Ppok .pptx

COPD

Chronic Obstructive pulmonary Diseas e  Two distinct processes are involved, most often in c ombination.  Chronic Bronchitis – dx on history  Emphysema – dx previously on histology, nowaday s clinically (good clinical-pathologic-radiologic cor relation)

Def: Chronic Bronchitis 

 1. 2. 3. 4.

Excessive tracheobronchial mucus production sufficient to cause cough with expectoration for most days of at least 3 months of the year for 2 consecutive years. Classification: Simple chronic bronchitis Chronic mucopurulent bronchitis Chronic bronchitis with obstruction Chronic bronchitis with obstruction and airway hyperreact ivity.

Def: Emphysema 

 1. 2. 3. 4.

Permanent abnormal distention of air spaces distal to the t erminal bronchiole with destruction of alveolar septa (cont aining alveolar capillaries) and attachments to the bronchi al walls. Classification: Centriacinar ( centrilobular) emphysema Panacinar emphysema Paraseptal emphysema Senile emphysema

Def: COPD  Chronic obstruction to airflow due to chronic bronc hitis and/or emphysema.  Degree of obstruction may be less when the patient is free from respiratory infection and may improve with bronchodilator drugs  Significant obstruction is always present

Epidemiology of COPD      

30% of smokers develop COPD 20% of adult males have COPD 15% of COPD patients are severely symptomatic 4 th leading cause of death (USA) Mortality rate still rising prevalence in low birth weight and low socioecon omic status  Tuberculosis in smokers predisposes to COPD

Pathogenesis:Effects of Smokin g -1  Oxidative stress: O2-, OH-,H2O2, HOCl; source of Fe2+  c atalizes production of OH- by neutrophils, eosinophils, alveo lar macrophages; tar (cigarettes) contains NO and induces i NOStoxic peroxynitrites  Elastin breakdown- activated neutrophils neutrophil elas tases and oxidants; -1-AT and metalloproteinase inhibitors (lung defenses) inactivated by smoke  Chemoattractant, upregulation of adhesion molecules  n eutrophil sequestration in lungs  expression of pro-inflammatory mediators: IL-8, NF-B  recruitment of N, B, E and T lymphocytes

Effects of smoking -2   levels of myeloperoxidase and eosinophilic cationic protei n  bronchoconstriction   levels of TGF- (transforming growth factor) fibrog

enesis  Lipid peroxidation and DNA damage point mutations 0f t he p53 gene locus epithelial dysplasia and lung

cancer   ciliary function  retained secretions;  airway resistance vagal-mediated smooth muscle contraction  Hypertrophy and hyperplasia of mucus secreting glands  secretions

Pathogenesis-3  Air pollution exacerbations of CB related to heavy polluti on with SO2 and NO2  Occupation  exposure to organic and inorganic dust or no xious gases accelerated decline in lung function  Infection  even mild viral respiratory infections ( rhino vir us) may be a major factor associated with etiology as well a s progression of disease; severe viral pneumonia early in life may lead to COPD  Genetic factors: - -1-antitrypsin deficiency PIZZ, PISZ, PI 00 (PI null null),  susceptibility to effects of smoking

Pathophysiology  Air trapping- RV and FRC elevated  Hyperinflation –TLC elevated   elastic recoil pressure  dynamic collapse of airways dur

ing expiration ineffective cough mechanism and pursed li ps breathing (emphysema)   compliance (emphysema)   airway resistance  Prolonged forced expiratory time (N=<6 seconds)

Pathology: CB  Hypertrophy of mucus-producing glands in submucosa of la rge cartilaginous airways  Goblet cell hyperplasia, mucosal and submucosal inflammat ory cell infiltrate, oedema, peribronchial fibrosis, intralumin al mucus plugs and increased smooth muscle in small airwa ys  The major site of airflow obstruction is in the small airways and the inflammatory infiltrate consists of neutrophils (in ast hma eosinophils)

Pathology : Emphysema 

1. 2. 3. 4.

in number and size of alveolar fenestrae eventual destr uction of alveolar septa and their attachments to terminal a nd respiratory bronchioles distention of alveolar spaces Centriacinar E- respiratory bronchioles (central) affected Panacinar E- central and peripheral portions of acinus affe cted Senile E- alveoli and alveolar ducts enlarge (> 50 Y) Periacinar/paraseptal E- distention of alveolar spaces adja cent to septal and pleural surfaces

Physical signs of COPD  Ronchi- in early disease present on forced expiration, later p resent in inspiration and expiration  Prolonged forced expiratory time (> 6 seconds)  Hyperinflation:  cardiac dullness, liver dullness displaced downwards,  A-P chest diameter,  heart and breath sound s, Hoover sign  Inspiratory crepitations (lung bases)  Pursed lips breathing ( dynamic airway collapse)  Use accessory respiratory muscles  Signs of cor pulmonale and PHT

Emphysema:ChronicBronchitis Emphysema = pink puffer Age (Dx) 60 + y Rest dyspnea mild-mod Exer dyspnea severe Cough ± Sputum scanty, mucoid Resp infect less often Resp failure terminal Cor pulmonale terminal

Chronic Bronchitis = blue bloater 50 ± y none moderate prominent large volume, purulent often repeatedly common

Emphysema:Chronic Bronchitis PHT (rest) 0-mild (exertion) moderate Build Asthenic, cachectic Hematocrit 35-45 Breath pattern use accesso ry muscles of respiration Sleep pattern Normal XRC Hyperinflation Bullae

Mild-moderate severe obese, cyanosed 50-55 do not use accessory muscles of respiration sleep apnea  bronchovascular markings

Emphysema:Chronic Bronchitis Blood gas: PaO2 ± 65 mm Hg PaCO2 35-40 Elastic recoil  AW resistance N- Diffusion Cap  FEV1  Bronchodilator response Poor

45-60 50-60 Normal  N-   Better but < 12% and 200ml

Spirometric classification of C OPD severity using post-bronch odilator FeV1

 Stage I (Mild): FeV1/FVC <0.7; FeV1 80% of pred icted  Stage II (Moderate): FeV1/FVC <0.7; FeV1 50- <8 0% of predicted  Stage III (Severe): FeV1/FVC <0.7; FeV1 30-<50%  Stage IV (Very severe): FeV1/FVC <0.7; FeV1 <30 % or <50% but chronic respiratory failure is present . (GOLD 2007)

Treatment: Goals of manageme nt -1  Recognition of disease (early Diagnosis and staging)  Smoking cessation (secondary prevention) nicotine replacem ent and Zyban  Improvement of breathlessness (Rx of airflow obstruction- b ronchodilator drugs) 1.Methylxanthines 2.Short and long-acting B2adrenergic agonists ( incidence of pneumonia with ICS and LABA combinations) 3.Short and long-acting Anticholinergics- BD of choice in COP D

Treatment -2  Respiratory infections –AB when sputum volume and/or p urulence (exacerbation of COPD); Influenza and Streptococ cus pneumoniae vaccination  Bronchopulmonary drainage and postural drainage (physioth erapy) for patients with CB  Oxygen therapy for patients with hypoxia (PaO2<55 mmHg, SaO2 <88% ) and erythrocytosis (Hematocrit>55)  Pulmonary rehabilitation and education ( improving quality of life)- exercise program and improved nutrition  Prevention and treatment of complications (cor pulmonale) a nd limitation of disease progression

Treatment -3  Glucocorticoids –only 10% of COPD patients show subjecti ve benefit and improved lung function (FeV1 increase of 20 % or more) on systemic GCs; with COPD exacerbation a co urse of prednisone 40 mg/d for 2 weeks are usually prescribe d  Inhaled GCs may  severity of exacerbations and need for h ospitalisation. Benefit of 10-14 day trial of 30-40mg prednis one for Stage III COPD patients remains to be proven.  Lung volume reduction surgery  Transplantation

Airway Diseases - COPD  Smoking  Hyperinflation  Airway collapse  Respiratory infection  Bronchospasm  Allergy  Inflammation

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