1. CHRONIC OBSTRUCTIVE PULMONARY DISEASE LECTURE NOTES PHCP 403(2017)

2. Definition:
Chronic obstructive pulmonary disease (COPD) is a disease state characterized by airflow limitation, that is not fully reversible. The airflow limitation is usually both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases.

3. COPD generally covers other disease labels including chronic obstructive airway disease (COAD), chronic obstructive lung disease (COLD).

4. The major risk factors for the development of COPD includes:
1. Smoking-Risk increases with increase in consumption.
2. Age—increasing age results in ventilatory impairment.
3. Gender—Male gender, due to high incidence of smoking
4. Occupation—Such as coal and gold mining, farming, grain handling and cement/cotton industries. .

5. Risk factors cont…..
5. Genetic factors—α1-antitrypsin deficiency is the strongest single genetic risk factor.
6. Air pollution---Death rates are higher in urban areas, indoor air pollution from burning biomass fuel is also implicated.
7. Socio-economic status—more common in individuals of low socio-economic status.
8. hyper-responsiveness-Smokers show increased levels of IgE, eosinophils and airway hyper- responsiveness but how this influence the development of COPD is unknown

6. PATHOPHYSIOLOGY
The airflow obstruction caused by COPD is usually progressive
It is attributed to pathologic changes in the lung that affect the proximal airways, peripheral airways, lung parenchyma, and pulmonary vasculature..
Alterations in tissue structure are caused by chronic inflammation that involves recruitment of inflammatory cells into the lung, as well as structural changes that result from repeated injury and tissue remodeling.

7. Pathophy. Cont.…
The magnitude of structural changes and tissue dysfunction varies among patients and is often distinguished by two major pheno-types that include chronic bronchitis and emphysema.
Chronic airflow limitation can result from both of these processes

8. AETIOLOGY
Tobacco smoking is the most important and dominant risk factor for the development of COPD. Other processes involved in pathogenesis of COPD are
Inflammation
Imbalance of proteinases and anti-proteinases, in
the lungs and
Oxidative stress

9. 1) Inflammation
It is characterized by chronic inflammation throughout the airways, parenchyma and pulmonary vasculature.
It is a different inflammation from that of asthma with an increase in neutrophils, macrophages, and T-lymphocytes (Particularly CD8).

10. These inflammatory cells cause the release of inflammatory mediators and cytokines such as leukotriene B4, Interleukins, and tumour necrosis.
The action of these mediators over a period of time damages the lungs and leads to the characteristic pathological changes.

11. 2) Proteinase and anti-proteinase inbalance.
It has been observed that α1-antitrypsin deficient individuals are at increased risk of developing emphysema.
In copd there is either an increased production /activity of proteinases or a decreased production/ activity of antiproteinases.
Proteolytic enzymes (proteinases) such as neutrophil elastin are released by macrophages or neutrophils. The antiproteinases inhibit the damage caused by the proteolytic enzymes .

12. The main antiproteinase is α1 –antitrypsin, also known as α1 –proteinase inhibitor. Cigarrete smoke inactivates these protein.

13. Oxidative stress
An imbalance of oxidants and antioxidants exist in COPD.
This state of oxidative stress contributes to the development of the disease by damaging the intracellular matrix, oxidizing biological molecules which cause cell destruction and promoting histone acetylation.

14. Clinical manifestation
Diagnosis
A diagnosis of COPD is usually considered in any patient who has symptoms of A cough, sputum production, dyspnea and a history of exposure to COPD risk factors
Diagnosis is confirmed with the use of spirometry
Clinical features
The two predominant features of COPD are emphysema and chronic bronchitis. Severity depends on which predominates.

15. Associated with cigarette smoke and air pollution
Chronic Bronchitis
 Associated with cigarette smoke and air pollution
chronic/recurrent cough with expectorations
Moderate dyspnea
Recurrent respiratory infections
Usually obese
blue bloater”
Retain CO2
Significant hypoxemia
Cyanosis
Peripheral oedema
end-stage chronic bronchitis
Polycythaemia
Cor pulmonale
“45 – 65 year old smoker”

16. α1 – antitrypsin deficiency
Emphysema
α1 – antitrypsin deficiency
Permanent change in anatomy with enlargement/destruction of alveoli leading to decreased gas exchange
Severe dyspnea is the primary complaint
“55 – 75 year old smokers”
“pink puffer”
Hyperventilates to compensate for hypoxia

18. INVESTIGATIONS
Lung function tests are used to assist in the diagnosis.
A Spirometer is used to measure lung volumes and flow rates. The main measurement made is the forced expiratory volume in the first second of exhalation(FEV1) Other test are ;
Vital capacity (VC): The volume of air inhaled and exhaled during maximal ventilation.
Forced vital capacity (FVC); The volume of air inhaled and exhaled during a forced maximal expiration after full inspiration.
Residual volume (RV):The volume of air left in the lungs after maximal exhalation.
Airflow obstruction is defined as.
FEV1 less than 80% of that predicted for the patient and FEV1/FVC less than 0.7.

19. Vital capacity decreases in bronchitis and emphysema.
Residual volume increases in both cases but tends to be higher in patients with emphysema due to air being trapped distal to the terminal bronchioles.
Chest radiographs reveals differences between the two disease states.
A patient with emphysema will have a flattened diaphragm with loss of peripheral vascular markings and the appearance of bullae.

20. A bronchitic patients will have increased bronchovascular markings and may also have cardiomegaly with prominent pulmonary arteries.
Additional investigations at diagnosis
Investigation
Chest X-ray To exclude other pathologies
Full blood count To identify anemia or polycythemia
Serial domiciliary peak flow To exclude asthma if there
is a doubt about
Measurements diagnosis

21. α-antitrypsin Particularly with early-onset disease or a
minimal smoking/family history.
CT scan of the thorax To investigate symptom that seem
ECG To assess cardiac status if features of cor- pulmonale
Pulse oximetry To assess need for oxygen therapy if FEV1 < 50% of predicted value.
Sputum culture To identify organisms if sputum is
persistently present
And purulent.

22. COPD
asthma

23. Clinical features differentiating COPD & asthma
Smoker or ex-smoker
Nearly all
possibly
Symptoms under age 35
rare
common
Chronic productive cough
uncommon
breathlessness
Persistent & progressive
variable
Night-time waking with breathlessness and/or wheeze
Significant diurnal or day-to-day variability of symptoms

24. TREATMENT
Drug treatment coupled with other measures such as physiotherapy and artificial ventilation have not been shown to improve the natural progression of COPD.
However, Quality of life and symptoms will improve with suitable treatment, also correct management of patients will lead to a reduction in hospital admissions and prevent prematured death

25. Smoking
Smoking being the most important factor in the development of obstructive airway disease .
Every smoker with a chronic airflow obstruction must be advised to stop.
Nicotine replacement therapy should be advised. The nicotine absorbed reduces the effects associated with reducing smoking such as irritability, sleep disturbances , fatigue, headache and increased appetite.

26. Antibiotics and Vaccines
Prophylactic antibiotics have no place in the management of COPD.Antibiotic therapy is vital if a patient develops purulent sputum. Pathogens involved are Streptococcus Pneumonia, Haemophilus influenza or Moraxella catarrhalis.

27. Prophylactic immunization
A single dose of Pneumococcal vaccine and annual influenza vaccinations have been shown to reduce hospitalisations and the risk of death in the elderly with chronic lung disease.
Bronchodilators
Bronchodilators in COPD are used to reverse airflow limitation. Their effectiveness should be assessed in each patient using respiratory function tests and by assessing any subjective improvement reported by the patients. Patients may experience improvement in exercise tolerance or relief of symptoms such as wheeze and cough,

28. Inhaled β2-adrenoceptor agonist
Selective β2-agonists should be tried initially since they provide rapid relief and have a low incidence of side effects. The effect of β2- agonists last for 4hours and they can be used either regularly or as required for symptom relief.
If patients remain symptomatic despite a short acting β2-agonist, then a long acting agent can be added (2 or more exacerbation/year)

29. Anticholinergic
In COPD, parasympathetic airway muscles tone is the major reversible component. Inhaled anticholinergic drugs reverse this vagal tone and have a significant bronchodilator effect, especially in the elderly e.g ipratropium bromide and tiotropium.

30. Theophyllines
They are weak bronchodilators but seems to have usefull additional physiologic effects in COPD as increased respiratory drive, improved diaphragmatic function and improved cardiac output.
Use of theophyllines should only be considered after a trial of short-acting with long acting bronchodilator.Care must be taken when prescribing theophylline, its clearance is affected by many factors, including cigarette smoking, viral pneumonia, heart failure and concurrent drug treatment such as macrolides antibiotics.

31. High-dose and nebulized bronchodilators
Patients with severe disease will benefit from higher doses of bronchodilators.
Corticosteroids
Patients with COPD show a poor response to corticosteroids and have a largely steroids-resistant pattern of inflammation. The long-term benefits of inhaled corticosteroids in COPD have been shown in patients with moderate to severe disease, with FEV1 less than 50% of predicted value.
Mucolytic
Mucolytic may be of benefit in stable COPD if there is a chronic cough that is productive of sputum.

32. COPD Exacerbations
An acute exacerbation of COPD is defined as an acute worsening of the patients chronic symptom (dyspnea, cough, sputum production) necessitating treatment.
The cause of acute exacerbations is believed to be as a result of respiratory tract infections, viral, or bacterial, air pollution or other environmental exposures.
Therapeutic interventions
Regular bronchodilator therapy, a short course of systemic corticosteroid therapy, and antibiotics. Bronchodilators are given when needed prn by a metered dose inhaler or nebulizer every 3 to 4 hours. A β2-agonist can be given with or without an anticholinergic agent.

33. Antibiotics
Antibiotics can be used to treat exacerbations of COPD associated with a history of more purulent sputum.
Corticosteroids
A short course of oral steroids has been shown to benefit FEV1 and reduce the duration of hospitalization. A suitable course is prednisolone 30mg every morning, given for 7-14 days.

34. Other treatments
Intravenous aminophylline can be considered .If there is an inadequate response to bronchodilators. Oxygen therapy is necessary to improve hypoxia.
In patients with hypoxic drive, the administration of high concentration oxygen will cause a fall in ventilation, carbondioxide retention and respiratory acidosis.
Intravenous hydration is given to take care of dehydration caused during an attack.
Chest physiotherapy is employed to mobilize secretions, promote expectoration and expand collapsed lung segments.Nebulised 0.9% sodium chloride has been used to help in this.

35. Treatment of cor-pulmonale
Treatment is symptomatic peripheral oedema is managed using thiazide or loop diuretics. Oxygen is used to treat hypoxemia and this should also promote a diuresis.
Domiciliary oxygen therapy
The aim is to improve oxygen delivery to cells increase alveolar oxygen tension and decrease the work of breathing to maintain a given Pao2.
It can be given in 2 ways:
Intermittent administration
To increase mobility and capacity for exercise and to ease discomfort, benefits emphysema.

36. Continues long-term oxygen therapy (LTOT)
LTOT of at least 15 hours per day improves survival in patients with severe irreversible airflow obstruction, hypoxemia and peripheral oedema.
PATIENT CARE
Pulmonary rehabilitation
Advice and support on smoking ceasation
Nutritional assessments
Aerobic exercise training
Breathing training
Education about medicines, nutrition, self-management of disease and lifestyle
Psychological support( depressed, anxious, fatigued.

37. SMOKING CEASATION
Nicotine replacement therapy
Long acting: Transdermal patches are considered to be most suitable for people who smoke regularly through the day. The 24 hour patch worn overnight, is better for people who crave nicotine first thing in the morning.
Heavy smokers should be started on high-dose patches.
Short acting: Several short acting NRT are available
Gum: Gum should be chewed slowly until the taste becomes strong, then allowed to rest between the and teeth to allow absorption.
Lozenges: Allowed to dissolve in the mouth and periodically moved around until completely gone. I

38. Mr. MA is a 61 –year- old retired dock worker whose medical history is COPD and chronic heart failure. He has recently started a pulmonary rehabilitation programme and asks you for advice on the best way to give up smoking. He currently smokes around 25 cigarettes a day and has been smoking since he was 20.
Q.1
a)Why is it important for Mr. MA to give up smoking?
b)What should be discussed when helping someone stop smoking? –
c)What non- pharmacological support will help Mr. MA in giving up?
d)Which smoking cessation product should be chosen
e) Is this choice safe in someone with cardiac disease?