Asthma/COPD Flashcards
objectives
Asthma Pathophys
- Smooth muscle dysfunction
- Airway inflammation
- Airway remodeling
- Fixed in a narrow position from collagen deposition
- Glands hypertrophied
Asthma pathophys: smooth muscle dysfxn
- exaggerated contraction
- increased smooth m. mass
- increased release of inflammatory mediators
- bronchoconstriction
- bronchial hyper-reactivity
- hyperplasia/hypertrophy
- inflmmatory mediator release
Asthma pathophys: Airway inflammation
- inflammatory cell infiltration/activation
- mucosal edema
- cellular proliferation
- epithelial damage
- basement membrane thickening
Asthma pathophys: Airway remodeling
- Cellular proliferation
- smooth m cells
- mucous glands
- inc matrix protein deposition
- basement membrane thickening
- angiogenesis
Asthma Phases
- acute response
- chronic/infammatory response
Asthma pathophys: acute response
- Bronchial hyperreacticity
- Mucosal edema
- Airway secretions
Asthma pathophys: chronic/inflammatory response
- Increase in inflammatory cell number
- LOTS of cells can release inflammatory medicators
- Steroids will control this
- Can lead to epithelial damage
Pathologic features associated with asthma
- Variable airflow obstruction
- Bronchoconstriction
- Edema
- Cough
- Airway hyperreactivity
- Airway inflammation (Eosinophils, mast cells, lymphocytes, neutrophils)
- Mucous hypersecretion
- Goblet cell metaplasia
- Submucosal gland hypertrophy
- Impaired mucous clearance
- Smooth muscle hypertrophy/hyperplasia
- Subepithelial matrix protein deposition
- Collagen deposition
asthma definition
- Inflammatory d/o of airways
- Reversible airflow obstruction
- Hyper-responsiveness
- Often viewed as atopic, allergic d/o with altered T cell function
- Best to view it as BOTH inflammatory AND smooth muscle d/o
- Variable severity and reversibility
- Tx should addres BOTH of these
- FH important!
asthma etiology
- Multifactorial
- Genetic
- FH of rhinitis, urticaria, eczema
- Viral infections
- Viral URI is the #1 cause of exacerbation = asthma attack
- Environmental
- Allergic: Pollen, molds, animal dander, dust mite
- Non-allergic: tobacco, chemicals, perfumes, cold, temp changes, pollution
- Others
- Drugs (BB and NSAID)
- GERD
- Rhinitis/sinusitis
- Food (rarely)
- Stress (more in adults)
- Genetic
other asthma facts
- Asthma is MC chronic childhood illness in US
- Increase in prevalence in 15 yrs by 58% overall
- 24million people have asthma (includes 7million children)
- Hospitalizations d/t asthma are preventable or avoidable with proper primary care
- Undertreatment and inappropriate therapy are the major contributors to asthma morbidity and mortality
- Underdiagnosed and treated, esp in children
- Over 500,000 hospitalizations/yr
- Over 6,000 deaths/yr
- Asthma is the third leading cause of preventable hospitalizations in US
- >100million days of decreased activity, 10million of lost school/ year
- 75% of those with asthma have persistent asthma and require daily controller med (far less receive these)
- Patients OVERESTIMATE the control of their asthma
- We need to tell them they should not be having symptoms
- Asthma mortality NOT directly related to severity
- d/t variability of asthma
- people with “mild” asthma may have SAME SEVERITY, just less often
asthma epidemiology
- 43% male; 57% female
- 67% at 18+; 33% 0-17 y/o
Ddx for children w/ asthma
- Allergic rhinitis and sinusitis
- Vocal cord dysfunction
- Vascular rings
- Laryngotracheomalacia
- Tumor or enlarged lymph nodes
- Viral bronchiolitis
- Cystic Fibrosis
- Bronchopulmonary dysplasia
- Aspiration due to gastroesophageal reflux
Ddx for adults w/ asthma
- Chronic obstructive pulmonary disease
- Congestive heart failure
- Pulmonary Embolism
- Mechanical obstruction (benign or malignant tumors)
- Pulmonary infiltration with eosinophilia
- Cough secondary to drugs (ACE inhibitors)
- Laryngeal dysfunction
Dx of asthma: important points
- Children with asthma are often mislabeled (bronchitis, bronchiolitis, croup, pneumonia) and may not get adequate therapy
- DX NOT NEEDED TO CONSIDER AND BEGIN TREATING ASTHMA SX!!
- Viral URI are MC precipitant of wheezing and cough in kids- do NOT preclude the dx of asthma= it is possible to have asthma and have it triggered by a viral illness!
- Recurrent episodes of cough and wheeze are almost always d/t asthma in both adults and kids
- Cough can be sole sx
asthma medical hx
- Episodic wheeze
- Chest tightness
- SOB
- Cough
- Sx worsen in presence of aeroallergens, irritants or exercise
- Sx occur or worsen at night, awakening pt
- Because you have a surge of cortisol in am naturally, then use it all day (little left at night)
- Pt has h/o allergic rhinitis or atopic dermatitis
- FH of asthma, allergy, sinusitis or rhinitis
4 stages of asthma
- Stage 1: Intermittent
- Stage 2: Mild Persistent
- Stage 3: Moderate Persistent
- Stage 4: Severe Persistent
4 stages of asthma–> Stage 1: Intermittent
- Symptoms less than a week
- Brief exacerbations
- Nocturnal symptoms not more than twice a month
- FEV1 or PEF ≥ 80% predicted
- PEF or FEV1 variability <20%
4 stages of asthma–> Stage 2: Mild Persistent
- Symptoms more than once a week- but less than once a day
- Exacerbations may effect activity and sleep
- Nocturnal symptoms more than twice a month
- FEV1 or PEF ≥ 80% predicted
- PEF or FEV1 variability 20-30%
4 stages of asthma–> Stage 3: Moderate Persistent
- Symptoms daily
- Exacerbations may affect activity and sleep
- Nocturnal symptoms more than once a week
- Daily use of short-acting beta-2 agonist
- FEV1 or PEF 60-80% predicted
- PEF or FEV1 variability >30%
4 stages of asthma–> Stage 4: Severe Persistent
- Symptoms daily
- Frequent exacerbations
- Frequent nocturnal asthma symptoms
- Limitation of physical activities
- FEV1 or PEF ≤60% predicted
- PEF or FEV1 variability >30%
asthma clinical sx
- Noisy/musical breath sounds
- Nocturnal awakenings
- Exertional dyspnea and “air hunder”
- Cough, SOB, wheeze
- Nasal flaring and grunting
- Suprasternal, intercostal and subcostal retractions
- Pallor, duskiness and cyanosis
Physical findings that increase probability of asthma
- Thoracic hyper-expansion on CXR
- Sounds of wheezing during normal breathing or a prolonged expiratory phase
- Increased nasal secretions, mucosal swelling, sinusitis, rhinitis or nasal polyps
- Atopic dermatitis, eczema
Therapeutic response that can strengthen dx of asthma
- Clinical improvement following bronchodilator and/or steroids
- So… when you don’t know but it sounds like asthma, give a bronchodilator and see if it helps sx
Making the Dx of asthma
- Recurrent sx
- Risk factors known
- Response to drug (bronchodilator or steroids)
- Other etiologies ruled out
goal of asthma tx
- Prevent chronic asthma sx and exacerbations in day and nigh
- Maintain normal activity; no limitations
- Have normal/near-normal lung fxn
- Prevent acute episodes
- Reduce ED visits and hospitalizations
- Have minimal SE on tx
- Enhanced adherance (simple meds)
Stepwise approach to managing asthma
- Gain control
- Maintain control
Gain control
- Preferred approach is to start therapy with more intensive program
- Suppresses airway inflammation and gain prompt control of reversible obstruction
- Ex: burst therapy steroids
- To do this, you need to define the severity of asthma
- Intervene with optimal medications
- Normalize activities, lung function and lifestyles
- Then try to “step down” tx to optimal levels
Maintain control
- f/u q 1-6 mos (usually q3-4)
- PFTs >=2x/yr
- “step down” long term control meds to achieve optimal control as safely and effectively as possible
- Keep it- Simple, Safe, Effective
Asthma tx
- No matter what ICS is ALWAYS in the treatment regime for persistent asthma
- Pts are candidates of Mainstay Therapy if the “RULES OF TWO” apply
- They are using a quick-relief inhaler >2x/wk
- They awaken d/t asthma >2x/month
- They refill their quick-relief inhaler Rx >2x/year
Where are the targets of asthma therapy?

current tx modalities of asthma
- Acute Tx or “Rescue” Therapies
- Chronic “controller” therapies
Acute Tx or “Rescue” Therapies
- Inhaled short acting β2 agonists (SABA) (Albuterol, Xopenex®)
- Systemic (injected) β2 agonists (epinephrine, terbutaline)
- Anticholinergics (Ipratropium bromide – Atrovent)
- Systemic steroids (Prednisone; PO preferred)
- 100% bioavailable; drug goes everywhere (not just lungs!)
- Oxygen, hospitalization, ventilation
Chronic “Controller” Therapies
- Inhaled corticosteroids (Flovent®, Pumicort©, Qvar®, Asthmanex®)
- Only about 2% is absorbed systemically (most goes directly to lungs)
- Long-acting bronchodilators (LABA) (Serevent®, Foradil®)
- NEVER use as monotherapy!
- Mast cell stabilizers (Intal®): not used often
- Leukotriene modifiers (Singulair®): good add-on therapy
- Combination therapies (Advair®, Symbicort®, Dulera®)
Asthma Medications
-
Long-term controller asthma meds are taken daily to achieve and maintain control of persistent asthma sx
-
Most effective long-term maintenance meds reduce inflammation!
- Inhaled steroids are best for persistent asthmatics
- ICS = First-line maintenance therapy for ALL persistent asthma, even mild
- Other classes of controller drugs, such as the LTM’s can be used, but they have limitations!
-
Most effective long-term maintenance meds reduce inflammation!
Inhaled Corticosteroids (ICS)
- ICS can decrease airway inflammation and bronchoconstriction of smooth muscle in mild to moderate asthmatics.
- Earlier tx with ICS appears to prevent pts from developing more prominent chronic lung changes and airway obstruction
- Long term use (> 2 yrs) significantly improves lung fxn
- Safe to use
Daily use of ICS can
- Diminish asthma sx; improvement will continue gradually
- decreases occurrence of severe exacerbations
- decreases use of quick-relief meds
- Improved lung fxn (PEF, FEV1, & airway hyperresponsiveness)
Effects of ICS on Inflammation
- Inhibits inflammatory mediator cells (decreases airway edema)
- Can reverse effects of airway remodeling
Long-Acting b2-Agonists (LABA)
- Safe and effective, easy to use, quick onset of action, well-tolerated
- Enhance benefits of ICS & more effective than ↑ ICS
- Treats nocturnal cough & exercise-induced bronchoconstriction for up to 12-14 hrs after use
- Enhance adherence and improve lung fxn
- NOT TO BE USED AS MONOTHERAPY!
Combination Therapies (ICS + LABA)
- Serevent® and Flovent® are available together in a DPI (Diskus® ) as Advair®(100/50, 250/50, 500/50)
- Clinical efficacy of a LABA & ICS is due to complementary actions of these two classes of drugs
- Treats BOTH inflammation and bronchoconstriction in a single device = IDEAL
Leukotriene Modifiers (LTM)
- Class of agents used in asthma therpay BUT limited long-term data exists
- Best used as add-on therapy, esp. for stuffiness and persistent cough
- Easy to dose, lack of perceived “steroid side effects”
Play a role in initial asthma tx, however, only a fraction of people treated with these agents appear to respond to therapy and they tend to have milder and more intermittent disease
asthma medical therapies
- Overall, short-acting bronchodilators account for over 50% of all asthma Rx among children and adults.
- Despite that asthma is now recognized as a chronic inflammatory disorder
- In Georgia, less than half of all asthmatics who need daily “controller” meds actually have them prescribed.
measuring effectiveness of asthma tx
- Improvement in lung fxn tests or PFT’s (spirometry: FEV1 > 6% or FEF25-75 > 35%)
- Improved AM/PM Peak Expiratory Flow
- Using Peak Flow Meters (measure speed & amt of air expelled in single puff)
- decrease use of “rescue” drugs (200 puffs per canister)
- Shouldn’t be using more than 4 canisters annually!
- decrease daytime and exercise-related resp. sx
- decrease nocturnal awakenings/cough
- Improved “quality of life”
Metered Dose Inhalers (MDI)
- MDI’s are mainstay for most asthma controller meds prescribed in US
- Small, portable, efficient, quick, & inexpensive to use (and lose!)
- When used with a spacer device, MDI’s deposit particles in small airways as effectively as nebs
- Effectively used at any age
- Technique is CRITICAL! Require SLOW INSPIRATORY flow rates
Typical MDIs
- Asthma spacers
- Dry Powder Inhalers (DPI’s)
- Diskus
Dry Powder Inhalers (DPI’s)
- Improved ease of use
- Impact of impending CFC phase-out
- decrease volume of inhaled powder
- Dose counters/indicators
- ↑ dose capacity in devices
- No dose to dose variation
Diskus®
- Open: Expose level underneath device
- Click: Push lever away until you hear or feel a click
- Inhale: Exhale, then bring device to lips and breathe in steadily & deeply thru inhaler. Airflow thru device ensures that dose is inhaled
- Close Diskus
Is My Asthma Well-Controlled?
- Have I visited the ER or hospital in past year?
- Do I use my rescue-inhaler more than 2x/wk?
- Have I found myself coughing or breathless in AMs and/or PMs?
- Do I limit my activities or miss work/school?
- Have I received Rx for oral prednisone >1x in past year?
COPD
- Chronic Obstructive Lung Disease
- Progressive airway obstruction
- Associated with smoking 90% of COPDers have smoked
- Not reversible
- Combination of chronic bronchitis, small airway obstruction and emphysema
COPD caused by
- Cigarette smoke (centrilobar emphysema)
- Alpha-1- antitrypsin deficiency (panacinar emphysema)
- Recurrent Airway infections
COPD incidence and mortality
- Approx 5% of Americans have COPD for a total of ≈12 million
- 125k deaths from COPD in ‘97
COPD symptoms in pt (esp over 40 y/o)
- Straw experiment
- How does it feel to take so long to breathe out?
- Shortness of breath, especially with exertion, resulting from being unable to expire completely…worsening over time
- This is worsened with exercise/exertion because patients are breathing faster
- Chronic, productive (especially in the morning) cough (can be a dry cough)
- Wheezing…patients will tell you this
- Chest tightness/heaviness
- Recurrent acute bronchitis
- Air hunger/increased effort to breathe
- Symptoms can happen late; after 50% of lung function is lost
COPD signs
- Hypoxemia
- Tachypnea
- Dyspnea on exertion
- Barrel chest/increased AP diameter
- Air trapping, widened rib spaces on CXR
- Wheezing (worse in exacerbation)
- Nail clubbing
- Peripheral edema (often later stage)- RHF
- Hypercapnea (later stage)
COPD spirometery
- Normal lung function (FEV1) declines by 30 ml per year after the age of 30
- In COPD- declines by 100ml per year
COPD risk factors
- Smoking
- Air pollution
- Occupational exposure
- Allergies
- Hereditary/Genetics
COPD mortality rate
- FEV1, BMI, Dyspnea, 6 minute walk (6MW) used as prognostic factors
- FEV1 = 1 Liter is 4 year prognosis
- End Stage COPD is approx. 1 year survival
- Oxygen
- Medicines
COPD Pathophys
- Combination of Chronic Bronchitis and Emphysema
- Narrowing of airway lumens and thickened walls
Chronic Bronchitis
- Clinical diagnosis
- Chronic cough and sputum production for at least 3 months of the year for at least 2 years.
- In the absence of any other disease.
- Caused by hypertrophy and hyperplasia of mucus secreting glands
- Intermittent dyspnea, copious sputum
Emphysema
- Morphologic Diagnosis
- Enlargement of airspaces distal to the conducting airways
- Bronchioles and alveoli walls are weakened
- Lysis of elastin and structural proteins
- Types
- Centrilobular- from smoking
- Panacinar- alpha 1 def
Centrilobular Emphysema
- Involves the Bronchioles
- With normal distal alveoli (except in severe dz)
- Exclusively found in smokers
- Central airway obstruction
- Upper lobe predominant
- Lung volume reduction surgery
Panacinar Emphysema
- Alpha-1 antitrypsin deficiency
- Genetic disease
- Patients have severe disease when compared to age/pack history
- Exacerbated by smoking
- Lower Lobe predominant
Pink Puffer = Emphysema
- Onset > age 50
- Dyspnea progressive, severe, constant
- Cough and sputum production mild, absent
- Weight loss
- Body habitus is thin, cachexia
- AP diameter increased/ barrel chest
- Percussion hyperresonant
- Auscultation diminished
- CXR- bulla, blebs, hyperinflation, hemidiaphragms are flattened
- Labs: EKG normal, ABG without hypercapnia or hypoxemia
- PFTs: increased TLC, increased RV, decreased diffusion capacity
Blue Bloater = Chronic Bronchitis
- Onset = after age 35
- Dyspnea is intermittent, mild to moderate
- Cough and sputum production persistent and severe
- No weight loss, can be obese, s/sx of RHF
- No increase in AP diameter
- Percussion normal
- Auscultation = wheezing, rhonchi
- PFTS: normal DLCO and RV/TLC
- CXR = Cardiomegaly, increased lung markings
- Labs – EKG with Rt Ventricular Hypertrophy, rt. Axis deviation
- Hypoxemia and hypercapnia are moderate to severe, resp acidosis
Ddx COPD
- CHF
- Chronic asthma
- Pulmonary embolism
- Bronchial asthma
- Bronchiectasis
- Cystic Fibrosis
- Central Airway obstruction
- Pulmonary Fibrosis
GOLD guideline criteria for COPD
- Stage 0: At Risk
- Stage I: Mild
- Stage II: Moderate
- Stage III: Severe
- Stage IV: Very Severe
GOLD guideline criteria for COPD: Stage 0
Stage 0: At Risk
- Chronic s/sx
- Exposure to risk factors
- Normal PFTs
- Treatment- influenza vac, avoid risk factors
GOLD guideline criteria for COPD: Stage I
- Stage I: Mild
- FEV1/FVC < 70%
- FEV1 >/= 80%
- With or without s/sx
- Treatment:
- Avoid risk factors
- Influenza vac.
- SABA prn
GOLD guideline criteria for COPD: Stage II
- Stage II: Moderate
- FEV1/FVC < 70%
- FEV1 btw 80 -50%
- With or without s/sx
- Treatment:
- Avoid risk factors, influenza vac.
- SABA prn
- Long acting Bronchodilator
Pulmonary Rehab
GOLD guideline criteria for COPD: Stage III
- Stage III: Severe
- FEV1/FVC < 70%
- FEV1 btw. 50- 30 %
- With or without s/sx
- Treatment:
- Avoid risk factors, influenza vac.
- SABA prn
- Long acting bronchodilator
- Pulmonary rehab
- ICS – if repeated exacerbations
- Evaluate for oxygen
- Daliresp (Roflumilast)
GOLD guideline criteria for COPD: Stage IV
- Stage IV: Very Severe
- FEV1/FVC < 70%
- FEV1< 30% or <50% with chronic respiratory failure
- Treatment:
- Avoid risk factors, influenza vac.
- SABA
- Long acting Bronchodilator
- Pulmonary rehab
- ICS
- O2
- ? Surgical candidate for lung volume reduction surgery.
- Consider hospice
COPD Tx w/ meds
- SABA
- Albuterol
- ProAir, Proventil 1-2 puff q4h prn
- Levalbuterol
- Xopenex 2 puffs TID prn
- Albuterol
- Long Acting Bronchodilators
- Tiotropium (spiriva)
- 1 puff qd
- Iprotropium bromide
- neb solu q6-8 h
- LABA: Salmeterol or formoterol
- use BID
- Theophylline
- Tiotropium (spiriva)
- ICS
- Beclomethasone
- Budesonide
- Fluticasone
- Combination Inhalers
- Advair
- Symbicort
- Dulera
- Oral Corticosteroids
COPD Dx work-up
- Complete PFT’s with ABG
- 6MW
- CXR - ? CT scan of Chest
- Alpha one antitrypsin level
- EKG
- ABG – resp. acidosis
- CBC
- BNP B-Type Natriuretic Peptide
- Echo
PFT for Obstructive COPD
- decrease in FEV1, FVC, ratio
PFT for hyperinflative COPD
- increase in RV, TLC
PFT for abnormal gas exchange COPD
- decrease in DLCO
COPD ABG
- decrease PaO2, increase in PaCO2
COPD clinical pearls
-
Methylxanthines
-
Theophylline
- narrow therapeutic window
- Cardiac sequelae if toxicities
- Sometimes works, sometimes doesn’t
-
Theophylline
- PO Albuterol is not safe from a cardiac standpoint (many COPD patients have concomitant cardiac disease)
- Watch out for pneumothorax due to bullae; do a CXR with unexplained worsening dyspnea
- In a young patient (age 40 or less) with COPD and a minimal or no smoking history, check an alpha-1 antitrypsin level…looking for a low level, indicating deficiency.
- This is a genetic cause of COPD
- Much higher incidence of COPD in HIV patients
- Discuss code status with all COPD patients…IN THE OFFICE
How to spot an acute exacerbation
- From patient’s baseline:
- Change in sputum color
- Increase in shortness of breath
- Increase in amount of sputum
- Also look for signs of infection:
- Fever, chills, hemoptysis, crackles/rales on lung exam
COPD Exacerbation
- CXR to rule out pneumonia as a cause for the exacerbation
- Check oxygen saturation!
- Decide whether or not to treat as an outpatient:
- PO steroids (prednisone)/bronchodilators
- PO Antibiotics
- Close follow up
COPD exacerbation Tx
- Hospitalized (hypoxemic, very dyspneic, fever, weakness)
- IV steroids, usually methylprednisolone, starting at 60mg IV Q6 hours, and taper…try not to dose less than Q8 hours for duration due to drug ½ life (transition to prednisone for discharge)
- Scheduled nebs; if on tiotropium (anticholinergic) do NOT use ipratropium
- When giving oxygen give only enough to get PaO2 above 60mmHg; this minimizes the danger of respiratory acidosis due to CO2 retention.
- Levalbuterol (q6 hours) or albuterol (q4 hours) nebs
- Mucolytic (guaifenesin) prn
- Sputum cultures, usually give antibiotics, covering for S. pneumo, H. flu, M. cat.
- Quinolones, cephalosporins, penicillins, macrolides
COPD smoking cessation options
- Nicotine replacement
- Behavioral modification
- Bupropion (Zyban, Wellbutrin)
- Varenicline (Chantix)
Smoking Cessation: other
- Patients need you to initiate the conversation…EVERY VISIT
- Medicare now reimburses for smoking cessation counseling
- If you don’t attempt it, you are not doing your job
- Bring them back for a smoking cessation visit
COPDer
- C: Corticosteroids (inhaled)
- 20% decrease in Acute exacerbations, but can increase risk of pneumonia
- O: Oxygen
- P: Prevention (Flu/Pneumovax, tob cessation)
- D: Dilators (Anticholinergic, SABA, LABA)
- E: Experimental (LVRS = lung volume reduction surgery)
- R: Rehabilitation