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MSK 1 > Bone and cartilage tissues > Flashcards

Bone and cartilage tissues Flashcards

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1
Q

What are some characteristics of bone?

A
  • highly specialized connective tissue
  • highly vascular
  • can absorb impact
  • constant remodeling (Wolf’s Law)
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2
Q

What are some risk factors for fractures?

A
  • history of falling
  • advanced age
  • female
  • BMI <25
  • decreased bone mineral density
  • nutrition
  • neoplasm
  • low PA level
  • smoking
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3
Q

What are some diseases that can cause bone fractures?

A
  • osteoporosis
  • osteomalacia
  • rickets
  • osteogenesis imperfecta
  • paget disease
  • ehlers-danos syndrome
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4
Q

What are the phases of healing for bones?

A

1) Inflammatory (several days)
2) Reparative (3-16wks)
3) Remodeling (months to years)

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5
Q

What are the clinical presentations of a fractures bone?

A
  • pain/ pain w/ WBing and loading
  • deformity
  • deep, dull ache
  • edema/bruising
  • could have major loss of function
  • pain response w/ ultrasound and/or tuning fork
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6
Q

What are primary and secondary fracture management techniques?

A

Primary:
- ORIF
- closed reduction internal fixation
- traction for realignment (halo)
- bone lengthening procedures

Secondary:
- no intervention (activity restrictions, brace, crutch, boot, sling)
- closed reduction and casting

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7
Q

What does PT address w/ fractures?

A

Treat impairments and functional limitations associated with fracture
- impaired ADLs
- ROM
- weakness

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8
Q

How do PTs manage fractures?

A

Start with mobilization, stretching, joint mobs, and then strengthening with short lever arms first

When appropriate, performing WBing activities to increase bone density

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9
Q

What is the healing prognosis timeline for fractures?

A

Children: 4-6 wks
Adolescents: 6-8 wks
Adults: 10-18 wks

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10
Q

What are stress fractures?

A
  • creep in bone from repetitive loading over time (bone can’t repair itself fast enough)

most common in LE (tibia, 2nd met, femur neck, pars interarticularis)

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11
Q

What is the clinical presentation of a stress fracture?

A
  • insidious onset with microtrauma
  • pain: cortical-local, trabecular-diffuse
  • does not improve with activity
  • tenderness on palpation
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12
Q

What are some interventions for stress fractures?

A
  • rest/immobilization
  • correct muscle imbalances
  • graduated return to training
  • promote shock absorption
  • orthotics prn
  • train muscle endurance
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13
Q

What is osteoporosis?

A

chronic, progressive disease characterized by low bone mass and deterioration of bone tissue

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14
Q

What score is considered an osteoporosis score?

A

-2.5 SD or less from mean for age and sex

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15
Q

What part of bone has 75% resistance to compression fractures?

A

cortical bone

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16
Q

When do bone mass changes occur?

A
  • peaks by mid 30s
  • bone loss begins several years prior to menopause

genetic factors contribute to 80% of women’s risk of osteoporosis

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17
Q

What are some risk factors of osteoporosis?

A

Non-modifiable:
- >50 years old
- Caucasian/Asian
- menopausal
- family history
- depression
- lactose intolerance

Modifiable:
- inactivity
- alcohol abuse, tobacco use
- medications
- low BMI
- diet

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18
Q

What are some secondary causes of osteoporosis?

A
  • renal insufficiency
  • cushings
  • hyperthyroidism
  • type II diabetes
  • osteomalacia
  • pagets disease
  • SCI
  • stroke
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19
Q

What are some risk factors for osteoporotic falls?

A
  • BMI <21
  • corticosteroids
  • personal history of fractures
  • 1st degree relative with fragility fractures
  • smoking
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20
Q

What is the difference between osteomalacia, osteopenia, and osteoporosis?

A

Osteomalacia:
- softening of bones

Osteopenia:
- decreased bone mass

Osteoporosis:
- low bone strength/density

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21
Q

When should BMD testing occur and how often?

A

ALL women over 65 and men over 70
- should occur every 2 years
- sooner in those with risk factors

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22
Q

What is some general treatment and prevention dietary advice for those with osteoporosis?

A

Nutrition:
- calcium
- vitamin D
- reduce caffeine
- vitamin K
- reduce excessive intake of vitamin A
- magnesium
- reduce alcohol consumption

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23
Q

What are some common medications taken for osteoporosis?

A

Antiresorptives:
- estrogen/HRT (for prevention ONLY)
- selective-estrogen receptor modulators (SERMS) (prevention & treatment)
- calcitonin (treatment)
- bisphosphonates (treatment and most common)

Anabolic PTH: builds up bone mass (treatment w/ daily injections)

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24
Q

What are some non-pharmacological interventions for fractures/osteoporosis?

A

Exercise:
- strengthening muscles (back and legs)
- WBing exercises
- flexibility
- strengthening exercises
- posture and balance

Orthotics
Gait training
Pain management

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25
What is the major contraindication for exercise and osteoporosis?
spinal FLEXION exercises - leads to vertebral fractures
26
What are some educational points for osteoporosis?
- avoid bending forward - carry loads close to the body - sleep with back straight - safe home environment - never twist with a load
27
How are vertebral factures managed?
- oral pain management - PT - kyphoplasty & vertebroplasty
28
What is the tidemark of articular cartilage and what are the 2 main components of articular cartilage?
Tidemark: edge of calcified zone that is before the deep zone Extracellular matrix: has fibrous proteins and ground substance Cells: chondrocytes
29
What are some properties of articular cartilage?
- avascular & aneural - gains nutrients through synovial fluid - superficial cells lay more flat than deeper cells - absorbs compression - resists tensile load - mainly type II cartilage
30
What are the 4 zones of fibers in articular cartilage?
- superficial: increased concentrations of fibrils; lays parallel - middle: fibers disorganized - deep: perpendicular to better resist secondary tensile loads - calcified: same as deep
31
What is in ground substance?
Proteoglycan chains: - glycosaminoglycan chains that are attached to core proteins that are attached to hyaluronan - negatively charged hydrophilic molecules that repel each other and draw water in 60% water
32
What are some biomechanics of articular cartilage?
Biphasic material that includes: - solid phase: fatigue resistant & sustains high stress & strains of loading - fluid phase: compliant & diffuses load over increased surface areas Viscoelastic material: - creep - initial loading = fluid phase - moves to solid phase after about 2.5-6 hours EXTREMELY slick to help with movement of joints
33
How does articular cartilage get its nutrients?
- through passive diffusion in the synovial fluid and compression-induced convection - basically squeezing in/out nutrients w/ load
34
What do chondrocytes do?
Synthesize, repair, remodel the extracellular matrix Activity is regulated by: - chemical factors - mechanotransduction - electrical fields w/in cartilage
35
How does immobilization affect articular cartilage?
- greater degeneration with longer, rigid periods of immobilization - cartilage does not completely recover after longer periods of immobilization
36
What are some aging affects in articular cartilage?
- chondral cell proliferation ceases at skeletal maturity - rate of synthetic activity is decreased - total number of chondrocytes is reduced - progressive decrease in tensile properties
37
How do OA and articular cartilage degeneration relate to one another?
- with mechanical OA, there is a decrease in tensile stiffness and diminished compressive properties with articular cartilage
38
What is the degree of cartilage repair dependent upon?
- extent of damage - nature of activity following damage
39
What does a lack of repair of articular cartilage result from?
- lack of blood flow - lack of inflammatory process - lack of chondrocyte mobility - ineffective matrix formation across lesion
40
How good is the repair of articular cartilage?
NOT good as new - only temporary - fibrocartilage characteristics - leads to eventual breakdown
41
What is the medical treatment of articular cartilage injury?
- NSAIDs - corticosteroid injections - viscosupplementation - regenerative medicines - total joint replacement
42
What is the rehabilitation process of articular cartilage injury?
After prolonged immobilization: - there is greater risk of injury during early phase (2-4 wks) - graded joint loading program - motion is lotion (AROM/PROM, unloaded, cyclic)
43
What is OA in a nutshell?
- articular cartilage failure with secondary components of inflammation - most common arthritis type - knees, hips, and hands most common places - multifactorial: genetic, metabolic, biochemical, and biomechanical
44
What is the pathology and disease process of OA?
- chondrocytes fail to repair damaged articular cartilage which leads to an unstable matrix - decreased water content makes the matrix stiff and brittle
45
What are some macro changes of OA?
- progressive cartilage loss - subchondral bone reaction/remodeling - osteophyte formation - synovial inflammation
46
What are the two different types of osteoarthritis?
Primary: Idiopathic - localized or generalized forms - localized OA most commonly affects the hands/hips/spine/knees/feet - generalized OA is three or more sites Secondary: - post-traumatic - congenital or development disorders - calcium pyrophosphate dihydrate deposition disease (CPPD) - others (paget disease, RA, gouty arthritis)
47
What is the etiology of OA?
Multifactorial: - aging - obesity - joint injury (trauma or repetitive microtrauma) - chronic low-grade inflammation - heredity/genetics
48
What are some risk factors of OA?
- age (50+) - sex (male <45, female >45) - family history - occupation/hobbies - past injuries - obesity
49
What are some clinical signs of OA?
- crepitus - bony enlargement - decreased ROM - malalignment or deformity - TTP - mild, localized joint effusion - impaired muscle performance - Gelling (morning stiffness for 5-10 minutes) - stiff after still, improved with movement - locking or giving way
50
What are some clinical symptoms of RA vs OA?
RA: - systemic autoimmune - symmetrical - morning pain/stiffness >30 minutes - small joints of hand (MCPs and PIPs) - boutonniere, swan-neck, and ulnar drift OA: - local joint disease - unilateral/asymmetrical - morning stillness <30 minutes - hand joints (PIPs and DIPs, thumb CMC)
51
What are some self-efficacy and self-management techniques for OA?
- stress reduction and coping strategies - weight loss - joint protection and energy conservation - maintain ROM and strength - use stronger and larger muscles when possible
52
What is the best exercise for OA?
NO BEST EXERCISE - is what pt will adhere to - mobility: ROM and stretching - strengthening: avoid pain and w/in pt tolerance (low intensity more reps) - neuromuscular training - aerobic conditioning: aquatic exercise
53
What is RA in a nutshell?
- progressive, systemic, autoimmune inflammation - often aggressive, devastating consequences - unknown etiology (auto immune, infection, smoking)
54
What are some characteristics of RA?
- symmetric synovitis - joint erosions, cartilage and bone destruction - multisystem extra-articular manifestations - onset usually slow & insidious over months - aggressive management leads to good control
55
What is the main cause of RA as an autoimmune disease?
- imbalance b/w pro/anti-inflammatory mediators - leads to chronic inflammation
56
What are the mediators of joint destruction in RA?
- cytokines (TNF) - chemokines (IL-1, IL-6) - MMP (VEGF)
57
What is the natural course of RA?
- undifferentiated polyarthritis - early RA - Mild disease - severe RA w/ deformities *25% require surgical treatment*
58
What are the diagnosis criteria for RA?
Four or more of the following must be present: - morning stiffness > 1 hour - arthritis of >3 joint areas of the 28 possible joints - arthritis of hand joints (MCPs, PIPs, wrists) - symmetric swelling - serum rheumatoid factor (antibody to IgG) - rheumatoid nodules - radiographic changes *first 4 have to be present for 6 weeks or more*
59
What are some of the typical joints involved in RA?
- wrist and MCP joints - index/middle MCP joints - PIP, MCP, MTP - elbows, shoulders - knees, ankles, hips *lumbosacral NOT involved* - atlanto-axial joint (C1-2), subluxation
60
Why is the atlanto-axial joint involved or affected with RA?
*Only purely synovial joint in spine* - could lead to spinal cord involvements
61
What are some extra-articular systemic manifestations of RA?
- MSK wasting - tenosynovitis, bursitis - osteoporosis, Rh nodules - vasculitis - pericarditis, myocarditis
62
What are the main deformities involved with RA in the hands?
- Swan-neck: DIPs - Boutonniere - Ulnar drift
63
What are some predictors of a poor prognosis in those w/ RA?
- presence of >20 inflamed joints - radiographic evidence of bone erosion - Rh nodules - high titers of RA factor and anti CCP - higher class of functional disability - persistent inflammation - advanced age of onset *40-85% of RA pts unable to work in 8-10 years*
64
What are some complications of RA?
- carpal tunnel - Baker's cyst - systemic vasculitis - peripheral neuropathy - cardiac and pulmonary involvement - risk of lymphomas is 3x greater - risk of infection due to disease and treatment
65
What is the main pharmacological treatment of RA?
DMARDs: - inhibit autoimmune response underlying RA - inhibits production of cytokines and cellular activation *Main DMARD is Methotrexate (Rheumatrex)*
66
What do some of the newer DMARDs do?
- inhibit key inflammatory mediators (TNF-alpha) - relatively selective
67
What is the new treatment paradigm for RA?
Patient education -> PT -> OT -> Orthopedic surgery
68
What are the main goals of PT in those w/ RA?
- decrease pain, inflammation - maintain functional ability and increase QoL - control systemic involvement - slow progression of disease - protect articular structures
69
How does PT manage RA?
- weight management - education on joint protection/energy conservation - avoid deforming positions and prolonged static positions - assistive devices - superficial heat - aquatic therapy
70
How does PT differ with acute vs subacute/chronic exacerbations of RA?
Acute: - respect pain & fatigue - Grade I-II joint mobs - active ROM through available ROM *NO stretching* - joint protection & energy conservation - modify ADLs prn Subacute/Chronic: - joint protection/energy conservation - flexibility and strength w/in joint tolerance - low load resistive training - low impact aerobic activity to tolerance *Vigorous stretching or manipulations contraindicated*

MSK 1 (4 decks)

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