allergies Flashcards
why does systemic anaphylaxis occur ?
due to a common stimuli of drugs , venom or foods
what is the route of entry ?
intravenous which can be directly or following absorption into the blood after oral intake
what can the response include
edema which is swelling , increased vascular permeability and laryngeal edema , circulatory collapse and death
what is acute urtucaria also known as?
wheal and flare
why does this occur ?
due to a common stimuli of past viral , animal hair , bee stings and allergy testing.
what is the route of entry ?
through the skin
what can occur ?
it can be systemic
what are the symptoms ?
increased blood flow , vascular permeability and swelling
what is seasonal rhino conjunctivitis also known as?
hay fever
what is the common stimuli ?
pollen and dust mite feaces
what is the route of entry ?
contact with the conjunctiva of the eye and nasal mucosa
what is the response ?
swelling of the conjunctiva and nasal mucosa and sneezing
what is the common stimuli of asthma ?
dander from cats , pollen and dust mite faeces
what is the route of entry ?
inhalation which leads to contact with muscosal of the lower airways
what is the response ?
bronchial constriction , increased mucus production and airway inflammation
what are the common stimuli of food allergy?
peanuts , shellfish , milk eggs and wheat
what is the route of entry for food allergies ?
oral
response ?
vomitting , diarrhoea and itching
what is pruitis ?
itching
what is IgE a prominent defense against ?
extracellular pathogens such as parasitic organisms like protazoans
what are the immediate hypersensitivity reactions involve ?
they are caused by the activation of mast cells and basophils as a result of IgE cross binding to the innocuous antigen.
what is sensitisation involve ?
the class switching to IgE production on the first contact with an allergen.
what are the common sensitising agents ?
proteases
what does the enzyme Der p 1 do ?
it cleaves the occludin in tight junctions and it enters the mucosa , it is then taken up by dendritic cells for antigen presentation and Th2 priming. The dendritic cell prime the T cells in the lymph and Th2 induces B cell switch to produce IgE. The plasma cell then travel back to the mucosa and produce Der p 1 specific IgE antibodies. The IgE binds to the FcERI receptor on mast cells. The Der p 1 specific IgE binds to the mast cells and this triggers degranulation. This leads to allergic symptoms.
how can basophils amplify the IgE production
they express FcεRI, and when they are activated by antigen cross-linking their FcεRI-bound IgE, they then express cell-surface CD40 ligand and secrete IL-4. The activated basophil provides contact and secretes signal to the B cell to stimulate IgE.production.
what is it that causes the contact between the cells ?
the CD40 and CD40L
what are most airborne allergens ?
highly soluble proteins that are carried on dry patches such as mite faeces
what two factors can lead to allergy susceptibility ?
environmental and genetic factors
what could count for the large increase in allergic diseases such as asthma recently ?
the environmental changes are having an impact on the people who gave a genetic predisposition to asthma
what is atopy ?
form of allergy in which a hypersensitivity reaction such as eczema or asthma may occur in a part of the body not in contact with the allergen
what cells can control our allergic responses ?
reg T cells so if these are faulty then this can lead to some allergic responses
where are mast cells found and what do they orchestrate ?
in the tissues and they orchestrate allergic responses
when mast cells are activated due to cross linking of the IgE to the allergen what occurs ?
they induce inflammatory reactions by releasing histamine which is a mediator stored in granules.
what does the response to the allergen depend on ?
the dose of the allergen
the entry route
what is different to IgE antibody to all the other antibodies ?
Most antibodies engage Fc receptors only after their antigen-binding sites have bound specific antigen, forming an immune complex of antigen and antibody. IgE is an exception, because it is captured by the high-affinity Fcε receptor (FcεRI) in the absence of bound antigen.
due to this where is IgE found in comparison to the other Ig’s ?
unlike other antibodies, which are found mainly in body fluids, IgE is mostly found fixed on cells that carry this receptor—mast cells in tissues, and basophils in the circulation and at sites of inflammation
how can IgE mediated allergies be treated ?
by inhibiting the effector pathways that lead to symptoms or desensitising techniques that aim at restoring biological tolerance.
what symptoms are seen when mast cells are activated in the GI tract ?
increased fluid secretion and increased peristalsis which leads to expulsion of gastrointestinal tract contents and diarrhoea and vomiting.
what symptoms are seen when the mast cells are activated in the eyes , nasal passages and airways ?
decreased airway diameter and increased mucus secretion. This leads to congestion and blockage of the airways and wheezing , coughing and phlegm occurs. There is also swelling and mucus secretion in the nasal passages and ocular itching and sneezing occurs.
what occurs when there are mast cells activated in the blood vessels ?
increased blood flow and increased permeability , this leads to increased fluid in the tissues which cause an increased flow of lymph to the lymph nodes. There’s an increase in cells and proteins in tissues and increased effector response in tissues. Hypotension can potentially lead to anaphylactic shock.
what is the immediate response due to ?
reaction is due to IgE-mediated mast-cell activation and starts within seconds of allergen exposure. It is the result of the actions of histamine, prostaglandins, and other preformed or rapidly synthesized mediators released by mast cells.
what does it depend on if a late response occurs ?
depends on allergen dose and on aspects of the cellular immune activation that are difficult to quantify.
what are the risk factors for developing an IgE mediated allergic response to food ?
- Immature mucosal immune system
- Early introduction of solid food
- Hereditary increase in mucosal permeability
- IgA deficiency or delayed IgA production
- Birth by caesarean
- Gastrointestinal infection
what do most of the drugs available for allergies do ?
they only treat the symptoms of the allergy and not the cause
how are anaphylaxis reactions treated ?
with epinephrine , adrenaline
how do antihistamines work ?
they inhibit the effects of mediators on specific receptors and . as a result inhibit the synthesis of these mediators.
what do corticosteroids do ?
they decrease the general anti inflammatory effects.
what does de sensitisation therapy to which is done by injection of a specific allergen ?
they cause the induction of regulatory T cells ( Th2 ).
how do anti - IgE antibodies work ?
they bind to the IgE Fc region and prevent it binding tot he Fc on mast cells and causing activation
immediate hypersensitivities are mediated by antibodies , what are the delayed type hypersensitive responses mediated by like cellular hypersensitive reactions ?
Th1 cells and CD8+ cytotoxic T cells
how long does it take for the cellular allergic responses to occur ?
three to five days
what does celiac disease have features of?
both an allergic response and autoimmunity
what is the molecular response to gluten recognition in celiacs
The peptides normally produced from gluten do not bind to the MHC class II molecules. An enzyme tissue transglutaminase ( tTG) modifies the peptides so they can now be processed and bind to the MHC class II. The bound peptide then activates gluten specific CD4T cells. The activated T cells can kill mucosal epithelial cells by binding to Fas. They also secrete IFN gamma which activates the epithelial cell to produce cytokines and chemokines that recruit other inflammatory cells.
what is celiac disease entirely depend on ?
the presence of the foreign antigen, gluten. It is not associated with a specific immune response against self anti- gens in the tissue—the intestinal epithelium—that is damaged during the immune response. Thus, celiac disease is not a classical autoimmune disease. But it does have some features of autoimmunity
