Transcript Inner-City Asthma Intervention

CHRONIC OBSTRUCTIVE
PULMONARY DISEASE
Chronic Obstructive Pulmonary
Disease (COPD)

Chronic Obstructive Airway disease (COAD)
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

Pulmonary function tests show :
1-Increased pulmonary resistance
2- Limitation of maximal expiratory
flow rates (reduced FEV1).
1.
EMPHYSEMA
2.
CHRONIC BRONCHITIS
3.
ASTHMA
4.
BRONCHIECTASIS

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

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
produces almost pure emphysema
deficiency

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--
Pathogenesis

2- Oxidant-antioxidant imbalance:
Smoking--Free O2 radicals--Deplete
Antioxidant in lung (superoxide dismutase,
glutathione)—Damage of lung tissue
Types of Emphysema
1-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
.
 Causes:
-Smoking
-Coal dust
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.
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.
4-Bullous Emphysema

--
Any form of emphysema which produces
large subpleural blebs or bullae (> 1cm).
- Localized accentuation of any one of the
type.
5-Interstitial Emphysema

Air penetration into the connective tissue
stroma of the :
- lung
- mediastinum or
- subcutaneous tissue.
6-Compensatory “Emphysema”

- Dilatation of alveoli in response to loss of
lung substance elsewhere.
-
Actually
hyperinflation
destruction of septal walls.
since
no
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.
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.
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.
Bronchiectasis
-
Permanent abnormal dilation of bronchi and
bronchioles,
- Usually associated with chronic necrotizing
inflammation
- Patients have fever, cough, foul–smelling
sputum.
- More common in left lung, lower lobes.
Causes:

Obstruction (tumor, mucus)

Congenital

Intralobar sequestration

Cystic fibrosis

Immotile cilia syndrome
 Necrotizing pneumonia

Kartaganer’s Syndrome
Asthma

-
Increased
responsiveness
of
tracheobronchial tree to various stimuli,
leading to paroxysmal airway constriction
- Unremitting attacks (status asthmaticus)
can be fatal.

Etiology :
1- Extrinsic
Factors (atopic, allergic); most
common
2-
Intrinsic
Factors
recognize mixed.
(idiosyncratic);
now

Basic Mechanism
- Bronchial plugging by thick mucous plugs
containing eosinophils, whorls of shed epithelium
(Curschmann’s spirals), and Charcot – Leyden
crystals (Eosinophil membrane protein);
- Distal air- spaces become over distended.

Histology:
-Thick basement membrane
-Edema and infiltration of the bronchial walls by
inflammatory
cells
with
prominence
eosinophils,
- Hypertrophy of bronchial wall muscle.
of

Therapeutic agents are aimed at increasing
cAMP levels either by :
-
increasing
epinephrine)
production
(ß-agonists,
e.g
or
- decreasing degradation (Methyl xanthines, e.g
theophylline).
-
Cromolyn
degranulation.
sodium
prevents
mast
cell
Allergic Bronchopulmonary
Aspergillosis

Occur in chronic asthmatics; hypersensitivity to
non – invasive Aspergillus.
Bronchocentric
mucus
granulomatous
impaction
of
bronchi,
inflammation,
eosinophilic
pneumonia.
Distinctive
(?Pathgnomonic)
promixal
bronchiectasis
Burden of Asthma

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Prevalence increasing in developed countries more than
developing or underdeveloped countries affecting 10 15% of population.
The number of children with asthma has increased sixfold 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%
Burden of Asthma

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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 US$6
billion.
At present Britain spends about US$1.8 billion
on health care for asthma and because of days
lost through illness
Burden of Asthma
Age-adjusted death rate per million
25
Under 5 years
20
15
10
5-14 years
5
0
1980
15-34 years
1985
1990
1995
19992000
2011
2010
Target
35-64 years
65 years and over
0
80
20
40
60
Deaths per Million
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)

Etiology and Pathogenesis

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Allergy
Airway hyperresponsiveness
Genetic factors
Asthma triggers
The Underlying Mechanism
Risk Factors (for development of asthma)
INFLAMMATION
Airway
Hyperresponsiveness
Airflow
Limitation
SymptomsRisk Factors (shortness of breath,
(for exacerbations) cough, wheeze)
Pathological changes
Genetic Factors
Candidate genes on chromosome 5q31-33
(IL4 GENE CLUSTER)
Responsible for production of cytokines ,IL3,IL4
,IL9 ,IL13, GM-CSF
Gene A
Gene D
Atopy
susceptible
Gene B
Gene C
Asthma
susceptible
Gene E
Asthma triggers
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Indoor allergens
Outdoor allergens
Occupational
sensitizers
Tobacco smoke
Air Pollution
Respiratory
Infections
Parasitic infections
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Socioeconomic factors
Family size
Diet and drugs
Obesity
Exercise
Acid reflux
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
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
Risk Factors for COPD
Host Factors

Genes (e.g. alpha1-antitrypsin deficiency)

Hyperresponsiveness
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Lung growth
Exposure

Tobacco smoke

Occupational dusts and chemicals
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Infections

Socioeconomic status
Pathogenesis of COPD
NOXIOUS AGENT
(tobacco smoke, pollutants, occupational
agent)
Genetic factors
Respiratory infection
Other
COPD
Noxious particles
and gases
Host factors
Lung inflammation
Anti-oxidants
Oxidative stress
Anti-proteinases
Proteinases
Repair mechanisms
COPD pathology
ASTHMA
COPD
Sensitizing agent
Noxious agent
Asthmatic airway inflammation
CD4+ T-lymphocytes
Eosinophils
Completely
reversible
COPD airway inflammation
CD8+ T-lymphocytes
Macrophages
Neutrophils
Airflow limitation
Completely
irreversible
Symptoms and Signs
Acute attack of asthma
Intermittent dyspnoea
Cough, sputum ,wheeze
Tachypnoea
Hyperinflated chest
Hyperresonant percussion
note
Diminished air entry
Widespread polyphonic
wheeze

Acute exacerbation of
COPD
Dyspnoea , cough ,sputum,
wheeze
Tachyponea
Use of accessory muscles
reduced cricosternal distance
<3cm
Reduced expansion
Hyperinflation
Hyperresonant percussion note
Quiet breath sounds
Wheeze , cyanosis
Cor pulmonale

Signs of severe attack of asthma
Inability to complete sentence
 Pulse>110
 Respiratory rate >25
 PEFR
<50%of predicted
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Signs of Life threatening attack
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Silent chest
Cyanosis
Bradycardia
Exhaustion
Confusion
Feeble respiratory effort
PEFR <33% of predicted
Low pH <7.35, PaO2< 8KPa , PaCO2>5KPa
Investigations for acute attack of
asthma
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Full Blood Count
Urine Complete and Electrolytes
PEFR (pt may be too ill to perform it well)
Arterial Blood Gases
Pulse oximetry
ECG
CXR
Investigations for Acute
Exacerbation of COPD
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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
Differential Diagnosis
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Asthma
COPD
Pneumothorax
Pulmonary edema
Upper respiratory tract obstruction
Pulmonary embolus
Anaphylaxis
Management Plan
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Immediate management to stabilize the patient
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Long term management of disease

Prevention of further attacks
Immediate management of acute
asthmatic attack
B2 Agonists
Salbutamol 5mg or Terbutaline 10mg nebulized
with O2
(se;tacchycardia,tremor,hypokalemia,arrythmia)
 Corticosteroids
Hydrocortisone 200 mg iv or Prednisolone 30 mg
oral (both if very ill)

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
Effects of Corticosteroids in Acute
Asthma
Systemic Corticosteroids
 Anti-inflammatory
 Late improvement in
outcomes (> 6 hrs)

Corticosteroids induce
transcriptional effects
synthesis of new proteins
Inhaled Corticosteroids
 Topical
 Early improvement in
outcomes (< 3 h)

Corticosteroids upregulating postsynaptic
adrenergic receptors
airway mucosa,
vasoconstriction decrease
airway mucosal blood
flow, mucosal
decongestion
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

Complications
Respiratory failure
 Treatment options;

Noninvasive Positive Pressure Ventilation
Intubation
Sedatives and Neuromuscular Blockers
PREVENTION
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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