Physical Agents Exam 1

Front 1

Physical Agents

Back 1

group of procedures using various forms of energy that are applied in systematic manner

Front 2

NAGI Model

Back 2

1965, pathology -> impairment -> functional limitations -> disability

Front 3

disability

Back 3

inability or limitation in actions usually expected in social roles that are customary to a person's status

Front 4

functional limitation

Back 4

restriction of ability to perform at level as a whole person in efficient manner

Front 5

impairment

Back 5

loss or abnormality in anatomic, physiologic or psychologic structure or function (swelling, pain)

Front 6

ICIDH Model

Back 6

WHO 1980, disease -> impairment -> disability -> handicap

Front 7

ICF Model

Back 7

2001, enablement model

-------------> health condition ------------------>

| body funct/struct <-> activity <-> particp|

|

environment + personal factors

can intervene at any leveI

Front 8

Goal of Inflammation

Back 8

Days 1-6. Controls effect of injury, dispose of microorganisms and foreign material, prepares area for repair, red and ready

Front 9

Signs of Inflammation

Back 9

redness, increased temperature, pain, swelling, loss of function

Front 10

Vascular Response to Injury

Back 10

occurs during inflammation: edema formation, initial vasoconstriction (5-10 mins), vasodilation, increase in histamine, increase in capillary permability, prostaglandin makes capillaries leaky

Front 11

margination and pavementing of WBC

Back 11

occurs during vascular response of inflammation stage, WBC stick and build up on vessel wall, neutrophils are first to arrive

Front 12

capillary hydrostatic pressure

Back 12

push fluids out of capillaries (arteriole end), increased in injury

Front 13

interstitial osmotic pressure

Back 13

pulls fluid in to capillaries in an attempt to dilute (venule end), increased in compression

Front 14

Hemostatic Response to Injury

Back 14

Co-occurs during inflammation, temporary plug to control blood loss (scab), small vessels retract due to norepinephrine, platelets aggregate, fibrin deposits and traps RBC to form clot, attracts monocytes, macrophages, neutrophils and fibroblasts, gives tensile strength to wound

Front 15

Cellular Response to Injury

Back 15

Occurs during inflammation, leukocytes are key

Early: PMN, neutrophils die and release digestive chemicals

Late: monocytes come to convert to macrophage

Front 16

Macrophage

Back 16

attract fibroblast, catalyst to move out of inflammation onto next stage, need oxygen

Front 17

Immune Response during injury

Back 17

occurs during inflammation, fights infection, cell mediated by leukocytes and T-lymphocytes, complement system: series of enzymatic proteins activated by antibody/antigen association and bacterial toxins from cells. MAC membrane attack complex is end product. Results: increased vascular permability, phagocytosis, chemotaxis of leukocytes

Front 18

Poliferation

Back 18

day 3-20, re-epithelialization, fibroplasia, wound contraction, neovascularization

Front 19

re-epithelialization

Back 19

regrowth of skin, basal cells detach from basement membrane and divide and move, migrate while holding parent cells, continue until the pull wound closed, superficial, can occur within 24-48 hrs for small wounds

Front 20

fibroplasia

Back 20

collagen production, allows for more tensile strength, immature, weak, day 21 is max production but 20% strength, 6 weeks 80% strength, need oxygen, just the right amount of stress and repair

Front 21

wound contraction

Back 21

myoblasts, pulls edges of the wound together, creates scar tissue, pulls edges together from all sides

Front 22

neovascularization

Back 22

endothelial buds and capillary loops, development of new blood vessels in area, old vessels may make new branches, granulation tissue, macrophages stimulate growth, looks pink/red

Front 23

Maturation

Back 23

Day 9 onward, fibroblasts disappear, balance of synthesis and lysis, remodeling along stress lines, weak hydrogen bonds replaced with covalent bonds, blood vessels disappear, water content decreases

Front 24

keloid scar

Back 24

scar extends beyond borders of original injury

Front 25

hypertrophic

Back 25

extra scar tissue within border of original injury

Front 26

Acute pain

Back 26

recent onset, short/predictable course, know the cause usually, correlated with inflammation, reminder not to use part, less than 3-6 mo

Front 27

chronic pain

Back 27

more than 3-6 months, original injury is healed, unknown cause sometimes, generally inflammation gone, not proportional to damage, psychological component, oversensitivity to pain

Front 28

hyperalgesia

Back 28

heightened stimulus

Front 29

allodynia

Back 29

something that should not be painful at all is painful

Front 30

Specificity Theory of Pain

Back 30

There is a specific receptor for every sensation, pain has own receptor, does not explain how pain in minimized

Front 31

Pattern Theory of Pain

Back 31

one kind of receptor but pain is determined by action potentials increasing in frequency

Front 32

Gate Control Theory

Back 32

receptors fire in patters but there are also specific types of receptors and free nerve endings which sense specific sensations, balance of excitatory and inhibitory

Front 33

nonnociceptive nerves

Back 33

sense not painful, good sensation, flower spray endings, mechanorecepts, pacinian, corpuscles,

Front 34

nociceptive nerve

Back 34

sense pain, activated by substance P

Front 35

Substance P

Back 35

attracts bradykinens and changes polarization to create action potential in nearby place to send sensation of pain

Front 36

A Delta fibers

Back 36

20% of nociceptors, myelinated with small diameter, 30 m/s, quick sharp pain

Front 37

C Fibers

Back 37

80% nociceptors, large diameter, 1-4 m/s, nonmyelinated, slow dull ache, bradykinens and prostiglandins cause firing

Front 38

A Beta Fibers

Back 38

nonnociceptors, not painful, large diameter, myelinated, 20-90 m/s

Front 39

Anterolateral System

Back 39

ascending system for sensory information, carry conscious info of pain, temperature and touch both well and poorly localized

Indirect: lateral spinothalamic and anterospinothalamic

Direct: spinoreticulothalamis

Front 40

Substantia gelatinosa (SG)

Back 40

interneurons, not affected by A delta or C fibers, activated by A beta to send info to T cell

Front 41

T Cell

Back 41

gate to pain, receives messages from SG and sends to brain, can be inhibited by A beta via the SG and is excited by A delta and C fibers

Front 42

lateral spinothalamic

Back 42

part of the anterolateral system, fast, noxious/sharp pain, not many stops, localized

Front 43

anterospinothalamic

Back 43

part of the anterolateral system, cruder, less localized, achey pain, many stops

Front 44

spinoreticulothalamic

Back 44

diffuse, poorly localized

Front 45

2nd order neuron

Back 45

t-cell to thalamus, anterolateral system

Front 46

first order neuron

Back 46

t-cell and SG

Front 47

Central pathways: brainstem to brain

Back 47

reticular formation, raphe nucleus of brainstem, periaqueductal gray matter of midbrain, limbic system, hypothalamus

Front 48

reticular formation

Back 48

brainstem to midbrain: arousal

Front 49

raphe nucleus of brainstem

Back 49

produces body's opiods and more importantly seratonin

Front 50

periaqueductal gray matter of midbrain

Back 50

manufactures and has receptors for opioids: endorphins and enkephalins

Front 51

limbic system

Back 51

emotion control, produce opioids

Front 52

hypothalamus

Back 52

ANS, controls mood, diencephalon

Front 53

3rd Order Neurons

Back 53

from thalamus (relay center for pain) to cortex (post central gyrus)

Front 54

Descending Pain Control Mechanism

Back 54

endogenous opiate theory: end endorphins for four hours and enkephalins for half hour

descending neurotransmitters: serotonin and norepinephrine influence T Cells

Front 55

Chronic Pain

Back 55

hyperirritability, decreased threshold, increased efferent output, viscerosomatic and somatovisceral connection, pain-spasm-pain cycle

Front 56

pain-spasm-pain cycle

Back 56

when a lot of A delta comes in quicky signal is sent to T cell and T cell sends signal to brain and to muscles to contract, muscle contraction causes more pain which causes more contraction, need to break cycle.

Front 57

treatments to decrease pain

Back 57

stimulate A beta fiber with a modality or technique, brief intense treatment to stimulate opioid, prolonged c fiber stimulation to stimulate endorphin release

Front 58

frequency of ultrasound

Back 58

above 20,000 Hz for therapy typically .7 to 3.3 MHz for depth of 2-5 cm

Front 59

attenuation

Back 59

ultrasound decreases in intensity as it travels through a material, 1/2 due to absorption, increases with collagen content

Front 60

continuous ultrasound

Back 60

used to produce thermal effects

Front 61

piezoelectric

Back 61

responds to the alternating current by expanding and contracting (in transducer of ultrasound machine)

Front 62

thermal effects of ultrasound

Back 62

increase temperature of deep and superficial tissues (proportional to coefficient of absorption and frequency), 3 MHz heats more but not as deep (1-2cm), 1 MHz heats less but deeper (3-5cm), SATP .5 W/cm^2 or greater

Front 63

duty cycle

Back 63

the proportion of the total treatment time that the ultrasound is on, can be either percentage or ratio, 1:5 means on 20% of the time and off 80% of the time

Front 64

spatial average temporal average (SATA) intensity

Back 64

the average output over the area of the transducer over the average of the on and off time

Front 65

Nonthermal effects of Ultrasound

Back 65

due to mechanical events, delivered in pulse mode with 20% or lower duty cycle, increase intracellular calcium levels, increase skin and cell permeability, increases histamine and chemotatic factor, promote macrophage response, can help heal fractures

SATP .1-.2 W/cm^2 1Mhz

Front 66

phonophoresis

Back 66

transdermal drug delivery using sound

Front 67

contraindications of ultrasound

Back 67

malignant tumor, pregnancy, over CNS tissue, joint cement, pacemaker, thromophlebitis, eyes, reproductive organs, plastic componenets

Front 68

adverse effects of ultrasound

Back 68

periosteal burn, burn in areas of impaired sensation, damage to epithelial lining of blood vessels, transmission of infection

Front 69

precautions of ultrasound

Back 69

acute inflammation, epiphyseal plates, fractures, breast implants

Front 70

acoustic streaming

Back 70

steady, circular dlow of cellular fluids induced by ultrasound

Front 71

cavitation

Back 71

the formation, growth and pulsation of gas-filled bubbles caused by ultrasound, expand during rarefaction and shrink during compression

Front 72

standing wave

Back 72

occur when the ultrasound transducer and reflecting surface are exact multiples of wavelengths apart, allowing reflecting wave to superimpose on incident wave

Front 73

effective radiating area

Back 73

ERA, area of transducer from which ultrasound energy radiates

Front 74

intensity of ultrasound

Back 74

power per unit area (W/cm^2)

Front 75

spacial average temporal peak

Back 75

SATP, average intensity/ERA, no heat when under .5W/cm^2

Front 76

physical properties of water

Back 76

buoyancy, specific heat/thermal conductivity, resistance/viscosity, hydrostatic pressures

Front 77

physiological effects of hydrotherapy

Back 77

cleansing (softens materials and exerts pressure), less trauma in weight bearing exercises, provide force in exercise (resistance), increases venous return (60% when in up to neck), decrease in heart rate, increases resistance to lung expansion, increased urine production, calming effect

Front 78

uses of hydrotherapy (5)

Back 78

superficial heating and cooling, exercise, edema control, wound care, burn care,

Front 79

contraindication of hydrotherapy (8)

Back 79

maceration around a wound (immersion), bleeding (immersion), superficial hot and cold contraindications

whole body: cardiac instability, infectious condition, bowel incontinence, severe epilepsy, suicidal patients

Front 80

adverse reactions of hydrotherapy (6)

Back 80

drowning, heat reactions (burning, fainting, bleeding), hyponatremia (loss of salt w/ burn patient), infection, aggravation of edema, exacerbation of asthma (if allergic to chemicals)

Front 81

hyperemia

Back 81

increase in blood to area causing increase in temp

Front 82

chronic inflammation

Back 82

simultaneous active inflammation, tissue destruction and healing (mononuclear cells and fibroblasts)

caused by reinjury, disease or infection

Front 83

factors affecting tissue healing ( 8)

Back 83

type/size/location, infection, vascular supply, movement, age, disease, medication, nutrition