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Medical Conditions 1 > Soft Tissue, Joint, and Bone disorders > Flashcards

Soft Tissue, Joint, and Bone disorders Flashcards

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1
Q

Marfan syndrome: pathogenesis

A
  • causes fragility of stretching tissues such as aorta
  • genetic defect on proteins associated with elasin (important for maintaining extensibility)
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2
Q

Marfan syndrome: clinical presentation

A
  • lanky person (long fingers, limbs etc)
  • silent killer effects blood vessels and aorta
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3
Q

Marfan syndrome: risk factors

A

risk is with parent

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4
Q

Ehlers Danlos Syndrome: pathogenesis

A
  • genetic
  • variants in specific genes that provide instructions for making collagen and related proteins
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5
Q

Ehlers Danlos Syndrome: risk factors

A
  • parents have it
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6
Q

Ehlers Danlos Syndrome: clincal presenation

A
  • joint laxity of capsule and other tissues
  • joint pain, hypermobility, subluxations
  • uterine and skin over stretchable,
  • can attack vessels
  • disabling musculoskeletal pain and scoliosis
  • joint instability
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7
Q

Hypertropic ossification: general/myositis ossifcans, and neurogenic HO

A
  • bone growth in nonosseous tissue or soft tissue
  • myositis ossifcans: specific to muscle
  • neurogenic HO: nervous tissue impairments
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8
Q

Hypertropic ossification risk factors

A
  • traumatic injury
  • previous h/o
  • hypertrophic osteoarthritis
  • ankylosing spondylitis
  • diffuse idiopathic skeletal hyperostosis
  • surgery
  • burns
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9
Q

Hypertropic ossification pathogenesis

A
  • pluripotent mesenchymal cells
  • mechanical stress
  • systemic factors
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10
Q

Hypertropic ossification clincal manifestation

A
  • progressive unexpected loss of ROM
  • often within 2 weeks of injury
  • inflammation
  • over 3-5 months there is a hard end feel
  • pain
  • causing to stop moving
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11
Q

Hypertropic ossification management

A
  • prevention (radiation, NSAIDs, diphophonates)
  • controlling hemoatoma, RICE
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12
Q

Rhabdomylosis overview

A
  • breakdown of skeletal muscle
  • release of creatine phosphokinase enzymes
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13
Q

Rhabdomylosis risk factors

A
  • strenuous activity
  • side effects from statins
  • linked to some herbal supplements
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14
Q

Rhabdomylosis pathogenesis

A
  • skeletal muscle breaks down
  • acute renal failure
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15
Q

Rhabdomylosis clincal manifestations

A
  • fatigue
  • myalgia
  • myoglobinuria (cola colored urine)
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16
Q

Rhabdomylosis management

A
  • lab results: abnormal renal fct and elevated creatine phosphokinase
  • re-hydration, dialysis
  • usually reversible
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17
Q

Myofascial Pain syndrome and Trigger points: risk factors

A
  • stress, injruy
  • overuse/overload
  • viseral pain and dysfunction
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18
Q

Myofascial Pain syndrome and Trigger points: pathogenesis

A
  • excessive ACh
  • inhibition of AChE
  • integrated TrP hypothesis
  • decreased pH
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19
Q

Myofascial Pain syndrome and Trigger points clincial manifestations

A
  • taut band in affected muscle
  • trigger points in muscle
  • referred pain
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20
Q

Myofascial Pain syndrome and Trigger points: management

A
  • good history and evaluation
  • look for structural or mechanical factors
  • metabolic and hormonal mgt
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21
Q

Myopathy hereditary causes

A
  • muscular dystrophy
  • congenital myopathy
  • myotonia
  • metabolic myopathy
  • mitochondrial myopathy
  • neurologic
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22
Q

acquired myopathy

A
  • inflammatory myopathy
  • endocrine myopathy
  • systemic illness myopathy
  • drug induced (stain)
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23
Q

Joint Disorders

A
  • Osteoarthritis
  • ## Degenerative Inter vertebral Disk Disease
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24
Q

Osteoarthritis overview

A
  • early joint space widening
  • subchondral bone sclerosis
  • subchondral bone cysts
  • osteophytes (out growths of bone)
  • Joint Space narrowing (once inflammation goes away)
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25
Q

Pathogenesis of osteoarthritis

A
  • synovial inflammation
  • loss of hyaline cartilage
  • hypertrophic changes in bone and joint capsule
  • focal calcifications of the cartilage
  • joint space narrows
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26
Q

Risk factors of osteoarthritis

A
  • genetic association influenced by environmental/nutrition
  • Participation in particular sports of occupations
  • joint laxity
  • connective tissue damage or disorder
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27
Q

osteoarthritis: radio graphic Findings (clinical Manifestations)

A
  • Joint space widening
  • subchondral bone sclerosis
  • subchondral bone cysts
  • osteophytes
  • joint space narrowing
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28
Q

American College of Rheumatology: osteoarthritis

A

knee pain with 3 of the following
1. older than 50
2. morning stiffness less than 30 minutes or crepitus with motion
3. bony tenderness
4. bony enlargement
5. no palpable warmth over knee

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29
Q

Clinical manifestations: osteoarthritis

A
  • bony enlargement
  • limited ROM
  • crepitus on motion
  • tenderness on pressure
  • joint effusion
  • malalignment
  • joint deformity
  • weight bearing joints usually
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30
Q

OA in IP joints of the fingers

A
  • Bouchards Nodes = PIP
  • Herberdens Nodes = DIP joints
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31
Q

OA: PT implications

A
  • symptoms may not equate with radiographic findings
  • POC based on clinical exam
  • side effect of OA meds: NSAIDs, corticosteriods
  • Joint protection
  • interventions: less WB
32
Q

Degenerative Disk Disease (DDD): Overview

A
  • degeneration at intervertebral disk articulations
  • no consensus on definition
  • begins early in life visble by age 30
  • > 1/2 of all Americans > 40 yrs have some type of DDD
33
Q

DDD risk factors

A
  • familial aggregation (some genes are identified)
  • excessive forces
  • potential risk factors: Psychosocial, smoking, height, atherosclerosis
34
Q

Pathogenesis: DDD

A
  • impaired cellular nutrition (compressive forces can cause this and loss of fluid)
  • reduced cellular viability
  • cellular senescence: cells/fibroblasts die
  • accumulation of degraded matrix macromolecules (scar tissue)
  • fatigue failure of the matrix
  • there are 3 stages
35
Q

DDD implications for PT

A
  • spinal stenosis often occurs with DDD (they will want to avoid extension)
  • exercise: careful assessment, abdominal strengthening, postural training, increased flexibility, aerobic conditioning
36
Q

Bone disorders:

A
  • Fracture
37
Q

4 categories of fractures?

A
  • sudden impact
  • stress or fatigue
  • insufficiency fracture (pathological in bones such as osteopenia, osteoporosis, Ca metabolism disorders)
  • Pathological fracture
38
Q

Fracture orientation types (describe + look at picture)

A
  1. transverse:
  2. oblique
  3. spiral
  4. comminuted
  5. Segmental
  6. Butterfly
39
Q

Patellar Fx

A
  • undisplaced
  • transverse
  • lower or upper pole
  • multifragmented (displaced vs non displaced)
  • Vertical
  • osteochondral
40
Q

FX: healing process

A
  1. hematoma formation: 48-72 hours after fx, clotting factors are initiated
  2. Cellular proliferation: osteogenic cells proliferate forming a fibrocartilage collar
  3. callous formation: collars unite and osteoblasts move to site
  4. ossification: bone replaces cartilage
  5. consolidation: excess bone is reabsorbed and remodelled based on mechanical stress
41
Q

Chondrolysis: overview

A
  • progressive cartilage degeneration
  • most often result of slipped capital femoral epiphysis (femoral head growth plate slips from the rest of the bone)
  • can result from infection, trauma, prolonged immobilization
42
Q

Chondrolysis: etiology-unkwown

A
  • theories suggest nutrition, mechanical, ischemia, abnormal chondrocyte metabolism, abnormal intracapsular pressure
43
Q

Clincal manifestations: Chondrolysis

A
  • progressive joint stiffness with loss of motion and pain
44
Q

medical management: Chondrolysis

A
  • imaging
  • NSAIDs, protective wt bearing, surgery
45
Q

Osteochondroses: overview

A
  • disorders of the epiphyses of growing children
  • common thread = avascular necrosis (no blood supply to the bone/cartilage) causing cell death
  • AKA epiphysitis, osteochondritis, aaseptic necrosis, ischemic, epiphyseal necrosis
46
Q

Examples of Osteochondroses

A
  1. kohler disease: fracture of navicular bone will normally affect growth plate and cut off blood supply
  2. Osgood-Schlatter Disease: bones grow and muscle don’t stretch
  3. Legg-Calve-Perthes Disease
47
Q

Osteochondritis Dissecans

A
  • localized subchondral necrosis followed by recalcification
  • a piece of articular cartilage and a fragment of bone separate and pull away from the bone
  • can end up with loose bodies in the joint causing stiffness/locking
  • most common at concave surfaces of synovial joints (medial femoral head, talar head, capitulum of humerus)
  • repetitive microtrauma causes ischemia and disrupts subchondral growth
  • Wilson sign: pain with knee extension and tibial IR and relieved with Tibia ER
48
Q

Osteonecrosis

A
  • AKA avascular necrosis and aseptic necrosis
  • death of bone and bone marrow due to loss of blood supply in absence of infection
  • ## femoral head most common sit: chandler disease
49
Q

Legg-Calve-Perthes disease

A
  • affects femur
  • blood spully to the femoral head is disrupted
  • causes a flattened head
  • femur does not sit correctly
  • pain stiffness, loss of ROM
50
Q

Pathophysiology of Legg-Calve-Perthes disease: stages of recovery

A
  • Avascular stage 1-2 weeks
  • revascularization/fragmentation stage 6-12 months
  • reparative stage 2-3 years
  • regenerative stage: final months
51
Q

Osgood-Schlatter Disease: Pathophysiolgy

A
  • Fibers of patellar tendon pull small pieces of immature bone from tibial tuberosity
  • tendonitis/tendonsis of patellar ligament
52
Q

Osgood-Schlatter Disease: risk factors

A
  • abnormal alignment
  • repetitive stress
  • indirect trauma
  • active adolescent (more common in boys 8-15 yrs; girls 8-13)
53
Q

Osgood-Schlatter Disease: clinical manifestations

A
  • aching pain at tibial tuberosity
  • aggravated by active knee extension or resisted knee flexion
  • often tight hamstrings, IT band, Triceps surae, quadriceps
  • can use a strap to compress and keep tendon in place
54
Q

Osgood-Schlatter Disease: PT implications

A
  • immobilization is not recommended
  • rest modification
  • time allowed for revascularization, healing, ossification
  • exercises to improve mechanical inefficiencies (stretching/strengthen)
  • Balance/coordination
  • knee sleeve, brace, or strap over tibial tuberosity
  • 90% respond well to conservative treatment
  • chronic, unresolved may need surgery
  • usually outgrow it
55
Q

Gout: overview

A
  • group of metabolic disorder
  • elevated serum uric acid, urate crystals in joints soft tissue and kidneys
56
Q

Gout risk factors

A
  • family history
  • age & increasing serum urate concentration
  • heavy alcohol consumption, obesity, HTN
  • hyperthriodism, renal insufficiency, Chemo pts
57
Q

pathogenesis: Gout

A
  1. Primary hyperuricemia: inherited disorder of uric acid metabolism
  2. Secondary Hyperuricemia: caused from other metabolic disorders, decreased renal fuction, neoplasm
  3. idopathic hyperuricemia
58
Q

clinical manifestations: gout

A
  • Asymptomatic hyperuricemia
  • acute gouty arthritis (most common, increase pain in 1 joint) redness, swelling, warmth
  • intercritical gout: next phase- asymptomatic but still hyperuricemia (months/yrs)
  • Chronic Tophaceous gout: return of symptoms, deposits of crystals in soft tissues
59
Q

gout management

A
  • great imitator: imitates other things
  • DD: septic arthritis, RA, neoplasm, triad of acute arthritis, hyperuricemia, response to meds allopurinol
  • presence of monosodium urate crystals in synovial fluid, CT, or other articular cartilage
60
Q
  1. osteomalacia
  2. osteopenia
  3. osteopetrosis
  4. osteoporosis
A
  1. softening of bone
  2. low bone mass
  3. increased bone density
  4. decreased bone density
61
Q

Osteoporosis: overview

A
  • most commone metabolic bone disorder
  • low bone mass/impaired bone quality
  • increased risk of skeletal deformity
  • increased of fracture
  • primary vs secondary
  • typically affects vertebral bodies
62
Q

Osteoporosis: diagnosis

A
  • history
  • medical imaging
  • bone mineral density testing
  • dual x-ray absorptiometry assessment DXA
  • radiographs or CT if suspected fracture
  • lab tests
63
Q

Osteoporosis: clinical manifestations

A
  • Posture: thoracic kyphosis, forward head, protuberant abdomen, posterior pelvic tilt, IR of shoulders, scapular protrusion, knee hyperextension
  • loss of height
  • change in facial appearance
  • muscle imbalance, muscle pain, and trigger points
64
Q

Osteoporosis: pathogenesis

A
  • strength depends on density and quality
  • BMD is measure of mass or minerals/volume of bone
  • quality depends on cells, matrix and minerals
65
Q

Osteoporosis: Risk factors

A
  • Nonmodifiable: age, ethnicity, family history, lactose intolerance
  • modifiable: exercise, tobacoo, caffeine, low body weight, diet, depression
66
Q

Commone meds associated with Osteoporosis:

A
  • corticosteriods
  • methotrexate
  • heparin/coumadin (blood thinners)
  • lasix (diuretic)
  • Depo-Provera
67
Q

Commone fracture sites with Osteoporosis:

A
  • vertebral compression fractures
  • hips
  • ribs
  • radius (fall)
  • femur
68
Q

treatment and prevention of Osteoporosis:
- diet

A
  • calcium/vitamin D
  • Eat more plants
69
Q

treatment and prevention of Osteoporosis:
- exercise

A
  • weightbearing
  • resistance
  • balance
  • whole body vibration
70
Q

treatment and prevention of Osteoporosis:
education

A
  • fall risk
71
Q

treatment and prevention of Osteoporosis: corrective surgery

A
  • kyphoplasty
  • vertebroplasty
72
Q

treatment and prevention of Osteoporosis:
medications bisphophonates

A
  • IV Aredia, zoledronate
  • Oral: risedronate; ibandronate, etidronate, alendronate, tiludronate
  • oral/IV: clodronic acid
73
Q

treatment and prevention of Osteoporosis:
medications other

A
  • hormonal therapy (ERT/HRT for women, testosterone for men)
  • estrogen agonist/antagonist: raloxifene/evista
  • calcitonin: nasal or injected
  • Parathryoid hormone
  • osteoprotegerin: decoy TNF receptor that prevents the enzymes that stimulate oasteoclast activity
74
Q

Pagets: overview

A
  • tends to occur in adults over 50
  • 2nd most common metabolic bone disease
  • bones will bow out and soft will be distorted
75
Q

Pagets: pathogenesis

A
  • increased osteoclast activity
  • osteoblasts cannot keep up
  • results: fibrotic bon, bone changes shape
76
Q

Pagets: clinical manifestations

A
  • insidious and slow progression
  • pain, skeletal, neurological, muscular, cardovascular
  • fatigue
  • tinnitus: ringing - bones in ear are affected
  • lightheaded, dizzy

Medical Conditions 1 (16 decks)

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