10 Asthma

Dr.
AKASH MISHRA
• 4 main points
– Chronic inflammatory disease
– Increased AHR to variety of stimuli
– Physiologically- reversible airway narrowing
– Clinically- wheeze, chest tightness, dyspnoea,
cough
Definition
• Asthma is a chronic inflammatory disease

characterized by increased airway hyper
responsiveness to a variety of stimuli
leading to narrowing of airways which is
reversible spontaneously or with therapy
• Currently 300 million people worldwide

suffer from asthma
Types
• Atopic asthma
– Positive family history
– Personal h/o atopy- rhinitis, urtiaria,eczema,
allegic conjunctivitis
– Increased IgE level in blood
• Non atopic asthma
– Lack family and personal h/o
– Normal IgE level
Etiology
• Stimuli that can trigger asthma are

– Allergens
• Pollen grains, house dust, mites dust
• Interact with mast cells
– Drugs
• Aspirin- shift in metabolism of arachnoid acid from
COX pathway to LOX pathway generating LTs
• B blockers
– Environment and air polllution
• Ozone, NO2, SO2
Etiology
• Stimuli that can trigger asthma contd..

– Occupational factors
• Industrial dust, metal salts
– Infections
• Mainly viral
Etiology
• Stimuli that can trigger asthma contd..

– Exercise
• Follows exercise and during it
• Depends on amount of ventilation and temperature
of the inspired air
– Emotional stress
• Due to effect on vagus nerve
Hygiene hypothesis
Pathophysiology
• Asthma is type I Hypersensitivity reaction

• The immune system is sensitized in first
exposure of allergen and the clinical
features appear from the following
exposures in a sensitized person
Pathophysiology
• Sensitization
Allergen enters the body
In genetically susceptible person,

produces TH2 reaction and produce
cytokines
Activates B cell to produce IgE
IgE specific to that allergen now

circulate bound to mast cells
Pathophysiology
• On repeated exposure of same allergen to

the sensitized person two phase reaction
occurs
– Early phase (immediate) reaction
– Late phase reaction
Pathophysiology
• Early phase reaction
Allergen enters a pre sensitized host

and binds to specific IgE bound to
mast cell
Mast cell is activated to release pre

formed mediators like histamine,
serotonin etc that leads to:
- Broncho constriction via activity of

cholinergic nerves
- Increased mucus production
- Vasodilation and increased
permeability
Pathophysiology
• Late phase reaction

– Continuation of early phase
– Requires no more exposure to allergen,
maintained by inflammatory cells
– Mast cell, epithelial cell and T cell in late
phase induce more inflammation with
recruitment of leukocytes, notably eosinophils,
neutrophils, and more T cells
– More mediators are released that lead to
• Epithelial damage
• More airway constriction
Pathophysiology
• Over time, repeated bouts of allergen

exposure and immune reactions result in
structural changes in the bronchial wall,
referred to as “airway remodeling”.
• Features of such remodelling are
– Overall thickening of airway wall
– Sub-basement membrane fibrosis , thickened
BM
– Increased vascularity
– An increase in size of the submucosal
glands
Pathophysiology
 With continued airway remodeling fibrosis occurs of

the airway too and not only basement membrane
leading to permanent airway obstruction
 Thus in conclusion
 Acute airflow obstruction is primarily attributed to
muscular broncho-constriction, acute edema, and
mucus plugging, with some contribution probably from
airway remodeling
 Chronic irreversible airway obstruction that occurs in
long term is mostly due to airway remodeling, mainly
fibrosis of airways
Clinical features: Symptoms
• H/O precipitating factors

• Dyspnoea
– Increases with increasing severity of asthma
• Cough
– Initially non productive
– Later produces thick stringy mucus
– Sometimes, cough may be ineffective leading
to mucus plugging so gasping and suffocation
Clinical features: Symptoms
• Wheeze
– Intially expiratory
– Later also inspiratory and even silent chest
when asthma much severe
• Chest tightness
• Cyanosis is a very late finding
• Symptoms are more in morning

• Start from childhood/ early age
• AE during changing season
Clinical features: Signs
• Not much
• Only due to acute attack
– Respiratory distress
– Wheeze
• 1st expiratory, later inspiratory too and silent chest
if acute and more severe
– Cyanosis – late sign
Diagnosis:
• Peak flow meters-simple, inexpensive and

widely found
• Ideally pt instructed to record the peak
flow readings after rising in the morning
and before retiring in the evening
• Similarly measurement of FEV1 and VC

by spirometry allows the demonstration of
airflow obstruction and following the
administration of bronchodilator confirms
the diagnosis.
Diagnosis
• Criteria for diagnosis is demonstration of

reversibility of airflow obstruction in patient
with suggestive symptoms
Airway hypersensitivity (AHR)
• Airway hypersensitivity (AHR) is integral to

the diagnosis of asthma and appears to be
related to airway inflammation.
• This includes exercises, cold air, dusts,
smoke and chemicals such as histamin
and methacholine.
• Helpful in pt presenting with the normal
lung function
Occupational asthma
• 2 hrs recording of peak flow preferably

including a period of time away from work
may establish diag.
• Bronchial provocation tests with the
suspected agent may be reqd.
• Skin prick tests or the measurement of
specific IgE may confirm sensitivity to the
suspected agent.
Diagnosis
• Cx-R:
– Unhelpful but point alternative diagnosis
– Acute asthma-hyperinflation
• Measure of allergic status
– Increased sputum and peripheral blood
eosinophils
– Increased IgE (if atopic)
– Skin prick test
Prevention
• Avoid allergens
• Avoid drugs that ppt asthma
• Change working environment if
occupational asthma
Medical management
• Patient education
• Avoid aggravating factors
• Drugs used
– Bronchodilators
• B2 agonist: Salbutamol, terbutaline, salmeterol, formeterol
• Alpha antagonist: tiotropium, ipratopium
– Steriods
• Inhaled (ICS): beclomethasone, budesonide, fluticasone
• Oral: In severe persistent asthma and Acute severe asthma
– Others
• Theophylline
• LT receptors antagonist : Zafirlukast, Montelukast
Medical management
• Step up and step down therapy for

persistent asthma
Medical management
Uses B agonist 3 times/week or more

Stepwise approach
• 1)Occasional use of inhaled B2 short acting
bronchodilator
– Mild intermittent asthma(symptoms < once a wk
for 3 mnths and fewer than 2 noctural
episodes/month)
– Inhaled short acting B2 agonist-on and as reqd
– H/o severe exacerbation-reclassification as
persistent asthma
• 2)Introduction of regular preventer therapy
– B2 agonist and inhaled corticosteroid
– Has experienced an exacerbation of asthma in
Steroid
• Starting dose: 400 microgm

beclometasone dipropionate(BDP)
• Budesonide can be used as BDP
• Fluticasone and Mometasone as useful as
above in half dose
• 3)Add on therapy
– Add on therapy beyond an ICS dose of 800
microgram /day BDP or equivalents in adults
– LABA (Salmeterol and Formoterol) acting at least 12
hrs 1st choice
– Similarly leucotrine receptor antagonist (montelukast
10 mg daily) can be used
• 4)poor control on moderate dose of inhaled steroid and

add on therapy:addition of a 4th drug
– ICS can be increased to 2000 microgram BDP/BUD
– Used with regular bronchdilators
• 5)continuous or frequent use of oral steroid
– Prednisolone-single dose in the morning is prescribed
in the lowest amount necessary to control the
symptoms
– Pt on long term corticosteroid (> 3 mnths) or receiving
> 3 or 4 courses per year will be at risk of systemic
side effects.
– Biphosphonates to prevent osteoporosis
• 6)step down therapy

• Once controlled inhaled or oral steroid should be titrated
to the lowest dose to control symptoms.
Medical management
 Exacerbations
 Characterized by increased symptoms, deterioration in
PEF and increase in airway inflammation
 For simple exacerbations, a 3 weeks course of oral
corticosteroid is given
 But acute severe asthma (PEF<50%) is an emergency
and requires
 B agonist nebulisation
 Systemic steriod
 If required IV MgSO4, IV Aminophylline
 Ventillator if respiratory failure
• Management of
acute severe
asthma
Nursing management
 Depend on the severity of disease

 If mild OPD management
 If acute severe asthma admission with ICU
 Family usually frightened, so calm them down
 Assess respiratory status by symptoms, signs,
SPO2, vitals
 Rule out H/O allergy before giving any medication
 O2 if required
 If requires intubation, assist the procedure and
closely monitor intubated patient

10 Asthma

Uploaded by

Copyright:

Available Formats

10 Asthma

Uploaded by

Document Information

Original Description:

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

10 Asthma

Uploaded by

Copyright:

Available Formats

Dr.

• Asthma is a chronic inflammatory disease

• Currently 300 million people worldwide

• Stimuli that can trigger asthma are

• Stimuli that can trigger asthma contd..

• Stimuli that can trigger asthma contd..

• Asthma is type I Hypersensitivity reaction

Allergen enters the body

In genetically susceptible person,

Activates B cell to produce IgE

IgE specific to that allergen now

• On repeated exposure of same allergen to

• Early phase reaction

Allergen enters a pre sensitized host

Mast cell is activated to release pre

- Broncho constriction via activity of

• Late phase reaction

• Over time, repeated bouts of allergen

 With continued airway remodeling fibrosis occurs of

• H/O precipitating factors

• Symptoms are more in morning

• Peak flow meters-simple, inexpensive and

• Similarly measurement of FEV1 and VC

• Criteria for diagnosis is demonstration of

• Airway hypersensitivity (AHR) is integral to

• 2 hrs recording of peak flow preferably

• Step up and step down therapy for

Uses B agonist 3 times/week or more

• Starting dose: 400 microgm

• 4)poor control on moderate dose of inhaled steroid and

• 6)step down therapy

 Depend on the severity of disease

You might also like