Respiration – 2021

✅ Correct Answer: Transpulmonary pressure

Explanation:
Transpulmonary pressure (Ptp) is defined as the difference between the alveolar pressure (Palv) and the intrapleural pressure (Pip):

This pressure represents the distending force that keeps the lungs expanded against the chest wall.

• When transpulmonary pressure increases → lungs inflate.

• When it decreases → lungs deflate.

It’s crucial in maintaining lung stability and preventing alveolar collapse.
At rest, intrapleural pressure is about –5 cm H₂O, and alveolar pressure is 0 cm H₂O (relative to atmosphere), making transpulmonary pressure +5 cm H₂O — enough to keep alveoli open.

❌ Interpulmonary pressure
Not a standard term; sometimes used interchangeably with alveolar pressure but does not describe the pressure difference.

❌ Interpleural pressure
Incorrect term — usually refers to intrapleural pressure, not the difference between pressures.

❌ Intrapleural pressure
This is the pressure within the pleural cavity, normally negative, but it is one of the components used to calculate transpulmonary pressure — not the difference itself.

❌ Atmospheric pressure
Pressure exerted by air in the environment; used as the reference point (0 cm H₂O) but not the pressure difference in question.

✅ Correct Answer: Henderson–Hasselbalch equation

Explanation:
The Henderson–Hasselbalch equation describes the relationship between the pH of a buffer solution, the acid dissociation constant (pKa), and the ratio of conjugate base to acid concentrations:

pH=pKa+log⁡([A−][HA])\text{pH} = \text{pKa} + \log\left(\frac{[\text{A}^-]}{[\text{HA}]}\right)pH=pKa+log([HA][A−]​)

When the concentrations of the acid (HA) and its conjugate base (A⁻) are equal, the ratio [A−][HA]\frac{[\text{A}^-]}{[\text{HA}]}[HA][A−]​ = 1, and since log⁡(1)=0\log(1) = 0log(1)=0:

pH=pKa\text{pH} = \text{pKa}pH=pKa

This condition represents the most effective buffering point, where the buffer resists changes in pH most efficiently.

❌ Water dissociation equation
Refers to the self-ionization of water (Kw=[H+][OH−])(K_w = [H^+][OH^-])(Kw​=[H+][OH−]), not related to acid–base buffer systems.

❌ Hardy–Weinberg equation
Used in population genetics, not chemistry or acid–base balance.

❌ Torricelli’s theorem
A physics principle about fluid flow velocity — unrelated to pH.

❌ pH log equation
A vague term — pH is defined as −log⁡[H+]-\log[H^+]−log[H+], but this does not relate to buffer equilibrium or pKa relationships.

✅ Correct Answer: 200

Explanation:
Lung compliance refers to the ease with which the lungs expand during inspiration — it is defined as the change in lung volume per unit change in transpulmonary pressure.

Compliance (C)=ΔVΔP\text{Compliance (C)} = \frac{\Delta V}{\Delta P}Compliance (C)=ΔPΔV​

• The total (combined) compliance of both lungs in a normal healthy adult is about 200 mL/cm H₂O.

• This means that for every 1 cm H₂O increase in transpulmonary pressure, the lung volume increases by approximately 200 mL.

This property is crucial for efficient ventilation, and it depends on:

• Elastic fibers in lung tissue, and

• Surface tension within the alveoli (reduced by surfactant).

Decreased compliance occurs in conditions like pulmonary fibrosis or acute respiratory distress syndrome (ARDS), while increased compliance is seen in emphysema.

❌ 1000, 800, 600, 400
These values are much higher than the physiological range for lung compliance. Typical compliance per lung is ~100 mL/cm H₂O; for both lungs combined, it’s about 200 mL/cm H₂O.

✅ Correct Answer: Strenuous exercise

Explanation:
A rightward shift of the oxygen–hemoglobin dissociation curve indicates that hemoglobin’s affinity for oxygen decreases, allowing more O₂ to be released to the tissues.
During strenuous exercise, several physiological changes occur that collectively cause this shift:

1. Increased temperature

2. Increased CO₂ (hypercapnia)

3. Decreased pH (acidosis) — due to lactic acid buildup

4. Increased 2,3-DPG (diphosphoglycerate) in red blood cells

These changes enhance oxygen unloading from hemoglobin to meet the higher metabolic demands of active muscles — an effect known as the Bohr effect.

❌ Low concentration of 2,3-DPG
Would shift the curve to the left, increasing hemoglobin’s affinity for oxygen and reducing release to tissues.

❌ Fetal hemoglobin
Has higher O₂ affinity, shifting the curve to the left, which helps the fetus extract oxygen from maternal blood.

❌ Low temperature
Also shifts the curve to the left, favoring oxygen binding rather than release.

❌ High pH
Alkalosis decreases H⁺ concentration, stabilizing oxyhemoglobin and shifting the curve to the left.

✅ Correct Answer: Alveolar capillary pressure remains greater than alveolar air pressure

Explanation:
In the lung’s lower (basal) region — Zone 3, the pulmonary circulation pressure is highest because of gravity.
The relationship between the three pressures in this zone is:

Partery>Pvein>PalveolusP_{\text{artery}} > P_{\text{vein}} > P_{\text{alveolus}}Partery​>Pvein​>Palveolus​

This means both arterial and venous pressures in pulmonary capillaries exceed the alveolar air pressure, allowing continuous blood flow through the capillaries.

Thus, in Zone 3, alveolar capillary pressure (blood pressure) is greater than alveolar air pressure, resulting in maximal and continuous perfusion — ideal for gas exchange.

❌ Alveolar air pressure remains greater than alveolar capillary pressure
This occurs in Zone 1 (apex), where alveolar pressure > arterial pressure, causing no blood flow.

❌ It is present in the apices of lungs
Zone 3 is located at the bases of the lungs, not the apices.

❌ It receives intermittent blood flow
That describes Zone 2, where arterial pressure > alveolar pressure > venous pressure, causing intermittent (pulsatile) flow.

❌ None of these
Incorrect, since Zone 3 clearly has continuous blood flow due to high capillary pressure.

✅ Correct Answer: Without large increase in pulmonary arterial pressure

Explanation:
During strenuous exercise, cardiac output may increase four- to fivefold to meet the body’s oxygen demands. The pulmonary circulation accommodates this massive increase in blood flow without a large rise in pulmonary arterial pressure — unlike the systemic circulation, which experiences a significant pressure increase.

This is achieved through three main adaptive mechanisms:

1. Recruitment of previously closed pulmonary capillaries: New capillary pathways open up, increasing the total cross-sectional area for blood flow.

2. Distension of pulmonary vessels: Existing capillaries widen (dilate), reducing resistance.

3. Increased pulmonary compliance: The thin, elastic pulmonary vessels expand easily to handle greater volume.

Together, these mechanisms maintain low pulmonary vascular resistance, ensuring efficient gas exchange even at high cardiac output.

❌ With large increase in systemic arterial pressure
True for systemic circulation during exercise, but not for pulmonary circulation — its pressure rises only slightly.

❌ With increase in pulmonary arterial pressure
A slight increase may occur, but the key feature is that it’s not large, due to the compensatory recruitment and distension of capillaries.

❌ With decrease in pulmonary arterial pressure
Incorrect — the pressure doesn’t decrease; it stays relatively stable or slightly increases.

❌ None of these
Incorrect — pulmonary circulation clearly adapts without a large increase in pressure.

✅ Correct Answer: Costophrenic angle

Explanation:
A pleural effusion refers to the accumulation of excess fluid in the pleural cavity — the space between the visceral and parietal pleura.
On a chest X-ray, the earliest and most sensitive sign of pleural effusion is blunting (obliteration) of the costophrenic angle.

• The costophrenic angle is the sharp angle formed by the junction of the diaphragm and the rib cage on either side.

• In a normal X-ray, this angle appears sharp and well-defined.

• Even a small amount of fluid (~200–300 mL) can cause this angle to appear dull or rounded.

• As fluid volume increases, the fluid level rises upward along the chest wall, sometimes forming a meniscus shape.

❌ Cardiophrenic angle
Formed between the heart border and diaphragm, it can also be obscured by fluid or fat, but it’s not the primary site for detecting pleural effusion.

❌ Infrasternal angle
Located anteriorly below the sternum — unrelated to pleural cavities.

❌ Base of the lungs
While fluid does collect at the base, the radiographic detection is done specifically at the costophrenic angle.

❌ Sternal angle
A surface landmark at the junction of the manubrium and body of the sternum (T4–T5 level), unrelated to pleural effusion.

✅ Correct Answer: Right intercostal nodes

Explanation:
The thoracic duct is the main lymphatic channel of the body, draining lymph from the entire body except the right upper quadrant (right side of head and neck, right upper limb, and right thorax).

It begins at the cisterna chyli (at the level of L1–L2 vertebrae) and ascends through the thorax to terminate at the junction of the left subclavian and left internal jugular veins.

The thoracic duct drains:

• Both lower limbs (right and left)

• Left side of thorax (via left intercostal and left bronchomediastinal trunks)

• Left upper limb (via left subclavian trunk)

• Left side of head and neck (via left jugular trunk)

The right intercostal nodes, however, drain into the right lymphatic duct, not the thoracic duct.

❌ Left bronchomediastinal trunk
✅ Drains into the thoracic duct from the left thoracic and mediastinal regions.

❌ Left intercostal nodes
✅ Drain into the thoracic duct along its posterior thoracic course.

❌ Right lower limb
✅ Drains via the cisterna chyli into the thoracic duct, since the thoracic duct handles both lower limbs.

❌ Left lower limb
✅ Also drains into the thoracic duct via the cisterna chyli.

✅ Correct Answer: pH meter

Explanation:
A pH meter is the instrument used to determine the pH value of a solution. It measures the hydrogen ion concentration (H⁺) indirectly using a pH electrode (glass electrode) and a reference electrode.

Here’s how it works:

• The glass electrode generates a potential (voltage) that depends on the H⁺ ion activity in the solution.

• This potential difference is compared to the reference electrode.

• The meter then converts the voltage difference into a pH value based on the Nernst equation.

This method provides accurate and quantitative pH readings, unlike pH paper or indicators, which give only approximate results.

❌ pH spectrometer
No such instrument exists; spectrometers measure light absorption, not pH.

❌ pH electrode
It’s a component of a pH meter, not the measuring device itself. It senses the H⁺ concentration but needs the pH meter to display the reading.

❌ pH balancer
A non-scientific term — refers generally to substances or systems that adjust pH, not measure it.

❌ pH detector
A vague term; not a recognized laboratory instrument for precise measurement.

✅ Correct Answer: In the form of bicarbonate ions

Explanation:
The majority of carbon dioxide (CO₂) produced by tissue metabolism is transported in the blood as bicarbonate ions (HCO₃⁻) — this accounts for about 70% of total CO₂ transport.

Here’s how it works:

1. Inside red blood cells, CO₂ reacts with water under the influence of carbonic anhydrase:

   CO₂+H₂O↔H₂CO₃↔H⁺+HCO₃⁻\text{CO₂} + \text{H₂O} \leftrightarrow \text{H₂CO₃} \leftrightarrow \text{H⁺} + \text{HCO₃⁻}CO₂+H₂O↔H₂CO₃↔H⁺+HCO₃⁻

2. The generated bicarbonate ions then diffuse out of the RBCs into the plasma, exchanged with chloride ions (Cl⁻) in the chloride shift (Hamburger phenomenon).

3. In the lungs, the process reverses — bicarbonate reenters RBCs, is converted back to CO₂, and is exhaled.

❌ In the form of carbaminohemoglobin
About 20–25% of CO₂ binds to hemoglobin’s amino groups (forming carbaminohemoglobin), but this is not the main transport form.

❌ In the form of carboxyhemoglobin
This compound results from carbon monoxide (CO) binding to hemoglobin, not CO₂.

❌ By binding to plasma proteins
CO₂ can attach to plasma proteins slightly, but this route contributes minimally to total CO₂ transport.

❌ By dissolving in plasma
Only about 5–7% of CO₂ is transported as dissolved gas directly in plasma.

✅ Correct Answer: Passive diffusion through the lipid bilayer

Explanation:
Oxygen (O₂) and carbon dioxide (CO₂) are small, nonpolar molecules, which allows them to dissolve in the lipid bilayer of the plasma membrane and move freely across it by simple (passive) diffusion.

This process:

• Requires no energy (ATP),

• Moves gases down their concentration gradients — O₂ into cells (where it’s lower) and CO₂ out of cells (where it’s higher), and

• Depends on partial pressure differences across the membrane, as described by Fick’s Law of Diffusion.

This passive movement is critical for gas exchange in the lungs and cellular respiration in tissues.

❌ Specific gas transport proteins
No carrier proteins are required for O₂ or CO₂ — both diffuse freely due to their nonpolar nature.

❌ Secondary active transport
Involves coupling one solute’s movement with another’s gradient (e.g., Na⁺–glucose cotransport), which is not how gases move.

❌ Primary active transport
Uses ATP to move ions against their gradients (e.g., Na⁺/K⁺ ATPase); gases do not require energy-dependent transport.

❌ Facilitated diffusion
Requires carrier or channel proteins (e.g., for glucose or ions); gases cross directly through the membrane, not via proteins.

✅ Correct Answer: The presence of cartilage

Explanation:
The presence or absence of cartilage is the key histological feature that distinguishes bronchi from bronchioles under the microscope.

• Bronchi contain irregular plates of hyaline cartilage in their walls, which help keep the airways open.

• Bronchioles, on the other hand, completely lack cartilage — instead, their walls are supported by smooth muscle that controls airway diameter through contraction and relaxation.

This transition marks the shift from the conducting zone with structural support (bronchi) to the smaller, more flexible airways (bronchioles).

❌ The presence of smooth muscle
Both bronchi and bronchioles contain smooth muscle, so it does not distinguish them.

❌ The type of epithelium
Both may have ciliated columnar or cuboidal epithelium, depending on size; epithelial type gradually changes but is not the defining feature.

❌ The type of cartilage
Only bronchi have cartilage, so “type” is irrelevant for bronchioles (they have none).

❌ The absence of glands
While bronchi have submucosal glands, and bronchioles generally lack them, this feature is secondary — the absence of cartilage is the most distinctive and reliable difference.

✅ Correct Answer: Great alveolar cells

Explanation:
Great alveolar cells, also known as Type II alveolar cells (Type II pneumocytes), are cuboidal epithelial cells found within the alveolar walls.
Their key features and functions include:

• Cuboidal shape — distinct from the thin, squamous Type I cells.

• Secretion of pulmonary surfactant, a phospholipid-rich substance that reduces surface tension and prevents alveolar collapse.

• Ability to divide and regenerate both Type I and Type II pneumocytes after lung injury, making them essential for alveolar repair.

Thus, the cuboidal shape and surfactant secretion are the hallmark features that identify these as Great (Type II) alveolar cells.

❌ Squamous alveolar cells
These are flattened cells — not cuboidal — and form the respiratory surface for gas exchange (Type I pneumocytes).

❌ Type 1 alveolar cells
Same as squamous alveolar cells — thin and flat, covering ~95% of alveolar surface area; do not secrete surfactant.

❌ Alveolar atria
These are spaces or passageways leading into groups of alveoli, not cellular structures.

❌ Alveolar sac
A cluster of alveoli that share a common opening — again, a structural space, not a cell type.

✅ Correct Answer: Carbonic anhydrase

Explanation:
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 (H⁺) ions:

CO₂+H₂O↔Carbonic anhydraseH₂CO₃↔H⁺+HCO₃⁻\text{CO₂} + \text{H₂O} \xleftrightarrow{\text{Carbonic anhydrase}} \text{H₂CO₃} \leftrightarrow \text{H⁺} + \text{HCO₃⁻}CO₂+H₂OCarbonic anhydrase​H₂CO₃↔H⁺+HCO₃⁻

This reaction is essential for:

• CO₂ transport in the blood (as bicarbonate),

• Regulation of blood pH through buffering, and

• CO₂ elimination in the lungs.

Carbonic anhydrase is abundant in red blood cells, renal tubular cells, and parietal cells of the stomach.

❌ Acetylcholinesterase
Breaks down acetylcholine into acetate and choline at neuromuscular junctions; unrelated to CO₂ transport.

❌ Alkaline phosphatase
Removes phosphate groups from molecules; found in liver, bone, and placenta, not involved in CO₂ hydration.

❌ Adenylate cyclase
Converts ATP to cyclic AMP (cAMP) — part of intracellular signaling, not acid–base balance.

❌ Protein kinase
Transfers phosphate groups to proteins (phosphorylation), regulating cellular activity; unrelated to bicarbonate formation.

✅ Correct Answer: The interrupted wall of lumen

Explanation:
The respiratory bronchioles are the first part of the respiratory zone of the lung — the region where gas exchange begins.
They are distinguished histologically by having an interrupted (discontinuous) wall, where alveoli open directly into the bronchiolar lumen.

Key features:

• Lined partly by ciliated cuboidal epithelium and partly by squamous alveolar cells.

• No cartilage or submucosal glands.

• Serve as a transition between the terminal bronchioles (conducting zone) and alveolar ducts (respiratory zone).

Thus, the presence of alveolar outpouchings (interruptions) in their walls is the hallmark feature that differentiates respiratory bronchioles from other bronchioles.

❌ The type of epithelium
Although respiratory bronchioles have a mix of ciliated cuboidal and alveolar epithelium, this overlap is not the key identifying feature — the interrupted wall is.

❌ The presence of glands
Bronchioles, including respiratory ones, lack submucosal glands — glands are found only in larger bronchi.

❌ The diameter of lumen
The lumen gradually narrows along the airway tree, but size alone does not define the respiratory bronchiole.

❌ The number of cells
Cell count is variable and non-defining; structure and wall composition are more diagnostic.

✅ Correct Answer: Klebsiella pneumoniae

Explanation:
Klebsiella pneumoniae is a Gram-negative encapsulated bacillus that frequently causes severe, necrotizing pneumonia in immunocompromised or debilitated patients, such as those with diabetes, chronic alcoholism, or prolonged hospitalization.

It is notable for producing:

• Thick, mucoid (“currant jelly”) sputum due to the organism’s polysaccharide capsule,

• Cavitary lesions on chest imaging, and

• High mortality, especially in hospital-acquired infections.

Klebsiella is part of the Enterobacteriaceae family and is also a common cause of UTIs and sepsis in immunocompromised individuals.

❌ Haemophilus influenzae
Common cause of pneumonia in children and COPD patients, but not specifically linked to immunocompromised states as much as Klebsiella.

❌ Legionella pneumophila
Causes Legionnaires’ disease, often from contaminated water sources, typically affecting elderly smokers or those with chronic lung disease — not necessarily the most common in immunocompromised patients.

❌ Staphylococcus aureus
Can cause post-influenza pneumonia or hospital-acquired pneumonia, but Klebsiella remains more classic in immunocompromised or alcoholic patients.

❌ Mycoplasma
Causes atypical pneumonia (“walking pneumonia”) in young adults, not immunocompromised individuals.

✅ Correct Answer: Small cell carcinoma

Explanation:
Small cell carcinoma (also known as oat cell carcinoma) of the lung is a highly malignant tumor strongly associated with smoking and characterized by specific genetic alterations, including:

• Chromosome 3p deletions, and

• Mutations in the tumor suppressor genes TP53 and RB (retinoblastoma gene).

These mutations contribute to uncontrolled cell growth and aggressive behavior.
Histologically, it consists of small round to oval cells with scant cytoplasm, “salt-and-pepper” chromatin, and neuroendocrine features (e.g., chromogranin A, synaptophysin positivity).

Clinically, it is often associated with paraneoplastic syndromes, such as:

• SIADH (due to ADH secretion),

• Cushing’s syndrome (due to ACTH secretion), and

• Lambert-Eaton myasthenic syndrome.

❌ Squamous cell carcinoma
Associated with chromosome 3q amplification and p16 (CDKN2A) alterations. It often arises centrally in the bronchi and shows keratin pearls histologically.

❌ Large cell carcinoma
Lacks specific molecular features; it is a diagnosis of exclusion among non–small cell carcinomas.

❌ Basal cell carcinoma
A skin cancer, not a lung tumor, typically involving PTCH1 gene mutations on chromosome 9q.

❌ Adenocarcinoma
Often shows KRAS, EGFR, or ALK mutations, not 3p deletions. It commonly occurs peripherally and is the most common lung cancer in nonsmokers.

✅ Correct Answer: Type 2 alveolar epithelial cells

Explanation:
Type II alveolar epithelial cells (also called Type II pneumocytes) are specialized cuboidal cells located within the alveolar walls.
Their main function is to synthesize and secrete pulmonary surfactant, a lipoprotein-rich substance composed primarily of dipalmitoylphosphatidylcholine (DPPC).

Surfactant reduces alveolar surface tension, preventing alveolar collapse (atelectasis) during exhalation and ensuring efficient gas exchange.
Type II cells also serve as progenitor cells, capable of dividing and differentiating into Type I pneumocytes after lung injury.

❌ Squamous epithelial cells of trachea
These are protective lining cells, not involved in surfactant secretion; the trachea is lined by pseudostratified ciliated columnar epithelium.

❌ Type 1 alveolar epithelial cells
These are thin, squamous cells that form the respiratory surface for gas exchange, not surfactant secretion.

❌ Endothelial cells
Line capillaries and facilitate gas diffusion; they play no role in surfactant production.

❌ Secretory cells
A general term; while many tissues have secretory cells, surfactant is specifically secreted by Type II pneumocytes.

✅ Correct Answer: Arachidonic acid

Explanation:
Prostaglandins are lipid mediators derived from arachidonic acid, a 20-carbon polyunsaturated fatty acid present in membrane phospholipids.
When cells are stimulated (e.g., by inflammation, trauma, or hormones), the enzyme phospholipase A₂ releases arachidonic acid from the membrane.
It is then converted into prostaglandins, thromboxanes, and prostacyclins through the cyclooxygenase (COX-1 and COX-2) pathways.

These molecules play important roles in:

• Inflammation (pain, fever, redness)

• Smooth muscle contraction

• Gastric mucosal protection

• Platelet aggregation regulation

❌ Nitric oxide
A gaseous signaling molecule synthesized from arginine, not a fatty acid. It mediates vasodilation, not prostaglandin formation.

❌ Arginine
An amino acid used for nitric oxide synthesis, urea cycle, and protein formation — not for prostaglandins.

❌ Glucose
A carbohydrate and main energy source; not directly involved in prostaglandin synthesis, which follows a lipid pathway.

❌ Oxygen
Although oxygen atoms are incorporated into prostaglandin molecules during COX-mediated reactions, it is not the substrate for synthesis — arachidonic acid is.

✅ Correct Answer: Brachiocephalic trunk

Explanation:
The sternal angle (Angle of Louis) is an important surface landmark located at the junction between the manubrium and body of the sternum, corresponding to the level of the T4–T5 intervertebral disc.

Several key anatomical structures lie in the plane of the sternal angle, including:

• Bifurcation of the trachea (forming the carina)

• Beginning and end of the aortic arch

• Bifurcation of the pulmonary trunk

• Arch of the azygos vein entering the superior vena cava (SVC)

• Division between the superior and inferior mediastinum

However, the brachiocephalic trunk arises below this level — from the ascending aorta — and therefore is not in the plane of the sternal angle.

❌ Pulmonary trunk bifurcation
Occurs exactly at the level of the sternal angle (T4–T5).

❌ Bifurcation of trachea
Also located at the sternal angle, forming the carina.

❌ Arch of azygos vein
Arches over the right main bronchus and opens into the SVC at the level of the sternal angle.

❌ Aortic arch
Begins and ends at the sternal angle — rising above it and returning at the same level.

✅ Correct Answer: Hypoxia

Explanation:
Hypoxia refers to a state of insufficient oxygen supply to body tissues despite adequate blood flow. It occurs when oxygen delivery or utilization is impaired.
Causes include:

• Low arterial PO₂ (as in high altitude or respiratory disease)

• Reduced hemoglobin concentration (anemia)

• Impaired blood flow (circulatory hypoxia)

• Inhibition of oxygen utilization (histotoxic hypoxia, e.g., cyanide poisoning)

If hypoxia becomes severe and prolonged, it can lead to cellular injury and death, particularly in high-demand tissues such as the brain and heart.

❌ Pulmonary embolism
It’s a cause of hypoxia, not the term for oxygen deficiency itself. It blocks pulmonary arteries, reducing oxygenation of blood.

❌ Asthma
A respiratory condition causing airway constriction and obstruction, which may lead to hypoxia, but it is not the term describing oxygen deficiency.

❌ Anemia
A condition of low hemoglobin concentration that can cause hypoxia, but it specifically refers to a blood disorder, not oxygen lack in tissues.

❌ Anoxia
Means complete absence of oxygen supply to tissues — a more extreme form of hypoxia, not the general term.

✅ Correct Answer: Stratified squamous non-keratinized

Explanation:
The vocal cords (true vocal cords) are lined by stratified squamous non-keratinized epithelium, which is well-suited for protection against mechanical stress caused by vibration during phonation.

• This type of epithelium provides durability while maintaining flexibility and moisture, essential for sound production.

• In contrast, most of the laryngeal mucosa (including the false vocal cords) is lined by pseudostratified ciliated columnar epithelium (respiratory type).

This change in epithelial type at the true vocal cords is a classic example of functional adaptation — a tougher epithelium where friction and trauma are greatest.

❌ Stratified squamous keratinized
Found in skin and lips, where protection from drying and abrasion is needed; not suitable for the moist internal environment of the larynx.

❌ Stratified cuboidal
Seen in ducts of sweat and salivary glands, not in respiratory or phonatory structures.

❌ Columnar ciliated
Lines most of the respiratory tract, including trachea and bronchi, but not the vocal cords themselves.

❌ Simple squamous
Present in alveoli and endothelium, specialized for gas exchange, not for friction resistance.

✅ Correct Answer: Carbon monoxide poisoning

Explanation:
Carbon monoxide (CO) poisoning leads to impairment of oxygen delivery to tissues because CO binds to hemoglobin with an affinity about 200–250 times higher than oxygen.

• This forms carboxyhemoglobin, which reduces the number of available binding sites for oxygen and also shifts the oxygen-hemoglobin dissociation curve to the left, meaning that the remaining oxygen is less readily released to the tissues.

• As a result, even though arterial PO₂ may appear normal, tissue hypoxia develops due to poor oxygen unloading — a state known as anemic hypoxia (due to reduced oxygen-carrying capacity).

❌ Previous history of cyanide poisoning
Cyanide affects cellular oxygen utilization by blocking cytochrome oxidase in mitochondria, causing histotoxic hypoxia, not impaired delivery of oxygen.

❌ Doing exercise early in the morning
Exercise increases oxygen demand, not its delivery impairment; in healthy individuals, oxygen transport remains efficient.

❌ Running a marathon at sea level
This increases oxygen consumption but does not impair delivery — blood oxygenation and perfusion are maintained.

❌ None of these
Incorrect, because carbon monoxide poisoning clearly impairs oxygen delivery despite normal arterial oxygen tension.

✅ Correct Answer: Phrenic nerve

Explanation:
The phrenic nerve (C3–C5) is the sole motor nerve supply to the diaphragm, the main muscle of inspiration.

• It originates mainly from the C4 spinal segment, with contributions from C3 and C5, remembered by the mnemonic “C3, 4, and 5 keep the diaphragm alive.”

• Injury to the phrenic nerve results in paralysis of the corresponding half of the diaphragm, which then moves upward (paradoxically) during inspiration due to unopposed pressure from the abdominal viscera.

• Such injury may occur during neck surgery, trauma, or mediastinal tumors compressing the nerve.

❌ Recurrent laryngeal nerve
A branch of the vagus nerve, it supplies the laryngeal muscles for phonation and airway protection — not the diaphragm.

❌ Supraclavicular nerve
A sensory nerve from the cervical plexus (C3–C4) that supplies skin over the shoulder and upper chest, not the diaphragm.

❌ Sympathetic trunk
Carries autonomic fibers controlling visceral and vascular tone, but has no role in diaphragm movement.

❌ Esophageal plexus
Formed by fibers of the vagus nerve, it supplies the esophagus and related structures, not the diaphragm’s motor control.

✅ Correct Answer: Sternal angle

Explanation:
The trachea bifurcates (divides into the right and left main bronchi) at the level of the sternal angle, which corresponds to the intervertebral disc between the T4 and T5 vertebrae.
At this point, an internal ridge called the carina marks the site of bifurcation — it is a sensitive area that triggers the cough reflex when irritated.

This anatomical landmark (the Angle of Louis) is important clinically and radiologically because it also corresponds to:

• The beginning and end of the aortic arch,

• The upper limit of the pericardium, and

• The division between the superior and inferior mediastinum.

❌ Gastroesophageal junction
Located much lower, around the T10–T11 level, where the esophagus enters the stomach — unrelated to tracheal anatomy.

❌ T4
Partially correct in reference, but the tracheal bifurcation is more precisely at the T4–T5 intervertebral disc, identified externally by the sternal angle.

❌ T6
Too low — this level is below the tracheal bifurcation, closer to the diaphragm.

❌ T3
Too high — the trachea lies higher in the neck and upper thorax at this level, not yet bifurcated.

✅ Correct Answer: Right bronchus

Explanation:
The right main bronchus is the most common site for foreign body aspiration because of its anatomical orientation:

• It is wider, shorter, and more vertical than the left bronchus.

• When a person inhales or accidentally aspirates an object, gravity and airflow dynamics favor entry into the right bronchial tree, particularly the right lower lobe bronchus in an upright person.

In children, this is clinically important because they frequently aspirate small objects such as coins, peanuts, or toy parts, leading to wheezing, coughing, or localized pneumonia if not promptly removed.

❌ Lobule of lung
Too distal — a large foreign body like a coin cannot reach this far into the lung parenchyma.

❌ Left bronchus
It is longer, narrower, and more horizontal, making foreign body entry less likely.

❌ Bronchioles
They are too small for a coin to pass into; only very small particles can reach this level.

❌ Trachea
A coin lodged in the trachea would cause immediate severe respiratory distress and stridor, not localized wheezing.

✅ Correct Answer: Has its own vein

Explanation:
A bronchopulmonary segment is the smallest functional and anatomical unit of the lung that can be surgically removed without affecting other segments.
Each segment is:

• Pyramidal in shape, with its apex facing the hilum and base toward the pleural surface.

• Supplied by its own segmental (tertiary) bronchus and segmental branch of the pulmonary artery — making it an independent functional unit for ventilation and perfusion.

However, pulmonary veins do not run within the segment. They lie in the connective tissue between adjacent segments and therefore drain more than one segment. This is why a bronchopulmonary segment does not have its own vein.

❌ Independent functional unit
True — each segment has its own airway and blood supply, functioning semi-independently.

❌ Segmental bronchus
True — each segment receives air through its own segmental bronchus branching from the lobar bronchus.

❌ Has its own artery
True — supplied by a segmental branch of the pulmonary artery accompanying the bronchus.

❌ Pyramidal in shape
True — the shape helps in surgical identification and removal during segmentectomy.

✅ Correct Answer: Downward movement of diaphragm

Explanation:
During inspiration, the diaphragm contracts and moves downward, flattening its dome shape. This action increases the vertical diameter of the thoracic cavity, allowing the lungs to expand and draw air in.

• The contraction of the diaphragm pulls its central tendon downward by about 1.5 cm during quiet breathing and up to 7 cm during deep inspiration.

• This downward movement increases the volume of the thoracic cavity and decreases intrapulmonary pressure, causing air to flow into the lungs.

❌ Upward movement of diaphragm
Occurs during expiration, not inspiration. The diaphragm relaxes and moves upward, reducing the vertical diameter of the thoracic cavity.

❌ Downward movement of ribs
Seen during forced expiration, as internal intercostal muscles pull the ribs downward and inward to reduce thoracic volume.

❌ Bucket handle movement
This refers to the lateral elevation of lower ribs (7th–10th), which increases the transverse diameter, not the vertical diameter.

❌ Pump handle movement
This involves the anterior and upward movement of upper ribs (2nd–6th), which increases the anteroposterior diameter, not the vertical diameter.

✅ Correct Answer: Above 1st rib

Explanation:
The apex of the lung extends into the root of the neck, above the level of the first rib and clavicle. It rises about 2.5 cm (1 inch) above the medial third of the clavicle, just posterior to the sternocleidomastoid muscle.
It is covered by a tough membrane called the suprapleural membrane (Sibson’s fascia), which protects it from injuries and maintains pleural integrity during respiration.

Clinically, this is important because penetrating injuries to the root of the neck (e.g., stab wounds or central line insertions) can damage the lung apex, causing pneumothorax.

❌ Below root of neck
The apex lies within the root of the neck, not below it.

❌ Below clavicle
It actually extends above the clavicle, not below it.

❌ Above 2nd rib
This is too low; the apex is above the 1st rib, not the 2nd.

❌ Below C1
The apex does not reach as high as the level of C1 vertebra; it’s closer to the neck of the 1st rib (around T1).

✅ Correct Answer: 1

Explanation:
The 1st rib is the shortest, broadest, and most curved of all ribs and has two distinct grooves on its superior surface separated by a small ridge called the scalene tubercle.

• The anterior groove transmits the subclavian vein, while

• The posterior groove transmits the subclavian artery and the lower trunk of the brachial plexus.

The scalenus anterior muscle inserts into the scalene tubercle between these grooves. This anatomical arrangement is crucial in understanding thoracic outlet anatomy, where compression of these structures can cause neurovascular symptoms.

❌ 2
The 2nd rib has a tuberosity for the serratus anterior muscle and is longer and thinner than the 1st rib. It does not have grooves for the subclavian vessels.

❌ 3
A typical rib, lacking any grooves for the subclavian artery or vein.

❌ 4
Also a typical rib; no special features for the subclavian artery.

❌ 6
A typical rib as well, with no grooves for subclavian structures.

✅ Correct Answer: Histotoxic hypoxia

Explanation:
Histotoxic hypoxia occurs when cells are unable to utilize oxygen effectively, despite adequate oxygen delivery and normal arterial oxygen saturation. This typically results from toxic interference with cellular respiration, such as cyanide poisoning, which inhibits cytochrome oxidase (Complex IV) in the mitochondrial electron transport chain.

• As a result, oxygen remains in the blood (high venous O₂ content), but ATP production halts, leading to cellular energy failure and tissue death despite “normal” oxygen levels.

❌ Circulatory hypoxia
Occurs when blood flow to tissues is reduced, such as in shock or heart failure. Oxygen delivery is limited due to impaired circulation, not due to toxic inhibition of cellular metabolism.

❌ Stagnant hypoxia
A subtype of circulatory hypoxia where local blood flow is sluggish or stagnant (e.g., due to venous obstruction or low cardiac output). Oxygen utilization by cells is intact, but delivery is reduced.

❌ Hypoxic hypoxia
Results from low arterial PO₂ (e.g., in high altitude, respiratory obstruction, or hypoventilation). The oxygen content in arterial blood is decreased, unlike histotoxic hypoxia where O₂ levels are normal.

❌ Anemic hypoxia
Occurs when hemoglobin concentration or oxygen-carrying capacity of blood is reduced (e.g., in anemia or carbon monoxide poisoning). The total oxygen content is low even though arterial PO₂ may be normal.

✅ Correct Answer: Acid and conjugate base

A buffer solution resists changes in pH when small amounts of acid or base are added. This property arises from the presence of a weak acid and its conjugate base (or vice versa).

• The weak acid neutralizes added bases, while the conjugate base neutralizes added acids.

• The Henderson–Hasselbalch equation,

  pH=pKa+log⁡([A−][HA])\text{pH} = \text{pKa} + \log\left(\frac{[\text{A}^-]}{[\text{HA}]}\right)pH=pKa+log([HA][A−]​)

  shows that the pH of a buffer depends on the ratio of acid to conjugate base concentrations, not just on one component alone.

❌ Weak and strong acid
A strong acid completely dissociates and destroys the buffering capacity. Buffer systems require partial ionization to maintain equilibrium, which a strong acid cannot provide.

❌ Strong acid
A strong acid has no ability to resist pH change because it dissociates fully, drastically altering [H⁺] concentration even with small additions.

❌ Weak acid
A weak acid alone cannot form a buffer; it needs its conjugate base to neutralize added H⁺ ions effectively.

❌ Weak base
Similarly, a weak base alone cannot form a buffer. A conjugate acid–base pair is necessary to resist both acid and base addition.

To break down phosphoglycerides, the body uses phospholipases — enzymes that cleave specific bonds in phospholipids.

These enzymes are essential for:

• Membrane remodeling

• Signal transduction (e.g., phospholipase C in IP₃/DAG pathway)

• Arachidonic acid release for prostaglandin synthesis

❌ Why Other Options Are Incorrect

• Sphingomyelinase: Breaks down sphingomyelin (a sphingolipid), not phosphoglycerides.

• Lipofructokinase: No such enzyme exists — possibly a distractor term.

• Transferase: Transfers functional groups but doesn’t hydrolyze phospholipids.

• Phosphatase: Removes phosphate groups, not the glyceride bonds.

The intra-alveolar septa are the thin walls that separate adjacent alveoli. They contain:

• Capillaries for gas exchange

• Connective tissue fibers (elastic and reticular)

• Cells such as type I and type II pneumocytes, fibroblasts, and macrophages (dust cells)

Dust cells are alveolar macrophages — phagocytic cells derived from monocytes. They play a key role in:

• Phagocytosing dust particles, pathogens, and debris

• Migrating to the bronchioles or lymphatic system to remove engulfed material

• Protecting alveolar surfaces from infection and inflammation

❌ Why other options are incorrect

• Sustentacular cells: Supportive cells found in olfactory epithelium, not in the alveoli.

• Columnar cells: Present in the respiratory epithelium of bronchi and bronchioles, not within the alveolar septa.

• Receptor cells: Found in the olfactory mucosa, responsible for smell detection — absent in lungs.

• Basal cells: Stem cells located in pseudostratified ciliated epithelium of the conducting airways, not in alveoli.

Acute Respiratory Distress Syndrome (ARDS) is a life-threatening condition marked by diffuse alveolar damage resulting in increased alveolar-capillary permeability. This causes protein-rich fluid leakage into the alveoli, leading to severe hypoxemia and non-cardiogenic pulmonary edema.

Key features:

• Acute onset of respiratory distress (within hours to days)

• Refractory hypoxemia (not improving with oxygen therapy)

• Diffuse alveolar infiltrates on chest X-ray — the classic “white lung” or “ground-glass appearance”

Mechanism:
Damage to the alveolar epithelium and capillary endothelium → leakage of plasma proteins → formation of hyaline membranes → decreased gas exchange and lung compliance → respiratory failure.

Common causes:

• Sepsis (most common)

• Aspiration

• Severe trauma

• Pancreatitis

• Shock

❌ Why other options are incorrect

• Pulmonary tuberculosis:

  • Produces localized lesions (typically in upper lobes) with cavitary changes, not diffuse “white-out” lungs.

  • Chronic, not acute presentation.

• Chronic bronchitis:

  • Involves mucus hypersecretion and airway obstruction, not alveolar flooding.

  • Chest X-ray may show increased bronchial markings, but not a uniform white lung.

• Emphysema:

  • Shows hyperinflated, translucent lungs with flattened diaphragm on X-ray — the opposite of white lung appearance.

  • Minimal parenchymal density.

• Pneumonia:

  • Causes localized consolidation (lobar or patchy), not diffuse bilateral opacities.

  • Usually accompanied by fever, cough, and sputum.

Bronchiectasis is a chronic condition characterized by abnormal, irreversible dilation of the bronchi due to destruction of the elastic and muscular components of the bronchial wall, usually following chronic infections or obstruction.

The key features in this question point to bronchiectasis:

• Difficulty breathing, especially in the morning or with positional changes: In bronchiectasis, mucus accumulates in dilated bronchi overnight, and when the patient changes position (e.g., sits up), it drains out, producing copious purulent sputum.

• Copious mucus production: A hallmark of bronchiectasis due to pooling of secretions in the dilated airways.

• Chronic productive cough and recurrent infections are also typical.

❌ Why other options are incorrect

• Chronic bronchitis:

  • Also causes a chronic productive cough but not large volumes of sputum or positional drainage.

  • The sputum is more mucoid and consistent rather than copious and purulent.

  • There is no bronchial dilation.

• Emphysema:

  • Characterized by destruction of alveolar walls and airspace enlargement, leading to dyspnea but minimal sputum.

  • Cough is usually dry; sputum production is not copious.

• Pneumonia:

  • Presents with acute onset of fever, chest pain, and productive cough.

  • Not a chronic condition; sputum is not persistently copious or positional.

• Asthma:

  • Causes episodic wheezing and dyspnea due to bronchial hyperreactivity.

  • Sputum is scant and viscous, not copious or position-dependent.

Contents of superior mediastinum (from anterior to posterior):

• Thymus or its remnants

• Veins: Right and left brachiocephalic veins and upper part of SVC

• Arteries: Arch of aorta and its three branches

  • Brachiocephalic trunk

  • Left common carotid artery

  • Left subclavian artery

• Nerves: Vagus, phrenic, and left recurrent laryngeal nerve

• Trachea, esophagus, and thoracic duct

❌ Why other options are incorrect

• Brachiocephalic veins: Present — drain into the superior vena cava within the superior mediastinum.

• Arch of azygos vein: Curves over the root of the right lung to drain into the superior vena cava. 

• Left common carotid: Present — arises directly from the arch of the aorta in the superior mediastinum.

• Arch of aorta: Present — a defining feature of the superior mediastinum.

🔹 Clinical Context:

A 65-year-old female develops chest pain and diffuse infiltrates on X-ray 3 days after admission to the ICU.

*The key clue here is the onset after hospitalization, which points toward an infection acquired within the hospital environment.

🏥 Nosocomial Pneumonia (Hospital-Acquired Pneumonia)

Definition:

• Pneumonia that develops ≥48 hours after hospital admission and was not incubating at the time of admission.

Common Causes:

• Gram-negative rods such as Pseudomonas aeruginosa, Klebsiella pneumoniae, E. coli

• Gram-positive cocci such as Staphylococcus aureus (especially MRSA)

Predisposing Factors:

• Mechanical ventilation (ventilator-associated pneumonia)

• Prolonged ICU stay

• Immunosuppression

• Advanced age

• Aspiration of oropharyngeal secretions

Radiologic Findings:

• Diffuse or patchy infiltrates (may be bilateral)

• Often involve dependent lung zones

❌ Why Other Options Are Incorrect:

• Granulomatous disease of lung:
  Chronic infections (e.g., TB, sarcoidosis) — not acute and not associated with recent hospitalization.

• Community-acquired pneumonia:
  Acquired outside the hospital; develops before or within 48 hours of admission.

• Interstitial disease of lung:
  Chronic, noninfectious (e.g., fibrosis); not an acute ICU complication.

• Lung abscess:
  Localized pus collection, not diffuse infiltrates; presents with cavity formation on imaging.

Inspiration involves the active enlargement of the thoracic cavity, allowing air to enter the lungs due to negative intrathoracic pressure.

🔹 Muscles Involved in Inspiration:

1. Primary Muscle:

   • Diaphragm — main inspiratory muscle (contracts → flattens → increases thoracic volume).

2. Accessory Muscles (during deep or labored breathing):

   • External intercostals → elevate ribs and expand thoracic cavity.

   • Sternocleidomastoid → elevates sternum.

   • Scalenus anterior (and medius, posterior) → elevate the first two ribs.

   • Serratus anterior → assists in elevating ribs when scapula is fixed.

These muscles aid inspiration by increasing the anteroposterior and lateral diameters of the thorax.

❌ Muscle Not Involved in Inspiration:

• Internal intercostal muscles (except intercartilaginous part)
  → Mainly active during forced expiration, pulling ribs downward and inward, reducing thoracic volume.

Only the intercartilaginous (parasternal) part may assist slightly in inspiration — but overall, the internal intercostals as a group are expiratory.

Pleuritis (pleurisy) refers to inflammation of the pleura, usually due to infection, autoimmune disease, or pulmonary infarction.
Inflammation increases capillary permeability, allowing proteins and cells to leak into the pleural space.

🧬 Types of Pleural Effusion:

Since pleuritis is an inflammatory process, it produces an exudative pleural effusion, meaning protein content > 30 g/L.

❌ Why the Other Options Are Incorrect:

• 20 g/L, 10 g/L, 5 g/L, 3 g/L:
  These values correspond to transudates, which occur in non-inflammatory conditions such as heart failure, cirrhosis, or nephrotic syndrome.
  In pleuritis, these protein levels would be too low.

Respiratory alkalosis occurs when the respiratory system removes too much CO₂ from the blood.
Let’s break this down:

🧬 Step-by-Step Mechanism:

1. CO₂ + H₂O ↔ H₂CO₃ ↔ H⁺ + HCO₃⁻

   • This equation shows how carbon dioxide is directly linked to acid production in the body.

2. When you breathe rapidly (hyperventilation), CO₂ is exhaled faster than it’s produced.
   ↓
   Less CO₂ remains in the blood.
   ↓
   The reaction shifts left, reducing H⁺ concentration.
   ↓
   Blood pH rises → alkalosis.

❌ Why the Other Options Are Incorrect:

• Retain excess amount of carbon dioxide:
  → Increases CO₂ → shifts equilibrium right → ↑ H⁺ → respiratory acidosis, not alkalosis.

• Retain excess amount of hydrogen ions:
  → Directly lowers pH → acidosis, not alkalosis.

• Remove excess amount of oxygen:
  → Doesn’t significantly affect pH since O₂ is not part of the main acid-base equation.

• Retain excess amount of oxygen:
  → Similarly, has minimal effect on acid-base status.

Caplan syndrome (also called rheumatoid pneumoconiosis) is a rare condition seen in individuals who have:

1. Pneumoconiosis – particularly coal worker’s pneumoconiosis (but can also occur with silica or asbestos exposure).

2. Rheumatoid arthritis – an autoimmune disease characterized by chronic joint inflammation.

Together, these conditions lead to the formation of multiple, well-circumscribed pulmonary nodules composed of central necrosis surrounded by fibrotic tissue.
These nodules resemble rheumatoid nodules found in other tissues.

🧬 Pathogenesis:

• Inhalation of coal dust or silica particles → chronic inflammation and fibrosis in the lungs.

• In the presence of rheumatoid arthritis, immune mechanisms amplify the response, leading to necrotizing nodular lesions in the lung parenchyma.

❌ Why Other Options Are Incorrect:

• Byssinosis and rheumatoid arthritis:
  → Byssinosis occurs due to cotton dust exposure in textile workers, causing airway narrowing — not associated with rheumatoid arthritis.

• Asbestosis and tuberculosis:
  → Asbestosis is a fibrotic disease due to asbestos fibers, predisposing to mesothelioma and bronchogenic carcinoma, not tuberculosis.

• Silicosis and tuberculosis:
  → This combination leads to Silicotuberculosis, a distinct condition — not Caplan syndrome.

• Berylliosis:
  → Caused by beryllium exposure in industries (aerospace, electronics); may resemble sarcoidosis but has no association with rheumatoid arthritis.

At sea level, the barometric (atmospheric) pressure — that is, the pressure exerted by the weight of the atmosphere — has a standard value of 1 atmosphere (760mmHg).

This standard pressure is used as a baseline for measuring other pressures in physiology, such as alveolar pressure, intrapleural pressure, and partial pressures of respiratory gases.

At high altitudes, barometric pressure decreases, leading to a lower partial pressure of oxygen, which explains altitude-related hypoxia.

❌ Why Other Options Are Incorrect:

• 1 mm of Hg:
  → Extremely small value; represents negligible pressure compared to atmospheric pressure.

• 760 atm:
  → Astronomically high; would crush any organism — 1 atm = 760 mmHg, not the other way around.

• 70 atm:
  → Way too high; such pressures are only found in deep-sea environments.

• 76 atm:
  → Unrealistic for atmospheric conditions on Earth.

Each intercostal space contains an intercostal neurovascular bundle, composed of:

• V → Intercostal vein

• A → Intercostal artery

• N → Intercostal nerve

These structures run in the costal groove along the inferior border of each rib, sandwiched between the internal intercostal and innermost intercostal muscles.

Therefore, when performing a thoracentesis (pleural effusion drainage) or inserting any needle into an intercostal space, the correct and safe approach is to insert the needle just above the upper border of the lower rib — i.e., above the superior border of the rib below the intended intercostal space.

This avoids injuring the intercostal vein, artery, and nerve, which lie inferior to the rib above.

❌ Why Other Options Are Incorrect:

• Parietal pleura:
  → The parietal pleura may be penetrated intentionally during pleural fluid drainage to access the pleural cavity — avoiding it is not the goal.

• Visceral pleura:
  → Lies directly on the lung surface and is not encountered during thoracentesis unless the lung is accidentally punctured (a complication).

• Pericardium:
  → Lies deeper and more medially, not at risk in the 3rd intercostal space lateral to the sternum.

• Lungs:
  → The lung may be injured if the needle goes too deep, but this is avoided by careful depth control, not by inserting the needle above the rib.

Innervation of diaphragm:

• The phrenic nerve (C3, C4, C5) provides motor innervation to the diaphragm.

• It also provides sensory innervation to:

  • The central part of the diaphragm

  • The mediastinal and diaphragmatic pleura

  • The pericardium

🩸 Mnemonic:
“C3, 4, 5 keep the diaphragm alive.”

❌ Why Other Options Are Incorrect:

• Iliohypogastric nerve:
  → Arises from L1; supplies abdominal wall muscles and skin, not the diaphragm.

• Intercostal nerves:
  → Supply intercostal muscles and sensory innervation to the peripheral part of the diaphragm, but not the main motor supply.

• Subcostal nerve:
  → The 12th thoracic nerve — supplies abdominal wall muscles, not the diaphragm.

• Vagus nerve:
  → Provides parasympathetic innervation to thoracic and abdominal organs — not the diaphragm.

🩸 Components of the anterior thoracic wall:

1. Sternum, consisting of:

   • Manubrium (upper part)

   • Body of sternum (middle, largest portion)

   • Xiphoid process (small, inferior portion)

2. Costal cartilages connecting ribs to the sternum.

3. Intercostal muscles lie between ribs but do not form the main bony structure.

Hence, when viewing an X-ray of the anterior thoracic wall, the sternum (manubrium + body + xiphoid process) is the key structure visualized in the midline.

❌ Why Other Options Are Incorrect:

• Intervertebral discs:
  → Found posteriorly between thoracic vertebrae, not in the anterior wall.

• Intercostal muscles:
  → They fill spaces between ribs but are not bony structures forming the anterior wall itself.

• Thoracic vertebrae:
  → Form the posterior wall of the thoracic cage.

• Ribs:
  → Contribute to lateral walls, not the anterior midline structure visualized in front.

Phospholipase A₂ (PLA₂) is a hydrolytic enzyme that specifically acts on phosphoglycerides (phospholipids) — major components of cell membranes.

✳️ Reaction Catalyzed by PLA₂:

It cleaves the ester bond at the C2 position of glycerophospholipids → releasing:

• A free fatty acid (commonly arachidonic acid)

• A lysophospholipid

This released arachidonic acid is the key precursor for eicosanoids (prostaglandins, thromboxanes, leukotrienes), which mediate inflammation and immunity.

❌ Why Other Options Are Incorrect:

• Synthesis of triacylglycerol (TAG):
  → Involves acyltransferases, not phospholipases.

• Breakdown of triacylglycerol (TAG):
  → Done by lipases (e.g., hormone-sensitive lipase, lipoprotein lipase), not PLA₂.

• Breakdown of sphingomyelin:
  → Done by sphingomyelinase, not phospholipase A₂.

• Breakdown of sphingolipid:
  → Involves ceramidase or glycosidases, not PLA₂.

Atopic asthma is a Type I hypersensitivity reaction mediated primarily by T helper 2 (Th2) cells.
These cells drive the allergic inflammatory response through cytokine release that activates other immune cells.

✳️ Mechanism:

1. Initial exposure to allergen → activates dendritic cells → present antigen to naïve CD4⁺ T cells.

2. These CD4⁺ T cells differentiate into Th2 cells.

3. Th2 cells release key cytokines:

   • IL-4 → stimulates B cells to produce IgE antibodies.

   • IL-5 → recruits and activates eosinophils.

   • IL-13 → promotes mucus production and airway hyperreactivity.

4. IgE binds to mast cells, leading to degranulation upon re-exposure to the allergen → bronchoconstriction, edema, and mucus secretion.

❌ Why Other Options Are Incorrect:

• T helper 1 (Th1) cells:
  → Involved in cell-mediated immunity and intracellular pathogen defense, not allergic inflammation.

• Neutrophils:
  → Prominent in non-atopic (intrinsic) asthma and severe chronic asthma, but not the main mediators in atopic asthma.

• Lymphocytes:
  → A general term that includes Th1, Th2, B cells, etc. — not specific enough.

• Monocytes:
  → Differentiate into macrophages; involved in chronic inflammation but not central to the IgE-mediated allergic mechanism of asthma.

Unlike the parietal pleura, which is pain-sensitive, the visceral pleura is insensitive to pain, temperature, or touch because it is innervated by autonomic (vasomotor) nerves derived from the pulmonary plexus.

✳️ Innervation details:

• Visceral pleura:

  • Supplied by autonomic nerves (both sympathetic and parasympathetic fibers) from the pulmonary plexus.

  • These fibers regulate vasomotor tone (blood flow) and glandular secretion, not somatic sensation.

  • Pain sensations from visceral pleura are not well localized and are often referred vaguely to the thoracic or upper abdominal region.

• Parietal pleura:

  • Costal pleura → intercostal nerves

  • Mediastinal pleura → phrenic nerve

  • Diaphragmatic pleura → lower intercostal nerves (peripherally) and phrenic nerve (centrally)

  • Highly sensitive to pain

❌ Why Other Options Are Incorrect:

• Collateral intercostal nerve / Only intercostal nerves:
  → These innervate parietal pleura (costal part), not visceral pleura.

• Somatic nervous system:
  → Supplies skeletal muscles and body wall structures; visceral pleura is under autonomic control, not somatic.

• Phrenic nerve:
  → Innervates mediastinal and central diaphragmatic pleura, not visceral pleura.

Asthma is best described as an atopic disease, which means it is associated with a genetic predisposition to develop hypersensitivity (allergic) reactions.

Key characteristics of atopic asthma:

• Type I hypersensitivity reaction (immediate hypersensitivity) mediated by IgE antibodies.

• Triggered by exposure to environmental allergens such as dust, pollen, pet dander, or mold.

• Activation of mast cells and eosinophils leads to the release of inflammatory mediators like histamine, leukotrienes, and prostaglandins.

• This causes bronchoconstriction, airway inflammation, and mucus hypersecretion, resulting in wheezing, shortness of breath, and coughing.

Asthma is often associated with other atopic conditions, including allergic rhinitis, eczema, and food allergies.

❌ Why Other Options Are Incorrect:

• Communicable disease: Asthma cannot be transmitted from one person to another.

• Contagious disease: Asthma is non-infectious and non-transmissible.

• Autoimmune disease: In autoimmune diseases, the immune system attacks the body’s own tissues. In asthma, the reaction is hypersensitivity to external allergens, not self-antigens.

• Malignant disease: Asthma is not cancerous; it is a chronic inflammatory disorder of the airways.

When a person lives at high altitude, the partial pressure of oxygen (PO₂) in the atmosphere decreases, leading to hypobaric hypoxia. The body responds through a series of short-term and long-term physiological adaptations, collectively known as acclimatization.

Key adaptive responses:

1. Increased ventilation: Hypoxia stimulates peripheral chemoreceptors (carotid bodies), increasing the rate and depth of breathing.

2. Increased red blood cell production: Hypoxia stimulates the kidneys to secrete erythropoietin, increasing RBC count and hemoglobin concentration for better oxygen transport.

3. Increased peripheral vascularization (angiogenesis): Over time, new capillaries form in tissues, especially in skeletal muscle, enhancing oxygen delivery and diffusion capacity to cells.

4. Increased 2,3-BPG (bisphosphoglycerate): Shifts the oxygen–hemoglobin dissociation curve to the right, facilitating oxygen release to tissues.

5. Cellular adaptation: Mitochondria increase in number and efficiency, improving oxygen utilization.

Thus, increased peripheral vascularization is a hallmark of long-term acclimatization, improving tissue oxygenation in a chronically low-oxygen environment.

❌ Why Other Options Are Incorrect:

• Decreased use of oxygen by tissues despite low PO₂: Incorrect — tissues become more efficient at oxygen utilization, not less.

• Decreased red blood cell count: Opposite effect — RBC count increases due to elevated erythropoietin levels.

• Decreased breathing rate: Acute hypoxia increases respiratory rate; long-term adaptation may fine-tune it but not decrease it below baseline.

• Decreased ventilation: Ventilation is increased due to ongoing stimulation of peripheral chemoreceptors and improved respiratory drive.

🩺 Clinical Correlation:
Failure to acclimatize can result in chronic mountain sickness (Monge’s disease), characterized by polycythemia, pulmonary hypertension, cyanosis, and right ventricular hypertrophy.
In contrast, individuals who successfully acclimatize exhibit enhanced oxygen delivery mechanisms — including angiogenesis, increased RBCs, and greater ventilation efficiency — allowing them to thrive in high-altitude environments.

Tobacco use—whether through smoking or smokeless forms—is the leading preventable cause of cancer worldwide, responsible for approximately 22% of all cancer-related deaths.

Tobacco contains over 7,000 chemicals, of which at least 70 are proven carcinogens, including polycyclic aromatic hydrocarbons (PAHs), nitrosamines, benzopyrene, arsenic, formaldehyde.

Cancers linked to tobacco use:

• Lung cancer (most strongly associated)

• Oral cavity, larynx, pharynx, and esophagus

• Pancreatic, bladder, kidney, and cervical cancers

❌ Why Other Options Are Incorrect:

• Environmental pollutants: Contribute to some cancers (e.g., asbestos → mesothelioma, benzene → leukemia), but the global burden is far lower than tobacco.

• Hydrocarbons: Present in smoke and industrial exposure, but not a standalone major cause like tobacco.

• Sun exposure: Major cause of skin cancers (especially melanoma), but accounts for a smaller proportion of global cancer deaths.

• Radiation: Causes cancers (e.g., thyroid, leukemia) but is responsible for a minor global percentage compared to tobacco-related malignancies.

Non-steroidal anti-inflammatory drugs (NSAIDs)—such as aspirin, ibuprofen, and naproxen—work primarily by inhibiting the cyclooxygenase (COX) enzymes, which are critical in the prostaglandin synthesis pathway.

Pathway overview:

• Arachidonic acid, released from membrane phospholipids by phospholipase A₂, can be metabolized by two main enzymatic routes:

  1. Cyclooxygenase (COX) pathway → produces prostaglandins, prostacyclin (PGI₂), and thromboxane A₂ (TXA₂).

  2. Lipoxygenase (LOX) pathway → produces leukotrienes.

There are two major isoforms of COX:

• COX-1: Constitutive enzyme; maintains physiological functions (gastric protection, platelet aggregation).

• COX-2: Inducible enzyme; expressed during inflammation and pain.

NSAIDs block both (non-selectively in most cases), thereby reducing prostaglandin synthesis → decreasing inflammation, pain, and fever.

❌ Why Other Options Are Incorrect:

• Lipooxygenase pathway: Not inhibited by NSAIDs; it produces leukotrienes, which are involved in asthma and allergic inflammation (targeted by anti-leukotriene drugs like montelukast).

• Thromboxane A₂: Its production depends on COX, but NSAIDs inhibit it indirectly by blocking the COX pathway, not specifically targeting thromboxane alone.

• Prostaglandins: Again, NSAIDs reduce prostaglandin synthesis but by inhibiting COX, not prostaglandins directly.

• Leukotrienes: Synthesized via lipoxygenase, so unaffected by NSAIDs.

The olfactory epithelium is a specialized region of the nasal mucosa located in the roof of the nasal cavity, along the superior nasal concha and part of the nasal septum.

It is a pseudostratified columnar epithelium with glandular cells and consists of three major cell types:

1. Olfactory receptor cells – These are bipolar neurons whose dendrites bear olfactory cilia that detect odorant molecules. Their axons pass through the cribriform plate to synapse in the olfactory bulb.

2. Supporting (sustentacular) cells – Columnar cells that provide mechanical and metabolic support to receptor neurons.

3. Basal cells – Small regenerative cells at the base of the epithelium that replace worn-out olfactory neurons and supporting cells.

Additionally, beneath the epithelium are Bowman’s (olfactory) glands, which are glandular structures that secrete a watery fluid to dissolve odorants, facilitating their detection.

❌ Why Other Options Are Incorrect:

• Pseudostratified columnar without glandular cells: Incorrect because Bowman’s glands are an essential feature of the olfactory mucosa.

• Stratified squamous: Found in regions of the nasal cavity exposed to friction, such as the vestibule, but not in the olfactory area.

• Simple cuboidal: Not found in the nasal cavity; typically lines ducts and small glandular passages.

• Simple columnar: Too simple for the complex sensory function of the olfactory epithelium.

The mediastinal surface of the left lung faces the heart and great vessels, and it bears several grooves and impressions formed by adjacent thoracic structures.

On the left lung, the key relationships are:

• Arch of aorta: Forms a superior curved groove over the hilum of the left lung.

• Descending thoracic aorta: Leaves a vertical groove posterior to the hilum.

• Left subclavian artery and left common carotid artery: Leave smaller impressions above the aortic arch groove.

• Heart (left ventricle and left atrium): Form the cardiac impression, which is deeper on the left lung.

Therefore, the arch of the aorta specifically produces the prominent curved groove on the mediastinal surface of the left lung, differentiating it from the right lung (which has a groove for the arch of the azygos vein).

❌ Why Other Options Are Incorrect:

• Arch of azygos vein: Related to the right lung, not the left; it arches over the right lung root to drain into the superior vena cava.

• Superior vena cava: Also related to the right lung; it lies anterior and to the right of the trachea.

• Ascending aorta: Lies more central and anterior in the mediastinum, making no direct groove on the left lung.

• Thoracic duct: Runs posterior to the esophagus and does not form a visible surface groove on the lung.

Course of the thoracic duct:

• Begins at the cisterna chyli (around T12) in the abdomen.

• Enters the thorax through the aortic hiatus (also at T12).

• Ascends through the posterior mediastinum, behind the esophagus, and between the aorta and azygos vein.

• At around T5, it crosses from the right side to the left, entering the superior mediastinum.

• Continues upward to terminate at the venous angle.

Therefore, the thoracic duct exits the posterior mediastinum at T5, marking its transition into the superior mediastinum.

❌ Why Other Options Are Incorrect:

• T12: This is the level where the thoracic duct begins (cisterna chyli and aortic hiatus), not where it exits the posterior mediastinum.

• T10: This is the esophageal hiatus level, still within the posterior mediastinum.

• T8: This is the caval opening level — associated with the inferior vena cava, not the thoracic duct.

• T2: Too high — by this point, the thoracic duct has already entered the superior mediastinum and is ascending toward the neck.

At sea level, the barometric (atmospheric) pressure is approximately 760 mmHg, which is equivalent to 1 atmosphere (atm). This value represents the pressure exerted by the weight of the air in the Earth’s atmosphere.

This standard is essential in respiratory physiology because:

• It allows calculation of partial pressures of gases (e.g., PO₂, PCO₂) using Dalton’s law.

• It serves as a baseline when comparing pressures in the lungs, pleural cavity, and blood gases.

For instance:

• Inspired air: PO2=21%×760=160 mmHg

• Alveolar air (after humidification and gas exchange): PO2≈104 mm

❌ Why Other Options Are Incorrect:

• 800 mmHg: Slightly higher than sea level — may occur below sea level, e.g., in deep valleys.

• 120 mmHg / 100 mmHg / 76 mmHg: These are far too low; such pressures occur only at very high altitudes, not at sea level, where oxygen availability would be dangerously reduced.

The term for the 8th to the 16th week of respiratory system development is the Pseudoglandular stage.

During this stage:

• The major parts of the conducting airways, up to the terminal bronchioles, are formed through extensive branching.
• The lung tissue has a glandular, or duct-like, appearance, which gives this stage its name (pseudo-glandular, meaning “false gland”).
• There are no respiratory bronchioles or alveoli yet, meaning gas exchange is not possible, and a fetus born at this time would not survive.

❌Why the other options are incorrect

Respiratory alkalosis results from hyperventilation, where the person exhales more CO₂ than normal. Since CO₂ is a major component of the body’s acid-base balance, excessive loss of it leads to a decrease in carbonic acid (H₂CO₃) formation, which in turn reduces hydrogen ion (H⁺) concentration and raises blood pH.

Here’s the chain of events:

1. Hyperventilation → excessive CO₂ exhalation.

2. ↓ CO₂ in blood (hypocapnia) → shift in equilibrium of CO₂+H₂O↔H₂CO₃↔H⁺+HCO₃⁻ toward the left, reducing H⁺ concentration.

3. ↑ pH → respiratory alkalosis.

The kidneys may compensate over hours to days by excreting more bicarbonate (HCO₃⁻) and retaining hydrogen ions to restore pH toward normal.

Common causes of respiratory alkalosis include:

• Anxiety or panic attacks (psychogenic hyperventilation)

• High altitude exposure

• Fever or sepsis

• Pulmonary embolism

• Salicylate poisoning (early phase)

❌ Why Other Options Are Incorrect:

• Compensatory alkalosis: Compensation occurs for acidosis, not as a primary event.

• Respiratory acidosis: Opposite situation — caused by hypoventilation and CO₂ retention.

• Metabolic alkalosis: Due to H⁺ loss or HCO₃⁻ gain (vomiting, diuretics), not breathing changes.

• Metabolic acidosis: Caused by acid gain or bicarbonate loss (e.g., DKA, diarrhea), not hyperventilation.

Respiratory acidosis occurs when alveolar ventilation decreases (hypoventilation), leading to retention of carbon dioxide (CO₂) in the blood.

Here’s what happens step by step:

1. Decreased ventilation → less CO₂ exhaled.

2. CO₂ accumulates in the blood → reacts with water to form carbonic acid (H₂CO₃).

3. H₂CO₃ dissociates into H⁺ and HCO₃⁻, increasing hydrogen ion concentration.

4. pH falls, resulting in acidemia.

CO₂+H₂O↔H₂CO₃↔H⁺+HCO₃⁻

The body compensates through renal mechanisms, increasing bicarbonate (HCO₃⁻) reabsorption and acid excretion, but this takes hours to days.

Common causes include:

• Chronic obstructive pulmonary disease (COPD)

• Respiratory muscle weakness

• CNS depression (sedatives, head injury)

• Airway obstruction

❌ Why Other Options Are Incorrect:

• Respiratory alkalosis: Caused by hyperventilation leading to decreased CO₂ and increased pH.

• Compensatory acidosis: Not a standard term; compensation occurs in respiratory acidosis, not as a separate condition.

• Metabolic alkalosis: Due to loss of H⁺ or gain of HCO₃⁻, as seen with vomiting or diuretic use.

• Metabolic acidosis: Caused by increased acid production (e.g., lactic acidosis, DKA) or bicarbonate loss, not by CO₂ retention.

Nicotine is the most damaging and addictive component of tobacco due to its powerful physiological and psychological effects. It acts as a potent stimulant of the autonomic nervous system and is the primary reason people develop dependence on tobacco products.

Here’s how nicotine causes harm:

1. Addiction: Nicotine stimulates nicotinic acetylcholine receptors in the brain, releasing dopamine in the reward pathways, leading to addiction and compulsive use.

2. Cardiovascular effects: It increases heart rate, blood pressure, and myocardial oxygen demand, predisposing to hypertension, atherosclerosis, and coronary artery disease.

3. Systemic toxicity: Chronic nicotine exposure causes oxidative stress, endothelial dysfunction, and carcinogenesis, both directly and indirectly through other tobacco compounds.

4. Gateway effect: Nicotine addiction reinforces long-term smoking behavior, exposing the user to thousands of additional harmful chemicals, including carcinogens like benzopyrene and nitrosamines.

❌ Why Other Options Are Incorrect:

• Arsenic: Present in small amounts in tobacco; it is carcinogenic but not the main addictive or systemic agent.

• Ammonia: Enhances nicotine absorption in the lungs but is not a major direct toxin in typical smoking concentrations.

• Butane: A hydrocarbon used in cigarette manufacturing; mainly a combustion product, not the core damaging compound in systemic terms.

• Lead: A toxic heavy metal found in some tobacco; can cause long-term effects, but its contribution is minor compared to nicotine’s widespread systemic harm.

The majority of oxygen transport in the blood is carried out by hemoglobin (Hb) inside red blood cells.

Here’s how oxygen is distributed in the blood:

• ≈ 98–99% of oxygen is bound to hemoglobin.

• ≈ 1–2% is dissolved directly in plasma.

Each hemoglobin molecule can bind four oxygen molecules (O₂) — one per heme group. This reversible binding allows hemoglobin to pick up oxygen in the lungs (where PO₂ is high) and release it in tissues (where PO₂ is low).

This efficient transport is due to the sigmoidal (S-shaped) oxygen dissociation curve, reflecting cooperative binding — once one O₂ molecule binds, hemoglobin’s affinity for the next increases.

❌ Why Other Options Are Incorrect:

• Bicarbonate ions: Transport carbon dioxide (CO₂), not oxygen.

• None of these: Incorrect — hemoglobin is clearly responsible.

• Albumin: Transports hormones, fatty acids, and drugs — not oxygen.

• Plasma: Carries only a small fraction of dissolved oxygen (about 0.3 ml O₂ per 100 ml blood), insufficient for body demands.

Asthma is a chronic inflammatory disorder of the airways characterized by reversible bronchoconstriction, airway hyperresponsiveness, and inflammation.
The key players in its immunopathogenesis are T-helper 2 (Th2) cells.

Here’s how Th2 cells contribute:

1. Th2 activation: Environmental allergens trigger dendritic cells to present antigens to naïve CD4⁺ T cells, which differentiate into Th2 cells.

2. Cytokine release: Th2 cells secrete cytokines such as:

   • IL-4: Stimulates B cells to produce IgE, which binds to mast cells.

   • IL-5: Recruits and activates eosinophils.

   • IL-13: Promotes mucus production and airway remodeling.

3. Result: Upon re-exposure to the allergen, mast cells degranulate, releasing histamine and other mediators — causing bronchoconstriction, edema, and airway inflammation.

❌ Why Other Options Are Incorrect:

• T-helper 1 (Th1) cells: Involved in cell-mediated immunity and defense against intracellular pathogens, not allergy.

• Natural killer (NK) cells: Target virus-infected or tumor cells; they play little to no role in allergic inflammation.

• Lymphocytes: A broad term encompassing multiple immune cell types (including Th1, Th2, B cells, etc.) — not specific enough.

• Monocytes: Differentiate into macrophages; they are involved in chronic inflammation but not the primary mediators in asthma.

https://www.researchgate.net/figure/Drawing-of-a-transverse-section-through-the-thorax-at-the-level-of-the-aortic-arch-shows_fig1_7851907

The transverse plane through the sternal angle (T4–T5) includes several classic landmarks:

• Arch of azygos vein draining into the SVC ✅

• Bifurcation of the trachea (carina) ✅

• Beginning and end of the aortic arch (hence nearby great vessels)

• Left common carotid artery (arising from the aortic arch) ✅

However, the right brachiocephalic trunk (innominate artery) does not lie at this plane. It originates from the aortic arch but then ascends and bifurcates behind the right sternoclavicular joint into:

• Right common carotid

• Right subclavian

That bifurcation is above the sternal angle, at the root of the neck, not at T4–T5.

❌ Why the others are in the vicinity

• Azygos vein drains into SVC → occurs at the T4–T5 level as it arches over the right lung root.

• Right common carotid artery → its proximal part (from brachiocephalic trunk) lies near this plane.

• Left common carotid → arises directly from the aortic arch at this level.

• Bifurcation of trachea → the carina is a classic T4–T5 landmark.

✅ Correct Answer: Face towards detector

Explanation of Correct Option:

• In a posteroanterior (PA) view of the chest X-ray, the X-ray beam passes from the back (posterior) to the front (anterior) of the patient.
• The patient’s chest (anterior surface) — including the face and sternum — is placed against the detector/film.
• This position minimizes heart magnification and provides a clear, accurate view of the lungs and mediastinum, which is why it’s the standard view for ambulatory patients.

Explanation of Incorrect Options:

❌ Midclavicular line towards detector

• The term describes a surface landmark, not the patient’s positioning. The entire anterior chest (not just the midclavicular line) should face the detector.

❌ Midaxillary line towards detector

• This position would produce a lateral view, not a PA view.

❌ Supinated against detector

• “Supinated” refers to the position of the hands/forearms, not the chest orientation during X-ray imaging.

❌ Back towards detector

• This describes an anteroposterior (AP) view, where the X-rays pass from front to back. It’s usually done for bedridden or critically ill patients, not for standard chest radiography.

✅ Correct Answer: T12

Explanation of Correct Option:

• The thoracic duct enters the posterior mediastinum through the aortic hiatus of the diaphragm at the level of T12.
• It travels upward between the aorta (on its left) and the azygos vein (on its right), posterior to the esophagus.
• This duct is the largest lymphatic vessel in the body, carrying lymph from most of the body (except the right upper quadrant) into the left venous angle (junction of the left subclavian and internal jugular veins).

Explanation of Incorrect Options:

❌ T10

• This is the level of the esophageal hiatus, through which the esophagus and vagal trunks pass — not the thoracic duct.

❌ L1

• The thoracic duct begins as the cisterna chyli around L1–L2, but it does not enter the thoracic cavity here.

❌ L2

• The cisterna chyli, the origin of the thoracic duct, is typically located at L2, below the diaphragm.

❌ T8

• This is the level of the caval opening in the diaphragm for the inferior vena cava, not related to the thoracic duct.

✅ Correct Answer: Pleural pressure

Explanation of Correct Option:

• Pleural pressure (also called intrapleural pressure) is the pressure in the thin fluid-filled space between the visceral pleura (covering the lungs) and the parietal pleura (lining the chest wall).
• It is normally negative (about –4 mmHg at rest) compared to atmospheric pressure, which keeps the lungs expanded against the chest wall.
• This negative pressure is crucial for maintaining lung inflation and preventing lung collapse (atelectasis).

Explanation of Incorrect Options:

❌ Transpulmonary pressure

• It is the difference between alveolar pressure and pleural pressure (P_alv – P_pl).
• It represents the distending pressure keeping the lungs open, not the pressure between pleural layers themselves.

❌ Intrapulmonary pressure

• Also known as alveolar pressure, it is the pressure within the airways and alveoli of the lungs, not between the pleural membranes.

❌ Intrathoracic pressure

• This is a broader term that refers to the pressure within the thoracic cavity, which may vary in different compartments (pleural, cardiac, vascular).
• It’s not specifically the pressure between the pleurae.

❌ Alveolar pressure

• It’s the pressure inside the alveoli of the lungs, which equalizes with the atmospheric pressure at the end of inspiration or expiration.

✅ Correct Answer: 2nd costal cartilage

Explanation of Correct Option:

• The pulmonary trunk arises from the right ventricle and carries deoxygenated blood toward the lungs.
• It runs upward, backward, and slightly to the left, and at the level of the 2nd costal cartilage, just below the sternal angle (T4/T5 vertebral level), it bifurcates into the right and left pulmonary arteries.
• This level corresponds roughly to the plane of Ludwig’s angle, which is a key anatomical landmark separating the superior and inferior mediastinum.

Explanation of Incorrect Options:

❌ 3rd intercostal space

• Lies below the actual level of bifurcation; by this point, the pulmonary trunk has already divided into pulmonary arteries.

❌ 1st intercostal space

• Too high; this space lies near the origin of the pulmonary trunk but not its bifurcation.

❌ 3rd costal cartilage

• Also too low; the bifurcation occurs above this level.

❌ 1st costal cartilage

• This level corresponds roughly to the origin of the pulmonary trunk from the right ventricle, not its division.

When blood reaches the lungs, what gas must leave hemoglobin so oxygen can bind and be carried to tissues?

✅ Correct Answer: Doctor taking entire control which is not apparent virtually

Explanation of Correct Option:

• The vertical model of the doctor–patient relationship is also called the paternalistic model.
• In this model, the doctor assumes full control over the medical decisions and acts in what they believe is the best interest of the patient.
• The patient plays a passive role, following the doctor’s advice without actively participating in decision-making.
• It’s termed “vertical” because the relationship is hierarchical — the doctor is in a superior (top) position, and the patient is in a subordinate (lower) one.

Explanation of Incorrect Options:

❌ Patient plays a mutual role in deciding the treatment plan

• This describes the mutual participation or shared model, where both doctor and patient cooperate in making decisions.

❌ Patient makes all the decisions on their own

• This represents the consumer or autonomous model, in which the patient is completely independent in decision-making.

❌ Doctor helps patient find their preferences

• This fits the interpretive model, where the doctor helps the patient clarify their values and preferences before making a choice.

❌ Doctor only provides facts to the patient

• This describes the informative model, where the doctor acts as a technical expert, providing all medical information but leaving decisions entirely to the patient.

✅ Correct Answer: Selective listening

Explanation of Correct Option:

Selective listening means paying attention only to parts of a message that interest you or confirm your own opinions, while ignoring other important details.

• This leads to misunderstanding, incomplete information exchange, and poor feedback, making it a key barrier to effective communication.

Explanation of Incorrect Options:

❌ Reasonable eye contact

• Promotes attentiveness and trust.
• Helps the speaker feel heard — enhances, not obstructs, communication.

❌ Selective reflection

• Involves reflecting key ideas to confirm understanding.
• A helpful technique for clarity, not a barrier.

❌ Active listening

• Means fully focusing, understanding, and responding thoughtfully.
• It improves communication effectiveness.

❌ Paraphrasing

• Restating what the other person said in your own words ensures mutual understanding.
• It is a facilitator, not an obstruction.

Pump Handle Movement

• Ribs involved: 2–6
• Axis: Transverse (through costovertebral and costotransverse joints)
• Movement: Upward and forward rotation of ribs
• Effect: Increases the anteroposterior diameter of the thoracic cavity
• Example: Sternum moves like a pump handle during inspiration

Bucket Handle Movement

• Ribs involved: 7–10
• Axis: Anteroposterior
• Movement: Upward and outward elevation of ribs
• Effect: Increases the transverse diameter of the thoracic cavity
• Example: Ribs move like the handle of a bucket

Caliper Movement

• Ribs involved: 11–12
• Axis: Vertical (near vertebral ends)
• Movement: Outward and backward (swinging open like calipers)
• Effect: Increases the lateral dimensions of the lower thorax
• Example: Floating ribs widen the lower thoracic aperture

✅ Correct Answer: Clara cells

Explanation:

Clara cells (also known as club cells) are non-ciliated, dome-shaped secretory cells found only in the bronchioles of the lower respiratory tract. Their main functions include detoxification, secretion of surfactant-like material, and regeneration of bronchiolar epithelium.

They are not present in the mucosal lining of the nasopharynx, which is part of the upper respiratory tract.

The nasopharynx is lined by pseudostratified ciliated columnar epithelium with goblet cells, specialized for filtering, warming, and humidifying inspired air — not for the detoxification or repair functions of Clara cells.

❌ Diffuse neuroendocrine cells (DNES):

These are present throughout the respiratory tract, including the nasopharynx, and play a role in local regulation via neuropeptides.

❌ Ciliated columnar cells:

These are the main cells of the respiratory epithelium in the nasopharynx, responsible for moving mucus and trapped particles toward the pharynx.

❌ Goblet cells:

Present in the nasopharynx, they secrete mucus that traps dust and microorganisms.

❌ Serous cells: