Chronic Obstructive Pulmonary Disease (COPD) is a common lung disease characterized by persistent respiratory symptoms and airflow limitation. It includes chronic bronchitis and emphysema. The main risk factor is cigarette smoking. Symptoms include dyspnea, cough, and sputum production. Diagnosis is confirmed by spirometry showing airflow limitation. Management involves smoking cessation, bronchodilators, pulmonary rehabilitation, oxygen therapy, and treating exacerbations with corticosteroids and antibiotics.

2. Chronic Obstructive Pulmonary Disease
(COPD)
Dr. Yousaf Hayat
( PG Trainee-Medcial A Unit, SGTH, Swat)
April 19, 2017

3. Definition;
• COPD is a disease state characterized by air flow limitation that is not fully
reversible.
• COPD is a common ,preventable and treatable disease that is characterized by
persistent respiratory symptoms and air flow limitation that is due to airway and
/ or alveolar abnormalities

4. COPD Includes:
• Chronic bronchitis
• Emphysema
• CHRONIC BRONCHITIS: is a clinical Dx defined by excessive secretion of the
bronchial mucous and is manifested by daily productive cough for 3 months or
more in at least 2 consecutive years.
• EMPHYSEMA:is a pathologic Dx that denotes abnormal and permanent
enlargement of air spaces distal to terminal bronchiols with destruction of their
walls and without obvious fibrosis.

5. PREVALANCE
• Prevalence of COPD is higher in smoker and ex smoker compared to non smoker.
• Higher in >40 years group compared to <40 .
• Higher in men's than women's.
• Estimated 384 million cases in 2010.
• 3 million deaths annually.
• With increasing prevalence of smoking in developing countries and aging
populations in high income countries the prevalence of COPD is expected to rise
over next 30 years.
• By 2030 predicted 4.5 million copd related deaths annually.

6. RISK FACTORS:
• Cigarette smoking
• Environmental tobacco smoke
• Occupational dusts, fumes & chemicals.
• Indoor air pollution from biomass fuel used for cooking and heating in poorly
ventilated building.
• Airway infections.
• Allergy
• Hereditary factors(alpha 1 anti trypsin deficiency).

7. PATHOLOGY,PATHOGENESIS & PATHOPHYSIOLOGY
Chronic inflammation and structural changes in large & small airways and lung
parenchyma ( mucous glands enlargement, goblet cells hyperplasia ,smooth
muscle hypertrophy, squamous metaplasia and bronchial hyperactivity, destruction
of gas exchanging air spaces, respiratory bronchioles , alveolar ducts and alveoli )
causes
• Mucous hyper secretion
• Air flow limitation
• Gas exchange abnormalities
• hyperinflation

8. CLINICAL FINDINGS
• SYMPTOMS
• Chronic and progressive dyspnea
• Cough-may be intermittent and may be non productive
• Chronic sputum production
• Wheezing and chest tightness
• Others. Fatigue, anorexia, weight loss or weight gain
• MMRC dyspnea scale

9. CLINICAL FINDINGS
• PHYSICAL FINDINGS
• INSPPECTION
• Barrel shaped chest
• Accessory respiratory muscle usage
• Prolonged expiration
• Expiration through pursed lips
• Paradoxical retraction of the lower intercostal spaces during inspiration(hoovers
sign)
• Tripod position to relieve dyspnea at end stage copd

10. CLINICAL FINDINGS
• PALPATION
• Decrease vocal fremitus
• PERCUSSION
• Hyper resonant chest
• Depressed diaphragm
• Diminished area of absolute cardiac dullness
• AUSCULTATION
• Prolonged expiration
• Reduced breath sounds

11. CLINICAL FINDINGS
• Wheezes or rhonchi
• Crackles if infection exists
• NOTE. Persistently localize wheeze and digital clubbing raise the possibility of
lung cancer

12. Pink Puffer v/s Blue Bloater

13. DIAGNOSIS
• INITIAL ASSESSMENT:

14. DIAGNOSIS
• LABARATORY FINDINGS:
• SPIROMETERY
• Spirometry provides objective information about pulmonary function and assess
the response to therapy. The presence of post bronchodilators FEV1/FVC <0.7
confirms the presence of persistent airflow limitation and thus of COPD.
• GOLD spirometric grading criteria of COPD severity

15. DIAGNOSIS
• ABCD ASSESSMENT TOOL consist of
• MMRC Questionnaire
• COPD assessment TEST(CAT)
• GOLD classification of severity of air flow
limitation
• Exacerbations Hx

16. DIAGNOSIS

17. DIAGNOSIS
• CBC
• Leukocytosis(suspecting infection)
• Erythrocytosis(in advance disease)
• ABGs
• No abnormality early in COPD
• Measurement is necessary when
1. Hypoxemia or hypercapnia is suspected.
2. FEV1 <40%
3. Signs of right heart failure
• Shows Respiratory acidosis with renal compensation

18. DIAGNOSIS
• Pulse oxymetry
• Serum Alpha 1 anti trypsin level
• ECG shows sinus tachycardia.in advance disease changes of cor pulmonale,AF,SVT
• IMAGING
• X-RAY chest
• Of Chronic bronchitis show non specific perivascular and peribronchial marking.
• Of Emphysema shows tubular heart shaddow,flatening of diaphragm and wide
intercoastal spaces.
• Its also important to exclude other causes such as Pneumonia,Pneumothorax,P.E
and pulmonary edema

19. DIAGNOSIS
• X-RAY chest

20. DIAGNOSIS
• CT CHEST
• More sensitive for Emphysema
• In advance stages when LVR or lung transplant are considered or
• As a part of lung cancer screening for smoker
• In Pul. HTN size of central pulmonary arteries.
• ECHOCARDIOGRAPHY
• In advance stages
• Pressure in pulmonary
Arteries.
• RV enlargement

21. COMPLICATIONS
• Acute bronchitis
• Pneumonia
• Pulmonary thromboembolism
• A.F ,Atrial flutter,SVT
• PUL- HTN
• Cor- Pulmonale
• Pneumothorax
• Chronic respiratory failure

22. PREVENTION
• Smoking cessation
• Elimination of long term exposure to tobacco smoke, inhaled toxines,indoor and
outdoor pollutions.
• Vaccination against influenza A(H1N1) annually and pneumococcal vaccine 5
yearly.

23. MANAGEMENT
• SMOKING CESSATION:
• Smoking cessation is single most important intervention in smokers with COPD
• Behavioral approaches. All individuals who smoke should be strongly encouraged
and supported to quit.
• NICOTINE REPLACEMENT: Nicotine gums,Transdermal patch,inhaler,nasal spray
• BUPROPION. Initiate 1 week before quit date.150 mg daily for 3 days then 150
mg B.D continue for 7-12 weeks.or in combination with nicotine patch.
• VARENICLINE.initiate 1 week before quit smoking date.
• Days 1-3, 0.5 mg PO daily, days 4-7,0.5 mg B.D ,day 8 to end of treatment 1 mg
b.d..if treatment is successful after 12 weks continue for another 12 weeks
• E-CIGARETTE

24. MABAGEMENT
• OXYGEN THERAPY:
• Supplemental oxygen for patients with resting hypoxemia is the only therapy with
evidence of improvement in the natural history of COPD.
• Proved benefits of home oxygen therapy in hypoxemic patients include longer
survival, reduced hospitalizations, and better quality of life.
• In pts with stable COPD and resting or exercise induced moderate desaturation
should not be prescribed LTOT routinely.
• INDICATIONS of LTOT for stable COPD
1. PaO2 at or below 7.3 kPa (55 mmHg) or SaO2 at or below 88%, with or without
hypercapnia confirmed twice over a three week period; or
2. PaO2 between 7.3 kPa (55 mmHg) and 8.0 kPa (60 mmHg), or SaO2 of 88%, if
there is evidence of pulmonary hypertension, peripheral edema suggesting
congestive cardiac failure, or polycythemia (hematocrit > 55%).

25. MANAGEMENT
• INHALED BRONCHODIALATORS:
• Bronchodilators do not alter the inexorable decline in lung function that is a
hallmark of COPD, but they improve symptoms, exercise tolerance,and overall
health status.
• Aggressiveness of bronchodilator therapy should be matched to the severity of
the patient's disease. It includes:.
• SABA:.Albuterol,Metaproterenol
• SAMA:.Ipratropium bromide
• LABA:.Formeterol,Salmeterol,Indacaterol,Vilanterol
• LAMA:.Tiotropium,Aclidium,Umeclidium,Glycopyronium
• SAMA is generally preferred over SABA as 1st line agent. Because of its no
sympathomimetic effect and long duration of action.

26. MANAGEMENT
• While SABA is less expensive, rapid onset of action and overall greater pts
satisfaction.
• Combination of SABA+SAMA has greater bronchodialation effect as compared to
either agent alone.
• long acting bronchodialators has superior bronchodialation effect than short
acting bronchodialators ..but are more expensive.
• LAMA has greater effect on exacerbation reduction compared with LABA and
health status.
• Combination of LABA & LAMA increase FEV1 and reduced exacerbation
compared to monotherapy or LABA+ICS

27. MANAGEMENT
• CORTICOSTEROIDS
• ICS alone can not be considered as 1st line therapy in COPD.
• ICS in combination with LABA and LAMA improved functional status and decrease
frequency of exacerbations.
• Regular treatment with ICS increases risk of pneumonia.
• OCS are not indicated in stable COPD .
• THEOPHYLLINE:-Oral theophylline is a fourth-line agent for treating COPD
patients who do not achieve adequate symptom control with inhaled
anticholinergic, beta- 2 - agonist, and corticosteroid therapies.
• Sustained-release theophylline improves hemoglobin saturation during sleep in
COPD patients and is a first-line agent for those with sleep-related breathing
disorders.

28. MANAGEMENT
• ANTIBIOTICS :.Antibiotics are commonly prescribed to outpatients with COPD for
the following indications:
• ( 1 ) to treat an acute exacerbation, (2) to treat acute bronchitis,and (3) to
prevent acute exacerbations of chronic bronchitis (prophylactic antibiotics).
• Options are:.
• Doxycycline 100mg every 12 hours,trimethoprim-sulfamethoxazole ( 1 60/800 mg
• every 12 hours), a cephalosporin (eg, cefpodoxime 200 mg every 12 hours or
cefprozil 500 mg every 12 hours), a macrolide eg, azithromycin 500 mg followed
by 250 mg daily for 5 days), a fluoroquinolone (eg, ciprofloxacin 500 mg every 12
hours), and amoxicillin-clavulanate (875/ 125 mg every 12 hours).
• Duration of therapy is 3-7 days
• In COPD patients subject to frequent exacerbations despite optimal medical
therapy, azithromycin (daily or three times weekly) and moxifloxacin (a 5 -day
course 1 week in 8 over 48 weeks) were modestly effective in clinical trials at
reducing the frequency of exacerbations.

29. MANAGEMENT
• PULMONARY REHABILITATIONS
• Graded aerobic physical exercise programs (eg, walking 20 minutes three times
weekly or bicycling) are helpful to prevent deterioration of physical condition and
to improve patients' ability to carry out daily activities.
• Training of inspiratory muscles by inspiring against progressively larger resistive
loads
• Pursed-lip breathing to slow the rate of breathing and abdominal breathing
exercises to relieve fatigue of accessory muscles of respiration.
• In a number of studies, pulmonary rehabilitation has been shown to improve
exercise capacity, decrease hospitalizations and enhance quality of life.

30. MANAGEMENT
• OTHER MEASURES
• Human alpha - ! -antitrypsin is available for replacement therapy in emphysema
due to congenital deficiency of alpha- 1-antitrypsin.
• Patients over 18 years of age with airflow obstruction by spirometry and serum
levels less than 1 1 mcmol!L (-50 mg/dL) are potential candidates for
replacement therapy. Alpha- 1 -antitrypsin is administered intravenously in a
dose of 60 mg/kg body weight once weekly
• In chronic bronchitis mobilization of secretion by systemic hydration and effective
cough training method.

31. MANAGEMENT

32. MANAGEMENT
• SURGERY FOR COPD:.
1. LUNG TRANSPLANTATION:
• Requirements for lung transplantation are severe lung disease, limited activities
of daily living, exhaustion of medical therapy,potential for pulmonary
rehabilitation, limited life expectancy without transplantation, adequate function
of other organ systems,
• The 2 –year survival rate after lung transplantation for COPD is 75%.
2. LVR SURGERY:. a surgical approach to relieve dyspnea and improve exercise
tolerance in patients with advanced diffuse emphysema and lung hyperinflation.
3. BULLECTOMY:. an older surgical procedure for palliation of dyspnea in patients
with severe bullous emphysema. Bullectomy is most commonly pursued when a
single bulla occupies at least 30-50% of the hemithorax.
4.LVR COILS/VALVES.

33. ACUTE EXACERBATION OF COPD
• Acute worsening of respiratory symptoms that results in additional therapy.
• CAUSES.
• Primary:.1) Tracheobronchial infections 2)Air pollution
• Secondary:.1)Pneumonia 2)P.E
3)Right heart failure 4)Pneumothorax
5)Pulmonary edema 6)Cardiac arrythmias

34. AECOPD

35. AECOPD

36. AECOPD
• TREATMENT:.
1. SUPPLEMENTAL O2.titrated to maintain Sao2 90-94% and Pao2 between 60 and
70 mmhg
2. SHORT ACTING BRONCHODIALATORS:. SABA with or without SAMA are
recommended the initial bronchodialators In AECOPD.
• inhaled ipratropium bromide ( 500 mcg by nebulizer, or 36 mcg by MDI with
spacer, every 4 hours as needed) plus beta-2-agonists ( eg, albuterol 2.5 mg
diluted with saline to a total of 3 mL by nebulizer, or MDI, 90 mcg per puff, four to
eight puffs via spacer, every 1 -4 hours as needed) .
• Long acting bronchodialators should be initiated as soon as possibble before
discharge from hospital.

37. AECOPD
3. SYSTEMIC CORTICOSTEROIDS:.oral prednisone 30-40 mg /day for 5-7 days
improve lung function(FEV1),oxygenation,shorten recovery time and
hospitalization duration.
4.ANTIBIOTICS.can shorten recovery time,reduced the risk of early
relapse,treatment failure and hospitalization duration.duration of therapy should
be 5-7 days.
• No risk of pseudomonas .then levofloxacin 750/day,or Moxifloxacin 400mg/day
or ceftriaxone 1gm/day
• Risk of Pseudomonas then tanzo 4.5gm QID,or ceftazidime 1gm TDS or cefepim
1gm BD or Ciprofloxacin.

38. AECOPD

39. PROGNOSIS
• BODE INDEX

40. COPD
• References
1. Harrisons principals of internal medicine
2. CMDT 2017
3. www.goldcopd.com
4. Medscape