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Chronic Obstructive Pulmonary Disease Dr Sana Al Mutairi

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					Chronic Obstructive Pulmonary Disease
Dr. Sana Al-Mutairi

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Case A: 60 yrs. Old with shortness of breath on exertion

Case B: 52 yrs old with shortness of breath on exertion
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Obstructive Lung disease:
Reduction of expiratory flow rates:

Normal FVE1 /FVC> 75-80%
COPD: Progressive expiratory air flow limitation.Resulting from destruction of lung parenchyma or irreversible damage to conducting airways.it is associated with abnormal inflammatory response of the lung to noxious particles or gases mainly cigarette smoking . -COPD has significant systemic consequences.

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Two major entities:
Chronic bronchitis Emphysema Now globally is the 4th killing Disease; by 2020 will be the third. Chronic bronchitis: Chronic productive cough for at least 3 month year for at least 2 successive year in absence of other causes.
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Emphysema :
Def:pathologically Permanent enlargement of air space distal to the terminal (non respiratory) bronchioles accompanied by destruction of the alveolar walls and without obvious fibrosis.

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Pathophysiology of chronic bronchitis
Due to increase inflammatory cells, oxidative stress, imbalance between proteinases and anti-proteinases ,get the following pathology: A. Chronic excessive mucus hypersecretion from: 1. Hypertrophy of sub-epithelial tracheobronchial mucus glands in cartilagenous airways (> 2mm diameter) 2. Goblet cells. B. Bronchiolitis in non-cartilagenous airways (<2mm) C. Bronchial smooth muscle hyperplasia. Excess mucus and excess collagen deposition in airways , mucosal edema, smooth muscles hyperplasia airways narrowing and increase its resistance. Non-uniform throughout the airwaysObstruction of expiratory flow in some areas leads to air trapping and hyperinflation.it is dynamic during exercise .V/Q mismatch. Thickening of pulmonary vasculature wall,endothelial dysfunction  pulmonary HPT,RV dysfunction

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Pathophysiology of emphysema
Loss of elastic recoil>increase lung compliance, peripheral airways allowed to be compresses leading to increase airways resistance, air trapping and hyperinflation. Nonuniform V/Q mismatch  hypoxaemia. Generally both : non-uniform V/Q mismatch : Hypoxaemia + hypercapnia

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Classification of Emphysema:

Centriacinar (proximal- centrilobular): Usually respiratory bronchioles usually, with cigarette smoking focal centrilobular , Or diffuse :with biological inactive dust. Panacinar:(panlobular) Dilatation of all the respiratory air spaces and of the secondary Lobule. Diffuse or focal. Diffuse may be as in protease inhibitors deficiency (α1 anti-trypsin); basal lobe. Bullae :emphysematous space > 1 cm diameter. Periacinar or paraseptal: Abnormal air space run along the edge of the acinar unit, abuts to a fixed structure e.g. Pleura , septum, vessels. **Systemic effect: systemic inflammation with skeletal muscle wasting exercise capacity limitation and worsen prognosis independent of PFT

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Risk factors for COPD
Cigarette smoking: most important. Accelerate decline of FEV1 50 – 70 ml yr. Chronic cough, sputum occur independent of airflow limitation. 2. Air pollution: a- Particulate matters: decline in PFT and symptoms of chronic bronchitis. b- Irritant: cellular change allergic response. c-indoor : domestic cooking :females in developing countries 3. Occupational: Organic and inorganic dust: grain handlers, Gold and coalminer. COPD related to work 19%, in non-smokers 31% Chronic bronchitis, decline in PFT 1.

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Risk factors for COPD: (cont)
4. Atopy and bronchial hyperponsiveness: genetically determined.Ig E and asthma 5. Hereditary: protease inhibitor deficincy. 6. Other risk factors. - Increasing age. - Sex : male - Low birth weight ,perinatal events ,childhood illness. - Socioeconomic - Diet: specially alcohol. Diagnosis : History : exposure to : smoking :pack-years. Dyspnea : modified MRC 0-4: predicts QOL and survival ----Productive cough.
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Physical examination
Mild disease : normal Progressive: labored breathing, pursed lips, accessory muscle, cyanosis. In acute exacerbation: sings of severe air flow obstruction. Pink buffer, blue bloater. Lab studies; CXR: 1. Can be normal chronic bronchitis

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Spirometry:
Severity of obstruction and reversibility. FEV1, FVC < 7o % perdicted post bronchodilator; not fully reversible RV  and FRC. Diffusion capacity:  in emphysema. ABG: Normal at early stage Hypoxic Hypoxic, hypercapnic Others: α1anti-trypsin:4th-5th decay exercise testing:out-proportional dyspnea to FEV1 C/T scan Echo, sleep study ,Respiratory muscle function

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Management
Investigation as above Case A: exacerbation with Hypercapnic Respiratory failure

Case B: emphysema with hypoxic respiratory respiratory failure.

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Treatment:
Exacerbation management Chronic stable management Adjuvant therapy Exacerbation
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2.

Identify the cause: infection, irritant exposure, non compliance with treatment Bronchodilators: Standard: - B2 agonist: salbutamol or terbutalin - Anticholinergic: ipratropium bromide - Xanthines: theophyline.

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Exacerbation (cont.)
3. Controlled Oxygen therapy: 1-2 liter min. Venti mask 24 – 28 % need to keep PaO2 60- 70 mm Hg (8-9) Kpa SaO2 > 90% without fall in PH
4. Corticosteroids: <20%, of COPD steroid responsive , give a trial: I.V or orally then shift to inhaler: Beclomethason or budesonide. No change in degree of severity of exacerbation but frequency of exacerbations.

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Exacerbation (cont.)
5. Antibiotics: broads spectrum: e.g.amoxacillian to cover H.Influenza. 6. Respiratory failure: Stable chronic respiratory failure can develop acute on top of chronic respiratory failure. May need assisted ventilation.

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Adjuvant therapy:
- Physiotherapy - Diuretics: CCF secondary to core pulmonale. - Cautious hydration.

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CHRONIC MANAGEMENT: stable COPD A-Maintain on bronchodilators: short : improve exercise tolerance long acting: improve health status Anti-cholinergic: improve health status < long acting ( !!Tiotropium) B-If steroid responsive or FEV1< 50%: inhaled steroid: frequecy of exacerbation / year and rate of deterioration in health status. C- mucolytic :debatable except ACC D- α1anti-trypsin augmentation : rate of decline in FEV1 E- anabolic steroid Improve exercise intolerance: to improve muscle function with exercise training. F-Oxygen therapy: LTOT 1. Increase survival. 2. Improve polycythemia ,exercise ,sleep,cognitive performance. 3. Improve PHT :modest decline yearly in PAP.
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Indication of LTOT:

Modified criteria:patient stable with PaO2 < 7.3 kPa(55mmHg-SaO2< 88%) 2. Patient with PaO2 7.3-7.8kPa (55-59SaO289%)with tissue hypoxia e.g. Oedema from CCF,impaired mental status, PHT or Core pulmonale 3. Palliation for preterminal respiratory failure of any cause. PaO2 < 7.3 Kpa.

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Indication of LTOT:
4. Others: - Patients desaturates on exercise PaO2 <7.3 Kpa or SaO2 85 – 90%. - Patient during sleep desaturates 5- Gray areas: if adequate PaO2 whose severe dyspnea relieved by low-flow O2 or their exertional capacity improve with supplemental O2.

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Adjuvant TREATMENT
Stop smoking. Avoid exposure to irritant, allergens. Flue vaccine. Pulmonary rehabilitation: Improve perception of dyspnea by improving metabolic load muscle training and decrease dynamic hyperinflation.
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Possible therapy:
A) – New bronchodilator : 1. Act as inhibitor to phosphodiestrase-4. 2. Combined B- adrenergic and dopaminergic agonist.

B) Use of anti oxidants:
To counteract oxidant effect and reactive oxygen species: e.g.: N –acetylanastole cystiene ,also as mucolytic.

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Future therapy (cont.)
(C) Anti-inflammatory:

inhibitor. D) Drugs opose reverse structural damage: e.g: retinoic acid.

- TNFα - Phosphodiesterase- 4

Surgery for COPD:
Bullectomy,LVRS Lung Transplant

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posted:4/28/2008
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