Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
43 Cards in this Set
- Front
- Back
|
What is hypersensitivity?
|
exaggerated or aberrant immune response to an antigen resulting in inflammation and tissue damage
|
|
|
What are hypersensitivity disorders?
|
disorders that are caused by aberrant immune responses
|
|
|
What is the most common disorder of immune system. Affects ~20% of population.
|
Type I Hypersensitivity
- often referred to as allergy or atopy. - occurs within min. after reexposure to antigen. - |
|
|
What antibody is involved with Type I Hypersensitivy?
|
IgE; Rapid IgE and mast cell mediated vascular and smooth muscle reaction that is often followed by inflammation.
- reaction affect various tissues depending on the route of Ag entry |
|
|
What are some examples of Type I hypersensitivity?
|
hay fever, food allergies, bronchial asthma, anaphylaxis
|
|
|
What is the general sequence of events in Type I hypersensitivity?
|
1 - production of IgE Ab.
2 - Binding of IgE ab to Fc receptors on mast cell 3 - Cross linking of bound IgE upon reexposure to Antigen. 4 - release of mast cells mediators |
|
|
What are the immediate effects of type I hypers.
|
5 - dilation of blood vessels, increased vascular permeability, smooth muscle contractions (BP drops)
|
|
|
What is the LAte response following immediate response in type I hypersens.
|
Inflammation (late reaction)
|
|
|
What is happening during the immediate response? be specific.
|
*vasoactive amines (histamine and serotonin) and proteases
- synthesis and secretion of *lipid mediators (prostaglandins and leukotrienes) |
|
|
What is happening during the last-phase rxn? be specific.
|
Synthesis and secretion of *cytokines (eg: TNFa, IL-4, IL-5, GM-CSF) and *chemokines (MIP-1a)
- infiltration of eosinophils, monocytes, and neutrophils |
|
|
Airways are protected by tight junction...so how do the dust mites get into to activate mast cell?
|
Der p 1 (of dust mite) is a protease that cuts the Tight junction and stimulates DC for APC and Th2 priming -> activate mast cell and triggers mast-cell degranulation
|
|
|
What are all clinical and pathologic features of immediate hypersensitivity reaction driven by?
|
mediators produced by mast cells
|
|
|
T/F Mediators produced in different amount and in diff. tissues are responsible for different immediate hypersensitivity syndromes.
|
true
|
|
|
The most sever form of immediate hypersensitivity is?
|
anaphylaxis
|
|
|
How do you treat Type I hypersensitivity?
|
if life threatening: epinephrine, theophylline for bronchial constriction - relaxes resp. tract
Cromolyn - blocks activity of mast cells desensitization to treat seasonal allergies (give tiny amount of allergy = desensitization) antihistamines = to decrease inflammation Corticosteroids for inflammation |
|
|
What ab is Type II sensitivity mediated by?
|
IgG
Occurs when host ab binds foreign Ag on cell surfaces or binds self Ag. - leads to the destruction of cells, inflammation, or interfere with normal cellular function. |
|
|
The diseases of Type II usualy are induced by foreign Ag. Explain Hemolytic Disease of the Newborn
|
maternal ab's targe fetal RBC's for destruction
- another ex: transfusion reactions - hemolytic anemia: drug binds RBC surface and serves as a target for anti-drug IgG ab |
|
|
Blood Transfusions Reactions can indcue Type II Hypersensitivity, how?
|
A, B, AB, O blood group antigens defined on basis of GLYCOPROTEINS ON RBC's. Ab's that react to blood groups are alwyas present. During transfusion from an incompatible donor, antibodies react against donor cells, and trigger complement activation, phagocytosis and inflammation.
|
|
|
What is a type II disease against SELF antigen?
|
Graves Disease - TSH receptor ab's stimulate TSH receptor to over produce thyroid hormone.
Myasthenia Gravis - Ach receptor ab's bind to and block the Ach receptor |
|
|
What therapeutic strategies for Hemolytic anemia, HDNB, and Graves, and MG?
|
Hemolytic Anemia: drug avoidance
HDNB: Anti-Rh Ab Graves Disease: radioactive iodine, anti-thyroid drugs, or thyroid removal Myasthenia Gravis: cholinesterase inhibitors and corticosteroids |
|
|
The 'basic' of Type II is: Host ab binds foreign ag on cells surfaces or binds self ag - and the ab assoc. with it is?
|
IgG
|
|
|
What ab does Hypersensitiivy III involve?
|
IgG
|
|
|
What is the main problem with Type III?
|
Type III Hypersensitivity/ Immune-Complex mediated: Ag-ab complexes clump and deposit in blood vessels or tissues attracting an acute inflammatory reaction.
|
|
|
What is an immune complex?
|
a complex consisting of an ag bound to it's specific ab
|
|
|
Larger aggregates fix complement and are cleared from circulation by phagocytes, but small complexes form in Ag excess deposit in ?
|
vessel or tissue - pathogenic potential determined by size, amount, affinity, and ab isotype
|
|
|
Where do the deposits generally accumulate?
|
at site where antigen is localized or at sites of turbulence* (vessel branches) or high pressure - so it can't get fixed.
thus, immune complex disease sometimes manifest as vasculitis, arthritis, or nephritis |
|
|
What are the 3 mechanisms of how immune complexes trigger inflammation?
|
1 - mast cell activation
2 - macrophages release TNFalpha and IL-1 that induce the inflammatory response 3 - C3a and C5a. - stimulate mast cells to release more histamine, serotonin, and chemotactic factors-attracts monocytes, neutrophils, and other leukocytes - cells bearing Fc receptors for IgG and IgE may be crucial for ab complex mediated hypersensitivity. |
|
|
What is the arthus rxn?
|
triggered in skin by IgG - immune complex formed there and local inflammatory rxn, with vascular perm. fluid and cells enter site
|
|
|
What is serum sickness and how is it type III?
|
is an classic example of transient immune complex -mediated syndrome
-caused by injection of foreign protein - so if given drug with ag that body can't handle - and 7-10 days later symptoms occur. ex: Antivenin (serum from horses immunized with snake venoms) Anti-lymphocyte globulin - an immunosuppressive agent used for transplant recipients... antibiotics (penicillin) Strepokinase (a bacterial enzyme) |
|
|
What type III hypersensitivity disease has IgG ab against ubiquitous self Ag in all nucleated cells
|
SLE - LUPUS
|
|
|
What are the therapeutic strategies for Serum sickness and LUpus?
|
serum sickness: drug avoidance, antihistaines, corticosteroids, etc...
Lupus: NSAID's corticosteroids, immunosuppressive agents, etc... |
|
|
Basic of Type III Hypersensitivity is: Type III hypersensitiviy/Immune complex mediated: Ag-ab complexes clump and aggregate near blood vessels attracting an acute inflammatory rxn. and uses what ab?
|
IgG
Immune Complex ex diseases: transient: serum sickness self ag: lupus (SLE) |
|
|
What Type of Hypersensitivity is cell mediated?
|
Type IV. : mediated by Ag specific T cells which induce macrophage infiltration in a sensitized indvidual. - DTH response to injected or absorbed Ag
2-3 days |
|
|
What is DTH?
|
Delayed Type Hypersensitivity - as the reaction takes 2-3 days to develop. Not antibody mediated but T cell mediated
Macrophages, CD8 T cells, and NK cells are impt. effector cells in the DTH response Activated CD8 cells destroy target cells on contact EX: TB test |
|
|
What are the 4 ways to contract TypeIV Hypersensitivity?
|
Tuburculin Type Hypers. - injected into the skin
Contact Hypersensitivity - absorbed by the skin' Chronic asthma - inhaled Granulomatous inflammation - indigestbible foreign material |
|
|
Explain the TB test and type IV hypersens.
|
Sm. amts of tuberculin are injected intradermally - within 24-72 hours T cell-mediated inflammatory rexn evolve in ind. previously exposed to M. TB.
- the response is mediated by Th1 cells and infiltrating inflammatory mediators, causing visible swelling. |
|
|
What is the major DTH Mechanism of Ag presentation?
|
Antigen is process by tissue macrophages and stimulates Th1 cells -> chemokines, cytokines, and cytotoxins.
|
|
|
Explain Contact Hypersensitivity?
|
absorbed in skin
- typically are highly reactivate sm. molecules (hapten) copmlexed with skin proteins and become internalized by APC's in the skin. - expecially if they cause itching that leads to scratching (poison ivy) can be elicited by either CD4 (helper) or CD8 (CTOXIC) cells -- inflammation occurs as a result of the inflammatory response initiated by T cells - 2 pahses of contact hypersensitivity - sensitization and eliciation |
|
|
What is the diff. between the sensitzation and elicitation phase of contact hypersensitivity?
|
sensitization: occurs during first exposure to Ag - takes 10-14 days to develop. - Langerhan's cells in skin (apc of the skin ) take up ag and present to T cells
Formation of CD4+ T cells memory t cells specific for the ag. ELICITATION: upon reexposure to Ag - develops within 24-48 hrs. - involves LC ag presentation to memory T cells at site of Ag entry - T cells release IFNgamma and pro-inflammatory cytokines, cytokines recruit macrophage, CTL, NK and other effector cells. |
|
|
Explain Chronic Asthma>
|
Mast cell degranulation leads to - *Th2* - (IL-5) and eosinophil influx.
Eosinophils activate and degranulate -> damaging tissue, and recrutiing more cells Chronic inflammation can cause irreversible damage and death |
|
|
*Explain Granulomatous Inflammation/Chron's Disease - has relevance to dentistry
|
Type of Inflammatory Bowel Disease (IBD) of the terminal ileum -
chronic inflammation ofthe bowel mucosa lesions, abdominal pain, diarrhea, rectal bleeding, weight loss, fever thought to be due to unresolved DTH Initial presentation may be in oral cavity and pharynx - 6% present with oral lesions at some time |
|
|
What therapeutic strategies are given for
TB Test injection Contact Hypersens. Chronic Asthma Crohn's Disease |
TB: self limiting
Contact Hyper: limit exposure, corticosteroids, antihistamines Chronic asthma: corticosteroid, bronchodilators, cromolyn, etc... Crohn's Disease: corticosteroids, immunosuppressants, etc... |
|
|
The "basics" of Type IV include:
Cell mediated rxn - mediated by ag specific T CELLS which induce macrophage infiltration in a sensitized individual. - DTH response to injected or absorbed ab 2-3 days later see symp. What are the ex. given in class? |
Ex: TB test, contact hypers. chronic as., and crohn's
|
