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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
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.
Pathophysiology of Asthma
Lungs look in Asthma
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
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
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
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.
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
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.
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.
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
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.
• 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
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.
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.
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.
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/
THANK YOU
Faculty of Pharmacy

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Drug therapy used in 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.
  • 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/