Hypersensitivity Flashcards
undesirable reactions produced by the normal immune system, including allergies and autoimmunity
Hypersensitivity
type I hypersensitivity
immediate, atopic, anaphylactic
type II hypersensitivity
antibody dependent
type III hypersensitivity
immune complex
type IV hypersensitivity
cell mediated or delayed type of hypersensitivity
also known as immediate or anaphylactic
hypersensitivity
Type I hypersensitivity
what are the reactions involved in type I hypersensitivity?
Skin (eczema), Eyes (conjunctivitis), Nasopharynx (rhinorrhea, rhinitis), Bronchopulmonary tissue (asthma), Gastrointestinal (gastroenteritis)
the range of symptoms in type I hypersensitivity?
minor inconvenience to death
the reaction takes ? from the time of exposure to the antigen in type I
15-30 minutes
type I delayed onset
6-8 hours
late phase reaction
leukotrienes
type I is mediated by ? antibody
IgE
primary cellular component in type I is?
Mast cell and Basophil
reaction is amplified and/ or modified by ? in type I
Platelets, Neutrophils and Eosinophils
? stimulated and release histamine?
Mast cells
mast cells stimulated and release ?
Histamine
are non-parasite antigens that can stimulate a type I hypersensitivity response
Allergen
term for the genetic trait to have a predisposition for localized anaphylaxis
Atopy
mechanism of type I
induce the synthesis of IgE then binds on surface of mast cell then reintroduced antigen interacts with IgE on mast cell causing cells to degranulate and release large amounts of histamine
produced by TH2 and upregulate production of IgE
IL-4
produced by TH1 and downregulate production of IgE
IFN-gamma
which mediator of type I
smooth muscle contraction & binds to the receptors on endothelial causes separation of junctions, increasing permeability
H1 receptors
which mediator of type I
mucus secretion and vasodilation
H2 receptors
which mediator of type I
Increases fluid secretion and peristalsis (diarrhea and vomiting)
degranulation in gastrointestinal tract
which mediator of type I
decrease in airway diameter (CONSTRICTION OF SMOOTH MUSCLE AROUND THHE BRONCHI, anaphylaxis) and mucus secretion
degranulation in lungs
which mediator of type I
increase blood flow and vascular permeability, causing edema
degranulation in along blood vessels
which mediator of type I
causes prolonged constriction of SM
Leukotrienes
which mediator of type I
can cause bronchoconstriction
Prostaglandins
? do not die
mast cells or basophils
? regenerate and synthesize new granules
degranulated cells
diagnosis for type I
prick and intradermal test (skin) and measurement of total IgE (measured by ELISA)
treatment for type I
Drugs
* non steroidal-inflammatories block histamin receptors
* antihistamines
* steroids
* Theophylline OR epinephrine -prolongs or increases CAMP levels in mast cells which inhibits degranulation
Immunotheraphy
* Desensitization (hyposensitization) also known as allergy shots
* Repeated injections of allergen to reduce the IgE on Mast cells and
produce IgG
- Over an extended period, injecting increasing dose of allergen
- Epi
vasoconstrictor, also relaxes SM
Epi
aka cytotoxic hypersensitivity and may affect variety of organs and tissue
type II
exogenous chemicals which can attach to cell membranes can also lead to type II
Haptens
diseases in type II
Drug-induced hemolytic anemia, granulocytopenia and thrombocytopenia and penicillin allergy
reaction time of type II
minutes to hours
type II is primarily mediated by antibodies of the?
IgM or IgG
rhogam ? of ? and after delivery within ?
28 weeks of gestation, 72 hours
diagnosis of type II
biopsy by immunofluorescence and staining pattern is normally smooth and linear, such as that seen in Goodpasture’s nephritis
treatment of type II
anti-inflammatory and immunosuppressive agents
type III is primarily mediated by?
IgG although IgM may also be involved
if the large amount of antigen and antibody complexes in the blood are not eliminated what will happen?
they can deposit in capillaries or joints and trigger inflammation
immunized rabbits with horse serum by repeated intradermal
reaction
Arthus
signs and symptoms of type III with horses for diphth and tetanus (HETEROLOGOUS SERUM)
antisera made with horses for diphth and tetanus (HETEROLOGOUS SERUM)
in type III the reaction may take?
3-10 hours after exposure
chronic bacterial, viral or parasitic infections
exogenous antigens
non-organ specific autoimmunity: e.g., systemic lupus erythematosus, SLE
endogenous antigens
? bind to immune complexes via FcR and phagocytize the complexes
polymorphonuclear leukocyte and macrophages
polymorphonuclear leukocyte and macrophages bind to immune complexes via FcR and phagocytize the complexes BUT if unable to phagocytize the immune complexes it can cause?
inflammation via C activation (C3a, C4a, C5a)
treatment for type III
anti-inflammatory agents
diagnosis of type III
examination of tissue biopsies for deposits of immunoglobulin and complement by immunofluorescence microscopy
pileup of pre-formed immune complexes on the basement membrane leads to lumy-bumpy deposits
serum-sickness
reaction involves sensitized T-cells
type IV
mediated by cells rather than abs
type IV
release cytokines to activate macrophages causing inflammation and tissue damage
Th1 cells
Continued macrophage activation can cause?
chronic inflammation resulting in tissue lesions, scarring, and granuloma formation
response time for type IV starts after?
48-72 hours
ARE ACTIVATED BY IF-GAMMA &TNF-BETA
macorphages
what activates macrophages?
IF-GAMMA &TNF-BETA
in VIVO diagnostic test for type IV?
cutaneous reaction (montoux) test and patch test (contact dermatitis)
in VITRO diagnostic test for type IV?
mitogenic response, lympho- cytotoxicity and IL-2 production
treatment of type IV
corticosteroids and immunosuppressive agents
edema, serum into tissue
wheal
erythema, dilation of BV
flare
another diagnostic test for type IV?
wheal and flare for 10-15 mins
aka allergy shots
desensitization
prolongs or increases CAMP levels in mast cells which inhibits degranulation
Theophylline or Epinephrine
