A diagnosis of COPD should be considered in any patient who has cough, sputum production, or dyspnea and/or a history of exposure to risk factors. The diagnosis is confirmed by spirometry. To help identify individuals earlier in the course of disease, spirometry should be performed for patients who have chronic cough and sputum production even if they do not have dyspnea. Spirometry is the best way to diagnose COPD and to monitor its progression and health care workers to care for COPD patients should have assess to spirometry.
air spaces distal to terminal bronchioles is (acini) respiratory bronchiole , alveolar duct , alveoli
Hypoxia in lung is special will induce pulmonary vasoconstriction that will elevate pulmonary hypertension, pressure overload right side heart failure
Definition It is defined as a persistent productive cough for at least 3 consecutive months in at least 2 consecutive yearsforms featuresSimple chronic bronchitis the productive cough raises mucoid sputum, but airflow is not obstructedChronic asthmatic bronchitis hyper-responsive airways with intermittent bronchospasm and wheezingChronic obstructive bronchitis develops chronic outflow obstruction Associated with emphysema
Pathogenesis of Chronic BronchitisPathogenesis of Chronic Bronchitis mucous gland hyperplasia,Cigarette smoking or other air pollutants lead to: 1-Hypertrophy and hyper secretion of bronchial mucous glands 2-Metaplastic formation of goblet cells 3-Infiltration by CD+8 lymphocytes ,macrophages and neutrophils
morphology The trachea in the mid- upper field is hyperemic the bifurcation & bronchi contain mucopurulent exudate secretion.
The severity of COPD also depends on the severity of dyspnea and exercise limitation. These and Investigation Spirometry Severity of COPD (GOLD scale) FEV1 % predicted Mild ≥80 Moderate 50–79 Severe 30–49 <30 or chronic respiratory failure Very severe symptoms CXR > hyperinflation FBC > polycythemia ABG > hypoxemia or hypercapnia
definition• It is permanent enlargement of air spaces distal to terminal bronchioles, accompanied by destruction of their walls.• not associate with fibrosisCauses:SmokingDeficinecy of a1 antitrypsin
Pathogenesis of Emphysema Tobacco smokeEmphysema arises as a consequence oftwo imbalances: free radicalProtease-antiprotease imbalanceOxidant-antioxidant imbalance INCRESE elastaseThe destructive effect of protease insubjects with low antiprotease activityleads to emphysema free radical Protease releaseFree radical → deplete the lungantioxidant mechanisms → tissuedamage
morphology The external surfaces of the upper lobes of both the right and left lungs have large bullae. Distal type. bullaeCystmore than1 cm.
the permanent enlargement of the airspace, accompanied by destruction of the septa
typestype features It involve the central or proximal parts of the aciniCentriacinar The lesions are more common and severe in the upper lobes This type is seen as a result of cigarette smoking It occurs more commonly in the lower lung zonesPanacinar The type of emphysema occurs in α1-antitrypsin deficiency The distal part of the acinus is involvedDistal Acinar It is seen adjacent to the pleura, along the lobular margins,scarring. Cystlike structures can be formed (bullae) The acinus is irregularly involvedIrregular It is associated with scarring Clinically asymptomatic The most common form of emphysema
Management & Investigation The same treatment & Investigation as the chronic bronchitis
Pulmonary Hypertension in COPD Chronic hypoxia Pulmonary vasoconstriction Muscularization Pulmonary hypertension Intimal hyperplasia Fibrosis Cor pulmonale Obliteration Edema Death
complicationI. Pulmonary hypertension; hypoxia-induced pulmonary vascular spasm loss of capillary surface area due to alveolar wall destructionII. Right side heart failureIII. Respiratory failure
S/S Patients present with dyspnea, and abnormal pulmonary function tests Patients with no bronchitisPatients with underlyingchronic bronchitis They have more severe dyspnea andThey have less dyspnea hyperventilationand retain more CO2 They are always hypoxic They have normal gasand cyanotic (blue exchange and adequatebloaters) oxygenation of hemoglobin (pink puffers)
Pulmonary hypertension: The pulmonary circulation is normally one of low resistance, with pulmonary blood pressures being only about one-eighth of systemic pressure. Pulmonary hypertension (when mean pulmonary pressures reach one- fourth or more of systemic levels) is most often secondary to a decrease in the cross- sectional area of the pulmonary vascular bed, or to increased pulmonary vascular blood flow
morphology A, Gross photograph of atheroma formation, a finding usually limited to large vessels. B, Marked medial hypertrophy. C, Plexogenic lesion characteristic of advanced pulmonary hypertension seen in small arteries.