24 Rhinitis Flashcards
What is rhinitis?
What is rhinitis?
Rhinitis is tissue inflammation and nasal hyperfunction that leads to nasal congestion, obstruction, rhinorrhea, nasal itching, and/or sneezing. Although rhinitis is generally not life-threatening, it is associated with significant loss of productivity and decreased quality of life.
How is rhinitis classified?
How is rhinitis classified?
Rhinitis may be classified into structural, noninflammatory, and inflammatory etiologies. Noninflammatory causes of rhinitis include nonallergic rhinitis, gustatory rhinitis, hormone induced rhinitis, atrophic rhinitis, CSF leak, and drug induced rhinitis. Inflammatory rhinitis includes allergic rhinitis, infectious rhinitis, nonallergic rhinitis with eosinophilia, nasal polyps, and rhinitis associated with systemic disease.
What are structural causes of rhinitis?
What are structural causes of rhinitis?
Concha bullosa, nasal polyps, septal deviation, adenoid enlargement, sinonasal tumors, and nasal foreign bodies can cause rhinitis. Nasal foreign body is a more common finding in the pediatric population. Nasal polyps are both structural and inflammatory in nature, with associated obstructive nasal symptoms, and may be accompanied by asthma or aspirin exacerbated respiratory disease.
How does one distinguish clear rhinorrhea of rhinitis from CSF leak?
How does one distinguish clear rhinorrhea of rhinitis from CSF leak?
CSF leak presents with clear rhinorrhea and oftentimes has a unilateral presentation. There is generally a history of preceding trauma though CSF leak can be spontaneous or idiopathic. Approximately 70% to 80% of CSF rhinorrhea is attributed to accidental trauma. If there is any doubt about a diagnosis CSF leak, qualitative β2-transferrin of nasal discharge is checked. β2 transferrin is found only in the CSF and its presence in nasal discharge therefore indicates CSF leak.
What is non-allergic rhinitis with eosinophilia (NARES) and how is it differentiated from allergic rhinitis?
What is non-allergic rhinitis with eosinophilia (NARES) and how is it differentiated from allergic rhinitis?
NARES is a perennial cause of rhinitis and common symptoms include congestion and clear nasal discharge. Nasal cytology demonstrates increased levels of eosinophils similar to allergic rhinitis, though these patients do not have sensitization on skin prick testing or specific IgE blood tests.
What is rhinitis medicamentosa and how is it treated?
What is rhinitis medicamentosa and how is it treated?
Rhinitis medicamentosa is rebound congestion that occurs with long-term use of intranasal decongestants that contain α-adrenergic compounds such as phenylephrine, oxymetolazine, or xylometolazine. Rebound effect is due to downregulation of α-adrenergic receptors as well as desensitization. Nasal sprays containing these medications should be limited to 3 to 5 days of use to avoid the rebound effect. Treatment of rhinitis medicamentosa involves weaning the intranasal decongestant spray, the addition of intranasal corticosteroids, and in some cases systemic corticosteroids. In refractory cases, inferior turbinate reduction may be needed.
What is hormonal rhinitis?
What is hormonal rhinitis?
Hormonal rhinitis is most often seen in pregnant women and about 20% to 30% of pregnant women will develop rhinitis of pregnancy. It is felt that rhinitis of pregnancy is due to changes in estrogen and progesterone though the mechanism remains undetermined. Symptoms generally resolve within 2 weeks after delivery. Hypothyroidism has also been implicated as a potential cause of chronic rhinitis.
What is atrophic rhinitis?
What is atrophic rhinitis?
Atrophic rhinitis is characterized by nasal dryness and congestion. Symptoms of atrophic rhinitis include crusting, purulent nasal discharge, nasal obstruction, and halitosis. This form of rhinitis typically presents in middle-aged populations. The cause of primary atrophic rhinitis is unknown and it is uncommon in North America, but has increased prevalence in areas with warm temperatures. Secondary atrophic rhinitis is seen in individuals who have undergone multiple aggressive sinonasal surgeries, but is also associated with trauma and granulomatous diseases. Secondary atrophic rhinitis is typically seen in an older population.
What is work-related rhinitis?
What is work-related rhinitis?
Work-related rhinitis is rhinitis that is associated with environmental exposures. Occupational rhinitis has a prevalence of approximately 5% to 15% worldwide. The rhinitis may be allergic or nonallergic and is further divided based on the substance causing the symptoms. Provoking substances may be irritants, corrosives or immunogens. Irritants include perfumes, paints, dust, and smoke. Corrosive rhinitis is associated with high levels of exposure to chemicals such as chlorine, sulfur dioxide, and ammonia. Immunologic exposure results in an IgE mediated response and include animal danders and grains. To diagnose work-related rhinitis it is helpful to have patients keep a diary of the timing of their symptoms.
What is gustatory rhinitis?
What is gustatory rhinitis?
Gustatory rhinitis is a noninflammatory rhinitis that presents with symptoms of rhinorrhea and/or postnasal drip following eating. It is more common with spicy or hot foods and is also more common in the elderly. Current prevalence is unknown and the mechanism is thought to be due to parasympathetic activation.
What are the common drugs associated with rhinitis?
What are the common drugs associated with rhinitis?
Angiotensin-converting enzyme inhibitors, β-adrenergic blockers, amiloride, hydralazine, many psychotropic medications, and phosphdiesterase-5 inhibitors.
What are “allergic salute,” “allergic shiners,” and “allergic gape”?
What are “allergic salute,” “allergic shiners,” and “allergic gape”?
Patients (particularly children) with persistent rhinorrhea often wipe the nose in an upward direction with the palm of the hand, which has been referred to as the allergic salute. Consequently, these patients may have a horizontal crease in the skin of the lower nose by the tip. Also, patients with allergic rhinitis can have darkened areas under their eyes, which are referred to as allergic shiners which are caused by swelling and congestion of small blood vessels beneath the skin. The allergic gape is a characteristic open mouth from nasal obstruction causing mouth breathing.
How can allergic rhinitis be differentiated from other causes of rhinitis?
How can allergic rhinitis be differentiated from other causes of rhinitis?
Generally seasonal allergic rhinitis has a seasonal variation and symptoms cease after the first frost. Physical exam findings suggestive of allergic rhinitis include pale, boggy nasal turbinates, allergic shiners, and allergic salute. Skin testing and specific IgE testing are also useful to differentiate allergic from nonallergic rhinitis. Nasal cytology may also be performed; however, this is not commonly used. Specific allergen challenges have also been utilized in research settings.
How is allergic rhinitis classified?
How is allergic rhinitis classified?
Allergic rhinitis is classified based on severity and frequency. Intermittent allergic rhinitis has symptoms on fewer than 4 days per week or for less than 4 weeks. Persistent allergic rhinitis is symptoms that occur for more than 4 days per week or more than 4 weeks. Severity is divided into mild and moderate/severe. Mild disease has normal sleep and no impairment of daily activities, sports, and leisure. Mild disease does not interfere with school and work. Moderate to severe disease must have at least one of the following present: sleep disturbance; impairment of daily activities, leisure, and/or sport; impairment of school or work; or troublesome symptoms.
Identify the classic seasons in which particular pollens are present.
Identify the classic seasons in which particular pollens are present.
- Tree: Spring
- Grass: Spring/Summer
- Weeds: Summer/Fall
What are general classes of medications available in the treatment of rhinitis?
What are general classes of medications available in the treatment of rhinitis?
Corticosteroids, both topical and systemic, are effective therapy for treatment of both inflammatory and noninflammatory causes of rhinitis. Topical and oral antihistamines are also available treatments. Intranasal anticholinergics are useful for rhinorrhea. Topical chromones that work as mast cell stabilizers and antileukotrienes may also be used in allergic rhinitis. Topical and oral decongestants are also available for temporary treatment of rhinitis over the counter, but have significant side effects if used extensively. See Table 24-1.
What is the pathophysiology of allergic rhinitis?
What is the pathophysiology of allergic rhinitis?
Allergens in the nasal mucosa are phagocytized by antigen presenting cells that present antigens to CD4 lymphocytes. Presentation to CD4 T-cells involves peptide presentation via the MCH class II complex. CD4+ T-cells then differentiate into a TH2 subset, where IL-4, IL-5, and IL-13 mediate eosinophil recruitment and survival. IL-4 and IL-13 are also necessary to promote the secretion of IgE from B-cells. The allergic response involves an early and late phase. Early phase reactions occur within minutes of exposure to the allergen and are due to release of preformed mediators in mast cells and basophils that are primed with IgE. Specific allergen binding promotes release of these mediators including histamine, tryptase prostaglandin D2, leukotriene C4, leukotriene B4, major basic protein, and platelet-activating factor. This results in symptoms of pruritus, sneezing, congestion, and rhinorrhea. Late phase reactions occur hours after allergen exposure and peak at 6 hours following exposure. Late reaction symptoms are primarily nasal congestion. Late phase reactions involve cellular infiltration and recruitment to the nasal mucosa and involve eosinophils, neutrophils, monocytes, and basophils, leading to longer-standing inflammation (Figure 24-1).
Figure text:
Immediate hypersensitivity diseases are initiated by the introduction of an allergen, which stimulates TH2 reactions and IgE production. IgE sensitizes mast cells by binding to FcεRI, and subsequent exposure to the allergen activates the mast cells to secrete the mediators responsible for the pathologic reactions of immediate hypersensitivity.
