inflammation and wound Flashcards
reversible injury
cell can fully recover and return to normal function
apoptosis and programmed cell removal
programmed cell death and does not release any inflammatory response
cell death and necrosis
unplanned cell death and causes inflammation
cellular injury mechanisms
hypoxic injury reperfusion injury oxidative stress genetics infections nutritional imbalances changes in atmospheric pressure environment chemical injury physical/mechanical force
hypoxic injury
anoxia or ischemia
can be caused by lack or oxygen or decrease blood flow or perfusion
anoxia or ischemia
reduced blood supply
reperfusion injury
restoration of circulation cause inflammation
oxidative stress
free radicals/ reactive oxygen species
chemical injury
drugs mead, mercury asbestos carbon monoxide air pollutants
physical/mechanical forces
blunt force injuries
results of cellular injury
- mitochondrial damage
- ATP depletion
- defects in membrane permeability
- disruption of calcium homeostasis
systemic manifestations of cell injury
fatigue malaise fever loss of appetite elevated plasma inflammatory response
hypo
decrease
hyper
increased
hypoxic
decreased oxygen
inflammation
itis
inflammatory response
second line of defence
non specific
activated by cellular injury or cell death
regardless of the trigger the process of inflammation will always be the same
goals of the inflammatory response
limit and control injury process
prevent and limit infection and further damage
initiate adaptive immune response
initiate healing
vascular responce to inflammation
blood vessel dilation
increased vascular permeability and leakage
- increase amount of blood enter and the blood flow dilates making capillary leaky and water and fluids come out of the capillary during inflammation
cellular response to inflammation
white blood cells adhere to capillary
phagocytosis
white blood cells stick to capillary wall then sneaks out and goes to area of inflammation
exudates
fluid, WBC and tissue debris
cellular component
neutrophils
monocytes, lymphocytes, macrophages, phagocytes, mast cells, platelets and other
chemical components
histamine, leukocytes, prostaglandins, bradykinin, complement, serotonin and clotting systems
5 signs of inflammation
red hot swollen loss of function pain
systemic manifestation of acute inflammation
- fever
- fatigue, anorexia and endogenous pyrogens
- leukocytosis
- elevated erythrocytes sedimentation rate (ESR)
chronic inflammation
- lasting 2 weeks or longer
- often related to an unsuccessful actor inflammatory response
- phagocytic cells (macrophages and lymphocytes rather than neutrophils)
immune and inflammatory substances (can further injure cells and delay healing) - fibroblast and scar tissue formation leading to loss of function (replace normal tissue)
systemic manifestation of chronic inflammation
same as acute
hyperplasia of spleen or lymph nodes
resolution
returning injured tissue to original structure and function
repair
replacement of destroyed tissue with scar tissue
healing process
primary intention
secondary intention
primary intention
wounds that heal under condition of minimal tissue loss
secondary intention
wounds that require a great deal more tissue replacement
factors affecting healing and tissue repair
- age
- blood supply
- temperature
- moisture
- nutrition
- tension on tissue
- drugs and stress hormones
- chronic disease
phases of healing
- inflammation
- proliferation and new tissue formation
- remodelling and maturation phase
inflammation
cleans up injured area
proliferation and new tissue
fibroblast proliferation
epithelialization
contraction
remodelling and maturation phase
cellular differentiation
scar tissue formation
scar remodelling
complication of wound healing
stenosis adhesions infection strictures and contractors excess scar formation dehiscence or evisceration
stenosis
narrowing
adhesion
scar tissue that sticks to other scar tissue
strictures and contractors
shortening of the skin - burns
excess scar formation
keloids
dehiscences or evisceration
closed wounds that have been open