Week 10 drugs only Flashcards
Exam 4
1
Q
Characteristic signs and symptoms of asthma:
A
Breathlessness
Tightness in the chest
Wheezing
Dysnea
Cough
2
Q
Underlying cause of asthma:
A
The underlying cause is immune-mediated airway inflammation.
3
Q
Chronic obstructive pulmonary disease (COPD)
A
is a chronic, progressive, largely irreversible disorder characterized by airflow restrictions and inflammation.
4
Q
Symptoms of COPD
A
Symptoms include chronic cough,
excessive sputum production,
wheezing,
dyspnea, and
poor exercise tolerance
5
Q
How does the inflammatory process of asthma begin?
A
The inflammatory process begins with binding of allergen molecules (e.g., house dust mite feces) to immunoglobulin E (IgE) antibodies on mast cells.
6
Q
When allergen molecules bind to IgE antibodies on mast cells in asthma, what happens?
A
This causes mast cells to release an assortment of mediators, including histamine, leukotrienes, prostaglandins, and interleukins.
7
Q
What are the two effects that mediators released by mast cells have during asthma?
A
These mediators have two effects.
- They act immediately to cause bronchoconstriction.
- In addition, they promote infiltration and activation of inflammatory cells (eosinophils, leukocytes, macrophages).
8
Q
What do the inflammatory cells do during asthma?
A
These inflammatory cells then release mediators of their own.
9
Q
What is the end result of airway inflammation?
A
The end result is airway inflammation characterized by edema, mucus plugging, and smooth muscle hypertrophy, all of which obstruct airflow.
10
Q
In addition to edema, mucus plugging and smooth muscle hypertrophy, what does inflammation produce?
A
Inflammation produces a state of bronchial hyperreactivity.
11
Q
Symptoms of COPD result largely from a combination of two pathologic processes:
A
- chronic bronchitis
- emphysema.
12
Q
Chronic bronchitis is defined by:
A
chronic cough and excessive sputum production
13
Q
What does chronic bronchitis result from:
A
results from hypertrophy of mucus-secreting glands in the epithelium of the larger airways
14
Q
Emphysema is defined by:
A
Emphysema is defined as enlargement of the air space within the bronchioles and alveoli brought on by deterioration of the walls of these air spaces.
15
Q
In a smal percentage of people, emphysema results from:
A
In a small percentage of the population, emphysema results from a genetic alteration that results in alpha-1 antitrypsin deficiency.
16
Q
Alpha-1 antitrypsin
A
Alpha-1 antitrypsin is a protease inhibitor that protects the lungs from enzymatic destruction by proteases.)
17
Q
Two main pharmacological classes of drugs for asthma and COPD:
A
- Anti inflammatory drugs
- Bronchodilators
18
Q
Principle antiinflammatory drugs are:
A
Glucocorticoids
19
Q
The principal bronchodilators are:
A
beta2 agonists
20
Q
For chronic asthma and stable COPD how are glucocorticoids administered? (route and timing)
A
For chronic asthma and stable COPD, glucocorticoids are administered on a fixed schedule, almost always by inhalation.
21
Q
For chronic asthma and stable COPD, how are Beta agonists administered?
A
Beta2 agonists may be administered on a fixed schedule (for long-term control) or as needed (PRN; to manage an acute attack). Like the glucocorticoids, beta2 agonists are usually inhaled.
22
Q
Most antiasthma drugs can be administered by inhalation: What are the three advantages of this route?
A
(1) Therapeutic effects are enhanced by delivering drugs directly to their site of action, (2) systemic effects are minimized, and
(3) relief of acute attacks is rapid.
23
Q
MDI
A
are small, handheld, pressurized devices that deliver a measured dose of drug with each actuation.
24
Q
When more than one inhalation is needed for MDIs, how should you take the medication?
A
When two inhalations are needed, an interval of at least 1minute should separate the first inhalation from the second.
25
Dry Powder Inhalers (DPIs)
Dry-powder inhalers (DPIs) are used to deliver drugs in the form of a dry micronized powder directly to the lungs.
26
How do MDIs compare with DPIs?
1. DPIs deliver more drug to the lungs
2. DPIs are breath activated.
3. Spacers are not used with DPIs
27
Nebulizer
A nebulizer is a small machine used to convert a drug solution into a mist.
28
What are the most effective drugs available for long term control of airway inflammation?
Glucocorticoids (e.g., budesonide, fluticasone)
29
How are glucocorticoids usually administered?
Administration is usually by inhalation but may also be IV or oral.
30
When do systemic glucocorticoids cause adverse effects?
When systemic glucocorticoids are used long term, severe adverse effects are likely.
31
In general, what do glucocorticoids do?
Glucocorticoids reduce respiratory symptoms by suppressing inflammation.
32
Specific antiinflammatory effects include of glucocorticoids include?
1. Decreased synthesis and release of inflammatory mediators (e.g., leukotrienes, histamine, prostaglandins)
2. Decreased infiltration and activity of inflammatory cells (e.g., eosinophils, leukocytes)
3. Decreased edema of the airway mucosa (secondary to a decrease in vascular permeability)
33
By reducing inflammation, what do glucocorticoids do?
1. reduce bronchial hyperreactivity and
2. decrease airway mucus production.
34
Therapeutic use of glucocorticoids:
they are especially effective for:
1. asthma prophylaxis and
2. for management of COPD exacerbations
35
What are the first line therapy for management of the inflammatory component of asthma?
Inhaled glucocorticoids
*most patients with persistent asthma should take these drugs daily
36
Who are oral glucocorticoids required for?
May be required for patients with moderate to severe persistent asthma or for management of acute exacerbations of asthma or COPD.
37
What is a serious problem with oral glucocorticoids? So when should these drugs be taken? How long should these meds be taken?
They have a potential for toxicity.
These drugs are prescribed only when symptoms cannot be controlled with safer medications (inhaled glucocorticoids, inhaled beta2 agonists)
Because the risk for toxicity increases with duration of use, treatment should be as brief as possible.
38
Adverse Effects of Inhaled Glucocorticoid:
1. Adrenal suppression
2. Oropharyngeal candidiasis
3. Dynsphonia
4. Slow growth of children and adolescents (but don't decrease adult height)
5. Increased risk for glaucoma and cataracts
6. May promote bone loss
39
Potential adverse effects of prolonged oral glucocorticoids include:
adrenal suppression,
osteoporosis,
hyperglycemia,
immunosuppression,
fluid retention,
hypokalemia,
peptic ulcer disease, and,
in young patients, growth suppression.
40
Prolonged glucocorticoid use and adrenal suppression:
prolonged glucocorticoid use can decrease the ability of the adrenal cortex to produce glucocorticoids of its own.
41
WHy is adrenal suppression life threatening
This can be life-threatening at times of severe physiologic stress (e.g., surgery, trauma, or systemic infection).
High levels of glucocorticoids are required to survive severe stress and because adrenal suppression prevents production of endogenous glucocorticoids,
42
At times of stress, what must patients with adrenal suppression be given?
Because high levels of glucocorticoids are required to survive severe stress and because adrenal suppression prevents production of endogenous glucocorticoids, **patients must be given increased doses of oral or IV glucocorticoids at times of stress.
43
When is adrenal suppression also a concern?
Adrenal suppression is also a concern when
1. discontinuing prolonged use of oral glucocorticoids or
2. when transferring from an oral route to an inhaled route.
44
It take months for full adrenal functioning, during that time, what must patients do?
it is important to decrease the dosage gradually. Throughout this time, all patients, including those switched to inhaled glucocorticoids, must be given supplemental oral or IV glucocorticoids at times of severe stress.
45
How are inhaled glucocorticoids administered?
Inhaled glucocorticoids are administered on a regular schedule—not PRN.
46
Leukotriene receptor antagonists (LTRAs)
Leukotriene receptor antagonists (LTRAs) suppress the effects of leukotrienes
47
Leukotrienes
Compounds that promote smooth muscle constriction, blood vessel permeability, and inflammatory responses through direct action and through recruitment of eosinophils and other inflammatory cells.
48
In patients with asthma, how do (LTRAs) work?
In patients with asthma, these drugs can decrease bronchoconstriction and inflammatory responses such as edema and mucus secretion.
49
Three LTRAs available and how are they taken?
1. Zileutin
2. Zafirlukast
3. Montelukast
**taken orally
50
How do current guidelines recommend taking leukotriene receptor antagonists?
1. second-line therapy if an inhaled glucocorticoid cannot be used and
2. as add-on therapy when an inhaled glucocorticoid alone is inadequate.
51
Zileuton- what does it do and what is it approved for?
What is does: Blocks leukotriene synthesis
Approved for: Asthma prophylaxis and maintenance therapy in adults and kids
52
Why can't zileuton not be used during an attack?
Because effects are not immediate, zileuton cannot be used to abort an ongoing attack.
53
What are zileutons less effective than?
Zileuton is less effective than an inhaled glucocorticoid alone and appears to be less effective than a long-acting inhaled beta2 agonist
54
Major adverse effects of LTRAs
TRAs can cause adverse neuropsychiatric effects, including depression, anxiety, agitation, abnormal dreams, hallucinations, insomnia, irritability, restlessness, and suicidal thinking and behavior.
55
What do Zafirlukast and Montelukast do?
What does Zileuton do?
Zafirlukast and montelukast: Block leukotriene receptors
Zileuton: blocks leukotriene synthesis
56
What is the most commonly used leukotriene modulator?
Montelukast
57
What is the Mast Cell Stabilizer Drug?
Cromolyn
58
Cromolyn (Mast Cell Stabilizer)
Cromolyn is an inhalational agent that suppresses bronchial inflammation.
59
What is Cromolyn used for?
The drug is used for prophylaxis—not quick relief—in patients with mild to moderate asthma.
60
How do the antiinflammatory effects of Cromolyn compare with glucocorticoids?
Antiinflammatory effects are less than with glucocorticoids; therefore cromolyn is not a preferred drug for asthma therapy.
61
What is the mechanism of action of Cromolyn?
Cromolyn suppresses inflammation; it does not cause bronchodilation.
62
What do Cromolyn do to mast cells?
Drug acts in part by stabilizing the cytoplasmic membrane of mast cells, preventing release of histamine and other mediators. In addition, cromolyn inhibits eosinophils, macrophages, and other inflammatory cells.
63
How is Cromolyn administered (route and frequency)?
By nebulizer
When administered on a fixed schedule, cromolyn reduces both the frequency and intensity of asthma attacks.
64
What is the safest of all antiasthma medications?
Cromolyn
65
Adverse effects of Cromolyn?
Cough
Bronchospasm
66
What are the newest drug category for management of airway inflammation? What do the meds end it?
Monoclonal Antibodies
End in 'mab'
67
What do bronchodilators do?
Bronchodilators provide symptomatic relief in patients with asthma and COPD but do not alter the underlying inflammation that is part of the disease process.
68
When is monotherapy with a bronchodilator appropriate?
Monotherapy with a bronchodilator is appropriate only when asthma is very mild and attacks are infrequent.
69
What are the most effective drugs available for relieving acute bronchospasm and preventing EIB?
Inhaled beta2 agonists
70
What is the mechanism of action of beta 2 agonists?
The beta2 agonists are sympathomimetic drugs that activate beta2-adrenergic receptors.
71
By activating beta 2 receptors in smooth muscle of the lung, what do beta 2 agonists do?
By activating beta2 receptors in smooth muscle of the lung, these drugs promote bronchodilation and thus relieve bronchospasm.
72
What do beta 2 agonists do with histamine?
Beta2 agonists have a limited role in suppressing histamine release in the lung and increasing ciliary motility.
73
How are beta agonists administered?
Orally or inhalation
74
Beta agonists inhaled agents, what are the groups?
1. Short Acting Beta Agonists (SABA)
2. Long-Acting Beta Agonists
75
What are SABA taken for?
1. taken PRN to abort an ongoing attack.
2. In patients with EIB, they are taken before exercise to prevent an attack from occurring.
76
For hospitalized patients undergoing a severe acute attack, what is the traditional treatment choice?
For hospitalized patients undergoing a severe acute attack, a nebulized SABA is the traditional treatment of choice
77
For patients in a outpatient setting undergoing a severe acute attack, how should SABA be administered?
SABA delivered with an MDI
78
What are considered life saving medications?
SABA
79
What happens if SABA is taken in excess?
tachydysrthmias
angina
seizures
Cardiac arrest
Death
80
How are LABA administered?
Dosing is done on a fixed schedule, not PRN.
81
What is preferred for patient with stable COPD?
LABAs are preferred over SABAs for patients with stable COPD.
82
In patients with asthma, how should LABAs be taken?
In patients with asthma, however, LABAs are not first-line therapy, and they must always be combined with a glucocorticoid.
83
Why is LABA use alone contraindicated in asthma?
Their use alone in asthma is contraindicated because LABA monotherapy has been associated with increased incidence of asthma-associated death.
(Although using a LABA alone is contraindicated for patients with asthma, LABAs can still be used alone in patients with COPD).
84
Systemic negative effects of SABAs?
Tachycardia, angina, and tremor—can occur but are usually minimal.
85
Example of Methylxanthines
1. Theophylline
2. Caffeine
3. Aminophylline
86
The most prominent actions of Methylxanthines?
1. (1) central nervous system (CNS) excitation and
(2) bronchodilation.
3. Other actions include cardiac stimulation, vasodilation, and diuresis.
87
What is the principal methylxanthine employed for asthma?
Theophylline
88
Benefits of Theophylline derive primarily from what?
Bronchodilation
89
Why must dosage of Theophylline be carefully controlled?
Theophylline has a narrow therapeutic range, so dosage must be carefully controlled.
90
What is the mechanism of action of Theophylline?
Theophylline produces bronchodilation by relaxing smooth muscle of the bronchi.
91
Safe dosing range of theophylline:
theophylline levels between 10 and 20 mcg/mL.
92
Theophylline levels between 20 to 25 produce what?
20 to 25 mcg/mL, relatively mild reactions occur (e.g., nausea, vomiting, diarrhea, insomnia, restlessness).
93
Theophylline levels above 30?
Serious adverse effects are most likely at levels above 30 mcg/mL. These reactions include severe dysrhythmias (e.g., ventricular fibrillation) and convulsions that can be highly resistant to treatment. Death may result from cardiorespiratory collapse.
94
What to do it theophylline toxicity is evident?
1. Dosing of theophylline should stop
2. Administer activated charcoal together with a cathartic (decreases absorption)
3. Ventricular dysrhythmias respond to lidocaine/amiodarone
4. IV benzo controls seizures
95
Drugs interactions with Theophyllines?
1. Caffeine
2. Tobacco and marijuana
3. Cimetidine
4. Fluoroquinolone antibiotics
96
Caffeine + Theophylline
Caffeine can intensify the adverse effects of theophylline on the CNS and heart.
In addition, caffeine can compete with theophylline for drug-metabolizing enzymes, causing theophylline levels to rise.
97
Tobacco and Marijuana + Theophylline
Smoking tobacco or marijuana can induce theophylline metabolism, resulting in increased drug clearance.
98
cimetidine and the fluoroquinolone antibiotics + theophylline
Can elevate plasma levels of theophylline primarily by inhibiting hepatic metabolism
99
How is theophylline available for use?
IV or oral use
100
When is IV theophylline used? How should it be administered?
Emergencies
Administration must be done slowly because rapid injection can cause fatal cardiovascular reactions.
101
Aminophylline (Methylxanthines)
Aminophylline is a theophylline salt that is considerably more soluble than theophylline itself.
102
How do anticholinergic drugs work? What are they approved for?
Anticholinergic drugs improve lung function by blocking muscarinic receptors in the bronchi, reducing bronchoconstriction.
These drugs are approved only for COPD.
103
First anticholinergic drug:
Ipatoptrium
104
Ipratoprium mechanism of action
Like atropine, ipratropium is a muscarinic antagonist. By blocking muscarinic cholinergic receptors in the bronchi, ipratropium prevents bronchoconstriction.
105
How does ipratropium compare to beta2 agonists?
Is less effective than the beta2 agonists.
Because ipratropium and the beta2-adrenergic agonists promote bronchodilation by different mechanisms, their beneficial effects are additive.
106
When do therapeutic effects of ipratropium begin?
Therapeutic effects begin within 30 seconds, reach 50% of their maximum in 3 minutes, and persist about 6 hours.
107
Most common adverse effects of ipratropium?
Dry mouth and irritation of the pharynx.
108
Tiotropium
Tiotropium is a LAMA approved for maintenance therapy of bronchospasm associated with COPD.
Not approved for asthma but has been used off-label for patients who have not responded to other medications.
109
How does ipratropium compare to tiotropium?
Compared with ipratropium, tiotropium is more effective and has a more convenient dosing schedule (once daily vs. 4 times daily).
110
What is tiotropium indicated for?
Tiotropium is indicated only for long-term maintenance.
111
When do therapeutic effects of tiotropium begin?
Therapeutic effects begin about 30 minutes after inhalation, peak in 3 hours, and persist for about 24 hours.
With subsequent doses, bronchodilation gets better and better, reaching a plateau after eight consecutive doses (8 days).
112
The goals for stopping acute severe exacerbations of asthma?
1. to relieve airway obstruction and hypoxemia and
2. to normalize lung function as quickly as possible.
113
Two ways in which pharmacological drugs for asthma and COPD can be taken:
1. Inhaled
2. Systemic
114
Anti inflammatory drugs include:
1. Glucocorticoids
2. Leukotriene antagonists
3. Mast cell stabilizer
4. Monoclonal antibodies
115
Bronchodilators include:
1. Beta 2 agonists
2. Anticholinergic
3. Methylxanthine (theophylline)
116
Three obvious advantages of inhaled glucocorticoids:
1. Therapeutic effect are enhanced
2. Systemic effects are minimized
3. Relief rapid of acute attacks
117
Three types of inhalers:
1. Metered Dose inhalers (MDIs)
2. Dry Powder Inhalers
3. Nebulizers
118
What is considered the most effective antiasthma drug available?
inhaled glucocorticoids
119
What are Inhaled Glucocorticoids used for:
Prophylaxis of chronic asthma
120
When should Glucocorticoids be taken?
Dosing must be on a fixed schedule, not as needed (PRN)
121
When are inhaled Glucocorticoids NOT used
Not used to abort an ongoing attack
122
Why are inhaled Glucocorticoids not useful during an ongoing attack?
Not used to abort on ongoing attack because beneficial effects develop slowly
123
Systemic Glucocorticoids- how are they taken/
IV or orally
124
When are Systemic Glucocorticoids used?
1. For pts with moderate to severe persistent asthma
2. for management of acute exacerbations of asthma or COPD
125
Why are systemic Glucocorticoids dangerous?
Potential for toxicity
126
Since systemic glucocorticoids have a potential for toxicity, when should they be used?
Should only be used when symptoms cannot be controlled with safer medications (inhaled glucocorticoids, inhaled beta 2 agonists)
127
How long should systemic glucocorticoids be used?
Treatment should be as brief as possible
128
Adverse Effects of systemic glucocorticoids:
1.Short term therapy
2. Long term therapy
3. Adrenal suppression
4. Osteoporosis
5. Hyperglycemia
6. Peptic ulcer disease
7. Growth suppression
129
Glucocorticoids reduce respiratory symptoms by suppressing inflammation. Specific antiinflammatory effects include:
* Decreased synthesis and release of inflammatory mediators (e.g., leukotrienes, histamine, prostaglandins)
* Decreased infiltration and activity of inflammatory cells (e.g., eosinophils, leukocytes)
* Decreased edema of the airway mucosa (secondary to a decrease in vascular permeability)
