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MSK Unit 2 > MSK Week 5 > Flashcards

MSK Week 5 Flashcards

1
Q

Phases of healing

A
  • Hemostasis
  • Inflammation
  • Proliferation
  • Remodeling
  • OCCURS SEQUENTIAL AND SIMULTANEOUS
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2
Q

What are MSK injuries?

A
  • Damage to MSK structures and nearby CT, blood vessels, nerves
  • Response to injury occurs sequentially and simultaneously
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3
Q

How do MSK injuries happen?

A
  • Direct trauma
  • Compressiong
  • Friction
  • Repeated over-stretching
  • Typically with a mechanical force
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4
Q

Hemostasis

A
  • 0 to up to 6-8 hours
  • Stop the bleeding
  • Cellular and vascular cascade causes local vasoconstriction
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5
Q

What is clot formation?

A

Stimulation of platelets and formation of fibrin

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6
Q

Inflammatory phase

A
  • 0 hours up to 2 weeks
  • Peak 2-3 hours
  • Clean up the wound site - prepare for construction
  • Begins as soon as chemical mediators start to move
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7
Q

Prominent inflammatory mediators

A
  • Histamine
  • Bradykinin
  • Serotonin
  • Lymphokines
  • Prostaglandins
  • Leukotrienes
  • Arachidonic acid
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8
Q

What is diapedesis?

A

Where cells squeeze through gaps in capillary wall to get where they need to go

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9
Q

What is chemotaxis?

A

Signaled by chemical agents in the area and they follow the train to get to the injury site

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10
Q

External factors that may affect the inflammatory phase - potentially derailing it

A
  • NSAIDs
  • Repetitive or forceful tasks
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11
Q

How do NSAIDs impact the inflammatory phase?

A
  • Can delay or hamper healing in MSK tissues (muscle, tendons, cartilage and bone)
  • Inflammation is a necessary step for healing and transition to proliferation
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12
Q

How to repetitive or forceful tasks impact the inflammatory phase?

A
  • Cause the acute inflammatory stage to continue, followed by fibrotic and structural tissue changes
  • Possibly also CNS reorganization resulting in movement disorders
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13
Q

Clinical signs during inflammatory phase

A
  • Swelling, redness, heat
  • Impairment or loss of function
  • Pain at rest, or with active motion, or with specific stress of the tissue
  • Potential for muscle guarding, self-splinting, protective posturing
  • W passive movement, pain is reported before tissue resistance reacher
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14
Q

Protective phase of rehab

A
  • Control pain, edema and inflammation
  • Restore full RPOM, prevent atrophy, maintain soft tissue joint integrity
  • Enhance function
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15
Q

PRICEMEN

A
  • Protection
  • Rest
  • Ice
  • Compression
  • Elevation
  • Manual therapy
  • Early motion - done safely
  • Medications
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16
Q

Proliferative phase

A
  • 4-22 days
  • Peak at 2-3 weeks
  • Rebuild damaged structures and strengthen the wound
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17
Q

When is the peak of the Proliferative phase?

A

When bulk of scar material is formed - continues for several months post-injury

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18
Q

What are the two tissue healing processes?

A
  • Regeneration - regrowth of original tissue
  • Repair - formation of a connective tissue scar
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19
Q

What are the 4 simultaneous processes of proliferation?

A
  • Epithelialization
  • Collagen production
  • Wound contraction
  • Neovascularization
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20
Q

Epithelialization

A
  • Only when the skin is involved
  • Reestablishes the epidermis
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21
Q

Collagen production

A
  • Limited tensile strength
  • Type III —> Type I
  • Excessive scarring may affect outcome
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22
Q

Wound contraction

A

If uncontrolled, contractures may result in

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23
Q

Neovascularization

A

New blood vessels (w/in 4 days)

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24
Q

Clinical signs during the Proliferative phase

A
  • Decrease in pain
  • Erythema resolved
  • No active effusion, residual swelling may persist
  • Increase in pain-free active and passive ROM
  • With passive movements, pain is felt at the point of tissue resistance
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25
Q

What is the intervention goal of the proliferation phase?

A

Create a strong extensible scar

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26
Q

How is a strong extensible scar going to be created during intervention?

A
  • Protection of the forming collagen
  • Direct collagen orientation to be parallel to the lines of force it must withstand
  • Prevent cross-linking and scar contracture
  • Modify faulty joint mechanics
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27
Q

Intervention approaches for Proliferative phase

A
  • Educate patients about signs/symptoms of over stress of healing tissues
  • Transition from passive interventions toward progressive stress of tissue - therapeutic exercise progression
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28
Q

How does loading the tissues help them heal?

A

Mechanotransduction

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29
Q

What is the 3 step process of Mechanotransduction

A
  • Mechanocoupling
  • Cell to cell communication
  • Effector cell response
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30
Q

Mechanocoupling

A

Mechanical trigger or catalyst

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31
Q

Cell to cell communication

A

Distribution of the message

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32
Q

Effector cell response

A

The tissue factory that produces and assembles

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33
Q

Remodeling Phase

A
  • Longest phase
  • Few days - 2 years
  • Modify scar tissue into its mature form
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34
Q

Clinical signs during the remodeling phase

A
  • Progression to pain-free function and activity
  • Pain is felt at end range of passive movements after tissue resistance met
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35
Q

Local factors affecting healing

A
  • Type, size, location of injury
  • Infection
  • Vascular supply
  • External forces (thermal agents, electromagnetic, mechanical pressure)
  • Movement (early, later)
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36
Q

Systemic factors that affect healing

A
  • Age
  • Disease or infection (diabetes, autoimmune)
  • Medications (antibiotics, corticosteroids)
  • Nutrition
  • Hormones
  • Fever
  • Oxygen
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37
Q

Acute, subacute and chronic timelines/additional names

A
  • Acute = 7-10 days; protective phase
  • Subacute = 10 days - 6 weeks; controlled motion
  • Chronic = 6 weeks - months; return to function
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38
Q

Structural components of muscle

A
  • Endomysium
  • Perimysium
  • Epimysium
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39
Q

What does the basal lamina serve as?

A

A scaffold for healing

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40
Q

What are satellite cells?

A

Muscle stem cells for regeneration and rebuilding

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41
Q

What is the myotendinous junction?

A

Where muscle proper is merging with the tendon proper - we get junction transition tissue

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42
Q

What are the contractile units of muscle?

A

Myofibers

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43
Q

Factors affecting muscle performance under load

A
  • Age
  • Temperature
  • Immobilization or disuse
44
Q

Muscle phases of healing

A
  • Destruction phase
  • Repair phase
  • Remodeling phase
45
Q

Destruction phase

A
  • Necrosis of damaged muscle tissue
  • Factors released, start hemostasis and inflammatory response
  • Vascular disruption - hematoma and edema begin
  • Leukocytes infiltrate and activation/proliferation of satellite cells (myoblasts)
46
Q

Repair phase

A
  • Hematoma formed
  • Inflammatory cells arrived and satellite cells proliferation continues
  • New myofibers are formed
  • Neuromuscular junction reestablished
47
Q

Remodeling phase

A
  • Regenerated tissue matures and tensile strength increases
  • Scar contracts and is reorganized
  • Type I returns to normal proportion over Type III
48
Q

Contusion

A
  • Blunt trauma
  • Hematoma (inter or intra muscular)
  • Myositis ossificans (calcified hematoma)
49
Q

Risk factors of strain

A
  • Inadequate flexibility
  • Inadequate strength or endurance
  • Muscle imbalances
  • Insufficient warm-up or fatigue
  • Inadequate rehab from past injury
50
Q

What is a distractive strain?

A

Excess pull, overstretch

51
Q

What tissues are impacted during eccentric motions that are not damaged during concentric and isometric motions?

A
  • Damage to sarcomere
  • Disrupt ECM
  • Intramuscular edema
  • Increased creatine kinase
52
Q

Grade I strain (First Degree)

A
  • Tear only a few musculotendinous fibers
  • Pain only with limited swelling
  • No loss of function
53
Q

Grade II Strain (2nd Degree)

A
  • Disruption of moderate number of fibers
  • Increased pain
  • Some loss of strength and function
54
Q

Grade III strain (3rd Degree)

A
  • Complete rupture of some musculotendinous units
  • Loss of function with little pain
  • MT junction site
55
Q

When is pain most pronounced in muscle injury?

A

Eccentric activation

56
Q

Muscle injury management

A
  • Protective phase
  • Controlled motion phase
  • Return to function phase
  • Re-injury prevention
57
Q

Protective phase management

A
  • PRICEMEN, patient education
  • PROM, AAROM, AROM
58
Q

Controlled motion phase management

A
  • AAROM, AROM, flexibility
  • Submaximal isometrics —> multiangle submaximal isometrics —> multiangle max isometrics —> PREs
  • Simple/safe balance, proprioception activities
  • corrective exercise of associated biomechanical deficiencies
59
Q

Return to function phase management

A
  • Endurance and maximizing strength, concentric —> eccentric training
  • General return to activity - 80% strength of unaffected contralateral
  • Speed, power, agility exercises
60
Q

Re-injury prevention management

A
  • Education on proper warm-up
  • Holistic conditioning
  • Maintenance of flexibility, strength
61
Q

Complications of muscle injury management

A
  • Immobilization/disuse - less force, less tolerance to lengthening
  • Reinjury
  • Fibrosis
  • NSAIDs induce impairment in functional capacity and histology when administered at later points
62
Q

Anatomy of Tendon

A
  • Glistening white
  • Collagen fibers in tightly packed bundles
  • Elastin
  • ECM: proteoglycans, GAGs
  • Parallel fibers
  • Avasular
  • Aneural
63
Q

Tissue tendon properties

A
  • Transmit force from muscle to skeleton
  • Store and release elastic energy
  • High tensile strength
  • Respond and adapt to loading, Mechanotransduction
  • Low metabolic rate —> very slow healing after injury
64
Q

Tendon mechanisms of injury

A
  • Loading
  • Overuse loads
  • After activity
65
Q

Loading mechanism of injury - tenodn

A
  • Sudden overload
  • Repetitive loading
  • Rapid unloading
66
Q

Overuse loads mechanism of injury - tendon

A
  • Tension + Compression
  • Shearing and friction
  • Fascicle on fascicle
  • Paratenon, retinacula, bone
67
Q

After activity mechanism of injury - tendon

A
  • Catabolism (24-36 hrs; break down)
  • Anabolism (24-80 hours; build up)
  • Adequate rest between exercise bouts
68
Q

Intrinsic factors for tendon injury risk factors

A
  • High body weight
  • Malalignments, imbalances, weakness, poor flexibility, poor form
  • Age
  • Gender
69
Q

Extrinsic factors for tendon injury risk factors

A
  • Excess volume, speed, magnitude of loading
  • Abrupt change to amount or type of load
  • Poor environmental conditions (like temperature)
  • Poor equipment
  • Medications
  • Prolonged immobilization
70
Q

Tendinopathy

A
  • Blanket term for tendon conditions arising from overuse
  • Absence of PG-mediated inflammation
  • Persistent, recalcitrant
  • Poor healing potential
71
Q

Specifics of tendinopathy - Blanket term for tendon conditions arising from overuse

A
  • Cumulative trauma
  • Weaken collagen cross-links
  • Degrade ECM and vascular elements
  • Does not follow the traditional phases of healing
  • Except vascular, proximal 1/3
72
Q

Chronic tendon injury stages

A
  • Stage I tendinitis
  • Stage II tendinosis
  • Stage III complete rupture
  • Stage IV tendinosis with other changes such as fibrosis or calcification
73
Q

Tendinitis

A
  • Pain, swelling, dysfunction of tendon
  • Broad term
74
Q

Tendinosis

A
  • Degeneration of tendon structures
  • Not well correlated with clinical symptoms
  • Pain not always present
  • Lower resistance to strain
75
Q

4 main histological changes of tendinosis

A
  • Angiofibroblastic hyperplasia
  • Disorganized and immature collagen
  • Hypercellularity and increased ground substance
  • Vascular hyperplasia and neo vascularization
  • Increase of neurochemicals
76
Q

What is angiofibroblastic hyperplasia?

A
  • New growth of blood vessels, fibroblast infiltration
77
Q

What is neurogenic inflammation?

A

Inflammation response caused by release of neural chemicals

78
Q

Clinical signs of tendon injury

A
  • Well localized with little referral beyond the tendon
  • Strong but painful (unless full rupture) in proportion to resistive load
  • Painful with stretch or palpation
  • Pain resolves quickly when load withdrawn
  • Unusual to be painful w/o load, at night or at rest
79
Q

What do opioid analgesics do?

A
  • Relieve moderate to severe pain
  • Act on CNS receptors in spinal cord and brain
80
Q

What pain receptor signals do opioid analgesics reduce?

A
  • Mu
  • Kappa
  • Delta
  • Sigma
81
Q

How do NSAIDs decrease inflammation?

A
  • Block PG/thromboxane/leukotriene synthesis —> inhibit cycle-oxygenate (COX) and PG synthase enzymes
  • Block vasodilation and inflammatory response
82
Q

How are NSAIDs anti-pyretic (fever reducer)

A
  • Block PGs that would elevate hypothalamic temperature control
83
Q

How do NSAIDs act as anti-thrombotic medication (anti-coagulant/blood thinner)?

A

Block COX —> thromboxanes that stimulate platelet aggregation

84
Q

How do NSAIDs relieve pain (mild-moderately)?

A
  • Don’t bind to opioid receptors
  • Block prostaglandins (PGs)
85
Q

COX-1 (+)

A
  • Helpful
  • Normal constituent of cells in hemostasis
  • GI mucoprotection
  • Regulate normal platelet activity
  • Renal and vascular homeostasis
  • Uterine function, embryo implantation
  • Regulation of sleep-wake cycle and body temp
86
Q

COX - 2 (-)

A
  • Produced by injured cells
  • Produces prostaglandins that mediate pain, inflammation, pyresis
  • Vasodilation and inhibition of platelet aggregation
  • Modulation of platelet aggregation
87
Q

Non-selective NSAIDs

A
  • COX-1 and COX-2 inhibitors
88
Q

Selective NSAIDs

A

Cox-2 inhibitors

89
Q

High potency opioid

A

Low does required for desired response

90
Q

Low potency opioid

A

High dose required for desired response - higher the dose, the more side effects

91
Q

What determines the dosage of over the counter NSAIDs?

A

Half-life

92
Q

Corticosteroids

A

Natural hormones produced by adrenal glands under control of hypothalamus - maintain fluid and electrolyte balance

93
Q

Cushing’s syndrome complications of excess use

A
  • Integ - delayed healing, velvet skin of the neck
  • Hypokalemia - K+ deficiency —> muscle weakness
  • MSK - myopathy and osteoporosis
  • Endocrine - hyperglycemia - high glucose levels, increased risk of infection neurological —> vertigo, headache, convulsions
  • Sensory - ophthalmic - glaucoma risk
  • Growth suppression
94
Q

What are DMARDs?

A

Disease specific modifying drugs - they inhibit immune system

95
Q

How do local aesthetics work?

A

By blocking peripheral nerve transporting the pain signal

96
Q

Neuropathic pain agents

A
  • Developed for treatment of seizure and depression
  • Increasingly used in management of chronic pain in place of opioids
97
Q

Muscle relaxers

A
  • Antispasmodic agents
  • Reduce muscle guarding and spasm due to MSK injury
98
Q

How can anticoagulants impact PT care?

A

Increased risk of bleeding/bruising; caution with manual therapy

99
Q

How would Hyperlipidemia meds impact PT care?

A
  • Myalgias
  • Myositis
  • Weakness
  • Paresthesias
  • Mimic MSK conditions
100
Q

How would cardiac medications impact PT care?

A
  • Suppression of normal HR, BP response to exercise
  • Require HR and BP throughout treatment
101
Q

How can anti-diabetic medications impact PT care?

A
  • Lower blood glucose levels
  • Synthetic insulin - supplement deficiency
  • Monitor blood glucose levels
102
Q

Symptoms of hypoglycemia

A
  • Sweating
  • Shaky
  • Irritability
  • Confusion
  • Rapid heart rate
  • Maybe hunger
103
Q

What do you do if a patient becomes hypoglycemic?

A

Provide glucose

104
Q

How do antidepressants impact PT care?

A
  • Time lag to effects
  • Increased depression during initial treatment
  • Mood changes
105
Q

How do antianxiety medications impact PT care?

A

Treat symptoms, not cause —> sedation

MSK Unit 2 (12 decks)

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