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Clinical Pathology (RIP) > T4 - L1 Allergic Diseases > Flashcards

T4 - L1 Allergic Diseases Flashcards

1
Q

what is an allergy/hypersensitivity?

A

an inappropriate immune response to:

  • innocuous antigens

in a

  • pre-sensitized (immune) host
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2
Q

which types of hypersensitivity of antibody mediated?

A

types 1-3

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3
Q

which types of hypersensitivity is cell mediated?

A

type 4

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4
Q

what antibodies feature in a type 1 (anaphylactic) hypersensitivity reaction?

A

IgE

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5
Q

what antibodies feature in a type 2 (cytotoxic) hypersensitivity reaction?

A

IgG

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6
Q

what antibodies feature in a type 3 (immune complex) hypersensitivity reaction?

A

IgG

IgM

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7
Q

what antibodies feature in a type 4 (delayed type) hypersensitivity reaction?

A

none

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8
Q

what type of antigen features in a type 1 (anaphylactic) hypersensitivity reaction?

A

exogenous

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9
Q

what type of antigen features in a type 2 (cytotoxic) hypersensitivity reaction?

A

cell surface

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10
Q

what type of antigen features in a type 3 (immune complex) hypersensitivity reaction?

A

soluble

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11
Q

what type of antigen features in a type 4 (delayed type) hypersensitivity reaction?

A

tissues and organs

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12
Q

what the response time of a type 1 (anaphylactic) hypersensitivity reaction?

A

15-30 minutes

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13
Q

what the response time of a type 2 (cytotoxic) hypersensitivity reaction?

A

minutes- hours

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14
Q

what the response time of a type 3 (immune complex) hypersensitivity reaction?

A

3-8 hours

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15
Q

what the response time of a type 4 (delayed type) hypersensitivity reaction?

A

48-72 hours

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16
Q

IgG/IgM Ab response against combined self/foreign antigen at the cell surface is which type of hypersensitivity?

A

type 2 (cytotoxic)

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17
Q

what are some clinical features of a type 2 (cytotoxic) hypersensitivity?

A
  • onset: minutes to hours

- cell lysis and necrosis

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18
Q

what is a common antigen of a type 2 (cytotoxic) hypersensitivity?

A

penicillin

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19
Q

what are three associated diseases of of a type 2 (cytotoxic) hypersensitivity?

A

Erythroblastosis fetalis

Goodpasture’s nephritis

Penicillin Mediated Autoimmune Haemolytic Anaemia

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20
Q

why type of sensitivity is referred to as cytotoxic?

A

type 2

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21
Q

what is haemolysis?

A

the rupture or destruction of red blood cells.

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22
Q

what is Erythroblastosis fetalis, and how does it occur?

A
  • Hemolytic disease of the newborn
  • mum is a different Rh blood type (e.g. mother is Rh- and newborn is Rh+)
  • mum’s antibodies attack fatal blood resulting in haemolytic in unborn child/immediately after birth
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23
Q

what are symptoms of Erythroblastosis fetalis seen in a newborn child?

A
  • life-threatening anemia because of a lack of oxygen in the blood.
  • jaundice
  • fevered
  • swelling
  • enlarged liver and spleen.
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24
Q

what is Goodpasture syndrome/Goodpasture’s nephritis?

A

antibodies attack the basement membrane in lungs and kidneys, leading to bleeding from the lungs and kidney failure.

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25
Q

a disease associated with type 1 (anaphylactic) sensitivity?

A

allergic asthma

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26
Q

a disease associated with type 3 (immune complex) sensitivity?

A

SLE

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27
Q

a disease associated with type 4 (delayed type) sensitivity?

A

contact dermatitis

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28
Q

IgG/IgM Ab against soluble antigen would result in why type of hypersensitivity reaction?

A

type 3 – immune complex deposition

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29
Q

what are some clinical features of type 3 (immune complex) hypersensitivity?

A
  • onset 3-8h

- vasculitis

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30
Q

what is the traditional cause of a type 3 (immune complex) hypersensitivity?

A

serum sickness

NB: [Serum used to be used as a treatment for tetanus but immune system recognizes
the fluid and subsequently causes SLE]

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31
Q

what is SLE?

A

Systemic lupus erythematosus (SLE)

- autoimmune disease

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32
Q

what are common symptoms of SLE?

A
  • painful/swollen joints
  • fever
  • chest pain
  • hair loss
  • mouth ulcers
  • swollen lymph nodes
  • fatigue
  • red rash most commonly on the face
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33
Q

Antigen specific T – cell mediated cytotoxicity is which type of hypersensitivity?

A

type 4 (delayed)

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34
Q

which type of hypersensitivity involves T cells?

A

type 4 (delayed)

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35
Q

what are some clinical features of a type 4 (delayed) hypersensitivity?

A
  • onset: 48-72h typically

- Erythema induration

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36
Q

how do we develop an allergy?

A
  • combination of environment and genetic factors
  • load od barrier function
  • sensitisation of the immune system
  • leading to IgE production
  • These antibodies travel to cells that release chemicals, causing an allergic reaction
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37
Q

what would be an immune response to parasitic disease?

A
  • increased levels of IgE
  • tissue inflammation (Eosinophilia & Mastocytosis [mast cells], Basophil infiltration)
  • CD4+ T cells secreting: IL4, IL5 & IL13
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38
Q

what type of cells are CD4+ T cells?

A

T helper cells

hey help the activity of other immune cells by releasing T cell cytokines.

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39
Q

what type of cells are CD8+ T cells?

A

Cytotoxic T cell

kills cancer cells, cells that are infected (particularly with viruses), or cells that are damaged in other ways.

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40
Q

what is the hygiene hypothesis?

A

lack of exposure to infectious agents and parasites increases susceptibility to allergic diseases by suppressing the natural development of the immune system

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41
Q

can allergic immune responses be inherited?

A

no they are polygenic diseases

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42
Q

can allergic immune responses be inherited?

A

no they are polygenic diseases

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43
Q

which antibody is responsible for allergies?

A

IgE

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44
Q

which cytokines are responsible for allergy?

A

Cytokine gene cluster IL3,5,9,13

45
Q

which cytokine receptors are responsible for allergy?

A

IL12R

IL4R

46
Q

what is FcεR1?

A
  • high-affinity IgE receptor
  • Crosslinking of the FcεRI via IgE-antigen complexes leads to degranulation of mast cells or basophils and release of inflammatory mediators.
47
Q

which cytokines work against allergies as part of the immune system?

A

IFNγ

TNF

48
Q

what is an allergen?

A

an antigen that initiates an IgE-mediated response

49
Q

describe a conventional immune response.

A
  • allergen processed
  • antigens presented to T-cells resulting in a cytokine release
  • Results in delineation of T-helper subsets into different types [Th2 drives allergic conditions]
50
Q

Genetic influences on the ‘allergic’ immune response are not sufficient for disease, ONLY susceptibility. What are the 4 groups of susceptibility genes for allergic disease?.

A

group 1: sensing the environment

group 2: barrier function

group 3: regulation of (atopic) inflammation

group 4: tissue response genes

51
Q

the first encounter of an allergen doesn’t always result in an IgE response, what does it result in instead?

A

First encounter results in innate & IgM response

52
Q

how are IgE antibodies produced?

A
  • An antigen (allergen) is recognized by both B-cell and Th2 cell
  • Th2 can signal to B-cell (IL4) which can cause it switch to IgE proliferation
53
Q

what is referred to as an “early priming event”?

A
  • a breach in the initial barrier so allergen can access the immune system
  • allergen taken up and antigens are presented by an antigen presenting cell (e.g. dendritic cell)
  • stimulates T cells (in lymph node) and they differentiate into different T cell subtypes to initiate immune response
54
Q

what is a Th2 cell?

A

a distinct lineage of CD4+ T helper cell that secretes:

IL-4, IL-5, IL-13

55
Q

what are the 4 basic subtypes of CD4+ T cell?

A

Th1
Th2
Th17
Treg

56
Q

what effector cytokines does Th1 secrete?

A

IFNy

IL-2

57
Q

what effector cytokines does Th2 secrete?

A

IL-4
IL-5
IL-13

58
Q

what effector cytokines does Th17 secrete?

A

IL-17
IL-21
IL-22

59
Q

what effector cytokines does Treg secrete?

A

IL-10

TGFβ

60
Q

which subtype of CD4+ T cell is the primary stimulator of a type 1 (anaphylactic) hypersensitivity reaction?

A

Th2

61
Q

what is the role of the Th2 T cell?

A
  • multiple cytokine release (IL-4 IL-5 IL-13)
  • innate inflammatory response
  • drive for IgE production

(activates innate and adaptive immune response)

62
Q

describe the mechanism of a type 1 allergic response

A
  • allergen detected by B and T cells
  • T cells secrete IL-4 which help the B cells differentiate into plasma cells
  • Plasma cell produces and secretes IgE
  • IgE attaches to and pops mast cells - producing all the hypersensitivity reactions e.g.:

low blood pressure
smooth muscle contractions
vomting
mucous secretion

63
Q

what stimulates mast cell and basophil degranulation?

A

IgE antibody

64
Q

what happens during mast cell and basophil degranulation?

A

release of preformed and

de novo synthesized inflammatory mediators

65
Q

what are clinical features of a IgE mediated allergic response?

A
  • fast onset: 15-30 min

- wheal and flare

66
Q

wheal and flare is a characteristic of which type of hypersensitivity?

A

type 1 (anaphylactic) hypersensitivity

67
Q

what are the characteristic cells that mediates the late phase response in an IgE/type 1 allergic response?

A

mainly Eosinophils

Th2 T cells also contribute

68
Q

during mast cell degranulation, what primary mediators (immediate/initial response) are released?

A

histamine

proteases

chemotactic factors (ECF and NCF)

69
Q

during mast cell degranulation, what secondary mediators (delayed/late-phase response) are released?

A

Arachnoid acid metabolites including leukotrienes

and prostaglandins

70
Q

what are the effects of histamine?

A
  • tachycardia
  • blood clots
  • gastric acide secretion (vomiting and diarrhoea)
  • blood vessel dilation (hypotension)
  • bronchoconstriction
  • inc permeability of capillaries
  • release of adrenaline
  • swelling and inflammation
71
Q

what is a protease?

A

an enzyme that helps proteolysis - protein catabolism by hydrolysis of peptide bonds

72
Q

what are chemotactic factors?

A

substances that stimulates locomotion/cellular migration

e.g. chemokine, complement proteins 3a and 5a

73
Q

what do leukotrienes do within an immune response?

A

trigger contractions in smooth muscles lining bronchioles

74
Q

what do prostaglandins do within an immune response?

A

local acting vasodilation

aggregation of blood platelets

75
Q

what conditions make up the atopic triad?

A

asthma
rhinitis
eczema

76
Q

shat is the difference between asthma and rhinitis?

A

Asthma affects lower airway

Rhinitis affects upper airways

77
Q

what are some symptoms of rhinitis?

A

Blocked nose, runny nose, sneezing and itchy nose - often with eye symptoms (Itching/burning, watery eyes, redness)

78
Q

what is the treatment of rhinitis?

A

Antihistamines

Nasal steroids

79
Q

what are triggers of non-allergic rhinitis?

A
  • vasomotor
  • infection
  • structural defects
  • drugs
  • hormonal treatment
  • polyps
80
Q

what is perennial allergic rhinitis?

A

you have it all year round

triggers such as dust mites, animals

81
Q

what is seasonal allergic rhinitis?

A

you get it with change of season e.g. hay fever

82
Q

a rhinitis triggered by dog fur is what type of rhinitis?

A

perennial

83
Q

what is asthma?

A

INFLAMMATION & HYPER-REACTIVITY of small airways

84
Q

immediate symptoms of asthma are mediated by which antibody?

A

IgE

85
Q

due to asthma, the airways can become damaged, is this due to the initial or late phase response?

A

late phase response

NB: DAMAGED AIRWAYS ARE HYPER-REACTIVE to non-allergic stimuli e.g. fumes

86
Q

which aero-allergic stimuli plays a key role in childhood asthma?

A

house dust mite

87
Q

describe the pathogenesis of asthma?

A
  • Allergens presented by APC to induce Th2 cells to secrete IL-4 to signal B-cells to make IgE Ab
  • IgE bind to mast cell via FCER1 = mast cell degranulation
  • release of histamine, leukotrienes, prostaglandins, cytokines, proteins and enzymes
    = allergic response
88
Q

what form of dermatitis is endogenous?

A

eczema

89
Q

what form of dermatitis is exogenous?

A

contact dermatitis

NB: this is not due to immediate exposure, a delayed reaction

90
Q

describe the pathogenesis of atopic dermatitis?

A
  • barrier disruption
  • allergen presented to T and B cells (T cells produce (IL-4 to stimulate B cell conversion into plasma cells = high IgE production)
  • T cell also produces IL-31 responsible for itching which results in more barrier disruption = cycle continues
91
Q

in atopic dermatitis which inflammatory cytokine is responsible for the itching sensation?

A

IL-31

92
Q

what is filaggrin and what is it’s role in the pathogenesis of atopic dermatitis?

A

Filaggrin binds to keratin fibres in epithelial cells to maintain epidermal homeostasis

Th2 Cells secrete IL-4/13 which inhibit the expression of Filaggrin leading to increased susceptibility of barrier disruption.

93
Q

which inflammatory cytokines, secreted by TH2, inhibit the expression of Filaggrin increasing the epidermis’ susceptibility to barrier disruption?

A

IL-4

IL-13

94
Q

with reference type 1 hypersensitivity, what is sensitisation?

A

induction of allergen

95
Q

how does sensitisation occur?

A
  • barrier disruption (allergen gains access to immune system)
  • taken up by antigen-presenting cell (APC)
  • APC travels to lymph nodes and presents antigens to naive T cells (Th0)
  • T cells stimulated to secrete IL-4 to differentiate to Th2
  • Th2 secretes IL-4 (positive feedback loop),5,13.
  • IL-4 stimulates class switch in B cells to produce IgE Ab
  • Mast cells have high affinity FCER1 receptor fir IgE that causes degranulation
96
Q

which inflammatory cytokine stimulates the differentiation of a naive T cell (Th0) to a Th2 cell?

A

IL-4

97
Q

which inflammatory cytokine stimulates the degranulation of eosinophils?

A

IL-5

98
Q

which inflammatory cytokine stimulates the class switch of B cells?

A

IL-4

99
Q

what is meant by “class switch” during sensitisation?

A

biological mechanism that changes a B cell’s production of immunoglobulin from one type to another

e.g. IgM to IgE

100
Q

Th2 plays central role in mediating delayed responses, what does it do?

A
  • stimulates eosinophils, memory cells
  • generates cytokines and chemokines
  • drives mast cells and basophils
101
Q

what tests can be done to diagnose an allergy?

A
  • take history
  • look for IgE in blood
  • skin-prick test
  • intra-dermal test
  • graded challenge test (most reliable)
  • basophil activation test
102
Q

what does the intra-dermal test involved?

A

The test involves injection of a small amount of the suspected allergen under the surface of the skin. After about 20 minutes the area is examined for a reaction at the site.

NB: Can only use negative control here since histamine can cause damage.

103
Q

what does the graded challenge test involve?

A
  • Start with tiny amount of suspected allergens and then keep doubling the dose
  • If the patient develops symptoms then stop it there and the diagnosis is found
  • if no symptoms, then they are not allergic to that substance
104
Q

what does the basophil activation test involve?

A
  • take patients blood (which contains basophils)
  • add allergen
  • When have allergen and reassess basophils again, there are increased levels of these
    markers: CD300a and CD203c
105
Q

advantages of a IgE specific blood test when trying to diagnose an allergy?

A

safe

- will not cause an allergic reaction.

106
Q

advantages of a skin prick test when trying to diagnose an allergy?

A
  • quick

- patient satisfaction (they know what they’re allergic to straight away)

107
Q

disadvantages of a IgE specific blood test when trying to diagnose an allergy?

A

false negatives and false positives possible

108
Q

disadvantages of a skin prick test test when trying to diagnose an allergy?

A
  • false negatives and false positives possible
  • risk of allergic reaction
  • antihistamines can inhibit skin prick response
109
Q

how do you treat a symptomatic allergy?

A

Antihistamines, Steroids, Adrenaline

immunosuppressive therapy if they don’t respond to above treatments

Clinical Pathology (RIP) (49 decks)

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