Treatement of Allergic Rhinitis Flashcards
What is triggered by inhalation of allergen in a person with sensitized immune system?
production of IgE.
What Does IgE bind to?
IgE binds to mast cells and basophils containing histamine.
What is the pharmacotherapy of allergic rhinitis based on?
Type of rhinitis present
Most prominent symptoms
Patient age
What is the most effective single therapy for A.R.
Glucocorticoid nasal spray (intranasal glucocorticoid)
What are the general MOA’s for medications for A.R.
Allergen avoidance Leuoktriene modifiers- Antihistamines Steroids Allergen immunotherapy.
MOA for INGC’s (intranasal glucocorticoids)
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
ADME of INGC’s
A: minimally systemic 1st gen- 10-50% bioavailability 2nd gen-<2% bioavailable D: N/A M: Hepatic - 1st pass met. E: N/a
Example of first generation INGC’s
Rhinocort, Nasacort,
Example of second generation INGC
Flonase, nasonex Veramyst
How soon should the pt expect an INGC to start working?
may take 3-5 days or even weeks before full relief is realized (onset-few hours).
Can an INGC be used PRN?
yes but not as efficacious as continued use.
When should an INGC be used vs. oral antihistamine?
Relieving congestion, relieving ocular symptoms, Raises threshhold for developing symptoms after exposure (when used continuously)
ADE of INGC
Nasal irritation, drying, burning, bleeding, Discomfort from throat runoff, Nasal septum perf.
Growth suppression in children.
DI of INGC
Fluticasone and strong CYP3A4 inhibitors. Adrenal suppression.
Forms of INGC’s that are new to market and Method of use for these
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)
Where are H1 histamine receptors located?
Throughout body, smooth muscles, vascular endothelial cells.
What is the function of H1 histamine receptors?
Systemic vasodilation and increased cell permeability
What Class of histamine receptors does the term antihistamine refer to?
H1
MOA oral antihistamines
Block action of Histamine at H1 receptors (inverse agonists-not antagonists)
What are the 2 categories of antihistamines?
1st gen-crosses BBB-causes sedation CNS side effects
2nd gem-does not cross BBB.
P’Kinetics of Oral antihx.
A: Rapid (10-30 min)
D: 60-70% protein bound
M: Minimal with exception of desloratadine (extensive 1st pass met)
E: Primarily urine
What is the duration of action for anthix.
1st gen: 1-6hours
2nd gen: 6-24 hours
Examples of 1st gen oral antihx.
OTC: Diphenhydramine (Benadryl), Chlorpheniramine, Clemastine, Brompheniramine.
Safety warnings with 1st gen oral antihix.
Lipophilic-easily cross BBB (CNS symp.)
Intellectual and motor function impairment
Not recommended for elderly.
ADE 1st gen Oral Antihix.
Anticholinergic: dry mouth, eyes, impotence, glaucoma.
CNS: sedation, confusion,
Misc: weight gain, hypersensitivity, prolonged QT interval
Examples of 2nd Gen antihx
Loratidine (claritin), Cetririzine (Zyrtec)
Compared to INGC’s is 2nd gen antihix more or less effective?
2nd gen antihx are less effective on nasal congestion than INGC’s
Onset of action for 2gen antihx
Onset of action-wtihin 1 hr.
Duration - long acting (dosed once daily)
MOA for 2gen antihx.
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
Safety of 2gen antihx.
Less sedating than 1st gen,
Anticholinergic effect varies (dry eyes mc)
Weight gain-stim of appetite
DI for 2nd gen Antihx.
St. John’s wort-decreases levels of loratadine/fexofenadine
MOA mast cell stabilizers
inhibits mast cell release of histamine. Blocks symptoms of immediate and late phase nasal allergen challenge. (useful for pt’s when exposure is imminent).
Efficacy of Cromolyn Sodium
less effective than INGC’s or 2nd gen antihistamines. Relief may require 2-4 weeks.
ADE cromolyn sodium
Increase in sneezing, burning, stinging irritation of nose. HA
Unpleasant taste
MOA Leukotriene modifiers
Inhibit cysteinyl leukotriene receptr-released from nasal mucosa upon allergen exposure
T/F Only zafirlukast (asthma med) is approved for use for AR?
F only Montelukast is approved for AR.
What is more effective INGC’s or Montelukast (a leukotriene Modifier)?
INGC’s
When is it best to use a leukotriene modifier?
Patients with concomitant asthma and pt’s who cannot tolerate/refuse nasal spray.
MOA ipratropium
anticholinergic-may also release sub P (vasoconstriction). Only reduced rhinorrhea.
When is it best to use Iproatropium (atrovent)
not first line! Useful with profuse rhinorrhea not otherwise controlled by INGC’s
MOA of Nasal decongestant sprays.
Potent direct-acting alpha-adrenergic agonist (periph vasc). produces local vasoconstriction and nasal decongestion.. NOT recommended as mono therapy. Caution - rhinitis medicamentosa
What causes rhinitis medicaments?
overuse of nasal decongestant spray causes down regulation of alpha adrenergic receptor after 3-7 days Results in rebound nasal congestion.
ADE nasal decongestant spray
Nasal burning discharge, sneezing, stinging
