C.o.P.D.

1. . C.o.P.D.

2. Kidney Brain • . G.I.T. Aging Sleep Skeletal system muscle Reproductive system Circulatory system

3. BY PROF.SAMIHA MOHAMED ABOU –BAKR. PROF. OF chest diseases El-Azhar

4. In Egypt 14.8 % of male deaths in 1987 were smoking related, compared to 8.9 percent 1974 also WHO found that five percent of Egyptian family income is spent, in one form or another, on smoking, and six million Egyptian smokers consume a total of 42 billion cigarettes annually a figure estimated to rise to 85 billion in the next century, and 439.000 of cigarette smokers in Egypt are children 10 years old

5. Genetically Chronic obstructive pulmonary disease (COPD) is polygenic devastating clinical problem. Although cigarette smoking is the major risk factor, only 10-20% of smokers develop symptomatic COPD. Alpha-1- antitrypsin (1-AT) deficiency is an important cause of lung disease, being associated with early onset adult emphysema The genotype most often responsible for this deficiency is homozygosity of PiZ but heterozygotes may also be affected.

6. Several genetic loci appear to exert a strong influence on lung function, probably through an effect on lung growth and development. Polymorphisms of the glutathione-S-transferase antioxidant genes may be associated with increased susceptibility to rapid lung function decline in smokers, according to North American researchers.

7. The theory of interplay . is that this inflammatory process which includes alveolar macrophages in some way releases neutrophil chemotactic factors known as (IL-8 ) causing neutrophils to emigrate from the blood space into the airspace to release elastase . In normal circumstances alpha-1-antitrypsin binds to the elastase and prevents it from binding to elastin thus destroying the structure of the lungs.

8. Neutrophils in the blood and air space release more active oxygen species in smokers, than in non smokers, these together with the 1017 oxidants in inhaled cigarette smoke inactivate the alpha-1-antitrypsin at its active site. This reduces the ability of alpha-1-antitrypsin to bind to elastase by a factor of approximately 2000 allowing active ealstase to bind to elastin and cause the enlargement of the airspace that is seen in emphysema. P-Selectin , L-seletin adhesions are important for the transport of inflammatory cells in the systemic circulation .

9. Glutathione is always in balance with its oxidised form and ,intracellur, it is part of the glutathione redox system which uses the enzyme glutathione peroxidase to detoxify lipid peroxideses and hydrogen peroxide . Reduced glutathione is sacrificed for oxidised glutathione .

10. C.O.P.D.is a mixture of 3 separate disease processes that together form the complete clinical and pathophysiological picture. These processes are chronic bronchitis, emphysema and, to a lesser extent, asthma. Each case of COPD is unique in the blend of processes; however, 2 main types of the disease are recognized.

12. According to GINA • What is the difference between asthma and COPD (chronic obstructive lung disease)?COPD is a collective name for chronic bronchitis and emphysema, two diseases that are almost always caused by smoking. Many of the symptoms of COPD are similar to those of asthma (e.g. breathlessness, wheezing, production of too much mucus, coughing).

13. COPD is generally a more serious disease than asthma, because the changes in the airways are much more difficult to treat, and it usually has a worse outcome. Unfortunately, COPD can cause greater long-term disability and have a greater effect on the heart and other organ systems than asthma.

14. COPD is an obstructive airway disease, and in this way it is quite like asthma. In fact, early in COPD development, you may have very similar symptoms to those seen in asthma

16. COPD is often misdiagnosed as asthma early in its development.While the obstructive nature of asthma and COPD may be similar in some ways, they are two very different diseases

17. Asthma and COPD differ in many ways. COPD is usually caused by cigarette smoking while asthma is not caused by smoking, although it will be worsened by smoking. Asthma is frequently associated with allergy while COPD is not. Asthma is usually highly responsive to medications, and avoidance of symptom triggers usually results in reversibility of airway obstruction.

18. In contrast, the airway obstruction in COPD rarely shows much reversibility with treatment. However, the progression of COPD may be stopped or slowed down with smoking cessation. An allergist or pulmonologist can tell the difference between asthma and COPD and offer appropriate treatment.

19. It should be realized that asthma and COPD can coexist. If you have asthma and smoke cigarettes for years, it would not be unusual for you to develop COPD. In this case, both COPD and asthma coexist. Therefore, both diseases must be treated at the same time

20. Asthma and COPD have important similarities and differences . Both are chronic inflammatory diseases that involve the small airways and cause airflow limitation , both result from gene-environment interactions and both are usually characterised by mucus and bronchoconstriction.

21. The similarities are striking, but the differences are also striking. For example, different anatomical sites are involved COPD affects both the airways and the parenchyma, whilst asthma affects only the airways. Both asthma and COPD involve the small airways and the structural changes in the small airways are responsible for much of the physiological impairment that occurs in these diseases .

22. Perhaps 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 . This is a very important distinction because the nature of the inflammation affects the response to pharmacological agents.

23. There is now ample evidence that inhaled corticosteroids are effective against the eosinophilic inflammation in asthma but largely ineffective against the primarily neutrophilic inflammation seen in COPD

24. In the definitions airway remodelling can occur in long-standing asthma, and results in partially reversible airflow obstruction. Therefore, in many (but not all) patients with long-standing asthma there is a component of chronic irreversible airflow obstruction with reduced lung function and incomplete response to a short-acting bronchodilator or to an oral or inhaled corticosteroid.

25. This makes the diagnosis of asthma sometimes challenging in older adults and it requires the adjustment of the goals of treatment with respect to the patient's age, as maintenance of normal lung function can no longer be a realistic goal.

26. It is therefore often challenging for the clinician to know which disease a patient has or what mix of diseases, since COPD is not one disease but rather a spectrum of diseases involving both the airways and parenchyma.

27. Because of the differences in the cells involved in asthma and COPD, and the relative lack of efficacy of pharmaceutical agents that can alter the progression of COPD (disease-modifying), 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

28. The treatment algorithm is based on severity for both asthma and COPD. For asthma, severity is based on symptom frequency and severity, lung function and healthcare utilisation. For COPD, the stages of severity are defined by lung function.

29. Chronic bronchitis • In this type, chronic bronchitis plays the major role. Chronic bronchitis is defined by excessive mucus production with airway obstruction and notable hyperplasia of mucus-producing glands.

31. Damage to the epithelium impairs the mucociliary response that clears bacteria and mucus. Inflammation and secretions provide the obstructive component of chronic bronchitis. In contrast to emphysema, chronic bronchitis is associated with a relatively undamaged pulmonary capillary bed.

32. Emphysema is present to a variable degree but usually is centrilobular rather than panlobular. The body responds by decreasing ventilation and increasing cardiac output. This V/Q mismatch results in rapid circulation in a poorly ventilated lung, leading to hypoxemia and polycythemia

33. Eventually, hypercapnia and respiratory acidosis develop, leading to pulmonary artery vasoconstriction and cor pulmonale. With the ensuing hypoxemia, polycythemia, and increased CO2 retention, these patients have signs of right heart failure and are known as "blue bloaters."

34. Emphysema • The second major type is that in which emphysema is the primary underlying process. Emphysema is defined by destruction of airways distal to the terminal bronchiole.

36. Pathology of emphysema involves • gradual destruction of alveolar septae • and of the pulmonary capillary bed, • leading to decreased ability to oxygenate • blood. The body compensates with • lowered cardiac output and • hyperventilation.

37. This V/Q mismatch results in relatively limited blood flow through a fairly well oxygenated lung with normal blood gases and pressures in the lung, in contrast to the situation in blue bloaters. Because of low cardiac output, however, the rest of the body suffers from tissue hypoxia and pulmonary cachexia. Eventually, these patients develop muscle wasting and weight loss and are identified as "pink puffers."

38. DIAGNOSIS • History: Patients with COPD present with a combination of signs and symptoms of chronic bronchitis, emphysema, and asthma. Symptoms include worsening dyspnea, progressive exercise intolerance, and alteration in mental status. In addition, some important clinical and historical differences can exist between the types of COPD

39. In the chronic bronchitis group, classic symptoms include the following: • Productive cough, with progression over time to intermittent dyspnea • Frequent and recurrent pulmonary infections • Progressive cardiac/respiratory failure over time, with edema and weight gain

40. In the emphysema group, the history is somewhat different and may include the following set of classic symptoms: • A long history of progressive dyspnea with late onset of nonproductive cough • Occasional mucopurulent relapses • Eventual cachexia and respiratory failure

41. Physical: Depending on the type of COPD, physical examination may vary. • Chronic bronchitis (blue bloaters) • Patients may be obese. • Frequent cough and expectoration are typical. • Use of accessory muscles of respiration is common

42. Coarse rhonchi and wheezing may be heard on auscultation. • Patients may have signs of right heart failure (ie, cor pulmonale), such as edema and cyanosis. • Because they share many of the same physical signs, COPD may be difficult to distinguish from CHF. One crude bedside test for distinguishing COPD from CHF is peak expiratory flow. If patients blow 150-200 mL or less, they are probably having a COPD exacerbation; higher flows indicate a probable CHF exacerbation.

43. Emphysema (pink puffers) • Patients may be very thin with a barrel chest. • They typically have little or no cough or expectoration. • Breathing may be assisted by pursed lips and use of accessory respiratory muscles; they may adopt the tripod sitting position. • The chest may be hyperresonant, and wheezing may be heard; heart sounds are very distant. • Overall appearance is more like classic COPD exacerbation.

44. Causes: In general, the vast majority of COPD cases are the direct result of tobacco abuse. While other causes are known, such as alpha-1 antitrypsin deficiency, cystic fibrosis, air pollution, occupational exposure (eg, firefighters), and bronchiectasis, this is a disease process that is somewhat unique in its direct correlation to a human activity.

45. Lab Studies: • Arterial blood gas • Arterial blood gas (ABG) analysis provides the best clues as to acuteness and severity. • In general, renal compensation occurs even in chronic CO2 retainers (ie, bronchitics); thus, pH usually is near normal. • Generally, consider any pH below 7.3 a sign of acute respiratory compromise

46. Serum chemistry • These patients tend to retain sodium. • Diuretics, beta-adrenergic agonists, and theophylline act to lower potassium levels; thus, serum potassium should be monitored carefully. • Beta-adrenergic agonists also increase renal excretion of serum calcium and magnesium, which may be important in the presence of hypokalemia. • CBC - Polycythemia

47. Imaging Studies: • Chest x-ray • Chronic bronchitis is associated with increased bronchovascular markings and cardiomegaly. • Emphysema is associated with a small heart, hyperinflation, flat hemidiaphragms, and possible bullous changes.