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Pathology > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

what is hypersensitivity

A

immune mediated disease caused by inflammation & not by infection

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2
Q

what type of environment is the immune system essential

A

where many harmful microorganisms/pathogens are present

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3
Q

what has the immune system evolved to protect the body against

A

pathogens:

  • viruses
  • bacteria
  • fungi
  • parasites
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4
Q

what are immune responses mediated by

A
  • a variety of cells

- soluble mediators that these cells produce

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5
Q

when can the immune system cause harm

A
  • when it is absent of suppressed, so the body is open to opportunistic infections which lead to immunodeficiency i.e. an immune deficient disease such as AIDS
    or
  • when the immune system responds in a very aggressive way in trying to alleviate the damage that he pathogen or other antigen causes, so the immune system does harm to our bodies
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6
Q

what are the components of the immune system as mixture of

A

chemicals and cells

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7
Q

name the two types of leukocytes which act as components of the immune system

A

lymphocytes & phagocytes

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8
Q

what are the lymphocyte components of the immune system

A

B cell
T cell
large granular lymphocyte LGL

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9
Q

what soluble mediator do B cells produce

A

antibodies

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10
Q

what soluble mediator do T cells produce

A

cytokines

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11
Q

what soluble mediator do large granular lymphocytes produce

A

cytokines

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12
Q

what are large granular lymphocytes also known as, and what are they involved in

A

natural killer cells

involved in defence against viruses

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13
Q

what are the phagocyte components of the immune system

A

mononuclear phagocyte
neutrophil
eosinophil

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14
Q

what soluble mediators do mononuclear phagocytes produce

A
  • cytokines

- complement

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15
Q

how do mononuclear phagocytes work

A

engulf antigens & sometimes destroy them
or
sometimes act as antigen presenting cells

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16
Q

how many % of leukocytes do neutrophils account for

A

70%

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17
Q

what property do neutrophils have

A

they are principle white cells of the blood, and also have a phagocytic property

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18
Q

where can neutrophils exist

A

they can exists within the blood, but can also leave blood & enter the tissues & phagocytose within the tissues

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19
Q

what are all the possible soluble mediators

A
  • antibodies
  • cytokines
  • inflammatory mediators
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20
Q

what are the two granulocytes

A

eosinophils

basophils

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21
Q

what are the auxiliary cells - components of the immune system

A

basophils
mast cells
platelets

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22
Q

what do the auxiliary cells - basophils, mast cells and platelets form

A

inflammatory mediators

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23
Q

what are T cells responsible for

A

cell mediator immunity

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24
Q

what type of mechanism are phagocytes a part of

A

innate defence mechanism

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25
Q

how do phagocytes destroy antigens and pathogens

A

by internalising them, and in order to destroy the engulfed particles, phagocytes have strong enzymes which if released to tissue can damage

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26
Q

give examples of phagocytes which internalise the antigens and pathogens and destroy them

A

monocytes (and macrophages) and polymorphonuclear neutrophils

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27
Q

what are the body’s first line of defence

A

barriers of our immune system within the body e.g. mucosal or skin barrier

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28
Q

what is the first defence of our body once a pathogen or antigen has passed the barriers of our immune system

A

phagocytes

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29
Q

what are B cells and T cells responsible for

A

recognition/detection of antigen

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30
Q

what are B cells/lymphocytes responsible for

A

antibody production

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31
Q

what do T helper cells produce

A

cytokines

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32
Q

what are cytokines

A

chemicals which regulate the immune system

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33
Q

what do type 1 T-helper cells (TH-1) cells do

A

activate/control macrophages

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34
Q

hat do TH-2 cells do

A

help B cells to divide and differentiate and make antibodies as well as produce cytokines

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35
Q

what do cytotoxic T cells (CTL or Tc) do

A

destroy virally infected cells and tumour cells

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36
Q

how do cytotoxic T cells (CTL or Tc) destroy virally infected cells and tumour cells

A

by recognising them via a mechanism and triggers a process of apoptosis and the cell dies

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37
Q

what do large granular lymphocytes (NK cells) have similar properties to and what are those properties

A

cytotoxic T cells

destroy virally infected cells and tumour cells

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38
Q

what do auxillary cells control

A

inflammation

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39
Q

what is the main purpose of inflammation

A

to attract leukocytes towards the site of infection

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40
Q

what is inflammation mediated by

A

a variety of other cells including mast cells and basophils

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41
Q

what do mast cells and basophils contain

A

granules

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42
Q

what do granules contain

A

soluble mediators of immunity

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43
Q

what are mast cells and basophils also capable of synthesising and secreting apart from soluble mediators of immunity

A

other mediators that control immune reactions

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44
Q

what do mast cells contain

A

histamine

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45
Q

what happens to blood vessels when histamine is released

A

dilate and become leaky

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46
Q

what is histamine

A

an inflammatory mediator which acts upon blood vessels

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47
Q

what are the variety of chemical mediators which are involved in the development of immune responses

A
  • antibodies and cytokines - produced by lymphocytes

- other serum proteins e.g. complement

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48
Q

what is opsonisation

A

process which acts in conjunction with antibodies which facilitates phagocytosis

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49
Q

how do some complement destroy bacteria

A

through process of lysis

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50
Q

what is the complement system a group of

A

about 20 serum proteins that interact with each other and other elements of the immune system

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51
Q

list the functions of the complement system

A
  • opsonisation of microorganisms e.g. bacteria
  • attraction of phagocytes
  • increased blood flow and increased vascular permeability
  • damage to cell membranes
  • release of mediators from mast cells
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52
Q

what does immune homeostasis require

A

a balance between:
- immunodeficiency (hypo-reactivity)
&
- immunopathology (hyperactivity)

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53
Q

what is immunodeficiency (hypo-reactivity) of the immune system, and give examples

A

suppressing of immune system which dampens down i.e. it is a poorly acting immune system e.g.

  • neutrophil disorders
  • antibody deficiency
  • complement deficiency
  • T-cell dysfunction
54
Q

what is immunopathology (hyperactivity) of the immune system, and give examples

A

immune system responds in too much of an aggressive manner e.g.

  • autoimmunity organ specific
  • allergies and asthma
  • pathogen induced pathology
55
Q

what types of immunodeficiency can there be

A
  • congenital - born with immunodeficient immune system
  • mostly acquired, mainly through organ transplants where strong drugs suppress the immune system or by diseases such as AIDS caused by a virus
56
Q

what are hypersensitivity reactions

A

exaggerated or inappropriate immune responses that lead to tissue damage, can be mild or life threatening

57
Q

what are the four types of hypersensitivity reaction recognised by Coombs and Gel 1963

A

type 1
type 2
type 3
type 4

58
Q

what type of hypersensitivity are the most common

A

type 1 mediated reactions

59
Q

briefly list the type of reaction associated with each type of hypersensitivity

A

type 1 - immediate hypersensitivity reaction
type 2 - antibody mediated reactions
type 3 - immune complex mediated reactions
type 4 - cell mediated reactions

60
Q

how long does it take for a type 1 hypersensitivity to occur

A

within minutes of exposure

61
Q

what is another word for type 1 hypersensitivity

A

atopy

62
Q

what causes type 1 hypersensitivity

A 
exposure to a variety of environmental antigens e.g. 
- pollen
- house dust mite 
- animal dander 
all termed allergens 
- mild hay fever (strong genetic link)
- severe anaphylaxis 
- allergens also contribute to asthma
63
Q

what is the meaning of an allergen

A

something that causes an allergy

64
Q

what is another word for hay fever

A

seasonal allergic rhinitis

65
Q

what are hay fever sufferers allergic to

A

airborne pollens ans spores

66
Q

what are the symptoms of hay fever

A
  • sneezing
  • rhinorrhoea (runny nose), nasal congestion
  • itching of the nose and eyes
  • watering of the eyes
  • wheezing and shortness of breathing
67
Q

when do symptoms of hay fever usually occur

A

between march and September

68
Q

when is tree pollen released and how many % does it affect

A

from march to may - spring affects 25% of sufferers

69
Q

when is grass pollen released and how many % does if affect

A

from may to late July - affects 90% of sufferers

70
Q

when is fungal spores released

A

until September

71
Q

what is the most important allergen in ‘house dust’

A

dust mite

72
Q

what causes the allergy from the dust mite

A

mite faecal pellets is what causes the allergy as they are similar size to pollen grains so give rise to similar symptoms to hay fever

73
Q

which period do dust mites cause allergy symptoms

A

all year round

74
Q

how severe is an anaphylaxis allergic reaction and what can it be caused by

A

very dangerous - life threatening

caused by particular foods especially nuts, insect bites or medicines

75
Q

how many of the population does anaphylaxis affect

A

1-3 per 10,0000 per year (rare)

76
Q

what are the early signs of an anaphylaxis allergic reaction

A

swelling and itching, the face may be flushed and wheals or hives (urticaria) bumps may erupt on the skin

77
Q

what are the later signs of an anaphylaxis allergic reaction

A
  • swelling of the face
  • difficulty breathing and wheezing due to laryngeal oedema (mucous membrane swell & airways gets blocked) or asthma
  • loss of colour, cold and clammy as blood pressure falls
  • collapse/loss of consciousness
78
Q

what is the emergency treatment for anaphylaxis

A

intramuscular pre loaded injection of adrenaline (epinephrine) followed by iv drip when they reach hospital of anti-histamine and corticosteroids

79
Q

what happens when someone encounters the allergen for the first time

A

they have no signs and symptoms at all

80
Q

what is type 1 hypersensitivity mediated by

A

mast cells

81
Q

what do mast cells display a high affinity receptor for

A

IgE

82
Q

what is IgE synthesised in response to

A

certain antigens (allergens)

83
Q

when allergens are deposited on the mucous membranes, what are they taken up by

A

taken up and processed by antigen presenting cells (e.g. dendritic cells or B cells)

84
Q

once the allergen is taken up by antigen presenting cells, what are they presented to

A

presented through an MHC receptor to TH2 cells which provide cytokine signals to (activate) B cells to produce IgE which binds to mast cells

85
Q

what is IgE

A

an antibody which is unusual, so if your allergic to something, you produce IgE

86
Q

what does cross linking of IgE by subsequent exposure to allergen (after the 2nd time) cause

A

calcium influx or cells and starts a mast cell degranulation

87
Q

what receptors do mast cells have

A

Fc receptors

88
Q

what is mast cell degranulation the major initiation of

A

the acute allergic reaction

89
Q

name some mast cell mediators

A
  • histamine
  • heparin
    and other factors
90
Q

what do the mast cell mediators, histamine and heparin cause

A
  • mucus secretion
  • vasodilation
  • oedema
91
Q

describe the whole type 1 mechanism

A
  • mast cells display a high affinity receptor for IgE
  • IgE is synthesised in response to certain antigens (allergens)
  • allergens are deposited on mucous membranes and taken up and processed by antigen presenting cells (e.g. dendritic cells or B cells)
  • allergen presenting to TH2 cells which provide cytosine signals to B cells to produce IgE Ig E binds to mast cells
  • cross linking of IgE by subsequent exposure to allergen causes mast cell degranulation
  • mast cell degranulation is the major initiation of the acute allergic reaction
  • mast cell mediators include, histamine, heparin and other factors
  • these causes, mucus secretion, vasodilation and oedema
92
Q

what two types of mediators do mast cells include

A

pre formed & newly formed mediators

93
Q

name some pre formed mast cell mediators

A
  • histamine
  • heparin
  • neutral protease
94
Q

name some newly formed mediators

A
  • leukotrienes
  • prostaglandin D2
  • platelet activating factor
95
Q

what does the degranulation of the mast cell cause

A

the allergy

96
Q

what is hay fever and anaphylaxis due to

A

the mast cell mediators

97
Q

what is type 2 hypersensitivity mediated by

A

antibody mediated response/hypersensitivity

98
Q

in type 2 hypersensitivity, what is the antibody directed against

A

membrane and cell surface antigens (autoantibodies) which recognise our cells as foreign

99
Q

in type 2 hypersensitivity, what do antigen-antibody reactions activate

A

complement, producing membrane damage

100
Q

in type 2 hypersensitivity mechanism, what do the antibodies bind to

A

the cell surface

101
Q

in type 2 hypersensitivity mechanism, what do phagocytes bind to the antibody via and what does it cause

A

their Fc receptor and causes phagocytosis of target cell

102
Q

in type 2 hypersensitivity mechanism, what does antibody binding also activate and what does this set up

A

complement, which sets up the inflammatory process within the tissue & automatically leads to organ destruction/cell lysis

103
Q

explain type 2 hypersensitivity antibody mediated mechanism on a blood vessel wall

A
  • the antibodies are recognising the epithelium that are making up the wall of the blood vessel as foreign
  • so they are binding onto those endothelial cells as they think it is foreign & initiate this inflammatory reaction
  • the phagocytes then come along to try to destroy this antigen
  • in doing so they release the toxic enzymes and chemicals into the vicinity of the blood vessel wall
  • and that produces lots of localised cell damage
104
Q

how do anti histamines work

A

antihistamines bind to the histamine receptor so that the histamine has got nothing to bind onto, so it works well by blocking histamine receptors

105
Q

describe the whole of type 2 hypersensitivity mechanism

A
  • antibodies bind to cell surface
  • phagocytes bind to the antibody via their Fc receptor
  • phagocytosis of target cell
  • antibody binding also activates complement which sets up the inflammatory process within the tissue
  • complement mediated cell lysis/destruction
106
Q

what occurs during haemolytic disease of the newborn

A
  • erythrocytes from a RhD+ foetus (first child) leak into the maternal circulation (who is RhD-), usually during birth which stimulates the production of anti-Rh antibody
  • during subsequent pregnancies, IgG antibodies are transferred across the placenta into the foetal (2nd child) circulation
  • if the foetus is again incompatible, the antibodies cause erythrocyte (red blood cell) destruction
107
Q

at which pregnancy does a haemolytic disease of a newborn occur

A

2nd or after

108
Q

instead of carrying out a blood transfusion on a baby who has haemolytic disease, what do hospitals do in order to avoid it from happening

A

after the first pregnancy, they treat the mother with a drug which takes out all the anti RhD+ antibodies, so when theres a 2nd baby, the antibodies are not able to cause haemolytic disease

109
Q

what is type 3 hypersensitivity mediated by

A

immune complex response mediated

110
Q

what does type 3 hypersensitivity cause excessive formation of

A

immune complexes eg persistent low grade infection, repeated inhalation of antigens

111
Q

give some examples of type 3 hypersensitivity

A
  • farmers lung

- immune complex glomerulonephritis

112
Q

what is farmers lung

A

when farmers are exposed to hay spores & hay spores form immune complexes & often happens in the lung so they end up with breathing difficulties

113
Q

what do immune complexes activate in type 3 hypersensitivity mechanism

A

complement

114
Q

what do immune complexes deposit within in type 3 hypersensitivity mechanism

A

tissues

115
Q

what and where a immune complexes degraded by in type 3 hypersensitivity mechanism

A

phagocytes, particularly in the liver and spleen

116
Q

what does excessive immune complex formation result in, in type 3 hypersensitivity mechanism

A

deposition in the tissues, particularly arterioles, kidneys and joints

117
Q

what do immune complexes induce in type 3 hypersensitivity mechanism

A

platelet aggregation and complement activation

118
Q

what does attempted phagocytosis cause in type 3 hypersensitivity mechanism

A

enzyme release and results in tissue damage

119
Q

in type 3 hypersensitivity mechanism, when theres an excess of immune complexes, what occurs

A

the immune system overloads and the phagocytes can’t cope with all those immune complexes & the immune complexes start to deposit in tissues such as lungs & kidneys which initiates this inflammatory reaction

120
Q

what type of hypersensitivity is type 4 hypersensitivity

A

delayed type

121
Q

how long does type 4 hypersensitivity take to develop after antigenic change

A

more than 12 hours (typically 12-48 hours)

122
Q

give examples of type 4 hypersensitivity

A
  • contact dermatitis = excema (coating of base metal)

- tuberculin reaction (mantoux test)

123
Q

what type of molecules do antigens in type 4 hypersensitivity include

A

large or small (haptens) linked to carrier molecules

124
Q

what other type of drug can cause a type 4 hypersensitivity

A

eye drops which treat an initial infection

125
Q

in type 4 hypersensitivity mechanism, what do antigen presenting cells (APC) resident in the skin process and migrate

A

process antigen & migrate to regional lymph nodes

126
Q

what do the antigen which has migrated to regional lymph nodes during type 4 hypersensitivity mechanism activate

A

T cells (CD4+ve)

127
Q

during type 4 hypersensitivity mechanism, where do sensitised T cells migrate back to

A

the skin, where they produce cytokines

128
Q

in type 4 hypersensitivity mechanism, what do cytokines attract

A

macrophages which cause tissue damage

129
Q

describe the whole of type 4 hypersensitivity mechanism

A
  • APC resident in the skin process antigen and migrate to regional lymph nodes where they activate T cells (CD4+ve)
  • sensitised T cells migrate back to the skin where they produce cytokines which attract macrophages which cause tissue damage e.g. contact dermatitis mediated by mast cells
130
Q

explain how type 4 hypersensitivity mechanism is used to test for TB immunity

A
  • injection of TB antigens (not the bacteria)
  • perform a skin test, to check if there was a reaction to the TB antigen, if there is, they do not need the vaccination as they have natural immunity and can react to the TB antigen
  • if there was no skin reaction, they need the TB vaccination
131
Q

what is hypersensitivity

A

exaggeration/inappropriate immune response mediated by 4 types

Pathology (20 decks)

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