INTERNAL MED COPD

AY 2020-2021 Dr. Jena Lynn Allan

1st Sem MIDTERMS Group 1: Magat, Matthew, Pulido

Trans Outline  Centrilobular emphysema

o Most frequently associated with cigarette smoking
1. COPD o Most prominent in the upper lobes and superior segments
a. Pathogenesis of lower lobes
b. Pathology o Focal
c. Pathophysiology o Enlarged air spaces found (initially) in association with
d. Airflow Obstruction respiratory bronchioles
e. Risk Factors  Panlobular emphysema
f. Clinical Presentation
o Abnormally large air spaces evenly distributed within and
g. Physical Finding
across acinar unit
h. Laboratory Finding
o Α1at deficiency
i. Treatment
j. Pharmacotherapy o Predilection for the lower lobes
k. Non Pharmacologic Therapies  Paraseptal emphysema
2. Exacerbations of COPD o 10–15% of cases and is distributed along the pleural
a. Patient Assessment margins with relative sparing of the lung core or central
b. Treatment of Acute Exacerbations regions
Pathophysiology
COPD  Persistent reduction in forced expiratory flow rates is the most
 Disease state characterized by persistent respiratory symptoms typical finding in COPD.
and airflow limitation that is not fully reversible.  Increases in the residual volume and the residual volume/total
 The classic definition of COPD requires the presence of lung capacity ratio, non-uniform distribution of ventilation, and
chronic airflow obstruction, determined by spirometry, that ventilation-perfusion mismatching.
usually occurs in the setting of noxious environmental Airflow Obstruction
exposures—most commonly cigarette smoking.  Reduced ratio of FEV1/FVC
 Emphysema  In contrast to asthma, the reduced FEV1 in COPD seldom
o An anatomically defined condition characterized by shows large responses to inhaled bronchodilators, although
destruction of the lung alveoli with air space enlargement improvements up to 15% are common
 Chronic bronchitis Hyperinflation
o A clinically defined condition with chronic cough and  “Air trapping”
phlegm  Increased residual volume and increased ratio of residual
 Small airway disease volume to total lung capacity
o Small bronchioles are narrowed and reduced in number  Progressive hyperinflation (increased total lung capacity) late
 Incidence in the disease
o Third leading cause of death Risk Factors
o Affects >10 million persons in the United States  Cigarette smoking
o accelerated decline in FEV1 in a dose- response
Pathogenesis relationship to the intensity of cigarette smoking, which is
 Airflow limitation, a major physiologic change typically expressed as pack-years
o Pack-years* of cigarette smoking is the most highly
 See Figure 1 (Appendix)
Pathogenesis of emphysema: significant predictor of FEV1 *(average number of packs of
1. Chronic exposure to cigarette smoke in genetically susceptible cigarettes smoked per day multiplied by the total number of
individuals triggers inflammatory and immune cell recruitment years of smoking).
within large and small airways and in the terminal air spaces of  Respiratory Infections
the lung. o important causes of COPD exacerbation
2. Inflammatory cells release proteinases that damage the  Occupational exposures
extracellular matrix supporting airways, vasculature, and gas o coal mining, gold mining, and cotton textile dust, have been
exchange surfaces of the lung. implicated as risk factors for chronic airflow obstruction
3. Structural cell death occurs through oxidant-induced damage  Ambient air pollution
4. Disordered repair of elastin and other extracellular matrix o prolonged exposure to smoke produced by biomass
components contributes to air space enlargement and combustion, a common mode of cooking in some countries
emphysema.  Passive/second hand smoke
 Genetics
Pathology o A1 Antitrypsin Deficiency
 Affect the large airways, small airways (≤2 mm diameter), and  M allele - normal α1AT levels
alveoli  S allele - slightly reduced α1AT levels
 Changes in large airways cause cough and sputum  Z allele - markedly reduced α1AT levels
production, while changes in small airways and alveoli are  null alleles - absence of any α1AT production
responsible for physiologic alterations o PiZ
 The major site of increased resistance in most individuals with  Individuals with two Z alleles or one Z and one null allele
COPD is in airways ≤2 mm diameter  most common form of severe α1AT deficiency.
 Emphysema is characterized by destruction of gas-exchanging
air spaces (respiratory bronchioles, alveolar ducts, and alveoli)
3 types: Clinical Presentation
 Three most common symptoms in COPD are cough, sputum
production, and exertional dyspnea
 Development of airflow obstruction is a gradual process, many
patients date the onset of their disease to an acute illness or
exacerbation
 Development of exertional dyspnea, often described as
increased effort to breathe, heaviness, air hunger, or gasping,
can be insidious
 As COPD advances, the principal feature is worsening dyspnea
on exertion
o Obvious bullae, paucity of parenchymal markings, or
hyperluscency suggests the presence of emphysema.
o Increased lung volumes and flattening of the diaphragm
suggest hyperinflation
o 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.
PROFESSOR’S INPUT

Physical Finding
 In patients with more severe disease, the physical examination
of the lungs is notable for a prolonged expiratory phase and
may include expiratory wheezing
 Signs of hyperinflation include a barrel chest and enlarged
lung volumes with poor diaphragmatic excursion as assessed
by percussion
 Patients with severe airflow obstruction may also exhibit use of
accessory muscles of respiration, sitting in the characteristic
“tripod” position to facilitate the actions of the
sternocleidomastoid, scalene, and intercostal muscles
 Patients may develop cyanosis, visible in the lips and nail beds
 Emphysema, termed “pink puffers”, are thin and noncyanotic
at rest and have prominent use of accessory muscles, and
patients with chronic bronchitis are more likely to be heavy and
cyanotic “blue bloaters”
Flattening of the diaphragm which suggests
 Advanced disease may be accompanied by cachexia, with
hyperinflation or “air trapping”.
significant weight loss, bitemporal wasting, and diffuse loss of
subcutaneous adipose tissue
5. Chest computed tomography (CT) scan
 Wasting is an independent poor prognostic factor in COPD
o Current definitive test for establishing the presence or
 Paradoxical inward movement of the rib cage with inspiration
absence of emphysema, the pattern of emphysema, and
(Hoover’s sign)
the presence of significant disease involving medium and
 Signs of overt right heart failure - Cor Pulmonale large airways.
Laboratory Finding GOLD 2020 for COPD
1. Pulmonary Function Test
o The hallmark of COPD is airflow obstruction
o Shows airflow obstruction with a reduction in FEV1 and
FEV1/FVC
o With worsening disease severity, lung volumes may
increase, resulting in an increase in total lung capacity,
functional residual capacity, and residual volume.
o The degree of airflow obstruction is an important prognostic
factor in COPD and is the basis for the GOLD spirometric
severity classification

Treatment

2. ABG STABLE PHASE COPD

o May demonstrate resting or exertional hypoxemia
o An important component of the evaluation of patients
presenting with symptoms of an exacerbation
3. CBC
o An elevated hematocrit suggests the presence of chronic
hypoxemia, as does the presence of signs of right
ventricular hypertrophy
The two main goals of therapy:
1. To provide symptomatic relief (reduce respiratory symptoms,
improve exercise tolerance, improve health status)
2. Reduce future risk (prevent disease progression, prevent and
treat exacerbations, and reduce mortality)

4. CHEST X-RAY

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 SYMP
TOM
ASSES
EXACERB SMEN
GROUP ATIONS T
PER YEAR m
C
M
A
R
T
C
A Low ≤1 0- <1
symptom (not leading 1 0
severity to hospital
Low admission)
exacerbat
ion risk
B High ≤1 ≥2 ≥1
symptom (not leading 0
severity to hospital
Low admission)
exacerbat
ion risk
C Low ≥2 or ≥1 0- <1
symptom (leading to 1 0
severity hospital
High admission)
exacerbat
ion risk
D High ≥2 or ≥1 ≥2 ≥1
symptom (leading to 0
severity hospital
High admission)
exacerbat
ion risk
Source: GOLD 2018 COPD guidelines
(Table was not included on the slides but it was explained)

Figure 2.86-6 Medication therapy for stable COPD.

Recommended pharmacologic treatment of stable COPD

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 is based on respiratory symptoms and exacerbation
frequency. Preferred treatment for the Diagnosis,
Management and Prevention of COPD, Global Initiative
for Chronic Obstructive Lung Disease (GOLD) 2017.

Pharmacotherapy
 Smoking Cessation
 Bronchodilators
o The primary treatment for almost all patients with COPD
and are used for symptomatic benefit and to reduce
exacerbations
o The inhaled route is preferred for medication delivery,
because side effects are less than with systemic
medication delivery

1. Anticholinergic Muscarinic Antagonists

o Short-acting ipratropium bromide improves symptoms with
acute improvement in FEV1
o Long-acting muscarinic antagonists (LAMA, including
aclidinium, glycopyrrolate, tiotropium, and umeclidinium)
improve symptoms and reduce exacerbations

2. Beta Agonists
o Short-acting beta agonists ease symptoms with acute
improvements in lung function
o Long-acting agents (LABA) provide symptomatic benefit
and reduce exacerbations, though to a lesser extent than a
LAMA

STEROIDS
 Inhaled Corticosteroids
o Reduce exacerbations
o Use has been associated with increased rates of
oropharyngeal candidiasis and pneumonia and in some
studies an increased rate of loss of bone density
PDE4 INHIBITORS
 Roflumilast
o Demonstrated to reduce exacerbation frequency in patients
with severe copd, chronic bronchitis, and a prior history of
exacerbations
OXYGEN
o Not indicated in all patients with COPD
o Supplemental O2 is the only pharmacologic therapy
demonstrated to decrease mortality rates in patients with
COPD
o For patients with resting hypoxemia (resting O2 saturation
≤88% in any patient or ≤89% with signs of pulmonary
hypertension or right heart failure), the use of O2 has been
demonstrated to have a significant impact on mortality
 Commonly Used Maintenance Medications in COPD (See Figure
2 Appendix)
Non Pharmacologic Therapies
1. Vaccination- influenza, pneumococcal
2. Pulmonary rehabilitation
o Comprehensive treatment program that incorporates
exercise, education, and psychosocial and nutritional
counseling
o Improve health-related quality of life, dyspnea, and exercise
capacity
3. Lung volume reduction surgery
o In carefully selected patients with emphysema, surgery to
remove the most emphysematous portions of lung
improves exercise, lung function, and survival
o Upper lobe-predominant emphysema and a low post-
rehabilitation exercise capacity are most likely to benefit
from LVRS.
o Fev1 <20% of predicted and either diffusely distributed
emphysema on ct scan or diffusing capacity of lung for
carbon monoxide (dlco) <20% of predicted have increased
mortality after the procedure, and thus are not candidates
for LVRS.
4. Lung transplantation
o Candidates for lung transplantation should have very
severe airflow limitation, severe disability despite maximal
medical therapy, and be free of significant comorbid
conditions such as liver, renal, or cardiac disease.

 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.

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 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
 Strongest single predictor of exacerbations is a history of a
previous exacerbation

Patients Assessment
 Quantification of the degree and change in dyspnea by asking
about breathlessness during activities of daily living and typical
activities for the patient
 Fever, change in character of sputum
 Physical examination should incorporate an assessment of the
degree of distress of the patient
 Patients with advanced COPD, a history of hypercarbia,
mental status changes (confusion, sleepiness), or those in
significant distress should have an arterial blood-gas
measurement
Treatment of Acute Exacerbations
1. Bronchodilators
o Treated with inhaled β agonists and muscarinic
antagonists. These may be administered separately or
together, and the frequency of administration depends on
the severity of the exacerbation
2. Antibiotics
o Streptococcus pneumoniae, Haemophilus influenzae, and
Moraxella catarrhalis
3. Systemic glucocorticoids
o Reduces the length of stay, hastens recovery, and reduces
the chance of subsequent exacerbation or relapse
o Current recommendations suggest 30–40 mg of oral
prednisolone or its equivalent typically for a period of 5–10
days in outpatients
4. Oxygen
o Supplemental O2 should be supplied to maintain oxygen
saturation ≥90%.
5. Mechanical Ventilatory Support
o Indicated for patients with severe respiratory distress

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 despite initial therapy, life-threatening hypoxemia, severe
hypercarbia and/or acidosis, markedly impaired mental
status, respiratory arrest, hemodynamic instability, or other
complications. REFERENCE:
1. Allan, J. (2020). COPD [video recording]

APPENDIX
Figure 1

Figure 2

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MDI: Metered Dose Inhaler
DPI: Dry Powder Inhaler

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