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Inflammation Part 1

Kyha Avery Pathophysiology Resp Therapy Inglés 46 fichas

What kind of exudate is this?

Fichas del conjunto (46)

  1. 1What is inflammation intended for?Intended to eliminate initial cause of cell injury/ eliminate necrotic cells/ tissues arising from the injury
  2. 2How does inflammation eliminate harmful agents?Walling off
    Neutralizing
    Enzymatically digesting
  3. 3What causes the degree of variation of response of inflammation?1.) Duration of Insult
    2.) Type of foreign antigen
    3.) Degree of Injury
    4.) Microenvironment
  4. 4What are the 5 cardinal signs of inflammation (occur at site of injury)? What causes them?1.) Heat (vasodilation which increases BF & increases heat)
    2.) Redness -vasodilation
    3.) Swelling - increased vascular permeability
    4.) Pain - increased vascular permeability- outflow of fluid into interstitial spaces
    5.) loss of function - increased vascular permeability- outflow of fluid into interstitial spaces
  5. 5What are the 2 types of inflammationVascular or cellular
  6. 6Describe vascular phase of inflammationIncreased BF
    Increased permeably
    Blood flow stasis & coagulation (slows down so it's more prone to clot)
    Redness/warmth/swelling
  7. 7Describe the cellular phase of inflammationSpecialized leukocytes
    Migrate to area of stimulation or injury
    Inactivate disease agents & remove debris
  8. 8Explain the vascular phase steps1.) Tissue injury
    2.) Vasoconstriction (BREIFLY)
    3.) Vasodilation (major effect)
    4.) Alterations in permeability, blood flow stasis & coagulation, exudate formation
    5.) Minor Injury-Transient
    Serious Injury - Sustained response
    Delayed Permeability - 4-24 hrs increased permeability
  9. 9When is exudate formed?During acute inflammation
  10. 10What are the different types of exudates? Explain themSerous - watery
    Hemorrhagic - bloody
    Fibrinous - thick sticky meshwork
    membranous - mucus membrane
    Purulent - pus (degraded WBCs, proteins & tissue debris)
    Chyle - milky lymph fluid
  11. 11Why are exudates beneficial?1.) Dilute Toxins
    2.) Causes pain - reduces movement
    3.) Delivers antibodies
  12. 12What kind of exudate is this?HemorrhagicWhat kind of exudate is this?
  13. 13What kind of exudate is this?FibrinousWhat kind of exudate is this?
  14. 14What kind of exudate is this?PurulentWhat kind of exudate is this?
  15. 15What kind of exudate is this?ChyleWhat kind of exudate is this?
  16. 16What kind of exudate is this?SerousWhat kind of exudate is this?
  17. 17What is an abscess composed of?Localized area of inflammation that contains purulent exudate surrounded by neutrophil layer
  18. 18What may eventually wall off the abscess?Fibroblasts
  19. 19Why are antimicrobials ineffective for abscesses?Because of the wall
  20. 20What is an ulceration?Site of inflammation where epithelial surface has become necrotic & eroded
  21. 21Explain BasophilsGranulocytes that have granules that contain histamine & other inflammatory chemical mediators. Circulate in the blood and bind to immunoglobulin E (Ige), triggers the release of histamine & vasoactive agents.
  22. 22What reactions are basophils more involved in?Allergic or hypersensitivity reactions
  23. 23Explain EosinophilsGranulocyte that circulates in the blood.
  24. 24What reactions are eosinophils involved in?1.) Parasitic - granules contain proteins that is highly toxic to parasites
    2.) Allergic reactions - control specific release of chemical mediators
  25. 25Mast cellsGranulocytes that develop in tissue sites. Release granules at site of inflammation. Granules contain histamine & other inflammatory mediators.
  26. 26What are mast cells involved inParasitic infections & allergic reactions
  27. 27What are plateletsSmall cell fragments that are involved in primary hemostasis. When activated they releases potent inflammatory mediators (increase vascular permeability & alter cell properties)
  28. 28Spontaneous activation of platelets has been lined to:SLE (Lupus)
    Arteriosclerosis
    migraines
  29. 29What is a Neutrophil, what does it contain, when does it arrive, and what does it do?Phagocytic Leukocyte. It is the primary Leukocyte. Arrives early at site of infection. Contains enzymes and antibacterial material. Destroys engulfed microbe dead tissues
  30. 30What is a monocyte? Precursor to what? Where is it released from?Monocyte is the biggest luekocyte. Precursor to macrophage and released from bone marrow to act as a macrophage
  31. 31Macrophages are what & what dot they contain?Phagocytic Leukocyte. Contain potent vasoactive mediators.
  32. 32Why do macrophages live longer?1.) Helps destroy causative agent
    2.) Helps resolve inflammatory response
    3.) Contribute to healing process
  33. 33Why are macrophages important in chronic inflammation?Wall off foreign material that cannot be
  34. 34Steps of the cellular phase1.) Adhesion & Margination
    2.) Transmigration
    3.) Chemotaxis
    4.) Activation & Phagocytosis
  35. 35What happens in the first cellular phase?Adhesion & Margination
    Leukocytes have been activated to engulf bacteria.
    Phagocytosis in 3 steps:
    1) Recognition & adherence
    2) Engulfment
    3) Intracellular killing
  36. 36What are Local signs & symptoms of infectionSwelling
    Exudate formation
    Abscess formation
    Ulceration
  37. 37What are some signs & symptoms of systemic infectionsHypotension
    Increased HR
    Labs: Increased WBC, Neutrophils, CRP
    Fever
  38. 38What else is CRP elevated in?MI, malignancies, auto-immune disorders
  39. 39what are the 5 results of acute inflammation?1.) Resolution of inflammatory event
    2.) Repairs tissue - wound healing
    3.) Fibroblasts wall of the area
    4.) Abscess forms
    5.) Progression to chronic inflammation
  40. 40Chronic inflammation lasts how long?Self perpetuating- lasts weeks, months or even years
  41. 41How does Chronic inflammation occur?Recurrent or progressive inflammatory process. Low grade response that doesn't trigger acute response
  42. 42What is there an increase in with chronic inflammation.1.) Influx of macrophages & lymphocytes NOT neutrophils
    2.) Proliferates fibroblasts not exudates
  43. 43What two pathways are there for Chronic inflammation?1.) Nonspecific
    2.) Granulomatous
  44. 44What occurs in Nonspecific Chronic Accumulation?1.) Diffuse accumulation of macrophages & lymphocytes
    2.) Ongoing chemotaxis keeps macrophages hanging around
    3.) Fibroblasts proliferate - scar formation
  45. 45How does Granulomatous Chronic Inflammation work?1.) Forms granuloma (small lesion with mass of macrophages surrounded by lymphocytes)
    2.) Forms around foreign body (splinters, microorganisms)
    How does Granulomatous Chronic Inflammation work?
  46. 46What is Systemic Inflammatory Response Syndrome (SIRS)Presents like sepsis. Systemic infection w/o an identifiable pathogen. Mass vasodilation that won't perfuse organs properly - leads to multi-organ failure.
    Hypoperfusion, hypotensive, shock

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Resp Therapy Pathophysiology Fichas sobre Inflammation Part 1, creado por Kyha Avery el 05/10/2023.
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Kyha Avery
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