Asthma Flashcards
1
Q
asthma word origin
A
“laboured breathing” (Greek)
2
Q
asthma resolved before 7 years old
A
permanently resolved
3
Q
asthma not resolved after 7 years old
A
permanently have asthma
4
Q
asthma is a (homogenous/heterogenous) disease
A
heterogeneous
5
Q
asthma is usually characterized by ___________________
A
chronic airway inflammation
6
Q
inflammation is cause of swelling of ________ –> narrower airway
A
bronchi
7
Q
It is defined by the history of respiratory symptoms such as _______, _________, _________ and _______ that vary over time and in intensity, together with
variable _________ airflow limitation
A
wheeze, shortness of breath, chest tightness and cough; expiratory
8
Q
meaning of GINA
A
Global Initiative for Asthma
9
Q
T/F
in asthma, coughing is a compensatory mechanism
A
T
10
Q
oxygenation of blood occurs in the _________
A
alveoli
11
Q
3 possible reasons for asthma
A
- inflammation
- bronchoconstriction
- hypersecretion of mucus
12
Q
2 types of asthma
A
- Extrinsic
- Intrinsic
13
Q
DETERMINE THE TYPE OF ASTHMA
triggered by allergen
A
extrinsic
14
Q
DETERMINE THE TYPE OF ASTHMA
more common in children w/allergic history
A
extrinsic
15
Q
DETERMINE THE TYPE OF ASTHMA
IgE production
A
extrinsic
16
Q
DETERMINE THE TYPE OF ASTHMA
triggers: non-allergic factors, irritants, emotions, exercise, weather, pollution
A
intrinsic
17
Q
DETERMINE THE TYPE OF ASTHMA
develops in adulthood
A
intrinsic
18
Q
DETERMINE THE TYPE OF ASTHMA
triggers mediator release from mast cells
A
intrinsic
19
Q
These are generally known as _______:
Mast cells
Eosinophils
TH2 cells
Basophils
Neutrophils
Platelets
A
Inflammatory cells
20
Q
These are generally known as _______:
Histamine
Leukotrienes
Prostanoids
PAF
Kinins
Adenosine
Endothelins
Nitric oxide
Cytokines
Chemokines
Growth factors
A
mediators
21
Q
These are generally known as _______:
Epithelial cells
Smooth muscle cells
Endothelial cells
Fibroblasts
Nerves
A
structural cells
22
Q
Effects on airway during asthma:
Bronchospasm
Plasma _______
________ secretion
AHR
_______ changes
A
exudation, Mucus, Structural
23
Q
in presence of allergen/non-allergen, increasing _________ cells or _______ in structural cells, increasing ________ (bronchoconstrictors) —> effect
A
inflammatory, change, mediators
24
Q
T/F:
Clinical Manifestations of asthma differs from one another
A
T
25
early response
immediately after exposure
26
late response
6 to 10 hours after exposure
27
most common cause of asthma
viral infection
28
NSAIDs, aspirin
problematic drugs that can trigger asthma
29
T/F: increasing mediators (bronchodilators) lead to asthma
F - bronchoconstrictors
30
Asthma triad
1. Wheezing
2. Dyspnea
3. Coughing
31
high-pitched whistling sound
Wheezing
32
T/F: asthma is often less evident at night or early morning
F - worse
33
confirmatory test or diagnosis for asthma
spirometry
34
Acc to GINA, patients with Clinical urgency, and a likely asthma diagnosis must be given
Empiric treatment with ICS and prn SABA
Review response
Diagnostic testing within 1-3 months
35
determine the degree of airway obstruction
Pulmonary function tests
36
Pulmonary function tests of asthmatic patients show reduced ______ and _____
FEV1/FVC ratio and PEF
37
PEF means
peak expiratory flow
38
FEV1 means
Forced expiratory volume in 1 second
39
measure of the FEV in the first second of exhalation
Forced expiratory volume in 1 second (FEV1)
40
patient inhales as deeply as possible and then exhales forcefully and
completely into a mouthpiece connected to a spirometer
Forced expiratory volume in 1 second (FEV1)
41
FVC meaning
Forced vital capacity
42
assessment of the maximum volume of air exhaled with maximum effort after maximum inspiration
Forced vital capacity (FVC)
43
total amt of air that can be forcefully exhaled; how much air
can the lungs hold
Forced vital capacity (FVC)
44
measures the
amount and rate of air a
person breathes in order to
diagnose illness or determine
progress in treatment
Spirometry
45
standard measurement
for lung function in asthma
Spirometry
46
apparatus in Spirometry
spirometer
47
normal FEV1/FVC ratio for adults
> 0.75 - 0.80 in healthy adults
48
normal FEV1/FVC ratio for children
> 0.90 in children
49
PEFR means
Peak Expiratory Flow Rate
50
Self assessment for the patient
Peak Expiratory Flow Rate (PEFR)
51
best measured in early morning, before medication administration
Peak Expiratory Flow Rate (PEFR)
52
Measures maximum flow rate that can be forced during expiration
Peak Expiratory Flow Rate (PEFR)
53
Peak Expiratory Flow Rate (PEFR) apparatus
Peak Flow Meter
54
Pulmonary function test that involves the whole body
Plethysmography
55
Allows to assess functional residual capacity (FRC pleth ) and primary airway resistance (sRaw) as primary measures
Plethysmography
56
primary measures in Plethysmography
functional residual capacity (FRC pleth ) and primary airway resistance (sRaw)
57
IDENTIFY DIAGNOSTIC TEST
In asthma = increased airway resistance, increased total lung capacity and residual volume, normal gas diffusion
Plethysmography
58
4 Pulmonary function tests
- Forced expiratory volume in 1 second (FEV1)
- Forced vital capacity (FVC)
- Peak Expiratory Flow Rate (PEFR)
- Plethysmography (Whole body)
59
Used to check severity of airway
Exhaled nitric oxide (FeNO)
60
noninvasive test measuring eosinophilic airway
inflammation.
Exhaled nitric oxide (FeNO)
61
It may also be useful in demonstrating insufficient anti- inflammatory therapy
Exhaled nitric oxide (FeNO)
62
to monitor adequacy of treatment & compliance
Exhaled nitric oxide (FeNO)
63
Exhaled nitric oxide (FeNO):
______ values indicate asthma type 2 airway inflammation, non-asthma conditions, late response to allergen or allergy
higher
64
Exhaled nitric oxide (FeNO):
______ values indicate smokers, bronchoconstriction, early phases of allergic reactions
lower
65
The long-term goals of asthma management are:
1. symptom control
2. risk reduction
66
Goals of asthma treatment:
to achieve good control of symptoms and
maintain normal activity levels
Symptom control
67
Goals of asthma treatment:
to minimize future risk of exacerbations, fixed airflow limitation and medication side-effects
Risk reduction
68
first-line treatment of asthma
β2-Agonists
69
stimulate β2-receptors, activating adenyl cyclase --> increases cyclic adenosine monophosphate (cAMP)
β2-Agonists
70
β2-Agonists
stimulate β2-receptors, activating ________ --> increases _________ (cAMP)
adenyl cyclase, cyclic adenosine monophosphate
71
β2-Agonists
increase in cyclic adenosine monophosphate (cAMP) causes: (3)
* bronchodilation,
* improved mucociliary clearance
* reduced inflammatory cell mediator release
72
β2-Agonists with a duration of 3 to 6 hours
SABA
73
β2-Agonists with a duration of over 12 hours
LABA
74
albuterol
SABA
75
terbutaline
SABA
76
formoterol
LABA
77
salmeterol
LABA
78
duration of SABA
3 to 6 hours
79
duration of LABA
over 12 hours
80
β2-Agonists
T/F: to reduce the occurrence of ADE, given tru inhalation
T
81
β2-Agonists
T/F: does not build-up tolerance
F - does
82
Olodaterol
LABA
83
Vilanterol
LABA
84
Indacaterol
LABA
85
prevent cholinergic nerve-induced bronchoconstriction and mucus secretion
Anticholinergics Muscarinic Receptor Antagonists
86
Anticholinergics Muscarinic Receptor Antagonists
prevent cholinergic nerve-induced _______ and ________
bronchoconstriction and mucus secretion
87
Anticholinergics Muscarinic Receptor Antagonists
Much (more/less) effective than β2 agonists in asthma therapy
less
88
inhibit only the cholinergic reflex component bronchoconstriction
Anticholinergics Muscarinic Receptor Antagonists
89
prevent all bronchoconstrictor mechanisms
β2-agonists
90
only used as an additional bronchodilator in patients with asthma that is not controlled by other inhaled medications
Anticholinergics Muscarinic Receptor Antagonists
91
atropine
Anticholinergics Muscarinic Receptor Antagonists
92
Ipratropium bromide
Anticholinergics Muscarinic Receptor Antagonists
93
T/F: Ipratropium bromide alone, will be enough to address symptoms of asthma
F - not enough
94
xanthine alkaloid
Theophylline
95
inhibit phosphodiesterase of airway smooth muscles --> cAMP
Theophylline
96
Theophylline
inhibit ________ of airway smooth muscles --> cAMP
phosphodiesterase
97
Theophylline
need (high/low) dose for bronchodilator effect
high
98
was widely prescribed as an oral bronchodilator several years ago, especially as it was inexpensive.
Theophylline
99
It has now fallen out of favor as side effects are common and inhaled β2 agonists are much more effective as bronchodilators.
Theophylline
100
side effects: N&V, headache, diuresis, palpitations, cardiac arrhythmia, epileptic seizures, and death
Theophylline
101
1,3-dimethylxanthine
theophylline
102
3,7-dimethylxanthine
theobromine
103
1,3,7-trimethylxanthine
caffeine
104
reducing inflammatory cell numbers and their activation in the airways
Corticosteroids
105
reduce eosinophils in the airways and sputum, and numbers of activated T-lymphocytes and surface mast cells in the airway mucosa.
Corticosteroids
106
Major effect of corticosteroids:
* switch off the _______ of multiple activated genes that encode ________ proteins such as: cytokines, chemokines, adhesion molecules, and inflammatory enzymes.
transcription; inflammatory
107
Increase expression of β2-receptors
Corticosteroids
108
Corticosteroids
reducing _________ numbers and their activation in the airways
inflammatory cell
109
causes decrease in encoded cytokines, chemokines, adhesion molecules, and inflammatory enzymes
Corticosteroids
110
Corticosteroids
reduce _______ in the airways and sputum, and numbers of activated __________ and _________ cells in the airway mucosa.
eosinophils; T-lymphocytes; surface mast
111
fluticasone
Inhaled Corticosteroids (ICS)
112
budesonide
Inhaled Corticosteroids (ICS)
113
are by far the most effective
controllers for asthma
Inhaled Corticosteroids (ICS)
114
their early use has revolutionized asthma therapy, effective in preventing asthma symptoms
Inhaled Corticosteroids (ICS)
115
hydrocortisone
Systemic Corticosteroids
116
methylprednisolone
Systemic Corticosteroids
117
treatment of acute severe asthma
Systemic Corticosteroids
118
prednisolone
Oral Corticosteroids
119
prednisone
Oral Corticosteroids
120
treat acute exacerbations of asthma
Oral Corticosteroids
121
best Corticosteroids due to localized effect
ICS
122
ICS are given ______ daily but some are given once daily
twice
123
Potent bronchoconstrictors:
* Microvascular leakage
* increase eosinophilic inflammation through the activation of cys-LT 1 –receptors
Cysteinyl leukotrienes (Cys-LTs)
124
Antileukotrienes:
inflammatory mediators are produced predominantly by ________ and, to a lesser extent, _______ in asthma.
mast cells; eosinophils
125
montelukast
Antileukotrienes
126
zafirlukast
Antileukotrienes
127
Block cys-LT 1 -receptors and provide modest clinical benefit in asthma.
Antileukotrienes
128
Antileukotrienes:
Block _________ and provide modest clinical benefit in asthma.
cys-LT 1 -receptors
129
less effective than ICS in controlling asthma and have less effect on airway inflammation
Antileukotrienes
130
Given orally once or twice daily and are well tolerated
Antileukotrienes
131
Antileukotrienes:
Given _______ once or twice daily and are well tolerated
orally
132
Cromolyn sodium
Cromones
133
nedocromil sodium
Cromones
134
inhibit mast cell and sensory nerve activation --> effective in blocking trigger-induced asthma
Cromones
135
Cromones:
inhibit ______ and _____ activation --> effective in blocking trigger-induced asthma
mast cell and
136
Cromones:
inhibit mast cell and sensory nerve activation --> effective in blocking ________-induced asthma
trigger
137
very safe and were popular in the treatment of childhood asthma, although now low doses of ICS are preferred as they are more effective and have a proven safety profile.
Cromones
138
T/F: Cromones are short acting with little benefit
T
139
useful for patients with coexisting allergic rhinitis; however, their role in the treatment of asthma remains unclear.
Antihistamines
140
compete with histamine for H1 -receptor sites on effector cells and thus help prevent the histamine-mediated responses that influence asthma.
Antihistamines
141
Antihistamines:
compete with _________ for H1 -receptor sites on effector cells and thus help prevent the _______-mediated responses that influence asthma.
histamine; histamine
142
Antihistamines:
compete with histamine for ___ -receptor sites on effector cells and thus help prevent the histamine-mediated responses that influence asthma.
H1
143
Magnesium sulfate is administered ________
intravenously
144
may be useful in some patients because of its modest ability to cause bronchodilation. When administered intravenously, it also improves respiratory muscle strength in hypomagnesemic patients
Magnesium sulfate
145
Magnesium sulfate:
may be useful in some patients because of its modest ability to cause bronchodilation. When administered intravenously, it also improves respiratory muscle strength in _________ patients
hypomagnesemic
146
Research has suggested that _____ may reduce admission rate and improve FEV1 in severe, acute asthma exacerbations and in stable, chronic asthma.
magnesium
147
as a stand-alone medication is indicated for anti-convulsant
Magnesium sulfate
148
using injected extracts of pollens or house dust mites has not been very effective in controlling asthma and may cause anaphylaxis
Immunotherapy
149
slowly expose px to their trigger factors to lessen the trigger
Immunotherapy
150
T/F: Immunotherapy has been shown to be effective
F
151
Xolair
Omalizumab
152
monoclonal antibody; very expensive
Omalizumab
153
T/F: Omalizumab is used as an add-on therapy
T
154
is an anti-IgE compound used for severe asthma and concurrent allergies
Omalizumab
155
Omalizumab is an anti-IgE compound used for (acute/severe) asthma and concurrent allergies
severe
156
T/F: Omalizumab is shown to reduce the number of exacerbations in patients with severe asthma and may improve asthma control
T
157
It is usually administered twice monthly as an injection in a specialty physician’s office.
Omalizumab
158
Omalizumab is usually administered _________ monthly as an injection in a specialty physician’s office.
twice
159
T/F: Life-threatening anaphylaxis has often been reported with Omalizumab
F - rarely
160
Pharmacologic options for treatment of Asthma: (3)
❑ Controller/ Preventers
❑ Reliever medication
❑ Add-on therapies
161
Medications For symptom relief, or before exercise or allergen exposure
Reliever
162
Medications that may also be given during an asthma attack to relieve bronchospasm
Reliever
163
Function: targets both domains of asthma control (symptom control and future risk)
Controller/Preventers
164
Mostly used for ICS-containing treatment
Controller/Preventers
165
Medications to to control symptoms, reduce airway inflammation, reduce future risks
Controller/Preventers
166
Frequency: regularly scheduled, e.g. twice daily
Maintenance treatment
167
Medications for patients on optimized controller medications with treatment of modifiable risk
factor
Add-on Therapies
168
Medications for patients with severe symptoms or persistent exacerbations
Add-on Therapies
169
Medications that are given when symptoms of patients are not well controlled
Add-on Therapies
