First Aid, Chapter 7 Hypersensitivity Disorders, Rhinitis

Question 1

What is the prevalence of AR?

Answer 1

15-25%

Question 2

What is the mean onset of age?

Answer 2

10

Question 3

What percentage of cases develop before age 20?

Answer 3

80%

Question 4

What is the breakdown of seasonal vs. perennial vs. mixed?

Answer 4

20% seasonal, 40% perennial, 40% mixed

Question 5

What percentage of rhinitis is allergic?

Answer 5

50%

Question 6

What is the most common chronic disease of childhood?

Answer 6

Allergic rhinitis

Question 7

Is allergic rhinitis male or female predominant?

Answer 7

male in childhood, no disparity in adulthood

Question 8

What countries are showing a more pronounced increase in allergic rhinitis?

Answer 8

industrialized countries

Question 9

What age group is the prevalence of AR increasing in fastest?

Answer 9

young age group (faster than adults)

Question 10

What data supports the hygiene hypothesis?

Answer 10

Decreased risk of allergen sensitization and clinical allergy associated with:

• The protective effect of the number of siblings
• A rural upbringing, with exposure to farmyard animals early in life (with higher endotoxin),
• Day care attendance
• Large family size
• Exposure to household pets

Question 11

What morbidity is associate with AR vs. the general population based on the 2010 National allergy survey assessing limitations study?

Answer 11

• Those with AR rate their health significantly lower
• Significant effect on sleep: Difficulty getting to sleep and/or waking up during the night
• Significant effect on daily life for more than 50% of patients with AR
• More of a limitation with work, with an estimated 20% decrease in productivity

Question 12

What do allergens do to the IgE receptor in AR?

Answer 12

Allergens cross-link the allergen-specific IgE receptor (FcεRI) on previously sensitized mast cells, which leads to degranulation. More recent evidence suggests that IgE may be made in nasal tissues and upper airway lymphatics even in the absence of systemic production.

Question 13

What mediators are released within 15 minutes in the immediate allergic response in AR? What cell releases them? What symptoms do they cause?

Answer 13

Mast cells release preformed mediators: histamine, proteases such as tryptase, and kinins such as kallidin and bradykinin. Mast cells also release newly formed mediators: prostaglandin-2 (PGD2) and leukotrienes (LT) LTC4, LTD4, and LTE4.
Acute symptoms are influenced by specific mediators:
-Histamine: Itch, sneeze, rhinorrhea
-PGD2: Nasal congestion
-Leukotrienes: Nasal congestion
-Kinins: Nasal congestion and/or blockage

Question 14

What happens in the late allergic response in AR?

Answer 14

Begins within 4–8 hours and can last for more than 24 hours. Cellular infiltrates occur with basophils, eosinophils, and infiltrating lymphocytes, especially Th2 CD4 T lymphocytes. Since the mast cell is less important, there is no increase in tryptase. Th2 cells release cytokines, such as IL3 and IL-5 (eosinophil factors), as well as IL-4 and IL-13 (IgE class switch). Nasal mucosal epithelial cells have been shown to generate granulocyte monocyte colony-stimulating factor (GM-CSF, an eosinophil growth factor) and stem cell factor (i.e., mast cell growth factor), as well as eotaxin and regulated on activation, normal T expressed and secreted (RANTES, also known as chemokine (C-C motif) ligand 5, or CCL5). Predominant symptoms include nasal congestion and mucus production.

Question 15

What percentage of asthmatics have AR? What percentage of AR have asthma? What abnormalities of the lower airway are seen in AR even without asthma?

Answer 15

Most asthmatics (80%) have AR. AR may be associated with lower airway abnormalities, such as basement membrane thickening, even in the absence of asthma. Up to 40%) of AR pts have asthma.

Question 16

Is exhaled nitric oxide increased in AR? in sinusitis?

Answer 16

increased in AR, decreased in sinusitis.

Question 17

What symptom is particularly prominent in the late-phase response of allergic rhinitis?

Answer 17

Nasal congestion.

Question 18

What does immunotherapy improve? What does it prevent?

Answer 18

Improves AR symptoms, decreases the risk of developing new sensitizations, and helps decrease the risk of developing asthma in children.

Question 19

How do intranasal steroids work?

Answer 19

They work by causing vasoconstriction, reducing mucosal edema, and inhibiting the expression of cytokines and mediators

Question 20

What is the PPV of history for diagnosing AR?

Answer 20

70%

Question 21

What does gustatory rhinitis stimulate to cause symptoms? What is a good treatment?

Answer 21

Vagal (parasymphathetic) innervation. Intranasal ipratropium.

Question 22

What phase response is blocked by intranasal steroids?

Answer 22

Early and late phases.

Question 23

What is NARES? What patient population does it occur in? What is a prodrome to? What is the treatment?

Answer 23

typical symptoms of AR and documented eosinophilia on nasal smear cytology in the absence of increased total or specific IgE. It occurs in middle-aged adults. These patients are prone to nasal polyps, and this condition may represent a prodrome to aspirin-exacerbated respiratory disease (AERD). NARES responds well to intranasal corticosteroids.

Question 24

What is atrophic rhinitis? What age does it occur in? What gender? What countries is the idiopathic form more common in? What are they colonized with? What are causes of secondary atrophic rhinitis? What are symptoms?

Answer 24

Atrophic rhinitis is a noninflammatory condition associated with loss of the normal secretory/humidifying function of the nose. It occurs more frequently in young to middle-aged patients, especially females at onset of puberty. The primary (idiopathic) form is more predominant in developing countries with a warm climate and is generally associated with microbial colonization (e.g., Klebsiella ozaenae). Secondary causes are frequent in the developed world and occur in those with a history extensive nasal and sinus surgeries, chronic granulomatous nasal infection, or irradiation). Symptoms of atrophic rhinitis include:  Nasal congestion  Nasal pain upon inspiration from excess mucosal dryness  Nasal crusting  A foul smell in the nasal vault (fetor)
Treatment may include nasal saline irrigation and topical antibiotics.

Question 25

What medications commonly cause medication-induced rhinitis?

Answer 25

 ASA and NSAIDs (as a feature of AERD)  β blockers and various other antihypertensive medications  Rhinitis medicamentosa: Prolonged use of intranasal decongestants (rebound congestion)  Angiotensin-converting enzyme (ACE) inhibitors  OCPs  Sildenafil  Intranasal cocaine or methamphetamine.

Question 26

What is the prevalence of pregnancy induced rhinitis in pregnant women? When does it occur in pregnant women? When does it resolve? Are intranasal steroids helpful?

Answer 26

Occurs in 1 in 5 pregnant patients, is not present prior to pregnancy, does not present before the second trimester, and usually resolves within 2 weeks postpartum. Intranasal steroids are not helpful.

Question 27

When should you check for CSF rhinorrhea?

Answer 27

Persistent unexplained rhinorrhea, particularly with a history of trauma and/or if unilateral, should trigger a search for CSF rhinorrhea (e.g., check β2-transferrin).

Question 28

What is the most common cause of rhinitis during pregnancy?

Answer 28

Pre-existing allergic rhinitis: About 1/3 of females with AR experience symptom exacerbation during gestation.

Question 29

Why can nasal congestion or rhinorrhea develop in hypothyroidism?

Answer 29

Release of thyroidstimulating hormone (TSH) results in increased edema in the turbinates.