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COPD
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- 3. COPD is a groupof lung diseases that cause airflow blockage and breathing-related problems. It is a progressive disease, meaning it gets worse over time.
- 4. COPD In the United States, COPDis the third leading cause of death.
- 5. COPD COPD is a majorcause of death worldwide, and it is estimated that 328 million people have COPD.
- 6. COPD forms The twomain forms of COPD are chronic bronchitis and emphysema
- 7. COPD The lungs arethe primary organs responsible for respiration, the process of taking in oxygen and releasing carbon dioxide. Respiration involves inhalation (inspiration), where the diaphragm contracts, expanding the chest cavity and drawing air into the lungs through the trachea, bronchi, and bronchioles to the alveoli. Exhalation (expiration) is primarily passive, with the chest cavity recoiling and forcing air out of the lungs. Gas exchange occurs in the alveoli, where oxygen diffuses from air into the blood and carbon dioxide diffuses from blood into air. The lungs also regulate blood pH, protect against infection, and produce surfactant to prevent alveoli from collapsing.
- 8. COPD pathophysiology COPD isa complex disease with a pathophysiology characterized by airway inflammation, air sac destruction, and small airway remodeling. These changes lead to airflow obstruction, chronic cough, dyspnea, gas exchange abnormalities, and, in advanced cases, right-sided heart failure
- 9. COPD Risk factors Smoking Exposureto secondhand smoke Exposure to air pollution Occupational exposure to dusts and fumes History of childhood respiratory infections Genetic predisposition Alpha-1 antitrypsin deficiency (AATD) Aging Low socioeconomic statusdust
- 10. COPD causes Smoking Air pollution Genetics Occupational exposures Historyof childhood respiratory infections
- 11. Smoking Smoking is theleading cause of COPD, accounting for about 80% of cases worldwide. Smoking damages the lungs and airways in multiple ways, leading to the development of chronic inflammation, air sac destruction, and small airway remodeling, the key pathophysiological features of COPD.
- 12. COPD causes Smoking triggers inflammationin the airways, leading to thickening of the walls, narrowing of the lumen, and increased mucus production. Smoking also generates excessive reactive oxygen species (ROS) that damage the elastin fibers in the airways, leading to airway collapse. Additionally, smoking disrupts the balance between proteases and antiproteases, leading to excessive protease activity that damages the alveolar walls, causing emphysema. These mechanisms contribute to the development and progression of COPD.
- 13. AAT deficiency AAT isa protease inhibitor, meaning it blocks the activity of proteases, enzymes that break down proteins. In the lungs, proteases play a role in the inflammatory response, and excessive protease activity can damage lung tissue. AAT helps to regulate protease activity and protect the lungs from damage. People with AATD have lower levels of AAT in their blood, making them more susceptible to lung damage from proteases
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- 15. COPD- stage 1 MildCOPD: People with mild COPD may have no symptoms or only mild symptoms, such as shortness of breath after exertion
- 16. COPD – stage2 People with moderate COPD may have more frequent shortness of breath, especially during exertion. They may also have a chronic cough or wheezing, increased phlegm
- 17. COPD - Stage3 People with severe COPD may have frequent shortness of breath, even at rest. They may also have wheezing, chest tightness, and fatigue, patient may need supplemental oxygen
- 18. COPD • Shortness of breath •Cough • Wheezing • Chest tightness • Fatigue • Mucous production • Heart failure at later stages
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- 21. COPD complications • Anemia •Right-sided heart failure • Muscle weakness • Lung infections • Bone thinning • Collapsed lungs • Bone thinning
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- 25. COPD – diagnosticmethods •Spirometry •Chest X-ray •Arterial blood gas (ABG) test •Body plethysmography •Alpha-1 antitrypsin (AAT) deficiency test •Pulse oximetry
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- 27. spirometry his is themost common test used to diagnose COPD. It measures how much air you can blow out of your lungs and how fast you can blow it out.
- 28. Pulse oximetry Pulse oximetryis a non-invasive method for measuring the oxygen saturation of your blood, which is the percentage of hemoglobin in your blood that is carrying oxygen. It is a quick, painless, and easy- to-use test that can be done in a doctor's office, hospital, or even at home.
- 29. ABGs This test measures theamount of oxygen and carbon dioxide in your blood. It can help to determine how severe your COPD is and whether you need oxygen therapy.
- 30. Electrocardiogram In COPD, ECG changescan occur due to the long-term effects of hypoxic pulmonary vasoconstriction (HPVC) upon the right side of the heart. HPVC is a narrowing of the blood vessels in the lungs, which can lead to pulmonary hypertension (high blood pressure in the lungs). Pulmonary hypertension can cause the right side of the heart to enlarge and weaken, which can lead to right ventricular hypertrophy (RVH).
- 31. Chest x ray Thistest can show if you have emphysema, which is one of the main causes of COPD. It can also rule out other lung problems, such as pneumonia.
- 32. COPD treatment • Bronchodilators: Thesemedications open up the airways and make it easier to breathe. • Antibiotics: These medications are used to treat lung infections. • Supplemental oxygen: This can help people with low levels of oxygen in the blood. • Vaccination: People with COPD should get a flu vaccine every year and a pneumonia vaccine once a year.
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- 34. Bronchodilators Bronchodilators form the cornerstoneof COPD treatment, working by relaxing the muscles surrounding the airways, allowing for easier airflow. Short- acting bronchodilators, such as albuterol (ProAir HFA, Ventolin HFA) and ipratropium (Atrovent HFA), provide rapid relief from acute symptoms, while long-acting bronchodilators, such as salmeterol (Advair HFA, Serevent HFA) and tiotropium (Spiriva), offer sustained symptom control over an extended period.
- 35. Anti inflammatory Inhaled corticosteroids, such as fluticasoneand budesonide (Symbicort HFA), combat the chronic inflammation that underlies COPD. By reducing inflammation, these medications help alleviate symptoms, improve lung function, and minimize the risk of exacerbations.
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- 40. Anti cholinergic Anticholinergics work byblocking muscarinic receptors, which are receptors for acetylcholine. By blocking these receptors, anticholinergics prevent acetylcholine from binding to them and exerting its bronchoconstrictor effects. This leads to relaxation of the muscles in the airways, allowing for easier airflow.
- 41. Leukotriene modifiers LTRAs workby binding to leukotriene receptors on immune cells and smooth muscle cells in the airways. By blocking these receptors, LTRAs prevent leukotrienes from exerting their inflammatory and broncho constrictive effects. This leads to reduced airway inflammation, mucus production, and airway constriction, which can help improve lung function and reduce symptoms in people with COPD.broncho- constrictive
- 42. expectorants Expectorants are thought towork by stimulating the production of mucus in the airways. They may do this by increasing the activity of the cilia, which are tiny hairs that line the airways and help to move mucus. Expectorants may also make mucus thinner by increasing the amount of water in it.
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- 45. COPD preventive methods Thebest way to prevent COPD is to avoid smoking and air pollution. Several lifestyle changes can help reduce the risk of COPD, such as eating a healthy diet and exercising regularly
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- 47. Chronic bronchitis is aprogressive lung disease characterized by persistent inflammation of the bronchial airways, leading to excessive mucus production and persistent cough. It is a major component of chronic obstructive pulmonary disease (COPD), a broader term encompassing obstructive lung diseases.
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- 50. Symptoms of chronicbronchitis - Shortness of breath - Chest tightness - Wheezing - Fatigue - Recurrent respiratory infections
- 51. Pathophysiology Chronic bronchitis arises fromchronic inflammation of the airways, primarily due to exposure to irritants like cigarette smoke, air pollution, and occupational dusts. This inflammation damages the cilia, tiny hair-like structures responsible for clearing mucus from the airways. Consequently, mucus accumulates, leading to cough and increased susceptibility to infections.
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- 53. complications Acute exacerbations: Worsening ofsymptoms requiring additional treatment - Respiratory failure: Severe impairment of lung function, requiring mechanical ventilation - Cor pulmonale: Right- sided heart failure due to chronic pulmonary hypertension - Lung cancer: Increased risk associated with chronic inflammation
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- 58. Emphysema - Emphysema isa type of chronic obstructive pulmonary disease (COPD), where the air sacs in the lungs (alveoli) become damaged and lose their elasticity. - The loss of elasticity causes the airways to collapse during exhalation, leading to difficulty in expelling air from the lungs.
- 59. causes Primary cause: Smoking isthe leading cause of emphysema, with long-term exposure to tobacco smoke being the primary risk factor. - Alpha-1 antitrypsin deficiency: Genetic factors can contribute to the development of emphysema, especially in individuals with a deficiency of the alpha-1 antitrypsin enzyme.
- 60. Pathophysiology Smoking-induced inflammation: Chronic exposure tocigarette smoke triggers inflammation in the airways, leading to the release of enzymes that break down elastin in the lungs. - Destruction of alveoli: Elastin breakdown results in the destruction of alveoli, reducing the surface area available for gas exchange.
- 61. Pathophysiology - Loss oflung elasticity: Reduced elasticity impairs the ability of the lungs to recoil during exhalation, causing air trapping.
- 62. symptoms - Shortness ofbreath, especially during physical exertion. - Persistent cough. - Wheezing. - Fatigue. - Weight loss.
- 63. Emphysema types Centriacinar emphysema Panacinaremphysema Paraseptal emphysema
- 64. Centriacinar emphysema Primarily affectsthe central or proximal parts of the acinus.
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