Bronchial

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

INTRODUCTION

CLASSIFICATION

RISK FACTORS
ASTHMA
Diagnosis

Treatment & Prevention

INTRODUCTION
 Introduction
4

 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.
 Introduction
5

 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".
CLASSFICATION
 Classification
7

 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
 Classification
8

 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
 Classification
9

 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
 Pathophysiology
10

I. Chronic inflammation

II. Airway Hyperresponsiveness

 Pathophysiology
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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
 Pathophysiology
12

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
 Pathophysiology
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I. Inflammation
 Environmental factors
 Viral infections: RSV, Mycoplasma,
Chlamydia
 Air pollution
 Allergens :house dust mite
 Pathophysiology
14

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.
Pathophysiology
15
Pathophysiology
16
RISK FACTORS
 Risk factors
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 Host factors:
 predispose individuals to, or protect
them from, developing asthma
i. Genetic
o Atopy
o Airway hyperresponsiveness
ii. Gender
iii. Obesity
 Risk factors
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 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
 Triggers
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 Asthma Triggers
 Allergens
 Virus Infections
 Drugs
 Exercise
 Food
 Air pollutants
 Physical factors
 GERD
 Stress
 Occupational factors
DIAGNOSIS
 Clinical manifestations
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 Symptoms
 Wheezing, dyspnea and cough.
 Variable – both spontaneously and with
therapy.
 Symptoms worse at night.
 Nonproductive cough
 Limitation of activity
 Clinical manifestations
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 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
Classification for asthma severity
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Grade Symptoms Night-time

Symptoms
Mild Symptoms ≤ 2 ≤ 2 times/month
intermittent times/week

Mild Symptoms ≥ 2 ≥ 2 times/month

persistent times/week
but ≤ 1/day
Moderate Daily Symptoms ≥ 1/week
persistent

Severe Continued Symptoms Frequent

persistent Limited physical activity
Clinical manifestations
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 Laboratory diagnosis
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 Pulmonary function
tests:
 Using Spirometry
 estimate degree of
obstruction
 ↓FEV1, ↓FEV1/FVC,
↓PEF.
 Laboratory diagnosis
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 CXR :
 hyperinflation,emphysema
 Arterial blood-gas analysis
 hypoxia & hypocarbia
 Skin hypersensitivity test
 Sputum & blood eosinophilia
 Elevated serum IgE levels
TREATMENT
 Management
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I. Non-Pharmacological

II. Pharmacological
 Non-Pharmacological
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 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
 Non-Pharmacological
31

 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
Pharmacological treatment
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 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
Pharmacological treatment
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 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
Pharmacological treatment
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 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.
Pharmacological treatment
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 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.
Pharmacological treatment
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 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
Pharmacological treatment
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 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
Pharmacological treatment
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 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.
Pharmacological treatment
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 Methylxanthines
 Adverse effects
o Anorexia, nausea, vomiting, abdominal
discomfort
o headache, and anxiety
o Seizures or arrhythmias
o Diuresis
 Doxyphylline
o long acting,oral
Pharmacological treatment
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 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.
Pharmacological treatment
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 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.
Pharmacological treatment
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 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
Pharmacological treatment
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 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
Pharmacological treatment
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 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.
Pharmacological treatment
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 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
Pharmacological treatment
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 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
Pharmacological treatment
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 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
Pharmacological treatment
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 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
Pharmacological treatment
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 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.
Pharmacological treatment
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 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
 Status asthmaticus
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(severe acute asthma)

 Severe airway obstruction
 Symptoms persist despite initial standard
acute asthma therapy.
o Severe dyspnea & unproductive cough
o Sweating , central cyanosis ,tachycardia
 Status asthmaticus
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(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
 Status asthmaticus
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(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
 Prophylaxis
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 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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thanks
Fo r W at ching