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Is it Asthma or COPD? Looking closer at your

patient

Susan Collazo APN-CNPThoracic SurgeryNorthwestern Memorial HospitalChicago, IL

Objectives

1. State one characteristic which is different between asthma and COPD

2. State at least one similarity between asthma and COPD

3. State one treatment option for COPD and/or asthma

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Asthma Prevalence

1 in 12 adults and 1:11 in children

4500 deaths annually

mediconweb.com/.../uploads/2010/10/asthma1.jpg

Airway Inflammation

The airways in asthma undergo significant structural remodeling including thickening of the reticular basement membrane.

www.intechopen.com

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In asthma: - Elevated IgE- Eosinophilic

infiltration- Reticular basemt

membrane thickening

- Smooth muscle hyperplasia

Allergic response in asthmaNote inflammatory mediators

http://what-when-how.com/acp-medicine

Asthma Triggers

Environmental

Genetics – relatedTo immune

response

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Differential Diagnosis

foreign body aspiration, tracheal stenosis or laryngotracheomalacia, vascular rings, enlarged lymph nodes or neck masses

COPD, congestive heart failure, airway masses, drug-induced coughing due to ACE inhibitors, vocal cord dysfunction

PEDS

Adults

Asthma symptoms

WheezingDyspneaChest tightnessCough

Triggers- Viral infections- Allergens- Tobacco smoke- Exercise- Stress

SymptomsVariable

AsthmaClassification

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Step-WiseApproach

To Asthma

Management

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Let’s define asthma

• Common chronic inflammatory disease of the airways

• Variable and recurring symptoms

• Reversible airflow obstruction and bronchospasm

• Trigger-induced – environmental or genetic

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Defining COPD

COPDEmphysema

Chronic Bronchitis

2014 GOLD Definition:

“…a common preventable and treatable disease characterized by persistent airflow limitation that is usually progressive and is associated with enhanced chronic inflammatory response in the airways and the lungs to noxious particles or gases.

Global Initiative for Chronic Obstructive Pulmonary Disease (GOLD). Global Strategy for Diagnosis, Management and Prevention of COPD. 2014.

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COPD structural changes

http://www.iappfind.com/app

Collazofile.com

Triggers

Indoor vsOutdoor

Triggers are Individualized

- Viral- Bacterial- Weather changes- Genetic (A1AT)

http://www.doctortipster.com

SYMPTOMS

•Chronic cough• usually the first symptom thatoccurs in COPD• initially intermittent

•Chronic expectoration

•Dyspnea• symptom for which patients withCOPD seek medical advice.• Persistent, daily, progressive overtime, exacerbated by exercise andrespiratory infections.

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Paraseptal Emphysema or

Bullous Emphysema

Radiographically

Collazofile.com

GOLD GUIDELINES 2014

Medications for COPD in the USA

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Asthma COPD

Decreased diffusing capacity DLCO – alveolar damage

Allergens

SIMILAR:Cough INFLAMMATIONWheezingShortness of breath

Exercise

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Inflammatory phenotypic differences between COPD and asthma, with cells listed in relative order of importance

COPD AsthmaNeutrophils EosinophilsMacrophages Mast cellsCD8+ T lymphocytes CD4+ T lymphocytesEosinophils Macrophages

Sutherland E & Martin RJ. Airway inflammation in chronic obstructive pulmonary disease:Comparisons with asthma. Allergy Clin Immunol 2003;112:819-27

Inflammation in both COPD and Asthma

SPIROMETRY

Spirometry in Asthma: Bronchial Reversibility

FEV1= Forced Expiratory Volume one second

Increases by more than 12 % or 200ml of predicted after inhalation of a B2 (bronchodilator reversibility)

- The more the variability the more certain you can be of diagnosis of asthma

- Spirometry during exacerbations may not demonstrate reversibility due to increase inflammation

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Effects of smoking on FEV1

I: Mild COPD •• FEV1/FVC < 0.7• FEV1 ≥ 80% predicted

II: Moderate COPD• FEV1/FVC < 0.7• 50% ≤ FEV1 < 80% predicted

III: Severe COPD• FEV1/FVC < 0.7• 30% ≤ FEV1 < 50% predicted

IV: Very Severe COPD• FEV1/FVC < 0.7• FEV1 < 30% predicted orFEV1 < 50% predicted pluschronic respiratory failure

At this stage, the patient may not be aware that their lung function is abnormal.

Symptoms usually progress at this stage, with shortness of breath typicallydeveloping on exertion.

Shortness of breath typically worsens at this stage and often limits patients’ dailyactivities. Exacerbations are especially seen beginning at this stage.

At this stage, quality of lifeis very appreciably impairedand exacerbations may belife-threatening.

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Mr Z, a 60y/o w 100pack-year smoking presents to your clinic. You perform spirometry. What is his GOLD classification?

PFTs of Ms. T :a 75y/o F present 40pack-year smoker who notes increase dyspnea

Asthma or

COPD?

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Early Spirometric screening can detect COPD

Zielinski J & Bednarek M. Early Detection of COPD in a High-Risk Population Using SpirometricScreening. Chest 2001; 119(3): 731-736.

By the time a COPD presents with complaints of dyspnea, more than ½ of the patient’s ventilatory reserve are irreparably lost.Free spirometry was offered to smokers >39y/o in Poland11,227 participants found

- 5.2% severe obstruction- 9.6% moderate obstruction- overall 30.6% obstruction of which >80% never knew

Subset of 2200 neversmokers had 14.4 % risk for obstruction.

GOLD GUIDELINES: Classification of COPD

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This is the DLCO of Ms. T. Is it low?What does that mean?

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How well does oxygen move or diffuse into your bloodstream from your lungs?Dependant on alveolar-capillary membrane :- Thickness – inflammation as with ILD or PD- destruction as in emphysema- hgb concentration

Diffusing Capacity

virtualmedic.wordpress.com

This is the DLCO of Ms. T. Is it low?What does that mean?

Vonk JM, Jongepier H, Panhuysen CIM, et al. Risk factors associated with the presence of irreversible airflow limitation and reduced transfer coefficient in patients with asthma after 26 years of follow up.

Thorax. 2003;58:322-327.

Population studies have shown that as many as 30% of patients with fixed airflow obstruction have a past history of asthma .

The presence of a normal diffusing capacity for carbon monoxide (DLCO) can be useful to differentiate patients with asthma from patients with COPD; nevertheless, patients with asthma and a history of smoking may also present a reduced DLCO.

The decreased DLCO may be directly related to the loss of alveolar-capillary surface area that is associated with emphysema

Asthma in the Elderly

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Asthma-COPD Overlap syndrome (ACOS)

SYMPTOMS:Cough, wheezing, sputum production, DOE, physical deconditioning

Louie S, Zeki AA, Schivo M et al. The Asthma–Chronic Obstructive Pulmonary Disease Overlap Syndrome. Expert Rev Clin Pharmacol 2013;6(2):197-219.

HAVE BEEN FOUND TO HAVE:- Experience frequent exacerbations,- Poor quality of life- A more rapid decline in lung function - High mortality- Consume a disproportionate amount of healthcare resources

than asthma or COPD alone

LUNG FUNCTION:Asthmatics with slightly lower DLCOCOPD w mild reversibility

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Asthma (severe) ACOS COPD

Demographics

>40 years

Women > men

Nonsmoker or <5 pack years

Obesity

Atopy typical

Rhinosinusitis

GERD

Frequent albuterol use

Exercise limited in between attacks

Dependence on prednisone

Hallmark problem: frequent exacerbations

>40 years; 50–65 years

Past or current smoker

>10 pack-years

Atopy present

Rhinosinusitis

GERD

Exercise very limited

Hallmark problem: very frequent exacerbations > COPD alone

≥65 years if not younger

Past or current smoker

>10 pack-years

No atopy

GERD

Multiple daily albuterol

Exercise very limited

Oxygen dependence

Hallmark problem: exacerbations and exercise intolerance

Louie S, Zeki AA, Schivo M et al. The Asthma–Chronic Obstructive Pulmonary Disease Overlap Syndrome. Expert Rev Clin Pharmacol 2013;6(2):197-219.

BOLD study = Burden of Obstructive Lung Disease

14 countries

4291 participants

23.3% Gold II COPD

>2/3 Woman

81%Previously

UnDx

Low Socio-econ

Severe childhdinfectx

Chest 2011; 139(4):752-763

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COPD Asthma

Onset Mid life Early or Late onset

Risk factors Smoking Atopy, irritant exposures, smoking

Symptoms Slowly progressive Intermittent

(i) Breathlessness On moderate/minimal effort On exacerbations

(ii) Cough Regularly On exacerbations

Family history May be present May be present

FEV1/FVC ratio <70% <70%

FEV1% predicted <80% <80%

Bronchodilator response Absent/present Present

Inflammatory cells

Neutrophils Eosinophils

Macrophages Neutrophils

CD8+ cells (Tc) Mast cells

CD4+ cells (Th2)

Structural changes

Airway smooth muscle + Airway smooth muscle +++

Peripheral airways All airways

Parenchymal destruction No parenchymal involvement

Epithelial metaplasia Epithelial shedding

Fibrosis++ (peribronchiolar) Fibrosis + (subepithelial)

Mucus secretion +++ Mucus secretion +

Steroid response +/− +++

Vonk JM, Jongepier H, Panhuysen CIM, et al. Risk factors associated with the presence of irreversible airflow limitation and reduced transfer coefficient in patients with asthma after 26 years of follow up. Thorax. 2003;58:322-327.

Goals of treatment in ACOS should be to:1. Control or reduce symptoms and impairment 2. Reduce risks, including acute exacerbations, decline

in lung function and adverse effects from drug treatments .

Goals of Treatment in ACOS

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Make an impact in Asthma-COPD

EDUCATION FOR A PARTNERSHIP IN CARE

Fellow providers

Patient

Public

1. Basic Facts About Asthma and COPD2. Role of Medications:

Understanding the difference betweenLong-term control medications:

- prevent symptoms, often by reducing inflammation

- Must be taken daily. - Do not expect them to give quick relief.

Quick-relief medications: - SABAs relax airway muscles to provide

prompt relief of symptoms. - Do not expect them to provide long-term

asthma control. - Using SABA >2 days a week indicates the

need for starting or increasing long-term control medications.

EDUCATION FOR A PARTNERSHIP IN CARE

EDUCATION FOR A PARTNERSHIP IN CARE

Patient skills in: - Importance of medication compliance- Reviewing MDI technique- Reviewing potential side-effects limiting daily use

• Identifying and avoiding environmental exposures that worsen the patient’s asthma/COPD; e.g., allergens, irritants, tobacco smoke;

• Immunize: virus (flu vax) or pneumonia (pneumovax)• Social Support

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REFERENCES

Global Initiative for Chronic Obstructive Pulmonary Disease (GOLD). Global Strategy for Diagnosis, Management and Prevention of COPD. 2014.

Lamprecht B, McBurnie MA, Vollmer W et al. COPD in never smokers: Results from the population-based burden of obstructive lung disease study. Chest 2011; 139(4):752-763.

Louie S, Zeki AA, Schivo M et al. The Asthma–Chronic Obstructive Pulmonary Disease Overlap Syndrome. Expert Rev Clin Pharmacol 2013;6(2):197-219.

NHLBI Guidelines for the Diagnosis and Management of Asthma (EPR-3), 2014.

Sutherland E & Martin RJ. Airway inflammation in chronic obstructive pulmonary disease:Comparisons with asthma. Allergy Clin Immunol 2003;112:819-27

Vonk JM, Jongepier H, Panhuysen CIM, et al. Risk factors associated with the presence of irreversible airflow limitation and reduced transfer coefficient in patients with asthma after 26 years of follow up. Thorax. 2003;58:322-327.

Zielinski J & Bednarek M. Early Detection of COPD in a High-Risk Population Using Spirometric Screening. Chest 2001; 119(3): 731-736.

Thanks to ILAPN

The CD4+ Th2 lymphocytes may have important role in maintaining this specific asthmatic airway inflammatory cascade [31–33]. Chronic inflammation in asthma results in bronchial remodelling characterized by basement membrane thickening, mucosal blood vessels proliferation, extracellular matrix proteins deposition, mucus gland stimulation, smooth muscle cell and myofibroblast proliferation, and finally defective epithelium regeneration and atrophy .

Sköld CM. Remodeling in asthma and COPD—differences and similarities. Clinical Respiratory Journal. 2010;4(supplement 1):20–27.

In elderly asthmatics the presence of emphysema is minimal, and airway remodeling is thought to be the main cause of fixed airflow obstruction