Chronic obstractive pulmunary disease (COPD)

Chronic obstractive pulmunary

1. Chronic Obstructive Pulmonary
Disease (COPD)
BY:
MUTEGEKI ADOLF

2. Outline
•INTRODUCTION
•TYPES
•PATHOLOGY
•RISK FACTORS
•CLINICAL FEATURES
•DIAGNOSIS
•MANAGEMENT
•COMPLICATION
•COPD AND ASTHMA

3. INTRODUCTION
Chronic obstructive pulmonary disease (COPD) is a lung disease
characterized
by chronic obstruction of lung airflow that interferes with normal
breathing and is not fully reversible.
•The more familiar terms ‘chronic bronchitis’ and ‘emphysema’ are
no longer used, but are now included within the COPD diagnosis.
•Such a diagnosis should be considered in any patient who has
symptoms of cough, sputum production, or dyspnea (difficult or
labored breathing), and/or a history of exposure to risk factors for
the disease.
•A COPD exacerbation is an acute worsening of the patient’s
respiratory
•symptoms needing a change in medications.

4. •It affects more than 5 percent of the population and is
associated with high morbidity and mortality
•It is the third-rankedcause of death in the United States,
killing more than 120,000 individuals each year
•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.

5. COPD includes
•1) Chronic Bronchitis
•2) Emphysema

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

7. Emphysema
Abnormal and permanent enlargement of the
airspaces distal to the terminal bronchioles that is
accompanied by destruction of the airspace walls,
without obvious fibrosis

8. Pathophysiology
•Chronic Bronchitis:Persistent inflammation of the
bronchi leads to increased mucus production,
narrowing of the airways, and airflow obstruction. The
cilia in the bronchi are damaged, reducing their ability
to clear mucus, leading to recurrent infections and
exacerbations.
•Emphysema:The destruction of the alveolar walls
leads to the loss of lung elasticity and collapse of the
small airways. This results in difficulty in exhaling air,
trapping air in the lungs, and reducing the ability to
take in fresh air.

9. PATHOLOGY
Airways
Chronic inflammation
Increased numbers of goblet cells
Mucus gland hyperplasia
Fibrosis
Narrowing and reduction in the number of small airways
Airway collapse due to the loss of tethering caused by alveolar wall
destruction in emphysema

11. Lung Parenchyma
•Emphysema affects the structures distal to
the terminal bronchiole, consisting of the
respiratory bronchiole, alveolar ducts,
alveolar sacs, and alveoli, known collectively
as the acinus.

13. Subtype of emphysema.
1. Centrilobularemphysema (Proximal
acinar)
•Abnormal dilation or destruction of the
respiratory bronchiole, the central portion
of the acinus. It is commonly associated
with cigarette smoking,

15. 2. Panacinaremphysema
•Refers to enlargement or destruction of all parts of
the acinus.
•Seen in alpha-1 antitrypsin deficiency and in
smokers

17. 3. Paraseptalemphysema
Distal acinar-the alveolar ducts are predominantly
affected.

19. Pulmonary vasculature
•Intimal hyperplasia and smooth musclehypertrophy
or hyperplasiathought to be due to chronic hypoxic
vasoconstriction of the small pulmonary arteries
•Destruction of alveoli due to emphysema can lead to
loss of the associated areas of the pulmonary capillary
bed and pruning of the distal vasculature

21. Genetics
Infections
Socio-economic status
Aging Populations
Risk Factors for COPD

22. Aetiology(Causes)
•Smoking:The most significant risk factor for COPD. Long-
term smoking leads to chronic inflammation, damage to the
airways, and destruction of lung tissue.
•Environmental and Occupational Exposures:Long-term
exposure to air pollution, chemical fumes, dust, and biomass
fuel smoke.
•Genetic Factors:Alpha-1 antitrypsin deficiency is a genetic
condition that can lead to COPD, particularly in non-
smokers.
•Infections:Recurrent respiratory infections in childhood may
contribute to the development of COPD later in life.

23. Clinical Presentations
•Chronic Cough:Often the first symptom, usually productive of
sputum.
•Dyspnea:Progressive shortness of breath, initially on exertion but
eventually even at rest.
•Wheezing:Due to narrowed airways.
•Chest Tightness:A common complaint, particularly during
exacerbations.
•Frequent Respiratory Infections:Individuals with COPD are prone to
frequent respiratory infections, which can exacerbate symptoms.
•Fatigue:Often due to the increased effort required to breathe.
•Cyanosis:Bluish discoloration of the skin and lips due to low oxygen
levels, seen in advanced stages.

24. Physical Examination
Inspection:
•Barrel-shaped chest ,
•Accessory respiratory muscle participate ,
•Prolonged expiration during quiet breathing.
•Expiration through pursed lips
•Paradoxical retraction of the lower interspaces during inspiration
(ie, hoover'ssign)
Tripod Position

26. Tripod Position
•Patients with end-stage
COPD may adopt
positions that relieve
dyspnea, such as leaning
forward with arms
outstretched and weight
supported on the palms
or elbows

27. Palpation:
•Decreased fremitus vocalis
Percussion :
•Hyperresonant
•Depressed diaphragm,
•Diminationof the area of absolute cardiac dullness.
Auscultation:
•Prolonged expiration ；
•Reduced breath sounds;
•The presence of wheezing during quiet breathing
Crackle can be heard if infection exist.

28. Differential diagnosis
•Asthma
•Congestive heart failure
•Pulmonary embolism
•Pulmonary TB

29. Diagnosis of COPD
chronic cough
shortness of breath
sputum
SYMPTOMS
tobacco
indoor/outdoor pollution
SPIROMETRY: Required to establish
diagnosis

30. The presence of a post-bronchodilator
FEV1/FVC < 0.70 confirms the presence of
persistent airflow limitation and thus of
COPD.
© 2015 Global Initiative for Chronic Obstructive Lung Disease

31. Investigation
•Spirometry: gold standard for diagnosis but if not available use all
available tools (history of exposure to risk factors + clinical symptoms +
any available investigations).
•History of exposure to risk factors
•CT Scan or Chest X-ray (Hyper-inflated lungs) -To assess the extent of lung
damage, including hyperinflation, flattened diaphragm, and areas of
emphysema
•Peak flometry(measures max. rate of air flow from the lungs)
•Echocardiography–when one suspects right-sided heart failure
secondary to COPD
•Arterial Blood Gas (ABG):To assess oxygen and carbon dioxide levels,
particularly in advanced disease
•Alpha-1 Antitrypsin Levels:In individuals with a family history of COPD or
non-smokers presenting with the disease.

32. Management
Treatment aims at:
•Removing risk factors and preventing further damage
•Relief of symptoms and prevention of the severity and frequency
of COPD exacerbations
•Improving the patients exercise tolerance and maintaining good
health
•Inhalers are the preferred formulation for the treatment of
COPD.
Explain to the patient that:
•COPD is chronic lung damage and there is no cure
•Treatment is to prevent exacerbations, further damage, and
infections

33. Non-pharmacological management
Advise the patient that:
•They must stop smoking –it is the only way to stop it from getting worse
•Reduce exposure to charcoal and wood/dung cooking smoke.
•Keep cooking areas well ventilated by opening windows and doors.
•Use alternative clean energy sources like Biogas, improved cooking stoves etc.
•Use masks for respiratory protection or stop working in areas with
occupational dust or pollution
•Physical exercise to train lung capacity (pulmonary rehabilitation) under
supervision
•Get treatment quickly in case of increased breathlessness, cough or sputum
•Physiotherapy is beneficial to improve exercise tolerance

34. Step 1: Mild
•Inhaled salbutamol 2 puffs 2-4 times a day, may be used
periodically for short periods.
•The main purpose of this treatment is to reduce or prevent
symptoms.
•If inhalers not available, consider:
•Aminophylline 200 mg twice daily.
Step 2: Moderate
•Inhaled salbutamol 2 puffs 2-4 times a day
•Plus inhaled steroid Beclomethasone100-400 micrograms 2-
4 times a day

35. Step 3: Severe
•As in step 2 plus ipratropium inhaler 2 puff 2-4
times a day
Note: If available, long acting bronchodilators
salmeteroland formeterolcan be used in moderate
and severe COPD in combination with inhaled
steroids

36. COPD exacerbations
•If more sputum, changed to more yellow/green coloured, and/or
breathlessness, temp >38°C and or rapid breathing (“bronchitis”),
then
•Treat with antibiotic e.g. amoxicillin 500 mg every 8 hours for 7-10
days or doxycycline 100 mg every 12 hours for 7-10 days
•Oral Prednisolone 40 mg once daily in the morning for 5 days. Do
NOT use oral steroids for extended periods in patients with COPD
•Refer urgently to hospital if: Rapid pulse (>100 beats per minute) or
breathing (>30 breaths per minute, Tongue or lips are “blue”
(central cyanosis), Confused, Failure to improve
•Give oxygen by nasal cannula (1-3 litres/min) if available, target
SpO2 88-92%

37. Note: Give oxygen with care (minimum flow required to
reach the target SpO2) because COPD patients are at risk
of hypercapnia(CO2 retention) which cause respiratory
depression and coma
Prevention
•Avoidance of Smoking:Key to preventing COPD.
•Avoidance of Respiratory Irritants:Such as air
pollution, chemical fumes, and dust.
•Early Detection and Management:In individuals with a
history of smoking or occupational exposures.
•Vaccinations:To prevent respiratory infections that can
exacerbate COPD.

38. Brief Strategies to Help the Patient Willing to Quit Smoking
1.ASK --Systematically identify all tobacco users at every visit
2.ADVISE -Strongly urge all tobacco users to quit
3.ASSESS -Determine willingness to make a quit attempt
4.ASSIST -Aid the patient in quitting
5.ARRANGE -Schedule follow-up contact.

39. Complications
•Pneumothorax
•Corpulmonale
•Exacerbations of copd
•Respiratory failure

40. COPD Comorbidities
•COPD patients are at increased risk for:
Cardiovascular diseases
Osteoporosis
Respiratory infections
Anxiety and Depression
Diabetes
Lung cancer
Bronchiectasis
•These comorbid conditions may influence mortality and hospitalizations and should be looked for
routinely, and treated appropriately.

41. COPD and Asthma
COPD
•Onset in mid-life
•Symptoms slowly
progressive
•Long smoking history
ASTHMA
•Onset early in life (often
childhood)
•Symptoms vary from day to day
•Symptoms worse at night/early
morning
•Allergy, rhinitis, and/or eczema
also present
•Family history of asthma

42. COPD is a leading cause of morbidity and mortality
worldwide, but with early detection, proper
management, and lifestyle changes, its progression
can be slowed, and quality of life can be significantly
improved.
END