EXAM 1: Lecture 11 - wound healing and surgical inflammation Flashcards
surgery = ____ of a wound
creation of a wound
what does disruption of tissue homeostasis lead to
inflammation
what is normal surgical inflammation
acute, local, short duration
what is abnormal surgical inflammation
prolonged (chronic), severe, signs of infection, or systemic signs
what are the 3 phases of wound healing
inflammation, proliferation, and remodeling
at how many days in wound healing will you see inflammation
4-6 days
at how many days in wound healing will you see proliferation
4-24 days
at how many days in wound healing will you see remodeling
21 days - 2 years
what is hemostasis
the body wanting to stop bleeding while maintaining perfusion
what are the 2 balances of hemostasis
vasoconstriction and vasodilation
what is endothelial cell disruption in hemostasis
immediate vasoconstriction, exposure of Von Willebrand factor (vWF) platelet activation and aggregation, and the coagulation cascade
what happens when endothelial cells release vasodilators
there is vasodilation to increase blood flow
what mediates vasodilation
histamine, NO, LTs, PGs, complement
what happens when there is post-capillary venule leakiness
increased inflammatory cell and inflammatory mediation infiltration leading to protein leakage (edema)
what happens with protein leakage
decreased osmotic pressure, increased blood viscosity, and increased interstitial pressure
T/F: Edema facilitates delivery of soluble factors and cells and can cause pain or loss of function
TRUE
what can cause vascular congestion
fluid loss to edema, hemoconcentration, and reduced velocity of blood flow
what is inflammation also called
debridement phase
what are the 2 phases of inflammation
early and late
what happens in the early phase of inflammation
neutrophil recruitment
what happens during the late phase of inflammation
monocyte transformation
what are the functions of inflammation
prepares the body for next phases of wound healing and removes dead tissue/foreign material
___1_ of trauma = intensity of __2___ = extent of ___3___ formed
- severity
- inflammation
- scar tissue
what do leukocytes do with inflammation
they are recruited from circulation by chemoattractants and initiate rolling, activation, tight adhesion, and transmigration of cells
what do neutrophils do for inflammation
neutrophil diapedesis is encouraged by increased capillary permeability
what is diapedesis
passage of blood cells through intact capillary walls
how quickly does neutrophil diapedesis happen
minutes and peaks 1-2 days after injury
why are neutrophils the first line of defense against contaminated wounds
they destroy debris and phagocytose bacteria
T/F: monocytes migrate from vasculature during inflammation
true!
T/F: macrophages change into monocytes
false, monocytes turn into macrophages
what do macrophages do for inflammation
pro-inflammatory functions, stimulate proliferation of dermal/endodermal/epithelial tissues and help with remodeling phase
how do we get resolution of inflammation
each of the pathways need to be halted or reversed and apoptosis of cells
what happens if there no resolution of inflammation
can lead to chronic, suppurative inflammation and a non healing wound OR proud flesh in horses
how is inflammation phase modulated by clinicians
- proper surgical debridement
- good hemostasis
- adequate drainage
- medications like NSAIDS or steroids
what causes proliferation of tissues
fibroplasia, angiogenesis, and epithelialization
what is fibroplasia and what does it do
formation of granulation tissue by fibrosis
gives a temporary barrier of infection
what are the 3 elements of granulation tissue
- macrophages
- fibroblasts
- blood vessels
what do macrophages do to make granulation tissue
debride, produce cytokines/growth factors that stimulate angiogenesis and fibroplasia
what do fibroblasts do to make granulation tissue
proliferate and make new extracellular matrix
what do blood vessels do to make granulation tissue
carry O2 and nutrients for cell metabolism and growth
what day in the healing process do you start to see granulation tissue
day 5
T/:F fibroblasts are directed by macrophages via cytokines and growth factors
true
what is angiogenesis
formation of new capillaries from pre-existing vessels
what regulates angiogenesis
macrophages and endothelium
_____ tissue hypoxia = _____ vessel ingrowth
increased tissue hypoxia = increased vessel ingrowth
what is epithelialization
when epithelium covers the wound
what is the purpose of epithelialization and how much growth is there per day
it reforms barrier of infection and about 0.1-0.2mm/day
what is wound maturation
continued epithelialization by thickening of the epidermis
how do wounds contract
fibroblasts differentiate into myofibroblasts under influence of growth factor and cytokines
what does remodeling mean
conversion of granulation tissue into scar tissue
what does MMP stand for and what is it
matrix metalloproteinases
it is collagenases, gelatinases, and stromelysins which is the demolition team for converting granulation in to scar
how long does remodeling take
may take up 1-2 years depending on the size of the wound
what are the 4 things that stop healing
- when wound edges meet
- tension surrounding skin > force of myofibroblasts
- reduced numbers of myofibroblasts
- granulation tissue is proliferative
what is “the rude unhinging of the machinery of life”
shock
what is shock
cascade of events that begins when cells/tissues are oxygen deprived from inadequate perfusion
what can shock lead to
SIRS and MOD
what does SIRS stand for
systemic inflammatory response syndrome
is SIRS normal?
Yes but it is a large overreaction to the situation
what causes SIRS
there are many causes leading to it. it can be infectious or non-infectious
what are 3 things that happen with SIRS
cytokine storm, leukocyte dysfunction, and delayed resolution of inflammation
what is the clinical definition of SIRS
must meet any 2 physiologic conditions with underlying pathologic cause
what are the possible causes that leads to a clinical definition of SIRS
- hyperthermia or hypothermia
- tachycardia
- tachypnea
- leukocytosis or leukopenia
- depression
what causes hyperthermia (fever)
IL-1, IL-6, TNF-alpha, PGE2 act on the hypothalamus
what causes hypothermia
shock from hypoperfusion or central blood sequestration
what is the cascade of tachycardia
vasodilation to hypotension to decreased CO to increased HR
what changes do we see on CBC
- leukopenia (<48h)
- leukocytosis (>48h)
- left shift (variable)
what is the cascade of tachypnea
hypoperfusion to anaerobic cellular metabolism to lactic acidosis to metabolic acidosis
what causes depression
cytokines and eicosanoids
what causes the stress response
IL-1 and TNF-alpha
what does IL-1 and TNF-a do to cause the stress response
increase in adrenocorticotropic hormone to increase corticosteroids
what do corticosteroids do to surgical healing
reduce it!!
