Unit 2 Weeks 5 MSK Flashcards

1
Q

What are the 4 phases of healing

A
  1. Hemostasis: stops bleeding
  2. Inflammation: prepares for healing
  3. Proliferation: rebuild
  4. Remodeling: strengthen scar tissue
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2
Q

Hemostasis Phase

A

Stops bleeding
- 0 to 6-8 hours
- MSK, CT, and blood vessels are damaged –> cellular cascade happens leading to local vasoconstriction
–> clot formation –> which then stimulates platelet formation of fibrin
–> Fibroblasts drawn to the area by growth factors to repair

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3
Q

Inflammatory Phase

A
  • Cleans up the wound site - and prepares the site for construction of new tissues
  • 0 to 2 weeks : peaks at 2-3 hours
  • This phase is stimulated by chemical mediators of the bleeding stage
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4
Q

What are the prominent Inflammatory mediators:

A

Histamines
Bradykinin
Serotonin
Lymphokines
Prostaglandins
leukotrienes
Arachidonic Acid

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5
Q

Diapedesis Vs. Chemotaxis

A
  • Diapedesis= cells (leukocytes, neutrophils, macrophages ect) squeeze through gaps in the capillary wall to get to where they need to go
  • Chemotaxis = signaled by chemical agents in the area and they go to the injury site
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6
Q

Clinical signs of inflammation

A
  • Rubor
  • Calor
  • Swelling
  • Dolor
  • functional loss
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7
Q

What is the Inflammatory Resolution

A
  1. Neutrophils apoptosis= as cells die they trigger more inflammation and more WBU influx which continues inflammation –> fibrosis and chronic inflammation –> the dead stuff needs to be cleared for inflammation to stop
  2. Macrophages gobble up dying cells and stop noxious stuff leaking from them that keeps inflammation going
  3. Macrophages then switch jobs to secreting an anti-inflammatory cytokine and suppresses release of pro-inflammation mediators and helps regenerate tissue or they leave the scene
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8
Q

What are some external factors that may affect inflammatory phase

A
  1. NSAIDS= can delay or hamper healing in musculoskeletal tissue, including muscle, tendons, cartilage and bone. Inflammation is necessary step for healing and transition to proliferative phase
  2. Repetitive of forceful tasks can 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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9
Q

What is the protective phase of rehab?

A
  • Control pain, edema, and inflammation
  • restore full PROM , prevent atrophy, maintain soft tissue joint integrity
  • Enhance function
  • PRICEMEM
    Protection
    Rest
    Ice
    Compression
    Elevation
    Manual Therapy
    Early motion
    Medications
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10
Q

Proliferative Phase

A
  • Rebuild damaged structures and strengthen the wound
    -4-22 days: peak 2-3 weeks
  • After phagocytes clear the injured area the construction begins
  • Tissue Healing Process in 2 ways
    1. Regeneration- regrowth of original tissue
    2. Repair- formation of a Connective tissue scar
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11
Q

What are the 4 Simultaneous processes of the Proliferative phase?

A
  1. Epithelialization= reestablishes the epidermis - occurs when skin is involved this doesn’t happen internally or with a ligament repair
  2. Collagen production= limited tensile strength
    –> Type 3 collagen has limited tensile strength and over time will be replaced by type 1
    –>Excessive scarring may affect the outcome
  3. Wound Contraction = if uncontrolled contractures may result
  4. Neovascularization = New blood vessels within 4 days
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12
Q

What are the Clinical Signs During Proliferative phase

A
  1. Decrease in pain
  2. Erythema Resolved
  3. No active effusion, those residual swelling may persist
  4. Increase in pain free active and passive ROM
  5. With passive movements pain is felt at the point of tissues resistance
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13
Q

True/False In the proliferative phase you want to transition from passive interventions toward progressive stress of tissue

A

True

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14
Q

What is the 3 step process of mechanotransudction when loading a tissue to help it heal

A
  • Process where MSK tissue convert mechanical load into a cellular response t build up those tissues
    1. Mechanocoupling: “mechanical trigger or catalyst
    2. Cell to cell communication “ distribution of the message
    3. Effector cell response: the tissue factory that produces and assembles
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15
Q

List the therapeutic exercise progression from Low to high

A
  1. Submaximal Isometrics
  2. Small arc submaximal concentric/eccentric pain free ROM
  3. Full ROM submaximal concentric
  4. Full ROM submaximal eccentric
  5. Functional/actively specific plane submaximal concentric
  6. Functional ROM submaximal eccentric
  7. OKC and CKC exercises concentrically then eccentrically
  8. Full ROM submaximal concentric isokinetic
  9. Full ROM submaximal eccentric isokinetic
  10. Functional ROM submaximal eccentric isokinetic
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16
Q

Remodeling phase

A

Modify the scar tissue into its mature form
- Toward the end of proliferative phase it goes full swing
- Few days to a few years
- Longest phase
- Process of collagen turnover- reabsorption and deposition
- Fibroblasts synthesize, deposit, and remodel ECM
- Myofibroblasts pull the wound edges together to contract the wound

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17
Q
  1. During the remodeling phase: at 3 weeks what is the tissue strength?
  2. At 3 months?
  3. What percentage of tensile strength will the scar be at after it is done in remodeling?
A
  1. 30%
  2. 80%
  3. The tissue will NEVER be 100% it will only go to 80% of the original strength
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18
Q

What are the clinical signs during the remodeling phase?

A
  • Progression to pain free function and activity
  • Pain felt at end range of passive movement after tissue resistance is met
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19
Q

What is Chronic Inflammation?

A

Failure to achieve healing through the natural phases
- How to manage it: 1. Address symptoms 2. Discover the root cause

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20
Q

What are the LOCAL factors affecting healing?

A
  • Type, size, location or injury
  • Infection
  • Vascular supply
  • External forces: thermal agents, electromagnetic, mechanical pressure
  • Movement: Early/later
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21
Q

What are the SYSTEMIC factors affecting healing?

A
  • Age
  • Disease or infection: diabetes/autoimmune
  • Medications: antibiotics/corticosteroids
  • Nutrition
  • Hormones
  • Fever
  • Oxygen
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22
Q

What are the Low to high potential of healing of the 6 different tissues

A
  1. Cartilage
  2. Meniscus/disc
    3.Ligament
  3. Tendon
  4. Bone
  5. Muscle
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23
Q

What are the 3 phases of healing and the time frames

A

Acute Phase: 7-10 days
Subacute Phase: 10 days-6 weeks
Chronic: 6 weeks - months

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24
Q

What is myotendinous Junction?

A

Muscle proper is merging with tendon

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25
Q

Basal Lamina

A

Serves as scaffolding for healing

26
Q

Satellite cells

A

Muscle stem cells that help with regeneration and rebuilding of the muscle

27
Q

Muscle Phases of healing

A
  1. Destruction phase
  2. Repair phase
  3. Remodeling Phase
28
Q

What is the Destruction Phase of muscle healing

A
  • Necrosis of damaged muscle tissue
  • Factors released, start hemostasis and inflammation response
  • Vascular disruption- hematoma and edema begin
  • Leukocytes infiltrate and activation/proliferation of satellite cells
29
Q

What is the repair phase of Muscle Healing

A
  • Hematoma formed
  • Inflammation cells arrived and satellite cells proliferation continues
  • New myofibers are formed
  • Neuromuscular junction reestablished
30
Q

What is the remodeling phase of muscle healing

A
  • Regenerated tissue matures and tensile strength increases
  • Scar contracts and is reorganized
  • Type 1 returns to normal proportion over type III
31
Q

What is a muscle strain?
What are the risk factors?

A
  1. It is excess pull or overstretch on a muscle: damages at the MT junction with immediate pain
  2. Risk factors include
    - Inadequate flexibility
    - Inadequate strength or endurance
    - Muscle imbalances
    - Insufficient warm up or fatigue
    - Inadequate rehab from past injury
32
Q

What happens during a Eccentric strain?

A

There is damage to sarcomere, disrupts ECM, intramuscular edema, increased creatinine kinase ( creatine kinase= signals muscle breakdown)
- Force eccentric reduction of 50-65% in 1-2 weeks

33
Q

What happens during a concentric strain?

A
  • Nothing like eccentric in the fact that there isn’t damage to the sarcomere ect.
  • Force concentric reduction is 10-30% hours after**
34
Q

Grade 1 Strain

A
  • Tear only a few musculotendinous fibers
  • Pain only with limited swelling
  • No function loss
35
Q

Grade 2 strain

A
  • Disruption of moderate number of fibers
  • Increased pain
  • Some loss of strength and function
36
Q

Grade 3 strain

A
  • Complete rupture of some musculotendinous units
  • Loss of function with little pain
  • MT junction site
37
Q

What are the Clinical signs of Muscle Injury?

A
  1. Almost always sudden onset/traumatic
  2. Pain most pronounced during eccentric activation
  3. Localized tenderness over myotendinous junction
  4. Possible swelling and ecchymosis
  5. AROM association joints may be restricted and painful
  6. Resisted strength testing; weak and painful
  7. Imaging: radiograph usu and MRI most accurate but not necessary
38
Q

What is the muscle injury management

A
  1. Protective phase: PRICEMEM, AROM, PROM, AAROM
  2. Controlled motion Phase: Submaximal isometrics–> multiangle submaximal isometrics–> multiangle max isometrics –> PREs : simple safe balance, proprioception activities
  3. Return to Function Phase: Endurance and maximizing strength, concentric–> eccentric training / speed agility exercises
  4. Re-injury Prevention: Education on proper warm up, holistic conditioning, maintenance of flexibility, strength
  5. Complications: Immobilization/disuse, reinjury, fibrosis, NSAIDS induce impairment
39
Q

Tendon Anatomy

A
  • Glistening white
  • Parallel fibers
  • Avascular
  • Aneural
40
Q

Positional Tendons vs. Energy Storing Tendon

A
  1. Positional= transmits force from muscle to create movement
  2. energy Storing= Can be put on a lot of stretch and store potential energy: they act like springs to create movement: seen more in bigger muscle groups
41
Q

T/F tendons do not heal rapidly after being injured

A

True
- Tendons has a slower metabolic rate than muscle which makes it have a very low healing process after injury

42
Q

What are intrinsic factors in tendon injury?

A
  • High body weight
  • Malalignments, imbalances, weakness, poor flexibility, poor form
  • Gender
  • Age
43
Q

What are extrinsic factors in tendon injury?

A
  • Excessive volume, speed, magnitude of loading
  • Abrupt change to amount of type of load
  • Poor enviornment conditions
  • Poor equipment
    -Medications
  • Prolonged immobilization
44
Q

Tendinopathy

A
  • Blanket term for tendon conditions arising from overuse
  • Cumulative trauma –> weaken collagen crosslinks –> degrade ECM and vascular elements–> does not follow the traditional phases of healing
  • Only vascular 1/3rd
  • Absent of PG-mediated inflammation
  • Persistent/ recalcitrant
  • Poor healing potential
45
Q

What is the Continuum of Chronic Tendon Injuries

A

Overlapping phases:
1. Stage 1 tendinitis
2. Stage 2 tendinosis
3. Stage 3 Complete rupture
4. Stage 4 Tendinosis with other changes such as fibrosis or calcification

46
Q

Tendinopathy (tendinitis)

A
  • Pain, swelling, dysfunction of tendon
  • No inflammation
  • Most tendinopathy has not PG-mediated inflammation
47
Q

Tendinosis

A
  • Degeneration of tendon structures
  • Tendon is yellow-brown or gray
  • Disorganized fibers
  • Lower resistance to strain
  • Pain isn’t always present
  • 4 Main Histological changes
    1. Angioblast hyperplasia
    2. Disorganized and immature collagen
    3. Hypercellularity and inc ground substance
    4. Vascular hyperplasia and neovascularization
    5. Increased neurochemicals
48
Q

What are the 3 presentations of degeneration?

A
  1. Excess load can lead to reactive tendinopathy which will resolve if load modified
  2. Unmodified load will progress to tendon disrepair which can be brought back load modification
  3. Unchecked will progress to degenerative tendinopathy
49
Q

Clinical signs of tendon injury

A

Localized with little referral beyond tendon
- Strong but painful proportion to resistive load
- Painful wit stretch
- Pain resolves quickly when load withdrawn
- Unusual to be painful without load at night or at rest

50
Q

Opioid Analgesics

A
  • Relieve moderate to severe pain
  • Act on CNS receptors in spinal cord and brain –> reduce transmission of pain receptors signals

Caution:
- increases threshold for noxious stimuli
- Sedation, respiratory depression, bradycardia,
- Orthostatic hypertension
- Cardiac /respiratory arrest
- High risk of dependency

51
Q

NSAIDs

A
  • Nonsteroidal anti-inflammatory Drugs
  • Acute and chronic MSK disorders
  • Block PGs
  • Decrease inflammation
  • Anti-pyretic
  • Anti- thrombotic
52
Q

COX-1 vs COX-2 effects

A

COX-1
- Normal constituent of cells in homeostasis
- GI mucoprotection
- Regulate normal platelet activity
- Renal and vascular homeostasis
- uterine function, embryo implantation

Cox-2
- produced by injured cells
- Produces prostaglandins that mediate pain, inflammation pyresis
- Vasodilation and inhibition of platelet aggregation
- Modulation of platelet aggregation

53
Q

What are the 2 types of NSAIDs

A
  1. Non-selective= COX-1 and COX-2 inhibitors
  2. Selective = COX-2 inhibitors
54
Q

Acetylsalicylic Acid (Aspirin)

A

Inhibits platelet aggregation

55
Q

What are NSAID Adverse Effects

A

Gastric irritation
renal dysfunction
skin reaction
bleeding/bruising
Liver disorders
Bone marrow depression
Perinatal effects
Headache, dizzy, lightheaded ect

56
Q

Acetaminophen

A

Good for OA*****
- It is a pain reducer/fever reducer
NOT AN ANTI-INFLAMMATORY

57
Q

Corticosteroids

A
  • Natural hormones produced by adrenal glands under control of hypothalamus - maintain fluid and electrolyte balance
  • Treat immunological and inflammatory MSK conditions
  • Cushing syndrome could happen by excessive use
  • commonly given as an injection
58
Q

DMARDs

A
  • Rheumatic Disease
  • Inhibits immune system
59
Q

Local Anesthetics

A
  • Block peripheral nerve transporting the pain signal
  • Greater effect on smaller nerves and lesser effect on larger nerves
60
Q

T/F the evidence on muscle relaxers is conflicting

A

True
- Can help reduce muscle guarding/spasm

61
Q
A