Hypersensativity

Question 1

Type 1 hypersensitivity

Immediate

Answer 1

1st exposure = Proliferation of IgE antibody which results in vasoactive amines and priming of mast cells
- TH2 mediated response

2nd exposure = recruitment of inflammatory cells and activation of mast cells

Histological lesions

• vascular dilation
• edema
• increased mucus production and inflammation

Known disorders

• anaphylaxis reactions
• bronchial asthma
• allergies

Question 2

Type 2 hypersensitivity

Antibody mediated

Answer 2

Production of IgG/ IgM binds to antigen on target cell tissues and promotes phagocytosis and lysis of targeted cell
- activation of compliment by Fc receptors on IgG/IgM induces phagocytosis

Histologic lesions

• phagocytosis and lysis of cells
• inflammation and functional derangement without cell or tissue injuries

Known disorders associated = autoimmune anemia and good pasture syndrome, MG, TPP, rheumatic fever, pernicious anemia, pemphigus vulgaris

Question 3

Type 3 hypersensitivity

Immune complex mediated

Answer 3

Deposition of antigen-antibody complexes which leads to compliment activation and recruitment of leukocytes by compliment products and Fc receptors
- releases enzymes and other toxic molecules into the blood stream

Histologic lesions

• inflammation
• necrotizing vasculitis and fibrinoid necrosis

Disorders associated

• SLE
• glomerulonephritis
• serum sickness

Question 4

Type 4 hypersensitivity

Cell-mediated

Answer 4

Activated T lymphocytes release cytokines and procure inflammation and recruitment of macrophages and CD8 T cells
- later macrophages and CD8-Tcells initiate cytotoxicity

Two types of Tcell reactions:

• 1) cytokine mediated CD4-Tcell
• 2) direct cytotoxic CD-8 T cells

Histologic lesions

• perivascular infiltrates
• edema
• granuloma formation
• cell destruction

Conditions associated

• contact dermatitis
• MS
• DM type 1
• TB activation

Question 5

3 events of immediate response in type 1

Answer 5

1) activation of TH2 cells Na production of IgE
2) sensitization of mast cells by IgE antibodies
3) activation of mast cells and release of mediators including vasoactive amines

Question 6

Immediate vs late phase reactions

Answer 6

Immediate:

• occurs within 30 minutes after allergen exposure
• goes away within 60 minutes
• stimulated by mast cell granule contents and lipid mediators

Late-phase

• occurs 2-8 hrs later and lasts several days
• stimulated by cytokines
• shows inflammation and tissue damage

Question 7

Dermatographic urticaria

Answer 7

is also called “skin writing”

Caused by release of histamine from mast cells without antigen exposure

Basic skin scratches result in over activation of hypersensitivity

Treatment = antihistamines if needed, otherwise benign

Question 8

Solar urticaria

Answer 8

“Sun allergies”

Acute sun exposure results in over hypersensitivity of histamine release from mast cells and causes a sunburn appearance

Question 9

Cholinergic urticaria

Answer 9

Type 1 hypersensitivity reaction to generalized heat

Veritable symptoms but can be life-threatening

Question 10

Cold urticaria

Answer 10

“Cold allergy”

Unknown cause of hypersensitivity type 1 due to cold

Variable symptoms but can be life threatening

Question 11

Insect bites and stings

Answer 11

Are usually an example of type 1 hypersensitivity to the toxin released from the bite
- NOT heavily histamine driven but more allergy to the toxin driven

Can occasionally be type 4 response if delayed symptoms

Question 12

Allergic contact dermatitis

Answer 12

Is usually type 4 but can be type 1

• type 1 = almost instantaneously
• type 4 = takes a couple days

Question 13

Principal mediates of hypersensitivity are what?

Answer 13

Histamine, proteases, PGE and leukotrienes

Question 14

3 phases of type 3 hypersensitivity

Answer 14

1) formation of immune complexes
2) deposition of immune complexes
3) inflammation and tissue injury