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Internal Med > Tissue Healing and Repair > Flashcards

Tissue Healing and Repair Flashcards

1
Q

Outcomes of acute inflammation

A
  • resolution (healed/normal)
  • chronic inflammation (progression from acute)
  • healed by fibrosis; NOT good, results in excessive fibrinogen and collagen that lessen the function of the area
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2
Q

Fibronectin

A

component of tissue healing

scaffold, tensile strengths, glues substances together

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3
Q

Proteoglycans

A

component of tissue healing

contains carbohydrates and sugars

secreted by fibroblasts early during the reaction

scaffolding and binds to growth factors

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4
Q

Elastin

A

becomes cross-linked to form fibrils or long sheets that provide tissue with elasticity

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5
Q

Collagen

A

structural support and tensile strength for almost all tissues and organs of body

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6
Q

What do mutations in collagen gene cause?

A

wide spectrum of diseases of bone, cartilage and blood vessels

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7
Q

Collagen type 1

A

predominant structural collagen of the body, 80-85% dermal collagen, scars, tendon, bone, dentin (teeth), joints; labrum

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8
Q

Collagen type 2

A

Predominant component of physis (growth plate) and hyaline cartilage (outer ear, nose), nucleus pulposus external annulus, labrum

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9
Q

Collagen type 3

A

vascular and visceral structures (blood vessels, GI tract, liver, uterus), other 15-20% dermal collagen, embryonic tissues

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10
Q

Collagen type 4

A

basement membranes (especially those in the developing fetus), glomeruli of kidney nephron

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11
Q

What collagen type is first deposited in wound healing

A

3

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12
Q

How does the type of tissue impact the healing process?

A

local blood supply is vital to bringing necessary materials and certain tissues (tendons, ligaments and cartilage) have a decreased blood supply, this the healing process may require additional time

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13
Q

What are growth factors

A

GFs are proteins that regulate cell proliferation, differentiation and migration

they do biosynthesis and degradation of proteins and angiogenesis (new blood cells made for the tissue)

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14
Q

Where are GFs found (give two specific examples)

A

they are produced by cells involved in the tissue repair response

platelets, fibroblasts, endothelial cells and macrophages (look these all come during inflammation response)

platelet-derived GF; platelet-rich plasma injected that speeds up healing process

fibroblast GF; proliferation of fibrogen and collagen

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15
Q

What is often the cause of chronic tissue injury and how as PTs should we treat it?

A

often causes by repeated stresses of moderate magnitude (back pain, tendinopathies, impingement, carpal tunnel)

identify and modify factors

  • movement and alignment
  • extrinsic factors (footwear, gravity)
  • others; psychosocial, medications, age, obseity
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16
Q

Phase 1 tissue healing

A

Homeostasis and degeneration

  • immediate
  • stop bleeding by initiating coagulation
  • platelets release GFs that summon inflammatory cells
  • degeneration phase; forms hematoma, necrosis of dead cells and starts inflammation
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17
Q

Phase 2 tissue healing

A

inflammation

  • inactivate injurious agents, break down and remove dead cells, initiate healing
  • replace injured tissue with healthy regenerated tissue, fibrous scar or both
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18
Q

Phase 3 tissue healing

A

Proliferation and migration

  • endothelial cells nearby proliferate to establish vascular network to transport oxygen and nutrients to support healing tissue
  • neurovascularization and angiogenesis
  • healing tissue called granulation tissue bc appearance is reddish granular layer of tissue

main cellular components; endothelia cells and fibroblasts

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19
Q

Phase 4 tissue healing

A
  1. tissue contraction
  2. contracture
  3. tissue regeneration
  4. tissue repair (scar tissue)
  5. special mention; chronic wounds
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20
Q
  1. Tissue contraction
A

(shrinking the wound)

newly formed extracellular matrix shrinks (contracts) the healing tissue

fibroblasts differentiate into myocytes (myofibroblasts) that contribute to shrinkage

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21
Q
  1. Contracture
A

joint contracture - abnormal shortening of tendons/ligaments (common in knees)

excessive shrinkage of healing tissue occurs

can limit mobility and organ function (can be disfiguring like burns healing)

prolonged immobilization or reconstructions can cause **arthrofibrosis - scarring that restricts and a thickened fibrotic capsule inhibits motion

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22
Q
  1. Tissue regeneration (what type of cells are involved)
A

process of replacement of dead parenchymal cells (primary fxn cells) by new cells to restore normal tissue fxn (parenchymal cells; functional tissue of a morbid growth)

only occurs if parenchymal cells can undergo mitosis (three different cell types)

  • permanent; regeneration does not occur and tissue can not divide, long-lived and irreplaceable (ex; cardiac myocytes or neurons)
  • labile; divide continuously
  • stable; normally do not divide but can be induced to undergo mitosis with appropriate stimulus
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23
Q
  1. Tissue repair - scar formation
A
  • when the cut, incision, damage, or trauma extends beneath the surface layer (epidermis)
  • structural integrity of the parenchymal (functional organ cells) tissue depends on the formation of connective tissue scar

important to minimize scare not just for cosmetics but bc they can interfere with organ function

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24
Q

Primary, Secondary and tertiary wound healing

A
  • primary; inital union of the edges of wound, progressing to complete healing without granulation
  • secondary; wound closure when edges are separated, granulation tissue fills gap and epithelium grows over granulation = scar
  • tertiary; granulation fills gap between edges, epithelium grows over granulation at a slower rate and produces larger scar (often suppuration, pus)
25
Q
  1. Chronic wounds (what are they and why do they happen?)
A

chronic wounds happen when wounds fail to heal normally and remain in the inflammatory and proliferative phases

possibly because the wrong biochemicals are present in the wrong amounts at the wrong time and fail to function effectively, or a deficiency in endogenous GFs responsible for stimulation cell migration, proliferation and extracellular matrix deposition

26
Q

What factors does tissue repair rely on

A
  • type of cell (permanet, liable, stable)
  • type of damage (lethal, sublethal)
  • other factors; nutrition, age, immunocompentency, vascualr supply, infection)
27
Q

Tissue repair: Lung

A

after lethal injury to alveolar cells, regeneration can occur only when the basement membrane remains in tact

if damage disrupts basement membrane, healing must be achieved by repair (fibrosis and scar formation - epithelial cells that may be dysfunctional)

certain injurious agents (asbestos) trigger the formation of scar tissue, leading to restrictive lung disease

28
Q

Tissue repair: Digestive tract

A
  • gut cells slough off into the inestinal tract and pass out of the body every 5 days or so
  • damages or injured cells are constantly leaving whereas healthy cells renew the GI
  • 3-4 weeks for complete turnover of gut cells
  • 2/3rds immune fxn and 90% of serotonin function take place in gut
29
Q

Tissue Repair; Peripheral nerves

A
  • when a nerve is cut, the peripheral portion rapidly undergoes a myelin degeneration and axonal fragmentation
  • within 24 hours, new axonal sprouts from the central stump are observed
  • microsurgical approximation (surgery to realign ends of nerves so they can rgow back together) of the nerve may result in re-innervation (aka successful nerve fxn again), especially those with gaps less then 3 mm (greater gaps it may not be possible)
  • the most important factor in achieving successful nerve regeneration after repair is the maintenance of the microtubules (basement membrane and connective tissue endoneurium/structural support) along which the new axonal sprouts can pass

-

30
Q

Skeletal muscles tissue regeneration

A

muscle tissue can regenerate, but restoration of normal structure and fxn is strongly dependent on the type of injury sustained

after transection, muscle fibers regenerate or growth of new independent fibers

contused or strained muscle is capable of self-repair, but the healing process is slow and often incomplete, = loss of strength and a high rate of reinjury at the site of the index injury

31
Q

Bone tissue types

A

80% cortical
20% cancellous bone (spongy intermeshing thin plates that are in contact with the bone marrow)

32
Q

When does loss of bone occur

A
  • an imbalance between destruction and production of bone cells
  • defective mineralization of bone matrix
33
Q

Bone fracture healing and repair

A
  1. immediate hematoma and inflammation
  2. granulation tissue and fibrocartilage formation

*reparative phase (6-12 weeks) - formation of soft callus around 2 weeks after injury

  1. ENCHONDRAL OSSIFICATION; fibrocartilaginous union (soft callus) is replaced by a fibrosseous union (bony callus)
  2. remodeling phase begins with no movement at site, with complete restoration of the medullary canal with mature lamellar bone

in the normal adult skeleton, approx, 10-30% of bone is replaced or remodeled to replace microfractures from stress and maintain mineral balance

34
Q

Factors that affect bone healing *

A
  • types of bone involved
  • fracture site and type
  • the treatment required (immobilization vs surgical repair, grafting)
    degree of soft tissue injury
    treatment complications
    other factors (vascular supply, nutritional status or immunocompetency)
35
Q

Tendon and ligament composition

A

78% water, 20% collagen 2% glycosaminoglycans

viscoeleastic characterisitcs can take compressive force

parallel fibers of type 1 collagen, small vascular supply,l snesory innervation

36
Q

What conditions may a tendon heal?

A
  1. proliferation of tenoblasts from the cut ends of the tendon

2, vascular ingrowth and proliferation of fibroblasts derived from the surrounding tissues

37
Q

Tendon healing porcess

A
  • HOMEOSTASIS PHASE begins immediately
  • INFLAMMATION PHASE during first 72 hours after injury or surgery
  • PROLIFERATION PHASE starts as early as 48 hrs after injury to 2-3 weeks after
  • 2 weeks into healing, collagen fibrils orient into thick bundles = strength (but immature and weak)
  • affected area remains immobilized to relieve stress and prevent re-ruptures and crosslinks
  • MATURATION / REMODELING PHASE around week 3; immature type 3 collagen replaced by mature type 1, aligns to lines of stress produced by the motion

scar tissue is weaker (more minor collagen types and decreased cross-links) causing impaired fxn, chance of reinjury and risk of osteoarthritis

38
Q

How many weeks for tendons and ligaments to regain normal strength after injury?

A

40-50 weeks

39
Q

Tendinopathy

A

a term used to denote clinical conditions with pain and pathologic changes

  1. tendinitis; implying an inflammatory process
  2. tendinosis; degenerative process with little or no inflammation but histopathologic changes in collagen matrix
40
Q

Chronic tendon disorders

A
  • overuse and chronic overload with repetitive microtrauma are the most common etiologic risk factors
41
Q

Ligament injury and healing

A
  • in many extraarticular ligaments (MCL), healing occurs by same process as tendons
  • some INTRAARTICULAR ligaments (ACL) have poor healing response
  • remodeling phase; continuous cycel of collagen synthesis and degradation (can take months to years), replacement tissue similar to scar tissue and does not have same properties of normal ligament
42
Q

Factors affecting ligament healing

A
  • the quality of the repaired tissue depends on load and stresses subjected to the ligament during the healing process (returning to sports too soon, too little load brought by prolonged immobilization)
  • NSAIDs have potential hindrance to heling and should be used judiciously
43
Q

Characteristics of Cartilage

A

aneural, avascular, alymphatic

44
Q

Types of Cartilage

A

articular (hyaline) - joint surfaces, bone apophyses; epiphyseal plates; costal cartilage (ribs); fetal skeleton

elastic - trachea (epiglottis); earlobe; ligamentum flavum

45
Q

articular (hyaline) cartilage

A

articular (hyaline) - joint surfaces, bone apophyses; epiphyseal plates; costal cartilage (ribs); fetal skeleton

46
Q

fibrocartilage

A

fibrocartilage - tendon and ligament insertion; meniscus; disc

47
Q

elastic cartilage

A

elastic - trachea (epiglottis); earlobe; ligamentum flavum

48
Q

fibroelastic cartilage

A

meniscus

49
Q

Cartilage healing

A

in adults without intervention, healing of articular cartilage occurs by fibrous scar tissue or fails to heal at all

fibrous scarring of the articular cartilage leads to local degenerative arthritis

50
Q

Menisci (knee) composition and development

A
  • fibrocartilaginous, 90% type 1 collagen
  • at birth, entire meniscus is vascular, by 9 inner 1/3 becomes avascular, by adulthood, outer 10-30% of vascularity remains

nerve fibers radiate into the outer 1/3 of the menisci

51
Q

Menisci tear (common causes and symptoms)

A

laceration causes; injury, degeneration

symptoms; pain, swelling, locking and catching, loss of motion

52
Q

Meniscal tears healing

A

heal by migration of cells from the synovial membrane adjacent to the meniscus (unknown mechanism)

management depends on type of tear and its location

meniscectomies - (surgery to remove damaged part) = biomechanical function alterations = alterations in normal loading mechanism of joint = increasing risk of osteoarthritic

53
Q

What are the two components of the synovial membrane

A

intimal (cellular layer of synoviocytes) layer next to the joint space

subintimal or supportive layer made of fibrous and adipose tissue

54
Q

Results of injuries to synovial membranes and other conditions

A

injury results in; hemorrhage, hypertrophy, hyperplasia of synovial lining and mild chronic inflammation

any type of immobilization leads to contraction of the capsule

synovial lining hypertrophies and forms adhesions between itself an adjacent articular cartilage

55
Q

Disc

A

outer third of annulus is innervated and blood supply restricted to peripheral outer annulus

56
Q

What is the source of people with low back pain

A

annulus

57
Q

Disc degeneration

A

cell senescence (inability to proliferate) is linked with degenerative disease, mostly in nucleus pulposus

  • nucleus pulposus begins to lose ability to absorb water
  • disc becomes dehydrated and then thick and fibrous
  • not able to absorb shock as well
  • tears called fissures form around the annulus
58
Q

Factors that impact disc healing

A
  • continued compressive forces to spine due to inactivity, weight gain, poor posture and poor tone of the muscles supporting the spine
  • changes in the extracellular matrix content affecting collagen fibers can reduce discs load-bearing capacity
  • calcification of the vertebral end plates is another factors thought to contribute to disc degeneration

Internal Med (15 decks)

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