Injury and Repair - Introduction Flashcards

1
Q

What are mechanisms of cell and tissue injury

A
  • ischemia
  • infection
  • immune reactions
  • genetic factors
  • nutritional factors
  • physical factors
  • mechanical factors
  • chemical factors
  • psychosocial factors
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2
Q

What is ischemia?

A
  • a lack of blood flow that is the underlying the minimus necessary to maintain cell homeostasis and metabolic function
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3
Q

What can cause ischemia?

A
  • arteriosclerosis
  • tourniquet
  • blood clotting g
  • anything that blocks blood flow or causes a blood vessel to be blocked o constricted
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4
Q

What are the effects from ischemia?

A
  • loss of function of impaired function
  • discoloration/palor
  • loss of sensation
  • cold
  • can cause a slowing/death of tissue
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5
Q

What is an infection caused by

A
  • bacteria, viruses and parasitic
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6
Q

what is primary injury vs secondary injury from infections

A
  • primary injury: as a result from the bacteria and can cause cell death
  • secondary injury: results of indirect effects of an infection such as inflammation
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7
Q

What is sepsis

A
  • toxins that get into the blood and then take over the body
  • releases endotoxins and cytokine, interleukin-1 and TNF (inflammatory markers)
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8
Q

how do viral infections kill cells?

A
  • direct cytopathic effect where the virus targets a cell and causes destruction
  • indirect cytopathic effect: causes a change in the cellular make up or internal changes
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9
Q

Immune reactions as a mechanism of cell death

A
  • antibody attachment
  • complement activation
  • activation of the inflammatory cells
  • innate immune system: saliva, flora in GI tract, mucus membranes, skin
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10
Q

Genetic factors as a mechanism of tissue injury and cell death

A
  • alteration in structure of number of chromosomes
  • single mutations of genes
  • multiple gene mutation
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11
Q

Nutritional factors as a mechanism of cell death

A
  • imbalances in essential nutrients can lead to cell injury of death
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12
Q

Physical factors as a mechanism of tissue injury and death

A
  • trauma and physical agent
  • extremes of physical agents such as temperature, radiation, and electricity, may damage cells
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13
Q

Mechanical factors as a mechanism of tissue injury and death

A
  • such as muscle forces pulling on bone causes it to be built up (benefits of mechanical factors
  • however some mechanical forces from bones for example can cause stress factors if it is too much force/too little/ or imbalanced
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14
Q

Chemical Factors as a mechanism of tissue injury and death

A
  • toxic substances that can be ingested or we can be exposed to
  • free radicals
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15
Q

Free radicals

A
  • can be helpful or harmful
  • oxidation can result in oxygen radicals and reactive oxygen
  • modulation of free radials: antioxidants, NO, exercise
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16
Q

Psychosocial factors and how they affect tissue healing

A
  • may influence an individual threshold values for tissue adaptation and injury
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17
Q

What are some cellular aging theories and explain

A
  • free radical theory: changes in aging are a result of exposure to free radicals
  • Telomere aging clock theory: the reduction of telomeres throughout the lifespan is though to be associated with aging
  • epigenetic clock theory: changes based on many factors that affect gene expression
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18
Q

What are the types of cell injury

A
  • reversible
  • irreversible
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19
Q

irreversible cell injury

A
  • Necrosis: internal cell death that is the result of a pathological reason
  • Apoptosis: signaled/planned cell death
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20
Q

reversible cell injury

A
  • stress to cells
  • altered functional demand/reversible cell injury
  • stress maintained
  • possible adaptations
  • atrophy, hypertrophy,hyperplasia, metaplasia, dysplasia
  • removal of stressor
  • return to normal cell
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21
Q

What are the components of tissue healing

A
  • fibronectin
  • proteoglycans and elastin
  • collagen
  • these molecules build structures for cartilage, ligaments, and tendons and depend on other factors
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22
Q
  • what are the factors affecting tissue healing
A
  • growth factors
  • nutrition
  • other factors: blood supply, sleep, infection/inflammation, stress, co morbidity
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23
Q

what are the phases of healing

A
  1. hemostasis and degeneration
  2. inflammation
  3. proliferation and migration
  4. remodeling and maturation
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24
Q

Hemostasis and degeneration:

A
  • 1st you must stop the bleeding and form a hematoma
  • possible necrosis
  • beginning of inflammation response once the clot is formed
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25
Inflammation- tissue healing stage
- begins once the clot is formed - purpose is to rid the causative agent, remove dead cells, and start healing the tissue - acute inflammation is good and chronic can be hazardous - in this stage vasodilation and increased permeability of the blood vessels - coordinated reaction f body tissues to cell injury and death - ends with the removal of initiating agent
26
what are some cellular causes of inflammation
- microbes - release of pro-inflammatory mediators from traumatic stimulation of nerves of mast cells - traumatic bleeding - cell death
27
What are clinical manifestations of inflammation
- redness, swelling, increased temperature - pain - decreased function of the affected site
28
What are some acute inflammation cellular infiltrate
- platelets - neutrophils - monocytes/macrophage - fibrocytes/fibroblasts - Endothelial cells
29
What are some chronic inflammation cellular infiltrate
- monocyte/macrophage - lymphocytes - plasma cells - fibrocytes/fibroblasts - endothelial cells
30
Acute Vs chronic inflammation: what happens to result in restitution of normal structure in acute inflammation
1. injury 2. injurious agent removed 3. labile or stable cells or little necrosis 4. restitution of normal structure and function
31
Acute vs chronic inflammation what happens to result in chronic inflammation
1. injury 2. acute inflammation 3a. injurious agent removed 3b.repeated episodes of acute inflammation 3c. injurious agent persists 4a. permanent cells or extensive necrosis 4b. chronic inflammation 4c. chronic inflammation 1 5. organization 6. scarring
32
Proliferation and Migration phase
- endothelial cells near edge begin to proliferate - establish a vascular network - neovascularization or angiogenesis: the endothelial cells bud out from vessels and form new capillary channels - granulation tissue: health vascular tissue/type of new connective tissue
33
Remodeling and maturation phase
- scar tissue is reduced and remodeled, living tissue smoother and stronger and less dense - the remodeling phase can take years as the skin first produces collagen fibers which are broken down and rearranged to withstand stress - over time, scare tissue grows stronger, relaxes and then lightens
34
What are the zones of cartilage starting with the one attached to the bone
- calcified - radial (best blood supply from the bone) - transitional - tangential (most injury as it is closer to where forces are applied) - articular surface
35
What is hyaline cartilage made of
- 75% water - chondrocytes - type 2 collagen 20% - glycoaminoglycans/proteoglycans 5% - cartilage is neural, avascular, and lymphatic
36
What are the three areas of growing cartilage
- growth plate: epiphysis - articular cartilage of joint surface - apophyses (such as in stood Schlatter diease)
37
How can injury occur to cartilage
can occur in skeletally immature children and adolescents - thought to be caused by hypertrophy and wearing of the hypertrophic zones of cartilage
38
What are the stages of bone healing
- hematoma - granulation tissue formation - callus formation - bone remodeling
39
Bone healing: hematome
- immediately after fracture - macrophages, neutrophils, and platelets release pro inflammatory cytokines such as TNF, bone morphogenetic proteins, platelet-derived growth factors, transforming growth factor, vascular endothelial growth factor and interleukins
40
Bone healing: granulation of tissue formation
- primary callus or fibrocartilaginous callus - occurs within 2 weeks of fracture - chondrogenesis - fibrin-rich granulation tissue formation - dependent on angiogenesis
41
Bone healing: callus formation
- endosteum and periosteum secrete fibroblast (over growth of bone) - the cartilaginous soft call begins to undergo endochondral ossification and medullary callus further supports the bridging soft callus
42
Bone healing: bone remodeling
- coupled remodeling- balance between osteoclasts and osteoblasts activity
43
What is the ideal process of bone healing
1. fracture reduction to restore the anatomy (closed = no surgery and open= surgery) 2. fracture fixation to achieve absolute or relative stability 3. [reservation of the blood supply to the bone and surrounding soft tissues 4. early and safe mobilization
44
Factors that influence bone healing
- blood supply - fracture characteristics - infection - age - smoking - comorbities - medications
45
Subluxation
- comes out of the joint space but is not fully dislocated - causes partial disruption - commonly occurs in more mobile joints
46
dislocation
- complete disruption of anatomic relationships - ligaments/tendons damaged - congenital most common at the hip
47
What is the anatomy of a tendon
- contain collagen fibrils (type 1) - tendons contain proteoglycan matrix - fibroblasts that are arranged in parallel rows
48
What is the basic functions of tendons
- tendons carry tensile forces from muscle to bone - they carry compressive forces when wrapped around a bone like a pulley
49
What is the blood supply in a tendon like
- vessels in perimysium (covering the tendon) - supply from the periosteal insertion - supply from surrounding tissue (muscle)
50
what is the anatomy of ligaments
- predominantly type 1 fibers - similar to tendon with hierarchical structure - collagen fibers are slightly less in volume fraction and organization - fibroblasts
51
What is the basic function of a ligament
- when bones move they keep them in alignment - resist some forces (the forces that muscle does not absorb)
52
What is the blood supply like in a ligament
- microvascularity from insertion sites - nutrition for cell population: necessary for matrix synthesis and repair - relies on bone and therefore the middle does not get as much blood supply
53
Ligament injury - grade 1: - grade 2: - grade 3:
- grade 1: stretching and small tears - grade 2: larger tear - grade 3: complete tear
54
Ligament injury: repair phases and length
- acute inflammation lasts about 2-3 days - proliferation or regenerative/repair phase (several weeks) - tissue remodeling phase (months-years)
55
What occurs during each repair phase in a ligament injury
- inflammation: platelets, WBCs, histamines, cytokines etc come to the area to bring nutrients and blood flow - Proliferation or regenerative phase: platelet-derived growth factor, transforming growth factor beta, vascular endothelial growth factor and fibroblast growth factor; fibroblast deposit collagen, proteoglycans, and other proteins and glycoproteins to the matrix - Tissue remodeling phase: tissue synthesis and degradation
56
Tendon injury
- Tendon rupture, tendinosis, tendinopathy, tendinitis
57
Tendon rupture vs tendinpathy
- attached muscle is max contracted with oblique and quick external stress - tendinopathy: overuse where tendon is repeated strained and then forms micro-tears
58
Spontaneous tendon rupture risk factors
- side effect of fluoroquinolone - > 60 yrs - heart, lung, kidney transplant - h/o tendinopathy, Mg deficiency, PVD, RA, DM, or strenuous sports
59
Tendinosis vs tendinitis
- tendinosis: chronic, no inflammation disorganized laying of collagen (failed healing process and thinner collagen fibers) , recovery 6-10 weeks - tendinitis: acute, inflammation, 6 days to 3 weeks recovery
60
tendon healing: controlled loading
- by cast immobilization = beneficial for tendon to bone healing (screwing tendons to bone) - by passive motion= for flexor tendon healing
61
What is the basic way muscle reheal
1. muscle degeneration, necrosis, hematoma, injured myofiber 2. inflammation: neutrophils, macrophages 3. muscle regeneration: SC proliferation, regenerated myofibers with centrally located myonuclei 4. muscle remodeling: TGF-B1, Fibroblasts, and CT formation; revascularization maturation of regenerated myofibers 5. extracellular matrix deposition, scar tissue formation; innervation of regenerated myofibers
62
Types of muscle injury
- muscle contusions from a force or smack - lacerations - strains - degenerative disease
63
Muscle repair: can it regenerate/what is needed for repair
- can regenerate but depends on extent of injury - basement membrane/sarcolemma sheath - satellite cells (adult muscle stem cells)
64
muscle repair phases
- degeneration/inflammation phase (1 couple days) - regeneration phase (begins 4-5 days post injury; peaks at 2 weeks, complete by 4) remodeling phase
65
strategies to improve repair of muscle
- factors: IGF, Platelet rich plasma (injection) - Stem cells: more severe - mechanics, stimulation: PROM, AAROM
66
Muscle strains
stretching or tearing of musculotendinous unit
67
Muscle strains types
1. mild/1st degree - stretching or minor tearing without loss of integrity - minor swelling - minimal loss of strength and movement 2. Moderate/2nd degree - partial tear with loss of function - pain, moderate disabilities, point tenderness, swelling, local hemorrhaging, abnormal motion 3. Severe/3rd degree - extends across entire cross section of muscle