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147 Cards in this Set
- Front
- Back
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What effect does TNF alpha have on dendritic cells?
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It tells them to get up and leave the tissue and migrate to the nearest lymph node and if it has digested an antigen it can present it to the CD4 cells
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What is the difference of taking OTC medications that take away the sickness symptoms?
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It makes you sicker longer. You are stopping the adaptive reactions and the body cannot fight what it is fighting
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What is the extreme pathological version of a systemic inflammatory response?
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Sepsis
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When does sepsis occur?
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When the infection reaches the blood stream
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What does the infection encounter when it enters the blood stream?
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The greatest amount of WBC
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What are LPS? what does it do?
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-Lipo-poly saccharides
-components of the cell wall of gram - bacteria -it is a endo/bacterial toxin -potent stimulator of an inflammatory response |
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What do LPS encounter in the blood stream? What does it cause?
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Complement proteins that trigger the complement system that causes inflammation
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What occurs when the LPS interact with the endothelium?
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They cause damage and trigger inflammatory response especially stimulating coagulation
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When septic blood hits the liver, what is the occurrence?
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The interaction with liver Kupfer cells that dump out the inflammatory cytokines IL 1, IL 6 and TNF alpha
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What local effects will inflammatory mediators have?
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o Vasodilation
o Increase permeability o Mobilization of other leukocytes |
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What manifestation is classic to septic shock?
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Decreased BP
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What occurs when vasodilation and increased permeability is spanned out to the entire circulatory system?
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Drop in BP
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Which cytokine has a huge involvement in the shock component of sepsis?
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TNF alpha
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In septic shock, what happens when your blood pressure drops?
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Not perfusing tissue and it gets damaged
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What is coagulopathy?
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Pathological coagulation
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What type of coagulation is a person in sepsis in danger of?
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DIC
-Disseminated inter vascular coagulopathy |
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What is disseminated inter vascular coagulopathy?
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It is a paradoxical coagulopathy!
-Situation that causes a wide spread activation of coagulation cascades and you to use up all of your coagulation factors -Causes hemorrhage!! |
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What is leukocytosis?
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Increase in the production and mobilization of WBCs particularly neutrophils
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What can a host cell do when a virus invades it?
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Can detect it early because it can see the presence of ds RNA and then tell other cells.
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All viruses at some point go through a stage of having what characteristic?
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double stranded RNA
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What 2 cytokines are released by the host cell when it detects the presence of a virus?
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Interferon alpha and beta
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WHat effects does interferon alpha and beta have?
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1. Have autocrine effects
--can increase production of enzymes designed to degrade viral RNA 2. Tells itself and its neighbors to produce enzymes that degrade viral RNA 3. stimulates to self and neighbor the production called MHC-1 protein 4. attract and activate nearby NK cells |
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WHat is MHC 1?
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Major histocompatability complex They are our generic self identity marker.
The way host cells communicates to immune system and tells it that it is a cell in the body. |
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What is MHC 1's function in a viral infection?
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Alerts the immune system that the host cell is a self cell and that it is infected with a particular virus
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What do NK cells do when they find virus infected cells? how are they attracted?
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Kill the cell
-and release a 3rd type of IF called IF gamma that increase the effects of IF alpha and beta -They are attracted by IF alpha and beta |
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What is the purpose of IF gamma? What releases it?
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It increases the effect of IF alpha and beta.
The NK cells |
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What does the innate system do in a viral infection, In general!?
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They will prevent the viral count from climbing. They cannot clear a viral infection!
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Other than the host cell releasing IF alpha and beta, how else can a viral infection be detected?
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When the virus reaches its lytic phase
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When a virus cell is in the lytic phase, what can it cause?
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An inflammatory response because it is tissue damage!
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What is inflammation always designed to do?
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Be short lived! trigger, explode and then healing
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When the source of the injury does not go away, what do you get?
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chronic inflammation, maladaptive!
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What is chronic inflammation synonymous with? WHy?
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Frustrated healing
-Because you have healing and acute inflammation happening at the same time |
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What is the best case scenario of acute inflammation?
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Complete resolution
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What is complete resolution?
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-source of injury is resolved
-all inflammatory mediators and cells have been cleared -you have regenerated all of your cells -complete normal function is regained |
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What occurs when an injury is resolved in tissues where the cells do not replicate?
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Do not get complete resolution
-Healing occurs with loss tissue replaced by connective tissue |
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What is healing through fibrosis?
What tissues heal this way? |
Healing occurs with loss of tissue replaced by connective tissue.
-Cardiac muscle heals this way |
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If inflammation is not interrupted in a chronic injury what type of healing will occur, even in replicating tissue?
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Will progress to fibrosis
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What is a pyogenic phase?
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a pus phase or formation of abssess that occurs in chronic inflammation.
-many neutrophils -but still heals through fibrosis |
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What is bad about fibrosis?
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You have a loss of function!
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What characterizes primary intention in healing?
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-Small wounds, minimal tissue, clean and closely apposed wound edges
-Involves sealing of wound at epithelial tissue and contraction or shrinkage of the wound |
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Describe secondary intention?
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Type of Big wound healing
-Large, not well approximated and not very clean wounds -Often times forms a scar |
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What healing intention type often causes a scar?
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Secondary intention
-have an amount of fibrotic tissue involved |
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Do the stages of healing differ for primary and secondary intentions?
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No, they are the same!
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What is the first phase of wound healing?
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Inflammatory phase
-injury is the wound |
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What is the second phase of wound healing?
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Reconstructive phase
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What is the reconstructive phase of healing?
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Destructive phase is replaced by the release of anti-inflammatory features and growth factors
-Esp macrophages -stimulate new capp beds -reconstruction of the tissue |
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What is the function of macrophages in the reconstructive phase?
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they act as growth factors and bring about a healing response
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What is the maturation stage of healing?
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The wound will undergo weeks and months of contractions
-A scar may just appear on the surface of the skin but the function may not have been lost |
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Is a scar total fibrotic tissue?
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No, it may appear so because it is a different color than the surrounding skin
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What is the reason that the source of injury must be relieved?
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Because it is the primary determining factor in successfully shutting off the inflammatory response
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What are some common causes of chronic inflammation?
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1. Persistant infections
--parasites, syphillis, certain fungi, viruses etc 2. prolonged exposure to a toxic agent (cigarette smoke) 3. Some endogenous agents (high cholesterol LDLs) 4. autoimmunity --you are the source of the injury (persistent attack) |
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How do some bacteria avoid being broken down by the immune system?
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They hide out in cells in our immune system, specifically macrophages.
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How can you interrupt a chronic inflammation?
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Fixed the problem or IMMUNE SUPPRESSION (treat the exaggerated response)
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What happens to shut down inflammation that goes wrong?
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1. neutrophils come and cause more damage
--debris the area and apoptose 2. Monocytes come in after --phagocytize the debris and are responsible for finishing up acute inflammatory response and trigger a shift to healing |
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why do neutrophils apoptose instead of necroses?
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They implode in on itself to not allow intracellular content to go into the ECF
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What WBC is designed to trigger the shift to turn off the inflammatory response to healing?
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macrophages!
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What is involved with shutting off the inflammatory response?
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1. inflammatory mediators have a short half life (degrade quickly)
2. Macrophages release 2 cytokines that are critical to turning off inflammation. |
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What are the two cytokines released by macrophages to turn of the inflammatory response?
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1. TGF beta
2. Interleukin 10 (IL 10) |
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What are Lapoxins?
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are arachidonic acid metabolites that have anti-inflammatory afffects
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In coming down from inflammation, what is released by mast cells, macrophages and endothelial cells that is an anti-inflammatory mediatory?
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Lapoxins!!
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Other than fibrosis, what is another outcome of chronic inflammation?
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Formation of granulomas
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What are granulomas?
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They are analogous to an abscess (filled with pus), but a granuloma is a collection of dead GRANULOCYTES
-usually not that large |
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What has been found to be a cause of chronic inflammation of adipose tissue?
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Obesity
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What are the Human Leukocyte Antigens?
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The major histocompatability complex 1 and 2
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What genes allow us to distinguish self from non-self?
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MHC genes
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Which MHC is found on every cell in the body except RBCs?
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MHC-1
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What information does MHC-1 cells signal to the immune system?
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The kind of cell that they came from and what kind of protein that the cell is making
ie. I am a lung cell producing cancer protein |
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The Antigen produced by MHC 1 is recognized by which cells?
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NK cells and Cytotoxic T cells
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What cells have the MHC 2 on them?
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These include macrophages, dendritic cells, and B lymphocytes
-They also have MHC1 |
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What does MHC2 tell the immune system?
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I am an official antigen presenting cell!!
-They present the antigens to helper T cells that unlock adaptive immune responses |
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Before MHC1's go the the surface of the cell, what do they do?
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They randomly attach to other proteins being made in the cell.
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When a helper T cells finds the particular B or T cell that is matched for the antigen presented to it, what does it tell those cells to do?
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It has the B or T cells to make many copies of itself!
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How many sets of copies are made of B and T cells once a Helper T cells has activated it?
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2 sets!
-One for memory and one as the effector group. |
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What starts off the adaptive immune response?
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MHC2 (presenter) cells presenting the antigen to the Helper T cell and then coming up with a response
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When the presenting cell has an antigen, what must it find in specific?
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the Helper T cell that is complimentary to the specific antigen
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What is the generation of clonal diversity?
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It is the creation of the multiple B and T cells once activated by the Helper T cell!
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In the thymus gland, many things are taking place. What is taking place there?
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The T cells are given either CD4 or CD8 and then its specific T cell receptor!
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When do we create the specific B and T cell for each antigen?
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Before we encounter then in nature!
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How many groups of genes code for the antigen binding site for the receptor?
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3 and randomly!
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What is the risk of random diversity of the 3 groups of genes that code for the antigen binding site?
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Might run the risk of producing self reactive T cell receptors
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How does the body help prevent the production of a self reactive clone? What is it called!?
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There are cells located adjacent to developing T and B cells that act as a diversion and deemed clonal deletion
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What is central tolerance?
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Our ability of our immune system to delete autoreactive B and T cells as they are produced
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How are the B cell receptors expresses? 2 ways?
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in the form of IgM and IgD
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Do IgM and IgD have the same antigen binding site? If so, what does it act as?
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Yes, it acts as the B cell receptor
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What form of pathogens predominate the EC space?
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forms of bacteria, fungi parasites etc
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What is the form of most intracellular pathogens?
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Viruses, but some very specific bacteria that can infect macrophages!
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What is an allergy?
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Immune response to a non harmful antigen in nature
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What 3 cytokines are released by the CD4 cell to stimulate expansion of the B or T cell?
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IL 4, 5, and 6
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What is the function of IgA?
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Antibodies in breast milk; passive immunity through breast feeding
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What is the function of IgD?
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Part of the B cell receptor
-Not sure if it has another function |
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Which antibody is present in all allergic reactions?
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IgE
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Which antibodies are the 2 key players in an adaptive immune response?
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IgM and IgG
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State the antibody that is the first to spike in the presence of illness?
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IgM is present in the acute phase of disease!
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The presence of which antibody in the body states that the person has had exposure to the antigen in the past?
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IgG
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What are 3 ways the antibody fights infection?
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1. Neutralization
2. Opsonization 3. Activation of the complement |
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What are the 2 sets of copies used for created by the release of IL 4,5 an6?
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-Have the memory B and T cells
-THe effector B and T cells |
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What is the last differentiation step of B and T effector cells?
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They convert into plasma cells that release antibodies!
They produce IgM antibodies, the same ones that were part of the B cell receptor with the particular antigen binding site |
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What are the 5 classes of antibodies?
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IgA, IgE, IgD, IgG, and IgM
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Which part of the antibody tells you about the class/function? The arms or the base?
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The base
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Can you have different classes of antibodies that work against the same antigen?
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Yes!
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Are all antibodies equally as powerful in each step of fighting infections?
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No, different classes are better at different functions!
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Which antibody has the strongest function in activating the complement system>
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IgM
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IgA is good at which function>
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Neutralization
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IgG is good at which steps of the immune response?
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Neutralization and opsonization
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What is the messiest response in the antibody mediated infection fight?
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The activation of the complement system by IgM
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which of the 3 steps in antibody mediated infection fighting is more silent?
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Opsonization and neutralization
-The functions of IgG |
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The second time you encounter a pathogen, which antibody response dominates!?
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IgG, it makes it less messy
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In a T cell response, what if the APC encounters the specific CD 8 cell first?
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Must be done only by the Dendritic cell! Will cause the CD8 T cell to release IL 2 on ITSELF and start clonal expansion on itself!!!
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In a T cell response, what if the APC finds CD4 first?
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It will activate the CD 8 to release IL-2 which will cause T cell receptor clonal expansion! Create 2 copies (effector and memory cells)
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Which APC is the only one that can present directly to the CD 8?
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The dendritic cell
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Which IL causes the T cells to have clonal expansion and which T cell releases it?
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IL-2 released by CD 8
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When the CD 8 effector clonal cells find the specific antigen what do they do?
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THey release a specific protein that degrades the protein membrane
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How many types of Helper Ts are there?
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2
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What is the function of TH-1?
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Responsible for fighting the INTRACELLULAR BACTERIA
-the infection of immune cells -They stimulate the macrophage to complete its phagocytic function and fuse its lysosome with the bacterial vesicle |
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Which immune cells are susceptible to a bacteria that can infuse the cell?
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Macrophages
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When the evolved bacteria gets inside the macrophage, what does it prevent?
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It prevents the fusion of the bacteria with the lysosome inside the macrophage and then the macrophage will proliferate and explode
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Which helper T is the gatekeeper of the immune response?
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Helper T 2
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In a second exposure to an infection, what is the rise of IgM in comparison to IgG?
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We produce a small burst of IgM in the acute phase, but the IgG is much higher in response to a second infection
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What is affinity?
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How tightly the antigen binds to the antibody?
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How does the affinity change from first exposure to the second exposure?
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It increases in the second exposure as well as the length of the exposure
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What is affinity maturation?
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The process of the body producing antibodies with more and more affinity to the antigen as it progresses
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What is class switching? Why does our body do this?
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qYour body switches the antibody that is produces against the same antigen!
-IgM to IgG -the different classes are the fighting the same infection in different ways and get a more affective response |
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What is the structure of IgM's in circulation?
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They are pentamers
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Which antibody has low affinity but high Avidity?
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IgM
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What is avidity?
Which antibody has the highest value for this? |
how any points of gravity you have on the antigen
-IgM because of its pentamer structure |
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How can you detect a virus present in the body that can't be detected in culture?
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You can do a serology test
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Do we produce antibodies against viruses?
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yes we do
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When can an antibody act against a viral infection?
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When the virus is in its lytic stage and it has exploded the cell and is floating in the EC space.
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What if you have a person with a large amount of IgM and no IgG?
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THey are in the acute phase of their infection and it is their first exposure
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What if a person has trace amount of IgM and a moderate amount of IgGs?
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They are in the chronic phase. or they have been immunized
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Define an alo-immune response.
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allergic reaction to some sort of graft tissue (transplant)
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What are the 3 inappropriate reactions of the body to a non-harmful substance?
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1. Allergic response
2. Aloimmune response 3. Autoimmune response |
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can you have an allergic response that involves more than one subtype of hypersensitivity reaction?
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yes
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What are type I hypersensitivity reactions?
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Classic Allergy (seasonal)
-hay fever, anaphylaxis (nut allergies) |
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Which exposure causes the hypersensitivity reaction?
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THe second response
-The first response presents the antigen and the cell produces IgE antibodies to react against the antigen in the second exposure. |
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Where do IgE antibodies sit?
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On the mast cell and causes the release of histamine and granulocytes in the exposure to the antigen
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Why are allergens really an unfortunate situation?
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Because the reaction gets stronger each exposure since the affinity to the antigen becomes stronger with each exposure
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Autoimmune hemolytic anemia is the prototypic disorder for which class of hypersensitivity?
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Type II:
Antibody mediated hypersensitivity |
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Describe the process of Type II hypersensitivity.
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-Antibody mediated hypersensitivity
-IgM and IgG bind to antigen on target cell or tissue causing phagocytosis by leukocytes (IgG) or complement system (IgM) -Mostly an attack of RBC causing anemia! |
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What is the hypersensitivity reaction that involves antigen-antibody complexes attaching to tissue and causing damage and thus and inflammatory response?
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Type III hypersensitivity
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Give an example of a disorder associated with Type III hypersensitivity.
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Post streptococcal glomerulonephritis
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Describe the hypersensitivity associate with transplant rejection? What is this type called?
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-Cell-mediated (type IV) hypersensitivity
-The antigen activates T cells that cause damage by activating inflammation and recruitment of phagocytic cells. -Direct cytotoxic T cell killing of antigen carrying cells |
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What part of the donor's tissue id attacked in a type IV hypersensitivity reaction?
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Their MHC proteins
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List the disease from Table 6-4 that are examples of Type II hypersensitivity reactions.
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1. Autoimmune hemolytic anemia
2. Autuimmune thrombocytopenic purpura 3. Pemphigus vulgaris 4. Vasculitis caused by ANCA 5. Goodpasture syndrome 6. Acute rheumatic fever 7. Myasthenia gravis 8. Graves disease (hyperthyroidism) 9. Insulin-dependent diabetes 10. Pernicious anemia |
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Which type II hypersensitivity is associated with myocarditis and arthritis?
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Acute rheumatic fever
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What is the clinical manifestation of pemphigus vulgaris (Type II)?
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bullae skin vesicles
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Muscle weakness and paralysis are associated with which diease?
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Myasthenia gravis
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