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.
Diffuse alveolar haemorrhage (DAH) is characterized by bleeding into the alveolar spaces caused by disruption of the alveolar-capillary basement membrane due to injury or inflammation of the small blood vessels in the lungs. Common initial symptoms include cough, hemoptysis, fever, and dyspnea. Diagnostic tests show increased DLCO on PFTs and progressively more hemorrhagic bronchoalveolar lavage samples. Treatment focuses on treating the underlying cause with glucocorticoids as the mainstay along with additional immunosuppressive agents or plasma exchange depending on the cause.
This document provides an overview of the diagnosis and management of Acute Respiratory Distress Syndrome (ARDS). It begins with defining ARDS and discussing the Berlin definition. It then covers risk factors, etiology, clinical course, pathophysiology, differential diagnosis, and management approaches. The management section emphasizes the importance of lung-protective ventilation with low tidal volumes to prevent ventilator-induced lung injury in ARDS patients.
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 summarizes various connective tissue disease-associated interstitial lung diseases. It describes common intrathoracic manifestations and imaging findings for conditions like rheumatoid arthritis, progressive systemic sclerosis, systemic lupus erythematosus, and polymyositis/dermatomyositis. For each condition, it lists typical radiological patterns seen on CT such as ground glass opacities, reticulation, consolidation, and honeycombing. Photomicrographs are also included to illustrate histopathological findings for some of the interstitial lung diseases.
The document discusses pleurisy and pleural effusions. It defines the pleura and pleural space, and describes different types of pleural syndromes including dry pleurisy, pleural effusion, pneumothorax, and fibrothorax. Common causes, symptoms, signs, and investigation findings for pleural effusions are outlined. Pleural fluid analysis is described to differentiate exudates from transudates. Differentials are provided for lymphocytic and eosinophilic pleural effusions.
Vasculitis refers to inflammation of blood vessels. The document discusses the classification, pathogenesis, clinical manifestations, investigations, and histopathology of various types of vasculitis. It classifies vasculitis based on vessel size (large, medium, small vessel) and cause (primary, secondary to infection, drugs, etc). Pathogenesis may involve infectious or non-infectious mechanisms like immune complex deposition, ANCA, or anti-endothelial cell antibodies. Investigations assess organ damage, immune mechanisms, and provide tissue diagnosis. Clinical features and histopathology vary depending on the type and organs involved in the vasculitis.
This document discusses pleural effusions, which occur when fluid accumulates in the pleural space between the lungs and chest wall. A small amount of fluid is normal but excess fluid can accumulate if the rate of fluid formation exceeds drainage by lymphatics. Effusions are classified as transudative or exudative based on their protein content and cell characteristics. Common causes of transudative effusions include heart failure and cirrhosis, while exudative effusions have infectious or inflammatory causes like pneumonia or cancer. Diagnosis involves physical exam, imaging like chest x-ray, and analyzing pleural fluid obtained via thoracentesis.
Interstitial lung disease is a general category that includes many different lung conditions. All interstitial lung diseases affect the interstitium, a part of the lungs' anatomic structure.
Some of the types of interstitial lung disease include:
Interstitial pneumonia: Bacteria, viruses, or fungi may infect the interstitium of the lung. A bacterium called Mycoplasma pneumonia is the most common cause.
Idiopathic pulmonary fibrosis : A chronic, progressive form of fibrosis (scarring) of the interstitium. Its cause is unknown.
Nonspecific interstitial pneumonitis: Interstitial lung disease that's often present with autoimmune conditions (such as rheumatoid arthritis or scleroderma).
Diffuse alveolar haemorrhage (DAH) is characterized by bleeding into the alveolar spaces caused by disruption of the alveolar-capillary basement membrane due to injury or inflammation of the small blood vessels in the lungs. Common initial symptoms include cough, hemoptysis, fever, and dyspnea. Diagnostic tests show increased DLCO on PFTs and progressively more hemorrhagic bronchoalveolar lavage samples. Treatment focuses on treating the underlying cause with glucocorticoids as the mainstay along with additional immunosuppressive agents or plasma exchange depending on the cause.
This document provides an overview of the diagnosis and management of Acute Respiratory Distress Syndrome (ARDS). It begins with defining ARDS and discussing the Berlin definition. It then covers risk factors, etiology, clinical course, pathophysiology, differential diagnosis, and management approaches. The management section emphasizes the importance of lung-protective ventilation with low tidal volumes to prevent ventilator-induced lung injury in ARDS patients.
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 summarizes various connective tissue disease-associated interstitial lung diseases. It describes common intrathoracic manifestations and imaging findings for conditions like rheumatoid arthritis, progressive systemic sclerosis, systemic lupus erythematosus, and polymyositis/dermatomyositis. For each condition, it lists typical radiological patterns seen on CT such as ground glass opacities, reticulation, consolidation, and honeycombing. Photomicrographs are also included to illustrate histopathological findings for some of the interstitial lung diseases.
The document discusses pleurisy and pleural effusions. It defines the pleura and pleural space, and describes different types of pleural syndromes including dry pleurisy, pleural effusion, pneumothorax, and fibrothorax. Common causes, symptoms, signs, and investigation findings for pleural effusions are outlined. Pleural fluid analysis is described to differentiate exudates from transudates. Differentials are provided for lymphocytic and eosinophilic pleural effusions.
Vasculitis refers to inflammation of blood vessels. The document discusses the classification, pathogenesis, clinical manifestations, investigations, and histopathology of various types of vasculitis. It classifies vasculitis based on vessel size (large, medium, small vessel) and cause (primary, secondary to infection, drugs, etc). Pathogenesis may involve infectious or non-infectious mechanisms like immune complex deposition, ANCA, or anti-endothelial cell antibodies. Investigations assess organ damage, immune mechanisms, and provide tissue diagnosis. Clinical features and histopathology vary depending on the type and organs involved in the vasculitis.
This document discusses pleural effusions, which occur when fluid accumulates in the pleural space between the lungs and chest wall. A small amount of fluid is normal but excess fluid can accumulate if the rate of fluid formation exceeds drainage by lymphatics. Effusions are classified as transudative or exudative based on their protein content and cell characteristics. Common causes of transudative effusions include heart failure and cirrhosis, while exudative effusions have infectious or inflammatory causes like pneumonia or cancer. Diagnosis involves physical exam, imaging like chest x-ray, and analyzing pleural fluid obtained via thoracentesis.
Interstitial lung disease is a general category that includes many different lung conditions. All interstitial lung diseases affect the interstitium, a part of the lungs' anatomic structure.
Some of the types of interstitial lung disease include:
Interstitial pneumonia: Bacteria, viruses, or fungi may infect the interstitium of the lung. A bacterium called Mycoplasma pneumonia is the most common cause.
Idiopathic pulmonary fibrosis : A chronic, progressive form of fibrosis (scarring) of the interstitium. Its cause is unknown.
Nonspecific interstitial pneumonitis: Interstitial lung disease that's often present with autoimmune conditions (such as rheumatoid arthritis or scleroderma).
This document discusses interstitial lung disease (ILD) associated with connective tissue diseases (CTDs). It begins by providing background on ILD and defining common presentations. It then discusses the classification of ILD and patterns associated with different CTDs. Common CTDs that can cause ILD are described such as systemic sclerosis, rheumatoid arthritis, and polymyositis/dermatomyositis. Risk factors, pathophysiology, epidemiology, clinical presentation, investigations including radiography and antibodies, and biomarkers for ILD associated with CTDs are summarized. Specific CT features that can help differentiate CTD-ILD from idiopathic pulmonary fibrosis are also outlined.
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 provides information about pleural effusions. It defines a pleural effusion as excess fluid buildup between the pleural layers outside the lungs. Normally a small amount of fluid is present and circulated, but over 25mL is considered an effusion. Effusions are classified as transudative or exudative based on their characteristics. Symptoms include chest pain and breathing difficulties. Diagnosis involves physical exam, imaging like x-rays, and fluid analysis. Management depends on the underlying cause but may include drainage, medication, or surgery in severe cases.
Sarcoidosis is a systemic granulomatous disease of unknown origin characterized by non-caseating granulomas that commonly affect the lungs. Pulmonary manifestations are present in 90% of patients and include bilateral hilar lymphadenopathy and pulmonary infiltrates. While two thirds of patients experience remission within ten years, one third have progressive disease that can lead to pulmonary fibrosis and, in rare cases, death. Computed tomography is more sensitive than chest x-rays in detecting lymph node enlargement and lung abnormalities associated with sarcoidosis.
Updates in Parapneumonic Effusion and EmpyemaGamal Agmy
The document discusses parapneumonic effusion and empyema. It classifies pneumonias and defines related terms like pleurisy, parapneumonic effusion, and empyema. It describes the pathophysiology of effusions in stages from pleuritis sicca to organization. Clinical presentation and differential diagnosis are also covered. Laboratory studies and imaging studies like chest radiography are important for diagnosing complicated parapneumonic effusions or empyemas to allow for optimal management.
FlashPath - Lung - Cryptogenic Organizing Pneumonia (Bronchiolitis Obliterans...Hazem Ali
This document discusses cryptogenic organizing pneumonia (COP), formerly known as bronchiolitis obliterans organizing pneumonia (BOOP). It presents the following key points:
1. COP is characterized by subacute onset of respiratory symptoms and radiologic evidence of patchy consolidation and nodularity. Histologically, it shows intraluminal plugs of granulation tissue (Masson bodies) in the respiratory bronchioles and alveolar ducts.
2. COP has an excellent prognosis and is usually steroid responsive. However, steroid resistance or relapse may occur after treatment is stopped.
3. The pathology of COP must be differentiated from other interstitial lung diseases that present similarly such as usual inter
This document discusses pulmonary hypertension (PH), defining it as a mean pulmonary artery pressure over 22 mmHg. PH is classified into 5 groups, with Group 1 being pulmonary arterial hypertension (PAH). PAH is defined by a mPAP over 25 mmHg and PCWP under 15 mmHg on right heart catheterization. Symptoms are nonspecific but include dyspnea and fatigue. Diagnosis involves echocardiogram, right heart catheterization, and tests like CT, V/Q scan, and PFTs. Treatments include diuretics, anticoagulants, oxygen, PAH-specific therapies like prostanoids, ERAs, PDE5is, and transplant for severe cases.
A 45-year-old male presented with a 2-month history of dry cough and 1-week history of shortness of breath. He was diagnosed with disseminated tuberculosis involving the lungs and massive pericardial effusion. He was started on anti-tuberculosis medications and steroids. He developed lower limb deep vein thrombosis and was started on anticoagulation. He underwent pericardial drainage and window procedure. His treatment plan includes continuing anti-TB medications, increasing warfarin dose, and educating the patient about medication adherence and side effect monitoring.
This document provides information on sarcoidosis, a multisystem chronic inflammatory disease characterized by non-caseating granulomas. It discusses the epidemiology, etiology, clinical presentation, pathology, diagnosis and systems involvement of the disease. Sarcoidosis most commonly affects the lungs and lymph nodes, presenting as bilateral hilar lymphadenopathy. The cause is unknown but believed to involve a disordered immune response in genetically predisposed individuals. Diagnosis is based on clinical features along with identification of non-caseating granulomas in biopsy specimens.
This document provides information on sarcoidosis, including its definition, epidemiology, etiology, clinical presentation, complications, diagnosis, and management. Some key points:
- Sarcoidosis is a granulomatous disease involving multiple organ systems that is thought to be due to an abnormal immune response in genetically predisposed individuals.
- Lungs are involved in over 90% of cases. Other commonly involved organs include lymph nodes, eyes, and skin.
- Diagnosis is based on compatible clinical presentation plus histological evidence of non-caseating granulomas. Bronchoalveolar lavage can also provide supportive evidence.
- Treatment is usually not needed for asymptomatic cases but may involve cort
This document provides information about hepatopulmonary syndrome (HPS). It defines HPS as the presence of liver disease, impaired oxygenation, and intrapulmonary vascular abnormalities. The pathophysiology involves widespread pulmonary vasodilatation leading to ventilation-perfusion mismatching and right-to-left shunting, causing hypoxemia. Clinical features include signs of liver disease in most patients and dyspnea in some. Diagnosis requires confirming the three criteria through tests like contrast echocardiography to detect intrapulmonary shunting.
This document outlines an approach to evaluating and diagnosing dyspnea. It begins by defining dyspnea and noting its high prevalence. Types of dyspnea like orthopnea and paroxysmal nocturnal dyspnea are described. The diagnostic approach involves obtaining a detailed history regarding onset, duration, patterns and associated symptoms. A physical exam assesses respiratory effort, oxygenation, and signs of heart failure. Initial tests may include EKG, chest x-ray, and bloodwork. Further tests are guided by initial findings and may include echocardiogram, pulmonary function tests, CT, or arterial blood gas. Treatment focuses on the underlying cause identified through diagnosis.
This document provides an overview of pleural effusion, including:
- Pleural effusion is abnormal fluid accumulation in the pleural space between the lungs and chest wall. Fluid builds up due to changes in pressure or permeability.
- Effusions are classified as transudative or exudative based on their mechanism and composition. Causes include infections, cancers, heart failure, and other conditions.
- Symptoms depend on the underlying cause but may include chest pain, difficulty breathing, and cough. Diagnosis involves physical exam, imaging like x-rays, and analyzing pleural fluid obtained via thoracentesis.
- Management consists of treating the underlying condition medically or surgically with drainage
This document provides an overview of sarcoidosis, including:
- It is a multisystem granulomatous disorder of unknown cause that commonly affects the lungs, skin and eyes.
- Risk factors include genetics and environmental exposures, and it has the highest rates in the United States and Sweden.
- Clinical presentation varies from asymptomatic to involvement of multiple organ systems. Lung involvement is most common and is staged based on chest x-ray findings.
- Diagnosis involves ruling out other causes and may include biopsy showing non-caseating granulomas. Treatment involves corticosteroids and prognosis is generally good with many experiencing remission.
This document discusses pleural effusions, including their mechanism, normal composition, differentiation between transudative and exudative effusions, and causes. It provides details on parapneumonic effusions and empyema, including classification and treatment approaches. Specific conditions discussed in detail include tuberculous pleural effusions, effusions in HIV patients, chylothorax, pseudochylothorax, and malignant pleural effusions. Useful pleural fluid tests are also summarized.
Pleural effusion is an abnormal collection of fluid in the pleural space that can be caused by various conditions. It is classified as a transudate or exudate based on the characteristics of the fluid. Investigation of pleural effusion involves examination of blood, chest x-rays, and analysis of pleural fluid obtained via thoracentesis to determine the cause and appropriate treatment. Common causes include cardiac failure, pneumonia, tuberculosis, malignancy, and liver or kidney diseases.
This document provides definitions and information about different types of dyspnea (shortness of breath). It discusses the pathophysiology and various causes of dyspnea like asthma, COPD, cardiac failure, pulmonary embolism. The document describes how to take history and examine patients presenting with dyspnea. It outlines investigations like chest imaging and laboratory tests. Differential diagnoses are provided for acute and chronic dyspnea. Management strategies for emergencies and exacerbations of conditions like asthma and COPD are briefly covered.
This document provides an overview of dyspnea, or shortness of breath. It defines dyspnea and outlines its physiological and clinical definitions. Common causes of dyspnea are then discussed, including pulmonary issues like COPD, pneumonia, and pulmonary embolism, as well as cardiac issues like heart failure, coronary syndromes, and dysrhythmias. The pathophysiology of how these conditions can stimulate breathing and cause the sensation of dyspnea is explained. Finally, the document discusses assessing and diagnosing patients presenting with dyspnea through clinical exams, investigations like chest x-rays, and determining if the cause is chronic or acute.
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
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
This document discusses interstitial lung disease (ILD) associated with connective tissue diseases (CTDs). It begins by providing background on ILD and defining common presentations. It then discusses the classification of ILD and patterns associated with different CTDs. Common CTDs that can cause ILD are described such as systemic sclerosis, rheumatoid arthritis, and polymyositis/dermatomyositis. Risk factors, pathophysiology, epidemiology, clinical presentation, investigations including radiography and antibodies, and biomarkers for ILD associated with CTDs are summarized. Specific CT features that can help differentiate CTD-ILD from idiopathic pulmonary fibrosis are also outlined.
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 provides information about pleural effusions. It defines a pleural effusion as excess fluid buildup between the pleural layers outside the lungs. Normally a small amount of fluid is present and circulated, but over 25mL is considered an effusion. Effusions are classified as transudative or exudative based on their characteristics. Symptoms include chest pain and breathing difficulties. Diagnosis involves physical exam, imaging like x-rays, and fluid analysis. Management depends on the underlying cause but may include drainage, medication, or surgery in severe cases.
Sarcoidosis is a systemic granulomatous disease of unknown origin characterized by non-caseating granulomas that commonly affect the lungs. Pulmonary manifestations are present in 90% of patients and include bilateral hilar lymphadenopathy and pulmonary infiltrates. While two thirds of patients experience remission within ten years, one third have progressive disease that can lead to pulmonary fibrosis and, in rare cases, death. Computed tomography is more sensitive than chest x-rays in detecting lymph node enlargement and lung abnormalities associated with sarcoidosis.
Updates in Parapneumonic Effusion and EmpyemaGamal Agmy
The document discusses parapneumonic effusion and empyema. It classifies pneumonias and defines related terms like pleurisy, parapneumonic effusion, and empyema. It describes the pathophysiology of effusions in stages from pleuritis sicca to organization. Clinical presentation and differential diagnosis are also covered. Laboratory studies and imaging studies like chest radiography are important for diagnosing complicated parapneumonic effusions or empyemas to allow for optimal management.
FlashPath - Lung - Cryptogenic Organizing Pneumonia (Bronchiolitis Obliterans...Hazem Ali
This document discusses cryptogenic organizing pneumonia (COP), formerly known as bronchiolitis obliterans organizing pneumonia (BOOP). It presents the following key points:
1. COP is characterized by subacute onset of respiratory symptoms and radiologic evidence of patchy consolidation and nodularity. Histologically, it shows intraluminal plugs of granulation tissue (Masson bodies) in the respiratory bronchioles and alveolar ducts.
2. COP has an excellent prognosis and is usually steroid responsive. However, steroid resistance or relapse may occur after treatment is stopped.
3. The pathology of COP must be differentiated from other interstitial lung diseases that present similarly such as usual inter
This document discusses pulmonary hypertension (PH), defining it as a mean pulmonary artery pressure over 22 mmHg. PH is classified into 5 groups, with Group 1 being pulmonary arterial hypertension (PAH). PAH is defined by a mPAP over 25 mmHg and PCWP under 15 mmHg on right heart catheterization. Symptoms are nonspecific but include dyspnea and fatigue. Diagnosis involves echocardiogram, right heart catheterization, and tests like CT, V/Q scan, and PFTs. Treatments include diuretics, anticoagulants, oxygen, PAH-specific therapies like prostanoids, ERAs, PDE5is, and transplant for severe cases.
A 45-year-old male presented with a 2-month history of dry cough and 1-week history of shortness of breath. He was diagnosed with disseminated tuberculosis involving the lungs and massive pericardial effusion. He was started on anti-tuberculosis medications and steroids. He developed lower limb deep vein thrombosis and was started on anticoagulation. He underwent pericardial drainage and window procedure. His treatment plan includes continuing anti-TB medications, increasing warfarin dose, and educating the patient about medication adherence and side effect monitoring.
This document provides information on sarcoidosis, a multisystem chronic inflammatory disease characterized by non-caseating granulomas. It discusses the epidemiology, etiology, clinical presentation, pathology, diagnosis and systems involvement of the disease. Sarcoidosis most commonly affects the lungs and lymph nodes, presenting as bilateral hilar lymphadenopathy. The cause is unknown but believed to involve a disordered immune response in genetically predisposed individuals. Diagnosis is based on clinical features along with identification of non-caseating granulomas in biopsy specimens.
This document provides information on sarcoidosis, including its definition, epidemiology, etiology, clinical presentation, complications, diagnosis, and management. Some key points:
- Sarcoidosis is a granulomatous disease involving multiple organ systems that is thought to be due to an abnormal immune response in genetically predisposed individuals.
- Lungs are involved in over 90% of cases. Other commonly involved organs include lymph nodes, eyes, and skin.
- Diagnosis is based on compatible clinical presentation plus histological evidence of non-caseating granulomas. Bronchoalveolar lavage can also provide supportive evidence.
- Treatment is usually not needed for asymptomatic cases but may involve cort
This document provides information about hepatopulmonary syndrome (HPS). It defines HPS as the presence of liver disease, impaired oxygenation, and intrapulmonary vascular abnormalities. The pathophysiology involves widespread pulmonary vasodilatation leading to ventilation-perfusion mismatching and right-to-left shunting, causing hypoxemia. Clinical features include signs of liver disease in most patients and dyspnea in some. Diagnosis requires confirming the three criteria through tests like contrast echocardiography to detect intrapulmonary shunting.
This document outlines an approach to evaluating and diagnosing dyspnea. It begins by defining dyspnea and noting its high prevalence. Types of dyspnea like orthopnea and paroxysmal nocturnal dyspnea are described. The diagnostic approach involves obtaining a detailed history regarding onset, duration, patterns and associated symptoms. A physical exam assesses respiratory effort, oxygenation, and signs of heart failure. Initial tests may include EKG, chest x-ray, and bloodwork. Further tests are guided by initial findings and may include echocardiogram, pulmonary function tests, CT, or arterial blood gas. Treatment focuses on the underlying cause identified through diagnosis.
This document provides an overview of pleural effusion, including:
- Pleural effusion is abnormal fluid accumulation in the pleural space between the lungs and chest wall. Fluid builds up due to changes in pressure or permeability.
- Effusions are classified as transudative or exudative based on their mechanism and composition. Causes include infections, cancers, heart failure, and other conditions.
- Symptoms depend on the underlying cause but may include chest pain, difficulty breathing, and cough. Diagnosis involves physical exam, imaging like x-rays, and analyzing pleural fluid obtained via thoracentesis.
- Management consists of treating the underlying condition medically or surgically with drainage
This document provides an overview of sarcoidosis, including:
- It is a multisystem granulomatous disorder of unknown cause that commonly affects the lungs, skin and eyes.
- Risk factors include genetics and environmental exposures, and it has the highest rates in the United States and Sweden.
- Clinical presentation varies from asymptomatic to involvement of multiple organ systems. Lung involvement is most common and is staged based on chest x-ray findings.
- Diagnosis involves ruling out other causes and may include biopsy showing non-caseating granulomas. Treatment involves corticosteroids and prognosis is generally good with many experiencing remission.
This document discusses pleural effusions, including their mechanism, normal composition, differentiation between transudative and exudative effusions, and causes. It provides details on parapneumonic effusions and empyema, including classification and treatment approaches. Specific conditions discussed in detail include tuberculous pleural effusions, effusions in HIV patients, chylothorax, pseudochylothorax, and malignant pleural effusions. Useful pleural fluid tests are also summarized.
Pleural effusion is an abnormal collection of fluid in the pleural space that can be caused by various conditions. It is classified as a transudate or exudate based on the characteristics of the fluid. Investigation of pleural effusion involves examination of blood, chest x-rays, and analysis of pleural fluid obtained via thoracentesis to determine the cause and appropriate treatment. Common causes include cardiac failure, pneumonia, tuberculosis, malignancy, and liver or kidney diseases.
This document provides definitions and information about different types of dyspnea (shortness of breath). It discusses the pathophysiology and various causes of dyspnea like asthma, COPD, cardiac failure, pulmonary embolism. The document describes how to take history and examine patients presenting with dyspnea. It outlines investigations like chest imaging and laboratory tests. Differential diagnoses are provided for acute and chronic dyspnea. Management strategies for emergencies and exacerbations of conditions like asthma and COPD are briefly covered.
This document provides an overview of dyspnea, or shortness of breath. It defines dyspnea and outlines its physiological and clinical definitions. Common causes of dyspnea are then discussed, including pulmonary issues like COPD, pneumonia, and pulmonary embolism, as well as cardiac issues like heart failure, coronary syndromes, and dysrhythmias. The pathophysiology of how these conditions can stimulate breathing and cause the sensation of dyspnea is explained. Finally, the document discusses assessing and diagnosing patients presenting with dyspnea through clinical exams, investigations like chest x-rays, and determining if the cause is chronic or acute.
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
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
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.
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.
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 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.
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.
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.
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.
Idiopathic Interstitial Pneumonia With Autoimmune Features(IPAF).pptxKefelegnNathan1
1) A 35-year-old female patient presented with shortness of breath and generalized body swelling for 1 month. She also had orthopnea and productive cough for the same duration.
2) Examination found bibasilar crackles, accentuated pulmonary component of S2, and echocardiogram showed severe pulmonary hypertension and RV dysfunction.
3) Investigations revealed elevated RF, ANA 1:100, diffuse bilateral pulmonary fibrosis and fibrosing mediastinitis on CT scan. A diagnosis of IPAF was made.
Pneumocystis pneumonia (PCP) is caused by Pneumocystis jiroveci and is an opportunistic infection affecting those with weakened immune systems. It is diagnosed through microscopic visualization of the organism in samples obtained noninvasively through induced sputum or bronchoalveolar lavage, or invasively through lung biopsy. Common symptoms include dyspnea, fever, and cough. Chest imaging often shows bilateral infiltrates and laboratory tests like lactate dehydrogenase are elevated. Treatment involves anti-fungal medications.
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.
Smoking Related Interstitial Lung DiseasesGamal Agmy
1) The document discusses several smoking-related interstitial lung diseases (SR-ILDs) including respiratory bronchiolitis (RB-ILD), desquamative interstitial pneumonia (DIP), pulmonary Langerhans cell histiocytosis (PLCH), and idiopathic pulmonary fibrosis (IPF).
2) These diseases are characterized by varying combinations of inflammation, fibrosis, cysts, and nodules seen on imaging and pathology. Clinical features often include cough and dyspnea. Prognosis and treatment depend on the specific disease.
3) There is significant overlap between the different SR-ILDs both clinically and radiographically. Smoking history and cessation are important for
This document provides a summary of an presentation on approaches to interstitial lung disease (ILD) and updates in idiopathic pulmonary fibrosis (IPF) management. It begins with an introduction to ILDs and the pulmonary interstitium. It then covers the pathogenesis, classification, epidemiology, clinical assessment including history, exams, tests and tissue sampling, and radiological and pathological findings of ILDs. A significant portion discusses IPF specifically, including prognosis, guidelines for diagnosis, and medical therapies including pirfenidone and nintedanib which have been shown to reduce lung function decline in clinical trials. It concludes with experience using pirfenidone in Saudi Arabia.
The document summarizes pulmonary involvement in people living with HIV. It finds that tuberculosis is the most common pulmonary manifestation, followed by bacterial pneumonia and Pneumocystis jirovecii pneumonia. The risk of specific opportunistic infections depends on CD4 count, with P. jirovecii pneumonia most common when CD4 is below 50 cells/mm3. Chest x-rays show findings characteristic of each disease, such as consolidation in tuberculosis and ground glass opacities in P. jirovecii pneumonia. The study aims to correlate pulmonary diseases with CD4 count in HIV-positive patients in India.
Systemic Lupus Erythematosus Female with (Diffuse Large B-Cell) Non-Hodgkin’s...asclepiuspdfs
Systemic lupus erythematosus (SLE) is an autoimmune disease with multisystem complications arising from both underlying disease activity and therapy-related side effects. SLE’s association with lymphoma is a well-established phenomenon. Studies have reported a higher incidence of lymphoma in the SLE population compared with healthy cohorts.[1,2] A 45-year-old woman with SLE presented with fever, cough, sputum, loss of appetite, and fatigue for 4 months. Before that time, her (SLE) symptoms had been well controlled on hydroxychloroquine, azathioprine, and small dose prednisone. Physical examination at initial evaluation was remarkable for bilateral inspiratory crackles. Laboratory investigations were normal. Computed tomography to chest showed bilateral cavitary pulmonary nodules and masses. Bronchoscopy with transbronchial biopsy was done. The histopathology showed diffuse large B-cell non-Hodgkin’s lymphoma. The patient referred to oncology service, where they started her on 4 cycles of R-CHOP by followed 4 cycles of high-dose chemotherapy. She underwent hematopoietic stem cell transplantation and achieved complete remissions.
Pulmonary/Thoracic Sarcoidosis by Dr. Malik Umer Farooq
What is pulmonary sarcoidosis? Sarcoidosis is a rare disease caused by inflammation. It usually occurs in the lungs and lymph nodes, but it can occur in almost any organ. Sarcoidosis in the lungs is called pulmonary sarcoidosis. It causes small lumps of inflammatory cells in the lungs.
The document provides information on the Global Initiative for Chronic Obstructive Lung Disease (GOLD) including its objectives to increase awareness of COPD, improve diagnosis and management, and stimulate research. It defines COPD as a preventable disease characterized by airflow limitation caused by an abnormal inflammatory response to noxious particles. The document also outlines the classification of COPD severity based on lung function tests, risk factors, pathogenesis, management approaches, and goals of reducing symptoms and disease progression.
Respiratory Manifestations in Systemic Lupus Erythematosus.pptxssusere39f231
This document summarizes the respiratory manifestations that can occur in patients with systemic lupus erythematosus (SLE). It describes several types of lung involvement including airway disease, parenchymal lung disease, vascular diseases, and pleural disease. Specific conditions discussed in detail include acute lupus pneumonitis, diffuse alveolar hemorrhage, interstitial lung disease such as lymphocytic interstitial pneumonia and organizing pneumonia, acute reversible hypoxemia syndrome, and pulmonary embolism. Treatment options are provided for some of the conditions.
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.
This document provides an overview of evidence-based medicine (EBM). It defines EBM as integrating the best available research evidence with clinical expertise and patient values. The key steps of EBM are outlined as formulating a clinical question using PICO (population, intervention, comparison, outcome), searching for evidence, appraising research studies, and applying the evidence to clinical problems. Study designs such as randomized controlled trials and systematic reviews are discussed. Methods for critically appraising studies including assessing validity and determining the clinical importance of results are also summarized.
1) The document discusses a lecture on evidence-based medicine (EBM) and critical appraisal.
2) EBM involves integrating the best available research evidence with clinical expertise and patient values. It includes formulating clinical questions, searching for evidence, appraising research, and applying the evidence to patient care.
3) The lecture reviews the principles of EBM and critical appraisal, including how to formulate answerable clinical questions using the PICO framework, search for evidence, and appraise different types of research studies.
This document provides an overview of scientific writing and research proposals. It discusses types of scientific publications such as journal articles, books, and conference posters. It emphasizes using clear, precise language and proper structure for scientific papers, including titles, introductions, methods, results, and references sections. The document also outlines the key elements of a good research proposal, such as stating the problem, reviewing previous literature, describing the methodology, presenting a timeline and budget, and listing references. Researchers are advised to write proposals that are coherent, informative, and clearly structured to convince readers of the significance and merit of the proposed research.
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.
1. The document provides an overview of evidence-based medicine (EBM) and the process of critically appraising research evidence. EBM involves integrating the best available research evidence with clinical expertise and patient values and preferences.
2. The key steps of EBM are outlined, including formulating a clear clinical question using PICO (population, intervention, comparison, outcome), searching for and appraising the evidence, and applying the results to the clinical problem.
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.
2. A 50-year-old current smoker with shortness of breath and cough showing findings on HRCT and PFTs would be diagnosed with RB-ILD based on surgical lung biopsy findings.
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.
Neuromuscular Disorders Respiratory Complications and AssessmentNahid Sherbini
This document discusses respiratory complications and management in patients with neuromuscular disorders. Key points:
- Duchenne muscular dystrophy is the most common childhood muscular dystrophy, causing progressive muscle weakness.
- Respiratory muscle weakness can occur independently of peripheral muscle weakness and should be evaluated through tests like PFTs, MIP, MEP, and cough assessment.
- Non-invasive ventilation may benefit those requiring short term or intermittent support, while invasive ventilation is preferred for acute respiratory failure due to risks of NPPV. Proper respiratory management can extend lifespans.
Hemoptysis is defined as the spitting of blood from the lungs or bronchial tubes. It can be classified based on severity from mild to massive. Common causes include infections like tuberculosis, cancers, vascular abnormalities and vasculitis. Initial management focuses on airway protection, oxygenation and circulation. Bronchoscopy helps identify the bleeding site and allows local measures like lavage, vasoconstrictors and tamponade. For persistent or massive bleeding, bronchial artery embolization or surgery may be needed. Precise localization through CT and arteriography guides definitive treatment.
The national lung screening trial /Nahid SherbiniNahid Sherbini
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.
Evaluation of preoperative pulmonary risk By Nahid SherbiniNahid Sherbini
- 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.
- 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.
- 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.
Control of Ventilation /Lung Physiology by Nahid SherbiniNahid Sherbini
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. Peripheral chemoreceptors in the carotid bodies also influence breathing in response to changes in blood oxygen and carbon dioxide levels.
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.
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.
share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
• Evidence-based strategies to address health misinformation effectively
• Building trust with communities online and offline
• Equipping health professionals to address questions, concerns and health misinformation
• Assessing risk and mitigating harm from adverse health narratives in communities, health workforce and health system
Promoting Wellbeing - Applied Social Psychology - Psychology SuperNotesPsychoTech Services
A proprietary approach developed by bringing together the best of learning theories from Psychology, design principles from the world of visualization, and pedagogical methods from over a decade of training experience, that enables you to: Learn better, faster!
ABDOMINAL TRAUMA in pediatrics part one.drhasanrajab
Abdominal trauma in pediatrics refers to injuries or damage to the abdominal organs in children. It can occur due to various causes such as falls, motor vehicle accidents, sports-related injuries, and physical abuse. Children are more vulnerable to abdominal trauma due to their unique anatomical and physiological characteristics. Signs and symptoms include abdominal pain, tenderness, distension, vomiting, and signs of shock. Diagnosis involves physical examination, imaging studies, and laboratory tests. Management depends on the severity and may involve conservative treatment or surgical intervention. Prevention is crucial in reducing the incidence of abdominal trauma in children.
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
Histololgy of Female Reproductive System.pptxAyeshaZaid1
Dive into an in-depth exploration of the histological structure of female reproductive system with this comprehensive lecture. Presented by Dr. Ayesha Irfan, Assistant Professor of Anatomy, this presentation covers the Gross anatomy and functional histology of the female reproductive organs. Ideal for students, educators, and anyone interested in medical science, this lecture provides clear explanations, detailed diagrams, and valuable insights into female reproductive system. Enhance your knowledge and understanding of this essential aspect of human biology.
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
Light House Retreats: Plant Medicine Retreat Europe
Dpld board reveiw final
1. DIFFUSE PARENCHYMAL LUNG
DISEASE
Dr Nahid Sherbini
Internal Medicine & Pulmonary Consultant
King Abdullah Medical Complex /Jeddah
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.
19. 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
36. DD
W (Wegner’s)
E (EP)
B (BOOP) COP
A (PAP, Aspiration)
L (Lymphoma)
L (Lipoid Pneumonia)
S (Sacroidosis)
37. Q.
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
38. PFT
•A restrictive defect :
(TLC), (FRC), (RV) ,(FVC) and (FEV1)
but usually the changes are in proportion to the
decreased lung volumes
Low DLCO
39. 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
40. 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.
41. Q.
An interstitial pattern onCXR accompanied by obstructive airflow
suggestive of :
a. Sarcoidosis
b. Diffuse alveolar hemorrhage
c. Pulmonary alveolar proteinosis
d. Combined pulmonary hypertension and ILD
e. All of the above
42. An interstitial pattern on CXR accompanied by obstructive
airflow suggestive of :
• Sarcoidosis
• Lymphangioleiomyomatosis
• HP
• PLCH
• Combined COPD and ILD
43. 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%.
44. Q.
Which of the following is false 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 may play role
D. Proposed pathogenesis include presence of microthrombi
,angiopathy and PE
E.All are False
45. The cause of PH in ILD is likely multifactorial.
The absence of a linear correlation between pulmonary function tests and
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
46. Q.
Which is true about BAL in ILDs ?
a. BAL is less 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
47. 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.
50. Q.
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 higly 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
51. 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.
52. 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.
56. 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
58. 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
60. Q .
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
61. 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
62. Q.
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
63. 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)
64. Q.
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
65. 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.
66. Q.
• 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.
67. What is the initial
diagnostic test ?
a. Serology for CTD
b. VATS
c. BAL
d. TBB
e. Serum precipitating
Ab
68. Q.
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
69. Q.
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
70.
71. 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)
74. 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.
77. 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)]
78. 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.
79.
80. 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.
82. Q.
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
83. 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)
84. Q
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.
85. NSIP EITHER
Idiopathic iNSIP OR Identifiable cause
• Connective tissue diseases
• Drugs
• Environmental/occupational exposures
• Immunocompromised hosts
• Infections
• Resolving acute lung injury
88. LIP
•idiopathic LIP
•Identifiable cause or underlying disease
Connective tissue disorders – esp. Sjögren
Immunodeficiency
Infections
Drugs/toxins
-Radiologically with GGO ,Cysts
89. Q.
• 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
91. Q.
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
92. 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.
93. Q.
• 40 y old female , progressive dyspnea for 5 m
• Abnormal CT Fig 1
• TBB reveals adenocarcinoma received cisplatin and gemcitabine EGFR
mutation positive , so started gefitinib . Her symptoms improve
• CT repeated after 2 m of treatment with no new symptoms except sob
Fig 2
• Bronchoscopy done and reveals lymphocytes 30 % CD4/CD8 3/3
• TBB Fig 3 ,Based on results what do you suggest ?
a. Begin Ganciclovir
b. Start radiation
c. Start Antibiotics
d. Stop gefitinib
96. Q.
• 40 y old female , progressive dyspnea for 5 m
• Abnormal CT Fig 1
• TBB reveals adenocarcinoma received cisplatin and gemcitabine EGFR
mutation positive , so started gefitinib . Her symptoms improve
• CT repeated after 2 m of treatment Fig 2
• Bronchoscopy done and reveals lymphocytes 30 % CD4/CD8 3/3
• TBB Fig 3 ,Based on results what do you suggest ?
a. Begin Ganciclovir
b. Start radiation
c. Start Antibiotics
d. Stop gefitinib
97. 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
98. 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
99. 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
100. Q.
• 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
101. Q.
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
102. 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
104. PPFE
• Idiopathic PPFE OR with Chemotherapy • Hematopoietic stem cell
transplant • Recurrent infections • Familial interstitial pneumonia
• Pleural and subpleural fibrosis with septal elastosis, predominantly
upper lobes
• HRCT: bilateral irregular pleuroparenchymal thickening, more
marked in upper and middle
• Spontaneous pneumomediastinum or pneumothorax common
• no effective treatment identified
• generally poor, most progress
105. Q
All true about Familial Interstitial Pneumonia/ Familial
Pulmonary Fibrosis except?
a. >2 % relatives
b. ~10% of interstitial pneumonia / pulmonary fibrosis
c. ~25% of these familial cases have identifiable
mutations
d. HRCT and histopathologic pattern is variable
e. None of the above
106. 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
107. 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
109. Q.
• 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
• Dx?
• Best treatment ?
110. 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
111. Q.
• 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
114. 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.
118. Q
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.
119. 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)
120. Q.
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
121. 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
122. Q.
• 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
123. A.
• MIP ,MEP
• To assess muscle weakness ?myositis or phrenic n palsy
• Dx shrinking lung syndrome
• Tx steroid , theophylline , beta agonist and immunosuppression
124. Q.
• 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
125. 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
126. Q.
About causes of pulmonary granuloma ,Which is true ?
a. Sarcoidosis
b. Fungal Infection
c. HP
d. GPA (Wegener)
e. All of the above
128. Q.
A 40 year old woman is seen in the office complaining of shortness of
breath in climbing a flight of stairs, which has been progressive over
the past four months. Her physical examination is unremarkable. Her
chest X-rays show bilateral hilar adenopathy, with a mild diffuse
infiltrate in the lung fields.What is the most likely diagnosis:
A. Interstitial pulmonary fibrosis (IPF)
B. Sarcoidosis
C.Wegener’s granulomatosis
D.Asbestosis
129. Q.
40 y old man complaining of progressive SOB for last 1 y . No fever
of haemoptysis . Redness and rash in the leg & Bilateral crackles on
chest examination . CXR show unilateral hilar opacity and bilateral
Interstitial Infiltrate. His laboratory test reveals only hypercalcemia
.Which of the following is correct ?
A.This stage I
B. Hypercalcemia is absolute indication for treatment
C. Spontaneous remission does not occur
D. MTX can be used as an alternative to steroids
E.All are true
130. Sarcoidosis
•A multisystem disorder of unknown cause
characterized by the presence of noncaseating
epithelioid cell granulomas.
•No identifiable cause for granulomas
•No other identifiable disease that may present
similarly
(Consensus Statement. AJRCCM 1999)
132. Sarcoidosis – Indication of
Steroids
•Pulmonary
Symptomatic stage II or III with moderate to severe PFT
impairment or progression
•Extrapulmonary
Cardiac
Neurologic
Ocular (not responding to topical therapy)
• Hypercalcemia
133. Q.
Diagnostic criteria for sarcoidosis include all of
the following EXCEPT?
A. Presence of noncaseating granulomas
B. Compatible clinico-radiologic features
C. Exclusion of identifiable causes of granulomas
D. Response to corticosteroid therapy
134. A.
•D.
•Systemic glucocorticoids may be indicated in an
attempt to halt progression of pulmonary function
decline but not in supporting any differential diagnosis
135. Q.
• A 38-year-old non-smoking and otherwise healthy farmer
complains of increasing cough and dyspnoea on exertion of almost
3 years’ duration. Due to acute clinical worsening with dyspnoea
even at rest and hypoxaemia (SpO2 of 88% on room air), the
patient was admitted to ER.There were no clinical and laboratory
signs of infection. PFT was not feasible.
• A chest radiograph in the next slide .
• A bronchoscopy with BAL was performed. It revealed a
predominance of lymphocytes and only occasional eosinophils and
macrophages.
• Open-lung biopsy in the next slide.
136.
137. Q.
Which statement is true regarding this condition ?
A. Biopsy is not diagnostic
B.TBB is not helpful in such case
C. BAL reveals low CD4/CD8 ratio (<1) which is a negative predictive
value for this disease
D.ACE level is diagnostic in stage I of the disease
e. None of the above
138. A.
• The case is typical of sarcoidosis in many respects.
• Diagnosis is usually made by a biopsy.
• Diagnostic yield of a transbronchial biopsy exceeds 80%.
• BAL may be helpful as well but high CD4/CD8 ratios (>4) are only
specific for sarcoidosis if combined with a transbronchial biopsy
that supports the diagnosis; a low CD4/CD8 ratio (<1) has a very
high negative predictive value for sarcoidosis.
• Serum markers such as ACE are sometimes used in the initial
evaluation and follow-up as a marker of activity but are not
diagnostic for the disease.
139. What is the Diagnosis?
LAM
Bronchiectasis
E
EG
140. 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
141. 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)
142. Q.
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
143.
144. 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
146. Q.
• 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
147. 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
148. 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
149. What is the name of this radiological
findings?
150. 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
152. 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
153. Q.
A 40-year-old woman is complaining of shortness of breath, dry cough, and
fever 39.4°C for the last 2 weeks. She is a social smoker and has recently
starting using the hot tub daily. She has used her hot tub last year without
any symptoms. Her husband and friends would join her in the hot tub they
claim to have no symptoms. She also owns some birds and works as a
chemist.
On physical examination, it is unremarkable except for some fine crackles in
both lung fields.Chest radiograph is normal and high-resolution
computerized tomography shows patchy ground glass opacities with ill-
defined nodules. Pulmonary function tests shows mild restriction with mild
gas transfer defect.
what is your diagnosis?
a. LIP
b. Acute hypersensitivity pneumonitis
c. Community-acquired pneumonia
d. Shrinking lung syndrome
154. Hypersensitivity pneumonitis
• Only 5% to 15% of individuals exposed repeatedly to an inhaled
antigen, usually <5 um in diameter, develop the disease.
• Genetics and environmental risk factors, such as concentration,
duration, frequency, particle size, solubility and variability,
influence the disease course.
• Appears to be less prevalent in smokers, partly due to a reduced
immunologic response to the antigen, but acute exacerbations in
smokers generally carry a poorer prognosis.
• Not a uniform disease.
155.
156. Q.
To which of the following patients is
the chest CT shown most likely to
belong?
a.79-year-old, non smoking female
with metastatic breast cancer
b.34-year-old, female smoker with
Langerhans’ cell histiocytosis
c.56-year-old, male smoker with
pneumococcal pneumonia
d.55-year-old, male bird-fancier with
hypersensitivity pneumonitis
e.63-year-old male with congestive
heart failure
157. Q.
A 36-year-old woman develops a mild dry cough and shortness of breath
during exercise. Pulmonary function testing shows FEV1 85% predicted, FVC
85% predicted,TLC 87% predicted andTLCO 65% predicted.A chest
radiograph and two HRCT images of the lung are shown below.
A bronchoalveolar lavage cell count of 650 per μL was found, with 84%
lymphocytes (CD4/ CD8 ratio 0.1), 4% eosinophils and 2% basophils. Based
on these findings, a differential diagnosis was made.
What is your next step in the management of this patient?
a. Search for precipitating IgG antibodies against antigens in the patient’s
serum.
b. Perform transbronchial lung biopsy.
c.Take a meticulous medical history of environmental exposures.
d. Prescribe inhaled corticosteroids.
e. Perform video-assisted thoracoscopic surgical lung biopsy.
158. • c.Take a meticulous medical history of environmental exposures.
• Diagnostic criteria for HP
1. History of appropriate exposure
2. Presence of serum precipitins), although the latter may seldom
be found in clinical practice due to low sensitivity.
3. Chest CT may reveal reticular, nodular or ground-glass opacities.
4. Pulmonary function tests may reveal a restrictive, obstructive or
mixed pattern along with a reducedTLCO.
5. Bronchoalveolar lavage usually shows lymphocytosis with a low
CD4/CD8 ratio.
159. Q.
A 33-year-old man presents with minor haemoptysis, fatigue, weight loss
and recurrent nasal bleeding.The chest radiograph discloses multiple dense
infiltrates, some with cavitation, and the serum cytoplasmic anti-neutrophil
cytoplasmic antibody (cANCA) test is positive with elevated anti-proteinase
3 (PR3) IgG.
Which of the following initial treatments is most appropriate for the
suspected disease?
a.Infiximab
b.Methotrexate
c.Azathioprine and prednisone
d.Cyclophosphamide and prednisone
e.Mycophenolate and prednisone
160. A. d
• This is a case of granulomatosis with polyangiitis.
• While glucocorticoid therapy alone extends the 5-month mean
survival of untreated cANCA-related vasculitis by only a few
months, the addition of immunosuppressive agents
(cyclophosphamide) to glucocorticoids is highly beneficial.
• Only localised or early systemic disease without the threat of vital
organ involvement may be treated with methotrexate and
glucocorticoids, based on the dosing regimen used in the NORAM
(Non renalWegener’s GranulomatosisTreated Alternatively with
Methotrexate) study, as this appears as effective as
cyclophosphamide and avoids the toxicity of the latter.
• TNF inhibition with infliximab may have a role in refractory disease
but not in routine induction regimens.