COPD lecture


Published on

Published in: Health & Medicine
  • Be the first to comment

  • Be the first to like this

No Downloads
Total views
On SlideShare
From Embeds
Number of Embeds
Embeds 0
No embeds

No notes for slide
  • Clinical defethion1- just productive caught 2-Chronic asthmatic bronchitis  associated hyperresponsive (hyperreactive) airways , bronchospasm3- - obstructive lesion
  • 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
  • COPD lecture

    1. 1. Free syriaRAHEEF ALATASSI
    2. 2. objectives chronic bronchitis :  definition  causes  path physiology  morphology  mechanism of obstruction  management  complication  S/S  Investigation Emphysema:  definition  Causes  path physiology  morphology  types  management  complication  S/S  Investigation Pulmonary hypertension:  Definition
    4. 4. 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
    5. 5. Causes
    6. 6. 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
    7. 7. morphology The trachea in the mid- upper field is hyperemic the bifurcation & bronchi contain mucopurulent exudate secretion.
    8. 8.  enlargement of the mucus-secreting glands
    9. 9. management Stop smoking > inhaled bronchodilator (anticholinergic agonist or b2 agonist) > combination > glucocorticosteroid > oxygen.
    10. 10. Complications: Pulmonary hypertension and cardiac failure Recurrent infections Respiratory failureS/S : cough , sputum ,frequent infections , intermittent dyspnea, wheeze. Some patients develop significant COPD with outflow obstruction: hypercapnia, hypoxemia, cyanosis
    11. 11. 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
    12. 12. Spirometry
    13. 13. EMPHYSEMA
    14. 14. 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
    15. 15. path physiology
    16. 16. Pathogenesis of Emphysema Tobacco smokeEmphysema arises as a consequence oftwo imbalances: free radicalProtease-antiprotease imbalanceOxidant-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
    17. 17. morphology The external surfaces of the upper lobes of both the right and left lungs have large bullae. Distal type. bullaeCystmore than1 cm.
    18. 18.  the permanent enlargement of the airspace, accompanied by destruction of the septa
    19. 19. 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
    20. 20. Management & Investigation The same treatment & Investigation as the chronic bronchitis
    21. 21. Pulmonary Hypertension in COPD Chronic hypoxia Pulmonary vasoconstriction Muscularization Pulmonary hypertension Intimal hyperplasia Fibrosis Cor pulmonale Obliteration Edema Death
    22. 22. complicationI. Pulmonary hypertension;  hypoxia-induced pulmonary vascular spasm  loss of capillary surface area due to alveolar wall destructionII. Right side heart failureIII. Respiratory failure
    23. 23. S/S  Patients present with dyspnea, and abnormal pulmonary function tests Patients with no bronchitisPatients with underlyingchronic bronchitis They have more severe dyspnea andThey 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)
    24. 24. 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
    25. 25. 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.