exam Flashcards
explain chronic pain
pain that has gone past the normal tissue healing time of 3 mos; has no protective purpose; no more inflammation
differentiate chronic and nociceptive pain and its relation to sensitization
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
PQRST nociceptive
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)
assessment procedures and purpose
central sensitization index (CSI)
tampa scale of kinesiophobia
pain catastrophizing scale
painDETECT - neuropathic vs CS
quantitative sensory testing
CSI
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
TSK
4 8 12 16 (+) used for checking (17px) consistency of px. response
higher = more kinesiophobia
37pts
PCS
30/52 clinically significant (13px)
rumination - 8, 9, 10, 11
magnification 6, 7, 13
helplessness
allodynia vs hyperalgesia
allodynia = pain when not pain
hyperalgesia = pain when pain
principles of altering pain memories (cognitive-targeted exercise therapy)
time contingent exercises
goal setting
addressing feared movements
motor imagery
make use of stress
address perceptions
painDETECT
0-12 neuropathic
12-19 not sure
19-38 CS
brain areas and parts that affect pain experience
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
gate control theory and CS
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
PSFS
functional scale (0-5)
SALIENCE
lower score less function
management principles
relax, exercise, self-regulate
parts of skin
epidermis (culugo sa batok)
dermis (papillary, reticular)
hypodermis (fat layer)
sensory receptors and levels, fx.
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
types of burns
thermal
electrical
radiation
chemical
inhalation
stages of wound healing
hemostasis
inflammation
granulation or proliferation
maturation or remodelling
zones jackson’s model
hyperemic
stasis
coagulation
types of burns and key features (color, pain, wound healing)
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
rule of 9s (adult and child)
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]
burn complications [9]
infection
metabolic complications
pulmonary complications
CV complications
heterotrophic ossification
neuropathy - d/t tight bandages, compression syndrome
pathological scars (keloid/hypertrophic) -> inc in collagen
contractures
techniques for wound care
debridement
medication
grafting
scar contracture correction
general rule for contracture mgmt; main movements to avoid
move away from position of comfort
flexion; plantarflexion
PT management techniques
ROM
ambulation
scar management
- pressure dressing
- breaking scar/ deep friction massage / wringing massage
conditioning exer
pressure sore risk factors
increased weight, decreased mobility, increased skin moisture, less protein intake, blood supply issues
describe pressure sore stages
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
general causes
diabetic neuropathy
arterial (regular, medial malleolus, lower calf)
venous (irreg, lateral aspect/dorsum of foot)
tests and measures for pressure ulcers and rationale
ankle-brachial index (ABI) - check loss of perfusion in LE
sensory testing (monofilament testing) - check for decrease in sensation
most effective treatments depending on type of ulcer
diabetic - foot care (know how to check)
arterial - smoking cessation
venous - compression therapy
main cause of DS and types
CH21
- trisomy 21
- mosaicism
- translocation
systemic affectations of DS [8]
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
pathokinesio issues of DS [5]
gross motor
fine motor
motor planning, balance, and coordination
physical clinical features [5]
clinodactyl pinky
simian crease
brushfield spots
flat facial profile
upward slanted eyes
ax for genetic conditions [2-but list items in framework (9)]
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
main cause of DMD
no dystrophin or dystrophin glycoprotein complex so cell has no protection
main clinical s&s of DMD
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
prognosis for DMD
most don’t make it past 18yo; wheelchair by 12
other types of MD
becker = better DMD
landouzy-dejerine (or FMD) - mostly facial muscle weakness and beevor sign
DM - DM1&2
tone mgmt and tx for genetic conditions
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
periodization
breaking down training phase into conditioning, transitioning, competition
emergency procedure [police]
protection, optimal loading, ice, compression, elevation
