This is a brief video on chronic obstructive pulmonary disease or COPD (with some comparisons to asthma).
I created this presentation with Google Slides.
Images were created or adapted from Wikimedia Commons.
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USMLE Step 2 CK 2CK Step 1 Step 3 board licensing exam Experience: Study Resources and Plan
Etiology Pathophysiology Presentation Diagnosis Chronic management Acute exacerbations Overview of Chronic Obstructive Pulmonary Disease (COPD) Smoking 90% of pts with COPD are/were smokers 20% of smokers get COPD Tobacco destroys elastin fibers → loss of elasticity → airway collapse Other environmental factors Poorly ventilated cooking fires Exhaust fires Occupational exposures (mining, chemical, textile industries) Genetic (suspect if patient is young, nonsmoker) alpha1-antitrypsin deficiency Etiology Pathophysiology Presentation Diagnosis Chronic management Acute exacerbations Pathophysiology Airway inflammation and irreversible bronchoconstriction Two components Most patients are a combination of both phenotypes Emphysema Fibrosis → low elasticity → hard to exhale (air is trapped) Accessory muscle use, increased work of breathing +/- weight loss, muscle wasting, cachexia Hyperinflated barrel chest Increased AP diameter Hyperresonance during percussion Prolonged expiration Airway collapse during expiration → increased resistance → increased effort → pursed lips Alveolar wall damage, remodeling → reduced surface area for gas transfer Tachypnea Pink complexion (no hypoxemia) → Pink puffers Chronic bronchitis Chronic productive cough Crackles, wheezing Prolonged expiration Cough for 3 months in two consecutive years Mucus production blocks larger airways Ciliary damage Increased goblet cells (which secrete mucus) → increased pulmonary vascular resistance → cor pulmonale (right ventricular strain) → Peripheral edema JVD Hepatosplenomegaly Inflammation → decreased gas transfer Low oxygen levels → a bluish color to the skin and lips Clubbing → Blue bloaters Etiology Pathophysiology Presentation Diagnosis Chronic management Acute exacerbations Pathophysiology By National Heart Lung and Blood Institute - National Heart Lung and Blood Institute, Public Domain, commons.wikime... By Nephron - Own work, CC BY-SA 3.0, commons.wikime... By Mikael Häggström - All used images are in public domain., Public Domain, commons.wikime... Pulmonary function tests ↓ FEV1 ( 80%), ↓ FVC , ↑ TLC because ↑ RV, ↓ DLCO Not reversible with bronchodilators ( 12% increase in FEV1 with albuterol) Not worsened with methacholine Other tests CXR: enlarged lungs, ↑ anterior-posterior diameter, flattened diaphragm, air trapping, translucent lung fields, rotated heart silhouette (RVH) CBC: erythrocytosis, ↑ hematocrit from hypoxemia EKG: right heart enlargement (RAE, RVH) from pulmonary hypertension ABG: ↑ pCO2, ↓ O2, respiratory acidosis BMP: ↑ bicarb to compensate A lateral chest X-ray of a person with emphysema: Note the barrel chest and flat diaphragm. By James Heilman, MD - Own work, CC BY-SA 3.0, commons.wikime... A severe case of bullous emphysema By © Nevit Dilmen, CC BY-SA 3.0, commons.wikime... Etiology Pathophysiology Presentation Diagnosis Chronic management Acute exacerbations Chronic management Based on severity (personalized) -Everyone (for mortality benefit) Smoking cessation Vaccines for influenza and pneumococcus Supplemental home O2 Mortality proportional to # O2 hours Up to ABG pO2 55, pulse ox 88% in all patients If cardiorespiratory signs of hypoxemia (high hematocrit, pHTN, cardiomyopathy): up to ABG pO2 60, pulse ox 90% in all patients Not higher so you don’t suppress hypoxic drive?? -Bronchodilators For rescue, use short-acting beta agonist (SABA: albuterol) Try both: long-acting muscarinic antagonist (LAMA, anticholinergics: ipratropium, aclidinium, umeclidinium, tiotropium) long-acting beta agonist (LABA: formoterol, olodaterol, salmeterol) In asthma, never use LABA w/o ICS Can add inhaled corticosteroids (ICS: budesonide) Can add PDE4-inhibitors (theophylline, roflumilast) Lastly, try oral steroids (prednisone) -Other Rehab can reduce dyspnea, improve exercise tolerance, but no mortality benefit Lung volume reduction surgery Transplant Etiology Pathophysiology Presentation Diagnosis Chronic management Acute exacerbations Acute exacerbations Supplement until SpO2 88-92% Nebulizer: ipratropium albuterol (often both) If no improvement, add PO or IV steroids Signs of infection? Purulent sputum? Up to half of all COPD exacerbations are caused by viruses, BUT Cover S pneumo, H flu, and Moraxella catarrhalis Consider amox +/ clav, TMP-SMX, azithromycin, doxycycline, fluoroquinolones, cephalosporins Last resort: intubation, mechanical ventilation