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BMS 615 Cardiovascular > Test 3: Wk13: 1 Airway Pharmacology - Salisbury > Flashcards

Test 3: Wk13: 1 Airway Pharmacology - Salisbury Flashcards

1
Q

treatment of choice for asthma

A

B2 adrenergic agonists

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2
Q

B2 adrenergic agonists are used for

A

rescue bronchodilators in asthma

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3
Q

3 Selective B2 Agonists

A

albuterol
pirbuterol
terbutaline

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4
Q

Long acting B2 agonists function

A

bronchodilation and bronchoprotection for more than 12 hrs

dose 2x daily

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5
Q

3 once daily B2 agonists

A

indacaterol
vilanterol
olodaterol

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6
Q

B2 agonists direct bronchodilator MOA

A

B2 expressed on bronchial SMCs
Gs adenylyl cyclase CAMP
bronchial SM relaxation

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7
Q

B2 Agonists Indirect bronchodilator MOA

A

Gs adenylyl cyclase cAMP PKA
mast cells decrease mediator release
decrease ACH release by cholinergic nerves

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8
Q

B2 Agonists anti-inflammatory effects

A

decrease mast cell mediator release and microvascular leakage

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9
Q

do B2 agonists help with chronic inflammation

A

no, corticosteroids still needed

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10
Q

SABAs stands for

A

Inhaled short acting B2 Agonists

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11
Q

Oral B2 agonists

A

increased side effects
resistant to COMT and MAO
useful in pts who cant use MDI

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12
Q

3 LABAs that have Bronchodilator action of more than 12 h and also protect
against bronchoconstriction for a similar period

A

salmeterol
formoterol
arformoterol

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13
Q

3 LABAs that have Duration of over 24 h (effective in COPD)

A

Indacaterol, vilanterol, and olodaterol

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14
Q

— can be combined with anticholinergics or ICSs

A

LABAs

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15
Q

can LABAs be used alone in asthma

A

no, they do not treat underlying chronic inflammation

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16
Q

in Asthma LABAs must be used with

A

ICSs

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17
Q

2 B2 Combination inhalers

A

fluticasone/salmeterol

budesonide/formoterol

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18
Q

Combination inhalers ensure — and allows for

A

Ensures they are delivered simultaneously to the same
cells in the airway this allows beneficial molecular
interactions between LABAs and ICS to occur.

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19
Q

ICS upregulate — receptors on bronchial SMCs

A

B2

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20
Q

Combination inhalers are used in

A

asthma and COPD

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21
Q

B2 agonists tolerance

A

occurs in non airway tissues

in asthmatic pts tolerance to the bronchodilator effects B2 agonists has not usually been found

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22
Q

5 Side effects of B2 agonists

A 
Muscle tremor
Tachycardia
Hypokalemia
Restlessness
Metabolic effects
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23
Q

Theophylline therapeutic index

A

narrow

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24
Q

Theophylline MOA (4)

A

Nonselective phosphodiesterase (PDE) inhibitor

Adenosine receptor antagonism

interleukin 10 release

inhibition of trscrptn factor NF-kB

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25
Q

Theophylline PDE inhibitor MOA

A 
Nonselective phosphodiesterase (PDE) inhibitor (↑ cAMP and cGMP→ smooth muscle cell relaxation,
PDE3, PDE4 and PDE5
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26
Q

Theophylline affects multiple on eosinophils

A

decrease number

increase apoptosis

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27
Q

Theophylline affects multiple on T-lymphocyte

A

decrease cytokines

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28
Q

Theophylline affects on Mast Cells

A

decrease mediators

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29
Q

Theophylline affects multiple on macrophages

A

decrease cytokines

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30
Q

Theophylline affects on Airway SMCs

A

bronchodilation

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31
Q

Theophylline affects on endothelial cells

A

decrease leak

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32
Q

Theophylline affects on respiratory skeletal muscles

A

possibly increase strength

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33
Q

Theophylline therapeutic range

A

5-15 mg/L

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34
Q

Theophylline metabolized by

A

lover, CYP1A2

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35
Q

Increased Clearance of Theophylline

A

CYP1A2 induction

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36
Q

Decreased Clearance of Theophylline

A

CYP1A2 inhibition

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37
Q

Theophylline Asthma

A

Reserved for patients who fail to respond to, or are
intolerant of, ꞵagonists.

Add to low dose ICS (better response than doubling the dose of
ICS)

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38
Q

Theophylline COPD:

A

Still used as a bronchodilator

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39
Q

Theophylline side effects (6)

A 
Nausea and vomiting
Headaches
Gastric discomfort
Diuresis
Cardiac arrythmias
Epileptic seizures
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40
Q

Muscarinic Cholinergic Antagonists Inhibit —receptors on bronchial smooth muscle and lead to a reduction in the — pathway

A

M3

M3 Gq PLC IP3 Ca2+

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41
Q

Muscarinic Receptor Antagonists clinical effects

A

reduce bronchoconstriction

reduce traheobronchial mucus secretion

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42
Q

Cholinergic antagonists have — effect on mast cells or the chronic inflammatory response

A

little

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43
Q

Muscarinic Receptor Antagonists Asthma:

A

anticholinergic agents are less effective than ꞵ2 agonists

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44
Q

Muscarinic Receptor Antagonists COPD:

A

anticholinergic drugs are as effective or more effective than ꞵ2 agonists

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45
Q

Anticholinergic drugs have an additive effect when combined with —

A

ꞵ2 agonists

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46
Q

3 Therapeutic Choices for Muscarinic Receptor Antagonists

A

Ipratropium (MDI)

Tiotropium (DPI)

Glycopyrronium bromide (DPI)

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47
Q

Muscarinic Receptor Antagonists Combination Inhalers

A

anticholinergic and ꞵ2 agonists:

albuterol/ipratropium

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48
Q

Muscarinic Receptor Antagonists Adverse effects:

A

generally well tolerated

systemic effects uncommon

bitter taste w/ ipratropium

Nebulized ipratropium may precipitate glaucoma

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49
Q

— has revolutionized the treatment of chronic

asthma

A

ICSs

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50
Q

1st line therapy for asthma

51
Q

ICSs in COPD

A

much less effective in COPD and should only be
used in patients with severe disease who have frequent
exacerbations.

52
Q

Corticosteroids MOA

A

anti-inflammatory effects

Ligand activated transcription factor

53
Q

Corticosteroids effect on eosinophils

A

decease numbers

increase apoptosis

54
Q

Corticosteroids effect on T-lymphocytes

A

decease cytokinesis

55
Q

Corticosteroids effect on mast cells

A

decrease numbers

56
Q

Corticosteroids effect on macrophages

A

decrease cytokines

57
Q

Corticosteroids effect on dendritic cells

A

decrease numbers

58
Q

Corticosteroids effect on epithelial cells

A

decrease cytokines

decrease mediators

59
Q

Corticosteroids effect on endothelial cells

A

decrease leak

60
Q

Corticosteroids effect on airway SMCs

A

increase B2 receptors

decrease cytokines

61
Q

Corticosteroids effect on mucus glands

A

decrease mucus secretion

62
Q

Corticosteroids have — direct effect on contractile responses of airway smooth muscle thus they are not rescue bronchodilator agents for asthma

A

no

they are not rescue bronchodilator agents for asthma

63
Q

improvement in lung function after ICSs is due to (3)

A

↓ chronic airway inflammation
↓ edema
↓ airway hyperresponsiveness.

64
Q

ICSs Rapid anti inflammatory effects

A

reduce airway hyperresponsiveness and inflammatory

mediator concentrations within a few hours.

65
Q

ICSs achieve maximal effects on airway in

A

several weeks or months

66
Q

Corticosteroids suppress inflammation in the airways but

A

do not cure the underlying disease.

67
Q

Corticosteroids potentiate the effects of β agonists on bronchial smooth muscle and

A

prevent and reverse β receptor desensitization in airways.

68
Q

Corticosteroids increase the transcription

A

of the β 2 receptor gene in human lung tissue

69
Q

— reduces ICSs from reaching systemic circulation

A

spacer chamer

70
Q

ICSs on COPD

A

respond if they have asthma

no effect on progression

no effect on mortality

reduce exacerbations in severe COPD

71
Q

Intravenous corticosteroids:

A

A cute asthma if lung function is less than 30%
predicted and in patients who show no significant
improvement with nebulized β 2 agonist.

72
Q

— is the steroid of choice because it has

A

Hydrocortisone
is the steroid of choice because it has
the most rapid onset (5 6 h after administration),
compared with 8 h with prednisolone.

73
Q

Local Side Effects of ICSs

A

Dysphonia

Oropharyngeal candidiasis

Cough

74
Q

Corticosteroids Systemic effects - long term oral corticosteroid
treatment (7)

A

HPA Axis suppression

fluid retention and wt gain

capillary fragility - hypertension

diabetes, cataracts, psychosis

Metabolic abnormalities

75
Q

Corticosteroids Therapeutic Choices

A

beclomethasone, triamcinolone, flunisolide, budesonide,
hemihydrate, fluticasone propionate, mometasone
furoate, ciclesonide , and fluticasone furoate.

76
Q

2 Cromones drugs

A

Cromolyn, nedocromil

77
Q

Cromones uses

A

Prophylactic anti inflammatory agents (inhalation delivery)

78
Q

Cromones action

A

mast cell stabilizers

79
Q

oral PDE4 inhibitor

A

Rofumilast

80
Q

Phosphodiesterase Inhibitor action

A

relax smooth muscle and inhibit inflammatory cells by increasing the levels of cAMP

81
Q

Roflumilast approved for

A

severe COPD

82
Q

Roflumilast side effects

A

diarrhea, headaches and nausea (limits its efficacy)

83
Q

Mediator antagonists

A

antihistamines

84
Q

Antihistamines evidence

A

since multiple mediators in action, inhibiting just H1 alone isnt enough to have an effect

85
Q

Cys-LTs cause

A

they induce bronchoconstriction, airway
hyperresponsiveness, plasma exudation, mucus
secretion, and eosinophilic inflammation

86
Q

5-LO Inhibitors Drug and MOA

A

Zileuton; inhibits 5-lipoxyfenase

87
Q

LT antagonists (3)

A

Montelukast
Pranlukast
Zafirlukast

88
Q

Antileukotrienes indication

A

mild to moderate asthma: improved lung function and reduced the use of a β 2 agonist

89
Q

Antileukotrienes compared to ICSs

A

Antileukotrienes are less effective

90
Q

Antileukotrienes is a benefit in

A

allergic rhinitis

91
Q

Antileukotrienes use in children

92
Q

Antileukotrienes and aspirin sensitivity

A

Should be beneficial in patients with aspirin sensitive

asthma (block the airway response to aspirin challenge)

93
Q

Antileukotrienes and exercise induced asthma

94
Q

Antileukotrienes in COPD

A

not effective

95
Q

Zileuton, zafirlukast and montelukast adverse effects

A

rare cases hepatic dysfunction

Churg Strass syndrome w/ zafirlukast and montelukast

96
Q

Immunomodulatory Therapies

A

Anti IgE receptor therapy

97
Q

is a humanized monoclonal antibody that binds

free IgE

A

Omalizumab

98
Q

Anti IgE receptor therapy prevents

A

prevents the binding of IgE to high affinity IgE receptors
(FcεR1) on mast cells and thus prevents their activation by
allergens

99
Q

Omalizumab used in

A

pts w/ severe asthma

100
Q

Omalizumab reduces requirement of

A

oral and or ICSs

101
Q

Omalizumab reduces

A

asthma exacerbations

102
Q

Allergic Rhinitis tx

A

Antihistamines

Ipratropium

Adrenergic agonists (Oxymetazoline, Phenylephrine,
Pseudoephedrine)

Montelukast

Corticosteroids (nasal spray)

103
Q

Antitussives

104
Q

Opioids are agonists of

A

Agonists of the mu (µ) opioid receptor.

105
Q

Opioids mechanism

A

μ opioid receptors in

medullary cough center to suppress cough

106
Q

— opioid is commonly used to suppress cough

107
Q

Opioids Adverse effects

A

sedation, constipation, opioid induced respiratory depression

108
Q

Dextromethorphan

A

Antitussive

Centrally active NMDA antagonist

109
Q

Dextromethorphan acts in

A

Acts in medullary cough center to suppress cough

110
Q

Dextromethorphan adverse effects

A

Hallucinations at high concentrations

abuse potential

111
Q

BENZONATATE

A

Antitussives
Inhibits stretch or cough receptors of vagal afferent fibers, which are located in the respiratory passages, lungs, and pleura

112
Q

Suppresses cough through a peripheral action.

A

BENZONATATE

113
Q

BENZONATATE adverse effect

A

Adverse effects: Dizziness

114
Q

Expectorant

A

Guaifenesin

115
Q

Guaifenesin action

A

•

Reduces the viscosity of mucus in airway

116
Q

Guaifenesin adverse effect

A

Adverse effect: Nausea

117
Q

Mucolytics (2)

A

N Acetylcysteine

Dornase Alfa

118
Q

N Acetylcysteine action

A

Acetylcysteine has a free sulfhydryl group that interacts
with disulfide bonds in mucus proteins (“opens up”
mucus proteins reduces Airway mucus viscosity)

119
Q

N Acetylcysteine is also useful for treating

A

cystic fibrosis

120
Q

N Acetylcysteine administration

121
Q

Dornase Alfa action

A

Is a DNase that reduces Airway mucus viscosity in patients with cystic fibrosis by breaking the long extracellular DNA molecules in mucus into smaller DNA fragments

122
Q

Dornase Alfa indication

A

cystic fibrosis

123
Q

Dornase Alfa adverse effect

BMS 615 Cardiovascular (49 decks)

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