Foundations 2, Week 1

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Foundations 2, Week 1
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2013-09-22 18:41:41
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Foundations 2, Week 1
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  1. What are the three layers of the blood vessel wall?
    • Tunica Intima: contains the endothelium (a single layer of squamous epithelial cells), the basal lamina of the endothelium, and loose connective tissue called the subendothelial layer.  Capillaries and postcapillary venules consist entirely of tunica intima.
    • Tunica Media: a layer of circumferentially layered muscle cells sandwiched between an internal and external elastic membrane. This layer is thick in arteries.
    • Tunica Adventitia: Layer of longitudinally arranged connective tissue (mostly collagenous with some elastic fibers).  This layer is thick in veins.  In thick veins and arteries, this layer also contains a network of vessels called the vas vasorum that supplies blood to the vascular walls and autonomic nerves called the nervi vascularis that contracts smooth muscles in the vessels.
  2. How does the wall and diameter of arterial vessels change from the aorta to the capillary?
    The diameter decreases from > 10 mm to as low as 4 micrometers. The tunica adventitia is consistently thinner than the tunica media.
  3. How does the wall and diameter of venous vessels change from the post capillary venule to the large veins?
    The diameter increases from 10 micrometers to as large as 10 mm. Some of the tunica adventitia is consistently thicker than the tunica media.
  4. How do arterioles differ from small arteries in structure and function?
    • Small arteries: Up to 8 layers of smooth muscle. The tunica intima has an internal elastic membrane.
    • Arterioles: have only 1 or 2 layers of smooth muscle. May not have a tunica intima.
  5. What is the function of precapillary sphincters?
    A precapillary sphincter is a slight thickening of the smooth muscle at the origin of a capillary bed from an arteriole, that adjusts the blood flow into each capillary.
  6. What are the constituents of the capillary wall?
    A single layer of epithelial cells and their basal lamina.
  7. What are the three types of capillaries and where might they be found?
    • Continuous capillaries: muscle and CNS
    • Fenestrated capillaries: endocrine glands and sites of fluid absorption
    • Discontinuous capillaries: liver, spleen, bone marrow - these are larger capillaries
  8. Name the most common vasoconstrictors.
    • Endothelins (ET-1, ET-2, ET-3)
    • angiotensin-converting enzyme (ACE)
    • prostaglandin H2
    • thromboxane A2
  9. Name the most common vasodilators.
    • Nitrous oxide (NO)
    • prostacyclin (PGI2 or prostaglandin I2)
    • PAF
    • Bradykinin (Platelet-activating factor)
  10. What is the structure and function of a pericyte?
    When present, pericytes (AKA Rouget cells) surround the capillary with branching cytoplasmic processes to provide vascular support. They are sometimes involved in pathogenesis (tumor angiogenesis and diabetic retinopathy).
  11. What are cytokines?
    Proteins released to affect the behavior of other cells by inducing transcription (including influencing differentiation) in an autocrine or paracrine manner. Also called Interleukins (IL-#) and Lymphokines.
  12. What are MHC class I molecules?
    • MHC class I molecules present fragments of proteins from the cell’s cytosol onto the cell’s surface, allowing other cells to recognize them as healthy or unhealthy.
    • Known as the cytosolic or endogenous pathway.
  13. What are MHC class II molecules?
    • MHC class II molecules present fragments of extracellular proteins, allowing for antigen presentation by APCs.
    • Known as the endocytic or exogenous pathway.
  14. What is CD?
    CD## = Cell Differentiation, a system for naming and characterizing cell surface molecules.
  15. What is an opsonin?
    Any molecule that enhances phagocytosis by marking an antigen for an immune response (ie, for phagocytosis or the complement system).
  16. Name the types of leukocytes from most numerous to least.
    • Neutrophils: 40%-70%
    • Lymphocyte (B and T cells): 20%-50%
    • Monocytes (become dendritic cells and macrophages): 2%-10%
    • Eosinophils: 1%-6%
    • Basophils: <1%
    • Remember! Never Let Monkeys Eat Bananas!
  17. Which cells are granulocytes?
    • Neutrophils
    • Eosinophils
    • Basophils
    • Never Eat Bananas (they are too grainy)
  18. How do neutrophils work?
    • Neutrophils bind bacteria and cancer cells, engulf them, and then destroy them with the toxic contents of their granules.
    • OR they can release granules to destroy pathogens without phagocytizing them.  
    • After phagocytosis, the pH of the lysosome is increased using HClO.
    • Neutrophils are attracted by cytokines released by endothelium, mast cells, and macrophages. They secrete additional cytokines as well.
  19. How do NK cells work?
    • NK cells are innate immunity lymphocyte that act about 3 days after an infection.
    • They respond to tumors and virus-infected cells.  
    • They are very similar to NK T cells, but lack the T-cell antigen receptors.  
    • NK cells have NKG2D receptors that bind to MIC ligands (expressed by unhealthy cells) and inhibitory receptors that bind to MHC class 1 ligands (expressed by healthy cells).
  20. How do monocytes work?
    Monocytes are stored in the spleen, but then move quickly to infection sites where they differentiate into macrophages and dendritic cells.
  21. What is Heparin?
    A powerful anticoagulant with the highest known negative charge density of any molecule.
  22. How do mast cells work?
    • Mast cells release histamines and heparin when triggered by IgE receptors on their surface.
    • They are similar in appearance and function to basophils despite having different progenitor cells.
  23. What is histamine?
    • An anti-inflammatory drug released by basophils and mast cells.
    • It increases vasodilation and recruits additional WBCs.
  24. How do basophils work?
    • Basophils release heparin and histamine when their receptors bind IgE.
    • They are often found near parasites.
    • When antigens or antibodies are detected, they release cytokines (including IL-4) to increase the production of effector T cells.
    • They play a role in allergens as well.
  25. How do eosinophils work?
    Eosinophils attack helminths, worms, and other multicellular parasites (detected through the IgE antibody) by releasing cationic granule proteins, reactive oxygen species (superoxide, peroxide, etc), and enzymes.
  26. What are the primary phagocytic cells?
    • Neutrophils (the most potent)
    • Dendritic cells
    • Macrophages
  27. What are the primary antigen-presenting cells?
    • Dendritic cells
    • Macrophages
    • B cells.
  28. How do macrophages work?
    • Macrophages engulf and then digest cellular debris, pathogens, and cancer cells.
    • They also stimulate lymphocytes and other immune cells to respond to pathogens.
    • They are produced from monocytes.
  29. What is IL-4?
    Interleukin 4 is a cytokine that induces differentiation of naive helper T cells (Th0 cells) to Th2 cells.
  30. What cytokine promotes the production of RBCs?
    Erythropoietin (EPO).
  31. What cytokine promotes the production of megakaryocytes?
    Thrombopoietin (TPO).
  32. What is a respiratory burst?
    • A respiratory burst (aka oxidative burst) is the rapid release of reactive oxygen species (superoxide radical (O2-) and hydrogen peroxide H2O2) and a metabolic change accompanied by an increase in oxygen consumption.
    • Occurs in neutrophils and macrophages when they phagocytose pathogens.
  33. How do B cells work?
    • B cells make antibodies against antigens and act as antigen-presenting cells (APCs)
    • B cells can develop into plasma cells and memory B cells after activation by antigen interaction.
  34. How do plasma cells work?
    In response to an antigen interaction, B cells can become plasma cells to release large volumes of antibodies.
  35. How do memory B cells work?
    Memory B cells last for an average of 10 years, retaining immunity and aiding in secondary responses should a pathogen reoccur.
  36. What are the different types of T cells?
    • T cells are any lymphocytes containing a T-cell receptor, including:
    • T helper cells (TH or CD4+ T cells): express the CD4 protein on their surface. They secrete cytokines when activated by MHC class II molecules.
    • Cytotoxic T cells: T cells expressing CD8 glycoprotein (CD8+ T cells), bind to cells with antigen-bound MHC class I molecules to destroy virally infected cells and tumor cells.
    • Memory T cells: persisting T cells that may express either CD4 or CD8 glycoproteins.
    • Regulatory T cells: (aka suppressor T cells) shut down T cells after an immune reaction, and shutdown auto-reactive T cells that escape negative selection in the thymus.
    • Natural Killer T cells: T cells that express NK properties as well.
  37. Name 3 ways pathogens can cause damage.
    • 1) By releasing exotoxins (like Vibrio Cholerae). Exotoxins can interact with membrane receptors, destroy cell membranes, or enter cells.
    • 2) By releasing endotoxins (like Yersinia pestis, which causes plague)
    • 3) By entering the cell and causing cell death (direct cytopathic effect, demonstrated by the influenza virus).
  38. What is the coagulation system?
    • Thrombocytes cause wounds to coagulate and release thrombocidens to kill pathogens in the region!
    • These platelets also release cytokines and chemokines to prepare other defenses and activate neutrophils.
  39. What are defensins?
    • Host defense peptides that are active against bacteria, fungi, and many viruses (especially phagocytosed pathogens).
    • They work by attaching to the pathogen membrane to create a pore that allows ions and nutrients to escape and enter.
    • α-defensins are mainly produced by neutrophils.  ß-defensins are primarily produced by epithelial cells.
  40. What are paneth cells
    Epithelial cells of the small intestine that secret defensins, lysozymes, and TNF-α.
  41. What are Lysozymes?
    Enzymes that damage bacterial cell walls.
  42. What are Endotoxins?
    Toxic lipopolysaccharides released by gram-negative bacteria when they are destroyed.
  43. What are Exotoxins?
    Powerful toxins secreted by bacteria, or released upon their destruction. Exotoxins can interact with membrane receptors, destroy cell membranes, or enter cells.
  44. What is TNF-α?
    • A pyrogen that is able to induce fever, apoptotic cell death, and inflammation.
    • It is able to inhibit tumorigenesis and viral replication.
  45. Describe the trafficking of a naive T cell into a lymph node and then it's re-entry into the bloodstream.
    When a T cell has seen an antigen, it downregulates a surface receptor.  If a T cell is missing the surface receptor, lymph nodes will reject them, allowing only naive T cells to enter.
  46. Describe the mechanisms of action of histamine in inflammation.
    • 1: Histamine is stored in the granules of platelets, basophils, and mast cells.  
    • 2: Histamine and serotonin granules are released from platelets during aggregation.
    • 3: Granule release from mast cells and basophils is stimulated by trauma, IgE-antigen interaction, or by the binding of C3a and C5a, substance P, IL-1 and IL-8 to their respective receptors on mast cells.
    • 4: Histamine induces increased vascular permeability by binding to H1 receptors on endothelial cells (causing contraction of myosin resulting in endothelial gaps).
  47. How does the complement system work?
    • C3 is converted to C3a and C3B through one of three pathways.  C3B then covalently bind to the surface of pathogens, labeling them for destruction by phagocytes.  Hence, defects in C3B are the most severe.  
    • Additionally, the pathogen can be destroyed directly by continuing the complement cascade on the pathogen surface.  C3B causes C3b2Bbto form, causing C5 to attach, which cleaves C5 to C5a and C5b. C5b binds to C6 and then to C7. This complex attaches to the lipid bilayer where C8 attaches, followed by a number of C9 molecules, which form a pore. (aka C3b-C5b-C6-C7-C8-C9{n} pore)
    • C3a and C5a are also active as anaphylatoxins, causing inflammation, chemotaxis, increased receptors, and increased wall adherence for WBCs. C5a is more stable and potent.  These anaphylatoxins can cause anaphylactic shock.
  48. How does the Alternate complement pathway work?
    C3 convertase iC3bBb is the converting enzyme.  The C3B molecule causes more C3B to attach through a positive feedback mechanism, making the cell very easy to identify.
  49. How does the Lectin complement pathway work?
    Mannose-associated serine proteases (2 MASP 1 and 2 MASP 2 - a total of 4) bind Mannose-binding lectin. This cleaves C4 to C4a + C4b, and C2 to C3b and C3a. C4b and C32a form C2aC4b classical C3 convertase, which cleaves C3.
  50. How does the Classical complement pathway work?
    C1 binds to a C-reactive protein on the pathogen surface. This creates the same C2aC4b classical C3 convertase, which cleaves C3.
  51. What role do phagocytic cells play in complement-mediated clearance of a pathogen?
    Macrophages and other phages have CR1 (Complement receptors) that bind C3b coated pathogens, allowing for phagocytosis.
  52. How does IL-2 T cell proliferation work?
    • Naive T cells express low affinity IL-2 receptors (having ß and gamma chains). Active T cells express high affinity IL-2 receptors (α, ß, and gamma chains) and secrete IL-2.
    • Antigen binding causes activation of the high affinity IL-2 receptor and secretion of IL-2.
    • IL-2 causes T cells to proliferate.  IL-2 is an interesting cytokine because it can also act in an autocrine fashion, activating its own receptors.
  53. Describe the Jak/Stat signal transduction pathway responsible for cytokine signaling.
    The JAK/STAT pathway consists of 2 Jak (a tyrosine kinase receptor) strands that bind a cytokine to dimerize, causing the JAK proteins to phosphorylate their strands and attract STAT proteins. 2 STAT proteins dimerize and then travel to the nucleus to induce transcription.
  54. What kind of receptors interact with chemokines?
    G-coupled receptors.
  55. What is IL-8?
    • Interleukin 8 is a chemokine that interacts with CXCR8 G-coupled receptors to attract neutrophils.
    • Think, "Interleukin 8! Don't be late!" -it's a chemokine that makes neutrophils hurry to their destination.
  56. How is Factor XII activated?
    Hageman factor (aka, clotting factor XII) is activated by exposure to negatively charged surfaces such as basement membranes, proteolytic enzymes, bacterial liposaccharides, and foreign materials.
  57. What does activated Factor XII activate?
    • Conversion of plasminogen to plasmin, which degrades fibrin clots.
    • Conversion of prekallikrein to kallikrein, which cleaves kininogen to kinins, which induce vasodilation. (ie, inflammation)
    • Activates the alternative complement pathway.
    • Activates the coagulation system.
    • Ie, degrades fibrin clots, causes inflammation, coagulation, and activates the alternative complement pathway.
  58. Identify these nuclear changes in necrosis:

  59. Identify these necrotic changes:
    • red=Karyolysis
    • yellow=karyorrhexis
    • black=pyknosis
    • blue=protein coagulation
    • green=acute inflammation
  60. How do bradykinins work?
    • Bradykinin causes inflammation through the release of prostacyclin, nitric oxide, and Endothelium-Derived Hyperpolarizing Factor.
    • Bradykinin is degraded by ACE, so ACE inhibitors increase the amount of bradykinin and promote vasodilation.
  61. What are the early activators of inflammation?
    • Histamine
    • Bradykinin
    • PAF
    • C3a
    • C5a
    • Leukotrienes
  62. What are the late activators of inflammation?
    • IL-1b
    • TNFa

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