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Hakeem khan
               Presented by,
Department of pharmacology
Luqman college of pharmacy
                   Gulbarga
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
   Allergy.
   Environmental factors.
   Emotional factors.
   Drugs.
CLINICAL FEATURES OF BRONCHIAL
   ASTHMA

1.   Coughing
2.   Wheezing & dyspnoea.
3.   Tightness in pain
4.   Labored expiration .
5.   Tachypnoea & tachycardia.
6.   signs of infection.
7.   Expiration time greater then inspiration time.
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
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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)
IMMEDIATE RESPONSE                     LATE-PHASE RESPONSE
     Eliciting agent: allergen or           Aggregation & activation of
   non-specific stimulus activates:     platelets, infiltration & activation of
                                             neutrophils, eosinophils,
                                            monocytes/macrophages :
    Mast cells, platelets, alveolar
  macrophages, causing release of:                                       lipocortin
                                                 PAF, LTC4, LTD4,
                                                 platelet factors &
                                                leukocyte products
 Spasmogens: H,      Chemotaxins:                  which cause:
 PAF, LTC4, LTD4,     LTB4, PAF,
    causing:          MNC, ECF-A
                     which cause:                                glucocorticoids
                                                 ODEMA, MUCOUS
                                                  SECRETION &
                        Reversed by β            BRONCHOSPASM
BRONCHOSPASM              agonists &
                         Theophylline
Major Cells Implicated in
Inflammatory Response

 Mast cells
 Lymphocytes
 Eosinophils
 Neutrophils
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
1. “Relievers”
    I. Short-acting bronchodilators
      A. β 2-adrenergic agents
      B. Anti-cholinergic (Parasympatholytic) agents

  2. “Controllers”
    1. Corticosteroids
    2. Long-Acting bronchodilators
      I. β 2-adrenergic agents
      II. Methylxanthines
    3. Mast cell stabilizers.
    4. Leukotriene inhibitors
    5. Anti-IgE monoclonal antibodies
“Relievers”
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
   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.
   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

   Tremor
   Palpitations and tachycardia
   Headache
   Insomnia
   Nervousness
   Dizziness
   Nausea
Anticholinergic (Parasympatholytic)
Bronchodilators
   Tertiary Ammonium Compounds:
    Atropine methonitrate.
    Scopolamine
   Quaternary Ammonium Compounds:
    Ipratropium bromide.
    Tiotropium bromide
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.
   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.
“Controllers”
Controllers
 Corticosteroids
 Long-Acting bronchodilators
    β2-adrenergic agents
    Methylxanthines
 Cromolyn sodium/Nedrocromil
 Leukotriene inhibitors
 Anti-IgE monoclonal antibodies
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.
Phospholipids
             (from cell membrane)

Corticosteroids         -
                  Phospholipase A2

              Arachidonic acid
                            Cyclooxygenase
   5-Lipoxyenase

                                            Prostacyclin (PGI2)
   Leukotrienes             PGE2
                                     PGH2
                            PGF2α
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
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
   albuterol
   Salmeterol
   Formoterol
   Salbutamol
   Terbutaline
   Bambuterol

       ASTHALIN 2,4 mg.
       VENTORLIN 2 Mg /5 ml syrup.
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
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
   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
   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
    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
   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
   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
   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
   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.
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:
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.
STEP –IV: High dose inhaled steroids
  added+Ipratropium.


STEP –V: Regular steroids+Beclomethasone (dose :
  800-2000ug).
Prednisolone may be given.
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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
 Chronic bronchitis.
 Emphysema.
 Bronchial asthma.
 Bronchiectasis.
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
   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
Emphysema
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.
1.   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?
   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?
   Bronchodilators –
     ○ Relaxes muscles around airways.


   Steroids
     ○ Reduces inflammation.



   Oxygen therapy
     ○ Helps with shortness of breath.
REFERENCES
1.   Sharma HL and Sharma KK “Principle of pharmacology” First
     edition 2007, Page no.658-667.

2.   RANG and DALE’S Pharmacology sixth edition 2007 page
     no.356-366.

3.   Tripathi KD “Essentials of medical pharmacology” sixth edition
     2008, page no. 213-230.

4.    F. S. K. “Essentials of pharmacotherapeutics” forth edition
     2007, Page no.544-552.

5.   www.google.com
6.   TEXT BOOK OF PATHOLOGY ,Fifth Edn ,H.Mohan,page
     no.485-494
642402 634249935653553750

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642402 634249935653553750

  • 1. Hakeem khan Presented by, Department of pharmacology Luqman college of pharmacy Gulbarga
  • 2. 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.
  • 3. CAUSES OR AGGRAVATING FACTORS  Allergy.  Environmental factors.  Emotional factors.  Drugs.
  • 4. CLINICAL FEATURES OF BRONCHIAL ASTHMA 1. Coughing 2. Wheezing & dyspnoea. 3. Tightness in pain 4. Labored expiration . 5. Tachypnoea & tachycardia. 6. signs of infection. 7. Expiration time greater then inspiration time.
  • 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.
  • 8. 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)
  • 9. IMMEDIATE RESPONSE LATE-PHASE RESPONSE Eliciting agent: allergen or Aggregation & activation of non-specific stimulus activates: platelets, infiltration & activation of neutrophils, eosinophils, monocytes/macrophages : Mast cells, platelets, alveolar macrophages, causing release of: lipocortin PAF, LTC4, LTD4, platelet factors & leukocyte products Spasmogens: H, Chemotaxins: which cause: PAF, LTC4, LTD4, LTB4, PAF, causing: MNC, ECF-A which cause: glucocorticoids ODEMA, MUCOUS SECRETION & Reversed by β BRONCHOSPASM BRONCHOSPASM agonists & Theophylline
  • 10. Major Cells Implicated in Inflammatory Response  Mast cells  Lymphocytes  Eosinophils  Neutrophils
  • 11. 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
  • 12. General Pharmacologic Approach to the Treatment of Asthma 1. “Relievers” I. Short-acting bronchodilators A. β 2-adrenergic agents B. Anti-cholinergic (Parasympatholytic) agents 2. “Controllers” 1. Corticosteroids 2. Long-Acting bronchodilators I. β 2-adrenergic agents II. Methylxanthines 3. Mast cell stabilizers. 4. Leukotriene inhibitors 5. Anti-IgE monoclonal antibodies
  • 14. Adrenergic Bronchodilators – Short- Acting Agents or sympathomimetics.  Catecholamine  Epinephrine  Isoproterenol  Isoetharine  Resorcinol agents  Metaproterenol  Saligenin agents Albuterol Pirbuterol Bitolterol
  • 15. 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.
  • 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.
  • 17. Side Effects Seen with Beta Agonist  Tremor  Palpitations and tachycardia  Headache  Insomnia  Nervousness  Dizziness  Nausea
  • 18. Anticholinergic (Parasympatholytic) Bronchodilators  Tertiary Ammonium Compounds: Atropine methonitrate. Scopolamine  Quaternary Ammonium Compounds: Ipratropium bromide. Tiotropium bromide
  • 19. 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.
  • 20. 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.
  • 22. Controllers  Corticosteroids  Long-Acting bronchodilators β2-adrenergic agents Methylxanthines  Cromolyn sodium/Nedrocromil  Leukotriene inhibitors  Anti-IgE monoclonal antibodies
  • 23. 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.
  • 24. Phospholipids (from cell membrane) Corticosteroids - Phospholipase A2 Arachidonic acid Cyclooxygenase 5-Lipoxyenase Prostacyclin (PGI2) Leukotrienes PGE2 PGH2 PGF2α
  • 25. 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
  • 26. 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.
  • 27. Adrenergic Bronchodilators – Long- Acting Agents  albuterol  Salmeterol  Formoterol  Salbutamol  Terbutaline  Bambuterol  ASTHALIN 2,4 mg.  VENTORLIN 2 Mg /5 ml syrup.
  • 28. 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
  • 29. 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®)
  • 30. 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.
  • 31. 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.
  • 32. 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
  • 33. 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
  • 34. 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
  • 35. 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.
  • 36. 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.
  • 38. 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.
  • 39. 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.
  • 40. STEP –IV: High dose inhaled steroids added+Ipratropium. STEP –V: Regular steroids+Beclomethasone (dose : 800-2000ug). Prednisolone may be given.
  • 42. 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.
  • 43. TYPES OF COPD  Chronic bronchitis.  Emphysema.  Bronchial asthma.  Bronchiectasis.
  • 44. 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.
  • 45. Primary Symptoms  Chronic Bronchitis Chronic cough Shortness of breath Increased mucus Frequent clearing of throat  Emphysema Chronic cough Shortness of breath Limited activity level
  • 48. 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.
  • 49. 1. 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.
  • 50. 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
  • 51. What medications are used to treat symptoms?  Bronchodilators – ○ Relaxes muscles around airways.  Steroids ○ Reduces inflammation.  Oxygen therapy ○ Helps with shortness of breath.
  • 52. REFERENCES 1. Sharma HL and Sharma KK “Principle of pharmacology” First edition 2007, Page no.658-667. 2. RANG and DALE’S Pharmacology sixth edition 2007 page no.356-366. 3. Tripathi KD “Essentials of medical pharmacology” sixth edition 2008, page no. 213-230. 4. F. S. K. “Essentials of pharmacotherapeutics” forth edition 2007, Page no.544-552. 5. www.google.com 6. TEXT BOOK OF PATHOLOGY ,Fifth Edn ,H.Mohan,page no.485-494