Paediatics Flashcards
1
Q
What age to paediatric physios typically see?
A
Up to the age of 21
2
Q
Where do peds physios work?
A
hospitals, clinics, treatment centers, schools and homes
*focus on treatment in childs environment
3
Q
What is the goal of peds physio?
A
Optimize partiicpation
4
Q
What is the APGAR scale?
A
used to assess newborn’s health, physical condition, need for immediate medical care
done 1 minute after birth, 5 minutes, and 10 minutes if the other was bad
scored 0-10, 0-3 = severely depression, 4-6=moderately depressed, 7-10 = excesslent
(low score= medical attention (ventilation), remains low = increased risk of neurological complications
see chart in book for scoring
Activity
Pulse
Grimace
Appearance
Respiration
5
Q
When do the lungs finish development?
A
32 weeks gestation
*before that - not enough surfactant to keep lungs open (harder to pull apart) = increased risk of atelectasis
6
Q
What is infant respiratory distress syndrome
A
type II alveolar cells typically produce surfactant, if this doesn’t happen, decrease surface tension = atelectasis = distress
7
Q
How do you classify the gestational age at extremely preterm, very preterm, moderate to late preterm, term birth?
A
extremely preterm - less than 28 weeks
very preterm: 28-32 weeks
moderate to late preterm: 32-37 weeks
term birth: 37 weeks (typically 38-41 weeks)
8
Q
What is preterm birth?
A
birth of a viable infant that occurs at fewer than 37 weeks of gestation
If combined with low-birth weight - significantly increases the risk for neuro impairments
9
Q
What is adjusted age and how do you calculate it?
A
based on 40 week gestation timeline
chronological age (weeks since birth) - number of weeks born prematurely (prior to 40 weeks gestation) = adjusted age
*this is the age that you should compare to child’s development - should catch up by the age of 2
10
Q
What are neonatal reflexes?
A
Involuntary response to a stimulus and appear during neonatal period that become integrated by the end of infancy (to the higher center controls)
can’t achieve milestones if these don’t do away
11
Q
What is the onset, integration, stimulus and response for ATNR reflex?
A
Onset - 20 weeks gestation
Integration - 5 months
Stimulus - turning head
Response - extension on UE and LE on side the face is turned to
12
Q
What is the onset, integration, stimulus and response for rooting reflex?
A
Onset - 28 weeks gestation
Integration - 3 months
Stimulus - lightly stroking perioral area
Response - movement of head and lips towards that stimulus
13
Q
What is the onset, integration, stimulus and response for suck-swallow reflex
A
Onset - 28 weeks gestation
Integration - 5 months
Stimulus - touch inside of mouth
Response - rhythmic sucking and swallowing
14
Q
What is the onset, integration, stimulus and response for palmar grasp reflex
A
Onset - 28 weeks gestation
Integration - 7 months
Stimulus - pressure against palm of hand
Response - flexion of fingers
15
Q
What is the onset, integration, stimulus and response for flexor withdrawal reflex
A
Onset - 28 weeks gestation
Integration - 2 months
Stimulus - Noxious stimulus to bottom of foot
Response - extension of toes, DF, hip and knee flexion on stimulus side
16
Q
What is the onset, integration, stimulus and response for crossed extension reflex
A
Onset - 28 weeks gestation
Integration - 2 months
Stimulus - noxious stimulus to bottom of foot
Response - flexion of LE on stimulated side and extension and adduction of LE on contralateral side
17
Q
What is the onset, integration, stimulus and response for galant (trunk incurvation) reflex
A
Onset - 28 weeks gestation
Integration - 3 months
Stimulus - stroke paravertebral skin in prone
Response - incurving of trunk towards stimuluated side
18
Q
What is the onset, integration, stimulus and response for moro reflex?
A
Onset - 28 weeks gestation
Integration - 5 months
Stimulus - sudden head drop backwards
Response - extension and abduction of UE with opening of hands and crying, may be followed by flexion and adduction of UE
19
Q
What is the onset, integration, stimulus and response for positive support reflex?
A
Onset - 35 weeks gestation
Integration - 2 months
Stimulus - feet in contact with floor or surface
Response - bilateral leg extension to support weight
20
Q
What is the onset, integration, stimulus and response for stepping reflex?
A
Onset - 37 weeks gestation
Integration - 4 months
Stimulus - supported upright with feet in contact with firm surface
Response - rhythmic high stepping movements
21
Q
What is the onset, integration, stimulus and response for Landau reflex?
A
Onset - 4-5 months after full term delivery
Integration - 24 months
Stimulus - supported in prone with hands under thorax
Response - head, neck, back, and LE extension
22
Q
What is the onset, integration, stimulus and response for STNR reflex?
A
Onset - 4 -6 months after full term delivery
Integration - 12 months
Stimulus - flexion or extension of cx spine
Response - flexion cx spine = UE flexion, LE extension, extension Cx = opposite
23
Q
What are the gross motor development milestones?
A
Roll - 3-6 months
Head control - 4months
Sit - 6 months
Crawl - 8-9 months
Cruising - 9 months
Standing - 9 months
Walking - 10-15 months
Stair climbing - 18-20 months
running - 2 years
kick a ball - 3 years
skipping 5 years
24
Q
What are common tests / measures for development scales
A
Alberta Infant Motor Scale - 0-18 months, motor skills
Bayley Scales of infant development (BSID) - 1-42 months, mental, motor, behaviour scales
Peabody development motor scale (PDMS-2) - 0-60 months (5 years), fine and gross motor skills
Bruininiks-oseretsky tests for motor performance (BOT-2) - 4-21 years, fine and gross motor skills - will follow longitudinally
use if 4 (even if overlap - to be able to track longitudinally
Also for activity and participation - PEDI, SFA, CHAC, PTSIB (same as CTSIB but peds)
25
What is the Alberta Infant Motor Scale?
0-18 months, observational and performance based on what the child does in different positions. 0-58 scoring.
screen for motor delays and direct rehab towards that - no indication of future performance
* not appropriate for child with CP
5th percentile for developmental delay (i.e., downs), same trajectory but happens later
26
How do you classify a developmental delay?
a child <5 years of age who is delayed by >1.5 SD in at least one of the following:
-ADLs and self help
-Cognition
-Motor and sensory function
-Social- emotional function
-Speech / language / communication
27
What is floppy infant syndrome?
global hypotonia and decrease antigravity strength - leads to dev delay
frog leg position in supine - abducted and fully externally rotated - arms are flaccif beside
Rag doll in ventral suspension
head lag on pull to sit
In womb - typically run out of space so develop flexor tone but premature babies don't get this - so they need to work on it. whereas typically work on extension out of womb.
28
What is down syndrome?
Genetic disorder caused by faulty cell divison resulting in an extra 21st chromosome
mild dev delay and mild to mod cognitive disability
distinict facial feature
-narrow eyes
-flattened nose
-small mouth and jaw
-protruding tongue
Increased risk for specific medical condition
-congenital heart malformations
-respiratory problems
-hearing and visual impairments
-ligamentous laxity and global hypotonia - careful with manipulation and mobilizations
*increased risk of SC injury cause transverse lig for AA is lax)
29
What is cerebral palsy?
Group of permanent disorders of development and movement and posture - non-progressive disturbances that occur in developing fetal or infant brain
motor can be accompanied by sensation, perception, cognition, communication, behaviour by epilepsy and secondary MSK problems
happen peri-natal or post-natal before 2 years
30
What are the risk factors of CP?
1 - prematurity - ventilation issues (decreased O2), PVL (white matter disorder) = spastic diplegia
2- atypical intrauterine growth (low - increased infection, high - materal diabetes birth weight)
3- infection (in-utero or post-natal)
4- infarction (increased risk of moms obese, older age, family Hx)
5- developmental defect (lissencephaly - flattened brain, microcephaly - small brain)
6- mutilple gestation
7- placental pathology
8- trauma (prenatal, perinatal (e.g., cord around throat), early postnatal - drop, shaken baby)
*more common in males, spastic more common
31
How do you diagnose CP?
No genetic or metabolic tests
based on clinical presentation and history
Imaging may be used to confirm
32
How do you classify CP?
impairment
-anatomic distribution (hemiplegia, diplegia, quadruplegia)
-type (spastic, dyskinetic, mixed)
Functional
-GMFCS
*NOT MUTUALLY EXCLUSION - helps communicate impairments and research
33
Describe the classification by impairment
Hemiplegia - one side of body
Diplegia - legs more than arms
Quadriplegia - arms, legs and trunk
Asymmetrical diplegia - legs more affected than arms, one side is more than other
34
Describe spastic CP
velocity dependent resistance to passive elongation
damage to cortex or white matter to and from sensorimotor cortex
most common type, diplegia most common
positive UMN signs
get scissoring gait (adductor spasticity), toe walking (PF spasticity)
35
Describe dyskinetic CP?
Ataxic
-movement disorder characterized by intention tremor, lack of muscle control, poor coordination of voluntary movements
-can walk without gait aid - may have balance difficulty
Athetosis
-movement disorder characterized by slow, continuous involuntary writhing movements
-common in distal extremity and mouth
-difficult to maintain stable position
-significant limitation in gross motor function
-postural instability as legs turn in too
-Chorea; movements are more rapid and jerky
Dystonic:
-damage to thalamus (relay center) and basal ganglia (pudemen and caudate)
-dystonia: involuntary muscle contractions leading to repetitive movements, abnormal fixed postures and disordered tone
-typically patterned and may include twisting or tremulous movements
- dystonic posturing - co-contraction of muscles causing a sustained abnormal posture
-triggered by voluntary movements
-limitations in gross motor function and fatigue due to high metabolic demand
36
Describe mixed CP
combo of spastic and dyskinetic
diffuse injury to motor cortex and basal ganglia
37
What is the gross motor function classification system?
focus on what the child CAN do
5 levels
-0-2
-2-4
-4-6
-6-12
-12-18
scale stably after age of 2
classified based on method of mobility
*see chart for scale
38
How do you do an assessment of CP
Motor function
-GMFM 88
-GMFM 66
*gold standard, 88 also validated for Downs
*can also use TUG for CP
-these are observational for gross motor function from 5months - 16 years
-appropriate for children whos motor skills are below or equal to a 5 year old without any motor disabilities
-high score is better
-dimensions - lying/rolling, crawling/kneeling, sitting, standing, walking/running/jumping
Spascity
-Modified ashworth scale
-modified tardieu scale
39
What are the interventions for CP
adress impairments
-bone development/deformity - hip dysplasia (esp GMFCS 5), scoliosis (?LLD - do in sitting), torsions
-balance
-coordination.
-motor planning
-ROM (flexbility, contractures)
-strength
-tone
-spasticity
Adress participation restrictions
-transfers, gait, stairs
-sports
-plauy
PT
-educaiton
-stretching
-exercise- strength, ROM, balance and coordaiont
-splinting
-orthosis
-assistance/ adaptive device - crutches, walkers, standaers, w/c
-gait, transfers and functional
40
What AFOs are commonly used for CP
solid AFO
-blocks all ankle at talocrural and subtalar
-rocker bottom
-limits knee extension movement (decreased hyperextension)
-Indications - post-surgery / botox, excessive DF, correctable equinois, dropp foot, increased med/lat stability
-*DO NOT USE FOR CROUCH GAIT. OR FIXED FOOT
Hinged AFO
-allows for controlled movement of ankle DF while still limting PF
-facilitates progression to foot flat position in early stance
-limits movement at subtalar
-limits knee extension moment (decrease knee hyperextension)
-Indications: correctable equinois, drop foot, knee hyperextension, subtalar OA
-DO NOT USE FOR CROUCH GAIT. OR FIXED FOOT OR BOTOX/LENGTHENING
Ground reaction AFO (GRAFO)
-blocks talocrural and limits subtalar
-provides knee extension moment (increase knee extension)
-DO NOT USE FOR DIXED KNEE FLEXION
-Indications: weak quads, overlengthening calf muscles, increase knee extension
41
What is the medical intervention for CP?
Bony realignemnt (osteotomy and fusion)
-botox - spasticity - lasts 3 months
-intrathecal baclofen - spastcity
-selective dorsal rhizotomy - spasticity
-serial casting - ROM
-ST (muscles and tendons) lengthening and tendon transfers - ROM
-percutaneous muscle/tendon release - ROM
-reconstruction - hip
42
What is the gait pattern for CP?
-true equinos - hip ext, knee ext, foot PF (calf spasticity)
- jumping = ant pelvic tilt, hip flex, knee flex, PF (hip flexor, hams and calf spasticity)
-crouch - increased hip flexion, knee flexion and DF (lengthened calf - over looked hip/knee)
43
What is Duchenne Muscular Dystrophy?
genetic disorder characterized by progressive weakening and degeneration
Due to mutation of the dystrophin gene - inherited in x-linked recessive pattern (1/3 arise from new genetic mutation)
M>F - live to 20-30s
44
How do you diagnose DMD?
Genetic testing
Creatine kinase
Muscle biopsy findings
45
What is the typical progression of DMD?
clinical signs apparent between 2-5 years
-early milestones achieved
-more apparent with higher level gross motor activiites (running, jumping)
progressive muscle wasting and weakness
-lower --> upper
-- run, walk, standing, T/F with legs difficult
-Proximal --> distal
--quads, DF
-muscles of face, eyes, speech, swallowing, and spincter not involved
46
What are the S + S of DMD?
Waddling gait.- wide stances, shift CoG over and circumduct
Gower's maneuver - used arms to push up to stand
Pseudohypertrophy of calves - enlargement due to fat deposits and connective tissue
Lumbar hyperlordosis - because weakness hip/knee (cog forward), weak abs, knees in hyperextension for stability
Wide stance with external rotation of LE - to increased Bos *Don't change this*
Toe walking - DF weak (gastroc tight)
47
What are the associated problems with DMD?
Cardio-respiratory function - weakness in muscles = decrease resp function, cariomyopathy = impaired strength/structure, under stress from constant contractions
Congitive - 30% non-progressive impairments
Obesity - dietary intake >energy expenditure, steroid therapy
GI system - constipation and impaction due to decrease motility
Spine - increased lordosis, increased scoliosis (w/c) - sometimes get surgery
48
What is the management for DMD?
Medical
steroids - increase risk of OP, weight gain, cataracts, slowing of physical growth
mechanical ventilation - BiPAP - 2 levels
surgery - scoliosis and spine stabilization, tendon release
PT
avoid agressive strengthening (esp eccentrics)
stretching / ROM
gait training
education on overexertion and energy conservation
respiratory exercises -breath stacking, assistive cough ,incentivee spirometer
transfer training
equipment selection
49
What is RA? Including etiology and epidemiology
Systemic inflam disease characterized by symmetrical polyarthritis - primarily a disease of the synovium
F>M, 3-45 onset which increases with age
autoimmune disease of unknown etiology - RF (antibodies that neutralize pathogen which attack normal tissue mistaken as foriegn) found in sera in 70%
-genetic basis
-high prevalence in smokers
50
What is the pathophys of RA?
Inflam of the synovium leads to joint effusion, pain, stiffness, loss of ROM - chronically leads to degradation of the articular cartilage
Synovial overgrowth of vascular granulation tissue (pannus) dissolves smooth cartilaginous surfaces - osteocytes and chondrocytes form
Joint surfaces become uneven
narrow of joint leads to pseudo-laxity
weakened joint capsule and ligaments - causes fraying of tendon sheath, ruptures = muscle imbalance
if advanced - tissue leads to adhesions, fibrosis or bony ankylosis (fusion) causing increasing immobility within the joint
51
What do the lab tests reveal in RA?
-acute phase reactants - increased C-reactive protein and erythrocyte sedimenation rate (ESR) - because active inflam
-autoantibodies present - RF (not all but usually more severe)
-complete blood count - RBC is decreased
-synovial fluid analysis - normal: transparent, yellowish, no clots, viscous. inflamed: cloudy, clots, less viscous
52
What do the radiographic findings reveal in RA?
-joint space - narrowed (uneven)
-bone - erosion, peri-articular osteopenia
-ST - rheumatoid nodules, swelling
53
What is the diagnostic criteria for RA?
*need at least 4
1. morning stiffness lasting at least 1 hour
2. ST swelling or fluid in at least 3 joints
3. at least one area swollen in wrist, MCP or PIP
4. Symmetrical arthritis
5. rheumatoid nodules
6. abnormal amounts of serum RF
7. erosions or bony decalcification on radiographs of the hand and wirst
54
What is the course of RA?
no cure, just manage disease
cycles of exacerbations and remission (<15 minutes of morning stiffness, no joint tenderness or effusion for at least 3 months)
55
What are the S + S for RA?
Systemic
Articular
Extra-articular
Impairments and complications - vascular, neurological, cardiopulmonary, ocular
56
What are the systemic S + S for RA?
morning stiffness - lasting >1 hour, generalized stiffness, progressively eases with movement, severity and duration of morning stiffness are directly related to degree of disease activity
Extreme fatigue - increased resting energy expenditure - due to chronic immune activation, leads to rheumatoid cachexia (loss of lean body mass as a result of RA) (also cause of deconditioning)
weight loss/loss of appetitive
fever
malaise
57
What are the articular S + S for RA?
bilateral and symmetrical pattern
effusion (swelling)
arthralgia (joint pain)
crepitus
deformity
loss of function
pseudo-laxity
eventually progresses to ankylosis/ fusion leading to immobility
58
What are the Cx S +S for RA?
Often involved
ROM limited in all planes (esp rotaiton)
C0/C1, C1/C2 and mid Cx - decreased ROM and potential instability
C1/C2 = life threatening - if transverse lig is lax = herniation of odontoid process into SC or C2 fractures into SC
If Cx neuro S +S - refer (MRI used to confirm)
59
What are the TMJ S +S for RA?
last joint involved
results in pain, swelling and limited ROM
can progress to ankylosis
60
What are the Shoulders S +S for RA?
GH, SC, AC involved
leads to distension and thinning of capsule and lig
joint surface erosion = shoulder instability and potential for shoulder subluxation
61
What are the elbows S +S for RA?
bilateral olecranon bursitis (in severe RA)
effusion between lat epicondyle and olecranon prominence
ulnar nerve entrapment
rheumatoid nodules
flexion contraction due to patient posturing
inflammation --> capsule and ligament distention and joint erosion --> instability
62
What are the wrists S +S for RA?
almost all RA patients
volar subluxation of wrist and hand on radius (piano key sign) --> may cause extensor tendon rupture
proximal row ulnar sublux, distal - radial --> loss of ulnar dev and compensatory ulnar drift of MCPs
carpal bone erosion
carpal tunnel syndrome common
decreased grasp and pinch strength
63
What are the MCP S +S for RA?
Commonly affected (almost ALL)
joint effusion
get zig zag effect
trigger finger - due to flexor tenosynovitis, friction with movement or tendon nodules
bunnel-littler test
-MCP in flexion/ extension with PIP flexion (limited both = capsule, limited in extension but not flexion = instrintic muscle tightness)
64
What are the PIP S +S for RA?
effusion common and easily palpable
swan neck - DIP flexion, PIP hyperextension and MCP flexion
-reflex muscle spasm
-volar capsule stretched --> lateral bands move dorsally --> tension on FDP by the hyperextend POP, flexes the DIP
-rupture of FD communis --> FDP to pull DIP into flexion
Boutonniere - DIP extension, PIP flexion, MCP extension
-chornic synovitis --> central slip (insertion of extensor digitorum communis into middle phalanx) lengthens, and volar slip of lateral bands --> PIP forced into flexion
65
What are the DIP S +S for RA?
Rarely affected
66
What are the Thumb S +S for RA?
Flail IP: loss of abiltiy to flex IP joint
Type 1 deformity: IP hyperextension (without CMC involvement) and MCP flexion - most common, Z-formity
Type 2: CMC subluxation and IP hyperextension - least common
Type 3: CMC subluxation and MCP hyperextension
67
What are the hip S +S for RA?
half have evidence of radiographical hip pathology
pain over greater trochanter due to trochanteric bursitis
68
What are the knee S +S for RA?
commonly involved in RA (knee has large amount of synovium)
knee ballottement test - press down on patella, sensation of bogginess
bulge test / brush test - upward on med aspect, then down on lat - postive if wave like movement to the med aspect of knee
accumulation of fluid may lead to baker's cyst
chronic synovitis - distension and laxity of joint capsule, colleteral and cruciate ligaments, erosion of joint surfaces, flexion contracture second to flexed posturing to avoid increase pain
69
What are the ankle S +S for RA?
Chronic synovitis leads to - hindfoot pronation, forefoot planus and flattened of med long arch, possible instability in subtalar joint requiring fusion
tarsal tunnel syndrome may develop
70
What are the feet S +S for RA?
synovitis of the MTP is common - may lead to metatarsalgia
calcaneous may erode or develop exostoses
hallux valgus and bunion may develop
Hammer toe, claw toe, mallet toe
morton's neuroma may develop
71
What could the muscle atrophy around the joint be due to in RA? Where is it most common
disuse, nerve impairment, myositis, steroid induced myopathy, selective attrition of unknown mechanism related to disease process (in type II fibers)
atrophy common in hand intrinsic. / quads
muscle weakness may be due to atrophy or reflex inhibition secondary to pain
72
What are the common sits of tenosynovitis in RA?
wrist flexors, thumb flexors, patella, achilles tendon
can lead to tendon rupture
73
What are rheumatoid nodules?
occur in 20-25 % of RA Paitents
associated with seropositive RF
found in subcutaneous tissue or deeper connective tissue
common where repeated mechanical pressure or pressure bearing areas (olecranon bursea, extensor surface of forearm, achilles tendon
74
what are the vascular complications of RA?
vasculitis (25-30%)
dermatological vasculitis - lead to focal ischemic skin lesions (discolouration) or ischemic ulcers
75
what are the neurological complications of RA?
peripheral neuropathy - develop secondary to mechanical compression of nerves or vasculities of vessels supplying the nerves
SC compression may arise due to inflam in Cx (ER)
76
what are the cardiopulmonary complications in RA?
increased morbidity and mortality risk due to CVD
accelerated atheroscleosis --> ischemic heart disease
pleuritis and pulmonary nodules may affect gas exchange
pulmonary nodules are related to rheumatoid modules elsewhere in the body and found in seropositive patients
77
what are the ocular complications in RA?
episcleritis (benign, self-limiting)
scleritis (serious = blindness)
get referred - have annual eye exam
78
What are the pharmacological innervations for RA? And the associated adverse effects
Goal: manage RA symptoms and halt or slow down disease progression (decrease pina, decrease inflam, decrease joint damage, preserve function)
NSAIDS
-analgesic (low), anti-inflam (high)
-adverse effects - GI and renal complications
Corticosteroids
-anti-inflam
-long term adverse effects - OP, muscle wasting, suppressed immune system, impaired wound healing, cataracts, glaucoma, hyperlipidemia, osteonecrosis, adrenal suppression
Disease modifying anti-rheumatic drugs (DMARDs)
-reduces disease progression, do not provide analgesic effects
-slow acting
-biological response modifiers (BRMs) - mimic activities of selective immune cells to reduce or block the inflam process (immunosuppression)
-increase risk of infections, malignancy, heart/lung conditions
79
What history is required for RA patients?
pain
joint inflam
joint stiffness - morning vs. prolonged
previous activity level
pattern and degree of fatigue
presence of co-morbidities
current meds
previous / current treatments
80
What are RA red flags (urgent referral)
claudication pain pattern
constitutional signs
focal or diffuse weakness
history of significant trauma
hot, swollen joint
neurogenic pain
81
What are the 4 objective measures on the SAJI of general level of inflam?
1. duration of morning stiffness (minutes)
2. bilateral grip strength testing (mmHg)
3. number of active joints
4. erythrocyte sedimentation rate - PT can't do
82
How do you tell if it is an active joint for RA?
effusion - 2 thumbs, 4 finger technique, palpation
joint line tenderness
stress pain - OP
STOP if one is positive
83
How do you tell if its a damaged joint for RA?
subluxation or deformity
bone on bone crepitus
loss of more than 20% of PROM
ligament instability
84
What are two common sensory impairments in RA?
Raynaud's disease - cold/stress induced, vasomotor constriction to affected areas, affects distal extremities
nerve compression - secondary to inflam or joint derangement
85
What are the C/I for the modalities of pain relief for RA?
Heat
-->superficial - do not apply on inflam, hot or swollen joints
--> deep - do not apply in acute stage of inflam
Cold
-don't use in raynaud's or cryoglobulinemia (when blood have cryoglobulin - insoluble at low temp)
Electrical agents
Rest
-not complete bed rest - lead to other problems such as deconditioning, depression, decrease bone and tissue health and increase risk for CV disease
86
What are the 3 types of orthoses, splints and braces?
1. functional splints- used to restore or improve function
2. corrective splints - used to improve joint alignment
3. resting splints - maintain joint alignment and reduce pain
87
What are the ROM and flexibility exercise C/I and indications?
daily AROM as tolerated
education to prevent contractures
NO stretching for active inflam joints
exercise time of day they feel best
if does not subside (pain induced by exercise) in 1 hour - regress
88
What are the strengthening exercise C/I and indications?
pain free
NONE for active inflamed joints
89
How long should RA patient do CV training for?
30 mins of mod exercise 5x/week or a total 150 mins / week
walks or bike is best and safe
90
What mobility aids could you modify to with RA patients?
weightbearing at forearm if wrist pain
-loft strand, elbow support or gutter
91
What orthosis may help with gait deformities in RA?
Orthotics or rocker bottom shoes, extra depth shoe toe box for greater support in rear foot (increased stability) and help in med long arch
92
What are the main goals initially in RA treatment?
decrease pain and swelling
optimize ROM and strength
optimize function
93
What is Systemic Lupus Erythematosus? Including epidemiology and etiology
An autoimmune disorder characterized by the production of autoantibodies
Can affect any organ
Most common
Presents with episodes of remission and relapse
F>M, onset during reproductive years (15-40)
Unknown, genetic predisposition and environment factors
94
What are the S+S for SLE?
Systemic - malaise, fever, fatigue
Skin - malar rash, discoid rash, photosensitivity
Hair - alopecia
Mucous membrane - oral or nasopharyngeal ulcers
Pulmonary - pleuritic chest pain and SOB
CV = pericarditis, hypertension, raynauds
Hematological - anemia, coagulation disorders (low platelet)
Neuropsychiatric - headaches, seizures, psychosis
Renal - proteinuria, cellular (urinary) casts
MSK - non-erosive arthritis (symmetrical, tenderness or effusion, common in peripheral joints), hand deformities (caused by true tendon or ligament laxity)
95
What is the criteria of diagnosis for SLE?
*must have at least 4 of 11
S - serositis - pleuritis or pericarditis
O - oral ulcers
A - arthritis - nonerosive of 2 or more joint
P - photosensitivity with UV exposure
B - blood disorders - low WBC, RBC, platelets
R - renal disorder - proteinuria or cellular casts
A - ANA - anti-nuclear antibody
I - immunologic disorder - abnormal immune tests
N - neurologic disorder - seizures or psychosis
M- malar rash - erythema over malar eminence, spare the nasolabial folds
D- discoid rash - erythematous raised patches
96
What is the medical management for SLE?
Analgesic - NSAIDs, acetaminophen
Corticosteroids - reduce inflam, suppress immune system
DMARDs - reduce inflam, suppress immune system
Biologics - reduce inflam, suppress immune system
97
What is the PT management for SLE?
Education - conservation techniques, protection from sun, S + S for progression
Aerobic exercise
Breathing techniques
Treatment for inflam
-manage pain / effusion - rest, modalities
-maintain joint ROM - ROM exercises, no stretching
-Joint protection - splints, positioning, assistive devices
-Strengthening - not during acute flares up, limited by fatigue
98
What is ankylosing spondylitis? Including epidemiology and etiology?
A chronic inflammatory arthritis of the axial skeleton - may progress to spinal fusion
M>F, 15-30
Autoimmune disease thought to have a genetic disposition and environmental trigger (infectious agent) - genetic (family history), or HLA-B27 gene associated with AS
99
What is the course of AS?
Onset - insidious, pain and stiffness in low back, SIJ, inflam - worse in morning, lasts 30-40 mins, sleep disturbed by pain
Progression - variable - mild to severe, periods of exacerbations and remission, progress from caudal to cephalad
100
What is the S + S of AS?
LBP and glute pain and stiffness
loss of ROM - e.g., girdle muscles as well (no scap post rot)
postural abnormalities - usually fused in flexion
tenderness over sites of enthesitis - insertion of muscle (inflam at that area)
Systemic
-fatigue
eye involvement - anterior uveitis (iritis)
cardiovascular involvement - decreased CO bc electrical irregularity = decreased HR
101
What are the postural changes in AS for advanced disease?
Increased tx kyphosis
decreased Lx lordosis
eye upward gaze due to cx flexion deformity
fixed thoracic cage
hip flexion and knee flexion in an attempt to maintain upright posture may lead to contracture
102
What are the main sites for enthesitis for AS?
Plantar fascia
Achilles
ITB
103
What are the lab tests for AS?
genetic testing - HLA B27 +ve
acute phase reactants - increased ESR, CRP
absence of RF RF -ve - seronegative spondyarthropathy
104
What are the radiographic findings for AS?
Sacroilitis - early - irregular SIJ spaces, subchondral bone erosions, increased sclerosis around SIJ. Advanced - SIJ thin or not visible
Syndesmophytes - bamboo spine - bony growth in outer fibrous ring of annulus, railroad track - long lig affected
Thoracic kyphosis
Enthesitis
Arthritis - hip
105
What does the physical exam consist of the AS?
observation
spinal ROM
peripheral ROM
chest expansion measurements
special tests
palpation
BASMI
106
What is the BASMI
Bath AS metrology index
1. cervical rotation
2. tragus to wall (cx retraction)
3. modified schober (lx flexion)
4. finger to floor lat flexion
5. intermalleolar distance
107
What are the self-report tools for AS?
Bath AS disease activity index
Bath AS functional index
108
What is the modified New York Criteria?
Clinical
-LBP present for 3 months; improved by exercises but not relieve dwith rest
-limitations in Lx motion in both sagittal and frontal planes
-limitation of chest expansion relative to normal values for age and sex
Radiological
-sacroilitis on xray
Diagnosis
-definite - if radiological plus one clinical
-probable - 3 clinical or radiological
109
What are the pharmacological, surgical and rehab interventions for AS?
Pharm
-NSAIDs, corticosteroids or biologics (not traditional DMARDs)
Surgical
-joint replacement, spinal surgery
Rehab
-pain - education, cryotherapy, thermotherapy (NOT INFLAM JOINTS), massage, electrophysical agents
-ROM - ROM exercises (NOT FLEXION), stretching, postural cues, adaptive equipment and assistive devices
-cardioresp - aerobic exercise, deep breathing, thoracic ROM, energy conservation techniques
110
What is osteoporosis? including epidemiology and classification?
a metabolic bone disease that presents with decreased bone mass (density) and micro architectural deterioration (quality)
F>M, post -menopause (50)
classification
1. primary - type 1 - postmenopausal (women 50-70), type 2 - senile (men and women over 70)
2. secondary - may be due to another primary condition or from treatment of another condition
risk factors
-non-modifiable - age, gender F>M, race (caucasian, asian), menopause, family history, small skeletal frame, amenorrhea (depending on cause)
-modifiable - sedentary lifestyle (inadequate loading), diet (deficient in calc and vit D), smoking, caffeine, alcohol abuse, amenorrhea (depending on cause)
111
What is the WHO criteria for diagnosis of OP?
Measuring bone mineral density (BMD) - used dual energy xray absorptiometry (DEXA) - t-scores (compared to young adult of same sex and how many SD)
>-1 : normal
-1 to -2.5 : osteopenia
<-2.5 : osteoporosis
<-2.5 and history of at least one OP fracture : severe OP
112
What is the impact of OP?
Bone fracture (mostly Tx / vertebral, hip, then radial and other)
Compression fractures - decrease in height
postural changes - increased in kyphosis, dowagers hump
Back pain
decrease mobility
113
What are the interventions for OP?
Postural education
falls prevention education
strength training
weight bearing exercises
lifestyle modifications (smoking cessation, moderate alcohol consumption)
diet / supplementation (calcium and vit D)
Pharmacological intervention
114
What is osteomalacia? Including etiology, S + S, interventions
Metabolic bone disease which results in softening of bones due to decalcification of bones
etiology - due to inadequate intestinal absorption of calcium, increase renal excretion of phosphorus or vit D deficiency
S + S
-pain, aching, fatigue, weight loss, weakness, possible deformities (increase Tx kyphosis, bowing of LE), high risk of fractures
Interventions
-pharmacological and/or nutritional interventions to address underlying etiology
-strength training
-bone protection strategies
115
What is Paget's disease? Including epidemiology, etiology, characteristics and interventions
A metabolic bone disease involving abnormal osteoclast and osteoblasts activity followed by disorganized remodelling - leads to enlarged and misshapen bones (which appear large, but lack structural integrity and strength)
M>F, typically >40 years old
unknown, thought to be linked to heredity (genetics), viral infection, and environmental factors
pain, misshapen bones, fractures, arthritis
pharmacological interventions for pain control and limiting osteoclast activity
postural re-ed
exercise therapy - strengthening, stretching, aerobic activity
116
What is osteomyelitis? Including etiology, S +S and interventions
Inflammation within bone caused by an infection
may be infected through blood stream, open fracture or surgery (mostly bacterial infection)
*more at risk of immunocompromised
Fever, tenderness, redness, warmth, swelling, loss of ROM in affected joints
Antibiotics, surgery, ROM exercises
117
What is osteogenesis imperfecta? Including epidemiology, etiology, characteristics and interventions
A genetic bone disorder characterized by fragile bones
M=F
Mutations in gene that affects bone formation, bone strength, and structure of other tissue
-affects type I collagen (low collagen production and abnormal collagen produced)
bone mineralization not necessarily affected
frequent fractures, bone deformity and bone pain, low bone density, short stature (decrease bone growth in length), scoliosis, ligament laxity, muscle weakness, fatigue, cardiac and resp issues, dental, vision and hearing problems
goals: minimize fractures, enhance indep function, and promote general health
fracture care
strengthening
aerobic conditioning
assistive devices
surgery if needed - ORIF, correct bone deformities, spine stabilization
diet
118
What are the precautions for osteogenesis imperfecta?
never pull or push on a limb, or bend it into an awkward position
when fracture is suspected, minimize handling of the affected limb
handle babies with extra care - lift behind buttock and legs and out shoulders, neck and head (NOT UNDER ARMPITS), do not lift by ankles
encourage to explore indep (not on soft surface)
support infants in a variety of positions
119
What are the functions of the skin?
protection - UV, infection, fluid loss
Temperature regulation
sensation
secretion of oils to lubricate skin
vit d synthesis
cosmetic appearance
120
What are burns? Including epidemiology and etiology?
A injury to tissue of the body caused by heat, cold, chemicals, electricity, friction or radiation
M>F, 16-40
Common cause - hot liquids, deaths - inhalation injuries
121
What are the two laters of skin?
Epidermis - avascular, free nerve ending
Dermis - deepest - BV, lymphatic, nerve endings, collagen and elastin - enclosed epidermal appendages (sweat glands, sebaceous glands, hair follicles)
122
What are the different ways to classify burns
depth
total body surface area
123
What is a superficial burns characteristics, depth and rate of healing?
see book
124
What is a superficial partial thickness burns characteristics, depth and rate of healing?
see book
125
What is a deep partial thickeness burns characteristics, depth and rate of healing?
see book
126
What is a full thickness burns characteristics, depth and rate of healing?
see book
127
What is a subdermal burns characteristics, depth and rate of healing?
see book
128
What is the rule of 9s?
see book for adult and children
129
What are the complications of burn injuries?
infection
pulmonary
metabolic
cardiovascular
heterotrophic ossification
neuropathy
amputation
pathological scars
130
What are the metabolic complications for burns?
increase metabolic activity
-decrease energy stores
-weight loss
-muscle atrophy
-increase evaporative heat loss
131
What are the associated complications for inhalation injury?
CO poisoning, tracheal damage, upper airway obstruction (constricting eschar), pulmonary edema, and pneumonia
132
What are the cardiovascular complications for burns?
increased cap permeability = fluid loss (intravascular --> interstitium), decrease CO (at risk for hypovolemic shock)
-usually resolves within 24 hours
-fluid replacement therapy helps manage
133
What is the most common areas for heterotopic ossification for burns
higher incidence in patients with larger TBSA burns
Elbow, hips, shoulders
134
What are the two types of neuropathy that can occur with burns?
Peripheral neuropathy
local - causes from Rx - tight bandage, poorly fitted splints, prolonged or inappropriate position (common in brachial plexus, ulnar, common peroneal)
polyneuropathy - larger TBSA burns
135
What are the types of pathological scars?
Hypertrophic - excessive scar that is raised, red and rigid
Keloid - type of hypertrophic that extends beyond the boundary of original wound
Scar contracture - leads to muscle contracture
Increased riskL
-deep partial thickness that heal spontaneouls
-full thickeness with incomplete coverage
136
What is the initial management for scars?
establish and maintain airway
prevent cyanosis, shock and hemorrhage
establish baseline
fluid replacement
clean patient and wound
examine injury
prevent and manage any pulmonary complication
137
What is the wound care for burns?
inspect
clean
debridement
prevent infection
138
What are the types of skin grafts
Auto - own skin (thighs and back) - either sheet (more cosmetic) or mesh (more SA)
Allo - same species
Xeno - from another species
139
What are the goals of positioning and splinting?
minimize edema, prevent contracture, preserve function
*position in elongated state or functional positioning*
140
What is the area of burn, position of contracture and suggested positioning and methods to do so?
See chart in book
141
How long do you discontinue joint movement above and below skin graft for burns?
3-5 days or when surgeon determines sage
142
What do you use to minimize edema and statis when upright during ambulation after a burn?
elastic wrap or TED (anti-emoblism) stockings
143
What is the ideal pressure of compression stockings? How long are they worn
25 mmHg
23 hours a day (not bathing) - 12 - 18 months
144
What is DM and what is it characterized by?
Characterized - hyperglycemia due to defective insulin action and/or secretion
beta cells of the pancreas produce and secrete hormone known as insulin - which helps regulate blood glucose and promote uptake
145
What is type 1 DM?
pancreas fails to produce sufficient (or any) insulin
children and adults - typically childhood onset
autoimmune abnormality that damages the islet cells of the pancrease
genetic predisposition and environment may be factor
146
What is type 2 DM? including risk factors
pancreas fails to produce sufficient insulin and resistance to insulin action (inadequate utilization)
onset in adulthood
Risk factors
-secondary to many dysfunctions
-obesity (BMI >30)
-high abdominal fat (high waist to hip ratio)
-poor diet
-sedentary lifestyle
147
What is hypoglycemia? including S + S
drop in blood glucose <3.9 mmol/L
caused by meds that incrases insulin secretion, not eating on time, restrictive caloric diets and increased PA
S + S
-autonomic - sweating, nausea, tremors, warmth, anxiety, palpitations, hunger
-neuroglycopenic - headache, blurred vision, confusion, weakness, fatigue, difficulty speaking, seizures, coma
148
How do you reduce risk of hypoglycemia with exercise?
educate on self-monitoring
insulin injections >1 hour before exercise
avoid injecting into exercising area
check blood glucose before and after exercise
exercise consistent time of day (after meal, not at night)
glucose rich snacks or drinks nearby
if <5.5mmol/L - 15:15 rule
149
What is hyperglycemia?
blood glucose >11mmol/L
due to lack of insulin present
regular exercise, diet and meds can have prevent
S + S
-polydipsia, polyphagia, polyuria, fatigue, blurred vision, delayed healing
150
Describe the cardiovascular complication for DM?
increase risk of CVD,CAD,MI, PVD, arteriosclerosis = ischemia of tissues and muscles
151
Describe the peripheral neuropathy complication for DM?
impaired function of peripheral nerves
affects sensory and motor neurons
glove and stocking distribution
poor balance due to sensorimotor distributions
may lead to charcot foot / high risks of ulcers / infection
152
What is Charcot foot?
bones weak and can fracture and not feel it with DM = deformity
153
Describe the autonomic neuropathy complication for DM?
impaired function of peripheral nerves of the ANS
blunted HR and BP
high resting HR
impaired peripheral vasodilation --> impaired sweating --> poor thermoregulation
increase incidence of orthostatic hypotension
increased risk of post-exercise hypotension
154
Describe the diabetic retinopathy complication for DM?
damage to retina caused by damage to small BV supplying the retina - leading cause of blindness
avoid - valsalva maneuver, heavy lifting, strenuous UE exercise, head down postures
155
Describe the diabetic nephropathy complication for DM?
kidney damage leading to loss of kidney function - high protein in urine = chronic kidney disease and kidney failure
may require dialysis or kidney transplant
156
What is the skin care advice for DM?
wash feet in lukewarm water with mild soap
dry (esp between toes)
used lanolin based lotion or petroleum jelly (not between toes)
use powder or cornstarch between toes if desired
never self treat
cut toenails straight or get someone else to do it
wear clean white socks
do not walk barefoot
do not apply heating or cold pack
157
What are the affects of exercise on DM?
increased insulin sensitivity, uptake
decerase insulin resistance
improve blood glucose control
decrease risk of diabetic complications
158
What are the parameters for aerobic and resistance exercise for DM?
aerobic
F - 3-7 days
I - 50-50 % of VO2R (12-16 RPE)
T - 20-60 mins
T - large muscle groups
Resistance
F - 2-3day with 48 break
I - 2-3 sets of 8 to 12 reps at 60-80% of 1RM
T - varies
T - tailor according to co-morbities and precautions
