Copd Part 1
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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.
![COPD
• The Global Initiative for Chronic Obstructive Lung Disease (GOLD) – a project initiated by the National
Heart, Lung, and Blood Institute (NHLBI) and the World Health Organization (WHO) defines COPD as
follows [1]:
• COPD is chronic obstructive disease of airways
that is characterized by airflow limitation that is
usually progressive and not fully reversible. It
associated with an enhanced chronic
inflammatory response in the airways and the lung
to noxious particles or gases.
Reference:
1. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease: Revised 2011. Global
Initiative for Chronic Obstructive Lung Disease (GOLD). www.goldcopd.org](https://image.slidesharecdn.com/copd-140520085018-phpapp01/85/Copd-Part-1-10-320.jpg)
Copd Part 1
- 1. Pratap Sagar Tiwari, MD, Internal Medicine, NMC COPD -PART 1
- 2. CASE SCENARIO • 55 years old male ,a chronic smoker with history of 20 pack years presented with complaints of dyspnea. • Note: 20 cig/day /year = 1 pack year • Copd is unlikely when it is < 10 pack/year.
- 3. STEP 1 • Lungs had Chronic exposure to cigarette smoke recruitment of inflammatory cells within the terminal airspaces of the lungs.
- 4. STEP 2 • These inflammatory cells release elastolytic proteinases that damage the extracellular matrix of the lung. Proteinases: examples are neutrophil elastase, Cathepsins etc Note: Cathepsins inhibitor: odanocatib neutrophil elastase inhibitor: sivelastat
- 5. STEP 3 & 4 • Loss of matrix cell attachment plus Oxidant stress leads to Structural cell death. • Ineffective repair of elastin and other extracellular matrix component Airspace enlargement
- 6. PATHOGENESIS OF EMPHYSEMA 1. Chronic exposure to cigarette smoke may lead to recruitment of inflammatory cells within the terminal airspaces of the lungs. 2. These inflammatory cells release elastolytic proteinases that damage the extracellular matrix of the lung. 3. Structural cell death result from oxidant stress and loss of matrix cell attachment. 4. Ineffective repair of elastin and other extracellular matrix component result in airspace enlargement.
- 8. EMPHYSEMA • Emphysema affects the structures distal to the terminal bronchiole, consisting of the respiratory bronchiole, alveolar ducts, alveolar sacs, and alveoli, known collectively as the acinus. • These structures in combination with their associated capillaries and interstitium form the lung parenchyma. • The part of the acinus that is affected by permanent dilation or destruction determines the subtype of emphysema. 1. Proximal acinar (centrilobular) emphysema 2. Panacinar emphysema refers to enlargement or destruction of all parts of the acinus. 3. In distal acinar (paraseptal) emphysema
- 9. • Smoking results in tracheo-bronchial mucous gland enlargement and goblet cell hyperplasia leading to cough and mucous production that defines chronic bronchitis. • Although not as prominent as in asthma, patient may have smooth muscle hypertrophy and bronchial hyperreactivity leading to airflow limitation. (Note: Goblet cells are glandular simple columnar epithelial cells whose function is to secrete gel forming mucins, which are the major component of mucus.)
- 10. COPD • The Global Initiative for Chronic Obstructive Lung Disease (GOLD) – a project initiated by the National Heart, Lung, and Blood Institute (NHLBI) and the World Health Organization (WHO) defines COPD as follows [1]: • COPD is chronic obstructive disease of airways that is characterized by airflow limitation that is usually progressive and not fully reversible. It associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases. Reference: 1. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease: Revised 2011. Global Initiative for Chronic Obstructive Lung Disease (GOLD). www.goldcopd.org
- 11. SUBTYPES OF COPD • Emphysema, chronic bronchitis, and chronic obstructive asthma. • Note: Extrapulmonary manifestations include impaired nutrition, weight loss and skeletal muscle dysfunction.
- 12. COPD :SUBTYPES • Emphysema is an anatomical condition characterized by abnormal and permanent enlargement of the airspaces distal to the terminal bronchioles that is accompanied by destruction of the airspace walls, without obvious fibrosis.1 • Chronic bronchitis is a clinically defined condition that is characterized as a chronic productive cough for three months in each of two successive years in a patient in whom other causes of chronic cough (eg, bronchiectasis) have been excluded .2 References: 1. Rennard SI. COPD: overview of definitions, epidemiology, and factors influencing its development. Chest 1998; 113:235S. 2. Celli BR, MacNee W, ATS/ERS Task Force. Standards for the diagnosis and treatment of patients with COPD: a summary of the ATS/ERS position paper. Eur Respir J 2004; 23:932.
- 13. • The National Asthma Education and Prevention Program (NAEPP) Expert Panel Report 3 gives the following definition of asthma. • Asthma is a chronic inflammatory disorder of the airways characterized by airflow limitation/obstruction that varies markedly , both spontaneously and with treatment. • There is a hyperresponsiveness to a wide range of triggers leading to excessive narrowing with consequent decrease in airflow and symptomatic wheezing and dyspnea. Reference: • GINA report, global strategy for asthma management and prevention 2006. Global Initiative for Asthma (GINA) file://www.ginasthma.org (Accessed on may 13, 2014).
- 14. EXTRA NOTES: • Patients with asthma whose airflow obstruction is completely reversible are not considered to have COPD. • Persons with chronic bronchitis, emphysema, or both are not considered to have COPD unless they have airflow obstruction. • Patients with airflow obstruction due to diseases that have a known etiology or a specific pathology (eg, cystic fibrosis, bronchiectasis, obliterative bronchiolitis) are not considered to have COPD .
- 15. CLINICAL FEATURES • COPD should be suspected in any patient over the age of 40 years who presents with symptoms of chronic bronchitis and/or breathlessness. • Cough and associated sputum production are usually the first symptoms, often referred to as a 'smoker's cough'. • Breathlessness usually brings about the first presentation to medical attention. • In advanced disease, enquiry should be made as to the presence of oedema (which may be seen for the first time during an exacerbation) and morning headaches, which may suggest hypercapnia.
- 16. MMRC
- 17. • In COPD there is air trapping (increased residual volume) AND hyperinflation (increased total lung capacity) late in the disease. Despite compensating for airway obstruction, hyperinflation can push the diaphragm into a flat position with a number of adverse effects. 1. Firstly, by decreasing the zone of apposition between the diaphragm and abdominal wall, positive abdominal pressure during inspiration is not applied as effectively to the chest wall, hindering ribcage movement and impairing inspiration. 2. Second, because the muscle of flat diaphragm are shorter than the normal curved diaphragm, they are less capable of generating Inspiratory pressure than normal. 3. Third, the flattened diaphragm (with increased radius if curvature, ) must generate greater tension to develop the pressure required to produce tidal breathing.
- 18. RISK FACTORS • Family history • Smoking history • Age at initiation • Average amount smoked per day since initiation • Environmental history
- 19. SYMPTOMS Dyspnea • Ask about the amount of effort required to induce uncomfortable breathing. Many individuals will deny symptoms of dyspnea, but will have reduced their activity levels substantially. Cough • Cough with or without sputum production. • The presence of chronic cough and sputum has been used to define chronic bronchitis. Wheezing • Wheezing occurring during breathing indicate the presence of airflow obstruction Acute chest illnesses • Inquire about occurrence and frequency of episodes of increased cough and sputum with wheezing, dyspnea, or fever.
- 20. BEDSIDE EXAMINATION IN EMPHYSEMA Inspection • Purse lip respiration • Barrel shape chest Palpation • Non localisation of apex beat • Diminished chest expansion • Diminished vocal fremitus Barrel shape chest Circular Horizontal ribs Wide subcostal angle Slight kyphosis Prominent sternal angle
- 21. BEDSIDE EXAMINATION IN EMPHYSEMA Percussion • Hyperresonant • Loss of liver and cardiac dullness Auscultation • Diminished breath sound • Wheeze and ronchi may be present • Force expiratory time prolonged
- 22. MUSCLES OF RESPIRATION Normal Respiration • Inspiration: Diaphragm, External Intercostal Muscles • Expiration: elastic recoil of the lungs Forceful Respiration • Inspiration: scalene muscles - Elevate the first two ribs, sternomastoids - Raise the sternum, alae nasi - Flare the nostrils, Pectoralis major and minor • Expiration: intercostal muscles and abdominal muscles
- 23. PURSE LIP BREATHING • Improves ventilation • Releases trapped air in the lungs • Keeps the airways open longer and decreases the work of breathing • Prolongs exhalation to slow the breathing rate • Relieves shortness of breath • Causes general relaxation
- 24. PHYSICAL EXAMINATION Other • Unusual positions to relieve dyspnea at rest • Digital clubbing suggests the possibility of lung cancer or bronchiectasis. • Mild dependent edema may be seen in the absence of right heart failure
- 27. END OF PART 1
Editor's Notes
- #4: Over 4000 chemical compounds are created by burning a cigarette – 69 of those chemicals are known to cause cancer. Carbon monoxide, nitrogen oxides, hydrogen cyanides and ammonia are all present in cigarette smoke.
- #8: As the bronchioles get smaller they divide into terminal bronchioles, these bronchioles mark the end of the conducting zone. The terminal bronchiole is the most distal segment of the conducting zone. Each of the terminal bronchioles divides to form respiratory bronchioles which contain a small number of alveoli. Alveoli only become present when the conducting zone changes to the respiratory zone. The respiratory zone is the site of O2 and CO2 exchange with the blood.
- #9: Emphysema affects the structures distal to the terminal bronchiole, consisting of the respiratory bronchiole, alveolar ducts, alveolar sacs, and alveoli, known collectively as the acinus. These structures in combination with their associated capillaries and interstitium form the lung parenchyma. The part of the acinus that is affected by permanent dilation or destruction determines the subtype of emphysema.Proximal acinar (centrilobular) emphysema refers to abnormal dilation or destruction of the respiratory bronchiole, the central portion of the acinus. It is commonly associated with cigarette smoking, but can also be seen in coal workers’ pneumoconiosis.Panacinar emphysema refers to enlargement or destruction of all parts of the acinus. Diffuse panacinar emphysema is most commonly a/w a-1 AT deficiency.In distal acinar (paraseptal) emphysema, the alveolar ducts are predominantly affected. Distal acinar emphysema may occur alone or in combination with proximal acinar and panacinar emphysema. When it occurs alone, the usual association is spontaneous pneumothorax in a young adult.