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Pharmacology - Exam 3 > Allergic Rhinitis > Flashcards

Allergic Rhinitis Flashcards

1
Q

How is allergic rhinitis treated?

A
  • allergen avoidance
  • pharmacotherapy
  • allergen immunotherapy (desensitization)
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2
Q

What is the best monotherapy for allergic rhinitis?

A
  • glucocorticoid nasal spray (INGCs)
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3
Q

What are INGCs particularly effective at txing?

A
  • nasal congestion
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4
Q

What are the 1st generation INGCs?

A
  • budesonide
  • triamcinolone
  • beclomethasone
  • flunisolide
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5
Q

What are the 2nd generation INGCs?

A
  • fluticasone propionate of furoate
  • mometasone
  • ciclesonide
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6
Q

What is the MOA of INGCs?

A
  • inhibit nasal inflam by inhibiting cytokines/chemokines
  • bind to intracellular glucocorticoid receptors of inflam cells to produce anti-inflam proteins & supress production of cytokines/chemokines
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7
Q

What is the ADME of INGCs?

A
  • A: minimal systemic
  • D: N/A
  • M: hepatic (1st pass metabolism)
  • E: N/E
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8
Q

What is the bioavailability of 1st gen INGCs?

A
  • 10-50%
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9
Q

What is the bioavailability of 2nd gen INGCs?

A
  • undetectable, <2%
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10
Q

What is the onset of INGCs?

A
  • few hours

- may take 3-5d or w before FULL RELIEF

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11
Q

T/F: Oral antihistamines are more effective than INGCs on nasal congestion.

A
  • False
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12
Q

What is the result of taking INGCs?

A
  • relieves congestion (i.e. nasal blockage, d/c, sneezing, itching, PND)
  • relieves ocular sx
  • can reduce response when taken prior to exposure
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13
Q

T/F: INGCs can be used PRN

A
  • True but not as effective
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14
Q

What are the ADE of INGCs?

A
  • local

i. e. nasal irritation, drying, burning, mech trauma, discomfort from run-off into throat, nasal septal perf

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15
Q

What are the potential drug interactions of INGCs?

A
  • fluticasone + strong CYP3A4 inhibitors (ritonavir in HIV + patient)
  • clinically significant adrenal suppression
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16
Q

What is seen in children taking INGCs?

A
  • growth suppression in excessive long-term beclomethasone
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17
Q

What is the new formulation for INGCs?

A
  • dry powder formulation in HFA propellent
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18
Q

What is the MOA of oral antihistamines?

A
  • block action of histamine at H1 receptor

- inverse agonist, not antagonist (bind receptor and causes the receptor to be inactive)

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19
Q

What are the categories of antihistamines?

A
  • 1st gen

- 2nd gen

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20
Q

Which antihistamine generation can cross BBB?

A
  • 1st

- cause sedation/CNS depression

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21
Q

What is the ADME of antihistamines?

A
  • A: rapidly absorbed (10-30m)
  • D: 60-70% protein bound
  • M: minimal except desloratadine
  • E: primarily urine
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22
Q

What is the duration of action of 1st gen oral antihistamines?

A
  • generally 1-6h
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23
Q

What is the duration of action of 2nd gen oral antihistamines?

A
  • 6-24h
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24
Q

T/F: All 1st gen oral antihistamines are available OTC

A

-True

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25
Q

What are the safety concerns with 1st gen oral antihistamines?

A
  • lipophilic (easily to X BBB)

- not recommended for elderly

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26
Q

What are the ADE of 1st gen oral antihistamines?

A
  • intellectual and motor function

- mostly driving performance

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27
Q

What are the side effects of 1st gen oral antishistamines?

A
  • anticholinergic effects (dry mouth/eyes, impotentce, urinary hesitancy, glaucoma)
  • CNS effects (sedation, rarlely stim usually in children, confussion in older pts, cognitive impairments)
  • wt gain
  • hypersensitivity
  • prolonge QT
  • ventricular arrhythmias
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28
Q

What are the 1st gen oral antihistamines?

A
  • diphenhydramine
  • chlorpheniramine
  • clemastine
  • brompheniramine
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29
Q

What are the 2nd gen oral antihistamines?

A
  • loratadine

- cetirizine

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30
Q

What makes a 3rd gen oral antihistamine?

A
  • metabolites of 2nd gen
31
Q

What were 2nd gen oral antihistamines developed for?

A
  • lipophobic to prevent unwanted CNS effects
32
Q

What is the onset of action for 2nd gen oral antihistamines?

A
  • w/in 1hr

- peak serum levels in 2-3hrs

33
Q

What is the duration of action for 2nd gen oral antihistamines?

A
  • long acting
34
Q

What is the MOA of 2nd gen oral antihistamines?

A
  • same as 1st (block H1 receptor)
  • decrease mast cell release
  • inhibition of inflam mediators (IL-4 and 13) [good for ashtma]
35
Q

What is the role of 2nd gen oral antihistamines?

A
  • popular option, most available OTC

- mild or intermittent sx

36
Q

_____ are less effective than _____, but equally or more effective than _____.

A
  • 2nd gen antihistamines are less effective than INGCs, but equally or more effective than cromolyn.
37
Q

What are the ADEs of 2nd gen oral antihistamines?

A
  • anticholinergic effects (dry eyes)

- ? wt gain

38
Q

What can 2nd gen oral antihistamines have a drug interaction with?

A
  • St. John’s wort
39
Q

What are the nasal antihistamines?

A
  • azelastine

- olopatadine

40
Q

What is the efficacy of nasal antihistamines?

A
  • antiinflam effect

- decrease nasal congestion

41
Q

What is the onset of action of nasal antihistamines?

A
  • < 15min
42
Q

How can nasal antihistamines be administered?

A
  • “on demand”
43
Q

Which is preferred, nasal antihistamines of INGCs?

A
  • INGCs
44
Q

What are the ADEs of nasal antihistamines?

A
  • bitter taste

- ? midly sedating

45
Q

What is the mast cell stabilizer?

A
  • cromolyn
46
Q

What is the MOA of mast cell stabilizers?

A
  • inhibits mast cell release of histamine
47
Q

What is the efficacy of mast cell stabilizers?

A
  • more effective than placebo

- less effective than INGCs or 2nd gen antihistamines

48
Q

What is the dosing schedule for mast cell stabilizers?

A
  • frequent
49
Q

How long does it take to achieve full relieve with mast cell stabilizers?

A
  • 2-4w
50
Q

What are the ADEs of mast cell stabilizers?

A
  • no serious

- increase in sneezing, burning, stinging, or irritation in nose, H/A, unpleasant taste

51
Q

What is the MOA of leukotriene modifiers?

A
  • inhibit cysteinyl leukotriene receptor which are released from nasal mucosa upon allergen exposure
52
Q

What are the antileukotriene agents or leukotriene modifiers?

A
  • montelukast (Singulair)
  • Zafirlukast (Accolate)
  • Zileuton (Zyflo)
53
Q

What are leukotriene modifiers tx for?

A
  • asthma
54
Q

Which leukotriene modifier is approved for tx of allergic rhinitis?

A
  • montelukast (Singulair)
55
Q

What is leukotriene modifiers efficacy when compared with INGCs?

A
  • less
56
Q

What is the place in therapy of leukotriene modifiers?

A
  • pts with concomitant asthma

- pts who cannot tolerate/refuse nasal sprays

57
Q

What is a side effect of leukotriene modifiers?

A
  • neuropsychiatric changes usually in children
58
Q

What is the MOA of ipatropium?

A
  • anticholinergic

- ? decrease release of substance P

59
Q

What is the efficacy of ipatropium?

A
  • only reduces rhinorrhea
60
Q

What is the place in therapy for ipatropium?

A
  • not recommended as 1st line therapy

- only in pts with profuse rhinorrhea, not otherwise controlled with INGCs

61
Q

What is the MOA of antitussives?

A
  • ? decrease cough associated with allergic rhinitis

- act on cough center in medulla oblongata

62
Q

What family are the substances in of antitussives?

A
  • morphine family
  • codine
  • dextromethorphan
63
Q

What are the general ADEs of antitussives?

A
  • GI

- neuro

64
Q

What will the antitussives interact with?

A
  • MAOIs

- ETOH

65
Q

What is a CI of antitussives?

A
  • concurrent MOAI use
66
Q

What is the MOA of nasal decongestant sparys?

A
  • direct-acting alpha-adrenergic agonist

- vasoconstriction –> nasal decong.

67
Q

What are the nasal decongestant sprays?

A
  • phenylephrine (Neo-Synephrine)
  • oxymetazoline (Afrin)
  • naphazoline (Privine)
68
Q

What is a side effect of nasal decongestant sprays?

A
  • rhinitis medicamentosa
69
Q

What is the physiology of rhinitis medicamentosa?

A
  • down regulation of alpha-adrenergic receptor after 3-7d
70
Q

What is a result from rhinitis medicamentosa?

A
  • rebound nasal congestion < 3d
71
Q

When are nasal decongestant sprays useful?

A
  • in combo with INGCs

- limited use to less than 3d

72
Q

When are oral (systemic) glucocorticoids indicated?

A
  • short course
  • severe allergic rhinitis sx that prevent sleeping or work
  • not to be given repeatedly or long term
73
Q

Describe the pathophysiology of allergic rhinitis

A
  • allergic inflam of nasal mucosa triggered by IgE production binding to mast cells & basophils containing & releasing histamine
74
Q

What are the medication classes used to treat allergic rhinitis?

A
  • glucocorticoids
  • oral antihistamines
  • antihistamine nasal sprays
  • mast cell stabilizers
  • leukotriene modifiers
  • ipatropium
  • antitussives

Pharmacology - Exam 3 (4 decks)

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