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					Asthma

Purpose of the theophylline:

         relaxes the airway smooth muscle
         inhibits synthesis and secretion of inflammatory mediators in mast and
          basophil cells

MOA of theophylline

       inhibits cyclic nucleotide phosphodieterases which increases cellular cAmp
         and cGMP
       competitive antagonist of adenosine

Side Effects

          narrow therapeutic range, high patient intervariablity in metabolism,
          requires therapeutic drug monitoring.
         Clearance can be decreased and or increased easily
         Toxic sx: headache, palpitations, dizziness, nausea, hypotension, restlessness,
          agitation
         Fatal intoxication can occur and seizure if plasma concentrations >40

Epinephrine inhaler:

         Bronchodilation

MOA of Epi:

         All 3 receptor types are activated

SE:

         Hallucinations, excitement, ataxia, incoordination, convulsions, fever, sinus
          tachycardia, urinary retention, dry mouth, deepening coma and cardio-
          respiratory collapse followed by death.
         May induce P450 enzymes

Albuterol in ER

         Short/Fast acting beta agonist
         Direct relaxation of airway smooth muscle

Nebulizer

         Used in acute exacerbations

MOA of Albuterol
       Direct relaxation of airway smooth muscles via beta2 adrenergic receptors 
        elevation of camp
       Increase K channel conductance leading to hyperpolarization and relaxation
       Inhibits inflammatory functions of mast cells, basophils, eosiniphils,
        neutrophils

   SE

       Increased HR, arrythmias, CNS effects

Why was GT given methylprednisolone?

       Acute exacerbations often require brief 5-10 day treatment (prednisone,
        methyl prednisolone)
       Side effects include mood disturbances, increased appetite, loss of blood
        glucose control, candidiasis
       Not recommended for chronic treatment


Why was the nebulized albuterol repeated in the ER every 2 hrs?

       Only last 2-6hrs

What is fluticasone? Its MOA?

       Glucocorticoid
       Do not relax airway smooth muscle and have little effect on acute
        bronchoconstriction
       Decrease airway inflammation
       Not for acute exacerbations


Why was GT given a prescription for fluticasone?

       To decrease airway inflammation

What is the reasoning behind replacing GT’s epinephrine inhaler with
albuterol?

       Albuterol has minimal side effects and works faster also more effective,
        better bronchodilator because it works directly on the beta 2’s.

After being prescribed fluticasone and albuterol, why does GT’s condition
improve?

       The medications are treating both the bronchoconstriction and inflammation
Although GT improves on the new meds, he still uses the albuterol inhaler 2-3
times per day. What change in meds might this suggest?
      He might need a ling acting beta agonist

What is a “spacer” and how is it used?

      Spacer devices can improve delivery with MDIs
      Limits number of larger molecules reaching mouth
      Reduces patient need to coordinate inhalation with MDI activation



Why was the theophylline replaced with salmeterol.

      Theophylline has lots of side effects and is a 3rd line rx for refractory asthma
       only

COPD

What is the difference between asthma and COPD?

      COPD involves primarily neutrophils as inflammatory mediators whereas
       asthma involves primarily eosinophils
      COPD shows progressive decline in lung function over time
      COPD shows progressive breakdown in connective tissue & matrix

What is the underlying cause of COPD?

      Cigarette smoking is primary cause for both


Why are some of the medications used to treat both conditions similar?

      Pharmacotherapy for both seeks to
          o Reduce or abolish symptoms
          o Improve airflow
          o Increase exercise capacity
          o Reduce number & severity of exacerbations
          o Generally improve health status


What is the reasoning behind prescribing albuterol and tiotropium?

      Albuterol is a short acting beta agonist
      Tiotropium is a anticholinergic--Inhalation powder (Spiriva)
      Long term, once daily, maintenance treatment of bronchospasm associated
       with COPD, including chronic bronchitis & emphysema
      Not indicated as rescue therapy
      Contraindicated in patients with history of hypersensitivity to atropine or its
       derivatives
      Most common side effect – dry mouth
      Currently considered first line treatment
   

Why might this patients condition have worsened over 2 yrs?

      Pharmacotherapy cannot modify the rate of decline in lung function
      Only treats the symptoms

What is the reasoning behind prescribing salmeterol?

      Not getting enough relief with current regimen and adding a long acting beta
       agonist is the next step



Antihistamines and Decongestants

Why does this patient develop seasonal rhinitis?

      Release of histamine/ IgE mediated hypersensititivy

Why does diphenhydramine relieve her symptoms?

      All H1 antagonists have similar actions – reversible, competitive inhibitors at
       H1 receptors
      Antagonizes constrictor action of histamine in respiratory smooth muscle
      Inhibits vasodilator effects on endothelial cells and vascular smooth muscle
      Blocks increased capillary permeability
      Blocks wheal & flare response
      Decreases itching
      Reduces secretion in cholinergically innervated areas such as respiratory
       tree
      Blocks portions of immediate hypersensitivity reactions related to histamine
      Does NOT prevent histamine release or bind to histamine that has already
       been released


Why does it cause drowsiness? Why does it cause dry mouth?

      First Generation
      Some of the first antihistamines
      High sedative and strong anticholinergic effects
           o Antagonizes ACh
           o Dry mouth, xerostomia, urinary retention
      Highly lipophillic, crosses BBB

What is the reason for switching her drugs?

      Decreased CNS penetration
      Ionized at physiologic pH and do not cross membranes
      High albumin binding – less free drug to enter CNS
      Less side effects



Why doesn’t loratidine produce drowsiness and dry mouth?

      b/c it is a 2nd generation drug

What is the difference between loratidine and loratidine D? What is the
reason for its use? How might it help RL’s symptoms, as opposed to plain
loratidine?

      loratidine D has a decongestant
      Decongestants are sympathomimetic amines which decrease swelling and
       congestion (via vasoconstriction), making breathing easier
      Indications: Relief of vasomotor rhinitis and acute rhinitis in upper
       respiratory infections


What is the MOA of pseudoephedrine?

      Mixed: Ephedrine and Pseudoephedrine. Activates a1 (vasoconstriction)
       and b(bronchodilation). Can act by direct and indirect MOA’s.
      Direct Acting
          o Sympathomimetic – a-adrenergic agonists
          o Vasoconstrictors
          o Phenylephrine, oxymetazoline,
      Indirect Acting
          o Sympathomimetic agents that act by being taken up into the
              prejunctional nerve terminal where they displace norepinephrine
              from storage vesicles
          o Norepinephrine is then released to postjunctional a-adrenergic
              receptors producing vasoconstriction

What other formulations of decongestants are available for RL?

•Phenylephrine

      Phenylephrine and pseudoephedrine are components of proprietary OTC
       allergy preparations
      Many are combined with a prescription antihistamine for relief of allergy
       symptoms (Claritin-D, Allegra-D)

•Phenylpropanolamine – similar to pseudoephedrine with less CNS effects. Also
suppresses appetite
   Banned sale due to risk of hemorrhagic stroke

				
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