Free WCC Exam Flashcards

Hemostasis (clotting), inflammation (0-3 days; redness, edema, neutrophils/macrophages), proliferation (granulation, angiogenesis, epithelialization), and maturation/remodeling (collagen reorganization, up to 1-2 years). Chronic wounds stall in the inflammatory phase.

Primary: clean approximated edges (sutured incision). Secondary: open wound heals by granulation and contraction from the base up. Tertiary (delayed primary): wound left open then closed later, used when infection or contamination is a concern.

Partial-thickness involves epidermis and possibly part of the dermis and heals mainly by epithelialization. Full-thickness extends through the dermis into subcutaneous tissue or deeper and heals by granulation, contraction, and epithelialization.

Stage 1: intact skin with non-blanchable erythema (localized). Stage 2: partial-thickness loss with exposed dermis, a viable pink/red wound bed or an intact/ruptured serum-filled blister. No slough or deeper tissue is visible.

Stage 3: full-thickness loss with visible subcutaneous fat; slough/eschar may be present but bone/tendon/muscle not exposed. Stage 4: full-thickness loss with exposed or palpable fascia, muscle, tendon, ligament, cartilage, or bone.

Full-thickness loss where the base is obscured by slough or eschar; true depth cannot be determined until the base is exposed. Stable (dry, adherent, intact) heel eschar should not be removed as it acts as a natural cover.

Persistent non-blanchable deep red, maroon, or purple discoloration of intact or blistered skin from damage to underlying soft tissue. May evolve rapidly to a full-thickness loss even with optimal care.

Predicts pressure-injury risk across six subscales: sensory perception, moisture, activity, mobility, nutrition, friction/shear. Lower total score means higher risk; a score of 18 or below generally indicates the patient is at risk.

Reposition bed-bound patients at least every 2 hours and use support surfaces. Wheelchair users should perform pressure-relief weight shifts about every 15-30 minutes plus a redistribution cushion. Keep the head of bed at 30 degrees or less to limit shear.

Friction is surface rubbing causing superficial damage. Shear is internal tissue distortion when skin stays fixed while deeper structures slide (e.g., sliding down in bed), occluding vessels and causing deep ischemic injury that often looks small at the surface.

Venous: medial gaiter (above ankle), shallow with irregular borders, heavy exudate, hemosiderin staining and edema, mild pain relieved by elevation. Arterial: distal/lateral or toes, punched-out, dry, pale base, severe pain, worse with elevation.

Located over pressure/bony points (plantar metatarsal heads), round punched-out with a callused rim, typically painless due to peripheral neuropathy. Management centers on offloading, glucose control, debridement, and infection monitoring.

Higher ankle systolic pressure divided by higher brachial systolic pressure. Normal 1.0-1.4; below 0.9 indicates arterial disease; below 0.5 is severe ischemia. ABI above 1.4 suggests non-compressible calcified vessels (common in diabetes).

Compression is first-line for venous ulcers to reduce edema and venous hypertension. Confirm adequate arterial perfusion first: full high compression is contraindicated when ABI is below 0.5-0.6 because it can cause tissue ischemia.

Capillary refill should return within about 3 seconds; prolonged refill, absent dorsalis pedis/posterior tibial pulses, dependent rubor, and pallor on elevation point to arterial insufficiency requiring vascular referral before aggressive debridement.

Granulation: beefy red, moist, bumpy (healthy). Slough: yellow/tan stringy nonviable tissue. Eschar: black/brown necrotic tissue, may be hard or soft. Epithelial: pink/pearly migrating edge. Document the percentage of each.

Undermining is tissue destruction extending under intact wound edges (described by clock position and depth). Tunneling/sinus tract is a narrow channel extending from the wound into deeper tissue. Both increase dead space and infection risk.

Measure length head-to-toe, width side-to-side perpendicular to length, and depth at the deepest point with a moistened applicator. Use a consistent body-clock orientation each visit so progression or deterioration is tracked accurately.

Maceration is white, soft, waterlogged periwound skin from excess moisture/exudate, predisposing to wound enlargement. Excoriation is mechanical or chemical loss of surface skin. Both signal a need for better exudate management and skin protection.

Wound bed preparation model: Tissue (debride nonviable tissue), Infection/inflammation (control bioburden), Moisture balance (manage exudate), Edge (advance non-migrating edges). Used to systematically identify why a wound is not progressing.

A balanced moist wound bed promotes faster epithelial migration, autolysis, and less pain than a dry bed. The goal is moisture balance: enough to keep the bed moist without macerating the periwound skin.

Fastest method; uses scalpel, scissors, or curette to remove devitalized tissue, performed only within scope and clinician competency. Contraindicated with stable dry heel eschar and used cautiously with anticoagulation or poor perfusion.

Uses the body's own enzymes and moisture-retentive dressings (hydrogel, hydrocolloid) to liquefy necrotic tissue. Selective and painless but slow; avoid in infected wounds that need faster bioburden control.

Enzymatic uses a topical agent (e.g., collagenase) to selectively digest necrotic tissue. Mechanical (wet-to-dry, irrigation, monofilament pads) is nonselective and can damage healthy tissue and cause pain; wet-to-dry is generally discouraged.

Do not debride stable, dry, intact eschar on an ischemic limb or heel without adequate perfusion; it serves as a protective cover. Establish blood flow (ABI/vascular evaluation) before removing necrotic tissue on an arterial wound.

Occlusive, moisture-retentive dressing for light-to-moderate exudate and autolytic debridement. Can stay in place 3-7 days. Avoid on infected wounds, heavily draining wounds, or fragile periwound skin.

Highly absorbent dressing derived from seaweed for moderate-to-heavy exudate and bleeding wounds (hemostatic). Forms a gel on contact; needs a secondary cover. Not for dry wounds because it can desiccate the bed.

Adds moisture to dry or minimally exudative wounds and supports autolytic debridement of slough/eschar. Soothes pain. Contraindicated for heavily draining wounds because it cannot manage excess exudate.

Absorbs moderate-to-heavy exudate, provides cushioning and thermal insulation, and protects the periwound. Useful under compression. Not ideal for dry or minimally exudative wounds where it offers little benefit.

Used to lower bioburden in critically colonized or locally infected wounds. They are an adjunct, not a substitute for debridement and systemic antibiotics when indicated, and should be reassessed rather than used indefinitely.

Core rule: add moisture to dry wounds (hydrogel), maintain moist wounds, and absorb heavily draining wounds (alginate, foam). The wrong choice causes either desiccation that stalls healing or maceration that enlarges the wound.

Applies controlled subatmospheric pressure to remove exudate, reduce edema, increase perfusion, and promote granulation. Contraindicated with untreated osteomyelitis, malignancy in the wound, exposed vessels/organs, and necrotic tissue/eschar present.

Delivers 100% oxygen at increased atmospheric pressure to raise tissue oxygenation. Evidence-supported uses include diabetic foot ulcers with hypoxia, osteoradionecrosis, and compromised flaps; it is an adjunct to standard wound care.

The gold-standard offloading method for plantar neuropathic ulcers because it redistributes pressure and forces adherence. Contraindicated with active infection, ischemia, or heavy exudate; removable walkers are an alternative when casting is unsafe.

Healing a pressure-related ulcer requires removing the causative mechanical load. Without offloading (cushion, total contact cast, heel protector, repositioning), even optimal dressings will not produce durable closure.

Increasing pain, erythema, warmth, edema, purulent or increased exudate, foul odor, friable/discolored granulation, and delayed healing. New stalled healing in a previously progressing wound suggests increased bioburden or biofilm.

Contamination: bacteria present, not replicating. Colonization: replicating bacteria without host response. Critical colonization/local infection: bioburden delays healing. Infection: invading organisms with a host response (signs/symptoms). Treatment escalates along this continuum.

A structured microbial community in a protective extracellular matrix that resists antibiotics and host defenses, often invisible. Suspected when a wound stalls despite appropriate care; managed by repeated debridement plus antimicrobial dressings.

Cleanse and debride first, then obtain a tissue biopsy or the Levine technique (rotate a swab over 1 cm² of viable wound bed with pressure). Avoid swabbing exudate, slough, or eschar, which yields surface flora rather than the infecting organism.

A wound that probes to bone, an ulcer over 2 cm², or one present for weeks without progress raises suspicion for underlying bone infection. Confirmation and antibiotic decisions require imaging and provider/specialist referral.

Normal saline or potable water is preferred for routine cleansing. Cytotoxic agents (full-strength povidone-iodine, hydrogen peroxide, sodium hypochlorite) can damage granulation tissue and fibroblasts and are generally avoided on clean healing wounds.

Protein, calories, vitamin C, vitamin A, and zinc support collagen synthesis and immune function. Albumin/prealbumin and unintended weight loss help screen risk; malnutrition prolongs the inflammatory phase and impairs closure.

Hyperglycemia impairs leukocyte function, angiogenesis, and collagen formation and contributes to neuropathy and peripheral arterial disease. Glycemic control is a core component of any diabetic wound plan, not a separate concern.

Surgical wound edge separation most often occurs around postoperative days 5-10, when collagen tensile strength is still low. Risk factors include infection, obesity, diabetes, smoking, poor nutrition, and excessive wound tension or coughing.

Dehiscence is separation of wound layers; evisceration is protrusion of internal organs through the opening (a surgical emergency). For evisceration: cover with sterile saline-soaked gauze, position to reduce tension, do not push organs back, and notify the surgeon immediately.

A wound failing to show measurable progress after about 2-4 weeks of appropriate therapy warrants comprehensive reassessment of wound, patient, and plan (using TIME and holistic factors) and consideration of advanced therapies or referral.

Track surface area, depth, tissue type percentages, exudate, and periwound status at consistent intervals (often weekly). A roughly 20-40% area reduction by week 4 is a common positive predictor of eventual closure.

Effective wound education uses teach-back, addresses health literacy, and covers offloading/repositioning, nutrition, glucose control, dressing technique, skin inspection, and which warning signs to report. Adherence barriers must be assessed, not assumed.

Document location, etiology, stage/classification, dimensions, tissue types, exudate, periwound, pain, odor, intervention, and patient response each visit. Accurate, objective records support continuity of care, reimbursement, and legal defensibility.

WCC certification validates wound knowledge but does not expand legal scope. Permitted interventions (e.g., sharp debridement) remain governed by the holder's professional license, state practice act, and employer policy.