UQ Mechanisms of Interventions Flashcards
1
Q
Define entrusbable professional activities (EPAs)
A
- Clinical activities that are expected at entry level
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
3
Q
What is the process of tissue differentiation
A
- Active vs PROM
- Contractile vs inert
- Special testing to confirm the tissue
- Tissue loading
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
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
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
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)
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
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
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
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
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
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
14
Q
What are the different pain timelines
A
- Acute: 24-48 hrs
- Sub-acute: 3-14 days
- Chronic: >3-6 mo
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
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
