exam Flashcards

1
Q

explain chronic pain

A

pain that has gone past the normal tissue healing time of 3 mos; has no protective purpose; no more inflammation

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2
Q

differentiate chronic and nociceptive pain and its relation to sensitization

A

chronic pain = central bc the issue usually lies with the CNS sensitivity to activity; central sensitization is usually triggered by mechanical stimuli but not thermal; nociceptive pain = peripheral sensitization so nerves around area of pain are sensitized, protective in nature ; usually triggered by both mechanical and thermal stimuli

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3
Q

PQRST nociceptive

A

provoking & quality & severity: stimuli proportional to pain increase (e.g., light touch = sensitive; pressing = painful); NSAIDs and analgesics work
region: localized to area of injury; surrounding areas may be a lil sensitive
time: sensitive esp when area is inflamed; but inflammation goes away soon enough (acute; sub-acute)

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4
Q

assessment procedures and purpose

A

central sensitization index (CSI)
tampa scale of kinesiophobia
pain catastrophizing scale
painDETECT - neuropathic vs CS
quantitative sensory testing

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5
Q

CSI

A

quality of pain; higher score = higher likelihood of CS
0-29 sub
30-39 mild
40-49 moderate (Nijs framework)
50-59 severe
60-100 extreme

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6
Q

TSK

A

4 8 12 16 (+) used for checking (17px) consistency of px. response
higher = more kinesiophobia
37pts

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7
Q

PCS

A

30/52 clinically significant (13px)
rumination - 8, 9, 10, 11
magnification 6, 7, 13
helplessness

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8
Q

allodynia vs hyperalgesia

A

allodynia = pain when not pain
hyperalgesia = pain when pain

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9
Q

principles of altering pain memories (cognitive-targeted exercise therapy)

A

time contingent exercises
goal setting
addressing feared movements
motor imagery
make use of stress
address perceptions

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10
Q

painDETECT

A

0-12 neuropathic
12-19 not sure
19-38 CS

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11
Q

brain areas and parts that affect pain experience

A

homunculus - little man (directory of motor neurons)
- pain cant be localized bc homuncular smudging occurs
amygdala - fear and negative emotion
- certain movements have negative emotions and experiences
brodmann area 312
- sensory information and experience can be transmitted to area 4 (motor)
A-beta fiber - touch
A-gamma fiber - ms contraction (pressure, stretch)
C fiber - pain, temp, itch

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12
Q

gate control theory and CS

A

dorsal horn wind-up
disinhibition of interneurons (aka interneurons that are supposed to be inhibiting the pain dont work like they should) usually prevent overflow of 2nd order neuron

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13
Q

PSFS

A

functional scale (0-5)
SALIENCE
lower score less function

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14
Q

management principles

A

relax, exercise, self-regulate

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15
Q

parts of skin

A

epidermis (culugo sa batok)
dermis (papillary, reticular)
hypodermis (fat layer)

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16
Q

sensory receptors and levels, fx.

A

meissners (p d) - discrimination
Krause (p d) - cold
Ruffini’s (p d) - warmth
Pacinian (r d) - pressure, vibration [Pacinian = Pressure]
Merkel’s (epi) - superficial sensation

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17
Q

types of burns

A

thermal
electrical
radiation
chemical
inhalation

18
Q

stages of wound healing

A

hemostasis
inflammation
granulation or proliferation
maturation or remodelling

19
Q

zones jackson’s model

A

hyperemic
stasis
coagulation

20
Q

types of burns and key features (color, pain, wound healing)

A

epidermal
- redness
- no intervention needed
superficial partial thickness (dermis)
- redness, warm
- most painful
- 7-10 days
deep partial thickness (reticular)
- bright pink or mottled red
- keloidal scar formation
full thickness (3rd deg)
- black, waxy white (ischemic)
- not sensitive to anything; dry, inelastic
- grafting; eschar presence
subdermal (electric)
- charred; past subcutaneous tissue

21
Q

rule of 9s (adult and child)

A

adult [child]
head - 4.5% one side [8.5% one side]
arms - 4.5% one side [4.5% one side]
leg - 9% one side [6.5% one side]
torso - 18 (9% superior; 9% inferior) [9% superior, inferior]
genitalia - 1% [same]

22
Q

burn complications [9]

A

infection
metabolic complications
pulmonary complications
CV complications
heterotrophic ossification
neuropathy - d/t tight bandages, compression syndrome
pathological scars (keloid/hypertrophic) -> inc in collagen
contractures

23
Q

techniques for wound care

A

debridement
medication
grafting
scar contracture correction

24
Q

general rule for contracture mgmt; main movements to avoid

A

move away from position of comfort
flexion; plantarflexion

25
Q

PT management techniques

A

ROM
ambulation
scar management
- pressure dressing
- breaking scar/ deep friction massage / wringing massage
conditioning exer

26
Q

pressure sore risk factors

A

increased weight, decreased mobility, increased skin moisture, less protein intake, blood supply issues

27
Q

describe pressure sore stages

A

1 - redness; no blanching
2 - no slough; skin breakage
3 - slough; deep crater
4 - undermining and tunneling; bone tendon muscle exposed
unstageable - covered in slough or eschar

28
Q

general causes

A

diabetic neuropathy
arterial (regular, medial malleolus, lower calf)
venous (irreg, lateral aspect/dorsum of foot)

29
Q

tests and measures for pressure ulcers and rationale

A

ankle-brachial index (ABI) - check loss of perfusion in LE
sensory testing (monofilament testing) - check for decrease in sensation

30
Q

most effective treatments depending on type of ulcer

A

diabetic - foot care (know how to check)
arterial - smoking cessation
venous - compression therapy

31
Q

main cause of DS and types

A

CH21
- trisomy 21
- mosaicism
- translocation

32
Q

systemic affectations of DS [8]

A

hypotonia (atlantoaxial, atlanto-occipital)
heart disease (ASD, VSD)
mild to moderate cognitive impairment
hematologic disorders
vision impairments
GI disorders (celiac, hirschsprung)
endocrinopathies (HYPOthyroidism, diabetes)
gross and fine motor, and language delays

33
Q

pathokinesio issues of DS [5]

A

gross motor
fine motor
motor planning, balance, and coordination

34
Q

physical clinical features [5]

A

clinodactyl pinky
simian crease
brushfield spots
flat facial profile
upward slanted eyes

35
Q

ax for genetic conditions [2-but list items in framework (9)]

A

gmfm-88
framework; check for:
- abnormal posture
- dysmorphic features & drooling
- primitive reflexes
- joint laxity (hypermobility) and flexibility
- antigravity test
- resistance to passive movement
- motor skills
- muscle strength
- fxal and endurance testing

36
Q

main cause of DMD

A

no dystrophin or dystrophin glycoprotein complex so cell has no protection

37
Q

main clinical s&s of DMD

A

LE > UE
proximal > distal
hypotonia, poor head control
toe walking, hard time running and climbing up stairs
ambulation delay
lumbar lordosis, scoliosis
AKHE contracture
pseudohypertrophy of calves
- scar tissue formation d/t release of creatine kinase
gower’s sign
pharyngeal weakness
waddling and trendelenburg gait
chronic respiratory failure
cardiac abnormalities

38
Q

prognosis for DMD

A

most don’t make it past 18yo; wheelchair by 12

39
Q

other types of MD

A

becker = better DMD
landouzy-dejerine (or FMD) - mostly facial muscle weakness and beevor sign
DM - DM1&2

40
Q

tone mgmt and tx for genetic conditions

A

facilitatory
- light moving touch
- Fast brushing
- Icing
- Proprioceptive Facilitatory Techniques
- Heavy joint compression
- Stretch
- Tapping
- Vestibular stimulation
inhibitory
- Slow rocking
- Slow stroking
- Light joint compression (approximation)
- Tendinous pressure
- Maintained stretch

41
Q

periodization

A

breaking down training phase into conditioning, transitioning, competition

42
Q

emergency procedure [police]

A

protection, optimal loading, ice, compression, elevation