Med surge

  1. Inflammatory Response
    • Neutrolizes and dilutes inflammatory agents
    • Removes necrotic materials
    • establishes an environmement for healing and repair
    • Inflammation is always present with infection; infection is not always present with inflammation
  2. Causes of Inflammatory response
    Heat, Radiation, trauma, Allergens, Infection
  3. Intensity of the response deponds on ..
    • Extent and severity of injury
    • reactive capacity of injured person
  4. Describe a vascular response.
    • Includes the blood
    • Arterials vasoconstrict after the release of histamine and other chemicals then vessels dilate(increase blood flow and filtration)
  5. What is chemotaxis?
    Chemotaxis- migration of WBC along a concentration gradient of chemotactic factors, substance that attract leukocytes to the site of inflammation. It ensures accumulation of neutrophils and monocytes at the focus of injury
  6. What are the components of Cellular response
    • neutrophills
    • Monocytes
    • Lymphocytes
    • Eosinophills and basophils
  7. Explain Neutrophils
    • 1st on site(few)
    • Phagocytsize bacteria and other foreign material and damaged cells.
    • short life span
    • pus is formed by accumulation of dead neutrophilles and digested bacteria
    • elevated WBC due to the bone marrow release immature fotms of neutrophils( band) into circulation; shift to the left)
  8. Explain Monocytes
    • 2nd on site -assist in phagocytosis
    • on entering tissue spaces monocytes tranform into macrophages
    • long life span and can multiply
  9. Macrophages?
    • clean the area befor healing can occur.
    • Cells may fuse to form a multi giant cells. Giants cells attempt to phagocyte particales too large macrophages
  10. Lymphocytes?
    • later at the cite
    • primary role is cell mediated immunity (b cells/t cells/ t helper cells) and humoral immunity (antibodies)
  11. Eosinophils??
    • released in large quantities in allergic reaction .
    • Release the chemical that act to control the effects of histamine and serotoni
    • Phagocytosis of allergen antibodies and anaphylactic shock
  12. Basophils
    • carry histamine and heparin in their granuales that are released during inflammation
    • limited phagocytic capabilities
  13. Local Response?
    Redness, Heat, Pain, swelling and loss of function
  14. Systemic Response
    • Increse WBC (shift to the left, malaise, nausea, fever, Anerexia.
    • Increase pulse and respirations (follows the rise in metabolism
    • changes due to complement activation and release of cytokines
    • Fever trigger cytokines
    • CHills (body attempt to increase temp and fever (hypathalmus)
  15. Formation of exudate
    consist of fluids and leukocytes that move from the circulation to the site of injury.
  16. vascular response
    • After cell injury, arterioles in area briefly undergo transiet vasoconstriction
    • afyer the release of histamine and other chemicals byt the injured cells, vessels dilate resulting in hyperemia(increase bloos)
  17. vasodilation?
    • results in hyperemia
    • increased blood flow in the area
    • raises filtration pressure
  18. vasodilation chemical mediators (vascular and chemical response)
    • endothelial cell retraction
    • increased capillary permeability
    • Movement of fluid from capillaries into tissue spaces
  19. Fluid in tissue spaces(vascular response)
    • inititally composed of serous fluid (blood/fluid)
    • later contains plasma proteins, primarily albumin(protein exert oncotic pressure that furthers draws fluid from blood vessels; tissues become edenatous)
  20. What are the chemical mediators
    • Histamine
    • serotonin
    • Kinin
    • complement system(major mediator of inflammation)
    • Prostoglandin(cellular response
    • leukocytes- ensures accumulation of neutrophils and monocytte at the focus of injury.
    • cytokines
  21. Explain the complement system
    enhanced phagocytosis, increase vascular permeability, chemataxis and cellular lysis
  22. Explain Prostaglandians
    • (can be synthesized from phosopholipis of cell membranes of most body tissues include blood cells
    • proinflammatory contributing to increased blood flows, edema and pain
  23. What are drugs that inhibit prostaglandin synthesis
    • NSiads( inhibits Prostogladis)
    • Asprin(work as a blood thinner)
    • Corticosteroids- weaken the immune system , blocks infection from showing
  24. Explain fever
    • trigger by the release of cytokines. they cause fever by their ability to initiate metabolic changes in the temp-regulating center(hypothalamus)
    • Benefits are increase killing of microorganism and increase phagocytosis and profilieration of t cells
  25. three types of inflammation
    • Acute
    • Subacute
    • Chronic
    • (Difference is duration)
  26. Explain an Acute inflammation
    doesnt know underlying cause(2-3 wks, neutrophils are predominent)
  27. Explain subacute inflammation
    same features as acute inflammation but last longer
  28. Explain Chronic Inflammation
    • 6months +
    • lyphocyte and macrophages,
    • may include changes in immune system
  29. stages of healing
    • regeneration
    • repair
  30. What is Regeneration?
    • replacement of lost cells and tissues with cells of rge same type.
    • Stable cells (liver, bone, kidney, pancrease) regenerate in response to injury
    • permenant cells (cardiac, neurons, skeletal) do not divide
  31. Repair?
    • healing as a result of lost cells being replaced with connective tissue
    • result in scar formation
  32. What is primary intention and what are their phases?
    • wound margins are neatly approximated (paper cut, surgical incisions)
    • initial phase(3-5 days) edges of the incision are 1st alligned and surtured in place. Fibrin clots, erythocyted, neutrophils fills the site
    • Granulation phase(5days- 3wks)- exudate, capillary sprout
    • Maturation phase- 7 days to yearS) scar contraction occurs, collagen fibers are organized and remodelung process occure. pale and avascular
  33. What is fibroblast
    immature cinnective tissue cells that migrate into the healing site and secrete collagen
  34. What is secondary intention
    • wounds that occur from trauma, ulceration and infection
    • large amoumy off exudate, extensive tissue lost, wide and irregular wound margin.
    • usually when wound opens up it is healed by secondary intention
  35. how does granulation occurs?
    Granulationtakes place from the edge inward and from the bottom of ound upward until detect is filled
  36. What is teritiary Intention
    • delayed primary intention
    • contaminated wound is left open surtured closed after infection is controlled
  37. How are wound classified
    • surgical/ nonsurgical
    • acute/chronic
    • deoth of tissue affected(superficial (epidermis), partail thickness(extends into the dermis) or full thickness(subcuantaous and fascia))
    • color of wound (red, yellow, black)
  38. Factors that delay wound healing?
    • Nutritional(vit. c (delay collagen fiber formation, protein((decrease tissue rpair, zinc(impair epithialization)
    • Inadequate blood supply, corticosteroids, infection, smoking obseity, diabetes, anemia,
  39. COmplication of Healing?
    • hypertopoc scars and keloid formation
    • contracture
    • dehiscence
    • excess granulation tissue
    • adhesion
  40. what is hypertropic scars and keloid formation?
    • inappropiately large red, raise and hard
    • keloid- greater protusion of scar tissue that extends beyond the wound edges, may form masses
  41. Contracture?
    necessary for healing but become abnormal when there is excessive contraction resulting in deformity or contracture. (wounds near joints/ burned area)
  42. Dehiscence?
    is the seperation adn disruption of previously joined wound. primary site burst open
  43. evisceration??
    intestines protrude over the wound
  44. excess granulation tissue?
    protrude above the surface of the healing wound
  45. adhesion?
    bands of scar tissue between or around the organ(abdominal cavity or between lungs)
  46. Pressure Ulcer
    a localized area(over a boney prominence) of tissue necrosis caused by unrelieved pressure that occulded blood flow to the tissue
  47. Factors that influence Pressure ulcers?
    • Intensity, duration, ability of tissue to tolerate presure, incidence.
    • most common area (heels and sacrum)
  48. what is shearing force?
    pressure exerted on the skin when it adheres to the bed and the skin layers slind in the direction of the body movement (wrinkles in the sheets/moving patient)
  49. Friction?
    2 surfaces rubbing against each other
  50. Stages of ulcer??
    • 1(minor)- skin is intact
    • 2 partial tickness, epidermis, dermis. superficial, blister
    • 3-subcutanous
    • 4(severe) full thickness, damage to muscles, bone
  51. How to measure a pressure ulcer?
    • 1st head to toe
    • 2nd side to side
    • 3rd is depth
  52. What is the Braden scale
    The risk of ulcers( from 23-0( no risk to very high risk)
Card Set
Med surge
Pathophysiologic Mechanism of Disease