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BRONCHIAL
ASTHMA
Introducation
 Asthma derived from Greek word
- To stay awake in order to breath
OR
Difficulty in breathing
 Asthma is a chronic inflammatory
disease in which patient suffers with
reversible episodes of airway
obstruction due to ...
 Early phase
(Acute)
-Due to bronchial
smooth muscle
spasm.
- Excessive
secretion of
mucus.
 Chronic phase
Continuous
In...
Clinical hallmarks
 Recurrent episodic coughing
 Shortness of breathing
 Chest tightness
 Wheezing
Symptoms are worsen...
Asthma described as two type
 Extrinsic
(Atopic extrinsic asthma)
It is associated with
exposure of specific
allergen
Ex:...
Pathophysiology
Allergen enter (Foreign body)
Immunological reaction (AG:AB Complex formation)
Circulation in blood
Basoph...
Whenever same allergen re exposed
Activation of AG:AB complex
Reacts with lung mast cells
(Degranulation of mast cells)
Sp...
Bronchial Tone
IgE-Antigen Complex
Basophil
Activation
Eosinophil
Activation
Chemical mediators
Histamine, LTC4, LTD4, LTB...
 It divided into two categories
1. Short term relievers.( Bronchodilators)
2. Long term controllers.
Asthma therapy
Bronchial Tone
Bronchoconstriction
Bronchodilitation
Bronchial Smooth Muscle
β2
SALBUTAMOL
β2 AGONISTS
5AMP
AC
ATP
THEOPHY...
Bronchial Tone
Bronchoconstriction
Bronchodilitation
Bronchial Smooth Muscle
IgE-Antigen Complex
Basophil
Activation
Eosin...
Drugs Used in Bronchial Asthma
1. Selective β2–
Agonists
Short acting
 Salbutamol,
 Terbutaline,
 Remiterol,
 Fenotero...
3. Anticholinergics
Ipatropium, Tiotropium, Oxitropium
4. Methyl Xanthines
Theophylline, Aminophylline, Diprophylline,
Cho...
 Mast Cell Stabilisers
Sodium Cromoglycate, Nedocromil, Ketotifen
 Leukotriene Modulators:
1. 5-Lipoxygenase Inhibitor :...
Sympathomimetic agents
 ß2 receptors are present in the airway
smooth muscle. cause Bronchodilatation
 These are only pr...
 Epinephrine:
 Rapid bronchodilator when SC/inhaled(320µg/puff)
 Onset of action 15min after inhalation
 Duration of a...
 Ephedrine: α,β1, β2
 Ephedrine has a longer action
 Oral activity
 Lower potency
 Pronounced central effects.
β2 Selective
 Short acting : Terbutaline, Salnutamol
 On inhalation they have rapid onset(1-5Min)
 Short duration of ac...
Long acting: Salmeterol, bambutarol
 Long acting but slow onset of action
 Preferred for maintenance therapy
 Not usefu...
ADR of Sympathomimetics
 By oral route stimulate β2 receptors in skeletal
muscle cause tremors, Orthostatic hypotension.
...
Antimuscurnic agent
 Less effective then β agonists
 MOA: By blocking M3 receptors on air way smooth
muscle and prevents...
Methyl Xanthenes
 MOA:
i) Inhibition of PDE 3,4. These enzyme are responsible
for metabolism of cAMP.
ii) Blockade of Ade...
 Pharmaco Kinetics:
 Oral/Parental
Food delay the rate of absorption
Well distributed
Cross placental & BBB
Metaboli...
ADR: Low therapeutic window, CNS stimulant drugs
Plasma levels 10-20µg/ml, Narrow safety
Restlessness, insomnia, headache,...
Corticosteroids (Controllers)
 Glucocorticosteriods induce synthesis of lipocotrin
which inhibits pholipaseA2 there by pr...
 Inhalator glucocorticosteriods such as
beclomethasone, budesonide and fluticasone are
used as prophylactic agents in ast...
Mast cell stabilizers
 Non bronchodilating, Non steroid drugs, used for prophylactic
treat.
MOA:
 Prevent degranulation ...
LT Modulators
 LT are powerful bronchoconstrictors.
 Action by preventing their synthesis or blocking
effect on cys LT r...
ADR:
 Head ache
 skin rashes
 rarely eosinophilia
 Zileuton cause hepatic toxicity.
Monoclonal anti IgE antibody
 MOA:- AG:Ab complex formation by AB action
 Omalizumab: Recombinant humanized
monoclonal a...
Miscellaneous
 NO: It dilate pulmonary blood vessels and
relax airway smooth muscle.
 Uses: For acute severe asthma and
...
RX Status asthmatics (Acute severe asthma)
 Status asthmatics a severe acute
asthma, which is a life threatening
conditio...
 Humidified O2 inhalation
 Neubulized β2 adrenergic agonist + anti
cholinergic agent
 Systemic glucocorticosteroids IV
...
DRUGS TO BE AVOIDED IN ASTHMA
 β adrenergic blockers
 Cholinergic agents
 NSAIDS ( cause hyperapoenia) except
paraceata...
Bronchial asthma (2)
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Bronchial asthma (2)

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Asthma treatment

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Bronchial asthma (2)

  1. 1. BRONCHIAL ASTHMA
  2. 2. Introducation  Asthma derived from Greek word - To stay awake in order to breath OR Difficulty in breathing
  3. 3.  Asthma is a chronic inflammatory disease in which patient suffers with reversible episodes of airway obstruction due to bronchial hyper responsiveness.
  4. 4.  Early phase (Acute) -Due to bronchial smooth muscle spasm. - Excessive secretion of mucus.  Chronic phase Continuous Inflammation, fibrosis, oedma, necrosis of bronchial epithelial cells. It has 2phases
  5. 5. Clinical hallmarks  Recurrent episodic coughing  Shortness of breathing  Chest tightness  Wheezing Symptoms are worsening at night
  6. 6. Asthma described as two type  Extrinsic (Atopic extrinsic asthma) It is associated with exposure of specific allergen Ex:- House dust, pollen It is episodic and less prone to develop to status asthmaticus.  Intrinsic (Non atopic extrinsic asthma) It is associated with some non specific stimulants Ex:- chemical irritants It is perenial and prone to develop to status asthmaticus.
  7. 7. Pathophysiology Allergen enter (Foreign body) Immunological reaction (AG:AB Complex formation) Circulation in blood Basophiles, Neutrophilis engulf Cause neutralization contd..,
  8. 8. Whenever same allergen re exposed Activation of AG:AB complex Reacts with lung mast cells (Degranulation of mast cells) Spasmogens release (Like Histamine,5HT,PGs,LT4, Cytokines)
  9. 9. Bronchial Tone IgE-Antigen Complex Basophil Activation Eosinophil Activation Chemical mediators Histamine, LTC4, LTD4, LTB4, Cytokines, Adenosine, PGD2, PAF, ECP and Neuropeptides Cause inflammation, oedema, bronchospasm, muscus secretion, epithelial damage Mast Cell Degranulation  In early phase these mediators leads to bronchoconstriction  In late phase inflammation, pulmonary oedema, mucous secretion bronchial hypersensivity and epithelial damage
  10. 10.  It divided into two categories 1. Short term relievers.( Bronchodilators) 2. Long term controllers. Asthma therapy
  11. 11. Bronchial Tone Bronchoconstriction Bronchodilitation Bronchial Smooth Muscle β2 SALBUTAMOL β2 AGONISTS 5AMP AC ATP THEOPHYLLINE M3 GTP GC cGMP Adenosine cAMP PDE
  12. 12. Bronchial Tone Bronchoconstriction Bronchodilitation Bronchial Smooth Muscle IgE-Antigen Complex Basophil Activation Eosinophil Activation Chemical mediators Histamine, LTC4, LTD4, LTB4, Cytokines, Adenosine, PGD2, PAF, ECP and Neuropeptides Cause inflammation, oedema, bronchospasm, muscus secretion, epithelial damage CARTICOSTEROIDS LT-ANTAGONIST Leukotrienes SOD. CROMOGLYCATE Stabilises Mast Cells Mast Cell Degranulation INFECTION NITRIC OXIDE DONORS
  13. 13. Drugs Used in Bronchial Asthma 1. Selective β2– Agonists Short acting  Salbutamol,  Terbutaline,  Remiterol,  Fenoterol,  Bitolterol Long-acting  Salmeterol,  Formoterol,  Bambuterol 2. Non-Selective Sympathomimetics  Adrenaline,  Ephedrine,  Isoprenaline,  Orciprenaline (Metaproterenol),  Isoetharine BRONCHODILATORS
  14. 14. 3. Anticholinergics Ipatropium, Tiotropium, Oxitropium 4. Methyl Xanthines Theophylline, Aminophylline, Diprophylline, Choline theophyllinate Anti inflammatory Drugs (Controllers) Corticosteroids 1. Oral : Prednisolone, Methylprednisolone 2. Parenteral : Methyl prednisolone, Hydrocortisone 3. Inhalational : Beclomethasome, Fluticasone, Triamcinolone, Budesonide, Flunisolide
  15. 15.  Mast Cell Stabilisers Sodium Cromoglycate, Nedocromil, Ketotifen  Leukotriene Modulators: 1. 5-Lipoxygenase Inhibitor : Zileuton 2. LT – Receptor Antagonists : Zafirlukast, Montelukast, Iralukast, Pranlukast  Monoclonal Anti-IgE Antibody Omalizumab  Miscellaneous: NO, Calcium channel blockers
  16. 16. Sympathomimetic agents  ß2 receptors are present in the airway smooth muscle. cause Bronchodilatation  These are only provide relief  M.O.A:  cAMP  Bronchodilatation  Release of broncho constricting mediators from mast cells Inhibit macrovascular leakage  Mucociliary clearance
  17. 17.  Epinephrine:  Rapid bronchodilator when SC/inhaled(320µg/puff)  Onset of action 15min after inhalation  Duration of action:60-90min. ADR:- Acts on β1 receptor cause  Tachycardia  Arrhythmias  Worsening angi  So rarely prescribed.
  18. 18.  Ephedrine: α,β1, β2  Ephedrine has a longer action  Oral activity  Lower potency  Pronounced central effects.
  19. 19. β2 Selective  Short acting : Terbutaline, Salnutamol  On inhalation they have rapid onset(1-5Min)  Short duration of action preferred for acute attack  Route: Inhalation 100-200µg/6hourly  Other MDI, Oral, IM, IV  Terbutaline is the only one drug safely used during the pregnancy.
  20. 20. Long acting: Salmeterol, bambutarol  Long acting but slow onset of action  Preferred for maintenance therapy  Not useful in acute attack due to slow onset of action Route: Inhalation 50µg twice daily. Formoterol:  Long acting  Rapid onset  Preferred for prophylaxis due to long acting Route: Inhalation 12-24µg twice daily
  21. 21. ADR of Sympathomimetics  By oral route stimulate β2 receptors in skeletal muscle cause tremors, Orthostatic hypotension.  Tachycardia (High dos also stimulate β1 receptors in heart)  Restlessness  Tolarance occurs.
  22. 22. Antimuscurnic agent  Less effective then β agonists  MOA: By blocking M3 receptors on air way smooth muscle and prevents Ach action. -They acts by cGMP levels in bronchial smooth muscle. Ipatropium:- -Poor absorption from bronchi into systemic circulation -Do not cross BBB. -Also mucus secretion Ipatropium + β2 (Salbutamol) work better in serve asthma and long duration of action
  23. 23. Methyl Xanthenes  MOA: i) Inhibition of PDE 3,4. These enzyme are responsible for metabolism of cAMP. ii) Blockade of Adenosine receptors.  Actions:  Theophyline exhibits bronchodilatory action  Anti Inflammatory  Immunomodulator  Respiratory stimulation  Diaphragmatic contractility  Mucociliary clearance
  24. 24.  Pharmaco Kinetics:  Oral/Parental Food delay the rate of absorption Well distributed Cross placental & BBB Metabolized in Liver Excreted in urine
  25. 25. ADR: Low therapeutic window, CNS stimulant drugs Plasma levels 10-20µg/ml, Narrow safety Restlessness, insomnia, headache, tremors Nausea, Vomiting Peptic ulcer Tachycardia, palpitation, hypotension, arrythimias Theophyline: potent vasodilator, reflex tachcardia, oral route Aminophyline: Slow IV infusion XanthenesGIT Diuresis Heart CNS 20µg/ml 40µg/ml 20µg/ml
  26. 26. Corticosteroids (Controllers)  Glucocorticosteriods induce synthesis of lipocotrin which inhibits pholipaseA2 there by preventing formation of mediators such as PGs,TAX2, LTand other mediators.  Actions: Anti allergic, anti inflammatory, immunosuppressant ( AG:AB reactions ), Mucosal oedema, bronchial hyperactivity, Enhance β adrenergic action by up regulation of β2 receptors in lung.
  27. 27.  Inhalator glucocorticosteriods such as beclomethasone, budesonide and fluticasone are used as prophylactic agents in asthma.  PK:  Well tolerated  less systemic side effects. Common side effects:  Dryness of mouth  Voice change  Oropharangeal candidiats. Systemic are used in acute severe and chronic severe asthma.
  28. 28. Mast cell stabilizers  Non bronchodilating, Non steroid drugs, used for prophylactic treat. MOA:  Prevent degranulation and release of chemical mediators from the mast cells.  They stabilize the mast cells by preventing transmembarane influx of Ca ions. PK:  Highly ionized  Least systemic absorption  well tolerated. Uses: Allergic asthma, allergic conjunctivitis, allergic rhinitis, allergic dermatitis. Ketotifen (Mast stab.+ Antihistamincs)
  29. 29. LT Modulators  LT are powerful bronchoconstrictors.  Action by preventing their synthesis or blocking effect on cys LT receptors  Synthesis inhibitors (Lipooxygenase) Zafirlukast,Montelukast  PK:  Well absorbed after oral administration  Highly bound to plasma protein  Metabolized by liver  Effective for prophylactic treat of mild asthma.
  30. 30. ADR:  Head ache  skin rashes  rarely eosinophilia  Zileuton cause hepatic toxicity.
  31. 31. Monoclonal anti IgE antibody  MOA:- AG:Ab complex formation by AB action  Omalizumab: Recombinant humanized monoclonal antibody.  Inhibit the binding site of IgE to mast cells and basophils  PK: administered parentarally  Uses: Moderate to severe asthma and allergic disorders.  Indicated for asthmatic patients who are not adequately controlled by inhalational corticosteroids.  ADR: Inj site redness, itching, stinging.
  32. 32. Miscellaneous  NO: It dilate pulmonary blood vessels and relax airway smooth muscle.  Uses: For acute severe asthma and management of pulmonary hypertension.  Ca channel blockers:  Broncho constriction ultimately involves some degree of ca into cells Nefedpine / Verapamil should provide relief in asthma.
  33. 33. RX Status asthmatics (Acute severe asthma)  Status asthmatics a severe acute asthma, which is a life threatening condition involving exhaustion, cyanosis, bradicardia,hypotension, dehydration and metabolic acidosis.
  34. 34.  Humidified O2 inhalation  Neubulized β2 adrenergic agonist + anti cholinergic agent  Systemic glucocorticosteroids IV (Hydrocortisone 200mgIV)  IV fluids to correct dehydration.  K supplements: To correct hypokalemia produced by repeated administration of salbutamol.  NaHCo3 (Sodium bicarbonate) to treat acidosis.  Antibiotics to treat infection
  35. 35. DRUGS TO BE AVOIDED IN ASTHMA  β adrenergic blockers  Cholinergic agents  NSAIDS ( cause hyperapoenia) except paraceatamol.

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