Study Guide to The PCE Written Exam

Prepared by PABC Members Jason Shane & Amanda Mrsic, Fall 2012
Prepared by Jason Shane and Amanda Mrsic. Hopefully the time (lets be honest, ridiculous amount
of time, lol) we spent making this will help you studying for the national exam.
(p.s. go to the end of the document for a good bye note...and a page count, yikes!)
SAMPLE LIST OF AREAS OF PRACTICE EVALUATED BY THE PCE
01.01. Neuromusculoskeletal (50%5%) (This list is not necessarily
exhaustive.)

SAMPLE LIST OF AREAS OF PRACTICE EVALUATED BY THE

PCE
01.01. Neuromusculoskeletal (50%5%) (This list is not
necessarily exhaustive.)
01.01.01 Muscle contusions/strains/tears/weakness
Mm Strains: majority occur in bi-articular mm at the mm-tendon jx,
most occur during eccentric loading; Rx: Acute Phase-PRICE,
crutches if in LE; Repair Phase-modalities, DTFs, strength,
stretching; Remodeling phase: strength (incr loading and velocity),
stretching (static and dynamic)

01.01.02 Pelvic floor dysfunction

Can be assessed via: digital, EMG, manometric, dynamometer,
RTUS real time ultra sound, MRI & biofeedback.
Rx: isolate PFM during exercise, avoid accessory mm use, eg.
Glutes, abs; overload the mm by holding longer with shorter rest
periods; weakness or laxity of PFM can occur during pregnancy or
childbirth further loss of elasticity and mm tone later in life (or
even after pregnancy) can lead to cystocele=herniation of bladder
into vagina, rectocele=rectum into vagina, uterine prolapse=uterus

into vagina; Sys of pelvic pain:pain down post thigh

ADD IN MORE INFO FROM PATHO LECTURE, FEMALE
REPRODUCTIVE PATHOLOGY
01.01.03 Ligament sprains/tears
Grade 2 syndesmotic ankle sprain (high ankle sprains)-Rx: Phase
1 (protection phase 2wks)) Goal to protect and decr inflam,
PRICE, NWB with crutches, modalities to decr edema, light ROM;
Phase 2 (management phase 2-4weeks) goal is normal mobility,
incr strength and fx ambulate (PWB w/o P), bilateral stance
training, joint mobs, strength training; Phase 3 (management) goal
to incr function and unilateral balance and strength; Phase 4
Return to sport
01.01.04 Tendonopathy, tendon ruptures/tears, tendonosis
Achilles tendonopathy, Rx-eccentric heel drop program,
footwear/orthoses, stretching/mobs
De Quervains Tenosynovitis= a tendinosis of the sheath or
tunnel that surrounds the tendons of EPB (O: lower post 1/3rd of
radius, I: base of prox. Phalynx of thumb) & APL (O:ulna, radius,
interos. Memb, I: base of 1st metacarpal) (mm which radially
deviate the thumb). To test for it tuck thumb in fist and ulnarly
deviate wrist, look for P along area of distal radius
APL, EPB, fray of sheath, scar tissue forms (inflamm, repair)
Lateral Elbow P=90% involve ECRB (O:lateral epi, I:post base of
3rd metacarpal, Fx:extends and abducts hand at the wrist), other
10% are b/w common extensor tendon and origin (tenoperiosteal
Jx) and origin of ECRL (O: lateral supracondylar ridge, I: dorsal
surface of base of 2nd metacarpal on radial side, Fx: extensor at
the wrist joint, abducts the hand at the wrist; usually symptomatic
with activities involving wrist and/or finger extension and/or
gripping; Test for it:P w/ resistied extension of D3; Rx: Acutecontrol P and inflame, rest, ice, US, tennis strap, TENS, Pt ed,

maintain mm length and mobility, AROM for elbow, wrist, and

hand; Repair-gently stress collagen via DTFM and eccentric
strength training, cont with stretches
01.01.05 Fasciitis, fascial tearing, myofascial restriction
P59 o sullivan
01.01.06 Joint derangements/dysfunction (e.g., loose bodies,
hypermobility, hypomobility)
Loose body: free floating piece of bone or cartilage; often result of
OA or chip fracture; typical symptom is locking or catching
Hypermobility: spondylosis (OA of joints in spine and narrowing of
foramina), listhesis (fracture and slip of cranial vert anteriorly),
lysis (fracture of pars)
Hypomoility: capsular patterns, Osullivan pg 4
01.01.07 Fractures, dislocations, subluxations
Shoulder (GH joint) dislocation: Rx-scapular stabilization/posture,
rotator cuff strengtheningfunctional rehab
Fractures:K&C pg 321-325
Comminuted fracture=fracture with more than 2 fragments
Subluxations: of AC joint, K&C pg 494; clavicle post and sup on
acromion
SLAP lesion= Superior Labral tear Anterior to Posterior
Bankart lesion=injury to ant/inf portion of glenoid labrum
01.01.08 Osteoporosis/osteopenia
DEPLETED BMD
W10X MORE THAN MEN ESP POST MENOPAUSE
FRACTURE OF:TSP, LSP FEMORAL NECK, PROX HUMERUS,
PROX TIB, PELVIS, DISTAL RAD
NORMAL = WITHIN -1 SD FOR BMD
OSTEOPENIA = -1 TO -2.5SD BMD

OSTEOPEROSIS = -2.5 SD AND BELOW

P37
01.01.09 Tumour/pathological fractures (ahh, the good old
tumour lectures, didnt realize we were studying to be
pathologists!)
Primary malignant tumors of soft tissues and bone are rare but
may occur in youth
Osteosarcoma=occur at either end of long bones, produce jt pain,
Agg:activity, X-ray:moth eaten appearance, Rx=surgery (Terry Fox
had this)
Primary malignant tumors are rare in bone, usually are secondary
Synovial sarcoma = usually in larger joints, P (often at night or w/
activity), swelling and instability, Rx:Sx +/- chemo/rad
Malignant tumors=may metastasize to bone
Mets from breast, lung, prostate, kidney, thyroid
Osteoid osteoma=benign bone tumor, exercise related bone P
and tenderness (often mistaken for bone #), characterized by
presence of night P and abolition of Sys with aspirin, CT scan
shows a central focus point, Rx:ablation, ethanol, laser
01.01.10 Degenerative joint disease
Mechanical change, jt disease and jt trauma
Degeneration of articular cartilage: hypertrophy of subchondral
bone and ht capsule (wt bearing jts)
Meds: corticosteroids and NSAIDS
OA: decreased jt space, dec cartilage height, osteophytes
PT goals: jt protection, improve jt mechanics, aquatics

01.01.11 Mechanical spinal abnormalities (e.g., low back pain,

scoliosis, postural dysfunction)
MEMORIZE THIS PICTURE, Im told it can be useful!!!

Posture: RSPT 518 Oct 8th

Posture and LBP: RSPT 544 Oct 13 (May Nolan lecture)

01.01.12 Inflammatory/infectious conditions of the

neuromusculoskeletal system (e.g., osteomyelitis)
OSTEOMYELITIS = INFLAMM RESPONSE IN BONE CAUSED
BY AND INFECTION; OSullivan pg 37, usually a staph aureus

infection
Goals: maintain joint function, cast care
MORE COMMON IN KIDS AND IMMUNE SUPRESSED, M>F
ANTIBIOTICS TO TREAT; SURGERY IF IN THE JT
TENDONITIS = INFLAMM DUE TO MICRO TRAUMA,
TENDINOSIS = CHRONIC TENDON DYSFUNCTION, common
sites supraspinatus, common extensor tendon of elbow, patella
BURSITIS-caused by overuse, trauma, gout, infection; S and S is
pain with rest, active and PROM are limited; Rx-flexibility, mobs,
thermal agents
01.01.13 Amputations (we spent a lot of time memorizing
this...sure would have been nice if they asked us a question
about it)
Causes: diabetes mellitus, PVD, trauma, congenital/correction of
deformity, tumors, infected TKR
Sites of amputation (the tricky ones): toe (ray resection), ankle
(symes)
Effects of:
1)Toe amputation-decreased power for push off, decrease
balance d/t decreased proprioception and BOS
2)Partial foot-lose forefoot lever, decrd balance, risk for tissue
breakdown secondary to incrd pressure on remaining WB surface
prosthesis: shoe filler, carbon fiber afo, complete prosthesis
3) ankle (Symes): goes through the jt, distal end of tip and fib
intact
-long lever, bulbous end, better than transtibial
-high risk of skin breakdown
prosthesis: similar to trans-tib, trap door to fit over maleoli, can
have partial patellar WB
4) transtibial - cant WB through the end, some ppl can achieve a
normal gait pattern

Prosthetic sockets: total surface bearing, patellar tendon bearing

Pressure sensitive: anterior/distal end of tib, fibula - head and end,
bottom of stump
pressure tolerant: post mm mass, patellar tendon, medial/lateral
flares
suspension: supracondylar, suprapatellar cuff, sleeve (req lots of
hand strength), locking pin, suction (1 way valve)
gait deviations:
stance: foot flat or foot slap, knee hyperextension or buckling,
early heel rise,
swing: inc/dec stride length, toe drag, lat/med whip, vaulting
5) knee disarticulation- thigh mm preserved, potential to WB
through the stump, prosthetic: trap door for condyles
6) transfemoral - no WB on end, takes 60% more energy to
ambulate with prosthesis compared to able body walking, may
require a gait aid, often asymmetrical gait, WB through Ischial
Tuberosities and hydrostatic loading, pressure sensitive areas=
end of residual limb, adductor tendon
Knee prosthesis: manual lock, mechanical/friction,
hydraulic/pneumatic/microprocessor
gait deviations:
stance: ABduction, lat trunk shift, excessive trunk lordosis, hip flex,
dec stance time,
swing: medial or lateral whips, circumduction, hip hike, vaulting
with good leg
7) hip disarticulation- probs require gait aid, asymm gait pattern
210% energy expenditure
8) hemipelvectomy
PT education: contracture prevention, knee or hip flex contracture
>20% will prevent prosthetic use, pain management, edema
control, shaping, fall prevention, foot care of remaining limb, falls
prevention (risk @ night)

NO PILLOWS under legs in supine or between legs for

transfemoral
Socket-supports body wt
Liner-interface b/w socket and limb
Suspension-system used to keep prosthesis on the residual limb
Socks-ensure proper fit
Shank/pylon-connects socket to foot, provides ht
01.01.14 Congenital malformations (e.g., talipes equinovarus,
hip dysplasia)
DUCHENNES MUSCULAR DYSTROPHY (P257)
X-LINKED RECESSIVE
MM WEAKNESS PROX TO DISTAL, DIE LATE ADOLESCENTS
+VE GOWERS
TALIPIES EQUINOVARUS = CLUB FOOT-plantar flexed
(talocrural), adducted, inverted (subtalar, talocalcaneal,
talonavicular, calcaneo-cuboid), supination at midtarsal joints
2 TYPES:
1) TALIPES EQUINOVARUS-ABNORMAL DEVELOPMENT HEAD
AnD NECK OF TALUS- hereditary or neuromuscular disorders;
2) POSTURALfeet squished in utero
Rx: casting and splinting or Sx
EQUINUS = PF FOOT
ETIOLOGY = CONGENITAL BONE DEFORMITY, CP,
CONTRACTURE OF CALF MM
01.01.15 Nerve compression (e.g., Carpal Tunnel Syndrome,
radiculopathy, spinal stenosis)
Radiculopathy=Sis & Sys depend on degree of compression and
may include P, tingling, numbness. Loss of nn conduction, mm

weakness, decrd skin sensation, and loss of reflex

SPINAL STENOSIS P60 -hypertrophy of spinal lamina,
ligamentum flavum, facets; vascular or neural compromise; also
see May Nolan L-Spine pg 15
Rx: joint mobs, flexion bias exercises, avoid extension, traction
THORACIC OUTLET - subclavian artery vein, brachial plexus,
vagus/phrenic N, sympathetic trunk
compress at : sup thoracic outlet, scalene triangle, clavicle and rib
1, pec minor and thoracic wall
Tx: restore mm imbalance, Sx

NERVE ENTRAPMENTulnar nerve-normally occurs in cubital tunnel, could be d/t trauma,

compression, thickend retinaculum in FCU, Sys medial elbow
pain, pos tinnel sign
median nerve-occurs in pronator teres, and under FDS, occurs
with repetitive gripping activities; aching pain, forearm pain
radial nerve-entrapment of distal branches (post interosseous
nerve) occurs in radial tunnel
CARPAL TUNNEL P48, can do Phalens test, long term
compression of median nerve can cause atrophy of thenar mm
01.01.16 Peripheral nerve injuries
WALLERIAN DEGEN - transection results in degen or axon and
sheath distal to site of injury
SEGMENTAL DEMYLINATION-axons are preserved but are
demylinated, remylelination restores fx, ex GBS
AXONAL DEGEN- axonal degeneration of axon cylinder and
myelin, distal to proximal, dying back of nerves,, ex-peripheral
neuropathy

P129-133
NEUROPATHY-any disease of nerves characterized by
deteriorating neural fx
TRAUMATIC
Expect to see motor, sensory, and potentially autonomic changes
(ex- ), and pain; an MRI or nerve conduction test is used to
confirm a peripheral nn injury
Neuropraxia= just a compression of the nerve, causes a transient
disruption, good recovery w/good prognosis which could take
minutes to weeks
Axonotemesis= disruption of axon but myelin sheath is still intact,
may cause paralysis of the motor, sensory, and autonomic. Mainly
seen in crush injury. Longer recovery with fair prognosis which can
take months
Neurotemesis=completely severed axon and sheath; recovery is
only possible with surgery with variable success; i.e. it may never
recover
Charcot Marie Tooth Disease=a hereditary motor and sensory
neuropathology causing extensive demyelination of motor and
sensory nerves of the foot
Presentation-slow progression of symmetric mm weakness,
atrophy of foot intrinsics, diminished deep tendon relfexes, pes
cavus/hammer toes, weak dorsiflexors and pronators
PT Rx: contracture management (stretching mm),
management/education on foot care
Bells Palsy=d/t latent herpes virus, days before onset Pt reports
pain around mastoid; virus causes inflam response over facial nn
Clinical manifestations-unilateral facial paralysis
Facial nn innervates-mm of facial expression, stapedius mm of
inner ear, sensory and autonomic fibers for taste (ant aspect of
tongue), tears, salivation

Rx: corticosteroids, estim?, protect eye

Thoracic Outlet Syndrome=an entrapment syndrome caused my
pressure on brachial plexus
Risks for getting it-posture, growth, trauma, body comp
Pathology-chronic compression of nn roots results in edema and
ischemia of nn roots-->neuropraxia and wallerian degen can occur
presentation-paraesthesia, weakness and pain in arm, neck pain
may radiate into face, scapula, ant chest; coldness, edema,
raynauds, fatigue in hand, distension of veins
Rx: correct posture, surgical mngmt if vasculature gets
compromised
Diabetic neuropathy=peripheral nn disorder in diabetes that
occurs w/o any other cause for neuropathy
Pathology-chronic metabolic disturbance affects nn and schwann
cells-->loss of both myelinated and unmyelinated axons
Presentation-symmetric, distal pattern of sensory loss, painless
paraesthesia with minimal motor weakness
Rx:control hyperglycemia, skin care, amputation
01.01.17 Neural tissue dysfunction/neuro-dynamic
dysfunction
DURAL TENSION kate kennedy
DOUBLE CRUSH - compress of N along several sites proximal
and distal H
SLR, PKB, ULTT, SLUMP ETC
01.01.18 Scars
Patho notes
Keloid scar: thick scar that goes beyond the margins of the
original wound
Hypertrophic: thick scars that do not extend beyond the boundary

of the original wound but has an excess amount of tissue in

relation to what is needed to replace the damaged dermis

01.02 Neurological (20%5%) (This list is not necessarily

exhaustive.)
01.02.01 Cerebral Vascular Accident/transient ischemic attack
P114-117
01.02.02 Acquired brain injury
TRAUMATIC=change in brain fx d/t external force; forces can
include blunt (MVA, fall, accel/decel), contusion, shearing,
bruising, axonal tearing, rotational forces, penetrating, blast
Hematomas:
Epidural-outside the dura, 90% assocd with skull fractures, most
often in temporal or temproparietal region, arterial bleed
Sub-dural-brain collects between brain and dura, often requires
surgical intervention (burr holes or craniotomy), venousl bleed
Intracranial-most common, blood within the brain
Diffuse axonal injury=shearing of the brains long connecting
nerve fibers; usually causes a coma, cant see on MRI; can affect
grey/white matter interfaces
Secondary brain injuries=cerebral blood flow is 50% less than
normal post injury, bruising, inflammation, incrd ICP
Intracranial pressure: normal is 0-10mm Hg, >20mm Hg is

BAAAD
Physio problem list:
Resp complications (decrd tidal volumes, small airway,
atelectasis), ICP, abnormal posture, mobility, contractures,
confusion/agitation, fatigue
Decerebrate posturing=indicates brain stem damage (lesions or
compression in midbrain) and lesions in cerebellem
Decorticate posturing= arms flexed, legs extended, damage to
areas including cerebral hemisphere, thalamus, cord, corticospinal
tract
Rx:
Initial medical management=prevent hypoxia, maintain adequate
BP, adequate fluids to maintain Mean Arterial Pressure, HOB 30
degrees
Nutrition: hypermetabolism, energy expenditure may be doubled
for up to 4 weeks
Other complications: 40% get post traumatic epilepsy; DVTs, and
PEs
Basal skull fracture=signs are blood or CSF out of nose or ears,
racoon eyes, bruising over mastoid (battle sign)
Coma=altered state of consciousness so that no amount of
stimulus or only pain will cause Pt to respond
Frontal lobe injury=disinhibition, memory impairment, anosmia
(cant smell), seizures, expressive aphasia)
Temporal lobe= receptive aphasia, dyslexia, dysgraphia, amnesic
syndromes, epilepsy

AND NON TRAUMATIC BRAIN INJURY

STROKE
ischaemic= 80% of strokes; could be d/t a thrombus (slower sys
to evolve) or embolism (occurs rapidly w/o warning); risk factors
are atherosclerosis, HTN, cardiac disease, diabetes, TIA=sudden
onset, last 24hrs, warning sign of stroke;majority have full stroke
w/i 1 year
hemorrhagic=20%, aneurysms and AV malformations, HTN, head
trauma, illicit drugs, bleeding disorders
Ss and Sys= confusion, headache, trouble speaking,
understanding speech, numbness or weakness on one side, cant
see, trouble walking, dizziness, loss of balance or coordination,
sudden severe headache
Rx: thrombolytic agents, Tissue Plasminogen Activator
(TPA)=activates plasminogen to digest fibrin which breaks down
the clot, TPA can salvage penumbral tissue if given within 3 hours;
mechanically widening an artery
White matter is not plastic, grey matter is
Lacunar strokes (infarcts)-subgroup of ischemic strokes, small
but deep in the brain; assocd with HTN and diabetes, correlation
with decreased cognition
What causes a stroke:
Arterial factors-artherosclerotic plaques, aneurysms, pressure on
artery walls
Venous factors-tendency for persons blood to clot quickly,
irritation or inflammation of lining of vein, DVTs
Penumbra=an area of the brain at risk for dying; is located
between an area of perfusion and necrosis
Progression of and Risk for a Stroke: ABCD Score; Age, Blood

pressure, Clinical features (hemi-weakness, speech problems),

Duration
Brain Stem stroke=not very common v. disabling b/c it can take
out ALL the ascending and descending tracts
Prevention of recurrent of stroke: anticoagulants (aspirin), lipid
lowering agents, lifestyle changes
cortex=grey matter and capable of neuroplasticity
Cortico-spinal tract-made up of white matter, is not plastic
CONCUSSION= a complex pathological process affecting the brain,
induced by traumatic biomechanical forces.
-mild form of brain injury (most common TBI)
-loss of conciousness may or may not be present
-diagnose with signs, behavioral change, cognitive impairment,
sleep disturbance
-baseline cognitive Ax: SCAT 2
-second impact syndrome- rare/fatal uncontrolled swelling of brain,
minor 2nd blow before initial symptoms are resolved
-post concussion syndrome: persistent symtoms
- 3+ consussions = 5X greater risk Alheimers, 3x memory deficits
-coup, contre-coup
- grade1: does not lose conciousness, dazed
- grade 2: no LOC, period of confusion, does NOT recall event
grade 3: loss of conciousness for short time, No memory of event,
requires eval asap
risk: contact sports, anti-coagulants, prior events
S&S: dizzy, headache, vomit, suddent weakness, nystagmus,
change in pupil size, emotional lability, memory loss, drowsy,
confused
post concussion syndorme: persistent sympoms: headache, dizzy,
irritable, memory, vision, concentration

TBI
***head down positioning is CONTRAINDICATED! for those with
traumatic brain injury******
positioning: limit neck flex and rotation
suctioning: pre/post oxygenation at 100%O2
resting splints 6-8hrs to prevent contractures
aspiration risks: turn feed tube off 20mins prior to Tx

01.02.03 Spinal cord injury

Id recommend you look over this section....

Causes of SCI: Traumatic; 40% are cervical incomplete

Non-trauma-cancer, infection and inflammation, motor neuron
disorders, vascular diseases (spinal cord infarcts); most are
parapalegic
Benefits of Sx: realignment, stabilization, early mobilization, early
rehab, less medical complications, decrd hospital stay

Reasons for Sx: unstable # or soft tissue injury, neuro sys getting
worse
Types of traumatic injuries: Hyperflexion, hyperextension, axial load,
rotation, penetrating injury
Myelopathy=refers to pathology of the spinal cord. When due to
trauma, it is known as spinal cord injury
Lumbar laminectomy=helps to decompress the cauda
equine/roots
Cauda equina syndrome:
-affects more than one nerve root, surgical emergency
-Usually presents with: bilateral leg pain/numbness, sacral root
problems, urinary retention, stool incontinence, absent reflexes
Mobility orders from doctor:
Spine stable=column is assumed unstable, +/- neuro deficits, t risk
for additional injury; Pt must: 1)maintain neutral spine at all times, 2)
bedrest, 3) HOB at zero degrees; 2-3 person turns at all times
Spine stable=confirmed spinal column, +/- neuro deficits, Pt must
maintain neutral spine at all times, Pt can turn independ with neutral
alignment, mob and rehab begins
Spine stable-no restrictions=injury decided stable by surgeon,
patient may do all mvmts of spine w/I comfort limits; Pt may be
taught to log roll with neutral spine
Important to classify SCI b/c: to define level and extent of injury,
gives a baseline, used for prognosis and outcome measure
ASIA:
Sensory exam-light touch and pin prick tested; Grade 0 Pts does not
reliably report being touched, Grade 1 Pt correctly reports being
touched and differentiating b/w sharp and dull BUT describes
feeling of sharpness as different, Grade 2 Pt normal
Hyperpathia=everything feels sharp
Deep Anal Pressure (DAP): if present, Pt has a sensory

incomplete injury ASIA B

Voluntary Anal Contraction=if present indicates motor incomplete
(AIS C)

Motor exam: 10 bilateral myotomes

C5 ABD/elbow flexors, C6 wrist extensors, C7 elbow ext, C8 thumb
ext/ ulnar dev, long finger flexors, T1 finger abductors
Level of lesion=defined as the most caudal segment of the spinal
cord with normal sensory and motor Fx on both sides of the body
Sensory level-most caudal segment w/bilateral score of 2 for both
light touch and pin prick
Motor level-most caudal segment with a grade greater than or equal
to 3 provided ALL segments above are grade 5
Clinical syndromes:
Complete injury=no sensory or motor Fx is preserved in the sacral
segments S4-S5; there may be dermatomes below the sensory
level and myotomes below the motor level that remain partially
innervatedKNOWN as Zone of Partial Preservation, the most
caudal segment with some sensory defines extent of ZPP
Anterior Cord Syndrome=loss of motor Fx, P and temp below
injury level; dorsal column is spared (i.e. kinesthesia, proprioception,
vibration)
Central Cord Syndrome=upper motor and sensory Fx more
impaired than LE; often associated with spinal canal stenosis
Brown Secard= one side of cord more damaged than the other;
IPSILATERAL loss of motor Fx and dorsal column Fx (reason is
they cross in medulla); CONTRALATERAL loss of P and temp
sensation a few levels below the lesion
Conus and Cauda Equina=spinal cord terminates at L1-L2; injuries
at conus can affect both conus and root resulting in a varied neuro

picture; i.e. mixture of UM and LMNL

Prognosis for neuro injuries: pinprick preservation (LE and sacral)
w/I 72hrs is good prognosticator of motor function to return and
ability to walk
SCI Effects on Resp Fx:
C4 is normally the level Pts need to breathe independently
T11 and below, normal vital capacity
Cough Fx: C1-C3 absent, C4-T1 non functional, T2-T4 poor, T5-T10
weak, T11 and below is normal
C2-C7 innervate accessory mm of breathing
T1-T11 intercostals
T6-L1 abdominals
Levels of injury:
C1-C4 Patterns of weakness-paralysis of trunk and UE, probably
diaphragm
Possible mvmts: neck mvmts, slight sh retraction and addn
Role of PT: ROM, spasticity management, neck strengthening,
chest physio, prevent contractures
Major mm innervated:
FULL: C1-C3 SCM, neck extensors, neck flexors
C2-C4 traps
PARTIAL: C3-C5 Lev scap, diaphragm, supraspinatus, infraspinatus
C4-C5 rhomboids
C5: patterns of weakness-sig imbalance around sh girdle, absence
of elbow ext, wrist pronation, ext, flex or any hand/finger movement
Possible mvmt-sh abd, flex, ext, elbow flexion and supination,
scapular add and abd
Full: all of the C4 mm plus diaphragm, rhomboids (C4-5 dorsal
scapular), levator scapula (C3-4 and dorsal scapular)
Partial: Deltoid, biceps, brachioradialis, teres minor (C5-6)

Hand Fx-use wrist splints and universal cuffs

C6: patterns of weakness-no wrist flexion, elbow ext, hand movt
Possible mvmt-radila wrist ext, some horiz adduction, can extend
elbow in some positions using ER of shoulder; have tenodesis grip
which permits a weak grasp w/o any hand mm
Slide board transfer possible, manual W/C possible, FIRST LEVEL
OF SCI to have potential to live in community w/o care
PT role: maximize strength for transfer to functional tasks, teach
trick mvmt strategis, ROM and stretching, prescribe equipment
C7-C8: patterns of weakness-limited grasp and release dexterity d/t
lack of intrinsic mm of hand
Mvmt possible-elbow ext (C7), wrist ext, DIP/PIP flex, MP flex (C8)
Triceps allow independent transfers, manual W/C, indep with
most/all ADLs
Hand function-C8 gives finger and thumb flexors (which are weak)
and no lumbricals
Thoracic paraplegia-intact UE Fx, mainly use W/C
Lumbar paraplegia-more motor sparing more efficient gait,
possible to have functional gait, if conus or cauda equina may have
flaccid bowel and bladder
2 tests for spasticity: Modified Ashworth, Tardieu
Lat spinothalamic- P and temp
Ant crude touch and pressure
Dorsal columns fine touch, stereognosis, vibration
Lateral corticospinal-the 90% that cross in the pyramid motor
Anterior corticospinal-the 10% cross at the level of innervations
motor

Autonomic effects of SCI on Heart and Lungs:

Sympathetic NS-Chain T1-L1, fight or flight, increases HR and BP
and blood flow to skeletal mm, RELAXES bronchial mm (one would
think it would contract them BUT if a bear was chasing you, you
would want the mm to relax to incr O2 supply)
Parasympathetic NS-craniosacral, primary interest in Vagus nerve;
decreases HR and contractility, decr blood flow to smooth mm,
contracts bronchial mm
With Level of injury T6 and above: (in general)
Sympathetic influence is dependent on level of injury (b/c it goes
from T1-L1)
Parasymp influence remains intact and UNOPPOSED via the vagus
nerve in injuries T6 and higher
Limits cardiac output and shunting of blood from inactive to active
ones
Blunting of heart rate often to only110-120bpm
Heart response is d/t vagal withdrawal rather than sympathetic drive
(normally sympathetic would drive up HR but it is no longer intact
there must rely on removing parasymp)
Spinal Shock=temporary suppression of all reflex activity below the
level of injury (24-48 hrs)
Neurogenic shock (T6 and above)=bodys response to sudden
loss of symp. control, therefore parasymp dominance, loss of
vasomotor control; 3 clinical signs are 1) bradycardia, 2)
hypotension, 3) Hypothermia
Rx for hypotension: volume resuscitation (saline), vasopressors (to
counter loss of sympathetic tone)
Health risks with SCI: DVT, pulmonary embolus, HO (2 main
contraindication for Rx are forced PROM and serial casting),

osteoporosis AND
Post traumatic syringomyelia=a formation of an abnormal tubular
cavity in the spinal cord; the dura tethers/scars to the arachnoid
blocking CSF flow, CSF is forced into the spinal cord progressively
enlarging the cyst which compresses the cord and its vascular
supply
Spastic bladder=injuries above the conus, messages will continue
to travel b/w bladder and spinal cord since reflex arc is still intact,
may be triggered by tapping, bladder can be trained to empty on
its own, bladder mngmt is either intermittent catheters or
condom/foley drainage
Flaccid bladder=in conus and cauda equina injuries, messages
dont travel b/w spinal cord and bladder since the reflex centre is
damaged, bladder loses ability to empty reflexively, bladder will
continue to fill AND must be catheterized
Misc info:
CVD is major cause of death in people surviving 30years+
L ventricular myocardial atrophy seen in SCI
100x higher rate of bladder cancer in people with SCI
Spasticity, common clinical characteristics: incrd mm tone or
firmness, incrd stretch reflex, uncontrolled mvmts

01.02.04 Tumour (Can you believe it, they put tumors on the
blueprint twice! Bah!)
tumor = neoplasm, benign or malignant, soft tissue or bone,
develop from or within tissue in a localized area - later they can
spread (mets)
epithelial = carcinoma
mesenchymal (type of undifferentiated loose connective tissue from

the mesoderm)= sarcoma

glial = glioma - most common site of tumors in the brain
lymphoid = lymphoma
hematopoietic= leukemia
melanocytic=melanoma
LUNG carcinoma - squamous metaplasia, squamous diplasia,
carcinoma in situ, invasive casrcinoma
COLON cancer = 2nd cause of death
BREAST = hormonal and genetic risk factors, axillary node disection
PROSTATE = in men over 50 usually, Tx: surgery, external beam
radiation, brachytherapy, androgen deprivation therapy
etiology = viruses, chemical agents, physical agents (radiation,
asbestos), drugs, hormones, alcohol
Tx: surgery, radiation, chemotherapy (usually in kids), biotherapy,
antiangiogenic therapy, hormonal therapy
kids: acute lymphocytic leukemia, non-hodgkins, hodgkins, brain,
small round blue cell, sarcoma (bone based - osteosarcoma,
ewings sarcoma)
Skin Cancer:
Basal Cell Carcinoma (BCC)=most common form of skin cancer,
low risk of spreading, translucent and red in color
Squamous Cell Carcinoma (SCC)=solid skin tumor, often volcano
shaped, high risk for mets
Malignant melanoma=most dangerous form of skin cancer; high
potential for mets
ABCD rule for melanoma- Asymmetry, Border, Color, Diameter

01.02.05 Degenerative neurological/neuromuscular disorders

(e.g., muscular dystrophies, amyotrophic lateral sclerosis,
Parkinson disease)
amyotrophic lateral sclerosis (Lou Gerigs)=a motor neurone
disease and gradual deterioration of BOTH UMN and LMN (may
have both flaccid and spastic paresis), characterized by rapidly
progressive weakness, muscle atrophy and fasciculations, muscle
spasticity, difficulty speaking (dysarthria), difficulty swallowing
(dysphagia), and decline in breathing ability.
amyotrophy-mm fiber atrophy
lateral-lateral column atrophy
sclerosis-sclerosis (harden/thickening) of those axons
Starts peripherally, moves central, mm groups are affected
asymmetrically
sensory system, cognition, bowel and bladder are spared
Rx:resp difficulties, complications of immobility, sy relief

Parkinson disease=chronic neurodegenerative disease,

reduction in dopamine produced by substantia nigra
Possible causes:infectious/post encephalitis (irritation and swelling
(inflammation) of the brain, most often due to infections), drug
induced
Dopamine normally inhibits Ach, without dopamine there is
excessive excitatory output
Motor disturbances: resting tremor, rigidity, akinesia/bradykinesia,
postural instability, impairments of voice, dexterity, balance, gait
Non-motor disturbances- pain, visual/spatial, proprioceptive,
postural hypotension,sleep disturbance, depression, anxiety,
fatigue, dementia
Limiting factors and contraindications to exercise: cardiac or resp
condition, MSK problems, postural hypotension, severe dyskinesia

DMD= issue with mm CT, fat infiltration, hypertrophy (esp in

calves) and weakness, dystrophyn affected (protein), Gowers sign
(difficulty standing up, uses on hand on leg to get up)
mutation in single gene on X chrmomsome
fail to produce dystrophin protein
dystrophin links sarcolemma to actin
mm cells replaced by fat and CT
pregessive symmetric mm wasting
CK levels high (necrotic mm)
normally diagnoses by 5, dead by ~20
gowers and calf pseudohypertrophy
-prox mm weakness, waddling gait, toe walking, lordosis, freq falls,
difficulty standing up and climbing stairs, lower IQ
-pelvic girlde then shoulder, scoliosis
PT: work on strength, independence, advocate
01.02.06 Demyelinating disorders (e.g., multiple sclerosis)
Multiple Sclerosis=an inflammatory disease in which the fatty
myelin sheaths around the axons of the brain and spinal cord are
damaged, leading to demyelination and scarring
typical onset 20-40yo
Sys: fatigue, mm weakness, paraesthesia, optic neuritis or
diplopia, vertigo, bowel and bladder, impaired cognition/memory,
pain, depression
Types:
Relapsing remitting new symptoms or old symptoms may
resurface or worse and it can be full or partial recovery relapses can
be days weeks or months recovery can be slow or instantaneous
Primary progressive there is a gradual worsening of symptoms
overtime may stabilize but no remission

Secondary progressive starts off as relapsing remitting then

steadily worsens
Progressive relapsing --there is a steady progression with attacks
PT Rx: treat vestibular dysfunction, posture, proprioception, core,
stretches
Contraindications and precautions to exercise: heat, fatigue,
pregnancy

01.02.07 Inflammatory/infectious conditions of nervous

system (e.g., meningitis, Lyme disease)
Lyme disease: from a bacteria, Borrelia burgdorferi, through ticks
may occur in stages,
stage 1) localized presentation, erythema, flu like
stage 2) neuro (headache and neck stiffness) MSK and cardiac
(tachy, brady, arrythmia, myocarditis) , may have Bells palsy
3) final stage long term neuro, with arthritis(1/3) and cognitive
deficits
Info: mimics other diseases like MS, fibromyalgia, chronic fatigue
syndrome, guillan barre
Rx: antibiotics to treat
PT management: relieve pain, prep deconditioned patients for
home ex, ed re FITT w/out exacerbating symptoms, improve
strength
meningitis: infectious disease that causes inflammation of
meninges (all 3: pia, arachnoid, dura)
Info: increased risk of infarctions, cortical veins may develop
thomboses, may be block of CSF secondary to scar tissue (can
cause hydrocephaly - excess amount of fluid in the brain) which
causes headache (the CARDINAL SIGN!)

Presentation: can present as acute (hrs-days)

sub acute (2wks plus)
chronic (1mo plus)
types:
1) aseptic (fungus, virus, parasite, can also get with: herpes syplex
2, ebstien barr, lupus)
2) tuberculosis: abcess or edema
3) bacterial: in child or infant is considered a medical emergency
Physical test for meningitis: patient supine, passively flex neck,
Brudzinskis sign: knees and hips will flex
Creutzfeldt Jakob disease=caused by prions; is bovine
spongiform encephalopathy in cows (mad cow disease); occurs in
young adults, is a movement disorder/dementia; it is rapidly
progressive and fatal
Pathology-contracted by ingestion or via the nose; incubates 58yrs
01.02.08 Post-polio syndrome (from Wikipedia) Ive been told
this is good to know...
Poliovirus attacks specific neurons in the brainstem and the
anterior horn cells of the spinal cord, generally resulting in the
death of a substantial fraction of the motor neurons controlling
skeletal muscles. In an effort to compensate for the loss of these
neurons, surviving motor neurons sprout new nerve terminals to
the orphaned muscle fibers. The result is some recovery of
movement and the development of enlarged motor units.[3]
The neural fatigue theory proposes that the enlargement of the
motor neuron fibres places added metabolic stress on the nerve
cell body to nourish the additional fibers. After years of use, this
stress may be more than the neuron can handle, leading to the
gradual deterioration of the sprouted fibers and, eventually, the

neuron itself. This causes muscle weakness and paralysis.

Restoration of nerve function may occur in some fibers a second
time, but eventually nerve terminals malfunction and permanent
weakness occurs.[3] When these neurons no longer carry on
sprouting, fatigue occurs due to the increasing metabolic demand
of the nervous system.[6] The normal aging process also may play
a role. There is an ongoing denervation and reinnervation, but the
reinnervation process has an upper limit where the reinnervation
cannot compensate for the ongoing denervation, and loss of motor
units takes place
01.02.09 Cerebellar disorders
-MS
- hereditary ataxia, Friedreichs ataxia
-neoplastic, metastatic tumors
-infection
-vascular: stroke
-developmental: ataxic cerebral palsy, arnold chiari syndrome
-trauma: TBI
-drugs: heavy metals
-chronic alcoholism; acute alcohol poisoning, effects GABA
receptors
1 archicerbellum lesions: central vestib system, gait and trunk ataxia
2 paleocerebellum lesions: hypotonia, trunk ataxia, ataxic gait
3 neocerebellum: intention tremor, dysdiadochokinesia, dysmetria,
dyssynergia, errors in timing
additional impairments: asthenia (generalized weakness),
hypotonia, motor learning impairments, cog deficits, emotional
dysregulation

01.02.10 Vestibular disorders

cause of dizziness: cardiovascular, neurological, visual,

psychogenic, cervicogenic, meds, vestibular
3 functions of vestibular: 1)gaze stabilization - objects in visual
field stay clear with head movement; 2)postural stabilization maintain balance and equlibrium; 3)resolution of sensory motor
mismatch (proprioception, vestibular and visual)= sea
sickness/motion intolerance
anatomy: semicircular canals x3; horizontal, anterior, posterior=
GAZE/ angular displacement of the head
otolith: utricle- detects horizontal plane motion, and sacculedetects sagittal plane motion; together detect acceleration and
deceleration= POSTURAL
vertigo= the subjective experience of nystagmus (room spinning
around you) - get it with BPPV
dizziness= discrepancy between R and L side, patient cant work out
where they are in space
oscillopsia=blurred vision
antibiotic= GENTOMYCIN = affects vestibular system
UVL-unilateral vestibular loss= peripheral dysfunction: causeinfection (vestib neuritis, labyrinthitis, disease (Menieres- too much
endolymph squishes structures in the ear S&S: low freq hearing
loss, tinnitis), trauma, BPPV)
presentation: dizziness, oscillopsia, imbalance
BPPV(UVL) = benign paroxysmal positional vertigo
- displaced otoconia go to the posterior canal
-presentation: brief transient vertigo when looking up/down, rolling to
that side in bed, sitting to supine
-Dix Hallpike maneuver to test - head 45 deg to test ear, 30 deg ext,
lower from sit to supine and keep for 30 sec +ve test nystagmusdelayed onset, brief and rotary
CIs arthritis, vertebral art insufficiency, 5Ds

Tx: modified Epley maneuver

BVL: causes: toxicity, bilat infection, vestibular neuropathy,
otosclerosis
BVL presentation: very poor balance, NO DIZZINESS
vestibular occular reflex= maintain stable vision during movement;
deficient with unilateral and bilateral vestibular loss
Central vestibular disorders= TIA, Stroke, head injury, brain tumor,
MS,
Ax: direction changing nystagmus
recovery dependent on cortical reorganization
motion sensitivity:
1) sensitivity to movement of the head - position change, repetitive
movement, car train or boat travel
2) sensitivity to moving visual field - visual vertigo, occular dizzness,
reading

01.02.11 Neuropathies (e.g., peripheral neuropathies, complex

regional pain syndrome)
peripheral neuropathy = injury to peripheral N that may be due to
injury or illness
-mononeuropathy, mononeuritis, polyneuropathy, autonomic
neuropathy, neuritis
most common cause is from diabetes. can also be due to injury or
other diseases like : lyme, HIV, shingles, Gullian-Barre

Complex Regional Pain Syndrome (formerly known as Reflex

Sympathetic Dystrophy)= a chronic pain condition believed to be

the result of dysfx in central or peripheral NS

Typical features: changes in the color and temp of the skin over
the affected limb or body part, with intense burning pain, skin
sensitivity, sweating, swelling, stiffness
Stage 1 (0-3 mo) puffy swelling, redness, warmth, stiffness,
allodynia, pos bone scan
Stage 2 (3-6 mo) incrd P and stiffness, firm edema, cyanosis,
atrophy, osteopenia on xray
Stage 3 (6mo plus) tight, smooth, glossy, cool, pale skin; stiffness
and contractures, nail and hair changes; severe osteopenia
PT Rx: prevention and early detection-> early ROM and use, P
and edema mngmt (desensitization, contrast baths, modalities),
education
01.02.12 Developmental/birth injuries (e.g., cerebral palsy,
myelomeningocele, Erbs palsy)
Cerebral Palsy:
CP: non progressive lesion of the brain that occurs before the age of
2, hearing and speech problems, hydroencephalus,
microencephaly, scoliosis, hip dislocation, mental retardation
anoxia, haemorrhage (intraventricular, periventricular leukomalacia most common ishcemic brain injury in premature babies) or brain
damage
risk factors: of mom is older, low birth wt, IVF (invitro fertilization)
mono, di, tri, quad, hemi
spastic: mm stiffness, dec ROM, movements limited to synergies primitive movement patterns- trouble start/stop movement
athetoid: slow twisting wide amplitude movements, changing of
mouth positions
ataxic: abnormal rate, range, force, duration of movements;
difficulty with rapid move, gait, fine motor, balance

dystonic: long sustained involuntary movements and postures

hypotonic: lack of tone, weakness
hip subluxation, spasticity of adductor longus and iliopsoas,
dislocate posteriorly
Tx: seating, botox to adductors, surgery, baclofen pump, tendon
release,
PT: manage atypical mm, habituation, not rehab, positioning,
orthotics, maintain ROM
Sitting modifications-put pummel between legs
Spina bifida: neural tube defect resulting in vertebral and/or spinal
cord malformation
1) spina bifida occulta - no spinal cord involvement, may be
indicated by hair tuft
2) spina bifida cystica - visible or open lesion
a)meningocele - cyst includes cerebrospinal fluid cord intact
b) myelomeningocele - cyst includes CSF and herniated cord tissue
-link between maternal decreased maternal decreased folic acid,
infection, exposure to teratogens (alcohol)
-hydrocephalus
- meningitis
-foot deformities -talipes equinovarus (club foot) esp with L4, L5
level
-latex allergy
Erbs palsy (waiters tip)
- C5, C6, injury in infants, usually come out of birth canal
- can affect: rhomboids, levator scapulae, serratus anterior, delts,
supraspinatus, infraspinatus, biceps, brachioradialis, brachialis,
supinator, long extensors of wrist, fingers, thumb
Rx: immobilization initially, gentle ROM, play exercises

Klumke (claw hand)

-C8,T1
effect: intrinsic mm of hand, flexors and extensors of wrist and
fingers
Median N palsy (ape hand)
- C6-8, T1 median N
- impairment of thenar mm
-cant ABduct and oppose thumb
01.02.13 Dementia, affective and cognitive disorders
Dementia:
Impairment in: memory, language, visual spatial skills, cognition,
personality
Most pts die of pneumonia
-Mini Mental State Exam (MMSI) is m
ost used outcome measure
PT concerns: prevent falls, retain motor activities, reduce
restlessness improve sleeping support for caregivers
01.02.14 Altered level of consciousness (e.g., coma, seizures)
Coma = lowest level of conciousness
- use GCS to assess; will not obey commands, open eyes, or
interpret words
Epilepsy/ seizures- disturbances in CNS
S&S: altered conciousness, motor activity (convulsions), sensory
phenomena, autonomic, cognitive
1)primary generalized seizures - bilateral and symmetrical w/out
local onset
a) tonic-clonic (grand mal) - dramatic, whole body - 2-5 mins
b) absence seizures (petit mal) - brief, almost imperceptible
LOC, come back to full conciousness, no change in posture, can

be up to 100/day
2) partial seizures
a) simple - usually one part of the body
- focal motor = clonic activity on specific area of body
- focal motor with march (Jacksonian) - orderly spread or march
of clonic movements; can progress to whole side
- temporal lobe seizure - episodic change in behavior, complex
hallucinations,
b) complex partial seizures - simple partial seizures followed by
impairment of consciousness

NEUROANATOMY (Admit it, this reminds you of coloring class, who doesnt like colored pens and
pencils)
Ascending Tracts:
Lat Spinothalamic-tests pain, hot/cold of limbs and trunk; receptors are free nerve endings
sharp P is A delta fibers, slow/dull are type C fibers; ascends in lateral white column of spinal cord,
crosses w/i 1-2 segments; finishes in parietal lobe (this lobe integrates sensory information from
different modalities); F HALF THE CORD has lesion, at the level there ipsilateral loss, and
contralateral loss below the lesion
Ant (ventral) Spinothalamic- crude touch and pressure; receptors are Merckel discs and Ruffini
corpuscles and free nerve endings; A delta and A beta; ascends in ant white column; crosses w/i 1-2
segments; finishes in parietal lobe as well; IF HALF THE CORD has lesion, at the level there
ipsilateral loss, and contralateral loss below the lesion

Dorsal columns (medial lemniscu)- 2-pt discrimination, fine touch, sterognosis, vibration; receptors
are pacinian corpuscles (vibration), merckelss disc, meissners (light touch); a beta; fibers cross in the
brain stem; lesion below medulla=ipsilateral loss; lesion above medulla=contralateral loss; finishes in
parietal lobe
Descending Tracts:
Lateral corticospinal=primary motor tract; 90% cross in pyramids (part of the brain stem); synapses in
ant horn cell in grey matter of spinal cord, goes out on an alpha motor neuron, terminates at the
neuromuscular junction; LESION above level of medulla where they cross-->loss of vol mvmt
contralateral to the lesion below level of medulla
Anterior corticospinal=primary motor; 10% that cross at level of innervation; target lower motor
neurons; start in frontal lobe; dont cross in the pyramids;travel in ventral white column; IF LESION is
on one side of the cord->loss of 10% voluntary mvmt contralateral to the lesion
Cerebral arteries:
Internal carotid artery= collateral supply is possible thru ant. and middle cerebral arteries;
deficit=contralat. hemiplegia and hemisensory disturbance, global aphasia (if dominant side), mentally
slow, contralateral homonymous hemianopia, partial Horners syndrome, gaze palsy (eyes to opp
side); is the main supply for ant cerebral a., post CA, middle cerebral a.
Anterior cerebral artery=weakness and sensory loss of contralat limbs, self care problems,
emotional lability
Middle cerebral artery= contralat hemiplegia, hemisensory loss, hemianopia, contralat neglect,
aphasia(impaired language abaility) if on dominant side, apraxia (disorder of motor planning, cant
carry out purposeful movements), impaired hearing, difficulty dressing, may also produce motor
speech dysfunction (Brocas area)
Vertebral artery= two join to form basilar artery; imp branches to watch for strokes PICA (largest
branch of vertebral a.), AICA, PCA
Post cerebral artery (PCA)= supplies occipital lobes; vision problems, CN III palsy, contralateral
hemiplegia, chorea (abnormal invol. mvmts, looks like dancing), hemiballismas (involuntary flinging

mvmts of extremities), hemisensory impairment, contralat homonymous hemianopia, difficulty with

naming and colors
Superior cerebellar artery= supplies cerebellum, limb ataxia, Horners syndrome (droopy eyelid, red
face), contralateral sensory loss
Ant inf cerebellar= supplies cerebellum, ipsilateral limp ataxia, ipsilateral horners, sensory loss,
facial weakness, paralysis of lateral gaze, and contralateral sensory loss of limbs and trunk
PICA=supplies cerebellum, disarthria (poor articulation while speaking d/t motor issues), ipsilateral
limb ataxia, vertigo, nystagmus, ipsilateral horners, sensory loss (p and temp) of face, pharyngeal and
laryngeal paralysis, contralateral sensory loss (p and temp) of trunk, visual sys (paralysis of vertical
eye mvmts and decrd pupillary light reflex)
Brocas(receptive) aphasia= Brocas area is located in the left frontal lobe
Wernickes(expressive) aphasia= Wernickes area is located in the left temporal lobe
Primary somatosensory= located in both parietal lobes, resp for all sensation
Primary visual=located in both occipital lobes
Primary auditory=located in both temporal lobes
Olfactory area=located in both temporal lobes
LEFT CVA mean most muscles on R side of body are affected. Also aphasias, used more reasoning,
numerical and scientific skills, spoken and written language, sign language.
RIGHT CVA means decreased musical and artistic awareness, spatial and pattern perception,
recognition of faces, emotional content of language (speak in montotnous voice), discriminating
smells, damage to right brodmanns area have difficulty differentiating smells
CRANIAL NERVES:
1 Olfactory- does smell; damage to can cause anosomia (inability to detect smells, seen with frontal
lobe lesions)
2 Optic- does vision; damage to can cause homonymous hemianopsia (hemianopic visual field loss
on the same side of both eyes. Hemianopias occur because the right half of the brain has visual

pathways for the left hemifield of both eyes, and the left half of the brain has visual pathways for the
right hemifield of both eyes)
3 Occulomotor- does pupillary reflexes; damage to can cause absence of pupillary constriction or
Horners syndrome (combination of drooping of the eyelid (ptosis) and constriction of the pupil
(miosis), sometimes accompanied by decreased sweating of the face on the same side; redness of
the conjunctiva of the eye is often also present)
4 Trochlear - turns adducted eye downwards
5 Trigeminal- V1 sensory on face, V2 opthalmic branch (touch with cotton), V3 motor mm of
mastication
6 Abducens - turns eye out
7 Facial-facial expression; damage to presents as inability to close eye, droopy corner of mouth,
difficulty speaking; innervates ant aspect of tongue
8 Vestibular- balance, gaze stability, auditory; damage to can cause vertigo, nystagmus, deafness
9 Glossopharyngeal- phonation (voice quality), swallowing; damage to can cause dysphonia (hoarse
or nasal voice); innervates the back of the tongue
10 Vagus- elevates the soft palate and controls position of uvula, gag reflex
11 Accessory (spinal) - innervates traps and SCM; damage to will cause inability to shrug ipsilateral
shoulder (traps) or inability to turn head to opp side (SCM)
12 Hypoglossal - tongue movement; damage to can cause dysarthria or deviation of tongue to the
weak side

SAMPLE LIST OF AREAS OF PRACTICE EVALUATED BY THE PCE

(continued)
01.03 Cardiopulmonary-vascular (15%5%) (This list is not necessarily
exhaustive.)
01.03.01 Heart disease/malformation/injury (e.g., arteriosclerosis,
blunt trauma, tamponade, aortic aneurysm)
valvular heart disease: valves break; failure of valved to open completely
thereby impede forward flow (stenosis), regurgitations(insufficiency): fail
valve to close-reverse blood flow

dilated cardiomyopathy: heart with increased mass, heart has trouble

pumping; risks: third trimester, alcohol
hypertrophic cardiomyopathy: hypertrophied heart, abnormalities in
filling ; young athletes at risk of dying; S&S chest pain, SOB, sudden
cardiac tamponade: compression of the heart due to blood or fluid buildup
in the pericardial sac, may occasionally be the result of puncture wound
through the heart during a procedure
Sys-jugular distension, hypotension, muffled heart sounds
arteriosclerosis=stiffening of the arteries; thickening and loss of elasticity hardening of arteries
artherosclerosis: plaques into lumen and weakened underlying artery;
heart attack, stroke, aortic aneurism; atheromas (plaques, cholesterol or
lipids) form within the intima of artery
aortic stenosis: calcification due to age or lipid accumulation;
consequences: heart murmur, hypertrophy, angina, syncope
aneurism: localized abnormal dilation of the wall of a blood vessel, all
aneurisms may rupture
causes; atherosclerosis, trauma, congenital defects
most common site: abdominal aortic aneurism
aortic dissection: chest pain, dissecting aneurism
Blunt trauma to the heart:
Flail Chest=multiple rib fractures, free floating rib section; Inspiration-flail
segment sucks in->lung, heart, mediastinum shift away, reducing air entry
into the unaffected lung; expiration-flail segments pushes outward->lung,
heart, mediastinum are pushed toward flail segment
Rx-pain control, intubation/ventilation if necessary, O2, airway clearance,
occasionally Sx
pneumothorax= collapse of the lung due to air in pleural space; can be
due to puncture of chest wall or lung spont bursts; hyperresonant

percussion; aspirate or chest tube

1)open - stabbed- air into pleural space; 2)tension - v.serious! - open
wound becomes sealed on expiration, air goes from affected lung into
pleural space - on inspiration air will stay in pleural space, increase
pressure on heart that can stop beating :(
spontaneous pneumothorax- spont rupture of air containing space of lungs
hemothorax- collapse of lung due to blood in pleural space ; less breath
sounds
01.03.02 Myocardial ischaemia and infarction (including surgical
interventions)
Terrible Triad: (3 Is)
1) Ischaemia= Inverted T waves, poor blood supply and hypoxia, occurs
w/i seconds of onset and is REVERSIBLE
2) Injury= Elevated ST segment, myocardial tissue injured during MI
occurs in 20-40mins, IS REVERSIBLE
Depressed ST segment: inj to myocardial tissue, can occur during angina
3) Infarction= abnormal Q waves and QS complexes, can also be tall R
waves
NOT REVERSIBLE, occurs 2hrs after onset
BRADYcardia <60bpm
TACHYcardia >100bpm

Ventricular fibrillation= incompatible with life = requires defib (shock!)

1degree AVblock= caused by prolonged conduction in AV node; P-wave
normal
2nd degree AV block (2 types, mobitz 1 and 2) =block occurs at occurs at
AV node and is transient; PR lengthens until totally blocked then NO QRS
follows a P causing a missed beat (MOBITZ type 1)
MOBITZ type 2: block occurs at bundle branches/bundle of His; abrupt
drop of QRS, but PR interval normal
3rd degree AV block: block at AV node, bundle of His OR bundle
branches; complete disassociation between atria and ventricles, this
produces independent atrial and ventricIular rate (atrial faster)
bundle branch block: in bundle branches and QRS is longer
01.03.03 Heart failure,
CHF: congestive heart failure
-heart is unable to pump blood at a rate required by tissues of the
body, or it does so at elevated filling pressures
- marked by breathlessness and abnormal retention of sodium and water
resulting in edema with congestion of lungs or peripheral circ or BOTH
two types: systolic; deterioration of contractile function
diastolic: cant accommodate ventricular blood volume
Right sided heart failure: common cause: L sided heart failure; damming
of blood in periphery, congestion of the portal system: liver damage and
enlarged spleen, dec flow in periphery, kidney and brain issues, pitting
edema

Left sided heart failure: due to: damming of blood in pulmonary

circulation; SOB when lying, nocturnal gasp of breath when sleeping,
kidney and brain dec perfusion
cor pulmonale: failure of the R side of heart; due to chronic severe pulm
HTN: emphysema and chronic bronchitis (COPD)
ischemic heart disease: caused by myocaridal ishcemia; S&S angina, MI,
sudden cardiac death 90% due to artherosclerosis
angina pectoris: paroxysmal (short and frequent) recurrent episodes of
chest discomfort caused by transient myocardial ischemia: stable,
unstable, prinzmetal(variant) occurs at rest
MI: release troponin and creatine kinase
01.03.04 Tumour (oh, sorry I was wrong, tumors are on the blueprint
THREE times!!!)
LUNG CANCER: 2 types:
1)small cell: 20-25%: develops in bronchial cell mucosa, spread rapidly,
and metastasize early
2) non-small cell:
1-squamous cell - spread slow, arise in central portion near hilum, mets
late
2- adenocarcinoma- 35-40%- slow to mod spread, early mets throughout
lungs brain and other organs
3- large cell - rapid spread, wide spread mets, kidney, liver, adrenals, poor
prognosis
risk: SMOKING YOU IDIOTS!
PT management: manage fatigue
Brain tumours= 2nd to stroke is #1 cause of death (in the brain)
50% chance of survival, kills more ppl than MS and lymphoma, sig cause

of death in kids (intra-tentorial)

1) intracerebral primary= tumors neurons dont proliferate (other cells
around proliferate)
2) intracerebral metastatic = come from lung, breast, prostate compensate by dec brain tissue vol, CSF vol and blood flow vol
3) Intra-spinal- signs: N root pain, worse at night, pain with cough, radicular
pain Tx: surgery or radiation
low grade astrocytoma - benign, good survival if treated early
anaplastic astryocytoma - aggressive
medulloblastomas - freq metastasize to other spots in brain and spine
neuronomas: a) schwannoma - cranial N 8 (vestibular)
S&S headache and seizure, nausea, vomit, cognition and behavior
01.03.05 Pneumonia (primary or post-operative/preventive)
inflammation of parenchyma of lungs (lung tissue); could be caused by 1)
bacterial, viral or fungal, 2) inhalation of toxic chemicals (smoke, dust,
gas), 3) aspiration; normally airborne pathogens
most are preceded by an upper respiratory infection followed by sudden
and sharp chest pain, coughs up green sputum, can also have dyspnea,
tachpnea
Rx: antibacterials/antibiotics, airway clearance techniques, antifungals (if
fungal infection), oxygen support, positioning
Hospital acquired pneumonia has a higher mortality rate than community
typical (sudden onset of symptoms - bacterial often, fever, sputum, physical
sign of consolidation) and atypical (walking- no symptoms, little sputum, min
chest signs)
aspiration: impaired consciousness- alc abuse, after surgery, neuro disease
01.03.06 Atelectasis (primary or post-operative/preventive)
Atelecatsis = collapse of normally expanded and aerated lung tissue at
any structural level involving all or part of the lung; can be patchy,
segmental or lobar distribution
can be due to: 1) blockage of bronchus/bronchiole, lung is prevented from

expanding due to: paralysis, diaphragmatic disorders, mucous or airway

obstruction, hypoventilation; 2) compression due to pneumothorax, pleural
effusion, space-occupying lesion (tumor) which prevents alveoli from
expanding; 3) postanesthetic - effects of anaesthesia and prolonged
recumbency
Presentation: x-ray=shifting of lung structures toward collapse, if involves
entire lobe may show a shadow; quiet breath sounds, possibly dyspnea,
tachypnea, cyanosis
Rx: identify underlying cause, suctioning if d/t secretions, chest tube if d/t
pneumo/hemo thorax or extensive pleural effusion
01.03.07 Adult/infant respiratory distress syndrome (e.g., acute lung
injury)
ARDS: acute respiratory failure with severe hypoxema as a result of
pulmonary or systemic problem; lung injury characterized by increased
permeability on alveolar capillary membrane; leakage of fluid and blood
into lung interstium and alveoli - INFLAMMatory reaction; alveolar edema
and collapse
causes: severe trauma; aspiration; embolism; indirect- happen after viral
infection or pneumonia
key feature on x-ray = WHITE OUT
Rx: PEEP to keep airways open, tackle underlying cause, PRONE position
SARS: severe acute respiratory syndrome = viral resp illness; unlike the
flu, will get pneumonia if you have SARS
abscess: infection leading to necrosis of lung tissue and cavity formation
IRDS: occurs in infants whose lungs have not fully developed; lack
surfactant - helps lungs inflate with air and keeps the sacs from collapsing
risks: prematurity, c-section, multiple preggers, blue baby, stop breathing,
grunts
Tx: deliver artificial surfactant

hypoxemic resp failure (gas exchange failure): arterial hypoxemia - low

blood O2, no inc in CO2, due to: pneumonia, ARDS, obstructive lung
disease, pulmonary embolism
hypercapnic resp failure: too much CO2 in the blood, leads to dec O2 in
the blood, due to dec ventilation (depress of resp ctr by drugs), acute
upper/lower airway obstruction, weak/impaired resp mm, SCI
01.03.08 Asthma
chronic inflamm of the lungs characterized by variable airflow limitation and
hyper-responsiveness; chronic inflamm disorder of airways - airway hyperresponsiveness: recurrent episode; wheezing, breathlessness, chest
tightness, coughing (often reversible unlike COPD)
smooth mm contraction
gas exchange normal, hyperinflated during attack, normal elastic recoil,
exercise capacity reduced, allergic exposure- child or adults
2 categories: 1)extrinsic- allergic or atopic - normally due to allergen; mast
cells release mediators which cause bronchospasm and hypersecretion KIDS more
2) intrinsic- non allergic- hypersensitivity to bacteria, virus, drugs, cold air,
ex , stress - ADULTS more
Rx: prevent triggers, pharmacological - inhaled corticosteroids
exercise induced: smooth mm constrict - upright, lean forward and pursed
lip breathing
01.03.09 Chronic obstructive pulmonary disease (e.g., emphysema,
bronchitis, bronchiectasis)
COPD= chronic resp condition characterized by progressive airway
obstruction that is not fully reversible, gas exchange is normal, always
hyperinflated, decreased elastic recoil, age of onset middle aged to older
adults
Rx: pharmacological 2 focuses, 1) smooth mm relaxation, 2) reduce airway

inflammation
O2 therapy, BUT NOT FOR Pts with pulmonary HTN, CHF
Bronchiectasis: irreversible destruction(necrosis) and dilation of the
airways with chronic bacterial infection; excess mucus, can be caused by
CF, TB, and endobronchial tumors; eventually alveoli replaced with scar
tissue due to chronic inflamm
Rx: bronchodilators, antibiotics, secretion clearance
Bronchitis: excess mucus production
Emphysema=pathological diagnosis, destruction of air spaces distal to the
terminal bronchiole with destruction of alveolar septa which causes merging
of alveoli into larger air spaces-->this reduces the surface area for gas
exchange; loss of airways and capillaries as well; Impact: hyperventilation
put the diaphragm at mechanical disadvantage (its flattened)

01.03.10 Restrictive pulmonary disease (e.g., fibrosis)

interstitial lung disease: stiff, less compliant lungs (not airway obstruction)
S&S dyspnea, severe O2 desaturation, finger clubbing, scarring on CT
Tx: O2 therapy, lung transplant, pulmonary rehab

pulmonary fibrosis: no known cause; TB, inhaling harmful particles,

radiation therapy, meds
idiopathic pulmonary fibrosis: scarring and fibrotic tissue
asbestosis: caused by inhaling harmful particles
pneumoconiosis (coal workers lung):
01.03.11 Tuberculosis
(mycobacterium tuberculosis)
infectious, inflamm systemic disease that affects lungs and may
dissemminate to involve kidneys, growth plates, meninges, avascular
necrosis of hip jt, lymph nodes and other organ.
airbourne particles
S&S: productive cough 3+wks, wt loss, fever, night sweats, fatigue,
bronchial breath sounds
TB skin test: inject in forearm: determine of bodys immune response has
been activated by TB before
medical management: 10 drugs
PT :thorough history and self protection (masks etc)
01.03.12 Pleural effusion
accumulation of fluid in the pleural space due to disease
- this can impair breathing by limiting expansion of the lungs
transudate: commonly due to heart fail - low protein, clear
exudate: formation of fluid by inflammation or disease, caused by infection
or cancer of the pleura - opaque
symptoms: SOB, chest pain, percussion - dull, decreased or ABSENT
breath sounds, may hear a pleural rub
may cause mediastinal shift
01.03.13 Pulmonary edema
increased fluid in extravascular spaces of the lungs; may be increased
hydrostatic pressure due to heart or kidney failure - pushes fluid out of
vessels, or increased alveolar permeability (drug induced, ARDS,

inhalation of noxious gas)

presents as stiffer lungs - inc work of breathing, and dyspnea
classic symptom: cough that produces a frothy pink tinged sputum
on auscultation: FINE CRACKLES
Pulmonary embolus=bloody sputum, dyspnea, incrd RR, SOB, cyanotic,
01.03.14 Cystic fibrosis
inherited autosomal disorder that effects all exocrine glands results in
defective Cl- excretion and Na+ absorption = THICK MUCUS
can get: recurrent chest infections, consolidation, atelectasis and thickened
bronchial walls
diagnose with fam history, sweat test - chloride content of sweat, 2 copies
of abnormal gene
respiratory symptoms most common; also get: finger clubbing,
breathlessness, delayed puberty and skeletal maturity, infertility in males,
symptomatic steatorrhea, diabetes mellitus, liver disease, osteoperosis
Tx: airway clearance techniques, bronchodilators, aggressive antibiotics
01.03.15 Peripheral arterial disease
account for 95% of arterial occlusive disease; artherosclerosis is the
underlying cause
Signs and symptoms-occur distal to site of narrowing or obstruction;
intermittent claudication, acute ischemia (pallor, pain paralysis, pulseless),
ulceration and gangrene, skin (shiny, thin, hairless); often occurs in feet
Outcome-decreased mobility d/t pain and loss of function or limb
PERIPHERAL VASCULAR DISEASE: (same as peripheral artery
disease)
-artherosclerotic obstruction of iliac, femoral, and politieal arteries in the legs
- feel pain during physical activity, most often in the calf
-pathologic conditions of blood vessels that supply extremities and major
abdominal organs

underlying cause: artherosclosis

S&S: intermittent claudication, dec pulses, uclers, cool skin, limit mobility,
pain or loss of function of limb
01.03.16 Venous disorders
THROMBOPHLEBITIS-partial or complete occlusion of a vein by a
thrombus with secondary inflammation
superficial or deep
DVT - can become pulm emboli S&S: tender calf (d/t thrombus in calf vein),
fever, test with Homans; risk is it may become a PE
CHRONIC VENOUS INSUFFICIENCY-inadequate venous return over a
prolonged period
cause: DVT trauma, obstruction by tumor,
damaged or destroyed valves lead to venous stasis, can get edema,
thickening brown skin and ulcers
Varicose veins=faulty valves cause abnormal dilation of veins leading to
twisting and turning of the vessel; at risk for thrombosis
************
Assisted Cough: Contraindications are ruptured diaphragm and inf vena
cava filter

Volumes (I dont even know how many times Ive memorized this diagram
over the years)
TIDAL VOLUME (TV): Volume inspired or expired with each normal breath.
(500mL)
INSPIRATORY RESERVE VOLUME (IRV): Maximum volume that can be
inspired over the inspiration of a tidal volume/normal breath. Used during
exercise/exertion. (2-3L)
EXPIRATORY RESERVE VOLUME (ERV): Maximal volume that can be
expired after the expiration of a tidal volume/normal breath.(1L)
RESIDUAL VOLUME (RV): Volume that remains in the lungs after a
maximal expiration. CANNOT be measured by spirometry(1L)
Capacities:
INSPIRATORY CAPACITY ( IC): Volume of maximal inspiration:
IRV + TV (2.5L-4L)
FUNCTIONAL RESIDUAL CAPACITY (FRC): Volume of gas remaining in
lung after normal expiration, cannot be measured by spirometry because it
includes residual volume:
ERV + RV(2L)
VITAL CAPACITY (VC): Volume of maximal inspiration and expiration:
IRV + TV + ERV = IC + ERV (3-4.5L)

TOTAL LUNG CAPACITY (TLC): The volume of the lung after maximal
inspiration. The sum of all four lung volumes, cannot be measured by
spirometry because it includes residual volume:
IRV+ TV + ERV + RV = IC + FRC (4-6L)

DEAD SPACE: Volume of the respiratory apparatus that does not

participate in gas exchange, approximately 300 ml in normal lungs.
--ANATOMIC DEAD SPACE: Volume of the conducting airways,
approximately 150 ml
--PHYSIOLOGIC DEAD SPACE: The volume of the lung that does not
participate in gas exchange. In normal lungs, is equal to the anatomic dead
space (150 ml). May be greater in lung disease.
FORCED EXPIRATORY VOLUME in 1 SECOND (FEV1): The volume of air
that can be expired in 1 second after a maximal inspiration. Is normally 80%
of the forced vital capacity, expressed as FEV1/FVC. In restrictive lung
disease both FEV1 and FVC decrease , thus the ratio remains greater than
or equal to 0.8. In obstructive lung disease, FEV1 is reduced more than the
FVC, thus the FEV1/FVC ratio is less than 0.8.

CARDIAC REHAB
3 goals: 1) restore optimal function
2) prevent progression of underlying processes
3) reduce the risk of sudden death and re-infarction
S&S of cardiopulmonary disease: pain in chest, neck, jaw, arms; SOB at
rest or mild exertion; dizzy or syncope; orthopnea (SOB while lying flat) or
nocturnal dyspnea, ankle edema, palpitations or tachycardia, intermittent
claudication, known heart murmur, unusual fatigue
exercises to avoid: NO VALSALVA! (or Hulk imitations); extensive upper
body activity; isometric/ static exercises;
phase 1: inpatient

phase 2: outpatient 12 week program

phase 3: in the community
cardiothoracic index=size of heart in relation to thorax

01.04 Multisystem (15%5%) (This list is not necessarily exhaustive.)

01.04.01 Episodic disease (e.g., oncology, HIV/AIDS, autoimmune
disorders, rheumatic diseases, haemophilia)
Oncology: (the Alliance is being sneaky this time, theyre calling it
oncology instead of tumors)
Staging cancer-TNM: Tumor (extent/spread), Nodes (lymph), Mets (distant
ones)
PT relevant Rx: PTs can teach Pts to stretch mm when radiation therapy
begins to mitigate occurrence of contactures
Physical activity:
During Rx-improves QOL, physical Fx, fatigue; Precautions-severe
anemia, immune compromised, severe fatigue
Following Rx-goals are to have appropriate weight, be physically active,
healthy diet
ACSM guidelines-prescription must be individualized according to cancer
survivors pre-Rx aerobic fitness, medical comorbidties, response to Rx,
and the neg side effects of Rx
Clinical presentation of cancer survivors: fatigue, myalgia, arthralgia, bone
health, peripheral neuropathy (impact on balance), deconditioning
Palliative Care: Goals are to provide comfort, support, maximize
independence; PTs can help with respiratory, stress reduction, education

AIDS: acquired immunodeficiency syndrome

-caused by hiv1 or 2; loss of immune system function; can get pneumonia,
Tb, malignancy, encephalitis, meningitis, dementia, herpes zoster
-reduction of CD4+ helper T cells
transmission through contact with infected body fluids: blood, saliva,
semen CSF, breast milk, vaginal/cervical secretions NOT:urine, sweat,
vomit
- diagnosed with clinical findings and systemic evidence
-AIDS - related complex (precursor to full blown AIDS)
-lab evidence: HIV -1 antibody test, CD4 cell count 200-500/ml
(normal = 800-1200/ml
- no cure
-med interventions = 1)multidrug antiviral therapy 2) symptomatic
treatment: maintain nutrition, maintain functional mobility, education,
- PT goals: use precautions when working, exercises- mod aerobic,
strength, avoid exhaustive, acute=reduce to mild levels, activity pacing,
energy conservation, stress management
Autoimmune disorders:
Guillan Barre Syndrome=antibody mediated demyelination of schwann
cells; see a generalized inflammatory response
Presentation: initially see a socks and gloves pattern of areas that initially
go numb; is perfectly symmetrical; maximal weakness occurs in 2-3 weeks
and takes months to recover; absent deep tendon reflexes
Rx: plasmapheresis, Iv administration of immunoglobulin (decreases the
immune response)
PT Rx: early on - prevent ulcers (posning), early PROM; later - mm
strength
Connective tissue disorders that may involve skin as well as organs:
Lupus erythematosus-can involve kidney, CNS, cardiac, pulmonary; on
skin may find BUTTERFLY rash, localized erythema and edema, alopecia

(loss of hair), photosensitivity, mucosal ulcers, Raynauds (fingers are cold

sensitive), effusion in joints; associated with positive serum antinuclear
antibodies (ANA)
Sclerodema-autoimmunity provokes massive fibrotic tissue response
which may lead to joint contractures, pulmonary fibrosis, GI dysmotility
(esp esophagus)
Dermatomyositis and polymyositis=inflam connective tissue disorders
characterized by proximal limb girdle weakness, often w/o P.
Dermatomyositis- affects both skin and mm; is also assocd. w/ a
photosensitive skin rash, purplish erythematous eruption over face (esp
upper eyelids), hands, forearms
Polymyositis- mm only
Haemophilia:
Type A-is the most common of hereditary clotting factor deficiencies
- X-linked recessive (Males have the condition, and the gene that causes it
is carried by women)
-If the mother carries the haemophilia gene and the father does not have
haemophilia: A male child will have a 50:50 chance of having haemophilia.
A female child will have a 50:50 chance that she will carry the haemophilia
gene.
If the father is affected by haemophilia and the mother is not a carrier:
A female child will be a carrier (she is known as an obligate carrier).
A male child will not be affected by the haemophilia gene and cannot pass
haemophilia onto his future children.
Presentation:profuse post circumcision bleeding, joint and soft tissue
bleeding, excessive bleeding, operative and post-traumatic hemorrhage
Signs and Symptoms
Big bruises;
Bleeding into muscles and joints, especially the knees, elbows, and
ankles;
Prolonged bleeding after a cut, tooth removal, surgery, or an accident.
Serious internal bleeding into vital organs, most commonly after a

serious trauma
Bleeding in the joints is the most common problem.
The symptoms of a joint bleed are as follows:
Tightness in the joint with no real pain.
Tightness and pain before any bleeding
Swollen and hot to touch, hard to move
All movement lost, severe pain
Bleeding slows after several days when the joint is full of blood
There can be disabling arthritis if this is not treated.
Rx: recombinant factor VIII infusion; note, before VIII available many Pts
received blood products in the 80s and died of AIDS and many got Hep C
Desmopressin (or DDAVP) can be used for sufferers of mild haemophilia
Rheumatic diseases:
Rheumatoid arthritis: synovitis is the main feature; synovium becomes
swollen and cells proliferate->a dense cellular membrane (pannus)
spreads over articular cartilage and erodes the underlying cartilage and
bone; over time the pannus may extend to the opposite articular surface
creating
1) fibrous scar tissue, 2) adhesions, 3) bony ankylosing; immobility and
consolidation (bones form a single unit) of a joint; bones can become
osteopenic and ligaments and tendons become damaged or ruptured;
surrounding mm deteriorate leaving joint unstable and prone to deformity
symmetrical pattern
Criteria for RA:
morning stiffness>1hr (6 weeks), arthritis of >/= 3 joints (6weeks), arthritis
of hand joints, symmetric arthritis (6weeks), rheumatoid nodules, serum
rheumatoid factor, radiographic changes
Have an abnormal antibody HLA-DR4 in 80% of people with RA
Increased risk:after mother gives birth, cigarette smoking, pollution
Clinical features:pain, fatigue, stiffness (decreased ROM), swelling, joint
deformity, mm atrophy

Management: Meds (DMARDs, NSAIDs, tylenol, cortisone)

Rehab: Acute phase-energy conservation, ice, splints, gentle ROM, NO
STRETCHING as it may stretch the synovial membrane and cause
irreversible damage
Chronic phase-relieve pain, i.e. modalities, splints, exercise (gentle ROM),
relaxation/rest; Reduce stiffness-gentle ROM, aquatic ex, heat; functional
exs, prevent deformity
Inflam conditions:-pain worse in morning, morning stiffness greater than
1hr
Non-Inflam condition-yes, after used, morning stiffness less than 30min
Joint count assessment=an indicator of the disease activity of RA
1) Joint effusion,
2) joint line tenderness
3) stress pain
Commonly affected joint in RA:
1)atlanto-axial joint (esp transverse lig)
Signs and symptoms of atlanto axial subluxation-clunking in repositioning
in Sharp Purser test, dysphagia, dizziness, blurred vision
2) TMJ-end stage may result in fusion of open bite
3) Shoulder-humeral head moves superiorly
4) AC joint
5) elbow-loss of extension, i.e. flexion deformity; superior radioulnar joint
commonly involved->erosion of radial head
6) hip (groin P, flexion deformity)
7) knee-bakers cyst, flexion deformity, valgus deformity, quad wasting
RHEUMATIC Cont:
Hallux valgus- 1st MTP synovitis, big toe is lateral, lig laxity and erosion,
sublux-> dislocation, prox phalanx drifts lat, causes pronation of midfoot
MTP subluxation- synovitis, displacement of the flexors, unopposed

extensors pull the prox phalanx into hyperext, metatarsal head prolapses
and get dislocation and lat drift of toes: Sign = callouses
Claw toe- MTP synovitis, MTP ext, PIP+DIP flex, often all toes except big
toe
Hammer toe--MTP and PIP synovitis, usually involves 2nd toe, flex of PIP
and hyperext of DIP (similar to boutinniere)
Mallet toe-- flex of DIP, affects longest toe
Swan neck (rheumatiod) flex of MCP(not always), hyperext of PIP, flex
DIP
Boutinniere- zig zag deformity - MCP hyperext (not always), flex of PIP,
hyperext of DIP
Gout=Genetic disorder of purine metabolism, inc serum uric acid
(hyperuricemia). Acid to crystals and deposits into jts, most= knee
and great toe of foot
Meds: NSAIDS, cox2-inhibitors, corticosteroids, ACTH
PT goals: injury prevention ed, fast intervention
Osteoarthritis=release of enzymes and abnormal biomechanical forces
cause fibrillation and damage of articular cartilage leading to cartilage loss;
increase in bone turn over->osteophytes
7 risk factors: age, sex (more women), genetic, obesity, physical inactivity,
injury, joint stress(occupation)
Dx by x-ray finding: 4 main features-1)joint space narrowing,
2)osteophytes, 3)subchondral cysts, 4)subchondral sclerosis
Sources of pain in OA-bone, soft tissue, inflammation, mm spasm
4 questions to diagnose OA: 1) pain most days in last month, 2) pain
over the last year, 3) worse with activity, 4) relieved with rest
3 tests indicative of OA of the knee: 1)flexion contracture, 2)abnormal
gait, 3)swipe test or patellar tap
Main joints it affects:
Spine-osteophytes in facet jts of l-spine can cause stenosis

Shoulder and Elbow-uncommon

Wrist-uncommon unless scaphoid fracture or avascular necrosis
Hand-PIP is Bouchard node, DIP is Hebernens node; CMC joints (esp
thumb)
Knee-most common jt affected by OA, varus, flexion contracture, crepitus
Hip-walk with trendelenburg, groin pain, osteophytes, flexion deformities
Types of FAI (femoral acetabular impingement):
Cam -decrease or absent waist of the jx of femoral neck and head; during
hip flexion the abnormal femoral head drives into acetabulum, most
common in young men
Pincer-d/t abnormal acetabulum that provides excessive cover of the
femoral head, retroverted or deep acetabulum; impingement occurs when
femoral neck pushes against overarching acetabulum; more common in
women age 30-40 years
Ankle-uncommon
Foot-first metatarsal joint; osteophytes can form at this jt causing hallux
valgus and rigidus, may have bunions
Rx: First line-exercise, weight loss, acetaminophen
Spondyloarthritis:
dont have a rheumatoid factor, common in the spine
Common features-inflammation in the spine (spondylitis and sacroilitis),
synovitis (affecting peripheral joints) typically unilateral, inflammatory of the
eye (iritis/uveitis and conjuctivitis), no rheumatoid factor (seronegative),
can be hereditary HLA-B27
Just flipping through this document before sharing it, is it me or is it
loooooong.
Psoriatic Arthris-Pt has psoriasis, M=F, can begin with kids,
Dactylitis=sausage like fingers d/t swelling; Enthesitis=usually in heels and
back

Chronic, erosive, inflamm most=digit jts and axial skeleton

Meds: acetaminophen, NSAIDs, DMARDs, corticosteroids, biological
response modifiers
PT goals: jt protections strategies, maintain jt mechanics, endurance
Enteropathic Spondylitis- assocd with ulcerative colitis (affects just the
lower half of the bowels) and Crohns disease (affects the whole digestive
system, its worse), may affect spine and SI joint
Reactive arthritis-triggered by infection (possibly STI) in bowel or GI tract,
hot swollen joints, may go away and come back
Ankylosing spondylitis-stiffness/fusing of the spine by inflammation,
disease of young adults; associated with genetic marker HLA B27
Features: MSK-sacroiliitis, enthesitis, synovitis; other signs-eyes, bowels,
lungs, heart
The hallmark sign is sacroiliitis; may also feel deep, dull pain in buttuck
area d/t inflammation of SI joint; fusion can occur over time
Enthesitis-inflammation of entheses leading to bony erosion and
overgrowth;
common sites are spine, hip, peripheral regions; syndesmophytes (bony
spurs on 2 sides of a joint) can also cause bony fusion and rigidity
(entheses=where tendons, ligs, and joint capsule attach to bone)
Synovitis-usually affects peripheral jts, commonly shoulders, hips, knees,
ankles
Clinical criteria of AS=LBP and stiffness for more than 3 months that
improves with ex but is not relieved with rest, limitation of motion of L-spine
(d/t pain, tissue contractures, mm guarding, fusing), limitation of chest
expansion (diaphragmatic breathing pattern), decreased strength d/t
disuse, joint effusion, and pain, flexion posture, fatigue d/t disease process,
cardiac involvement, decrd vital capacity
Quick overview:

onset before 40, low back pain, sacroiliitis, kyphotic deformitiy Csp, Tsp,
dec lumbar lordosis, M>F
Meds: NSAIDS, corticosteroids, cytotoxic, tumor necrosis factor
Diagnosis HLA-B27
PT goals: trunk flexibility, endurance, increase resp function (relaxation)
Physical Ax-posture (tragus to wall), lateral trunk flexion, trunk flexion
(modified schobers), trunk extension (smythe test), trunk rotation, chest
expansion, cervical mobility
Spondyloarthritis Rx:
Meds-DMARDs, NSAIDs, corticosteroids, biologics
Physical Management-control/decrease inflammation, P management,
reduce stiffness/increase ROM, posture correction, increase mm strength
and endurance, increase cardio
Juvenile Idiopathic arthritis=signs and Sys must be present for 6 weeks
to make diagnosis, avoid resisted exs with active disease, P does not
indicate joint damage; improved strength (non-active period of the disease)
reduces P and increases stability
complete remission in 75% of kids if occurs before age 16
Sys-joint pain, stiffness, warm swollen joints, eye issue (uveitis), HLAB27, fatigue, Erythrocyte sedimentation rate, rheumatoid factor
Inflamm back pain-usually prolonged, >60min, max P and stiffness in
early AM, chronic, age of onset 12-40 years, radiographs show sacroilitis,
syndesmophytes, and spinal anklosis
Mechanical back pain-minor <40min, max P and stiffness late in the day,
activity worsens Sys, acute/chronic, 20-65 yrs, radiographs show
osteophytes, disc space narrowing, misalignment
01.04.02 Metabolic disorders/conditions (e.g., diabetes)
DIABETES

Hypoglycemia=dizzy, nausea, weak, sweating profusely (this rules out

orthostatic hypotension)
Hyperglycemia=blurred vision, fatigue, thirst, frequent urination

01.04.03 Chronic pain/fibromyalgia

Chronic pain= pain that persists past the normal time of healing
Chronic fatigue syndrome=may be viral
Dx: by exclusion; persistent or relapsing fatigue for at least 6 months, not
resolved with bed rest, reduces daily activity by at least 50%
Rx: Analgesics, anti-inflamm, NSAIDS, nutrition, psych support
PT Rx: check ex tolerance
Fibromyalgia=chronic pain syndrome affecting mm and soft tissue (nonarticular rheumatism)

Etiology: unknown
Sys-headaches, sensitivity to stimuli, fatigue, myalgia (mm pain),
generalized aching, sleep disturbances
Anxiety and depression are common; more common in women
11 of 18 points: Occiput (suboccipital insertions), low cervical (ant aspects
of intertransverse spaces at C5-C7), Traps (mid-pt of upper border),
Supraspinatus (at origin), Second rib (lateral to 2nd costochondral
junction), lateral epicondyle, gulteal, greater trochanter, knee (at medial fat
pad proximal to joint line)
Rx:anti-inflamm, mm relaxants, pain meds, psycholgical support, nutrition
PT Rx: energy conservation, aquatic therapy
01.04.04 Lymphodema= lymph accumulating in tissues
2 types:
Primary-rare, inherited condition caused by problems with the dvlpmt of
lymph vessels
Secondary-d/t identifiable damage to or obstruction of normally functioning
lymph vessels and notes;ex-Sx, radiation, parasitic infections
Fx of lymph system: removal from body tissues of fluid, proteins, bacteria,
viruses
smooth mm in walls contract to move lymph
Risk factors: radiation, age, axillary node dissection, arm infection/injury,
obesity, weight gain since operation
Prevention: skin care (avoid trauma/injury to reduce infection), activity (and
maintain body wt), avoid limb constriction, avoid extreme temperatures
Role of PTs: exercise (weight loss), education on what to avoid (BP cuffs),
educating on signs and symptoms
Rx:compression garments, manual lymph drainage, manage risk factors
[Cording=tight fibrous bands that go from axilla to elbow or wrist and
restrict ROM]
01.04.05 Sepsis

body has severe response to bacteria or other germs; whole body

inflammatory state; have SIRS and a proven infection
SIRS= systemic inflammatory response syndrome; whole body
inflammatory state
- diagnose with body temp, HR, RR, WBC count
01.04.06 Obesity
Excess body fat; BMI=weight (kg)/height (m)^2
overweight BMI= 25-29.9
OBESITY= BMI > or = to 30
morbidly obese > or = to 40
skin caliper test fat greater than 1 inch is excess
health risks associated with obesity: HTN, hyperlipidemia, type 2 diabetes,
cardiovascular disease, glucose intolerance, gallbladder disease, menstrual
irreg, infertility, cancer
abdominal obesity=independent predictor of morbidity and mortality
cause: excess calorie intake, psych/enviro factors, genetic factors, endocrine
and metabolic disorders
lifestyle modifications, behavior therapy, pharmacology, surgery
exercise=moderate intensity 40-60% progress to 50-70% HRR, 5-7d/wk, 4560mins, circuits or aquatics
01.04.07 Pregnancy and post partum conditions
NORMAL = gain 20-30lbs
PT can teach relaxation and breathing ex, provide ed
postural changes = kyphosis, forward lean in Csp, lumbar lordosis
balance change, lig laxity (hypermobile SI - teach jt protections
teach exercises to maintain abdominal and pelvic floor mm
Diastasis recti abdominis= lateral separation or split of rectus
abdominus; separation from midline >2cm sig; ab wall dec support; get
back pain

pelvic floor disorders= due to stretching; can lead to partial or total organ
prolapse
- cystocele : herniation of bladder into vagina
- rectocele: herniation of rectum into vagina
- uterine prolapse: bulge of uterus into vagina
pelvic pain, urinary incontinence, pain with sexual intercourse
PT= pelvic floor mm ex, postural re-ed,
low back and pelvic pain
PT: teach body mechanics, balance activity and rest, massage, modalities
for Pain
SI dysfunction
-post pelvic pain, buttock pain, may radiate to leg, pain with sit, walk, stand
PT: external stabilization, ed on no single leg WB
varicose veins
PT elevate extremities, elastic stockings
preeclampsia= preg induced, acute HTN after 24wks gestation
PT evaluate for S&S: HTN, edema, headache, visual disturb, hyperreflex
Csection
PT: TENS for incision pain, breathing ex, gentle ab ex, pelvic floor ex,
postural ex, ambulation, prevent incisional adhesions (scar massage)

01.04.08 Burns
Superficial

Partial Thickness
Full thickness
Zones:
Zone of coagulation=pt of maximum damage, irreversible tissue loss
zone of stasis=decrd tissue perfustion, potentially salvageable
zone of hyperemia=increased perfusion, will recover unless sepsis occurs
Effects of burns:
CV: Increased capillary permeability->interstitial edema; peripheral
vasoconstriction; hypovolemia; myocardial depression->hypotension and
decreased organ perfusion
Resp:bronchoconstriction, ARDS
Metabolism: increased 3x
Immune system: compromised
Renal: b/c of loss of fluids, vasoconstricsion, decrd GFR, incrd myoglobin
gets processed by kidneys and can block tubules
Signs of inhalation injury: singed eyebrows/nasal hairs/burnt face, black
oral/nasal discharge, swollen lips, hoarse voice, abnormal oxygenation, Hx
of being enclosed in closed room
Inhalation injury process:w/i 24hrs upper airway obstruction/pul edema; 2448 just pulmonary edema; 48 hrs plus bronchiolitis, alveolitis, pneumonia,
ARDS
Mngmt of inhalation injury: early mobilization, breathing exs, post drainage
Rx of burns: first 2-3 weeks AROM and PROM to maintain range,
positioning, edema management, encourage ambulation, scar
management BECAUSE
as early as 1-4 days can get a scar tissue contracture
Contraindications to exercise: exposed joint, fresh skin graft, DVT,
compartment syndrome
Sx:
Split Thickness Skin Graft=uses skin graft, stitched, glued or sutured in
place; immobile for 5 days

Full Thickness Skin Graft=skin transplant

Skin graft Rx: scar massage, sun protection, ROM, pressure garments,
strengthening can begin in 3-4 weeks
Scar from burns: 3 stages 0-4 weeks Fibroblastic/proliferative, 4-12 weeks
early remodeling, 12-40 weeks late remodeling/maturation
Factors influencing scar: age, smoking, type of tissue, nutrition
Therapeutic mngmt of scar: pressure garments, massage, moisture
01.04.09 Wounds/ulcers
Ulcers
Causes: Pressure (round sore), shearing (abrasion/scrape), friction
(blisters can be a sign), deep tissue damage from banging or bumping
(purple or bruising)
4 Stages of wounds: 1 reddened (non blanchable), 2 skin is broken, small
crater, 3 deep crater,might be infected, may be black, dead tissue 4 deep
through mm to the bone or joint

01.04.10 Skin conditions (e.g., dermatitis, psoriasis)

Psoriasis=an autoimmune disease that affects the skin. It occurs when the
immune system mistakes the skin cells as a pathogen, and sends out
faulty signals that speed up the growth cycle of skin cells; i.e profound
cutaneous inflammation and epidermal hyperproliferation
Plaques frequently occur on the skin of the elbows and knees, but can
affect any area, including the scalp, palms of hands and soles of feet, and
genitals. In contrast to eczema, psoriasis is more likely to be found on the
outer side of the joint.
Fingernails and toenails are frequently affected (psoriatic nail dystrophy)
and can be seen as an isolated sign. Psoriasis can also cause
inflammation of the joints, which is known as psoriatic arthritis. Between

1030% of all people with psoriasis also have psoriatic arthritis

5 Cardinal morphologic features: 1) placque (raised lesions), 2) well
circumscribed margins, 3) bright salmon red color, 4) silvery micaceous
(shiny) scales, 5) symmetric distribution
Complications: pruritus (desire to scratch), severe psoriasis is associated
with increased risk of CVD and shortened lifespan
Rx: Topical creams containing glucocorticoids, tars, vitamin D or A;
phototherapy with UV light; systemic therapy with immunosuppressive
drugs such as methotrexate or cyclosporine; systemic prednisone usually
not used
Eczema (means boiling over)=is a form of dermatitis, or inflammation of
the epidermis (the outer layer of the skin); is an itchy, red, scaly disorder
Two types:
1) Atopic dermatitis (endogenous eczema)-is an intensely itchy
inflammatory skin disorder associated with atopy (predisposition toward
developing certain allergic hypersensitivity reactions): asthma, hayfever,
and allergic conjunctivitis
Presentation: itchiness is the most outstanding feature; can also be
erythema, lichenification (thickening skin lines), excoriations (scratching or
picking at skin)
3 Phases:
Infantile (2mo-2years)-facial and extensor distribution
Childhood-dry skin, flexural distribution (popliteal and cuboid fossa)
Adult-atopic dermatitis generally improves with age, less flexural
distribution, primarily affect the hands
Rx: avoid irritating factors, moisturizers, topical glucocurticoids, oral
antihistamines, UV
2) Contact dermatitis (exogenous eczema)
a) allergic contact dermatitis-immune hypersensitivity to an allergen in
contact with the skin (e.g. nickel, poison ivy)
b) irritant contact dermatitis-contact of skin with something that primarily

causes direct local irritation (harsh detergents, chemicals)

Seborrheic dermatitis (dandruff)=occurs in areas of higher sebaceous
gland activity (oily areas) such as scalp, face, central chest and back; is
probably due to an excessive immune response to a yeast; Rx: antifungals
Associated disorders: seen frequently in PD patients and Pts with
neurologic disorders that decrease their mobility (eg stroke, TBI, SCI), as
well as HIV infection

01.04.11 Tumours (covered elsewhere)

01.04.12 Competing diagnoses (management of 1 diagnosis is

changed by 2 diagnosis)
Graves disease= hyperthyroidism, autoantibodies stimulate the thyroid
(TSH receptor), T3 and T4 (these inhibit the secretion of TSH) will be high,
affects men>women
Sy:fever, wt loss, exercise intolerance, goiters, bulging eyes
(exophthalmos), tachycardia, decrd fertility
Rx: betablockers for HR, anti-thyroid drug therapy, radioactive Iodine, Sx
removal of thyroid
Hashimoto thyroiditis= hypothyroid, autoimmune destruction of thyroid
gland, T3 and T4 are low, TSH is high; affects men>women
Sy: wt gain, cold intolerance, round puffy face, bradycardia, constipation,
depression
Rx: thyroid hormone replacement
Addisons=autoimmune process against the adrenal cortex, fatal if not
treated, great prognosis if treated

Sys-weakness, fatigue, anorexia, hyponatremia, hypoglycemia,

hyperpigmentation
Rx-replace missing adrenal hormone with aldosterone and cortisol
Cushings disease=chronic gluccocorticoid (cortisol) excess (usually
iatrogenic in Pts taking them for immunosuppression, can also get from
cancer of adrenal gland
Sys-moon face, central obesity, abdominal striations
Rx: surgical if caused by tumor (tumor in pituitary or adrenal gland)

PAEDS:
Slipped capital femoral epiphysis=growth plate slips off the head of the femur
Developmental milestones Sullivan pg 247
Ifnt reflexes diminsih/gone 2-6mo

PRACTICAL COMPONENT
LIST OF FUNCTIONS EVALUATED BY THE PCE
(This list is not necessarily exhaustive.)

02.01 ASSESSMENT AND EVALUATION (35%5%)

Data Collection
Obtain the following client information and interpret implications for
intervention:
02.01.01.01 Past and current history (e.g., medical, surgical, developmental,
psycho-social, current status/symptoms, concurrent and past treatments)
02.01.01.02 Results of tests and diagnostic procedures (e.g., imaging,
laboratory tests, functional capacity evaluation, pulmonary function tests)
02.01.01.03 Medications (past and current)
02.01.01.04 Home/work/leisure/play environments, family and community
support systems and resources
02.01.01.05 Client expectations and goals
Tests/Measurements
02.01.02.01 Select and justify evaluation/assessment procedures based on
client needs and expectations, responses, and best available evidence
02.01.02.02 Perform selected physiotherapy evaluations/assessments in a
safe and accurate manner including handling all monitoring devices,
equipment, or lines attached to or around client
02.01.02.03 Examine and evaluate neuromusculoskeletal, neurological,
cardiopulmonary-vascular, integumentary and other systems using
appropriate tests and measures
02.01.02.04 Examine and evaluate mental status (e.g., cognition, memory),
hearing, and visual acuity as they relate to clients participation in
physiotherapy programs and attainment of goals
02.01.02.05 Screen for contraindications and precautions for treatment
planning (e.g., medical issues; psychosocial issues; safety issues; language
comprehension; educational needs; risk factors and mediators)
02.01.02.06 Observe clients response to the physiotherapy
evaluation/assessment and respond accordingly
02.01.02.07 Assess client need for assistive, adaptive, and protective devices
(e.g., positional supports, mobility aids, orthotic or prosthetic devices)

LIST OF FUNCTIONS EVALUATED BY THE PCE (continued)

(This list is not necessarily exhaustive.)
02.02 INTERPRETATION, PLANNING, INTERVENTION, AND REEVALUATION (50%5%)
Data Interpretation
02.02.01.01 Develop a list of physiotherapy differential diagnoses and
determine the most probably cause of clients problem
02.02.01.02 Identify indications, barriers, precautions, and contraindications
to treatment, using the best available evidence
02.02.01.03 Determine need for physiotherapy treatment, collaboration,
consultation, or referral
Prognosis
02.02.02.01 Determine the potential for recovery or decline with or without
physiotherapy intervention
Goal Setting and Care Planning
In consultation/collaboration with the client and family:
02.02.03.01 Establish short-and long-term goals that are client-centred; and
specific, measurable, attainable, relevant and time-based (SMART)
02.02.03.02 Identify which aspects of intervention involve consultation,
collaboration, delegation, and/or referral
02.02.03.03 Prioritize clients problems and associated treatments within the
context of available resources
02.02.03.04 Select and justify treatments and procedures, using the best
available evidence and considering environmental factors, safety factors,
family/cultural factors, and clients impairments, activities and participation
levels
02.02.03.05 Identify appropriate outcome measures for use in determining
efficacy of intervention
02.02.03.06 Identify aspects of treatment that can be performed by client
independently or with caregiver/family assistance
02.02.03.07 Schedule treatments to optimize clients response (e.g., time of

day, medication timing)

02.02.03.08 Facilitate procurement of client equipment and aids
02.02.03.09 Participate in interprofessional continuum of care planning and
follow-up care with client, family and other care givers
Implementation
Use the following interventions in a safe, effective, and ethical manner with
individuals or groups:
02.02.04.01.01 Exercise with or without equipment (e.g., passive, active
assisted, active, resisted, neuromuscular, vestibular, muscle patterning, PNF)
NORMAL ROM
Vestibular exercises
PNF patterns: (Yes, they may still ask you about this what year is it again,
1980?)
UPPER EXTREMITY
D1 Flexion UE
flexion, (horiz) adduction, external rotation
Close your hand, turn & lift up and across your face "Grab your seat belt",
verbal cue for D1 Flexion UE
D1 Extension UE
extension, (horiz) abduction, internal rotation
Open your hand, turn & push down and out "Fasten your seat belt"
verbal cue for D1 Extension UE
D2 Flexion UE
flexion, (horiz) abduction, external rotation
Open your hand, turn & lift up and out "Pizza man"
verbal cue for D2 Flexion UE

D2 Extension UE
extension, (horiz) adduction, internal rotation
Close your hand, turn & push down and across "sword in the side"
verbal cue for D2 Extension UE
LOWER EXTREMITY
D1 Flexion LE
flexion, adduction, external rotation
Foot up, turn & lift up and across "cross leg on opp knee foot bottom up" kick
soccer ball
verbal cue for D1 Flexion LE
D1 Extension LE
extension, abduction, internal rotation
Foot down, turn & push down and out
verbal cue for D1 Extension LE
D2 Flexion LE
flexion, abduction, internal rotation
Foot up, turn & lift up and out "going over a hurdle"
verbal cue for D2 Flexion LE
D2 Extension LE
extension, adduction, external rotation
Foot down, turn & push down and across "cross feet with toes pointed at
ankles"
verbal cue for D2 Extension LE
Capsular patterns-Osullivan pg 4

02.02.04.01.02 Joint mobilization

go through doc made by classmates

open and closed pack positions

CIs - cancer, acute arthritis, fracture, dislocation, bone disease, inflammation,
empty/bony end feel, anticoagulant/steroid use, sign of ze BUTT, vertebral
artery insufficieny, CV lig instability
02.02.04.01.03 Joint manipulation
CIs - fracture, jt instability, inflammation, inflamm jt disease, bone disease,
open wound, poor circulation, sensory deficit in area, spasm or inc pain with a
test pull (pre manip hold), unsure gen health/diagosis, anti coag,
hemophiliacs, cant relax
02.02.04.01.04 Soft tissue techniques (e.g., massage, friction,
stretching)
Friction-CI: ossification, infection, skin breakdown, inflam skin/jt disease
Stretching- CI: acute inflam/infection, unhealed fracture, jt effusion, recent
corticosteroid injection to the involved tissue, in the direction of hypermobility,
specific to certain surgeries ex-hip replacement
PNF Stretching=the use of inhibition techniques to assist mm elongation;
when the stretch reflex is activated in a mm being recruited, the mm on the
opp side is inhibited
massage:
CIs - autoimmune diseases during flare ups, fever, haemorrhage, flu,
migrane headache, serious psych diagnosis, recent surgery, acute RA, sickle
cell disease
relative CIs (DOC Clearance) - cancer, stroke, bleed disorders, CHF, HTN,
kidney stones
02.02.04.01.05 Fitness/conditioning/endurance exercise programs
02.02.04.01.06 Functional activity training
02.02.04.01.07 Posture training

02.02.04.01.08 Positioning
02.02.04.01.09 Gait/mobility education and training with or without
equipment

Cane - widen base of support, help balance,

Quad cane - not that good for stairs
Crutches - help with lateral stability and improve balance
Forearm crutches - allows for use of hands, but need more arm strength to
use
Normal gait : stance 60%, swing 40%
4 POINT GAIT - 3 points of support on ground at all times; 1 aid advanced,
then opposite LE advanced, can be done with CRUTCHES OR CANES, slow
stable gait
2 POINT GAIT - similar to 4 point only 2 points of contact maintained at all
times, less stable, req better balance CRUTCHES OR CANES

- one leg and contralateral aid advance at same time (ex R cane and L leg
together, then L cane and R leg together
3 POINT GAIT - 3 points of support on floor, NWB, PWB (<80% cant use
CANE), FeWB on affected LE
- pt1) affected LE advanced, pt2) wt transferred to floor through aid (both
cruches at the same time or walker), pt3)unaffected leg advanced, and wt
returned to unaffected leg
STEP TO, or STEP THROUGH, can be done with CRUTCHES OR WALKER

02.02.04.01.10 Neurodynamic techniques (e.g., nerve gliding/flossing

exercises)
nerve gliding/flossing - do not Ax or treat in presence of CNS signs:
myotomes, dermatomes, reflexes
peripheral N conduction signs: Ax but dont treat
dont treat if worsening or undiagnosed symptoms
KEEP READING, THERES GOOD STUFF BELOW, COLLEGE
GUIDELINES...

LIST OF FUNCTIONS EVALUATED BY THE PCE (continued)

(This list is not necessarily exhaustive.)
02.02.04.01.11 Balance training/proprioceptive training
Balance=ability to maintain COG over base of support; 3 things necessary
for balance are visual, vestibular, proprioception
Proprioception=sensations of jt mvmt (kinesthesia)
and joint position
02.02.04.01.12 Sensory training (e.g., desensitization, protective education,
sensory integration)

02.02.04.01.13 Techniques to optimize oxygen transport and facilitate airway

clearance (e.g., positioning, suctioning, secretion clearance, forced expiratory
techniques)
Auscultation-know 6 points antrly and 10 points postrly
02.02.04.01.14 Mechanical agents (e.g., traction, continuous passive
movement, compression garment and devices, vasopneumatic devices)
Traction-incrd IVF diameter, pain inhibition, decreased mm spasm, mm
stretching; Indications-nerve root compression, disc pathology, degeneration,
jt dsfx, hypomobility, pain;
CI-fracture, infection/inflam, pain with manual traction, signif trauma w/o
xrays, SCI signs and Sys
02.02.04.01.15 Conductive thermal agents (e.g., contrast baths, whirlpools,
paraffin wax, hot packs, ice/cold)
02.02.04.01.16 Electrical agents (e.g., EMG biofeedback, iontophoresis,
transcutaneous electrical nerve stimulation [TENS], neuromuscular electrical
nerve stimulation [NMES], interferential current [IFC], high voltage pulsed
current [HVPC])
02.02.04.01.17 Electromagnetic energy agents (e.g., shortwave diathermy,
LASER, ultraviolet)
02.02.04.01.18 Acoustic agents (e.g., ultrasound)
02.02.04.01.19 Protective, adaptive, or assistive devices (e.g., tape, splints,
orthotics, prostheses)
02.02.04.02 Recognize and respond to the adverse effects of intervention
(e.g., pain, deterioration in client status) and/or non-adherence
Education/Communication/Advocacy
02.02.05.01 Communicate the purpose and results of physiotherapy
evaluation/assessment, proposed treatment procedures, expected outcomes

and progress to client, family, and healthcare and other service providers and
verify their understanding of same
02.02.05.02 Use teaching and communication strategies with clients and
family members that respect culture, learning, communication, language
style, and abilities
02.02.05.03 Educate client, family, and healthcare and other service
providers in safe and effective physiotherapy techniques and use and care of
equipment as appropriate
02.02.05.04 Educate the client, family/significant others about the condition,
self-management, coping and prevention strategies
02.02.05.05 Educate client regarding credibility of external educational
materials/resources
02.02.05.06 Assist, and where necessary advocate on behalf of, client in
obtaining access to necessary services, funding, equipment, and treatment
within the continuum of care
02.02.05.07 Educate client, family, and healthcare and other service
providers about transitions (e.g., change in level of care, care provider or care
funder), other services, and discharge plans
Intervention Progression
02.02.06.01 Assess client satisfaction and response to treatment with
appropriate outcome measures and benchmarks
02.02.06.02 Perform re-evaluations/re-assessments at appropriate intervals
or based on changes in client status as appropriate
02.02.06.03 Adjust, revise, or discontinue treatment plan when goals are
achieved, clients status changes, or treatment is no longer effective

LIST OF FUNCTIONS EVALUATED BY THE PCE (continued)

(This list is not necessarily exhaustive.)

02.03 PROFESSIONAL RESPONSIBILITIES (15%5%)

Professional Accountability
02.03.01.01 Respect the knowledge, rights, confidentiality, and dignity of
client and family
02.03.01.02 Adhere to professional and regulatory codes of ethics/conduct
and standards of practice
02.03.01.03 Participate in processes that evaluate and improve quality and
outcomes of services
Communication and Collaboration
02.03.02.01 Secure informed consent for evaluation/assessment and
treatment
02.03.02.02 Participate in collaborative health care service delivery (e.g.,
rounds, specialty care clinics or meetings)
02.03.02.03 Consult and collaborate with healthcare and other service
providers to ensure services to clients are coordinated and clients needs are
met
Professional Judgment and Reasoning
02.03.03.01 Recognize and practice within the scope and limitations of self
and profession
02.03.03.02 Demonstrate continuing competence (e.g., reflective practice,
self-directed learning)
Practice Management
02.03.04.01 Document all relevant aspects of care including client
evaluation/assessment, treatment plan, progress notes and discharge plan
02.03.04.02 Adhere to federal and provincial laws regarding storage,
protection, disclosure of information, business practices, etc.
02.03.04.03 Assign tasks, guide, and supervise activities of support
personnel as needed
yah, we went there, we actually went the the Colleges website to find this!!!!
CPTBC Practice Standard No 3. Assignment of Task to a Physical Therapist

Support ASSIGNMENT OF TASK TO A PHYSICAL THERAPIST SUPPORT

WORKER
Assignment of Task: Transfer of a component of a physical therapy treatment
plan to a physical therapist support worker (PTSW).
Physical Therapist Support Worker: an individual who works under the direction
and
supervision of a physical therapist.
Supervision: the means by which the physical therapist monitors the
performance of the PTSW.
An individual who does not work under the direction and supervision of a
physical therapist is not considered a PTSW.
1. The physical therapist must obtain informed consent from each patient for
the involvement of a PTSW in the delivery of their physical therapy treatment
plan. PTSW must be made aware that patient consent can be revoked at any
time.
2. The physical therapist must explain to each patient the relationship between
the physical therapist and the PTSW for the purpose of clarifying the difference
in roles and responsibilities as they relate to patient assessment and treatment.
3. The physical therapist must ensure the PTSW is competent (has the
knowledge, skills and abilities) to carry out the assigned tasks.
4. The physical therapist is responsible for the physical therapy task(s)
assigned to the PTSW.
5. The assigned task must be recorded in the clinical record in accordance with
the Practice Standard on Clinical Records.
6. To determine the appropriate level of supervision the physical therapist must
exercise clinical judgment. The following factors should be considered:
Patient preference, practice setting, complexity of the assigned task and
environment, competencies of the PTSW, acuity of the patients condition,
degree of judgment and decision making required to carry out the task, level of
risk associated with the task, and patients cognitive status.
7. Assigned tasks must be within the physical therapists level of competence
and be within the physical therapy scope of practice.
8. The physical therapist must ensure that the PTSW has been instructed in

standard infection control measures CPTBC Practice Standard No 3.

Assignment of Task to a Physical Therapist Support Worker
9. The physical therapist must ensure that the PTSW is aware of patient
confidentiality
standards and College Bylaws
10. The physical therapist must be available for consultation. If unavailable, the
physical therapist must arrange for transfer of supervision to another physical
therapist.
11. The physical therapist must instruct the PTSW to recognize any adverse
treatment reactions, cease treatment and immediately report to the supervising
physical therapist.
12. The physical therapist must reassess the patient at timely intervals.
13. The physical therapist must make any changes to the treatment plan and
record the changes in the clinical record.
14. Physical therapists must NOT assign any physical therapy task which has
an evaluation component that immediately influences the treatment program. A
physical therapist must not assign the following tasks to PTSW:
Interpretation of referrals, diagnosis, or prognosis
Performance of assessment/evaluative procedures
Interpretation of assessment findings
Discussion of physical therapy diagnosis or treatment rationale with anyone
other than the physical therapist
Planning or initiating physical therapy treatment goals or programs
Tasks requiring a physical therapists clinical judgment
Modification of treatment beyond established limits
Completion of documentation that is the physical therapists responsibility
Electro-physical agents (except neuromuscular stimulation or TENS)
Teaching of the assigned task to another person
Discharge planning

02.03.04.04 Procure and maintain safe and effective equipment

02.03.04.05 Ensure client safety in all aspects of assessment/evaluation and

intervention
02.03.04.06 Use routine precautions for infection control in all aspects of
client interaction
02.03.04.07 Manage and administer physiotherapy practice using ethical
business practices
02.03.04.08 Establish and manage a transparent prioritization process when
demand exceeds ability to deliver services

Sign of the Buttock:RONFISS; Rheumatic fever, Osteomyelitis, Neoplasm, Fracture, Ishiorectal

abcess, Septic bursitis, Septic arthritis
Synovium = oct 18th
lines inner surfaces of joints, prod synovial fluid, lines tendons and form sheaths, forms bursae
injury =contusion or compression, friction or stress
intervertebral disc
annulus fibrosis = outer layer vascular and nerves ; nucleus pulposus inside jelly
degen disc disease P due to facet jt compress, pain on N root, injury to annulus and to end plates
cartilage:
hyaline: between joints ;
elastic: resp system and ear;
fibrocartilage: meniscus (even force distribution)
insertion cartilage: tendons and ligaments
- heal by repair of adj cells from synovium and labrum
Imaging:
X-rays: penetrates soft tissue, doesnt penetrate bone
X-ray arthrogram: dye injected into jt to see it
Fluoroscopy: live action x-ray
CT: 2D x rays made into 3D by the computer
MRI: magnets used to align and alter the H nuclei in water: detects change in magnetic field

Bone scan: detect BMD, and check for mets, fractures, infections
Ultrasound: soft tissues LIKE THE BABIES!!!!!!
Floroquinolones: broad spec antibiotics for COPD, pneumonia, GU infections: inc risk of tendon
ruptures (and corticosteroids)
Osteomyleitis: infection of bone: get it with sepsis, open trauma, infected surgical implant; children at
highest risk
Effects of Aging:
Sarcopenia: reduction and mm mass and function
Tendons: less metabolic active, more wear and tear, more cross linking, less of strength at enthesis;
Achilles and supraspinatus most prone to injury with age
IMMOBILIZATION:
Effects of bed rest on mm: dec mito, dec red blood supply, fat infiltration, dec strength, atrophy and
contractures
Bones: osteopenia
Ten and lig: disorganization of parallel arrays and less strong
Cartilage: loss of thickness; synovium: adhesions form between synovium and cartilage; synovium:
inflamed, fatty infiltration; less jt fluid production

Patellar dislocation: due to tight lat retinaculum, weak VMO, direct blow
Ganglion: pocket of synovial fluid
Contracture: shortening of soft tissue: ex dupuytren's
Adhesion: abnormal adherence of collagen fibers
Reflex mm guarding: myofacial trigger points, Pain mm guard around it
Intrinsic mm spasm: prolonged contraction of mm in resp to circulatory and metabolic changes and it
is contracted
Myofacial compartment syndrome: fascia too small to accommodate for mm growth, can cause
mm necrosis

Rhabdomyolosis: mm compressed and starts breaking down, myoglobin accumulates and backs up
in the kidneys, can get kidney failure
Protein balance for mm: contact and stretch release MGF mm growth factor, take steroids; GH,
testosterone, IGF-1; cortisol = breaks down mm,
Mm training: increased cross sectional area, dec fat, inc angle of pennation, resistance training: dec
number of mitochondria (mito used or endurance energyt prod), more caps, more type 2 mm fibres
Satellite cell: mm stem cell; on the periphery, activated by exercise and trauma, and can completely
regenerate mm myofibres
Tenocytes: get more collagen align into rays, progenitor cells: repair of tendon
Pacinian corpuscles: strength, tension, in jt capsule and free N endings
EIMD: how long, magnitude and vel of strain affect EIMD; age, gender affect it too; ECCENTRIC
DOMS peak 48hrs after, not correlated with markers of mm damage
Repeated bout effect: adaptation of mm after eccentric EIMD, after 2nd bout indirect markers of mm
damage are reduced
MO=bone formation in the mm; same as HO(neuro)
Deformation curve, toe, linear, elastic, deformation
Types of Collagen:
Collagen type 1 = tendon, end scar strongest
Collagen type 2 = hyaline cartilage
Collagen type 3 = granulation tissue, scar
Achilles rupture; 35, 70, risks: age BMI, sport, male
Jumpers knee, patellar tendon tendinopathy, lots in kids
Tennis elbow: lat epicondylitis, ECRB
Golfers elbow:med epicondylitis

Tib post tendinopathy: compressed under med mal, if hyperpronate can irritate
BONES:
Types: flat, tubular, irregular (vertrebral bones), sesamoid bones(develop in tendons), supernumerary
(centre of talus os trigonum)
Osteomalacia defect in mineralization of collagen matrix Vit d deficiency (rickets - kids)
Pagets disease: 2nd most common bone disease., excessive osteoclast, abnormal regeneration
Ostopetrosis: v rare, inherited, deficiency of carbonic anhydrase, body inability to resorb bone
Osteochondrosis: disorders of epiphyseal growth plates
Kohlers disease: avascular necrosis of navicular
Osgood slatters: irritation to tibial tuberosity, or pull bone off
Legg-Calve-Perth: necrosis of femoral head put in adduction
Osteochondritis dessicans: sub chondral necrosis of bone followed by recalcification, bone and
cartilage can pull away
Salter Harris fracture = fracture of the growth plate
Congenital hip dysplasia: malformation of the hip present at birth; hip dislocation, asymm leg
postions
Marfans: lack of fibrilin , long hands, genetic
Larsen syndrome: prominent forehead and wide spaced eyes, genetic disorder, multiple jt
dislocations
Osteogenesis imperfecta: brittle bone disease
Achondroplasia: dwarfism, impaired cartilage formation and effects growth factor for bones growing.
Multiple epiphyseal dysplasia: cluster of disorders effect epiphysial growth plates, short stature and
limbs
Acromegaly: overactive pituitary gland
Fibrillation: loss of normal smooth surface, rough edges into tiny fibrils
SCOLIOSIS:
3 kinds 1) Idiopathic, 2) Congenital, 3) Neuromuscular; can be structural or functional
Rx: Education, bracing, stretching, strengthening, posture
Scoliosis Kisner Colby...page 396/7...
Scoliosis usually involves the thoracic and lumbar regions. Typically, in right-handed individuals, there
is a mild right thoracic, left lumbar S-curve, or a mild left thoracolumbar C-curve. There may be

asymmetry in the hips, pelvis, and lower extremities. Structural scoliosis involves an irreversible
lateral curvature with fixed rotation of the vertebrae (Fig. 14.13A).
Rotation of the vertebral bodies is toward the convexity of the curve. In the thoracic spine, the ribs
rotate with the vertebrae so there is prominence of the ribs posteriorly on the side of the spinal
convexity and prominence anteriorly on the side of the concavity.
CARDIORESP
Types of breathing:
breath stacking: stacking little breaths on top of one another when a deep breath is too painful
active cycle of breathing: diaphragmatic breaths with a hold at the top, then to normal breathing,
repeat cycle then 3 huffs
autogenic drainage: use breathing to clear secretions
flutter: breath out thru device, vibrations from device will loosen secretions
diaphragmatic breathing: post op, obstructive or restrictive
segmental breathing: improved vent to hypo-ventilated lung areas
pursed lip breathing: help blow off CO2, inc tidal vol, red resp rate, red dyspnea; for COPD
BREATH SOUNDS: p20 reid and cheung
bronchial breath sounds: hollow, high pitched, harsh: consolidated pneumonia or lobar collapse
normal: soft and low pitched
decreased or absent: pleural effusion, hemothorax, pneumothorax, emphysema, obese or elderly
crackles: fine: atelectasis, interstitial pulmonary fibrosis;
coarse: retained secretions
wheezes: asthma, COPD
will have inc FRC: vol of air remaining in lungs at end of ordinary exp with age
p38 R&C
ABGs
p178 O Sullivan
normal range
pH7.35-7.45 lower=resp or metabolic acidosis; high: metabolic or resp alkalosis
PaCO2 35-45mmHG
high= resp acidosis (from hypoventilation - COPD, flail chest,
neuromuscular disorders, sleep apnea) :help with secretion clearance

low = resp alkalosis (hyperventilation, pain or anxiety or breathlessness); mechanical vent

PaO2 80-100mmHG
HCO3 22-28

decreased: metabolic acidosis; increased: metabolic alkalosis

resp compensation mins to hours

renal compensation is 1-5 days
metabolic acidosis: renal failure, lactic acidosis, ketoacidosis
metabolic alkylosis: sodium base overload, potassium depletion, vomiting
HAEMODYNAMICS:
WBC low: lethargic, bruise easy
Hb 85-110: put on iron; below 85= transfusion
low: fatigue, dizzy, headache, lack of concentration
platelets: low = thrombocytopenia, get lots of bruising, and get small bleeds; Normal platelet count is
150-450,000/uL of blood
IRN: looks at coagulation and clotting time of blood low levels: will have restricted activity or bed rest
potassium: reg mm tissue, digestion and metabolism low: hypokalemia- weak, fatigue, vomit,
nausea ; high:hyperkalemia - min symptoms
sodium; reg blood vol, blood pressure, osmitic equlib, pH
low; hyponatrimia: headaches, confusion, mm spasm, seizures
high; hypernatrima: S&S of dehydration
magnesium: high: hypermagnesemia- nausea, vom, mm weakness
low: mag deficiency - mm cramps, hyperactive reflexes, remors and overall weakness
calcium: low - hypocalcemia, prolonged QTwave
high - kiney stones, groans, bones (risk of #) thrones: diarhhea, psyc overtones
arterial line: measure BP, blood sampling for ABGs, admin meds
pulmonary arterial line: vena cava into R atrium, pulm art or pulm cap: meausre pulm art pressure,
pulmonary capillary wedge pressure (L art pressure), right atrial pressure, CO
LINES:

PICC - peripherally inserted central catheter: treatments such as chemo or antibiotics, samples of
blood, no freq needles; have to wait to mobilize until PICC insertion cleared by x-ray, close off before
shower or hydrotherapy
central venous line: sits at vena cava: monitors R atrial pressure, venous tone and circ blood vol.,
central venous pressure normal = 5-12
gtube= facial trauma- tube for feeding, turn feed off before PT treatmet
TPN: total parental nutrition, amino acids and lipids
lumbar drain: drains CSF
continuous bladder irrigation: contin flow of fluid, prevents obstruction and cleaning, bag higher than
bladder
hemodyalisis: removes wastes and extra fluid in blood and returns clean blood to patient: renal
insufficiency anget rid of antibodies in plasma
intracranial pressure ICP: 10-15mmHg
infarction: necrosis develops distal to occlusion of an artery
embolism: passage of any material capable of getting lodged in a blood blood vessel
pulmonary infarctions: death of lung tissue S&S: SOB, chest pain,
edema: presence of excess fluid in interstitial space; anasarca: total body edema
effusion: excess fluid in body cavities
transudate: low in proteins
exudate: high in protein

OUTCOME MEASURES:
Kurtzke Expanded Disability Scale- for MS
Expanded Disability Status Scale (EDSS)=MS
Oswestry Disability Index=lower back pain
Hoehn and Yahr Classification of Disability=Parkinsons
Unified Parkinsons Disease Rating Scale (UPDRS)=Parkinsons
Disability Rating Scale (DRS)=Traumatic Brain Injury
Fugl-Meyer Motor strength test=stroke

Stroke Impact Scale (SIS)=evaluates how stroke has impacted health and life from Pts perspective; a
questionnaire
Rivermead mobility index=functional mobility following stroke
The Community Balance and Mobility Scale=detect high level balance and mobility deficits
The Dynamic Gait Index=Assesses individuals ability to modify balance while walking in the presence
of external demands
The Functional Independence Measure=measures the level of a patient's disability and indicates how
much assistance is required for the individual to carry out activities of daily living.
Barthel scale or Barthel ADL index is an ordinal scale used to measure performance in activities of
daily living (ADL)
Knee injury and OA Outcome Scale (KOOS)=evaluates s/t and l/t Pt relevant outcomes of knee injury
that can result from post-traumatic OA (ACL injury, meniscus injury)
McMaster Toronto Arthritis Patient Preference Disability Questionnaire (MACTAR)=assesses
disability in Pts with RA
********
PCE Electro Review
Interferential Current:
Low voltage, medium intensity
2 sinusoidal waves alternating current
Each wave = slightly different frequencies and interfere with one another in tissues creating
new wave (linear super-position)
Series of wave packets (beats)
Balanced, symmetrical, biphasic, amplitude modulated
Can output 50-90mA (other machines = much lower) NO THORACIC APPLICATION OVER
50mA
Used for pain, edema, increases blood flow, muscle stimulation
Motor = 1-10Hz; Sensory (pain) = 80-150Hz
20-40mins
TENS

Low voltage, low intensity

Gate control theory or extrasegmental
Conventional:
o High frequency (80-150Hz), low pulse duration (60microsec.)
o Comfortable tingle
o Acute analgesic effect only while machine on
o Electrodes bracket pain
Acupuncture-like:
o Low frequency (5-10Hz), high pulse duration (200microsec)
o Motor twitch
o Chronic pain 4-6 hours analgesia
o Electrodes on motor point (want twitch)
LASER
-3 features of a laser: Monochromaticity (all photons have a single wavelength), coherence (all
photons travel in same phase and direction), collimation (minimal divergence over distance)
Used to increase tissue healing, decrease pain, decrease inflammation (wound
management)
Choose laser head based on depth of lesion (red-near infrared = 1-5mm; near-mid infrared =
5-10mm)
Dose: acute = 2J/per point; chronic = 4 J/per point (look at WALT)
Frequency: acute = <1000kHz; chronic = >1000kHz
Continuous or pulsed (laser lasts longer)
Contact or noncontact (scanning/grid)
Wear eyewear
Heat:
2 fibers for perception of thermal sensation (warmth and heat (>45deg. C)
Major source of heat gain = metabolism (also absorption of radiation from environment, etc.)
Heat loss major source = radiation (also exhalation, evap. of sweat, urine)
Thermoregulation is controlled by the hypothalamus
As you get hotter, metabolism increases Van Hoft (in body temperature >45C = protein
damage)

Therapeutic effects of superficial tissue heating: tissue healing, pain relief, reduction of
muscle spasm, sedative effect, increased joint ROM, facilitates fine movements
Paraffin wax baths 6-8layers, 15minutes (contraindications skin infections or acute
inflammation of underlying joints should not receive wax; dermatitis can get worse)
Contrast bath (hot then cold then hot) produces blood flow to tissues good sensory
stimulation (no evidence of reduction of local edema) treatment starts and ends with immersion in
hot water hot = 3-4mins, cold = 1min (repeat 3-4X)
Whirlpool gating effect stimulation of moving water may gently debride wounds (may
sometimes increase edema dependent position?)
Superficial heat precautions local burns, altered thermal sensation, ischemic disease
restricting local circulation, DM, PVD, altered heat loss mechanism (ex: obesity), fungus,
exacerbation of dermatitis or eczema, malignancies, open wounds)
COLD
Cooling reduces metabolic rate enhances survival of vulnerable cells that have survived the
initial injury reduces edema (allows vulnerable cells to remain closer to O2 supply), reduces sharp
pain (blocks nerve conduction) little value for chronic pain (doesnt affect those fibers)
Mild cooling can increase isometric strength, but greater cooling can reduce this strength,
cooling reduces tremor, can reverse conduction block associated with demyelination of peripheral
nerves (heating exacerbates it) ex: MS
Therapeutic uses: recent injuries, pain, muscle spasm, spasticity, muscle strengthening,
chronic inflammatory conditions, chronic edema
Check for allergic reaction to cold after 1 minute and after 5 minutes
Dangers/contraindications: ice burn, peripheral nerve damage, frostbite, reduced peripheral
blood supply (can further damage tissue), cold sensitivity (Reynauds, cold urticaria)
UV
Contraindications = photosensitivity, skin cancer, and CT disorder (be aware of drugs causing
photosensitivity)
Used to treat: psoriasis, eczema, vitilago, pruritus (secondary to liver/kidney disease), acne,
photodermatoses, wound healing, atopic dermatitis
On eyes can cause conjunctivitis or photokeratitis (inflammation of cornea) cataracts are
caused by chronic exposure to UV

HVPC
High voltage, high peak intensity, low average intensity
Monophasic (can build up a bigger net charge)
Frequency = 1-200Hz, pulse width fixed (5-65microsec.), peak current is high (higher risk of
burning), but long interpulse interval so charge has a chance to dissipate allowing safer application
(total current is very low)
Mainly used for: decreased pain, decreased edema, increased wound healing, muscle
stim. (enhances oxygenation, blood flow and tissue formation)
High voltage = more comfortable and large punch = better at punching away or bringing in
molecules
Wound healing = 50-100Hz (submotor), edema reduction = 5-20Hz (want twitch), muscle stim
= 35-65Hz, pain = same parameters as TENS
Galvanotaxis can repel molecules or attract desired cells based on polarity
Dont use for inflammation (dont want to add energy to injury)
For acute edema active red on edema and set it as negative to push away positive proteins
OR put it on muscle twitch on motor point and nerve trunk (chronic)
Wound healing one electrode in wound and one 10-20cm away
Phonophoresis (dont need to know) and Iontophoresis
Phonophoresis (dont need to know) using US to enhance delivery of topically applied drugs
avoid risks of IV, reduce risk of OD, local Rx, easy method to terminate and bypass liver
o Primary uses: decrease tissue inflammation, reduce pain
o 3 common meds local anesthetics, anti-inflammatories, counter-irritants
Iontophoresis method of Rx using current flow between two electrodes to push ions through the
skin barrier
o Current is direct current
o Positively charged drug can be made to cross the skin away from positive electrode
o Under the anode may get an acidic reaction (hardening of skin over time (sclerotic) and under
cathode may get alkaline reaction (softening and burning of skin) but most electrodes have
buffering agents to prevent this
o Keep the cathode larger (current density is therefore lower and skin is less likely to burn)
o Used for: hyperhidrosis, MSK inflammatory disorders, plantar fasciitis, TMJ disorders,
ischemic skin ulcer, fungal infections, bursitis and tendonitis

o Contraindications include over damaged skin or open lesions, allergy to therapeutic ions, impaired
sensation, over electric implants
Short Wave Diathermy
Therapeutically heat body tissues at any depth
2 types of electromagnetic fields producing the heat (electrostatic and electromagnetic)
thermal and non-thermal effects
Physiological effects of pulsed SWD: increased tissue healing, enhance nerve
regeneration, pressure ulcers, chronic low back pain, soft tissue injuries (some evidence it can
be used for pain, muscle spasm, chronic inflammation, delayed wound healing, chronic infection)
- 2 main indications for application = OA and ankle sprain
Main contraindications = metallic implants and pacemakers (implanted devices)
Can get burns (unequal spacing, perspiration, etc.) patient should just feel mild, comfortable
warmth
EMG Biofeedback:
Nerve conduction testing estimates velocity of depolarization along an alpha motor neuron
In skeletal muscle, normally silent at rest (short burst of electrical activity during needle
insertion)
reduced insertional activity seen in fibrotic or severely atrophied muscle (when put needle in), increased activity when a muscle is irritable
Abnormal electrical activity at rest suggests neuropathy or myopathy and is indicated by
fibrillation potentials (rapid, irregular contractions of muscles), positive sharp waves, or fasciculation
potentials
Surface EMG provides information about muscle activity (in order to uptrain or downtrain
activity)
Used to: improve control over defective muscles or improve control over stressed
muscles (ex: hemiplegia, SCI, spasticity, dystonia, recovering peripheral nerve injuries)
Used as a tool not a treatment
NMES:
The use of electrical stimulation to generate an action potential in a nerve leading to
contraction of skeletal muscle - Pulsed and biphasic

Used for: pain modulation, edema management, decrease spasticity, muscle

strengthening
Parameters: pain = same as TENS intensity can be turned up to sensory or motor threshold,
edema = same as HVPC intensity to muscle twitch, muscle stim and spasticity = 35-65Hz
intensity to tetany
On:off time set based on muscle grade of strength grade 5 muscle strength = 1:1 and grade
1 = 1:5
Electrode placement anode = nerve trunk (or muscle belly), cathode = motor point (or
muscle belly) can surf cathode to get the right spot (1/3 proximal, 2/3 distal for motor point)
Side effects: rhabdomyelosis, ischemic colitis, inappropriate ICD discharge
12-15 contractions per session
Ultrasound:
Sound waves
Maintain contact and keep head moving and perpendicular to tissue
Parameters: frequency 1MHz (deep) and 3MHz (superficial); intensity (0.5 acute and 2 = high
for chronic while 1-1.2 = moderate for chronic), pulsed (acute) and continuous (chronic); acute = 510mins, chronic = 20 minutes
Apply to area not larger than 2-2.5xERA (ERA = area producing 5% or more of max. power
output higher = better) Used for thermal effects: decreased pain, decreased joint stiffness, improved blood
flow, promote healing (decreases inflammation) and non-thermal effects: wound healing,
inflammation and soft tissue healing
Contraindications: implantable devices, malignancy, bleeding disorder, infection, DVT, dont
use on Medtronic stimulation system
Functional Electrical Stimulation
Used for: treatment of disuse atrophy, increasing ROM, re-educating muscle, managing
spasticity, gait orthoses, improving motor recruitment, increasing muscle endurance, reeducating gait
Individuals with CNS condition benefit from this stroke, MS, SCI, CP, PD, TBI and orthopedic
conditions or conditions resulting from deconditioning
Individuals who cannot benefit LMNL, peripheral nerve lesions, motor neuron disease, GBS,
polio and post-polio syndrome, fixed contractures

joint

Especially used for drop-foot stimulation (reduce fall risk) and improving subluxation of GH

Estim Contraindications:
Areas where it could affect electrical devices (ex: pacemaker)
Low back/abdomen/acupuncture points of pregnant women
Areas of malignancy
Acute hemorrhage
DVT or thrombophlebitis
CVA or TIA
TB
Osteomyelitis
Chest if cardiac issues
Neck/head region in people with seizures
Damaged/at risk skin areas
Infection
Recently radiated areas
Impaired sensory awareness
Acute inflammation
Trans-thoracically or trans-cerebrally
Cognition impairments
NMES contraindicated to chest, intercostals, and lower abdomen
****
NERVES
Common Peroneal branches:
Common peroneal in popliteal fossa: Sensory
Superficial peronealMotor
Peroneus brevis, Peroneus longus,
Cutaneous sensory:
Lower leg: Anterolateral
Foot: Dorsum of foot and big toe
Medial & Intermediate dorsal cutaneous nerves of foot
Deep peroneal- Motor branches in leg

Tibialis anterior, Extensor hallucis & Extensor digitorum longus, Peroneus tertius
Lateral terminal branch in foot
Extensor digitorum brevis
Tibial nerve:
-branch of the sciatic nerve, passes through the popliteal fossa to pass below the arch of soleus.
-In the popliteal fossa the nerve gives off branches to:
-motor= gastrocnemius, popliteus, soleus and plantaris muscles
-cutaneous=become the sural nerve (distal branch of the tibial nerve and supplies the back of the leg
and lateral side of the foot and little toe)
Below the soleus muscle the nerve lies close to the tibia and supplies the:
-motor= tibialis posterior, the flexor digitorum longus and the flexor hallucis longus.
In the foot it divides into the:
1) Medial plantar (calcaneal) nervecutaneous: supplies the heel and medial sole of the foot
motor: abductor hallucis, the flexor digitorum brevis, the flexor hallucis brevis
2) Lateral plantar nervecutaneous:to the lateral sole and lateral one and one half toes (like the ulnar nerve).
motor: quadratus plantae, flexor digiti minimi, adductor hallucis, the interossei, three lumbricals. and
abductor digiti minimi.

ECGs, what is the issue with three PVCs in a row=>Ventricular tachycardia=>which can b/co
ventricular fibrillation, VERY BAD! Prob that the atria are not contracting because no wave
Cyanosis=bluish discoloration of skin and nailbeds of fingers and toes alont with cold and moist
palms; caused by excess deoxygenated hemoglobin in the blood
Apraxia = disorder of the brain and nervous system that is a person is unable to perform tasks and
movements when asked
Verbal apraxia-inability to produce motor patterns resulting in speech; in the absence of
impaired understanding , mm paralysis/ weakness or intellect
Ideational apraxia: Cannot carry out learned complex tasks in the proper order, such as
putting on socks before putting on shoes due to mis-identification

 motor apraxia= disorder of voluntary movement notwithstanding the in absence of paralysis

or mm weakess
constructional apraxia - unable to draw objects in absence of paralysis

Astereognosis (tactile agnosia) = inability to identify held objects in the absence of language or
sensory loss
Right brain is dominant for body awareness
Anosognosia= a lack of awareness or a denial of a neurologic defect or illness in general, especially
paralysis, on one side of the body (like a limb). It may be attributable to a lesion in the right parietal
lobe.
Somatognosia= Inability to correctly identify or orient the parts of one's body or the body of another.
Expressive aphasia=Brocas
Receptive aphasia=Wernickes

CEREBELLAR:
cerebellar ataxia - jerky innaccurate, uncoordinated movement, w/ normal strength and no hypertonia
dysmetria= overshoot the intended goal
dysarthria - trouble with speaking, slurred due to lack of motor coordination
intention tremor - tremor when initate movement
dysdiadochokinesia- inability to perform rapid alternating movements
NON CEREBELLAR:
athetosis - slow continuous involuntary movements
chorrea- rapid repeated jerky coarse movements
dystonia- frequent maintained contraction of hypertonic mm
hemiballsmus - sudden stabbing movements of one side of the body
fasiculation - twitching of mm fibers in single motor neuron unit (often visible on surface, occur with
LMNL)

fibrillation - abnormal contraction of a single mm, only visible with EMG, and seen with dying neurons
Huntingtons chorea= genetic disorder with writhing (choreoform) movements including limbs, speech
(sound drunk) due to loss of neurotransmitters and GABA
Korsokoffs syndrome = genetic metabolic injury due to malnutrition or alcoholism, cant make new
memories, characterized by confabulation
spastic hypertonia (spasticity) - velocity dependent increase in resistance to passive movement
rigid hypertonia - velocity INDEPENDENT increase resistance to passive movement

Metabolic syndrome=pre cursor to Type 3 diabetes, abd obesity, high trigylcerides, low HDLs, HTN,
high fasting plasma glucose
Glaucoma=loss of peripheral vision first, followed by central blindness
Cataracts=a clouding of the lens, gradual loss of vision, central vision is lost first, then peripheral

Resistance exercise is contra-indicated in Pts with signif:

Bony mets, osteoporosis, low platelet count (<20,000)

Lumbar plexus-draw out

If I Get Laid F*$k Off Sex (Hey, kids may be reading this ;)

Nerve

Segm
ent

Innervated
muscles

Cutaneous branches

Iliohypogastric

T12L1

Transversus
abdominis
Abdominal
internal oblique

Anterior cutaneous
ramus
Lateral cutaneous
ramus

Ilioinguinal

L1

Genitofemoral

L1,
L2

Lateral femoral
cutaneous

L2,
L3

Obturator

L2-L4

Anterior scrotal
nerves in males
Anterior labial nerves
in females
Cremaster in
males

Femoral ramus
Genital ramus
Lateral femoral
cutaneous

Obturator
externus (ADduct
thigh, LAT rotate)

Cutaneous ramus

 Adductor longus
Adductor brevis
Gracilis
Pectineus
Adductor magnus
Femoral

L2-L4

Iliopsoas
Pectineus
Sartorius
Quadriceps
femoris

Short, direct muscular

branches

T12L4

Psoas major
Quadratus
lumborum
Iliacus
Lumbar
intertransverse

Anterior cutaneous
branches
Saphenous

PES ANSERINE: (medial side of knee)

Saratorius....................Femoral
Gracillis........................Obtorator
Bursae = pes anserine burase
semiTendinosis............Tibial
SGT FOT

BRACHIAL PLEXUS
From

Nerve

Roots[
2]

Muscles

Cutaneous

roots

dorsal
scapular
nerve

C5

rhomboid muscles
and levator scapulae

roots

long thoracic
nerve

C5,
C6,C7

serratus anterior

uppe
r
trunk

nerve to the
subclavius

"C5",C
6

subclavius muscle

uppe
r
trunk

suprascapul
ar nerve

C5, C6

supraspinatus and
infraspinatus

later
al
cord

lateral
pectoral
nerve

C5,
C6, C7

pectoralis major (by

communicating with
the medial pectoral
nerve)

later
al
cord
(term
inal
N)

musculocuta
neous nerve

C5,
C6, C7

coracobrachialis,
brachialis and biceps
brachii

becomes the lateral

cutaneous nerve of
the forearm

later
al
cord

lateral root of
the median
nerve

C6, C7

fibres to the median

nerve

post
erior
cord

superior/upp
er
subscapular
nerve

C5, C6

subscapularis (upper
part)

post
erior
cord

thoracodorsa
l
nerve(middle
subscapular
nerve)

C6,
C7, C8

latissimus dorsi

post

lower /

C5, C6

subscapularis (lower

erior
cord

inferior
subscapular
nerve

part ) and teres major

post
erior
cord

axillary
nerve

C5, C6

anterior branch:
deltoid and a small
area of overlying skin
posterior branch:
teres minor and
deltoid muscles

posterior branch
becomes upper
lateral cutaneous
nerve of the arm

post
erior
cord
(term
inal
N)

radial nerve

C5,
C6,
C7,
C8, T1

triceps brachii,
supinator, anconeus,
the extensor muscles
of the forearm, and
brachioradialis

skin of the posterior

arm as the posterior
cutaneous nerve of
the arm

medi
al
cord

medial
pectoral
nerve

C8, T1

pectoralis major and

pectoralis minor

medi
al
cord

medial root
of the
median
nerve

C8, T1

fibres to the median

nerve
all flexors of forearm
except FCU, part of
FDP,

portions of hand not

served by ulnar or
radial

medi
al
cord

medial
cutaneous
nerve of the
arm

C8, T1

front and medial skin

of the arm

medi
al
cord

medial
cutaneous
nerve of the

C8, T1

medial skin of the

forearm

forearm
medi
al
cord
(term
inal
N)

ulnar nerve

C8, T1

flexor carpi ulnaris,

the medial two bellies
of flexor digitorum
profundus, the
intrinsic hand
muscles except the
thenar muscles and
the two most lateral
lumbricals

the skin of the medial

side of the hand and
medial one and a
half fingers on the
palmar side and
medial two and a half
fingers on the dorsal
side

The main portion of the MEDIAN NERVE supplies the following muscles:
Superficial group:
Pronator teres
Flexor carpi radialis
Palmaris longus
Intermediate group:
Flexor digitorum superficialis muscle
The anterior interosseus branch of the median nerve supplies the following muscles:
Deep group:
Flexor digitorum profundus (only the lateral half)
Flexor pollicis longus
Pronator quadratus
Hand
median nerve supplies:1st and 2nd lumbrical muscles, muscles of the thenar eminence by a recurrent
thenar branch.
The rest of the intrinsic muscles of the hand are supplied by the ulnar nerve.
The median nerve innervates the skin of the palmar side of the thumb, the index and middle finger,
half the ring finger, and the nail bed of these fingers.
The lateral part of the palm is supplied by the palmar cutaneous branch of the median nerve, which
leaves the nerve proximal to the wrist creases. This palmar cutaneous branch travels in a separate

fascial groove adjacent to the flexor carpi radialis and then superficial to the flexor retinaculum. It is
therefore spared in carpal tunnel syndrome.
The muscles of the hand supplied by the median nerve can be remembered using the mnemonic,
"LOAF" for Lumbricals 1 & 2, Opponens pollicis, Abductor pollicis brevis and Flexor pollicis brevis.
(NB: OAF are the thenar eminence)

Lumbo -Sacral plexus

Nerve

Segme
nt

Innervated muscles

Superior
gluteal

L4-S1

Gluteus medius
Gluteus minimus
Tensor fasciae latae

Cutaneous branches

Inferior gluteal

L5-S2

Posterior
cutaneous
femoral

S1-S3

Gluteus maximus
Posterior cutaneous
femoral
Inferior cluneal nerves
Perineal branches

Direct branches
from plexus
Piriformis

S1-2

Piriformis

Obturator
internus

L5-S1

Obturator internus

Quadratus
femoris

L5-S1

Quadratus femoris

L4-S3

Semitendinosus (Tib)
Semimembranosus (Tib)
Biceps femoris
Long head (Tib)
Short head (Fib common peroneal)
Adductor magnus (medial
part, Tib)

Sciatic
Sciatic

Tibal
L4-S3

Common
fibular
(peroneal)

Fibular
L4-S2

Lateral sural cutaneous

Communicating fibular

Superficial
fibular

L5-S2

lateral compartment
Peroneus longus (runs
post to lat malleolus)
Peroneus brevis

Medial dorsal cutaneous

Intermediate dorsal
cutaneous

Deep

L4-S2

anterior compartment

Lateral cutaneous nerve of

fibular
(peroneal)

and dorsum of foot

Tibialis anterior
Extensor digitorum
longus
Extensor digitorum brevis
Extensor hallucis longus
Extensor hallucis brevis
Peroneus tertius

big toe
Intermediate dorsal
cutaneous

DEEP Posterior
compartment
Triceps surae
Plantaris
Popliteus
Tibialis posterior
Flexor digitorum longus
Flexor hallucis longus
SUPERFICIAL post
compartment
Gastrocnemius and
soleus (S1-2)

Medial sural cutaneous

Lateral calcaneal
Medial calcaneal
Lateral dorsal cutaneous

Medial
plantar
(from tibial
nerve)

Abductor hallucis
Flexor digitorum brevis
Flexor hallucis brevis
(medial head)
Lumbrical (first and
second)

Cutaneous to medial
plantar aspect of foot

Lateral
plantar
(from tibial
nerve)

Flexor hallucis brevis

(lateral head)
Quadratus plantae
Abductor digiti minimi
Flexor digiti minimi
Lumbrical (third and

Cutaneous to lateral plantar

aspect of foot

Tibial nerve

L4-S3

fourth)
Plantar interossei (first to
third)
Dorsal interossei (first to
fifth)
Adductor hallucis
Pudendal and
coccygeal
Pudendal
(Pudendal
plexus)

S2-S4

Muscles of the pelvic

floor:
Levator ani
Superficial transverse
perineal
Deep transverse perineal
Bulbospongiosus
Ischiocavernosus
Sphincter anus externus
Urethral sphincter

Coccygeal
(Coccygeal
plexus)

S5-Co1

Coccygeus

Inferior rectal
Perineal
Posterior scrotal/labial
Dorsal penis/clitoris

Anococcygeal
Dorsal branches

sural nerve: formed by the junction of the medial sural cutaneous (from tibial nerve) with the
peroneal anastomotic branch of the lateral sural cutaneous nerve (from common fibular nerve)

Layers of the Anterior Forearm

All median nerve except FCU and medial half of FDP
1. Superficial
pronator teres
flexor carpi radialis
palmaris longus
flexor carpi ulnaris (ulnar nerve)
2. Intermediate
flexor digitorum superficialis (ulnar nerve is medial half)
3. Deep -innervated by ant. interosseous nerve which is branch of median nerve
pronator quadratus
flexor digitorum profundus
flexor pollicis longus
All innervated by RADIAL nerve:
triceps, brachoradialis,

All mm listed below are innervated by post interosseous nerve which is a branch of the radial
nerve
supinator
1. Extend hand (carpi)
extensor carpi radialis brevis
extensor carpi radialis longus
extensor carpi ulnaris
2. Extend medial 4 digits (fingers)
extensor digitorum
extensor indicis
extensor digiti minimi
3. Extends thumb (pollex) (snuff box)
abductor pollicis longus
extensor pollicis brevis
extensor pollicis longus
Muscles of Anterior Compartment:
INNERVATED by Median Nerve except FCU
1. Superficial
pronator teres
flexor carpi radialis
palmaris longus
flexor carpi ulnaris (INNERVATED BY ULNAR NERVE)
2. Intermediate
flexor digitorum superficialis
3. Deep
pronator quadratus
flexor digitorum profundus 1 and 2
flexor pollicis longus
thenar eminence (OAF): opponens pollicus, ABD policus, flex pollicus brevis
1st 2 lumbrical; LOAF
ULNAR NERVE:

Hypothenar eminence (OAF)- opponens DM, ABductor DM, Flexor DM brevis

Interossei- Pad, and Dab
ADDuctor pollicis
3rd and 4th lumbricals
FCU
medial of FDP
FCU
Ranchos los amigos: -does not predict improvement over long term, helps understand behaviour and
progression of brain injury over time, useful for therapist, PT, and family; 1=no response, 5=confused,
10=normal

OUTC
OME

NO RESPONSE:
Does not respond to voices, sounds, light, or touch; appears in a deep
sleep.

II

GENERALIZED RESPONSE:
Limited, inconsistent, non-purposeful responses; first reaction may be to
deep pain; may open eyes but will not seem to focus on anything in
particular

III

LOCALIZED RESPONSE:
Inconsistent responses but purposeful in that reacts in a more specific
manner to stimulus; may focus on a presented object; may follow simple
commands.

IV

CONFUSED, AGITATED:
Heightened state of activity; confusion; unable to do self-care; unaware of
present events. Reacts to own inner confusion, fear, disorientation;
excitable behavior may be abusive or aggressive.

CONFUSED, INAPPROPRIATE, NON-AGITATED:

Appears alert; responds to commands; follows tasks for 2-3 minutes but
easily distracted by environment; frustrated; verbally inappropriate; does
not learn new information.

VI

CONFUSED APPROPRIATE:
Follows simple directions consistently; needs cueing; can relearn old
skills; serious memory problems but improving; attention improving; selfcare tasks performed without help; some awareness of self and others.

VII

AUTOMATIC APPROPRIATE:
If physically able, can carry out routine activities but may have robot-like
behavior, minimal confusion, shallow recall; poor insight into condition;
initiates tasks but needs structure; poor judgement, problem-solving and
planning skills; overall appears normal.

VIII

PURPOSEFUL APPROPRIATE:
Alert, oriented; recalls and integrates past events; learns new activities
and can continue without supervision; independent in home and living
skills; capable of driving; defects in stress tolerance, judgment; abstract
reasoning persist; many function at reduced levels in society.

Glasgow coma scale: eye opening, verbal response, motor response; from 0-15, less than 8 is
severe head injury

second rib = superior angle of scapula

Well, thats it. If you actually made it to the end of this document, congrats. I feel pretty confident
youll not only pass but kill the written exam. By the way, not sure if you counted, but this doc is 89
pages long. Whoa, can you say OCD!
Jason