Respiration – 2018

✅ Correct Answer:

Macrophages plus monocytes

Dust cells, also known as alveolar macrophages, are specialized phagocytic cells found on the alveolar surface of the lungs. They originate from blood monocytes that migrate into the alveoli and differentiate into macrophages.

Their main function is to phagocytose inhaled particles, including dust, bacteria, and carbon particles (especially in smokers or people exposed to polluted air). When filled with these particles, they appear as darkly pigmented “dust cells.”

❌ Incorrect Options:

• Eosinophils and red blood cells — ❌ Eosinophils play a role in allergic reactions and parasitic infections, not dust clearance.

• Macrophages plus erythrocytes — ❌ Red blood cells don’t form part of these immune cells; however, macrophages may engulf RBCs during hemorrhage (forming heart failure cells), which are different from dust cells.

• Lymphocytes and plasma cells — ❌ These are part of the adaptive immune system and mainly function in antibody production, not phagocytosis.

• Neutrophils and silica — ❌ Silica damages macrophages, leading to fibrosis (silicosis), but it doesn’t create dust cells.

✅ Correct Answer:

Sternal angle

The trachea bifurcates into the right and left main bronchi at the level of the sternal angle, which corresponds posteriorly to the intervertebral disc between T4 and T5.
This point is also known as the angle of Louis and serves as a key anatomical landmark for several important thoracic structures — including the beginning and end of the aortic arch and the upper border of the pericardium.

❌ Incorrect Options:

• Gastroesophageal junction — ❌ Lies much lower, at the level of T10–T11, where the esophagus enters the stomach.

• T3 — ❌ Too high; at this level, the trachea is still in its upper thoracic course, well above the carina.

• T4 — ❌ Close, but the bifurcation occurs at the T4–T5 junction, precisely marked by the sternal angle, not at T4 alone.

• T6 — ❌ Too low; at T6 the trachea has already divided into main bronchi.

✅ Correct Answer:

Superior vena cava

The mediastinal surface of the right lung bears grooves for structures that lie in close contact with it within the mediastinum. The groove for the superior vena cava (SVC) is a prominent feature on this surface. It runs vertically in front of the hilum, marking the position where the SVC descends to enter the right atrium.

Other impressions on the right lung’s mediastinal surface include those for the right atrium, azygos vein (arching over the hilum), and esophagus (posteriorly).

❌ Incorrect Options:

• Subclavian artery — ❌ This leaves a groove on the apex of the lung, especially on the left, not on the mediastinal surface.

• Descending aorta — ❌ This structure lies posterior to the left lung, producing a deep groove on the left lung’s mediastinal surface, not the right.

• Arch of aorta — ❌ Also indents the left lung, curving over the left hilum — not the right.

• Diaphragm — ❌ Forms the diaphragmatic surface (base) of both lungs, not the mediastinal surface.

✅ Correct Answer:

Centriacinar

Centriacinar (centrilobular) emphysema is the most common type seen in smokers. It primarily affects the respiratory bronchioles in the central or proximal parts of the acinus, while the distal alveoli are relatively spared.

This pattern is strongly associated with chronic smoking and typically involves the upper lobes, especially the apical segments. The pathogenesis involves oxidative damage and inflammation from tobacco smoke, leading to destruction of alveolar walls and loss of elastic recoil.

❌ Incorrect Options:

• Panacinar — ❌ Involves uniform destruction of the entire acinus, from respiratory bronchiole to alveolus. It is characteristic of α₁-antitrypsin deficiency, not smoking, and affects the lower lobes more severely.

• Paraseptal — ❌ Affects the distal alveoli near the pleura or septa. It is often linked to spontaneous pneumothorax in young adults, not to smoking directly.

• Septal — ❌ Not a standard category; the term “paraseptal” covers this type of distribution.

• None of these — ❌ Incorrect because centriacinar emphysema has a well-established link with smoking.

✅ Correct Answer:

Vertebral arch

The sclerotome portion of a somite gives rise to the mesenchymal cells that form the vertebral column. Specifically, the mesenchyme surrounding the neural tube (dorsal part of the sclerotome) condenses to form the vertebral arch — the bony structure that encloses and protects the spinal cord.

Meanwhile, the ventral part of the sclerotome surrounds the notochord to form the vertebral body. Thus, different regions of the same sclerotome contribute to distinct parts of each vertebra.

❌ Incorrect Options:

• Vertebral body — ❌ Formed by the ventral sclerotome surrounding the notochord, not the neural tube.

• Notochord — ❌ Derived from axial mesoderm, not sclerotome mesenchyme; it induces vertebral formation but does not arise from it.

• Sternum — ❌ Arises from somatic mesoderm (sternal bars) in the ventral body wall, not from sclerotome tissue.

• Ribs — ❌ Develop from the costal processes of thoracic vertebrae, lateral extensions of sclerotome cells, not from the tissue directly surrounding the neural tube.

✅ Correct Answer:

Nucleus pulposus

During the 3rd week of embryonic development, the notochord forms from mesodermal cells that migrate through the primitive node. It acts as the primary axial support of the embryo and serves as an inductive signaling center for the development of the neural tube and vertebral column.

In adults, the notochord largely disappears, but its remnants persist as the nucleus pulposus, the gelatinous core of the intervertebral disc. This central part provides cushioning and flexibility to the vertebral column.

❌ Incorrect Options:

• Transverse process — ❌ Formed from the vertebral arch and costal processes derived from sclerotome, not from the notochord.

• Vertebral arch — ❌ Develops from posterior extensions of sclerotome cells, forming the bony ring around the spinal cord.

• Vertebral body — ❌ The notochord contributes transiently to the center of vertebral bodies during formation, but it is replaced by bone, not retained.

• Sternum — ❌ Arises from somatic mesoderm (sternal bars), completely unrelated to the notochord.

✅ Correct Answer:
Henderson–Hasselbalch equation

The Henderson–Hasselbalch equation relates the pH of a buffer solution to the pKa of the acid and the ratio of the concentrations of conjugate base to acid. It is given by:
pH = pKa + log([A-] / [HA])

When the concentrations of acid ([HA]) and base ([A-]) are equal, their ratio becomes 1, and log(1) = 0, making:
pH = pKa

This means the solution’s pH equals the acid’s pKa when the buffer is balanced — the point of maximum buffering capacity.

❌ Incorrect Options:

• Water dissociation equation: Refers to Kw = [H+][OH-] = 10^-14 at 25°C, which applies to pure water, not buffer systems.

• Hardy-Weinberg equation: Belongs to genetics, describing allele frequencies (p^2 + 2pq + q^2 = 1), not acid–base chemistry.

• pH log equation: This simply defines pH as pH = -log[H+]; it does not describe acid–base equilibrium.

• None of these: Incorrect, because the Henderson–Hasselbalch equation clearly fits the described relationship.

✅ Correct Answer:

Endothoracic

This statement is not true — the endothoracic structure is not a surface of the parietal pleura; rather, it refers to the fascia (endothoracic fascia) that lines the inner surface of the thoracic wall, separating the costal pleura from the thoracic cage. It provides a loose connective tissue layer that allows the pleura to move during respiration.

The true surfaces of the parietal pleura are:

• Costal pleura — lines the inner aspect of ribs and intercostal spaces.

• Diaphragmatic pleura — covers the superior surface of the diaphragm.

• Mediastinal pleura — covers the lateral surface of the mediastinum.

• Cervical (cupula) pleura — extends into the root of the neck above the first rib.

❌ Incorrect Options:

• Diaphragmatic — ❌ True surface. Covers the diaphragm and separates pleural cavity from abdominal viscera.

• Mediastinal — ❌ True surface. Forms the lateral boundary of the mediastinum and reflects onto the lung as pleura.

• Cervical — ❌ True surface. Extends into the neck, forming the pleural cupula.

• Costal — ❌ True surface. Lines the inner thoracic wall and ribs.

✅ Correct Answer:

Superior mediastinum

The superior mediastinum is the upper compartment of the mediastinum, located above the sternal angle (T4–T5 level) and below the thoracic inlet. It contains several vital structures, including the trachea, esophagus, thoracic duct, arch of the aorta and its branches, superior vena cava, vagus and phrenic nerves, and part of the thymus. These structures pass through or are continuous with those in the posterior mediastinum as they descend.

❌ Incorrect Options:

• Posterior mediastinum — ❌ Contains the descending thoracic aorta, azygos and hemiazygos veins, thoracic duct, and esophagus, but not the trachea (which ends at T4–T5). The presence of the trachea differentiates the superior mediastinum.

• Anterior mediastinum — ❌ Lies in front of the pericardium, containing loose connective tissue, thymic remnants, lymph nodes, and fat, but no trachea, esophagus, or thoracic duct.

• Inferior mediastinum — ❌ A general division that includes anterior, middle, and posterior parts; the specific structures in question (trachea + esophagus + thoracic duct) are best grouped under the superior part.

• Middle mediastinum — ❌ Contains the heart enclosed by pericardium, roots of the great vessels, and main bronchi, not the trachea or thoracic duct.

✅ Correct Answer:

L1

The cisterna chyli is a dilated sac-like structure that marks the beginning of the thoracic duct, the body’s main lymphatic channel. It lies anterior to the bodies of L1 and L2 vertebrae, usually to the right of the aorta and posterior to the right crus of the diaphragm. It receives lymph from the intestinal trunk and lumbar lymphatic trunks, collecting lymph from the lower limbs, pelvis, and abdomen before it ascends as the thoracic duct through the diaphragm.

❌ Incorrect Options:

• T10 — ❌ This level corresponds roughly to the esophageal hiatus of the diaphragm, not where the cisterna chyli lies.

• T4 — ❌ This is the level of the sternal angle and carina, far above the abdominal location of the cisterna chyli.

• T8 — ❌ The caval opening for the inferior vena cava passes at T8, again in the thoracic region, not the retroperitoneum.

• L3 — ❌ Too low; the cisterna chyli lies above this level, typically opposite L1–L2 vertebrae.

✅ Correct Answer:

Bronchopulmonary segment cannot be removed

This statement is not true. Each bronchopulmonary segment is a structurally and functionally independent unit of the lung. Because it has its own segmental (tertiary) bronchus and pulmonary artery branch, it can be surgically removed (segmentectomy) without affecting the adjacent segments. This is often done in cases of localized infections or tumors.

❌ Incorrect Options:

• Bronchopulmonary segment is supplied by segmental bronchus — ✅ True. Each segment receives air through its own segmental bronchus, making it an anatomically distinct area.

• Bronchopulmonary segments share venous drainage — ✅ True. While arteries and bronchi are segmental, the pulmonary veins run in the intersegmental septa and therefore drain adjacent segments together, leading to shared venous drainage.

• Bronchopulmonary segment is pyramidal in shape — ✅ True. Each segment is pyramidal, with its apex directed toward the hilum and its base toward the pleural surface.

• Bronchopulmonary segment has its own artery — ✅ True. Each segment has a segmental branch of the pulmonary artery, accompanying the segmental bronchus.

According to the World Health Organization (WHO):

• Roughly one in four people globally are infected with Mycobacterium tuberculosis (the bacteria that cause TB).

• This means about 25% of the world’s population has latent TB infection — they carry the bacteria but do not show active symptoms.

Only a small fraction (about 5–10%) of those infected will develop active TB disease during their lifetime, especially if their immune system becomes weak.

Correct Answer:
✅ Phospholipid

• Explanation: The cell membrane (plasma membrane) is primarily composed of phospholipids, which form a bilayer structure. Each phospholipid molecule has:

  • A hydrophilic (polar) head, and

  • Two hydrophobic (nonpolar) fatty acid tails.
    This amphipathic nature allows the membrane to be selectively permeable, flexible, and fluid. Among phospholipids, phosphoglycerides (like phosphatidylcholine and phosphatidylethanolamine) are the most common subclasses.

Incorrect Options:

❌ Phosphoglycerides

• These are a subclass of phospholipids, not the main group name — the broader category “phospholipid” is correct.

❌ Sphingolipid

• Found in smaller amounts, particularly in myelin sheaths and neuronal membranes, but not the most abundant overall.

❌ Glycolipid

• Present in the outer leaflet of the membrane, important for cell recognition, but they make up a small fraction of total membrane lipids.

❌ None of these

• Incorrect — the correct and most common lipid type is clearly phospholipid.

Correct Answer:
✅ Atypical pneumonia

• Explanation: In HIV-positive or immunocompromised patients, pneumonia caused by atypical organisms — especially Pneumocystis jirovecii (formerly Pneumocystis carinii) — is common. This type of pneumonia presents with:

  • Fever, cough with sputum, and dyspnea

  • Diffuse infiltrates on chest X-ray rather than lobar consolidation

  • Wheezing or crackles due to alveolar involvement and interstitial inflammation
    Atypical pneumonia differs from typical pneumonia by having less abrupt onset and less purulent sputum, with organisms such as Mycoplasma, Legionella, Chlamydophila, and Pneumocystis jirovecii.

Incorrect Options:

❌ Typical pneumonia

• Caused by Streptococcus pneumoniae and similar bacteria; produces lobar consolidation and thick purulent sputum, more common in healthy adults.

❌ Aspiration pneumonia

• Occurs when gastric contents or oropharyngeal secretions are aspirated, typically involving dependent lobes (like right lower lobe), not associated specifically with HIV.

❌ Bronchopulmonary pneumonia

• Involves patchy consolidation around bronchi; more typical of bacterial infections in debilitated patients, not the interstitial pattern of atypical pneumonia.

❌ Pneumoconiosis

• A noninfectious occupational lung disease caused by inhalation of dust (e.g., silica, asbestos, coal) — not related to infection.

Correct Answer:
✅ Nosocomial pneumonia

• Explanation: Nosocomial (hospital-acquired) pneumonia develops 48 hours or more after hospital admission and was not incubating at the time of admission. It commonly affects patients who are hospitalized for other reasons — such as this man with cardiac arrest — especially if they are on ventilators, have reduced consciousness, or are immunocompromised.

  • Common causative organisms include Pseudomonas aeruginosa, Klebsiella pneumoniae, Staphylococcus aureus (MRSA), and E. coli.

  • It typically presents with fever, productive cough, chest pain, and new infiltrates on chest X-ray after 48–72 hours of hospitalization.

Incorrect Options:

❌ Community acquired pneumonia

• Occurs outside hospital settings or within 48 hours of admission. Not applicable here since symptoms appeared after 72 hours.

❌ Interstitial lung disease

• A chronic, noninfectious condition involving fibrosis, not an acute infection.

❌ Chronic pneumonia

• Refers to long-standing infections like tuberculosis or fungal pneumonia; this patient’s presentation is acute.

❌ None of these

• Incorrect, since nosocomial pneumonia clearly fits the scenario.

Correct Answer:
✅ Right bronchus

• Explanation: The right main bronchus is wider, shorter, and more vertical than the left bronchus. Because of this anatomy, any aspirated foreign body — like a coin — is most likely to enter and become trapped in the right main bronchus. This occurs especially in children, where coordination of swallowing is not fully developed, increasing aspiration risk.

Incorrect Options:

❌ Left bronchus

• Longer, narrower, and more horizontal, making it less likely for objects to enter.

❌ Trachea

• A foreign body may briefly lodge here but usually either causes immediate choking or passes into one bronchus — most often the right.

❌ Bronchioles

• Far too small to trap a large object like a coin; only very small particles reach this level.

❌ Lobule of lung

• A microscopic structural unit, not a likely site for a large aspirated object.

Correct Answer:
✅ Right bronchus

• Explanation: The right main bronchus is wider, shorter, and more vertical than the left. Because of this anatomical orientation, inhaled foreign bodies (such as a broken tooth) most commonly enter and lodge in the right bronchus. It acts like a straight continuation of the trachea, making it the natural path for aspirated objects.

Incorrect Options:

❌ Left bronchus

• Longer, narrower, and more oblique — less likely for foreign bodies to enter.

❌ Trachea

• Objects may momentarily lodge here but usually pass into one of the main bronchi. Lodging here often causes choking and is not the most common final site.

❌ Bronchioles

• Too small for large objects like a tooth; smaller particles (like food or fluid) might reach this level.

❌ Terminal bronchus

• Anatomically incorrect term — the last conducting bronchioles are terminal bronchioles, which are far too narrow for a large foreign body.

Correct Answer:
✅ Has its own vein

• Explanation: A bronchopulmonary segment is the smallest functional, independent unit of the lung that can be surgically removed without affecting adjacent segments. Each segment is supplied by:

  • A segmental (tertiary) bronchus, and

  • A branch of the pulmonary artery.
    However, the veins (pulmonary veins) are intersegmental, meaning they lie in the connective tissue between adjacent segments and drain blood from more than one segment. Thus, a bronchopulmonary segment does not have its own vein.

Incorrect Options:

❌ Independent functional unit

• Correct characteristic — each segment functions independently and can be surgically isolated.

❌ Has its own artery

• True — each segment is supplied by its own segmental branch of the pulmonary artery.

❌ Segmental bronchus

• True — each segment is ventilated by a tertiary (segmental) bronchus.

❌ Pyramidal in shape

• True — each segment is roughly pyramidal, with its apex toward the hilum and base toward the pleural surface.

Correct Answer:
✅ Epithelium

• Explanation: The trachea and esophagus can be distinguished by their epithelial lining, especially in the upper chest (cervical and upper thoracic region):

  • Trachea: lined by pseudostratified ciliated columnar epithelium with goblet cells, designed for air conduction and mucus clearance.

  • Esophagus: lined by non-keratinized stratified squamous epithelium, adapted to resist friction from food passage.
    Thus, the epithelium is the key histological feature that differentiates them.

Incorrect Options:

❌ Adventitia

• Both trachea and esophagus have an outer adventitia; it doesn’t help distinguish them.

❌ Submucosa

• Both structures contain seromucous glands in the submucosa; not a reliable differentiating feature.

❌ Mucosa

• Both have mucosal layers, but the difference lies specifically in the type of epithelium within it.

❌ Muscle

• Both have muscle layers (trachea: smooth muscle posteriorly; esophagus: skeletal upper → smooth lower), but this difference is secondary; the epithelium provides the clearest distinction.

Correct Answer:
✅ True ribs

• Explanation: The first seven pairs of ribs (1–7) are called true ribs because each one articulates directly with the sternum through its own costal cartilage. These ribs form the main protective framework of the thoracic cage.

Incorrect Options:

❌ Floating ribs

• Ribs 11 and 12 are floating ribs — they do not attach to the sternum at all.

❌ Atypical ribs

• Ribs 1, 2, 10, 11, and 12 are atypical due to unique structural features.

❌ Typical ribs

• Ribs 3 to 9 are typical ribs, not all seven of the first ribs.

❌ False ribs

• Ribs 8–10 are false ribs — they attach to the sternum indirectly through the costal cartilage of the rib above.

Correct Answer:
✅ Klebsiella

• Explanation: Klebsiella pneumoniae is a Gram-negative bacillus and a common cause of lobar pneumonia in alcoholics and debilitated patients. It often produces a thick, mucoid, blood-stained (“currant jelly”) sputum due to necrosis and hemorrhage in the lung tissue.

  • The right lower lobe is a frequent site of infection.

  • The cold sore (caused by herpes simplex virus reactivation) often appears with fever or stress but is not the causative agent — it’s just a clue that the patient is immunocompromised or under stress.

  • The bronchial breath sounds and lobar haziness on X-ray confirm consolidation typical of lobar pneumonia.

Incorrect Options:

❌ Streptococcus pneumoniae

• The most common cause of community-acquired pneumonia but classically affects healthy adults; sputum is rust-colored, not thick and mucoid.

❌ Staphylococcus aureus

• Causes bronchopneumonia or multiple lung abscesses, often post-influenza, not classic lobar consolidation in alcoholics.

❌ Escherichia coli

• A rare cause of pneumonia, usually hospital-acquired in severely ill or ventilated patients.

❌ Legionella

• Causes Legionnaires’ disease, with high fever, hyponatremia, diarrhea, and confusion — not the “currant jelly” sputum pattern.

Correct Answer:
✅ 6 mEq/L

• Explanation: In respiratory acidosis, hypoventilation (as may occur after brain trauma) leads to CO₂ retention → increased carbonic acid (H₂CO₃) formation → H⁺ accumulation in the blood. To compensate, H⁺ ions move into cells and K⁺ ions move out through the H⁺/K⁺ exchanger, resulting in hyperkalemia.

Thus, the serum potassium value rises above normal (3.5–5.0 mEq/L) and can reach around 6 mEq/L in moderate-to-severe acidosis.

Incorrect Options:

❌ 2.5 mEq/L

• Indicates hypokalemia, which occurs in alkalosis, not acidosis.

❌ 3.5 mEq/L

• Lower limit of normal; does not reflect the expected rise in potassium during acidosis.

❌ 4 mEq/L

• Normal potassium; no significant acid–base disturbance effect.

❌ 4.5 mEq/L

• Slightly normal; not consistent with hyperkalemia due to acidosis.

Correct Answer:
✅ Ca and K

• Explanation: In respiratory alkalosis, there is excessive loss of CO₂ due to hyperventilation, leading to increased blood pH. This causes two key ionic shifts:

  • Calcium (Ca²⁺): More calcium binds to plasma proteins (like albumin) as hydrogen ions decrease, resulting in decreased ionized calcium levels → can cause tingling, numbness, and muscle cramps.

  • Potassium (K⁺): Hydrogen ions move out of cells to buffer the alkalosis, and potassium moves into cells, leading to hypokalemia.

Thus, both Ca²⁺ and K⁺ levels are disrupted in respiratory alkalosis.

Incorrect Options:

❌ Mg and Na

• Sodium and magnesium are not significantly altered in respiratory alkalosis.

❌ Ca and Na

• Sodium levels remain relatively stable; only calcium and potassium are affected.

❌ Selenium

• Trace element, not involved in acid–base or electrolyte balance.

❌ K and Na

• Potassium may fall, but sodium is typically unaffected.

Correct Answer:
✅ C-shape cartilage plate in adventitia

• Explanation: The trachea does contain C-shaped hyaline cartilage rings, but they are located in the submucosa, not in the adventitia. These cartilaginous rings provide structural support and prevent tracheal collapse during inspiration. The adventitia is the outermost connective tissue layer, which anchors the trachea to surrounding tissues.

Incorrect Options (these are correct statements about tracheal structure):

❌ Epithelial lining resting on a thick basement membrane

• True. The trachea is lined by pseudostratified ciliated columnar epithelium with goblet cells resting on a distinct thick basement membrane.

❌ Fibroelastic membrane in deep membrane lamina propria

• True. The fibroelastic membrane (elastic tissue) helps maintain tracheal flexibility during breathing.

❌ Epithelium consists of columnar ciliated cells

• True. The epithelium has ciliated columnar cells, goblet cells, basal cells, and brush cells.

❌ Seromucous glands in submucosa

• True. These seromucous glands produce mucus and serous secretions that help trap and remove debris from inspired air.

Correct Answer:
✅ Lack of surfactant in alveoli

• Explanation: In Acute Respiratory Distress Syndrome (ARDS), injury to the alveolar–capillary membrane (from causes such as sepsis, trauma, or aspiration) leads to damage and loss of type II pneumocytes, which are responsible for surfactant production. The resulting loss of surfactant causes alveolar collapse (atelectasis), reduced lung compliance, and severe hypoxemia that is resistant to oxygen therapy. Thus, impaired surfactant function is a key mechanism in ARDS pathophysiology in both adults and neonates (though causes differ).

Incorrect Options:

❌ Deficiency of angiotensin converting enzyme

• ACE is produced in the lungs, but its deficiency does not cause ARDS.

❌ Carbon dioxide tension

• High or low CO₂ levels are consequences, not causes, of respiratory failure.

❌ Pulmonary embolism

• Can cause acute dyspnea and hypoxia, but not diffuse alveolar damage or surfactant loss characteristic of ARDS.

❌ Oxygen tension

• Low oxygen tension (hypoxemia) results from ARDS, not a cause of it.

Correct Answer:
✅ Downward movement of diaphragm

• Explanation: During inspiration, the diaphragm contracts and moves downward, increasing the vertical diameter of the thoracic cavity. This creates negative intrathoracic pressure, drawing air into the lungs. The diaphragm’s descent is responsible for about 75% of the inspiratory volume during quiet breathing.

Incorrect Options:

❌ Upward movement of diaphragm

• This occurs during expiration, when the diaphragm relaxes, reducing thoracic volume.

❌ Downward movement of ribs

• Happens during forced expiration, not inspiration.

❌ Bucket handle movement

• Increases the transverse diameter, not the vertical one.

❌ Pump handle movement

• Increases the anteroposterior diameter, not the vertical one.

Correct Answer:
✅ 7–10

• Explanation: The bucket-handle movement involves the lower ribs (7–10). When these ribs are elevated during inspiration, their curved shafts swing upward and outward, increasing the transverse diameter of the thoracic cavity. This movement is essential for side-to-side expansion of the chest, allowing more air to enter the lungs.

Incorrect Options:

❌ 10–12

• Ribs 11 and 12 are floating ribs and do not participate in the bucket-handle movement.

❌ 3–8

• Ribs 3–6 primarily show pump-handle movement, which increases the anteroposterior diameter.

❌ 1–7

• The upper ribs (1–6) are more involved in pump-handle movement rather than transverse expansion.

❌ 2–6

• Again, mainly the pump-handle type movement, not the bucket-handle movement.

Correct Answer:
✅ Elevation of shafts of ribs

• Explanation: The bucket-handle movement occurs primarily in the lower ribs (7–10) during inspiration. When the shafts of these ribs are elevated, they swing outward and upward — similar to a bucket handle being lifted. This movement increases the transverse diameter of the thoracic cavity, allowing greater lung expansion.

Incorrect Options:

❌ Depression of vertebral ends of ribs

• This would occur during expiration, not inspiration.

❌ Lateral movement of vertebral ends

• The vertebral ends act as pivot points; they don’t move laterally during normal respiration.

❌ Medial movement of vertebral ends

• There’s no inward (medial) motion of vertebral ends during breathing — the movement happens mainly at the shaft and sternal ends.

❌ Elevation of sternal end

• This movement is part of the pump-handle mechanism (upper ribs 2–6), which increases the anteroposterior diameter, not the transverse diameter.

Correct Answer:
✅ Above 1st rib

• Explanation: The apex of the lung extends into the root of the neck, rising about 2–3 cm above the medial third of the clavicle and above the level of the first rib. It is covered by the cervical pleura (cupula), which is reinforced by the suprapleural membrane (Sibson’s fascia). This anatomical relationship is clinically important — injuries to the root of the neck (like stab wounds or central line insertion) can damage the apex of the lung and cause pneumothorax.

Incorrect Options:

❌ Below root of neck

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

❌ Below clavicle

• It actually rises above the clavicle by about 2–3 cm.

❌ Above 2nd rib

• True but imprecise; the specific landmark is above the 1st rib, not 2nd.

❌ Below C1

• Too high anatomically; the apex does not reach this cervical level.

Correct Answer:
✅ Over 3900

• Explanation: The natural tobacco plant and its smoke contain more than 3,900 chemical compounds, and over 60 of these are known carcinogens (cancer-causing). When tobacco is burned, additional toxic substances are formed — including carbon monoxide, formaldehyde, benzene, hydrogen cyanide, and nitrosamines — which contribute to cardiovascular disease, cancer, and respiratory illnesses.

Incorrect Options:

❌ Around 1000

• Too low; this underestimates the number of identified compounds in tobacco smoke.

❌ Around 100

• Far fewer than the true number of constituents.

❌ Over 2000

• Closer, but still below the established figure of over 3,900 compounds.

❌ Below 50

• Completely incorrect — even a single cigarette releases hundreds of chemicals.

Correct Answer:
✅ Hydrogen ion concentration

The pH of a solution is defined as the negative logarithm (base 10) of the hydrogen ion concentration:
pH = -log10 [H+]

This means that as the concentration of hydrogen ions increases, the pH decreases (the solution becomes more acidic).
For example, if [H+] = 1 × 10^-7, then pH = 7, which is neutral.

Incorrect Options:

❌ Hydroxyl ion concentration
This determines pOH, not pH.
pOH = -log10 [OH-], and pH + pOH = 14

❌ Strong acid
pH is not defined as the log of an acid itself — it depends on the [H+] produced by the acid in solution.

❌ Weak base
A weak base affects hydrogen ion concentration indirectly, but pH is not defined using base concentration.

❌ Weak acid
Similarly, pH depends on how much H+ the acid releases, not on the total concentration of the acid molecules.

Correct Answer:
✅ Inferior vena cava

• Explanation: The inferior vena cava (IVC) passes through the central tendon of the diaphragm at the level of T8 (the caval opening). A stab wound reaching this region can injure the IVC, leading to massive venous hemorrhage because of its large size and direct connection to the right atrium. The IVC opening also allows the right phrenic nerve to pass through.

Incorrect Options:

❌ Inferior phrenic artery

• Supplies the diaphragm but does not pass through it; it runs along the inferior surface of the diaphragm.

❌ Azygos vein

• Passes through the aortic hiatus with the aorta at the T12 level, posterior to the diaphragm — not through the central tendon.

❌ Hemiazygos vein

• Also passes through the aortic hiatus (T12) or sometimes pierces the left crus of the diaphragm, not the central tendon.

❌ Aorta

• Passes through the aortic hiatus at T12, behind the diaphragm, not through the central tendon.

Correct Answer:
✅ 1st rib

• Explanation: The first rib is short, broad, and most curved. It has two grooves on its superior surface:

  • Anterior groove → for the subclavian vein

  • Posterior groove → for the subclavian artery and the lower trunk of the brachial plexus
    These grooves are separated by the scalene tubercle, where the scalenus anterior muscle attaches.

Incorrect Options:

❌ 2

• The second rib has a tuberosity for the serratus anterior muscle but no grooves for major vessels.

❌ 3, 4, 6

• These are typical ribs with no specialized grooves for subclavian vessels.

Correct Answer:
✅ Histotoxic hypoxia

• Explanation: Histotoxic hypoxia occurs when cells are unable to utilize oxygen properly despite its adequate delivery and saturation. This usually results from toxic substances (like cyanide or carbon monoxide) that inhibit enzymes of cellular respiration, particularly cytochrome oxidase in the electron transport chain. As a result, oxygen remains unused in the blood and tissues, leading to elevated venous oxygen content.

Incorrect Options:

❌ Circulatory hypoxia

• Caused by decreased blood flow (e.g., heart failure or shock), leading to insufficient oxygen delivery to tissues.

❌ Stagnant hypoxia

• Similar to circulatory hypoxia; due to sluggish or stagnant blood flow, not enzyme inhibition.

❌ Hypoxic hypoxia

• Due to low oxygen tension in arterial blood (e.g., high altitude, respiratory disease).

❌ Anemic hypoxia

• Occurs when oxygen-carrying capacity of blood is reduced due to low hemoglobin levels or abnormal hemoglobin.

Klebsiella pneumoniae is the most common cause of pneumonia in alcoholics. It is a Gram-negative, encapsulated bacillus that belongs to the Enterobacteriaceae family.

In chronic alcoholics, several factors predispose to Klebsiella infection:

• Impaired cough and gag reflexes, increasing the risk of aspiration

• Compromised immune function

• Poor nutrition and altered oropharyngeal flora

Pathogenesis:
Klebsiella typically causes lobar pneumonia, often affecting the upper lobes. The infection leads to tissue necrosis, abscess formation, and production of thick, blood-tinged sputum — classically described as “currant jelly” sputum due to its viscous, dark-red appearance caused by hemorrhage and necrosis.

On imaging, the affected lobes may show bulging fissures because of the heavy exudate.

❌ Why the Other Options Are Incorrect:

• Streptococcus pneumoniae:
  The most common cause of community-acquired pneumonia overall, but not specifically associated with alcoholism. Usually causes rust-colored sputum and less necrosis.

• Pseudomonas aeruginosa:
  Common in hospital-acquired pneumonia, especially in cystic fibrosis, burn patients, or those on ventilators, but not specifically in alcoholics.

• Staphylococcus aureus:
  Often a secondary infection following influenza or viral pneumonia; tends to cause multiple abscesses rather than the lobar consolidation typical of Klebsiella.

• Haemophilus influenzae:
  Common in COPD patients and children, but not classically linked to alcoholism.

A hamartoma is the most common benign tumor of the lung. It’s composed of a disorganized mixture of tissues that are normally present in the lung, such as cartilage, fat, connective tissue, and epithelial elements.

Hamartomas are often peripheral in location and are usually discovered incidentally on chest imaging.
On an X-ray or CT scan, they characteristically show “popcorn calcification” — a distinctive, irregular pattern of calcification due to the cartilaginous component.

Histologically, they are well-circumscribed, slow-growing, and noninvasive, which differentiates them from malignant lung tumors.

❌ Why the Other Options Are Incorrect:

• Hemangioma:
  A benign vascular tumor, more common in the liver or skin than in the lungs. Pulmonary hemangiomas are rare.

• Hepatoma:
  Another name for hepatocellular carcinoma, a malignant liver tumor, not related to the lungs.

• Adenoma:
  Although benign glandular tumors (adenomas) can occur in the lungs (e.g., bronchial adenomas), they are less common than hamartomas and may sometimes behave in a locally invasive manner.

• Fibroma:
  A benign tumor of fibrous tissue, which is rare in the lung parenchyma.

Ketonuria means the presence of ketone bodies (like acetoacetate, β-hydroxybutyrate, and acetone) in the urine.

In diabetes mellitus, especially type 1, there is an insulin deficiency. Without sufficient insulin, glucose cannot enter cells for energy. As a result, the body begins breaking down fats through lipolysis to produce energy.

This fatty acid oxidation in the liver leads to excessive production of ketone bodies, which are acidic in nature. When they accumulate in the blood, they lower the blood pH, causing metabolic acidosis, specifically diabetic ketoacidosis.

When the blood levels of ketones rise above the renal threshold, they appear in the urine — hence ketonuria.

❌ Why the Other Options Are Incorrect:

• Respiratory acidosis:
  Caused by CO₂ retention due to hypoventilation (e.g., COPD). It has nothing to do with fat metabolism or ketone production.

• Metabolic alkalosis:
  Characterized by increased blood pH (opposite of acidosis), often from vomiting or loss of H⁺ ions, not ketone accumulation.

• Inorganic acidosis:
  This term is nonspecific; diabetic ketoacidosis results from organic acids (ketone bodies), not inorganic acids.

• Hypokalemia:
  Although potassium disturbances can occur in diabetes, ketonuria specifically points toward acid production, not directly low potassium levels.

A modern-day doctor should embody a patient-centered approach, meaning that the patient’s needs, values, preferences, and well-being are at the heart of all clinical decisions.

This approach represents a shift from older, disease-centered or hospital-centered models. Instead of focusing solely on curing the illness, patient-centered care emphasizes healing the person, through empathy, communication, shared decision-making, and respect for individual differences.

It also involves holistic care — considering physical, psychological, and social aspects — and ensuring patients feel heard, understood, and involved in their treatment plans.

❌ Why the Other Options Are Incorrect:

• Hospital-centered:
  Focuses more on institutional goals, resources, and efficiency than on individual patient welfare — not aligned with modern ethics.

• Wealth-centered:
  Prioritizing profit over patient care is unethical and contradicts the Hippocratic Oath and professional integrity.

• Time-centered:
  While time management is important, prioritizing speed over patient understanding can compromise care quality.

• Judgemental:
  Doctors must be empathetic, nonjudgmental, and culturally sensitive; judgment impedes trust and effective communication.

In the respiratory system, β₂-adrenergic receptors are found predominantly in bronchial smooth muscles. When these receptors are stimulated (for example, by β₂ agonists like salbutamol), they cause bronchodilation — widening of the airways and easing airflow.

In contrast, inhibiting or blocking β₂ receptors leads to bronchoconstriction. This principle becomes important in the treatment of glaucoma, where β₂ receptor inhibition reduces aqueous humor production in the ciliary body of the eye, thereby lowering intraocular pressure.

However, this same inhibition can have undesirable effects on the lungs — namely, airway narrowing. That’s why non-selective beta-blockers (which block both β₁ and β₂ receptors) can worsen asthma or COPD by triggering bronchospasm.

Thus, while β₂ inhibition is useful in glaucoma, it can be harmful in respiratory conditions, making this a key example of how pharmacologic receptor targets in one organ system can have significant effects in another.

❌ Why the Other Options Are Incorrect:

• Alpha-2:
  These receptors primarily reduce sympathetic outflow when activated. Their inhibition doesn’t significantly affect aqueous humor or airway tone.

• Alpha-1:
  Found in vascular smooth muscle; their blockade causes vasodilation, not a change in intraocular pressure or bronchodilation.

• Beta-1:
  Located mainly in the heart. Inhibition reduces heart rate and contractility but has minimal respiratory or ocular effect.

• Beta-3:
  Found mostly in adipose tissue; associated with lipolysis and thermogenesis, not relevant to eye or airway physiology.

The pleura consists of two layers — the parietal pleura (lining the thoracic wall) and the visceral pleura (covering the lungs directly).
Lymphatic drainage differs significantly between these two layers due to their distinct locations and embryological origins.

• The parietal pleura drains into lymph nodes of the thoracic wall, such as intercostal, parasternal, and diaphragmatic nodes.

• The visceral pleura, on the other hand, is tightly adherent to the lung and shares its lymphatic drainage — meaning lymph from the visceral pleura flows into the pulmonary lymphatic system.

Lymph from the visceral pleura first drains into pulmonary lymph nodes located within the lung parenchyma, which then drain into the bronchopulmonary (hilar) nodes, and ultimately into the tracheobronchial nodes located around the bifurcation of the trachea.
These tracheobronchial nodes form the main collecting point for deep lymphatic drainage of the lungs and visceral pleura.

❌ Why the Other Options Are Incorrect:

• Diaphragmatic lymph nodes:
  Drain portions of the parietal pleura, especially over the diaphragm, and do not receive lymph from the visceral pleura.

• Paravertebral lymph nodes:
  Lie along the vertebral column and primarily drain the posterior thoracic wall, not the lungs or visceral pleura.

• Prevertebral lymph nodes:
  Found in front of the vertebral column, associated with major vessels and sympathetic trunks, mainly draining deep thoracic and abdominal structures, not pulmonary tissue.

• Axillary lymph nodes:
  Drain the upper limbs, chest wall, and breast, including parts of the parietal pleura, but not the visceral pleura covering the lungs.

Although the right and left hila differ slightly, their general spatial arrangement is consistent:

• The bronchus lies posteriorly

• The pulmonary artery lies anterior to the bronchus

• The pulmonary veins lie most anterior and inferior

Right Lung Hilum:

• The eparterial bronchus (to the upper lobe) is located above the pulmonary artery.

• The hyparterial bronchus (to the middle and lower lobes) lies below it.

• Both pulmonary veins lie anterior and inferior to the bronchi and arteries.
  Thus, overall, the bronchus remains posterior and superior to the pulmonary veins.

Left Lung Hilum:

• The main bronchus lies posterior to the pulmonary artery.

• The pulmonary veins are anterior and inferior to both the artery and bronchus.

❌ Why the Other Options Are Incorrect:

• The main bronchus is posterior to the pulmonary artery and inferior to the pulmonary veins
  → The pulmonary veins are the lowest structures in the hilum; the bronchus lies above, not below, them.

• The main bronchus is posterior to pulmonary veins and inferior to the pulmonary artery
  → Partly right about being posterior, but wrong in saying it’s inferior to the veins — it’s superior instead.

• The main bronchus is in the middle of pulmonary artery and veins
  → The bronchus lies behind both, not between them.

• The main bronchus is anterior to pulmonary artery and veins
  → The bronchus is posterior, not anterior.

The transmission of TB depends on whether viable bacilli are present in the airways, allowing the bacteria to spread via droplet nuclei during coughing or sneezing.

🔹 Latent Tuberculosis (Non-transmissible Form)

In latent tuberculosis, the bacteria are present in the body but remain dormant (inactive) within granulomas formed by the host’s immune system.

• There is no bacterial replication and no destruction of lung tissue.

• No bacilli are expelled in sputum, since the infection is not active in the respiratory tract.

• Individuals are asymptomatic, and their chest X-rays are usually normal or show healed lesions.

Hence, latent TB cannot be transmitted to others.

❌ Why the Other Options Are Incorrect:

• Secondary (Reactivation) Tuberculosis:
  Occurs when dormant bacilli become active again, typically in the apical regions of the lungs.
  This form produces cavitary lesions filled with bacteria.
  The patient coughs up bacilli, making them highly infectious.

• Primary Tuberculosis:
  The initial infection in a previously unexposed person, commonly seen in children.
  Forms a Ghon focus in the lower part of the upper lobe or upper part of the lower lobe.
  While often asymptomatic, progressive cases can involve bacilli in the airways — making them potentially transmissible.

• Miliary Tuberculosis:
  A disseminated form caused by widespread hematogenous spread.
  The lungs are often involved along with other organs.
  If the bacilli reach the alveoli, airborne transmission can occur.

• Abdominal Tuberculosis:
  Usually results from swallowed sputum from pulmonary TB or hematogenous spread.
  Involves the intestines, mesenteric lymph nodes, or peritoneum.
  Though not a common source of airborne infection, it still involves active bacilli, hence not entirely non-transmissible.

The thoracic inlet is the upper opening of the thoracic cavity, through which structures pass between the neck and the thorax.

It is bounded by:

• Anteriorly: upper border of the manubrium sterni

• Posteriorly: body of the first thoracic vertebra (T1)

• Laterally: first pair of ribs and their costal cartilages

🔹 Major Structures Passing Through the Thoracic Inlet:

From the neck to the thorax:

• Trachea

• Esophagus

• Apices of the lungs and pleura

• Thymic remnants (vestiges)

• Great vessels: brachiocephalic veins, subclavian arteries, common carotid arteries

• Nerves: vagus, phrenic, recurrent laryngeal, and sympathetic trunks

🔹 Why the 5th Ventral Thoracic Nerve Does Not Enter:

The 5th ventral thoracic nerve (T5) arises from the 5th thoracic spinal segment.

• It emerges from the intervertebral foramen at the level of the fifth thoracic vertebra, well below the thoracic inlet.

• It runs laterally and anteriorly along the intercostal space as part of the intercostal nerves.

• It does not ascend upward toward the neck or pass through the thoracic inlet.

Hence, it remains entirely within the thoracic cavity — not entering or exiting through the thoracic inlet.

❌ Why the Other Options Are Incorrect:

1. Apices of the lungs

   • The apices project slightly above the level of the first rib and extend into the root of the neck.

   • Therefore, they do pass through the thoracic inlet.

2. Thymic vestiges

   • The thymus originates in the neck (from the third pharyngeal pouch) and descends into the thorax during development.

   • Its remnants (vestiges) can extend into or through the thoracic inlet.

3. Esophagus

   • The esophagus begins at the lower border of the cricoid cartilage (C6) in the neck and passes through the thoracic inlet into the thoracic cavity.

4. Trachea

   • The trachea begins just below the larynx at C6 and descends into the thoracic cavity through the thoracic inlet, where it continues to the carina at the sternal angle.

Aminophylline is a phosphodiesterase (PDE) inhibitor and a derivative of theophylline, both of which belong to the methylxanthine class of bronchodilators.

It is sometimes used as an adjunct therapy in chronic obstructive pulmonary disease (COPD) and asthma, especially when other drugs fail to provide adequate control.

🔹 Mechanism of Action:

• Inhibition of phosphodiesterase (PDE)
• Adenosine receptor antagonism
• Anti-inflammatory effects
• Improves diaphragmatic contractility

⚠️ Clinical Considerations:

• Toxicity signs: nausea, vomiting, seizures, and arrhythmias.

• Drug interactions: metabolism affected by smoking, macrolides, and certain anticonvulsants.

❌ Why the Other Options Are Incorrect:

• Long-acting corticosteroid

  • Example: Fluticasone or Budesonide.

  • These are anti-inflammatory, not bronchodilators.

  • They work by suppressing airway inflammation, not by inhibiting PDE.

• Tiotropium

  • A long-acting muscarinic antagonist.

  • Blocks M3 receptors to cause bronchodilation.

  • No effect on phosphodiesterase.

• Albuterol (Salbutamol)

  • A short-acting β₂-adrenergic agonist.

  • Stimulates β₂ receptors → increases cAMP → bronchodilation.

  • However, this occurs through receptor activation, not PDE inhibition.

• Zileuton

  • A 5-lipoxygenase inhibitor used in asthma, not COPD.

  • Decreases leukotriene synthesis → reduces inflammation and bronchoconstriction.

  • No action on phosphodiesterase.

Tiotropium is a long-acting muscarinic antagonist used as a maintenance therapy for chronic obstructive pulmonary disease (COPD) and sometimes for severe asthma.

It works by blocking M3 muscarinic receptors in the airway smooth muscle, preventing acetylcholine-mediated bronchoconstriction.

Unlike short-acting antimuscarinics such as ipratropium, tiotropium dissociates very slowly from M3 receptors, resulting in 24-hour bronchodilation with once-daily dosing.

This makes it ideal for long-term management of COPD, a condition characterized by persistent airflow limitation and chronic bronchoconstriction.

🔬 Mechanism of Action:

1. Antagonizes M3 receptors → inhibits bronchial smooth muscle contraction.
2. Reduces mucus secretion and airway hyperreactivity.
3. Improves airflow and reduces COPD exacerbations.

❌ Why the Other Options Are Incorrect:

• Ipratropium

  • Also an antimuscarinic bronchodilator, but short-acting.

  • Used mainly for acute symptom relief or in combination with β₂-agonists.

  • Duration: 4–6 hours, not suitable for long-term control like tiotropium.

• Terbinafine

  • An antifungal agent (inhibits squalene epoxidase).

  • Used for dermatophytosis (tinea infections), not respiratory diseases.

  • No bronchodilator activity.

• Salbutamol (Albuterol)

  • A short-acting β₂-adrenergic agonist.

  • Provides rapid bronchodilation — useful for acute asthma attacks, not long-term COPD maintenance.

  • Duration: 4–6 hours only.

• Prednisone

  • A systemic corticosteroid used for anti-inflammatory effects in acute exacerbations of asthma or COPD.

  • Not a bronchodilator and not used chronically due to systemic side effects (immunosuppression, hyperglycemia, osteoporosis).

Epinephrine, a key sympathomimetic hormone released by the adrenal medulla, acts on both alpha and beta adrenergic receptors throughout the body. However, its cardiac effects are primarily mediated through β₁-adrenergic receptors.

🔹 Mechanism of Action:

When epinephrine binds to β₁ receptors on the sinoatrial (SA) node, atrioventricular (AV) node, and ventricular myocardium, it activates Gs proteins, which stimulate adenylyl cyclase, leading to increased cAMP levels.

This cascade:

1. Increases Ca²⁺ influx through L-type calcium channels → enhances myocardial contractility (positive inotropy).

2. Increases the rate of depolarization in the SA node → increases heart rate (positive chronotropy).

3. Enhances conduction velocity through the AV node → increases cardiac output overall.

Therefore, β₁ receptor activation by epinephrine directly leads to increased cardiac output and contractility.

❌ Why the Other Options Are Incorrect:

• Alpha 1 Receptors

  • Located mainly on vascular smooth muscle, not the heart.

  • Activation → vasoconstriction → increases peripheral resistance and blood pressure, but does not directly enhance cardiac contractility.

  • Indirectly increases afterload, which can even reduce stroke volume.

• Alpha 2 Receptors

  • Found primarily on presynaptic nerve terminals.

  • Activation → inhibits norepinephrine release, leading to decreased sympathetic output.

  • Result: Decreased rather than increased cardiac stimulation.

• Beta 2 Receptors

  • Located mainly in bronchial smooth muscle and vascular smooth muscle of skeletal muscle.

  • Activation → bronchodilation and vasodilation, not enhanced cardiac contractility.

  • Although epinephrine binds to them, their cardiac contribution is minor compared to β₁.

• Beta 3 Receptors

  • Found mainly in adipose tissue; involved in lipolysis and thermogenesis.

  • Minimal role in cardiac physiology.

  • Some are found in the heart, but their activation actually reduces contractility (negative inotropic effect).

A Ghon focus refers to a localized area of caseating granulomatous inflammation caused by Mycobacterium tuberculosis.
The location of this lesion helps determine the type or stage of tuberculosis:

🔹 Primary Tuberculosis

• Occurs upon first exposure to the organism.

• The Ghon focus typically forms in the lower part of the upper lobe or the upper part of the lower lobe of the lung — areas with good lymphatic drainage.

• When combined with regional lymph node involvement, it forms a Ghon complex.

🔹 Secondary (Post-Primary) Tuberculosis

• Results from reactivation of dormant M. tuberculosis bacilli, often years after the primary infection.

• This reactivation tends to occur in the apices (upper lobes) of the lungs because:

  • These regions have the highest oxygen tension, ideal for the aerobic mycobacteria.

• Hence, a Ghon focus in the apical region signifies secondary tuberculosis.

The lesions in secondary TB are typically more cavitary, caseating, and may lead to fibrosis or hemoptysis.

❌ Why the Other Options Are Incorrect:

• Miliary Tuberculosis

  • Represents disseminated TB where bacilli spread through the bloodstream.

  • Produces tiny millet seed–like lesions throughout multiple organs (lungs, liver, spleen).

  • Lesions are numerous and diffuse, not localized to the apices.

• Primary Tuberculosis

  • The initial infection, with Ghon focus in lower lobes (not apices).

  • Occurs commonly in children and immunocompetent hosts.

  • May remain latent or heal with calcification (Ghon complex).

• Latent Tuberculosis

  • Represents dormant infection without active disease.

  • No radiological or histologic evidence of an active Ghon focus — bacteria remain contained within granulomas.

  • If reactivation occurs → becomes secondary TB.

• Lung Abscess

  • Localized suppurative necrosis (pus-filled cavity) due to bacterial infection (e.g., Staphylococcus aureus, Klebsiella).

  • Not caused by M. tuberculosis, and the pathology is purulent, not granulomatous.

The upper respiratory tract (URT) includes all structures from the nose down to the larynx:
➡️ Nose → Nasal cavity → Pharynx → Larynx (above vocal cords).

An upper respiratory tract infection refers to inflammation or infection involving these regions.
The most common examples are:

• Pharyngitis (sore throat)

• Rhinitis (common cold)

• Sinusitis

• Tonsillitis

• Laryngitis

Among the given options, pharyngitis fits perfectly as a typical URTI — usually caused by viruses (e.g., adenovirus, rhinovirus, coronavirus, influenza) or bacteria (e.g., Streptococcus pyogenes).

🔬 Why the Other Options Are Incorrect:

• Bronchiolitis

  • Involves the small bronchioles → lower respiratory tract.

  • Common in infants (often caused by RSV) — symptoms include wheezing and respiratory distress.

  • Not part of the upper airway.

• Tuberculosis (TB)

  • A chronic infection caused by Mycobacterium tuberculosis, primarily affecting the lungs (lower respiratory tract).

  • Can spread systemically, but not considered a URTI.

• Laryngitis

  • Borderline case: the larynx lies at the junction of upper and lower tracts.

  • It’s sometimes classified as an URTI, but pharyngitis is far more common and classic.

• Pneumonia

  • Infection of the alveoli and lung parenchyma → definitely a lower respiratory tract infection.

  • Presents with productive cough, fever, and dyspnea.

The trachea extends from the lower border of the cricoid cartilage (C6) in the neck down to the level of the sternal angle (T4–T5 vertebral level) within the thorax.
At this point, it bifurcates into the right and left main bronchi — a ridge called the carina marks this division.

Anatomical Extent of the Trachea:

• Upper limit: Lower border of the cricoid cartilage (C6).

• Lower limit: Sternal angle (T4–T5) — at the level of the carina.

From here:

• The right main bronchus is shorter, wider, and more vertical → foreign bodies often enter this side.

• The left main bronchus is longer, narrower, and more horizontal.

Clinical Relevance:

• The carina is a sensitive mucosal ridge—stimulation (e.g., by a suction catheter or aspirated material) triggers a strong cough reflex.
• On chest X-rays, the carina is used as a radiological landmark. Its displacement may indicate pathology (e.g., enlarged lymph nodes, masses, or bronchial deviation).

❌ Why the Other Options Are Incorrect:

• Lower lobe of lungs:

  • The trachea divides into bronchi before entering the lungs. The bronchi then continue into lobar and segmental branches within the lungs.

  • Therefore, the trachea does not extend as far down as the lung lobes.

• Lung hila:

  • The main bronchi, not the trachea, enter the lung hila. The bifurcation occurs above the hila at the level of the sternal angle.

• Diaphragm:

  • The diaphragm lies much lower, around T8–T10 vertebral level (depending on phase of respiration). The trachea ends far above this.

• T6:

  • Slightly lower than the actual bifurcation. The trachea typically ends at T4–T5, not T6.

  • While there may be minor variation with inspiration (carina may descend slightly), T4–T5 remains the standard anatomical level.

The trachea is a tubular structure composed of C-shaped rings of hyaline cartilage that keep the airway open. These rings are incomplete posteriorly, meaning that the posterior surface is flat, unlike the curved anterior and lateral surfaces formed by cartilage.

Structure of the Trachea:

• The trachea has 16–20 C-shaped cartilaginous rings.

• The open part of the “C” faces posteriorly, toward the esophagus.

• The gap between the ends of the cartilage is bridged by smooth muscle fibers known as the trachealis muscle, and connective tissue.

This design gives the trachea both rigidity and flexibility:

• Rigidity (from cartilage) prevents collapse during inspiration.

• Flexibility (from the flat posterior wall) allows the esophagus behind it to expand anteriorly as food passes through.

Functional Importance of the Flat Posterior Surface:

1. Allows esophageal expansion:
   When swallowing, the esophagus can bulge forward into the tracheal space without obstruction.
2. Aids in cough reflex:
   The trachealis muscle contracts during coughing, narrowing the tracheal lumen to increase the velocity of expelled air.
3. Prevents airway collapse:
   Despite being soft, the posterior wall remains supported by adjacent structures and smooth muscle tone.

❌ Why the Other Options Are Incorrect:

• All surfaces:

  • Only the posterior one is. The rest (anterior and lateral) are rounded due to cartilaginous rings.

• Anterior:

  • The anterior surface is convex and formed by cartilage, not flat. It lies behind the sternum and muscles of the neck.

• Lateral:

  • Both lateral surfaces are curved, shaped by the rounded sides of the cartilage rings and adjacent to the lobes of the thyroid gland.

• Medial:

  • The term “medial surface” is not typically applied to the trachea because it’s a midline structure. There’s no distinct medial surface — only anterior, posterior, and lateral.

The trachea is a vital component of the respiratory tract, extending from the lower border of the cricoid cartilage (C6) down to the level of the sternal angle (T4–T5), where it bifurcates into the right and left main bronchi.

Anatomically, it lies within the superior mediastinum and partly continues into the thoracic inlet before bifurcating just above the heart.

Detailed Anatomy:

1. Location and Extent

• Begins at the lower border of the cricoid cartilage (C6 vertebral level).

• Ends at the carina (T4–T5 level), where it divides into the main bronchi.

• The portion above the sternal angle lies in the superior mediastinum.

2. Relations of the Trachea:

• Anteriorly:

  • Sternum (manubrium)

  • Thymus (in children or remnants in adults)

  • Left brachiocephalic vein

  • Arch of the aorta (crosses obliquely)

• Posteriorly:

  • Esophagus

• Laterally:

  • Pleura, lungs, and great vessels (e.g., common carotid arteries, brachiocephalic artery on right, arch of aorta on left)

3. Structure:

• Consists of C-shaped hyaline cartilage rings, open posteriorly, bridged by trachealis muscle (smooth muscle).

• The trachealis muscle allows the esophagus (just behind it) to expand during swallowing.

Clinical Relevance:

• The carina is a highly sensitive ridge at the tracheal bifurcation; irritation here triggers cough reflex.

• Tracheostomy is typically performed below the cricoid cartilage but above the sternal notch to maintain airway access.

• Compression of the trachea may occur due to enlarged thyroid, aortic aneurysm, or mediastinal tumors—hence, its anatomical position is clinically significant.

❌ Why the Other Options Are Incorrect:

• Posterior to the esophagus:

  • The trachea is anterior to the esophagus. Food passes behind the trachea, not in front of it.

• Anterior mediastinum:

  • The anterior mediastinum contains fat, connective tissue, lymph nodes, and the thymus (in children), not the trachea.

• Inferior mediastinum:

  • The inferior mediastinum lies below the plane of the sternal angle, containing structures like the heart (middle part) and esophagus (posterior part)—the trachea ends above this level.

• Middle mediastinum:

  • Contains the heart, pericardium, roots of great vessels, and main bronchi, but not the trachea itself.

  • The carina lies at the boundary between the superior and middle mediastina, but most of the trachea is within the superior mediastinum.

Both Thromboxane A₂ (TXA₂) and Prostaglandins (PGs) are eicosanoids, meaning they are derived from arachidonic acid through the cyclooxygenase (COX) pathway.
Despite sharing a common precursor, they exert opposing physiological effects—especially in the regulation of hemostasis and vascular tone

Thromboxane A₂ (TXA₂):

• Site of production: Synthesized by platelets.

• Major actions:

  • Promotes platelet aggregation — enhances clot formation by activating nearby platelets.

  • Causes vasoconstriction — narrows blood vessels, helping to reduce blood loss during injury.

• Physiological role:

  • Pro-coagulant and pro-thrombotic; it helps form a stable hemostatic plug at injury sites.

Prostaglandins (particularly PGI₂ or prostacyclin):

• Site of production: Synthesized by vascular endothelial cells.

• Major actions:

  • Inhibits platelet aggregation — prevents excessive clotting.

  • Causes vasodilation — maintains blood flow and prevents unnecessary vessel constriction.

• Physiological role:

  • Anti-thrombotic and vasoprotective; it ensures blood remains fluid within intact vessels.

Key Concept – The Balance:

The body maintains a delicate equilibrium:

• TXA₂ (from platelets) → promotes clotting and constriction.

• PGI₂ (from endothelium) → inhibits clotting and promotes dilation.

This balance ensures hemostasis without causing thrombosis.

❌ Why the Other Options Are Incorrect:

• Thromboxane A₂ decreases platelet aggregation while prostaglandins increase it:

  • TXA₂ increases aggregation, PGI₂ decreases it.

• Thromboxane A₂ causes vasodilation while prostaglandins cause vasoconstriction:

  • TXA₂ causes vasoconstriction, while prostacyclin (PGI₂) causes vasodilation.

• Thromboxane A₂ mediates allergic reactions while prostaglandins do not:

  • Allergic reactions are mainly mediated by histamine, leukotrienes, and bradykinin, not thromboxane A₂.

• Thromboxane A₂ mediates pain while prostaglandins do not:

  • Prostaglandins, particularly PGE₂, are actually key mediators of pain and inflammation. TXA₂ has no significant role in pain transmission.

The Tuberculin Skin Test (TST)—also known as the Mantoux test—is the best test to assess tuberculosis (TB) at the community level.

At the community level, public health officials are primarily concerned with identifying latent TB infections or estimating the prevalence of TB exposure in a population. The Mantoux test fulfills these criteria because it is:

1. Inexpensive – requires minimal resources.

2. Easily administered – a small intradermal injection of purified protein derivative (PPD) into the forearm.

3. Simple to interpret – the size of the induration (not redness) after 48–72 hours indicates exposure.

4. Scalable for field use – can be applied in mass surveys without needing advanced lab infrastructure.

This makes it ideal for epidemiological surveys and community-level screening, even though it is not the most specific or confirmatory test for active TB disease.

How it works:

• The TST measures a delayed-type (Type IV) hypersensitivity reaction to tuberculin (PPD).

• A person previously infected or vaccinated (BCG) will have sensitized T-cells that release cytokines upon exposure, causing induration.

• The diameter of induration (commonly ≥10 mm for general population, ≥5 mm for immunocompromised, ≥15 mm for low-risk individuals) indicates a positive result.

Purpose at the community level:

• To estimate the prevalence of latent TB infection  in a population.

• To identify high-risk groups and plan targeted public health interventions.

❌ Why the Other Options Are Incorrect:

• Interferon Gamma Release Assay (IGRA):

  • A blood test measuring interferon-γ released by T-cells in response to TB antigens.

  • Advantages: More specific than TST, unaffected by BCG vaccination.

  • Limitations: Expensive, requires laboratory setup, not feasible for large-scale community surveys in resource-limited settings.

  • Use: Preferred in individual testing in high-income or specialized settings, not for population-level screening.

• Sputum Culture:

  • Gold standard for diagnosis of active TB.

  • Takes weeks for growth and identification, requires lab facilities, biosafety precautions, and trained personnel.

  • Used for diagnosis and drug sensitivity testing, not for mass screening.

• Chest X-ray:

  • Useful for detecting active pulmonary TB lesions, but expensive and not portable for large community-based studies.

  • Requires electricity, equipment, and trained radiologists for interpretation.

  • May show non-specific findings and cannot differentiate latent infection from active disease.

• Gene Xpert (CBNAAT):

  • A molecular test detecting Mycobacterium tuberculosis DNA and rifampicin resistance.

  • Highly sensitive and specific, gives results within hours.

  • Limitation: Costly, equipment-dependent, not feasible for community-wide use—ideal for clinical diagnosis, not epidemiological surveys.

What Tropicamide does and why it’s used in eye exams
Tropicamide is an antimuscarinic (parasympatholytic) agent used topically in the eye. It blocks muscarinic receptors on the iris sphincter and the ciliary muscle. The functional consequences are:

• Temporary loss of sphincter activity → the circular smooth muscle that would normally constrict is inhibited, so the aperture of the eye becomes larger and allows better visualization of internal structures.

• Temporary paralysis of accommodation → the ciliary muscle relaxes, which helps in some parts of the exam (e.g., refraction in children, fundus view).

Clinical properties that make it ideal for routine exams

• Rapid onset: Works within minutes.

• Short duration: Effects typically wear off within a few hours (commonly around 4–6 hours), so normal vision returns the same day.

• Well tolerated for diagnostic use: Side effects are usually transient (photophobia, blurred near vision) but generally acceptable for brief diagnostic procedures.

Practical use

• Widely used by ophthalmologists and optometrists for funduscopy, retinal exam, slit-lamp exam when dilation is needed, and sometimes for refraction when temporary cycloplegia helps.

• Because the effect is short, patients don’t have to miss much time or endure prolonged visual disability.

❌ Why the Other Options Are Incorrect:

Ipratropium

• Class & use: An inhaled antimuscarinic bronchodilator used for obstructive airway disease (COPD/asthma).
• Why not: It is formulated and delivered for the respiratory tract, not the eye. It is not used as a diagnostic in routine ophthalmic exams.

Propranolol

• Class & use: A non-selective beta-blocker used for hypertension, arrhythmias, migraine prophylaxis, etc.
• Why not: It does not induce the temporary change needed for ocular visualization. (Topical beta-blockers like timolol are used to reduce intraocular pressure in glaucoma — that’s a therapeutic use, not for dilation during an exam.)

Atropine

• Class & use: A potent antimuscarinic that does produce dilation and cycloplegia.
• Why not for routine exam: Duration is the problem. Atropine’s ocular effects are very long-lasting (days to a week or more), causing prolonged blurred vision and light sensitivity. Because of this prolonged impairment, atropine is reserved for specific therapeutic purposes (e.g., treating uveitis, inducing prolonged cycloplegia in amblyopia therapy), not for routine diagnostic dilation.

Opioids

• Class & use: μ-opioid receptor agonists used for analgesia.
• Why not: Opioids typically cause pupil constriction (miosis), the opposite of what’s needed to allow an examiner a wider view of internal eye structures. They are not used to facilitate eye exams.

Ischemic hypoxia occurs when there is reduced blood flow to tissues, leading to inadequate oxygen delivery despite normal oxygen content in the blood. The most common cause is thrombosis, where a blood clot blocks a vessel and prevents perfusion of downstream tissues. This is the underlying mechanism in myocardial infarction and ischemic stroke.

❌ Why Other Options Are Incorrect:

• Increased P02 of arterial blood: This would improve oxygenation, not cause hypoxia.

• Vasculitis: Can reduce perfusion but is less common compared to thrombosis.

• Hemorrhage: Causes hypovolemic (circulatory) hypoxia, not directly ischemic hypoxia.

• Poisoning: E.g., cyanide poisoning → histotoxic hypoxia (cells can’t use oxygen), not ischemic.

The heart is enclosed within the pericardium and is located in the middle mediastinum.

• The mediastinum is divided into superior and inferior.

• The inferior mediastinum is further divided into anterior, middle, and posterior parts.

• The middle mediastinum contains the heart, pericardium, roots of the great vessels (ascending aorta, pulmonary trunk, superior vena cava), and main bronchi.

❌ Why Other Options Are Incorrect:

• Posterior mediastinum: Contains structures like the descending thoracic aorta, esophagus, thoracic duct, azygos/hemiazygos veins, not the heart.

• Inferior mediastinum: General term; heart is in the middle division of it.

• Anterior mediastinum: Lies between sternum and pericardium; contains thymus (in children) and lymph nodes, not the heart.

• Pleural cavity: Surrounds the lungs, not the heart.

The posterior and inferior borders of the lungs meet at approximately the level of T10 vertebra in the mid-scapular line.

• Inferiorly, the lung border lies at rib 6 in the midclavicular line, rib 8 in the midaxillary line, and T10 posteriorly.

• This corresponds to the lower margin of the lung in quiet breathing, above the costodiaphragmatic recess.

• During deep inspiration, the lower border may descend further, but in standard anatomical description, T10 is the landmark.

❌ Why Other Options Are Incorrect:

• T12: Too low; this corresponds more to the pleural reflection, not the lung border.

• T4: Level of the sternal angle; corresponds to the division of the mediastinum and tracheal bifurcation, not the lung border.

• T8: Too high; in the midaxillary line lungs end at rib 8, but posteriorly they extend lower.

• T6: Level of inferior border in the midclavicular line, not posteriorly.

Leukotrienes are synthesized from arachidonic acid via the 5-lipoxygenase pathway. The enzyme 5-lipoxygenase (5-LOX), with the help of FLAP (5-lipoxygenase–activating protein), first converts arachidonic acid into 5-hydroperoxy-eicosatetranoic acid (5-HPETE).

• This compound is the first committed product in the leukotriene pathway.

• From 5-HPETE, subsequent conversions occur, producing leukotriene A4 (LTA4) and then other leukotrienes (LTB4, LTC4, etc.), which are important in inflammation and hypersensitivity reactions.

❌ Why Other Options Are Incorrect:

• 5-hydroxy-eicosatetranoic acid (5-HETE): This is a reduced metabolite of 5-HPETE, not the first product.

• Prostaglandin G2 (PGG2): Belongs to the cyclooxygenase pathway, not leukotriene synthesis.

• Leukotriene A4 (LTA4): Formed later from 5-HPETE, not the first product.

• Leukotriene B4 (LTB4): A downstream leukotriene derived from LTA4; not the initial product.

Spirometry records dynamic lung volumes — air that can be inhaled and exhaled. Residual volume (RV) is the amount of air remaining in the lungs after maximal forced expiration. Because this air cannot be exhaled, it cannot be directly measured by spirometry. Instead, RV is estimated using indirect methods such as:

• Helium dilution test

• Nitrogen washout technique

• Body plethysmography

Other lung volumes (tidal volume, inspiratory capacity, expiratory reserve volume, and vital capacity) all involve air that moves in or out of the lungs and thus can be measured by spirometry.

❌ Why Other Options Are Incorrect:

• Expiratory reserve volume (ERV): Can be measured by asking the patient to exhale maximally after a normal expiration.

• Inspiratory capacity (IC): Measurable by inspiring maximally after a normal expiration.

• Vital capacity (VC): Maximum air exhaled after maximum inspiration — directly measurable.

• Tidal volume (TV): Normal quiet breathing volume — directly recorded on spirometry.

During exercise, cardiac output can increase 3–4 times the resting level. One might expect pulmonary arterial pressure to rise steeply, but the pulmonary circulation accommodates the increased flow efficiently by:

• Recruitment of additional pulmonary capillaries (previously closed capillaries open up).

• Distension of already open capillaries (capillary diameter increases).

These mechanisms lower resistance and allow for greater blood flow with only a slight rise in pulmonary arterial pressure. This is crucial to prevent pulmonary edema and to maintain efficient gas exchange even under high flow states.

❌ Why Other Options Are Incorrect:

• Sometimes decreased, sometimes increased pulmonary pressure:  Pulmonary pressure does not decrease during exercise, it rises slightly in a predictable manner.

• Massive increase in pulmonary pressure: Would cause pulmonary edema and impaired oxygenation.

• No increase in pulmonary pressure: There is a small but definite increase.

• Decrease in pulmonary pressure: Physiology doesn’t allow for decreased pulmonary artery pressure when flow increases.

Smooth muscle is distributed along the respiratory tract but in varying amounts:

• Bronchi → Terminal bronchioles: Smooth muscle is well developed. Function: regulate airway diameter (bronchoconstriction/dilation) and control airflow distribution.

• Respiratory bronchioles → Proximal alveolar ducts: Smooth muscle becomes discontinuous and patchy. Function: provide limited control of airflow and maintain airway patency.

• Distal alveolar ducts: Smooth muscle completely disappears. At this level, the structure is optimized purely for gas exchange, where the thinnest possible wall is required to minimize diffusion distance for oxygen and carbon dioxide.

• Alveoli: Absolutely no smooth muscle, only type I and type II pneumocytes with elastic fibers for recoil.

Thus, the disappearance of smooth muscle at the distal part of the alveolar duct ensures efficient, unobstructed diffusion across the alveolar–capillary membrane.

❌ Why Other Options Are Incorrect

• Present throughout the respiratory system: Wrong — not present in alveoli or distal alveolar ducts.

• Alveoli: True that alveoli lack smooth muscle, but smooth muscle already disappears before this, at the distal alveolar duct.

• Terminal bronchioles: Rich in smooth muscle, crucial for airflow resistance regulation.

• Bronchi: Contain smooth muscle plus cartilage for airway patency.

Vital capacity (VC) is the maximum amount of air that can be exhaled after a maximal inspiration. It represents the greatest possible change in lung volume. It is calculated as:

VC=TV+IRV+ERV

• Tidal Volume (TV): Normal breath (~500 mL).

• Inspiratory Reserve Volume (IRV): Extra air you can inhale after a normal inspiration.

• Expiratory Reserve Volume (ERV): Extra air you can exhale after a normal expiration.

Residual volume (RV) is not part of VC, because it cannot be exhaled.

❌ Why Other Options Are Incorrect

• Tidal volume + expiratory reserve volume + residual volume: Includes RV (not part of VC).

• Residual volume + tidal volume + expiratory reserve volume: Again includes RV.

• Tidal volume + inspiratory reserve volume: Leaves out ERV.

• Tidal volume + expiratory reserve volume: Leaves out IRV.

Residual volume (RV) is the amount of air that remains in the lungs after maximal (forceful) exhalation.

• In normal healthy adults, this value is approximately 1200 mL.

• It cannot be expelled voluntarily and cannot be measured directly by spirometry.

• RV is essential to keep the alveoli open and allow continuous gas exchange between breaths.

❌ Why the other options are incorrect:

• 2000 mL: Too high — no standard physiological measurement matches this for RV.

• 1500 mL: Slightly higher than the actual RV; this could vary in pathology but not in normal lungs.

• 500 mL: This corresponds to tidal volume (normal breath in/out), not residual volume.

• 800 mL: Lower than the true average for RV in adults.

• Residual volume (RV) is the amount of air that remains in the lungs after maximal (forceful) exhalation.

• This volume cannot be measured directly by spirometry because it cannot be exhaled.

• In adults, RV is typically around 1.2 L.

• Its physiological role is to prevent lung collapse (atelectasis) and ensure continuous gas exchange between breaths.

❌ Why the other options are incorrect:

• Functional residual capacity (FRC): Volume left after normal (tidal) exhalation, not after forceful exhalation.

• Expiratory capacity: Maximum volume that can be exhaled after a normal inspiration, not the residual.

• Total lung volume (TLC): The maximum lung capacity (~6 L), not the leftover volume after exhalation.

• Tidal volume (TV): The ~500 mL exchanged in normal quiet breathing, not what remains after maximal exhalation.

• Functional residual capacity (FRC) is the volume of air remaining in the lungs after a normal (tidal) exhalation.

• It is the sum of expiratory reserve volume (ERV) and residual volume (RV).

• In an average adult, FRC is about 2.5 L.

• FRC provides a buffer that maintains consistent gas exchange between breaths, preventing large fluctuations in blood gases.

❌ Why the other options are incorrect:

• Expiratory capacity: Maximum volume of air that can be exhaled after a normal inspiration—not the air left behind.

• Total lung volume (TLC): Maximum volume lungs can hold (≈6 L)—not what remains after quiet expiration.

• Residual volume (RV): Air left in lungs after a maximal exhalation—not after a normal one.

• Tidal volume (TV): Air exchanged in a single quiet breath (~500 mL)—not the volume left behind.

• Tidal volume (TV) is the volume of air moved in or out of the lungs during a normal, quiet breath.

• In a healthy adult, this is approximately 500 mL per breath.

• It represents the baseline ventilation and is crucial for maintaining gas exchange at rest.

• Other lung volumes (like inspiratory capacity, vital capacity, and residual volume) are measured during forced or maximal breathing, not in a single quiet breath.

❌ Why the other options are incorrect:

• Forced vital capacity (FVC): Maximum air forcibly exhaled after a full inspiration—not a single quiet breath.

• Inspiratory capacity (IC): Maximum air that can be inspired after a normal expiration—larger than tidal volume.

• Total lung volume (TLC): The maximum volume the lungs can hold (includes all lung volumes)—far greater than tidal volume.

• Residual volume (RV): Air remaining in lungs after maximal expiration—cannot be exchanged in normal breathing.

• The primary cells infected in tuberculosis are alveolar macrophages.

• When Mycobacterium tuberculosis is inhaled, it reaches the alveoli, where it is phagocytosed by macrophages.

• The bacteria, however, survive inside macrophages by inhibiting phagolysosome fusion, allowing them to replicate.

• This intracellular survival triggers a cell-mediated immune response. Activated helper T cells (Th1) release IFN-γ, which stimulates macrophages to form granulomas that wall off the infection.

• The persistence of infected macrophages is key to the formation of caseating granulomas in TB.

❌ Why the other options are incorrect:

• Cytotoxic T cells (CD8+): Involved in killing infected cells, but not the primary site of TB infection.

• Helper T cells (CD4+): Crucial for immune response (release IFN-γ), but they are not directly infected first.

• Neutrophils: Important in acute bacterial infections, but TB is chronic and primarily macrophage-based.

• B cells: Produce antibodies, but TB defense is mainly cell-mediated, not humoral.

• Mycoplasma pneumoniae is the most common cause of atypical pneumonia, especially in children, adolescents, and young adults.

• Unlike typical bacterial pneumonia, which presents with sudden onset, high fever, and productive cough, atypical pneumonia is characterized by:

  • Gradual onset

  • Low-grade fever

  • Dry cough

  • Patchy infiltrates on chest X-ray (disproportionate to clinical findings)

• M. pneumoniae lacks a cell wall → not visible on Gram stain and resistant to beta-lactam antibiotics (like penicillins).

• Treatment often involves macrolides (azithromycin, clarithromycin) or tetracyclines.

❌ Why the other options are incorrect:

• Streptococcus pneumoniae: Causes typical lobar pneumonia (sudden onset, rusty sputum).

• Haemophilus influenzae: Causes bronchopneumonia, often in COPD patients.

• Klebsiella pneumoniae: Causes severe, necrotizing pneumonia with “currant jelly sputum,” common in alcoholics/diabetics.

• Staphylococcus aureus: Causes bronchopneumonia and post-viral pneumonia, not atypical.

The primitive body cavity (intraembryonic coelom) appears during the 3rd week as a single horseshoe-shaped cavity. Initially, it is continuous, but as development progresses, partitions form to divide it into separate cavities.

• By the 5th week, the process of partitioning is well-advanced, and the coelom becomes separated into the pericardial cavity, pleural cavities, and peritoneal cavity.

• This partitioning involves the septum transversum, pleuropericardial folds, and pleuroperitoneal membranes, which help establish the definitive cavities.

❌ Why the other options are incorrect:

• 3rd week: The intraembryonic coelom appears, but it is still a single primitive cavity, not yet divided.

• 4th week: The body folding process occurs, but cavities are still continuous.

• 6th week: Cavities are already separated by this time; the division was established earlier.

• None of these: Incorrect, because the division does occur at a definite time (5th week).

The alveoli are extremely rich in elastic fibers, which are essential for their function. These fibers surround the alveolar walls and allow the lungs to expand during inspiration and recoil during expiration. This elastic recoil is what helps push air out of the lungs efficiently without excessive muscular effort.

• The fine elastic fiber network also maintains the structural integrity of the alveoli, preventing collapse while allowing flexibility.

• Damage to these fibers (e.g., in emphysema) leads to loss of recoil, air trapping, and obstructive lung disease.

❌ Why the other options are incorrect:

• Bronchioles: Have smooth muscle to regulate airway diameter but relatively fewer elastic fibers compared to alveoli.

• Trachea: Mainly supported by C-shaped hyaline cartilage rings and smooth muscle, not dominated by elastic fibers.

• Bronchi: Contain some elastic tissue, but their walls are reinforced by cartilage and smooth muscle, not primarily elastic fibers.

• Larynx: Contains hyaline and elastic cartilage, but not abundant elastic fibers in the connective tissue framework like in alveoli.