COPD and related problems.

COPD is an umbrella term for various clinical entities with multiple causes resulting in airflow limitation that is not fully reversible. COPD is better defined as a clinical syndrome characterized by chronic respiratory symptoms, structural pulmonary abnormalities (airways disease, emphysema, or both), lung function impairment (primarily airflow limitation that is poorly reversible), or any combination of these. Early definitions of COPD distinguished different types (ie, chronic bronchitis, emphysema, asthma), a distinction that is not included in the current definition.

It is the third highest cause of death. Although in most areas men suffer more from this disease in other areas women are it’s major target. For a period there is an interaction between the environment and genetic susceptibility. Logically this is the period when prevention strategies should be instigated.

In persons without obstruction who are exposed to cigarette smoking, the presence of cough, sputum, and dyspnea and the detection of a low diffusing capacity of the lung for carbon monoxide (DLco) are associated with an increase in the risk of COPD.

Similarly, in persons without obstruction who have a baseline value for forced expiratory volume in 1 second (FEV1 ) at the low end of the normal range, a reduction in FEV1 that exceeds 40 ml per year (normal rate of loss after the third decade of life, <25 ml per year) over an 18-month period is associated with an increase by a factor of 36 in the risk that COPD will develop in the next 5 years. Patients in this “silent” stage constitute a group that can be labeled as having “pre-COPD.”

COPD remains underdiagnosed, primarily because it usually is considered to be a disease of the elderly. The disorder should be recognized at an earlier age because earlier interventions, such as smoking cessation, can normalize lung-function decline. Improving the quality of air in many cities and early use of bronchodilators i.e. before the age of fifty may prevent obstruction in the lungs. The treatment of younger patients who have mild disease (i.e., earlier treatment) may provide the greatest benefit over time.

  • Who is at risk?
  1. Cigarettes’ exposure. Those who smoked cigarettes throughout a 25 year observation period were more likely than never smokers to develop COPD (36 versus 8 percent) . Smoking tobacco through a Chinese water pipe (narghile or hookah or sheesha) is also associated with an increased risk of COPD. Smoking both tobacco and marijuana synergistically increases the risk of COPD and respiratory symptoms.
  2. Environmental exposure to particulate matter, dusts, vapors, fumes, or organic antigens may also be a risk factor for COPD. Why have women become more likely to develop COPD? Women are exposed to biosmoke when, in poor areas. they cook on wood smoke, cow dung, peat and coal. Occupational exposure to chemical disinfectants (eg, glutaraldehyde, bleach, hydrogen peroxide, alcohol, and quaternary ammonium compounds) is associated with an increased risk of COPD among nurses; women tend to have more atopy but less smoking. Check this out against smoking in rural Asia and the subcontinent among women.
  3. Atopy and asthma are predictors of COPD specially when they develop at a young age.
  4. Antioxidant deficiency — There are limited data suggesting that a deficiency of antioxidant vitamins (eg, vitamins C and E) may be a risk factor for COPD.
  5. Pulmonary tuberculosis may contribute to airflow obstruction via endobronchial infection and subsequent bronchostenosis or via lung parenchymal destruction with loss of airway tethering. In a study of 8784 Chinese subjects aged 50 or older, radiographic evidence of prior pulmonary tuberculosis was associated with an increased risk for airflow obstruction, independent of cigarette smoking, biomass fuel exposure, and prior diagnosis of asthma.
  6. Antioxidant related enzymes — Genetic variation in antioxidant enzyme function or regulation may affect risk for COPD. In particular, the genes for glutathione S-transferases P1 and M1, glutamate cysteine ligase, and superoxide dismutase appear to be involved.
  7. Family history. Patients with COPD are more likely to have first degree relatives who have bronchorespiratory hyper responsiveness to smoke.
  8. Respiratory symptoms. The three cardinal symptoms of COPD are dyspnea, chronic cough, and sputum production and the most common early symptom is exertional dyspnea. Less common symptoms include wheezing and chest tightness 
  9. Combination of symptoms. Those who present with episodes of increased cough, purulent sputum, wheezing, fatigue, and dyspnea that occur intermittently, with or without fever. Diagnosis can be problematic in such patients. The combination of wheezing plus dyspnea may lead to an incorrect diagnosis of asthma. Conversely, other illnesses with similar manifestations are often incorrectly diagnosed as a COPD exacerbation (eg, heart failure, bronchiectasis, bronchiolitis).
  10. COPD derives from various lifelong, dynamic, and cumulative gene–environment interactions (e.g., smoking, inhalation of other pollutants, prematurity, respiratory infections, and dietary insufficiency

Preventive strategies.

  1. Implement, monitor, and enforce strict control of airborne exposure in the workplace
  2. Initiate intensive and continuing education of workers, managers, clinicians, and legislators
  3. Promote smoking cessation since smoking aggravates exposure to other particles and gases
  4. Improve ventilation in areas where biomass fuels are used for cooking and promote use of clean fuels

When is the disease established and advanced?

  1. Once such airflow limitation occurs, the diagnosis of COPD is confirmed.
  2. FEV1, expressed as a proportion of reference values, defines the severity of airflow limitation.
  3. The intensity of dyspnea.
  4. The presence or absence of cachexia.
  5. An assessment of the capacity to perform activities of daily life, provides additional prognostic information.
  6. A history of exacerbations, especially two or more in a year or an episode requiring hospitalization, predicts future exacerbations and poor outcomes,

What else should we look for?

Patients with COPD often have certain coexisting conditions, including ischemic heart disease, atrial fibrillation, heart failure, osteoporosis, lung cancer, gastroesophageal reflux, anxiety, and depression. Most of these disorders are characteristically seen in the elderly, but in patients with COPD they occur at younger ages.

How does a CT scan of the chest help?

Chest CT detects and quantitates the emphysema phenotype, classically known as
the “pink puffer” phenotype but better defined as the MOLT (multiorgan loss of tissue) phenotype, which is frequently associated with loss of mesenchymal tissue (bone, muscle, and fat). Patients with this phenotype are at increased
risk for lung cancer.

What else will a CT scan tell us?

  1. The presence of heterogeneous, predominantly upper-lobe emphysema identifies good candidates for bronchoscopic or surgical lung-volume reduction.
  2. CT also detects airway luminal narrowing and wall thickening associated with cough, phlegm production or discoloration, and exacerbations of COPD.
  3. It can identify bronchiectasis,
  4. early-stage lung cancer,
  5. interstitial lung abnormalities,
  6. coronary calcifications, cardiomegaly,
  7. enlargement of the pulmonary vasculature,
  8. thoracic-wall and mediastinal abnormalities, osteoporosis, sarcopenia, and hiatal hernia, all of which affect health status and could be the target of specific therapies.

First measure the resting oxygen saturation. A resting oxygen saturation of less than 90% should prompt measurement of arterial blood gases to determine whether supplemental oxygen is needed. In patients with dyspnea on exertion, physiological testing can be informative.

Hyperinflation is determined by measuring lung volumes, with air trapping indicated by a ratio of residual volume to total lung capacity that exceeds the normal value of 0.35. A low ratio of inspiratory to total lung capacity (<0.25) is associated with an increased risk of death and, when accompanied by dynamic hyperinflation, is a determinant of the severity of dyspnea.

A low DLco (an indirect measure of emphysema) is a good predictor of oxygen desaturation, coexisting pulmonary hypertension, and lung cancer.

A 6-minute walking distance of less than 350 m is associated with increased mortality. Cardiopulmonary exercise testing helps differentiate cardiac from respiratory compromise and can be used to guide pulmonary rehabilitation.

The multidimensional BODE index, which consists of the integration of four variables (body-mass index, degree of airflow obstruction, degree of dyspnea, and exercise capacity [6-minute walking distance]), provides better prognostic information (higher scores indicate a greater risk of death) than the FEV1 alone.

The initial Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines used the forced expiratory volume in one second (FEV1; expressed as a percentage of predicted) to stage disease severity.

Endotypes, Biomarkers, and Treatable Traits

An endotype is a disease subtype defined functionally and pathologically by a molecular mechanism or by treatment response. Endotypes should be identified by means of validated biomarkers. Currently, only two blood tests meet this criterion for COPD endotypes that constitute treatable traits.

  1. The first test is the serum level of alpha1 -antitrypsin, which should be measured in all patients. A low level indicates a genetically determined COPD endotype that responds to long-term replacement of the missing protein.
  2. The second test is the blood eosinophil count. In patients with frequent exacerbations despite appropriate bronchodilator treatment, the blood eosinophil count helps predict the response to inhaled glucocorticoids. Eosinophil counts higher than 300 per cubic millimeter indicate a good response, values between 100 and 300 per cubic millimeter suggest a moderate response, and a low eosinophil count (<100 per cubic millimeter) is associated with minimal benefit and an increase in the risk of pneumonia.

Primary and Secondary Prevention.

  1. Stop smoking.
  2. Reduce ambient pollution.
  3. Vaccines for influenza
  4. Improve and change methods of cooking.

How to begin treatment?

Assess the Modified Medical Research Council dyspnea scale score or COPD Assessment Test

Most patients with mild symptoms (a score of 0 or 1 on the modified Medical Research Council dyspnea scale [scores range from 0 to 4, with higher scores indicating more severe dyspnea] or a score of <10 on the COPD Assessment Test [scores range from 0 to 40, with higher scores indicating greater severity of symptoms]) and fewer than two exacerbations per year do well with exposure control, increased physical activity, vaccinations, and use of long-acting bronchodilators.

The presence of more intense symptoms and the occurrence of more frequent exacerbations should prompt a more detailed evaluation and specialized management, with consideration of a referral for pulmonary rehabilitation, which improves health status, reduces dyspnea, and increases exercise capacity.


The Global Initiative for Chronic Obstructive Lung Disease suggests an initial approach based on the intensity of symptoms and the history of exacerbations, with a subsequent algorithm that includes a blood eosinophil count for adjustment.
of therapy.

  1. A long-acting muscarinic antagonist (LAMA) such as  ipratropium, triotropium ,  umeclidinium, aclidinium, is the initial drug of choice for patients with mild disease and no exacerbations. If the patient has more severe dyspnea, severe airflow obstruction, and lung hyperinflation.
  2. Combine a LAMA with a selective long-acting beta2-agonist (LABA) such as salmeterolformoterol, vilanterol) if the patient has more severe dyspnea, severe airflow obstruction, and lung hyperinflation, combining the two agents in a single inhaler to simplify treatment.
  3. Start therapy with a combination of a LABA and an inhaled glucocorticoid in patients with a history of asthma, wheezes, rhinitis, polyps, or allergies; a history of exacerbations; an elevated blood eosinophil count (>150 per cubic millimeter); or a combination of these findings.
  4. Monotherapy is not recommended because of evidence that use of an inhaled glucocorticoid (fluticasone propionate) alone is associated with an increased risk of death, as compared with the combination of fluticasone and salmeterol.
  5. For patients who have repeated exacerbations while receiving maximal inhaled therapy or who have side effects from inhaled glucocorticoids, oral macrolides are useful. Be careful if the QT is prolonged or if there are arrhythmias.
  6. Use a phosphodiesterase inhibitor roflumilast, which lowers exacerbation rates among patients with severe COPD.
  7. Trials of mepolizumab and benralizumab have shown marginal benefits in patients with COPD and exacerbations. Oral antioxidants are popular in Europe and the Far East but not in the rest of the world.

You must also be aware of surgical and bronchoscopic options for reducing lung volumes and treating acute exarcerbations of the disease and pulmonary rehabilitation maneuvers.

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I am a Professor of Medicine and a Nephrologist. Having served in the Army Medical College, Pakistan Army for 27 years I eventually became the Dean and Principal of the Bahria University Medical and Dental College Karachi from where I retired in 2016. My passion is teaching and mentoring young doctors. I am associated with the College of Physicians and Surgeons Pakistan as a Fellow and an examiner. I find that many young doctors make mistakes because they do not understand how they should answer questions; basically they do not understand why a question is being asked. My aim is to help them process the information they acquire as part of their education to answer questions, pass examinations and to best take care of patients without supervision of a consultant. Read my blog, interact and ask questions so that I can help you more.

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