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Pharm Kay Exam 2 > Asthma > Flashcards

Asthma Flashcards

1
Q

definition of asthma

A

increase responsiveness of trachea and bronchi to various stimuli causing reversible airway narrowing

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2
Q

4 main asthma triggers

A

control status
H/o exacerbation
enviornmental triggers
seasonal, genetic, immunologic RF

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3
Q

what are the enviornmental triggers of asthma

A 
exercise
smoke
cold-induced
occupational
drug induced--B-blockers, ASA/NSAID
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4
Q

what are the seasonal/genetic/immunologic triggers

A 
URI
recurrent sinus infection
atopic asthma
allergic rhinitis
PND
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5
Q

what is the early phase of asthma attack

A

bronchospasm + mucosal edema after initiating event
followed by wheeze, SOB, cough, edema
within 1-2hrs

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6
Q

what do early phase asthma attacks respond to

A

MDI

nebulized bronchodilators

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7
Q

what is the late phase asthma attack

A

mucosal inflammation & increase mucous production

within 4-6hrs

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8
Q

what do late phase asthma attacks respond to

A

anti-inflammatory (Steroids)

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9
Q

what are asthma related deaths due to?

A 
lack of access
lack of AAP
underuse of steroid
overuse of brochodilator
underestimation of severity
lack of measure of airway obstruction
non-adherence
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10
Q

if you are using a SABA >2 times a week what is indicated

A

anti-inflammatory therapy

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11
Q

what are the most effective anti-inflammatory agents

A

ICS

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12
Q

what can be added to ICS if they aren’t enough

A

LAMA

LABA

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13
Q

what is the final step when all common therapies have been attempted

A

immunologic and avoidance of triggers

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14
Q

why don’t we use epinephrine & isoproterenol?

A

cardiac stimulation via B1–tachy/arrythmias common

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15
Q

why don’t we use albuterol, metaproterenol, terbutaline in pill forms?

A

worse ADR’s w/ skeletal muscle tremor and nervousness

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16
Q

what are the rescue therapies?

A

SABA
SAMA
steroids

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17
Q

what are the maintenance therapies

A 
ICS
LABA
LAMA
leukotriene
mast-cell stab.
Immunotherapy
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18
Q

why do we prefer inhalers?

A

fast onset
small dose
better ADR profile

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19
Q

what are the 4 inhalers?

A

MDI
Soft Mist
Dry Powder
Neb

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20
Q

what is good about soft mist?

A

formulation propelled forward

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21
Q

what do you have to do prior to MDI use?

A

shake

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22
Q

what can be used w/ MDI to help get more drug into lungs?

A

VHS or spacer

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23
Q

who should use dry powder inhalers?

A

ppl w/ technique issues of MDI

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24
Q

example of inhaler wrapped in foil?

A

advair

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25
Q

example of inhaler not in foil?

A

proair

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26
Q

how should you breathe when using MDI, soft mist inhaler?

A

slow and deep

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27
Q

how should you breathe when using an DPI?

A

quick and deep

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28
Q

SABA drugs

A

albuterol

Levabuterol

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29
Q

what forms does albuterol come in?

A

DPI and HFA

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30
Q

what form does levabuterol come in?

A

dpi

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31
Q

MOA of SABA

A

stimulate adenylyn cyclase–increase cAMP–relax smooth muscel to allow for vasodilation

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32
Q

how fast do SABA’s work?

A

5 min w/ peak @30m-60min

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33
Q

clinical indications for SABA

A

relieve broncohspasm

prophylactic for working out

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34
Q

how often can you take albuterol ?

A

2 puffs q4-6hrs

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35
Q

dosage of neb albuterol

A

1.25-5mg in 3mL saline q4-8hrs

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36
Q

are nebs more effective?

A

no

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37
Q

when is a pt taking too much albuterol and then what should we do?

A

2x/wk

anti-inflammatory tx

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38
Q

ADR of albuterol

A

tachycardic
palpitations
tremor

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39
Q

what increases ADR’s of albuterol

A

high doses

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40
Q

what is the rescue therapy (antimusc)

A

nebulized ipratropium + albuterol

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41
Q

when does rescue therapy need to be initiated?

A

FEV1 or PEF <50% or no response to albuterol alone

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42
Q

what systemic steroids do we use?

A

prednisone
Methylprednisolone
dexamethasone

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43
Q

benefits of dexamethasone

A

longer 1/2 life
high potency
tolerated more by pts

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44
Q

MOA of steroids

A

inhibit production of inflammatory cytokines and reduce bronchial reactivity

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45
Q

clinical indication of steroids

A

exacerbation

use w/ SABA +/- ipatropium

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46
Q

ADRs of steroids

A

insomnia
nervousness
increase appetite
hyperglycemia

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47
Q

what ICS do we use

A

budesonide

Fluticasone

48
Q

what is the only ICS neb?

A

budesonide

49
Q

what ICS is a prodrug?

A

Ciclesonide

50
Q

where is ciclesonide activated?

A

in the long

51
Q

clinical indications of ICS

A

presistent asthma

52
Q

what dose ICS should we use?

A

low!

53
Q

what if low dose ICS + albuterol isn’t enough?

A

increase to medium dose or add LABA

54
Q

what should we do before medium/high dose ICS?

A

try LABA or leukotriene modifier

55
Q

what is the most potent long-term controller of asthma symptoms?

A

ICS

56
Q

pt ed for ICS

A

rinse mouth after use

take 1-2 weeks before effective

57
Q

what are budesonide, fluticasone, and ciclesonide substrates of

A

CYP3A4

58
Q

what pt population/med is bad to combine with ICS?

A

HIV meds–COBI

59
Q

HIV patients on ICS can develop what condition

A

cushings b/c too much steroid d/t inability to metabolize it

60
Q

ADR of budesonide, fluticasone, and ciclesonide

A 
dysphonia
OP candidiasis
skeletal effects--stunts growth
increase risk osteoporosis
occular issues
skin issues
61
Q

how can budesonide, fluticasone, and ciclesonide effect the eyes?

A

increase IOP–glaucoma

increase cataract formation

62
Q

what do budesonide, fluticasone, and ciclesonide do to the skin?

A

increase risk of bruising/purpura

63
Q

what are the LABAs

A

salmeterol

Formoterol (NEB)

64
Q

what is the only SOLO laba inhaler?

A

salmeterol

65
Q

MOA of LABA’s

A

lipid soluble–dissolves in smooth muscle cell membrane to slowly release

66
Q

what type of agonist is formoterol

A

full agonist

67
Q

what type of agonist is salmeterol

A

partial

68
Q

what is the BB warning for salmeterol

A

increase risk of severe asthma attack & death if used solo

69
Q

should you ever use salmeterol alone?

A

no! medical negligence

70
Q

what is salmeterol a substrate of?

A

3A4

71
Q

if CYP3A4 inhibitor is present and you use salmeterol, what are the effects?

A

tachycardia

palpitations

72
Q

what is the LAMA

A

tiotropium

73
Q

MOA of LAMA

A

long-acting antimuscarinic

74
Q

what is a SAMA

A

ipatropium

75
Q

when should we use tiotropium

A

add on to high dose ICS + LAba

76
Q

minimum age for LAMA

A

12

77
Q

ADR of lama?

A

dry mouth

pharyngeal irritation

78
Q

how do leukotrienes exacerbate asthma

A

chemotaxis of inflammatory cells
produce mucous and edema in the airway
bronchoconstriction

79
Q

what do leukotrienes result from

A

5-lipoxygenase on arachidonic acid

80
Q

what is the 5-lipo inhibitor

A

zileuton

81
Q

do we use zileuton?

A

no

82
Q

2 drugs that are cysteinyl leukotriene receptor antagonist

A

Zafirlukast

Montelukast

83
Q

what is the only leukotriene modifer we use

A

montelukast (tablet)

84
Q

ADR of montelukast

A

hA

neuropsych effects

85
Q

what patient population is montelukast best for?

A

those w/ allergies

86
Q

what does montelukast NOT do to help asthma

A

no effect on smooth muscle tone

87
Q

when should montelukast be taken? exacerbation or prophylatically

A

prophylactically

88
Q

MOA of theophylline

A

bronchodilator

blocks PDE

89
Q

what is theophylline a substrate of

A

1A2

90
Q

what drugs inihibit 1A2

A

ciprofloxacin
amiodarone
OCP
cimitidine

91
Q

what pt RF decrease ability to clear theophylline

A

<1yr
>60yr
concurrent dz
drug interactions

92
Q

what theophylline conc causes increase pulm fcn

A

10mcg/mL

93
Q

what theophylline conc causes anorexia, N/V, abdominal pain, anxiety, HA

A

> 15-20mcg/mL

94
Q

what theophylline conc causes seizures and arrythmias

A

> 40mcg/mL

95
Q

what anti-IgE antibody do we use

A

Omalizumab (SQ)

96
Q

MOA of omalizumab

A

IgG binds to free IgE in circulation and blocks its attachment to surface of mast and basophils

97
Q

clinical use of omalizumab

A

pts >6 w/ mod-severe asthma w/ allergic components

98
Q

serious ADR of omalizumab

A

anaphylaxis

99
Q

how do we give the 1st 3 injections of omalizumab

A

monitored!

100
Q

what med should pts w/ eosinophilic phenotype get?

A

IL-5 antibodies

101
Q

IL-5 antibody drugs

A

mepolizumab
reslizumab
benralizumab

102
Q

MOA of mepolizumab and Reslizumab

A

bind to IL-5 and decrease survival of eosinophils/basophils to decrease airway inflammation

103
Q

MOA of benralizumab

A

bind to IL-5 causing apoptosis of eosinophils/basophils to decrease airway inflammation

104
Q

IL-4 antagonist

A

Dupliumab (SQ)

105
Q

MOA of duplimuab

A

bind to IL-4 receptor to inhibit signaling of cytokines to decrease inflammation drivers

106
Q

what pts should get dupliumab

A

mod-severe asthma + eosinophilic phenotype

107
Q

what are contract indicated when on dupliumab

A

live vaccines

108
Q

what ADR has been reported with dupliumab

A

eosinophila–E-GPA (pneumonia, vasculitis)

109
Q

what NSAID should asthma pts use

A

celecoxib

110
Q

do we go low & slow dosing for asthma?

A

NO

111
Q

once we control pts asthma symptoms how long do we stay at that level

A

3 months

112
Q

how many months should each step down be until we reach a lowest dose?

A

3 months

113
Q

Risks of asthma in pregnancy

A 
preeclampsia
preterm birth
LBW or IGUGR
congeital malformation
perinatal death
114
Q

drugs in pregnancy for asthma

A

SABA (C)
LABA (C)
ICS (B)

115
Q

how frequently should pregnant pts w/ poor asthma control be seen ?

A

1-2wks

Pharm Kay Exam 2 (3 decks)

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