Patho Unit 1

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Author:
rstoth
ID:
101929
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Patho Unit 1
Updated:
2011-09-15 17:20:57
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cell inflammation
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chapter 3
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  1. acute inflammation
    • adaptive response
    • short duration
    • fluid & plasma out
    • leukocytes (neutraphils) in
  2. chronic inflammation
    • longer duration
    • proliferation of blood vessels, tissue necrosis, fibrosis
  3. endothelial cells in inflammation
    • produce antiplatelet antithrombotic agents
    • vasodilators & vasoconstrictors
    • selective permeable barrier to stimuli
    • regulate leukocyte extravasation by expression of adhesion molecules
    • synthesis of inflammatory mediators
    • cell proliferation through secretion CSF
    • production of growth factors stimulate angiogenesis
  4. platelets in inflammation
    • release inflammatory mediators
    • increase vascular permeability
    • alter chemotactic, adhesive & proteolytic properties of endothelial cells
  5. leukocytes in inflammation
    • granulocytes- cytoplasmic granules, multi-lobed nucleus
    • agranulocytes- single nucleus
  6. neutrophils in inflammation
    • first cells to appear
    • engulf through phagocytosis
    • oxygen-dependent metabolic pathways generate toxic oxygen & nitrogen
    • last 24-48 hrs
  7. eosinophils in inflammation
    • appear 2-3 hrs after neutrophil
    • contain protein highly toxic to parasitic worms
    • interact w/ basophils in allergic reaction
    • long life span
    • active in chronic
  8. basophils & mast cells
    • allergic reactions mediated by IgE
    • triggers release histamine & vasoactive agents
    • mucosal surfaces of lung, GI, dermis
    • activation of mast cells: release of contents(histamine, proteases, cytokines, IL), synthesis of lipid mediators from cell membrane precursors (prostaglandin, platelet-activating factor), stimulation of cytokine synthesis by other inflammatory cells
  9. monocyte/macrophage
    • single kidnet shaped nucleus
    • produce prostaglandins, platelet activating factor, inflammatory cytokines & growth factors
    • life span 3-4x longer granulocytes
    • destroy causitive agent
    • aid in signaling of immunity
    • resole inflammatory process
    • initiating of healing process
  10. lymphocytes and plasma cells
    • immune-mediated inflammation by infection & injury
    • work w/ macrophage to stimulate each other to activation
    • activated B-lymphocytes develop plasma cells that produce antibodies against antigens
  11. selectin CAM
    adhesion leukocytes to endothelial wall
  12. integrin CAM
    promote cell-to-cell & cel-to-extracellular matrix interactions
  13. adhesion molecules
    • immuloglobulins
    • interact w/ integrins to recruit leukocytes
  14. cardinal signs of inflammation
    • rubor
    • tumor (swelling)
    • calor (heat)
    • dolor (pain)
    • loss of function
  15. vascular stage
    • vasoconstriction followed rapidly by vasodliation/ increased vascular permeability w/ leakage of protein-rich fluids into extravascular tissue
    • induced by histamine & nitric oxide
    • loss of fluid makes blood thicker concentrating blood components, slowing of flow, & clotting
    • fluid shift dilates offending agent
    • histamine, bradykinin & leukotrienes cause contraction of endothelial cells and separation of intracellular junctions
  16. patterns of responses
    • immediate transient-rapid, reversible, short duration (15-30 min);leakage in venules
    • immediate sustained- several days; all levels of microcirculation; direct damage to endothelium
    • delayed hemodynamic- increased permeability after delay 2-12 hours; injuries due to radiation (sunburn)
  17. cellular stage of acute inflammation
    • 1. margination & adhesion
    • 2. transmigration
    • 3. chemotaxis
    • 4. activation & phagocytosis
  18. margination & adhesion
    • leukocytes slow migration, adhere to endothelium & move along edge of blood vessel
    • cytokines cause endothelial cell lining to express adhesion molecules that bind the carb on leukocytes (tethering)
  19. transmigration
    adhesion causes endothelial cells to seperate allowing leukocyte to extend pseupodia & go through vessel wall & migrate to tissues
  20. chemotaxis
    leukocyte wanders through tissue guided by gradient of chemoattractants (chemokines, debris)
  21. phagocytosis
    recognition, adherence & intracellular killing
  22. opsonization
    enhanced binding of antigen due to antibody
  23. plasma derived mediators
    • made in liver
    • acute phase proteins, coag factors, complement factors
    • products of coag/fibrinolysis system & protein of complement
  24. cell-derived mediators
    • normally sequestered in intracellular granules (histamine) or
    • newly made in response to stimulus (cytokines)
  25. vasoactive amines-histamine & serotonin
    • stored in preformed molecules in mast cells
    • H-dilation of arterioles & increases permeability of venules; principal mediator of transient phase
    • serotonin- vasoactive mediator in platelet granules
  26. arachidonic acid metabolites (prostaglandins, leukotrienes)
    • corticosteriods block action preventing release
    • prostaglandins potentiate mediators
    • NSAIDs block prostaglandin pathway
    • leukotriene- slow & sustained constriction of bronchioles
  27. Omega-3 polyunsaturated fatty acids
    partial replacement of omega-6 arachidonic acid blocking prosta & leuko production
  28. platelet activating factor
    • stimulates neutrophils, nonocyte, endothelial cell & vascular smooth muscle
    • enhances serotonin release
    • enhances leukocyte adhesion, chemotaxis, & synthesis of mediators
  29. cytokines
    • low-molecular-weight proteins
    • source of TNF & IL-1 by activated phagocytes
    • fever, hypotension, high HR, anorexia, release of neutrophils into circulation & increased corticosteriods
  30. chemokines
    • chemoattractants- recruit & direct inflammatory & immune cells
    • chemotactic gradient binding proteoglycans on endothelium
    • response to bacterial toxin & cytokines
  31. nitric oxide
    • relaxation of vascular smooth muscle
    • antagonism of platelet adhesion, aggregation & degranulation
    • regulator of leukocyte recruitment
  32. oxygen-derived free radicals
    • increase expression of cytokines & endothelial adhesion
    • produces endothelial cell damage- increase of vascular permeability, inactivate antiproteases, produce injury to rbc's
  33. serous exudate
    • watery fluids low in protein
    • from plasma
  34. hemorrhagic exudates
    • severe tissue injury
    • leakage of rbc from capillaries
  35. fibrinous exudates
    • fibrinogen
    • form thick sticky meshwork
  36. membranous exudates
    • mucous membranes
    • necrotic cells in fibropurulent exudate
  37. purolent exudate
    degraded white cells, proteins, tissue debris
  38. abcess
    central necrotic core contining purulent exudate surrounded by layer of neutrophils
  39. ulceration
    epithelial surface becomes necrotic & eroded
  40. resolution
    • replacment of injures cells & return of tissues to normal structure & function
    • neutralization of inflammatory mediators, normal vascular permeability & stopping of leukocyte infiltration
  41. chronic inflammation
    • infiltration of mononucleur cells & attempted repair by angiogenesis
    • low-grade infection/irritants unable to penetrate deeply or spread rapidly
    • adipose tissue source of TNF & insulin resistance
  42. granuloma
    • massing of macrophages surrounded by lymphocytes
    • foreign bodies
    • poorly digested & controlled by inflammatory mechanisms
    • coalese (clump) & form giant cell
  43. acute phase response
    • change concentrations plasma proteins
    • skeletal muscle catabolism
    • negative nitrogen balance
    • high sed rate
    • high leukocytes
  44. acute-phase proteins
    • stimulated by cytokines
    • CRP-binds to & targets cell for destruction
    • SAA (serum amyloid A)- starts transfer HDL from liver to macrophage to utilize for energy; rise in fibrinogen causes rbc to form stacks & increase sed rate
  45. WBC response
    • shift to left-increase in immature neutrophils
    • bacteria-neutrophilia
    • parasitic-eosinophilia
    • viral-neutropenia & lymphocytosis
  46. heat production
    • metabolism source of heat production
    • epi & norepi-shift metabolism to heat production instead of energy
    • shivering-hypothalmus 3-5x increase
  47. heat loss
    • AV shunts-sympathetic nervous system
    • radiation- air or vacuum; 60% of loss
    • conduction- transfer to molecules (blood cariies from inner core to outer)
    • convection-circulation of air currents
    • evaporation-sweating
  48. fever definition
    cytokine-induced upward displacement of set point in hypothalmus
  49. pyrogens
    act directly & immediately on hypothalmus to increase set point
  50. neurogenic fever
    • damage to hypothalmus
    • resistant to therapy no sweating
  51. purpose of fever
    • signal infection
    • enhance immune function
    • inhibit microbial growth
  52. fever patterns
    • intermittent-return to normal once in 24 hrs
    • remittent-no return to normal varies few degree in either direction
    • sustained- above normal minimal variations
    • relapsing-one or more episodes of fever w/ several days between
  53. prodromal fever
    non-specific complaints (fatigue, HA, malaise, aches)
  54. second-stage (chill) fever
    generalized shaking though temp rising
  55. third stage (flush) fever
    vasodilation
  56. fourth stage fever (defervescense)
    sweating
  57. causes of manifestations of fever
    • increase in BMR
    • increased need ofr oxygen
    • use of body proteins & fat as energy
    • HA-vasodilation of cerebral vessels

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