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Karteikarten

Inflammation 2

Rachael Jones 2. Pharmacology and therapeutics AD1 Englisch 85 Karten

Karten in diesem Stapel (85)

  1. 1Where are neuropeptides released form?Sensory neurones
  2. 2What do neuropeptides produce?Neurogenic inflammation
  3. 3Give 2 neuropeptides that activate mast cells.1. Neurokinin A
    2. Substance P
  4. 4What is Calcitonin gene-related peptide (CGRP)?A potent vasodilator that is a neuropeptide
  5. 5What 2 functions can the same neurone do in relation to causing inflammation?1. Send signals to the spinal cord causing the release of neurotransmitter
    2. Act locally, eg cause vasodilation
  6. 6What are cytokines and where are they released from?Protein or polypeptides produced and released from immune inflammation
  7. 7What is the most potent substance in the body and what does this mean?Cytokines
    Very little is required to cause a response
    Sub nanomolar (<1x 10^-9M)
  8. 8How many cytokine exist but how many main sub-groups are there?Over 100 exist
    Split into 4 main groups
  9. 9When are cytokines upregulated?During inflammation
  10. 10What do cytokines do?Act at kinase-linked receptors or GPCRs to coordinate inflammatory response
  11. 11What are the 4 main groups of cytokines?1. Interlukins
    2. Interferons
    3. Chemokines
    4. Colony Stimulating Factors
  12. 12What are the 2 sub groups of interleukins?1. Pro-inflammatory
    2. Anti-inflammatory
  13. 13Give 2 examples of pro-inflammatory interleukins.1. Tumour necrosis factor (TNF) alpha
    2. Interleukin (IL) -1 family
  14. 14When are pro-inflammatory interleukins released?During inflammation
  15. 15What is the role of pro-inflammatory interleukins?Stimulate synthesis and release of other cytokines
  16. 16When are pro-inflammatory interleukins implicated?1. Rheumatoid arthritis
    2. Irritable bowel disease
  17. 17Give 4 examples of anti-inflammatory interleukins.1. Transforming growth factor (TGF) beta
    2. IL-4
    3. IL-10
    4. IL-13
  18. 18What is the function of anti-inflammatory interleukins?Switch off the inflammatory response once the harmful substance has been removed
  19. 19What makes up the interferons class of cytokines?Several different proteins
  20. 20Give the 3 most well studied interferons.1. IFN alpha
    2. IFN beta
    3. IFN gamma
  21. 21Roughly how many proteins make up the IFN alpha family?About 20
  22. 22When are interferons released?In response to viral infection and other pathogens, activate anti-viral processes
  23. 23What could be used in the future to treat viral infections?Recombinant interferons
    (eg Virbagen Omega- feline immunodeficiency)
  24. 24What do chemokines do?Control migration of leukocytes
    Some also have other effects eg mast cell degranulation
  25. 25How many chemokines have been identified?More than 40
  26. 26How do some viruses exploit the chemokine system?Produce proteins that can mimic chemokines or antagonise their receptors
  27. 27What process are chemokines involved in?Chemotaxis
  28. 28Name a virus that exploits the chemokine system by binding to a chemokine receptor.HIV
  29. 29Where do colony stimulating factors bind to to cause proliferation and differentiation into specific blood cells?Haemopoietic stem cells
  30. 30Give 3 examples of colony stimulating factors.1. Granulocyte-macrophage CSF
    2. Granulocyte CSF
    3. Macrophage CSF
  31. 31What are colony stimulating factors used for clinically?Stimulate the production of leukocytes
    eg. post chemotherapy
  32. 32What are eicosanoids generated from?Phospholipids
  33. 33What are the precursors of eicosanoids?20 carbon fatty acids (20C)
  34. 34What are eicosanoids involved in?Physiological processes
    - Major involvement in inflammation
  35. 35What drugs target eicosanoids?NSAIDs
    Glucocorticoids
  36. 36What is the enzyme that converts phospholidpids into arachidonic acid?Phospholipase A2
  37. 37Give 3 categories that arachidonic acid can be converted into.1. Prostaglandins
    2. Thromboxanes
    3. Leukotrienes
  38. 38What are classed as prostanoids?Prostaglandins and thromboxanes
  39. 39Give 5 factors that can stimulate phospholipase A2 (PLA2).1. Bradykinin
    2. Antigen-antibody binding on mast cells
    3. Thrombin
    4. Complement C5a
    5. Cell damage
  40. 40What is the nomeclature for prostaglandins?PG= prostaglandin
    Letter = basic structure
    Number = numbr of C=C double bonds
  41. 41Give the 4 main prostaglandins to be aware of.1. PGD2
    2. PGE2
    3. PGF2alpha
    4. PGI2
  42. 42What is the name of teh enzyme that converts arachidonic acid into PGG2 and PGH2?Cyclooxygenase
  43. 43What converts PGH2 to PGD2, PGE2, PGF2alpha and PGI2?D
  44. 44What determines what prostaglandin that is produced?What enzymes that are expressed in the cells
  45. 45What happens toSpontaneously decays to inactive metabolite within about 5 mins
  46. 46Why are the prostaglandins metabolised to inactive metabolites within minutes?Restrict inflammation to the local area
  47. 47As well as prostaglandins what else can be produced from PGH2?Thromboxanes
  48. 48What form is cyclooxygenaseTwo isoforms - 1 and 2
  49. 49When is isoform 1 of cyclooxygenase found?Normally in most cells
  50. 50When is isoform 2 of cyclooxygenase found?Not normally found, expression induced inflammatory factors
  51. 51What can cause the increase the expression of isoform 2?Cytokines
  52. 52What are the most important prostaglandins in inflammation?PGE2 and PGI2
  53. 53What is the affect of PGD2?1. Relaxation of vascular smooth muscle
    2. Constriction of bronchial muscle
    3. Relaxation of GI and uterine muscle
  54. 54What is the effect of PGE2?1. Vasodilation
    2. Bronchial dilation
    3. Hyperalgesia
    4. Produces fever
    5. Promotes platelet aggregation
    6. Inhibition of gastric acid secretion and increased gastric mucous secretion
  55. 55What effect does PGF2alpha have?1. Vasoconstriction
    2. Bronchial constriction
    3. Luteolysis in some species
    4. Uterus contraction
  56. 56What effect does PGI2 have?1. Vasodilation (potent)
    2. Hyperalgesia
    3. Inhibit platelet aggregation
    4. Modulates kidney function
  57. 57What is the enzymes that converts PGH2 to thromboxane A2?TXA2 synthase
  58. 58How does thromboxane A2 get converted to thromboxane B2?Spontaneous hydrolysis within 30 seconds
  59. 59Is thromboxane B2 inactive or active?Inactive
  60. 60Give 3 functions thromboxane A2 can do.1. Vasoconstriction
    2. Broncho constriction
    3. Induce platelet aggregation
  61. 61What does the conversion of TXA2 to TXB2 do?Limits the ability of TXA2 to complete its function
  62. 62What is the name of the enzyme that converts arachidonic acid into 5-HPETE?5-lipoxygenase
  63. 63What does 5-HPETE get converted to?Leukotriene A4
  64. 64What are the two leukotrienes that leukotriene A4 can be converted to?1. Leukotriene B4
    2. Leukotriene C4
  65. 65What are classed as cysteinyl leukotrienes?Leukotriene (LT) C4
    LT D4
    LT E4
    LT F4
  66. 66Where are leukotrienes produced?Leukocytes, lung, mast cells and platelets
  67. 67What are the 2 different receptors for leukotrienes?1. BLT for LTB4
    2. CysLT for otehrs
  68. 68What does LTB4 do?Causes activation and targeting of leukocytes and cytokine production
  69. 69What so the Cysteinyl-LTs do?Cause bronchoconstriction and vasodilation (but coronary vasoconstriction)
  70. 70Name 2 CystLT receptor antagonists.1. Zafirlukast
    2. Montelukast
  71. 71What are zafirlukast and montelukast used for in human medicine?Treating asthma (preventitive not for acute attacks)
    - recommended use to complement glucocorticoid or bronchodilator therapy NOT on own
  72. 72As well as arachidonic acid, what else can be made from phospholipids in the plasma membrane?Platelet activating factor
  73. 73What is the path for the production of platelet activating factor?Acyl-PAF
    -enzyme: phospholipase A2
    Lyso-PAF
    PAF
  74. 74What is the function of PAF?- Activate platelets and acts on several other cell types
    - Stimulate TXA2 production by platelets
    - Vasodilation, increases vascular permeability, activation of leukocytes, activation and aggregation of platelets, bronchial constriction
  75. 75Give an example of a PAF receptor antagonist.Lexipafant
    (Rupatadine is a PAF and H1 receptor antagonist)
  76. 76What is the main source and main effect of histamine?MS: mast cells, basophils
    ME: Vasodilation, increase vascular permeability
  77. 77What is the main source and main effect of Prostaglandins?MS: mast cells, leukocytes
    ME: Vasodilation, pain, fever
  78. 78What is the main source and main effect of leukotrienes?MS: mast cells, leukocytes
    ME: increase vascular permeability, leukocyte activation and chemotaxis
  79. 79What is the main source and main effect of PAF?MS: Leukocytes, mast cells
    ME: Vasodilation, increase vascular permeability, leukocyte activation and chemotaxis
  80. 80What is the main source and main effect of nitric oxide?MS: Macrophages, endothelium
    ME: Vasodilation, increase vascular permeability
  81. 81What is the main source and main effect of Interleukins?MS: Mast cells, marcophages
    ME: coordinate inflammatory response
  82. 82What is the main source and main effect of Chemokines?MS: mast cells, leukocytes
    ME: leukocyte activation and chemotaxis
  83. 83What is the main source and main effect of Bradykinin/kallidin?MS: Plasma
    ME: increase vascular permeability, pain, vasodilation
  84. 84What is the main source and main effect of anti-inflammatory interleukins?MS: leukocytes, macrophages
    ME: Suppress expression of pro-inflammatory mediators, promote healing
  85. 85What is the main source and main effect of Thromboxane A2?MS: platelets
    ME: platelet aggregation, vasoconstriction

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Beschreibung
2. Pharmacology and therapeutics AD1 (Anti-inflammatories SF) Karteikarten am Inflammation 2, erstellt von Rachael Jones am 28/10/2016.
Erstellt von
Rachael Jones · Okt 2016
Aktualisiert
7 Jan 2017
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1
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