NCOI UNIT 3 WOUNDS AND BURNS EXAM QUESTIONS WITH COMPLETE SOLUTIONS 100% VERIFIED LATEST UPDATE
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Module
NCOI
Institution
NCOI (NCOI)
NCOI UNIT 3 WOUNDS AND BURNS EXAM QUESTIONS WITH COMPLETE SOLUTIONS 100% VERIFIED LATEST UPDATE
Keloid
Overgrowth of collagenous tissue from at site of a previous injury
Vitiligo
Total loss of pigmentation in an area of skin
Lack of melanin, unknown cause
Actinic keratosis
premalignant skin ...
Overgrowth of collagenous tissue from at site of a previous injury
Vitiligo
Total loss of pigmentation in an area of skin
Lack of melanin, unknown cause
Actinic keratosis
premalignant skin lesions
Pre-cancerous
Risk factors for Squamous cell Carcinoma
pipe, cigar, and cigarette smoking
Immunosuppression leads to dramatic increase in the incidence
Bacterial Skin Infections
When the balance between the host and microorganisms is changed. This can occur as
a primary infection after a break in the skin. Or, a secondary infection can occur in
already damaged skin or as a sign of a systemic disease
Staphylococcus aureus and group A β-hemolytic streptococci are the major types of this
responsible for primary and secondary skin infections.
Streptococci cause impetigo, erysipelas, cellulitis, and lymphangitis. S. aureus causes
impetigo, folliculitis, cellulitis, and furuncles
,Viral Skin Infections
These are hard to treat. When this infects a cell, a skin lesion may develop.
Herpes simplex, herpes zoster, and warts are the most common viral infections
affecting the skin
Fungal skin infections
Most infections are relatively harmless in healthy adults, but they can cause
embarrassment and distress.
Infections are easy to diagnose. A microscopic examination showing the appearance of
hyphae (threadlike structures) in a skin scraping mounted in 10% to 20% potassium
hydroxide (KOH) indicates an infection. A Wood's light examination of hair infected with
certain fungi will fluoresce blue to green.
Stevens Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN)
Rare, life-threatening diseases.
They are violent immune responses that often occur as a severe adverse reaction to
either a medication or, more rarely, an infection. The result is the acute destruction of
the epithelium of the skin and mucous membranes.
Typically occur 4 to 21 days after starting use of the offending drug.
Clinical manifestations of Stevens Johnson syndrome
fever, cough, headache, anorexia, myalgia, and nausea, precede skin and mucous
membrane findings by 1 to 3 days.
Skin involvement starts as an erythematous, macular rash with purpuric
centers. Over a period of hours to days, the rash merges to form blisters with sheet-like
epidermal detachment.
, Seborrheic Keratosis
Round, oval patches, sometimes irregular looking
Looks like they are stuck on the skin.
NOT PRECANCEROUS
Initial phase
Lasts 3-5 days
Edges of incision are aligned
Blood fills the incision area, which forms matrix for WBC migration
Acute inflammatory reaction occurs
The area of injury is composed of fibrin clots, erythrocytes, neutrophils (both dead and
dying), and other debris. Macrophages ingest and digest cellular debris, fibrin
fragments, and RBCs.
Extracellular enzymes derived from macrophages and neutrophils help digest fibrin.
As the wound debris is removed, the fibrin clot serves as a meshwork for future capillary
growth and migration of epithelial cells.
Granulation Phase
Fibroblasts migrate into site and secrete collagen.
Wound is pink, vascular, and FRAGILE.
Surface epithelium begins to regenerate.
Maturation phase and scar contraction
Begins 7 days after injury and continues for several months/years
Fibroblasts disappear as wound becomes stronger
Mature scar forms
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