COPD Dr.S.Nandakumar. Professor of Medicine FOM, AIMST
Pre Test What is COPD ? What is Asthma ? How to differentiate these two ? Main etiology for COPD Symptoms ? Name two drugs used to treat COPD ?
Facts About COPD Cigarette smoking is the primary Cause of COPD. The WHO estimates 1.1 billion smoker worldwide, increasing to 1.6 billion by 2025 in low middle-income countries. In 2000,the WHO estimated 2.74 million deaths worldwide from COPD. In 2020 COPD will be the 3rd most common cause of death
Chronic Obstructive Pulmonary Disease (COPD) COPD is a disease state characterized by airflow limitation that is not fully reversible. The airflow limitation is usually both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases and associated with systemic manifestations. This definition does not use the terms chronic bronchitis and emphysema and excludes asthma (reversible airflow limitation).
Diagnosis of COPD It should be considered in patients over the age of 35 who have a risk factor, generally smoking, and who present with exertional dyspnoea, chronic cough, regular sputum production, frequent bronchitis or wheeze. The presence of airflow obstruction should be confirmed by performing spirometry.
Chronic Obstructive Pulmonary Disease (COPD) Chronic bronchitis Defined as the presence of cough and sputum production for at least 3 months in each of 2 consecutive years, is not necessarily associated with airflow limitation. Emphysema Defined as destruction and dilatation of the alveoli, is a pathological term that is sometimes (incorrectly) used clinically. Chronic bronchitis without airflow limitation is not included in COPD
Disease Trajectory of a Patients with COPD Symptoms Exacerbations Deterioration End of Life
Risk Factors Cigarette smoking Hyper responsiveness of airways Infection- ??? childhood Occupational exposure ??? Air pollution ??? Passive smoking Alpha 1 anti trypsin deficiency
Pathophysiology Smoking - activates macrophage – cytokines – inflammation Smoking – mucous gland hyperplasia – metaplasia - excess mucous production – edema – airway narrowing Reduced surfactant – airway narrowing or collapse Fibrosis
Pathophysiology of COPD Airflow obstruction – reduced FEV1/FVC ( COPD Vs BA ) Air trapping due to loss of elastic recoiling -– hyperinflation – impaired respiration Non uniform ventilation leads to ventilation perfusion mismatch -hypoxemia
Figure 7. 24 Diagrammatic representation of breath sounds Figure 7.24 Diagrammatic representation of breath sounds. (A) Vesicular. (B) Bronchial. Note the gap between inspiration and expiration and change in pitch and the blowing, tubular quality of bronchial breath sounds. © 2005 Elsevier 11
Figure 5.48 Timing of vesicular breathing. © 2005 Elsevier 12 12
Figure 5.49 Timing of bronchial breathing. © 2005 Elsevier 13 13
ASTHMA & COPD Asthma COPD Asthma COPD Onset in mid-life. Symptoms slowly progressive. Long smoking history. Dyspnoea during exercise. Largely irreversible airflow limitation. COPD Asthma COPD Onset early in life (often childhood). .Symptoms vary from day to day. .Symptoms at night/early morning. .Allergy, rhinitis, and/or eczema also present. .Family history of asthma. .Largely reversible airflow limitation. Asthma
Comparisons of asthma & COPD CD 4+ lymphocytes eosinophils mast cells Vary over time and in severity cough wheeze breathlessness chest tightness COPD CD 8+ lymphocytes macrophages neutrophils Persistent and progressive over time cough Wheeze Breathlessness sputum Patho- physiology: chronic inflammation Clinical history: symptoms Slide 8 • COPD differs from asthma in both the type of inflammation involved and in the pattern of respiratory symptoms caused
Risk factors that lead to asthma development Predisposing Factors atopy gender indoor allergens - dust mites - pet animal - cockroach - fungi outdoor allergens - pollens - fungi occupational sensitizers Contributing Factors respiratory infections diet air pollution - outdoor - indoor Smoking - passive - active Slide 18 GINA, Guidelines 1998
Common occupational agents flour / grain dust (bakery) paint, glue or plastic fumes soldering flux natural rubber latex wood dust Slide 19 • A large number of agents encountered in the workplace may provoke or exacerbate asthma • Some agents induce allergic asthma through stimulating the formation of a specific serum IgE (taking many years to cause the disease); some cause an immediate antigen-antibody response and others result in airway hyperresponsiveness because of a direct irritant effect on the airway wall • Typically, PEF measurements improve as soon as the patient is away from the workplace
Asthma - an inflammatory disease Normal Asthma Slide 13 • Asthma is a chronic inflammatory disorder of the airways • This bronchoscopic view of an airway shows the normal appearance of a healthy airway, contrasted with inflammation (reddening and swelling) and narrowing of the asthmatic airway • Microscopic examination of biopsy and lavage samples taken through the bronchoscope has established that inflammatory changes are present in asthma of all grades of severity, including recently diagnosed asthma
Inducers Inflammation Airway Hyperresponsiveness Airflow Limitation Allergens, Chemical sensitisers, Air pollutants, Virus infections Inflammation Triggers Allergens, Exercise Cold Air, SO2 Particulates Symptoms Cough Wheeze Chest tightness Dyspnoea Airway Hyperresponsiveness Airflow Limitation Slide 16 • Inflammation of the airways not only causes symptoms associated with widespread, variable airflow obstruction, it also results in an increase in airway hyperresponsiveness to a variety of stimuli (triggers) • Environmental and genetic influences in asthma (inducers) act mainly by provoking airway inflammation, rather than directly stimulating airway hyperresponsiveness • Triggers of bronchoconstriction, which are factors that provoke contraction of the sensitised airway wall, include a wide range of stimuli, such as exercise, cold air and pollen • Allergens can act as both inducers and triggers Barnes PJ
Indicators for Considering a COPD Diagnosis Indicators for Considering a COPD Diagnosis Chronic cough Present intermittently or every day. Often present throughout the day; seldom only nocturnal. Chronic sputum production Any pattern of chronic sputum production may indicate COPD. Acute bronchitis Repeated episodes. Dyspnoea that is Progressive (worsens over time). Persistent (present every day). Worse on exercise. Worse during respiratory infections. History of exposure to risk factors Tobacco smoke …. (including popular local preparations). Occupational dusts and chemicals. Smoke from home cooking and heating fuel. CLINICAL FEATURES OF COPD
Clinical features – physical examination Early stage – no findings Barrel chest Pursed lip breathing Tripod position Prolonged expiratory phase & wheeze Predominant emphysema – pink puffers Ch. Bronchitis – blue bloaters Signs of right heart failure
Diagnosis Of COPD SPIROMETRY The diagnosis should be confirmed by When performing spirometry, measure: Forced Vital Capacity (FVC) and Forced Expiratory Volume in one second (FEV1). Calculate the FEV1/FVC ratio. Patients with COPD typically show : a decrease in both FEV1 and FEV1/FVC With limited/no reversibility after bronchodilators However, both symptoms and spirometry should be considered when developing an individualized management strategy for each patient.
Assessment of severity of COPD MILD AIRFLOW OBSTRUCTION MODERATE AIRFLOW OBSTRUCTION SEVERE AIRFLOW OBSTRUCTION FEV1 50-80% PREDICTED FEV1 30-49% PREDICTED FEV1 <30% PREDICTED
Other tests… ABG X ray chest CT thorax Alpha 1 AT
GOLD Classification of COPD Stage 0 At Risk normal spirometry Chronic symptoms (cough and sputum production) Stage I Mild COPD FEV1 / FVC < 70% but FEV1 > or equal to 80 % predicted With or without chronic symptoms cough and sputum production. Stage II Moderate COPD :FEV1/FVC<70% 30% < or equal FEV1<80% predicted (IIA:50% < or equal FEV1<80% ) (IIB:30% < or equal FEV1<50% ) With or without chronic symptoms (cough, sputum production and dyspnea) Stage III Severe COPD FEV1 /FVC < 70% FEV1 < 30% predicted or FEV1 <50% predicted +presence of respiratory failure or clinical signs of right heart failure. At this stage, quality of life is very impaired and exacerbations may be life-threatening.
Goals of COPD management Prevent disease progression . Relieve symptoms. Improve exercise tolerance. Prevent and treat complications. Reduce mortality.
Assess and Monitor Disease A detailed medical history. Spirometry. Chest X-ray. Arterial blood gas measurement. Alpha-1 antitrypsin deficiency screening.
Smoking cessation is the single most effective And cost-effective – Reduce Risk Factors Smoking cessation is the single most effective And cost-effective – intervention to reduce the risk of developing COPD and slow its progression – nicotine patch or Bupropion Smoking Prevention Avoid occupational Exposures
Management of stable COPD Patient education. Pharmacologic Treatment. - Bronchodilators, - Corticosteroids, - Antibiotics, - Mucolytic -- Respiratory Stimulants Non-Pharmacologic Treatment - Rehabilitation, - Oxygen Therapy, - Surgical Treatments (Bullectomy)
“Bronchodilator medications are central to the symptomatic management of COPD” GOLD Report 2003
How Do Bronchodilators Work? Reverse the increased bronchomotor tone Relax the smooth muscle Reduce the hyperinflation Improve breathlessness
“All guidelines recommend inhaled bronchodilator as first line therapy. Chest 2000; 117: 23S-28S
Mode of Action Increased cholinergic tone is the only reversible component of COPD Normal airways have less degree of vagal cholinergic tone
Mode of Action (Contd.) Therefore, the need for anticholinergic drugs that will act as muscarinic receptor antagonist and block the acetylcholine induced bronchoconstriction
Mode of Action (Contd.) Anticholinergics may also reduce mucus hypersecretion Anticholinergic have no effect on pulmonary vessels, and therefore do not cause a fall in PaO2 Drugs of Today 2002; 38(9): 585-600
“Combining bronchodilators with different “Patients with moderate to severe symptoms of COPD require combination of bronchodilators” “Combining bronchodilators with different mechanisms and durations of actions may increase the degree of bronchodilation GOLD Report 2003
Algorithm for the management of COPD Mild Short acting bronchodilator – as required Tiotropium Long acting beta agonist assess with symptoms and spirometry Tiotropium+LABA LABA + tiotropium Add -Inhaled steroids -Theophylline Severe
Management Of Acute Exacerbation Home Management Bronchodilators: Increase dose and/or frequency of existing bronchodilator therapy. Can add anticholinergic until symptoms improve. Glucocorticosteroids: If baseline FEV1 < 50% predicted, add 40 mg oral prednisolone per day for 10 days to the bronchodilator regimen. Antibiotics: When symptoms of breathlessness and cough are increased and sputum is purulent and increased in volume, provide antibiotic coverage , taking into account local patterns of antibiotic sensitivity.
Indications for Hospital Admission for Acute Exacerbations .Marked increase in intensity of symptoms, such as sudden development of resting dyspnea Onset of new physical signs (e.g. Cyanosis, peripheral edema) Failure of exacerbation to respond to initial medical management Newly occurring arrhythmias .Older age
Management of acute exacerbation Bronchodilators + anticholinergics Antibiotics Corticosteroids Oxygen Mechanical ventilation
Carry home message.. Definition COPD v ASTHMA Risk factors Clinical features Management
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