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HLTH3200 > Healing and Repair > Flashcards

Healing and Repair Flashcards

1
Q

What are the outcomes of injury

A
  • Tissue Injury
  • Apoptosis (no inflammation) or Necrosis (acute inflammation)
  • Healing (removal of injured tissue / noxious agent, regeneration and repair)
  • Chronic Inflammation (failure to remove injured tissue / noxious agent)
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2
Q

What is wound healing

A
  • Wound: Circumscribed injury caused by external force, possibility to occur in all tissue types (skin, eyes, bone and organs)
  • Healing: Body’s response to injury, attempt to restore normal structure and function, replacement of damaged tissue by new healthy tissue, highly organised / predictable
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3
Q

What is regeneration of tissues dependent on

A
  • Proliferation capacity of tissues
  • Driven by growth factors
  • Integrity of extracellular matrix
  • Presence of stem cells differentiating to mature cells
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4
Q

List classifications of cells based on replication potential

A
  • Labile tissues
  • Stable / quiescent tissues
  • Permanent tissues
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5
Q

What are labile tissues

A
  • Cells are continuously lost and replaced
  • Replacement by stem cells and proliferation of mature cells
  • Cells remain in cell cycle, can proliferate rapidly after injury if stem cells are preserved
  • Example: Basal layer of epidermis, haematopoietic stem cells
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6
Q

What are stable / quiescent tissues

A
  • Minimal replicative activity in normal state
  • Mitotically divide when stimulated
  • Fully differentiated cells leave cell cycle at Go
  • Proliferating stable cells divide symmetrically, both daughter cells are differentiated
  • Long lived cells, slow turn-over
  • Example: Parenchymal cells (renal tubule epithelium) and mesenchymal cells (fibroblasts)
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7
Q

What are permanent tissues

A
  • Terminally differentiated post-mitotic cells
  • Cannot re-enter the cell cycle (non-proliferative)
  • “No” capacity to divide, replaced by scar tissue
  • Exit cell cycle before G1 and are unable to re-enter
  • Example: Cardiac myocyte’s, skeletal muscle, neurons
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8
Q

Why is regeneration in healing important

A
  • Growth (proliferation) and differentiation of new cells
  • Replacement of damage or dead cells by cells identical to ones lost
  • Complete restoration of original tissue with restoration of normal function
  • Proliferation of parenchymal tissues and replacement of cells by surrounding specialised cells
  • Labile and stable / quiescent tissues
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9
Q

Why is repair in healing important

A
  • Healing outcome in which tissues do not return to their normal architecture and function
  • Replacement of damaged cell with scar tissue (connective tissue)
  • Helps to hold organ together (function not restored)
  • Involves, granulation tissue formation and contraction of the wound, begins within 24h of injury
  • Proliferation of connective tissue and replacement of lost tissue by granulation tissue (scar tissue)
  • Permanent tissue
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10
Q

What mechanisms are involved in repair and regeneration in healing

A
  • Monocyte chemotaxis (chemokine, TNF, PDGF, FGF)
  • Fibroblast migration / replication (PDGF, EGF, TNF, IL-1, FGF)
  • Angiogenesis (VEGF, angio-proteins, EGF)
  • Collagen synthesis (TNF-beta, PDGF)
  • Collagenase secretion (PDGF, FGF, TNF)
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11
Q

What is the function of skin and the layers

A
  • Functions: Protection, thermoregulation, sensation and metabolic functions
  • Layers: Epidermis, dermis and hypodermis
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12
Q

What is the epidermis

A
  • Stratified squamous epithelium
  • Basal layer contains keratinocytes / melanocytes
  • Basal cells divide and move up through layers (change appearance / differentiate)
  • Barrier and protection against foreign bodies and substances, retains moisture
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13
Q

What is the dermis

A
  • Connective tissue, many fibroblasts (production and maintenance of structural elements of skin)
  • Thin (hair, sweat / sebaceous glands) and thick (none of above)
  • Papillary Layer: Loose connective, BV, nerves, sensory receptors
  • Reticular Layer: Dense, irregular collagenous connective
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14
Q

What is the hypodermis

A
  • Adipose connective tissue
  • Large blood vessels
  • Fibroblasts (synthesise collagen and elastin)
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15
Q

What is keratin

A
  • Keratinocytes: Rapidly deciding stem cells
  • Keratinised Squamous Epithelium: Water in cell cytoplasm mainly replaced by keratin, outer layer contains dead cells, epidermis of the skin
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16
Q

List the phases of wound healing

A
  • Haemostasis / Coagulation
  • Inflammation
  • Proliferation or Granulation
  • Maturation or Remodelling
17
Q

What is haemostasis and coagulation

A
  • Vessel rupture and bleeding
  • Vascular response (5-10min)
  • Platelets aggregate
  • Growth factors, hormone and cytokine release
  • Vasoconstriction occurs to limit blood loss
  • Platelet degranulation and release of cytokines and growth factors
  • Fibrin formation and coagulation
  • GFs increase size / number of cells, inhibit apoptosis, initiate proliferation, migration and differentiation
18
Q

What are the 3 types of inflammation

A
  • Early: Commences 2-3h and peaks at 2-3 days, edema, neutrophil infiltration and degradation of necrotic cells, complement activation, cytokine repair
  • Late: Monocyte infiltration, differentiation of monocytes into macrophages, lymphocyte infiltration and cytokine repair
  • Chronic: Uncontrolled, pathological
19
Q

What is proliferation / granulation

A
  • Proliferation: 3-5 days following injury, overlaps with inflammatory phase
  • Granulation: Inflammatory cells, fibroblasts and keratinocytes, neo-vasculature, collagen, proteoglycans
  • Scar Formation: Epithelialisation, fibroplasia, angiogenesis and wound contraction
20
Q

What are the steps involved in scar formation (proliferation / granulation)

A
  • Epithelialisation: Migration, formation of epithelium, basal cell proliferation, seal between wound / environment
  • Fibroplasia: Migration of fibroblasts, attach fibrin matrix, deposit collagen, elastin, fibronectin
  • Angiogenesis: Formation of BV, increased perfusion of healing factors, scar formation and resorption
  • Wound Contraction: Day 5-15, centripetal movement of wound edges, concurrent with collagen synthesis
21
Q

What is maturation / remodelling

A
  • 5-7 days after injury
  • Remodelling of ECM
  • Fibroblasts initiate collagen lysis
  • Increasingly organised collagen
  • Restoration of tensile strength of injured skin
  • Vascular maturation and progressive vascular regression
22
Q

What are factors that affect wound healing

A
  • Type, location and extend of injury
  • Infection
  • Nutrition
  • Steroids
  • Mechanical Factors
  • Poor blood supply (ischaemia)
  • Movement
  • Exposure to UV light facilitates healing
  • Foreign bodies
  • Ionising radiation / chemo
  • Uncontrolled Diabetes
  • Age
23
Q

What is cutaneous wound healing and types of repair

A
  • Cutaneous: Relating to, or affecting the skin

- Types of Repair: Primary and secondary intention

24
Q

What is healing by first intention

A
  • Clean and uninfected
  • Surgically incised (wounds with opposed edges)
  • Without much loss of cells and tissues
  • Epithelial regeneration is principal mechanism of repair
  • Edges of wound are approximated by surgical sutures
  • Disruption of epithelial basal membrane
  • Complications infrequent
  • Results in a linear / hairline scar
25
Q

What is healing by second intention

A
  • Separated irregular edges
  • Open with large tissue defect
  • At times infected
  • Inflammatory reaction more intense
  • Complications frequent
  • Fibrosis, larger area of granulation tissue
  • Wound contraction mediated by action of myo-fibroblasts
  • Melanocytes do not migrate into healing wounds leading to hypo-pigmentation
26
Q

How does healing of a laceration occur

A
  • Laceration: Deep cut / tear of skin, initial haemorrhage
  • Signs: Damaged cells, plasma in wound, neutrophils, increase BV / capillary permeability
    Healing:
  • Clot and scab form
  • Macrophages clean up debris
  • New capillaries formed
  • Fibroblasts deposit new material to replace the old
  • Neutrophils replace macrophages
  • Epithelial cells grow and scab falls off
  • Remodelling phase
27
Q

What are aberrations of healing

A
  • Keloids: Healing with excessive fibrosis, excess granulation/excess collagen, grow beyond borders of original wound, don’t resolve spontaneously, genetic
  • Hypertrophic Scarring: Accumulation of excess collagen, decreased lysis, scars stay within limit of original wound, tend to regress spontaneously, generally seen soon after tissue injury
28
Q

How do different tissues heal

A
  • Mucosal: Good regeneration, lost and replaced continuously, some bacteria delay wound healing and some are beneficial
  • Nervous: Nerve cells not replaced in CNS, scar tissue can slow nerve conduction
  • Solid Organs: Tissue replaced by fibrous scar

HLTH3200 (14 decks)

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