HYPERSENSITIVITY

ALLERGIC REACTIONS.
HYPERSENSITIVITY

 It is an exaggerated immune
response.
 Sensitisation occurs on first exposure
to the Antigen.
 Allergic response occurs on re
exposure to the same/cross reacting
antigen.
Type 1 Hypersensitivity.

 Also known as ANAPHYLACTIC

REACTION.
 An Ag induces IgE Ab .
 IgE Ab bind firmly to receptors on
mast cells & basophils.
 Re exposure to the same Ag causes
release of mediators leading to
immediate allergic reaction.
IMMEDIATE PHASE

 Pollen,animal dander,certain foods e.g

nuts,shellfish etc.& various drugs
cause production of large amounts of
IgE in certain individuals.
 On re-exposure,cell bound
IgE,crosslinks & degranulation of mast
cells occurs releasing chemical
mediators of anaphylaxis.
CLINICAL
MANIFESTATIONS.
 Asthma
 Edema.
 Erythema(wheal & flare).
 Itching.
 These occur within minutes,d/t release
of histamine.
LATE PHASE.

 Occurs after about 6 hrs. of exposure.

 Leukotriens(SRS-A)are synthesised
after degranulation of mast
cells,causing influx of neutrophils
&eosinophils.
 Complement is not involved in these
reactions.
CLINICAL
MANIFESTATIONS.
 Urticaria (hives).
 Eczema.
 Rhinitis & conjunctivitis(hay fever).
 Asthma.
 Diarrhea(in those who ingest
allergens).
 Hay fever(in those who inhale
allergens).
Imp.Mediators of
anaphylaxis.
 HISTAMINE.
 SLOW REACTING SUBSTANCE OF
ANAPHYLAXIS(SRS-A).
 EOSINOPHIL CHEMOTACTIC FACTOR
OF ANAPHYLAXIS(ECF-A).
 SEROTONIN.
 PROSTAGLANDINS.
 THROMBOXANES.
TYPE 2
HYPERSENSITIVITY.
 Also called CYTOTOXIC
HYPERSENSITIVITY.
 Antigen is part of cell membrane.
 Ab directed at Ag activates
complement.
 A membrane attack complex is formed
that damages cell membrane.
CAUSATIVE FACTORS.

 Hemolytic anaemias.
 ABO Transfusion reactions.
 Drugs e.g
Penicillin,quinidine&phenacitin.
 Infections e.g Mycoplasma
pneumoniae can induce Ab that cross
react with RBC resulting in haemolysis.
 Good pasture’s syndrome.
TYPE 3
HYPERSENSITIVITY.
 Also known as IMMUNE COMPLEX
HYPERSENSITIVITY.
 Immune complexes persist &get
deposited in tissue.
 Complement is activated &results in
inflamation & tissue damage.
Manifestations.

 ARTHUS REACTION.
 Inflamation causedby deposition of
immune complexes at a localised site.
 ALLERGIC ALVEOLITIS.
 FARMER’S LUNG.
 CHEESE WORKER’S LUNG.
 WOOD WORKER’S LUNG.
 WHEAT MILLER’S LUNG.
SERUM SICKNESS.

 A systemic inflamatory response d/t

deposition of immune complexes in
many areas of the body.
IMMUNE COMPLEX
DISEASES.
 GLOMERULONEPHRITIS.
 RHEUMATOID ARTHRITIS.
 SYSTEMIC LUPUS ERYTHEMATOSIS.
TYPE 4
HYPERSENSITIVITY.
 CELL MEDIATED HYPERSENSITIVITY.
 It is due to cell mediated immunity.
 Can be transferred by T-cells.
TYPES OF DELAYED
HYPERSENSITIVITY.

 CONTACT HYPERSENSITIVITY.
 Caused by chemicals
e.gNickle,formaldehyde,plant
materiale.g poison ivy,poison
oak,topically applied drugs e.g
sulphonamides,neomysin,cosmetics&s
oaps .
TUBERCULIN TYPE
HYPERSENSITIVITY.
 Occurs due to Ag of microorganisms.
 Tuberculin test is a typical example.
 PPD. Is injected I/D .
 Ina pt. who is previously exposed to
infection redness & induration reaches
a peak in 48-72 hrs.
COMPLEMENT
DEFICIENCY STATES.
 Deficiency of C5-C8---infections by
Neisseriae sp.
 Def.of C3b---recurrent pyogenic
infections.
 Def.of C1 Esterase inhibitor—
angioedema.
 Def.Of decay accelerating factor—
Haemolysis resembling Paroxysmal
Nocturnal Haemoglobinuria.