Pathology Terms Flashcards

(343 cards)

1
Q

Analgesics

A

Drugs that relieve pain

  • Analgesia = absence of normal sense of pain
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2
Q

Anti-pyretics

A

Drugs that reduce fever

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3
Q

Anti-inflammatory drugs

A

Drugs that reduce inflammation (inflammation does not equal fever)

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4
Q

Opioids

A

Any synthetic narcotic drug derived from opium

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5
Q

Salicylates

A

Aspirin (ASA)

Available OTC (non-opioid)

PTA Implications: Increase risk of bleeding/bruising

DO NOT mix with anticoagulants

Children - DO NOT use to treat chicken pox or flu like symptoms

Pharmacotherapeutics
- Relieves pain (not visceral or severe pain)
- Reduce fever
- Reduces inflammation
- Used as an anticlotting factor

Adverse Reactions
- Gastric Distress
- Nausea/vomiting
- Bleeding
- Hearing Loss

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6
Q

Aceteaminophen

A

Pharmacotherapeutics
* Reduce fever (antipyretic)
* Relieve headache, muscle pain, general pain
* Treat flu-like symptoms

Adverse Reactions
* Liver toxicity*
* Skin rash
* Hypoglycemia
* Neutropenia

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7
Q

NSAIDs; nonsteroidal anti-
inflammatory drugs

A

Examples: Ibuprofen (Advil), Naproxen (Naprosyn, Aleve)

  • Not an anti-coagulant, BUT can enhance anti-coagulant substances
  • Reduce inflammation
  • Provide pain relief
  • Reduce fever

Common use:
- Post-op
- Painful musculoskeletal conditions
- Treatment of inflammatory rheumatic disease

Adverse Reactions
* Abdominal pain, bleeding
* Drowsiness, headache
* Bladder infection, hematuria
* HTN, heart failure

May need to schedule patient according to timing of
medication dosage
* Peak dosage is usually about 2 hours after administration

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8
Q

Opioids versus Opium

A

Opioid (Natural): Ex. Heroin, opium, morphine, and codeine

Opioids (Synthetic): Ex. Demerol, Oxycodone,
Fentanyl, Methadone, Percodan, Percocet

Pharmacotherapeutics
* Pain relief in acute, chronic, and terminal illnesses
* Reduce anxiety
* Control diarrhea
* Suppress cough

Drug Interactions
* Sedatives and anesthetics*
* Antidepressants and anticholinergics*

Adverse Reactions
* Respiratory depression*
* Hypotension*
* Pupil constriction
* Flushing
* Nausea/vomiting
* Hypertension
* Tachycardia
* Anxiety
* Headache

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9
Q

Anesthetics

A

Ex. General - ketamine, propofol, fentanyl; Local - Lidocaine, cocaine; Topical - Lidocaine

Any of the “caines” are anesthetics

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10
Q

Patient Controlled Analgesia (PCA)

A

Self-administered, physician pre-determined dosage of morphine analgesia through PCA Pump.

Common side effects: Drowsiness, Confusion, Decreased, respiration

  • As treating PTA, need to monitor patient’s
    demeanor and ability to safely or effectively
    participate in treatment
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11
Q

Clinical Application: Medicine Use

A

Monitoring pain
* What questions to ask?
* Monitoring patient’s use of medications
* Subjective and can be noted
* DO NOT make recommendations, even for OTC drugs
* What are some non-pharmacological methods of
pain control available to the PTA??
* PTA can administer hot and cold, vibration, TENS, and
Iontophoresis
* Exercise releases endorphins that bind to opioid receptors in the brain

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12
Q

Antihistamines

A

Examples:
* Ethanolamines: Benadryl
* Alkylamines: Dimetapp
* Phenothiazines: Phenergan
* Piperidines: Zyrtec

Drug Reactions
* Epinepherine
* Aminogylcosides
* CNS depressants

Adverse Reactions
* CNS depression
* Dizziness, fatigue, & muscle weakness
* Tachycardia & arrhythmias
* Gastric distress

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13
Q

Corticosteriods

A

Naturally occurring hormones produced by adrenal
cortex and gonadal tissue

Primary use is reducing inflammation. Also immunosuppressants (which is how the inflammation is reduced)

All steroids will end in “-one.”

  • Glucocorticoids (cortisol)
  • Ex: Cortisone, Dexamethasone, Hydrocortisone
  • Decrease inflammation for local or systemic conditions (immunosuppression)
  • Mineralocorticoids (aldosterone)
  • Commonly used in inhalers
  • Ex: Fludrocortisone acetate, Aldosterone
  • Androgens (testosterone); causes masculinization
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14
Q

Corticosteroids- Adverse effects

A
  • Changes in sleep, mood
  • GI irritation
  • Hyperglycemia
  • Na & H2O retention*
  • Impaired wound healing*
  • Hyperlipidemia
  • Cushing’s syndrome* (hormonal disorder caused by prolonged exposure to high levels of cortisol, leading to conditions such as obesity, high BP, diabetes, and osteoporosis)
  • facial puffiness and weight gain
  • Increased susceptibility to infection*
  • Steroid induced myopathy (muscle weakness, wasting)
  • Osteoporosis (inhibits bone mineralization)*
  • Connective tissue breakdown*
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15
Q

Corticosteroids: PTA Implications

A
  • Inflammation and Infection
    -Given early TBI, some SCI
  • Increased susceptibility to infection
  • Intensive Care Setting
  • Infection, impaired wound healing, ICU-acquired paresis, muscle weakness
  • Intraarticular Injections
  • No joint should have more than 3-4 injections, avoid movements that may aggravate symptoms for 2-3 days
  • Exercise
  • Promote weight bearing, closed chain, educate on proper footwear
  • Monitoring Vitals
  • Due to electrolyte imbalance, monitor during aerobic exercise due to CV demand, also fluid retention may lead
    to HTN
  • Steroids, nutrition, stress
  • Increase dietary intake of calcium, vitamin D
  • May interfere with insulin -> regular glucose monitoring (steroid-induced DM)
  • Psychologic considerations
  • Mood changes, changes in adipose tissue distribution, thinning of skin, stretch marks
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16
Q

Anti-Gout Medications

A

Only medicine we need to remember: Colchicine

Decrease uric acid in the blood

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17
Q

Rheumatoid Drugs

A

Disease Modifying Anti-Rheumatoid Drugs (DMARDS)

  • Don’t need to know specific ones currently

Disease Modifying Osteoarthritic Drugs
(DMOADs)

Viscosupplementation
(nondrug)
* Injection: Hyalgan and Synvisc
* Used to help restore viscosity
and elasticity, (reduce friction)

Oral: Glucosamine and Chondroitin Sulfate

Indications for Use
* Improve viscosity and function of the synovial fluid
* Protect articular cartilage

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18
Q

Fibromyalgia

A

Chronic, generalized muscle pain
syndrome

Diffuse soft-tissue pain and physical
findings of multiple tender points

at least 11/18 bilateral tender points*

Systemic problem with widespread
multiple tender points

6 million people in U.S. affected
 Most common MS disorder
◦ Periods of exacerbation and remission
◦ 20-55 years old, women > men
◦ Chronic fatigue syndrome – early form of the condition

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19
Q

Fibromyalgia Syndrome

A

*Experience pain from stimuli not
normally perceived as painful:
- Due to lowered pain thresholds
- Unbalanced autonomic nervous system
response to physical, chemical, and
physiologic stressors

  • Not just muscle pain (systemic) affects other systems of the body in various ways.
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20
Q

Fibromyalgia: Implications for the PTA

A

Modalities for pain relief
◦ US, Hi-Volt galvanic stimulation, pulsed US
with IFC

 Aerobic exercise, resistance exercise

 Flexibility training

 Gentle stretching (during the day to
reduce fatigue)

 Strategies for work modification &
ergonomics

 Aquatic Therapy

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21
Q

Referred Pain

A
  • Pain arising from deep body structures
    but felt at another, distant site
  • Sensory nerves from the skin and
    internal organs converge within the
    spinal cord pathway
  • Visceral organs refer sensations to skin
    in neurological patterns
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22
Q

Sclerotome

A

areas of bone
innervated by a particular nerve root

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23
Q

Nociceptor

A

Noci - pain

specialized sensory receptor that responds to actual or potential tissue damage and send a signal to the spinal cord and brain

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24
Q

3 Types of Nociceptors

A

3 distinct types of
free nerve endings that respond to
different stimulus:

High Threshold Mechanoreceptor (Mechanical - pressure, stretch)

  • Fiber Type: A-Delta: small myelinated neurons [Fast]
    -Responds to: Strong mechanical stimulation
    -Sensation: sharp ‘pricking’, well localized

Mechanothermal Nociceptor (Thermal - hot/cold)

-Fiber Type: A-Delta [Fast]
-Responds to: Strong mechanical stimulation; Noxious heat
-Sensation: sharp ‘pricking’, well localized

Polymodal Nociceptor (Chemical - acids, inflammatory mediators)

  • Fiber Type: C [Slow]
    -Responds to: Strong mechanical stimulation; noxious heat; irritant chemicals
    -Dull aching, burning; Poorly localized
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25
Nerve vs Tract
Nerve is in the periphery while a tract is central
26
Pain Perception: Ascending Pathways
To become aware of pain, noxious stimuli must travel from the dorsal horn of the spinal cord to the brain 2 Tracts responsible for this transmission:  Spinothalamic [fast pain] – spinal cord to the thalamus  Thalamus acts a general relay station sending stimuli to the somatosensory cortex where sharp, discriminative and localized sensations are perceived  Spinoreticulothalamic [reticular pain] – spinal cord to the reticular formation of the brainstem to the thalamus
27
Pain Perception: Descending Pathways
Modulates pain ◦ Not completely understood ◦ Evidence shows our body produces natural endogenous opiates to inhibit perception of pain ◦ Ex: serotonin, dopamine ◦ Release of the opiates is stimulated by pain, intense exercise, laughter, relaxation, meditation, acupuncture, and electrical stimulation
28
Chronic Pain Disorders
- Can be psychologically based - Result of a general medical condition - Chronic post op pain  i.e. phantom limb pain Medical Management ◦ Caring for the whole person  Identifying the mechanism for pain  Pain perception  Psychological impact
29
Chronic Pain Disorders: Implications for the PTA
◦ Counterproductive to speculate whether the pain is real or not ◦ Creating and working within mutually accepted goals ◦ Focus on improving functional outcomes (rather than pain) ◦ Dealing with chronic anxiety & depression in the patient ◦ Monitor for fear avoidance behavior  Pt. education: pain does not equal new injury
30
Osteoporosis
Means porous bones - Systemic condition and metabolic disease involving diffuse loss of bone density and strength ' Combination of decreased bone mass and micro damage to the bone structure that results in a susceptibility to fracture - Bone reabsorption exceeds bone formation - Declined osteoblast function
31
Osteoporosis: Risk Factors - Non-modifiable
 Non-modifiable ◦ Female  Post-menopause ◦ Age > 50 ◦ Caucasian/Asian ◦ Thin, small-frame (less cortical bone) ◦ Family history/genetics
32
Osteoporosis: Risk Factors - Modifiable
Modifiable: ◦ Sedentary lifestyle ◦ Diet and nutrition ◦ Low calcium intake ◦ Smoking ◦ Excessive alcohol intake (> 2 drinks / day) ◦ Excessive caffeine intake (equivalent to > 3 cups of caffeinated coffee) ◦ Excessive tobacco use ◦ Certain medications (Ex. Corticosteroids) Low Body weight and BMI
33
Osteoporosis: Signs and Symptoms
Loss of height, postural changes, back pain and fracture*  Marked thoracic spine kyphosis and “dowager’s hump”  Fractures, commonly in the wrist, hip, vertebral compression factures  Low back and neck pain
34
Vertebral Compression Fracture (VCF)
Fracture of the anterior portion of a vertebrae (commonly seen in people with osteoporosis)
35
Osteoporosis: Tests and Measures
History: vitamin, calcium intake, use of corticosteroids Bone mineral density testing (BMD) Imaging studies ◦ DXA: dual energy x-ray absorptiometry - (-1.0 or higher is normal, -2.5 or lower is osteoporosis) Radiograph: to diagnose fractures
36
Osteoporosis: Treatment
 Prevention is best*  Calcium, magnesium and vitamin D supplements  Regular exercise: aerobic and resistance training provide weight- bearing to bone  Lifestyle changes to decrease risk factors ◦ Minimize caffeine, alcohol, tobacco, adequate nutrition
37
Osteoporosis: Physical Therapy Intervention
Pt. Education - Spinal extension exercises - Heat, massage, spinal support to reduce pain Contraindications - include spinal flexion exercises, mobilization techniques, traction
38
Common Fractures
Greenstick: an incomplete bone fracture where the bone bends and cracks on one side but does not break completely through Spiral: a broken bone that occurs when a bone is twisted, causing the break to coil around it like a corkscrew Comminuted: a break where the bone shatters into multiple pieces Transverse: a bone break that occurs at a right angle, or horizontally, across the long axis of the bone Compound: a broken bone that pierces the skin, creating an open wound Compression: a break in a spinal vertebra (bone) that causes the bone to collapse or compress
39
Specific Fractures
Colles' Fracture: a break in the large forearm bone (radius) near the wrist Boxer's Fracture: a break in the neck of one of the five metacarpal bones in the hand, most commonly the fifth metacarpal near the pinky finger. It is often caused by punching something with a closed fist FOOSH (Fall On Outs Stretched Hand): an injury that occurs when a person falls onto an outstretched hand, causing a break in the bones of the wrist, elbow, or arm Skaters or Snow Border's: in the feet, ankles, or lower legs, due to repetitive impact and landings Avulsion: a bone break where a small piece of bone is pulled away from its main body by a tendon or ligament
40
Osteogenesis Imperfecta [OI] (Brittle Bone Disease)
[not needed for this class] a genetic disorder present from birth where bones are improperly formed due to a defect in collagen
41
ORIF (Open Reduction, Internal Fixation)
a surgical procedure used to treat bone fractures. During an ORIF, the surgeon makes an incision to realign the broken bones (open reduction) and then uses hardware like screws, plates, or rods to hold them in place (internal fixation).
42
Fractures: Healing Time - Bone
◦ 3-4 days- Fractured edges become necrotic. Osteoblasts mobilize in the area (inflammatory phase). ◦ Approx. up to 2 weeks: Osteoblasts form soft callus (reparative phase). ◦ 3-4wks- Hard callus develops. ◦ 3-4 months to years: Fracture is healed, but bone continues to remodel
43
Fractures: General Rehab Principles
Following a fracture there is usually a period of immobilization ◦ Blood clot prevention ◦ Promoting fracture repair  Avoiding substances like nicotine that inhibit fx repair ◦ Monitor for neurovascular and integumentary changes during this period  Compartment syndrome
44
Fractures: Rehab in the Acute Setting
Early Mobilization ◦ Transfer training ◦ Strength training ◦ ROM  Reduces risk of DVT/PE, skin breakdown, pneumonia and decline in mental status  Decrease in LOS  Quicker discharge home
45
Fractures: Complications
 May heal in a bad position: Mal-union  May take longer than usual: Delayed union  Failure to heal: Non-union  Loss of blood supply to area will limit healing (Avascular necrosis)  Emboli (Clot, Plaque, air, etc.)
46
Complications: Osteomyelitis
- Infection may develop in bone if open fracture or external fixation. Look for signs of osteomyelitis and report  Unusual redness, increased pain, swelling, drainage from a external fixator pin site.
47
Resporbtion
Ca+ out of bones
48
Osteoarthritis (OA)
Degenerative Joint Disease (DJD), degenerative arthritis, osteoarthrosis, OA  Breakdown of hyaline cartilage [covers ends of bones] [articular cartilage is a subtype of hyaline cartilage]  Non-inflammatory, slow, progressive damage and loss of articular cartilage  Joint spaces narrow, eventually produces bony remodeling and overgrowth (spurs)  Affects weight-bearing joints; most commonly hips, knees, shoulder, cervical, lumbar spine, hands  Primary – unknown cause, defect in articular cartilage  Secondary – known cause, trauma, infection, hemarthrosis, osteonecrosis  Most common joint disease ◦ 60% of men, 70% of women after age 65 yrs ◦ Approx. 40 million people in U.S.  Most common indication for total joint replacements
49
Progression of OA
 Loss of articular cartilage: leads to inflammation, bony overgrowth, ligament laxity, progressive muscle weakness and atrophy  Cartilage becomes thin and soft, begins to flake off and enter joint cavity  Damaged tissues stimulate enzymes that accelerate the degenerative process  Surface defects appear and expose underlying bone, which then becomes sclerotic  Joint space narrows
50
Osteoarthritis Clinical Manifestations (s/s)
 *Bony enlargement, limited ROM, crepitus on motion, tenderness on pressure, joint effusion, malalignment, joint deformity  Pain on weight bearing  Stiffness after inactivity (sitting, sleeping) ◦ Morning stiffness of 5-10 minutes  Muscle atrophy, weakness, and spasm  Reduced or loss of function  Inflammation, edema with acute exacerbations  Slow and gradual progression of pain - Joints may enlarge and present with nodes. ◦ Buochard nodes on proximal IP joints ◦ Heberden nodes on distal IP joints
51
OA: Medical Treatment
 Medications: NSAIDS  Supplements: Glucosamine  Injections of Corticosteroids and medications based on hyaluronic acid  Joint aspiration to remove fluid  Bracing  Dietary changes-weight loss and exercise  Joint replacement surgery  Education
52
Osteoarthritis: PT Interventions
 Prevention: Healthy lifestyle -> exercise, weight reduction  Improve functional status  Reduce pain, muscle spasms  Modalities  Maintain/improve ROM, flexibility, strengthening, aerobic conditioning ◦ Consider aquatic exercise and less loaded activities (low-impact)  Patient education (about disease, safe exercises)  Assistive devices as needed
53
OA-Surgical Treatment
 Removal of bone spurs (Resection)  Transplantation of new cartilage  Autologous Chrondrocyte Implantation (ACI) [Cartilage from oneself grown in a petri dish and put back into the body where needed]  Osteochondral Autograft Transplantation (OATs) [a surgical technique to repair damaged joint cartilage and underlying bone by taking plugs of healthy tissue (cartilage + bone) from a non-weight-bearing area of the patient's joint and transplanting them into a defect site]  THA (THR)  TKA (TKR)
54
Post-Op Physical Therapy
 Observation of Precautions  **Posterolateral Hip Replacement: NO flexion > 90, IR, or adduction  Exercise to restore strength and function, functional training.  TKA require techniques to improve range of motion
55
RHEUMATOID ARTHRITIS (RA)
 Chronic systemic inflammatory disease with articular and non-articular findings  Chronic polyarthritis  Affects many systems (MSK, CVP, GI)  Unsure of exact cause  Autoimmune disease  Connective tissue (cartilage, adipose, osseous tissue, etc. blood) disease
56
RHEUMATOID ARTHRITIS (RA): Risk factors
◦ Genetic predisposition and environmental triggers ◦ Women>Men ◦ Age (25-50 yrs)
57
RHEUMATOID ARTHRITIS (RA): Clinical Manifestations
Clinical Manifestations  Symptoms begin insidiously and progress slowly  Systemic manifestations: ◦ Morning stiffness, symmetrical, B/L joint involvement, joint swelling, rheumatoid nodules  Articular symptoms  Other complaints: ◦ Weight loss ◦ Fatigue ◦ Diffuse musculoskeletal pain ◦ Weakness  Course can vary considerably  Joints ◦ Multiple joints involved bilaterally ◦ Warm, swollen, painful, stiff ◦ After rest periods, stiff lasting > 30 minutes  Soft tissue ◦ Synovitis (of the synovial membrane), bursitis, tendonitis, neuritis, etc.  Spine ◦ Early involvement of cervical spine ◦ subluxation
58
RHEUMATOID ARTHRITIS (RA): Pathology
Hand deformities are associated with ulnar drift Swan neck deformities and Boutonniere deformities Swan Neck Deformity: a deformity of the finger characterized by hyperextension of the proximal interphalangeal joint (PIP) and flexion of the distal interphalangeal joint (DIP). Boutonniere Deformity: a deformity of the fingers in which the proximal interphalangeal joint (PIP) is flexed and the distal interphalangeal joint (DIP) is hyperextended. Pathology: Body believes synovial tissue to be foreign and attacks it, causing inflammation and joint effusion (swelling). This distends the joint. Enzymes cause breakdown of joint tissues)
59
RHEUMATOID ARTHRITIS: Medical Management
 Early treatment is vital to long term outcomes  Lab testing: elevated erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP)  Mainstay of treatment is PT and drug therapy  Treatment goals: ◦ Reduce pain ◦ Maintain mobility ◦ Minimize edema, stiffness, and joint destruction - Can also use STRONG isometric to not only prevent atrophy but to also reduce pain by STRENGTHENING the muscles.  Pharmacotherapy ◦ Analgesics ◦ NSAIDs: long term use can cause stomach/GI issues. ◦ Corticosteroids: ◦ Note: Corticosteroids can cause delayed wound healing and osteoporosis ◦ Anti Rheumatic Drugs (DMARDs) ◦ Biologic Response Modifiers (BRMs) ◦ Immunosuppressants (methotrexate)
60
GOUT
Represents a genetic heterogeneous group of metabolic disorders  Elevated level of serum uric acid (hyperuricemia)  Uric acid changes into crystals and deposits in peripheral joints (knee and great toe)  Predominantly viewed as form of arthritis
61
Risk Factors
 Middle aged men  Family history  Heavy alcohol consumption  Obesity  Fasting  Medications  Renal insufficiency  HTN  Hypothyroidism  Diet: rich in purines (shellfish, trout, sardines, meat, asparagus, beans, peas, spinach)
62
Gout: Implications for the PTA
 *Swollen, hot joint is always of concern  Need to distinguish between gout and septic joint as a septic joint is an orthopedic emergency  During acute attack: rest, elevation, protection of involved joint
62
Gout: Medical Management
 Goals: ◦ End acute attacks and prevent recurrent attacks ◦ Correct the hyperuricemia  Pharmacotherapy ◦ NSAIDS ◦ Corticosteroids (occasionally intraarticular injections) ◦ Meds to lower the concentration of uric acid (colchicine [kowl-chuh-seen])  Dietary changes, weight loss and monitor ETOH intake
63
Gout: Clinical Manifestations
 Disease occurs in 4 stages  Most common s/s: acute, monoarticular, inflammatory arthritis manifested by exquisite joint pain, occurring suddenly at night  1st MTP common site; ◦ Other sites: ankle, instep, knee, wrist, elbow
64
Gout: Medications
 Allopurinol ◦ Slows rate at which body makes uric acid  Colchicine ◦ Given during acute phase, less common 2’ narrow therapeutic range, many side effects
65
ANKYLOSING SPONDYLITIS
 Also called Marie-Strumpell disease; one of several inflammatory arthropathy of the axial skeleton  Progressive inflammatory arthritis leading to calcification and fusion (ankylosis) of the joints of the spine, sacroiliac joint  Men 2-3x more than women; 15 – 30 years of age; Caucasian and Native American populations  Approx. 2 million people in US
66
ANKYLOSING SPONDYLITIS: Etiology and Diagnosis
 Autoimmune  Genetic component  Seronegative for rheumatoid factor (It's NOT RA)  Clinical manifestations, radiographic findings, MRI to identify sacroiliitis ◦ Bamboo spine ◦ Dagger sign
67
ANKYLOSING SPONDYLITIS: Signs and Symptoms
 Insidious (proceeding in gradual, subtle way - negative way) onset of low back, buttock, hip pain, > 3 months  Tenderness over spinous processes and sacroiliac areas  Ankylosis – fusion or stiffening of the joints; mainly spine and sacroiliac joint, can also be shoulders, hips, knees  “Bamboo spine” - affected joints become fibrosed and calcified, intervertebral discs replaced with bony material, spine loses mobility and appearance of bamboo ◦ Inflammation in synovial joints of spine, enthesitis  "Dagger Sign" - A bright, white (radio-dense) line running vertically down the center of the vertebrae on a frontal X-ray. It's formed by bone building up in the ligaments connecting the back of the vertebrae.  Early stages: ◦ Fatigue, back pain, stiffness, sciatic nerve pain ◦ Symptoms greater in morning; alleviated with movement  As disease progresses: ◦ Lumbar curve lessens, thoracic curve becomes pronounced ◦ Head and neck move forward, hips flexed backwards ◦ Ribcage expansion affected if costovertebral joints are ankylosed
68
ANKYLOSING SPONDYLITIS: Medical Management
 Goal: reduce inflammation and stiffness  Maintain mobility, proper posture, exercise  Medications to reduce pain and inflammation ◦ NSAIDs, analgesics, muscle relaxants ◦ DMARDS  Surgery - rarely
69
ANKYLOSING SPONDYLITIS: Implications for the PTA
Ankylosing - fusion [Ankylosaursus - "Fused Lizard" or "Stiff Lizard"]  Maintain mobility of the spine, especially into extension, proximal peripheral joints ◦ Flexibility exercises  Modalities and postural training may be used for pain relief.  Aerobic exercise, stretching, pulmonary exercises ◦ Chest expansion exercises ◦ Balance  Aquatic therapy; emphasize extension  AVOID ◦ High-impact activities; contact sports, high-risk activities ◦ Flexion activities
70
POLYMYALGIA RHEUMATICA
Description ◦ ‘pain in the muscles’ ◦ Chronic and systemic; associated with giant cell arteritis ◦ Diffuse pain and stiffness; neck, low back, shoulders and legs, proximal joints of shoulder and pelvic girdles Etiology (Not necessary to know) ◦ Unknown ◦ Possible genetic ◦ Possible environmental factors  Virus?
71
Polymyalgia Rheumatica: Treatment
Signs and Symptoms (No need to know at this time)  Treatment ◦ *Medications to reduce pain and blood clotting
72
Polymyalgia Rheumatica: Implications for the PTA
Focused on improving functional activity, reducing pain and stiffness, light to moderate aerobic conditioning, and tissue mobilization with exercises and modalities as well as possibly evaluating the patient’s home or work situation.
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SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)
 Chronic, inflammatory, autoimmune disease, affecting multiple organ systems ◦ skin, bones, joints, NS, kidneys, lungs, blood, blood vessels, other organs  Remissions and exacerbations  Sudden or delayed onset  Women > men (10:1)  Different forms: ◦ *Systemic Lupus – most common* ◦ Discoid Lupus – affects only the skin ◦ Drug-induced Lupus – triggered by medications
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SYSTEMIC LUPUS ERYTHEMATOSUS (SLE): Etiology
 Unknown, cause; immunologic, environmental, hormonal, genetic factors  Autoimmune response that leads to production of circulating autoantibodies ◦ Production of antibodies against its own cells (tissue components)  React to DNA, RNA, nuclear proteins  Deposit immune complexes in connective tissue  Produces inflammation and tissue damage
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SYSTEMIC LUPUS ERYTHEMATOSUS (SLE): Signs and Symptoms
 Musculoskeletal system ◦ Arthralgias, arthritis ◦ Fever, weight loss, malaise, fatigue  Cutaneous ◦ Facial rash (butterfly rash / malar rash), rash on sun-exposed areas, vasculitis  Cardiopulmonary system ◦ Pleuritis, pericarditis, dyspnea
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SYSTEMIC LUPUS ERYTHEMATOSUS (SLE): Treatment
 No cure  Mild cases ◦ Anti-inflammatory medications  Severe cases ◦ Corticosteroids and immunosuppressants ◦ Avoid aggravating factors  Observe for side effects of corticosteroids(edema, weight gain, bruising) long-term use-> osteoporosis, myopathy, tendon rupture, diabetes
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SYSTEMIC LUPUS ERYTHEMATOSUS (SLE): Implications for the PTA
 Skin care, prevention of skin breakdown  Generalized fatigue – activity pacing, energy conservation  Follow a prescriptive exercise plan (muscle strengthening, endurance), avoid excessive bed rest, protect joints  Treatment frequently includes posture reeducation, strengthening, and ROM and stretching.
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SpondylOSIS (osis - condition, process, disease, abnormal state)
Degenerative change in the spine = Osteoarthritis of the spine ◦ Commonly affects the neck ◦ Result in bone spur growths that can put pressure on spinal nerves or the spinal cord Etiology ◦ Aging process  Laxity in spinal ligaments, herniated discs ◦ Previous spinal injury ◦ Faulty Posture
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SpondylOSIS: Clinical Presentation
 Pain: may be referred  Pain with movement  Pain in sacroiliac region, buttocks, and hips  Muscle spasms  Altered sensation and paresthesias  Limited range of motion/hypomobility  Osteophyte formation
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SpondylOSIS Treatment
 Analgesics, anti-inflammatories  Decompressive surgery  Cortisone injections Physical Therapy Intervention  Restore function through postural re- education and exercises  Reduce pain with use of heat, massage, relaxation exercises  Modalities  Patient education
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SpondylOLYSIS (-lysis - loosening, dissolving, decomposition, or breakdown)
◦ Structural deformity in the pars interarticularis of lumbar spine vertebrae ◦ Usually occurs at L4/L5 or L5/S1 ◦ Incidence is 3-7% of the U.S. population, increases with athletes in contact sports or gymnastics ◦ CAN CAUSE anterior slipping of the L5 vertebra over the sacrum called spondylolisthesis (Grade 1 – 4)
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SpondyLOLYSIS: Signs and Symptoms
◦ May be clinically absent ◦ Discovered on radiograph
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SpondyLOLYSIS: Etiology
Etiology ◦ Cause unknown ◦ Repeated microtrauma from gymnastics, weight lifting, football ◦ Genetic defect ◦ Spina bifida occulta
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SpondyLOLYSIS: Treatment
◦ Analgesics ◦ Spinal fusion ◦ No extension exercises ◦ Dynamic stabilization exercises of trunk/spinal stabilization, abdominal strengthening
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SpondylolisTHESIS (-thesis - to put, place)
Description ◦ Vertebra becomes anteriorly disPLACED ◦ Usually affects L4/L5 or L5/S1 ◦ Age of onset usually > 40, women > men (3:1)  Etiology ◦ Disc degeneration and bone disease (arthritis) ◦ Birth defect or trauma to vertebral column
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SpondylolisTHESIS: Signs and Symptoms & Medical Treatment
Signs and Symptoms ◦ Low back pain, referred pain ◦ Muscle spasm ◦ Increased lumbar lordosis ◦ Step deformity-one spinous process palpated anterior to next Medical Treatment ◦ Analgesics ◦ Spinal fusion
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SpondylolisTHESIS: Physical Therapy Intervention
 Exercise – avoid extension that may add stress  Abdominal strengthening  Postural re-education  Modalities for pain relief  Abdominal binder  Patient education
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Kyphosis
Exaggeration of the normal posterior thoracic curvature  Excessive rounding > 45-50 degrees (20-40 degrees is normal) ◦ Can have rounded shoulders, forward head, and Dowager’s hump
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Kyphosis: Etiology
◦ Can be from posture or disease ◦ Chronic spasticity of pectoralis major and minor, serratus anterior, weak rhomboid major and minor ◦ Osteoporosis in older persons ◦ Tuberculosis of vertebral bodies, ankylosing spondylitis, cancer, benign tumors, spina bifida, cerebral palsy, poliomyelitis
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Kyphosis: Signs and Symptoms
◦ Asymptomatic until hump becomes obvious ◦ Mild back pain and fatigue ◦ Decreased mobility of the spine ◦ Rounded back and shoulders ◦ Chest may cave in, head moves forward
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Kyphosis: Treatment & Physical Therapy Intervention
Treatment ◦ Exercises ◦ Bracing ◦ Spinal fusion Physical Therapy Intervention  Strengthening of the back muscles  Stretching of the chest muscles  Postural education Kyphosis
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Scoliosis: Structural vs. Functional
 Structural ◦ Fixed curvature of spine due to vertebral rotation, asymmetry of ligamentous supporting structures ◦ Unknown (80% of cases) in adolescents or a congenital malformation of the spine and diseases ◦ Idiopathic  Functional (Postural, reversible) ◦ Caused by pain, poor posture, leg length discrepancy, muscle spasm ◦ Disappears when the cause is remedied ◦ Appears to change configuration when the
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Adam's Test
Scoliosis Test - Adam's rib was taken out to create Eve -Rib hump shows when person bends forward at the waist and hump/unevenness is observed from posterior view in person with scoliosis.
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Scoliosis – Medical management
Treatment ◦ Prevention of postural or idiopathic structural scoliosis ◦ Monitoring every 2-6 months for curves < 25 degrees ◦ Body / back brace if curve is > 25-45 degrees ◦ Surgery if curve is > 45 degrees ◦ Spinal fusion
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Scoliosis: Implications for the PTA
 Exercise programs: strengthening – trunk extensors, abdominals, gluteals to reduce muscle imbalances  Stretching; iliopsoas, low back extensors, lateral trunk flexors on concave side  Skin care with braces  Post Op ◦ Following physician protocol ◦ Segmental Stabilization vs. Harrington Bods
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Kyphoscoliosis
 Scheuermann’s disease  Structural deformity affecting adolescents between 12 & 16  Most common cause of kyphosis in adolescence  In the aging population, develops 2’ poor posture, disk degeneration, vertebral compression fractures, endocrine disorders, arthritis Clinical Manifestations  Adolescent kyphosis is usually asymptomatic  Prominent vertebral spinous processes  Tenderness and stiffness of spine  Tightness of pectoral, hamstring, and hip flexor muscles
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Lordosis
◦ Aka hyperlordosis, saddleback, or swayback ◦ Exaggeration of the normal anterior curvature of the lumbar spine ◦ Can lead to degenerative disc disease or herniated discs in the lumbar spine Etiology ◦ Postural compensation for added abdominal mass, girth, as in pregnancy and obesity ◦ May accompany spinal disease such as osteoporosis or spondylolisthesis
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Atrophy vs. Hypertrophy
Reduction in cell size Increase in cell size
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Metaplasia
Change of cell from one type to another
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Hyperplasia vs. Hypoplasia/Involution
Increase in number of cells Decrease in number of cells
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Muscular Atrophy
Description- ▫ muscle wasting with decrease in muscle cell diameter * Etiology ▫ Prolonged inactivity, poor nutrition, motor nerve dysfunction * Signs and Symptoms ▫ Muscle appears smaller, “looser”, “flattened” ▫ Decreased strength * Treatment ▫ Physical exercises/strengthening activities
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Types of Strains
Grade 1 ▫ Damage to less than 5% of muscle fibers ▫ Requires 2-3 weeks of rest Grade 2 ▫ More extensive damage but not complete rupture ▫ Requires 3-6 weeks of rest Grade 3 ▫ Complete rupture of the muscle ▫ 3 months of rehab ▫ If sports related: usually a surgical repair
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Tendinitis
▫ Inflammation of a tendon from microtrauma ▫ Usually due to repetitive motion/overuse, direct blows, or excessive tensile forces Treatment ▫ Rest, ice, analgesics, anti-inflammatories ▫ ROM activities
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Bursitis
▫ Inflammation of the bursa (from overuse, trauma, gout or infection) Symptoms ▫ Pain w/ rest, limited ROM Diagnosis ▫ By clinical exam -swelling, pain Medical Management ▫ NSAIDS, acetaminophen, steroid injection PTA Role ▫ Flexibility exercises, ROM, STM, modalities
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Plantar Fasciitis
* chronic inflammation of plantar fascia Clinical Manifestations: * pain along medial border of calcaneous, pain is worse in a.m. * Possible increase of sx's with ankle DF Medical Management: * NSAIDS, acetaminophen, steroid injections (last resort) Interventions: * modalities, flexibility/stretching, joint mobilization, night splint, strengthening of invertors *Consider strengthening of inverter muscles as they help maintain the arch. Tib. Post & Ant. (main) and others(?)
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Achilles Tendinitis
Clinical Manifestations * overuse, repetitive trauma (overloading of tendon) Interventions * acetaminophen, NSAIDS, PT
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Achilles Rupture
Definition/Etiology: * occurs with sudden eccentric-concentric contraction * Usually 3-4 cm proximal to insertion * Men (age 20-50 yrs) * h/o corticosteroid injections Clinical Manifestations: * defect/gap of tendon, (+)Thompson Test Medical Management: ▫ Non-surgical (usually a period of immobilization) ▫ Surgical * Interventions: modalities, ROM, flexibility, strengthening activities
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Medial Tibial Stress Syndrome (MTSS)
* aka Shin splints , anterior tibial periostitis Definition ▫ Musculotendinous overuse condition (ant. tibialis, extensor hallucis longus, post. tibialis) ▫ Caused by abnormal biomechanical alignment, poor conditioning, improper training methods ▫ Found often in runners (hard/uneven surfaces) Conservative Treatment ▫ Rest, ice, stretching, strengthening
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Osgood-Schlatter Syndrome
Knee pain in growing adolescents, caused by fibers of the patella tendon pulling small bits of bone from the tibial tuberosity ▫ More common in boys 10-15 years Symptoms: knee pain, aching below (tibial tubercle), inflammation of patellar tendon ▫ Aggravated by activity Treatment: activity modification, decrease pain/swelling
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Patellar Tendinitis
aka Jumper’s knee, Runner's Knee Clinical Manifestations: * Pain directly over the patellar tendon * Pain with activities, particularly jumping * May be exacerbated by quadriceps tightness Interventions: * Protection phase: Rest, NSAIDs, modalities, gentle ROM, Stretching * Controlled motion and return to function phase: strengthening, dynamic control, pain free mobility, LE stability * Other: Braces or support straps, taping
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Rotator Cuff: Tendonitis
Clinical Manifestations: * Minor pain; can radiate down the side of the arm * Sudden pain with reaching activities/overhead activities * Pain at night * Loss of strength Interventions: * Rest, NSAIDs, steroid injections * PT: limit overhead activities, ROM, posture, strengthening, stretching
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Rotator Cuff: Tendonitis - Impingement
 In laborers, athletes, those that have repeated overhead activities, faulty posture  Special tests: Hawkins Kennedy test, Neer’s impingement  Hawkin's Kennedy  Neer's  Treatment: Rest, ice, activity modification -> strengthening (scap. stabilization), posture -> return to activity
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Rotator Cuff Tears
Clinical Presentation * Pain and weakness with overhead movement especially abduction Clinical Tests: * Drop Arm test (RC Tear), Empty Can (for supraspinatus) Surgery: may need ABD. pillow, NSAIDS, PT
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Lateral Epicondylitis
Affects Extensors Common Manifestations: -Lateral Elbow Tendinopathy -Tennis Elbow Symptoms ▫ Pain over lateral epicondyle, usually with gripping activities/repetitive wrist extension ▫ Extensor carpi radialis brevis muscle -> may also involve extensor digitorum Management * Protection phase: decrease pain, immobilization prn, cross-friction massage, STM, passive stretching * Controlled motion and return to function phase: -passive stretching/flexibility, cross-friction massage, dynamic resistance exercises, strengthening
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Medial Epicondylitis
Affects Flexors and Pronator Teres Common Manifestation: - Bowler’s or Golfer’s Elbow  Involves common flexor/pronator tendon  Repetitive movements into wrist flexion  Less common than lateral epicondylitis Treatment * Refer to lateral epicondylitis treatment phases
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DeQuervain’s Tenosynovitis
Special Test: Finklestein's Test - tuck thumb into closed fist and ulnar deviate. * Inflammation of the abductor pollicis longus & extensor pollicis brevis (EPB) * Clinical Manifestations: Pain on radial side of wrist, increased with ulnar deviation, painful nodules, + Finkelstein Test * Interventions: Activity modification, bracing, RICE, stretching
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Dupuytren’s Contracture
* Formation of a flexion contracture, palmar nodules, and thickening band/cord of palmar fascia ▫ Usually involves 4th and 5th digits * Risk Factors: Diabetes*, heredity, DM, seizures, ETOH use, increased age * Nonsurgical Treatment * Surgical Treatment
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Ankle sprains: Mechanisms of Injury
95% of all ankle sprains involve lateral ligaments Combination of PF, inversion & adduction of the foot & ankle * ATFL * CFL * PTF: rarely torn, strongest of lateral ligaments Stepping off a curb, stepping on a rock or into a hole
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Ankle sprains: Clinical Manifestations
* (+) Anterior drawer test - assesses the anterior talofibular ligament * (+) Talar tilt test - assesses the calcaneofibular ligament * Ecchymosis (bruising) * Swelling * Pain * Proprioception deficit * Decreased ROM * Restricted ambulation
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Classification of Ankle Sprains
Grade I * No loss of function with minimal tearing of ligament, usually the anterior talofibular Grade II * Some loss of function, partial disruption of anterior talofibular & calcaneofibular Grade III * Complete loss of function, complete tear of ATFL and CFL
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Ankle Sprain: Interventions
1st & 2nd degree can be effectively managed non-operatively 3 Phases of intervention *Protection Phase - PRICE, gentle ROM (sagittal plane) pain free, pt. education, Isometrics (stronger ones can be used because we are talking about injured ligaments, not muscle) * Controlled Motion Phase - Continue with splinting, gait training, mobilizations, ROM, therex (avoid end-range), stretching of gastroc-soleus, balance activities, strengthening * Return to Function Phase - Strengthening with elastic bands, neuromuscular reeducation – add instability, unstable surface training, weight-bearing activities, return to sport/activity training
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Knee Ligament Injuries
Grade I * An incomplete stretching of collagen fibers Grade II * Partial loss of ligament fiber continuity * A few may be completely torn, but most of the ligament remains intact Grade III * Completely torn * No continuity of the ligament
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ACL Injury Etiology
* Females > males Common mechanism: rotational -Contact: force applied to lateral aspect of knee resulting in a large valgus movement * May also injure MCL and medial meniscus - Noncontact: a) Tibia externally rotates on a planted foot b) forceful hyperextension of the knee Clinical Manifestations * Depending on the grade of the injury * ACL is intracapsular increased joint effusion * Joint instability Special Tests * Lachman Test (+) * Anterior Drawer Test (+) * Pivot Shift Test (+)
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ACL Injury Interventions
Operative management * Different procedures - * Autograft procedures - Gracilis tendon - Semitendinosus tendon - Patellar tendon Non-Operative Management * Progresses at a faster pace than surgery: Strengthening muscles to help stabilize knee
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Posterior Cruciate Ligament (PCL) Injuries
Method of Injury Caused by posterior tibial force – fall on flexed knee, hyperflexion of knee, hyperextension with foot planted Clinical Examination * Posterior Drawer Test * Godfrey Tibial Sag Test Treatment * Conservative – RICE, bracing, quad strengthening post acute phase * Surgical – autograft, allograft, limit knee flexion acutely ↓ stress on graft
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MEDIAL/Lateral COLLATERAL LIGAMENT INJURIES
* Most common ligament injuries seen * Usually from a direct contact to the lateral knee * Grade III MCL injuries are usually associated with an ACL lesion as well * Do not forget the medial meniscus and MCL are attached to each other * The Unhappy Triad (terrible triad) Clinical Manifestations * Patient may hear a pop * Swelling * Possible ecchymosis (sweating) * Impaired gait * Pain * Positive Valgus/Varus test
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MENISCAL Tears (Not important now)
5 main types of tears * Horizontal * Longitudinal* (complete or incomplete) * Degenerative * Flap* (81% meniscal tears) * Radial
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Menisci
* C-shaped or semicircular fibrocartilage on the tibial plateau * Contain primarily (90%) Type I collagen * Function of the menisci * Stability, shock absorption, load transmission, nutrition, lubrication, reduce jt. stress
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Meniscal Injury: Clinical Presentation
* Mechanism of Injury: Weight bearing with rotation or hyperflexion * Pain, clicking and possible locking Clinical Tests * Apley’s compression test * McMurray’s test
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Meniscal Injury: Management
* Options are related to the location of the tear (red on red, red on white, or white on white) as well as the ability of the meniscus to repair itself Surgical indications: * Symptoms affecting ADLs * (+) finding on clinical exam * Failure of conservative Rx * Absence of other causes for knee pain * Lesion in vascular outer third of medial or lateral meniscus
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Meniscal Surgeries
Menisectomy * Avoid a total removal, usually partial Meniscal repair * Usually associated with an ACL repair * Usually WB more rapidly after peripheral zone repair * Meniscal transplantation * Allografts used restore normal function * Excellent results with proper indications followed
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PATELLOFEMORAL PAIN SYNDROME (PFPS)
The undersurface of the patella can wear on the femoral surface causing pain. If the patella tracks laterally it is more likely to wear since the lateral femoral condyle is more prominent Anterior knee pain - Usually provoked by physical activity (running, squatting, stair climbing) * Women are affected 2x more than men Causes are multifactorial * Overuse injuries (Open chain quad with heavy weights and activities such as bicycling with seat low) * Patellar instability and lateral tracking * Direct trauma * Joint degeneration * Soft tissue length and strength imbalances
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Patellofemoral Tracking
Patellofemoral Malalignment – resulting in increased Q angle and can cause lateral tracking of the patella. Causes include: 1. Patellar Position – patella alta 2. Tight IT band/lateral retinaculum 3. ↑external tibial torsion 4. Femoral anteversion 5. Foot pronation 6. # 3-5 together = miserable malalignment 7. VMO insuffciency 8. Hip abductor weakness
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PFPS Treatment
Primarily conservative treatment (PT) * Taping * Patellar braces * Foot orthotics * Patella mobilizations * Strengthening and stretching - hamstrings, rectus gastroc
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Shoulder Dislocations
* ‘Unidirectional instability’ ‘Hypermobility’ * 95% occur in anterior-inferior direction * UE is abducted, forcefully externally rotated * Causes tearing of inferior glenohumeral ligament, anterior capsule, and occasionally glenoid labrum * Most commonly dislocated joint in the body * May be atraumatic or traumatic (usually associated with complete rupture of RC) * High recurrence rate
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Shoulder: Anterior Dislocations - Clinical Presentations
* Humeral head in anterior inferior position upon observation * Pain, muscle guarding * Tests to check for anterior instability: * Apprehension Test * Anterior Drawer Test * Anterior Load and Shift
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Shoulder: Anterior Dislocations - Interventions
Non-operative * Initial protection of 4-6 weeks, occasionally immobilized * Avoid motions that reproduce the dislocation: abduction, horizontal abduction and ER Operative * Anterior capsulolabral reconstruction (Bankart Repair) * ROM limited per physician orders * Shoulder strengthening
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Shoulder: Labral Tears - Clinical Manifestations
* Shoulder pain, pain with overhead activities, weakness, instability * SLAP Tear * Locking, popping catching or grinding * Pain with movement or lifting * Clinical tests: Biceps load test, Slide test * Bankart Lesion * Shoulder pain not localized, but worsens when the arm is held behind the back * Weakness & instability * Clinical tests: Clunk tests
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Shoulder: Labral Tears
SLAP * Superior Labrum Anterior and Posterior * Commonly in pitchers * May also involve the biceps tendon Bankart lesion * At anteroinferior labrum * Coincides with anterior dislocation of the GH joint * Involves glenohumeral ligament
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Shoulder: Labral Tears - Interventions
SLAP Tear - Nonsurgical * NSAIDs and PT for 3 to 6 months - Surgical * Arthroscopic * Immobilized 2-4 weeks * Follow post-op protocol, Avoid biceps strengthening and stretching since attaches to labrum Bankart Lesion - Nonsurgical * Not very effective; recurrent instability rate 17-96% under 30y old - Surgical * Arthroscopic or open, but does not significantly improve shoulder functionality * 1/3 of stabilized shoulder experienced dislocation after 8-10y
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AC Joint Separations
* The area between the clavicle and the acromion separates * Mechanism of injury - Most common is from a fall directly onto the shoulder or outstretched arm - Identified with a visible deformity, may also need a radiograph * Clinical tests: Step deformity and Positive piano key sign *Treatment - Non-surgical * Sling * Ice * Medications for pain - Most return to near full function. If full function does not return, then surgery will be the option
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AC Joint Separation: Grades
Grade 1 * Simple sprain of the AC ligament * Normal appearance on radiograph Grade 2 * Tear of the AC ligament & sprain of the coracoclavicular (CC) ligament Grade 3 * Tears of both ligaments and significant deformity
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Ulnar Collateral Ligament Tear
- Elbow MCL - Commonly affects baseball pitchers - Usually due to repetitive valgus stress * In particular pitchers, but can include, cheerleading, gymnastics and wrestling Symptoms * Pain along the medial side * May have a popping noise; catching * Occasionally swelling, if ruptured ecchymosis * Loss of elbow motion
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Ulnar Collateral Ligament Tear
Non-surgical Treatment * Medications for pain * Treat initially with rest and activity modification * Movement analysis * Strengthening exercises (elbow flexors) * Taping (for return to activity) Surgery * Failed conservative treatment * Arthroscopic if joint is not unstable * If acute injury * Direct repair * If chronic injury * May need to replace the ligament & reconstruction * Tommy John Surgery
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Spine Pathologies - Disc - Incidence
* Incidence - ↑ in middle age (less than 45 y/o). Higher incidence in men. Less common in elderly, but disc are deteriorating so there is some risk. * Contributing Factors: * ↑ forces on the disc * Improper body mechanics – bending, lifting, posture * ↑ body weight/↓ overall fitness level
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Spine Pathologies - Disc - Signs & Symptoms
Signs & Symptoms * LBP – unilateral, bilateral, generalized * ↑ or radiates with sitting/ forward flexion * ↓ or centralizes with walking, trunk extension * Is affected by side bending if spinal nerve is laterally or medially impinged Radicular Sx * Along dermatomes or along sciatic nerve * Pain, paresthesias, hypethesias * Muscle weakness along myotome
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Spine Pathologies - Disc - Objective Examination
* Posture – lateral shift (correctable?), ↓ lordosis, forward bend, weight bears on hands in sitting * Palpation – tenderness, spasms, edema * AROM – LOM, affect of ROM on pain (centralizes or peripheralizes) * Compression/Distraction * Quadrant Test * SLR + if LBP at 30 – 60 ̊ * Slump Test * Neurological * Tests for Malingering (pt. faking sx's) * Waddell’s - tests for symptom magnification * Hoover Test – cup hands in heels to determine if trying to lift LE
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Spine Pathologies - Disc - Diagnostic Tests
Diagnostic Tests * Radiographs (rule out fracture, not diagnostic for herniation) * MRI * Myelogram * EMG
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Spine Pathologies - Disc - Treatment
Conservative * Modalities * Exercise, normalize WB, progress to spinal stabilization * McKenzie Exercises (performed by standing and leaning back) * Education * Nerve glides (flossing) * Oral Medication/Epidural Injections * Spinal Supports Surgical * Discectomy – posterior/anterior approach * Laminectomy with discectomy * Surgeon could choose to fuse affected vertebrae * Microdiscetomy –minimally invasive * Disc Replacement * IDET-intradiscal electothermal therapy
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Sacroiliac Joint (SI) Injuries
* Falls * Disease-Ankylosing spondylitis * Muscular forces acting on pelvis: check for weakness(stabilizers-abs, gluts) and tightness of muscles * Remember that tightness in the hip can transmit forces to the pelvis * (hamstrings, hip flexors, rotators of hip)(if tight-stretch, while stabilize pelvis) * Pregnancy and ligamentous laxity * Improper lifting or twisting * LLD
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Sacroiliac Joint (SI) Injuries - Related Terms
* Anterior and posterior torsion (rotation) - One side of pelvis (ilium) is rotated (not the whole pelvis turns - remember SI Joints) (No need to know these for test) * Upslip vs. Downslip - Entire side slips up or down * Innominate outflare (ASIS out) * Innominate inflare (ASIS in)
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Sacroiliac Joint (SI) Injuries - Clinical Tests
1. Posture: pelvic asymmetry 2. Palpation 3. Testing hip and abdominal muscles 4. FABER (Flexion, ABduction, ER) test SI joint motion-is it hypermobile or hypomobile? * A. Forward Flexion test- research shows not good method * B. Compression and Distraction Tests * C. Injections of local anesthetic by physician
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Cerebrovascular Accident (Stroke)
“CVA”, a stroke, or a “brain attack”  Sudden, focal disruption in cerebral blood flow, with death of brain tissue leading to irreversible brain damage  Symptoms last more than 24 hours  Men > women  Leading cause of disability and 3rd leading cause of death in the US
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Transient Ischemic Attack
Stroke symptoms that last LESS than 24 hours
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CVA: Etiology/Risk Factors
- Cerebrovascular disease; primary cause  Damage to blood vessels of brain - Risk Factors  Increased age (> 55 yrs.)  Race: increased in African Americans  Men > Women  Family h/o stroke  HTN  Heart disease  DM  Cigarette smoking
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Types of CVA
Hemorrhagic CVA  Ruptured blood vessel  Aneurysm ruptures -> blood seeps into surrounding tissue and creates pressure -> symptoms dependent upon which area of the brain is affected Ischemic CVA (Most common, 85% of strokes)  Blood clot in cerebral arteries/branches  Atherosclerosis leads to an embolus -> clot travels and blocks a smaller blood vessel in the brain -> lack of oxygen leads to brain tissue necrosis
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Stroke Procedure: F.A.S.T.
Face is uneven, weak, or numb Arm is weak or numb Speech is strange Time to call 911
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CVA: Impairments
Impairments will vary depending on the area, but may include:  Aphasia Expressive: ‘Broca’s’= interrupted/awkward words Receptive: ‘Wernicke’s’ = fluent, spontaneous speech, impaired auditory comprehension Global: combo of expressive & receptive  Dysphagia: difficulty swallowing  **may lead to aspiration (incr. risk of respiratory distress & pneumonia)
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Circle of Willis
a vital ring of arteries at the base of the brain that connects the internal carotid and vertebrobasilar systems, acting as a crucial "bypass" or collateral pathway to ensure continuous oxygenated blood supply to the brain, even if one of the major arteries becomes blocked, preventing or reducing the impact of strokes and ischemia
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Left vs Right side brain damage:
Left: - Right side paralysis - Speech and memory deficits - Cautious and slow behavior Right: - Left side paralysis - Perceptual and memory deficits - Quick and impulsive behavior
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Stroke Possible Impairments
Aphasia Expressive: ‘Broca’s’= interrupted/awkward words (sometimes called "non-fluent") Receptive: ‘Wernicke’s’ = fluent (as in words just flow out - doesn't make sense), spontaneous speech, impaired auditory comprehension Global: combo of expressive & receptive Dysphagia: difficulty swallowing  **may lead to aspiration (incr. risk of respiratory distress & pneumonia) Hemiparesis: one-sided weakness Hemianopsia: loss of vision Flaccidity: transient decrease or lack of resistance to PROM (immediately after spinal shock after injury) Spasticity: increased resistance to PROM (spasticity is always associated with CNS disorder) (velocity dependent)
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CVA: Treatment
 Immediate medical attention, within 90 minutesafter onset of symptoms  Imaging: CT Scan  *Clot-busting medications: tPA (tissue plasminogen activator) - Clot-busters are not anti-cuagulants  Anticoagulants for ischemic type  Control of hypertension and brain bleeds for hemorrhagic type  Reduce hypertension and blood cholesterol, anticoagulants or antiplatelet treatment
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CVA: PT Intervention
* May begin in ICU if indicated for bed mobility and range of motion, progressing to strengthening exercises and ambulation as tolerated * Training on how to use the affected and neglected extremities * Gait training and adaptive equipment as necessary * Follow precautions
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Transient Ischemic Attack (TIA)
 Brief episode of impaired brain functioning due to a temporary reduction of blood flow  Individual remains conscious  Complete recovery in 24 hours with no residual dysfunction; > 24 hours is a CVA  Can indicate development of CVA or stroke (1/3 of patients)  Etiology, signs and symptoms, and treatment are the same as those of a CVA
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Traumatic Brain Injury (TBI)
 a head injury, with external physical force affecting brain function  Impairment of cognition and physical function which can be temporary or permanent  Initially, diminished/altered state of consciousness  Behavior and emotional changes
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Traumatic Brain Injury (TBI): Etiology
 Open injuries - meninges are breached and the brain is exposed  Closed head injuries  Epidural or subdural hematoma occurs -> blood creates pressure on brain tissue -> ischemia of brain tissue  Edema of brain tissue -> diffuse pressure on brain -> increased intracranial pressure - Primary injury: direct damage to brain - Secondary injury: bleeding or something after the fact
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Traumatic Brain Injury (TBI): Coup – contrecoup injury
The brain hits one part of the brain as well as the directly opposing part of the brain  Creates a shearing effect
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TBI Signs and Symptoms
 Mild to severe range  Loss of consciousness, seizures, coma, death  Headaches, dizziness, nausea and vomiting  Altered cognition, changes in personality or emotions, retrograde or posttraumatic amnesia, post-traumatic stress disorder, anterograde amnesia (can't make new memories)  Glasgow Coma Scale (level of conciousness)  (3-15 scale; lower = more impaired 3 = coma, doesn't go lower)
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TBI Impairments
 Cognition/Arousal  Memory  Anterograde (after the accident)  Retrograde (before the accident)  Hypertonicity and hypotonicity  Possible fractures and soft tissue injuries  Strength and ROM issues
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PT Intervention for TBI
* Treatment will begin in the ICU * PROM, progressing to more active strengthening with transfer training, wheelchair training, and gait training * Must be aware of the patient’s cognitive deficits in order to communicate with and teach the patient appropriately
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PT Interventions post Concussion
 Rest and recovery  Restore strength and activity tolerance  Eliminate dizziness and improve balance  Reduce and eliminate headaches  Return to normal sport/activity
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Multiple Sclerosis (MS)
 Autoimmune disorder  Chronic, progressive demyelination of neurons of the brain, spinal cord, cranial nerves (of CNS), sclerotic plaques  Periods of remissions and exacerbations  Women > men (at least 2:1); onset between 20 - 50 years old  Fluctuating periods. Both relapsing-remitting (most common) and primary progressive  Exacerbations related to stress, heat, fatigue, infections
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MS Etiology
 Genetic defect reducing the ability of T-cells to turn off the immune response -> autoimmune attack on the myelin -> scar tissue causes plaques which build up in spinal cord and brain -> disruption of brain function and neural transmission
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MS- Categories
Relapsing-Remitting  Characterized by attacks (most common 85%), exacerbation/remission, may have minimal long-term impairment - Up and down on graph with gradual progression overtime Primary progressive  Steady decline in function with min recovery -Acute onset, steady straight curve progression Secondary progressive  50% change into this from R-R. into progressive -Starts out as up-down and turns into straight curve on graph (Combo of first two ^) Progressive relapsing  Rarest form, progressive with periodic acute relapses - straight progressive curve with large ups, but no valleys.
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MS Signs and Symptoms
 Demyelination causes the primary symptoms  Paresthesias, vision disturbances (diplopia), progressive muscle weakness, cognitive impairments, and bladder and bowel dysfunctions, fatigue (especially in afternoons)  Secondary symptoms result from primary symptoms  Tertiary symptoms include social and psychological functioning
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MS: Treatment
 Team approach including physicians, psychologists, social workers, physical therapists, occupational therapists, speech therapists, and family  Medications to reduce the development of new brain lesions and slow down disease progression (ABC drugs)  Corticosteroids  Avoid exacerbating factors: infections, trauma, pregnancy, stress
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MS: PT Management
* Treatment focuses on maintaining mobility and the quality of life, * Reduce fatigue: stretching, aerobic exercise, and education regarding fall prevention and energy conservation techniques. * May need to avoid heat * Coordination exercises * Limit strengthening/resistive: may increase fatigue
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Parkinson’s Disease (PD)
 Chronic, progressive, degenerative neurologic disorder of the basal ganglia  Produces syndrome of abnormal movements  Deficiency of dopamine and degeneration of substantia nigra ▪ Dopamine ▪ Regulates voluntary movements, emotions, mood, motivation
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PD Signs and Symptoms
 Slowly progressing  Tremors – “pill-rolling” Most common initial manifestation  Cogwheel/Lead-pipe rigidity  Bradykinesia  Akinesia: movement initiation  Slowness of voluntary movements  Gait changes: narrow, shuffling  Flexed posture  Decreased balance  Masklike appearance of the face  Mentation deficits: slowing of thought, depression, dementia  Muffled speech  Difficulty with chewing and swallowing  Deconditioning  Parkinson's Gait  Resting Tremor
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Parkinson’s Disease- Treatment
Incurable  Prescribed medications to slow the development of dopamine : levodopa / carbidopa-levodopa (sinemet) , or anticholinergic medications(control tremors)  Surgery  Deep brain stimulation, stem cell implantation  Speech therapy for speaking and swallowing  Occupational therapy for ADLs
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PT Intervention for Parkinson’s Disease
* Treatment focuses on addressing the patient’s functional deficits, promote independence * Range of motion exercises, strengthening, balance training, gait training, posture, flexibility, spinal flexibility * Instruction in use of assisted devices to maximize the patient’s mobility * Manage home environment
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Huntington's Disease (HD)
 Autosomal dominant, progressive degenerative disorder  [Genetic] Caused by mutation of the gene which produces huntingtin protein  Motor disturbances, mental deterioration, abnormal behavior  Slow progression from 10 - 30 years before death, symptoms appear in the 30s and 40s  1 in 20,000 in U.S. affected
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Huntington's Disease (HD) Signs and Symptoms
 Chorea - involuntary, purposeless, rapid or jerky motions of the arms and face (Herky jerky)  Dystonia – increased muscle tone, involuntary movements with rotation (writhing)  Myoclonus – involuntary twitching and spasm  Movement tics – brief muscular spasms on the face  Abnormalities of eye movements  Parkinson – like movements – rigidity and tremors  Dysarthria: decreased rate and rhythm of speech
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PT Intervention for (HD)Huntington's Disease
* Treatment focuses on maintaining independence for as long as possible * Apraxia becomes severe – may lose ability to perform ADLs * Strength, flexibility, and endurance training; progressing through wheelchair training or ambulation with assistive devices, positioning * Education regarding fall prevention and energy conservation techniques for both the patient and the family.
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Seizure Disorders: Decription
 Epilepsy and epileptic syndromes  Explosive episodes of uncontrolled and excessive electrical activity in the brain which results in multiple involuntary muscle contractions  Diagnosis of epilepsy requires 2 seizures occur without a known cause
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Seizure Disorders: Etiology
 Abnormalities within the neurons or with the balance of the neurotransmitters, which cause the neurons to be triggered all at one time  Unknown, possibly genetic factors involved  Head trauma or brain tumors  Infections, high fevers
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Seizure Disorders: Potential Causes
 Medical Conditions Hyponatremia, hypernatremia, hypoglycemia  Neurologic Conditions Stroke, brain tumor, meningitis  Drug Induced Seizures Drug or alcohol withdrawal  Illnesses Eclampsia, renal failure, sickle cell disease
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Type of Seizures
 Absence seizures – “petit mal”, with brief loss of consciousness, staring  Atonic – temporary, sudden loss of muscle tone, collapses  Myoclonic / myotonic, Clonic/tonic-”grand mal”– jerking and twitching, loss of consciousness  Simple partial – emotion and sensation changes, consciousness maintained  Complex partial – altered level of consciousness, staring, twitching
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Seizure Disorders: Treatment
 Prescribed medications acting on neurotransmitters  Barbiturates : Phenobarbital (long acting), Pentobarbital  Benzodiazepines: Diazepam (Valium), Lorazepam (Ativan)  Dilantin, Tegretol, Lamictal  Vagal nerve stimulation  Surgery to remove the affected area of brain  Ketogenic diet, gene therapy, stem cell research
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Seizures: Safety
 What do you do if your patient had a seizure while you were treating them????  SAFETY!!! Both the patient and you! Protection  Remove all objects from the area  Do NOT restrain them  If they are standing lower them to the ground safely  Turn them on their side if able to allow for vomit to exit the mouth  DO NOT put your anything in patient’s mouth  Vitals, length of seizure time  **Status Epilepticus -> Medical Emergency, seizure > 30 minutes
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Epilepsy vs Seizure disorder
A seizure is a single electrical event in the brain, while epilepsy (or a seizure disorder) is a chronic neurological condition defined by recurrent, unprovoked seizures, meaning they happen without an immediate trigger like fever or injury. Not every seizure means epilepsy; a provoked seizure (due to infection, trauma, drugs) may not lead to epilepsy, but recurring, spontaneous seizures diagnose the disorder.
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PT Intervention for Seizure Disorders
* Treatment is aimed at the injuries or conditions resulting from the seizure, such as fractures or developmental delays. * may include work on mobility, stretching, strengthening and balance. It is important to be aware of seizure precautions if a patient has had a prior neurological injury
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Alzheimer’s Disease
 Progressive degenerative disease of the brain  Destroys cerebral cortex neurons  Leads to dementia  500,000 new cases diagnosed each year
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Alzheimer’s Disease: Etiology
 Exact cause unknown  Risk increased with advancing age, genetics, atherosclerosis  Plaques and amyloid accumulate in brain tissue -> neurofibrils break down and become tangled -> nerve impulse transmission prevented -> function of sections on the cerebral cortex destroyed  Neurofibrillary tangles detectable at autopsy
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AD Signs and Symptoms
 Loss of memory, inability to concentrate, impairment of reasoning, apathy, personality changes  Warning signs: memory loss, problems with language, disorientation, difficulty completing familiar tasks, distorted judgment, problems with abstract thinking, misplacing things, mood, behavior, and personality changes  Sundowning - increase in symptoms at the end of the day
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AD Treatment
 Prevention including healthy diet, higher education [challenging your brain]  Medications  Stem cell research  Massage  Supportive environment, and long term
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PT Intervention for AD
* Goal is to maintain functional independence for as long as possible by encouraging activity, as the disease may lead to inactivity due to the cognitive restrictions. * Strengthening, balance activities, maintain ROM * Due to the patient’s cognitive status, the therapist must use short, clear, and concise instructions. * Short and simple exercise sessions
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Dementia
Types: Lewy body, senile, vascular, and dementias precipitated by other diseases  Progressive brain deterioration  Decline of mental facilities (thinking, remembering, communicating)  Affect a wide age range
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PT Intervention for Dementia
* Treatment is aimed at the neurological and musculoskeletal manifestations, and must be adjusted due to the patient’s cognitive status by using short instructions and a familiar location. * Work on stretching, strengthening, endurance, balance and coordination, as well as ambulation may be indicated.
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Amyotrophic Lateral Sclerosis (ALS)
 Also called Lou Gehrig’s Disease (baseball player) - Degeneration and demyelination of MOTOR neurons  Acute onset; Leads to general paralysis and immobility; progresses rapidly, with death usually in 3 - 10 years (Steven Hawking had a different form of ALS and lived for roughly 50)  50% have cognitive impairments  Mainly occurs between 40 and 60 years of age, with men > women; 2 case per 100,000  5th decade or later
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ALS Signs and Symptoms
Begins with weakness and rapid atrophy (not from disuse) of hands, forearms, legs and eventually spreading to rest of the body Severe fatigue Paralysis Difficulty with speech, chewing, swallowing, breathing
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ALS Treatment: Medical Treatment
 Medications to control muscle spasms  Assistance with breathing including intermittent positive pressure ventilation (IPPV) or tracheostomy
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PT Intervention for ALS
"Palliative" care "Goal is to maintain independence and functional independence for as long as possible * Work on functional mobility, including wheelchair evaluation and training if needed * Home modifications and assistive devices * Strengthening and stretching * Low-impact aerobic exercise * Breathing exercises, postural drainage, chest PT
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Spinal Cord Injury (SCI)
 Damage to the vertebrae, neural tissue  Loss of movement and sensation distal to injury site  Quadriplegia or paraplegia  Men > women 4:1; ages 15 - 25  12,000 new cases each year in the U.S.
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Spinal Cord Injury: S & Sx
Immediate Phase (Don't need to know the specifics of the phases) Lasts up to 2 hours after the injury Spinal shock, with no movement, sensations, or reflexes below the level of the injury Edema in the spinal cord -> hemorrhage and death of gray and white matter cells -> ischemia of spinal cord Acute phase  From 2 – 48 hours after injury  Hemorrhage continues -> increased inflammation and edema -> free radical production -> damaged tissue -> immune system response -> neural and glial cell damage Subacute phase  From 2 days – 2 weeks after injury  Phagocytes clean-up debris and destroy myelin -> scarring -> barrier for axon regeneration  Intermediate Phase  From 2 weeks – 6 months after injury  Scarring matures -> axon regeneration Chronic Phase  From 6 months – the end of lifetime  At 1-2 years, symptoms and deficits occurs  Bone density loss, pressure ulcers, depression, suicidal thoughts, hostility, substance abuse
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SCI Impairments
 Impairments will vary depending on the injury, but can include  Impaired sensation Temperature Light touch Kinesthetic  Impaired motor function  Impaired bowel & bladder  Ipsilateral and contralateral depending on the injury
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SCI: Autonomic Dysreflexia*
 A medical EMERGENCY in SCI patients  Above the T6 level  Diaphoresis (excessive sweating) along nerves above T6, high blood pressure, increased HR  Usually associated with a full bladder or blocked catheter  Sit patient up and check for noxious stimulus and get help!!!! Order of operations (MUST FOLLOW): 1) Sit them up if they're lying down, check for pinched catheter - lower blood pressure to brain (DON'T lay them back down if they have orthostatic hypotension) 2) Check for (painful or uncomfortable) noxious stimulus 3) Get help or Call 911!
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PT Intervention for Spinal Cord Injuries
* Treatment focuses not only compensatory movements, but also on recovery. * Strategies include functional electrical stimulation and passive range of motion, progressing to more active strengthening and balance training. * Treatment also includes transfer training, wheelchair training, and gait training
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12 Cranial Nerves (Order)
PNS PPT slide 4, (Picture on Phone)
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12 Cranial Nerves - Pneumonic
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Lower Motor Neuron (LMN) Injuries
 Cell body of the alpha motor neuron  Axons that arise from the anterior horn  Motor Endplate of the Neuron (where it hits muscle)  Muscle fibers innervated by that axon
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Relationship of Nerve & Muscle to Disease and Trauma
- mesis = to cut PNS PPT. Slide 7 (Picture on Phone)
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Guillain-Barré Syndrome
Also known as: "Acute/Ascending Idiopathic Demyelinating Polyneuropathy" (AIDP) Rapidly progressing inflammatory disease in which the immune system affects the neural tissue - related to the immune system but not an autoimmune disease - can be recovered from. Etiology  Unknown  Related to autoimmune response preceding viral infection or immunization Signs & Symptoms  Numbness or tingling in feet and hands  Followed by progressive muscle weakness beginning in legs and traveling up the trunk, down the arms to the face, usually bilaterally, with possible complete paralysis  Vision, speech, and breathing may be impaired  Absent deep tendon reflexes  High level of proteins in the cerebrospinal fluid
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Guillain-Barré Syndrome: Treatment
 No known cure  Plasmapheresis to reduce the autoimmune response and remove toxins  Intravenous immunoglobulin to restore immune defenses  Manage symptoms of dehydration and skin breakdown  Psychological support for patient and family - PT Treatment follows the pace of peripheral nerve recovery, and usually begins with patient and family education in range of motion exercises to prevent contractures, progressing through wheelchair training or ambulation with assistive devices, strengthening, and balance and coordination activities. It is important not to overfatigue a patient. - Holly Frances recover video documenting getting the condition 3 wks after pregnancy.
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Post-Polio Syndrome
 NOT a re-infection of the Polio virus  Seen in some patients who have had poliomyelitis earlier in life  Appears an estimate of 35 years after infection  Exhibited in 28.5 to 64% of previous polio patients  Increased occurrence due to polio epidemic in 1940s and 1950s - Previously injured nerves force healthy nerves to pick up the slack and after a couple decades those healthy nerves are overworked and start to break down causing Post-Polio Syndrome.
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Post-polio syndrome: S & Sx and Treatment
 Develop slowly  Weakness and decreased muscular endurance, “post-polio progressive muscular atrophy”  Fatigue, loss of energy, myalgia  Decreased concentration, mental exhaustion  Respiratory, speech, and swallowing problems  Joint problems, inflammation; leads to decreased mobility and function Treatment  No cure  Medications not effective  Manage physical effects of weakness through lifestyle changes - Energy conservation techniques including rest and use of a wheelchair - Low-impact aerobic program Strengthening program without fatiguing
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Peripheral Neuropathy
- Umbrella term Disease of the peripheral nerves  Affects motor, sensory, autonomic systems  > 20 million affected; more common in older adults Etiology (Don't need to memorize)  Unknown; inherited  Diabetes mellitus, Guillain-Barre  Alcoholism  Autoimmune diseases  Kidney failure, thyroid dysfunction, cancer  Environmental toxins; Infections  Long-term medications  Vitamin B deficiency, malnutrition
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Peripheral Neuropathy: S & Sx and Treatment
 "Glove and Stocking Pattern"  Sudden or gradual, > in distal lower extremities  Mild to severe and debilitating  Pain during regeneration of nerves  Weakness and atrophy, fasciculations, cramping  Altered sensation: “Glove” distribution, vibratory, touch, pressure, temperature, numbness, kinesthetic  Decreased balance, coordination, mobility  Decreased weight bearing -> bone degeneration  Hypotension -> dizziness, poor balance  Facial muscle weakness -> swallowing, eating difficulties  Bowel / intestinal symptoms  Can result in skin breakdown, amputation Treatment  Team approach  Treat underlying cause  Lifestyle changes  Medications to decrease pain  Orthopedic shoes - Treatment begins with PT evaluation of muscle strength, skin sensation. The treatment plan may include orthotics, wound care, prevention of contractures, gait training, balance training, strengthening, endurance, and patient education.
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Myasthenia Gravis (Grave muscle disease/disorder)
 Autoimmune disease  Neurologic disorder characterized my impaired transmission of motor neurons  Antibodies are produced that attach and destroy acetylcholine receptors in the neuromuscular junction  Excessive amount of cholinesterase ▪ Enzyme that deactivates acetylcholine  Stimulation of muscles is prevented leading to progressive weakness  Respiratory muscles affected Review: Acetylcholine (ACh) is a vital neurotransmitter for muscle contraction, learning, memory, and autonomic functions like heart rate, digestion, and glandular secretions, acting as a chemical messenger between neurons and other cells in both the central and peripheral nervous systems
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Myasthenia Gravis: S & Sx and Treatment
Signs and Symptoms  Facial weakness and loss of expression  Muscles of eyes, mouth, throat, neck affected  Vision impaired  Fatigue - Use "Sleepy" the dwarf as an illustration Treatment  Pharmacotherapy - Focused on functional activities, including activities of daily living, with possible adaptive equipment, breathing exercises, and occasional exercise programs, being very careful to avoid fatigue.
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Bells’ Palsy
 AKA Idiopathic Facial Paralysis  Common clinical condition  20 of 100,000 people each year  Most common between ages 15 to 45  *Affects the (7th) Facial Nerve unilaterally
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Bell's Palsy: S & Sx and Treatment
 Days before severe pain in the area of the mastoid  Facial paralysis that develops rapidly  Dry eye on the affected side  Increased sensitivity to sound on the affected  Also affects salivation and lacrimation (flow of tears) Management:  Prophylactic administration of high dose steroids for 5 days f/b a tapered dose for 5 days  Treatment should begin no later than 10 days after onset  Antiviral medications  95.7% recovery rate  Use of an eye patch to protect the cornea  Electrical stimulation should NOT be used  Twice daily exercise program
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Thoracic Outlet Syndrome (TOS)
 Those with TOS have vague symptoms  Remains a controversial diagnosis  It is complex and poorly defined  Patient’s are labeled  It is an entrapment syndrome  Places pressure on the structures in the outlet  Brachial Plexus fibers  Subclavian artery  Chronic compression of the spinal roots, proximal plexus and arteries  Compression between the clavicle and first rib  Impinging musculature  Results in edema and ischemia n the nerves Review: The brachial plexus is a complex network of nerves originating from the lower neck (C5-T1 spinal nerves) that controls movement and sensation in the shoulder, arm, forearm, and hand, running from the spine through the armpit to the limb. Review: The subclavian artery is a major blood vessel located beneath the collarbone (clavicle) that supplies oxygen-rich blood to the head, neck, and arms, with distinct left and right arteries originating from the aorta and brachiocephalic trunk, respectively, transitioning into the axillary artery at the first rib. Issues like narrowing (stenosis) or blockage can cause symptoms such as arm fatigue, pain, numbness, dizziness, and visual changes, often due to conditions like atherosclerosis or thoracic outlet syndrome.
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Thoracic Outlet Syndrome (TOS): Sub-divisions
Neurogenic  Compression of the brachial plexus Vascular  Compression of subclavian vessels Disputed  Nonspecific w/chronic pain & symptoms of plexus involvement
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Thoracic Outlet Syndrome (TOS): S & Sx
 Signs & symptoms reflect the structures that have been compressed  Paresthesias and pain in the arm *Primarily nocturnal  *Upper Plexus injury (C5 to C7) * Pain in neck and radiating to face  *Lower Plexus injury (C7 to T1) * Pain numbness in posterior neck down the arm  Weakness in muscles that correspond to the impaired nerve root  Coldness & Edema in arm & hand * Raynaud’s Phenomenon - a condition causing blood vessels, usually in fingers and toes, to narrow (vasospasm) in response to cold or stress, leading to color changes (white, blue, then red), numbness, and tingling as blood flow is restricted and then returns
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Thoracic Outlet Syndrome (TOS): Tests & Treatments
Tests:  Provocative tests are used to elicit symptoms  They have a high false (+) rate  Maneuvers are performed bilaterally  TOS tests  Radiographic test  NCV testing Treatment: - Conservative  When symptoms are mild  Postural and breathing exercises  Strengthening traps, levator scap & rhomboids  Avoiding overhead activities - Surgical  Reserved for cases that are refractory to postural & exercise correction  Vascular compromise  6 different procedures & 6 different approaches ▪ Scalenectomy ▪ Clavicle resection
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Ulnar Nerve Entrapment
Cubital Tunnel Syndrome  Elbow - Causes  Mobile nerve over the epicondyle  Leaning on the elbow for long periods  Fluid build up  Direct trauma Compression @ Guyon’s Canal  Wrist - Cause  Soft tissue tumors (ganglion cyst)  Repetitive trauma ▪ Like using a jack hammer  Chronic pressure ▪ Bicyclists
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Ulnar Nerve Entrapment: S & Sx
 Numbness in the 4th & 5th fingers  Weakness in grip and decreased coordination  Depending on how long, muscle atrophy in hypothenar muscles
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Carpal Tunnel Syndrome (CTS)
 Most common entrapment neuropathy  Compression of the median nerve  3.5 cases per 1000 individuals  Prevalence 2.1%  70% of all CTS cases occur in women  500,000 surgeries performed annually 10 Structures that go through the Carpal Tunnel: Median Nerve, Flexor PIP (4) and DIP (4) tendons, and Flexor pollicis longus.
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CTS – Clinical Manifestations and Management
Clinical Manifestations  Symptoms in the Median Nerve distribution  Pain may be located in the forearm and radiate into the thumb, index and middle fingers  Nocturnal pain is hallmark  Thenar weakness in advanced cases Management  Must be distinguished between cervical radiculopathy or ulnar neuropathy  (+) Phalen’s test  (+) Tinel’s test  NCV Testing  No universally accepted treatment  Median Nerve Glides
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Complex Regional Pain Syndrome (Reflex Sympathetic Dystrophy
Review: Sympathetic NS - fight or flight response  Also known as Causalgia, Reflex Sympathetic Dystrophy  Chronic pain condition  Continuous, intense pain out of proportion to the severity of the injury  Most often affects one arm, leg, hand, or foot Etiology  Unknown  Sympathetic nervous system can play a role  Immune response triggering inflammatory response - inflammation triggers more pain - turns into positive feedback cycle.
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Complex Regional Pain Syndrome: S & Sx and Treatment
S & Sx  Pain that begins in a portion of a limb and can spread to the entire limb  Changes in color and temperature of the skin  Intense burning pain, skin sensitivity, sweating, swelling Treatment  Focused on pain relief  Corticosteroids, opiates, antidepressants (CNS depression)  Sympathetic nerve block, spinal cord stimulation, intrathecal drug pumps  No drug or combination of drugs have produced consistent long-term improvement in symptoms
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Physical Therapy Intervention for Complex Regional Pain Syndrome
Early mobilization of the limb post-surgery Modalities to decrease pain and hypersensitivity Tactile desensitization activities Exercise, reduce guarding of affected limb Physical Therapy is sometimes controversial , can be unsuccessful
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Bacterial Infection Treatment Terms
bactericidal - kills bacteria bacteriostatic - inhibits the growth of bacteria iatrogenic - disease caused from the unclean hands of healthcare workers
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Staphylococcal Infections
* Staph bacteria among most common bacterial pathogens normally residing on the skin *Staph aureus * Leading cause of nosocomial and community acquired infections * Risk Factors: Direct contact with colonized surfaces * Most common locations: Nares, skin, axilla, perineum, vagina, oropharynx * Diabetics, HIV+, IV drug users, hemodialysis patients, chronic skin lesions, surgical/burn patients, RA, corticosteroid therapy
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Staphylococcal Infections: Pathogenesis and Clinical Signs
* S.aureus cannot invade through intact skin * May enter through damaged skin * Usually produces an abscess or other skin infections – cellulitis, boil-like lesions * Fever, chills, and symptoms with the affected body part
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Staph Infection Treatment
- I.V. ABx of Vancomycin (Currently only thing that can kill this bacteria) * Requires contact isolation * Often used in the treatment of total joint infections Note: Primary reason for anti-biotic resistance is not taking the full course of anti-biotics.
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Vancomycin-Resistant Enterocci (VRE)
* Usually in the urine * s/s: bloodstream infection (sepsis), UTI, abscesses, wound infections * Treated similarly to MRSA
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Anti-biotic Resistant Staph Infections
* Methicillin-Resistant Staph Aureus (MSRA) * VRE Special Implications for the PTA * -handwashing, cleaning of equipment
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Clostridium Difficile “C-Diff”
* An anaerobic spore forming bacillus – inflammation of colon -> mild diarrhea to severe colon inflammation and possible death * Occurring exclusively in the presence of prolonged exposure to antibiotics * Primarily transmitted in health care facilities * Fecal- oral route * Requires contact isolation * Pathogenesis- Change in the protective flora * Induced by ABx * Acute and persistent diarrhea **Anti-biotic DO NOT CAUSE C-diff. Everyone has C-diff. Your good natural gut bacteria keeps usually keeps it at bay, but anti-biotics kill your good gut bacteria, allowing room for C-diff to grow. (Suddenly empty apartment block illustration)
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PT Interventions for MRSA, VRE, & C Diff
Proper hand washing Cleaning all the equipment that came into contact with the patient Contact Isolation techniques observed: Wear gloves and gown Do NOT use hand foams when working with a patient with C-Diff. Must wash hands.
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Tuberculosis (TB)
is an infectious, inflammatory systemic disease that affects the lungs and may disseminate to involve lymph nodes and other organs * It is characterized by caseous (cheesy) necrosis and subsequent cavity formation typically in the lungs. (Myobacterum tuberculosis) * Risk Factors * Immunocompromised: HIV infection * Over 65 years of age * Economically disabled persons * It becomes established in the lungs from inhaled droplet * TB is an easily spread (contagious) disease.
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TB: Implications for the PTA
Stay alert to prevention of spread Fit masks (N95 or better) PPD : usually required yearly Confine care to the patients room (negative pressure room with door closed at all times)
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Cytomegalovirus (CMV)
- Description: AKA herpes virus type 5, CMV * Most common congenital virus in U.S.; 1 in 150 infants affected, 1 in 5 develop permanent disability * Related to herpes viruses - Etiology: Present in all body fluids, transmission through close contact with infected fluids * May be passed to fetus through pregnancy or breast milk
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Cytomegalovirus (CMV): S & Sx and Treatments
- Signs and Symptoms: May or may not be present; may mimic influenza * Newborn symptoms: low birth weight, microcephaly, respiratory problems, mental and motor delays, seizures * Immunocompromised: colitis, pulmonary infections, encephalitis, neuropathy, retinitis * Organ transplant patients (you're on immunosuppressants to keep the body from rejecting the new organ) - Treatment * Infants treated with antiviral medication to prevent hearing loss * Antiviral medications for complications
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Cytomegalovirus (CMV): PT Interventions
* Physical therapy not directly indicated * Handwashing * If pregnant, do not work with patients who have CMV
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Hepatitis
* Group of liver infections and diseases caused by various viruses Several types * Hepatitis A (HAV) * Hepatitis B (HBV) * Hepatitis C (HCV) * Hepatitis D (HDV) * Hepatitis E (HEV) * Hepatitis G (HGV) * Alcoholic Hepatitis
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Hepatitis B
Symptoms * Loss of appetite, nausea and vomiting * Weakness, fatigue, joint and muscle pains, aching * Fever, skin rash * Jaundice, dark-colored urine Treatment * Prevention, vaccinations * Medications - antivirals PT Interventions * Not directly indicated * Standard Precautions * Immunizations *Hep B can stay on surfaces for 7 days
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Hepatitis C
* > 85% develop chronic form * Etiology * Transmitted via infected blood * RNA virus, transmitted through blood * Most common in those persons who use IV drug use or have multiple sexual partners
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Hep C
Signs and Symptoms * Usually mild * Reduction in appetite, abdominal pain, tenderness over liver region * Muscle and joint pain * Jaundice, cirrhosis Treatment * Prevention * Medications (can't miss a dose) * Harvoni * Possible liver transplant if severe PT Intervention: Since there is no real cure - Treatment of associated arthritis and fibromyalgia.
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HIV/AIDS
* HIV = human immunodeficiency virus * AIDS: progressive destruction of cell-mediated T- cell immunity * CD4 count (asymptomatic CD4= 500 or more) * Etiology: blood-borne pathogen * Transmitted via blood and bodily fluids: sexually, shared hypodermic needles, blood transfusions (1980s) *Secondary / opportunistic infections (Important to know these): * Pneumonia, herpes simplex and zoster, non-Hodgkin’s, CMV, candidiasis, Karposi sarcoma * Treatment * Pharmacology: HAART (highly active antiretroviral therapy) * Focus on disease prevention
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Herpes Zoster (Shingles)
Reactivation of the Herpes Varicella (chicken pox) virus If you had chicken pox prior you can't catch shingles. HOWEVER, if you never had chicken pox you CAN CATCH it from someone with shingles.
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Shingles
Clinical Manifestations * Vesicular eruption * Unilaterally * Dermatomal pattern * Usually the trunk or the 5th cranial nerve Symptoms * Fever, chills, malaise, tingling along the dermatome * Severe neuralgic pain * Scarring and degenerative changes involving the nerve trunks, ganglia, and skin * May lead to postherpetic neuralgia
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Lice: Parasite
Description: Lousiness or pediculosis * Is an infestation by Pediculus humanus * Usually from shared personal item (comb) Clinical Manifestations * Severe itching * Small grayish, white nits in the hair Treatment * cleaning solutions (specialized shampoo) Implications for the PTA * Contact isolation
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Scabies
* Highly contagious skin eruption caused by mites * Common public health problem * The female mite burrows into the skin and deposits eggs which hatch in a few days * Transmitted skin to skin contact or via contaminated objects * Can spread rapidly Clinical Manifestations- Intense pruritus (itching) * Excoriated skin * Mites are found in the interdigital web spaces, flexor aspects of the wrist, axillae, waistline, nipples in females and genitalia in males and umbilicus * Treated via medication Implications for the PTA * Prevention of transmission * Gloves, gowns, & hand washing * Single use BP cuffs * Thorough disinfection of equipment
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Health Care Worker Vaccinations
Hep B Flu COVID MMR Measles TDAP: Tetnus, DPtheria Varicella (Chicken Pox)
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Gastroesophageal Reflux Disease (GERD)
* Esophagitis * Which may be a result of reflux of infectious agents, chemical irritants, physical agents, or gastric juices * Acid flowing backward from the stomach * Reflux esophagitis is most common type * Wide range of foods and lifestyle factors contribute * Heartburn, reflux, belching, dysphagia, and painful swallowing * Pain may radiate to the back, neck or jaw * Often occurs 30-60 minutes after a meal
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GERD - Treatment
Medications * Acid suppressing inhibitors (Proton Pump Inhibitors) -meds ending in prazole: Esomeprazole(Nexium), omeprazole(Prilosec) * OTC drugs usually help to block the histamine or neutralize stomach acid -meds ending in tidine: cimetidine(Tagament), Famotidine(Pepsid), Rantidine(Zantac), Maalox, Mylanta
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GERD - Treatment
* Lifestyle Modifications * Wearing loose clothing * Avoiding caffeine, nicotine, alcohol, NSAIDS and ASA (aspirin) * Avoiding meals near bedtime or naptime * Elevation of bed at night, Sleep on Left side at night * Remain upright 3 hours after a meal * Avoid large meals
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GERD: Implications for the PTA
* Exercise is important especially for those overweight * Exercise may worsen symptoms * Strenuous exercise can inhibit gastric & sm. intestine emptying * Positioning * Take care when implementing interventions in supine position * Encourage LEFT sidelying or head-elevated positions
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Crohn’s Disease
* Inflammatory Bowel Disease * Chronic lifelong inflammatory disorder * Can affect any segment of the intestinal tract * Characterized by diseased areas * Periods of exacerbation & remission *Bi-polar colon disorder with periods of diarrhea and constipation. Clinical Manifestations * Begins with low grade fever, malaise, weight loss, diarrhea & abdominal cramping or pain * Followed by an obstructive phase with persistent bloating and distention
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Crohn’s Disease - Implications for the PTA
* Understanding the pain may mimic other MS pains * Dehydration * Monitor for signs of dehydration (dry lips, hands, headache, disorientation) * Psychological impact of the disease and the patient's susceptibility to emotional stress * Stress management, relaxation techniques
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Cirrhosis
* Description * Progressive liver disease that destroys liver cells * Fibrous scar tissue replaces cells * Liver functions deteriorate, damage is irreversible * Death can occur 5-15 years after diagnosis without transplant * Etiology * Chronic alcohol abuse * Viral hepatitis B and C * Autoimmune or metabolic diseases *important disease progression to know: - Ascites (fluid in peritoneal cavity)
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Cirrhosis: PTA Implications
* Physical therapy may be indicated for associated decreases in strength, endurance, mobility, and function. * Observe for fluid retention, ask about any changes in health status/weight gain * Prevent increased intra-abdominal pressure * Prevent injury from falls * Many patients with decreased aerobic capacity
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Biliary Conditions
All conditions related to the gallbladder * Cholelithiasis (gallstones created from cholesterol) * Choledocholithiasis (presence of gallstones in the bile duct. * Cholangitis (infection of the biliary [bile] tree) * Cholecytitis (inflammation of the gallbladder) * Cholecystectomy (surgical removal of the gallbladder)
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Carcinomas
* Cancerous * Can occur in the mouth, esophagus, stomach, liver, pancreas, colon
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Colostomy
* Surgery moving one end of the large intestine through the abdomen * Stool drains into colostomy bag * Done after bowel obstruction or bowel resection
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Bariatric Surgery
- Done for obesity 3 Options: * Lap Band * Roux-en-Y (bypass) - ‘gold standard’ * Vertical sleeve gastrectomy
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Bariatric Surgery: Lap Band
* Bands are placed around the stomach * Fastened around the upper portion of the stomach * Limits & controls the amount of food you eat * Slows the emptying process Pros * Least traumatic * Reversible * Adjustable * No dumping syndrome (happens when food, especially sugary food, moves too quickly from the stomach to the small intestine, causing cramping, diarrhea, nausea (early symptoms 10-30 mins after eating), or weakness, shakiness, and rapid heartbeat (late symptoms 1-3 hrs after eating) due to blood sugar shifts) Cons * Slower initial weight loss * Regular f/u required for optimal results * Can have band slippage
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Bariatric Surgery: Roux-en-Y (Bypass)
* Creates a smaller stomach pouch * The attaches a y shaped section of the small intestine to the large intestine * Bypassing much of the small intestine Pros * Gold Standard * Rapid Weight loss * Reduction in weight related health concerns Cons * Complex operation * Not reversible * Risk of intestinal leaking * Deficiency in mineral absorption
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Bariatric Surgery: Sleeve Gastrectomy
* Mostly done for those too heavy to have the other 2 options * The structure of the stomach is changed * Now shaped like a tube * Restricts amount of calories ingested * 75-80% of the stomach is excised Pros * Rapid weight loss * Portion of stomach producing hunger hormones is removed * Limited stomach expansion * Reduced risk of vitamin deficiency Cons * Not reversible * May be considered investigational by some insurance companies
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Organ of Corti
In the cochlea ◦ Essentially the organ of hearing ◦ Contains 2 types of receptors cells  Inner and outer hair cells ◦ Inner hair cells  Function as auditory receptor cells ◦ Frequency dependent
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Vestibular Anatomy - Vestibule
 Vestibule ◦ Contains 2 swellings (these needed for balance)  Utricle for horizontal plane movement  Saccule head position with respect to gravity  Otoconia ◦ The inertia of the otoconia causes the gel to lag behind the movement of the skull and bends the hair cells.
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Vestibular Anatomy
 Innervation provided by CN VIII ◦ Vestibular portion -> balance information  Analyzes information about the position or movement of the head in space  Functions ◦ Maintain balance ◦ Coordinates eye, head and body  Semicircular Canals ◦ 3 anterior, posterior and lateral ◦ Arranged in 3 planes ◦ Lie roughly at right angles to each other ◦ Ampulla  Enlargement at the base of each canal  Cupula resides with in the ampulla  Lymph lags behind and activates or deactivates the cupula
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Visual Anatomy: Fovea
Area highly condensed cones
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Visual Anatomy: Blind spot
Area where the optic nerve and blood vessels enter and leave the eye
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Visual Anatomy: Retina
Contains the photoreceptors  Rods mediate light perception ◦ The image on the retina is inverted and reversed
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Visual Pathways:
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Visual Pathways: Optic nerve
From the eye to the chiasm Cranial Nerve II (purely sensory - no motor function)
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Visual Pathways: Optic Chiasm
the crossing of nerve fibers at front of head. an X-shaped neural structure at the base of the brain, located below the hypothalamus and just above the pituitary gland, where the optic nerves partially intersect PPT 8 Special Sensory Disorder slide 23* A - Optic nerve damage B - D -
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Visual Pathways: Optic tracts
Prior to interaction with the lateral geniculate nucleus
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Optic Reflexes
 Light Reflexes ◦ Light causes the pupil to contract  Convergence ◦ Eyes move toward the midline so the image remains focused on the fovea  Accommodation ◦ Increasing the thickness of the lens to maintain focus on the fovea  Pupillary constriction ◦ To regulate the depth of the focus
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Cataracts
 It is a cloudy or opaque area of the lens of the eye  Usually develops slowly  Most common cause of age related vision loss  Progressively reduced visual acuity  Blurring  Photosensitivity  The pupil appears white, opaque in appearance
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GLAUCOMA
 Defined as damage to the optic nerve due to increased intraocular pressure  Common severe condition
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MACULAR DEGENERATION
 A progressive deterioration of the macula of the retina  Destructive changes of the yellow pigmented area surrounding the central fovea (central vision)
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Nystagmus
 An involuntary constant movement of the eyes that is visible to others  Can affect one or both eyes  Movements can be in any direction - Variety of causes: tumors, alcohol abuse (too much to drink - not long term usage), congenital, head trauma, other diseases.
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Hemianopsia
 Loss of half of the visual field  Classified by the missing field ◦ Homonymous (same half of each field)  Ranges from mild to severe ◦ Which portions of the visual pathways are damaged  Causes include: ◦ Stroke ◦ Trauma ◦ Tumors ◦ Seizures, migraines ◦ Infections ◦ Toxin exposure
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Tinnitus
Ringing or buzzing in the ears Cranial Nerve 8 - VestibuCochlear  Caused by: ◦ Vascular abnormalities ◦ Medications ◦ Stimulants (caffeine or nicotine)  It is actually a symptom  Treatment is focused on decreasing symptoms rather than a cure  Implications for the PTA ◦ Difficulty concentrating or hearing
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VERTIGO
Type of vertigo: Benign Paroxysmal Positional Vertigo (BPPV)  Episodic intense vertigo related to head position  Benign because it is NOT the sign of disease process but a mechanical disorder of the labyrinths Most common cause of vertigo  Increased fluid pressure within the labyrinth may dislodge the otoconia  Head trauma or infection may also be responsible ◦ Preceding by months or years *NOT the kind of patient you want to sit up if dizzy  Common Characteristics ◦ Episodic sensation of intense vertigo with head position changes ◦ Sensation stops after 20-30 sec in static position ◦ Nausea w/vertigo w/reports of spinning inside the head ◦ Autonomic changes such as sweating, feeling like passing out  Common Characteristics Con’t ◦ Sensation of movement of the environment and blurred vision ◦ Reports of disequilibrium during typical activities ◦ Waking up dizzy at night after rolling over in bed ◦ Symptoms during head movement or bending forward during typical activities *Dix Hallpike Maneuver - Special Test - Beginning of Epley's or Semont maneuvers which is to treat it. - Also medications for vertigo - Or canalith repositioning - usually done by PT
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Meniere’s Disease
 Endolymphatic hydrops ◦ Disorder relating the membranous inner ear due to an over accumulation of endolymph ◦ Most common syndrome ◦ Characterized by:  Episodic vertigo  Fluctuating hearing loss  Sensation of fullness in the ear  Tinnitus  Implications for the PTA ◦ Psychological issues because unpredictable attacks  Social phobias  Insecurities  Anxiety
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Peripheral Vascular Disease (PVD)
◦ Diseases of the blood vessels (arteries and veins) supplying the extremities  Typically affects the LEs > UEs  Most commonly a result of atherosclerosis  May be a side effect of atherosclerosis to the arteries supplying abdominal organs ◦ Atherosclerosis of the peripheral arteries ◦ Diabetes, cigarette smoking, hypertension, hyperlipidemia, gender (males) ◦ Inflammatory disorders, vasculitis  Hypertension, reduced urine output, kidney damage  Ischemia of both large and small intestines  Gastrointestinal symptoms  Intermittent claudication* ◦ Classic symptom of PAD, generally occurs in calves [No pain, no gain - gotta push them to max tolerable pain] ◦ If pain at rest = more severe  Gangrene
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PVD: Treatment & Interventions
Treatment  Prevention – reduce risk factors  Angioplasty  Bypass surgery  Medications ◦ Statins (cholesterol lowering) ◦ Antiplatelet drugs (decrease risk for thrombus formation/clotting)- low dose aspirin  Amputation PT Interventions  Treatment of arterial insufficiency disorders ◦ Arterial insufficiency ulcers, gangrene  Monitor pain with exercise  Do NOT heat area or perform massage  Positioning, Buerger-Allen exercises ◦ pain will likely ↑ with legs elevated  Exercise programs ◦ Graded treadmill protocols  Skin inspection  NO constrictive or compressive garments  **Interventions will differ for venous disorders  ABI (Ankle Brachial Index) - comparison of BP in arm and ankle to check for PVD).
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Raynaud’s Disease/Phenomenon
◦ Periodic temporary, severe, arterial vasospasms in superficial tissues causing pallor/cyanosis of digits in response to cold temperature S & Sx:  Skin turns blue to white to red  Cyanosis, numbness and sensation of cold  Signifies ischemia  As circulation is restored ◦ Affected area turns purplish red followed by pain  Skin may ulcerate
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Deep Vein Thrombosis (DVT)
Partial occlusion or complete occlusion of a VEIN by a thrombus (clot) with 2⁰ inflammatory reaction in the wall of the vein If clot breaks free it goes up veins (which get bigger as they go towards the heart) and can cause a pulmonary embolism Special Test: Homan's sign - pain in calf when ankle dorsiflexed passively > test no longer considered sensitive and specific to rule a DVT in or out.
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DVT: Anticoagulants
Heparin ◦ Measured by Partial Thromboplastin Time (PTT)  A blood test that looks at how long it takes for blood to clot ◦ Usually normal 24 hours after initiated ◦ Low Molecular Weight Heparin (LMWH) Coumadin ◦ Measured by International Normalized Ratio (INR)  A calculation used to monitor individuals who are being treated with the blood-thinning medication - *If it clots too quickly you need more medication, if it's too fast you need less
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Varicose Veins
◦ Abnormal dilation of veins from incompetent valves ◦ Superficial or deep veins affected ◦ Legs, esophagus, rectum ◦ Blood flow is turbulent and slow favoring clotting which can lead to thrombus formation ◦ Spider veins Signs and Symptoms ◦ Symptoms develop gradually  Fatigue or ache in the legs at the end of the day, ankles may swell, leg cramping at night ◦ Condition progresses  Veins appear bluish-purple, bulbous and tortuous, hard to the touch, pain worsens and is noted earlier in the day  Ulcers may form near the ankle
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Blood Disorders: Glycemia
 **Blood sugar levels decrease with insulin and with exercise. Avoid treatment shortly after insulin is given or before eating**  Hypoglycemia ◦ 70 mg/dL or less ◦ s/s: blurred vision, fatigue, pale skin, HA, hunger, shaking, sweating, trouble concentrating, loss of consciousness - "Did you take your insulin right before therapy?" - If they did you need to monitor them as insulin will reduce blood sugar.  Diabetic Ketoacidosis (DKA) [Very high hyperglycemia] ◦ >300 mg/dL ◦ s/s: flushed, thirsty, fruity breath, rapid breathing, abdominal pain, vomiting, confusion *Both hypo and hyperglycemia can lead to coma and death
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Red Blood Cells (RBCs)
- ability of blood to carry oxygen ◦ Erythrocytes ◦Decreased:  Anemia, blood loss, dietary insufficiency, chemotherapy, various disorders and diseases ◦Increased:  Polycythemia vera (disorder bone marrow), dehydration, severe diarrhea, poisoning, high altitude, chronic heart disease
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White Blood Cells (WBCs)-
cells that fight infection ◦ Leukocytes ◦Decreased:  Infection, bone marrow suppression or failure, AIDS, alcoholism, diabetes, autoimmune disease ◦Increased:  Indicates infection, inflammation, tissue necrosis, leukemia, tissue trauma or stress, burns, dehydration  <1000/mm3 No exercise; wear protective mask*  <5000/mm3 No exercise permitted  4800-10,800 mm3 normal range in adults  no activity restrictions  >5000 mm3 Light exercise, progress as tolerated - Too high - also don't exercise
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Hematocrit and Hemoglobin
◦ Hematocrit (HCT)  Is a PERCENTAGE of whole blood occupied by RBCs ◦ Normal range for adults ◦ Hemoglobin (HgB)  Measures oxygen carrying capacity of RBCs - DIRECT COUNT of RBCs ◦ Normal range for adults Exercise Guidelines ◦ Hematocrit  <25% No exercise permitted  >25% Light exercise permitted  30-32% Add resistive exercise ◦ Hemoglobin  <8 g/dL No exercise permitted  8-10 g/dL Light exercise permitted  >10 g/dL Resistive exercise permitted
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Platelets
Clotting potential ◦ Decreased  Anemia, use of antibiotics, toxic effect of many drugs, pneumonia or other infections, HIV infection, cancer, chemo, bone marrow replacement ◦ Increased  Inflammation, infection, cancer, splenectomy, trauma, RA, heart disease, cirrhosis, recovery from bone marrow suppression
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Cardiac Enzymes and Markers: Troponin
Molecule specific to muscle tissue & is specific to myocardial injury * If Troponin levels are elevated we are not allowed to do cardio
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Rhabdomyolysis (CPK skeletal tissue)
When body runs out of energy stores and the body breaks down skeletal muscle tissue for energy.
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Blood pH
pH Measure of blood acidity (acidic< [7.35-7.45 > alkaline)]
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Leukocytosis/Leukopenia
increase in white cell count/reduction of white cell count
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Polycythemia
increase in red blood cells
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Thrombocytopenia
reduced number of platelets
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Layers of the Skin
3 Layers: Epidermis Dermis Hypodermis
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Tissue Repair: 2 Methods
Regeneration  Replacement of destroyed tissue by the same kind of cells Fibrosis  Repair by dense fibrous connective tissue (scar tissue) Determination of method  Type of tissue damaged  Severity of the injury
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Events in Tissue Repair
Capillaries become very permeable  Introduce clotting proteins  Wall off injured area from bacteria and other harmful substances  Scar – clot was exposed to the air and dries Formation of granulation tissue  New capillaries form delicate pink tissue  Contains phagocytes and fibroblasts (building blocks)  New collagen fibers are formed (scar tissue) Regeneration of surface epithelium
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Pressure Ulcer Stages
Stage 1: Skin is unbroken but inflammed Stage 2: Skin is broken to epidermis or dermis Stage 3: Ulcer extends to subcutaneous fat layer Stage 4: Ulcer extends to muscle or bone. - Undermining is likely.
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Braden Scale
Risk scale for Pressure Ulcers Factors: - Mobility - Activity - Sensory Perception - Moisture - Friction-Shear - Nutrition - Tissue Perfusion and Oxygenation
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Venous Ulcers
Venous Ulcers - Occur due to impaired venous circulation Etiology  Trauma, varicose veins, thrombosis occur and impair the venous return system  Risk factors include heart disease, DVT, obesity, genetic defects of valves Signs and Symptoms  Irregular shape, on lower leg  Yellow, white, gray, but not black (as in arterial ulcers), exudate (a mass of cells and fluid that has seeped out of blood vessels or an organ)  Edema and cellulitis can also be present Treatment  Debridement  Surgery
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Arterial Ulcers
 Ischemic ulcer, diabetic ulcer  Seen with peripheral vascular disease and diabetes Etiology  Reduction in oxygenation perfusion of tissue -> lack of oxygenated blood to skin, muscles, other tissues -> gangrene and ischemic ulcers  Risk factors are heredity, smoking, high blood pressure, diabetes mellitus, hypercholesterolemia, atherosclerosis, peripheral neuropathy, reduced joint range of motion, obesity, poor footwear Signs and Symptoms  Absence of arterial pulses, night pain, absence of hair, pallor when elevated  Circular shape, “punched out”  Rarely bleed, slow or fail to heal  Necrotic tissue, black eschar Treatment  Surgery  Hyperbaric oxygen therapy (HBOT)  Debridement of necrotic tissue  Dietary and lifestyle changes  Possible amputation
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Neuropathic (diabetic) Ulcers
Results from the simultaneous action of many contributing factors  Peripheral neuropathy -60% of ulcers due to lack of sensation  Peripheral vascular disease - 50% of the cases there is some vascular limitations
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Basal Cell Carcinoma
 Arises in basal layer of epidermis  Most common form  Least dangerous due to slow growth - Does not easily invade blood or lymph vessels  If untreated, can invade other tissues Risk factors  Excessive exposure to sunlight (natural or artificial)  Fair skin and light-colored hair and eyes  Personal or family history of skin cancer, past radiation treatments, immunosuppression, chronic exposure to arsenic Signs and Symptoms  Elevated, firm nodule  Pearly or ivory white with central depression  Painless  As progresses – more prominent, bleed, form crusts
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Squamous Cell Carcinoma
 Second most common form of skin cancer  More prevalent in those > 50 years old  Men > women; 3:1  95% curable when detected early  History of excessive exposure to sunlight (natural or artificial)  Fair skin, light-colored hair and eyes  Personal or family history of skin cancer, past radiation treatments, immunosuppression, chronic exposure to arsenic, smoking, chewing tobacco Signs and Symptoms  Irregular borders that develop ulcerated center  Thickened, rough, crusted, may bleed  Usually on face, neck, scalp, ears, lips, shoulders, arms, upper back and trunk  In the mouth – red or ulcerated sore or white patch
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Malignant Melanoma
 Develops from melanocytes in basal layer of the epidermis or from benign melanocytic mole (nevus)  Extremely malignant, grows quickly, extending down to tissues, metastasizes to regional lymph nodes and other organs  Accounts for 74% of deaths from skin cancer  May develop from a preexisting nevus or appear as new in normal skin  Exposure to UV radiation, history of severe sunburn (especially during childhood)  Fair skin, light-colored hair and eyes  Multiple moles  Family history  Older age Signs and Symptoms  Lentigo melanoma, superficial spreading melanoma, nodular melanoma  Skin lesions with mixed flat and raised portions, irregular shape, dark brown or black lesions, variations of color, itching, mole > 6 mm diameter, bleeding from lesion  Lesion with above characteristics may suddenly appear
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Kaposi’s Sarcoma
 Malignant, rare, seen in patients that have AIDS (secondary opportunistic infection)  Originates in blood vessels and connective tissue of dermis; mouth, nose, throat, and other linings Etiology  Kaposi’s sarcoma-associated herpes virus (KSHV) in patient’s with HIV  Corticosteroids and immunosuppressive medications
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PT Intervention for Skin Cancers
 Wound care may be indicated after surgical removal  May be able to identify possible cancerous sites on skin  Important for early detection  Improve chances for survival  Strengthening, ambulation, endurance, and mobility, especially in patients with AIDS and Kaposi’s sarcoma
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The only kind of wound that can be "staged" are pressure ulcers
Stage 1, 2, 3,4 - Pressure ulcers. Others cannot be staged like this. Burn degrees are not "stages"
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Burn Degrees
1st Degree (Superficial) Burn  Previously called “first – degree”  Only epidermis is damaged  Red, swollen, tender  Healing in only a few days  Sunburn 2nd Degree (Superficial partial-thickness) Burn  Previously called “second-degree”  Epidermis and upper dermis are damaged  Swelling, redness, blistering, pain  Healing in 10 days – regrowth may occur because epithelial cells are still present  Minimal scarring may form 3rd Degree (Deep partial thickness) Burn  Previously called “third degree”  Damage to epidermis and dermis to reticular layer  Blood vessels, hair follicles and sweat glands  Red, white severe edema, heal in 3-5 weeks  Keloid and hypertrophic scarring 4th Degree Type I (Full-thickness) Burn  Previously called “fourth degree”  Destroys entire skin layers, down to fat tissue  Eschar, leathery, numb (damage to nerve endings)  Damage to lymphatic vessels (little swelling seen)  Requires skin-grafting  Healing several months  Regeneration not possible (Full-thickness) Burn 4th Degree Type II (Sub-dermal) Burn  Also previously called “fourth degree”  Destroys entire skin layers, including fat, muscle, bone  Caused by flame or electrical shock  Require surgery, skin grafting, possible amputation  Can be lethal
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Burns: Deep partial thickness burn scarring
Hypertrophic  Excess collagen production  Raised  Do not grow beyond boundaries of original scar Keloid  Excess collagen production  Raised  Extend beyond wound site
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Electrical Burns
 Current passes through body through blood vessels and nerves  Line of least resistance  Extensive damage to blood vessels, heart, kidneys, nerves  Gangrene and spinal cord damage  Not immediately evident
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Burns: Rule of Nines*
 Way to determine the extent of burns  Body is divided into 11 areas for quick estimation  Each area represents about 9% Weaker degree burns can still be dangerous if they cover enough of the body. Totals: - Anterior and posterior head and neck, 9% - Anterior and Posterior UEs, 18% (9% each limb) - Anterior and Posterior trunk, 36% (18% each side) - Perineum, 1% - Anterior and Posterior LEs, 36% (18% each limb)
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Burns: Complications
 Infection  Cardiac arrest  Smoke inhalation (smoke isn't just dirty, can also be hot enough to burn lungs)  Inhalation of noxious chemicals  Pneumonia  Hypothermia  Scarring
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*The deeper the burn wound the less surface area needed for it to be fatal
In other words, the severity level of the burn can trump the size of the area burned.
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PT Intervention for Burns
 Sharp debridement by PT (necrotic tissue)/Non-sharp debridement PTAs can do, whirlpool, pulsed lavage, dressing changes  Prevention of deformity through stretching and range of motion  Precautions for maintaining sterile environment, disturbing skin graft  Prevention of atrophy through cardiovascular exercises *Position patient away from position of the burn. Ex) Right side of neck burn means neck shouldn't be placed in right side flexion.
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Cellulitis
 Also called erysipelas, necrotizing fasciitis (severe)  Infection and inflammation of the skin and subcutaneous tissues  If left untreated can spread to blood and become systemic  Higher incidence with chronic diseases and conditions  Etiology  Strep and Staph  MRSA Cellulitis & Necrotizing Fasciitis - Necrotizing fasciitis is a serious bacterial infection that spreads rapidly and destroys the body's soft tissue. - Commonly called a "flesh-eating infection" by the media, this rare disease can be caused by more than one type of bacteria. These include group A Streptococcus (group A strep), Klebsiella, Clostridium, E. coli, Staphylococcus aureus
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Frost Bite
 Thermal Injury  Overexposure to the cold air or water  2 major forms  Localized injuries (frostbite)  Systemic injuries (hypothermia)  Initial vasoconstriction in the skin to protect the core  When tissue temps drop below 35.6° F - Ice crystals form in the tissues and expand extracellular spaces - With compression of cells, cell membrane rupture, interrupting enzymatic and metabolic activities
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Traumatic Injuries
Hemorrhage -Loss of a large amount of blood in a short period, externally or internally.  Hemorrhage may be arterial, venous, or capillary Contusion - A bruise; an injury with no break in the skin, characterized by discoloration, pain, and swelling Ecchymosis  Skin discoloration consisting of a large, irregularly formed hemorrhagic area with colors changing from blue-black to greenish brown or yellow; commonly called a bruise Petechia - Minute, pinpoint hemorrhagic spot of the skin.  A petechia is a smaller version of an ecchymosis
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Hemotoma
- Blood loss into a tissue, organ or other confined space. - Elevated, localized collection of blood trapped under the skin that usually results from trauma
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Functions of the Urinary System
* Acid-base balance in the blood * Blood pressure regulation - Production of renin (enzyme) - Increase volume → increase BP * Red blood cell production - Stimulated by erythropoietin * Activation and conversion of vitamin D * Storage and transportation of urine - Ureters, urinary bladder, urethra - Blood Pressure Fall in BP > Release of Renin > Release of Angiotensinogen (Angiotensinogen/Angiotensinogen I/Angiotensinogen II) > Vasoconstriction or Aldosterone Release > BP increase or Sodium retention leading to BP increase.
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Renal Failure
Failure of the kidneys to perform their physiologic functions adequately Acute renal failure * Abrupt, sudden reduction in renal function * If untreated, renal functions cease within a couple weeks Chronic renal failure (end stage renal disease) * Insidious and gradual, irreversible * Accompanied by dysfunction of other organs * Renal failure – significant loss of function * Renal insufficiency – diminished to 25% of normal function * Uremia – accumulation of waste products in the blood Signs and Symptoms * General malaise and weakness; progressing to severe fatigue * Changes in mental status * Oliguria (urinating a lot), anuria (inability to urinate) * Weight loss * Edema * Sensation loss in hands and feet * Severe bruising * Anemia * Malnutrition * Renal bone disease from dysfunction of platelets
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Urinary Tract Infections (UTI)
Cystitis (Bladder Infection) Pyelonephritis (Kidney Infection) * UTIs affect more than 11.3 million women per year * 5-30% of the older adult population * Mostly in females * Urethra is shorter and closer to the entrances of the rectum and vagina * Bacteria that result in most UTIs are acquired from the large bowel * Catheterization * Accounts for 40% of nosocomial infections * *Most common cause is "holding it in" for too long/too much Clinical Manifestations * Frequency * Urgency * Dysuria (peeing at night) * Nocturia * Fever, chills, & malaise * Increased confusion among the elderly Implications for the PTA * May not be able to fully participate depending on the severity of the infections * Note any changes in mental status * Awareness of symptoms to educate on early recognition * At risk for infections elsewhere * Catheters should not be place on floor * Urinary retention is a risk factors for UTI, so assist patient to bathroom as necessary
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Endocrine vs Exocrine Glands
Endocrine  Ductless glands  Anterior pituitary, thyroid, adrenals, parathyroid  Hormones released into blood Exocrine  Release products into body’s surface or cavities through ducts
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Hypothyroidism
 Underactive thyroid gland leading to deficiency of thyroid hormone secretion in adulthood  Cretinism, Hashimoto’s disease, congenital aplasia, secondary and tertiary Signs and Symptoms  Myxedema (Gull’s disease) = edema, obesity, intolerance to cold, decreased energy  Slowed metabolic rate, slowed mental processes  Muscle weakness  Thinning hair or hair loss
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Diabetes Mellitus (DM) [Diabetes]
 Lack of production of insulin by pancreas [Type I]; inability of the body to utilize insulin [Type II] Type I diabetes: insulin dependent  Most often seen in children  Autoimmune with a genetic component Type II diabetes: non-insulin dependent (NIDDM) - Having high blood sugar levels more often that you should  Most common  Most often seen in adults, and in certain ethnic populations - African- or Asian- Americans, Pacific Islanders, Latin descent - > 45 years of age, sedentary, hypertension, high cholesterol, poor diet, obesity Blood Glucose Levels: Fasting Plasma Glucose - Normal: <100 mg/dL - Prediabetes: 100-125 mg/dL - Diabetes: >125 mg/dL 2 Hr Oral Glucose Tolerance Test - Normal: <139 mg/dL - Prediabetes: 140-199 mg/dL - Diabetes ≥200 mg/dL Signs and Symptoms  Occur suddenly and more severely in Type 1; more gradually in Type 2  Glucose in urine  Blurred vision  Weight loss, increased appetite  Nausea, vomiting, abdominal pain  Amenorrhea, erectile dysfunction  *3 P's of Diabetes - Polyuria - excessive or an abnormally large production or passage of urine - Polydipsia - excessive thirst - Polyphagia - excessive hunger
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Diabetes Complications and long-term effects
 Diabetic coma - Can result from both hyperglycemia and hypoglycemia  Bone disease - Osteoporosis  Cardiac and vascular diseases - Cerebrovascular disease, ischemic changes in the limb, renal disease, reflex sympathetic dystrophy, Dupuytren’s contracture, limited joint mobility, gangrene to extremities  Renal disease - Reduced function to kidneys  Eye problems - Glaucoma, retinopathy, cataracts  Diabetic amyotrophy - Proximal muscle weakness  Diabetic neuropathy - Foot drop, susceptible to injury due to loss of sensation to the skin, “stocking” or “glove” parasthesias, carpel tunnel syndrome, Charcot’s joint * complication of diabetes-related neuropathy (nerve damage). It can cause serious symptoms like fractures and ulcers (convexity in the arch of the foot picture)
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Diabetes PT Interventions
 Exercise programs to improve blood pressure, weight loss, decrease heart rate and cholesterol levels, help body utilize insulin  Orthotic assessment, wound care for ulcers  Strengthening and lengthening of ankle musculature  Modalities to decrease pain  Rehabilitation for amputations  Pay particular attention to medication compliance  Sensory testing and patient foot care and inspection
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Comparison of Hypo- and Hyper- Glycemia (Picture on Phone)
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