10-9 Bronchodilators and Asthma Drugs - Martin Lecture & DSA Flashcards
1
Q
What is asthma?
A
Asthma is currently viewed primarily as an inflammatory illness that results in bronchial hyperreactivity and bronchospasm
2
Q
Why are drugs so important in controlling asthma?
A
recommendations for prevention and treatment of asthma emphasize control of the inflammatory component as the underlying problem
- reserve bronchodilators primarily for symptomatic use.
The inflammatory component and the airway narrowing of asthma are largely reversible
- drug therapy plays a significant role in the management of the disease
3
Q
Why is inflammation so pervasive in allergic asthma?
A
immediate hypersensitivity-type reactions can be continuously present at a sub-threshold level
- resulting in mild-to-moderate inflammation without overt bronchoconstriction
4
Q
If inflammation is continuously present in allergic asthma, why is overt bronchospasm intermittent?
A
Overt bronchospasm then occurs upon exposure to a specific allergen or to a variety of nonspecific stimuli, e.g., cold air, dust, air pollution, exercise, etc
5
Q
What is going on in COPD?
A
disease characterized by the presence of airflow obstruction due to chronic bronchitis or emphysema
- airflow obstruction is generally progressive
- may have airway hyperreactivity
- may be partially reversible
6
Q
How is drug therapy helpful in treating COPD?
A
useful in addressing the reversible component of COPD
- induce bronchodilation
- decrease inflammatory reaction
- facilitate expectoration
7
Q
What are the anti-inflammatory classes of drugs useful in asthma and related respiratory disease?
A
corticosteroids
cromolyn-like compounds
anti-leukotriene drugs
8
Q
What are the bronchodilators helpful in treating asthma and related respiratory diseases?
A
b-adrenergic agonists,
muscarinic receptor antagonists
methylxanthines
9
Q
In addition to bronchodilators and anti-inflammatories, what other types of drugs are helpful in addressing some respiratory disease?
A
decongestants, antitussives, expectorants and mucolytic agents
10
Q
What happens in allergy that causes release of inflammatory mediators?
A
Allergen-specific IgE binds to Fc receptors on mast cell.
When allergen comes in contact with IgE, the mast cell is activated and releases a large number of mediators.
- enormous variety of mediators is released, each having more than one potent effect on airway inflammation.
11
Q
Why are antihistamines not very effective in controlling allergic asthma?
A
many different mediators released
pharmacological blocker of any one mediator is ineffective in alleviating the symptoms or progression of asthma or the inflammatory component of other respiratory diseases
Corticosteroids, which can block many of the key steps in the inflammatory process, come closest to this ideal therapy
12
Q
Mast cells release many inflammatory mediators, but why do airways become responsive to non-specific stimuli?
A
asthmatic airways respond to allergen challenge with an immediate airway narrowing and mast cell infiltration.
Reactive hyperemia, edema, and cellular inflammation become evident within hours of challenge
- frequently associated with a second, usually more severe, rise in airways resistance
- influx of white cells and changes in airways function may persist for days and weeks after a single challenge and can result in heightened bronchial sensitivity to a number of stimuli
13
Q
What changes due to enzyme release from inflammatory cells contribute to bronchial sensitivity?
A
damage to the respiratory epithelium
enhanced neuropeptide release
exposed afferent nerve endings that can evoke enhanced vagal responses
14
Q
Other than mast cells, what cells contribute to inflammation in asthma?
A
Inflammatory cells other than mast cells implicated in the pathogenesis of asthma include eosinophils, neutrophils, macrophages, lymphocytes, and platelets.
15
Q
To sum, what are the 4 key features of asthma?
A
- Mast cell activation associated with early bronchospasm
- Inflammatory cell infiltration with subsequently mediator release
- Epithelial cell damage
- Increased responsiveness of the airways to a variety of non‑specific stimuli
16
Q
What are the immediate mediators from mast cells? What are the effects?
A
Preformed:
Histamine, TNF-a, Proteases, Heparin
Effects:
Bronchoconstriction, itch, cough, vasodilation, edema
17
Q
What are the lipid mediators from mast cells? What are the effects?
A
Mediators - lipids work in minutes
Leukotrienes, Prostaglandins
Effects:
Bronchoconstriction, chemotaxis, mucus secretion
18
Q
What are the cytokine mediators from mast cells? What are their effects?
A
Cytokines - start working in hours:
Interleukins, GM-CSF
Effects:
Bronchoconstriction, chemotaxis, inflammatory cell proliferation
19
Q
Why is aerosol delivery of asthma drugs beneficial?
A
pathophysiology of asthma appears to involve the respiratory tract alone.
- effective treatment could be achieved if drug administration was restricted to the lungs.
Aerosol application of drugs to the lungs can produce a high local concentration in the lungs with a low systemic absorption
- significantly improving the therapeutic ratio by minimizing side effects.
- both b2-agonists and corticosteroids have potentially serious side effects when delivered systemically.
20
Q
What percentage of asthmatic patients can be managed by aerosols?
A
Probably more than 90% of asthmatic patients who are capable of manipulating inhaler devices can be managed by aerosol treatments alone.
21
Q
What is are some important factors that determine effective deposition of drug into lung?
A
Particle size:
>10 mm deposit in mouth and oropharynx
<0.5 mm are inhaled and then exhaled
1-5 mm deposit in small airway and are most effective.
Rate of breathing and breath holding are important.
The recommendation technique is that a slow, deep breath be taken and held for 5 - 10 sec
22
Q
How much of a dose of aerosol drugs for asthma reach the lung? Why is this important in formulating drugs for asthma, etc.?
A
under ideal conditions only 2 - 10 % of drug is deposited in lungs
- most of the remainder is swallowed
to have minimal systemic side effects, an aerosolized drug should be either poorly absorbed from the GI tract or be rapidly inactivated by first-pass liver metabolism.
- ipratropium Br is complexed to a salt and permanently charged, and cannot be absorbed will in the GI tract or cross membranes well
23
Q
What are the different devices for aerosol delivery?
A
Metered Dose Inhalers (MDI) - with spacer device
Nebulizers
Dry powder inhalers
24
Q
How do MDIs work?
A
pressurized canister with a metering valve that delivers drug with hydrofluoroalkane (HFA) propellant, co-solvents, and/or surfactants
Spacer devices that attach to the MDI markedly improve the ratio of inhaled to swallowed drug and reduce need for coordination.
Valved holding chambers (VHCs) have one-way valves that prevent the patient from exhaling into the device, minimizing the need for coordinated activation and inhalation.
25
What are the advantages of MDIs? Disadvantages?
low cost and portability
disadvantages include need for hand-lung coordination making it more difficult for young children and the elderly to use
26
What are the advantages of nebulizers?
preferred for severe asthma exacerbations with poor inspiratory ability
do not require hand-lung coordination
Nebulizer therapy can be delivered by face mask to young children or older patients who are confused.
27
What are the advantages and disadvantages of dry powder inhalers?
require relatively high air flow to suspend the powder
can be irritating when inhaled
28
What are the 2+ major classes of bronchodilators?
**b-Adrenergic Agonists:**
_Short-Acting_ _b__2-selective adrenergic agonists (SABA)_
_Long-Acting_ _b__2-selective adrenergic agonists (LABA)_
also:
**_Nonselective agonists_**
Epinephrine (\*important emergency uses)
29
What are beta 2 agonists preferred for?
preferred therapy for bronchoconstriction
DOC for rapid relief of bronchospasm
Highly effective and safe for intermittent, prophylactic treatment of asthma.
These are the only agents shown to be immediately effective for relieving bronchoconstriction during acute, severe asthma.
30
What is the current emphasis for beta adrenergic agonists?
Intermittent use on an as-needed basis for relief of acute, severe bronchospasm in asthma and COPD
Not general prophylaxis
31
What is the MOA for beta adrenergic agonists?
Stimulate b2-adrenergic receptor on surface of bronchiolar smooth muscle cells.
b2-adrenergic receptor couples to Gs protein and activates adenylyl cyclase enzyme leading to increased cellular levels of cyclic AMP.
Cyclic AMP stimulates phosphorylation cascade that leads to decreased intracellular calcium and smooth muscle relaxation.
Also inhibit mediator release from mast cells.
32
What are the problems associated with overuse of beta adrenergic agonists?
Side effects intensify with overuse
- greater danger is the tendency to continue to self-medicate during periods when symptoms are escalating
- decreasing receptor sensitivity to agonist activity with increasing use
To avoid a medical emergency, patients should be encouraged to seek medical attention as soon as possible after they detect a decline in the efficacy of their usual therapeutic regimen
33
What are the rapid acting short duration beta 2 adrenergic agonists? What is their onset and duration?
**Albuterol**
Levalbuterol - l-isomer of albuterol
Pirbuterol
Terbutaline
onset\<15 min
duration: 2-4 hr
34
What popular term applies to rapid acting-short duration
b2-adrenergic agonists? What are they good at?
These agents are used as “rescue inhalers”
They are relatively fast at relieving bronchospasm,
but have a relatively short duration of action.
35
What are some long acting b2-selective agonists (LABA)?
salmeterol
formoterol
36
What is the onset and duration of salmeterol and formoterol?
Long Acting b2-Selective Agonists (LABA)
slower onset
duration \> 12 hours of useful bronchodilation
37
What are salmeterol and formoterol used for?
useful to control nighttime asthma attacks, also now used BID for prevention
## Footnote
**not suitable for treatment of acute bronchospastic attacks because onset of action is too slow**
38
What are some less or nonselective b-adrenergic agonists?
epinephrine
isoproterenol
metaproterenol
isoetharine
racemic epinephrine
39
What are epinephrine, isopreterenol, metaproterenol and isoetharine used for?
Because of their very short duration of action and their lack of b2-selectivity, these agents are not frequently used.
Low-strength epinephrine inhalers sometimes prescribed for mild asthma
40
What is racemic epinephrine used for?
aerosol used for pediatric patients
41
What can happen with long-term use of LABA?
Continued use of a LABA may cause down-regulation of b2 receptors with loss of the protective effect from rescue therapy with a short-acting agent.
42
What should LABAs be used with?
LABA should not be used for monotherapy in patients with persistent asthma, especially in children.
LABA should be used in asthma only in combination with an inhaled corticosteroid.
43
When should use of LABAs be stopped?
**Stop use of a LABA, if possible, once asthma control is achieved and maintain the use of an asthma-controller medication such as an inhaled corticosteroid**
44
What should be anticipated with beta adrenergic agonists used in oral therapy for bronchodilation?
Oral administration increases incidence of adverse side effects:
muscle tremor, cramps, cardiac tachyarrhythmias, metabolic disturbances, hypokalemia
45
What are some appropriate situations for oral therapy?
brief therapy in children with upper respiratory tract infections who cannot manipulate inhaler
in severe asthma exacerbations where inhaler cannot be used or when aerosol is irritating
oral albuterol and terbutaline are available
46
What are some adverse side effects of beta-adrenergic agonists?
(all side effects are made more minimal by inhalation route)
Skeletal muscle tremor (most frequent side effect)
CNS: restlessness, apprehension, anxiety, tremors
CVS: tachycardia, dysrhythmias, hyper- or hypotension
- hypokalemia (d/t skeletal mm vasodilation, drives K+ uptake)
worsen hyperglycemia in diabetics
47
What drug interactions should you look out for with beta adrenergic agonists?
drug interactions with thyroid, digitalis, methylxanthines
48
What is the DOC for anaphylactic reactions?
epinephrine
49
How should epi be administered for anaphylaxis?
Give SQ (or IM or IV with dextrose)
50
What are the effects of epinephrine, and what receptors mediate these effects?
Bronchodilation (mediated by b2 receptors)
Vasoconstriction (mediated by a1 receptors)
- maintains BP & decreases edema
Inhibition of mediator release (b2 receptors)
51
What are the treatments for anaphylaxis, in addition to epi?
Albuterol via nebulizer
IV fluids
Oxygen
Secondary therapy
52
What are the drugs for secondary treatment of anaphylaxis?
H1 antagonist - diphenhydramine
H2 antagonist - ranitidine
Corticosteroid - hydrocortisone, methylprednisolone
Aminophylline
NE, glucagon - for hypotension
53
What is ipratropium bromide?
Bronchodilator - a quaternary muscarinic receptor antagonist
54
Why does the route of administration matter with ipratroprium Br?
If given parenterally, effects are like atropine
But, only given as inhaled aerosol
- few side effects, even when swallowed because is poorly absorbed from GI and does not cross into brain
- quaternary amine- poor diffusion across membranes
55
Why is ipratropium Br an important drug, considering what receptors it works on?
Parasympathetic - mediated bronchospasm is a significant component of airway resistance in some asthmatics and COPD patients
especially psychogenic exacerbations
56
In addition to ipratropium Br, what is another anticholinergic bronchodilator?
tiotropium (Spiriva)
**Anticholinergic Agents**
**Ipratropium bromide (Atrovent)**
**Tiotropium (Spiriva)**
Aclidinium (Tudorza Pressair)
57
How long is bronchodilation caused by cholinergic antagonists versus beta agonists?
Bronchodilation develops more slowly and is usually less intense than that produced by b-agonists.
Useful bronchodilation lasts up to 6 hours.
58
What is the principle use of ipratropium?
Tx for COPD
59
What is Combivent?
ipratropium Br + albuterol
60
In addition to bronchodilation, what is another use for cholinergic antagonists?
Also used intranasally to reduce secretions in the upper and lower respiratory tract in allergic rhinitis and chronic postnasal drip syndrome.
61
What is tiotropium? What is the dosing, what is it used for, and what kind of device is it?
newer long-acting agent (QD dosing) used for maintenance therapy in chronic bronchitis and emphysema; dry powder inhaler device
62
What are the methylxanthines? What substances contain them?
**theophylline**, caffeine, theobromine
found in coffee, tea, chocolate, cocoa, colas
63
What are the cellular actions of methylxanthine bronchodilators?
adenosine receptor antagonists
block cyclic AMP degradation – PDE inhibitor
lower intracellular calcium
hyperpolarize cell membranes
64
What is the clinical effect of theophylline?
Bronchodilation
65
What other effects of theophylline, in addition to bronchodilation, are there?
CNS stimulation, modest peripheral vasodilation, improved skeletal muscle contractility, and a thiazide-like diuresis
66
What is the therapeutic use of theophylline?
Formerly a first-line agent for treatment of asthma
Now has a far less prominent role
67
Why is theophylline no longer a prominent drug in treating bronchospasm?
benefits are modest
narrow therapeutic window
considerable variation in absorption and elimination between different patients
monitoring of plasma concentrations is often required
68
What condition can be improved with theophylline?
Nocturnal asthma can be improved with slow-release theophylline, but inhaled corticosteroids and salmeterol are probably more effective.
69
What is the name of the IV formulation of theophylline?
aminophylline
70
What is the rationale beihind using corticosteroids in treating asthma?
In asthma (and some COPD) an **inflammatory response** is responsible for the underlying disease process.
So many inflammatory mediators are involved that a blocker of any given autocoid or cytokine, e.g., antihistamine, is ineffective in alleviating the symptoms of asthma.
Corticosteroids block many of the steps involved in the inflammatory cascade.
71
What is the MOA for corticosteroids?
**General anti-inflammatory response**
corticosteroids are steroid receptor agonists that bind to intracellular receptors that translocate to the cell nucleus and positively or negatively regulate gene transcription. This takes time.
corticosteroids inhibit the production and release of cytokines, vasoactive and chemoattractive factors, lipolytic and proteolytic enzymes, decrease mobilization of leukocytes to areas of injury, and decrease fibrosis.
72
What are the inhaled corticosteroids?
Beclomethasone dipropionate (Beclovent)
Budesonide dipropionate (Pulmicort)
Ciclesonide (Alvesco)
Flunisolide (AeroBid)
Fluticasone (Flovent)
Mometasone (Asmanex Twisthaler)
Triamcinolone acetonide (Azmacort)
73
What are the systemic corticosteroids? Administration route?
IV or oral:
Prednisone
Methylprednisolone
Hydrocortisone
74
Why is inhalation important for administration of corticosteroids?
Corticosteroids have potentially important adverse side effects.
Aerosol delivery of the steroid has significantly improved the safety of treatment for moderate to severe asthma
75
Who is a candidate for inhaled corticosteroids therapy?
Asthmatics who require inhaled b-adrenergic agonist therapy 3 - 4 or more times weekly are candidates for inhaled steroid therapy.
76
How do current preparations of inhaled corticosteroids differ? How are they the same? How does this impact dosing?
Available preparations have equivalent efficacy and potential side effects
- differ in the amount of drug aerosolized per inhaler activation, i.e., high-dose and low-dose.
Therefore, the dose of inhaled steroid must be empirically determined for each patient.
77
What happens to asthmatics who use inhaled corticosteroids?
Asthmatic patients maintained on inhaled corticosteroids show improvement of symptoms and lower requirements for “rescue” with a bronchodilator
78
When is systemic therapy with corticosteroids indicated for bronchospasm?
Systemic (i.v. or oral) steroid therapy is used in severe asthmatic attacks requiring hospitalization
79
How is systemic corticosteroid therapy administered to asthmatics?
For severe asthma, **prednisone or methylprednisolone** is given i.v., followed by oral doses and gradual tapering of the dose.
For acute, sever exacerbations, oral prednisone is administered for 1 -2 weeks.
Longer treatments require tapering of the dose to account for hypothalamic-pituitary-adrenal suppression.
80
What are the potential side effects of corticosteroids?
HPA suppression - low risks until high doses
Bone resorption - modest risks
Carbohydrate and lipid - minor risks
Cataracts and skin thinning - dose-related
Purpura - dose-related
Dysphonia - usually resolves
Candidiasis - use spacer device and rinse mouth
Growth retardation - of concern in children
81
What are some combination products that are useful?
Fluticasone propionate + Salmeterol (Advair Diskus, Advair HFA)
Budesonide + Formoterol
(Symbicort HFA)
Mometasone + Formoterol (Dulera)
Not useful for acute bronchospastic attack
Cost Range: ~$145-$175/month
82
What are the components of COPD?
Emphysema and chronic bronchitis
Alveolar destruction is the main pathophysiological component (irreversible component)
Some patients have inflammation and bronchospasm (reversible components)
83
What are the treatments for COPD?
smoking cessation
Drug therapy is applicable to the reversible component of COPD:
Inhaled ipratropium bromide or tiotropium - especially useful in patients with a vagally-mediated psychogenic component.
Inhaled b2-adrenergic agonists - as with asthma, continuous (overuse) of bronchodilators may be associated with worsening of symptoms.
A subgroup of COPD patients may benefit from corticosteroid therapy, but generally mixed results of steroids in COPD.
84
What is step-up treatment for COPD?
Dividing patients into groups A - D, depending on severity of disease.
85
What is cromolyn Na? What does it do?
Cromolyn sodium (Intal)
Cromolyn sodium is an anti-inflammatory agent that indirectly inhibits antigen-induced bronchospasm and directly inhibits the release of histamine and other autocoids from sensitized mast cells.
May suppress the activating effects of chemoattractant peptides on eosinophils, neutrophils, and monocytes.
86
Are cromolyn compounds good for controlling acute bronchospasm?
Cromolyn compounds do not directly relax smooth muscle, therefore they are not useful for control of acute bronchospasm
87
How are cromolyn compounds used clinically in treatment of bronchospasm?
Cromolyn compounds are primarily **prophylactic**. When inhaled several times daily, they inhibit both the immediate and late asthmatic responses to antigenic challenge or exercise.
88
How are leukotriene inhibtors used clinically?
Alternative or adjunctive therapy to low-dose corticosteroids for mild persistent asthma.
Useful as oral prophylaxis in exercise-induced asthma
89
What are some leukotriene inhibitors?
Zafirlukast
LTD4 receptor antagonist
**Montelukast**
LTD4 receptor antagonist
90
What is the role of leuklotrienes in airway inflammation?
Role of leukotrienes in airway inflammation:
leukotriene (LT) autocoids are important mediators of inflammatory reactions and anaphylaxis.
Leukotrienes are lipid mediators derived from arachidonic acid in the 5-lipoxogenase pathway.
LTs are synthesized by eosinophils, mast cells, macrophages, and basophils.
LTB4 is a potent neutrophil chemoattractant.
LTC4 and LTD4 exert many effects known to occur in asthma including bronchoconstriction, increased bronchial reactivity, mucosal edema, and mucus hypersecretion.
91
What is omalizumab?
Omalizumab/Xolair is the first monoclonal antibody directed against IgE and is the first biologic therapy targeted for use for the treatment of asthma. It is a chimeric monoclonal antibody specific for IgE and is used for the treatment of moderate to severe allergic asthma
92
What is the MOA for Xolair?
Omalizumab binds to human IgE's high affinity Fc receptor, preventing the binding of IgE to a variety of cells associated with the allergic response and lowering free serum IgE concentrations. Avoiding the bridging between IgE and cells associated with allergic response prevents degranulation of such cells and, thereby, the release of inflammatory mediators. The early phase of allergic response is prevented as omalizumab prohibits IgE's binding to mast cells, preventing mast cell degranulation. The late phase of allergic response is prevented when the IgE-anti-IgE complex is unable to bind to FcepsilonRI receptors on monocytes, eosinophils, dendritic cells, epithelial cells, and platelets, thus interfering with mediator/cytokine release. Omalizumab has been found in clinical trials to reduce free serum IgE concentrations by more than 90%, considerably suppress eosinophils in induced sputum, and blunt both early and late phase allergic responses
93
How is omalizuman administered? What is an important side effect?
adminstered by SQ injection
Side effect: life-threating hypersensitivity reaction to drug
94
What is allergic rhinitis?
Seasonal allergic rhinitis (hay fever) is caused by deposition of allergens on the nasal mucosa resulting in immediate hypersensitivity reactions. This reaction is different from asthma in that larger foreign particles are usually involved that do not become inhaled into the lower airways.
95
What is the treatment for allergic rhinitis?
Treatment of allergic rhinitis is similar to that for asthma. **Topical corticosteroids** delivered as an aqueous **nasal spray** (*beclomethasone, budesonide, flunisolide, fluticasone, mometasone, triamcinolone*) or ***cromolyn*** **sodium** can be highly effective with minimal side effects.
**antihistamines** (H1 histamine receptor antagonists) produce considerable, though incomplete, symptom relief.
**Nasal decongestants** that are a-adrenergic agonists that cause vasoconstriction via activation of a1-adrenergic receptors are found in many, many over-the-counter preparations. Rebound congestion is a problem with these agents.
Sympathomimetic Agents (a-agonists)
Phenylephrine (Neo-Synephrine)
Pseudoephedrine (Sudafed) *access restricted in most states because of diversion to manufacture methamphetamine.*
96
How is COPD treated?
Patients with active inflammation with bronchospasm and excessive mucus production can obtain relief of symptoms with **inhaled ipratropium or tiotropium combined with a b2-adrenergic agonist.**
## Footnote
**Ipratropium bromide + albuterol is available as a combination (Combivent)**
97
What therapy is contraindicated in COPD?
Monotherapy with inhaled corticosteroids is not approved for use in COPD
98
What is triple therapy for COPD?
tiotropium, formoterol or salmeterol, and fluticasone or budesonide
- superior to treatment with 1 or 2 agents in relieving symptoms such as dyspnea and in improving lung function
99
What is the treatment for emphysema due to alpha-1 antitrypsin deficiency?
Purified a1-antiproteinase (Prolastin) is available for IV replacement.
100
What is cough?
Cough is a nonspecific sign of upper or lower airway irritation or inflammation and is mediated through reflex vagal pathways
Multiple factors may cause cough, such as airway hyperactivity, smoking, infection, neoplasms, foreign bodies, "postnasal drip", esophageal reflux, or irritation of the sinuses, upper airway and eardrum.
101
What is an indication for use of antitussive therapy?
Nonproductive cough that is irritating to the throat and self‑perpetuating or exhausting to the patient
102
What are the classes and agents for antitussive therapy?
Opioids:
Codeine
Dextromethorphan
Non‑opioids:
Benzonatate (Tessalon)
Diphenhydramine (Benylin)
103
What is the MOA for opioids in controlling cough?
Opioids are believed to act at the CNS level, by suppression of the cough reflex.
May act at non-opioid receptor site.
104
What is the MOA for non-opioid antitussives?
Local anesthetics and demulcents probably act directly on nerve endings in the pharynx. Antihistaminics mechanism is unknown.
105
What is the therapeutic rationale behind using expectorants and mucolytic agents?
Stimulation of secretion in the respiratory tract is of theoretic value in the treatment of chronic irritating cough
106
What is the MOA for expectorants and mucolytic agents?
mechanism of action of expectorants is unknown whereas the mucolytic agent is thought to act by facilitating the depolymerization of mucopolysaccharides in dried airway secretions.
107
What are the expectorants?
guaifenesin
potassium iodide and iodinated glycerol
108
How does guaifenesin work?
claimed to enhance the output of respiratory tract fluid by reducing adhesiveness and surface tension facilitating the removal of viscous mucus.
As a result, nonproductive coughs become more productive and less frequent.
There is a lack of convincing studies to document efficacy.
109
How does potassium iodide and iodinated glycerol work?
Iodides enhance the secretion of respiratory fluids, thus decreasing the mucus viscosity.
- may stimulate breakdown of fibrinoid material in inflammatory exudates.
Objective evidence of clinical efficacy is lacking.
Because of the potential for adverse effects, other agents are usually preferred.
110
Why is recombinant DNAse useful in treating cystic fibrosis?
(dornase alfa, Pulmozyme) a recombinant DNAse has become available as a nebulizer solution for treatment of cystic fibrosis.
Inspissated secretions containing large numbers of inflammatory cells lodge in the smaller airways causing obstruction in cystic fibrosis.
- a substantial portion of the purulent material is due to the DNA from the nuclei of lysed cells.
Inhaled DNAse has been shown to aid in clearing these secretions.
