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ALLERGIC RHINITIS
DR.B.KRISHNA SANTOSH,ASSOCIATE
PROFESSOR OF ENT,GSL MEDICAL
COLLEGE
Definition
 Multifocal
 igE
 Type1 hsn
 Of nasal mucosa
 To various allergens
 Inheritance-
 If one parent has h/o allergy-20-40% chance
 If both parents- 50-70% chance.
 Seasonal
 Perennial
 Occupational
 Common durring adolosence
 More common in males
 Genetic
 Focal sensitivity of nasal mucosa
 igA deficiency state
 Environmental factors
 psychology
 Pollen and dust.
 Fungus
 Danders
 Miscellaneous
 Allergens-
 Pollens
 Molds-fungal spores,aspergillus,
curvalaria,alternaria.
 Insects-cockroach,bed
bugs,houseflies,musquitoes.
 Animal dander-cat,doghorse,rabbit,guinea pig.
 House dust.
 Dustmite-in matresses.dermatophagoides.
 Foods- eggs,strawberries,nuts or fish,milk,
wheat.
Pollen common culprits
Flowers
Grasses and trees
Pets / animal dander
 Primary response :- allergic challenge in less
than 24 hrs.
 Late phase :- after 48 hrs
 Histamine secretion leads to sneezing, watery
discharge, itching.
 Pg,ld,n-mucous secretion and blockage.
 Eosinophils, mononuclear cells lead to
mucopurulent discharge.
 Ag + ige
 Degranulation release of mediators
 First response-rapid phase, sneezing,watery
discharge,itching.
 Late phase-noseblock,mucosal
secretion,inflamatory phase.- sub acute,
chronic.
 Preformed mediators
 Newly synthesized membrane derived lipid
mediators.
 Antigen molecules cross react with ige.this
cross linking allows formation of a calcium
channnel and the calcium influx triggers the
events that lead to histamine release .
Clinical features
 Nasal pruritis
 Paroxyms of sneezing
 Rhinorrohea
 Bilateral nasal stuffiness
 Seasonal > Perennial
 Mostly school children
 Assoc symp- cough, wheezing,chest
tightness,dyspnoea,eye
irritation,pruritis,eczematous dermatitis.
 Allergic salute, allergic shiners.
 Pale mucosa,boggy, blue tinged.
 Thin watery discharge
 Polyps
 Superadded imfection
 Complications-polyps,sinusitis,cobblestone
conjunctiva,edema of lids,allergic shiners.
 Serous otitis media,granular
pharyngitis,hoarseness of voice, bronchial
asthma.
Allergic salute
Investigations
 Cbp- eosinophils are raised.
 Nasal smear show-eosinophils
 Intranasal provacation test- crude method
(nasal challenge test).
 Specific ige antibody tests
 Skin test or invitro method.
Skin test
 prick or intradermal skin test
 Wheal(induration) ,flare ( erythema)which is
maximal at 15-20 mins.
 Detects presence of ige ab in tissueand shows
biologic activity.
In vitro tests
 RAST-it is a invitro test and measures the
specific igE concentration in patients serum.
 ELISA
TREATMENT
 AVOIDANCE –
 Pollen-close windows, remain in ac
 Animal dander- remove pets, HEPA Filter
(highefficiency particulate arresting ).
 Dust mite-encase pillows, matresses.
 Remove carpets.
 Molds- avoid gardening.
Drug therapy
 Anti histamines :-
 1st gen-chlorpheneramine,dimenhydramine.
 2nd gen-loratidine,cetrizine
 3rd gen-fexofenadine,levocetrizine.
 Topical-azelastine.
 Nasal decongestants-
 Pseudoephedrine,phenylephrine.
 Topical – xylo,oxy metazoline.
 Corticosteroids-anti inflamatory action.
 Systemic
 Topical-fluticasone, mometasone,
beclomethasone, nasal sprays.
 Mast cell stabilisers-sodium cromoglycate,
 Prophylaxis,stabilise the mast cell.
 Anti cholinergic agents
 Ipatropium bromide
 Donot cause rhinitis medicamentosa
 Mainly helps in treatment of post nasal drip
and rhinorrohea.
 Leukotriene modifiers
 Monteleukast-leukottriene inhibitor
 Zileuton-5-lipo oxygenase inhibitor.
 Anti ige antibody therapy-
 Omalizumab,
 Immunotherapy
 Repeated longterm injections of allergens.
 Circulating levels of ige antibodies increase
slightly during first few months but later on
decrease to substantially lower levels than
prior to injection.
 Subcutaneous injections gradually increasing
doses.weekly or twice a week.
 Surgery
 Inferior turbinectomy
 Laser , cryosurgery
 Electrocautery
 Chemical cautery
 Submucous diathermy.
 THANKYOU

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Allergic rhinitis

  • 2. Definition  Multifocal  igE  Type1 hsn  Of nasal mucosa  To various allergens
  • 3.  Inheritance-  If one parent has h/o allergy-20-40% chance  If both parents- 50-70% chance.
  • 5.  Common durring adolosence  More common in males  Genetic  Focal sensitivity of nasal mucosa  igA deficiency state  Environmental factors  psychology
  • 6.  Pollen and dust.  Fungus  Danders  Miscellaneous
  • 7.  Allergens-  Pollens  Molds-fungal spores,aspergillus, curvalaria,alternaria.  Insects-cockroach,bed bugs,houseflies,musquitoes.  Animal dander-cat,doghorse,rabbit,guinea pig.  House dust.  Dustmite-in matresses.dermatophagoides.  Foods- eggs,strawberries,nuts or fish,milk, wheat.
  • 11. Pets / animal dander
  • 12.  Primary response :- allergic challenge in less than 24 hrs.  Late phase :- after 48 hrs  Histamine secretion leads to sneezing, watery discharge, itching.  Pg,ld,n-mucous secretion and blockage.  Eosinophils, mononuclear cells lead to mucopurulent discharge.
  • 13.  Ag + ige  Degranulation release of mediators  First response-rapid phase, sneezing,watery discharge,itching.  Late phase-noseblock,mucosal secretion,inflamatory phase.- sub acute, chronic.
  • 14.
  • 15.  Preformed mediators  Newly synthesized membrane derived lipid mediators.
  • 16.
  • 17.  Antigen molecules cross react with ige.this cross linking allows formation of a calcium channnel and the calcium influx triggers the events that lead to histamine release .
  • 18.
  • 19. Clinical features  Nasal pruritis  Paroxyms of sneezing  Rhinorrohea  Bilateral nasal stuffiness  Seasonal > Perennial  Mostly school children  Assoc symp- cough, wheezing,chest tightness,dyspnoea,eye irritation,pruritis,eczematous dermatitis.
  • 20.  Allergic salute, allergic shiners.  Pale mucosa,boggy, blue tinged.  Thin watery discharge  Polyps  Superadded imfection  Complications-polyps,sinusitis,cobblestone conjunctiva,edema of lids,allergic shiners.  Serous otitis media,granular pharyngitis,hoarseness of voice, bronchial asthma.
  • 22. Investigations  Cbp- eosinophils are raised.  Nasal smear show-eosinophils  Intranasal provacation test- crude method (nasal challenge test).  Specific ige antibody tests  Skin test or invitro method.
  • 23. Skin test  prick or intradermal skin test  Wheal(induration) ,flare ( erythema)which is maximal at 15-20 mins.  Detects presence of ige ab in tissueand shows biologic activity.
  • 24. In vitro tests  RAST-it is a invitro test and measures the specific igE concentration in patients serum.  ELISA
  • 25. TREATMENT  AVOIDANCE –  Pollen-close windows, remain in ac  Animal dander- remove pets, HEPA Filter (highefficiency particulate arresting ).  Dust mite-encase pillows, matresses.  Remove carpets.  Molds- avoid gardening.
  • 26. Drug therapy  Anti histamines :-  1st gen-chlorpheneramine,dimenhydramine.  2nd gen-loratidine,cetrizine  3rd gen-fexofenadine,levocetrizine.  Topical-azelastine.  Nasal decongestants-  Pseudoephedrine,phenylephrine.  Topical – xylo,oxy metazoline.
  • 27.  Corticosteroids-anti inflamatory action.  Systemic  Topical-fluticasone, mometasone, beclomethasone, nasal sprays.  Mast cell stabilisers-sodium cromoglycate,  Prophylaxis,stabilise the mast cell.
  • 28.  Anti cholinergic agents  Ipatropium bromide  Donot cause rhinitis medicamentosa  Mainly helps in treatment of post nasal drip and rhinorrohea.
  • 29.  Leukotriene modifiers  Monteleukast-leukottriene inhibitor  Zileuton-5-lipo oxygenase inhibitor.  Anti ige antibody therapy-  Omalizumab,
  • 30.  Immunotherapy  Repeated longterm injections of allergens.  Circulating levels of ige antibodies increase slightly during first few months but later on decrease to substantially lower levels than prior to injection.  Subcutaneous injections gradually increasing doses.weekly or twice a week.
  • 31.  Surgery  Inferior turbinectomy  Laser , cryosurgery  Electrocautery  Chemical cautery  Submucous diathermy.