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CHRONIC OBSTRUCTIVE PULMONARY DISEASE

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Title: CHRONIC OBSTRUCTIVE PULMONARY DISEASE


1
CHRONIC OBSTRUCTIVE PULMONARY DISEASE
2
Chronic Obstructive Pulmonary Disease (COPD)
  • Chronic Obstructive Airway disease (COAD)

3
DEFINITION
  • COPD is a disease state characterized by
    increase in resistance to airflow due to partial
    or complete obstruction of airway at any level
    from the trachea to respiratory bronchiole.
    Changes are usually irreversible esp. in chronic
    bronchitis and emphysema.
  • - Predominant symptom Dyspnoea
  • - Predominant cause Smoking

4
  • Pulmonary function tests show
  • 1-Increased pulmonary resistance
  • 2- Limitation of maximal expiratory flow rates
    (reduced FEV1).

5
  1. EMPHYSEMA
  2. CHRONIC BRONCHITIS
  3. ASTHMA
  4. BRONCHIECTASIS

6
  • Emphysema.
  • -Abnormal permanent enlargement of the distal
    air spaces due to destruction of the alveolar
    walls and loss of respiratory tissue.
  • -Obstruction is caused by lack of elastic
    recoil.

7
  • Etiology
  • 1- Most common cause is smoking produces
    combination of emphysema and chronic inflammation
  • 2- Genetic deficiency of alpha1 antitrypsin (Pi
    locus on chromosome 14) alpha-1-antitrypsin
    deficiency produces almost pure emphysema

8
  • Pathogenesis
  • 1- Protease-antiprotease imbalance
  • . Alpha1 antitrypsin present in serum,
    tissue fluids, macrophages
  • . Inhibitor of proteases (esp. elastase
    secreted by neutrophils during inflammation)
  • .Stimulus--TNF,IL8--Increased
    neutrophils--Release of proteases(elastase,protein
    ase-3,cathepsin-G)--Elastic lung tissue
    destruction

9
Pathogenesis
  • 2- Oxidant-antioxidant imbalance
  • Smoking--Free O2 radicals--Deplete
    Antioxidant in lung (superoxide dismutase,
    glutathione)Damage of lung tissue

10
Types of Emphysema1-Centroacinar (Centrilobar)
Emphysema
  • -- Affects central (proximal) parts of the
    acini (respiratory bronchioles) but spares the
    distal alveoli.
  • - More severe in upper lobes, especially apical
    segments
  • .

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  • Causes
  • -Smoking
  • -Coal dust

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2-Panacinar (Panlobar) Emphysema
  • -- Uniform enlargement of the acini in a
    lobule.
  • - May not necessarily involve entire lung
  • - Predominantly lower lobes.
  • - Alpha -1- antitrypsin deficiency is
    prototype.

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3-Paraseptal (Distal Acinar) Emphysema
  • -- Proximal acinus normal, distal part
    involved
  • - Most prominent adjacent to pleura and along
    the lobular connective tissue septa.
  • - Probably underlies spontaneous
    pneumothorax in young adults.

18
4-Bullous Emphysema
  • -- Any form of emphysema which produces large
    subpleural blebs or bullae (gt 1cm).
  • - Localized accentuation of any one of the type.

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5-Interstitial Emphysema
  • Air penetration into the connective tissue
    stroma of the
  • - lung
  • - mediastinum or
  • - subcutaneous tissue.

21
6-Compensatory Emphysema
  • - Dilatation of alveoli in response to loss of
    lung substance elsewhere.
  • - Actually hyperinflation since no destruction
    of septal walls.

22
7-Senile Emphysema
  • - Change in geometry of lung with larger
    alveolar ducts and smaller alveoli.
  • - No loss of lung tissue hence not really an
    emphysema.

23
Chronic Bronchitis
  • - Clinical definition persistent cough with
    sputum production for at least three months in at
    least two consecutive years.
  • - Can occur with or without evidence of airway
    obstruction
  • - Smoking is the most important cause.

24
  • Basic Mechanism
  • Hypersecretion of mucus
  • Histology
  • -Increased numbers of goblet cells in small
    airways as well as large airways.
  • -Increased size of submucosal glands in large
    airways (Reid index ratio of thickness of
    mucosal glands to thickness of wall between
    epithelium and cartilage)
  • -Peribronchiolar chronic inflammation.

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Bronchiectasis
  • - Permanent abnormal dilation of bronchi
    and bronchioles,
  • - Usually associated with chronic necrotizing
    inflammation
  • - Patients have fever, cough, foulsmelling
    sputum.
  • - More common in left lung, lower lobes.

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Causes
  • Obstruction (tumor, mucus)
  • Congenital
  • Intralobar sequestration
  • Cystic fibrosis
  • Immotile cilia syndrome
  • Necrotizing pneumonia
  • Kartaganers Syndrome

34
Asthma
  • - Increased responsiveness of tracheobronchial
    tree to various stimuli, leading to paroxysmal
    airway constriction
  • - Unremitting attacks (status asthmaticus) can
    be fatal.

35
  • Etiology
  • 1- Extrinsic Factors (atopic, allergic) most
    common
  • 2- Intrinsic Factors (idiosyncratic) now
    recognize mixed.

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  • Basic Mechanism
  • - Bronchial plugging by thick mucous plugs
    containing eosinophils, whorls of shed epithelium
    (Curschmanns spirals), and Charcot Leyden
    crystals (Eosinophil membrane protein)
  • - Distal air- spaces become over distended.

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  • Histology
  • -Thick basement membrane
  • -Edema and infiltration of the bronchial
    walls by inflammatory cells with prominence of
    eosinophils,
  • - Hypertrophy of bronchial wall muscle.

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  • Therapeutic agents are aimed at increasing
    cAMP levels either by
  • - increasing production (ß-agonists, e.g
    epinephrine) or
  • - decreasing degradation (Methyl xanthines,
    e.g theophylline).
  • - Cromolyn sodium prevents mast cell
    degranulation.

46
Allergic Bronchopulmonary Aspergillosis
  • Occur in chronic asthmatics hypersensitivity
    to non invasive Aspergillus.
  • Bronchocentric granulomatous inflammation, mucus
    impaction of bronchi, eosinophilic pneumonia.
  • Distinctive promixal bronchiectasis
    (?Pathgnomonic)

47
Burden of Asthma
  • Prevalence increasing in developed countries more
    than developing or underdeveloped countries
    affecting 10 -15 of population.
  • The number of children with asthma has increased
    six-fold in the last 25 years
  • Between 100 and 150 million people around the
    globe
  • 5.1 million people in the UK have asthma
  • In South Asia (including Pakistan) rough
    estimates indicate a prevalence of between 10
    and 15

48
Burden of Asthma
  • World-wide, the economic costs associated with
    asthma are estimated to exceed those of TB and
    HIV/AIDS combined.
  • In the United States, for example, annual asthma
    care costs (direct and indirect) exceed US6
    billion.
  • At present Britain spends about US1.8 billion on
    health care for asthma and because of days lost
    through illness

49
Burden of Asthma
Age-adjusted death rate per million
Under 5 years 5-14 years 15-34 years 35-64
years 65 years and over
0 20 40
60 80
Deaths per Million
50
CLASSIFICATION OF ASTHMA
  • EXTRINSIC
  • Implying a definite external cause
  • Atopic individuals
  • Positive skin prick test
  • More common
  • Early onset in childhood
  • INTRINSIC OR CRYPTOGENIC
  • Late onset (middle age)

51
Etiology and Pathogenesis
  • Allergy
  • Airway hyperresponsiveness
  • Genetic factors
  • Asthma triggers

52
The Underlying Mechanism
Risk Factors (for development of asthma)
INFLAMMATION
AirwayHyperresponsiveness
Airflow Limitation
Symptoms- (shortness of breath, cough, wheeze)
Risk Factors(for exacerbations)
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Pathological changes
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Genetic Factors
  • Candidate genes on chromosome 5q31-33
  • (IL4 GENE CLUSTER)
  • Responsible for production of cytokines ,IL3,IL4
    ,IL9 ,IL13, GM-CSF

57
Asthma triggers
  • Indoor allergens
  • Outdoor allergens
  • Occupational sensitizers
  • Tobacco smoke
  • Air Pollution
  • Respiratory Infections
  • Parasitic infections
  • Socioeconomic factors
  • Family size
  • Diet and drugs
  • Obesity
  • Exercise
  • Acid reflux

58
Burden of COPD
  • The global burden of COPD will increase
    enormously over the foreseeable future as the
    toll from tobacco use in developing countries
    becomes apparent.
  • In UK and USA COPD occurs in
  • 18 male smokers
  • 14 female smokers
  • 6-7 those who have never smoked

59
Direct and Indirect Costs of COPD, (US
Billions)
  • Direct Medical Cost 18.0
  • Total Indirect Cost 14.1
  • Mortality related IDC 7.3
  • Morbidity related IDC 6.8
  • Total Cost 32.1

60
Risk Factors for COPD
  • Host Factors
  • Genes (e.g. alpha1-antitrypsin deficiency)
  • Hyperresponsiveness
  • Lung growth
  • Exposure
  • Tobacco smoke
  • Occupational dusts and chemicals
  • Infections
  • Socioeconomic status

61
Pathogenesis of COPD
  • NOXIOUS AGENT(tobacco smoke,
    pollutants, occupational agent)
  • Genetic
    factors

  • Respiratory infection
  • Other
  • COPD

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Symptoms and Signs
  • Acute exacerbation of COPD
  • Dyspnoea , cough ,sputum, wheeze
  • Tachyponea
  • Use of accessory muscles
  • reduced cricosternal distance lt3cm
  • Reduced expansion
  • Hyperinflation
  • Hyperresonant percussion note
  • Quiet breath sounds
  • Wheeze , cyanosis
  • Cor pulmonale
  • Acute attack of asthma
  • Intermittent dyspnoea
  • Cough, sputum ,wheeze
  • Tachypnoea
  • Hyperinflated chest
  • Hyperresonant percussion note
  • Diminished air entry
  • Widespread polyphonic wheeze

65
Signs of severe attack of asthma
  • Inability to complete sentence
  • Pulsegt110
  • Respiratory rate gt25
  • PEFR
  • lt50of predicted

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Signs of Life threatening attack
  • Silent chest
  • Cyanosis
  • Bradycardia
  • Exhaustion
  • Confusion
  • Feeble respiratory effort
  • PEFR lt33 of predicted
  • Low pH lt7.35, PaO2lt 8KPa , PaCO2gt5KPa

67
Investigations for acute attack of asthma
  • Full Blood Count
  • Urine Complete and Electrolytes
  • PEFR (pt may be too ill to perform it well)
  • Arterial Blood Gases
  • Pulse oximetry
  • ECG
  • CXR

68
Investigations for Acute Exacerbation of COPD
  • Full Blood Count
  • Urine Complete and Electrolytes
  • PEFR (pt may be too ill to perform it well)
  • Arterial Blood Gases
  • Pulse oximetry
  • ECG
  • CXR
  • Blood cultures (if Pyrexial)
  • Sputum for culture

69
Differential Diagnosis
  • Asthma
  • COPD
  • Pneumothorax
  • Pulmonary edema
  • Upper respiratory tract obstruction
  • Pulmonary embolus
  • Anaphylaxis

70
Management Plan
  • Immediate management to stabilize the patient
  • Long term management of disease
  • Prevention of further attacks

71
Immediate management of acute asthmatic attack
  • B2 Agonists
  • Salbutamol 5mg or Terbutaline 10mg nebulized with
    O2
  • (setacchycardia,tremor,hypokalemia,arrythmia)
  • Corticosteroids
  • Hydrocortisone 200 mg iv or Prednisolone 30 mg
    oral (both if very ill)

72
Immediate management of acute asthmatic attack
  • Additional management in Life threatening attack
  • Nebulize with Anti cholinergics (Ipratropium 0.5
    mg add to B2agonist)
  • Aminophylline
  • 250 mg (5mg/kg) I/V over 20 mins
  • I/V B2 agonists
  • Salbutamol or Terbutaline 0.25mg over 10 mins

73
Effects of Corticosteroids in Acute Asthma
  • Systemic Corticosteroids
  • Anti-inflammatory
  • Late improvement in outcomes (gt 6 hrs)
  • Corticosteroids induce transcriptional effects
    synthesis of new proteins
  • Inhaled Corticosteroids
  • Topical
  • Early improvement in outcomes (lt 3 h)
  • Corticosteroids up-regulating postsynaptic
    adrenergic receptors airway mucosa,
    vasoconstriction decrease airway mucosal blood
    flow, mucosal decongestion

74
Complications
  • Respiratory failure
  • Type I continuous O2
  • Type II controlled O2
  • Intubation and ventilation
  • Cor pulmonale
  • Pneumothorax (ruptured bulla bullous lung
    disease, Indication of surgery)
  • Chest infection (pneumonia)
  • Polycythemia

75
Complications
  • Respiratory failure
  • Treatment options
  • Noninvasive Positive Pressure Ventilation
  • Intubation
  • Sedatives and Neuromuscular Blockers

76
PREVENTION
  • Elimination of risk factors
  • Patient education and information
  • Advice on not missing the dose
  • Proper management plan
  • Addition of mast cell stabilizers like sodium
    cromoglycate and nedocromil and leukotriene
    antagonists e.g montelukast and zafirlukast to
    traditional therapy

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