In these slides you can get all the information related to therapy of Bronchial asthma.

1. Drug therapy USED
IN
BRONCHIAL ASTHMA
Submitted By :
Abu Bakr Ansari
Pharm. D 5th Year
Roll No. 1601096001
Enroll No. 1600100627
Submitted To :
Dr. Mohd Ahmad Sir
Associate Professor
Integral University, Lucknow
Faculty of Pharmacy

2. Bronchial Asthma
• Asthma as an inflammatory illness
• In the year 2015, an estimated of nearly 65 million
people in India suffered from asthma
• Asthma is a condition in which your airways
narrow and swell and may produce extra mucus.
This can make breathing difficult and trigger
coughing, a whistling sound (wheezing) when you
breathe out and shortness of breath.

3. Pathophysiology of Asthma

4. Lungs look in Asthma

5. Causes
 Airborne allergens, such as pollen,
dust mites, mold spores, pet dander or
particles of cockroach waste
 Respiratory infections, such as the
common cold
 Physical activity
 Cold air
 Air pollutants and irritants, such as
smoke

6. Symptoms
 Shortness of breath
 Chest tightness or pain
 Wheezing when exhaling, which is a common sign of
asthma in children
 Trouble sleeping caused by shortness of breath,
coughing or wheezing
 Coughing or wheezing attacks that are worsened by a
respiratory virus, such as a cold or the flu

7. Approaches to Treatment
• Prevention of antigen-antibody reaction
• Neutralization of IgE - Omalizumab
• Suppression of inflammation and bronchial
hyperactivity - corticosteroids
• Prevention of release of mediators – mast cell
stabilizers
• Antagonism of released mediators – Leukotriene
antagonists, antihistamines and PAF antagonists.
• Blockade of constrictor neurotransmitter -
anticholinergics
• Mimicking dilator neurotransmitter - sympathomimetics
• Directly acting bronchodilators – methylxanthines

8. Classification
I. Bronchodilators
A. β2 Sympathomimetics: Salbutamol, Terbutaline,
Bambuterol, Salmeterol, Formoterol,Ephedrine.
B. Methylxanthines: Theophylline
(anhydrous),Aminophylline, Choline theophyllinate,
Hydroxyethyl theophylline, Theophylline
ethanolate of piperazine, Doxophylline.
C. Anticholinergics: Ipratropium bromide,Tiotropium
bromide.
II. Leukotriene antagonists
Montelukast, Zafirlukast.

9. III. Mast cell stabilizers
Sodium cromoglycate, Ketotifen.
IV. Corticosteroids
A. Systemic: Hydrocortisone, Prednisolone and
others.
B. Inhalational: Beclomethasone dipropionate,
Budesonide, Fluticasone propionate,
Flunisolide, Ciclesonide.
V. Anti-IgE antibody
Omalizumab

10. Sympathomimetics
Adrenergic drugs cause bronchodilatation through β2
receptor stimulation → increased cAMP formation in
bronchial muscle cell → relaxation. In addition,
increased cAMP in mast cells and other inflammatory
cells decreases mediator release.Since β2 receptors on
inflammatory cells desensitize quickly, the contribution
of this action to the beneficial effect of β2 agonists in
asthma where airway inflammmation is chronic, is
uncertain, and at best minimal. Adrenergic drugs are
the mainstay of treatment of reversible airway
obstruction, but should be used cautiously in
hypertensives, ischaemic heart disease patients and in
those receiving digitalis. They are the most effective
and fastest acting bronchodilators when inhaled.

11. Salbutomol (Albuterol)
highly selective β2 agonist; cardiac side effects are less
prominent.Selectivity is further increased by inhaling the
drug. Inhaled salbutamol delivered mostly from
pressurized metered dose inhaler (pMDI) produces
bronchodilatation within 5 min and the action lasts for
2–4 hours. It is, therefore, used to abort and terminate
attacks of asthma, but is not suitable for round-the-
clock prophylaxis. Muscle tremors are the dose related
side effect. Palpitation, restlessness, nervousness,
throat irritation and ankle edema can also occur.
Hypokalaemia is a possible complication. Salbutamol
undergoes presystemic metabolism in the gut wall, oral
bioavailability is 50%.
Dose: 2–4 mg oral, 0.25–0.5 mg i.m./s.c., 100–200 µg by
inhalation.

12. Terbutaline
It is similar to salbutamol in properties and use.
Dose: 5 mg oral, 0.25 mg s.c., 250 µg by inhalation.
Methyl Xanthines
• The main compounds in methyl xanthine family are theophylline
and it’s compounds.
• But they are not used as the first line drug in treatment of asthma.
• They are primarily used in the treatment of COPD.
• All these compounds are derived from plant sources as:
1. Caffeine
2. Theophylline
3. Theobromine

13. Leukotriene Antagonists
Drugs
• There are mainly two leukotriene
antagonist drugs. They are:
1. Montelukast
2. Zafirlukast
• Both these two drugs are within the
chemical family of Cysteinyl
Leukotrienes antagonists.

14. • Both the drugs are well absorbed orally.
• They bound with plasma very highly, so the volume of
distribution is very low.
• They are extensively metabolized by CYP2C9
and CYP3A4 isoenzymes in liver.
• Plasma half life: Montelukast: 3-6 hours.
 Zafirlukast: 8-12 hours.
• Montelukast and zafirlukast are very safe drugs.
• They produce very few side effects like headache and
rashes.
• Very few cases of Churg-Strauss syndrome
(vasculitis with eosinophilia) has been reported.
Pharmacokinetics
Side effect

15. Mast Cell Stablizers
• Sodium cromoglycate
• Kitotifen
 1. Sodium cromoglycate:
• Sodium cromoglycate is not absorbed orally.
• It is absorbed as an aerosol through metered dose inhaler.
• Only a small fraction is absorbed systemically.
• Rest of the portion is rapidly excreted unchanged in urine
and bile.
 2. Kitotifen:
• It is absorbed orally.
• Bioavailability is 50% due to first pass metabolism.
• It is largely metabolized.
• Plasma half life is 20-22 hours.

16. Anti – IgE Antibody Drugs
 Omalizumab
• It is used only in severe extrinsic asthma.
• It is very expensive, so use of it is restricted for:
1. Resistant asthma patients.
2. Patients giving positive skin test.
3. Patients with raised IgE level who require frequent
hospitalization.

17. MoA
• The drug omalizumab is actually a humanized
monoclonal antibody.
• It is administered i.m or s.c.
• It neutralizes free IgE in circulation without
activating mast cells and other inflammatory cells.
• So IgE level in plasma is down and so, mast cell-
IgE mediated
 histamine (inflammatory mediators) release is
inhibited.
• So bronchoconstriction occurs.

18. References
 https://www.mayoclinic.org/diseases-
conditions/asthma/symptoms-causes/
 https://www.healthline.com/health/asthm
a
 Textbook of Essential Medical
Pharmacology, Tripathi K.D., Page no.
222-231
 https://www.slideshare.net/Parasuraman
Parasuraman/drugs-used-in-bronchial-
asthma/

19. THANK YOU
Faculty of Pharmacy