This document provides information on diffuse parenchymal lung disease (DPLD) and idiopathic interstitial pneumonias (IIPs). It begins with an overview of common IIPs including idiopathic pulmonary fibrosis (IPF), other IIPs, familial IIP, IIP with autoimmune features, and smoking-related ILDs. It then discusses diagnosing other ILDs through clinical, radiological findings and management approaches. Specific ILDs covered include CTD-associated ILDs, diffuse cystic lung diseases like lymphangioleiomyomatosis, pulmonary Langerhans cell histiocytosis, pulmonary alveolar proteinosis, and diffuse alveolar damage
Segmental anatomy of lungs , anatomy of mediastinum and secondary lobuleGamal Agmy
The document discusses the segmental anatomy of the lungs and secondary lobule. It notes that there are approximately 23 generations of dichotomous branching from the trachea to the alveolar sacs. The secondary lobule is described as the basic anatomic unit of pulmonary structure and function, measuring 1-2 cm and containing 5-15 pulmonary acini. It is supplied by a terminal bronchiole in the center and surrounded by connective tissue septa and two lymphatic systems. Diseases typically manifest in either the centrilobular or perilymphatic areas based on how they enter the lungs.
The document discusses the pulmonary interstitium, which is the connective tissue within the lungs. It has three main functions: supporting the lung, fluid balance, and repair/remodeling. The interstitium is made up of a thin portion forming barriers between alveoli and capillaries, and a thick portion where fluid can accumulate. The thick portion contains extracellular matrix, macrophages, and fibroblasts. There are three zones of interstitial tissue: peripheral, axial, and parenchymal. Fluid balance in the interstitium is regulated by Starling forces and leakage can occur if pressures are too high. Remodeling of the matrix is also important for lung biology and chronic inflammation. The document then provides examples of
Bronchiectasis is the irreversible dilatation of the airways. There are different types including cylindrical, varicose, and cystic bronchiectasis. CT scans are useful for diagnosis and can show signs like the signet ring sign, lack of bronchial tapering, and visibility of peripheral airways. Pseudo-bronchiectasis can occur due to artifacts or conditions like tumors, broncholithiasis, or post-irradiation fibrosis. Common causes of diffuse bronchiectasis include cystic fibrosis, sarcoidosis, nontuberculous mycobacterial infections, and immotile cilia syndrome. Idiopathic bronchiectasis and recurrent childhood infections are common
The document discusses interstitial lung disease (ILD), including its common features, types, causes, diagnostic approach and treatment. It describes various ILD types such as idiopathic pulmonary fibrosis and sarcoidosis. Imaging and biopsy are used to diagnose ILD and determine prognosis. Treatment involves identifying and removing environmental causes, suppressing inflammation, and managing complications like right heart failure.
This document provides a detailed summary of various patterns seen on HRCT scans of the lungs including reticular, nodular, ground glass, mosaic and honeycombing patterns. It describes the characteristic radiological features of different interstitial lung diseases such as UIP, NSIP, COP, RB-ILD, DIP, LIP, AIP and others. Key diagnostic criteria and differentiating features between these conditions are discussed. HRCT images demonstrating examples of the described patterns are also included.
Endobronchial ultrasonography (EBUS) allows visualization of tissues outside the airway wall using ultrasound probes inserted into the bronchoscope. There are radial and convex probes used for different applications. EBUS is used to stage lung cancer by examining lymph nodes and determining tumor invasion depth. It can also identify peripheral lung lesions. Convex probe EBUS specifically allows real-time guided biopsy of mediastinal structures and lymph nodes. The procedure involves identifying the target with ultrasound imaging and advancing a TBNA needle under real-time visualization to obtain tissue samples for diagnosis. Potential complications are rare and include pneumothorax and bleeding.
This document discusses computed tomography (CT) imaging findings of various chest diseases, including pleural diseases, chest wall diseases, and mediastinal diseases. It describes how CT can be used to identify and characterize pleural effusions, pleural thickening, asbestos-related pleural disease, and tumors of the pleura. It also discusses chest wall abnormalities such as pectus excavatum, pectus carinatum, and Poland syndrome. Finally, it provides guidance on using CT findings to localize diseases within the mediastinum and differentiate various mediastinal abnormalities.
Segmental anatomy of lungs , anatomy of mediastinum and secondary lobuleGamal Agmy
The document discusses the segmental anatomy of the lungs and secondary lobule. It notes that there are approximately 23 generations of dichotomous branching from the trachea to the alveolar sacs. The secondary lobule is described as the basic anatomic unit of pulmonary structure and function, measuring 1-2 cm and containing 5-15 pulmonary acini. It is supplied by a terminal bronchiole in the center and surrounded by connective tissue septa and two lymphatic systems. Diseases typically manifest in either the centrilobular or perilymphatic areas based on how they enter the lungs.
The document discusses the pulmonary interstitium, which is the connective tissue within the lungs. It has three main functions: supporting the lung, fluid balance, and repair/remodeling. The interstitium is made up of a thin portion forming barriers between alveoli and capillaries, and a thick portion where fluid can accumulate. The thick portion contains extracellular matrix, macrophages, and fibroblasts. There are three zones of interstitial tissue: peripheral, axial, and parenchymal. Fluid balance in the interstitium is regulated by Starling forces and leakage can occur if pressures are too high. Remodeling of the matrix is also important for lung biology and chronic inflammation. The document then provides examples of
Bronchiectasis is the irreversible dilatation of the airways. There are different types including cylindrical, varicose, and cystic bronchiectasis. CT scans are useful for diagnosis and can show signs like the signet ring sign, lack of bronchial tapering, and visibility of peripheral airways. Pseudo-bronchiectasis can occur due to artifacts or conditions like tumors, broncholithiasis, or post-irradiation fibrosis. Common causes of diffuse bronchiectasis include cystic fibrosis, sarcoidosis, nontuberculous mycobacterial infections, and immotile cilia syndrome. Idiopathic bronchiectasis and recurrent childhood infections are common
The document discusses interstitial lung disease (ILD), including its common features, types, causes, diagnostic approach and treatment. It describes various ILD types such as idiopathic pulmonary fibrosis and sarcoidosis. Imaging and biopsy are used to diagnose ILD and determine prognosis. Treatment involves identifying and removing environmental causes, suppressing inflammation, and managing complications like right heart failure.
This document provides a detailed summary of various patterns seen on HRCT scans of the lungs including reticular, nodular, ground glass, mosaic and honeycombing patterns. It describes the characteristic radiological features of different interstitial lung diseases such as UIP, NSIP, COP, RB-ILD, DIP, LIP, AIP and others. Key diagnostic criteria and differentiating features between these conditions are discussed. HRCT images demonstrating examples of the described patterns are also included.
Endobronchial ultrasonography (EBUS) allows visualization of tissues outside the airway wall using ultrasound probes inserted into the bronchoscope. There are radial and convex probes used for different applications. EBUS is used to stage lung cancer by examining lymph nodes and determining tumor invasion depth. It can also identify peripheral lung lesions. Convex probe EBUS specifically allows real-time guided biopsy of mediastinal structures and lymph nodes. The procedure involves identifying the target with ultrasound imaging and advancing a TBNA needle under real-time visualization to obtain tissue samples for diagnosis. Potential complications are rare and include pneumothorax and bleeding.
This document discusses computed tomography (CT) imaging findings of various chest diseases, including pleural diseases, chest wall diseases, and mediastinal diseases. It describes how CT can be used to identify and characterize pleural effusions, pleural thickening, asbestos-related pleural disease, and tumors of the pleura. It also discusses chest wall abnormalities such as pectus excavatum, pectus carinatum, and Poland syndrome. Finally, it provides guidance on using CT findings to localize diseases within the mediastinum and differentiate various mediastinal abnormalities.
This document discusses the approach to interstitial lung diseases (ILD) and diffuse parenchymal lung diseases (DPLD). It begins by reviewing the spectrum of ILD and DPLD, identifying clues from clinical presentation to make a diagnosis, and reviewing common radiographic findings. Key points include that ILD involves the pulmonary interstitium located between the epithelial and endothelial basement membranes. Clinical presentation of DPLD/ILD often involves dyspnea, cough, and abnormal chest imaging. Diagnosis involves considering history, physical exam, pulmonary function tests, imaging like chest radiographs and CT, and tissue sampling. Management depends on the specific diagnosis but may include treatments like corticosteroids, immunosuppressants, anti
This document discusses the approach to bullous lung disease. It defines a bulla as a large air-containing space within the lung larger than 1 cm in diameter. Bullae can occur with emphysema, pulmonary fibrosis, or in otherwise normal lungs. HRCT is useful for evaluating the size, number and relationships of bullae. Pulmonary function testing may show obstructive lung disease, hyperinflation and reduced diffusion capacity. For surgical candidates, bullectomy or lung volume reduction surgery may be considered to treat symptoms or complications like spontaneous pneumothorax.
1. Lung development begins in the fourth week of gestation and progresses through five stages - embryonic, pseudoglandular, canalicular, saccular, and alveolar.
2. Key molecular regulators of lung development include fibroblast growth factors, sonic hedgehog, retinoic acid, transforming growth factor beta, Wnts, platelet-derived growth factor and vascular endothelial growth factor.
3. Transcription factors such as NKX2-1, GLI genes, FOX family, GATA6 and SOX family also play important roles in lung development by regulating cell proliferation, branching morphogenesis and epithelial cell differentiation.
This document describes the anatomy of the lungs and pleura. It discusses the borders and lobes of the lungs, noting key landmarks like the apex and angles of Louis. It also details the fissures that divide the lungs into lobes, such as the oblique and transverse fissures. The document outlines the segmental bronchi and notes their anterior and posterior divisions. Furthermore, it describes the layers of the pleura, including the parietal and visceral pleura. Several important surface anatomy landmarks are indicated, such as Traube's area, Kronig's isthmus, and the bare area of the heart. In closing, the upper border of the liver is delineated starting at the 6th rib.
This document discusses radiology signs of pneumomediastinum. It begins by defining pneumomediastinum and listing potential sources where air can originate from, both intrathoracic and extrathoracic. It then describes several common radiographic signs seen with pneumomediastinum, including the thymic sail sign, ring around the artery sign, and ginkgo leaf sign. Examples of each sign are shown through radiograph and CT images. Other signs like the continuous diaphragm sign, tubular artery sign, and Naclerio's V sign are also defined. The document emphasizes the importance of recognizing these signs on imaging for diagnosing pneumomediastinum.
This document discusses pulmonary infiltrative eosinophilia (PIE) syndrome. It begins by introducing eosinophilic pneumonias as disorders characterized by pulmonary and/or blood eosinophilia. It then discusses the classification of eosinophilic pneumonias into six categories: Loeffler's syndrome, drug-induced eosinophilia, idiopathic acute eosinophilic pneumonia, tropical pulmonary eosinophilia, chronic eosinophilic pneumonia, and allergic bronchopulmonary aspergillosis. For each category, it provides information on pathogenesis, clinical features, investigations, treatment and prognosis. It concludes by discussing idiopathic hypereosinophilic syndrome.
This document provides information about Pickwickian Syndrome, also known as Obesity Hypoventilation Syndrome. It defines the condition as a combination of obesity, low blood oxygen levels during sleep, and high blood carbon dioxide levels during the day due to abnormally slow or shallow breathing. The document outlines the objectives of teaching about the syndrome, provides details on its history, epidemiology, anatomy and physiology of the lungs, classification, pathophysiology, clinical manifestations, diagnosis, treatment, nursing management, and prognosis. It also includes sections on the definition, history discovered in 1956, and epidemiology being more common in obese males and certain ethnicities.
This document provides an overview of CT chest imaging, including standard CT, high-resolution CT, and their indications. It discusses CT chest anatomy and windows. Common lung pathologies seen on standard CT like bronchial carcinoma, collapse, and metastasis are described. Interpretation of high-resolution CT focuses on patterns such as reticular, nodular, ground glass opacity, and consolidation. Specific findings including honeycombing, tree-in-bud, mosaic attenuation, and crazy paving are explained. The document concludes with a discussion of low attenuation patterns including emphysema, lung cysts, and bronchiectasis.
1) Respiratory failure is a condition where the lungs cannot properly oxygenate the blood and remove carbon dioxide, classified as Type I (hypoxemic) or Type II (hypercapnic).
2) It can result from problems affecting gas exchange in the lungs, respiratory control centers in the brain, or the chest wall muscles.
3) Common causes of Type I respiratory failure include pneumonia, ARDS, and severe asthma, while Type II is often due to conditions that decrease breathing, such as COPD.
This document discusses ground-glass opacities seen on CT scans. It defines ground-glass opacities as a hazy increase in lung opacity while preserving bronchial and vascular markings. Various pathologies can cause ground-glass opacities by partially filling the airspaces. The document then describes different patterns of ground-glass opacities including diffuse, patchy, focal, halo, and peripheral distributions. For each pattern, common diseases that may present with that appearance are listed and briefly characterized.
Cavitary lung lesions can have various causes including cancer, infection, autoimmune disease, vascular embolism, and trauma. On imaging, characteristics like wall thickness, inner contour, location, and other associated findings provide clues to the underlying etiology. Malignant processes tend to have thicker walls over 15mm while benign lesions usually have thinner walls under 4mm. Infectious cavities often have irregular inner walls and may contain fluid levels. Autoimmune diseases typically cause multiple bilateral nodules. The clinical context is also important for determining the most likely diagnosis.
This document describes the mediastinal lymph node stations according to the 2009 IASLC lymph node map. It provides detailed definitions for each lymph node station, including anatomical boundaries and examples of enlarged lymph nodes in each station seen on CT scans. Key lymph node stations described include supraclavicular (1), superior mediastinal (2-4), aortic (5-6), inferior mediastinal (7-9), hilar (10), interlobar (11), lobar (12), segmental (13), and subsegmental (14) nodes. Diagrams and CT images are provided to illustrate lymph node locations.
radiological anatomy of thoracic lymph nodesHaseeb Manzoor
The document summarizes the radiological anatomy of thoracic lymph nodes according to the mapping system proposed by the International Association for the Study of Lung Cancer in 2009. It defines 14 specific lymph node stations within 7 mediastinal zones, and provides images to illustrate the location and borders of each station. Non-regional thoracic lymph nodes are also discussed, including internal mammary, intercostal, juxtavertebral, and diaphragmatic nodes.
The document summarizes the anatomy of the tracheobronchial tree. It begins by describing the trachea, noting its length, cartilage rings, and bifurcation into left and right bronchi. It then discusses the structure and branching of the bronchi, bronchioles, and alveoli. Key details are provided on cartilage, muscle, epithelium, blood supply, and the segmentation of the lungs into bronchopulmonary segments. References are listed at the end.
The document describes the anatomy of neck spaces. It discusses that the neck can be divided into suprahyoid and infrahyoid spaces based on the hyoid bone. Specific spaces described include the sublingual, submandibular, buccal, masticator, parotid, pharyngeal mucosal, parapharyngeal, visceral, anterior cervical, posterior cervical, carotid, retropharyngeal, prevertebral, and danger spaces. The spaces are delineated by layers of cervical fascia including the superficial, middle, and deep layers. Understanding these neck spaces is important for diagnosing conditions and limiting the spread of infections and tumors.
Bronchiectasis is a lung condition characterized by abnormally widened airways that make the lungs vulnerable to infection. The document discusses the types, signs and symptoms, investigations including CT scans and sputum analysis, and treatment approaches for bronchiectasis such as antibiotics, airway clearance techniques, anti-inflammatory therapies, and in some cases surgery. The goals of treatment are to improve symptoms, reduce complications and exacerbations, and decrease morbidity and mortality through managing both the condition and any underlying causes.
1. The document describes the anatomical locations and classifications of mediastinal lymph nodes. It discusses 10 different lymph node stations located in the mediastinum, including the supraclavicular, upper and lower paratracheal, prevascular, subaortic, para-aortic, subcarinal, paraesophageal, pulmonary ligament, and hilar lymph nodes.
2. Conventional mediastinoscopy allows biopsy of stations 2L, 2R, 4L, 4R, and 7 while extended mediastinoscopy provides access to deeper stations 5 and 6. Endoscopic ultrasound with fine needle aspiration provides sampling of stations 7, 8, and 9.
3. Accurate lymph node
Hypoxia is O2 deficiency at the tissue level. A pathological condition in which the whole body as a whole or a region of the body is deprived of adequate oxygen supply. It is the decrease below normal levels of oxygen in inspired gases, arterial blood, or tissues, without reaching anoxia.
2. High altitude. Low hemoglobin level. Decreased oxygen supply to an area. Low oxygen carrying capacity. P
This document provides an overview of diffuse parenchymal lung disease (DPLD) and idiopathic interstitial pneumonias (IIPs). It discusses the classification of IIPs including idiopathic pulmonary fibrosis (IPF), nonspecific interstitial pneumonia (NSIP), respiratory bronchiolitis-associated interstitial lung disease (RB-ILD), and others. It also covers the clinical presentation, diagnostic approach involving history, physical exam, pulmonary function tests, radiological findings on high-resolution CT, and role of bronchoscopy with bronchoalveolar lavage in evaluating these conditions. Key points like reduced diffusing capacity on pulmonary function tests and honeycombing on imaging in IPF
Based on the information provided:
- The patient has a UIP pattern on HRCT consistent with IPF.
- His occupational exposure to asbestos 35 years ago could be contributing to the fibrosis.
- His rheumatoid arthritis is seronegative so unlikely the cause.
- A multidisciplinary discussion including review of HRCT, pulmonary function tests and clinical history is needed to determine if he meets criteria for a confident diagnosis of IPF. Given his occupational exposure, other ILDs need to be considered or excluded as well.
This document discusses the approach to interstitial lung diseases (ILD) and diffuse parenchymal lung diseases (DPLD). It begins by reviewing the spectrum of ILD and DPLD, identifying clues from clinical presentation to make a diagnosis, and reviewing common radiographic findings. Key points include that ILD involves the pulmonary interstitium located between the epithelial and endothelial basement membranes. Clinical presentation of DPLD/ILD often involves dyspnea, cough, and abnormal chest imaging. Diagnosis involves considering history, physical exam, pulmonary function tests, imaging like chest radiographs and CT, and tissue sampling. Management depends on the specific diagnosis but may include treatments like corticosteroids, immunosuppressants, anti
This document discusses the approach to bullous lung disease. It defines a bulla as a large air-containing space within the lung larger than 1 cm in diameter. Bullae can occur with emphysema, pulmonary fibrosis, or in otherwise normal lungs. HRCT is useful for evaluating the size, number and relationships of bullae. Pulmonary function testing may show obstructive lung disease, hyperinflation and reduced diffusion capacity. For surgical candidates, bullectomy or lung volume reduction surgery may be considered to treat symptoms or complications like spontaneous pneumothorax.
1. Lung development begins in the fourth week of gestation and progresses through five stages - embryonic, pseudoglandular, canalicular, saccular, and alveolar.
2. Key molecular regulators of lung development include fibroblast growth factors, sonic hedgehog, retinoic acid, transforming growth factor beta, Wnts, platelet-derived growth factor and vascular endothelial growth factor.
3. Transcription factors such as NKX2-1, GLI genes, FOX family, GATA6 and SOX family also play important roles in lung development by regulating cell proliferation, branching morphogenesis and epithelial cell differentiation.
This document describes the anatomy of the lungs and pleura. It discusses the borders and lobes of the lungs, noting key landmarks like the apex and angles of Louis. It also details the fissures that divide the lungs into lobes, such as the oblique and transverse fissures. The document outlines the segmental bronchi and notes their anterior and posterior divisions. Furthermore, it describes the layers of the pleura, including the parietal and visceral pleura. Several important surface anatomy landmarks are indicated, such as Traube's area, Kronig's isthmus, and the bare area of the heart. In closing, the upper border of the liver is delineated starting at the 6th rib.
This document discusses radiology signs of pneumomediastinum. It begins by defining pneumomediastinum and listing potential sources where air can originate from, both intrathoracic and extrathoracic. It then describes several common radiographic signs seen with pneumomediastinum, including the thymic sail sign, ring around the artery sign, and ginkgo leaf sign. Examples of each sign are shown through radiograph and CT images. Other signs like the continuous diaphragm sign, tubular artery sign, and Naclerio's V sign are also defined. The document emphasizes the importance of recognizing these signs on imaging for diagnosing pneumomediastinum.
This document discusses pulmonary infiltrative eosinophilia (PIE) syndrome. It begins by introducing eosinophilic pneumonias as disorders characterized by pulmonary and/or blood eosinophilia. It then discusses the classification of eosinophilic pneumonias into six categories: Loeffler's syndrome, drug-induced eosinophilia, idiopathic acute eosinophilic pneumonia, tropical pulmonary eosinophilia, chronic eosinophilic pneumonia, and allergic bronchopulmonary aspergillosis. For each category, it provides information on pathogenesis, clinical features, investigations, treatment and prognosis. It concludes by discussing idiopathic hypereosinophilic syndrome.
This document provides information about Pickwickian Syndrome, also known as Obesity Hypoventilation Syndrome. It defines the condition as a combination of obesity, low blood oxygen levels during sleep, and high blood carbon dioxide levels during the day due to abnormally slow or shallow breathing. The document outlines the objectives of teaching about the syndrome, provides details on its history, epidemiology, anatomy and physiology of the lungs, classification, pathophysiology, clinical manifestations, diagnosis, treatment, nursing management, and prognosis. It also includes sections on the definition, history discovered in 1956, and epidemiology being more common in obese males and certain ethnicities.
This document provides an overview of CT chest imaging, including standard CT, high-resolution CT, and their indications. It discusses CT chest anatomy and windows. Common lung pathologies seen on standard CT like bronchial carcinoma, collapse, and metastasis are described. Interpretation of high-resolution CT focuses on patterns such as reticular, nodular, ground glass opacity, and consolidation. Specific findings including honeycombing, tree-in-bud, mosaic attenuation, and crazy paving are explained. The document concludes with a discussion of low attenuation patterns including emphysema, lung cysts, and bronchiectasis.
1) Respiratory failure is a condition where the lungs cannot properly oxygenate the blood and remove carbon dioxide, classified as Type I (hypoxemic) or Type II (hypercapnic).
2) It can result from problems affecting gas exchange in the lungs, respiratory control centers in the brain, or the chest wall muscles.
3) Common causes of Type I respiratory failure include pneumonia, ARDS, and severe asthma, while Type II is often due to conditions that decrease breathing, such as COPD.
This document discusses ground-glass opacities seen on CT scans. It defines ground-glass opacities as a hazy increase in lung opacity while preserving bronchial and vascular markings. Various pathologies can cause ground-glass opacities by partially filling the airspaces. The document then describes different patterns of ground-glass opacities including diffuse, patchy, focal, halo, and peripheral distributions. For each pattern, common diseases that may present with that appearance are listed and briefly characterized.
Cavitary lung lesions can have various causes including cancer, infection, autoimmune disease, vascular embolism, and trauma. On imaging, characteristics like wall thickness, inner contour, location, and other associated findings provide clues to the underlying etiology. Malignant processes tend to have thicker walls over 15mm while benign lesions usually have thinner walls under 4mm. Infectious cavities often have irregular inner walls and may contain fluid levels. Autoimmune diseases typically cause multiple bilateral nodules. The clinical context is also important for determining the most likely diagnosis.
This document describes the mediastinal lymph node stations according to the 2009 IASLC lymph node map. It provides detailed definitions for each lymph node station, including anatomical boundaries and examples of enlarged lymph nodes in each station seen on CT scans. Key lymph node stations described include supraclavicular (1), superior mediastinal (2-4), aortic (5-6), inferior mediastinal (7-9), hilar (10), interlobar (11), lobar (12), segmental (13), and subsegmental (14) nodes. Diagrams and CT images are provided to illustrate lymph node locations.
radiological anatomy of thoracic lymph nodesHaseeb Manzoor
The document summarizes the radiological anatomy of thoracic lymph nodes according to the mapping system proposed by the International Association for the Study of Lung Cancer in 2009. It defines 14 specific lymph node stations within 7 mediastinal zones, and provides images to illustrate the location and borders of each station. Non-regional thoracic lymph nodes are also discussed, including internal mammary, intercostal, juxtavertebral, and diaphragmatic nodes.
The document summarizes the anatomy of the tracheobronchial tree. It begins by describing the trachea, noting its length, cartilage rings, and bifurcation into left and right bronchi. It then discusses the structure and branching of the bronchi, bronchioles, and alveoli. Key details are provided on cartilage, muscle, epithelium, blood supply, and the segmentation of the lungs into bronchopulmonary segments. References are listed at the end.
The document describes the anatomy of neck spaces. It discusses that the neck can be divided into suprahyoid and infrahyoid spaces based on the hyoid bone. Specific spaces described include the sublingual, submandibular, buccal, masticator, parotid, pharyngeal mucosal, parapharyngeal, visceral, anterior cervical, posterior cervical, carotid, retropharyngeal, prevertebral, and danger spaces. The spaces are delineated by layers of cervical fascia including the superficial, middle, and deep layers. Understanding these neck spaces is important for diagnosing conditions and limiting the spread of infections and tumors.
Bronchiectasis is a lung condition characterized by abnormally widened airways that make the lungs vulnerable to infection. The document discusses the types, signs and symptoms, investigations including CT scans and sputum analysis, and treatment approaches for bronchiectasis such as antibiotics, airway clearance techniques, anti-inflammatory therapies, and in some cases surgery. The goals of treatment are to improve symptoms, reduce complications and exacerbations, and decrease morbidity and mortality through managing both the condition and any underlying causes.
1. The document describes the anatomical locations and classifications of mediastinal lymph nodes. It discusses 10 different lymph node stations located in the mediastinum, including the supraclavicular, upper and lower paratracheal, prevascular, subaortic, para-aortic, subcarinal, paraesophageal, pulmonary ligament, and hilar lymph nodes.
2. Conventional mediastinoscopy allows biopsy of stations 2L, 2R, 4L, 4R, and 7 while extended mediastinoscopy provides access to deeper stations 5 and 6. Endoscopic ultrasound with fine needle aspiration provides sampling of stations 7, 8, and 9.
3. Accurate lymph node
Hypoxia is O2 deficiency at the tissue level. A pathological condition in which the whole body as a whole or a region of the body is deprived of adequate oxygen supply. It is the decrease below normal levels of oxygen in inspired gases, arterial blood, or tissues, without reaching anoxia.
2. High altitude. Low hemoglobin level. Decreased oxygen supply to an area. Low oxygen carrying capacity. P
This document provides an overview of diffuse parenchymal lung disease (DPLD) and idiopathic interstitial pneumonias (IIPs). It discusses the classification of IIPs including idiopathic pulmonary fibrosis (IPF), nonspecific interstitial pneumonia (NSIP), respiratory bronchiolitis-associated interstitial lung disease (RB-ILD), and others. It also covers the clinical presentation, diagnostic approach involving history, physical exam, pulmonary function tests, radiological findings on high-resolution CT, and role of bronchoscopy with bronchoalveolar lavage in evaluating these conditions. Key points like reduced diffusing capacity on pulmonary function tests and honeycombing on imaging in IPF
Based on the information provided:
- The patient has a UIP pattern on HRCT consistent with IPF.
- His occupational exposure to asbestos 35 years ago could be contributing to the fibrosis.
- His rheumatoid arthritis is seronegative so unlikely the cause.
- A multidisciplinary discussion including review of HRCT, pulmonary function tests and clinical history is needed to determine if he meets criteria for a confident diagnosis of IPF. Given his occupational exposure, other ILDs need to be considered or excluded as well.
The CT scan shows bilateral, basal-predominant reticular opacities and honeycombing. Given the patient's history of asbestos exposure, though brief, the radiological findings are most consistent with a diagnosis of asbestosis. Asbestosis is the correct answer.
Pulmonary sarcoidosis is a multisystem inflammatory disease of unknown etiology characterized by non-caseating granulomas. It most commonly affects the lungs, skin, eyes and lymph nodes. The pathogenesis involves accumulation of inflammatory cells and T lymphocytes forming granulomas that can damage tissues. Diagnosis is based on clinical features, radiological evidence of non-caseating granulomas on biopsy with other causes excluded. Treatment depends on severity and organ involvement but may include corticosteroids.
This document provides an overview of interstitial lung disease (ILD), also known as diffuse parenchymal lung disease. It discusses the epidemiology, diagnostic approach, classification, and treatment of ILD. The diagnostic approach involves obtaining a thorough history, physical exam, pulmonary function tests, imaging like chest X-rays and HRCT, and tissue sampling via bronchoscopy or surgical lung biopsy. ILDs can be classified as idiopathic interstitial pneumonias, granulomatous diseases like sarcoidosis, connective tissue disease-associated, and those related to occupational or environmental exposures. Treatment depends on the underlying cause but may include immunosuppression, antifibrotic drugs, managing comorbid
Interstitial lung disease (ILD) is a group of disorders causing scarring of the lungs. Idiopathic pulmonary fibrosis is the most common ILD, accounting for around half of cases. It generally affects older adults and smokers and causes shortness of breath, cough, and lung function decline. Diagnosis involves imaging, pulmonary function tests, and biopsy. Approved treatments are pirfenidone and nintedanib, which can slow disease progression, but prognosis remains poor with median survival of 3-4 years. Nonspecific interstitial pneumonia is another ILD that may be idiopathic or associated with connective tissue diseases.
Interstitial lung disease (ILD) is a group of diseases causing fibrosis in the lungs, leading to stiffness and difficulty in breathing and oxygen delivery to the bloodstream. This presentation gives an overview on "Diagnosis of ILD". For more information, please contact us: 9779030507.
This document provides an overview of connective tissue disease (CTD)-associated interstitial lung disease (ILD). Some key points:
- ILD is a common pulmonary complication in patients with CTDs like systemic sclerosis (SSc), rheumatoid arthritis (RA), and systemic lupus erythematosus (SLE). It can occur concurrently with or after diagnosis of the CTD.
- The pathogenesis involves autoimmune mechanisms, genetic factors, environmental exposures, and inflammatory cytokines that cause lung inflammation and fibrosis.
- SSc has the highest rate of ILD of all CTDs, affecting 40-80% of patients. Antibodies to topoisomerase I are associated with increased
This document discusses idiopathic pulmonary fibrosis (IPF), a chronic, progressive fibrosing interstitial pneumonia of unknown cause associated with a histopathologic pattern of usual interstitial pneumonia (UIP). It defines IPF and outlines the diagnostic criteria, which involves ruling out known causes, abnormal pulmonary function tests, characteristic radiologic findings on high-resolution computed tomography (HRCT), and surgical lung biopsy showing UIP pattern. HRCT features that are consistent and inconsistent with UIP are described. Guidelines for management of IPF are provided, including recommendations for pirfenidone and nintedanib based on recent clinical trials. Lung transplantation is the only treatment that increases long-term survival for patients with IPF.
This document provides an overview of interstitial lung disease (ILD). ILD encompasses over 200 lung disorders that involve scarring or damage to the lungs' interstitium. Progressive fibrosis can occur in some ILDs and is associated with worse outcomes. Idiopathic pulmonary fibrosis is the most common progressive ILD and is characterized by lung scarring. Progressive-fibrosing ILD describes patients with fibrotic ILDs that may deteriorate despite treatment. Diagnosis involves evaluating symptoms, imaging, pulmonary function tests, biopsies and labs to identify the specific ILD and develop a treatment plan which may include immunosuppressants or removing environmental exposures.
The document discusses diffuse parenchymal lung diseases (DPLDs), a heterogeneous group of conditions that affect the lungs. Key points:
- DPLDs include idiopathic pulmonary fibrosis, which has characteristic radiologic and histologic patterns. It typically presents with progressive breathlessness.
- Sarcoidosis is a multisystem granulomatous disorder characterized by non-caseating granulomas. It commonly causes bilateral hilar lymphadenopathy and lung infiltrates.
- Pulmonary eosinophilia refers to lung abnormalities and blood eosinophilia. It includes conditions like Churg-Strauss syndrome and acute eosinophilic pneumonia.
Children's interstitial lung disease (chILD) involves the alveoli and surrounding tissues, leading to gas exchange issues. It was previously called interstitial lung disease but diffuse infiltrative lung disease is a more accurate term. Common causes of chILD include surfactant dysfunction disorders, lung growth abnormalities, neuroendocrine cell hyperplasia of infancy, and pulmonary interstitial glycogenosis. Diagnosis involves clinical evaluation, imaging like HRCT, pulmonary function tests, and sometimes lung biopsy. Management is generally supportive care though corticosteroids may help in some cases. Prognosis depends on the underlying condition but some forms of chILD have high mortality.
This document discusses various idiopathic interstitial pneumonias (IIPs), including their definitions, histological features, radiographic appearances, treatments, and prognoses. It covers common IIPs such as idiopathic pulmonary fibrosis (IPF), nonspecific interstitial pneumonia (NSIP), desquamative interstitial pneumonia (DIP), respiratory bronchiolitis-associated interstitial lung disease (RB-ILD), acute interstitial pneumonia (AIP), and cryptogenic organizing pneumonia (COP). Lung biopsy is an important tool to distinguish between IIPs and make treatment decisions, but larger tissue samples are often needed due to sampling errors with transbronchial biopsies
This document provides an overview of interstitial lung disease (ILD). ILD involves the lung parenchyma between the alveoli and small airways. There are over 200 known ILDs classified into groups based on predominant inflammation/fibrosis or granulomatous reaction. Idiopathic pulmonary fibrosis is the most common ILD and has a poor prognosis. Diagnosis involves clinical history, imaging like HRCT, pulmonary function tests showing restriction, and sometimes lung biopsy. Management focuses on identifying and removing causes, suppressing inflammation, and lung transplantation for severe cases.
1) The patient presents with a history of recurrent chest infections and inspiratory crackles on examination. Imaging and pulmonary function tests are required to diagnose interstitial lung disease.
2) Idiopathic pulmonary fibrosis is a chronic, progressive form of interstitial lung disease of unknown cause characterized by fibrosis of the lungs. It carries a poor prognosis with median survival of 3 years.
3) Diagnosis requires ruling out other causes through history, imaging showing reticular opacities and honeycombing, and lung biopsy if imaging is not definitive. Treatment focuses on managing complications, vaccination, oxygen therapy and consideration of lung transplantation in advanced cases.
This document discusses the diagnosis of interstitial lung disease (ILD). It defines ILD as a collection of over 100 lung disorders that share clinical, radiographic, and pathological features. ILD is classified based on patterns seen on histology and radiography. Risk factors include age, smoking, occupation, and family history. Signs and symptoms include dyspnea, cough, chest pain, and digital clubbing. Diagnostic tests involve pulmonary function tests, chest imaging like HRCT, bronchoscopy, and surgical lung biopsy. HRCT is more sensitive than chest x-rays and can identify patterns like ground glass opacities and cysts that indicate different diseases.
Interstitial lung disease with rheumatological diseasesMohamed Alfaki
1) Interstitial lung disease (ILD) can occur in several rheumatological diseases in children and is a major cause of morbidity and mortality.
2) ILD most commonly involves pulmonary fibrosis and presents diagnostic challenges requiring close collaboration between specialists.
3) Diagnostic testing for ILD includes HRCT, PFTs, BAL, and biopsy though genetic testing has reduced need for biopsy in some cases. Treatment involves immunosuppression.
1. Interstitial lung diseases (ILDs) involve the lung parenchyma including the alveoli, capillaries, and tissues between them.
2. Patients commonly present with progressive dyspnea, cough, and interstitial opacities on imaging.
3. A thorough evaluation includes pulmonary function tests, imaging, biopsy, and ruling out other known causes to identify the underlying ILD.
The document discusses interstitial lung disease (ILD). It begins with an introduction and overview of ILD pathogenesis, epidemiology, approach, specific diseases, management and follow up. It then discusses in more detail the classification, pathogenesis, epidemiology, clinical approach, radiographic patterns and specific ILDs such as idiopathic pulmonary fibrosis and granulomatous lung diseases like sarcoidosis and hypersensitivity pneumonitis. Laboratory tests and imaging findings that can help diagnose and characterize ILD are also summarized.
This document provides an overview of key aspects of clinical research papers, including their typical structure and components. It outlines the main sections such as the title, abstract, introduction, methods, results, discussion, and references. It also describes important considerations for study design, including defining the study population and ensuring internal and external validity. Common study designs like randomized controlled trials and how to properly implement randomization and blinding are covered.
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This document discusses novel treatment options for asthma, focusing on biologic-based targeted therapies. It summarizes the four approved type-2 targeted biologic therapies that target IL-5 and IgE, as well as IL-4 and IL-13. These target key pathways involved in type-2 inflammation like eosinophil recruitment and activation. Emerging therapies also target other inflammatory pathways like IL-17. Characterization of inflammatory biomarkers and phenotypes helps identify patients that may benefit most from specific targeted therapies.
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3. Users' guides are provided for critically appraising different study designs, focusing on whether the results are valid and assessing the magnitude and precision of the treatment effect. Factors like randomization, blinding, follow-up, and equal treatment of groups
1. Transbronchial biopsy is the least invasive approach to obtain a histologic diagnosis for a 60-year-old man with shortness of breath, a history of smoking, and basilar crackles. Objective parameters like 6MWT, DLCO, FVC, and HRCT can assess progression of the disease. Lung transplantation is the best curative treatment.
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3. A 40-year-old man with rapid deterioration and bilateral infiltrates on CXR would be diagnosed with acute eosin
Pneumonia can be categorized as community-acquired pneumonia (CAP), healthcare-associated pneumonia (HCAP), hospital-acquired pneumonia (HAP) including ventilator-associated pneumonia (VAP). HCAP refers to patients who received recent healthcare but did not stay overnight in the hospital. CAP occurs in people acquired in the community with an annual rate of 5.16 to 6.11 cases per 1000 persons increasing with age. Streptococcus pneumoniae is the most common worldwide cause of CAP. Pneumonia pathogens can be typical bacteria like S. pneumoniae or atypical organisms such as Legionella spp, Mycoplasma pneumoniae, and Chlamydophila pneumoniae.
This study analyzed 29 cases of Middle East Respiratory Syndrome Coronavirus (MERS-CoV) in Saudi Arabia from March to May 2014. Most cases were male Saudi nationals over age 40. Common symptoms were fever, cough and shortness of breath. Patients had abnormal chest imaging and laboratory abnormalities including low white blood cell count. Ten patients (34%) died, generally being older, male smokers with more severe symptoms and worse laboratory and blood gas values. MERS-CoV disproportionately affected health care workers through close contact with infected patients.
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Neuromuscular Disorders Respiratory Complications and AssessmentNahid Sherbini
This document discusses respiratory complications and management in patients with neuromuscular disorders. Key points:
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The National Lung Screening Trial (NLST) compared low-dose CT screening to chest x-ray (CXR) screening for lung cancer in high-risk individuals. Over 53,000 participants were randomized to receive either low-dose CT or CXR screening annually for three years. The primary endpoint was lung cancer mortality. An interim analysis found that low-dose CT screening reduced lung cancer mortality by 20% compared to CXR, with fewer advanced stage cancers detected in the CT group. However, the false positive rate was high at around 95% for both screening methods.
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- A thorough preoperative evaluation involves reviewing the patient's history, performing a physical exam, and testing like arterial blood gases, chest x-ray, and pulmonary function tests to determine their risk level. Assigning a risk level helps guide risk reduction strategies in high risk patients.
- Pulmonary complications are a major cause of postoperative morbidity and mortality. The risk depends on patient-related factors like age, smoking history, COPD, asthma, obesity, sleep apnea, and heart failure as well as procedure-related factors like the surgical site and duration of anesthesia.
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This document discusses asthma management during pregnancy. It begins by describing how pregnancy can affect asthma severity, noting that prior asthma severity predicts severity during pregnancy. It then explains how asthma can impact pregnancy outcomes like preterm delivery. The rest of the document covers general asthma care during pregnancy, including monitoring, education, trigger avoidance, and medications. It notes most asthma medications are category B or C but are generally considered safe in pregnancy with monitoring. Inhaled short-acting beta agonists are recommended for acute exacerbations. The goal is preventing acute episodes and optimizing lung function to reduce risks.
The document summarizes the neural control of breathing. It discusses how breathing is regulated by central neuronal networks in the brainstem and spinal cord to meet metabolic demands. The central neurons in the medulla and pons form the basic respiratory center that produces and controls respiration. These centers integrate input from higher brain areas, mechanoreceptors, and peripheral chemoreceptors. They regulate breathing frequency and tidal volume through motor neurons that control respiratory muscles. Chemical control of breathing also occurs through central and peripheral chemoreceptors that sense changes in blood gases like oxygen and carbon dioxide to modulate ventilation.
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PGx Analysis in VarSeq: A User’s PerspectiveGolden Helix
Since our release of the PGx capabilities in VarSeq, we’ve had a few months to gather some insights from various use cases. Some users approach PGx workflows by means of array genotyping or what seems to be a growing trend of adding the star allele calling to the existing NGS pipeline for whole genome data. Luckily, both approaches are supported with the VarSeq software platform. The genotyping method being used will also dictate what the scope of the tertiary analysis will be. For example, are your PGx reports a standalone pipeline or would your lab’s goal be to handle a dual-purpose workflow and report on PGx + Diagnostic findings.
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Discuss and demonstrate the approaches with array and NGS genotyping methods for star allele calling to prep for downstream analysis.
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The biomechanics of running involves the study of the mechanical principles underlying running movements. It includes the analysis of the running gait cycle, which consists of the stance phase (foot contact to push-off) and the swing phase (foot lift-off to next contact). Key aspects include kinematics (joint angles and movements, stride length and frequency) and kinetics (forces involved in running, including ground reaction and muscle forces). Understanding these factors helps in improving running performance, optimizing technique, and preventing injuries.
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This guideline is directed principally toward new Molecular Entities that are
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because the population to be treated is known to include substantial numbers of
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Travel Clinic Cardiff: Health Advice for International TravelersNX Healthcare
Travel Clinic Cardiff offers comprehensive travel health services, including vaccinations, travel advice, and preventive care for international travelers. Our expert team ensures you are well-prepared and protected for your journey, providing personalized consultations tailored to your destination. Conveniently located in Cardiff, we help you travel with confidence and peace of mind. Visit us: www.nxhealthcare.co.uk
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Post-Menstrual Smell- When to Suspect Vaginitis.pptx
Dpld board reveiw 2019 final
1. DIFFUSE PARENCHYMAL LUNG
DISEASE
Dr Nahid Sherbini
Internal Medicine & Pulmonary Consultant
Certified from Harvard Medical School in Practice of clinical Research
2. LearningTargets -I-
•To elaborate the general diagnostic approach to
ILDs and Classifications
•To diagnose IPF and understand treatment
options
•To recognize forms of IIP and clinical relevance
3. DPLD I
Idiopathic Interstitial Pneumonias (IIPs)
• IPF
• Other IIPs
• Familial IP
• IP with autoimmune features (IPAF)
• Smoking-related ILDs
6. Introduction
(ILDs) are a heterogeneous group of
disorders that are classified together
because of similar clinical, radiographic,
physiologic, or pathologic manifestations .
8. What is the Pulmonary Interstitium?
•between the epithelial and
endothelial basement
membrane
•Expansion of the interstitial
compartment by
inflammation with or
without fibrosis
• Necrosis
• Hyperplasia
• Collapse of basement
membrane
• Inflammatory cells
9. Pathogenesis
The pathogenesis of ILDs is unknown.
But more and more facts have shown that
immune cells and their cytokines play an important
role in the course of ILDs.
21. Physical examinations
•Bilateral basilar, crepitant velcro-like rale
•wheezing, rhonchi and coarse rales are occasionally
heard
•with advanced disease, patients may have tachypnea
and tachycardia
•At last, pulmonary hypertention and cor pulmonale
may be exist
26. Q. 1
Classical HRCT findings for IPF , All true except :
a. Traction Bronchiectasis
b. Basal , Sub pleural , Central
c. Honeycombing
d. Reticular Pattern
27. Images courtesy of W. Richard Webb, MD.
Basal and peripheral reticulationReduced lung volume
38. DD
W (Wegner’s)
E (EP)
B (BOOP) COP
A (PAP, Aspiration)
L (Lymphoma)
L (Lipoid Pneumonia)
S (Sacroidosis)
39. Q. 2
55 year male with history of SOB and dry cough over 6 months. He
smokes occasionally . PFT Restrictive pattern with reduced capacity .
HIS HRCT show GGO with traction bronchiectasis .
Which of the following is the most likely diagnosis?
A. NSIP
B. UIP
C. RB-ILD
D. LIP
41. Q.3
In interstitial lung diseases, lung function tests most often show:
A. Reduced carbon monoxide diffusing capacity (DLCO)
B. Increased total lung capacity (TLC)
C. Airflow obstruction
D. Elevated arterial PCO2
43. PFT
•A restrictive defect :
(TLC), (FRC), (RV) ,(FVC) and (FEV1)
but usually the changes are in proportion to the
decreased lung volumes
Low DLCO
44. PFT
• A reduction (DLCO) is a common, but nonspecific finding in ILD- , the
severity of the DLCO reduction does not correlate well with disease
prognosis, unless the DLCO is less than 35 %.
• Due to effacement of the alveolar capillary units but more importantly, to
the extent of mismatching of ventilation and perfusion of the alveoli.
• In some ILDs, i.e sarcoidosis , there can be considerable reduction in lung
volumes and/or severe hypoxemia but normal or only slightly reduced
DLCO
45. Moderate to severe reduction of DLCO in the presence of
normal lung volumes in a patient with ILD suggests one
of the following:
a. Combined emphysema and ILD
b. Combined ILD and PVD
c. Pulmonary Langerhans cell histiocytosis
d. Pulmonary lymphangioleiomyomatosis
e. All of the above
Q.4
46. Q. 5
An interstitial pattern onCXR accompanied by obstructive airflow
suggestive of :
a. Sarcoidosis
b. Diffuse alveolar hemorrhage
c. Pulmonary lymphoangioliomatosis
d. Combined COPD and ILD
e. All of the above
47. An interstitial pattern on CXR accompanied by obstructive
airflow suggestive of :
• Sarcoidosis
• Lymphangioleiomyomatosis
• HP
• PLCH
• Combined COPD and ILD
48. 6MWT
•6MWT have correlated with prognosis in several studies of IPF
• Pulse oximetry desaturation to 88 during the 6MWT is
associated with a median survival of 3.21 y compared with a
median survival of 6.63 y in those who did not desaturate
below 89%.
49. Q. 6
Which of the following is true regarding Pulmonary hypertension in
ILDs ?
A.The cause of PH in ILD is likely multifactorial.
b.There is a linear correlation between PFT and PH in ILD.
C. Genetic predisposition not play a role
D. Proposed pathogenesis include presence of vaso-dilation
,angiopathy and PE
E.All are False
50. The cause of PH in ILD is likely multifactorial
The absence of a linear correlation between PFT
PH in ILD suggests that other factors may play a role ,These include the
following:
1.Vasoconstriction and vascular remodeling;
2.Perivascular fibrosis and vascular destruction;
3.Hypoxemia, both nocturnal and exertional;
4.Thrombotic angiopathy and pulmonary emboli;
5.Elevated pulmonary capillary wedge pressure resulting from peripheral
vascular occlusive disease, which has been described in both IPF and
sarcoidosis and/or diastolic dysfunction;
6.Microvascular inflammation and injury;
7.Pathobiological process (ie, vascular granulomas in sarcoidosis, PH of
Langerhan's cell histiocytosis); and
8.Genetic predisposition and varying gene expression
51. Q. 7
Which is true about BAL in ILDs ?
a. BAL is likely to be helpful in patients with a radiographic pattern
suggestive of IPF.
b. BAL does not have an established role in the assessment of ILD
progression or response to therapy
c. Consist normally of macrophages >85%, lymphocytes 10-15%,
neutrophils ≤3%, eosinophils ≤1%, epithelial ≤5%
d. High CD4 /CD8 ratio in sarcoidosis and rheumatoid lung while
reveals low ratio in HP .
e. All are true
52. Q.
Which of the following associated with neutrophilicCellular pattern
in BAL ?
A. IPF
B. HP
C. COP
D. Drug induced Pneumonitis
E. Radiation Pneumonitis
53. ROLE OF BRONCHOALVEOLAR
LAVAGE (BAL)
•The lavage fluid is sent for cell counts, cultures for
mycobacterial, viral and fungal pathogens, and cytological
analysis.
•Virtually all patients presenting with hemoptysis and
radiographic ILD should undergo BAL to confirm an alveolar
source of bleeding and identify any infectious etiologies.
56. Q. 8
Which is true regardingVATS use for diagnosing ILDs ?
A. Low diagnostic accuracy
B. More morbidity and mortality than open lung biopsy
C. Role of BAL andTBBX is highly diagnostic in all IIP
D. Ideal biopsy include two or more surgical wedge biopsies with
areas of normal lung and samples should measure 3-5 cm in length
and 2-3 cm in depth
E. None of the above
57. Video AssistedThoracic Surgery (VATS)
ChangAC, et al. AnnThorac Surg. 2002.74;1942-1946.Rena O, et al. Eur JCardiothorac Surg. 1999;16:624-627.
• VATS is the preferred procedure for obtaining a lung biopsy
High diagnostic accuracy
Less morbidity and mortality than open lung biopsy
BAL andTBBx limited to excluding other IPF mimickers
• Ideal biopsy
Two or more surgical wedge biopsies with areas of normal lung
Samples should measure 35 cm in length and 23 cm in depth
• Outpatient thoracoscopic lung biopsy can be a safe and effective
procedure for patients with interstitial or focal lung disease
Diagnosis obtained in 61/62 patients
72.5 % discharged home within 8 hours
22.5% discharged home within 23 hours
ATS/ERSConsensus Statement. AmJ Respir Crit Care Med. 2000;161:646-664.
58. Probability of Histologic Diagnosis of Diffuse Diseases
Surgical
Biopsy
1. Granulomatous diseases
2. Malignant tumors/lymphangitic
3. DAD (any cause)
4. Certain infections
5. Alveolar proteinosis
6. Eosinophilic pneumonia
7.Vasculitis
8. Amyloidosis
9. EG/HX/PLCH
10. LAM
11. RB/RBILD/DIP
12. UIP/NSIP/LIP COP
13. Small airways disease
14. PHT and PVOD
Often
Sometimes
Rare
Transbronchial
Biopsy
Courtesy of Kevin O. Leslie, MD.
62. Q. 9
• 55 y old , 30 y pack history
• Progressive dyspnea and cough
• Was working in plastic factory for
the last 30 y
• Bilateral infiltrate in chest
radiograph and cyst
• Surgical biopsy shown
What is true about the nature of the
disease ?
a.This stage carry good prognosis
b. Respond to Steroids
c. Changing his work will be
beneficial
d. Poor Prognosis
63. Q.
• 55 y old , 30 y pack history
• Progressive dyspnea and cough
• Was working in plastic factory for
the last 30 y
• Bilateral infiltrate in chest
radiograph and cyst
• Surgical biopsy shown
What is true about the nature of the
disease ?
a.This stage carry good prognosis
b. Respond to Steroids
c. Changing his work will be
beneficial
d. Poor Prognosis
• Fibrosis with honeycombing
• Architectural destruction
• Peripheral and basal distribution
• Patchy (i.e. normal and abnormal lung)
• Fibroblastic foci UIP
65. Average survival diagnosis of IPF is
approximately 2.5–3.5 years1 from diagnosis
Onset of symptoms
Initial visit
Kaplan-Meier plot of the survival
probability in IPF patients (n=238)2
1. Ley B et al.Am J Respir Crit Care Med 2010 October 8 2. KingTE et al. Am J Respir Crit Care Med 2001; 164: 1171-1181
67. Q .10
Which of the following conditions cause UIP pattern in
HRCT ?
a. IPF
b. Chronic HP
c. Drug Induced
d. Infections e.gTB
e. All of the above
68. Establish Diagnosis
Multi-Disciplinary Team (MDT)
Discussion
Clinical
• Symptoms
• Smoking history
• Exposures
• Features of CTD
• Examination
Investigations
• CXR
• CTThorax
• Blood tests
• Lung Function
Pathology
• Bronchoalveolar
lavage
• Surgical lung biopsy
69. Q.11
A confident diagnosis of idiopathic pulmonary fibrosis
(IPF) requires which one of the following?
A. Surgical lung biopsy
B. Usual interstitial pneumonia (UIP) pattern on lung
biopsy or HRCT.
C. Failure to respond to corticosteroid therapy
D. Evidence of disease progression
70. To Diagnose
•1. Exclude identifiable causes of ILD (e.g.,
occupational or environmental exposures, drugs
&radiation, CTDs)
•2. UIP pattern shown by: a) HRCT or b) Surgical
lung biopsy, in the absence of HRCT features
inconsistent with UIP Diagnostic Criteria for IPF
(ATS/ERS/JRS/ALAT statement. AJRCCM 2011)
71. Q. 12
73-year-old retired insulating engineer presents with a 6-m
history of increasing dyspnoea. He worked with asbestos for 2
years, 35 years ago. He has seronegative rheumatoid arthritis,
clubbing and basal crackles on chest examination.The CT scan
is shown below.
Which one of the following is the most likely diagnosis?
a. Idiopathic pulmonary fibrosis
B. Asbestosis
c. Rheumatoid lung
d. Lung adenocarcinoma
e. Bronchiectasis
72. A. Idiopathic pulmonary fibrosis
• Asbestosis is unlikely because the patient’s asbestos exposure was only
2 years in duration and his disease began more than 20 years later.The
absence of pleural plaques is evidence against asbestosis, in which
more than 95% of patients have pleural plaques demonstrable on chest
CT.
• Rheumatoid lung with interstitial fibrosis is unlikely in seronegative
disease, and clubbing is uncommon in rheumatoid pulmonary fibrosis.
• Lung adenocarcinoma remains a possible diagnosis but in this case is
less likely than IPF and the CT does not suggest the presence of a
cancer.
• Bronchiectasis is unlikely in the absence of cough and sputum
production and clubbing seldom occurs nowadays except in patients
with cystic. Bronchiectasis is not a prominent feature in the presented
CT.
73. Q 13
• 70 year-old never-smoking man, who is former office worker,
complains of a dry cough and progressive sob (NYHA class III) for
6 m. He takes 20 mg enalapril daily for hypertension. He has no
other diseases. He has not kept animals, or been exposed to dust
or fumes. Auscultation revealsVelcro rales over both lung bases.
There is no clubbing. Pulmonary function tests cannot be
performed because of impressive, possibly psychogenic,
hyperventilation.While breathing room air,ABG shows PaO2 72
mmHg, PaCO2 41 mmHg, pH 7.36 and SaO2 94%. His chest CT
image is shown below.
74. Q13
What is the initial
diagnostic test ?
a. Serology for CTD
b. VATS
c. BAL
d. TBB
e. Serum precipitating
Ab
75. Q 14
In patients with suspected idiopathic pulmonary fibrosis, the most
valuable measure is:
A. Bronchoscopy
B. ESR
C.Trial of steroids
D.Video-assisted thorascopic surgery (VATS)
E. None of the above
76. Q 15
75-year-old female is referred for dyspnoea on exertion and chronic cough
that have worsened progressively over the past 12 months. Pulmonary
function testing reveals an FVC of 72% predicted, FEV1 of 80% predicted
andTLCO of 38% predicted.The chest radiograph shows bilateral interstitial
basal infiltrates. On HRCT, bilateral reticular opacities and clustered basal
honeycombing are found. Open-lung biopsy reveals randomly distributed
foci of usual interstitial pneumonia surrounded by normal lung parenchyma.
What is the most appropriate therapy for this patient?
a. Pirfenidone
b. Bosentan
C. Acetylcysteine
d. Prednisolone/azathioprine
e. Supportive care
77.
78. The recommendation against the use of the
following agents for the treatment of IPF
• Anticoagulation
• Imatinib
• Combination prednisone, azathioprine, and N-
acetylcysteine
• Selective endothelin receptor antagonist (ambrisentan
• Phosphodiesterase-5 inhibitor (sildenafil)
• Dual endothelin receptor antagonists (macitentan,
bosentan)
(ATS/ERS/JRS/ALAT Guideline.AJRCCM 2015)
79. Q.
InAscend and CAPACITYTrial ,What is most common reported side
effect of Perfinidone compared to placebo?
A. Vomiting
B. Insomnia
C. Rash
D. Headache
E. Nausea
80. Q
Pooling the results ofAscend , Capacity 1 and Capacity 2 ,Which is
false ?
a. Improve dyspnoea
b. Reduce mortality
c. Reduce decline in 6 MWT
d. Decrease all cause mortality
e. Reduce decline in FVC
83. ASCEND: Key inclusion criteria
40–80 years of age
Definite UIP on HRCT, or possible UIP on HRCT plus definite or
probable UIP on surgical lung biopsy
Extent of fibrotic changes greater than extent of emphysema on
HRCT scan
FVC ≥50% and ≤90% predicted
DLCO ≥30% and ≤90% predicted
FEV1/FVC ratio ≥0.8
6MWT distance ≥150 m
King TE Jr, et al. N Engl J Med 2014;370:2083-2092.
85. TOMORROW: Annual rate of decline in
FVC
Difference between nintedanib 150 mg bid and placebo: p=0.064 vs placebo (pre-specified primary multiplicity-corrected
analysis [closed testing procedure]); p=0.014 vs placebo (pre-specified hierarchical testing procedure).
Richeldi L, et al. N Engl J Med 2011;365:1079–1087.
-0.19
-0.17
-0.21
-0.16
-0.06
-0.30
-0.25
-0.20
-0.15
-0.10
-0.05
0.00
Placebo
(n=83)
Nintedanib
50 mg qd
(n=85)
Nintedanib
50 mg bid
(n=86)
Nintedanib
100 mg bid
(n=85)
Nintedanib
150 mg bid
(n=84)
AnnualrateofFVCdecline,L/year
[Mean(SE)]
86. TOMORROW: Preservation of health-related
quality of life
5.46 4.67
2.18
1.48
-0.66
-4
-2
0
2
4
6
8
Placebo
(n=79)
Nintedanib
50 mg qd
(n=76)
Nintedanib
50 mg bid
(n=82)
Nintedanib
100 mg bid
(n=82)
Nintedanib
150 mg bid
(n=75)
ChangeinSGRQtotalscore
[Mean(SE)]
*
*p=0.007 vs placebo.
SGRQ, St George’s Respiratory Questionnaire.
Richeldi L, et al. N Engl J Med 2011;365:1079–1087.
87.
88. All-cause mortality over 52 weeks: Pooled data
from INPULSIS®
Placebo
Nintedanib 150 mg bid
HR 0.70
(95% CI; 0.43, 1.12)
p=0.1399
Richeldi L, et al. N Engl J Med 2014;370:2071–2082.
90. Q 16
About GERD in patients with IPF ,Which of the
following statement correct ?
a. GERD is common (60-90%) in IPF
b. Majority (50-75%) asymptomatic.
c. May contribute to fibrosis progression, AE.
d. Some studies suggest use of GERD medications to be
an independent predictor of longer survival time in IPF,
associated with slower decline in FVC, decreasedAE.
e. All are true
91. Treatment of IPF
• “We suggest that clinicians use regular antacid
treatment for patients with IPF.”
• “ lung transplantation in patients with IPF.”
• “The committee did not make a recommendation
regarding treatment of PH in patients with IPF.”
(ATS/ERS/JRS/ALAT Guideline. AJRCCM 2015)
92. Q 17
Which of the following is true regarding NSIP?
A. NSIP is a specific disease entity.
B. Prognosis associated with NSIP and UIP are
similar.
C. NSIP is commonly associated with
connective tissue diseases.
D. NSIP commonly manifests cystic lung lesions
on HRCT.
93. NSIP EITHER
Idiopathic iNSIP OR Identifiable cause
• Connective tissue diseases
• Drugs
• Environmental/occupational exposures
• Immunocompromised hosts
• Infections
• Resolving acute lung injury
96. LIP
•idiopathic LIP
•Identifiable cause or underlying disease
Connective tissue disorders – esp. Sjögren
Immunodeficiency
Infections
Drugs/toxins
-Radiologically with GGO ,Cysts
97. Q 19
• A 50-year-old man, current smoker and HIV with CD4 500, has been complaining
of shortness of breath and non-productive cough for 5 months. He is previously
treated with antibiotics but his symptoms have failed to improve. In the
emergency department, he is noted to be hypoxic on room air and crackles on
auscultation of his lungs. His WBC 16,000; Hgb 14; Plt 300; LDH 500.He had a chest CT
which showed below
• The cell count from the bronchial alveolar lavage reveals eosinophils 5%,
lymphocytes 15%, neutrophils 15%.The transbronchial biopsy shows
inflammatory intraluminal plugs consisting of granulation tissue with fibroblasts
and myofibroblasts in connective matrix, in small airway, ducts and alveoli with
mild interstitial inflammation.There is preservation of architecture and uniform
appearance. What is your presumptive diagnosis?
a. Chronic eosinophilic pneumonia
b. Cryptogenic organizing pneumonia
c. Desquamative interstitial pneumonia
d. Pulmonary Oedema
e. Acute eosinophilic pneumonia
99. Q 20.
The patient has been discharged on prednisone 20 mg PO daily for 4 weeks.
He has not been compliance to his medications and he comes in
complaining of fatigue and shortness of breath. He is noted to have oxygen
saturation of 95% on room air and afebrile. Repeat radiographs show new
central sparing infiltrates on the left lung.Cultures have been obtained
which has been negative. What would be the next appropriate step?
a. Prednisone 20 mg PO daily
b. Solumedrol 1 g IV daily for 3 days
c. Piperacillin–Tazobactam 3.375 mg IV every 6 hours with vancomycin 1 g
IV every 12 hours
d. Cellcept 1,000 mg PO every 12 hours
e. Amphotericin B
100. A.
• Answer: A. Prednisone 20 mg PO daily
• The patient appears to have a relapse, which manifests as worsening
symptoms with reoccurrence of prior or new infiltrates.They are
common during steroid taper.
• Predictors of relapse include delayed treatment and mild increases
with alkaline phosphatase and gammaglutamyltransferase.
• Proposed taper of medications include prednisone 0.75 mg/kg/day for 4
weeks; followed by 0.5 mg/kg/day for 4 weeks, and then 20 mg daily
for 4 weeks, 10 mg for 6 weeks, and 5 mg daily for 6 weeks. If relapse
occur while dose <20 mg daily, increase dose to 20 mg daily and slowly
taper accordingly.
• Treatment of COP includes steroids from 0.75 to 1.5 mg/kg/day with
usual duration of up to 1 year.
101. Q.
• 25 y old lady not known to have
any medical illness , history of
recurrent abortions, presented
with dyspnea , admitted to ICU
CT shown - Bronchoscopy done
Which is true about this
condition?
a. Good prognosis
b. Bronchoscopy will not help in
diagnosis
c. Need high dose steroids
d. Complements will be normal
102. DAD
• Histologic pattern of ALI characterized by diffuse involvement with
edema, hyaline membranes, and acute interstitial inflammation
(exudative phase) evolving to loose organizing fibrosis and type II
pneumocyte hyperplasia (organizing phase).
• HRCT: Diffuse ground-glass and/or consolidative opacities
• Management: depends on the clinical context, corticosteroids
commonly used when non-infectious
• Prognosis: high short-term mortality
103. Acute Interstitial Pneumonia
Idiopathic (“Hamman Rich syndrome”)
Identifiable cause or underlying disease:
• Infections
•Toxic inhalants
• Drugs
• CTDs/vasculitides/alveolar hemorrhage
• Acute radiation reaction
• Acute exacerbation in ILDs
Histo – Septal thickening
and proliferation of spindle cells
104. Q 23
• 40 y old female teacher , Hypothyroidism and hypoadrenalism on
treatment, presented with shortness of breath ,cough a typical chest
pain and haemoptysis- minimal amount. History of Raynaud's and
generalized fatigability .No fever . No other systemic symptoms
• Looks Sick , Fully Oriented , BP 90/60 P130 Afebrile Spo2 90 %
• CVS S1, loud S2 with pansystolic murmur , Chest bilateral crackle and
L L oedema
• Leukopenia ,Mild elevation of transaminase
• CXR show Cardiomegaly and bilateral lung infiltrate
• Previous CT one y back :Interstitial lower lobes infiltrates with traction
bronchiectasis
• Echo Severe Pulmonary HTN 90 and dilated RA ,RV normal LV
• RHC ,ANA Positive ,all other autoimmune profile were negative
105. Q 23.
What is suggested treatment ?
A. Sildenafil ,Bosentan and Pirfenidone
B. illoprost , Bosentan and steroids
C. Lasix , Steroids ,Sildenafil and illoprost
D. Bosentan , illoprost ,Lasix and Steroids
E. Steroids only
106. Autoimmune-features ILD
(Interstitial Pneumonia with
Autoimmune Features (IPAF) )
.
Classification criteria:
• Presence of an interstitial pneumonia (by HRCT or SLBx) •
Exclusion of alternative etiologies and,
• Does not meet criteria of a defined connective tissue and, disease
and,
• At least one feature from at least 2/3 domains: clinical (e.g.,
Raynaud’s), serologic, morphologic (HRCT or SLBx features)
ERS/ATS statement. ERJ 2015
108. Q. 24
Which is true about Familial Interstitial Pneumonia/ Familial Pulmonary
Fibrosis?
a. >20 % relatives
b. ~40% of interstitial pneumonia / pulmonary fibrosis
c. ~25% of these familial cases have identifiable mutations
d. Specific HRCT and histopathologic pattern
e. None of the above
109. Familial Interstitial Pneumonia/
Familial Pulmonary Fibrosis
Evolving recommendations regarding
genetic testing for those with early onset
(<50 yr), positive family history, suspicious
extrapulmonary features
Borie et al. Eur Respir Rev 2017
110. Q 25
Which one of the following interstitial lung diseases is related to smoking?
A. LAM
B. Desquamative interstitial pneumonia
C. UIP
D. NSIP
E. DAD
111. Q
Which one of the following interstitial lung diseases is
NOT related to smoking?
A. Acute eosinophilic pneumonia
B. Desquamative interstitial pneumonia
C. Respiratory bronchiolitis –ILD
D. Hypersensitivity Pneumonitis
E. IPF
113. Q. 26
• 40 y old ,nurse ,15y pack history
• Progressive SOB
• No fever or haemoptysis
• RR 27 SPO2 93%RA
• Chest bilateral crepitation
• Normal Labs including ESR & ANA
• CT Shown
• Best treatment
a. Observation & Stop Smoking
b. Stop Smoking & Steriods
c. Steriods and azathioprin
d. Perfinedone
114. RB-ILD
• numerous pigmented macrophages
• Relatively uniform appearance
• Most are smoking-related
• HRCT: GGOs ± reticular opacities;
sometimes cysts, or and vague
nodules
• Management: smoking cessation,
corticosteroids
• Prognosis: generally good, up to 30%
mortality
115. Q 27
• 44 y old came with dyspnea on exertion and cough. Has been told
she has emphysema. Attempt of tobacco cessation failed.
• Physical examination reveals crackles
• Her radiographic ,pathology shown
• Which of the following is most likely ?
a. COPD
b. Goodpasture Syndrome with diffuse pulmonary haemorrhage
c. Pulmonary Langerhans histiocytosis
d. DIP
118. Combined Pulmonary Fibrosis and
Emphysema (CPFE)
•Upper lung emphysema and lower lung fibrosis
•Typically male smokers
•Relatively preserved spirometry and lung volumes with
low DLCO
•Increased incidence of pulmonary hypertension –
associated with increased mortality
•“Pulmonary fibrosis” includes UIP, NSIP, RB-ILD, DIP,
etc.
122. Q 28
Respiratory manifestations in CTD is characterized by
which one of the following?
A. Obstructive lung disease is not seen.
B. Lung biopsy is usually needed.
C. SLE involves the lung more often than other CTDs.
D. Acute exacerbation can occur in patients with CTD-
ILDs.
123. Rheumatic Disease ILD
•RA 20 - 30 %
•PM/DM 20 - 50 %
More common with anti-synthetase antibodies
•Systemic sclerosis 45 % (“clinically significant”)
More common in diffuse disease; topoisomerase-1
antibodies
•SLE 2 - 8 %
Usually in patients with multisystem disease
•MCTD 20 – 60 %
•Sjögren to 25 %
(Castelino et al. Arthritis ResTher 2010)
124. Q 29
45 year old man known case of PM/DM , presented with three
weeks history of dyspnea on exertion ,progressive and
associated with dry cough ,weight loss and loss of appetite He
has a history of Raynaud’s. Physical Examination show ankle
joint swelling, HRCT show bilateral interstitial infiltrate diffuse
predominantly upper lobes with traction bronchiectasis ILD.
What is true about this disease?
a. 2-5 % of PMDM patients will have it
b. UIP pattern is the commonest to be found in HRCT
c. Anti –jo antibodies positive
d. Obstructive ventilatory defect in PFT
e. None of the above
125. AntiSythestase Syndrome
•Subset (16-30%) of patients with PM/DM
• Characterized by relatively acute onset, constitutional
symptoms, Raynaud’s, “mechanic’s hands”, arthritis,
ILD.
•anti-Jo-1 (anti-histidyl–tRNA synthetase)
• Associated with ↑ risk of ILD Usually NSIP > UIP > OP;
sometimes LIP, DAD, etc
•Can be more refractory to treat than other PM/DM-
associated ILD
126. Q 30
• 30 y lady with SLE , Co progressive SOB 3 m , no other respiratory
symptoms . OnWarfarin for previous DVT. Examination is normal
• PFT FEV1 55% ,FVC 58% FEV1FVC 0.78 TLC 68%
RV 100%
DLCO 77% adjusted to alveolar volume 100%
• CXR small lung volume without lung infiltrates or effusion
What is the next to do ?
a. Echo
b. VQ scan
c. Maximum Inspiratory and Expiratory Pressure
d. Bronchoscopy
127. A.
• MIP ,MEP
• To assess muscle weakness ?myositis or phrenic n palsy
• Dx shrinking lung syndrome
• Tx steroid , theophylline , beta agonist and immunosuppression
128. Q 31
• 66 y old lady with Systemic sclerosis , Raynaud's
• Never smoker , work as a secretary
• Examination reveals Spo2 93% , diffuse skin thickening and
telangactasia upper limb digitals
• FVC 60%
• HRCT bilateral basal ground glass opacities
What is the best treatment ?
a. Cyclophosamide
b. Cyclosporine
c. Steroids
d. Azathioprine
129. A.
• B.
• RCT
• 49% improved with cyclophosphamide Vs 26%
Clin Rheumatol. 2006 Mar;25(2):205-12. Epub 2005 Oct 14.
A randomized unblinded trial of cyclophosphamide versus azathioprine in
the treatment of systemic sclerosis.
Nadashkevich O1, Davis P, Fritzler M, Kovalenko W
131. Diffuse Cystic Lung Disease
• Cyst = a round parenchymal lucency with a well defined
thin-wall (<2 mm), usually contain air • Focal/multifocal
vs diffuse
•Cavity = a lucency within pulmonary consolidation, a
mass, or a nodule. (thick wall)
•Emphysema = focal areas of low attenuation without
visible walls
Fleischner Society, 2008
132. Mechanism of Cyst Formation
•Elastolysis mediated by matrix metalloproteinases
MMPs) – LAM, PLCH
• Destruction of the bronchial wall and progressive
luminal dilatation – PLCH
•Airway narrowing and check valve mechanism – LIP,
amyloidosis
• Hamartoma-like cystic alveolar formation – BHD
• Cavitation of nodule (inflammatory/infectious,
neoplastic)
133. Q 32
Which of the following radiographic features is
least likely to be found in Langerhans’ cell
histiocytosis of the lung?
a.Nodules ranging in size up to 10 mm
b.Bilateral reticulonodular opacities
c.Pneumothorax
d.Pleural effusion
e.Honeycomb lung
134.
135. Langerhans’ cell histiocytosis
(LCH)
d. Pleural effusion
1. Early , Centrilobular nodules (2–10 mm in size) and
2. Reticular and nodular opacities with a predominantly bilateral
symmetric upper- to mid-lung distribution.
3. Late ,Cysts develop and become the dominant imaging finding.
Cysts vary in size but usually are smaller than 1 cm may result
in bullous formation, which then predisposes the patient to
recurrent spontaneous pneumothorax. In advanced LCH,
honeycomb changes can occur.
4. Pleural effusions are rare.
Zaveri et al. 2014
137. Q 33
• 56 y F , smoker
• Secretary
• Progressive SOB for last 2 y
• Childhood asthma with FH of asthma
• Not on any medications
• Chest examination reduced breath
sounds -No skin lesions
• Previous- 1 y - CXR reported as
increase lung volume.
• FVC 79% FEV1 46% DLCO 60
What is the most likely diagnosis?
a.LAM
b.PLCH
c. Birt-Hogg-Dude syndrome
d.LIP
138. LAM
• Proliferation of abnormal
smooth muscle cells (LAM cells
– HMB-45+)
• Sporadic andTSC-related
forms; caused by mutation in
theTSC genes
• Mostly women
• High risk of pneumothorax: 60-
80%
• PFT:Typically obstructive
139. Diagnosis and Management -
LAM
CT chest findings plus any one or more of the following:
• Biopsy of lung or extrapulmonary LAM
• Renal angiomyolipomas
• Chylothorax (seen in 20-40% during course)
•Tuberous sclerosis complex (TSC)
• High serumVEGF-D level, >800 pg/mL Management
140. What is the name of this radiological
findings?
141. PAP
• Most are 20-60 y of age (median ~40)
• Nonspecific presentation: insidious onset DOE, cough - sometimes
asymptomatic
• Fever, fatigue, weight loss, chest pain, haemoptysis
• Inspiratory crackles in 20- 50%
• Serum LDH, surfactant A and D, KL-6 (mucinlike glycoprotein) -
common, nonspecific
• Anti-GM-CSF antibodies detectable in serum & BAL fluid in most
cases of acquired PAP
• PFTs: a restrictive defect, reduced DLCO
• Whole Lung Lavage
143. Radiation-induced Lung Injury
After radiation therapy in patients with lung cancer and mediastinal
lymphoma, radiologic abnormalities occur in 60-90%; 5-15%
symptomatic.
Radiation pneumonitis - symptoms 4-12 weeks after irradiation
Radiation fibrosis - 6-12 months after irradiation
• Imaging: radiographic abnormalities confined to radiation field
with “straight line” effect
• Management: symptomatic pneumonitis, prednisone 40-60 mg/d x
2 wk, then taper over 4-12 wk