1. Dr. Shaikh Mujeeb Ahmed Assistant Professor AlMaarefa College
Bronchial Asthma
IMS 423 BLOCK
Dr. Shaikh Mujeeb Ahmed
Assistant Professor
AlMaarefa College

2. Intended Learning Outcomes
Describe pathophysiology of Bronchial asthma
Enumerate the predisposing factors for asthma
Describe the clinical features of asthma
Interpret the spirometry results lab results and correlate with severity of the disease.

3. Epidemiology
According to epidemiological studies asthma affects 1-18% of population of different countries.

4. What is Asthma?
Asthma is a chronic inflammatory disease of the airways characterized by variable recurring symptoms,
air flow obstruction, and
bronchial hyper responsiveness.
Asthma is a disease that affects the lungs. It causes repeated episodes of wheezing, breathlessness, chest tightness, and nighttime or early morning coughing. If someone has asthma, he or she has it all the time, but asthma attacks will occur only when something bothers the lungs. We know that if someone in the family of a person with asthma has asthma, other family members are more likely to have it too.   In most cases, we don’t know what causes asthma, and we don’t know how to cure it; however, it can be controlled.
Asthma can be controlled by knowing the warning signs of an attack, staying away from things that trigger an attack, and following the advice from a healthcare provider. 4

6. Airway obstruction Episodic wheezing Difficulty breathing,
Chest tightness, and
Cough that often is worse at night and in the early morning.

7. Types of Asthma Extrinsic – initiated by type I hypersensitivity
Atopic
Intrinsic – Non immune mechanisms
Respiratory tract infections
Exercise,
Ingestion of aspirin,
Emotional upset, and
Exposure to bronchial irritants such as cigarette smoke.

8. Some allergens which may cause asthma
Spittle, excrements,
hair and fur
of domestic
animals
House-dust mites which live in carpets, mattresses and upholstered furniture
Plant pollen
Dust of book depo-sitories
Pharmacological agents (enzymes, antibiotics, vaccines, serums)
Food components (stabilizers, genetically modified products)

9. Etiology & Pathogenesis
Early phase response
Late phase response

10. Etiology & Pathogenesis

11. Extrinsic (Atopic) Asthma
Allergen
Mast cells release
inflammatory
mediators
WBCs enter region
and release more
Type I hypersensitivity
Mast cells’ inflammatory mediators cause acute response within 10–20 minutes
Airway inflammation causes late phase response in 4–8 hours

12. Role of T lymphocytes T - Lymphocytes TH 1 - Lymphocytes
B - Lymphocytes
Plasma Cells
Ig G & Ig M
Ig E

13. Intrinsic (Nonatopic) Asthma
Respiratory infections
Epithelial damage, IgE production
Exercise, hyperventilation, cold air
Loss of heat and water may cause bronchospasm
Inhaled irritants
Inflammation, vagal reflex
Aspirin and other NSAIDs
Abnormal arachidonic acid metabolism

14. Aspirin and other NSAIDs

15. Airway Obstruction in Asthma
inflammatory
airway
mediators
inflammation
increased
epithelial
impaired
airway
injury
mucociliary
responsiveness
function
bronchospasm
edema
airflow limitation

16. Pathologic anatomy Macroscopic changes:
viscous mucous/ mucopurulent phlegm
airway dyskinesia with zones of spastic contraction and paralytic expansion of bronchi
obstruction of airway lumen
lung emphysema, pneumosclerosis
RV and RA hypertrophy and dilation

17. Microscopic changes:
Bronchial wall infiltration with mast cells, eosinophils, basophils and T-lymphocytes
Edema of mucous and submucous tunics
Destruction of bronchial epithelium
Hypertrophy of bronchial smooth muscles,
Hyperplasy of submucous glands
Microvessels dilation

19. Muscles
cells Ciliated
Goblet
cells
Bronchial glands
Cartilage
Bronchioles (section)

20. Mucosal edema
Mucus secretion increase
Muscle contraction
Asthma

21. Risk Factors for Developing Asthma
Genetic characteristics
Occupational exposures
Environmental exposures
Risk Factors for Developing Asthma 21

23. Diagnosing Asthma: Medical History
Symptoms
Coughing
Wheezing
Shortness of breath
Chest tightness
Symptom Patterns
Severity
Family History
Diagnosing Asthma: Medical History 23

24. Diagnosing Asthma Troublesome cough, particularly at night
Awakened by coughing
Coughing or wheezing after physical activity
Breathing problems during particular seasons
Coughing, wheezing, or chest tightness after allergen exposure
Colds that last more than 10 days
Relief when medication is used
Diagnosing Asthma 24

25. Diagnosing Asthma Wheezing sounds during normal breathing
Hyperexpansion of the thorax
Increased nasal secretions or nasal polyps
Atopic dermatitis, eczema, or other allergic skin conditions
Diagnosing Asthma

26. Diagnosing Asthma: Spirometry
Test lung function when diagnosing asthma
Diagnosing Asthma: Spirometry 26

27. Spirometry Measurement of Forced expiratory volume (FEV1 )
forced vital capacity (FVC)
FEV1/VC
Peak Expiratory Flow rate (PEFR)

30. Pulmonary Function Tests

32. Reversibility Test

33. Inhalational challenge test
Administration of sequential increasing conc. of either histamine , methacholine or mannitol.

34. Diurnal variation in PEFR

35. Exercise induced Asthma

36. Allergic skin testing
X-ray chest
Induced sputum differential eosinophil count - >2%
FENO

37. Management
Asthma is extremely common and causes considerable morbidity. The aims of treatment are to:
Abolish symptoms
Restore normal or best possible lung function
Reduce the risk of severe attacks
Enable normal growth to occur in children
Minimize absence from school or employment.

38. This involves: patient and family education about asthma
patient and family participation in treatment
avoidance of identified causes where possible
use of the lowest effective doses of convenient medications to minimize short-term and long-term side-effects.

39. Control of extrinsic factors
Measures must be taken to avoid causative allergens such as the house-dust mite, moulds and certain food stuffs (e.g eggs ,checolate), particularly in childhood.
Active and passive smoking should be avoided, as should beta-blockers in either tablet or eye drop form.
Individuals intolerant to aspirin may benefit by avoiding salicylates and should avoid NSAIDs.

40. 50% of individuals sensitized to occupational agents may be cured if they are kept permanently away from exposure. The remaining 50% continue to have symptoms that may be as severe as when exposed to materials at work, especially if they were symptomatic for a long time before the diagnosis was made.
This emphasises:
the importance of the rapid identification of extrinsic causes of asthma and their removal wherever possible (e.g. occupational agents, family pets)
once extrinsic asthma is initiated, it may become self-perpetuating possibly by non-immune mechanisms.

41. Drug treatment
The mainstay of asthma therapy is the use of therapeutic agents delivered as aerosols or powders directly into the lungs The advantages of this method of administration are that drugs are delivered direct to the lung and the first-pass metabolism in the liver is avoided; thus lower doses are necessary and systemic unwanted effects are minimized.
Both national and international guidelines have been published on the stepwise treatment of asthma based on three principles:

42. Asthma self-management with regular asthma monitoring using peak flow meters and individual treatment plans discussed with each patient and written down.
The appreciation that asthma is an inflammatory disease and that anti-inflammatory (controller) therapy should be started even in mild cases.
Use of short-acting inhaled bronchodilators (e.g. salbutamol and terbutaline) only to relieve breakthrough symptoms. Increased use of bronchodilator treatment to relieve increasing symptoms is an indication of deteriorating disease.

43. Drugs used in asthma Quick relief medication
short acting β2 agonist (salbutamol, terbutaline)
oral steroids
Anticholinergic agents
Long-acting relief/disease controllers
- Long-acting β2 agonists - salmeterol, formoterol
- Sodium cromoglicate (mast cell stabilizer)
- Leukotriene modifiers
Other agents with bronchodilator activity
Theophylline preparations

44. Steroid-sparing agents
- Methotrexate
- Ciclosporin
- Gold
- Intravenous immunoglobulin
- Anti-IgE monoclonal antibody - Omalizumab

45. Asthma severity classification
Clinical course, severity
Daytime asthma symptoms
Nighttime awakenings
FEV1, PEF
Intermittent
< 1 /week
2 and < /month
>80% predicted. Daily variability < 20%
Mild persistent
 1 /week but not daily
> 2 /month
>80% predicted. Daily variability – 20-30%
Moderate persistent
Daily
> 1 /week
> 60 but < 80% predicted. Variability>30%.
Severe persistent
Persistent, which limit normal activity
<60% predicted. Variability > 30%.

46. Level of Asthma control

49. Managing Asthma: Peak Expiratory Flow (PEF) Meters
Allows patient to assess status of his/her asthma
Persons who use peak flow meters should do so frequently
Many physicians require for all severe patients

50. Managing Asthma: Peak Flow Chart
People with moderate or severe asthma should take readings:
Every morning
Every evening
After an exacerbation
Before inhaling certain medications
Managing Asthma: Peak Flow Chart
Source: “What You and Your Family Can Do About Asthma” by the Global Initiative For Asthma Created and funded by NIH/NHLBI

51. A stepwise approach to the management of asthma
Step 1: Occasional use of inhaled short-acting β2-adrenoreceptor agonist bronchodilators
Step 2: Introduction of regular ‘preventer’ therapy
Step 3: Add-on therapy
Step 4: Poor control on moderate dose of inhaled steroid and add-on therapy: addition of a fourth drug
Step 5: Continuous or frequent use of oral steroids

53. Acute severe asthma Patients with acute severe asthma typically have:
inability to complete a sentence in one breath
respiratory rate ≥ 25 breaths per minute
tachycardia ≥ 110 beats/min (pulsus paradoxus, is not useful as it is only present in 45% of cases)
PEF < 50% of predicted normal or best.

54. Features of life-threatening attacks are:
a silent chest, cyanosis or feeble respiratory effort
exhaustion, confusion or coma
bradycardia or hypotension
PEF < 30% of predicted normal or best (approximately 150 L/min in adults).

55. Treatment of severe asthma
At home
The patient is assessed. Tachycardia, a high respiratory rate and inability to speak in sentences indicate a severe attack.
If the PEFR is less than 150 L/min (in adults), an ambulance should be called. (All doctors should carry peak flow meters.)
Nebulized salbutamol 5 mg or terbutaline 10 mg is administered.
Hydrocortisone sodium succinate 200 mg i.v. is given.
Oxygen 40-60% is given if available.
Prednisolone 60 mg is given orally.

56. At hospital The patient is reassessed. Oxygen 40-60% is given.
The PEFR is measured using a low-reading peak flow meter, as an ordinary meter measures only from 60 L/min upwards. Measure O2 saturation with a pulse oximeter.
Nebulized salbutamol 5 mg or terbutaline 10 mg is repeated and administered 4-hourly.
Add nebulized ipratropium bromide 0.5 mg to nebulized salbutamol/terbutaline.
Hydrocortisone 200 mg i.v. is given 4-hourly for 24 hours.

57. terbutaline 1.5-5.0 μg/min, or magnesium sulphate 1.2-2 g over 20 min.
Prednisolone is continued at 60 mg orally daily for 2 weeks.
Arterial blood gases are measured; if the Paco2 is greater than 7 kPa, ventilation should be considered.
A chest X-ray is performed to exclude pneumothorax.
One of the following intravenous infusions is given if no improvement is seen:
salbutamol 3-20 μg/min, or
terbutaline μg/min, or
magnesium sulphate g over 20 min.

58. Arterial blood gases should always be measured in asthmatic patients requiring admission to hospital. Pulse oximetry is useful in monitoring oxygen saturation during the admission and reduces the need for repeated arterial puncture. Features suggesting very severe life-threatening attacks are:
a high Paco2 > 45
severe hypoxaemia Pao2 < 60 despite treatment with oxygen
a low and falling arterial pH.

59. A Public Health Response to Asthma: Interventions
Medical management
Education
Environment
Schools
A Public Health Response to Asthma: Interventions