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Ranks as the fourth leading cause of death worldwide, trailing behind CVD, pneumonia & HIV/AIDS**
Future of COPD
COPD is expected to grow globally 1. Due to increase in life expectancy of the population more than 60 yrs 2. Increased usage of cigarette smoking
COPD - Definition
Airflow is usually progressive & is associated with inflammatory response of the lungs to noxious particles or gases primarily caused by smoking
1. Large barrel shaped chest 2. Prominent accessory respiratory muscles in neck are used for respiration 3. Low flat diaphragm 4. Diminished breath sound
Diagnosis of COPD
Should be considered in any individual who has 1. Symptoms of cough 2. Sputum production 3. Dyspnoea 4. History of exposure to risk factors for the disease 5. Family history of chronic respiratory illness
Detecting COPD
1. Air containing volume of the lung 2. The ability to move air into & out of the lung 3. The rate at which gases diffuse between the lung & blood 4. Blood levels of oxygen & carbon dioxide
http://seniorhealth.about.com/od/respiratorycond/a/test_copd.htm
Detecting COPD
Exposure to cigarettes/ environmental pollution Family history of chronic respiratory illness Presence of cough/sputum/dyspnoea
Despite the burden of COPD it has received limited recognition from both patients & physicians*
More than half of the COPD patients are misdiagnosed or treated as having asthma**
*Resp Med 2002;96;S2-s12 **News-Misdiagnosis of COPD- national Jewish medical research center
Asthma
Starts at any age Sniffing, nasal discharge Can be linked to few Specific trigger factors (symptoms are not consistent) Inhaled corticosteroids & if needed addition of bronchodilators
Nasal symptoms Rarely present with nasal symptoms Smoking Triggers 80% of patients are smokers Respiratory tract infections Quitting smoking helps (symptoms are consistent) Bronchodilators
www.about-copd.com
Asthma
Inflammation Airway hyperresponsiveness
Emphysema
Destruction of alveolar walls Reduced elasticity & recoiling of capillaries for gas exchanges
Reversibility Inflammation
Mostly reversible Yes, responsive to antiinflammatory therapy Adrenergic/sympathetic responds to adrenergic bronchodilators
Poorly reversible airflow limitations associated with cystic fibrosis & fibrosis due to tuberculosis are not included in the definition of COPD but should be considered in differential diagnosis
As the disease progress there is fibrosis & increased deposition of collagen in the walls resulting in loss of cilia function
1. Genetic factor- hereditary deficiency of alpha1 antitrypsin, a inhibitor of protease 2. Sex- More prevalent in males 3. Airway hyperresponsiveness
1. Smoking (lowers the maximally attainable lung function in adulthood) 2. Socioeconomic status (indoor cooking in rural areas using biomass,
impaired growth of lungs, inc rate of infection)
3. Occupation (COPD attributable to work is 19.2%) 4. Environmental pollution 5. Recurrent pulmonary infections 6. Diet
According to WHO 75% of deaths from COPD that occur in developed countries are directly related to smoking *
Smokers are more likely to have upper & lower respiratory tract infections than nonsmokers
1. Contributes to inflammatory response 2. Leads to exaggeration of normal protective inflammatory response leads to tissue destruction impairs defence mechanisms 3. Also leads to imbalance of proteinase & antiproteinase in the lungs - Positioning for Metadec 4. Oxidative stress Positioning for LycoRed
Inflammatory cells (macrophages, neutrophils) release a combination of proteinase and on the other hand decrease the activity of antiproteinases by oxidation due to free radicals
Presence of Oxidative stress markers evident from the exhaled air from the lungs & urine of smokers
Free radicals Oxidizes variety of biological molecules Leads to cell dysfunction & death Damages the extra cellular matrix Activates proteinases
Stages of COPD
Stage 1: lung function at 50% of normal capacity or higher; health is not greatly affected Stage 2: Lungs function at 35-49% of normal capacity; health is significantly impacted Stage 3: Lung function at less than 35%; health is severely affected
www.about-copd.co/html/copd-complications.php3
A. B. C.
Primary care Level (Primary health centers, dispensaries, general practice clinics) Secondary Care Level (District level hospitals and clinics Tertiary Care Level (Medical colleges, large corporate, institutional and specialty hospitals)
http://www.indiachest.org/copd_guidelines/algorithm.html
Management of COPD
3. Mucolytic 4. Antioxidant therapy (only on N-acetylcysteine-reduces the nos of exacerbations) 5. Antibiotic therapy 6. Oxygen treatment 7. Anabolic steroids for pulmonary rehabilitation
Exercise training- endurance (aerobic) & strength exercises Education- self management & adherence to the treatment plan Psychosocial & behavioral intervention- Anxiety & depression is
common in these patient Nutritional & Anabolic Therapy Weight loss & muscle wasting are present in 25-30% of the stable patients but it contributes to morbidity & mortality
www.about-copd.co/html/copd-complications.php3
Heart disease : Occurs if low oxygen levels develop in the blood it leads to strain on the heart, making it work harder ultimately results in heart diseases & heart attacks
Sleep disorders: leads to sleep disorder, insomnia, nightmares and chronic fatigue
www.about-copd.co/html/copd-complications.php3
Skeletal muscle wasting: The systemic effects limits the exercise capacity of the patients and worsens the prognosis leading to skeletal muscle wasting as Weight loss & being underweight are associated with decreased diffusing capacity
1. Nutritional screening
2. BMI-weight(Kg)/height (m2)
Underweight (BMI<21 kg.m-2) Normal weight (BMI 21-25 kg.m-2) Overweight (BMI 25-31 kg.m-2)
www.about-copd.co/html/copd-complications.php3
www.about-copd.co/html/copd-complications.php3
1. Reduced or altered contractile activity 2. Negative energy balance due to a) Raised energy expenditure b) Reduced dietary intake 3. Reduced testosterone levels 4. Hypoxia or hypoxaemia & acidosis 5. Glucocorticoids 6. Increased pro-inflammatory cytokines
Eur Resp J 2003;;22 52s-63s
Weight loss is an important determinant of 1. Functional capacity due to muscle atrophy & weakness 2. Health status- reduced exercise tolerance & dyspnoea 3. Mortality 4th leading cause of death & prevalence is further increasing
Loss of fat free mass is observed in 20-40% of patients with COPD
Significant weight loss has been found to begin on an average 3.5 years before death
Following the onset of unintended weight loss mortality reaches 30% in 3 years and 50% in 5 years
Chest 2002;122:421-428
Malnutrition is associated with severe COPD in * 10-26% OPD patients Upto 47% hospitalized patients with acute respiratory failure
*Chest 1998;jul;114;19-28
Reversal of weight loss has been associated with improved outcomes, incld inc muscle strength, exercise capacity & survival
Restoration of body weight may be difficult to achieve and to maintain using nutritional intervention alone
Chest 2002;122:421-428
Anabolics have been associated with significant improvement 1. Muscle performance 2. Weight 3. Pulmonary function 4. Reduction in breathlessness
(Oxandrolone 20mg/day for 1month)
Anabolics are effective adjunct to facilitate weight restoration in patients with COPD
(Oxandrolone 20mg/day for 4month)
Chest 2002;122:421-428
Mechanism of action
1. Increases muscle mass 2. Erythrpoeitic effect 3. Reverses the diaphragmatic muscle weakness specifically induced by glucocorticosteroids
Trial 1 : Chest Nov 2003 Nandrolone decanoate 50mg every 15 days for 8 weeks N=63 male patients
Significant rise in fat free mass compared with placebo Increases maximal breath intake Improvement in muscle function & exercise capacity Significant increase in erythrocyte count results in better oxygen delivery to tissue
Trial 1 Safety
Nandrolone decanoate was able to antagonize the loss of diaphragm force induced by long term low dose methylprednisolone administration
Trial 1 Conclusion
A short term course of Nandrolone decanoate had an overall positive effect on the body composition with improvement in muscle function, exercise capacity and improvement in erythropoietic parameters. Also restored the pulmonary impairment attributed to the use of glucocortosteroids
Trial 2 : Am J Resp Crit Care Med 1995; oct;1268-1274 Nandrolone decanoate 50mg to men & 25 mg to women, every 15 days for 8weeks N=217 patients
Nutritional supplementation alone predominately increased fat mass whereas anabolic steroid increased muscle mass Respiratory muscle strength improved more in the combination therapy (Nutrition + Nandrolone)
Trial 2 Conclusion
Nutritional supplementation and anabolic steroid resulted in some benefits for patients with moderate to severe COPD
Conclusion
The reduction in diaphragm force generation in the methylprednisolone group was completely abolished by the addition of Nandrolone decanoate
Conclusion
Nandrolone decanoate in part reversed the loss of diaphragm force generating capacity in emphysematous hamsters treated with methylprednisolone & reversed the fiber atrophy completely
Metadec