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Kin 2236 Athletic Injuries > Lecture 5: Tissue Types and Healing > Flashcards

Lecture 5: Tissue Types and Healing Flashcards

1
Q

Why don’t we use the term acute anymore?

A

B/c all injuries are technically acute because something initiates them

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2
Q

Chronic injury

A

At some point, if injuries don’t heal, they are called chronic

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3
Q

Traumatic injuries

A

aka acute

  • occur SUDDENLY and have a clearly DEFINED cause or ONSET (know exactly then it happened)
  • occur when tissue loading is enough to cause sudden IRREVERSIBLE deformation of the tissue
  • usually in high speed sports with or without contact
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4
Q

Overuse injuries

A
  • occur slowly over time (secondary to repetitive movement)
  • repeated overloading can accumulate over time to exceed tissue threshold (even if individual incidences don’t cause injury)
  • in aerobic sports that need long training schedules or in technical sports where a movement is repeated many times
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5
Q

Extrinsic/External Injury Factors

A
  • makes us SUSCEPTIBLE
  • originating outside the anatomical limits of tissue/person
  • ex. increased training duration, increase in FITT, not enough rest, inappropriate shoes, field conditions
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6
Q

Intrinsic vs Extrinsic Factors

Not enough rest

A

Extrinsic – could be due to practice too much or too much school

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7
Q

Intrinsic/Internal Injury Factors

A
  • PREDISPOSES us to injury
  • belonging to or lying within a given part person/tissue
  • ex. flat feet, knee alignment, tight hamstrings
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8
Q

Muscle Characteristics

A
  • contractile tissue with main function to generate power
  • well vascularized = good O2 and nutrients; good for healing; bleeds lots
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9
Q

What structures are affected by strains?

A

Muscle

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10
Q

What structures are affected by contusions?

A

Muscle
Bone
Cartilage

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11
Q

What structures are affected by sprains?

A

Ligaments

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12
Q

What structures are affected by ruptures?

A

Muscle
Ligament
Tendon

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13
Q

What structures are affected by lacerations?

A

Muscle
Ligament
Tendon

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14
Q

What structures are affected by fractures?

A

Bones

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15
Q

What structures are affected by tendonosis/itis?

A

Tendons

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16
Q

Things to consider with strains

A
  • % of fibres torn
  • ability to move through range - stretch
  • Oxford Scale (strength generated out of 5)
  • pain – sometimes more is better (no pain could mean worse tear)
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17
Q

Oxford Scale

A

Grading Muscle STRENGTH
Out of 5

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18
Q

Oxford Scale
Grade 5

A

Normal

  • Full strength
  • can resist throughout available range compared to other side
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19
Q

Oxford Scale
Grade 4

A

Good

Near full strength through available range when compared to other side

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20
Q

Oxford Scale
Grade 3

A

FAIR

Full R.O.M against gravity only
- can’t take any resistance

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21
Q

Oxford Scale
Grade 2

A

Poor

Can complete full available range with GRAVITY ELIMINATED
- to eliminate gravity: change plane of movement (ex. biceps - go lateral to medial instead of up and down)

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22
Q

Oxford Scale
Grade 1

A

Trace

Able to palpate (feel) muscle contraction when patient tries to contract

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23
Q

Oxford Scale
Grade 0

A

Nothing happens when patient tries to contract

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24
Q

Isometric Contraction

A

muscle contraction where length of muscle is CONSTANT

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25
Q

Concentric Contraction

A

muscle SHORTENS while contracting against resistance

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26
Q

Eccentric Contraction

A

muscle LENGTHENES while contracting against resistance
- greater risk of injury

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27
Q

How do muscle injuries generally happen?

A
  1. Distension (strains/pulled muscle)
  2. Direct trauma (contusion/laceration)
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28
Q

Muscle strains

A
  • usually happen at musculotendinous junction
  • more common in 2 jt. msucle (sart
  • strains happen due to forcible stretching of a muscle (either passively or when muscle is activated)
  • active contraction + passive stretch = STRAIN
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29
Q

Ecchymosis

A

Bruising from strains (b/c muscle is well vascularized)

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30
Q

Grade I Strain

A
  • usually 10-20% of muscle fibres torn/stretched
  • near full ROM w/ some discomfort near the end
  • good strength (4-5 on Oxford scale)
  • slight pain/discomfort
  • no palpable divot
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31
Q

Grade II Strain

A
  • usually 20-80% of fibres torn
  • significant DECREASE in ROM with discomfort near end
  • poor strength (50% or 2-3 on Oxford scale)
  • significant pain/discomfort
  • can have palpable divot
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32
Q

Grade III Strain

A
  • 80%+ of fibres torn to complete rupture
  • Poor range of motion
  • Poor strength (0-1 on Oxford scale)
  • variable pain (complete rupture = no tension on muscle = no pain b/c no attachment)
  • initial pain
  • large gap or muscle retraction
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33
Q

Muscle Contusions

A

Bruising
- can be any muscle (most common in quads)
- ecchymosis is common due to vascularity of muscles
- all result in internal bleeding
- can be intramuscular or intermuscular

34
Q

Intramuscular contusions

A
  • NO injury to FASCIA = blood trapped in muscle
  • significantly LONGER HEALING TIME
  • increased compartment pressure = decreased flow/O2/nutrients
  • chemical irritation (pain due to acidity of blood)
35
Q

Intermuscular contusions

A
  • fascia is injured
  • blood flows out btwn muscles = ecchymosis faster
  • HEALS FASTER (no increased pressure = more blood flow, increased healing)
  • blood can be absorbed (no irritation)
36
Q

Characteristics of Tendons

A
  • connective tissue that attaches muscle to bone
  • function: transfer force from muscle to skeleton
  • 65-80% Type I collagen (less elastin than ligaments)
  • arranged into parallel bundles of different sizes
37
Q

Overuse Tendon Injuries

A

Tendinitis
Tenosynovitis
Paratenonitis
Tendinosis
Bursitis
Periotitis

38
Q

Traumatic Tendon Injuries

A

hot, red and painful = inflmaed

laceration (skate)
penetrating injury (stab)
rupture (Achilles, quads)
acute tendon strain/tear
- tendonitis

39
Q

Tendinitis

A
  • inflammation of the tendon
  • acute inflammation

relatively rare and over diagnosed

40
Q

Paratenonitis

A

inflammation, pain and crepitation of the paratenon as it slides over the structure

41
Q

Acute irritation of the tendon is usually triggered by

A

Extrinsic Factors: rub from equipment, “too much, too soon”, increase in FITT

Intrinsic Factors: rub over bone

42
Q

Tendinopathy

A

general term used to refer to pain and reduced function in tendons
- could be traumatic or overuse injury

43
Q

Tendinitis to Tendinosis

A

over time, tendinitis –> tendinosis

If repetitive overuse continues and an inflamed/irritated tendon fails to heal, the tendon begins to degenerate

Primary concern changes from tendon inflammation to tendon degeneration = tendinosis

44
Q

Tendinosis

A
  • chronic pathological changes due to repetitive micro-trauma (no time to heal = breakdown)
  • NO inflammatory cells
  • characteristic changes in collagen fibre structure
  • abnormal vascularity
45
Q

Tendinosis Collagen Changes

A

Normal tendon
- collagen fibres lined up
- many nuclei

Tendinosis (breaks down faster)
- collagen fibre disarray (not lined up)
- loss of parallel bundles
- fewer cell nuclei

46
Q

Tendinosis Vascular Changes

A

Normal tendon
- well-developed, evenly spaced vasculature

Tendinosis (not evenly spaced)
- hyper vascularity
- increased # of poor-quality blood vessels (neovascularization)

47
Q

Characteristics of Ligaments

A
  • connect one bone to another
  • made predominantly of collagen (higher amount of elastin than tendons
  • passive stabilizers
  • usually TRAUMATIC mechanism of injury
  • well innervated = position, movement and pain (very important for proprioception and rehab)
48
Q

Types of Ligaments

A

Intra-articular
Capsular
Extra-capsular

49
Q

Intra-articular ligaments

A

inside a jt or jt capsule
- total rupture will NOT heal
- blood supply from ends - minimal to middle portion
- ex. ACL

50
Q

Capsular ligaments

A

Ligament projects as a thickening of a jt. capsule
- total rupture = excellent healing
- good blood supply
- ex. MCL, ATFL (anterior talofibular lig.)

51
Q

Extra-capsular ligaments

A

Outside of jt. capsule
- similar to intra-articular
- unlikely to heal total ruptures w/o surgery
- ex. LCL, CFL (calcaneofibular lig)

52
Q

Structure/morphology of ligaments

A
  • wave or crimp across ligament
  • built into structure of ligament
  • injury cam be closely correlated to load-deformation curve
  • 3 phases of curve
53
Q

3 phases of ligament curve

A
  1. Toe region
  2. Linear region
  3. Rupture region
54
Q

Toe Region and Early Linear Region

A

Ligaments (stress vs strain curve)

  • initial concave region
  • represents normal physiological range of strain = 0-2% of length (crimp stays the same)

Early Linear Region = 2-4% of length
- due to flattening of crimp

Repeated cycling of stretch in this range is reversible

55
Q

Late Linear Region

A

Ligaments

  • pathological IRREVERSIBLE ligament elongation
  • will see tears in ligament as cross-links are disrupted
  • early part = mild/grade 1 sprain (<50% torn)
  • 2nd part = grade 2 sprain (50-80% torn and obvious laxity)
56
Q

Rupture Region

A

Ligaments

  • failure point at about 10%
  • complete rupture
  • grade 3
  • decreased pain (if totally torn)
57
Q

Things to consider with sprains

A
  • % of fibres torn
  • ability to move through range - stretch
  • laxity on testing and end point
  • pain (sometimes more is better)
58
Q

Grade I Sprain

A
  • full ROM
  • slight pain
  • NO jt. laxity (good stability)
  • has an endpoint
59
Q

Grade II Sprain

A
  • significant loss of ROM
  • significant pain on palpation
  • SOME jt. laxity
  • has an endpoint
60
Q

Grade III Sprain

A
  • loss of motion (swollen)
  • pain of palpation (variable)
  • GROSS laxity
  • has NO endpoint
61
Q

Open Fractures

A

aka Compound fractures

  • bone breaks through surrounding tissue
  • usually a medical emergency
62
Q

Closed Fractures

A

aka Simple fractures

  • little or no displacement of bone through surrounding tissue
63
Q

Greenstick fractures

A

incomplete fracture

common in CHILDREN

64
Q

How to tell btwn a fracture and contusion?

A

Direct pressure = pain w/ contusion and fracture

Indirect pressure = pain with fracture (ex. fractured hand, pushing down on finger would tell; fractured fibula would be shown by pressure from rotating ankle)

65
Q

Phases of Healing

A
  1. Inflammatory Phase
  2. Repair Phase
  3. Remodeling Phase
66
Q

Inflammatory Phase

A

Phase 1 of Healing

  • days 1 - 4 on injury
  • cellular injury = altered metabolism + release of chemical mediators/proteins
    • cause inflammatory response
67
Q

Repair Phase

A

Phase 2 of Healing

  • day 4 to 6 weeks after injury
  • lay tissue down and repair
68
Q

Remodeling Phase

A

Phase 3 of Healing

  • week 6 to 2/3 years after injury
69
Q

Primary Damage

A
  • damage at a time of injury (immediately irreversible)
70
Q

Secondary Damage

A
  • damaged by released proteins (in tissues around)
  • damage as a result of body processes (edema, damage due to decreased blood flow, decreased oxygen)
71
Q

Steps of Injury

A
  1. Injury to cell
  2. Chemical mediators liberated (histamines, leukotrienes, cytokines)
  3. vascular rxns. (vascontsriction -> vasodilation/hyperemia -> exudate -> creates stasis)
  4. Margination (platelets and leukocytes (neutrophils) adhere to vascular wall)
  5. Diapedesis
  6. Phagocytosis
  7. Clot Formation
72
Q

Histamines

A

cause vasodilation and cell permeabilitu

73
Q

Leukotrines

A

responsible for margination/diapedesis
- stuff moving out of capillaries to tissue

74
Q

Cytokines

A

helps attract phagocytes to remove waste from tissue

75
Q

Diapedesis

A

Passage of fluid, proteins and neutrophils through cell wall

Forms exudate (fluid matrix where healing can start)

76
Q

Signs/Symptoms of Inflammation

A
  • redness
  • swelling (b/c of exudate)
  • pain
  • local heat
  • loss of function
77
Q

Cycle of injury

A

pain, muscle spasm and ischemia increases the possibility of atrophy over time

Stop one and stop the rest

78
Q

Repair (Fibroblastic) Phase

A
  • 72 hours to 6 weeks
  • proliferative and regenerative healing = formation of connective tissue repair and repair of injured tissue
  • fibroplasia begins within the first few days and inflammatory signs should decrease
  • growth of endothelial capillary buds into wound is stimulated by lack of O2 (new growth allows increased O2 and blood flow)
  • body lays down Type 3 collagen (not as good as Type I)
  • weak tensile strengtjh
79
Q

Remodeling/Maturation Phase

A
  • usually firm, strong non-vascular scar by end of 3 weeks
  • long-term process (6 weeks to years)
  • increased stress and strain = collagen changes to type I and begins realignment
  • critical that injured structures be exposed to progressively increasing loads (work up to aggressive AROM and strengthening to facilitate remodeling and realignment)
  • watch out for pain and swelling post-exercise
80
Q

Wolf’s Law

A

Remodeling/Maturation phase

bone and soft tissue will respond to they physical demands placed on them = they will align

Kin 2236 Athletic Injuries (20 decks)

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