This document provides an overview of bronchial asthma, including its classification, pathophysiology, risk factors, diagnosis, and treatment. It begins with an introduction defining asthma as a chronic inflammatory airway disease characterized by wheezing and reversible airway obstruction. It then covers asthma's classification into allergic and non-allergic types, risk factors like genetics and environment, and diagnostic tests like spirometry and allergy testing. The bulk of the document focuses on treatment approaches, including non-pharmacological methods and a wide range of pharmacological options targeting inflammation and bronchodilation. It concludes with guidance on managing severe exacerbations and the goals of prophylaxis.

1. Dr. Sameh Ahmad Muhamad abdelghany
Lecturer Of Clinical Pharmacology
Mansura Faculty of medicine
Bronchial
asthma
Management

2. 2
ASTHMA
INTRODUCTION
CLASSIFICATION
RISK FACTORS
Diagnosis
Treatment & Prevention
CONTENTS

3. INTRODUCTION

4. 4
Introduction
 Asthma is a chronic inflammatory disorder
of the airways that is characterized:
o clinically by recurrent episodes of wheezing,
breathlessness, chest tightness, and cough,
particularly at night/early morning.
o physiologically by widespread, reversible
narrowing of the bronchial airways and a
marked increase in bronchial
responsiveness.

5. 5
Introduction
 In 2015, 358 million people globally had
asthma, up from 183 million in 1990.
 It caused about 397,100 deaths in 2015,
most of which occurred in the developing
world.
 Asthma was recognized as early as Ancient
Egypt.
 The word "asthma" is from the Greek
ἅσθμα, ásthma, which means "panting".

6. CLASSFICATION

7. 7
Classification
 A heterogenous disorder.
 Atopic /extrinsic /allergic ( 70%):
o Most common type
o Environmental agent: dust, pollen,
food, animal dander
o Family history - present
o Serum IgE levels - increased
o Skin test with offending agent –wheal
flare

8. 8
Classification
 Non-atopic/ intrinsic /non-allergic( 30%)
 Triggered by respiratory tract infection
 Viruses - most common cause
 Family history uncommon
 IgE level normal
 No associated allergy
 Skin tests NEGATIVE
 Cause- hyperirritability of bronchial tree

9. 9
Classification
 Drug induced asthma
 Several pharmacologic agents
 Aspirin sensitive asthma
o Increased bronchoconstrictor leukotrienes.
o sensitive to small doses of aspirin.
o Inhibits COX pathway, without affecting
LPO pathway

10. 10
Pathophysiology
I. Chronic inflammation
II. Airway Hyperresponsiveness

11. 11
Pathophysiology
I. Inflammation
 Chronic inflammatory state
 Involves respiratory mucosa from trachea
to terminal bronchioles, predominantly in
the bronchi.
 Activation of mast cell , infiltration of
eosinophils & T-helper type 2 (Th2)
lymphocytes

12. 12
Pathophysiology
I. Inflammation
 Exact cause of airway inflammation is
unknown.
 Thought to be an interplay between
endogenous and environmental factors.
 Endogenous factors
 Atopy
 Genetic predisposition to IgE mediated
type I hypersensitivity
 The major risk factor for asthma
 Genetics

13. 13
Pathophysiology
I. Inflammation
 Environmental factors
 Viral infections: RSV, Mycoplasma,
Chlamydia
 Air pollution
 Allergens :house dust mite

14. 14
Pathophysiology
II. Airway Hyperresponsiveness (AHR)
 The excessive bronchoconstrictor response
to multiple inhaled triggers that would
have no effect on normal airways.
 Characteristic physiologic abnormality of
asthma.

15. 15
Pathophysiology

16. 16
Pathophysiology

17. RISK FACTORS

18. 18
Risk factors
 Host factors:
 predispose individuals to, or protect
them from, developing asthma
i. Genetic
o Atopy
o Airway hyperresponsiveness
ii. Gender
iii. Obesity

19. 19
Risk factors
 Environmental factors:
 influence susceptibility to development of
asthma in predisposed individuals,
precipitate asthma exacerbations, and/or
cause symptoms to persist
o Indoor allergens , Outdoor allergens
o Occupational sensitizers
o Tobacco smoke , Air Pollution
o Respiratory Infections
o Diet

20. 20
Triggers
 Asthma Triggers
 Allergens
 Virus Infections
 Drugs
 Exercise
 Food
 Air pollutants
 Physical factors
 GERD
 Stress
 Occupational factors

21. DIAGNOSIS

22. 22
Clinical manifestations
 Symptoms
 Wheezing, dyspnea and cough.
 Variable – both spontaneously and with
therapy.
 Symptoms worse at night.
 Nonproductive cough
 Limitation of activity

23. 23
Clinical manifestations
 Signs
 ↑ respiratory rate, with use of accessory
muscles
 Hyper-resonant percussion note
 Expiratory rhonchi
 No findings when asthma is under control or
b/w attacks

24. 24
Classification for asthma severity
Grade Symptoms Night-time
Symptoms
Mild
intermittent
Symptoms ≤ 2
times/week
≤ 2 times/month
Mild
persistent
Symptoms ≥ 2
times/week
but ≤ 1/day
≥ 2 times/month
Moderate
persistent
Daily Symptoms ≥ 1/week
Severe
persistent
Continued Symptoms
Limited physical activity
Frequent

25. 25
Clinical manifestations

26. 26
Laboratory diagnosis
 Pulmonary function
tests:
 Using Spirometry
 estimate degree of
obstruction
 ↓FEV1, ↓FEV1/FVC,
↓PEF.

27. 27
Laboratory diagnosis
 CXR :
 hyperinflation,emphysema
 Arterial blood-gas analysis
 hypoxia & hypocarbia
 Skin hypersensitivity test
 Sputum & blood eosinophilia
 Elevated serum IgE levels

28. TREATMENT

29. 29
Management
I. Non-Pharmacological
II. Pharmacological

30. 30
Non-Pharmacological
 Reduce exposure to indoor allergens
 Avoid tobacco smoke
 Avoid vehicle emission
 Identify irritants in the workplace
 Explore role of infections on asthma
development, especially in children and
young infants

31. 31
Non-Pharmacological
 Influenza Vaccination
o should be provided to patients with asthma
when vaccination of the general population is
advised
o routine influenza vaccination of children and
adults with asthma does not appear to protect
them from asthma exacerbations or improve
asthma control

32. 32
Pharmacological treatment
 Classification of drugs
 Bronchodilators : rapid relief, by relaxation of
airway smooth muscle
 β2 Agonists
 Anticholinergic Agents
 Methylxanthines
 Controllers : inhibit the inflammatory process
 Glucocorticoids
 Leukotrienes pathway inhibitors
 Cromones
 Anti-IgE therapy

33. 33
Pharmacological treatment
 β2 Agonists in asthma
 Potent bronchodilators.
 Usually given by inhalation route.
 Effects:
o Relaxation of airway smooth muscle
o Inhibition of mast cell mediator release
o Reduction in plasma exudation
o Increased mucociliary transport
o Inhibition of sensory nerve activation
 No effect on airway inflammation

34. 34
Pharmacological treatment
 β2 Agonists in asthma
a) Short-Acting β2 Agonists
 E.g salbutamol , terbutaline
 Convenient,rapid onset,without significant
systemic side effect
 Bronchodil. of choice in acute severe asthma
 Used for symptomatic relief
 Only treatment required for mild, intermittent
asthma.
 Use >2 times a week indicates need of a regular
controller therapy.

35. 35
Pharmacological treatment
 β2 Agonists in asthma
b) Long-Acting β2Agonists
 E.g salmeterol, formoterol
 Duration of action - >12 hrs.
 Used in combination with inhaled corticosteroid
therapy.
 Improve asthma control and reduce frequency
of exacerbations.
 Should not be used as monotherapy (increased
mortality).
 Not effective for acute bronchospasm.

36. 36
Pharmacological treatment
 Anticholinergic agents
 E.g Ipratropium bromide, tiotropium.
 Prevent cholinergic nerve induced
bronchoconstriction.
 Less effective than β2 agonists.
 Response varies with existing vagal tone.
 Use in asthma
o Intolerance to inhaled β2 agonist.
o Status asthmaticus –additive effect with β2
agonist

37. 37
Pharmacological treatment
 Anticholinergic agents
 Ipratropium:
o slow,bitter taste
o precipitate glaucoma
o paradoxical bronchoconstriction
 Tiotropium:
o longer acting, approved for treatment of COPD.
o Dryness of mouth

38. 38
Pharmacological treatment
 Methylxanthines
 Medium potency bronchodilator
 E.g Theophylline, theobromine, caffeine
 Recently interest has declined in this class of
drugs:
o Side effects
o Need for plasma drug levels
o Pharmacokinetics
o Availability of other effective drugs
 Still widely used drugs especially in developing
countries due to their lower cost.

39. 39
Pharmacological treatment
 Methylxanthines
 Adverse effects
o Anorexia, nausea, vomiting, abdominal
discomfort
o headache, and anxiety
o Seizures or arrhythmias
o Diuresis
 Doxyphylline
o long acting,oral

40. 40
Pharmacological treatment
 Corticosteroids in asthma
 Effective drugs for treatment of asthma.
 Development of inhaled corticosteroids is a
major advance in asthma therapy.
 Used prophylactically as a controller therapy.
 Reduce the need for rescue β2 agonist.
 Benefit starts in 1week but continues up to
several months.
 If asthma not controlled at low dose of ICS then
addition of long acting β2 agonist is more
effective than doubling steroid dose.

41. 41
Pharmacological treatment
 Corticosteroids in asthma
 Effects: Broad anti-inflammatory effects:
o Marked inhibition of infiltration of airways by
inflammatory cells.
o Modulation of cytokine and chemokine
production
o Inhibition of eicosanoid synthesis
o Decreased vascular permeability.
o Potentiate effect of β2 agonist.

42. 42
Pharmacological treatment
 Corticosteroids in asthma
 Inhaled corticosteroids( ICS)
o Use of β2Agonists >2 times a week indicates
need of a ICS
o E.g Beclomethasone , Budesonide , Fluticasone

43. 43
Pharmacological treatment
 Corticosteroids in asthma
 Inhaled corticosteroids( ICS)
 Adverse effects:
o Oropharyngeal candidiasis, dysphonia
o Decreased bone mineral density.
o Skin thinning, purpura
o Growth retardation in children

44. 44
Pharmacological treatment
 Corticosteroids in asthma
 Systemic steroids in asthma
 Indication
1. Acute exacerbation(lung function <30%
predicted)
2. Chronic severe asthma
 A 5-10 day course of prednisolone 30-
45mg/d is used.
 1% of patients may require regular
maintenance therapy.

45. 45
Pharmacological treatment
 Leukotrienes pathway inhibitors
a) Inhibition of 5-lipoxygenase, thereby
preventing leukotriene synthesis. Zileuton.
b) Inhibition of the binding of LTD4 to its
receptor on target tissues, thereby preventing
its action. E.g Zafirlukast, montelukast.
 Oral route.
 Adverse effects
o Liver toxicity
o vasculitis with eosinophilia

46. 46
Pharmacological treatment
 Leukotrienes pathway inhibitors
 They are less effective than ICSs in
controlling asthma
 Use in asthma
o Patients unable to manipulate inhaler devices.
o Aspirin induced asthma.
o Mild asthma – alternative to ICS.
o Moderate to severe asthma – may allow
reduction of ICS dose

47. 47
Pharmacological treatment
 Cromones
 E.g Cromolyn sodium & nedocromil sodium
 On chronic use (four times daily) reduce the
overall level of bronchial reactivity.
 have no effect on airway smooth muscle tone
and are ineffective in reversing asthmatic
bronchospasm; they are only of value when
taken prophylactically.
 Inhalation route

48. 48
Pharmacological treatment
 Cromones
 May act by stabilization of Mast cells with
inhibition of mediator release
 Uses
o Asthma - Prevention of asthmatic attacks in
mild to moderate asthma
 Adverse effects
o Well tolerated drugs
o Minor side effects- throat irritation, cough, and
mouth dryness, rarely, chest tightness, and
wheezing

49. 49
Pharmacological treatment
 Anti-IgE therapy:
 Omalizumab
 recombinant humanized monoclonal antibody
targeted against IgE.
 Action:
o IgE bound to omalizumab cannot bind to IgE
receptors on mast cells and basophils, thereby
preventing the allergic reaction at a very early
step in the process.

50. 50
Pharmacological treatment
 Anti-IgE therapy:
 Use in asthma
o Persons >12 years of age with moderate-to-
severe persistent asthma.
 Omalizumab is not an acute bronchodilator and
should not be used as a rescue medication or as
a treatment of status asthmaticus.
 Expensive drug
 Has to be given under direct medical
supervision due to the risk of anaphylaxis

51. 51
Status asthmaticus
(severe acute asthma)
 Severe airway obstruction
 Symptoms persist despite initial standard
acute asthma therapy.
o Severe dyspnea & unproductive cough
o Sweating , central cyanosis ,tachycardia

52. 52
Status asthmaticus
(severe acute asthma)
 Treatment of Status asthmaticus
 High conc. of oxygen through facemask
 Nebulised salbutamol in oxygen given
immediately
 Ipratopium bromide + salbutamol
nebulised in oxygen,who don’t respond
within 15-30 min

53. 53
Status asthmaticus
(severe acute asthma)
 Treatment of Status asthmaticus
 Terbutaline s.c. or i.v.
 excessive coughing or too weak to inspire
adequately.
 Hydrocortisone hemisuccinate i.v. ,
followed by infusion.
 Endotracheal intubation & mechanical
ventilation if above ttt fails

54. 54
Prophylaxis
 Preservation of the environment, healthy
life-style (smoking cessation, physical
training) – are the basis of primary asthma
prophylaxis.
 These measures in combination with
adequate drug therapy are effective for
secondary prophylaxis.

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thanksF o r W a t c h i n g