Musculoskeletal System Healing Flashcards
1
Q
Tissues of the MSK System
A
Muscle
Bone
Tendon
Ligament
Cartilage
2
Q
Muscle Strain
A
Tears in muscle fibers
3 Grades
3
Q
Muscle Strain Grade I
A
Only a few fibers are torn, painful, muscle has complete function
4
Q
Muscle Strain Grade II
A
Greater Number of fibers torn, severe pain, swelling observed, loss of strength, loss of ROM, bruising may be evident
5
Q
Muscle Strain Grade III
A
Muscle tears into two separate pieces or is torn away from the tendon, considerable pain and swelling, may be an obvious dent or gap at the site of injury, loss of strength and ROM
6
Q
Muscle Repair
A
After injury the healing process set up two competitive events:
1. Regeneration of muscle fibers
2. Production of fibrous scar tissue
Phases: Destruction, Repair (Regeneration, Remodeling
7
Q
Muscle
Destruction Phase
A
After rupture hemorrhage and edema occur
* Degenerative changes and necrosis occur at the site of injury
* An inflammatory reaction is initiated and the necrotic area is invaded
by:
* Macrophages (clear debris)
* T-lymphocytes (release cytokines and growth factors)
* Cytokines and GF’s aid in activation of satellite cells
8
Q
Muscle
Destruction Phase
A
- Satellite cells are activated
- Eventually will transform into myoblastic cells → myotubes → new muscle fibers
- Formation of a connective tissue scar by fibroblasts occurs at the
central zone of injury - Type III collagen
9
Q
Muscle
Regeneration Phase
A
- Begins 3-6 days post injury
- Peaks at 7-14 days
- Satellite cells proliferate and differentiate into myoblasts
- Occurs at both sides of the injury
- Ultimately form multinucleated myotubes
- Myotubes attempt to join injured myofibers on the opposite side of
the injury - These regenerating muscle cells begin to pierce through the scar
10
Q
Muscle
Remodeling Phase
A
- Tensile strength of healing tissue occurs over time
- Greater amount of type III collagen
- The tissue remodels as type III collagen is replaced with type I
- Collagen cross links stabilize and gain strength
11
Q
Muscle
Remodeling Phase
A
- Scar formation, muscle regeneration, orientation of new fibers have
been enhanced in animal models when subjected to controlled
movement compared to immobilization - Muscle may undergo low-force exercise designed to prevent atrophy and maintain muscle tone
12
Q
Skeletal muscle pathology
Myasthenia Gravis
A
- Disorder of the neuromuscular transmission, characterized by fluctuating
weakness and fatigability of skeletal muscle - Peak incidence occurs in women 20-30 years old and men 50-60 years old
– ratio of women to men is 3:2 - Autoimmune disease – the presence of specific anti-ACh receptor antibodies, which block the normal binding site for Ach
- The receptors at the motor endplate are decreased in number and those that remain are altered in shaped resulting in decreased function.
13
Q
Myasthenia Gravis
A
- Clinical manifestations are variable from
mild to severe - Include muscle weakness and
fatigability - The fluctuating weakness tends to be
more evident in the proximal muscles
14
Q
Myasthenia Gravis
A
- Cranial muscles (eyelids and muscles
controlling eye movements) are the first
to show weakness resulting in diplopia
(double vision) and ptosis (drooping
eyelid) - Chewing can produce fatigue
- Difficulty with swallowing can occur
- Aspiration of food can become
common
15
Q
Myasthenia Gravis Tx
A
Acetylcholinesterase inhibitor medication reduces the weakness but does not treat the underlying disease
Administration of the medication is tailored to the individual needs of the
client throughout the
Immunosuppression
using corticosteroids
(prednisone)
~Adverse side effects of using
high doses of corticosteroids
include weight gains,
hypertension, osteoporosis
Plasmapheresis can be used to remove the anti-AChR antibody
16
Q
Myasthenia Gravis Prognosis
A
Prognosis is variable with periods of remission and exacerbation and the symptoms fluctuate in intensity throughout the day
A severe MG crisis can require mechanical ventilation due to weakness of the respiratory muscles
17
Q
Muscular Dystrophy (MD)
A
- Mutation in the gene that creates the protein dystrophin and dystrophin-associated protein complex
18
Q
Duchenne’s MD (DMD)
A
X-linked recessive (males are affected clinically and females are carriers) with onset at 1-4 years, rapid progression, loss of walking 9-10 years, death late teens.
Severe crippling, Deformities and Contractures
19
Q
Becker’s MD (BMD)
A
X-linked recessive, onset 5-10 years, slowly progressive, walking maintained past teens, death in 20s
Using hands to push on legs to stand
20
Q
MD Clinical Manifestations
A
- Muscular weakness, wasting, hypotonia
- Child has difficulty getting off the floor
- Gower’s sign – client places hands on thighs and walks up legs)
- Frequent falls, difficulty climbing stairs, walks with a waddle gait (proximal
muscle weakness)
21
Q
MD Clinical Manifestations Cont’d
A
- Walks on toes (weakness and contracture of anterior tibialis and peroneals)
- Increased lumbar lordosis
(hip extensor weakness) - Positive Trendelenburg’s sign (weak hip abductors)
22
Q
MD Tx
A
- Treatment – none known to halt progression of disease
- Treatment is directed at maintaining function in the unaffected muscle groups
as long as possible.
* Glucocorticoid therapy (prednisolone)
tends to slow the progression of the
disease state.
- Treatment is directed at maintaining function in the unaffected muscle groups
23
Q
MD in PT
A
Maintain activity level
Avoid repetition of strenuous activities
Respiratory Monitoring
Provide ambulation/pool therapy for endurance
Info on assistive devices
24
Q
Bone cells
A
- Osteogenic cells
- Develop into osteoblasts
- Found in the deep layers of the periosteum and bone marrow
- Osteoblasts
- Bone formation
- Found in the periosteum and endosteum
- Osteocytes
- Maintain mineral concentration of bone matrix
- Entrapped in the bone matrix
- Osteoclasts
- Bone resorption
- Bone surfaces
25
Bone Modeling
* The process by which bones change their shape in response to physiologic influences or mechanical forces
* May widen or change it’s axis by the removal or the addition of bone in response to biomechanical forces
* Example – tennis player
* Cells likely responsible for sensing physical stimuli - osteocyte
26
Osteocytes
* Bone mass is rapidly lost under unloading conditions
* Bed rest
* Local denervation of muscle
* Hind-limb unloading
27
Who has higher bone mineral density?
Active children and adults
Reduced long-term fracture risk
28
Bone Remodeling
* Bone is a living organ that undergoes remodeling throughout life
* In homeostatic equilibrium, resorption and formation of new bone
matrix are balanced
* Old bone is continuously replaced by new bone
29
Bone Remodeling Cont'd
* Activation, Resorption, Formation (ARF)
* Activation of the osteoclasts
* Resorption of bone by osteoclasts
* Formation of new bone by osteoblasts
* Activated by 3 circumstances
* Release minerals in response to low serum calcium levels
* Repair skeletal microdamage
* Balance the mechanical and mass needs of the skeleton
30
What are the 3 primary influences affecting this remodeling process?
(1) mechanical stresses; (2) calcium and phosphate levels in the extracellular fluid; and (3) hormonal levels of parathyroid hormone, calcitonin, vitamin D, cortisol, growth hormone, thyroid hormone, and sex hormones
31
Bone - Calcium
* Regulated by parathyroid hormone (PTH)
* Secreted by the parathyroid gland to
increase calcium levels
* Calcitonin
* Secreted by the thyroid
* Acts to decrease calcium
* PTH – stimulates osteoclasts to resorb
bone, releasing calcium into the blood
* Calcitonin inhibits the effects of PTH on
osteoclasts
32
Bone
Micro-damage
* Main theory for remodeling is the repair of micro-damage
* Fatigue micro-cracks that occur throughout
the skeleton
* Increasing evidence suggests the osteocyte may
sense micro-cracks in the bone
* Micro-cracks may cause local osteocyte
apoptosis
* Adjacent osteocytes release signaling molecules
* Studies where apoptosis was inhibited, resorption was diminished
33
Rickets
* A softening of bones as a result of a deficiency
or impaired metabolism of vitamin D,
phosphorus or calcium,
* Can lead to fractures and deformity
34
Osteoporosis
* Low bone mass and skeletal deterioration
* Increase susceptibility of fractures
* Marked increase in bone resorption with rapid bone loss
35
Osteoporosis Incidence/Risk
* Women > men
* Increased age
* Body size
* Family history
* Post-menopausal
* Low levels of calcium and vitamin D
* Low activity level
* Tobacco and ETOH abuse
36
Osteomyelitis
Inflammation of bone caused by an infectious organism such as bacteria, but fungi, parasites, and viruses can also cause skeletal infections (spine, pelvis, and arms/legs often affected)
37
Fracture healing
* Process involving the local response of various growth factors
and cytokines resulting in the control of osteoclasts and
osteoblasts
* Direct or indirect healing pathways
38
Indirect Fx Healing
Sequential steps of tissue differentiation, resorption of the surface of the Fx, uniting the Fx fragments by a callus, and long-lasting remodeling
39
Indirect Fx Healing
* Inflammatory phase
* Initial disruption of bone
* 3-4 days
* Repair phase (proliferative phase)
* 1-4 months
* Remodeling phase
* 1-4 years
40
Bone
Inflammatory Phase
Hematoma formation
Coagulates around the fracture ends and within the medulla
Forms a template for callus formation
41
Bone
Repair Phase
Formation of a cartilaginous callus
-Later undergoes mineralization, resorption, bone replacement
Capillary ingrowth
Fibroblasts transform the hematoma into granulation tissue
42
Bone
Repair Phase Cont'd
* Cartilaginous callus is replaced with
woven bone
* At the end of the phase bone union has
been achieved
* The structure differs from the original
bone
43
Bone
Remodeling Phase
* Biomechanic stability has not yet been restored
* A second resorptive phase initiated
* Remodels the hard callus into a lamellar bone
structure with a central medullary cavity
* Balance of hard callus resorption by osteoclasts and
lamellar bone deposition by osteoblasts
44
Direct Fx Healing
Stable fixation and compression without an apparent callus
45
Direct Fx Healing
* Requires correct anatomical reduction of the fracture
ends without any gap
* Often the primary goal of open reduction internal fixation surgery
* Remodeling of the lamellar bone, Haversian canals, and
blood vessels
* Bone on one side of the cortex unites with bone on the other side of the cortex to re-establish mechanical
continuity
46
Stress Fx
* One of the most common
overuse injuries
* Excessive repetitive
loading without adequate
periods of rest
* Increases osteoclast
activity
* Osteoblast lag time
* Intrinsic risks
* Age
* Race
* Gender
* Extrinsic
* Malnutrition
47
Tendon Function
Transmit force from muscle to bone
Store elastic energy when stretched
Resist passive motions to increase joint stability
48
Effects of age on tendon
* During maturation (<20 years):
* Cross-links increase
* Collagen fibril diameter increases
* Older age (>60 years):
* Tensile strength and stiffness begin to decrease
* Decreased collagen content
49
Effects of immobilization on tendon properties
* To maintain the normal mechanical properties of the tendon, there
must be regular loading
* Without this, the tendon becomes weaker
* Collagen content decreases
* Cross-links decrease
* Cells and fibers become disorganized
* Increased deformation with normal tensile loads
50
Acute Tendon Injury
* Injuries caused by sudden loading/excessive force
* Lacerations
* Partial thickness rupture
* Full thickness rupture
* Compressive forces
* Repetitive loading/tissue microtrauma
51
Chronic Tendon Injury
* Compressive forces
* Repetitive loading/tissue microtrauma
52
Ligament Function
* Passive guidance of bones during
normal function
* Joint stability during external loading
* Proprioception
* Energy conservation
53
Effects of immobilization on ligament
properties
* Load-sensitive structures
* Immobilization causes a rapid deterioration in strength and stiffness
* 6-9 weeks = 50% loss in strength and stiffness
* Bone is also affected by immobilization
* Leads to atrophy of the ligament
* Increased cell catabolic activity
54
Effects of exercise on ligament properties
* Loading of a biological tissue stimulates collagen production
* May increase strength and stiffness of a ligament 10-20%
55
Effects of age on
ligament properties
* Prior to skeletal maturity:
* Ligaments are more viscous, have a
smaller cross-sectional area and
are less stiff.
* Increased risk for injury at the bony
insertion
56
Ligaments on Middle age
Decreased viscosity, increased
collagen cross-linkages,
decreased elasticity
57
Ligaments in Old age
* Ligaments lose mass, stiffness
and strength
* Ligaments more prone to
excessive creep
* Joint laxity
* Changes due to aging process, or
change in activity? Both
58
Injury to Ligament
* Mechanism of injury (MOI) must involve enough force to rupture collagen fibers
* Direction of force will dictate if a ligament could be injured
* Other structures often involved if a ligament has been damaged
59
Ligament Grade I Sprain
* Ligament has been lengthened beyond it’s yield point, but no major damage
* Pain with stressing the ligament, but no laxity noted
60
Ligament Grade II Sprain
* Ligament has been lengthened with some disruption of ligament fibers
* Pain with stressing the ligament, some laxity noted
61
Ligament Grade III Sprain
* Ligament has been lengthened with complete or nearly complete disruption of the ligament fibers
* Significant joint laxity with stressing the ligament, may be an absence of pain
62
Ligament Healing
Bleeding/clotting
* Injury damages the blood supply to the ligament
* Platelets cause a blood clot to form
* Fibrin clot leads to vasodilation, infiltration of inflammatory cells
* Lasts for hours-days (~3)
63
Ligament Healing
Inflammation
* Initiated by fibrin clot formation
* Macrophages and other inflammatory cells remove debris
* The process attracts fibroblasts to the area
* Lasts up to 5 days
64
Ligament Healing
Proliferation/fibroplasia
* Fibroblasts begin to produce a scar matrix
* Still predominately type I collagen, but a higher amount of types III, V and IV
* Decrease STIFFNESS and strength
* While inflammation is still present, scar tissue is more viscous
* Lasts for up to 6 weeks
65
Ligament Healing
Maturation/remodeling
* Scar matrix contracts
* Scar tissue behavior is less viscous, more elastic
* Scar tissue continues to remodel based on the forces applied to the joint
* Some conversion to type I collagen, but never exactly resembles ligament tissue
* Alignment of scar tissue fibers dependent on forces applied
* Lasts up to 12 months post injury
66
Implications for rehabilitation during the inflammatory phase
* Anti-inflammatory modalities may help to limit
damage to other joint structures and decrease
pain and swelling
* Whether or not this influences scar formation is
unknown
* Some degree of immobilization may be necessary to allow for the scar tissue to form a “bridge”
between the two ends of the ligament
67
Implications for rehabilitation during the Proliferative Phase
* Controlled motion is necessary to stimulate adequate scar formation and
prevent scar tissue adhesions
* May need to focus on correcting:
* Altered biomechanics
* Altered posture/alignment
* Compensatory movements/postures
68
Implications for rehabilitation during Maturation/Remodeling
* Focus is to continue gradual increase in normal forces to the ligament
* Promotes improved scar tissue quality
* Promotes improved alignment of scar tissue fibers
69
Cartilage
* Essentially non-vascular tissue that does not contain nerves
* Composed of chondrocytes and matrix (collagen, elastin, ground substance)
* Resistant to deformation and readily withstands compressive forces
70
Articular
(hyaline)
cartilage
* Devoid of blood vessels, lymphatic channels, and innervation
* Purpose is to distribute joint loads over a wide surface, reducing the stress per unit area
– Intense stress localization promotes
cartilage degeneration
– Abnormal joint articulation increases the stress on the joint surface resulting in
cartilage failure – leading cause of osteoarthritis
* Allow movement of opposing joint surfaces
with minimal friction/wear – fluid film provides
joint lubrication
71
Nutrition of articular
cartilage
* Cartilage is nourished by synovial fluid contained in the joint
* This is accomplished by diffusion and the pumping action of the compression and decompression associated with joint
movement
* Periods of inactivity (bed rest) at the joint can
lead to articular cartilage damage
72
Articular cartilage response to injury
* Repair process progresses slowly reflecting the lack of
vascularization
* Better repair is evident at the superficial tangential zone and the deep zone
* Cells of inflammation/repair enter the region via the synovial membrane and pass through the fluid
* Repair is mediated by chondrocytes and results in fibrocartilage formation
73
Articular cartilage response to injury Cont'd
* Injuries often do not result in adequate repair
* Surgical repair of articular cartilage often includes drilling into the subchondral bone, inducing vascular damage and initiating an
aggressive inflammatory response in the bone
that spills into the cartilage
* Traumatic damage can include slippage of
cartilage or the release of cartilage fragments
from the joint surface
74
Osteoarthritis
* Degenerative joint disease
* Articular cartilage breaks down because of an imbalance between the mechanical stresses and the ability of the joint structure to handle the loads
75
Osteoarthritis Cont'd
* Mechanical wear and tear leads to gradual breakdown of the articular cartilage
* As a result, excessive forces are applied to the other parts of the joint
* Results in narrowing of joint space, sclerosis of the subchondral bone, and osteophyte formation
76
Osteoarthritis Immobilization
* Immobilization can also promote articular cartilage degeneration
– Articular cartilage is dependent upon repetitive loading/unloading to promote movement of nutrients and wastes
– Absence of such movement will result in structural weakening of the cartilage
77
Rheumatoid Arthritis (RA)
* Autoimmune induced chronic, systemic
inflammatory disease resulting in tissue destruction
* About 80% of individuals with RA are rheumatoid factor positive
78
RA
* Complaints of fatigue, weight loss, weakness, and general diffuse musculoskeletal pain
* Multiple joints are involved with symmetrical bilateral presentation
* Joint subluxation and deformity
* Rheumatoid nodule formation at areas of
pressure (elbow, Achilles tendon, heart, lung, GI tract
79
RA Diagnosis
Exhibits 4 or more of the following:
* Morning stiffness at least 1 hour for 6 weeks
* Swelling in 3 or more joints for 6 weeks
* Swelling of wrist, hand for 6 weeks
* Radiographic evidence of symmetrical joint swelling
* Erosions of bones of hands and decalcification
* Rheumatoid nodules
* Presence of rheumatoid factor
80
RA Tx
* Treatment goals:
* Reduce pain
* Maintain mobility
* Minimize stiffness, edema, joint destruction
81
OA
Age of onset: >50
Pain: Worse during or after activity
Stiffness: Worse during or after activity | Usually <30min in morning
Joint characteristics: Hard and bony
Primary joints affected: DIP, CMC of thumb, knees | Not symmetrical
Associated signs: Heberden's nodes, Bouchard's nodes
82
RA
Age of onset: 30-50
Pain: Inactivity, worse in morning
Stiffness: Worse in the morning | >30 min
Joint characteristics: Soft, tender, warm
Primary joints affected: PIP, MCP, Elbows, ankles, wrists | Symmetrical
Associated signs: Ulnar deviation, Boutonniere deformity, Swan-neck deformity
