OS 216

Bronchial Asthma Trans 09B Exam # 2

Jenifer R. Otadoy-Agustin, MD, FPCP, DPSAAI
01/21/2019

OUTLINE II. WHAT IS ASTHMA?

I. Burden of asthma A. DEFINITION OF ASTHMA
II. What is asthma? • Asthma is a heterogenous disease usually characterized by
III. How is asthma diagnosed? chronic airway inflammation.
IV. How do we assess and control severity? • It is defined by the history of respiratory symptoms such as
V. What are the treatment options? wheeze, shortness of breath, chest tightness and cough that vary
VI. Asthma flare-ups (exacerbations) over time and in intensity, together with variable expiratory
VII. Primary Prevention airflow limitation (GINA, 2017).
Heavily lifted from 2021 trans.
Asthma is characterized by chronic airway inflammation,
I. BURDEN OF ASTHMA respiratory symptoms (cough, wheeze, shortness of breath,
• Asthma is a common chronic disease that affects more than and chest tightness), and a variable expiratory airflow
300M individuals worldwide. limitation.
• Increasing prevalence
• Major cause of school and work absence B. PATHOGENESIS OF ASTHMA
• Health care expenditure on asthma is very high

1. What is the prevalence of adult asthma in the Philippines?

A. <10% B. 10-15% C. 15-20% D. >20%
Answer: C

2. True or False: Asthma is a common and potentially serious

chronic disease that can be cured.
Answer: False. Asthma cannot be cured

A. WHAT IS KNOWN ABOUT ASTHMA?

• Asthma is a common and potentially serious chronic disease
that imposes a substantial burden on patients, their families and
the community.
• Asthma can be controlled but not cured.
• It causes respiratory symptoms, limitation of activity, and flare-ups
(attacks) that sometimes require urgent health care and may be
fatal.
• Asthma causes respiratory symptoms that vary over time in
their occurrence, frequency and intensity Figure 1.The interplay of genetic and environmental factors is crucial in the
o cough development of asthma. Concomitant respiratory infections that target the
lower airway increase an individual’s risk to develop asthma.
o wheezing
o shortness of breath
o chest tightness
• Symptoms are associated with variable expiratory airflow, i.e.,
difficulty breathing air out of the lungs due to:
o Bronchoconstriction (airway narrowing)
o Airway wall thickening
o Increased mucus
• Symptoms may be triggered or worsened by factors such as:
o viral infections
o allergens
o tobacco smoke
o exercise
o stress
• Asthma can be effectively treated
• When asthma is well-controlled, patients can:
o Avoid troublesome symptoms during the day and night
o Need little or no reliever medication
o Have productive, physically active lives
o Have normal or near-normal lung function
o Avoid serious asthma flare-ups (also called exacerbations, or
severe attacks) (GINA, 2017)

Figure 2. Pathogenesis of asthma. Dendritic cell presents antigen to Th0.

Th0 differentiates into Th2 and causes a Th2 response. Inflammatory
mediators are released, leading to bronchial hyperresponsiveness and
airway obstruction.

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C. PATHOPHYSIOLOGY OF ASTHMA

Figure 3. Pathophysiology of asthma. Structural alteration is caused by

accumulation of inflammatory cells, deposition of ECM proteins, thickening,
leading to epithelial damage. Epithelial damage, increased muscle mass
(through cellular hypertrophy and hyperplasia), and angiogenesis (due to
VEGF) lead to airway remodeling. Release of inflammatory mediators and
increased mucus secretion lead to edema, which causes airway narrowing.
Figure 5. Histology of a normal bronchiole vs. a bronchiole of an asthmatic
patient. Notice that there is an evident decrease in lumen size because of
subeptithelial membrane thickening, airway smooth muscle hyperplasia, and
angiogenesis. Increased mucus production also contributes to
bronchoconstriction. (BV – blood vessel, Ep – epithelium, Sm – smooth
muscle, Bm – basement membrane)

III. HOW IS ASTHMA DIAGNOSED?

• Diagnosis of asthma is based on identifying both a history of a
characteristic pattern of respiratory symptoms (wheezing,
dyspnea, chest tightness, and cough) and evidence of variable
expiratory airflow limitation (from bronchodilator reversibility
testing or other tests).
• Document evidence for the diagnosis in the patient’s notes,
preferably before starting controller treatmen
It is often more difficult to confirm the diagnosis after treatment
has been started
• Asthma is usually characterized by airway inflammation and
airway hyperresponsiveness, but these are not necessary or
sufficient to make the diagnosis of asthma.
• See Appendix A for the diagnosis of asthma flowchart

A. RESPIRATORY PATTERNS
SYMPTOMS THAT INCREASE PROBABILITY OF
ASTHMA
• Increasedprobability that symptoms are due to asthma if:
o More than one type of symptom (wheeze, shortness of breath,
cough, chest tightness)
o Worse at night or in the early morning
o Vary over time and in intensity
o Triggered by viral infections, exercise, allergen exposure,
changes in weather, laughter, irritants such as car exhaust
fumes, smoke, or strong smells

SYMPTOMS THAT DECREASE PROBABILITY OF

ASTHMA
• Decreased probability that symptoms are due to asthma if:
o Isolated cough with no other respiratory symptoms
Figure 4. Airway remodeling in asthma. Mast cells degranulate upon contact o Chronic production of sputum
of allergen with the surface IgE. This releases inflammatory mediators, o Shortness of breath associated with dizziness, light-
leading to stimulation of the Th2 response, recruitment of leukocytes, headedness or peripheral tingling
macrophages, and eosinophils. This causes airway damage/inflammation o Chest pain
(chronic phase). Chronic inflammation leads to mucus gland hyperplasia, o Exercise-induced dyspnea with noisy inspiration (stridor)
collagen deposition, smooth muscle hyperplasia and hypertrophy (remodeling
phase).

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PHYSICAL EXAMINATION
• The PE findings in asthmatic patients are usually normal,
however, in exacerbations, wheezing may be present on
auscultation, especially on forced expiration (most common
symptom)
• It should be noted that wheezing could also be found in other
conditions:
o respiratory infections
o COPD
o upper airway dysfunction
o endobronchial obstruction
o aspirated foreign body
• Wheezing may also be absent during severe asthma
exacerbations (‘silent chest’)

Case 1
55/F Non-smoker
Cough x 3 weeks (+) HTN, DM2, enalapril 6 months
Awakens her at night (-) rhinitis symptoms
Difficulty sleeping Normal CXR, PFTs (normal)
Figure 7. Typical spirometric tracings. FEV1 is lower than normal in asthmatic
(-) shortness of breath
patients but this increases upon administration of a bronchodilator.
(-) exertion

3. Is this Asthma? No • Asthma is characterized by variable expiratory airflow limitation

4. What is the diagnosis? Most common etiologies of chronic cough wherein lung function may vary between completely normal and
are upper airway cough syndrome, asthma, and GERD severely obstructed in the same patient.
• Poorly controlled asthma is associated with greater variability in
lung function than well-controlled asthma.
• Airflow limitation could be assessed through a spirometer or a
peak flow meter if a spirometer is unavailable.
• Airflow limitation can be confirmed through the measurement of
FEV1/FVC:
o Healthy adults: >0.75 – 0.80
o Children: >0.90 in children

Table 1. Sample spirometry results.

PRE %PRED POST %CHg
FVC 4.59 97 4.53 -1
FEV1 3.85 93 4 4
FEV1% 83.9 96 88.3 5

• Variability refers to improvement or deterioration in symptoms and

lung function.
• This could be identified over the course of one day (diurnal
variability), day to day, visit to visit or through a reversibility test
using a rapid acting bronchodilator.
• Excessive bronchodilator reversibility:
Figure 6. Asthma differentials in pediatric vs adult patients. Infections are o Adults: increase in FEV1>12% and >200mL
common differentials. o Children: increase >12% predicted
• Excessive diurnal variability from 1-2 weeks twice-daily PEF
B. VARIABLE EXPIRATORY AIRFLOW LIMITATION monitoring (daily amplitude x 100/daily mean, averaged)
• Significant increase in FEV1 or PEF after 4 weeks of controller
Case 2 treatment
30/F Similar episodes over • Referring to Table 1, is the patient asthmatic or not?
Dyspnea the last 2 yrs o FEV1/FVC = 3.85/4.59 = 83.88%
Chest tightness ~2x/month ♦ No airflow limitation, therefore the patient is not asthmatic,
Cough with clear sputum Trigger: Exercise assuming that the patient is an adult
Frequent runny nose More frequent last December o Bronchodlator reversibility = (4-3.85)/3.85 = 0.04 = 4%
History of eczema (-) medications • Conform variation in lung function: depends on increase 12% or
This is her first consult (-) smoking, alcohol 200 mL increase from pre to post bronchodilator
PE findings:
Bilateral wheezes on forced expiration
T: 36.6 C, HR: 86, RR: 18/min, BP: 120/80

5. Is this asthma? It may be asthma (dyspnea, chest tightness,

and cough)
6. Are the Hx and PE enough to diagnose asthma?
No; variable airflow limitation needs to be demonstrated.

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• Assess asthma severity is assessed after patient has been on

controller treatment for several months.
• Severity is not static – it may change over months or years or as
different treatments become available.

Figure 8. Reversibility test using a rapid acting bronchodilator.

Reversible is significant if >12%. Figure 10. Asthma severity and treatment (See Appendix B for clearer
picture). Steps 1 & 2 = mild. Step 3 = moderate asthma (Low dose ICS +
LABA). Steps 4 & 5 = severe.
IV. HOW DO WE ASSESS CONTROL AND SEVERITY?
A. ASTHMA CONTROL
V. WHAT ARE THE TREATMENT OPTIONS?
• Two domains:
A. GOALS OF TREATMENT
1. Symptom control over the last 4 weeks
• The long-term goals of asthma management are:
2. Risk factors for poor outcomes, including low lung function
o Symptom control: to achieve good control of symptoms and
maintain normal activity levels
Case 3 o Risk reduction: to minimize future risk of exacerbations, fixed
20/F comes home from college dorm airflow limitation and medication side-effects
Compliant with her long term medications and denies night time
• Achieving these goals requires a partnership between patient and
symptoms
their health care providers
Doing well and only having asthma symptoms if she forgets her
o Ask the patient about their own goals regarding their asthma
medications prior to work out. o Good communication strategies are essential
Using salbutamol 3-4x/week, but not requiring rescue medications o Consider the health care system, medication availability,
No emergency room visits or prednisone therapy
exercise
included
cultural and personal preferences and health literacy

WE
7. What is the level of her asthma control? Partly controlled;
Uses a reliever: salbutamol (a short-acting β-agonist) 3-4x/week
not B. ASTHMA TREATMENT OPTIONS
• Patient Education (always indicated)
• Allergen Avoidance (when indicated)
• Pharmacotherapy
• Immunotherapy
• Non-pharmacologic Interventions:
o Avoidance of tobacco smoke exposure
o Physical activity
o Occupational asthma
o Avoid medications that worsen asthma
o Remediation of dampness or mold in homes
Figure 9. GINA 2017 assessment of symptom control. Note that this excludes o Allergy work up
reliever taken before exercise, because many people take this routinely • Patient-MD partnership
(rescue medications).
C. THE CONTOL-BASED ASTHMA MANAGEMENT
B. ASSESSMENT OF RISK FACTORS FOR POOR CYCLE
ASTHMA OUTCOMES
• Independent (of the level of symptom control) risk factors for poor
asthma outcomes
o Ever intubated for asthma
o Uncontrolled asthma symptoms
o Having ≥1 exacerbation in last 12 months
o Low FEV1 (measure lung function at start of treatment, at 3-6
months to assess personal best, and periodically thereafter)
o Incorrect inhaler technique and/or poor adherence
o Smoking
o Elevated FeNO in adults with allergic asthma
o Obesity, pregnancy, blood eosinophilia

C. ASTHMA SEVERITY
• Asthma severity is assessed retrospectively from the level of
treatment required to control symptoms and exacerbations Figure 11. The control-based asthma management cycle. Asthma treatment
is a continuous cycle: assess, adjust treatment, and review response.

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D. ASTHMA SEVERITY AND TREATMENT (GINA, 2017) Reliever: Short-acting β-agonist (SABA)
STEP 1: AS NEEDED INHALED SHORT-ACTING β2 • A reliever (used for acute exacerbations)
AGONIST (SABA) • Drug of choice for treatment of acute asthma exacerbations and
Initial controller treatment for adults, adolescents and episodes: effective in 15 min, until 4-6 hrs
children 6-11 years • Examples: Salbutamol (aka Albuterol in the US), Levalbuterol,
• Controller medications - used daily for maintenance treatment Terbutaline, Fenoterol
• Start controller treatment early
o For best outcomes, initiate controller treatment as early as STEP 3: ONE OF TWO CONTROLLERS + AS-NEEDED
possible after making the diagnosis of asthma INHALED RELIEVERS
• Indications for regular low-dose inhaled corticosteroid (ICS): Controllers (choose only 1)
o Asthma symptoms more than twice a month • Low dose ICS/LABA
o Waking due to asthma more than once a month o Ex: fluticasone propionate/salmeterol xinafoate (Seretide)
o Any asthma symptoms plus any risk factors for exacerbations • Medium/high dose ICS + LTRA (or + theophylline)
• Consider starting at a higher step if: • Formoterol is a controller and a reliever
o Troublesome asthma symptoms on most days
o Waking from asthma once or more a week, especially if any Reliever: Short-acting β-agonist (SABA)
risk factors for exacerbations
• SABA
• If initial asthma presentation is with an exacerbation:
• Low dose ICS/formoterol
o Give a short course of oral steroids and start regular controller
o Used as both maintenance and reliever
treatment (e.g. high dose ICS or medium dose ICS/LABA, then
o Ex: budesonide/formoterol fumarate dehydrate (Symbicort)
step down)
STEP 4: TWO OR MORE CONTROLLERS + AS-NEEDED
Low, Medium, and High dose inhaled corticosteroids for INHALED RELIEVER
adults and adolescents (≥12 years) Controllers (choose 2 or more)
• Medium/high ICS/LABA – added to decrease requirement for
steroids: less adverse reactions
• Add tiotropium
• High dose ICS + LTRA (or + theophylline)

Reliever
• SABA
• Low dose ICS/formoterol
o Used as both maintenance and reliever

STEP 5: HIGHER LEVEL CARE AND/OR ADD-ON

TREATMENT
• Anti-IgE (omalizumab)
• Anti IL-5 (SC mepolizumab or IV reslizumab)

Figure 12. Low, medim and high dose corticosteroids for adults and
adolescents (≥12 years). MUST MEMORIZE ACCORDING TO MA’AM para
Omalizumab
daw alam kung ano yung low, medium, and high doses. Budesonide,
Beclometasone, and Fluticasone are available in the Philippines. CFC –
cholorofluorocarbon, HFA – hydrofluoroalkane. Smaller particles at a smaller
dose are able to go into the airway so low amount is needed to achieve the
dose.

STEP 2: LOW-DOSE CONTROLLER + AS-NEEDED

INHALED SABA
Controllers (choose only 1)
• Inhaled corticosteroids (ICS)
o First line controller medications for asthma
o Most potent and most effective Figure 13. Omalizumab prevents the binding of the allergen to the IgE, thus
o Ex: Fluticasone (Flixotide) inhibiting the release of allergic reaction mediatora (histamine and
o Refer to Figure 10 for the doses leukotrienes), ultimately inhibiting inflammation and constriction of the
• Leukotriene receptor antagonists (LTRA) airways. Bound IgE cannot complex with mast cells preventing
degranulation and resulting into decreased in symptoms.
o Alternative controller
o May be used for Pxs with both asthma and allergic rhinitis
o Ex: Montelukast
• Theophylline
o Another alternative controller
o Less effective than ICS

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Figure 17. Proper use of dry turbo inhalers.

Figure 14. Omalizumab binds to circulating IgE, decreasing cell-bound IgE

and downregulates the expression og high affinity receptors. Thus, there is
decreased tissue infiltration of eosinophils and decreased mediator release.
There is decreased asthma symptoms and exacerbations.

D. REVIEWING RESPONSE AND ADJUSTING

TREATMENT
• How often should asthma be reviewed?
o 1-3 mos after treatment started, then every 3-12 mos
o During pregnancy, every 4-6 weeks
o After an exacerbation, within 1 week
• Stepping up asthma treatment
o Sustained step-up, for at least 2-3 months if asthma poorly
controlled
§ Important: first check for common causes (symptoms not
due to asthma, incorrect inhaler technique, poor adherence)
o Short-term step-up, for 1-2 weeks, e.g. with viral infection or
allergen Figure 18. Provide hands-on inhaler training.
§ May be initiated by patient with written asthma action plan
• Stepping down asthma treatment VI. ASTHMA FLARE-UPS (EXACERBATIONS)
o Consider step-down after good control maintained for 3 A. MANAGEMENT OF WORSENING ASTHMA AS A
months CONTINUUM
o Find each patient’s minimum effective dose, that controls both • Self-management within a written asthma action plan
symptoms and exacerbations • Management in primary care
• Asthma action plan & asthma control zone (Appendix C & D) • Management in the emergency department and hospital
• Proper use of inhalers • Follow-up after any exacerbation

B. WRITTEN ASTHMA ACTION PLANS (APPENDIX E)

C. IDENTIFY PATIENTS AT RISK OF ASTHMA-RELATED

DEATH
• Patients at increased risk of asthma-related death should be
identified
o Any history of near-fatal asthma requiring intubation and
ventilation
o Hospitalization or emergency care for asthma in last 12
Figure 15. Proper use of metared dose inhalers. months
o Not currently using ICS, or poor adherence with ICS
o Currently using or recently stopped using OCS
♦ (indicating the severity of recent events)
o Over-use of SABAs, especially if more than 1 canister/month
o Lack of a written asthma action plan
o History of psychiatric disease or psychosocial problems
o Confirmed food allergy in a patient with asthma
• Flag these patients for more frequent review
Figure 16. Proper use of dry powder inhalers.

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D. MANAGING EXACERBATIONS IN PRIMARY OR

ACUTE CARE (APPENDIX F)

E. FOLLOW-UP AFTER AN EXACERBATION

• Follow-up all patients regularly after an exacerbations until
symptoms and lung function return to normal
o Patients are at increased risk during recovery from an
exacerbation
• Exacerbations often represent failures in chronic asthma care and
they provide opportunities to review the patient’s asthma
management
• At follow-up visit(s), check:
o The patient’s understanding of the cause of the flare-up
o Modifiable risk factors, e.g. smoking
o Adherence with medications, and understanding of their
purpose
o Inhaler technique skills
o Written asthma action plan

VII. PRIMARY PREVENTION

• The development and persistence of asthma are driven by gene-
environment interactions
• For children, a ‘window of opportunity’ exists in utero and in early Hoo does volcanic
life, but intervention studies are limited
• For intervention strategies including allergen avoidance ash cause
o Strategies directed at a single allergen have not been effective
o Multifaceted strategies may be effective, but the essential
components have not been identified
asthma
• Current recommendations are
o Avoid exposure to tobacco smoke in pregnancy and early life

IT 40mm particles
o Encourage vaginal delivery
o Advise breast-feeding for its general health benefits
o Where possible, avoid use of paracetamol (acetaminophen)
and broad-spectrum antibiotics in the first year of life
A mucus secretion
REFERENCES bronchoconstr
END OF TRANS 27 irritant gases
Congratulations, UP MRX!!!

Please don’t forget to submit your Shots!

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APPENDIX

APPENDIX A. Flowchart for the diagnosis of asthma

APPENDIX B. Asthma severity and treatment

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APPENDIX C. Prescribing an asthma action plan

APPENDIX D. Assessment of control zone

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APPENDIX E. Written asthma action plans

APPENDIX F. Management of asthma in exacerbation

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