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Asthma For a better control. Dr Hatem Al Mubarak, MD, FRCPC, FACCP Pulmonary Specialist Al Jazira and Central Hospital Abu Dhabi, UAE. Asthma for a better control. Definition Epidemiology of asthma Pathophysiology and asthma evolution Diagnosis of asthma Asthma classification

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Slide1 l.jpg

Asthma

For a better control

Dr Hatem Al Mubarak, MD, FRCPC, FACCP

Pulmonary Specialist

Al Jazira and Central Hospital

Abu Dhabi, UAE


Asthma for a better control l.jpg
Asthma for a better control

  • Definition

  • Epidemiology of asthma

  • Pathophysiology and asthma evolution

  • Diagnosis of asthma

  • Asthma classification

  • Treatment of asthma

  • Clinical Scenarios and discussion


Definition l.jpg
Definition

A chronic inflammatory disorder of the airways in which many cells play a role that causes recurrent episodes of wheezing, breathlessness, chest tightness and cough ic but variable airflow limitation that is at least partly reversible either spontaneously or with treatment. The inflammation also causes. These symptoms associates with widespread and associated increase in airway responsiveness to variety of stimuli.


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Venn diagram of obstructive lung disease

Chronic Bronchitis

Emphysema

Airflow limitation

Asthma


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Epidemiology and Risk Factors

  • For all age group : incidence 2.65-4/1000 per year.

  • Children : 4.3-18/1000 per year

  • Adult : 2.1/1000 per year

  • Mortality (1985-1987) between 1.3-9.3 /100,000 of total population

  • Danish follow-up study showed cigarette smoking, age, presence of blood eosinophilia, impairment of lung function and degree of reversibility contribute to asthma mortality


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Age and Sex Distribution of Asthma

16

14

12

10

8

6

4

2

0

Individuals per 1000

0 10 20 30 40 50 60 70 80

Female

Male


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Prevalence of self-reported asthma, children aged 13-14 years

12 months prevalence of self-reported asthma with a written questionnaire, for children aged 13-14 years . International Study of Asthma and Allergies in Childhood (ISAAC) including 463,801 children in 56 countries


Asthma evolution hypothesis l.jpg
Asthma Evolution Hypothesis years

Genetic

Predis-

position

+

Airway

Inflammation

Hyper-

responsiveness

Sensitisation

+

Asthma

Environmental

Factors

Maternal Smoking

Indoor/outdoor

Allergens

Environmental

Factors

Smoking, cold air

Indoor/outdoor

Allergens, viral

infection


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Asthma Evolution Hypothesis years

Genetic

Predis-

position

Asthma


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The Genetic of Asthma years

  • 20-25% Increase in prevalence of asthma among first degree relative of asthmatics compare to general population (4%)

  • Monozygotic twins (50%) dizygotic twins (33%)

  • Doesn’t follow any medelian pattern

  • Genetic researches provided evidence of several atopic phenotypes (eosinophil count, skin testing, atopic cytokines)


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Asthma Evolution Hypothesis years

Genetic

Predis-

position

+

Asthma

Environmental

Factors

Maternal Smoking

Indoor/outdoor

Allergens



Atopy l.jpg
Atopy years

  • Atopy is characterized by

    • Elevated IgE level

    • Detection of IgE against common allergens

    • Positive skin test against common allergen

  • Asthmatic are more atopic than non-asthmatic

  • Increase airway hyperresponsiveness is associated with increase in atopy


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Atopy in asthma years

  • House dust mite is the most common allergens

  • Increases in prevalence of asthma in New Guinea when adult exposed to house dust mite.

  • Association between the level of house dust mite in the bed room of babies during the first year of life and asthma in at 8 years of age.

  • Cats more than any other animals is a risk for asthma

  • Children expose to furry cat are at twice the risk for developing asthma

  • Other allergens including grass, tree pollen, and cockroaches


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Asthma risk factors years

  • Exercise: occur because of water loss from the airway wall

  • Occupation: e.g.; wood dust, formaldehyde, latex, animal allergens

  • Drugs: NSAID, possible biphosphonate, ß-blocker

  • Premenstrual asthma : associated with late luteal phase


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Smoking and asthma risk years

  • Passive smoking

    • It the second major risk after atopy

    • Parental ,especially maternal, smoking is associated with increase risk of asthma in children

    • Smoking >10cig/day increase asthma by 2.5 times at 12 years of age

    • Increase four-fold of the level of IgE from cord blood of newborn of mothers who smoke (even in absence of atopy)


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Asthma Evolution Hypothesis years

Genetic

Predis-

position

+

Sensitisation

Asthma

Environmental

Factors

Maternal Smoking

Indoor/outdoor

Allergens


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Th1 and Th2 Balance years

Bacterial Infection

TB, Measles, HepA

Rural Environment

Widespread use of antibiotics

Western lifestyle

Diet

Sensitisation to allergens

Parasitic infection

Th1

Th0

Th2

Allergic

disease

Protective

immunity


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Asthma Evolution Hypothesis years

Genetic

Predis-

position

+

Airway

Inflammation

Sensitisation

Asthma

Environmental

Factors

Maternal Smoking

Indoor/outdoor

Allergens


Slide20 l.jpg

Mast years

cell

Smooth Muscle

PGD2, LTC4/D4

Histamine, Tryptase

Eosinophils

Cytokines

Mast

cell

Acute Asthma

B-cell

Chronic Asthma

APS

TH2


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Asthma Evolution Hypothesis years

Genetic

Predis-

position

+

Airway

Inflammation

Hyper-

responsiveness

Sensitisation

+

Asthma

Environmental

Factors

Maternal Smoking

Indoor/outdoor

Allergens

Environmental

Factors

Smoking, cold air

Indoor/outdoor

Allergens, viral

infection



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Case 1 years

  • 22 years old lady came to your office with cough for several weeks with no associated sputum. She deny any other symptoms but remember she use to have similar symptoms when she was young. She also noticed that she get tired slighter sooner that her class mate in sports event.

  • Examination was normal and her PEF was normal

  • Does this patient have asthma?


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Diagnosis of asthma years

Wheeze

Chest

tightness

Asthma

Cough

Nocturnal

symptoms

Difficulty

In breathing


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Canadian Asthma Consensus yearsDiagnosis and Evaluation of Asthma in Adult

  • Spirometry: improvement of FEV1 by

    • 12% and 200ml from the base line after inhalation of short acting ß2 agonist

    • 20% and 250ml after 10-14 days on inhaled or systemic glucocorticosteroid

    • 20% and 250 ml with spontaneous variability

  • Peak Expiratory Flow

    • 20% or more variability between highest and lowest values ( morning and afternoon, before and after bronchodilator)


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Spirometry in asthma years

Normal FVC

Normal FEV1

Normal Ratio

Normal or mild low FVC

low FEV1

low Ratio

Normal Asthma


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Canadian Asthma Consensus yearsDiagnosis and Evaluation of Asthma in Adult

  • Airway Hyperresponsiveness

    • Methacholine neubelizer provocation test to evaluate the airway response

    • Positive test is there is a drop of more than 20% of FEV1 in a methacholine concentration of less than 8mg/ml

    • Negative methacholine can exclude asthma


Methacholine provocation test l.jpg
Methacholine Provocation Test years

FEV1 Base line

PC20

20% Drop

FEV1

Normal Saline 0.25mg/ml 0.5 mg/ml 1mg/ml 2mg/ml 4mg/ml 8mg/ml

Methacholine Concentration


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Asthma Evolution years

Primary

Prevention

Secondary

Prevention

Secondary

Prevention

Secondary

Prevention

Genetic

Predis-

position

Regular

Anti-inflammatory

treatment

Avoidance

Treatment of

exacerbation

+

Airway

Inflammation

Hyper-

responsiveness

Sensitisation

+

Asthma

Environmental

Factors

Maternal Smoking

Indoor/outdoor

Allergens

Environmental

Factors

Smoking, cold air

Indoor/outdoor

Allergens, viral

infection



2 agonist l.jpg
ß2 agonist years

  • ß2 receptors are present in all smooth muscles of the airways

  • Direct effect causing

    • Smooth muscle relaxation

    • Reduction in neurotransmitter

    • Increase ciliary clearance

    • Decrease the microvascular leakdecrease edema

  • Salbutamol, terbutaline,fenoterole, metaprotanole

  • Does not have anti inflammatory effect

  • Drug of choice in both children and adult for the relief of acute asthma symptoms


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ß2 agonist years

  • Side effects

    • Mild tremor (affect on skeletal muscle receptors)

    • Tachycardia( affect on cardiovascular)

    • Hypokalemia ( increase K+ entry to skeletal muscle)

  • No evidence that it increase or induce serious arrhythmias or other cardiac abnormalities


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ß2 agonist years

  • No evidence that regular four times a day with SAß2 is better than as needed approach in any degree of asthma severity

  • Regular SAß2 is associated with masking underlying inflammation  increase hyperresponsiveness worsening severity


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Long acting ß2 years

  • It have more sustained action

  • It enhance the effect of inhaled steroids

  • Salmeterol and formoterol

  • Not recommended for relief of acute symptoms and exacerbation

  • Does not increase airway hyperresponsiveness and it have some anti-inflammatory effect


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Theophylline years

  • Phosphodiestterase inhibitors increase in cAMP bronchodilators

  • Adenosine receptors antagonist CNS stimulation, cardiac arrhythmias,diuresis

  • Stimulation of adrenaline release

  • Less effective than ß2 agonist in acute exacerbation and it is more recommended in chronic asthma (especially if nocturnal symptoms present)


Anticholiergics l.jpg
Anticholiergics years

  • Muscarinic receptors antagonist and inhibit cholinergic receptors that cause bronchoconstrection

  • Less effective than ß2 but it has additative effect

  • Are more effective in acute than chronic asthma

  • More effective in asthmatic who have element of fixed airway

  • Ipratropium, oxitropium and tiotropium bromide


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Affect of anticholinergic yearson smooth muscle

Vagus Nerve

Anticholinergic

Acetylcholine


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Cromones years

  • It may affect chloride channels that expressed in mast, nerve and some inflammatory cells

  • Inhibit mediators release from mast cells by membrane stabilization

  • Effect on sensory nerve ending in the airways

  • Prophylactic treatment and should be given regularly

  • Preferred agent in children


Antileukotrienes l.jpg
Antileukotrienes years

  • LTC4,LTE4 and LTD4 are products of inflammatory cells that cause bronchoconstrition

  • 40 times more potent that histamine or methacholine to cause bronchoconstriction

  • Blocking leukotriens receptors cause bronchodilatation and decrease eosinophils

  • Zafirlukast, pranlukast and montelukast

  • Reduce allergen-exercise-cold induced asthma by 50-70%

  • Complete response in aspirin-induced asthma


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Corticosteroids years

  • Action occur through activation of glucocoticosteroid receptors (GCSr) which found in all body cells

  • When bound to receptors it decreases gene production for many pro and inflammatory cytokines

  • Systemic (parental/oral) or inhaled are the two major form


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Systemic corticosteroids years

  • Reserved for moderate to sever cases

  • Oral bio availability is very high with complete GI absorption.

  • Parental route reserved if oral rout can’t be tolerated


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Inhaled corticosteroid years

  • They are as effective as low to moderate dose of systemic steroids with much lesser side effects

  • Lipophilic: very high binding affinity and fast first pass liver metabolism

  • five inhaled corticosteroids (ICS) currently available

    • Fluticasone propionate (Flexotide, Flovent)

    • Beclomethasone 17,21-dipropionate ( Beclovent, QVAR)

    • Triamcinolone (Azmacort)

    • Flunisolide (AeroBid)

    • Budesonide (Pulmicort)


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Corticosteroids side effects years

  • Local side effect:

    • oral candidiasis occur in 10%

    • Increase risk with poor technique,concomitant use of antibiotics and reduce by use of spacer and rinsing mouth.

    • Dysphonia (30%) in people who use their voice a lot

    • Doesn't have any effect on airway mucosa


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ICS side effects years

  • Hypothalamic-pituitary-adrenal axis

    • No effect was seen with doses of BDP<1500g/day or budesonide <1600 g/day

    • Only 2 cases reported with adrenal insufficiency ( very high dose of budesonide of 6400 g/day)


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ICS side effects years

  • Osteoporosis

    • ICS shown to have some effect on osteocalcin (bone formation) and hydroxyproline (bone resorption) in doses of budesonide>2000 g/day

    • Bone densitometry carried out in adult asthmatic on various doses of ICS and it showed no increase bone loss

  • Does not cause growth retardation in children

  • Children on ICS were shorter on average than children not on ICS at 2 years of age, but all of them had the same height at 6 years of age


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ICS side effects years

  • Posterior subcapsular cataract

    • Usually there is no risk

    • Risk slightly increase with high doses of ICS and use of MDI

  • Risk of lung infection

    • Risk of lung infection is not increased

    • Does not increase the risk of TB re-activation

  • Risk of skin bruising increase with height doses of ICS ( from 22% to 47%) in older population



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Case 2 years

  • 64 years old gentleman who was known to have asthma for several years on inhaled corticosteroids ( MDI) .

  • You are seeing him for the first time, his history and exam revealed moderate persistent asthma not will controlled because he claim he can’t use the apparatus. Throat exam showed oral condidiasis and chest exam .


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Pressurized metered-dose inhaler years

  • Pressurized in a crystal suspension in liquid mixture of chloroflucarbones(CFC)

  • The mixture boil off rabidly as soon as they leave the container with velocity of 30m/sec

  • Newer form ban the CFC and use non-CFC solution

  • Laryngeal deposition is 25% with some MDI



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Dry-powder inhaler years

  • Depends on patient inspiratory effort

  • DPI

    • Spinhalers

    • Rotahaler

    • Diskhalers

    • Reservoir dry-powder inhalers


Neubelizers l.jpg
Neubelizers years

  • Two type of neubelizer; Jet and ultrasonic

  • Ultrasonic use sound wave vibration through liquid to form fountain of droplets

  • Jet neubelizer result from steam of compressed air or oxygen that push liquid drug through small capillaries to become like steam

  • Usually 50% of neubelized solution is left in apparatus and can’t be utilized


Slide60 l.jpg

Deposition% years

Loss in air

Apparatus

GI

Lung

MDI DPI Nebulizer



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Case 3 years

  • 29 years old male was diagnosed to have asthma for several years that was controlled in budesonide 200mcg bid with MDI. In the last week he noticed that he is having more cough and occasionally awaking up in the middle of the night with cough. After assessing possible excerbating factors what will be your next step?



Treatment goals l.jpg
Treatment Goals years

  • Achieve and maintain control of symptoms

  • Minimize frequency of asthma attacks

  • Prevent emergency visits to doctors or ER

  • Achieve and maintain normal activity level

  • Optimise asthma therapy with minimum side effects

    • Minimize the need of ß2 agonist

    • Step down use of ICS


Mild intermittent asthma l.jpg
Mild intermittent Asthma years

If symptoms>2/week, nocturnal >2/month

Go to next step 

Moderate Persistent

Rescue medication with

Short ß2 agonist

Sever Persistent

Mild Persistent


Mild persistent asthma l.jpg
Mild persistent asthma years

If symptoms>6/week, nocturnal >4/month

Go to next step 

Short ß2 agonist is needed

Inhaled corticosteroid

Beclomethasone or budesonide 200-800g

Or fluticasone 100-400 g

Or

Sodium cromolyn

Moderate Persistent

Sever Persistent

Mild intermittent


Moderate persistent asthma l.jpg
Moderate persistent asthma years

If symptoms continual, nocturnal daily

Go to next step 

Short ß2 agonist is needed

double Inhaled corticosteroid

Beclomethasone or budesonide 800-2000g

Or fluticasone 400-1000 g

Or

Inhaled corticosteroids with

long acting ß2 agonist

Sever Persistent

Mild Persistent

Mild intermittent


Sever persistent asthma l.jpg
Sever persistent asthma years

Short ß2 agonist is needed

double Inhaled corticosteroid

Beclomethasone or budesonide 800-2000g

Or fluticasone 400-1000 g

Or

Inhaled corticosteroids with

long acting ß2 agonist

With

Theophylline or antileukutriens or high dose

Anticholinergic

If worse symptoms

Systemic steroid

Moderate Persistent

Mild Persistent

Mild intermittent



Case 4 l.jpg
Case 4 years

  • 33 years old male presented to emergency with 3 days of progressive dyspnea. He could not sleep the night before because of cough and breathlessness. He is known to have asthma but he is not taking regular treatment. He smoke a pack aday. He deny fever, chest pain or previous history of heart disease

  • Exam showed patient in moderate distress, BP130/90, pulse 120/min, O2 90%

  • Chest exam showed decrease air entry at right with wheeze bilaterally

  • What is your management?


Clinical features of acute asthma l.jpg
Clinical Features of Acute Asthma years

  • History of exacerbating factors ( infection, allergens)

  • History of previous symptoms could be absent but mostly with history of uncontrolled asthma. Dyspnoea, orthopnea and PND could be present

  • Presence of chest pain could indicate asthma complication ( pneumothorax, collapse ,CAD or pneumomediastinum)

  • History of previous ICU or intubations considered high risk


Hospital management in acute asthma l.jpg
Hospital management in acute asthma years

Assess severity,ß2 agonist,O2, systemic steroids

Repeat assessment

Life threatening

asthma

improvement

Partial or no

improvement

Continue treatment

admit

Response maintain

improvement

worsening

ICU

discharge


Case 5 l.jpg
Case 5 years

  • 26 years old lady 12 weeks pregnant came to you regarding her asthma treatment. She have mild persistent asthma taking fluticason 250mcg bid

  • She is worry about her baby as she was told that steroids is not good during pregnancy.

  • What will be your advice


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