COPD v. AsthmaMATT GENTHER

COPD

Chronic Obstructive Pulmonary Disease (COPD) Chronic bronchitis and Emphysema

Two forms of COPD with specific pathologic lung changes

Progressive irreversible airflow limitation

Associated with abnormal inflammatory lung response (McCance & Huether, 2010)

COPD

Tobacco smoke is the most common cause of COPD

Other causes include Air pollutants, genetic factors, respiratory infections and

occupational exposures (Postma, et al., 2014).

COPD is the third leading cause of death in the United states 12-16 million Americans report to have been diagnosed (Kim &

Criner, 2013)

Most common to report Age 65+, current and former smokers, women, hx of asthma, people

with low incomes and individuals with less than high school income (McCance and Huether, 2010)

COPD – Chronic Bronchitis

Defined as being associated with chronic cough and sputum production At least 3 months per year for 2 consecutive years

With increased exacerbation rate and accelerated decrease in lung function (Kim & Criner, 2013)

Chronic Bronchitis (CB) primary risk factor is smoking (42%) but can be found in 4-22% of non-smokers (Kim & Criner, 2013) Potential risk factors include inhalation of biomass fuels, dust, and

chemical fumes.

COPD – Chronic Bronchitis

Epidemiology of CB, high prevalence of patients with COPD

14-76% of all patients with COPD

10 million people in the US

Majority between 44-65 years of age (Kim & Criner, 2013)

Image (Buggy, 2007)

COPD – Chronic Bronchitis

Inspired irritants increase mucous and number of goblet cells in airway Creating thicker secretions

Increased mucous promotes bacterial cell growth

Embedded secretions impair airway function

Bronchial walls become inflamed leading to wall narrowing and bronchospasm (McCance & Huether, 2010)

Initially only the large bronchi are affected though all airways are involved Obstruction greater on expiration

Profusion mismatch traps gas in distal lungs

Decrease tidal volume, hypoventilation, and hypercapnia (McCance & Huether, 2010)

COPD – Chronic Bronchitis

Clinical manifestations:

Decreased exercise tolerance, wheezing, shortness of breath

Productive cough, frequent pulmonary infections, and copious thick sputum production. (McCance & Huether, 2010)

Forced expiratory volume (FEV1) and forced vital capacity (FVC) are declined in CB

Image (Kim & Criner, 2013)

COPD – Chronic Bronchitis

Diagnosis is based on a history of symptoms, physical exam, chest radiography and blood gas analysis (McCance & Huether, 2010)

Prevention is the best treatment because damage is irreversible Smoking cessation before the damage is great is a mainline defense

Decreases goblet cell hyperplasia (Kim & Criner, 2013)

Antibiotics, mucolytics, corticosteroids, oxygen therapy and bronchodilators are first line medications for CB Reduction of exacerbations, increase lung function and decreasing

the infectious and inflammatory response of the body are the mechanisms of treatment (Poole, Black & Cates, 2012)

COPD Emphysema

Emphysema is characterized by destruction of alveolar walls and enlargement of gas exchange airways (acini)

Elastic recoil is lost due to aging

Most likely cause of emphysema before old age is secondary to smoking (McCance & Huether, 2010)

COPD – Emphysema

Three classifications of Emphysema: Panacinar, Parasceptal and Centroacinar. Panacinar emphysema destroys entire alveolus uniformly, mostly

found in lower lungs

Parasceptal emphysema involves alveolar ducts and sacs in the peripheral lung

Centroacinar emphysema starts in the bronchioles and spreads towards the periphery (Higginson, 2010)

COPD – Emphysema

1-2% of cases are due to a lack of alpha-1 antitrypsin, in which alveoli lose elasticity

More commonly, noxious stimuli inhalation leads to emphysema

Cigarette smoke is the most common causing inflammatory response Neutrophils, macrophages and lymphocytes produce chemicals that

decrease the elasticity in cells, creating fewer larger alveoli (Higginson, 2010)

Inhaled toxins and air pollutants also know to cause emphysema

COPD – Emphysema

Emphysema is a progressive non-reversible disease of the alveoli

Hypoxemia causes the lungs to go through pulmonary hypoxic vasoconstriction

The constriction leads to pulmonary hypertension and eventual right sided heart failure, cor pulmonale (Higginson, 2010)

COPD – Emphysema

Clinical manifestations: Dyspnea upon exertion and at rest, some unproductive coughing,

thin stature and prolonged expiration

Barrel chest, hyperresonant percussion, pursed lip breathing and tripod breathing positioning (McCance & Huether 2010)

Diagnosis is based on respiratory signs and symptoms Pulmonary function test

Size and shape of chest, breathing pattern, shortness of breath, clubbing of fingers, auscultation and percussion

X-ray, CT scans, arterial blood gases and EKG (Bailey, 2012)

COPD - Emphysema

Smoking cessation primary mechanism to stop damage of emphysema

Oxygen therapy, pulmonary rehab, bronchodilators, corticosteroids, and surgery used to treat disease

Disease is irreversible

Treatments used to reduce symptoms, dyspnea and hypoventilation

Asthma

Chronic disorder of the airway, involving interactions of airway obstruction, bronchial hyperresponsiveness and inflammation (McCance and Huether, 2010)

This heterogeneous syndrome affects 300 million individuals worldwide Airways suffer from chronic inflammation and small bronchial

diameter (Aguilar, Walgama & Ryan, 2014)

Asthma

Asthma occurs at all ages, half of all cases are found in children

Familial disorder linking over 100 genes with susceptibility

Eosinophils, mast cells, leukotrienes, and bronchial hyperresponsiveness increase the production of IgE IgE plays a role in hypersensitivity and allergic response (Aguilar,

Walgama & Ryan, 2014)

Risk factors: family history, exposure to pollutants and smoking, respiratory viral infections, and obesity (McCance & Huether, 2010)

Prevention and treatment of allergic rhinitis may prevent asthma (McCance & Huether, 2010)

Asthma

Inflammation causes wheezing, breathlessness, chest tightness and coughing Most often at night or early morning

Episodes are widespread in lungs, resolve either spontaneously or with treatment (Postma, et al., 2014)

Expiratory flow is decreased by airway obstruction causing air trapping

Decreased alveolar perfusion causes hypoxia and respiratory acidosis and can lead to respiratory failure (McCance & Huether, 2010)

Asthma

Host factors

Male sex in childhood, female sex in adulthood

Family history of COPD

(Family) history of asthma Family history asthma/atopy

Genetic constitution Genetic constitution

Airway hyperresponsiveness Airway hyperresponsiveness

Atopy —

Low lung function Low lung function

Overweight —

Perinatal factors

Maternal smoking Maternal smoking

Maternal diet —

Mode of delivery —

Childhood exposures

Viral respiratory infections Respiratory tract infections

No breastfeeding —

Microbial deprivation Maternal smoking

Environmental tobacco smoke exposure Indoor air pollution

Air pollution —

Adult exposures

Occupational exposures Occupational exposures

Cigarette smoking Cigarette smoking

Outdoor air pollution Outdoor air pollution

— Indoor air pollution

Asthma

Pulmonary function tests are normal in between exacerbations

During attacks chest constricts, expiratory wheeze is present, dyspnea, coughing, tachycardia, prolonged expiration, and tachypnea

Prolonged bronchospasm can lead to status asthmaticus Acidosis can follow PACO2 rises and can cause sudden death

(McCance & Huether, 2010)

Asthma

Diagnosis based on attacks, family history, allergies and an decreased FEV1, FVC and total lung capacity

Classified by severity: intermittent, mild persistent, moderate persistent and severe consistent (McCance & Huether, 2010)

Treatment includes avoiding allergens, short acting beta agonist inhalers for acute exacerbations, anti-inflammatory medications, and corticosteroids (Postma, et al., 2014)

COPD v. Asthma: Study Questions

1. Which form of emphysema damages the entire acinus and tends to not be associated with smoking?

a. Centriacinar emphysema

b. Panacinar emphysema

c. Paraseptal emphysema

d. Cor pulmonale

2. Which cells are NOT associated with inflammation and destruction of alveolar elasticity?

a. Neutrophils

b. Macrophages

c. Fibroblasts

d. Lymphocytes

COPD v. Asthma: Study Questions3. Increased mucous production found in CB is associated with?

a. Goblet cell hyperplasia

b. Inflammatory cytokines

c. Pneumonia

d. Hypoventilation

4. Which group has a decreased risk for asthma?

a. Children of parents that smoke

b. Children living in cities

c. Children with many allergies

d. Children that live in rural areas

5. Pulmonary hypertension causes?

a. Left sided heart failure

b. Right sided heart failure

c. Diabetes

d. Tuberculosis

References

Aguilar, P., Walgama, E., & Ryan, M. (2014). Other asthma considerations. Otolaryngologic Clinics Of North America, 47(1), 147-160. doi:10.1016/j.otc.2013.08.015

Bailey, K. (2012). The Importance of the Assessment of Pulmonary Function in COPD. Medical Clinics Of North America, 96(4), 745-752.

Buggey, T. (2007). Storyboard for Ivan's morning routine. Diagram. Journal of Positive Behavior Interventions, 9(3), 151. Retrieved December 14, 2007, from Academic Search Premier database

Hadjiliadis, D. (2011). Emphysema. Retrieved from http://www.nlm.nih.gov/medlineplus/ency/imagepages/17055.htm

Hadjiliadis, D. (2011). Cor pulmonale. Retrieved from http://www.nlm.nih.gov/medlineplus/ency/imagepages/17055.htm

Higginson, R. (2010). COPD: pathophysiology and treatment. Nurse Prescribing, 8(3), 102-110.

References

Kim, V., & Criner, G. (2013). Chronic bronchitis and chronic obstructive pulmonary disease. American Journal Of Respiratory & Critical Care Medicine, 187(3), 228-237. doi:10.1164/rccm.201210-1843CI

McCance, K., & Huether, S. (2010). Alterations of Pulmonary Function. In Pathophysiology: The biologic basis for disease in adults and children (6th ed., pp. 1266-1309). Maryland Heights, Mo.: Mosby Elsevier

Poole, P., Black, P., & Cates, C. (2012). Mucolytic agents for chronic bronchitis or chronic obstructive pulmonary disease. Cochrane Database Of Systematic Reviews, (8), doi:10.1002/14651858.CD001287.pub2

Postma, D., Reddel, H., ten Hacken, N., & van den Berge, M. (2014). Asthma and chronic obstructive pulmonary disease: similarities and differences. Clinics In Chest Medicine, 35(1), 143-156. doi:10.1016/j.ccm.2013.09.010