Rhinitis: by Khairunnisa
Rhinitis: by Khairunnisa
Rhinitis: by Khairunnisa
BY K H A I R U N N I S A
Lets ZOOM in
into nasal cavity
NASAL CAVITY
where all the action takes place:
air conditioning humidification, warming or cooling incoming
airstream
filter the incoming airstream of microorganisms and pollutants
immune function preventing infection by airborne
microorganisms
olfaction sense of smell
voice quality affects voice resonance
Cleanse
Vibrissae lining the nasal vestibule
filter large particulate
Goblet cells in the epithelium secrete
mucous
Thinner deeper layer
- allows cilia to beat with less
resistance
Thicker outer layer
- traps airborne particulate
- contains inflammatory mediators,
leukocytes
PARANASAL SINUS
a group of four pairedair-filled spacesthat surround
thenasal cavity.
ALLERGIC RHINITIS
ALLERGIC RHINITS
WHO GETS ALLERGIC RHINITIS?Allergic rhinitis, also known as "hay
fever," affects approximately 20 percent of people of all ages. The risk of
developing allergic rhinitis is much higher in people with asthma or eczema
and in people who have a family history of asthma or rhinitis.
It is an IgE-mediated immunologic response of nasal mucosa to air-borne
allergens.
HERE IS
ANOTHE
R
CL A SSI
F I C ATI O
PATHOGENESIS
Mediated by type-1 hypersensitivity reaction
involves the excess production of IgE antibodies
Basically, allergic response occurs in two phases Subsequent reaction to allergen early phase
Late phase
SENSITISATION
In atopies, allergen molecules are inhaled and presumably not completely
cleared by mucociliary system
They reach antigen presenting cell(APC) in the nose dendrites cell or
langerhan cells
They capture the antigen and process it and present it to nave T-cell in the
local lymph nodes
They also activate B lymphocytes, encourage them to proliferate, migrate to
the nasal lining and produce IgE antibody
Once produced, the IgE is rapidly taken up, mainly by mast cells
Thus armed, mast cells are able to response to subsequent allergen contact
A. EARLY PHASE
Antigen combine with IgE antibody causes degranulation of the mast cells
provoking inflammatory response
Secretion of histamine, leukotriene, Pg and others mediators
These mediators are responsible for symptomatology of allergic disease
sneezing, rhinorrhoea, itching, vascular permeability, vasodilation, glandular
secretion
B. LATE PHASE
The release of cytokines causes an influx of inflammatory cells (mainly
eosinophils) by chemotaxis
The main symptoms are nasal congestion and hypersensitivity
Eosinophils increase local vascular permeability and mucus secretion,
causes further inflammatory cell influx
Endothelial cells recruitment of leukocytes to the site of allergic response
by releasing chemotactic factors and modulating adhesion molecules
CAUSES
1. Genetic susceptibility (i.e. family history)
2. Environmental factors (e.g. dust, mold exposure)
3. Exposure to allergens (e.g. pollens, animal dander, food)
4. Passive exposure to tobacco smoke (especially in early childhood)
5. Diesel exhaust particles (in urban areas)
.In infancy and childhood food allergens such as milk, eggs, soy, wheat,
dust mites, and inhalant allergies such as pet dander are the major causes of
allergic rhinitis and the comorbidities of atopic dermatitis, otitis media with
effusion, and asthma.
.In older children and adolescents - pollen allergens become more of a
causative factor.
Clinical findings
to determine whether the patient is atopic and the
causative allergen
A. HISTORY
Onset, duration, type, progression, severity of symptoms;
Possible trigger of symptoms;
Family history of atopy - allergies, eczema, asthma
Thorough allergy history
determine if symptoms are seasonal or perennial
reproducibility of symptoms on exposure to inciting factor
use of medications- antihistamines, intranasal corticosteroids
history of anaphylaxis
Environmental exposure
Occupational exposure
Associated ocular, pharyngeal, systemic symptoms
e.g. recurrent rhinosinusitis, ear infections, asthma flare-ups, gastrointestinal symptoms, skin
rashes, hives
B. EXAMINATION .
Inspection of the ears, throat and nasal passages
Typical findings in seasonal allergies
bluish, pale, boggy turbinates
wet, swollen mucousa
nasal congestion with nasal obstruction
In perennial allergies
nasal congestion
normal nasal examination
Anatomic abnormalities
deviated nasal septum
concha bullosa
nasal polyps
CONT,
If nasal polyps are suspected, an endoscopic nasal exam is also warranted.
Other possible physical findings include conjunctivitis, eczema, and,
possibly, asthmatic wheezing.
Common findings in children - allergic shiners (dark circles under the
eyes), facial grimacing, mouth breathing, and the nasal salute (constant
rubbing of the tip of the nose with the hand).
In this age group, a concomitant otitis media with effusion is also a
possibility.
C. CONFIRMATORY TESTS.
Allergy testing
to establish objective evidence of atopy
to determine the causative allergens
to determine the specific therapeutic recommendations
Skin testing
Skin prick test (epicutaeneous)
most commonly used
allows for uniformity in testing procedure
DIFFERENTIAL DIAGNOSIS
Infectious Rhinitis (Acute or Chronic)
Perennial Nonallergic Rhinitis (Vasomotor Rhinitis)
Pollutants and Irritants
Hormonal Rhinitis
Rhinitis Medicamentosa(medication induced)
Anatomical Deformity
e.g. deviated nasal septum, concha bullosa, nasal polyps
TREATMENT
ENVIRONMENTAL CONTROL
1. Reduce household humidity to below 50%
2. Wash bed linens in hot water
3. Remove carpets and pets from the most often used living areas,
especially bedrooms
4. Encase pillows, mattresses, and box springs in hypoallergenic coverings
(for dust mite protection)
5. In poor and urban settings, eliminate cockroaches
6. For airborne allergens (e.g., animal dander), air purifiers can be used.
PHARMACOTHERAPEUTIC MEASURES
1. Antihistamines
2. Intranasal corticosteroid
3. Systemic corticosteroid
4. Decongestants
5. Intranasal anticholinergics
6. Intranasal cromolyn
7. Leukotriene inhibitors
Immunotherapy
attempts to increase the threshold level of
symptom appearance after allergen exposure
believed to be due to
increase in blocking antibodies
regulation of immune cascade
Viral Rhinitis
Associated with other presentations of viral infection
headache, malaise, body ache, cough
Occupational Rhinitis
Caused by irritants in the work environment
e.g. dust, ozone, sulphur dioxide, ammonia
Vasomotor Rhinitis
Presents with
nasal obstruction, clear nasal drainage
Associated with
temperature changes, eating, chemical or odour exposure, alcohol use
Rhinitis Medicamentosa
Presents with nasal obstruction worsening over many years
Typically associated with long-term vasoconstrictive nasal spray use
B.
Surgical Measures
1.
2.
Turbinate surgery
Arigatooo