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Pharmacology > Exam 2 - PULMONARY DRUGS > Flashcards

Exam 2 - PULMONARY DRUGS Flashcards

1
Q

How are aeresolized drugs delivered? (3)

A

-nebulizer, dry poweder inhalant, metered powder inhalant

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2
Q

Disadvantages to aeresolized drugs (3)

A
  • correct dose?
  • alteration of breathing pattern?
  • deposition of drug in oral mucosa?
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3
Q

Asthma features

A

-bronchoconstriction, airway infammation, airway hyperresponsiveness, hypersecretion of mucous

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4
Q

Atopy

A
  • refers to inhereted predispostion for certain conditions (asthma, allergic rhinitis, eczema)
  • underlies almost all asthma in children, most in adults
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5
Q

COPD

A

chronic lung condition in which airflow limitation is not reversible

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6
Q

COPD – tx goals (4)

A
  • reduce inflammation
  • relieve bronchoconstriction
  • reduce risk of/treat infection
  • control cough
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7
Q

B-2-adrenergic-agonists

A
  • for tx of acute bronchoconstriction

- stimulate B2 receptors in smooth mus of bronchioles and bronchii

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8
Q

B2 agonist – method of action

A
  • stim B2 receptors = increase in activity of adenylcyclase
  • adenyclyclase leads to increase in production of intracellular cyclic AMP
  • AMP activates protein kinase A……relaxation bronchioles
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9
Q

Epinephrine

A
  • alpha, B1, B2
  • acute bronchoconstriction, rapid therapeutic effect
  • also treats bronchiolitis, RSV, and status asthmaticus – severe prolonged asthma that is unresponsive to standard drug tx
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10
Q

ultra short acting B2 adrenergic agonists (2)

A
  • 2-3 hrs

- isoproterenol, isoetharine

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11
Q

short-acting B2 adrenergic agonists (3)

A
  • 3-6 hours

- metaproterenol, terbutaline, pirbuterol

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12
Q

Intermediate acting (3)

A
  • 8 hours

- albuterol, levalbuterol, bitolterol

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13
Q

long acting (LABAs) (2)

A
  • 12 hours

- salmeterol, formoterol

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14
Q

Levalbuterol

A
  • intermediate acting

- B2 selectives usually mixture of R and S isomers. Only the R isomer activates the B2 receptor

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15
Q

Formoterol

A
  • highly selective B2, long acting
  • highly lipophilic, enters cell as “depot” and gradually released into aqueous phase to activate B2 receptors resulting in long duration of action
  • aqueous phase activity NOT demonstrated by salmeterol
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16
Q

Tolerance

A
  • if short acting B2 agonists overused, tolerance occurs because B2 receptors become unresponsive to stimulation
  • can be reversed through use of inhaled corticosteroids
  • no tolerance observed with LABA
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17
Q

Inhaled Anticholinergics – MOA

A
  • blocks muscarinic cholinergic receptors (non-specific anti-cholinergic) aka M-receptor antagonsits
  • cause decrease in formation of cGMP, decreasing contractility of smooth ms in lung, inhibiting bronchoconstriction & mucus secretion
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18
Q

Inhaled anticholinergics – most common use

A

-symptomatic relief of COPD

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19
Q

Inhaled Anticholinergics – names (3)

A
  • ipratropium bromide (atrovent)
  • ipatropium + albuterol (combivent)
  • tiotropium (spiriva)
20
Q

Inhaled anti-cholinergics – side effects

A

-dry mouth, nervousness, headache, GI upset, worsening of glaucoma, prostatic hypertrophy

21
Q

tiotropium (spiriva)

A
  • longer acting structural analog of ipratropium bromide
  • approved for maintenance of COPD
  • long action thought to be due to slowed dissociation rate from M receptors
22
Q

Inhaled Corticosteroids

A
  1. suppress inflammation in airways, decreases mucous cell secretions, reduce edema, assist in repair of damaged epithelium
  2. increase number and sensitivity of B2 receptors – restores/enhances effectiveness of B2 agonists
23
Q

Corticosteroid Facts

A
  • in most acute severe asthma attacks, IV administration of CS offers little advantage over PO dosing
  • full action takes 48-72 hrs
  • oral CS should not be taken for 7-10 days with doses titrated down, should not D/C rapidly
24
Q

Inhaled v Systemic Corticosteroids

A
  • inhaled even at high doses, no sig serious adverse effects
  • long term systemic: adrenal gland atrophy, peptic ulcer, hyperglycemia, osteopenia/osteoporosis, aseptic necrosis of hip, immune supression
  • unpleasant effects: “moon face”, redistribution of weight, thin skin, acne, fatigue, GI disturbance
25
Q

Inhaled Corticosteroids (names – 5)

A
  • fluticasone (Flovent)
  • budesonide (Pumicort)
  • triamcinolone (Asmacort)
  • Flunisolide (Aerobid)
  • beclomethasone (Qvar, Beclovent)
26
Q

Oral Corticosteroids (2)

A
  • methylprednisolone (Depo-Medrol)

- prednisone (Deltasone, etc)

27
Q

Fluticasone propionate (Flovent)

A
  • outside of airway, bioavailability is minimal
  • Why? subject to rapid inactivation by liver, metabolite produced is largely inactive, has limited affinity for glucocorticoid receptor
28
Q

`Combination Agents (2)

A
  • contain both corticosteroid and bronchodilator (LABA)
  • fluticasone and salmeterol (Advair diskus)
  • budesonide and formoterol (Symbicort)
29
Q

Methylxanthines – additional effects

A
  • bronchodilators chemically related to caffeine
  • additional effects: inhibit pulm edema by decreasing vascular permeability, increase ability of cilia to clear mucous
  • Non-pulm effects: increased CO, peripheral vasodilation, mild diuretic effect, CNS stimulation
30
Q

Methylxanthines – how given, why decline in use

A

-PO or IV however use has declined to to narrow margin of safety and significant adverse effects and toxicity

31
Q

Mast Cell Stabilizers - MOA

A
  • inhibit release of histamine from mast cells
  • used as prophylaxis to prevent acute asthma attacks
  • short half life (2.5 hrs), must be used long term for sig benefit
32
Q

Mast Cell Stabilizers – names (2)

A
  • Cromolyn (Intal)

- Nedocromil (Tilade)

33
Q

Leukotrienes – what are they, how formed

A
  • strong chemical mediators of bronchoconstriction, inflammation, mucous secretion
  • formed by lipoxygenase pathway of arachidonic acid metabolism in response to cell injury
34
Q

Leukotriene Modifiers – what they do, names (3)

A
  • counteract effects of leukotrienes
  • indicated for long term tx of asthma, allergies
  • zileuton (Zyflo), montelukast (singulair), zafirlukast (accolate)
35
Q

zileuton (Zyflo)

A

-reduces formation of leukotrienes by blocking lipoxygenase

36
Q

montelukast (Singulair) and zafirlukast (Accolate)

A

block leukotriene receptors

37
Q

Immunosuppressant Monoclonal Antibody (1)

A

=omalizumab (Xolair)

  • binds to IgE, preventing attachment to mast cells and basolphils – prevents release of pro-inflammatory & pro-allergic substances
  • mainly rx for pts with severe, persistent asthma that can’t be controlled even w high doses of CS
38
Q

Mucolytics/Expectorants (uses, names (3))

A
  • used to reduce viscocity of bronchial mucus, aid in its removal
  • OTC: guaifenesin (Robitussin, etc)
  • RX: acetylcysteine (Mucomyst), dornase alfa-recombinant (Pulmozyme)
39
Q

Antitussives (uses, types)

A
  • dampen cough reflexes
  • Opiods: codeine, hydrocodone, bitartrate (Hydocan)
  • Non-Opiods: bensonatate (Tessalon), dextromethorphan (Pediacare, etc)
  • most used in combination w other agents like mucolytic/expectorant
40
Q

Repiratory Distress Syndrome (RDS)

A
  • condirtion in which lungs not producing surfactant
  • occurs mostly in preemies
  • surfactant allows alveoli to remain open during respiration, produced by type II alveolar cells
  • Colfosceril (Exosurf), ceractant (Survanta)
41
Q

Respiratory Synctial Virus (RSV) (tx options, prevention)

A
  • virus affecting infants, young childruns
  • tx with both selective and non-selective B-adrenergic drugs, O2, ribavirin, supportive care, etc
  • Prevention: monthly injection of RSV antibodies during peak RSV season to reduse risk of infection
42
Q

Anaphylaxis (what, S/S)

A
  • severe, sometimes life threatening allergic reactions to a variety of agents (foods, stinging insects, medication)
  • S/S: flushing, urticaria, pruritis, bronchospasm, cramping, hypotension
43
Q

Anaphylaxis (tx)

A
  • epinephrine S.C. or I.M.mg
  • a-agonist activity: increased peripheral vascular resistance, reverse vascular permeability
  • B-agonist: bronchodilation, positive iontotropic effect
44
Q

Pathophysiology of Anaphylaxis

A
  • first exposure –> IgE formation
  • IgE attached to mast cells/basophils –> mediators eg histamine are released from mast cells
  • Mediators –> smooth muscle constriction (leads to bronchospasm, cramping), increased vascular permeability (50% shift of vascular volume to tissues)
  • -> vasodilation
45
Q

Why must serum drug levels be monitored with methylxanthines?

A

peptic ulcer, renal dysfunction, seizure disorders, tachycardia, GERD

Pharmacology (4 decks)

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