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2. Asthma is a major cause of impaired
quality of life with impact on work
and recreational, as well as physical
activities, and emotions.

3. "a chronic inflammatory disorder of the
airways” caused by reversible airways
obstruction.
3

4. • Inflammatory airways disorder involving mast
cells, eosinophils, PMN’s, epithelial cells, macrophages and T
cells.
• This inflammation leads to clinical sequelae of episodic
bronchospasm (wheezing), breathlessness, chest tightness
and cough.
• Episodes are usually associated with variable airflow
obstruction that is reversible.

5. is "a chronic inflammatory disorder of the airways in
which many cells and cellular elements play a role.
The chronic inflammation is associated with airway
responsiveness that leads to recurrent episodes of
wheezing, breathlessness, chest tightness, and
coughing, particularly at night or in the early
morning. These episodes are usually associated with
widespread, but variably, airflow obstruction within
the lung that is often reversible either
spontaneously or with treatment.

6. 1. Episodic or chronic symptoms of airflow
obstruction: breathlessness, chest
tightness, wheezing, and cough.
2. Complete or partial reversibility of airflow
obstruction, either spontaneously or following
bronchodilator therapy.
3. Symptoms frequently worse at night or in the early
morning.
6

7. 4. Prolonged expiration and diffuse wheezes on physical
examination.
5. Limitation of airflow on pulmonary function testing
or positive bronchoprovocation challenge.

8. 1. Bronchial muscle contraction, triggered by a variety
of stimuli.
2. Mucosal swelling/inflammation, caused by mast cell
and basophil degranulation resulting in the release
of inflammatory mediators.
3. Increased mucus production.

9.  Airflow limitation which is usually reversible
spontaneously or with treatment.
 Airway hyperresponsiveness to a wide range of
stimuli.
 Inflammation of the bronchi with T
lymphocytes, mast cells, eosinophils with
associated plasma exudation, oedema, smooth
muscle hypertrophy, matrix deposition, mucus
plugging and epithelial damage.

10. Airway lumen
Mucous gland narrowing Epithelial
hypertrophy damage
and
hyperplasia
Airway smooth-
Muscle hypertrophy,
hyperplasia, and
bronchoconstriction
Edema
Inflammatory
Inflammatory
cell infiltration
cell
Mucus infiltration
hypersecretion
Vascular
Thickening dilation
of basement
membrane Goblet cell
hyperplasia
10

11. GENDER:
• From childhood till 20 : more in male.
• From 20 till 40 : approximately equal.
• After 40 : more in females.

12. Explanations :
• greater prevalence of atopy in
young boys.
• smaller airway size in young boys
compared to girls.

13. Classification:
Asthma is a complex disorder of the conducting
airways that most simply can be classified as:
■ extrinsic – implying a definite external cause.
■ intrinsic – when no causative agent can be
identified.

14. Extrinsic asthma:
1) Occurs most frequently in atopic individuals
who show positive skin-prick reactions to
common inhalant allergens such as dust
mite, animal danders, pollens and fungi.
2) Positive skin-prick tests to inhalant allergens
are shown in 90% of children and 70% of adults
with persistent asthma.
14

15. 3) Childhood asthma is often accompanied
by eczema (atopic dermatitis).
4) A frequently overlooked cause of late-
onset asthma in adults is sensitization to
chemicals or biological products in the
workplace.

16. Intrinsic asthma:
1) Often starts in middle age (‘late onset’).
2) Nevertheless, many patients with adult-onset
asthma show positive allergen skin tests and
on close questioning give a history of
respiratory symptoms compatible with
childhood asthma.

17. • Non-atopic individuals
may develop asthma in middle age from
extrinsic causes such as sensitization to
occupational, intolerance to nonsteroidal anti-
inflammatory drugs (NSAID’S) such as aspirin or
because they were given β-adrenoceptor-
blocking agents for concurrent HTN or angina
that block the protective effect of endogenous
adrenergic agonists.

18. Extrinsic causes must be
considered in all cases of
asthma and, where
possible, avoided.

19. HISTORY AND PHYSICAL EXAMINATION :
• Asthma may develop at any age
although new-onset asthma is less
frequent in the elderly compared to
other age groups.
• Asthma is diagnosed before the age of
seven years in approximately 75 percent
of cases.

20. • Thus, clinicians treating adolescents and adults will
often encounter patients whose diagnosis of
asthma was made (correctly or incorrectly) years
earlier.
• Many adolescents experience a remission of
childhood asthma symptoms around the time of
puberty, with recurrence several years later.

21. Historical information:
Some patients will report or present with the
classic triad of symptoms:
1) Wheeze (high-pitched whistling sound, usually
upon exhalation).
2) Cough (typically worsening at night).
3) Shortness of breath or difficulty breathing.

22. • "Wheezing" does not have a standard
meaning for patients and may be used by
those without a medical background to
describe a variety of sounds, including
upper airway noises from the nose or
throat.

23. • Cough may be dry or productive
of mucoid or pale yellow sputum
(made discolored by the presence
of eosinophils).

24. • Some describe chest tightness
or a band-like constriction. In
contrast, chest pain is
uncommonly used to describe
the sensation of asthma.

25. • Because the symptoms of asthma are
also seen in a myriad of other
respiratory diseases, it may be difficult
to be certain of the diagnosis of
asthma based upon history alone.

27. 1) Episodic symptoms:
Asthmatic symptoms characteristically come
and go, with a time course of hours to
days, resolving spontaneously with removal
from the triggering stimulus or in response to
anti-asthmatic medications.

28. 2) Characteristic triggers:
Respiratory symptoms triggered by
exercise, cold air, and exposure to allergens
are suggestive of asthma.

29. 3) Personal or family history of atopy:
A strong family history of asthma and
allergies or a personal history of atopic
diseases (specifically, atopic
dermatitis, seasonal allergic rhinitis and
conjunctivitis, or hives) favors a diagnosis of
asthma in a patient with suggestive
symptoms.

30. 4) History of asthmatic symptoms as a
child:
As previously mentioned, recollection of
childhood symptoms of chronic
cough, nocturnal cough in the absence of
respiratory infections, or a childhood
diagnosis of "chronic bronchitis" or "wheezy
bronchitis" favors asthma.

31. Allergens that typically trigger asthma symptoms include:
• Dust, molds, furred animals, cockroaches, and pollens.
• Other irritant-type exposures (eg, cigarette smoke, strong
fumes, changes in weather, airborne chemicals or dusts) are non-
specific and do not favor a diagnosis of asthma over other
respiratory diseases.
• Similarly, viral infections are common triggers for
asthma, although they can trigger exacerbations in other chronic
respiratory conditions as well.

33. historic features lessen the prior probability
of asthma.
• Onset of symptoms after age 50
• Lack of improvement following anti-
asthmatic medications:
• History of cigarette smoking

34. Symptoms:
 Intermittent dyspnoea.
 Wheeze.
 Cough (often nocturnal) and sputum.

35. Ask specifically about?
1. Precipitants?
Cold air, exercise, emotion, allergens (house dust
mite, pollen, animal fur), infection, drugs (eg:
aspirin, NSAID’s, B-blockers).
2. Diurnal variation in symptoms or peak flow?
Marked morning dipping of peak flow is common
and can tip the balance into a serious
attack, despite having normal peak flow at other
times.

36. 3. Exercise?
Quantify the exercise tolerance.
4. Disturbed sleep?
Quantify as nights per week (a sign of severe
asthma).
5. Acid reflux?
This has a known association with asthma.
36

37. 6. Other atopic disease?
Eczema, hay fever, allergy, or family history.
7. The home (especially the bedroom)?
Pets? Carpet? Feather pillows or duvet?
Floor cushions and other soft furnishing?
37

38. 8. Occupation?
If symptoms remit at weekends or
holidays, something at work may be a
trigger. Ask the patient to measure his
peak flow at intervals at work and at home
(at the same time of day) to confirm this.
9. Days per week off work or school?
38

40. • Tachypnoea.
• Audible wheeze.
• Hyperinflated chest.
• Hyperresonant percussion note.
• Diminished air entry.
• Widespread, polyphonic wheeze.
40

41. 1- Widespread, high-pitched, musical
wheezes are characteristic of
asthma, although these findings are not
specific.
2- Wheezes are heard most commonly on
expiration, but can also occur during
inspiration.
41

42. 3- Asthmatic wheezing usually involves
sounds of multiple different
pitches, starting and stopping at
various points in the respiratory cycle
and varying in tone and duration over
time.
42

43. 4- It is different from the monophasic
wheezing of a local bronchial narrowing
(eg, due to an aspirated foreign body or
bronchogenic cancer), which has single
pitch and repeatedly begins and ends at
the same point in each respiratory cycle.
43

44. 5- Transmission of expiratory noises from the
upper airway (eg, larynx, pharynx) can mimic
wheezing and is often described as wheezing
by patients. However, these noises are
typically loudest over the neck and greatly
diminished over the chest.
44

45. 6- A history of intermittent symptoms typical of
asthma (as described above) plus the finding
on physical examination of characteristic
musical wheezing (present in association
with symptoms and absent when symptoms
resolve) strongly point to a diagnosis of
asthma.
45

46. 7- Importantly, the presence or
absence of wheezing on physical
examination is a poor predictor of
the severity of airflow obstruction in
asthma.
46

47. 8- Wheezing may be heard in patients with
mild, moderate, or severe airway
narrowing, while widespread airway
narrowing may be present in individuals
without wheezing.
Thus, the presence of wheezing alerts one to
the likely presence of airway narrowing, but
not its severity.
47

48. Physical findings that suggest severe airflow
obstruction in asthma, include:
1. Tachypnea.
2. Tachycardia.
3. Prolonged expiratory phase of respiration
(decreased I:E ratio).
4. A seated position with use of extended
arms to support the upper chest ("tripod
position").
48

49. 5. Use of the accessory muscles
of breathing
(eg, sternocleidomastoid)
during inspiration.
AND
6. A pulsus paradoxus (greater
than 12 mmHg fall in systolic
blood pressure during
inspiration) are usually found
only during acute asthmatic
attacks.
49

50. • However, these signs are
insensitive manifestations of
severe airflow obstruction; as
their absence does not exclude
the possibility of a severe
asthmatic attack.
50

51. Acute severe asthma:
• The term ‘status asthmaticus’ was defined as
asthma that had failed to resolve with
therapy in 24 hours.
• Although this term is still used occasionally, it
has been mainly discarded and replaced by
‘acute severe asthma’, i.e. severe asthma that
has not been controlled by the patient’s use
of medication.
51

52. Patients with acute severe asthma
typically have:
1- Inability to complete a sentence in one
breath.
2- Respiratory rate ≥ 25 breaths per minute.
3- Tachycardia ≥ 110 beats/min (pulsus
paradoxus, is not useful as it is only present
in 45% of cases)
4- PEFR < 50% of predicted normal or best.
52

53. Features of life-threatening attacks are:
1- A silent chest, cyanosis or feeble respiratory
effort.
2- Exhaustion, confusion or coma.
3- Bradycardia or hypotension.
4- PEFR < 30% of predicted normal or best
(approximately 150 L/min in adults).

54. • 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.
54

55. Features suggesting very severe life-
threatening attacks are:
• A high Paco2 > 6 kPa.
• Severe hypoxaemia Pao2 < 8 kPa despite
treatment with oxygen.
• A low and falling arterial pH.
55

56. 56

57. 1- A pale, swollen nasal lining on otoscopic
examination of the nasal cavities
suggests associated allergic rhinitis.
57

58. 2- Nasal polyps, which appear as
glistening, gray, mucoid masses within the
nasal cavities, should prompt questioning
about concomitant aspirin sensitivity and
chronic sinusitis. Since triad asthma
(asthma, nasal polyps, and aspirin sensitivity)
is uncommon in childhood, the finding of
nasal polyps in an adolescent with similar
respiratory symptoms should lead to
consideration of alternative
diagnoses, specifically cystic fibrosis.
58

59. Nasal polyps in nostril
Nasal polyps appear as fixed, glistening, gray or
white, mucoid masses in the nasal cavities.
59

60. 3- Clubbing is not a feature of asthma; its
presence should direct the clinician
toward alternative diagnoses such as
interstitial lung disease, lung cancer, and
cystic fibrosis.
60

61. PULMONARY FUNCTION TESTING
• Pulmonary function tests are critical tools
in the diagnosis of asthma.
• Measurement of peak expiratory flow rate
and spirometry are the two pulmonary
function tests most often used in the
diagnosis of asthma.

62. Peak expiratory flow rate:
The peak expiratory flow rate (PEFR) is •
measured during a brief, forceful exhalation.
Simple and inexpensive (approximately $20) •
equipment can be used to measure the PEFR;
the patient can be taught to monitor PEFR
routinely at home.

63. • However, the resulting measurements
are highly dependent upon the patient's
expiratory effort and technique.
• Thus, it is important that the clinician
assess the patient's use of the monitor
and effort level and correct any
mistakes.
63

64. • In addition, the patient's peak flow
values may vary depending upon the
particular brand of peak flow meter.
• The PEFR maneuver can be performed
sitting or standing.
64

65. • Proper technique involves taking a
maximally large breath in, putting the
peak flow meter quickly to the mouth
and sealing the lips around the
mouthpiece, and blowing as hard and
fast as possible into the meter.
65

66. • For PEFR, the effort does not need to be
sustained beyond one to two seconds.
• The patient should perform the
maneuver three times and record the
highest of the three measurements.
66

67. • A peak flow
meter is
small, inexpen
sive, and easy
for most
patients to
use.
67

68. • Personal best PEFR:
Peak flow monitoring can be used to establish a
patient's "personal best" peak flow. Each
patient must establish his or her own personal
best PEFR value, ideally by recording
measurements at least twice daily for two
weeks (or more). If possible, this should be done
when the patient is feeling well and free from
asthma symptoms.

69. • The personal best PEFR is used to define
the patient's normal peak flow
range, which is between 80 and 100
percent of the personal best. Readings
below this range indicate airway
narrowing, a change that often occurs
before the onset of symptoms and can
alert the patient to a change in asthma
control.
69

70. • Interpretation of PEFR variability :
There is some variability inherent in measurements of
peak flow. This may be as much as 15 to 20 % with
repeated measurements, even in individuals without
asthma. PEFR results that vary little over time (less than
20 % of the maximal value) argue against the diagnosis
of asthma, particularly if reported symptoms are
associated with unchanging peak flow measurements.
In contrast, peak flow values that repeatedly fall by
more than 20 % when symptoms are present and return
to baseline as symptoms resolve are consistent with
asthma.
70

71. • A single peak flow determination made in the
doctor's office at the time that a patient is
experiencing respiratory symptoms, if reduced from
the normal predicted value, is suggestive of asthma.
However, it is not diagnostic, because a reduced peak
flow is not specific for airflow obstruction and can be
seen with other pulmonary processes. A reduced
peak flow that improves by more than 20 %
approximately 10 minutes after administration of a
quick-acting bronchodilator (eg, inhaled albuterol) is
also confirmatory evidence favoring the diagnosis of
asthma.
71

72. ASTHMA MONITORING RECOMMENDATIONS:
The NAEPP recommend that patients use a peak
flow meter to:
 Regularly monitor lung function and response
to treatment over the short- and long-term.
 Determine the severity of an asthma attack.
 Assess response to treatment during an attack.

73. • Patients should use an
asthma diary to record
their daily peak flow
meter
readings, exposure to
potential asthma
triggers, asthma
medication use, and
asthma symptoms.
73

74. 74

75. HOW TO USE A PEAK FLOW METER:
• PEFR monitoring should be performed on a regular
basis, even when asthma symptoms are not
present.
• PEFR should also be checked if symptoms of
coughing, wheezing, or shortness of breath
develops.
• Patients should demonstrate PEFR measurement
with their healthcare provider to verify that their
technique is accurate.
75

76. Getting the best readings:
Several steps are important to make sure the peak flow
meter records an accurate value:
1. The peak flow meter should read zero or its lowest
reading when not in use.
2. Use the peak flow meter while standing up
straight.
3. Take in as deep a breath as possible.
4. Place the peak flow meter in the mouth, with the
tongue under the mouthpiece.

77. 5. Close the lips tightly around the
mouthpiece.
6. Blow out as hard and fast as possible; do
not throw the head forward while blowing
out.
7. Breathe a few normal breaths and then
repeat the process two more times. Write
down the highest number obtained. Do not
average the numbers.
77

78. • Normal values for men and women are
based upon height and age.
• Normal values for adolescents are
based upon height.
78

79. Limitations of PEFR:
Despite its usefulness, there are several
shortcomings of the PEFR that should be
kept in mind.
79

80. 1. Mild airflow obstruction may be present
when the peak flow remains within the
normal range.
2. Reduced peak flow measurements may be
seen in both obstructive and restrictive
diseases. Spirometry and lung volumes are
necessary to distinguish the two.
80

81. 3. Peak flow measurements are not sufficient to
distinguish upper airway obstruction (eg, vocal cord
dysfunction) from asthma. Spirometry is needed for
this.
4. The validity of PEFR measurements depends entirely
upon patient effort and technique. Errors in
performing the test frequently lead to
underestimation of true values, and occasionally to
overestimation.
81

82. 5. Home PEFR monitoring is
unsupervised. Patients may produce
higher values with appropriate
coaching.
6. Peak flow meters cannot be routinely
calibrated, unlike spirometers.
Thus, results will vary somewhat
among different instruments.
82

83. A zone scheme
similar to a
traffic
light
system be
used to illustrate a
plan upon which
patients can base
self-management
decisions.
83

84. • GREEN (80 to 100 % of personal
best) signals "all clear". When
readings are within this range
and symptoms are not
present, the patient is advised
to adhere to his or her regular
maintenance regimen.
84

85. • YELLOW (50 to 80 % of personal best)
signals "caution", since the airways are
somewhat obstructed. The patient should
implement the treatment plan decided
upon with the clinician to reverse airway
narrowing and regain control. The wide
range represented by the yellow zone can
be subdivided above and below the 65
percent level if desired.
85

86. • RED (below 50 % of personal best)
signals "medical alert". Bronchodilator
therapy should be started
immediately, and the clinician should
be contacted if PEFR measures do not
return immediately to the yellow or
green zones.
86

87. Spirometry:
• Spirometry, which includes measurement
of forced expiratory volume in one
second (FEV1) and forced vital capacity
(FVC), provides additional information
that is useful in the diagnosis of asthma.
• Spirometry can be completed in 10 to 15
minutes with no risk to the patient.

88. 88

89. The results of spirometry can be used to
determine the following:
1. Distinguish normal from abnormal lung
function.
2. Categorize abnormalities into obstructive or
restrictive patterns.
3. Characterize the severity of the abnormality.
4. Assess the reversibility of the obstructive
abnormality if the testing is repeated after
administration of a bronchodilator.

90. • The forced vital capacity (FVC), which is
the total volume of air exhaled.
• The FEV1, which is the volume exhaled in
the first second of expiration.
• The ratio of FEV1 to FVC, or FEV1/FVC
ratio.
90

91. Bronchodilator response (baseline spirometry):
• Administer bronchodilator (at least 400mcg
salbutamol or bricanyl, e.g. 4 puffs using a
spacer device e.g. volumatic spacer or 5mg
by nebuliser). Then perform spirometry again
after 15 minutes. An increase in FEV1 of
>12% and >200mls suggests significant
reversible airflow obstruction) with 95 %
certainty.
• A steroid trial (30 - 40mg prednisolone daily
for 2 weeks or 1,000 μg of inhaled
corticosteroid for three months) may also be
appropriate to assess bronchodilator
reversibility if asthma is still suspected.

92. • Having identified the presence of airflow
obstruction by a reduction in FEV1/FVC, the
severity of airflow obstruction is then
categorized by the degree of reduction of the
FEV1 below normal and is graded as
mild, moderate, severe, and very severe
according to the following categories.
(Note: these are categories used for pulmonary
function interpretation and are NOT the same as
categories used to stage asthma severity):
92

93. • FEV1 80 to 99 % : mild obstruction.
• FEV1 51 to 79 % : moderate obstruction.
• FEV1 36 to 50 % : severe obstruction.
• FEV1 less than 35 % : very severe
obstruction.
93

94. Flow-volume curves in obstructive and restrictive
lung disease
Sample flow-volume curves during a maximal forced expiration in normals and
in obstructive and restrictive lung disease. The normal expiratory portion of
the flow volume curve is characterized by a rapid rise to the peak flow
rate, followed by a nearly linear fall in flow as the patient exhales toward
residual volume. With obstructive disease, maximal expiration begins and ends
at higher lung volumes and lower flow rates than normal. With restrictive
disease, the lung volumes and flow rates are reduced but the flow in relation
to lung volume is actually higher than normal.
94

95. • Bronchoprovocation testing.
• Exhaled nitric oxide.
95

96. OTHER LABORATORY TESTS
Other laboratory
studies, including chest
radiography, blood tests, and
tests for allergy, are sometimes
useful in the diagnosis of
asthma.
96

97. Chest radiography:
• The chest radiograph is almost always normal
in patients with asthma.
• Many clinicians favor obtaining a chest
radiograph for new-onset asthma in the
adult, for the purpose of excluding the
occasional alternative diagnosis (eg, the
mediastinal mass with tracheal compression or
congestive heart failure).
97

98.  In contrast, CXR is definitely recommended in the
evaluation of severe or "difficult-to-control"
asthma, for the detection of co-morbid conditions
(eg, ABPA, eosinophilic pneumonia, or atelectasis
due to mucus plugging).
 In addition, CXR is indicated in patients presenting
with features that are atypical for asthma, including
any of the following:
98

99. • Fever.
• Chronic purulent sputum production.
• Localized wheezing.
• Hemoptysis.
• Weight loss.
• Clubbing.
• Inspiratory crackles.
• Significant hypoxemia.
• Airflow obstruction that does not reverse
with bronchodilators.
99

100. Blood tests:
• No blood tests are available that assess the
presence or absence of asthma or gauge its
severity. However, a complete blood count
(CBC) with differential white blood cell
analysis to screen for eosinophilia or
significant anemia may be helpful in certain
cases.
100

101. • An elevated eosinophil percentage by
automated cell sorter is best confirmed by
manual differential (to exclude erroneous
classification of neutrophils as eosinophils).
Markedly elevated eosinophil percentages
(>15 percent) should prompt consideration of
alternative diagnoses, including parasitic
infections (eg, Strongyloides), drug
reactions, and syndromes of pulmonary
infiltrates with eosinophilia.

102. • Significant anemia can cause dyspnea that is
unresponsive to asthma therapies and would
require further evaluation to determine the
causative process.
• A one-time measurement of the serum
alpha-1 antitrypsin level is recommended in
the lifelong non-smoker with persistent and
irreversible airflow obstruction, to exclude
emphysema due to alpha-1 antitrypsin
deficiency.
102

103. 103