Preface

Agam is a group of budding medicos, who are currently doing their under graduation in
various Medical Colleges across Tamil Nadu and Pondicherry. The group was initiated on 18th
November 2017, in the vision of uniting medicos for various social and professional causes.

We feel delighted to present you Agam pharmacology notes prepared by Agam Divide and
Rule 2019 Team to guide our fellow medicos to prepare for university examinations.

This is a reference work of 2017 batch medical students from various colleges. The team
took effort to refer many books and make them into simple notes. We are not the authors of the
following work. The images used in the documents are not copyrighted by us and is obtained from
various sources.

Dear readers, we request you to use this material as a reference note, or revision note, or
recall notes. Please do not learn the topics for the 1st time from this material, as this contain just the
required points, for revision.
Acknowledgement

On behalf of the team, Agam would like to thank all the doctors who taught us Pharmacology.
Agam would like to whole heartedly appreciate and thank everyone who contributed towards the
making of this material. A special thanks to Kareeshmaa H C, who took the responsibility of leading
the team. Agam heartily thanks Bala Diwakar T, for his contribution towards making this material.
 INDEX

Chapter 1: Drugs for Cough and Bronchial

Asthma.

Essay
1. Bronchial Asthma Drugs Classification.
Inhalation Steriods. Anti IgE Antibody…………… 1

Short Notes
2. Sympathomimetic Drugs……………………………… 4
3. Mechanism and Pharmacological Action
of Methylxanthine……………………………………….. 5
4. Mast Cell Stabilizers……………………………………… 7
5. Treatment of Status Asthmaticus………………….. 8

Short Answers
6. 2 Opioid Antitussives…………………………………….. 9
7. 2 Leukotriene Antagonists…………………………….. 9
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1. DRUGS FOR BRONCHIAL ASTHMA

INHALATIONAL CORTICO STEROIDS (ICS)

• They are glucocorticoids with high topical and low systemic activity
• They have poor absorption and marked first pass metabolism
• It has been Advocated as step one for all the asthma patients to
prevent bronchial remodeling but currently they are not necessarily
used in mild and episodic asthma patients.
• Peak effect is seen after 4-7 days of administering ICS and the effects
persists for few weeks after discontinuation.
• Dosage: initially 100 - 200µg BD, titrate dose upward for every 3 – 5
days, maximum dose of 400µg QID, beyond which no further benefit
generally occurs.
• They are safe during pregnancy.

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FUNCTIONS:

i. Suppress bronchial inflammation.

ii. Increases the peak expiratory flow rate
iii. Reduce need for β2 agonist inhalations
iv. Prevent episodes of acute asthma

ADVERSE DRUG EFFECTS:

▪ Hoarseness of voice
▪ Dysphonia
▪ Sore throat
▪ Symptomatic/ asymptomatic oropharyngeal candidiasis
*prevention: ADR can be minimized by usage of spacers and
gargling of mouth after every dose. Oral candidiasis can be
prevented/ treated by topical nystatin or clotrimazole.*
▪ Dose> 600µg/day causes mood changes, osteoporosis, growth
retardation in children, early cataract, etc.

DRUGS

❖ Beclomethasone dipropionate:
Effective in perennial rhinitis
❖ Budesonide:
Non-halogenated glucocorticoid with high topical: systemic activity
ratio
They are preferred in severe cases
Contraindicated in presence of nasal infection and nasal ulcers.
❖ Fluticasone propionate:
High potency

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Longer duration
Negligible oral bioavailability
Preferred in patients requiring higher doses

❖ Flunisolide:
Topical steroid used for prophylaxis and treatment of seasonal
and perennial rhinitis.
❖ Ciclesonide:
It is a prodrug that is cleaved by esterases in the bronchial
epithelium to release the active moiety.
Oral bioavailability <1%

ANTI IgE ANTIBODY

Omalizumab:
❖ Humanized monoclonal antibody against IgE.
❖ Administered via subcutaneous route
❖ Mechanism of action: it neutralizes free IgE in circulation without
activating mast cells and other inflammatory cells. On antigen
challenge little IgE is available bound to the mast cell receptors t
trigger mediator release and cause bronchoconstriction.
❖ Uses: reduces exacerbations and steroid requirement in severe
extrinsic asthma. It is reserved for resistant asthma patients with
positive skin tests or raised IgE levels that require frequent
hospitalization.
❖ Very expensive.

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2. SYMPATHOMIMETICS
❖ These β2 agonist are used in treatment of asthma
❖ The drugs are:
▪ Salbutamol
▪ Terbutaline
▪ Bambuterol
▪ Salmeterol
▪ Formoterol
❖ β2 agonist must be cautiously used in hypertensives, ischemic heart
disease patients and in those receiving digitalis.
❖ They are the most effective and fastest acting bronchodilators when
inhaled.

Mechanism of action:

beta agonist

beta receptors

increases cAMP

relaxation of muscle and

decresed asthma mediators

release from mast cells

❖ Ephedrine: oral sympathomimetic (α+β1+β2) action used in mild to

moderate chronic asthma.

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3. METHYLXANTHINES

• PHARMACOLOGICAL ACTIONS
➢ CNS: caffeine is more active than theophylline in producing these effects
▪ Stimulates higher centres
▪ Increases alertness
▪ Allays fatigue
▪ Produces sense of well being
▪ Higher doses causes nervousness, panic, restlessness, excitement

➢ CVS:
▪ Increases heart rate, force of contraction and cardiac output.
▪ At higher doses causes cardiac arrhythmias.
➢ SMOOTH MUSCLE: theophylline is more potent than caffeine
▪ Relaxation – bronchodilatation
➢ KIDNEY:
▪ Mild diuretic
▪ Increases renal blood flow and GFR
➢ SKELETAL MUSCLE:
▪ Enhances contraction
▪ Relieves fatigue
▪ Facilitate neuromuscular transmission
➢ GIT:
▪ Increased gastric acid secretion
▪ Increased digestive enzyme secretion
➢ METABOLISM:
▪ Increase in BMR
➢ INFLAMMATORY CELLS:
▪ Decreased release of histamines, cytokines and other mediators.

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• MECHANISM OF ACTION

a. Release of calcium from sarcoplasmic reticulum, especially in cardiac

and skeletal muscle
b. Inhibition of phosphodiesterases
(Phosphodiesterases degrade cyclic nucleotides intracellularly)

inhibition of PDE

↑ conc of cyclic nucleotides

1. bronchodilatation
2. cardiac stimulation
3.vasodilation
4. mediator release inhibition

c. Blockade of adenosine receptors causes bronchodilatation and

attenuate mediator release.

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4. MAST CELL STABILIZERS

▪ Sodium chromoglycate
• Synthetic chromone derivative which inhibits degranulation of mast
cells by trigger stimuli.
• Long term treatment deceases cellular inflammatory response
• Bronchial hyper reactivity is reduced to variable extents.
• Bronchospasm induced by allergens, cold air, exercise may be
attenuated
• Uses:
➢ Bronchial asthma
➢ Allergic rhinitis
➢ Allergic conjunctivitis
• ADR:
➢ Bronchospasm
➢ Throat irritation
➢ Cough
▪ Ketotifen
• Antihistaminic with some chromoglycate like action
• Stimulation of immunogenic and inflammatory cells and mediator
release are reduced.
• ADR:
➢ Sedation
➢ Dry mouth
➢ Dizziness
➢ Nausea
➢ Weight gain.

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5. TREATMENT OF STATUS ASTHMATICUS

It is a life threatening condition.

Upper respiratory tract infection is the most common precipitant.

TREATMENT:
❖ Hydrocortisone hemisuccinate 100mg ( or equivalent dose of
another glucocorticoid) i.v. stat , followed by 100- 200mg 4-8 hourly
infusion; may take 6 hours to act
❖ Nebulised Salbutamol(2.5 – 5 mg)+ ipratropium bromide 0.5mg
intermittent inhalations driven by oxygen
❖ High flow humidified oxygen inhalation
❖ Salbutamol/ Terbutaline 0.4 mg i.m./ s.c. may be added , since
inhaled drug may not reach smaller bronchi due to severe narrowing/
plugging with secretions
❖ Intubation and mechanical ventilation, if needed
❖ Intensive antibiotic therapy for treating chest infections
❖ Saline+ sodium bicarbonate/ lactate infusion to correct dehydration
and acidosis

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6. Two Opioid Antitussives

i. Codeine
ii. Ethylmorphine
iii. Pholcodine

7. Two Leukotriene Antagonists

i. Montelukast
ii. Zafirlukast

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