Basics: Anatomy, physiology (incl pigment), wound healing, scars Flashcards

1
Q

List the functions of the skin

A

1) Barrier - to environment extremes, thermal injury, pathogens, UV light 2) Thermoregulation 3) Immune function 4) Vitamin D metabolism 5) neurosensory 6) cosmetic / social function

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2
Q

List the ways that skin is involved in thermoregulation

A

1) Vaso-motor: i) hypothalamus control of periperhal vasoconstriction and vasodilation AND ii) superficial (hot, radiation) vs. deep (cool) venous shunting AND iii) glomus bodies AV shunts 2) Sweating (evaporation) 3) Subcutaneous fat insulation 4) Sebum prevents water loss 5) Other ? not skin - piloerection and shivering

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3
Q

What skin structures arise from the ectoderm?

A

Epidermis Epidermal appendages: pilosebaceous unit, eccrine and apocrine sweat glands Keratinocytes Nail unit

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4
Q

What skin structures arise from the mesoderm?

A

Dermis Macrophages, langerhaan’s cells, mast cells, fibroblasts Adipocytes vessels

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5
Q

What skin structures arise from neuroectoderm

A

Melanocytes Nerves, nerve endings Merkel cells

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6
Q

What are the epidermal appendages? When do they develop?

A

Pilosebaceous unit: hair follicle, sebaceous gland, arrector pilli muscle Eccrine sweat gland Apocrine (odour) gland Develop 9-16 weeks

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7
Q

What is a keratinocyte and what are the layers in the epidermis and their function?

A

Keratinocyte is the primary cell type of the epidermis, produces keratin Stratum basale - for replicating Stratum spinosum - for Stratum granulosum - for storing melanosomes and contains granules to produce keratin Stratum lucidum (only palm, sole) - non viable, extra protection Stratum corneum - non-viable, for protection

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8
Q

What is a melanocyte and what is its function

A

a melanocyte is a specialized cell of neuroectodermal origin (neural crest cell) located along basal layer- function is to produce melanin, stored in melanosomes, transferred to keratinocytes, in order to protect DNA from UV radiant damage

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9
Q

What is a langerhan’s cell, it’s function and locaiton?

A

A langerhaan’s cell is located in the papillary epidermis malphigi layer (also: appendages in dermis, oral/vag muscosa, LN, tymus ) and it’s function is as a specialized antigen presenting cell to TH cells for immunie function

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10
Q

Describe the anatomy of the dermis

A

Located below the epidermis, the epidermal rete ridges interdigitate with the dermal papillae. The epidermis and dermis are adherent via hemi-desmosomes. The dermis has 2 layers: papillary (superficial, loosely less organized collagen) and reticular (deeper, densely organized collagen and vessels)

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11
Q

What are the functions of the dermis?

A

1) Nourish the epidermis 2) Protection of deeper structures 3) Provide strength, pliability and elasticity to skin 4) Wound healing

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12
Q

Compare and contrast eccrine and apocrine glands

A

Function

  • eccrine - secrete sweat, thermal control
  • apocrine - secrete odour, activated by bacteria, vestigial sexual function

Location

  • eccrine - most concentrated palms/soles/axillae but cover most of body except mucous membranes, lips, glans penis, labia minora and clitoris
  • apocrine - anogenital region, axilla, areola

Excretion promoted by:

  • eccrine: cholingeric stimulation
  • apocrine: adrenergic stimulation

Release to:

  • eccrine - direct to skin
  • apocrine - to hair follicle
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13
Q

Describe the phases of wound healing, dominant cell type, dominant cytokines, duration

A

Inflammatory - 0 - 5 days

  • Overall: hemostasis and acute inflammatory infiltrate
  • 5 processes occur: vasoconstriction (including platelet plug and coagulation cascade and fibrin production), vasodilation, chemotaxis, cell migration and cellular response
  • Dominant cells: neutrophils (phagocytosis, bacterial killing) and macrophages (critical for inflammatory phase; phagocytosis, bacterial killing, antigen presentation, cytokine release critical for next phases)
  • Cytokines: PDGF, EGF, IL-1

Proliferative - 5 days to ~ 3 weeks

  • Overall: fibroplasia, granulation, epithelialization, angiogensis, contraction
  • 4 major processes occur:
    • Connective tissue framework by fibroblasts: collagen synthesis and production, elastin synthesis and production, extracellular matrix production (chondroitin sulfate, heparain sulfate, dermatin sulfate)
    • Granulation: occurs in open wounds
    • Epithelialization: mobilization, migration, mitosis, maturation
    • Angiogenesis
    • Contraction
  • Dominant cell type: fibroblast, other cells = myofibroblast
  • Dominant cytokines: TGF-b, VEGF, TNF

Maturation - 3 wks - 1 yr

  • Overall: movement neutral collagen balance and reorganization
  • Major process is collagen reorganization to more parallel, organized fibres to reach mature wound levels of type I and type III (from immature wound at I:III of 2:1 to normal of 4:1)
  • 50% tensile strength @ 3 wks and 80% by ~ 60 days
  • Dominant cell: decreasing cellular populations
  • Dominant cytokine: TGF-b
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14
Q

What is granulation tissue?

A

Granulation tissue is formed in open healing wounds due to the process of neovascularization - capillaries, macrophages, fibroblasts, embeded in loose matrix of HA, collagen, fibronectin

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15
Q

List local factors that modify wound healing

A
  • oxygen tension
  • infection
  • foreign body
  • radiation
  • chronic wound
  • malignancy
  • moisture
  • temperature
  • iatrogenic (surgical technique and wound mechanism)
  • fistula/sinus tract
  • Mechanical stress
  • Denervation
  • Edema
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16
Q

List systemic factors that modify wound healing

A
  • Genetic: age, skin type, sebaceous quality / thickness, inherited disorders
  • Nutrition: macro (caloric, protein malnutrition), anemia, micro (Fe, Cu, Zn, Vit C, Vit E)
  • Comorbidities: DM, PVD, CAD, ESRD, cirrhosis, obesity
  • Immunosuppression
  • Drugs:
    • immunosuppressants: chemotherapy, steroids
    • smoking
    • alcohol
  • Psychosocial
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17
Q

List medications & toxins that impair / influence wound healing

A
  • Anti-inflammatories: NSAIDs, colchicine - decrease collagen synthesis
  • Steroids: decrease angiogensis, wound contraction, macrophage activation
  • Chemotherapeutics
  • Smoking
  • Lathyrogens
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18
Q

Describe the location and function of melanocytes

A
  • Derived from NCCs and migrate to epidermis week 10
  • Located basal layer epidermis, also appendages (hair follicles), uveal tract, leptomeninges, mucous membranes
  • Function: produces tyrosinase (only cell) to synthesize melanin, package in melanosomes, transfer to keratinocytes
  • Function of melanin is to prevent DNA damage from radiant UV light (repair DNA damage and scavenge free radicals)
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19
Q

Describe and classify melanin

A
  • High molecular weight pigmented polymer synthesized by melanocytes and stored in melanosomes
  • Melanin is synthesized from tyrosine (+/- cysteine) using tyrosinase, via intermediate DOPA.
  • Produced in ER, packaged into melanosomes in golgi, transferred via dendrites to keratinocytes
  • 3 types: eumelanin, pheomelanin, neuromelanin
    • Eumelanin: brown/black, found in skin/hair, synthesized from tyrosine and tyrosinase
    • Pheomelanin: yellow/red, found in blond/red hair; synthesized from tyrosine & cysteine by tyrosinase
    • Neuromelanin: black, in neural tissue, exact role uncertain
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20
Q

Compare melanocytes, nevus cells, melanoma cells

A
  • Melanocytes become nevus cells when they leave the epidermis and go to dermis
    • Both produce melanin via similar mechanisms, but they do differ on the following:
  • Shape:
    • Melanocytes: dendritic
    • Nevus cells: round
    • Melanoma: round
  • Grouping
    • Melanocytes: solitary
    • Nevus cells: clusters
    • Melanoma: clusters or sheets
  • Nucleai
    • Melanocytes: Small, regular
    • Nevus cells: small, regular
    • Melanoma: large, irregular, hyperchromatic
  • Mitoses
    • Melanocytes: rare
    • Nevus cells: rare
    • Melanoma: common
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21
Q

What are the 4 pigments in control of skin colour?

A
  • Melanin - from melanocytes - brown/black
  • Oxyhemoglobin - from intravascular RBCs and iron breakdown prods - red
  • Deoxyhemoglobin - intravascular - blue
  • Carotin - dietary sources - orange
  • Note that bile is a pigment not responsible for skin colou
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22
Q

Describe skin colour

A
  • Skin and hair colour is determined by the size and number of MELANOSOMES within keratinocytes
    • # melanocytes is constant and does not affect pigment
  • Factors that influence melanin production (and therefore size/# of melanosomes) are:
    • Genetic determinants
    • Hormonal: melanocyte stimulating hormone, ACTH, liptropin - not major influence in healthy adults
    • Paracrine - melanotropins are secreted by keratinocytes and act locally on melanocytes
    • UV radiation stimulates melanotropin release
  • Skin colour can be constitutive (genetically pre-determined colour or facultative (genetically pre-determined response to UV radiation - UV dependent)
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23
Q

DEFINE TISSUE EXPANSION

A
  • process of using an inflatable (usually silicone) device to provide donor tissue that maintains qualities of donor site such as colour, sensation, hair-bearing, thickness
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24
Q

LIST ADVANTAGES IF TISSUE EXPANSION

A
  • follows principle of reconstructing like with like
  • can be hair-bearing, similar colour, similar thickness, sensate
  • reliable
  • minimal donor site morbidity
  • can be repeated
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25
Q

LIST DISADVANTAGES OF TISSUE EXPANSION

A
  • takes time - preliminary operation, multiple expansions
  • not immediately available
  • requires multiple stages
  • some morbidity - scarring or pressure alopecia, scars, contour defect (skeletal), forms capsule
  • some operative risks of placement and expansion - hematoma, seroma, infection, exposure, skin necrosis
  • aesthetically displeasing while TE in situ
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26
Q

LIST CONTRAINDICATIONS TO TE PLACEMENT

A
  • infection
  • malignancy
  • radiation
  • unstable soft tissue
  • poor compliance
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27
Q

describe the physiologic property of skin that is employed for TE

A
  • utilizes the visco-elastic property of “creep”
    • mechanical creep is 70% of expansion - whereby tissue is expanded by water displacement from cells and ground substance, increased inter-cellular space in gap junctions, cellular stretch (hypertrophy)
    • biological creep is 30% of expansion - whereby reorientation of existing tissue and regeneration of new tissue including cellular hyperplasia
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28
Q

describe the histological changes that occur to each tissue layer during tissue expansion

A
  • epidermis - increased thickness - hypertrophy, acanthosis, hyperkeratosis
  • dermis - changes occur at reticular dermis - hypoplasia, atrophy (thinner), increased space between NV structures, reorientation of collagen fibres parallel, elastic may rupture of fibrose
  • subcutaneous fat - atrophy (thinner)
  • muscle - atrophy, may fibrose
  • vasculature - capillary dilatation (in reticular dermis), Increased vessel number, length, calibre; increased VEGF, increased blood flow (especially in capsule) - regarded as delay
  • bone: resporption of outer cortex (especially children)
    *
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29
Q

WHAT ARE THE 4 ZONES OF TISSUE EXPANDER CAPSULE?

A
  1. INNER ZONE: macrophages and fibrin
  2. CENTRAL ZONE: elongated fibroblasts and myofibroblasts
  3. TRANSITION ZONE: loose collagen
  4. OUTER ZONE: blood vessels and collagen
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30
Q

WHAT ARE PRINCIPLES OF PRE OP PLANNING OF TE PLACEMENT?

A
  • choose the expander: round, rectangular, crescent
    • aim for length of TE = length of defect; width of TE = 2-2.5x width of defect; area of TE = > 2x area of defect
    • for advancement, arc of circumference needs to be length of defect + length of TE
    • rectangular ~ 38% increase; crescent ~ 32% increase; round = ~ 25% increase
  • plan in reverse
  • choose skin/tissue to be expanded
  • choose scars / incision placement - radial, border, remote
  • orient TE parallel to long axis of defect
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31
Q

describe fundamentals of operative procedure OF TE

A
  • prophylactic antibiotics,
  • TE pocket dissection following prophylactic hemostasis
  • irrigation of pocket w/ bacitracen
  • soaking of TE in bacitracen
  • single touch technique of TE placement
  • use of closed-suction drains
  • 2 layer close
  • expansion of 10-20% TE volume
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32
Q

list reasons to pause TE and reasons to stop or remove TE

A
  • pause
    • pain, neurapraxia, seroma, pressure on underlying non-critical structures, spread scar
  • Stop / remove
    • infection, hematoma, dehiscence, exposure, skin ischemia, pressure on underlying critical structures
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33
Q

Describe the embryology of skin

A

Skin formed by Ectoderm and mesoderm

ECTODERM

  • Pilosebaceous unit
  • Apocrine unit
  • Nail unit
  • Eccrine gland
  • Epidermis

NEUROECTODERM

  • melanocytes, nerves, merkel cells, specialized sensory

MEDOSERM

  • fibroblasts
  • macrophage
  • mast cell
  • lagherhans cell
  • vessels
  • fat cells

from ECTODERM:

  • Stratum germinativum
    • forms basal cells, suqamous cells
    • epithelial germ cell
      • forms apocrine, sebaceous glands and hair
    • ecrrine germ cells
      • eccrine glands
        *
34
Q

What is the pidermis, what cells compose it and in what layers

A

Def. Stratified sqaumous keratinized epithelium

Epidermis is composed of cells:

Keratinocytes > melanocytes > Lnagerhans > Merkel

Epidermis is divided into 2zones, 5 layers (in palm.sole, 4 layers elsewhere wihtout lucidum)

Stratus malpighii

  • Basal
  • Spinosum
  • Granulosum

Stratum corneum

  • lucidum
  • corneum
35
Q

What are keratinocytes

A

Form predominant cell in epidermis

  • Proliferate in basal layer - interconnected via hemidesmosome, desmosomes
  • Form more intercellular connections (spines) in spinosum layer
  • Develop granule fo rkeratin formaton in granulosum
36
Q

Where are melanocytes located in the body

A
  • Uveal tract
  • Retina
  • Leptomeninges
  • Hair Follicles
  • Epidermis (basal layer)
37
Q

WHat is the function of melanocytes

A

Produce melanin to protect skin from UV damage

Melanocytes produce melanin and package in melanosomes and distribtue these via dendrites to keratinocytes

38
Q

What is the function of langerhans cells

A

APC to TH cells - >key for delayed type 4 hypersensitivty allergic reaction and allograft rejection

Located in

  • dermis, epidermal appendage
  • LN, thymus
  • oral mucosa, vagina
39
Q

What is the function of merkel cell

A

Mechanoreceptor

Merkel cells are located

  • lips, nose
  • genitalia
  • volar digits, nail bed
  • hair follicles
40
Q

Whatis the DEjunction and what diseases occur at the DE jx

A

Dermal-epidermal junction

Composed of

  • lamina lucida (thin adherent to BM)
  • lamina densa (thicker, connects epidermis to dermis via hemidesmosomes)

Bullous diease occur at DE jx

41
Q

What is the function of the dermis, layers and its composition

A

Fx

  • nourish epidermis
  • strength, pliability of skin
  • wound healing
  • protect deeper structrues

Dermis composed of:

  1. Connective tissue matrix
  2. Ground substance
  3. Cellular components

Layers PR 31

Papillary - thin, collagen type 3, elastin, collagen

Reticular - thick, collagen type 1, elastin, dense collagen parallel bundles, epidermal ppendages, vessels, nerve endings

42
Q

What forms the connective tissue matrixof the dermis

A
  • Collagen
    • forms 70% of CT matrix
    • type 1 collagen in retcular dermis, type 3 collagen in papillary dermis
    • 4:1 type 1 ; type 3 collagen in adult skin vs immature scar is 2:1
  • Elastin
    • resists deformational forces
    • thin in papillary dermis, thicker in reticular dermis
43
Q

How is collagen formed/structure

A
  • Fibroblasts produce collagen as a chain of Gly-X-Y, where X or Y are proline, hydroxylprline, hydroxylysine
  • triple helix is formed bychains of Gly-X-Y, glycosylated and released from fibroblasts as a procollagen
  • Procollagen is cleaved a terminal amino acids and then names tropocollagen
  • Tropocollagent hen forms into collagen fibrils, which coalesce in fiber
44
Q

What types of collagen are there and where are they located?

A
  • Type 1 - most abundant - reticular dermis
  • type 2 - hyaline cartilage, eye
  • type 3 - papillary dermis
  • type 4 - basement membrane
45
Q

What forms the ground substance in the dermis

A
  1. GAGs
  2. Structural proteins (fibronectin)

Fx

  • wound helaing - first 3days
  • fluid homeostasis
46
Q

What cells comprise the dermis

A
  • Fibroblats
    • main cell component
    • produce/degrade colagen/elastin/ground subs
  • Mast cell
    • key for type 1 hypersensitivity rn
    • release granule of vasoactive mediator
  • Macrophage
    • APC, phagocytes
    • key for tumoricidal and bacteriocidal fx and wound healing
  • Plasma cells, lymphocytes
47
Q

what comprises a pilosebaceous unit

A
  • hair ofllicle
  • arector pilli muscle
  • sebaceous gland (apocrine gland in axilla and anogenital regions)
48
Q

What is hair and what are three types of hair

A

Keratinized structure made by hair follicle

3types

  • Lanugo - fine hypopigmented ahru shed by fetus prior to birth
  • Velus - fin ehair appearing replacign lanugo hai in post natal period covers most of body

Terminal - coarse, after puberty, replace velus hairs

49
Q

What are phases of hair growth

A

Anagen - most hairs in this phase of growth

Catogen - buld degrades and separates from papilla

Telogen - resting phase

50
Q

What are sebaceous glands, their location, fx

A

Glands secrete sebum, generally into duct opening into hair follicle

Named differently based on locatoin (montgomery-areola, meibomian - eyelid, fordyce - lip vermilion)

  • located everywhere except palms, soles
  • highest # face/scap
  • inhibited by mite dermodex folliculorum
  • inflammed by FA breakdown of P.acnes

Function

  • sebum retains moisture, antibacterial/fungal
51
Q

What is the composition of sweat

A

water

electrolyte

glycogen

sialomucin

52
Q

Contrast apocrine and eccrine glands

A
  • First appear and greatest density
    • E: palm, sole. Highest palm sole axilla
    • A: scalp. Highest anogenital, axilla, areola
  • Function
    • E: thermoregulation, cholinergic
    • A: scent, adrenergic
    • both release sweat
      • E: directly to skin
      • A: into hair follicle via duct
  • Absent E gland in nonhair bearing areas ie. labia minora, glans penis, clitoris, lips
53
Q

WHat are 3 sources of nail growth

A
  1. Germinal matrix - most of growth from flattened proliferating keratinized cells
  2. Sterile matrix - add epidermal cells to verntral plate
  3. Dorsal roof of eponychium - shiny layer of dorsal plate
54
Q

What are the 5plexus of blood supply in the skin

A

Subepidermal

dermal

Subdermal

Subcutaneous

Fascial

55
Q

What are two types of nerves in the skin

A

Somatic (afferent) - pain, touch, temperature, vibration, proprioception

Autonomic (Efferent) - sudomotor, vasomotor, pilomotor

56
Q

What are the sensory receptors in the skin

A

FREE NERVE ENDINGS

  • unmyelinated axon - pain, temp, touch
  • Merkel cell mechanoreceptor - light touch

ENCAPSULATED RECEPTORS

  • Meissner - light pressure
  • Pacinian - deep pressure vibration
  • Ruffini - heat, proprioception, vibration
  • Krause - cold
57
Q

What are the functions of the skin

A
  1. Protection / Barrier
  2. Thermoregulation
  3. Vitamin D production
  4. Sensory stimuli detection
  5. Cosmesis
58
Q

How does the skin function as a protective barrier

A

Against noxious stimuli

  • UV light (melanin, stratum corneum)
  • Low voltage (stratum corneum)
  • mechanical F (sub cut, dermis)
  • Toxins (lipids content of skin, s. corneum, langerhans, tcell, tight cell jx

Against microorganisms

  • Physical barrier (s. corneum, dermis,desquam)
  • Chemical barrier (sebum)
  • Immunologic (langerhans, macrophage)
  • Normal skin flora (corynebacterium/diphteroid, GPC s. epidermis/aureus, GNB acinetobacter, malssezia dermatophyte
59
Q

How does skin fx as thermoregulation

A

Regulation of water loss

  • s.corneum

Regulation of temperature

  • shivering
  • hypodermis/fat insulation
  • eccrine glands
  • glomus bodies mcirocirculation
  • piloerection
  • altered macrocirculation
60
Q

What are 3 physical properties of skin

A

VTE

Viscoelastic - creep, stress relaxation, recoil, recruitment

Tension - stretch, striae, blanching

Extensibility - RSTL (borges), Langers lines

61
Q

Describe the Viscoelastic property of skin

A
  • Creep = stretching from constant force over time
    • Mechanical - strecthing b/c displaced fluid b/w GS/collagen
    • Biologic - stretching b/c new tissue generated
  • Stress relaxation =load required to keep strecth reduced over time

Initial strecth acheived by extensibility of elastin but collagen resists deformation

62
Q

Describe the tension property of skin

A

Tension defined as stored force in stretched skin to return back to normal relaxed state

Tension lines are perpendicular to muscle.

With excess tension, get stretching, striae, blanching

63
Q

Describe the principle of extensibility

A

Skin is extensible perpendicular to langers lines (which represent lines of maximal tension =langers lines)

Langer line = line of maximum tension

Borges Relaxed skin tension lines = line of minimal tension = maximal extensibility

Scars a best parallel to line of maximal extensibitlity = RSTL

64
Q

Classify wound healing

A
  • Type
    • primary
    • delayed primary
    • secondary
    • partial thickness
  • Timing
    • acute
    • chronic
  • Normal vs abnormal
    • Abnormal wound healing
      • overgrowth
      • undergrowth
      • pigmentation
      • contour
65
Q

Differentiate 1’ 1’delayed, 2’ and partial thikness wound healing

A
  • Primary
    • wound closed by approximation of epidermis/dermis wihtin hours of creation
    • MMP responsible for remodeling collagen
  • Primary delayed
    • wound closed after debridement by host defenses or medical inervention
    • collagen tensile strength same as if 1’ closed
  • Secondary
    • heals by contractino and epitheliazation
    • myofibroblasts
  • Partial thickness
    • heals by epitheliazation from appendages, no collagen deposition
66
Q

Describe phases of wound healing (timing, cytokines, cells involved)

A
  • Inflammatory phase (day 0-4)
    • Cells: PML (PMN, macrophage, Lymphocyte)
    • Cytokine: PEI1 (pDGF, EGF, IL1)
    • Vasoconstriction, Coag cascade, platplug
  • Proliferative (day 4- wk 3)
    • Cells: fibroblast
    • Cytokine: TT (TGFB, TNF)
    • Collagen and GS deposition
    • increase tenisle strength 50% 3wk 80% 8wk
  • Remodeling/maturation (3wk - 1yr_
    • Cell: fibroblast ->transform to myofibroblast
    • Cytokine : TGFb
    • Contraction
    • Collagen replaced type3 ->type 1 til 4:1 ratio reached
67
Q

Describe the detailed events in the inflammatory phase of wound healing

A
  • Tissue injury
    • blood extravastion, constriction, coag cascade
  • Coagulation = fibrin
    • platelet plug formed
    • platelets release PDGF, TGFB, PF4 to attract fibroblast, endothelial cell, macrophage
    • Coag casde end product - fibrin = matrix for cell migration
  • Early inflammation (24hrs) = leuk migration
    • Leukocyte migration (PMN, macrophage, Lymphocyte) to debride wound and prevent infection
      • margination - roll/adhere to endotheial cells with selectins/Integrins
      • diapedesis - move through wall -integrins
      • chemotaxis - migrate to chemicals released by tissue damage/bacteria/platelets to remove debris
  • Late inflammation/proliferation
    • Macrophage - dominates at 48-72h - phagocyte, GF producer for + fibroblast, endothelial cell, SM cell
    • Lymphocyte - last to arrive 72hr b/c IL-1 - for collagen remodelling?
68
Q

Describe detailsed events of proliferative phase in wound healing

A
  • Proliferation - 72hrs
    • Macrophage stimulate fibroblasts via PDGF, TGFb, PF4
    • Lymphocyte - mediate collagen/ECM remodel
    • Fibroblast - day 3- 4wk - increase collagen deposition linear growth
    • Myofibroblast - day 3 to 21 - actin monofilament intracell system - deposit collagen to maintain contracted position
  • Epitheliazation
    • mobilization
    • migration
    • mitosis
    • maturation - no appendages
    • stimualted by EGF, bFGF
69
Q

What are matrix molecules invovled in wound healing

A
  • Collagen
    • exposed colagen attract platelets
    • foundation of ECM
  • Fibronectin
    • key for leukoctye migration, cell-cell interaction. In basal lamina. made by fibroblasts/macrophage
  • PG, GAG
    • compose the GS
    • 4 types of GAGs: chondroitin sulfate, heparan sulfate, keratan sulfate, HA
70
Q

How does nutrition modify wound healing

A

Anabolic event needs

  • Protein - for inflammtory phase
  • Glucose - leukocytes
  • Essential FA
  • Minerals
    • Zinc - prolif fibroblast epithelial
    • Manganese - procollagen formation
    • Copper - crosslinking collagen
    • iron - hydroxylation Pro Lys
  • Vitamins
    • A (retinoid acid) :
      • fibroplasia, collagen syn/croslink, epithe. Needed to supplement monocyte/macrophage dysfx caused by steroids. Oral 25000IU/day
    • C (ascorbic acid):
      • cofactor for collagen syn (hydroxylation proline.lysine
      • OHlysine - crosslink fibrils
      • OHproline - exocytosis of collagen
    • B6 (pyroxidine
      • collagen crosslinking
    • B1 thiamine and B2 riboflavin
      • syndromes ass with poor wound healing
    • E
      • antioxidant - no evidence for use in surgical wounds
71
Q

What drugs modify wound healing

A
  • Anti-inflammatory
    • NSAID ASA block PG = inhibits collagen syn
  • Steroids
    • inhibits inflammatory phase (macrophage), decrease contraction, angiogenesis, wound infection
  • Colchicine
    • arrest cell replication
  • Chemotherapy
    • decrease fibroblast prolif
    • wait 1wk post op before starting
72
Q

What toxins modify wound healing

A
  • Lathyrogen
    • found in ground peas
    • inhibit crosslinkning
  • smoking
    • vascoonstriction, Hb-O2 curve shifted left
73
Q

How does DM affect wound healing

A
  • Neuropathy - altered endoneurial blood flow
  • Glycosylated Hb - increase viscosity and affinity of O2 for Hb
  • Atheroscleroiss of tibial/peroneal arteries
  • Phagocytes impaired
  • high venous backflow increase transudate/edema
74
Q

List microvascular diseases that impair wound healing

A
  • Occlusive arterial D
    • buerger disease (thromboangitis obliterans)
    • microembolism
  • Vasospastic D
    • raynaud
  • Vasculisits
    • scleroderma
    • SLE
  • Hematologic D
    • cryoglobulinemia
    • PCV
75
Q

What local factors impair wound healing

A
  • Cancer
  • Doctor skill
  • Edema
  • Foreign body - nidus for infection
  • Growth factors
  • Hydration - use semipermeable occlusive dressing
  • Infection
    • Mechanical stress
  • Nerve (denervation) - high collagenase activity
  • Oxygen - impairs fibroblasts if PO2<40mmHg
  • Radiation
76
Q

How does radiation impair wound healing

A

Acute

  • occlusion and stasis of small vessels, drop in collagen sythese by fibroblasts and drop in tensile stregnth

Chronic

  • cell malfx and necrosis

Safe to allow for wound healing 6months post radiation

77
Q

How do HTS and Keloid differ from normal scar

A
  • Collagen nodules
  • rich vasculature
  • thick epidermis
  • high mesenchymal density
78
Q

What general factors impair wound healing

A

INTAKE

  • nutrition
  • smoking
  • drugs

PATIENT

  • Age
  • inherited disorders
  • Systemci disease: DM, cardiac/renal, Obesity
  • Microvascular D
  • Hematocrit
79
Q

Compare HTS and keloid scar

A

Genetics

  • familial inheritance Keloid>HTS

Race/Gender

  • black>caucasian , F>M for Keloid only

Age

  • young 10-30 or keloid/HTS

Borders

  • wihtin borders (HTS)
  • outside of borders(keloid)

natural history

  • Keloid appear months after injury, rarely disappear, face,ear lobe, chest
  • HTS appear early, improve with time, flexor surface

Etiology

  • Keloid - immune dysfx. higher HA, collagenase, less apoptosis, high response to TGFb
  • HTS - timing/tension of closure. high collagenase

Histology

  • Keloid:broad pink thick bundles of collagenw ith whorls/nodule, eosinophils, mast cells, lymphocytes
  • HTS: no bundles but nodules present. Myofibroblasts found despite ocntraction finished, increased vascularity

Collagen

  • HTS fine parallel fibers, 6x normal synthesis
  • Keloid thick random fibers, 20x normal synthesis

Elastin

  • HTS reduced, Keloid abundant

Cells/vessels

  • HTS increaed # w myofibroblasts, Keloid not T excpt higher fibroblast proliferation
    *
80
Q

List ways to prevent poor scar formation

A
  • align incision parallell to RSTL
  • tension free closure
  • timely removal of sutures
  • avoid UVA/B damage
  • moist environment
  • scar massage
  • silicone sheet
81
Q

What are non -surgical tratment options for managing scars

A
  • Intralesional steroid
    • kenalog (triamcinolone 10mg/ml, 40mg/ml
    • decrease fibroblast actviity/#, increase collagenase
    • inject qmonth x4
    • max 120mg adult, 40mg kid
    • S/e telangiectasia, hypopig atrophy, necrosis
  • Pressure garment
    • pressure must exceed 25mmHg
    • need 6-24m of treatment
  • Silicone sheeting
    • for symptomatic keloid
    • need 2-6mths of tx
  • RTX
    • reduce keloid reucrrence post excision, 7days post op
  • PDL
    • in combo w injection of steroid effetciv efor keloid
  • Intralesional 5-FU
  • Intralesional IFNa
  • Cryosurgery
  • Surgical excision
    • Should be combined with
      • RTx - recurrence <5%, start 7dys postop
      • kenalog - pre,intra,post <50% recurence
      • Imiquimod - topicaly q2d
    • simple intralesional excision
    • re-orientate scar -Z 2 or 4 flaps, W, M
    • Serial excision
  • dermabrasion
82
Q

List differences between fetal and adult wound healing

A

Fibroblasts

  • Adult - more collagenase
  • Fetal - more collagen synthesized

Repair rate

  • faster in fetal

Inflammation

  • Fetal - reduced in early gestation

VEGF

  • Fetal - rapid expression

Matrix - fetal

  • more HA to stimulate fibroblast migration
  • more type 3 collagen, thinner collagen fibers, less distance b/w fibers