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Dr Musa Almakawi -COPD

In the name of Allah the most gracious and merciful.

Today were going to talk about COPD. Before starting the lecture, COPD is smoke related disease, probably 85 % of COPD patients are smoker ( this is in west) But in Jordan, It might be 90% or 95% because here we dont have mining or other industrial exposure. Smoking Related Death In a worldwide, it is about 5.4 millions per year, one death every seconds due to smoking, out of this amount, there are 1.7 millions died due to Cardiovascular Diseases (CVD), 1 million due to COPD, and 80,000 due to lung cancer. In United States, about 443,000 died every year because of smoking. Smokers generally die 15 years earlier than non-smoker. So if anyone of you smoking, you have to take back this survival rate point as consideration . And a diabetic patients usually die 10 years earlier compared to non-diabetic patients. So, a smoker die earlier than a diabetic patient.

Chronic Obstructive Pulmonary Disease (COPD)


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Chronic Obstructive Pulmonary Disease (COPD) it means that there is an airway obstruction and chronic disease. It comprises of 2 diseases, and well start by definition, COPD is a disease state characterized by airflow limitation or airflow obstruction that is not fully reversible ( DD: Bronchial Asthma - Chronic Obstruction but reversible with Tx. Majority of them have normal pulmonary function, they can lead a normal life) and it usually progressive (DD: Bronchial Astma Intermittent) and associated with abnormal inflammatory response of the lungs to noxious particles or gases (from cigarette). It is preventable and treatable but not cureable. There is Tx to reduce the symptoms indicated because the disease is irreversible, you cannot return the patient into normal after tx. The Tx is usually a symptomatic treatment. It gives some quality of life, but It cannot be cured. So we have two type of COPD which is 1) Chronic Bronchitis 2) Emphysema (Both are smoke related) Chronic Bronchitis is defined clinically by the presence of cough and sputum production for at least 3 months in each year for two consecutive years without underline lung disease for example to those who have (5.33) will have cough and sputum but this is not COPD. When you have a patient that have a chronic bronchitis but he dont have any obstruction in airway. This is not COPD, He does have the symptoms but the pulmonary function is normal. So to diagnose COPD,
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you have to check pulmonary function regarding any obstruction in aiwarys. The other disease is Emphysema, which is a permanent airspace englargement beyond the terminal bronchioles with destruction of alveolar septa. If you go back to anatomy of bronchiole tree, you have conducting airways starting from trachea down to 17 generations because each one in a dichotomous way , will give two branches. This is a conducting airway from here to here. And this is the part where Chronic Bronchitis usually occur. But majority of inflammation happen small airways which are about 2mm of diameter. While emphysema is related in transitional and respiratory zone (including some part of terminal bronchioles until alveolar sacs) where the gas exchange unit started. So in Emphysema, it is the destruction of alveolar wall, while Chronic Bronchitis is the inflammation of conduting airways.

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Comparisons between Asthma and COPD

Asthma
Caused by Sensitizing Agent (Grass pollen, tree polen, animal fur) Inflammation:-CD4+ T Lymphocytes - Eosinophils (good response towards steroid either inhale or systemic good in tx) Completely / Partially reversible

COPD
Caused by Noxious Agent ( toxin in smoker) Inflammation:-CD8+ Lymphocytes - Macrophages -Neutrophils ( no response towards steroid- difficult in tx) Completely irreversible

COPD in USA

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Some statistic in USA about COPD (we dont have a local statistic, thats why we use USA statistic.)

There are 12.1 million adults has COPD in 2001 Estimated number now up to 16 millions About 14 million is undiagnosed because most of they patient they dont go to see the physicians unless they have advance disease or another complication. Usually they have cough related to smoking, they have short breath, and they said Because e are smokers, we are getting older, So this is half of natural history . Because the symptoms of COPD is cough and sputum production. If you ask the patient about the cough, they will deny it. But if you ask him does he clear his troat in the morning, and he says yes. So this means that hes having a Chronic Bronchitis (CB) . When you face the same thing, you might be having CB, but at your age, it does not happen because COPD is a middle-age disease. About 124,816 deaths in 2002 in USA ( the 4th leading cause of death in USA at that time) In 2008, it became the 3rd leading cause of death in USA If you see the statistics here, the six common killers, all are turning down or at least, leveling except COPD which has been increasing steadily since 1970. As you can see for example, Heart disease, stroke and accidents are getting less, cancer and stroke are almost level and Diabetes is fluctuating. But COPD is increasing.

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Not only that, By gender, in female, the number of death due to COPD you are catching up males by years statistically. The reason that even in the west, during 60s and 70s female were not accepted to smoke. Only males who usually smoke during the era but not for females. However, nowadays thing are different, females are also participating in smoking like males causing the rates between both are similar. The prevelance of smoking in males are getting down while females are getting up, and now they are equal. Thats why, mortality of male and female in year 2000 are similar. The risk factor for COPD especially in Jordan like I said, is caused by

1. smoking MOSTLY (90%) 2. Some host factors (Less than 1%) - Rarely they have alpha-1 antitrypsin/alpha-1 antiprotease deficiency (It is inherited). Usually they have emphysema but quite different from smoker related emphysema by having symptoms at early 40s. But if they smoke, and have alpha1antitrypsin deficiency, they would have symptoms at their early 30s. If they are non-smoker, there is replacement for alpha-1 antitrypsin. - It might also cause by airway hyperresponsiveness which is a main feature of asthma. The airway is constricted due to response against non-specific stimuli like histamine or methacoline. For smoker, the chance of COPD is higher. - Lung growth. Those who has a lung infection during neonatal period or childhood period, the lung wouldnt grow properly, and smoking at the same time, are tend to have COPD.
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3. Exposures - The most important thing is, tobacco smoke is the major factor of COPD. And this is in our hand, If we stop smoking, well stop COPD and other diseases. Even if you escape COPD (not all smokers have COPD about 20% ), you might have lung cancer, coronary disease, and other problems - Occupational- Working outdoors like Farming and mining may expose you to COPD. - Indoor and outdoor air pollution, - Infections - Socieconomic status- Poor people tends to have COPD more than rich people as rich people usually buy and eat fresh fruits and vegetables which act as antioxidants. But it doesnt mean that you smoke and take antioxidants you can escape COPD. Some poor people tend to spend their money more in cigarette rather than feeding. In the west, they are usually poor, they smoke and take alcohol and also poor nutrition, which mainly cause COPD. Prevalance in Jordan Statistic In Jordan, this was during 2007, for adults above age 18 years old, there were 49.6% Males smokers and 10.5% Females smokers (this is quite not true because female smoker tend to hide their habit of smoking). Even in University Street, you can see many people smoking and also Shisha-ing (aragella) along the street. For school children (13-15 years), In 1999, a study was done,
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saying that 25% of males are smoker as well as 10.5% of females. But theyre an experiment smoker (which means theyd tried smoke once or more-not like regular smoker). This is the problem usually once when they try to smoke cigarette for the first time , they will start get addicted. In 2007, the prevalence increased, as males smoker became 37% while female smokers 26%. In the west, prevalence of smoker is decreasing by year nowadays, but not in third year country like Jordan which is increasing. Last year, it was the first time in United States, for the prevalence of smoking becoming less than 20 % which is about 19%. But In Jordan, you can see about 80% of physicians are smoker, especially anesthetist and surgeons. And our hospital for example, Im sure more that 80% of anesthetist and surgeons are smoker. And in medical department, we have 50 members, only one is smoking . Pathology and Pathogenesis As you said, the COPD, the main things is the airway obstruction, the cough and sputum production. Why do we cough? Because toxin in tobacco smoke leads to hypertrophy of the mucus secreting lung if you remember histology of airways there are lined by pseudostratified ciliated columnar epithelium and you have mucous gland. As you go down, youll get Goblet Cell in the smaller airways, there is hypertrophy in goblet cell and secreting mucous gland. And the toxin leads to inhibition of ciliary function, which have an important function as I said bronchiole tree is lined by pseudostratified ciliated columnar epithelium and these cilia,
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they beat in an ordinal manner from down to up, about 30 beats/second, as to propel the mucous and irritants that go down. So the toxin from smoking will inhibit the ciliary function which cause the production of sputum and cough. The airflow limitation & Hyperinflation (Because the destruction of alveolar septa , that leads to shortness of breath) If the patient has emphysema that will affect gas exchange unit, because the conducting airways has nothing to do with gas exchange of Oxygen and Carbon Dioxide. But in emphysema, youll have pulmonary hypertension that leads to hypoxia, that might cause cor-pulmonale (right ventricular hypertrophy) with or without failure of secondary disease. And they might end with respiratory failure.

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Diagnosis Clinical features As clinical problem we go for clinical symptoms and signs in the patient. Anyone who is middle age and he has chronic cough, sputum production or shortness of breath(Dyspnea) and if he has risk factors we have to consider COPD. Example of risk factors are smoker or occupation( job that deal with highly exposure to irritants or chemicals) And as I said the cough, we ask the patient in early morning did they cough and clear their throat . This cough of COPD and this usually above 40 years old of age if he is younger than that, probably you think of other like bronchial asthma although he is a smoker. Q: does the cough occur only in early morning? Not necessarily but usually started in the morning but they can cough at anytime. Bcoz probably during sleep the mucus secretion increase it retain there and they are not conscious so the mucus start to accumulate and they start coughing to clear their airways. We have two types of COPD Chronic Broncitis(Blue Bloaters)- usually this patient have cough and sputum production especially obese patient. Typical history that this obese is a smoker and he will tell you that he start to have cough and sputum production. If they have cold in winter they have more shortness of breath , cough and sputum production usually stay for 3 or 4 days and these symptoms can goes ten days or two weeks later on they start having shortness
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of breath and coughing all day around. And they are called Blue Bloaters bcos they have the tendency to have cyanosis. Emphysema(Pink Puffers)-usually they have very thin airways but they dont have cyanosis instead have worst shortness of breath although they are maintaining their oxygenation and their lungs are hyper inflate These are the extremes but majority of patients they have emphysema and chronic bronchitis at the same time if both are smoker related

If you suspect a patient to have COPD, we have to comfirm bcoz as we said he might have emphysema without COPD, or he might have chronic bronchitis without COPD. Bcoz COPD means chronic obstructive airways disease so we have to demonstrate that there is airways obstruction, and the only way to determine it is by doing Pulmonary Function Test . We measure it by calculating Force Expiratory Volume of the first second(FEV1) / Force Vital Capacity (FVC) ratio. Normal people if you take a deep breath and you exhale
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forcefully most people they can exhale about 80% or more of their vital capacity in the first second, these people(patients) bcoz they have airways obstruction, they cannot expel that amount so the FEV1/ FVC is less than 70%.

So all COPD they have this ratio reduce, the FEV1 have absolute value is variable according to the severity of the disease. If we measure the airways resistance it is increase bcoz by logic if we have narrow airways the resistance in that airways will be higher. The total lung capacity is increase. The residual volume, which is the amount of air remains after force expiration normally theres 20% of total lung capacity remained . But this patient might have 30% or 40% or more.

The Diffusion capacity which is a measurement across the gas exchange unit that will differentiate a patient to have COPD of Emphysema or Chronic bronchitis. The ratios is reduce, the FEV1 is reduce, there is increase airway resistance, total lung capacity is increase especially in emphysema but even chronis bronchitis have but more to emphysema, the residual volume is increase but more in emphysema, while in diffusion lung capacity in chronic bronchitis is normal, while in emphysema it is reduce bcoz the diffusion capacity it measure the gas exchange across the gas exchange unit and chronic bronchitis we said is a disease of conducting airways has nothing to do with gas exchange. While emphysema is a disease of gas exchange unit which is started after the terminal bronchioles, the respiratory bronchioles, the alveolar ducts and the alveolar sacs.
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So you have an airways obstruction with the reduce diffusion capacity.

Pic A Usually we measure the diffusion capacity of carbon monoxide this means that predominantly an emphematous patient.

Pic B

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Pic C The above Pic A is example of normal graph of spirometry . We look for the first three parameter, the sex of the patient, the height and the age. The computer will tell you what are the predictive value or PRED(third line from the table) for that person. Usually we do spirometry before(PRE-RX) and after using bronchodilator(POST-RX). So we do spirometry as a baseline then we give a bronchodilator usually we give Salbutamol to differentiate whether it is asthma or non-asthma. Bcoz asthma is reversible while COPD is not reversible. So this is (Pic A) a pretreatment between before and after giving the bronchodilator any value between 80% an 100% of within predictive is within normal limit and the ratio FEV1/FVC is 79 and it is above 70 so this is normal spirometry. This is typical spirometry(Pic B) of asthmatic patient. The ratio was low which is 69 and within normal range and improve after givin bronchodilator which is 80.So there is significant improvement. While in COPD (Pic C) the ratio is reduce. The ratio before giving bronchodilator was 63 and there is no improvement after giving bronchodilator which is 59. So this is irreversible airways obstruction which confirmed COPD.

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This is a normal chest x-ray you can see the diaphragm is dome shape and presence of bronco vascular marking.

This is a chest x-ray of of an emphysematous person, there is hyperinflation the lungs are larger and the background is blacker and you dont see the bronco vascular margin bcoz of enlargement air
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spaces. But the chest x-ray is not sensitive. The most sensitive is the high resolution CT scan.

This is typical of hight resolution CT scan. You can see lots of holes here, these are the centrilobular emphysema and usually effect on the upper lobe rather than the lower lobe

This is the panacinar emphysema , you can see this is relatively normal and you cant see vascular marking and increase largeness

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Sometimes it can go into what we call bullous emphysema very large airspaces compare to the normal lungs tissue.

Treatment The first thing in treatment of COPD is to prevent the disease progression the only thing that can prevent or stop disease progression is stopping smoking. If you stop smoking the disease will not progress and will not go back to normal but at least the disease will not progress further and we have to make every effort to convince the patient to stop smoking. Smoking is an addiction and qualifies the criteria of addiction there is physical and mental dependence on nicotine. So if you stop there are withdrawal symptoms. So if the patient tried and he fail, we can assist him by giving nicotine replacement or we can use antidepressant or varinicline( which is nicotine receptor agonist). But all these, the success rate are probably 20% or 30%. We have to give them the vaccines to prevent infections, they have to take the influenza vaccines every one cup and they have to take the pneumococcal vaccines once in their life. We can improve the pulmonary function by
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giving medical treatment, and the main treatment we gave bronchodilators either the 2 agonist with short acting or long acting depend on the stage of the disease or anticholinergic drugs wither short acting like Ipratropium or the long acting like Tiotropium. Inhaled cortical streroid can be given especially those who have frequent exacerbation and they have moderately severe disease there is evidence that that giving inhale cortical steroid might improve their symptoms. While in asthma the main steroid treatment is the inhaled cortical steroid. Sometimes we have some surgical treatment for certain disease. Normally about the age of 25 we reach the maximum pulmonary function after that we start losing FEV1. Normal people they lose about 20ml to 30ml of their FEV1 every year. For example for someone whose 25years and hes 170cm his FEV1 probably around 3.5 liter, if he lived to the ages of 75 after 50 years he will lose about 20ml to 30ml every year so he lose about 1 liter of FEV1, so at age 75 his FEV1 is 2.5 liter. If your FEV1 is below 2 liter cant even tolerate pneumonectomy(removal of one lung). While a smoker who is susceptible to have COPD and probably some genetic predisposition (bcoz why some people develop COPD in smoker and others are not) as I said 20% to 30% person only may develop COPD they lose between 50ml-70ml every year. So if we take average of 60ml after 50 years he lose 60ml every year so probably 60ml times 50 about 3 liters. So at the age of 75 his FEV1 left is 0.5 liter and if you have FEV1 less than 1 liter you are probably dead. So this is the susceptible smoker of how the FEV1 drop, this is not susceptible even if he smoke

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Smoking Cessation and FEV1 Decline


2.9
Post bronchodilator FEV1

2.8 2.7 2.6 2.5 2.4


2 1y r 2y r 3y r Sc re en 4y r 5y r
Sustained Quitters Continuing Smokers

Anthonisen et al. JAMA 1994;272:14971505

At any stage if you stop smoking at least after years you stop smoking and lose back only 20ml only not like the 50ml or 70ml that you lose if you continue to smoking. So it is not late to quit smoking even if you have advance diseases. You will not go back to normal but at least you have some improvement and maintain you function. So this is FEV1(above line) those who have sustain quitters stop smoking and continue stop smoking their FEV1 remain relatively stationary, while those who continue to smoke their FEV1 dropping every year. So the management of COPD according to these rate all COPD have to avoid the risk factors and should have vaccination. We add the bronchodilator like I said Salbutamol or the long acting bronchodilators Salmeterol and Formoterol and the anticholinergic drugs. If they have severe disease we start adding inhale cortical steroid. If they ended up with respiratory failured we will use oxygen long therapy at home. The treatment option surgical which is rarely, is done by lung volume reduction surgery. We have what we called the bullectomy if he has large bulla(a large air-filled space) and lung transplant. Nobody is doing lung transplant for COPD if related to smoking but those who have 1
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antitrypsin defiency if they are not smoker and develop respiratoy failure they can be candidates for lung transplant. The lung volume reduction surgery for those who have emphysema not chronic bronchitis bcoz smoke related to emphysema they are affecting the upper lobes of the lungs. So the upper lobes are hyperinflated and they are compressing the relatively normal lung tissue in the middle and lower zone. So the ideas is to remove this upper lobe to give more space for the relatively lung tissue and that will improve the dynamic of the diaphragm. Making the diaphragm to become normal dome shape and thus help in breathing. This surgery is only done for emphysema patient bcoz this disease affecting the upper lobe of the lung.

Acute Exacerbations For the COPD patients, the most dreadful and fearful thing is acute exacerbation which will have increase shortness of breath, cough, sputum production , any three of those, for 48 hours, this is an exacerbation. Usually theyre related to infections that might be viral (however about 50 % are not related to infection) and the other might be related to inviral cause. This disease may be mild or chronic that require ICU admission or assisted ventilation. 1) And the main therapy is we have to get an oxygen therapy because theyre hypoxic. We also have to give the bronchodilator through nebulization in acute exacerbation .

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2) And we have tp get the antibiotics as well which will recover the bacteria like Haemophilus Influenza or Moroxilla Cataralist (not suree!) or Strep Kimon(not sure!). 3) Corticosteroids are given systemically either orally or parentally according to severity. 4) if they do not response they might need assisted ventilation of non-invasive or mechanical ventilation. Those with advance disease with time, they develop chronic respiratory failure, not only during acute exacerbation, but during their usual days

Respiratory Failure Anyone who has Pa O2 < 55mmHg(7.3kPa) ( providing hes not an exacerbation) PaO2 ( Arterial Oxygen Partial Pressure ) of between 55 mmHg and 60mmHg(7.3-8kPa) plus Corpulmonale (by clinically, or ECG) or if he has erythrocytosis (secondary Polycythemia) because theyre hypoxic as the body try to produce more haemoglobin, more erythopoetin to compensate the hypoxia. So if its between 55 and 60 plus, hes a candidate for Long Term Oxygen Therapy (LTOT) , you have to use the oxygen all the day and night at home. And the oxygen is provided by either in Cylinder (which is changed every 48 hours) or nowadays we have Oxygen Concentrater (A machine that is pluged into electricity, it will take the atmospheric air, take nitrogen out of it, and will leave the oxygen. This is expensive relatively but more practical for the patient. And there are
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many studies has shown the long term oxygen therapy (LTOT) for those who have respiratory failure do improve in their survival . First study was done by medical research council, has shown that those with RF, if theyre given LTOT, they survive longer than who did not received LTOT.

-The End-

*Alhamdulillah! Sorry for any mistake or confusion in our notes.

-Wan Muhammad Najib -Amar Adam

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