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Winter 2024 MSK 1 > Unit 2 Week 6 MSK > Flashcards

Unit 2 Week 6 MSK Flashcards

1
Q

Wolffs Law

A
  • Bones are organized to resist the load placed on them
  • More resistance you place on bone the more stress you place the more the bone is going to remodel
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2
Q

Bone= `

A

Bone is a highly specialized connective tissue
- Highly vascular
- Most ridged of connective tissue
- Can absorb impact
- Dynamic tissue which undergoes constant remodeling in response to different mechanical/physiological stimulation

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3
Q

What are some of the diseases that can increase the likelihood of a fracture

A

Osteoporosis
Osteomalacia
Rickets
Hyperparathyroidism
Hypogonadism
Osteogenesis Imperfecta
Scruvy
Marfans syndrome/ Ehlers - Danos syndrome
Pagets Disease
Medications: Corticosteroids, antirheumatics, anti-seizures

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4
Q

Bone healing phases

A
  1. Inflammatory= several days - including hematoma formation and angiogenesis, fibrosis union
  2. Reparative= 3-16 weeks - cartilage formation including calcification, cartilage removal and bone formation
  3. Remodeling= months to years
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5
Q

Fractures Clinical Presentation

A
  • Unusual Pain after trauma
  • Deformity of alignment
    Pain with weight bearing or loading or tenderness at the bone region
  • Dull deep ache: sharp severe
  • edema
  • Bruising
  • Crepitus that is atypical, unusual, or unexpected
  • IF A PATIENT HASN’T PROGRESSED WITH THERAPY BE SUSUPISICOUS A FRACTURE MAY NOT SHWO UP ON IMAGING DUE TO SWELLING
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6
Q

Fractures: PT interventions

A
  • Immobilization phase, transfer training ADLs and gait per MD order
  • treat impairment and functional limitations associated with fractures: Impaired ADL’s, ROM, weakness
  • Address balance if necessary
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7
Q

Fracture Prognosis

A
  1. Healing: children 4-6 weeks, Adolescents 6-8 weeks , Adults 10-18 weeks
  2. Dependent on bone and type of fracture
  3. Negative predictors for normal healing: smoking, diabetes, corticosteroids, ETOH, renal and vascular insufficiency
  4. Other complications: poor stabilization, damage to blood supply, infection
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8
Q

Stress Fractures

A
  • Caused by creep in the bone results from sustained loading: repetitive loading over time which will gradually exceed the bones ability to repair itself
  • Tibial stress fractures are the most common
  • Bone stress or strain can lead to increased osteoclastic activities/ increase absorptic activity which may predispose the bone to microdamage
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9
Q

Stress fracture Clinical Presentation

A
  • History- insidious onset with microtrauma
  • Does not improve with activity
  • (+) Hop or Percussion test
  • (+) Tuning fork
    -(+) US
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10
Q

Fracture Interventions

A
  • Rest/immobilization
  • Correct muscle imbalances
  • Graduated return to training
  • promote shock absorption
  • Orthotics PRN
  • Train muscle endurance
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11
Q

Osteoporosis

A

A chronic progressive disease characterized by low bone mass and microarchitectural deterioration of bone tissue leading to decreased bone strength enhanced bone fragility and consequent increase in fracture incidence
2 types
1. Primary
2. Secondary

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12
Q

Primary vs. Secondary Osteoporosis

A
  1. Primary= most common, occurs both genders, all ages, happens most often in post menopausal woman
  2. Secondary= Associated with conditions and medications
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13
Q

Risk factors of Osteoporosis

A

Non-Modifiable
- >50 y/o
- Caucasian/Asian
- Menopausal
- Family h/o Osteoporosis
- Depression
- Lactose intolerant

Modifiable
- Inactivity, Immobilization, sedentary lifestyle
- Tobacco/caffeine
- Medications
- Low BMI, small body frame
- Diet
- Eating disorders

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14
Q

Risk Factors for Osteoporotic Falls: NOF

A

Major
- Body weight < 70 kg or BMI < 21
- Corticosteroids
-Personal history of fractures as adults
- first degrees relative with fragility fracture
- Currently smoking

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15
Q

Osteomalacia

A

Softening of bone

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16
Q

Osteopenia

A

Low bone mass

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17
Q

Osteoporosis

A

Decreased bone density

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18
Q

BMD Testing Recommendations

A

All woman 65+
Men >= 70

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19
Q

Osteoporosis General treatment/Prevention Recommendations

A

Calcium and Vitamin D= augmentation of other agents, given to all osteoporosis patients

Caffeine= may reduce calcium absorption

Vitamin K = May help with bone metabolism and reducing urinary calcium exertion

Vitamin A and magnesium are beneficial

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20
Q

Osteoporosis Pharmacological Management

A
  • Anti-resorptive= decrease amount of bone that is lost
  • Anabolic= build up bone mass
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21
Q

Hormone replacement therapy for Osteoporosis

A
  • Recommended for prevention only
  • Increased BMD
  • Decrease in hip, vertebral, and other osteoporotic fracture rates
  • Increased risk of CV evens, venous thromboembolism and breast CA, decrease in colon CA
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22
Q

Osteoporosis : Selective Estrogen Receptor Modulators
SERMS

A
  1. prevention and treatment of postmenopausal OP vertebral fracture risk
  2. Daily or oral dosing
  3. Modest increase in BMD of spine and hip; decreases bone turnover
  4. Side effects= hot flashes, leg cramps, increased VTE
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23
Q

Calcitonin

A
  • Not approved for prevention
  • Nasal spray
  • only for patients who can’t tolerate other agents
  • Minimally inhibits bone resorption
24
Q

what are contraindicated Exercises with osteoporosis ?

A
  • Flexion exercises
  • B/c it can lead to vertebral fracture: bending forward places compressive forces on the anterior part of the vertebrae which will contribute to compression fractures
25
Q

How does articular cartilage get its nurtients?

A
  • nutrient supply + get rid of wastes through synovial fluid
  • Which is facilitated by loading and unloading of the tissue
26
Q

What is articular cartilage?

A
  • Smooth surface at the ends of bones
  • Tidemark line is where that articular cartilage affixes to the subchondral bone
  • AVASCULAR
    -ANEURAL
  • NO PERICONDRIUM
27
Q

What are the 2 main components of Articular Cartilage

A
  1. Extracellular Matrix- fibrous proteins/ground substance
  2. Chondrocytes
    - superficial chondrocytes are more elongated/flattened and will lay parallel to the surface where as the deeper cells are more round
    - Deeper chondrocytes will produce higher volumes of proteoglycans but their rate of turn over is slower than proteoglycans
    - Chondrocytes make all the extra cellular matrix components: they keep up the matrix/produce the matrix and clean up the wastes of the matrix
28
Q

What are the 4 zones of the Articular cartilage Fibers

A
  1. Superficial or tangential zone: highest concentration of fibrils/aligned parallel to the surface
  2. Middle/ transitional: fibers appear disorganized
  3. Deep Zone: perpendicular to surface
  4. Calcified cartilage zone: fibers perpendicular to the surface
    –> Deeper zones better fiber orientation to resist secondary tensile loads
29
Q

What is ground substance

A
  • Proteoglycan chains- push out against each other
  • Negatively charged hydrophilic molecules - repel each other
  • Drawls water in
  • Highest concentration of Ps in middle zones
    Fluid concentration lowest in deepest regions
    Water gives the cartilage its ability to absorb compressive loads
30
Q

Biphasic material of cartilage

A

Solid phase= it is fatigue resistant and sustains high stress and strains of loading

Fluid Phase= is compliant and able to diffuse load over increased surface area

31
Q

T/F cartilage is a viscoelastic material

A

True

32
Q

Which happens first fluid phase of cartilage or solid phase?

A

1st fluid phase happens and can support 90% of the load for about 15 minutes –> then switches to solid phase for the next 2-6 hours

33
Q

Where does cartilage get its nutrition?

A

Synovial fluid exchange

34
Q

T/F cartilage is avascular

A

True

35
Q

What do chondrocytes do?

A

Chondrocytes are the main source of metabolism within cartilage
- their job is to synthesize repair and remodel the extracellular matrix
- Chondrocyte activity is regulated by chemical factors

36
Q

T/F cartilage will have greater degeneration if it is not loaded and kept in immobilization

A

True - greater degeneration of cartilage happens if the joint is rigidity immobilized
- Cartilage won’t heal if it is subjected to a very long period of immobilization longer than 6+ weeks

37
Q

How does cartilage do with aging?

A

Chondrocyte activity decreases with age
- rate of synthetic activity decreased
- chondral cell proliferation ceases

38
Q

Cartilage repair

A
  • Chondrocytes are metabolically active
  • degree of repair success depends on
    1. extent of damage
    2. Nature of activity following damage
39
Q

Cartilage Treatment

A

least to most aggressive:
1. Oral medications
2. corticosteroid injections
3. viscosupplements
4. regenerative medicine; stem cell transplant
5. Microfracture and grafting procedures
6. Arthrocentesis/arthroscopy
7. Arthrodesis
8. Total joint replacement

40
Q

What is the Pathology/Disease Process of OA

A

Chondrocytes fail to repair damaged articular cartilage –> unstable matrix ( if the matrix is unstable it cannot accept compressive loads)
- Chondrocytes injured , metabolism decreases, and then decreased proteoglycans
- Increased proteases that increase chondrocyte death decrease ECM production
- Decreased water content becomes stiff and brittle
PROGRESSIVE CARTILAGE LOSS PENETRATIN TO SUBCHONDRAL BONE–> INFLAMMATORY RESPONSE

41
Q

Primary OA

A

-Localized or generalized forms
- Localized OA most commonly affects the hands, hips, spine, knees, feet
- generalized OA = 3 or more jointsS

42
Q

Secondary OA

A
  • Happens because of some disease/injury
43
Q

What is the Multifactorial Etiology of OA

A
  • Aging
  • Obesity
  • Joint injury: trauma or repetitive microtrauma
  • Chronic low grade joint inflammation
  • Heredity/genetics
44
Q

Risk factors of OA

A
  • Age 50+
  • Male <45 / Female > 45
  • family history
  • Occupation
  • Past injuries, congenital/developmental conditions
  • obesity
45
Q

Clinical Signs of OA

A

History:
1. Risk factors
2. Insidious onset
3. Painful joint , deep ache
4. Asymmetrical Involvement
5. Impaired mobility
Activity and participation limitations

Physical Exam :
1.crepitus- feels crunchy, crackly, grinding
2. Bony enlargement
3. Decreased range of motion
4. malalignment of deformity
5. tenderness to palpation
6. Mild, localized joint effusion
7. Impaired muscle performance
8. Impaired balance
9. impaired gait and transfers

46
Q

What is gelling?

A

morning stiffness for 5-10 minutes
stiff after still, improved with movement
l

47
Q

Differential diagnosis of OA

A

It could present like
- RA
- Gout
-CPPD Calcium pyrophosphate crystal deposition disease
- Septic Joint
- Polymyalgia rheumatica

48
Q

What might you see on a radiographic elevation of OA

A
  • reduced joint space
  • osteophyte formation
  • subchondral sclerosis
  • subchondral cysts ( fluid filled sac within subchondral bone)
49
Q

Clinical Symptoms of RA

A
  1. Systemic Autoimmune
  2. Symmetrical
  3. Can occur at any age
  4. Morning or pain/stiffness >30 minute s
  5. Constitutional symptoms
  6. Small joints of hand MCPs and PIPs
  7. X-rays: periarticular osteoporosis, joint space narrowing , juxtaarticular erosion, large cystic erosions of bone, bony proliferation, marked deformities

Swan neck deformity= proximal interphalangeal (PIP) joint hyperextension and flexion of the distal interphalangeal (DIP) joint.

Boutonniere deformity=flexed at the proximal interphalangeal joint (PIP) and hyperextended at the distal interphalangeal joint (DIP)

50
Q

Clinical Symptoms of OA

A
  • Local Joint disease
  • Unilateral/asymmetrical
  • More common as you get older
  • morning pain/stiffness <30 minutes
  • No constitutional symptoms
  • Hand joints : PIPs and DIPs, thumb CMC
  • X-rays: joint space narrowing, osteophytes, subchondral sclerosis and cysts

Bouchard and Heberden’s nodes

51
Q

OA Pharmacological Management

A

Strongly recommend:
1. Oral NSAIDs
2. Topical NSAIDs
3. I-A steroids

Strongly Against:
1. Bisphosphonates
2. Glucosamine
3. Hydroxychloroquine
4. Methotrexate
5. TNF inhibitors
6. IL-1Receptors antagonists
7. PRP
8. Stem cell injections
9. chondroitin
10. I-A hyaluronic acid

52
Q

OA Physical, Psychosocial, Mind and body Management

A

Strongly recommended
1. Exercise
2. Self management programs
3. Weight loss
4. Tai chi
5. Cane
6. TF knee brace
7. 1st CMC orthosis

Strongly Against
1. TENS

53
Q

RA

A
  • Progressive, systemic, autoimmune inflammation
  • Often aggressive, devastating consequences
  • Unknow etiology

Characterized by:
- systemic synovitis- chronic polyarthritis
- joint erosion , cartilage and bone destruction
- Multisystem- extra articular manifestations
- onset usually slow and insidious over months
- in 15%-20% may have rapid or acute
- aggressive management leads to good control

54
Q

RA Diagnosis ACR Criteria

A
  1. Morning stiffness> 1 hour
  2. Arthritis of hand joints MCPs, PIPs, wrists
  3. symmetric swelling
  4. Serum rheumatoid factor - RA factor
  5. Rheumatoid nodules
  6. Radiographic changes

first 4 criteria has to be present for 6 or more weeks

55
Q

T/F the lumbosacral is involved in RA

A

False only the atlanto axial is involved because it is a synovial joint

56
Q

Typical joints involved in RA

A
  • Wrist joints/MCP
  • Index and middle metacarpophalangeal joint
  • PIP
  • MCO
  • MTP
  • Elbow/shoulders
  • Knees, ankles, hips,
  • ATLANTO-AXIAL JOINT
57
Q
A

Winter 2024 MSK 1 (6 decks)

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