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Advanced Orthopedics > UQ Mechanisms of Interventions > Flashcards

UQ Mechanisms of Interventions Flashcards

1
Q

Define entrusbable professional activities (EPAs)

A
  • Clinical activities that are expected at entry level
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2
Q

Levels of the entrustment scale

A
  • Not competent to perform skill (remediate)
  • Competent with direct supervision
  • Competent to perform w/o direct supervision (independent)
  • Proficient: able to teach others
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3
Q

What is the process of tissue differentiation

A
  • Active vs PROM
  • Contractile vs inert
  • Special testing to confirm the tissue
  • Tissue loading
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4
Q

Steps in the intervention framework

A
  • A) Identify patients priority problem & impairment
  • B) Link impairment to an objective measure that links to the patient’s problem
  • C) Choose intervention framework & deliver, consider phases (tissue healing…) or approaches (symptom modulation…)
  • D) Re-test, repeat A&B to reassess the intervention
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5
Q

Describe Muller physical stress theory (PST)

A
  • The application of force over a given area of tissue during movement results in stress to the tissue
  • Stress = force/area, where force may be applied in any direction
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6
Q

What is the traditional pathoanatomical (Biomechanics) model

A
  • Confirm the 3 R’s & validate their pain experience
  • Reproducible sign
  • Region of origin
  • Reactivity level
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7
Q

Describe normal pain behavior if it’s mechanical

A
  • Constant or intermittent
  • Onset: acute or gradual
  • Directly proportional to activity (tissue loading)
  • Movements in one direction may increase vs movements in another direction may decrease or abolish (response pattern)
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8
Q

Describe normal pain behavior if it’s chemical

A
  • Constant
  • Onset: acute
  • Inflammation signs: edema, rubor, calor, tenderness
  • All movements are painful
  • No activity, no movement, & no position decrease the pain
  • Generally speaking over TIME chemical pain decreases
  • ***If not decreasing over time suspect NON-MSK pain
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9
Q

Describe what acute pain responds to and what is most sensitive to chemical irritation following a trauma

A
  • Acute pain = response to chemical, thermal, or mechanical stimulus
  • Chemical irritation: Periosteum & joint capsule, subchondral bone, tendon, & pigment, muscle & cortical bone, synovium & articular cartilage
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10
Q

Describe Melzack and Walls Gate Theory

A
  • OPEN gate = facilitate
  • CLOSED gate = inhibit
  • Basic concept: If we stimulate large fibers we close the gate to the small nociceptive fibers
  • Application: TENS, STM, even vibration/shaking your hand
  • This theory does not explain post amputation pain
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11
Q

Describe the mature organism model to understand pain

A
  • Perception of input
  • “Scrutinized” by the Brain (Interpretation past experience)
  • Output = response as behavior
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12
Q

Define pain

A
  • Disturbed sensation that may cause disability, suffering, or distress
  • IASP Def: an unpleasant sensory & emotional experience associated with actual or potential tissue damage, or described in terms of such damage
  • PTs use tests & measurers to determine a cause or a mechanism for an individual’s pain & to assess the intensity, quality, & temporal & physical characteristics associated with the pain
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13
Q

IASP’s 6 points about pain

A
  • Pain is always a personal experience that is influenced to varying degrees by biological, psychological, & social factors
  • Pain & nociception arre different phenomena
  • Through life experiences individuals learn the concept of pain
  • A person’s report of an experience as pain should be respected
  • Although pain usually serves an adaptive role it may have adverse effects on function & social & psychological well-being
  • Verbal description is only one of several behaviors to express pain; inability to communicate does not negate the possibility that a human or a nonhuman animal experiences pain
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14
Q

What are the different pain timelines

A
  • Acute: 24-48 hrs
  • Sub-acute: 3-14 days
  • Chronic: >3-6 mo
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15
Q

Pain mechanistic interventions for PT and the pharmacologic intervention that pairs with it

A
  • Nociceptive: exercise, massage, TENS; topical analgesic, NSAIDs, opioid, channel blocker
  • Nociplastic: education, exercise, massage, manipulation, TENS; SNRI, tricyclic antidepressant
  • Neuropathic: exercise; Gabapentinoid
  • Psychosocial: education, exercise, massage; SNRI, tricyclic antidepressant
  • Motor: education, exercise, manipulation; muscle relaxant
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16
Q

Define nociceptive pain

A
  • Pain that arises from actual or threatened damage to non-neural tissue & is due to the activation of nociceptors
  • Classic tissue based pain usually proportional to the forces involved (tissue loading/unloading)
  • Can be constant or intermittent, can be sharp with aggravating activity or at rest a dull ache or throb
  • Not electric or shooting type of pain
  • Objective: rule in/out with movement restrictions & special tests
17
Q

Define peripheral neurogenic pain

A
  • Pain caused by a lesion or disease of the peripheral somatosensory nervous system, pathology to the peripheral nerve or surrounding interfacing tissue (ex: blood flow to the nerve)
  • Will have positive neurodynamic signs & palpation of nerve elicits noxious stimulation
  • Described as sharp electric, shooting type of pain
  • Dermatomal or cutaneous distribution for specific nerve
  • Objective: near signs that correlate with a peripheral nerve (sensory or motor), pos. neurodynamic signs (active & passive, part away from the “hot” spot), pos. palpation of nerve elicits noxious stimulation (direct vs compression vs distraction), pressure algometry
18
Q

Define central nociplastic pain

A
  • Pain that arises from altered nociception despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors
  • Disproportionate pain with disproportionate aggravating or easing factors, diffuse tenderness & multiple psychosocial factors
19
Q

What are the different nociceptor types

A
  • Type A: Delta fibers
  • Type B fibers
  • Type C fibers: chemical, mechanical, thermal
20
Q

Describe management of identified physical dysfunctions for nociceptive pain

A
  • *Early motion after injury & teach patients tissue loading & unloading strategies
  • Boom Bust cycle vs teaching “Sore but safe”
  • Modalities to reduce tissue irritability: cold, Estim, compression
  • Gentle mobilization
21
Q

What factors BEYOND the BIO are thought to affect a persons pain experience?

A
  • Mental status
  • Traumatic events
  • An individuals understanding of pain
22
Q

Interventions for peripheral neurogenic pain with manual therapy

A
  • Patient education: reduce fear & calm the nervous system
  • Overall physical activity = increased blood flow
  • Gentle motion: nerve glides
  • Unload the nerve containers: OMPT & self mobilization
  • Modalities tor educe/unload any stress on nerve or blood flow (axoplasmic flow)
23
Q

Describe exercise and effects on neuropathic pain

A
  • Can be considered a disease modifying treatment in neuropathic pain conditions by promoting healing of injured tissues
  • Regular aerobic exercise increases anti-inflammatory cytokines & the expression of M2 macrophages which secrete anti-inflammatory cytokines at the site of injury
  • ^can also decrease expression of M1 macrophages & inflammatory cytokine production at the site of injury
  • In people w/ diabetic neuropathy, a decrease in pain is associated with increased growth of epidermal nerve fibers after a regular exercise program
24
Q

Lists some altered sensory testing

A
  • Pain pressure thresholds
  • 2-point discrimination
  • Laterality
  • Vibration, Hot, Cold away from site
  • Localization, Graphesthesia, Sterognosis
25
Q

Define central sensitization

A
  • Increased responsiveness of nociceptive neurons in the central nervous system to their normal or sub threshold afferent input
26
Q

Define peripheral sensitization

A
  • Increased responsiveness & reduced threshold of nociceptive neurons in the periphery to the stimulation of their receptive fields
27
Q

Define allodynia

A
  • Pain due to a stimulus that does not normally provoke pain
28
Q

Define hyperalgesia

A
  • Increased pain from a stimulus that normally provokes pain
29
Q

Does the weather affect your pain

A
  • Yes
  • 24 hrs for ION channel changes
30
Q

Describe neurobiology of pain

A
  • Ion channels can change in 24 hrs
  • Only exist at nerves where no myelin
  • Consider tissue injury that strips the myelin = increase sensitivity
31
Q

Where does neuroplasticity occur

A
  • Ion channels (everywhere)
  • Dorsal horn spinal cord
  • Brain
32
Q

Observations of central nociplastic neuroplasticity

A
  • Hypervigilance
  • Fatigue
  • Neglect
  • Smudging: motor and/or sensory
33
Q

Describe PNE interventions for nociplastic pain

A
  • Pain neuroscience education & cognitive functional therapy
  • Help people make sense of pain
  • Overall explaining pain or helping people in chronic pain understand pain corresponds to increased pain thresholds & increased conditioned pain modulation (AKA central inhibition)
  • Education challenges maladaptive cognitions/behaviors & beliefs which in turn alters central pain processing
34
Q

Metaphors to help explain central pain without saying its all in your head

A
  • Sensitive alarm system
  • Radio tuning
  • Freeway, Rush hour
35
Q

Describe TENS interventions for nociplastic pain

A
  • TENS activates central inhibitory pathways & reduces central sensitization simultaneously to reduce pain & hyperalgesia
    -Studies show the high and low frequency TENS analgesia activates multiple central pathways
36
Q

Manual therapy as an intervention for nociplastic pain

A
  • Massage activates descending inhibitory pathways using oxytocin to produce analgesia
  • Joint mobs
  • Manipulation reduces central excitability measured by reduced temporal summation in the region of primary hyperalgesia & reduced secondary hyperalgesia in those with chronic pain
  • Therapeutic dry needling
37
Q

Slide 61

A
38
Q

Describe different motor pattern changes

A
  • Motor inhibition/muscle weakness: strength & facilitation exercise, Estim
  • Motor facilitation/muscle tension, tone, spasm: manual therapy to reduce spasm
  • Motor behaviors volitional: consider reflexive pain response vs fear avoidance; PNE, relaxation training, reciprocal inhibition exercise, TENS, graded activity/exposure
  • Sub-optimal tissue loading: focus on mechanical re-loading; optimal activity dosing
39
Q

Slide 67-75

A

Advanced Orthopedics (29 decks)

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