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HYPERSENSITIVITY
By HARSHAL S BEHADE
Msc R.G.B.C RTMNU
(Jr and Sr. college teacher)
Introduction
 “An exaggerated or undesirable response/reactions by the immune
system to a drug or other substances”
Types:-
 There are four types
 Hypersensitivity type 1 immediate type
 Type 2 antibody mediated
 Type 3 immune complex mediated
 Type 4 delayed type
Hypersensitivity 1 immediate type
 When allergen are entered into the body, our immune responses or immune
system’s are activates and on working immediately.
 It occurs in two phases:-
a) Sensitisation phase
b) Effector phase
Sensitisation phase
 Alergens enter into the body.
 So we have two types of antigen
presenting cells
 1. Dendritic cells
 2. Macrophages
 They breaks allergen into antigen
peptides.
And they show that antigen peptide
To T-cell with the help of MHC-II molicule
 Then TH cells detects these antigen
peptide with the help of CD4 receptors.
 Once it detects then TH cells
differentiate into TH2 cells.
 These TH2 cells releases Interlukins
molicules as IL-4, IL-5,IL-13.
 This IL-5 molicules develop & activates
Eosinophils.
 Remaining Interlukins 4 & 13 are differentiate
B cells into IgE secreating Plasma cells and Memory cells.
 These plasma & memory cells secreates IgE antibody.
 Some receptors are present in circulating Mast cells FCeRI
(high affinity FC receptors)
So these IgE antibody binds that receptors.
2nd :- Effector phase
 In this phase that allergen enters into the body again or second time (or
introduced again ).
 This is known as shocking dose.
 Allergen directly encounters the F(ab) region of IgE molecule present on Mast
cell.
 & binds with that Fab region
 Then cross linking occurs in IgE molecule & the mast cell initiates into
degranulation.
Three changes occurred in mast cell:-
 1. It releases granules contained Histamine and Proteases.
 2. Membrane phospholipase A2 activates by this activity,
 Then they are converted into Arachidonic acid.
 This arachidonic acid makes Prostglandins (D2) by Cox pathway,
 And Leukotriens (B4,C4,O4) by Lox pathway.
 3. also one signal going to Nucleus & then Cytokines gene activates.
 Then this cytokines & chemokines are released.
 So these histamine, protease, prostaglandins, leukotriens, cytokines,
chemokines are our Modulators.
Modulators
 These produces our immune response immediately and this occurs within a
minute after repeat exposure.
 These responses are in the form of
 1. Vasodilation
 2. Increases vascular permeability
 3. and smooth muscles contraction
 These immediate responses occurred by granular prostaglandins and
leukotriens.
Next is a late phase reaction
(Inflamation)
 After repeate exposure to allergen the inflammation occures in 2-24 hrs,
 by cytokines and chemokines.
1. Leukocytes infiltration
2. Epithilial damages
3. Bronchospasm, occures
Menifestations:-
 Systemic anaphylaxis (allergy on full body)
 Localized anaphylaxis
 Systemic:-
 Within minutes after exposure itching(red ness), hives, vomiting, abdominal cramps, diarrhea &
larrhengial abstraction follows and the patient may go into shock & even die within hour’s.
 Allergens : 1. venom ( bee, ants etc)
 2. Drugs ( penicillin, Insuline etc)
 3. Antitoxins
 4. See foods
 5. Nuts
 Drug of choice:- Adrenaline = 0.5ml
Localised anaphylaxis:- (atopy)
 A. Allergic Rhinitis (Hey fever)
 Most common atopic disorder.( it affects 10% populations)
 Ex. Symptoms :- high secretion of Cunjuctiva, nasal mucosa, upper respiratory
tract infections, sneezing, coughing.
 B. Asthama:-
 Second most common atopic disorder
 Lower respiratory tract infection involved
 Symptoms:- Bronchospasm, Breathlessness.
 Asthama if allergic then caused by pollen dust fumes, insect products, viral
antigens.
 If it is Intrinsic then coused by excessive exercise, temperature change.
c.Food allergy
 Someone are allergic by food like nuts, eggs, seafoods.
 Symptoms: - food poisoning l;ike , vomiting, diarrhea, Atopic urticaria.
 D. Atopic dermatitis
 Erruption on skin filled by pus
 Symptoms:- Erythromatus skin, (eruption which are filled with pus)
 E. Drug allergy:- 1.penicillin, 2. Sulphonamide

Treatments
 Avoid contact with known allergens (pollen etc.)
 Hyposensitisation:-
 It was known about the allergy & if we take regular doses intradermaly introduce
in the skin or body then the effect may less then IgG antibody secreats apart from
IgE.
 Monoclonal Anti Ig-E
 Drugs:- 1. Antihistamine
2. Adrenaline
3. Cortisone
4. Theophyline
5. Cromolyn solution.
Thank you

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HYPERSENSITIVITY(1).pptx

  • 1. HYPERSENSITIVITY By HARSHAL S BEHADE Msc R.G.B.C RTMNU (Jr and Sr. college teacher)
  • 2. Introduction  “An exaggerated or undesirable response/reactions by the immune system to a drug or other substances”
  • 3. Types:-  There are four types  Hypersensitivity type 1 immediate type  Type 2 antibody mediated  Type 3 immune complex mediated  Type 4 delayed type
  • 4. Hypersensitivity 1 immediate type  When allergen are entered into the body, our immune responses or immune system’s are activates and on working immediately.  It occurs in two phases:- a) Sensitisation phase b) Effector phase
  • 5. Sensitisation phase  Alergens enter into the body.  So we have two types of antigen presenting cells  1. Dendritic cells  2. Macrophages  They breaks allergen into antigen peptides. And they show that antigen peptide To T-cell with the help of MHC-II molicule
  • 6.  Then TH cells detects these antigen peptide with the help of CD4 receptors.  Once it detects then TH cells differentiate into TH2 cells.  These TH2 cells releases Interlukins molicules as IL-4, IL-5,IL-13.  This IL-5 molicules develop & activates Eosinophils.
  • 7.  Remaining Interlukins 4 & 13 are differentiate B cells into IgE secreating Plasma cells and Memory cells.  These plasma & memory cells secreates IgE antibody.  Some receptors are present in circulating Mast cells FCeRI (high affinity FC receptors) So these IgE antibody binds that receptors.
  • 8. 2nd :- Effector phase  In this phase that allergen enters into the body again or second time (or introduced again ).  This is known as shocking dose.  Allergen directly encounters the F(ab) region of IgE molecule present on Mast cell.  & binds with that Fab region  Then cross linking occurs in IgE molecule & the mast cell initiates into degranulation.
  • 9. Three changes occurred in mast cell:-  1. It releases granules contained Histamine and Proteases.  2. Membrane phospholipase A2 activates by this activity,  Then they are converted into Arachidonic acid.  This arachidonic acid makes Prostglandins (D2) by Cox pathway,  And Leukotriens (B4,C4,O4) by Lox pathway.  3. also one signal going to Nucleus & then Cytokines gene activates.  Then this cytokines & chemokines are released.  So these histamine, protease, prostaglandins, leukotriens, cytokines, chemokines are our Modulators.
  • 10. Modulators  These produces our immune response immediately and this occurs within a minute after repeat exposure.  These responses are in the form of  1. Vasodilation  2. Increases vascular permeability  3. and smooth muscles contraction  These immediate responses occurred by granular prostaglandins and leukotriens.
  • 11. Next is a late phase reaction (Inflamation)  After repeate exposure to allergen the inflammation occures in 2-24 hrs,  by cytokines and chemokines. 1. Leukocytes infiltration 2. Epithilial damages 3. Bronchospasm, occures
  • 12. Menifestations:-  Systemic anaphylaxis (allergy on full body)  Localized anaphylaxis  Systemic:-  Within minutes after exposure itching(red ness), hives, vomiting, abdominal cramps, diarrhea & larrhengial abstraction follows and the patient may go into shock & even die within hour’s.  Allergens : 1. venom ( bee, ants etc)  2. Drugs ( penicillin, Insuline etc)  3. Antitoxins  4. See foods  5. Nuts  Drug of choice:- Adrenaline = 0.5ml
  • 13. Localised anaphylaxis:- (atopy)  A. Allergic Rhinitis (Hey fever)  Most common atopic disorder.( it affects 10% populations)  Ex. Symptoms :- high secretion of Cunjuctiva, nasal mucosa, upper respiratory tract infections, sneezing, coughing.  B. Asthama:-  Second most common atopic disorder  Lower respiratory tract infection involved  Symptoms:- Bronchospasm, Breathlessness.  Asthama if allergic then caused by pollen dust fumes, insect products, viral antigens.  If it is Intrinsic then coused by excessive exercise, temperature change.
  • 14. c.Food allergy  Someone are allergic by food like nuts, eggs, seafoods.  Symptoms: - food poisoning l;ike , vomiting, diarrhea, Atopic urticaria.  D. Atopic dermatitis  Erruption on skin filled by pus  Symptoms:- Erythromatus skin, (eruption which are filled with pus)  E. Drug allergy:- 1.penicillin, 2. Sulphonamide 
  • 15. Treatments  Avoid contact with known allergens (pollen etc.)  Hyposensitisation:-  It was known about the allergy & if we take regular doses intradermaly introduce in the skin or body then the effect may less then IgG antibody secreats apart from IgE.  Monoclonal Anti Ig-E  Drugs:- 1. Antihistamine 2. Adrenaline 3. Cortisone 4. Theophyline 5. Cromolyn solution.