Inflammation and Healing Flashcards
Erythrocytes
RBCs
do not migrate to injury
ROLE: O2 transport
Hemoglobin specifically transports the O2
Leukocytes
WBCs migrate to the injury
clear debris - PHAGOCYTOSIS to prep for healing
each one is specialized for a task in early or later stages of inflammation
Monocyte becomes Macrophage once out of capillary WBC
PHAGOCYTOSIS - eating dead stuff
prominent in CHRONIC inflammation
come and go quickly in acute inflammation
too many is BAD = chronic infla
Lymphocyte WBC
bacteria killer - come and go within 1-2 days
if chronic it sticks around
too many is bad = chronic infla
Eosinophil
if high count - scary
allergic reaction or parasite infection
too many is bad = chronic
Neutrophil
bacteria killer - come and go in a couple of days
acute inflammation/ NL
Basophil
acute inflammation/ NL releases histamine (inc BF to area)
Mast Cells
found in CT (not blood)
releases HISTAMINE/Heparin in response to tissue injury and infla
present in NL infla process
Platelets
1st cells to injury site and promote blood clotting
even come to site when skin is intact
PDGF - platelet derived growth factor creates PRP (platelet rich plasma) which can be injected into injury to speed up healing process
Chemotactic Signaling
platelets send out chemical messages than an injury is present
the signal is PDGF
Fibroblasts **
Spew Collagen**
found in CT and forms collagen fibers
Good - but too much is not always good
EPA’s inc their activity: US/laser
Inflammation
1-6 days
prepares the wound for healing to occur
some EPAs try to trigger/restart this process
Inflammation Signs
heat, pain, swelling, redness, loss of function
Resolve QUICKLY! prevent chronic inflammation
Vascular Inflammation Response
Brief VC (5-10min) to not lose blood
VD and inc permeability to clean up and bring troops
Extravasation, Histamine, Hageman Factor, Bradykinin, Prostaglandin
Extravasation
the process of a leukocyte migrating form the vessel to the tissue
Histamine = VD
VD**
released by Mast, plateets and basophils
VD to inc vascular permeability leading to edema
Hageman Factor (clot factor XII)
enzyme found in blood that helps to stop local bleeding
Bradykinin
mediated the inflammatory process
inc VD**
maybe some pain regulation
Prostaglandin
attracts leukocytes
chemotactic signaling - attracts WBCs (troops)
pain - receptors sensitized
Hemostatic Inflammation Response
limit local bleeding and fluid drainage
seal damaged vessels
platelets - 1st to promote clot and PDGF
collect fibrin and collagen to help clot
Cellular Inflammation Response
Mast and platelets release chemotactic agents to attract leuk. Destroy neutrophils to break down fibers, mediate immune response, macrophage - phagocytose and attract fibroblasts
PT goals with Inflammation
Protect area and Prevent Inflammation
Proliferation
“Fibroblastic Phase”
rebuilds damaged tissue and strengthen the wound
4 steps: epithelialization, collagen production, wound contraction, neovascularization/angiogenesis
Epithelialization
if open wound - reestablishment of epidermis, provides protection, healthy cells migrate to cover wound
Collagen Production
fibro eat Ca and spew collagen which is thin, weak, unorganized (type III) which tolerates early and controlled movement.
Day 12 type III is replaced by type I which is more mature and stronger - still unorganized
Wound Contraction
pulls edges of site together for smaller area of scar
myofibroblasts have contractile properties and pull good skin together
can have contracture
Contractures
uncontrolled wound contraction
inc resistance to passive stretch
Neovascularization/ Angiogenesis
Development of new bld vsls to area helps healing and supply of O2 and nutrients
Form a capillary loop which is weak and often immob helps protect these was they grow
pink/bright red
Maturation/ Remodeling
modifies scar tissue into its mature form
Maturation Response
collagen reabsorbed if off direction
longest phase up to 1 yr
changes in size, form, strength of scar (become white)
Type I coll replace type III need O2 - also need a balance between synthesis of new and lysis of III
Induction Theory
scar mimics tissue its healing
Tension Theory
internal and external stressed placed on area determine final structure
tension during healing can inc tensile strength
immobilization reduces tensile strength and collagen structure
1st phase EPAs
cryo, compression, iontophoresis, laser, TENS, e-stim
2nd phase EPAs
inc BF - heat, diathermy
inc cell metab - laser, estim, US*
3rd phase EPAs
US*, laser, CPM, traction, NM e-stim
Acute Infla
sequence of healing continuous and within expected time frame
Chronic Inflammation
delay in processs because repeat trauma, poor perfusion/oxygenation, immune response to foreign material or RA
local factors to wound healing
type/size/location wound dimension infection vascular supply external forces movement
Systemic factors of wound healing
age
disease
medications
nutrition - smoking
