Exam 1 Healing Flashcards
microtrauma
overuse, cyclicnloading or friction injury
macrotrauma
impact or contact injury, large insult and immediate tissue disruption
things that cause inflammation
physical
chemical
ischemia
allergies
physical agents like thermal and radiation
foreign bodies like splinters
infection
nutritional
genetic
effects of inflammation
local :
redness
warmth
swelling
pain
loss of function
systemic:
malaise, fatigue, headache, anorexia, fever
Cardinal signs of inflammation
erythema
heat
edema
pain
loss of function
3 phases of healing
inflammation
proliferation
maturation
also (hemostasis)/ stabilizing prior to inflammaiton
protection phase
first 1-6 days
immediate protective response that attempts to destroy, dilute, or isolates the cells that may be at fault
Acute stage of inflammation
vascular changes
discharge
early fibroblastic activity
clinical signs:
inflammation
pain before tissue resistance
what is the vascular response to acute inflammation?
transient vasoconstriction occurs at the injured vessels
chemical mediators(histamine and serotonon) release
vasodilation and increased permeability make up the vascular response
Local swelling due to increase permability
pain is from the increased pressure
inflammation vascular response
1.vasoconstriction
2.vasodilation
3.growth of the fibrin lattice
4.enter leukocytes
5.enter platelets (first 24-36 hrs)
inflammation chemical mediators
RELEASED FROM INFLAMMATORY CELLS OR DERIVED FROM PLASMA
histamine
platelet activating factor
cytokines
Plasma cell derived chemical mediators
blood coagulation
firbrinoclytic
complement
What forms clots?
platelets
release prothorombin start the fibrin lattice
what is the cell response to acute inflammation?
leuokcytes move to the area and remove and eliminate stimulus
hemostatic response in inflammation
platelets scab over the area
fibrin
makes a cross linked lattice to seal off whole
why does edema occur?
results from an increase in fluid within the extravascular spaces
as permability increases the fluid becomes exudate
exudate
fluid being released from wound
sanginous fluid
red due to RBC
serosanguinous
yellow or pink
rbcs present
serous or watery
thin or clear yellow consists of protein
purulent
cloudy indicates infection or high WBC
catarrhal
clear
fibrinous
yellow or pink
goals of proliferation
epithelization
collagen production
wound contracture
neovascularization
fibroblastic activity in proliferation phase
scar formation
fibroplasia
symotoms of inflammation subside
what is epithelization
establishment of a epidermis, prevent electrolyte loss and chance of infection
what is resolution
the process that occurs when min tissue damage occured. damaged cells will recover, ex. sunburn
primary intention
features wound contracture
epithelization willnot provide adequate
secondary intention
healing by indirect union, gap between edges
ex. butterly or sutures
rely on epithelization for tissue healing
what is fibroplasia
collagen production
presence of infection or excessive stress will put the wound back into inflammation
regeneration
the process of mitosis in damged tissue
angiogenisis
regrowth of blood vessels
what types of collagen are present in maturation?
type 1 and 3
with chronic inflammation
tension theory
internal and external stresses can determine the scars final tissue structure
what are the outcomes of healing ?
- complete recovery
- healing by scar formation
3.formation of an abscess - chronic inflammation
complications of healing
infection
ulcers
spasm
chronic inflammation
adhesions
abscess
what causes chronic inflammation
-extensive nercosis
-inflammatory agent persists
-repeated episodes of acute inflammation in same tissue
-persistent immune rxn
chronic inflammation
can aid in healing but struggle to return to full function
chronic inflammation destorys tissue
how much muscle is lost per day of immobilization
1 to 3 %
immobiity effects of cardiovascular
raises 0.5 beats per min per day
decreased stroke volume of up to 15%
