors

• Diminished biceps reflex

❌ Incorrect Options:

• VII — ❌ The facial nerve, a cranial nerve, not related to cervical vertebrae.

• IV — ❌ The trochlear nerve, another cranial nerve, not spinal.

• V — ❌ The trigeminal nerve, also cranial, supplies facial sensation, not the neck or upper limb.

• X — ❌ The vagus nerve, descends in the neck but is not compressed between vertebrae.

✅ Correct Answer:

Superior thyroid artery

The trachea receives its blood supply from branches of the inferior thyroid artery (a branch of the thyrocervical trunk) and the superior thyroid artery (a branch of the external carotid artery).
The upper part of the trachea is primarily supplied by the superior thyroid artery, while the lower part is supplied by branches from the inferior thyroid artery.

These arteries form a rich anastomotic network along the trachea, ensuring continuous blood flow even if one source is compromised.

❌ Incorrect Options:

• Internal thoracic artery — ❌ Supplies the anterior chest wall, breast, and pericardium, not the trachea.

• Common carotid artery — ❌ A major neck vessel that divides into internal and external carotid arteries; it doesn’t give direct branches to the trachea.

• Coronary artery — ❌ Supplies the heart, not the trachea.

• None of these — ❌ Incorrect, since the superior thyroid artery does contribute to tracheal supply.

✅ Correct Answer:

Immunity to disease

A positive Mantoux test indicates that the person has been exposed to Mycobacterium tuberculosis and has developed cell-mediated (Type IV) hypersensitivity, meaning the immune system recognizes TB antigens.
This does not confirm active disease — it only shows immunologic sensitization due to:

• Past infection (latent TB)

• BCG vaccination

• Or active infection (current TB disease)

Thus, a positive result reflects immunity or prior exposure, not necessarily active illness.

❌ Incorrect Options:

• Passive disease — ❌ Not a recognized term; TB infection is either latent or active, not “passive.”

• Presence of TB — ❌ The test cannot differentiate between active and latent TB — it just shows exposure.

• Active disease — ❌ Diagnosis of active TB requires clinical evidence, chest X-ray, and microbiological confirmation, not just a skin test.

• No infection — ❌ A negative Mantoux test** suggests lack of exposure or anergic immune response, not a positive one.

✅ Correct Answer:

Mantoux skin test

The Mantoux skin test (also called the tuberculin skin test) is used to detect prior exposure or infection with Mycobacterium tuberculosis.
It involves an intradermal injection of purified protein derivative (PPD) into the forearm. After 48–72 hours, the site is examined for induration (raised, firm swelling) — not redness.

A positive result indicates immune sensitization to TB antigens, suggesting past infection, vaccination (BCG), or latent TB, but not necessarily active disease.

❌ Incorrect Options:

• Mycoplasma test — ❌ Used for diagnosing Mycoplasma pneumoniae, unrelated to tuberculosis.

• Positive test — ❌ Describes a result, not the name of the test itself.

• Negative test — ❌ Same as above — this is an outcome, not the procedure.

• TB skin test — ❌ A general term, but the formal and specific name is the Mantoux test.

✅ Correct Answer:

Nadolol

Nadolol is a non-selective β-adrenergic antagonist (β-blocker), meaning it blocks both β₁ (cardiac) and β₂ (bronchial, vascular, and metabolic) receptors.
Because of this non-selectivity, it can reduce heart rate and contractility (β₁ effect) but may also cause bronchoconstriction (β₂ effect), making it contraindicated in asthma and COPD.

It is used for:

• Hypertension

• Angina pectoris

• Long-term control of arrhythmias

❌ Incorrect Options:

• Bisoprolol — ❌ A β₁-selective blocker (cardioselective), primarily affecting the heart.

• Metoprolol — ❌ Also β₁-selective, safer in patients with mild airway disease.

• Salbutamol — ❌ A β₂-agonist, not an antagonist; it relaxes bronchial smooth muscle (used in asthma).

• Atenolol — ❌ Another β₁-selective blocker with minimal β₂ effect.

✅ Correct Answer:

Recurrent laryngeal nerve

The recurrent laryngeal nerve, a branch of the vagus nerve (cranial nerve X), runs in close proximity to the trachea.

• On both sides, it ascends in the tracheoesophageal groove — the narrow space between the trachea and esophagus.

• It supplies all intrinsic muscles of the larynx (except the cricothyroid) and provides sensory innervation below the vocal cords.

Because of its close anatomical relationship, the recurrent laryngeal nerve is vulnerable to injury during thyroid, tracheostomy, or esophageal surgeries, which can result in hoarseness or loss of voice.

❌ Incorrect Options:

• Left phrenic — ❌ Passes anterior to the root of the lung and along the pericardium, not near the trachea.

• Left vagus — ❌ Lies more laterally to the trachea and gives off the recurrent laryngeal branch that loops around the aortic arch.

• Suprarenal — ❌ Refers to the adrenal glands, located in the abdomen, far from the trachea.

• Subclavian — ❌ The right recurrent laryngeal nerve loops around the right subclavian artery, but the artery itself is not near the trachea.

✅ Correct Answer:

Streptococcus pneumoniae

Streptococcus pneumoniae is the most common cause of community-acquired pneumonia (CAP) worldwide. It is a Gram-positive, lancet-shaped diplococcus that often colonizes the upper respiratory tract and causes pneumonia when host defenses are compromised.

Typical clinical presentation includes:

• Sudden onset of fever and chills

• Productive cough with rust-colored sputum

• Pleuritic chest pain

• Lobar consolidation on chest X-ray

❌ Incorrect Options:

• Staphylococcus pneumoniae — ❌ No such species exists; the correct organism is Streptococcus pneumoniae. Staphylococcus aureus can cause pneumonia, but usually hospital-acquired or post-influenza, not community-acquired.

• Haemophilus influenzae — ❌ Can cause CAP in elderly or COPD patients, but it’s not the most common cause.

• Rubella — ❌ A viral exanthem (German measles), not a respiratory infection.

• HIV — ❌ A virus causing immunodeficiency, not pneumonia itself; it increases susceptibility to other infections.

Intercostal veins are not superficial structures — they lie within the intercostal spaces, specifically in the costal groove of the corresponding rib, along with the intercostal artery and nerve.

Their arrangement from superior to inferior is remembered by the mnemonic VAN:

Vein – Artery – Nerve

All of them lie deep to the internal intercostal muscle and superficial to the innermost intercostal muscle, not superficial to the entire intercostal space.

❌ Why the Other Options Are Correct:

• Supreme intercostal vein → brachiocephalic vein: True. It drains the 1st intercostal space into the brachiocephalic vein.

• Most drain into azygos vein: True. Right posterior intercostal veins usually drain into the azygos vein; left ones into hemiazygos or accessory hemiazygos.

• Posterior veins are 11 in number: True. There are 11 pairs of posterior intercostal veins corresponding to the 11 intercostal spaces.

• They have valves: True. Intercostal veins contain valves to prevent backflow.

Morphine is an opioid analgesic that depresses the respiratory center in the medulla oblongata. This leads to hypoventilation, meaning the patient breathes less frequently and less deeply.

Because of this:

• CO₂ accumulates in the blood (↑ PaCO₂).

• This shifts the carbonic acid–bicarbonate buffer toward increased H⁺ concentration.

• Result: ↓ pH → Respiratory acidosis.

🔬 Mechanism Summary:

CO₂+H₂O↔H₂CO₃↔H⁺+HCO₃⁻

⬆ CO₂ → ⬆ H⁺ → ⬇ pH (acidosis)

❌ Why the Other Options Are Incorrect:

• Respiratory alkalosis:
  Occurs when CO₂ is lost due to hyperventilation (e.g., panic attack), not retained as in this case.

• Metabolic acidosis:
  Caused by increased acid production or loss of bicarbonate, not by CO₂ retention.

• Hyperkalemia / Hypokalemia:
  These are electrolyte disorders and may occur secondarily but are not the main issue here. The primary disturbance is respiratory acidosis due to hypoventilation.

🩺 Clinical Connection:
A respiratory rate below 12/min after opioid administration indicates respiratory depression.
This can progress to coma and death if not reversed.

Beta agonists are the main class of bronchodilators used in conditions such as asthma and chronic obstructive pulmonary disease (COPD).
They act by stimulating β₂-adrenergic receptors in the bronchial smooth muscle, leading to increased cAMP and smooth muscle relaxation, which results in bronchodilation.

Types of β₂-agonists:

• Short-acting (SABA): Salbutamol (albuterol), Terbutaline — used for acute relief of bronchospasm.

• Long-acting (LABA): Salmeterol, Formoterol — used for maintenance therapy alongside corticosteroids.

They also decrease airway resistance and improve mucociliary clearance, making breathing easier.

❌ Why the Other Options Are Incorrect:

• Adrenergic agonists:
  This term is too broad — it includes both alpha and beta agonists. Alpha agonists mainly cause vasoconstriction, not bronchodilation. Only β₂-adrenergic agonists specifically dilate bronchi.

• Anti-leukotriene:
  These drugs (e.g., montelukast) reduce inflammation and prevent bronchoconstriction, but they do not directly relax smooth muscle to cause bronchodilation.

• Corticosteroids:
  These are anti-inflammatory, not direct bronchodilators. They reduce airway inflammation and edema but work over hours or days, not immediately.

• Anti-histamine:
  Used in allergic reactions, they block H₁ receptors to reduce mucus secretion and swelling but do not dilate bronchi significantly.

🩺 Clinical Connection:
In acute asthma attacks, short-acting β₂-agonists (like salbutamol) are the first-line treatment for rapid bronchodilation.
In contrast, long-acting β₂-agonists are used for maintenance, but always in combination with inhaled corticosteroids to prevent tolerance and control inflammation.

Atropine is a competitive antagonist of muscarinic acetylcholine receptors (M₁, M₂, and M₃).
When it blocks M₃ receptors in the bronchial smooth muscle, it prevents acetylcholine-induced bronchoconstriction and reduces mucus secretion—thereby promoting bronchodilation.

Mechanism summary:

• Normal M₃ activation: Acetylcholine binds → smooth muscle contraction → bronchoconstriction and increased secretions.

• With atropine: M₃ receptor blocked → smooth muscle relaxation → bronchodilation and dry airways.

❌ Why the Other Options Are Incorrect:

• Acetylcholine:
  It stimulates M₃ receptors, causing bronchoconstriction and increased glandular secretion — opposite of inhibition.

• Bethanechol:
  A muscarinic agonist, not an antagonist. It activates M₃ receptors, mainly used for urinary retention and intestinal atony, not for respiratory dilation.

• Salbutamol:
  A β₂-adrenergic agonist, which causes bronchodilation via sympathetic stimulation — not by blocking M₃ receptors.

• Propranolol:
  A non-selective β-blocker, which can actually worsen bronchoconstriction by blocking β₂ receptors — contraindicated in asthma and COPD.

🩺 Clinical Connection:
In COPD, muscarinic antagonists (like ipratropium and tiotropium, derived from atropine) help keep airways open by blocking M₃-mediated bronchospasm, improving airflow and reducing symptoms.

Clara cells are non-ciliated, dome-shaped epithelial cells located mainly in the terminal and respiratory bronchioles.

Their key role is to secrete a surfactant-like material, which reduces surface tension within the bronchioles—helping to prevent airway collapse, especially during expiration.

Additionally, Clara cells perform several important functions:

• Detoxification: They contain cytochrome P450 enzymes that degrade harmful inhaled substances.
• Regeneration: They act as progenitor cells for the bronchiolar epithelium, replacing damaged ciliated or secretory cells.
• Immune protection: They secrete Clara cell secretory protein (CCSP), which has anti-inflammatory properties.

❌ Why the Other Options Are Incorrect:

• Regenerating new cells:
  While Clara cells do have regenerative capacity, this is not the main mechanism preventing lung collapse. The surfactant secretion plays the key role in maintaining airway stability.

• Inflating alveoli:
  Inflation of alveoli occurs through negative intrathoracic pressure during inspiration, not through Clara cell activity.

• Entrapping bodies:
  This refers more to macrophages or mucociliary clearance, not Clara cells.

• Forming memory:
  This is a function of the adaptive immune system (B and T lymphocytes), which is unrelated to the structural mechanics of lung collapse.

🩺 Clinical Connection:
Damage to Clara cells (e.g., due to smoking or toxic inhalants) can impair surfactant secretion and epithelial repair, leading to bronchiolar obstruction and increased susceptibility to respiratory diseases such as chronic bronchiolitis.

The alveolar-capillary (respiratory) membrane is the site of gaseous exchange between the alveolar air and the blood in the pulmonary capillaries. Its total thickness is extremely thin—ranging from 0.2 to 2.5 micrometers (µm)—to facilitate efficient diffusion of gases according to Fick’s law.

This membrane is composed of six layers (from alveolar air to blood plasma):

1. Alveolar fluid with surfactant

2. Alveolar epithelial cell (Type I pneumocyte)

3. Epithelial basement membrane

4. Interstitial space

5. Capillary basement membrane

6. Capillary endothelial cell

In many regions, the two basement membranes fuse, making the membrane even thinner (~0.2 µm), allowing rapid exchange of O₂ and CO₂.

❌ Why the Other Options Are Incorrect:

• 0.2 to 2.5 picometers:
  A picometer (10⁻¹² m) is subatomic in scale—thousands of times smaller than atoms. Such a measurement is far too small for biological structures.

• 0.2 to 2.5 millimeters:
  A millimeter (10⁻³ m) is 1000 times thicker than a micrometer. A membrane this thick would completely prevent gas diffusion, making respiration impossible.

• 0.2 to 2.5 nanometers:
  A nanometer (10⁻⁹ m) is far too thin for a cellular barrier.

• 0.2 to 2.5 meters:
  Obviously unrealistic — this is the height of a human, not a microscopic structure [lol :)]

🩺 Clinical Connection:
Conditions like pulmonary edema, fibrosis, or inflammation thicken the alveolar membrane, impairing gas exchange and leading to hypoxia despite normal ventilation.

Type II pneumocytes (also called Type II alveolar cells) are specialized cuboidal epithelial cells found in the alveoli of the lungs.
Their primary function is to synthesize and secrete pulmonary surfactant, a phospholipoprotein-rich substance that reduces surface tension within the alveoli, preventing their collapse during expiration.

Surfactant production begins around 24–28 weeks of gestation and becomes adequate by 34 weeks, which is why premature infants are at risk for neonatal respiratory distress syndrome (NRDS) due to insufficient surfactant.

❌ Why the Other Options Are Incorrect:

• Type I pneumocytes:
  These are squamous epithelial cells that form the thin alveolar walls for gas exchange. They do not produce surfactant but facilitate diffusion of gases.

• Lymphocytes:
  White blood cells involved in immune defense, not in alveolar structure or surfactant production.

• Hepatocytes:
  Liver parenchymal cells responsible for metabolism, detoxification, and bile secretion, unrelated to the lungs.

• Macrophages:
  In the lungs, they are called alveolar macrophages (dust cells) and function in phagocytosis of debris and pathogens, not surfactant synthesis.

🩺Clinical Connection:
Surfactant deficiency leads to alveolar collapse (atelectasis), causing impaired gas exchange. Administration of exogenous surfactant or maternal corticosteroids can significantly improve outcomes in preterm infants

In the peripheral tissues, carbon dioxide (CO₂) is produced as a metabolic byproduct and diffuses into red blood cells. Inside the RBCs, carbonic anhydrase catalyzes the following reaction:

CO2​+H2​O⇌H2​CO3​⇌H++HCO3−​

Most of the CO₂ is converted to bicarbonate ions (HCO₃⁻), which then diffuse out of the RBCs into the plasma in exchange for chloride ions (a process called the chloride shift).

Thus, the majority of CO₂ in the blood (about 70%) is transported as bicarbonate (HCO₃⁻), not as dissolved CO₂ or bound to hemoglobin.

❌Why the Other Options Are Incorrect:

• In combination with carbonic anhydrase:
  Carbonic anhydrase is an enzyme, not a transport form. It facilitates the conversion of CO₂ to bicarbonate but does not carry CO₂ itself.

• In combination with H₂CO₃:
  Carbonic acid (H₂CO₃) is unstable and quickly dissociates into H⁺ and HCO₃⁻. Only a very small fraction of CO₂ exists in this transient form.

• In combination with Hb:
  About 20–25% of CO₂ is carried as carbaminohemoglobin (HbCO₂), where CO₂ binds to the globin part of hemoglobin. This is significant but not the main form.

• CO in the blood:
  Carbon monoxide (CO) forms carboxyhemoglobin, not involved in normal CO₂ transport. This option is unrelated and pathologic.