Respiratory Pathology — MCQs
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Which of the following is a causative agent of Farmer's Lung?
Which of the following conditions is a cause of granulomatous lung disease?
In Kartagener syndrome, all are seen except?
What is the most common pattern of pneumonia seen in Klebsiella infection?
Mesothelioma is most commonly caused by?
Potato nodes are a feature of which condition?
Which of the following is NOT a feature of primary tuberculosis?
Liver cirrhosis is associated with which type of emphysema in PIZZ phenotype mutation?
What is true about adenocarcinoma of the lung?
Which of the following would most likely be observed in the lung during an autopsy of a 2-week-old infant who died of neonatal respiratory distress syndrome?
Respiratory Pathology Indian Medical PG Practice Questions and MCQs
Question 381: Which of the following is a causative agent of Farmer's Lung?
- A. Thermophilic Actinomycetes (Correct Answer)
- B. Aspergillus Fumigatus
- C. Actinobacter
- D. Aspergillus Flavus
Explanation: **Explanation:** **Farmer’s Lung** is a classic example of **Hypersensitivity Pneumonitis (Extrinsic Allergic Alveolitis)** [1][2]. It is a Type III and Type IV hypersensitivity reaction occurring in the lung parenchyma (alveoli and distal airways) due to the inhalation of organic dusts [1]. 1. **Why Option A is Correct:** The primary causative agents of Farmer’s Lung are **Thermophilic Actinomycetes** (specifically *Saccharopolyspora rectivirgula*, formerly *Micropolyspora faeni*). These bacteria thrive in damp, warm environments like **moldy hay** or grain. When a farmer handles this hay, the spores are inhaled, leading to an inflammatory immune response in the lungs. 2. **Why Other Options are Incorrect:** * **Aspergillus fumigatus (B):** While it causes various lung conditions (ABPA, Aspergilloma, or Invasive Aspergillosis), it is specifically the agent for **Malt Worker’s Lung** (when found in moldy barley). * **Actinobacter (C):** This is a Gram-negative bacterium typically associated with nosocomial (hospital-acquired) infections like VAP or septicemia, not hypersensitivity pneumonitis. * **Aspergillus flavus (D):** Known primarily for producing **Aflatoxin** (linked to Hepatocellular Carcinoma) and causing fungal sinusitis or keratitis, rather than Farmer's Lung. **NEET-PG High-Yield Pearls:** * **Histopathology:** Characterized by the "Triad" of interstitial pneumonitis, non-caseating **ill-defined granulomas**, and bronchiolitis obliterans. * **Other HP Types:** * *Bird Fancier’s Lung:* Avian proteins (droppings/feathers) [2]. * *Bagassosis:* Moldy sugar cane (*Thermoactinomyces sacchari*) [2]. * *Humidifier Lung:* Contaminated water in AC units. * **Diagnosis:** High-resolution CT (HRCT) shows "ground-glass opacities" or a "mosaic pattern." Management primarily involves antigen avoidance and corticosteroids. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 60-61. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 332-333.
Question 382: Which of the following conditions is a cause of granulomatous lung disease?
- A. Hypersensitivity pneumonitis (Correct Answer)
- B. Sarcoma
- C. Bronchogenic carcinoma
- D. Bronchogenic cyst
Explanation: ### Explanation **Correct Option: A. Hypersensitivity Pneumonitis (HP)** Hypersensitivity pneumonitis is an immunologically mediated inflammatory lung disease caused by an exaggerated immune response to inhaled organic antigens (e.g., *Farmer’s lung*, *Bird fancier’s lung*) [1, 2]. * **Pathogenesis:** It involves both Type III (immune complex) and **Type IV (delayed-type) hypersensitivity** reactions [1]. * **Morphology:** The hallmark histological finding in the subacute and chronic phases is the presence of **loosely formed, non-caseating granulomas** located in the interstitium and peribronchiolar areas, often accompanied by chronic interstitial inflammation (lymphocytes and plasma cells) [1]. **Incorrect Options:** * **B. Sarcoma:** These are malignant tumors of mesenchymal origin (e.g., angiosarcoma). While they can metastasize to the lungs, they present as neoplastic cell proliferation, not granulomatous inflammation. * **C. Bronchogenic Carcinoma:** This refers to primary lung cancer (e.g., Squamous cell or Adenocarcinoma). It is characterized by malignant epithelial cells, architectural distortion, and necrosis, but not granulomas. * **D. Bronchogenic Cyst:** This is a congenital anomaly resulting from abnormal budding of the foregut. It is a fluid-filled cyst lined by ciliated columnar epithelium; it is not an inflammatory or granulomatous process. **NEET-PG High-Yield Pearls:** * **Differential Diagnosis of Lung Granulomas:** Always remember the mnemonic **"S-T-H"** for non-caseating granulomas: **S**arcoidosis (well-formed), **T**uberculosis (usually caseating), and **H**ypersensitivity Pneumonitis (loosely formed) [1, 3]. * **Key Histology for HP:** Look for the "Triad": Interstitial pneumonitis, Bronchiolitis, and **Non-caseating granulomas** [1]. * **Clinical Clue:** HP is reversible if the offending antigen is removed early, unlike many other interstitial lung diseases. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 701-702. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 332-333. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 700-701.
Question 383: In Kartagener syndrome, all are seen except?
- A. Bronchiectasis
- B. Situs inversus
- C. Bronchial asthma (Correct Answer)
- D. Sinusitis
Explanation: **Explanation:** Kartagener Syndrome is a subset of **Primary Ciliary Dyskinesia (PCD)**, an autosomal recessive disorder characterized by a structural defect in the **dynein arms** of cilia. This defect leads to impaired ciliary motility (immotile cilia syndrome). **Why Bronchial Asthma is the correct answer:** Bronchial asthma is a chronic inflammatory airway disease characterized by reversible bronchoconstriction and airway hyperresponsiveness, typically driven by Type I hypersensitivity [1]. It is **not** caused by ciliary dysfunction. While patients with Kartagener syndrome have chronic respiratory symptoms, the underlying mechanism is mucus stasis due to immotile cilia, not the allergic/inflammatory pathway seen in asthma [2]. **Analysis of other options:** * **Situs Inversus (B):** During embryogenesis, normal ciliary beat is required for the proper left-right positioning of internal organs. Lack of ciliary motion leads to random organ placement; in 50% of PCD cases, this results in Situs Inversus (the defining feature of Kartagener syndrome). * **Bronchiectasis (A) & Sinusitis (D):** Effective ciliary action is essential for the "mucociliary escalator." When cilia are immotile, mucus stagnates in the sinuses and bronchi, leading to recurrent infections. Chronic infection and inflammation eventually cause permanent dilation of the bronchi (Bronchiectasis) [3] and chronic Sinusitis. **NEET-PG High-Yield Pearls:** * **The Triad:** Kartagener Syndrome = Situs inversus + Bronchiectasis + Sinusitis. * **Infertility:** Males are infertile due to immotile spermatozoa (flagella defect); females may have reduced fertility due to impaired ciliary action in the fallopian tubes. * **Diagnostic Gold Standard:** Electron microscopy showing absence or abnormality of **dynein arms** (inner or outer). * **Screening Test:** Low levels of nasal Nitric Oxide (nNO). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 689-690. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 688-689. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 690-691.
Question 384: What is the most common pattern of pneumonia seen in Klebsiella infection?
- A. Lobar Pneumonia (Correct Answer)
- B. Bronchopneumonia
- C. Interstitial Pneumonia
- D. Miliary Pneumonia
Explanation: **Explanation:** **1. Why Lobar Pneumonia is Correct:** *Klebsiella pneumoniae* is a classic cause of **Lobar Pneumonia**, a pattern characterized by diffuse inflammation and consolidation involving an entire lobe of the lung [1]. The organism possesses a thick, prominent polysaccharide capsule that protects it from phagocytosis, leading to an intense inflammatory response. This results in the production of thick, mucoid, and blood-stained sputum (classically described as **"Currant Jelly Sputum"**). The heavy inflammatory exudate often causes the affected lobe to swell, leading to the characteristic **"Bulging Fissure Sign"** on chest X-ray. **2. Why Other Options are Incorrect:** * **Bronchopneumonia:** This pattern involves patchy consolidation centered around bronchioles. While many Gram-negative bacteria cause bronchopneumonia, *Klebsiella* is specifically notorious for its rapid progression into a confluent lobar pattern. * **Interstitial Pneumonia:** This is typically caused by viruses (e.g., Influenza, RSV) or atypical bacteria (e.g., *Mycoplasma pneumoniae*). It involves the alveolar walls rather than the alveolar spaces [1]. * **Miliary Pneumonia:** This refers to multiple, tiny, millet-seed-sized lesions spread hematogenously, most commonly seen in Miliary Tuberculosis. **3. Clinical Pearls for NEET-PG:** * **Risk Groups:** Most common in chronic alcoholics, diabetics, and elderly patients (due to aspiration of oropharyngeal flora) [1]. * **Complications:** *Klebsiella* is highly destructive and frequently leads to **abscess formation** and cavitation (unlike *Streptococcus pneumoniae*, which rarely causes necrosis). * **Radiology:** Look for the "Bulging Fissure Sign" (usually the minor fissure). * **Gram Stain:** Shows Gram-negative, encapsulated, "plump" bacilli. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, p. 715.
Question 385: Mesothelioma is most commonly caused by?
- A. Asbestosis (Correct Answer)
- B. Silicosis
- C. Anthracosis
- D. Coal workers pneumoconiosis
Explanation: **Explanation:** **1. Why Asbestosis is Correct:** Malignant Mesothelioma is a rare neoplasm of the mesothelial cells, most commonly affecting the pleura [1], [5]. There is a heavy causal link between **asbestos exposure** and mesothelioma; approximately 80% of cases report a history of exposure [1]. The pathogenesis involves the inhalation of asbestos fibers (particularly the sharp, needle-like **amphibole** type), which reach the periphery of the lung, migrate to the pleura, and induce chronic inflammation and oncogenic damage. It is important to note that while asbestos is the primary cause of mesothelioma, the most common cancer associated with asbestos exposure is actually **Bronchogenic Carcinoma** [2]. **2. Why Incorrect Options are Wrong:** * **Silicosis (Option B):** Caused by inhalation of crystalline silica. It is associated with an increased risk of **Tuberculosis** (Silicotuberculosis) and lung cancer, but not mesothelioma. * **Anthracosis (Option C):** This is the asymptomatic accumulation of carbon pigment in the lungs of city dwellers and smokers. It does not lead to malignancy. * **Coal Workers' Pneumoconiosis (CWP) (Option D):** Caused by chronic inhalation of coal dust. While it can lead to Progressive Massive Fibrosis (PMF) and "Black Lung," it is not a risk factor for mesothelioma [3]. **3. High-Yield Clinical Pearls for NEET-PG:** * **Latent Period:** Mesothelioma has a long lag period (25–40 years) after initial exposure [5]. * **Smoking Link:** Unlike bronchogenic carcinoma, the risk of mesothelioma is **not** increased by smoking [1]. * **Morphology:** Look for **Ferruginous bodies** (asbestos bodies) in the lungs—golden-brown, fusiform rods with a translucent center [3]. * **Markers:** Calretinin, WT-1, and Cytokeratin 5/6 are positive immunohistochemical markers for mesothelioma. * **Imaging:** Classically presents as diffuse pleural thickening and pleural plaques [3], [4]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 221-222. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 286. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 698-699. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, p. 699. [5] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 339-340.
Question 386: Potato nodes are a feature of which condition?
- A. Sarcoidosis (Correct Answer)
- B. Tuberculosis
- C. Carcinoid
- D. Lymphoma
Explanation: **Explanation:** **Sarcoidosis (Correct Answer):** "Potato nodes" is a classic radiological and pathological description for the massive, symmetrical, and non-adherent **bilateral hilar lymphadenopathy** seen in Sarcoidosis. These nodes are typically firm, discrete, and rubbery, resembling potatoes on a chest X-ray or CT scan [1]. Pathologically, they are characterized by **non-caseating granulomas**. The lack of periadenitis (inflammation of surrounding tissue) ensures the nodes remain distinct and do not matted together, unlike in infectious processes [1]. **Incorrect Options:** * **Tuberculosis:** Characterized by **caseating granulomas**. Lymph nodes in TB tend to be "matted" due to periadenitis and necrosis, rather than discrete "potato-like" structures. It usually presents with unilateral or asymmetrical lymphadenopathy. * **Carcinoid:** This is a neuroendocrine tumor typically presenting as a polypoid endobronchial mass. While it may cause obstructive features, it is not associated with the specific "potato node" morphology. * **Lymphoma:** While lymphoma causes significant lymphadenopathy, the nodes are often described as "bulky" or "conglomerate." In Hodgkin Lymphoma, nodes may be rubbery, but the term "potato nodes" is specifically reserved for the classic presentation of Sarcoidosis in medical literature. **NEET-PG High-Yield Pearls for Sarcoidosis:** * **Schaumann bodies:** Laminated concretions of calcium and proteins. * **Asteroid bodies:** Stellate inclusions within giant cells. * **Kveim-Siltzbach Test:** Historically used skin test (now largely replaced by biopsy). * **Biochemical marker:** Elevated **Serum ACE** (Angiotensin-Converting Enzyme) levels. * **Staging:** Stage I specifically refers to Bilateral Hilar Lymphadenopathy (BHL) alone. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 700-701.
Question 387: Which of the following is NOT a feature of primary tuberculosis?
- A. Apical lung cavity (Correct Answer)
- B. Ghon's focus
- C. Paratracheal lymphadenopathy
- D. Heals spontaneously by fibrosis
Explanation: **Explanation:** The distinction between primary and secondary tuberculosis (TB) is a high-yield topic for NEET-PG. **Why Option A is the correct answer:** **Apical lung cavities** are the hallmark of **Secondary (Reactivation) Tuberculosis**, not primary TB. Secondary TB occurs in a previously sensitized host, typically localized to the apices of the upper lobes where high oxygen tension favors the growth of *Mycobacterium tuberculosis*. The intense hypersensitivity reaction leads to tissue necrosis and cavitation [1]. **Analysis of incorrect options:** * **B. Ghon’s focus:** This is a 1–1.5 cm area of gray-white inflammation/consolidation found in the subpleural region of the mid or lower lung zones. It is the classic initial lesion of **Primary TB** [1]. * **C. Paratracheal lymphadenopathy:** In primary TB, the bacilli drain via lymphatics to the regional (hilar and paratracheal) nodes. The combination of the Ghon focus and involved nodes is called the **Ghon Complex** [1]. * **D. Heals spontaneously by fibrosis:** In 90-95% of immunocompetent individuals, the cell-mediated immune response successfully arrests the infection, leading to fibrosis and often calcification (Ranke Complex) [2]. **NEET-PG Clinical Pearls:** 1. **Ranke Complex:** Ghon Complex + Radiologic Calcification. 2. **Simon’s Focus:** Initial secondary TB lesion at the lung apex. 3. **Epithelioid Granuloma:** The characteristic histological feature, driven by **IFN-gamma** (secreted by TH1 cells) activating macrophages [2]. 4. **Primary TB** is usually asymptomatic or presents as a mild flu-like illness, whereas **Secondary TB** presents with "B-symptoms" (night sweats, weight loss, and hemoptysis) [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 379-380. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 380-381.
Question 388: Liver cirrhosis is associated with which type of emphysema in PIZZ phenotype mutation?
- A. Centriacinar
- B. Panacinar (Correct Answer)
- C. Paraseptal
- D. Multifocal
Explanation: **Explanation:** The question describes a classic presentation of **Alpha-1 Antitrypsin Deficiency (AATD)**. Alpha-1 Antitrypsin (AAT) is a protease inhibitor synthesized in the liver that protects the lungs from neutrophil elastase [2][4]. **1. Why Panacinar is correct:** In individuals with the **PiZZ phenotype** (the most severe homozygous form), the AAT protein is misfolded [2]. This leads to two consequences: * **In the Lungs:** A lack of circulating AAT results in unchecked elastase activity, which destroys the alveolar walls throughout the entire acinus [1][4]. This characteristically produces **Panacinar (Panlobular) emphysema**, typically involving the **lower lobes** of the lungs [1][3]. * **In the Liver:** The misfolded proteins cannot be secreted and aggregate within the endoplasmic reticulum of hepatocytes, leading to **liver cirrhosis** [2]. **2. Why other options are incorrect:** * **Centriacinar (Centrilobular):** This is the most common type of emphysema, but it is primarily associated with **cigarette smoking** and typically affects the upper lobes [1][3]. It involves the proximal part of the acinus (respiratory bronchioles). * **Paraseptal (Distal Acinar):** This involves the distal part of the acinus near the pleura [3]. It is associated with spontaneous pneumothorax in young adults and is not linked to AATD. * **Multifocal:** This is not a standard pathological classification for emphysema related to genetic protease deficiencies. **High-Yield Clinical Pearls for NEET-PG:** * **Histology:** Liver biopsy in PiZZ patients shows **PAS-positive, diastase-resistant globules** in hepatocytes. * **Genetics:** The *SERPINA1* gene on chromosome 14 encodes AAT [2]. * **Radiology:** AATD emphysema shows a predilection for the **basal (lower) segments**, whereas smoking-related emphysema favors the apical segments. * **Clinical Clue:** Suspect AATD in a young, non-smoker presenting with emphysema and signs of liver failure. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 684-685. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 856-858. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, p. 683. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 683-684.
Question 389: What is true about adenocarcinoma of the lung?
- A. More common in females (Correct Answer)
- B. Not associated with smoking
- C. Associated with central cavitations
- D. Most common in the upper lobes
Explanation: **Explanation:** Adenocarcinoma is currently the most common histological subtype of lung cancer overall, regardless of gender or smoking status [2]. 1. **Why Option A is correct:** While lung cancer incidence is generally higher in males due to historical smoking patterns, **adenocarcinoma** is the most common subtype found in **females** and **non-smokers** [2]. In women who develop lung cancer, adenocarcinoma is significantly more prevalent than squamous cell or small cell carcinoma. 2. **Why the other options are incorrect:** * **Option B:** While adenocarcinoma is the most common type in non-smokers, it is still **strongly associated with smoking**. Most patients with adenocarcinoma are, or were, smokers; however, the correlation is less intense than that seen with squamous cell or small cell carcinoma [2]. * **Option C:** Adenocarcinomas are typically **peripheral** lesions [1]. **Central cavitation** is a classic hallmark of **Squamous Cell Carcinoma**, often due to rapid growth and central necrosis [1]. * **Option D:** Adenocarcinoma does not have a specific predilection for the upper lobes; it is primarily characterized by its **peripheral location** in the lung parenchyma, often involving the pleura [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Driver Mutations:** Frequently associated with **EGFR** mutations (common in Asian non-smoking females), **ALK** rearrangements, and **KRAS** mutations (common in smokers) [1]. * **Precursor Lesion:** Atypical Adenomatous Hyperplasia (AAH) $\rightarrow$ Adenocarcinoma in situ (AIS, formerly Bronchioloalveolar carcinoma) [1]. * **Microscopy:** Shows gland formation and/or mucin production (detected by PAS or Mucicarmine stains). * **Marker:** **TTF-1** (Thyroid Transcription Factor-1) is a highly specific positive immunohistochemical marker. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 335-336. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 721-723.
Question 390: Which of the following would most likely be observed in the lung during an autopsy of a 2-week-old infant who died of neonatal respiratory distress syndrome?
- A. Alveoli filled with neutrophils
- B. Dense fibrosis of the alveolar walls
- C. Enlarged air spaces
- D. Hyaline membranes and collapsed alveoli (Correct Answer)
Explanation: **Neonatal Respiratory Distress Syndrome (NRDS)**, also known as Hyaline Membrane Disease, is primarily caused by a deficiency of **surfactant** (produced by Type II pneumocytes) [1]. Surfactant normally reduces alveolar surface tension; its absence leads to high surface tension, causing widespread **atelectasis (alveolar collapse)** [1]. 1. **Why Option D is Correct:** The resulting alveolar hypoxia and acidosis cause endothelial and epithelial damage. This leads to the leakage of plasma proteins (fibrin) into the alveolar spaces. This fibrin, mixed with necrotic cell debris, forms the characteristic eosinophilic, waxy **hyaline membranes** that line the collapsed alveoli [1]. 2. **Why Incorrect Options are Wrong:** * **Option A (Neutrophils):** This is characteristic of bacterial pneumonia. While NRDS infants are at risk for secondary infections, the primary pathology of NRDS is non-inflammatory [1]. * **Option B (Dense Fibrosis):** This is a feature of chronic lung diseases or the late "organizing" stage of ARDS [2]. While prolonged oxygen therapy in NRDS can lead to Bronchopulmonary Dysplasia (BPD) involving fibrosis, it is not the acute autopsy finding of NRDS. * **Option C (Enlarged Air Spaces):** This describes emphysema or compensatory overinflation, the opposite of the diffuse collapse seen in NRDS. **High-Yield Clinical Pearls for NEET-PG:** * **Risk Factors:** Prematurity (most common), Maternal Diabetes (insulin inhibits surfactant synthesis), and Cesarean section (lack of "vaginal squeeze" stress which triggers surfactant release) [1]. * **Diagnosis:** L/S (Lecithin/Sphingomyelin) ratio **< 2:1** in amniotic fluid indicates lung immaturity. * **X-ray Finding:** Classic **"Ground-glass appearance"** with air bronchograms. * **Treatment Complication:** Therapeutic oxygen can lead to **Retinopathy of Prematurity (ROP)** and **Bronchopulmonary Dysplasia (BPD)**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 465-467. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 679-681.
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