c2: inflammation

  1. 5 signs of inflammation
    • pain 
    • redness
    • swelling
    • heat
    • loss of function
  2. circulatory changes during inflammation (6)
    • vasodilation
    • constriction of arteriolar smooth muscles
    • active hyperemia
    • increased hydrostatic pressure
    • congestion
    • hemodynamic changes: RBC rouleux formation and margination of WBC
  3. Hemodynamic Changes (3) during inflammation
    • 1. margination of neutrophil
    • 2. adhesion of platelets releasing mediators of coagulation
    • 3. pavementing of leukocytes to endothelium
  4. cytokines
    adhesion molecules that facilitate leukocytes to adhere to endothelium during inflammation
  5. 4 vessel wall changes
    • 1. increased hydrostatic pressure inside congested blood vessels
    • 2. slow circulation reducing oxygen and nutrients to endothelial cells
    • 3. adhesion of leukocytes and platelets to endothelial cells
    • 4. release of soluble mediators
  6. types of mediators and inflammation
    • plasma derived: circulate inactively in blood, activated during inflammation
    • cell derived: stored in granules of platelets and leukocytes
  7. steps of inflammatory response
    • mast cells and platelets release histamine
    • capillary leaks causing increase in vascular permeability
    • phagocytes engulf bacteria
    • platelets move out of capillary to seal wounded area
  8. histamine
    • quick reaction/ short action mediator (amine)
    • from platelets and mast cells
    • increases vascular permeability
    • vasodilation
    • increase phagocytosis
    • pain
    • inactivated by histaminase
  9. what is bradykinin
    • from plasma through Hageman factor (coagulation factor)
    • similar to histamine function
    • incrs. vascular permeability
    • pain
    • longer lasting
  10. Hageman factor
    • AKA coagulation factor
    • produces: bradykinin, plasmin, fibrin
  11. complement system
    group of plasma proteins produced in liver that enhances antibodies and phagocytosis to clear damaged cells and promote inflammation. Circulates in inactive form
  12. end product of complement system
    produce MAC to cause cell lysis
  13. complement proteins C3a and C5a produce
    • C3a: anaphylatoxins + opsonin
    • C5a: anaphylatoxin + chemotaxis
  14. opsonin
    signaling chemicals that facilitate phagocytosis
  15. anaphylatoxins
    • chemicals that release histamine, vasodilation, vascular permeability
    • released by C3a and C5a
  16. complement fragments promote?
    chemotaxis
  17. chemotaxis
    attraction of white cells to area of inflammation
  18. Arachidonic acid is derived from and metabolized thru
    derived from membrane phospholipids and metabolized through lipoxygenenase pathway and cyclooxygenase pathway
  19. lipoxygenase pathway products
    • leukotrienes: promote chemotaxis and vascular permeability. present in anaphylactic shock, bronchospasm
    • lipoxins: inhibit chemotaxis, negative regulator of leukotriene, vasodilation
  20. cyclooxygenase pathway products
    • prostaglandins: smooth muscle contraction, pain and fever, vascular permeability
    • thromboxane: platelet aggregation (clots), vasoconstriction
    • prostacyclin: counteracts thromboxane
  21. transudate
    leakage of plasma fluid into interstitial vessel. result of increased permeability
  22. exudate
    transudate + proteins + inflammatory cells (WBC)
  23. extravasation of fluids leads to
    • inc vascular permeability
    • inc hydrostatic pressure, (edema)
    • emigration of leukocytes, releasing exudate
    • chemotaxis
  24. how leukocytes migrate from vessels, emigration of leukocytes (4)
    • 1. adhesion of leukocytes
    • 2. insertion of pseudopods between endothelial cells
    • 3. passage through basement membrane
    • 4. ameboid movement toward chemotactic stimuli
  25. phagocytosis process (4)
    • 1. bacterium opsonized (coated with phagocytic chemicals)
    • 2. bacteria is engulfed by PMN
    • 3. Degranulation: phagocytic vacuoles and lysosomes digest bacterium
  26. pus
    dead leukocytes mixed with tissue debris and lytic enzymes
  27. types of inflammation cells (5)
    • polymorphonuclear neutrophils
    • eosinophils
    • basophils 
    • macrophages
    • platelets
    • lymphocytes
    • plasma cells
  28. polymorphonuclear neutrophil
    • first responders to acute inflammation
    • cytokine production: interleukin -1 --> hypothalamus --> fever
  29. eosinophils
    • 2-3% of WBC
    • appears 2-3 days after PMN
    • allergy, parasites
    • chronic
  30. basophils
    • <1% of WBC
    • allergy
    • from mast cells
  31. macrophages
    • derived from blood monocytes
    • appears 3 - 4 days after onset
    • chronic inflammation
    • involved in phagocytosis
  32. platelets
    fragments of megakaryocytes
  33. 7 types pathological forms of inflammation
    • serous inflammation
    • fibrinous inflammation
    • purulent inflammation
    • ulcerative inflammation
    • pseudomembranous
    • chronic
    • granulomatous
  34. serous inflammation
    • early stage of most inflammation 
    • joint swelling in rheumatoid arthritis, herpes, pneumonia
    • exudation of serum
    • mild
  35. fibrinous inflammation
    • exudate rich in fibrin
    • severe
    • strep throat (bacterial infection)
  36. purulent inflammation
    • exudate with pus
    • contains dead PMN and necrotic tissue remnants
  37. three types of purulent inflammation
    • abscess: localized collection of pus enclosed in capsule
    • sinus: rupture abscess containing a cavity that drains puss
    • fistula: a channel connecting two hollow cavities/organs or to the surface of the body
  38. ulcerative inflammation
    ulcer: loss of epithelial lining in hollow organs
  39. pseudomembranous inflammation
    • ulcerative inflammation + fibropurulent
    • contain exudate composed of pus, fibrin, cellular debris and mucus
  40. chronic inflammation
    • fibroblast proliferation
    • scarring by deposit of collagen
    • fibrosis: hardening of tissue, usually associated with lung disease
    • occurs after acute
  41. granulomatous inflammation
    • granulomas
    • consists of lymphocytes, macrophages, and multinucleated giant cells
    • common in TB
  42. granuloma
    • a type of chronic inflammation with many lymphocyte, macrophages (epithelioid cells), and multinucleated giant cells
    • not preceded by acute inflammation
    • present in TB patients
  43. what are the cytokines/pyrogenes released from leukocytes/macrophages during inflammation (2)
    • IL-1
    • tumor necrosis factor
  44. describe the pathogenesis of fever
    • 1. leukocytes + macrophages release  IL - 1 and tumor necrosis factor
    • 2. IL-1 and TMF enter hypothalamus releasing prostaglandins which cause fever.
    • can be inhibited by aspirin
  45. mitotic cell cycle
    • Go: resting phase
    • G1: growth
    • S: DNA synthesis
    • G2: growth and preparations for division
  46. quiescent facultative mitotic cells
    • cells that do not divide regularly but can be stimulated to proliferate
    • ex. parenchymal cells of liver
    • stops at G0 phase
  47. nondividing postmitotic cells
    • cells that cannot divide
    • ex. neurons, myocardial cells
  48. cells participating in wound healing
    • macrophages
    • myofibroblasts
    • fibroblasts 
    • angioblasts
  49. what cells are involved in wound healing
    • myofibroblasts: contract, secret matrix substances
    • macrophages: contract, secret matrix
    • fibroblasts: extracellular matrix including fibronectin and collagens (III,II,I)
    • angioblasts: blood vessel precursors
  50. what is granulation tissue
    connective tissue rich in macrophages,
  51. types of wound healing
    • first intention
    • secondary intention
  52. first intention
    • healing for small wounds
    • scar --> leukocytes --> granulation tissue (fibroblast, macrophage) --> small scar
  53. secondary intention
    • prolonged wound healing
    • exposed granulation tissue delays healing tremendously
  54. what happens when there's healing complications
    • deficient scar formation: slow scar formation usually seen in diabetic pts as a result of ischemia
    • wound dehiscence: separation of tissue margins
    • excess scar formation
    • keloids leftover type III collagen
  55. cyclooxygenase pathway inhibited by
    aspirin
  56. most abundant WBC
    PMN polymorphonuclear neutrophil
  57. Platelets release
    • histamine
    • coagulation proteins
    • cytokines
    • growth factors
  58. what is platelet-derived growth factor (PDGF)
    factor that promotes proliferation of connective tissue
  59. opsonization
    facilitated phagocytosis of bacteria
  60. angiogenesis
    formation of new blood vessels
Author
tanyalequang
ID
333757
Card Set
c2: inflammation
Description
notes on reading and ppt
Updated