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ASTHMA
BY: Dr. Akhilesh Sah
INTRODUCTION
 Bronchial asthma is a chronic respiratory Inflammatory disease
characterized by airway inflammation and bronchial
hyperresponsiveness, resulting in recurrent episodes of wheezing,
chest tightness, coughing, and dyspnea.
 Particularly at night and in the early morning
 It affects approximately 334 million people worldwide and is one of
the most common chronic diseases in both children and adults
 There are several types of asthma, including allergic asthma, non-
allergic asthma, exercise-induced asthma, occupational asthma,
and nocturnal asthma.
 Mainly due to atopy
 Atopy refers to the genetic tendency to develop allergic
diseases such as allergic rhinitis, asthma and atopic
dermatitis (eczema). Atopy is typically associated with
heightened immune responses to common allergens,
especially inhaled allergens and food allergens
Etiology
Host factors:
Atopy
Genetic: genes predisposing to airway hyperresponsiveness
Sex: more in males 2:1
Environment factor
Allergens: mites, fur, animals, fungi, mold
Infection
Seasonal
Diet : peanuts, eggs wheat
Pollution and smoke
Cont.
Others
- Psychosocial factors
- Drugs: aspirin, beta blockers
- Pollutants: smoke, mosquito coil, sprays, perfume etc
- Other allergens
Pathology
Cont
 In asthma, the airways become inflamed and
hyperreactive, leading to narrowing of the air passages
and difficulty breathing.
 The inflammation is characterized by increased numbers
of immune cells (e.g. eosinophils, T cells) and release of
inflammatory mediators (e.g. histamine, leukotrienes,
prostaglandins) that cause swelling, mucus production,
and smooth muscle contraction in the airways.
 The remodeling of the airways over time due to chronic
inflammation can lead to irreversible damage and
decreased lung function.
Clinical feature
 Wheezing
 Chest tightness
 Breathlessness
 Cough: productive cough
 Use of accessory muscles
 Symptoms may be worse at night and patients typically awake in the early
morning hours
 Hyperinflatted chest
Intrinsic asthma : non allergic, non atopic, due to infection, aspirin,
A minority of asthmatic patients (~10%) have negative skin tests to common
inhalant allergens and normal serum concentrations of IgE.
Extrinsic asthma : Allergic asthma, atopic, high serum IgE
Investigation / Diagnosis
 Lung function test / spirometry :
reduced FEV1 , FEV1 /FVC ratio , PEF(peak expiratory flow)
Reversibility is demonstrated by a >12% and 200-mL increase in FEV1 15 min after
an inhaled short-acting β2 –agonist(SABA)
 Hematologic Tests Blood tests are not usually helpful. Total serum IgE and
specific IgE to inhaled allergens (radioallergosorbent test [RAST]) may be
measured in some patients. Blood test usually done to determine infection
 Imaging : Chest Xray and ct chest
 Skin tests
 Exhaled NO :Fractional exhaled nitric oxide (FENO) : to detect
eosinophilic
Complication
 AE asthma
 Pneumonia
 Pneumothorax
 Respiratory failure
 Decreased lung function
TREATMENT
Goals
 • Minimal (ideally no) chronic symptoms, including nocturnal
 • Minimal (infrequent) exacerbations
 • No emergency visits
 • Minimal (ideally no) use of a required β2-agonist
 • No limitations on activities, including exercise
 • Peak expiratory flow circadian variation
CONT
The stepwise approach to the management of asthma
Step 1: Occasional use of inhaled short-acting β2-
adrenoreceptor agonist bronchodilators(SABA)
-For patients with mild intermittent asthma (symptoms less than once a
week for 3 months and fewer than two nocturnal episodes per month)
- Salbutamol, terbutaline
- Used as required
Step 2: Introduction of regular preventer therapy
Regular anti-inflammatory therapy: inhaled ICS such as beclometasone,
budesonide, fluticasone, mometasone, should be started in addition to
SABA on as required basis
- Has experienced exacerbation asthma for 2 years
- Used SABA three times a week or more
- Reports symptoms three times a week or more
- Is awakened by asthma 1 night/week
Step 3: Add-on therapy
ADDING lABA(long acting beta 2 agonist)
Step 4: Poor control on moderate dose of inhaled glucocorticoid and
add-on therapy: addition of a fourth drug
Leukotriene receptor antagonists(montelukast, zafirlukast), long-acting
antimuscarinic agents(ipratropium bromide), theophyllines or a slow-
release β2-agonist may be considered
 Step 5: Continuous or frequent use of oral glucocorticoids
prednisolone therapy (usually administered as a single daily dose in the
morning) should be prescribed in the lowest amount necessary to control
symptoms
Step-down therapy
Once asthma control is established, the dose of inhaled (or oral)
glucocorticoid should be titrated to the lowest dose at which effective
control of asthma is maintained. Decreasing the dose of glucocorticoid by
around 25–50% every 3 months is a reasonable strategy for most patients
Exacerbations of asthma
increased symptoms, deterioration in lung function, and an
increase in airway inflammation.
Exacerbations are most commonly precipitated by viral
infections
Management of acute severe asthma
Oxygen : above 92%
High doses of inhaled bronchodilators: SABA via nebulizer, MDI,
Systemic glucocorticoids: IV Hydrocortisone/ oral Prednisolone
Asthma.pptx

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Asthma.pptx

  • 2. INTRODUCTION  Bronchial asthma is a chronic respiratory Inflammatory disease characterized by airway inflammation and bronchial hyperresponsiveness, resulting in recurrent episodes of wheezing, chest tightness, coughing, and dyspnea.  Particularly at night and in the early morning  It affects approximately 334 million people worldwide and is one of the most common chronic diseases in both children and adults  There are several types of asthma, including allergic asthma, non- allergic asthma, exercise-induced asthma, occupational asthma, and nocturnal asthma.  Mainly due to atopy
  • 3.  Atopy refers to the genetic tendency to develop allergic diseases such as allergic rhinitis, asthma and atopic dermatitis (eczema). Atopy is typically associated with heightened immune responses to common allergens, especially inhaled allergens and food allergens
  • 4.
  • 5. Etiology Host factors: Atopy Genetic: genes predisposing to airway hyperresponsiveness Sex: more in males 2:1 Environment factor Allergens: mites, fur, animals, fungi, mold Infection Seasonal Diet : peanuts, eggs wheat Pollution and smoke
  • 6. Cont. Others - Psychosocial factors - Drugs: aspirin, beta blockers - Pollutants: smoke, mosquito coil, sprays, perfume etc - Other allergens
  • 8. Cont  In asthma, the airways become inflamed and hyperreactive, leading to narrowing of the air passages and difficulty breathing.  The inflammation is characterized by increased numbers of immune cells (e.g. eosinophils, T cells) and release of inflammatory mediators (e.g. histamine, leukotrienes, prostaglandins) that cause swelling, mucus production, and smooth muscle contraction in the airways.  The remodeling of the airways over time due to chronic inflammation can lead to irreversible damage and decreased lung function.
  • 9. Clinical feature  Wheezing  Chest tightness  Breathlessness  Cough: productive cough  Use of accessory muscles  Symptoms may be worse at night and patients typically awake in the early morning hours  Hyperinflatted chest
  • 10. Intrinsic asthma : non allergic, non atopic, due to infection, aspirin, A minority of asthmatic patients (~10%) have negative skin tests to common inhalant allergens and normal serum concentrations of IgE. Extrinsic asthma : Allergic asthma, atopic, high serum IgE
  • 11. Investigation / Diagnosis  Lung function test / spirometry : reduced FEV1 , FEV1 /FVC ratio , PEF(peak expiratory flow) Reversibility is demonstrated by a >12% and 200-mL increase in FEV1 15 min after an inhaled short-acting β2 –agonist(SABA)  Hematologic Tests Blood tests are not usually helpful. Total serum IgE and specific IgE to inhaled allergens (radioallergosorbent test [RAST]) may be measured in some patients. Blood test usually done to determine infection  Imaging : Chest Xray and ct chest  Skin tests  Exhaled NO :Fractional exhaled nitric oxide (FENO) : to detect eosinophilic
  • 12.
  • 13.
  • 14. Complication  AE asthma  Pneumonia  Pneumothorax  Respiratory failure  Decreased lung function
  • 16. Goals  • Minimal (ideally no) chronic symptoms, including nocturnal  • Minimal (infrequent) exacerbations  • No emergency visits  • Minimal (ideally no) use of a required β2-agonist  • No limitations on activities, including exercise  • Peak expiratory flow circadian variation
  • 17. CONT The stepwise approach to the management of asthma Step 1: Occasional use of inhaled short-acting β2- adrenoreceptor agonist bronchodilators(SABA) -For patients with mild intermittent asthma (symptoms less than once a week for 3 months and fewer than two nocturnal episodes per month) - Salbutamol, terbutaline - Used as required
  • 18. Step 2: Introduction of regular preventer therapy Regular anti-inflammatory therapy: inhaled ICS such as beclometasone, budesonide, fluticasone, mometasone, should be started in addition to SABA on as required basis - Has experienced exacerbation asthma for 2 years - Used SABA three times a week or more - Reports symptoms three times a week or more - Is awakened by asthma 1 night/week
  • 19. Step 3: Add-on therapy ADDING lABA(long acting beta 2 agonist) Step 4: Poor control on moderate dose of inhaled glucocorticoid and add-on therapy: addition of a fourth drug Leukotriene receptor antagonists(montelukast, zafirlukast), long-acting antimuscarinic agents(ipratropium bromide), theophyllines or a slow- release β2-agonist may be considered
  • 20.  Step 5: Continuous or frequent use of oral glucocorticoids prednisolone therapy (usually administered as a single daily dose in the morning) should be prescribed in the lowest amount necessary to control symptoms Step-down therapy Once asthma control is established, the dose of inhaled (or oral) glucocorticoid should be titrated to the lowest dose at which effective control of asthma is maintained. Decreasing the dose of glucocorticoid by around 25–50% every 3 months is a reasonable strategy for most patients
  • 21.
  • 22.
  • 23.
  • 24. Exacerbations of asthma increased symptoms, deterioration in lung function, and an increase in airway inflammation. Exacerbations are most commonly precipitated by viral infections
  • 25.
  • 26. Management of acute severe asthma Oxygen : above 92% High doses of inhaled bronchodilators: SABA via nebulizer, MDI, Systemic glucocorticoids: IV Hydrocortisone/ oral Prednisolone