Hyper sensitivity and autoimmunity Flashcards

1
Q

What cells are involved in innate immunity?

A

Phagocytes, easoinophils, basophils, mast cells etc.

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2
Q

What receptors are involved in innate immunity?

A

Complement, Cytokines

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3
Q

What cells are involved in adaptive immunity?

A

B cells

T cells

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4
Q

What receptors are involved in adaptive immunity?

A

Ig, Cytokine, Complement

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5
Q

What is complement?

A

Group of proteins present in blood plasma and tissue fluid that combine with antigen - antibody complexes to bring about the lysis of cells.

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6
Q

What is hypersensitivity?

A

Normal, beneficial components of immune system respond in an exaggerated / inappropriate manner to (usually ) environmental organisms that shouldn’t do any harm usuallly .

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7
Q

In hypersensitivity, the tissue damage is not caused by the environmental organism, but by the response itself. What is this called?

A

Bystander response.

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8
Q

Which types of hypersensitivity and antibody mediated?

A

I , II, III

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9
Q

Which type of hypersensitivity is due to the inappropriate action of Th1 cells?

A

IV

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10
Q

What is type 1 hypersensitivity ?

A

Allergy

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11
Q

In type 1 hypersensitivity, how can the allergen be exposed?

A

Airborne, Ingested, Injected, Skin Contact

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12
Q

What does IGE do in type 1 inflammatory?

A

IGE -> binds to mast cells -> releases inflammatory mediators.

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13
Q

The inflammatory mediators in type 1 inflammation create an early phase response and a late phase response. What preformed mediators are involved in the early phase response?

A

Histamine, heparin, easoniphil and neutrophil chemotactic factors.

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14
Q

The inflammatory mediators in type 1 inflammation create an early phase response and a late phase response. What newly synthesised meditators are involved?

A

Prostaglandins.

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15
Q

Allergy isn’t just IGE. Its also due to lots of factors, genetic environmental etc. All of this plus symptoms makes an allergy. What is it called when theres IGE but no symptoms (commoner than allergy)

A

Atopy

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16
Q

When may type 2 hypersensitivity occur?

A

When wrong blood is infused.

17
Q

In type two hypersensitivity, IgG and IgM antibodies are directed on antigens of the surface of the cells / fixed within tissues. Where do these antigens come from?

A

External (exogenous ) or derived from self

18
Q

The antibody + antigen creates tissue damage. Name 3 ways this could happen. (Type two hypersensitivity)

A

Complement activation
Antibody dependant cellular cytotoxicity
Effects target cell function ( Inhibition or stimulation)

19
Q

Why do conditions arise in type 3 hypersensitivity?

A

Abnormal deposition of immune complexes.

20
Q

What are immune complexes? (type 3)

A

Antigen + Antibody (Ag or Ab)

21
Q

In type three hypersensitivity, where are the antigens from?

A

Exogenous or self antigen

22
Q

Describe the physiology of immune complexes destruction ( type 3).

A

Immune complex -> blood stream -> Liver/ spleen -> Destroyed by fixed phagocytes

23
Q

Why may the journey of immune complexes get pathological problems in type three hypersensitivity?

A

Predisposing factors in antigen / immune response to antigen.

24
Q

What is the pathology of type 3 hypersensitivity?

A

Abnormal immune complex formation -> Precipitates in tissues -> inflammation.

25
Q

Type three hypersensity - explain serum sickness.

A

Systemic - deposits of immune complexes in many tissues.

26
Q

Type three hypersensitivity - explain ARTHUS reaction.

A

Local - deposits form in local tissue.

27
Q

In type 4 hypersensitivity - what does the body struggle to respond too?

A

Microorganism - may have evolved to evade immune response.

Hapten + Carrier

28
Q

Explain happen + carrier in type 4 hypersensitivity.

A

Hapten is exogenous low molecular antigen that is too small to produce an immune response, so it binds to an endogenous host protein (which provides bulk)

29
Q

During type four hypersensitivity, what does the body do?

A

1) produces Th1.
2) this produces cytokines ( interleukin - 2 & beta - inferon)
3) these activate macrophages and are responsible for cell mediated immunity.
4) inflammation

30
Q

What is cell mediated immunity?

A

Immunity that does not involved antibodies, but involved phagocytes and cytokines etc.

31
Q

What are autoimmune diseases?

A

group of clinical disordered characterised by tissue/ organ damage, mediated by incorrect immune mechanisms targeted at self antigens.

32
Q

What is broken down for autoimmune disorder to arise?

A

Tolerance

33
Q

What are the two types of tolerance

A

central tolerance - auto reactive t and b cells deleted during cell maturation
peripheral tolerance - inhibition of auto reactive cells that escape the central tolerance process

34
Q

what is physiological autoimmunity?

A

beneficial self recognition - like antibodies recognising other antibodies are regulating their production and activity.

35
Q

WHAT 5 factors are involved in aetiology of autoimmune disease?

A
1 - genetic
2 - immune regalarotry factors 
3 - hormonal factors
4- environmental factors 
5 - others - eg. age, disease, trauma
36
Q

Name four pathogenic mechanisms in autoimmunity.

A

1 - T cells or B cells activated
2 - (auto) antibody activation of complement mediated inflammation
3 - immune - complex formation
4 - recruitment of innate immune components

37
Q

what leads to broken tolerance

A

1 or more environmental factor (e.g. infection) + 1 or more genetic factor (specific HLA allele)

38
Q

what organs may be affected by autoimmune disorders”

A

thyroid
stomach
adrenal

39
Q

what non - organ specifics may be affected by autoimmune disorders?

A

muscles
skin
joints