EXSS 366 Exam 1 Study Set: Key Terms & Definitions

Inflammatory response

acute phase

fibroblastic

repair phase

maturation

remodeling phase

healing process is a

continuum

8 events of inflammatory response (overlapping)

- primary injury

- ultrastructural changes

- chemical mediation

- hemodynamic changes

- metabolic changes

- permeability changes

- leukocyte migration

- phagocytosis

what forms a hematoma

- initial injury leads to the destruction of cells and vascular damage

- collection of cell debris and hemorrhaged blood from disrupted capillaries -> hematoma

what is the vascular response to injury

vasoconstriction to promote clotting

what begins production of thrombin

damage to endothelial cells that compose the vessel

what does thrombin do

converts fibrinogen to fibrin

what does fibrin do

adhere to the edges of the damaged endothelial cells to create a mesh that traps platelets and reduces the loss of RBC

main responsibilities of chemical mediators present after initial injury

- vasodilation

- increase permeability

- increase activity of leukocytes

histamine

- released from mast cells, basophils, and platelets

- vasodilation of arterioles and increased permeability of venules

Kinins (bradykinin)

-dilate arterioles, have strong chemotactic properties, stimulate prostaglandins

- chemotaxis = attraction of leukocytes to microbes

serotonin

vasoconstriction

leukotrienes

- cause smooth muscle contraction

- endothelial cells contract (promotes margination of leukocytes)

Heparin

- inhibits coagulation by preventing conversion of prothrombin to thrombin

vasodilation

- increases total blood volume

- slows blood through the area -> collection of leukocytes

- expands space between endothelial cells easing transport of leukocytes out of vessel

increased permeability

- combination of vasodilation and smooth muscle contraction

- increase gaps between endothelial cells -> facilitates movement of leukocytes into extracellular space

________ allows leukocytes to adhere to vessel walls better (margination)

slower blood flow from vasodilation

gaps in endothelial cells from from

smooth muscle contraction induced by chemical mediators

diapedesis

leukocytes pass through gaps into extracellular space

first leukocytes to arrive

PMNs

PMNs

- polymorphonuclear neutrophils

- smaller, faster, and very numerous

- first line of defense

- short lived (~7hrs)

- do not reproduce

macrophages

- arrive later

- death of PMNs release chemical mediators that attract macrophages

- live for months

- can reproduce

- release chemical mediators to continue inflammatory response

2 special considerations during inflammatory response

- secondary cellular injury

- edema formation

secondary cellular injury - enzymatic injury

- contents of lysosomes from destroyed cells break down membranes of healthy cells on periphery of injury

secondary cellular injury - metabolic injury

- result of prolonged ischemia which leads to deficiency in ATP prodxn

- cells switch to glycolysis/anaerobic metabolism

- hypoxia (insufficient O2) and inadequate fuel delivery

- vessel damage

- slowed blood flow from chemical mediators

- inadequate waste removal

- build up of lactic acid and decreased cell pH

secondary cellular injury can ultimately lead to

(if severe enough) cell death = greater injury & greater hematoma to clean up

edema formation

- accumulation of fluid portion of blood in tissue

- occurs when a disruption in normal fluid dynamics (exchange of fluid btwn capillaries and tissue)

normal fluid dynamics

- fluid is constantly exchanged between capillaries and extracellular spaces

- 2/3 of fluid returned to capillary

- 1/3 of fluid absorbed by lymph vessel & eventually drains back into venous system

2 factors that make movement of fluid possible

- H2O molecules diffuse through capillary wall 80x faster than the flow of blood through the capillary

- capillary filtration pressure

capillary filtration pressure

gradient of intravascular and extravascular pressure

(CHP + TOP) - (THP + COP)

- balance of hydrostatic pressure and tissue oncotic pressure from capillary and tissue

- net result determines which way fluid flows

hydrostatic pressure

- pressure exerted by a column of water

- pushes water

- more water = more pressure = more pushing

CHP

- capillary hydrostatic pressure

- forces fluid out of capillary

THP

- tissue hydrostatic pressure

- forces fluid out of tissue

oncotic pressure

- pressure resulting from attraction of fluid by free proteins (think osmotic pressure in plants)

- more free protein = more pressure = more pulling

COP

- capillary oncotic pressure

- pulls fluid into capillary

TOP

- tissue oncotic pressure

- pulls fluid into tissue

intravascular pressure

- pressure to move fluid into tissue

- CHP + TOP

Extravascular pressure

- pressure to move fluid into capillary

- THP + COP

In healthy tissue

intravascular pressure > extravascular pressure

- 1/3 of fluid has to be handled by lymph vessels

capillary filtration pressure is different depending on location:

arteriole (intravascular>) or venule (extravascular>)

capillary filtration pressure after injury

- increase in concentration of free protein increases TOP

- greater movement of fluid into tissue resulting in greater edema and tissue swelling

fibroblastic-repair phase

- can only occur once the inflammatory phase has performed its function: remove debris and isolate injury

larger hematoma =

longer for repair to begin

- importance of limiting secondary injury

- importance of limiting edema formation

2 types of repair

- reconstitution and replacement

reconstitution

reproduction of identical cells

- occurs most readily with labile cells (skin, GI tract)

replacement

reproduction of non-identical cells, scar formation

- occurs most readily with stabile cells (muscle, ligament, tendon)

granulated tissue is

- created to allow tissue healing to occur

- delicate tissue composed of capillaries, fibroblasts, and collagen

- accomplished during the vascular and collagenization phases

vascular phase

- production of large number of blood vessels to provide adequate oxygen and nutrients to repair injured tissue

- takes 4-6 days

- driven by capillary budding

capillary budding

- endothelial cells in adjacent uninjured vessels begin to divide rapidly

- the new cells push between existing cells, advancing into the injured area; forms capillary buds

- adjacent capillary buds move towards each other

capillary arch

- once adjacent capillary buds meet, they form a capillary arch

- blood begins to flow through the arch

- flow of blood through the capillary arch stimulates additionally capillary budding and the process continues

capillary arcade

- eventually a capillary arcade, network of capillary arches, is formed

- capillary expands into the entire area of injury

- must be present for collagenization phase to begin; network will diminish once collagenization is complete; pruning

collagenization phase

- process of producing and laying down collagen in the injured area

- requires a great amount of oxygen

- energy requirements of the fibroblasts

- O2 is an essential building block of collagen

collagen is produced by

fibroblasts

- travel along the edges of the capillary arcade

- attracted to the area by the presence of macrophages

collagen

- fibrous protein in all types of connective tissue

- primary solid substance of ligaments, tendons, and scar tissue

- initial collagen produced is type III and is not as strong as that found in ligaments/tendons

amount of _____ at injury site can affect healing by...

oxygen affects the amount of collagen produced, the tensile strength of the collagen

- both increase with greater O2 delivery

how to increase O2 availability during healing

collagen is only able to best resist forces that are

in line with the orientation of the fiber

contraction occurs by two processes

(fibroblastic-repair)

- collapsing of the capillary arcade

- increased activity of myofibroblasts

collapse of capillary arcade

- collagen is a relatively inactive tissue and does not require a lot of O2

- extensive capillary network no longer needed

increased activity of myofibroblasts

-fibroblasts that have the ability to contract

- accumulate at the edges of the wound and pull towards the center

restructuring

- collagen is reorganized to a more parallel arrangement

- alginment is more inline with the forces exerted on the tissue; able to provide greater tensile strength

- important time for stress to be placed on tissue; dangerous for immobilization; active ROM and stress in all planes of motion is important

- type III collagen is replaced by type I (greater tensile strength

special considerations for contraction and restructuring phase

- scar tissue produced by collagen is relatively inelastic

similar to structure and fxn of ligaments and tendons but not muscle

- muscle tissue has satellite cells

- remain dormant in muscle tissue

- lack cytoplasm and proteins, but can serve as the nuclei for new muscle cells aiding in the repair of the muscle tissue

maturation-remodeling phase

- marked by strengthening of the scar and return to preinjury conditions

- collagen continues to be swtiched from type III to type I

- removal of fibroblasts, myofibroblasts, and macrophages

- importance of balancing stress and protection of the tissue

ligaments

- provide stability and proprioceptive information to a joint

- similar collagen structure to tendons

-ligaments are flatter, collagen fibers are more compact

ligament healing

- bleeding/inflammation (72 hrs)

- extraarticular- subcutaneous space

- intraarticular - joint capsule

- vascular proliferation and collagen synthesis (~6 weeks)

- scar maturation (12 months)