ASTHMA & COPD

Asthma

• Asthma is a chronic inflammatory

disorder of the airways causes recurrent
episodes of coughing, wheezing,
breathlessness, and chest tightness.
• These episodes are usually associated
with widespread but variable airflow
obstruction that is often reversible either
spontaneously or with treatment.
Asthma

• Definition of asthma
• a chronic inflammatory disease of the
airways in which many cells/cellular
elements play a role, including, mast cells
eosinophils, T-lymphocytes, macrophages,
neutrophils, and epithelial cells
• airway inflammation causes recurrent
episodes of wheezing, breathlessness, chest
tightness, and coughing, particularly at night
or in the early morning.
Signs and Symptoms
• Wheezing due to airstream turbulence and
vibration of mucus
• Rapid breathing and shortness of breath
(dyspnea)
• Coughing
• Chest tightness
• Hyperinflation of thorax, voluntary at first to
dilate airways; secondarily as a result of
incomplete emptying
• Markedly reduced FEV1 (forced expiratory
volume)
• Attacks typically last from a few minutes to
several hours and are often associated with
exercise or sleep
Etiology of Asthma
• Two types of asthma have been
described:
• Extrinsic, or allergic asthma (atopic asthma)
• Mediated by IgE
• Usually begins in childhood, less common in adults
• Usually associated with atopy
• Sensitization to allergens is key feature
• increased indoor play and exposure to indoor
allergens
• Decreased childhood infections inhibits normal
development of immune system leading to increases
in allergic responses?
• Intrinsic, or idiopathic asthma
• More common in adults
• Usually not associated with atopy
• Patients may have nasal polyps, asprin sensitivity,
sinusitis
• Attacks may be precipitated by infection, exercise,
inhaling cold air, emotional factors
Asthma Triggers
• Can be physical, chemical,
environmental or pharmacologic in
nature
• Common triggers include:
• mold
• pollen
• house dust mites
• pet dander
• cock roach antigens
• cigarette smoke
• perfume and other chemicals (e.g. cleaners)
• viral infections
• cold air
• exercise
• aspirin
Pathophysiology

• Well recognized as an inflammatory

condition
• Chronic airway inflammation results in:
• increased smooth muscle cell proliferation and
hypertrophy leading to thickening of the airway
wall
• increased mucous production
• airway edema
• End result is partial airway obstruction and
difficulty in airflow movement
Pathophysiology

• Other features:
• Presence of inflammatory mediators may
increase airway reactivity and induce
bronchospasm
• contraction of smooth muscle surrounding
medium-sized bronchi and bronchioles
Pathophysiology

• Other features:
• Presence of inflammatory mediators may
increase airway reactivity and induce
bronchospasm
• contraction of smooth muscle surrounding
medium-sized bronchi and bronchioles
Traditional Asthma Theory
• Asthma was traditionally thought of as
resulting from altered
adrenergic/cholinergic balance:
• 2 Agonist drugs (albuterol, etc) give rapid,
effective relief in asthma attacks
• Cholinergic muscarinic antagonists also
provide relief (atropine, ipratropium
bromide)
• Asthmatics appear to have partial blockade
of -adrenergic receptors (or a reduced or
defective population)
• Evidence against the -blockade theory
of asthma
• -Blockade in normal subjects does not
 Revised Asthma Theory
• Asthmatics have an imbalance of
adenosine receptor subtypes (A1
predominates over A2):
• Inhalation of adenosine in asthmatics but not in
normal subjects causes bronchoconstriction
• Adenosine A2 receptor may be inactive or
underrepresented in asthmatics
• Theophylline, an adenosine receptor
antagonist, is effective in the treatment of
asthma
• Antagonizes both receptor Adenosine

subtypes, but because A1

predominates, blockade of
A1 Receptor A2 Receptor
its effects (bronchoconstriction) Theophylline
gives relief
Constriction Dilation
Asthmatics
Current Asthma Theory
• Inflammatory mediators are responsible
for bronchoconstriction
• Leukotrienes, prostaglandins, cytokines (IL4,
IL5)
• Released by macrophages, mast cells, T
lymphocytes
• Promote the migration and activation of other
inflammatory cells, most notably eosinophils
• Eosinophils also release substances that damage
tissue and promote hyperreactivity
• Current and future therapies are directed at
interfering in these pathways
• Zafirlukast (Accolate) is LTD4 and LTE4
receptor blocker
• Zileuton (Zyflo) is a 5-lipoxygenase inhibitor
that blocks LTD4 and LTE4 synthesis
Diagnosis of Asthma
• Made on the basis of spirometry:
• Spirometry measurements (FEV 1 , FVC, FEV
1 /FVC) taken before and after the patient
inhales a short-acting bronchodilator
• Helps determine whether there is airflow obstruction
and whether it is reversible over the short term
• Generally valuable in children over age 4; however,
some children cannot conduct the maneuver adequately
until after age 7
Diagnosis of Asthma
• Made on the basis of spirometry:
• Measures the maximal volume of air forcibly exhaled
from the point of maximal inhalation (forced vital
capacity, FVC) and the volume of air exhaled during
the first second of the FVC (forced expiratory volume
in 1 second, FEV 1 )
• Airflow obstruction is indicated by reduced FEV 1 and
FEV 1 /FVC values relative to reference or predicted
values
• Significant reversibility is indicated by an increase of
>12 percent and 200 mL in FEV 1 after inhaling a short-
acting bronchodilator
Diagnosis of Asthma
• Key indicators in patient history
suggestive of asthma and need for
diagnostic spirometry include:
• Wheezing—high-pitched whistling sounds
when breathing out—especially in children
• History of any of the following:
• Cough, worse particularly at night
• Recurrent wheeze; recurrent difficulty in breathing
• Recurrent chest tightness
• Reversible airflow limitation and diurnal variation
as measured by using a peak flow meter
Diagnosis of Asthma
• Key indicators in patient history
suggestive of asthma and need for
diagnostic spirometry include:
• Symptoms occur or worsen in the presence
of:
• Exercise; viral infection
• Animals with fur or feathers; house-dust mites (in
mattresses, pillows, upholstered furniture,
carpets)
• Mold; pollen; smoke (tobacco, wood)
• Changes in weather; Strong emotional expression
(laughing or crying hard)
• Airborne chemicals or dusts; Menses
• Symptoms occur or worsen at night,
awakening the patient
Classification of Asthma

• Based on severity:
• Step 1 = intermittent
• Step 2 = mild persistent
• Step 3 and 4 = moderate persistent
• Step 5 and 6 = severe persistent
Treatment

• The primary goal is prevention of life-threatening asthma by early

• recognition of signs of deterioration and early intervention. As
• such, the principal goals of treatment include: 2
• • Correction of significant hypoxemia
• • Rapid reversal of airflow obstruction
• • Reduction of the likelihood of relapse of the exacerbation or
• future recurrence of severe airflow obstruction
• • Development of a written asthma action plan in case of a
further
• exacerbation
Pharmacologic Therapy
• 2 types of asthma medications:
• “quick relievers”
• short-acting beta 2 agonist inhalers
• “long-term “controllers”
• inhaled corticosteroids
• long acting beta 2 agonist inhalers
• oral beta 2 agonists
• Theophylline
• cromolyn/nedcromil
• leukotriene modifiers
 Drugs Used in Asthma

 Bronchodilator Drugs
 a. Adrenergic agonists
 Adrenergic drugs used for the management of acute and
chronic asthma are adrenaline (activates both α and β
adrenoceptors), isoproterenol(selective for βadrenoceptor),
 Salbutamol, Albuterol, terbutaline, and salmeterol, that are
relatively selective for β2adrenoceptors that do not cause
excessive cardiac stimulation.
 These agents are used both to reverse acute episodes of
bronchospasm and prophylactically to maintain airway
patency over the longterm.
 Bronchodilators..
 Inhaled, short-acting (SABA): albuterol, bitolterol,levalbuterol, pirbuterol
 Inhaled, longacting (LABA): salmeterol, formoterol
 Oral, long acting: albuterol, terbutaline
 MOA
 Adrenomimetics enhance the production of cAMP by activating
adenylylcyclase, the enzyme that converts adenosine triphosphate(ATP) to cAMP.
 AdverseEffects
 Even after inhalation, effective amount scan reach the systemic circulation and
cause side effects (e.g.,tachycardia,hyperglycaemia,hypokalemia)
 They ↑HR, tremors, chest pain by acting on beta1 receptors
 During chronic administration, the sensitivity of bronchial musculature is likely to
decline.
 ClinicalUses
 Adrenaline(non-selective adrenoceptor agonist) is used in the treatment of
acute anaphylaxis.
 Isoproterenol (non-selective β adrenoceptor agonist) is used principally by
inhalation for the management of bronchospasm. It is also used intravenously
for asthma and as a stimulant in cardiac arrest.
 Terbutaline, albuterol, salmeterol and other β2 adrenoceptor agonists are used
primarily in the management of asthma.
 Terbutaline and albuterol have very rapid onset of action and are indicated for
acute symptom relief.
 •Salmeterol, in contrast, has a slow onset of action but a long duration of
action (duration: 12 h; onset ~20 min), it is thus used as prophylactic therapy
only, not to reverse acute symptoms
 Phosphodiesterase Inhibitors
 Theophylline and its more soluble ethylenediamine salt,

aminophylline, act by inhibition of phosphodiesterase

 Phosphodiesterase are enzymes that inactivate cAMP and

cyclic guanosine monophosphate (cGMP), second

messengers that mediate bronchial smooth muscle
relaxation.
 Increases cyclic AMP levels cause bronchodilation and

inhibition of chemical mediator release from mastcells

 Decreases secretions and stimulates respiration
 In bronchial asthma, theophylline can be given orally for
prophylaxis or aminophylline parenterally to control the attack.
 Theophylline has a narrow therapeutic index and produces side
effects that can be severe, even life threatening
 Theophylline is usually administered orally having highly
variable oral absorption, and multiple drug interactions
 Plasma levels must be monitored, Sustained release
preparations preferred
 Over dosage produces cardiac and CNS stimulation, and may
cause seizures. Toxicity can be fatal
 Anticholinergic Drugs/Antimuscarinic
 Act by inhibiting M3 receptor found in airway smooth muscle, mucus glands,
and airway epithelium.
 Ipratropium bromide
 Is a synthetic muscarinic blocking agent used for the treatment of some
respiratory disorders
 Is used via inhalation in the treatment of chronic obstructive pulmonary disease
and to a lesser extent, asthma.
 Ipratropium has as lower onset of action (1–2hours for peak activity) than
β2-adrenoceptor agonists, thus more suitable for prophylactic use.
 Ipratropium is as effective as β2 adrenoceptor agonists, in chronic obstructive
pulmonary disease but less effective in asthma
 It is poorly absorbed and lacks sufficient effectiveness in allergic bronchospasm
 The most prevalent peripheral side effects associated with
ipratropium are drymouth, headache, nervousness, dizziness, nausea,
and cough.
 short-acting used in COPD (asthma)
 Additive effects when used with beta 2-agonists. Used as MDI or
nebulizer
 Tiotropium
 Long-acting anticholinergic:
 •Recently approved for use in COPD
 Ipratropium PLUS Albuterol: combines a short-acting anticholinergic
PLUS SABA 2 agonist
 Anti-inflammatory Drugs
 Corticosteroids
 All corticosteroids (Adrenal gland hormone derivatives) have the same general
mechanism of action
 Act by inhibiting cytokine and mediator release, attenuation of mucus
secretion, upregulation of β adrenoceptor numbers, inhibition of IgE synthesis,
attenuation of eicosanoid generation, decreased microvascular permeability,
and suppression of inflammatory cell influx and inflammatory processes.
 The effects of the steroids take several hours to days to develop, so they
cannot be used for quick relief of acute episodes of bronchospasm.
 Used in inflammatory and allergic conditions.
 Decrease inflammation, airway edema, mucus production and increase
responsiveness to beta 2 agonists.
 Clinical Uses
 Inhaled corticosteroids, including triamcinolone acetonide, budesonide
beclomethasone dipropionate, fluticasone, flunisolide are indicated for maintenance
treatment of asthma as prophylactic therapy butarenot effective for relief of acute
episodes of severe bronchospasm.
 Inhalation limits systemic toxicity; Inhaled-MDI or dry-powder, Usual dose: 1-2puffs 2-
4X per day
 MDIs-use as pacer (rinse mouth after use)
 Possible SE: adrenalsuppression, boneloss
 Systemic corticosteroids, including hydrocortisone, prednisone and prednisolone, are
used for the shortterm treatment of asthma exacerbations that do not respond to β2
adrenoceptor agonists and aerosol corticosteroids.
 •Systemic corticosteroids, along with other treatments, are used to control status
asthmaticus.
 Systemic glucocorticoids for asthma
 Systemic steroids (IV or oral) used in high-dose, short-term
“pulses” to control acute exacerbations
 Short-term therapy for acute exacerbations; chronic use if unable
to control symptoms otherwise.
 IV: for acute attack needing emergency care, admission
 Side Effects
 Range from minor to severe and life threatening.
 The nature and severity of side effects depend on the route, dose,
and frequency of administration, as well as the specific agent used.
 (3)AlternativeTherapies
 A number of medications useful in the treatment of asthma are
neither strictly bronchodilators nor anti-inflammatory agents.
 They are classified as alternative asthma therapies
 Leukotriene Modulators
 MastCellStabilizers
 These drugs, used prophylactically to decrease the frequency and
severity of asthma attacks and are NOT indicated for
monotherapy.
 They are used along with adrenomimetic bronchodilators,
corticosteroids, or both.
 Leukotriene Inhibitors
 Anti-inflammatory drugs that interfere with the inflammatory actions of the
leukotrienes.
 The cysteinyl leukotrienes are generated in mast cells, basophils, macrophages, and
eosinophils thus decrease eosinophil infiltration, mucus production, airway edema,
bronchoconstriction.
 Zafirukast and montelukast (Singulair) block leukotriene receptors. (Preferred);
Cysteinyl leukotriene (LTC4,LTD4,&LTE4) receptor antagonists
 Zileutronblockstheenzymerequiredfortheformationofleukotrienes;Leukotriene(LTB4)s
ynthesisinhibitor
 Drugs are indicated for the chronic treatment and control of asthma
(Prophylaxis/maintenance).
 These mediators are powerful bronchoconstrictors and stimulate mucus secretion
and microvascular leakage, both of which contribute to airway obstruction.
 MOA
 Montelukast and zafirlukast are competitive antagonists of these receptors.
 In contrast, zileuton suppresses synthesis of the leukotrienes by inhibiting
5-lipoxygenase, a key enzyme in the bioconversion of arachidonic acid to
the leukotrienes.
 Zileuton also blocks the production of leukotriene B4
 Clinical Uses
 Montelukast, zafirlukast, and zileuton are indicated for the prophylaxis and
chronic treatment of asthma only because of their long onset of action (3-
14 days).
 All the three agents are administered orally.
 Leukotriene Inhibitors
 Side effects
 Zafirlukast and montelukast are well tolerated but acute vasculitis,
eosinophilia, and a worsening of pulmonary symptoms may occur in
rare cases.

 Zafirlukast increases plasma concentrationsof warfarin and decreases

the concentrations of theophylline and erythromycin.
 Dyspepsia is the most common side effect of zileuton.
 •Liver transaminase levels are elevated in a small percentage of
patients taking zileuton.
 •Zileuton inhibits the metabolism of theophylline
 (b) Mast Cell Stabilizers
 Cromolyn and Nedocromil
 Cromolyn and Nedocromil are chemically related drugs called chromones
that are used for the prophylaxis of mild or moderate asthma
 Both are administered by inhalation and have very good safety profiles,
making them particularly useful in treating children
 Are used almost exclusively for the prophylactic treatment of mild to
moderate asthma and should not be used for the control of acute
bronchospasm
 They are effective in about 60 to 70 of children and adolescents with
asthma, but less effective in older patients and in patients with severe
asthma
 It may take up to 4 to 6 weeks of treatment for Cromolyn sodium to be
effective in chronic asthma, but it is effective after a single dose in exercise
induced asthma
 Cromolyn and nedocromil inhibit the physiological effects of
antigen-antibody reaction on mastcells that triggers allergic
reactions by inhibiting the release of histamine.
 Administration as nebulized or MDI

 Have no effect on the histamine receptors giving best results

before large amounts of histamine is released (prophylactic)

 Clinical Indication:Prevent symptoms of

1.Severebronchial asthma (for control of asthma (NOT

effective in acute attacks)
2.Exercise-induced bronchospasm
3.Allergicrhinitis 4.Mastocytosis
(c)IgE Blockers
 Monoclonal antibodies e.g.Omalizumab
 Omalizumab (Xolair),binds to circulating IgE
 Inhibits the binding of IgE to mast cells but does not

activate IgE already bound to these cells and thus does not
provoke mast cell degranulation.
 It may also inhibit IgE synthesis by B lymphocytes(Down-

regulates mast cell receptors for IgE)

 Inhibits binding of IgE to mast cells, preventing release of

inflammatory mediators
 STATUS ASTHMATICUS
 •Status asthmaticus is a life-threatening exacerbation of asthma symptoms that is
unresponsive to standard therapy.
 It must be treated very aggressively, and hospitalization may be necessary.
 A provocative factor such as prolonged allergen exposure or a respiratory infection often
precedes status asthmaticus.
 A rapid increase in the daily use of bronchodilators to control acute symptoms is a
danger sign of an impending crisis.
 •Treatment includes
 •oxygen
 Inhaled short-acting β2 agonists and
 Oral or parenteral corticosteroids.
 Subcutaneous β2 agonists can be given to those who respond poorly to inhaled
adrenomimetics.
 Inhaled ipratropium may be effective in some patients.
 Global strategy for diagnosis, management, & treatment of
Obstructive Lung Disease (GOLD Criteria)
 •“PulmonaryFunctionTests”(PFTs)areusedtoevaluatelungfunction:
 •diagnose and stage disease
 •Monitor efficacy of treatment or progression of disease
 •FEV1
 •Staging determines treatment strategy
 •Stage1–Mild
 •Stage2–Moderate
 •Stage3–Severe
 •Stage4–Verysevere
CATEGORY SYMPTOMS THERAPY
 A (mild) Less Short-acting bronchodilator –
SABA -Anticholinergic
 B (moderate) More Add to short acting-LABA or -
Anticholinergic
 C (severe) Less InhaledGC + LABA or Long acting
anticholinergic
 D (very severe) More InhaledGC + LABA and/or Long
acting anticholinergic
 QuickreliefvsLong-Term
 Quick
 Shortactingbetaagonist(SABA)
 Anticholinergics
 IV&oralglucocorticoids
 Long-term
 Longactingbetaagonists(LABA)
 Methylxanthines
 InhaledGCs
 Cromolyn
 Anti-IgE
 Leukitrienemodifiers
 Medications–Asthma&COPD
 •DonotreducemortalitybutreducesymptomsandimprovequalityoflifeQoL
 •AddressBOTHbronchoconstriction&inflammation:
 •Bronchodilators
 •beta2agonists
 •methylxanthines
 •Anticholinergics
 •Anti-inflammatory
 •glucocorticoids(steroids)
 •cromolyn
 •leukotrienemodifiers
 •IgEblockers
 Management of asthma: Acute exacerbation
 •Inhaled

beta2agonistsforacutereliefofbronchospasm(MDIwithspacer
ornebulizedsolution)
 •IVororalsteroidtherapy
 •SupplementaloxygentokeepO2sats>95%
 •SQepinephrineifunabletouseinhaled
 •Mayrequirehospitalization
 Route Medication
 Inhaled
 MDI–aerosol
 MDI-powder
 Nebulizer Beta-2agonists(short&longacting),
Anticholinergics, Glucocorticoids
 Oral Methylxantines, Leukotrienemodulators
 Injection Glucocorticoids, Beta-2agonists
 Patient Education
• Key in helping patients control their asthma
and stay out of the hospital
• Should teach and reinforce at every
opportunity:
• Basic facts about asthma
• Roles of medications
• Skills: inhaler/spacer/holding chamber use, self-
monitoring
• Environmental control measures
• When and how to take rescue actions
COPD

• Disease state characterized by airflow limitation

• Airflow limitation is
• not fully reversible
• Usually progressive
• Associated with abnormal inflammatory response of the lungs
to noxious particles or gases
• Caused by a mixture of small airway disease (obstructive
bronchiolitis) and parenchymal destruction (emphysema)
• Relative contribution of each varies from patient to patient
• Chronic Inflammation is present and causes remodeling and
narrowing of small airways
• Destruction of the parenchyma
• Loss of alveolar attachments to the small airways
• Decreases lung elastic recoil
• The above changes lead to a diminishment in the ability of the
airways to remain open during expiration
• In the past COPD has been viewed as the overlapping of
Chronic Bronchitis and Emphysema
• However movement away from this view
Obstructive vs Restrictive
Pulmonary Disease
• Obstructive diseases impair exhalation
• Asthma, bronchitis, emphysema
• Obstructive diseases reduce FEV/FVC ratio
• vital capacity does not change (may even increase)
• Restrictive diseases impair inhalation
• Pneumonia, pulmonary fibroses (black lung)
• Due to fluid accumulation, loss of elasticity
• Restrictive diseases reduce volume (vital capacity)
but do not affect FEV/FVC ratio
Chronic Bronchitis: Clinical
Characteristics
• Chronic bronchitis is characterized by
the excessive production of mucus with
productive cough
• Blockade of bronchioles by mucus,
inflammation and edema
• Presentation
• Early onset (20-30 yrs) with cigarette
cough, morning cough
• Diagnosis usually occurs at 50-60 yrs
• Smoking is the most significant risk factor
• Repeated respiratory infections are common
• Productive cough, copious, often purulent sputum,
late onset dyspnea
• Patient is typically obese
Chronic Bronchitis:
Pathophysiology
• Repeated irritation and inflammation leads
to bronchiolar smooth muscle hypertrophy
and reduction in airway diameters
• Increase in size and number of submucosal mucus
glands and goblet cells
• Goblet cells proliferate in bronchioli, which normally do not
contain mucus-secreting cells
• Mucus is thick and difficult to clear from airways
• Ciliary action is impaired by inflammation, resulting
in poor clearance of mucus, leading to repeated
bacterial infections
• Hypoventilation common
• Elevated blood CO2 and reduced O2, cyanosis
• Often termed “blue bloaters”
• Loss of respiratory drive unexplained
• Death results from right heart failure (cor
pulmonale) due to pulmonary hypertension,
Emphysema: Clinical
Characteristics
• Emphysema results from
acinar distension and
destruction of alveolar
membranes
• Loss of surface area for gas
exchange
• Later onset than CB (30-40
yrs)
• Diagnosis usually occurs at 60-70
yrs
• Minimal history of cough
• Chief complaint is shortness
of breath
• Patients typically hyperventilate
to maintain normal blood gases
• “pink puffers”
Differentiation of Asthma,
Chronic Bronchitis, and
Emphysema
Symptom Asthma Bronchitis Emphysema
Principal Intermittent Chronic cough,
Dyspnea
complaint bronchospasm copious sputum
Reversible with
β2-agonists Yes No No

Allergic
Frequently No No
component
Inflammation Yes Yes Alveoli only
Sputum Copious,
During attacks Little
production continuous
Constant,
Cough After attack No
productive
Childhood 20-30 yr 30-40 yr
Age of onset (allergic); adult (Diagnosis at 50 (Diagnosis at 60
(nonallergic) yr+) yr+)
Thin, barrel-
Body build Varied Obese
chested
Hypoxic During attack Yes No
Management of COPD

• General Concepts
• Smoking Cessation
• Exercise training
• Pharmacotherapy
• Does not modify long-term decline in lung function
• Medications decrease symptoms and/or complicatons
• Bronchodilators
• Can be given PRN or scheduled to prevent or reduce
symptoms
• Inhaled preferred
• In contrast to asthma, fully normal
pulmonary function cannot be attained
 Management of COPD
First Choice Second Choice
Patient A PRN ipratropium OR Long-acting anticholinergic or Long-
PRN Albuterol acting 2-agonist OR ipratropium +
Albuterol
Patient B Long-acting Long-acting anticholinergic + Long-
anticholinergic OR acting 2-agonist
Long-acting 2-
agonist
Patient C Inhaled corticosteroid Long-acting anticholinergic + Long-
+ Long-acting 2- acting 2-agonist
agonist OR Long-
acting anticholinergic
Patient Inhaled corticosteroid Inhaled corticosteroid + Long-acting
D + Long-acting 2- anticholinergic
agonist OR Long- OR Inhaled corticosteroid + Long-acting
acting anticholinergic 2-agonist + Long-acting anti-cholinergic
OR
Inhaled corticosteroid + Long-acting 2-
agonist +Theophylline OR Long-acting
Pharmacotherapy

• Principle Therapies
• Beta2 agonists
• Anticholinergics
• Theophylline
• Combination of above
• Choice between above agents depends on
patient individual response in terms of
safety and effectiveness
Pharmacotherapy

• Long acting bronchodilators are more

effective and convenient than short acting,
but much more expensive
• Combining drugs with different
mechanisms and durations of action may
increase the degree of bronchodilation for
equivalent or lesser side effects.
• Theophylline is effective in COPD, but due
to its potential toxicity, inhaled
bronchodilators are preferred when
available.