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Year 3 > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

what is hypersensitivity?

A

Hypersensitivity is a group of disorders where the normally beneficial components of the immune response act in an exaggerated or inappropriate fashion to environmental antigens which do not normally cause tissue damage. The exaggerated response directed at the antigen rather than the antigen itself is responsible for the tissue damage which results.

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2
Q

type 1 hypersensitivity =

A

allergy

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3
Q

immunoglobulin in type 1 hypersensitivity

A

IgE

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4
Q

phases of type 1 hypersensitivity

A

sensitisation

reaction

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5
Q

treatment of type 1 hypersensitivity

A

antihistamines
corticosteroids
adrenaline
allergen avoidance

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6
Q

atophy triad

A

eczema
asthma
hayfever

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7
Q

what is atopy?

A

genetic tendency to develop allergic diseases

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8
Q

describe atopic dermatitis

A
  • Common in children
  • Exposed and flexor surfaces
  • Degranulation of basophils and mast cells in response to sensitised IgE
  • “Leaky” skin allows more allergen in and water out
  • Dry and itchy
  • Itch leads to further infection/inflammation
  • Itch worse at night
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9
Q

type 2 hypersensitivity

A

cytoxic

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10
Q

type 3 hypersensitivity

A

immune mediated

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11
Q

type 4 hypersensitivity

A

cell mediated

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12
Q

what is contact dermatitis

A
  • Haptens cross stratum corneum
  • Langerhans cells present to TH1 cells
  • Langerhans cells are APC that site on cell surfaces
  • TNF alfa and IL 1, 13 and 18
  • LCs become differentiated Dendritic cells presenting allergenic epitope and multiply
  • More aggressive response 2nd time
  • Reexposure will not result in anaphylaxis
  • Acquired immune response not innate
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13
Q

effector mechanism in type 1 hypersensitivity

A

mast cell activation

eosinophil activation

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14
Q

antibody in type 11 hypersensitivity

A

IgG

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15
Q

type 2 hypersensitivity effector mechanism

A

cell or matrix associated complement
FcR+ cells

cell surface receptor
Ab alters signalling

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16
Q

example of type 2 hypersensitivity

A

drugs

chronic urticaria

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17
Q

immunoglobulin in type 3 hypersensitivity

A

IgG

18
Q

effector mechanism in type 3 hypersensitivity

A

complement

phagocytes

19
Q

example of type 3 hypersensitivity

A

arthus reaction

20
Q

type 4 hypersensitivity immune reactant

A

Th1 cells

21
Q

effector mechanism in type 4 hypersensitivity

A

macrophage activation

22
Q

example of type 4 hypersensitivity

A

contact dermatitis

tuberculin reaction

23
Q

describe the production of IgE

A

• IgE produced by plasma B cells in lymph nodes, or
locally at site of inflammation
• IgE located mostly in tissue (hence low serum
concentration), bound to Mast Cell surface
through high affinity IgE receptor Fc!RI
• Certain antigens and routes of delivery appear to
favour IgE production. Transmucosal at low doses
is often a common route.
• CD4+ T cells of the Th2 phenotype that produce
IL4 cytokines favour IgE responses
• Th2 T cells also force B cells to switch the
isotype of the Ig they secrete from IgM to IgE

24
Q

what do CD8 cytotoxic cells produce?

A

IFNgamma

TNF-a

25
Q

what are the functions of the things CD8 cells produce?

A

target cell lysis

26
Q

what do CD4 Th1 cells produce?

A

IFN-g
GM-CSF
TNF-a

27
Q

what are the functions of the things Th1 cells produce?

A

macrophage activation

28
Q

what do CD4 Th2 cells produce

A

IL4

IL5

29
Q

what are the functions of the things Th2 cells produce?

A

b cell activation

30
Q

features of allergic asthma

A 
• Bronchial constriction
• Increased secretion of fluid and mucus,
trapping inhaled air
• Chronic inflammation may ensue with
continued presence of Th2 T cells,
eosinophils, neutrophils.
• Chronic asthma driven originally by
specific allergen, but may then result in
hyperreactive airways to other irritants
such as cigarette smoke and other
pollutants
31
Q

describe the effects of ingested allergens

A

• Ingested allergens leads to two main symptoms
• Activation of GI Mast cells results in
transepithelial fluid loss and smooth muscle
contraction: diarrhea and vomiting
• If allergen enters bloodstream, generalised
disseminated rash, Urticaria, (hives).
• In severe cases of food allergy, eg nuts and
shellfish, life threatening generalised anaphylaxis
and cardiovascular collapse may occur

32
Q

chemical mediators of allergic responses

A 
• Mast cells granules contain a wide range of
inflammatory mediators
• Lipids
• Toxic mediators
• Cytokines
• enzymes
33
Q

lipids in allergic response

A

• Prostaglandins, increase vascular permeability, increase body temperature. Platelet activating Factor, increase adhesion between endothelium and neutrophils. Leukotrienes, attract and activate neutrophils, increase vasc permeability

34
Q

toxic mediators in allergic response

A

Histamine, increase vascular permeability, and promotes movement of fluid from the vasculature by constricting vascular smooth muscle.

35
Q

cytokines in allergic respoonse

A 
• IL-4, IL-13; amplify Th2 response
• IL-3, IL-5, GM-CSF; promote
eosinophil activation and production
• TNF-#; pro-inflammatory, activates
endothelium
Chemokine MIP-1#; attracts
macrophages and neutrophils
36
Q

enzymes in allergic response

A
  • Tryptase
  • Chymase
  • Cathepsin G
  • Carbopeptidase
  • Remodel connective tissue matrix
37
Q

describe type 2 hypersensitivity

A
  • Type II reactions are the result of antibodies, usually IgG, binding to components of cell membranes or extracellular matrix.
  • Can be self-components, or exogenous components
38
Q

give examples of type 2 hypersensitivty endogenous

A

• Self: Goodpasture’s syndrome, antibodies bind to basement membrane collagen type IV, glomerulonephritis in kidney, pulmonary haemorrhage in lung

39
Q

describe type 3 hypersensitivity

A
  • As with Type II, Type III are caused by antibody, usually IgG, but also sometimes IgM.
  • Type III antibodies directed to soluble antigens
  • Formation of antibody-antigen complexes is a normal part of immune response.
  • Usually cleared by reticuloendothelial system (RES): macrophages, neutrophils in liver spleen and bone marrow that ingest and degrade immune complexes
  • Excess immune complex deposition in tissues leads to pathology
40
Q

sites of immune complex deposition in type 3 hypersensitivity

A
  • Sites of immune complex (IC) deposition are not necessarily the sites from where the antigen is derived.
  • Glomeruli : kidney, filtration process makes it very common site in IC deposition, damage driven by complement activation
  • Blood vessel walls: IC accumulate on veins and arteries, causes vasculitis, often seen as skin lesions if close to surface
  • Synovial membranes: Rheumatoid arthritis, in which the IgG of the immune complexes can become an antigen itself, and IgM Rheumatoid Factor antibodies develop.
  • Skin: common site for IC deposition, causes rashes.
  • Systemic sites: in case of Systemic Lupus Erythematosus (SLE) IC deposits in kidney, joints, skin, vasculature, muscle and other organs.
41
Q

describe type 4 hypersensitivity

A
  • Unlike I, II & III, Type IV reactions are entirely cell-mediated
  • Complement does not play a role in Type IV.
  • Most Type IV reactions are caused by CD4+ delayed type hypersensitivity (DTH) reactions. ‘Delayed’ refers to reaction occurring 2 to 4 days after antigen exposure
  • Macrophages that cause damage are not specific, harm infected and non-infected tissue

Year 3 (164 decks)

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