H380 Fall 2017

Compare and Contrast: Asthma VS COPD

Criteria Asthma COPD
Cigarettes a Heterogenous disease = combination of clinical manifestations + preventable and treatable disease
dayWhat is it? along with reversible expiratory airflow limitation or bronchial + persistent airflow limitation that is usually progressive
(definition) hyperresponsiveness + enhanced chronic inflammatory response in the airways and
+ lung disease that causes inflammation with variable episodes lungs
of airflow obstruction. + primarily cause = cigarette smoking and other noxious
particles and gases

Risk Factors / affects mostly women (62%) 3rd leading cause of death
Etiology O.A. undiagnosed 133,000 deaths per year
Genetic factors = atopy; genetic predisposition to develop an Cigarette smoking
allergic: immunoglobulin E oHyperplasia (↑ in cell production)/ goblet cells
 Male children ↑ mucus
obesity ↓ airway diameter
 Hygiene hypothesis (infant expose early to infection; use few ↑ difficulty of clearing secretions
antibiotics, exposed to other children, pets and live in rural oReduces ciliary activity; cause loss of cilia
setting helps the immune response fare better against asthma) oProduces abnormal dilation of distal air space w/
Cockroaches, furry animals, fungi, pollen, molds (in/outdoors destruction of alveolar walls.
Exercise-induced asthma oRemodeling
oExpose to cold, dry air during activity (swimming in Change structure of lungs by chronic inflammation
heated pool in door better) oStimulates SNS
 exercise induced bronchospasm. ↑ HR
oAfter vigorous exercise Causes peripheral vasoconstriction
oCause by hyperventilation which changes mucosa with ↑ BP and cardiac workload
cooling and rewarming of air/ capillary leaking in airway o↓ hemoglobin function
wall. o↑ platelet aggregation
 Air Pollutants oCompounds problems in CAD
o Aerosol sprays oCarbon monoxide
o Cigarette smoke/ wood smoke ↓ O2 – carrying capacity
 Accelerated decline of lung functioning ↑ HR
 ↑ severity of disease Impairs psychomotor judgment and performance
 Pt. < responsive to Tx. Reducing chances of oPassive smoking = environmental tobacco smoke
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 controlling the disease (ETS) = secondhand smoke
o Exhaust fumes (vehicle) ↓ pulmonary function
o Oxidants ↑ respiratory symptoms
o Perfume ↑ Risk of lung and nasal sinus cancer
o Sulfur dioxides Pneumonia (SLRTI)
 Occupational Exposure mo/yrs to develop, gradual ↑ Occupational & Environmental- intense / prolonged
o Agriculture, farming oDust, vapors, irritants, fumes at job
o Industrial chemicals and plastics oHigh levels of urban air pollution
o Laundry detergents oCoals, other biomass (fossil) fume used indoors for
o Metal salts cooking and heating in poor ventilated areas
o Paints, solvents Severe recurring respiratory Infection
o Pharmaceutical agents oImpair normal defense mechanisms (starts in
o Wood and vegetable dusts childhood/ ↑ in adulthood)
 Viral respiratory tract infections (causing alter oHIV
tracheobronchial system, ↑ inflammatory cell growth, edema oTuberculosis
of airways; major triggering factor of AAA Alpha1-antitrypins (AAT) Deficiency
 Rhinitis (improves w/ Tx.) oGenetic RF (3% have AAT)
 Chronic sinusitis (inflammation of mucous membranes) oAutosomal recessive disorder
o Tx. = removal of lg. nasal polyps Serum protein produced by liver / found in lungs
 Drugs and Food Additives An α1 protease inhibitor to protect normal lung tissue
o Asthma triad; nasal polyps, asthma, sensitivity to aspirin protease attacks during inflammation of smoke and
and NSAIDs infection
 Wheezing occur w/in 2 hrs. Tx. Prolastin (IV weekly) slow progression
 Found in foods, beverages, and flavorings Affect people of European descent
 Rhinorrhea, congestion, tearing, angioedema Can have DNA, Screening of siblings, serum for
 Oral beta adrenergic blockers (metoprolol); eye drops genetic testing
(timolol) – cause bronospasm  Aging
 ACE inhibitors (lisinopril) causes coughing o Emphysema common with physiologic changes in
 Tartrazine – yellow dye no. 5 O.A. lung tissue
 Sulfiting agents in food (fruit, beer, wine), preservatives (on Loss elastic recoil (thoracic cage changes causing
veggies), sanitizing agents osteoporosis and calcification of costal cartilages)
 Rare in adults Chest wall stiffens (affects ventilation; harder to breath)
 GERD Altered G.E. (alveoli ↓ peripheral airways ↓G.E. & PaO2
o Common in people with asthma = trigger  Low exercise tolerance

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 bronchoconstriction and aspiration; treat GERD 1ST Asthma
because asthma meds worsen GERD o Pathologic and functional overlap with COPD
 Psychologic factors o Called Asthma-COPD overlap syndrome
o Stress = bronchoconstriction via stimulation of o Equal in men and women because of smoking
cholinergic reflex pathways
o Extreme emotional expressions (crying, laughing, anger,
fear) leads to hyperventilation and hypocapnia (↓ CO2 in
blood causing deep breathing)
o Asthma can trigger panic, anxiety, and stress
What causes it? 1st persistent inflammation of airways because of exposure to combination of Chronic bronchitis (cough and sputum > 3
Pathophysiolog allergens or irritants mo. for 2 yrs.) and Emphysema (destruction of alveoli and
y Limit airflow cause bronchoconstriction, hyperresponsiveness, have several structural abnormalities
edema of airways not fully reversible; airflow limited during forced exhalation
Inflammatory cells involved are mast cells (start), loss elastic recoil
macrophages, eosinophils, neutrophils, T and B lymphocytes, Airflow obstruction due to mucous hypersecretion, mucosal
epithelial cells edema, and bronchospasm
Trigger by Allergen in Early Phase Response (EPR) Lung disease that systemic causing chronic inflammation
 1st step: trigger Chronic inflammation primary process
 2 mast cell degranulation  1st inhalation of noxious particles and gases like
 3 release IgE smoking
 4 Release leukotrienes, histamine, cytokines,  2nd neutrophils, macrophages, and lymphocytes
prostaglandins, and nitric oxide may cause mediators released causing damage to lung tissue.
 Vasodilation of blood vessels ↑ capillary  3rd airways inflamed caused by oxidants that inactivate
permeability (runny nose) antiproteases and stimulate mucus secretion fill the
 Itching (nerve cells) lungs with fluid
 Bronchial spasms / narrowing of airway (smooth  4. Parenchyma destroyed (imbalance b/w proteinase
muscle) and anti-proteinase)
 Mucus production (goblet cells)  Supporting structures of lungs destroyed
 Occur 30 -60 m after exposure  Air goes in easily, but remains in the lungs (smaller
 Last-phase response (LPR) airways)
 Recur 4 to 6 hrs. after initial attack  Bronchioles tend to collapse (lungs overinflated)
 Occurs in 50% of patients  Causes barrel-shaped chest, dyspnea, limited exercise
 More severe than EPR; last 24 hr/longer ability
 May lead to irreversible lung damage  Impaired G.E. = hypoxemia and hypercapnia (increased
 Corticosteroids effective Tx. CO2)

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 Causes remodeling changing subepithelium
  Air entrapment = destroyed alveoli create bullae (lg. air
fibrosis, smooth muscle hypertrophy of airways, spaces in parenchyma) and blebs (air spaces in pleurae)
lg. amt. of mucus, inflammation, angiogenesis  Caused problems with perfusion and ventilation not
 Inflammation mediators to EPR G.E.
 Vascular congestion  Common characteristics
 Edema formation  Overproduction of mucus cause COUGH in
 Production of thick, tenacious mucus predominant chronic bronchitis patients
 Bronchial muscle spasm  Dysfunction of cilia
 Thickening of airway walls  Overinflation of lungs
 Impaired G.E. (stimulate inflammatory mediators and
enlarges submucosal glands)
 Pulmonary vascular changes
 Vasoconstriction of small pulmonary arteries
 Thick blood vessel in later phase
 Increase pressure on pulmonary circulation due to loss
in alveolar walls and capillaries =
 Causes pulmonary hypertension
Coexists with CVD
Cachexia (skeletal muscle wasting)
Osteoporosis
Diabetes
Metabolic syndrome
Clinical  Unpredictable and variable diagnosis includes
Manifestations Recurrent episodes of wheezing, breathlessness, cough,  chronic intermittent cough (first symptom) or sputum
dyspnea, and chest tightness after exposure or trigger production
may be abrupt or gradual  progressive dyspnea when moving present daily
last-minute hours  exposure to risk factors
expiration prolonged 1:3; 1:4 (inspiratory – expiratory ratio) common complaints early stage
 bronchospasm, edema, mucus in the bronchioles occur  not able to take deep breaths
because of narrow airways  heaviness in chest
air takes longer to move out produces wheezing, air trapping,  gasping for air
hyperinflation  air hunger
most common  dyspnea interferes with daily activities
 cough  can’t walk fast as peers

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  shortness of breath (dyspnea) Late Stage COPD
 wheezing dyspnea at rest
 chest tightness over distended alveoli increasing air entrapment
 variable airflow obstruction causes diaphragm to flatten
cough variant asthma patient breeze from partially inflated lungs
 cough is the only symptom decreased abdominal breathing; causes chest breather by rely
 bronchospasm not severe enough to cause airflow on intercostal and accessory muscles
obstruction but increases bronchial tone and irritate wheezing (laryngeal) and chest tightness (follow activity)
stimulated cough receptors advanced COPD
 fatigue (highly prevalent)
 weight loss occurs with adequate caloric intake
 anorexia occurs
 Paroxysmal coughing may be so severe that patient faints
or fractures ribs
 prolonged expiratory respiratory phase, wheezes, ↓
breath sounds
 ↑ Anterior-posterior diameter (barrel chest) chronic air
trapping
 Tripod position (right with arms supported on fixed
surface)
 Pursed lip breathing (use accessory muscles like neck to
aid w/ inspiration)
Polycythemia and cyanosis
Hypoxemia = PaO2 < 60; SO2 < 88%
Increased production of red blood cells
Bluish-red color of skin
Hemoglobin concentrations may reach 20 g/dL (200 g/L) or
more
 Low hemoglobin and hematocrit = chronic anemia

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Diagnostic Spirometry  Hx. and physical exam for both
Studies Peak expiratory flow rate (PEFR) = aid to diagnose and monitor Spirometry confirms the presence of airflow obstruction and
asthma determines the severity of COPD
Chest x-ray (look for foreign body in airway like pneumonia);  FEV1/FVC ratio < 70% (in one minute)
may have fever, chills, upper airway stridor  FEV1 = severity of COPD
Oximetry  expressed as a percentage
Allergy testing (determine sensitivity to specific Allergens  The lower the FEV1 the sicker the patient.
Blood levels of eosinophils highly suggestive to specific
Increased residual volume
allergens
 Give patient SABA
CBC laboratory Chest x-ray = show flat diaphragm due to hyperinflated
lungs
6-minute walk test = used for exercise-induced hypoxemia
COPD Assessment Test (CAT) 88% SaO = room air;
measure daily impact of COPD
Clinical COPD Questionnaire (CCQ)
ABGs assess in severe stages > 50% FEV1
 ↑ HCO3, low PaO2, elevated PaCO2, low-normal pH
Echocardiogram or multigated acquisition (MUGA) (cardiac
blood pool) scan
 Evaluate right and left sided ventricular function
Sputum for culture and sensitivity
 Collected for acute exacerbation and doesn’t respond to
antibiotic therapy


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Clinical Steps to treating Asthma
management– 1. use SABA as needed
medical/surgical 2. use low-dose ICS (preferred) /LTRA or theophylline
/drugs 3. use low-dose ICS + LABA or Medium-dose ICS (preferred)
(Collaborative low dose of ICS + LTRA or theophylline, or zileuton
Interventions) 4. Medium dose of ICS and LABA (preferred) medium dose of
ICS + either LTRA, theophylline, or zileuton
5. High dose ICS and LABA and omalizumab for allergens
6. High dose ICS and LABA and corticosteroid and omalizumab
for allergens

Must used
Complications Severe; life threatening exacerbation  Cor pulmonale
to look for  RR > 30/min  Exacerbations of COPD
 Dyspnea at rest, feeling of suffocation  Acute respiratory failure
 Pulse > 120/min  Peptic ulcer disease
 PEFR is 40% at best  Depression/anxiety
 Seen in ED or hospitalized
Life-threatening asthma
 Too dyspneic to speak
 Perspiring profusely
 PEFR < 25%
 Admitted to ICU
Mediation for  Short-acting bronchodilators
exacerbations  Oral systemic corticosteroids
 Antibiotics
 Supplemental oxygen therapy
Independent For spirometry usage; have patient to stop taking bronchodilator  Acute Respiratory Failure caused by exacerbations and
Nursing medication for 6 to 12 hrs. before test; help determine if discontinuing bronchodilator or corticosteroid medication
Interventions/ medication is working; ↑ 200 mL or 12% on breathing which increases cough and dyspnea
Implementation  Assess the severity of the disease at diagnosis and initial
/Education Tx.
 Monitor periodically to control disease
Comparison of 1. Age Usually <40 yr (onset). 1. Usually 40-50 yr (onset).
asthma and 2. Smoking Hx. Not causal. 2. long history of smoking (>10-20 pack-years)
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COPD 3. Health and family Hx of allergy, rhinitis, eczema 3. Family history of asthma; lung or liver disease without
4. Clinical symptoms Intermittent, worse at night or early smoking history (α1-antitrypsin deficiency). Infrequent
morning. allergies. Exposed to environmental pollutants.
5. Dyspnea only during exacerbations or poor control. 4. Slowly progressive and persistent
6. Sputum Infrequent. 5. Dyspnea during exercise.
7. Disease course Stable (with exacerbations). 6. have sputum often
8. ABGs are normal 7. Progressive worsen
9. pH is ↑ Early in exacerbation, then ↓ if prolonged/ severe; ↓ 8. advanced COPD
PaO2, PaCO2 early signs; PaCO2 increases during exacerbation ++++ low-normal pH and PaO2
10. Chest x-ray reveal hyperinflation ++++ High-normal PaCO2 with high HCO3− (compensated
11. lungs are often normalized respiratory acidosis)
12. both have increase lung capacity 9. pH, PaO2, is N→↓PaCO2 = N→↑
13. both have increased residual volume 10. Chest x-ray reveal cardiac enlargement, flattened
14. both have decrease FEV1 diaphragm.
15. FEV1/FVC normal to decrease 11. never normalized
15. ↓ < 70%

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