Week 1 Flashcards
Epidermis Layers
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- Stratum Corneum= horny layer all dead keratinocytes accounts for 3/4ths of the thickness of epidermis
- Stratum Lucidum= only in the soles and palms of the hands contains few layers of dead keratinocytes
- Stratum granulosum= 3-5 flattened cell rows with increased concentration of keratin.
- 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
- 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
What is the Basement Membrane
acts as scaffolding for epidermis + selective filter for substances moving between dermis and epidermis
–> Stratum Basale and dermis attach by the thin basement membrane
How thicc is the Epidermis
0.06-0.6 mm
How thicc is the Dermis
2-4mm
Which is vascular and avascular: Dermis Vs. Epidermis
Dermis= Vascular
Epidermis= Avascular
Absence of Inflammation
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
Chronic Inflammation
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
Hypogranulation/ Non-advancing Wound Edges
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
Hypergranulation
Granulation tissue that goes above the wound opening
- pressure
- silver nitrate
- surgery
Dehiscence
A separation of wound margins due to insufficient collagen production of tensile strength
Hypertonic Scarring/keloid
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
Contractures
Pathologic shortening resulting in deformity
–> prevention= movement
Angioblasts
Build new blood vessels
Keratinocytes
epithelialize the wound
Fibroblasts
Build granulation tissue
Myofibroblasts
Cause wound contracture
Cells of the Epidermis
Merkel cells= Light touch sensation Langerhans Cells= Infection fighters
Melanocytes= skin color
Appendages= hair, sebaceous, sudoriferous glands
Cells of the Dermis
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
Inflammatory Stage Vascular Response
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
Inflammatory Phase Cellular Response
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
Proliferative Phase: 4 Crucial Events
- Angiogenesis= building new blood vessels
- Granulation tissue= temporary lattice work of connective tissue that will allow for contraction and epithelialization across the wound
- Wound Contraction= when the wound starts to pull together and become smaller
- Epithelialization= keratinocytes marching across the wound to heal it
Maturation and Remodeling Stage
- rapid collagen synthesis
- old collagen destroyed and cleared
- Scar strength is only at 80% of original strength
Induction theory
scar tissue tries to mimic the surrounding tissue
Tension theory
like wolfs law the more tension and stress placed on tissue it will cause fibers to align
Primary Intention
Simple and quickest
- clean wound
- Small wound like a paper cut
- heals within 1-14 days
Epithelialization can start within 24 hours
Secondary Intention
- 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
Delayed Primary Closure (Tertiary)
Dirty wound left open for cleaning
- closed by surgeon
- Skin graft, sutures after being open
- Should close in 1-2 weeks after suturing
Chronic wound healing
A wound induced by varying causes whose progression through the phases of healing is prolonged or arrested for any reason
Roles of Epidermis
- 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
What kind of environment does a wound like?
Moist
Benefits of a covered wound
- moist environment
- Traps fluid
- exposed wounds more inflamed
Local factors of a wound
- 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
Systemic Factors of a Wound
- Takes into account the overall health that will
- Age
- Comorbidities
- Medications: steroids, immunosuppressants,
- Lifestyle Choices
- Nutrition
- Obesity
- Aging Skin
Aging Skill Epidermis
- 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
Aging Skill Dermis
- 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
Futcher’s Line
- Sharp demarcation between darkly pigmented and lightly pigmented skin in the upper extremity
- Follows spinal nerve distribution
Midline Hypopigmentation
- Lines of hypopigmentation over the sternum
- Lessens with age
Nail Pigmentation
- Diffuse nail pigmentation or linear dark bands on the nail
- May appear brown, blue, or blue-black
Palmar Changes
- Creases may be hyper pigmentated
- May contain hyperkeratotic papules or pits in the creases
Dermatosis Papulosa Nigra
- Brown to Black
- Flesh Moles do not require treatment although some seek cosmetic excision
- Family history more common on females
Plantar Changes
- Hyperpigmented macules may vary in color and distribution
- May present with irregular borders
