Unit IV: alterations in the intergumentary system

Tissue repair

Response to tissue injury, attempting to restore normal body structure and function.
Overlaps the inflammatory process

• tissue regeneration

• fibrous tissue repair

What is tissue regeneration?

Replacement of injured tissue with cells of the same type; leaves little to no evidence of injury;

• only labile and stable cells can do this

  • labile cell : cells of the skin, oral cavity, vagina, urinary tract, bone
    marrow, and other cells that continue to divide and replace throughout
    life)

  • stable cells: cells that normally stop dividing when growth ceases
    but can regenerate if needed- includes cells in the liver, kidney, smooth muscle cells, and vascular endothelial cells

What is a labile cell

cells of the skin, oral cavity, vagina, urinary tract, bone

What is a stable cell

cells that normally stop dividing when growth ceases but can regenerate if needed- includes cells in the liver, kidney, smooth muscle cells, and vascular endothelial cell

What are permanent or fixed cells?

nerve cells, skeletal muscle cells, and cardiac muscle cells, they cannot regenerate

What is fibrous tissue repair?

Repair occurring with severe/persistent injury, by replacement with connective tissue; involves granulation tissue and scar formation

• ii. Involves the generation of granulation tissue and formation of scar tissue

  • 1. Granulation tissue is moist, red, and contains lots of capillaries.

• iii. Scar tissue formation builds on the granulation tissue:

  • 1. Fibroblasts migrate to the site of injury and proliferate

  • 2. Deposition of collagen and other extracellular matrix components

  • 3. As the scar matures, vascular degeneration occurs and turns the
    granulation tissue into a pale, avascular scar

Choose the best description of granulation tissue

Moist, red tissue containing many capillaries; forms during the proliferative phase of wound healing

What is primary intention?

• well approximated edges

• no tissue loss

• ex: sutured surgical incision

What is secondary intention?

• occurs with greater loss of tissue and/or contamination

• slower and forms large amounts of scar tissue

• edges not well approximated

Phases of wound healing

• inflammatory

• proliferative

• remodeling

Inflammatory phase of wound healing:

1. Begins at the time of injury and lasts 2-3 days
2. Prepares the wound environment for healing**
3. Includes hemostasis and the vascular and cellular phase of inflammation
a. hemostasis phase: The clot formed during hemostasis loses fluid and becomes a hard scab protecting the area
b. _______ phase: Neutrophils and macrophages are required to remove debris

Proliferative phase (wound healing)

1. Second phase of wound healing (begins 2-3 days after injury, up to 3 weeks, if would healing by primary intention);

2. focus of this phase is building new tissue to fill the wound

3. Fibroblast cells are the key players in this phase. (Connective tissue cells that synthesize/secrete collagen and other substances
   needed for wound healing.)

4. Fibroblasts and vascular endothelial cells proliferate to form
   granulation tissue. The tissue has many new capillary buds that
   bleed easily.

5. The capillaries in the granulation tissue are semipermeable and allow plasma proteins and WBCs to leak into the tissues.

6. Final step: epithelialization- migration, proliferation, and differentiation of epithelial cells at wound edges. This is to form a
   new surface layer that is similar to the one destroyed during the
   injury.

7. The epithelial cells migrate under and between the scab until a significant portion of the wound has been covered with epithelial
   tissue. Then the scab lifts off

8. Collagen synthesis peaks within 5-7 days and can continue for several weeks. By week 2, WBCs have mostly left the area, the
   edema has decreased, and the new small vessels have degenerated

fibroblasts

Connective tissue cells that synthesize and secrete collagen and other substances needed for wound healing

What is epithelialization-

migration, proliferation, and differentiation of epithelial cells at wound edges.

• This is to form a new surface layer that is similar to the one destroyed during the
  injury.

What phase is granulation tissue formed?

proliferative phase

Remodeling phase of wound healing

1. Starts ~ 3 weeks after injury and may continue for > 6 months.
2. Continued remodeling of scar tissue by the synthesis of collagen by fibroblasts and the lysis of collagen by enzymes
3. Most wounds do not regain full tensile strength.
4. Keloid formation: Genetic component; more common in African
Americans

What is a keloid

Excess scar tissue formation with a genetic component; more common in African Americans

Who is more prone to keloids?

african americans

Do most wounds regain full tensile strength?

most wounds do not regain full tensile strength

What are some factors that affect wound healing

• malnutrition (wound healing takes lots of nutrients and minerals)

• blood flow and oxygen delivery (good blood flow needed for regeneration)

• impared inflammatory response

• infection

• wound separation

• foreign bodies

• bite wounds

How does maluntrition affect wound healing?

a. Need adequate proteins, carbs, fats, vitamins, and minerals to heal wounds.
b. Protein deficiencies prolong the inflammatory process
c. Carbohydrates are needed for energy for WBCs
d. Fats are needed for synthesis of new cells
e. Vitamins A & C are needed for collagen synthesis

How does blood flow and oxygen delivery affect wound healing?

a. Wounds need adequate blood flow to deliver nutrients and cells and remove waste, bacteria, and other debris
b. Edema or preexisting health conditions may decrease blood flow
c. Molecular oxygen is required for collagen synthesis- Hypoxia prevents wound healing
d. Wounds with ischemic tissue become infected more frequently than wounds with good blood flow

How does Impaired Inflammatory and Immune Response affect wound healing?

a. immunosuppressive drugs
b. Genetic disorders that impair immunity
c. Other conditions: Diabetes Mellitus- High glucose levels impair wound healing.

How does Infection, Wound Separation, & Foreign Bodies affect wound healing?

a. Infection impairs all phases of wound healing
b. All wounds are contaminated at the time of injury, but normal body defenses can handle mild contamination and destroy the microorganisms.
c. Approximation of wound edges enhances wound healing and prevents infection.
d. Foreign bodies introduce bacteria to the wound- delay healing and may cause infection.

How do bite wounds affect wound healing?

a. Infection risk!!!
b. Type of animal, location of the bite, and type of injury all determine whether the wound becomes infected.
c. Adult bites have greater risk of infection than bites from children.
d. All bite wounds should be evaluated.

Wound healing and age:

Neonates and children:

Children wound healing is similar to adults
b. Neonates may have an immature immune system
c. Adequate nutrition is necessary

Wound healing in older adults:

a. Wound healing may be progressively impaired with aging
b. Reduced collagen and fibroblast synthesis
c. Impaired wound contraction
d. Slower reepithelialization of open wounds
e. Structural and functional changes
f. Effects of sun exposure
g. Possibly more co-morbidities

What classification of burn is this?

a. Only the outer layer of the epidermis.
b. Red/pink, dry, painful- Usually no blisters
c. Skin maintains ability to function
d. Heals in 3-10 days (quick healing)
e. Example: Mild sunburn

first degree superficial

What classification of burn is this?

a. Involve the epidermis and various degrees of the dermis
b. Painful, moist, red, blistered
c. Blisters are important to prevent the loss of water and superficial dermal cells.
d. Underneath blisters: weeping, pink/red, sensitive skin
e. Heal in approximately 1-2 weeks

second degree superficial partial-thickness

What classification of burn is this?

a. Entire epidermis and dermis
b. Structures originating in the subcutaneous layer (hair follicles, sweat glands) remain intact
c. Very painful
d. Mottled pink, red, or waxy white with blisters and edema
e. Blisters are flat and appear dry
f. Tactile sensation may be lost or diminished
g. Heal in approximately 1 month, usually with a scar, and there may be loss of some
sensation.

second degree full-thickness

What classification of burn is this?

a. Extend into subcutaneous tissue- may involve muscle and bone
b. Thrombosed vessels may be seen under the skin
c. Vary in color: waxy white, yellow, tan, brown, red, or black
d. Hard, dry, and leathery
e. Extensive edema to burned area and surrounding tissues
f. No pain
g. Regeneration, if possible (smaller areas), may take several weeks. Large areas may require skin grafts.
h. Permanent scarring

nerve endings destoryed

third degree full-thickness

Systemic complications

• Hemodynamic(blood pressure, heart rates) instability

  • electric burns may cause cardiac arrythmias

  • capillaries are injured and fluid is lost

• Respiratory system dysfunction

  • common w/ smoke inhalation

  • synged nasal hairs or soot

• Hypermetabolic response

  • healing wounds takes a lot of nutrients, healing takes a lot of calories

    • burn victims are on high calorie diets

• Dysfucntion of other organ systems

  • stress ulcer (curling ulcer):

  • sepsis: large burn = loss of first major line of defense (skin)

System compilications

Hemodynamic(blood pressure, heart rates) instability

a. May begin almost immediately
b. Capillaries are injured and fluid is lost from the vascular, interstitial, and cellularcompartments
c. Hypovolemic shock → Decrease in cardiac output and impaired perfusion to vital organs
d. Electrical burns may cause cardiac arrhythmias

What is a hypovolemic shock (burns)

Decrease in cardiac output and impaired organ perfusion to vital organs from fluid loss through injured capillaries after a burn

System complications:

Respiratory System Dysfunction

a. Common with smoke inhalation
b. Irritation and ulceration of mucous membranes in the respiratory system,
bronchospasm, and edema
c. May have thermal injury to the respiratory passages
d. Manifestations of inhalation injury:
i. Hoarseness
ii. Drooling
iii. Unable to handle secretions
iv. Hacking cough
v. Labored, shallow breathing
vi. Smokey odor to breath

System complications:

Hypermetabolic Response

a. Stress of burn injury increases metabolic demand and nutritional requirements
b. Stress-related hormones (catecholamines and cortisol) are released
c. Heat production is increased
d. Increased oxygen consumption, increased glucose use, and protein and fat wasting
e. Peaks 7-17 days after the burn
f. Nutritional support is necessary

System complications:

Dysfunction of Other Organ Systems

a. Renal insufficiency- May occur as a result of hypovolemia, damage to kidneys from burn, or medications
b. GI- Gastric dilation and decreased peristalsis. Potential complication: acute ulceration of stomach and duodenum (Curling ulcer)
c. Neurologic changes- Caused by periods of hypoxia, hypovolemia, trauma, etc. May see confusion, memory loss, insomnia, lethargy, or combativeness.
d. Musculoskeletal effects- Fractures at the time of the incident, deep burns, scarring, and contractures.
e. Sepsis- Severe, overwhelming, systemic infection. Skin is the body’s first line of defense against infection

What is a curling ulcer?

acute ulceration of stomach and duodenum

What is a pressure injury?

Ischemic lesions of the skin and underlying structures caused by unrelieved pressure that impairs the flow of blood and lymph

• may occur in any area with prolonged pressure, but bony prominences are more at risk.

• At risk populations: Older adults, people with quadriplegia, and critically ill individuals.

Mechanisms of development: PRESSURE INJURY

I. Pressure around capillaries exceeds pressure inside capillaries, and blood flow is obstructed.
II. If pressure is applied more than 2 hours, the lack of blood flow and the buildup of metabolic wastes causes irreversible tissue damage.
III. Greatest pressure is on the surface of the bone. Extensive underlying tissue damage can be present when a small, superficial skin lesion is first noticed.
IV. Factors contributing to development:
a. Shearing forces- Sliding of one tissue layer over another. The skeleton moves, but the skin remains fixed to a surface. This causes injury and thrombosis of vessels.
b. Friction- Damaging the skin at the epidermal-dermal interface. Happens when someone in bed uses their elbows/heels to help them move.
c. Moisture- Weakens the cell wall and changes the protective pH of the skin. Makes
the skin more susceptible to pressure, shear, and friction injury

What are shearing forces?

Sliding of one tissue layer over another. The skeleton moves, but the skin remains fixed to a surface. This causes injury and thrombosis of vessels.

What is friction (pressure injury)

• Damaging the skin at the epidermal-dermal interface.

  • Happens when
    someone in bed uses their elbows/heels to help them move

How does moisture cause a pressure injury?

Weakens the cell wall and changes the protective pH of the skin. Makes the skin more susceptible to pressure, shear, and friction injury

Prevention of pressure injury

• I. Identifying risk factors

  • a. Sensory perception impairments

  • b. Exposure to moisture

  • c. Urine/fecal incontinence

  • d. Altered nutrition/hydration

  • e. Altered mobility

  • f. Altered circulatory status

  • g. Presence of shear and friction forces

• II. Frequent position changes

• III. Meticulous skin care

• IV. Provide adequate nutrition/hydration

• V. Frequent assessment

What description best fits a stage I pressure injury

Non-blanchable area of skin redness or purple discoloration without a break in the skin.

• Non blanchable (if we were to push on it, it would stay red)

What description best fits a stage II pressure injury

• Partial-thickness loss of skin layers involving the epidermis.

• Looks like an intact or ruptured blister or open/shallow crater

What description best fits a stage III pressure injury

• Full-thickness loss of skin extending through the epidermis and exposing
  subcutaneous tissues.

• Deep crater with no tunneling and undermining.

What description best fits a stage IV pressure injury

• Full thickness of skin and subcutaneous tissue are lost, exposing muscle, bone, or both.

• Deep crater that may include necrotic tissue, slough, or eschar. Tunneling and undermining often present.

  • undermining: can stick q-tip under edge

  • tunneling: can stick q-tip fully under/through

Unstageable pressure injury

• Full-thickness loss of tissue, but base of wound is covered by slough and/or
  eschar.

• The stage cannot be determined because the base of the wound is not visible due to the slough/eschar

• necrotic tissue

slough

Necrotic tissue that can obscure the base of a wound, preventing pressure injury staging

eschar

Dry, dead/necrotic tissue that can obscure the base of a wound, preventing pressure injury staging

Deep tissue injury

• Localized area of non-blanchable, deep red or purple discoloration.

• May resemble a blood-filled blister. May be intact or nonintact. Due to intense or prolongedpressure or shearing force.

Skin cancer

Rising incidence of skin cancer in the U.S. due to increased sun exposure and thinning ozone
layer.

Regular self-examination is key!

Examine all existing and new nevi (moles) regularly for ABCDE:
• Asymmetry
• Border irregularity
• Color variation
• Diameter > 6 mm (pencil eraser)
• Evolution (changing over time)
Observe for other alterations, such as itching and/or bleeding

What is ABCDE (melanoma sceening)

• Asymmetry
• Border irregularity
• Color variation
• Diameter > 6 mm (pencil eraser)
• Evolution (changing over time)
Observe for other alterations, such as itching and/or bleeding

What kind of melanoma is being described?

• Malignant tumor of melanocytes;

• rapidly progressing and metastatic;

• risk factors include fair skin, family history, freckling on upper back, and history of >3 sunburns before age 20 (USUALLY IN SUN EXPOSED SKIN)

• manefestations:

  • a. Melanomas are usually slightly raised and brown/black
    b. Irregular borders and uneven surfaces
    c. Usually arise from preexisting nevi or new mole growths
    d. Possibly surrounding erythema, inflammation, tenderness
    e. May ulcerate and bleed

• Colors:

  • blue

  • red

  • white

  • can change colors

• 4 types, most common: superficial spreading melanoma

malignant melanoma

Basal cell carcinoma

• Neoplasm of nonkeratinizing cells of the epidermis basal layer;

• most common skin cancer;

• non-metastasizing but can spread deep/wide if untreated

• usually seen on head and neck, often in skin that has hair

• may also be seen on chest or back (less common)

• may be pinkish, translucent papule that extends over time

• may have shiny, waxy border

Squamous cell carcinoma

• Second most common malignant skin tumor;

• increased UV exposure risk;

• has risk of metastasis, unlike basal cell carcinoma

• usually on sun exposed surfaces: nose, forehead, ear, lower lip, back of hand

• red-scaling, keratotic, slighlty elevated lesion

• irregular border

• usually with a shallow, chronic ulcer

• later stages have larger ulcerations, persistent crusts, and erythematous (red) borders

• crusty type apperance

• dark skinned people rarely affected

• occupational risks: exposure to arsenic, industrial tars, coal, and paraffin

Malignant melanoma manefestations:

slightly raised, brown/black
irregular borders, uneven shading
arise from preexisting nevi or new nevi
may have erythema, inflammation, tenderness, ulceration, or bleeding

colors:

blue-melanoma growth
red-inflammation
white-scar tissue formation

basal cell carcinoma location and manifestations

head and neck
chest or back less common
pinkish, translucent papule with shiny, waxy border

squamous cell carcinoma location and manifestations

sun-exposed areas
red, scaling, keratotic, slightly elevated
irregular border
shallow, chronic ulcer