Pharmacotherapy of asthma and copd 1.pptx

Amity Institute of Pharmacy
Pharmacotherapy of Asthma And
COPD
Advanced Pharmacology II
M.PHARM (Pharmacology)
SEM 2
BY: ABHINAV SINGH
1

Disorders of Respiratory
Function
• Mainly disorder of the respiratory system
are :
1. Brochial asthma
2. cough
3.allergic rhinitis
4.Chronic obstructive pulmonary disease
(COPD) also k/a emphysema
2

What is Bronchial Asthma?
Bronchial asthma is a chronic respiratory
disease characterized by inflammation and
narrowing of the airways in the lungs, which
causes difficulty in breathing.
The inflammation causes the airways to
become hyperreactive to certain triggers, such
as allergens, irritants, and exercise, leading to
symptoms such as wheezing, coughing, chest
tightness, and shortness of breath.
3

Clinical Feature
• Wheezing: a high-pitched whistling sound when
breathing out
• Shortness of breath: a feeling of breathlessness
or difficulty in breathing
• Chest tightness: a sensation of tightness or
pressure in the chest
• Coughing: a persistent cough, especially at night
or early in the morning
• Difficulty in breathing: breathing is rapid and
shallow with a feeling of suffocation
4

• These symptoms may occur intermittently or
persistently, and they may be triggered by certain
factors such as:
1. Allergens: such as pollen, dust mites, animal dander,
and molds
2. Irritants: such as tobacco smoke, air pollution, and
strong odors
3. Exercise: physical activity or exertion can cause
symptoms in some people
4. Respiratory infections: such as the common cold or flu,
which can aggravate asthma symptoms
5. Emotional stress: stress or anxiety can also trigger
asthma symptoms in some people.
5

Risk Factor
• Genetics: asthma tends to run in families, and certain
genetic variations may make a person more susceptible
to the condition.
• Allergies: people with allergies are more likely to develop
asthma, as the inflammation caused by allergies can
trigger asthma symptoms.
• Environmental factors: exposure to pollution, dust, and
other environmental irritants can increase the risk of
developing asthma, especially in children.
• Respiratory infections: certain respiratory infections,
such as the common cold or flu, can increase the risk of
developing asthma or exacerbate existing symptoms.
• Obesity: being overweight or obese can increase the risk
of developing asthma, especially in women.
6

• Occupational exposure: exposure to certain chemicals,
dust, or fumes at work can increase the risk of
developing occupational asthma.
• Smoking: smoking or exposure to secondhand smoke
can increase the risk of developing asthma or
exacerbate existing symptoms.
• Physical activity: in some people, physical activity or
exercise can trigger asthma symptoms.
• Stress: emotional stress or anxiety can trigger asthma
symptoms in some people.
7

Airway innervations
• Afferent nerves (sensory)
1. Irritant receptors in upper airways
2. C-fiber receptors in lower airways
Stimulated by: exogenous chemicals
physical stimuli (cold air)
Endogenous inflammatory mediators
* Efferent nerves( motor)
Parasympathetic supply
M3 receptors in smooth muscle and glands
8

Anti-Asthmatic drugs
• Anti- Asthmatic Drugs:
• These drugs are used to relieve the acute episodic attacks
of asthma like bronchodilators, quick relief medications.
• To reduce the frequency of attacks and nocturnal
awakenings.(anti-inflammatory drugs , control therapy)
• Bronchodilators:
• Quick relief medications.
• Treat acute episodic attack of asthma.
• Short Acting Beta2- agonists
• Antimuscarinics
• Xanthine preparations
9

• Anti- inflammatory agents:
(control medications or prophylactic therapy)
Reduce the frequency of attacks
• Corticosteroids
• Mast cell stabilizers
• Leukotrienes antagonists
• Anti-IgE monoclonal antibody
• Long acting β2-agonists
10

Anti-asthmatic drugs
• Bronchodilators: (quick relief medications)
This are used to relieve acute attack of
bronchoconstriction
1. β2-adrenoreceptor agonists
2. antimuscarinics
3.xanthine preparations
11

• Mechanism of action (β2 adrenoreceptor agonist)
• The mechanism of action of beta-2 agonists involves
binding to and activating the beta-2 adrenoreceptors,
which are coupled to a G protei2n that ultimately leads to
the activation of the enzyme adenylate cyclase.
Adenylate cyclase then converts ATP to cyclic AMP
(cAMP), which activates protein kinase A (PKA) and
ultimately leads to relaxation of the smooth muscle cells
in the bronchioles.
• Inhibit mediators release from mast cells.
• Increase mucus clearance.
12

• Classification of β agonists:
• Non Selective β agonists:
Epinephrine – isoprenaline
• Potent bronchodilator
• Rapid action
• s.c or inhalation
• Has short duration of action 60-90 min
• Drug of choice (Hypersensitivity reactions)
Selective β2- agonists (Preferable)
• Salbutamol
• Terbutaline
• Salmeterol
• Formeterol
13

Non Selective β agonists:
• Disadvantages
• Not effective
• Hyperglycemia
• Cvs side effects : tachycardia, arrhythmia, hypertension
• Skeletal muscle tremor
• Not suitable for asthmatic patients with hypertension or heart failure.
• Contraindications:
• CVS patients , diabetic patients
14

Selective β2- agonists
• Drug of choice for acute attack of asthma
• Can be given orally, parentrally
Short acting β2 agonists
• E.g salbutamol,terbutaline
Long acting β2 agonists
• E.g salmeterol, formeterol
Advantage of β2 Agonists
• Minimal CVS side effects
• Suitable for asthmatic patients with hypertension or heart failure
Disadvantages of β2 Agonists
Nervousness , tachycardia on over dose
Skeletal muscle tremors 15

Muscarinic antagonists
• Ipratropium- tiotropium
• Acting by blocking muscarinic receptors
• Aerosol inhalation
• Quaternary Derivative of atropine
• Does not enter diffuse into the blood.
• Delayed onset of action
• Ipratropium has short duration of action 3-5hr
• Titropium has longer duration of action (24hr).
• Pharmacodynamics
• Are short-acting bronchodilator
• Inhibit bronchoconstriction and mucus secretion
• Less effective than beta 2 agonists
• No anti-inflammatory action
• Uses:
• Main choice in chronic obstructive pulmonary disease (COPD)
• In acute severe asthma combined with beta2 agonists & steroids.
16

Methylxanthines
• Theophylline- aminophylline
• Mechanism Of action :
• These are phosphodiesterase inhibitors
• Increase cAMP – bronchodilation
• Adenosine receptors antagonists
• Increase diaphragmatic contraction
• Stabilization of mast cell membrane.
Pharmacological effects:
• Bronchial muscle relaxation
• Increase contraction of diaphragm- improve ventilation
• CVS: increase heart rate, increase force of contraction
• GIT: increase gastric acid secretions
• Kidney: increase renal blood flow ,weak diuretic action
17

Pharmacokinetics:
• it is metabolized by cyt p450 enzymes in liver
• Half life = 8 hours
• Drug interaction
-Enzyme inducers: as phenobarbitone-rifampicin-- increase metabolism of theophylline--
decrease half life.
Uses:
• Second line drug in asthma (theophylline)
• For status asthmatics( aminophylline, given slow infusion)
Side effects:
• Low therapeutic index narrow safety margin
• Cvs effects: hypotension, arrhythmia
• GIT effects: nausea & vomiting
• CNS effects: tremors, nervousness, insomnia, convulsions
18

• Glucocorticoids:
MOA: -Inhibition of phospholipase A2
-decrease prostaglandin and leukotrienes
-decrease number of inflammatory cells in airways.
-Mast cell stabilization- decrease histamine release
-Decrease capillary permeability and mucosal edema.
-Inhibition of antigen-antibody reaction
-Upregulate beta2 receptors (have additive effects to beta2 agonists)
Routes of administration:
-inhalation
Eg: budesonide & fluticasone, beclomethasone
-given by inhalation,given by metered-dose inhaler
-have first pass metabolism
-best choice in asthma, less side effects
• orally: prednisone, methyl prednisolone
• Injection: hydrocortisone, dexamethasone.
• Systemic corticosteroids are reserved for a;
• Status asthmaticus (i.v)
• Using inhaled beta2 agonists 3 times /week
• Or waking one night/week. 19

*Side effects due to systemic corticosteroids:
-adrenal suppression
-growth retardation in children
-Osteoporosis
-fluid retention, weight gain ,hypertension
-hyperglycemia
-susceptibility to infections
-glaucoma
-cataract
-fat distribution, wasting of the msucles
-psychosis
20

Mast Cell Stabilizers:
• E.g: Cromolyn-Nedocromil
• Act by stabilization of mast cell membrane.
• Given by inhalation(aerosol, microfine powder, nebulizers)
• Have poor oral absorption
• Pharmacodynamics:
• Not bronchodilators
• Are not effective in acute attack of asthma
• Prophylactic anti inflammatory drug
• Reduce bronchial hyper reactivity.
Uses:
-prophylactic therapy in asthma
-allergic rhinitis.
-conjunctivitis.
Side effects:
-Bitter taste
-Minor upper respiratory tract irritation(burning sensation , nasal congestion)
21

Leukotrienes’s antagonists
• Leukotrienes:
-produced by the action of 5-lipoxygenase on arachidonic acid
-synthesized by inflammatory cellsfound in the airways(eosinophils, macrophages, mast cell)
-Leukotriene –B4: chemotaxis of neurophills
*Cysteinyl leukotrienes C4,D4 &E4:
Bronchoconstriction
Increase bronchial hyper-activity
Mucosal edema, mucus hypersecretion.
Leukotriene receptor antagonist:
E.g: zafirlukast, montelukast, pranlukast
-are selective , reversibile, antagonists of cysteinyl leukotriene receptors
-taken orally
-are bronchodilators
-have anti-inflammatory action
Less effective than inhaled corticosteroids
Use: not effective to relieve acute attack of asthma
Prophylaxis of mild to moderate asthma
Aspirin-induced asthma
Antigen and exercise inducd asthma
22

• Omalizumab:
• Is a monoclonal antibody directed against
human IgE
• Prevents IgE binding with its receptors on
mast cells & basophils.
• Decrease release of allergic mediators
• Used for treatment of allergic asthma
• Expensive not first line therapy.
23

Drugs Used in COPD
• COPD is a chronic irreversible airflow obstruction, lung damage and inflammation of the air
sacs(alveoli).
• Smoking is a high risk factor.
24
Treatment: – Inhaled bronchodilators
– Inhaled glucocorticoids
– Oxygen therapy
-Antibiotics specifically macrolides such as azithromycin to
reduce the number of exacerbations.
-Lung transplantation

25

26

• References:
• KD. Tripathi 8th edition.
• Leung, J. M., & Sin, D. D. (2017). Asthma-COPD overlap syndrome:
pathogenesis, clinical features, and therapeutic targets. BMJ
(Clinical research ed.), 358, j3772. https://doi.org/10.1136/bmj.j3772
• Hoshino, T., Toda, R., & Aizawa, H. (2009). Pharmacological
treatment in asthma and COPD. Allergology international : official
journal of the Japanese Society of Allergology, 58(3), 341–346.
https://doi.org/10.2332/allergolint.09-RAI-0117
27

• Thank You!!
28

Pharmacotherapy of asthma and copd 1.pptx

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