COPD (chronic obstructive pulmonary disease) is a prevalent and treatable condition that causes increasing airway obstruction and tissue deterioration.
It is linked to structural lung abnormalities caused by chronic inflammation induced by prolonged exposure to toxic particulates or gases, most notably cigarette smoke.
Chronic inflammation promotes airway constriction and diminished lung recoil. Dyspnea, cough, and sputum production are common signs of the disease. Symptoms can range from being asymptomatic to respiratory distress.
Epidemiology
COPD is present predominantly in smokers and individuals more than 40 years of age. Incidence increases with age and is presently the third most prevalent cause of mortality and morbidity worldwide.
In 2015, the incidence was 174,000,000, and around 3.2 million fatalities were attributable to COPD worldwide. However, due to COPD misdiagnosis, the prevalence is underestimated.
Anatomy
Pathophysiology
It is an inflammatory disease that affects the airways, pulmonary vasculature, and lung parenchyma. It is believed that the process involves oxidative stress and protease-antiprotease instabilities. Emphysema represents the anatomical alterations seen in COPD, in which most alveolar sacs are destroyed, resulting in obstructive physiology.
Neutrophils and macrophages are activated, releasing a variety of inflammatory mediators. An irritant produces an inflammatory response. Excess proteases and oxidants cause the deterioration of the air sacs. Elastin degradation by proteases results in a lack of elastic recoil and airway collapse during expiration.
The forced expiratory volume (FEV1) decreases due to an inflammatory response and airway obstruction, while airflow restriction and decreased gas exchange are carried on by tissue damage. Imaging examinations frequently reveal hyperinflation of the lungs, which results from air getting trapped when the airways collapse during expiration.
Elevated levels of carbon dioxide are brought on by the inability to exhale completely. A common symptom of disease progression is impairment in gas exchange. CO2 retention is caused by a decrease in the ventilation or an increase in physiological dead space. Hypoxemia-induced diffuse vasoconstriction may lead to pulmonary hypertension.
Etiology
Acute COPD exacerbations are frequent and typically spurred on by triggers, such as bacterial, viral, or environmental stimuli.
A spike in inflammation and air embolism frequently requires corticosteroids and bronchodilators as treatment.
Prolonged exposure to toxic chemicals or particles results in COPD. The primary cause of COPD worldwide is cigarette smoking.
Genetics
Prognostic Factors
The prognosis depends on adherence to therapy, which includes quitting smoking and avoiding other hazardous gases.
The prognosis of patients with other comorbidities, such as pulmonary hypertension, cardiovascular illness, or lung cancer, is often worse.
Dyspnea and airflow restriction is typically progressive conditions.
COPD (chronic obstructive pulmonary disease) is a prevalent and treatable condition that causes increasing airway obstruction and tissue deterioration.
It is linked to structural lung abnormalities caused by chronic inflammation induced by prolonged exposure to toxic particulates or gases, most notably cigarette smoke.
Chronic inflammation promotes airway constriction and diminished lung recoil. Dyspnea, cough, and sputum production are common signs of the disease. Symptoms can range from being asymptomatic to respiratory distress.
COPD is present predominantly in smokers and individuals more than 40 years of age. Incidence increases with age and is presently the third most prevalent cause of mortality and morbidity worldwide.
In 2015, the incidence was 174,000,000, and around 3.2 million fatalities were attributable to COPD worldwide. However, due to COPD misdiagnosis, the prevalence is underestimated.
It is an inflammatory disease that affects the airways, pulmonary vasculature, and lung parenchyma. It is believed that the process involves oxidative stress and protease-antiprotease instabilities. Emphysema represents the anatomical alterations seen in COPD, in which most alveolar sacs are destroyed, resulting in obstructive physiology.
Neutrophils and macrophages are activated, releasing a variety of inflammatory mediators. An irritant produces an inflammatory response. Excess proteases and oxidants cause the deterioration of the air sacs. Elastin degradation by proteases results in a lack of elastic recoil and airway collapse during expiration.
The forced expiratory volume (FEV1) decreases due to an inflammatory response and airway obstruction, while airflow restriction and decreased gas exchange are carried on by tissue damage. Imaging examinations frequently reveal hyperinflation of the lungs, which results from air getting trapped when the airways collapse during expiration.
Elevated levels of carbon dioxide are brought on by the inability to exhale completely. A common symptom of disease progression is impairment in gas exchange. CO2 retention is caused by a decrease in the ventilation or an increase in physiological dead space. Hypoxemia-induced diffuse vasoconstriction may lead to pulmonary hypertension.
Acute COPD exacerbations are frequent and typically spurred on by triggers, such as bacterial, viral, or environmental stimuli.
A spike in inflammation and air embolism frequently requires corticosteroids and bronchodilators as treatment.
Prolonged exposure to toxic chemicals or particles results in COPD. The primary cause of COPD worldwide is cigarette smoking.
The prognosis depends on adherence to therapy, which includes quitting smoking and avoiding other hazardous gases.
The prognosis of patients with other comorbidities, such as pulmonary hypertension, cardiovascular illness, or lung cancer, is often worse.
Dyspnea and airflow restriction is typically progressive conditions.
COPD (chronic obstructive pulmonary disease) is a prevalent and treatable condition that causes increasing airway obstruction and tissue deterioration.
It is linked to structural lung abnormalities caused by chronic inflammation induced by prolonged exposure to toxic particulates or gases, most notably cigarette smoke.
Chronic inflammation promotes airway constriction and diminished lung recoil. Dyspnea, cough, and sputum production are common signs of the disease. Symptoms can range from being asymptomatic to respiratory distress.
COPD is present predominantly in smokers and individuals more than 40 years of age. Incidence increases with age and is presently the third most prevalent cause of mortality and morbidity worldwide.
In 2015, the incidence was 174,000,000, and around 3.2 million fatalities were attributable to COPD worldwide. However, due to COPD misdiagnosis, the prevalence is underestimated.
It is an inflammatory disease that affects the airways, pulmonary vasculature, and lung parenchyma. It is believed that the process involves oxidative stress and protease-antiprotease instabilities. Emphysema represents the anatomical alterations seen in COPD, in which most alveolar sacs are destroyed, resulting in obstructive physiology.
Neutrophils and macrophages are activated, releasing a variety of inflammatory mediators. An irritant produces an inflammatory response. Excess proteases and oxidants cause the deterioration of the air sacs. Elastin degradation by proteases results in a lack of elastic recoil and airway collapse during expiration.
The forced expiratory volume (FEV1) decreases due to an inflammatory response and airway obstruction, while airflow restriction and decreased gas exchange are carried on by tissue damage. Imaging examinations frequently reveal hyperinflation of the lungs, which results from air getting trapped when the airways collapse during expiration.
Elevated levels of carbon dioxide are brought on by the inability to exhale completely. A common symptom of disease progression is impairment in gas exchange. CO2 retention is caused by a decrease in the ventilation or an increase in physiological dead space. Hypoxemia-induced diffuse vasoconstriction may lead to pulmonary hypertension.
Acute COPD exacerbations are frequent and typically spurred on by triggers, such as bacterial, viral, or environmental stimuli.
A spike in inflammation and air embolism frequently requires corticosteroids and bronchodilators as treatment.
Prolonged exposure to toxic chemicals or particles results in COPD. The primary cause of COPD worldwide is cigarette smoking.
The prognosis depends on adherence to therapy, which includes quitting smoking and avoiding other hazardous gases.
The prognosis of patients with other comorbidities, such as pulmonary hypertension, cardiovascular illness, or lung cancer, is often worse.
Dyspnea and airflow restriction is typically progressive conditions.
https://www.ncbi.nlm.nih.gov/books/NBK559281/
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