Bronchial Asthma

Nathir M Obeidat

Bronchial Asthma Definition

Bronchial asthma is a clinical syndrome characterised by recurrent episodes of airway obstruction, which resolve spontaneously or as a result of treatment.

The reversibility of the airway obstruction in asthma is the feature that distinguishes it from other forms of obstructive lung diseases.

Definition of Bronchial Asthma

• A chronic inflammatory disease of the airways in which

many cells play a role, in particular, mast cells, eosinophils

and T lymphocytes.

• In susceptible individuals this inflammation causes

recurrent episodes of wheezing, breathlessness, chest

tightness and cough, particularly at night and or early

morning.

•These symptoms are associated with airflow limitation that

is at least partially reversible either spontaneously or with

treatment.

Asthma Phenotypes

Total number of persons Percent

Current Asthma Prevalence: United States, 2001-2010

One in 12 people (about 26 million, or 8% of the U.S. population) had asthma in 2010, compared with 1 in 14 (about 20 million, or 7%) in 2001.

Year

Risk Factors for Developing Asthma

Genetic characteristics

Occupational exposures

Environmental exposures

Risk Factors for Developing Asthma:

Genetic Characteristics

Atopy

The body’s predisposition to develop an antibody

called immunoglobulin E (IgE) in response to

exposure to environmental allergens

Can be measured in the blood

Includes allergic rhinitis, asthma, hay fever, and

eczema

Pathophysiology of Bronchial Asthma

• It is a Complex interaction of cells and mediators, which lead to:

1- Inflammation

2- Bronchial hyperresponsiveness

3- Airflow limitation

4- Variability.

5- Reversibility

Inflammation 1

• It is a result of interaction of Cellular changes which includes:

1- Cells such as epithelial cells, mucous glands , endothelial cells and myofibroblasts.

2- Resident cells such as bone marrow-derived mast cells and macrophages.

3- Infiltrating cells such as eosinophils, CD4 , neutrophils , basophils and platelets.

Inflammation 2

- The above cells will lead to generation of mediators that can induce bronchoconstriction.

- These mediators includes histamine ,platelet activating factor, and some derivatives of arachidonic cascade such as PGD2 ,C4 ,D4, E4 (LTC4,LTD4 ,LE4).

- Infiltration of airways by mast cells, eosinophils, activated T lymphocytes and neutrophils

Inflammation 3

- Mast cells as aresult of IgE – Mediated stimulation also release mediators

- Cytokines most of which are product of lymphocytes and macrophages

- Edema of the airway mucosa is due to inflammation and increased capillary permeability.

Inflammation 4

• Death from severe asthma usually occurs from blockage of airways by mucous plugging.

• The presence of mucous plug is associated with hyperplasia and metaplasia of goblet cells

Airway Hyper responsiveness

- It is an exaggerated bronchoconstrictive response by the airways to a variety of stimuli such as histamine , methacholine ,cold air ,and environmental irritants.

- It is not known whether bronchial hyperreacyivity ( BHR) is acquired or is present at birth.

- it is thought that inflammation is the stimulus for BHR

- The degree of BHR usually correlates with the clinical severity of asthma

AIRWAY OBSTRUCTIONCauses

- Acute bronchoconstriction

- Mucous plugging of airways

- Bronchial wall edema

- Inflammatory cell infiltration

- Airway wall remodeling

- Smooth muscle hypertrophy

Airflow limitation

• Defined as FEV1/FVC <75%.

• During remission this can be normal.

• Age Dependent.

• Needs spirometry for assement of severity of the disease.

ATOPY• Defined as genetic susceptibility for developing

immunoglobilin IgE directed to epitopes expressed on common environmental allergens such as dust mites , animal proteins, pollens, and fungi.

• Atopic asthma has seasonal variation and avoidance of the offending antigens may result in dramatic improvement.

• Atopy manifests as allergic asthma, allergic rhinitis , allergic sinusitis with eosinophilia and high serum IgE level

Variability• Defined as a diurnal variation of PEEFR of 20%.

• This is diagnostic for asthma.

• The degree of variability is proportional to the severity of asthma.

• A high degree of variability signals unstable asthma that demands increased medications

Direct Medical Care

Hospital stay

Intensive care

Emergency department

Primary care

Medications

Indirect Costs

Social security

Loss of work output

Loss of school days

Impact on individual / family / society

Cost of asthma

GINA Guidelines 2010

Diagnosis• History

• Physical Examination

• PFT

- Vitalogram

- Spirometry

- FVL

- Lung Volumes

- DLCO

- PFM

- ABG

Diagnosis

• CXR

• IgE Level and Eosinophills

FVL

• Location of the changes :

- Above the line (Expiratory Arm)

Or

- Below the line (Inspiratory arm)

• Shape of the Loop

SPIROMETRY

• Volume-time tracing.

• Flow-volume tracing.

Asthma:

Treatment options & guidelines

Goals of Treatment of Asthma

• In spite of Immunotherapy, No real hope for cure of Bronchial Asthma.

But

• Treatment can achieve Asthma control and decrease exacerbations.

• No asthma attacks

• No emergency visits

• Minimal need for quick relief (as needed) ß2-agonist

• Maintain normal physical activity including exercNo chronic

symptoms ise

• Maintain lung function as close to normal as possible

• Minimal (or no) adverse effects from medicine

GINA Guidelines 2010

Treatment objectives

Domains of Asthma Control

Impairment of Function :

1- Subjective Impairment:

- Frequency and intensity of symptoms.

- Limitations of daily activities.

2- Objective Impairment:- Variations and Severity of Impairment of lung function.

Future risk:- Likelihood of exacerbations.

- Progressive loss of lung function.

- Adverse effects from medications.

Control of airway inflammation

BMJ. 2006 Apr 1; 332(7544): 767–771

fumarate

Is the Pathophysiological impact of Asthma limited to the Large Airways?

Adapted from Haughney J, Price D, Kaplan A, et al.. Respir Med.

2008;102(12):1681-93.

Asthma Control

Assessment

Uncontrolled

Incorrect Diagnosis

Incorrect Inhaler

Technique

Inadequate Treatment

Poor Adherence

• Large vs Small Airway

• Role of Small Airway Disease

• Phenotypes

Pharmacological therapy

Controllers

Inhaled corticosteroids

Inhaled long-acting 2-agonists

Inhaled cromones

Oral anti-leukotrienes

Oral theophyllines

Oral corticosteroids

Relievers

Inhaled fast-acting 2-agonists :

• Albuterol• Fenoterol

Inhaled anticholinergics

• Ipratropium bromide

The choice of treatment should be guided by:

Level of asthma control

Current treatment

Pharmacological properties and availability of the various

forms of asthma treatment

Economic considerations

Cultural preferences and differing health care systems need to be considered

controlled

partly controlled

uncontrolled

exacerbation

LEVEL OF CONTROL

maintain and find lowest controlling step

consider stepping up to gain control

step up until controlled

treat as exacerbation

TREATMENT OF ACTION

TREATMENT STEPSREDUCE INCREASE

STEP

1STEP

2STEP

3STEP

4STEP

5

RED

UC

EIN

CR

EASE

Beta 2-Adrenoceptor agonists are the most powerful known bronchodilators and play a pivotal role in every step of this

algorithm.

Hanania N. Current Opinion in Pulmonary Medicine 2010,

Review Response and Adjusting the Dose

• 2-4 weeks after starting controller therapy.

• 1-3 months regular visit.

• 4-6 weeks regular visit in Pregnancy.

• within 1 week after exacerbation.

The frequency of visits depends on:

1. Initial levelof control

2. previous response to treatment.

3. His ability and willingness to be engaged in self – management plan.

Stepping Up Treatment

• Sustained step up every 2-3 months

If symptoms persists or exacerbation in spite of 2-3 months controller therapy.

• Before stepping up consider:

1. Incorrect Inhaler Technique

2. Adherence

3. Modified risk ( Smoking)

4. Symptoms of comorbid condition(AR,GERD)

Day to Day Adjustment

• By The Patient’s himself.

• Smart Symbicort.

Stepping Down Approach

• When Asthma is controlled Well.

• Asthma controlled achieved for 3 months.

• You aim to find the lowest dose of treatment that maintain:

1. symptoms free

2. no exacerbation

3. minimize side effects.

Step down Technique

• Appropriate Timing ( no infection ,no travell no Pregnancy).

• Document the baseline , symptoms and PFT.

• Reduce ICS dose by 20-50% EVRY 2-3 months

Treating Modifiable Risk Factoers• Decrease Exacerbation Risk by

optimizing medications.

• Self monitoring of symptoms and by using PEF.

• Avoid Tobacco smoke Exposure.

• Confirmed Food Allergy: Avoidance and availability of Epinephrine.

• For Severe Asthma : Refer to especial centre.

Asthma Exacerbation

• Exacerbations of asthma are episodes of progressive increase in shortness of breath, cough, wheezing, or chest tightness

• Exacerbations are characterized by decreases in expiratory airflow that can be quantified and monitored by measurement of lung function (FEV1 or PEF)

• Severe exacerbations are potentially life-threatening and treatment requires close supervision

Asthma Exacerbations Management

Primary therapies for exacerbations:

• Repetitive administration of rapid-acting inhaled β2-

agonist

• Early introduction of systemic glucocorticosteroids.

• Oxygen supplementation

Closely monitor response to treatment with serialmeasures of lung function

GINA Guidelines 2010

Non Pharmacological Strategies and interventions• Smoking Cessation Advice.

• Regular Physical Activities.

• Avoid NSAIDs and Aspirin.

• Occupational Asthma.

Treatment in special Population’s contexts

• Pregnancy

• Elderly

• Allergic Rhinitis and Sinusitis

• Obesity

• GERD

• Anxiety

• Aspirin induced Respiratory distress.

Identifying patients at high risk of Asthma related death

• Asthma needed Intubation and Ventilations.

• Asthma Hospitalization or ICU care for Asthma in the last 12 months.

• Currently not on ICS or poor inhaler adhirence.

• currently using or recently stopping OCS.

• Over use of SABA more than canister/month

• Lack of written Asthma action plan.

• confirmed food aleergy.