Anti asthma drugs

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Dr. Jahid
Anti-Asthma Drugs

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Anti Asthma drugs
▪ Definition: Asthma is characterized
clinically by recurrent bouts of -
✓ Shortness of breath
✓ Chest tightness
✓ Wheezing
✓ Often associated with coughing
▪ Asthma take place by chronic airway inflammation
and airway become hyper-responsiveness.

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▪ Types of bronchial Asthma:
▪ MILD ASTHMA: symptoms occur only
intermittently, as on exposure to
allergens or air pollutants, on
exercise, or after viral upper
respiratory infection.
▪ SEVERE ASTHMA: associated with
more frequent and severe symptoms
call acute asthmatic attacks, or
“asthma exacerbations.”

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▪ Types of bronchial Asthma:
✓ Asthma associated with specific allergic
reactions
✓ Asthma not associated with known allergy
✓ Drug-Induced Asthma
✓ Occupational Asthma
Kumar V, and Stanley L. Robbins Basic Pathology. 8th ed. Philadelphia: Saunders/Elsevier.; 2013.

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The hallmark of acute asthmatic attacks, or
“asthma exacerbations” includes-
▪ Contraction of airway smooth muscle
▪ Marked increase in bronchial responsiveness to inhaled
stimuli
▪ Thickening of the bronchial mucosa from edema
▪ Hyperplasia of secretory, vascular, and smooth
muscle cells
▪ Inspissation of viscid mucus plugs in the airway lumen

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Activity-1
A. Compare and contrast histology of bronchus with hyper
responsive pathological bronchus of a asthma patient.

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Pathogenesis of Asthma
Exposure to allergen TH2 cells stimulates B cells
synthesis of IgE: binds to mast cells in the airway mucosa.
Re-exposure to allergen/antigen Ag-Ab interaction on
the surfaces of the mast cell triggers:
Mediators of anaphylaxis:
histamine, tryptase, PGD2
cytokines: LTC4, LTD4 PAF.
Immediate
contraction of the airway
&
Vascular leakage
Early asthmatic response
TH2 cells
cytokines: IL4,5,13
Eosinophils & Neutrophils
ECP, MBP, Protease, PAF
Influx of inflammatory cells
with an increase in bronchial
reactivity

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▪ The classic atopic form of asthma is associated
with an excessive TH2 reaction against environmental
antigens.
TH2 cells
IL-4 stimulates B cells
to produce IgE
IL-5 activates
eosinophils
IL-13 stimulates
mucus production and also
promotes IgE production by
B cells
▪ eosinophils and neutrophils
releases-
▪ eosinophil cationic protein (ECP)
▪ major basic protein (MBP)
▪ proteases, and platelet-activating
factor
▪ Increased in bronchial reactivity

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Activity-2
B. Discuss the role IgE on bronchial mucosa to become hyper
responsive bronchus.
C. List important effector proteins mediate such action.
▪Katzung B.G. Basic and clinical Pharmacology. Mcgraw-Hill Tata, 12th edition, p 339-350.

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Aims of treatment
▪ Prevention of exposure to allergens
▪ Dilatation of narrow bronchi
▪ Reduction of bronchial inflammation and
hyperactivity

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Anti Asthma drugs
▪ Short-term reliever
▪ (agents relax airway
smooth muscle)
▪ β2 -adrenoceptor agonist
▪ Methylxanthine
derivatives
▪ Antimuscarinic agents
▪ Long-term controller:
▪ (anti-inflammatory
agents)
▪ Corticosteroid
▪ Inhibitor of mast cell
▪ Leukotriene pathway
antagonist

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Sympathomimetic
▪ Sympathomimetic agents that have been widely used in
the treatment of asthma include :
▪ Epinephrine
▪ Ephedrine
▪ Isoproterenol
Epinephrine is an effective,
rapidly acting bronchodilator
when injected subcutaneously
or as Inhaler.
▪ Maximal bronchodilation is
achieved 15 minutes
▪ after inhalation and lasts
60–90 minutes.
▪ tachycardia,arrhythmias,
and worsening of angina
pectoris are troublesome
adverse effects
▪ Still drugs of choice in
bronchospasm of
anaphylaxis
Ephedrine has a longer duration of
action.
▪ more pronounced central
effects,
▪ and much lower potency.
Isoproterenol is a potent
nonselective β1 and β2
bronchodilator
▪ maximal bronchodilation
within 5 minutes
▪ and has a 60- to 90-minute
duration of action
▪ high doses of inhaled
isoproterenol causes cardiac
arrhythmias.

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Anti Asthma drugs
▪ Beta 2 agonist drugs…….
▪ Short acing: (3-6 hr)
▪ Salbutamol (Inhaler, Tablet)
▪ Terbutaline (Inhaler, Tablet, subcutaneous inj.)
▪ Metaproterenol
▪ Pirbuterol
▪ Levalbuterol
▪ Long acting : (12 hr)
▪ Salmeterol
▪ and Formoterol
▪ Ultral Long acting : (24 hr)
▪ Indacaterol.

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Anti Asthma drugs
▪ Short acting:
✓ Bronchodilatation occur by 15-30 mins and lasts
for 3-4 hours. 2-4 puffs 2-4 times daily.
✓ Suitable for emergency use.
▪ Long-acting:
✓ high lipid solubility
✓ long-term treatment
✓ not suitable for acute relief
✓ enhance local but not systemic action of
corticosteroids
✓ Oral or inhaler (combined with corticosteroid)

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Anti Asthma drugs; Salbutamol
▪ Mechanism of Action…
▪ Stimulate β2 receptor of the
bronchial smooth muscle.
▪ (+) of the Adenylate Cyclase
enzyme via Gs coupled receptor.
▪ Increased intracellular cyclic-AMP
▪ Smooth muscle relaxation
▪ Broncho dilatation occurs.
Receptor + drug
stimulation of the G-protein
adenylate cyclase stimulation
ATP
C-AMP
Protein kinase A
Broncho Dilation.
Salbutamol

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Anti Asthma drugs
▪ Adverse effects with β2 -adrenoceptor agonist-
▪ Least with inhaled preparations
▪ tachycardia, arrythmias (β1)
▪ tremors (β2)
▪ Tolerance
▪ Hypoxemia.

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Methylxanthines
▪ Their major source is beverages (tea and coffee).
▪ Theophylline is the prototype, it is water insoluble
but it’s salts are water soluble.
▪ The important methylxanthines are –
▪ Theophylline
▪ Aminophylline
▪ Theobromine
▪ Caffeine.
Theophylline is 1,3-dimethylxanthine; theobromine is
3,7 dimethylxanthine;

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Mechanism of action:
1. On Smooth muscle
▪ They act by inhibition of
phosphodiesterase enzyme.
▪ This results in decreased
breakdown of cyclic AMP.
▪ So the concentration of cyclic
AMP is increased, results
bronco dilatation.
▪ Inhibition of PDE4 in inhibiting
release of cytokines and
chemokines.
Bronchial Tone
Bronchoconstriction
Bronchodilation
cAMP
ATP
AC
PDA-4
AMP

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Anti Asthma drugs
2. Inhibition of cell surface receptors for
adenosine
▪ Methylxanthines blocks adenosine actions
▪ Adenosine is known to cause smooth muscle
contraction and histamine release.
3. Enhancement Of Histone Deacetylation

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Pharmacological effects
A. Central Nervous System Effects:
▪ Caffeine: cause mild cortical arousal with increased
alertness and deferral of fatigue.
▪ Very high doses: cause medullary stimulation,
convulsions, and even death.
A. Cardio vascular System Effects:
▪ Methylxanthines have positive chronotropic and
inotropic effects on the heart.
▪ Increased cardiac output, increased blood pressure.
▪ Decrease blood viscosity and may improve blood flow.
C. Effects on Gastrointestinal Tract
The methylxanthines stimulate secretion of both gastric
acid and digestive enzymes.

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D. Effects on Kidney
Theophylline act as a weak diuretics by increased
glomerular filtration and reduced tubular sodium
reabsorption.
E. Effects on Smooth Muscle
The bronchodilation produced by increasing
concentrations of intracellular cAMP and, in some
tissues, cGMP.
F. Skeleton Muscle
❖ Strengthen diaphragm  improve contractility 
improve ventilatory response to airflow obstruction.

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Anti Asthma drugs
▪ Clinical uses
• *** Acute asthma
• Theophylline improves long-term control of asthma
✓ Long-term treatment
✓ Orally well absorbed, rapid
✓ short T½
✓ Sustained released preparations can produced
therapeutic blood level for 12 hours.
• NARROW THERAPEUTIC WINDOW
• *use only with therapeutic drug monitoring
facilities

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▪ Toxicity
• 1. CNS: nervousness, tremors, insomnia,anxiety
convulsions.
• 2. CVS:
• inhibition of presynaptic adenosine receptors 
 catecholamines
• inhibition of phosphodiesterase   cAMP
• tachycardia,  CO, arrythmias ( TPR,  BP).

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Ipratropium Bromide
▪ Anticholinergics (Antimuscarines)
✓ It competitively blocks the action of acetylcholine on
the muscarine receptors (M2) of the bronchial wall.
✓ Reduced secretion of mucus that occurs in response
to vagal (efferent) activity in bronchus
✓ Poorly absorbed, does not enter CNS
✓ minimal systemic side-effects.
✓ Increased efficacy if combined with nebulized β2
agonist in severe acute asthma.
✓ Longer-acting antimuscarinic agents, tiotropium and
aclidinium, are approved for maintenance therapy of
COPD.

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Activity-3
A. Discuss the cascades of smooth muscle relaxation with the
emphasis on role of Ca++, ATP/GTP phosphorylation and activation of
protein kinase G (PKG).

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STEROIDS
▪ Inhaled corticosteroids are labeled as
“ controllers”.
▪ Steroids used in inhalation route:
✓ Beclomethasone
✓ Budesonide
✓ Fluticasone
✓ Triamcinolone
▪ Oral agents:
✓ Prednisolone
▪ Intravenous agents:
✓ Methylprednisolone

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Activity-4
1. Discuss synthesis of Eicosanoids.
2. Enlist products of Cyclooxygenases pathway
3. Enlist Products of Lipoxygenase
▪Katzung B.G. Basic and clinical Pharmacology. Mcgraw-Hill Tata, 13th
edition, p 435-450.

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leukotrienes
phospholipase A2
Arachidonic acid
Phospholipids
lipoxygenase
COX 1
PG
Synthesis of mediators derived from
arachidonic acid : Prostaglandins
PHOSPHOLIPASE A2

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Mechanism of action
1. Anti-inflammatory effects
▪ Glucocorticoids inhibits Phospholipase A2
enzyme and block formation of Arachidonic acid.
▪ Therefore synthesis of prostaglandins (PG),
leukotriens (LT), TxA2 etc are stopped.
▪ They inhibit function of leukocytes and
macrophase.
2. Steroids produce permissive effect
3. Reduce bronchial response and reactivity
4. Reduce frequency of exacerbations

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Anti Asthma drugs
▪ Clinical uses:
▪ Prophylaxis/long-term treatment -
inhalational agents
▪ Acute, severe asthma
– - IV Hydrocorticone
– - Oral prednisolone

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Anti Asthma drugs
▪ Side-effects:
▪ Inhalational agents
– - minimal systemic toxicity
– - oropharyngeal candidiasis
– - hoarseness of voice
– - cataracts & osteoporosis in long-term
▪ Oral agents
– - Acute adrenal insufficiency
– - Cushing’s syndrome etc
• [avoid using oral agents > 3 week
• use alternate day therapy
• taper dose when stopping treatment)

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Anti Asthma drugs
▪ Sodium cromoglycate, nedocromil and
ketotifen
▪ These drugs have no effect on airway smooth muscle
tone and are ineffective in reversing asthmatic
bronchospasm.
▪ They are only effective when taken
prophylactically.
▪ And allergic rhinoconjunctivitis
▪ Water soluble, so cant given orally.
▪ They are given as metered dose inhalation form.
▪ They are used for antigen and exercise induced
asthma.
▪ When combined with inhaled steroids can improve
asthma control.

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▪ Mechanism of action
• Cromolyn and nedocromil alter the function of delayed
chloride channels in cell membranes.
• inhibiting cell activation (mast cells and eosinophils)
• inhibition of cough (by inhibiting vegus nerve )
• inhibit the early and the late response to antigen
challenge.
Sodium cromoglycate, nedocromil
▪ Adverse effects:
▪ These include throat irritation, cough, and mouth
dryness.
▪ Serious adverse effects are rare. Reversible dermatitis,
myositis, or gastroenteritis occurs in less than 2% of
patients.

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▪ Clinical uses
• 1. Asthma
✓ Prophylaxis for allergic asthma
✓ Prophylaxis before exercise
✓ reduce severity and frequency of attacks
✓ most suitable for young patients with
extrinsic asthma
• 2. Allergic rhinitis
• 3. Allergic conjunctivitis

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Anti Asthma drugs
❖ Leukotriene Pathway Inhibitors
▪ Leukotriene B4 is a potent neutrophil
chemoattractant
▪ LTC4 and LTD4 exert many effects-
▪ including bronchoconstriction
▪ increased bronchial reactivity
▪ mucosal edema

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leukotrienes
phospholipase A2
Arachidonic acid
Phospholipids
5-lipoxygenase
COX 1
PG
Synthesis of mediators derived from
arachidonic acid : Prostaglandins
PHOSPHOLIPASE A2

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▪ Arachidonic acid 
lipoxigenase  leukotrienes
▪ Leukotriene receptor
antagonists:
▪ Montelukast
▪ Zafirlukast
▪ 5-lipoxygenase inhibitor:
(Synthesis inhibitor)
▪ Zileuton.

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• Effects:
✓ reduce inflammation (less potent than inhaled
steroids)
✓ reduced bronchial reactivity
✓Reduce fequency of exacerbation (equally
effective as inhaled steroids)
❖ Clinical uses
✓ Prophylaxis
✓ Aspirin induced asthma
✓ Orally effective
❖ Side-effects
✓ Zileuton – liver toxicity
✓ Montelukast- headache, rash

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Anti Asthma drugs

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▪ An entirely new approach to the treatment of
asthma target by targeting IgE antibody.
▪ Omalizumab (an anti-IgE monoclonal antibody)
inhibits the binding of IgE to mast cells
▪ and does not activate IgE already bound to these
cells and thus does not provoke mast cell
degranulation.
▪ Omalizumab’s most important effect is reduction of the
frequency and severity of asthma exacerbations
Omalizumab

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Cough: forced expiration against a closed glottis which
suddenly opens to expel air and unwanted material from the
respiratory tract may be voluntary or involuntary.
Irritation to mucosal surface lining respiratory tract.
Impulses relayed via afferent vagus nerve
Relay in cough centre in brain
Efferent's via vagus nerve
Integration with the diaphragm, glottis,muscles of chest and
abdomen.

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A. Opioid
• Suppress the cough reflex by direct action on the cough
center in meu opoid receptor in the medulla.
• and also decreases the rate and/or tidal volume of
respiration
• Examples: codeine, Pholcodine, Morphine, Methadone.
Productive cough-do not use cough suppressants
Use expectorants and mucolytics
Goodman, L.S., Gilman, A., Hardman, J. G., Gilman, A. G., & Limbird, L. E, in Goodman & Gilman's the
pharmacological basis of therapeutics. 2011, McGraw-Hill, Health Professions Division.: Newyork. p. 1057-
1059.

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▪ Dextromethorphan-has a central action on NMDA
receptor and also on the medullary cough centre.
▪ Structurally related to morphine but little or no analgesic
properties.
▪ And minimal (little) sedative activity.
▪ Do not depress respiratory center.
▪ Antitussive effects may persist for up to 5 hours.
Benzonatate: a local anesthetics, act peripherally by inhibiting the
stretch receptors located in the respiratory passages, lungs and
pleura.
Adverse effect: Dizziness, dysphagia, seizure and cardiac arrest.
pharmacological basis of therapeutics. 2011, McGraw-Hill, Health Professions Division.: Newyork. p. 1057-1059.

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Antitussives: Side Effects
 A. Opioid
▪ Sedation, nausea, vomiting, constipation
▪ They should be used with caution in patients
taking monoamine oxidase inhibitors
▪ its use in children less than 6 years of age has
been banned by the FDA.
 B. Dextromethorphan
 Dizziness, nausea
abuse of its purified (powdered) form has been
reported to lead to serious adverse events including
death.
Goodman, L.S., Gilman, A., Hardman, J. G., Gilman, A. G., & Limbird, L. E, in Goodman & Gilman's
the pharmacological basis of therapeutics. 2011, McGraw-Hill, Health Professions Division.: Newyork.
p. 1057-1059.

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Expectorants-act by increasing the volume of
secretions in respiratory tract so that they may be
more easily removed by ciliary action and coughing.
e.g. guaifenesin
Mucolytics- considered to reduce sputum viscosity
e.g.N-acetylcysteine, bromhexine, carbocysteine,
methyl cysteine
pharmacological basis of therapeutics. 2011, McGraw-Hill, Health Professions Division.: Newyork. p. 1057-1059.

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The viscosity of pulmonary mucus secretions depends on
the concentrations of mucoproteins and deoxyribonucleic
acid (DNA). Binds together by disulphide bridge.
While mucoprotein is the main determinant of viscosity
in normal mucus, in purulent inflammation the mucoid
concentration of DNA increases (due to increased cellular
debris) and so does its contribution to mucoid viscosity,
which is firmly attached to the lining of bronchioles and
bronchi
Adverse effects of increased mucus accumulation are
1. Increase the "lumen narrowing" effects of bronchial
constriction
2. Enhance the overall inflammatory process
3. Potentiate persistent coughing
Acetylcysteine-probably reduces viscosity by
splitting the disulphide bonds in mucoproteins.

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▪ References:
▪ Katzung B.G. Basic and clinical Pharmacology. Mcgraw-Hill
Tata, 12th edition, p 339-350.
▪ Goodman, L.S., Gilman, A., Hardman, J. G., Gilman, A. G.,
& Limbird, L. E, in Goodman & Gilman's the pharmacological
basis of therapeutics. 2011, McGraw-Hill, Health Professions
Division.: Newyork. p. 1057-1059.
▪ Kumar V, and Stanley L. Robbins Basic Pathology. 8th ed.
Philadelphia: Saunders/Elsevier.; 2013.

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