This document discusses chronic obstructive pulmonary disease (COPD). It defines COPD as a chronic, progressive lung disorder characterized by limited airflow. The document covers the pathogenesis of COPD, which involves inflammation and damage to lung tissue from cigarette smoke exposure. This leads to emphysema and obstruction of small airways. The clinical presentation of COPD typically includes cough, sputum production, and shortness of breath with exertion. Physical examination may reveal prolonged expiration in severe cases. The major risk factor for COPD is cigarette smoking.
This document provides information on a 70-year-old male patient admitted with chronic obstructive airway disease (COAD). It outlines the patient's history, examination findings, treatment and nursing care plan. The nursing diagnoses identified include ineffective breathing, impaired gas exchange, alteration in bowel habit, alteration in activities of daily living, risk for infection, risk for nutritional deficiencies, and knowledge deficit.
COPD is a chronic lung disease characterized by obstructed airflow caused by conditions like emphysema and chronic bronchitis. Risk factors include cigarette smoking, genetics, and air pollution. Symptoms include excessive cough, shortness of breath, wheezing, and fatigue. Diagnosis involves assessing symptoms, examining lungs, and tests like chest X-rays, pulmonary function tests, and blood gas analysis. Treatment focuses on preventing further lung damage by quitting smoking, using bronchodilators and steroids, antibiotics for infections, and exercises to clear airways and strengthen breathing. Complications can be respiratory failure, pneumonia, and depression if not properly managed.
Restrictive lung diseases (interstitial lung diseases)
Histological Structure of Alveoli
The wall of the alveoli is formed by a thin sheet of tissue separating two neighbouring alveoli.
This sheet is formed by epithelial cells and intervening connective tissue.
Collagenous , reticular and elastic fibres are present.
Between the connective tissue fibres we find a dense, anastomosing network of pulmonary capillaries. The wall of the capillaries are in direct contact with the epithelial lining of the alveoli.
Neighbouring alveoli may be connected to each other by small alveolar pores (pores of Kohn).
The epithelium of the alveoli is formed by two cell types:
Alveolar type I cells (small alveolar cells or type I pneumocytes) are extremely flattened and form the bulk (95%) of the surface of the alveolar walls.
Alveolar type II cells (large alveolar cells or type II pneumocytes) are irregularly (sometimes cuboidal) shaped.
They form small bulges on the alveolar walls.
Type II alveolar cells contain are large number of granules called cytosomes (or multilamellar bodies), which consist of precursors to pulmonary surfactant (the mixture of phospholipids which keep surface tension in the alveoli low) .
Cilia are absent from the alveolar epithelium and cannot help to remove particulate matter which continuously enters the alveoli with the inspired air. Alveolar macrophages take care of this job. They migrate freely over the alveolar epithelium and ingest particulate matter.
FUNCTIONS OF PULMONARY CELLS
Type I pneumocytes
Permeable to Oxygen and CO2, do not divide
Type II pneumocytes
Reserve cells
secrete pulmonary surfactant
Serve as repair cells
Alveolar macrophages
Phagocytosis
Pores of Kohn (allow passage of Macrophages)
This document discusses risk factors, prevalence, symptoms, and management of chronic obstructive pulmonary disease (COPD) and asthma. It provides statistics on the increasing mortality rates of COPD compared to declines in other causes of death. Studies from Pakistan show the frequency of asthma, allergic rhinitis, and their relationship to socioeconomic status. The document examines the pathology and inflammatory processes of COPD compared to asthma and how these differences impact clinical presentation and therapy.
Chronic Obstructive Pulmonary Disease (COPD) is an umbrella term used to describe progressive lung diseases including emphysema, chronic bronchitis, and refractory (non-reversible) asthma. This disease is characterized by increasing breathlessness
This document provides information on a 70-year-old male patient admitted with chronic obstructive airway disease (COAD). It outlines the patient's history, examination findings, treatment and nursing care plan. The nursing diagnoses identified include ineffective breathing, impaired gas exchange, alteration in bowel habit, alteration in activities of daily living, risk for infection, risk for nutritional deficiencies, and knowledge deficit.
COPD is a chronic lung disease characterized by obstructed airflow caused by conditions like emphysema and chronic bronchitis. Risk factors include cigarette smoking, genetics, and air pollution. Symptoms include excessive cough, shortness of breath, wheezing, and fatigue. Diagnosis involves assessing symptoms, examining lungs, and tests like chest X-rays, pulmonary function tests, and blood gas analysis. Treatment focuses on preventing further lung damage by quitting smoking, using bronchodilators and steroids, antibiotics for infections, and exercises to clear airways and strengthen breathing. Complications can be respiratory failure, pneumonia, and depression if not properly managed.
Restrictive lung diseases (interstitial lung diseases)
Histological Structure of Alveoli
The wall of the alveoli is formed by a thin sheet of tissue separating two neighbouring alveoli.
This sheet is formed by epithelial cells and intervening connective tissue.
Collagenous , reticular and elastic fibres are present.
Between the connective tissue fibres we find a dense, anastomosing network of pulmonary capillaries. The wall of the capillaries are in direct contact with the epithelial lining of the alveoli.
Neighbouring alveoli may be connected to each other by small alveolar pores (pores of Kohn).
The epithelium of the alveoli is formed by two cell types:
Alveolar type I cells (small alveolar cells or type I pneumocytes) are extremely flattened and form the bulk (95%) of the surface of the alveolar walls.
Alveolar type II cells (large alveolar cells or type II pneumocytes) are irregularly (sometimes cuboidal) shaped.
They form small bulges on the alveolar walls.
Type II alveolar cells contain are large number of granules called cytosomes (or multilamellar bodies), which consist of precursors to pulmonary surfactant (the mixture of phospholipids which keep surface tension in the alveoli low) .
Cilia are absent from the alveolar epithelium and cannot help to remove particulate matter which continuously enters the alveoli with the inspired air. Alveolar macrophages take care of this job. They migrate freely over the alveolar epithelium and ingest particulate matter.
FUNCTIONS OF PULMONARY CELLS
Type I pneumocytes
Permeable to Oxygen and CO2, do not divide
Type II pneumocytes
Reserve cells
secrete pulmonary surfactant
Serve as repair cells
Alveolar macrophages
Phagocytosis
Pores of Kohn (allow passage of Macrophages)
This document discusses risk factors, prevalence, symptoms, and management of chronic obstructive pulmonary disease (COPD) and asthma. It provides statistics on the increasing mortality rates of COPD compared to declines in other causes of death. Studies from Pakistan show the frequency of asthma, allergic rhinitis, and their relationship to socioeconomic status. The document examines the pathology and inflammatory processes of COPD compared to asthma and how these differences impact clinical presentation and therapy.
Chronic Obstructive Pulmonary Disease (COPD) is an umbrella term used to describe progressive lung diseases including emphysema, chronic bronchitis, and refractory (non-reversible) asthma. This disease is characterized by increasing breathlessness
The document discusses several disorders of the pleura and lungs, including pleural effusions, pneumothorax, and mesothelioma. Pleural effusions can be transudative or exudative depending on disturbances to Starling forces or increased vessel permeability. Pneumothorax can be spontaneous due to bleb rupture or tension pneumothorax from a flap-like pleural tear. Mesothelioma is a malignant tumor of the pleura associated with asbestos exposure that encases the lung.
Obstructive diseases : Chr.by
Obstruction to airflow out of the lungs
Due to partial or complete obstruction in airway.
Increase in lung compliance and
Decrease in lung elasticity.
Restrictive diseases : Chr by
reduced expansion of lung parenchyma with problems in getting air in the lungs.
Lung compliance is decreased
Elasticity is increased: once air is in the lungs it comes out rapidly on expiration.
Etiopathogenesis and pharmacotherapy of COPD
a. the pathophysiology of selected disease states and the rationale for drug therapy;
b. the therapeutic approach to management of these diseases;
c. the controversies in drug therapy;
d. the importance of preparation of individualised therapeutic plans based on diagnosis;
e. needs to identify the patient-specific parameters relevant in initiating drug therapy,
and monitoring therapy (including alternatives, time-course of clinical and laboratory
indices of therapeutic response and adverse effects);
f. describe the pathophysiology of selected disease states and explain the rationale for
drug therapy;
g. summarise the therapeutic approach to management of these diseases including
reference to the latest available evidence;
h. discuss the controversies in drug therapy;
i. discuss the preparation of individualised therapeutic plans based on diagnosis; and
j. identify the patient-specific parameters relevant in initiating drug therapy, and
monitoring therapy (including alternatives, time-course of clinical and laboratory
indices of therapeutic response and adverse effects).
Asthma
A chronic relapsing inflammatory disorder characterized by:
Hyper-reactivity of the respiratory tree to various stimuli leading to
Reversible airway obstruction
Obstruction produced by combination of :
Constriction of bronchial musculature (bronchospasm)
Mucosal inflammation (edema)
Excessive secretion of mucus.
Clinically Manifested by :
Difficulty in breathing (Dyspnea)
Wheeze (a soft whistling sound during expiration)
Difficulty in expiration.
Asthma is:
Episodic and reversible airway disease
Primarily targets the bronchi and terminal bronchioles
MC chronic respiratory disease in children
Two types:
Extrinsic asthma (allergic, atopic)
Intrinsic asthma (non-allergic asthma or idiosyncratic asthma)
Obstructive lung diseases such as chronic bronchitis, emphysema and asthma are characterized by airflow limitation caused by inflammation and obstruction of the airways. The main risk factor is smoking. Signs and symptoms include shortness of breath, cough, wheezing and excess mucus production. Treatment focuses on reducing symptoms, improving lung function and preventing exacerbations through medications, breathing exercises, smoking cessation and pulmonary rehabilitation. Nurses play an important role in patient education, monitoring for complications and promoting lung expansion through airway clearance techniques.
COPD refers to chronic bronchitis and emphysema, two commonly co-existing lung diseases where the airways become narrowed leading to limited airflow. The main causes are smoking, occupational exposures, air pollution, and genetic conditions. Symptoms include chronic cough, sputum production, wheezing, chest tightness, and shortness of breath. Management includes bronchodilators, corticosteroids, oxygen therapy, promoting exercise, and controlling complications to improve lung function and general health.
This document provides an overview of chronic obstructive pulmonary disease (COPD), including its definition, causes, symptoms, diagnosis and treatment. COPD is a progressive lung disease characterized by limited airflow. The two main types are chronic bronchitis and emphysema. Smoking is the leading cause of COPD. Symptoms include cough, shortness of breath, wheezing and frequent respiratory infections. Diagnosis involves medical history, physical exam, lung function tests and chest imaging. Treatment focuses on medications, oxygen therapy and managing symptoms. Quitting smoking can prevent further progression of COPD.
Chronic obstructive pulmonary disease (COPD) is characterized by irreversible airway obstruction and lung impairment. The two most common conditions are chronic bronchitis and emphysema. Chronic bronchitis involves excessive mucus production due to smoking-induced airway inflammation. Emphysema is the abnormal enlargement of airspaces due to an imbalance between the protease elastase and its inhibitor. Symptoms include a productive cough, shortness of breath, and signs of pulmonary hypertension. Treatment involves smoking cessation, oxygen therapy, bronchodilators, steroids, and antibiotics for infections.
COPD, also known as chronic obstructive pulmonary disease, is a slowly progressive lung disease characterized by chronic obstruction of lung airflow that is not fully reversible. It involves conditions such as chronic bronchitis and emphysema. The main causes of COPD are tobacco smoke and air pollution. Symptoms include chronic cough, sputum production, wheezing, shortness of breath, and fatigue. Management involves smoking cessation, bronchodilators, pulmonary rehabilitation, exercise, and lifestyle changes. Nursing care focuses on techniques to improve breathing and clear airways, administering medications, nutrition, changing positions, and health education.
Chronic obstructive pulmonary disease (COPD) refers to two lung diseases, chronic bronchitis and emphysema, that are typically caused by smoking and result in limited airflow. The document discusses the definition, causes, symptoms, diagnosis, and management of COPD. It notes that COPD is the 4th leading cause of death and involves inflammation and narrowing of the airways leading to shortness of breath. Treatment focuses on improving ventilation, removing secretions, managing complications, and improving overall health.
Chronic obstructive pulmonary disease (COPD) is a chronic respiratory disease in horses characterized by decreased work performance, chronic coughing, abnormal lung sounds, and cardiac dysfunction. Pathologically, there is varying degrees of bronchiolitis and pulmonary emphysema. COPD is caused by a hypersensitivity reaction to allergens like mold spores found in hay and straw. Clinically, affected horses cough, have increased respiratory rates, and abdominal breathing. Treatment focuses on reducing allergen exposure, using corticosteroids to reduce inflammation, bronchodilators for temporary relief, and antibiotics for secondary infections. There is no cure for COPD and treatment aims to control symptoms palliatively.
Chronic obstructive pulmonary disease (COPD) is characterized by progressive airflow limitation that is not fully reversible. It includes chronic bronchitis and emphysema. COPD is caused by noxious particles or gases like cigarette smoke that trigger an inflammatory response in the lungs. Symptoms include chronic cough, sputum production, shortness of breath, and wheezing. Diagnosis involves spirometry to detect airflow obstruction and chest imaging to rule out other conditions. Treatment focuses on smoking cessation and medications like bronchodilators and corticosteroids to relieve symptoms and prevent exacerbations.
This document discusses obstructive pulmonary disorders including asthma and chronic obstructive pulmonary disease (COPD). It covers the causes of these conditions such as smoking, occupational exposures, air pollution, and genetics. The pathophysiology of COPD involves damage to airways and air sacs causing airflow limitation. Symptoms include coughing, wheezing and shortness of breath. Management involves medical treatment to improve ventilation, oxygen therapy, and surgery in some cases. Nursing care focuses on managing symptoms and preventing complications like infection.
1) Emphysema, chronic bronchitis, asthma, and bronchiectasis are obstructive lung diseases. Emphysema and chronic bronchitis are often grouped together as chronic obstructive pulmonary disease (COPD) since most patients have features of both, likely due to cigarette smoking.
2) COPD is a major public health problem and the fifth leading cause of death worldwide. Heavy cigarette smoking and environmental pollutants are significant risk factors.
3) Emphysema is characterized by irreversible destruction of lung tissue and airspace enlargement. It is classified according to anatomical location within the lung lobe. Chronic bronchitis involves inflammation and mucus buildup in the bronchi.
This document discusses COPD (chronic obstructive pulmonary disease), including its definition, symptoms, pathology, diagnosis, management, and treatment. Some key points include:
- COPD is characterized by persistent respiratory symptoms and airflow limitation usually caused by significant exposure to noxious particles or gases. It involves chronic inflammation in the airways, lung parenchyma, and pulmonary vasculature.
- Diagnosis is based on spirometry showing airflow limitation that is not fully reversible. Severity is classified based on lung function tests and exacerbation history.
- Management focuses on smoking cessation, vaccinations, pulmonary rehabilitation, pharmacologic therapy including bronchodilators and inhaled corticosteroids,
This document discusses chronic bronchitis, which is an obstructive lung disease characterized by a persistent productive cough for at least three months in consecutive years. Chronic bronchitis is often caused by cigarette smoking and air pollution and is clinically grouped with emphysema as chronic obstructive pulmonary disease (COPD). The document describes the clinical features, pathogenesis, gross and microscopic pathology, cytology, differential diagnosis, and management of chronic bronchitis. Chronic bronchitis involves inflammation and mucus hypersecretion in the large airways that can lead to bronchial dilation over time.
This document provides an overview of pulmonary aspergillosis, caused by inhalation of the fungus Aspergillus. It discusses the main types including aspergilloma (fungal ball in a pre-existing lung cavity), allergic bronchopulmonary aspergillosis (ABPA, an immune response in people with asthma or cystic fibrosis), and invasive aspergillosis which occurs in immunocompromised people. The pathology, risk factors, clinical features, diagnosis and treatment are described for each type. ABPA is characterized by severe asthma attacks, mucus plugs and bronchial obstruction visible on chest imaging.
Pathology basic introduction to pathology of common lung diseases for underg...Sufia Husain
The document provides an overview of common lung diseases for undergraduate dental students and nurses. It discusses the pathology of diseases such as bronchial asthma, chronic bronchitis, emphysema, bronchiectasis, pneumonia, tuberculosis, and lung tumors. For bronchial asthma, it describes the characteristic airway inflammation and reversible airway constriction. It notes that chronic bronchitis and emphysema often co-exist and are commonly caused by cigarette smoking. Emphysema involves the permanent enlargement of airspaces due to alveolar wall destruction. Tuberculosis is caused by the bacterium Mycobacterium tuberculosis and forms characteristic granulomas. Lung tumors are often carcinomas, with non-small
COPD is a chronic lung disease characterized by airflow limitation and breathing-related problems. It encompasses chronic bronchitis and emphysema. The main risk factor is cigarette smoking, which causes an inflammatory response and destruction of lung tissue over time. Symptoms include cough, sputum production, shortness of breath, and wheezing. Diagnosis involves pulmonary function tests and chest imaging. Treatment focuses on smoking cessation, bronchodilators, corticosteroids, oxygen therapy, breathing exercises, and managing exacerbations.
The document discusses several disorders of the pleura and lungs, including pleural effusions, pneumothorax, and mesothelioma. Pleural effusions can be transudative or exudative depending on disturbances to Starling forces or increased vessel permeability. Pneumothorax can be spontaneous due to bleb rupture or tension pneumothorax from a flap-like pleural tear. Mesothelioma is a malignant tumor of the pleura associated with asbestos exposure that encases the lung.
Obstructive diseases : Chr.by
Obstruction to airflow out of the lungs
Due to partial or complete obstruction in airway.
Increase in lung compliance and
Decrease in lung elasticity.
Restrictive diseases : Chr by
reduced expansion of lung parenchyma with problems in getting air in the lungs.
Lung compliance is decreased
Elasticity is increased: once air is in the lungs it comes out rapidly on expiration.
Etiopathogenesis and pharmacotherapy of COPD
a. the pathophysiology of selected disease states and the rationale for drug therapy;
b. the therapeutic approach to management of these diseases;
c. the controversies in drug therapy;
d. the importance of preparation of individualised therapeutic plans based on diagnosis;
e. needs to identify the patient-specific parameters relevant in initiating drug therapy,
and monitoring therapy (including alternatives, time-course of clinical and laboratory
indices of therapeutic response and adverse effects);
f. describe the pathophysiology of selected disease states and explain the rationale for
drug therapy;
g. summarise the therapeutic approach to management of these diseases including
reference to the latest available evidence;
h. discuss the controversies in drug therapy;
i. discuss the preparation of individualised therapeutic plans based on diagnosis; and
j. identify the patient-specific parameters relevant in initiating drug therapy, and
monitoring therapy (including alternatives, time-course of clinical and laboratory
indices of therapeutic response and adverse effects).
Asthma
A chronic relapsing inflammatory disorder characterized by:
Hyper-reactivity of the respiratory tree to various stimuli leading to
Reversible airway obstruction
Obstruction produced by combination of :
Constriction of bronchial musculature (bronchospasm)
Mucosal inflammation (edema)
Excessive secretion of mucus.
Clinically Manifested by :
Difficulty in breathing (Dyspnea)
Wheeze (a soft whistling sound during expiration)
Difficulty in expiration.
Asthma is:
Episodic and reversible airway disease
Primarily targets the bronchi and terminal bronchioles
MC chronic respiratory disease in children
Two types:
Extrinsic asthma (allergic, atopic)
Intrinsic asthma (non-allergic asthma or idiosyncratic asthma)
Obstructive lung diseases such as chronic bronchitis, emphysema and asthma are characterized by airflow limitation caused by inflammation and obstruction of the airways. The main risk factor is smoking. Signs and symptoms include shortness of breath, cough, wheezing and excess mucus production. Treatment focuses on reducing symptoms, improving lung function and preventing exacerbations through medications, breathing exercises, smoking cessation and pulmonary rehabilitation. Nurses play an important role in patient education, monitoring for complications and promoting lung expansion through airway clearance techniques.
COPD refers to chronic bronchitis and emphysema, two commonly co-existing lung diseases where the airways become narrowed leading to limited airflow. The main causes are smoking, occupational exposures, air pollution, and genetic conditions. Symptoms include chronic cough, sputum production, wheezing, chest tightness, and shortness of breath. Management includes bronchodilators, corticosteroids, oxygen therapy, promoting exercise, and controlling complications to improve lung function and general health.
This document provides an overview of chronic obstructive pulmonary disease (COPD), including its definition, causes, symptoms, diagnosis and treatment. COPD is a progressive lung disease characterized by limited airflow. The two main types are chronic bronchitis and emphysema. Smoking is the leading cause of COPD. Symptoms include cough, shortness of breath, wheezing and frequent respiratory infections. Diagnosis involves medical history, physical exam, lung function tests and chest imaging. Treatment focuses on medications, oxygen therapy and managing symptoms. Quitting smoking can prevent further progression of COPD.
Chronic obstructive pulmonary disease (COPD) is characterized by irreversible airway obstruction and lung impairment. The two most common conditions are chronic bronchitis and emphysema. Chronic bronchitis involves excessive mucus production due to smoking-induced airway inflammation. Emphysema is the abnormal enlargement of airspaces due to an imbalance between the protease elastase and its inhibitor. Symptoms include a productive cough, shortness of breath, and signs of pulmonary hypertension. Treatment involves smoking cessation, oxygen therapy, bronchodilators, steroids, and antibiotics for infections.
COPD, also known as chronic obstructive pulmonary disease, is a slowly progressive lung disease characterized by chronic obstruction of lung airflow that is not fully reversible. It involves conditions such as chronic bronchitis and emphysema. The main causes of COPD are tobacco smoke and air pollution. Symptoms include chronic cough, sputum production, wheezing, shortness of breath, and fatigue. Management involves smoking cessation, bronchodilators, pulmonary rehabilitation, exercise, and lifestyle changes. Nursing care focuses on techniques to improve breathing and clear airways, administering medications, nutrition, changing positions, and health education.
Chronic obstructive pulmonary disease (COPD) refers to two lung diseases, chronic bronchitis and emphysema, that are typically caused by smoking and result in limited airflow. The document discusses the definition, causes, symptoms, diagnosis, and management of COPD. It notes that COPD is the 4th leading cause of death and involves inflammation and narrowing of the airways leading to shortness of breath. Treatment focuses on improving ventilation, removing secretions, managing complications, and improving overall health.
Chronic obstructive pulmonary disease (COPD) is a chronic respiratory disease in horses characterized by decreased work performance, chronic coughing, abnormal lung sounds, and cardiac dysfunction. Pathologically, there is varying degrees of bronchiolitis and pulmonary emphysema. COPD is caused by a hypersensitivity reaction to allergens like mold spores found in hay and straw. Clinically, affected horses cough, have increased respiratory rates, and abdominal breathing. Treatment focuses on reducing allergen exposure, using corticosteroids to reduce inflammation, bronchodilators for temporary relief, and antibiotics for secondary infections. There is no cure for COPD and treatment aims to control symptoms palliatively.
Chronic obstructive pulmonary disease (COPD) is characterized by progressive airflow limitation that is not fully reversible. It includes chronic bronchitis and emphysema. COPD is caused by noxious particles or gases like cigarette smoke that trigger an inflammatory response in the lungs. Symptoms include chronic cough, sputum production, shortness of breath, and wheezing. Diagnosis involves spirometry to detect airflow obstruction and chest imaging to rule out other conditions. Treatment focuses on smoking cessation and medications like bronchodilators and corticosteroids to relieve symptoms and prevent exacerbations.
This document discusses obstructive pulmonary disorders including asthma and chronic obstructive pulmonary disease (COPD). It covers the causes of these conditions such as smoking, occupational exposures, air pollution, and genetics. The pathophysiology of COPD involves damage to airways and air sacs causing airflow limitation. Symptoms include coughing, wheezing and shortness of breath. Management involves medical treatment to improve ventilation, oxygen therapy, and surgery in some cases. Nursing care focuses on managing symptoms and preventing complications like infection.
1) Emphysema, chronic bronchitis, asthma, and bronchiectasis are obstructive lung diseases. Emphysema and chronic bronchitis are often grouped together as chronic obstructive pulmonary disease (COPD) since most patients have features of both, likely due to cigarette smoking.
2) COPD is a major public health problem and the fifth leading cause of death worldwide. Heavy cigarette smoking and environmental pollutants are significant risk factors.
3) Emphysema is characterized by irreversible destruction of lung tissue and airspace enlargement. It is classified according to anatomical location within the lung lobe. Chronic bronchitis involves inflammation and mucus buildup in the bronchi.
This document discusses COPD (chronic obstructive pulmonary disease), including its definition, symptoms, pathology, diagnosis, management, and treatment. Some key points include:
- COPD is characterized by persistent respiratory symptoms and airflow limitation usually caused by significant exposure to noxious particles or gases. It involves chronic inflammation in the airways, lung parenchyma, and pulmonary vasculature.
- Diagnosis is based on spirometry showing airflow limitation that is not fully reversible. Severity is classified based on lung function tests and exacerbation history.
- Management focuses on smoking cessation, vaccinations, pulmonary rehabilitation, pharmacologic therapy including bronchodilators and inhaled corticosteroids,
This document discusses chronic bronchitis, which is an obstructive lung disease characterized by a persistent productive cough for at least three months in consecutive years. Chronic bronchitis is often caused by cigarette smoking and air pollution and is clinically grouped with emphysema as chronic obstructive pulmonary disease (COPD). The document describes the clinical features, pathogenesis, gross and microscopic pathology, cytology, differential diagnosis, and management of chronic bronchitis. Chronic bronchitis involves inflammation and mucus hypersecretion in the large airways that can lead to bronchial dilation over time.
This document provides an overview of pulmonary aspergillosis, caused by inhalation of the fungus Aspergillus. It discusses the main types including aspergilloma (fungal ball in a pre-existing lung cavity), allergic bronchopulmonary aspergillosis (ABPA, an immune response in people with asthma or cystic fibrosis), and invasive aspergillosis which occurs in immunocompromised people. The pathology, risk factors, clinical features, diagnosis and treatment are described for each type. ABPA is characterized by severe asthma attacks, mucus plugs and bronchial obstruction visible on chest imaging.
Pathology basic introduction to pathology of common lung diseases for underg...Sufia Husain
The document provides an overview of common lung diseases for undergraduate dental students and nurses. It discusses the pathology of diseases such as bronchial asthma, chronic bronchitis, emphysema, bronchiectasis, pneumonia, tuberculosis, and lung tumors. For bronchial asthma, it describes the characteristic airway inflammation and reversible airway constriction. It notes that chronic bronchitis and emphysema often co-exist and are commonly caused by cigarette smoking. Emphysema involves the permanent enlargement of airspaces due to alveolar wall destruction. Tuberculosis is caused by the bacterium Mycobacterium tuberculosis and forms characteristic granulomas. Lung tumors are often carcinomas, with non-small
COPD is a chronic lung disease characterized by airflow limitation and breathing-related problems. It encompasses chronic bronchitis and emphysema. The main risk factor is cigarette smoking, which causes an inflammatory response and destruction of lung tissue over time. Symptoms include cough, sputum production, shortness of breath, and wheezing. Diagnosis involves pulmonary function tests and chest imaging. Treatment focuses on smoking cessation, bronchodilators, corticosteroids, oxygen therapy, breathing exercises, and managing exacerbations.
Chronic obstructive pulmonary disease (COPD) refers to two lung diseases, chronic bronchitis and emphysema, that are commonly found together. In COPD, less air flows in and out of the airways due to damage to the airways and air sacs. The main risk factor is tobacco smoking. Symptoms include shortness of breath, cough, and sputum production. Treatment focuses on smoking cessation and medications to improve breathing.
The document discusses COPD and its comorbidities. It defines COPD as a disease characterized by persistent airflow limitation associated with an inflammatory response in the lungs to noxious particles. COPD has several risk factors and a variable natural history. The key pathological changes occur in the central and peripheral airways, lung parenchyma, and pulmonary vasculature. This leads to several physiological abnormalities including airflow limitation, gas exchange impairment, pulmonary hypertension, and systemic effects. Diagnosis requires symptoms, risk factor exposure, and confirmation of persistent airflow limitation on spirometry. Assessment aims to determine disease severity and impact on health status and risk of future events. Comorbidities commonly occur and should be actively managed.
Chronic obstructive pulmonary disease (COPD) is characterized by persistent airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and lungs. The major risk factors are cigarette smoking and exposure to occupational dusts and chemicals. Clinically, COPD most commonly presents with exertional dyspnea, chronic cough, and sputum production that typically worsens over time. Pathologically, COPD involves chronic inflammation in the airways and lung parenchyma, along with the destruction of lung tissue seen in emphysema.
CHRONIC OBSTRUCTIVE PULMONARY DISEASE BY AKRAM KHANAkram Khan
This document provides information on Chronic Obstructive Pulmonary Disease (COPD). It defines COPD as a disease characterized by airflow obstruction caused by chronic bronchitis or emphysema. The main causes are cigarette smoking, infections, and occupational exposures. Symptoms include cough, sputum production, and dyspnea. Diagnosis involves spirometry and chest imaging. Management focuses on smoking cessation, bronchodilators, corticosteroids, oxygen therapy, lung surgery for severe cases, and dietary modifications. Nursing care includes assessing respiratory status, teaching breathing techniques and airway clearance, administering medications, and addressing nutrition.
COPD is characterized by airflow limitation caused by chronic inflammation in the lungs. It affects over 80 million people worldwide and is predicted to become the third leading cause of death by 2020. The main risk factors are tobacco smoke and indoor air pollution. Symptoms include cough, sputum production and exertional dyspnea. Diagnosis involves lung function tests showing reduced FEV1 and FEV1/FVC ratio. Management focuses on smoking cessation and bronchodilators.
Chronic obstructive pulmonary disease (COPD) is characterized by airflow limitation caused by emphysema and chronic bronchitis. The Global Initiative for Chronic Obstructive Lung Disease defines COPD as usually progressive airflow limitation associated with lung inflammation from noxious gases. Spirometry showing irreversible or partially reversible airflow limitation is used to diagnose COPD. Major risk factors include cigarette smoking and occupational exposures. As COPD progresses, patients experience symptoms like cough and dyspnea, and examination may reveal prolonged expiration and barrel chest from lung hyperinflation.
This document provides an overview of chronic obstructive pulmonary disease (COPD) and acute exacerbations of COPD. It discusses the definition and types of COPD, risk factors like cigarette smoking, pathophysiology, clinical features, diagnostic tests, management, and complications. Acute exacerbations are characterized by increased symptoms, worsening lung function, and deteriorating health status, which can lead to respiratory failure if not properly treated. Management of exacerbations focuses on oxygen supplementation, bronchodilators, corticosteroids, antibiotics, hydration, and monitoring for complications.
Chronic obstructive pulmonary disease (COPD) refers to chronic bronchitis and emphysema, diseases where the airways become narrowed over time due to damage from cigarette smoke or other noxious particles. The main symptoms are shortness of breath, cough, and sputum production. A diagnosis is made through pulmonary function tests showing airflow obstruction. Treatment focuses on smoking cessation and medications to relieve symptoms and prevent exacerbations.
This document provides an overview of chronic obstructive pulmonary disease (COPD). It defines COPD as a progressive lung disease characterized by airflow limitation. The document discusses the causes of COPD, including cigarette smoking which is the primary cause in over 90% of patients. It also examines the pathophysiology of the two main types of COPD - chronic bronchitis and emphysema. The clinical evaluation and diagnostic tests used to diagnose COPD are outlined, including the use of spirometry to confirm airflow limitation. Treatment objectives for COPD and its management are briefly mentioned.
Chronic obstructive pulmonary disease (COPD) is a progressive lung disease characterized by persistent respiratory symptoms and limited airflow. The document defines COPD and its components of chronic bronchitis and emphysema. It describes the respiratory anatomy and physiology. Risk factors for COPD include cigarette smoking, occupational exposures, and genetic factors. The diagnosis is made through spirometry and imaging. Treatment focuses on smoking cessation, bronchodilators, pulmonary rehabilitation, and managing exacerbations.
Atelectasis, restrictive and obstructive pulmonary disease.pptxTeshaleTekle1
Atelectasis is the collapse of lung tissue caused by inadequate expansion of air spaces. It is classified into three forms: resorption, compression, and contraction atelectasis. Resorption occurs when an obstruction prevents air from reaching distal airways, causing absorption of existing air and alveolar collapse. Compression results from fluid, blood, or air accumulation in the pleural cavity compressing the lung. Contraction occurs when fibrosis affects lung or pleural expansion. Chronic obstructive pulmonary disease (COPD) includes emphysema and chronic bronchitis. Emphysema is characterized by destruction of alveolar walls leading to enlarged air spaces, while chronic bronchitis involves inflammation of the large airways and
This document provides an overview of COPD and emphysema pathogenesis. It discusses:
1. The case of a 55-year-old male smoker presenting with dyspnea and a history of 20 pack-years of smoking.
2. The pathogenesis of emphysema, which involves chronic smoke exposure leading to lung inflammation and damage, structural cell death, and ineffective repair of lung tissue.
3. Definitions and classifications of COPD, emphysema, and chronic bronchitis from leading health organizations.
This document provides an overview of chronic obstructive pulmonary disease (COPD), including its definition, pathophysiology, epidemiology, and clinical correlates. It describes the main types of COPD such as chronic bronchitis and emphysema. Key points include that COPD is mainly caused by cigarette smoking and is characterized by irreversible airflow limitation. The document discusses the role of inflammation, proteinases, oxidative stress and genetic factors in COPD pathogenesis. It also outlines how COPD affects lung function and physiology through changes in volumes, capacities, elastic recoil and gas exchange.
This document discusses chronic obstructive pulmonary disease (COPD), describing its pathology and the changes that occur in the lungs. COPD involves pathological changes in the central airways, peripheral airways, lung parenchyma, and pulmonary vasculature. In the central airways, there is goblet cell and mucous gland hyperplasia leading to excessive mucus production. In the peripheral airways, bronchiolitis and fibrosis occur. Emphysema involves the destruction of lung parenchyma and loss of alveoli. Changes in the pulmonary vasculature include intimal hyperplasia, smooth muscle hypertrophy, and destruction of the capillary bed. Smoking is a major risk factor for COPD
Emphysema is a chronic lung disease that destroys alveoli, causing shortness of breath and fatigue. It decreases lung capacity to oxygenate blood and remove carbon dioxide, overloading the heart. Treatment includes quitting smoking, medications, oxygen supplementation, and surgery.
Atelectasis is lung collapse from airway blockage or lack of surfactant, causing decreased lung function. Asthma is characterized by bronchiole constriction from allergic reactions or irritants, making expiration difficult. Tuberculosis causes lung fibrosis and damage over time.
Various lung diseases can cause hypoxia from inadequate oxygen exchange. Oxygen therapy is effective for hypoxia from low oxygen levels or impaired diffusion but less
A common, preventable and treatable disease, characterized by persistent respiratory symptoms and airflow limitation that are usually progressive and associated with an enhanced chronic inflammatory response in the airways and/or alveoli due to significant exposure to noxious particles or gases. (Vogelmeier et al., 2017).
Similar to Chronic obstructive pulmonary by dr shailesh gupta & NIKHIL A KUMAR (20)
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Kat...rightmanforbloodline
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.
Does Over-Masturbation Contribute to Chronic Prostatitis.pptxwalterHu5
In some case, your chronic prostatitis may be related to over-masturbation. Generally, natural medicine Diuretic and Anti-inflammatory Pill can help mee get a cure.
2. • Chronic obstructive pulmonary disease (COPD) is
• A chronic ,Slowly progressive disorder characterized by
airflow limitation that is not fully reversible.
3. • COPD includes
• Emphysema-- an anatomically defined condition
characterized by destruction and enlargement of the
lung alveoli;
• chronic bronchitis, a clinically defined as a
productive cough that last for 3 months or more for
at least 2 years
4. • chronic bronchitis without chronic airflow
obstruction is not included in COPD.
• COPD is the third leading cause of death and
affects >10 million persons in the United
states
5. PATHOGENESIS
• Airflow limitation, major physiologic change in
COPD,
• result from both small airway obstruction and
emphysema.
• small airways become narrowed by cells
hyperplasia , mucus, and fibrosis.
6. • airway fibrosis due to activation of
transforming growth factor β (TGF-β )
• While lack of TGF-β may contribute to
parenchymal inflammation and emphysema.
7. • pathogenesis of emphysema---
• Chronic exposure to cigarette smoke leads to
•
•
•
• inflammatory and immune cell recruitment
•
inflammatory cells release elastolytic and other proteinases
that damage the extracellular matrix of the lung.
8. Structural cell death (endothelial and epithelial cells)
through oxidant-induced cigarette smoke damage as
well as indirectly via proteolytic loss of matrix
attachment.
•
• Ineffective repair of elastin and other extracellular
matrix components result in air space enlargement
that defines pulmonary emphysema.
9.
10. INFLAMMATION AND EXTRACELLULAR
MATRIX PROTEOLYSIS
• exposure to oxidants from cigarette smoke,
macrophages and epithelial cells become
activated,
• Produce proteinases and chemokines that attract
other inflammatory and immune cells.
11. • Other mechanism of macrophage activation
occurs via
• oxidant-induced inactivation of histone
deacetylase-2, shifting the balance toward
acetylated or loose chromatin.
12. • resulting in transcription of matrix
metalloproteinases, proinflammatory cytokines
such as
• interleukin 8 (IL-8), and
• tumor necrosis factor α (TNF-α);
• this leads to neutrophil recruitment.
13. • CD8+ T cells are also recruited in response to
cigarette smoke and
• release interferon-inducible protein-10 (IP-10),
• leads to macrophage production of macrophage
elastase (matrix metalloproteinase-12 (MMP-12).
14. • cigarette smoke–
• impaired macrophage phagocytosis,
• induced loss of cilia in the airway epithelium
• Which predispose to bacterial infection with
neutrophilia.
15. • Cigarette smoke oxidant-mediated structural cell death
occurs via a variety of mechanisms including
• rt801 inhibition of mammalian target of rapamycin
(mTOR),
• leading to cell death ,inflammation and proteolysis.
• Cigarette smoke impairs macrophage uptake of
apoptotic cells, limit repair.
16. PATHOLOGY
• Cigarette smoke exposure affect ---
• large airways
• small airways (≤2 mm diameter), and
• alveoli.
17. • Changes in large airways cause cough and sputum,
•
• changes in small airways and alveoli are responsible
for physiologic alterations.
• Emphysema and small airway pathology are present
in most persons with COPD;
18. • LARGE AIRWAY—
• Cigarette smoking results in ---
• mucus gland enlargement and
• goblet cell hyperplasia,
• leading to cough and mucus production
• but these abnormalities are not related to
airflow limitation.
19. • Goblet cells not only increase in number but in extent
through the bronchial tree.
• Bronchi undergo squamous metaplasia, predisposing
to carcinogenesis and disrupting mucociliary clearance.
• But not prominent as in asthma, patients.
20. • Patient have smooth-muscle hypertrophy and bronchial
hyperreactivity leading to airflow limitation.
• Neutrophil influx associated with purulent sputum of
upper respiratory tract infections.
21. SMALL AIRWAYS
• The major site of increased resistance in most
individuals with COPD is in airways ≤2 mm diameter.
Characteristic cellular changes include
• goblet cell metaplasia, these cells replacing
• surfactant-secreting Clara cells.
• Smooth-muscle hypertrophy
22. • These abnormalities cause luminal narrowing
by
• fibrosis,
• excess mucus,
• edema, and
• cellular infiltration.
23. Reduced surfactant increase surface tension at the air-
tissue interface, predisposing to airway narrowing and
collapse.
Respiratory bronchiolitis with mononuclear
inflammatory cells collecting in distal airway tissues
cause proteolytic destruction of elastic fibers in
respiratory bronchioles
24. LUNG PARENCHYMA
• Emphysema--- characterized by destruction of gas-
exchanging air spaces, i.e., the respiratory bronchioles,
alveolar ducts, and alveoli.
• Their walls become perforated and obliterated with
coalescence of small air spaces into a larger air spaces.
25. • Macrophages accumulate in respiratory bronchioles of
all young smokers
• In smokers Bronchoalveolar lavage fluid contains five
times macrophages as compare to nonsmokers.
26. • macrophages comprise >95% of the total cell count and
• neutrophils, nearly absent in nonsmokers’ lavage,
account for 1–2% of the cell
• T lymphocytes, particularly CD8+ cells,are also increased
in the alveolar space of smokers.
27. • Emphysema is classified into --
• centriacinar
• panacinar.
28. • Centriacinar emphysema,
• most frequently associated with cigarette smoking,
is characterized by enlarged air spaces.
• Most prominent in the upper lobes and superior
segments of lower lobes
29. • Panacinar emphysema
• abnormally large air spaces evenly distributed
within and across acinar units.
• Panacinar emphysema is usually observed in
patients with α1AT deficiency,
• which has a predilection for the lower lobes.
30. PATHOPHYSIOLOGY
most typical finding in COPD –
• reduction of forced expiratory flow rates .
• Increases residual volume and
• residual volume/total lung capacity ratio,
• and ventilation-perfusion mismatching.
31. AIRFLOW OBSTRUCTION
• Airflow obstruction also known as airflow
limitation
• determined by spirometry,
• involves forced expiratory maneuvers after the
subject has inhaled to total lung capacity.
32. • Key parameters obtained from spirometry
include
• the volume of air exhaled within the first second
of the forced expiratory maneuver (FEV1)
• The total volume of air exhaled during the entire
spirometric maneuver (forced vital capacity
[FVC]).
33. • Patients with airflow obstruction related to COPD
have a chronically reduced ratio of FEV1/FVC.
• In contrast to asthma, the reduced FEV1 in COPD
seldom shows large responses to inhaled
bronchodilators,
• Asthma patients can also develop chronic (not fully
reversible) airflow obstruction.
34. • HYPERINFLATION
• Lung volumes are routinely assessed in pulmonary
function testing.
• In COPD there is “air trapping” (increased residual
volume and increased ratio of residual volume to total
lung capacity) and
• progressive hyperinflation (increased total lung
capacity) late in the disease.
35. • hyperinflation push the diaphragm into a flat position
with a number of adverse effects.
• First, by decreasing the zone of apposition between the
diaphragm and the abdominal wall,
• positive abdominal pressure during inspiration is not
applied as effectively to the chest wall,and impairing
inspiration.
36. Second, because the muscle fibers of the flattened
diaphragm are shorter than those of a more normally
curved diaphragm,
they are less capable of generating inspiratory pressures
than normal.
37. • Third,
• the flattened diaphragm(with increased radius of
curvature, r) generate greater tension (t)
• to develop the transpulmonary pressure (p) required to
produce tidal breathing.
• follows Laplace’s law, p = 2t/r.
38. RISK FACTORS
• 1. CIGARETTE SMOKING—
• cigarette smoking is a major risk factor,
• longitudinal studies have shown accelerated decline in
FEV1 in a dose-response relationship to the intensity of
cigarette smoking,
39. • Which is expressed as pack-years (average number of
packs of cigarettes smoked per day multiplied by the
total years of smoking).
• This dose-response relationship between reduced
pulmonary function and cigarette smoking intensity
• accounts for the higher prevalence rates of COPD with
increasing age.
40. 2. OCCUPATIONAL EXPOSURES—
including
• coal mining,
• cotton textile dust,
risk factors for chronic airflow obstruction.
• coal miners, coal mine dust exposure was a significant
risk factor for emphysema in both smokers and
nonsmokers.
41. 3. AIR POLLUTION—
• increased respiratory symptoms in those living in urban
compared to rural areas, which relate to increased
pollution in the urban.
• Prolonged exposure to smoke produced by biomass
combustion—a common mode of cooking in some
countries—significant risk factor for COPD among
women in those countries.
42. 4.GENETIC CONSIDERATIONS—
• cigarette smoking is the major environmental risk
factor for the development of COPD.
• Severe α1AT deficiency proven genetic risk factor for
COPD;
• α1 Antitrypsin Deficiency --Many variants of the
protease inhibitor (PI or SERPINA1) locus that encodes
α1AT .
• The common M allele is associated with normal α1AT
levels.
43. • The S allele, associated with slightly reduced α1AT
levels, and
• the Z allele, associated with markedly reduced α1AT
levels.
• Individuals with two Z alleles or one Z and
• one null allele are referred as PiZ, which is the most
common form of severe α1AT deficiency.
45. In advances COPD---
• dyspnea on exertion ,and
• breathless doing simple activities of daily living.
• Pursed-lip breathing
• Contraction of the sternomastoid and scalene
muscles on insipiration.
46. CLINICAL PRESENTATION cont--
PHYSICAL FINDINGS
• early stages of COPD, patients usually have an entirely
normal On physical examination.
• Current smokers have signs of active smoking, including
an odor of smoke or nicotine staining of fingernails.
• patients with severe disease, on physical examination
prolonged expiratory phase with expiratory wheezing.
47. • Patients with severe airflow obstruction may also exhibit
use of accessory muscles of respiration, sitting in the
characteristic “tripod” position
• To facilitate the actions of the sternocleidomastoid,
scalene, and intercostal muscles.
• Patients may develop cyanosis, visible in the lips and nail
beds.
48. • patients with predominant emphysema, termed “pink
puffers,” are thin and noncyanotic at rest and have
prominent use of accessory muscles,
• patients with chronic bronchitis are heavy and cyanotic
(“blue bloaters”),
49. • Other feature of Advanced disease
• cachexia, with significant weight loss,
• bitemporal wasting, and
• diffuse loss of subcutaneous adipose tissue.
• This syndrome has been associated with both inadequate
oral intake and elevated levels of inflammatory cytokines
(TNF-α).
50. • patients with advanced disease have paradoxical
inward movement of the rib cage with inspiration
(Hoover’s sign),
• result of alteration of the vector of diaphragmatic
contraction on the rib cage as a result of chronic
hyperinflation.
• Clubbing of the digits is not a sign of COPD
51. LABORATORY FINDINGS
• The hallmark of COPD is airflow obstruction
• Pulmonary function testing shows airflow obstruction
with a reduction in FEV1 and FEV1/FVC ,
• lung volumes may increase, resulting in an increase in
total lung capacity, functional residual capacity, and
residual volume.
52. • In patients with emphysema, the diffusing capacity is
reduced,
• Due to lung parenchymal destruction characteristic of
the disease.
• Radiographic studies may assist in the classification of
the type of COPD,
• Obvious bullae, paucity of parenchymal markings, or
hyperlucency suggests the presence of emphysema
53. • COPD cannot be diagnosed on a chest radiograph but
useful in excluding other pathology
• In moderate and severe COPD the chest radiograph
typically shows
• Hypertranslucent lung field
• Low flat diaphragams
• Prominent pulmonary artery shadows
54. .
• Increased lung volumes and flattening of the diaphragm
suggest hyperinflation but do not provide information
about chronicity of the changes.
•
• Computed tomography (CT) scan is the current
definitive test for establishing the presence or absence
of emphysema .
55. • Recent guidelines have suggested
• testing for α1AT deficiency in all subjects with COPD
or asthma with chronic airflow obstruction.
• Measurement of the serum α1AT level is a initial test.
• subjects with low α1AT levels, the definitive diagnosis
of α1AT deficiency
• requires protease inhibitor (PI) type determination.
56. • This is typically performed by isoelectric focusing of
serum, which reflects the genotype at the PI locus for
the common alleles and many of the rare PI alleles as
well.
• Molecular genotyping of DNA can be performed for
the common PI alleles (M, S, and Z).
57. TREATMENT
• STABLE PHASE COPD
Only three interventions—
• smoking cessation,
• oxygen therapy in chronically hypoxemic patients,
• and lung volume reduction surgery in selected patients
with emphysema.
58. • All other current therapies are directed at
improving symptoms
• and decreasing the frequency and severity of
exacerbations.
59. • PHARMACOTHERAPY
• Smoking Cessation It has been shown that middle
aged
• smokers who were able to successfully stop smoking
significant improvement in the rate of decline in
pulmonary function,
• returning to annual changes similar to that of
nonsmoking patients.
60. • All patients with COPD should be strongly urged to quit
smoking and educated about the benefits of quitting.
• There are three principal pharmacologic approaches to
the problem:
• 1.nicotine replacement therapy available as gum,
transdermal patch, inhaler, and nasal spray; and
61. • Bupropion—norepinephrine-dopamine reuptake
inhibitor (NDRI) ana nicotinic anatogonist,
• It reduces the nicotine craving and withdrawal
symptom.
• Epileptic seizures are the most common side effect
• varenicline--a nicotinic acid receptor
agonist/antagonist– it reduces cravings and
decreases the plesurable effect of tobacco products.
62. • Food and drug administratio (FDA) approved the use
of vernicline for up to 12 weeks
• If smoking cessation has been achieved continued
another twelve weeks.
• Mild nausea is the most common side effect
• And other common side effect include-
headche,difficulty sleeping and nightmares
63. • Bronchodilators—
• bronchodilators are used for symptomatic patients with
COPD.
• inhaled route is preferred for medication delivery
because the incidence of side effects is lower
• than that seen with the use of parenteral medication
delivery.
64. • Anticholinergic Agents—
• Ipratropium bromide improves symptoms and produces
acute improvement in FEV1.
• Tiotropium-- long-acting anticholinergic, has been
shown to improve symptoms and reduce exacerbations.
• Studies of both ipratropium and tiotropium have failed
to demonstrate that either influences the rate of decline
in FEV1.
65. --
• Beta Agonists—
• provide symptomatic benefit.
•
• Long-acting inhaled β agonists, such as salmeterol or
formoterol, and more effective than ipratropium
bromide.
• The main side effects are tremor and tachycardia
66. • Glucocorticoids—
• chronic use of oral glucocorticoids for treatment of
COPD is not recommended because of an unfavorable
benefit/risk ratio.
Inhaled Glucocorticoids associated with
• increased rates of oropharyngeal candidiasis
• and increased rate of loss of bone density
67. The chronic use of oral glucocorticoids is associated with
significant side effects,
• including osteoporosis,
• Weight gain,
• cataracts,
• glucose intolerance,
• and increased risk of infection..
68. Theophylline—
• Theophylline improve expiratory flow rates and vital
capacity
• and improvement in arterial oxygen and carbon dioxide
levels in patients with moderate to severe COPD.
69. • Nausea
• tachycardia and
• Tremor
• is a common side effect
roflumilast--
• is selective phosphodiesterase4 (PDE4) inhibitor
• used to reduce exacerbation frequency in COPD
patients with chronic bronchitis and a prior history of
exacerbations;
70. Oxygen—
• Supplemental O2 is commonly prescribed for patients
with exertional hypoxemia and nocturnal hypoxemia.
• And patients with resting hypoxemia (resting O2
saturation ≤88% or <90% with signs of pulmonary
hypertension or right heart failure).
71. • Other Agents—
• N-acetyl cysteine used in patients with COPD for both
its mucolytic and antioxidant properties.
• Specific treatment in the form of IV α1AT augmentation
therapy is available for individuals with severe α1AT
deficiency.
• α1AT augmentation therapy is not recommended for
severely α1AT-deficient persons with normal
pulmonary function and a normal chest CT scan.
72. • Lung Transplantation—
• COPD is currently the second leading indication for lung
transplantation.
• Current recommendations are that candidates for lung
transplantation
• should have severe disability despite maximal medical
therapy and
• be free of comorbid conditions such as liver, renal, or
cardiac disease.
73. TREATMENT OF ACUTE EXACERBATIONS—
Bronchodilators
• patients are treated with an inhaled β agonist, with the
addition of an anticholinergic agent.
• the frequency of administration depends on the
severity of the exacerbation.
• Patients are often treated initially with nebulized
therapy, as such treatment is easier to administer in
older patients or in respiratory distress.
74. Oxygen
• Supplemental O2 should be supplied to keep arterial
saturations ≥90%.
• 24-28% via mask ,2 litres/min by nasal prong
check ABGs within 60 min and adjust according to
pao2 and paco2/pH
75. Glucocorticoids—
• the use of glucocorticoids
• reduce the length of stay, and
• reduce the chance of subsequent exacerbation or
• relapse for a period of up to 6 months.
• The GOLD guidelines recommend--
30–40 mg of oral prednisolone or its equivalent for a
period of 10–14 days.
76. Mechanical Ventilatory Support—
• noninvasive positive pressure ventilation (NIPPV) in
patients with respiratory failure, results in a significant
reduction in
• mortality rate,
• need for intubation,
• complications of therapy, and
• hospital length of stay.
77. Invasive (conventional) mechanical ventilation via an
endotracheal tube is indicated for patients with severe
respiratory distress despite initial therapy,
• life-threatening hypoxemia,
• severe hypercarbia and/or acidosis,
• markedly impaired mental status,
• Respiratory arrest,
• hemodynamic instability, or other complications.