COPD (Chronic obstructive pulmonary disease
Definition: COPD is a group of chronic and slowly progressive respiratory disorders characterized by reduced maximal expiratory flow during forced exhalation. With variable degree of reversibility and bronchial hyper reactivity. COPD comprises emphysema and chronic bronchitis, which most often present in combination. Emphysema----permanent and destructive enlargement of air spaces distal to the terminal bronchioles without obvious fibrosis and with loss of normal architecture.1Friday, February 10, 2006Friday, February 10, 2006Friday, May 06, 2011 Chronic bronchitis----presence of cough productive of sputum not attributable to other causes on most days for at least 3 months over 2 consecutive years, with clinically significant airflow limitation.
Caucasian more affected than African American. Prevalence peaks in the seventh and eighth decades. Males are more frequently affected than females.EPIDEMIOLOGY
There is a higher prevalence of COPD among persons with lower socioeconomic status and in those with history of low birth weight. It¶s the 4th cause of death in the US (mortality is still rising).
. Limited studies available in developing countries.
Pathological changes of COPD and emphysema typically coexist. This leads to regular expectoration of sputum. In advanced cases. The epithelial layer may become ulcerated and when the ulcer heals squamous cells may replace the columnar cells leading to widespread fibrosis of the bronchial wall and narrowing in the small airways. There is infiltrations of the walls of the bronchi and bronchioles with chronic inflammatory cells predominantly the CD8. Leading to development of air flow limitation
. mainly in the larger bronchi. the bronchi are inflamed and pus is seen in the lumen. Chronic bronchitis: The most consistent fining in chronic bronchitis is hypertrophy and increase in number of the mucus secreting glands of the bronchial tree.
Pathophys««.whilst the distal alveolar ducts and alveolar are well preserved (common presentation) Pan -acinar emphysema: This is less common. Loss of lung elastic recoil result increase TLC .Emphysema
Emphysema is classified according to the site of damage. Irregular emphysema. Here distension and destruction appear to involve the whole of the acinus.and decrease gas transfer.
. the lung become a mass of bullae. Leading to expiratory air flow limitation and trapping. Occurs in alpha 1 antitrypsin deficiency. Centri . There is scarring and damage affecting the lung parenchyma patchily without particular regard for acinar structure..acinar emphysema: Distention and damage of lung tissue is concentrated around the respiratory bronchioles .
. Causing loss of elastic recoil and air flow limitation.Chronic bronchitis
The most consistent pathological finding is hypertrophy and increase of the mucus secreting glands of the bronchial tree and is evenly distributed throughout the lung mainly in the larger bronchi. If smoking is stopped earlier the condition is reversible. The walls of the bronchi and bronchioles are infiltrated with acute inflammatory cells predominantly CD8.Pathophys«. If not leads to squamous metaplasia and fibrosis of the bronchial walls. The epithelial cells become ulcerated and when it heals squamous cells replace the columnar cells-. At times they become inflamed and pus is seen in the lumen.scarring and narrowing in small airways. Leading to increased mucus production and regular expectoration of sputum.
The smoke has an adverse effect on surfactant.smokers. Alpha 1 antitripsin is a major serum anti protease which can be inactivated by cigaratte smoking. These granulocytes are capable of releasing elastases and proteases. favoring overdistension of the lungs.Pathogenesis
Cigarette smoking Smokers bronchi. and alveoli are infiltrated by neutrophil granulocytes. which possibly help to produce emphysema. bronchioles. The hypertrophyof mucus glands in the larger airway is thought to be due to irritation resulting from inhalation of cigarette smoke.
.which are absent in non.
. However prompt use of antibiotics and routine influenza vaccinations are appropriate.Infection
Patients with COPD cope badly with infection often is a cause of acute exacerbations. The precise mechanisms are not clear. Repeated infections are associated with development of progressive airflow limitation that characterizes disabling COPD.Pathogenesis««.
Those who dvlp dizs are usually cigarette smokers. Not all develop chest disease. its function is to inhibit neutrophil elastase. a proteolytic enzyme capable of destroying alveolar wall connective tissue.Pathogenesis«.Alpha ±Antitrypsin deficiency
It is produced by the liver. There are three phenotypes MM (normal) MZ (heterozygous) and ZZ (homozygous) 1:5000 child in BR.. Accounts for 2% of emphysema cases. Is born with homozygous deficiency.
Frequent infective exacerbations Symptoms can be worsened by cold. foggy weather. With advance dizs breathlessness become severe even after mild exercise.Clinical features
Symptoms. and atmospheric pollutions.
. Wheezes and breathlessness following many years of a smokers cough. Cough with production of sputum.
Clinical features«. Patients who remain responsive to CO2 are usually breathless and rarely cyanosed ( pink puffers) PTs who become insensitive to CO2 are often oedematous and cyanosed (blue blotters) PTs with hypercapnea may have peripheral vasodilatation with bounding pulse. Chest expansion is poor. In severe cases.coarse Flapping tremors confusion. tachypnoea.
. loss of normal cardiac and liver dullness. lungs are hyperinflated.Signs
In mild dizs just a wheeze. prolonged expiration. Intercostal in drawing on inspiration. drowsinesseventually papilloedema. use accessory muscles. High PaCo2 >70mmHg -.
. Renal hypoxia will lead to activation of RAAS resulting in water and salt retention.Complications
Respiratory failure Occurs when PaO2 is less than 60mmHg or PaCO2 more than 55mm Hg Persistent hypercarpnia and hypoxemia lead to constriction of pulmonary artery and subsequent pulmonary arterial hypertension.
Heart disease secondary to disease of the lung. Charactrerised by: pulmonary hypertension.Complications«.
History of breathlessness and sputum production in a chronic smoker. Signs of overinflated lungs.
. Hyperinflated lungs. No individual clinical feature is diagnostic.
PEFR is low. Tall P wave (P. or H. FEV/FVC ratio is reduced. Pneumoniae. Blood gases. pulmonale) Alpha 1-trypsin levels.Investigations
Lung function tests. Lung volume may be normal or increased CXR. Low diaphragm presence of bullae. hyperinflated lungs. ECG. Sputum examination Strep. Haemoglobin and PCV ±elevated secondary to hypoxemia. Moraxella catarrhalis are causative of exacerbations. influenzae . N 2-4g/L
Long term value of steroids not known. Inhaled steroids beclometasone 4mg twice a day.4 mg four times daily. Anti muscarinic agents: more prolonged bronchodilatation effect.ipatropium 0. 2mg twice daily . Oxytropium. Corticosteroids May improve airway function Prednisolone 30mg daily for two weeks then review.Treatment
Stop smoking.d Antibiotics: During exacerbations are recommended
. Broncholdilators: Beta adrenergic agonist Salbutamol.
Give Oxygen Type 11 failure high carbondioxide don¶t give O2 will remove O2 drive. stimulant or artificial ventilation
.Treatment««. PH should no fall below 7.
Treatment of respiratory failure: Type 1 failure low oxygen high carbon dioxide..25 give resp.