Chapter 10 - Tissue Response to Injury Flashcards
5 signs of inflammation
redness (rubor) swelling (tumor) pain (dolor) temp (calor) loss of function (function lease)
inflammatory response phase lasts
about 4 days
inflammation caused by
cellular injury results in altered metabolisms and liberation of materials that initiate inflammation
injury causes altered metabolisms and release of materials and chemicals that initiate inflammation
1st responders of inflammation
leukocytes, phagocytic cells, exudates
Phases of inflammatory response
vascular reaction, phagocytosis, formation of a clot
vascular reactions
immediate vasoconstriction followed by vasodilation
initial effusion last 24-36 hours
chemical mediators: histamine, leukotaxin, necrosis, leukocytes
histamine
released from mast cells; vasodilation, increased cell permeability, sensitizes pain receptors
Leukotaxin
margination; increases cell permeability locally to allow for diapedesis
Diapedesis
movement of wbc out of small arterial walls
Necrosin
phagocytic activity; amount of swelling that occurs directly related to extent of vessel damage
Leukocytes
neutrophils and macrophages - cause release of bradykinin and prostaglandin
Bradykinin
increased permeability, pain, stimulates release of prostaglandin
Prostaglandin
increases permeability of blood vessels and tissue (increased space for WBC’s to move)
three phases of the healing process
inflammatory response phase, fibroblastic repair phase, maturation-remodeling phase
margination
neutrophils and macrophages line up along the cell wall
cytokines
attrack phagocytes to site of inflammation
vascular reaction
vascular spasm, formation of a platelet plug, blood coagulation, growth of fibrous tissue
what state does immediate vasoconstriction cause
local anemia, followed by rapid hyperemia because of vasodilation
formation of platelet plug
platelets adhere to collagen fibers that stick out due to injury.. create sticky matrix that sticks to more platelets and leukocytes to eventually form a platelet plug
formation of a clot
damaged cell–>thromboplastin –>prothrombin changed to thrombin –> fibrinogen changed to fibrin –> clot shuts off blood supply to injured area
clot formation begins when?
12 hours after injury and completed within 48 hours.
initial flammatory phase lasts
2-4 days
Chronic inflammation
neutrophils present during normal acute inflammation are replaced with macrophages, lymphocytes, and fibroblasts, and plasma cells.
this causes damage to occur to the healthy cells around the dead cells - damage to the CT - causes necrosis and fibrosis.
forms granulation tissue
PMN’s
polymoprhonuclear neutrophils - first on the scene - kill bacteria - will die off and create a toxic environment
mononuclear phagocytes / macrophages
after PMN’s.
once debris is removed from site of injury
blood coagulates, exudates coagulates to form fibrin network to localize injury, epithelial cells migrate to edges and fibroblasts enter to regrow capillaries
granulation tissue
fibroblasts, collagen, capillaries
extracellular matrix
callagen, elastin, ground substance, proteoglycans, glycosaminoglycans
fibroblastic repair phase
fibroplasia - scar formation - can last 4-6 weeks
as the fibrin clot breaks down..
granulation tissue is formed. capillaries grown into the area, and fibroblasts accumulate lay down parallel to capillaries
fibroblasts
synthesize extracellular matrix and begin to randomly deposit collagen fibers to form the scar. Type III collagen is most common
tensile forces
tensile forces help strengthen the collagen and lead it into the maturation phase, presence of fibroblasts is diminished
maturation-remodeling phase
long-term process. realignment or remodeling of the collagen fibers according to the subjected tensile forces
types of repair
resolution: little no damage - normal restoration
granulation: initially laying down of type III - changes to type 1 in 2 weeks
regneration: new cells of same type are generation and capable of performing same function
factors that impede healing
extent of injury, edema, hemorrhage, poor vascular supply, separation of tissue, muscle spasm, corticosteroids, keloids, infection, humidity, climate, health, age, nutrition
Vitamin C and healing
collagen synthesis, immune system function
vitamin K and healing
clotting
Vitamina A and healing
immunue system function
zinc and healing
enzyme system
oxygen tension
relates to neurovascularization of wound, which translates into optimal saturation and maximal tensile strength development
microtears
overuse
macro tears
acute
Wolff’s law
bone and soft tissue will respond to the physical demands placed on them, causing them to remodel or realign along line of tensile force
cell organelles
mitochondria, ribosomes, endoplasmic reticulum, centrioles, golgi apparatus, microtubules
4 types of soft tissue
epitheial
connnective
muscle
nervous
soft tissue adaptations
metaplasia, dysplasia, hyperplasia, atriphy, hypertrophy
metaplasia
coversion of one kind of tissue into a form that is not normal for that tissue
dysplasia
abnormal development of tissue
hyperplasia
excessive proliferation of normal cells in the normal tissue arrangement
cartilage healing properties
limited healing capacity
ligament healing
first 72 hours: loss of blood and attraction of inflammatory cells
extra-articular ligament
bleeding occurs in subQ
intra-articular ligament
bleeding occurs inside joint capsule until clotting or pressure causes cease
full ligament healing may take
12 months
factors affecting ligament healing
surgery, active exercise, strengthening of surrounding muscles (all these are good for the ligament)
Muscle healing
long healing time
tendon healing
begins as one mass that is adhered to surrounding tissues (2nd week) eventually elongates into separate structure by the third week
nerve healing
regneration is impossible
unless the injury does not affect the cell body
3-4 mm per day
bone healing
affected by torsion, bending, and compression
bone healing after fracture
week 1: fibroblasts laying down collagen network
weeks 3-8: immobilization
osteoblastic/clastic activity - 2-3 years after
chondroblast cells
begin producing fibrocartilage, creating a callus b/w broken bones
osteoblats
form cancellous bone trabeculae which eventually replaces cartilage
osteoclasts
cells that resorb bone - clean up debris
remodeling
fibrous cartilage replaced by fibrous bone and them lamellar bone
referred pain
occurs away from a actual site of irritation
types of referred pain
myofascial pain, sclerotomic pain, dermatomic pain
myofascial pain
trigger points are small hyper-irritable area within a muscle in which nerve impulses bombard the CNS and are expressed as referred pain
sclerotomic pain
deep, aching, poorly localized pain from area of bone or fascia,
single nerve root
can cause affective changes
dermatomic pain
area of skin supplied by a single nerve root; pain is sharp and well-localized, projects mainly to thalamus and is relayed directly to the the cortex (skips autonomic and affective responses)
nociceptors
pain receptors/free nerve endings, sensitive to mechanical, thermal, chemical energy
first order-primary afferents
transmit impulses from nociceptor to dorsal horn of spinal cord
a-alpha and a-beta
large - diameter
a-delta and C
small-diameter, transmit sensation of pain and temperature
a-deltas
transmit ‘fast pain’, C transmits ‘slow pain’
secondary order afferents
carry sensory messages from dorsal horn to brain
input from a-betas/deltas, and C’s.
serve large receptor fields
third order afferents
carry info from the thalamus to the cerebral cortex
seratonin
active in descending pathways
norephinephrine
inhibits pain transmission b/w first and second order neurons
enkephalins
found in descending pathways
beta-endorphins
found in CNS
Gate Control Theory
sensory inför from alpha-beta fibers overrides or inhibits the ‘pain info’ carried along a-deltas and C affront fibers, thus inhibiting or ‘closing the gate’ to the transmission of pain info to 2nd order neurons
T-cell (located in dorsal horn) only lets one sensation through at a time, so strong sensory information traveling along alpha-beta fibers can affect the SG(substantial gelintinosa) which can send inhibitory signals to the T-cell and close the gate before the pain stimuli (a-deltas or C fibers) can be transmitted to 2nd order neurons
occurs at spinal cord level.
afferent pathway
Central Biasing
‘Descending pathway pain control’
previous experience, emotional influences, sensory perception, main influence perception of pain - brain can release neurotransmitter
Release of Beta-Endorphins
painful stimuli release B-endorphin opiates from hypothalamus and anterior pituitary.
strong analgesic effects
efferent pathway
Visual Analog Scale
lines that represent limits of pain.
pain charts
2-dimensional graphic chart to assess location of pain
mcgill pain questionnaire
78 words that describe pain, which are grouped into 20 sets and divided into 4 categories representing dimensions of the pain experience
activity pain indicators
64-question self report tool to assess impairment associated with pain
numeric rating scale
1-10
phagocytosis
disposing of injury byproducts
