Synopsis on chronic obstructive pulmonary disease (COPD)

1. Chronic Obstructive
Pulmonary Disease
(COPD)
______________________________
Aminu Arzet
Department of Internal Medicine
Nelson Mandela School of Medicine
University of K-Natal
Durban
27th March,2015

2. ICU 2B/Respiratory unit presentation
Inkosi Albert Luthuli Central Hospital
(IALCH)
DURBAN

3. Introduction
COPD Is a lung disease characterized
by persistent, progressive airway
obstruction, that leads to poor airflow
in and out of lungs, with resultant
reduction in FEV1and FEV1/FVC ratio.
The lung function impairment is fixed,
but some reversibility can be achieved
by using bronchodilator/other therapies

4. Introduction Continuation
Its associated with shortness of
breath, cough, and sputum production,
which is due to chronic inflammatory
response in the airways and lungs to
noxious substances.
It commonly involve narrowing of
small airways(small airway disease) and
breakdown of lung tissue,with resultant
entrapment of air (emphysema).

5. Epidemiology
COPD is a leading course of morbidity
and mortality world over
It affects about 5% of world
population (330 million people)
In 2012, it ranked as the 3rd leading
cause of death, killing over 3 million
people globally.

6. Epidemiology Continuation
The number of deaths is projected to
increase due to higher smoking rates
and an aging population globally.
It resulted in an estimated economic
lost of about $2.1 trillion across the
globe in 2010 .

7. Risk Factors
Cigarette smoking is the major risk
factor for COPD
Occupational exposure to dust and
chemicals
Environmental pollution from Car
exhaust, tobacco smoke, wild fire/bush
burning, poorly ventilated indoor
cooking fires using biomass fuel(BMF).

8. Risk factor continuation
Genetic makeup of individual- Alpha1
antitrypsin deficiency
Recurrent bronchopulmonary
infections
Socioeconomic status-commoner
among less privileged.

9. Pathophysiology
Air ways obstruction occur as a result
of chronic inflammatory response to
inhaled noxious substances and
recurrent infection.
There is excessive release of
inflammatory mediators like
Nuetrophils, Macrophages,
Lymphocytes, Histamines, Leukotrienes,
Cytokines,Chemokines, free radicals,etc

10. Pathophysiology Cont.
The irritation causes mucus gland to
become thickened, blocking the air way,
at same time producing excessive
mucus secretion, which clog the airways
the more
Inflammation/fibrosis of small airways
due to recurrent infection/Irritation is
termed as small airway disease, and this

12. Pathophysiology Cont.
Alveolar wall destruction due to
breakage of alveolar attachment, and
lost of elasticity with resultant decrease
in elastic recoil, are another cause of air
entrapment, and emphysema ensued.
In addition to aforementioned,
Pulmonary capillary bed damage and
attendant pulmonary edema, amplify
the airflow limitation.

14. Pathophysiology Cont.
Lung damage also occur due to break
down of lung tissue by inflammatory
cells and released proteases, which are
insufficiently inhibited, due to lack of
Alpha1antitrypsin(anti protease).
Alpha1antrypsin deficiency is
genetically mediated, but cigarette
smoking is believed to potentiate that,
by stimulating release of free radicals
and inflammatory cells.

15. Clinical features
 Symptoms: Include shortness of
breath, cough, sputum production,
dyspnoea, and wheeze.
 Signs:
 Pink puffers-Thin body build, with
expiratory pursed -lip breathing
 Blue bloaters–cyanosis with mild
activity

16. Clinical features Patients
 Patient who have chronic cough and
sputum production with a history of
exposure to risk factors, should be
tested for airflow limitation, even if they
do not have dyspnea .

17. Physical examination
 Pt has large, barrel shaped chest,
Prominent accessory respiratory
muscles in the neck.
 Low, flat diaphragm, causing costal
margin retractions on inspiration.
 Hyperimplated lungs with diminished
breath sounds, distant HS, prolonged
expiration with generalized wheezes
predominantly on expiration.

18. Physical examinations cont
 Depressed liver, which is not
enlarged.
 In ‘blue bloater’ type of COPD, patient
may also have:
Cyanosis at rest or mild exertion.
Pedal oedema
Crackles at lung bases.
Loud second heart sound in pulmonary area
(difficult to hear in COPD).

19. Physical examinations cont
 In ‘pink puffer’ type of COPD patient
may also have:
expiratory pursed-lip breathing, thin
body build and tendency to lean
forward over a support to assist
breathing

20. Investigations
 Plain chest X-ray shows
1. Low flattened diaphragms.
2. An obtuse costophrenic angle.
4. A reduction in size and numbers
of pulmonary vessels, particularly
in the periphery of the lung.
5. Vessel distortion producing
increased branching, angles or
bowing of vessels

21. CT CHEST
 It shows areas of low attenuation
without obvious margins or walls.
 Abnormal vascular configuration.
 CT Scan is the most sensitive and
specific imaging technique for
assessing Emphysema

22. Diagnosis
 Clinically based on dyspnoea,
Chronic cough and exposure to risk
factors.
 Spirometry is the gold standard.
 Post bronchodilator FEV1/FVC < 70%
or FEV1 < 80% of predicted value,
confirms the presence of airflow
limitation that is not fully reversible.

25. Spirometry:
Decreased FEV1, FEV1/FVC,
Lung volumes:
Increased Total Lung Capacity
Increased Residual Volume
Increased RV/TLC

26. Additional investigations
1.Bronchodilator reversibility testing
2. Glucocorticosteroid reversibility
testing
3. Arterial blood gas measurement
4. Alpha1 antitrypsin deficiency
screening

27. Additional investigations cont.
Alpha 1 antitrypsin screening is done
in the fallowing settings:
- COPD develops under 45
- COPD develops in non-smoker
- Strong family history of COPD
Normal: >150 mg/dL , In disease: <45
mg/dL

28. Differential diagnosis
 Asthma-due to bronchoconstriction
 Congestive Heart Failure
 Bronchiectasis
 Tuberculosis
 Obliterative Bronchiolitis

29. Management
First is to determine the severity of the
disease, and total health condition of the
patient.
Consider the following aspects of the
disease separately:
 current level of patient’s symptoms
 severity of the spirometric abnormality
 frequency of exacerbations
 presence of comorbidities.

30. Symptoms assessment
COPD symptoms are chronic and
progressive dyspnea, cough, and sputum
production that can vary from day to day.
In symptoms assessment these
features are objectively graded using
the fallowing scoring systems:

31. Stmptoms assesement cont.
1. COPD Assessment Test (CAT): An
8 items measure of health status
impairment in COPD
2. Clinical COPD Questionnaire (CCQ):
This is self administered questionnaire,
developed to measure clinical control in
patients with COPD.

32. Symptoms assesement cont
3. Modified British Medical Research
Council(mMRC) Questionnaire: It also
assesses health status and predicts
future mortality risk. It has a score of
0-4

34. Two or more exacerbations within the
last year
One or more Hospitalization for a
COPD exacerbation
FEV1 < 50 % of predicted value
are indicators of high risk patient.

38. Stage Characteristics Recommended Treatment
All * Avoidance of risk factor (s)
* Influenza vaccination
0: At risk * Chronic Symptoms
(cough, Sputum)
* Exposure to risk factors
* Normal spirometry
Mild COPD * FEV1/FVC < 70% *Short acting B/dilator
* FEV1  80% predicted when needed or SAMA
* With or without symptoms

39. Therapy at Each Stage of COPD
Stage Characteristics Recommended Treatment
Moderate FEV1 50 -79% *Regular treatment * Inhaled Gluccocorti
COPDD with one or more costeorodis +
bronchodilators LABA or LAMA
* Rehabilitation Symptoms and lung
function response

40. Therapy at Each Stage of COPD
Stage Characteristics Recommended Treatment
Severe COPD FEV1 30-49% * Regular treatment with LABA+
and or LAMA
Very Severe FEV1<30% * Inhaled glucorticosteroids if
COPD significant symptoms or repeated
exacerbations.
* Treatment of complications.
* Consider surgical treatments -
lung volume reduction /transplant
* Long-term oxygen therapy if
in respiratory failure
* Rehabilitation- exercise,
*Health Education-cessation of smoking

44. COPD Comorbidities
COPD patients are at increased risk for:
CVS disease like Corpulmonale
Osteoporosis
Respiratory infections
Anxiety and Depression
Diabetes
Lung cancer
Bronchiectasis

45. Prognosis
Prognosis is generally poor, unless if
detected early and management start
in early stage.

46. THANK YOU

47. Reference
•GOLD 2014/2006 document
•Kumar and ckerk
•Harrison
•Davidsons
•British medical journal
•Wikipedia