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Pharm Exam 3 > Treatement of Allergic Rhinitis > Flashcards

Treatement of Allergic Rhinitis Flashcards

1
Q

What is triggered by inhalation of allergen in a person with sensitized immune system?

A

production of IgE.

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2
Q

What Does IgE bind to?

A

IgE binds to mast cells and basophils containing histamine.

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3
Q

What is the pharmacotherapy of allergic rhinitis based on?

A

Type of rhinitis present
Most prominent symptoms
Patient age

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4
Q

What is the most effective single therapy for A.R.

A

Glucocorticoid nasal spray (intranasal glucocorticoid)

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5
Q

What are the general MOA’s for medications for A.R.

A 
Allergen avoidance
Leuoktriene modifiers-
Antihistamines
Steroids
Allergen immunotherapy.
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6
Q

MOA for INGC’s (intranasal glucocorticoids)

A

Inhibit inflammation of nose by inhibiting cytokines/chemokines.
Binds to intracellular GC receptors of inflammatory cells. Change of the receptor activates genes to transcribe mRNA for anti-inflammatory proteins. Suppresses transcription of cytokine/chemokine genes surpasses inflammation

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7
Q

ADME of INGC’s

A 
A: minimally systemic 
1st gen- 10-50% bioavailability
2nd gen-<2% bioavailable
D: N/A
M: Hepatic - 1st pass met.
E: N/a
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8
Q

Example of first generation INGC’s

A

Rhinocort, Nasacort,

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9
Q

Example of second generation INGC

A

Flonase, nasonex Veramyst

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10
Q

How soon should the pt expect an INGC to start working?

A

may take 3-5 days or even weeks before full relief is realized (onset-few hours).

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11
Q

Can an INGC be used PRN?

A

yes but not as efficacious as continued use.

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12
Q

When should an INGC be used vs. oral antihistamine?

A

Relieving congestion, relieving ocular symptoms, Raises threshhold for developing symptoms after exposure (when used continuously)

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13
Q

ADE of INGC

A

Nasal irritation, drying, burning, bleeding, Discomfort from throat runoff, Nasal septum perf.
Growth suppression in children.

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14
Q

DI of INGC

A

Fluticasone and strong CYP3A4 inhibitors. Adrenal suppression.

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15
Q

Forms of INGC’s that are new to market and Method of use for these

A

Dry powder formations (HFA).
MOU: Tilt head back, dispense spray, hold breath, exhale through mouth. (different than spray INGC’s which you tild head down)

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16
Q

Where are H1 histamine receptors located?

A

Throughout body, smooth muscles, vascular endothelial cells.

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17
Q

What is the function of H1 histamine receptors?

A

Systemic vasodilation and increased cell permeability

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18
Q

What Class of histamine receptors does the term antihistamine refer to?

A

H1

19
Q

MOA oral antihistamines

A

Block action of Histamine at H1 receptors (inverse agonists-not antagonists)

20
Q

What are the 2 categories of antihistamines?

A

1st gen-crosses BBB-causes sedation CNS side effects

2nd gem-does not cross BBB.

21
Q

P’Kinetics of Oral antihx.

A

A: Rapid (10-30 min)
D: 60-70% protein bound
M: Minimal with exception of desloratadine (extensive 1st pass met)
E: Primarily urine

22
Q

What is the duration of action for anthix.

A

1st gen: 1-6hours

2nd gen: 6-24 hours

23
Q

Examples of 1st gen oral antihx.

A

OTC: Diphenhydramine (Benadryl), Chlorpheniramine, Clemastine, Brompheniramine.

24
Q

Safety warnings with 1st gen oral antihix.

A

Lipophilic-easily cross BBB (CNS symp.)
Intellectual and motor function impairment
Not recommended for elderly.

25
Q

ADE 1st gen Oral Antihix.

A

Anticholinergic: dry mouth, eyes, impotence, glaucoma.
CNS: sedation, confusion,
Misc: weight gain, hypersensitivity, prolonged QT interval

26
Q

Examples of 2nd Gen antihx

A

Loratidine (claritin), Cetririzine (Zyrtec)

27
Q

Compared to INGC’s is 2nd gen antihix more or less effective?

A

2nd gen antihx are less effective on nasal congestion than INGC’s

28
Q

Onset of action for 2gen antihx

A

Onset of action-wtihin 1 hr.

Duration - long acting (dosed once daily)

29
Q

MOA for 2gen antihx.

A

Blocks action of histamine at H1 receptor.
Variety of anti-inflammatory properties
Decreasd mast cell mediator release
Inhibition of IL-4, IL-13 some benefit on asthma

30
Q

Safety of 2gen antihx.

A

Less sedating than 1st gen,
Anticholinergic effect varies (dry eyes mc)
Weight gain-stim of appetite

31
Q

DI for 2nd gen Antihx.

A

St. John’s wort-decreases levels of loratadine/fexofenadine

32
Q

MOA mast cell stabilizers

A

inhibits mast cell release of histamine. Blocks symptoms of immediate and late phase nasal allergen challenge. (useful for pt’s when exposure is imminent).

33
Q

Efficacy of Cromolyn Sodium

A

less effective than INGC’s or 2nd gen antihistamines. Relief may require 2-4 weeks.

34
Q

ADE cromolyn sodium

A

Increase in sneezing, burning, stinging irritation of nose. HA
Unpleasant taste

35
Q

MOA Leukotriene modifiers

A

Inhibit cysteinyl leukotriene receptr-released from nasal mucosa upon allergen exposure

36
Q

T/F Only zafirlukast (asthma med) is approved for use for AR?

A

F only Montelukast is approved for AR.

37
Q

What is more effective INGC’s or Montelukast (a leukotriene Modifier)?

A

INGC’s

38
Q

When is it best to use a leukotriene modifier?

A

Patients with concomitant asthma and pt’s who cannot tolerate/refuse nasal spray.

39
Q

MOA ipratropium

A

anticholinergic-may also release sub P (vasoconstriction). Only reduced rhinorrhea.

40
Q

When is it best to use Iproatropium (atrovent)

A

not first line! Useful with profuse rhinorrhea not otherwise controlled by INGC’s

41
Q

MOA of Nasal decongestant sprays.

A

Potent direct-acting alpha-adrenergic agonist (periph vasc). produces local vasoconstriction and nasal decongestion.. NOT recommended as mono therapy. Caution - rhinitis medicamentosa

42
Q

What causes rhinitis medicaments?

A

overuse of nasal decongestant spray causes down regulation of alpha adrenergic receptor after 3-7 days Results in rebound nasal congestion.

43
Q

ADE nasal decongestant spray

A

Nasal burning discharge, sneezing, stinging

Pharm Exam 3 (4 decks)

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