chemical agents

physical forces

microbes

• only occurs in living tissues
• only occurs in multicellular organisms
• series of dynamic, coordinated events
• normally:  protective, beneficial role

calor

rubor

tumor

dolor

functio laesa

connective tissue

blood/lymph vessels

WBC's

hyperemia

exudation

emigration

fluid leaks from blood vessels to tissues

can create swelling and pain

movement of WBC to tissues

"diapedisis"

INFLAMMATORY CHEMICAL MEDIATORS

released from

injured tissues

mast cells

macrophages

neutrophils

INFLAMMATORY CHEMICAL MEDIATORS

molecules

histamine

prostaglandins

leukotrienes

INFLAMMATORY CHEMICAL MEDIATORS

cause

vasolialation (hyperemia)

increase vascualr permeability (exudation)
emigration of WBC to area via chemotaxis

LEWIS TRIPLE RESPONSE

intial response

vasocontriction

white line

LEWIS TRIPLE RESPONSE

Response 1

flush

capillary diation

dull red line

LEWIS TRIPLE RESPONSE

Response 2

flare

arteriolar dilation

bright red, irregular zone surr

LEWIS TRIPLE RESPONSE

Response 3

weal

increase vessel permeability

raised area surr. stroke = edema

overlaps w/ exudation

SPHINCTERS

type of innervation

HYPEREMIA

direct response to injury

1st:  increased blood to capillaries

2nd:  increased blood to arterioles

EXUDATION

short-term response

cells:  release of chemical mediators

mast cells

histamine

increase vessel leakiness

EXUDATION

long term response

increase vessel permeability

pain

EXUDATION

affects of protein-rich fluid entry

• edema, swelling:  tumor (dolor)
• increase fluids:  dilutes toxins
• increase protein: 
  • antibodies, host defense
  • fibrinogen:  clot formation, wound healing
  • lymmphatic capillaries:  take up extra fluid

EMIGRATION

characteristics

mast cells:  chemoattractants for WBC

WBC move from vessel to tissue

diapedisis

EMIGATION

diapedesis:  types of movement/shape

• blood vessel:  spherical, margniation/pavementing
• connective tissue:  amoeboid

removal of injury causing agent

healing:  repair

restoration of normal

• rapid removal of causative agent
• minimal death and damage
• favorable local conditions
  • adequate blood & lymphatic vessels
  • adequate #'s of functioning WBC

stem cells

quiescent cells (fibroblast)

non-dividing cells (nerves)

phagocytic:  neutrophils, mactrophages

nonphagocytic:  myofibroblast, angioblast, fibroblasts

NEUTROPHIL

characteristics

intitial injury

bacteria

short-term

MACROPHAGES

long term

chemical mediators

pericytes

precursors of new blood vessels

fibronectin

type III collagen

type  collagen

WOUND HEALING

1st intention

1ST INTENTION

starting point

blood clot

debris

sutures

1ST INTENTION

2-4 hours

acute inflammatory response

hyperemia

exudation

emigration

1ST INTENTION

3-7 Days

macrophages:  cytokines, growth factors

granulation time

1ST INTENTION

week 2

granulation tissue:  figronectin, type III collagen

macrophages:  fewer, less secretion

BV:  no longer dilated, less redness

1ST INTENTION

week 3-6

granulation tissue:  fibronecting, type III collagen

scar:  replaced by type I collagen

1ST INTENTION

epidermal changes

• normal skin:  contact inhibition prevents lateral movement
• wound: 
  • loss of contact inhibition
  • cells move laterally to cover wound surface
  • granulation tissue in dermis

2ND INTENTION

characteristics

large defects

gaping wounds

myofibroblast:  active but not effective

no approximation of wound edges

granulation tissue:  exposed

delayed healing

• site of wound:  skin vs brain
• mechanical factors:  wound edges
• size of wound
• infection
• circulatory state
• nutritional and metabolic status
• age

• deficient scar formation
• excessive granulation tissue:  proud flesh
• excessive scar tissue formation:  keloid
• contractures