Exam 2 - PULMONARY DRUGS Flashcards
1
Q
How are aeresolized drugs delivered? (3)
A
-nebulizer, dry poweder inhalant, metered powder inhalant
2
Q
Disadvantages to aeresolized drugs (3)
A
- correct dose?
- alteration of breathing pattern?
- deposition of drug in oral mucosa?
3
Q
Asthma features
A
-bronchoconstriction, airway infammation, airway hyperresponsiveness, hypersecretion of mucous
4
Q
Atopy
A
- refers to inhereted predispostion for certain conditions (asthma, allergic rhinitis, eczema)
- underlies almost all asthma in children, most in adults
5
Q
COPD
A
chronic lung condition in which airflow limitation is not reversible
6
Q
COPD – tx goals (4)
A
- reduce inflammation
- relieve bronchoconstriction
- reduce risk of/treat infection
- control cough
7
Q
B-2-adrenergic-agonists
A
- for tx of acute bronchoconstriction
- stimulate B2 receptors in smooth mus of bronchioles and bronchii
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
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
10
Q
ultra short acting B2 adrenergic agonists (2)
A
- 2-3 hrs
- isoproterenol, isoetharine
11
Q
short-acting B2 adrenergic agonists (3)
A
- 3-6 hours
- metaproterenol, terbutaline, pirbuterol
12
Q
Intermediate acting (3)
A
- 8 hours
- albuterol, levalbuterol, bitolterol
13
Q
long acting (LABAs) (2)
A
- 12 hours
- salmeterol, formoterol
14
Q
Levalbuterol
A
- intermediate acting
- B2 selectives usually mixture of R and S isomers. Only the R isomer activates the B2 receptor
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
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
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
18
Q
Inhaled anticholinergics – most common use
A
-symptomatic relief of COPD
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
- suppress inflammation in airways, decreases mucous cell secretions, reduce edema, assist in repair of damaged epithelium
- 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
Inhaled Corticosteroids (names -- 5)
- fluticasone (Flovent)
- budesonide (Pumicort)
- triamcinolone (Asmacort)
- Flunisolide (Aerobid)
- beclomethasone (Qvar, Beclovent)
26
Oral Corticosteroids (2)
- methylprednisolone (Depo-Medrol)
| - prednisone (Deltasone, etc)
27
Fluticasone propionate (Flovent)
- 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
`Combination Agents (2)
- contain both corticosteroid and bronchodilator (LABA)
- fluticasone and salmeterol (Advair diskus)
- budesonide and formoterol (Symbicort)
29
Methylxanthines -- additional effects
- 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
Methylxanthines -- how given, why decline in use
-PO or IV however use has declined to to narrow margin of safety and significant adverse effects and toxicity
31
Mast Cell Stabilizers - MOA
- 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
Mast Cell Stabilizers -- names (2)
- Cromolyn (Intal)
| - Nedocromil (Tilade)
33
Leukotrienes -- what are they, how formed
- strong chemical mediators of bronchoconstriction, inflammation, mucous secretion
- formed by lipoxygenase pathway of arachidonic acid metabolism in response to cell injury
34
Leukotriene Modifiers -- what they do, names (3)
- counteract effects of leukotrienes
- indicated for long term tx of asthma, allergies
- zileuton (Zyflo), montelukast (singulair), zafirlukast (accolate)
35
zileuton (Zyflo)
-reduces formation of leukotrienes by blocking lipoxygenase
36
montelukast (Singulair) and zafirlukast (Accolate)
block leukotriene receptors
37
Immunosuppressant Monoclonal Antibody (1)
=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
Mucolytics/Expectorants (uses, names (3))
- used to reduce viscocity of bronchial mucus, aid in its removal
- OTC: guaifenesin (Robitussin, etc)
- RX: acetylcysteine (Mucomyst), dornase alfa-recombinant (Pulmozyme)
39
Antitussives (uses, types)
- 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
Repiratory Distress Syndrome (RDS)
- 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
Respiratory Synctial Virus (RSV) (tx options, prevention)
- 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
Anaphylaxis (what, S/S)
- severe, sometimes life threatening allergic reactions to a variety of agents (foods, stinging insects, medication)
- S/S: flushing, urticaria, pruritis, bronchospasm, cramping, hypotension
43
Anaphylaxis (tx)
- epinephrine S.C. or I.M.mg
- a-agonist activity: increased peripheral vascular resistance, reverse vascular permeability
- B-agonist: bronchodilation, positive iontotropic effect
44
Pathophysiology of Anaphylaxis
- 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
Why must serum drug levels be monitored with methylxanthines?
peptic ulcer, renal dysfunction, seizure disorders, tachycardia, GERD
