Allergic Rhinitis Flashcards
1
Q
How is allergic rhinitis treated?
A
- allergen avoidance
- pharmacotherapy
- allergen immunotherapy (desensitization)
2
Q
What is the best monotherapy for allergic rhinitis?
A
- glucocorticoid nasal spray (INGCs)
3
Q
What are INGCs particularly effective at txing?
A
- nasal congestion
4
Q
What are the 1st generation INGCs?
A
- budesonide
- triamcinolone
- beclomethasone
- flunisolide
5
Q
What are the 2nd generation INGCs?
A
- fluticasone propionate of furoate
- mometasone
- ciclesonide
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
7
Q
What is the ADME of INGCs?
A
- A: minimal systemic
- D: N/A
- M: hepatic (1st pass metabolism)
- E: N/E
8
Q
What is the bioavailability of 1st gen INGCs?
A
- 10-50%
9
Q
What is the bioavailability of 2nd gen INGCs?
A
- undetectable, <2%
10
Q
What is the onset of INGCs?
A
- few hours
- may take 3-5d or w before FULL RELIEF
11
Q
T/F: Oral antihistamines are more effective than INGCs on nasal congestion.
A
- False
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
13
Q
T/F: INGCs can be used PRN
A
- True but not as effective
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
15
Q
What are the potential drug interactions of INGCs?
A
- fluticasone + strong CYP3A4 inhibitors (ritonavir in HIV + patient)
- clinically significant adrenal suppression
16
Q
What is seen in children taking INGCs?
A
- growth suppression in excessive long-term beclomethasone
17
Q
What is the new formulation for INGCs?
A
- dry powder formulation in HFA propellent
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)
19
Q
What are the categories of antihistamines?
A
- 1st gen
- 2nd gen
20
Q
Which antihistamine generation can cross BBB?
A
- 1st
- cause sedation/CNS depression
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
22
Q
What is the duration of action of 1st gen oral antihistamines?
A
- generally 1-6h
23
Q
What is the duration of action of 2nd gen oral antihistamines?
A
- 6-24h
24
Q
T/F: All 1st gen oral antihistamines are available OTC
A
-True
25
What are the safety concerns with 1st gen oral antihistamines?
- lipophilic (easily to X BBB)
| - not recommended for elderly
26
What are the ADE of 1st gen oral antihistamines?
- intellectual and motor function
| - mostly driving performance
27
What are the side effects of 1st gen oral antishistamines?
- 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
28
What are the 1st gen oral antihistamines?
- diphenhydramine
- chlorpheniramine
- clemastine
- brompheniramine
29
What are the 2nd gen oral antihistamines?
- loratadine
| - cetirizine
30
What makes a 3rd gen oral antihistamine?
- metabolites of 2nd gen
31
What were 2nd gen oral antihistamines developed for?
- lipophobic to prevent unwanted CNS effects
32
What is the onset of action for 2nd gen oral antihistamines?
- w/in 1hr
| - peak serum levels in 2-3hrs
33
What is the duration of action for 2nd gen oral antihistamines?
- long acting
34
What is the MOA of 2nd gen oral antihistamines?
- same as 1st (block H1 receptor)
- decrease mast cell release
- inhibition of inflam mediators (IL-4 and 13) [good for ashtma]
35
What is the role of 2nd gen oral antihistamines?
- popular option, most available OTC
| - mild or intermittent sx
36
_____ are less effective than _____, but equally or more effective than _____.
- 2nd gen antihistamines are less effective than INGCs, but equally or more effective than cromolyn.
37
What are the ADEs of 2nd gen oral antihistamines?
- anticholinergic effects (dry eyes)
| - ? wt gain
38
What can 2nd gen oral antihistamines have a drug interaction with?
- St. John's wort
39
What are the nasal antihistamines?
- azelastine
| - olopatadine
40
What is the efficacy of nasal antihistamines?
- antiinflam effect
| - decrease nasal congestion
41
What is the onset of action of nasal antihistamines?
- < 15min
42
How can nasal antihistamines be administered?
- "on demand"
43
Which is preferred, nasal antihistamines of INGCs?
- INGCs
44
What are the ADEs of nasal antihistamines?
- bitter taste
| - ? midly sedating
45
What is the mast cell stabilizer?
- cromolyn
46
What is the MOA of mast cell stabilizers?
- inhibits mast cell release of histamine
47
What is the efficacy of mast cell stabilizers?
- more effective than placebo
| - less effective than INGCs or 2nd gen antihistamines
48
What is the dosing schedule for mast cell stabilizers?
- frequent
49
How long does it take to achieve full relieve with mast cell stabilizers?
- 2-4w
50
What are the ADEs of mast cell stabilizers?
- no serious
| - increase in sneezing, burning, stinging, or irritation in nose, H/A, unpleasant taste
51
What is the MOA of leukotriene modifiers?
- inhibit cysteinyl leukotriene receptor which are released from nasal mucosa upon allergen exposure
52
What are the antileukotriene agents or leukotriene modifiers?
- montelukast (Singulair)
- Zafirlukast (Accolate)
- Zileuton (Zyflo)
53
What are leukotriene modifiers tx for?
- asthma
54
Which leukotriene modifier is approved for tx of allergic rhinitis?
- montelukast (Singulair)
55
What is leukotriene modifiers efficacy when compared with INGCs?
- less
56
What is the place in therapy of leukotriene modifiers?
- pts with concomitant asthma
| - pts who cannot tolerate/refuse nasal sprays
57
What is a side effect of leukotriene modifiers?
- neuropsychiatric changes usually in children
58
What is the MOA of ipatropium?
- anticholinergic
| - ? decrease release of substance P
59
What is the efficacy of ipatropium?
- only reduces rhinorrhea
60
What is the place in therapy for ipatropium?
- not recommended as 1st line therapy
| - only in pts with profuse rhinorrhea, not otherwise controlled with INGCs
61
What is the MOA of antitussives?
- ? decrease cough associated with allergic rhinitis
| - act on cough center in medulla oblongata
62
What family are the substances in of antitussives?
- morphine family
- codine
- dextromethorphan
63
What are the general ADEs of antitussives?
- GI
| - neuro
64
What will the antitussives interact with?
- MAOIs
| - ETOH
65
What is a CI of antitussives?
- concurrent MOAI use
66
What is the MOA of nasal decongestant sparys?
- direct-acting alpha-adrenergic agonist
| - vasoconstriction --> nasal decong.
67
What are the nasal decongestant sprays?
- phenylephrine (Neo-Synephrine)
- oxymetazoline (Afrin)
- naphazoline (Privine)
68
What is a side effect of nasal decongestant sprays?
- rhinitis medicamentosa
69
What is the physiology of rhinitis medicamentosa?
- down regulation of alpha-adrenergic receptor after 3-7d
70
What is a result from rhinitis medicamentosa?
- rebound nasal congestion < 3d
71
When are nasal decongestant sprays useful?
- in combo with INGCs
| - limited use to less than 3d
72
When are oral (systemic) glucocorticoids indicated?
- short course
- severe allergic rhinitis sx that prevent sleeping or work
- not to be given repeatedly or long term
73
Describe the pathophysiology of allergic rhinitis
- allergic inflam of nasal mucosa triggered by IgE production binding to mast cells & basophils containing & releasing histamine
74
What are the medication classes used to treat allergic rhinitis?
- glucocorticoids
- oral antihistamines
- antihistamine nasal sprays
- mast cell stabilizers
- leukotriene modifiers
- ipatropium
- antitussives
