Soft Tissue Injury Flashcards

1
Q

What are the three stages of wound healing?

A
  1. Cleanup phase
  2. Repair phase: Production of fibrous tissue and attempt to restore.
  3. Final stage of reorganization, remodeling, maturation.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe the first stage of wound healing?

A

Hemorrhage, edema, clot formation lead to removal of cellular debris, dead tissue, foreign material. Must be effective for second (repair phase) to happen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe second period of wound healing.

A

Production of fibrous tissue, skin defect seals, cut tendon ends unite, broken ends of bone join. Anatomical integrity. But disorganized and poor mechanical properties.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe 3rd stage of wound healing.

A

Maturation, reorganization, and remodeling. Organized, compact, functionally efficient. Fractured bones regain supportive strength and lacerated tendons regain tensile strength.

Depends on degree of injury, age and health of patient, type of treatment, etc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are mediators of inflammatory response in clean-up stage?

A

Histamine and serotonin from basophils, mast cells, platelets. They increase vascular permeability and dilatation enabling PMN leukocytes to migrate into area of trauma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Within a few minutes to hours of injury, which additional mediators are released?

A

Kinins (cause pain by stimulating nerve endings).

Prostaglandins 2-6 hours after injury.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Which mediator is a chemotaxis promoter?

A

Prostaglandins (attract more cells by migration to injured tissue).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Growth factors such as _______ are present in early wound and important in chemotaxis and mitogenesis.

A

Platelet derived growth factor which comes from wound clot.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Granulocytes are followed by which other inflammatory cells at the end of the first 24 hours?

A

Lymphocytes, monocytes, and later by macrophages.

These release lysosomal enzymes which cleave macromolecules.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What role does arachidonic acid play in wound healing in cleanup phase?

A

ADA is released by lysosomal enzymes and is a precursor for prostaglandin synthesis from cell membranes.
This sustains inflammatory response and toxic material can be broken down enzymatically.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Cleanup phase lasts how long?

A

3-4 days.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe the repair phase: What happens with blood vessels? With collagen?

A

Capillaries grow into trauma area and fibroblasts produce collagen. Local growth factors stimulate cell division and protein synthesis.
Collagen production is rapid and reaches peak during second week slowing down by day 14.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Maturation phase: When does it start? What happens with collagen? What happens with vessels?

A

Begins 2 weeks after injury and lasts several months or years. Collagen synthesis and breakdown approaches steady state. Fibers become mature and oriented along tension lines (adding to mechanical strength).

Vascularity diminishes and capillary loops in scar tissue are obliterated.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Maturation phase: When does it start? What happens with collagen? What happens with vessels?

A

Begins 2 weeks after injury and lasts several months or years. Collagen synthesis and breakdown approaches steady state. Fibers become mature and oriented along tension lines (adding to mechanical strength).

Vascularity diminishes and capillary loops in scar tissue are obliterated.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What prolongs wound healing?

A
  • Greater trauma
  • Contaminating wound with foreign material
  • Impaired blood supply (from vascular injury or indirectly from swelling which causes additional tissue death from ischemia)
  • Infection (esp by anaerobic clostridial organisms)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Most important local growth factor in MSK system for wound healing?

A

Bone morphogenetic proteins

Acid-stable, heat-labile proteins. They are present in bone and released when bone is resorbed by osteoclasts. In local environment, stimulate osteoprogenitor cells to become osteoblasts and produce new bone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Other important growth factors for wound healing?

A

Transforming growth factor b. Platelet derived growth factor. Insulin like growth factor 1 and basic fibroblast growth factor.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Other important growth factors for wound healing?

A

Transforming growth factor b. Platelet derived growth factor. Insulin like growth factor 1 and basic fibroblast growth factor.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Why do alcoholics not heal wounds and fractures well?

A

Poor wound healing from chronic malnutrition. Inadequate supply of amino acids methionine and cysteine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Why is a vitamin C deficiency bad for wound healing?

A

Vitamin C important for collagen formation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the affect of ACTh and cortisone on wound healing?

A

Adverse effect. These diminish inflammatory response and surpress fibroplasia. Gain in wound tensile strength is retarded.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the affect of ACTh and cortisone on wound healing?

A

Adverse effect. These diminish inflammatory response and surpress fibroplasia. Gain in wound tensile strength is retarded.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Why do children have more rapid healing of fractures?

A

Growth hormone.

Also it is important in heterotropic bone formation seen in patients with head injuries.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Nicotine has what affect on wound healing?

A

Negative effect on bone healing.

25
Q

NSAIDs impair what in wound healing? Why?

A

Impair bone healing because certain prostaglandins are important in bone formation.

26
Q

What is effect of immobilization on injury?

A

Leads to poorer tensile strength in ligament, adhesions in tenson, formation of poorer quality of tissue in cartilage and osteoporosis in bone. Immobilizatoin is necessary but restoring mobility as soon as possible is best.

27
Q

What are two requirements for tendons to work correctly in normal human body?

A

Great tensile strength and ability to glide easily through surrounding tissue.

28
Q

In order for tendons to have great tensile strength, they need what substance?

A

Abundance of collagen which can lead to adhesions to surrounding tissue which impairs gliding function.

29
Q

In order for tendons to have great tensile strength, they need what substance?

A

Abundance of collagen which can lead to adhesions to surrounding tissue which impairs gliding function.

30
Q

What makes it difficult for tendons and ligaments to heal?

A

Limited blood supply and high functional demands.

Bulk of tissue mass is longitudinally oriented collagen fibers and between bundles=sparse fibrocytes.

31
Q

Describe healing process of a tendon:

A
  1. Clean laceration
  2. Inflammatory exudate and influx of macrophages, fibroblasts, capillary buds.
  3. In fibroblastic repair phase, collagen is randomly oriented.
  4. During maturation phase, fibers become arranged parallel to line of tendon pull.
  5. Adhesions occur between tendon and sheath determining future gliding function of tendon.
32
Q

Protection from excessive stress would disrupt

A

blah

33
Q

Why are tendons and ligament injuries immobilized?

A

Ligaments and tendons heal better with mobilization. However, they need to be protected from excessive stress that would disrupt repair.

34
Q

What is time span of tendon and ligament repair?:

A

Collagen formation in tendon and ligament begins at 4-5 days.

Tensile strength increases steadily after about two weeks. Strength is not sufficient to permit heavy loading for 4-5 weeks.

35
Q

What are four main components of articular cartilage?

A

Chondrocytes, collagen, protein polysacchardie, water.

36
Q

Which part of cartilage has a low turnover in adult? Which has high turnover?

A

Cellular turnover rate is exceedingly low as is turnover of collagen component.

Protein polysaccharide is being constantly synthesized and degraded.

37
Q

Why does articular cartilage not heal well?

A

Absence of vessels within cartilage and low mitotic activity of chondrocytes.

38
Q

Which heals better: A) Lower defect extending partway through cartilage. B) Upper defect extending completely through cartilage and into subchondral bone.

A

Healing is less complete in partial thickness defect. Full thickness injury is vascularized by subchondral vessels which enhances healing.

39
Q

Which heals better: A) Lower defect extending partway through cartilage. B) Upper defect extending completely through cartilage and into subchondral bone.

A

Healing is less complete in partial thickness defect. Full thickness injury is vascularized by subchondral vessels which enhances healing.

40
Q

Partial thickness defects: Healing facts

A
  1. Necrosis of a few cartilage cells adjacent to lesion and loss of mucopolysaccharide from this area.
  2. Defect fills with fibrin but the inflammatory response in absence of blood vessels is limited.
  3. Between 48 hours and two weeks, mitotic activity in cartilage cells adjacent to defect but they don’t really help with healing.
  4. Cartilage defect filled with cells that are elongated and fibrous in appearance which arise from flattened cells of superficial zone of articular cartilage. Under stimulus of injury can act as perichondrium.
    - -These elements may remain fibrous or may appear like fibrocartilage or even become hyaline cartilage.
41
Q

Full thickness defects facts:

A
  1. Vascular tissue dervied from bone and marrow is available to wound.
  2. Defect is filled with blood which clots.
  3. Necrosis of cartilage cells adjacent to injury that is seen in superficial defect.
  4. By 48 hours, there is in growth of vascular granulation tissue from marrow in cartilage defect.
  5. Accumulation of increasing amounts of fibrous tissue and collagen.
  6. Bone formation occurs up to level of previous subchondral bone but not into area of articular cartilage.
  7. In time, surface of defect is covered by several layers of flattened cells, presumably derived from superficial layer of cells of adjacent intact cartilage.
42
Q

Full thickness defects facts:

A
  1. Vascular tissue dervied from bone and marrow is available to wound.
  2. Defect is filled with blood which clots.
  3. Necrosis of cartilage cells adjacent to injury that is seen in superficial defect.
  4. By 48 hours, there is in growth of vascular granulation tissue from marrow in cartilage defect.
  5. Accumulation of increasing amounts of fibrous tissue and collagen.
  6. Bone formation occurs up to level of previous subchondral bone but not into area of articular cartilage.
  7. In time, surface of defect is covered by several layers of flattened cells, presumably derived from superficial layer of cells of adjacent intact cartilage.
  8. Tissue eventually becomes more fibrous and less vascular: fibrous tissue, fibrocartilage, or hyaline cartilage.
43
Q

Stable and accurate reduction helps with cartilage healing in what way?

A

It allows early mobilization which promotes better cartilage formation.

44
Q

Undisplaced fracture has intact what?

A

Surrounding soft tissues (periosteum) which provide some mechanical stability and contribute to healing.

45
Q

Which growth factors are released by clot? Which growth factors are released by bone ends of fractured bone?

A

PDGF=released by clot.

TGFbeta and BMP released by bone ends.

46
Q

Describe healing process of bone fracture.

A
  1. Inflammatory reaction to trauma=>polymorphonuclear cells and macrophages. Removal of bone debris (osteoclasts) takes longer than removal of soft-tissue debris and may not be completely for months to years.
  2. In 48 hours, vascular tissue invades fracture area. Most of these come from soft tissue. Some from marrow cavity.
  3. Cells produce new subperiosteal bone along outer surface of shaft. Bone acts as anchor for callus that will bridge fracture gap.
  4. Activated periosteal cells and endosteum and marrow cells will join fibrous and vascular invasion of clot to form callus.
47
Q

What is a fracture callus?

A

Fusiform mass of repair tissue that envelops broken ends of fractured bone. Pluripotent stem cells are mesenchymal in origin. These cells produce collagen, fibrous tissue, cartilage, and bone.

Progression of callus:

  1. Granulation tissue
  2. Fibrous tissue
  3. Cartilage
  4. Woven bone
  5. Lamellar bone
48
Q

Regulatory mechanisms that determine amount of each tissue formed during healing of fracture are:

A

pH, mechanical loading, oxygen tension, electrical events, cyclic nucleotides, growth factors, etc.

49
Q

Regulatory mechanisms that determine amount of each tissue formed during healing of fracture are:

A

pH, mechanical loading, oxygen tension, electrical events, cyclic nucleotides, growth factors, etc.

50
Q

Which phase of bone healing does Wolff’s law play a role?

A

Maturation or re-modeling phase.

51
Q

Two examples of how location of fracture can affect callus formation.

A

Fracture through region of cancellous bone (metaphyseal region of proximal tibia)=>Little external callus.

Fracture through well vascularized cortical bone (clavicle)=abundant callus formation.

52
Q

Two examples of how location of fracture can affect callus formation.

A

Fracture through region of cancellous bone (metaphyseal region of proximal tibia)=>Little external callus.

Fracture through well vascularized cortical bone (clavicle)=abundant callus formation.

53
Q

What is effect of motion at fracture site?

A

Compression of fracture site is helpful.

Tensile loads (bending bone back and forth pulling on one side of fracture then the other) is not good and causes scar.

Fracture in shear (bone ends slide back and forth past one another)=Body forms fibrocartilage (tissue that normally uses in joints where there is a lot of shear loading).

Excessive motion=Impair fracture healing by cartilaginous tissue or fibrous tissue.

54
Q

For fractures where there is no motion at fracture site, callus may be _____.

A

Minimal or absent.

Bone healing progresses to maturation phase in which fracture site is remodeled away.

Primary union=long and gradual process.

55
Q

Cancellous bone heals faster or slower than cortical bone?

A

Cancellous bone heals faster than cortical bone.

56
Q

Middle or distal thirds of tibia usually heal fast or slow? Why?

A

Poor blood supply. Heal slow.

57
Q

What is malunion?

A

Fracture healing in non-anatomical position.

58
Q

What is nonunion?

A

Fracture does not heal by bone union but by fibrous tissue formation. Can lead to pseudarthrosis (false joint) in which bone ends are covered with fibrocartilaginous tissue and fracture site contains fluid filled space which resembles a joint.

Treatment: bone grafting, stimulation by electrical currents, mechanical stimulation,

59
Q

What is nonunion?

A

Fracture does not heal by bone union but by fibrous tissue formation. Can lead to pseudarthrosis (false joint) in which bone ends are covered with fibrocartilaginous tissue and fracture site contains fluid filled space which resembles a joint.

Treatment: bone grafting, stimulation by electrical currents, mechanical stimulation.