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adhesive capsulitis meaning

inflammation of shoulder capsule due to adhesions

etiology

cause of disease

primary cause of adhesive capsulitis

unknown, associated with diabetes mellitus, thyroid, cardiopulm issues

secondary cause of adhesive capsulitis

trauma, immobilization, CRPS (complex regional pain syndrome), RA (rheumatoid arthritis), RC tear, bicipital tendonitis

most common presentation for adhesive capsulitis

40-60 (middle age) woman with diabetes mellitus

adhesive capsulitis symptoms

pain with loss of ER, restricted elevation, loss of ROM

adhesive capsulitis treatment

acute: pharmaceuticals, modalities, grade 1-2 mobs (if allowed by state), isometrics, pendulums, progressive resistive exercises (PRE)

chronic: grade 3-4 mobs, working thorugh pain free ROM and increasing strength

adhesive capsulitis key words

female, middle age (40-60), diabetes, pain with loss of ROM, loss of ER, can’t reach overhead

cerebral palsy most common cause

hypoxia to brain (lack of oxygen to tissue) AKA prenatal cerebral hypoxia

cerebral palsy anatomy

hypoxic brain, increased spasticity, motor delays, hip dislocation, upper motor neuron

cerebral palsy etiology

prenatal cerebral hypoxia, maternal malnutrition, infection or rh incompatibility, CVA, trauma to brain, infection following birth, brain tumor

cerebral palsy symptoms

spasticity, hyperreflexive, abnormal tone, abnormal reflex response, impaired voluntary muscle control and mobility (might require AD), one or all extremities, ataxia (cerebellum) or athetosis (basal ganglia), mild to severe

cerebral palsy treatment

depends on symptoms, pharmaceuticals (Seizure meds, botox or baclofen), orthotics, AD, work with OT, caregiver communication (position/handling), stretching, strengthening, mobility, splinting, maximize independence.

cerebral palsy key words

hypoxia, spasticity/hyperreflexia (toe walking), delayed developmental milestones or primitive reflexes, pediatric patient

diabetes mellitus type 1 anatomy

mainly associated with pancreas and unable to produce insulin, islet of langerhans, pancreatic beta cells, insulin receptors to reduce blood glucose.

DM

diabetes mellitus

DM type 1 etiology

exact cause unknown, WBCs attack pancreatic beta cells, most common in children and teens, occurs in 5-10% of individuals with DM

DM type 1 symptoms

polyphagia (extreme hunger), rapid weight loss, polyuria, polydipsia (extreme thirst), ketoacidosis (high acid due to excessive accumulation of ketones), fatigeu, blurred vision, sweet, fruity breath, abrupt onset.

DM type 1 treatment

exogenous insulin, glucose sensor, nutritional management, PT interventions: light ex 50-60% max HR, strengthening, mobility, cardiovascular exercise, exercise might elevate blood glucose.

normal blood glucose

70-100 mg/dL

hypoglycemia

<70 mg/dL, give sugar and wait 15 mins

hyperglycemia

>180 mg/dL, give insulin and wait 15 mins

DM type 1 key words

polyuria, polydipsia, pancreatic beta cells, hyperglycemia/hypoglycemia, needs exogenous insulin, metabolic ketoacidosis, metabolic disease

W/C seat height

heel to popliteal fold and add 2 inches (avg 19.5-20.5)

W/C seat depth

posterior buttocks to popliteal fold and subtract 2 inches (avg 16 in)

W/C seat width

widest part of hips and add 2 in (avg 18 in)

W/C back height

seat to floor of axilla. and subtract 4 in (avg 16-16.5 in)

W/C arm rest height

elbow flexed 90 deg and add 1 in (avg 19 in above chair seat)

axillary crutches positioning

6 in anteriorly, 2 in laterally, 2 in (3 fingers) under axilla, 20-25 deg elbow flexion with grip at ulnar styloid

meaasurementstings

20-25 deg elbow flex at ulnar styloid

cane measurements

uninvolved side, 20-25 deg flex at ulnar styloid

quad cane measurements

uninvolved side, legs facing out, 20-25 deg flex at ulnar styloid

forearm (loftstrand) crutches

1-1.5 in below olecran process, 6 in anterior 2 in lateral, 20-25 deg flex at ulnar styloid

OA anatomy

synovial joints, most common join disease, most common in hips and knees, PIP and DIP joints

OA etiology

primary OA: happens through aging process

secondary OA: results from trauma, obesity, DM type 2, joint injuries and neuromuscular disorders

OA symptoms

osteophy formation, unilateral or bilateral, antalgic gait, genu varus, crepitus, pain and stiffness in the morning that decreases throughout the day, PIP and DIP joint

Bouchard’s nodes

PIP joint

Heberden’s nodes

DIP joint

OA treatment

pain meds, steroid injections, strengthen, modalitites (heat and ice, e-stim), stretching, ergonomics, aquatic therapy, scope with debridement, joint replacement

OA key words

unilateral, hip-knee/WB joints, crepitus (crackling), Bouchard’s or Heberden’s nodes, osteophytes, subsides within 30 minutes in the morning

CVA anatomy

brain

most common CVA etiology

ischemic (thormbus, embolus)

CVA etiology

inschemic (thrombus, embolus), hemorrhagic (subdural, subarachnoid, intracerebral), transient ischemic attack (TIA), most common cause is hypertension. other causes is birth control, DM, obesity, high cholesteral, smoking

CVA symptoms

hemiplegia, hemiparesis, balance deficits, dysphagia, cognitive deficits, difficulty ambulating, depends on side

L CVA

R hemiparesis/hemiplagia, wernicke’s aphasia (temporal lobe), broca’s aphasia (frontal lobe), apraxia (motor planning), L vs R discriminiation deficits, R heminopsia, processing deficits, frustration and overly cautious

R CVA

L hemiparesis/hemiplegia, L side neglect, decreased attention span, decreased spatial awareness, judgment deficits, memory deficits, emotional swings (lability), impulsive, decreased abstract reasoning, L hemianopsia (vision)

CVA treatment

depends on stroke type and region, control HTN, balance, ROM, postural control and awareness, neurodevelopmental treatment (NDT), PNF, fall prevention, safety in home, amb, spasticity management, functional mobility

CVA key words

which side, which region, aphasia, apraxia, language = L side, spatial deficits, lack of attention, emotional lability = R side

PVD

peripheral vascular disease

PVD anatomy

narrowing blood vessels - usually due to atherosclerosis (plaque buildup)

PVD etiology

primary: atherosclerosis, DM, smoking, hyperlipidemia, inactivity/obesity, HTN, injury/surgery, family PMH

PVD symptoms

intermittent claudication (brought on by exercise, relieved with rest), legs tired with prolonged exertion, loss of sensation (numb/tingling), pain at rest, poor circulation (slow healing, cold extremity), weak pulse, loss of hair

PVD treatment

anticoagulants/antiplatelets/thrombolytics, statins, improve walking distance/tolerance, recumbent bike, ROM, PRE, improve functional independence, low cholesterol diet, angioplasty, bypass

PVD key words

intermittent claudication, pain when walking relieved with rest, worse with prolonged activity, atherosclerosis, pain and cramping in calves with exercise, poor circulation/sensation, cold extremities

types of ulcers

arterial ulcer, venous insufficiency ulcer, neuropathic ulcer

neuropathic ulcers anatomy

integument, peripheral nerves (lack of sensation), most likely affect feet

neuropathic ulcer etiology

DM type 2, any other peripheral neuropathy causing loss of sensation at bottom of feet

neuropathic ulcer symptoms

ulcer on WB part of foot, oval or circle, good granulation, little to no wound bed necrosis, exudate (fluid that leaks out into blood vessels), not painful due to lack of sensation, edema to area, cold skin, shiny skin, dry around wound bed, inelastic skin, no protective sensation in foot

Wagner ulcer grade classification scale

0-5, for neuropathic ulcers

Wagner ulcer grade 0

no open wound, pre-ulcerative lesions, healed ulcer, exhibits bone deformity

Wagner ulcer grade 1

superficial ulcer, no subcutaneous involvement

Wagner ulcer grade 2

deep ulcer going to subcutaneous tissue, tensons, ligaments, joint capsule might be exposedWagner ulcer grade

Wagner ulcer grade 3

deep ulcer with abscess, osteitis, or osteomyelitis

Wagner ulcer grade 4

gangrene of 1 digit

Wagner ulcer grade 5

gangrene of foot requiring amputation (disarticulation)

neuropathic ulcer treatment

patient education (inspect feet every day, properly sized footwear, cushioned shoes, seamless socks), maintain cleanliness in LE, check nothing in shoes before putting on, caregiver education (inspect feet), wound care education (dressing determined by exudate present and taking photos to see if wound changes), sensory testing - monolilament, debridement, antibiotics and pharmacological management

neuropathic ulcers key words

DM, peripheral neuropathy, loss of sensation, wagner grade classification, feet/foot, monofilament testing

conduction heat transfer

direct contact between 2 objects of different temperatures, transfers faster through water

conduction heat transfer examples

cold pack, ice massage, cryo-cuff/gameready, paraffin, moistheat

convection heat transfer

heat transfer due to moving air/water over body part, capable of transferring large amounts of heat, make sure pt has good circulation

convection heat transfer examples

fluidotherapy, hot/cold whirlpool

conversion heat transfer

heat is transferred from one form (nonthermal) to another (thermal), requires a medium

conversion heat transfer examples

ultrasound, diathermy

evaporation heat transfer

heat absorbed and changed into water vaopr, cooling the skin, coolant evaporates due to skin heating up

evaporation heat transfer example

vapocoolant spray

radiation heat transfer

transfer of energy from radiation energy (light usually) to heat, take into account energy source,, distance between light and skin, size of treatment area

radiation heat transfer examples

infrared light, laser, UV light

RC tear anatomy

SITS - supraspinatus (most injured), infraspinatus, teres minor, subscapularis

RC tear etiology

increase in age (tissues lose strength/vascularity), traumatic injury or overuse injury

RC tear symptoms

pain with movements that put tension on muscle/tendon, wprse with partial tears, pain with elevation, mobility deficits, crepitus, pain at night (esp when lying on affected side)

supraspinatus test

empty can test, drop arm test

infraspinatus test

infraspinatus test, ER lag

teres minor test

hornblower’s sign

subscapularis test

lift-off test, bear hug, belly press

RC tear treatment

depends on size of tear and extent of loss of mobility/function, surgery, pain meds, PTROM/gentle ROM until 6 wks, slowly add PRE and AROm 6-12 weeks, ROM and strength and endurance 12 weeks+, overall work on scapular stabilization, activity modification, postural re-ed, slowly improving ROM

RC tear key words

special test names positive, supraspinatus, pain in shoulder, decreased mobility, traumatic event, full/partial thickness