RHINITIS | PROPOSED MECHANISM |
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Non-Allergic Rhinitis: | Â |
Vasomotor Rhinitis | CNS stimulation leading to inhibition of the sympathetic nervous system response and enhancement of the parasympathetic response[33]. |
   Gustatory Rhinitis | Muscarinc receptor stimulation[45]. |
   Infectious Rhinitis | Typically viral or bacterial induced inflammation[20]. |
   Non-allergic rhinitis with eosinophilia syndrome (NARES) | Eosinophilia leading to direct nasal mucosal damage and decreased mucocilliary clearance[48–53]. |
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   Annoyance | Subjective without evidence of inflammation. |
   Irritant | Substance P induced neutrophilic inflammation. |
   Corrosive | Agent directly damages nasal mucosa. |
   Allergic | IgE mediated. |
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   Hormonally induced Rhinitis | Increased circulating blood volume and possible hormonal influences (e.g. estrogen, progesterone) leading to vascular pooling and smooth muscle relaxation causing nasal congestion. |
   Rhinitis Medicamentosa | Direct mucosal damage by alpha-adrenergic agent causing loss of ciliated cells and interstitial edema[64, 65]. |
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   Primary Atrophic Rhinitis | Infectious i.e. Klebsiella ozaenae |
   Secondary Atrophic Rhinitis | Identifiable causes: Chronic sinusitis, turbinate surgery and irradiation |