Week 3 Flashcards
Hypersensitivity Reactions
- immune system going wrong
- sensitization of immune system by repeated exposure to allergen = immune reaction
Antigens = allergens
- harmless allergens to most people
- susceptible individuals, the immune system over-reacts
Most common hypersensitivity reaction
Type I
Type I hypersensitivity reaction + which antibody (2)
IgE mediated (most)
can by Th1 cell mediated (contact materials)
IgE mediated responses = which condition
Atopy
Atopic triad
- atopic asthma
- allergic rhinitis
- atopic dermatitis
Atopic disease
IgE mediated hypersensitivity
have one of the triad = more likely to have another
First exposure to allergen - type I hypersensitivity
the first exposure = sensitization
- produces IgE Abs to the allergen
Re-exposure to allergen - Type I
allergen binds to IgE Abs = activates mast cell = histamine and cytokines = allergic reaction
Type I hypersensitivity - inhalation (location, symptoms, atopic condition)
- repiratory tract (upper and lower)
- overproduction of mucous, sneexing, congestion, bronchial smooth muscle constriction
- rhinitis (hay fever) asthma
Type I hypersensitivity - injection (location, symptoms, atopic condition)
- skin, bloodstream
- local inflammation, systemic inflammation
- urticaria (hives), anaphylaxis
Type I hypersensitivity - Ingestion (location, symptoms, atopic condition)
- gastrointestinal tract
- intestinal smooth muscle constriction
- systemic inflammation - allergen enters blood
- gastroenteritis (vomit, diarrhea), anaphylaxis
Anaphylaxis - what
- medical emergency
- anaphylaxis is a severe potentilaly life threatening allergic reaction
- requires immediate attention’-
- edema, dispnea, widespread shock
Anaphylactic shock
- low blood pressure from dilation of blood vessels
- temporarily controled by epi injection
anaphylaxis - CNS symptoms
- lightheadedness
- loss of consiousness
confusion
headache - anxiety
Anaphyllaxis - respiratory symptoms
- SOB
- wheezes
- hoarsness
- pain with swallowing
Anaphylaxis- GI
- cramps abdominal pain
- diarrhea
- vomiting
Diagnosis of IgE hypersensitivity (3)
1) increased serum IgE levels
2) skin prick test or skin patch test
3) biopsy of GI tissue
Desensitization therapy
- allergy shots
- principle: divert immune response from IgE to IgG
- mechanism is unclear but seems to have something to do with different route of entry for the allergen
- side effects: redness, irritation at injection site, systemic reactions (less common more serious), throat swelling, wheezing, anaphylaxis, etc.
Hypersensitivity Type II - mediated by which antibody
IgG or IgM - cell surface antigens
Hypersensitivity type II - destroys allergen HOW (3)
- opsonization and phagocytosis
- antibody dependent cellular cytotoxicity
- complement activation
Opsonization
when a cell is tagged to make it more likely to be destroyed by phagocytosis
antibody dependent cellular cytotoxicity
IgG bonds to surface cells with antigen and attract killer T cells
complement activation
- complement system
- causes lysis of the antigen by attacking its membrane complex/phagocytosis
- recruitments of neutrophils and monocytes + enzymes = tissue damage
Rh incompatibility - hypersensitivity type II
- pregnancy if a woman has Rh - blood and her baby has Rh + blood
- mom’s body will react to babies blood as a foreign substance, create antibodies against it = don’t cause problems during first pregnancy, but cause problems to second and later pregnancies = attack blood cells = hemolytic anemia in baby
- prevent with immune globulin injections
Hypersensitivity III reactions - antibody
- immune complex mediated
- localized inflammation (complement system)
- produce damage when come into contact with vessel lining/deposited into tissues = inflammatory response, recruitment of neutrophils/inflammatory cells = injury to tissue
Hypersensitivity III reacitons - consequences
- vasculitis (seen in autoimmune disorders)
- kidney damage (acute glomerular nephritis)
Post streptococcal glomerulonephritis (6)
- body responds to nephrogenic streptococcus by forming these immune complexes with a human antibody
- immune complexes deposited into nephrons glomeruli/ in situ formation of antigen/antibody formation
- rapid deterioration of kidney function following glomerulonephritis
- children 1-2 weeks after sore throat/skin infection
- infiltration of neutrophils and other recruited cells = renal failure, acid base imbalance, HTN, electrolyte imbalance
- hematuria (tea coloured urine), edema, HTN
Type IV reactions - antibody?
cell mediated
Type IV hypersensitivity reactions
- cell mediated
- delayed (24 hours later)
- T cells are activated by antigens
- must be a previous exposure to amount a reaction to second exposure (ex poison Ivy)
- release cytokines that act on vascular endothelium = visible lesion on skin
Type IV hypersensitivity reaction - examples (2)
- Tuberculin skin test
- Poison Ivy
Self antigen
antigen expressed on your own cells
auto-reactive cells
- T or B cells that bind to a self antigen
Autoantibody
antibody that binds to a self-antigen
Immune tolerence
- self tolerence - delete self-reactive immune cells
Central tolerance
deletion of self-reactive T cells in the Thymus and B cells in the bond marrow are eliminated
Peripheral tolerance
maintenance of tolerance in secondary tissue (spleen and lymph nodes) = deletion of self-reactive cells via apoptosis, suppression of T cells that escape central tolerance
Autoimmune - defined
when the body loses self tolerance = attacks own cells
Factors that influence autoimmunity (3)
- genes
- environment (trigger)
- gender (mostly women)
environmental factors for autoimmunity (4)
- infection
- toxins
- stress
- food
infection and autoimmunity - strep EX
- antibodies for certain strep antigens can resemble self-antigens on heart + kidney = innflamation of heart and kidney
classification of autoimmunity (2)
- organ specific autoimmune diseases
- systemic autoimmune diseases
classifications can overlap
Organ specific autoimmune diseases + example
- target antigen present in a specific organ
- EX Grave’s disease, hasimotos, type I diabetes, Multiple sclerosis
Systemic autoimmune diseases + examples
- target an antigen present on many organs-
- EX: systemic lupus erethomatosis, rheumatoid arthritis
Grave’s disease - hyperthyroidism
- overactive thyroid
- immune system attacks thyroid = causes it to make more thyroid hormone than the body needs
- antibody = thyroid stimulating immunoglobbin = tells thyroid to make more hormone
Type I diabetes mellitus - autoimmune
- chronic autoimmune destruction of insulin producing beta cells
- islets of langerhans
- reduced insulin production = hyperglycemia
- not known what triggers this immune response (ex a trigger event, previous viral illness, clusters in different times of year)
Multiple sclerosis
myelin sheath of nerve fibres in brain and spinal cord destroyed by autoreactive T cells
- disease causes permanent damage and destruction to nerves
- inflammatory T cells trigger injury of axons and myelin sheath (autoimmune process)
Treatment for autoimmune disease (6)
- dependent on type of tissue involved, effect or mechanism involved, magnitude of disease process
- immunosuppression (NSAIDS, prednisone)
- plasmapheresis (remove antibodies) = temp fix
- block MhC with similar peptide (mimic)
- use antibodies that block B cells and/or T cells
- disease-specific treatments (insulin for T1D, joint replacements for rheumatoid arthritis)
