Bronchial Asthma Undergraduate Level

2. “Chronic inflammatory disease of the airways
which develops under the allergens influence,
associates with bronchial hyper responsiveness
and reversible obstruction and manifests with
attacks of dyspnea, breathlessness, cough,
wheezing & chest tightness.”
Definition

3. • Complex etiology
• Multiple environmental and genetic factors
• Childhood infections
• Indoor pollution
• Dietary deficiency of antioxidants
• Exposure to pets in early life
• Allergen exposure
• Communal
• Industrial
• Occupational
• Natural
• pharmacological.
Etiology

4. Some allergens which may cause
asthma
House-dust mites which
live in carpets, mattresses
and upholstered furniture
Spittle, excrements,
hair and fur
of domestic
animals
Plant pollen
Pharmacological
agents (enzymes,
antibiotics,
vaccines, serums)
Food
components
(stabilizers,
genetically modified
products)
Dust of
book
depo-
sitories

5. •ATOPY
“Genetic abnormalities which lead to excessive
production of allergen-specific antibodies (IgE) is called
atopy “ -
• Trigger-factors
• Simultaneous penetration of large quantity of allergen
• viral respiratory infection
• Hyperventilation
• Physical exertion
• Emotional stress
• becoming too cold, adverse weather conditions
• Some medicines (aspirin, b-blockers).

6. Asthma pathophysiology is quite difficult and
insufficiently studied. Undoubtedly, in most cases
the disease is based on 1 type hypersensitivity
reaction. The genesis of any allergic reaction may
be divided into immune, pathochemical and
pathophysio-logic phases.
Pathophysiology

7. After involving into the airways allergens activate immunocompetent cells.
As a result B-lymphocytes produce antibodies of Ig E class. In case of asthma
T-lymphocytes are inhibited, so the activation of B-lympocytes and Ig E
production are excessive, exceeding normal needs.
Immune phase
B-cell
Allergens
T-cell
Allergen-specific
IgE

8. Further these antibodies bind to the surface of mast cells, basophils and
eosinophils of bronchial mucous.When a new portion of allergen involves the
respiratory system, it interacts with IgE-antibodies.
This is a
first,
immune
phase of
allergic
reaction.

9. As a result of antigen-antibody reaction the peculiar
“explosion” occurs.The membranes of mast cells, basophils
and eosinophils of bronchial mucous wreck with output of
biologically active substances (histamine, serotonin,
chemotaxis factors, heparin, proteases, thromboxane,
leukotrienes, prostaglandins),
Pathochemical phase
These induce
1. Inflammation
2. Mucous edema
3. Spasm of smooth myocytes,
4. Glands hypersecretion,
5. Viscous exudate formation in
bronchial lumen.

10. ATOPIC/ EXOGENOUSASTHMA---------------------------------------
The indicated mechanism is specific for atopic (exogenous)
asthma genesis.
NONATOPIC/ ENDOGENOUSASTHMA------------------------------
In addition to this, autosensitisation of damaged pulmonary
tissue, neuropsychic disturbances, corticoid insufficiency,
adrenergic imbalance, impairment of arachidonic acid
metabolism, genetic and some other factors probably play a
certain role in genesis of nonatopic (endogenous) asthma.

11. Macroscopic changes:
1. viscous mucous/ mucopurulent phlegm
2. zones of spastic contraction
3. obstruction of airway lumen
4. Emphysematous lung
5. RV and RA hypertrophy
Pathologic
anatomy

12. 1.Bronchial wall infiltration with mast cells, eosinophils,
basophils andT-lymphocytes
2.Edema of mucousa and submucousa
3.Destruction of bronchial epithelium
4.Hypertrophy of bronchial smooth muscles
5.Hyperplasia of submucous glands
6.Microvascular dilatation
Microscopic changes:

13. By etiology:
• exogenous (atopic)
• endogenous (non-atopic).
By clinical course
• intermittent (beginning, early)
• persistent (chronic, late).
Depending on frequency of exacerbations, limitations of
patient’s physical activity and lung function persistent
asthma is divided into
• Mild
• moderate
• severe.
Classification

14. Asthma severity classification
Clinical course,
severity
Daytime asthma
symptoms
Night time
awakenings
FEV1, PEF
Intermittent < 1 /week
2 and <
/month
>80% predicted.
Daily variability <
20%
Mild
persistent
 1 /week
but not daily
> 2 /month
>80% predicted.
Daily variability –
20-30%
Moderate
persistent
Daily > 1 /week
> 60 but < 80%
predicted.
Variability>30%.
Severe
persistent
Persistent,
which limit
normal activity
Daily
<60% predicted.
Variability > 30%.

15. GINA GUIDELINES:
In recommendations of Global Initiative for Asthma (GINA) asthma is
classified on the base of control assessment and is divided into
• well-controlled
• partially controlled
• uncontrolled.
Asthma control is considered as:
• daytime symptoms  2 /week;
• ability to engage in normal daily activity
• absence of night time awakenings
• need for bronchodilators administration  2 /week;
• Absence of asthma exacerbations
• normal or near normal lung function parameters.

16. Classic signs and symptoms of asthma are:
1. Attacks of expiratory dyspnea
2. Shortness of breath
3. Cough
4. Chest tightness
5. Wheezing & Rhonchi
Clinical manifestations

17. PRODROMAL
PEAK OF
EXACERBATION
REVERSAL OF
CHANGES

18. ACUTE SEVERE
ASTHMA
• PEF 33-50%
• RR> 25/min
• HR >110/min
• Inability to
complete
sentence in one
breath
LIFETHREATENING
FEATURES
• PEF 33-50%
• Normal paCO2
• Silent chest/
Cyanosis
• Feeble respiratory
effort
• Bradycardia/
arrythmia
• Hypotension
• Exhaustion,
confusion, coma
NEAR FATAL
ASTHMA
• Raised PaCO2
• Requiring
mechanical
ventilation

19. The severe and prolonged asthma exacerbation with
• intensive progressive respiratory failure
• hypoxemia, hypercapnia
• respiratory acidosis, increased blood viscosity and the
most important sign is blockade of bronchial b2-receptors.
Stages:
1st-----------refractory response to b2-agonists
2nd --------- “silent” lung because of severe bronchial
obstruction and collapse of small and intermediate bronchi;
3rd-----------The hypercapnic coma.
STATUS ASTHMATICUS

20. Persistent asthma causes:
1. fibrosing bronchitis
2. small bronchi deformation
and obliteration
3. emphysema
4. pneumosclerosis,
5. chronic respiratory failure
6. chronic cor pulmonale.
complications of asthma
exacerbations:
1. pneumothorax
2. lung atelectasis
3. pneumonia
4. acute or subacute cor
pulmonale
5. Status Asthmaticus
Asthma complications
Asthma in childhood leads to growth inhibition
and thoracic deformation.

21. 1. CBC:
• Eosinophilia & moderate leukocytosis in blood.
2. IgE levels:
• Raised
3. SPUTUM DR:
• Inflammatory cells
• Curschmann's spirals (viscous mucus which copies small bronchi)
• Charcot-Leyden crystals (crystallized enzymes of eosinophils and
mast cells)
Investigations Lab Data

22. 1. hyperlucency of lung
fields
2. low standing and limited
mobility of diaphragm
3. expanded intercostal
spaces
4. horizontal rib position.
Chest X-ray

23. especially in
case of severe,
persistent asthma,
shows hypertrophy
of right heart
chambers.
ECG
Right axis deviation,
Rs type complex in V1 lead,
low amplitude R in V5-V6 leads

24. •forced expiratory
volume in 1 second
(FEV1) peak
expiratory flow (PEF),
which are measured
spirometry at forceful
expiration.
Lung function assessment

25. FEV1 and PEF
directly depend
on bronchial
lumen size and
elastic
properties of
surrounding
lung tissue.
Expiration
Inspiration
PEF
Volume
FEF
FEF
PIF
Flow

26. Increase in FEV1 and PEF after inhalation of bronchodilators (b2-agonists) of
15% and more is specific for asthma.

27. PEF also can be measured with the help of individual
devices – peak flow meters

28. Typical clinical
manifestations
and lung
function
assessment are
sufficient for
diagnosis of
asthma.
Diagnosis

29. Asthma is to be differentiated with a number of
diseases manifesting with dyspnea –
•cardiac
•uremic
•Hysteria, anxiety
•systemic vasculitis
•broncho-carcinoma
•carcinoid
•COPD
Differential diagnosis

30. In contrast to bronchial, in case of cardiac
asthma
the signs of
severe heart
disease and
pulmonary
congestion
can be found.

31. Drug therapy
Antiinflammatory drugs
(basic)
Bronchodilators
2 drug categories are used:
Are divided into:
hormone-containing
(corticosteroids)
nonhormone-containing
(cromones, leukotriene
receptor antagonists)
3 groups:
anticholinergic drugs
b2-agonists
methylxanthines

32. STEP UP & STEP DOWN
TREATMENT ???

33. High dose inh steroids
& regular
bronchidilators
Regular oral
corticosteroids
Low to moderate dose inh
steroids & LABA or
Leukotriene rec antagonists
Occasional temporary
step ups will be needed
Low dose inhaled steroids Consider step down if symptoms
controlled for > 3 months
Occasional inhaled short acting
beta agonosts
Withdraw anti inflammatory if
paient well for 6 months

34. Bronchodilators
b2-agonists
Anticholinergic
drugs
Smooth
muscle
relaxation
Stimulates
b2-adrenergic
receptors of bronchi
reduce tonus
of vagus
Methylxanthines
inhibit phosphodiesterase

35. Inhaled b2-agonists - basic drug group among
bronchodilators.
•Short-acting (duration of action 5-6 h) b2-
agonists - salbutamol - are used for quick relief
•Long-acting (> 12 h) b2-agonists - salmeterol -
are used for prevention of asthma symptoms.

36. •Cell membrane stabilization
•Inhibition of Inflammatory mediators
•Restoring the sensivity of b2-receptors.
Corticosteroids

37. 1. Cromones (cromolyn sodium – intal, and nedocromil)
2. Leukotriene receptor antagonist (montelukast,
zafirlukast)
3. Anticholinergic drugs (ipratropium bromide, atrovent)
4. Methylxanthines (aminophylline, theophylline)

38. Combined inhaled drugs (corticosteroids with b2-
agonists) – seretide, simbicort – with use of delivery
devices (nebulisers, turbuhalers, spasers, spinhalers,
sinchroners) enhance the effectiveness of asthma
therapy.

39. 1. Oxygen
2. Systemic corticosteroids: (Hydrocortisone 200mg or
Methylprednisolone 125mg every 6h IV or Prednisolone 50
mg/day)
3. Inhalations of short-acting b2-agonists – Salbutamol 5mg or
Fenoterol 2mg through nebulaser – 3 times at 1st hour, then once
an hour till distinct improvement of patient’s condition is
achieved; then 3-4 times a day.
4. Inhaled anticholinergic drugs or Aminophylline IV.
5. If ineffective - Mechanical ventilation.
Management of
asthmatic status

40. In case of early detection and adequate
treatment the prognosis for the disease
is favourable.
It becomes serious in severe persistent
and poorly controlled (insensitive for
corticosteroids) asthma.
Prognosis