Soft Tissue, Joint, and Bone disorders Flashcards
(76 cards)
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)
2
Q
Marfan syndrome: clinical presentation
A
- lanky person (long fingers, limbs etc)
- silent killer effects blood vessels and aorta
3
Q
Marfan syndrome: risk factors
A
risk is with parent
4
Q
Ehlers Danlos Syndrome: pathogenesis
A
- genetic
- variants in specific genes that provide instructions for making collagen and related proteins
5
Q
Ehlers Danlos Syndrome: risk factors
A
- parents have it
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
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
8
Q
Hypertropic ossification risk factors
A
- traumatic injury
- previous h/o
- hypertrophic osteoarthritis
- ankylosing spondylitis
- diffuse idiopathic skeletal hyperostosis
- surgery
- burns
9
Q
Hypertropic ossification pathogenesis
A
- pluripotent mesenchymal cells
- mechanical stress
- systemic factors
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
11
Q
Hypertropic ossification management
A
- prevention (radiation, NSAIDs, diphophonates)
- controlling hemoatoma, RICE
12
Q
Rhabdomylosis overview
A
- breakdown of skeletal muscle
- release of creatine phosphokinase enzymes
13
Q
Rhabdomylosis risk factors
A
- strenuous activity
- side effects from statins
- linked to some herbal supplements
14
Q
Rhabdomylosis pathogenesis
A
- skeletal muscle breaks down
- acute renal failure
15
Q
Rhabdomylosis clincal manifestations
A
- fatigue
- myalgia
- myoglobinuria (cola colored urine)
16
Q
Rhabdomylosis management
A
- lab results: abnormal renal fct and elevated creatine phosphokinase
- re-hydration, dialysis
- usually reversible
17
Q
Myofascial Pain syndrome and Trigger points: risk factors
A
- stress, injruy
- overuse/overload
- viseral pain and dysfunction
18
Q
Myofascial Pain syndrome and Trigger points: pathogenesis
A
- excessive ACh
- inhibition of AChE
- integrated TrP hypothesis
- decreased pH
19
Q
Myofascial Pain syndrome and Trigger points clincial manifestations
A
- taut band in affected muscle
- trigger points in muscle
- referred pain
20
Q
Myofascial Pain syndrome and Trigger points: management
A
- good history and evaluation
- look for structural or mechanical factors
- metabolic and hormonal mgt
21
Q
Myopathy hereditary causes
A
- muscular dystrophy
- congenital myopathy
- myotonia
- metabolic myopathy
- mitochondrial myopathy
- neurologic
22
Q
acquired myopathy
A
- inflammatory myopathy
- endocrine myopathy
- systemic illness myopathy
- drug induced (stain)
23
Q
Joint Disorders
A
- Osteoarthritis
- ## Degenerative Inter vertebral Disk Disease
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)
25
Pathogenesis of osteoarthritis
- synovial inflammation
- loss of hyaline cartilage
- hypertrophic changes in bone and joint capsule
- focal calcifications of the cartilage
- joint space narrows
26
Risk factors of osteoarthritis
- genetic association influenced by environmental/nutrition
- Participation in particular sports of occupations
- joint laxity
- connective tissue damage or disorder
27
osteoarthritis: radio graphic Findings (clinical Manifestations)
- Joint space widening
- subchondral bone sclerosis
- subchondral bone cysts
- osteophytes
- joint space narrowing
28
American College of Rheumatology: osteoarthritis
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
29
Clinical manifestations: osteoarthritis
- bony enlargement
- limited ROM
- crepitus on motion
- tenderness on pressure
- joint effusion
- malalignment
- joint deformity
- weight bearing joints usually
30
OA in IP joints of the fingers
- Bouchards Nodes = PIP
- Herberdens Nodes = DIP joints
31
OA: PT implications
- 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
Degenerative Disk Disease (DDD): Overview
- 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
DDD risk factors
- familial aggregation (some genes are identified)
- excessive forces
- potential risk factors: Psychosocial, smoking, height, atherosclerosis
34
Pathogenesis: DDD
- 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
DDD implications for PT
- spinal stenosis often occurs with DDD (they will want to avoid extension)
- exercise: careful assessment, abdominal strengthening, postural training, increased flexibility, aerobic conditioning
36
Bone disorders:
- Fracture
37
4 categories of fractures?
- sudden impact
- stress or fatigue
- insufficiency fracture (pathological in bones such as osteopenia, osteoporosis, Ca metabolism disorders)
- Pathological fracture
38
Fracture orientation types (describe + look at picture)
1. transverse:
2. oblique
3. spiral
4. comminuted
5. Segmental
6. Butterfly
39
Patellar Fx
- undisplaced
- transverse
- lower or upper pole
- multifragmented (displaced vs non displaced)
- Vertical
- osteochondral
40
FX: healing process
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
Chondrolysis: overview
- 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
Chondrolysis: etiology-unkwown
- theories suggest nutrition, mechanical, ischemia, abnormal chondrocyte metabolism, abnormal intracapsular pressure
43
Clincal manifestations: Chondrolysis
- progressive joint stiffness with loss of motion and pain
44
medical management: Chondrolysis
- imaging
- NSAIDs, protective wt bearing, surgery
45
Osteochondroses: overview
- 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
Examples of Osteochondroses
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
Osteochondritis Dissecans
- 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
Osteonecrosis
- 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
Legg-Calve-Perthes disease
- 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
Pathophysiology of Legg-Calve-Perthes disease: stages of recovery
- Avascular stage 1-2 weeks
- revascularization/fragmentation stage 6-12 months
- reparative stage 2-3 years
- regenerative stage: final months
51
Osgood-Schlatter Disease: Pathophysiolgy
- Fibers of patellar tendon pull small pieces of immature bone from tibial tuberosity
- tendonitis/tendonsis of patellar ligament
52
Osgood-Schlatter Disease: risk factors
- abnormal alignment
- repetitive stress
- indirect trauma
- active adolescent (more common in boys 8-15 yrs; girls 8-13)
53
Osgood-Schlatter Disease: clinical manifestations
- 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
Osgood-Schlatter Disease: PT implications
- 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
Gout: overview
- group of metabolic disorder
- elevated serum uric acid, urate crystals in joints soft tissue and kidneys
56
Gout risk factors
- family history
- age & increasing serum urate concentration
- heavy alcohol consumption, obesity, HTN
- hyperthriodism, renal insufficiency, Chemo pts
57
pathogenesis: Gout
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
clinical manifestations: gout
- 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
gout management
- 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
1. osteomalacia
2. osteopenia
3. osteopetrosis
4. osteoporosis
1. softening of bone
2. low bone mass
3. increased bone density
4. decreased bone density
61
Osteoporosis: overview
- 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
Osteoporosis: diagnosis
- history
- medical imaging
- bone mineral density testing
- dual x-ray absorptiometry assessment DXA
- radiographs or CT if suspected fracture
- lab tests
63
Osteoporosis: clinical manifestations
- 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
Osteoporosis: pathogenesis
- strength depends on density and quality
- BMD is measure of mass or minerals/volume of bone
- quality depends on cells, matrix and minerals
65
Osteoporosis: Risk factors
- Nonmodifiable: age, ethnicity, family history, lactose intolerance
- modifiable: exercise, tobacoo, caffeine, low body weight, diet, depression
66
Commone meds associated with Osteoporosis:
- corticosteriods
- methotrexate
- heparin/coumadin (blood thinners)
- lasix (diuretic)
- Depo-Provera
67
Commone fracture sites with Osteoporosis:
- vertebral compression fractures
- hips
- ribs
- radius (fall)
- femur
68
treatment and prevention of Osteoporosis:
- diet
- calcium/vitamin D
- Eat more plants
69
treatment and prevention of Osteoporosis:
- exercise
- weightbearing
- resistance
- balance
- whole body vibration
70
treatment and prevention of Osteoporosis:
education
- fall risk
71
treatment and prevention of Osteoporosis: corrective surgery
- kyphoplasty
- vertebroplasty
72
treatment and prevention of Osteoporosis:
medications bisphophonates
- IV Aredia, zoledronate
- Oral: risedronate; ibandronate, etidronate, alendronate, tiludronate
- oral/IV: clodronic acid
73
treatment and prevention of Osteoporosis:
medications other
- 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
Pagets: overview
- tends to occur in adults over 50
- 2nd most common metabolic bone disease
- bones will bow out and soft will be distorted
75
Pagets: pathogenesis
- increased osteoclast activity
- osteoblasts cannot keep up
- results: fibrotic bon, bone changes shape
76
Pagets: clinical manifestations
- insidious and slow progression
- pain, skeletal, neurological, muscular, cardovascular
- fatigue
- tinnitus: ringing - bones in ear are affected
- lightheaded, dizzy
