Purpose of the theophylline:
relaxes the airway smooth muscle
inhibits synthesis and secretion of inflammatory mediators in mast and
MOA of theophylline
inhibits cyclic nucleotide phosphodieterases which increases cellular cAmp
competitive antagonist of adenosine
narrow therapeutic range, high patient intervariablity in metabolism,
requires therapeutic drug monitoring.
Clearance can be decreased and or increased easily
Toxic sx: headache, palpitations, dizziness, nausea, hypotension, restlessness,
Fatal intoxication can occur and seizure if plasma concentrations >40
MOA of Epi:
All 3 receptor types are activated
Hallucinations, excitement, ataxia, incoordination, convulsions, fever, sinus
tachycardia, urinary retention, dry mouth, deepening coma and cardio-
respiratory collapse followed by death.
May induce P450 enzymes
Albuterol in ER
Short/Fast acting beta agonist
Direct relaxation of airway smooth muscle
Used in acute exacerbations
MOA of Albuterol
Direct relaxation of airway smooth muscles via beta2 adrenergic receptors
elevation of camp
Increase K channel conductance leading to hyperpolarization and relaxation
Inhibits inflammatory functions of mast cells, basophils, eosiniphils,
Increased HR, arrythmias, CNS effects
Why was GT given methylprednisolone?
Acute exacerbations often require brief 5-10 day treatment (prednisone,
Side effects include mood disturbances, increased appetite, loss of blood
glucose control, candidiasis
Not recommended for chronic treatment
Why was the nebulized albuterol repeated in the ER every 2 hrs?
Only last 2-6hrs
What is fluticasone? Its MOA?
Do not relax airway smooth muscle and have little effect on acute
Decrease airway inflammation
Not for acute exacerbations
Why was GT given a prescription for fluticasone?
To decrease airway inflammation
What is the reasoning behind replacing GT’s epinephrine inhaler with
Albuterol has minimal side effects and works faster also more effective,
better bronchodilator because it works directly on the beta 2’s.
After being prescribed fluticasone and albuterol, why does GT’s condition
The medications are treating both the bronchoconstriction and inflammation
Although GT improves on the new meds, he still uses the albuterol inhaler 2-3
times per day. What change in meds might this suggest?
He might need a ling acting beta agonist
What is a “spacer” and how is it used?
Spacer devices can improve delivery with MDIs
Limits number of larger molecules reaching mouth
Reduces patient need to coordinate inhalation with MDI activation
Why was the theophylline replaced with salmeterol.
Theophylline has lots of side effects and is a 3rd line rx for refractory asthma
What is the difference between asthma and COPD?
COPD involves primarily neutrophils as inflammatory mediators whereas
asthma involves primarily eosinophils
COPD shows progressive decline in lung function over time
COPD shows progressive breakdown in connective tissue & matrix
What is the underlying cause of COPD?
Cigarette smoking is primary cause for both
Why are some of the medications used to treat both conditions similar?
Pharmacotherapy for both seeks to
o Reduce or abolish symptoms
o Improve airflow
o Increase exercise capacity
o Reduce number & severity of exacerbations
o Generally improve health status
What is the reasoning behind prescribing albuterol and tiotropium?
Albuterol is a short acting beta agonist
Tiotropium is a anticholinergic--Inhalation powder (Spiriva)
Long term, once daily, maintenance treatment of bronchospasm associated
with COPD, including chronic bronchitis & emphysema
Not indicated as rescue therapy
Contraindicated in patients with history of hypersensitivity to atropine or its
Most common side effect – dry mouth
Currently considered first line treatment
Why might this patients condition have worsened over 2 yrs?
Pharmacotherapy cannot modify the rate of decline in lung function
Only treats the symptoms
What is the reasoning behind prescribing salmeterol?
Not getting enough relief with current regimen and adding a long acting beta
agonist is the next step
Antihistamines and Decongestants
Why does this patient develop seasonal rhinitis?
Release of histamine/ IgE mediated hypersensititivy
Why does diphenhydramine relieve her symptoms?
All H1 antagonists have similar actions – reversible, competitive inhibitors at
Antagonizes constrictor action of histamine in respiratory smooth muscle
Inhibits vasodilator effects on endothelial cells and vascular smooth muscle
Blocks increased capillary permeability
Blocks wheal & flare response
Reduces secretion in cholinergically innervated areas such as respiratory
Blocks portions of immediate hypersensitivity reactions related to histamine
Does NOT prevent histamine release or bind to histamine that has already
Why does it cause drowsiness? Why does it cause dry mouth?
Some of the first antihistamines
High sedative and strong anticholinergic effects
o Antagonizes ACh
o Dry mouth, xerostomia, urinary retention
Highly lipophillic, crosses BBB
What is the reason for switching her drugs?
Decreased CNS penetration
Ionized at physiologic pH and do not cross membranes
High albumin binding – less free drug to enter CNS
Less side effects
Why doesn’t loratidine produce drowsiness and dry mouth?
b/c it is a 2nd generation drug
What is the difference between loratidine and loratidine D? What is the
reason for its use? How might it help RL’s symptoms, as opposed to plain
loratidine D has a decongestant
Decongestants are sympathomimetic amines which decrease swelling and
congestion (via vasoconstriction), making breathing easier
Indications: Relief of vasomotor rhinitis and acute rhinitis in upper
What is the MOA of pseudoephedrine?
Mixed: Ephedrine and Pseudoephedrine. Activates a1 (vasoconstriction)
and b(bronchodilation). Can act by direct and indirect MOA’s.
o Sympathomimetic – a-adrenergic agonists
o Phenylephrine, oxymetazoline,
o Sympathomimetic agents that act by being taken up into the
prejunctional nerve terminal where they displace norepinephrine
from storage vesicles
o Norepinephrine is then released to postjunctional a-adrenergic
receptors producing vasoconstriction
What other formulations of decongestants are available for RL?
Phenylephrine and pseudoephedrine are components of proprietary OTC
Many are combined with a prescription antihistamine for relief of allergy
symptoms (Claritin-D, Allegra-D)
•Phenylpropanolamine – similar to pseudoephedrine with less CNS effects. Also
Banned sale due to risk of hemorrhagic stroke