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Karteikarten

Inflammation

Marielle83 Veterinary Pathology BVMS Englisch 55 Karten

Inflammation

Karten in diesem Stapel (55)

  1. 1Shediak-Higashi syndrome?Defective phago-lysosomal fusion (cats, cows, minks, killer whales)
  2. 2Interaction b/w lymphocytes and macrophages in chonic inflammation?Activated T lymphocytes recruit inflammatory cells (through TNF and other) and activate macrophages (through INF gamma). In return, activated macrophages stimulate T cells by presenting antigens and via secretion of inflammatory mediators (like IL12).
  3. 3Name the cell-derived mediators of inflammationPlatelets, neutrophils, monocytes/macrophages, mast cells
    +
    Pre-existing (intracellular granules)
    E.g. histamine in mast cells
    Synthesized de novo (PGs, cytokines)
  4. 4Name some plasma derived mediators of inflammationE.g. complement proteins, kinins
    - Made in liver
    - Circulate as inactive precursors
  5. 5What stimulates mediators?Necrotic material (PAMPs and DAMPs)
    +
    Proteins of complement, kinin, and coagulation systems
  6. 6Which vaso-active amine is mainly released by mast cells but also basophils and platelets?Histamine
  7. 7What is the effect of histamine release?Dilation of arterioles & increased permeability of venules
    (via binding to H1 receptors on endothelium)
  8. 8Which vaso-active amine is mainly released by platelets and neuroendocrine cells in an inflammatory response and what stimulates its release?Serotonine stimulated by platelet aggregationWhich vaso-active amine is mainly released by platelets and neuroendocrine cells in an inflammatory response and what stimulates its rele...
  9. 9What are the 2 major classes of eicosanoids?Cyclooxygenase pathway (PGs)
    Lipoxygenase pathway (LTs and lipoxins)
  10. 10Leukotrienes- produced by lipoxygenases, secreted by leukocytes have effects on?Vasculature (permeability, constriction)
    Chemotaxis (call in other cells)
    Smooth muscle (bronchospasm)
  11. 11Lipoxins - produced by lipoxygenase have what effect in inflammation?INHIBITORS of inflammation (particularly inhibit leukocyte recruitment)
  12. 12Prostaglandins - produced by actions of cyclooxygenases: COX-1 (constitutively expressed) and COX-2 (inducible) prostacyclin, thromboxane have effects on?Vasculature (dilation, constriction)
    Platelets (aggregation or inhibition)
    Smooth muscle
    Chemotaxis
    Pain / fever
  13. 13Out of COX-1 and COX-2, which one is always activated and which one only activated in inflammation?COX-1 Always
    COX- 2 Inflammation
  14. 14Which pathway does NSAIDs act on and which eicosanoid pathway does it not have an effect on?Cyclooxygenase pathway! (COX-inhibitors)
    No effect on Lipoxygenase pathway
  15. 15Cytokines TNF and IL-1 are relased from activated macrophages in response to what?Physical injury
    Endotoxins and other microbial products
    Immune complexes
    etc.
  16. 16Complement system functions? (3)Inflammation(C3a, C5a)
    Phagocytosis (C3b is opsonin)
    Cell lysis (deposition of MAC on cell)
  17. 17What are kinins?Vasoactive peptides e.g. bradykinin with similar effects to histamine
  18. 18Can you live a normal life without factor XII (Hageman factor) ?Yes
  19. 19True or false: Inflammatory mediators are long-acting and require a specific STOP signalFalse
    Short half-lives with rapid decay or proteolysis
  20. 20List two effects of histamineVasodilation
    Increased vascular permeability
  21. 21What stimulates the release of inflammatory mediators?Microbial products (PAMPs), necrotic material (DAMPs), other mediators
  22. 22What are the 2 pathways of the arachidonic acid metabolism, and what is produced by each?Cyclooxygenase: PGs
    Lipoxygenase: leukotrienes and lipoxins
  23. 23Where does arachidonic acid come from?Cell membranes
  24. 24How are lipoxins different from the other classes of eicosanoids?Inhibition of inflammation
  25. 25Which part of the arachidonic acid pathway do cortocosteroids inhibit?Entire thing (NSAIDS inhibit Cox-1 and Cox-2; not lipoxygenase)
  26. 26Where do "plasma-derived" proteins actually come from?Originally made in liver; circulate in inactive form
  27. 27List 2 effects of cytokines tnf and IL-1Leukocyte recruitment
    Fever
  28. 28What is the key step in complement fixation that is common to all pathways?C3 proteolysis
  29. 29What are the 3 functions of the complement system? And what proteins are most involved with each function?Inflammation (C3a and C5a)
    Phagocytosis (C3b)
    Cell lysis (MAC attack complex)
  30. 30What mediator is involved in eliciting pain?Bradykinin
  31. 31Activation of what substance is involved in activating the four systems involved in inflammation?Hageman factor (Factor XII)
  32. 32List the 3 major pathogen routes of entry into lungInhaled (aerogenous)
    Hematogenous
    Direct entry
  33. 33List 4 types of pneumonia and their route of entryBronchopneumonia (inhaled)
    Interstitial (inhaled or hematogenous) Granulomatous (inhaled or hematogenous) Embolic (hematogenous)
  34. 34Name the etiologies involved in enzootic pneumonias and shipping feverEnzootic pneumonia = mycoplasmas (ovipneumoniae and hyopneumoniae)
    Shipping fever = Mannheimia hemolytica
  35. 35List two causes of granulomatous pneumoniaFungal: blastomycosis, histoplasmosis, coccidiomycosis, cryptococcosis
    Mycobacterium bovis
  36. 36Recall a predisposing condition for aspiration pneumoniaMegaesophagus, handfeeding, cleft palate, downer animal
  37. 37Identify two predisposing conditions in a cow for embolic pneumoniaHepatic abscesses
    Vegetative valvular endocarditis
  38. 38Identify two predisposing conditions in a cow for embolic pneumoniaHepatic abscesses
    Vegetative valvular endocarditis
  39. 39What is the origin of the neoplastic cells in Jaagsiekte (OPA)Alveolar epithelial cells (type II pneumocytes and Clara cells)
  40. 40What bug is the cause of shipping fever?Mannheimia haemolytica
  41. 41What type of pneumonia is shipping fever?Acute fibrinous bronchopneumonia
    (can also be suppurative or fibrinosuppurative)
  42. 42BALT?Bronchus Associated Lymphoid Tissue
  43. 43Metaplasia?The reversible replacement of one differentiated cell type with another mature differentiated cell type
  44. 44Gross findings at interstitial pneumonia?Diffuse distribution and large lungs that do not deflate, rubbery texture "meaty"
  45. 45Gross findings in granulomatous pneumoniaMultifocal firm nodules (any lobe) with white/grey/tan crumbly material
  46. 46Which pathogens may cause suppurative bronchopneumonia?P. multocida
    B. bronchiceptica
    A. pyogenes
    Strep spp.
    Distemper virus
    Parainfluenza virus
  47. 47Which type of pneumonia may be ventilator induced?Interstitial
  48. 48Which bacteria is the major cause of granulomatous pneumonia?Mycobacterium bovis
  49. 49Which parasites may cause granulomatous pneumonia?Dictycaulus
    Muelleria capillaris
  50. 50Via what route does embolic pneumonia enter the lungs?Haematogenous
  51. 51What are the 3 possible causes of embolic pneumonia?Vegetative valvular endocarditis
    Hepatic abscesses
    Any septicaemia
  52. 52How could you grossly differentiate b/w embolic pneumonia and for example tumours or an M. capillaris infection?Lesions in embolic pneumonia are soft like normal tissue and not nodular
  53. 53Jaagsiekte is what type of cancer, and what is the cause?Pulmonary adenocarcinoma
    Jaagseikte Sheep Retrovirus (JSRV)
  54. 54List the events in the resolution of acute inflammationNeutralisation/decay/degradation of chemical mediators
    Normalisation of vascular permeability
    Cessation of leukocyte migration
  55. 55Name 4 types of inflammatory stimuliInfectious agents
    Tissue damage
    Foreign bodies
    Immune reactions

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BVMS Veterinary Pathology Karteikarten am Inflammation, erstellt von Marielle83 am 03/12/2014.
Erstellt von
Marielle83
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