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NCOI UNIT 3 WOUNDS AND BURNS EXAM QUESTIONS WITH COMPLETE SOLUTIONS 100% VERIFIED LATEST UPDATE

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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 ...

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  • July 23, 2024
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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 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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