Download Free Medical Chronic Obstructive Pulmonary Disease-COPD PowerPoint Presentation

Chronic Obstructive Pulmonary Disease-COPD PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical titled "Chronic Obstructive Pulmonary Disease (COPD)" by Mikael Jones, Pharm.D., BCPS.

This medical talks about Chronic obstructive pulmonary disease (COPD), a chronic respiratory disease characterized by airflow limitation that is not fully reversible. COPD includes chronic bronchitis, emphysema, and small airway disease. It is usually caused by long-term exposure to irritating gases or particulate matter, such as cigarette smoke, air pollution, or workplace dust and chemicals.

The primary symptoms of COPD include shortness of breath, coughing, and sputum production. As the disease progresses, it can lead to respiratory failure, heart disease, and other complications. COPD is a major cause of morbidity and mortality worldwide, and it is estimated to be the third leading cause of death globally.

There is currently no cure for COPD, but there are treatments that can help manage the symptoms and slow the progression of the disease. These treatments include bronchodilators, inhaled corticosteroids, oxygen therapy, and pulmonary rehabilitation. Quitting smoking and avoiding other environmental irritants can also help prevent the development and progression of COPD.

Tags : Chronic Obstructive Pulmonary Disease, COPD, chronic respiratory disease, chronic bronchitis, emphysema, small airway disease, Emergency Medicine, Emergency Medicine

Published on : Apr 14, 2023 | Views : 1453 | Downloads : 6

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Chronic Obstructive Pulmonary Disease (COPD) Mikael Jones, Pharm.D., BCPS NUR 652
Slide 2-

COPD Disease state characterized by airflow limitation Airflow limitation is not fully reversible Usually progressive Associated with abnormal inflammatory response of the lungs to noxious particles or gases Caused by a mixture of small airway disease (obstructive bronchiolitis) and parenchymal destruction (emphysema) Relative contribution of each varies from patient to patient Chronic Inflammation is present and causes remodeling and narrowing of small airways Destruction of the parenchyma Loss of alveolar attachments to the small airways Decreases lung elastic recoil The above changes lead to a diminishment in the ability of the airways to remain open during expiration In the past COPD has been viewed as the overlapping of Chronic Bronchitis and Emphysema However movement away from this view
Slide 3-

Obstructive vs Restrictive Pulmonary Disease Obstructive diseases impair exhalation Asthma, bronchitis, emphysema Obstructive diseases reduce FEV/FVC ratio vital capacity does not change (may even increase) Restrictive diseases impair inhalation Pneumonia, pulmonary fibroses (black lung) Due to fluid accumulation, loss of elasticity Restrictive diseases reduce volume (vital capacity) but do not affect FEV/FVC ratio
Slide 4-

COPD: Epidemiology Affects >14 million adults in U.S. (5% of population) 12 million with chronic bronchitis (~90%) 1.65 million with emphysema (~12%) 4th Leading cause of mortality 80-90% of COPD is linked to cigarette smoking 15-20% of smokers develop COPD Other risk factors include occupational exposures (dust, smoke, mining, textile manufacturing), and air pollution
Slide 5-

Chronic Bronchitis: Clinical Characteristics Chronic bronchitis is characterized by the excessive production of mucus with productive cough Blockade of bronchioles by mucus, inflammation and edema Presentation Early onset (20-30 yrs) with cigarette cough, morning cough Diagnosis usually occurs at 50-60 yrs Smoking is the most significant risk factor Repeated respiratory infections are common Productive cough, copious, often purulent sputum, late onset dyspnea Patient is typically obese
Slide 6-

Chronic Bronchitis: Pathophysiology Repeated irritation and inflammation leads to bronchiolar smooth muscle hypertrophy and reduction in airway diameters Increase in size and number of submucosal mucus glands and goblet cells Goblet cells proliferate in bronchioli, which normally do not contain mucus-secreting cells Mucus is thick and difficult to clear from airways Ciliary action is impaired by inflammation, resulting in poor clearance of mucus, leading to repeated bacterial infections Hypoventilation common Elevated blood CO2 and reduced O2, cyanosis Often termed “blue bloaters” Loss of respiratory drive unexplained Death results from right heart failure (cor pulmonale) due to pulmonary hypertension, or respiratory failure
Slide 7-

Emphysema: Clinical Characteristics Emphysema results from acinar distension and destruction of alveolar membranes Loss of surface area for gas exchange Later onset than CB (30-40 yrs) Diagnosis usually occurs at 60-70 yrs Minimal history of cough Chief complaint is shortness of breath Patients typically hyperventilate to maintain normal blood gases “pink puffers” Environmental risk factors: smoking, dust inhalation, pollution Patients are typically thin, sometimes “barrel-chested”
Slide 8-

Differentiation of Asthma, Chronic Bronchitis, and Emphysema
Slide 9-

Four Components of COPD Management Assess and monitor the disease Reduce Risk Factors Manage stable COPD Manage Exacerbations
Slide 10-

Assess and Monitor Disease Diagnosis based on History of exposure to risk factors The presence of airflow limitation that is not fully reversible, with or without the presence of symptoms Therefore consider workup for patients who have chronic cough and sputum production even in the absence of dyspnea Spirometry is used to diagnosis COPD
Slide 11-

Assess and Monitor Disease Spirometry
Slide 12-

Assess and Monitor Disease Severity of COPD Gold 1 Mild FEV1 80% predicted Gold II Moderate FEV1 50-79% predicted Gold III Severe FEV1 30-49% predicted Gold IV Very Severe FEV1 <30%
Slide 13-

Assess and Monitor Disease Staging of COPD patients uses a combination of Spirometetry and patient report of symptom severity Number of exacerbations per year Modified Medical Research Council Questionnaire for Assessing the Severity of Breathlessness (mMRC) Used to capture symptom impact on function
Slide 14-

Assess and Monitor Disease Modified Medical Research Council Questionnaire for Assessing the Severity of Breathlessness (mMRC)
Slide 15-

Assess and Monitor Disease Use Spirometry and mMRC to place a patient into 1 of 4 categories
Slide 16-

Assess and Monitor Disease Patient Group A- Low Risk, Less symptoms Gold 1 or 2 and/or 0-1 exacerbations per year and mMRc 0-1 Patient Group B-Low Risk, More symptoms Gold 1 or 2 and/or 0-1 exacerbations per year and mMRc ≥2
Slide 17-

Assess and Monitor Disease Patient Group C High Risk, Less Symptoms Gold 3 or 4 and/or ≥2 exacerbations per year and mMRc 0-1 Patient Group D-Low Risk, More symptoms Gold 3 or 4 and/or ≥2 exacerbations per year and mMRc ≥2
Slide 18-

Risk Factor Reduction Reduction exposure to Tobacco smoke Occupational dusts and chemicals Indoor and outdoor pollutants SMOKING CESSATION Reduces risk of developing COPD Stops its progression! Offer smoking cessation to every patent
Slide 19-

Management of COPD General Concepts Smoking Cessation Exercise training Pharmacotherapy Does not modify long-term decline in lung function Medications decrease symptoms and/or complicatons Bronchodilators Can be given PRN or scheduled to prevent or reduce symptoms Inhaled preferred In contrast to asthma, fully normal pulmonary function cannot be attained
Slide 20-

Management of COPD
Slide 21-

Pharmacotherapy Principle Therapies Beta2 agonists Anticholinergics Theophylline Combination of above Choice between above agents depends on patient individual response in terms of safety and effectiveness
Slide 22-

Pharmacotherapy Long acting bronchodilators are more effective and convenient than short acting, but much more expensive Combining drugs with different mechanisms and durations of action may increase the degree of bronchodilation for equivalent or lesser side effects. Theophylline is effective in COPD, but due to its potential toxicity, inhaled bronchodilators are preferred when available.
Slide 23-

Anticholinergics Available agents Ipratropium bromide Inhaler and nebulized solution Tiotropium Dry powder inhlaer Aclidinium Clinical Pharmacology anticholinergic agent that blocks the effects of acetylcholine at muscarinic receptors in the airways, reducing vagal-mediated bronchoconstriction Tiotropium has a duration of action of more than 24 hours Ipratropium lasts up to 8 hours from administration Aclidinium is does every 12 hours
Slide 24-

Anticholinergics Safety Contraindications Hypersensitivity to products For Ipratropium, allergy to peanuts or soybeans Product contains soya lecithin Warning/Precautions Use in caution in diseases which anticholinergics can exacerbate the diseasse Myashenia gravis, narrow angle glaucoma, benign prostatic hyperplasia, bladder neck obstruction 74% of Tiotropium is eliminated unchanged via the urine; use caution in renal failure (monitor for excessive antcholinergic symptoms)
Slide 25-

Anticholinergics Safety Adverse Effects poorly absorbed from the lungs so little systemic effects are observed therefore adverse effects are minimal dry mouth unpleasant taste cough urinary retention
Slide 26-

Anticholinergics Patient Education Educate on how to use inhaler Tiotropium uses a capsule to hold the dry powder inhaler. The capsule is placed in the inhaler device Tiotropium vs. Ipratropium Tio given once daily vs Iprat q6-8 hours Tio= better compliance Iprat= much less expensive
Slide 27-

Beta2 Agonists See asthma lecture for specific details Short-acting beta 2 agonists have a shorter duration of action (4-6 hours) than ipratropium Long-acting beta 2 agonists have a duration of action of 12 hours Arformoterol is nebulized Twice daily Indacterol once daily Formoterol twice daily Salmeterol twice daily
Slide 28-

Theophylline See Asthma handout Use is limited by toxicity Inhaled anticholinergics or beta agonists are preferred over theophylline
Slide 29-

Roflumilast Sectively inhibit phosphodiesterase-4 (PDE4) leading to an accumulation of cyclic AMP (cAMP) within inflammatory and structural cells Anti-inflammatory effects include suppression of cytokine release inhibition of lung infiltration by neutrophils and other leukocytes.
Slide 30-

Roflumilast Used as adjunctive therapy in severe COPD associated with chronic bronchitis Dosed 500mg po daily Adverse effects Weight loss/ Diarrhea Insomnia Anxiety, depression Avoid in patients with history of depression with suicidal behavior/ideation
Slide 31-

Inhaled Corticosteroids See asthma lecture Reserved for patients in Patient Categories C and D May reduce exacerbations
Slide 32-

COPD Exacerbations Most common causes Infection of the tracheobronchial tree Air pollution Unknown Factors Presentation Increased breathlessness Increased sputum production Change in sputum quality Malaise, insomnia, fatigue Signs of Severe exacerbation Use of accessory respiratory muscles. Paradoxical chest wall movements. Worsening or new onset central cyanosis. Development of peripheral edema. Hemodynamic instability. Signs of right heart failure. Reduced alertness.
Slide 33-

COPD Exacerbations