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Clin Phar II Lec > Asthma > Flashcards

Asthma Flashcards

1
Q

asthma word origin

A

“laboured breathing” (Greek)

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2
Q

asthma resolved before 7 years old

A

permanently resolved

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3
Q

asthma not resolved after 7 years old

A

permanently have asthma

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4
Q

asthma is a (homogenous/heterogenous) disease

A

heterogeneous

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5
Q

asthma is usually characterized by ___________________

A

chronic airway inflammation

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6
Q

inflammation is cause of swelling of ________ –> narrower airway

A

bronchi

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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

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8
Q

meaning of GINA

A

Global Initiative for Asthma

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9
Q

T/F
in asthma, coughing is a compensatory mechanism

A

T

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10
Q

oxygenation of blood occurs in the _________

A

alveoli

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11
Q

3 possible reasons for asthma

A
  1. inflammation
  2. bronchoconstriction
  3. hypersecretion of mucus
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12
Q

2 types of asthma

A
  • Extrinsic
  • Intrinsic
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13
Q

DETERMINE THE TYPE OF ASTHMA
triggered by allergen

A

extrinsic

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14
Q

DETERMINE THE TYPE OF ASTHMA
more common in children w/allergic history

A

extrinsic

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15
Q

DETERMINE THE TYPE OF ASTHMA
IgE production

A

extrinsic

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16
Q

DETERMINE THE TYPE OF ASTHMA
triggers: non-allergic factors, irritants, emotions, exercise, weather, pollution

A

intrinsic

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17
Q

DETERMINE THE TYPE OF ASTHMA
develops in adulthood

A

intrinsic

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18
Q

DETERMINE THE TYPE OF ASTHMA
triggers mediator release from mast cells

A

intrinsic

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19
Q

These are generally known as _______:
Mast cells
Eosinophils
TH2 cells
Basophils
Neutrophils
Platelets

A

Inflammatory cells

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20
Q

These are generally known as _______:
Histamine
Leukotrienes
Prostanoids
PAF
Kinins
Adenosine
Endothelins
Nitric oxide
Cytokines
Chemokines
Growth factors

A

mediators

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21
Q

These are generally known as _______:
Epithelial cells
Smooth muscle cells
Endothelial cells
Fibroblasts
Nerves

A

structural cells

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22
Q

Effects on airway during asthma:
Bronchospasm
Plasma _______
________ secretion
AHR
_______ changes

A

exudation, Mucus, Structural

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23
Q

in presence of allergen/non-allergen, increasing _________ cells or _______ in structural cells, increasing ________ (bronchoconstrictors) —> effect

A

inflammatory, change, mediators

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24
Q

T/F:
Clinical Manifestations of asthma differs from one another

A

T

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25
Q

early response

A

immediately after exposure

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26
Q

late response

A

6 to 10 hours after exposure

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27
Q

most common cause of asthma

A

viral infection

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28
Q

NSAIDs, aspirin

A

problematic drugs that can trigger asthma

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29
Q

T/F: increasing mediators (bronchodilators) lead to asthma

A

F - bronchoconstrictors

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30
Q

Asthma triad

A
  1. Wheezing
  2. Dyspnea
  3. Coughing
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31
Q

high-pitched whistling sound

A

Wheezing

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32
Q

T/F: asthma is often less evident at night or early morning

A

F - worse

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33
Q

confirmatory test or diagnosis for asthma

A

spirometry

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34
Q

Acc to GINA, patients with Clinical urgency, and a likely asthma diagnosis must be given

A

Empiric treatment with ICS and prn SABA

Review response

Diagnostic testing within 1-3 months

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35
Q

determine the degree of airway obstruction

A

Pulmonary function tests

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36
Q

Pulmonary function tests of asthmatic patients show reduced ______ and _____

A

FEV1/FVC ratio and PEF

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37
Q

PEF means

A

peak expiratory flow

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38
Q

FEV1 means

A

Forced expiratory volume in 1 second

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39
Q

measure of the FEV in the first second of exhalation

A

Forced expiratory volume in 1 second (FEV1)

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40
Q

patient inhales as deeply as possible and then exhales forcefully and
completely into a mouthpiece connected to a spirometer

A

Forced expiratory volume in 1 second (FEV1)

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41
Q

FVC meaning

A

Forced vital capacity

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42
Q

assessment of the maximum volume of air exhaled with maximum effort after maximum inspiration

A

Forced vital capacity (FVC)

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43
Q

total amt of air that can be forcefully exhaled; how much air
can the lungs hold

A

Forced vital capacity (FVC)

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44
Q

measures the
amount and rate of air a
person breathes in order to
diagnose illness or determine
progress in treatment

A

Spirometry

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45
Q

standard measurement
for lung function in asthma

A

Spirometry

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46
Q

apparatus in Spirometry

A

spirometer

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47
Q

normal FEV1/FVC ratio for adults

A

> 0.75 - 0.80 in healthy adults

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48
Q

normal FEV1/FVC ratio for children

A

> 0.90 in children

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49
Q

PEFR means

A

Peak Expiratory Flow Rate

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50
Q

Self assessment for the patient

A

Peak Expiratory Flow Rate (PEFR)

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51
Q

best measured in early morning, before medication administration

A

Peak Expiratory Flow Rate (PEFR)

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52
Q

Measures maximum flow rate that can be forced during expiration

A

Peak Expiratory Flow Rate (PEFR)

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53
Q

Peak Expiratory Flow Rate (PEFR) apparatus

A

Peak Flow Meter

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54
Q

Pulmonary function test that involves the whole body

A

Plethysmography

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55
Q

Allows to assess functional residual capacity (FRC pleth ) and primary airway resistance (sRaw) as primary measures

A

Plethysmography

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56
Q

primary measures in Plethysmography

A

functional residual capacity (FRC pleth ) and primary airway resistance (sRaw)

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57
Q

IDENTIFY DIAGNOSTIC TEST
In asthma = increased airway resistance, increased total lung capacity and residual volume, normal gas diffusion

A

Plethysmography

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58
Q

4 Pulmonary function tests

A
  • Forced expiratory volume in 1 second (FEV1)
  • Forced vital capacity (FVC)
  • Peak Expiratory Flow Rate (PEFR)
  • Plethysmography (Whole body)
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59
Q

Used to check severity of airway

A

Exhaled nitric oxide (FeNO)

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60
Q

noninvasive test measuring eosinophilic airway
inflammation.

A

Exhaled nitric oxide (FeNO)

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61
Q

It may also be useful in demonstrating insufficient anti- inflammatory therapy

A

Exhaled nitric oxide (FeNO)

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62
Q

to monitor adequacy of treatment & compliance

A

Exhaled nitric oxide (FeNO)

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63
Q

Exhaled nitric oxide (FeNO):

______ values indicate asthma type 2 airway inflammation, non-asthma conditions, late response to allergen or allergy

A

higher

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64
Q

Exhaled nitric oxide (FeNO):

______ values indicate smokers, bronchoconstriction, early phases of allergic reactions

A

lower

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65
Q

The long-term goals of asthma management are:

A
  1. symptom control
  2. risk reduction
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66
Q

Goals of asthma treatment:
to achieve good control of symptoms and
maintain normal activity levels

A

Symptom control

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67
Q

Goals of asthma treatment:
to minimize future risk of exacerbations, fixed airflow limitation and medication side-effects

A

Risk reduction

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68
Q

first-line treatment of asthma

A

β2-Agonists

69
Q

stimulate β2-receptors, activating adenyl cyclase –> increases cyclic adenosine monophosphate (cAMP)

A

β2-Agonists

70
Q

β2-Agonists
stimulate β2-receptors, activating ________ –> increases _________ (cAMP)

A

adenyl cyclase, cyclic adenosine monophosphate

71
Q

β2-Agonists
increase in cyclic adenosine monophosphate (cAMP) causes: (3)

A
  • bronchodilation,
  • improved mucociliary clearance
  • reduced inflammatory cell mediator release
72
Q

β2-Agonists with a duration of 3 to 6 hours

A

SABA

73
Q

β2-Agonists with a duration of over 12 hours

A

LABA

74
Q

albuterol

A

SABA

75
Q

terbutaline

A

SABA

76
Q

formoterol

A

LABA

77
Q

salmeterol

A

LABA

78
Q

duration of SABA

A

3 to 6 hours

79
Q

duration of LABA

A

over 12 hours

80
Q

β2-Agonists
T/F: to reduce the occurrence of ADE, given tru inhalation

A

T

81
Q

β2-Agonists
T/F: does not build-up tolerance

A

F - does

82
Q

Olodaterol

A

LABA

83
Q

Vilanterol

A

LABA

84
Q

Indacaterol

A

LABA

85
Q

prevent cholinergic nerve-induced bronchoconstriction and mucus secretion

A

Anticholinergics Muscarinic Receptor Antagonists

86
Q

Anticholinergics Muscarinic Receptor Antagonists
prevent cholinergic nerve-induced _______ and ________

A

bronchoconstriction and mucus secretion

87
Q

Anticholinergics Muscarinic Receptor Antagonists
Much (more/less) effective than β2 agonists in asthma therapy

A

less

88
Q

inhibit only the cholinergic reflex component bronchoconstriction

A

Anticholinergics Muscarinic Receptor Antagonists

89
Q

prevent all bronchoconstrictor mechanisms

A

β2-agonists

90
Q

only used as an additional bronchodilator in patients with asthma that is not controlled by other inhaled medications

A

Anticholinergics Muscarinic Receptor Antagonists

91
Q

atropine

A

Anticholinergics Muscarinic Receptor Antagonists

92
Q

Ipratropium bromide

A

Anticholinergics Muscarinic Receptor Antagonists

93
Q

T/F: Ipratropium bromide alone, will be enough to address symptoms of asthma

A

F - not enough

94
Q

xanthine alkaloid

A

Theophylline

95
Q

inhibit phosphodiesterase of airway smooth muscles –> cAMP

A

Theophylline

96
Q

Theophylline
inhibit ________ of airway smooth muscles –> cAMP

A

phosphodiesterase

97
Q

Theophylline
need (high/low) dose for bronchodilator effect

A

high

98
Q

was widely prescribed as an oral bronchodilator several years ago, especially as it was inexpensive.

A

Theophylline

99
Q

It has now fallen out of favor as side effects are common and inhaled β2 agonists are much more effective as bronchodilators.

A

Theophylline

100
Q

side effects: N&V, headache, diuresis, palpitations, cardiac arrhythmia, epileptic seizures, and death

A

Theophylline

101
Q

1,3-dimethylxanthine

A

theophylline

102
Q

3,7-dimethylxanthine

A

theobromine

103
Q

1,3,7-trimethylxanthine

A

caffeine

104
Q

reducing inflammatory cell numbers and their activation in the airways

A

Corticosteroids

105
Q

reduce eosinophils in the airways and sputum, and numbers of activated T-lymphocytes and surface mast cells in the airway mucosa.

A

Corticosteroids

106
Q

Major effect of corticosteroids:
* switch off the _______ of multiple activated genes that encode ________ proteins such as: cytokines, chemokines, adhesion molecules, and inflammatory enzymes.

A

transcription; inflammatory

107
Q

Increase expression of β2-receptors

A

Corticosteroids

108
Q

Corticosteroids
reducing _________ numbers and their activation in the airways

A

inflammatory cell

109
Q

causes decrease in encoded cytokines, chemokines, adhesion molecules, and inflammatory enzymes

A

Corticosteroids

110
Q

Corticosteroids
reduce _______ in the airways and sputum, and numbers of activated __________ and _________ cells in the airway mucosa.

A

eosinophils; T-lymphocytes; surface mast

111
Q

fluticasone

A

Inhaled Corticosteroids (ICS)

112
Q

budesonide

A

Inhaled Corticosteroids (ICS)

113
Q

are by far the most effective
controllers for asthma

A

Inhaled Corticosteroids (ICS)

114
Q

their early use has revolutionized asthma therapy, effective in preventing asthma symptoms

A

Inhaled Corticosteroids (ICS)

115
Q

hydrocortisone

A

Systemic Corticosteroids

116
Q

methylprednisolone

A

Systemic Corticosteroids

117
Q

treatment of acute severe asthma

A

Systemic Corticosteroids

118
Q

prednisolone

A

Oral Corticosteroids

119
Q

prednisone

A

Oral Corticosteroids

120
Q

treat acute exacerbations of asthma

A

Oral Corticosteroids

121
Q

best Corticosteroids due to localized effect

A

ICS

122
Q

ICS are given ______ daily but some are given once daily

A

twice

123
Q

Potent bronchoconstrictors:
* Microvascular leakage
* increase eosinophilic inflammation through the activation of cys-LT 1 –receptors

A

Cysteinyl leukotrienes (Cys-LTs)

124
Q

Antileukotrienes:
inflammatory mediators are produced predominantly by ________ and, to a lesser extent, _______ in asthma.

A

mast cells; eosinophils

125
Q

montelukast

A

Antileukotrienes

126
Q

zafirlukast

A

Antileukotrienes

127
Q

Block cys-LT 1 -receptors and provide modest clinical benefit in asthma.

A

Antileukotrienes

128
Q

Antileukotrienes:
Block _________ and provide modest clinical benefit in asthma.

A

cys-LT 1 -receptors

129
Q

less effective than ICS in controlling asthma and have less effect on airway inflammation

A

Antileukotrienes

130
Q

Given orally once or twice daily and are well tolerated

A

Antileukotrienes

131
Q

Antileukotrienes:
Given _______ once or twice daily and are well tolerated

A

orally

132
Q

Cromolyn sodium

A

Cromones

133
Q

nedocromil sodium

A

Cromones

134
Q

inhibit mast cell and sensory nerve activation –> effective in blocking trigger-induced asthma

A

Cromones

135
Q

Cromones:
inhibit ______ and _____ activation –> effective in blocking trigger-induced asthma

A

mast cell and

136
Q

Cromones:
inhibit mast cell and sensory nerve activation –> effective in blocking ________-induced asthma

A

trigger

137
Q

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.

A

Cromones

138
Q

T/F: Cromones are short acting with little benefit

A

T

139
Q

useful for patients with coexisting allergic rhinitis; however, their role in the treatment of asthma remains unclear.

A

Antihistamines

140
Q

compete with histamine for H1 -receptor sites on effector cells and thus help prevent the histamine-mediated responses that influence asthma.

A

Antihistamines

141
Q

Antihistamines:
compete with _________ for H1 -receptor sites on effector cells and thus help prevent the _______-mediated responses that influence asthma.

A

histamine; histamine

142
Q

Antihistamines:
compete with histamine for ___ -receptor sites on effector cells and thus help prevent the histamine-mediated responses that influence asthma.

A

H1

143
Q

Magnesium sulfate is administered ________

A

intravenously

144
Q

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

A

Magnesium sulfate

145
Q

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

A

hypomagnesemic

146
Q

Research has suggested that _____ may reduce admission rate and improve FEV1 in severe, acute asthma exacerbations and in stable, chronic asthma.

A

magnesium

147
Q

as a stand-alone medication is indicated for anti-convulsant

A

Magnesium sulfate

148
Q

using injected extracts of pollens or house dust mites has not been very effective in controlling asthma and may cause anaphylaxis

A

Immunotherapy

149
Q

slowly expose px to their trigger factors to lessen the trigger

A

Immunotherapy

150
Q

T/F: Immunotherapy has been shown to be effective

A

F

151
Q

Xolair

A

Omalizumab

152
Q

monoclonal antibody; very expensive

A

Omalizumab

153
Q

T/F: Omalizumab is used as an add-on therapy

A

T

154
Q

is an anti-IgE compound used for severe asthma and concurrent allergies

A

Omalizumab

155
Q

Omalizumab is an anti-IgE compound used for (acute/severe) asthma and concurrent allergies

A

severe

156
Q

T/F: Omalizumab is shown to reduce the number of exacerbations in patients with severe asthma and may improve asthma control

A

T

157
Q

It is usually administered twice monthly as an injection in a specialty physician’s office.

A

Omalizumab

158
Q

Omalizumab is usually administered _________ monthly as an injection in a specialty physician’s office.

A

twice

159
Q

T/F: Life-threatening anaphylaxis has often been reported with Omalizumab

A

F - rarely

160
Q

Pharmacologic options for treatment of Asthma: (3)

A

❑ Controller/ Preventers
❑ Reliever medication
❑ Add-on therapies

161
Q

Medications For symptom relief, or before exercise or allergen exposure

A

Reliever

162
Q

Medications that may also be given during an asthma attack to relieve bronchospasm

A

Reliever

163
Q

Function: targets both domains of asthma control (symptom control and future risk)

A

Controller/Preventers

164
Q

Mostly used for ICS-containing treatment

A

Controller/Preventers

165
Q

Medications to to control symptoms, reduce airway inflammation, reduce future risks

A

Controller/Preventers

166
Q

Frequency: regularly scheduled, e.g. twice daily

A

Maintenance treatment

167
Q

Medications for patients on optimized controller medications with treatment of modifiable risk
factor

A

Add-on Therapies

168
Q

Medications for patients with severe symptoms or persistent exacerbations

A

Add-on Therapies

169
Q

Medications that are given when symptoms of patients are not well controlled

A

Add-on Therapies

Clin Phar II Lec (3 decks)

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