Microbio-final-lect 2 (nov17) – Flashcards
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| Hypersensitivity |
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| Any immune response against a foreign antigen exaggerated beyond normal |
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| The 4 types of Hypersensitivity |
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| Type I (immediate, anaphylactic) Type II (cytotoxic) Type III (immune-complex mediated) Type IV (delayed or cell-mediated) |
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| Allergies |
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| (stimulated by antigens --> allergens = allergic antigens) |
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| Relationship: allergies and antigens |
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| allergies are localized or systemic reactions that result from release of inflammatory molecules in response to an antigen |
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| Time it takes for allergies to develop |
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| Develop within seconds or minutes following exposure to antigen |
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| Specific Antibody associated with allergies |
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| Antibody involved is IgE |
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| Cells involved withType I (immediate, anaphylactic)? How? |
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| Th2 is involved in Type I. Th2 puts out IL-4 and stimulates B cell. B cells becomes plasma cell, which secretes IgE. |
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| Relationship: TH2, IL-4, B-cells, plasma cell and IGe |
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| Th2 is involved in Type I. Th2 puts out IL-4 and stimulates B cell. B cells becomes plasma cell, which secretes IgE |
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| Mast cells |
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| Found in sites close to body surfaces e.g. skin, intestinal walls, and airways. |
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| Process of an allergic reaction |
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| Th2 puts out IL-4 and stimulates B cell. B cells becomes plasma cell, which secretes IgE. IgE bends to mast cells, basophils, and eosinophils. Now cells are sensitized, or primed. Degranulation then occurs, and allergic reactions take place. |
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| Mast cells: features |
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| large granules in cytoplasm ? Granules contain a mixture of potent inflammatory chemicals |
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| Mast cells released during degranulation |
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| Histamine, kinins and Proteases |
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| Fnx: Histamine, Kinins and Proteases |
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| (all are mast cells that are involved in degranulation) Histamine - smooth muscle contraction, increased vascular permeability and irritation Kinins - smooth muscle contraction, inflammation and irritation Proteases - damage tissue and activate complement |
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| Mast cells that are synthesized in response to inflammation |
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| Leukotrienes and Prostaglandins |
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| Fns: Leukotrienes and Prostaglandins |
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| (both are mast cells that are synthesized in response to inflammation) Leukotrienes - slow, prolonged smooth muscle contraction Prostaglandins - some contract smooth muscle, others relax it |
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| Basophils |
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| Granules filled with inflammatory chemicals similar to chemicals in mast cells |
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| Basophils: fnx |
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| *(sensitized basophils)-bind IgE and degranulate in same way as mast cells. |
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| Eosinophils |
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| Granules that contain inflammatory mediators and leukotrienes that contribute to the severity of a hypersensitivity response (allergic reaction) |
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| Relationship: Mast cells and Eosinophils in hypersensitivity response |
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| Mast cell degranulation stimulates the release of eosinophils. Which migrate to the site of mast cell degranulation where eosinophils degranulate. |
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| A form of allergic rhinitis is also known as? |
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| Hay Fever = allergic rhinitis |
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| Typical severity of Type I hypersensitivity reactions |
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| usually mild and localized |
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| Site of reactions is dependent upon |
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| Portal of entry |
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| Inhaled allergens may cause |
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| hay fever (allergic rhinitis) |
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| Type I hypersensitivity - upper respiratory tract response (distinguish signs and symptoms) |
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| watery nasal discharge (sign) sneezing (sign and symptom) and excessive tear production (sign and symptom) itchy throat and eyes (symptom) |
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| The etiological agents of Upper Respiratory response |
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| Etiologic agents: mold spores, pollens, flowering plants, some trees, and dust mites |
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| Inhaled allergens that are small and can reach lungs may cause |
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| asthma - lower respiratory tract response |
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| Lower Respiratory response: Signs/Symptoms |
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| Signs/symptoms: wheezing, coughing, excessive mucus production, and constriction of smooth muscles of bronchi |
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| Ingested allergens (examples) |
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| Ingested allergens - foods e.g. strawberries, peanuts, shellfish, cow's milk |
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| Food allergies: |
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| Signs/symptoms: diarrhea, uticaria (wheal and flare) = hives and other GI signs and symptoms e.g. swollen lips, abdominal cramps, nausea ? Peanuts and shell fish can cause anaphylaxis |
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| What causes anaphylaxis |
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| food allergies to: Peanuts and shell fish |
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| A skin allergen (Type 1) aka: |
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| Local dermatitis |
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| Eczema |
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| Eczema (atopic dermatitis) - elevated IgE levels, reddened skin rash, and periodic intense itching. Causative allergen unclear. |
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| Type 1 skin hypersensitivity produces? how? |
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| Produces uticaria - due to release of histamine and other mediators into nearby skin and tissue and serum leakage from blood vessels |
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| Treatment of Type I Hypersensitivity |
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| Administer drugs that counteract inflammatory mediators released by degranulation |
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| Treatment for Asthma |
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| treated with inhalant containing corticosteroid and bronchodilator |
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| Antihistamines Fnx: |
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| neutralize histamine |
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| What does Epinephrine do |
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| Epinephrine (adrenalin, bronchodilator, adrenergic antagonist) - neutralizes many of the mechanisms of anaphylaxis |
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| How does Epinephrine alleviate asthma |
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| Relaxes smooth muscles and reduces vascular permeability |
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| When is Epinephrine |
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| Used in emergency treatment of severe asthma and anaphylactic shock |
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| Epinephrine replacements |
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| albuterol and salmeterol |
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| Describe Type 2 (cytotoxic response) |
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| Results when an immune response destroys cells. Often due to combined activities of complement and antibodies. |
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| 2 examples of Type 2 (cytotoxic) immune response |
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| 1. Destruction of RBCs following incompatible blood transfusion 2. Rh System and Hemolytic Disease of Newborns |
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| Blood types (4): |
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| Blood types A, B, AB, O |
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| Describe interaction of blood types and what permits multiple interaction? |
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| Blood type A can receive from type A or O, type B can receive from B or O, type AB can receive from A, B, AB, or O, type O can receive from O. • Cannot receive blood for other blood types due to antibodies present that fight against foreign blood types. |
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| Cause of Type 3 immune response |
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| Due to formation of antigen-antibody complexes = immune-complexes |
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| Type III (immune-complex mediated): systemic related conditions |
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| Systemic lupus erythematosus (SLE) ? Rheumatoid arthritis (RA) |
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| Type III (immune-complex mediated): localized related conditions |
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| Hypersensitivity pneumonitis Glomerulonephritis |
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| Hypersensitivity pneumonitis |
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| Individuals become sensitized upon antigen inhalation deep into lungs --> stimulating antibody production |
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| Hypersensitivity pneumonitis: allergen examples |
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| Allergens e.g. mold spores (from moldy hay, mushrooms), dust from pigeon feces or old books ? Subsequent inhalation of same antigen stimulates immune complex formation --> complement activation |
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| Glomerulonephritis |
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| ( type 3) Deposition of immune complexes circulating in bloodstream glomeruli (small blood vessels in kidneys) walls ? Damage to glomerular cells impedes blood filtration ? Result: kidney failure and ultimately death |
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| Type IV (delayed or cell-mediated) |
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| Inflammation resulting from contact with certain antigens occurring after 12-24 hours |
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| Type IV (delayed or cell-mediated): result from which specific interactions |
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| Results from interactions of antigens, APCs, and T cells ? Delay in response reflects time macrophages and T cells take to migrate and proliferate at site of antigen location |
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| Type IV (delayed or cell-mediated): 4 examples |
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| 1.Tuberculin response 2.Allergic contact dermatitis 3.Graft rejection 4. |
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| (Tuberculin response) *Type 4: An Individual never infected or vaccinated will display what type of response? |
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| no response when tuberculin injected to skin |
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| (Tuberculin response) *Type 4: An Individual - past exposure |
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| Red, hard swelling = induration surround by erythema develops |
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| Allergic contact dermatitis |
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| Cell-mediated immune response --> intensely irritating skin rash ? Response triggered by chemically modified skin proteins (foreign to body) |
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| Allergic contact dermatitis: example |
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| Can occur when hapten e.g. oil (from poison ivy and related plants) binds to proteins on skin |
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| Allergic contact dermatitis: what occurs in severe cases |
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| Severe cases - Tc cells destroy so many skin cells that develop acellular, fluid-filled blisters |
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| Allergic contact dermatitis: examples of haptens |
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| haptens - formaldehyde, cosmetics, metal jewelry - containing nickel, chrome, and latex (gloves) |
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| Allergic contact dermatitis: treatment drug |
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| Can be treated with corticosteroids |
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| Type 1 examples **less than 30min before clinical signs** |
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| anaphylatic shock from drug injections and insect venom common allergic conditions: hay fever and asthma |
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| In terms of portal of entry: Systemic vs. Local anaphylaxis |
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| Systemic: usually via injection Local: usually ingested (food) or inhaled (pollen) |
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| Type 2 (cytotoxic reactions) usually involve which two types of antibodies: |
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| IgG or IgM |
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| The most common cytotoxic hypersensitivity reactions are: |
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| transfusion reactions (involving blood) |
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| Individuals with Type A have what antibodies? |
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| anti-B antibodies |
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| Individuals with Type B have what antibodies? |
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| Anti-A bodies |
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| Individuals with Type O have what antibodies? |
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| both A and B antibodies |
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| Individuals with Type AB have what antibodies? |
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| no antibodies to either A or B |
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| Rh+ |
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| those that posses the antigen |
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| Rh- |
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| those that lack the RBC antigen |
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| What will occur if blood from an Rh+ donor is given to an Rh- recipient? |
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| the donor's RBC's stimulate the production of anti-Rh antibodies in the recipient. If the recipient then receives Rh+ RBCs in a subsequent transfusion, a rapid, serious hemolytic reaction will develop. |
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| Describe the interaction of an Rh+ child and a Rh- mother |
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| The Rh- mother can become sensitized to this antigen during birth when the placental membranes tear and the fetal Rh+ RBCs enter the maternal circulation, causing the mother's body to produce anti-Rh antibodies of the IgG type |
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| Describe the interaction of an Rh+ child and a Rh- mother of a subsequent pregnancy |
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| the mothers anti-Rh antibodies will cross the placenta and destroy the fetal RBCs. The fetal body responds to this immune attack by produing large numbers of immature RBCs called erythroblasts (aka Hemolytic disease of the newborn). **IgG antibodies cross the placenta and destroy fetal RBCs |
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| Hemolytic disease of the newborn can cause the child to develop which conditions at birth |
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| stillbirth or jaundiced child (severe anemia) |
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| If father and mother are Rh+ and child is +/-, (1st child)- will there be hemolysis |
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| no hemolysis |
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| If father is +, mother is -, and child is +: hemolysis? 1st child? 2nd child? |
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| no hemolysis for 1st child, but yes for 2nd child and subsequent children. |
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| Prevention of hemolytic disease of newborn |
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| Administration of anti-Rh serum (Rhogam) to Rh negative pregnant women |
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| Would Rh- or + women receive anti-Rh serum (Rhogam) |
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| Rh- |
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| Describe RhoGAM (anti-Rh immune globulin) and what it prevents |
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| administered to at risk mother at 1st pregnancy - within 1st 24-72 hours (preferable within 1st few hours) after delivery or abortion of Rh positive child ? Helps activate and remove fetal Rh+ cells before mother's immune system can react and she becomes sensitized ? Destroys any fetal RBCs that entered maternal body ? Sensitization of mother does not occur and subsequent pregnancies are safer |
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| The primary antigens involved in Type 3 (immune complexes) |
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| IgG |
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| The potential result of Glomerulonephritis |
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| kidney failure and ultimately death |
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| Why is the reaction of a Type 4 response delayed |
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| It takes time for the T cells and macrophages to migrate to an accumulate near the foreign antigens. |
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| If the recipient has (or has had) a previous infection by tuberculosis bacteria, what will be the reaction |
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| an inflammatory reaction to the injection of these antigens will appear on the skin in 1-2 days |
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| Allergic contact dermatitis is associated with which type of immune response |
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| Type 4 (delayed-cell -mediated hypersensitivity) |
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| A patch test is associated with which type of immune response |
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| Type 4 ( to identify the environmental factors causing dermatitis-samples of the materials will be patched to the skin for 48hrs) |
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| Autograft |
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| *most successful - taking a burn patients uninjured skin to culture extensive sheets of new skin |
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| Isograft |
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| *2nd most successful a tranplant between twins (whom have identical genetic makeup) |
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| Allografts |
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| *3rd most successful ( usually btwn Genetically different member of same species) -grafts between people who are not identical twins |
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| Xenograft: |
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| -different species. Least successful. - graft taken from tissues or organs that have been transplanted from animals |
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| graft rejection by host (recipient) |
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| -Rejection of transplanted tissues or organs - normal immune response against foreign MHC glycoproteins on surface of graft cells |
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| Which cells are responsible for recognition of foreign proteins in a graft |
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| Tc cell mediated recognition of foreign MHC proteins |
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| Which MHC class is associated with grafts |
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| Mainly MHC Class I |
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| The mechanism of Tc cells in grafts |
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| Host Tc cells release IL-2 • Amplifies Th and Tc cells specific to foreign antigens on the donated cells ? Tc cells bind to the grafted tissue and secrete lymphokines that begin the rejection process within 2 weeks of transplantation |
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| Likelihood of graft rejection depends on |
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| degree of "foreignness" of graft to recipient |
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| Graft versus host disease (GVHD) |
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| Occurs when donated bone marrow cells regard patient cells as foreign and produce an immune response against patient cells |
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| What happens if: donor and recipient differ in MHC class I molecules |
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| grafted T cells attack all of recipient's tissues ? Produce destructive lesions in skin and intestines |
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| What happens if donor and recipient differ in MHC class II molecules |
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| grafted T cells attack host APCs of host ? Leads to immunosuppression |
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| Describe Privileged sites |
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| - a site that does not stimulate an immune response to a graft or transplant AKA immunologically privileged site |
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| What are the privileged sites |
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| Brain lack lymphatic vessels, brain blood vessel walls impermeable to lymphocytes e.g. T cells ? Cornea - lacks extensive blood vessels ? Eyes and testes - contain naturally high levels of immunosuppressive molecules ? Other sites - either lack dendritic cells or express low levels of MHC molecules, so AP does not occur |
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| What is not a privileged sit but is not usually rejected |
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| Fetus |
