Internal medicine. Lec #: 4 Date: COPD-Definition

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1 Internal medicine Topic: COPD Dr: mousa malkawy Lec #: 4 Date: COPD-Definition A disease state characterized by airflow limitation that is not fully reversible and usually it is progressive and associated with abnormal inflammatory response of the lungs to noxious particles or gases. It is a preventable but not treatable disease. Although asthma is a chronic and obstructive disease but it s not classified as a chronic obstructive pulmonary disease (COPD). COPD is not fully reversible, but asthma is reversible one. the inflammatory response in COPD differ from that of asthma; in asthma the main cells are CD4+ with eosinophiles, basophiles and mast cells while COPD the main inflammatory cells are CD8+ with neutrophiles. COPD is smoke related and only in 10% it s not related to smoke. Unlike asthma, COPD can t be curable or once the pt has COPD he will never go back to mild or reverse his condition, but some associated symptoms can be relieved by medication. COPD-Classification COPD could be a component of one of two inflammatory diseases leading to airflow limitation at the level of small airways : 1. The first component is obstructive bronchiolitis (chronic bronchitis) where there s inflammation mainly in the small airway with fibrosis lead to narrowing and airflow obstruction. 2. The second component is emphysema where there s destruction of the elastic tissue in the lung and walls of alveoli, so the alveoli that are normally patent by the elastic tissue will be collapsed leading to airflow obstruction. To diagnose a pt with COPD he\she must have permanent airflow limitation by pulmonary function test, what ever the cause of airflow limitation (it may be a from of ch.bronchitis, emphysema or both). 0

2 Chronic bronchitis CLINICALLY: The presence of cough and sputum production most of the day for at least 3 months in 2 consecutive years without the presence of underlying parenchymal disease or other causes for the cough or the sputum. Chronic bronchitis define clinically, any one who is smoker with cough and sputum production for 3m for 2 consecutive years is diagnosed as chronic bronchitis. In some lung disease like bronchiectsis or interstitial lung diseases there s a cough most of the day, but we don t consider them as a chronic bronchitis because there s underlying parenchymal pathology in those diseases or the cough and sputum here is explained by other diseases. Most of the pt in chronic bronchitis denies the presence of cough and sputum as they consider it as a part of smoke, but if you ask them do you cough early morning to clear your airways they say yes, which is characteristic for chronic bronchitis. Emphysema Permanent airspace enlargement beyond the terminal bronchioles where gas exchange take place due to alveolar destruction. Emphysema is diagnosed pathologically, not clinically. In the pic, look where the pathology of emphysema take place, it s distal to terminal bronchiole where gas exchange take place (respiratory bronchiole, alveolar ducts and alveolar sacs ) 1

3 To understand COPD better Ch. Bronchitis affects the airways (mainly small airways) while emphysema affects the air sacs and parenchyma of the lung. In COPD, less air flows in and out of the airways because of one or more of the following: 1. The airways and air sacs lose their elastic quality 2.The walls between many of the air sacs are destroyed This is mainly the effect of emphysema (1+2) 3. The walls of the airways become thick and inflamed (swollen) 4.The airways make more mucus than usual, which tends to clog the airways. This is mainly the effect of ch.bronchitis (3+4) In emphysema, the walls between many of the air sacs are damaged, causing them to lose their shape, elasticity and become floppy. This damage also can destroy the walls of the air sacs, leading to fewer and larger air sacs instead of many tiny ones. In chronic obstructive bronchitis, the lining of the airways is constantly irritated and inflamed. This causes the lining to thicken. Lots of thick mucus forms in the airways, making it hard to breathe. If you look at this diagram, you will see that there s overlap between asthma, emphysema, chronic bronchitis and COPD. For example you might have pt have chronic bronchitis but without COPD, bcz he doesn t has airflow obstruction like area 1 and 11. You might have pt with emphysema (diagnosed by C.T scan) and you do pulmonary function test then you find that there's no airway obstruction so this is emphysema without COPD Some pts have both asthma and COPD, like those who are already asthmatic and they are smoker so they will get asthma and emphysema at the same time. In COPD you must have airflow limitation by pulmonary function test. 2

4 Prevalence - risk factors Burden of COPD is like this 12.1 million adults has COPD in 2001 Estimated number now is 16 millions 14 million undiagnosed this is bcz most of the pts justify and relate their cough to smoke itself and consider it normal so they will be undiagnosed until the symptoms become severe enough to make them go for diagnosis. 4th leading cause of death in USA it's predicted if the same rate of smoking is continuing, at year 2020 COPD will become the 3 rd leading cause of death. So it's a lethal disease different from asthma. This figure is just to show you that most of the killing diseases are going down, heart diseases and stroke are decreasing, and stroke doesn't increase but in COPD the rate of death are increasing. Here to show you that the prevalence of COPD related death is increasing in females, and this bcz smoke among females is increasing. 3

5 Clinical Risk Factors Smoking the most important single risk factor, 90% of COPD is related to smoke. But 20% of smokers develop COPD and that's due to other factors affect each smoker separately including genetic factor. Airway hyperresponsiveness Environmental exposures those who exposed to dust and air pollution are more likely to develop COPD. Atopy like asthma, atopic diseases increase the risk. Antioxidant deficiency (vit. C & E) Bronchopulmonary dysplasia (neonatal chronic lung disease) like those who are born prematurely are more likely to develop this disease. Except for smoking, the rest are considered minor factors. Molecular and genetic risk factors Alpha one anti-protease deficiency this is very rare disease, less than 1% of COPD is related to this factor, pts develop emphysema due to this in the 40yrs of their age but if they are smoker, smoke will accelerate the development of emphysema earlier in the late twenties and early thirties. Gene polymorphisms : mostly the genes that are affected are : Tumor necrosis factor alpha Microsomal epoxide hydrolase Transforming growth factor beta 1 In the case of gene polymorphism, this will make COPD run in families (familial) and of course increase the risk in first degree relatives especially those who are smokers. Risk Reduction Smoking cessation the most important, if you want to prevent COPD just stop smoking bcz if COPD happened you will not be fine again bcz of the permanent damage in the lung. Exposure avoidance Physical activity those who are smokers and they are on regular exercises are less likely to develop COPD Anti-inflammatory therapy (ICS, Statins) so far studies shows that inhaled corticosteroids doesn t affect the airway obstruction which happen in COPD, but it can prevent the exacerbation of COPD, also few studies have shown that Statins will decrease the progression of COPD but it's not proved so far. N-acetylcysteine like vit C, E. N-acetylcysteine which act as anti oxidant may help in decreasing the risk. Prevalence of Smoking in Jordan Adults above age 25 year : Males 48% Females 10.5% School children year " those who are experimenting smoking for the first time " : Males 26% Females 11.5% 4

6 Pathology of COPD M C h a n g e s i n L a r g e A i r w a y s o f C O P D P a t i e n t s u c u s h y p e r s e c r e t i o n N e u t r o p h i l s i n s p u t u m G o b l e t c e l l h y p e r p l a s i a S q u a m o u s m e t a p l a s i a o f e p i t h e l i u m N o b a s e m e n t m e m b r a n e t h i c k e n i n g? M a c r o p h a g e s M u c u s g l a n d h y p e r p l a s i a? C D 8 + l y m p h o c y t e s L i t t l e i n c r e a s e i n a i r w a y s m o o t h m u s c l e S o u r c e : P e t e r J. B a r n e s, M2 0D Here if you notice the pathology will affect large and small airways: Large airways increase Neutrophiles in sputum and macrophages which both driven by CD8+ cells, S.M and B.M not largely affected (unlike asthma), mucous and goblet cells hyperplasia leading to mucous hypersecretion. Small airways Why COPD is progressive and irreversible, bcz as you see we have structural changes in addition to fibrosis affecting small airways (peribronchial fibrosis) leading to airways narrowing and limitation which is not reversible, B.M is not thickened as in asthma which is reversible, so fibrosis is permanent change which is not reversible make COPD irreversible C h a n g e s i n S m a l l A i r w a y s i n C O P D P a t i e n t s I n f l a m m a t o r y e x u d a t e i n l u m e n D i s r u p t e d a l v e o l a r a t t a c h m e n t s T h i c k e n e d w a l l w i t h i n f l a m m a t o r y c e l l s - m a c r o p h a g e s, C D 8 + c e l l s, f i b r o b l a s t s L y m p h o i d f o l l i c l e P e r i b r o n c h i a l f i b r o s i s S o u r c e : P e t e r J. B a r n e s, M2 1D 5

7 Changes in the Lung Parenchyma in COPD Patients Here the changes that happens in COPD at the Level of parenchyma (Emphysema), you see alveolar Wall and Septa destruction that Normally give support to the Airways, the damage Result in Reduce elasticity and collapsed Airways. Alveolar wall destruction Loss of elasticity Destruction of pulmonary capillary bed? Inflammatory cells macrophages, CD8 + lymphocytes Source: Peter J. Barnes, 22 MD A S T H M A A l l e r g e n s C O P D C i g a r e t t e s m o k e Y Y Y E p c e l l s M a s t c e l l A l v m a c r o p h a g e E p c e l l s C D 4 + c e l l ( T h 2 ) E o s i n o p h i l B r o n c h o c o n s t r i c t i o n A H R C D 8 + c e l l ( T h 1 ) N e u t r o p h i l S m a l l a i r w a y n a r r o w i n g A l v e o l a r d e s t r u c t i o n R e v e r s i b l e A i r f l o w L i m i t a t i o n I r r e v e r s i b l e 2 3 S o u r c e : P e t e r J. B a r n e s, M D. This is to show you the difference between asthma and COPD, in asthma the inflammatory response mediated by CD4+ " eosinophiles, mast cells" although there is airflow limitation but it's at the level of bronchi "large airways" and it's reversible so we don't consider it as apart of COPD. In COPD the inflammatory response mediated by CD8+ (macrophages, neutrophiles) in addition to airflow limitation in the small airways with alveolar destruction that is not reversible 6

8 First pic: in a + b: this is pathology of a smoker who didn't develop COPD, as we said 20% of smokers develop COPD but not all of them. In c + d: here is a late stage where there are excessive exudates in the airways with peribronchial fibrosis leading to permanent airflow limitation. Second pic: this is emphysema related to smoke; the emphysema which is developed due to smoke is centriacinar (centrilobular) which affect the respiratory bronchiole, while emphysema due to alpha one antiprotease deficiency is panacinar (pan lobular) affect the respiratory bronchiole, alveolar ducts and sacs. Diagnosis of COPD done mainly by 1. Clinical feature 2. Pulmonary function test 3. Radiology COPD-diagnosis 1. Clinical features the most important one that we depend on when we diagnose COPD, any one who has cough, sputum production with SOB and he is smoker ( more than 20 pack/year ) or has risk factors he is candidate to have COPD. 7

9 D i a g n o s i s o f C O P D S Y M P T O M S c o u g h s p u t u m s h o r t n e s s o f b r e a t h E X P O S U R E T O R I S K F A C T O R S t o b a c c o o c c u p a t i o n i n d o o r / o u t d o o r p o l l u t i o n S P I R O M E T R Y 2 7 One phenotype of COPD where there is predominantly ch.bronchitis is what is called Blue Bloater, these pts are usually obese, smoker, have cor pulmonale and chronic respiratory failure, they are cyanosed and edematous as a result of right sided heart failure and cor pulmonale all of theses are character of blue bloater The other phenotype is what is called pink buffer, pt here have predominantly emphysema, those pts have severe shortness of breath but the don't have cyanosis and they are thin. Most of the cases in COPD have both component ch.bronchitis and emphysema bcz both of them are related to smoke. 8

10 D ifferen tia l D ia g n o sis: C O P D a n d A sth m a C O P D O n s e t in m id -life S y m p to m s s lo w ly p ro g re s s ive L o ng s m o k in g h is to ry D y s p n e a d u rin g e x e rc is e L a rg e ly irre v e rs ib le a irflo w lim ita tio n A s th m a O n s e t e a rly in life (o fte n c h ild h o o d ) S y m p to m s va ry fro m d a y to d a y a n d u s u a lly w o rs e a t n ig h t O th e r a to p ic d is e a s e s o r fa m ily h is to ry o f a to p y. L a rg e ly re v e rs ib le a irflo w lim ita tio n 30 This to differentiate between asthma and COPD just by history and clinical features alone. 1. We haven't seen pts who have COPD less than 40yrs of age but majorities of asthma are young and children. 2. Asthma is intermittent disease while COPD is chronic and progressive. 3. smoking history is much more important in COPD 2. Pulmonary function tests Once we suspect COPD we do pulmonary function test to confirm, bcz pts might have chronic bronchitis without COPD, COPD as we said mean that we have airway obstruction and this is confirmed by pulmonary function test which is done by spirometer. 9

11 Remember these terms: FEV1 (forced expiratory volume at one second): maximum volume of air that can be forced out or expired within one second after taking deep breath. FVC (forced vital capacity): This measures the amount of air you can exhale with force after you inhale as deeply as possible. TLC (total lung capacity): the volume of the lung achieved at the end of maximal inspiration. TLC = RV (residual volume) + IRV (inspiratory reserved volume) + TV (tidal volume) + ERV (expiratory reserved volume) TV: the amount of air inspired or expired with each breath (normal passive breath not forced one). IRV: maximum amount of additional air that can be inspired from the end of normal inspiration. ERV: maximum amount of additional air that can be expired from the end of normal expiration RV: the volume of air remains in the lung after maximal expiration. VC (vital capacity): TLC-RV, volume achieved by maximal forceful expiration after maximal inspiration Pulmonary function test FEV1/FVC < 70 COPD FEV1 Airway resistance Total lung capacity Residual volume Diffusion capacity chronic bronchitis emphysema variable increased increased increased normal decreased The hallmark of COPD is a reduction in FEV1/FVC ratio, the normal ratio is >= % which mean that70%-80% of inspired air must be expired at 1 st second, in COPD it's a must to find this ratio (< 70%) and that's bcz there's obstruction which prevent more than 70% of the inspired air to be expired. This is called vital capacity maneuver where we ask the pt to take deep breath and expire it and measure the expired air during the first second. 10

12 FEV1 alone is variable among COPD pts according to the severity. Airway resistance is increased TLC is increased, RV is increased especially in emphysema bcz there's more air stay in the lung that not fully expired as the normal person does. Diffusion capacity, if the pt is predominantly has ch.bronchitis then diffusion capacity is normal while in emphysema the diffusion capacity is decreased this is bcz in emphysema the pathology is at the site where gas exchange take place ( distal to terminal bronchiole) which mean decrease gas exchange, but in ch.bronchitis those sites will not be affected. According to this we can determine the severity of COPD as following Stage I: Mild FEV1/FVC < 0.70 FEV1 > 80% Stage II: Moderate FEV1/FVC < % < FEV1 < 80% Stage III: Severe FEV1/FVC < % < FEV1 < 50% Stage IV: Very Severe FEV1/FVC < 0.70 FEV1 < 30% or FEV1 < 50% plus chronic respiratory failure 11

13 3. Radiology This is C.T scan shows centrilobular emphysema, you can notice dark spots which indicate smoke pigments, and it usually affects the upper lobes of the lungs This is x-ray shows extreme emphysema, you can see low flat diaphragm with hyper-inflated lungs. This is more severe one with subpleural emphysematous spaces; this type could lead to pneumothorax if these could rupture. This is panlobular emphysema which mostly affects the lower lobes of the lung, its characteristic of alpha one antiprotese deficiency. 12

14 This is bullous emphysema, where small bulla coalesce together to form large bullae. Treatment and management of COPD Goals of COPD Management 1. Relieve symptoms the most important goals, if these two are Achieved all others will be improved. 2. Prevent disease progression 3. Improve exercise tolerance 4. Improve health status 5. Prevent and treat complications 6. Prevent and treat exacerbations 7. Reduce mortality 13

15 Prevent disease progression Treatment A. Smoking cessation: the only thing that can prevent disease progression is probably smoking cessation, if you stop smoking the disease will stay as it is and it will not deteriorate more, you will not go back to normal but you will keep the pulmonary function as it is or it might improve a little in the first one or two years. B. Vaccines: all smokers who have COPD should receive the influenza vaccine and probably the pneumococcal vaccine, the evidence for influenza vaccine is stronger but usually we give pneumococcal once and we give influenza annually. Improve pulmonary function Medical treatment Rehabilitation Surgical treatment Treat complications Smoking cessation It's advisable that any physician who sees pts to ask pts about smoking even if the disease that the pts come for is not smoke related, and they found by adopting this policy (ask the pts to quit smoking) that high percent of smokers will quit smoking, we have to adopt what is called the five As: Ask the pt if he is smoker, advice him to quit smoking even if this disease is not smoke related, assess his willingness to quit smoking, assist pts in quitting smoking bcz some pts tell you that they tried to quit but they failed so if they failed you can offer them 1.nicotine replacement therapy 2.nicotene patches or gum 3. Give them antidepressant which is useful in smoking cessation 4. Recently varenicline was introduced which is nicotine receptor agonist 30-40% of smoker might quit only by assisting them in quitting, and you have to arrange for follow up for these pts. 14

16 FEV 1 (%) Relative to Age 25 Age Indeterminate Symptoms Disability Death 2 Susceptible Smokers Not Susceptible 1 Stopped smoking at 45 (mild COPD) Stopped smoking at 65 (severe COPD) Age (years) Courtesy of D.O Donnell.. Adapted from Fletcher CM, Peto R. Br Med J. 1977;1:1645. As I said only 20% of smokers develop COPD, and this is probably genetically determined. around the age of twenty we reach the maximum pulmonary function, after the age of 20 we start aging process then we will get a decline in our FEV1, in normal people after the age of twenty they will loss around ml of their FEV1 every year. In COPD pts there is what is called rapid accelerator, they loss ml of their FEV1 every year. Number 1 in the box above, this person is not susceptible (not smoker = no COPD) so he is probably can live around age 90 with reasonable pulmonary function. Number 2 in the box, those who are susceptible (smoker) by age of 60 they will die, but if they stopped smoking at age of 45 (# 3) they will go back and only loss ml of their FEV1 every year after quitting instead of the 70-80ml lost when they were smokers and they will live around the age of 80 instead of 6o. So it's not late to quit smoking bcz if you quit you will have more years to live. Smoking Cessation and FEV 1 Decline Post bronchodilator FEV Sustained Quitters Continuing Smokers This is to show you that after you quit smoking (the upper line) the FEV1 will improve in the first year and after that it will start to decline again as usual (20-30 ml/ year). 2.4 Screen 2 1yr 2yr 3yr 4yr 5yr Anthonisen et al. JAMA 1994;272:

17 Medical treatment In medical treatment of COPD we do stage treatment according to the symptoms: As we said before we start treatment with smoking cessation and then we offer vaccination this is applied for all stages of COPD pts. If pts have mild symptom we give them short acting beta two agonist If pts have moderate symptoms we give them long acting beta two agonist + anticholinergic medication. If pts have severe symptoms we give them inhaled corticosteroids in addition to the previous protocol (long acting beta two agonist + anticholinergic medication) If pts have very severe symptoms we add long term oxygen therapy if they have respiratory failure in addition to the previous protocols (inhaled corticosteroids + long acting beta two agonist + anticholinergic medication) Protocols here differ from that in asthma, in asthma we used inhaled corticosteroids in initial stages but here inhaled corticosteroid is used in severe and very severe cases. 16

18 Surgical Treatment Lung volume reduction surgery Bullectomy Lung transplantation we do it only if the pt have alpha one antitrypsin deficiency. Lung volume reduction surgery: we use this type of surgery only in very severe cases of smoke related emphysema but not in ch.bronchitis, we do pulmonary function test and we find that FEV1 is less than 30% which indicate a very severs case then we do high resolution C.T scan and if we find that emphysema predominantly affecting the upper lobes of the lung which is characteristics finding in smoke related emphysema ( centrilobular emphysema) then we can remove the severely affected upper lobes of the lung which give more space for the relatively normal lung tissue down which then improve oxygenation, exercise tolerance and survival. So this type of surgery is only done in severe cases of smoke related emphysema and it must affect predominantly the upper lobes of the lung. If the pt has large bullous that compress the normal lung tissue we do what is called Bullectomy, but these are very rare. 17

19 Acute Exacerbations of COPD Definition: COPD exacerbation is a period in the natural course of the disease that is characterized by a worsening of a patient's baseline symptoms -- such as dyspnea, cough and/or sputum production. Signs and Symptoms of a COPD Exacerbation The main symptom of an acute exacerbation of COPD is abrupt increase in breathlessness (SOB) for h which is often accompanied by the following: Increased cough and sputum production Change in the color and/or thickness of the sputum the major ones. Wheezing Chest tightness Fever Causes of COPD Exacerbation: Infection, Air Pollution The top two causes of an exacerbation are infection (50% of exacerbation is due to infection and mainly it's bacterial) of the airways or lungs and air pollution (environmental factors). In one-third of all COPD exacerbation cases, however, the cause cannot be identified. Therapy for Acute Exacerbations Oxygen therapy : we use this if the pt have chronic respiratory failure to correct hypoxemia Bronchodilators : Bronchodilator dosages are increased during acute exacerbations to decrease acute bronchospasm, usually we give nebulizers of short acting beta two agonist and anticholinergic therapy Antibiotics: Approximately 50% of acute exacerbations are due primarily to the bacterial infection, most important of these are Streptococcus pneumoniae (causing pneumonia), Haemophilus influenzae (causing flu), and Moraxella catarrhalis (causing pneumonia). We always give antibiotic in COPD exacerbation even if the cause is not related to infection. 18

20 We decide the type of antibiotic according to the severity of infection. In asthma we don't give antibiotic for exacerbation, bcz exacerbation of asthma is only due to viral infection. Corticosteroids Assisted ventilation-mechanical ventilation : Patients with acute exacerbations of COPD have a risk for developing respiratory failure. Respiratory failure occurs when respiratory demand exceeds the ability of the respiratory system to respond. Without aggressive intervention at the point of respiratory failure, the patient can die. Mechanical ventilation: Mechanical ventilation is a means by which air is pushed into a patient's lungs by the ventilator instead of the patient using his respiratory muscles to draw in air. Mechanical ventilation therefore reduces or eliminates the patient's work of breathing, and the patient continues to receive air into his lungs and passively exhale without any work. There are two commonly used methods for mechanical ventilation in COPD: noninvasive and invasive. Invasive Ventilation the more traditional means is invasive ventilation: an endotracheal tube, a small-diameter plastic tube, is placed into the trachea and then connected to a ventilator, which pushes air into the lungs. Invasive ventilation can be administered to patients who are unconscious or heavily sedated, and it is more effective than noninvasive ventilation. Noninvasive Ventilation Noninvasive ventilation is used in a conscious, cooperative patient. In this method, oxygen is delivered through a mask that forms a seal around the nose or mouth and nose. The advantages are that the mask can be periodically removed and the patient's natural protection against secretions getting into the lower airway is preserved. Respiratory Failure and COPD If pts have respiratory failure with stable COPD we have to supply them with oxygen Respiratory failure has two type 1. Type one respiratory failure (hypoxemic): here there is decrease in PaO2 only, PaO2 < 55mmhg (7.3 kpa). 2. Type two respiratory failure (hypercapnic): here there's decrease in PaO2 and increase in PaCO2, PaCO2 > 55mmhg (7kPa). 19

21 Now if a pt has (PaO2 < 55 mmhg) or (PaO2 between mmhg + evidence of chronic hypoxemia such as polycythemia or cor pulmonale) they are candidate for long term oxygen therapy, those therapy include one of two : o We give them oxygen cylinder that can be replaced every 24-48h or o We give them what is called oxygen concentrators, a machine that provide oxygen that have higher concentration than that found in the ambient air by taking the atmospheric air and keep the nitrogen out of it, characterized by easy accessibility than the oxygen cylinder These studies have shown that pts who have COPD with chronic respiratory failure, giving them oxygen will improve the survival in these pts. This slide shows those who have type two respiratory failure if it's transient, bcz some pts during exacerbation they retain Co2 and after exacerbation they recur to type one those who have chronic or transient type two failure the mortality rate will be higher than those who have type one failure. 20

22 Prognostic Factors BMI & FFMI if a COPD pt has low body mass index (<=21) the mortality rate is higher than that who has high body mass index Airway hyperresponsiveness Acute exacerbations Respiratory failure All these increase mortality rate in COPD pts Hypercapnea BODE index The most important prognostic factor we depend on is the percentage predicted of FEV1, the more the reduction the more severe the disease is and the higher mortality rate is. BODE index B: BMI O: airway obstruction D: Dyspnea E: Exercise capacity 4 year survival 0-2 points 80% 3-4 points 67% 5-6 points 57% 7-10 points 18% 21

23 COPD and Co-Morbidities COPD is considered as asystemic disease, accordingly COPD patients are at increased risk for: Myocardial infarction, angina Osteoporosis Respiratory infection Depression Diabetes Lung cancer تم بحمده تعالى Thx for all 22

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