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Biophysical Agents > Unit 1 Lecture > Flashcards

Unit 1 Lecture Flashcards

1
Q

define physical agents

A

energy and material applied to help in rehabilitation

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2
Q

list general examples of physical agents

A

hot packs
cold packs
ice massage
paraffin
electrical stimulation
whirlpool
ultrasound

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3
Q

what are the 3 categories of physical agents?

A

thermal agents
mechanical agents
electromagnetic agents

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4
Q

define thermal agents

A

hot and cold
transfers energy to produce an increase or decrease in tissue TEMPERATURE

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5
Q

what are the 2 categories of thermal agents?

A

thermotherapy and cryotherapy

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6
Q

describe thermotherapy and the agents used

A

heat and speed up
increases circulation
increases metabolic rate
promotes soft tissue extensibility
decreases pain

agents: hot pack, paraffin, ultrasound (deep and superficial heating agents)
ultrasound is continuous

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7
Q

describe cryotherapy and the agents used

A

cold and slow down
decreases circulation
decreases metabolic rate
decreases pain

agents: cold packs, ice massage

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8
Q

define mechanical agents

A

apply force to increase or decrease PRESSURE on the body

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9
Q

describe agents used in the mechanical category

A

water - hydrotherapy
traction - decreases inflammation
compression - changes fluid pressure, controls or reverses edema
*ultrasound is pulsed - facilitates tissue healing, transdermal drug penetration

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10
Q

define electromagentic agents

A

apply energy in the form of electromagnetic radiation or electrical current

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11
Q

describe agents used for electromagnetic radiation

A

UV radiation
infrared radiation
laser
diathermy (superficial and deep heat)

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12
Q

describe the agent used for electrical currents

A

E-stim for
pain modulation
muscle strengthening
reduce edema
tissue healing

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13
Q

how are physical agents used in rehabilitation?

A

they have a direct effect on the level of impairment
can be used in addition to other interventions (such as exercise/stretching) to make the effectiveness greater

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14
Q

describe factors to be considered when determining a physical agent to use

A

!plan of care developed by PT
physician’s referral
medical diagnosis
medical history
indications of use
precautions/contraindications
level of risk

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15
Q

define contraindications

A

conditions under which a certain treatment should NOT be applied

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16
Q

define precautions

A

conditions under which a certain treatment should be applied with special limitations or care

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17
Q

what are general precautions and contraindications?

A

pregnancy - changing temperature of womb can be dangerous
malignancy - heat can spread cancer cells
pacemaker/implanted electronic device - electrical currents can effect the device’s function
impaired sensation - cannot tell if something is too hot, cold, painful, etc.
impaired mentation - cannot communicate whether something is too hot, cold, painful, etc.

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18
Q

define and describe the importance of evidence-based practice

A

the use of the current best evidence in making decisions about the care of individual patients

importance: able to provide the best possible patient care

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19
Q

how has history influenced the use of physical agents?

A

new uses of agents have been discovered as a result of increased understanding of the biological processes underlying disease, dysfunction, and recovery

this has also led to other agents and applications falling out of favor

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20
Q

define inflammation and repair

A

a multifactorial process dependent on
source of injury
site of injury
state of local homeostasis
whether the injury is acute (short-term) or chronic (ongoing)

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21
Q

what is the goal of the inflammation and repair process?

A

to remove what is causing the inflammation, replace the damaged tissue, and facilitate growth of new tissue

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22
Q

what are the 3 phases of inflammation and repair?

A

inflammation phase
proliferation phase
maturation phase

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23
Q

describe the inflammation phase

A

first phase
goal: prep the wound
days 1-6
immediate response to destroy, dilute, or isolate what may be a fault when tissue is altered by disease or trauma

4 responses: vascular, hemostatic, cellular, immune

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24
Q

what are the cardinal signs of inflammation?

A

hyperemia - increased vascularity/blood flow (RED/HOT)
swelling - vasodilation/blockage of lymphatic drainage/fluid into interstitial spaces
pain - physical pressure or chemical irritation
loss of function

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25
Q

describe the vascular response

A

first response of inflammation phase
(1) involved vessels constrict to reduce blood loss for 5-10 minutes
(2) neighboring uninjured vessels start vasodilation - this and an + in capillary permeability is initiated by histamine (released by platelets/mast cells/basophils & attracts leukocytes), bradykinin (vasodilator), and prostaglandins (sensitizes pain receptors/can cause fever/ NSAIDS (advil/tylenol) can stop production)
(3) hageman factor - enzyme that activates coagulation, vasoconstriction, and increased permeability of plasma proteins/ blood flow slows, blood thickens, and blood vessels stick together/neutrophils migrate to the injured area: margination - line the walls of vessels, pavementing - lay down in layers, diapedesis - begin to squeeze through vessel walls, emigration - migrate from blood vessels to perivascular tissues
(4) edema occurs because of an unbalanced increased capillary hydrostatic pressure (pulling in fluid), interstitial osmotic pressure (pushing fluid out), venule permeability, and/or overwhelmed lymphatic system

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26
Q

describe the fluid types associated with edema during the vascular response of the inflammation phase

A

transudate - formed first, very few cells and proteins
exudate - extravascular fluid becomes cloudy and vicious, high content of cellular debris and lipids

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27
Q

describe the hemostatic response

A

second response of inflammation phase
works to control blood loss
(1) immediately after injury platelets enter the area and bind to collagen, releasing fibrin to stimulate blood clotting
(2) platelets release Platelet-Derived Growth Factor (PDGF) which helps with fibroblasts (which make collagen), macrophages, monocytes, and neutrophils
(3) fibrin and fibronectin form with collagen cross links to make fibrin lattice (temporary plug/band-aid) - provides sole strength during this phase
monocytes: leuokocytes with a single nucleus that become macrophages when they move from the capillaries into tissue spaces/seen 24-48 hours after injury/make chemicals that remove necrotic tissue and bacteria/promotes cell growth
macrophages: essential for wound healing/release substances that enhance the killing microorganisms and signal for more to come to the area/may also attract fibroblasts

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28
Q

describe the cellular response

A

third response during inflammation phase
(1) migrate into the area hours after injury - leukocytes (neutrophils, basophils, eosinophils) are delivered to the area by circulation and clear in the injured site of debris to get ready for tissue repair
neutrophils: highest concentration in blood/present most initially after injury/rid the area of debris and bacteria by phagocytosis/release enzymes for debridement process/present for 24 hours
basophils: release histamine/contribute to increased vascular permeability
eosinophils: some activity in phagocytosis

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29
Q

describe the immune response

A

4th response in the inflammation phase
mediated by cellular and humoral response
activation of the complement system make bacteria more susceptible to phagocytosis, cell lysis, and death/increase vascular permeability

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30
Q

describe the achievements of the inflammation phase

A

(1) fibrin lattice is formed - limits blood loss and initially strengthens wound
(2) neutrophils and macrophages clean out damaged tissues
(3) endothelial cells and fibroblasts are brought to the area

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31
Q

describe the proliferation phase

A

second phase
days 3-20
goal is to cover the wound and strengthen the injury site

4 responses: epithelialization, collagen production, wound contraction, neovascularization

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32
Q

describe epithelialization

A

first response of proliferation phase
very weak for several weeks
(1) reestablishment of the epidermis that begins early when the wound is superficial/can be resurfaced in approximately 48 hours (longer ones take longer)
if wound is deep, this phase will begin after collagen production and neovascularization
(2) uninjured epithelial cells from the margins of the damaged area reproduce and migrate over the injured area to provide a protective barrier that prevents fluid loss and decreases the risk of infection

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33
Q

describe collagen production

A

2nd phase of proliferation phase
(1) fibroplasia (growth of fibrous tissue) takes place in connective tissue and fibroblasts migrate to the injured area to synthesize procollagen
fibroblasts initially produce a thin, weak collagen structure with no organization (type lll) - can tolerate early, controlled motion, but disruptions means more inflammation and collagen (more collagen causes excessive scarring
(2) collagen fibers form and begin to strengthen the injured area/can also facilitate endothelial cells and macrophages for wound healing
(3) granulation tissue is formed and as it increases in amount there is a reduction in the size of the fibrin clot - this helps to build a more lasting structure

34
Q

describe the time frame of collagen production in the collagen production response

A

day 7 - more collagen present - increased strength
day 12 - type lll > type l
day 21 - collagen production is maximal, but wound strength is at 20% of normal
6 weeks later - wound strength is at 80% of normal

35
Q

describe wound contraction

A

3rd response of proliferation phase
healing of the wound UNDERNEATH the skin
begins at day 5 and peaks at 2 weeks - myofibroblasts attach to margins of intact skin and pull the epithelial layer inward
shape and size of wound influences rate of closure (square - fast/ circle - slow)

36
Q

describe the types of healing during the wound contraction response

A

healing by primary intention - wound is closed with sutures and heals without wound contraction

healing by secondary intention - heals on its own

healing by delayed primary intention - heals on its own at first and then is closed by sutures

37
Q

describe the neovascularization response

A

occurs as a result of angiogenesis
development of new blood supply to injured area - vessels supply oxygen and nutrients
must be careful with early aggressive motion to prevent microhemorrhaging

38
Q

describe the maturation phase

A

3rd phase
day 9+
longest phase - may take over a year
(1) water content declines and scar is white in appearance (type l collagen)

39
Q

describe the types of collagen

A

type l - mature scars/inelastic/organized and patterned/STRONG (bone, skin, tendons)
type ll - collagen in cartilage (ex - ear)
type lll - unorganized and WEAK (GI tract, uterus, blood vessels)

40
Q

keloid scars

A

extend beyond the margins of the injury into surrounding tissue

41
Q

hypertrophic scars

A

raised, but stays within the margins of the wound/inelastic

42
Q

define acute inflammation

A

occurs immediately after tissue damage and is short term

43
Q

define chronic inflammation

A

a simultaneous progression of acute inflammation, tissue destruction, and healing/long-term

44
Q

can physical agents affect or modify tissue healing?

A

yes

45
Q

describe local factors that influence healing

A

location - how far/close to a good blood supply
size - how big/small injury is
vascular supply
use of physical agents
movement

46
Q

describe systemic factors that influence healing

A

age
disease
medication
nutrition

47
Q

describe the healing of cartilage

A

limited healing due to the lack of lymphatics, blood supply, and nerves

48
Q

describe the healing of tendons and ligaments

A

occurs at different rates due to location, type of injury, nearby structures, immobilization, and whether or not there is damage to the tendon sheath

49
Q

describe the healing of skeletal muscle

A

regeneration in humans has not been documented after trauma

50
Q

describe the healing of bone

A

will heal with or without rigid fixation

51
Q

name and describe the 6 phases of bone healing

A

(1) impaction - energy from injury effect bone
(2) induction - activation of cells with osteogenic capabilities
(3) inflammation - starts after injury/present until fibrous union is present
(4) soft callus - bony fragments united by fibrous or cartilagenous tissue
(5) hard callus - (3 weeks - 4 months) sticky, hard callus over area of fracture/new bone unites with fragments
(6)**bone remodeling - occurs when bone is clinically and radiologically healed (can take months-years)

52
Q

what is pain?

A

interaction between neurological, psychological, sociological, and mechanical factors & unpleasant sensory/emotional experience

53
Q

describe acute pain

A
  • response to a noxious stimuli causing pain that lasts less than 6 months and is mediated through rapidly conducting pathways
  • causes increased muscle tone, HR, and BP
  • pain is present as long as stimulus is present
54
Q

describe chronic pain

A
  • persists beyond the normal time for tissue healing
  • decreases levels of enkephalins (endorphins)
  • increased quantities of and sensitivity to nociceptors
55
Q

define hyperalgesia

A

hurts more than it should

56
Q

define allodynia

A

hurts when it shouldn’t

57
Q

describe referred pain

A

feeling pain in 1 area because of an issue in another area

usually referred
(1) from a nerve to its area of innervation
(2) from 1 area to another derived from the same dermatome

58
Q

describe neuropathic pain

A
  • occurs as a direct response to something that affects/damages the nerves
  • described as burning/sharp and may occur with numbness, prickles, itching, weakness of lower extremities, pain in feet, balance issues, etc.
59
Q

describe nociceptive pain

A
  • caused by stimulation of pain receptors by chemical, thermal, or mechanical stimulus
  • associated with ongoing tissue damage and is present for those with chronic pain due to weakened tissues
60
Q

describe dysfunctional pain

A

very little is known about this type
- pain that serves no purpose
- can be associated with fatigue, sleep problems, depression, impaired physical/mental state

61
Q

describe psychogenic pain

A

no injury, but real and physical symptoms
-psychological role of pain to a large degree

62
Q

define anaglesia

A

absence of pain

63
Q

describe nociceptors

A

(1) release neuropeptides (like substance P) when activated
(2) convert initial stimulus into electrical activity as action potentials via transduction
(3) action potentials spread from nociceptors along AFFERENT nerves towards the spinal cord
(4) nociceptors give rise to 2 first-order AFFERENT nerve fibers: A-Delta and C-Fibers

64
Q

describe C-Fibers group IV afferents

A
  • small diameter and unmyelinated - transmit action potentials slowly and have a slow onset after initial stimulus response
  • 80% of afferent pain-transmitting fibers
  • mechanical, thermal, and chemical stimulation can cause sweating, nausea, and increased HR and BP
  • long lasting pain/dull, throbbing, tingling, aching, tapping, burning
  • emotional component
    reduced by opiates
65
Q

describe A-Delta fibers group lll afferents

A
  • small diameter and myelinated - transmits action potentials rapidly and have a quick onset after initial stimulus exposure
  • 20% of afferent pain-transmitting fibers
  • sensitive to high intensity mechanical stimulation and some response to heat and cold
  • short term pain/sharp, stabbing, pricking
  • no emotional component
    **not usually blocked by opiates*
66
Q

describe A-Beta fibers

A
  • have large, myelinated axons that conduct impulses faster than A-Delta and C-Fibers
  • found in skin, bones, and joints
    -can cause normal stimuli to cause pain
  • respond to vibration, stretching the skin, and mechanoreception (body movements) which don’t usually cause pain
67
Q

describe the use of the central pathways from the periphery to the cortex

A

(1) step one:
- first order afferents (A-Delta and C-Fibers) project from the periphery to the dorsal horn of the spinal cord
- they can be direct synapse or synapse by interneurons (T-cells) with second order neurons
- T-cells in SC receive excitatory input from nociceptors and inhibitory input from sensory nerves/fibers this determines whether pain will be felt or not
- excitatory impulses dominate = pain/ inhibitory impulses dominate = no pain

(2) step two:
- second order neurons carry information in pathways located in the anterolateral aspect of the SC
- carries information on temperature and touch/has 2 divisions:
- lateral spinothalmic tract: sharp pain/localization
- anterospinothalmic tract: prolonged aching pain/emotional
- most will cross the midline and project to the thalmus where they will synapse with third order neurons

(3) step three:
- third order neurons project from the thalmus to the cortex where pain is brought to the conscious level

68
Q

what is the pattern theory

A

all nerve endings transmit all types of stimuli

69
Q

what is the specificity theory?

A

there are specific nerve endings that only respond to certain stimuli

70
Q

describe the pain-spasm-pain cycle

A
  • pain causes T-cell activation which can increase muscle spasm by spinal cord reflex (because T-cells synapse with anterior motor neurons to cause muscle contractions)
  • ongoing muscle contractions can lead to a build up of tissue irritants and fluid
  • the contracted muscle muscle may compress nociceptors and increase impulses
    this creates the cycle
71
Q

what is the normal role of the SNS and its responses to pain?

A
  • prepares body for fight or flight
  • responses to pain: sweating, increased HR/BP
72
Q

what happens if there is an overstimulation of the SNS?

A
  • can develop abnormal responses to pain due to an acute injury or an injury that does not get better
  • can lead to severe pain, vasomotor responses (regulates BP), and sweating
73
Q

what’s another name for that pain that causes overstimulation of the SNS?

A

complex regional pain syndrome (CRPS)

74
Q

name and describe the types of CRPS

A

type 1 - after a trivial/minor injury
type 2 - after a serious injury

75
Q

what are signs/symptoms of CRPS?

A
  • severe pain (more than should be present)
  • hyperesthesia
  • allodynia
  • trophic skin changes
  • loss of function
76
Q

describe substance P

A
  • usually found in C-Fibers
  • neurotransmitter involved in transmission of neuropathic and inflammatory pain
  • involved in nociceptive processing at the SC level
77
Q

describe the gate control theory

A
  • balance of excitatory and inhibitory inputs to T-cells in the SC
  • T-Cells get excitatory inputs from C-Fibers and A-Delta’s & inhibitory inputs from A-Beta nonnociceptor afferents
  • increased activity of A-Beta’s causes T-cells to close the spinal “gate” to the cerebral cortex which stops pain (ES, traction, massage, compression)
78
Q

describe the endogenous opioid system

A
  • opiopeptins (endorphins) bind to specific receptors in the nervous system
  • opiopeptins/opiate receptors found in certain areas of the brain and limbic system
  • opiopeptins found at dorsal horn of spinal cord (superficial layers) and nerve endings of C-Fibers
  • opiate receptors may inhibit the release of substance P from C-Fiber terminals and decrease pain at the spinal cord level
    STIMULATION OF OPIOPEPTINS AND OPIODS ALWAYS HAVE AN INHIBITORY EFFECT*
79
Q

describe what to look for to measure/objectify pain

A

location
severity
quality
24 hour time scale
what makes it better or worse?
does pain have an effect on what patient can do?
use body diagrams

80
Q

describe the pharmacological approaches to pain management

A

(1) NSAIDS (aspirin) - for analgesic and inflammatory pain long term use > GI irritation/bleeding
(2) acetaminophen (tylenol) - for mild to moderate pain long use/big doses > liver damage
(3) opioids (hydrocodone, oxycodone, codeine) - post-op pain, acute pain, malignancy pain, chronic pain
(4) antidepressants - for chronic pain and depression
(5) spinal anaglesia - drugs into epidural or subarachnoid space of SC
(6) local injection - for local inflammation/pain - short term relief
(7) exercise
(8) cognitive behavioral therapy

81
Q

how are physical agents used to manage pain?

A

may help with:
- changing metabolic rate
- stopping pain causing chemicals
- excitation of A-Beta fibers
- pain gating at SC
less side effects and no dependency

Biophysical Agents (3 decks)

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