Holly's Set

AD

Recognition • Common in SCI >T6 • Respons to some noxious stim • s/sx o severe HTN o bradycardia o profuse sweating above level o HA o Nausea o Piloerection o Red and blotchy skin Response • Place in UPRIGHT position • Attempt to ID and removenoxious stim - cathetder, scoks, shoes, etc • Monitor VS abd call for med assistance

sports PT high school hockey player with Chrons and small bowel resection- high risk for what?

a. Reactive arthritis/Reiter's syndrome= similar RA whereby body's immune system mistakenly attacks joints and causes joint pain and stiffness as well as deformity. Affects larger joints and lower spine especially SIJ.

subtalar capsular

limitation varus

13 y/o girl- ACL reconstruction with ortho. What is GREATEST influence on candidacy for surgery?

skeletal immaturity

1. Inpatient PT after brain damage from MVA. Physical therapist finds patient trying to use her comb on the mirror. What is perceptual deficit here?

somatoagnosia

1. neck pain d/t MVA. Determine function of deep cervical flexors using cranio cervical flexion test. Expected findings when normal?

1. xpected findings when normal? a. During active chin tuck, the pressure in stabilizer cuff increases to 22 and pt can hold for 10 s

1. Manual w/c C5 quadriplegia. What w/c most appropriate?

a. Manual with handrim projections: but not primary mode due to limited UE innervation and associated endurance

Rinnes versus Webers test

a. Rinne's test: compare bone conduction with air conduction if BC is greater than AC, the pt is experiencing conductive deafness. If AC is greater than BC, the pt. is experiencing sensorineural deafness. i. Weber's= holding turning fork on vertex of head and ask what ear is louder.

tibfib capsular

when stressed

tinea pedis

• (aka athlete's foot) o Superficial fungal infection very contagious! o Etiology = prolonged moistness, excessive sweating o S+S = itching, redness, peeling skin btwn toes, odor, pain o Tx = antibiotics, prevention (wear shoes in locker room, change socks freq, etc.)

eczema

• (aka dermatitis) o Chronic skin inflammation d/t immune abnormality, allergic rxn, or external irritant o Etiology = higher risk in kids but can grow out of it o S+S = red or brown, itchy, lichenified skin plaques o Tx = corticosteroids, antibiotics, anti-inflammatories, avoid extreme temps, stress management

knee goni

• FLEX & EXT: supine o F: lat. fem. Epicondyle o SA: Gr. Troch. MA: Lat. malleolus

wagner ulcer scale

0 • No open lesion BUT maybe pre-ulcerative lesion • Healed ulcers • Bony deformity 1 • Superficial ulcer - NO sub-Q tissue 2 • Deep ulcer - THROUGH sub-Q • Potential bone, tendon, lig, joint capsule seen 3 • Deep ulcer • Infection present osteitis, abcess, osteomyelitis 4 • Gangrene digit 5 • Gangrene of foot requiring disarticulation

talocrural LP CP

10* PF, midway max INV and EV Max DF

distal radioulnar LP CP

10* SUP 5* SUP

scoliosis age

13-14 in males. And 11-13 in females.

PT adjusts on/off time e-stim. For muscular re-education what do ya use

1:5

H&Y PD scale

1= UL 2= BL/ midline 3= BL impaired balance 4= bilateral severe 5= confined to bed or w/c

1. PT administers Mini-Mental Exam. Minimum score to avoid classified in cognitive impairment

24

knee LP CP

25* FLEX Full EXT, ER tibia

hip LP CP

30* FLEX, 30* ABD, slight ER Full EXT, IR

GH LP, CP

30* FLEX, 55* horizontal ADD ABD and ER

oxygen therapy

50/50 rule - if pO2 < 50 and if pCO2 >50 then MECHANICAL VENT IT ISSSSSS!!!

ottawa knee rules

55 y/o+ isolated patellar tenderness w/o other tenderness tender at fibular head inability to F knee to 90 deg inability to WB immediately after/ED

ulnohumeral LP CP

70* FLEX, 10* SUP EXT

proximal radioulnar LP CP

70* FLEX, 35* SUP 5* SUP

spinocerebellar tract

= ipsi subconscious proprioception, muscle tension, posture, joint sense ♣ Ventral = trunk, UEs and LEs; this is the dumb one that crosses and re-crosses ♣ Dorsal = mostly LEs ascending

scoliosis

About • Lateral curvature of the spine c-shaped or s-shaped o Usually in thoracic or lumbar regions o Named based on side of CONVEXITY ♣ If ROT present, also towards this side o Can also have associated kyphosis or lordosis • Usually quantified via Cobb method with standing x-ray • Vertebral column, rib cage, supporting ligs, muscles are all affected • Classification o Idiopathic = 80% OF CASES!! unknown etiology ♣ Infantile - 0-3 ♣ Juvenile - 4-puberty ♣ Adolescent - 12 for girls, 14 for boys ♣ Adult - skeletal maturation o Functional = other abnormalities in body affect spine ♣ NON-structural aka can be corrected with lateral bend (eg leg length discrep) o Neuromuscular = developmental patho causes issue in spine (eg Marfans, CP) ♣ STRUCTURAL aka cannot be fixed lateral shift o Degenerative = occurs due to normal aging process (HNP, osteophyte formation) ♣ STRUCTURAL aka lateral shift cannot fix cuz its spine itself Etiology • Typically idiopathic (80% of cases) • Contributing factors = altered spine development in utero, NM diseases, inhereitence as autosomal dominant trait • usually diagnosed 10-13 yo • the curve says it alll o small curve aka <10deg = girls and boys same likelihood o large curve aka >30 degrees = GIRLS more likely o curves <20 degrees = rarely cause problems o if curve >40/50* when reach skeletal maturity = will keep prog as adult o once >60 degrees = pulmonary insufficiency, sig pain, impairment lung capacity, degenerative changes S/Sx • STRUCTURAL CURVE o Asymmetries of shoulder, scaps, pelvis, skinfolds • JUVINILE IDIOPATHIC o Usually THORACIC and CONVEX to RIGHT o May progress quickly o MAYBE rib hump (on conVEX side) o Not pain usually until curve has progressed - usually 2/2 structures AROUND spine that get affected cuz weird relationship NOT spine itself Imaging • X-ray = ant and lat; stand and bent over • Scoliometer = measures curve • Cobb method = measures curve too • Bone scan or MRI = r/o conditions like infections, neoplasms, spondy, HNP, comp fxs Exam • Adams fwd bend test • Scoliometer Mgmt • FOCUS = depends on magnitude of curve and progression o Not progressing = no action o Note: typically does not progress after bone growth is complete as long as not >40* • PT = posture, flexibility, muscle strengthening, stretching, shoe lifts, bracing, respiratory function • BRACE = 25-40* • SX = REQUIRED WHEN >40* CURVE o Posterior spinal fusion and harrington rod o PT after = breathing, posture, flexibilty, general strength and resp muscle function Outcome • PT should improve • Prognosis dep on age of onset and severity curve • Early intervention = best possible outcome Comp • TORTICOLIS = see later

antithrombolytic

Action • inhibit platelet aggregation and clot formation bleeding risk

AC LP, CP

Arms at side 90* shld ABD

SC LP CP

Arms at side Max shld elevation

TROUSSEAU'S SIGN

BP cuff occludes, patient's hypocalcemia and subsequent neuromuscular irritability will induce spasm of the muscles of the hand and forearm. The wrist and metacarpophalangeal joints flex, PIP/DIP extend, and the finegrs ADD

Thumb ROM

CMP ABD 70 F 15 E 20 opp tip thumb base 5th MCP F 50 IP F 80

ANKLE ROM

DF 20 PF 50 INV 35 EV 15

mid tarsal capsular

DF>PF>ADD>IR

accessibility requirements

Doorway Min = 32 in width Max = 24 in depth Threshold <3/4 in = slide door <1/2 in = other doors Carpet ½ in pile or less Hallway clearance 36 in width Ramp 12 in run every 1 in rise 8.3% grade w/c turning radius (u-turn) 60 in width 78 in length Fwd reach w/c Low = 15 in High = 48 in

1st MCP capsular

E>F

capsular pattern GH

ER>ABD>ER

capsular pattern A-O

EXT SB equal

hip ROM

F 120 E 30 ABD 45 ADD 30 IR ER 45

knee ROM

F 135

ROM elbow

F 150 E 0

LE tension tests

Flexion, ABD, DF= sciatic and tibial Flexion, DF, EV= TIBIAL Flexion, DF, IN= SURAL Flexion, IR, PF, INV= Common Fibular N Flexion, DF= spinal nerve root

w/c components

Frame • ultralight = sports; NO POSTURE support • standard/lightweight = can self-propel, can sit comfortably • hemi frame = self-propel using LES! • One-hand drive frame = self-propel via ONE UE! • Amputee frame = can self-propel BUT COM shifted BACK • Power w/c = can NOT self-propel BUT can operate the device themselves • Geri chair = can NOT self-propel AND can NOT operate power w/c • Reclining frame = cannot WS or sit up-right ; mod-severe trunk involvement • Tilt-in-space = cannot sit upright or perform WS ; issues with sliding, EXT tone Headrest • Planar (flat) posterior = used with reclining/tilt-in-space OR hyper-EXT neck • Curved Back Inserts • Sling back = pt needs NO postural support and NO neuro deficits • Planar back = pt needs MILD-MOD trunk support • Curved back = pt needs MOD trunk support • Custom molded = pt needs SIG postural support 2/2/ severe postural concerns • Removable back insert = folding w/c • Back height below inf angle scap = pt can self-propel AND good trunk control • Back height above inf angle scap = pt CAN self propel BUT needs more spinal support ORRRR they have a power device with little/no trunk control Seat inserts • Sling = pt needs NO postural support and NO neuro deficits • Planar = NO DEFORMITY • Curved = pt needs MILD-AGGRESSIVE trunk support (inc contact area) • Custom molded = correct pelvic obliquity or fixed asymmetrical deformity • Removable = folding w/c • Bevel (undercut) = for peeps who self-propel via Les Trunk supp • Planar lateral = MILD-MOD lateral support • Contoured/curved = needs TOTAL CONTACT (worse) • Chest strap = needs trunk support for falling fwd • Chest harness = needs chest and shoulder support Armrests • Removable • None = pt needs NO UE or trunk support • Full length arms o pt does sit>stand o pt needs postural support o pt uses lap board • tubular or single posted arms o min support UEs o easy access wheels o easy arm removal • fixed/non-removeable = durable UE support Wheel locks / brakes • Toggle/lever brackes = pt can operate I • Brake extension = gives extra leverage OR makes so pt can reach • Attendant op brakes = breaks the person pushing uses Handrims • Small diameter = good strength ; good for speed • Large diameter = some weakness • Rim projections = stick out from rim to help pt with grip • Covered rims = gives more friction for pt for better grasping Footrests • Standard = full ROM feet and ankles • Adjustable = not full ROM foot/ankles • One-piece footboard = additional support needed • Custom foot box = need custom for some reason (eg windswept) Power mobility controls • Joystick • Proportional control = speed changes based on joystick displacement • Non-proportional control = speed stays same no matter displacement • Sip-and-puff = switch based where force inhale/exhale controls • Head control = controlled with head o Can be proportional or non-prop other • Bariatric chair = 300-1000 lbs • Solid cushions = lightweight, high shear o Viscoelastic, polyurethane, honeycomb • Liquid cushions = heavier, limits shear; NOT if incontinent o Gel or water filled • Air filled = light, need diligent monitoring of inflation; need trunk stability o Roho, bye bye decubiti

claudication scale

Grade 1 Def discomfort - but only initial or modest level Grade 2 MOD discomfort - CAN distract Grade 3 INTENSE pain - cannot distract Grade 4 Excruciating an unbearable pain

subtalar ROM

INV 5 EV 5

US technique

Intensity: -Spatial averaged intensity beam non uniformity ratio BNR: 2:1- 8:1- higher move to avoid burns F 3Hz superficial 1 Hz deeper duty cycle on time/ (one+off) *100 continuous: heating pulsed: non thermal, 20% duration: dam of head* (#heads ) * (1 min or 2-3 min) thermal 2-3x/week non thermal: 1x/day

1. Trochanteric bursitis 1 week treated, no resolution, problems in gait. Weakness of quad and altered sensation at greater trochanter. Most likely cause of problem?

L4 nerve root compression

recent stroke R hemisphere, pusher syndrome. Would lean

Left

RLA

Levels of Cognitive Functioning Scale • classify level of injury based on where the pt best meets the criteria for each level • analyzes COGNITION I - No response II - General response III - Local response IV - Confsued and agitated V - confused and inapprop VI - confused and approp VII - automatic and approp VIII - purposeful-approp

CN XI spinal accessory

M = voluntary: SCM, trap T = shoulder shrug

CN VI abducens

M = voluntary: lateral rectus of eyeball T = lateral gaze (aka ABD eyes)

carpometacarpal LP

Midway FLEX/EXT and ABD/ADD

facet LP, CP

Midway btw FLEX and EXT EXT

subtalar, mid tarsal, tarsoMT LP CP

Midway btw movement extremes SUP

MTP LP CP

Neutral Full EXT

talocrural capsular

PF>DF

RLA gait

Phase Beginning phase Ending phase Function IC Heel touches ground Heel touches ground Deceleration LR Following IC Other foot coming off to swing Shock absorption; transfer BW MS Other foot lifted Body weight over forefoot Support BW over stance limb TS Heel rise Other foot strikes ground (IC) Body progression beyond foot PSw IC opp limb Ipsilateral toe off Accelerate progression ISw Foot lifted from ground Max knee flexion swing; swing foot opp stance foot Bringing limb fwd from behind MSw Max knee flexion Tibia perp to ground (vertical) Foot clearance TSw Tibia vertical Just before IC Completes limb advancement

RBC, leukocytes, platelets, PTT, HCt, Hgb

RBC 4-5.6x10^6 leuko 3.5-9x10^3 platelet 165-415*10^3 PTT 26.3-39.4 HCt 35-46% Hub 12-16

CN VIII vestibulococchlear

S = hearing and balance of the ear T = hear watch ticking (record distance they begin to hear; + cant hear 18-24 in; diff B) Hearing tests - Weber and Rinne (use tuning fork) Balance and coordination tests

ULTT4

Shoulder depression, 10-90* ABD, elbow flexion, forearm sup, and RD, forearm sup, wrist ext, finger ext, shoulder ER CL cervical SB Ulnar

MCP LP CP

Slight FLEX Fingers = Full FLEX Thumb = full OPP

IPJ LP CP

Slight flexion Full EXT

TB

TB About • Highly contagious infectious disease spread through airborne transmission • Largely infects lungs • Also can infect brain, spine, kidneys • LATENT = infected but no sx and not contagious • ACTIVE = symptomatic; either latent back or recetn exposure to contagious person Etiology • Caused by mycobacterium tuberculosis bacteria - multiple antibiotic resistant strains • RISK = weak immune system S/Sx • ACTIVE in lungs o Fever o Chills o Fatigue o Weight loss o Dec appetite o Night sweats o Persistent cough >3 weeks o Bloody sputum o Chest pain associated with deep breathing or coughing o Abnormal lung sounds - pleural effusion o Enlarged lymph nodes o Clubbing of digits later

barthel index, BBS, functional reach, POMA

a. Barthel Index: 10 ADLs 0-100 in increments of 5. 100= independent i. BBS: 14 tasks, 56 max, 45-fall risk ii. Functional reach: risk for falls iii. POMS: balance and gait 28 max. 19 risk for falls

elderly pt spinal stensosis- how to diff from intermittent vascular claudication

a. Bicycle/ van Gelderen's test: stress LE vascular system w/o causing central canal or foraminal stenosis

1. Limitation in movement SLR in supine. Then flexes knee and NO additional movement.

a. Likely gluteal bursitis: also indicate abscess, tight glute max, tight posterior capsule

1. Knee capsular tightness and limited ability to attain full flexion. An initial intervention to employ should emphasize sustained mobilization in lP position. What is best choice?

a. Posterior glide and IR of the tibia.

cerebral thrombosis 4 days ago: dec. pain/Temp of ipsilateral face, nystagmus, vertigo, nausea, dysphagia, ipsi Horner's syndrome, CL loss pain/T. what location

a. Posterior inferior cerebellar artery: Wallenbergs syndrome= PICA= branch vertebral artery

77 y/o female diazepam for anxiety and fall risk- due to what side effect

a. Sedation, impaired balance, dec NM function, dec central processing

1. therapist suspects that pt recovering from MCA stroke exhibiting HHA. Would test would confirm this?

a. Visual confrontation test with a moving finger: visual field is examined using confrontation test. Pt sits opposite the therapist and is instructed to maintain his/her gaze on therapist nose. Therapist slowly brings the finger/pen in pt field of view from R/L side and indicates when and where can see target. i. Ocular pursuit: penlight in H pattern to extremes of gaze

1. 66 y/o female with RA. F at PIP and hyperextension at MCP and DIP

a. boutonniere = slip of extensor hood i. swan neck is due to contraction of intrinsic mm or tearing of volar plate ii. mallet: rupture extensor tendon iii. ulnar drift: weakening capsololigamentous structure

RLD

classification of disorders where there is difficulty getting air IN aka a REDUCTION in lung volumes • Eg tumor, IPF, scarring lungs, pneumonia, MS pathos, NM pathos.... • More below in clinical templates

intermittent compression facts phsyiological

during compression: arterial blood flow reduced. venous flow and lymphatic flow enhanced -interstitial P increased: fluid into lymph system deflation: arterial flow increases

renal failure Sx

i. hypocalcemia, hyperkalemia, elevated BUN/Creatinine/Mg/uric acid

z test

o Z-test = EST or COMP mean of 2 pops when noram dist AND pop variance is KNOWN

capsular pattern SC and A

pain end range

cholesterol levels

total <200 LDL <100 HDL 40-60 TRG <150

stroke

• Summary o Ischemic stroke (thrombus, embolus, lacunar) vs. hemorrhagic stroke (intracerebral, subdural, subarachnoid) o L CVA wkns/paralysis on R, impaired processing, heightened frustration, aphasia, dysphagia, motor apraxia o R CVA wkns/paralysis on L, poor attention span, impaired awareness and judgement, spatial deficits, emotional lability, impulsive behavior • Diagnosis o Condition that produces symptoms interruption of cerebral circulation (ischemic vs. hemorrhagic) d/t stroke in evolution (gradual) or a complete stroke (abrupt) resulting in cerebral insufficiency, destruction of brain tissue, and neuro deficit o Injured structures prolonged ischemia to artery in brain that disrupts blood flow and damages the supplied tissues • Inference o Contributing factors modifiable (HTN, atherosclerosis, heart disease, diabetes, cholesterol, smoking, obesity) vs. non-modifiable (age, race, fam hx, sex) risk factors; 73% are > 65 y/o • Confirmation o Clinical presentation hemiplegia or hemiparesis, sensory, visual, perceptual impairments, balance abnormalities, dysphagia, aphasia, cognitive deficits, incontinence, emotional lability o Imaging MRI, CT (delayed), PET, US o Additional info r/o w/chest x-ray (lung disease) and electrocardiogram (heart problems) • Examination o Additional findings differences in R (judgement, emotions) vs. L (aphasia, dysphagia, motor apraxia), coma and death are most severe complications, common to have residual deficits • Management o Tx meds (thrombolytics and anticoagulants if ischemic), PT (positioning, sensory awareness, ROM, muscle re-ed, balance) • Outcome o PT outcome depends on overall health, level of cognition and motivation, motor recovery, residual deficits, and fam support o Long-term effects range from spont recovery to permanent disability, 1st 3 mo are most critical but can cont to improve for 2-3 yrs • Comparison o Transient ischemic attach (TIA) similar to CVA but only lasts for a brief period of time and don't have permanent neuro deficits; indicates increased risk for future CVA

TNM

• TNM system = one of most commonly used o T - primary TUMOR o N - lymph NODE involvement o M - presence of METASTASIS

NMES to quads only feel tingles- what to change

increase pulse duration

trapeziometacarpal capsular

ABD>E

legg calve perthes dx

About 5-7 y/o • Degenraton of femoral head 2/2 AVN • 4 stages o condensation o fragmentation o re-ossification o remodeling Etiology • trauma, genetic predisposistion, synovitis, vascular abnormalities, infection S/Sx • pain • decreased ROM • antalgic gait • (+) trendelenberg sign Tx • variable based on clinical presentation • FOCUS = relieve pain, MAINTAIN FEM HEAD IN CORRECT POSISTION, improve ROM • Orthodics or surgery may also be indicated

tarsal tunnel syndrome

About • tarsal tunnel = medial aspect ankle; flexor retinaculum goes over o Tom - posterior tibialis o Dick - flexor digitorum longus o And - post tibial artery o Very - vein o Nervous - tibial nerve o Harry - flexor hallucis • Syndrome is a compression of the tibial nerve as is passes through tarsal tunnel of love • MOI o Intrinsic - tumor, scar tissue o Extrinsic - crash injury, severe ankle sprain o Tension factors - pes planus, hind-foot valgus deformity S/Sx • Pain, numbness and paresthesia in foot • antalgic gait • rest typically makes better but it doesn't go away • may see atrophy • light touch and temp may be diminished • severe - trophic skin changes Imaging • EMG or NCV - neuropathy confirmation • MRI or US - can actually tell you the structure which is causing Exam • Look at family hx of neuropathies or deformities • special testing o tinel sign tibial nerve • r/o planar fasciitis

pneumothorax

About • Accumulation AIR in the pleural cavity (space between lung and chest wall) - COLLAPSES LUNG • Increase in pressure in pleural space partial collapse lung impaired gas exchange decreased oxygenation of blood • TENSION PNEUMOTHORAX = damaged tissue causes 1-way valve in chest resulting in large inc. in pressure o MEDICAL EMERGENCY S/Sx • Varies widely - asymptomatic to life threatening • Chest pain • SOB • Hypoxemia • Cyanosis • Hypotension • Decreased breath sounds and decreased fremitus on auscultation • If LARGE = mediastinal shift

PFPS

About • General term for ANTERIOR KNEE PAIN • Can also be called chondromalacia patella ranges from softening articular cartilage of patella to complete cartilage destruction exposing subchondral bone • Caused by abnormal tracing of the patella in the trochlear groove places increased and misdirected forces o Esp when patella pulled too far laterally in EXT • Note: can occur post-op rehab after ACL (lots of quad work and imbalances) Etiology • Unknown really • Extremely common in adolescents • Direct association with activity level Repetitive overuse • When in older peeps = associated with OA • increased risk o females > males o during growth spurt (adolescence) o runners who just upped mileage o overweight • factors which cause inc. forces o decreased quad strength (esp. VMO) o pronation feet o knee valgus o dec. LE flexibility (iliopsoas, HS, gastroc., VLO) o patellar instability o tibial torsion or femoral anteversion o patella alta o insufficient lateral femoral condyle S/Sx • gradual onset anterior knee pain (retropatellar) • usually after increasing physical activity • exacerbated by stairs, jumping (may be "burning") • pain prolonged sitting • point tenderness over lateral border patella • swelling • crepitus when push down patella into groove • pain up and down stairs • VMO may look week Imaging • Not commonly used • X-ray to r.o fx or look at configuration joint • Arthrogram / arthroscopy to look at articular cartilage Exam • Make sure to look at everything you need to ID the cause hip strength, alignment (q-angle, foot architecture), gait and running mechanics, dynamic patella tracking o q-angle = angulation measuring from mid-patella to ASIS and tibial tubercle ♣ males = 13* ♣ females = 18* • Special tests o Clarkes sign = push prox. to upper pole patella and have pt contract (+) won't be able to cuz pain o Patellar grind test o Patella glide test • DD = r/o referred pain of hip, Osgood-schlauttters, neuroma, patellar tendonitis, plica syndrome, infection knee joint Mgmt • Med mgmt. = conservative • PT o FOCUS = depends on what is causing bad PF tracking o In general, control edema, stretch whats tight, strengthen what's weak, patella mobility, activity modification o Strength should emphasize VMO and decreasing compressive forces at patella o AVOID deep squat - aggrevating • PHARM = acetomet, NSAIDs, steroid injections • HEP = important; make sure compliance to doing what they need to do Outcome • Prognosis is good with the RIGHT treatment that is addressing the true cause • May suffer from periodic aggravations • Return PLOF ~4-6 weeks

PVD

About • Narrowing of lumen of blood vessels causing reduction in circulation - can be EITHER arteries or veins • Typically 2/2 atherosclerosis • Damage walls fatty plaque buildup hard and narrowing vessels • Compounded by emboil or thrombi Etiology • PRIMARY FACTOR = athlerosclerosis • Other = phlebitis (vein inflammation), injury/sx, autoimmune dz, DM, smoking, hyperlip, inactivity, HTN, (+) family hx, inc age, obesity S/Sx • Diff dep what vessel is affected and how much blood flow comp • Early = intermittent claudication o Inc. pain when walking a certain distance, BUT could also present as legs "giving out" • Tingling and numbness • Pain at rest and while sleeping • Slowed healing • Changes skin coloring • Dec skin temp • Absence hair • Weak / absent pulse Add findings • Ischemic rest pain - 2/2 combo of PVD and inadequate perfusion • Common to also have comorbidities of - DM, CAD (PVD limits BEFORE CAD in exercise) • Higher risk comp - DVT, insufficiency ulcers, gangrene, amputation Imaging / additional info for diagnosis • Blood tests - CBC< BUN, creatine and electrolyte studies • Doppler US - determine flow status • MRI, angiogram, arteriogram - can be used to assist • ABI o >0.90 = normal o 0.70-0.90 = MILD disease o 0.50-0.70 = MOD disease o <0.50 = SEVERE disease • rubor of dependency test • pulse ox • treadmill exercise test Mgmt • need all the peeps • PHARM = anti-coagulants, anti-platelets, thrombolytics (goal = reduce mobility and comp) • PT EDU SUPER IMPORTANT - disease process, skin care, limb protection, risk factor reduction • PT o Initially = walking, AROM, isometrics o Walking program - get them to MAX PAIN; essentially building up that tolerance and collateral circ ♣ Goal = longer walking, less rest, eventually 30 min straight o 4-6 weeks = start resistance exercises • SX = more severe cases - balloon angioplasty, endarectomy, stent implant, bypass sx Outcome • Pt really has to want to get better - then PT is effective • These are high risk pts - permanent sensory changes, gangrene, amputation, MI AND CVA • Symptomatic PVD = death rate ~30% in 5 years, ~50% in 10 year

PF

About • Plantar fascia = Broad CT structure that spans from calc to met heads on plantar surface foot o Assists with medial arch support o Windlass mech for force production / pushoff • Inflammation / chronic overuse of the plantar fascia at PROX insertion at medial tubercle of calcaneus • Excessive tension overtime can create chronic inflammation and micro tears • ADB hallucis, flexor digitorum brevis and quadratus plantae also originate at medial tubercle so can become irritated/inflamed too Etiology • Acute = excessive loading • chronic = irritation due to EXCESSIVE PRONATION • Factors that contribute o Excessive pronation in stance phase o Tightness foot and calf muscles o Obesity o High arch o Person in endurance sports o Occupation with a lot of walking • most common in pts 40-60 yo (middle aged) • can occur in younger peeps, but usually in combo with calcanea apophysitis S/Sx • severe tenderness at insertion • can radiate up to calf and down to toes • pain WORSE IN MORNING (contracted, stiff, cold) • after long periods inactivity / standing • pain walking barefoot • may be bony growths near insertion o NOT the same as heel spur syndrome • usually unilateral tightness calves too Imaging • initially nothing • if not getting better after 6-8 weeks then MRI to confirm dx • x-ray and bone scan r/o fx • rheumatology workout r/o systemic etiology • EMG to r/o neurology Exam • Make sure to biomechanically look at gait, observation foot posture, posterior cord tightness, gait disturbances, training routine Mgmt • PT o heel cup, deep friction massage, massage using tennis ball, medial longitudinal arch taping, joint mobs, strengthen instrinsic and extrinsic muscles o night-tension splints maybe o PREV = heel-cord stretching, avoid sudden intensity changes, orthodics for hyperpronation • PHARM = corticosteroid injections, anti-inflammatory meds • SX = super rare Outcomes • Should return PLOF ~8 weeks • Total resolution ~12 months • PT, orthodics, splinting, pharm, MD follow-up all super important to get better • Recurrence may occur

sponylolisthesis

About • Spondylosis = age related degeneration of discs • Spondylolysis = unhealed fracture of one or both pars interarticularis which is between the superior and inferior articulating processes • Spondylolisthesis = anterior slippage of vertebrae 2/2 healed elongation of the pars following a fracture o Classification ♣ Ischemic = fatigue fracture of pars ♣ Degenerative = degeneration of disc or facet • Dis the one we talking about ♣ Traumatic = acute injury or fracture of facet joint or complex ♣ Congenital = issues with shape of bone and structures cause issues ♣ Pathologic = metabolic or neoplastic process effects elements o Classification ♣ Grade 1 - <25% ♣ Grade 2 - 25-50% ♣ Grade 3 - 50-75% ♣ Grade 4 - 75-100% ♣ Grade 5 - 100% aka spondyloloptosis • Caused by WEAKENING of joints - allows fwd slippage of the top vertebrae on the bottom on • Most common for DEGENERATIVE = L4-L5 o remember: L5-S1 is traumatic in adolescent gymnasts • if you get sx due to STENOSIS not really slipping o slipping makes it so its unstable and the facets are hitting together so osteophyte formation o deprives the nerves causing ISCHEMIA and POOR NOURISHMENT o L4 is the nerve affected usually!!! • PLL, ALL, IV disc, vert periosteum and bone could also be affected Etiology • Caused by ARTHRITIS and DEGENERATIVE changes of the spine • IV disc loses height facets inc size and develop bone spurs spinal stenosis weaken spine slippage vertebrae (limited still doe) S/Sx • >50 y/o • more common African Americas; WOMEN • back pain primary sx • increases with exercise, lifting OH, prolonged standing, getting out of car, etc • severe and may radiate depending on stenotic area • may have sensory and motor loss - follow derm/myo pattern • usually don't have sig neuro deficits but could happen Imaging • X-rays = confirm • CT scan or MRI = r/o other shit Exam • make sure to CHECK NEURO, and coordination may be good too, ask about bowel and bladder function Mgmt • med mgmt. = education, meds, activity mod, PT • PT = Willam's flexion exercises may be indicated o extension causes them pain usually o need to strengthen abs and reduce lumbar lordosis o core stabilization o inc flexibilty bracing or corset may relieve intra-discal pressure • PHARM = NSAIDs (pain and inflammation), corticosteroids (severe), maybe epidural injections if oral meds fail • SX = when cons fails, pain disabling, DEF when neuro sx are badddd o Decompression w/ or w/out spinal fusion Outcome • Usually successful with PT • May or may not have additional slippage o Note: if is worsens, doesn't mean neuro sx get worse

TMJ

About • TMJ = articulation of condyle of mandible and mandibular fossa; MENISCUS which is cushion between 2 surfaces o Articular disc separates joint into UPPER and LOWER compartments ♣ UPPER = gliding / translation ♣ LOWER = rolling / rotation ♣ Condyles first ROLLS for first 10-15 mm, then will TRASLATE WITH ROT for next 40 mm • If translation restricted, can have up to 20-25 mm opening NEED BOTH FOR FUNCTION o Posterior disc and posterior apparatus are HIGHLY innervated what leads to pain • BILATERAL (2 sides CANNOT function independently 1 another), condylar, synovial hinge joint • Very powerful for chewing but also fine motor control for speaking and swallowing • Weak stability if TMJ is dislocated them MEDICAL EMERGENCY • Disc displacement o Ant or med is predominant o 1 = displacement WITH reduction ♣ reciprocal clicks during opening and closing o 2 = displacement WITHOUT reduction (locked position) ♣ EXTREMELY painful, no joint noises, hypomobile (can roll but no glide) o 3 = displacement with OA ♣ clicking through entire range, near norm opening • injury Results from injury, derangement or incongruence of TMJ ITSELF, discs, and/or the supporting structures around it • Over time the meniscus of the TMJ becomes compressed, wearing away so that bone is rubbing • Etiology • Pt typically 20-40 yo • FEMALES > males • 3 primary etiological factors o predisposing factors o triggering factors o perpetuating / sustaining factors • can occur 2/2 to injury/trauma to joint, congenital abnormalities, internal derangement, arthritis, dislocation, disc degeneration, metabolic conditions, stress • risk factors o chewing one side o eating tough food o clenching o grinding teeth (bruxism) o gum chewing and nail biting S/Sx • either bilateral or unilateral • persistent or recurring pain • muscle spasm • abnormal or limited jaw movement • HA • tinnitus (ringing ears) • clinical manifestations are related to CAUSE!! o Popping and clicking when opening o Locking TMJ o Restriction of unaffected side o movement towards affected Imaging • X-ray, MRI, mandibular kinesiology, CT scan, dental examination Exam • Ask Review of sx, PMH, Social hx, Eating habits • upper quarter screening • TMJ loading • Condyle-meniscus relationship • Special test o Forced biting = bite on rolled gauze; testing for INFLAMMATION ♣ (+) = pain on OPP side o Retrussive overpressure = compress joint with hand; testing for INFLAMMATION ♣ (+) = pain o knuckle test = test of opening Mgmt • PHARM = analgesics, NSAIDs, muscle relaxants, antianxiety meds • Maybe splint for realignment • PT = based on etiology o In general: education, posture retraining, modalities, STM, joint mobs o US ok over TMJ and masseter but NOT over temporalis • SX = condylectomy, osteotomy, arthrotomy, arthroscopy, reduction subluxation, joint debridement Outcomes • PT should help to improve • Previous diagnosis = increased risk (but If you do what you're supposed to then not so much)

IPJ capsular

F>E

MCP and IP capsular

F>E

knee capsular

F>E

ulnohumeral capsular pattern

F>E

radio humeral capsular pattern

F>E>sup>pro

ULTT 1

Shoulder depression, ABD 110*, elbow ext, forearm sup, wrist ext, finger and thumb ext CL cervical SB Median nerve, anterior interosseous

T-sp L-sp capsular pattern

SB and ROT>ext

CA staging

Stage 0 ONLY in layer of CELLS it began Carcinoma in situ Stage 1 TISSUE of origin No lymph node No metastasis Stage 2 ADJACENCT tissues Maybe lymph nodes MICROmetastesis Stage 3 ADJECENT tissues and FIXATION to deeper structures PROBS metastatic lymph nodes Stage 4 Mets BEYOND primary site - bone or another organ

distal radioulnar capsular

full ROM pain at extremes

1. stroke early recovery of RUE with mod spasticity of biceps and finger flexors. Voluntary movement evident in elbow F and shoulder ABD thru ½ range. BEST choice for initial exercise?

a. WB on extended RUE with wrist and fingers extended: early intervention stretching and positioning the RUE into extension with wrist and fingers extended. To dec. developing flexor spasticity. This activity promotes extensor activity in triceps and shoulder stabilizers.

exam with ulnar nerve palsy. What find most consistent with hypothesized dx?

a. Wasting of hypothenar eminence i. I said PIP joint hyperextension and slight F of DIP- this is rupture of FDS.

postural drainage

anterior apical: sitting posterior apical: sitting and leaning forward upper lobe anterior: supine pillow under knee L post segment upper lobe: inclined head SL R R post upper lobe: AL 1/4 turn L lingual: head declined 1/4 turn on R middle lobe: head decline 1/4 turn on L anterior lower lobe: declined supine pillow knees posterior lower lobe: declined prone pillow under tummy lateral sements: head declined SL superior segments lower lobe: prone pillow under tummy

do not take coumadin with

aspirin (acetylsalicylic acid) b/c both are anticoagulants

pulmonary edema

excess fluid in lungs; often when LV is unable to pump blood out to body well • ACUTE = MEDICAL EMERGENCY - extreme SOB, wheezing or gasping, anxiety, cough with sputum, chest pain, palp

pleural effusion

excess fluid in pleural cavity 2/2 medical conditions which cause inc. fluid production or dec. absorption • Large = SOB, chest pain, cough, fever

1. Weakness secondary to femoral nerve injury. Examine from IC to foot flat. MOST likely observe?

forward trunk lean compensate weak quads

1. PT attempts to implement a formal exercise program for a pt. 3 weeks following cardiac transplantation. Which physiological response should PT anticipate based on transplantation?

increased resting HR, due to lack PS

capsular pattern TMJ

limited mouth openin

brainstem infarction: left lateral medullary syndrome- what sx?

loss of pain and temperature R side (spinothalamic tract) -they cross at spinal cord

contact dermatitis

o Superficial irritation of skin d/t poison ivy, latex, soap, jewelry, rubber, etc. o Etiology = exposure to mechanical, chemical, environmental, or biological agents o S+S = tching, burning, redness o Tx = remove source of irritation, topical steroids

DCML

o proprioception, vibration, 2-pt discrimination, graphesthesia ♣ Fasiculus cuneatus (UE, trunk and neck) and gracilis (LE) ascending

rule of 9s

o used to est total amount of surface area damaged by burn o does NOT account for severity cannot predict prognosis or outcomes o Adult ♣ Head and neck = 9% ♣ Ant trunk = 18% ♣ Post trunk = 18% ♣ B ant arm, forearm, and hand = 9% ♣ B post arm, forearm, and hand = 9% ♣ Genital region = 1% ♣ B ant leg and foot = 18% ♣ B post leg and foot = 18%

recent onset steroid induced myopathy- what is most difficult

proximal mm affected so would be climbing stairs

R hemiplegia observed in GT. Performs side stepping towards hemiplegic side. May expect compensate for weak abductors by:

towards unaffected to unweight affected and use of momentum

1. 18 y/o male sustained patella fx in MVA. Knee maintained in extension using straight knee immobilizer. MOST likely gait deviation?

vaulting

CF

• Autosomal recessive genetic disease of exocrine glands (aka both parents must have and give to child) • Primarily effects LUNGS, PANCREAS, LIVER, INTESTIES, SINUSES, also reproductive systems o Lungs and digestive systems usually most affected • Affects ion transport, causing glands to overproduce thick mucous, norm secretions, sodium and chloride o Epithelial cells are impermeable to chloride - creating elevation sodium chloride and pancreatic enzymes • MOST COMMON LETHAL DISORDER OF WHITE PEOPLE • Mutation of the CF transmembrane conductance regulator (CFTR) protein on chromosome 7 • Normally allows chloride to pass through membrane • Vary with progression of disease • Most consistent sx = Salty tasting skin / high salt content in sweat • Persistent and productive cough • Frequent lung infections • Wheezing • SOB • Poor growth / weight gain even though appetite good • Frequent greasy, bulky stools • Most common complication = exacerbation COPD • PFT testing o Dec FEV1 (can't get out fast) o Dec FVC (dec air out at all) o Inc FRC and RV (air getting trapped) • Hypoxemia and hypercapnia develop 2/2 alteration in perfusion • May get barrel chest, pectus carnietum and kyphosis deformities • Usually have pancreas issues - enzyme deficiency, degeneration, eventual progressive fibrosis • Issues with digestion and absorption nutrients • Airway obstruction can cause pulmonary HTN, atelectasis, pneumonia, lung abscess • Can lead to BRONCHIETASIS - dilation of the bronchus 2/2 chronic inflammation • Sever comp = cirrhosis, DM, pneumothorax, cardiac patho, pancreatitis, cor pulmonale, intestibal obstruction • MEDS = anti-biotics, nutrition supplements, pancreatic enzyme replacement, mucolytics, bronchodilators • PT = ESSENTIAL o AWC, breathing techniques, assisted cough, ventilitory muscle training (acapella with IMT + flutter valve to jar lose secretions); general exercise indicated EXCEPT once gets severe NEED to educate pts how to help with chest PT at home; may get manual percussor

gout

• Complex form arthritis - HIGH LEVELS URIC ACID • Uric acids froms in body as purine in foods is broken down • As levels inc around joints, TOPHI (crystals) form inflammation and joitn swelling More common in males - bog toe, knee, ankles

iontophoresis ions

Acetic acid Calcific deposits Myositis ossificans - Calcium chloride Scar tissue Keloids Muscle spasms - Copper sulfate Fungal infection + Dexamethasone Inflammation - Iodine Scars Adhesive capsulitis - Lidocaine Analgesia Inflammation + Magnesium sulfate Muscle spasms Ischemia + Salicylates Muscle and joint pain Plantar warts - Zinc oxide Healing Dermal ulcers Wounds +

radoiocarpal LP CP

Neutral, slight UD Wrist EXT, RD

adrenal

o outer portion cortex and inner portion medulla ♣ Cortex = fluid and water balance, stress response, immune system, sex development and funct, metabolism • Androgen pubic hair growth and masculinity • Aldosterone (mineralcorticoid) inc. NA in blood, pee out K+ • Cortisol (glucocorticoid) food met, anti-inflammatory ♣ Medulla = stress/symp reponses • epinephrine inc. HR, <3 contraction force, vasodilation skeletal muscle • norepinephrine vaso-constriction skin, viscera, muscles

intermittent compression: UE/LE

• Inflation pressure = ~30-80 mmHg o UEs = 30-60 mmHg o LEs = 40-80 mmHg o Should NOT exceed DBP

spinothalamic tract

♣ Anterior (ASTT) = CRUDE touch and firm pressure ♣ Lateral (LSTT) = pain and temp ascending

Cerebellum

coordinates movement and assists w/maintenance of balance and posture Impairments on IPSILATERAL SIDE = ataxia (loss of control of movement), nystagmus, tremor, hyper-metria (overshooting), poor coordination, postural reflex, balance, and equilibrium deficits

lymph node pathology

♣ Lymphadenitis = infection and inflammation of lymph node; acute or chronic ♣ Lymphandenomegaly = enlargement of lymp nodes • 2/2 CA, infections, allergic rxns ♣ Lymphadenopathy = dx which affects #, size, consistency lymph nodes

pos ionotropic agents

Action • Inc force and velocity <3 contraction, slow HR, decrease conduction velocity through AV node, dec symp activation • No NOT inc MVO2 AE: arrythmias

PE response

Recognition • s/sx o SOB o Cough (sometimes with bloody sputum) o Chest pain which worsens with deep breathing o Lightheaded / dizzy o Tachypnea o Rapid and irregular HR o Fever o Diaphoresis o Anxious o Cyanosis o Clammy skin o Leg pain and swelling Response • EMS CALLED IMMEDIAELY!!! • Cont. to monitor VS until they get there

1. PT reading report of ABG: FiO2= .21, PaO2= 53, PaCO2= 30, pH= 7.48, bicarbonate=24. What does this indicate?

a. Respiratory alkalosis. i. Increased pH= alkalosis. ii. CO2 viewed as acid if low = less acid= alkalosis. iii. If metabolic a HIGH bicarbonate value would be anticipated!!

RCT

o comparison a specific intervention to control condition ♣ Randomized into control vs experimental group • Control = no tx or standard default tx • Exp = gets the intervention ♣ Want the groups to be as equivalent at baseline as possible ♣ Randomization reduces any bias and inc prob that it actually came from intervention

cross sectional study

o data/observations made AT ONE POINT in time ; all subjects tested at rel same time ♣ Aims to describe relationship between disease/condition + factors fo interetes that exist in a certain pop AT THAT TIME ♣ Describe prevalence, demo associations CANNOT dist newly occurring and long-est conditions, ID causal relationships about what lead

parathyroid

o maintenance Ca and phosphate levels in blood (clotting, NM excitability, cell membrane perm) ♣ Parathormone moves Ca and Ph from bones to BLOOD (stim HYPOcalcemic)

laceration/bleeding response

Recognition • ARTERIAL bleeding = spurting blood, bright red (oxygenated) • VENOUS bleeding = flowing, more purple (de-oxy) Response • Apply gloves first • Apply pressure with sterile towel UNTIL bleeding ceases o Arterial bleed = intermittent pressure to artery just prox • If excessive blood flow - elevate above heart level • DO NOT do prolonged pressure with tourniquet • Call EMS = severe bleed, spurting bleed, >10 mins

1. cc runner has AL leg pain. Progressively worsened since increase in training. Symptoms appear at later stages of runs and persist 2-3 hours after completion. Denis LE paresthesias. Tib anterior is tender and taut. Resisted DF strong but reproduces the pain. MOST likely dx?

a. Chronic exertional compartment syndrome: result of transiently elevated anterior cpt P that restricts blood flow to mm. tender AL leg region and taut ant compartment. Rearfoot strike associated with this due to increased mm activity of tib anterior. Tx require change in footwear, training surface, or re run training

1. Pt with several motor and sensory abnormalities exhibits signs of ANS dysfunction. What is NOT an indicator of increased S involvement?

a. Constriction of the pupils is a PS response. Also dec. HR, stimulate digestion, constrict lungs, and stimulate other internal organs. b. SNS does have anxiety, distractibility, mottled/cold/shiny skin, rapid HR, dilation of lungs, inc. muscle tension/strength, rapid and shallow breathing To decrease: maintained touch, massage, rocking, deep breathing, generalized warmth, midline pressure

pain left lateral face, limited passive and active mouth opening ROM. Passive lateral deviation full both sides. What is the reason?

a. Decreased flexibility in mm of mastication on the left i. Lateral deviation does not require a significant lengthening in muscles of mastication as primary motion of mandible is sligh tanterior translation of the mandibular condyle w/o increasing the distance b/w the body of the mandible and upper palate. 1. Unilateral capsular and intraarticular restrictions would result in deflection of mandible toward side of restriction with opening and would limit lateral deviation away from side of restriction d/t decreased anterior translation of mandibular condyle. 2. Anterior disc displacement would not limit mouth opening.

pt on bed rest in acute for over one month—what would be most effected after immobilization?

a. Extensor muscles of the LE: i. LE>UE. Extensors strength decreases by 20% and knee flexor non-significant decrease.

pt demonstrates large amplitude, sudden flailing motions of arm and leg on one side of the body primarily involvement in axial and proximal joint muscles. What clinical term BEST describes the pt's behaviors?

a. HEMIBALLISMUS- HEMI should have been the clue i. Chorea: rapid, irregular rand jerly involuntary movements

meneire's dx

a. Head tilt to one side: this is unilateral vestibular hypofunction—also (conjugate eye torsion, skew deviation, abnormal weight shifts to one side) b. Meneire's would include: hearing loss, tinnitus, vertigo >30 min

1. major medical center in acute care. Most common infection transmitted to health care workers?

a. Hep B: thru exposure to blood and blood products and infected body fluids

catheter in internal jugular veing thru VC to RA, permtis removal of blood samples, administration meds, monitor CVP it is called what

a. Hickman catheter= indwelling RA catheter

PT notices pt with transfemoral amputation takes a longer step with prosthetic limb than CL limb. What is the MOST likely cause:

a. Hip flexion contracture: dec. hip extension in late stance on prosthetic side so shorter step on uninvolved side versus involved i. Fear and insecurity would be bilateral shorter steps

most appropriate functional goal for 5 y/o with high lumbar lesion L2 myelomeningocele and minimal cognitive involvement?

a. Household ambulation with RGO and Lofstrand crutches: physiological benefits include imporved CV and musculoskeletal functions. Too high EE for community ambulation. I said KAFO but inadvertent hip flexion can happen with these.

10 year hx MS 3+ extensor tone in bilateral LE. w/c rec?

a. Tilt in space wheel care with pelvic belt: needs hip control to maintain hips in flexion. And tilt in space keeps in w/c when extensor spasms are active.

traumatic injury to R hand had flrxor tendon repair to fingers. When should PT intervention begin?

a. Within a few days after surgery to preserve tendon gliding- early passive and active exercises promote collagen remodeling to allow free tendon gliding. Prevent adhesions from forming that would restrict free tendon gliding. Early initiation of strengthening is CO.

Sever's disease

a. calcaneal apophysitis: inflammation of growth plate in the heel. In adolescence.

1. Foot in subtalar neutral. Medial border of foot higher than lateral along MT. this is called

a. forefoot varus= inverted position in relation to rearfoot. Low arches often have this.

PT in acute care reviews results of lab testing for one of their patients. Pt was dehydrated- what does this effect

a. increased BUN: assess kidney function. Indicative of dehydration, renal failure, heart failure. Normal 10-20 mg. i. Hgb and HCt would be increased

thyroid

o = rate of fuel burning ♣ thyroxine (T4) + triiodothyronine (T3) inc met ♣ calcitonin moves Ca from blood to BONE (stim HYPERcalcemia)

cancer s/s

o C - change in bowel/bladder o A - a sore that will not heal o U - unusual bleeding / discharge o T - thickening / lump develops o I - indigestion or difficulty swallowing o O - obvious change wart / mole o N - nagging cough / hoarseness o Unexplained weight loss, fatigue, anorexia, pain, weakness

onchychomyosis

o Fungal infection, usually in toenails and nail beds o Etiology = manicures/pedicures, wet footwear, impaired immune system o S+S = yellow/brown nails, hyperkeratosis and hypertrophy of nail o Tx = manual debridement, anti-fungals

ROM requirement in gait

o Hip flexion = 0-30* (max at TSw, IC and LR) o Hip ext = 0-10* (max at TS) o Knee flexion = 0-60* (max at ISw) o Knee ext = 0* (max at IC, TS) o Ankle DF = 0-10* (max at MS) o Ankle PF = 0-20* (max at PSw)

ovaries and testes

o Ovaries = menstrual cycle, pregnancy, sex development ♣ estrogen (ovarian follicles) development and maintenance female qualities (breasts, reproductive cycles) ♣ progesterone (corpus luteum) maintain uterus lining o Testes = secrete androgens (testosterone) for sperm, sex development

superficial reflexes

o POLY-SYNAPTIC reflex (aka long) = sensory signal must reach SC and ascend to the brain for processing then has to descend SC to reach motor neurons o Typically graded as present or absent; ALWAYS comp B o Abdominal (T8-L1) = stroke each quadrant of abd toward umbilicus ♣ Norm = dev of umbilicus towards stimulus o Corneal (trigeminal/facial) stroke cornea ♣ Norm = both eyes blink o Cremasteric (L1-2) = scratch skin of upper med thigh ♣ Norm = ipsi testicle rise o Gag (glossopharyngeal/vagus) = stim each side back of throat ♣ Norm = gag (sometimes absent is normal too) o Plantar (L5-S1) = stroke sole of foot from heel to ball ♣ Norm = toes flex ♣ Abnormal = Babinski (splaying toes)

compression garments

o Prevent DVT = 16-18 mmHg o Scar tissue control = 20-30 mmHg o Edema control = 30-40 mmHg

quad vs ischial containment socket

o Quadrilateral socket ♣ Wider med/lat and narrower ant/post ♣ Posterior wall is angled fwd to provide some initial hip flexion and also something for glute/HS to push off of during gait • Comes UNDER ischial tuberosity - has ischial seat • The anterior wall is high and has a bulge in order to push it back against this ♣ The medial wall stops medial movement and pushes residual limb against lateral wall ♣ Issue: distal femur moves back and forth hitting Lateral wall o Ischial containment socket ♣ Narrower med/lat and wider ant/post ♣ Overall, this contains structures more LOCKS pelvis into residual limb • The post wall goes higher on this socket, pocketing the glute max and ischial tub (more WB on end of residual limb and not here) • The lateral wall encompasses the greater troch as well as the TFL, lateral HS and VL put on stretch to reduce AP movmt femur • The medial wall encompasses the ischial ramus and provides counter-presssure to lateral wall (which now goes over the greater troch) in turns promotes more ADD of the residual limb

S3-4

o S3 (lub-dub-BOOM) = vibrations from DISTENDED ventricle walls 2/2 passive blood flow for atria during rapid filling phase EARLY diastole --Healthy young children = NORMAL - "physiologic" 3rd heart sound --Adults = ABNORMAL - "ventricular gallop" (WORSE) • May be associated with HF, or non-compliant ventricle mass o S4 (DA-lub-dub) = pathologic sounds of vibration ventricle wall END diastole and beg atrial contraction --ABNORMAL - "atrial gallop" • May be associated with HTN, stenosis, scar from MI

jerk test

o Test: posterior instability with clunk; posterior labral lesion with pain o Position: sitting, shld elevated to 90*, IR, elbow bent o PT gives axial compression force through elbow while horizontally ADD shld (+) clunk or jerk; pain

SI joint capsular pattern

pain stressed

1. respiratory assessment- best position to measure chest excursion in inspiration

supine

wrist goni

• FLEX: sitting supported, arm 90*, elbow 90* o F - lateral aspect wrist at triquetrum o SA - midline ulna (olecranon) o MA - midline 5th metacarpal • EXT: sitting supported, ABD 90*, elbow 90* o Same as flexion • RD: sitting supported, ABD 90*, elbow 90* o F - capitate dorsal aspect wrist o SA - lateral epicondyle o MA - midline 3rd digit o FIRM or HARD UD: sitting supported, ABD 90*, elbow 90*

resp involvement SCI

• (to C8 will still have some resp compromise!!!) o High cervical = phrenic nerve / diaphragm stimulator (3, 4, 5); mech vent o Paralysis of abdominals = paradoxical; belly bulging o Reduce cough effectiveness use binder, teach assistive cough techniques, positioning and drainage (PRONE IS GREAT!)

hypothermia and frostbite response

• Asses body temp via palpation; asses verbal and motor response • HYPOTHERMIA o Move to warm room and take off any wet clothing o Attempt to warm - STARTING WITH CORE • Call EMS if = LOC, body <95* F • FROSTBITE o Immerse in WARM (not hot) water OR warm via body heat Do NOT do massage over area - can cause inc tissue damage

SCI bowel and bladder

• Bladder o UMN (T11-12 and ABOVE) = NEUROGENIC -aka signals can be received from the bladder and go up, BUT supraspinal control cannot come back down --REFLEXIVELY PEE since the reflex arc is still intact --Can either by hypertonic or hypotonic o LMN (T12 or BELOW) - ARREFLEXIC --aka signals can't even get to the SC so you lose all reflex and everything to pee --FLACCID • Bowel o Neurogenic bowel o reflexic bowel = uses suppositories and digital stim o non-reflexic = muscle straining and manual evac

TSA

• Candidates = severe degeneration of humeral head and glenoid, severe pain, have failed conservative measures o Could be due to waer and tear, inflammation, injury, previous surgery • Types o TOTAL = both glenoid and humerus o HEMI = replacement head and neck of humerus o REVERSE TOTAL = reversing convex-concave rule ♣ When pt has DYSFUNCTIONAL rotator cuff ♣ DELTOID INTEGRITY super important cuz it basically becomes prime mover • Uses ANTERIOR approach subscap. detached for easier access o Wide variation protocols BUT lets talk about Neer's ♣ Isometrics = start 3 weeks post ♣ Active = 6 weeks post ♣ NO AROM FIRST PHASE - just ROM and AAROM (wand, pendulums) ♣ NO IR OR ER >35/40* - ~2-3 weeks o WB restrictions on arm ♣ Limitations lifting or closed chain activities PHARM = anti-coagulation and PAIN

position to relieve dyspnea

• Choice position dep on circumstances • TRIPOD = optimizes LTR of diaphragm and closes the chain so you can use the pecs and UP to elevate the ribs • REVERSE TRANDELENBERG (supine with head above trunk) = decreases weight abdominal contents on diaphragm so reduced resistance • SEMI-FOWLERS (supine, HOB 45*) = CHF or other cardiac positions

cardiac rehab indications/ CI

• Clinical indications o MED STABLE post-MI o STABLE angina pectoris o CABG o PTCA o COMPENSATED HF o Cardiomyopathy o Heart transplant o Other cardiac sx (valve repair, pacemaker, etc) o PAD o HIGH RISK CAD - DM, dyslip, HTN, obesity o End stage renal disease • CONTRAINDICATIONS o UNSTABLE angina o Resting SBP > 220 RO restign DBP >110 o Orthostatic BP drop >20 mmHg WITH SYMPTOMS o Critical aortic stenosis o Acute systemic illness or fever o Uncontrolled arrhythmias o 3rd degree AV block without pacemaker o acute pericarditis or myocarditis o recent embolisim o thrombophlebitis o restign ST seg depression or elevation >2mm o UNCOMP CHF o Ortho or metabolic conditions which would prohibit

deceberate and decorticate

• Decerebrate Rigidity = trunk and extremities are in EXTENSION o Corticospinal tract lesion in BRAINSTEM • Decorticate Rigidity = UEs in flexion and LEs in extension (red nucleus spared) o At level of diencephalon o MORE FUNCTIONAL ABILITIES here

elbow goni

• FLEX: supine o Fulcrum - lateral epicondyle of humerus o Stationary - lateral midline of humerus using acromion as reference o Moving - lateral midline of radius using radial styloid process as reference o SOFT end feel • EXT: supine with arm over edge of table if needed for full ROM o Same landmarks as FLEX HARD end feel

insulin related illness and response

• HYPOGLYCEMIA = low blood glucose o RAPID onset o Pale and moist skin o Rapid HR o Shallow breathing o Dizziness o HA o Altered vision o Hinger o Excted and agitated behavior o Confusion o Seizure o LOC • HYPERGLYCEMIA = elevated blood glucose o GRADUAL onset o Thirst o Freq urination o Glucose in urine o Can lead to KETOACIDOSIS if left untreated diabetic coma ♣ LIFE THREATENING ♣ Fruity smelling breath ♣ Deep, labored breathing ♣ n/v ♣ dry tongue • HYPO = inject some sugar o If not conscious = admin IV o REST until blood glucose levels normal again • KETOACIDOSIS = call EMS! Likely need injection of insulin o Do NOT give them sugar!!!!

8-9 months

• Hands and knees in prone • Does NOT tolerate supine position • Moves from sitting to prone • Sits without hand support longer periods • pivots in sitting • pulls at furniture to stand, can lower from there • crawling • cruising = walking along furniture • activie supination • radial-distal grasp • inferior pincer grasp • takes objects out of container Points and pokes with index finger

myocarditis

• INFLAMMATION and weakness of MYOCARDIUM! • Can lead to sx of HEAT FAULRE • Usually VIRAL - flu, coxsackie virus, adenovirus • BACTERIA - polio, rubella, Lyme disease • Dep on cause and severity • Arrhythmias • Chest pain • SOB • Fatigue • Signs of fever - HA, muscle aches, sore throat, diarrhea, rashes • FOCUS = underlying disease OR decreasing workload of <3 • Meds = antibiotics, anti-inflmatories, diuretics (dec preload), beta blockers (dec symp), calcium channel blockers (dec workload) • SEVERE = sx implant LVAD, intra-aotic balloon pump

cholinergic meds

• Inc cholinergic activity • Direct = mimic ACh • Indirect = inhibtat ACh-ase (which normllay breaks down) WHO: • Glaucoma • Dementia d/t AD • Post-op dec GI motility • MG • Reversal anticholinergic toxicity Side effects: • GI distress • Impaired vision • PARASYMP effects o Bronchoconstriction o Bradycardia o Flushing • Dec HR and dizziness PT • Pts with AD and MG may be better in thereapy if on these meds • Duvoid, Pilocar, Aricept, Prostigmin, Cognex

pregnancy exercise recomendation

• Mild-mod exercise routines - min 3x/week o 50-60% max HR (mild/mod) for ~30 min o don't exercise to exhaustion!! have decreased O2 available to them • NWB preferred • Don't do exercises where there could be abdominal trauma or LOB (esp 3rd trimester) • No exercises in supine after 1st trimester!!!! • Avoid prolonged periods of motionless standing • Need ~300 kcal/day extra make sure adequate diet • Don't overheat hydrate, good clothing, optimal environment • Changes last ~4-6 weeks post-partum make sure to ease back into old routines

SCI C8-L2

• Muscles o C8 = finger flexors (active grip and release) o T1 = finger ABD and ADD o T2-L1 = postural trunk and abdominal muscles (stability and balance) o L2 = hip flexion and ADD • Functionality o Essentially, from C6 on you have the same functional capabilities, just the manner that you achieve them is diff an how long it takes to gain them. o Bed mobility = indep o Trasnfers = indep; min A-I with floor o WS = Mod I w/ depression WS o w/c mgmt = I o w/c mobility = min A-mod I curbs; mod I down steps; max-min A up steps o Gait = range from exercise only to community amb; RGOs, HKAFOs, KAFos, and AFOs ♣ RGO = T12-L4!!; B HKAFO = T9-L1/2 o Feeding, grooming = independent self-care o Dressing batthig, bowel/bladder = mod I independent driving w/ hand controls, independent stowing w/c

SCI L3

• Muscles = quads (knee ext) • Functionality o Independent all self care o Potential functional ambulation o Can ambulate with crutches and AFOs Need w/c for sports and high level activities (work, parenting, etc)

HF

• Progressive condition -- <3 cannot maintain normal CO to get blood to body o AKA HEART FAILING AS A PUMP! (Ventricles weak / dilated) • Can be R or L sided or both o R sided --Due to anything abstracting flow to lungs pulmonary HTN (cor pulmonale since from lungs), right valve disease, right vent infarct --Cause BACKUP INTO BODY o L sided = where typically begins Types • SYSTOIC (EF reduced - HfrEF ) = issue pumping OUT • DIASTOLIC (EF preserved/norm - HfpEF ) = issue with FILLING --Causes BACKUP INTO L vent L atrium pulm vein LUNGS ---When body trys to compensate for all this, does all the wrong things symp system activated and renin-angio cycle goes off (keep in mind with tx) o CHF = end stage; when backed up into liver, abdomen, LEs, lungs • Either acute or chronic • Usually develops AFTER other conditions have weakened the heart • CAUSED BY ANYTHING OBSTRUCTING FLOW OR MAKING HEART SUCK • CAD, HTN (of body or lungs), DM, MI, abnormal heart valves, cardiomyopathy • R SIDE (think backup into body) o Decreased SBP o DEPENDENT EDEMA o liver engorgement o ASCITES o Fatigue o Anorexia o Bloating o S3 o Cyanosis o JVD o WEIGHT GAIN • L SIDE (think backup into LUNGS) o Decreased SBP o DYSPNEA o DRY COUGH o Orthopnea o PND o Fatigue o Weakness o PULMONARY RALES (B and symmetrical at bases and progresses up) o S3 sometimes S4 o enlarged heart o acute pulm edema o WEIGHT GAIN o BNP released (hormone when heart muscle stretched) • Treating underlying cause can help (eg fixing valve causing issue) • Most cases it is a BALANCE of meds, devices and lifestyle changes to get <3 to contract normally • Meds = ionotropes (contraction - digitalis), diuretics (unload fluid and dec preload), ACE inhibitors (stop angio to 2 - dec afterload), beta blockers (stop symp tone inc, dec HR) • Sx = severe cases o CABG, valve repair, ICD, biventricular pacemaker, IABP (balloon inserted into aorta from femoral a, inflates (diastole) and deflates (systole) with heat), LVAD (mechanical circulation device which replaces function of failing heart), heart transplant (last chance effort - remember its dennervated after) • Lifestyle changes = stop smoking, restrict sodium, healthy weight, limit alc and fluids, dec stress, mod exercise Class 1 (mild) NO limitation No fatigue, palpitation, dyspnea Class 2 (mild) SLIGHT limitation Good at rest, ORDINARY ACT causes fatigue, palpitation, DOE Class 3 (mod) MARKED limitation Good at rest, LESS THA ORDINARY causes fatigue, palpitation, DOE Class 4 (severe) UNABLE TO CARRY OUT any physical activity w/out discomfort Sx cardiac insufficiency at rest - physical activity makes way worse

subtalar goni

• Subtalar INV & EV: prone o F: Middle of malleoli o SA: Midline calf MA: Midline calcaneus

Bells palsy

• Summary o Acute onset of sensory and motor deficits in facial nerve (CN VII) distribution muscles of facial expression and sometimes saliva and tear production, taste to ant 2/3 tongue o Self-limiting, not life-threatening usually have spontaneous recovery w/in wks or mos • Diagnosis o Condition that produces symptoms d/t abnormal compression (inflammation, edema) on facial nerve (muscles of facial expression, tear and saliva production) o Injured structures facial nerve (CN VII) • Inference o Contributing factors virus (herpes simplex, Epstein-Barr, varicella zoster, HIV) • Confirmation o Clinical presentation onset can be sudden or gradual, affect 1 side of face, start w/stiffness and tightness, facial droop, decreased taste, altered tear and saliva production, auditory sensitivity o Imaging MRI or CT to ID source of pressure, blood tests to r/o o Additional info hx for r/o and ID exposure risks, EMG of facial nerve, dx w/testing of facial nerve (looking for asymmetries) • Management o Tx pt ed, monitoring, anti-inflammatories, PT (massage, stretching, moist heat, bioFB, NMES) o Home care massage, stretching, strengthening, eye protection

polyneuropathy

• Summary o Damage or disease of multiple peripheral nerves ♣ DM is most common cause o Usually starts in dist LEs, symmetrically, and may progress prox o Electromyography and nerve conduction testing used to determine location and extend of nerve damage • Diagnosis o Condition that produces symptoms damage or disease of multiple peripheral nerves d.t DM, age, drugs, alcohol abuse, AIDs, environmental toxins, inherited conditions o Injured structures peripheral nerves (esp. in extremities), can be motor, sensory, or both • Confirmation o Clinical presentation starts distally, usually symmetrical, can progress proximally, N+T, "stocking"/"glove" pattern, loss of proprioception and vibration, wkns and atrophy, constipation, loss of B+B control, OH o Imaging electromyography and nerve conduction testing o Additional info assess sensation, strength, DTRs, and coordination

anterior cord syndrome

• Summary o Incomplete SC lesion damage to ant 2/3 of SC o Traumatic incident (ex: fx, dislocation) pressure or damage to ASA o Bilat loss of motor function and pain and temp sensation below lesion d/t damage to corticospinal and spinothalamic tracts • Diagnosis o Condition that produces symptoms incomplete SC lesion (c/s flex injury or ASA infarction) that damages the ant 2/3 of the SC o Injured structures compression and damage to ant SC and ASA resulting in loss of blood flow to corticopinal (motor) and spinothalamic (pain and temp) tracts • Inference o Contributing factors usually traumatic incident (fx or dislocation) or vascular insufficiencies • Confirmation o Clinical presentation complete loss of motor control and pain and temp sensation below level of lesion, ANS dysfunction (bowel and bladder, sexual dysfunction) o Imaging MRI, X-ray, CT o Additional info thorough neuro exam, can use ASIA scale • Management o Tx immobilization and stabilization, methylprednisolone (limit swelling), orthosis, PT (ROM, respiratory management, pressure relief, pt ed, functional mobility; eventually strengthening, transfers, AD use, compensatory techniques, w/c training) • Outcome o PT outcome needs extensive PT, recovery depends on level of lesion, don't expect a lot of neuro recovery o Long-term effects best outcomes if see improvements w/in 1st 24 hrs, high mortality and poor functional outcomes

post polio syndrome

• Summary o Occurs in 25-50% of pts w/poliomyelitis o Symptoms muscle wkns, atrophy, fatigue, muscle and joint pain o Multidisciplinary tx control symptoms and improve daily function • Diagnosis o Condition that produces symptoms wkns occurring years after recovery from poliomyelitis o Injured structures polio starts as a viral attack to the ant horn cells in SC, subsequent death of motor nerves and atrophy of muscles; collateral sprouting helps recover strength but eventually high demands result in deterioration and another onset of wkns • Inference o Contributing factors 25-50% of pts who had polio get PPS; more common in F and pts who had severe cases of polio • Confirmation o Clinical presentation muscle wns, atrophy, fatigue, and sometimes muscle or joint pain, usually affects previously affected muscles, symptoms worse in cold or w/activity o Imaging electromyography, muscle biopsy o Additional info must have prev hx of polio followed by period of recovery and then gradual onset of new symptoms • Management o Tx meds for fatigue (IV immunoglobulin, anticholinesterases), PT (strength and endurance, avoid overexertion, energy conservation, orthoses, ADs) o Home care aerobic exercise, strength, and endurance training every other day • Outcome o PT outcome PT improves function and QOL o Long-term effects tend to have normal lifespan but does affect QOL, usually progresses slowly w/ periods of stability

trigeminal neuralgia

• Summary o Usually d/t abnormal pressure on or irritation of trigeminal nerve (CN V) o Symptoms usually unilateral, episodic or constant, sudden pain (sharp, jolting, stabbing, shock-like, persistent aching or burning) o Dx-testing is usually inconclusive, dx based on hx • Diagnosis o Condition that produces symptoms abnormal pressure or irritation to trigeminal nerve, often d/t swollen blood vessel, tumor, or MS o Injured structures trigeminal nerve (CN V) injury d/t pressure or demyelination usually near where it exits BS • Confirmation o Clinical presentation unilateral, episodic or constant, sudden onset of pain (sharp, jolting, stabbing), spasm, tics, may be triggered by touch or sound, aching or burning, symptoms can be progressive and severe ♣ Common is F and people > 50 y/o o Imaging magnetic resonance angiography o Additional info hx to ID cause

pericarditis

• Swelling and irritation of PERCARDIUM of heart - often caused VIRAL infections • Sx = sharp chest pain with radiation, pain wirse with coughing, lying down of inhaling deeply, SOB, heart palpitations, weaknes, fatge, fever, cough • PERICARDIAL RUB ON AUSCULTATION!

fx response

• assess peripheral pulse and sensation - nerve and vascular integrity • apply support to site with firm object to stabilize position and immobilize jt • pt should avoid mvmt of extremity • PT shoud NOT try to re-align fx • If open, cover with sterile towel or dressing If spinal fx = DO NOT MOVE PT

Rood's Theory

• based on reflex stimulus model: motor output is the result of past and present sensory input SENSORIMOTOR • Goal of homeostasis is achieved using key patterns to enhance MC want pt to be able to do task w/out stim o Key patterns = developmental sequence developed by Rood for synergy recovery • Tx includes sensory stimulation to facilitate or inhibit a response o Facilitation = approximation, joint compression, icing, light touch, quick stretch, resistance, tapping, traction o Inhibition = deep pressure, prolonged stretch, warmth, prolonged cold • Constructs o Heavy work = performing activity AGAINST gravity or resistance --Used to develop stability --Used to strengthen POSTURAL muscles o Light work = performing an activity WITHOUT resistance --Used to develop controlled mvmt and skilled function --Used for EXTREMITIES o Use sensory stim for motor output o movement considered autonomic and non cognitive o need homeostasis of all symptoms takes into account autonomic nervous system and environment o tactile stim to facilitate normal movement o environment influences treatment o exercise must give proper sensory feedback in order to be therapeutic response must be correct and advance motor learning ♣ once achieved, stim should be withdrawn

10-11 months

• brief stands w/out support • pulls to stand using half-kneel • can pick up objects from supported standing • creeps = bear walk • walks w/hands held - one or both fine pincer grasp (thumb and forefinger)

anti-eleptic meds

• reduce/eliminate seizure activity in brain • inhibit firing certain cerebral neurons o Barbiturates, benzodiazepine, carboxylic acid, hydantoins, iminostilibenes, succinimides Indication: Seizures Side effects: • Ataxia • Skin issues • Behavior changes • GI distress • Blurred vision • Weight gain PT: • Know how to repond to seizure • Know AEs of the meds • Watch enviornemnt nosies, lights • Secpma;, Neurontin, Dilantin, Tegretol, Celontin, Klonopin, Depakote

6-7 months

• rolls supine to prone • holds weight on 1 hand to reach for toy • HEAD CONTROL lifts head in supine and can control head while pulled to sitting • Can get to sitting and sit independently • May crawl backwards • Radial-palmar grasp • "rakes" to pick up objects Voluntary release to transfer objects in hands

5-8 years

• skip • jumping games (hop-scotch, jump rope) • hand preference 7-9 yo = mature adult gait

sprain vs strain

• sprain = acute injury to ligament o grade 1 = mild pain and swelling, little to no tear o grade 2 = mod; min instability, decreased ROM o grade 3= complete tear • strain = acute injury to muscle o grade 1 = local pain, min tenderness, min swelling o grade 2 = local pain, mod swelling and tenderness, impaired motor function o grade 3 = palpable defect; severe pain, poor motor function

effect size index

• stat which rep effect size using standardized value o = (diff between 2 groups) / STD one of the groups o Interpretation ♣ <0.1 trivial effect ♣ 0.1-0.3 small effect ♣ 0.3-0.5 mod effect ♣ >0.5 large effect

NCV

• stimulation of peripheral nerve to determine APs and ability to send signals/measure how fast o r/o peripheral neuropathy, carpal tunnel, demylination patho, peripheral nerve compression

APGAR scale

• total scores calculated at 1 min and 5 min after birth - HIGH SCORES ARE GOOD o 7-10 good o </= 3 low immediate med attention

2 years

• tricycle • tip-toe • catching • hopping (1-foot) • turns knob, closes jars, large buttons • child-scissors w/ help • 12-15 piece puzzles Folds clothes and paper

unilateral neglect

• unilateral neglect = the one side of body essentially doesn't exist o L side most common - lesion to R inf parietal or sup temporal lobe

echocardiography

• way to non-invsevly eval functioning heart via real-time images o Electrocardiogram = machine that uses SOUND WAVES to generate the pic o Tells Size and function ventricles, septal thickness, function walls, valves and chambers o TRANSTHORACIC ECG (TEE) = places US transducer on chest and into esophagus in order to get closer image of <3 since theyre both in close proximity (non-invasive)

RGO

♣ Designed to permit reciprocal gait instead of swing through (4 point gait pattern) ♣ Does this through the use of a cable system to assist with advancement of the other LE while the other is in stance ♣ Primarily for those with parapalegia • SCI = T9-L1 (says C8-T12 but rare) ♣ Designs • LSU RGO = 2 cable system coupling the passive hip flexion and extension movements that advance LEs • Isocentric RGO = uses bar balance system located at lumbosacral level of orthosis • Advanced reciprocating gait orthosis system (ARGO) = low-profile push-pull cables system (1) that provides reciprocating gait at hips and ALSO assists with standing through hip and knee extension assist mechanism • Walkabout = reciprocator at inner thigh

hypo and hyperglycemia

♣ Hyperglycemia (> 180-200 mg/dl) increased thirst, freq. urination, can lead to ketoacidosis (life-threatening, dyspnea, fruity breath, dry mouth, confusion, N+V, LOC) ♣ Hypoglycemia (< 70 mg/dl) hunger, shaky, sweaty, dizzy, clumsy, HA, LOC, counter w/ingestion of carbs/sugars ♣ Exercise response increased blood glucose uptake, should ingest carb snack prior to exercise to avoid hypoglycemia

bainbridge reflex

♣ Inc venous return STRETCH receptors of the RA VAGAL afferent signals to cardiovascular center in medulla INHIBITS Parasymp activity INCREASED HR • Think: want to pump all that extra blood out of heart

waveforms and intervals ECG

♣ P wave = atrial depolarization ♣ PR interval = time atrial depol and conduction SA to AV node • Normal: 0.12 - 0.20 secs (3-5 little boxes) ♣ QRS complex = ventricular depol., atrial repol. • Normal: 0.06 - 0.10 secs ♣ QT interval = time for both vent depol and repol • Normal: 0.20 - 0.40 secs dep on HR ♣ ST segment = isoelectric period following QRS ♣ T wave = ventricular repolarization

dialysis

♣ peritoneal dialysis = have catheter that stays in abdomen; peritoneal membrane acts as filter • fluid into cavity 20 mins - stays 4 hours - 20 min drain ♣ hemodialysis = taking blood out of body and filtering it with machine then putting it back in • 3x/week - 3-5 hours • PT imp o Mod tx based on fluid and electrolyte schedule o Standard precautions o Very fatigued before - very fatigued after o BEST = morning after getting done o Monitor VS closely - RPE may actually be best o Do NOT put cuff over the arm where fistula is o Not supposed to do mobilization DURING hemodialysis (Mandel said diff but okay) o Energy conservation and breathing skills education

Vertebral-basilar artery

♣ pons, midbrain, cerebellum, medulla, thalamus, occipital cortex • loss of consciousness • comatose/vegetative state • locked in syndrome (aka pseudocoma) pt aware but cannot move or communicate verbally 2/2 complete paralysis of nearly all voluntary muscles in the body except for vertical eye movements and blinking • Wallenberg syndrome (lat med infarct) ipsi facial pain and temp, ipsi ataxia, vert, CL pain and temp body, horners syndrome (decreased pupil size, a drooping eyelid and decreased sweating on the affected side of the face) • vertigo, nystagmus • syncope • ataxia • dysphagia • dysarthria

MI

About • Blood flow to one of coronary arteries SEVERELY REDUCED or CUT OFF • Causes irreversible NECROSIS to the area myocardium artery supplies • Extent of damage is dep on DURATION ischemia, THICKNESS tissue involved o Blood gets Epi first then down to endo (if gets to endo then we know it was worse AND this is gonna be the area more likely to get injured cuz the blood flow isn't there to be reproduced quickly) o Ischemia injury infarct o TRANSMURAL = full thickness o NONTRANSMURAL = sub-endocardidal area (inner 1/3 of myocardium) • 3 zones o zone of infarct = tissue dead o zone of hypoxic injury = a little damaged o zone of ischemia = had some O2 debt but iight • LAD = most common; gets septum and L vent • RCA = rome of the RV (marginal branch) and posterior-inf LV (posterior interventricular) Etiology • Typically due to RUPTURED atherosclerotic plaque OR blood clot blocks bloodflow • UNCOMMON = spasm of coronary artery • PRIMARY risk factors = pt or fam hx heart disease, smoking, physical inactivity, stress, HTN, high cholest, DM, obesity • Occurs more freq in morning and in Nov and Dec since peeps stuffing their faces S/Sx • Location and severity determine sx and overall acute clinical picture -- If you start to get any of these, CALL. Most people wait too long • 2/3 of peeps get PRODROMAL sx days to weeks before event - unstable angina, SOB, fatigue • Chest discomfort - pressure, squeezing, pain (MOST COMMON!!!) does NOT get better with rest/nitroglyc • Anxous • Pale • SOB (women more likely) • Discomfort upper body - arms, shoulder, neck, jaw, back • Nausea / vomiting (women more likely) • Dizziness • Sweating • Palpitations • Silent MIs happen too Add findings • At risk for complications - ARRYTHMIAS (~90% pts post MI), hypotension, pericarditis, impaired CO, pulmonary edema, CHF, pericarditis, cardiogenic shock , recurrent infarct, sudden death Imaging / add info for diagnosis • 12 lead EKG = PRIMARY o inverted t-wave = 50/50 chance ischemia, look at chest pain o ST depression = DEF ischemia, PENDING sub-endocardial, transmural infarction, see blood levels o ST elevation = DEF injury, acute infarction, check blood • Blood test o CPK - peaks at 24 and then gone day 2 o Troponin - stays longer o AST o Lactate dehydrogenase (LDH) • Chest radiograph, radio-nucleotide imaging, amylase level - could help Tx • Treatment varies from meds to sx - dep on severity and amount heart damage • Meds ACUTE = anticoagulants, beta-blockers, ACE inhibtors, thrombolytics, pain relievers, anti-HTN, cholesterol lowering meds, estrogen (in women) o Note: morphine actually really good, pain relief AND drops preload • PT = cardiac rehab once stable o Exercise test in 3 days to determine exercise guidelines o Need to get to 5 METS before can leave hosp. then it cont. to OP setting • SX = coronary angioplasty with stenting, CABG • Lifestyle changes Outcome • Cardiac rehab should help to get them back functioning ADLs • Long term outcome dep on - PLOF, extent and damage, age, CV disease, hypotension, co-morbities, abnormal treadmill exercise test

emphysema

About • DESTRUCTION ALVEOLAR WALLS over time - turn into large, irregular pockets with holes o Blebs = pockets of air in alveolar spaces o Bullae = pockets of air in lung parenchyma • Elastic fibers which hold open bronchioles destroyed COLLAPSING during EXHALE no air can escape lungs air trapping inc. in TLC, RV, Dec in VC and flow rates • 3 classifications o centilobulbar = destroys bronchioles in UPPER lung, alveolar sacs remain intact o panlobilbar = destroys air spaces in the acinus; LOWER LUNGS o paraseptal = destroys alveoli in lower lungs and causes blebs in periphery • PINK PUFFER TYPE OF COPD! Etiology • Primary risk factors = chronic bronchitis, lower resp. infection, smoking, genetic predisposition • SMOKING = leading cause • RARE cases = genetic disorder of protein alpha-1-antitrypsin o Without this, enzymes cause progressive lung damage and cause issues S/Sx • Can be asymptomatic until middle age - often diagnosed between 55-60 y/o • SOB • Wheezing • Chronic cough • Barrel chest • Inc subcostal angle • Inc fwd shoulder 2/2 tight pecs 0 • Inc use accessory muscles • Increased RR - with this dx, they inc. this in order to compensate and try to keep O2 and CO2 at proper levels (and are successful for a little until they get resp muscle fatigue) • Pursed lip breathing • Fatigue - they are ALWAYS overworking • Reduced exercise capacity • Decreased breath sounds BUT not really rales and rhonchi like in blue bloater • Probs have anxiety and other things like that going on 2/2 issues breathing • Possible complication = rupture of bullae/blebs which could lead to pneumonia and cor pulmonale Imaging • X-ray - eval shape and spacing lungs • Planogram - detect bullae • Bronchogram - eval mucous ducts and possible enlargement of bronchi • ABGs -may indicate decreased PaO2 • DIAGNOSIS= physical exam, pt. history, PFTs o Dec FEV1, VC, FVC (can't get air out) o Inc. TLC, RV, FRC (air trapping) Tx • MEDS = bronchodilators, anti-inflammatories, mucolytic expertorants, mast cell stabilzers, antihistamines, inhaled steroids, supplemental O2, antibiotics (if bacteria infection) • Lifestyle modifications - energy conservation, pursed lip breathing, • PT = Pulmonary rehab = AWC, breathing exercises, endurance and strength training • SX = lung volume reduction, bullectomy (dilated air-spaces aka bullae and blebs in lung parenchyma are removed), lung transplant Outcome • May require PT Intermittently to max functional abilty and pulmonary function • This is progressive - will need ongoing care • Life expectancy dec with severe exp slowing <1L during FEV1 Comp • BRONCHIECTASIS = chronic inflammation and dilation of bronchi and destruction walls o Associated with chronic infection o CF, sinusitis, Kartagener's syndrome, endobroncial tumors all inc risk o Chronic cough with sputum, hemoptysis, wheezing, dyspnea, recurrent resp infections o TX = PT, bronchodilators, antibiotics

sarcoidosis

About • Growth of small, abnormal collections of inflammatory cells (granulomas) within organs • Can affect any of the bodys organs - commonly lungs, lymph nodes and skin • When multiple form within the same organ - will affect function • If affects brain, heart - serious complications

bicipital tendonitis

About • Inflammatory process long head of the biceps tendon • Usually due to repeated ABD and ER humeral head - causes irritation o Leads to inflammation, edema, microscopic tears, degeneration o Damaged cells do not have time to heal tendonitis o Degeneration of the tendon causes loss of normal alignment of fibers Individual strands become intertwined or break • Common in sports or work with frequent OH motion - baseball pitching, swimming, rowing, gymnastics, tennis Etiology • Caused through repetitive OH activity and motion • Direct trauma to tendon with ABD and ER - humeral head migrates anteriorly • Ex high risk athletes = baseball pitchers, swimmers, tennis, gymnasts, rowers • Can also be caused 2/2 other shoulder pathology o Rotator cuff disease, impingement syndrome, intra-articular pathology (eg labral tear) S/Sx • Deep ache in front of or on top of shoulder • May spread down into biceps • Worse with OH activity or heavy lifting • Resting typically decreases pain • Pain to palpation over the groove • (+) biceps resistance test, Yergesons, Speeds • Catching or slipping may indicate tear of transverse humeral ligament (runs over biceps tendon in groove) • Shoulder instability and subluxation seen more with term chronic tendonitis • Could also accompany impingement syndrome, rotator cuff tendonitis, other forms GH instability Imaging • NONE confirm • MRI can view but that's expensive • Plain x-rays may show calcification in groove or Subacromial spurring; could also do of spine and elbow to r/o any other diagnoses Exam • PMH, what do they do daily and shit • Look at dexterity and coordination • May wanna look at DTRs too • Special tests o Biceps resistance test = pain to resisted shld flex with elbow ext and sup o Yergasons = arm ADD, elbow flexed, resist supination and ER o Speeds = arm flexed to 90, forearm supinated, resist shoulder flexion at forearm • Mgmt • Medical mgmt. o Primary goal = relieve pain, reduce inflammation, regain full ROM o Rest/immobilization in brace or splint maybe initially for short period of time o Avoid all OH motion, reaching and lifting • PT o GOAL = restore full ROM without pain o Not usually done initially - needs to calm down (get out acute phase) o Pt may benefit from iontophoresis or phonoporesis o Once out acute, stretch and strengthen affected muscle groups ♣ Allows tendon to function properly, improve healing, prevention recurrent injury • SX = rare; only when failed over 6 months o Arthroscopic decompression and acriomoplasty with anterior acromionectomy • Pharm = NSAIDs (pain and inflammation) Outcome • Overall prognosis depends on level of involvement • Most have positive outcomes and can return to PLOF • Usually return 6-8 weeks

lateral epicondylitis

About • Irritation, inflammation, or degeneration to the common extensor tendon muscles (at lateral epicondyle) • Repetitive overuse wrist ext. - particularly EXT CARPI RADIALIS BREVIS o Produces tensile stress microscopic tearing and damage o Does not allow for proper healing so more damage o Overtime may lead to formation of adhesions o Other muscles = ED, ECRL, ECU • Racquet sports or throwing Etiology • MOI = rep wrist EXTENSION AND SUPINATION against resistance • Best seen with racket sports (backhand in tennis), overuse with painting, hand tools, gardening, etc • May be caused by faulty mechanics or poor equipment • Most common = 30-50 yo (normal loss extensibility with aging) • MALES > females S/Sx • PRIMARY SYMPTOM = PAIN along lateral aspct of elbow • Point tenderness over lateral epicondyle • May radiate down into dorsum hand • Increases with wrist flexion and elbow extension (stretching); as well as active wrist ext, RD • Difficulty holding or gripping objects; insufficient forearm strength • Usually no limits ROM unless severe Imaging • Nah Exam • Look into what they do that may be contributing • Special tests o Cozens = Pt makes a fist, pronates, RD and ext wrist against resistance with elbow slightly flexed o Mill's test = push into more wrist flexion with elbow ext and forearm pron o Lateral epicondylitis test = resisted middle finger extension at IP joint with elbow ext and forearm pronated Mgmt • Medical mgmt. = o Initially = protection, RICE o Avoid all activities that aggrevate o Phonophoresis (hydrocortisone); iontophoresis (dexamethasone) o Sometimes resting splints • PT o Increase strength, endurance and flexibility of elbow, wrist, and hand muscles o ALWAYS PAIN FREE!!!! o Counter-force bracing = Strap 2-3 cm distal to epicondyle can help to dec. some of the tension (wean off prior to RTP) • Pharm = NSAIDs Outcome • Overall outcome favorable - should return to PLOF and activities without restrictions • Common recurrence • May have to have sx if does not get better 2-3 months with conservative tx

cor pulmonale

About • PULMONARY HEART DISEASE (aka heart issue caused by lung issue) R sided HF!!! • Increased afterload / pulmonary TN causes o Hypertrophy of the RV since the lungs are f'd (working hard to try to get blood in there) o Dilation of RV o Changes in BO Etiology • Pulmonary HTN - S/Sx • CARDINAL SX = progressive SOB, esp with exertion • INITIALLY = sx more related to underlying patho o Fatigue o Palpitations o Atypical chest pain o Cough o Tachypnea o Inc chest diameter o Hyperresonance with percussion • As progresses, get more R side HF sx o Swelling LEs o JVD Tx • SUPPLEMENTAL O2 - SaO2 > 90 (O2 in blood) ; PaO2 > 60 mmHg (O2 in tissues) • Meds = diuretics, anticoagulation

angio II receptor antagonist

Action • BLOCK angiotensin 2 receptors • Limit vasoconstriction and limit aldosterone hormone (water and salt) Indication • HTN • CHF AEs • Dizziness • Back and leg pain • Angina pectoris PT imp • MIN IMPLICATIONS Ex • ALL THE -SARTANS!

thrombolytics

Action • BREAKDOWN CLOTS - convert plasminogen to plasmin o Plasmin = breaks down clots

opiod agents

Action • Stimulates opiod receptors within CNS - stops pain impulses from reaching destination • Certaindrugs also used for dependency, withdrawl symtoms Indications • Moderate to severe pain various origins • Induces conscious sedation prior to diagnostic procedure • Mgmgt opiod dependence • Refleif sereve and persistent cough (codeine) AEs • Mood swings • Sedation • Confusion • Vertigo • Dulled cognitive function • OTH • Constipation • Incoordination • Physical dependence • Tolerance PT imp • Monitor for AEs - esp respiratory depression • Tx scheduled 2 hours from dose - max effects pain relief • May not accurately report if something is painful Ex. • Roxanol (morphine) • Demerol (meperidine) • OxyContin (oxycodone) • Sublimaze (fentynal) • Paveral (codeine)

meniscus tear

About • Menisci = C and O shaped fibrocartilage structures which help with shock absorption and load distribution o firmly attached to tibia; thick on the outside and thin on the inside • Medial is more commonly injured since attached to capsule so LESS mobile • Typically tear as result of trauma - in isolation or in conjunction • MOI = twisting of knee while flexes and planted OR hyperflexion o Older = degeneration then pivoting • Types o Bucket-handle/longitudinal can be squeezed back together with WB o Oblique some features of longitudinal and radial... can detach and left with loose fragment or roll up in joint and cause locking o Degenerative wear and tear of joint with age... loss of cell matrix and weakening of fibers, replacement is slow... damage is faster than repair process o Radial o Horizontal tear from inside out... see separation btwn layers in cartilage • Blood supply o Outer 1/3 = red-red and is GREAT o Middle 1/3 = red-white and DECE o Inner 1/3 = white-white and BLAH Etiology • Sports, esp with quick cutting and pivoting • Older - more likely to have degenerative tears • Pt with knee instability also more prone S/Sx • Joint line pain • Swelling LATER (ACL is immediate) • Catching or locking • Sometimes a mechanical block • Traumatic = sudden onset; degenerative = gradual onset Imaging • Diagnosed by arthroscopy • MRI = test of choice Exam • special tests o Appleys o McMurrays o Thessalys o bounce home Mgmt • several considerations - age, activity level, location, type/extent tear • CONS = palliative modalities and strength, limited WB • SX = full or partial meniscectomy, repair, transplantation o Repair = when in outer peripheral (red-red zone so more vascular), more active peeps o Menisectomy = older pts, lesion avascular portion

SLE

About • Autoimmune reaction where the body attacks its own CONNECTIVE tissues (also can have systemic effect) • high levels of autoantibodies (ANA) form immune complexes inflammatory response further tissue destruction Etiology • immunoregulatory disturbance from genetic, enviornemntal, iral, hormonal factrs • environmental = UV exposure, infection, antipiotics (penicillin, sulfa drugs), extreme stress, immunization, pregnancy o DECREASE THESE RISK FACTORS FOR LESS EXACURBATION PERIODS • more common in women (10-15x!!!) • 15-40 yo S/Sx • period of remission and exacerbation • DIVERSE based on involvement • Arthralgias • Malasise • Fatigue • HA • RED BUTTERFLY RASH ON FACE and rash on sun-exposed areas of body • Alopecia • Kidney invokvement, heart involvement, lungs, other organs pericarditis, endocarditis, myocarditis, neuphritis, neurological issues o POORER PROGONISS • FMS • Skeletal deformities = UD and subluxed IP joints of hand • CNS involvement depression, irritability, emotional instability, seizures Imaging • Microscopic fluorescent techniques = detect ANA In body • Antideoxyribonucleic acid antibodies test = done if POSITVE FOR ANA • Physical presentation • DIAGNOSIS = at least 4/14 characteristics given by the American rheumatisism association Mgmt • Reverse autoimmune response • GEN = avoid UV, avoid stress, good nutrition, ongoing med supervision • PHARM salicylates (pain and inflame reduc), indomethiacin, NSAID, antimalarial, corticosteroids, immunosuppressive therapies • PT = slow resumption act after period of remission, energy conservation, pacing, relaxation tech, prevent deformity Outcome • Course is highly unpredictable • Overall prognosis is good BUT can remain acute and becoe fatal in rare cases

pleural effusion detailed

About • Buildup of FLUID IN THE PLEURAL SPACE btw lungs and chest cavity (aka surrounding lungs) o Type of fluid in there dep on cause • This can push the pleura against lungs - hard to breathe, maybe cause atelectasis • EMPYEMA = fluid gets infected and turns to abscess Etiology • Usually 2/2 a variety of med conditions - CHF, pneumonia, renal or liver dz, CA, PE, autoimmune disorder • PLEURITIS = inflammation of visceral and parietal pleura (lining of the lungs) o Can be caused by VIRAL infection, PNEUMONIA, PE, autoimmune disease (RA, lupus) S/Sx • Often asymptomatic unless large • SOB • Chest pain • Cough • If infected - dry cough, fever, chills • Additional Sx of whatever caused pleural effusion • MUSCULTATION = dec. breath sounds, dec. fremitus, egophony (say e hear a), pleural friction rub

RLD in detail

About • CLASSIFICATION of many disorder where basic premise is can't get air IN! o Aka many conditions cause - either pulmonary or extrapulmonary • Impairment in lung expansion and reduction in pulmonary ventilation • FEV1/FVC = >75% (they dont have an issue getting air out, they just didn't have a lot of air in to begin with to get out) Etiology • Abnormal lung parenchyma - atelectasis, pneumonia, pulmonary fibrosis, pulmonary edema, ARDS • Abnormal pleura - pleural effusion, pleural fibrosis, pneumothorax, hemothorax • Disorders affecting ventilitory pump - dec resp drive, neurologic and NM diseases, muscle disease or weakness, thoracic deformity or trauma, CT disorder, pregnancy/obesity/ascites S/Sx • Varies based on underlying cause - but often a lots of sx are common • Pathogenesis = dec compliance, dec lung volumes, inc WOB! • Decreased chest mobility • Dec breath sounds • SOB / DOE • Tachypnea - rapid, shallow breathing pattern • Resp muscle weakness AND inc accessory muscle use • Ineffective cough • Hypoxemia • Reduced exercise tolerance Add findings • May become unable to deeply inhale 2/2 poor lung expansion • As progresses, resp. muscle fatigue will lead to impaired alveolar ventilation, CO2 retention • Initially DOE, but eventually will have at rest too • Complications / advanced progression = hypoxemia, pulmonary HTN, cor pulmonale, severe dec oxygenation, vent failure Imaging / add info for diagnosis • Chest radiograph - lung structure, evidence fibrosis, infiltrates, tumor, deformity • ABGs - hypoxemia (dec PaO2), and hypocapnia • PFT testing o Impaired VC o Dec FVC (air out, cu they don't have air to get out) o Dec TLC (can't get air in) o Dec expiratory reserve volume (again, don't have and air in to get out) o Reduced FRC o NORMAL RV (opp. COPD which gets trapping) o Normal exp. flow rates (nothing blocking it from coming out) Tx • PT = GOALS to max gas exchange, max function o Body mechanics, posture training, resp. muscle strengthening, relaxation, energy conservation tech o Breathing, coughing, AWC • Mech. vent, supplemental O2, nutrition support Outcome • Outcome is based on etiology • Most eventually progress to resp. failure • Some may be candidates for lung transplant at the end • IPF = high mortality rate ~4-6 years into diagnosis

asthma

About • Chronic inflammation of the airways o Big 3 = bronchoconstriction, airway edema, mucous plugs • Caused by INC SENSITIVITY to various stimuli • What happens: antigen trigger immune system calls in mast cells mediators like histamine released SMOOTH MUSCLE CONTRACTION (so foreign cant get in), CELL MEMB PERM INC (more blood to get rid of irritants) Etiology • Factors that trigger o Resp infections o Allergens - pollen, mold, animal dander, feathers, food, dust o Exposure cold air o Excitement/stress o Exercise (EIA) S/Sx • DEPENDS on level of restriction • MILD o Wheezing o Chest tightness o Slight SOB • SEVERE (can result in resp failure if left untreated) o Dyspnea o Flaring nostrils o Diminished wheezing o Anxiety o Cyanosis o Inability to speak Tx • REDUCE EXPOSURE TO TRIGGER • 2 classes of meds o ANTI-INFLAMMATORY = interrupt bronchial inflammation PREVENTATIVE ♣ Inhaled corticosteroids, cromolyn sodium, leukotriene modifiers o BROCHODILATORS = dilate airways by relaxing smooth muscles ♣ Beta-adenergic agonists, methylxanthins, anticholinergics • PT = caregiver edu, airway clearance (do NOT do percussion with these peeps, makes worse), relaxation, endurance and strength training

club foot

About • Deformity where toe points down and forefoot turns inward Etiology • Unknown but theories • familial tendency • positioning in utero or lack of movement • often accompanies other neuromuscular abnormalities - spina bifida, arthrogyphosis S/Sx • adduction forefoot • varus at Hindfoot • equinus at ankle Tx • splinting and serial casting • GOAL = restore proper positioning • SX = if failed the casting

GH instability

About • Excessive translation of humeral head on glenoid • SUBLUXATION = joint laxity; >50% of humeral head goes over rim but does not leave • DISLOCATION = humeral head all the way out o 80% of these detach the glenoid labrum BANKHART LESION Etiology • combo of forces stress ant capsule, GH lig, RTC cause humerus to move anteriorly • ant dislocation most common ABD and ER S/Sx • SUBLUX o Feeling shoulder popping in and out o Pain and paresthesia o Arm feels dead o Capsular tenderness o Swelling o (+) apprehension test • DISLOC o Severe pain and paresthesia o Other arm holding it o Limited ROM o Weakness o Visible shoulder fullness Tx • Immobilization 3-6 weeks • RICE and NSAIDs • ROM and isoMETRIC strengthening • Progress to PRE focusing on IR, ER and scapular stabilizers

pulmonary edema detailed

About • Fluid collects in ALVEOLI / LUNGS • Very difficult to breathe • ACUTE = MEDICAL EMERGENCY - CALL 911!!! o Extreme SOB, profuse sweating, bubbly/wheezing or gasping during breath, cyanotic, rapid, irregular pulse, pink, frothy sputum, drop in BP! Etiology • Typically, due to L vent failure o Blood gets backed up into pulmonary veins and capillaries capillary walls alveoli • Non-cardiac = fluid leaks from capillaries WITHIN alveoli since the cap themselves become MORE PERMEABLE o Could be from pneumonia, toxins, meds, smoke, ARDS, living high elevations S/Sx • Develop suddenly or slowly dep on cause • ACUTE o EXTREME SOB (lying down makes WORSE - inc venous return / <3 pooling) o Feeling suffocating or drowning o Wheezing or gasping for breath o Anxiety o Restlessness o Apprehension o Coughing o Red, frothy sputum o Vest pain (if cardiac cause) o Rapid, irregular pulse • CHRONIC o SOB worsens when lying down or activity o Weight gain o LE swelling o Fatigue Imaging • Chest xray - primary • Blood test, CKH, echocardiogram - try to find out cause Tx • Variable dep on cause • Supplemental O2, meds

dequarvians synovitis

About • Inflammation of the ABD POLLICIS LONGUS and EXT POLLICUS BREVIS at the anatomical snuffbox • The tendons have a synovial sheath around them and run through the anatomical tunnel od the EXT reticulum and radial styloid process o Inflammation results in IMPINGMENT here • MOI = repetitive activities of thumb ABD and EXT (racket sports, heavy lifting); direct trauma; structural anomalies • WOMEN > men (esp. new mothers) S/Sx • Localized pain and tenderness at snuffbox • may occasionally radiate into forearm • gradual or sudden onset • worse with activity and resistance • better with rest • edema may be there • severe cases edema - may get nerve entrapment of superficial branch radial nerve Imaging • no lab or imaging studies commonly used Exam • look at ADLS for provocative things they're doing • special test o finklestein

lateral ankle sprain

About • Lateral ankle complex = 3 bands o ATFL = PF and INV; ant translation of talus on fibula ♣ Most likely to be injured o CFL = INV in neutral o PTFL = post translation of talus ♣ strongest one! • MOI = sig inv and PF / varus force • Note: deltoid lig. complex (med) is stronger so usually a sprain that is enough to rupture all those causes a fx of medial malleolus first Etiology • #1 risk factor for ankle sprain is a previous ankle sprain o dec. prop and remaining joint laxity • sports with cutting and jumping • deconditioned • poor proprioception • obesity S/Sx • Sig pain / tenderness lateral aspect of ankle, esp. ATFL • Pain limits strength assessment • Pain with INV and PF (stretched structures) • AROM limited (need to be done to r/o Achilles tendon rupture • Antalgic gait • Ligamentous laxity • Ecchymosis laterally • Edema Imaging • MRI not usually done unless other issues • X-ray - use Ottawa ankle rules Exam • Important hx = PMH, meds, fam Hx, current sx, etc • Special tests o anterior drawer = ATFL - anterior translation o talar tilt = talus moved into ADD • Makes sure to r/o neurovascular complications, Achilles tendon rupture o Thompsons test o Distal pulses o Sensory integrity Mgmt • Medical mgmt. = conservative; RICE o Sx = not usually indicated unless other issues o May use crutches initially to progress to FWB • PT = increase ROM, inc. prop and balance, dec. edema, PRE, joints mobs if capsular tightness, functional activities, gait, agility, modalities, x-friction massage AFTER inflammation gone o Make sure to work on peroneals = dynamic ankle stability o Complete functional test before RTP • Pharm = pain mgmt. (acetometaphone, NSAIDs) outcome • Should heal quickly - back to prior level 2-6 weeks • May need to do period taping/bracing with return initially • Long term effects = residual laxity will inc risk of recurrence

anyeurism

About • Localized ABNORMAL DILATION / BALLOONING of blood vessel - usually an artery • Common sites o Thoracic aortic (TAA) o Abdominal aortic (AAA) o Brain vessels (usually in circle of willis) Etiology • Congenital defect • Weakness in wall - typically 2/2 HTN • CT disease (eg Marfans) • Trauma • Infection S/Sx • VARIES based on place • AAA= usually asymptomatic, general abdominal or LBP if yes o Low back, abdominal pain o Nausea and vomiting o Lightheaded o Tachycardia o When ruptured = hypovolemic shock - FATAL o If large -- pulsating near belly button • TAA o Jaw, neck, back chest pain o Coughing / hoarseness o SOB • CEREBRAL o Fatigue o LOB o Speech and vision issues o rupture = subarachnoid hemorrhage ♣ severe and sudden HA ♣ nausea and vomiting ♣ stiff neck, seizure ♣ LOC ♣ AMS ♣ double vision Imaging • US, CT, MRI, echocardiography, angiography • Rupture brain = lumbar puncture to see if blood in CSF

MCL sprain

About • MCL runs from slightly above medial femoral epicondyle to medial aspect shaft of tibia o Thick and flat, fan-shaped band • PRIMARY stabilizer MEDIAL side - valgus stress and ER tibia (esp. when knee flexed) o Actually has good secondary support system when WB since closed down joint space and adding stability • Often involves injury to other structures - ACL and/or meniscal damage • Grading o Grade 1 = o Grade 2 = PARTIAL tear; laxity is present ♣ Medial capsular lig. also involved o Grade 3 = full tear Etiology / Contrib factrs • MOI = Contact or noncontact, fixed foot, tibia rotation injury valgus + tibial ER • Participation contact activities, high level of agility • Muscle weakness resulting in poor dynamic stabilization S/Sx • Pain and sig tenderness medial aspect knee • Possible dec. strength • Possible dec. proprioception • Slight to mod swelling (more severe swelling could indicate cruciate or meniscal involvement) • Antalgic gait • Decreased ROM - inability to fully ext or flex knee • Feels unstable • (+) valgus stress test Imaging • MRI - can see but $$$$$$ (only done when really necessary for other shit) Exam • MOI important • special test o (+) valgus stress test - done at 0* and 30* (worse if more laxity and 0 since CP pos) o also make sure to r/o cruciate or meniscal involvement with special tests Mgmt • med = usually CONSERVATIVE o full length KI or hinge brace and crutches to limit WB - use until pt can ext knee joint (can do SLR with no ext lag) • PT = dec inflammation, protection knee joint and lig, ROM, strengthening o Cross friction to healing lig good for alignment fibers o NOT at prox attachment - potential bone periosteal disruption o RTP = full ROM, ambulation with no limp, no swelling, competence with all agility and functional testing • PHARM = acetometaphine and NSAIDs (pain mgmt.) • SX = rarely required since well-vascularized

idiopathic pulmonary fibrosis

About • MICROSCOPIC DAMAGE TO ALVEOLI causing irreversible SCARRING o You have abnormal wound healing -- Makes it stiff and thick and less flexible so breathing harder Etiology • Most idiopathic • Chronic exposure dust, asbestos, sugar cane, bird and animal droppings • Radiation lung or breast CA • Chemo drugs • Certain anti-arrhythmic meds - amiodrone, propnolol • Antibiotics - nitrofurantoin, sulfasalazine S/Sx • SOB - esp. during or after activity • Dry cough ONCE MORE ADVANCED • Fatigue • Unexplained weight loss • Aching muscles and joints Tx • Combo corticosteroid + immunosuppressents • Lung transplant when advanced • Try to improve QOL

congenital hip dysplasia

About • Malalignment of the femoral head in acetabulum • Develops during 3rd trimester in utero Etiology • Curtural pre-disposistion • Mal-posistion in utero • Environmental and genetic influences S/Sx • Asymmetrical hip ABD • Tightness and apparent shortening involved side • Testing = Ortolanis, Balow's, diagnostic US Tx • Depends on age, severity, initial attempt to reposition • CONS = Try to reposition the femoral head through constant harness, bracing, splinting or traction • SX = open reduction and then app of hip spica cast

OA

About • Most common type of joint disease • Chronic degenerative disease PRIMARILY hands, knees, hips (WB joints) • Affects ARTICULAR CARTILAGE • NOT just wear and tear - there are also secondary inflammatory changes which occur • Degeneration articular cartilage breakdown chondrocytes disruption cartilage matrix - decreased joint space reactive new bone formation (deformity and thickening subchondral bone) • Excessive loading of healthy joint OR normal loading unhealthy joint Etiology • Primary = idiopathic o Intact joints, no Hx which supports getting it • Secondary = degeneration due to some predisposing condition o Has already adversely affected the articular cartilage and subchondral bone o Relatively young individuals • typically, middle aged - pretty much all have (80-90%) by the time you're >65 yo o <55 yo = mostly males o >55 = mostly females • risk factors o age o overweight o trauma / infection / other joint injuries o occupational or athletic overuse (repetitive microtrauma) o genetic factors o inflammatory arthritis o NM and metabolic disorders S/Sx • Typically, bilateral Hands (DIP and PIP), knees, hips, spine • gradual onset deep and achy joint pain (MAIN reason seek med attention) • increased pain after exercise and with weather changes o progresses to morning stiffness and pain at rest too • enlarged joints o Heberdens (bony swelling at DIP) or Bouchards (PIP) nodes (more common women) • crepitus • stiffness • decreased ROM and functionality • crepitus • may see malalignment later • deviated gait pattern • NOT erythema or warmth • Increased incidence sprains and strains around joints with it Imaging • Typically, just use clinical exam findings • Radiographs may show decreased joint space • NOT blood tests Exam • Do tests you would do on old peeps too (TUG, BERG) • Make sure to look at QOL and functional impact Mgmt • GOAL = reduce pain, promote joint function, protect joint • Med mgmt. o Visco-supplementation = injections hyaluronic acid for lubrication o Glucocorticoid injections = sparing use for sx o Education nutrition and weight reduction • PT = intermittent for help with Sx and functionality o AROM, PROM, heat, ice, education, decrease weight, energy conservation, body mechanics • PHARM = acetometaphine, corticosteroids, NSAIDs • SX = range arthroscopic to total joint Outcome • PT can assist periods of exacerbation BUT this is a chronic degenerative condition which we cannot change • Degree of disability depends on site and rate of progression (usually slow) • OA of knee is leading cause of disability in older persons

spinal stenosis

About • Narrowing of lumbar vertebral or IV foramina • Sx due to compression of SC or the nerve roots • Structural changes = degeneration, HNP, osteophyte formation, hypertrophy of structures (eg lig flavum) • other etiologies = trauma, compression fx, systemic conditions (tumor, ankylosing spondy), iatrogenic factors (laminectomy, discectomy) • Classification o Primary = congenital; small percentage o Secondary = narrowing 2/2 AQUIRED changes of foramina Etiology • Certain congenital defects and conditions inc. risk • AGE = PRIMARY RISK FACTOR for secondary stenosis S/Sx • Gradual onset and worsening LBP • Maybe unilateral radiculopathy, Paresthesia, weakness, diminished reflexes • Worse with extension • Decreased with flexion (increased space) stopped posture • NEUROGENIC CLAUDCATION SX • RARE: B radiculopathy, ataxia, balance dysfunction, bowel/bladder issues, hyperreflexia Imaging • MRI - best since can diff soft tissues • CT myelogram - inject dye to see; can see SC, nerve roots, areas of compression Mgmt • PHARM = NSAIDs, muscle relaxants • SX = cons fail, sx badddd o Lumbar laminectomy • PT = improve function and pain mgmt, strength, flexibility, endurance, spinal stabilization, modalities, use AD, EDUCATION, weight loss may be recommended

CAD

About • Narrowing or blockage (aka atherosclerosis) of CORONARY ARTERIES • Usually develops slowly and goes undiagnosed or unnoticed for years Etiology • Damage/injury to inner wall fatty plaque buildup (cholesterol, cell waste) harden narrow artery impede blood flow • ORRRR the plaque could rupture platelets to site for more clumping • Basically, whatever it is causes a block and then that could lead to MI • Risk factors o High blood levels LDL (>70) o low blood levels HDL o type 2 DM o smoking o obesity o low physical activity o genetic factors, HTN, hypo-thyroidisim also S/Sx • NEED ~70% OCCLUSION OF AN ARTERY TO ACTUALLY GET SX!!! • Angina • SOB • Other Sx • Full blockage = MI Imaging / diagnosis • Cardiac cath. with coronary angiography - aka injecting dyes through cardiac caths. and looking at with x-ray imaging is MOST accurate • CT and MRI can also give pics (non-invasive) Tx • Aggressive modification risk factors • PHARM = anti-platelets (ASA, clopidogrel - ic supply by dec. buildup), ACE inhibitors (dec. afterload), angiotension II receptor blockers (dec afterload), statins o ACUTE = M (morphine), O (O2), N (nitroglycerine), A (ASA) • SX = for pts high risk mortality o percutaneous angioplasty, CABG, endarectomy • PT = formal multi-phase rehab program o Educate target HR and self-monitoring status during exercise

cellulitis

About • Noncontagious bacterial skin infection - DERMAL AND SUBQ LAYERS • commonly - strep and staph • uncommonly - pneumococcus, oseudomonias, clostridium • can become SYSTEMIC if not caught early Etiology • weakned immune system - meds (corticosteroids, chemo), meds conditions (HIV, leukemia) • HIGH RISK = impaired blood / lymph flow (venous HTN, lymphedema, obesity) • Tyocally 2.2 break in skin (bacteria can now enter) pts with DM can get without break S/Sx • Local rednes, warmth, tenderness • progressive edema • red streaks away from primary infection site • weeping • serous drainage • systemic signs if worsens - fever, chills, aches, swollen and tender lymph nodes Exam • blood sample analysis = WBCs will be elevated but cant r/I ALONE • wound culture = tells specific bacteria at fault

anterior compartment syndrome

About • Occurs when pressure in anterior compartment of lower leg increases secondary to SWELLING o Tibaialis anterior, extensor hallucis longus, extensor digitorum longus, peroneus tertius • Results in occlusion blood flow ischemia and damage the longer it goes • Acute = often cause by trauma, MEDICAL EMERGENCY; damage usually worse • Chronic = 2/2 atheltci exertion; NOT med emergency S/Sx • Tightness and tenderness over muscle belly of tibialis anterior • does NOT decrease with elevation or pain meds • pain INCREASES passive stretching or active use muscles • may have paresthesia/numbness along dist of deep peronral nerve Imaging • compartment pressure testing = needle into compartment and measuring pressure o for ACUTE • for chronic, measurements compared before and after Exam • r.o DVT, fx, peripheral nerve injury

impingement syndrome

About • One of MOST COMMON injuries of shoulder • Rep micro-trauma from OH activities • Throwing, swimming, racket sports susceptible Etiology • Humeral head an RTC attachments migrate up into acromion and coroco-humeral ligament S/Sx • Discomfort / mild pain deep in shoulder • Painful arc 60-120* • Tenderness over greater tib and bicipital groove • (+) impingement sign, Neers, empty can/full can Tx • RICE, NSAIDs, activity modifications • Strengthening RTC and scapular stabilizers

PE

About • One or more arteries in lung (aka pulmonary arteries) become BLOCKED 2/2 CLOT! • Usuallly a couple clots to actually cause blockage • Causes dec. perfusion in lung tissue ischemic tissue body can't get good O2 • Can be life-threatening but prompt treatment helps to dec. risk Etiology • Usually caused by blood clots for LEs which dislodge and travel in bloodstream S/Sx • Vary greatly - deps on how much lung, size clot, overall health of pt • Sudden onset SOB - nothing really makes it better • Chest pain -- worse with eating, deep breathing, coughing, bending • Coughing up pink sputum • Wheezing • Unilateral LE swelling • Excessive sweating • Rapid or irregular pulse • Lightheadedness / fainting Imaging • V-Q san - nuclear imaging readiomucleotide substance injected to see blood-flow through lungs • Spinal CT scan - 3D images to confirm presence/location • MRI, diagnostic US - to see if any elsewhere • Pulmonary angiography - most conclusive and accurate, but complication high so ONLY when other tests not conclusive Tx • ACUTE = anticoagulants and anti-thrombolytics • Sx = remove clot, filter at IVC • PREVENTION = anticoagulants, get moving, compression socks, water

medial epiconydlitis

About • Overuse injury - tendons are overworked and become inflamed • Could also tech be from trauma causing inflammation too • Commonly occurs as result of repetitive WRIST FLEX and forearm PRONATION o Flexor carpi ulnaris and pronator teres main hoes o finger flexors and other anterior compartment muscles are the sometimes side-hoes • all those tendons share insertion at the flexor bundle at MEDIAL EPICONDYLE • ulnar nerve can also become irritated right here too • often seen in golfers, other racket sports Etiology • activities which require repetitive wrist FLEXION and GRIPPING • pts with poor flexibility strength and endurance of forearm flexors more at risk • other factors = improper equipment, improper technique S/Sx • gradual onset (unless traumatic incident caused obvi) • pain and tenderness over medial epicondyle • pain with resisted wrist flexion, pronation, and gripping - passive wrist extension • may also be weakness of these movements • if ulnar nerve affected - pain and paresthesia's into 4th and 5th fingers Imaging • not usually used • x-ray = normal; use only if traumatic • MRI - can tell damage but don't need Exam • Make sure to assess ulnar collateral ligament integrity as can mimic sx Mgmt • Initial = RICE, anti-inflammatories, bracing, massage, stretching • Bracing = cock-up splint to limit wrist movement; counterforce brace to dec tension at insertion • Once pain subsides = strength (ECCENTRIC!!) • Cortisone shot may help - short term • Sx = maybe (debridement) Outcomes • Large majority do well with conservative • To prevent recurrence - make sure they keep good strength and flexibility, limit provoking activities

HTN

About • PERSISTENT elevation of BP (BP measures the force of blood against arterial walls) o SBP = pressure during CONTRACT heart; DBP = pressure during RELAX heart o ADULT = SBP>140 mmHG, DBP > 90 mmHg o CHILD = SBP/DBP consistently > 95 percentile BP distribution o Adult Classification ♣ Normal <120 / <80 ♣ Prehypertensive 120-139 / 80-89 ♣ Stage 1 HTN 140-159 / 90-99 ♣ Stage 2 HTN >160 / >100 • PRIMARY / ESSENTIAL = no known cause • SECONDARY = due to known cause (usually renal disease) • Isolated systolic HTN (ISH) = when older pts have ONLY elevated SBP but DBP same Etiology • Risk factors = Black, men, post-menopausal women, fam hx HTN • Conditions like pregnancy, DM, sleep apnea also inc risk • Modifiable risk factors = smoking, sedentary, stress, smoking, ETOH, high salt diet S/Sx • Often asymptomatic until complications develop in the organs • S4 = EARLY SIGN • SEVERE HTN = sig CNS sx (confusion, cortical blindness, hemiparesis, seizures), CV sx (chest pain, dyspnea), RENAL involvement

piriformis syndrome

About • Piriformis = flat, oblique muscle; ABD and ER hip o Sciatic nerve runs underneath it o Greater sciatic foramen inferior piriformis distal along midline post thigh splits • Syndrome = Result of compression or irritation to PROX sciatic nerve due to the muscle o Inflammation, spasm or contracture, trauma, scarring, entrapment • Commonly mistaken for LBP - "psuedosciatica" Etiology • 50% have hx of local trauma - contusion, THA • abnoraml gait mechanics, inc lumbar lordosis, long sitting, participation a lot of physical activity S/Sx • imprecise pain location - first in mid-buttock then radicular to sciatic nerve dist • hip, coccyx, groin pain also may • exacerbated prolonged sitting • worse acitvites with IR and ADD • paina dn weakness resistance testing ER and ABD • radicular sx worse with SLR and better with traction • present super similar to L5-S1 disc Imaging • clinical diagnosis of EXCLUSION! • Imaging to r/o shit Exam • Make sure to r/o other dx - troch bursisits, myofascial pain Mgmt • Typically CONS - pain mgmt • PT = modalities, STM, mobs, strain/counterstrain, muscle energy, addressing SI dysfunction, leg length discrep, other biomech factors; grad strengthening as pain decreases • SX = piriformis tendon release, sciatic neurolysis o LAST RESORT Outcomes • Typically respond well to PT intervention - able to return no issues • Return dep on - severity and chronicity, pt compliance • Can be disabling long-term if not addressed

bronchiectasis

About • Progressive OBSTRUCTIVE lung disease • AIRWAYS/BRONCHI (not alveoli) scarred from chronic inflammation which results in THINNING/DILATION of bronchial wall • IRREVERSIBLE • Typically associated with chronic infections, aspiration, CF!!!, immune system impairment Etiology • Injury to airways or lung infection - pneumonia, whooping cough, measles, TB, fungal infections S/Sx • Consistent PRODUCTIVE cough • Hemoptysis • Weight loss • Anemia • Crackles • Wheezes • Loud breath sounds Tx • Meds = antibiotics, bronchodilators, expectorants (thins the mucous/increases secretion of it), mucolytics (dissolves mucous)

achilles tendonitis

About • Repetitive overuse disorder microtears of collagen fibers • Can be on surface or in substance • MOST OFTEN @ avascular zone - distal 1/3 of tendon; 2-6 cm above insertion tendon Etiology • Repetitive overload often changes in intensity or bad mechanics • Limited flexibility / strength gastroc/soleus complex • Pronated or cavus foot • Running, bball, gymnastics, dancing • INCREASES likelihood of rupture S/Sx • Aching / burning posterior heel • Tenderness tendon • Pain with increased activity • weakness 2/2 pain • Swelling / thickening of tendon • Morning stiffness Tx • Initially = RICE, NSAIDs, analgesics as needed • Heel lift and cross training may limit tensile load • Prevention = heel cord exercises, approp. soft-soled foot-ware, ECCENTRICS, avoid sudden training changes

RTC tear

About • Rotator cuff = supra, infra, subscap., teres minor o All work together for dynamic stability GH joint o Supra = greatest support and mobility; depresses humeral head, ABD o Infra = ER, ext o Subscap = IR, depression o Teres minor = ER • Acute traumatic incident OR Chronic degeneration o Chronic = Pts >50 more susceptible - decrease in elasticity and blood supply o Trauma = FOOSH or strain to shoulder during push/pull activities • Typically supra is involved o More severe = infra, subscap • Classification o Full thickness = all the way through tendon o Partial thickness = only a portion of tendon o Acute o Chronic o Degenerative S/Sx • pain and weakness = most common o pain = C5 dermatome o chronic = more general with certain activities / motions o traumatic = more acute and specific • partial tear = GREATEST pain (tension on remaining structures) • small-partial tear = pretty functional • full tear = maybe arm positioned in IR and ADD; sig functional deficits • shoulder instability / stiffness • GH grinding with mobility • Crepitus • Night pain - esp. when lying on involved side Exam • special tests o drop arm (supra) o empty can (supra) Mgmt • failure to treat may necessitate sig activity modification, surgery, adhesive capsulitis or degenerative changes • PT o PRIMARY FOCUS = prevent adhesive capsulitis, strengthen UE muscles o Restore normal mobilyt, restore strength, scapular stability, postural re-ed, modifications • SX = usually only when conservative methods fails o Types = arthroscopic, kinda arthroscopic, full open o Immobilized in sling ~4-6 weeks o PROM AAROM AROM o Isometrics isotonics functional o Return to function ~9-12 months • PHARM = analgesics, anti-inflammatories, local cortisone injections

angina

About • TRANSIENT sensation pressure or discomfort from MYOCARDIAL ISCHEMIA o O2 demand > O2 supply • Types o Stable = PREDICTIBLE; happens with same amount of activity every time ♣ Responds to: rest or nitroglycerine ♣ Only lasts like 15 min or so usually o Unstable = UNPREDICTIBLE; more intense, lasts longer, happens w/ less exertion, occurs rando at rest, etc ♣ NOT responsive to nitroglycerine • Syndromes o Angina of effort = happens at predictable level of activity o Walk-through angina = gets it when you first start walking but as you cont if goes away o Prinzmetal (variant) = due to CORONARY ARTERY SPASM ♣ Typically associated with CAD o Nocturnal = when you sleep o Postprandial = after you eat since not the gut is taking all your blood Etiology • <3 isn't getting enough blood - usually 2/2 CAD • risk factors = have CAD, fam hx heart disease, smoking, physical in-activity, stress, HTN, high cholesterol, DM, obesity S/Sx • pressure, heaviness, fullness, burning or aching behind sternum • could also be felt in neck, jaw, back, shoulders and arms (usually L side) • difficulty breathing / SOB • nausea or vomiting • sweating • anxiety or fear (angina equivalents) • usually TRIGGERED by exertion, strong emotion; BETTER with rest Imaging / diagnosis • 12 lead EKG - most common; would see T-WAVE INVERSION (may have to do exercise one for some peeps) • diagnosis usually confirmed but finding PATHO CAUSING

chronic venous insufficiency

About • Veins and valves in LE suck and now BLOOD CAN'T GET BACK TO <3 • Leads to LE blood pooling (aka venous HTN) inc fluid interstitial spaces overload lymphatics edema • Accum of protein rich fluid causes local inflammation, hypoxia and fibrotic changes venous stasis ulcer snd poor wound healing Etiology • Weak or damaged valves • Altered pressure gradient from the fluid backup / HTN • Risk factors o Female o Age o Obesity o Pregnancy o Prolonged sitting or standing S/Sx • Leg swelling (edema) • Varicose veins • Aching, heaviness or cramping • Itching or redness skin • Ulcers (medial aspect, more wet) • BETTER with elevation, WORSE with dependency • Untreated = brawny skin discoloration Imaging • Venous US - bidirectional color-flow studies to see flwo patern and structures Tx • Compression stocking • ELEVATION LEGS (dependency makes worse) • Varicose vein stripping - persistent pain or skin ulcers 2/2 poor circulation

trochanteric bursitis

About • acute or cumulative trauma to the lateral hip causing irritation to troch bursa o acute = contusion related to direct impact (falls, impact sports) o chronic = associated with constant friction and tightness of lateral structures (running, etc) • troch bursa = between the greater troch, glute med and ITB Etiology • factors that may contribute o leg length discrepancy (longer leg ??) o lateral hip sx o sports that involves running or contact • WOMEN > men • Can also happen to sedentary peeps too S/Sx • Pain at lateral hip • point tenderness • worse with WBing, direct pressure to area • passive hip ER, ABD - resisted flex and ABD = reproduction • may also have pain-related weakness Imaging • MRI or dx US - may be helpful in differentiating from glute med tendonitis • X-ray = r/o shit per usual Exam • Make sure to r/o similar diagnoses o Sciatic pain, ITB friction syndrome, femoral head AVN Mgmt • PHHARM = anti-inflammatories , anesthetic agents, local injection • SX = uncommon • PT = stretching (ITB, TFL, ERs, quads, hip flexors), STM, modalities, education stretch and activity modifications, gait abnormalities addressed, things necessary to prevent Outcomes • Typically respond well to CONS tx • Full return PLOF when sx reside • Combo injection + PT = GREAT!!!! • Sx recurrence possible - stay on your shit

UCL sprain

About • aka game-keepers thumb, skiers thumb • UCL of thumb = located on medial aspect of MCP thumb; important stabilizer • MOI = excessive valgus at MCP joint thumb • Graded 1-3 S/Sx • Pain, tenderness, bruising over the medial aspect MCP • Instability • Weakness with grasping objects Imaging • X-ray - r/o fx or dislocation • US or MRI - if lig tear is present Exam • Special test o Ulnar collateral ligament instability test = Place the thumb in extension and apply a valgus force through the MCP joint of thumb ♣ (+) excessive valgus movement

myositis ossificans

About • calcification in the muscle belly • MOI = typically, not treating a muscle strain or contusion as you should (not adding ice, adding heat, doing STM too soon) o Disrupt healing and lead to abnormal bone growth • Usually in muscel prone to traumatic injury - quads, HS • Bone begins to grow 2-4 weeks after injury and mature within 3-6 months S/Sx • INITIAL STAGE POST INJURY (just like a normal contusion) o pain functional activities o stiffness and pain after rest o swelling tenderness, bruising • FEW WEEKS LATER o Noticeable hard lump in muscle belly o Increase pain o Decrease ROM Imaging • X-ray - PRIMARY (3 weeks after injury) • MRI and US - help to confirm Exam • Medical and physical exam • r/o other conditions - osteosarcoma, chondroma

osteomyelitis

About • infection with in the BONE • usually 2/2 staph • exposure = DIRECT contamination or SECONDARY o direct = fx, sx, puncture o secondary = came from somewhere else in body • can result in structural damage that results in needing amputation • at risk = pts with shitty immune system, DM, sickle cell, elderly, undergoing hemodyaliysis S/Sx • systemic = fever and chills • local = pain, edema and erythema • sx tend to be generalized or vague - makes definitive dx hard • if 2/2 wound infection - change in exudate, delayed healing - may be seen Imaging • bone biopsy - MOST DEFINITIVE • blood tests, x-ray, MRI, US, CT, bone scan, PET scan - more info but dont make conclusion Exam • make sure to really eval. everything

resp alkalosis

About • pH is abnormally HIGH - alkalemia o since this is resp we know acid (CO2) was too LOW • ACUTE = PaCO2 Low, pH high, HCO3 normal • CHRONIC = PaCO2 low, pH approaching norm, HCO3 (???) compensates Etiology • HYPERVENTILATION - fast removal CO2 hypocapnia H+ levels decrease • PE, hyperthyroidism, sepsis, meds {catacholamines, nicotine), high altitude, internal infleuences (CNS reponse to fear, trauma, pain, anxiety) S/Sx • INITIAL = related to underlying patho • Tachypenia • Tachycardia • Hyperventilation • Dizziness • SEVERE o seqizures o cyanosis (if also hypoxic) Imaging • ABGs - serum CO2 and O2 • Metabolic blood panel - ssereum electrolytes • Urine pH

resp acidosis

About • pH is abnormally LOW - acidemia o since this is resp. we know TOO MUCH ACID caused it • ACUTE = pH is still out of whack and body has not yet attempted to compensate o PaCO2 is HIGH, pH is LOW o Emergent 2/2 buildup of CO2 • CHRONIC = body has compensated by increasing HCO3 from kidneys o pH in normal range (probs still near low), HCO3 value higher as compensation Etiology • HYPOVENTILATION - CO2 not out of body hypercapnia HCO3 levels decrease • Common etiologies = pulm disease, meds that SUPRESS breathing, RLD (severe scoliosis, morbid obesity), conditions that cause resp. muscle weakness (GB, ALS) S/Sx • INITIAL = vague, more closely related to underlying patho. • As progresses o Lethargy o Confusion o AMS o Cyanosis Imaging • ABGs - serum CO2 and O2 • Metabolic blood panel - serum electrolytes • Urine pH

OSTEOCHONDRITIS DISSECANS

About • subchondral bone and articular cartilage SEPARATE from the end of the bone • severe cases - bone may detach and freely float in joint • not sure - but think due to loss of blood flow to the area 2/2 microtruma o causes subchondral bone to die and sep so then articular cartilage prone to more damage • usually KNEE but elbow and ankle happen too S/Sx • VARIES based on degree of detachment • Pain with functional acitivities • Joint popping or locking • Weakness • Swelling • Decreased ROM Imaging • X-ray - confirms • CT or MRI - assist to better visualize the cartilage damage Exam • Thorough med history • r/o similar conditions - arthritis • special test o wilsons test - pt sits with knees over table; bend to 90*, IR the tibia, have pt EXT leg until they feel pain ♣ (+) patient reports pain in the knee about 30° from full extension and ER tibia back to neutral pain disappears

RA

About • systemic autoimmune disorder of the CT • CHRONIC INFLMMATION synovial mebranes, tendon sheaths, ARTCICULAR cartilage • Inflammation synovial membrane formation granulation tissues protein degrading enzymes erosion artivulr cartilage destricution, adhesions, fibrosis of joints Etiology • UNKNOWN but probs. genetic with some viral or bacterial trigger • 80% have POSITIVE RF FACTOR - conflicts with immunuloglobin antibodies in blood • WOMEN 3x MORE LIKELY!! • Usualy 30-50 yo S/Sx • SMALLER PERIPHREAL JOINTS FIRST • Periods of exacerbation and remission • EARLY o Fatigue o B involvement o Tenderness small joints o Low grade fever o Pain with motion o Morning stiffness • LATE o Progression to larger joints o Disease of the heart o Deformities (radial of the wrist, ulnar deviation of the fingers) o Subluxation and contractures • Extrarticualr manifestation o Pericarditis o Anemia o Tearing of tendons o OP o Swan neck and boutineeres deformities o Compression and peripheral neuropathies o Depression o Pleurisy (inflammation lining lung) o Skin changes o Anorexia Imaging • Blood work = RF, ESR, WBC count, Hgb, Hct • Synovial fluid analysis = content synovial fluid in joint • X-rays = joint space and extent of decalcification Exam • Mgmt • Early mgmt is CTITICAL so stop long term progression • PHARM = corticosteroids, NSAIDs, DMARDS • PT o Acute stage ♣ Eduation = regular rest, pain reflif, posisitoning, relaxation positioning, joint protection, splinting, energy conservation ♣ AVOID resistive exercises and deep heating, active stretching o Chronic = improve functional capacity, endurance and strength ♣ NO AGGRESSIVE STRETCHING Outcome • Need PT intermittently • We cannot halt progression buut gve beter QOL and help with function

antihyperlipidemia

Action • 5 classes o STATINS (most common) = inhibit enzyme that makes cholesterol, breaks down LDL, dec triglycerides, inc HDL o Bile acid sequestrants o Nicotinic acid o Cholesterol absorption inhibitors o Fibric acid derivitors Indication • Hyperlipidemia • Atherosclerosis • Prevention coronary event those with CAD, DM, PVD AEs • HA • GI distress • Myaligia • Rash PT imp • Excise with this its gooooood (also helps inc HLD) Ex • -STATINS - Lipitor (atorvastatin), Zocor (simvastatin) • tricor (fenofibrate)

antihistamine

Action • BLOCK histamine effects • Dec nasal congestion, mucosal irritation, symptoms of common cold, sinusitis, conjunctivitis, allergies

anti-arrythmic agents

Action • Class 1 = sodium channel blockers - control cardiac excitement and conduction • Class 2 = beta blockers - limit symp activity by blocking B-adrenergic agents • Class 3 = prolonged repol by inhibiting sodium AND potassium o Considered most effective • Class 4 = calcium channel blockers - depress depol and slow conduction through AV node Indication • Cardiac arrhythmias AEs • ARRYTHMIAS! • Dizziness • Hypotension PT imp • Make sure pts adhere to dosing schedule • Immediately report and AEs Ex • Class 1 = quinidine, lidocaine • Class 2 = Tenormin (atenolol) • Class 3 = cordarone (damiodrone) • Class 4 = Cardizem (diltiazem)

Ca Ch Blockers

Action • DECREASE ENTRY OF CA into muscle cells • Dec contraction, vasodilation, dec MVO2 Indication • HTN • Angina pectoris • Arrhythmias • CHF AEs • Dizziness • HA • Hypotension • Peripheral edema PT imp • MONITOR WITH RPE • Caution rising up 2/2 dizziness / OTH • Observe signs and sx HF! - peripheral edema, weight gain, dyspnea Ex • Norvasc (amlodipine) • Procardia (nifedipine) • Calan (verapamil) • Cardizem (diltiazem)

mucolytic

Action • Dec viscocity of mucous - ALTER COMPOSISTION and consistency so easier to expectorate • Admin by NEBULIZER

bronchodilator

Action • GOAL: STIMULATE SYMP (dilation/relaxation) or INHIBIT PARASYMP (relative dilation) o Symp = inc cAMP - dilation and inhibits mast cells o Parasymp = inc cGMP - constriction and stimulates mast cells (inc constriction and inc cell memb perm) • Anticholinergics = BLOCK Parasymp • Adrenergic / sympathomimetics = STIM SYMP o Non-selective; B2 selective (Short acting, Long acting) • Xanthins = like caffine

diuretics

Action • INC EXCRETION WATER AND SALT • Reduction plasma voume dec BP • Classification o Thiazide o Loop o Potassium sparing Indication • HTN • Edema with CHF • Pulmonary edema • Glaucoma AEs • Dehydration • Hypotension • Electrolyte imbalance • Polyuria • Inc LDLs • Arrhythmias PT imp • Caution rising up 2/2 dizziness / OTH • Monitor for electrolyte balance - weakness, cramping Ex • Thiazide = diuril (chlorothizide) • Loop = Lasix (SUPER POTENT - need to take K+) • Potassium sparing = dyrenium (triamterene)

antiinflammatory

Action • INHIBIT production inflammatory cells, suppress release inflamm mediators, REVERSE cell membrane perm • Prevention inflammatory-mediated bronchoconstriction!! REDUCE AIRWAY EDEMA • Inhaled corticosteroids • Leukotriene modifiers • Mast-cell stabilizers

expectorant agent

Action • Reduce viscosity and increases volume of secretions • Helps to loosen mucous - better cough, cilia work better

ACE-I

Action • Suppress enzyme which converts angiotension 1 angiotension 2 o Angiotension 2 = potent vasoconstrictor and also stimulates aldosterone to keep salt therefore H2O • DEC BP AND AFTERLOAD Indication • HTN • CHF AEs • Hypotension • Dizziness • DRY COUGH • HYPERKALEMIA - super high can inc risk MI/death • HYPONATREMIA (low Na) - confusion, weakness, weakness, loss energy PT imp • Caution rising up 2/2 dizziness / OTH • Don't inc exercise too much for those with HF Ex • ALL THE -PRILS!

non opiod agents

Action • Promote a reduction of prostaglandin - dec. inflammatory process, dec. uterine contractions, lowers fever, minimizes impulse formation pain fibers Indications • Mild to moderate pain various origins • Fever • HA • Muscle ache • Inflammation (NOT acetomethaphine) • Primary dysmenorrhea • Reduce risk MI (ASA only) AEs • Nausea • Vomiting • Abdominal pain • GI distress or bleeding • Ulcer formation • Potential Reye syndrome in children (ASA only) PT imp • Inc. risk for masked pain allow more movement than they actually have • STOMCH PAIN c/o should be taken seriously, refer PCP ulcers, GI distress Ex. • Tylenol (acetometaphine) • Non-steroidal inflammatories (NSAIDs) • ASA (acetylsalicylic acid) • Aleve (naproxen) • Advil (ibuprofen) • Celebrex (celecoxib)

salter harris fx classification

I: entire epiphysis: shearing, torsion, avulsion- relocated and immobilized II: entire epiphysis and portion metaphysics: most common- shear or avulsion with ANGULAR force. relocated and immobilized III: portion of epiphysis: growth plate partially FUSED. relocated and immobilized ~ ORIF IV: portion of epiphysis and portion metaphysics: similar III. ORIF. V: COMPRESSION. compression/crush injury. found after the fact no immediate intervention- NWB if acute.

hypoxemia

Mild 60-80 mmHg Moderate 40-60 mmHg Severe <40 mmHg

CDT

Occurs in 2 diff phases • Phase I = intensive acute treatment; outpatient o Certified lymp specialist - 4-6 weeks • Phase II = self-management • Note: may need to return to phase I whenever there is a resurgence of S+S Manual lymphatic drainage (MLD) = move lymh around bloakcages and to areas it can be drained • Start prox and work distally • Stroke should always be towards working lymph nodes Compression therapy = maintains reduction from MLD • Improves reabsorption ability capillaries, reduces filtration of fluids into interstitium, softens fibrotic tissues • Phase I = short-stretch bandages low resting pressure so no constriction • Phase II = combo compression garments (day) and bandages (night) o Garments only fitted once size plateaued • higher pressures distally Exercise • Inc vessel contractions, ind fluid uptake, mucles pump, inc deep breathing (imp thoracic duct flow) • Must be carefully monitored • Low impact, aerobic activities • Trunk prox extremity distal extermities trunk again deep breathing • Can use compression garments/bandages while exercising Skin care = PREVENTION • Insepected, cleansed thoroughly, apply lotion, low or neutral pH Contraindications to CDT = Acute infection, cardiac

quadrant pain

RUQ • Hepatomegaly • Duodenal ulcer • Cholecystisis • Pneumonia • Hepatitis • Biliary stones LUQ • Gastric ulcer • Perforated colon • Pneumonia • Spleen injury • Spleen rupture (+ Kerhs sign) • Aortic aneurysm RLQ • Kidney stone • Urethral stone • Meckel diverticulum • Appendicitis (+ McBurney point) • Cholycycstitis • Intestinal obstruction LLQ • Perforate colon • Ileitis • Sigmoid diverticulitis • Kidney stone • Urethral stone • Intestinal obstruction

obstructed airway response

Recognition • Ask if they are choking o if speak, cough, breathe = NO INTERVENTION but stay close o if cannot = INTERVENE Response • check mouth, get out anything in there • go behind pt, hands clasped, between belly button and diaphragm • give foreful, inward and upward thrusts UNTIL object out • if LOC = place in supine, perform rescue breathing thrusts • CHILD <1 yo o Recumbent prone over therapist arm, head supported o 4 forceful blows interscapular region with heel of hand o Turn over, 4 thrusts to lower sternum with 2 fingers o Repeat until expulsion

shock response

Recognition • Caused by LOSS OF PERFUSION to organs • Often 2/2 excessive bleeding, excessive heat, mvmt supine to vertical • s/sx o pale, moist, cool skin o diaphoresis o shallow and irreg. breathing o weak and rapid pulse o HYPO-tension o Low body temp o Weakness o Dizziness o n/v o dilated pupils o anxiety o AMS o Syncope Response • Remove source shock, monitor BP, HR, RR • Cardiopulm resuscitation is necessary • SUPINE with LEGS ELEVATED • Cold compress to forehead or blanket • Avoid exertion until sx gone

burn response

Recognition • Causes = heat, chemical, electricity • Therapist should ID o Source o Location o Extent • Classified according to depth and rule of 9s Response • Attempt to remove source if possible • If CHEMICAL = use WATER to dilute o CAREFUL not to wash into unaffected area o If from dry powder, brush off skin • THERMAL = run under COOL water for several min o BUT if LARGE = do NOT use cold water - could cause hypothermia • ELECTRICAL = asses HR and RR; monitor signs of cardiac arrest • Removes all clothing but NOT if attached to burn area • Place clean towel or dressing over wound to prevent infection • Call EMS if extensive OR involves face, hands, perineum, feet, resp system

allergic reaction

Recognition • Mild - moderate = not usually life threatening o Itchy skin, redness, rash, hives o Areas of swelling o Itchy and watery eyes, runny nose, sneezing o HA • SEVERE o Swelling face or mouth o Diff swallowing / speaking o Chest tightness and pressure o Tachycardia o Abdominal pain o N/V o AMS o Dizziness / syncope • Common allergens = pollen, dust, eggs, shellfish, milk, wheat, soy, nuts, insect stings, chemicals, latex, meds Response • Severe = LIFE THRETENING • Try to remove source • Check airway • Begin cardiopulm resuscitation if necessary • If use emergency med - assist in injection / ingestion o NOT orally if trouble breathing • Call EMS IS HAVING ISSUES DIFF OR SWALLOWING

concussion response

Recognition • Mild TBI 2/2 to blow to the head • s/sx - can be immediate or delayed o memory loss, confusion o drowsiness o behavior or personality changes o light or noise sensitivity o HA o Impaired vision o n/v o lack coordination o dizziness o LOC Response • Do NOT allow back to physical activity until CLEARED by medical professional • EMS contacted IMMEDIATELY if demos: o Extreme drowsiness o LOC o HA that will not improve o One pupil larger than other o Slurred speech o Weakness / numbness / loss coordination o Repeated n/v o Convulsions or seizures o Inc. confusion o Restlessness / agitation

stroke response

Recognition • s/sx o dropping or numbness one side face o numbness or weakness 1 arm o slurred speech o altered vision o HA o Dizziness o Lack coordination o Confusion o LOC Response • CALL EMS immediately • Note time to Sx started meds • If go away after few min = still seek tx, they probs had a TIA (still serious)

P ulcer staging

Stage 1 • INTACT, UNBALANCABLE ERYTHEMA (redness does not go away with pressure) • Inc. warmth or coolness • altered coloration Stage 2 • PARTIAL THICKNESS - full epidermis and SOME dermis • Red or pink wound bed • Abrasion, BLISTER, shallow crater • NO slough or bruising Stage 3 • FULL THICCNESS loss of epidermis, dermis NOT FASCIA • Can't see bone and tendon • DEEP CRATER, lack of epithelization wound edges • May have necrosis, undermining/tunneling, SLOUGH Stage 4 • FULL THICKNESS of epidermis, dermis, fascia • Can see muscle/tendon/bone etc. • Slough, ESCHAR, undermining/tunneling • Inc. risk OSETOMYELITIS Unstageable • Full thickness tissue loss which is COVERED by slough or eschar • Cannot determine depth until all the shit is out of the way o NEVER REMOVE ESCHAR ON THE HEELS!!! This is the body's natural, biological cover o You CANNOT reverse-stage- it's a HEALED stage 3 pressure ulcer

cataracts vs glaucoma

a. Cataracts= clouding of lens= gradual loss of vision. Central lost first then peripheral. i. Glaucoma is reversed!

1. Pt rehabbing from bone marrow transplant referred to PT for instruction in exercise program. Plans to use O2 sat to gain additional objective data related to pt's tolerance. Assuming O2 sat 95% at rest. What would be MOST appropriate.

a. Discontinue with O2 sat is below 90% (PO2 of 60=hypoxemia)

reviews results of PFT for 58 y/o male admitted to hospital. TLC is increased when compared to established standards. What would produce this type of result?

a. Emphysema: lunges become hyper-inflated due to loss of elastic recoil, obstruction to airflow seen as increase in TLC, RV, and FRC.

PT treats pt. with end stage renal dx for general deconditioning. Which other Sx would this pt MOST likely demonstrate?

a. Increased urine output and anemia: kidneys have dec. ability to filter fluids. Also role in production of erythropoietin, so ESRD display signs of anemia.

1. indep community ambulation realistic functional goal for ASIA A for what level SCI?

a. Lower lumbar L4-5: exhibit adequate ROM, strength of residual mm, CV endurance. Bil AFO and canes.

insidious onset LBP. Dysfunction of lumbar facet test?

a. Lumbar quadrant test: places lumbar facet in maximally closed and most provocative position

A PT works with a pt. who has been instructed to take NSAID to help control arthritis. Therapist educates that overuse of NSAIDs can result in GI damage. Side effect caused by inhibition of which hormone?

a. Prostaglandins: hormones that protect stomach lining by inhibiting gastric acid secretion and increasing production of mucous.

Pt decides to exercise a pt with LE lymphedema using aquatic therapy. Hydrostatic pressure by water can be expected to do which of the following?

a. Reduce effusion and assist venous return: pressure exerted on immersed object is equal on all surfaces. As depth increases so does hydrostatic pressure. Increased pressure limits effusion and assists VR and can induce bradycardia. i. Buoyancy: relative weightlessness and assists in joint unloading and active movement. ii. Hydromechanics of water: increase R of water as speed increases iii. How water >35 deg C can increase CV demands at rest and with exercise

1. : PT reads medical record that pt. suspected CVD had positive graded exercise test. What data most influential when concluding a positive test?

a. ST segment changes: ischemia of the ventricles >1 mm downslope= positive

2 mo. Hx worsening shoulder pain and stiffness without known injury to shoulder. Unable to move shoulder while perofrming ADLs= adhesive capsulitis. What is best choice of PT intervention?

a. STRETCHING exercises= moderate evidence to support based on CPG. b. Weak= modalities and joint mobilizations

A pt has developed a thick eschar 2/2 full thickness burn, what antibacterial agent MOST effective?

a. Sulfamylon: penetrates thru eschar and provides antibacterial control i. Silver nitrate and nitrofurazone= superficial agents that attack surface organisms. ii. Panafil is keratloytic enzyme used for selective debridement

hyperthyroidism- what to monitor with exercise

a. Tachycardia and dyspnea- hypermetabolic state associated with exercise intolerance and impaired cardiopulmonary function. Sx include dyspnea, fatigue, tachycardia, arrhythmia. Can aggravate preexisting HD.

Pt works with pt status post L CVA with R hemiplegia. Most difficult position

a. ½ knee with involved leg posterior- bc responsible for increased BW

Anterior cerebral artery (ACA)

ant frontal lobe, med frontal and parietal lobes • contra LE motor and sensation, (LE>UE) • bowel and bladder • behavioral inhibition • neglect • aphasia (can't speak) • apraxia (can't control mvmt) • agraphia (can't write) • perseveration (repeating things)

NMES

facilitate skel mm activity ♣ Electrodes • Over the muscel and in parallel • Ideally 1 electrode over motor point strongest contraction with least current • Sep by min 2 in ♣ AMPLITUDE = dep on desired strength of contraction; TRY to set to 40-60% MVC • General muscle strength = forceful contraction • Recovering from recent sx = maybe a little less ♣ PULSE DURATION = >200 microsecs (already set with Russian) • Needs to be high enough to overcome rel low capacitance motor nerve fibers AND to get to the depth of fibers • Shorter = more comfortable for smaller muscles o Note: as pulse duration is shortened, need HIGHER amp to produce same strength contraction • Longer = better for larger muscles ♣ FREQUENCY = 30-50 bps • Sufficient to produce a tetanic contraction • Higher freq = more rapid contraction (aka fatigue) NOT stronger contraction ♣ DUTY CYCLE = on time: 6-10 secs / off-time 5x longer -- 10/50 (10 on/50 off) • Make sure to tell the pt to CONTRACT WITH the on times • May want to dec length off times based on pt progress • Need off-time to promote relaxation and limit fatigue ♣ RAMP TIME = ramp of 1-4 for on time 6-10 - 2 sec • Makes onset of stim more comfortable ♣ TREATMENT TIME = want to do 10-20 contractions - 10-20 mins • Want to do MIN 3x/week

descending tracts extrapyramidal

gross, automatic mvmts; do NOT pass through pyrimids and have many interconnections ♣ Damage = paralysis, hypertonicity, exaggerated DTRs, clasp-knife reaction ♣ Reticulospinal = +/- of voluntary and reflex activity via alpha and gamma motor neurons • Regulator mvmt ♣ Tectospinal = CL postural tone associated w/ visiual/auditory stimuli • turn head toward stem ♣ Vestibulospinal = ipsi postural adjustments to head movement, - flexor tone and FACILITATES EXT • arm out when you fall ♣ Rubrospinal = postural tone, FACILITATES FLEXORS and - extensor tone

likelihood ratios

o (+) likelihood ratio = How much more likely a (+) test is to be found in people w/the condition than in people w/out it ♣ If test has high (+) likelihood ratio shifts towards diagnosis ♣ A likelihood ratio of > 1 indicates the test result is associated with the disease.(shifts towards diagnosis) • High like >10 = good; could really shift you • Close to 1 = not good o (-) likelihood ratio = How much more likely a (-) test is to be found in people w/out the condition than in people w/it ♣ Considered the most useful statistic when reporting the diagnostic accuracy of clinical tests ♣ A likelihood ratio <1 indicates that the result is associated with absence of the disease. • Tests where the likelihood ratios lie close to 1 have little practical significance as the post-test probability (odds) is little different from the pre-test probability.

pituitary gland

o (aka master gland) = controls other glands, affected by seasons and emotions, Secretes endorphins (reduce pain), controls ovulation ♣ Anterior = adenohypophysis produces and secretes hormones • Growth hormone (GH) growth and protein synthesis • Follicle-stim hormone (FSH) estrogen and spermatogenesis • Luteinizing hormones (LH) ovulation, making estrogen and testosterone • Thyroid-stim hormone (TSH) making more T3 and T4 (thyroid hormones) • Adrenocorticotrophic (ATCH) making more cortisol (adrenal steroids) • Prolactin lactation ♣ Posterior = neurohypophysis really just stores and then secrete hormones as hypothalamus tells it to • Oxytocin uterus contractions, mild release • anti-diuretic reduces urine output, inc. BP (vasoconstriction) ♣ All regulated by hypothalamus except prolactin (stim cervix and nipples) and ADH (dec water)

ABI

o >1.3 RIGID arteries - need US test to check for PAD o 1.0-1.3 NORMAL - no blockage o 0.8-0.99 MILD blockage - beginning PAD o 0.4-0.79 MOD blockage - may be associated with intermittent claudication WITH EXERCISE o <0.4 SEVERE blockage - suggests severe PAD and may have claudication pain AT REST

acute wound dx

o Abrasion = scaping skin superficial layers; MOI is friction + shear o Avulsion (degloving) = tension makes skin come off underlying surfaces; serious o Incisional wound = sharp object causes; most often assocated w/ surgery o Laceration = wound or irregaulr tear; associated with trauma ♣ MOI = shear, tension, high force compression o Penetrating = wound which enters interior of organ or cavity o Puncture = sharp object penetrates skin and underlying tissues; relatively little damage; risk for contam/infection o Skin tear = force/trauma causes fragile skin to tear

adrenal dysfunction

o Addison's dx = HYPO-function adrenal cortex ♣ Dec. production cortisol (food met) + aldosterone (Na in blood, K out) ♣ S+S = metabolic dysfunction, fluid and electrolyte imbalances, hypotension, weakness, anorexia, weight-loss, altered pigmentation • Untreated = shock and maybe death ♣ Tx = synthetic hormone replacement o Cushings = HYPERfunction adrenal gland ♣ Excessive cortisol production 2/2 excessive ACTH production pituitary gland OR take a lot of corticosteroids ♣ S+S (over years) = moon face, buffalo hump, truncal obesity, purple abdominal striae, hyperglycemia, growth failure, acne, small dick, depression, poor conc, memory loss ♣ Tx = pharm blocking production, radiation, chemo, sx o Rehab considerations ♣ Signs of stress / exhaustion don't exacerbate condition ♣ Call MD if signs inc. ICP meds may need to be altered ♣ OTH common with long-term cortisol therapy ♣ Report sleep disturbances to MD ♣ Inc. incidence OP, bone fxs, degenerative myopathy, tendon ruptures, ataxic gait ♣ Delayed wounds healing (cortisol dec. inflammation)

high f airway oscillation

o Aka acapella and flutter which combine positive exp pressure and high freq airway vibrations to mobilize secretions o Procedure ♣ Put device in mouth ♣ Inhale ~75% ♣ Hold breath 2-3 secs ♣ Exhale 3-4 secs ♣ Do 10-20 breaths ♣ Remoe device and COUGH / HUFF 3x (raises secretions) o Precautions / contra ♣ Increased WOB tolerance (COPD, acute asthma) ♣ Elevated ICP ♣ Hymodynamic instability ♣ Recent facial, oral, skull sx or trauma ♣ Acute sinusitis ♣ Nosebleed ♣ Esophageal sx ♣ Active hemoptysis ♣ Nausea ♣ Middle ear patho / tymp membrane rupture ♣ Untreated pneumothorax

skin graft terms

o Allograft (hemograft) = temp skin from another human o Autograft = permanent graft from donor site on own body o Heterograft (xenograft) = temp skin graft from another species o Full-thickness graft = dermis + epidermis o Split-thickness graft = ONLY epidermis + superficial layer dermis o Sheet graft = skin graft transferred directly from unburned donor site to prepped recipient site o Mesh graft = skin graft altered to create mesh-like pattern so larger area o Donor site = site where HEALHTY skin taken; used as graft o Recipient site = site burned and requires graft o Eschartomy = sx; opens or removes eschar to reduce pressure surrounding, interstitial edema; enhance circ o Z-plasty = sx; eliminates scar contracture

reliability

o Alternate forms (parallel) reliability = assesses consistency / agreement of measurements obtained with diff forms of tests ♣ Allows tests to be interchangeable (equivalent measures) ♣ Ex: NPTE is given several times through year and they are all similar difficulties o Internal consistency = extent to which all the items on a thing actually measure what they are supposed to measure ♣ Ex: functional assessment scale includes only items that relate to person's function o Intra-rater reliability = ONE PERSON getting similar results over time o Inter-rater reliability = SEVERAL PEEPS getting similar measurements (agreement of diff peeps) o Test-retest reliability = consistency measurements made on ONE PERSON - OVER TIME - SEP occasions ♣ Affected by: time btw, fatigue or learning, changes in characteristic being measured

THA approaches

o Anterolateral = access through TFL and glute med ♣ Some of hip ABDs released ♣ Hip dislocated ANT ♣ No hip flex >90, no ext, no ADD, no ER o Direct lateral = splits TFL and vastus lateralis ♣ Release ANT glute med but keeps POST part ♣ MINIMIZES dislocation risk non-compliant pts ♣ No hip flex >90, no ext., no ER, no ADD o Posterolateral = split glute max ♣ Release short ERs and hip ABD goes ant (preservation ABDs) ♣ Dislocate POST ♣ MOST COMMON ♣ HIGHEST dislocation risk - youre messing with posterior capsule ♣ No hip flex >90, ADD, IR

typical etiologies of nerve entrapment

o Axillary = humeral neck fx, ant shld dislocation o Musculocutaneous = clavicle fx o Radial = humeral fx, compression in radial tunnel o Median = pronator teres entrapment, carpal tunnel o Ulnar = compression arcade of struthers (prox to elbow), cubital tunnel (@ elbow), Guyon's canal o Femoral = THA, displaced acetabular fx, ant dislocation femur, hysterectomy, appendectomy o Sciatic = trauma to butt, THA, accidental injection to nerve o Obturator = THA, fixation of femur fx o Peroneal = femur, tibia, or fibula fx, positioning during sx o Tibial = tarsal tunnel entrapment, popliteal fossa compression o Sural = fx of calcaneus or lat malleolus

phase 1 cardiac rehab

o Begins with physician referral when MED STABLE ♣ No new or recurrent chest pain in 8 hours ♣ No new signs uncomp HF - dyspnea at rest, B basilar crackles ♣ No new, significant, abnoram heart rhthym or ECH changes 8 hours ♣ Stable Ck and troponin levels o Pt education, self-care eval, cont monitoring VS, frou discussions, LOW LEVEL exercsies o Trend = 2-5 days long • MODE = progressive supervised o Level walking = 2-3 mets o Up and down steps or treadmill = 3-4 METS • INTENSITY = RPE <13 o Post MI = HR < 120 OR <20 beats above resting o Post sx = <30 beats above resting • DURATION o Intemittant: 3-5 mins o Progress to 10-15 mins cont • FREQUENCY o Days 1-3 = 3-4x o Days 4+ = 2xday inc duration • PRORGESSION o Adequate inc HR o Adequate rise SBP (10-40 mmHg) o No new arrhythmias or ST change ECG o No cardiac sx o Expected outcomes ♣ Prevent bed rest issues ♣ Walk 5-10 min cont, 1000 ft, 4x daily ♣ Walk up and down 1 flight stairs INDEP (5 METS!!!) ♣ Know safe HR and RPE limits ♣ Recog abnoraml sigsn and symptoms ♣ Promate return to ADLs ♣ Prep pt home support

properties of water

o Buoyancy = UPWARD force on body when immersed EQUAL to amount of water displaced ♣ Think: anti-gravity o Resistance to movement = INCREASES in prop to speed o Specific gravity of 1 = peeps tend to float since peeps are <1 o Specific heat = ability of a fluid to store heat ♣ Water is 1 while air is .001 sooooo water retains heat 1,000x better than air o Total drag force = force exerted on person's body which normally OPPOSES direction of body' motion ♣ Comprised of profile drag, wave drag, surface drag o Viscosity = thickness essentially ♣ Great viscocity = greater force required to create mvmt of fluid

standard precautions

o Care of all pts REGARDLESS of infection or diagnosis o Combine universal and body substance isolation precautions o Apply to all blood and bodily fluids, secretions, excretions o HAND WASHING = plain soap for routine, antimicrobial for specific stated in policy o GLOVES = wear them; change them when you come into contact; wash hands in between change o MASK = wear during activities where splash risk o GOWN = wear when splash risk o PT CARE EQUIPTMENT = make sure you don't transfer germs; make sure sanitized before re-use OCC HEALTH AND BLOODBORNE PATHO = don't recap sharp objects and make sure in sharps

central and peripheral vertigo

o Central = injury or disease to BRAIN -neuro sx present (diplopia, hemianopsia, weakness, numbness, ataxia, dysarthria) -Ex: meningitis, migraines, trauma/tumor, cerebellar degeneration (alcohol), MS o Peripheral = injury/issues to inner ear -episodic and short duration, sweating, N+V, tinnitus, ear fullness CAUSED by something -Ex: BPPV, Meniere's, infection, tumor/trauma, metabolic disorders (DM), acute alcohol intoxication

non prob sampling

o Convenience sampling = readily available to researcher o Purposive sampling = subjects deliberately selected based on criteria o Quota sampling = pop dividied into subgroups - chose the one theyre interested in, then NON RANDOLY select select subjects (convenience) o Snowball sampling = current subjects recruit new subjects ♣ Used when characteristic is rare - diff and costly to ID peeps with

dermis

o Dermis = vascularized, lymph system present, high water content, provides nutritional support to epi, houses growth factors, thermoregulation, immune cells, sensory assist ♣ Layers • Papillary - healing/immune elements • Reticular - functional stuff (collagen, vasculature, nerve endings, glands) ♣ Cells • WBC • Fibroblasts - make collaged, elastin • Mast cells - histamine mediated inflammation • Macrophages

gangrene

o Dry ♣ Loss of vascular supply leading to local tissue death ♣ Etiology = blood vessel disease (DM, athersclerosis) ♣ S+S = not painful, dark brown or black nonviable mass of tissue ♣ Tx (serious med condition) = meds, sx, hyperbaric O2 o Wet ♣ Has associated bacterial infection ♣ Etiology = post burn, frostbite, or severe injury that gets infected and stops blood flow ♣ S+S = swelling, change in color from red to brown/black, blisters w/pus, fever, general malaise ♣ Tx (serious med condition) = meds, sx, hyperbaric O2

t test

o ESTIMATING or COMPARING 2 pop mean when pop norm dist AND pop variance UNKNOWN

Lobes Cx

o Frontal = intellect, orientation, voluntary movement (PMA and precentral gyrus), Broca's area (L side -- speech/expression), executive functions, personality, judgement, reasoning -Imp = CL weakness, apraxia (cant perform mvmts w/ goal in mind), perseveration, loss executive functions, apathy, inhibited o Parietal = touch, kinesthesia, vibration, language comprehension, provides meaning and perception ♣ Imp = abnormal mvmt patterns or lack of mvmt planning, somatosensory deficits Temporal = auditory processing, Wernicke's area (L side -- receptive), speech, seems to me like does a lot of interpretation (emotional and visual -- recognizing/categorizing things), memory ♣ Imp = affects short and long term mem - do more demos; remembering steps will be har o Occipital = visual processing, judgement of distance, 3D vision ♣ Imp = RECEPTION (not perception) of visual stuff so don't use diagrams and shit and you may have to modify the environment

HKAFO

o Hip-knee-ankle-foot orthosis (HKAFO) ♣ Indications: hip, foot, knee, ankle weakness ♣ B KAFOs with extension to hip joint and pelvic band ♣ Controls rot, ABD, ADD at hip ♣ Heavy and restricts pts to swing-to or swing through gait pattern (3-pt gait pattern) • shift lift kick step • Pts must keep hip extended - rest on iliofemoral ligaments

coccydynia

o Hypermobility of joint btwn coccyx and sacrum after childbirth ♣ Etiology = childbirth ♣ S+S = difficulty sitting, LBP, SIJ pain, pain with bowel mvmts, dyspareuinia, hemorrhoids ♣ Tx = heat, joint mobs, MFR, METs, core strength, cushions

scar management

o Hypertrophic scarring = imbalance btw collagen synthesis and lysis ♣ Common with severe burns ♣ Complications = contracture, adhesions, hypersensitivity, functional limitation, poor cosmesis o Assessment = tonometer, rating scale, location, sensation texture, pigmentation, vascularity, pliability, height o Friction massage = loosen adhesions, dec. sensitivity improved pliability ♣ CAUTION: not too soon or too much o Compression garments = sustained compression for balance synthesis and lysis ♣ 15-35 mmHg, 22-23 hrs/day ♣ recommended for burns requiring >14 days to heal begin btw 2 weeks and 2 months

thyroid dysfunction

o Hypo-thyroisisim = dec. thyroid hormone in blood ♣ Slows metabolism ♣ Etiology = Hashimoto's thyroiditis, underdeveloped thyroid gland ♣ S+S (everything dec.) = fatigue, PROX. weakness, dec. HR, weight gain, constipation, delayed puberty, slowed growth/development, cold intolerance ♣ Tx = oral replacement therapy o Hyper-thyroidism = inc. thyroid hormones in blood ♣ Speed up metabolism ♣ Etiology = GRAVES DISEASE (most specific cause) • Common women >20 but can happen to anyone • Autoimmune dx - antibodies stim thyroid and make overactive ♣ S+S (everything inc.) = inc. nervousness, excessive sweating, weight-loss, inc. BP, exophalmos, myopathy, chronic periarthris, enlarge gland (goiter), palpitations, tremor, heat intolerance ♣ Tx = pharm, radio-active iodine, Sx o Postpartum thyroiditis = Painless inflammation of thyroid after childbirth ♣ Phase 1 (mo. 1-4) = get hyperthyroidism (anxious, irritable, heat sensitive) ♣ Phase 2 (4-8 mo.) = hypothyroidism (dry skin, cold sensitivity, depression) • Easier to catch in this phase

parathyroid dysfunction

o Hypopara = decreased secretion or low level parathormone ♣ Not enough Ca in blood (stays in bones), too much phosphate in blood ♣ S+S = hypocalcemia, neurological Sx (seizures, cog defects, short, tetany muscle pain, cramps), compromised breathing, cardiac arrhythmias potential HF, INC NM ♣ Tx = IV Ca for rapid elevation (acute), pharm mgmt and diet modification (chronic) o Hyperpara = inc production ♣ Disruption Ca, Ph, bone metabolisim (Ca out of bones and into blood) ♣ S+S = renal stones, kidney damage, depression, memory loss, muscle wasting, bone deformity (brittle), myopathy, arthiris, gout, DEC NM excitability ♣ Tx = diuretics or absorption meds to dec Ca dast (acute), sx to remove, pharm (chronic)

hypo/hyper pituitary

o Hypopituitarisim = dec. or absent hormone secretion from anterior gland; RARE ♣ S+S (vary) = short (dwarf), delayed growth/puberty, sex/reproductive disorders, DM ♣ Tx = replace the hormone affects, OTH o Hyperpituitarisim = excessive secretions one or more homrones ♣ S+S (vary) = gigantisim/acromegaly, hair growth, abnormal lactation, amenorrhea, infertility, impotence, CPS, osteophyte formation ♣ Tx = tumor resection, sx, radiation, hormone suppression/replacement o Rehab considerations ♣ Abulate/exercise w.in 24 hrs of sx ♣ Inc awareness hypoglycemia ♣ w/ HYPOpit OTH, B HHA

mm active by phase

o IC ♣ Ankle DF (pre-tibs) = place ankle in DF and act to slowly lower to ground (eccentric) ♣ Quads = ext knee ♣ HS = stabilize the knee (prevent hyperextension) and also stabilize the pelvis ♣ Hip EXT and ABDs = stabilize trunk and pelvis over leg o LR ♣ Ankle DF = ECC lowering of foot ♣ Quads = ECC control knee flexion • Later on become CONC to to draw femur fwd over tibia ♣ PF + post tib = turn on LATER to ECC control tibia rolling over foot and pronation ♣ Hip ext = CONC to produce hip extension o MS ♣ PF = ECC to control DF ♣ KNEE MUSCLE ACTIVITY IS MIN ♣ Quads = CONC for CKC ext (TKE) ♣ Hip ABD = stabilize pelvis, prevent CL hip drop ♣ Iliopsoas = ECC control hip extension o TS ♣ PF = CONC for propulsion ♣ KNEE MUSCLE LIMITED ♣ Hip ABD = stabilize pelvis ♣ Iliopsoas = ECC slow hip ext o PSw = ALL ABOUT TOE OFF!!! And CONC contraction to bring that leg fwd!! ♣ PF = PEAK!! For toe off ♣ HS = CONC for knee flexion in swing phase (momentum of body also helps) ♣ Hip flexors (iliopsoas, RF, sartorius, ADD long) = CONC hip flexion o ISw = all about foot clearance ♣ DF = CONC to clear foot ♣ HS = CONC flex the knee for clearance ♣ Hip flexors = CONC to advance hip fwd o MSw ♣ DF = CONC for foot clearance ♣ KNEE AND HIP ACT min since fwd momentum helps the limb o TSw = all about prep for IC ♣ DF = CONC for foot clearance ♣ Ankle INVERTERS (tib ant, post tib) = CONC in prep for IC ♣ Quads = CONC to ext knee ♣ HS = ECC to slow rate of knee extension ♣ Hip EXT = ECC slow rate of hip flexion and prep for IC

wound healing phases

o Inflammatory phase (1-10 days) ♣ Platelets come and start clotting Temp repair re-est. homeostasis ♣ Mast cells, neutrophils, leukocytes cleans wound bed ♣ Re-epithemilzation tissue rest and permanent processes AFTER wound bed clean • Begins ~24 hrs after injury BUT cant see until like 3 days later o Proliferative phase (3-21 days) ♣ Signaled by new tissue formation ♣ Capillary beds and granulation tissues fill wound bed ♣ Keritinocytes, endothelial cells and fibroblasts collagen matrix ♣ SKIN INTEG RESTORED - WOUND CLOSURE THROUGH EPITHELIZATION, WOUND CONTARCTION o Maturation / remodeling phase (7 days-2 years) ♣ Starts when granulation tissue and epithelial diff begin to appear in wound bed ♣ Fiber reorg and contraction shrink and thin scar ♣ Collagen lysis and synthesis scar tissue remodeling and strengthened ♣ New tissue initially only has ~15% original strength - progresses to ~80% ♣ Hypertrophic scarring = BAD for this phase; makes it take longer Eg burns - without heals ~4-8 weeks; with ~2 years

measures of distribution

o Kurtosis = "peakedness" of a distribution ♣ High kurtosis = sharp peak, long fat tails ♣ Low jurtosis = round peak, shot thin tails o Normal = bell shaped curve ♣ Most data clustered around mean ♣ Mean, median and mode are all same • 68% fall w/in 1 STD above and below mean • 95% fall w/in 2 STD of mean • 99% fall w/in 3 STD of mean

droplet precautions

o LARGE particles; DROP AFTER 3 FT; transmitted through MUCOUS MEMBRANES (cough, sneeze, talking, suctioning) ♣ Private room UNLESS staying with other person that has same ♣ Maintain 3 ft between OR be wearing a mask ♣ Room door can be OPEN ♣ Limit transport outside room ♣ Bacterial: haemophilis influenza, Neisseria meningitides (meningitis, neumonia, sepsis), diphtheria, mycoplasma pneumonia, pertussis, step A ♣ Viral: adenovirus, influenza, mumps, parvovirus B19, rubella

classification: neuropraxia, axonotmesis, neurotmesis

o Neurapraxia = mildest form of injury - CONDUCTION BLOCK 2/2/ MYELIN DYSFUNCTION --Everything is intact nerve conduction prox and distal still works --s/s = pain, min atrophy, numbness or more, diminished proprioception --recovery = rapid and complete (4-6 weeks) o Axonotmesis = med severe injury - REVERSIBLE DAMAGE to nerve fibers -Damage to axons but everything around is fine (anatomically still intact) -potential for spontaneous recovery regrow @ 1mm/day o Neurotmesis = most severe damage - IRREVERSIBLE DAMAGE --Everything f'd axon, myelin, CT --s/sx = flaccid paralysis, wasting, loss of motor/sensory --no spontaneous recovery, sx may allow for some recovery (sensory before motor)

scales of measurement

o Nominal (classification scale) = values of variable are mutually exclusive and exhaustive aka you can only be assigned to 1 category ♣ QUALITATIVE not quant ♣ Ex: blood type, type of breath sound, type of arthritis o Ordinal (ranking scale) = data is ranked based on property of variable; intervals btw may not be equal or known ♣ Ex: MMT, assistance levels, pain, joitn laxity o Interval = intervals btw adjacent variable points are equal, but there IS NOT A 0 ♣ Ex: temp, some developmental and functional tests o Ratio = intervals btw adjacent points are equal, and THERE IS A TRUE 0 ♣ Ex: ROM, distance walked, time to complete activity, nerve conduction velocity

predictive values

o Not the most useful statistic, some aren't even using it anymore o Predictive values are significantly affected by the prevalence of the disease in the pts being examined ♣ For predictive values to apply: prevalence of disorder in clinical population HAS to be identical to the prevalence in the study population ♣ If you are working in pop with SAME pop as what in study, good to use that data o Negative predictive value = proportion of ALL pts with (-) test results who are actually (-) o Positive predictive value = proportion of ALL pts with (+) test results who are actually (+)

PFT interpretation

o OBSTRUCTIVE VENT IMPAIRMENT --DEC exp flows --Airways narrowing during exhalation causes RED max air flows vs max volume displaced from lungs --FEV1/FVC < 70% !!!! --Further classified • >100% possible normal variant • 70-100% mild obstruction • 60-70% mod obstruction • 50-60% mod-severe obstruction • <50% severe obstruction --pathologies: asthma, emphysema, chronic bronchitis o RESTRICTIVE VENT IMPAIRMENT --RED lung volumes (TLC, FVC, FEV1) and relatively normal exp flow rates - CANT GET AIR IN! --Inferred from spirometry when FVC is reduced and FEV1/FVC = >80% or normal! Pathologies: interstitial lung disease, pleural diseases, chest wall deformities, obesity, pregnancy, NM disease, tumor

model to develop clinical question

o P - pt or problem ♣ What is the target pt population or the problem of interest o I - intervention ♣ What intervention or form of therapy needs to be evaluated ♣ Could also refer to diagnosis / prognosis o C - comparison ♣ What comparision or control tx are being compared to primary intervention o O - outcome ♣ Whatc hanges would suggest that intervention effective, prognostic factor is important or diagnostic test is accurate

central vs. peripheral nystagmus

o Peripheral = 2/2 peripheral lesion ♣ Unidirectional eye mvmt - fast segment is OPP lesion ♣ Fixation STOPS vertigo and nystagmus ♣ SIGNIFICANT vertigo ♣ Finite period of time although that time varies; recurrent o Central = 2/2 central lesion BS/cerebellum ♣ Bidirectional or unidirectional eye mvmt ♣ Fixation does NOT help ♣ MILD vertigo ♣ Can be chronic

inherited metabolic disorders

o Phenylketonuria (PKU) = amino acid/organic acid metabolic disorder ♣ Excess phenylalanine d/t enzyme mutation affects BRAIN ♣ Etiology = genetic (auto rec), most common in white people ♣ S+S = intellectual disability, gait disturbance, hyperactive, psychoses, abnormal odor, lighter color ♣ Tx = dietary restriction of phenylalanine o Tay-Sachs Disease = lysosomal storage disorder ♣ Absence of hexosaminidase A leading to GM2 buildup in brain ♣ Etiology = auto rec, most common in Ashkenazi jews ♣ S+S = miss developmental milesones at ~6 mo, deteriorate in motor and cognitive skills ♣ Tx = none; try to do genetic testing to simply avoid it (die by 5 y/o) o Mitochondrial Disorders ♣ Etiology = inherited or spontaneous mutations leading to impaired function of proteins in mitochon ♣ S+S = dec coordination, wkns, visual and hearing problems, learning disabilities, issues w/organs, dementia ♣ Tx = variable (relieve symptoms, slow disease process) o Wilson's Disease = RARE; hepatolenticular degeneration ♣ Decreased ability to metabolize copper accumulates in organs and tissues ♣ Etiology = genetic (auto rec) Eastern European, southern Italians ♣ S+S (~4-6 yo) = rings in iris, degenerative brain changes (esp BG), hepatitis, athetoid movements, ataxic gait, emotional and behavior changes, atrophy, contracture, fx, osteomalacia with time ♣ Tx = vit B6 and D-penicillamine (promote Copper excretion); prevent hepatic disease

preload, after load, SV, CO, VR

o Preload = tension in vent wall AT END OF DIASTOLE ♣ Reflects VENOUS FILLING o Afterload = FORCES WHICH IMPEDE bloodflow out of heart ♣ Aka PVR, compliance of aorta, mass and viscosity of blood o SV = VOLUME of blood pushed of LV with EACH PUMP ♣ Normal = 60 - 80 mL (dep on sex, age, activity) o CO = AMOUNT of blood pumped out PER MINUTE ♣ CO = SV x HR ♣ Normal (at rest) = males: 4.5 - 5.0 L/min; females: slightly less • With exercise can increase up to 25 L/min!!!! o Venous return = blood that returns to RV each minute ♣ Similar in volume to CO (must equal CO when averaged overtime since system is a loop)

healing by intention

o Primary = smooth, clean edges approximated and closed w/ sutures, staples, adhesives OR epithelial migration ♣ Acute wounds, min tissue loss, superficial partial thickness wounds • Blisters, abrasions, surgical incision, laceration, puncture ♣ Min scarring and heal quickly o Secondary = wounds heal on own w/o superficial closure - granulation tissue fills, contracts and scars ♣ Sig tissue loss or necrosis, irregular or nonviable wound margins that cannot be reapproximated, infection or debris contamination ♣ Often associated with patho - DM, ischemic conditions, pressure damage, inflammatory disease ♣ Req ongoing wound care, larger scars o Tertiary intention = delayed primary intention healing ♣ Wounds at risk for complication are temporarily left open until risk factors are alleviated then close wound

KAFO

o Provides support and stability to knee and ankle o Diff kinds ♣ Metal: 2 metal uprights connecting from shoe/ankle with both calf an thigh bands ♣ Plastic: plastic thigh shell connect to plastic AFO through 2 metal upright bars Craig scott- no pelvic band

RPE

o RPE 13-14 ~70% max HR on treadmill or cycle ergometer o RPE 11-13 upper limit prescribed training HR early in cardiac rehab

debridement

o Red-yellow-black system ♣ Red = protect ♣ Yellow = remove exudate and debris, absorb drainage ♣ Black = debride necrotic tissue o Selective = removal of ONLY non-viable tissue ♣ Sharp = use scalpel, scissors, forceps; fastest removal • Can do when cellulitis or sepsis ♣ Enzymatic = use topicals; slow removal • Infected or non-infected wounds ♣ Autolytic = use body's own mechanisms w/help of films, hydrocolloids, hydrogels, and alginates • Non-invasive and pain-free but slow • NOT appropriate w/infections o Non-selective = removal of BOTH viable and non-viable tissue ♣ Wet-to-dry dressings = use moistened gauze, let it dry, rip it off • Mod amounts exudate and necrotic tissue (only on 100% slough!) • Painful and often removes granulation tissue ♣ Hydrotherapy = whirlpool to soften and loosen • AEs = maceration, edema from dependency, systemic effects (hypotension) ♣ Wound irrigation = pressurized fluid (ex: pulse lavage) • Good for infections or loose debris

o Rhythmic initiation o Contract relax = o Hold relax = o Hold relax active movement (HRAM) = o Repeated contractions o Rhythmical rotation = o Rhythmic stabilization o Shortened held resisted contraction (SHRC) o Alternating isometrics (AI) = o Slow reversal = o Slow reversal hold o Agonistic reversals (AR) o Normal timing o Timing for emphasis o Resisted progression = resistance to pelvis, hips o

o Rhythmic initiation = passive AAROM AROM resisted --for initiation; when hypertonia exists --mobility o Contract relax = max contraction of antagonist at end range - "push into my hand" (concentric) --to increase ROM --mobility o Hold relax = isometric contraction at end range - "don't let me move you" --to increase ROM (used when pt is in pain) --mobility o Hold relax active movement (HRAM) = Isotonic contraction to shortened position w/ 10 sec isometric contraction followed by relaxation to lengthened position and quick stretch back into isotonic --Aka replication --improved initiation AND this one is really good with PD truncal rigidity --mobility o Joint distraction = manual traction applied throughout motion --to increase ROM --Mobility o Repeated contractions = quick-stretch followed by isometric or isotonic contraction --to initiate movement or help strengthen --mobility o Rhythmical rotation = passive technique; slowly rotate joint about longitudinal axis --decrease tone - relaxation --Mobility o Rhythmic stabilization = isometric contractions in all directions around a joint - "don't let me twist/turn you" --Stability o Shortened held resisted contraction (SHRC) = isometric contraction shortened range --Improvement postural extensors (superman) --Stability o Alternating isometrics (AI) = isometric contraction alternating from one side to the other, NO REST --Aka stabilizing reversals --for increased strength and endurance --stability o Slow reversal = slow and resisted concentric contractions --Aka dynamic reversal --Stability, controlled mobility, skill o Slow reversal hold = slow and resisted concentric contractions w/isometric hold btwn them --Aka dynamic reversal hold --Stability, controlled mobility, skill o Agonistic reversals (AR) = SLOW concentric contraction against resistance followed by eccentric contraction -Aka combination of isometrics (CI) --Controlled mobility, skill o Normal timing = resistance prox so distal can move --to improve coordination --skill o Timing for emphasis = isotonic and isometric contractions to STRONG muscles --strengthen weak muscles using overflow --Skill o Resisted progression = resistance to pelvis, hips or extremity while walking --to improve coordination, strength, endurance during gait --skill PNF = Kabat

airborne precautions

o SMALL particles (like air, dust) which are infectious ♣ Private room - monitored air pressure ♣ 6-12 air changes per hour ♣ Door CLOSED pt STAYS IN ROOM ♣ N-95 mask worn in room (personal fit and no facial hair) ♣ LIMIT time outside room ♣ Measles, varicella, TB

SpO2

o STOP ACTIVITY = IF SpO2 <90 in acutely ill or <85 in chronic lung dx pts --Discus with MD about adding or inc. supplemental O2 Est the percent of arterial O2 saturation of hemoglobin by sensor on finger or earlobe - SpO2

steps in testing hypothesis

o Sate null and alternate hypothesis o Select approp test statistic o Select level of significance for test (eg p<0.05) o Calc test stat from sample data o Interpret results = compare p-value associated with test stat to sig level ♣ If p-value </= level of significance = REJECT NULL in favor of alternate ♣ If p-value > level of significance = DO NOT reject null hypothesis

sampling-probabilit

o Simple random sampling = table of random numbers or random number generator ♣ Not most statistically efficient method and may not be rep since luck of draw o Systematic sampling = picking every nth subjet ♣ Size interval based on size pop and desired sample size ♣ Super simple o Stratified random sampling (proportional/quota) = pop divided into subgroups then a simple random sample is taken from each ♣ Assures sample will rep key subgroups + overall pop o Cluster sampling = pop divided into clusters or areas, random samle of clusters is selected, ALL units in that selected cluster are measured ♣ Less costly, more efficient

electrotherapy

o Size ♣ Small electrodes = over small areas of body small muscles that need low stimulation • Inc current density • Inc impedance • Dec current flow ♣ Large electrodes = larger areas of body or larger muscles which need hig levels stim • Dec current density • Dec impendence • Inc current flow o Current density = influenced by size of electrode and distance apart ♣ Same size = current density underneath each is same ♣ Unequal size = current more conc under small electrode ♣ Close proximity = current more dense superficial ♣ Further apart = more dense in deeper tissues o Placement ♣ Monopolar technique = wound, iontophoresis, edema • Active = over target; typically smaller electrode • Dispersive = site away ♣ Bipolar technique = weakness, NM facilitation, spasms, ROM • 2 active electrodes over target area; equal in size

spinotectal, olivary, reticular

o Spinotectal = assists with movement head and eyes towards a stimulus (spino-visual reflexes) o Spino-olivary = info from cutaneous and proprioceptive organs (to cerebellum) o Spinoreticular = consciousness (goes to reticular formation) ascending

incontinence types

o Stress UI = lose 2/2 activities which INC intraabdominal pressure (cough, sneeze, etc) o Urge UI = loss urine after sudden, intense urge to void ♣ COMMMON in geriatric population ♣ Etiology = detrustor muscle overactivity, overactive bladder, changes smooth muscle, inc sensitivity to ACh, Association with MS, SCI, CVA, PD ♣ S+S = conditioned reflex (key in lock) ♣ Tx = behavior modification - get rid of that urge , biofeedback, pelvic floor strengthening, bladder retraining, pharm o Overflow UI = loss when intra-bladder pressure exceeds urethras ability to hold in ♣ Etiology = outflow obstruction (prolapsed organ, enlarged prostate, chronic const, neurological dz) ♣ S+S = difficult initiating stream, weak and dribbled stream ♣ Tx = sx for obstruction, double voiding (weakness), intermittent cath if fails o functional UI = person can't or does not want to make it to the bathroom ♣ etiology = decrease mental awareness, dec. mobility, rarely seen in isolation ♣ at risk populations: Restricted mobility and dexterity, environmental barriers, mental and psychosocial disability, pharmacological influence ♣ Tx = alleviate underlying issue, behavioral toileting schedule

JRA

o Summary o AI disorder in kids < 16 y/o immune cells attack joints and organs local and systemic effects o F > M, usually dx as toddlers or early adolescents o Persistent joint swelling, pain, stiffness o Diagnosis o Condition that produces symptoms arthritis in kids < 16 that causes inflammation and stiffness in joints o Injured structures autoimmune o Inference o Contributing factors genetic possibly triggered by environmental factors o Confirmation o Clinical presentation systemic involvement, + rheumatoid factor and antinuclear antibody, joint swelling, pain, and stiffness ♣ Pauciarticular (< 4 joints) vs. polyarticular (> 4 joints, symmetrical) vs. systemic (fever, chills, rash, myalgia, polyarthritis, anemia, pericarditis, myocarditis, hepatosplenomegaly,, lymphadenopathy) o Imaging blood tests (RF, ANA, HLA-B27), ESR

fibromyalgia

o Summary o Nonarticular rheumatic condition w/pain d/t tender points in muscles, tendons, and ligs o Affects all ages, 75% F o Widespread pain all over body >/= 11/18 tender points o Diagnosis o Condition that produces symptoms rheumatology syndrome or or nonarticular rheumatic condition o Injured structures dysfunction w/in stress system, ANS, immune system, and/or reproductive and hormone systems o Inference o Contributing factors diet, sleep, infection, stress, environmental and occupational factors, trauma, genetics o Confirmation o Clinical presentation widespread hx of pain throughout body, axial pain, pain in at least 11/18 tender points measured w/dolorimeter (occiput, low c/s, trap, supra, 2nd rib, lat epi, gluts, greater troch, knee), fatigue, memory and visual impairment, sleep disturbances, IBS, HA, anxiety/depression o Imaging no tests, possibly correlates w/substance P (pain transmission) o Additional info dx if meet American College of Pheumatology criteria and has symptoms > 3 mo o Management o Tx meds to normalize ANS, psychotherapy, lifestyle management, nutritional support, stress management, pt/fam ed is key, avoid straining, aqua therapy, energy conservation, relaxation o Outcome o PT outcome common for symptoms to remain unchanged despite intervention o Long-term effects "moderate" symptoms for rest of life

burn depth

o Superficial = outer epidermis only ♣ redness, light edema ♣ heals in 2-5 days (no scar or peeling) o Superficial partial thickness = epidermis and upper dermis ♣ painful, blister (SUNBURN) ♣ heal in 5-21 days (min-no scar) o Deep partial thickness = epidermis and most of dermis ♣ Discolored, broken blisters, swelling ♣ nerve damage (less pain) ♣ heal in 21-35 days (hypertrophic or keloid scarring may occur) o Full thickness = all of epidermis and dermis, some damage to subcutaneous fat ♣ eschar, min pain ♣ may need grafts ♣ heal in weeks to months o Subdermal = epidermis, dermis, and subcutaneous fat, may involve muscle and bone ♣ req multiple sx and extensive healing o NOTE: Level of pain varies based on depth ♣ Superficial partial thickness are most painful!!

TLSO

o Taylor (flexion/extension control) = pelvic band connects 2 posterior upright which end midscap; has anterior abdominal closure and axillary straps ♣ TWO 3-pt pressure systems are coupled tighter to LIMIT BOTH FLEX AND EXT in the lumbar and thoracic spine o Jewett (flexion control) = 3-pt pressure system is created with 2 pads - one across sternum and other at pubic symphysis, with the counter force being provided by single pad posteriorly ♣ Promotes hyperextension and restricts fwd. flexion o Plastic body Jacket (flexion-extension-lateral-rotary control) = well fitted body jacket that will RESTRICT MOTION ALL PLANES ♣ Anterior and lateral trunk containment elevate intra-abdominal pressure and decrease demand on vertebral discs ♣ Variety of modifications for comfort - anterior chest cutouts, altering pelvic trim lines, etc. ♣ Uses = post-surgical, during acute trauma

froments sign

o Test: ulnar nerve compromise or paralysis (ADD pollicis) o Position: sitting, paper between thumb and index finger o PT tries to pull paper out o (+) flex DISTAL phalanx as compensation o (+) hyperextension at MCP JEANNE"S SIGN!!!

burn types

o Thermal = via conduction or convection o Electrical = entrance and exit wound ♣ Complications cardiac arrhythmias, resp. arrest, renal failure, neurologic damage, fas o Chemical = cont. until substance is removed/diluted ♣ Sulfuric acid, lye, hydrochloric acid, gas ♣ Iontophoresis related burns occurs when skin pH < 3 or > 5 (beyond normal tolerance) • usually under negative electrode, d/t skin erosion from excessive current, prolonged duration, poor electrode placement o Radiation = exposure to external radiation; alters DNA

US thermal vs. non thermal effects

o Thermal effects ♣ Acceleration met. rate ♣ Modulation pain ♣ Red muscle spasm ♣ Dec joint stiffness ♣ Alteration nerve conduction velocity ♣ Inc circulation ♣ Inc soft tissue extensibility o Non-thermal effects = due to cavitation and acoustic microstreaming ♣ Cavitation = bubbles which expand and compress 2/2 US pressure • Stable = vibrate and do not burst • Unstable = change size and burst o Typically doesn't happen with therapy US ♣ Acoustic microstreaming = unidirectional movement of fluids along cell membranes 2/2 US ♣ Inc cell and skin membrane perm ♣ Inc intracellular calcium levels ♣ Facilitation tissue repair ♣ Promotion normal cell function

hepatitis

o VIRAL is most common -- A, B, C, D, E, G o Hep A = transmitted by close contact or feces ♣ Get FLU LIKE SX! ♣ Does NOT progress to chronic - usually recover 6-10 weeks o Hep B = through needles and sex, body fluids ♣ NO SX ♣ Does have TX so most cases DO NOT progress ♣ tx = hep B immunoglobulin, immunization • HBIG within 24 hours - vaccination series at 1 and 6 months (3 doses) • Already vaccinated = get the vaccination again o Hep C = through needles and sex, body fluids ♣ NO S+S - But - inc freq getting manifestation like Hashimotos thyroiditis, DM, corneal abrasion ♣ Does NOT HAVE TX - MOST PROGRESS TO CHRONIC!!! OR lead to cirrhosis o Rehab considerations ♣ Make sure to have all immunizations and IF INFECTED then get tx ASAP ♣ Standard precautions EXCEPT for those with A and E - they get ENTERIC precautions • Wash hands with SOAP AND WATER before and after - think cuz feces transmission ♣ Arthralgia may be noted and they wont respond like normal to therapy ♣ Teach energy conservation and pacing skills

benzos

o Xanax, valium, atrivan, halicon, dalmane ♣ Action: CNS depressor through GABA ♣ PT imp = dependence, rebound insomnia, may disturb intellectual function and motor dexterity, withdrawal seizures may occur upon cessation and withdrawal from this ish sucksssss

burn zones

o Zone of coagulation = most severe injury area; irreversible damage o Zone of stasis = surrounds zone of coag.; less severe; reversible damage o Zone of hyperemia = surround zone of stasis; has inflammation but will fully recover with no damage

epidermis

o avascular, 5 layers, top is dead cells takes about 14-21 (2-3 weeks) days to go from bottom to top ♣ Layers • Stratum Corneum - callus forms here • Stratum Lucidum • Stratum Granulosum - lipid molecules so this layer is a waterproof barrier • Stratum Spinosusm - bundles of keratin (Tonofibrils) that stand against friction and shear • Stratum Basale - produces fingerprints and the germinal keratinocytes for regeneration of the epidermis ♣ Cells • Melanocytes - pigment, UV protection • Merkel cells - light touch • Langerhans - fight infection

metabolic acidosis

o body's pH drops below 7.35; too much CO2 or too little HCO3 ♣ Etiology = renal failure, lactic acidosis, starvation, diabetic or alc ketoacidosiss, severe diarrhea, poisoning ♣ S+S = hypervent (blow off CO2), vomiting, diarrhea, HA, weakness, malaise, hyperkalemia, cardiac arrhythmias • Untreated = coma, eventual death ♣ Tx = manage cause, correct imbalances, admin sodium bicarb

cholecystitis/cholelithiasis

o cholelithiasis = gallstone o Cholecystitis = inflammation for the gallbladder ♣ Usually caused by gallstones impacted in cyctic duct go figure o S+S = RUQ pain - can radiate to INTERSCAPULAR REGION, tenderness, rebound pain, jaundice, fever, N/V, rigidity

hypothalamus

o control ANS (temp, appetite, sweating, sex, rage, fear, BP, sleep) and pituitary gland ♣ Essentially has hormones with either release or inhibit pituitary hormones ♣ Regulated by CNS and circulating hormone levels

pancreas

o endocrine (blood sugar and storage reg) and exocrine (digestion) tissues ♣ islets of Langerhans produce hormones • alpha cells = glucagon sugar INTO blood and out of liver o stim when HYPO-glycemic • beta cells = insulin sugar OUT OF blood and into fat cells o stim when HYPERglycemic

descending tracts- pyramidal

o fine, skilled mvmts; passes through medullary pyramids; descends directly ♣ Damage = + Babinski, no sup abd or cremasteric reflex, loss of fine motor movement ♣ Corticospinal = voluntary mvmt • Anterior = IPSI voluntary; discrete and fine mvmts • Lateral = CL voluntary fine mvmt ♣ Corticobulbar = runs from the cortex to motor nuclei of cranial nerves; innervates motor muscles of the face

Meningitis

o inflammation of meninges of brain and SC Bacterial form is a med emergency dead in hours Signs = fever, HA, vomit, stiff/painful neck, pain in l/s and post thigh, Brudzinski's sign (neck flex hip and knee flex), Kernig's sign (pain w/hip flex and knee ext), light sensitivity ♣ Dx = lumbar puncture ♣ tx = w/antibiotic, antimicrobial, and steroids

L hemisphere Cx

o language, movement, logical, rational, math calculations, positive emotions ♣ Think: more organized and logical aka I am L brain minus the math shit and the logical shit and the positive emotions thing (so am I actually L brain ?)

normal pH, PaCO2, PaO2, SaO2

o pH 7.35-7.45 o PaCO2 35-45 mmHg o PaO2 97 mmHg --- BUT if 60+ yo, then subtract age over 60 from 80 (eg 65 yo = 75) o SaO2 >90%

case control study

o peeps who have disease are matched with comparison group of those who do not have; look at history btw the 2 to see ♣ Retrospective, observational ♣ Odds ratio = association btw exposure and occurrence of disease • Ratio of odds of exposure in diseased vs odds of exposure in non-diseased subjects

cohort study

o peeps with a risk factor or exposure are followed over a specific period of time to comp occurrence in exposure vs unexposed ♣ Longitudinal, observational study • Prospective = future • Retrospective = looking from past ♣ Relative risk = measure of association btw exposure and disease • Ratio incidence rate exposed vs control ♣ Limitation = excessive length, influence other variables

w/c measurements

o seat height = user's heel to popliteal fold + 2 in ♣ standard = 19.5-20.5 in o seat depth = back of butt to popliteal fossa along LATERAL thigh - 2 in ♣ standard = 16 in o seat width = largest part butt + 2 in ♣ standard = 18 in o back height = seat of chair to floor of axilla - 4 in ♣ should be BELOW inferior angle of scap ♣ MAKE SURE THAT CUSHION IS ON WHEN MEASURE IF HAVE ONE! ♣ Standard = 16-16.5 in o Armrest height = seat of chair to elbow when pt elbow flexed to 90* + 1 in ♣ MAKE SURE THAT CUSHION IS ON WHEN MEASURE IF HAVE ONE! ♣ Standard = 9 in above chair seat

contact precautions

o through direct or indirect contact ♣ DIRECT = you touched them ♣ INDIRECT = you touched something they touched ♣ Private room unless same organism ♣ Gloves when enter and CHANGE before leaving AND if you contact he infectious shit ♣ Wear a gown if close contact is possible ♣ Limit transport out of room ♣ LET PT HAVE THEIR OWN EQUIPTEMNT ♣ Wound infections, drug-resistant bacteria, c-diff, e-coli, shugilla, hep A, impetigo, herpes simplex, scabies, zoster, ebola

tetraplegia pt insidious onset pain inferior GH joint with swelling and warmth, erythema and limited ROM. high serum alkaline phosphatase.

septic arthritis and ectopic bone formation

proximal radioulnar capsular

sup>pro

mckenzie side glide test

used to determine if disc dysfunction with nerve root involvement versus postural disorder

evoked potentials

• 2 sets of electrodes; records time for impulse to reach brain o r/o MS, brain tumor, acoustic neuroma, SCI

PET

• 2D and 3D brain scan imaging that takes pics of ACTIVITY o r/o circulatory patho, met dysfunction, tumors, blood flow, brain changes following drug/alc abuse

cardiomyopathy

• 3 types o DILATED = chambers blown out --impaired SYST function 2/2 overstretch o HYPERTROPHIC = myocardium too thick --impaired DIASTOLIC o RESTRICTIVE = abnormal stuff in the myocardium impaired DYSTOLIC BUT contract fine S/S: • EARLY = none • Breathlessness • Swelling legs, ankles, feet • Bloating abdomen 2/2 fluid backup • Fatigue • Irregular heartbeat • Lightheadedness Fainting oDILATED: Meds = want to help contraction or decrease the stretch if possible ♣ ACE inhibitors, beta blockers, digoxin (cardiac glycoside which messes with Ca and K in heart so contraction is better), diuretics • Hypertrophic o Med = slow HR and stabilize rhythm ♣ Lopressor (aka Metoprolol beta blocker), calcium channel blocker • Restrictive o Meds = improve sx ♣ Diuretics, anti-HTN, antiarrhythmic

normal and abnormal blood volume

• : 4.5 - 5.0 L o Hypovolemia = deceased blood volume --Causes = bleeding, dehydration 2/2 vomiting, diahhrea, sweating, severe burns, diuretics --s/sx = OTH, tachycardia, elevated body temp o hypervolemia = fluid overload or increased blood plasma --causes = excess fluid intake (IV or blood transfusion), sodium or fluid retention (HF, kidney disease) --s/sx = swelling in legs, ascites, fluid in lungs

CT scan

• = brain scan imaging, produces cross sections of brain (2D image) o r/o vascular malformation, tumors, cysts, HNP, hemorrhage, epilepsy, encephalitis, spinal stenosis, intracranial bleeding, head injury

terminate ETT

• ABSOLUTE INDICATIONS TO TERMINATE TEST o Drop in SBP >10 mmHg from baseline despite inc in workload WITH other evidence ISCHEMIA o Mod severe angina (scale 3 or 4) o Inc nervous system symptoms (eg ataxia, dizziness) o Signs poor perfusion (pallor, cyanosis) o Sustained v-tach o 1.0 mmST elevation in leads without diagnostic Q wave • RELATIVE indications for terminating exercise test o Drop in SBP >10 mmHg from baseline despite inc workload with NO SIGNS ischemia o Arrhythmias (NOT v-tach) - multifocal PVCs, supraventricular tachy, heart block, bradycarrythmias o Fatigue, SOB, wheezing, leg cramps, claudication o Development bundle branch block ror intraventricular conduction delay o Inc in chest pain o Hypertensive response - SBP > 250 and/or DBP > 115

heart murmur

• Abnormal swishing sound when auscultating - INC TURBULENCE!! FF • INNOCENT = blood flows rapidly 2/2 activity, pregnancy, fever, anemia • ABNORM = TURBULENT blood flow o Damaged / narrow valve, hole, rheumatic fever, endocarditis, calcified valves, MVP • INNONCENT = nothing • ABNORMAL o Cyanosis o Limb edema o SOB o JVD o Chest pain o Dizziness o Fainting • INNOCEN = nah • ABNORMAL = dep on underlying cause o Meds = digoxin (inc strength and eff contraction), anticoagulants, diuretics, anti-HTN o SX = valve replacement, patching if defect is causing

monitoring devices

• Arterial line = monitoring device attached to cath inserted into ARTERY o Used to measure BP or obtain blood samples ♣ MORE ACCURATE o PT imp ♣ Careful with mobilization ♣ If DISPLACED - apply direct pressure to stop bleeding and call nurse • CVP catheter (central or PICC line) = catheter placed through veins to RA or SVC! o Measures PRESSURE o Eval RV function, RA filling pressure, circulating blood volume • Indwelling RA catheter (Hickman) = cath inserted through cephalic or int jugular vein into SV or RA o LONG-TERM ADMIN of substances into venous system - chemo, parental nutrition, antibiotics • ICP monitor = measures pressure exerted aganist skull o Types of monitors ♣ Epidural sensor = between skull and dural tissue • Cannot drain CSF OUT ♣ Subarachnoid bolt = through dura mater and into subdural space ♣ Intraventricular cath = catheter into VENTRICLE (most accurate) • Oximeter = photoelectroc device which measures O2 content of TISSUES o Usualy on finger or ear o PT imp ♣ Look at while doing exercise and changes in position - activity tolerance • Pulmonary artery cath (Swan-ganz) = cath through vein to PULMONARY ARTERY o Cont measurements pulmonary artery pressure o PT imp ♣ Not easily mobile ♣ Avoid excessive movement of head, neck extremities

alpha adrenergic agents

• BLOCK alpha-1-adrenergic receptors (A1 = peripheral receptors) • REDUCE PVR - dilation arterioles and veins, dec BP indication • HTN • BPH AEs • Dizziness • Palpitations • OTH • Drowsiness - you're blocking all receptors

balance tests

• Berg Balance Scale = fall risk o 14 tasks each scored 0-4 static, transitional and dynamic activities o score < 45/56 = FALL RISK •Fregly-Graybiel Ataxia Test Battery = higher-level balance!!! o 8 conditions, pass/fail stand on beam, and walk on beam, 2 leg, 1 leg, walking, rhomberg) o does NOT help to ID cause of dysfunction • Fugl-Meyer Sensorimotor Assessment of Balance Performance Battery = for pts with hemipalegia o 7 items, each scored 0-2 o 14 still does not mean normal balance (dumb) • Functional Reach Test = stand a reach fwd 3x and average o Age-related standards if below their age then FALL RISK ♣ 20-40 = 14.5-17 in ♣ 41-69 = 13.5-15 in ♣ 70-87 = 10.5-13.5 • Rhomberg Test = assess balance and ataxia o stand w/feet together and EO followed by EC for 30 sec ♣ EO = all 3 systems together (if vestib patho then staring at object will make better) ♣ EC = vestib and somto stressed more o Ataxia + (+) rhomberg = SENSORY ataxia, not cerebellar o Sharpened Rhomberg = same but in tandem stance for 30 sec ♣ Further stress on somatosensory and vestibular systems • Timed Up and Go (TUG) Test = assess mobility, balance, and fall risk o stand up and walk 10 ft and back ♣ < 10 sec = normal ♣ >20 sec = limit of function indep and increased fall risk ♣ >30 sec = high fall risk • Tinetti Performance Oriented Mobility Assessment = screen for falls o 1st part = sit<>stand (no arms), immediate stand balance EO EC, slight push standing, turn 360* o 2nd part = normal gait then fast but safe gait o score < 19/28 = HIGH fall risk (lower the score, the worse the fall risk)

tunnel littler or reticular ligament test

• Bunnel-littler test o TEST: differentiation of intrinsic muscles or capsular tightness limiting motion at the PIP o Position: sitting o 1 - MCP in EXT then flex the PIP and measure distance o 2 - MCP in FLEX then flex the PIP and measure distance o (+) capsular restriction = both restricted same o (+) intrinsic muscle tightness = motion increases when MCP joint flexed (ext MCP stretches intrinsic hand muscles so makes sense) • tight retinacular ligament test o test: retinacula ligaments o position: sitting o 1 - PIP in neutral, try to flex the DIP o 2 - PIP inflexion, try to flex the DIP o (+) joint capsule = limited in both o (+) retinacula ligaments = limited while extended

experimental designs

• Clinical trial = tests how well methods of screening, prevention, diagnosis, treatment of a dx work in peeps o Completely randomized design (Parallel groups design) = subjects randomly assigned diff groups, each group gets unique intervention; outcome diff groups compared at end • Crossover design = subject receives BOTH tx in random order sep by period of no tx o Each subject serves as own control • Factorial design = 2 or more independent variables investigated with diff subjects assigned to various combos level of the independent variable • pretest-posttest control group design = compares outcomes 2 or more groups formed randomly; test before and after o basic format RCT • posttest only control group design = compares randon group only AFTER treatment • randomized control trial = clinical trail; peeps rando assigned to EXP or CON group • repeated measures design (within subjects) = same group of subjects under multiple conditions o serve as own control • sequential clinical trial = data analyzed as becomes available so it can stop once shows sig diff btw tx • single-subject design = permits drawing conclusions about tx effects based on SINGLE pt response • Quasi-experimental design = research WITHOUT control group, random assn, or both

LOC

• Coma = unconscious, unresponsive to stimuli • Stupor = general unresponsiveness, arousal from repeated stimuli (pain) • Obtundity = state of sleep, decreased alertness, delayed responses • Delirium = disorientation, confusion, agitation, loudness • Clouding of consciousness = quiet behavior, confusion, poor attention, delayed responses • Consciousness = alert, aware, oriented, has memory

chronic fatigue syndrome

• Complex condition where a person is super fatigued an have various other things • diagnosis of EXCLUSION • criteria according to disease control o history of at least 6 months unexplain, prolonged, svere fatigue unrelieved by rest o 4/8 additional sx ♣ self-reported memory/cog defecit interefeing with life ♣ persistent/ recurrent sore throat ♣ painful / enlarged axillary / cervical nodes ♣ unexplained muscle pain ♣ migrating joint pain with no signs inflammation ♣ malaise >24 hours HA which changespattern / severity

cardiac biomarkers

• Creatne kinase (CPK-MB) = aerobic enzyme skeletal muscle, brain, MYOCARDIUM o Increases ~4 hours after, PEAK 24 hours, NORMAL day 2 o Used to detect acute and subacute • Troponin-1 = protein that's HIGHLY specific for necrosis of HEART o Increases ~4 hrs after, PEAK 12-24 hours, STAYS like 5-10 days after o Good to monitor and if MI suspected days ago • Myoglobin = small marker sensitive to skeletal and cardiac muscle necrosis o Elevated <24 hors o Acute MI only

cardiac arrest response

• Determine if pt. responsive • Call EMS if unresponsive, have 2nd person locate AED • Perform CPR until EMS or AED arrives • Use AED once 5!!! Cycles of CPR have been completed • Make sure pts chest is exposed for application of pads - follow AED commands If AED plans to shock pt., move away and clear immediate area

brachial plexus

• Dorsal scapular = rhomboids, levator scap • Long thoracic = serratus anterior • Nerve to subclavius = subclavis • Suprascapular = infraspinatus, supraspinatus • Lateral pectoral = pec major (clav head) • Musculocutaneous = coracobrachialis, biceps, brachialis • Median = forearm flexors + 5 muscles in hand • Median pectoral = pec major (sternal head), pec minor • Ulnar = FCU, FDP, small muscles of hand • Subscapular = subscapularis • Thoracodorsal = lats • Lower subscap = subscap, teres major • Axillary = deltoid, teres minor • Radial = brachioradialis, triceps, supinator, wrist ext, anconeus

peptic ulcer dx

• EROSION of the mucosa 2/2 acid > protection o Etiology = h-pylori and NSAIDS o S+S = epigastric pain, heart burn, N/V, bleeding, bloody stools, pain in waves relieved by eating ♣ If caused by h-pylori = bad breath, rosacea, flushing ♣ Complications = perforation, obstruction, malignancy o Tx = pharm, Sx if intense o Rehab considerations ♣ Make sure to monitor EVERYONE WITH HX ULCERS for signs of bleeding ♣ Monitor fatigue, pallor, exercise tolerance ♣ HR INCREASE AND BP DECREASE MAY BE SIGNS OF BLEEDING ♣ BACK PAIN = perforated ulcer post stomach or duodenum ♣ RAD PAIN MIDTHOR TO RUQ = blood and acid in cavity 2/2 perforrated ulcer

EMG detailed

• Evaluation of motor units through intramuscular needles or surface electrodes o Aka youre looking at: anterior horn cell, axons, NM junctions, muscle fibers innervated o Intramuscular EMG = small or deep muscles, need to record single motor unit potential • NORMAL o relaxed muscle = electrical silence o contracting muscle = APs begin to appear ♣ as strength contraction increases more muscel fibers produce APs ♣ full contraction disorderly group APs at varying rates and amplitudes • ABNORMAL o Associated with a variety of med conditions - ALS, carpal tunnel, DMD, GB, MG, peripheral neuropathy, poliomyelitis o Spontaneous = at rest ♣ Fibrillation potentials = twitching YOU CAN SEE; very irregular • LMN disease - ALS, SMA, ♣ Positive sharp wave • De-nervated muscle disorders at rest - ALS, MS, etc. • Primary muscle disease (aka affects muscles themselves) - DMD, etc. ♣ Fasciculation's = rapid twitching of individual muscle fibers; CAN'T SEE with eye • Irritation/degeneration anterior horn cell • Nerve root compression or muscle spasms ♣ Repetitive discharges • Myopathies (issue with muscle themselves) • Lesion anterior horn cells and peripheral nerves o Voluntary ♣ Polyphasic potentials • Myopathies (issue with muscles themselves) • Muscle or peripheral nerve involvement

expected outcomes pulmonary rehab

• Expected outcome o Inc exercise tolerance o Inc peak O2 uptake o Inc endurance time o Inc functional walking distance o Inc muscle strength and endurance o Reduce DOE o Can do ADLs o Improve QOL o Reduce anxiety and depression

internal vs. external validity

• External validity = degree results of research can be generalized to pop.circumstances BEYOND what was in stidy o Threats: interaction tx with specif type subjects, place (setting), and time (hx) which exp is performed • Internal validity = degree that intervention evaluated (IND) is the cause of the outcome (DEP) and NOT cuz of other factors o Threats: history, maturation, attrition, testing, instrumentation, regression to mean

TL spine goni

• FLEX and EXT: o Double inclinometer method ♣ Zero them out before them have them do the motion ♣ Calculation = difference between 2 o Tape measure = MOST COMMON ♣ Align between SP C7 and T1 - record distance ♣ Bend fwd/back while tape unwinds - record 2nd distance ♣ Calculation = difference between 2 • Lateral FLEX: standing, feet shoulder width apart o F - SP S2 o SA - per to ground o MA - SP T1 • ROT: sitting on chair with no back o F - center top of head o SA - parallel to imainry line btw iliac crests MA - imaginary line between acromial processes

hip goni

• FLEX: supine o F - Gr. Troch. o SA - Trunk Midline o MA - Lat. Fem. Condyle • EXT: prone o same landmarks as FLEX • ABD: supine, *Keep toes pointed twd ceiling to prevent ER* o F - ASIS o SA - Contralat. ASIS o MA - Mid-Patella • ADD: supine o same landmarks as ABD, *drop contra. leg off table* • IR & ER: sitting o F - Center of patella o SA - Perpendicular to ground (pointed straight ↓ to floor) MA - Midline b/t malleoli

synergies

• Flexor o UE scap elevation and retraction, shoulder abd and ER, elbow flex, forearm sup, wrist flex, finger and thumb flex w/add ♣ More common o LE hip abd and ER, knee flex, ankle DF w/sup, big toe ext (others flexed 2/2 spasticity) • Extensor o UE scap depression and protraction, shoulder add and IR, elbow ext, forearm pron, wrist ext, finger and thumb flex w/add (think: waiters tip hand) o LE hip ext, add, and IR, knee ext, ankle PF w/inv, toe flex and add ♣ More common

HALO

• GREATEST reduction in cervical motion; cranial ring secured to skull by 4 pins, ring attached by 4 metal bars to plastic vest worn continuously o Estimated reduction in all cervical motions is 90-95% o Can also provide distraction forces to aid in spinal stabilization an reduction of load o Common uses ♣ Cervical SCI to prevent further damage ♣ During recovery period of dislocation o Wear until spine becomes stable

COPD:

• GROUP of lung diseases the BLOCK AIRFLOW 2/2 narrowing of the arterial tree o AIR CANNOT GET OUT!!! • 2 main conditions: o Emphysema (pink puffer) = alveolar wall destruction o Chronic bronchitis (blue bloater) = hypertrophy mucous secreting glands; inflammation bronchial walls • Can also refer to damage caused by chronic asthmatic bronchitis • Progression = alveolar destruction, subsequent air trapping • INCREASED TOTAL VOLUME - INCREASED RESIDUAL VOLUME • FEV1/FVC = <75% (they have an issue getting air out and they have a lot of air in there since air trapping etiology • Majority - long term smoking or exposure to other irritants • RARE cases = genetic disorder of protein alpha-1-antitrypsin S/S • Excess mucous production • Chronic productive cough (only productive blue bloater) • Wheezing • SOB • Fatigue • Reduced exercise capacity TX: • MEDS = bronchodilators, inhaled steroids, supplemental O2, antibiotics (if bacteria infection) • SX = lung volume reduction, bullectomy (dilated air-spaces aka bullae and blebs in lung parenchyma are removed), lung transplant • Lifestyle modifications • Pulmonary rehab = AWC, breathing exercises, endurance and strength training

heat illness response

• Heat exhaustion = less serious, can progress to heat stroke o Profuse sweating o Moist and pale skin o Nausea o HA o Dizziness o Muscle cramps o Weakness o Rapid and shallow breathing o WEAK and rapid pulse • Heat stroke = medical emergency if not treated properly o Dry skin o Flushed color o Nausea o HA o Labored breathing o STRONG and rapid pulse o Elevated temp o Contractona d dilation of pupils o Convulsions o AMS o Possible LOC • Placed in shaded or covered area • Monitor VS • Remove or loosen outer clothing • Use ice bag / cold compress on pts forehead, neck, groin • Water or electrolyte solution if STILL CONSCIOUS o NO DO GIVE SALT TABLETS - can neg. effect electrolyte balance • EMS called if experiencing heat stroke or condition is worsening

gastritis

• INFALMMATION of the inner wall of the stomach (gastric mucosa) o EROSIVE GASTRITIS = bleeding from the gastric mucosa 2/2 stress, NSAIDs, alcohol, alcohol, etc ♣ S+S = indigestion, N/V, coughing up blood ♣ Tx = removal stim, pharm, sx last resport o NON-EROSIVE GASTRITIS = usually caused by H-PYLORI INFECTION ♣ S+S = Usually asymptomatic ♣ Tx = MUST be treated AGGRESSIVELY - h-pylori is a carcinogem (PPI, antibiotics) o Rehab considerations ♣ Blood in the stool = MD referral ♣ Educate make sure to take meds with food and water ♣ AVOID ASA CONTAINING COMPOUNDS

Rheumatic Fever

• INFALMMATORY DISEASE which can develop as comp from badly taken care of strep (a certain type) • can DAMAGE VALVES and cause HF!! • streptococcus pyogenes or group A strep causes strep or scarlet fever S/S • they result from INFLAMMATION OF whatever structure it is • red, swelling • fever • painful joints • heart palpitations • chest pain • SOB • Skin rash • GOALS = destroy the virus, relieve sx, control inflammation • Antibiotics, anti-inflammatories

endocarditis

• INFLAMMATION ENDOTHELIUM (innermost layer) which lines <3 and valves • When untreated, can damage or DESTROY the valves life-threatening • Caused by BACTERIA - enters blood through needles, catheters, dental procedures, gum disease, STDs, inflammatory bowel disease • At risk = damaged valve, artificial valve, other heart defects • May develop slowly dep on cause • Fever • Chills • Heart murmur • Fatigue • SOB • Weightloss • Blood in urine • Skin petechiae = tiny purple, red, or brown spots on the skin • ANTIBIOTICS • Sx = if persistent infection or to replace a damaged valve

RPP

• Index of myocardial O2 consumption and coronary blood flow • Provides and easy to measure correlate to onset of ischemia or development of ECG abnormalities • Generally sx occur at a reproducible RPP value • Procedure o Measure SBP and HR during the same exercise workload o RPP = SBP x HR ♣ Typically recorded with x 10^3 after since it's a big numero ♣ Eg HR = 150, SBP = 170, RPP = 25.5 x 10^3

pneumonia

• Inflammation of THE LUNGS / ALVEOLAR SACS o Diff btw this and pulm. edema is this is caused by INFECTION!! • CAUSED BY INFECTION -- Bacteria, viral, fungal, parasitic infection • Variable dep on cause • SOB • Fever • Cough • Sweating • Shaking chills • Chest pain that FLUCT WITH BREATHING • HA • Muscle pain • Fatigue • FOCUS = get rid of the cause • Rest and drink plenty of liquids

bronchitis

• Inflammation of bronchi - HYPERTROPHY OF MUCOUS SECRETIG GLANDS o Increased mucous production insufficient oxygenation since blockage • When CHRONIC = BLUE BLOATER type of COPD o Characterized by productive cough for 3 months over last 2 years etiology • ACUTE = cold virus, exposure to smoke, air pollutants • CHRONIC = cig smoke primarily; also exposure in workplace S/S • Persistent cough with PRODUCTION THICK SPUTUM o Worse in morning and damp weather • Increase accessory muscle use with breathing • Wheezing • Dyspnea • Cyanosis • Increased pulmonary artery pressure • Persistent resp infection TX: • FOCUS = relief sx and improve breathing • ACUTE = rest, fluids, warm and moist air, cough suppressants (blocks cough reflex), acetopmetaphine, ASA • CHRONIC o Meds = antibiotics, anti-inflammatory, bronchodilators o Lifestyle changes = stop smoking, avoid irritants, wear a mask if the cold sets you off, air humidifier o Pulm rehab = AWC, breathing exercises, endurance and strength training

K level amputee

• K0 = NOT a potential user for ambulation or transfers o Feet: none o Knee: none • K1 = potential HOUSEHOLD ambulator o Transfers, ambulate level surfaces, fixed cadence, limited or unlimited household ambulator o Feet: SACH, single axis o Knee: single axis, constant friction mechanism • K2 = potential LIMITED COMMUNITY ambulator o Traverse low level barriers (curbs, stairs, uneven surfaces), limited community ambulator o Feet: flexible keel, multi-axial o Knee: polycentric, constant friction mechanism • K3 = COMMUNITY ambulatory using VARIABLE CADENCE including THER-EX or vocation o Variable cadence, unlimited community, traverse most environmental barriers, use beyond simple locomotion o Feet: energy storing, dynamic response foot, multi-axial foot o Knee: pneumatic/hydraulic, microprocessor, variable friction mech • K4 = HIGH ACTIVITY user who EXCEEDS normal ambulation skills o Exceeds basic ambulation skills, exhibits high impact, stress or energy levels, typical child, athlete, or active adult o Feet: all o Knee: all

Cx L hemi, R hemi, BS, cerebellum stroke

• L hemisphere = wkns/paralysis of R side, increased frustration, decreased processing, possible aphasia, dysphagia, and motor apraxia, decreased L/R discrimination, R hemianopsia • R hemisphere = wkns/paralysis of L side, decreased attention span, awareness, judgement, abstract reasoning, and spatial orientation, L hemianopsia, memory deficits, L inattention, emotional lability, impulsive behaviors • BS = unstable vitals, decreased consciousness and ability to swallow, B wkns/paralysis • Cerebellum = decreased balance, coordination, and postural adjustments, ataxia, nausea, nystagmus

O2 Hgb dissociation curve

• LEFT = INCREASED affinity aka Hb will hold on to O2 (clingy af) o Increased pH more base o Decreased temp hypothermic, metabolic rate slowed o Decreased pCO2 • RIGHT = DECREASED affinity aka Hb will cut that bish O2 off o "my right hand will bitch slap a hoe to cut her off" o Decreased pH more acid o Increased temp hyperthermic and metabolic rate increases o increased pCO2 Like with exercise!! dumping O2 into tissues (why you get all red ???)

lumbar and sacral plexus

• Lumbar plexus = psoas major, psoas minor, QL • Sacral plexus = piriformis, sup and inf gemelli, obturator internus, quadratus femurs • Sciatic (tibial) = ST, SM, BF (long) • Sciatic (tibial) = BF (short) • Sup glut = glut med and min, TFL • Inf gluteal = glut max • Deep peroneal = TA, EDL, EHL, peroneus tertius, EDB (anterior compartment) • Superficial peroneal = peroneus longus and brevis (lateral compartment) • Femoral = RF, VL, VM, VI, iliacus, sartorius, pectineus • Obturator = adductor longus, magnus, brevis, obturator externus, gracilis • Tibial = soleus, popliteus, plantaris, tibialis post, gastroc, FHL, FDL (posterior compartment) • Med plantar = abd hallucis, lumbrical 1, FDB, FHB • Lat plantar = abd, flex, and opponens digiti minimi, dorsal and plantar interossei, quadratus plantae, adductor hallucis, lumbricals 2-4

phase 2

• MODE = rhythmic activities, large muscle groups, continuous and safe o Walk, hike, run, jog, bike, ski, dance, jump rope, etc • INTENSITY = HR, METs RPE o Note: generally want >10 beats/min BELOW known ischemic / angina threshold o HR ♣ Without entry test = resting HR + 20 bpm ♣ Usually target HR zone • Method 1: percent of max HR o Lower THR = maxHR x 55% o Upper THR = max HR x 90% • Method 2: heart rate reserve (HRR) or karvonen formula o Lower THR = [(HR max - HR rest) x 40%) + HR rest o Upper THR = ([HR max - HR rest) x 60%) + HR rest o METS ♣ 1 MET = 3.5 mLO2/kg/min ♣ you have to measure max METS in test for this ♣ Lower MET = [(MET max - MET rest) x 40%) + MET rest ♣ Upper MET = ([MET max - MET rest) x 60%) + MET rest o RPE (SPECIFIC TO MODE OF EXERCISE) ♣ Really good when can't use HR - beta blockers, heart transplant ♣ 12-16 = 40-85% ♣ initial phase = 11-13 ♣ later = 14-16 • DURATION o 1st month (training phase) = 15-20 min continuous or intermittent o months 2-5 (improvement) = 25-30 mins o 6 months + (maintenance) = 40+ mins o interval training may be approp for those who cannot do cont • FREQUENCY = 3/5 days/week o Anticipated outcomes ♣ Promote active lifestyle ♣ Improved functional capacity ♣ Lower CV risk factors ♣ Improve sx and physiological response to exercise ♣ Mod unhealthy behaviors ♣ Improve pt understanding of safety issues during exercise

muscle relaxation agents

• Muscle relaxation WHO • Spasm cont, toncic contraction SE • Sedation • Drowsiness • Dizziness • n/v • HA • Tolerance • Dependence PT • AES • Train them while theyre on their meds so it sticks • Valium, flexeril, paraflex

anti-spasciticty meds

• Muscle relaxation • Agents bind selectively to CNS or w/in skeletal muscel cells themselves WHO: Inc tone, spastcity, SCI, CVA, MS SE: • Drowsiness • Confusion • HA • General muscle weakness • Hepatotoxicity w/ dantrium • Tolerance • Dependence Sedation PTschedule approp • Balance btw dec it and then losing function • Baclofen, Valium/Diazepam, Dantrium, Zanaflez

SCI C7-8

• Muscles o C7 = triceps, pronators, wrist flexors, muscle which attach to thoracic wall and shld now full (serratus, lats, pecs, biceps, RTC) o C8 = finger flexors (active grip and release) • Functionality o GAME CHANGER o Bed mobility = INDEPENDENT o Transfers = mof I slide board; mod A-mod I w/ car; max-mod from floor ♣ Aka w/ a lot of work they can get up from floor o WS = mod I o w/c mgmt = may req A with cushion adjustment, anti-tip levers, w/c maintenance o w/c mobility = power w/c mod I smooth, ramp, rough; dep-max A curbs can drive with hand controls!!! man mod I smooth, ramp; min A-mod I rough; mod-min curbs, dep-max steps o gait = N/A o ROM/positioning = min A-mod I o Feeding = mod I with adaptive equipt o Grooming = mod I o Dressing = in bed mod I upper and lower body dressing In w/c min A lower body (C7), mod I upper/lower (C8) o Bathing = mod I USING CHAIR o Bladder = male: mod I in bed or w/c; female: mod I in bed, mod A in w/c o Bowel = min A-mod I with equiptment o Can drive with hand controls and stow w/c by self o Still lacking trunk control WHEELIE SKILLS!!

SCI C5

• Muscles = biceps (brachialis, brachioradialis), deltoid, serratus, pecs, rhomboids, shoulder ERs (infraspinatus) • Functionality = o Bed mobility = mod-max A o Transfers = max A with slide board ♣ Unlikely to be able to do I transfers o WS = dep in manual w/c; mod I with power (same as C4) ♣ Pressure relief limited tilt in space or recline o w/c mgmt = dep o w/c mobility = max A-dep manual w/c MAY be mod I on smooth surface fwd BUT need power W C for comm ambulation o gait = N/A o ROM/positioning = dep o Feeding = min A with adaptive equipment o Grooming = min A w/ adaptive for face; mod-max for hair o Dressing = dep o Bathing = dep Bowel/bladder = dep

SCI C4

• Muscles = upper traps, SCM, diaphragm (partially - 3,4,5 keep alive) • Functionality = essentially dep with everything, mod I with power w/c o Bed mobility = dep o Transfers = dep o WS = dep in manual w/c; mod I with power o w/c mgmt = dep o w/c mobility = mod I with power (would need head or breath control), dep with manual o gait = N/A o ROM/positioning = dep o Feeding = dep o Grooming = dep o Dressing = dep o Bathing = dep o Bowel/bladder = dep o May need respiratory assistance Teach to self-direct care

SCI C6

• Muscles = wrist extension (tenodesis), traps (shoulder depression), subscap (IR), teres minor (IR and add), • Functionality o Bed mobility = min A-mod I w/ equipment (can rach midline + move self around fixed arm) o Transfers = min A-mod I with slide board; dep w/ w/c loading to car and dep with floor transfers ♣ High motivation needed - very tiresome o WS = mod I w/ power recline/tilt; min A-mod I w/ side to side/fwd lean WS o w/c mgmt = some assistance required o w/c mobility = w/ power w/c mod I in smooth, ramp, and rough terrain power w/c, dep curbs w/ manual w/c mod I smooth; mod-min A ramps/rough terrain; max-mod curbs o gait = N/A o ROM/positioning = mod A-mod I o Feeding = mod I with adaptive equiptment o Grooming = mod I with adaptive equiptment o Dressing = mod I upper body; min A lower body putting on, mod A taking off lower body ♣ Aka can dress self but it takes 10 years o Bathing = min A upper; mod A lower - USING CHAIR o Bladder = min A male bed or w/c; mod A female in bed o Bowel = mod A with equiptment o Aka thye have self care capabilities but its not always efficicent CAN DRIVE - needs hand controls and something to help with stowing

PAD

• NARROWING ARTERIES of aorta, periphery • Can be stenotic, occlusive, aneurysmal • PRIMARY = athlerosclerosis and thromboembolytic processes which alter structure and function S/S • fatigue, aching, numbness, pain mostly in butt, thigh, calf, foot • felt at rest or walking (intermittent claudication) • poor healing wounds (lateral aspect leg) • distal hair loss • trophic skin changes • hypertrophic nails TX: • asymp = modification lifestyle factors • disabling intermittent claudication o revascularization processes = angioplasty, stent, lasers, atherectomy devices) o sx = a

CVA tests/measures

• NIH Stroke scale = assessment of acute CVA relative to impairment • Functional Independence Measure (FIM) = assess mobility and ADLs to determine level of burden • Stroke Impact Scale = assess physical and social disability • Fugl-Meyer Assessment of Physical Performance = motor, sensory, and balance impairment and pain and ROM

development milestones newborn-1 mo.

• Physiologic flexion • Lift head briefly • Head to side • Head lag pull to sit • Reflex standing and walking • Regards object sin direct line of sight and follows to midline Hands fisted and mvmts jerky

psoriasis

• Plaque o Chronic autoimmune disease (T cells) of skin o Etiology = genetic, sunlight, stress, alcohol, smoking, HIV, meds o S+S = red, raised blotches, itchy and flaky o Tx = control symptoms and prevent infection

mm of exhalation

• Quiet breathing is mostly PASSIVE • Forceful breathing requires some muscle help o Muscles = rectus abdominis, EO, IO, transverse abdominis o DEPRESS the ribs and COMPRESS abdominal contents pushes the diaphragm UP!!

OI

• RARE connective tissue disorder that impairs collagen synthesis (making collagen) o Impairs TYPE 1 collagen o Reduces collagen production 20-50% • THIS AFFECTS BONES (makes brittle) AND ALL CT IN THE BODY o Compromises growth, hearing, CP function, joint integrity o DELAYED DEVELOPMENTAL MILESTONES • There are 4 types vary in severity DIAGNOSIS is made through tests below, exam, personal and family medical history • Type 1 = mild o Near normal growth and appearance o Freq fxs ceases after puberty o Mild or mod fragility o No deformity o Blue sclera o Easy bruising o Triangular face o Possible hearing loss o Most are COMMUNITY ambulators • Type 2 = MOST SEVERE o Child dies in utero or early child birth o Sig fragilty CT o Multiple fxs o Extreme deformities o Soft skull • Type 3 = severe o BUT greater ossification of skull o Sig growth retardation o Progressive deformities o Triangular face o Blue sclera o Sig limitations functional mobility o Only 26% become HOUSEHOLD ambulators • Type 4 = milder but more than type 1 o Mild - mod fragility o Hypermobile joints o OP o Fx easily prior to puberty - some improve at that time o May or may not have shorter stature o Near normal sclera o Bowing long bones (Rickets in legs) o Barrel-shaped rib cage (impaired resp function) o Possible hearing loss o Brittle teeth o Near normal life expectancy o 57% are HOUSEHOLD ambulator; 26% are COMMUNITY DELAYED EVELOPMENTAL MILESTONES with all • Skin biopsy = tells collagen and type OI • X-ray and bone scan = evidence of deformities or fxs bone densitometry = measure bone mass, est fx risk certain body sites

CPR

• Recognition o Unresponsive o No breathing, no normal breathing / gasping o No pulse palpated within 10 secs • CPR sequence o Compression airway breathing • Compression rate o 100-120 / min • Compression depth o Adult = min 2 in o Children = min 1/3 chest AP depth; ~2 in o Infants = min 1/3 AP depth; ~1.5 in • Chest wall recoil o Allow complete recoil before next compression o Rotate compressors every 2!!!! Minutes • Compression interuptions o Minimize BUT if must do then def <10 secs • Airway o Head tilt chin lift o If suspected trauma jaw thrust • Compression to vent ratio (until advanced airway placed) o Adults = 30:2 BOTH 1-2 rescuers o Children/infants = 30:2 if 1 rescuer; 15:2 if 2 rescuers

CI to pregnancy exercise

• Relative anemia, arrhythmias, chronic bronchitis, unmanaged type 1 diabetes, extremely over or under weight, poorly controlled HTN, seizures, or hyperthyroidism • Absolute hemodynamically unstable, RLD, incompetent cervix, high risk for premature labor, preeclampsia, persistent bleeding, placenta previa

dopamine replacement meds

• Relieve PD sx • Go across BBB and then turn into dopamine WHO: • PD, parkinsonisim Side effects: • Arrhythmias (levodopa) • GI distress • OTH • Dyskinesias • Mood and behavior changes • Tolerance PT • Scheudl 1 hour after admin ON TIME • Monitor BP since OTH • Sinemet or madopar (levodopa) symmeterel

ARDS

• SUDDEN RESP FAILURE 2/2 FLUID ACCUMULATION in the ALVEOLI • Usually occurs in vulnerable peeps already chronically ill or sig injury • Severe SOB develops HOURS to A FEW DAYS after original provocation • FATAL in 25-40% of peeps who develop it • Survivors may not REGAIN function for A YEAR OR MORE! Etiology • Mechanical cause = fluid leakage btw smallest vessels of lungs into alveoli • Normal = protective membrane BUT inflammation can undermine integrity • Conditions which can injure lungs and lead to this: o Severe viral / bacteria pneumonia o Infection through blood (sepsis) o HF o Multiple or massive blood transfusions o Serious head or chest injury o Fx of long bones can cause fat embolism o PROLONGED USE SUPPLEMENTAL O2! o Accident inhalation vomit of chemicals (ammonia, chlorine) o Smoke inhalation o Near drowning o AE CA drug or other meds o Drug OD (heroin most common) o Shock S/S • Varies based on cause and severity • SEVERE SOB • Labored and rapid breathing • HYPOtension • Confusion • Extreme fatigue • Cough • Fever TX: • Make sure to determine cause - determines tx and chance of survival • FIRST GOAL = O2 to lungs (supplemental O2, mech. vent) • THEN = treat underlying condition o Meds = prevent and tx infection, relieve pain, provide sedation, prevent blood clots

forearm goni

• SUP: sitting with elbow flexed to 90* o Fulcrum - MEDIAL to ulnar styloid process o Stationary - Parallel to anterior midline of humerus o Moving - ventral aspect distal radius o FIRM end feel • PRON: sitting, elbow 90* flex o Fulcrum - LATERAL ulnar styloid process o Stationary - parallel to anterior midline of humerus o Moving - dorsal aspect diatl radius FIRM or HARD

Sn and Sp

• Sensitivity = % of people who TEST POS who actually HAVE disease o SnNout = if test NEGATIVE, then rule OUT ♣ Since test is very good at catching +, we know that if they get a (-) then they def don't have it • Specificity = % of peeps who TEST NEG who DO NOT HAVE disease o SpPin = if test POSITIVE, then rule IN ♣ Since text is very good at catching -, we know that if they get a (+) then they def have it

atherosclerosis

• Slow progressive BUILDUP FATTY PLAQUES on inner walls of arteries • This can overtime restrict blood flow and cause clot • Exact cause unknown BUT we have suspicions • Damage/injury to inner wall fatty plaque buildup (cholesterol, cell waste) harden narrow artery impede blood flow (inner lipid core and then fibrous cap over it) • Risk factors o High blood levels LDL (>70) o low blood levels HDL o type 2 DM o smoking o obesity o low physical activity o genetic factors, HTN, hypothyroidism also • VARIES based on severity and artery affected • CORONARY = angina • CEREBRAL = numbness or weakness of extremities, diff speech/slurred, drooping face muscles • PERIPHREAL = intermittent claudication • Lifestyle changes = stop smoking, exercise more, eat healthy, manage stress • Meds = antiHTN, antiplatelet, antilipidemic • SX = angioplasty, endarectomy, bypass

epilepsy

• Summary o Abnormal activity of brain's nerve cells d/t brain injury electrical discharges resulting in epileptic seizures o Wide variety of symtoms mood distrurbance, staring, LOC, uncontrollable jerking of extremities, muscle stiffening, loss of muscle control o Prodromal period (rare) can occur hrs or days prior, include mood changes, sleep disturbances, lightheadedness, irritability, difficulty concentrating , aura (min before) o Electroencephalogram measures electrical activity of brain, most common test for dx • PT should stay calm, prevent injury, remove objects near pt, time seizure, max comfort, keep others away, no restraints, nothing in their mouth, no food, water, or meds, call 911 if longer than 5 min • Post-seizure person lays on L side until fully alert, stay w/pt until recovery (5-20 min), be aware of pts who are at risk • Diagnosis o Condition that produces symptoms chronic CNS disorder characterized by epileptic seizures d/t abnormal neuronal activity from trauma, disease, genetics, and developmental disorders o Injured structures injury to brain • Confirmation o Clinical presentation wide variety; mood disturbances, staring, LOC, uncontrollable jerking of extremities, muscle stiffening, loss of muscle control; seizure (1 seizure doesn't mean have epilepsy) o Imaging electroencephalogram o Additional info PMH, physical and neuro exam to r/o syncope, metabolic conditions, movement disorders, migraine

myasthenia gravis

• Summary o Autoimmune disorder affecting transmission of NM signals o Present w/skeletal muscle wkns but other neuro functions (sensation, reflexes) are normal ♣ Affects prox > dist usually limb and ocular musculature • Diagnosis o Condition that produces symptoms autoimmune disorder affecting transmission of NM signals o Injured structures immune cells attack nerve receptors in NMJ • Inference o Contributing factors thymus gland abnormalities; affects F (20-30s) > M (50-60s) • Confirmation o Clinical presentation muscle wkns and fast fatigue w/fast recovery after rest, normal neuro signs (reflexes, sensation), ocular (diplopia, ptosis), facial expression, chewing, swallowing, speech, worse w/activity, heat, illness, stress, pregnancy, and menstruation, respiratory crisis (req vent) o Characteristics fluctuating mild to severe symptoms, prox more affected than dist, difficulty w/speech, swallowing, and chewing, eyelid wkns, diplopia, ptosis, can have exacerbations and remissions o Imaging blood test (antibodies), electromyography, CT or MRI of thymus o Additional info differentiate from hyperthyroidism and botulism, assess ocular and facial muscles, neuro testing, pulmonary function • Management o Tx meds (streroids to depress immune function, acetylcholinesterase inhibitor), sx thymus removal, PT (strength and endurance, avoid overexertion)

HD

• Summary o Chronic progressive genetic disorder fatal in 15-20 yrs post-manifestation o Degeneration and atrophy of BG (striatum) and cerebral cortex o Enlarged ventricles d/t atrophy of BG, mental deterioration, speech disturbances, ataxic gait • Diagnosis o Condition that produces symptoms degeneration and atrophy of BG (striatum) and cortex o Injured structures affects BG and cortex, decrease in GABA and ACh neurons so cannot modulate movement resulting in chorea, bradykinesia, and rigidity • Inference o Contributing factors genetic (autosomal dominant) on chromosome 4 (gene IT-15) • Confirmation o Clinical presentation usually 35-55 y/o, movement disorder, affective dysfunction, cognitive impairment, starts w/involuntary choreic movement, mild personality alteration, unintentional facial expression (tongue out, grimace, raised eyebrows), ataxic, choreoathetoid movement of extremities and trunk, speech disturbances, mental deterioration, eventual rigidity, dementia, and incontinence o Imaging MRI, CT, DNA testing o Additional info fam hx • Examination o Additional findings may need to be admitted to psychiatric facility for severe depression and suicide • Management o Tx meds (anticonvulsants, antipsychotics, Haldol, Reserpine, Perphenazine), PT (pt/fam ed, relaxation, functional movement, balance, postural stability, AD, positioning), OT, ST • Outcome o PT outcome max functional outcomes w/in disease process o Long-term effects fatal 15-20 yrs after manifestation, end-stage has total physical and mental incapacitation

sciatica

• Summary o Compression of sciatic nerve d/t herniated disc inflammatory response and subsequent damage o LBP and gluteal pain that radiates down back of thigh o Increased pain w/lifting, sitting, FB, or twisting • Diagnosis o Condition that produces symptoms PL protrusion of IV disk against NR; sciatica involves L4-S3 o Injured structures inner NP bulges through outer AF, hits sciatic nerve and causes inflammation and damage via compression • Inference o Contributing factors d/t natural aging, common in 40-60 y/o • Confirmation o Clinical presentation LBP and gluteal pain (dull, aching, or sharp, can be gradual or sudden onset) that radiates down back of thigh, N+T to dermatomal distribution, limited l/s ROM, TTP and muscle guarding o Imaging myelogram, discography, CT, MRI o Additional info SLR test should reproduce symptoms • Examination o History o Tests and measures o Additional findings increased pain w/sitting, lifting, twisting, and bending; prolonged bedrest will make pt worse (contraindicated) • Management o Tx rest, decrease disc pressure, pt ed, meds (NAIDs, steroid injections), PT (biomechanics, lumbar and core stabilization, McKenzie exercises, aerobic exercise) • Outcome o PT outcome improve w/conservative tx in 2-4 mo o Long-term effects may need sx (laminectomy, discectomy, chemonucleolysis) if neuro symptoms increase or don't improve

TOS

• Summary o D/t compression and damage to brachial plexus nerves, subclavian vascular supply, and/or axillary artery o Contributing factors presence of cervical rib, abnormal 1st rib, postural deviations, scalene hypertrophy or spasm, elongated c/s TPs o 2-3x F > M, 30-40 y/o • Diagnosis o Condition that produces symptoms neurovascular compression of brachial plexus usually btwn interscalene triange and inf border of axilla o Injured structures compression and damage to brachial plexus nerves (can progress to neurapraxia and axonotmesis), subclavian vascular supply, and/or axillary artery • Inference o Contributing factors presence of cervical rib, abnormal 1st rib, postural deviations, scalene hypertrophy or spasm, elongated c/s TPs, chronic UE hyperabd, body comp, degenerative disorders • Confirmation o Clinical presentation diffuse pain in arms (worst at night), paresthesias in fingers, wkns, muscle wasting, poor posture, edema, discoloration, pain may radiate up into neck or down o Imaging N/A, only to r/o o Additional info Adson maneuver, Wright test, Roos test, Halstead maneuver, Allen test, costoclavicular and hperabd tests • Examination o Additional findings difficulty sleeping, carrying, lifting OH • Management o Tx anti-inflammatory meds, PT (posture, breathing, stretching ant and strengthening post, joint mobs, body mechanics), sx if conservative fails after 3-4 mo (75% successful) • Outcome o PT outcome usually return in 4-8 wks

vestibular disorders

• Summary o D/t disruption of sensory info processed by inner ear and brain w/respect to body's control of balance and eye movement o Peripheral > central o Diverse effects range from spont. recovery to permanent disability • Diagnosis o Condition that produces symptoms disruption to vestibular system d/t injury to processing area, genetic, environmental, and idiopathic etiology ♣ Ex: Meniere', BPPV, labyrinthitis, ototoxicity, acoustic neuroma o Injured structures peripheral (dysfunction of auditory vestibular structures of inner ear) > central (NS dysfunction) • Inference o Contributing factors ear infection, whiplash, head injury, idiopathic (older) • Confirmation o Clinical presentation variable (intermittent or persistent, single time or recurring), many resolve w/o intervention, vertigo, dizziness, nausea, altered balance, auditory changes, difficulty w/cognition, memory, coordination o Imaging N/A, r/o w/MRI or CT o Additional info vestibular testing (vestibule-ocular reflex, Dix-Hallpike, electronystagmography, videonystagmography), balance testing (postural sway, gait, etc.), auditory testing by audiologist • Examination o Additional findings falls, irritability, decreased self-esteem or depression in impairments have been persistent • Management o Tx meds (vestibular suppressants (benzo, anticholinergics, antihistamines), steroids (prednisone), antibiotics15 or antivirals), nutrition (fluid balance), psychological counseling (coping), sx, vestibular rehab/PT (habituate to symptoms via adaptation, substitution, cognitive, and symptom prediction, balance, proprioception, vestibuloocular reflex training) --Ex: gaze stabilization w/head movement, SLS on variable surfaces, gait w/variable surfaces and head movements o Home care symptom accommodation and habituation exercises • Outcome o PT outcome usually successful, earlier initiation helps decrease falls, need to set realistic goals and emphasize habituation (instead of full recovery) Long-term effects large range from spont recovery to permanent disability

TBI

• Summary o D/t open head injury w/penetration through skull or closed head injury where brain makes contact w/skull 2* to sudden, violent accel/decel o Injury can include swelling, axonal injury, hypoxia, hematoma, hemorrhage, and ICP changes o High risk ages (M>F) 0-4, 15-19, >65 • Diagnosis o Condition that produces symptoms d/t open or closed head injury or 2* to anoxia (near drowning, cardiac arrest) o Injured structures 1* damage at site of impact, 2* damage d/t metabolic and physiologic rxns, injuries include swelling, axonal injury, hypoxia, hematoma, hemorrhage changes in ICP • Inference o Contributing factors falls and MVAs, M > F, ages 0-4, 15-19, > 65 y/o • Confirmation o Clinical presentation altered consciousness, cognitive and behavioral deficits, changes in personality, motor impairments, changes in tone, speech and swallowing issues o Imaging CT or MRI, x-ray of c/s o Additional info full neuro eval (mental, CN, tonal assessment, pupillary reactivity), GCS, RLA levels of cognitive functioning • Examination o Additional findings HO, contractures, monitor ICP, skin breakdown, DVT, • Management o Tx stabilize pt and control ICP, possible sx, meds (vasoconstrictors, psychotropic, hypertensive, and antispasticity agents), PT (sensory stim, ROM, functional mobility, behavioral training, compensatory strategies, vestibular rehab, WC/AD/orthotic use) o Home care consistency is key, community re-integration • Outcome o Long-term effects depends on degree of damage, many have lifelong deficits and many others die

PD

• Summary o Degenerative disorder resulting in decreased dopamine production w/in substantia nigra of BG o Hypokinesia, difficulty initiating or stopping movement, festinating and shuffling gait, bradykinesia, poor posture, cogwheel or lead pip rigidity o Dopamine replacement therapy (Levadopa, Sinemet, Madopar) decrease bradykinesia, rigidity, and tremor • Diagnosis o Condition that produces symptoms disturbance of balance and voluntary movement d/t decreased dopamine production (and subsequent ACh imbalance) in substantia nigra of BG o Injured structures dopamine-producing neurons in substantia nigra (subcortical grey matter) of BG • Inference o Contributing factors unknown; genetic defect, CO toxicity, other neurodegenerative diseases (AD, HD) • Confirmation o Clinical presentation increased risk w/age, resting (pill-rolling) tremor, balance distrbances, trouble w/bed mobility, trouble w/fine motor control and ADLs (dressing, writing, etc.), bradykinesia, akinesia (initiation), festinating and shuffling gait, poor posture, dysphagia, cogwheel or leadpipe rigidity, "freezing" during speech, ambulation, etc., mask-like facial expression o Imaging N/A, can only use to r/o o Additional info hard to dx bc slowly progreses over 20-30 yrs • Examination o Additional findings stooped posture, increased fall risk • Management o Tx meds for rigidity, bradykinesia, and tremor (Sinemet, Levdopa, Madopar), PT (functional mobility, VC and oral FB are key, balance, gait, rotation, respiratory therapy), OT, ST o Home care regular exercise routine is very helpful • Outcome o Long-term effects doesn't ususally affect lifespan if dx btwn 50-60 y/o but have worsening symptoms, deconditioning, and complications leading to death

MS

• Summary o Demyelination of myelin sheaths plaque development, decreased NCV, eventual failure of impulse transmission o Visual problems, paresthesias, sensory changes, clumsiness, wkns, ataxia, balance dysfunction, fatigue o Intervention regulation of activity level, relaxation and energy conservation techniques, normalization of tone, balance activities, gait training, core stabilization • Diagnosis o Condition that produces symptoms demyelination resulting in decreased efficiency of nerve impulse transmission o Injured structures myelin sheaths of nerves in brain and SC, lesions are randomly scattered throughout CNS • Inference o Contributing factors unknown; genetics, viral infection (autoimmune response), environmental factors (temperate climate), 2x F > M, white, 20-35 y/o • Confirmation o Clinical presentation relapsing-remitting (85%) vs. secondary-progressive vs. primary-progressive vs. progressive-relapsing, initially have visual problems, paresthesias, and sensory changes, clumsy, wkns, ataxia, balance issues, fatigue o Imaging hard to dx early, MRI and CSF testing o Additional info dx if experience 2 separate attacks and evidence of 2 separate lesions • Examination o Additional findings emotional lability, depression, dementia, psychological problems, spasticity, tremor, wkns, paralysis, sexual dysfunction, loss of bowel and bladder control • Management o Tx meds (ABC (immunomodulary)), PT (relaxation, energy conservation, normal tone, balance and gait, postural stability, pt/fam ed, AD/WC use), OT, ST o Home care submax exercise/endurance program, aquatics • Outcome o PT outcome heat, stress, infection, trauma, and pregnancy can influence exacerbations o Long-term effects permanent damage and disability, die from 2* complications (atrophy, pressure sores, contracture, fx, renal infection, pneumonia), un-tx will need WC in 15 yrs, high suicide

CTS

• Summary o Greatest risk 35-55 y/o; F > M o Often get APB atrophy followed by thenar muscles o Confirm dx w/electromyography, Tinel's sign, Phalen's test • Diagnosis o Condition that produces symptoms formed by transverse carpal lig, scaphoid, trapezium, hamate, pisiform, and ligs; median nerve, 4 FDP and FDS tendons, and FPL tendon pass through the tunnel; CTS d/t compression of median nerve in tunnel o Injured structures compression (normal pressure = 2-10 mm Hg, but CTS can be > 30 mm Hg) of median nerve in carpal tunnel causing ischemia of nerve and sensory and motor disturbances in distribution • Inference o Contributing factors edema, inflammation, tumor, fibrosis, repetitive use, RA, pregnancy, diabetes, trauma, tumor, hypothyroidism, wrist injury, congenital tunnel narrowing, B6 deficiency • Confirmation o Clinical presentation 35-55 y/o, F > M, sensory changes and paresthesia in hand, night pain, hand wkns, atrophy (APB, thenar), decreased grip strength, clumsiness, decreased wrist mobility o Imaging electromyography, electroneurographic studies o Additional info Tinel's, Phalen's, tethered median nerve stress test • Examination o Additional findings unrelieved compression creates neurapraxia w/demyelination and eventual axonotmesis and Wallerian degeneration; may present w/ape hand deformity • Management o Tx meds (methylprednisolone), corticosteroids, splinting PT (stretching, carpal mobs), sx if conservative fails (release carpal lig), post-op PT for 6-8 wks (initially avoid wrist flex and gripping (4 wks), always avoid RD) • Outcome o PT outcome conservative should improve in 4-6 wks, post-op tx lasts 6-8 wks o Long-term effects range from none to debilitating, depends on degree of severity • Comparison o Compression in tunnel of Guyon on ulnar nerve d/t leaning on hands, repetitive gripping, or trauma; get paresthesias in ulnar nerve distribution

ALS

• Summary o Highest risk btwn 40-70 y/o; M > F o UMN and LMN involvement w/wkns progressing from dist to prox o Usually live for 2-5 yrs post-dx 20-30% survive > 5 yrs • Diagnosis o Condition that produces symptoms chronic degenerative disease w/UMN and LMN resulting in demyelination, axonal swelling, and atrophy in cortex, premotor areas, sensory cortex, and temporal cortex o Injured structures rapid degeneration of pyramidal cells in cortex and cell bodies of LMN resulting in denervation of muscle fibers, atrophy, and wkns • Inference o Contributing factors 90% unknown, genetic (autosomal dom), virus, metabolic disturbance, lead and aluminum toxicity; M > F, 40-70 y/o • Confirmation o Clinical presentation LMN signs from dist to prox (asymmetric muscle wkns, cramps, atrophy, fasciculations); UMN signs (incoordination, spasticity, clonus, + Babinski); bulbar involvement (dysarthria, dysphagia, emotional lability); fatigue, oral motor impairment, fasciculations, spasticity, motor paralysis, respiratory paralysis o Imaging electromyography, muscle biopsy, CT o Additional info symptoms w/UMN and LMN involvement, no sensory impairment, must r/oMS, SC tumors, progressive MD, Lyme disease, syringomyelia • Examination o Additional findings preserved sensation, eye movement, and bowel and bladder function • Management o Tx supportive care and symptomatic therapy, meds (riluzole/Rilutek, anticholinergic, antispasticity, antidepressants), PT (low-level exercise, energy conservation, mobility, AD and WC use, improve function, pt/fam ed), OT, ST, respiratory therapy, nutritional therapy • Outcome o PT outcome can help w/function but cannot stop disease progression o Long-term effects rapidly progressing, usually only live for 2-5 yrs post-dx d/t respiratory failure • Comparison o Muscular dystrophy (MD) progressive muscle degeneration w/o sensory component d/t absence of dystrophin w/in skeletal muscle; presents early in life w/atrophy, contractures, and cardiac and respiratory wkns

SCI C7

• Summary o Impaired cough and ability to clear secretions, altered breathing pattern, poor endurance o Outcomes indep w/feeding, grooming, dressing, self-ROM, WC mobility, transfers, driving w/adapted car o Lowest innervated muscles triceps, EPL and EPB, extrinsic finger exts, FCR • Diagnosis o Condition that produces symptoms usually d/t traumatic injury to SC from compression or flex/ext of spine w/o rot o Injured structures displacement or compression of SC w/subsequent hemorrhage and vascular damage, get 2* damage from biochemicals and inflammation, C7 is most dist segment of SC w/both sensory and motor intact • Inference o Contributing factors MVA, violence, falls, M > F, white, 15-30 y/o • Confirmation o Clinical presentation immediate spinal shock (total depression of NS function (days) w/flaccid paralysis and loss of sensation and reflexes), halo device to stabilize spine, spasticity, AD, thermoregulation problems, impaired cough and ability to clear secretions, altered breathing, poor endurance, risk of contractures and impaired skin integrity o Imaging x-rays, myelogram o Additional info MOI, full neuro exam • Examination o Additional findings OH, pressure sores, spasticity, HO, AD, sexual dysfunction, respiratory complications, pain management • Management o Tx acutely need to medically stabilize pt (methylprednisolone), inpatient rehab (positioning, ROM, respiration) for 6-8 wks, compensatory techniques, WC/AD use, transfers, community reintegration • Outcome o PT outcome should be indep living w/adaptive equipment (feeding, grooming, dressing, self ROM, WC mobility, transfers, driving) o Long-term effects no cure, ongoing MS and CP issues, 40% have life expectancy > 45 yrs

central cord syndrome

• Summary o Incomplete SC lesion often d/t c/s hyperext injury o Motor loss in UE > LE o Most common incomplete lesion accounts for ~30% of all incomplete forms of tetraplegia • Diagnosis o Condition that produces symptoms damage to central aspect of SC resulting in incomplete SC lesion often d/t hyperext of c/s o Injured structures bleeding into central gray matter of SC • Inference o Contributing factors usually c/s hyperext, can also be c/s spondylosis, narrowing or congenital defect of c/s, tumor, RA, syringomyelia, M > F, > 50 y/o • Confirmation o Clinical presentation motor loss in UE > LE, rarely affects sacral segments, 55-85% resolve any bowel and bladder issues in 6 mo o Imaging MRI, CT, x-ray • Examination o Additional findings all present differently based on location of lesion; may have AD, spasticity, neurogenic bowel and bladder, allodynia, and pressure ulcers • Management o Tx meds (Methylprednisolone (w/in 8 hrs for improved neuro recovery), BP meds, antispasticity, anticonvulsants, anticoagulants, antidepressants) physiatry, PT (functional mobility, AD use, balance, proximal stabilization, strength, endurance), OT, vocational counseling, social services • Outcome o PT outcome assist to max functional outcomes o Long-term effects younger pts do better than older pts, early hand function, improvement in strength, and no LE involvement indicate better outcomes • Comparison o Anterior cord syndrome (ACS) affects ant 2/3 of SC d/t c/s flex or ASA; injury complete loss of motor function (corticospinal) and pain and temp (spinothalamic) below lesion; worst prognosis (10-15% achieve functional recovery)

CRPS

• Summary o Increase SNS activity norepinephrine vasoconstriction pain and increased peripheral sensitivity o M:F = 1:3; all ages but 35-60 y/o most common o Intense burning and chronic pain that spreads pros • Diagnosis o Condition that produces symptoms disturbance in SNS leading to increase peripheral NE and increased pain/sensitivity in extremity (usually after some sort of trauma) o Injured structures sensory nerve fibers (symp efferents) • Inference o Contributing factors trauma, sx, CVA, TBI • Confirmation o Clinical presentation intense, burning, and chronic pain ♣ Stage I (acute - edema, stiffness, dryness), II (dystrophic - constant pain, cont edema, trophic skin changes), III (atrophic - hardened edema, atrophic changes in fingers and toes) o Imaging x-rays, thermographic studies • Examination o Additional findings progresses to bone demineralization and ankylosis muscle atrophy, spasm, contracture, depression, anxiety • Management o Tx meds (NSAIDs, corticosteroids, amitriptyline, baclofen, bisphosphonate), sx (symp block), PT (pt/fam ed, desensitization, aqua, relaxation techniques) o Home care stretching, ROM, light WB activity • Outcome o PT outcome better if begin early in disease process to break pain cycle o Long-term effects can spont resolve or cont for yrs

DS

• Summary o Manifestations hypotonia, flattened nasal bridge, Simian line (palmar crease), epicanthal folds, enlarged tongue, developmental delay o Usually detect 60-70% of women carrying child w/Down o Exercise is key to avoid inactivity and obesity • Diagnosis o Condition that produces symptoms trisomy 21 d/t nondisjunction, translocation, or mosaicism resulting in 47 chromosomes o Injured structures chromosome 21 • Inference o Contributing factors unknown etiology; increased maternal age, environmental factors (virus, paternal age, meds) • Confirmation o Clinical presentation intellectual disability, hypotonia, flattened nasal bridge, almond eyes, abnormal ears, Simian line, epicanthal folds, enlarged tongue, CHD, developmental delay, MS disorders o Imaging o Additional info triple screen during pregnancy (Alpha-fetoprotein, HCG, unconjugated estrogen) via amniocentesis, umbilical blood sample, or chorionic villus sampling; karyotype • Examination o Additional findings 2* complications such as C1-2 instability, sensory, hearing, and visual impairments, umbilical hernia, respiratory compromise, AD, celiac disease, epilepsy, constipation, blood, dermatologic, and MS disorders • Management o Tx achieve max function, focus of PT on developmental delay, hypotonia, lig laxity, and poor strength o Home care need routine exercise, positioning is key • Outcome o Long-term effects shorter life expectancy, 80% live to 55 y/o

GB

• Summary o Motor wkns (dist to prox), sensory impairment, possible respiratory paralysis o Unknown etiology possibly autoimmune response to respiratory infection, flu, immunization, or sx o Usually have full recovery 20% have remaining neuro deficits, 3-5% die from respiratory complications • Diagnosis o Condition that produces symptoms temp inflammation and demyelination of peripheral nerves resulting in motor wkns (dist prox), sensory impairment, and possible respiratory paralysis o Injured structures myelin sheaths of peripheral nerves (motor > sensory) get attacked by autoantibodies • Inference o Contributing factors unknown; autoimmune response (flu, virus, immunization, bacterial infection, sx) • Confirmation o Clinical presentation M > F, white > AA, young adults and 50-80 y/o, distal symmetrical motor wkns and mild dist sensory impairments, progress towards UEs and head, peak symtoms in 2-4 wks, may have absence of DTRs, muscle and respiratory (life-threatening) paralysis, and inability to speak and swallow, usually have 2-4wk static period followed by gradual recovery (mo-yrs) o Imaging CSF sample • Examination o Additional findings 30% require respiratory assistance, may also have bladder wkns, deep muscle pain, and ANS symptoms (arrhythmia, postural hypotension, heart block) • Management o Tx possible hospitalization (trach, cardiac monitoring), meds (immunosuppressants (no corticosteroids), narcotics), PT (ROM, positioning, light exercise, avoid overexertion/fatigue, breathing, ADs/WV/orthotics, functional mobility) o Home care breathing exercises, incentive spirometry • Outcome o PT outcome recovery can take 3-12 mo o Long-term effects most have full, but slow, recovery; 3-5% die from respiratory complications • Comparison o Polyneuropathy progressive condition affecting nerves, usually d/t DM, develops slowly, bilaterally, and symmetrically, usually starts w/sensory loss in dist. LEs

SCI L3 para

• Summary o Partial innervation of gracilis, iliopsoas, QL, RF, sartorius and full UE use o Additional findings sexual dysfunction, non-reflexive bladder, need for bowel program, UTIs, muscle contracture, pressure sores o Should be able to live indep. w/ed for management of disability • Diagnosis o Condition that produces symptoms usually d/t traumatic injury to SC from compression or flex/ext of spine w/o rot o Injured structures displacement or compression of SC w/subsequent hemorrhage and vascular damage, get 2* damage from biochemicals and inflammation, L3 is most dist. segment of SC w/both sensory and motor intact • Inference o Contributing factors MVA, violence, falls, M > F, white, 15-30 y/o • Confirmation o Clinical presentation immediate spinal shock (total depression of NS function (days) w/flaccid paralysis and loss of sensation and reflexes), spinal orthosis for stability, spasticity, full use of UEs, hip flex, add, and knee ext o Imaging lab tests (CBC, electrolytes), x-ray, CT, MRI o Additional info thorough neuro exam, rectal tone and perianal sensation, cutaneous abd reflex, bulbocavernous reflex, Babinski • Examination o Additional findings sexual dysfunction, nonreflexive baldder, bowel program, flaccid paralysis below lesion, risk of pain, UTI, contracture, and pressure sores • Management o Tx stabilization of airway and IV methylprednisolone, TLSO, PT (transfers, bed mobility, WC/AD use, ROM, strengthening, balance, orthotics), OT, physiatry, nutrition, counseling • Outcome o PT outcome 4-8 wks inpatient rehab, should have indep function from WC and ambulation level, outcome based on emotional stability, co-morbidities, and motivation o Long-term effects increased risk of osteoporosis, pressure ulcers, HTN, and HO, pneumonia is leading cause of death

cauda equina

• Summary o Peripheral nerve injury resulting from damage and loss of function of 2 or more nerves in cauda equina can be d/t compression of NRs from spinal structure pathology, trauma, infectious conditions, tumor, iatrogenic factors o Self-limiting but longer pt has symptoms prior to tx, complete recovery is less likely • Diagnosis o Condition that produces symptoms peripheral nerve injury resulting from damage and loss of function of 2 or more nerves in cauda equina o Injured structures cauda equina (paired lower l/s, s/s, and c/s NRs that extend beyond conus medullaris (~L1) and provide sensation to "saddle area", LE motor innervation, parasymp to bowel and bladder, voluntary control of sphincters) • Inference o Contributing factors compression d/t spinal structure pathology, trauma, infection, tumor, iatrogenic factors • Confirmation o Clinical presentation altered reflexes, pain, decreased strength and sensation; can also get severe back pain, functional impairment, diminished sensation in saddle region, bowel and bladder dysfunction, sexual dysfunction; onset can be gradual or rapid; more common in adults but can also happen in kids o Imaging MRI, x-ray or CT o Additional info LE strength, sensation, and DTRs, perineal sensation, reflexes, and rectal tone • Management o Tx nerve root decompression via radiation or chemo for tumor, anti-inflammatory or antibiotics; PT (ther ex, functional mobility, coordination, sensory stim, orthotic, AD training) • Outcome o PT outcome based on degree of damage, cont PT until pt has reached realistic goals o Long-term effects self-limiting but longer w/o tx, the worse the outcome

ALZ Dx

• Summary o Progressive disorder leading to deterioration and irreversible damage w/in cerebral cortex and subcortical areas of brain o Starts w/changes in higher cortical functions trouble w/memory, concentration, and new learning o Typical course 7-11 yrs w/death from infection or dehydration • Diagnosis o Condition that produces symptoms progressive neuro disorder resulting in loss of neurons in cortex and subcortical areas of brain o Injured structures breakdown of nerves d/t neurofibrillary tangles, amyloid plaques, cerebral atrophy • Inference o Contributing factors unknown; possibly low levels of NTs, higher aluminum levels, genetic inheritance, autoimmune disease, abnormal amyloid processing, virus • Confirmation o Clinical presentation change in higher cortical function (memory, concentration, learning), loss of orientation, word finding difficulties, emotional lability, depression, poor judgement, impaired ability to perform self-care; behavioral and motor problems (aphasia, apraxia, perseveration, agitation, violent or socially unacceptable behavior) in middle phase; eventually lose all ability to learn and long term memory; end-stage has severe intellectual and physical destruction, incontinence, functional dependence, inability to speak, seizures o Imaging req postmortem biopsy o Additional info need 2 of following symptoms - deficits in cognition, memory, related cognitive functioning • Examination o Additional findings high risk of infection and pneumonia; contractures, decubui (ulcer), fx, pulmonary compromise • Management o Tx meds (Tacrine/Cognex, donepezil/Aricept, rivastogmine/Exelon) to inhibit acetylcholinesterase, alleviate cognitive symptoms, and control behavioral changes (only last 6 mo, have bad side effects), PT (pt/fam ed, max function, safety, functional mobility, gait training), long term care facility o Home care cont w/activity as tolerated, compensatory strategies for memory, exercise, participate in ADLs • Outcome o PT outcome helpful but cannot alter course of disease o Long-term effects death d/t infection and dehydration in 7-11 yrs • Comparison o Multi-infarct dementia step-like symptoms, > 70, M > F, increased risk w/HTN, neuro deficits (hemiplegia, emotional lability)

CP

• Summary o Spastic (UMN damage) vs. athetoid (BG damage) o Motor delays, abnormal muscle tone and control, reflex abnormalities, poor postural control, balance impairments o 50-60% of kids have intellectual disability and epilepsy • Diagnosis o Condition that produces symptoms group of non-progressive movement disorders d/t brain damage o Injured structures hypoxic and ischemic injuries disrupt normal metabolism resulting in global damage to fetus; classified by neuro dysfunction and limb involvement; spastic (UMN) vs. athetoid (BG) • Inference o Contributing factors multifactorial etiology, prenatal (Rh incompatability, maternal malnutrition, hypothyroidism, infection, diabetes, chromosome abnormalities) vs. perinatal (premature birth, breech delivery, low birth weight, prolapsed cord, placenta abruption asphyxia) vs. postnatal (CVA, head trauma, neonatal infection, brain tumor) risk factors; most common risk factor = prenatal cerebral hypoxia • Confirmation o Clinical presentation common NM disorder of posture and controlled movement w/variable presentation, high or low tone or athetoid movement, monoplegia vs. hemiplegia vs. quadriplegia, motor delays, abnormal tone and motor control, abnormal reflexes, poor postural control, intellectual disability, vision, hearing and perception impairments o Imaging electroencephalography (EEG) • Examination o History maternal pregnancy course, risk factors o Additional findings complications (aspiration, pneumonia, contractures, scoliosis), 50-60% have intellectual disability • Management o Tx meds (anti-spasticity, -anxiety, -convulsant), PT (sensory integration, normalize tone, pt/fam ed, positioning, strengthening, balance, mobility, AD/WV/orthotic use) • Outcome o PT outcome max functional outcomes, should ambulate by 8 o Long-term effects non-progressive but permanent condition, mild-mod CP have normal lifespans but most die by 10 if severe • Comparison o Arthrogryposis multiplex congenital (AMC) occurs in utero, non-progressive, born w/multiple contractures, normal intelligence and lifespan but have trouble living indep

ankylosing spondy

• Summary o Systemic inflammation of spine and larger peripheral joints o M:F = 2-3:1; 20-40 y/o onset o Recurrent and insidious onset of back pain morning stiffness, impaired spinal ext • Diagnosis o Condition that produces symptoms chronic inflammation that destroys lig-bone junction w/subsequent fibrosis and ossification o Injured structures SIJ, IV discs, spine, costovertebral and apophyseal joints, connective tissue, larger peripheral joints • Inference o Contributing factors progressive systemic disorder, genetic (HLA-B27) and environmental influence, M > F, 20-40 y/o • Confirmation o Clinical presentation LBP, morning stiffness, dec spinal ext and joint ROM, flattened spinal curves o Imaging x-ray (bamboo spine) • Examination o Additional findings iritis, uveitis, A-A instability, CP issues • Management o Tx meds (NSAIDS, DMARDs (methotrexate), indomethacin), PT (postural, energy conservation, ROM (esp ext), aqua, low impact) • Outcome o Long-term effects slow progression over 15-25 yrs, stiffness and joint limitation •

Erb's palsy

• Summary o Usually affects muscles supplied by C5 and C6 loss of function of RTC, deltoid, brachialis, coracobrachialis, and biceps o Brachial plexus injury in newborn d/t difficult delivery d/t large baby, breech position w/prolonged labor, or use of forceps o Flaccid paralysis (aka waiter's tip deformity) loss of shoulder function, elbow flex, forearm sup, hand in pinch grip • Diagnosis o Condition that produces symptoms upper brachial plexus injury from over-stretching usually d/t difficult birth (can also occur in adults) o Injured structures injury of brachial plexus (avulsion, rupture, neuroma, neurapraxia) at Erb's point (C5-C5) and affecting muscles of shoulder and elbow • Inference o Contributing factors difficult delivery (large baby, breech, forceps), d/t over-stretching of brachial plexus • Confirmation o Clinical presentation flaccid paralysis (aka waiter's tip deformity) resulting in loss of shoulder function, elbow flex and sup, and hand held in pinch grip o Imaging MRI, EMG, NCS o Additional info active movement scale, Gilbert Shoulder Classification, Pediatric Outcome Data Collection Instrument • Examination o History labor and delivery (infants) vs. MOI (adults) • Management o Tx OT and PT (ROM, strengthening, UE functional activities), may perform sx in conservative tx fails (splint 3-4 wks) • Outcome o Long-term effects 9/10 recover conservatively (3-4 mo), nerves regenerate at fixed rate (1 in/mo) • Comparison o Klumpke's palsy brachial plexus injury (C7, C8, T1) from traction of UE in abd; present w/elbow flex and sup, wrist ext, MCP hyperext, and IP flex resulting in "claw-hand"

DMD

• Summary o X-linked recessive trait manifests in M, F are carriers o Waddling gait, prox muscle wkns, toe walking, pseudohypertrophy of calf, difficulty w/stairs o Usually has rapid progression w/inability to ambulate by 10-12 y/o and death in teenage yrs (sometimes in 20s) • Diagnosis o Condition that produces symptoms progressive NM degenerative disorder d/t mutation of dystrophin gene (Xp21) leading to replacement of muscle w/fat and connective tissue o Injured structures abnormal dystrophin results in weakening of cell membranes and destruction of myofibrils • Inference o Contributing factors X-linked recessive (M get it, F carry it) • Confirmation o Clinical presentation begins at 2-5 y/o in M, waddling gait, prox muscle wkns, clumsy, toe-walking, excessive lordosis, pseudohypertrophy of gastroc, trouble getting off floor (Gowers'), cognitive and behavioral deficits, lose ability to walk by 10-12 y/o (rapid progression) o Imaging electromyography, muscle biopsy • Examination o Additional findings disuse atrophy, contracture, scolioisis, weight gain, cardio and respiratory impairments, MS deformity, GI dysfunction • Management o Tx maintain function as long as possible, meds (glucocorticoids, immunosuppressants), PT (assess MMT often, use ADs and orthotics, respiratory care, positioning, pt/fam ed and support) • Outcome o Long-term effects death d/t cardiorespiratory problems in teens or 20s

type I and II errors

• Type I error (alpha error) = researcher error when they reject null and SHOULD NOT HAVE o Saying that there is a diff / relationship when there is NOT o When level of sig at 0.01, there is a 1% chance of a type I error o FALSE POSITIVE FINDING - saying that it is there when it is not • Type II error (beta error) = researcher error where they do NOT reject null, when they SHOULD HAVE o Saying that there isn't a diff / relationship when there ISSSSS o FALSE NEGATIVE FINDINGS - saying that there isn't when there is

Brunstrom

• USE synergy patterns to assist w/developing movement combos outside of synergy patterns but ONLY to certain point • key terminology o limb synergy = group of muscles which produces predictable pattern in flex or ext o Associated reactions = involuntary and automatic movement as result of intentional active or resistive movement of ad different body part (happens when you overwork them) o Overflow = muscle activation of involved extremity d/t intense action of an uninvolved muscle/group o homolateral synkinesis = flexion of involved UE will facilitate flexion of involved LE o Raimiste's phenomenon = involved LE will abd or add w/applied resistance to uninvolved LE in the same direction o Souques' phenomenon = raising involved UE > 100* w/elbow ext will produce ext and abd of fingers • Stages of recovery = progression through abnormal tone, reflex activity and voluntary mvmt o 1 no volitional movement o 2 basic limb synergies beginning of spasticity o 3 synergies performed voluntarily MAX SPASTICITY o 4 decreasing spasticity not all movement is in synergies ex: hand behind back o 5 more decreased spasticity indep from limb synergies ex: hand behind head o 6 isolated joint movements have coordination They're pretty near normal

vestibule-ocular and -spinal reflexes

• Vestibuloocular reflex (VOR) = supports gaze stabilization through eye movement that counters mvmtsof the head o eyes stay still while head moves • Vestibulospinal reflex (VSR) = stabilize body while head is moving manage upright posture o Righting and equilibrium reactions, postural control during walking

4-5 months

• WB on ext arms in prone and pivots to reach toys • rolls to SL • plays with feet to mouth • head steady in sitting and turns head • can sit alone briefly • bears all weight through legs in supported standing grasps and releases toys uses ulnar-palmar

q angle

• angulation measuring from midpatella to ASIS and tibial tubercle o males = 13* o females = 18*

NDT, Bobath

• based on the hierarchical model of neurophysiological function abnormal posture and tone caused by lack of supraspinal inhibition (cortex not overriding cuz effed) • constructs o need to learn to control mvmt through activities which promote NORMAL mvmt patterns and integrate FUNCTION o NO COMPENSATION or using of the reflexes / associated reactions o Use developmental sequence o Use Reflex inhibiting postures (RIPs) = static positions that inhibit abnormal tone and reflexes ♣ Gives them a feeling of "normal" o Use Key points of control = specific points (shoulder, pelvis, hand, foot) that influence and facilitate posture, alignment, and control ♣ Proximal points of control = start here ♣ Distal points of control = progression o Balance of muscle groups during intervention o Use rotation o Move in and out of midline to give orientation to midline

apraxia

• cannot performed purposeful learned mvmts -- no sensory or motor impairment stopping o constructional apraxia = cannot reproduce geometric figures and designs ♣ cannot visually analyze HOW TO PERFORM a task o ideational apraxia = cannot form initial motor plan and sequence tasks ♣ proprioceptive input necessary for mvmt is impaired ♣ ex: given screwdriver and try to use as pencil; do tasks out of order o ideomotor apraxia = person can plan but NOT perform task ♣ may have automatic mvmt BUT cannot impose additional mvmt on command ♣ ex: when you ask them to show you how to brush teeth, they cannot BUT they can tell you

lymphedema

• chronic, incurable condition characterized by accumulation of protein-rich fluid (aka lymph) in body, esp in extremities • types o Primary = abnormal development of lymphatic system (females, LEs) ♣ Ex: absence of vessels, decreased number, increased size (valves incompetent), Milroys (inherited in infancy; B LE edema) o Secondary = result of another disease or injury that damages lymphatic system ♣ Ex: trauma, sx, radiation, tumor, BREAST CA SX (most common), filariasis (tropical parasite) • 2 types of insufficiencies o Dynamic = there's too much fluid in the system, results in PITTING EDEMA (compressible); MOST COMMON --Ex: chronic venous insufficiency, CHF, pregnancy o Mechanical = injury makes it so system has difficulty transporting, results in NON-PITTING EDEMA (harder and not compressible) o Combined = both inc in fluid AND dec transport capacity Dx: • medical hx, physical exam, BUT imaging tech can help o direct/indirect lymphography o lymphoscintigraphy preferred o CT, MRI help to see tumors which may be causing

measurement validity

• degree to which a measurement represents what it is actually supposed to represent o Face validity = appears to test what it is supposed to ♣ Not good enough for us but important for the pt so they can see how it relates o Content validity = degree to which a measurement reflects ALL THINGS IMPORTANT to that particular construct ♣ Ex: McGill pain > VAS cuz McGill gives intensity, location, quality and duration too o Construct validity = ability of a tst to measure an abstract construct ♣ Evidence is provided through logical argument based on theoretical and research evidence • Known groups method = look at its abilty to diff btw known hgh level and known low levels • Convergent = look at 2 tests supposed to measure SAME construct and determine relationship o Ex: MMT measureing innervation status of muscel -- We could prove it has construct validity is compare relationship btw MMT and EMG • Discriminant = look at relationship between 2 tests which are supposed to measure DIFF constructs o Criterion-related validity = abilty of 1 test (target test) to predict results of another test when the other test is a godl standard ♣ Concurrent = compared at SAME TIME • Ex: HR by palpation peripheral pulses and EKG ♣ Predictive = score on target test is used to predict score on future godl standard test • Ex: use GPA / GRE to predict doing well in grad school / NPTE ♣ Prescriptive = score on target test determines approp intervention • Judged based on successful outcome of treatment

milwaukee

• designed to promote re-alignment of the spine due to scoliotic curve or kyphosis o Custom made and extends from pelvis to upper chest (TLSO) ♣ Also have a CTLSO version which has a neck ring and occipital pad connected to 4 upright bars o Corrective padding also applied to severe areas of curve o Another type of brace to correct scoliosis like this Boston Brace

lipedema

• disease affecting size and distribution of adipose tissue o usually symmetric and in LEs, cannot lose weight like if just obesity Think: women who have "big legs" o S+S (usually arise during times of sig hormone change) = tenderness to palpation, column-like fat dist in LEs, inc edema throughout day o Tx = weight mgmt, CDT

drug admin

• enteral = GI o oral most common bc easy to perform on own and allows a slow, controlled release of drug o sublingual o rectal • arenteral = outside GI o inhalation o topical o transdermal o injection ♣ IV = 100% bioavailable ♣ inta-arterial ♣ subQ ♣ IM muscle soreness ♣ intrathecal = into sheath; CNS w/ no BBB

active cycle breathing

• forced exp technique) = couples breathing with huff cough o Helps secretion clearance those with asthma (idea behind it is you are mobilizing secretions) ♣ Release SLOW = LOW volume = smaller peripheral airways ♣ Release FAST = HIGH volume = LARGER peripheral airways

GERD

• incompetent lower esophageal sphincter which causes acid and stomach contents to come back up o Rehab considerations ♣ Don't do exercises which inc sx ♣ Recumbent bike probs not best ♣ Some of the postural drainage positions are not good ♣ L side lying is better ♣ Pathos like chronic bronchitis, asthma, IPF all may have GERD as a sx ♣ Tight clothing, exercise, constipation may all make GERD worse

nosocomial infection

• infection acquired DURING a hospitalization o Primary factor = proper hand washing

3-4 years

• jumping • fast (mature) running • stairs (alternating) • matching drawing

hippocampus

• memory (HOW to do something), learning language o CONSOLIDATION of memory -decides where to send it o DECLARITIVE memory HOW to do

EMG

• needle inserted; records electrical activity from brain and SC to peripheral nerve o r/o muscle patho, nerve patho, SC disease, denervated muscle, LMNL

spinal corset

• numerous designs made from fabric, elastic, laces and Velcro o Provide Intraabdominal pressure and posture reinforcement promote stability for clients o Can help to relieve pain associated w/ mid and LB pathologies (eg post-partum or SI instability) o Some have a moldable plastic insert or metal uprights more mechanical stability

p value

• probability that a particular stat result could have happened by chance o When SMALLER than stated level of alpha (level or significance) REJECT NULL o When LARGER than stated level of alpha (level of sig) DON'T reject null (accept it)

GCS

• uses to assess pts w/suspected head injury in order to classify the injury from mild to severe • analyzes CONSCIOUSNESS • Eye opening (4) o None o To pain o To speech o Spontaneous • Motor response (6) o None o Extensor o Flexor o General withdrawal o Localizes pain o Obeys commands • Verbal response (5) o None o Incomprehensible o Inappropriate words o Confused conversation o Oriented • Score (E+M+V) = 3-15 o > 8 - severe brain injury and coma o 9-12 - mod brain injury o 13-15 - mild brain injury

autogenic drainage

• usng controlled breathing to mobilze secretions o Requires patience to learn - not good kids or peeps not motivated/ easily distracted o Procedure Sittin in chair with back support Controlled breathing 3 lung volumes • Unsticking phase = slowly breathe in through nose LOW volumes - 2-3 sec hold - exhale into exp reserve volume o Allow collateral ventilation air to get behind secretions • Collecting phase = breathe TV - 2-3 sec holds • Evacuating phase = deep insp low-mid insp reserve volume - breath holds - HUFF Exhaled through pursed lips - control exp flow rate Ave tx tme = 30-45 mins

12-15 months

• walking w/out support fast, sideways • creeps or hitches up stairs • turns over containers • use crayons adaptively grasps throws in sitting

BPPV

•repeated episodes of vertigo lasting only a couple secs 2/2 changes in head position o Etiology = otoconia (crystals) are free-floating in semi-circular canal (most common = posterior) o POSISTIONAL nystagmus present o Testing -Dix-Hallpike = posterior and anterior canals • Sittin, head 45* lay supine ext head back 30* • Observe eyes for nystagmus / sx direction it goes towards tells you canal involved o <60 sec = canalisthiasis o >60 secs = cupulolithiasis -Head roll test (supine roll) = horizontal canal o Treating = Epplys (begins with dx-hallpike then you keep em spinning around for canal), Liberty-sermont maneuver (when you literally throw them around - for cupulo), Brandt-Daroff exercises (HEP) , BBQ roll (horizontal canal), forced prolonged positioning maneuvers Aka repositioning maneuvers where you move those crystals back to where they belong

conventional TENS

♣ BREIF pain relief - only DURING TX when current being generated ♣ Use when trying to tx pain in first couple sessions ♣ Works by GATE CONTORL THEORY: stim a-beta to stim SG inhibits bad t-cell (pain sens) ♣ FREQ = 100 Hz (high) ♣ PULSE DUR = 100 microsecs (short) ♣ AMP = sensory threshold • Turn intensity up until you get twitch then take a notch down ♣ TX TIME = 20-30 mins ♣ Pt sensation: mild tingling under and btw the electrodes

osteomalacia

♣ Bones become soft d/t Ca or phosphorus deficiency (matrix fine just not hardening) ♣ Etiology = inadequate Ca absorption, increased phosphorus loss in renal excretion, vit D deficiency ♣ S+S = aching, fatigue, weight loss, kyphosis, bowing of LEs ♣ Tx = nutrition, supplements (vit D or phosphate)

case series/report

♣ Case series = COLLECTION of observatiosn similar cases ♣ Case report = in-depth descrption of an INDIVIDUALS condition or response to tx • Can help to generate future research topics • CANNOT test hypothese of est cause/effect relatioships

dx diabetes

♣ Classic S+S + random test of >200 (aka test done any point in day) ♣ 2 occasions of + diabetes testing • Fasting plasma glucose = 8 hrs after last meal o normal < 100 mg/dl o DM > 125 • Oral glucose tolerance = 2 hrs after eating sugar o normal < 140 mg/dl o DM > 200 • A1c testing = average over past 2-3 months o normal < 5.7% o DM > 6.5%

stages of ML

♣ Cognitive = high concentration/cognitive work, problem solve to meet goal, lots of errors, inconsistency, high reps for improvement ♣ Associative = decreased errors and need for concentration, skill refinement, increased coordination, lots of practice, reliance on internal over external FB ♣ Autonomous = automatic, error-free, distractions don't impact activity, can multi-task, internal FB >> external

acupuncture like tens

♣ DELAYED ONSET and LONGER lasting pain relief - ~30 min AFTER tx is done ♣ NOT used during ADLs ♣ Works by endogenous opiate pain control theory: You are treating pain with pain - stim mild painful sens to brain which will stim brain to block pain like runners high ♣ FREQ = 1-5 Hz (low) ♣ PULSE DUR = 200 microsecs (long) ♣ AMP = enter into motor - SEE TWITCHING ♣ TX TIME = 2-20 mins (20-45 mins according to SCB) • Short period when first start to see if it will work then grad increase ♣ Pt sensation: uncomfortable, burning, muscle twitching

chemoreceptor reflex

♣ Decrease in O2, increase in CO2, drop in pH stimulate RESPIRATORY CENTERS • Increase RATE and DEPTH of breathing • This then ensues activation of the PARASYMP system o Reduces HR o Reduces <3 contractility ♣ In case of persistent hypoxia, CNS will be DIRECTLY stimulated inc in SYMP activity • In chronic hypoxia, you have the decreased levels or O2 but also INCREASED CO2 so this is a game changer!! • You want to increase RR and depth of breath to blow off CO2 BUT • Also want to increase HR inorder to get O2 to all the deprived tissues

dressings

♣ Hydrocolloids = gel backed by strong film or foam adhesive Properties • MOST occlusive -- .NO infected wounds • Anchors to surrounding skin • Protection from contamination • Moderate absorption • NO secondary dressing required • Waterproof surface Indications • Partial and full thickness wounds • Granular or necrotic wounds ♣ Hydrogels = gel + sheet or amorphous form Properties • MIN ABSOPRTION o Amorphous = gives moisture to dry wounds o Sheet = maintains moisture • Reduce pressure and diminish pain • Coupling agent for US • Requires 2* dressing Indications • Superficial or partial thickness wounds with MIN drainage ♣ Foam dressings = hydrophilic layer in contact with wound and hydrophobic layer on outside Properties • Moderate absorption through hydrophilic layer • Adhesive and non-adhesive forms • Moist environment for healing • Protection dn cushioning • Autolytic debridement Indications • Partial and full-thickness wounds w/ varying levels exudate • Secondary over amorphous hydrogel ♣ Transparent film = thin, impermeable film Properties • Highly elastic • Allow visual inspection • Moist environment • Resist shear and frictional forces • NOT absorbent at all • Don't need 2* dressing Indications • Superficial or partial thickness wounds with MIN drainage • NO infection ♣ Gauze = most common Properties • Impregnated = has something in it (zinc, antimicrobials, etc) • Non-occlusive • Readily available • Can modify layers for changing wound • Frequent dressing changes • Increased infection rate Indications • Infected or non-infected wounds any size • Wet-to-wet • Wet-to moist • Wet-to dry ♣ Alginates = turns to gel w/in wound to stim healing Properties • Highly absorptive • Non-occlusive • Autolytic debridement • Protects contamination • Non-adherent • Need 2* dressing • CANNOT used on exposed tendon or bone Indications • Partial or full thickness draining wounds (eg pressure or venous ulcers) • Infected wounds o Moisture (most absorptive least) ♣ need some for healing but too much causes maceration ♣ Alginate semipermeable foam hydrocolloid hydrogel semipermeable film o Occlusion (most least) ♣ Hydrocolloid hydrogel semipermeable foam semipermeable film impregnated gauze alginate gauze

decipher HR intensity

♣ Max HR = max HR during graded exercise test ORRRR from age predicted (220-age) ♣ Method 1: percent of max HR • Lower THR = maxHR x 55% • Upper THR = max HR x 90% ♣ Method 2: heart rate reserve (HRR) or karvonen formula • Lower THR = [(HR max - HR rest) x 40%) + HR rest • Upper THR = ([HR max - HR rest) x 60%) + HR rest

stages of motor control

♣ Mobility = initiate movement through functional ROM; NO TONE ABNORMAL • Head righting present ♣ Stability = maintain position via co-contraction • Ex: unsupported sitting with midline control • Head righting + protective extension (large and fast perturbation) ♣ Controlled mobility = ability to move w/in a WBing position or rotate about a long axis • Ex: WS in modified plantigrade • Head righting + protective extension + tilting (large and slow perturbation) ♣ Static dynamic = proximal hold with distal control; can unweight an extremity for performance • Ex: sitting on SB and can lift leg • Head righting + protective extension + tilting + postural fixation ♣ Skill = ability to consistently perform functional tasks and manipulate the environment w/normal postural reflexes and balance reactions • Ex: ADLs, community locomotion • Head righting + protective extension + tilting + postural fixation

wound modalities

♣ Negative pressure wound therapy (NPWT) (aka vacuum-assisted closure/VAC) = foam in wound attached to pump to help w/ closure and drainage • Indications: chronic/acute wounds which cannot be closed by 1* intention o Dehisced wounds, full-thickness, partial-thickness, partial-thick burns, flaps, grafts • Contra = malignancy, bad vascularity, large amounts eschar, untreated osteomyelitis, fistulas, exposed arteries. veins, uncontrolled pain ♣ Hyperbaric O2 = closed chamber which delivers 100% O2 at high pressure • Indications: osteomyelitis, diabetic wounds, crush injuries, compartment syndromes, necrotizing soft tissue infection, thermal burns, radiation necrosis, comprised flaps and grafts • Contra = terminal illness, untreated pneumothorax, active malignancy, pregnancy, seizures, emphysema, certain chemo agents --Growth factors = topicals which facilitate healing by stim specific cells • Indications: neuropathic ulcers into/through subQ w/ good circulation so wound healing • Contra = closed wounds, hypersensitivity to product, hx neoplasm at application site ♣ US = low intensity, pulsed duty cycle • Inflammatory and proliferative phase= stim fibroblasts, endothelial WBC activity enhance strength and elasticity scar tissue ♣ High voltage pulsed current (HVPC) = monophasic DC • Negative (cathode) BACTERIA ACTION since it either acts on the bacteria themselves OR it stimulates WBCs to come and fight infection (galvantotaxis). CAN USE ON INFECTIONS. • Positive (anode) HEALING ACTION as it attracts fibroblasts and other cells for granulation • If you're getting results and then they suddenly stop - SWITCH POLARITY for like a week and see if it helps.

cervical traction

♣ POSISTION -- Supine or prone • supine = separation posterior structures o more common ♣ traction force doesn't have to overcome gravty ♣ pt more relaxed o can adjust flexion, rot and SB to focus on specific segment AND comfort • extended = separation anterior strctures • sitting = flexion and ext can be controlled by pt position o TOWARD traction force = more flexion o AWAY from traction force = more extension • Relative amount of flexion influences specific spinal levels o Upper cervical = 0-5* o Midcervical = 10-20* o Low cervical = 25-35* ♣ Have to wear head halter - make sure its pulling on occiput, careful TMJ ♣ MODE -- Static vs intermittent • Intermittent = reduction pain and inc ROM ♣ FORCE • Dep on goals and influenced by pt position • Initial = no more than 10 lbs • Stretch soft tissue, disc, spasm = 7-10% pt BW (11-15 lbs) • Joint distraction = 13-20% pt BW (20-30 lbs) • NO MORE THAN 30 LBS LIKE EVER!! ♣ DURATION • Vary from 5-30 min o Disc related = 10 min or less o Other spinal conditions = can move up to 30 • PRIMARY DET FACTORS = pt tolerance and changes in sx

grip types

♣ POWER = strong or forceful grip needed; stabilization against palm of hand • Fingers in flexion, hand in UD and wrist in EXT • Cylindrical = entire hand around; fingers and thumbs separated (soda can) • Fist = smaller cylinder; fingers and thumb overlap (hammer) • Spherical = entire hand around; fingers sep and greater thumb opp (baseball) • Hook = flex your IPs too (grabbing pail) o Controlled by forearm flexors and extensors ♣ PRECISION aka prehension = accurate or precise movements, uses MCP and IP joints on RADIAL side hand • Digital prehension (3-fingered pinch) = thumb + index + middle finger (hold pencil) • Lateral prehension = thumb + lateral side index finger (hold key) • Tip prehension (tip pinch) = thumb + tip of any finger (hold a needles) o Thumb is in opposition

AFO

♣ Solid AFOs = no ankle joint • Anterior trim line = max stability through control DF, PF, inv, ev • Posterior leaf spring = trim line is thin and POSTERIOR to malleoli o helps with DF and prevents foot drop o pt needs to have adequate med/lat support themselves • Position of calf shell in relation to footplate can effect knee (aka ankle joint angle) o Great ankle DF = more knee flexion o Greater PF = more knee extension ♣ Articulating AFOs = have ankle joint that moves • Allows movement ot tibia over ankle in gait • Diff deigns have diff control of ankle movement o Overlap, Gillette (most common), Oklahoma (tear-drop), Plantar flexion stop ♣ Tone-reducing AFO = has footplate which reduces pressure over areas which stimulate inc tone, applying pressure over muscle insertions and inhibiting stretch ♣ Floor reaction orthosis (FRO) AFO = utilizes joint moments from GRF to create stability at knee • Prevents tibial progression (and promotes extension and therefore stability) by: o Ankle in slight PF extension moment at knee o Length and rigidity of footplate o Proximal anterior shell • Clients = weak quads (instead of LLB or KAFOs), weak tib ant or peroneals

systematic review/meta analysis

♣ Systematic review = looking at all lit; has explicit method to search, analyze, appraise, and summarize • EX: Cochrane systematic review - specific for health care and health care policy ♣ Meta analysis = systematic review which uses statistical technique to derive est of effect size • Essentially pools systematic reviews and gives overall effectiveness of tx • Minimizes problem of small sample size pooling inc overall sample zise

signs ischemia or infarct

♣ T-wave inversion = may or may not indicate ischemia • 50/50 chance ischemia Chest pain can clue us in! • occurs hours or days after MI 2/2 delay in repol. produced by injury • may also occur with R and L bundle branch blocks, after CVA • normal juvenile t-wave pattern in children and some adults ♣ ST-depression (4mm horizontal depression) = DEF ischemia; possible non-STEMI • SUBENDOCARDIAL • Non-STEMI = no ST elevation, but still infarcted o Check blood levels for confirmation • Could also be due to DIGITALIS toxicity or hypokalemia ♣ ST-elevation = DEF injury/inflammation; good chance we also have an infarct • Earliest sign TRANSMURAL infarct (at this point it's not transmural though) • STEMI = ST Elevation Myocardial Infarction o check blood levels for confirmation o STEMI alert = heart muscle is dying; act fast to avoid MI • Could also indicate benign early repol in healthy heart ♣ Q-wave (in not aVR) = DEF infarct (Signifies loss of positive voltage due to necrosis) • Significant abnormal = longer than 0/04 msec and larger than 1/3 amplitude of the R wave • Transmural MI

brief intense TENS

♣ Used to MIN PAIN DURING ther-ex, activity or procedure which may be painful ♣ Serves as a distraction ♣ FREQ = 150-250 Hz (high) ♣ PULSE DUR = 300 microsecs (long) ♣ AMP = pain threshold • Should be sufficient for sig paresthesia or motor response • May have to inc if they habituate ♣ TX TIME = 15 min or however long procedure is

baroreceptor reflex

♣ What happens when ..... • DECREASE in arterial pressure (dec stretch) decreased baroreceptor firing autonomic neurons in medulla respond: o INCREASE SYMP OUTFLOW - increase in BP due to: ♣ Inc HR ♣ Inc contractility ♣ Arterial vasoconstriction ♣ Venoconstriction • INCREASE in arterial pressure (inc stretch) increased baroreceptor firing medualla o INREASE PARASYMP!!! - decrease in BP due to: ♣ Dec in HR ♣ Small dec in contractility

HR determination count

♣ counting from R to R or P to P using the fat black lines • 300 - 150 - 100 - 75 - 60 - 50

MAS

♣ grading spasticity • 0 - no increase in tone • 1 - slight increase in tone, catch and release or min resistance at end range • 1+ - slight increase in tone, catch and release or min resistance through < ½ range • 2 - increased tone through > ½ range, parts easily moved • 3 - considerable increase in tone, passive movement is difficult • 4 - rigid

practice (ML)

♣ integral to ML repeated performance of activity to learn/perfect a skill ♣ Massed = practice time > rest time ♣ Distributed = rest time =/> practice time ♣ Constant = practice under uniform conditions ♣ Variable = practice under differing conditions ♣ Random = varying practice among different tasks ♣ Blocked = consistent practice of 1 task ♣ Whole training = practice entire task ♣ Part training = practice component(s) of task

Middle cerebral artery

♣ outer cerebrum (gets all lobes), BG, internal capsule, putamen, pallidum, lentiform nucleus • MOST COMMON AND THE WORST ONE!! • contra wkns and sensation (face and UE>LE) • aphasia o Broca's = cant speak o Wernicke's aphasia = cant UNDERSTAND o Global = cant do either • homonymous hemianopsia (field loss same side both eyes - this type coming from nerve) • apraxia (cant plan mvmt) • flat affect (R side) • spatial relations • body schema • anosognosia (non-dom hemi -- lack of insight)

vasalva

♣ resultant DECREASE in CO and BP (heart doesn't really have blood to pump out - decreased pressure) sensed by BARORECEPTORS INCREASED SYMP stimulation • reflexively INCREASE HR and myocardial contractility ♣ when the glottis opens, venous return and BP INCREASE, as well as <3 contractility since all the blood slings in sensed by baroreceptors (inc pressure) PARASYMP stimulation • DECREASE HR • Increases intrathoracic pressure • increases intraabdominal pressure • decreases venous return

Posterior cerebral artery

♣ temporal lobe, occipital and occipitoparietal cortices, midbrain, subthalamic nucleus, basal nucleus, thalamus • HHA (CORTICOL aka its coming from the brain itself) • contra pain and temp sensory loss • contra hemiplegia IF large lesion (parapalegia not as bad in this one) • weird mvmts cuz cerebellum o ataxia, athetosis, choreiform movement o hemiballismus (intermittent, large scale mvmts one side of body) • cant recognize shit o visual agnosia (cant recognize objects) o anomia (cant recall names of everyday objects) o prosopagnosia (cant recognize faces) • memory impairment • thalamic pain syndrome = ipsi abnorm pain, temp, touch, and prop

TMJ LP, CP

Mouth slightly open (freeway space) Clenched teeth

SCI lesions

--Anterior cord syndrome = compression and damage anterior SC; anterior spinal artery • Spinothalmic = loss of pain and temp • Corticospinal = loss sense and motor function --Brown-Sequard's syndrome = hemisection SC; 2/2 GSW or stabbing • paralysis and loss of vibration and position sense (corticospinal, dorsal columns) on ipsi side • loss of pain and temp (lat spinothalamic) on contra side --Central cord syndrome = compression damage CENTRAL part SC; MOI cervical hyperext • Spinothalamic = pain and temp • Corticospinal = motor below • UE >>> LE ; motor >>> sensory --Posterior cord syndrome = uncommon; compression PSA • DCML = loss of proprioception, 2-pt discrimination, stereognosis --Cauda equina injuries = below L1; getting nerve roots so PERIPHREAL nerve injury • flaccidity, areflexia, impaired bowel and bladder • full recovery NOT typical long way for axonal regeneration --sacral sparing = some of innermost tracts remain innervated • sensation of saddle area, mvmt toe flexors, anal contraction

dyspnea scale

0 None 0.5 Very, very slight 1 Very slight 2 Slight breathlessness 3 Moderate 4 Somewhat severe 5 Severe breathlessness 6 7 VERY severe breathlessness 8 9 Very, very severe breathlessness 10 MAX

lymphedema staging

0 • latent • no visible edema transport has been affected 1 • reversible • pitting edema worse with exercise, diminishes w/elevation and rest 2 • spont irreversible • non-pitting edema - does not change • fibrotic changes • Stemmer's sign!!! (can't lift skin on forefoot) 3 • lymphostatic elephantiasis • extensive non-pitting edema and fibrotic changes • have deep skin folds, hyperkeratosis (thickening skin), papilloma (wart-like growth) • infection is common and stemmers is still positive

angina scale

1 Light, barely noticeable 2 Moderate, bothersome 3 Moderately severe, very uncomfortable 4 Most severe or intense pain ever felt.

renal failure

= kidneys DECREASE glomerular filtration rate (GFR) so toxins are not gotten rid of o etiology = 2/2 DM, HTN, posion, trauma, genetics nephrons damaged so cant filter blood o stages of kidney disease ♣ stage 1 = kidney damage, norm GFR (>90) ♣ stage 2 = MILD dec GFR (60-89) ♣ stage 3 = MOD dec GFR (30-59) ♣ stage 4 = SEVERE red GRF (15-29) ♣ stage 5 = failure (GRF <15) o acute renal failure = damage occurs quickly ♣ etiology = dec. blood flow (prerenal), obstruction after kidney (postrenal), primary damage renal tissues (intrarenal) ♣ S+S = inc BUN and cretine, oliguria, kyperkalemia, sodium retention ♣ Tx = gmmt etiology, pharm, diuretics, nutritional support, hydration, hemodialysis/transfusions when necessary o chronic renal failure = damage over time ♣ etiology = DM, HTN, glomerulopathies, obstructive uropathy, interstitial nephritis, polycystic kidney disease) ♣ tx = conservative mgmgt (utirion, hydration, avoid protein, pharm), renal replacement therapy (hemodyalisis, organ transplant o end stage = basically totally gone; need dialysis

meds for a-fib, angina, HTN, thrombus

A-fib-by depressing the electrical conductivity, digitalis can effectively prevent the conduction of atrial arrhtmias into the ventricles. Also used for CHG. i. Angina uses anti-ischemic drugs: B blockers, Ca channel blockers, nitrates ii. HTN uses diurects, vasodilators iii. Thrombus formation: thrombolytic, anti platelet meds

colles fx

About • transverse fx of distal radius o lunate acts as wedge shear force DORSAL displacement of radius • MOI = FOOSH o Note: lots of diff fx can occur from this • Damage to shit on ulnar side may occur - ulnar collateral lig, styloid process • Peeps with OP at sig risk of developing this S/Sx • "dinner fork: or "bayonet" deformity • pain and edema close prox to fx site Imaging • x-ray - will show deformity OR area of increased bone density when not bad enough to have deformity • MRI - when lig. or soft tissue damage suspected Exam • MOI, current sx really important • Visual inspection, careful exam

frozen shoulder

About • Inflammation and fibrotic thickening ANTERIOR joint capsule, rotator cuff, Subacromial bursae, deltoid • Inflammation adhesion capsule thickens decrease in joint space dec. in joint fluid adhesion and migration to humeral head contracture • Classification o Primary = spontaneous o Secondary = results from underlying condition • 3 stages o freezing (2-9 months) - ACUTE o frozen (lasts 4-12 months) - CHRONIC o thawing (lasts 12-24 months) Etiology • Middle aged pop (peak = 40-60 yo) • Females > males • Primary = No known etiology o Associated with conditions such as DM (11% of peeps with), thyroid abnormalities, CP conditions • Secondary = Result from trauma, immobilization, CRPS, RA, abdominal disorders, psychogenic disorders o Ortho things that may initiate = supraspinatus tendonitis, partial tear rotator cuff, bicipital tendonitis S/Sx • Typically UNILATERAL (85-90%) • Restricted AROM and PROM - all motions but esp ER>ABD>IR • May also see spasms around the shoulder • Loss of reciprocal arm swing • Disuse muscle atrophy over time • Acute phase o Progressive loss of motion o Pain in C5 dermatome o Night pain o PROM limited 2/2 pain and guarding • Chronic phase o Pain localized around C5 derm. still - but less intense o NO night pain o PROM limited due to CAPSULAR stiffness Imaging • arthrogram - detects dec. fluid volume o norm = 16-20 mL o with AC = 5-10 mL • other tests only for DD Exam • Important hx = PSH/PMH, fam hx, current sx, health status, social hx and habits, occupation, leisure activities, social support system • Make sure to r/o concomitant system, rheumatologic, inflammatory, metastatic, infectious disorders Mgmt • Medical mgmt. = varies o Usually self- limiting process that recovers on own with time o Injection corticosteroid o Sx = to breakup adhesions or release muscles adhered to joint ♣ LAST RESORT! • PT o Acute phase = ice/heat, GENTLE mobs, PRE, pendulums, isometric strengthening ♣ Careful not to overstretch - can set back o Chronic phase = US, HIGHER grade mobs, PNF to inc pain-free range o HEP = yep ♣ Acute = AVOID ABD at home - damage Subacromial tissue • Pharm = control of pain - NSAIDs, acetometaphine, long acting analgesics or narcotics for pain relief Outcome • Usually prescribed for 3-5 months after dx • Usually non-linear recovery • Usually resolves 1-2 years; may have some residual loss ROM after • Long term effects o 7-14% experience some permanent loss ROM but asymptomatic and doesn't usually impair functional mobility

anticoagolants

Action • Stop fibrin fibrinogen • Inhibit platelet aggregation and thrombus formation bleeding risk

achilles tendon rupture

About • typically occurs 1-2 in above the insertion at the calcaneus (distal 1/3 - avascular zone) • incidence: 30-50 yo WITHOUT hx calf or heel pain • typically will be unable to stand • (+) Thompson test (squeeze the calf and the foot wont PF) • Achilles tendon is largest and strongest tendon in the body • Made of tendinous portion gastroc/soleus, attached to insertion at calcaneal tuberosity • Probs occurs in tendons that have degenerative changes more susceptible o Begins with HYPOvascularity o Combines with the repetitive trauma Etiology • MOI is EITHER o Pushing off WB LE with EXT knee and DF foot (stretch of gastroc-soleus) o Forceful ECC contraction • Highest incidence = 30-50 yo; NO hx calf or heel pain; rec activities or weekend warriors • Contributing factors / risk factors o >30 y/o - more avascular d/t aging changes o more common in men (probs just d/t involvement in high-risk activities) o Plays sports with quick-changing footwork - b-ball, football, tennis, softball o Poor stretching routine o Tight calf muscles o Improper shoe wear during high-risk activities o Altered foot biomechanics - inc. pronation/flattened arch o History of corticosteroid injections at tendon S/Sx • Swelling over distal tendon • Palpable defect in tendon above insertion o Complete tear = palpable gap • Pain and weakness with PF o Will NOT be able to do WB calf-raise • May limb • c/o "pop" or "snap" with SEVERE pain • (+) Thompson test - squeeze calf in prone and no DF • MD may do O'Brien needle test to confirm rupture Imaging • get an x-ray to r/o avulsion fx or bony injury • MRI = location tear and severity Exam • Important hx = MOI, PMH, meds, current health status, social history and habits, occupation, living environment, social support system • Tests/measures o Anthropometric - measure edema or use palpation o Arousal, attention, cognition o ADs - will they have to use crutches ? o Gait, locomotion, balance - safety with or withouth AD; biomechanics o Integ - SENSATION o Joint and mobility - thomposon , other special tests o Muscel performance - strength and characteristics of muscle contraction o Pain o ROM o Sensory integration - prop and kinesthesia o Self-care and home mgmt . Mgmt • Medical mgmt. = EITHER conservative or surgical o Conservative ♣ immob through serial casting ~10 weeks ♣ heel lift ~3-6 months • ensures max healing without stress to tendon o SX = self-explanatory; they suture it back together if quick turnaround since injury; otherwise may bridge using tissue from another place ♣ Note: you wanna do this sx fast or else the tendon recedes up ♣ Cast / brace 6-8 weeks! • PT = BOTH cases, start once cast is off o ROM, stretch, ice, AD training, endurance programming, gait training, strength, plyos, skill specific training o They're doing HEP ~6-7 months • Pharm not really indicated for this unless NSAIDs, acetometaphine or narcotis for pain relief Outcome • Pt should return to PLOF ~6-7 months!!! • Long term effects o Without Sx = higher rate re-rupture (40%) and incomplete return PLOF o Surgical = risk surgical infection BUTTTT low re-rupture (0-5%) AND HIGHER rate RTP

beta blockers

Action • BLOCK B-adrenergic receptors • Can either by selective or non (B1 = heart, B2 - lungs) • Dec MVO2 by dec HR and contractility Indication • HTN • Angina • Arrhythmias • HF • Migraines • Essential tremor AEs • Bradycardia • Arrhythmias • Fatigue • Depression • Dizziness • Weakness • Blurred vision PT imp • MONITOR VIA RPE - BP and HR will be diminished • Caution rising up 2/2 dizziness / OTH Ex • All the -olols - atenolol, Lopressor (metoprolol), Inderal (propranolol)

RTC tendonitis

About • typically, impingement of supraspinatus tendon just prox to insertion at greater tubercle • Caused by INABILITY of supra musel to DEPRESS humeral head in glenoid fossa o Causes sup migration of hum head since now the biceps is unrestrained pulling up • Types o Primary impingement = intrinsic or extrinsic factors WITHIN Subacromial space o Secondary = getting sx from something outside (eg poor posture, instability) • Further classification o Stage 1 = <25 yo, local inflammation, edema, min bleeding around o Stage 2 = 25-40 yo, progressive deterioration tissues surround RTC o Stage 3 = 40+ end stage, disruption and/or rupture numberous structures • Bicipital and infra tendonitis and bursitis may also contribute (all in that same little space) • Note: often presents in association with IMPINGMENT SYNDROME Etiology • Inc. risk: EXCESSIVE OH ACTIVITY!! - swimming, tennis, baseball, painting, etc • excessive use UE after a period where didn't use at all can also contribute • peeps 25-40 yo MOST COMMON for this condition S/Sx • difficulty with OH activities - feel weak • dull ache following periods of activity • painful arc ABD: 60-120 • pain with palpation • pain with stretching of involved muscles or active contraction of them • pain often inc. at night and they can't sleep on that side • difficulty with reaching, dressing, etc. Imaging • MRI - can ID presence but $$$ so not common • X-rays in ER - can slow calcific deposits or bony abnormalities Exam • Make sure to look at joint play and POSTURE, look at PMH so see if anything could be maybe causing a decrease in that subacromial space • Special tests o Empty can - supra o Neers impingement o Hawkins-Kennedy - impingement o Jobe test o Tendonitis vs bursitis test Mgmt • PT o Acute = ice, activitiy modification, rest ROM o Progression = strengthen (start at side, use AAROM) o ALWAYS IN PAIN-FREE RANGE - dependent on adequate blood supply and O2 o Make sure that shoulder is all strong when you start OH activities!! o Shoulder shrugs and pushup when ABD to 90* = elevation of acromion so not hitting RTC ♣ Works on serratus ant and upper traps • PHARM = analgesics and NSAID for pain Outcome • Conservative = return to function ~4-6 weeks • Depends on stage • If fails, you may have sig activity mod or sx • Prolonged inflammation may lead to tear

corticosteroids

Action • REDUCE INFALMMATION • Provide hormonal, anti-inflammatory, and metabolic effects • Vasoconstriction results from stabilizing lysosomal membrane and enhancing effects of catecholamine's Indications • Replacement therapy endocrine dysfunction • Anti-inflammatory and immunosuppressive effects • Tx rheumatic, respiratory, other various disorders AEs • Muscle atrophy • GI distress • Glaucoma • Adrenocoricol suppression • Drug-unduced Cushing syndrome • Weakening/breakdown bone, ligament, tendon, skin • Mood changes • HTN PT imp • Wear a mask since immune system weak • Be aware toxicity signs moon face, buffalo hump, personality changes • Risk OP and muscle wasting • When injected, careful cuz ligament/tendon weakening/laxity Ex. • Dermacort (hydrocortisone or cortisol) • Cordrol (prednisone) • Pediapred (prednisolone) • Medrol (methylprednisone) • Decadrol (dexamethasone) • Nasonex (mometasone)

DMARD

Action • slow or halt progression rheumatic disease • induce remission by o MODIFYING THE PATHOLOGY o INHIBITING immune response

1. PT administers special test of pinch test. What nerve?

Anterior interosseous nerve: Flexor pollicis longus- branch of the median nerveAnterior interosseous nerve: Flexor pollicis longus- branch of the median nerve

breathing patterns

Apnea ABSENCE spontaneous breathing Biot's Irregular - breaths vary in depth and rate with period of apnea Often associated with inc. ICP or damage to medulla (resp. center there) Bradypnea Slower than normal rate May be associated w/ neurologic or electrolyte disturbance, infection, high level CV fitness Cheyne-Stokes (periodic) Dec rate and depth of breathing with periods of apnea Can occur 2/2 CNS damage Eupnea NORMAL RATE AND DEPTH Hyperpnea INCREASED rate and depth Hypopnea DECREASED rate and depth Kussmaul's Deep and fast breathing Often associated with metabolic acidosis (trying to blow off CO2) Paradoxical Chest wall moves in with inhalation and out with exhalation (opp. norm) Due to chest trauma or paralysis of diaphragm Tachypnea Faster than normal resp. rate (ONLY RATE)

spine ROM cervical

F/E/SB 45 ROT 60

radoiocarpal capsular

F=E

hip capsular pattern

F>ABD>IR

lab values of platelets, WBC, hemoglobin to CI exercise

Exercise testing and training is CI in pt with CA whose platelets are <50,000 WBC <3,000, Hgb <10 g/dL

testing sensations

Examine superficial and deep sesn first, then cortical make sure to vary the time youre testing and giving them time btw and not fatiguing them can do derm and peripheral nerve regions • Superficial sensations o Light touch o Temperature o Pain • Deep sensations o Kinesthesia: direction and extent movement o Proprioception: iD static x o Vibration • Cortical sensations o Localization of touch o Bilateral simultaneous stimulation o Two-point discrimination o Stereognosis o Barognosis o Semmes Weinstein monofilaments = OBJECTIVE data regarding protective sensation ♣ Should be done when pt AT RISK for sensory impairments ♣ 4.17 = 1g NORMAL sensation ♣ 5.07 = 10g NO protective sensation (cant sense trauma, WBing NEED protective footware) ♣ 6.10 = 75g totally INSENSATE foot

ROM shoulder

F 180 E 60 ABD 180 IR 70 ER 90

wrist ROM

F 80 E 70 RD 20 UD 30

T and L spine ROM

F 80 E 25 SB 35 ROT 45

radiohumeral LP CP

FULL EXT, FULL SUP 90* elbow FLEX, 5* SUP

primitive reflexes

Galant • 30 weeks gest - 2 months • Lateral flexion trunk to side of stim when swipe shoulder to hip • Interferes: sitting balance, lead to scoliosis Pos Support • 35 weeks gest - 2 months • Weight on balls of feet when upright leg and trunk ext • Interefers: standing and walking, balance rxns, WS in standing • Can lead to ankle PF contractures Walking reflex • 38 weeks gest - 2 months • Supported upright, soles on firm recipricol flex/ext of legs • Interferes: standing and walking, balance rxns and WS standing, development smooth, coord, recipricol mvmts LEs rooting • 28 weeks gest - 3 months • Touch cheek turn head that way with mouth open (finding nipple) • Interferes: oral-motor development, midline head control, optical righting, visual tracking, social interaction palmar grasp • Birth - 4 months • Pressure ulnar side hand flexion fingers (grip) • Interferes: grasping and releasing voluntarily, WBing open hand moro • 28 weeks gest - 5 months • Head drops ext arm ABD, fingers open, then cross trunk into ADD, cry (dropping) • Interferes: sitting balance reactions, protective reponses sitting, eye-hand coord, visual tracking startle • 28 weeks gest - 5 months • Loud sudden noise moro BUT elbows flex, hands closed • Interferes: sitting balance, protective reponses, eye-hand coord, visual tracking, social interaction, attention ATNR • Birth - 6 months • Head to side ext UE front of face, flex UE behind head • Interferes w: feeding, visual tracking, midline hand use, B hand use, rolling, crawling • Possibly leads to skeletal deformities (scoliosis, hip sublux/dislocation) TLR • Birth - 6 months • Supine body and ext in ext • prone body and ext in flex • Interferes w: rolling initiation, prop on elbows when prone, flex trunk and hips supinesit, balance in sitting or standing STNR • 6 - 8 months • Head flexed arms flexed and legs ext; head ext arms ext and legs flexed • Interferes w: prop on arms in prone, quadruped positioning, crawling, sittign balance when looking around, use hands when looking at objects in hand plantar grasp • 28 weeks gest - 9 months • Pressure base of toes toe flexion • Interferes: ability to stand flat feet, balnce rxns and WS in standing

CN III oculomotor

M = voluntary: eyelid levator; sup, med, inf recti; inf oblique Autonomic: smooth muscle of eyeball (constrictor pupillae and ciliary muscles) T = up, down and medial gaze (move something in front of them; observe for - tracking, asym, ptosis) Reaction to light

CN XII hypoglossal

M = voluntary: muscles of tongue T = stick out tongue (deviates TOWARDS injured side)

CN IV trochlear

M = voluntary: sup oblique T = down and in gaze (move object; + cant depress and/or c/o diplopia)

digits ROM

MCP F 90 MCP HYPEREXT 45 PIP F 100 DIP F 90 DIP hypertext 10

spina bifida

Myelomeningocele • Summary o Occulta (incomplete fusion of post vertebral arch w/no neural tissue protrusion) vs. meningocele (incomplete fusion of post vertebral arch w/neural tissues/meninges protruding) vs. myelomeningocele (incomplete fusion of post vertebral arch w/meninges and SC protruding) o 75% of defects in lumbosacral region L5-S1 is most common o Elevated alpha-fetoprotein (AFP) in blood during prenatal testing (gestation wk 16) probable neural tube defect • Diagnosis o Condition that produces symptoms congenital defect (usually in l/s) from neural tube failing to close by 28th day of gestation, 3 classifications (occulta < meningocele < myelomeningocele) o Injured structures sac/cyst protruding from spine (may or may not be covered by skin) containing herniated meninges, CSF, and SC via defect in vertebrae • Inference o Contributing factors poor prenatal care (diabetes, low folic acid (esp in 1st 6 wks), alcohol/drug use), genetic predisposition • Confirmation o Clinical presentation sac protruding from infant's back, motor and sensory loss below lesion, hydrocephalus, Arnold-Chiari type II (cerebellum and BS in SC),clubfoot, bowel and bladder, scoliosis, learning disabilities, deficits in perception, attention, memory, and problem solving o Imaging US, AFP blood testing • Examination o Additional findings increased risk of meningitis, hemorrhage, and hypoxia, hydrocephalus, clubfoot, neuropathic fx, visual problems, osteoporosis, kyphosis, hip dislocation, latex allergy • Management o Tx immediate sx to repair defect and place shunt for hydrocephalus, PT (positioning, ROM, pt/fam ed, developmental milestones, balance, mobility, AD/WC use), OT • Outcome o Long-term effects near normal life w/consistent healthcare

CN II: optic nerve

S = sight T = visual eye fields (ID objects or items from distant object)

1: olfactory nerve

S = smell T = ID familiar odors (sitting, eyes closed/blindfolded)

OTH response

Recognition • 2/2 venous pooling in legs when supine/sitting stand • Causes DEC perfusion to the brain • s/sx o DIZZZINESS o SYNCOPE o Altered vision o Nausea o Confusion Response • Lie down in supine position with LEGS ELEVATED

seizures response

Response • Place pt is safe location and position WITHOUT restraining mvmts • RR and quality should be monitored • Make sure airway stays patent - NO OBJECT IN PT MOUTH • When convulsions subside, turn pt. head so no aspiration

CN VII facial

S = taste: anterior tongue M = voluntary: facial muscles *Autonomic = lacrimal, submandibular, sublingual glands T = close eyes tight Smile and show teeth Whistle and puff cheeks ID familiar tastes

CN V trigeminal

S = touch and pain skin of face (V1, V2, V3) mucous membranes nose, sinus, mouth anterior tongue M = voluntary: muscles of mastication T = corneal reflex Face sensation (+ absent; cant diff sharp/dull) Clench teeth push down on jaw jaw jerk reflex

CN X vagus

S = touch and pain: pharynx, larynx, bronchi Taste: tongue, epiglottis M = voluntary: muscles of palate, pharynx, larynx Autonomic: thoracic and abdominal viscera T = gag reflex (this has to do with MOTOR part being effed up) Ability to swallow Say "ahhh"

CN IX glossopharyngeal

S = touch and pain: posterior tongue, pharynx Taste: posterior tongue M = voluntary: select muscle of pharynx Autonomic: parotid gland T = gag reflex (this has to do with SENSORY part effed up) Ability to swallow

capsular pattern C spine

SB and ROT>EXT

ULTT3

Shoulder depression, ABD 10*, elbow ext, forearm pron, wrist flexion, UD, finger and thumb flexion, shoulder IR CL cervical SB Radial

ULTT2

Shoulder depression, ABD 10*, elbow ext, forearm sup, wrst ext, finger and thumb ext, shoulder ER CL cervical SB Median nerve, musculocutaneus nerve, axillary nerve

topical agents burn care

Silver sulfadiazine • w/ or w/out dressings - applied directly to wound • painless • effective against YEAST • does NOT penetrate eschar Silver nitrate • non-allergenic • painless application, painful removal • poor penetration • ELECTROLYTE IMBALANCES!!! Povidone-iodine • ANTIFUNGAL - NOT effective against pseudomonas • Painful app, easily removed with water • May impair THYROID FUNCT Mafenide acetate • PENTRATES ESCHAR • w/ or w/out occlusive dressings • METABOLIC ACIDOSIS and may comp resp function • May inhibit epithelization Gentamicin • w/ or w/out dressings • ototoxic and nephrotoxic • caused resistant strains Nitrofurazone • BACTERIOCIDAL • May lead to overgrowth fungus / pseudomonas • Painful application

lung volumes

TLC: Sum of ALL lung volumes - air in lungs AFTER MAX INSP TLC = RV + VC TLC = FRC + IC VDVolume of air which does NOT participate in gas exchange (part of residual volume) RV: Gas left in lungs AFTER MAX EXHILATION ~25% lung volume RV Total volume of air inspired and expired during NORM QUIET BREATH ~10% lung volume FRC Volume of air in lungs AFTER NORMAL EXHILATION FRC = ERV + RV ~40% lung volume IR MAX volume of air which can be inhaled AFTER normal TV ~50% total lung volume ERV MAX volume of air which can be expelled AFTER normal TV ~15% total lung volume VC Volume change which occurs between max inhalation and max exhalation AKA the volume a person can achieve when they breathe ALL THE WAY out and ALL THE WAY in (everything but dead space) VC = TV + IRV + ERV IC Max amount of air which can be INHALED AFTER you NORMAL TIDAL EXHILATION IC = IRV + TV ~60% lung volume FVC Volume of air EXPIRED after you just max inhaled FEV MAX volume of air exhaled in SPECIFIC PERIOD OF TIME Usually FEV1 (1 sec) but can be 2 or 3 of the FVC maneuver talked about above PEF MAX FLOW of air during beginning of a forced expiratory maneuver VE minute ventilation Amount of air expired in ONE MINUTE VE = TV x RR

Pt with Achilles tendonitis- notes foot and ankle appear to be pronated. What is this in NWB foot

a. ABD, DF, Eversion

1. which orthosis MOST EE ambulation in child with L1-3 spina bifida

a. RGO with rolling walker: grade 3/5 for hip flexors, adductors, and knee extensors, and grade 3 or less for hip extensors and knee flexors: RGO will assist with hip F and E

1. Pt recovering from stroke for spastic hypertonia in more involved UE. What muscles during early to middle recovery?

a. Shoulder adductors, forearm pronators, flexors of elbow, wrist, hand i. Antigravity muscles

pusher syndrome

affects CL side of lesion hemiplegic side

shoulder goni

all firm • FLEX: supine o Fulcrum - Greater Tuberosity / acromial process o Stationary - Parallel w/ Thorax o Moving - Lateral Epicondyle • EXT: prone o Same landmarks as FLEX • ABD: supine o Fulcrum - ANT Acromion o Stationary - Parallel w/ Sternum o Moving - Medial Epicondyle • IR & ER: supine o Fulcrum - Olecranon Process o Stationary - Perpendicular to floor o Moving - Along Ulna towards Ulnar Styloid Process • Hz ADD: sitting o Fulcrum - Top of Acromion o Stationary - Pointed out to the side (parallel w/ floor) Moving - Lateral Epicondyle

activities that precipitate SI dysfunction

anterior torsion innominate: squatting/lifting, pregnancy, hip 90 axial loads, golfing/tennis posterior torsion innominate: vertical thrust, sprint starting x, fall onto ischial tub, unilateral standing sacral dysfunction: postural abnormalities, fall on sacrum/coccyx, carrying load in ambulation, childbirth trauma, loss balance, sitting with rotation and lifting

ottawa ankle and foot rules

bone tenderness posterior edge/tip lat/medial malleolus extended 6 cm proximally inability to take 4 steps immediately and in ED OR bone tenderness base 5th MT/navicular and 4 steps thing

peripheral nerve lesions

compression, fx, compartment syndrome, laceration, penetrating trauma, traction, MVA, cold o Pathophys for degeneration = muscles exhibit: --Altered response ACh wasting sarcoplasm and loss of fibrils --Total loss muscle over time replacement fibrous tissues o Double crush syndrome = 2 sep lesions along same nerve; more severe sx o Mononeuropathy = 1 nerve lesion ♣ associated conditions: trauma or entrapment o Neuroma = abnormal growth nerve cells ♣ Associated: vasculitis, AIDS, amyloidosis o Peripheral neuropathy = impairment/dysfunction peripheral nerves ♣ Associated conditions: diabetic perihreal neuropathy, trauma, alcoholisim o Polyneuropathy = diffuse nerve dyscuntion which is typically symmetrical and 2/2 patho not traums ♣ Associated conditions: GB, peripheral neuropathy, use neutrotoxic drugs, HIV o Wallerian degeneration = DISTAL degeneration of MYLIN SHEATH and AXON

how to calculate current density

current amplitude divided by surface area

what happens with: hyperkalemia, hypermagnesemia, hypernatremia, hypercalcemia

hyperkalemia: respiratory paralysis or cardiac arrest hypermagnesemia: hypotension and resp depression hypernatremia: thirst hypercalcemia: constiplation, pain, nausea, vomiting

1. 67 y/o with neck pain, recommends x-ray to r/o cervical spine fx. What finding prompted this? a. Fall from a 4 foot step ladder. Based on Canadian c-spine rule high risk factors that mandate radiography are:

i. Combo of age >65, hx dangerous MOI ii. Low risk factors: paresthesias in extremities and simple rear end collision and ability to actively rotate head 45 deg

stress fx

insidious onset of pain associated with change in equipment or training and exacerbated with activity localized bony tenderness and palpable periosteal thickening pain at fracture site with percussion or vibration at a distance from the fx joint ROM maintained point tenderness on tibia and pain with 3 point stress

concussion

mild TBI • injury to head, may temporarily lose consciousness, damage to reticular activating system (affects vital signs) • Grade 1 = no LOC, have transient confusion (15 min), full memory o remove from play and return in 1 wk if no symptoms • Grade 2 = moderate head injury, confusion > 15 min, retrograde and anterograde amnesia o remove from play and return after 2 wks if no symptoms o should have CT scan if gets worse • Grade 3 = 2/2 diffuse axonal injury; LOC, TAKE TO ER for neuro exam!! o need to be symptom-free for at least 1 mo before RTP

R hemisphere Cx

nonverbal processing and communication, artistic ability, concept comprehension, hand-eye coordination, spatial relationships, kinesthetic awareness, music, negative emotions, body image ♣ Think: more creative

HIV

o o Risk factors unprotected sex, IV drug use, mom to fetus o 3 stages acute HIV infection, clinical latency, AIDS o Leading causes of death AIDS-related/opportunistic infection, non-AIDS-defining cancers, liver disease, CV disease o Diagnosis o retrovirus that attacks immune system (CD4+ and T-cells); HIV uses cells, CD4 antigen to replicate, further weakening the immune system o Injured structures T-cells first, then monocytes, macrophages, microglia, cervical cells, epithelial cells (GI) o Inference o Contributing factors contact w/blood, semen, vaginal secretions, breast milk often from sex or needles o Confirmation o Clinical presentation stage I (acute - asymptomatic, flu-like, rapid CD4 drops, highly contagious), stage II (latency - tx (ART) keeps virus in check, ~10 yrs), stage III (AIDS - CD4 < 200 cells/mm3, 3 yr survival, opportunistic infections) o Imaging blood tests (Western blot)

mccill pain questionnaire

o Pain assessment tool, 4 parts, 70 Q ♣ MOST WIDELY USED! ♣ Valid and reliable o Part 1 = marking where on body + int vs ext o Part 2 = chose word which best describes o Part 3 = pattern of pain, factors that inc or dec o Part 4 = intensity 0-5

ruling out vs confirming dx

o Ruling out a disease: ♣ High sensitivity > 90 ♣ (-) likelihood ratio <0.10-0.20 ♣ Likelihood ratio <1 indicates test result is associated with absence of the disease o Confirming a disease: ♣ High specificity >90 ♣ (+) likelihood ratio >5-10 ♣ Likelihood ratio >1 indicates test result is associated with the disease

gaze stability exercises- VOR

o adaptation of VOR ♣ make sure sped >/= 2 Hz so actually working VOR like supposed to ♣ VORx1 = card still, head moving ♣ VOR x2 = head and card move opp o Substitution of VOR = using VSR, VCR, brain, other things ♣ VOR x1 BUT move card slow (using smooth pursuit now) or move head (target VSR now) ♣ Imagined targets = look at thumb, close eyes, move head, try to keep eyes on thumb while move • Using central programming to override ♣ Gaze shift = move eyes btw 2 targets • Central programming ♣ Use of visual / sensory cues (eg flashlight, visual scanning)

metabolic alkalosis

o body's pH rises above 7.45; too much HCO3 or too little CO2 ♣ Etiology = cont vomiting, ingestion antacids, diuretic therapy, hypokalemia, NG suctioning ♣ S+S = nausea, diarrhea, confusion, muscle fasciculation, cramping, hyperexcitatbility, convulsions, hypoventilation (want to keep CO2) • Untreated = comatose, seizures, resp parlysis ♣ Tx = manage cause, correct imbalance, admin potassium chloride

lumbar traction

position: supine: stenosis prone: HNP mode: static vs. intermittent force: spasm/disc= 25% BW sep of vertebrae= 50% duration 5-30 min. disc <10 min

ROM forearm

pronation 80 sup 80

c spine goni

• FLEX and EXT: sitting, thoracic and lumbar supported o F - external auditory meatus o SA - perp to ground o MA - nose • Lateral flexion: sitting F - SP C7 o SA - perp to ground o MA - occipital protuberance • ROT o F - center of top of head o SA - acromion MA - tip of the nose

transverse tarsal goni

• ADD/ABD (Transverse Tarsal INV/EV): *Stabilize calcaneus* o F: 2" distal to middle of malleoli o SA: Tibial tuberosity MA: Parallel to 2nd MT

2-3 months

• Head control - can lift to 90* briefly • rolls prone to supine • can put some weight on forearms in prone • strong ATNR • needs full support to sit - may have head lag to get there still • poor WBing in standing reflexive grasp palmar

mm of inspiration

• Principle muscles = diaphragm and EXTERNAL intercostal Accessory muscles = SCM, scalenes, pec major (sternocostal portion), pec minor, serratus anterior

nitrates

• Smooth muscle RELAXTION and DILATION peripheral vessels DECREASE ISCHEMIA AE: OTH

16-24 months

• squats • walk backwards • pick up toys from floor w/out falling • ascends/descends stairs (cannot alternate - 2 yo = 2 feet each step) • kick and throw ball • 24 months = immature running (fast walking, no flight pahse) • Fold paper, string beads, stacks cubes Hold crayon thumb and finger

paget dx

♣ Heightened osteoclast activity enlarged but weak bone ♣ Etiology = genetic and geographic, pts > 50 y/o ♣ S+S = MS pain w/bony deformities ♣ Tx = bisphosphonates (inhibit bone resorption), exercise, weight control, cardiac fitness