respiratory pharmacology

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thedewhub
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300197
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respiratory pharmacology
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2015-04-07 16:49:02
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respiratory pharmacology
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respiratory pharmacology
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respiratory pharmacology
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  1. Inhalation Therapy
    • Advantage is delivery of effective doses with minimal systemic absorption
    • Rapid onset
    • Optimum size of particles is 2 Optimum size of particles is 2-5μm
    • – Larger are deposited in oropharnyx
    • – Smaller remain suspended and expelled
  2. - limitations
    Only 5% of drug enters lower airway
  3. Inhalation Devices
    •  Metered dose inhalers (mdi)
    • – Drug propelled from a canister Drug propelled from
    • a canister
    • – Difficult for patient to coordinate
  4. Dry powder inhalers
    • – Fewer additives/ no propellant
    • Requires less coordination
    • – Can cause local irritation and cough
  5.  Nebulizer
    • – Jet or ultrasonic
    • – Can deliver higher doses
  6. Spacer chambers
    • – Reduce the velocity and the size of particles
    • – Increase proportion of drug entering lower
    • airway
    • – Reduce need for coordination
  7. Airway Pharmacology
    •  Bronchodilators
    •  Anti-Inflammatory Agents Inflammatory Agents
    •  Mucolytics
  8. Bronchodilators
    •  Beta2-adrenergic agonists
    • – Sympathomimetics
    •  Methylxanthines
    •  Anti-cholinergics- copd
  9. Beta2-Agonists
    •  Stimulation of beta2 receptors causes
    • smooth muscle relaxation in proximal and
    • distal airways
    • – Lowers intracellular Ca Lowers intracellular Ca
    • – Inhibits phosphoinositide hydrolysis
    • – Opens Ca-activated K channel that repolarizes
    • the smooth muscle cell the smooth muscle cell
  10. Beta2-Agonists Additional Effects:
    •  Prevent mediator release from mast cells
    •  Prevent microvascular leakage and mucosal
    • edema
    •  Increase mucous secretion and mucociliary
    • clearance
    •  Prevent acetylcholine release
  11. Beta2-Agonists Mode of Administration
    •  Inhalation
    • – Nebulized, mdi, dry powder
    • – Onset < 5 minutes
    • Duration of action 3-4 hours
    •  Oral
    • – No advantage with more side effects No advantage with more side effects
    •  Intravenous
    • – No advantage with more side effects
  12. Albuterol
    •  MDI 90 μg/act
    • – HFA preparation uses hydrofluoroalkane as HFA preparation uses hydrofluoroalkane as
    • propellant rather than CFC
    •  Nebulized .083 % in 3cc solution Nebulized .083 % in 3cc solution
    •  DPI not available
  13. Beta2-Agonists  Adverse effects:
    •  Tremor due to stimulation of beta Tremor due to stimulation of beta receptors 2 receptors
    • in skeletal muscle
    • Tachycardia due to stimulation of atrial
    • beta2 and beta1 receptors at high doses
    •  Hypokalemia due to increased K uptake by Hypokalemia due to increased K uptake by
    • skeletal muscle
    •  Hypoxemia due to pulmonary artery
    • vasodilation
    •  Increased shunt
  14. Beta2-Agonists Tolerance
    • due to the mast cell stabilization
    • effect but not the bronchodilator effect has
    • been demonstrated
    •  Down-regulation of beta receptors does regulation of beta receptors does
    • occur - but is not clinically significant
    •  Down-regulation of beta receptors is regulation of beta receptors is minimized by inhaled corticosteroids
  15. Beta2-Agonists Clinical Use
    •  Acute bronchodilator effect and protection against
    • bronchial challenge
    •  Short-acting agents are intended for “as needed”
    • use
    • – Albuterol and pirbuterol
    •  Long-acting preparations for nocturnal symptoms acting preparations for nocturnal symptoms
    • and severe, persistent asthma
    • – Salmeterol and formoterol
  16. Salmeterol and Formoterol LABA
    •  Formoterol DPI 12 μg/act bid
    •  Salmeterol DPI 50 Salmeterol DPI 50 μg/act bid
    •  No prn use
  17. Beta2-Agonists Levalbuterol
    •  ‘R’ isomer of albuterol isomer of albuterol
    •  Selection of pulmonary beta2 receptors only
    • – Lower incidence of paradoxical bronchospasm
    • – Less cardiovascular side effects??
    •  Nebulized formulation @ .63-1.25 mg q 6-8
    • hour
  18. Beta2-Agonists Epinephrine
    • – Beta2 stimulation at low dose stimulation at low dose
    • – Alpha1 and beta1 stimulation at high dose
    •  Treatment of choice for anaphylaxis
    • Treatment of choice for anaphylaxis
    •  Not first line therapy for asthma as it has no
    • added benefit over albuterol
  19. Racemic Epinephrine
    •  Indicated for treatment of upper airway
    • edema, laryngospasm or vocal cord edema
    •  Mechanism of action is vasoconstriction -
    • not bronchodilation not bronchodilation
    •  Nebulized @ .05 ml/kg/dose diluted in 5 ml
    • NSS
  20. Anticholinergics
    •  Mechanism of Action
    •  Muscarinic antagonists that inhibit reflex Muscarinic antagonists that inhibit reflex
    • bronchoconstriction
    •  Decrease intrinsic vagal tone of airways
    •  No anti-inflammatory effect
  21. Ipratropium Bromide
    •  Mode of Administration
    •  Available in mdi (18 Available in mdi (18
    • μg/act) and nebulized g/act) and nebulized
    • (0.5mg) formulations
    •  Onset of bronchodilationin 30-60 minutes with duration of action 4-6 hours
    • – Tiotropium DPI available for once daily use
    •  No tachyphylaxis
  22. Ipratropium Bromide Clinical Use
    • – Proven to slow the loss of pulmonary function Proven to slow the loss of pulmonary function
    • in COPD (Lung Health Study)
    • Not recommended for rescue use in asthma
    •  Adverse Effects
    • – Virtually no side effects as there is no systemic Virtually no side effects as there is no systemic
    • absorption (not receptor-mediated
  23. Anti-Cholinergics
    •  Atropine
    • May be useful prior to bronchoscopy to decrease secretions
    •  Usually given intramuscularly
    •  Glycopyrrolate- antimuscarininc- decreases bronchial secretion
  24. Methylxanthines
    • Theophylline and Aminophylline
    •  Mechanism of action:
    •  Phosphodiesterase inhibition leads to Phosphodiesterase inhibition leads to increased intracellular cAMP
    • Adenosine receptor antagoist
    •  Catecholamine Release
    •  Prostaglandin Inhibition
    •  Calcium Influx Calcium Influx
  25. Theophylline
    •  Bronchodilator effect at therapeutic
    • concentrations is weak
    •  Inhibits mast cell degranulation
    •  Increases mucociliary clearance Increases mucociliary clearance
    •  Prevents mucosal edema
    •  Increases the contractility of the diaphragm- better for emphysema
  26. Theophylline
    •  Narrow therapeutic index
    •  Metabolized in the P450 system Metabolized in the P450 system
    • – Many drug interactions
    •  Adverse effects
    • – Nausea, vomiting, tremor, seizure, behavioral
    • disorders
  27. Aminophylline
    •  Intravenous and oral preparation Intravenous and oral preparation
    •  No advantage over theophylline except
    • convenience of intravenous dosing and
    • short half-life
    •  Indicated for severe, refractory
    • bronchospasm
    •  Check levels frequently Check levels frequently
  28. Corticosteroids
    •  Modification of ester ring of glucocorticoids
    • made them topically effective
    •  Inhibit secretion of leukotrienes,
    • prostaglandins cytokines prostaglandins, cytokines
    •  Inhibit degranulation of eosinophils
    •  No effect on mast cells/degranulation
    •  No effect on the contractile response of
    • airways
  29. Corticosteroids routes
    •  Oral
    • – Prednisone converted to prednisolone in liver Prednisone converted to prednisolone in liver
    •  Intravenous
    • – Prednisolone slower onset than hydrocortisone
  30. Inhaled Corticosteroids effect
    •  No immediate effect
    •  Chronically reduce the acute constrictor Chronically reduce the acute constrictor
    • response to bronchial challenge
    •  Increase beta Increase beta receptors
    • 2 receptors
    •  Systemic effect determined by what fraction deposited in oropharnyx and then metabolized in liver
  31. Inhaled Corticosteroids
    •  No upper limit on dose except for increased No upper limit on dose except for increased
    • systemic effect
    •  Fluticasone and budesonide most Fluticasone and budesonide most commonly used high dose inhalers
    •  MDI and dry powder preparation
  32. Corticosteroids
    •  Inhaled steroids are indicated in chronic
    • asthma if beta agonist is required more than
    • 3 times a week
    •  Assessment of steroid responsiveness
    • required if prolonged oral or high dose inhaled therapy is planned
  33. Corticosteroids
    •  Side effects
    • – Adrenal suppression
    •  Effect on bone evident
    • – Fluid retention hypertension glucose Fluid retention, hypertension, glucose intolerance, increased appetite, capillary fragility gastritis cataracts psychosis fragility, gastritis, cataracts, psychosis, osteoporosis, dermal thinning
    • – Hoarseness, oral candidiasis, cough Hoarseness, oral candidiasis, cough
  34. Leukotriene Antagonists
    •  Leukotrienes are bronchoconstrictors and
    • chemotactic for neutrophils
    •  Inhibit cysteinyl leukotrienes
    • – Arachidonic acid metabolites which release Arachidonic acid metabolites which release
    • mast cells and eosinophils
    •  Peak plasma concentration in 3 Peak plasma concentration in 3-4 hours 4 hours
    •  Few P450 drug interactions even though hepatically cleared
  35. Leukotriene Antagonist
    •  Leukotriene modifiers are effective against
    • exercise and allergen induced bronchospasm
    •  Not effective as rescue bronchodilator Not effective as rescue bronchodilator
    •  Montelukast 10 mg po qhs
    • Other agents have significant hepatotoxicity
  36. Cromolyn Sodium
    •  Mast cell stabilizer?
    •  Inhibits bronchoconstriction mediated by sensory nerves/neurogenic inflammation
  37. Nedocromil Sodium
    •  Reduces airway hyperresponsivenes
    •  Similar action and efficacy
    • to cromolyn
    • • No absorption/side effects
    • • Variable efficacy
  38. Antihistamines
    •  Used to treat allergic rhinitis
    •  May decrease asthma exacerbations that are May decrease asthma exacerbations that are
    • triggered by post-nasal drip and allergic
    • rhinitis
  39. Mucolytics
    •  Acetylcysteine
    •  Free sulfhydryl groups react with disulfide Free sulfhydryl groups react with disulfide
    • linkages in bronchial secretions
    •  3-5 ml of 20% solution via nebulizer 5 ml of 20% solution via nebulizer
    •  Not proven effective by inhalation
    •  If given orally, decreases COPD
    • exacerbations
    • – Decreases bacterial colonization?
  40. Mucolytics
    •  Dornase alfa ( rh-DNAse)
    •  Hydrolyzes extracellular DNA Hydrolyzes extracellular DNA
    • – Increased protein content of CF secretions due
    • to degenerating inflammatory cells and bacteria to degenerating inflammatory cells and bacteria
    •  FDA approved for use in cystic fibrosis
    • – decreases frequency of exacerbations and decreases frequency of exacerbations and
    • hospitalizations
  41. Bad Actors
    •  Beta Blockers
    •  ACE Inhibitors ACE Inhibitors
    •  Amiodarone

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