WK1 ( CH-13): Skin and Wound Healing Flashcards

1
Q

Describe the normal structure and function of the epidermis.

A

I. Structure ( ascending):
a. Basement Membrane
b. Stratum Basale: single row of keratinocytes
c. Stratum Spinosum: more mature keratinocytes
d. Stratum Granulosum: 3-5 layers of flattened cell rows with increasing concentrations of keratin.
e. Stratum Lucidum: few layers of dead keratinocytes
f. Stratum Corneum: “horny” layer, consists of dead keratinocytes.

II. Function:
a. Physical and chemical barrier
b. Regulates fluid.
c. Provides with light touch sensation.
d. Assists with thermoregulation.
e. Assists with excretion.
f. Critical to endogenous Vitamin D production.
g. Contributes to appearance.

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2
Q

Describe the normal structure and function of the dermis.

A

I. Structure:
a. Papillary Dermis: loosely woven fibers embedded in ground substance.
b. Reticular Dermis: dense irregularly arranged connective tissue.
II. Function
a. Supports and nourishes epidermis.
b. Houses epidermal appendages: hair, glands.
c. Assists with infection control.
d. Assists with thermoregulation.
e. Provides sensation.

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3
Q

Describe the normal structure and function of the subcutaneous tissue.

A

I. Structure:
a. Adipose tissue: highly vascular, loose connective tissue that stores fat.
b. Fascia: highly fibrous connective tissue that be regularly or haphazardly arranged.

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4
Q

State the main cells located within each layer of the integument and describe their functions.

A

I. Epidermis:
a. Keratinocytes (90%): produce keratin, a protective protein.
b. Melanocytes: produce melanin to protect from UV radiation
c. Merkel Cells: mechanoreceptors providing information on light touch sensation.
d. Langerhans’ Cells: fight infection by engulfing foreign material.
II. Dermis:
a. Fibroblasts: produce collagen and elastin.
b. Macrophages and white blood cells: help fight infection.
c. Mast Cells: release of inflammatory mediators like histamine.
III. Subcutaneous Tissue:
a. Stores fat, provides energy, cushioning, insulation, and stores fat soluble vitamins ( A,D,E,K). Separation of deep structures, facilitate movement.

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5
Q

Describe the normal structure of deeper tissues that may be exposed in open wounds including muscle, tendon, ligament, joint capsule, and bone.

A

I. Muscles: regularly arranged fibers surrounded by fascia. Rich vascular supply which makes muscle appear dark red, bleeds easily under trauma.
II. Tendons: regularly arranged collagen that may be enclosed in sheaths.
III. Ligaments and Joint Capsules: dense connective tissue, that may be regular or irregular. Glistening and white.
IV. Bone: Healthy shine, smooth, milky white, hard when probed.

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6
Q

Differentiate between viable and nonviable tissues that may be present in an open wound.

A

I. Unviable:
a. Muscles: appears gray or black in color.
b. Tendons, Joint capsule, and ligaments: dry, leathering, dark in color, and may not be continuous.
c. Bone: moth-eaten, irregular surface, bruised, dark discoloration.

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7
Q

Differentiate between superficial, partial-thickness, and full-thickness wounds.

A

I. Superficial: affect only the epidermis. Like an abrasion.
II. Partial-thickness: involve the epidermis and the dermis. Like a second degree burn that blisters and peels.
III. Full-thickness: extends through the epidermis and dermis into subcutaneous tissue. Can be subcutaneous or subdermal if deeper tissues are wounded.

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8
Q

If a wound extends only into the epidermis, will it bleed profusely? Explain your answer.

A

I. No, the epidermis does not have blood supply

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9
Q
  1. Your patient presents with an open blister on the posterior heel secondary to poor-fitting shoes. What tissues are involved with this type of injury?
A

I. Epidermis and Papillary dermis layer are involved.

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10
Q

How does the dermis assist with temperature regulation?

A

I. If the body is cold the blood superficial vasculature of the dermis constricts to divert blood to the body’s core. If the body is hot, the vessels dilate to dissipate heat into the environment.

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11
Q

Your patient presents with a burn on his right arm after accidentally submerging his arm in a deep fat fryer. Based on the normal functions of the integument, describe the implications this injury will have acutely.

A

I. The patient may be at risk of infection. Patient may become dehydrated quicker if they’re not given fluids. The patient may require a blanket to stay warm. May be unaware of touch.

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12
Q

Describe the vascular response of inflammation.

A

I. Injured blood vessel walls allow fluid called transudate to leak out into the interstitial space, causing edema.
II. Local blood vessels reflexively constrict for several minutes to reduce blood loss.
III. Platelets aggregate at the site of injury are activated by contact with damaged endothelial cells lining vessel walls and exposed collagen. They release cytokines, growth factors and chemotactic agents.
i. Cytokines like interleukin-1 and tumor necrosis factor alpha are signaling proteins.
ii. Growth factors are hormone like and control cell growth, differentiation, and metabolism.
iii. Chemotactic agents attracts cells necessary for wound repair.
IV. Vasodilation continues within 30 minutes and inflammatory mediators continue to reach the wounded area; this rich fluid is called exudate.
V. Histamine is released by mast cells which increases vessel wall permeability and short-term vasodilation. Prostaglandin release by injured cells induce a longer lasting vasodilation. This leads to the cardinal signs of inflammation: tumor, calor, rubor, dolor, functio laesa.

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13
Q

State the cells involved in the inflammatory phase and describe their functions.

A

I. PMN’s: first cells to site of injury, release chemotactic agents, kills bacteria, cleans wound.
II. Macrophages: directs repair process, assists with cleaning wound and eliminating bacteria. Secretes growth factors and MMP’s.
III. Mast Cells: secretes enzymes and inflammatory mediators.

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14
Q

Describe the proliferative phase of wound healing.

A

I. Consists of 4 crucial events:
i. Angiogenesis: formation of new blood vessels.
ii. Granulation tissue formation: MMP’s are responsible for clearing up debris from inflammatory phase. Then highly vascularized tissue called granulation tissue is laid down, it is like a supplementary lattice that fills the void left by the MMP’s.
iii. Wound contraction: Some fibroblasts in the wound become myofibroblasts and begin contracting the wound.
iv. Epithelialization: keratinocytes at the wound margins and epidermal appendages begin to multiply and migrate across the wound bed.

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15
Q

State the cells involved in the proliferative phase and describe their functions.

A

I. Angioblasts: forms new blood vessels
II. Fibroblasts: builds granulation tissue.
III. Myofibroblasts: causes wound contraction.
IV. Keratinocyte: reepthelializes wound surface.

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16
Q

Describe the maturation and remodeling phase of wound healing.

A

I. Granulation tissue is further strengthened and matured. Collagen synthesis continues at a rapid rate, and old collagen is broken down. Scar tissue is at most 80% as strong as original tissue.

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17
Q

Differentiate between wound closure by primary, secondary, and delayed primary wound closure.

A

I. Primary
i. When a wound is clean and organized it heals faster, like a surgical incision which is then physically approximated.
II. Secondary
i. Irregular wound shapes and sizes are more difficult to heal.
III. Delayed Primary
i. A combination of primary and secondary closure. A wound is cleansed then observed, then it is surgically closed.

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18
Q

Explain why absence of inflammation and chronic inflammation occur.

A

I. Absence of Inflammation
i. May occur due to immunocompromised status due to some underlying pathology or condition like HIV, AIDS, malnourishment, age.
II. Chronic Inflammation
i. Can be self-perpetuating where lymphocytes and macrophages continuously signal more inflammatory cells into the area. Could be due to the presence of a foreign body in the wound area, repetitive mechanical trauma, and using cytotoxic agents.

19
Q

Compare and contrast hypogranulation and hypergranulation.

A

I. Hypogranulation:
i. A wound that fails to build granulation tissue resulting in a pothole wound.
II. Hypergranulation:
i. When granulation tissue formation continues after the wound defect has been filled.
III. Interventions
i. Gently wipe wound edges with gauze after each change, lightly filling pothole type wounds, serial debridement, surgical excision.
ii. Pressure over hypergranular tissue, silver nitrate, surgical excision

20
Q

Compare and contrast hypertrophic scarring, keloids, contractures, and wound dehiscence.

A

I. Hypertrophic scarring: overproduction of immature collagen during the proliferative and maturation phases of healing.
II. Keloids: excessive production of collagen, keloids extend beyond the confines of the original wound and rarely regress.
III. Contractures: pathology shortening of a scar resulting in tissue deformity.
IV. Dehiscence: insufficient scar formation, the separation of wound margins.

21
Q

1Your patient sustains a partial-thickness chemical burn. How do you think the body will reepithelialize the defect?

A

I. A partial thickness burn would affect the epidermis and dermis which would require epithelialization from the wound margins and epidermal appendages located in the dermis.

22
Q

1You are working with a patient who had a total knee replacement. Five days after surgery the knee becomes infected and is surgically debrided. One week after debridement the surgeon decides to surgically close the wound. This is an example of what type of healing?

A

I. Delayed primary closure, or tertiary intention.

23
Q

1You have been working with a patient with a pressure ulcer daily for the last 3 weeks. Initially, the wound appeared as a crater and was 1.0 cm deep. Today when you remove the bandage, you notice the granulation tissue has risen above the skin surrounding the wound.
I. How would you describe this tissue?
II. What can you do to improve the wound bed?

A

i. Hypergranular
ii. Applying pressure, Silver nitrate, a different kind of dressing.

24
Q

1Define the terms transudate and exudate.

A

I. Transudate is a collection of fluid caused by increased vascular permeability. Exudate is a mixture of transudate and cells.

25
Q

Describe the processes by which polymorphonuclear neutrophils (PMNs) arrive at the zone of injury during inflammation.

A

I. They marginate and force their way into the interstitial space through the blood vessels. Then they migrate to the area of injury along chemical gradients.

26
Q

Describe the process of angiogenesis.

A

I. Angioblasts bud and grow from endothelial cells adjacent to the wound into the injured area. VEGF is a powerful stimulator for this.

27
Q

What is granulation tissue?

A

I. A temporary scaffolding created by fibroblasts consisting of water, proteoglycans, and fibers.

28
Q

How does wound contraction occur?

A

I. Myofibroblasts pull the wound margins closer together.

29
Q

Provide two reasons why a wound may be chronically inflamed.

A

I. Foreign debris in the wound bed and repeated trauma

30
Q

Suppose you are working with a patient who sustained burns to the neck and face when trying to relight a pilot light. You notice that he chooses to keep his neck flexed when sitting and lying down. How may this hinder his recovery? Describe two interventions you might try to prevent this from happening.

A

I. It may result in a contracture which would not allow fibers to be properly repositioned and cause adaptive shortening of deep fibers and structures.
II. AROM cervical extension, limit pillows.

31
Q

Your patient is referred to physical therapy for wound management with a full thickness pressure ulcer. Describe the normal wound healing process you can expect this patient’s wound to undergo during treatment.

A

I. The wound should pass through the 3 phases of wound healing, inflammation, proliferation, maturation, and remodeling.

32
Q
  1. State the difference between an acute and a chronic wound.
A

I. Acute: induced by surgery or trauma in otherwise healthy individuals. Predictable.
II. Chronic: a wound induced by varying causes, whose progression through healing phases is prolonged or arrested because of underlying conditions.

33
Q
  1. Describe wound characteristics associated with delayed wound healing.
A

I. Mechanism of onset, time since onset, wound location, wound dimensions, temperature, wound hydration, necrotic tissue, and infection.

34
Q
  1. Compare and contrast colonization and infection.
A

I. Infection: the invasion and multiplication of microorganisms in body tissues
II. Colonization: presence of microbes, does not imply infection.

35
Q
  1. Describe local factors associated with delayed wound healing.
A

I. Circulation: inadequate blood flow increases risk of infection; blood must reach wound bed.
II. Sensation: sensory deficits cause a failure to recognize and relieve pressure, irritation, or overt trauma which may lead to tissue damage.
III. Mechanical Stress: pressure, shear, friction perpetuate neuropathic and pressure ulcers.

36
Q
  1. Describe systemic factors associated with delayed wound healing.
A

I. Age: with age the body becomes worse at healing for a myriad of reasons.
II. Inadequate Nutrition
III. Comorbidities.
IV. Medication
V. Behavioral risk taking
VI. Inappropriate wound management

37
Q
  1. Describe methods to enhance delayed wound healing.
A

I. Maintain wound in moist, warm environment.
II. Do not use antiseptics unless recommended.

38
Q
  1. Identify two problems with the following statement: If left open to the air, chronic wounds will eventually heal.
A

I. Wounds heal faster in warm, moist environments.
II. Chronic wounds are not self-limiting and require aggressive interventions.

39
Q
  1. Does wound pain correlate with wound severity?
A

I. No. A patient may have severe wounds that are painless due to sensory nerve dysfunction.

40
Q
  1. Should a patient with an open wound who is undergoing chemotherapy receive physical therapy for wound care? Why or why not?
A

I. Yes. The patient is at risk for delayed wound healing and aggressive interventions should be instated.

41
Q
  1. Do all 80-year-old individuals heal at the same rate? Why or why not?
A

I. No. People are different but generally older individuals heal slower than younger people.

42
Q
  1. You are working with two patients with open wounds. Patient X is a 20-year-old college student who sustained a laceration to the forehead after falling off her mountain bike yesterday. The wound measures 7.0 * 0.8 cm and has some debris in the wound bed. Patient Y is a 68-year-old patient with diabetes who noticed a wound on the bottom of his foot 6 months ago. The wound measures 2.5 * 2.0 cm and is free of necrotic tissue. Which patient’s wound do you think will heal faster and why?
A

I. Patient X due to region of injury, age, and lack of comorbidities.

43
Q

You are working with a 66-year-old patient with diabetes who has an ulcer on the bottom of his foot. The wound has slowly but steadily decreased in size over the last 3 months using “good” local wound care and non-weight-bearing with crutches. Last week the wound was 0.5 cm in length, 0.4 cm in width, and 0.1 cm in depth, about a quarter of its original size. When you assess the wound today, there are no open areas, only a pink scar where the wound was previously located. The patient wishes to stop using his crutches and begin training for the upcoming Senior Olympic basketball trials. What is your response and why?

A

I. The patient should wait. Even thought the wound is closed it is still maturing and therefore is more susceptible to reinjury. NWB training would be best.

44
Q

Where do blisters occur ?

A

between the dermis and the epidermis.