Exam #2 Flashcards

0
Q

Risk factors for COPD

A

1: smoking: usually takes about 20 pack years to see signs

  • environmental exposures
  • genetics
  • other (poor nourishment, socioeconomic status, chronic asthma, repeated lower respiratory tract infections, ..)
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1
Q

Definition of COPD

A

a common, preventable and treatable disease, is characterized by persistent airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and lungs to noxious particles or gases. Exacerbations and comorbidities contribute to the overall severity in individual patients.
inability to get air OUT is characteristic of this

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2
Q

what are comorbidities for COPD?

A
cardiovascular disease
osteoporosis & depression
metabolic syndrome and diabetes
lung cancer
GERD (independent risk factor for exacerbation & associated w/worse health status)
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3
Q

screening and diagnosis of COPD

A

should be suspected in any adult over 40 y.o. with…

  • classic symptoms (chronic cough, chronic sputum production, dyspnea –> progressive, persistent & usually worse on exertion)
  • exposure to risk factors for the disease (smoking history, usually > 20 pack years, occupational dust & chemicals)
  • family history of COPD (especially alpha 1 antitrypsin deficiency)

spirometry (gold standard) should be considered in all patients suspected of COPD

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4
Q

What parameters are evaluated with spirometry?

A

FVC (forced vital capacity): maximum volume of gas (L) that can be expired forcefully after a maximum inspiration
FEV1 (forced expired volume in 1 sec): volume of gas (L) expired during first second of FVC

performed 15 minutes AFTER administration of a SABA (short acting beta agonist)

have to do this 3 times, because you need 2 to be reproduceable

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5
Q

How do you use spirometry to diagnose COPD?

A

FEV1/FVC ration < 0.70 (post SABA) confirms presence of persistent airflow limitation
grading: % predicted FEV1 (post SABA) indicates severity of obstruction

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6
Q

What information can you get fro pulmonary function tests? (PFT)

A
total lung capacity (amt of air in lungs at full inspiration)
residual volume (amt of air left in lungs after maximal expiration) - both of these increase with air trapping (emphysema)
diffusion capacity (DLCO): gas-transfer function of the lungs. reduced value consistent with emphysematous changes
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7
Q

What is the GOLD grading of airflow limitation?

A

ALL levels have FEV1/FVC < 0.70 (all measurements are post-bronchodilation)

Gold 1 (mild): FEV1 % predicted >/= 80%
Gold 2 (moderate): 50-79%
Gold 3 (severe): 30-49%
Gold 4 (very severe): < 30%
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8
Q

How do you figure out what quadrant a COPD patient is in? (A, B, C or D)

A

Go to the quadrant that is most severe
Gold classification of airflow limitation 1 or 2 means bottom, 3 or 4 means top
0 or 1 exacerbation that did not require hospitalization means bottom, 2 or more OR one that caused hospitalization means top
CAT score < 10 = left side
CAT score >/= 10 = right side
A = 0-1 exacerbation or GOLD 1 or 2 and CAT < 10
B = 0-1 exacerbations or GOLD 1 or 2 and CAT >/= 10
C = >/= 2 exacerbations (or 1 hospitalization) or GOLD 3 or 4 and CAT < 10
D = >/= 2 exacerbations (or 1 hospitalization) or GOLD 3 or 4 and CAT >/= 10

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9
Q

what do gold copd patient groups mean?

A

A: low risk, less symptoms
B: low risk, more symptoms
C: high risk, less symptoms
D: high risk, more symptoms

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10
Q

What is CAT?

A

COPD assessment test

self-administered

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11
Q

what is MMRC?

A

modified medical research council dyspnea scale
another scoring method for COPD quadrant, used when CAT isn’t available (CAT is preferred). This is more specific for dyspnea

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12
Q

What are the goals of treatment of stable COPD?

A
reduce symptoms *** (relieve symptoms, improve exercise tolerance, improve quality of life)
reduce risk (prevent progression, prevent & treat exacerbations, reduce mortality)
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13
Q

What are non-pharmacological recommendations for stable COPD?

A
smoking cessation
vaccinations (yearly flu and pneumococcal for people 65 yrs and older OR 19-64 years old if chronic lung disease or smoker)
pulmonary rehabilitation
oxygen
surgery
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14
Q

what is the only intervention for COPD that has been proven to slow the progression of the disease?

A

smoking cessation

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15
Q

what is pulmonary rehabilitation?

A

comprehensive multidisciplinary program: exercise, smoking cessation, nutrition counseling, education
increases QOL, recovery from exacerbation, increases exercise capacity & possibly survival, decreases hospitalizations, depression/anxiety and breathlessness

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16
Q

what kind of surgery can be done for COPD?

A

lung volume reduction surgery (LVRS): parts of lungs are resected to reduce hyperinflation
usually upper lobes of lung - then air can expand better
OR transplant (lung)

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17
Q

When should long-term oxygen therapy be used?

A

patients with documented hypoxemia +/- complications of chronic hypoxemia: > 15 hrs/day is needed (24 hrs is ideal)
can improve mortality
can improve symptoms
can reverse long term complications

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18
Q

what are pharmacological options for management of stable COPD?

A

inhaled bronchodilators: (mainstay of therapy)
-beta 2 agonists: SABA & LABA
-anticholinergics: SAMA and LAMA
inhaled corticosteroids (ICS)
phosphodiesterase-4 (PDE-4) inhibitor: roflumilast (Daliresp)
oral bronchodilators (theopylline)

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19
Q

bronchodilator therapy pearls

A

mainstay of therapy - all improve symptoms & exercise tolerance
not proven to alter progression of disease
combining beta2 agonists + cholinergic antagonists can result in improved efficacy with reduced risk for SE
long acting are more convenient & effective than short acting
decrease hospitalizations & exacerbations & improve QOL

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20
Q

how do you manage stable COPD for patient groups A, B, C and D

A
All patients should have SABA prn for acute symptoms
Group A
first choice: SABA prn (or SAMA prn)
alternative: LAMA or LABA or SABA + LAMA
other possible treatments: theophylline
Group B
first choice: LAMA or LABA
alternative: LAMA + LABA
other possible treatments: SAMA or SAMA + SABA or theophylline

Group C:
first choice: ICS + LABA or LAMA
alternative: LABA + LAMA or LAMA + roflumilast or LABA + roflumilast
other possible treatments: SAMA or SAMA + SABA or theophylline
Group D:
first choice: ICS + LABA + LAMA or LAMA alone
alternative: ICS + LABA + LAMA or inhaled CS + LABA + roflumilast or LABA + LAMA or LAMA + Roflumilast
other possible treatments: SAMA or SAMA + SABA or theophylline, carbocyteine, N-acetylcysteine

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21
Q

What are inhaled beta 2 agonists for stable COPD?

A
LABAs (first choice option alone for group B patients, CI: severe hypersensitivity to milk proteins)
salmeterol
formoterol
indacaterol
olodaterol
aformoterol
SABA (first choice option prn alone for group A, prn for all groups)
albuterol
levalbuterol
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22
Q

What are inhaled anticholinergics for stable COPD

A

LAMA: (first choice option for groups B, C and D. use with caution in pts with narrow-angle glaucoma and men with BPH. caution or CI: severe hypersensitivity to milk proteins)
tiotropium
aclidinium
umeclidinium
SAMA: first choice prn for group A; “other” option group B-D
iprotropium

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23
Q

What are combination bronchodilators for stable COPD?

A

SAMA + SABA: iprotroprium + albuterol (combivent resimat): alternative choice for A; “other” options B-D
LAMA + LABA: umeclidinium + vilanterol (Anoro Ellipta): alternative choice for groups B and C. CI: severe hypersensitivity to milk proteins

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24
Q

Theophylline

A

low efficacy and side effects, not recommended unless other bronchodilators are unavailable or unaffordable
available in tablets, capsules & liquid
dose-dependent side effects: tremor, tachycardia, insomnia, nervousness, irritability, GI, seizures, cardiac arrhythmias
watch out for drug interactions

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25
Q

inhaled Corticosteroid pearls

A

decrease exacerbations, improve symptoms, lung function, and QOL (does not alter progression of disease)
add on therapy for patients at high risk for exacerbations or frequent exacerbations (1st choice option in combination with LABA for groups C & D)
not recommended as monotherapy
side effects: increased risk for pneumonia (?), increased thrush, bruising and hoarseness
risk for worsening symptoms if discontinued

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26
Q

combination ICS + LABA products

A

budesonide + formoterol (symbicort): FDA-approved for COPD
fluticasone + salmeterol (Advair diskus): 250/50 dose FDA-approved for patients w/COPD. CI: severe hypersensitivity to milk proteins
fluticasone furoate + vilanterol (Breo Ellipta): FDA-approved for COPS. CI: severe hypersensitivity to milk proteins

inhaled combinations (ICS + LABA) have been shown to be more efficacious than either agent alone.

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27
Q

Roflumilast

A

selective phosphodiesterase (PDE) - 4 inhibitor
decrease PDE4 –> decrease cAMP metabolism –> increase cAMP in lung cells
FDA indicated to reduce the risk of COPD exacerbations in patients w/severe COPD associated w/chronic bronchitis and a history of exacerbations
alternative choice for groups C and D patients per GOLD guidelines
500 mcg tablet po once daily
$270/month
CI: moderate to severe liver impairment (Childs Pugh B & C)
warnings: watch out for worsening insomnia, depression, anxiety, suicidal thoughts
adverse effects: diarrhea, weight loss, nausea, headache, back pain, insomnia, dizziness, psychiatric adverse effects
DI: do not use with potent CYP450 inducers, use cautiously with CYP3A4 and dual CYP1A2/3A4 inhibitors

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28
Q

daily antibiotic therapy & COPD

A

one large study of Azithromycin 250mg po daily vs placebo for 1 yr showed significant reduction in time to & rate of exacerbations BUT
not recommended in guidelines due to risk > benefits
(small increase risk for hearing loss, possible antibiotic resistance, small increase risk for cardiac death - fatal heat arrhythmia)

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29
Q

how do you monitor response to therapy in COPD?

A
repeat spirometry is not reliable
options:
patient reported symptoms/activity level
CAT score
6 minute walk test
QOL questionnaires
other scoring tools
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30
Q

what are patient education points for COPD?

A

smoking cessation (mention it every time you see them)
purpose of medications
expected outcome (benefit) from medications
side effects
timing & techniques (MDI/DPI)

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31
Q

What is an acute exacerbation of COPD?

A

an acute event characterized by a worsening of the patient’s respiratory symptoms (dyspnea, cough and/or sputum) beyond normal day-to-day variation & leads to a change in medication
precipitating factors: respiratory infection, environmental exposure, non-adherence

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32
Q

What are the consquences of a COPD exacerbation?

A
negative impact on QOL
impact on symptoms and lung function
increased economic cost
increased mortality
accelerated lung function decline
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33
Q

how do you manage an acute exacerbation of COPD?

A

oxygen: titrate to improve patient’s hypoxemia w/target saturation of 88-92%
bronchodilators: SABA w/or without SAMA preferred
hospitalized/ED patients; administration by nebulizer tends to be easier
outpatient management: MDI + spacer is effective
antibiotics: considered in hospitalized or ED patients w/increased sputum purulence AND increased dyspnea or sputum volume
treat for 5-10 days
benefits: decreased treatment failure, decreased mortality (in ICU patients)
systemic corticosteroids:
recommended in all COPD patients w/exacerbation
prednisolone/predisone 40 mg po daily X 5 days (*** know this **)
benefits: shorten recovery time, improve lung function & arterial hypoxemia reduce risk of early relapse, treatment failure, & length of hospital stay
watch for SE: hyperglycemia, edema, psych (insomnia, psychosis, anxiety)

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34
Q

Management of acute exacerbations of COPD and VTE prophylaxis

A

COPD exacerbation = major risk factor for VTE

may use heparin, enoxaparin, dalteparin, fondaparinux… until hospital discharge

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35
Q

asthma statistics

A
1 out of 11 children (US)
1 out of 12 adults (US)
females > males
young > old
black children > white children
lower ed & income > higher ed & income
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36
Q

characteristics of asthma

A

chronic inflammatory disorder of the airway
mast cells, eosinophils, neutrophils, macrophages & epithelial cells play a role
inflammation leads to recurrent episodes of cough, wheezing, breathlessness, and chest tightness
widespread, variable, reversible airflow obstruction

bronchoconstriction
airway hyperresponsiveness
edema

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37
Q

how do you diagnose asthma?

A

symptoms
med history
physical exam (increased nasal secretion, mucosal swelling, use of accessory muscles, hyperexpansion of thorax, atopic dermatitis, eczema)
spirometry: FEV1/FVC reduced
positive bronchodilator reversibility test (after SABA - tells us airway obstruction is reversible - necessary for diagnosis of asthma)

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38
Q

when should we use spirometry with asthma?

A

initial assessment
after treatment has been started & symptoms have stabilized
loss of asthma control
every 1-2 years

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39
Q

what are the goals of asthma treatment?

A
reduce impairment (reduce symptoms, minimal need of rescue inhaler, few night-time awakenings, optimal lung function, maintain normal daily activities)
reduce risk (prevent exacerbations/ need for hospitalization, prevent reduced lung growth in children/loss of lung function in adults, optimize medications & minimize adverse effects)
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40
Q

classification of asthma severity in 0-4 yrs old

A

Intermittent: symptoms 2 days/week but not daily, 1-2/month nighttime awakenings, > 2 days/week but not daily use of SABA, minor limitation of activity, >/=2 exacerbations in 6 months requiring oral systemic glucocorticoids OR >/= 4 wheezing episodes/per lasting >1 day and risk factors for persistent asthma

Moderate: daily symptoms, 3-4/month nighttime awakenings, daily SABA use, some limitation with activity - same exacerbation/risk as mild

Severe: symptoms throughout the day, >1 time/week nighttime awakenings, SABA several times/day, extremely limited activity, same risk as mild

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41
Q

classification of asthma severity in 5-11 y.o.

A

intermittent: symptoms 85%, FEV1 > 80%, 0-2 exacerbations requiring oral systemic glucocorticoids/yr
mild: symptoms > 2 days/week but not daily, 3-4/mo night time awakenings, >2 days/week SABA use but not daily, minor limitations with activities, FEV1/FVC > 80%, FEV1 > 80%, > 2 exacerbations in 1 year
moderate: daily symptoms, < 1/week but not nightly nighttime awakenings, daily SABA use, some limitations of activity, FEV1/FVC 75-80%, FEV1 60-80%, same risk as mild
severe: symptoms throughout the day, often 7 times per week nighttime awakenings, several times/day SABA use, extremely limited activity, FEV1/FVC < 75%, FEV1 < 60%, same risk as mild

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42
Q

classification of asthma severity in >/= 12 y.o.

A

intermittent: symptoms 80%, exacerbations requiring oral systemic glucocorticoids 0-2/yr
mild: > 2 days/week but not daily symptoms, 3-4/month nighttime awakenings, >2 days/week but not daily SABA use, minor limitations with activity, lung function FEV1/FVC normal, FEV1 > 80%, > 2 exacerbations in 1 year requiring oral systemic glucocorticoids
moderate: daily symptoms, < 1/week but not nightly nighttime awakenings, daily SABA use, some limitations with activity, FEV1/FVC reduced < 5%, FEV 60-80%, same risk as mild
severe: symptoms throughout the day, often 7 times/week nighttime awakenings, several times/daySABA use, extremely limited activity, FEV1/FVC reduced > 5%, FEV1 < 60%, same risk as mild

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43
Q

Step therapy

A

intermittent: step 1
mild persistent: step 2
moderate persistent: step 3 or 4
severe persistent: step 5 or 6

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44
Q

Step therapy for 0-4 y.o.

A

ALL have SABA prn
Step 1: SABA prn
Step 2: preferred: low dose ICS
alternative: montelukast or cromolyn
step 3: preferred: medium-dose ICS
step 4: preferred: medium dose ICS AND either montelukast or LABA
step 5: preferred: high-dose ICS and either montelukast or LABA
step 6: preferred: high dose ICS and either montelukast or LABA AND oral corticosteroids
step up if needed (first check adherence & environmental control) assess control, step down if possible (and asthma is well controlled at least 3 months)
patient education & environmental control at each step

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45
Q

step therapy for 5-11 y.o.

A

SABA for all
patient education & environmental control at each step
step 1: preferred SABA prn
step 2: preferred: low dose ICS
alternative: LTRA (leukotriene receptor antagonist: montelukast), Cromolyn, nedocromil, or theophylline
step 3: preferred: medium-dose ICS or low dose ICS + LABA, LTRA, or thephylline
step 4: preferred: medium-dose ICS + LABA, alternative: medium-dose ICS + either LTRA or theophylline
step 5: preferred: high-dose ICS + LABA, alternative: high-dose ICS + either LTRA or theophylline
step 6: preferred: high-dose ICS + LABA + oral corticosteroid, alternative: high-dose ICS + either LTRA or theophylline + oral corticosteroid

step up if needed (first check adherence & environmental control & comorbid conditions) assess control. step down if possible (and asthma is well controlled at least 3 months)
steps 2-4, consider SQ allergen immunotherapy for allergic patients

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46
Q

step therapy for >/= 12 y.o.

A

patient education and environmental control at each step
SABA prn for all patients
step 1: preferred SABA prn
step 2: preferred: low dose ICS, alternative: cromolyn, nedocromil, LTRA or theophylline
step 3: preferred: medium-dose ICS OR low-dose ICS + LABA, alternative: low-dose ICS+LTRA, theophylline or zileuton
step 4: preferred: medium-dose ICS + LABA, alternative: medium-dose ICS + LTRA, theophylline or zileuton
step 5: preferred: high dose ICS + LABA, and consider omalizumab or patients who have allergies
step 6: preferred: high-dose ICS + LABA + oral corticosteroid and consider omalizumab for patients who have allergies
step up if needed (first, check adherence and environmental control, and comorbid conditions) assess control. step down if possible (and asthma is well controlled at least 3 months)

steps 2-4: consider sq allergen immunotherapy for allergic patients
use of beta 2 agonists > 2 days/week for symptom control indicates inadequate control & the need to step up treatment

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47
Q

What are the categories of asthma medications?

A

Quick Relief:
SABA (short acting beta agonists)
short acting anticholinergic
systemic corticosteroids

Long Term Control Medications:
Inhaled corticosteroids
LABAs (long acting beta agonists)
Cromolyn
leukotriene modifiers
methlxanthines
immunomodulators
systemic corticosteroids
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48
Q

Asthma medication terminology
MDI
HFA
DPI

A

MDI - meter dosed inhaler
HFA - hydrofluoroalkane (propellant that’s used to get medication out)
DPI- dry powder inhaler (discus)
spacer - attach it to MDI to help patient use it appropriately
nebulizer

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49
Q

SABAs

A

drug of choice for acute bronchospasm
sole treatment for intermittent asthma
therapy of choice for exercise induced bronchospasm (EIB)
albuterol HFA (proventil, ventolin, proair)
levalbuterol HFA (xopenex) (L-enantiomer of albuterol)
Albuterol nebulizer
levalbuterol nebulizer
Adverse effects: tachycardia, tremor, hypokalemia, hyperglycemia, inhaled route leads to few systemic side effects
therapeutic considerations:
not for long term daily use
increase in use or lack of effect indicates diminished control of asthma
inhalation route preferred (oral therapies are available)
all patients w/asthma should have SABA available

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50
Q

Anticholinergics

A

Role in therapy:
drug of choice for bronchospasm due to beta-blocker medication
alternative for patients intolerant to SABA
used in combination w/SABA during acute exacerbation
ipratropium HFA (atrovent)
Ipratropium nebulizer
Iprotropium/albuterol inhaler (combivent Respimat)
Ipratropium/albuterol nebulizer
Adverse effects: dry mouth & respiratory secretions, blurred vision (if sprayed in eyes), less cardiac stimulation than SABAs
Therapeutic considerations: increase in use or lack of effect indicates diminished control of asthma, not for long term daily use in asthma, does not work for exercise induced bronchospasm

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51
Q

Oral corticosteroids

A

Role in therapy: short courses “bursts” used to establish control with initiation of therapy or during exacerbation
may be used in severe persistent asthma (step 6 for every age group)
Methylprednisolone
prednisolone
prednisone
adverse effects: short term use: glucose abnormalities, increased appetite, fluid retention, weight gain, facial flushing, mood changes, hypertension, adrenal suppression, osteoporosis, skin thinning, growth suppression
Therapeutic considerations: burst should be continued until patient achieves 80% of peak expiratory flow or symptoms resolve, other equipotent doses of systemic corticosteroids may be used, different dosages for daily use, tapering with daily use, not with bursts

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52
Q

inhaled corticosteroids

A
role in therapy:
drug of choice for persistent asthma
long term prevention of symptoms, suppression, control and reversal of inflammation
beclomethasone HFA
Budesonide DPI
Budesonide nebulizer
Flunisolide
Flunisolide HFA
fluticasone HFA
Fluticasone DPI
mometasone DPI
triamcinolone
adverse effects: cough, dysphonia, oral thrush, at high doses, systemic side effects may occur
Therapeutic considerations: reduce risk of thrush by use of spacer/holding chamber with MDI, rinse mouth after inhalation, Dexamethasone is not used as an ICS due to high absorption & long term suppressive side effects
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53
Q

Long acting beta agonists

A

role in therapy:
long term prevention of symptoms in addition to ICS
prevention of exercise induced bronchospasm
do NOT use for acute symptoms
potential for uncommon, severe, life threatening or fatal exacerbation when used as monotherapy in asthma
Salmeterol
Formoterol
adverse effects: tachycardia, tremor, hypokalemia, prolongation of QTc
Therapeutic considerations:
do not use for acute symptoms
Do not use as monotherapy
May provide more control when added to ICS compared to increasing dose of ICS

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54
Q

what are some combination medications available? (LABA + ICS)

A

fluticasone/salmeterol (Advair) DPI
Budesonide/formoterol (Symbiocort)
Mometasone/formoterol (Dulera)

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55
Q

Cromolyn

A

Role in therapy:
long term prevention of symptoms in mild persistent asthma as an alternative to ICS
preventive treatment prior to exposure to exercise or known allergen
Adverse effects: cough and irritation
Therapeutic considerations:
safety is primary advantage of cromolyn
Therapeutic response will typically occur in 2 weeks, but max benefit may not be seen in 4-6 weeks
dose of MDI cromolyn may be inadequate for asthma; nebulizer may be preferred

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56
Q

Leukotriene modifiers

A

Role in therapy:
alternative treatment for persistent asthma
may be used in exercise induced bronchospasm, aspirin-induced asthma, and allergic asthma
Leukotriene Receptor antagonists:
Montelukast
Zafirlukast
5-Lipoxygenase inhibitor:
Zileuton
adverse effects: Antagonists: headache | Inhibitor: GI upset, headache, hepatoxicity
Therapeutic considerations:
monitor liver function with zafirlukast and zileuton
Administer zafirlukast at least 1 hr before or 2 hrs after meals
be aware of drug interactions with zafirlukast & zileuton
also approved for allergic rhinitis

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57
Q

Methylxanthines

A

Theophylline
Role in therapy:
long term control & prevention of symptoms in mild persistent asthma (as an alternative to ICS) or as an adjunctive with ICS in moderate to severe asthma
have to calculate dose
adverse effects:
insomnia, gastric upset, aggravation of ulcer/gerd, increase in hyperreactivity in children
Toxicities: tachycardia, nausea, vomiting, tachyarrhythmias, central nervous system stimulation, headache, seizures, hematemesis, hyperglycemia, hypokalemia
Therapeutic considerations:
regular serum monitoring is necessary (narrow therapeutic window, severe toxicity)
steady-state concentrations = 5-15 mcg/mL
food affects absorption
many drug-drug/drug disease interactions

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58
Q

Immunomodulators

A

Role in therapy:
long term control and prevention of symptoms in adults (>/=12 yrs) who have moderate or severe persistent allergic asthma inadequately controlled with ICS
Omalizumab
only for > 12 y.o.
adverse effects: pain & bruising at injection sites, anaphylaxis
Therapeutic considerations:
monitor following injections due to potential for anaphylaxis
administer no more than 150 mg in one injection
refrigerate

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59
Q

tiotropium in asthma

A

long acting anticholinergic bronchodilator
widely used for COPD, but not included in asthma guidelines
reserve for poorly controlled asthma despite ICS/LABA

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60
Q

Assessing control of asthma 0-4 y.o.

A

well controlled: 2 days/week symptoms, >/= 1 time/month nighttime awakening, > 2 days/week SABA use, some limitations of activity, 2-3 /yr exacerbations requiring oral systemic glucocorticoids
very poorly controlled: symptoms throughout the day, >/= 1 time/week nighttime awakenings, several times/day SABA use, extremely limited activities, > 3/yr exacerbations requiring oral systemic glucocorticoids

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61
Q

assessing control of asthma 5-11 y.o.

A

well controlled: 80% lung function FEV1, >80% FEV1/FVC, 0-1/yr exacerbations requiring oral systemic glucocorticoids
Not well controlled: > 2 days/week; multiple times on /= 2 times/month nighttime awakenings, some limitations in activity, 60-80% lung function FEV1, FEV1/FVC 75-80%, >/=2/yr exacerbations requiring oral systemic glucocorticoids
very poorly controlled: symptoms throughout the day, nighttime awakenings >/= 2 times/week, SABA use several times/day, extremely limited activity, lung function < 60%, FEV1/FVC /= 2 /yr exacerbations requiring systemic glucocorticoids

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62
Q

assessing control of asthma > 12 y.o.

A

well controlled: 80% lung function FEV1, Asthma control test >/= 20, 0-1/yr exacerbation requiring oral systemic glucocorticoids
not well controlled: > 2 days/week symptoms, 1-3 times/week nighttime awakenings, SABA use > 2 days/week, some limitations with activities, 60-80% FEV1 lung function, ACT 16-19, >/= 2/yr exacerbations requiring oral systemic glucocorticoids
very poorly controlled: symptoms throughout the day, nighttime awakenings >/= 4 times/week, SABA use several times/day extremely limited activity, FEV1 < 60%, ACT /= 2/yr exacerbations requiring oral systemic glucocorticoids

63
Q

changes based on control

A

well controlled: maintain current step, regular follow up every 1-6 months, consider step down if well controlled for at least 3 months
not well controlled: review adherence, inhaler techniques, environmental controls
step up 1 step
reevaluate in 2-6 weeks
very poorly controlled: review adherence, inhaler techniques, environmental controls, consider short course of oral systemic corticosteroids, step up 1-2 steps, reevaluate in 1-2 weeks.

64
Q

common comorbid conditions that may affect asthma

A
GERD
obesity
obstructive sleep apnea
stress
depression
65
Q

patient education topics for asthma

A

basic facts about asthma
role of medication (difference b/t rescue & maintenance medication)
patient skills: inhaler technique, environmental exposures, self-monitoring, asthma action plan
self-management education: improves patient outcomes, cost-effective
How to integrate self-management: active partnership, written asthma plan, repetition

66
Q

what is an asthma action plan?

A

instructions for daily management: long term medication, environmental control measures
how to manage worsening asthma: signs/symptoms, medications to take
typically recommended for patients with: moderate or severe persistent asthma, severe exacerbations, poorly controlled asthma

67
Q

what is an asthma exacerbation?

A

episodes of progressively worsening SOB, cough, wheezing, and/or chest tightness
decreased lung function

68
Q

what factors increase risk of asthma-related death?

A

history of near-fatal asthma requiring intubation
hospitalized or ED visit for asthma in past year
currently using or having recently stopped using oral corticosteroids
not currently using ICS
over-use of SABAs
history of psychiatric disease or psychosocial problems
poor adherence with asthma medications/asthma action plan
food allergy in a patient with asthma

69
Q

what are the signs of a mild or moderate exacerbation of asthma?

A
talks in phrases, prefers sitting to lying, not agitated
increased respiratory rate
no use of accessory muscles
pulse = 100-120 bpm
O2 saturation 90-95%
PEF > 50% predicted/best
70
Q

what are the signs of a severe or life threatening asthma exacerbation?

A
talks in words, sits hunched forward, agitated
RR > breaths/min
accessory muscles in use
pulse > 120 bpm
O2 saturation < 90%
PEF </= 50% of predicted/best

Life threatening: drowsy, confused, or silent chest

71
Q

mild to moderate exacerbation treatment for asthma

A

SABA 4-10 puffs by MDI + spacer, repeat every 20 minutes for 1 hour
Prednisolone:
adults 1 mg/kg, max 50 mg
children 1-2 mg/kg, max 40 mg
controlled oxygen
target: 93-95% adults
target 94-98% children
assess response at 1 hour
discharge is symptoms improve, PEF improving, O2 saturation > 94% on room air, adequate resources at home
arrange at discharge: SABA, controller (check inhaler technique & assess adherence), prednisolone (adults 5-7 days, children 3-5 days), follow up in 2-7 days

72
Q

severe/ life threatening asthma exacerbation treatment

A

transfer to acute care facility
while waiting give SABA, Oxygen, systemic corticosteroids
ED management:
Assess: airway, breathing, circulation (ABC)
if drowsiness, confusion, silent chest are present –> transfer to ICU
if above symptoms are not present, classify as mild/moderate vs severe
ED management for mild/moderate
SABA, consider ipratropium, O2, oral corticosteroids
ED management for severe: SABA, ipratropium, O2, oral or IV corticosteroids, consider IV magnesium, consider high dose ICS
reassessment in ED: measure lung function in all patients after 1 hr., if FEV1 or PEF is 60-80% of predicted or personal best & symptoms have improved –> consider discharge planning
if FEV1 or PEF < 60% of predicted or personal best OR lack of clinical response –> continue treatment & reassess frequently

73
Q

exercise induced bronchospasm (EIB)

A

asthma symptoms occurring during or after exercise
warm up period before exercise
if symptoms are only during/after exercise:
SABA, tolerance may develop with regular use
LTRA (prior to)
Cromolyn (prior to)
If symptoms occur unrelated to exercise or risk of exacerbation: ICS, LTRA

74
Q

pregnancy and asthma

A

1:1:1 ration of patients whose asthma improves, worsens and does not change during pg
albuterol = rescue drug of choice
budesonide = control drug of choice/ICS of choice
formoterol = LABA of choice
okay to keep patient on ICS/LABA if well controlled

75
Q

What are the health consequences of smoking?

A

cancers, pulmonary diseases, cardiovascular diseases, reduced fertility in women, erectile dysfunction, diabetes, RA, cataract, osteoporosis, impaired immune functions

76
Q

What are the compounds in tobacco smoke?

A

4800 compounds including 11 proven human carcinogens
gases: carbon monoxide, hydrogen cyanide, ammonia, benzene, formaldehyde
particles: nicotine, nitrosamines, lead, cadmium, polonium-210
Nicotine is the addictive element, but it does not cause the ill health effects

77
Q

Nicotine absorption & pH

A

absorption is pH dependent
nicotine is a weak base
in acidic environment, Nicotine is ionized so poorly absorbed across membranes
In alkaline media, nonionized so well absorbed across membranes. At physiological pH, 31% of nicotine is unionized, so readily absorbed

78
Q

how long does it take nicotine to reach your brain after you smoke?

A

11 seconds - enforces desire to smoke, because you immediately feel the effects

79
Q

how is nicotine metabolized?

A

70-80% –> cotinine
10% other metabolites (cotinine & other metabolites excreted in urine)
10-20% excreted unchanged in urine
metabolized primarily through CYP450 system

80
Q

What is the half life of nicotine?

A

2 hours - quick, so it gets into the system quickly & leaves the system quickly, making you want another cigarette soon
cotinine has half life of 16 hours, so you can measure cotinine levels if you want to know if someone has been smoking recently

81
Q

how is nicotine excreted?

A

through kidneys
pH dependent - higher with acidic pH
through breast milk, too.

82
Q

drug interactions with smoking

A

not an interaction with nicotine
most interactions occur due to CYP P450 induction: (clopidogrel, olanzapine - these levels will be decreased b/c cigarette smoke causes induction of CYP P450)
Pharmacodynamic interactions may alter expected response of some medications: (beta blockers, opioids - may need higher doses of both if patients are smoking)
consider DI when patients stop, quite or alter smoking

83
Q

smoking and hormonal contraceptives

A

increased risk of serious cardiovascular adverse effects:
-stroke
-myocardial infarction
-thromboembolism
does NOT decrease efficacy of hormonal contraceptives
women who are 35 or older and smoke at least 15 cigarettes/day are at significantly elevated risk.

84
Q

nicotine pharmacodynamics

A

binds to receptors in brain & other sites in body
predominantly stimulatory effects
CNS (pleasure, arousal, enhanced vigilance, improved task performance, anxiety relief) , exocrine glands, adrenal medulla, peripheral nervous system, cardiovascular system (increase heart rate, increase cardiac output, increase blood pressure, coronary vasoconstriction, cutaneous vasoconstriction), GI system, neuromuscular junctions sensory receptors, other organs
appetite suppression, increased metabolic rate, skeletal muscle relaxation

85
Q

what are the neurochemical and related effects of nicotine?

A

neurotransmitters that are affected by nicotine:
dopamine –> pleasure, appetite suppression
norepinephrine –> arousal, appetite suppression
acetylcholine –> arousal, cognitive enhancement
glutamate –> learning, memory enhancement
serotonin –> mood modulation, appetite suppression
beta endorphin –> reduction of anxiety and tension
GABA –> reduction of anxiety and tension

86
Q

Nicotine addiction

A
tobacco users maintain a minimum serum nicotine concentration in order to:
prevent withdrawal symptoms
maintain pleasure/arousal
modulate mood
Users self-titrate nicotine intake by:
smoking/dipping more frequently
smoking more intensely
obstructing vents on low-nicotine brand cigarettes
87
Q

what are the effects of nicotine withdrawal?

A
irritability/frustration/anger
anxiety
difficulty concentrating
restlessness/impatience
depressed mood/depression
insomnia
impaired performance
increased appetite/weight gain
cravings
88
Q

What are the 2 parts of tobacco dependence?

A

physiological: addiction to nicotine - need medications for cessation
behavioral: habit of using tobacco - need behavior change program
treatment should address the physiological and behavioral aspects of dependence

89
Q

What are non-pharm methods of quitting tobacco use?

A
  • cold turkey
  • unassisted tapering (reduced frequency of use, lower nicotine cigarettes, special filters or holders)
  • assisted tapering (QuitKey: computer developed taper based on patient’s smoking level, includes telephone counseling support)
  • formal cessation programs (self-help programs, individual counseling, group programs, telephone counseling [1-800-QUIT-NOW], web-based counseling [smokefree.gov, quitnet.com],
  • acupuncture therapy
  • hypnotherapy
  • massage therapy
90
Q

what are the 1st line therapies for quitting tobacco use?

A

Nicotine replacement therapy (NRT): gum, patch, lozenge, nasal spray, inhaler
Psychotropics: sustained-release bupropion
Partial nicotinic receptor agonist: varenicline

91
Q

tobacco cessation in pregnancy

A

Clinical Practice Guidelines make no recommendations regarding use of medications in pregnant smokers: insufficient evidence of effectiveness.
category C: varenicline, bupropion SR
category D: prescription formulations of NRT
“Because of serious risks of smoking to the pregnant smoker and the fetus, whenever possible, pregnant smokers should be offered person to person psychosocial interventions that exceed minimal advice to quit.”

92
Q

when is pharmacotherapy NOT recommended for smoking cessation?

A

smokeless tobacco users
individuals smoking fewer than 10 cigarettes per day
adolescents (nonprescription sales (patch, gum, lozenge) are restricted to adults >/= 18 y.o.). NRT use in minors requires a prescription
recommended treatment is behavioral counseling

93
Q

what is the rationale for nicotine replacement therapy use?

A

reduces physical withdrawal from nicotine
eliminates the immediate, reinforcing effects of nicotine that is rapidly absorbed via tobacco smoke
allows patient to focus on behavioral and psychological aspects of tobacco cessation
so helps prevent cravings and symptoms of withdrawal

94
Q

What are precautions of NRT use?

A

patients with underlying cardiovascular disease: recent myocardial infarction (within past 2 weeks), serious arrhythmias, serious or worsening angina
NRT products may be appropriate for these patients if they are under medical supervision.

95
Q

Nicotine gum: what is it made of and what is the dosing

A

resin complex: nicotine, polacrilin
sugar-free chewing gum base
contains buffering agents to enhance buccal absorption of nicotine
available: 2 mg, 4 mg; original, cinnamon, fruit and mint (various) flavors
dosing: based on time to first cigarette (TTFC) as an indicator of nicotine dependence: if patient smokes w/in 30 minutes of waking, they need 4 mg, if they can wait 30 minutes before 1st cigarette, 2 mg is more appropriate

96
Q

What is the recommended usage schedule for nicotine gum?

A

Weeks 1-6: 1 piece q 1-2 h
Weeks 7-9: 1 piece q 2-4 h
Weeks 10-12: 1 piece q 4-8 h
do not use more than 24 pieces per day

higher chance of success when patients follow scheduled dosing rather than just when they feel craving

97
Q

what are the directions for use for nicotine gum?

A

chew each piece very slowly several times
stop chewing at first sign of peppery taste or slight tingle in mouth (~15 chews, but varies)
park gum between cheek and gum to allow absorption of nicotine across buccal mucosa
resume slow chewing when taste or tingle fades
when taste or tingle returns, stop & park gum in different place in mouth
repeat chew/park steps until most of the nicotine is gone (taste or tingle does not return; generally 30 minutes)

98
Q

additional patient education for nicotine gum

A

to improve chances of quitting use at least 9 pieces of gum daily
effectiveness of nicotine gum may be reduced by some foods and beverages: coffee, wine, juices, soft drinks
* do not eat or drink for 15 minutes before or while using nicotine gum*
chewing gum will not provide some rapid satisfaction that smoking provides
chewing gum too rapidly can cause excessive release of nicotine resulting in: lightheadedness, nausea and vomiting, irritation of throat and mouth, hiccups, indigestion
side effects of nicotine gum include: mouth soreness, hiccups, dyspepsia, jaw muscle ache
nicotine gum may stick to dental work: discontinue use if excessive sticking or damage to dental work occurs

99
Q

what are advantages and disadvantages of nicotine gum?

A

advantages: might serve as an oral substitute for tobacco, might delay weight gain, can be titrated to manage withdrawal symptoms, can be used in combination with other agents to manage situational urges
disadvantages: need for frequent dosing can compromise adherence, might be problematic for patients with significant dental work, proper chewing technique is necessary for effectiveness and to minimize adverse effects, gum chewing might not be acceptable or desireable for some patients

100
Q

What are nicotine lozenges made of?

A

nicotine polacrilex formation: delivers ~25% more nicotine than equivalent gum dose
sugar free mint, cherry flavors
contains buffering agents to enhance buccal absorption of nicotine
available in 2mg and 4 mg
dosing based on TTFC: if you smoke w/in 30 minutes of waking, use 4mg, if you can wait 30 min, use 2 mg.

101
Q

what is the dosing of nicotine lozenges?

A

weeks 1-6: 1 lozenge q 1-2 h
weeks 7-9: 1 lozenge q 2-4 h
weeks 10-12: 1 lozenge q 4-8 h
do not use more than 20 lozenges per day

102
Q

directions for nicotine lozenge use

A

use according to recommended dosing schedule
place in mouth and allow to dissolve slowly (nicotine release may cause warm, tingling sensation)
do not chew or swallow lozenge
occasionally rotate to different areas of the mouth
lozenges will dissolve completely in about 20-30 minutes

103
Q

patient education for nicotine lozenges

A

to improve chances of quitting, use at least 9 lozenges daily during first 6 weeks
the lozenge will not provide the same rapid satisfaction that smoking provides
the effectiveness of the lozenge may be reduced by some foods & beverages: coffee, wine, juices, soft drinks
do not eat or drink for 15 minutes before or while using the nicotine lozenge
side effects: nausea, hiccups, cough, heartburn, headache, flatulence, insomnia

104
Q

nicotine lozenge pros and cons

A

advantages: might serve as an oral substitute for tobacco, use might delay weight gain, can be titrated to manage withdrawal symptoms, can be used in combination with other agents to manage situational urges
disadvantages: need for frequent dosing can compromise adherence, GI side effects (nausea, hiccups, heartburn) might be bothersome

105
Q

Transdermal nicotine patch - what’s the deal

A

nicotine is well absorbed across the skin
delivery to systemic circulation avoids hepatic first-pass metabolism
plasma nicotine levels are lower and fluctuate less than with smoking
NicoDerm CQ: 24 hr nicotine delivery, OTC, 7, 14 or 21 mg strength
Generic: 24 hr nicotine delivery, OTC + Rx, 7, 14, 21 mg strength

106
Q

directions for use of nicotine patch

A

choose an area of skin on the upper body or upper outer part of the arm
make sure skin is clean, dry, hairless & not irritated
apply patch to different area each day
do not use same area again for at least 1 week
remove patch from protective pouch
peel off half of backing from patch
apply adhesive side of patch to skin
peel off remaining protective covering
press firmly with palm of hand for 10 seconds
make sure patch sticks well to skin, especially around edges
wash hands (nicotine on hands can get into eyes or nose & cause stinging or redness)
do not leave patch on skin for more than 24 hrs - doing so may lead to skin irritation
adhesive remaining on skin may be removed with rubbing alcohol or acetone
dispose of used patch by folding it onto itself, completely covering adhesive area

107
Q

dosing of nicotine patch

A
Heavy smoker ( 10 cigarettes/day)
Step 1 (21 mg X 6 weeks)
Step 2 (14 mg x 2 weeks)
Step 3 (7 mg x 2 weeks)

only difference is that Generic says for heavy smoker, step 1 is 4 weeks long instead of 6 weeks long.

Light smoker:
step 2 (14 mg x 6 weeks)
step 3 (7 mg X 2 weeks)
108
Q

patient ed for nicotine patch

A

water will not harm the patch if it is applied correctly, patients may swim, bathe, shower or exercise while wearing patch
do not cut patches to adjust dose (nicotine may evaporate from cut edges, patch may be less effective)
keep new & used patches out of reach of children & pets
remove patch before MRI procedures
side effects: mild itching, burning, tingling
additional possible side effects: vivid dreams or sleep disturbances, headache
after patch removal, skin may appear red for 24 hrs. If it stays red for more than 4 days, or if it swells or a rash appears, contact health care provider - do not apply new patch
local skin reactions: (redness, burning, itching), usually caused by adhesive, up to 50% of patients experience this reaction, fewer than 5% discontinue therapy, avoid use in patients with dermatologic conditions (e.g., psoriasis, eczema, atopic dermatitis)

109
Q

nicotine patch pros and cons

A

advantages: once daily dosing associated with fewer adherence problems, of all NRT products, its use is least obvious to others, can be used in combination with other agents, delivers consistent nicotine levels over 24 hrs
disadvantages: when used as monotherapy, cannot be titrated to acutely manage withdrawal symptoms, not recommended for use by patients with dermatologic conditions

110
Q

nicotine nasal spray - what’s the deal?

A

aqueous solution of nicotine in a 10-ml pray bottle
each metered dose actuation delivers 50 mcL spray, 0.5 mg nicotine
~ 100 doses/bottle
rapid absorption across nasal mucosa
works more quickly than the rest of the nicotine replacement products

111
Q

what is the dosing & administration of nicotine nasal spray?

A

one dose = 1 mg nicotine (2 sprays, one 0.5 mg spray in each nostril)
start with 1-2 doses/hour
increase prn to maximum dosage of 5 doses per hour or 40 mg (80 sprays); ~ 1/2 bottle) daily
for best results, patients should use at least 8 doses daily for the first 6-8 weeks
termination: gradual tapering over an additional 4-6 weeks

112
Q

directions for using nicotine nasal spray

A

press in circles on sides of bottle & pull to remove cap
prime the pump (before first use), re-prime (1-2 sprays) if spray not used for 24 hours
blow nose (if not clear)
tilt head back slightly & insert tip of bottle into nostril as far as comfortable
breathe through mouth and spray once in each nostril
do not sniff or inhale while spraying
if nose runs, gently sniff to keep nasal spray in nose
wait 2-3 minutes before blowing nose
avoid contact with skin, eyes and mouth: if contact occurs, rinse with water immediately, nicotine is absorbed through skin & mucus membranes

113
Q

patient education for nicotine spray

A

what to expect (first week):
hot peppery feeling in back of throat or nose
sneezing, coughing, watery eyes, runny nose
side effects should lesson over a few days
regular use during the first week will help in development of tolerance to the irritant effects of the spray
if side effects do not decrease after a week, contact health care provider

114
Q

pros and cons for nicotine spray

A

advantages: can be titrated to rapidly manage withdrawal symptoms, can be used in combination with other agents to manage situational urges
disadvantages: need for frequent dosing can compromise adherence, nasal administration might not be acceptable/desirable for some patients; nasal irritation often problematic, not recommended for use by patients with chronic nasal disorders or severe reactive airway disease

115
Q

nicotine inhaler: what’s the deal

A

nicotine inhalation system consists of mouth piece, cartridge with porous plug containing 10 mg nicotine and 1 mg menthol
delivers 4 mg nicotine vapor, absorbed across buccal mucosa

116
Q

nicotine inhaler dosing

A

start with at least 6 cartridges/day during first 3-6 weeks
increase prn to maximum of 16 cartridges /day
in general, use 1 cartridge every 1-2 hours
recommended duration of therapy is 3 months
gradually reduce daily dosage over the following 6-12 weeks

117
Q

nicotine inhaler directions for use

A

align marks on the mouthpiece
pull and separate mouthpiece into 2 parts
press nicotine cartridge firmly into bottom of mouthpiece until it pops down into place
line up the marking on the mouthpiece again & push the two pieces back together so they fit tightly
twist top to misalign marks & secure unit
during inhalation, nicotine is vaporized and absorbed across oropharyngeal mucosa
inhale into back of throat or puff in short breaths
nicotine in cartridges is depleted after about 20 minutes of active puffing (cartridge does not have to be used all at once - try different schedules to find what works best, open cartridge retains potency for 24 hours)
mouth piece is reusable; clean regularly with mild detergent

118
Q

nicotine inhaler patient education

A

side effects: mild irritation of the mouth or throat, cough, headache, rhinitis, dyspepsia
severity generally rated as mild, and frequency of symptoms declined with continued use
use inhaler at room temperature; in cold environments, the delivery of nicotine vapor may be compromised
use the inhaler longer and more often at first to help control cravings (best results are achieved with frequent continuous puffing over 20 minutes)
effectiveness of the nicotine inhaler may be reduced by some foods and beverages
do not eat or drink for 15 minutes before or while using the nicotine inhaler

119
Q

nicotine inhaler pros and cons

A

advantages: might serve as an oral substitute for tobacco, can be titrated to manage withdrawal symptoms, mimics the hand to mouth ritual of smoking, can be used in combination with other agents to manage situational urges
disadvantages: need for frequent dosing can compromise adherence, cartridges might be less effective in cold environments

120
Q

Bupropion SR

A

(Zyban, generics)
nonnicotine cessation aid
sustained-release antidepressant
oral formulation
MOA: atypical antidepressant thought to affect levels of various brain neurotransmitters: dopamine, norepinephrine
clinical effects: decrease cravings for cigarettes, decrease symptoms of nicotine withdrawal

121
Q

buproprion warnings & precautions

A

neuropsychiatric symptoms & suicide risk:
changes in mood ( e.g. depression & mania)
psychosis/hallucinations/paranoia/delusions
homicidal ideation/hostility
agitation/aggression/anxiety/panic
suicidal ideation or attempts
completed suicide
**advise patients to stop taking bupropion SR and contact a health care provider immediately if symptoms such as agitation, hostility, depressed mood, or changes in thinking or behavior that are not typical are observed or if the patient develops suicidal ideation or suicidal behavior
should be used with caution in the following populations:
patients with elevated risk for seizures, including: severe head injury, concomitant use of medications that lower the seizure threshold (e.g., other bupropion products, antipsychotics, tricyclic antidepressants, theophylline)
severe hepatic impairment
patients with underlying neuropsychiatric conditions

122
Q

Bupropion SR dosing

A

To ensure that therapeutic plasma levels of the drug are achieved, patients should begin therapy 1-2 weeks PRIOR To quit date
initial treatment: 150mg po q AM for 3 days
then: 150 mg po bid for 7-12 weeks
doses must be administered at least 8 hours apart
tapering not necessary when discontinuing therapy

123
Q

bupropion adverse effects

A

common side effects: insomnia, dry mouth

less common, but reported side effects: tremor, skin rash

124
Q

bupropion pros and cons

A

advantages: oral dosing is simple & associated w/fewer adherence problems, might delay weight gain, bupropion might be beneficial in patients with depression, can be used in combination with NRT agents
disadvantages: seizure risk is increased, several CI & precautions preclude use in some patients, patients should be monitored for neuropsychiatric symptoms

125
Q

Varenicline

A

(chantix)
Nonnicotine cessation aid
partial nicotinic receptor agonist
oral formulation
MOA: binds with high affinity & selectivity at alpha4beta2 neuronal nicotinic acetylcholine receptors: stimulates low-level agonist activity, competitively inhibits binding of nicotine
clinical effects: lowers symptoms of nicotine withdrawal, blocks dopaminergic stimulation responsible for reinforcement & rewards associated with smoking

126
Q

Varenicline warnings & precautions

A

neuropsychiatric symptoms and suicidality:
changes in mood, psychosis/hallucinations/paranoia/delusions, homicidal ideation/hostility, agitation/anxiety/panic, suicidal ideation or attempts, completed suicide
***patients should be advised to stop taking varenicline and contact a healthcare provider immediately if agitation, hostility, depressed mood, or changes in thinking or behavior that ar enot typical for the patient are observed, or if the patient develops suicidal ideation or suicidal behavior
BLACK BOX WARNING

127
Q

what is the dosing of varenicline?

A

Patients should begin therapy 1 week prior to their quit date. the dose is gradually increased to minimize treatment-related nausea and insomnia
day 1-3 0.5 mg qd
day 4-7 0.5 mg bid
day 8 to end of treatment1 mg bid (up to 12 weeks)

128
Q

what are the adverse effects of varenicline?

A

common: nausea, sleep disturbances (insomnia, abnormal dreams), constipation, flatulence, vomiting
nausea & insomnia are most common - titrating dose up helps avoid that

129
Q

Varenicline patient education

A

doses should be taken after eating, with a full glass of water
nausea and insomnia are usually temporary side effects
if symptoms persist, notify your health care provider
may experience vivid, unusual or strange dreams during treatment
use caution driving, drinking alcohol, and operating machinery until effects of quitting smoking with varenicline are known.

130
Q

varenicline pros and cons

A

advantages: oral dosing is simple and associated with fewer adherence problems, offers a different MOA for persons who have failed other agents
disadvantages: should be taken with food or a full glass of water to reduce incidence of nausea, patients should be monitored for potential neuropsychiatric symptoms, post-marketing surveillance data indicate potential for neuropsychiatric symptoms and adverse effects not shown to be prevalent in randomized trials

131
Q

Combination pharmacotherapy for smoking cessation

A
regimens with enough evidence to be recommended first-line
combination NRT (long-acting formulation [patch] produces relatively constant levels of nicotine) PLUS short-acting formulation (gum, inhaler, nasal spray) 
allows for acute dose titration as needed for nicotine withdrawal symptoms

Bupropion SR + Nicotine patch

132
Q

electronic cigarettes

A

deliver nicotine containing aerosol vapor
solution typically contains; propylene glycol or glycerol, nicotine, flavoring agents
marketed as “healthier” versions of cigarettes, aides for smoking cessation, method for circumventing smoke free laws
NOT regulated by FDA
wide variability in nicotine concentrations, solution used, volume of solution in product, delivery systems, battery, additives/flavors
substancs found in e-cigarette solutions: aldehydes, metals, volatile organic compounds
conflicting data on efficacy for smoking cessation

133
Q

what to tell patients about electronic cigarettes

A
  • safest to use conventional products (NRT, bupropion, varenicline)
  • if failed, intolerant of, or refuses traditional treatment, support attempt to quit with electronic cigarettes
  • likely less toxic, but unregulated, contain toxic materials, and are not regulated by FDA
  • do not use in public
  • set quit date for e-cigarette
134
Q

5 A’s

A
Ask - about tobacco use
Advise - tobacco users to quit
Assess - readiness to make a quit attempt
Assist - with quit attempt
Arrange - follow-up care
135
Q

Brief smoking cessation counseling

A

Ask, advise, refer
ask about tobacco use
advise tobacco users to quit
refer to other resources who assist & arrange (patient receives assistance with follow-up counseling arranged from other resources such as tobacco quitline)
brief interventions have been shown to be effective
in the absence of time or expertise: ask, advise & refer to other resources such as local group programs or the toll free quitline 1-800-quit-now

136
Q

Not ready to quit counseling strategies

A
5 R's - methods for enhancing motivation
Relevance
Risks
Rewards
Roadblocks
Repetition
Tailored, motivational messages

with help from a clinician, the odds of quitting approximately doubles

137
Q

N-acetylcysteine

A

Mucolytic
reduces cross linking by reducing disulfide bones - has a free thiol group.
SE: administered by inhalation or intratracheal instillation (giving high dose). Bronchospasm (especially with asthmatics, because they have twitchy airways. Low pH is a trigger that can cause bronchospasm)
Can cause bronchoconstriction
CI in patients with advanced bronchitis because mucus is already liquid –> harder for mucociliary escalator to work.
Poor efficacy - not that much better than inhaling humidified air or instilling saline

138
Q

Dornase alpha

A

Pulmozyme
mucolytic
recombinant human DNase
hydrolyzes extra cellular DNA, decreases mucus viscosity, increases clearance, decreases obstruction & infection risk
SE: wheezing, laryngitis (upper airway irritation), increase antibiotic effects b/c DNA can chemically alter them & if there’s less DNA, then there is more active antibiotics.
Specific nebulizers so dornase alpha goes where mucus is - NOT in peripheral airways or stuck in the throat.

139
Q

hypertonic saline

A

expectorant
promotes fluid flow from epithelium into mucus (osmotic stimuli)
SE: inhalation administration, bronchoconstriction because hypertonicity can stimulate sensory nerve endings- most likely to happen in asthmatics

140
Q

mannitol

A

not approved in US
expectorant
promotes fluid flow from epithelium into mucus (osmotic stimuli)
SE: inhalation administration, broncho constriction because hypertonicity can stimulate sensory nerve endings - most likely to happen in asthmatics.

141
Q

guaifenesin

A
expectorant
irritates gastric mucosa
increases respiratory secretions
decreases viscosity
SE: nausea, vomiting, HA
142
Q

codeine

A

centrally acting antitussive
increases cough threshold, decreases cough reflex
acts on mu receptors in CNS
decreases nerve ending sensitivity
acts at doses BELOW those required for analgesia
SE: nausea, vomiting, constipation, dizziness, mental clouding, abuse potential

143
Q

hydrocodone

A

centrally acting antitussive
increases cough threshold, decreases cough reflex
acts on mu receptors in CNS
decreases nerve ending sensitivity
acts at doses BELOW those required for analgesia
SE: nausea, vomiting, constipation, dizziness, mental clouding, abuse potential

144
Q

dextromethorphan

A

opiate derivative
centrallly acting anti-tussive
no analgesic or additive properties. Codeine is more effective

145
Q

levopropoxyphene napsylate

A
opiate derivative
centrally acting antitussive
l-isomer of dextro propoxyphene
SE: drowsiness, sedative, GI upset
more tolerable & less problematic than codeine
146
Q

benzonatate

A

peripherally acting anti-tussive
decreases sensitivity of cough receptors to stimulants
related to procaine (local anesthetic). Inhibits pulmonary stretch receptors

147
Q

Menthol

A

peripherally acting antitussive

local anesthetic effect on sensory nerves - stretch receptors (numbing cough receptors)

148
Q

3 mechanisms of bronchodilators

A

direct relaxation of airway smooth muscles (beta 2 agonists)
amplification of relaxation pathways (methylxanthines)
inhibition of bronchoconstrictor stimuli (muscarinic antagonists)
act rapidly (within minutes)

149
Q

SABAs

A
albuterol
levalbuterol
metaproterenol
pirbuterol
terbutaline
150
Q

LABAs

A

formoterol

salmeterol

151
Q

ultra LABA

A

indacaterol

152
Q

non-selective beta 2 agonist

A

epinephrine

isoproterenol

153
Q

Beta 2 agonists

A

relax airway smooth muscle
inhibit mediator release
facility mucociliary transport –> increase ciliary function –> good to work harder & faster in order to clear mucus

154
Q

methylxanthines

A

work by amplifying cAMP dependent pathways by blocking breakdown of cAMP
Theophylline
aminophylline
(old drug)
inhibits adenosine receptors, decrease airway smooth muscle contraction, decrease mast cell degranulation
improve ventilatory muscle performance
stimulate cilia to help clear mucus
SE: nausea, vomiting, tachycardia, dysrhythmias, CNA (like caffeine) - restlessness, insomnia, learning impairment in children, brain damage’seizures in children