Bronchial asthma is a chronic inflammatory disorder of the airways characterized by variable and reversible airflow obstruction. It presents with recurrent episodes of wheezing, breathlessness, chest tightness and cough, particularly at night or in the morning. The inflammation and airway hyperresponsiveness are due to environmental antigens triggering an immune response. Diagnosis is made based on clinical features and confirmed with spirometry showing reversibility with bronchodilators. Management follows a stepwise approach starting with short-acting bronchodilators and adding preventive medications such as inhaled corticosteroids as needed to control symptoms.

1. BRONCHIAL ASTHMA
ASHARA T
BOT 2018

2. LEANRING OBJECTIVES
* Defenition
•Clinical features
•Pathophysiology
•Diagnosis
•Investigation
•Management
•Pharmacotherapy
•prognosis

3. ASTHMA
Asthma is the chronic inflammatory disorder of the airway , in which cells and
cellular elements play a role.
“ Airway hyper responsivness causing variable and reversible airflow
obstruction’’

4. Age>40

5. Asthma is chronic inflamatory response
CLINICAL REPRESENTATION PHYSIOLOGICAL REPRESENTATION
- Recurrent episodes of wheezing,
breathlessness, chest tightness and
cough particularly at morning/night.
widespread, reversible narrowing of
the bronchial airways and a marked
increase in bronchial responsiveness.

6. CLASSIFICATION
1 . Atopic/ Extrinsic- ( ~70%)
IgE mediated immune response to environmental antigens
2. Non Atopic/Intrinsic ( ~30%)
Triggered by non immune stimuli- Infections( viral), exercise, aspirin,
psychological stress or inhaled irritants
The ultimate humoral and cellular mediators of airway obstructions are common to both atopic
and non atopic forms and hence they are treated in a similar way.

7. PEAK EXPIRATORY FLOW RATE (PEFR ):- maximam speed of expiration
as measured with peak flow meter.
normal PEFR should be 20%.

8. CLINICAL FEATURES
Typical symptoms include
Episodes of wheezing
chest tightness
Breathlessness
Cough
-Particularly if the symptoms are worse at night/early morning
-Occur in response to exercise/allergen exposure/cold air
- Personal or family history of asthma or atopic disorder
-Otherwise unexplained low FEV1 or PEFR
-Otherwise unexplained peripheral eosinophilia

9. Following features decrease probability of BA-
- Isolated cough with no other respiratory symptoms
- Chronic sputum production
- Cardiac symptoms
- Significant smoking history
- Voice disturbance

10. Clinical representation
.MILD ASTHMA PERSISTANT
ASTHMA
NOCTURNAL
ASTHMA
COUGH VARIANT
ASTHMA
Patient with mild
asthma are usually
asymptomatic
between
exacerbations.
Patient with persistent
asthma report ongoing
breathlessness and
wheeze but these are
variable, with the
symptoms fluctuating
over period by period.
characteristically
displays a diurnal
pattern ,with
symptoms and lung
function being worse
in the early morning.
Cough , wheeze disturb
sleep
Cough may be
dominant symptom.
The lack of wheeze or
breathlessness may led
to delay in reaching
diagnosis.

11. Signs
*Increased RR, +/- use of accessory muscles
*Hyper resonant percussion note may be elicited
*On auscultation, expiratory rhonchi ,wheeze.
*During, severe attacks, airflow may be so insufficient to produce rhonchi-
SILENT CHEST
*No findings in between attacks or when asthma is under control

13. PATHOPHYSIOLOGY
Airway hyper reactivity (AHR)- tendency for airways to narrow excessively in response to
triggers that have little or no effects in normal individuals.
Other factors likely to be important in the behavior of airway smooth muscle include the
degree of airway narrowing and neurogenic mechanism .
Common examples include
* allergens(produce igE)
* house dust
* pest such as cat,dog
* cockroaches and fungi etc………

16. ASTHMA FACTORS
Allergens
Viruses
Drugs
Exercise
Food
GERD( gastroeosophageal reflux disease)
Stress
Occupational factors( toxic substances )

18. * Some patient with asthma have similar inflammatory response in the upper airway.
* History of sinusitis, sinus head ache ,a blocked or runny nose and loss of sense of smell.
* In some circumstances the appearance of asthma is triggered by medications such as beta
blockers and other non steroidal anti inflammatory drugs (NSAIDs).
* Aspirin sensitive patient may report symptoms following alcohol and food containing
salicylates :-ASPIRIN INDUCED ASTHMA
* Other contraceptive pills,cholinergic agents and prostaglandin f2alpha .
*Betel nuts similar to methacholine can aggravate asthma .

19. INVESTIGATIONS
Usually a clinical diagnosis by spirometry ,
-estimates degress of obstruction
- ↓ FEV1, ↓ FEV1/FVC.
- > 15% increase in FEV1, 15 minutes after
bronchodilator use ( to check the reversibility).
- ↓PEFR ( diurnal variation of PEFR of more than 20% is considered diagnostic.)

20. -Chest x-ray - Hyperinflated lungs
-Hypoxia and hypercarbia ( severe asthma)
-skin prick test( allergy skin test) :- presence of atopy may be demonstrated
-Sputum and blood eosinophilia
-↑ IgE levels
-assessment of eosinophilic airway inflamation-eosinophilic count<2% or exhaled breathe
nitric oxide (FEno)
- methacholine challenge test

21. MANAGEMENT
1- SETTING GOALS
Asthma is chronic inflammatory disorder but may be controlled with appropriate treatment in
the majority of the patients .

22. THE STEP WISE APPROACH TO THE MANAGEMENT
OF ASTHMA
1-OCCASIONAL USE OF
INHALED SHORT ACTING
BETA 2 ADRENORECEPTORS
AGONIST BRONCHO
DILATORS.
2-INTRODUCTION TO
REGULAR PREVENTER
THERAPY
3-ADD ON THERAPY
4-POOR CONTROLED TO
MODERATE DOSE OF
INHALED STEROID AND
ADD ON THERAPY
ADDITION OF 4TH DRUG
5-CONTINOUS OR
FREQUENT USE OF ORAL
STEROIDS

25. EXACERBATION OF ASTHMA
* The course of asthma may be punctuated by exacerbation with increased
symptoms , deterioration in lung function , and an increase in airway
inflammation.
* It is most probably seen with viral infections , moulds (Alternaria and
Cladosporium),pollens and air pollution are also implicated.
* Most of the attacks are characterised by a gradual deterioration over several
hours to day but some appear with little or no warning :-BRITTLE ASTHMA.
*Patient appears to have a blunted perception of airway narrowing and fail to
appreciate the early signs of deterioration.

26. STATUS ASTHMATICUS
 Severe airway obstruction
 Symptoms persist despite standard acute asthma therapy
 Severe dyspnea
 Sweating, central cyanosis, tachycardia
 Upper respiratory tract infection - most common precipitant

27. MANAGEMENT
MILD(PEFR >75%) –MODERATE (PEFR 50-75%) EXACERBATIONS.
Short course of ‘rescue’ oral corticosteroids (prednisole 30-60mg daily) therefore are often
required to regain control .
Tapering of the dose to withdraw treatment is not necessary ,unless given for more than 3
weeks .

28. MANAGEMENT
ACUTE SEVERE ASTHMA ( PEFR < 50%)
* arterial blood gas analysis is essential to determine the PaCO2.
* High conc. of O2 through face mask( 60%).
* Nebulised salbutamol 5mg in O2 immediately
* Ipratropium bromide 0.5mg + salbutamol 5mg nebulised in O2, who don’t respond
within 15-30 min
* prednisolone 40mg orally (hydrocortisone 200mg Iv )
• Endo tracheal intubation & mechanical ventilation if all Respiration fails.
• Measurement of PEAK EXPIRATORY FLOW RATE (PEFR) is mandatory.

29. Potassium supplement is necessary because salbutamol can lower serum potassium.
if patient improves other options may considered:- intravenous magnesium PEF<30 %.
 correct fluid and electrolytes. ( especially k+)

30. PHARMACOTHERAPY
1. BRONCHO DILATORS.
a) short acting beta2 adrenoreceptors agonists(SABA ).
Salbutamol
b) Long acting beta2 adrenoreceptors agonists (LABA)
Salmeterol,formoterol
c) Methylxanthines
Theophyllinate (anhydrous ),aminophylline, choline theophyllinate.
d)Anticholinergic drugs
Ipratropium bromide, tiotropium bromide

31. 2) LEUKOTRIENE ANTAGONISTS :- montelukast, zafirlukast.
3) mast cell stabilizers :- sodium cromoglycate , ketotifen.
4) corticosteroids :-
a) inhalations :- beclomethasone dipropionate, fluticasone propionate.
b) systemic :- hydrocortisone ,prednisolone
5)ANTI IgE antibody :- omalizumab

33. PROGNOSIS
* The outcome from acute severe asthma is generally good
* Death is fortunately rare
* Failure to recognize the severity of an attack ,on the part contributes delay
in delivering appropriate therapy and interventions.
* Prior to discharge the patient should be stable
* PEFR<75%
* Self management
* Avoidance of trigger factors.

34. REFERENCES
1)Davidsons’s principles and practice of medicine
22nd edition
chapter 19 – respiratory disease
2) Harrison’s principles of internal medicine
19th edition
section 2- disease of respiratory system.