EXAM 1: Skin and Wound Healing Flashcards

1
Q

Thickness of dermis & epidermis

A
  • epidermis: .06-.6 mm
  • dermis: 2-4 mm
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2
Q

How many days to get from the basal lamina to the surface of the epidermis?

A

15-30 days

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3
Q

List the 5 layers of the Epidermis

A

Stratum Corneum
Stratum Lucidum
Stratum Granulosum
Stratum Spinosum
Stratum Basale

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4
Q

Characteristics of Stratum Corneum

A
  • multiple layers of dead, flattened, interlocking keritinocytes
  • relatively dry
  • water resistant, not waterproof
  • 3/4 epidermis
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5
Q

Characteristics of Stratum Lucidum

A

glassy layer in thick skin only
- only in soles of feet and palms of hands

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6
Q

Characteristics of Stratum Granulosum

A
  • Keratin fibers develop as cells become thinner and flatter
  • where water resistant barrier begins!!
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7
Q

Characteristics of Stratum Spinosum

A
  • Keratinocytes bound together by maculae adherers attatched to tonofibrils of cytoskeleton
  • LANGERHANS cells and melanocytes present
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8
Q

Characteristics of Stratum Basale

A
  • Deepest layer attached to basal lamina in basement membrane
  • contains epidermal basal (stem) cells, MELANOCYTES, and merkel cells
  • where keritinocytes are born
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9
Q

Action of each type of cell:
Merkel Cells
Langerhans Cells
Melanocytes
Mast Cells
Fibroblasts

A
  • Merkel: light touch sensation (epi)
  • Langerhans: immune response (epi)
  • Melanocytes: melanin producing cells in basal layer of epidermis
  • Mast cells: secrete chemical mediators for inflammatory response (a scratched, raised bump = mast cell release) (dermis)
  • Fibroblasts: produce collagen and elastin fibers
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10
Q

Role of Epidermis

A
  • Avascular (doesn’t bleed)
  • Provides a physical and chemical barrier (PROTECTION)
  • Regulates fluid (its water resistant so it can regulate sweat output)
  • Provides light touch sensation (merkle cells)
  • Thermoregulation (sweat glands)
  • Waste disposalL excretion of sweat
  • Critical to vit. D production (for bone formation)
  • Comesis/ appearance
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11
Q

Layers of the dermis

A

Papillary Dermis & Reticular Dermis

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12
Q

T or F: The dermis can not regenerate itself

A

TRUE

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13
Q

Role of Dermis

A
  • support and nourish epidermis
  • house epidermal appendages (hair & sebaceous & sudoriferous)
  • assist with infection control
  • assist with thermoregulation
  • provide sensation
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14
Q

Blisters:

A

occur from friction between epidermis and dermis when a collection of fluid builds up between the two

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15
Q

Subcutaneous Tissues:
- Adipose tissue:
- Fascia:
- Deeper Lymphatics :
- Muscules :
- Tendons:
- Bone:

A
  • Adipose tissue: fat; stores ADEK, for insulation and cousining, energy source, highly vascularized, WHITE TO YELLOW IN COLOR
  • Fascia: connective tissue, highly fibrous
  • Deeper Lymphatics :
  • Muscules : vascular duhhhh
  • Tendons: collagen fibers that can be in sheaths; SHINY GLOSSY AND BRIGHT WHITE
  • Bone: SHINY SMOOTH MILKY WHITE
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16
Q

Wound Classifications based on depth

A
  • superficial: epidermis
  • partial-thickness: epidermis & superficial dermis (BLISTER, wagner grade 1 ulcer)
  • full-thickness: epidermis, dermis, & subcutaneous tissue (wagner grade 1, 2-5 ulcer, full thickness burn, stage 3 pressure injury
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17
Q

Phases of Wound Healing, Purpose, and Length

A
  • Inflammation: to CONTROL BLEEDING, fight germs and bacteria that have entered due to an open area (3-6 days!) STARTS IMMEDIATELY
  • Proliferation: GROWTH and production of cells TO CLOSE THE WOUND, 48 hrs after injury
  • Remodeling/Maturation: RAPID COLLAGEN SYNTHESIS, OLD COLLAGEN DESTROYED (by collagenase); months - 2 yrs after wound is closed
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18
Q

Responses of the Inflammatory Stage

A

Vascular Response
&
Cellular Response

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19
Q

Localized Edema Cause

A

caused by transudate leaking from the vessel walls and causes pressure to stop bleeding

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20
Q

What inflammatory response are platelets involved in?

A

Both Cellular and Vascular (Platelet aggregation: laying down matrix to stop bleeding)

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21
Q

Macrophages

A

fight bacteria and direct repair process

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22
Q

Mast Cells

A

from dermis & produce histamine that allows for short term vasodilation

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23
Q

How long after constriction does vasodilation occur??

A

after 30 min

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24
Q

Exudate formation

A

from a mixture of water, protein, waste, chemical mediators

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25
Q

What allows for short term vasodilation?

A

Histamine release

26
Q

What allows for long term vasodilation?

A

Prostaglandin release

27
Q

S & S of Inflammation

A
  • rubor
  • pallor
  • calor
  • dolor
  • tumor/edema/ swelling
  • decreased function due to swelling
28
Q

Proliferation 4 Crucial Events

A
  1. Angiogenesis: new blood vessels
  2. Granulation tissue formation: temp. lattice work of vascularized connective tissue that will fill a wound and allow for contraction and epithelialization across wound
  3. Wound Contraction: wound pulls together
  4. Epithelialization: karitinocytes march across wound to close completely; VERY SLOW
29
Q

T or F: amount of wound contraction is affected by shape and depth

A

TRUE

  • circular wounds contract slowest
  • deeper wounds contract more than partial thickness
30
Q

Cells to know:
Angioblasts
Fibroblasts
Myofibroblasts
Keratinocytes

A

Angioblasts: build new blood vessels
Fibroblasts: build granulation tissue
Myofibroblasts: causes wound contraction
Keratinocytes: re-epithelialize wound surface

31
Q

Maturation and Remodeling stage events

A
  • rapid collagen synthesis, old gets destroyed
  • collagen fiber orientation (2 theories)
32
Q

What are the two theories of maturation and remodeling stage

A
  • Induction theory:
  • Tension theory: wolf’s law for bone, Davis’s law for skin
33
Q

Scar strength - what phase and what %

A

Maturation and remodeling
- 80% strength for fully mature scar
- 64% strength with repeat healing
- 10% strength when wound first clothes

34
Q

Types of Closures

A

Primary Closure/Intention

Secondary Closure/Intention

Delayed Primary Closure/Tertiary Intention

35
Q

Primary Closure/Intention

A
  • SIMPLIST AND QUICKEST
  • 1-14 days to heal
  • clean wound, edges approximated
  • paper cuts, small cutaneous wounds, surgical
36
Q

Secondary Closure/Intention

A
  • granulation matrix built
  • acute wounds 14 days, chronic wounds 30 days
  • Tx: PT intervention
37
Q

Delayed Primary Closure/Tertiary Intention

A
  • dirty wound left open for cleaning
  • closed by surgeon
  • should close with 1-2 wks of suturing
38
Q

Chronic Wound

A

a wound induced by varying causes, whose progression through the phases of healing is prolonged or arrested for any reason

39
Q

Charges of:
wound
chronic wound

A

wound = negative
chronic wound = loses negative charge

40
Q

what stage of healing cant it get to with chronic inflammation

A

Proliferation Stage
- caused by foreign body bc they signal more inflammation
- repetitive microtrauma
- cytotoxic agents (betadine into wound is BAD)

41
Q

Hypogranulation

A
  • no epitheliazation so hole doesn’t fill
  • epiboly formation: wound edges rounded
42
Q

Hypergranulation

A
  • elithelial cells cant climb hill so no closure
  • tx: silver nitrate to cauterize wound
43
Q

Dehiscence

A

surgical wound splits open due to insufficient collagen production or tensile strength

44
Q

Hypertrophic Scarring/Keloid

A

overproduction of collagen
- most common in wounds that cross joints
- prolonged proliferation stage

45
Q

Best Tx for contractures

A

PREVENTION

46
Q

were doing great :)

A

thats all LOL

47
Q

Maceration:

A

white, wrinkly, and soggy venous wounds

48
Q

Local & Systemic Factors that SLOW healing

A

Local Factors
- Oxygen
- external/internal stressers (pressure & edema & absent sensation & infection)

Systemic Factors
- Age
- Comorbidities
- Meds (steroids, immunosupp., NSAIDS
- smoking/sedentary/alcohol abuse
- nutrition: lack of protein

49
Q

What happens to the epidermis when you age?

A
  • skin gets thinner and clearer
  • thickening of stratum corneum (for sun protection)
  • decreased langerhans cells
  • atrophy of basal membrane and flattening of dermal epidermal dermal junction making it more frail and can tear easily
50
Q

what happens to the dermis when you age?

A
  • decreased vascularization
  • damage to collagen and elastin fibers
  • decreased SNS input
51
Q

Whats the skin color scale called?

A

The Fitzpatrick Skin Type Scale

52
Q

Type 1 vs Type 6: which has the most…

  • Melanin Content
  • Risk for skin cancers, vascular damage, solar condition, actinic aging
  • Risk for hyper/o pigmentation, trauma, keloid scarring
A
  • most melanin content: type 6 (darkest)
  • risk for skin cancers…: type 1
  • risk for hyperpigmentation: type 6
53
Q

Futcher’s (Voigt’s) line

A
  • sharp demarcation btw darkly pigmented and lightly pigmented skin in the UE
  • follows spinal nerve distribution
54
Q

Midline hypopigmentation

A
  • like of hypopigmentation over the sternum
  • lessens with age
55
Q

Nail pigmentation

A
  • diffuse. nail pigmentation or linear dark bands on the nail
  • brown, blue, black
56
Q

Palmar Changes

A
  • creases may be hyperpigmented
  • may contain hyperkeratoic papules or pits in the creases
57
Q

Plantar changes

A
  • hyperpigmented macules may vary in color and distribution
  • irregular borders
58
Q

Dermatosis Papulosa Nigra

A
  • brown to black papules
  • flesh moles do not require tx
  • family history, >females
59
Q

is the dermis vascular or avascular ?

A

vascular

60
Q

What is induction theory?

A

The theory that scar tissue will mimic the surrounding tissue is