Lecture 10 Flashcards

1
Q

What are hypersensitivity reactions

A

Abnormal or undesirable state of immune reactivity which has deleterious effects on the host = immunopathology

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2
Q

What are the 4 classifications of hypersensitivity

A
  1. Type I or Immediate hypersensitivity
  2. Type II or antibody-mediated cytotoxic hypersensitivity
  3. Type II or immune complex hypersensitivity
  4. Type IV or delayed-type hypersensitivity (DHT)
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3
Q

Describe the 2 phases of immediate hypersensitivity (type I)

A

Phase 1
- Individual first sensitised to allergen
- Allergen-specific B cells mage IgE
- IgE binds to mast cells
Phase 2
- Upon subsequent exposure to allergen mast cells degranulate
-Rapid release of inflammatory molecules from mast cels
- Synthesis of other mediators

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4
Q

Where are Ag encountered that induce hypersensitivity type I

A

Mucosal sufaces

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5
Q

What is Atopy

A

Genetic predisposition to type I hypersensitivity

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6
Q

What do atopic individuals have predisposition to overreact to

A

Th2 immunity, high levels of IL-4, IgE

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7
Q

What are the main players in hypersensitivity

A

Th2 cells, IL-4, IgE, mast cells and eosinophils

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8
Q

Eosinophils in type I hypersensitivity

A

Large presence of eosinophils, attracted to mast cell degranulation products, presence of eosinophils at site is regarded as hall mark of type I

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9
Q

What happens to eosinophils in type I hypersensitivity

A

Degranulate to release own mediators

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10
Q

How are eosinophils activated

A

Mast cells and Th2 cells produce IL-5 and eotaxins which mobilise eosinophils from the bone marrow, eosinophils release complex array of molecules that contribute to acute inflammation, eosinophils exacerbate inflammation caused by mast cells

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11
Q

What are the clinical signs of hypersensitivity type I.

A

Hay fever, rash, itchy skin, asthma ect

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12
Q

What does Type I hypersensitivity result from

A

Excessive release of inflammatory mediators from mast cells, eosinophils and basophils

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13
Q

Clinical sings of atopy in dogs and cats (5)

A
  1. Pruritus or itching
  2. Licking of paws
  3. Over grooming
  4. Erythema (redness) and alopecia
  5. Thickening and increased pigmentation
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14
Q

When does anaphylaxis occur

A

When a section becomes systemic

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15
Q

How to diagnose type I hypersensitivity (5)

A
  1. Clinical history, age, breed, environment
  2. Allergin exkursion
  3. Comercial serum ELSIA
    Intradermal skin testing
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16
Q

How to treat type I hypersensitivity (4)

A
  1. Avoid exposure to allergen
  2. Corticosteriods, su press inflammation
  3. Immunotherapy, allergy shots, Th2 to Th1, induce tolerance
  4. Anaphylaxis
17
Q

What do type II antibodies react to

A

Surface of normal cells

18
Q

with Type II what are normal cells destroyed by

A

Complement or cytotoxic cells

19
Q

Type II: what can lesions result from

A

Destruction of the cells - delayed

20
Q

How do blood transfusions work

A

RBCs have surface antigen

21
Q

What happens if there is transfusion of miss matched blood

A

Stimulates an immune response, RBCs are agglutinated and lysed by Ab + complement, NK cels or removed by phagocytic cells

22
Q

What are the major groups of blood to species

A
Canine: DEA 1.1 and 1.2,7
Feline: A, B 
Equine: A, C, Q
Bovine: B, J
Ovine: B, R
23
Q

What causes haemolytic disease of the new born

A

Female sensitised to foetal ‘foreign’ blood group antigen during pregnancy as it makes Ab against foetal antigens. Suckling newborn absorbs colostral antibodies. Ab generated against foetal antigens react with antigens on blood cells of newborn causing rapid haemolyosis of newborn blood cells

24
Q

How do immune complex form with type III

A

Immune complexes forms as a result of antigen-antibody completes ant this activated complex

25
Q

Type III: what does sensitisation wiht Ag increase with

A

Increased circulating Ab

26
Q

Type III; what type of cells are recruited

A

Phagocytic cells

27
Q

Type III: where are immune complexes deposited

A

At site of Ag penetration

28
Q

Type III: what does it cause

A

Pain, oedema, thrombosis, local inflammation, haemorrhage and sometimes necrosis

29
Q

What are types I-III mediated by

A

Ab

30
Q

What is type IV mediated by

A

Cell mediated and had prolonged onset

31
Q

Where to type IV cells home

A

To the tissue site of Ag exposure and release of IFNy and other cytokines/chemokines

32
Q

What is ‘immunological’ contact dermatitis

A

Soluble molecules called happens penetrate skin and attach to proteins of epidermis

33
Q

What are the main players in ‘immunological’ contact dermatitis

A

Cytokines and T cells

34
Q

What is the Arthus reaction

A

Localised type III hypersensitivity

35
Q

What is serum sickness

A

Example of type III hypersensitivity