87745
Description
Mind Map by tanitia.dooley, updated more than 1 year ago
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Created by tanitia.dooley
almost 12 years ago
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Hypersensitivity
types 2,3 & 4
- Type II
- Caused by IgM/IgG Abs to cell surface and
extracellular matrix proteins: Abs interact with
complement components and effector cells such as
macrophages and neutrophils=results in tissue damage
via mechs nor malls active against foreign Ags
- Eg. Reactions against incompatible blood
transfusions, autoimmune haemolytic
anaemia (sensitised to patients own RBS,
often drug induced), good pastures
syndrome (Ab against basement mem
proteins produce nephritis)
- Haemolytic disease of the newborn
- Occurs when mother has become sensitised to Ag
on the infants erythrocytes. Rhesus D commonly.
1. Sensitiation of the mother during the birth of the
first rhesus +ve baby 2. Subsequent children have
an increased risk of being affected-Ab crosses
placenta and goes to babies RBCs
- Child shows high bilirubin levels from haemoglobin
breakdown, lower erythrocyte counts (because
RBCs lysed), enlarged spleen and liver (tried to
make more RBC to make up for ones removed) &
potentially lower growth (lack of O2)
- Prophylaxis: rhesus -ve mothers given
anti rhesus D Abs immediately after
birth- thought it works by removing
infact Rh +ve erythrocytes (Ag) from
mothers circa preventing sensitisation
- Prophylaxis: rhesus -ve mothers given
anti rhesus D Abs immediately after
birth- thought it works by removing
infact Rh +ve erythrocytes (Ag) from
mothers circa preventing sensitisation
- Child shows high bilirubin levels from haemoglobin
breakdown, lower erythrocyte counts (because
RBCs lysed), enlarged spleen and liver (tried to
make more RBC to make up for ones removed) &
potentially lower growth (lack of O2)
- Occurs when mother has become sensitised to Ag
on the infants erythrocytes. Rhesus D commonly.
1. Sensitiation of the mother during the birth of the
first rhesus +ve baby 2. Subsequent children have
an increased risk of being affected-Ab crosses
placenta and goes to babies RBCs
- Haemolytic disease of the newborn
- Eg. Reactions against incompatible blood
transfusions, autoimmune haemolytic
anaemia (sensitised to patients own RBS,
often drug induced), good pastures
syndrome (Ab against basement mem
proteins produce nephritis)
- Myasthenia gravis
- Extreme muscle weakness-Abs to
the Ach receptors present on muscle
mem=reduced signal transmission
- Extreme muscle weakness-Abs to
the Ach receptors present on muscle
mem=reduced signal transmission
- Caused by IgM/IgG Abs to cell surface and
extracellular matrix proteins: Abs interact with
complement components and effector cells such as
macrophages and neutrophils=results in tissue damage
via mechs nor malls active against foreign Ags
- Type III
- Caused by IgM/IgG Abs against soluble Ags. Ab/Ag complexes
normally removed efficiently. In these reactions complexes that
persist are deposited in circ or tissues and cause inflammation.
Frequent complication in autoimmune disease.
- A lot of Ag little Ab
- A lot of Ag little Ab
- 3 categories: Persistent infection-Ag is
microbial and infects kidney and
infection organs/ autoimmunity against
self Ag in kidney joints and skin/inhaled
Ag from mould plant or animal Ag affects
the lung
- Complexes interact with basophils and
platelets to induce amino release eg
histamine=inflammation. Macriohage
stimulation results in cytokine release (TNF,
IL-1), complement activation and inflammation
- Extrinsic allergic alveolitis
- Farmers lung caused by Abs to actinomycete fungi present in
moudly hay or pidgeon fanciers lung with Abs to pidgeon Ags.
Ag is inhaled and immune complexes form in
alveoli=complement activation, inflammation ad fibrosis follows
- Farmers lung caused by Abs to actinomycete fungi present in
moudly hay or pidgeon fanciers lung with Abs to pidgeon Ags.
Ag is inhaled and immune complexes form in
alveoli=complement activation, inflammation ad fibrosis follows
- Arthurs reaction
- Hyper-immunise animal to get high Ab levels-give Ag usually to skin
or give suspected Ag to a patient by intradermal injection and look for
inflammation. Local immune complexes activate complement and
mast cell degranulation=local inflammation, movement of fluid and
proteins into tissues and blood vessel occlusion (raised area of skin)
- Hyper-immunise animal to get high Ab levels-give Ag usually to skin
or give suspected Ag to a patient by intradermal injection and look for
inflammation. Local immune complexes activate complement and
mast cell degranulation=local inflammation, movement of fluid and
proteins into tissues and blood vessel occlusion (raised area of skin)
- Caused by IgM/IgG Abs against soluble Ags. Ab/Ag complexes
normally removed efficiently. In these reactions complexes that
persist are deposited in circ or tissues and cause inflammation.
Frequent complication in autoimmune disease.
- Type IV
- Delayed type hypersensitivity
- Mediated by TH1 cells which produce cytokines
(TNFa, IFNy, IL-12, IL-15=inflammation)
- Can be shown experimentally by transferring T cells between
animals (from sensitised animal to non-sensitised=animal
becomes sensitised even in absence of Ag)
- Can be shown experimentally by transferring T cells between
animals (from sensitised animal to non-sensitised=animal
becomes sensitised even in absence of Ag)
- Mediated by TH1 cells which produce cytokines
(TNFa, IFNy, IL-12, IL-15=inflammation)
- 3 types
- Contact hypersensitivity (48-72 hrs)
- Characterised by inflammatory reaction in the skin following
contact with allergen (Nickel, chromate & small organic chemicals
for example DNCB). Small molecules to generate a response this
must act as haptens (small group of chemical bound to carrier)
- Allergen enters skin and binds protein carrier-now big
enough to be recognised- langerhans cell migrate to lymph
node: Ag is presented to CD4 generating memory cells and
effector cells- these cells can migrate to the skin where
reaction can be set off if person in contact with Ag again
- Elicitation phase- subsequent time- Ag presentation to primed T
cells in the tissue- T cells respond by making cytokines (TNFa &
IFNy) which promotes tissue swelling or oedema of the tissue and
cell adhesion molecule expression on the vasculature. Causes
cytokine release from kerratinocytes including IL1, IL6 &
chemoattractant cytokines resulting in inflammatory cell recruitment
- Elicitation phase- subsequent time- Ag presentation to primed T
cells in the tissue- T cells respond by making cytokines (TNFa &
IFNy) which promotes tissue swelling or oedema of the tissue and
cell adhesion molecule expression on the vasculature. Causes
cytokine release from kerratinocytes including IL1, IL6 &
chemoattractant cytokines resulting in inflammatory cell recruitment
- Allergen enters skin and binds protein carrier-now big
enough to be recognised- langerhans cell migrate to lymph
node: Ag is presented to CD4 generating memory cells and
effector cells- these cells can migrate to the skin where
reaction can be set off if person in contact with Ag again
- Characterised by inflammatory reaction in the skin following
contact with allergen (Nickel, chromate & small organic chemicals
for example DNCB). Small molecules to generate a response this
must act as haptens (small group of chemical bound to carrier)
- Granulomatous hypersensitivity (21 days)
- Seen in many T cell mediated disease. Macrophages
are activated but are unable to destroy an Ag which
persists. Activation persists and the macrophage form
large epitheloid cells which can fuse into giant
multinuclear cells (granuloma)=Form large collections
of cells and the products from these activated cells
can damage tissues
- Diseases which can show granulomatous type
IV reactions: -Leprosy-borderline skin reactions
-Tuberculosis: mycobacterium tuberculosis
-Crohns disease: granulomatous reaction in the
gut, nature of any infectious agent is unknown
- Seen in many T cell mediated disease. Macrophages
are activated but are unable to destroy an Ag which
persists. Activation persists and the macrophage form
large epitheloid cells which can fuse into giant
multinuclear cells (granuloma)=Form large collections
of cells and the products from these activated cells
can damage tissues
- Contact hypersensitivity (48-72 hrs)
- Delayed type hypersensitivity
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