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Principles of Disease > Autoimmunity and Hypersensitivity > Flashcards

Autoimmunity and Hypersensitivity Flashcards

1
Q

Define hypersensitivity

A

Components of immune system act in an exaggerated fashion to harmless environmental antigens

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2
Q

What is responsible for tissue damage in hypersensitivity?

A

The exaggerated immune response as opposed to the antigen itself

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3
Q

Which hypersensitivity mechanisms are mediated by antibodies?

A

1,2,3

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4
Q

What is the 4th type of of hypersensitivity caused by?

A

Th1 Cells

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5
Q

What is type 1 sensitivity also known as?

A

Allergy

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6
Q

How does allergy arise?

A

Inappropriate synthesis of IgE by the immune system

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7
Q

What are the different sources of environmental antigens that IgE is directed against?

A

Airborne, Ingested, Injected or encountered through skin contact

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8
Q

Is synthesis of IgE on its own enough to cause the clinical allergy?

A

No there are other factors involved such as Environmental influences, hormonal and neurological factors and immune regulatory factors

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9
Q

What is the word given for the production of excessively high levels of IgE to a harmless stimuli, but no related symptoms?

A

Atop, no allergy (which is the presence of associated symptoms)

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10
Q

What is the pathogenesis of type 1 hypersensitivity?

A

Allergen exposure,
Mast cell +allergen specific IgE
Release of inflammatory mediators (histamine - preformed and prostaglandins - newly formed)

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11
Q

What is type 2 hypersensitivity mediated by?

A

IgG or IgM antibodies - directed against antigens found on the surface of cells or fixed within certain tissues

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12
Q

In type two disorders, why is the distinction between hypersensitivity and autoimmunity slightly blurred?

A

Antigens can be exogenous or derived from self

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13
Q

How does damage to tissue arise after the antibody has bound to the relevant antigen?

A

Complement activation
Fc Binding of immunoglobulin and stimulation of phagocytes
Antibody dependant cellular cytoxicity
Effects on target cell function - inhibition of function, stimulation

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14
Q

How do clinical conditions arise with type 3 hypersensitivity?

A

Mediated by the actions of antibody - abnormal deposition of immune complexes in tissues

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15
Q

What is the source of antigen in type 3 hypersensitivity?

A

Exogenous or Self

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16
Q

Describe the movement of immune complexes

A

Access bloodstream on formation, transported whilst being attached to red blood cells to the liver and spleen where fixed phagocytes take up and destroy the complexes

17
Q

Immune complex formation can be described as pathological or physiological, describe the means by which they can be described as pathological

A

Complexes precipitate out into tissues and cause inflammation

  1. Systemic illness - immune complexes deposited in many tissues - SERUM SICKNESS
  2. Localised disorder, complexes form locally in tissues - ARTHUS REACTION
18
Q

What are the cytokine products of Th1 cells?

A

Interleukin- 2 and interferon of these cells

19
Q

How is type 4 sensitivity triggered?

A

Contact with inert environmental substances

OR

As a reaction to certain microorganisms

20
Q

Why do the inert environmental substances or microorganisms cause this type 4 hypersensitivity response?

A

Immune system finds it hard to destroy the environmental agents or the infectious agents such as mycobacteria

The environmental agent itself will produce no great adverse effect on its own, immune response causes tissue damage.

21
Q

How do non-infectious environmental agents cause a a stimulus sufficient in size to incite an immune response?

A

They bind to host proteins to create an antigenic stimulus sufficient in size to incite the stimulus sufficient in size.

22
Q

What is the low molecular weight agent called?

A

A HAPTEN

23
Q

What is the host protein called?

A

A CARRIER

24
Q

What is the carrier needed for?

A

A sufficient antigenic bulk

25
Q

Why is type 4 hypersensitivity called the delayed type hypersensitivity?

A

48-72 hour delay between antigen exposure and clinical effect

26
Q

What is the pathogenesis for type 4 hypersensitivity?

A

Hapten + carrier / Microorganism

Antigen uptake and presentation

Th1 antigen recognition / cytokine production (overactivity and dysregulation)

Inflammation

27
Q

How is tolerance achieved?

A

Deletion of autoreactive T and B cells during maturation (central tolerance)

Deletion of autoreactive T and B cells which escape the central tolerance process (peripheral tolerance)

28
Q

What is a requirement for the development of autoimmune disease?

A

Breakdown in one or more of the processes of tolerance

29
Q

What are examples of physiological autoimmunity?

A

T cells recognise antigen which is complexed with self molecules

Antibodies can recognise and bind other portions of other antibodies - regulating their production and activity.

Other - age, trauma, malignant disease

30
Q

How does clinical autoimmune disease arise?

A

Aetiological factor in association with disordered and dysregulated immune effector mechanisms

31
Q

What are the effector mechanisms involved in autoimmunity?

A

They are identical to those which operate in normal immune responses and therefore comprise

T cell activity
B cell activity (antibodies)
Autoantibody activation of complement - mediated inflammation
Immune complex formation
Recruitment of innate immune components (phagocytes/ cytokines/ NK cells)

32
Q

What are the autoimmunity aetiologies?

A

Genetic factors - (inheritance of particular HLA types, familial predisposition)

Immune regulatory factors - (defective tolerance induction, defective peripheral tolerance mechanisms)

Hormonal factors (particularly female hormones)

Environmental factors (infectious agents, sunlight, drugs, chemicals, nutritional factors)

‘Other’ factors (age, trauma, malignant disease)

33
Q

What is the pathogenesis of a autoimmunity?

A

Initiating event (environmental) i.e infection

Genetic susceptibility / predisposition (inheritance of particular HLA alleles)

Breakdown of self tolerance

Autoreactivity involving humoural and cellular mechanisms

TISSUE DAMAGE

34
Q

Are autoimmune endocrine disorders organ specific on non - organ specific?

A

Organ specific

35
Q

Are connective tissue disorders organ specific on non - organ specific?

A

Non-organ specific

36
Q

Can autoimmune disorders lead to hyper function as opposed to hypo function?

A

Yes for example the thyroid

Principles of Disease (48 decks)

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