COPD vs Asthma.

differences between COPD and Asthma.

1. Copd vs Asthma Dr mrinmoy roy Dnb pgt medicine

2. definition Asthma has been defined as “a chronic inflammatory disorder of the airways in which many cells and cellular elements play a role. Chronic inflammation is associated with airway hyper-responsiveness that leads to recurrent episodes of wheezing, breathlessness, chest tightness, and coughing, particularly at night or in the early morning. These episodes are usually associated with widespread, but variable, airflow obstruction within the lung that is often reversible either spontaneously or with treatment. Asthma, therefore, is characterised by hyper-responsive airways and reversible airways obstruction. COPD is characterised by airflow limitation that is not fully reversible. Airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lung to noxious particles or gases. COPD is almost always a disease of smokers, becoming more prevalent with increasing age.

3. Symptoms: eg . cough, wheeze, shortness of breath, chest tightness and sputum production. These symptoms are similar for asthma and COPD, although there is generally more sputum production in COPD Pattern of symptoms : Nocturnal symptoms and on awakening in early morning suggest asthma. Asthma can be seasonal, associated with pollen and other trigger factors. COPD, on the other hand, does not vary much in severity during the year. Asthma tends to be episodic, while COPD is persistent.

4. Precipitating and/or aggravating factors : Both asthma and COPD can be worsened by respiratory infections. Asthma can often be associated with exposure to known allergens (indoor and outdoor). Age of the home, location, heating system, moulds or mildew and furnishings can be important both in distinguishing COPD from asthma and also in identifying precipitating factors. Both asthma and COPD can be aggravated by occupational chemicals, irritants ( eg . tobacco smoke, air pollutants, occupational chemicals, dusts, etc ), changes in weather and exposure to cold air while episodes associated with emotions and stress are more likely to be associated with uncontrolled asthma. the most important difference between asthma and COPD is the nature of inflammation, which is primarily eosinophilic and CD4-driven in asthma, and neutrophilic and CD8-driven in COPD

5. Family history: Patients with asthma often have a string family history of asthma, allergy, sinusitis, rhinitis, eczema, or nasal polyps in close relatives. COPD does not show any strong familial association apart from the obvious links with smoking . Following a history and examination, routine investigations would be chest X-ray, full blood count, ESR, routine biochemistry, IgE and alpha-1 anti- trypsin.sputum for c/s. Chest x-ray appearances in both asthma and COPD can both show hyperinflation, but in asthma there will be no bullae or structural changes. High-resolution CT of thorax may be helpful in providing a more detailed image of any structural changes suggestive of emphysema. If the IgE is raised, RAST testing or skin prick allergy testing will help confirm the diagnosis of asthma and identify allergens. Serum IgE and eosinophils may be raised in asthma. RAST tests and skin allergy tests can be positive in asthma but will usually be normal in COPD. Alpha-1 anti-trypsin deficiency is a genetic defect which may contribute to early onset COPD.

6. Exercise: Patients complaining of breathlessness on exercise may have exertional dyspnoea or exercise-induced asthma. Exercise-induced asthma is a condition in which vigorous physical activity triggers acute airway narrowing in people with heightened airway reactivity. A more accurate description would be exercise- induced bronchospasm. Exercise-induced asthma is defined as a transient increase in airway resistance following six to eight minutes of vigorous exercise and is usually at its worst three to 15 minutes after vigorous exercise. Dyspnoea on exertion due to COPD, on the other hand, is present from the start of exercise and causes a fixed degree of dyspnoea.   Development of disease and treatment : Asthma quite often appears in childhood or early adulthood, while the onset of COPD is later in life, almost always in smokers. Asthma is episodic in nature without being progressive, although poorly controlled asthma may cause airway remodelling with a fixed reduction in lung functions and poorer response to bronchodilators. COPD has a progressive course.  

7. Differences in brief

8. SPIROMETRY the definitive investigation is pulmonary function testing (PFT) with assessment of reversibility. Simple spirometry would be sufficient in straightforward cases, but full PFTs should be done if the diagnosis is unclear. Both asthma and COPD will give an obstructive pattern , but asthma should show reversibility. Reversibility means that the FEV1 (forced expiratory volume in 1 second) and FVC (forced vital capacity) will increase by at least 12-15% after bronchodilator treatment, while in COPD the improvement in FEV1 will be far less.

9. PFT

10. Other investigations The Functional Residual Capacity is increased in hyperinflation and is this is characteristic of COPD.   Diffusing capacity, or transfer factor, is most useful in differentiating asthma from COPD, being normal in asthma but always reduced in COPD. If the diagnosis is unclear and spirometry is normal or slightly abnormal a methacholine or histamine challenge should be carried out when asthma is suspected. This should only be carried out if the FEV1 is more than 65% of the predicted value. A positive test will display hypersensitivity while a negative test will rule out asthma. It is important to remember that asthma and COPD are not mutually exclusive

11. treatment the approach to the treatment of asthma and COPD is different. The essential difference is that the treatment of asthma is driven by the need to suppress the chronic inflammation, whereas in COPD, treatment is driven by the need to reduce symptoms. Asthma management quick-relief medications (bronchodilators) such as short-acting beta agonists, ipratropium , and oral and intravenous corticosteroids allergy medications such as allergy shots (immunotherapy) and omalizumab . long-term asthma control medications such as inhaled corticosteroids, leukotriene modifiers, long-acting beta agonists, combination inhalers bronchial thermoplasty long-acting beta2-agonists (LABAs) are used in combination with anti-inflammatory - inhaled corticosteroids (ICs) in asthma. LABAs may be used alone in patients with COPD. The isolated use of a beta2-agonist in asthma is contraindicated and is associated with a poor prognosis. Anti-leukotrienes , such as montelukasts , can reduce eosinophilic inflammation through inhibition of the lipoxygenase pathway. The bronchodilator effect of anti-leukotrienes is discrete, and the use of these drugs is reserved for asthmatic patients; however, there is no concrete clinical applicability of these drugs in COPD

12. continuing Copd management medications such as bronchodilators, inhaled steroids, combination inhalers, oral steroids, phosphodiesterase-4 inhibitors, theophylline , and antibiotics lung therapies , including oxygen therapy and pulmonary rehabilitation programs involving education, exercise training, nutritional advice, and counseling to increase your quality of life surgeries such as lung volume reduction surgery (removing areas of damaged lung tissue to increase space in the chest cavity for the remaining healthy lung tissue), lung transplant (replacing diseased and damaged lungs with healthy, donated lungs), or bullectomy (removal of abnormally large air spaces from the lungs to help improve breathing . vaccination Short-acting beta2-agonists (SABAs) are the first-line treatment for COPD; however, the use of SABAs as a rescue medication in asthma is appropriate.LABA causes functional improvement (increased FEV1). Xanthines , such as theophylline, have moderate bronchodilator effects, immunomodulatory properties and anti-inflammatory effects, which increase sensitivity to corticoids in the nucleus of inflammatory cells through the histone deacetylase pathway. However, the clinical effects of xanthines , which are associated with a reduced therapeutic range and an increased risk of severe side effects, have reduced the clinical applicability of these drugs. The use of xanthines is increasingly reserved for severe cases, especially in patients with COPD

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