Unit 1 Lecture Flashcards
1
Q
define physical agents
A
energy and material applied to help in rehabilitation
2
Q
list general examples of physical agents
A
hot packs
cold packs
ice massage
paraffin
electrical stimulation
whirlpool
ultrasound
3
Q
what are the 3 categories of physical agents?
A
thermal agents
mechanical agents
electromagnetic agents
4
Q
define thermal agents
A
hot and cold
transfers energy to produce an increase or decrease in tissue TEMPERATURE
5
Q
what are the 2 categories of thermal agents?
A
thermotherapy and cryotherapy
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
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
8
Q
define mechanical agents
A
apply force to increase or decrease PRESSURE on the body
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
10
Q
define electromagentic agents
A
apply energy in the form of electromagnetic radiation or electrical current
11
Q
describe agents used for electromagnetic radiation
A
UV radiation
infrared radiation
laser
diathermy (superficial and deep heat)
12
Q
describe the agent used for electrical currents
A
E-stim for
pain modulation
muscle strengthening
reduce edema
tissue healing
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
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
15
Q
define contraindications
A
conditions under which a certain treatment should NOT be applied
16
Q
define precautions
A
conditions under which a certain treatment should be applied with special limitations or care
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.
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
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
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)
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
22
Q
what are the 3 phases of inflammation and repair?
A
inflammation phase
proliferation phase
maturation phase
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
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
25
describe the vascular response
***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
26
describe the fluid types associated with edema during the vascular response of the inflammation phase
transudate - formed first, very few cells and proteins
exudate - extravascular fluid becomes cloudy and vicious, high content of cellular debris and lipids
27
describe the hemostatic response
***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
28
describe the cellular response
***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
29
describe the immune response
***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
30
describe the achievements of the inflammation phase
(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
31
describe the proliferation phase
***second phase***
**days 3-20**
goal is to cover the wound and strengthen the injury site
4 responses: epithelialization, collagen production, wound contraction, neovascularization
32
describe epithelialization
*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
33
describe collagen production
*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
describe the time frame of collagen production in the collagen production response
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
describe wound contraction
*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
describe the types of healing during the wound contraction response
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
describe the neovascularization response
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
describe the maturation phase
*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
describe the types of collagen
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
keloid scars
extend beyond the margins of the injury into surrounding tissue
41
hypertrophic scars
raised, but stays within the margins of the wound/inelastic
42
define acute inflammation
occurs immediately after tissue damage and is short term
43
define chronic inflammation
a simultaneous progression of acute inflammation, tissue destruction, and healing/long-term
44
can physical agents affect or modify tissue healing?
yes
45
describe local factors that influence healing
location - how far/close to a good blood supply
size - how big/small injury is
vascular supply
use of physical agents
movement
46
describe systemic factors that influence healing
age
disease
medication
nutrition
47
describe the healing of cartilage
limited healing due to the lack of lymphatics, blood supply, and nerves
48
describe the healing of tendons and ligaments
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
describe the healing of skeletal muscle
regeneration in humans has not been documented after trauma
50
describe the healing of bone
will heal with or without rigid fixation
51
name and describe the 6 phases of bone healing
(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
what is pain?
interaction between neurological, psychological, sociological, and mechanical factors & unpleasant sensory/emotional experience
53
describe acute pain
- 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
describe chronic pain
- persists beyond the normal time for tissue healing
- decreases levels of enkephalins (endorphins)
- increased quantities of and sensitivity to nociceptors
55
define hyperalgesia
hurts more than it should
56
define allodynia
hurts when it shouldn't
57
describe referred pain
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
describe neuropathic pain
- 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
describe nociceptive pain
- 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
describe dysfunctional pain
*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
describe psychogenic pain
*no injury, but real and physical symptoms*
-psychological role of pain to a large degree
62
define anaglesia
absence of pain
63
describe nociceptors
(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
describe C-Fibers group IV afferents
- 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
describe A-Delta fibers group lll afferents
- 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
describe A-Beta fibers
- 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
describe the use of the central pathways from the periphery to the cortex
(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
what is the pattern theory
all nerve endings transmit all types of stimuli
69
what is the specificity theory?
there are specific nerve endings that only respond to certain stimuli
70
describe the pain-spasm-pain cycle
- 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
what is the normal role of the SNS and its responses to pain?
- prepares body for fight or flight
- responses to pain: sweating, increased HR/BP
72
what happens if there is an overstimulation of the SNS?
- 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
what's another name for that pain that causes overstimulation of the SNS?
complex regional pain syndrome (CRPS)
74
name and describe the types of CRPS
type 1 - after a trivial/minor injury
type 2 - after a serious injury
75
what are signs/symptoms of CRPS?
- severe pain (more than should be present)
- hyperesthesia
- allodynia
- trophic skin changes
- loss of function
76
describe substance P
- usually found in C-Fibers
- neurotransmitter involved in transmission of neuropathic and inflammatory pain
- involved in nociceptive processing at the SC level
77
describe the gate control theory
- 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
describe the endogenous opioid system
- 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
describe what to look for to measure/objectify pain
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
describe the pharmacological approaches to pain management
(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
how are physical agents used to manage pain?
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*
