Exam 3 Study Guide Flashcards
Peripheral vascular disease - PVD
General term of disrupted arterial or venous blood flow to the extremities
Causes are multifactorial – smoking, cardiac disease, DM, HTN, ↑ cholesterol & triglycerides, obesity, & sedentary lifestyle
Arterial Insufficiency
lack of blood flow to a region
Venous Insufficiency
inadequate drainage of venous blood
Arterial ulcer clinical presentation
lower extremities (Lateral malleoli, dorsum of foot & toes), size is partial to full thickness, wound base is necrotic & pale, lacks granulation, dry gangrene, drainage is minimal, painful and skin is cool to the touch.
> 1.0 <1.3 ABI reading
Normal
0.8-1.0 ABI reading
Mild peripheral arterial occlusive disease
<0.6 ABI reading
Intermittent Claudication
0.5-0.8 ABI reading
Moderate peripheral arterial occlusive disease
< 0.5 ABI readings
Severe occlusive disease
< 0.26 ABI readings
Resting ischemic pain
<0.02 ABI readings
Gangrenous extremity
Venous Ulcers
Inadequate drainage of venous blood resulting in edema, skin abnormalities & ulcerations
Venous ulcers clinical presentation
mostly located on Medial malleolus, small, shallow, irregular margins, wound bed is red and granulation tissue present, moderate to large quantity of drainage, generally painless, skin temp may be elevated.
Pitting edema grading scale 1+
up to 2mm depression, rebounding immediately.
Pitting edema grading scale 2+
3-4mm of depression, rebounding in 15sec or less
Pitting edema grading scale 3+
5-6mm of depression, rebounding in 60sec
Pitting edema grading scale 4+
8mm of depression, rebounding in 2-3 minutes.
Diabetic Neuropathy
weight-bearing surface of the foot, anesthetic, round & over a bony prominence, size is variable, wound bed is discolored, granulation is central with less necrotic tissue, drainage is minimal unless infected, rimmed by callus, painless.
Autonomic Neuropathy
Decreased or absent sweat and oil production, dry and inelastic skin, increased susceptibility to skin breakdown and injury, heavy callus formation.
Pressure Ulcers
Results from unrelieved pressure, friction, shear or stress, associated with poor mobility, dehydration, hypotension, decreased sensation, incontinence.
Pathogenesis of pressure ulcers
compression of capillaries occluding blood flow to and lymphatic drainage from tissues, occurs with pressure higher than 32 mmHg, muscle and tendon tolerate less pressure than skin.
Clinical presentation of pressure ulcers
circular pattern over bony prominence, greatest ischemia near bone, generally not painful
Stage 1 pressure wound
intact skin, non-blanchable erythema, warm skin temp, firm or boggy tissue feel, pain and itching
Stage 2 Pressure wound
partial-thickness wound with loss of dermis, shallow open ulcer or open/ruptured serum filled blister, red or pink wound bed but adipose is not visible
Stage 3 Pressure wound
Full thickness tissue loss, but not through fascia, undermining or tunneling may be present
Stage 4 pressure ulcer
Full-thickness loss, undermining, tunneling, or sinus tracts, exposed or easily palpable bone, tendon, or muscle.
Unstageable pressure ulcer
full-thickness skin or tissue loss, extent of tissue damage cannot be determined due to slough or eschar.
External risk factors for pressure ulcers
pressure with shear or moisture
intrinsic risk factors for pressure ulcers
Maceration, decreased skin resilience, malnutrition, decreased circulation, decreased sensation. Impaired mobility/activity, incontinence, altered level of consciousness
Phases of wound healing
Inflammation, repair, remodeling
Inflammation phase 1
normal immune response, injury to 10 days. Goals are to limit the extent of tissue damage, limit the spread of infection, remove necrotic tissue, debris, and pathogens.
Proliferation phase 2 timing and goals
day 3 to day 20, rebuilding structure and framework of the wound, fragile.
what happens during proliferation phase 2
new tissue from fibroblasts turn into collagen, re-epithelialization &/or contraction
Maturation/remodeling phase 3 timing and goals
day 9 up to 2 years, obtain complete wound healing & strength
whats happening during Maturation/Remodeling phase 3
epithelial cells continue to turn into type 1 collagen, granulation tissue is replaced by less vascular tissue, scar formation
role of oxygen in wound healing
oxygen is needed at the cellular level, decreased oxygen means increased likely hood for infection
What can limit perfusion
edema, necrosis, vasoconstriction
what can improve perfusion
warmth, avoid smoking, hydration, controlling pain & anxiety
Role of moisture in wound healing
dry wounds delay healing, wound hydration is most important external factor
Primary Skin Lesion
1st to appear, visually recognizable structure
Secondary skin lesion
when changes occur to a primary lesion (Scale, crust, thickening, erosion, ulcer, scar, fissure)
Signs and symptoms of skin lesions
Pruritis (itching)
Xerosis/Xeroderma (dry skin)
Urticaria (hives)
Rash (eruption of skin)
Blisters (could be friction or bacteria)
Changes in appearance of nails
Changes in skin pigmentation, turgor, texture
Causes of skin disease
Hereditary factors
Physical trauma
Systemic origin
Burns
Dehisced surgical wounds
Neoplasm
Reaction to radiotherapy
Contact with infective organism or injurious agent
Reaction to medication
Atopic Dermatitis
Most common type of eczema - chronic inflammatory skin disease. Results of dry irritable skin with impaired immune function
Diagnosis of atopic dermatitis
increased IgE and food allergies
Treatment of atopic dermatitis
Education, hygiene, moisture, avoidance of irritant, topical or systemic pharmacology.
Contact Dermatitis
Presents pruritis, erythema, and edema, primary treatment is to remove the causative agent, secondary treatment is avoidance, lubrication, topical agents.
Stasis Dermatitis
Development of areas of very dry, thin skin, often with small shallow ulcerations, result of vascular insufficiency. Initially presents with edema of legs, tissue becomes hypoxic & dies. Itching, heaviness in legs, brown-stained skin, open shallow lesions
Impetigo (bacterial infection)
superficial skin infection. Can be caused by staph or strep, hot and humid weather, close contact, poor hygiene, and trauma. Treatment with antibiotics
Cellulitis (bacterial infection)
Rapid spreading acute inflammation & infection of skin & subcutaneous tissue (strep or staph). Present in adults with DM, malnutrition, steroid therapy, presence wounds/ulcerations, lymphedema, obesity.
Herpes Simplex
Type 1 - Cold sore
Type 2 - Genital warts
Herpes Varicella-Zoster Virus (VZV)
Varicella (chicken pox) – fluid filled vesicles
Herpes Zoster (shingles) – blister like lesions
14 to 21 days
Verrucae (warts)
Common benign infection of skin & adjacent mucous membranes (HPV), transmission through direct contact. white/black dots.
Fungal infections
Invade stratum corneum, hair & nails
Superficial infections, live on not in skin.
Tinea corporis
Ringworm
Tinea capitis
Scalp
Tinea cruris
jock itch
tinea pedis
athletes foot
Candida
yeast infection
Seborrheic Keratosis (benign tumor)
basal cells, waxy smooth or raised yellow to dark tone lesions
Nevi (moles) (benign tumor)
pigmented or nonpigmented lesions of melanocytes
Actinic Keratosis (premalignant)
results years of sun exposure, abnormal well defined crusty like skin
Bowen Disease (premalignant)
can occur any where, persistent brown to reddish brown well-defined lesions
Basal Cell Carcinoma
Slow growing epithelial skin tumor originating from undifferentiated basal cells (Lack keratin). Rarely metastasize. Prolonged sun exposure, immunosuppression, & genetics.
Squamous Cell Carcinoma
2nd most common, invasive, risk is UV damage of DNA of epidermal nuclei
Malignant Melanoma
Neoplasm of melanocytes, can occur anywhere. there are 4 subtypes.
Psoriasis (autoimmune)
Chronic inherited, recurrent, inflammatory disease, triggered by mechanical, UV or chemical injury, stress, smoking & endocrine changes
Signs and symptoms of psoriasis
Dry, Itchy, cracking lesions
Functions of the epidermis
protection and regulation
function of dermis
provides strength, support, and blood to epidermis, “true skin”
Hypodermis
stabilization, loose adipose and connective tissue, provides padding especially over bony areas
Gauze indications
More reasons not to use than to use. Can be used as a secondary dressing, especially if changed frequently or if exudate is heavy
Gauze Disadvantages
No specific contraindications, but there are generally much better choices. Wet-to-Dry = Pain & Trauma
Impregnated Gauze indications
Good as a primary dressing over new sutures to prevent them catching or sticking
Impregnated Gauze disadvantages
Not very absorptive, may be greasy to wound bed
Transparent Films indications
Facilitates a moist environment, While in place, can protect skin from shearing, friction, & incontinence.
Transparent Films disadvantages
Can tear skin upon removal.(No deep or highly exudating wounds)
Foam indications
Highly absorptive.
Help to create an occlusive environment for moist wound healing.
Foam disadvantages
Should not be used alone on a dry wound unless used in combination with a “wet” product (i.e. gel)
Hydrogels indications
Increase moisture, soften necrotic tissue, support autolytic debridement. Good for stage 2 or 3 dry
Hydrogels disadvantages
Only minimally absorptive. Non-adherent (needs a secondary dressing).
Hydrocolloids indications
Most occlusive & moisture retentive; best for mild-to-moderately exudating wounds
Hydrocolloids disadvantages
Discontinue with increased exudate, hyper-granulation, or infection
Alginates indications
Absorb 20-30x their weight., can be used on infected wounds
Alignates disadvantages
Permeable to bacteria; require a secondary dressing
Hydrofibers indications
very absorbent, do not dry out or stick to the wound.
Skin substitutes indications
resemble skin structure and function. Useful for wounds that don’t respond to conventional dressings
Skin substitutes disadvantages
Very expensive! May require a secondary dressing or surgical fixation
Enzymatic debriders indications
slowly debride eschar
Enzymatic debriders disadvantages
Santyl needs added moisture to work (Vashe?)
Tape foam
Flexibility and stretch, comfortable, effective for swelling
Non adhesive tape
wrapping and securing bandages, adheres to self, does not adhere to skin
paper tape
Gentle, less adherent, affordable, breathable, sensitive skin, labeling
transparent tape
Sticks to anything, waterproof, easy to tear, strongest adhesive for skin, pliable. Leaves residue however
cloth/fabric tape
Sticks to skin, no residue, affordable, breathable, high strength, labeling. not waterproof, difficult to tear.
First Degree Burn
thickness is superficial, depth is to the epidermis, characteristics include pain, redness, mild swelling.
Second degree burn
Thickness is superficial partial, depth is to the dermis (papillary region), characteristics are pain, blisters, severe swelling.
Third degree burn
Thickness is deep partial, depth is to the dermis (reticular region), characteristics are white, leathery.
Third and fourth degree burn
Full thickness/subdermal, depth is to the hypodermis, characteristics are charred, insensate, eschar formation.
Zone of Coagulation
Cells are irreversibly destroyed, skin grafting, eschar is present and increased risk of infection
Zone of Stasis
Cells may die within 1-2 days without treatment.
Zone of hyperemia
Minimal cell damage, may recover in a few days without long lasting damage.
Heterotopic Ossification
the formation of extraskeletal bone in muscle and soft tissues, 20% burns are at increased risk, most common in elbows, hips, shoulders
Heterotopic Ossification signs and symptoms
Pain, tenderness, decreased ROM, a pathologic hard end feel
Autograft
The skin is donated by the patient
Xenograft
Graft skin is taken from another species
Allograft
Graft skin is taken from individual of the same species
Epidermal healing
Cells migrate from the surrounding epidermis into the wound, & stop when they bump into other epidermal cells (contact inhibition)
Dermal healing
scar formation, categorized by inflammation, proliferation, remodeling.
Superficial burn
sunburn, only cell damage to epidermis, skin appears erythematous, dry, free of blisters, & tender to touch.
Superficial Partial thickness burn
Epidermis & upper dermis are damaged, presence of intact blisters, extremely painful
Deep partial thickness burn
Epidermis is destroyed, dermis is severely damaged, wound bed is white, more white = deeper, very painful
Full thickness burn
All epidermal & dermal layers destroyed, possible subcutaneous fat layer, eschar will be present from black, red or white
Serous
thin watery appearance with few cells
Sanguineous
Maybe called “bloody”
Thin, bright red
Serosanguineous
Thin, watery, Pale pink
Purulent
Thin (seropurulent) or thick
Opaque tan to yellow
sweet smell
pseudomonas infection
ammonia smell
proteus infection
Induration
Abnormal hardening of the tissue caused by consolidation of edema.
