ASTHMA

What is Asthma?
• It is an inflammatory condition characterized by having narrowing of
respiratory passage ways, which can cause difficulty in breathing and
sometimes can become fatal.
• Underlying causes are not completely known, probable causes are
• Atopic triad: Certain individuals who have genetic predisposition where
they have more of allergic or hyper responsiveness to specific types of
allergens
a) Asthma
b) Atopic dermatitis
c) Allergic rhinitis
• Extrinsic and intrinsic asthma based on presence or absence of IgE
antibodies
• Extrinsic (eosinophilic, IgE mediated) asthma
• Common in children
• Associated with genetic predisposition
• Precipitated by known allergens
• Intrinsic (non-IgE mediated) asthma
• Develops in adulthood
• Triggered by non-allergenic factors like viral infections, mucosal irritants,
emotional upsets and exercise
Common trigger factors
• Allergens: Pollens, molds, house dust mites, pets.
• Industrial chemicals: Isocyanate containing paints, aluminum hair
spray.
• Drugs: Aspirin, Ibuprofen and other prostaglandin inhibitors, β-
blockers.
• Other triggers: Wood or grain dust, cotton dust, cigarette smoke.
• Miscellaneous: Cold air, exercise, hyperventilation, viral respiratory
tract infection, stress.
Pathophysiology
• Refer diagram from notebook
Pathophysiology
• Allergens comes in contact with antigen presenting cells (dendritic
cells, macrophages)
• Dendritic cells phagocytosis these allergens, also activate particular
gene (MHC2 molecule) chromosome 6.
• Dendritic cell then takes MHC2 complex with the particular allergen
and bring it to the T-helper 2 cell (TH2)
• T-helper 2 cell will react to the dendritic cell and foreign antigen will
bind to T cell receptor on TH2 cell.
• Also CD4 molecule on TH2 cell with interact with MHC2 molecule.
Pathophysiology
• TH2 cell will undergo inappropriate type of reaction due to underlying
genetic or environmental condition and produces two important
chemicals interleukin-4 and interleukin-5.
• Interleukin-4 activates plasma cells to produce specific type of
antibodies i.e. it increases IgE antibodies.
• IgE antibody bind to mast cells with Fc epsilon R1 receptor. Once they
bind it triggers mast cell to undergo degranulation.
• When it degranulates it starts producing inflammatory mediators
histamines and leukotrienes.
Pathophysiology
• Interleukin-5 activates eosinophils which will release leukotrienes and also
going to release cytokines which are going to attract more white blood cells.
• It also produces proteases which over time start to cause tissue damage to
respiratory tract (so proteases is important in chronic cases)
• All of this takes place in mucosa and sub mucosa of the bronchioles.
Histamines and leukotrienes from mast cells and eosinophils starts affecting the
bronchioles and causes
Bronchoconstriction
Mucous buildup
Inflamed mucosa
Increase vascular permeability
Clinical presentation
• Generally present with cough.
• Chest tightness
• Dyspnoea
• Sometimes have difficulty in speaking
• Hyperinflation of lungs
• Wheezing
Diagnosis
• Pulmonary function test (PFT) is considered as gold standard for diagnosis of
asthma.
• If patients have symptoms of asthma then PFT is done.
• Here, in patients with Asthma FVC (forced vital capacity) is lower but FEV1
(forced expiratory volume at 1 second) is even lower.
• If FEV1/FVC<75% then some obstructive pattern is interpreted.
• In symptomatic patients after this test bronchodilator(SABA) will be
administered.
• FEV1 ≥12% after SABA administration → Asthma
• FEV1 <12% after SABA administration → COPD
Diagnosis
• In asymptomatic patients after this test bronchoconstrictor
(Methacholine) will be administered this is known as Methacholine
challenge.
• FEV1 drops 20% or more after Methacholine administration from the
original → Asthma
• Asthma patients will have increased eosinophil count.
• Asthma patients will have increased IgE antibodies.
• Chest x-ray has no importance in asthma diagnosis it is done just to
rule out pneumonia. In asthmatic patients hyperinflation will be seen
in chest x-ray.
Treatment
• Treatment should be directed towards reducing inflammation and
increasing bronchodilation.
• Treatment aims should include a lack of day and nighttime symptoms,
no asthma exacerbations, no need for rescue medication, normal PEFs
and no unwanted side effects from medication.
Treatment
• Relievers
• Preventers
What are releivers?
• Bronchodilators
• Rescue medications
• Quick relief of symptoms
• Used during acute attacks
• Action lasts 4-6 hrs

Not for regular use

Releivers
• Short acting 2 agonists
Salbutamol100 mcg:
1 or 2 puffs as necessary

Levosalbutamol 50 mcg :
1 or 2 puffs as necessary

• Anti-cholinergics
Ipratropium bromide

• Xanthines
Theophylline
• Adrenaline injections
Preventers
• Anti-inflammatory
• Takes time to act (1-3 hours)
• Long-term effect (12-24 hours)
• For regular use ( whether symptoms present or not)
• Prevent airway remodeling
Preventers
• Leukotriene inhibitors
• Corticosteroids
• Monteleukast
• Prednisolone
• zafirleukast
• Budesonide
• Beclomethasone • Mast cell stabilizers
• Fluticasone • Sodium cromoglycate
• Long acting beta 2 agonists • Combinations
(LABA) Salmeterol/Fluticasone
• Salmeterol Formoterol/Budesonide/
• formoterol Salbutamol/Beclomethasone
Aerosol delivery systems

• Metered dose inhalers

• Dry powder inhalers (Rotahaler)

• Spacers / Holding chambers

Classification of Asthma severity
 Part 4: Long-term Asthma Management
Stepwise Approach to Asthma Therapy -
Adults RULE OF THUMB

Outcome: Asthma Control Outcome: Best

Possible Results

Controller:
 Daily inhaled
corticosteroid
Controller:  Daily long –acting  When asthma is
inhaled β2-agonist controlled,
Controller:  Daily inhaled reduce therapy
Controller: corticosteroid  plus(if needed)
Daily inhaled
None corticosteroid
 Daily long-acting
inhaled β2-agonist -Theophylline-SR
 Monitor
-Leukotriene
-Long-acting inhaled
β2- agonist
-Oral corticosteroid

Reliever: Rapid-acting inhaled β2-agonist prn

STEP 1: STEP 2: STEP 3: STEP 4: STEP Down
Intermittent Mild Persistent Moderate Persistent Severe Persistent

Alternative controller and reliever medications may be considered (see text).

Bronchodilators
• Mainstay of management of athma
• Stimulate beta receptors and cause bronchodilation
• May also stimulate receptors present in the heart resulting in
tachycardia and palpitations
• Used for symptomatic relief from wheezing and breathlessness
• Salbutamol and levosalbutamol commonly used
Other bronchodilators
• Terbutaline- both inhaled and oral
• Theophylline – available only orally
Inhaled corticosteroids
• Mainstay for prevention of asthma
• Started at low dose and increased if symptoms persisti
• Dose should be reduced once symptoms are improved
• Oropharyngeal side effects like candidiasis are common at higher
doses of steroids
Inhaled anticholinerics
• Block muscarinic receptors in the bronchial smooth muscle
• Decrease secretions
• Used as add-on therapy with bronchodilators
• Slower onset of action than beta agonists but last longer
• Tiotropium – longer acting
• Anticholinergic side effects
Effects of corticosteroids
Oral corticosteroids
• Used only if symptoms not controlled with highest dose of inhaled
steroids
• Given as a single morning dose to minimise adrenal suppression
• Attempt to withdraw once stabilised
• Short courses of high-dose oral steroids during exacerbations
LABA
• Used in conjunction with SABA and not as substitute
• Combine with low-dose steroids instead of increasing steroid dose
• Can control nocturnal and early morning symptoms
• Tremors are the major side effect
Leukotriene antagonists
• Leukotriene receptor antagonists – monteleukast andzafirleukast
• Leukotriene synthesis inhibitor – zileuton
• Improve PFT’s, decrease nocturnal awakenings, decrease
bronchodilator use
• Hepatitis major side effect
Patient Care
• Understanding of action of each of the medications
• Education in the use of inhalational device
• Individual self-management plan for each patient
Monitoring disease
• Spirometry
• Physical examination
• Symptoms monitoring
• Use of inhalational device
Monitoring therapy
• Watch for tachycardia and tremors
• Change of voice, candidiasis
• Adrenal suppression
• Electrolytes, bloodglucose
• Theophylline toxicity
• Liver functions
• Thank you