Alergic Rhinitis Flashcards
Allergic rhinitis
an IgE-mediated immunologic response of nasal mucosa to airborne allergens and is characterized by watery nasal discharge, nasal obstruction, sneezing and itching in the nose.
Two clinical types
Seasonal
Perennial
Seasonal Allergic Rhinitis
Symptoms appear in or around a particular season when the pollens of a particular plant, to which the patient is sensitive, are present in the air.
Perennial Allergic Rhinitis
Symptoms are present throughout the year.
AETIOLOGY
Inhalant allergens
Genetic predisposition
Seasonal allergens
pollens from trees, grasses and weeds.
Perennial allergens
molds, dust mites, cockroaches and dander from animals. Dust includes dust mite, insect parts, fibres and animal dan- ders. Dust mites live on skin scales and other debris and are found in the beddings, mattresses, pillows, carpets and upholstery.
PATHOGENESIS
genetically predisposed individuals ➡️Inhaled allergens produce specific IgE antibody➡️ fixed to the blood basophils or tissue mast cells by its Fc end➡️ On subsequent exposure, antigen combines with IgE antibody at its Fab end ➡️degranulation of the mast cells ➡️release of several chemical mediators ➡️symptomatology of allergic disease ➡️vasodilation, mucosal oedema, infiltration with eosinophils, excessive secretion from nasal glands or smooth muscle contraction
priming affect
mucosa earlier sensitized to an allergen will react to smaller doses of subsequent specific allergen
Nonspecific nasal hyper-reactivity is seen in patients of allergic rhinitis why ?
Nasal mucosa gets “primed” to other nonspecific antigens to which patient was not exposed ➡️increased nasal response to normal stimuli resulting in sneezing, rhinorrhoea and nasal congestion
Clinically, allergic response occurs in
Acute or early phase
Late or delayed phase
Acute or early phase
within 5–30 min, after exposure to the specific allergen
consists of sneezing, rhinorrhoea nasal blockage and/or bronchospasm.
It is due to release of vasoactive amines like histamine.
Late or delayed phase
It occurs 2–8 h after exposure to allergen without additional exposure. It is due to infiltration of inflammatory cells—eosinophils, neutrophils, basophil, monocytes and CD4 + T cells at the site of antigen deposition causing swelling, congestion and thick secretion
In the event of repeated or continuous exposure to allergen
acute phase symptomatology over- laps the late phase.
Usually the onset is at
12–16 years of ag
Age group and sex predilection
There is no age or sex predilection
cardinal symptoms of seasonal nasal allergy
paroxysmal sneezing
nasal obstruction,
watery nasal discharge
and itching in the nose
par- oxysmal sneezing
10–20 sneezes at a time
Itching may also involve
eyes, palate or pharynx
Symptoms of perennial allergy
frequent colds, persistently stuffy nose, loss of sense of smell due to mucosal oedema, postnasal drip, chronic cough and hearing impairment due to eustachian tube blockage or fluid in the middle ear
Nasal signs
- transverse nasal crease
- pale and oedematous nasal mucosa which may appear bluish.
- Turbinates are swollen.
- Thin, watery or mucoid discharge is usually present.
transverse nasal crease produces a sign called
allergic salute
transverse nasal crease
a black line across the middle of dorsum of nose due to constant upward rubbing of nose simulating a salute
Ocular signs
oedema of lids, congestion and cobble- stone appearance of the conjunctiva, and dark circles under the eyes
allergic shiners
dark circles under the eyes
Otologic signs
retracted tympanic membrane or serous otitis media as a result of eustachian tube blockage
Pharyngeal signs
granular pharyngitis due to hyperplasia of submucosal lymphoid tissue. A child with perennial allergic rhinitis may show all the features of pro-
longed mouth breathing as seen in adenoid hyperplasia.
Laryngeal signs
hoarseness and oedema of the
vocal cords.
DIAGNOSIS is based on
New Allergic Rhinitis and Its Impact on Asthma (ARIA) clas- sification
ARIA is baesd on
duration and severity of disease
Duration of symptoms is subdivided into
intermittent or persistent
severity of disease is subdivided into
mild, moderate or severe.
Intermittent Symptoms are presen
– Less than 4 days a week or
– For less than 4 weeks
Persistent: Symptoms are present
– More than 4 days a week or
– For more than 4 week
Mild
None of the following symptoms are present
Moderate to severe
– Sleep disturbance
– Impairment of daily activities, leisure and sport – Impairment of school or work
– Troublesome symptoms
One or more of the above symptoms are present
INVESTIGATIONS
Total and differential count Nasal smear. Skin tests Radioallergosorbent test (RAST) Nasal provocationtest
Total and differential count
Peripheral eosinophilia may be seen but this is an inconsistent finding.
Nasal smear.
large number of eosinophils
Nasal eosinophilia is also seen in certain
nonallergic rhi- nitis, e.g. NARES (nonallergic rhinitis with eosinophilia syndrome).
Skin tests aim
identify specific allergen
Skin tests types
prick, scratch and intradermal tests
Skin prick test.
This is an excellent method to demon- strate the allergen. A drop of concentrated allergen solution is placed on the volar surface of the forearm or back and a sharp needle pricked into the dermis through the drop. It introduces the allergen into the dermis. A positive reaction is manifested by the for- mation of a central wheal and a surrounding zone of erythema (flare) within 10–15 min. Simultaneously a control test is performed with histamine and the diluent used in allergen solution
There is a good correlation between the skin tests and
specific IgE measure- ments.
Radioallergosorbent test (RAST)
in vitro test and measures specific IgE antibody concentration in the patient’s serum.
Nasal provocationtest
A crude method is to challenge the nasal mucosa with a small amount of allergen placed at the end of a toothpick and asking the patient to sniff into each nostril and to observe if allergic symptoms are repro- duced.
COMPLICATIONS
1.Recurrent sinusitis because of obstruction to the sinus ostia.
2. Formation of nasal polypi in about 2%.
3. Serous otitis media.
4. Orthodontic problems and other ill-effects of prolonged
mouth breathing especially in children.
5. Bronchial asthma. Patients of nasal allergy have four times more risk of developing bronchial asthma Twenty to thirty per cent of patients with rhinitis have asthma
TREATMENT
- Avoidance of allergen. 2. Treatment with drugs. 3. Immunotherapy.
Treatment with drugs
Antihistaminics Sympathomimetic drugs (oral or topical) Corticosteroids Sodium cromoglycate Anticholinergics Leukotriene receptor antagonists Anti-IgE.
Sympathomimetic drugs
Pseu- doephedrine and phenylephrine are often combined with antihistaminics for oral administration.
Topical use of sympathomimetic drugs
Phenylephrine, oxymetazoline and xylo- metazoline are often used to relieve nasal obstruction
Side effects of topical nasal decongestant
severe rebound congestion. Patient resorts to using more and more of them to relieve nasal obstruction. This vicious cycle leads to rhi- nitis medicamentosa.
Topical steroids
beclomethasone dipropio- nate, budesonide, flunisolide acetate, fluticasone and mometasone
Steroids are effective in
late-phase allergic reaction as inhibit recruitment of inflammatory cells into the nasal mucosa
Topical steroids side effects
mucosal atrophy and even septal perforation
promote growth of fungus
Anticholinergics
Ipratropium bromide has been used as nasal spray to control rhinorrhoea. There are no systemic side effects.
Leukotriene receptor antagonists
montelu- kast, pranlukast and zafirlukast
They block cysteinyl leukotriene type receptors. They are well-tolerated and have few side effects.
Anti-IgE.
reduces the IgE level and has an anti- inflammatory effect. Omalizumab is such a drug. It is indicated in children above 12 years who have moder- ate to severe asthma. It is not yet approved for allergic rhinitis.
Immunotherapy
hyposensitization is used when drug treatment fails to control symptoms or produces intolerable side effects.
Immunotherapy procedure
Allergen is given in gradu- ally increasing doses till the maintenance dose is reached. Immunotherapy suppresses the formation of IgE. It also raises the titre of specific IgG antibody. Immunotherapy has to be given for a year or so before significant improvement of symptoms can be noticed. It is discontinued if uninter- rupted treatment for 3 years shows no clinical improvement.
Routes for immunotherapy
Subcutaneous immunotherapy is often used but now sub- lingual and nasal routes are also being employed
Advantage of sub- lingual and nasal routes in immunotherapy
with doses 20–100 times greater than used by the subcutaneous route.
A step care approach is recommended by ARIA for aller- gic rhinitis treatment.
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