Your SlideShare is downloading. ×
Hypersensitivity
Hypersensitivity
Hypersensitivity
Hypersensitivity
Hypersensitivity
Hypersensitivity
Hypersensitivity
Hypersensitivity
Hypersensitivity
Hypersensitivity
Hypersensitivity
Hypersensitivity
Hypersensitivity
Hypersensitivity
Hypersensitivity
Hypersensitivity
Hypersensitivity
Hypersensitivity
Hypersensitivity
Upcoming SlideShare
Loading in...5
×

Thanks for flagging this SlideShare!

Oops! An error has occurred.

×
Saving this for later? Get the SlideShare app to save on your phone or tablet. Read anywhere, anytime – even offline.
Text the download link to your phone
Standard text messaging rates apply

Hypersensitivity

1,836

Published on

0 Comments
2 Likes
Statistics
Notes
  • Be the first to comment

No Downloads
Views
Total Views
1,836
On Slideshare
0
From Embeds
0
Number of Embeds
0
Actions
Shares
0
Downloads
176
Comments
0
Likes
2
Embeds 0
No embeds

Report content
Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
No notes for slide

Transcript

  • 1. HypersensitivityClassificationHypersensitivity reactions are classified into four types:type I, type II, type III (immediate reactions)type IV (delayed reactions)
  • 2. Type I Hypersensitivity AllergensInhalants: Pollen grains, Fungal allergensInjectants: drugsContact: Antiseptic spray
  • 3. Type I hypersensitivity is known as immediate or hypersensitivity. The reaction may involve:■ Skin (urticaria and eczema),■ Eyes (conjunctivitis),■ Nasopharynx (rhinorrhea, rhinitis),■ Bronchopulmonary tissues (asthma)■ Gastrointestinal tract (gastroenteritis).
  • 4. ■ The mechanism of reaction involvesproduction of IgE, in response to certainantigens (allergens).■ IgE has very high affinity for its receptoron mast cells and basophils.■ A subsequent exposure to the same allergencross links the cell-bound IgE and triggersthe release of various active substances.
  • 5.  Cross-linking of IgE Fc-receptor is important in mast cell triggering. Mast cell degranulation is preceded by increased Ca++ influx, which is a crucial process.
  • 6. Mediators of Immediate Hypersensitivity Preformed mediators in granules:Hypersensitivity Table 1 Mediators of I bronchoconstriction, mucus secretion, histamine vasodilatation, vascular permeability tryptase proteolysis ECF-A attract eosinophil and neutrophils Newly formed mediators: leukotriene B4 basophil attractant leukotrieneC4, same as histamine ( 1000x more potent) D4 prostaglandins
  • 7. Diagnostic tests for immediatehypersensitivity■Skin (prick and intradermal) tests.■Measurement of Total IgE andspecific IgE antibodies: measured byELISA.
  • 8. Treatment A- Avoidance of exposure. B- Symptomatic treatment. C- Immunotherapy
  • 9. Symptomatic treatment1-Antihistamines which block histamine receptors.2-Chromolyn sodium inhibits mast cell degranulation, by inhibiting Ca++ influx.3-Late onset allergic symptoms, particularly bronchoconstriction which is mediated by leukotrienes, are treated with leukotriene receptor blockers or inhibitors of the cyclooxygenase.4-Symptomatic, although short term, relief from bronchoconstriction is provided by bronchodilators (inhalants).
  • 10. Type II hypersensitivity ■ Also known as cytotoxic hypersensitivity and may affect a variety of organs and tissues.■ The antigens are normally endogenous, althoughexogenous chemicals (haptens) which can attach to cell membranes can also lead to type II hypersensitivity. ■ Primarily mediated by IgM or IgG classes → ◘Complement mediated lysis. ◘Phagocytes and Killer cells may also play a role (ADCC).
  • 11. Types A- RBCs lysis:  1- Incompatible blood transfusion.  2- Erythroblastosis faetalis:  3- Autoimmune hemolytic disease. B- WBCs lysis:  1- Granulocytopenia.  2- S.L.E. C- Platelet destruction:
  • 12. Type III Hypersensitivity (immune (complex hypersensitivity■ It is mediated by soluble immunecomplexes. They are mostly of the IgG,although IgM may also be involved.■ The antigen may be: ■ exogenous (chronic bacterial, viral or parasitic infections). ■ endogenous (non-organ specific autoimmunity: e.g. (SLE).
  • 13. Mehanism■ The Ag is soluble and not attached to the organ involved.■ Soluble Ag-antibody complexes which pentrate the enothelium of blood vessel and deposited on the vascular basement membrane.■ This will stimulate the complement and chemotactic factors like C5a is released which attract neutrophils which infitrate the area and release lysosomal enzymes leading to destruction of the basement membrane.
  • 14. Types:Arthus reaction -1:Serum sickness -2:Hypersensitivity pneumonitis -3:Posstreptococcal glomerulonephritis -4Autoimmune disease: RA , SLE -5
  • 15. Type IV Hypersensitivity■ Type IV hypersensitivity is also known as cellmediated or delayed type hypersensitivity.■ The classical example of this hypersensitivity istuberculin (Montoux) reaction which peaks 48hours after the injection of antigen (PPD or oldtuberculin). The lesion is characterized byinduration and erythema.
  • 16. ■ Mechanisms of damage in delayed hypersensitivityinclude T lymphocytes and monocytes and/ormacrophages. Cytotoxic T cells cause direct damagewhereas Th1 cells secrete cytokines which activatecytotoxic T cells and recruit and activate monocytes andmacrophages, which cause the bulk of the damage. Thedelayed hypersensitivity lesions mainly contain monocytesand a few T cells.■ Major lymphokines involved in delayed hypersensitivityreaction include monocyte chemotactic factor, Il-2,interferon-gamma, TNF alpha/beta, etc.

×