Hypersensitivity reaction, bph

1. HYPERSENSITIVITY REACTION
MAN BAHADUR RANA
BPH
ACAS,NEPAL

2. 2
Definition
Any tissue damaging Immune reactions. Hypersensitivity can
occur to certain individual who have previous contact with
the antigen, when exposed to second dose of the same
antigen.
The Initial dose of the antigen adequate to sensitize the host
immune cells is called Sensitizing dose
The Subsequent dose of same antigen adequate to produce
abnormal immune response is called Shocking dose
: Antigen able to cause Hypersensitivity is called Allergen
Hypersensitivity reactions

3. 3
Classification
On the Basis of Mechanisms and time taken for the
appearance of hypersensitivity rxns, Gels and Coombs
(1963) classified hypersensitivity rxns
I, II, III, IV (Type V is also now added)
Basis of time required by sensitized host to respond to the
shocking dose of antigen, hypersensitivity rxns can be
categorized into two main groups
Immediate hypersensitivity rxns whihc manifest in few
minutes to few hours
Delayed Hypersensitivity rxns which manifest Usually after
24 hours
Hypersensitivity reactions

4. 4
Hypersensitivity type I
Type I hypersensitivity is also called Anaphylactic
Hypersensitivity or Anaphylaxis or simply as allergy and the
components of type I hypersensitivity include allergens, IgE
and Mast cells or Basophils
The first contact with the antigen (allergen) induces preferential
production of abnormal amount of IgE mediated by IL-4 and
IL-13. IgE bind through their Fc port receptors on cell
surface of Mast Cells and Basophils which are found
throught the body tissue and circulations.
Second contact with the same antigen crosslinks the membrane
bound IgE on mast cells and basophils, causing
degranulation, thus releasing the Primary (Histamine,
serotonin, Proteases, Eosinophil chemotactic factor etc) and
Secondary (prostglandins, Bradykinins, Cytokines
etc)pharmacologic mediators.
The effects of these mediators are vasodilation, smooth muscle
contraction and setting up an inflammatory condition.
Hypersensitivity reactions

5. 5
Hypersensitivity type I(Mechanism)
Hypersensitivity reactions
1. Sensitisation
2. Waiting
Period(2-3 weeks)

6. 6
Hypersensitivity type I
Hypersensitivity reactions
3. Effector Phase

7. 7
Hypersensitivity type I
Hypersensitivity reactions

8. 8
Hypersensitivity type I
Clinical manifestations
Hypersensitivity reactions
• Localized anaphylaxis and Atopy
In localized type I hypersensitivity, the reaction is limited to
specific target tissue or organ often involving the
epithelial surface at the site of allergen entry
– cutaneous anaphylaxis – wheal & flare
– Skin (urticaria and eczema)
– Eyes (Conjunctivitis)
– Nasopharynx (allergic rhinitis or hay fever)
– Gastrointestinal tract(Gastrointeritisfood allergies)
– Bronchopulmonary tissues(asthma)
Atopy: Hereditary tendency to manifest localized anaphylaxis.

9. 9
Hypersensitivity type I
Clinical manifestations
Systemic Anaphylaxis
Hypersensitivity reactions
In systemic anaphylaxis a generalized vasodilation
and smooth muscle contraction occurs.
mast cells degranulation occurs all over body with 3
potentially fatal Rx
• laryngeal edema – fluid leaking out → swelling
• bronchiole constriction → suffocation
• peripheral edema → shock from fluid loss

10. 10
Hypersensitivity type II
Type II hypersensitivity reaction involve Ab mediated
destruction of cell or cellular dysfunction
Specific IgG or IgM bind with antigens, that may be
microbial products or drugs( like penicillin) passively
adsorbed on a self cell surface, foreign cells surface
antigens or autoantigens. The antibodies attached to
antigens mediate the destruction of cells or tissue,
inflammation or cellular dysfunction. The destruction or
dysfunction occurs by activation of complement that
kills cells by making pores, ADCC mainly by NK cells,
and by increased phagocytosis (frustrated phagocytsis
by opsonization)
Hypersensitivity reactions

11. 11
Hypersensitivity type II
Clinical significance
1. Autoimmune Hemolytic Anemia
2. Transfusion reaction (Transfusion of incompatible blood
group
3. Erythroblastosis Fetalis (Rehesus incompatibility when
Rh negative mother gives birth to Rh positive baby)
4. Drugs induced hemolytic anemia
5. Goodpasteur’s disease (Autoimmune disease,
Autoantibodies to lungs and basement membrane
6. Grave’s disease (Cellular dysfunction of follicles of
thyroid gland)
Hypersensitivity reactions

12. 12
Hypersensitivity type II
A. Target cell Depletion or Destruction without Inflammation
Hypersensitivity reactions

13. 13
Hypersensitivity type II
C. Antibody mediated cell dysfunction
1. Grave’s disease
Hypersensitivity reactions

14. Hypersensitivity reaction type III
Immune complex  Inflammation
Ag  free Exogenous or Endogenous
Ab IgG or IgM
14
Hypersensitivity reactions

15. Hypersensitivity reaction type III
Ag-Ab complex complement activation + inflammatory
cells Inflammatory reaction
15
Hypersensitivity reactions

16. Type of Hypersensitivity reaction type III
1. Generalized / Systemic reactionSerum sickness like
2. Localized Reaction  Arthus Reaction
16
Hypersensitivity reactions

17. Hypersensitivity reaction type III
17
Hypersensitivity reactions

18. Hypersensitivity reaction type III
18
Hypersensitivity reactions

19. Hypersensitivity reaction type III
Generalized ReactionsSerum sickness
• May last for 7-10 days.
• •Bacterial, Viral and Parasitic infection produce serum
sickness.
• •Important Diseases
• Post Streptococcal Glomerulonephritis
• SLE
• Polyarthritis nodusa
• Rheumatoid arthritis
• Drugs
19
Hypersensitivity reactions

20. Hypersensitivity reaction type III
1. Localized Reaction  Arthus Reaction
Farmer’s lung disease
Bird Fancier’s disease
20
Hypersensitivity reactions

21. Hypersensitivity reaction type IV
Delayed type or cell mediated (Th1 cell)
Th1 cells cytokinesLarge influx of non specific
inflammatory cells (Macrophages)
Slow evolving (24-72 hours)
21
Hypersensitivity reactions

22. Hypersensitivity reaction type IV-Mechanism
22
Hypersensitivity reactions

23. Hypersensitivity reaction type IV-Mechanism
23
Hypersensitivity reactions
b. Effector phase

24. Hypersensitivity reaction type IV
Granuloma
Tuberculin test
Contact dermatitis
24
Hypersensitivity reactions

25. Hypersensitivity reaction type IV-Mechanism
25
Hypersensitivity reactions
b. Effector phase

26. Hypersensitivity reaction type IV-inducing
pathogens and Antigens
Intracellular Bacteria
M. tuberculosis, M. leprae, Listeria monocytogens,
Brucella abortus
Intracellular fungi
Candida albicans, Histoplasma capsulatum, Cryptococcus
neoformans
Intracellular Parasites
Leishmani sp, Pneumocystis carinii,
26
Hypersensitivity reactions

27. Hypersensitivity reaction type IV-inducing
pathogens and Antigens
Intracellular Viruses
Herpes Simplex virus, Small pox virus, Measles Virus
Contact Antigens
Picryl Chloride, Hair dyes, Nickel salts, Poison ivy, Poison
oak
27
Hypersensitivity reactions