CHRONIC OBSTRUCTIVE PULMONARY DISEASE

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CHRONIC OBSTRUCTIVE PULMONARY DISEASE
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Chronic Obstructive Pulmonary Disease (COPD)

• Chronic Obstructive Airway disease (COAD)

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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

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

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

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• 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.

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• 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

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• 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

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Pathogenesis

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

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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.

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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.

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6-Compensatory Emphysema

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

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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.

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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.

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• 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

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Asthma

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

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• 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.

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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)

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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

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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

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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
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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)

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Etiology and Pathogenesis

• Allergy
• Airway hyperresponsiveness
• Genetic factors
• Asthma triggers

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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

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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

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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

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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

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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

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Pathogenesis of COPD

• NOXIOUS AGENT(tobacco smoke,
  pollutants, occupational agent)
• Genetic
  factors
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  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

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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

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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

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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

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Differential Diagnosis

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

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Management Plan

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

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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)

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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

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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

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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

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Complications

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

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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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