Respiratory Pathology — MCQs

A 45-year-old man incurs blunt chest trauma. On examination, he has marked right chest wall pain. A chest radiograph shows a fractured 7th rib on the right side. Over the next 2 days, he has subcutaneous soft tissue swelling with nonpainful crepitus on palpation of the right chest wall. Leakage of which of the following is most likely producing this swelling?

Respiratory Pathology Indian Medical PG Practice Questions and MCQs

Question 231: In primary pulmonary hypertension, what is the basic abnormality in gene?

A. Bone morphogenic protein receptor II (Correct Answer)
B. Endothelin
C. Homeobox gene
D. PAX - 11

Explanation: **Explanation:** **Primary Pulmonary Hypertension (PPH)**, now classified as Idiopathic Pulmonary Arterial Hypertension (IPAH), is characterized by a sustained increase in pulmonary artery pressure without an identifiable secondary cause. **Why Option A is Correct:** The fundamental genetic abnormality in approximately 75% of familial cases and 25% of sporadic cases of IPAH is a mutation in the **Bone Morphogenetic Protein Receptor Type II (BMPR2)** gene [1], [2]. BMPR2 is a member of the TGF-β receptor superfamily [2]. Under normal conditions, BMPR2 signaling inhibits the proliferation of vascular smooth muscle cells and promotes apoptosis. When mutated (loss-of-function), there is **unchecked proliferation of smooth muscle cells** and endothelial cells within the pulmonary arteries, leading to the characteristic "plexiform lesions" and vascular narrowing [1], [2]. **Why Other Options are Incorrect:** * **Option B (Endothelin):** While Endothelin-1 levels are often *elevated* in pulmonary hypertension (causing vasoconstriction), it is a mediator of the disease process rather than the primary genetic abnormality [1]. * **Option C (Homeobox gene):** These genes are primarily involved in anatomical development and segmentation during embryogenesis (e.g., HOX genes), not the pathogenesis of PPH. * **Option D (PAX-11):** PAX genes are transcription factors involved in organogenesis (e.g., PAX-6 in eye development). There is no established link between PAX-11 and pulmonary hypertension. **Clinical Pearls for NEET-PG:** * **Inheritance:** BMPR2 mutations follow an **Autosomal Dominant** pattern with low penetrance (only 10-20% of carriers develop the disease) [2]. * **Histology:** Look for **Plexiform lesions** (tufts of capillary formations) which are the hallmark of advanced pulmonary hypertension. * **Demographics:** Classically affects young females (20–40 years). * **Clinical Sign:** Loud P2 (pulmonary component of the second heart sound) and right ventricular hypertrophy [3]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 324-325. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 706-707. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, p. 707.

Question 232: A 63-year-old woman with chronic bronchitis presents with shortness of breath. A chest X-ray reveals a 2-cm 'coin lesion' in the upper lobe of the left lung. A CT-guided lung biopsy is obtained. Which of the following describes the histologic features of this lesion if the diagnosis is hamartoma?

A. Benign neoplasm of epithelial origin
B. Disorganized benign neoplasm of mesenchymal origin (Correct Answer)
C. Ectopic islands of normal tissue
D. Granulation tissue

Explanation: ### Explanation **Correct Answer: B. Disorganized benign neoplasm of mesenchymal origin** A **pulmonary hamartoma** is the most common benign tumor of the lung [1]. By definition, a hamartoma is a mass composed of tissues normally present at that site, but growing in a disorganized, haphazard fashion [1]. In the lung, these lesions are predominantly **mesenchymal** in origin. Histologically, they consist of mature **cartilage** (most common component), connective tissue, fat, and smooth muscle, often interspersed with clefts lined by respiratory epithelium [1]. **Why the other options are incorrect:** * **Option A:** While hamartomas contain epithelial-lined clefts, these are usually entrapped respiratory epithelium rather than the primary neoplastic component [1]. The lesion is primarily mesenchymal. * **Option C:** This describes a **Choristoma** (heterotopia), which is normal tissue found in an abnormal anatomical location (e.g., pancreatic tissue in the stomach wall). A hamartoma is normal tissue in its *correct* location, just disorganized. * **Option D:** Granulation tissue is a feature of wound healing and chronic inflammation (consisting of fibroblasts, capillaries, and inflammatory cells), not a neoplastic growth like a hamartoma. ### NEET-PG High-Yield Pearls: * **Radiology:** Classically presents as a solitary **"coin lesion"** on chest X-ray. On CT, the presence of **"popcorn calcification"** is pathognomonic. * **Demographics:** Usually discovered incidentally in adults (40–60 years). * **Genetics:** Often associated with chromosomal aberrations involving **6p21 or 12q14-15** (HMGA1/HMGA2 genes) [1]. * **Clinical Significance:** Most are peripheral and asymptomatic; they are significant primarily because they must be differentiated from bronchogenic carcinoma. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 727-728.

Question 233: Which of the following hormonal levels is NOT increased in small cell carcinoma of the lung?

A. ACTH
B. Growth hormone (Correct Answer)
C. ANF
D. AVP

Explanation: Small cell carcinoma (SCC) of the lung is a high-grade neuroendocrine tumor derived from **Kulchitsky cells** (APUD cells) [2]. Due to its neuroendocrine origin, it is the lung cancer most frequently associated with **Paraneoplastic Syndromes** resulting from the ectopic secretion of hormones [1], [3]. **Why Growth Hormone (GH) is the correct answer:** Ectopic secretion of Growth Hormone is **not** typically associated with small cell carcinoma. Instead, excessive GH (or Growth Hormone-Releasing Hormone) leading to Acromegaly or Hypertrophic Osteoarthropathy is more commonly linked to **Carcinoid tumors** or **Adenocarcinomas**. **Analysis of Incorrect Options:** * **ACTH (Adrenocorticotropic Hormone):** SCC is the most common cause of ectopic ACTH secretion, leading to **Cushing Syndrome** [1], [3]. Patients often present with hypokalemia and hyperglycemia rather than classic "buffalo hump" features due to the rapid progression of the malignancy. * **AVP (Arginine Vasopressin/ADH):** SCC frequently secretes ADH, causing **SIADH** (Syndrome of Inappropriate Antidiuretic Hormone) [1], [3]. This leads to dilutional hyponatremia, which can manifest as confusion or seizures. * **ANF (Atrial Natriuretic Factor):** SCC can also ectopically produce ANF, which contributes to natriuresis and hyponatremia, often mimicking or exacerbating the clinical picture of SIADH. **NEET-PG Clinical Pearls:** * **Small Cell Carcinoma:** Strongly associated with smoking; central location; "Oat cell" appearance; **Azzopardi effect** (DNA staining of vessel walls); and **Lambert-Eaton Myasthenic Syndrome** (antibodies against voltage-gated calcium channels) [2]. * **Squamous Cell Carcinoma:** Associated with **PTHrP** (Parathyroid Hormone-related Protein) leading to **Hypercalcemia** [3]. Remember: **S**quamous = **S**tones (Hypercalcemia). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 725-727. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 337-338. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 338-339.

Question 234: Pancoast tumors are known to cause which of the following complications?

A. Increased sweating
B. Wasting of muscles of the hand (Correct Answer)
C. Destruction of lower ribs
D. Bony metastasis

Explanation: **Explanation:** **Pancoast tumor** (Superior Sulcus Tumor) is a bronchogenic carcinoma (usually squamous cell or adenocarcinoma) located at the extreme apex of the lung. The clinical manifestations, known as **Pancoast Syndrome**, result from the local invasion of structures surrounding the thoracic inlet [1]. **Why the correct answer is right:** The tumor frequently involves the **Brachial Plexus**, specifically the lower roots (**C8, T1**) [1]. Involvement of the T1 nerve root leads to the denervation of the **intrinsic muscles of the hand** (interossei, thenar, and hypothenar muscles), resulting in weakness and **wasting (atrophy)**. This is often accompanied by pain radiating down the ulnar aspect of the arm [1]. **Analysis of Incorrect Options:** * **A. Increased sweating:** Incorrect. Pancoast tumors typically cause **Horner’s Syndrome** due to involvement of the cervical sympathetic chain [1]. This results in **anhidrosis** (lack of sweating) on the affected side, not increased sweating. * **C. Destruction of lower ribs:** Incorrect. Due to its apical location, the tumor involves the **upper ribs** (typically the 1st and 2nd ribs), not the lower ribs [1]. * **D. Bony metastasis:** While lung cancer can metastasize to bones, Pancoast syndrome is defined by **local invasion** rather than distant metastasis [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Horner’s Syndrome Triad:** Ptosis, Miosis, and Anhidrosis (due to sympathetic chain involvement) [1]. * **Most common cell type:** Historically Squamous Cell Carcinoma, but Adenocarcinoma is now frequently reported. * **Differential Diagnosis:** Always rule out Pancoast tumor in an elderly smoker presenting with shoulder pain and hand weakness. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 334-335.

Question 235: What is the most likely precursor to bronchiectasis?

A. Tuberculosis
B. Carcinoma
C. Bronchial adenoma
D. Necrotising pneumonia (Correct Answer)

Explanation: **Explanation:** **Bronchiectasis** is defined as the permanent, abnormal dilation of bronchi and bronchioles caused by the destruction of muscle and elastic supporting tissue [1]. This destruction results from a vicious cycle of **chronic infection and inflammation.** **Why Necrotizing Pneumonia is the correct answer:** The most common precursor to bronchiectasis is a severe, necrotizing infection. **Necrotizing pneumonia** (often caused by *Staphylococcus aureus*, *Klebsiella*, or *Pseudomonas*) causes intense inflammatory infiltration and tissue necrosis [2]. This destroys the structural integrity of the bronchial walls. Once the elastic and muscular components are replaced by fibrous tissue, the airways lose their recoil and become permanently dilated [1]. **Analysis of Incorrect Options:** * **Tuberculosis (A):** While TB is a major cause of bronchiectasis in developing countries (often leading to Traction Bronchiectasis), it is considered a specific chronic infection rather than the primary acute pathological precursor compared to the rapid destruction seen in necrotizing pneumonia [1]. * **Carcinoma (B) & Bronchial Adenoma (C):** These represent **localized** causes of bronchiectasis [1]. They cause airway obstruction, leading to distal pooling of secretions and secondary infection. While they can lead to bronchiectasis, they are much less common precursors than primary necrotizing infections. **NEET-PG High-Yield Pearls:** * **Gold Standard Investigation:** High-Resolution CT (HRCT) scan showing the **"Signet Ring Sign"** (bronchus diameter > accompanying pulmonary artery). * **Kartagener Syndrome:** A classic triad associated with bronchiectasis: Situs inversus, chronic sinusitis, and bronchiectasis (due to Primary Ciliary Dyskinesia). * **Commonest Site:** Lower lobes, bilaterally (except when caused by localized obstruction) [1]. * **Allergic Bronchopulmonary Aspergillosis (ABPA):** Characterized by **central/proximal bronchiectasis** and "finger-in-glove" appearance on X-ray [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 321-322. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, p. 715.

Question 236: Eggshell calcification of lymph nodes is suggestive of which condition?

A. Asbestosis
B. Berylliosis
C. Stannosis
D. Coal worker pneumoconiosis (Correct Answer)

Explanation: **Explanation:** **Eggshell calcification** refers to a distinctive radiological pattern where calcium deposits form in the periphery of hilar or mediastinal lymph nodes. **1. Why Coal Worker’s Pneumoconiosis (CWP) is correct:** While classically associated with **Silicosis** (the most common cause), eggshell calcification is also a recognized feature of **Coal Worker’s Pneumoconiosis** [1]. In CWP, the inhalation of coal dust leads to the formation of coal macules and nodules [1]. When these involve the lymph nodes, chronic inflammation can lead to peripheral calcification [2]. In the context of this specific question, CWP is the most appropriate choice among the provided options. **2. Why the other options are incorrect:** * **Asbestosis:** Characterized by **pleural plaques** (calcified or non-calcified) and ferruginous bodies [1]. It typically involves the lower lobes and does not cause eggshell calcification. * **Berylliosis:** A granulomatous disease (similar to Sarcoidosis) [1]. While it can cause hilar lymphadenopathy, eggshell calcification is not a classic hallmark. * **Stannosis:** A benign pneumoconiosis caused by tin oxide [1]. It presents with dense, punctate opacities on X-ray but does not typically involve lymph node calcification. **Clinical Pearls for NEET-PG:** * **Differential Diagnosis for Eggshell Calcification:** Silicosis (Most common), Coal Worker’s Pneumoconiosis, Sarcoidosis (5% of cases), treated Lymphoma, and occasionally Blastomycosis. * **Silicosis vs. CWP:** Silicosis significantly increases the risk of **Tuberculosis** (Silicotuberculosis) because silica impairs macrophage function [1]. * **Caplan Syndrome:** The combination of a pneumoconiosis (usually CWP) and Rheumatoid Arthritis, presenting with large necrobiotic nodules in the lungs [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 695-698. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 331-332.

Question 237: Which of the following is characteristic of adult respiratory distress syndrome?

A. Diffuse alveolar damage (Correct Answer)
B. Interstitial tissue inflammation
C. Alveolar exudates
D. Interstitial fibrosis

Explanation: **Explanation:** **Adult Respiratory Distress Syndrome (ARDS)** is a clinical syndrome characterized by the sudden onset of severe hypoxemic respiratory failure and bilateral pulmonary infiltrates in the absence of heart failure [2]. **Why Option A is Correct:** The histological hallmark and morphological manifestation of ARDS is **Diffuse Alveolar Damage (DAD)** [2]. DAD occurs in three phases: 1. **Exudative Phase (Acute):** Characterized by capillary congestion, edema, and the formation of **hyaline membranes** (composed of fibrin and necrotic cell debris) lining the alveolar walls [1]. 2. **Proliferative/Organizing Phase:** Type II pneumocyte proliferation and fibroblast infiltration. 3. **Fibrotic Phase:** Extensive collagen deposition [1]. **Why Other Options are Incorrect:** * **Option B (Interstitial tissue inflammation):** While some inflammation occurs, it is not the defining characteristic. ARDS primarily involves damage to the alveolar-capillary unit. * **Option C (Alveolar exudates):** While edema fluid is present, "alveolar exudate" is a non-specific term more characteristic of bacterial pneumonia (consolidation) [3]. * **Option D (Interstitial fibrosis):** This is a late-stage sequela of ARDS or a feature of chronic restrictive lung diseases (like IPF), not the primary diagnostic characteristic of the syndrome itself [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Pathogenesis:** Triggered by damage to **alveolar capillary endothelium** and **Type I pneumocytes** [2]. * **Key Histology:** Waxy, eosinophilic **Hyaline Membranes** are the most characteristic finding in the acute phase [1]. * **Berlin Criteria:** Acute onset (<1 week), bilateral opacities on imaging, and $PaO_2/FiO_2$ ratio $\leq 300$ mmHg. * **Common Causes:** Sepsis (most common), diffuse pulmonary infections, gastric aspiration, and severe trauma. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 679-681. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 691-692. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 317-318.

Question 238: Which of the following statements is true regarding non-specific interstitial pneumonia?

A. Honeycombing on CT scan
B. More common in male smokers
C. Fibroblastic foci are characteristic
D. Most often associated with connective tissue disease (Correct Answer)

Explanation: ### Explanation: Non-Specific Interstitial Pneumonia (NSIP) **Non-specific Interstitial Pneumonia (NSIP)** is a distinct pattern of chronic interstitial lung disease characterized by a uniform (homogenous) histological appearance, unlike the patchy nature of Usual Interstitial Pneumonia (UIP) [1]. #### Why the Correct Answer is Right: **Option D** is correct because NSIP is the most common interstitial lung disease pattern associated with **Connective Tissue Diseases (CTDs)** such as Systemic Sclerosis (Scleroderma), Rheumatoid Arthritis, and SLE [2]. While it can be idiopathic, identifying an NSIP pattern should always prompt a clinical search for an underlying autoimmune disorder [2]. #### Why Other Options are Incorrect: * **Option A (Honeycombing):** Honeycombing is a hallmark of **UIP/Idiopathic Pulmonary Fibrosis (IPF)**. In NSIP, CT scans typically show symmetric, subpleural **Ground Glass Opacities (GGO)** with lower lobe predominance [1]. Honeycombing is rare or absent in NSIP [1]. * **Option B (Male Smokers):** NSIP typically affects **non-smoking females** in their 40s–50s [1]. In contrast, IPF (UIP pattern) is more common in elderly male smokers. * **Option C (Fibroblastic Foci):** These are the hallmark histological feature of **UIP**. NSIP is characterized by **temporal homogeneity** (all lesions are at the same stage of development), showing either uniform inflammation (Cellular NSIP) or uniform collagen deposition (Fibrotic NSIP) [1]. #### NEET-PG High-Yield Pearls: * **Histology:** "Uniformity" is the keyword. Look for diffuse interstitial chronic inflammation or fibrosis without the "spatial and temporal heterogeneity" seen in UIP [1]. * **Prognosis:** NSIP has a significantly **better prognosis** than UIP/IPF and responds well to corticosteroids [1]. * **Radiology:** Ground-glass opacities are the dominant feature; "subpleural sparing" is a highly specific sign for NSIP. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 693-695. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 333-334.

Question 239: A 67-year-old male with a history of chronic smoking presents with hemoptysis and cough. Bronchoscopic biopsy from a centrally located mass shows an undifferentiated tumor histopathologically. Which immunohistochemical marker would be most useful to make a proper diagnosis?

A. Cytokeratin (Correct Answer)
B. Parvalbumin
C. HMB-45
D. Hep-par1

Explanation: **Explanation:** The clinical presentation of a 67-year-old male smoker with a central lung mass and hemoptysis strongly suggests a primary bronchogenic carcinoma, most likely **Squamous Cell Carcinoma** or **Small Cell Carcinoma** [1]. When a tumor is histologically "undifferentiated," immunohistochemistry (IHC) is essential to determine the cell of origin [2]. **1. Why Cytokeratin is the correct answer:** Cytokeratins (CK) are intermediate filaments found in the intracytoplasmic cytoskeleton of **epithelial tissue**. Since the vast majority of primary lung cancers (95%) are carcinomas (epithelial in origin), Cytokeratin is the primary marker used to confirm that a poorly differentiated mass is indeed a carcinoma rather than a sarcoma or lymphoma. **2. Why other options are incorrect:** * **Parvalbumin:** This is a calcium-binding protein used primarily as a marker for specific renal tumors (e.g., Chromophobe Renal Cell Carcinoma) or certain muscle/nerve tissues. It has no role in diagnosing lung carcinoma. * **HMB-45:** This is a highly specific marker for **Melanoma**. While melanoma can metastasize to the lung, the central location and smoking history point toward a primary epithelial lung malignancy. * **Hep-par1:** This is a specific marker for **Hepatocytes** and is used to diagnose Hepatocellular Carcinoma (HCC). **High-Yield Clinical Pearls for NEET-PG:** * **Central Lung Tumors:** Squamous Cell Carcinoma and Small Cell Carcinoma (Both are strongly associated with smoking) [1]. * **Peripheral Lung Tumors:** Adenocarcinoma (Most common type in non-smokers and females). * **Specific IHC Markers for Lung Cancer:** * **Adenocarcinoma:** TTF-1 (+), Napsin A (+). * **Squamous Cell Carcinoma:** p40 (+), p63 (+), CK5/6 (+) [3]. * **Small Cell Carcinoma:** Chromogranin (+), Synaptophysin (+), CD56 (+) [2]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 336-337. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 337-338. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 723-724.

Question 240: A 45-year-old man incurs blunt chest trauma. On examination, he has marked right chest wall pain. A chest radiograph shows a fractured 7th rib on the right side. Over the next 2 days, he has subcutaneous soft tissue swelling with nonpainful crepitus on palpation of the right chest wall. Leakage of which of the following is most likely producing this swelling?

A. Acid
B. Air (Correct Answer)
C. Blood
D. Lymph

Explanation: **Explanation:** The clinical presentation of **nonpainful crepitus** (a crackling sensation) and soft tissue swelling following blunt chest trauma and a rib fracture is pathognomonic for **Subcutaneous Emphysema**. **1. Why Air is the Correct Answer:** When a rib fractures, the sharp bony fragments can lacerate the underlying parietal pleura and the lung parenchyma. This creates a communication between the airways and the chest wall. If air escapes the lung but cannot exit the body, it tracks along the fascial planes into the subcutaneous tissues. The sensation of "bubbles" or "crackling" (crepitus) on palpation is caused by the displacement of this trapped air within the soft tissues. Interstitial emphysema through traumatic rupture of an airway may spread to the subcutis, giving this characteristic spongy crepitus [1]. **2. Why Incorrect Options are Wrong:** * **Acid:** Gastric acid leakage occurs in esophageal rupture (Boerhaave syndrome), which typically presents with severe retrosternal pain and mediastinitis, not localized chest wall crepitus following trauma. * **Blood:** Leakage of blood into the soft tissues (hematoma/ecchymosis) causes tense, painful swelling and discoloration. Blood is a fluid and does not produce the characteristic "crackling" crepitus associated with gas. * **Lymph:** Leakage of lymph (chylothorax) usually occurs due to thoracic duct injury. It results in a pleural effusion rather than subcutaneous crepitus. **Clinical Pearls for NEET-PG:** * **Hamman’s Sign:** A "crunching" sound heard over the precordium synchronous with the heartbeat, indicating **pneumomediastinum** (air in the mediastinum). * **Radiology:** On a chest X-ray, subcutaneous emphysema appears as radiolucent (black) streaks outlining muscle bundles (e.g., the "Ginkgo leaf sign" over the pectoralis major). * **Management:** Small amounts of subcutaneous air are usually self-limiting and reabsorb spontaneously once the underlying air leak (like a pneumothorax) is addressed. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 327-328.

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