Inflammation-Hypersensitivity Reactions Flashcards Preview

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Flashcards in Inflammation-Hypersensitivity Reactions Deck (19)
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1
Q

What mediates Type I Hypersensitivity reactions?

A

IgE antibodies

2
Q

What is Type I also known as?

A

Immediate anaphylaxis

3
Q

What are the types of anaphylaxis?

A

General: bronchoconstriction, contraction of smooth muscle, increases in vascular permeability, often fatal, rare

Local: operates via binding of allergen to IgE antibodies on surface of mast cells or basophils; release of histamine causes clinical signs of acute inflammtion

4
Q

What mediates Type II Hypersensitivity reactions?

A

IgG or IgM antibodies reacting with cell surface antigens or haptens

5
Q

What are the 4 main modes of cell destruction in Type II hypersensitivity?

A
  1. phagocytosis of antibody-coated cells by liver, splenic, or tissue macrophages
  2. complement-mediated lysis of antibody-coated cells
  3. antibody-dependent cell-mediated cytotoxicity by killer cells
  4. surface receptor endocytosis or down regulation
6
Q

What phases do all hypersensitivity reactions have?

A

Sensitation phase: previous exposure, develop specific immune response

Effector phase: pathology

7
Q

what are the ways in which Type II hypersensitivities can be taken care of (good or bad)?

A
  • -Opsonization via IgG antibodies
  • -Opsonization or lysis via complements (kick off the MAC or C3b can causes phagocytosis)
  • -Antibody-dependent cell-mediated cytotoxicity (ADCC) (IgG, killer cells have FcR that bind tissue cell)
  • -Receptor blockade/removal (antibody doesnt allow hormone to bind or antibody/receptor complex gets internalized)
  • -Antibody-mediated cellular dysfunction (antibody causes cell to perform or not perform, regardless of stim by hormones)
8
Q

What is the overall pathway of the Type III Hypersensitivity reaction?

A

Ag-Ab complex>deposition>neutrophil and macrophage activation by FcR>complement cascade

9
Q

What is the basis of Type III hypersensitivity?

A

combination of soluble antigen with circulating IgG or IgM antibodies to form “immune complexes”

10
Q

What is an Arthus reaction?

A

immune complexes are formed locally in blood vessels and tissues

11
Q

What is the characteristic lesion of Type III hypersensitivity?

A

vasculitis

12
Q

What is Type IV hypersensitivity also known as?

A

Cell-mediated Delayed Type Hypersensitivity (DTH)

13
Q

What mediates Type IV hypersensitivity?

A

T cells and macrophages

14
Q

Does the individual have to be sensitized for a Type IV reaction?

A

Yes

15
Q

What is DTH an extension of?

A

Normal T cell mediated immune responses

16
Q

What are some examples of Type IV hypersensitivity?

A

Jones Mote (cutaneous basophil hypersensitivity)
Tuberculin reaction
contact sensitivity

17
Q

What is a Type IV hypersensitivity reaction due to?

A

activation of specific T cells which release lymphokines to attracte macrophages and more lymphocytes

18
Q

What may happen to a lesion in chronic DTH?

A

development of epitheloid cells or giant cells (macrophages for both)

These cells along with T cells kill infected cells, causing caseous necrosis at center of reaction

19
Q

What happens to the lesion if the organism is killed? If not?

A

Killed: lesion is repaired by fibrosis
Not: caseous necrosis is walled off by CT, forming granuloma; lesion can become calcified or liquefied