Asthma, Antiasthmatic drugs, Pharmacodynamics , Pharmacokinetics, Side effects, Uses and MCQS for GPAT, NIPER, Pharmacist and Drug inspector exam

Asthma, Antiasthmatic drugs, Pharmacodynamics , Pharmacokinetics, Side effects, Uses and MCQS for GPAT, NIPER, Pharmacist and Drug inspector exam

Bronchial Asthma:

It is chronic condition in which a person’s airways become inflamed swell, narrow and produce extra mucus which make difficulty in breathing.

Sign and symptoms:

Coughing, shortness of breath, chest tightness and wheezing sound (whistling sound in airways).

Risk factor that trigger Asthma:

Allergies, cold air, stress, irritants (household sprays, perfumes etc.), indoor and outdoor allergens, respiratory infections etc.

Inflammatory mediators in Asthma:

The inflammation in Bronchial Asthma is initiated by mast cells (present in lungs). The inflammatory reaction produces mediators like histamine, protease enzyme, prostaglandins, interleukins, leukotriene’s etc. These mediators together cause mucosal edema, constrict bronchial smooth muscles which will make breathing difficult.

Classification of Drugs for Asthma:

Sr. No. Drugs Mechanism of action Pharmacokinetics Side Effects Uses
1 Bronchodilators        
A Beta sympathomimetic




It stimulates β2 receptors of inflammatory cells, increased cAMP formation in bronchial smooth muscle cell and it will decrease the release of inflammatory mediators and dilates the bronchial smooth muscle. Highly selective short acting β2 agonist. It is fastest acting bronchodilators, produces bronchodilation in 5 minutes and the action lasts for 2-4hrs. Hypokalemia, tachyphylaxis throat irritation, nervousness, palpitation,   restlessness, ankle edema. and muscle tremors. Use for symptomatic relief, prevention of bronchospasm due to bronchial asthma and chronic bronchitis.
Salmeterol Same as above It is first long acting β2 agonist. Slow onset of action. Headache, dizziness, cough, runny nose, stuffed nose, nervousness and ear pain Used by inhalation  for maintenance therapy and nocturnal asthma
  Formeterol Same as above It is also long acting β2  agonist and acts for 12hr. It hs faster onset of action as compared to Salmeterol. It is used on regular morning evening schedule for round the clock bronchodilation.
  Bambuterol Ester prodrug of terbutline has same mechanism of action It is metabolised by hydrolysation in plasma and lungs by pseudocholinestrase enzyme to release active drug over 24 hrs. Headache and feeling restless. It is used in nocturnal and chronic asthma.
 B Methyl Xanthines        
  Theophylline, Aminophylline, Choline theophylline, Hydroxyethyl theophylline and Doxophylline. It is natural bronchodilator. It inhibits the phosphodiesterase enzyme, it also cause an intracellular increase in levels of cAMP and cGMP. This signal   results in bronchial smooth muscle relaxation, pulmonary vessel vasodilation, CNS stimulation and cardiac stimulation. Well absorbed orally, do no accumulate in organs and tissues, metabolised by liver.  t1/2 is of 7-12 hrs and 2% of drug administered excreted unchanged in urine. Gastric pain (with oral), rectal inflammation (with rectal suppostries), pain at the site of injection(i.m) and rapid iv can cause sudden death, convulsions and arrythmia Used in COPD, bronchial astma and apnoea in premature infants.
 C Anticholinergics        
  Ipratropium bromide, Tiotropium bromide Bronchodilation by blocking cholinergic constrictor tone. Poorly absorbed through g.i.t. The bioavailability of drug by inhalation is 0.03-6.9%. About 90% of inhaled dose is swallowed. T1/2 is of 2-3 hrs. Dry mouth, upset stomach, vomiting, nosebleed, muscle pain. Used for COPD and bronchial asthma.
2 Leukotriene antagonists        
  Montelukast, Zafirlukast Competitively antagonise cysLT1 receptor mediated bronchoconstriction, increased vasodilation. These drugs inhibit leukotriene enzyme arachidonate 5 lipoxygenase , antagonise  leukotriene receptor which opposed the action of leukotriene inflammatory mediators which are responsible for bronchoconstriction, inflammation and in mucus secretion. Aggression, anxiety, hallucinations, depression, insomnia. Used for prophylactic therapy of mild to moderate asthma.
3 Mast cell stabilizers        
  Sodium chromoglycate, Ketotifen It inhibits degranulation of mast cells of liver. It also inhibits the release of mediators like histamine, leukotrienes and interleukins which cause bronchoconstrictions. It is not absorbed orally, administered as meterd dose inhalers. Half-life is of 8.5hrs. Cough, throat irritation and  bronchospasm Allergic rhinitis, allergic conjunctivitis and in long term prophylaxis in mild to moderate bronchial asthma.
4 Corticosteroids        
 A Systemic corticosteroids:

Hydrocortisone, predinisolone

These drugs bind with the cell nucleus to regulates that control transcription of pro-inflammatory gene products by reducing inflammation caused by inflammatory mediators. It acts in 6-24 hrs. Increased appetite, weight gain, changes in mood, increased growth of body hairs and cataract. and blurred vision Used in bronchial asthma, staus asthmaticus and in COPD.
 B Inhalational corticosteroids
  Beclomethasone Same as above Rapidly absorbed from pulmonary, nasal and GI tssue.   Undergoes extensive first pass metabolism in the liver. 87% drug bind to protein Sneeing, nasal irritation Effective in perennial rhinitis
  Budesonide Same Greater first pass metabolism than beclomethasone. Small fractionis absorbed is rapidly metabolised. Itching of throat, nasal irritation, sneezing, throat dryness. Used in seasonal perennial allergies.
  Fluticasone same At higher dose systemic effects produce due to absorption from lungs. Same Used at higher doses in severe cases.
  Ciclesonide Same It is absorbed from lungs. Bioavailability is 1%. Extensively bound to plasma proteins. Unpleasant tase in mouth, dry mouth, hoarse voice, mild itching or skin rash. Used to prevent difficult breathing, chest tightness, coughing and wheezing.
4 Anti- IgE antibody Human monoclonal antibody. It neutralizes free igE in circulation without activating mast cells and inflammatory cells.  






No benefits noted in allergic asthma.



1.What causes an asthma attack

a. Allergens

b. Smoke

c. Irritants

d. All of the above

2. Which one of the following anti-asthmatic drugs can cause arrhythmia and convulsions.

a. Prednisolone

b. Zafirlukast

c. Theophylline

3. Which anti-asthmatic drugs can cause cataracts.

a. Salmeterol

b. Salbutamol

c. Prednisolone

d. Montelukast

4. Which drugs are short-acting β2– agonist

a. Salbutamol

b. Prednisolone

c. Terbutaline

d. a&c

5. Which drugs are long-acting β2 – agonist

a. Salbutamol

b. Formoterol

c. Salmeterol

d. b&c

6. Asthma is characterized by recurrent episodes of

a. Wheezing

b. Chest tightness

c. Coughing

d. All of the above

7. Identify leukotriene inhibitors

a. Zafirlukast

b. Salbutamol

c. Theophylline

d. Ipratropium

8. Which anti-asthmatic drugs show first pass metabolism

a. Budesonide

b. Salmeterol

c. Beclomethasone

d. a&c

9. Which anti asthmatic drugs act as bronchodilators

a. Salbutamol

b. Ipratropium

c. Theophylline

d. All of above

10. Which is natural bronchodilator

a. Theophylline

b. Prednisolone

c. Budesonide

d. Ipratropium

11. Which is drug inhibit (phosphodiesterase) enzyme

a. Theophylline(Methyl Xanthine)

b. Salbutamol

c. Terbutalline

d. Ipratropium

12. Acute attack of asthma treated with

a. Bronchodilators

b. Steroids

c. Methyl xanthines

d. Anticholinergics

13. Side effects of β-2 agonist

a. Hypokalemia

b. Tachyphylaxis

c. Muscle tremor

d. All of above

14. LT1 Receptor antagonist used in asthma

a. Zafirlukast

b. Montelukast

c. Both

d. None

15. Which drug inhibit 5- lipoxygenase enzyme.

a. Salbutamol

b. Montelukast

c. Ketotifen

d. Flutikasone



1. d

2. d

3. c

4. d

5. d

6. d

7. a

8. d

9. d

10. a

11. a

12. a


14. c


References: ‘K.D. Tripathi’, 8thedition 2018, page no-242-251.

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