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MSK Unit 2 > MSK Week6 > Flashcards

MSK Week6 Flashcards

1
Q

Functions of bone

A
  • Support structures and provide shape to the body
  • Protect vital structures
  • Allow movement and anchors for muscle
  • Provide mineral storage
  • Contribute to blood cell formation in the red marrow
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2
Q

True or false: bone is highly specialized connective tissue, highly vascular, most rigid of the connective tissues

A

True

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3
Q

Risk factors for fracture

A
  • History of fall or trauma
  • Advanced age
  • Female
  • BMI <25
  • Decreased BMD
  • Nutrition (vitamin D, calcium, caffeine)
  • Hormonal factors
  • Neoplasm
  • Low physical activity level
  • Smoking
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4
Q

Phases of Repair for Bone

A
  • Inflammatory - several days (hematoma formation, angiogenesis; fibrous union)
  • Reparative - 3-16 weeks (cartilage formation w/ calcification, cartilage removal and bone formation)
  • Remodeling - months to years
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5
Q

Primary fracture management

A
  • ORIF
  • Closed reduction internal fixation
  • External fixator (complicated fx’s)
  • Traction for realignment (halo)
  • Bone lengthening procedures (ilizarov)
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6
Q

Secondary fracture management

A
  • No intervention: activity restriction, brace, crutch, boot, sling
  • Closed reduction and casting: less infection, wait & see
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7
Q

What do healing factors depend on?

A

The bone involved and type of fracture

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8
Q

General healing time frame - children, adolescents, adults

A

Children - 4 to 6 weeks
Adolescents - 6 to 8 weeks
Adults - 10 to 18 weeks

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9
Q

Negative predictors for normal healing

A
  • Smoking
  • Diabetes
  • Corticosteroids
  • EtOH
  • Renal and vascular insufficiency
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10
Q

Other complications to fracture prognosis

A
  • Poor stabilization
  • Damage to blood supply
  • Infection
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11
Q

What are stress fractures caused by?

A

Creep in the bone that results in cyclic or sustained loading 0 repetitive loading over time, which gradually exceeds the bones ability to repair itself

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12
Q

Gold standard diagnostic for stress fractures?

A

Bone scan

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13
Q

Where are stress fractures most common?

A

Lower extremities
- Tibia, 2nd met, femoral neck, interarticularis

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14
Q

Interventions for stress fractures

A
  • Rest/immobilization
  • Correct muscle imbalances
  • Graduated return to training
  • Promote shock absorption
  • Orthopedics prn
  • Train muscle endurance
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15
Q

What is osteoporosis?

A
  • A chronic, progressive disease characterized by low bone mass and microarchitechtural deterioration of bone tissue, leading to decreased bone strength, enhanced bone fragility and a consequent increase in fracture incidence
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16
Q

Primary osteoporosis

A
  • Most common
  • Occurs in both genders at all ages
  • More often in menopausal women
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17
Q

Secondary osteoporosis

A

More associated with conditions or medications

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18
Q

Bone strength

A

Related to bone mass and other factors
- Remodeling frequency (bone turnover)
- Bone size and area
- Bone micro architecture
- Degree of bone mineralization

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19
Q

How much resistance to compression fractures does cortical bone account for?

A

Up to 75%

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20
Q

Osteoporosis bone pathophysiology

A
  • Imbalance of bone resorption and remodeling
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21
Q

Non modifiable risk factors

A
  • > 50 y.o
  • Caucasian/Asian
  • Menopausal or post menopausal
  • Family history of osteoporosis
  • Lactose intolerance
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22
Q

Modifiable risk factors to osteoporosis

A
  • Inactivity, immobilization, sedentary lifestyle
  • Excessive EtOH, tobacco, caffeine
  • Medications (steroids, immunosuppressants, anticoagulants)
  • Low BMI, small body frame
  • Diet (deficiency of Ca, Mg, Vit D, Vit C)
  • Eating disorders
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23
Q

Osteomalacia

A
  • Softening of the bones
  • Disorder of mineralization of newly formed bone - weak and more prone to fracture, vitamin D deficient and low phosphate
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24
Q

Osteopenia

A
  • Low bone mass
  • Less bone loss than osteoporosis
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25
Q

Osteoporosis

A
  • Decreased bone density (strength)
  • Deterioration of bone tissue and decreased bone strength
  • Includes osteopenia
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26
Q

Major risk factors for osteoporotic falls

A
  • Body weight < 70kg or BMI <21
  • Corticosteroids
  • Personal history of fractures as adult
  • First-degree relative with fragility fracture
  • Current smoking
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27
Q

Minor risk factors for osteoporotic falls

A
  • Early menopause
  • Nutrition
  • Decreased activity
  • EtOH
  • Impaired vision
  • Dementia
  • Poor health
  • Recent falls
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28
Q

Pharmacological management of osteoporosis

A
  • Antiresorptives - estrogens/HRT, selective estrogen receptor modulators, calcitonin, biphosphates
  • Anabolic PTH
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29
Q

What do antiresorptives do?

A

Decrease amount of bone lost

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30
Q

What does anabolic PTH do?

A

Build up bone mass

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31
Q

Nutrition general treatment and prevention recommendations of osteoporosis

A
  • Calcium - decrease bone loss
  • Vitamin D - reduced risk of hip and non-vertebral fx
  • Calcium AND Vitamin D
  • Caffeine - may reduce calcium absorption
  • Vitamin K - may help with bone metabolism and reducing urinary calcium excretion
  • Vitamin A - high levels = increased risk of hip fx
  • Magnesium
  • ETOH - can suppress osteoblasts; mod intake = decreased risk of hip fx
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32
Q

Non-pharmacological interventions for osteoporosis

A
  • Rehabilitation
  • Avoiding substances
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33
Q

Rehabilitation interventions for osteoporosis

A
  • Exercise —> strengthen muscles: back and legs
  • Orthotics
  • Gait training
  • Pain management
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34
Q

What types of exercises can be done to help osteoporosis?

A
  • Weight bearing - walking.hopping, light jog; maintain BMD
  • Flexibility
  • Strength - weights, resistance bands, water resistance
  • Postural and balance
    ** Best is combo of all **
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35
Q

Patient education for osteoporosis

A
  • Body mechanics - help prevent falls and fxs
  • Make the home environment safe
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36
Q

Management of vertebral fractures

A
  • Conservative - oral pain management, PT
  • Surgical - kyphoplasty, vertebroplasty (inject cement to help restore vertebral body height; last resort)
37
Q

What is the tidemark line of articular cartilage?

A

Where articular cartilage affixes to the subchondral bone

38
Q

What are the two main components of articular cartilage?

A
  • Extracellular matrix
  • Cells (chondrocytes)
39
Q

What are chondrocytes responsible for?

A
  • Making all the extracellular matrix components
  • Produce matrix, maintain matrix surrounding it, break down any waste products within the matrix
40
Q

Qualities of articular cartilage

A
  • A few mm thick
  • No blood or nerve supply
  • No pericondrium
41
Q

How does articular cartilage get their nutrient supply and get rid of waste?

A

Through synovial fluid, which is facilitated by the loading and unloading of the tissue

42
Q

Qualities of deeper chondrocytes

A
  • Produce higher volumes of proteoglycans
  • Rate of turnover is slow
43
Q

What makes up the extracellular matrix?

A
  • Fibrous proteins
  • Ground substance
44
Q

Qualities of superficial chondrocytes

A

More elongated and will lay parallel to the surface

45
Q

What are the four zones of articular cartilage fibers?

A
  • Superficial/tangential zone
  • Middle/transitional zone
  • Deep zone
  • Calcified cartilage zone
46
Q

Superficial or tangential zone

A
  • Highest concentration of fibrils
  • Aligned parallel to the surface
47
Q

Middle or transitional zone

A

Fibers appear disorganized

48
Q

Deep zone

A

Fibers perpendicular to surface

49
Q

Calcified cartilage zone

A
  • Fibers perpendicular to the surface
  • Deeper zones better fiber orientation to resist secondary tensile loads
50
Q

Ground substance

A
  • Proteoglycan chains
  • Negatively charged hydrophilic molecules
  • Water
  • Highest concentration of PGs in middle zones
  • Fluid concentration lowest in deepest regions
51
Q

What does water do for cartilage?

A

Gives cartilage the ability to absorb compressive loads

52
Q

Proteoglycan chains

A
  • Glycosaminoglycan (GAG) chains
  • Core protein
  • Hyaluronan
53
Q

Negatively charged hydrophilic molecules

A
  • Repel each other
  • Draw water in (swelling pressure) - resisted by collagen fibril network
54
Q

Biphasic material

A
  • Solid phase
  • Fluid phase
55
Q

Solid phase

A

Fatigue resistant, sustains high stress and strains of loading

56
Q

Fluid phase

A
  • Compliant, able to diffuse load over increased surface area
  • Where the load is being accepted and being managed by the movement of fluid within the cartilage
57
Q

Viscoelastic material

A
  • Time-dependent behavior (creep)
  • Initial loading, fluid phase supports 90% of load (15 min)
  • Transfer to solid phase over 2.5-6 hours
  • Fluid flow reversed when load removed
58
Q

Combination of lubrication for articular cartilage

A
  • Fluid film between articulating surfaces
  • Boundary lubricant bound to/absorbed on articular surface
59
Q

Fluid film condition

A

In fast low load

60
Q

Boundary condition

A

In slow severe load

61
Q

Nutrition of articular cartilage

A
  • Avascular and alymphatic
  • Synovial fluid exchange
  • Passive diffusion
  • Compression - induced convection
  • Reciprocal loading essential for tissue health
62
Q

Compression-induced convection

A

Reciprocal loading and unloading is constantly squeezing fluid in and out, like a sponge

63
Q

Synovial fluid exchange

A
  • Nutritional products
  • Respiratory gasses
  • Systemic signaling molecules - hormones and inflammatory molecules
  • Waste products
64
Q

What is activity regulated by?

A
  • Chemical factors
  • Mechanotransduction
  • Electrical fields within cartilage
65
Q

Metabolism of articular cartilage

A
  • Chondrocytes are main source —> synthesize, repair, remodel extracellular matrix
  • PGs are broken down/synthesized at higher rate than collagen
66
Q

Skeletal maturity and aging

A
  • Chondral cell proliferation ceases
  • Rate of synthetic activity decreased
  • Total number of chondrocytes reduced
67
Q

Osteoarthritis

A
  • Collection of pathologies
  • Impacts articular cartilage, subchondral bone, joint capsule, synovial membrane, ligaments and periarticular muscles
68
Q

Mechanically - OA cartilage

A
  • Decreased tensile stiffness
  • Diminished compressive properties
69
Q

Early phase of OA

A

Increase synthesis/turn over of matrix to keep up with ongoing damage

70
Q

Advanced disease - OA

A
  • Altered distribution of cells, eventual cell die off
  • More of the load on solid phase —> more damage
  • Subchondral bone may become exposed as cartilage layer completely wears away
71
Q

Cartilage repair - Chondrocytes

A
  • They’re metabolically active
  • Maintaining matrix
  • Respond to changes in mechanical stimuli
  • Often not able to prevent cartilage matrix loss
72
Q

What does the degree of repair success of cartilage depend on?

A
  • Extent of damage
  • Nature of activity following damage
73
Q

What would cause lack of repair for cartilage?

A
  • Lack of blood flow
  • Lack of inflammatory process
  • Isolated from sources of stem cells
  • Lack of chondrocytes mobility
  • Ineffective matrix formation across lesion
74
Q

When is there a greater risk of injury for cartilage?

A
  • During early phase of healing (2 to 4 weeks)
75
Q

Treatment for OA

A
  • Medical (medications and such)
  • Rehabilitation
  • Surgical/procedural
76
Q

What happens after prolonged immobilization (about 6 weeks +) or known cartilage injury?

A
  • Mindful of degradation of connective tissue
  • Greater risk of injury during early phase
  • Graded joint loading program (acceleration loading can be damaging)
  • Motion is lotion —> A/Prom, unloaded, cyclic
77
Q

Post surgical/post procedural treatment for OA

A
  • Protocol driven
  • Surgical repairs typically have WB restriction period
  • Injections will have minimal restrictions
78
Q

What type of exercises give more shear forces?

A

Closed kinetic chain exercises

79
Q

Arthrocentesis

A

Flushing the joint with saline - bad long term outcomes

80
Q

Arthroscopy

A
  • Flush joint
  • Clear debris, loose bodies
  • Shave down raggedy cartilage - smooth things out
  • A clean up
81
Q

Arthrodesis

A

Fuse the joint - more common in small joints where total joint replacement can’t be done

82
Q

Clinical presentation of stress fractures

A
  • History —> insidious onset w/ microtrauma
  • Pain —> Cortical-local; trabecular - diffuse
  • Does not improve w/ activity
  • Tenderness on palpation
  • (+) hop or percussion test
  • (+) tuning fork
83
Q

PT interventions for fractures - immobilization phase

A
  • Transfer training
  • ADL’s
  • Gait
  • Per MD order
84
Q

PT interventions for fractures - If ORIF

A
  • Watch for screws, wires, refracture and infection
85
Q

What will most fractures have associated with them?

A
  • Soft tissue injuries —> examine the soft tissue upon cast removal or when appropriate
86
Q

What impairment and functional limitations are associated with fractures?

A
  • Impaired ADLs
  • Decreased ROM
  • Weakness
87
Q

How should you begin with mobility after immobilization?

A

Begin stretch/mobilize with short lever ROM and joint mobilization

88
Q

What is weight bearing and resumption of activity based on?

A

Communication with the ortho MD

MSK Unit 2 (12 decks)

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