Exam 1 671

Viscoelastic properties

creep

stress relaxtion

pre-conditioning

stretch model

tear the tissue so we can elongate it

growth model

apply stimulus to the tissue of moderate lengthening over time it will grow that way

immobilization of CT (no trauma)

decrease in collagen biosynthese, enzyme activity, MRNA for type I & III collagen, GAGs, HA

increase in collagen degradation, expression of MMP, weak cross links

Contracture

adaptive shortening of periarticular tissue

collagen reorganization

myofibrils activation

muscle shortening = loss of sarcomeres

Adhesion Formation

loss of gliding

scar formation b/t two tissues that normally glide or unfold on each other

Biomechanical changes of CT following Imm.

decreased tissue stiffness

decreased load ton failure

increased joint stiffness

stages of wound healing

inflammation (0-5 days, recruit neutrophils/macrophages)

fibroplasia (5-28, repair, fibroblasts secrete collagen

maturation (28-365, remodeling, improving tensile strength of collagen)

Precontemplation

no thought to change

contemplation

exposed to idea of change, but no action

preparation

actively making plans

action

performing the behavior change

maintenance

incorporation the behavior change into lifestyle

Eliciting change talk

Desire for change

Ability to change

Reason to change

Need for change

Commitment

Activation

Taking steps

MI Core Skills

Open ended questions

Affirmations

Reflections

Summary

MI guiding principles

Resist righting reflex

Understanding the pt own motivations

Listen with empathy

Empower the patient

Spirit of MI

collaboration

compassion

acceptance

evocation

Models for behavior change

Health belief

social cognitive theory

self-determination theory

transtheoretical model of change

bone mineral strongest in

compression, made of hydroxypatite

bone matrix strongest in

tension, made of collagen

open fracture

any break in skin that extends down to the bone

higher infection risk

more soft tissue damage = longer healing time

closed fracture

skin intact

less infection risk, less soft tissue damage

SH type I

fracture through growth plate

SH type II

fracture exits through metaphysis

SH type III

fracture exits through epiphysis (intra-articular)

SH type IV

transverse, across the growth plate (intra-articular)

which SH fractures are usually surgical

Type III & IV

fracture healing stages

inflammation (1-3 days, fracture hematoma)

soft callus (osteogenic repair cells infiltrate hematoma, Chondroblasts form cartilage, sticky, cells differentiate into osteoblasts)

hard callus (6-12 weeks, clinical union)

remodeling (bones responds to stress, osteoblasts lay down new bone along lines of stress, osteoclasts reabsorb poorly located bones)

factors that affect fracture healing

age

site & configuration

initial displacement

blood supply

what happens to a fracture if there is poor blood supply?

prolonged healing process (scaphoid tibia)

Treatment options for fractures

immobilization: used for non-displaced fractures

closed reduction: realigning fracture without surgically opening the site

open reduction: surgically opened in order to be reduced, internal fixation is placed

common fracture sites

proximal humerus

distal radius

scaphoid

hip

femur

tibia

ankle

malunion

unacceptable alignment

nonunion

shows no signs of healing by 3 months

infection

common in open fractures and diabetes

compartment syndrome

tissue pressure > venous pressure

complex regional pain syndrome

pain, swelling, autonomic dysfunction, burning aching pain out of proportion to injury

Primary bone healing

direct contact b/t fragments

occurs 2 weeks from injury

rigid compression fixation

no callus formation

stable fracture site

secondary bone healing

callus formation

casting/ IF

most common

motion minimized not eliminated

Stress sharing

NOT rigid fixation

callus formation

faster healing

includes casts, IM rods, external fixators

stress shielding

rigid fixation

NO callus formation

no motion at fracture site

includes plates/screws

Management phases for fracture

Phase1 protected Motion

Phase 2 early motion

Phase 3 Functional recovery

Phase 4 return to activity

Phase 1 protected motion

immobilization

ROM of non-involved joints above/below

WB status

Edema control

Education

Phase 2 early motion

WB status

Immobilization

begin joint ROM

Address other impairments

Phase 3 functional recovery

imm. usually discontinued

progress to full joint ROM as tolerated

begin strengthening: isometrics to isotonics

begin neuromuscular reeducation

address functional deficits

Phase 4 return to activity

return to all functional mobility

Low frequency TENS mechanisms

activates mu-receptors in RVM, SC periphery

uses serotonin and activates 5-HT2 and 5HT3 receptors in spinal cord

High frequency TENS mechanism

activates o-opioids receptors in RVM and SC

reduces glutamate and aspartate release

increases concentration of beta endorphins and methionine encephalin in CSF

reduces substance P in SC and periphery

for sensory stim when do we use high freq.

when we want to produce a constant tingling sensation

what happens when we want motor stim at a high frequency?

constant contraction (becomes uncomfortable, need on/off times)

What happens when we want motor stim at a low frequency?

a strong twitch is produced

what happens with noxious stim at a high freq.

constant strong and uncomfortable