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Defination
it is an chronic inflammatory airway disease with
episodic occurence of
1. paroxysmal(sudden recurrence)dyspnoea(shortness of
breath)
2. wheezing(high pitched whilstling sound made during
breathing) and
3. cough(sudden forceful hacking sound to release air and
clear irritation in throat or airway).
4. chest tightness
leading to variable expiratory airflow limitation.
• It is disease characterized by an increased
responsiveness of airways to various stimuli.
• It results from narrowing of the airways
produced by a combination of muscle spasm,
mucosa oedema and viscid bronchial secretion.
• The airflow limitation is generally reversible
spontaneously or with treatment.
Triggers
• Inhalation – dust, pollens, pets
• Air pollutants – cigarette smoke, perfumes
• Emotional – Stress
• Genetic factors
• Exercise induced
• Food induced - GERD
• Climate – cold
• Drugs – aspirin, beta-blockers
• Viral infections
• Occupational induced – wood, chemicals
Types
• Early onset/ Extrinsic/ Atopic/ Allergic
• Late onset/ Intrinsic/ Non-atopic/ Idiosyncratic
Extrinsic Intrinsic
Early age of onset Late age of onset
External allergens have strong role No role of external allergens
Positive personal / family history Negative personal / family history
Increased serum IgE levels Normal serum IgE levels
Skin hypersensitivity reaction positive Skin hypersensitivity reaction negative
Responds well to inhaled corticosteroids Requires higher doses of to inhaled
corticosteroids
Other types
• Exercise induced
• Food induced - GERD
• Climate – cold
• Drugs induced – aspirin, beta-blockers
Pathophysiology
Summary of Pathophysiology
Bronchial
hyper-
responsive
ness
Narrowing
of airways
Symptoms
Cells &
triggers
Constriction
of smooth
muscles
Symptoms
On Examination
• Observation :
- Respiratory rate is increased
- Use of accessory muscles
- High-pitched polyphonic expiratory and
inspiratory rhonchi are audible
- Very severe attacks the airflow may be
insufficient to produce rhonchi - "silent chest“
- Hyperinflated chest – pegion chest deformity
- Cynosis
- Use of accessory muscles of breathing.
• Palpation:
- TVF – decreased
- TVR – decreased
- No tracheal shifts
- Tracheal tug
- Chest expansion reduced
- Chest deformity – pegion chest - depression
on either side of the sternum
• Auscultation:
- Wheezing on expiration but may also occur upon
inspiration.
- Prolonged expiration and high pitched wheezing
- Crackles heard if sputum is present
- Breath sounds diminished if reduced airflow
- Wheezing absent in severe asthma
• Percussion:
- Hyper – resonant ( hyper inflated chest )
- Reduced diaphragmatic excursion ( normal level
5-6 cm )
PEFR
• Peak flow meter is device which is specially
designed for asthama patients.
• It records the peak or max flow during forced
expiration.
• PEFR- it is the max speed of expiration which is
measured by the peak flow meter to record
the persons ability to forcefully breath out.
• Not used in children below 5yr.
Gardes of Asthama depending upon
PEFR levels
• Grade 1 – GREEN – 80-100% peak flow
- no coughing, chest tightness or breathing
difficulty, routine treatment can be continued.
• Grade 2 – YELLOW – 50-80% peak flow
- acute exacerbation present, night time awakening
symptoms, medication dose be increased.
• Grade 3 – RED - <50% peak flow
- bronchodilators should be taken immediately,
begin oral steroids, PEF should return to
green/yellow within 2-4 hrs.
Changes in PFT
• FVC reduced
• FEV1 reduced
• FEV1 / FVC < 70% - Obstructive condition
• If, FEV1 > 12% / 200 ml in 10 to 15 min after
administration of 200 to 400 µg salbutamol
bronchodilator – Confirmatory Asthama.
If, FEV1 < 12-15% after administration of
bronchodilator – COPD Condition.
• PFT varies with age, height, diurnally, post-
exercise, post-bronchodilator treatment
• Skin hypersensitivity tests - development of a
wheal and flare reaction to intradermal
injections of common allergens. Distinguish
atopic from non-atopic subjects.
• ABG - hypoxaemia and hypocarbia in acute
attack & hypercarbia in severe acute.
X-ray Changes
• over-distended lungs due to over-inflation.
Lungs appear hyperinflated.
• Costophrenic and cardiophrenic angle
obliterated
• Intercostal space increased
• Bronchial wall thickening
• Excessive air trapping
• Bronchial luminal narrowing
Structural Impairements
• Inflammation – mast cell hyperactivity – degranulation of mast cell
– release of histamine – bronchoconstriction
• Increased of IgE antibodies ( type 1 hypersensitivity )
• Submucosal oedema
• Increased mucous production ( mucus plugs )
• Hypertrophy of submucosal glands, bronchial smooth muscle
• Hyperplasia, hyperactivity and hypertrophy of goblet cells(mucous
producing cells)
• Complications - like pigeon chest, lobar or segmental collapse,
pneumothorax and mediastinal and subcutaneous emphysema may
be seen.
• Cynosis , PaCO2 > 50 mm Hg.
Functional Impairements
• Difficulty to talk,walk
• Coughing
• Breathlessness
• Increased breathing
• Reduced chest expansion
• Increased work of accessory muscles
Medical Management
Beta adrenergic agonist(beta2)
- SABA – salbutamol,
terbutaline,
- LABA – salmeterol,
formeterol
• Anticholinergics
-ipratropium bromide
• Methyxantine - theophylline
• Anti IgE antibody
- omalizumab
• Corticosteroids
- inhaled – beclomethasone,
budesonide
- oral – prednisolone
• Anti-histamines
- cetrizine
• Leukotrienes anatagonist
- montelukast
Inhalers
• Meter dose inhalers – children>12yr
• Meter dose inhalers with spacer – children>4yr
• Meter dose inhalers with spacer and face mask
– children<4yr
• Dry powder inhaler
• Nebulizer
Oxygen therapy
To correct hypoxaemia, rise in PaCO2 levels,
respiratory acidosis, respiratory muscle fatigue
Status Asthamaticus
• It is a condition in which severe airway obstruction and
asthmatic symptoms persist despite the initial
administration of standard acute asthma therapy.
• Severe dyspnoea and unproductive cough.
• Patient adopts an upright position fixing the shoulder
girdle to assist the accessory muscles of respiration.
• Physical signs include sweating, central cyanosis,
tachycardia and pulsus paradoxus.
• Severe & unremitting form of disease may prove to be
fatal.
Asthama

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Asthama

  • 1.
  • 2. Defination it is an chronic inflammatory airway disease with episodic occurence of 1. paroxysmal(sudden recurrence)dyspnoea(shortness of breath) 2. wheezing(high pitched whilstling sound made during breathing) and 3. cough(sudden forceful hacking sound to release air and clear irritation in throat or airway). 4. chest tightness leading to variable expiratory airflow limitation.
  • 3. • It is disease characterized by an increased responsiveness of airways to various stimuli. • It results from narrowing of the airways produced by a combination of muscle spasm, mucosa oedema and viscid bronchial secretion. • The airflow limitation is generally reversible spontaneously or with treatment.
  • 4. Triggers • Inhalation – dust, pollens, pets • Air pollutants – cigarette smoke, perfumes • Emotional – Stress • Genetic factors • Exercise induced • Food induced - GERD • Climate – cold • Drugs – aspirin, beta-blockers • Viral infections • Occupational induced – wood, chemicals
  • 5. Types • Early onset/ Extrinsic/ Atopic/ Allergic • Late onset/ Intrinsic/ Non-atopic/ Idiosyncratic Extrinsic Intrinsic Early age of onset Late age of onset External allergens have strong role No role of external allergens Positive personal / family history Negative personal / family history Increased serum IgE levels Normal serum IgE levels Skin hypersensitivity reaction positive Skin hypersensitivity reaction negative Responds well to inhaled corticosteroids Requires higher doses of to inhaled corticosteroids
  • 6. Other types • Exercise induced • Food induced - GERD • Climate – cold • Drugs induced – aspirin, beta-blockers
  • 8.
  • 9. Summary of Pathophysiology Bronchial hyper- responsive ness Narrowing of airways Symptoms Cells & triggers Constriction of smooth muscles
  • 11. On Examination • Observation : - Respiratory rate is increased - Use of accessory muscles - High-pitched polyphonic expiratory and inspiratory rhonchi are audible - Very severe attacks the airflow may be insufficient to produce rhonchi - "silent chest“ - Hyperinflated chest – pegion chest deformity - Cynosis - Use of accessory muscles of breathing.
  • 12. • Palpation: - TVF – decreased - TVR – decreased - No tracheal shifts - Tracheal tug - Chest expansion reduced - Chest deformity – pegion chest - depression on either side of the sternum
  • 13. • Auscultation: - Wheezing on expiration but may also occur upon inspiration. - Prolonged expiration and high pitched wheezing - Crackles heard if sputum is present - Breath sounds diminished if reduced airflow - Wheezing absent in severe asthma • Percussion: - Hyper – resonant ( hyper inflated chest ) - Reduced diaphragmatic excursion ( normal level 5-6 cm )
  • 14. PEFR • Peak flow meter is device which is specially designed for asthama patients. • It records the peak or max flow during forced expiration. • PEFR- it is the max speed of expiration which is measured by the peak flow meter to record the persons ability to forcefully breath out. • Not used in children below 5yr.
  • 15. Gardes of Asthama depending upon PEFR levels • Grade 1 – GREEN – 80-100% peak flow - no coughing, chest tightness or breathing difficulty, routine treatment can be continued. • Grade 2 – YELLOW – 50-80% peak flow - acute exacerbation present, night time awakening symptoms, medication dose be increased. • Grade 3 – RED - <50% peak flow - bronchodilators should be taken immediately, begin oral steroids, PEF should return to green/yellow within 2-4 hrs.
  • 16. Changes in PFT • FVC reduced • FEV1 reduced • FEV1 / FVC < 70% - Obstructive condition • If, FEV1 > 12% / 200 ml in 10 to 15 min after administration of 200 to 400 µg salbutamol bronchodilator – Confirmatory Asthama. If, FEV1 < 12-15% after administration of bronchodilator – COPD Condition. • PFT varies with age, height, diurnally, post- exercise, post-bronchodilator treatment
  • 17. • Skin hypersensitivity tests - development of a wheal and flare reaction to intradermal injections of common allergens. Distinguish atopic from non-atopic subjects. • ABG - hypoxaemia and hypocarbia in acute attack & hypercarbia in severe acute.
  • 18. X-ray Changes • over-distended lungs due to over-inflation. Lungs appear hyperinflated. • Costophrenic and cardiophrenic angle obliterated • Intercostal space increased • Bronchial wall thickening • Excessive air trapping • Bronchial luminal narrowing
  • 19.
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  • 21. Structural Impairements • Inflammation – mast cell hyperactivity – degranulation of mast cell – release of histamine – bronchoconstriction • Increased of IgE antibodies ( type 1 hypersensitivity ) • Submucosal oedema • Increased mucous production ( mucus plugs ) • Hypertrophy of submucosal glands, bronchial smooth muscle • Hyperplasia, hyperactivity and hypertrophy of goblet cells(mucous producing cells) • Complications - like pigeon chest, lobar or segmental collapse, pneumothorax and mediastinal and subcutaneous emphysema may be seen. • Cynosis , PaCO2 > 50 mm Hg.
  • 22. Functional Impairements • Difficulty to talk,walk • Coughing • Breathlessness • Increased breathing • Reduced chest expansion • Increased work of accessory muscles
  • 23. Medical Management Beta adrenergic agonist(beta2) - SABA – salbutamol, terbutaline, - LABA – salmeterol, formeterol • Anticholinergics -ipratropium bromide • Methyxantine - theophylline • Anti IgE antibody - omalizumab • Corticosteroids - inhaled – beclomethasone, budesonide - oral – prednisolone • Anti-histamines - cetrizine • Leukotrienes anatagonist - montelukast
  • 24. Inhalers • Meter dose inhalers – children>12yr • Meter dose inhalers with spacer – children>4yr • Meter dose inhalers with spacer and face mask – children<4yr • Dry powder inhaler • Nebulizer Oxygen therapy To correct hypoxaemia, rise in PaCO2 levels, respiratory acidosis, respiratory muscle fatigue
  • 25. Status Asthamaticus • It is a condition in which severe airway obstruction and asthmatic symptoms persist despite the initial administration of standard acute asthma therapy. • Severe dyspnoea and unproductive cough. • Patient adopts an upright position fixing the shoulder girdle to assist the accessory muscles of respiration. • Physical signs include sweating, central cyanosis, tachycardia and pulsus paradoxus. • Severe & unremitting form of disease may prove to be fatal.