Integument Flashcards

1
Q

Skin Changes in Older Adult

A
  • Loss of subcutaneous tissue
  • Dermal thinning
  • Decreased elasticity causes wrinkles and sagging
  • Turgor decreased
  • Inability to respond to heat and cold quickly
  • Increased risk for heat stroke and hypothermia
  • Loss of oil and sweat gland causes dry itchy skin
  • Flat brown macules on hands and arms
    “Liver spots”
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2
Q

Skin Changes in Older Adult

A
  • Keratosis caused by hyperpigmentation
  • Seborrheic keratosis
  • Dark raised lesions
  • Actinic keratosis
  • Reddish raised plaques on areas of high sun exposure can become malignant
  • Skin tags
  • Hair and nail growth decreases
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3
Q

Lesions

A
  • Characteristics of lesions helpful in diagnosing
  • Can be cause by systemic diseases or infections, allergies
  • Location, length of time present, and any changes occurring help with diagnosis
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4
Q

Skin Colour

A
  • Can be a sign or symptom of an number of disorders
  • Result of varying levels of pigmentation
  • Exposure to sun causes a buildup in melanin, causing light skin to tan which can impair changes
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5
Q

Skin Colour

A

Erythema
- Reddening of skin
- Caused by blushing, fever, inflammation, hypertension
Cyanosis
- Bluish discoloration of skin and mucous membranes
- Results from poor oxygenation of hemoglobin, lack of adequate RBCs or hemoglobin

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6
Q

Skin Colour

A

Jaundice
- Yellow to orange color visible in skin and mucous membranes
- Usually results from a liver disorder
Pallor
- Paleness of skin
- Caused by shock, fear, anemia, anger, or hypoxia

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7
Q

Integumentary System: Diagnostic Tests

A
Biopsy
Culture and sensitivity
Skin scraping
Patch test
Wood’s light examination
Blood work
Photographs
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8
Q

Bacterial Infections

A
  • Primary infection – relate to resident flora
  • Secondary infection- developing in wounds or lesions
  • Often arise from the hair follicle where bacteria accumulate and grow to cause a localized
    infection
  • Systemic infection if invade into deeper tissue
  • Many nosocomial infections of wounds or open lesions are often the result of bacteria (staph aureus-MRSA)
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9
Q

Foliculitis

A
  • Often caused by Staphylococcus aureus
  • Infection begins at the skin surface and extends
    into hair follicle
  • Bacteria release enzymes and chemicals that cause inflammation
  • Commonly seen on the scalp and extremities, face of bearded men, legs of women who shave, eyelids (stye)
    Contributing factors include: poor hygiene, nutrition, prolonged moisture, trauma
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10
Q

Furuncle (boil)

A
Infection of the hair follicle
- Carbuncle—group of infected hair
follicles
- Often from Staphylococcus aureus
- Deep red nodule that gets larger
and becomes a cyst.
- May cause fever, chills, or malaise
- Contributing factors include: poor
hygiene, skin trauma, excessive moisture, and systemic diseases (diabetes)
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11
Q

Cellulitis

A
  • Localized infection of the dermis and subcutaneous layers
  • May occur following a wound or an extension of furuncles
  • Spreads as a result of spreading factor substance called “hyaluronidase” from the organism
  • Breakdown of fibrin network and other barriers
  • Cellulitis is red swollen, painful
  • May also experience : fever, chills, malaise, headache,
    swollen lymph glands
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12
Q

Acute Necrotizing Fasciitis

A
  • Highly virulent Group A beta hemolytic streptococcus
  • Also termed “Flesh Eating Disease”
  • Rapid tissue invasion resulting from the secretion of proteases & enzymes that destroy the tissue. They also produce toxins that cause toxic shock.
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13
Q

Acute Necrotizing Fasciitis

A
  • Often a history of minor trauma or infection in the skin and subcutaneous tissue of an extremity.
  • Surperficial facia in the subcutaneaous tissue and
    fascia surrounding the skeletal muscle become edematous and necrotic with occlusion of small blood vessels leading to gangrene
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14
Q

Acute Necrotizing Fasciitis

A
  • S&S : Infected area is inflamed, painful and increases in size rapidly as dermal gangrene occurs.
  • Systemic toxicity develops with fever, tachycardia, hypotension, mental confusion and disorientation
  • Possible organ failure
  • Mortality rate 40 -60%
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15
Q

Fungal Infections

A
  • Fungi are plantlike organisms that live in soil, on animals, on humans
  • Dermatophypes are fungi that live on stratum corneum, hair, and nails and cause superficial skin infections.
  • Superficial fungal skin infections are often referred to as ringworm or tinea.
  • Fungal disorders are also called Mycoses
  • Transmission – direct or indirect
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16
Q

Fungal Infections: Contributing Factors

A
  • Moist areas
  • Use of broad spectrum antibiotics
  • Presence of diabetes mellitus
  • Immunodeficiencies
  • Nutritional deficiencies
  • Pregnancy
  • Increasing age
  • Iron deficiency
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17
Q

Dermatophyte (Tinea)

A

Tinea pedis
- Athlete’s foot (soles of feet, toes, toenails. Pruritis and foul odour, mild scaliness to deep fissures)
Tinea curis
- Groin infection (inner thigh and buttocks “jock itch”)

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18
Q

Viral Infections

A
  • Pathogens that have RNA or DNA cores surrounded by a protein coat
  • Depend on live cells for reproduction
  • Viruses that cause skin lesions either increase cell growth or cause cellular death
  • Increase in viral skin disorders may be related to some commonly used drugs
    (birth control, corticorsteroids and antibiotics)
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19
Q

Warts

A
  • Lesions caused by the Human papillomavirus (HPV)
  • Often found on the skin and mucous membranes
  • Nongenital warts are considered benign lesions
  • Genital warts may be precancerous
  • Transmitted through skin contact : viral shedding
  • Most are round, raised, rough grey surface.
  • Resolve spontaneously
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20
Q

Warts: Common Types

A
  • Common : anywhere on skin and mucous membranes
  • Plantar : on the soles of feet , finger and face
  • Condylomata acuminate (venereal warts) : glans of the penis, anal area, vulva (cauliflowerlike pink or purple)
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21
Q

Parasitic Infections

A
  • Skin invaded by parasites or insects
  • Often associated with crowded or unsanitary living conditions
  • Most common parasites are mites and lice
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22
Q

Pediculosis

A
  • Infestation of lice
  • Transmission : contact with an infected person or contact with clothing or linen infested with
    parasites.
  • Causes intense itching and skin irritation
  • Three types live on humans
  • Pediculosis corporis—body lice
  • Pediculosis capitus—head lice
  • Pediculosis pubis—pubic lice (crabs)
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23
Q

Scabies (Sarcoptes scabiel)

A
  • Female mite
  • Transmission: generally skin to skin contact but the mite can live for 2 days on clothing and linens
  • Outbreaks frequently occur in shelters, dormitories and long term care facilities.
  • Occurs up to 4 weeks after contact
  • Infestation between fingers and inner surfaces of wrist, elbow, axillae, nipple, penis, belt line, and gluteal crease
  • Small red mite burrows into skin
  • Pruritus common at night; increased risk of infection
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24
Q

Infections/ Infestations: Diagnosis

A
  • Culture and sensitivity
  • Scrapings and microscopic examination
  • Ultraviolet light inspection
  • Visual inspection
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25
Q

Pressure Ulcers

A
  • Ischemic lesions of the skin and underlying tissue caused by external pressure the impairs the flow of blood and lymph
  • Ischemia causes tissue necrosis and eventual ulceration
  • Necrotic tissue elicits an inflammatory response with a possible secondary bacterial infection
  • Tend to develop over bony prominences or areas exposed to pressure, friction & shearing
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26
Q

Pressure Ulcers: Risk Factors

A
  • Older adults
  • Limited mobility from injury or hospitalization
  • Paralysis
  • Incontinence
  • Nutritional deficits
  • Chronic illnesses (renal failure, anemia)
  • Edema
  • Infections
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27
Q

Patho and Manifestations

A
  • Pressure distorts capillaries and interferes with bld flow
  • Reactive hyperemia occurs (brief)
  • Platelets clump in endothelial cells surrounding capillaries and form microthrombi Ischemia and hypoxia occurs
  • Cells and tissue in immediate area die and become necrotic
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28
Q

Shearing Forces

A
  • One tissue layer slides over another
  • Stretching and bending cause injury and thrombosis
  • Cause: HOB elevated or pulling
  • Skin and superficial fascia remain fixed to bed sheet
  • Deep fascia and bony skeleton slide in the direction of movement
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29
Q

Contact Dermatitis

A

Caused by exposure to an allergen or direct chemical irritation

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30
Q

Atopic Dermatitis (Eczema)

A
  • Common in infancy
  • May persist into adulthood
  • Atopic refers to inherited tendency toward allergic conditions
  • Family history of eczema, allergic rhinitis or hay fever, asthma
  • Indicates genetic component
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31
Q

Atopic Dermatitis: Pathophysiology

A
  • Chronic inflammation results from allergens

- Eosinophilia and inc. serum IgE levels indicate allergenic basis

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32
Q

Atopic Dermatitis: Manifestations; Children

A
  • Pruritic lesions, moist, red, vesicular and covered with crusts
  • Location- symmetrically on face, neck, extensor surfaces (arms, legs, buttocks)
33
Q

Atopic Dermatitis: Manifestations; Adult

A
  • Affected skin dry and scaling with lichenification (thick and leathery patches)
  • Moist and red in folds
  • Location – flexor surfaces arms and legs (antecubital areas), hands and feet
34
Q

Atopic Dermatitis: Diagnostic Tests; Allergy testing - Complications

A
  • 2nd infections due to scratching and disseminated viral infections (herpes)
  • Affected areas more sensitive to many irritants
  • Marked temp changes aggravate and cause exacerbations (dry winters, hot humid summers)
35
Q

Psoriasis

A
  • Chronic inflammatory skin disorder of unknown origin
  • Familial tendency
  • Onset in teens
  • Increased cellular proliferation leading to thickening of dermis and epidermis
  • Epidermal shedding occurs quicker then normal
  • Silvery placques form while base remains erythermatous d/t inflammation and vasodilation
36
Q

Herpes Simplex

A
  • Most common cause of cold sores, fever blisters
  • Herpes simplex virus type I
  • Spread by direct contact with saliva or fluid of lesion
37
Q

Herpes Simplex: Patho

A
  • Primary infection may be asymptomatic but virus remains in latent stage in sensory nerve
    ganglion of trigeminal nerve
  • Maybe reactivated by infection, common cold, sun exposure or stress
  • Painful vesicle – ruptures and forms crust
  • Healing spontaneously in 2-3 weeks
38
Q

Herpes Simplex: Medications

A
  • Initially asymptomatic
  • Reactivation – preliminary burning or tingling sensation along the nerve at lips
  • Painful vesicle until rupture
  • Crusted
39
Q

Herpes Simplex: Diagnostic Tests; Complications

A

Diagnostic tests
- none
Complications
- Keratitis spreading virus to eye and cause infection and ulceration of cornea
- Herpetic whitlow – painful infection of fingers

40
Q

Herpes Zoster (Shingles)

A
  • Caused by varicella-zoster virus (VZV)
  • Usually seen in adults years after having chicken pox or varicella as child
  • Can occur in children post chicken pox
41
Q

Herpes Zoster (Shingles): Patho

A
  • Usually affects one
    cranial nerve or dermatone (a cutaneous area innervated by a spinal nerve) on one side of body
  • Immune deficient clients - lesions spread locally
42
Q

Herpes Zoster (Shingles): Diagnostic Tests; Complications

A

Diagnostic tests
- Based on location and look of rash
Complications
- Visual impairment – involvement of ophthalmic division of trigeminal nerve
- Neuralgia – in older individuals this pain may continue after lesions are gone

43
Q

Burns

A
  • An injury in which a transfer of energy to the human body results in tissue loss, damage or irreversible destruction.
  • May be mild or life threatening
  • Causes an acute inflammatory response, release of chemical mediators resulting in a:
  • Major fluid shift
  • Edema
  • Decreased blood volume
44
Q

Types of Burns

A
  • Thermal
  • Dry heat—flame
  • Moist heat—steam or hot liquid
  • Chemical
  • Acid or alkaline agents
  • Electrical—current or voltage
  • Radiation—sunburn or radiation treatment of cancer
45
Q

Severity of Burn

A
  • Cause of the burn
  • Temperature
  • Duration of the contact
  • Extent of the burn surface
  • Site of the injury
46
Q

Burn Classification

A
  • Classified by depth of damage
  • Percentage of body surface area involved
  • Partial thickness – superficial (1st
    degree)
  • Partial thickness – deep (2nd degree)
  • Full thickness – ( 3rd and 4th degree)
47
Q

Classifications of Burn Depth

A
  • Partial thickness - Superficial—first degree
  • Epidermal layer (superficial)
  • Sunburn, UV light, minor flash injury, minor radiation burn associated with cancer treatment
  • Appear red and painful but heal without a scar
  • May also experience chills, headache, nausea and vomiting.
48
Q

Classification of Burn Depth

A
  • Partial-thickness – deep- second degree
  • Superficial—dermis
  • Surface appears red, moist with blister formation
  • Pain in response to temperature and air is usually severe
  • Pigment changes are common
  • Blanches with pressure
  • Deep—dermis plus hair follicles
  • Surface appears pale and waxy and moist or dry
  • Large, easily ruptured blisters
  • Areas of pain and decreased sensation
  • Sebaceous and sweat glands intact
  • Healing more than 21 days
49
Q

Classification of Burn Depth

A
  • Full-thickness burn—third and fourth degree
  • All layers of skin
  • Extend to subcutaneous fat, connective tissue, muscle, and bone
  • Appears pale, waxy, yellow, brown, mottled charred, or non blanching red
  • Wound surface is dry, leathery and firm to the touch.
  • Pain and touch receptors destroyed
  • The damaged tissue called
  • Eschar shrinks causing pressure on edematous tissue beneath it.
  • Require skin grafts for healing – no cells available for reproduction - Prolonged contact with flames, steam, chemicals or high voltage electrical current.
50
Q

Percentage of Body Surface Area

A
  • Provides a guideline for fluid replacement and therapeutic interventions.
  • “Rule of Nines”
  • Method for rapid calculation of area affected
  • Body parts are assigned a value of nine or a multiple of nine
  • Are approximations and can be revised
  • Adjustments often made for children
51
Q

Effects of Burns

A

Serious burns have many effects both local and systemic including:

  • Shock
  • Respiratory Problems
  • Pain
  • Infection
  • Metabolic Needs
52
Q

Major Burns: Cardiovascular System

A

Cardiac rhythm alterations
- Burns of more than 40% TBSA cause significant myocardial
dysfunction including decreased myocardial contractility and
decreased cardiac output causing a falling BP. (hypovolemia)
- Called BURN SHOCK (hypovolemic shock)
- Loss of potassium ions from the injured cells also contribute
to cardiac dysrhythmia
Peripheral Vascular compromise
- Direct heat damage to blood vessels
- Circulation impaired due to edema and peripheral
vasoconstriction resulting in necrosis of the underlying
tissues
- RBC destruction

53
Q

Major Burns: Shock

A
  • No bleeding with burns – tissue and blood coagulate or solidify
  • Inflammatory process occurs
  • When large burn – inflammatory response results in massive shift of water, protein and electrolytes causing fluid excess or edema.
  • Difficult to maintain blood volume until inflammation subsides
  • Prolonged or recurrent shock may cause kidney failure or damage to organs
54
Q

Major Burns: Respiratory System

A
  • Inhalation injury ranging from mild respiratory inflammation to massive pulmonary failure
  • Carbon monoxide
  • Smoke inhalation
  • Interstitial Pulmonary Edema
  • Upper airway thermal injury

Pneumonia may result because of decreased ventilation, inflammation in respiratory tract and immobility.

55
Q

Major Burns: Immune System

A
  • Impairs active components of cell-mediated and humoral immunity
  • Decrease in serum immunoglobulins
  • Decrease in serum protein
  • These put the client in a state of Acquired immunodeficiency and risk for infection for up to 4 weeks following the injury.
  • Infections can develop causing death despite intense antimicrobial therapy
56
Q

Major Burns: Integumentary System

A

Impairs normal physiological function of the skin
If the microcirculation:
- Remains intact, it will cool and protect deeper layers
- Is lost, continues to burn even if heat source removed
- Thickness of the dermis and epidermis varies from one area to another in the body – damage in one area may not occur in another based on temperature.

57
Q

Major Burns: GI System

A
  • Curling’s ulcer – acute ulcer of the stomach or duodenum (pain, hematemesis, occult blood in the stool)
  • Paralytic ileus - lack of intestinal motility (gastric distension, nausea, vomiting and hematemesis)
58
Q

Major Burns: Urinary System

A
  • Early stages – renal blood flow and glomerular filtration rates reduced from decreased intravascular blood volume and release of ADH.
  • Urine output decreases while serum creatinine and blood urea nitrogen (BUN) increases .
  • Dark brown urine due to release of large amounts of dead or damaged erythrocytes which could occlude renal tubules ultimately leading to renal failure.
59
Q

Major Burns: Metabolism

A
Ebb phase
- Decreased metabolic state
- First 3 days of injury
Flow phase
- Hypermetabolic state
- Increased BMR—twice normal rate
- Body weight and heat decrease
- Persists after wound closure and may reappear
60
Q

Major Burns: Infection

A
  • Major concern for patients with burns
  • Ready made source of infection within glands and hair follicles (normally present microbes)
  • Opportunistic organisms (bacteria and fungi) waiting to invade open areas with decreased defensive barriers and reduced blood flow.
  • Infection increases tissue loss.
  • Common microbes: pseudomonas aeruginosa, Staphylococcus aureus, Klebsiella and candida
61
Q

Major Burns: Infection

A
  • Only give antibiotics once microbe has been identified
  • Risk of infection and toxins spreading throughout the body septic shock.
  • Prevention – excision or removal of the damaged tissue and skin grafting since few epithelial cells are available for direct healing.
62
Q

Major Burns: Healing

A
  • The recovery period may continue for weeks and months
  • Scar tissue occurs even with skin grafting and impairs function as well as appearance
  • Hypertrophic scar tissue is common.
  • Children may require additional surgeries to accommodate growth.
63
Q

Major Burns: Healing

A

Healing involves 4 phases

  • Hemostasis
  • Inflammation
  • Proliferation
  • Remodeling
64
Q

Major Burns: Phase 1 Hemostasis

A
  • Immediately following the injury
  • Platelets in contact with the injury – aggregate and degranulate
  • Fibrin deposited, trapping platelets and thrombus formed
  • Thrombus and local vasoconstriction lead to hemostasis
65
Q

Major Burns: Phase 2 Inflammation

A
  • Local vasodilation and an increase in capillary permeability
  • Neutrophils infiltrate the wound and peak at 24 hours
  • Monocytes then predominate - convert macrophages which consume pathogens
66
Q

Major Burns: Phase 3 Proliferation

A
  • Within 3 – 4 days postburn – fibroblasts are the major cell within the wound
  • Peak in numbers by day 14
  • Granulation tissue begins
  • Epithelial cells cover the wound
  • Lasts until complete reepithelialization occurs
67
Q

Major Burns: Phase 4 Remodeling

A
  • May last for years
  • Collagen fibers are reorganized into compact areas
  • Scars contract and fade in colour
  • When burn injury extends into dermal layer may result in hypertrophic scar or keloid
68
Q

Major Burns: Hypertrophic Scars, Keloid

A

Hypertrophic Scar
- Overgrowth of dermal tissue that remains within the boundary of the wound.
Keloid
- Scar that extends beyond the boundaries of the original wound.

69
Q

Major Burns: Diagnostic Tests

A
  • Cultures Urinalysis
  • Complete blood count
  • Serum electrolytes
  • Total protein and albumin
  • Arterial blood gases
  • Pulse oximetry
  • Chest x-ray and flexible bronchoscopy
  • Electrocardiogram
70
Q

Skin Cancer

A
Two main types of cancer:
Melanomas
Non-melanoma
- Basal cell carcinoma
- Squamous cell carcinoma
71
Q

Melanoma

A
  • Starts in the melanocytes
  • Can be anywhere but increased on trunk, neck, legs, face
  • Melanoma is suspected in any nevus that shows:
  • Change in appearance
  • Change in border
  • Change in color
  • Increase in diameter
72
Q

Melanoma Risks

A
  • Most skin cancers are caused by exposure to UV radiation
  • UV rays change the genetic material in the cells
  • Increased risk with fair skin, freckling and light hair
  • Moles Family history
73
Q

Melanoma Risks

A

Personal history of melanoma
Immune suppression
Gender
Age

74
Q

Melanoma

A

Precursor lesion is a dysplastic nevi (mole)
Change in the color or size of a nevus occurs in 70% of people diagnosed with melanoma
- A asymmetry
- B border irregularity
- C color variation
- D diameter greater than 6 mm

75
Q

Basal Cell

A
  • Develop from basal cells
  • Slow growing
  • Rarely spread
76
Q

Squamous Cells

A
  • Common on sun exposed areas
  • More aggressive that basal cells
  • Painless, malignant
77
Q

Basal & Squamous Cell Risks

A
  • Psoriasis treatment
  • Smoking
  • HPV infection
  • Reduced immunity
78
Q

Warning Signs of Skin Cancer

A
  • A sore that does not heal
  • A change in shape, size, color, or texture of a lesion
  • New moles or odd shaped lesions that develop
  • A skin lesion that bleeds repeatedly, oozes fluid or itches