Airway Diseases
May 2013
Mekelle
Chronic Obstructive
Pulmonary Disease
COPD
Definition
 COPD- a disease state
characterized by airflow limitation
that is not fully reversible
 The airflow lim...
 COPD includes
 Chronic bronchitis
 Emphysema
 Small airway disease
 COPD is the fourth leading cause
of death in the...
Risk factors
 In the west
 Most important is cigarette smoking
 In developing countries
 Role of household fuels and i...
 Occupational exposure
 Air Pollution
 Genetic- α-1 Antitrypsin Deficiency
 Regarding smoking
 The degree of damage to the lung (FEV loss) is
proportional to the amount of cigarettes smoked.
 No...
 Regarding asthma and COPD
 Dutch hypothesis – asthma and COPD are two diseases
in the same spectrum
 British hypothesi...
Natural history
 Risk of mortality from COPD is closely associated with
reduced levels of FEV1
 FEV1 is a marker of obst...
 Obstruction leads to hyperinflation.
 Hyperinflation leads to impaired diaphragmatic
function.
Pathology
 Cigarette smoke exposure may
affect the large airways, small
airways ( 2 mm diameter), and
alveolar space
 La...
 Patterns
 Emphysema
 Defined in anatomic terms
 Destruction of the airways
 Pan or centri acinar pattern
 Chronic b...
Diagnosis
 Consider COPD in any patient with combination of
these symptoms
 Dyspnea
 Chronic cough
 Chronic sputum pro...
 Physical examination is rarely
diagnostic in COPD
 Wheezes here and there
 With severe airflow obstruction-
 use of accessory muscles of respiration- tripod
position
 Cyanosis
 Systemic wastin...
Laboratory findings
 CXR can be normal or some times shows some hyperinflation.
 Don’t rule out COPD b/c you have a norm...
 Hct – for erythrocytosis
 ECG and Echo – for Cor pulmounale
Stage of COPD
 We use spirometric parameters
 GOLD staging
Management plan has four components
 Assess and monitor disease
 Reduce risk factors
 Manage stable COPD
 Manage exace...
Assess and monitor
 Stage of the disease
 Use spirometry and clinical features
 Risk factor reduction
 Smoking cessation
Stable COPD
 Bronchodilators – anticholinergics, beta agonist
 Inhaled corticosteroids- for patients with frequent
exace...
Treatment of exacerbations
 Exacerbations are a prominent
feature of the natural history of
COPD
 The frequency of exace...
Treatment includes-
 Bronchodilators
 Antibiotics
 Glucocorticoids
 Oxygen therapy
 Mechanical ventilation
 Home O2 therapy for resting and nocturnal
hypoxemia
 Lung volume reduction surgery
Asthma
Asthma
 Asthma is a syndrome characterized by
airflow obstruction that varies markedly,
both spontaneously and with treat...
Prevalence
 ~10–12% of adults and 15% of children affected by the
disease
 can present at any age
 peak age is 3 years
 Children with asthma – the asthma can subside as
they grow older.
 Adults with asthma-rarely so
 The severity of asthm...
Etiology
 Asthma is a heterogeneous disease with interplay
between genetic and environmental factors
Genetic predisposition suggested by-
 familial association of asthma
 high degree of concordance for asthma in identical...
 Atopy is the major risk factor for
asthma
 Allergic rhinitis and atopic dermatitis
 Allergens
 House dust mite
 Intrinsic Asthma or nonatopic asthma-~10% have
negative skin test to common inhalant allergens and
normal serum concentr...
Pathogenesis
 Asthma is associated with a
specific chronic inflammation of
the mucosa of the lower airways
 The degree o...
Clinical features
 Wheezing,
 dyspnea, and
 Cough
These are variable, both spontaneously and with therapy
 Symptoms ma...
 Physical signs
 wheezes
Diagnosis
 Simple spirometry confirms airflow
limitation with
 a reduced FEV1,
 FEV1/FVC ratio,
 PEF
 Reversibility i...
 Aims of treatment
 For the patient to have
 No or minimal symptoms esp. nocturnal
 No emergency OPD visits
 No frequ...
Treatment
Two groups of drugs are used
 Bronchodilators
 beta 2-adrenergic agonists,
 anticholinergics, and
 theophyll...
Management of chronic asthma
 Avoid triggers
 Pharmacotherapy –stepwise
therapy
 Patient education
Goals
 Reduce impai...
Treatment of chronic
asthma
First try to determine severity.
This can be done by looking at
 Reported symptoms over the p...
 Then stratify your patient by the severity to either
 Intermittent
 Mild persistent
 Moderate persistent
 Severe per...
Adjusting therapy
 Assess the status of the patient after 2-4 weeks of
therapy.
 If improving step down the treatment
 ...
Management of acute severe asthma
 The best strategy for management of acute exacerbations of
asthma is early recognition...
 Look for simple clinical severity indicators
 Degree of dyspnea
 Can the patient finish a sentence?
 Degree of desatu...
Provide
High flow oxygen therapy to keep
oxygen saturation >90%
High dose inhaled short acting beta
agonists are the mai...
 Start systemic glucocorticoids if there is not an immediate and
marked response to the inhaled short-acting beta agonist...
 For patients with respiratory failure, it is necessary to intubate and
institute ventilation
 Consider antibiotics if s...
Refractory asthma
 A small proportion of patients (~5%
of asthmatics) are difficult to
control despite maximal inhaled
th...
Chronic obstructive pulmonary disease   copy
Chronic obstructive pulmonary disease   copy
Chronic obstructive pulmonary disease   copy
Chronic obstructive pulmonary disease   copy
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Chronic obstructive pulmonary disease copy

  1. 1. Airway Diseases May 2013 Mekelle
  2. 2. Chronic Obstructive Pulmonary Disease
  3. 3. COPD Definition  COPD- a disease state characterized by airflow limitation that is not fully reversible  The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases
  4. 4.  COPD includes  Chronic bronchitis  Emphysema  Small airway disease  COPD is the fourth leading cause of death in the USA
  5. 5. Risk factors  In the west  Most important is cigarette smoking  In developing countries  Role of household fuels and indoor pollution have important contribution.
  6. 6.  Occupational exposure  Air Pollution  Genetic- α-1 Antitrypsin Deficiency
  7. 7.  Regarding smoking  The degree of damage to the lung (FEV loss) is proportional to the amount of cigarettes smoked.  Not all smokers develop COPD ( 15%) only; outlining individual susceptibility  Second hand (passive) smokers are also at risk
  8. 8.  Regarding asthma and COPD  Dutch hypothesis – asthma and COPD are two diseases in the same spectrum  British hypothesis – different entities
  9. 9. Natural history  Risk of mortality from COPD is closely associated with reduced levels of FEV1  FEV1 is a marker of obstruction
  10. 10.  Obstruction leads to hyperinflation.  Hyperinflation leads to impaired diaphragmatic function.
  11. 11. Pathology  Cigarette smoke exposure may affect the large airways, small airways ( 2 mm diameter), and alveolar space  Large airway changes cause cough and sputum (i.e. the symptoms),  small airways and alveolar
  12. 12.  Patterns  Emphysema  Defined in anatomic terms  Destruction of the airways  Pan or centri acinar pattern  Chronic bronchitis  Defined in clinical terms  Based on symptoms
  13. 13. Diagnosis  Consider COPD in any patient with combination of these symptoms  Dyspnea  Chronic cough  Chronic sputum production  History of exposure to risk factors
  14. 14.  Physical examination is rarely diagnostic in COPD  Wheezes here and there
  15. 15.  With severe airflow obstruction-  use of accessory muscles of respiration- tripod position  Cyanosis  Systemic wasting  Later on  Signs of right sided heart failure  Sometimes  Features of systemic inflammation ( ischemic heart disease osteoporosis ….), poor sleep
  16. 16. Laboratory findings  CXR can be normal or some times shows some hyperinflation.  Don’t rule out COPD b/c you have a normal CXR  Pulm Function tests  Low FEV1/FVC  Low peak flow  Some reversibility might be there in the obstruction
  17. 17.  Hct – for erythrocytosis  ECG and Echo – for Cor pulmounale
  18. 18. Stage of COPD  We use spirometric parameters  GOLD staging
  19. 19. Management plan has four components  Assess and monitor disease  Reduce risk factors  Manage stable COPD  Manage exacerbations
  20. 20. Assess and monitor  Stage of the disease  Use spirometry and clinical features
  21. 21.  Risk factor reduction  Smoking cessation
  22. 22. Stable COPD  Bronchodilators – anticholinergics, beta agonist  Inhaled corticosteroids- for patients with frequent exacerbations  Vaccination- influenza and pnuemococcal  Non pharmacotherapies- pulmonary rehabilitation, lung volume reduction surgery, lung transplantation
  23. 23. Treatment of exacerbations  Exacerbations are a prominent feature of the natural history of COPD  The frequency of exacerbations increases as airflow obstruction increases  Exacerbations are commonly considered to be episodes of increased dyspnea and cough and change in the amount and
  24. 24. Treatment includes-  Bronchodilators  Antibiotics  Glucocorticoids  Oxygen therapy  Mechanical ventilation
  25. 25.  Home O2 therapy for resting and nocturnal hypoxemia  Lung volume reduction surgery
  26. 26. Asthma
  27. 27. Asthma  Asthma is a syndrome characterized by airflow obstruction that varies markedly, both spontaneously and with treatment  Narrowing of the airways is usually reversible, but in some patients with chronic asthma there may be an element of irreversible airflow obstruction
  28. 28. Prevalence  ~10–12% of adults and 15% of children affected by the disease  can present at any age  peak age is 3 years
  29. 29.  Children with asthma – the asthma can subside as they grow older.  Adults with asthma-rarely so  The severity of asthma does not vary significantly within a given patient
  30. 30. Etiology  Asthma is a heterogeneous disease with interplay between genetic and environmental factors
  31. 31. Genetic predisposition suggested by-  familial association of asthma  high degree of concordance for asthma in identical twins The severity of asthma is also genetically determined Environmental factors-in early life determine which atopic individuals become asthmatic
  32. 32.  Atopy is the major risk factor for asthma  Allergic rhinitis and atopic dermatitis  Allergens  House dust mite
  33. 33.  Intrinsic Asthma or nonatopic asthma-~10% have negative skin test to common inhalant allergens and normal serum concentrations of IgE  Usual adult onset
  34. 34. Pathogenesis  Asthma is associated with a specific chronic inflammation of the mucosa of the lower airways  The degree of inflammation is poorly related to disease severity and may be found in atopic patients without asthma
  35. 35. Clinical features  Wheezing,  dyspnea, and  Cough These are variable, both spontaneously and with therapy  Symptoms may be worse at night  Typical physical signs are inspiratory, and to a great extent expiratory, rhonchi throughout the chest
  36. 36.  Physical signs  wheezes
  37. 37. Diagnosis  Simple spirometry confirms airflow limitation with  a reduced FEV1,  FEV1/FVC ratio,  PEF  Reversibility is demonstrated by a >12% or 200 mL increase in FEV1 15 min after an inhaled short-acting beta 2-agonist or, in some patients, by a 2- to 4-week trial of oral
  38. 38.  Aims of treatment  For the patient to have  No or minimal symptoms esp. nocturnal  No emergency OPD visits  No frequent use of salbutamol  No limitation of activity
  39. 39. Treatment Two groups of drugs are used  Bronchodilators  beta 2-adrenergic agonists,  anticholinergics, and  theophylline  Controllers  Glucocorticoids  Antileukotriens  Cromones  antiIGE  Immunotherapy
  40. 40. Management of chronic asthma  Avoid triggers  Pharmacotherapy –stepwise therapy  Patient education Goals  Reduce impairment
  41. 41. Treatment of chronic asthma First try to determine severity. This can be done by looking at  Reported symptoms over the previous two to four weeks  Night symptoms  Current level of lung function (FEV1 and FEV1/FVC values)  Number of exacerbations requiring oral glucocorticoids per year  Emergency visits
  42. 42.  Then stratify your patient by the severity to either  Intermittent  Mild persistent  Moderate persistent  Severe persistent  Then institute therapy by the level of severity
  43. 43. Adjusting therapy  Assess the status of the patient after 2-4 weeks of therapy.  If improving step down the treatment  If not step up the ladder.
  44. 44. Management of acute severe asthma  The best strategy for management of acute exacerbations of asthma is early recognition and intervention, before attacks become severe and potentially life threatening  Treatment starts with assessment of severity of attack
  45. 45.  Look for simple clinical severity indicators  Degree of dyspnea  Can the patient finish a sentence?  Degree of desaturation?  Paradoxic breathing, accessory muscles  Mental status  Silent chest  Level of V/S derangement
  46. 46. Provide High flow oxygen therapy to keep oxygen saturation >90% High dose inhaled short acting beta agonists are the main stay of therapy (nebulized or via metered dose inhaler) Add inhaled anticholinergics if no
  47. 47.  Start systemic glucocorticoids if there is not an immediate and marked response to the inhaled short-acting beta agonists  Slow infusion of aminophylline may be effective in patients not responding to high dose bronchodilators  Make frequent (every one to two hours) objective assessments of the response to therapy until definite, sustained improvement is documented
  48. 48.  For patients with respiratory failure, it is necessary to intubate and institute ventilation  Consider antibiotics if signs of pneumonia
  49. 49. Refractory asthma  A small proportion of patients (~5% of asthmatics) are difficult to control despite maximal inhaled therapy  Some of these patients will require maintenance treatment with oral corticosteroids  The most common reason for poor control of asthma is

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