Week 1 Flashcards

1
Q

Epidermis Layers
Top to Bottom

A
  1. Stratum Corneum= horny layer all dead keratinocytes accounts for 3/4ths of the thickness of epidermis
  2. Stratum Lucidum= only in the soles and palms of the hands contains few layers of dead keratinocytes
  3. Stratum granulosum= 3-5 flattened cell rows with increased concentration of keratin.
  4. Stratum Spinosum= consists of several rows of mature keratinocytes- cells in spinosum and Basale receive nutrients from diffusion across basement membrane- only mitotically active cells in the epidermis
  5. Stratum Basale= single row of keratinocytes continuously dividing cells that produce the protective protein keratin

Basement Membrane
–> cells journey from Stratum Basale to Stratum Corneum is 15-30 days

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2
Q

What is the Basement Membrane

A

acts as scaffolding for epidermis + selective filter for substances moving between dermis and epidermis
–> Stratum Basale and dermis attach by the thin basement membrane

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3
Q

How thicc is the Epidermis

A

0.06-0.6 mm

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4
Q

How thicc is the Dermis

A

2-4mm

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5
Q

Which is vascular and avascular: Dermis Vs. Epidermis

A

Dermis= Vascular

Epidermis= Avascular

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6
Q

Absence of Inflammation

A

Leads to a chronic wound
Can be caused by:
-medical condition
-old age
- malnourished
- HIV/AIDS

–> proliferation will not start
–> inflammation is necessary to heal

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7
Q

Chronic Inflammation

A

Persistent signs of inflammation
- redness
- painful
- inflammation
- Cardinal signs of inflammation
Causes:
- foreign body, repetitive mechanical trauma, cytotoxic agents
Prevention of the proliferative phase of healing

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8
Q

Hypogranulation/ Non-advancing Wound Edges

A

Can’t fill wound
- Epiboly formation
- NOn advancing edges= keratinocytes will only march around the edges and eventually they will think healing is complete and will stop
Causes= repetitive trauma, wound dehydration, local hypoxia
Treatments:
- offload wound
- keep wound moisturized

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9
Q

Hypergranulation

A

Granulation tissue that goes above the wound opening
- pressure
- silver nitrate
- surgery

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10
Q

Dehiscence

A

A separation of wound margins due to insufficient collagen production of tensile strength

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11
Q

Hypertonic Scarring/keloid

A

Over production of collagen and the overproduction of skin goes outside of the wound margins
- At risk wounds are wounds that cross joints, prolonged proliferation stage, burns

Treatment:
–> Hypertonic= compression dressings/ silicone gel pads/ scar mobilization/ steroid injections
–> Keloid= Z plasty/ radiation/ compression

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12
Q

Contractures

A

Pathologic shortening resulting in deformity
–> prevention= movement

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13
Q

Angioblasts

A

Build new blood vessels

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14
Q

Keratinocytes

A

epithelialize the wound

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15
Q

Fibroblasts

A

Build granulation tissue

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16
Q

Myofibroblasts

A

Cause wound contracture

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17
Q

Cells of the Epidermis

A

Merkel cells= Light touch sensation Langerhans Cells= Infection fighters
Melanocytes= skin color
Appendages= hair, sebaceous, sudoriferous glands

18
Q

Cells of the Dermis

A

Mast cells= secrete chemical mediators for inflammation
Macrophages/WBC’s= immune response and kill pathogens
Fibroblasts= produces collagen and elastin fibers
Sensory receptors= temperature, vibration, pressure and touch

19
Q

Inflammatory Stage Vascular Response

A

Vascular Response
1. Transudate leaks from vessels to interstitial space of the injury to cause edema
2. Local Blood vessel constriction
3. Platelets aggregate to injury site to form a plug and help stop the bleeding and releasing chemical mediators
4. chemical mediators bring more cells to the area to help healing
–> Growth factor= control cell growth, differentiation, and metabolism.
–> Cytokines= signaling protein during the inflammatory phase of wound healing
–> Chemotactic Agents= substances that attract cells necessary for wound repair to the area

20
Q

Inflammatory Phase Cellular Response

A

After 30 minutes vasoconstriction vessels dilate to allow more fluid into the interstitial space which allows for more inflammatory cells to reach area
–> exudate = H2O, macrophages, lymphocytes, PMN’s, proteins, electrolytes, enzymes, inflammatory mediators, GH all of this makes exudate
1. PMN’s migrate toward zone of injury within 12-24 hours
- secrete inflammatory mediators + attract more PMN’s which stimulates fibroblasts +PMN’s secrete enzymes that break down damaged tissue and kill bacteria
2. macrophages kill pathogens
- Macrophages signal extent of injury attracting more cells
- macrophages produce growth hormone
3. Mast cells activate inflammatory cells
- Histamines= short
- Prostaglandins= long

21
Q

Proliferative Phase: 4 Crucial Events

A
  1. Angiogenesis= building new blood vessels
  2. Granulation tissue= temporary lattice work of connective tissue that will allow for contraction and epithelialization across the wound
  3. Wound Contraction= when the wound starts to pull together and become smaller
  4. Epithelialization= keratinocytes marching across the wound to heal it
22
Q

Maturation and Remodeling Stage

A
  • rapid collagen synthesis
  • old collagen destroyed and cleared
  • Scar strength is only at 80% of original strength
23
Q

Induction theory

A

scar tissue tries to mimic the surrounding tissue

24
Q

Tension theory

A

like wolfs law the more tension and stress placed on tissue it will cause fibers to align

25
Q

Primary Intention

A

Simple and quickest
- clean wound
- Small wound like a paper cut
- heals within 1-14 days
Epithelialization can start within 24 hours

26
Q

Secondary Intention

A
  • granulation matrix must be built
  • Signs of progression through stages of healing noted in acute wounds within 14 days and for chronic wounds 30 days
  • increased time and scarring
    PT intervention
    Extra:
  • healing occurs by coagulation, inflammation, macrophage migration, granulation tissue production, wound contraction, and epithelialization
27
Q

Delayed Primary Closure (Tertiary)

A

Dirty wound left open for cleaning
- closed by surgeon
- Skin graft, sutures after being open
- Should close in 1-2 weeks after suturing

28
Q

Chronic wound healing

A

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

29
Q

Roles of Epidermis

A
  • Provides a physical and Chemical Barrier
    -Regulates fluid
  • Provides light touch sensation
  • Assists in thermoregulation
  • Assist with waste disposal
    -Critical to endogenous Vitamin D production
    -Contributes to cosmesis/appearance
30
Q

What kind of environment does a wound like?

A

Moist

31
Q

Benefits of a covered wound

A
  • moist environment
  • Traps fluid
  • exposed wounds more inflamed
32
Q

Local factors of a wound

A
  • These factors directly influence the wound
  • Oxygenation
  • circulation: O2 is needed for cellular metabolism, angiogenesis, keratinocytes functioning and epithelialization, ect
  • External and internal stressors: edema & pressure
  • Absent sensation
  • Infection
33
Q

Systemic Factors of a Wound

A
  • Takes into account the overall health that will
  • Age
  • Comorbidities
  • Medications: steroids, immunosuppressants,
  • Lifestyle Choices
  • Nutrition
  • Obesity
  • Aging Skin
34
Q

Aging Skill Epidermis

A
  • Atrophy of epidermis: makes skin more see through
  • Thickening of stratum corneum: helps protect from UV
  • Decrease in Langerhan cells: decreases in immune function of the skin
  • Atrophy of basal membrane
  • flattening of epidermal dermal junction: causes changes in thermoregulation and making skin more frail
35
Q

Aging Skill Dermis

A
  • Decreased vascularization : decreased in number of capillaries loops and epithelial cells that line the avascular structures
  • damage to collagen and elastin fibers: makes skin more disorganized causing the skin to be easily damaged
  • Decreased sympathetic nervous system input
36
Q

Futcher’s Line

A
  • Sharp demarcation between darkly pigmented and lightly pigmented skin in the upper extremity
  • Follows spinal nerve distribution
37
Q

Midline Hypopigmentation

A
  • Lines of hypopigmentation over the sternum
  • Lessens with age
38
Q

Nail Pigmentation

A
  • Diffuse nail pigmentation or linear dark bands on the nail
  • May appear brown, blue, or blue-black
39
Q

Palmar Changes

A
  • Creases may be hyper pigmentated
  • May contain hyperkeratotic papules or pits in the creases
40
Q

Dermatosis Papulosa Nigra

A
  • Brown to Black
  • Flesh Moles do not require treatment although some seek cosmetic excision
  • Family history more common on females
41
Q

Plantar Changes

A
  • Hyperpigmented macules may vary in color and distribution
  • May present with irregular borders