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3B week 1 - abnormal urine > organ specific autoimmunity > Flashcards

organ specific autoimmunity Flashcards

1
Q

what is a type 1 hypersensitivity reaction

A

immediate reaction and involves immunoglobulin E (IgE) mediated release of antibodies against the soluble antigen -> atopy and allergies

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2
Q

what is a type 2 hypersensitivity reaction

A

antibody-mediated immune reaction in which antibodies (IgG or IgM) are directed against cellular or extracellular matrix antigens

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3
Q

what is a type 3 hypersensitivity reaction

A

immune-complex mediated -> immune response in which antigen-antibody complexes accumulate in the tissues and cause inflammation and tissue damage

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4
Q

what is a type 4 hypersensitivity reaction

A

cell-mediated reaction that can occur in response to contact with certain allergens -> it does not involve the participation of antibodies but is due primarily to the interaction of T cells with antigens.

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5
Q

what are the immune effectors of autoimmune disease

A
  1. T cells -> cytotoxic and T helper
  2. B cells -> make autoreactive self antibodies
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6
Q

what are the 2 parts of the antibody fragement

A
  1. Fab (light chain)
  2. Fc (heavy chain, constant region)
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7
Q

what antibodies are normally involved in autoimmune reactions (2)

A

IgG and IgE

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8
Q

what does the complement cascade ultimately lead to

A

formation of the membrane attack complex

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9
Q

function of membrane attack complex

A

creates pores in the pathogen leading to lysis

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10
Q

how to natural killer cells attack pathogens

A

Fc region of antobodies that have been bound to pathogens can bind to NKCs leading to the release of cytotoxic granules onto the pathogen leading to it lysing

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11
Q

how does type II autoimmunity wrok

A

antibodies (IgG and IgM) bind self antigens on tissue -> complement activation, NKCs, etc. -> tissue damage and inflammation

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12
Q

examples of type II autoimmune diseases (10)

A
  1. haemolytic anaemia
  2. thrombocytopenia
  3. goodpasture’s syndrome
  4. pemphigus vulgaris
  5. acute rheumatic fever
  6. guillian barre
  7. grave’s disease
  8. myesthenia gavis
  9. RA
  10. T2DM
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13
Q

what types of autoimmunity hypersensitivity does RA have

A

type 2, 3 and 4

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14
Q

how does type 3 autoimmunity work

A

antibodies bind soluble self antigens and form immune complexes -> get stuck in small vessels -> immune cells recruited in response to blockage

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15
Q

examples of type III autoimmune diseases (5)

A
  1. SLE
  2. RA
  3. post strep glomerulonephritis
  4. Reactive arthritis
  5. henoch-schonelin purpura
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16
Q

how does type 4 autoimmunity work

A

cell mediated i.e. does not involve antibodies -> self-reactive cytotoxic T-cells released due to evasion of thymus selection -> these will release cytokines and perforin leading to cell tissue death

17
Q

examples of type 4 autoimmune conditions (3)

A
  1. T1DM
  2. RA
  3. multiple sclerosis
18
Q

why is type 4 hypersensitivity sometimes known as “delayed” hypersensisitivity

A

delay in processing -> antigen taken up but APCs but it takes a few days for the antigens to be presented to T helper cells and produce cytokines -> these are required for the self cytotoxic T-cells to bind

19
Q

how does type 1 autoimmunity work

A

allergy (not strictly autoimmunity) -> immediate reaction to allergen presentation in the body, histamine release

20
Q

what cell secretes IgE and where does it bind

A

secreted by B cells and binds to IgE receptors on mast cells and eosinophils -> histamine release

21
Q

what does the release of histamine in T1 reaction lead to

A

local inflammation -> vasodilation and porus epithelial lining to allow other immune cells to reach the pathogen

22
Q

how can T1 hypersensitivity lead to anaphylaxis

A

large scale release of histamine leads to airway narrowing and reduction of blood pressure through vasodilation -> breathing disfficulties, feeling lightheaded, confusion etc.

23
Q

what type of autoimmune reaction is anti-glomerular basement membrane disease

A

type II -> release of cryptic antigens due to damage to the lung from smoking, antibodies released which also bind to the BM in the glomerulus

24
Q

what happens in goodpasture’s syndrome

A

auto antibodies bind in the kidney and lung -> leads to haemorrhage so haematuria/ coughing up blood

25
Q

what does glomerulonephritis often result from

A

immune complex deposition e.g. by Hep B, C, malaria etc. -> type III reaction (also seen w SLE leading to lupus nephritis)

26
Q

what is IgA made in response to

A

infection of mucosal srufaces

27
Q

how does IgA nephropathy occur

A

IgA with unusual sugars made -> these sugars trigger auto-antibody reactions and causes immune-complex formation -> T3 reaction

frequent colds and infections increase IgA produciton

28
Q

what are the antigens presented on to the T helper cells

A

MHC/HLA

29
Q

what is central tolerence

A

the destruction of T cells that recognise self antigens when being educated in the thymus

30
Q

where do immature T cells differentiate

A

in the thymus

31
Q

what is negative selection (central tolerance)

A

when an immature T-cell binds strongly to a self MHC peptide they are negatively selected and destroyed in the thymus

32
Q

is there a genetic link to autoanitbody formation

A

yes e.g. AnkSpn - HLA B27; goodpasture’s - HLA DR2 etc.

33
Q

why might an infection trigger and autoimmune disease

A

normally self reactive T cells dont last long, however, is there is a infection then cytokines are made to combat this but these can also cause the proliferation of the self reactive T cells

34
Q

examples of autoimmune conditions that tend to arise post infection (5)

A
  1. guillian barre
  2. myocarditis
  3. grave’s disease
  4. rheumatic fever
  5. ank spn
35
Q

5 methods of treatment for autoimmune diseases

A
  1. removal of antibodies by plasmapheresis or IgG therapy
  2. anti inflammatory drugs - NSAIDs, steroids, biologics
  3. immunosuppressives
  4. restore/reverse specific damage e.g. insulin for T1DM, carbimazole etc.
  5. DMARD
36
Q
A

3B week 1 - abnormal urine (5 decks)

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