I Obstructive Pulmonary Disorders blockage obstacle to flow a Manifested by increased resistance to airflow b Classification according to locations i Due to disorders in wall of airway lumen asthma acute and chronic bronchitis ii Due to loss of lung parenchyma emphysema 1 Parenchyma tissue of lung formed by alveoli iii Due to airway lumen disorders bronchiectasis bronchiolitis cystic fibrosis acute tracheobronchial obstruction epiglotitis croup II Luminal Wall Disorders a Asthma i NOT COPD Due to reversibility ii Affects 5 12 of U S this is a high percentage iii Most common chronic disease in children iv High risk populations African Americans inner city residents poolution smog premature low birth weight babies surfactant v Risk Factors 5 11 14 1 Genetic atopy structural smaller airways chromosomes a Atopy allergic genetic asthma 2 History of hay fever and eczema positive skin tests for allergens family history allergic asthma vi Pathogenesis 1 Reversible airway obstruction partial complete 2 Airway inflammation Increased airway responsiveness to certain stimuli vii viii Pathogenesis immunohistopathologic 1 Airway epithelium denudation lose outer layer making epitherlial node 2 Collagen deposition beneath basement membrane 3 Edema Mast cell activation inflammation histamine Inflammatory cell infiltrates neutrophils eosinophils 4 lymphocytes ix Classification 1 Intrinsic non allergic elevated IgE but Ag Ab reactions not directly involved a Inside the body 2 Extrinsic allergic dogs cat pollen a Outside the body x Clinical manifestations 1 Wheezing chest tightness dyspnea dry productive cough 2 Increased sputum production thick tenacious scant viscid xi Extrinsic asthma 1 30 50 of cases 2 IgE mediated response is common 3 Atopic clinical manifestations elevated IgE allergic rhinitis and eczema positive family history of allergy attacks associated with seasonal environmental occupational exposure 4 30 50 of cases xii Extrinsic Mechanism of Action Ag Ab complex 1 Immediate phase initiated by exposure to specific Ag with previously sensitized mast cell in airway mucosa Ag reacts with Ab on mast cells causing mast cells to release chemical mediators 2 Chemical mediators released histamine slow reacting leukotrienes of anaphylaxis prostaglandins bradykinins serotonin eosinophilic chemotactic factors a Prostaglandins vasodilate b Chemotactic Factors chemicals that transport esosinophils basophils and mast cells 3 Normal respiratory epithelium is denuded and replaced by goblet cells 4 Alterations in epithelial integrity holes damaged leaky 5 vessels Increased microvascular permeability mucosal edema inflammatory exudates bronchoconstriction and leakage 6 Late phase recruit leukocytes release more mediators to cause more epithelial damage 7 Epithelial damage hypertrophied smooth muscle edema mucus gland hypertrophy and mucus in lumen 1 Physical cough wheezing hyperinflated chest decreased breath sounds a Hyperinflated chest especially in kids stress on the lungs because you re trying to bring in so much air 2 Sputum exam Charcot Leyden crystals from crystallized enzymes on eosinophilic membranes eosinophils Curschmann spirals mucus casts in bronchioles a Charcot Leyden Crystals look like purple flowers under microscope b Curschman spirals are mucus that builds in bronchioles and becomes hardened fibrotic spiral like 3 X ray hyperinflation with diaphragm flattening 4 Pulmonary function test decreased forced expiratory volumes peak expiratory flow rate xiii Diagnosis xiv Treatment 1 Avoid triggers b Bronchitis i Acute bronchitis 2 Environmental control remove allergens air purifiers air conditioners a Air purifiers to filter the air 3 Preventive therapy prevent attacks and permanent 4 Desensitization allergen specific immunotherapy 5 Oxygen therapy small volume nebulizers opens up the damage lungs 6 Drugs beta 2 agonists corticosteroids leukotriene modifiers mast cell inhibitors 1 Acute inflammation of trachea and bronchi ii Chronic bronchitis more often with overweight patients 1 Type B COPD blue bloater cyanotic and edema all over the body Anasarca 2 Chronic recurrent productive cough for 3 months in 2 successive years 3 Persistent irreversible 4 Typical patient overweight men women onset 30 40 years 5 Commonly associated with emphysema 6 Etiology tobacco smoke repeated airway infections genetic predisposition physical chemical irritant inhalation due to occupation perhaps 7 Pathogenesis a Chronic bronchial mucosa inflammation and swelling results in scarring b Bronchial mucus gland goblet cell hyperplasia increased mucus production mucus combine with purulent exudate bronchial plugs to form mucus plug Increased bronchial wall thickness resistance increases breathing work increased oxygen demands c d Pulmonary hypertension bronchial wall inflammation with pulmonary vessel vasoconstriction possible right heart failure 8 Chronic manifestations a Clinical manifestations dyspnea on exertion excess sputum chronic cough more severe in mornings excess body fluid edema hypervolemia late cyanosis 9 Diagnosis via chest X ray increased bronchial vascular markings congested lung fields previous pulmonary infection evidence III Parenchymal Disorders a Emphysema a Normal x ray is a dark gray black means air fluid 10 Management a Stop smoking reduce exposure to irritants b Adequate rest proper hydration c Physical reconditioning treadmill stationary bike alternating rest and exercise d Bronchodilator therapy i Type A COPD Pink puffer puff through pursed lips ii Onset 1 50 years old hereditary alpha 1 antitrypsin deficiency in lung iii Etiology 2 50 years old develops over time 1 Smoking 70 pack year alveolar damage due to lung inflammation which causes proteolytic enzyme release inactivates protective alpha 1 antitrypsin 2 Air pollution 3 Certain occupations mining welding working with near asbestos 4 Alpha 1 antitrypsin deficiency should be found normally in the body and its proteases and makes sure we don t have too much elastase but we do need some a Alpha 1 anti trypsin liver protein serine protease inhibitor inhibits leukocyte proteases elastase protects lungs by preventing elastase from breaking down elastic tissue 5 Genetic or environmental Inflammatory cells neutrophils macrophages release proteolytic enzymes leading to alveolar damage 2 Reduction in pulmonary capillary bed impaired exchange of oxygen and carbon dioxide between alveoli and capillaries 3 Loss of elastic tissue in lung decreased