asthma and chronic obstructive pulmonary disease

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SEMINAR ON ASTHMA& COPD : 

SEMINAR ON ASTHMA& COPD ABDUL RAZZAQ M.PHARMA(PHARMACHEMISTRY) DEPARTMENT OF PHARMACHEMISTRY LUQMAN COLLEGE OF PHARMACY GULBARGA

ASTHMA : 

ASTHMA The asthma is derived from the Greek word meaning" difficulty in breathing”. Asthma is physiologically characterized by increased responsiveness of trachea and bronchi to various stimuli and by widespread narrowing of the airways. Chronic inflammatory disorder of the airway. Usually reversible, but not yet curable. Contraction of bronchial smooth muscles. Edema of mucosa.

CAUSES OR AGGRAVATING FACTORS : 

CAUSES OR AGGRAVATING FACTORS Allergy. Environmental factors. Emotional factors. Drugs.

Slide 4: 

CLINICAL FEATURES OF BRONCHIAL ASTHMA Coughing Wheezing & dyspnoea. Tightness in pain Labored expiration . Tachypnoea & tachycardia. signs of infection. Expiration time greater then inspiration time.

Slide 5: 

ASTHMA FACTS About 17 million or 4 % Americans have asthma. Rate of asthma increased 75% between 1980 and 2008. Most common chronic childhood disease, affecting about 5 million children. 14 people die each day from asthma. Nearly 2 million emergency room visits each year. Male: Female ratio is 2:1.

Pathophysiology of Asthma : 

Pathophysiology of Asthma

Chemicals Involved in Inflammation : 

Chemicals Involved in Inflammation IgE Histamine Tryptase Leukotrienes (LTC4) Platelet activating factor (PAF) Prostaglandins (PGD2) Interleukins (IL-4, IL-5) Granulocyte-macrophage colony stimulating factor (GM-CSF) Tumor Necrosis Factor (TNF) Major Basic Proteases (MBP) Eosinophil Cationic Protein (ECP)

Major Cells Implicated in Inflammatory Response : 

Major Cells Implicated in Inflammatory Response Mast cells Lymphocytes Eosinophils Neutrophils

General Goals of Asthma Therapy : 

General Goals of Asthma Therapy Prevent chronic symptoms and asthma exacerbations during the day and night Maintain normal activity levels Have normal or near-normal lung function Have no or minimal side effects while receiving optimal medications

General Pharmacologic Approach to the Treatment of Asthma : 

General Pharmacologic Approach to the Treatment of Asthma 1. “Relievers” I. Short-acting bronchodilators A. 2-adrenergic agents B. Anti-cholinergic (Parasympatholytic) agents 2. “Controllers” 1. Corticosteroids 2. Long-Acting bronchodilators I. 2-adrenergic agents II. Methylxanthines 3. Mast cell stabilizers. 4. Leukotriene inhibitors 5. Anti-IgE monoclonal antibodies

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“Relievers”

Adrenergic Bronchodilators – Short-Acting Agents or sympathomimetics. : 

Adrenergic Bronchodilators – Short-Acting Agents or sympathomimetics. Catecholamine Epinephrine Isoproterenol Isoetharine Resorcinol agents Metaproterenol Saligenin agents Albuterol Pirbuterol Bitolterol

Beta-2 Adrenergic Agonists – Short acting agents : 

Beta-2 Adrenergic Agonists – Short acting agents Mode of administration: Inhaled/ Parenteral Modes of action: Here it leads to increase c AMP Formation in bronchial muscle cell leading to relaxation &decrease mediator release. Relax airway smooth muscle Decrease vascular permeability May modulate mediator release from mast cells and basophiles.

Slide 16: 

Role in therapy: Medication of choice for treatment of acute exacerbations of asthma and useful in the pretreatment of exercise-induced bronchospasm (EIB) Used to control episodic bronchoconstriction Increased used – or even daily use of these agents is a warning of deterioration of asthma and indicates the need to intensify regular anti-inflammatory therapy. Dose:2-4 mg oral,0.25-0.5 i.m/s.c.

Side Effects Seen with Beta Agonist : 

Side Effects Seen with Beta Agonist Tremor Palpitations and tachycardia Headache Insomnia Nervousness Dizziness Nausea

Anticholinergic (Parasympatholytic) Bronchodilators : 

Anticholinergic (Parasympatholytic) Bronchodilators Tertiary Ammonium Compounds: Atropine methonitrate. Scopolamine Quaternary Ammonium Compounds: Ipratropium bromide. Tiotropium bromide

Anticholinergic (Parasympatholytic) Bronchodilators : 

Anticholinergic (Parasympatholytic) Bronchodilators Role in therapy: Additive effect when nebulized together with a rapid-acting beta-2 agonist for exacerbations of asthma Ipratropium can be used an alternative,who experience adverse effects such as tachycardia, arrhythmias, and tremors from beta-2 agonists. Side effects: Dryness of the mouth and bitter taste.

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Dose: 40-80 ug. as in aerosol form by inhalation SPASMOLYSIN 0.32 MG TAB. Ipratopiam bromide: onset & (late peak 60-90 min). Duration of action 4-6 hr. Marketed preparations: 20 ug /puff metered dose inhaler. 2 puff 3-4 times daily. IPRANASE 0.084 % nasal spray 1-2 sprays in each nostrils 2-3 times daily.

Slide 21: 

“Controllers”

Controllers : 

Controllers Corticosteroids Long-Acting bronchodilators 2-adrenergic agents Methylxanthines Cromolyn sodium/Nedrocromil Leukotriene inhibitors Anti-IgE monoclonal antibodies

Inhaled Glucocorticoids : 

Inhaled Glucocorticoids Mechanisms of action: They inhibit the formation and release of cytokines and chemical mediators & reduces bronchial hyper reactivity. Inhibition of the release of prostaglandins and leukotrienes thus preventing the smooth muscle contraction and mucous secretions also suppresses inflammatory responses due to AG:AB reaction. Role in therapy: Most effective anti-inflammatory medication for the treatment of asthma.

Inhaled Glucocorticoids Examples : 

Inhaled Glucocorticoids Examples Beclomethasone dipropionate:BECLATE INHALER 50 Ug. Dosage: 200-1000µg BD. Budesonide:PULMICORT 100,200,400Ug/metered dose. Dosage: 200-400µg BID –QID. Flunisolide SYNTARIS 25 µg Per actuation nasal spray.. Fluticasone : FLOMIST50 ug per actuation nasal spray. 100-500µg(max-1000 ug ) Tramcinolone acetonide 400-2000µg

Systemic Glucocorticoids : 

Systemic Glucocorticoids Mode of administration: Oral Parenteral Mechanisms of action: They inhibit the formation and release of cytokines and chemical mediators & reduces bronchial hyper reactivity. Inhibition of the release of prostaglandins and leukotrienes thus preventing the smooth muscle contraction and mucous secretions also suppresses inflammatory responses due to AG:AB reaction. Role in therapy: Long-term oral Glucocorticoids therapy may be required to control severe persistent asthma. E.g. Hydrocortisone and methylprednisolone.

Adrenergic Bronchodilators – Long-Acting Agents : 

Adrenergic Bronchodilators – Long-Acting Agents albuterol Salmeterol Formoterol Salbutamol Terbutaline Bambuterol ASTHALIN 2,4 mg. VENTORLIN 2 Mg /5 ml syrup.

Adrenergic Bronchodilators – Long-Acting Agents : 

Adrenergic Bronchodilators – Long-Acting Agents Modes of administration: Inhaled Oral Mechanisms of action: Here it leads to increase c AMP Formation in bronchial muscle cell leading to relaxation &decrease mediator release. Effects persists for at least 12 hours

Adrenergic Bronchodilators – Long-Acting Agents : 

Adrenergic Bronchodilators – Long-Acting Agents Role in therapy: Long-acting inhaled beta-2 agonists should be considered when standard introductory doses of inhaled Glucocorticoids fail to achieve control of asthma . Because long-term treatment with these agents does not appear to influence the persistent inflammatory changes in asthma, this therapy should be combined with inhaled Glucocorticoids Fluticosone propionate – salmeterol and bedesonide-formoterol inhalers (Advair®)

Adrenergic Bronchodilators – Long-Acting Agents : 

Adrenergic Bronchodilators – Long-Acting Agents Its action starts within 5 min & lasts for 2-3 hours. systemic adverse effect : For e.g., cardiovascular stimulation, skeletal muscle tremors, and hypokalemia, palpitation. Dose: 5 mg oral,0.25 mg sc,250 ug by inhalation. BRICAREX 2.5 mg tab,3 mg/5 ml syrup.

Methylxanthines : 

Methylxanthines Mode of administration Oral or Parenteral Mechanisms of action Inhibition of phosphodiasterase III and IV. These are responsible of metabolism of cAMP.(Bronchodilation,cardiac stimulation & vasodilation occur.) Blocking of adenosine receptor on airway muscles (A1) and those present on mast cells (A3).it contract bronchial muscles,depresses cardiac pace maker& inhibit gastric secretion . Role in therapy Sustained release theophylline is effective in controlling asthma symptoms and improving lung function.

Methylxanthines : 

Methylxanthines Pharmacokinetic: Theophyllene-half life 7-12 hrs. Preparations & doses: 100-300 mgTDS.oral THELONG 100,200 Mg SR tab. AMINOPHYLLINE 250-500 Mg Side effects : Gastrointestinal symptoms – nausea, vomiting CNS – Seizures Cardiovascular – tachycardia, arrhythmias Pulmonary – stimulation of the respiratory center

Leukotriene modifiers : 

Leukotriene modifiers A relatively new class of anti-asthma drugs that include cysteinyl leukotriene 1 (CysL T1) receptor antagonists. e.g. montelukast, zafirlukast 5-lipoxeygenase inhibitor : e.g. zileuton

Leukotriene modifiers : 

Leukotriene modifiers Mode of administration Oral Mechanism of action Receptor antagonists block the CysLT1 receptors on airway smooth muscle and thus inhibit the effects of cysteinyl leukotrienes that are release from mast cells and eosinophils

Leukotriene modifiers : 

Leukotriene modifiers Role in therapy These agents have a small and variable bronchodilator effect, reduce symptoms, improve lung function, and reduce asthma exacerbations. Leukotriene modifiers are less effective than long-acting inhaled beta-2 agonists therapy.

Leukotriene modifiers : 

Leukotriene modifiers Side effects These drugs are usually well tolerated, and few if any effects have been recognized. Zileuton has been associated with liver toxicity. GIT Disturbances. Half life- montelukast-3-6hr 10 mg OD & zafirlukast - 8-12 hr 20 mg BD. EMLUCAST 4 mg tab.

Slide 37: 

IgE Antibodies

Anti-IgE Antibodies : 

Anti-IgE Antibodies Agents directed at diminishing the production of IgE through effects on interleukin 4 or on IgE itself have been evaluated Recombinant human monoclonal antibody that forms complexes with free IgE blocks the interaction of IgE with mast cells and basophiles. E.g. Omalizumab.

TREATMENT: : 

TREATMENT: STEP UP APPROACH:- STEP – I:Short acting β-agonist are given. STEP –II: Short acting β-agonist +Beclomethasone BID or fluticasone . Dose:50-200 ug/BID. STEP –III: Short acting β-agonist +Beclomethasone BID or fluticasone. Here salmiterol may be added. 50ug BID.

Slide 40: 

STEP –IV: High dose inhaled steroids added+Ipratropium. STEP –V: Regular steroids+Beclomethasone (dose :800-2000ug). Prednisolone may be given.

Slide 41: 

COPD

What is COPD?? : 

What is COPD?? A set of lung diseases that limit air flow and is not fully reversible. COPD patients report they are “hungry” for air. Usually progressive and is associated with inflammation of the lungs as they respond to noxious particles or gases. Potentially preventable with proper precautions and avoidance of precipitating factors. Symptomatic treatment is available.

TYPES OF COPD : 

TYPES OF COPD Chronic bronchitis. Emphysema. Bronchial asthma. Bronchiectasis.

Major Clinical features of COPD : 

Major Clinical features of COPD 1. Chronic Bronchitis is characterized by Chronic inflammation and excess mucus production. Presence of chronic productive cough. 2. Emphysema is characterized by Damage to the small, sac-like units of the lung that deliver oxygen into the lung and remove the carbon dioxide. Chronic cough.

Primary Symptoms : 

Primary Symptoms Chronic Bronchitis Chronic cough Shortness of breath Increased mucus Frequent clearing of throat Emphysema Chronic cough Shortness of breath Limited activity level

Normal versus Diseased Bronchi : 

Normal versus Diseased Bronchi

Emphysema : 

Emphysema

What can cause COPD? : 

What can cause COPD? Smoking is the primary risk factor Long-term smoking is responsible for 80-90 % of cases Smoker, compared to non-smoker, is 10 times more likely to die of COPD. Prolonged exposures to harmful particles and gases from: Second-hand smoke, Industrial smoke, Chemical gases, vapors & fumes. Dusts from grains, minerals & other materials.

Ways to prevent or slow the progression of COPD : 

Ways to prevent or slow the progression of COPD Stop smoking, if you smoke, to prevent further damage to your body Smoking cessation is critical for all severities of COPD 2. Avoid or protect yourself from exposures to Second-hand smoke and Other substances such as chemical vapors, fumes, mists, dusts, and diesel exhaust fumes that irritate your lungs.

How is COPD Treated? : 

How is COPD Treated? COPD can be managed, but not cured. Treatment is different for each individual and is based on severity of the symptoms Early diagnosis and treatment can Slow progress of the disease Relieve symptoms Improve an individual’s ability to stay active Prevent and treat complications Improve quality of life

What medications are used to treat symptoms? : 

What medications are used to treat symptoms? Bronchodilators – Relaxes muscles around airways. Steroids Reduces inflammation. Oxygen therapy Helps with shortness of breath.

REFERENCES : 

REFERENCES Sharma HL and Sharma KK “Principle of pharmacology” First edition 2007, Page no.658-667. RANG and DALE’S Pharmacology sixth edition 2007 page no.356-366. Tripathi KD “Essentials of medical pharmacology” sixth edition 2008, page no. 213-230. F. S. K. “Essentials of pharmacotherapeutics” forth edition 2007, Page no.544-552. www.google.com TEXT BOOK OF PATHOLOGY ,Fifth Edn ,H.Mohan,page no.485-494

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Thank you