The document provides a comprehensive overview of chronic obstructive pulmonary disease (COPD), detailing its definition, epidemiology, pathophysiology, symptoms, diagnosis, and management strategies. It emphasizes the importance of smoking cessation, pulmonary rehabilitation, and the management of exacerbations, while also highlighting the economic burden and public health challenge posed by COPD. Additionally, the document discusses the association of comorbidities and conditions such as asthma-COPD overlap syndrome (ACOS) in the clinical context of COPD.

1. Chronic Obstructive Pulmonary
Disease (COPD)
By: Dr Ibrahim Ahmed Nur
Senior house officer (SHO)
KIU
Date: 09-09-2022

2. Outline
• Introduction
• Epidemiology
• Pathphysiology
• Clinical features
• Diagnosis
• Management
• Complication
• COPD exacerbation
• ACOS (Asthma-COPD Overlap Syndromes)

3. #Question 1
• A patient with a post-bronchodilator FEV1/FEVC of 65% and FEV1 of 70%
presents with a COPD Assessment test (CAT) score today of 11 and has never had
a COPD exacerbation. Which of the following best stages and assigns a risk
category for this patient’s COPD?
GOLD grade Risk category
A. 2 B
B 1 A
C. 2 D
D. 1 B

4. Introduction
• COPD is the 3rd leading cause of death in the world (GOLD Guidelines 2021).
• More than 3 million people died of COPD in 2012 accounting for 6% globally
(WHO)
• Prevalence of COPD in Uganda was 16% this was highest in people aged 30-39
years (Fresh air Uganda survey, Lancet Global Health 2015)

6. Burden of COPD
• COPD represents an important public health challenge that is both preventable
and treatable.
• The burden of COPD is projected to increase in coming decades due to
continued exposure to COPD risk factors and the aging of the world’s
population.
• COPD is associated with significant economic burden.

7. Definition of COPD
A common, preventable and treatable disease, characterized by persistent respiratory
symptoms and airflow limitation that are usually progressive and associated with an
enhanced chronic inflammatory response in the airways and/or alveoli due to
significant exposure to noxious particles or gases. (Vogelmeier et al., 2017).

8. COPD includes
1. Chronic Bronchitis
2. Emphysema
Chronic Bronchitis
Emphysema

9. Chronic bronchitis
Defined as a chronic productive cough for three months in each of the two
successive years in a patient in whom other causes of chronic cough have been
excluded.

10. Emphysema
Abnormal and permanent enlargement of the airspaces distal to the terminal
bronchioles that is accompanied by destruction of the airspaces walls , without
obvious fibrosis.
Emphysema has 4 morphologic patterns:
1. Centriacinar.
2. Distal acinar, or paraseptal
3. Panacinar.
4. irregular

14. Pathophysiology
• COPD is an inflammatory condition involving the airways, lung parenchyma, and
pulmonary vasculature
Emphysema: one of the structural changes seen in COPD where there is
destruction of the alveolar air sacs (gas-exchanging surfaces of the lungs) leading
to obstructive physiology.
• An irritant (e.g., smoking) causes an inflammatory response, Neutrophils and
macrophages are recruited and release multiple inflammatory mediators, Oxidants
and excess proteases leading to the destruction of the air sacs, The protease-
mediated destruction of elastin leads to a loss of elastic recoil and results in airway
collapse during exhalation Air trapping

15. Loss of elasticity Air trapping Increase in end expiratory volume Barrel chest

16. Genetics and COPD
Alpha 1-antitrypsin deficiency is a genetic condition (caused by misfolding of the
mutated protein which can accumulate in the liver) that is responsible for about 2%
of cases of COPD.
In this condition, the body does not make enough of a protein alpha 1-antitrypsin.
Alpha 1-antitrypsin protects the lungs from damage caused by protease enzymes,
such as elastase and trypsin, that can be released as a result of an inflammatory
response to tobacco smoke.

17. Chronic bronchitis
• Mucous gland hyperplasia is the histologic hallmark of chronic bronchitis.
• Airway structural changes include atrophy, focal squamous metaplasia, ciliary
abnormalities, variable amounts of airway smooth muscle hyperplasia, inflammation,
and bronchial wall thickening

18. • Damage to the endothelium impairs the mucociliary response that clears bacteria
and mucus.
• Inflammation and secretions provide the obstructive component of chronic
bronchitis.
• Neutrophilia develops in the airway lumen, and neutrophilic infiltrates accumulate
in the submucosa.
• The respiratory bronchioles display a mononuclear inflammatory process, lumen
occlusion by mucus plugging, goblet cell metaplasia, smooth muscle hyperplasia,
and distortion due to fibrosis.
• These changes, combined with loss of supporting alveolar attachments, cause
airflow limitation by allowing airway walls to deform and narrow the airway
lumen.

19. • 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.
• Eventually, hypercapnia and respiratory acidosis develop, leading to pulmonary
artery vasoconstriction and cor pulmonale.
Alveolar hypoxia pulmonary vasoconstriction Pulmonary HTN
Reduced blood to LV Reduce LV out put reduce in circulatory
volume Activation RAAS Fluid retention
• With the ensuing hypoxemia, polycythemia, and increased CO2 retention, these
patients have signs of right heart failure and are known as "blue bloaters."

21. Clinical features
Symptoms
The characteristic symptoms of COPD are chronic and progressive dyspnea, cough
and sputum production that can be variable from day to day.
Dyspnea: progressive persistent and worse with exercise.
Chronic cough: May be intermittent and may be unproductive.
Chronic sputum production: COPD patients commonly coughs up sputum.

22. Other symptoms
• Wheezing
• Chest tightness
• Wt. loss
• Respiratory infection

23. Examination
Bossily benign exam
• Barrel chest
• Prolonged expiratory phase
• Pursed lip breathing, accessory muscle use.
• Tachypnea.
• clubbing

24. • Hyper resonant
• Decreased breath sounds
• Wheezing

25. • Paradoxical retraction of the lower interspaces during inspiration (ie, hoover’sign)
• Tripod position- pt with end stage COPD adopt positions that relieve dyspnea,
such as leaning forward with arms outstretched and weight supported on the palms
or elbows.

26. Extreimities:
Clubbing
Lower extremity edema in RHF
Skin: central cyanosis

27. Diagnosis
• Full history
• Full examination
• CXR
• CBC
• ABGs
• PFT
• Alpha 1 AT level
• ECG and ECHO

28. CXR :-
 Hyperinflation, bullae, flat hemidiaphragm
 Also its important to exclude lung cancer
 interstitial markings & bullae

31. • Decreased FEV 1
• Decreased FEV1/FVC <0.7
• Minimal or no response to SABD (less than 12%)

34. Assessment of symptoms

36. Combined tool (ABCD assessment tool)

38. Example
Consider two patients:
 Both patients with FEV1 < 30% of predicted
 Both with CAT scores of 18 and mMRC dyspnoea scale of 2
 But, one with 0 exacerbations in the past year and the other with 3
exacerbations in the past year.

39. PATIENT 1:
 FEV1 < 30% of predicted: GOLD GRADE 4
 0 exacerbations in the past year: GOLD GROUP A or B
 CAT scores of 18 and mMRC dyspnoea scale of 2: GOLD GROUP B
PATIENT 1: GOLD GRADE 4 GROUP B
PATIENT2:
 FEV1 < 30% of predicted: GOLD GRADE 4
 3 exacerbations in the past year: GOLD GROUP C or D
 CAT scores of 18 and mMRC dyspnoea scale of 2: GOLD GROUP D
PATIENT 2: GOLD GARDE 4 GROUP D

40. BODe index
• BODe index is a simple grading system for COPD
• Using body mass index (BMI), airflow Obstruction, Dyspnoea, and Exercise
capacity as its scoring variables.
• It has been shown to be better than FeV1 at predicting risk of hospitalization and
death in patients with COPD, as it is multidimensional.
• Patients are scored as having a BODe index of 0–10
• Higher scores indicating a higher risk of death.
• It is being increasingly used, with recommendations to calculate it in the clinical
setting to give prognostic information (Celli Br et al. New Engl J Med 2004; 350:
1005–1012).

42. Differential diagnosis

43. •Management

44. Principles
• To relieve symptoms.
• To decrease the frequency and severity of acute attacks.
• To slow progression of disease
• Improve quality of life
• To prolong survival

45. management

46. General management
• Smoking cessation (critical in slowing lung function decline)
• Vaccinations for:
• Pneumococcal pneumonia
• Influenza
• Pulmonary rehabilitation:
• Improve symptoms and quality of life
• Reduces frequency of exacerbations
• Components: exercise training, nutritional counselling and psychosocial support
• O2 therapy:
• If O2 saturation is < 88% in a stable patient (PO₂ < 55 mm Hg)
• If concurrent pulmonary hypertension, right-sided heart failure, or polycythemia

51. Why low concentration O2 given in COPD? Or what happens
when high flow O2 given?
o In COPD, the patient is dependent on hypoxic drive for respiration.
o High flow oxygen blunts the chemo responsiveness of the respiratory center in the
medulla (part of the brainstem) and thus aggravates respiratory failure (Type 2
respiratory failure). To avoid this, low flow oxygen is given

55. Surgical intervention
• Surgery is reserved for severe cases not controlled with medical therapy to
improve quality of life.
• Bullectomy: removal of giant bullae to relieve local compression
• Lung volume reduction: resection of the most diseased parts of the lung to
decrease hyperinflation
• Lung transplant: indicated in end-stage lung disease

56. Oxford Handbook of
Respiratory Medicine
Page: 197

57. Exacerbation of COPD
• Canadian Thoracic Society defined: “a sustained worsening of dyspnea, cough
or sputum production leading to an increase in the use of maintenance medications
and/or supplementation with additional medications
• It is an acute event characterized by a worsening of the patient’s respiratory
symptoms that is beyond the normal day to day variations and leads to change of
medication.

58. Causes of exacerbation
• Infective
1. Viral e.g. RSV, Rhinoviruses, influenza, parainfluenza
2. Bacterial(50%) H.influenza, S.pneumoniae, moraxela cataharis,mycoplasma
pneumonia
• Non-infective –air pollution, pulmonary embolism, pneumothorax, sedatives, heart failure or
arrhythmia.

60. Assessment of severity of exacerbation
• Classified as:
• Mild: Treated with short acting bronchodilators(SABDs) only
• Moderate: Treated with SABDs plus antibiotics and/or oral corticosteroids)
• Severe: Patients require hospitalization or visit the emergency room, may be also
be associated with acute respiratory failure.
• Blood eosinophil count may also predict exacerbation rates (in patients treated
with LABA without ICS).

64. Oxford Handbook of
Respiratory Medicine
Page: 203

67. COPD AND COMMORBIDITIES
• The presence of comorbidities should not alter COPD treatment
• Comorbidities should be treated per usual standards regardless of the presence of
COPD
• Cardiovascular diseases are common and important comorbidities in COPD
• Lung cancer is frequently seen in patients with COPD and is a major cause of
death

68. Covid 19 and COPD

69. •Asthma-COPD Overlap Syndrome (ACOS)

70. ACOS
 characterized by persistent air flow limitation with:
 several features usually associated with asthma
 several features usually associated with COPD
 ACOS is therefore identified in clinical practice by the features that it shares with
both asthma and COPD.

72. #Question 1
• A patient with a post-bronchodilator FEV1/FVC of 65% and FEV1 of 70%
presents with a COPD Assessment test (CAT) score today of 11 and has never had
a COPD exacerbation. Which of the following best stages and assigns a risk
category for this patient’s COPD?
GOLD grade Risk category
A. 2 B
B 1 A
C. 2 D
D 1 B

73. REFERENCES
• GOLD Guidelines 2021
• Oxford Handbook of Respiratory Medicine (4th edition)
• Up-to-date 2021

74. • THANKS FOR LISTENING