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RHINITIS

BY K H A I R U N N I S A

DEFINITION RHINITIS OR CORYZA


Irritation and inflammation of the mucous membrane inside the nose
This inflammation characterized by one or more of the following
symptoms
itching
Nasal congestion
Sneezing
Runny nose
Postnasal drip(the sensation that mucous is draining from the sinuses
down the back of the throat)

LETS HAVE A LOOK INSIDE OUR NOSE

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.

Themaxillary sinusesare located under theeyes;


thefrontal sinusesare above the eyes;
theethmoidal sinusesare between the eyes and
thesphenoidal sinusesare behind the eyes.

OK NOW, ITS TIME TO LEARN ABOUT


TYPES OF RHINITIS
ALLERGIC
RHINITIS
NON ALLERGIC
RHINITIS

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.

Seasonal versus perennial allergic rhinitis


Seasonal Allergic Rhinitis
Symptoms occur during certain seasons,
depending on the pollination time of plants
pollens from trees, grasses, and weeds,
as well as spores from fungi and molds
Perennial allergic rhinitis
Symptoms are present throughout the year
Common allergens include: dust mites,
cockroaches, animal dander, and fungi
or molds
Infections and nonspecific irritants may
aggravate the
condition and cause
complications
e.g. rhinosinusitis, otitis media with effusion

HERE IS
ANOTHE
R
CL A SSI
F I C ATI O

ALLERGIC RHINITIS SYMPTOMS


The symptoms of allergic rhinitis vary from person to person. Although the term
"rhinitis" refers only to the nasal symptoms, many people also experience
problems with their eyes, throat, and ears. In addition, sleep may be disrupted.
Symptoms may include the following:
Nose Watery nasal discharge, blocked nasal passages, sneezing, nasal itching,
postnasal drip, loss of taste, facial pressure or pain
Eyes Itchy, red eyes, feeling of grittiness in the eyes, swelling and blueness of the
skin below the eyes (called "allergic shiners")
Throat and ears Sore throat, hoarse voice, congestion or popping of the ears,
itching of the throat or ears
Sleep Mouth breathing, frequent awakening, daytime fatigue, difficulty performing
work

When an allergen is present year round, the predominant symptoms include


postnasal drip, persistent nasal congestion, and poor quality sleep.

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.

Diagnosis of allergic rhinitis


Most allergy rhinitis patient can be diagnosed by a
combination of
History
Examination
Confirmatory tests

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

Impact of symptoms on quality of life

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

Intradermal testing (intradermal dilutional testing - IDL)


used when skin prick test is equivocal
uses quantitative 1:5 serial dilutions

In vitro testing - Allergen specific IgE testing

equivalent to skin testing in efficacy(commonly used in research)


do not require patient to be free from antihistamines/ other medications that
may interfere with skin testing

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

Tumours, Foreign Bodies

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

Indications for use


long-term pharmacotherapy
inadequacy or intolerability of pharmacotherapy
significant allergen sensitivities

OTHER TREATMENT CONSIDERATION


The first aspect of treating patients who have not responded well
to therapeutic measures, including immunotherapy, is
determining to what degree therapeutic compliance has
occurred.
The next steps are to adjust drug dosages, try one or two other
agents, and consider combination therapy.
In addition, the physician should determine whether allergy
exposure has increased and should also review the
environmental control measures.
Finally, it may be necessary to reconsider the diagnosis and reevaluate the patient.

NON ALLERGIC RHINITIS

The term non-allergic rhinitis is commonly applied to a diagnosis of


any nasal condition which the symptoms are identical to those seen
in allergic rhinitis but an allergic aetiology has been excluded.
Occur more frequently in adult than children
Typically presents with
Clear Rhinorrhea
Nasal Obstruction
+/- sneezing, itching, watery eyes

Relevant history to ask include:


OTC nasal spray use
History of trauma
Work or chemical exposure
History of intranasal drug use

Red flags of Neoplasms


Epistaxis
Pain
Unilateral symptoms

TYPE OF NON ALLERGIC RHINITIS


Viral rhinitis
Occupational rhinitis
Vasomotor rhinitis
Nonallergic rhinitis with eosinophilia
Rhinitis Medicamentosa
Rhinitis During Pregnancy
Vasculitides, Autoimmune & Granulomatous
Diseases

Viral Rhinitis
Associated with other presentations of viral infection
headache, malaise, body ache, cough

Nasal drainage is often clear or white


can be accompanied by nasal congestion and sneezing

Occupational Rhinitis
Caused by irritants in the work environment
e.g. dust, ozone, sulphur dioxide, ammonia

Typically presents with


Nasal dryness, reduced airflow, rhinorrhea, sneezing

Vasomotor Rhinitis
Presents with
nasal obstruction, clear nasal drainage

Associated with
temperature changes, eating, chemical or odour exposure, alcohol use

Nonallergic Rhinitis with Eosinophilia (NARES)


Presents with
nasal obstruction, congestion
eosinophilia on nasal smears
not associated with allergies

Patients frequently experience exacerbations, developing


sinusitis, polyposis

Rhinitis Medicamentosa
Presents with nasal obstruction worsening over many years
Typically associated with long-term vasoconstrictive nasal spray use

Leading to rebound rhinitis

Rhinitis during Pregnancy


The increase in oestrogen leads to rise in hyaluronic acid, resulting in oedema and
congestion
There is an increase in mucous glands and decrease in cilia, causing a decrease in
mucous clearance and consequent congestion
Usually most severe during the 2nd and 3rd trimesters

Vasculitides, Autoimmune and Granulomatous Diseases


PE

a)External : previous trauma


b) Internal: nasal septal position, turbinates,
rhinorrhea, nasal polyposis, masses. chronic
inflammation, vasculitis, and septal perforation
Due to: systemic problems.
Ex: Wegener granulomatosis, cocaine abuse

in-depth examination: rigid or flexible nasal endoscope

TREATMENT OF NONALLERGIC RHINITIS


A. Nonsurgical Measures
1. Irritant avoidance
2. Saline irrigation: intranasal stasis crusting. efficacy of intranasal topical
medication & ciliary
function.
3. Topical intranasal steroids: eosinophil & neutrophil chemotaxis, mast cell-related
reactions, intracellular edema.
4. Adrenergic agents: phenylamines (oral agents), imidazolines (topical agents).
5. Additional agents: Anticholinergic agents (ipratropium bromide), cromolyn sodium.

B.

Surgical Measures
1.

Septal procedures: Septal perforations

2.

Turbinate surgery

Arigatooo

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