Discuss the definition, risk factors and management of BA and COPD

1. BRONCHIAL ASTHMA AND
CHRONIC OBSTRUCTIVE
PULMONARY DISEASE

2. OBJECTIVES
1. Discuss bronchial asthma and COPD, including their
causes, risk factors, and pathophysiology.
2. Describe common symptoms of bronchial asthma and
COPD
3. Discuss triggers and exacerbating factors for both
conditions, such as allergens, irritants, infections, and
smoking.
4. Discuss the management of bronchial asthma and COPD

3. Case scenario
A case of JS, 65/Male from Tacloban City who worked as a
mechanic but already retired. Patient presented to the clinic
complaining of increasing shortness of breath over the past few
months. He also reports a chronic cough with sputum production,
especially in the mornings. He notes that he has been
experiencing more frequent exacerbations lately
(+) hypertension
(+) allergies to dust
(+) smoker of 40 pack years
(+) occasional heartburn

4. Case scenario
Vital Signs: BP 140/90 mmHg, HR 88 bpm, RR 24cpm, O2 saturation
88% on room air
(+) weak looking (+) dyspneic at rest
Chest and lungs: use of accessory respiratory muscles, prolonged
expiratory phase, diffuse wheezing, diminished breath sounds on
auscultation
CVS: regular rate and rhythm, no murmurs or gallops.
Other Systems: No significant findings.

6. BRONCHIAL ASTHMA
-syndrome characterized by airflow obstruction leading to
excessive narrowing with consequent reduced airflow and
symptomatic wheezing and dyspnea
-narrowing of the airways is usually reversible
PREVALENCE: ~10–12% of adults and 15% of children
affected by the disease

8. PATHOLOGY
-AIRWAY INFLAMMATION from
trachea to terminal bronchioles
-AIRWAY REMODELLING may lead
irreversible narrowing of the
airways
-AIRWAY RESPONSIVENESS- the
characteristic physiologic
abnormality of asthma and
describes the excessive
bronchoconstrictor response to
multiple inhaled triggers

9. CLINICAL FEATURES
-wheezing, dyspnea, and coughing
-symptoms worse at night, awaken in the early
morning hours
-inspiratory, and to a greater extent expiratory,
rhonchi throughout the chest, and there may be
hyperinflation

10. DIAGNOSIS
-obstructive symptoms or history of variable respiratory
symptoms
- Evidence of variable expiratory airflow limitation
• FEV1 increases after inhaling a bronchodilator by
>200ml and 12% of the pre-bronchodilator value –
significant bronchodilator responsiveness or
reversibility
• FEV1 increases by > 12% and 200ml from baseline
after 4 weeks of anti-inflammatory treatment

12. TREATMENT
-CONTROLLER MEDICATIONS - used to reduce airway inflammation,
control symptoms, and reduce future risks such as exacerbations and
decline in lung function
-RELIEVER ( RESCUE) MEDICATIONS - as-needed relief of
breakthrough symptoms, including during worsening asthma or
exacerbation, also recommended for short-term prevention of
exercise-induced bronchoconstriction.
-ADD-ON THERAPHIES FOR PATIENTS WITH SEVERE ASTHMA
-considered when patients have persistent symptoms and/or
exacerbations despite optimized treatment with high dose controller
medications (usually a high dose of ICS plus a
LABA)

13. GINA 2023 Pocket guide

14. GINA 2023 Pocket guide

17. ACUTE SEVERE ASTHMA
CLINICAL FEATURE
-increasing chest tightness, wheezing, and dyspnea NOT
OR poorly relieved by reliever inhaler with increased
ventilation, hyperinflation, and tachycardia.
-marked fall in spirometric values and PEF
-ABG : show hypoxemia, and normal or rising pCO2
which is an indication of impending respiratory failure

18. ACUTE SEVERE ASTHMA
TREATMENT
-High Oxygen to achieve o2sats >90%
-Mainstay: high doses of SABA ( nebulizer/MDI)
-Impending respiratory failure: IV B2agonists;
prophylactic intubation
-No sedatives

19. Chronic obstructive pulmonary disease (COPD) is defined as a disease state characterized
by persistent respiratory symptoms and airflow limitation that is not fully reversible
COPD includes:
emphysema, an anatomically defined condition characterized by destruction of the
lung alveoli with air space enlargement;
chronic bronchitis, a clinically defined condition with chronic cough and phlegm;
small airway disease, a condition in which small bronchioles are narrowed and
reduced in number
The classic definition of COPD requires the presence of chronic airflow
obstruction, determined by spirometry, that usually occurs in the setting of noxious
environmental exposures—most commonly cigarette smoking.

20. ■ CIGARETTE SMOKING
 cigarette smoking was a major risk factor for
mortality from chronic bronchitis and
emphysema.
 accelerated decline in FEV1 in a doseresponse
relationship to the intensity of cigarette smoking,
which is typically expressed as pack-years
 the higher prevalence rates of COPD with
increasing age
 Pack-years of cigarette smoking is the most
highly significant predictor of FEV1 but only 15%
of the variability in FEV1 is explained by pack-
years.
■ AIRWAY RESPONSIVENESS AND COPD
 A tendency for increased bronchoconstriction in response to a variety of
exogenous stimuli, including methacholine and histamine, is one of the
defining features of asthma However, many patients with COPD also share
this feature of airway hyperresponsiveness.
 considerable overlap between persons with a history of chronic asthma and
smokers with COPD in terms of airway responsiveness, airflow obstruction,
and pulmonary symptoms.
 Asthmatics with reduced lung function early in life were more likely to meet
spirometric criteria for COPD in early adulthood.
 Patients with features of both asthma and COPD have been described as the
asthma-COPD overlap syndrome.
 Both asthma and airway hyperresponsiveness are risk factors for COPD.
■ RESPIRATORY INFECTIONS
 Respiratory infections are
important causes of COPD
exacerbations
 recent studies have suggested that
childhood pneumonia may lead to
increased risk for COPD later in
life.
■ OCCUPATIONAL EXPOSURES
 Several specific occupational exposures, including
coal mining, gold mining, and cotton textile dust,
have been implicated as risk factors for chronic
airflow obstruction.
 coal mine dust exposure was a significant risk
factor for emphysema in both smokers and
nonsmokers.
■ AMBIENT AIR POLLUTION
 Some investigators have reported increased
respiratory symptoms in those living in urban
compared to rural areas, which may relate to
increased pollution in the urban settings.
 Prolonged exposure to smoke produced by biomass
combustion—a common mode of cooking in some
countries—also appears to be a significant risk
factor for COPD among women in those countries.
■ PASSIVE, OR SECOND-HAND, SMOKING EXPOSURE
 In utero, tobacco smoke exposure also contributes
to significant reductions in postnatal pulmonary
function.
 Although passive smoke exposure has been
associated with reductions in pulmonary function,
the importance of this risk factor in the
development of the severe pulmonary function
reductions often observed in COPD remains
uncertain.
■ GENETIC CONSIDERATIONS
...ἀ1 Antitrypsin Deficiency ...
 The common M allele is associated with normal α1
AT levels.
 The S allele, associated with slightly reduced α1 AT
levels, and
 the Z allele, associated with markedly reduced α1
AT levels
 Null alleles, which lead to the absence of any α1 AT
production through a heterogeneous collection of
mutations.
 Individuals with two Z alleles or one Z and one null
allele are referred to as PiZ, which is the most
common form of severe α1 AT deficiency.
 The clinical laboratory test used most frequently to
screen for α1 AT deficiency is measurement of the
immunologic level of α1 AT in serum

21. PATHOPHYSIOLOGY
-Small airways may become narrowed by cells (hyperplasia and
accumulation), mucus, and fibrosis, and extensive small airway
destruction has been demonstrated to be a hallmark of advanced
COPD.
-Persistent reduction in forced expiratory flow rates is the most
typical finding in COPD.
-Increases in the residual volume and the residual volume/total
lung capacity ratio, non-uniform distribution of ventilation, and
ventilation-perfusion mismatching also occur.

22. CLINICAL FEATURES
-Cough, sputum production, exertional dyspnea
-Expiratory wheezes
-Signs of hyperinflation ( barrel chest/enlarged
lung volumes)
-Tripod sitting position
-Emphysema- pink puffers, thin, noncyanotic at rest
-Chronic bronchitis – heavy and cyanotic (blue bloaters)
-Hoover sign – in advanced copd,; paradoxical inward
inspiratory movement of rib cage

23. -Hallmark of COPD is
airflow obstruction
-Airflow obstruction
with a reduction in FEV1
and FEV1/FVC
-degree of airflow
obstruction is an
important prognostic
factor in COPD
LABORATORY FINDINGS

24. ....
 prolonged expiratory phase and may include expiratory wheezing
 barrel chest and enlarged lung volumes with poor diaphragmatic excursion
 use of accessory muscles of respiration, sitting in the characteristic “tripod”
position
 cyanosis, visible in the lips and nail beds.
 patients with predominant emphysema, termed “pink puffers,” are thin and
noncyanotic at rest and have prominent use of accessory muscles
 patients with chronic bronchitis are more likely to be heavy and cyanotic (“blue
bloaters”)
 cachexia, with significant weight loss, bitemporal wasting, and diffuse loss of
subcutaneous adipose tissue
 paradoxical inward movement of the rib cage with inspiration (Hoover’s sign)
PHYSICAL FINDINGS

25.  An elevated hematocrit suggests the presence of chronic hypoxemia...
 Obvious bullae, paucity of parenchymal markings, or hyperlucency on
chest x-ray suggests the presence of emphysema. Increased lung
volumes and flattening of the diaphragm suggest hyperinflation
 Chest computed tomography (CT) scan is the current definitive test for
establishing the presence or absence of emphysema, the pattern of
emphysema, and the presence of significant disease involving medium
and large airways
 Measurement of the serum α1 AT level is a reasonable initial test
 Molecular genotyping of DNA can be performed for the common PI
alleles (M, S, and Z).
LABORATORY FINDINGS

26. STABLE PHASE COPD
The two main goals of therapy are:
1. to provide symptomatic relief...
2. reduce future risk...
 Only three interventions—smoking
cessation, oxygen therapy in
chronically hypoxemic patients, and
lung volume reduction surgery (LVRS)
in selected patients with emphysema—
have been demonstrated to improve
survival of patients with COPD.

28. It has been shown that middle-aged smokers who were able to successfully stop
smoking
experienced a significant improvement in the rate of decline in pulmonary function,
often returning to annual changes similar to that of nonsmoking patients.
There are three principal pharmacologic approaches to the problem:
1.nicotine replacement therapy available as gum, transdermal patch, lozenge, inhaler,
and nasal spray;
2.bupropion;
3.varenicline, a nicotinic acid receptor agonist/antagonist.
PHARMACOTHERAPY
Smoking Cessation

29. EXACERBATIONS OF COPD
 prominent feature of the natural history of COPD.
 episodic acute worsening of respiratory symptoms, including increased
dyspnea, cough, wheezing, and/ or change in the amount and character of
sputum.
 may or may not be accompanied by other signs of illness, including fever,
myalgias, and sore throat.
 strongest single predictor of exacerbations is a history of a previous
exacerbation
Other factors, such as an elevated ratio of the diameter of the pulmonary
artery to aorta on chest CT, and gastroesophageal reflux, are also associated
with increased risk of COPD exacerbations.

32. The initiation of noninvasive positive-pressure
ventilation (NIPPV) in patients with respiratory
failure, defined as Paco2 >45 mmHg, results in a
significant reduction in mortality rate, need for
intubation, complications of therapy, and hospital
length of stay.
Contraindications to NIPPV include:
 cardiovascular instability
 impaired mental status
 inability to cooperate
 copious secretions or the inability to clear
secretions
 craniofacial abnormalities or trauma precluding
effective fitting of mask
 extreme obesity
 significant burns.
Mechanical Ventilatory Support
Invasive (conventional) mechanical ventilation via
an endotracheal tube is indicated for patients with:
 severe respiratory distress despite initial
therapy
 life-threatening hypoxemia
 severe hypercarbia and/or acidosis
 markedly impaired mental status
 respiratory arrest
 hemodynamic instability, or other
complications...

33. REFERENCES:
● HARRISONS PRINCIPLES OF INTERNAL MEDICINE, 20TH
EDITION
● GLOBAL INITIATIVE FOR ASTHMA POCKET GUIDE FOR
ASTHMA MANAGEMENT AND PREVENTION
● GLOBAL STRATEGY FOR PREVENTION, DIAGNOSIS AND
MANAGEMENT OF COPD: 2024 Report