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Allergic Rhinitis
by Rolex R Maklago
Lecturer: Dr. Okwiri N
Powerpoint Templates
Page 2
Outline
✓ General Considerations
✓ Causes
✓ Classification
✓ Pathogenesis
✓ Clinical Features
✓ Investigations
✓ Differential Diagnoses
✓ Treatment
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General Considerations
• Allergy occurs as an adverse immune response
to usually harmless substances e.g. mold
spores, pollen after repeated contact
• Allergic Rhinitis refers an Ig-E-mediated
inflammatory reaction in the nasal mucous
membranes to one or more allergens
• Common allergic condition affecting up to 25%
of the population in US
• The condition is associated with considerably
high economic costs attributable to direct costs
on prescription and non-prescription drugs
• Although not life threatening, it significantly
diminishes quality of life among sufferers
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General Considerations cont.
• The onset of Allergic Rhinitis can be at any age.
• Highest incidence is in adolescence; decreases
with advancing age.
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Causes
1. Genetic susceptibility i.e. family history
2. Environmental factors e.g. mold, dust exposure
3. Exposure to allergens e.g. animal dander,
pollen, foods
4. Exhaust particles e.g. diesel exhaust
5. Passive exposure to tobacco smoke, especially
in early childhood
In infancy and childhood; otitis media, OME and
asthma occur as comorbidities
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Classification
a) Seasonal Allergic Rhinitis
• Symptoms occur or increase during certain
seasons. For example, season when plants
pollinate. Molds cause symptoms during fall;
trees pollinate in the spring
• Major symptoms are itching of the nose, ears
eyes and throat; sneezing, watery rhinorrhea,
nasal congestion (blockage), red and watering
eyes
• Worse in the morning; aggravated by dry and
windy conditions
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Classification
b) Perennial Allergic Rhinitis
• Constant symptoms with little seasonal
variation
• Nasal congestion, blockage and postnasal drip
are predominant; less of sneezing, rhinorrhea
and eye symptoms
• May be influenced by seasonal pollen,
nonspecific irritants, infections, food allergens
and indoor inhalants (cockroaches, dust mites,
mold spores)
OTHER CLASSIFICATIONS
1. Intermittent (<4 d/wk or <4 weeks) and
persistent (>4 d/wk or >4 weeks)
2. Minimal, moderate, severe changes to QOL
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Classification
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Pathogenesis
• Type I hypersensitivity reaction – an atopic
reaction involving excess production of IgE ab
• Sensitization to a specific allergen induces IgE
ab production through T-cel, B-cell and plasma
cell cascade
• Subsequent exposure leads to attachment of
antigen to 2 specific abs on surface of mast cells
(prevalent in resp and GIT mucosa, eye
subconjunctiva & subcutaneous skin layer).
• It then causes degranulation of mast cells to
release inflammatory mediators e.g. histamine,
leukotriene
• Release of histamine causes predominant
symptoms of allergic rhinitis (sneezing, itching,
rhinorrhea) –early phase (10-15 min)
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Pathogenesis cont.
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Pathogenesis cont.
• Release of leukotrienes and cytokines causes
influx of inflammatory cells, mainly Eθ, leading
to a prolonged and enhanced allergic cascade.
• It sets in in 4-6 hours and last for as long as
48hrs
• The mediators also cause a priming effect –
hyperactivity to both specific and non-specific
irritants
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Clinical Features
• Clear and watery nasal discharge
• Postnasal drip
• Itching of nose, eyes and throat
• Bluish pale, boggy turbinates
• Nasal congestion (predominant in perennial)
• Wet and swollen mucosa
• Nasal obstruction
• DNS, nasal polyps and concha bullosa may be
present as additional symptom contributors
• Nasal salute and allergic shiners under the eye
Additionally
• Associated ear infections, recurrent
rhinosinusitis, GIT symptoms, skin rashes,
asthma flare-ups
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Investigations
• Hx and PE is mostly adequate
• Allergic testing – in vitro serum assays, skin
testing
1. In vitro serum assays –
radioallergosorbent (RAST) test and
allergen-specific serum IgE testing
2. Skin Testing -skin prick test
-intradermal testing
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DDx
➢ Perennial non-allergic rhinitis e.g. vasomotor
rhinitis
➢ Infectious rhinitis (acute/chronic)
➢ Hormonal rhinitis (hypothyroidism, pregnancy)
➢ Anatomic deformity e.g. nasal polyp, DNS
➢ Foreign body
➢ Tumor
➢ Rhinitis medicamentosa – medication-induced
topical rhinitis
Powerpoint Templates
Page 15
Treatment
Avoidance and Environmental Controls
• Reduce household humidity
• Remove carpets and pets from most used
living areas e.g. bedroom
• Wash bed linens in hot water
• Air purifiers to remove airborne allergens
• Encase mattresses and pillows
• Eliminate cockroaches in poor and urban
settlements
Pharmacotherapy
• Antihistamines as the first line of therapy
e.g. diphenhydramine, chlorpheniramine
and hydroxyzine
• Intranasal and systemic corticosteroids
e.g budenoside and fluticasone
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Page 16
Treatment cont.
• Intranasal
anticholinergics eg
ipratropium bromide
to control rhinorrhea
• Intranasal cromolyn
before onset of
symptoms
• Leukotriene inh eg
Montelukast
Immunotherapy
• a gradual increase in
the dose of the
antigen(s) given until
either a mild systemic
symptom or a large
local reaction at the
subcutaneous injection
site occurs
Powerpoint Templates
Page 17

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Allergic rhinitis

  • 1. Powerpoint Templates Page 1 Powerpoint Templates Allergic Rhinitis by Rolex R Maklago Lecturer: Dr. Okwiri N
  • 2. Powerpoint Templates Page 2 Outline ✓ General Considerations ✓ Causes ✓ Classification ✓ Pathogenesis ✓ Clinical Features ✓ Investigations ✓ Differential Diagnoses ✓ Treatment
  • 3. Powerpoint Templates Page 3 General Considerations • Allergy occurs as an adverse immune response to usually harmless substances e.g. mold spores, pollen after repeated contact • Allergic Rhinitis refers an Ig-E-mediated inflammatory reaction in the nasal mucous membranes to one or more allergens • Common allergic condition affecting up to 25% of the population in US • The condition is associated with considerably high economic costs attributable to direct costs on prescription and non-prescription drugs • Although not life threatening, it significantly diminishes quality of life among sufferers
  • 4. Powerpoint Templates Page 4 General Considerations cont. • The onset of Allergic Rhinitis can be at any age. • Highest incidence is in adolescence; decreases with advancing age.
  • 5. Powerpoint Templates Page 5 Causes 1. Genetic susceptibility i.e. family history 2. Environmental factors e.g. mold, dust exposure 3. Exposure to allergens e.g. animal dander, pollen, foods 4. Exhaust particles e.g. diesel exhaust 5. Passive exposure to tobacco smoke, especially in early childhood In infancy and childhood; otitis media, OME and asthma occur as comorbidities
  • 6. Powerpoint Templates Page 6 Classification a) Seasonal Allergic Rhinitis • Symptoms occur or increase during certain seasons. For example, season when plants pollinate. Molds cause symptoms during fall; trees pollinate in the spring • Major symptoms are itching of the nose, ears eyes and throat; sneezing, watery rhinorrhea, nasal congestion (blockage), red and watering eyes • Worse in the morning; aggravated by dry and windy conditions
  • 7. Powerpoint Templates Page 7 Classification b) Perennial Allergic Rhinitis • Constant symptoms with little seasonal variation • Nasal congestion, blockage and postnasal drip are predominant; less of sneezing, rhinorrhea and eye symptoms • May be influenced by seasonal pollen, nonspecific irritants, infections, food allergens and indoor inhalants (cockroaches, dust mites, mold spores) OTHER CLASSIFICATIONS 1. Intermittent (<4 d/wk or <4 weeks) and persistent (>4 d/wk or >4 weeks) 2. Minimal, moderate, severe changes to QOL
  • 9. Powerpoint Templates Page 9 Pathogenesis • Type I hypersensitivity reaction – an atopic reaction involving excess production of IgE ab • Sensitization to a specific allergen induces IgE ab production through T-cel, B-cell and plasma cell cascade • Subsequent exposure leads to attachment of antigen to 2 specific abs on surface of mast cells (prevalent in resp and GIT mucosa, eye subconjunctiva & subcutaneous skin layer). • It then causes degranulation of mast cells to release inflammatory mediators e.g. histamine, leukotriene • Release of histamine causes predominant symptoms of allergic rhinitis (sneezing, itching, rhinorrhea) –early phase (10-15 min)
  • 11. Powerpoint Templates Page 11 Pathogenesis cont. • Release of leukotrienes and cytokines causes influx of inflammatory cells, mainly Eθ, leading to a prolonged and enhanced allergic cascade. • It sets in in 4-6 hours and last for as long as 48hrs • The mediators also cause a priming effect – hyperactivity to both specific and non-specific irritants
  • 12. Powerpoint Templates Page 12 Clinical Features • Clear and watery nasal discharge • Postnasal drip • Itching of nose, eyes and throat • Bluish pale, boggy turbinates • Nasal congestion (predominant in perennial) • Wet and swollen mucosa • Nasal obstruction • DNS, nasal polyps and concha bullosa may be present as additional symptom contributors • Nasal salute and allergic shiners under the eye Additionally • Associated ear infections, recurrent rhinosinusitis, GIT symptoms, skin rashes, asthma flare-ups
  • 13. Powerpoint Templates Page 13 Investigations • Hx and PE is mostly adequate • Allergic testing – in vitro serum assays, skin testing 1. In vitro serum assays – radioallergosorbent (RAST) test and allergen-specific serum IgE testing 2. Skin Testing -skin prick test -intradermal testing
  • 14. Powerpoint Templates Page 14 DDx ➢ Perennial non-allergic rhinitis e.g. vasomotor rhinitis ➢ Infectious rhinitis (acute/chronic) ➢ Hormonal rhinitis (hypothyroidism, pregnancy) ➢ Anatomic deformity e.g. nasal polyp, DNS ➢ Foreign body ➢ Tumor ➢ Rhinitis medicamentosa – medication-induced topical rhinitis
  • 15. Powerpoint Templates Page 15 Treatment Avoidance and Environmental Controls • Reduce household humidity • Remove carpets and pets from most used living areas e.g. bedroom • Wash bed linens in hot water • Air purifiers to remove airborne allergens • Encase mattresses and pillows • Eliminate cockroaches in poor and urban settlements Pharmacotherapy • Antihistamines as the first line of therapy e.g. diphenhydramine, chlorpheniramine and hydroxyzine • Intranasal and systemic corticosteroids e.g budenoside and fluticasone
  • 16. Powerpoint Templates Page 16 Treatment cont. • Intranasal anticholinergics eg ipratropium bromide to control rhinorrhea • Intranasal cromolyn before onset of symptoms • Leukotriene inh eg Montelukast Immunotherapy • a gradual increase in the dose of the antigen(s) given until either a mild systemic symptom or a large local reaction at the subcutaneous injection site occurs