Term
*What are the exogenous environmental factors that affect the immune system: |
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Definition
Viral diseases HIV and knock down the T helper cells, radiation knock out stem cells, any cortisol medications knock down the immune system. Women have highest amount of autoimmune disease; good diet |
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Term
1. What is the difference between active acquired immunity and passive acquired immunity in terms of longevity of immunity? Why is this? Give two examples of active acquired immunity and two examples of passive acquired immunity. |
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Definition
Active acquired: have for the rest of your life (Ex: natural exposures, mumps, measles, chicken poxs; Immunizations: necessary) Produce memory cells t cells, but sometimes you need a booster shot if there is a change in the antigen.
Passive acquired: get the antibodies (ex: from mom through placenta, breast fed, or snake bite.) Only last weeks maybe months. |
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Term
2. Distinguish between primary and secondary immune responses in terms of: 1) response time; 2) types of antibodies involved; and 3) levels of antibodies in the blood. |
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Definition
Primary: 1) 5 days for sufficient immune response. Level of antibodies are low compared to secondary. Most are IGM
Secondary: 1) in 24 hr period. High amount of antibodies. IGG. |
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Term
What are lymphocytic stem cells? Are they immunocompetent? What is meant by the term “immunocompetent”? |
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Definition
Lymphocytic: stem cell produced by bone marrow. Can differentiate into B or T cells to be immunocopentant: T cells can respond to antigen. |
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Term
Where do lymphocytic B stem cells become immunocompetent? T stem cells? What types of immunocompentent T cells are produced? |
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Definition
-in the bersal equivalent in the bone marrow.
T stem cells in the thymus.
-Types: cytotoxic t cells
-Helper t cells t4 or cd4 or helper t cells |
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Term
5. Cytotoxic T-cells (CTL, Tc) are also labeled T-8 or CD8 cells. Why? |
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Definition
B/c they have the coreceptor |
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Term
T-helper cells (TH) are also called T-4 or CD4 cells. Why? |
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Definition
B/c they have the cd4 coreceptors |
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Term
6. When considering the major histocompatibility complex, Class I molecules are encoded in what region? Class II molecules? |
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Definition
-HLAA, HLAB, HLAC region of MHC complex on chrom 6.
Class 2: HLADR, HLADQ, HLADP |
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Term
7. On what cells are Class I molecules found? Class II molecules? |
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Definition
Class 1: all class 1 HLA cells except the red blood cells bc they have their own way of identifying themselves.
Class 2: T cells, antigen presenting cells (macrophages/dendritic cells)
8. Know the 7 steps in the activation of the humoral arm of the immune system (i.e., 7 pt essay question) |
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Term
. What are the two “working ends” of an antibody? |
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Definition
Fat end and thick end
Fat end, antigen binding sight |
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Term
What are the three possible actions of the Fc end of the antibody? |
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Definition
Thick end: activate the compliment system, involved in transporting ternal antibodies for fetal circulation through placenta or intestinal cell, binding or optimization to the surface of PMN
-Polymorphonuclear
- types: neutrophils and eosinophils
Neutrophils: phagocitic cells |
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Term
. What subset of helper T cells plays a major role in activating the cytotoxic arm of the immune system? |
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Definition
2 types of helper cells: th1 and th2
Th2: will activate B cells to plasma cells to produce antibodies
TH1 cell: involed in acvtiation of cytotoxic arm |
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Term
12. What are the main target cells for CTLs? |
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Definition
Virus infected cells with intracellular bacteria: TB, rikettsia, clamydia, malaria, allagraphs and transplant tissue |
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Term
13. What are the two routes in which cytotoxic killer cells (Tc, CTC) are activiated? |
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Definition
1) independently of the TH1 cells with an antigen presenting cell
2) combination of APC presenting the antigen in its class 2 hla antigen to the cd4 which releases cytokines, at the same time the
Class 1= CDA
Class 2= CD4 |
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Term
14. How do CTLs recognize a cell infected with a virus? |
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Definition
-By docking to the virally infected cells and bringing a piece of the virus onto its class 1.
The infected cell presents a peptide which is recognized and the cell ends up committing suicide= optosis. |
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Term
16. What are the two main target cells for natural killer (NK) cells. |
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Definition
-viruses
-host cells that have become cancerous |
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Term
What type(s) of antibodies are found in the serum of the following blood types: A, B, AB, O? When do these develop within a person? What Class of antibodies are these? Can they pass through the placenta? |
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Definition
Blood type A: B
Blood Type B: A
Around 6 months
IGM can’t pass through the placenta but the IgG’s can. |
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Term
In a paternity suit, the child is blood type AB and the mother is type A. The alleged father of the child is blood type O. Does the mother have a case? |
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Definition
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Term
The parents of a child are Rh-positive, yet the child is Rh-negative. What must be the genotype of the parents? |
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Definition
Homozygous dd= 25% chance that they’ll be dd |
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Term
22. Can hemolytic disease of the newborn (HDN) be caused by incompatibility of the ABO blood group? What is the usual blood type of the mother? What characteristic of this blood type increases the risks for HDN? |
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Definition
Yes it can;
Mother is blood type O
Characteristic: paternal contains anti A and anti B which tend to be IgG class and can cross the placenta and hemolysis fetal red blood cells. |
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Term
. In Rh-HDN, explain how sensitization occurs. At the time of this sensitization (i.e., first pregnancy), why can’t the Rh antibodies cross the placenta from the mother’s side and enter the child’s circulation? 28 |
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Definition
sensititation: first pregnancy due to fetal maternal hemorage , during prenatalbleed.
Primary Immune response.
-IgM response so it can’t cross over. |
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Term
24. In subsequent pregnancies, HDN can cause the condition of kernicterus. What is it? How is it caused? Why is it not a problem during pregnancy? Why is it a problem after birth? |
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Definition
kernicterus: a high concentration of billirubin and can collect in brain and cause samage besides just jaundice. During birth the concentration is cleared by the placenta and cleared by mom but after birth the liver can’t handle all of the billirubin and accumulates in the fatty tissue in skin and brain. |
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Term
25. In subsequent pregnancies, HDN causes severe anemia in the fetus. Why? Why does this lead to hepatomegaly and splenomegaly? |
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Definition
Because mom’s already got antibodies and they can cross over early in fetal development and they can begin to wipe out the fetal red blood cells. The fetus tries to compensate by producing red blood cells through other tissues but they’re immature hydrops fetalis |
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Term
26. A complication of severe HDN causes fetal tissue to become swollen and is usually fatal—what is it called? |
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Definition
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Term
When is Rh immunoglobulin (RhIG or RHOgam) given to the mother to prevent HDN? How does RhIG prevent HDN? |
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Definition
Rh Immunoglobulin: depends on the mother’s Dr. because there’s slight controversy on when the injection should be given. |
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