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Pharmacology > Chapter 10: Pulmonary > Flashcards

Chapter 10: Pulmonary Flashcards

1
Q

Three main respiratory disorders that are responsive to treatment

A

Asthma Allergic rhinitis Cough

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2
Q

Respiratory disorders that are less responsive to treatment

A

COPD Chronic bronchitis

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3
Q

What are bronchodilators usually used for

A

treat reversible bronchospasm in asthma

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4
Q

What receptors do bronchodilators stimulate

A

beta-1, beta-2, alpha-1 adrenergic receptors

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5
Q

stimulation of beta-1

A

cardiac stimulation

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6
Q

stimulation beta-2

A

vasodilation and bronchial dilation

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7
Q

stimulation of aplpha-1

A

bronchodilation, vasoconstriction, pressor effects

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8
Q

What may occur if HR>130

A

ventricular arrythmias

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9
Q

prolonged administration or excessive dosing of bronchodilators can cause

A

metabolic acidosis d/t increase in serum lactic acid

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10
Q

Directions for MDI formulations

A

wait 3-5 minutes between inhalations shake inhaler before use

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11
Q

LABA stand for

A

long acting beta-2 agonists

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12
Q

LABA mechanism of action

A

Stimulates beta-2 receptor to causes relaxation of bronchial, uterine, vascular smooth muscle

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13
Q

LABA clinical uses

A

control reversible airway obstruction prevent exercise induces asthma prevent bronchospasm in COPD emphysema

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14
Q

Examples of LABAs

A

salmeterol (Serevent Diskus)

bitolterol (Tornalate)

formoterol (Foradil)

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15
Q

Can LABAs be used for acute asthma attacks

A

No

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16
Q

LABA contraindications

A

preexisting arrhythmias angina palpitations chest pain narrow angle glaucoma

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17
Q

Types of bronchodilators

A

LABAs

SABAs

Xanthine derivatives

Anticholinergics

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18
Q

Why are LABAs prescribed with corticosteroids

A

increased risk of asthma related death with monotherapy of one or the other

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19
Q

LABA pharmacokinetics

A
  • absorption: not much absorbed systemically as most action is in the lungs
  • distribution: 90% protein bound
  • metabolism: any that is absorbed systemically is metabolized by liver
  • excretion: varies half-life: varies
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20
Q

Formoterol onset, excretion, half-life

A
  • Onset: 1-3 minutes
  • Excretion: urine
  • Half-life: 10 hours
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21
Q

salmeterol onset, excretion, half-life

A
  • Onset: 20 minutes
  • excretion: feces
  • half-life: 3-4 hours
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22
Q

duration of all LABAs

A

12 hours

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23
Q

Bitolterol excretion, half-life

A
  • excretion: feces and urine
  • half-life: 3 hours
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24
Q

LABA adverse reactions

A
  • CV: palpitations, tachycardia GI: nausea, heartburn, GI distress, diarrhea
  • META: hypoglycemia, hypokalemia PULM: cough, dry throat
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25
Q

Conscientious considerations for LABAs

A

excessive use causes tolerance

not monotherapy

dosing is critical in children

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26
Q

LABA interactions

A

beta-blockers can decrease effectiveness

tricyclics

lasix

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27
Q

what should be considered equally for patients older than 5 who have moderate persistent asthma or asthma not controlled on lows dose ICS

A

increasing ICS adding LABA

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28
Q

What is the recommendation for a a patient older than 5 with severe persistent asthma or asthma inadequately controlled on step 3 care

A

combination of ICS and LABA

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29
Q

what does SABA stand for

A

short acting beta-2 agonist

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30
Q

SABA mechanism of action

A

stimulate beta-2 receptors in the lung causing relaxation of bronchial smooth muscle

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31
Q

SABA clinical uses

A

acute asthma exercised induced bronchospasm COPD

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32
Q

Are SABAs recommended for daily use

A

No

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33
Q

Examples of SABAs

A

albuterol (Ventolin, Proventil)

metaproterenol (Alupent)

pirbuterol (Maxair)

terbutaline (Brethine)

levabuterol (Xopenex)

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34
Q

SABA contraindications

A

preexisting arrythmias

angina

narrow angle glaucoma

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35
Q

SABA pharmacokinetics

A
  • absorption: inhaled - gradually from bronchi, oral - rapid from GI tract
  • metabolism: liver
  • excretion: urine
  • half-life: inhaled - 2.7-5 hours, oral - 2-3.8 hours
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36
Q

onset of action for SABAs

A

15-30 minutes

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37
Q

What is the preferred agent to combine with ICS for patients 12 and older

A

LABAs

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38
Q

SABAs adverse reactions

A
  • CV: HTN, tachcardia, palpitations, arrhythmias, chest pain, MI, increased BP followed by decresed BP, doaphoresis, chills, skin blanching
  • GI: N/V
  • NEURO: headache, nervousness, tremor, dizziness
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39
Q

SABA interactions

A

lasix

beta blockers

MAOIs

tricyclics

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40
Q

How long should you wait between SABA and MAOI

A

2 weeks

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41
Q

Are SABAs scheduled regularly

A

No

not advised for daily use only prn

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42
Q

indications of poor asthma control with SABAs

A

usage more than twice/week to control bronchospasm needing refills sooner than allowed

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43
Q

What is the first choice for asthma control

A

Albuterol d/t lower incidence of side effects

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44
Q

Xanthine derivatives mechanism of action

A

directly relaxes bronchial airways relaxes pulmonary blood vessels increases the force of contraction of diaphragmatic muscles

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45
Q

examples of xanthine derivatives

A

theophylline

aminophylline

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46
Q

xanthine derivatives clincal use

A

weak bronchodilators

reserved for patients who are on maximal therapy with safer medications

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47
Q

Xanthine derivative pharmacokinetics

A
  • absorption: rapid and complete orally distribution: freely in fat free tissues
  • metabolism: aminophylline to theophylline then to caffein in liver
  • excretion: renal half-life: 4-8 hours
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48
Q

Do Xanthine derivatives cross placenta

A

Yes, and enter breast milk

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49
Q

what increases half-life of xanthine derivatives

A

smoking

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50
Q

dosage of xanthine derivatives

A

titrate to keep serum levels at 5-12mch/mL

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51
Q

xanthine derivatives adverse effects

A
  • CV: arrhythmias, angine, palpitations, TACHYCARDIA
  • GI: N/V, anorexia, cramps, increased GI acid
  • NEURO: seizures, anxiety, headache, restlessness, tremors, CNS stimulation
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52
Q

xanthine derivatives interactions

A

caffeine, herbls (St. John’s Wort) and ephedra increase levels

beta blockers decrease levels

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53
Q

xanthine derivatives contraindications

A

hyperthyroidism

geriatric

obesity

preexisting arrhythmias

angina

palpitations

narrow-angle glaucoma smokers

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54
Q

xanthine derivatives conscientious considerations

A

can occur near usual therapeutic leves

levels should be monitored every 6-12 months and when condition changes

serious side effects can occur with no preceding signs

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55
Q

Xanthine derivatives patient education

A

hydration to minimize airway secretions

avoid OTC cough medicine

take with H2O if GI upset occurs

call if effect seems to be waning

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56
Q

anticholinergics mechanism of action

A

cause bronchodilation and inhibit nasal secretions

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57
Q

anticholinergic clinical uses

A

prevent acute bronchospasm (bronchitis)

emphysema

rhinorrhea

COPD

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58
Q

examples of anticholinergics

A

ipratropium (Atrovent)

tiotropium (Spiriva)

Ipratropium/albuterol (Combivent)

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59
Q

Ipratropium pharmacokinetics

A
  • absorption: not much systemic
  • metabolism: liver, if absorbed
  • excretion: feces half-life: 1.5-4h
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60
Q

tiotropium pharmacokinetics

A
  • absorption: not much systemic
  • metabolism: largely unchanged if absorbed
  • excretion: urine half-life: 5-6 days
61
Q

anticholinergic adverse effects

A
  • EENT: worsen angle-closure glaucoma causing severe eye pain and blurry vision
  • GI: nausea
  • GU: worsen enlarged prostates and bladder neck issues
  • NEURO: headache
  • PULM: cough, dry nose/mouth, nasal irritation
62
Q

anticholinergic interactions

A

ipratropium can create additive anticholinergic effects

63
Q

anticholinergic contraindications

A

narrow angle glaucoma

enlarged prostate

bladder blockages

sensitivity to atropine

64
Q

anticholinergic patient education

A

MDI: wait 3-5 min between inhalations and shake spiriva

wont work for acute attacks

do not use OTC decongestants for 3-5 days

65
Q

signs of serious allergic reaction to anticholinergics

A

itching/rash

swelling of lips/tongue/throat

blurry vision/halos d/t corneal and conjunctival congestion

66
Q

Types of steroids

A

inhaled corticosteroids

systemic-oral corticosteroids

67
Q

what is the most effective drug class for long-term treatment of asthma

A

inhaled corticosteroids

68
Q

clinical uses of ICS

A

prophylactic asthma treatment

allergic rhinitis

69
Q

ICS mechanism of action

A

anti-inflammatory effects are believed to be mediated through glucocorticoid receptors widely expressed in most cell types throughout the body

70
Q

Examples of ICS for asthma treatment

A

Beclomethasone (QVAR)

Budesonide (Pulmicort)

Flunisolide (Aerobid)

Triamcinalone (Azmacort)

fluticasone (Flovetnt)

mometasone (Asmanex)

71
Q

Examples of ICS for allergic rhinitis

A

Beclomethasone (Beconase)

Ciclesonide (Omnaris)

Triamcinolone (Nasacort)

Fluticasone propionate (Flonase)

72
Q

What action of ICS is potentially responsible for systemic side effects

A

if it is swallowed instead of rinsed, it is absorbed in GI tract

escapes first pass metabolism and enters circulation in active form

73
Q

ICS pharmacokinetics:

absorption, distribution, metabolism

A
  • absorption: pulmonary, nasal, GI tissue
  • distribution: 87% protein bound
  • metabolism: extensive first pass metabolism in liver
74
Q

Beclomethason

excretion and half-life

A
  • excretion: feces
  • half-life: 15 hours
75
Q

dexamethasone

excretion and half-life

A
  • excretion: urine
  • half-life: 3.5-4 hours
76
Q

fluocinolone

excretion and half-life

A
  • excretion: urine
  • half-life: 1.3-1.7 hours
77
Q

mometasone

ecretions and half-life

A
  • excretion: excreted in bile
  • half-life: 5.8 hours
78
Q

ciclesonide

excretion and half-life

A
  • excretion: multiple organs
  • half-life: 0.7 hours
79
Q

LABA dosing

salmeterol (severent diskus)

bitolterol (Tornalate)

formoterol (Foradil)

A

Page 161

80
Q

SABA dosing

albuterol (Ventolin, Proventil)

metaproterenol (Alupent)

pirbuterol (Maxair)

terbutaline (Brethine)

levalbuterol (Xopenex)

A

p. 162

81
Q

Anticholinergic dosing

ipratropium (Atrovent)

tiotropium (Spiriva)

A

p. 164

82
Q

ICS dosing for asthma

beclomethasone (QVAR)

budesonide (Pulmicort)

flunisolide (AeroBid)

fluticasone (Flovent)

mometasone (Asmanex)

triamcinolone (Azmacort)

A

p. 166

83
Q

Systemic oral corticosteroids dosing

hydrocortisone (Solu-Cortef)

prednisone (Deltasone)

methylprednisone (Solu-Medrol)

A

p. 167

84
Q

Leukotriene modifyers dosing

zarfirlukast (Accolate)

montelukast (Singulair)

A

p. 170

85
Q

ICS dosing for rhitinits

beclomethasone (Beconase)

ciclesonide (Omnaris)

triamcinolone (Nasacort)

budesonide (Rhinocort)

flunisolide (Nasarel)

mometasone furoate (Nasonex)

fluticasone propionate (Flonase)

A

p. 166

86
Q

Oxygenase Inhibitors dosing

zileuton (Zyflo CR)

A

p. 171

87
Q

first generation for chronic/seasonal rhinitis dosing

brompheniramine (Dimetane)

clemastine (Tavist)

chlorpheniramine (Chlor-Trimeton)

diphenhydramine (Benadryl)

A

p. 173

88
Q

second generation for chronic/seasonal rhinitis

cetirizine (Zyrtec)

desloratidine (Clarinex)

fexofenadine (Allegra)

loratidine (Claritin)

levocetirizine (Xyzal)

A

p. 173

89
Q

Antitussive dosing

Coricidin

Delsym

Duratuss DM

Hycotuss

Tussionex

Tessalon

Hycodan

A

p. 174

90
Q

dosing of intranasal products

azelastine (Astelin)

ipratropium bromide (Atrovent)

oxymetazoline (Afrin)

beclomethasone (Beconase AQ)

triamcinolone (Nasacort AQ)

budesonide (Rhinocort Aqua)

fluticasone (Flonase, Veramyst)

mometasone (Nasonex)

ciclesonide (Omnaris)

A

p. 175

91
Q

ICS adverse reactions

A
  • EENT: intranasal: naal burning, mucosal dryness, localized fungal infections, sore throat, ulceration of nasal mucosa, bloody nose, nasal candidiasis, eye pain
  • MISC: acute allergic reaction manifests as urticaria, bronchospasm, and angioedema
  • PUL: inhalation: throat irritation, dry mouth, hoarseness, cough, transient bronchospasm, esophageal candidiasis
  • SYSTEMIC: osteoporosis, reduced growth in children, thining of skin, cataracts
92
Q

ICS interactions

A

anything that inhibits CYP450 will increase levels

93
Q

ICS contraindications

A

hypersensitivity

94
Q

Are ICS used to treat acute or chronic asthma

A

preventing exacerbations of chronic asthma

95
Q

oral systemic corticosteroids mechanism of action

A

suppress inflammation and normal immune response system

96
Q

oral corticosteroids clinical uses

A

asthma (short term)

COPD

replacement therapy for adrenal insufficiency

CHron’s

97
Q

examples of oral corticosteroids

A

hydrocortisone (Solu-Cortef)

prednisone (Deltasone)

methylprednisolone (Solu-Medrol)

98
Q

oral corticosteroid ccontraindications

A

serious fungal, viral, or tubercle skin infection

99
Q

oral corticosteroids mechanism of action

A
  • absorption: rapid from any site
  • distribution: 65-91% protein bound
  • metabolism: hepatic converts from inactive to active state
  • excretion: urine
  • half-life:
    • prednisone: 2.5-3.5 hours
    • methylprednisolone: 3-3.5 hours
    • hydrocortisone: 1.5-2 hours
100
Q

what is the best time of day to take oral corticosteroids

A

3:00 pm

101
Q

oral corticosteroid adverse reactions

A
  • DERM: acne, facial flushing, delayed wound healing
  • ENDO: suppress growth (aldolescents), cause Cushing’s syndrome, induce DM
  • GI: heartburn, abdominal distention, increased appetitie, diarrhea, constipation
  • MISC: high dose can be immunosuppressive (monitor for infection)
  • NEURO: insomnia, nervousness, mood swing, psychosis
102
Q

oral corticosteroids interactions

A

insulin/oral hypoglycemics (increases BG_

ethanol increased gastric mucosal secretions

103
Q

oral corticosteroid patient education

A

take with food if GI upset

prevent side effects by rinsing mouth after dose

104
Q

Types of inhaled anti-inflammatory agents

A

Leukotriene receptor agonists (LTA)

oxygenase inhibitors

monoclonal antibodies

mast cell stabilizers

105
Q

mast cell stabilizers mechanism of action

A

inhibits antigen-induced bronchospasm

106
Q

Mast cell stabilizers conscientious consideration

A

monitor for possibility of reduction of other astma medications in 2-4 weeks

not for acute attacks (prophylactic)

consider pretreatment with bronchodilators to increase effectiveness

107
Q

examples of sodium cromoglycates

A

Cromolyn (Intal)

nedocromolyn (Tilade)

taken off market in 2010 for depleting ozone

108
Q

mechanism of action for leukotriene modifiers

A

help reverse the ability of leukotriene to constrict airway smooth muscle through inflammatory processess

(asthma, allergy, airway edema/bronchoconsriction)

109
Q

2 types of leukotriene modifiers

A

LTA

5-lipoxygenase inhibitors

110
Q

Examples of leukotriene receptor agonists

A

montelukast (Singulair) - >12

zafirlukast (Accolate) - >5

111
Q

leukotriene receptor agonists mechanism of action

A

blocks leukotriene’s recptor so the enzyme that responds to it to cause inflammation can’t

112
Q

leukotriene receptor agonists clinical uses

A

long-term treatment for mild persistent asthma

as part of combo therapy with corticosteroids for moderate persistent asthma

113
Q

leukotriene receptors agonists pharmacokinetics

A
  • absorption: food reduces (take on empty stomach)
  • distribution: 90-99% protein bound (peak concentration in 3hr)
  • metabolism: liver CYP450 pathway
  • excretion: urine if metabolized, feces if not
  • half-life:
    • zafirlukast: 10 hours
    • montelukast: 2.5-5 hours
114
Q

leukotriene receptor agonists adverse reactions

A
  • EENT: pharyngitis, rhinitis
  • GI: gastritis, GI upset, serious liver dysfunction (rare)
  • HEM: eosinophil condition
  • NEURO: headache, weakness
    • PULM: cough, may cause CHURG-STRAUSS syndrome (rare pulmonary vasculitis)
115
Q

leukotriene receptor agonist contraindications

A

impaired liver function or disease

116
Q

leukotrien receptor agonists patient education

A

take even during asymptomatic periods

not for acute attacks

regular PFTs will be needed

117
Q

Things to monitor when patient is on oxygenase inhibitor

A

LFTs periodically during 1st year

ALT q3 months for 1st year, then periodically

118
Q

Monoclonal antibodies mechanism of action

A

Bind to IgE receptors on mast cells and eosinophils preventing release of mediators to the allergic response

reduces/prevents number of asthma exacerbations

119
Q

monoclonal antibodies clinical uses

A

moderate-persistent asthma if reactive to periennial allergens or are not controlled by ICS

120
Q

example of monoclonal antibody

A

omalizumab (Xolair)

121
Q

Xolair pharmacokinetics

A
  • absorption: SQ injection (slowly absorbed)
  • distribution: serum protein
  • metabolism: hepatic
  • excretion: hepatic and reticuloendothelial
    • half-life: 26 days
122
Q

when is Xolair’s peak effect seen

A

7-8 days

123
Q

Xolair dosing

A

p. 172

124
Q

Xolair adverse reactions

A
  • DERM: urticaria at injection site
  • EENT: sinusitis, pharyngitis
  • MISC: malignant neoplasms, viral infections, ANAPHYLAXIS
  • NEURO: headache
125
Q

Xolair interactions

A

none

126
Q

Benefit to combination products

A

may increase benefit and decrease cost

127
Q

Bronchodilator/anti-inflammatory combinations

A

salmeterol/fluticasone (Advair)

albuterol/ipratropium (Combivent)

128
Q

Advair/Combivent contraindications

A

heart disease

HTN

CHF

siezures

allergies to soy (soybeans and peanuts)

129
Q

combinations using inhaled steroids

A

clinical differences in potency

adjust dosing when switching from on to another

delivery device influences effect (MDI, DPI. etc)

130
Q

types of medications used to treat chronic/seasonal allergic rhinitis

A

antihistamines

antitussives

131
Q

antihistamines action

A

decrease histamine-mediated contraction of smooth muscle of the bronchi, intestine, and uterus

132
Q

antihistamine clinical uses

A

prevent allergic response mediated by histamine

133
Q

examples of first generation antihistamines

A

diphenhydramine (Benadryl)

chlorpheniramine (Chlor-Trimeton)

134
Q

examples of second generation antihistamines

A

certirizine (Zyrtec)

desloratidine (Clarinex)

allegra

claritin

135
Q

antihistamine interactions

A

antacids with calcium and magnesium will decrease absorption

136
Q

What is the best antihistamine

A

No one is better than any other

137
Q

antihistamine pharmacokinetics

A
  • absorption: rapid after oral
  • distribution: 60-70% protein bound
  • metabolism: minimal
  • excretion: feces and urine
  • half-life: wide ranging (p. 173)
138
Q

antihistamine adverse reactions

A
  • CV: potential for QT elongation
  • GI: N/V, GI distress
  • GYN: dysmenorrhea
  • NEURO: somnolence, headache, fatigue
139
Q

antitussive mechanism of action

A

act on cough center in the medulla by elevating its threshold for the cough reflex

140
Q

clinical uses of antitussives

A

cough suppression

throat irritation

141
Q

what are antitussives often combined with

A

benzocaine in throat lozenges

142
Q

examples of antitussives

A

dextromethorphan (Delsym)

guaifenesin/hydrocodone (Hycotuss)

diphenhydramine/dextromethorphan (Duratuss DM)

143
Q

antitussive pharmacokinetics

A
  • absorption: rapid from GI tract
  • distribution: into CFS
  • metabolism: liver
  • excretion: renal
144
Q

antitussives adverse reactions

A
  • GI: abdominal discomfort, constipation, GI upset, nausea
  • NEURO: dizziness, drowsiness
145
Q

antitussive interactions

A

can cause MAOI toxicity

alcohol could cause respiratory distress

146
Q

antitussive patient education

A

danger to children

dont drink alcohol

147
Q

examples of intranasal steroids

A

beclomethasone (Beconase AQ)

triamcinalone (Nasacort AQ)

budesonide (Rhinocort Aqua)

fluticasone (Flonase, Veramyst)

mometasone (Nasonex)

ciclesonide (Omnaris)

148
Q

examples of other non-steroid intranasals

A

azelastine (Astelin) - antihistamine

ipratropium bromide (Atrovent) - anticholinergic

oxymetazoline (Afrin) - sympathomimetic

149
Q

pregnancy. geriatric, pediatric considerations

A

p. 175-176

Pharmacology (28 decks)

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