This document provides information about chronic obstructive pulmonary disease (COPD) including its definition, causes, diagnosis, management, and related conditions like emphysema and bronchiectasis. COPD is a progressive lung disease characterized by limited airflow in the lungs. The primary cause is cigarette smoking which leads to an abnormal inflammatory response in the lungs. Symptoms include breathlessness, chronic cough, and sputum production. Spirometry is required for diagnosis and shows airflow limitation. Management involves smoking cessation, bronchodilators, steroids, vaccines, and oxygen supplementation during exacerbations. Related conditions like emphysema and bronchiectasis are also discussed.

1. DR.Bilal Natiq Nuaman,MD
C.A.B.M.,F.I.B.M.S.,D.I.M.
2016-2017
Chronic obstructive
pulmonary disease
1

2. Definition
Chronic obstructive pulmonary disease (COPD) is
a preventable and treatable disease state
characterized by airflow limitation that is not
fully reversible.
The airflow limitation is usually progressive and
is associated with an abnormal inflammatory
response of the lungs, primarily caused by
cigarette smoking.
Although COPD affects the lungs, it also
produces significant systemic consequences.
2

3. 3

4. ➢Major cause of death and disability
➢4th leading cause of death
➢COPD is the only chronic disease that is
showing progressive upward trend in both
mortality and morbidity
➢It is expected to be the third leading cause of
death by 2020
COPD
GENERAL FACTS
4

5. % Change in Age Adjusted Death Rate
5

6. 6

7. ➢COPD should be suspected in any patient
over the age of 35 years who presents with
symptoms of persistent cough and sputum
production and/or breathlessness.
➢Depending on the presentation important
differential diagnoses include asthma,
tuberculosis, bronchiectasis and congestive
cardiac failure.
7

8. ➢ Breathlessness usually heralds the first presentation to
the health professional.
➢ In advanced disease, the presence of edema and
morning headaches indicative of hypercapnia.
➢ Crackles may accompany infection but if persistent raise
the possibility of bronchiectasis.
➢ Finger clubbing is not consistent with COPD and should
alert the physician to potentially more serious pathology.
(CA Lung)
8

9. ➢Some patients with severe COPD may
demonstrate signs consistent with corpulmonale
(raised jugular venous pressure, loud P2 due to
pulmonary hypertension, tricuspid regurgitation,
pitting peripheral edema and hepatomegaly) and
its presence usually indicates a poor prognosis.
9

10. Skeletal muscle wasting and cachexia may
occur in advanced disease, while some
patients may also be overweight.
The body mass index (BMI; weight/height²)
should be calculated during the initial
examination.
10

11. 11

12. 12

13. 13

14. COPD clinical phenotypes
Chronic Bronchitis
(Blue Bloaters)
EmPhysema
(Pink Puffers)
14

15. 15

16. Pink Puffers
➢Thin and
dyspnic , and
maintain PaCO2
until the late
stage of
disease.
➢EMPHESEMA
16

17. Pursed lip breathing occur in
emphysema not in chronic bronchitis
17

18. EMPHYSEMA
Pathological definition
permanent dilatation of air spaces
distal to terminal bronchioles,
accompanied by destruction of
their walls
18

19. 19

20.
1. CENTRIACINAR (Centrilobular):
Central part of the acinus (respiratory bronchioles)
is affected, while distal alveoli is spared. Upper
lobes, particularly apical segments are involved
Cause: Cigarette smoking
2) PANACINAR (Panlobular):
Entire acinus (from respiratory bronchiole to distal
alveoli affected) , Affects lower lobes
Cause: α-1 antitryPsin deficiency
Types of emphysema
20

21. Pathogenesis of Emphysema
21

22. Clinical Features
➢No cyanosis (pink)
➢Presents with severe dyspnea (puffer)
➢Have a barrel chest.
➢X-ray shows large volume lung, Heart is
seems buried and diaphragm pushed down.
Alveoli can rupture ! pneumothorax.
➢Don’t usually have cough or expectoration
PINK PUFFER
22

23. 23

24. 24

25. BLUE BLOATER
Develop and
tolerate
hypercapnia
earlier and may
develop edema
and 2‘
polycythemia.
CHRONIC
BRONCHITIC
25

26. CHRONIC BRONCHITIS
➢Defined clinically
Persistent cough with sputum
production for at least 3 months in
at least 2 consecutive years, with
exclusion of other causes like
Bronchiectasis .
26

27. PATHOGENESIS
SMOKING
4-10 times more common in heavy smokers
✓ a smoking history of more than 20 pack years
➢Smoke and other irritants cause
Hypertrophy of submucosal glands--- hypersecretion
of mucus
Increase in goblet cells
↑predisposition to infection
27

28. Clinical Features
➢Cyanosed (Blue)
➢Edematous (Bloater)
➢Productive Cough
➢CorPulmonale – heart failure
➢Usually dyspnea triggered by infection
➢Respiratory acidosis
Blue bloater
28

29. 29

30. Diagnosis of COPD
SYMPTOMS
cough
sputum
dyspnea
RISK
FACTORS
tobacco
SPIROMETRYEXAMINATION

31. Criteria of Dx
1-PFT : OBSTRUCTIVE LUNG PATTERN
➢FEV1 ↓ <80%
➢FVC low-normal 70-80%
➢FEV1/ FVC ↓ <70%
31

32. 2-Negative reversibility test (Post-
bronchodilator FEV1 <15% (200ML)
increase following administration of
bronchodilator or trial of
corticosteroids) .
32

33. DLCO: Transfer Factor
• Asthma high
• Chronic bronchitis normal
• Emphysema low
33

34.
Other tests
➢Hemoglobin level and packed cell volume (PCV) can
be elevated as a result of persistent hypoxemia
causing secondary polycythemia.
➢Arterial blood gases (ABGs) determine the degree of
hypoxia and hypercapnia.
➢CXR can be normal or show hyper-expanded lung
fields with low flattened diaphragms and the presence
of bullae (emphysema).
➢ECG can show advanced cor pulmonale
➢ Alpha-antitrypsin level and phenotype may be helpful
(young non smokers, lower lobe emphysema, a family
history of chest problems). 34

35. 35

36. Disease Progression of a Patients
with COPD
Symptoms
Exacerbations
Exacerbations
Exacerbations
Deterioration
End of Life
36

37. 37

38.
Management of
COPD
38

39. 39

40. 40

41. Smoking cessation
➢The only
intervention
proven to
decelerate the
decline in
FEV1. 41

42. Pharmacotherapy
BRONCHODILATORS
➢Decrease airway muscle tone
➢Three types (short & long acting):
● Anticholinergics (inhaled)
● Beta-2 agonists (inhaled)
● Methylxanthines (po)
42

43. Bronchodilators
Short Acting Beta2 Agonist (SABA)
➢e.g. Salbutamol
➢Improve pulmonary function/SOB/exercise
performance
➢Combination SABA’s and anticholinergics
produce better bronchodilation
➢For patients with MILD symptoms
● SOB on exertion
43

44. Bronchodilators
Long Acting Beta2 Agonist (LABA)
➢e.g.– Formoterol, Salmeterol
➢For patients who still have symptoms
on SABA’s (MODERATE disease)
➢More sustained effect on PFT’s, chronic
SOB
➢Early evidence these may prolong time
between exacerbations
44

45. Inhaled anticholinergics
inhaled ipratropium bromide is preferred over
beta-2 agonists by many as the bronchodilator of
choice in COPD for the following reasons:
➢Its minimal cardiac stimulatory effects compared
to those of beta agonists
➢Its greater effectiveness than either beta agonist
or methylxanthine bronchodilators in most studies
of patients with COPD
45

46. 46

47. Steroids
Inhaled steroid
➢Not recommended as first line therapy
➢No consistent effect on decreasing inflammation
➢Consider inhaled form in those with mod-severe
disease
➢Consider in those who have maximal
bronchodilator therapy
➢Inhaled corticosteroids are currently
recommended in severe disease( FEV1 <50%) who
report two or more exacerbations requiring
antibiotics or oral steroids per year . 47

48. 48

49. 49

50. Additional measures
➢Vaccines. Patients with COPD should receive a single
dose of the polyvalent pneumococcal polysaccharide
vaccine and yearly influenza vaccinations.
➢ a1-Antitrypsin replacement. Weekly or monthly
Infusions of a1-antitrypsin have been recommended for
patients with serum levels below 310mg/L and
abnormal lung function. 1
➢ Heart failure should be treated with diuretics .
➢ Secondary polycythemia requires venesection if the
PCV is >55%.
50

51. SURGERY
➢Bullectomy : young with emphysema
➢Lung Volume reduction surgery (LVRS):
emphysema
➢Lung transplant
Have been used for severe COPD
51

52. 52
Emergency treatment
Emergency treatment
Exacerbations of COPD are characterized by an acute worsening
of symptoms, with
increased breathlessness,
sputum volume and
sputum purulence.
They may occur spontaneously or as a result of infections.
Mild exacerbations can be managed at home but patients with
severe exacerbations require admission to hospital.
key adverse features that indicate a severe exacerbation :
(confusion, cyanosis, severe respiratory distress).

53. 53
Patients admitted to hospital should have
• Chest X-ray,
• Arterial blood gas measurement,
• ECG (to exclude comorbidities),
• Full blood count and
• Urea and electrolyte measurements.
• Culture of sputum
• Blood cultures should be taken if the patient is
pyrexial and
• Theophylline level should be measured in patients
on theophylline therapy.

54. 54
Bronchodilator therapy
is usually given by nebulizer, using a
combination of salbutamol 2.5 – 5.0 mg and
ipratropium 500 mcg

55. ORAL STEROIDS
ORAL STEROIDS are useful during exacerbations
(rule of 15)
PREDINSOLON 15 mg TWICE DAILY GIVEN FOR 15
DAYS MAY BENEFIT 15% OF PATIENTS WITH
COPD EXACERBATION
55

56. 56
Antibiotics
Common bacteria associated with COPD exacerbation
include
Haemophilus inluenzae,
Streptococcus pneumoniae and
Moraxella catarrhalis.
Treatment
Augmentin(amoxicillin and clavulanic acid),
or doxycycline, or ciprofloxacin or clarithromycin.

57. 57
Emergency oxygen
treatment should be commenced using controlled oxygen (e.g.
28% Venturi mask in pre-hospital care or 24% Venturi mask in
hospital settings), with an initial target saturation of 88–92%
pending urgent blood gas assessment to determine the patient’s
ventilatory status (pH and PCO2)

58. 58
Ventilatory support
if the pH is below the normal range (<7.35) then
noninvasive ventilation (NIV) should be employed

59. BRONCHIECTASIS
A destructive lung disease characterized by:
● Abnormal & permanent dilatation of medium sized
bronchi
● An associated, persistent and variable inflammatory
process producing damage to bronchial elastic and
muscular elements
59

60. PATHOLOGY
Neutrophil proteases
(acute infection in a normal or compromised host)
⇩
Epithelial injury
+
Structural protein damage
⇩
Damaged, dilated airway
⇩
Mucous retention / chronic, recurrent infection
⇩
Ongoing inflammation / tissue damage / repair
60

61. 61

62. 62

63. 63

64. Physical signs
➢ 1-normal chest exam. If bronchiectatic airways
do not contain secretions and there is no
associated lobar collapse .
➢ 2-coarse crackles if there is secretions .
➢ 3- deviated trachea toward side of lesion ,
dullness ,↓breath sound if there is collapse .
➢ 4- bronchial breathing : advanced scarring .
64

65. INVESTIGATIONS
1-Sputum culture
For pseudomonas aeruginosa , fungi , and
mycobacteria .
2- Radiology
CXR : early stage normal
Advanced thickened airway walls , cystic
spaces , pneumonic consolidation or collapse .
SPIRAL CT SCAN of chest is much more
sensitive .
3-Assessment of ciliary function
65

66. management
➢1-airway obstruction : inhaled bronchodilators and
corticosteroids .
➢2- physiotherapy
Patients should adopt a position in which the lobe to
be drained is uppermost.
Deep breathing followed by forced expiratory
maneuvers (the 'active cycle of breathing'
technique) is of help in allowing secretions in the
dilated bronchi to gravitate towards the trachea,
from which they can be cleared by vigorous
coughing.
66

67. 'Percussion' of the chest wall with cupped
hands may help to dislodge sputum, and a
number of mechanical devices are available
which cause the chest wall to oscillate, thus
achieving the same effect.
The optimum duration and frequency of
physiotherapy depends on the amount of
sputum but 5-10 minutes once or twice daily
is a minimum for most patients.
67

68. 68

69. 3- antibiotics
Oral ciprofloxacin 500-750 mg bid
Or ceftazidime by IV inj. Or infusion 1-2 gm 8-
hourly.
4- surgery
Only in unilateral , single lobe in young patient
69

70. THANK YOU
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