Injury and Healing Handout Flashcards

(51 cards)

1
Q

steps in soft tissue healing

A
  1. bleeding, degeneration, disruption (sec-min)
  2. clot formation (min-hrs)
  3. inflammation (min-days)
  4. repair, regeneration (hrs-mos)
  5. remodeling (mo-yrs)
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2
Q

what is the process of bleeding, degeneration & disruption? (timeline)

A

immediately following injury. proteases are released by myofiber degeneration.

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3
Q

what do proteases get released by/do?

A

released by myofiber degeneration. do auto-digestion of damaged tissue; chemotaxis of neutrophils and macrophages to the area.

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4
Q

what does vessel injury cause?

A

it exposes clotting factors and platelets to collagen; activation of complement and kinin, plasmin generation and stimulates platelet degranulation

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5
Q

process of clot formation?

A

min- hrs. clot of fibrin, platelets, red cells, debris. scaffolding for fibroblast repairs.

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6
Q

inflammation process?

A

min-days. protective. eliminate necrotic cells and tissues from insult, initiate repair

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7
Q

cardinal signs of inflammation?

A

heat, redness, swelling, pain, loss of fxn. esp prominent in acute inflammation.

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8
Q

what is acute inflammation?

A

rapid in onset, short duration, lasts mins-days, predominantly neutrophilic leukocyte accumulation

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9
Q

what is chronic inflammation?

A

days to yrs. influx of lymphocytes & monocytes (tissue macrophages), associated vascular proliferation/fibrosis (scarring)

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10
Q

macrophage fxn?

A

induce local inflammatory response. stimulate cytokine release, chemotactic factors from T cells. recruit progenitor and satellite cells

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11
Q

what cytokines do MP stimulate?

A

IL-1, 6, 8 and IGF-1

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12
Q

repair/regeneration process?

A

hours to months.

  1. proliferation
  2. tissue repair by reneration
  3. scar tissue contraction
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13
Q

proliferation process?

A

hours-wks. prolif of surrounding fibroblasts, migration into wound. produce collagen matrix. phagocytes digest. granulation tissue with neovascularization. myofibroblasts contract.

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14
Q

what do phagocytes do?

A

release enzymes to digest exudage, fibrin clot and debris (clot easily disrupted)

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15
Q

granulation tissue modification

A

vascular budding & recanalization restores vasc connections in 3-4 days. granulation tissue bridges gaps days 7-10. spread of area of inflammation and edema into surrounding normal tissue 21 days. 6 weeks back to normal.

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16
Q

labile tissue repair results in?

A

regeneration with complete restoration of form and function. eg bone marrow, most surface epithelia, bones

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17
Q

permanent tissue repair results in?

A

replacement with connective tissue and scar formation. eg skeletal muscles, cartilage.

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18
Q

scar tissue contraction process?

A

after 2 weeks, can withstand typical stresses. 3+ mo near normal strength

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19
Q

remodeling process?

A

months-years. 6 mo fibrils more oriented to lines of stress. 1-2 years = final remodeling

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20
Q

bone healing process?

A
  1. bleeding
  2. clot formation
  3. inflammatory stage
  4. repair stage
  5. remodeling stage
    + variables
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21
Q

bleeding timeline?

A

seconds-minutes

22
Q

clot formation process?

A

minutes-hours. w hematoma formation

23
Q

inflammatory stage process? inhibitors?

A

hours-days. prostaglandin infiltration. fibroblasts lay down stroma. granulation tissue formation. altered by prostaglandin inhibitors, cytotoxic meds.

24
Q

process of infiltration of inflammatory cells and fibroblasts? where?

A

prostaglandin mediated. inflammatory cells = macrophages, monocytes, lymphocytes, PMNs. also fibroblasts. proliferation is under periosteum and in breached medullary canal

25
fibroblasts do what? inhibited by what?
lay down stroma to support vasc growth. inhibited by nicotine.
26
granulation tissue formation includes?
tissue formation + vascular ingrowth and mesenchymal cell migration
27
repair stage of bone takes how long?
1-2 weeks to 3+ mo
28
steps of repair?
1. osteoclasts and osteoblasts invade blood clot 2. collagen matrix forms, osteoid forms soft callus 3. hard callus formation 4. consolidation 5. bony gaps bridged 6-12 mo
29
how do osteoclasts and osteoblasts invade blood clot?
osteoclasts burrow thru debris at fracture line. osteoblasts fill remaining spaces.
30
how does soft callus form?
ostoid (unmineralized, organic portion of bone matrix) is secreted. 2-6 weeks.
31
how is hard callus formed?
4 to 12+ weeks, mineralization of matrix
32
upper vs lower extremity union?
4-6 weeks union for upper extremity. 8-12 weeks for lower.
33
consolidation process?
callus maturation. 12-26 weeks. woven bone becomes laminar bone.
34
remodeling stage process?
1-2 years. thicker lamellae re: stress. reabsorption of under loaded areas. medullary reformation.
35
which deformities remodel better?
angular better than rotational
36
what are some variables in bone healing?
1. bone type (cancellous > cortical) 2. fracture type (spiral > transverse) 3. blood supply (good > poor) 4. age (young > old) 5. general health
37
how does hyaline cartilage heal?
heals with fibrocartilage and fibrous tissue (has inferior weight bearing properties)
38
apophysitis due to?
overuse/repetitive stress of growth plate. irritation, rarely causes avulsion.
39
common location and what they are? treatment?
patellar, calcaneous, hip, elbow. treatment = relative rest.
40
osgood schlatter?
patellar tendon insertion on tibial tubercle
41
sever's?
achilles insertion on calcaneous
42
sinding-larsen-johansson
patellar tendon origin on inferior patellar pole
43
ASIS?
sartorius
44
AIIS?
rectus femoris
45
little leaguer's elbow?
medial epicondyle
46
ankle sprain etiology?
forced ankle inversion
47
ankle sprain exam?
anterior drawer test, squeeze test, external rotation test += suspicious for high ankle sprain
48
squeeze test results?
pain at ankle --> high ankle sprain. pain at knee --> maisonneuve fracture
49
loose bodies etiology? treatment?
usually traumatic, occasionally metaplastic. surgical or observation
50
loose bodies stx?
swelling & locking, or asymptomatic
51
UCL sprain
throwing athletes. valgus stress in 20 degrees of flexion causes pain and potentially increased laxity (if higher grade injury)