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Medical Conditions 1 > Injury and Repair - Introduction > Flashcards

Injury and Repair - Introduction Flashcards

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USMLE® Step 1 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
Q

Inflammation- tissue healing stage

A
  • 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
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26
Q

what are some cellular causes of inflammation

A
  • microbes
  • release of pro-inflammatory mediators from traumatic stimulation of nerves of mast cells
  • traumatic bleeding
  • cell death
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27
Q

What are clinical manifestations of inflammation

A
  • redness, swelling, increased temperature
  • pain
  • decreased function of the affected site
28
Q

What are some acute inflammation cellular infiltrate

A
  • platelets
  • neutrophils
  • monocytes/macrophage
  • fibrocytes/fibroblasts
  • Endothelial cells
29
Q

What are some chronic inflammation cellular infiltrate

A
  • monocyte/macrophage
  • lymphocytes
  • plasma cells
  • fibrocytes/fibroblasts
  • endothelial cells
30
Q

Acute Vs chronic inflammation: what happens to result in restitution of normal structure in acute inflammation

A
  1. injury
  2. injurious agent removed
  3. labile or stable cells or little necrosis
  4. restitution of normal structure and function
31
Q

Acute vs chronic inflammation what happens to result in chronic inflammation

A
  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
  3. organization
  4. scarring
32
Q

Proliferation and Migration phase

A
  • 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
Q

Remodeling and maturation phase

A
  • 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
Q

What are the zones of cartilage starting with the one attached to the bone

A
  • calcified
  • radial (best blood supply from the bone)
  • transitional
  • tangential (most injury as it is closer to where forces are applied)
  • articular surface
35
Q

What is hyaline cartilage made of

A
  • 75% water
  • chondrocytes
  • type 2 collagen 20%
  • glycoaminoglycans/proteoglycans 5%
  • cartilage is neural, avascular, and lymphatic
36
Q

What are the three areas of growing cartilage

A
  • growth plate: epiphysis
  • articular cartilage of joint surface
  • apophyses (such as in stood Schlatter diease)
37
Q

How can injury occur to cartilage

A

can occur in skeletally immature children and adolescents
- thought to be caused by hypertrophy and wearing of the hypertrophic zones of cartilage

38
Q

What are the stages of bone healing

A
  • hematoma
  • granulation tissue formation
  • callus formation
  • bone remodeling
39
Q

Bone healing: hematome

A
  • 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
Q

Bone healing: granulation of tissue formation

A
  • primary callus or fibrocartilaginous callus
  • occurs within 2 weeks of fracture
  • chondrogenesis
  • fibrin-rich granulation tissue formation
  • dependent on angiogenesis
41
Q

Bone healing: callus formation

A
  • 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
Q

Bone healing: bone remodeling

A
  • coupled remodeling- balance between osteoclasts and osteoblasts activity
43
Q

What is the ideal process of bone healing

A
  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
Q

Factors that influence bone healing

A
  • blood supply
  • fracture characteristics
  • infection
  • age
  • smoking
  • comorbities
  • medications
45
Q

Subluxation

A
  • comes out of the joint space but is not fully dislocated
  • causes partial disruption
  • commonly occurs in more mobile joints
46
Q

dislocation

A
  • complete disruption of anatomic relationships
  • ligaments/tendons damaged
  • congenital most common at the hip
47
Q

What is the anatomy of a tendon

A
  • contain collagen fibrils (type 1)
  • tendons contain proteoglycan matrix
  • fibroblasts that are arranged in parallel rows
48
Q

What is the basic functions of tendons

A
  • tendons carry tensile forces from muscle to bone
  • they carry compressive forces when wrapped around a bone like a pulley
49
Q

What is the blood supply in a tendon like

A
  • vessels in perimysium (covering the tendon)
  • supply from the periosteal insertion
  • supply from surrounding tissue (muscle)
50
Q

what is the anatomy of ligaments

A
  • predominantly type 1 fibers
  • similar to tendon with hierarchical structure
  • collagen fibers are slightly less in volume fraction and organization
  • fibroblasts
51
Q

What is the basic function of a ligament

A
  • when bones move they keep them in alignment
  • resist some forces (the forces that muscle does not absorb)
52
Q

What is the blood supply like in a ligament

A
  • 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
Q

Ligament injury
- grade 1:
- grade 2:
- grade 3:

A
  • grade 1: stretching and small tears
  • grade 2: larger tear
  • grade 3: complete tear
54
Q

Ligament injury: repair phases and length

A
  • acute inflammation lasts about 2-3 days
  • proliferation or regenerative/repair phase (several weeks)
  • tissue remodeling phase (months-years)
55
Q

What occurs during each repair phase in a ligament injury

A
  • 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
Q

Tendon injury

A
  • Tendon rupture, tendinosis, tendinopathy, tendinitis
57
Q

Tendon rupture vs tendinpathy

A
  • attached muscle is max contracted with oblique and quick external stress
  • tendinopathy: overuse where tendon is repeated strained and then forms micro-tears
58
Q

Spontaneous tendon rupture risk factors

A
  • side effect of fluoroquinolone
  • > 60 yrs
  • heart, lung, kidney transplant
  • h/o tendinopathy, Mg deficiency, PVD, RA, DM, or strenuous sports
59
Q

Tendinosis vs tendinitis

A
  • 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
Q

tendon healing: controlled loading

A
  • by cast immobilization = beneficial for tendon to bone healing (screwing tendons to bone)
  • by passive motion= for flexor tendon healing
61
Q

What is the basic way muscle reheal

A
  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
Q

Types of muscle injury

A
  • muscle contusions from a force or smack
  • lacerations
  • strains
  • degenerative disease
63
Q

Muscle repair:
can it regenerate/what is needed for repair

A
  • can regenerate but depends on extent of injury
  • basement membrane/sarcolemma sheath
  • satellite cells (adult muscle stem cells)
64
Q

muscle repair phases

A
  • degeneration/inflammation phase (1 couple days)
  • regeneration phase (begins 4-5 days post injury; peaks at 2 weeks, complete by 4)
    remodeling phase
65
Q

strategies to improve repair of muscle

A
  • factors: IGF, Platelet rich plasma (injection)
  • Stem cells: more severe
  • mechanics, stimulation: PROM, AAROM
66
Q

Muscle strains

A

stretching or tearing of musculotendinous unit

67
Q

Muscle strains types

A
  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

Medical Conditions 1 (16 decks)

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