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Resp - mine > Immunology > Flashcards

Immunology Flashcards

1
Q

what is vaccination

A

the DELIBERATE exposure to an antigen to induce immunologically-mediated resistance to the disease through the induction memory

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2
Q

what is immunisation

A

the process through which an individual develops immunity/memory to a disease

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3
Q

what types of immunity are there

A

passive and active

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4
Q

what is active immunity

A

protection against a disease produced by the body’s OWN immune system

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5
Q

how long does active immunity last

A

usually permanent

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6
Q

give examples of methods of gaining active immunity

A

vaccination, via infection

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7
Q

what is passive immunity

A

protection against a disease TRANSFERRED from another person or animal

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8
Q

give examples of methods of gaining passive immunity

A 
breast milk (IgA)
placental transfer (IgG)
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9
Q

what cells are involved in production of memory

A

memory B and T cells
memory CTLs
long-lived plasma cells

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10
Q

what type of T cell is involved in producing memory

A

CD4+

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11
Q

what is needed for memory to be produced (______ & _____ of the immune system)

A

stimulation & maturation of the immune system AFTER exposure to antigen

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12
Q

what cells are involved in the PRIMARY adaptive immune response

A

T and B cells

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13
Q

in what state do T and B memory cells survive in the body and for how long

A

dormant for years

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14
Q

how do T and B cells reactivate

A

rapidly

clonal proliferation + expansion then the differentiate into effector cells or memory cells

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15
Q

what have B memory cells already undergone

A

Ig class switching and hypermutation

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16
Q

what properties of T and B memory cells have been enhanced

A

cell adhesion and chemotaxis

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17
Q

compare active vaccination to memory generated by natural infection

A

immune response is stimulated in the SAME way

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18
Q

what types of active vaccination are there

A

live attenuated

inactive

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19
Q

describe the features of inactive vaccines

A

can’t replicate inside the host

requires multiple doses

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20
Q

what is the response to inactive vaccines

A

ANTIBODY bases (not T cells)

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21
Q

describe the features of live attenuated vaccines

A

very effective
single dose
may cause infection immunocompromised host

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22
Q

what infections can vaccine NOT be developed for

A

chronic/latent infections (e.g HIV, Herpes, Hep C)

rapidly evolving infections (e.g. HIV, flu)

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23
Q

what are adjuvants

A

mixtures of inflammatory substances required to stimulate immune responses to co-administered vaccine

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24
Q

what are the hallmarks of immune deficiency

A

(SPUR)

Serious infections
Persistent infections
Unusual infections
Recurrent infections

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25
Q

what counts as a serious infection

A

unresponsive to ORAL antibiotics

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26
Q

what counts as an unusual infections

A

unusual organism and/or site

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27
Q

what counts as a recurrent infection

A

2 major infection OR 1 major and 1 minor infections in one year

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28
Q

how are immunodeficiencies

A

secondary and primary

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29
Q

compare primary and secondary immunodeficiencies

A

secondary is common, subtle and often involves more than 1 component of the immune system

primary is rare with a strong family history

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30
Q

give examples of causes of secondary immunodeficiencies

A 
extremes of life
infection (HIV, measles)
treatment (steroids, chemo, immunosuppressants) 
 cancer
malnutrition 
renal insufficiency/dialysis
diabetes (type 1 + 2)
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31
Q

innate immune system immunodeficiencies involve what cells

A

phagocytes (neutrophils + macrophages)

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32
Q

what are the 5 steps in a phagocyte life cycle

A
  1. Mobilisation from bone marrow or within tissues
  2. adhesion and migration into tissues
  3. Recognition of the organism
  4. Phagocytosis and killing of organism
  5. Activation of other components of immune system
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33
Q

what NORMALLY happens during the 1st step of phagocyte life cycle

A

stem cells differentiate then mature before leaving the bone marrow

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34
Q

what NORMALLY happens during the 2nd step of phagocyte life cycle

A

up regulation of endothelial adhesion markers (selections & intergrins) allow transendothelial migration

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35
Q

what NORMALLY happens during the 3rd step of phagocyte life cycle

A

recognition of organism via PRR:PAMP (direct) OR opsonins (indirect)

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36
Q

what NORMALLY happens during the 4th step of phagocyte life cycle

A

killing happens after engulfment when free radicals are released via an oxidative burst

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37
Q

what NORMALLY happens during the 5th step of phagocyte life cycle

A

macrophages secrete IL-12 which induces TH1 to secrete INF-gama which feedbacks to the phagocyte stimulating the oxidative pathway (free radicals)

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38
Q

what can go wrong during the 1st step of the phagocyte life cycle (2 ways)

A
  1. failure to DIFFERENTIATE = reticular dysgenesis which results in infant death
  2. failure to MATURE = kostmann syndrome (NO neutrophils)
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39
Q

what can go wrong during the 2nd step of the phagocyte life cycle

A

failure to recognise activation markers on endothelial cells = leukocyte adhesion deficiency

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40
Q

what does leukocyte adhesion deficiency result in

A

neutrophils CANNOT EXIT the bloodstream leading to high levels within the blood but NONE in the tissues

41
Q

what can go wrong during the 3rd step of the phagocyte life cycle

A

defect in RECOGNITION or OPSONIN = less affective phagocytosis

42
Q

what does issues in the 3rd step of the phagocyte life cycle result in

A

no significant disease

43
Q

what can go wrong during the 4th step of the phagocyte life cycle

A

failure of the oxidative killing mechanism resulting in chronic granulomatous disease

44
Q

what is chronic granulomatous disease

A

inability to generate O2 free radicals (ROS/RNS)

45
Q

How is hronic granulomatous disease diagnosed

A

via NBT test

46
Q

what can go wrong during the 5th step of the phagocyte life cycle (3)

A
  1. INF-gamma receptor deficiency
  2. IL-12 deficiency
  3. IL-12 receptor deficiency
47
Q

what is autoimmunity

A

presence of immune responses to self-tissues/cells

48
Q

what are the 3 main causes of autoimmune disease

A

immune regulation
environment
gene

49
Q

how does immune regulation result in autoimmune disease

A

it is responsible for maintaining self tolerance

50
Q

how does environment result in autoimmune disease

A

molecular mimicry

51
Q

what is molecular mimicry

A

cross-reactivity between antigens expressed by pathogens and self, usually caused by infection

52
Q

how do genes result in autoimmune disease (2 types)

A

monogenic disorders

complex genetic interplay

53
Q

give an example of a monogenic autoimmune disorder

A

IPEX Syndrome

54
Q

what is IPEX Syndrome

A

failure of peripheral tolerance due to defective regulatory T cells

55
Q

give an example of complex genetic interplay autoimmune disorder

A

HLA genes

56
Q

what are HLA genes

A

associated with but not a prerequisite for autoimmune disease

57
Q

describe what tolerance is and why it is required

A

some T cells mutate to recognise self and foreign, tolerance mechanisms ensure these cells are eliminated before they are able to mature and harm self

58
Q

give examples of type 1 autoimmune conditions (Gel Coombs classification)

A

none

59
Q

give examples of type 2 autoimmune conditions (Gel Coombs classification)

A

Grave’s disease

Goodpasture’s syndrome

60
Q

give examples of type 3 autoimmune conditions (Gel Coombs classification)

A

SLE (lupus)

61
Q

give examples of type 4 autoimmune conditions (Gel Coombs classification)

A

type 1 diabetes
coeliac disease
Rh arthritis

62
Q

what is a hypersensitivity reaction

A

immune response that results in bystander damage to self

63
Q

what is a hypersensitivity reaction an exaggeration of

A

normal immune mechanisms

64
Q

what is type 1 hypersensitivity reaction

A

immediate hypersensitivity (allergy)

65
Q

what is type 1 hypersensitivity reaction characterised by

A

enhanced sensitivity to normally innocuous substances leading to physiological damage

66
Q

what Ig_ is involved in type 1 hypersensitivity reaction

A

IgE

67
Q

what is an allergy

A

IgE-mediated response to an external antigen (allergen)

68
Q

what are the clinical features of a type 1 hypersensitivity reactions

A

occurs quickly (mins- 1 or 2 hrs)
presentation depends on site of contact
rash, angiodema,anaphylaxis

69
Q

what immune cells are involved in type 1 hypersensitivity reactions (3)

A

B cells
T cells
Mast cells

70
Q

what is the role of B cells in type 1 hypersensitivity reactions

A

recognises antigen and produces SPECIFIC IgE antibodies

71
Q

what is the role of T cells in type 1 hypersensitivity reactions

A

helps B cells to produce antibodies

72
Q

what T cells are involved type 1 hypersensitivity reactions

A

Th2

73
Q

what is the role of mast cells in type 1 hypersensitivity reactions

A

express receptors for the Fc region of the IgE antibody, residual antibodies will remain even after the antigen is cleared. if the allergen is re-encountered it will bind to the IgE coated surface, disrupting the membrane and causing the release of vasoactive substances

74
Q

give an example of an type 1 hypersensitivity reactions

A

asthma, hay fever, allergic rhinitis

75
Q

what is he gold standard test for allergy

A

skin prick test

76
Q

give the management options of allergy (5)

A 
targeted avoidance
sodium cromoglycate
antihistamines 
leukotriene receptor agonist
corticosteroids
77
Q

what is the role of sodium cromoglycate in the treatment of allergy

A

mast cell stabilisers

78
Q

what is an type 2 hypersensitivity reaction

A

direct cell killing due to cell bound antigen

79
Q

what is type 2 hypersensitivity reactions also known as

A

antibody dependent hypersensitivity

80
Q

what causes type 2 hypersensitivity reactions

A

IgM or IgG binding to a self antigen or a foreign antigen which is attached to a human cell

81
Q

what cells are involved in an type 2 hypersensitivity reaction

A

B cell

IgM or IgG

82
Q

what antibodies are involved in type 2 hypersensitivity reaction

A

IgM

IgG

83
Q

what does the bound antibody interact with in an type 2 hypersensitivity reaction, what does these interacts result in

A

complement or the Fc receptor on macrophages

activation of complement (causing cell lysis + opsonisation)
opsonisation (antibody mediated phagocytosis)

84
Q

what is the management of type 2 hypersensitivity reactions

A

plasmapheresis

immunosuppression

85
Q

give examples of type 2 hypersensitivity reactions

A

immune haemolytic anaemias

86
Q

give examples of immune haemolytic anaemias

A

drug induced haemolysis

acute haemolytic transfusion reaction

87
Q

what is type 3 hypersensitivity reaction

A

immune complex mediated

88
Q

describe what happens during a type 3 hypersensitivity reaction

A

immune complexes which are trapped within the body attract inflammatory cells which cause damage to the body

89
Q

what cell are involved in a type 3 hypersensitivity reaction

A

B cells
IgG
neutrophils

90
Q

what Ig_ is involved in a type 3 hypersensitivity reaction

A

IgG

91
Q

what causes immune complexes to form

A

in the presence of excess antigen, antibodies will bind together to form immune complexes

92
Q

what is the management of type 3 hypersensitivity reactions (3)

A 
avoidance
decrease inflammation (corticosteroids)
decrease antibody production (immunosuppression)
93
Q

Give an example of type 3 hypersensitivity reactions

A

Hypersensitivity pneumonitis (______ lung)

94
Q

what is type 4 hypersensitivity reactions

A

delayed

95
Q

what mediates type 4 hypersensitivity reactions

A

T cells.

96
Q

what cells are involved type 4 hypersensitivity reactions

A

Th1 cells

macrophages

97
Q

explain what happens during a type 4 hypersensitivity reaction

A

initial exposure to the antigen results in the generation of “primed” Th1cells. subsequent exposure activated “primed” cells which recruit macrophages

98
Q

give examples of type 4 hypersensitivity reaction (4)

A

autoimmune
. type 1 diabetes
. rheumatoid arthritis

non-autoimmune
. contact dermatitis (e.g. poison ivy)
. sarcoidosis

Resp - mine (18 decks)

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