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57 Cards in this Set
- Front
- Back
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what are fixed macrophages
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WBC that don't travel from the blood and leak out into the tissue instead they are already in the tissue
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true or false there is some conversion of monocytes to macrophages in the blood
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true
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what are some of the fixed macrophages
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histocytes
tissue macrophages (lymph nodes) alveolar macrophages (lungs) kupffer cells (liver) |
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what are the steps to inflammation
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vasodilation
increased capillary permeability clotting of interstitial fluid migration of granulocytes/monocytes |
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what are the macrophage and tissue lines of defense in responses to inflammation
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tissue macrophages - 1st line
neutrophile invasion - 2nd line macrophage invasion - 3rd line increase in # of WBC produced to fight infection (increased granulocyte/monocyte production) - 4th line |
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what do factors released from activated macrophages do
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they release factors that reach the bone marrow and cause the production of more WBC
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during normal conditions what is the distribution of WBC
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there is a large pool of WBC in the marrow and a small amount in the tissue and capillaries
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during an infection what is the distribution of wbc
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the pool in the bone marrow is decreased and more WBC are in circulation and tissue (this is called leukocytosis)
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what is leukocytosis
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increase in the amount of WBC due to them being a defense cell and trying to fight off infection.
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what is leukocytosis an indication of
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infection, acute inflammation and trauma
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what is Leukemia
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abnormal # of WBC and an increased WBC count
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what is Leukopenia
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decrease in # of WBC may be caused by defective bone marrow, HIV infection
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what is the main role of Eosinophils
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involved in parasitic infections
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what is eosinophilia
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this occurs when a person has a higher than normal level of Eosiniphils and is an indication that they are fighting off a parasitic infection
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what is the difference between basophils and mast cells
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basophils become mast cells when they enter tissue
basophils = blood mast cells = tissue both release heparin (anticoagulant) and histamine (alergin) |
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what causes basophils/mast cells to degranulate
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they have a sticky surface upon which antibodies can sit and whenever the body is exposed to an allergin which is specefic to that antibody the allergen binds and the basophils/mast cells degranulate releasing histamine and heparin
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what is agranulocytosis
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complete absence of granulocytes and this is due to a defective bone marrow and the person will be prone to infections
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what is lymphocytic leukemia
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leukemia that effects lymph tissue responsible for making leukocytes
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what is myelogenous leukemia
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leukemia that effects bone marrow and therefore effects cells made by bone marrow
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what is the difference between acute and chronic leukemia
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acute - progresses quickly and if untreated person will die
*acute progresses quickly because all of the WBC are undeffrentiated (not functional) chronic leukemia - may take years to develope *with chronic leukemia the cancer cells are partially diffrentiated meaning some of the cells are still fucntional |
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why is someone with leukemia as prone to infection as someone with leukopenia
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because eventhough they have a large number of WBC they are not fucntional
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what happens to people with myelogenous leukemia
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the cancer cells would slowly replace the bone marrow cells and the person would develope anemia b/c their bone marrow is no healthy and is therefore no longer producing RBC. Bleeding would also occurs because their marrow is no longer making Platelets
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where are antigens and how are they obtained
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antigens are on the RBC and they are inherited
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where are antibodies and how are they obtained
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antibodies are in the plasma and occur spontaneously
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what happens when an antigen antibody reaction occurs
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for example if someone with type B blood was given type A blood this would occurs due to the person with type B having antibodies for type A. what occurs is the antibody sticks to the antigen of the donors RBC and this results in the either immediate blood transfusion reaction or clumps form and macrophages can phagocytos the clumps causing hemolysis of the blood
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who's blood gets hemolyzed when agglutination/antigen antibody reaction occurs
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the donors blood gets hemolyzed because there are far more antibodies in the reciepient, and the donors antibodies will get diluted resulting in hemolysis of the donors blood
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where is the Rh antigen
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on the surface of the cell
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where is the Rh antibody
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in the plasma of Rh negative cells that have been exposed to Rh positive cells
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what is the main difference with the Rh system and the OAB system
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OAB - spontaneously developes antibodies
Rh - antibodies are developed only after exposure |
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why is there only a mild transfusion reaction when someone who is Rh negative first gets Rh positive blood
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the recepient will develope Rh antibodies 2-4 months after they receive the transfusion and since RBC have a lifespan of 120 days most of the RBC would have already died on their own
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who can Rh+ people give blood to
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only Rh+
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who can Rh- give blood to
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anyone
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how can a recepient die from a transfusion reaction
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due to clump formation
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what happens to the Hemoglobin of RBC when a transfusion reaction occurs
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increased release of hemoglobin since the blood is being broken down this will result in extra presure on the kidney causing acute renal failure (the hemoglobin would be excreted through the urine). jaundice may also occur due to the excess bilirubin from hemoglobin breaking down
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what is the cause a Erythroblastosis fetalis
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a blood mismatch between mother and fetus
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why is it that in the 2nd pregnancy the Rh+ baby can be harmed
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the Rh antibodies of the mom can pass through the placenta cause hemolysis of the baby's cells (baby will be anemic and have jaundice)
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how is Erythroblastosis fetalis prevented
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the mom can be given artificial Rh antibodies so she never makes her own
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how is Erythroblastosis fetalis treated
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by giving the fetus Rh- blood
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what are the stages of hemostasis
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vascular constriction
formation of platelet plug blood coagulation clot retraction and permanent closure |
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what occurs during vascular constriction
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immediate response to bleeding
decrease in BV size decrease in leakage of blood short lived and not a permanent solution |
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what occurs in the formation of platelet plug
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when there is a cut damaged tissue exposes collage. collagen attracts platelets and causes them to become activated. the platelets attract more platelets by releasing thromboxan A2..
PLATELET PLUG IS NOT STRONG ENOUGH AND REQUIRES REINFORCEMENT |
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how do platelets attract more platelets
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release thromboxane A2
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what occurs during blood coagulation
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fibrin fibers reinforce the platelet plug
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during normal conditions which one dominates procoagulants or anticoagulants
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procoagulants
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during a vessel injury which one dominates procoagulants or anticoagulants
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procoagulants
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what are the steps to the formation of fibrin
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Prothrombin Activator + Ca converts prothrombin to thrombin.
Thrombin converts fribrinogen to fibrin monomer. fibrin monomer + Ca gets converted into the loose fibrin network fibrin stabilizing factor converts the loose fibrin network into the tight fibrin network |
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how does thrombin promote the fibrin network formation
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thrombin has positive feed back loop of its own production
thrombin activates fibrin stabilizing factor thrombin converts fibrinogen to fibrin monomer |
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what is the role of the liver in clotting
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the liver produces prothrombin and fibrinogen both are used in clotting
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why does liver disease lead to bleeding
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since the liver produced prothrombin and fibrinogen w/o them there will not be proper clot formation therefore bleeding will occur
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what is the role of platelets in clotting
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platelets are important because they have receptors on the surface upon which prothrombin binds
platelets also release fibrin stabalizing factor they are needed for clot formation |
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what is the rate limiting step in the formation of fibrin
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prothrombin activator
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what is factor 10 a
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prothrombin activator
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what kind of trauma is the intrinsic factor related to
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internal trauma
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what kind of trauma is the extrinsic factor related to
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external injury
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what are both the intrinsic and extrinsic factor related to
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formation of prothrombin activator
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what is hemophilia and how is it treated
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hemophilia is the lack of factor 8
and their intrinsic pathway is not fucntional and can't make prothrombin activator therefore bleeding will occur b/c no clot formation. it is treated by giving factor 8 or blood transfusions |
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what must heparin join in order to be a strong anticoagulant and what does it do
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heparin must join with antithrombin 3
it will remove thrombin and inhibit platelets from activating |
