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Internal Medicine I EXIMIUS

COPD 2021
DR. JENA LYNN ALAN November 2019

COPD  Emphysema is characterized by destruction of gas-


 disease state characterized by persistent respiratory symptoms exchanging air spaces (respiratory bronchioles, alveolar
and airflow limitation that is not fully reversible ducts, and alveoli)
 The classic definition of COPD requires the presence of chronic
airflow obstruction, determined by spirometry, that usually 3 types:
occurs in the setting of noxious environmental exposures— 1.Centrilobular emphysema
most commonly cigarette smoking -most frequently associated with cigarette smoking
- most prominent in the upper lobes and superior
 Emphysema segments of lower lobes
- an anatomically defined condition characterized by - focal
destruction of the lung alveoli with air space - enlarged air spaces found (initially) in association with
enlargement respiratory bronchioles
 Chronic bronchitis 2. Panlobular emphysema
- a clinically defined condition with chronic cough and - abnormally large air spaces evenly distributed within and
phlegm across acinar unit
 Small airway disease - α1AT deficiency
- small bronchioles are narrowed and reduced in - predilection for the lower lobes
number 3. Paraseptal emphysema
 third leading cause of death - 10–15% of cases and is distributed along the pleural
 affects >10 million persons in the United States margins with relative sparing of the lung core or central regions

PATHOPHYSIOLOGY
PATHOGENESIS
 Persistent reduction in forced expiratory flow rates is the
 Airflow limitation, a major physiologic change
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

AIRFLOW OBSTRUCTION
 reduced ratio of FEV1/FVC
 In contrast to asthma, the reduced FEV1 in COPD seldom
shows large responses to inhaled bronchodilators,
although improvements up to 15% are common
 air trapping”
 increased residual volume and increased ratio of residual
volume to total lung capacity
 progressive hyperinflation (increased total lung capacity)
late in the disease

RISK FACTORS
Pathogenesis of emphysema: 1. Cigarette smoking
1. Chronic exposure to cigarette smoke in genetically - accelerated decline in FEV1 in a dose- response
susceptible individuals triggers inflammatory and immune cell relationship to the intensity of cigarette smoking, which is
recruitment within large and small airways and in the terminal typically expressed as pack-years
air spaces of the lung - Pack-years* of cigarette smoking is the most highly
2. Inflammatory cells release proteinases that damage the significant predictor of FEV1
extracellular matrix supporting airways, vasculature, and gas *(average number of packs of cigarettes smoked per day
exchange surfaces of the lung multiplied by the total number of years of smoking).
3.Structural cell death occurs through oxidant-induced damage 2. Respiratory Infections
4. Disordered repair of elastin and other extracellular matrix - important causes of COPD exacerbations
components contributes to air space enlargement and 3. Occupational exposures
emphysema - coal mining, gold mining, and cotton textile dust, have
been implicated as risk factors for chronic airflow
PATHOLOGY obstruction
 affect the large airways, small airways (≤2 mm diameter), 4. Ambient air pollution
and alveoli - prolonged exposure to smoke produced by biomass
 changes in large airways cause cough and sputum combustion, a common mode of cooking in some
production, while changes in small airways and alveoli are countries
responsible for physiologic alterations 5. Passive/second hand smoke
 The major site of increased resistance in most individuals 6. Genetics
with COPD is in airways ≤2 mm diameter A1 Antitrypsin Deficiency
M allele - normal α1AT levels

TRANSCRIBER GROUP 1 1
Internal Medicine I EXIMIUS
COPD 2021
DR. JENA LYNN ALAN November 2019

S allele- slightly reduced α1AT levels


Z allele- markedly reduced α1AT levels
null alleles-absence of any α1AT production

PiZ - Individuals with two Z alleles or one Z and one null allele
- most common form of severe α1AT deficiency.

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, 2. ABG
can be insidious - may demonstrate resting or exertional hypoxemia
 As COPD advances, the principal feature is worsening dyspnea - an important component of the evaluation of patients
on exertion presenting with symptoms of an exacerbation
3. CBC
PHYSICAL FINDING - An elevated hematocrit suggests the presence of chronic
 In patients with more severe disease, the physical examination hypoxemia, as does the presence of signs of right
of the lungs is notable for a prolonged expiratory phase and ventricular hypertrophy
may include expiratory wheezing
 signs of hyperinflation include a barrel chest and enlarged lung CHEST X-RAY
volumes with poor diaphragmatic excursion as assessed by  Obvious bullae, paucity of parenchymal markings, or
percussion hyperlucency suggests the presence of emphysema.
 Patients with severe airflow obstruction may also exhibit use of  Increased lung volumes and flattening of the diaphragm suggest
accessory muscles of respiration, sitting in the characteristic hyperinflation
“tripod” position to facilitate the actions of the  Chest computed tomography (CT) scan is the current definitive
sternocleidomastoid, scalene, and intercostal muscles test for establishing the presence or absence of emphysema,
 Patients may develop cyanosis, visible in the lips and nail beds the pattern of emphysema, and the presence of significant
 emphysema, termed “pink puffers,” are thin and noncyanotic disease involving medium and large airways
at rest and have prominent use of accessory muscles, and
patients with chronic bronchitis are more likely to be heavy and TREATMENT
cyanotic “blue bloaters” STABLE PHASE COPD
 Advanced disease may be accompanied by cachexia, with The two main goals of therapy:
significant weight loss, bitemporal wasting, and diffuse loss of 1. to provide symptomatic relief (reduce respiratory
subcutaneous adipose tissue symptoms, improve exercise tolerance, improve health
 wasting is an independent poor prognostic factor in COPD status)
 paradoxical inward movement of the rib cage with inspiration ` 2. reduce future risk (prevent disease progression,
(Hoover’s sign) prevent and treat exacerbations, and reduce mortality)
 Signs of overt right heart failure- cor pulmonale
LABORATORY FINDING
1. Pulmonary Function Test
- The hallmark of COPD is airflow obstruction
- shows airflow obstruction with a reduction in FEV1 and
FEV1/FVC
- With worsening disease severity, lung volumes may
increase, resulting in an increase in total lung capacity,
functional residual capacity, and residual volume.
- The degree of airflow obstruction is an important
prognostic factor in COPD and is the basis for the GOLD
spirometric severity classification

TRANSCRIBER GROUP 1 2
Internal Medicine I EXIMIUS
COPD 2021
DR. JENA LYNN ALAN November 2019

NONPHARMACOLOGIC 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
PHARMACOTHERAPY
o FEV1 <20% of predicted and either diffusely distributed
 Smoking Cessation
emphysema on CT scan or diffusing capacity of lung for
 Bronchodilators
carbon monoxide (DLCO) <20% of predicted have
- the primary treatment for almost all patients with COPD
increased mortality after the procedure, and thus are not
and are used for symptomatic benefit and to reduce
candidates for LVRS
exacerbations
- The inhaled route is preferred for medication delivery,
4. Lung Transplantation
because side effects are less than with systemic
o candidates for lung transplantation should have very
medication delivery
severe airflow limitation, severe disability despite maximal
medical therapy, and be free of significant comorbid
1. Anticholinergic Muscarinic Antagonists
conditions such as liver, renal, or cardiac disease
o Short-acting ipratropium bromide improves symptoms
with acute improvement in FEV1
 Only three interventions—smoking cessation, oxygen therapy
o Long-acting muscarinic antagonists (LAMA, including
in chronically hypoxemic patients, and lung volume reduction
aclidinium, glycopyrrolate, tiotropium, and umeclidinium)
surgery (LVRS) in selected patients with emphysema—have
improve symptoms and reduce exacerbations
been demonstrated to improve survival of patients with COPD
2. Beta Agonists
EXACERBATIONS OF COPD
o Short-acting beta agonists ease symptoms with acute
 prominent feature of the natural history of COPD
improvements in lung function
 episodic acute worsening of respiratory symptoms, including
o Long-acting agents (LABA) provide symptomatic benefit
increased dyspnea, cough, wheezing, and/ or change in the
and reduce exacerbations, though to a lesser extent than a amount and character of sputum
LAMA
 strongest single predictor of exacerbations is a history of a
previous exacerbation
Steroids
1. Inhaled Corticosteroids
PATIENT ASSESSMENT
o reduce exacerbations
 quantification of the degree and change in dyspnea by asking
o use has been associated with increased rates of
about breathlessness during activities of daily living and typical
oropharyngeal candidiasis and pneumonia and in some activities for the patient
studies an increased rate of loss of bone density  fever, change in character of sputum
 physical examination should incorporate an assessment of the
PDE4 Inhibitors
degree of distress of the patient
o roflumilast
 Patients with advanced COPD, a history of hypercarbia, mental
o demonstrated to reduce exacerbation frequency in
status changes (confusion, sleepiness), or those in significant
patients with severe COPD, chronic bronchitis, and a prior distress should have an arterial blood-gas measurement
history of exacerbations

Oxygen
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

TRANSCRIBER GROUP 1 3
Internal Medicine I EXIMIUS
COPD 2021
DR. JENA LYNN ALAN November 2019

Specific attention should be focused on tachycardia, tachypnea, use 2. Antibiotics


of accessory muscles, signs of perioral or peripheral cyanosis, the o Streptococcus pneumoniae, Haemophilus influenzae, and
ability to speak in complete sentences, and the patient’s mental Moraxella catarrhalis
status
3. Systemic glucocorticoids
o reduces the length of stay, hastens recovery, and reduces the
The presence of hypercarbia, defined as a Pco2 >45 mmHg, has
chance of subsequent exacerbation or relapse
important implications for treatment (discussed below).
o Current recommendations suggest 30–40 mg of oral
 The need for inpatient treatment of exacerbations is suggested prednisolone or its equivalent typically for a period of 5–10
by the presence of respiratory acidosis and hypercarbia, new or days in outpatients
worsening hypoxemia, severe underlying disease and those
whose living situation is not conducive to careful observation 4. Oxygen
and the delivery of prescribed treatment o Supplemental O2 should be supplied to maintain oxygen
saturation ≥90%.
TREATMENT OF ACUTE EXACERBATIONS
1. Bronchodilators 5. Mechanical Ventilatory Support
o treated with inhaled β agonists and muscarinic antagonists. o indicated for patients with severe respiratory distress despite
These may be administered separately or together, and the initial therapy, life-threatening hypoxemia, severe hypercarbia
frequency of administration depends on the severity of the and/or acidosis, markedly impaired mental status, respiratory
exacerbation arrest, hemodynamic instability, or other complications

TRANSCRIBER GROUP 1 4
SUBJECT EXIMIUS
TOPIC 2021
PROFESSOR DATE

TRANSCRIBERS ROX 5

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