Presentation1 Pathology

HYPERSENITIVITY REACTIONS
Tejaswini Salunkhe
Roll no. 64
2nd Yr BHMS CBDC
Definition
 Sensitised response to subsequent antigenic stimuli
in inappropriate or exaggerated manner, leading to
tissue damage, diseade or even death.
 Hypersensitivity refers to injurious consequences in
sensitized host, following cintact with specific
antegens
Allergy
 The term allergy was originally used by Von Pirquet
 Allergy means an altered state of reactivity to an antigen and include both
types of immune responses, protective as well as injurious.
The individual should have contact with antigens (Allergen)
Initial response sensitize the immune system
Priming of B and T lymphocytes
Sensitizing or primary dose
Subsequent contact with allergen causes hypersensitivity
Shocking case
classification
a) Immediate hypersensitivity reaction
b) Delayed hypersensitivity reaction
coombs and Gell classified hypersensitivity reaction into 4 types based on
different mechanism of pathogenesis
1) Type 1 (Anaphylactic)
2) Type 2 (cytotoxic or cell stimulating)
3) Type 3 (immune complex or toxic complex disease)
4) Type 4 (delayed or cell mediated hypersensitivity)
Type 1. Anaphylactic, IgE or reagin dependant
 Causes :
1. Injections
2. Antibiotics or other drugs
3. Insect stings
 Treatment :
Adrenline is to be administered subcutaneously or intramuscularly. Dose
being repeated if necessary.
1. Type 1
(Anaphylactic, IgE or reagin dependent)
 IAntibodies are fixed on surface of tissue cells i.e. is most cell and
basophilic in somaliland individual. The antigen combines to with fixed
antibodies, leading to release of pharmacologically Active substances
(Vasoactive amines) and produces the clinical reaction.
 If sensitization is the most infective when the antigen is introduced
parenterally but may occur by any route including ingestion/Inhalation.
very minute dose can sanitize the hart.
 There should be an interval of atleast (2-3 weeks) between the
sensitizing does and shocking dose.
 The shocking antigen must be identical or immunologically closely
related to the sensitizing antigen.
 The clinical features of anaphylaxis are the same with antigen but the way
between spaces. The clinicals effects are due to samooth muscle contraction
and increased vascular permeability.
 Tissues or organs predominantly invove in the anaphylactic reaction are kniwn
as target tissue or shock.
 Other chancges are oedema, decreased coagulability of lood, fall in blood
pressure and temperature, leucopenia and thrombocytopenia.
 Symtoms and signs of anaphylactic shock:
1. Itching of scalp and tongue
2. Flushing of skin over the whole body
3. Difficulty in breathing
4. Nausea, vomiting, abdominal pain, diarrhea.
5. Sometimes blood in stool
6. Acute hypotension
7. Loss of consciousness and death follow.
Cutaneous Anaphylaxis
 When a smaal dose of antigen is administered intradermally
to asensitized host, there will be a local wheal and flare
response.
 The wheal is pale, central area of puffiness due to oedema,
because is surrounded by a flare caused by hyperthermia
and subsequent erythema.
 Cutaneous anaphylaxis is used in testing for hypersensitivity
and in identifying allergen respnsilble in atopic diseases.
 Ib highly sensitized individual, even the skin test may lead to
serious and even fatal reaction. Hence a syringe loaded with
adrenaline should be always be kept ready whenever a skin
test is performed to detect anaphylactic hypersensitivity.
Mechaniom of Anaphylaxis
 IgE molecules are bound to surface

receptors on most cells and basophils
 Following exposure to shocking chose ,the

antigen molecules combine with cell bound
IgE
 This cross linking increases permeability of
cells to calcium ions and leads to
degranulation with release of biologically
active substances contained in the granules
 The manifestation of anaphylaxis are due to
pharmacological mediation because are of a
kind
 Primary Secondary
Mediators Mediators
Primary mediators
 With are the preformed contents of mast

cell and basophil granule
 [ Histamin , serotonin,
eosinophil ,chemotactic factor of
anaphylaxis , neutrophils chemotaxtic
factor , heparin and various proteolytic
enzyme]
Secondary mediators
 Because are nearly formed upon simulation

by mast cells ,basophils and others
leucocyte.
 [ slow reacting substance of anaphylaxis ,
prostaglandin and platelets abdicating
factor , and cytokines such as IL3,IL4 ,
IL5,IL6,GM-CSF]
Anaphylactoid reaction
 Inteauenous injection of peptone , teypoin and

certain other subjects prouokes a clinical reaction
resembing anaphylactic shock .this is termed as
anaphylactoid reaction.
 The clinical resemblance to due to some chemical
mediators participating in oth reaction.the only
difference is that anaphy lactoid shock has no
immunological basis and is a nonspecific mechanism
involving the activation of complement and the
release of anaphylatoxins
 ATOPY :-
It was introduced by coca to referto
naturally occurring familial hypersensitivities
of human beings , typified by hay fever and
asthma . The antigens commonly involved in
atopy and characteristically inhalance Eg -
pollenhouse dust or ingestants Eg - eggs ,
milk.
some of them are contact allergens to
because theskin and conjuncative are exposed
These atopens are generally not good

antigens when injected parenterally, but
 Antibiodies, formerly termed as “regain “
antibiodies . Atopic sensitization is developed
spontageneously following natural contactwith
atopens . Its is difficult to induce atopy
artificially
 Predioposition to atopy is generatically

determined , probably linked to MHC henotype.
Atopy therefore sums in families
 What is inherited is not sensitivity to
paricularantigen but a tendency to produce IGE
antibiodies in usually large quantities
 Bottlefed infants tend to develop atopy in later
like more often than breastfed babies
1] It cannot be demonstrated by the

conuentional serological reactions such as
precipitationor complement fixation radio
allergosorbent test (RAST),ELLSA , passive
aqqluknation
2]IgE is homocytoteopic ie , species specific
only humans IgE can fix to the surface of human
cells
3]IgE is hea sensitive and is inactivated at56 C
in 2-4 hours
4] Atopic antibodies does not pass through
placenta.
 Atopic sensitivity is due to ever production of
IgE antibodies this is often associated with the
deficient of IgA . This association has led to the
suggestion that IgA deficiency may predilopose
to atopy.
 the distribution of lymphocytes capable of
syntheoixing IgA and IgE is doosly parallel
eopecially in submuoosa .In normal induduals ,
the inhalent and inqests antigents are deals with
by IgA
 Lining the respiratory and intestinal mucosa and
therefore they do not come into contact with the
potential IgE producing cells . When IgA is
deficient, the antigens cause massive stimulation
of IgE forming cells , leading to over production of
IgE.
 The symptoms of atopy are cause by the release

of pharmacologically active outs following the
combination of antigen and the cell fixed IgE
 The clinical expression of atopic reaction is

usually determined by partial of entry of the
Causes :- conjunctivitis
Rhinitis
gastrointestinal symptoms and
dermatitis
Urticaria

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HYPERSENITIVITY REACTIONS

Initial response sensitize the immune system

Priming of B and T lymphocytes

Sensitizing or primary dose

Subsequent contact with allergen causes hypersensitivity

 IgE molecules are bound to surface

 Following exposure to shocking chose ,the

 With are the preformed contents of mast

 Because are nearly formed upon simulation

 Inteauenous injection of peptone , teypoin and

These atopens are generally not good

 Predioposition to atopy is generatically

1] It cannot be demonstrated by the

 The symptoms of atopy are cause by the release

 The clinical expression of atopic reaction is

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