Chapter 10: Pulmonary Flashcards Preview

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Flashcards in Chapter 10: Pulmonary Deck (149):
1

 

 

Three main respiratory disorders that are responsive to treatment

 

 

Asthma Allergic rhinitis Cough

2

 

 

Respiratory disorders that are less responsive to treatment

 

 

COPD Chronic bronchitis

3

 

 

What are bronchodilators usually used for

 

 

treat reversible bronchospasm in asthma

4

 

 

What receptors do bronchodilators stimulate

 

 

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

5

 

 

stimulation of beta-1

 

 

cardiac stimulation

6

 

 

stimulation beta-2

 

 

vasodilation and bronchial dilation

7

 

 

stimulation of aplpha-1

 

 

bronchodilation, vasoconstriction, pressor effects

8

 

 

What may occur if HR>130

 

 

ventricular arrythmias

9

 

 

prolonged administration or excessive dosing of bronchodilators can cause

 

 

metabolic acidosis d/t increase in serum lactic acid

10

 

 

Directions for MDI formulations

 

 

wait 3-5 minutes between inhalations shake inhaler before use

11

 

 

LABA stand for

 

 

long acting beta-2 agonists

12

 

 

LABA mechanism of action

 

 

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

13

 

 

LABA clinical uses

 

 

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

14

 

 

Examples of LABAs

 

 

salmeterol (Serevent Diskus)

bitolterol (Tornalate)

formoterol (Foradil)

15

 

 

Can LABAs be used for acute asthma attacks

 

 

No

16

 

 

LABA contraindications

 

 

preexisting arrhythmias angina palpitations chest pain narrow angle glaucoma

17

 

 

Types of bronchodilators

 

 

LABAs

SABAs

Xanthine derivatives

Anticholinergics

18

 

 

Why are LABAs prescribed with corticosteroids

 

 

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

19

 

 

LABA pharmacokinetics

 

 

  • 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

20

 

 

Formoterol onset, excretion, half-life

 

 

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

21

 

 

salmeterol onset, excretion, half-life

 

 

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

22

 

 

duration of all LABAs

 

 

12 hours

23

 

 

Bitolterol excretion, half-life

 

 

  • excretion: feces and urine
  • half-life: 3 hours

24

 

 

LABA adverse reactions

 

 

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

25

 

 

Conscientious considerations for LABAs

 

 

excessive use causes tolerance

not monotherapy

dosing is critical in children

26

 

 

LABA interactions

 

 

beta-blockers can decrease effectiveness

tricyclics

lasix

27

 

 

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

 

 

increasing ICS adding LABA

28

 

 

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

 

 

combination of ICS and LABA

29

 

 

what does SABA stand for

 

 

short acting beta-2 agonist

30

 

 

SABA mechanism of action

 

 

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

31

 

 

SABA clinical uses

 

 

acute asthma exercised induced bronchospasm COPD

32

 

 

Are SABAs recommended for daily use

 

 

No

33

 

 

Examples of SABAs

 

albuterol (Ventolin, Proventil)

metaproterenol (Alupent)

pirbuterol (Maxair)

terbutaline (Brethine)

levabuterol (Xopenex)

34

 

 

SABA contraindications

 

 

preexisting arrythmias

angina 

narrow angle glaucoma

35

 

 

SABA pharmacokinetics

 

 

  • 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

36

 

 

onset of action for SABAs

 

 

15-30 minutes

37

 

 

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

 

 

LABAs

38

 

 

SABAs adverse reactions

 

 

  • 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

39

 

 

SABA interactions

 

 

lasix

beta blockers

MAOIs

tricyclics

40

 

 

How long should you wait between SABA and MAOI

 

 

2 weeks

41

 

 

Are SABAs scheduled regularly

 

 

No

not advised for daily use only prn

42

 

 

indications of poor asthma control with SABAs

 

 

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

43

 

 

What is the first choice for asthma control

 

 

Albuterol d/t lower incidence of side effects

44

 

 

Xanthine derivatives mechanism of action

 

 

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

45

 

 

examples of xanthine derivatives

 

 

theophylline

aminophylline

46

 

 

xanthine derivatives clincal use

 

 

weak bronchodilators

reserved for patients who are on maximal therapy with safer medications

47

 

 

Xanthine derivative pharmacokinetics

 

 

  • 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

48

 

 

Do Xanthine derivatives cross placenta

 

 

Yes, and enter breast milk

49

 

 

what increases half-life of xanthine derivatives

 

 

smoking

50

 

 

dosage of xanthine derivatives

 

 

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

51

 

 

xanthine derivatives adverse effects

 

 

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

52

 

 

xanthine derivatives interactions

 

 

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

beta blockers decrease levels

53

 

 

xanthine derivatives contraindications

hyperthyroidism

geriatric

obesity

preexisting arrhythmias

angina

palpitations

narrow-angle glaucoma smokers

54

 

 

xanthine derivatives conscientious considerations

 

 

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

55

 

 

Xanthine derivatives patient education

 

 

hydration to minimize airway secretions

avoid OTC cough medicine

take with H2O if GI upset occurs

call if effect seems to be waning

56

 

 

anticholinergics mechanism of action

 

 

cause bronchodilation and inhibit nasal secretions

57

 

 

anticholinergic clinical uses

 

 

prevent acute bronchospasm (bronchitis)

emphysema

rhinorrhea

COPD

58

 

 

examples of anticholinergics

 

 

ipratropium (Atrovent)

tiotropium (Spiriva)

Ipratropium/albuterol (Combivent)

59

 

 

Ipratropium pharmacokinetics

 

 

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

60

 

 

tiotropium pharmacokinetics

 

 

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

61

 

 

anticholinergic adverse effects

 

  • 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

 

 

anticholinergic interactions

 

 

ipratropium can create additive anticholinergic effects

63

 

 

anticholinergic contraindications

 

narrow angle glaucoma

enlarged prostate

bladder blockages

sensitivity to atropine

64

 

 

anticholinergic patient education

 

 

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

 

 

signs of serious allergic reaction to anticholinergics

 

itching/rash 

swelling of lips/tongue/throat

blurry vision/halos d/t corneal and conjunctival congestion

66

 

 

Types of steroids

 

 

inhaled corticosteroids

systemic-oral corticosteroids

67

 

 

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

 

 

inhaled corticosteroids

68

 

 

clinical uses of ICS

 

 

prophylactic asthma treatment

allergic rhinitis

69

 

 

ICS mechanism of action

 

 

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

70

 

 

Examples of ICS for asthma treatment

 

Beclomethasone (QVAR)

Budesonide (Pulmicort)

Flunisolide (Aerobid)

Triamcinalone (Azmacort)

fluticasone (Flovetnt)

mometasone (Asmanex)

71

 

 

Examples of ICS for allergic rhinitis

 

 

 

 

Beclomethasone (Beconase)

Ciclesonide (Omnaris)

Triamcinolone (Nasacort)

Fluticasone propionate (Flonase)

72

 

 

What action of ICS is potentially responsible for systemic side effects

 

 

 

 

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

escapes first pass metabolism and enters circulation in active form

 

73

 

 

ICS pharmacokinetics:

absorption, distribution, metabolism

 

 

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

74

 

 

Beclomethason

excretion and half-life

 

 

  • excretion: feces
  • half-life: 15 hours

75

 

 

dexamethasone

excretion and half-life

 

 

  • excretion: urine
  • half-life: 3.5-4 hours

76

 

 

fluocinolone

excretion and half-life

 

 

  • excretion: urine
  • half-life: 1.3-1.7 hours

77

 

 

mometasone

ecretions and half-life

 

 

  • excretion: excreted in bile
  • half-life: 5.8 hours

78

 

 

ciclesonide

excretion and half-life

 

 

  • excretion: multiple organs
  • half-life: 0.7 hours

79

LABA dosing

 

salmeterol (severent diskus)

bitolterol (Tornalate)

formoterol (Foradil)

 

 

Page 161

80

SABA dosing

albuterol (Ventolin, Proventil)

metaproterenol (Alupent)

pirbuterol (Maxair)

terbutaline (Brethine)

levalbuterol (Xopenex)

 

 

p. 162

81

Anticholinergic dosing

 

ipratropium (Atrovent)

tiotropium (Spiriva)

 

 

p. 164

82

ICS dosing for asthma

 

beclomethasone (QVAR)

budesonide (Pulmicort)

flunisolide (AeroBid)

fluticasone (Flovent)

mometasone (Asmanex)

triamcinolone (Azmacort)

 

 

 

p. 166

83

Systemic oral corticosteroids dosing

 

hydrocortisone (Solu-Cortef)

prednisone (Deltasone)

methylprednisone (Solu-Medrol)

 

 

p. 167

84

Leukotriene modifyers dosing

 

zarfirlukast (Accolate)

montelukast (Singulair)

 

 

p. 170

85

ICS dosing for rhitinits

 

beclomethasone (Beconase)

ciclesonide (Omnaris)

triamcinolone (Nasacort)

budesonide (Rhinocort)

flunisolide (Nasarel)

mometasone furoate (Nasonex)

fluticasone propionate (Flonase)

 

 

p. 166

86

Oxygenase Inhibitors dosing

 

zileuton (Zyflo CR)

 

 

p. 171

87

first generation for chronic/seasonal rhinitis dosing

 

brompheniramine (Dimetane)

clemastine (Tavist)

chlorpheniramine (Chlor-Trimeton)

diphenhydramine (Benadryl)

 

 

p. 173

88

second generation for chronic/seasonal rhinitis

 

cetirizine (Zyrtec)

desloratidine (Clarinex)

fexofenadine (Allegra)

loratidine (Claritin)

levocetirizine (Xyzal)

 

 

p. 173

89

Antitussive dosing

 

Coricidin

Delsym

Duratuss DM

Hycotuss

Tussionex

Tessalon

Hycodan

 

 

p. 174

90

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)

 

 

p. 175

91

 

 

ICS adverse reactions

 

 

 

  • 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

 

 

ICS interactions

 

 

anything that inhibits CYP450 will increase levels

93

 

 

ICS contraindications

 

 

hypersensitivity

94

 

 

Are ICS used to treat acute or chronic asthma

 

 

preventing exacerbations of chronic asthma

95

 

 

oral systemic corticosteroids mechanism of action

 

 

suppress inflammation and normal immune response system

96

 

 

oral corticosteroids clinical uses

 

 

asthma (short term)

COPD

replacement therapy for adrenal insufficiency

CHron's

97

 

 

examples of oral corticosteroids

 

 

hydrocortisone (Solu-Cortef)

prednisone (Deltasone)

methylprednisolone (Solu-Medrol)

98

 

 

oral corticosteroid ccontraindications

 

 

serious fungal, viral, or tubercle skin infection

99

 

 

oral corticosteroids mechanism of action

 

  • 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

 

 

what is the best time of day to take oral corticosteroids

 

 

3:00 pm

101

 

 

oral corticosteroid adverse reactions

 

  • 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

 

 

oral corticosteroids interactions

 

 

insulin/oral hypoglycemics (increases BG_

ethanol increased gastric mucosal secretions

103

 

 

oral corticosteroid patient education

 

take with food if GI upset

prevent side effects by rinsing mouth after dose

104

 

Types of inhaled anti-inflammatory agents

 

Leukotriene receptor agonists (LTA)

oxygenase inhibitors

monoclonal antibodies

mast cell stabilizers

105

 

 

mast cell stabilizers mechanism of action

 

 

inhibits antigen-induced bronchospasm

106

 

 

Mast cell stabilizers conscientious consideration

 

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

 

 

examples of sodium cromoglycates

 

 

Cromolyn (Intal)

nedocromolyn (Tilade)

taken off market in 2010 for depleting ozone

108

 

 

mechanism of action for leukotriene modifiers

 

 

 

 

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

(asthma, allergy, airway edema/bronchoconsriction)

109

 

 

2 types of leukotriene modifiers

 

 

 

 

LTA

5-lipoxygenase inhibitors

110

 

 

Examples of leukotriene receptor agonists

 

 

montelukast (Singulair) - >12

zafirlukast (Accolate) - >5

111

 

 

leukotriene receptor agonists mechanism of action

 

 

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

112

 

 

leukotriene receptor agonists clinical uses

 

 

long-term treatment for mild persistent asthma

as part of combo therapy with corticosteroids for moderate persistent asthma

113

 

 

leukotriene receptors agonists pharmacokinetics

 

  • 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

 

 

leukotriene receptor agonists adverse reactions

 

 

  • 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

 

 

leukotriene receptor agonist contraindications

 

 

impaired liver function or disease

116

 

 

leukotrien receptor agonists patient education

 

 

take even during asymptomatic periods

not for acute attacks

regular PFTs will be needed

117

 

 

Things to monitor when patient is on oxygenase inhibitor

 

 

LFTs periodically during 1st year

ALT q3 months for 1st year, then periodically

118

 

 

Monoclonal antibodies mechanism of action

 

 

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

reduces/prevents number of asthma exacerbations

119

 

 

monoclonal antibodies clinical uses

 

 

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

120

 

 

example of monoclonal antibody

 

 

omalizumab (Xolair)

121

 

 

Xolair pharmacokinetics

 

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

122

 

 

when is Xolair's peak effect seen

 

 

7-8 days

123

 

 

Xolair dosing

 

 

p. 172

124

 

 

Xolair adverse reactions

 

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

125

 

 

Xolair interactions

 

 

none

126

 

 

Benefit to combination products

 

 

may increase benefit and decrease cost

127

 

 

Bronchodilator/anti-inflammatory combinations

 

 

salmeterol/fluticasone (Advair)

albuterol/ipratropium (Combivent)

128

 

 

Advair/Combivent contraindications

 

 

heart disease

HTN

CHF

siezures

allergies to soy (soybeans and peanuts)

129

 

 

combinations using inhaled steroids

 

 

clinical differences in potency

adjust dosing when switching from on to another

delivery device influences effect (MDI, DPI. etc)

130

 

 

types of medications used to treat chronic/seasonal allergic rhinitis

 

 

antihistamines

antitussives

131

 

 

antihistamines action

 

 

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

132

 

 

antihistamine clinical uses

 

 

prevent allergic response mediated by histamine

133

 

 

examples of first generation antihistamines

 

 

diphenhydramine (Benadryl)

chlorpheniramine (Chlor-Trimeton)

134

 

 

examples of second generation antihistamines

 

 

certirizine (Zyrtec)

desloratidine (Clarinex)

allegra

claritin

135

 

 

antihistamine interactions

 

 

antacids with calcium and magnesium will decrease absorption

136

 

 

What is the best antihistamine

 

 

No one is better than any other

137

 

 

antihistamine pharmacokinetics

 

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

138

 

 

antihistamine adverse reactions

 

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

139

 

 

antitussive mechanism of action

 

 

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

140

 

 

clinical uses of antitussives

 

 

cough suppression

throat irritation

141

 

 

what are antitussives often combined with

 

 

benzocaine in throat lozenges

142

 

 

examples of antitussives

 

 

 

dextromethorphan (Delsym)

guaifenesin/hydrocodone (Hycotuss)

diphenhydramine/dextromethorphan (Duratuss DM)

143

 

 

antitussive pharmacokinetics

 

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

144

 

 

antitussives adverse reactions

 

 

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

145

 

 

antitussive interactions

 

 

can cause MAOI toxicity

alcohol could cause respiratory distress

146

 

 

antitussive patient education

 

 

danger to children

dont drink alcohol

147

 

 

examples of intranasal steroids

 

beclomethasone (Beconase AQ)

triamcinalone (Nasacort AQ)

budesonide (Rhinocort Aqua)

fluticasone (Flonase, Veramyst)

mometasone (Nasonex)

ciclesonide (Omnaris)

148

 

 

examples of other non-steroid intranasals

 

azelastine (Astelin) - antihistamine

ipratropium bromide (Atrovent) - anticholinergic

oxymetazoline (Afrin) - sympathomimetic

149

 

 

pregnancy. geriatric, pediatric considerations

 

 

p. 175-176