asthma common disease

1. ASTHMA
Ass. Prof .Dr: MUHAMMED WAHEEB AL,OBAIDY
CONSULTANT CHEST PHYSCIAN.
MEDICAL COLLEGE –UNIVERSITY OF BAGHDAD.2017

2. Objective
• Provide a clear definition of asthma
• Recognise the burden of asthma at a global level
• Recognise the burden of asthma in our country or region
• Describe the pathogenesis of asthma
• Differentiate the pathogeneses of asthma and COPD
• Identify the major host and environmental causes of asthma

3. Objective
• Recognise the key signs and symptoms of asthma
• Differentiate the diagnosis of asthma with that of other major
respiratory diseases, including COPD, bronchiolitis, bronchiectasis
and tuberculosis
• Understand the diagnostic role of spirometry and peak expiratory flow
(PEF) measurements
• Recognise the diagnostic challenges of asthma
• Identify the goals of asthma treatment
• Understand each of the four components of asthma management
• Understand the asthma ‘step up/step down’ treatment sequence
• Assess and manage severe asthma attacks. MUHAMMED WAHEEB 2017
•

4. The Definition
• Asthma is a chronic inflammatory disease of the
airways characterized by hyper-responsiveness of
the tracheo-bronchial tree to a multiplicity of
stimuli.
• Asthma is manifested physiologically by
widespread narrowing of the air passages which
may be reversed spontaneously or in response to
treatment.
• Clinically asthma is manifested by paroxysms of
dyspneoa, cough, & wheezing.
Harrison Text book of Internal Medicine

5. Prevalence of Asthma
• Asthma is a very common disease.
• Current estimates suggest that 300 million people
world-wide suffer from asthma and an additional
100 million may be diagnosed by 2025.
• The prevalence of Asthma is rising in many parts
of the world, e.g. in the USA prevalence increased
from 3-4% to about 10-12% of adults and about
15% of children.
• In the U.K. the prevalence is around 7%
• There are no studies demonstrating the
prevalence of Asthma in Iraq.
GINA Guidelines 2004

6. Prevalence continued
• In the middle east the prevalence is about
5.8%.
• In Kuwait 8.5%, Iran5.5%, Turkey 7.4%, Saudi
Arabia 5.6%.
• Asthma is more common in children, about
half the cases develop before the age of 10
years, another third before the age of 40.
GINA Guidelines 2004

7. Prevalence of clinical asthma
GINA 2014
In this report an arbitrary figure of 50% of the prevalence of ‘current wheezing’ in children (self-reported
wheezing in the previous 12-month period in 13- to 14-year old children) has been used as the prevalence of
"clinical asthma’. The prevalence rates for ‘clinical asthma’ reported in this report represent a conservative
estimate. Data from: International Study of Asthma and Allergies in Childhood (ISAAC) and the European
Community Respiratory Health Survey (ECRHS).

8. Prevalence of asthma
0 2.5 5 7.5 10 12.5 15 17.5
China/Taiwan/Mongolia
South East Asia
South Asia
Central America
North Africa
Central Asia/Pakistan
East Africa
Scandanavia/Baltic
West Africa
Middle East
Japan/Korea
Western Europe
Balkans/Turkey/Caucasus/Mediterranean
Southern Africa
South America
Caribean
North America
Oceania
United Kingdom
%
GINA 2014
In this report an arbitrary figure of 50% of the prevalence of ‘current wheezing’ in children (self-reported
wheezing in the previous 12-month period in 13- to 14-year old children) has been used as the prevalence of
‘clinical asthma’. The prevalence rates for ‘clinical asthma’ reported in this report represent a conservative
estimate. Data from: International Study of Asthma and Allergies in Childhood (ISAAC) and the European
Community Respiratory Health Survey (ECRHS).

9. Etiology of Asthma
• Asthma is a heterogeneous disease with genetic
and environmental factors playing a role.
• Environmental factors include viruses,
occupational exposure and allergens playing a
role in both the initiation and continuation of the
disease.
• Henry Salter in 1860 suggested “distinct traces of
inheritance are seen in 2 cases out of 5.
• Many studies now suggest that first degree
relatives have a 20-25% chance of developing
Asthma.
Harrison Text Book of Internal Medicine

10. Aetiology

11. Classification Of Asthma
1.Allergic Asthma ( atopic)( extrinsic)
It is often associated with a personal family history of
allergic disease + increased level of IgE in serum positive response
to provocation test .
-It is usually early –onset & typically episodic .
2. Idiosyncratic Asthma (non- atopic ) (intrinsic):
3. Many patients have disease not fit clearly
into either of the above ( mixed group).
Harrison Text book of Internal Medicine

12. Pathogenesis Of Asthma
• Asthma results from a state of persistent sub-acute
inflammation of the airways.
• The airways are edematous & infiltrated with
eosinophils( which seems to play an important role),
neutrophils , & lymphocytes .
• Physiologic & clinical features of asthma derive from
an interaction among the resident & infiltrating cells
in the airways.

13. Asthma mechanism- role of inflammatory cells
macrophage
Antigen
phagocytosis B Lymphocytes
Cell to cell contact
Antibodies
Interleukin-1
Growth of specific Lymphocytes
Mast cell
binding
IgE
IgA
IgG
IgD
IgM
•Eosinophils
•Mediators
-Histamine
-PAF
-Leukortriense
-Protaglandins
GINA 2004

14. Mucus
hypersecretion
Hyperplasia
Eosinophil
Mast cell
Allergen
T cell
Vasodilatation
New vessels
Plasma leak
Oedema
Neutrophil
Mucus plug
Macrophage/
dendritic cell
Bronchoconstriction
Hypertrophy / hyperplasia
Cholinergic
reflex
Epithelial shedding
Subepithelial
fibrosis
Sensory nerve
activation
Nerve activation
Inflammation and tissue damage in Asthma
Barnes PJ

15. Major cells are :
Mast cells ; Eosinophils ; Lymphocytes ; & Epithelial cells
Less important cells :
Neutrophils ; macrophages ; basophiles . …..
Each of the major cells types can produce mediators &
Cytokines to initiate & amplify both acute inflammatory &
The long- term effects.

16. Mediators
• Histamine
• Leukotriens
• Prostaglandins
• Thromboxane
• PAF
• Bradykinins
• Tachykinins
• Endothelins and others.

17. Mediators released produce an intense
, immediate inflammatory reaction
involving :
1. Bronchoconstruction
2. Vascular congestion
3. Edema formation
4. Increased mucus production
5. Impaired mucociliary transport.
6. Structural changes ( fibrosis , smooth muscle
hyperplasia , angiogenesis ,mucus hyperplasia)

18. Changes in the airway
Davidson Text book of Internal Medicine

19. Stimuli That Incite Asthma
1.Allergens.
2.Pharmacologic Stimuli.
3.Environment & Air Pollution..
4.Occupational Factors.
5.Infections.
6.Exercise..
7.Emotional.
Coexisting conditions that can aggravate asthma :
1. Rhinitis 2. sinusitis 3. GERD .

20. Allergens
• Most of the allergens that provoke asthma are
airborne.
• Immune mechanisms appear to be causally
related to the development of asthma in 25-35%
of all cases & contributory in ~ another third.
• Important allergen such as house dusts mites, cat's
allergen & pets ,cockroach allergen.
• Smoking increase the risk of asthma by about 4 times.

22. Aspirin-sensitive asthma
• Aspirin & other NSAID can result in asthma
exacerbation in some (~10%) patients , most of such
patients have severe Asthma & nasal polyps. The
affected patients develop rhinorrhea & nasal
congestion .
• They may benefit from leukotriene modifying agents
and other drugs e.g. B- blockers .

23. Exercise –induced Asthma
• Exercise is common precipitant of acute episodes of asthma.
• Typically the attacks follow exertion & do not occur during it.
• Short sprints are more likely to induce the episodes.
• The challenge test consist of a short ( 6-8 min) exercise ,&
Spirometry is checked before & at 0,5,10,15, 20, or 30 minutes
after exercise.
• A 20% decrease in FEV1 confirms the diagnosis.
• Approximately 10% of the athletes on U.S. Olympic teams in
recent years had exercise- induced asthma.
• It dose not evoke any long – term squeal ,nor dose it increase
airway reactivity.

24. Infections
• Respiratory infections are the most common stimuli that
evoke acute exacerbations of asthma.
• Viruses & not bacteria are the major stimuli.
• In children RCV & par influenza virus are most important.
• In older children & adult , rhinovirus & influenza virus are the
commonest .

25. Occupational asthma
• Occupational asthma is the most common form of occupational
respiratory disorders & should be considered in all adult
asthmatics .
• It is especially important from to enquire whether symptoms
improve during time away from work , e.g. Weekends or
holidays .
• Atopic individuals & smokers at high risk .
• The diagnosis can be reached by performing 2- hourly peak flow
recording ; skin prick tests or the measurement of specific IgE
may confirm the diagnosis .
• Bronchial provocative tests with the suspected agent may be
necessary .
• Workplace visit to identify & rectify exposure , & to trigger
screening of other employees.

26. • Workers most commonly reported to occupational
asthma schemes .
* Paint sprays * Bakers & pastry-makers
* Welders * Food processing
* Chemical workers * Animal handlers
* Timber workers * Nurses

27. • Most frequent reported causative agents
*Isocyanates * Flour& grain dust
* Colophony & fluxes * Latex
* Animals * Aldehydes
* Wood dust

28. Nocturnal asthma
• Occurrence of asthma
symptoms at night or
early morning
• Circadian rhythm
• Exposure to triggers at
day time leads to
broncho-spasm at night
• Sleep Apnea?
• Sinusitis ?
• GERD ?
• Increase venous return?

29. Clinical Presentation Of
Asthma
1. Triad of cough + dyspnea + wheezing ( in up to90%)
usually episodic .
2. Dry cough : It may be the sole presentation ( cough-variant
asthma ) , as many as 30-50% in children who complaint from
chronic cough will developed wheeze (75%) in the next 5-7
years & 13% of adult >50 years .
3. Exertional dyspnea.
4. Asymptomatic .
Davidson Text book of Internal Medicine

30. Asthma is a variable disease
Symptoms and use of
reliever medication
Time
Exacerbation
Oral course of
corticosteroids
Effect of inhaled
corticosteroids during
periods of worsening
Exacerbation
GINA 2004

31. DIAGNOSIS OF ASTHMA

32. Clinical features in adults that
influence the probability of asthma
• MORE THAN ONE OF THE FOLLOWING
SYMPTOMS :
Wheeze , breathlessness , chest tightness , & cough ,
particularly if :
* symptoms worse at night early morning
* symptoms in response to exercise ,
allergens & cold air .
* symptoms after taking aspirin or B-blockers.
From BTS 2008

33. Clinical features cont.
• History of atopic disorders .
• Family history of asthma or atopic disorders.
• Widespread wheeze on auscultation .
• Otherwise unexplained low FEV1 or PEF .
• Otherwise unexplained peripheral
eosinophilia .
From BTS 2008

34. Making a diagnosis of
asthma
Compatible clinical history + either or :
• FEV1 >= 15% ( & 200 ml) increase following
bronchodilator trial of corticosteroids .
• > 20% diurnal variation on > 3 days in a week
for 2 weeks on PEF diary .
• FEV1 >= 15 % decrease after 6 min of exercise
----------------------------------------------------------------
GINA accepts an increased FEV1 12%GINA 2004

35. Peak flow(PEFR) measurement
• The fastest flow rate of air
during a forced expiration
• PEFR = 600L/min in healthy
adult male
• = 450L /min in healthy female
& children
• AM-PM variation in healthy
person < 20%
• PEFM, easy to use, repeatable,
inexpensive

36. Importance of long term peak flow
measurements
• To establish diagnosis and
treatment
• To assess severity of an
exacerbation
• To assess response to
treatment
• To evaluate how well
asthma is controlled
• To alert patient to need
for possible change in
treatment

37. Typical Spirometric (FEV1) Tracings
1
Time (sec)
2 3 4 5
FEV1
Volume
Normal Subject
Asthmatic (After Bronchodilator)
Asthmatic (Before Bronchodilator)
Note: Each FEV1 curve represents the highest of three repeat measurements
GINA 2004

38. Increased loss of FEV1 in asthma
Lange P et al, NEJM 1998
No asthma (n = 5480)
Asthma (n = 314)
Age (years)
Height-adjustedFEV1(L)
Male non-smokers
p <0.001
Epidemiology / pathology

39. Measuring Airway Responsiveness
GINA 2004

40. Other Diagnostic methods
Enhanced bronchoconstriction( AHR) to a variety of direct
Or indirect stimuli e.g.
1. Exercise
2. Cold air
3. Dusts , smoke ,& chemicals.
4. Histamine & methacholine ( provocative test).
5. Challenge test using adenosine ( may be more specific).

41. Other investigations:
1. Eosinophilia( sputum or blood)
2. IgE ( total or specific).
3. Skin tests
4. Pulmonary function test ( for Dx & evaluations)
5. CXR
6. ABG.

42. Differential Diagnosis Of
Asthma
COMMON :
1. Acute bronchitis
2. Aspiration( foreign body)
3. Bronchial stenosis
4. Cardiac failure
5. Chronic bronchitis
6. Cystic fibrosis
7. Eosinophilic pneumonias

43. D. Dx ( cont.)
Uncommon :
1. Airway obstruction e.g. external or internal
2. Carcinoid syndrome
3. Pulmonary embolism
4. Systemic vasculitis
5. Endobronchial sarcoid
6. Systemic mastocytosis.

44. What are the deference between
asthma & COPD(Chronic Bronchitis)
ASTHMA COPD
ONSET Mainly childhood mid-late adult life
smoking Usually nonsmoker almost invariably smoker
Chronic cough & sputum Absent Frequent
Dyspnea on effort Variable & reversible constant , poorly
reversible
Nocturnal symptoms Relatively common Uncommon
Airflow limitation Diurnal variability Normal
Response to
bronchodilator
Good poor
Davidson Text book of Internal Medicine

45. Ancillary tests in the D. Dx. between
stable asthma & COPD
TEST ASTHMA COPD
Reversibility to
bronchodilator & /or
corticosteroids
Usually present usually absent
TLV + RV usually normal Increase
DLco normal
AHR might be increase
allergy test Often + often -
CXR usually normal usually abnormal
sputum eosinophilia neutrophilia
Exhaled NO increase usually normal
Davidson Text book of Internal Medicine

46. Management Of Asthma
1. Patients education :
Patients & their parents (children)should be educated for :
1. The nature of the disease
2. the deference between reliever & controller .
3. proper using of the inhaler .
4. the uses of a peak flow meter .
5. about corticosteroids

47. Education changes patient
expectations
Satisfactionwithcontrol(%ofpatients)
Before After
0
10
20
30
40
50
60
70
Being shown GINA guidelines
58%
(n=301)
satisfied
25%
drop
33%
(n=173)
satisfied
Haughney et al. Prim Care Respir J 2004

48. Management cont.
2. Avoidance of precipitating factors:
Desensitization :
There is little evidence of its benefit in asthma ,
& there is attendant risk .
Davidson Text Book of Internal Medicine

49. Classification of Asthma Severity
CLASSIFY SEVERITY
Clinical Features Before Treatment
Symptoms Nighttime
Symptoms PEF
STEP 4
Severe
Persistent
STEP 3
Moderate
Persistent
STEP 2
Mild Persistent
STEP 1
Intermittent
Continuous
Limited physical activity
Daily
Use b2-agents daily
Attacks affect activity
> 1 time a week
but < 1 time a day
< 1 time a week
Asymptomatic and
normal PEF between
attacks
Frequent
>1 time week
>2 times a months
< 2 times a month
< 60% predicted
Variability >30%
> 60% - <80% predicted
Variability >30%
<80% predicted
Variability 20-30%
³ 80% predicted
Variability <20%
The presence of one of the features of severity is sufficient to place a patient in that category.
GINA 2004

50. Management of chronic
Asthma
Step 1 :
In patients with mild to moderate asthma ( occasional use
of inhaled short –acting B2 agonist (ISABA) e.g. salbutamol,
terbutaline
Step 2 :
When the pat. use ISABA more than once daily .
ISABA used as required + regular inhaled steroids (ICS).
e.g. beclomethasone ; budesonide ( up to 800 mcgd) or
fluticasone ( up to 400 mcg d ).
- Or leukotriene modifier .
Davidson’s Text Book of Internal Medicine

51. Management cont.
Step 3:
1-Medium- high dose of ICS ( 800-2000 mcg|d) + ISABA or
2-Low dose of ICS + long – acting B2 – agonist e.g.
salmeterol ; formoterol or
3-Low dose of ICS + leukotriene modifier .
Step 4 :
Like step 3 plus one or more of :
a. Leukotriene receptor antagonist.
b. Inhaled ipratropium bromide or oxitropium.
c. Long –acting oral B2 – agonist .
d. Sodium cromoglycate or nedocromili.
Davidson’s Text Book of Internal Medicine

52. Management cont.
Step 5:
When a patient in exacerbations of asthma .
Short courses of `rescue` oral corticosteroids (30-60mgd
of prednisolone ) often required .
Indications for `rescue` courses include:
1. Symptoms & PEF progressively worsening day by day
2. PEF < 60%
3. Onset or worsening of sleep disturbance.
4. Persistence of morning until midday.
5. Symptoms severe enough to require nebulised or
injected bronchodilators
Davidson’s Text Book of Internal Medicine

53. TREATMENT
Avoid or control triggers
STEP 1: INTERMITTENT
Avoid or control triggers
STEP 2: MILD PERSISTENT
Avoid or control triggers
STEP 3: MODERATE PERSISTENT
Avoid or control triggers
STEP 4: SEVERE PERSISTENT
CONTROLLER: daily medications
• Inhaled steroid
• Or possibly cromone, SR theophylline
or anti-leukotriene
RELIEVER
• Rapid-acting Inhaled
ß2-agents as needed
(max. 3-4 times/day)
CONTROLLER: daily medications
• Inhaled steroid plus long-acting inhaled
ß2-agents
• Consider adding, SR theophylline, ICS at
higher doses or anti-leukotriene
RELIEVER
• Rapid-acting Inhaled
ß2-agents as needed
(max. 3-4 times/day)
RELIEVER
• Rapid-acting Inhaled
ß2-agents as needed
(max. 3-4 times/day)
RELIEVER
• Rapid-acting Inhaled
ß2-agents as needed
(max. 3-4 times/day)
CONTROLLER: daily multiple medications
• Inhaled steroid plus long-acting inhaled ß2-
agents plus either
Oral steroid, SR theophylline or LTRA
CONTROLLER: none
Step up
if not controlled (after
check on inhaler
technique and
compliance)
Step down
when
controlled
•Patient education
essential at every
step
•Reduce therapy if
controlled for at
least
3 months
•Continue
monitoring
GINA 2004

54. GINA 2004

55. Clinical Control of Asthma
No (or minimal)* daytime symptoms
No limitations of activity
No nocturnal symptoms
No (or minimal) need for rescue medication
Close to Normal lung function
No exacerbations
_________
* Minimal = twice or less per week
GINA 2004

56. Deaths and hospital days fell
despite increase in patients
eligible for asthma treatment
Haahtela et al. Thorax 2006
450
400
350
300
250
200
150
100
50
0
Valueoftheindex
Share of asthmatics
Drug cost per patient
Deaths
Number of hospital days
Finnish Asthma Programme 2005

57. Asthma care can be improved
at no additional overall cost
250
200
150
100
50
0
Costs(million€)
1611 €/patient 1031 €/patient
1993 2003
218 million € 213.5 million €
Disability pension
Medication
Hospital days
Doctor visits
25%
10%
37%
28%
43%
21%
20%
16%
Patients are being treated effectively outside the hospital
Haahtela et al. Thorax 2006Finnish Asthma Program 2005

58. Why don’t patients comply with
treatment?
 Difficulties with inhaler devices
 Too complex regimen e.g
multiple doses or multiple drugs
 Side effects
 Cost of medication
 Dislike of medication(taste,
odour or shape)
 Distant health services and
pharmacies
 Misunderstanding or lack of
instructions
 Dissatisfaction with health care
professionals
 Poor supervision, training or
follow-up
 Inappropriate expectations
 underestimation of severity
 Cultural issues
 Fear of addiction
 Attitude toward ill health
 religious issues
Drug factors Non drug factors

59. Management of acute
severe asthma :
Features of acute severe asthma:
1. PEF 33-50 % of predicted ( < 200 l min)
2. Respiratory rate > 25 min
3. Heart rate > 110 min
4. Inability to complete sentences in one breath.

60. Features of Life- threatening
asthma :
1. PEF < 100 Lmin
2. SaO2 < 92% or PaO2 < 8 Kpa ( 60 mmHg )
3. Normal PaCO2
4. Silent chest .
5. Cyanosis
6. Feeble respiratory effort
7. Bradycardia or arrhythmias
8. Hypotension
9. Exhaustion
10. Confusion
11. Coma
Near- fatal Asthma
Raised PaCO2 &or requiring mechanical ventilation
GINA 2004

61. Treatment of acute severe
Asthma
1. Oxygen therapy :
High concentration to maintain SaO2 > 92%
2. Inhaled bronchodilators: (high dose)
a. short- acting B2 –agonist ( metered dose inhaler
through a spacer or nebulizer e.g. salbutamol.
b. Ipratropium bromide ( provide additional effect)
Davidson’s Text Book of Internal Medicine

62. 3. Systemic corticosteroids :
Oral prednisolone 30-60 mg d or I.V. Hydrocortisone 200mg
initially
4. Other :
I.V. Fluids ( if the pat dehydrated )
potassium supplementation
Subsequent management :
1. I.V. magnesium 1.2- 2.0 g 20 min
2. I.V. aminophylline
3. I.V. leukotriene receptor antagonist
Davidson’s Text Book of Internal Medicine

63. Conclusions
• Asthma is common and has a big impact – worldwide
• Impact of asthma can be reduced
• Global asthma severity assessments are unreliable
• Physicians underestimate severity
• Patients overestimate control
• Asthma control instruments have predictive validity
• Poor asthma-control score is associated with:
– Big impact on patient’s life
– Increased exacerbations, admissions, doctor visits

64. Monitoring of the patients
1. PEF every 15-30 min
2. Pulse oximetry
3. Arterial blood gases (ABG)
4. CXR

65. Indications for assisted
ventilation
1. Coma
2. Respiratory arrest
3. Deterioration of ABG
PaO2 < 8 Kpa
Pa CO2 > 6 kpa
low PH
4. Exhaustion ; confusion ; drowsiness

66. Asthma in pregnancy
* Asthma during pregnancy has unpredictable course:
13 improve ; 13 worsen.
* It represents the greater danger to the fetus :
- intrauterine growth restriction & low birth weight.
- preterm birth .
- high perinatal mortality.
- neonatal hypoxia .
• Uncontrolled asthma associated with more maternal :
Hypertension ; hyperemesis ; pre-eclampsia ; vaginal
bleeding ; complicated labour .
Davidson’s Text Book of Internal Medicine

67. Asthma in pregnancy (cont):
Good safety for:
B2- agonist; inhaled steroids; theophyllines;
oral prednisolone & chromones .
Oral leukotriene receptor antagonist should
not be stopped in women have previously
controlled before pregnancy .
Women on prednisolone > 7.5 mg / d should
receive hydrocortisone 100 mg 6-8 h during
labour.
Davidson’s Text Book of Internal Medicine

68. Asthma in pregnancy (cont):
* Prostaglandin F2 alpha may induce
bronchospasm !!
* During breastfeeding medication can be used
normally.
Davidson’s Text Book of Internal Medicine

69. Thank You