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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
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

Pharmacology (28 decks)

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