anti-asthma drugs

1. ASTHMA
PRESENTED BY
P.GANESH
M-pharmacy
Dept. Of Pharmacology
GITAM Institute of Pharmacy
GITAM UNIVERSITY
Visakhapatnam
2016-2017

2. CONTENTS
• Introduction
• Pathophysiology
• Signs and symptoms
• Causes
• Anti-asthmatic agents.
• Mechanism and dosage.
• Pharmacokinetics, side effects and therapeutic uses.

3. Asthma is a condition where in an increased responsiveness of bronchial
smooth muscles to various stimuli resulting in narrowing of airways occurs.
Asthma is a common long term inflammatory disease of the airways of the lungs.
 It is a long term respiratory condition, in which the airways may unexpectedly and
suddenly narrow, often in response to an allergen, cold air, emotional stress.
Asthma is of two types
A. Extrinsic Asthma(Atopic)
It occurs due to exposure to allergens and chemical irritants.
It must be seen in childhood.
B. Intrinsic Asthma(Non-atopic)
Here the occurrence is unknown, in some cases may be due to stress and
exercise.
According to the World Health Organization, about half the cases are due to genetic
susceptibility and half result from environmental factors.

4. PATHOPHYSIOLOGY
• Asthma may be caused due to several factors like allergens and chemical irritants which
stimulate the mast cells to release of inflammatory mediators like histamine, prostaglandins,
leukotrienes, etc..
Bronchi
β2 receptor
Deactivation of adenylcyclase
Decrease cAMP Bronchial constriction

5. SIGNS AND SYMPTOMS
Wheezing.
shortness of breath.
chest tightness.
coughing.
 Sputum.
A physical or mental feature which is regarded as indicating a condition of disease

6. CAUSES
• Asthma is associated with exposure to indoor allergens. (Dust)

7. CAUSES
Genetic
Family history is a risk factor for asthma, with many different genes being implicated.
If one identical twin is affected, the probability of the other having the disease is
approximately 25%.
Some genetic variants may only cause asthma when they are combined with specific
environmental exposures.

8. ANTI-ASTHMATIC DRUGS
I. Bronchodilators II. Anti-inflammatory III. Anti-IgE antibody
A. Adrenergic A. Glucocorticoids. Ex. Omalizumab
receptor agonist. Ex. Beclomethasone.
Ex. Salbutamol, salmeterol Fluticasone.
B. Anti-muscarinic. B. Leukotriene inhibitors.
Ex. Ipratropium bromide Ex. Montelukast, Zileuton.
C. Phosphodiesterase C. Mast cell stabilizer
inhibitor. Ex. Cromolyn sodium.
Ex. Theophylline
Aminophylline

9. ADRENERGIC RECEPTOR AGONIST
• Short acting
Salbutamol:
it is a β2 adrenergic receptor agonist. It is preferred drug for asthma.
Mechanism of action:
Salbutamol selectively binds to results in activation of GS which results
Resulting in increase cAMP levels stimulation of g-protein couple receptor
Which relaxes bronchial smooth muscle by reducing ca+ dependent coupling action
bronchial dilation
β2

10. • Pharmacokinetics
Salbutamol is readily absorbed from GIT following oral administration.
It under goes first pass metabolism in liver. The drug is excreted unchanged in urine.
 it shows rapid onset of action when given inhalation.
Duration of action by inhalation route is 4-6hrs.
side effects:
Nervousness, insomnia, headache, nausea and drowsiness.
Therapeutic uses:
Used for the treatment of acute asthma.
It is used in hyperkalaemia especially in patient with renal failure.

11. • Terbutaline: Its mechanism action is similar to that of salbutamol.
Pharmacokinetics:
When given orally gets absorbed to an extent of 33-50% of the total dose and
lasts for about for 8hrs.
Therapeutic uses: it is preferred drug for quick relief of asthma.
Contraindication: if the pregnant women we should not given.

12. Class of drug Mechanism of
action
side effects Therapeutic
uses
Pharmacokineti
cs
Dosage and
route
Anticholinergic
agents
(ipratropium
bromide)
Inhibits Broncho
constrictive action
of Ach by binding
muscarinic receptor
Dry mouth,
bad taste
Used in COPD It is poorly
absorbed from
GIT on oral
administration
40-80µg t.i.d,
inhalation.
Phosphodiester
ase inhibitors
(theophylline)
It inhibits PDE,
which is responsible
for the degradation
of cGMP.
Nausea,
vomiting.
In mild to
moderate
asthma.
It is well
absorbed on
upon oral
administration.
It distributed to
all parts of body
and crosses
placenta.
100-300µg t.i.d,
By oral.

13. II. ANTI-INFLAMMATORY
Glucocorticoids:
These are a class of steroids. They are the primary drugs used in treatment of asthma.
Mechanism of action:
They inhibit the release of prostaglandins and leukotrienes and thus preventing the
construction of smooth muscle and mucus secretion.
Adverse effects: Dysphonia (difficulty in voice production), sore throat.
Therapeutic uses:
The are used in severe asthma.
Dosage: 200µg 3-4times/day

14. Mast cell stabilizer:
These drugs are safe and effective for mild to moderate asthma.
Mechanism of action:
They act by inhibiting the degranulation of mast cells and other inflammatory cells,
there by preventing the release of mediators like interleukins, leukotrienes, histamine
etc.
Pharmacokinetics
Cromolyn and Nedocrmolyn are poorly absorbed in GIT.
So that’s why they are administered by inhalation route.
Side effects: wheezing, headache, throat irritation and joint swelling etc...
Therapeutic uses:
Used in treatment for mild to moderate asthma.

15. III. ANTI-IGE ANTIBODY
• Omalizumab:
it is recombinant humanized monoclonal antibody, which acts against
immunoglobulin E (IgE).
Mechanism of action:
It inhibits the binding of IgE to its receptor on mast cells and their by preventing
allergen-induced activation of mast cells.
Pharmacokinetics
After SC administration, Omalizumab is absorbed with an average absolute
bioavailability of 62%. Following a single SC dose in adult and adolescent patients
with asthma, Omalizumab was absorbed slowly, reaching peak serum concentrations
after an average of 7-8 days.
Side effects:
Reaction at site of injection.

16. Thank you