87784
Description
Mind Map by tanitia.dooley, updated more than 1 year ago
|
Created by tanitia.dooley
over 11 years ago
|
|
Allergy
and atropy
- Allergy- A form of immediate or type 1 hypersensitivity
reaction (IgE-production and mast cell activation)
- Atropy- propensity of an individual to produce IgE Abs in
response to environmental stimuli and develop strong immediate
hypersensitivity reactions (strong genetic component)
- Atropy- propensity of an individual to produce IgE Abs in
response to environmental stimuli and develop strong immediate
hypersensitivity reactions (strong genetic component)
- Hayfever-most common, caused by inhalation
of allergens. Disease of the upper respiratory
tract. Clinical features include leukocyte
infiltration, coughing and difficulty in breathing
- Allergic conjunctivitis- often associated
with hay fever, itchy, irritated eyes
- Asthma- immediate hypersensitivity reaction
in the lung-reversible airway obstruction,
bronchial inflammation. Difficulty in breathing
- Eczema, Urticaria- allergic reaction in
skin occurs when allergens come into
direct contact with skin or after an
allergen enters the system circ
- Anaphylaxis- systemic immediate
hypersensitivity reaction characterised
by edema, bronchoconstriction and/or
hypotension (fall in blood pressure)
- Allergens
- House dust mites (their excreta), tree and
grass pollen, food proteins especially egg and
peanut, cat & dog dander-shed skin and
hair-the allergen is a saliva protein, drugs
- Dust mites
thrive in warm
humid
conditions-
bedding etc
feed on dead
kin and body
fluids you
excrete while
you sleep
- Wild grasses
- House dust mites (their excreta), tree and
grass pollen, food proteins especially egg and
peanut, cat & dog dander-shed skin and
hair-the allergen is a saliva protein, drugs
- Mechanisms
- 1. Exposure to allergen 2. Activation of Th2 cells 3. IgE class switching in B-cells
4.Secretion of IgE 5. Binding of IgE to Fc on mast cells 6.Following re-exposure to
Ag=cross linking of IgE 7.Activation of mast cells= degranulation and release of mediators
- Mediators
- Histamine, platelet-activating factor,
leukotrienes, prostaglandin D
- Early response= vasodilation, edema, bronchospasm/
late response=cellular recruitment, inflammation
- Early response= vasodilation, edema, bronchospasm/
late response=cellular recruitment, inflammation
- Histamine, platelet-activating factor,
leukotrienes, prostaglandin D
- Mast cell cytokines: IL-3 promotes mast cell
proliferation, TNFa promotes inflammation, IL4 & IL13
promote TH2 differentiation, IL5 promotes eosinophil
recruitment further eosinophil production and activation
- time course graph
- Production of IgE
- IgE Ab is produced by B-cells stimulated with a Ag, IgE
binds to mast cells, IgE binds to Fc receptor on mast cells,
forming a multi-valent binding site for the Ag. The same Ag
that stimulated B cells and IgE production subsequently
binds to IgE on mast cells=degranulation. Atopic individual
produce high levels of IgE following exposure to Ag. Normal
individuals produce lower levels and or other isotopes
- IgE Ab is produced by B-cells stimulated with a Ag, IgE
binds to mast cells, IgE binds to Fc receptor on mast cells,
forming a multi-valent binding site for the Ag. The same Ag
that stimulated B cells and IgE production subsequently
binds to IgE on mast cells=degranulation. Atopic individual
produce high levels of IgE following exposure to Ag. Normal
individuals produce lower levels and or other isotopes
- 1. Exposure to allergen 2. Activation of Th2 cells 3. IgE class switching in B-cells
4.Secretion of IgE 5. Binding of IgE to Fc on mast cells 6.Following re-exposure to
Ag=cross linking of IgE 7.Activation of mast cells= degranulation and release of mediators
- Activation of Th2 cells
- IgE synthesis is dependent on
activation of CD4+ T cells that
secrete IL-4 & IL-13. Cytokines
from type 2 T cells promote Ab
class switchibg in B cells. T cells
also secrete IL-5 and eotaxin which
are involved in the recruitment and
activation of eosinophils which are
involved in the late phase of
immediate hypersensitivity
- IgE synthesis is dependent on
activation of CD4+ T cells that
secrete IL-4 & IL-13. Cytokines
from type 2 T cells promote Ab
class switchibg in B cells. T cells
also secrete IL-5 and eotaxin which
are involved in the recruitment and
activation of eosinophils which are
involved in the late phase of
immediate hypersensitivity
- Mast cells
- Mature mast cells are found throughout
the body. Contains many pre-formed
granules that contain histamine and other
mediators. Following Ag cross-linking of
Fc receptor bound IgE, there is three
types of biological response -secretion of
pre-formed mediators from granules
-synthesis of further mediators -cytokine
synthesis
- Mature mast cells are found throughout
the body. Contains many pre-formed
granules that contain histamine and other
mediators. Following Ag cross-linking of
Fc receptor bound IgE, there is three
types of biological response -secretion of
pre-formed mediators from granules
-synthesis of further mediators -cytokine
synthesis
- Eosinophils
- Migrate to sites of inflammation (move
towards IL5). They secrete proteins (eg
major basic protein) from granules- these
proteins can directly damage host cells
- Migrate to sites of inflammation (move
towards IL5). They secrete proteins (eg
major basic protein) from granules- these
proteins can directly damage host cells
- Genetic susceptibility
- IgE synthesis and atopy generally runs in families.
The propensity to produce IgE is influenced by the
inheritance of several genes (multi-genetic)
- Candidate genes: IL4 & 13-promote IgE class
switching/ IL5 promotes eosinophil growth or
activation/ MHC class II-certain alleles regulate T cell
response to different Ags/ TNFa-mast cell mediator
(inflammatory)/Fc receptor-mast cell receptor
- Candidate genes: IL4 & 13-promote IgE class
switching/ IL5 promotes eosinophil growth or
activation/ MHC class II-certain alleles regulate T cell
response to different Ags/ TNFa-mast cell mediator
(inflammatory)/Fc receptor-mast cell receptor
- IgE synthesis and atopy generally runs in families.
The propensity to produce IgE is influenced by the
inheritance of several genes (multi-genetic)
- Treatment
- Anaphylaxis-Adrenaline which can be life-saving reverses
bronchoconstriction, vasodilation & improve cardiac
output/Antihistamines-antagonism of histamine receptors
- Asthma- corticosteroids-block the production of
inflammatory cytokines/ sodium
cromolyn-inhibits release of mast cell mediators
- Hayfever-
antihistamines most
common treatment
- Skin reactions- cutaneous corticosteroids
- Anaphylaxis-Adrenaline which can be life-saving reverses
bronchoconstriction, vasodilation & improve cardiac
output/Antihistamines-antagonism of histamine receptors
Want to create your own Mind Maps for free with GoConqr? Learn more.