Week 5

Question 1

What is bone growth stimulated by?

Answer 1

Weight bearing positions

Question 2

What are some normal skeletal alignment changes in an infant?

Answer 2

0-18 mo: varus knees
3-4 years: valgus knees

Question 3

What is Salter-Harris Classification?

Answer 3

Fracture injuries near the growth plate

1) S: slip (epiphysis separated from shaft)
2) A: above
3) L: lower
4) T: through (epiphysis & metaphysis)
5) R: rammed

Question 4

Describe Developmental Dysplasia of the Hip

Answer 4

Infant positioning impacts the
formation of the acetabulum, results in head of the femur not securely seated
in the acetabulum.
Often confirmed with ultrasound
(Increases risk of breech delivery or large baby)

• Three types:
  1)Unstable Hip Dysplasia: Hip is positioned normally but can be dislocated.
  2) Subluxation or Incomplete Dysplasia: Femoral head in partial contact with
  acetabulum but is partially displaced.
  3) Complete: Femoral head is fully out of acetabulum.

Question 5

List the etiology, pathogenesis, clinical presentation, and diagnostics of Developmental Dysplasia of the Hip

Answer 5

1. Etiology:
   Genetic predisposition
   Breech presentation during birth
   First-born child or family history
   Maternal hormone influence (e.g., relaxin)
2. Pathogenesis:
   Abnormal development or dislocation of the hip joint
   Shallow or poorly developed acetabulum
   Instability of the femoral head in the acetabulum
3. Clinical Presentation (Signs & Symptoms):
   Asymmetry in hip abduction or leg length discrepancy
   Positive Ortolani and Barlow tests in infants
   Limited range of motion in the affected hip
   Hip “click” or “clunk” during movement
4. Diagnostics:
   Ultrasound for infants (younger than 6 months)
   Ortolani’s Maneuver
   hip flexion and adduction to
   dislocate head of femur, then hip
   flexion and abduction to relocate (Ortolani “Click”-only in first month)

Question 6

List the medical/surgical management, precautions/red flags, and PT management of Developmental Dysplasia of the Hip

Answer 6

1. Medical/Surgical Management and Medication:
   Pavlik Harness: hip is braced into
   flexion and abduction until the
   femoral head molds into the
   acetabulum and joint capsule
   tightens.
2. Precautions/Red Flags:
   Monitor for avascular necrosis after treatment
   Risk of joint stiffness or dislocation recurrence
   Delayed intervention may cause long-term gait abnormalities or arthritis
3. Physical Therapy Management:
   Post-surgical rehabilitation for mobility and strength
   Hip stabilization exercises and gait training
   Stretching and ROM exercises to maintain flexibility
   Education on proper positioning and movement

Question 7

List the etiology, pathogenesis, clinical presentation, and diagnostics of scoliosis

Answer 7

1. Etiology:
   Idiopathic (unknown) 80%
   Adolescent Idiopathic Scoliosis:
   >30* curve is more common in girls at a rate of 10 to 1
   A) Osteopathic (wedge vertebrae)
   B) Myopathic (strength imbalance)
   C) Neuropathic (cerebral palsy)
2. Pathogenesis:
   Lateral curvature of the spine with possible rotation of vertebrae
   Structural abnormalities can worsen during growth spurts
   Progressive deformity affecting posture, balance, and spinal alignment
3. Clinical Presentation (Signs & Symptoms):
   Visible spinal curvature or uneven shoulders/hips
   Rib hump with forward bending (Adam’s forward bend test)
4. Diagnostics:
   Physical examination with Adam’s test
   X-rays to measure Cobb angle (curvature severity)
   PT scoliometer

Question 8

List the medical/surgical management, precautions/red flags, and PT management of scoliosis

Answer 8

1. Medical/Surgical Management and Medication:
   Bracing is indicated in curves 25-45
   degrees; Boston TLSO imaged here
   Surgical rodding and fusion
   recommended with curves greater
   than 45 degrees
   Organ compromise with severe curves,
   60 degrees or more (Pulmonary insufficiency, impaired cardiac function)
2. Precautions/Red Flags:
   Rapid progression during growth spurts
   Neurological symptoms (e.g., weakness, numbness, bowel/bladder dysfunction)
   Severe pain or functional limitations may indicate a more serious condition
3. Physical Therapy Management:
   Core strengthening and spinal stabilization exercises
   Stretching for tight muscles (e.g., hamstrings, hip flexors)
   Postural education and correction
   Breathing exercises (especially for rib cage rotation)
   Tailored exercise program to prevent curve progression and improve function

Question 9

List the etiology, pathogenesis, clinical presentation, and diagnostics of Degenerative Kyphoscoliosis

Answer 9

(Scheuermann’s disease)

1. Etiology:
   structural deformity classified by anterior wedging of 5 degrees or more of three adjacent thoracic bodies and affects adolescents aged 12 to16 years and is the most common cause of structural kyphosis in adolescence
2. Pathogenesis:
   Progressive spinal curvature due to collapse of vertebral bodies and intervertebral discs
   Combined lateral curvature (scoliosis) and excessive forward bending (kyphosis)
   Spinal instability and altered biomechanics lead to further degeneration
3. Clinical Presentation (Signs & Symptoms):
   Stooped posture with spinal deformity
   Chronic back pain, often worse with movement or prolonged standing
   Decreased height
   Minimal pain
   Schmorl’s nodes: local extrusion of nucleus pulpous through the cartilage and into vertebral body
4. Diagnostics:
   X-rays to assess spinal curvature, disc space narrowing, and vertebral fractures
   MRI or CT scans to evaluate nerve compression and disc degeneration
   Bone density scan (DEXA) if osteoporosis is suspected

Question 10

List the medical/surgical management, precautions/red flags, and PT management of Degenerative Kyphoscoliosis

Answer 10

1. Medical/Surgical Management and Medication:
   Pain management with NSAIDs, muscle relaxants, or opioids in severe cases
   Bracing to provide support and reduce pain
   Surgical intervention (e.g., spinal decompression, fusion) for severe cases or nerve compression
   Osteoporosis treatment (e.g., bisphosphonates, calcium, vitamin D supplements)
2. Precautions/Red Flags:
   Progressive neurological symptoms (e.g., leg weakness, bowel/bladder dysfunction)
   Severe, worsening back pain unresponsive to conservative treatment
   Increased risk of falls and fractures due to spinal instability and poor posture
3. Physical Therapy Management:
   Postural correction exercises to improve alignment
   Core and back strengthening exercises to support the spine
   Stretching to relieve muscle tightness, especially in the chest and hips
   Gait and balance training to reduce fall risk
   Education on proper body mechanics and ergonomics to reduce strain on the spine

Question 11

List the etiology, pathogenesis, clinical presentation, and diagnostics of Down Syndrome

Answer 11

1. Etiology:
   Genetic condition caused by an extra copy of chromosome 21 (trisomy 21)
   Risk factors include advanced maternal age
2. Pathogenesis:
   Extra chromosome affects development, leading to physical and intellectual disabilities
   Delayed motor and cognitive development
   Increased risk of congenital heart defects, hypothyroidism, and other medical conditions
3. Clinical Presentation (Signs & Symptoms):
   Flattened facial features, small head, short neck
   Hypotonia (low muscle tone) and joint laxity
   Developmental delays (cognitive, motor, speech)
   Short stature and a single deep crease across the palm
4. Diagnostics:
   Prenatal screening (e.g., nuchal translucency, noninvasive prenatal testing)
   Postnatal karyotype analysis to confirm trisomy 21
   Echocardiogram to detect congenital heart defects

Question 12

List the medical/surgical management, precautions/red flags, and PT management of Down’s syndrome

Answer 12

1. Medical/Surgical Management and Medication:
   Regular monitoring for associated health conditions (e.g., heart defects, thyroid function)
   Early intervention programs (speech, occupational, and physical therapy)
   Surgical correction for congenital heart defects if needed
   Medications for associated conditions (e.g., thyroid hormone replacement)
2. Precautions/Red Flags:
   Monitor for atlantoaxial instability (risk of spinal cord injury)
   Increased susceptibility to infections due to immune system abnormalities
   Risk of early-onset Alzheimer’s disease in adulthood
3. Physical Therapy Management:
   Early intervention to address hypotonia and motor delays
   Strengthening exercises for postural stability and motor skills development
   Gross motor skill training (e.g., crawling, walking, coordination exercises)
   Gait training and balance exercises to improve mobility
   Educating caregivers on promoting functional independence

Question 13

Give some examples of muscular dystrophies

Answer 13

All of them have a genetic origin (dystrophin, glycoprotein, complex)

1) Duchenne MD (most common): x-linked recessive (affects males).
Onset 2-4 yo
Rapidly progressive (death in 20’s)
2) Becker MD: x-linked recessive
Onset 5-10 yo
Slowly progressive, lifespan into adulthood
3) Limb-girdle MD: autosomal recessive
Onset varies
Slowly progressive, mild impairment

Question 14

List the etiology, pathogenesis, clinical presentation, and diagnostics of Duchenne’s MD

Answer 14

1. Etiology:
   
   • Genetic disorder caused by mutations in the dystrophin gene (X-linked recessive)
   • Primarily affects males
2. Pathogenesis:
   
   • Lack of dystrophin protein leads to muscle fiber damage and progressive muscle degeneration
   • Muscle weakness starts in the lower limbs and gradually affects other muscle groups
3. Clinical Presentation (Signs & Symptoms):
   
   • Delayed motor milestones (e.g., walking, running)
   • Progressive muscle weakness, beginning in the legs (falls, waddling gait) (proximal weakness)
     *. Winging scapula
   • Gower’s sign (using hands to push off thighs to stand up)
   • Pseudohypertrophy of calves (enlarged but weak muscles)
   • Eventual loss of ambulation (usually by early teens)
4. Diagnostics:
   
   • Elevated creatine kinase (CK) levels in blood tests
   • Genetic testing for dystrophin gene mutations
   • Muscle biopsy showing absence of dystrophin
   • Electromyography (EMG) to assess muscle function

Question 15

List the medical/surgical management, precautions/red flags, and PT management of Duchenne’s MD

Answer 15

(AVOID eccentric exercises)

1. Medical/Surgical Management and Medication:
   
   • Corticosteroids (e.g., prednisone) to slow muscle degeneration
   • Cardiac and respiratory monitoring (as heart and lung muscles weaken)
   • Assisted ventilation as respiratory muscles weaken
   • Orthopedic interventions (e.g., braces, spinal fusion for scoliosis)
   • Gene therapy and emerging treatments (e.g., exon-skipping therapy)
2. Precautions/Red Flags:
   
   • Monitor for respiratory complications and cardiac issues (e.g., cardiomyopathy)
   • Avoid excessive physical strain, which can accelerate muscle damage
   • Pay attention to scoliosis and respiratory decline in the later stages
3. Physical Therapy Management:
   
   • Gentle strengthening and stretching exercises to maintain mobility
   • Range of motion (ROM) exercises to prevent contractures
   • Use of orthotics and assistive devices to enhance mobility
   • Respiratory exercises to maintain lung function
   • Education on energy conservation techniques and caregiver training

Question 16

Describe spinal muscular atrophy

Answer 16

(Genetic autosomal recessive, anterior horn cell degeneration “motor”)

Type 1: Respiratory failure, early death
Type 2: Intermediate, significant functional impairment, power mobility
Type 3: Mildest form, independent ambulators, slow progression

Question 17

List the etiology, pathogenesis, clinical presentation, and diagnostics of spinal muscular atrophy

Answer 17

1. Etiology:
   
   • Genetic disorder caused by mutations in the SMN1 gene (autosomal recessive)
   • Leads to a deficiency of the survival motor neuron (SMN) protein
2. Pathogenesis:
   
   • Loss of motor neurons in the spinal cord and brainstem
   • Progressive muscle weakness and wasting of skeletal muscles
   • Severity varies depending on the type of SMA (Type I–IV)
3. Clinical Presentation (Signs & Symptoms):
   
   • Muscle weakness and atrophy, typically affecting proximal muscles
     *. Secondary scoliosis
   • Hypotonia (floppy baby syndrome in infants)
   • Difficulty with swallowing, breathing, and motor functions
   • Delayed motor milestones (e.g., sitting, standing, walking)
4. Diagnostics:
   
   • Genetic testing to identify SMN1 gene mutations
   • Electromyography (EMG) to assess motor neuron activity
   • Muscle biopsy may show denervation
   • Elevated creatine kinase (CK) levels may be present but are not diagnostic

Question 18

List the medical/surgical management, precautions/red flags, and PT management of spinal muscular atrophy

Answer 18

1. Medical/Surgical Management and Medication:
   * Nusinersen (Spinraza) and gene therapy (Zolgensma) to slow disease progression
   * Supportive care (e.g., respiratory support, feeding tubes)
   * Orthopedic management for scoliosis and joint contractures
   * Medications to manage symptoms and improve quality of life
2. Precautions/Red Flags:
   
   • Respiratory decline (monitor for breathing difficulties)
   • Difficulty with feeding and risk of aspiration
   • Regular monitoring for scoliosis and joint contractures
3. Physical Therapy Management:
   
   • Range of motion (ROM) exercises to prevent contractures
     
     • Pulmonary exercises
   • Strengthening exercises tailored to avoid fatigue
   • Postural and respiratory exercises to maintain lung function
   • Use of adaptive equipment (e.g., braces, wheelchairs) for mobility
   • Family and caregiver education on positioning, mobility, and home exercises

Question 19

List the etiology, pathogenesis, clinical presentation, and diagnostics of Congenital Muscular Torticollis

Answer 19

1. Etiology:
   
   • Likely caused by intrauterine positioning or birth trauma
   • Shortening or fibrosis of the sternocleidomastoid (SCM) muscle
   • Associated with other musculoskeletal abnormalities (e.g., hip dysplasia)
2. Pathogenesis:
   
   • Unilateral tightening of the SCM muscle leading to head tilt (toward the affected side) and rotation (toward the opposite side)
   • Can lead to plagiocephaly (flattening of the head) due to consistent head position
     *. Developmental delay and hip dislocation
3. Clinical Presentation (Signs & Symptoms):
   
   • Cervical side bending toward the involved side and rotation away from the involved side
   • Palpable tightness or lump in the SCM muscle
   • Limited range of motion in neck rotation and lateral flexion
   • Possible facial or skull asymmetry (plagiocephaly)
4. Diagnostics:
   
   • Physical examination for head tilt and limited neck ROM
   • Ultrasound may be used to confirm SCM muscle involvement

Question 20

List the medical/surgical management, precautions/red flags, and PT management of Congenital Muscular Torticollis

Answer 20

1. Medical/Surgical Management and Medication:
   * Conservative treatment with physical therapy as the primary intervention. Responds well to PT but 16% of cases require surgery
   * Surgery (e.g., SCM release) may be considered if severe or unresponsive to therapy after 1 year of age
   * Positioning techniques to reduce plagiocephaly
2. Precautions/Red Flags:
   
   • Monitor for worsening neck range of motion or development of plagiocephaly
   • Be alert for signs of other conditions like cervical spine issues or hip dysplasia
   • Delay in treatment can lead to persistent deformity and functional limitations
3. Physical Therapy Management:
   
   • Positioning and stretching exercises to lengthen the SCM muscle
   • Strengthening exercises to improve neck muscle balance and symmetry
   • Positioning strategies to encourage head rotation and avoid prolonged pressure on one side
   • Parent education on stretching, positioning, and handling techniques to promote active movement
   • Monitoring and addressing any secondary issues like plagiocephaly

Question 21

What are the types of Congenital Muscular Torticollis?

Answer 21

1. Postural Torticollis: This is the mildest form and involves a head tilt with no muscle tightness or mass in the sternocleidomastoid (SCM) muscle. It is typically positional and can be corrected more easily.
2. Muscular Torticollis: This form involves tightness in the SCM muscle but no palpable mass. The muscle shortening causes the head to tilt to one side and turn toward the opposite side.
3. Sternocleidomastoid Mass: In this type, a fibrotic mass or “tumor” is present in the SCM muscle, leading to significant muscle shortening and more severe restriction of neck movement.
4. Postnatal Muscular Torticollis: This form develops after birth, usually as a result of birth trauma, muscle injury, or other conditions that affect the neck muscles.

Question 22

List the etiology, pathogenesis, clinical presentation, and diagnostics of Brachial Plexopathy

Answer 22

1. Etiology:
   
   • Typically traction injury of the brachial plexus within a difficult birth
   • A) Erb’s palsy: c5-6 injury: the arm is maintained in a position of abduction and internal rotation at the shoulder with lower arm pronated and fingers flexed “waiter’s tip” position
     *. B) Klumpe’s palsy: c8-T1, position in pronation, elbow flexion, no grasp
2. Pathogenesis:
   
   • Damage to the brachial plexus nerves (C5–T1) affecting motor and sensory function in the shoulder, arm, and hand
   • Can involve different parts of the brachial plexus (upper, middle, lower trunks)
   • Nerve damage may lead to weakness, paralysis, or sensory loss
3. Clinical Presentation (Signs & Symptoms):
   
   • Weakness or paralysis in the shoulder, arm, or hand (depending on nerve involvement)
   • Numbness, tingling, or loss of sensation in the affected limb
   • Pain or burning sensation in the shoulder, arm, or hand
   • Muscle atrophy in chronic cases
4. Diagnostics:
   
   • Electromyography (EMG) and nerve conduction studies to assess nerve function
   • MRI or CT to evaluate for structural damage (e.g., tumors, compression)
   • Physical exam focusing on muscle strength, reflexes, and sensation

Question 23

List the etiology, pathogenesis, clinical presentation, and diagnostics of Osteogenesis Imperfecta (OI)

Answer 23

1. Etiology: (Rare brittle bone disease)
   
   • Genetic disorder, most commonly autosomal dominant. Short stature is common
   • Caused by mutations in genes collagen synthesis affecting bone and connective tissue, mostly autosomal dominant
     *. Four types at least:
     A) Type I: most common, least severe
     B) Type III: Triangular face, progressive
     deformity, w/c dependent teens
2. Pathogenesis:
   
   • Defective or insufficient collagen leads to fragile bones that break easily
   • Affects not only bones but also teeth, skin, and connective tissues
   • Varying degrees of severity based on OI type (Type I–IV being most common)
3. Clinical Presentation (Signs & Symptoms):
   
   • Frequent fractures with minimal trauma
   • Bone deformities (e.g., bowing of long bones, scoliosis)
   • Blue sclera (bluish tint in the whites of the eyes)
   • Short stature and joint hypermobility
   • Hearing loss in some cases (due to middle ear bone malformations)
4. Diagnostics:
   
   • Clinical assessment based on history of fractures and physical signs
   • Genetic testing to confirm collagen gene mutations
   • X-rays showing fractures in different stages of healing
   • Bone density testing (DEXA) to assess bone fragility

Question 24

List the medical/surgical management, precautions/red flags, and PT management of Brachial Plexopathy

Answer 24

1. Medical/Surgical Management and Medication:
   * Pain management (NSAIDs, opioids, neuropathic pain medications)
   * Physical therapy and rehabilitation for nerve recovery and muscle strengthening
   * Surgical intervention (e.g., nerve grafts, nerve transfer) for severe cases or persistent dysfunction
   * Steroids or immunosuppressants in cases of inflammatory brachial plexopathy
2. Precautions/Red Flags:
   
   • Monitor for progressive weakness or paralysis
   • Signs of autonomic dysfunction (e.g., Horner’s syndrome)
   • Chronic pain or failure to recover may indicate the need for surgical evaluation
3. Physical Therapy Management:
   
   • Positioning and Range of motion (ROM) exercises to prevent contractures and maintain mobility
   • Strengthening exercises to motor function
   • Sensory re-education for any loss of sensation

Question 25

List the medical/surgical management, precautions/red flags, and PT management of Osteogenesis Imperfecta (OI)

Answer 25

1. Medical/Surgical Management and Medication: * Bisphosphonates (e.g., pamidronate) to increase bone density * Orthopedic interventions (e.g., rodding surgery to stabilize bones) * Physical aids (e.g., braces, wheelchairs) to support mobility * Pain management with analgesics or physical modalities * Regular monitoring for hearing loss and dental issues (dentinogenesis imperfecta) 2. Precautions/Red Flags: * High risk of fractures, especially during routine activities * Avoid aggressive physical therapy or manual techniques that could cause fractures * Respiratory issues due to chest deformities in severe cases 3. Physical Therapy Management: * Gentle low-impact exercises to improve muscle support around joints (AQUATIC THERAPY) * Range of motion (ROM) exercises to maintain joint flexibility without excessive force * Aquatic therapy for safe, supported movement * Education on safe handling and positioning to prevent fractures * Functional training to improve mobility with assistive devices and adaptive equipment

Question 26

List the etiology, pathogenesis, clinical presentation, and diagnostics of Arthrogryposis Multiplex Congenita

Answer 26

1. Etiology: (underlying cause unknown) * Non-progressive condition caused by fetal akinesia (lack of movement in the womb) * Three types: A) Contracture syndromes B) Amyoplasia C) Distal arthrogryposis 2. Pathogenesis: * Decreased fetal movement leads to abnormal joint development and contractures * Can develop to scoliosis. Talipies equinovarus “cleft foot” can also occur * Multiple joint deformities present at birth, affecting movement and function 3. Clinical Presentation (Signs & Symptoms): * Multiple joint contractures, especially in the limbs (e.g., clubfoot, extended knees, flexed elbows) * Muscle weakness or absence * Limited or absent range of motion in affected joints * Typically involves symmetrical deformities in the arms and legs 4. Diagnostics: * Prenatal ultrasound may show decreased fetal movement and joint contractures * Physical examination at birth for joint stiffness, deformities, and muscle weakness * X-rays to assess bone and joint involvement * Genetic testing if a hereditary condition is suspected

Question 27

List the medical/surgical management, precautions/red flags, and PT management of Arthrogryposis Multiplex Congenita

Answer 27

1. Medical/Surgical Management and Medication: * Orthopedic surgery (e.g., tendon releases, osteotomies) to improve joint function * Serial casting or bracing to correct deformities and maintain alignment * Pain management, if needed, following surgeries * Assistive devices (e.g., orthotics, wheelchairs) to enhance mobility 2. Precautions/Red Flags: * Monitor for respiratory complications due to thoracic deformities * Be cautious with aggressive stretching, as it may cause skin or joint damage * Ensure appropriate post-surgical rehabilitation to prevent recurrence of contractures 3. Physical Therapy Management: * Stretching and range of motion (ROM) exercises to maintain joint mobility * Strengthening exercises to maximize functional muscle use * Adaptive equipment and assistive devices to promote independence in mobility * Splinting and bracing to prevent contractures and improve joint alignment * Family education on home exercises and proper handling techniques to support long-term function

Question 28

List the etiology, pathogenesis, clinical presentation, and diagnostics of Marfan Syndrome

Answer 28

1. Etiology: * Genetic mutation, in fibrilin-1 gene connective tissue development. usually autosomal dominant * Caused by mutations in the FBN1 gene, affecting the production of fibrillin, a protein important for connective tissue integrity 2. Pathogenesis: * Soft tissue injury that affects multiple systems, particularly the skeletal, cardiovascular, and ocular systems * Heart valve defect and aortic aneurysm 3. Clinical Presentation (Signs & Symptoms): * Tall stature with long limbs and fingers (arachnodactyly) and characteristic facial features *. Scoliosis * Overgrowth of bone to above average height * Joint hypermobility and flat feet * chest deformities (pectus excavatum) * Lens dislocation (ectopia lentis) and myopia * Cardiovascular issues: aortic dilation, aortic aneurysm, mitral valve prolapse 4. Diagnostics: * Clinical evaluation based on physical characteristics and family history * Genetic testing for FBN1 mutation * Echocardiogram and MRI to assess the aorta and heart valves * Eye examination to check for lens dislocation and other abnormalities

Question 29

List the medical/surgical management, precautions/red flags, and PT management of Marfan Syndrome

Answer 29

1. Medical/Surgical Management and Medication: * Beta-blockers or angiotensin receptor blockers (ARBs) to reduce aortic stress * Regular cardiovascular monitoring (echocardiograms) to track aortic dilation * Surgery for aortic aneurysms or severe mitral valve prolapse * Corrective lenses or surgery for vision problems * Orthopedic interventions for severe skeletal deformities (e.g., scoliosis) 2. Precautions/Red Flags: * Risk of aortic dissection or rupture (medical emergency) * Avoid contact sports or high-impact activities that stress the aorta * Monitor for sudden chest, back, or abdominal pain (signs of aortic dissection) 3. Physical Therapy Management: * Postural correction and exercises to address scoliosis and chest deformities * Joint stabilization exercises to strengthen muscles and improve joint support * Avoidance of high-intensity or high-impact activities to protect the cardiovascular system * Stretching and strengthening exercises to improve overall function without overstressing joints * Education on proper body mechanics and activity modifications to reduce strain on the aorta and joints

Question 30

Label these

Answer 30

1) spina bifida occulta: (least severe, only bony vertebra affected) 2) spina bifida myelomeningocele: (most sever, malformation of spinal cord, meninges, and vertebra) 3) spina bifida meningocele: meninges and bony vertebra

Question 31

List the etiology, pathogenesis, clinical presentation, and diagnostics of Spina Bifida

Answer 31

1. Etiology: (3 types: occulta, cystica “meningocele”, and myelomeningocele) * Congenital anomaly which occurs when the embryologic development of the spinal cord fails to close the neural tube, before the 28th day of gestation. * Multi factorial risk factors include folic acid deficiency during pregnancy, genetics, and environmental influences 2. Pathogenesis: * Incomplete formation of the vertebral arches, leaving part of the spinal cord exposed * Motor and sensory deficits similar to spinal cord injury. (Flaccid paralysis): under L2 more peripheral (Spasticity): above L2 “CNS” 3. Clinical Presentation (Signs & Symptoms): * Varies by type: * Spina Bifida Occulta: Often asymptomatic, may have a small dimple, tuft of hair, or birthmark at the site * Meningocele: Sac of fluid protrudes through the spine but doesn’t involve the spinal cord; may have mild symptoms * Myelomeningocele: Severe symptoms including paralysis, loss of sensation below the lesion, bowel/bladder dysfunction, and hydrocephalus * Bowel and bladder issues, scoliosis congenital or acquired, UE fine motor & perceptual deficits, risk of pressure breakdown, cleft foot, VP shunt *. LATEX allergy 4. Diagnostics: * Prenatal screening via maternal serum alpha-fetoprotein (AFP) test and ultrasound * Postnatal diagnosis through physical exam and imaging (e.g., MRI, ultrasound) to assess spinal defect * Amniocentesis may be performed for further confirmation during pregnancy

Question 32

List the medical/surgical management, precautions/red flags, and PT management of spina bifida

Answer 32

1. Medical/Surgical Management and Medication: * Surgical closure of the spinal defect shortly after birth (for myelomeningocele) * Ventriculoperitoneal (VP) shunt to manage hydrocephalus * Bladder and bowel management programs * Assistive devices (e.g., braces, wheelchairs) for mobility * Ongoing medical monitoring for complications (e.g., hydrocephalus, urinary tract infections) 2. Precautions/Red Flags: * Monitor for signs of shunt malfunction (headache, vomiting, lethargy) * Risk of skin breakdown due to immobility and loss of sensation * Increased risk of latex allergies in individuals with spina bifida * Bowel and bladder dysfunction may lead to urinary tract infections or kidney damage 3. Physical Therapy Management: * Early intervention with mobility and strengthening exercises * Range of motion (ROM) exercises to prevent contractures * Gait training, bracing, or assistive devices based on functional level * Positioning and adaptive equipment to prevent deformities and enhance independence * Education on skin care, mobility techniques, and prevention of secondary complications (e.g., pressure sores)

Question 33

List the etiology, pathogenesis, clinical presentation, and diagnostics of Neurological Sequelae

Answer 33

1. Etiology: (AKA Hydrocephalus) * Result of primary neurological injury or illness (e.g., stroke, traumatic brain injury, spinal cord injury, infections like meningitis, multiple sclerosis) * Arnold-Chiari Malformation type II 2. Pathogenesis: * Damage to the central or peripheral nervous system leads to long-term complications * Secondary effects may include impaired neural pathways, inflammation, or scarring * Neurological sequelae can affect motor, sensory, cognitive, and autonomic functions 3. Clinical Presentation (Signs & Symptoms): * Spinal cord tethering (watch for neurological changes –tonal and cognitive changes, marked decline in function, scoliosis) * Motor impairments: muscle weakness, spasticity, paralysis * Sensory impairments: numbness, tingling, loss of proprioception * Cognitive deficits: memory loss, difficulty with problem-solving, attention deficits * Emotional changes: depression, anxiety, personality changes * Autonomic dysfunction: bladder/bowel issues, blood pressure regulation problems 4. Diagnostics: * Clinical assessment based on history of the primary condition * Neurological examination to assess motor, sensory, and cognitive functions * Imaging (MRI, CT scan) to evaluate brain or spinal cord damage * Electromyography (EMG) or nerve conduction studies for peripheral nerve involvement

Question 34

List the medical/surgical management, precautions/red flags, and PT management of Neurological Sequelae

Answer 34

1. Medical/Surgical Management and Medication: * VP shunt *Wheelchair mobility *Independent pressure relief *Independent self-catheterization *Flexibility and strengthening **caution for joint overuse *Often kids that require KAFO for ambulation will abandon ambulation when they reach teen years. Energy conservation perspective. 2. Precautions/Red Flags: * Increased risk of secondary complications such as contractures, pressure sores, and infections * Monitor for changes in neurological status, such as sudden worsening of symptoms * Risk of falls, aspiration, or other injuries related to motor and sensory impairments 3. Physical Therapy Management: *Positioning is essential for the young child for prevention of deformity ◦ Often tend to posture in a frog legged position ◦ Use hand-made supports and/or splinting *Handling techniques for: ◦ head/trunk control ◦ righting and equilibrium reactions ◦ transitional mobility * should have a standing system by 9 mo to 1 yo (standing frame, HKFAOs, AFO…)

Question 35

What are the bone classifications?

Answer 35

(206 bones in the adult skeleton) 1) Flat bone: thin and curved bone; serves as a point of attachment for muscles and protects internal organs (sternum, ribs, scapula, cranial bones) 2) Irregular bone: complex shape, protects internal organs from compressive force (vertebra, facial bones) 3) Long bone: cylinder shaped, longer than it is wide, functions as a lever (femur, humerus, phalanges) 4) Sesamoid bone: small round bone embedded in a tendon, protects the tendon from compressive forces (patella) 5) Short bone: cube shaped that is equal width, length and thickness. Provides limited motion (carpals, tarsals)

Question 36

Describe diaphysis, epiphysis, epiphyseal plate, periosteum, spongy bone, trabeculae

Answer 36

*Diaphysis - tubular shaft that runs between the proximal and distal ends of a long bone *Epiphysis - wide section at each end of a long bone; filled with spongy bone and red marrow *Epiphyseal plate - (also, growth plate) sheet of hyaline cartilage in the metaphysis of an immature bone; replaced by bone tissue as the organ grows in length *Periosteum - fibrous membrane covering the outer surface of bone and continuous with ligaments *Spongy (cancellous) bone - trabeculated osseous tissue that supports shifts in weight distribution *Trabeculae - sections of the lattice-like matrix in spongy bone

Question 37

Describe compact bone, endosteum, medullary cavity, lacunae, and articular cartilage

Answer 37

*Compact (cortical) bone - dense osseous tissue that can withstand compressive forces *Endosteum - delicate membranous lining of a bone’s medullary cavity *Medullary cavity - hollow region of the diaphysis; filled with yellow marrow *Lacunae - spaces in a bone that house an osteocyte *Osteon (Haversian system) - basic structural unit of compact bone; made of concentric layers of calcified matrix *articular cartilage - thin layer of cartilage covering an epiphysis; reduces friction and acts as a shock absorber

Question 38

Describe the bone cells

Answer 38

1) Osteogenic cells: develops into osteoblasts (endosteum, cellular layer of periosteum) 2) Osteoblast cells: bone formation (endosteum, cellular layer of periosteum, growing portions of bone) 3) Osteocyte: maintains mineral concentration of matrix (entrapped in matrix) 4) Osteoclast: bone reabsorption (endosteum, cellular layer of periosteum, old injured or unneeded bone)

Question 39

Explain Intramembranous ossification

Answer 39

compact and spongy bone develops directly from sheets of mesenchymal cells (flat bones of the face, most of the cranial bones, and the clavicles)

Question 40

Explain endochondral ossification

Answer 40

bone develops by replacing hyaline cartilage. (Cartilage does not become bone, but serves as a template to be completely replaced by new bone) Endochondral ossification takes much longer than intramembranous ossification. (Ex: Bones at the base of the skull and long bones form via endochondral ossification.)

Question 41

What are the zones of bone growth in order?

Answer 41

reserve zone - region closest to the epiphyseal end of the plate and contains small chondrocytes within the matrix proliferative zone - contains stacks of slightly larger chondrocytes zone of maturation and hypertrophy - older and larger zone of calcified matrix - zone closest to the diaphysis, are dead because the matrix around them has calcified, restricting nutrient diffusion

Question 42

What is the role of calcium in bone health?

Answer 42

Needed to make calcium phosphate and calcium carbonate which form hydroxyapatite crystals that give bone its hardness

Question 43

What is the role of vitamin D in bone health?

Answer 43

Calcium absorption

Question 44

What is the role of vitamin K in bone health?

Answer 44

Supports bone mineralization

Question 45

What is the role of magnesium in bone health?

Answer 45

Structural component of bone

Question 46

What is the role of fluoride in bone health?

Answer 46

Structural component of bone

Question 47

What is the role of omega-3 fatty acids in bone health?

Answer 47

Reduces inflammation that may interfere with osteoblast formation

Question 48

What is the normal calcium level? What happens if it’s too much/little?

Answer 48

Normal (10mg/dL) 1) too much: Thyroid releases calcitonin, osteoclast activity is inhibited, Ca2+ reabsorption in kidneys decreases, Ca2+ in blood decreases 2) too little: Parathyroid gland releases PTH, osteoclasts release Ca2+ from bone, calcium is reabsorbed from urine in kidneys, absorbed in small intestine via vitamin D synthesis, Ca2+ in blood increases

Question 49

How does exercise affect bone tissue?

Answer 49

*Mechanical stress stimulates the deposition of mineral salts and collagen fibers. *People who exercise regularly have greater bone density than those who are more sedentary *Resistance training has a greater effect than cardiovascular activities. *Resistance training is especially important to slow down the eventual bone loss due to aging and for preventing osteoporosis. *Wolff’s Law!!!

Question 50

How does Growth Hormone affect the skeletal system?

Answer 50

Increase length of bones, improves mineralization and bone density

Question 51

How does Thyroxine affect the skeletal system?

Answer 51

Stimulates bone growth and promotes synthesis of bone matrix

Question 52

How do Sex Hormones affect the skeletal system?

Answer 52

Promote osteoblastic activity and production of bone matrix, responsible for adolescent growth spurt, promotes conversion of epiphyseal plate epiphyseal line

Question 53

How does Calcitriol affect the skeletal system?

Answer 53

Stimulates absorption of calcium and phosphate from digestive tract

Question 54

How does Parathyroid Hormone affect the skeletal system?

Answer 54

Osteoclast proliferation and resorption of bone by osteoclasts, indirectly increases calcium absorption by small intestine

Question 55

How does Calcitonin affect the skeletal system?

Answer 55

Inhibits osteoclast activity and stimulates calcium uptake by bones

Question 56

Explain the types of bone fractures

Answer 56

A) open or compound: tears through skin B) closed or simple: skin is intact 1) Transverse: straight across long axis of bone 2) Oblique: angle that is not 90 3) Spiral: bone segments are pulled apart from twisting motion 4) Comminuted: several breaks 5) Impacted: one fragment is driven into another from compression 6) Greenstick: partial fracture where one side of the bone is broken

Question 57

Briefly state the stages of bone repair

Answer 57

1) broken blood vessels lead to fracture hematoma 2) internal and external calluses form from cartilage 3) cartilage gradually replaced by trabecular bone 4) remodeling occurs to replace immature bone with mature bone

Question 58

What are the phases of bone remodeling?

Answer 58

1) Quiescent phase – bone at rest. 2) Activation phase – Retraction of bone lining cells (mature osteoblasts) and digestion of endosteal membrane by collagenase. Recruitment and activation of osteoclasts to initiate bone resorption. 3) Resorption phase - Osteoclasts begin to dissolve minteral material and decompose osteoid matrix. Approx 2 – 4 weeks during each remodeling cycle. 4) Reversal phase – Bone resorption transition to bone formation. Mononuclear cells (monocytes, osteocytes, preosteoblasts) recruited to begin new bone formation. 5) Formation phase – Osteoblasts release and synthesize new osteoid matrix. 6) Mineralization phase – new matrix is mineralized with calcium and phosphorous. Quiescent phase begin again.

Question 59

How does thyroid hormone affect bone?

Answer 59

Stimulate bone resorption and formation (ex: bone loss in hyperthyroidism)

Question 60

Describe factors of the systemic regulation of bone remodeling?

Answer 60

*Genetic factors – 60 – 80% of bone mass is genetically determined. African American > White > Asian *Mechanical factors – Load, stress, physical activity *Vascularization – supply blood, oxygen, nutrients *Nutritional factors – Calcium, caffeine, alcohol, excess salt. *Hormonal factors

Question 61

What is Osteoporosis? And what causes it?

Answer 61

*Osteoporosis is a very common metabolic disorder of the skeleton where the bone mineral density (BMD) is reduced *Bone microarchitecture is disrupted and the amount and variety of noncollagenous proteins in bone is altered *Increased risk of fracture. *Causes: *Primary (postmenopausal/senile) *Secondary cause (nutrition, endocrine, drug, malignancy, chronic disease, idiopathic)

Question 62

What can contribute to the bone strength and mass loss in Osteoporosis?

Answer 62

1) Failure to reach an optimal peak bone mass as a young adult 2) Excessive resorption of bone after peak mass has been achieved 3) An impaired bone formation response during remodeling

Question 63

What can the defect in osteoblast function in Osteoporosis be the consequence of?

Answer 63

1) Cellular senescence 2) Decrease in the synthesis or activity of systemic and local growth factors

Question 64

What are the risk factors of Osteoporosis?

Answer 64

1) Noncontrollable risks: *Female gender *Small frame *Advanced age *Hormone levels *Genetics *Predisposing medical condition 2) Controllable risks: *Cigarette smoking *Excessive alcohol intake *Inactive lifestyle *Excessive caffeine intake *Lack of weight-bearing exercise *Drugs (eg, steroids, heparin) *Poor health *Low weight *Calcium-poor diet *Low vitamin D levels

Question 65

What is the treatment for Osteoporosis?

Answer 65

1) Treatment: *Drug therapy – bisphosphonates (reduce bone resorption) *Hormone therapy *Lifestyle and behavioral remedies *Nutrition & supplementation *Exercise 2) Physical therapy for osteoporosis: (slow down the effects) *Weight bearing exercises to strengthen bone & muscles *Proper posture to protect spine from fracture *Optimize alignment for ADL *Improve balance to reduce risk of falling (Intensive or high-impact exercise not recommended)

Question 66

What is Osteomalacia/Rickets? And what causes it?

Answer 66

It is softening of bones due to incomplete or impaired mineralization of osteoid Rickets: children Osteomalacia: adults Causes: *Lack of sun exposure *Poor nutritional intake *Drug-induced altered bone mineralization or vitamin D deficiency *Kidney or liver disorders (involved in activating vitamin D) *Vitamin D deficiency in older adults is the most common cause of osteomalacia

Question 67

What is the treatment for Osteomalacia?

Answer 67

1) Treatment: *Drugs and supplementation (Vitamin D, calcium) *Lifestyle and behavioral remedies *Nutrition – eat foods high in Vitamin D *Exercise 2) Physical therapy (similar to osteoporosis): *Weight bearing exercises to strengthen bone & muscles *Proper posture to protect spine from fracture *Optimize alignment for ADL *Improve balance to reduce risk of falling (Intensive or high-impact exercise not recommended)

Question 68

List the etiology, pathogenesis, clinical presentation, and diagnostics of Osteomyelitis

Answer 68

1. Etiology: * Bacterial infection, most commonly caused by Staphylococcus aureus. The bacteria seeds in the vascular areas of the bone * Acute (more common in children): Hematogenous spread (ESPECIALLY IF THERE IS UNEXPLAINED CELLULITIS) * Chronic (more common in adults): immune compromised 2. Pathogenesis: * Bacteria invade bone tissue, causing inflammation and necrosis. (Periosteum inflammation) * Infection disrupts normal bone remodeling and leads to abscess formation * Can cause pathological fracture due to bone poor quality 3. Clinical Presentation (Signs & Symptoms): * Pain not always an indicator * Acute: Localized bone pain and tenderness * Swelling, redness, warmth over the affected area * Fever, malaise, and chills * Chronic: Persistent or intermittent bone pain * Possible drainage from sinus tracts or open wounds * Signs of systemic infection may be absent in chronic cases 4. Diagnostics: * Elevated WBC, ESR, CRP * Blood cultures to identify the causative organism * X-rays may show bone periosteal changes * pain and limited ROM, fever, erythema, swelling, heat * Bone biopsy, scan or MRI to confirm

Question 69

List the medical/surgical management, precautions/red flags, and PT management of Osteomyelitis

Answer 69

1. Medical/Surgical Management and Medication: * 1st thing to do: Surgical debridement Longterm IV antibiotics Prosthetic removal, implantation of antibiotic beads (6 weeks), revision surgery *. Prophylactic considerations: Prior to surgery and Prior to dental work (for those with increased risks) 2. Precautions/Red Flags: * Monitor for signs of systemic infection (fever, chills, worsening pain) * Risk of chronic osteomyelitis, especially in immunocompromised patients or those with poor circulation (e.g., diabetics) * Risk of sepsis or spread to other organs if untreated * Delayed healing or recurrence if infection is not fully eradicated 3. Physical Therapy Management: * Post-surgical rehabilitation to restore function and mobility * Weight-bearing restrictions to avoid stressing the affected bone during healing * ROM exercises to prevent joint stiffness and muscle atrophy * Strengthening exercises once infection is controlled and healing progresses * Education on wound care and infection prevention, especially in diabetic patients or those at risk of recurrence

Question 70

List the etiology, pathogenesis, clinical presentation, and diagnostics of Spondylodiskitis

Answer 70

1. Etiology: * Infection that affects the vertebral spine components *. Intervertebral disk most commonly *. Adults-post-op diskectomy (takes out the herniated part of the disc) *. Children-hematogenous after respiratory or urinary tract infection *. Clinical presentation as with osteomyelitis *. Must consider vertebral osteomyelitis potentially underlying-MRI 2. Pathogenesis: * Infection begins in the disc space and spreads to adjacent vertebral bodies * Inflammation leads to disc and bone destruction, abscess formation, and potential spinal instability * Chronic cases can lead to fibrosis, deformity, and spinal cord or nerve root compression 3. Clinical Presentation (Signs & Symptoms): * Severe, localized back pain that worsens with movement and is not relieved by rest * Fever, chills, and malaise (more common in acute cases) * Neurological symptoms (e.g., weakness, numbness) if abscess or spinal deformity compresses nerves * Stiffness or limited range of motion in the spine 4. Diagnostics: * Elevated inflammatory markers (ESR, CRP) * Blood cultures to identify the causative organism * MRI is the gold standard for early detection, showing disc space narrowing, vertebral destruction, and abscess formation * X-rays and CT scans may show disc space collapse or vertebral changes in later stages * Biopsy of the disc space or vertebrae for culture and definitive diagnosis

Question 71

List the medical/surgical management, precautions/red flags, and PT management of Spondylodiskitis

Answer 71

1. Medical/Surgical Management and Medication: * Bedrest (acute phase), antibiotics long term * Bracing to immobilize the spine (TLSO, Hip Spica “child”) * Surgical intervention 10-20% or cases * Pain management with NSAIDs or analgesics 2. Precautions/Red Flags: * Monitor for neurological deficits (e.g., weakness, numbness, bladder/bowel dysfunction), which may indicate spinal cord compression * Risk of sepsis or systemic spread if the infection is untreated * Spinal instability or deformity may occur if the infection progresses * Ensure complete antibiotic course to prevent recurrence 3. Physical Therapy Management: * Early mobilization, within weight-bearing limits, to prevent deconditioning and maintain spinal mobility * Postural exercises to improve spinal alignment and reduce pain * Gradual strengthening and stabilization exercises for spinal musculature once the infection is under control * Pain management techniques (e.g., heat, stretching) to reduce discomfort * Patient education on activity modification, avoiding excessive loading of the spine during recovery

Question 72

List the etiology, pathogenesis, clinical presentation, and diagnostics of Infectious arthritis

Answer 72

1. Etiology: * Bacterial infection of the joint, most commonly caused by Staphylococcus aureus * NOT = reactive arthritis (Reiter's syndrome) *. Local response with joint destruction and sepsis (can be irreversible) *. Risks-penetrating trauma, chronic joint damage *. Chondoral damage within hours (URGENT) *. Joint aspiration for culture and sensitivity *. I & D common 2. Pathogenesis: * Infection enters the joint through the bloodstream, direct inoculation (e.g., surgery, trauma), or contiguous spread from nearby infection * Pulmonary risk due to abnormal joint synovium “surface” * If untreated, can result in irreversible joint destruction and systemic infection 3. Clinical Presentation (Signs & Symptoms): * Acute onset of severe joint pain, swelling, and warmth, typically in one joint (commonly the knee, hip, or shoulder) * Fever, chills, and systemic symptoms (more common in bacterial causes) * Limited range of motion due to pain and joint effusion * Redness over the affected joint 4. Diagnostics: * Joint aspiration (arthrocentesis) to analyze synovial fluid for white blood cells, bacteria, and crystals * Synovial fluid culture to identify the causative organism * Elevated inflammatory markers (ESR, CRP) * Blood cultures if systemic infection is suspected * X-rays or ultrasound to assess joint effusion and any bony involvement

Question 73

List the medical/surgical management, precautions/red flags, and PT management of Infectious Arthritis

Answer 73

1. Medical/Surgical Management and Medication: * Immediate administration of intravenous (IV) antibiotics based on the causative organism (e.g., vancomycin for Staphylococcus aureus) * Oral antibiotics for several weeks after IV therapy * Joint drainage via needle aspiration, arthroscopy, or open surgery if needed * Pain management with NSAIDs or analgesics * Surgical debridement in severe cases or if infection involves prosthetic joints 2. Precautions/Red Flags: * Delay in treatment can lead to irreversible joint damage and sepsis * Monitor for worsening systemic symptoms (e.g., fever, chills, sepsis) * Risk of recurrence, especially in patients with prosthetic joints or immunosuppression * Prolonged or untreated infections can lead to joint deformity and loss of function 3. Physical Therapy Management: * Early passive range of motion (ROM) exercises once the infection is under control to prevent joint stiffness and maintain mobility * Gradual introduction of active exercises to restore strength and function * Gait training and use of assistive devices if weight-bearing joints are affected * Pain management techniques (e.g., ice, gentle stretching) during recovery * Education on joint protection and activity modification during rehabilitation

Question 74

List the etiology, pathogenesis, clinical presentation, and diagnostics of the Infectious (Inflammatory) Muscle Disease-Myositis: Inclusion Body Myositis (IBM)

Answer 74

1. Etiology: * Autoimmune and degenerative components where the muscle fibers degenerates leading to weakness (from staphylococcus aureus) *. In rare cases can be from parasite or medications * Primarily affects older adults (usually >50 years old) * Exact cause unknown, but genetic predisposition and environmental factors may contribute 2. Pathogenesis: * Inflammatory cells invade muscle tissue, leading to chronic muscle degeneration * Characterized by both inflammatory (T-cell-mediated) and degenerative changes (vacuoles, protein deposits in muscle fibers) * Gradual muscle atrophy and weakness, especially in distal muscles (e.g., wrists, fingers) and quadriceps 3. Clinical Presentation (Signs & Symptoms): * Often misdiagnosed *. Extreme cases: rhabdomyolysis *. Slow, progressive muscle (months to years) * can be an early sign of malignancy * Weakness in the forearm and finger flexors, affecting grip and fine motor tasks * Dysphagia (difficulty swallowing) in some patients * Muscle atrophy and reduced reflexes in affected areas 4. Diagnostics: * Elevated inflammatory marker creatine kinase (CK) levels, though usually only mildly elevated * Muscle biopsy showing characteristic inflammatory infiltrates, rimmed vacuoles, and protein inclusions * Electromyography (EMG) to detect abnormalities in muscle electrical activity * MRI to visualize muscle inflammation and atrophy * Genetic testing to rule out other muscular dystrophies if suspected

Question 75

List the medical/surgical management, precautions/red flags, and PT management of the Infectious (Inflammatory) Muscle Disease-Myositis: Inclusion Body Myositis (IBM)

Answer 75

1. Medical/Surgical Management and Medication: * No definitive cure or highly effective treatment * Corticosteroids, immunosuppressants, or intravenous immunoglobulin (IVIG) may be tried but often have limited effectiveness in IBM * Focus on managing symptoms and slowing progression * Physical therapy to maintain mobility and strength * Supportive care for dysphagia (e.g., swallowing therapy, dietary modifications) 2. Precautions/Red Flags: * Pulse pain + station = red flag *. Progressive loss of function, especially in the legs and hands * Increased risk of falls due to quadriceps weakness * Monitor for swallowing difficulties and aspiration risk * Limited response to immunosuppressive therapies compared to other types of myositis 3. Physical Therapy Management: * Gentle, sub max exercises to maintain muscle function without overexertion * AVOID ECCENTRIC EXERCISE * Balance and gait training to reduce fall risk * Adaptive equipment (e.g., canes, walkers, hand grips) to assist with daily activities and improve independence * Education on energy conservation and activity pacing to manage fatigue and prevent overexertion

Question 76

List the etiology, pathogenesis, clinical presentation, and diagnostics of the Infection of Bursae and Tendons, Bursitis

Answer 76

1. Etiology: * Inflammation of the bursa (fluid-filled sac that reduces friction between tissues) * Causes include repetitive motions, prolonged pressure on joints, injury/trauma, or underlying conditions like gout or rheumatoid arthritis (NOT ALWAYS INFECTIOUS) * Can also result from infection (septic bursitis) 2. Pathogenesis: * Inflammation causes the bursa to swell, leading to pain and limited movement * Chronic irritation can result in thickening of the bursa walls and ongoing inflammation * If untreated, can lead to long-term pain and reduced joint mobility 3. Clinical Presentation (Signs & Symptoms): * Localized pain and tenderness over the affected joint (commonly shoulder, elbow, hip, knee, or heel) * Cardinal signs of inflammation * Pain with movement or pressure over the affected area * Limited range of motion in the affected joint 4. Diagnostics: * Clinical examination based on history and localized pain/tenderness * Imaging (ultrasound or MRI) to confirm bursal inflammation or fluid accumulation * Aspiration of bursal fluid for analysis in cases of suspected infection (septic bursitis) or crystal-induced bursitis (e.g., gout)

Question 77

List the medical/surgical management, precautions/red flags, and PT management of the Infection of Bursae and Tendons, Bursitis

Answer 77

1. Medical/Surgical Management and Medication: * Rest, ice, and NSAIDs (e.g., ibuprofen, naproxen) for pain and inflammation * Corticosteroid injections into the bursa to reduce inflammation in severe or persistent cases * Antibiotics (Florquinolone): but they can damage soft tissue like tendons * Aspiration or surgical drainage in cases of infection or chronic bursal swelling * Surgery in rare cases for chronic, non-responsive bursitis 2. Precautions/Red Flags: * Monitor for signs of septic bursitis (fever, redness, and severe pain) * Avoid repetitive movements or activities that exacerbate symptoms * Ensure proper technique or posture during activities to prevent recurrence 3. Physical Therapy Management: * Gentle range of motion (ROM) exercises to maintain or restore joint mobility * Strengthening exercises to support muscles around the affected joint and reduce stress on the bursa * Education on activity modification and ergonomic adjustments to prevent flare-ups * Soft tissue mobilization and stretching exercises to relieve tension around the affected area * Gradual return to activity with a focus on proper body mechanics

Question 78

List the etiology, pathogenesis, clinical presentation, and diagnostics of skeletal tuberculosis

Answer 78

1. Etiology: (it is 15% of extra pulmonary TB) * Caused by Mycobacterium tuberculosis infection, typically spreading from pulmonary TB * Hematogenous spread * Risk factors include immunosuppression, malnutrition, and living in areas with high TB prevalence 2. Pathogenesis: * Infection leads to granulomatous inflammation in bones and joints * Progressive destruction of bone and cartilage, with caseous necrosis * can go in spine and cause injury 3. Clinical Presentation (Signs & Symptoms): * pain stiffness and joint effusion * Lower thoracic and lumbar spine most common, can escalate to "Pott" paraplegia * begins in cancellous bone but spreads 4. Diagnostics: * Biopsy, aspiration and culture to identify Mycobacterium tuberculosis * Elevated inflammatory markers (ESR, CRP)

Question 79

List the medical/surgical management, precautions/red flags, and PT management of skeletal tuberculosis

Answer 79

1. Medical/Surgical Management and Medication: * Rifampicin (prolonged treatment) * Some cases require Surgical intervention 2. Precautions/Red Flags: * Monitor for signs of spinal cord compression (e.g., paralysis, bowel/bladder dysfunction) in spinal TB * Risk of permanent joint deformity or disability if untreated * Drug resistance if anti-tubercular therapy is not completed or improperly followed 3. Physical Therapy Management: * Gentle range of motion (ROM) exercises to maintain joint mobility and prevent stiffness * Gradual strengthening exercises to restore muscle function after infection is controlled * Postural correction and spinal stabilization exercises for spinal TB patients, especially after surgery * Gait training and functional mobility exercises for patients with joint TB * Education on activity modification and joint protection to prevent further damage during recovery

Question 80

What are some Special Implications for the Therapist for MSK infections

Answer 80

1) Rest and protection of healing tissues 2) Weight bearing considerations-proper methods of moving, transferring, and positioning themselves 3) AROM once resolving (AROM can increase compressive forces as if weightbearing)

Question 81

List Developmental and Genetic MSK Disorders:

Answer 81

Down's Syndrome Scoliosis Spina bifida Developmental dysplasia of the hip Muscular dystrophy Spinal muscular atrophy Torticollis Brachial plexus palsy Osteogenesis imperfecta Arthrogryposis multiplex congenita Marfan Syndrome

Question 82

List Metabolic MSK Disorders:

Answer 82

Osteoporosis Osteomalacia/Rickets Paget Disease

Question 83

List MSK Infections:

Answer 83

Osteomyelitis Infections involving prostheses Infectious arthritis Myositis Skeletal tuberculosis

Question 84

List the etiology, pathogenesis, clinical presentation, and diagnostics of Paget’s disease

Answer 84

1. Etiology: * Unknown exact cause, but likely related to genetic factors and possible environmental triggers (e.g., viral infections) * More common in older adults, especially men 2. Pathogenesis: * Abnormal bone remodeling due to increased osteoclastic activity followed by disorganized osteoblastic activity * Leads to excessive bone resorption and formation, resulting in structurally weak and enlarged bones * Affects certain bones more frequently (e.g., pelvis, spine, skull, femur, tibia) 3. Clinical Presentation (Signs & Symptoms): * Often asymptomatic in early stages * Bone pain and joint stiffness (most common symptoms) * Bone deformities (e.g., bowed legs, enlarged skull) * Increased risk of fractures due to weakened bone structure * Nerve compression symptoms (e.g., hearing loss if the skull is affected, due to cranial nerve compression) 4. Diagnostics: * Elevated serum alkaline phosphatase (ALP) levels, indicative of increased bone turnover * X-rays showing characteristic bone changes (thickened bone, deformities) * Bone scans to identify areas of active bone remodeling * MRI or CT may be used to assess complications like nerve compression

Question 85

List the medical/surgical management, precautions/red flags, and PT management of Paget’s disease

Answer 85

1. Medical/Surgical Management and Medication: * Bisphosphonates (e.g., alendronate, risedronate) to inhibit bone resorption * Calcitonin as an alternative treatment if bisphosphonates are not tolerated * Pain management with NSAIDs or analgesics * Surgery for severe deformities, fractures, or nerve compression (e.g., joint replacement or osteotomy) 2. Precautions/Red Flags: * Monitor for increased risk of fractures in affected bones * Neurological complications due to nerve compression (e.g., hearing loss, vision changes) * Rare risk of osteosarcoma (malignant bone tumor) in longstanding disease * Cardiovascular complications from increased blood flow to affected bones 3. Physical Therapy Management: * Strengthening exercises to support muscles around affected bones and reduce load on joints * Low-impact activities (e.g., swimming, walking) to maintain mobility without overstressing bones * Balance training to reduce fall risk, especially with lower limb deformities * Postural correction and stretching exercises to manage musculoskeletal pain and stiffness * Education on safe movement and body mechanics to prevent fractures or injury