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Flashcards

Test 4: Part 2

Brianne Schmiegelow Animal Physiology Undergraduate English 83 cards

Cards in this deck (83)

  1. 1What is coprophagia?Eating of feces
    Some species do this to recover the vitamin Bs that the colon can't absorb
  2. 2What accounts for up to 10% of our caloric intake?The absorption of small fatty acids in the large intestine that are produced by bacteria fiber digestion
  3. 3How is the digestive system controlled?Both neural and hormonal control
  4. 4What is the Enteric NS?Nervous system of the digestive system that controls glands, muscles, and motility
  5. 5What determines the length of digestion in the stomach?Amount and type of food
    Detected by stretch and chemoreceptors
    Carbohydrates - fast (<1hr)
    Proteins - intermediates
    Fats - slow (up to 6 hr)
  6. 6What is CCK?Hormone secreted by the small intestine when fat or acid-rich chyme from the stomach enters
    Causes the gallbladder to contract, sending stored bile to the small intestine
    Causes pancreas to release digestive enzymes
    Slows stomach emptying so chyme can be neutralized and emulsified a little at a time
    Stimulates satiety
  7. 7What is secretin?"first hormone"
    Release by small intestine is stimulated by the presence of acid
    Circulates and stimulates pancreas to secrete bicarbonate for neutralization (SI not as well protected as the stomach) and so the enzymes work best (neutral/alkaline)
    Slows down stomach emptying
  8. 8What are the two types of incretins? What do they do?GIP and GLP
    Stimulate insulin secretion
    Secreted in response to glucose in the small intestine
  9. 9Who doesn't respond to GIP?People with NIDDM because of lack of receptors
  10. 10What does GLP do?Inhibits acid secretion and stomach-emptying
    Increases satiety
    Increases insulin, decreases glucagon
  11. 11Hormones don't play a role in ______ motility. Control is via _________ and _______.Large intestine
    Enteric NS and ANS
  12. 12What can stimulate/inhibit defecation?Anxiety can do both!
    Coffee stimulates
  13. 13What is the innate immune system?System that provides an immediate, non-specific response
    Found in all plants and animals
  14. 14What is the adaptive immune system?System that is activated to specifically attack pathogens that evade/survive the innate response
    Specificity is carried into the future by immunological memory
  15. 15What is immunological memory?System that carries specificity into the future which enables faster, stronger attack next time that pathogen is seen
    How vaccinations work!
  16. 16What are PAMPs?Pathogen-associated molecular patterns
    Include LPS (lipopolysaccharide) from gram- membranes and peptidoglycan from gram+ walls and double-stranded RNA from viruses
    Trigger phagocytosis by the innate system
  17. 17What are PRRs?Pattern recognition receptors
    Receptors in innate system cells that recognize the PAMPs common to many microbes
  18. 18What are neutrophils?WBCs that are produced in the marrow
    Mobile, short-lived, and the 1st to arrive at infection sites (within minutes), biggest component of pus
    Attracted by cytokines and exit the bloodstream by diapedesis
  19. 19What's the most abundant type of WBC?Neutrophils
  20. 20What are macrophages?Derivatives of monocytes
    Mobile, long-lived phagocytes
  21. 21What are organ-specific phagocytes?Phagocytes that are often tethered and found in the liver, spleen, lymph nodes, lungs, and brain
  22. 22Fever is part of innate immunity. How?It is induced by pyrogens released by WBCs in response to PAMPs
    Increases body temp above the optimal growth temp for many microorganisms
    Leads to release of heat shock proteins
  23. 23What are heat shock proteins? What is their role?Family of proteins released in stressful conditions that cause production of inflammatory cytokines
    Cytokines increase metabolism which increases production and activity of phagocytes, speeds up multiplication of lymphocytes, increases antibody and cytokine production, and increases WBC release by marrow
  24. 24What are interferons?Polypeptides that are produced by virus-infected cells to boost immune activity
    Activate Natural Killer Cells
    Confers short-acting, non-specific resistance to viral infection on nearby cells
  25. 25What are natural killer cells? (NKCs)WBCs that are activated by interferons
  26. 26What is the purpose of the complement system?To help clear pathogens and bad cells from the body and to work with adaptive immunity
  27. 27How does the complement system work?When activated, the system initiates an enzyme cascade that results in the formation of MACs to kill pathogenic cells
  28. 28What are MACs?Membrane attack complexes
    Large pores formed by complement proteins that perforate and lyse pathogenic cells
  29. 29What are antigens?Molecules that can elicit an immune response
    Immune system can distinguish self from non-self antigens and NORMALLY only makes antibodies against nonself
  30. 30What are lymphocytes?A class of WBCs that include T cells, B cells, and natural killer cells
    Produced by the thymus, spleen, and lymph nodes
  31. 31What are T cells?Cells produced by the thymus that provide cell-mediated immunity
    Constitute 65-85% of lymphocytes in blood
    Attack infected host cells, cancer cells, and foreign cells
  32. 32What are B cells?Lymphocytes that secrete antibodies into blood and lymph which provide humoral immunity
    Have antibodies on their surface that are receptors for antigens
    When bound to the antigen, they are stimulated to divide and secrete antibodies
  33. 33What happens when B cells divide?Some become plasma cells, some become memory cells
  34. 34What are plasma cells?Cells derived from B cells that produce about 2000 antibodies per second
    Provide active immunity
  35. 35What are memory cells?Cells derived from B cells that provide a rapid, strong antibody response to subsequent exposures to an antigen
  36. 36What is the complement cascade?A process triggered by the binding of B cells to antigens
    B cells and their products serve as signals for MACs and phagocytes to carry out killing
  37. 37What are antibodies?Proteins called immunoglobulins
    5 types, basic structure is a "Y"
  38. 38What are the 5 types of antibodies?IgG, IgE, IgM, IgA, and IgD
  39. 39What is Fab?The variable region of antibodies at the tips of the "Y" arms that binds antigens and confers antibody specificity
  40. 40What is Fc?The stem part of the "Y" that is constant among different antibodies
    Activates other parts of the immune system
  41. 41How many antibody molecules does each person have?10^20
    (With a few million different specificities)
  42. 42What is antigen specificity based on?Shape
    An antibody binds to an antigen that fits into its binding pocket
  43. 43What is opsonization?Labeling of a pathogen for phagocytosis or complement attack
    Antibodies do this because they can't kill on their own
  44. 44What do antibodies use opsonization on?Gram negative bacteria, viruses, and host cells recognized as non-self
  45. 45What are MHCs?The Major Histocompatibility Complex
    4 gene complex on Chromosome 6
    Produce cell surface proteins that display self peptides normally made by a cell or non-self peptides normally originating from a pathogen
    Are on the surface of all the body's cells EXCEPT mature RBCs
  46. 46What forms the basis for histocompatibility typing?MHC genes have multiple alleles, creating many possible MHC types
    Basis of organ compatibility
  47. 47What do MHCs produce?2 types of antigen-presenting proteins: Class 1 and Class 2
  48. 48What are class-1s?Antigen-presenting molecules produced by MHCs in all cells except RBCs
    Display peptides normally made by a cell on the cell's surface
    Interacts with CD8 coreceptor on killer Ts which (normally) recognize these peptides as self and leave them alone
  49. 49What happens if a killer T's antigen is presented by a class-1 protein?The killer T takes out the cell with the help of the complement system because it indicates it's a bad self cell
    Killer Ts have to have found a class 1 with a foreign antigen to bind to the cell
  50. 50What happens if killer Ts respond to self antigens?They are (normally) deleted or inactivated
  51. 51What are class-2s?Antigen-presenting proteins produced by MHCs that are expressed by professional antigen-presenting cells
  52. 52What are pro APCs?Professional antigen-presenting cells
    Include macrophages, dendritic cells, and B cells
    Phagocytize antigens then digest them into small pieces (epitopes) which are presented by class-2s on their surface
  53. 53What do pro APCs have on their surface?Class-1 and Class-2 proteins
  54. 54Which cells can activate a killer or helper T that has never seen its antigen before? How?Dendritics
    When a naive helper T binds to its antigen and a class-2 MHC, a dendritic cell activates it with ILs which leads to secretion of antibodies, memory cells, and plasma cells
  55. 55What is CD4?A coreceptor on helper Ts that interacts only with class-2s on dendritic cells
  56. 56What do activated helper Ts do?Stimulate other cells with ILs
  57. 57What are NKCs?Natural killer cells
    Lymphocytes that can kill virus-infected and tumor self cells that are opsonized and lack class-1 MHC antigens
  58. 58How do intracellular microbes and tumors become resistant to killer T actions? What kills them then?They down-regulate class-1 molecules
    NKCs recognize these cells and attack them with MACs, granzymes, and perforins
  59. 59What is affinity maturation?When a B cell binds to an antigen, it undergoes programmed point mutations of its variable region genes at a rate 10^6x higher than normal
    If the new Bs bind longer and tighter to the epitope, they will divide more and survive longer, so this fine-tunes the shape of the Fab antigen pocket (binds epitope better)
    The better-fit Bs become plasma and memory cells
  60. 60What is immunological tolerance?The ability to produce antibodies against non-self while tolerating self
    BEGINS at about 1 month of life
  61. 61Where does T cell tolerance first develop? B cell?Thymus
    Marrow
  62. 62What is AIRE?Autoimmune regulator
    A transcription factor in the thymus that causes the thymus to express peptides produced by most other tissues, creating a profile of self-antigens
  63. 63What happens to new Ts that bind to the selfs produced by AIRE?They are deleted!
  64. 64Why do dendritics migrate to the cortex of the thymus?To help present self-antibodies to developing Ts for potential deletion in the event that they bind to selfs
  65. 65What happens to B cells in marrow that bind selfs?They undergo receptor editing, meaning they reshuffle gene expression to make new receptors
    If it still bind self, they will undergo apoptosis
  66. 66What is peripheral tolerance?Outside the thymus, naive T cells that recognize self-antigens undergo apoptosis (clonal deletion), usually in the lymph nodes
    And/or Ts, Bs that bind selfs are inactivated and circulate without function until they die (ANERGY)
  67. 67What are autoreactive Ts?Killer Ts that attack self-antigens
  68. 68Which self-antigens are normally hidden from the blood? What happens if the body has exposure to these?Lens protein in the eye, those in joints, etc.
    Exposure results in production of autoantibodies and attack from autoreactive Ts
  69. 69What is FAS?A surface receptor on killer Ts that increases during infection
  70. 70What is FAS ligand?Produced by killer Ts a few days after an infection begins
    Binds to FAS and triggers apoptosis of the killer Ts
  71. 71What are Tregs?Suppressor T cells
    Cells that shut down immune attack after a disease to deter autoimmunity
    Secrete cytokines that suppress other immune cell activity
  72. 72What happens if you have a deficiency of Tregs?Severe autoimmunity, immunopathology, and allergy
  73. 73What is the primary antibody response?On first exposure to a pathogen, there is a latency of 5-10 days before specific antibodies are made, then antibody levels decline after a few weeks
    Induced by vaccines
  74. 74What is the secondary antibody response?A response caused by subsequent exposure to the same antigen that causes much more rapid and sustained antibody production
  75. 75What is passive immunity?Protection produced by transfer of antibodies from a donor to a recipient
    Used to treat snakebite, rabies, tetanus, and hepatitis
  76. 76How does passive immunity occur with babies?Occurs naturally before and after birth (most in breastmilk)
    Some antibodies from the mother pass the placenta to the fetus during pregnancy and provide passive immunity
  77. 77What is colostrum?Produced by a mother during the first 2-3 days of nursing
    Contains her antibodies and gives her immunity to the infant
  78. 78When does a specific immune response develop? When do vaccines take?1 month
    15 months
  79. 79What happens when you have an autoimmune disease?Autoreactive T cells are formed and B cells produce autoantibodies
  80. 80What happens in Hashimoto's?Antibodies attack thyroglobulin which is normally hidden from immune surveillance
  81. 81What happens in thrombocytopenia?Platelets are destroyed because they combine with the victim's medications
    An example of a self-antigen that is otherwise tolerated with a foreign antigen that is not
  82. 82What happens in rheumatoid arthritis?Antibodies are produced that are directed against other antibodies
  83. 83What happens in Type I diabetes to make it autoimmune?Self-antigens are presented to a helper T by a class-2 molecule causing them to be activated

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Test 4
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