Flashcards in Chapter 19 Deck (31)
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hypersensitivity
an ABNORMAL antigenic response results from a prior exposure to a foreign substance antigen called an allergen
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hypersensitivity: type 1 - anaphylactic
- signs show within 30 minutes. IgE binds to mast cells or basophils and causes degraulation of mast cells or basophil and release of reactive substances such as histamines
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anaphylactic: localized
Symptoms: hives, hay fever, asthma--from inhaled or ingested allergens like food or pollen
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anaphylactic: systemic
anaphylactic shock, released mediators cause enlargement of blood vessels and a sudden extreme drop of BP (shock), usually from drug injections, insect stings
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desensitization
achieved by repeated injects of the antigen, which leads to the formation of blocking IgG antibodies
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mediator
Are released chemicals (histamines) which cause the observed allergic reactions
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prostoglandin
type of mediator, affect smooth muscles of the respiratory system and increase mucus secretion
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hypersensitivity: type 2 - cytotoxic
- signs show between 5-12 hours. Antigen causes formation of IgM and IgG antibodies that bind to target cell; when combined with action of complement, it destroys target cell. EX: transfusion reactions; Rh incompatibility (hemolytic disease of the newborn)
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hemolytic disease of the newborn
When dad is Rh+ and mom is Rh-, there is a 50% chance the child will be Rh+.
If the child is Rh+, the mother can become sensitized to this antigen during birth when placental membranes tear and fetal Rh+ RBCs enter maternal circulation, causing mother's body to produce anti-Rh antibodies of the IgG type.
If the fetus in a subsequent pregnancy is Rh+, mothers anti-Rh antibodies will cross placenta and destroy fetal RBCs.
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RhoGAM
HDNB is prevented today by passive immunization of the Rh- mother at the time of delivery of any Rh+ infant with anti-Rh antibodies. These anti-Rh antibodies combine with any fetal Rh+ RBCs that have entered mother's circulation, so it is less likely she'll become sensitized to the Rh antigen.
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ABO blood group system
4 principle types of blood: A, B, AB, O.
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hypersensitivity: type 3 - Immune complex reactions
- occurs within 3-8 hours; antibodies and antigens form complexes that cause damaging inflammation. EX: glomerulonephritis - inflammation damage to kidney glomeruli
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hypersensitivity: type 4 - Delayed cell-mediated, or delayed hypersensitivity
: occurs between 24-48 hours. Antigens activate Tc that kill target cells. EX: rejection of transplanted tissues, contact dermatitis (poison ivy), chronic diseases (tuberculosis)
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allergic contact dermatitis
usually caused by haptens that combine with protiens (amino acid lysine) in the skin of some peope to produce an immune response, such as reactions to poison ivy, cosmetics, metals in jewelry, latex,
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autoimmune disease
loss of self-tolerance, immune system reacts to self-antigens and causes damage to one's own organs
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cytotoxic immune reactions
Involve antibody reactions to cell-surface antigens. EX: Graves' disease, myasthenia gravis
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immune complex autoimmune reactions
systemic lupus erythematosus, rheumatoid arthritis
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cell-mediated autoimmune reactions
MS, insulin-dependent diabetes mellitus, psoriasis
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autograft
one's own tissue is grafted to another part of the body
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isograft
transplantation between identical twins
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allograft
transplantation between people that are not identical twins
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xenograft (xenotransplant)
grafts from animals
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HIV infection
retrovirus, has 2 identical strands of RNA, enzyme reverse transcriptase, and an envelope of phospholipid. Envelope has glycoprotein spikes (gp120)
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T cells
an immune system cell that plays a central role in cell-mediated immunity
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infectivity of HIV
attachment to the target cell depends on the glycoprotein spike (gp120) combining with the CD4+ receptor.
Gp41 participates in fusion of the HIV with the cell. Following fusion with the cell, an entry pore is created.
After entry, the viral envelope remains behind and the HIV uncoats, releasing the RNA core for directing synthesis of the new viruses.
in the host cell, viral RNA is released and transcribed into DNA by the enzyme reverse transcriptase.
This viral DNA then becomes integrated into the chromosomal DNA of the host cell. can either become active or latent.
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latent infection
viral dna is integrated into cellular DNA and forms a provirus that can later be activated to produce infective viruses.
A subsetof HIV-infected cells, instead of being killed, become long-lived memory T cells in which the resevoir of latent HIV can persist for decades.
This ability to become a provirus / latent virus shelters it from the immune system
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active infection
provirus is activated, allowing it to control the synthesis of new viruses, which bud from host cell.
Final assembly takes place at the cell membrane, taking up viral envelope proteins as the virus buds from the cell.
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cell-cell fusion
another way for HIV to evade immune system, by which the virus moves from an infected cell to an adjacent uninfected cell.
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transmission of HIV
transmitted by sexual contact, breast milk, contaminated needles, transplacental infection, artificial insemination, and blood transfusion.
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CXCR4 and CCR5
best known chemokine coreceptors that are required for HIV to be infective.
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