ANTIASTHMATIC DRUGS

-I

Col Waqar Aslam (Retd), SI(M)

Professor of Pharmacology
CKMC Kharian Cantt
1
 Objectives
1. Define bronchial asthma & discuss its pathophysiology

2. Classify drugs used in treatment of bronchial asthma

3. Elucidate their pharmacokinetics & pharmacodynamics

4. Explain effects of Antiasthmatic drugs on their effectors

5. Describe their adverse effects and toxicity

6. Enlist contraindications for use of Antiasthmatic drugs

7. Elaborate drug management of Acute Severe Asthma

2
 DEFINITION
Bronchial Asthma is a chronic inflammatory
disease of airways characterized by:
1. Bronchial hyper-responsiveness
2. Bronchoconstriction
3. Increased bronchial secretions
4. Mucosal edema
5. Mucus plugging
6. Airways remodeling
7. Allergens influence
8. Reversible obstruction
3
 EPIDEMIOLOGY
• 5-20% (Global Asthma Report)

• 350 million suffer

• 250 thousand die

• Air pollution

4
 ETIOLOGY OF ASTHMA
• Allergens:
• Molds
• House dust mites
• Plant pollen & animal hair
• Pharmacological agents:
• Aspirin & chemicals
• Infectious stimuli:
• Viruses
• Airborne stimuli:
• Industrial smoke
• Diesel Fumes
• Irritants:
• Tobacco
• Cold weather
5
• Stress
ASSOCIATION WITH MEDICATION

• Aspirin & other NSAIDs:

• 10% cases
• Related with shift of arachidonic acid
metabolism

• from COX pathway generating prostaglandins

• to LOX pathway generating cystenyl leukotrienes

• Beta-Adrenoceptor Antagonists:
• Even when administered topically
as eye drops
6
FUNCTIONAL ANATOMY & PHYSIOLOGY
OF RESPIRATORY TRACT

• Conducting airways, from nose to alveoli,

connect the external environment with the
extensive, thin and vulnerable alveolar surface
• Inhaled air is filtered, heated to
body temperature & moisturized
• Airway patency is maintained by
cough reflex and by reinforcing
cartilage rings

7
 PATHOPHYSIOLOGY OF
ASTHMA

• Airway hyperreactivity
• Bronchoconstriction
• Chronic airway inflammation
• Oedematous wall with infiltration of inflammatory
cells like eosinophils, lymphocytes
• Mast cells & T-lymphocytes/cytokines
• Clumps of shed airway epithelium are present in
airway lumen
• Lumen occluded by mucus plug
• Airway remodeling
8
 DIAGNOSIS
• History: • X-ray chest:

• Physical examination:

• Spirometry:
• FEV1
• PEF

• Allergy testing:
• Skin prick test
• Patch Test

• Lab investigations:
• Blood (eosinophils & IgE)
• Sputum (eosinophilia)

• Challenge:
9
• Methacholine
 SYMPTOMS
• Wheeze
• Cough
• Chest tightness
• Dyspnea
• Airflow obstruction
• Variable over short periods of time
• Reversible with treatment

10
 TYPES OF BRONCHIAL ASTHMA
• Extrinsic Asthma:
• Allergic type

• Episodic Extrinsic Asthma

• Less prone to status asthmaticus

(acute severe asthma)

11
TYPES OF BRONCHIAL ASTHMA (Cont ….)

• Intrinsic Asthma:
• It tends to be perennial (long lasting)

• Status Asthmaticus is more common

• Associated with COPD

12
 ROUTES OF DRUG DELIVERY

• Oral:

• Inhalation:

• Parenteral:
13
INHALATION DRUG DELIVERY DEVICES

14
 ASTHMA SEVERITY CLASSIFICATION

Severity Daytime Night time FEV1, PEF

symptoms awakening

Intermittent ‹ 1 /week 2 & ‹ /month › 80% predicted

Mild
persistent ≥ 1/week but › 2 /month › 80% predicted
not daily

Moderate
persistent Daily › 1 /week 60% - 80%
predicted

Severe
persistent Persistent Daily ‹ 60% predicted

15
 CLASSIFICATION OF
ANTIASTHMATIC DRUGS
1. Bronchodilators:
i. Sympathomimetic Drugs:
a. Non-selective alpha & β Adrenoceptor Agonists
● Epinephrine
● Ephedrine
b. Non-selective β Adrenoceptor Agonists
● Isoproterenol (Isoprenaline)
c. Selective β2 Adrenoceptor Agonists
● Salbutamol (Albuterol)
● Salmeterol
● Formoterol
● Terbutaline
● Metaproterenol (Orciprenaline) 16
ii. Methylxanthines:
• Theophylline
• Theobromine
• Caffeine
• Aminophylline

iii. Antimuscarinic Agents:

• Ipratropium Bromide
• Tiotropium Bromide

17
2. Leukotriene Pathway Inhibitors:
i. Leukotriene Receptor Antagonists:
• Montelukast
• Zafirlukast
• Pranlukast
ii. 5-Lipoxygenase Enzyme Inhibitor:
• Zileuton

18
3. Mast Cell Stabilizers:
• Sodium Cromoglycate (Cromolyn)
• Nedocromil
• Ketotifen

4. Anti-IgE Recombinant Humanized

Monoclonal Antibody:
• Omalizumab

19
5. Corticosteroids:
i. Systemic:
• Hydrocortisone
• Prednisolone
ii. Inhalational:
• Beclomethasone dipropionate
• Triamcinolone acetonide
• Budesonide
• Fluticasone propionate
• Flunisolide

20
APPROACH TO TREATMENT
1. Prevention of Antigen – Antibody reaction

2. Hyposensitization

3. Prevention of release of mediators

4. Antagonism of released mediators

5. Mimicking dilator neurotransmitter

6. Suppression of inflammation

7. Blockade of constrictor neurotransmitter

21
 CONTROL ASSESSMENT
 Daytime symptoms ≤ 2 /week

 Absence of night time awakenings

 Ability to engage in normal daily activity

 Need bronchodilators administration ≤ 2 / week

 Absence of asthma exacerbations

 Normal/near normal lung function parameters

22
 MANAGEMENT OF ASTHMA
1. Adrenoceptor agonists or Sympathomimetics:
• Used as relievers or bronchodilators

2. Corticosteroids:
• Used as controllers or anti-inflammatory agents

23
 BRONCHODILATORS
i. Sympathomimetic:
• Non-selective alpha & β Adrenoceptor Agonists
• Epinephrine
• Ephedrine
• Non-selective β Adrenoceptor Agonists
• Isoprenaline (Isoproterenol)
• Selective β2 Adrenoceptor Agonists
• Salbutamol (Albuterol)
• Salmeterol
• Formoterol
• Terbutaline
• Metaproterenol
• Bambuterol 24
 BRONCHODILATORS
• Selective β2 Adrenoceptor Agonists:
• Short Acting (SABA):
• Salbutamol
• Terbutaline
• Long Acting (LABA):
• Salmeterol
• Formoterol
• Bambuterol INHALER
Preferred route of administration

25
 SYMPATHOMIMETIC AGENTS
(ADRENERGIC AGONISTS)

DIRECT MIXED INDIRECTLY

ACTING ACTING ACTING

UPTAK
NON- RELEASING MAO COMT
SELECTIVE E
SELECTIVE AGENTS INHIBIT INHIBIT
INHIBIT

ephedrine
dopamine amphetamine
pargylin
α1-phenylephrine α1 α2- oxymetazoline
cocaine entacapone
α2-clonidine β1 β2- isoprenaline
β1-dobutamine α1 α2 β1 β2- epinephrine
β2-salbutamol α1 α2 β1- norepinephrine
26
• Phenylethylamine is basic structure of all
sympathomimetic agents

• It has an aromatic benzene ring attached to

ethylamine side chain

• Addition of hydroxyl group ( OH) at carbon

atom 3 & 4 results in catachol nucleus

• Catachol nucleus attached to ethylamine side

chian forms compounds collectively called
catacholamines (epinephrine, norepinephrine,
dopamine & isoproterenol) 27
 OH 3

4
OH
β α
Catechol Nucleus
CH2 CH2 NH2
Greatest adrenergic activity

PHENYLETHYLAMINE
Ethyl group Amine
28
Potency H H
COMT
BA HO β α
DOA
3 C C NH2
CNS

Increses
4 OH H Beta receptor
Direct activity
HO acting
MAO
agonists

NOREPINEPHRINE

29
 H H
HO
C C NH

OH H CH3
HO

EPINEPHRINE:

30
 ISOPRENALINE:

H
CH
HO 3
C C NH CH
CH
OH H 3

HO
Catachol Ethylamine side chain
31
 H
HOH2C
3 C C NH

4 OH H C(CH3)3

HO

SALBUTAMOL:

32
 H
HOH2C
C C NH

OH H C

HO
O

SALMETROL:

33
 SYMPATHOMIMETICS
• MECHANISN OF ACTION: (β2 adrenoceptor agonists)
1. Activate adenylyl cyclase
• Increased formation of intracellular cAMP leading to
• Increased protein kinase A activity
• Decreased calcium conc due to its removal from cytosol into
intracellular stores & out of the cell
• Inhibition of PLC-IP3-Ca++pathway
• Inactivation of MLC kinase, activates MLC phosphatase
• Also increase membrane potassium conductance
• Relax airway smooth muscle resulting in bronchodilation
2. Inhibit release of mediators from mast cells
3. Inhibit microvascular leakage
4. Increase mucociliary transport

34
 PHARMACOKINETICS
• Short Acting: Salbutamol & Terbutaline (SABA)
• Route of administration: Inhalation (MDIs)

• 100 – 400 doses per inhaler

• 10 – 20% of administered dose is absorbed

• Particle size:

• < 0.5 µm exhaled

• < 2 µm clinical benefit uncertain

• Optimum size is 2 – 5 µm

• 5 - 10 µm efficacy is reduced
35
• > 10 µm deposit in oral cavity
 PHARMACOKINETICS (Contd….)

• Onset of action: 1 – 5 min

• Excretion: Kidneys (unchanged & metabolites)
• Half Life & DoA: 3 – 4 hours
• Dose: 100 – 200 µg (max 4 times/day)
• Nebulizer: 2.5 – 5 mg
• Tablets: 1 (2 mg) x BD or TDS
• S/C: Terbutaline 0.25 mg
36
 PHARMACOKINETICS (Contd….)

• Long acting: Salmeterol & Formoterol (LABA)

• High lipid solubility

• Duration of action: 12 hours

• Not to be used as monotherapy

37
 SYMPATHOMIMETICS
• Uses:
• Short Acting Drugs (SABA):
• Acute Asthma
• Children < 5 years & elderly may benefit from
spacer device
• Inhalation & I/V
• Long Acting Drugs (LABA):
• Chronic Asthma/Prophylaxis
• Night symptoms control
• Oral/inhalation
• Less benefit in COPD

38
 SYMPATHOMIMETICS (cont…)
Adverse Effects (Oral Route):
•Tachycardia (st. directly cardiac β2 receptors/VD/reflex)
•Tremors (st. β2 receptors in sk muscles)
Vagal withdrawal
•Muscle cramps
•Tolerance to β2 agonist activity
• Hypokalemia (Na+K+ ATPase drives K+ into the cells)
•Nervousness

•Headache

•Weakness

•Elevated serum glucose levels (glycogenolysis)

39
MCQs

40
MCQ 1.
A young adult reported in ER with acute
attack of bronchospasm. Physician decided to
administer a drug that relieves
bronchospasm within short time. Which one
of the following drugs is used as “reliever” in
bronchial asthma:

A.Montelukast

B.Omalizumab

C.Prednisolone

D.Salbutamol
41
MCQ 2:
Physician prescribes a drug to a known asthmatic.
However the interval between the doses is short
because of its short half-life. Which one of the
following beta-2 agonists is most likely prescribed:

A. Formoterol
B. Bambuterol
C. Salmeterol
D. Salbutamol

42
MCQ 3:
A 35 years old known asthmatic patient was brought to
ER with acute attack of bronchospasm. His friend
informed that the man had taken few tablets advised to
him by a quack in his village. Which one of the
following drugs was most probably taken by this man
that can induce an acute attack of bronchial asthma in
susceptible individuals:
A. Aminophylline
B. Aspirin
C. Montelukast
D. Prednisolone
43
MCQ 4.
Which one of the following drugs is used as
“controller” in bronchial asthma:
(C-1)

A.Aminophylline

B.Montelukast

C.Prednisolone

D.Salbutamol
44
MCQ 5:
A known asthmatic complained about frequent episodes of
bronchospasm at midnight. His physician advised inhaler that
contains a long acting beta-2 agonist with a corticosteroid.
Justification for such a combination of Long acting beta-2
agonists with steroids is that beta-2 agonists: (C-2)

A. are only available in combination with steroids

B. do not have their own anti-inflammatory effect

C. have their bioavailability enhanced by steroids

D. therapeutic effect is enhanced by combination

45
 SEQs
SEQ 1:
Write classification of drugs used in
Bronchial Asthma.

SAQ 2:
Write MOA of Salbutamol

SAQ 3:
Enlist adverse effects of beta-2 agonists

46
ANTIASTHMATIC DRUGS - II

47
 METHYLXANTHINES
• Main source is beverages
• Tea …….. Theophylline
• Coffee …. Caffeine
• Cocoa …. Theobromine

•• Substituted
Cost derivatives:
effective drugs
• Enprofylline
• Efficacy in attenuating three
• Doxofylline
• cardinal
Salts: features of asthma:
• • Aminophylline
Airway (ethylene diamine)
hyper-responsiveness
• Oxtrifylline
•
• Airway inflammation
Acepifylline
• Airflow obstruction
48
 MOA: (Methylxanthines)
1. Inhibit PDE enzyme
i. Increase cAMP & cGMP
ii. Relaxation of smooth muscle
2. Inhibit cell surface adenosine receptors
i. Adenosine; autacoid that causes bronchoconstriction &
release of histamine from airway smooth muscle
ii. Theophylline blocks adenosine receptors
iii. Stimulation of cardiac function
3. Interleukin-10 cytokine release (anti-inflammatory action)
4. Reduce immune & inflammatory activity of specific cells
5. Histone deacetylase activation ( steroids action)
6. Reduce diaphragmatic fatigue
Immune modulatory effect

49
 Therapeutic Uses: (Methylxanthines)
1. Acute asthma
i. slow i/v
ii. Risk of cardiotoxicity
2. Chronic asthma
i. Prophylaxis for long term control of asthma
ii. Maintenance therapy with inhaled steroids
3. Apnea of newborn
i. Preterm infants
• Rectal preparations available
i. Elderly
ii. Infants
• Sustained release preparations also available 50
Drug Interactions: (Methylxanthines)

1. Hepatic metabolism

2. Rapid elimination of theophylline by:

i. Phenytoin

ii. Oral contraceptives

iii. Smoking

3. Reduced clearance by:

i. Cimetidine

ii. Macrolides

iii. Viral infection 51

 Adverse Effects (Methylxanthines)

1. Narrow therapeutic index

2. Therapeutic drug monitoring (TDM) required

3. Optimum range : 5-15 mcg/L for theophylline

4. > 20 mcg/L
• GIT: Anorexia, nausea, vomiting, abdominal discomfort
• CNS: Insomnia, anxiety, headache, seizures

• CVS: Palpitations, tachycardia, arrhythmias

5. Neonates are at high risk due to slow clearance

6. Rate of infusion monitoring 52

 Adverse Effects (Methylxanthines)

• Nausea & vomiting ………. PDE4 inhibition

• Gastric discomfort ……….. “ “
• Headache ………………… “ “
• Behavioral disturbances … “ “
• Diuresis …………………… A1 receptor antagonism
• Epileptic seizures ………… “ “
• Cardiac arrhythmias …….. PDE4 inhibition & A1

53
 ANTICHOLINERGICS
• Selective in action
• Inhibit the effect of:
• Acetyl choline

• Muscarinic receptors

• Efferent ending of vagus nerve

• atropine
• Atropine • scopolamine
• hyoscyamine

• Ipratropium Bromide Datura stramonium

54
MECHANISM OF ACTION (ANTICHOLINERGICS)

1. Blockade of muscarinic receptors:

i. Bronchi
ii. Bronchioles

2. Block direct constrictor effect of Ach on

bronchial smooth muscle mediated via:
2+
i. M3-Gq-PLC-IP3-Ca pathway

3. Decrease mucus viscosity

4. Increase mucociliary clearance

55
 USES (ANTICHOLINERGICS)

1. Acute Severe asthma (status asthmaticus)

2. Chronic Asthma

3. COPD

4. Prophylaxis
• Inhalation
 More effective

 Less toxic

 Lesser dose required

56
 (ANTICHOLINERGICS)

• Ipratropium is drug of choice in:

• Chronic Bronchitis

• Clears mucus by expectoration

• Side effects:
• Dryness of mouth, nausea, blurred vision, dysuria
Contraindications:
• Glaucoma

• Urinary retention

57
LEUKOTRIENE RECEPTOR ANTAGONISTS
• Montelukast & Zafirlukast: Oral
• Mechanism of action:
• Leukotrienes contribute to increased secretions
& edema of bronchial passages
• LTD4 is 1000 times more potent than histamine

• Inhibit cysteinyl-leukotriene type-1 receptors

(Cys LT1 receptors)
• Inhibit physiologic actions of LTC4, LTD4, LTE4
(SRS-A; slow-reacting substance of anaphylaxis)
58
 USES

• Prophylaxis and long term treatment of:

1. Antigen induced asthma

2. Exercise induced asthma

3. Aspirin induced asthma

59
 PHARMACOKINETICS
• Half life (T½):
• Montelukast: 6 hrs

• Zafirlukast: 10 hrs

• Extensive plasma protein binding

• Metabolism:
• CYP 450

60
 TOXICITY
• Churg-Strauss syndrome:
• Asthma
• Eosinophilia
• Vasculitis
• Several cases reported
 Rare vasculitis that is associated with
increased circulating eosinophils and
asthma, it may effect:
 Heart, Peripheral nerves, Kidneys
 Reported in asthmatics with or without
concomitant corticosteroid therapy 61
• Rare cases of hepatic dysfunction reported

with use of these agents

• So hepatic enzymes should be monitored

62
 Asthma and Mast Cell Activation
• Chronic inflammatory disease of the airways:
• Increased mast cells in airways smooth muscle
• Activation of mast cells
• Infiltration of eosinophils & T helper cell lymphocytes
• Mast cell activation by allergens & physical
stimuli releases:
• Bronchoconstrictor mediators
• Histamine
• Leukotriene D4
• Prostaglandin D2
63
 MAST CELL STABILIZERS
• Sodium Cromoglycate ….. Inhalation
• Nedocromil
Oral
• Ketotifen
• Properties:
• Inhibit release of cytokines from mast cells due to
antigen-antibody reaction
• Prevent release of:
• Histamine
• Serotonin
• SRS-A
• Mast cell stabilizers do not have bronchodilator effect
• Once mediator has been released, are not effective
• So their use is prophylactic only
64
• Administered mostly by inhalation
• Only 10% of the administered dose is absorbed
• Uses:
• Prophylaxis of asthma
• Allergic
• Exercise induced
• Irritant induced

• Allergic rhinitis
• Nasal spray

• Allergic conjunctivitis
• Eye drops
65
 ADVERSE EFFECTS
• Cough
• Headache
• Nausea
• Rashes
• Irritation & bronchospasm due to powder
• Rarely anaphylaxis
66
 OMALIZUMAB
• Anti-IgE Recombinant Humanized Monoclonal Antibody

• First biological drug approved for treatment of asthma

• Binds to IgE receptors on mast cells , lymphocytes

& blocks binding of IgE

• Also binds & neutralizes free IgE in serum

• It is very expensive drug

• Clinical trials are limited 67

 CORTICOSTEROIDS

• Routes of administration:
• Hydrocortisone I/V
• Prednisolone Oral
• Betamethasone Inhalation
• Beclomethasone Inhalation
• Budesonide Inhalation
• Fluticasone Inhalation
68
 MECHANISM OF ACTION
• Enter target cells

• Bind to glucocorticoid receptor in cytoplasm (GR)

• Steroid-GR complex moves into the nucleus

• Binds to specific sequences of target genes

• Resulting in its influence on gene transcription

69
 (MECHANISM OF ACTION)

• Anti-inflammatory action:
• Decrease mucosal edema
• Reduce mucus secretions
• Reduce capillary permeability
• Stabilize mast cells
• Block immune response
• Decrease antibody formation
• Antagonize histaminergic & cholinergic responses
• Enhance β2 adrenoceptor responsiveness to

agonists (catecholamines) 70
 USES
• Acute severe asthma (Status asthmaticus):
• Hydrocortisone
• I/V
• Acute asthma:
• Prednisolone
• Oral
• Chronic asthma:
• Prophylaxis
• Beclomethasone
• Inhalation
71
 (USES)

• Seasonal allergic rhinitis with cough &

bronchospasm:
• Oral
• Prednisolone (Deltacortril)
• Nasal spray
• Beclomethasone (Rino clenil)
• Inhalation
• Fluticasone (Seretide)
• Non-infected inflammatory conditions of
nose:
• Nasal drops:
• Betamethasone (Betnesol)
72
 SIDE EFFECTS
• Oral candidiasis:
• Inhalers

• Hoarseness of voice

• Saline gargles

• Suppression of hypothalamic-pituitary-
adrenal (HPA) axis
• Cushing’s syndrome
73
 SIDE EFFECTS (Cont ….)

• HPA axis suppression occurs with:

• Prednisolone
• oral
• Dose > 10 mg/day
• For many months
• Beclomethasone
• Inhaled
• Dose > 2000 µg daily
• For months or years
• Other inhaled steroids
• Equivalent dose & duration to beclomethasone

74
 (SIDE EFFECTS)
• Fluid retention
• Increased appetite
• Weight gain
• Osteoporosis
• Capillary fragility
• Hypertension
• Peptic ulceration
• Diabetes 75
 (SIDE EFFECTS)

• Cataract
• Psychosis
• Tendency of adverse effects of steroids
tends to increase with age

• In aspirin-sensitive asthmatic patients,

anaphylaxis to I/V hydrocortisone

• Growth suppression in children

76
 STATUS ASTHMATICUS

Acute Severe Asthma

•Acute exacerbation of asthma
•Not responsive to treatment with bronchodilators
•Life threatening situation
•May lead to respiratory failure
•Cardiac arrest can occur
•Requires immediate & aggressive corrective therapy
•Metabolic acidosis reduces effectiveness of β agonists
•I/V NaHCO3 added if blood pH is low

77
 STATUS ASTHMATICUS (Cont ….)

• Decrease in PO2 level corrected with O2

• Nebulization of albuterol for first few hours continuously
• Switched to intermittent albuterol every 02 hours
• I/V corticosteroids
• Inhaled ipratropium every 06 hours
• Magnesium Sulfate (MgSO4) has been used I/V in a
mean dose of 50 mg/Kg with satisfactory results in
adults and children
• If still no response to treatment:

• GA with inhaled anesthetics which are potent bronchodilators 78

MCQs

79
MCQ 1:
Which one of the following drugs may lead
to severe adverse effect when used daily for
several weeks for severe asthma?

n Beclomethasone by aerosol
n Albuterol by inhaler (C-2)
n Cromolyn sodium by aerosol
n Prednisolone by mouth

80
MCQ 2:
Which one of the following drugs is a
prophylactic agent used in bronchial
asthma that stabilizes mast cells:

n Aminophylline
n Cromolyn sodium
n Epinephrine (C-1)
n Ipratropium

81
MCQ 3:
Asthma is characterized by reversible
narrowing of the air ways, which of the
following will relieve acute attack of asthma
by bronchodilation?

A. Beclomethasone
B. Theophylline (C-1)
C. Montelukast
D. Omalizumab
82
MCQ 4:
Methylxanthines exert which one of the
following actions at the cellular or molecular
level:
(C-1)

A. Agonistic action at Adenosine receptors

B. Antagonistic action at glycine receptors

C. Intracellular release of potassium

D. Inhibition of phosphodiesterase

83
MCQ 5:
A 10-year-old patient has severe asthma & was
hospitalized 5 times between the ages 7 and 9. He is
receiving out-patient medications since last several
months that have greatly reduced the frequency of
severe attacks but child’s growth is visibly effected.
Which one of the following drugs is most likely
responsible for this observation of physician?

nAlbuterolby aerosol
nBeclomethasone by aerosol (C-2)
nCromolyn by inhaler
nPrednisolone by mouth

84
MCQ 6: 18 years old boy is a known asthmatic.
His condition is worse during spring season.
Doctor advises him medicine that acts as a
prophylactic drug that prevents release of
mediators of allergy and inflammation by the
inflammatory cell due to its action on their cell
membranes. Which one of the following is most
likely the drug prescribed to this patient:

A. Cromolyn sodium

B. Montelukast (C-2)

C. Salbutamol

D. Theophylline 85
MCQ 7:
A 16 years old girl is brought to medical OPD
complaining of muscle tremors and tachycardia.
Condition is especially worse after taking
medication which was prescribed by a doctor
when she developed bronchospasm during a
school visit to the flower market. Which one of
the following drugs may be responsible for her
condition:

A. Beclomethasone

B. Ipratropium (C-2)

C. Montelukast
86
D. Salbutamol
MCQ 8:
A known asthmatic 16-year-old boy is
brought to ER with bronchospasm after
taking aspirin for headache. Which one of
the following drugs is useful to relieve his
condition:
A. Aminophylline
B. Cromolyn sodium (C-2)
C. Montelukast
D. Omalizumab 87
MCQ 9:
A 15 years old girl is brought to emergency
dept with severe bronchospasm, wheezing
and extreme difficulty in breathing. Her
parents inform the doctor that recently she
has suffered such attacks repeatedly,
especially after visiting the nearby garden.
Which one of the following drugs can relieve
her condition rapidly:

A. Beclomethasone
B. Ketotifen (C-3)
C. Montelukast
D. Salbutamol 88
 SEQs

SEQ 1: Write MOA & adverse effects of

Methylxanthines

SEQ 2: Write a note on Leukotriene Pathway Inhibitors

SEQ 3: Write management of Acute Severe Asthma

SEQ 4: Justify use of Salmeterol with corticosteroids

SEQ 5: Why nonselective beta blockers and Aspirin

not used
in asthma 89