DRUGS USED IN ASTHMA

By group 1
PATHOPHYSIOLOGY ASTHMA
Asmathic bronchoconstriction mediated by
mediator release from IgE-sensitized mast
cells and other cells involved in imunologic
responses.
Mediators include:
LTC4 &LTD4, LTB4 (Chemoanthractant)
Cause chronic inflamatory
DRUGS USED IN
ASTHMA
Bronchodilatorβ agonist, muscarinic
antagonist, methylxanthine
 Anti-inflamatory drugsrelease inhibitor, steroid,

slow anti-inflamatory drugs, antibodies

 Leukotrien antagonist lipoxygenase inhibitor,

reseptor inhibitor
Preventive treatment control the inflamatory
process in the air way
Β-AGONIST SELECTIVE
Albuterol

Terbutaline Short acting

Metaproterenol

Salmeterol

Formoterol Long acting

Given by orally & inhalation

Inhalations reduce systemic effect &
effective dose delivering locally in airway
smooth muscle
B- AGONIST NON SELECTIVE

 Epinefrin
 Efedrin
 isoproterenol
MECHANISM

Β-agonist stimulating adenilyl cyclase &

increase cAMP in the smooth muscle cells
Increasing of cAMP powerful bronchodilator
response
CLINICAL USES

 Short acting β-agonist acute episode

bronchospasm, the drugs of choice for asthma, the
most effective bronchodilator & not for
prophylaxis
 Long acting β-agonist for prophylaxis not for
acute episode bronchospasm
TOXICITY

 Tremor
 High dosagesignificant effect to β1 agonist
 Inhalationtachycardia
 Excessive of short acting β-agonist loss
responsive (tolerance, tachypylaxis)
 COPD patients normal dosage cardiac
disease & arrythmias
METHYLXANTHINE

Purine derivatives
Found an plantscaffein(coffee),
theophylline (tea), Theobromine (cocoa)
Theophylline the only one substance that
important in asthma treatment
Givenorally, promt release & slow release
form
Metabolism with P450 hepatic enzyme
CON’TD

Clearance:
a.age highest in young

b.Smoking statushigher in smoker

c.Concurrent with the other drugs inhibit or

induce hepatic enzyme
MECHANISM

Methylxanthine inhibit phospodiesterase

(PDE) PDE can’t degrades cAMP to
AMP so cAMP increase.
Inhibit adenosin reseptor in CNS
The mechanism is not so clear
EFFECT

 Bronchodilator
 Strength contraction of diaphragm
 CNS stimulating
 Cardiac stimulating
 Vasodilatations
 Increase blood pressure (release of
norepinephrine)
 Increase gastrointestinal motility
CLINICAL USES

 Asthma
 Slow releasecontrol nocturnal asthma
TOXICITY

 Common gastrointestinal distress, tremor,

insomnia
 Overdosage nausea, vomiting,
hypotension, cardiac arrythmias, convulsions
 Β blocker antidote severe cardiovascular
toxicity from theophylline
MUSCARINIC ANTAGONIST

 Atropine
 Ipatropium aerosol
 Tiotropium longer acting-analog
MECHANISM

 Ipratropium competitive block muscarinic

reseptor in airways & effective prevents
bronchoconstrictions by vagal discharge
EFFECT

 Reverse bronchoconstriction in same asthma

patients children
 COPD
 No effect on the inflamatory aspect of asthma
CLINICAL USES

 It’s useful in 1/3 -2/3 of ashmatic patient

 Acute broncospasme
 COPDwith acute episodes of
bronchospasm
TOXICITY

 Excessive dosage atropine like effect (dry

mouth, blurred vision, retention of urine,
constipation)
 Systemic effects are small
 Not cause tremor n arrythmia
 ATP

Bronchodilation
AC + Beta agonist

+ cAMP

Bronchial tone PDE - Theophyline

AMP

Acetylcholine + + Adenosine

- -
Muscarinic
Theophyline
antagonists

Bronchoconstriction
ARIGATO