Study Guide PCE Jason Shane Amanda Mrsic

8/9/2019 Study Guide PCE Jason Shane Amanda Mrsic

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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 (let’s 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, DTF’s, 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 orchildbirth 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


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maintain mm length and mobility, AROM for elbow, wrist, andhand; 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 ofOA 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, O’sullivan pg 4

01.01.07 Fractures, dislocations, subluxations

Shoulder (GH joint) dislocation: Rx-scapular stabilization/posture,

rotator cuff strengtheningàfunctional 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


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OSTEOPEROSIS = -2.5 SD AND BELOWP37

01.01.09 Tumour/pathological fractures (ahh, the good old

tumour lectures, didn’t 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 Sy’s 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


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

scoliosis, postural dysfunction)

MEMORIZE THIS PICTURE, I’m 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; O’Sullivan pg 37, usually a staph aureus


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infectionGoals: 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 - can’t WB through the end, some ppl can achieve a

normal gait pattern


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Prosthetic sockets: total surface bearing, patellar tendon bearingPressure 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/microprocessorgait 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)


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NO PILLOWS under legs in supine or between legs fortransfemoral

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=Si’s & Sy’s depend on degree of compression and

may include P, tingling, numbness. Loss of nn conduction, mm


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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 wallTx: restore mm imbalance, Sx

NERVE ENTRAPMENT-

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

compression, thickend retinaculum in FCU, Sy’s 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 interosseousnerve) occurs in radial tunnel

CARPAL TUNNEL P48, can do Phalen’s 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


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P129-133NEUROPATHY-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 weeksAxonotemesis= 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 andsensory 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

Bell’s 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


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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,

raynaud’s, 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


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of the original wound but has an excess amount of tissue inrelation to what is needed to replace the damaged dermis

01.02 Neurological (20%±5%) (This list is not necessarilyexhaustive.)

01.02.01 Cerebral Vascular Accident/transient ischemic attack

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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 brain’s long connecting

nerve fibers; usually causes a coma, can’t 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


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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 toareas 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, andPE’s

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

(can’t smell), seizures, expressive aphasia)

Temporal lobe= receptive aphasia, dyslexia, dysgraphia, amnesic

syndromes, epilepsy


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AND NON TRAUMATIC BRAIN INJURYSTROKE

ischaemic= 80% of strokes; could be d/t a thrombus (slower sy’s

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

S’s and Sy’s= confusion, headache, trouble speaking,

understanding speech, numbness or weakness on one side, can’t

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 person’s blood to clot quickly,

irritation or inflammation of lining of vein, DVT’s

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


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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


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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


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incomplete injury ASIA BVoluntary 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 spinalcord 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 partiallyinnervated…KNOWN 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


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picture; i.e. mixture of UM and LMNLPrognosis 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 Pt’s 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 normalC2-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 contracturesMajor 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)


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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 ADL’s

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


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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 intactthere 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)=body’s 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),


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osteoporosis ANDPost 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 onits own, bladder mngmt is either intermittent catheters or

condom/foley drainage

Flaccid bladder=in conus and cauda equina injuries, messages

don’t 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 SCISpasticity, 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


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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


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Secondary progressive – starts off as relapsing remitting thensteadily 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

deficitsInfo: 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!)


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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,Brudzinski’s 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 5-

8yrs

01.02.08 Post-polio syndrome (from Wikipedia) I’ve been toldthis 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

http://en.wikipedia.org/wiki/Poliovirushttp://en.wikipedia.org/wiki/Poliovirushttp://en.wikipedia.org/wiki/Brainstemhttp://en.wikipedia.org/wiki/Brainstemhttp://en.wikipedia.org/wiki/Brainstemhttp://en.wikipedia.org/wiki/Anterior_horn_%28spinal_cord%29http://en.wikipedia.org/wiki/Anterior_horn_%28spinal_cord%29http://en.wikipedia.org/wiki/Anterior_horn_%28spinal_cord%29http://en.wikipedia.org/wiki/Motor_neuronhttp://en.wikipedia.org/wiki/Motor_neuronhttp://en.wikipedia.org/wiki/Motor_neuronhttp://en.wikipedia.org/wiki/Skeletal_musclehttp://en.wikipedia.org/wiki/Skeletal_musclehttp://en.wikipedia.org/wiki/Skeletal_musclehttp://en.wikipedia.org/wiki/Post-polio_syndrome#cite_note-NINDS-2http://en.wikipedia.org/wiki/Post-polio_syndrome#cite_note-NINDS-2http://en.wikipedia.org/wiki/Post-polio_syndrome#cite_note-NINDS-2http://en.wikipedia.org/wiki/Metabolismhttp://en.wikipedia.org/wiki/Metabolismhttp://en.wikipedia.org/wiki/Metabolismhttp://en.wikipedia.org/wiki/Metabolismhttp://en.wikipedia.org/wiki/Metabolismhttp://en.wikipedia.org/wiki/Post-polio_syndrome#cite_note-NINDS-2http://en.wikipedia.org/wiki/Skeletal_musclehttp://en.wikipedia.org/wiki/Skeletal_musclehttp://en.wikipedia.org/wiki/Motor_neuronhttp://en.wikipedia.org/wiki/Motor_neuronhttp://en.wikipedia.org/wiki/Anterior_horn_%28spinal_cord%29http://en.wikipedia.org/wiki/Anterior_horn_%28spinal_cord%29http://en.wikipedia.org/wiki/Brainstemhttp://en.wikipedia.org/wiki/Brainstemhttp://en.wikipedia.org/wiki/Poliovirus


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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, Friedreich’s 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

http://en.wikipedia.org/wiki/Post-polio_syndrome#cite_note-NINDS-2http://en.wikipedia.org/wiki/Post-polio_syndrome#cite_note-NINDS-2http://en.wikipedia.org/wiki/Post-polio_syndrome#cite_note-NINDS-2http://en.wikipedia.org/wiki/Post-polio_syndrome#cite_note-khan-5http://en.wikipedia.org/wiki/Post-polio_syndrome#cite_note-khan-5http://en.wikipedia.org/wiki/Post-polio_syndrome#cite_note-khan-5http://en.wikipedia.org/wiki/Post-polio_syndrome#cite_note-khan-5http://en.wikipedia.org/wiki/Post-polio_syndrome#cite_note-NINDS-2


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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 saccule-detects 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 can’t work out

where they are in space

oscillopsia=blurred vision

antibiotic= GENTOMYCIN = affects vestibular system

UVL-unilateral vestibular loss= peripheral dysfunction: cause-infection (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 nystagmus-

delayed onset, brief and rotary

CI’s arthritis, vertebral art insufficiency, 5D’s


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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


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the result of dysfx in central or peripheral NSTypical 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, Erb’s palsy)

Cerebral Palsy:

CP: non progressive lesion of the brain that occurs before the age of2, 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


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dystonic: long sustained involuntary movements and postureshypotonic: 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

Erb’s 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


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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

-can’t 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


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be up to 100/day2) 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 doesn’t like colored pens andpencils)

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

http://en.wikipedia.org/wiki/Sensory_systemhttp://en.wikipedia.org/wiki/Sensory_systemhttp://en.wikipedia.org/wiki/Sensory_systemhttp://en.wikipedia.org/wiki/Sensory_systemhttp://en.wikipedia.org/wiki/Sensory_modalityhttp://en.wikipedia.org/wiki/Sensory_modalityhttp://en.wikipedia.org/wiki/Sensory_modalityhttp://en.wikipedia.org/wiki/Sensory_modalityhttp://en.wikipedia.org/wiki/Sensory_modalityhttp://en.wikipedia.org/wiki/Sensory_modalityhttp://en.wikipedia.org/wiki/Sensory_systemhttp://en.wikipedia.org/wiki/Sensory_system


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Dorsal columns (medial lemniscu)- 2-pt discrimination, fine touch, sterognosis, vibration; receptorsare pacinian corpuscles (vibration), merckels’s 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; don’t 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 Horner’s 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 (disor der of motor planning, can’t

carry out purposeful movements), impaired hearing, difficulty dressing, may also produce motor

speech dysfunction (Broca’s area)

Vertebral artery= two join to form basilar artery; imp branches to watch for strokes PICA (largestbranch 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


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mvmts of extremities), hemisensory impairment, contralat homonymous hemianopia, difficulty withnaming and colors

Superior cerebellar artery= supplies cerebellum, limb ataxia, Horner’s syndrome (droopy eyelid, red

face), contralateral sensory loss

Ant inf cerebellar = supplies cerebellum, ipsilateral limp ataxia, ipsilateral horner’s, 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 andlaryngeal paralysis, contralateral sensory loss (p and temp) of trunk, visual sy’s (paralysis of vertical

eye mvmts and decrd pupillary light reflex)

Broca’s(receptive) aphasia= Broca’s area is located in the left frontal lobe

Wernicke’s(expressive) aphasia= Wernicke’s 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 brodmann’s area have difficulty differentiating smells

CRANIAL NERVES:

1 Olfactory- does smell; damage to can cause anosomia (inability to detect smells, seen with frontallobe 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


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pathways for the left hemifield of both eyes, and the left half of the brain has visual pathways for theright hemifield of both eyes)

3 Occulomotor- does pupillary reflexes; damage to can cause absence of pupillary constriction or

Horner’s 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


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dilated cardiomyopathy: heart with increased mass, heart has troublepumping; 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

Sy’s-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 defectsmost 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


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percussion; aspirate or chest tube1)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 surgicalinterventions)

Terrible Triad: (3 I’s)

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 100bpm


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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: can’t 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


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Left sided heart failure: due to: damming of blood in pulmonarycirculation; 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


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of death in kids (intra-tentorial)1) intracerebral primary= tumors neurons don’t 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 spineneuronomas: 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,

tachpneaRx: 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


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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 hyper-

responsiveness: 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 more2) 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


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inflammationO2 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 (it’s 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


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pulmonary fibrosis: ⅔ no known cause; ⅓ 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, avascularnecrosis 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 body’s 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,


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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 MUCUScan 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


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underlying cause: artherosclosisS&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 Homan’s; 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 venacava filter


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Volumes (I don’t even know how many times I’ve 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)


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TOTAL LUNG CAPACITY (TLC): The volume of the lung after maximalinspiration. 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


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phase 2: outpatient 12 week programphase 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, they’re calling it

“oncology” instead of tumors)

Staging cancer-TNM: Tumor (extent/spread), Nodes (lymph), Mets (distant

ones)

PT relevant Rx: PT’s can teach Pt’s 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, bonehealth, peripheral neuropathy (impact on balance), deconditioning

Palliative Care: Goals are to provide comfort, support, maximize

independence; PT’s can help with respiratory, stress reduction, education


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(loss of hair ), photosensitivity, mucosal ulcers, Raynaud’s (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 (espupper 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 haemophiliagene.

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


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serious traumaBleeding 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 80’s 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

creating1) 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


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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

ex’s, prevent deformity

Inflam conditions:-pain worse in morning, morning stiffness greater than

1hrNon-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 repositioningin 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-baker’s 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


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extensors pull the prox phalanx into hyperext, metatarsal head prolapsesand 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


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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 Sy’s must be present for 6 weeks

to make diagnosis, avoid resisted ex’s 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 16Sy’s-joint pain, stiffness, warm swollen joints, eye issue (uveitis), HLA-

B27, 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


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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 supportPT Rx: check ex tolerance

Fibromyalgia=chronic pain syndrome affecting mm and soft tissue (non-

articular rheumatism)


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Etiology: unknownSy’s-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, nutritionPT 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,

virusessmooth 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 PT’s: 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


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body has severe response to bacteria or other germs; whole bodyinflammatory 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 30morbidly 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, surgeryexercise=moderate intensity 40-60% progress to 50-70% HRR, 5-7d/wk, 45-

60mins, 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

Documents

Study Guide PCE Jason Shane Amanda Mrsic