Exam 1 Blood, Lymphatics, & Immunity 2

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Exam 1 Blood, Lymphatics, & Immunity 2
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2012-09-11 19:35:53
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A&P 2402 Exam #1 Pt 2 Lymphatics & Immunity
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  1. Explain the roles of the skin & mucos membranes in providing defenses against pathogens
    They play the role of Surface Barriers as the First Line of defense against invaders
  2. Describe the different types of phagocytes.
    • Ingest and destroy foreign cells and matter
    • Macrophages
    • Neutrophils: get rid of bacteria
    • Eosinophils: get rid of parasites
    • Mast Cells
  3. Describe the role of Natural Killer (NK) cells.
    Attack non-self cells (cancer cells-secrete preforins & granzymes) & virus cells (-secrete interferon)
  4. What are the Inflammatory response signals.
    • Redness (Erythema)
    • Heat
    • Swelling (Edema)
    • Pain
    • Loss of Function
  5. Explain an Inflammatory response.
    • 1. Vasodilation (brings in more leukocytes)-heat, swelling, redness
    • 2. Increse in blood vessel Permeability-increase swelling more & PAIN!
    • 3. Mobilize Phagocytes (chemotaxis)-increse swelling even more & PAIN!
  6. What is the process involved in phagocyte mobilization?
    • 1. Leukocytosis (more leukocytes)
    • 2. Margination (adhere to side of capillary wall)
    • 3. Diapedisis ("walk"/move along capillary wall)
    • 4. Chemotaxis (traveling of phagocytes to localized area)
  7. List the inflammatory chemicals and discuss their functions
    • Histamine & Seratonin cause blood vessels near wound
    • to constrict
  8. List the antimicrobial proteins and describe their function.
    Interferons (a, b, g-activate MAC cells) & Complement (classical & alternative-activate MAC cells). Attack microorganisms directly and stop reproduction of pathogens
  9. Explain how fever helps protect the body.
    Caused by the body's release of chemicals that stimulate the action of WBCs (first line of defense) by increasing the body's temperature
  10. Inflammatory Process: Kinins
    • Vascular Permeability (molecule with greatest inflammatory response)
    • Vasodilation
    • Pain
    • Chemotaxis
    • NO Clotting
    • NO Fever
  11. Inflammatory Process: Interlukins
    • Vascular Permeability
    • NO Vasodilation
    • NO Pain
    • NO Chemotaxis
    • Clotting (stimulates platelet production)
    • Fever
  12. Inflammatory Response:Histamine
    • Vascular Permeability
    • NO Vasodilation
    • NO Pain
    • NO Chemotaxis
    • NO Clotting
    • NO Fever
  13. Inflammarory Response:Thrombin
    • Vascular Permeability
    • NO Vasodilation
    • NO Pain
    • NO Chemotaxis
    • Activates Clotting
    • NO Fever
  14. Inflammatory Process: Complement
    • NO Vascular Permeability (only molecule w/o permeability)
    • NO Vasodilation
    • NO Pain
    • Chemotaxis
    • NO Clotting
    • NO Fever
  15. Inflammartoy Process: Tumor Necrosis Factors (TNFs)
    • Vascular Permeability
    • NO Vasodilation
    • NO Pain
    • NO Chemotaxis
    • Clotting (stimulates platelet production)
    • NO Fever
  16. What is the relationship between capillaries & lymphatic vessels?
    Capillaries feed into collecting vessels->feed into trunks->blind sacs close contact with capillaries->protein free fluid is absorbed->fluid moves into BUT NOT OUT OF lymph capillary->enter lymphatic system
  17. How does the lymph normally flow?
    The lymph flows upward to empty into large veins of the neck.
  18. Where are the majority of B cells?
    B cells are found in the Spleen & Lymph Nodes.
  19. Where are the majority of T cells?
    T cells are found in the Thymus.
  20. What is the structure & function of the Spleen?
    • Structure: Located in left hypochondriac region protected by ribcage
    • HIGHLY VASCULAR
    • Red Pulp (engourged with RBCs)
    • White Pulp (lymphocyte & macrophage group)
    • Function: RBC Production
    • Removes old RBCs & platelets from blood
    • Stores platelets & recycled RBC waste
    • Interaction site for lymphocytes & antigens
  21. What is the struture & function of the Thymus?
    • Structure: Located between aortic arch & superior mediastinum (right above the main artery invisible on adults)
    • Function: Influences the martuation of immature lymphocytes into mature T cells
  22. What is the MALT & why is its location important to its function?
    Mucosae-associated lymphatic tissue. It is located in areas of body that are vulnerable to invasion by pathogenic bacteria.
  23. The main protein in blood plasma is____
    Albumin constitutes about 60% of plasma protein.
  24. What part of the body does erythropoietin (EPO) target to increase erythropoiesis?
    Bone Marrow
  25. What part of the hemoglobin molecule is recycled to form bile?
    A portion of the heme group
  26. Which formed element can be described as cytoplasmic fragments?
    Platelets
  27. In adults, RBC production occurs in _____.
    Red bone marrow is the site of erythrocyte production.
  28. These three can stimulate erythrocyte production:
    • 1) a drop in normal blood O2 levels
    • 2) testosterone
    • 3) erythropoietin
  29. _________ results from a vitamin B12 deficiency
    Pernicious anemia
  30. On a blood smear slide prepared using Wright's stain, you observe a large cell with a U-shaped nucleus and pale blue cytoplasm. This cell is most likely a(n)______.
    Monocyte
  31. Athletes who choose to use industry-produced EPO as a performance-enhancing drug to increase the effects of their naturally-produced EPO, will experience _______.
    decreased production of EPO by their kidneys. (powerful hormone secreted by kidneys)
  32. What are three functional characteristics of leukocytes?
    • 1) amoeboid motion
    • 2) diapedesis
    • 3) positive chemotaxis
  33. A person who lacks agglutinogens A and B would have blood type ____.
    O
  34. What are the three formed elements of the blood/red bone marrow?
    • 1) erythrocytes (RBCs)
    • 2) leukocytes (WBCs)
    • 3) platelets (fragments)
  35. What are the two most abundant components of whole blood, in order from most abundant and second-most abundant, are _______. (think about tube after removed from centrifuge)
    Plasma, erythrocytes
  36. A test tube of blood goes unused in the lab, and the stagnant blood coagulates. This is due to which pathway of blood clotting?
    Intrinsic pathway
  37. In the lab, the tech determines the pt's blood type. Pt's blood agglutinates in anti-A antibodies, but has no reaction in anti-B or anti-D antibodies. What is the pt's blood type?
    A-
  38. Besides the HCT, what other component of blood could be measured to give a better understanding of O2-carrying capacity?
    Hemoglobin encourages the transportation of O2 to organs in the body.
  39. What are the differences between non-specific & specific immunity?
    • Non-specific:
    • Respond to any “non-self" cell
    • Rapid response
    • No memory developed
    • Specific:
    • Recognize then destroy specific antigens
    • Delayed response
    • Memory developed
  40. What is an antigen?
    ANY substance that can initiate an immune response (NON SELF)
  41. What are antigenic determinant?
    • Surface proteins found on antigens that allow Antibody & activated lymphocyte binding.
    • One antigen can have 100 determinants.
  42. Describe clonal selection of B-cells.
    • Primary Immune Response
    • –First exposure of immunocompotent B-cell to a single antigen in lymph or blood
    • -Activates B-cell through surface receptor binding
    • Begins clonal selection of B-cells
    • Cell division (expansion)
    • •All cells have IDENTICAL surface receptor
    • Memory B-cell is made
    • “Cloned” B-cells differentiate into plasma cells & produce antigen specific antibodies
  43. Describe differentiation of B-cells.
    • Secondary Immune Response
    • Second exposure to SAME antigen
    • Memory B cells are activated through surface receptor binding
    • Cell division
    • •All cells have IDENTICAL surface receptor
    • Differentiation of B-cells to plasma cells
    • Antigen specific antibodies are made
  44. Compare and contrast primary & secondary immune responses.
    • Primary Immune Response:
    • Activates B-cell thru surface receptor binding
    • Clonal selection of B-cell
    • B-cells differentiate into plasma & antigen specific antibodies
    • Lag time: 3-6 days, Peak ~10 days
    • Secondary Immune Response:
    • Activates MEMORY B-cell thru surface receptor binding
    • No clonal selection
    • B-cells differentiate into plasma & antigen specific antibodies
    • Lag time: 12 hrs, Peak 2-3 days
  45. What is the difference between Active Immunity & Passive Immunity?
    • Active= body mounts immune response
    • –Natural = due to normal exposure to infectiveagents
    • –Artificial = vaccine
    • Passive= person given preformed antibodies
    • –Natural = mother to fetus/infant
    • –Artificial = injection
  46. Describe the structure of an antibody.
    • 4 protein chains (2 heavy & 2 light)
    • Variable regions has antigen binding site with variable protein structure
    • Constant regions allows two or more antibodies to bind together or to cell surface
    • Complement binding sites found ONLY on heavy chain constant region
  47. What are the 5 classes of antibodies?
    • (MADGE)
    • IgM, IgA, IgD, IgG, IgE
  48. What are the functions of the 5 classes?
    • IgM: first to peak during a primary immune response
    • IgA: protects mucosal barriers
    • IgD: along with IgM, this is a B-cell receptor
    • IgG: Main antibody of both primary and secondary immune response
    • IgE: Involved in allergies
  49. What are the similarities & differences between CTLs & NK cells?
    • CTL is MHC restricted for activation
    • NK cells DO NOT express antigen specific receptors
    • CTLs make memory cells but NKs don’t
    • Both use perforins & granzymes to cause cell death
    • NKs recognize target cells by two receptor model
  50. What is the cause & cellular physiology of Graft Rejection?
    • Caused by a cell mediated immune response to MHCs on the graft tissue.
    • •Sensitization stage
    • –T-cells respond & activate
    • –Major APC is dendritic cell from graft
    • •Effector stage
    • –CTLs & NKs cause cell lysis
    • –Flooding of graft with cytokines
  51. What is the cause and cellular physiology of Acute Hypersensitivities?
    • Caused by an allergic reaction
    • Sensitization stage
    • –Antigen exposure
    • –B-cell differentiates to plasma cell that secretes IgE
    • –IgE binds to mast cells & basophils (becomes fixed)
    • Secondary Response
    • –More antigen invades body
    • –Antigen binds fixed IgE
    • –Mast cells & basophils DEGRANULATE
    • –Histamine is released
    • •Vasodilation & fluid release
    • •Mucus production
    • •Bronchioles constrict
  52. What is the link among the non-specific & specific imune system?
    Both go thru the same process of attacking the antigen, however the non-specific immune system has a shorter time span and does not create a memory t-cell. The specific immune system is a longer process, however it creates memory t-cells

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