Allergic Rhinitis and Cough Flashcards
ANS sympathetic activation
constricts arterioles
reduces mucosal thickness
widens airway allowing more air to enter
ANS parasympathetic activation
dilates arterioles
increases mucosal thickness
increases stuffiness and runny nose
Immune Defense
first line
cleans and conditions inhaled air
lined with mast cells (release histamine)
Antigen Antibody Response
allergen interacts with IgE + mast cells
release of mediators –> vasodilation, increased vascular permeability, production of nasal secretions
sensory nerve stimulation = itching
vagal stimulation = sneezing
Mast Cell Mediators
histamine
eosinophil chemotactic factor
leukotienes
Histamine
stimulates irritant receptors
pruritus
vascular permeability
mucosal permeability
smooth muscle contraction
Eosinophil Chemotactic Factor
influx of inflammatory cells
Leukotrienes
smooth muscle contraction
vascular permeability
mucus secretion
chemotaxis
neutrophil chemotaxis
Late Phase Reaction
4-8 hrs after initial exposure
caused by cytokines
persistent chronic symptoms
hyper responsive, inflamed mucosa
Seasonal Rhinitis Guidelines
- monotherapy with an intranasal corticosteroid (ages 12+)
- intranasal corticosteroid > leukotriene receptor antagonist (ages 15+)
- intranasal corticosteroid + intranasal antihistamine for initial treatment of mod-sev cases (ages 12+)(weak)
Nasal Steroids
Benefits include symptom control, improved quality of life, better sleep, cost-saving if used as monotherapy, targeted local effect.
Patient preference will play a large role.
Oral Antihistamines
Second generation (nonsedating) agents should be used in patients with primary complaints of sneezing and itching.
Relief of eye symptoms, OTC status and the availability of lower cost generics may be advantages.
Intranasal Antihistamines
Evidence is strong but studies were of short duration. May consider these agents as optional.
Immunotherapy
Recommended in patients who have inadequate response to with pharmacologic therapy with or without environmental controls