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39 Cards in this Set
- Front
- Back
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Is it possible to be hypersensitive to an antigen without previous exposure?
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No; you have to have been exposed to an antigen at least once before your body can become hypersensitive to it.
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What is the most significant way Type 4 hypersensitivity is different from types 1-3?
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Type 4 is carried out by T cells and mediators rather than antibodies. It is also delayed in its response.
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What type of reaction is involved in Type 1 hypersensitivity?
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Allergic; if severe enough, can cause anaphylactic shock. Type 1 is also the fastest reaction.
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What are the 3 main immune players involved in a Type 1 hypersensitivity response?
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1. mast cells
2. eosinophils 3. IgE (also basophils) |
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Atopic animals (Type 1)
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Produce excessive amounts of IgE, making them prone to allergies. Certain breeds are pre-disposed (terriers, dalmatians, Irish setters)
React strongly to antigen w/ Th-2 response--Th-2 produces IL-4, which increases antibody class switch to IgE Genetic predisposition (were parents atopic?) Excess IgE attaches to and coats mast cells |
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Mast cells in Type 1
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Allergen binds to IgE on surface of mast cell and cross-links IgE molecules. This stimulates the cell to degranulate, secreting heparin + histamine.
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Effects of mast cell granules (Type 1)
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INFLAMMATION
Increase capillary permeability--> swelling/edema Vasodilation--> increased blood flow to site--> redness/heat Smooth muscle constriction--> can cause respiratory or gastrointestinal distress Stimulate secretions like mucous, saliva, tears; liquid in intestine Irritate nerve endings--> pruritis (itching) Chemotaxis of eosinophils |
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Eosinophils (Type 1)
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Degranulate at reaction site and contain more inflammatory substances
Secrete IL-4 and cytotoxic substances that kill bacteria |
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Local allergic reactions (Type 1)
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Very fast--degranulation within seconds and clinical signs within minutes
Severity of clinical signs depends on site of reaction Ex: skin = less severe Upper respiratory = more severe (wheezing, increased secretions) Intestinal tract = more severe (spastic contraction of smooth muscles--> pain, colic; diarrhea from increased secretions) |
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Systemic allergic reaction (Type 1)
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If mast cells are stimulated all over body (i.e. from intravenous injection of an allergen), body can go into anaphylactic shock
Primary concern = constriction of smooth muscles of large vessels (pulmonary vein, aorta, etc.)--> blood flow stops---> animal must be treated within minutes or it may die Constriction of bronchi Increased urination, diarrhea |
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Epinephrine (Type 1)
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Used to reduce anaphylactic shock
Relaxes smooth muscles, restores breathing, counter-acts vasodilation of capillaries |
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Testing for allergies
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Skin test
Inject a small amount of antigen intradermally Wheal & Flear reaction If IgE present, inflammation, red skin If no inflammation, no IgE, no allergy |
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Treatment for allergies
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Best treatment is avoidance of allergen
Antihistamines prevent allergic reactions, but do not work well in treating an ongoing reaction Corticosteroids inhibit an allergic reaction by suppressing the immune system Desensitization therapy (i.e. allergy shots) --used if allergen cannot be removed from animal/environment of animal --serial injections of antigen administered to animal --very small amount of antigen injected every 3-4 days for a long period of time --Th-2 response switches to Th-1 --Th-1 stimulates B cells and B cells stop producing IgE/class-switch |
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What type of reaction is involved in Type 2 hypersensitivity?
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Cytotoxic
The immune response (antibodies) kills normal cells. |
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What are the 2 main immune system players in Type 2?
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IgM + IgG
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Blood Types (Type 2)
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RBCs have proteins on membranes called blood group antigens, or erythrocyte antigens (EA)
There are differences in RBC proteins among individuals of the same species--they have the same function but are different in structure. There are also differences between different species. Different protein types are inherited |
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Blood transfusion w/ compatible donor (Type 2)
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Donor and recipient have same blood group-->no immune response
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Blood transfusion w/ incompatible donor without having had a previous transfusion (Type 2)
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Without previous transfusion of donor's blood type, there are no natural antibodies in existence, so incompatible blood type is accepted at first--primary immune response takes time.
By day 10-20, antibodies against the incompatible blood group are made, but by that time, all of the donor RBCs are gone. Thus, transfusion can be successful. |
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Blood transfusion w/ incompatible donor type that recipient HAS had previous exposure to (previous transfusion) (Type 2)
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Antibodies against donor blood type are already present in the body, so secondary immune response is launched.
Antibodies form Complement --Activated/Fixed: cause mast cells to release chemicals from granules--> lysis of incompatible RBCs--> anemia --Inactivated: opsonization of incompatible RBCs--> removed from circulation via phagocytosis of macrophages in spleen + liver (Kuppfer cells)--> clotting/anemia All RBCs transfused are quickly destroyed (most likely by lysis) Outcomes: Hemoglobinuria-- hemoglobin from lysed RBCs accumulate in kidney + urine--> hemoglobin is toxic to kidney cells Hemoglobinemia-- free hemoglobin in blood Anaphylactic shock due to chemicals released from mast cells-- very difficult to reverse |
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Pre-existing natural antibodies to a blood type prior to a transfusion (Type 2)
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Certain viral, protozoan, or helminth infections have antigens that are similar to proteins on RBC (allows some infectious agents to avoid the immune system)
May cross-react w/ incompatible blood groups |
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Cross-Matching Test (Type 2) for blood transfusions
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Wash down RBCs from donor and remove the serum components via light suspension
Mix with sample of recipient RBCs in vitro --if no antibodies, nothing happens--> donor match --if antibodies present, lysis (via C') or agglutination (RBCs clump) within 30 minutes--> donor incompatible |
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Cross-Matching in horses (Type 2)
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RBCs might have antibodies, but they may not cross-link with each other--> no lysis or agglutination--> false negative
This does NOT mean there won't be a reaction in the body--additional testing required Coomb's Test (antiglobulin test) --additional reagent used: anti-equine immunoglobulin antibodies If antibodies present, will cross-react--> linkage/clumping within 15-20 minutes |
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Hemolytic disease of newborns (neonatal isoerythrolysis) (Type 2)
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Occurs if mother has antibodies to newborn's RBC type
Antibodies consumed by newborn via colostrum--> lyse offspring's RBCs Very similar reaction to that of an incompatible blood transfusion Anemia--> lethargy Hemoglobinurea--> collapses quickly Common in horses |
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Why does the mother have antibodies against her newborn's blood group in the case of neonatal isoerythrolysis?
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During parturition, there is trauma and mother is exposed to RBCs of newborn. This is not a problem with her first offspring as colostrum is gone before she is able to produce antibodies.
If second offspring has the same blood group as the first, it may be affected. It may take several offspring to develop enough antibodies to do harm |
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Test for hemolytic disease (Type 2)
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Coomb's test
Take a sample of serum from mother and RBCs from father Esp. important prior to breeding |
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Who would make a good donor for the anemic foal?
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NOT sire--father has same blood group as foal so RBCs would still be attacked
Dam is good donor because she does not make antibodies against her own RBCs. Mother's blood must be washed first to prevent transfer of more antibodies. Discard the plasma and re-suspend the RBCs in saline, then transfuse |
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RBC destruction due to drugs
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Some drugs stick to RBCs when they're metabolized.
If animals have antibodies against drug metabolites, RBCs are destroyed along with antigen on drug when immune complex forms. So, need to start transfusion slowly if drug is still in system. Stop if clumping develops. Very difficult to reverse this reaction |
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RBC destruction due to some viral infections
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Viruses stick to RBCs. Antibodies against the virus also destroy RBCs when immune complex forms.
Ex: Equine Infectious Anemia |
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3 immune players of Type 3 Hypersensitivity
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1. IgM
2. IgG 3. Neutrophils |
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Cause of Type 3 hypersensitivity
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Excessive formation of immune complex (Ag + Ab)
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Local Type 3 reaction
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Arthus reaction
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Inflammation of tissue (Type 3)
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Excessive immune complexes activate C'
By-products of C' activation have inflammatory effects--> dilate capillaries--> increased permeability of capillaries--> swelling/edema, and attract neutrophils Neutrophils release proteolytic enzymes at site--> tissue destruction --If severe, thrombo (small blood clot) formation--> tissue destruction/necrosis? (ex: cat ear tip falls off) Macrophages may follow neutrophils |
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Speed of Type 3 hypersensitivity reaction
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Slower reaction--signs occur within 1 hour
[vs. Type 1--attracts eosinophils, signs occur within minutes] |
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Glomerulonephritis (Type 3)
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Immune complexes can get stuck or deposit in glomeruli of kidneys
Depending on size of immune complex--can get stuck in different parts of the glomerulus or produce different types of lesions If antigens are circulating for too long (prolonged antigenemias), they can alter the function of the glomerulus via: --deposit in basal membranes of glomerulus, causing them to become thickened --stimulate endothelial cells in glomerulus to proliferate --cause Mesangial cells to proliferate |
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Immune complexes deposit in vessels (Type 3)
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Inflammation of vessels
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Immune complexes deposit in joints (Type 3)
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Arthritis
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Immune complexes stick to (Type 3): RBCs, thrombocytes, lymphocytes
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RBCs--> anemia
Thrombocytes--> clotting Lymphocytes--> decreased # of lymphocytes in circulation (lymphopenia) |
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Do Type 3 reactions permanently damage organs?
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They can cause permanent damage to these organs but most of the time they are able to recover
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Mechanism of Type 3 reaction (general)
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Inject Ag into dermis--> local Type 3 hypersensitivity
Ab to Ag is circulating (IgM + IgG) Some Ag will diffuse and come in close contact with capillary--Ab in circulation increase permeability and will pour into site where Ag is More C' is fixed--> more neutrophils attracted to site--> more inflammation (excluding smooth muscle contractions) |
