08/2-7, COURSE III: PULMONOLOGY

2012SEM Obstructive Airway Disease

1 ASTHMA
Year 2

I. OVERVIEW  negative skin tests to common allergens and

ASTHMA normal concentrations of IgE
 Syndrome characterized by airflow obstruction  usually show later onset of disease (adult-
due to inflammation in the airways that make onset asthma)
them more responsive to a wide range of  commonly have nasal polyps and is aspirin-
triggers causing: sensitive
o excessive narrowing  reduced  usually have more severe, persistent asthma
airflow  symptomatic wheezing  C. Infections
dyspnea  viral infections common as triggers but it is
 one of the most common chronic diseases still uncertain as an etiology
globally associated with urbanization (in  atypical bacteria i.e. Mycoplasma and
developing countries) Chlamydophilia in severe asthma but
 genetic predisposition is a likely cause for evidence is not very convincing
people affected by asthma D. Genetic Considerations
 can present at any age: peak age of 3 years  Asthma is polygenic
 In childhood, 2:1 male to female ratio; in  Polymorphisms of genes on chromosomes
adulthood sex ratio has equalized 5q including T helper 2 (TH2) cells,
interleukin (IL)-4, IL-5, IL-9 and IL-13 which
II. ETIOLOGY are associated with atopy.
 Interplay between genetic & environmental  Novel genes involved in asthma: ADAM-33,
factors: DPP-10 and GPRA though not yet clear
E. Environmental Factors
Table 1. Risk Factors & Triggers Involved in Asthma.  Interacts greatly with genetic predisposition
Endogenous Environmental Triggers F. Hygiene Hypothesis
Factors Factors  Lack of infections in early childhood preserves
Genetic Indoor Allergens TH2 cell (associated with atopy), whereas
predisposition Allergens exposure to infections and endotoxin results in a
Atopy Outdoor URTI shift towards protective TH1 immune response
allergens G. Diet (needs further studies)
Airway Occupational Exercise &  Increased risk of asthma for patients with diets
hyperresponsiveness sensitizers hyperventilation low in antioxidants i.e. Vit. C and A, magnesium,
Gender Passive Cold air selenium and omega-3 polyunsaturated fats (fish
smoking oil) or high in sodium and omega-6
Ethnicity? Respiratory Sulfur dioxide & polyunsaturates
infections irritant gases  Vitamin D deficiency predispose to the
Obesity? Drugs (ß- development of asthma
blockers,  Obesity, particularly in women, but mechanisms
aspirins) are unknown
Early viral infections? Stress H. Air Pollution
Irritants  Pollutants i.e. sulfur dioxide, ozone, diesel
(household particulates act as triggers though role in the
sprays, paint etiology is still uncertain
fumes) I. Allergens
A. Atopy  Inhaled allergens, i.e. house dust mites, animal
 Due to the genetically determined production dander (particularly cats) are common triggers of
of specific IgE antibody towards environmental asthma symptoms and also implicated in allergic
allergens sensitization
 major risk factor for asthma J. Occupational Exposure
 Asthmatics commonly suffer from other atopic  Chemicals i.e. toluene diisocyanate and trimellitic
diseases, i.e. allergic rhinitis (found in over anhydride may lead to sensitization independent
80% of asthmatic patients) and atopic of atopy
dermatitis (eczema)  Animal allergens in laboratory workers
 allergens are usually proteins that have  Fungal amylase in wheat flour in bakers
protease activity:  Occupational asthma symptoms improve during
o house dust mites (Dermatophagoides weekends and holidays
pteronyssinus) K. Other Factors
o cat & dog fur  Lower maternal age
o cockroaches  Duration of breast-feeding
o grass & tree pollens  Prematurity and low birthweight
o rodents  Inactivity
o Unlikely to contribute to the recent global
B. Intrinsic Asthma increase in asthma prevalence
 or nonatopic asthma  Acetaminophen consumption in childhood but
remains unexplained

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1 ASTHMA
Year 2
III. Pathology
Symptoms and Signs(Pathophysiology of Disease 6th
Edition)
The variability of symptoms and signs is an indication of
the tremendous range of disease severity, from mild and
intermittent disease to chronic, severe, and sometimes
fatal asthma.
1. Cough—Cough results from the combination of
airway narrowing, mucus hypersecretion, and the
neural afferent hyperresponsiveness seen with
airway inflammation. It can also be a
consequence of nonspecific inflammation after
superimposed infections, particularly viral, in
asthmatic patients. By virtue of the compressive
narrowing and high velocity of airflow in central
airways, cough provides sufficient shear and
propulsive force to clear collected mucus and
retained particles from narrowed airways.
2. Wheezing—Smooth muscle contraction,
together with mucus hypersecretion and
retention, results in airway caliber reduction and
prolonged turbulent airflow, producing
auscultatory and audible wheezing. The intensity
of wheezing does not correlate well with the
severity of airway narrowing; as an example, with
extreme airway obstruction, airflow may be so
reduced that wheezing is barely detectable if at
all.
3. Dyspnea and chest tightness—The
sensations of dyspnea and chest tightness are
the result of a number of concerted physiologic
changes. The greater muscular effort required to
overcome increased airway resistance is
detected by spindle stretch receptors, principally
of intercostal muscles and the chest wall.
Hyperinflation from airway obstruction results in
thoracic distention. Lung compliance falls, and
the work of breathing increases, also detected by
chest wall sensory nerves and manifested as
chest tightness and dyspnea. As obstruction
worsens, increased / mismatching produces
hypoxemia. Rising arterial CO2 tension and, later,
evolving arterial hypoxemia (each alone or
together as synergistic stimuli) will stimulate
respiratory drive through the peripheral and
central chemoreceptors. This stimulus in the
setting of respiratory muscle fatigue produces
progressive dyspnea.
4. Tachypnea and tachycardia—Tachypnea and
tachycardia may be absent in mild disease but
are virtually universal in acute exacerbations.
Pathology (Pathophysiology of Disease 6th Edition)
5. Pulsus paradoxus—Pulsus paradoxus is a fall
of more than 10 mm Hg in systolic arterial
pressure during inspiration. It appears to occur as
a consequence of lung hyperinflation, with
compromise of left ventricular filling, together with
augmented venous return to the right ventricle
during more vigorous inspiration in severe
obstruction. With increased right ventricular end-
diastolic volume during inspiration, the
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ADZU-SOM II
intraventricular septum is moved to the left,
compromising left ventricular filling and output.
The consequence of this decreased output is a
decrease in systolic pressure during inspiration,
or pulsus paradoxus.
6. Hypoxemia—The presence of increasing /
mismatching with airway obstruction produces
areas of low / ratios, resulting in hypoxemia.
Shunt is unusual in asthma.
7. Hypercapnia and respiratory acidosis—In
mild to moderate asthma, ventilation is normal or
increased, and the arterial PCO2 is either normal
or decreased. In severe attacks, airway
obstruction persists or increases and respiratory
muscle fatigue supervenes, with the evolution of
alveolar hypoventilation and increasing
hypercapnia and respiratory acidosis. It is
important to note that this can occur in the face of
continued tachypnea, which is not equivalent to
alveolar hyperventilation.
8. Obstructive defects by pulmonary function
testing—Patients with mild asthma may have
entirely normal pulmonary function between
exacerbations. During active asthma attacks, all
indices of expiratory airflow are reduced,
including FEV1, FEV1/FVC (FEV1%), and peak
expiratory flow rate (Figure 9–20). FVC is often
also reduced as a result of premature airway
closure before full expiration. Administration of a
bronchodilator results in the improvement of
airflow obstruction. As a consequence of the
airflow obstruction, incomplete emptying of lung
units at end expiration results in acute and
chronic hyperinflation; total lung capacity (TLC),
functional residual capacity (FRC), and residual
volume (RV) can be increased. Pulmonary
diffusing capacity for carbon monoxide (DLCO) is
often increased as a consequence of the
increased lung (and lung capillary blood) volume.
9. Bronchial hyperresponsiveness—Bronchial
provocation testing reveals nonspecific
hyperresponsiveness in virtually all asthmatics,
including those with mild disease and normal
routine pulmonary function testing. Bronchial
hyperresponsiveness is defined as either (1) a
20% decrease in FEV1 in response to a provoking
factor that, at the same intensity, causes less
than a 5% change in a normal individual; or (2) a
20% increase in the FEV1 in response to an
inhaled bronchodilating drug. Methacholine and
histamine are the agents for which standardized
provocation testing has been established. Other
agents have been used to establish specific
exposure sensitivities; examples include sulfur
dioxide and toluene diisocyanate.
 Airway mucosa is thickened, edematous, and
infiltrated with inflammatory cells, principally
lymphocytes, eosinophils, and mast cells.
 Hypertrophied and contracted airway smooth
muscle is seen.
 Bronchial and bronchiolar epithelial cells are
frequently damaged, in part by eosinophil
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products such as major basic protein and
eosinophil chemotactic protein, which are
cytotoxic for epithelium.
 Epithelial injury and death leave portions of the
airway lumen denuded, exposing autonomic and
probably noncholinergic, nonadrenergic afferents
that can mediate airway hyperreactivity.
 Secretory gland hyperplasia and mucus
hypersecretion are seen, with mucus plugging of
airways a prominent finding in severe asthma.
 Even in mildly involved asthmatic airways,
inflammatory cells are found in increased
numbers in the mucosa and submucosa, and
subepithelial myofibroblasts are noted to
proliferate and produce increased interstitial
collagen; this may explain the component of
relatively fixed airway obstruction seen in some
asthmatics.
Pathology(Robbin’s)
Lung overinflation with patchy atelectasis, occlusion of
airways by mucus plugs
Microscopically, edema + inflammatory infiltrate in
bronchial walls with numerous eosinophils. Hypertrophy of
wall musculature.
(+) whorled mucous plugs (Curschmann’s spirals)
(+) crystalloid debris of eosinophil membranes (Charcot-
Leyden Crystals)
IV. Clinical Features
 Characteristic Symptoms
o Wheezing
o Dyspnea
o Coughing (variable – spontaneously
and with therapy)
o Symptoms may be worse at night
o Patients typically awake in the early
morning hours
o Difficulty in filling lungs with air
o Increased mucus production in some,
with typically tenacious mucus that is
difficult to expectorate
o Increased ventilation
o Use of accessory muscles of
ventilation
o Prodromal symptoms may precede
an attack:
 Itching under the chin
 Discomfort between
scapulae
 Inexplicable fear (impending
doom)
V. Diagnosis
A. Lung Function Tests
 Simple spirometry
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o Confirms airflow limitation with
↓FEV1, FEV1/FVC ratio, PEF
 Whole body plethysmography
o ↑ airway resistance, ↑ total lung
capacity and residual volume
o gas diffusion usually normal but there
may be a small increase in gas
transfer in some
B. Airway Responsiveness
 ↑ AHR measured by methacholine or
histamine with calculation of provocative
concentration reduces FEV1 by 20%
(PC20)
 rarely useful but can be used as
differential diagnosis of chronic cough
and in the setting of normal pulmonary
function tests
 occasional exercise testing is done to
demonstrate postexercise
bronchoconstriction
C. Hematologic tests
 Not usually helpful
 Total serum IgE and specific IgE to
inhaled allergens may be measured in
some
D. Imaging
 Chest X-ray usually normal but in more
severe patients may show hyperinflated
lungs
o In exacerbations, there may be
evidence of pneumothorax
o Lung shadowing usually
indicates pneumonia or
eosinophilic infiltrates in
patients with
bronchopulmonary aspergillosis
 High resolution CT
o Bronchiectasis in severe
asthma
E. Skin Tests
 Skin prick tests to common inhalant allergens
positive in allergic asthma and negative in
intrinsic asthma
 Not helpful in diagnosis but in persuading patients
to undertake allergen avoidance measures
F. Exhaled Nitric Oxide
 Noninvasive test to measure eosinophilic airway
inflammation
 Typically elevated in asthma
 A test of compliance with therapy
 Useful in demonstrating insufficient anti-
inflammatory therapy
VI. Differential Diagnosis
 Upper airway obstruction by a tumor or
laryngeal edema vs. severe asthma
o R/O asthma if (+) stridor localized in
large airways
o Dx confirmed: flow-volume loop with
↓inspiratory and expiratory flow and
bronchoscopy for site of upper airway
narrowing
 Endobronchial obstruction by a foreign body
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o Persistent wheezing in a specific area (exercise-induced control underlying

of the chest asthma) if taken inflammation
 Left ventricular failure prior to exercise - improve asthma
o (+) wheezing similar to asthma - used in high control and reduce
o (+) basilar crackles, R/O asthma doses by nebulizer exacerbations
 Eosinophilic pneumonias and systemic or via a metered- when added to ICS
vasculitis, i.e. Churg-Strauss syndrome and dose inhaler with - widespread use
polyarteritis nodosa spacer of fixed
o (+) wheezing combination
 COPD inhalers that
o Show less variability, never contain a
completely remit, show much less (or corticosteroid and
no) reversibility to bronchodilators a LABA, proven to
o 10% have features of asthma be highly effective
 ↑ sputum eosinophils and a in asthma control
response to oral
corticosteroids Mortality Increased use of Lack of
 patients have both diseases Risks rescue SABAs concomitant use of
concomitantly reflect poor asthma ICS with LABAs
VII. Treatment control
 Aims:
o Minimal (ideally no) chronic symptoms, o Side Effects:
i.e. nocturnal  Muscle tremors& palpitations,
o Minimal (infrequent) exacerbations usually in the elderly
o No emergency visits  Small fall in plasma potassium
o Minimal (ideally no) use of a required due to ↑ uptake by skeletal
B2-agonist muscle cells
o No limitations on activities, i.e. exercise 2. Anticholinergic Therapy
o Peak expiratory flow circadian variation o Muscarinic receptor antagonists i.e.
<20% ipratropium bromide to prevent
o (Near) normal PEF cholinergic nerve-induced
o Minimal (or no) adverse effects from bronchoconstriction and mucus
medicine secretion
o Much less effective than B2-agonists
A. BRONCHODILATOR THERAPIES since they inhibit only the cholinergic
 act primarily on airway smooth muscle to reverse reflex component of bronchoconstriction
the bronchoconstriction of asthma o Only used as an additional
3 Types (B2-adrenergic agonists, bronchodilator in uncontrolled asthma by
anticholinergics, and theophylline): other inhaled medications
o High doses may be given by nebulizer in
1. B2-Adrenergic Agonists (most effective) severe asthma only following intake of
o Activate B2-adrenergic receptors (widely B2-agonists due to its slower onset of
expressed in airways) by coupling with bronchodilation
G-proteins and adenyl cyclase resulting o Side effects: usually not a problem
to ↑ intracellular cAMP  relaxes since there is little or no systemic
smooth muscle cells & inhibits mast cell absorption; most common is dry mouth;
proliferation in the elderly, urinary retention &
o Mode of action: act as functional glaucoma
antagonists to reverse and prevent 3. Theophylline
contraction of airway smooth-muscle o Widely prescribed as oral bronchodilator
cells in the past since it is inexpensive
o Clinical Use:usually given by inhalation o At present, bronchodilators replaced
to reduce side effects. theophylline for reasons of efficacy and
due to its side effects
Features Short Acting B2 Long Acting B2 o Bronchodilator effect due to inhibition of
Agonists Agonists (LABAs) phosphodiesterases in airway smooth-
(SABAs) muscle cells increasing cAMP but has
Examples albuterol Salmeterol side effects
terbutaline formoterol o At lower doses, has anti-inflammatory
Duration of 3-6 hrs 12 hrs effects by activating histone
action deacetylase-2
Features - rapid onset of - given twice daily o Clinical Use: oral theophylline given as
bronchodilation - should be given a slow-release preparation 1x or 2x daily
- useful in with ICS therapy for a more stable plasma concentration:
preventing EIA since they do not  Additional bronchodilator
(severe asthma) when 10-20
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mg/L plasma concentration are with fewer side effects);

required although associated
with side effects
 Low doses (plasma
concentration: 5-10 mg/L) have
additive effects to ICS for
severe asthma
 Withdrawal of theophylline may
cause deterioration in asthma
control
 At low doses, it is well-tolerated
 IV aminophylline (soluble salt of
theophylline) used to treat
severe asthma but largely
replaced by high doses of
inhaled SABAs (more effective,
occasionally used (slow IV
infusion) in patients with severe
exacerbations that are
refractory to SABAs.
o Side Effects (>10 mg/L plasma
concentration): nausea, vomiting,
headaches (due to phosphodiesterase
inhibition); diuresis and palpitations; at
high concentrations: cardiac
arrhythmias, epilectic seizures, death
(due to A1-receptor antagonism)
B. CONTROLLER THERAPIES (Pharmacologic)
(See Table below)

Inhaled Systemic Anti- Cromones Steroid- Anti-IgE Immuno-

Corticosteroids Corticosteroids leukotrienes Sparing therapy
(ICS) Therapies
- most effective -IV hydrocortisone or - montelukast - - to reduce - Omalizumab -use extracts of
anti- methylprednisolone and zafirlukast cromolynsodiu the is a blocking pollen or house
inflammatory for acute severe block cys-LT1 m&nedocromil requirement antibody that dust mites for
agents for asthma (inflammatory sodium inhibit for OCS in neutralizes specific
asthma in any - Oral mediators mast cell and patients with circulating IgE immunotherapy
severity & age Corticosteroids produced by sensory nerve severe without -not very
Mode of action: (OCS)  prednisone mast cells and activation asthma binding to effective and
-↓ or prednisolone 30- eosinophils in - effective in - cell-bound may cause
inflammatory 45mg 1x daily for 5- asthma; a blocking Methotrexate IgE and anaphylaxis
cell numbers & 10 days to treat potent trigger-induced , inhibits IgE- -reduce side
their activation acute exacerbations bronchoconstric asthma i.e. cyclosporine mediated effects by
in airways of asthma, no tor) receptors EIA and A, reactions sublingual
- ↓eosinophils in tapering of dose - less effective allergen- and azathioprine, - ↓ number of dosing
the airways & needed than ICS in sulfur dioxide- gold and IV exacerbations
sputum & Side Effects: controlling induced gamma in severe
numbers of - systemic: truncal asthma & have symptoms globulin but asthma and
activated T obesity, bruising, less effect on - relatively have no long- may improve
lymphocytes & osteoporosis airway have little term benefit asthma
surface mast diabetes, inflammation benefit in the and control
cells ↓AHR in hypertension, gastric but are useful long-term associated -very
chronic ICS ulceration, proximal as an add-on control of with a expensive;
therapy myopathy, therapy in some asthma due to relatively suitable for
- molecular depression, patients their short high risk highly
mechanisms cataracts uncontrolled duration of effects selected
(further reading, - use steroid-sparing with low-dose action (at least patients who
Harrison’s, therapies ICS, although 4x daily by are not
p.2111) less effective inhalation) controlled on
Clinical Use: -In postmenopausal than LABAs -very safe & maximal
- given 1x- women on - given 1x or 2x popular in doses of
2x/day maintenance OCS, daily and are treatment of inhaler
-rapidly improve monitor bone density well tolerated childhood therapy
symptoms & to determine need asthma, - 3-4 month
lung functions for preventive although now trial to show
-effective in treatment with low doses of objective
preventing EIA bisphosphonates or ICS are benefit
& nocturnal & estrogen preferred - given as a
severe - For noncompliant subcutaneous
exacerbations patients, IM injection
- given as first- triamcinolone every 2-4
line therapy for acetonide is used weeks with
persistent but proximal significant
asthma myopathy is a major side effects,
Side Effects: problem with this anaphylaxis
- have minimal therapy. occasionally
systemic effects seen
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Year 2

-local:
hoarseness, oral
candidiasis
-at highest
recommended
doses, some
suppression of
plasma &
urinary cortisol
concentrations
 Alternative Treatments (Nonpharmacologic)
o Hypnosis, acupuncture, chiropraxis,
breathing control, yoga, speleotherapy VIII. Management of Chronic Asthma

 Respiratory failure, intubate & institute

ventilation; may benefit from halothane if
unresponsive to conventional bronchodilators
 Sedatives never given as they depress
ventilation
 Antibiotics not routinely given unless
(+) signs of pneumonia

B. Refractory Asthma

 Difficult to control asthma despite maximal

 Stepwise Therapy
 Mild persistent asthma – ICS 2x/daily, start with
intermediate dose, i.e. 200 ug bid of
beclomethasone dipropionate (BDP)
IX. Asthma Classifications
A. Acute Severe Asthma
 Clinical Features:
 Increasing chest tightness
 Wheezing
 Dyspnea, often not or poorly relieved by
usual reliever inhalers
 In severe exacerbations,
(+) cyanosis, (+) breathless
 PE: ↑ ventilation, hyperinflation, tachycardia,
pulsus paradoxus may be present (rarely
useful),
 marked ↓spirometric values & PEF.
 Arterial blood gases – hypoxemia, ↓PCO2
(hyperventilation); normal or ↑ PCO2
indicates impending respiratory failure
 CXR – not usually informative; may show
pneumonia or pneumothorax
 Treatment:
 High concentration O2 by face mask
 High doses of SABAs either via nebulizer or
metered-dose inhaler with spacer
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inhaled therapy
 2 major patterns: persistent symptoms w/ poor
lung function & normal or near normal function
but w/ intermittent, severe exacerbations
 In severely ill patients w/ impending
respiratory failure, IV B2-agonists, add
inhaled anticholinergic if no satisfactory
response
 In patients who are refractory to inhaled
therapies, slow infusion of aminophylline;
monitor blood levels, esp. when already
treated w/ oral theophylline
 IV magnesium sulfate or by nebulizer +
inhaled B2-agonists are effective & well
tolerated but not routinely recommended
 Impending respiratory failure, prophylactic
intubation
X. Review Questions
1. All of the following statements about asthma are correct
EXCEPT which?
A. its severity remits or exacerbates with or without
therapy
B. It is a disease of airway hyperreactivity
C. It can be triggered by viral infections, exercise or
emotions
D. The presence of wheezing is diagnostic
E. Inhaled symphatomimetics are effective therapy
2. A 15-year-old adolescent who has asthma wakes up in
the middle of the night with an acute asthma attack. He
comes in the emergency room for therapy. On PE, he is
afebrile, has normal RR, but is noted to be wheezing. His
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PEFV is 70% of predicted. Therapy for this adolescent

should include all of the following EXCEPT

A. Aerosolized albuterol every 20 minutes

B. Measurement of oxygen saturation by oximetry
C. Peak flow measurements after albuterol aerosol
D. Prednisone if he fails to respond to aerosolized
albuterol
E. Arterial blood gas analysis

3. Which of the following are derived from eosinophil

membrane proteins diagnostic of bronchial asthma?

A. Bronchial submucosal gland hyperplasia

B. Charcot-Leyden crystals
C. Copious purulent sputum
D. Alpha1 – antitrypsin deficiency

4. The goals of pharmacotherapy for asthma management

are to reduce acute asthma episodes and maintain long-
term control of persistent asthma. Two major groups of
medications are used, one with a directly positive effect on
the other’s efficacy. Whichmedication group affects both
pathophysiologies?

A. Anti-inflammatory drugs
B. Proton-pump inhibitors
C. Bronchodilators
D. H2-blockers

5. A 6-year-old boy presents at your primary care office

with an elevated temperature,bilateral ear pain, and
irritability. He has a history of asthma. What instructions
are quiteimportant for antipyretics and analgesics before
leaving the office?
A. Administer only acetaminophen for fever and
discomfort.
B. Administer twice the recommended dose for the
first 2 days.
C. Administer half the recommended dose for the
first 2 days.
D. Administer only NSAIDs for fever and discomfort.

Answer Key:
1. D. Wheezing can occur in many other diseases not just
asthma.
2. E. Arterial blood gas analysis is indicated if PEFV drops
below 25% of predicted or if his asthma episode does not
respond to therapy and admission to the hospital is
planned.
3. B. Found in sputum of bronchial asthma
4. A. Reducing inflammation also reduces
bronchoconstriction
5. A. In about 25% of clients with asthma, aspirin and other
nonsteroidal anti-inflammatory drugs (NSAIDs) can
precipitate an asthma attack and should be avoided.

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