Immune Mediated Tissue Damage Flashcards

1
Q

Whats the difference between immunity and hypersensitivity

A

Immunity is fighting the infection which is a good thing whereas hypersensitivity is when the immune response causes damage to the host tissue which is harmful to the health of the individual

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2
Q

Table he mentioned. This is a big chunk of this module

A
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3
Q

Fishback’s description of Anaphylaxis

A
  1. IgEs are pre made, that is they are made before the superantigen exposure take place.
  2. Cell injury is attributed to Th2 cells
  3. Ployclonal response
  4. Degranulation: antigen binds with IgE then crosslinks with another IgE causing degranulation of mast cells which release mainly histamine.
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4
Q

What is released in Anaphylaxis

A
  1. Mast cells releases histamine, protease and chemotactic factors
  2. Cytokines are made IL-1,3,4,5,6
  3. Products of arachidonic acid: Prostaglandins and leukotrienes.
  4. PAF (he said it is more powerful than histamine)
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5
Q

What happens in the first exposure in regards to Anaphylaxis

A

Mast cells are loaded up with IgEs

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6
Q

What counteracts the histamine released by mast cells

A

Eosinophils make histaminase to regulate the effects of histamine.

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7
Q

Clinical significance of eosinophils

A

If there is a patient will elevated blood count of eosinophils then we have to consider 2 conditions

  1. Allergies
  2. Parasitic infections
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8
Q

What are the 2 components that characterize the anaphylaxis

A

There are 2 parts of the anaphylaxis response:

  1. Immediate reaction
  2. Late-phase reaction

Immediate reaction is due to the factors discussed previosuly whereas the late phase reaction is mainly due to prostaglandins and leukotrienes

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9
Q

Describe the process of Anaphylaxis in detail

A

Important thing to note: during the first exposure there is class switching from IgM to IgE

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10
Q
A

Important: people with chronic asthma since childhood have obstruction and hyperinflation

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11
Q
A

High power - lungs - asthma

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12
Q

What are the receptors on mast cells to which antigen-bound IgE bind to and cause degranulation

A

Fc receptors

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13
Q

What is a long term pathology associated with type I hypersensitivity reactions

A

In people with chronic asthma since childhood their lungs undergo remodeling due to chronic inflammation such that the smooth muscles around their bronchioles undergo hypertrophy.

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14
Q

What antibodies are in type II hypersensitivity

A

IgM or IgG (no IgE!, thats only in type I)

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15
Q

What did Fishback mention about type II hypersensitivity

A
  1. It can cause increase in IgM and/or IgG. This leads to binding and activation and MAC can then be attached to a cell which leads to its lysis.
  2. NK cells can be activated by a phenomenon known as the antibody-dependent cell-mediated cytotoxicity
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16
Q
A

This is a picture of the glomeruli in Goodpasture Syndrome.

  1. IgG or IgM antibodies are made against collagen, specifically type IV collagen
  2. Collagen IV is found in the basement membrane which is found all over the body but the organs it affects the most are the lungs and the glomeruli
17
Q

What happens in type III

A

Antibodies are IgG and IgM but the antigen this time is solouble. Immune complexes are formed, these are most often formed in situ and are filtered out in the capillaries. Skin and kidneys are most commonly affected

18
Q

What is lupus classified under

A

Sytemic Lupus Eryhtmatosus is classified under type III

19
Q
A

Post Streptococcal Nephrotitus

20
Q

Remember that in type III it is the neutrophils that are causing the problems since they are recruited as C3a and C5a binds and recruites neutrophils

A
21
Q

Explain type IV hypersensitivity reaction

A
  1. Antibodies are not involved at all, T cells are involved specifically Th1 cells.
  2. Th1 release cytokines recrutiting more macrophages that form Langhans Giant cells
22
Q

Explain the structure of a granuloma

A
  1. Langhaans cells shown in U
  2. The macrophages inside has more cytoplasm so they appear different
  3. Outside are the lymphocytes
  4. The whole thing is encapusilated by a fibrous, sometimes calcified fibrous layer.

This is observed in infections like TB and Herpes

23
Q

Caseouting granuloma

A
24
Q
A

Type IV hypersensitivity in the skin

25
Q
A

Contact Dermatitus which is a type IV reaction. This picture specifically is for Poison Ivy