exam Flashcards

(42 cards)

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
PT management techniques
ROM ambulation scar management - pressure dressing - breaking scar/ deep friction massage / wringing massage conditioning exer
26
pressure sore risk factors
increased weight, decreased mobility, increased skin moisture, less protein intake, blood supply issues
27
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
28
general causes
diabetic neuropathy arterial (regular, medial malleolus, lower calf) venous (irreg, lateral aspect/dorsum of foot)
29
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
30
most effective treatments depending on type of ulcer
diabetic - foot care (know how to check) arterial - smoking cessation venous - compression therapy
31
main cause of DS and types
CH21 - trisomy 21 - mosaicism - translocation
32
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
33
pathokinesio issues of DS [5]
gross motor fine motor motor planning, balance, and coordination
34
physical clinical features [5]
clinodactyl pinky simian crease brushfield spots flat facial profile upward slanted eyes
35
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
36
main cause of DMD
no dystrophin or dystrophin glycoprotein complex so cell has no protection
37
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
38
prognosis for DMD
most don't make it past 18yo; wheelchair by 12
39
other types of MD
becker = better DMD landouzy-dejerine (or FMD) - mostly facial muscle weakness and beevor sign DM - DM1&2
40
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
41
periodization
breaking down training phase into conditioning, transitioning, competition
42
emergency procedure [police]
protection, optimal loading, ice, compression, elevation