Treatment of Obstructive Lung Disease Flashcards Preview

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Flashcards in Treatment of Obstructive Lung Disease Deck (20)
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Goals of asthma therapy

•Reduce the frequency and intensity of asthma symptoms

•Cough, chest tightness, wheezing, dyspnea

•Decease use of rescue short acting beta agonists

•Reduce night-time symptoms and awakenings

 •Prevent exacerbations

•Prevent long term consequences of poorly controlled asthma


Well controlled asthma characteristisc

  • sx = (less than or equal to) 2x/wk
  • nighttime sx = 2x/mo
  • SABA use =2x/wk except for exercise
  • peak flow near normal
  • oral steroid = 1x/yr
  • urgent care visit = 1x/yr


Long-term control medications for asthma

  • Inhaled glucocorticoids – preferred long-term control medication for the treatment forpersistent asthma
  • Long-acting inhaled beta2-agonists –preferred supplementary long-term control agent for use with inhaled glucocorticoids
  • Leukotriene modifiers
  • Omalizumab (anti-IgE) –biologic response modifier


Short-term relief in Asthma

•Short acting beta2-agonists – preferred treatment to relieve symptoms and to prevent exercise-induced asthma.

•Anticholinergics – approved for use in COPD but not asthma; used as secondary reliever for significant asthma exacerbations.

•Systemic glucocorticoids – used to manage severe acute asthma exacerbations and occasionally for continued use in managing severe asthma.


B-adrenergic agonist pharmacokinetics

  • •Clinical pharmacology: albuterol, terbutaline, salmeterol, formoterol. Used to treat asthma and COPD.
  • Route: inhaled, injectable and oral 
  • rapid onset of action: minutes for albuterol and formoterol (slightly longer for salmeterol)
  • duration of action:
    • •quick relievers:  4 - 6 hours (albuterol)
    • •long-term controllers:  long acting ß-agonists last ~12 hours (salmeterol, formoterol)


B-adrenergic agonsits MOA/benefit

•  mechanism of action: ß-adrenergic receptor stimulation

•  beneficial effect:  bronchodilation via smooth muscle relaxation; inhibits production of respiratory secretions


Anticholinergics MOA/pharmacokinetics

•mechanism of action: cholinergic receptor   inhibition

•beneficial effect - bronchodilation via smooth   muscle relaxation –inhibits production of   respiratory secretions

•Clinical pharmacology: atropine, ipratropium, tiotropium; approved for use in COPD but not in asthma

--Route: inhaled

–rapid onset of action: minutes

•duration of action: –Quick relievers: up to 6 hours (ipratropium) –Long-term controllers: up to 12 hours (tiotropium)


Systemic glucocorticoids MOA/benefits

  • mechanism of action: phospholipase   inhibition;  inhibition of cytokine synthesis
  • beneficial effect :
    • anti-inflammatory - reduces cellular infiltration, particularly eosinophils, mast cells, lymphocytes
    • vasoconstrictor - reduces edema



Systemic glucocorticoids pharmacokinetics

Clinical pharmacology: hydrocortisone, prednisone, prednisolone, methylprednisolone. Used to treat acute exacerbations of asthma.

  •  Route: oral or parenteral

  •  onset of action: 30 - 60 minutes

  •  metabolism: half-life 2 -3 hours

  •  peak of action: approximately 8 hours

  •  duration of action: hydrocortisone=12-24 hrs & prednisolone=36-48


Inhaled glucocorticoids MOA/pharmacokinetics

•Used as the preferred long-acting control agent to treat asthma and for the treatment of COPD, if repeated COPD exacerbations noted.

  •Route: inhaled

•duration of action: requires once to twice   daily administration to maintain effect •mechanism of action: phospholipase   inhibition; inhibition of cytokine synthesis •beneficial effect

–anti-inflammatory - reduces cellular   infiltration, particularly eosinophils, mast cells, lymphocytes;

–vasoconstrictor - reduces edema



Asthmatic combination therapy

  • Inhaled products are now available that combine an inhaled corticosteroid plus long acting ß-adrenergic agonist for benefits of both in the same delivery device. 


Leukotriene modifiers MOA/pharmacokinetics

•  mechanism of action:

  leukotriene D4 antagonist – montelukast,

  5-lipoxygenase inhibition – zileuton

•  beneficial effect

  bronchodilator effect

  anti-inflammatory effect due to leukotriene
  blocking effect

  attenuates exercise-induced asthma

•administered by the oral route
•onset of action: 30 - 60 minutes
•metabolism: half-life 6 hours; hepatic   metabolism
•duration of action: 12-24 hours


Immunomodulator (omalizumab)


•Approved for allergic asthma, requires parenteral (subcutaneous) administration

•binds to IgE to reduce likelihood of allergic response by inhibiting binding of IgE to mast cells.

•An adverse effect associated with anti-IgE is anaphylaxis which may occur shortly after or several hours after administration.


Cromolyn/nedocromil MOA/pharmacokinetics

  • Route: inhaled route

  •  half-life:  20 minutes; excreted   unchanged

  •  mechanism of action: inhibition of mast cell mediator release

  •  beneficial effect: preventative therapy for exercise-induced   asthma can prevent allergen-induced   pulmonary response


Theophyllines MOA/benefits

  •  mechanism of action: inhibition of phosphodiesterase

  •  beneficial effect: bronchodilator effect and some anti-inflammatory activity


Theophylline: pharmacokinetics

  •  Route: oral or IV

  •  metabolism: half-life 7 hours; hepatic

  •  duration of action: 12 - 24 hours after single dose


Theophylline adverse effects

  • caffeine-like effects such as irritability, gastrointestinal distress
  • very narrow therapeutic range and requires blood level monitoring to individualize dose.
  • Significant adverse effects can include seizures and irreversible neurologic damage
  • multiple drug interactions


COPD therapeutic options

  • Smoking cessation has the greatest capacity to influence the natural history of COPD. 
  • Pharmacotherapy and nicotine replacement reliably increase long-term smoking abstinence rates.
  • All COPD patients benefit from regular physical activity 


COPD medications (6 + subtypes + combos)


First-line tx for each category of COPD severity (A --> D)


  • A ==> SAMA (SAmuscarinic antagonist)  prn or SABA prn
  • B ==> LAMA or LABA
  • C ==> ICS + LABA or LAMA
  • D ==> ICS + LABA or LAMA