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Principles of disease > Hypersensitivity & Autoimmunity > Flashcards

Hypersensitivity & Autoimmunity Flashcards

1
Q

Define Hypersensitivity

A

immune response acts in exaggerated or innapropriate fashion to environmental antigens and cause tissue damage (bystander damage)

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2
Q

Which types of hypersensitivity are mediated by antibodies?

A

Types I, II & III

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3
Q

What is type 1 hypersensitivity also called?

A

“allergy”

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4
Q

How does Type 1 hypersensitivity arise?

A

enviromental antigens (allergens) are mistaken for pathogens
IgE is innapropriately synthesised

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5
Q

What does the allergen-specific IgE released during type 1 hypersensitivity do?

A

Triggers mast cells to release inflammatory mediators like histamine & prostaglandins

(prostaglandins = lipids made at sites of tissue damage/infection, involved in dealing with injury and illness)

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6
Q

What are the consequences of type 1 hypersensitivity?

A

Mucosal Oedema
Capillarly leakage
vasodilation

(basically inflammation)

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7
Q

What factors influence allergic problems?

(think what factors all immune responses arise from)

A
  • Genetic factors
  • Hormonal & neurological influences
  • Enviromental Influences
  • Immune regulatory factors
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8
Q

Why isn’t the presence of IgE alone enough for an allergic reaction to occur?

A

Clinical allergy arises through many factors not just immune regulatory factors
IgE can or be associated with symptoms or might not

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9
Q

What is it called when IgE is present but no symptoms occur?

A

Atopy
State of sub-clinical immune sensitisation

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10
Q

What antibodies mediate Type 2 hypersensitivity?

A

IgG & IgM antibodies

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11
Q

Why is the line between type 2 hypersensitivity & autoimmune blurred?

A

In type 2, IgG & IgM antibodies can bind to exogenous or self antigens

(exogenous antigens = antigens that have entered body from outside)

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12
Q

How does type 2 hypersensitivity occur?

A
  • IgG & IgM antibodies target antigens on surface of cells or within tissues
  • cause tissue damage
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13
Q

How do antibodies in type 2 hype cause tissue damage?

A
  • complement activation triggers cell lysis
  • Fc receptors on phagocytes bind to immunoglobulin & phagocytic activity is stimulated
  • ADCC (antibody dependant cellular cytotoxicity)
  • inhibit/stimulate cell function
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14
Q

What is immune complex formation?

A

Antigens & antibodies from complexes together

Transported to liver/spleen and destroyed by phagocytes.

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15
Q

How does type 3 hypersensitivity occur?

A

Predisposing factors in Ag or Ab cause immune complex to precipitate into tissues & cause inflammation

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16
Q

What are the 2 types of inflammation in type 3 hypersensitivty?

A

Serum sickness - immune complexes deposited throughout many tissues
Arthus reaction - complexes formed locally in tissues

17
Q

What causes type 4 hypersensitivity?

A

Environmental substance with phagocytic resistance or infectious micro-organism that evades immune system
Th1 cells overreact (having trouble destroying the foreign substances)
Inappropriate action of Th1 cells.

18
Q

Why do non-infectious enviromental agents need to bind to a host protein to triger type 4 hype?

A

Non-infectious EV agents Too low molecular weight to produce substantial antigenic stimulus in order to trigger immune response.

19
Q

What is a Hapten? (think type 4 hype)

A

non-infectious EV agent bound to host protein

20
Q

What is a Carrier? (think type 4 Hype)

A

host protein bound to low mw EV agent

21
Q

Define an autoimmune disease.

A

tissue/organ damage controlled by abnormal cellular or humoral immunological mechanisms against autoantigens

22
Q

Describe autoantigen specificity

A

Systemic - diffuse, spread throughout body, affects multiple organs

Organ specific - directed against 1 organ

23
Q

Define tolerance?

A

Immune system avoids producing damaging reaction against self-antigens

(Unresponsiveness of immune system toward certain substances or tissues that are normally capable of stimulating immune response)

24
Q

Define central tolerance:

A

Deletion of auto-reactive T&B cells during cell maturation

(auto reactive = produced by organism and acting against own cells or tissues)

25
Q

Define peripheral tolerance:

A

Inhibiting activity of autoreactive cells that escape central tolerance.

26
Q

In what cases is immune self-recognition not damaging?

A

T cells can recognise antigens complexed to self molecules
Antibodies can recognise and bind to eachtoher to regulate production and activity

27
Q

What is physiological autoimmunity

A

processes of self-recognition that are normal & beneficial

28
Q

What factors make up the aetiology of autoimmune disorders?

A
  • Genetic factors
  • immune regulatory factors
  • hormonal factors
  • environmental factors
    Age
    Trauma
    Malignant disease
29
Q

what are immune regulatory factors that help cause autoimmune disorders?

A

defective central or peripheral tolerance mechanisms

30
Q

What is an early phase response?

A

Occurs within minutes
Involves preformed mast cell mediators (e.g histamine, heparin & chemotactic factors)

31
Q

Whats a late phase response?

A

Takes hours or days
Newly synthesised mediators like prostaglandins
Th2 cytokines
Eosinophil mediators

32
Q

What immune effector mechanisms can go wrong to cause an autoimmune disease?

A
  • Cellular (T cell) & antibody (B cell) activity
  • autoantibody activation of complement-mediated inflammation
  • immune complex formation (type 3 hype)
  • recruitment of innate immune components (phagocytes/cytokines/Nkc etc)
33
Q

Summary of the steps of an autoimmune disorder:

A
  • initiating EV agent [infection] and genetic susceptibility factors e.g. inheritance of particular HLA (Human leukocyte antigen) alleles.
  • breakdown of self tolerance
  • auto-reactivity (humoral/cellular)
  • Tissue damage
34
Q

Do autoimmune disorders only cause damage?

A

Some cause hyperfunction (hyperthyroidism)

35
Q

How do overlap disorders occur?

A

Autoimmune disorders often occur together
Can/cannot be organ specific

36
Q

What are the pathogenic mechanisms of autoimmune disease?

A
  • Immune complex formation
  • Antibody mediated
  • Cell-mediated
  • Recruitment of innate immune components (neutrophils, macrophages etc)
  • complement system
37
Q

List some oran specific diseases:

A
  • Pernicious anaemia (stomach)
  • Addison’s disease (adrenal insufficiency)
  • Hashimotos thyroiditis (thyroid insufficiency)
  • Primary myxoedema (thyroid shrinking)
  • Thyrotoxicosis (overactive Thyroid)
38
Q

List some non-organ specific diseases:

A

-Muscles = Dermatomyositis (muscle shrinking/skin rash)
- Skin = Scleroderma
- Kidneys = SLE (lupus)
- Joints = Rheumatoid arthritis

Principles of disease (47 decks)

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