1.

Epidermis

PART I — ANATOMY AND PHYSIOLOGY OF THE INTEGUMENTARY SYSTEM 2. Dermis

3. Subcutaneous tissue (hypodermis)

I. Overview of the Integumentary System

The integumentary system is the largest organ system of the body, composed of the: III. Epidermis

• Skin General Characteristics

• Hair • Outermost layer

• Nails • Avascular (no blood vessels)

• Sweat (sudoriferous) glands • Receives nutrients via diffusion from dermis

• Sebaceous (oil) glands • Composed of stratified squamous epithelium

Primary Functions • Constantly regenerates

1. Protection Rationale:
Avascularity reduces bleeding from minor injuries while still allowing rapid cell turnover for
2. Thermoregulation
repair.
3. Sensation

4. Metabolism (vitamin D synthesis)

A. Cell Types of the Epidermis
5. Excretion
1. Keratinocytes
6. Immune defense
• Most abundant cell
7. Fluid balance
• Produce keratin (a fibrous protein)
Rationale:
Function:
Because the integumentary system interfaces directly with the external environment, it
Keratin provides waterproofing, strength, and resistance to abrasion.
plays a critical role in homeostasis, infection prevention, and early detection of systemic
disease.

2. Melanocytes

II. Skin: Structure and Organization • Located in the stratum basale

The skin (cutaneous membrane) has three major layers: • Produce melanin
Function of Melanin:

• Absorbs ultraviolet (UV) radiation 2. Stratum Spinosum

• Protects DNA from damage • Cells connected by desmosomes

Rationale: • Provides strength and flexibility

Increased melanin reduces risk of UV-induced skin cancer.

3. Stratum Granulosum
3. Langerhans Cells
• Keratinization begins
• Immune cells (macrophage type)
• Cells flatten and lose nuclei
• Derived from bone marrow

Function:
4. Stratum Lucidum
• Capture antigens
• Present only in thick skin (palms, soles)
• Activate immune response
• Provides extra protection

4. Merkel Cells
5. Stratum Corneum
• Associated with sensory nerve endings
• Dead, flattened, keratinized cells
Function:
• Primary protective barrier
• Light touch sensation
Rationale:
• Texture discrimination This layer prevents fluid loss and blocks pathogens and chemicals.

B. Layers (Strata) of the Epidermis IV. Dermis

From deepest to most superficial: General Characteristics

1. Stratum Basale • Highly vascular

• Single layer of dividing cells • Provides strength and elasticity

• Responsible for cell regeneration • Contains nerves, glands, blood vessels, hair follicles
 • Sensory receptors

A. Layers of the Dermis

1. Papillary Layer V. Subcutaneous Tissue (Hypodermis)

• Thin, superficial layer Composition

• Contains capillaries and nerve endings • Loose connective tissue

• Forms fingerprints • Adipose (fat) tissue

Function: Functions

• Nourishes epidermis 1. Insulation

• Sensory perception 2. Energy storage

3. Shock absorption

2. Reticular Layer 4. Anchors skin to underlying structures

• Thicker, deeper layer Rationale:

Loss of subcutaneous fat increases risk of hypothermia and pressure injuries.
• Dense connective tissue

• Contains:
VI. Skin Appendages
o Collagen (strength)

o Elastin (elasticity)
A. Hair
Rationale:
Loss of elastin and collagen leads to wrinkles and sagging. Structure

• Shaft (visible portion)

B. Structures Found in the Dermis • Root (below surface)

• Hair follicles • Follicle

• Sebaceous glands Functions

• Sweat glands • Protection (scalp, eyelashes)

• Blood vessels • Sensory input

 • Thermoregulation (piloerection) Clinical Link:
Overactivity → acne vulgaris

B. Nails
2. Sweat (Sudoriferous) Glands
Structure
a. Eccrine Glands
• Nail plate
• Distributed throughout body
• Nail bed
• Produce watery sweat
• Lunula
Function:
• Cuticle (eponychium)
Primary thermoregulation mechanism
Functions

• Protect fingertips
b. Apocrine Glands
• Aid fine motor skills
• Located in axilla, groin
Clinical Significance:
• Secrete protein-rich sweat
• Clubbing → chronic hypoxia
Clinical Link:
• Spoon nails (koilonychia) → iron-deficiency anemia Bacterial breakdown causes body odor

C. Glands of the Skin VII. Thermoregulation

Skin regulates body temperature via:

1. Sebaceous Glands • Vasodilation → heat loss

• Secrete sebum • Vasoconstriction → heat conservation

• Usually associated with hair follicles • Sweating → evaporative cooling

Functions of Sebum: Rationale:

Failure of thermoregulation leads to heat stroke or hypothermia.
• Lubricates skin and hair

• Inhibits bacterial growth

VIII. Sensory Functions of the Skin
Receptors Detect: Rationale:
Older adults are at increased risk for skin tears, pressure injuries, and infections.
• Touch

• Pressure
PART III – INTEGUMENTARY SYSTEM
• Pain
Inflammatory and Immunologic Skin Disorders
• Temperature

• Vibration
I. Overview of Inflammatory and Immunologic Skin Disorders
Clinical Importance:
Neuropathy (e.g., diabetes mellitus) reduces sensation and increases injury risk. Inflammatory and immunologic skin disorders result from abnormal activation of the
immune system, leading to inflammation, hypersensitivity reactions, or autoimmune
destruction of skin components.
IX. Metabolic and Immune Functions
These disorders may involve:
Vitamin D Synthesis
• Epidermis
• UV exposure converts precursors into vitamin D
• Dermis
• Essential for calcium absorption and bone health
• Skin appendages

• Systemic immune involvement

Immune Defense
They often present with:
• Langerhans cells initiate immune response
• Erythema (redness)
• Intact skin prevents microbial entry
• Pruritus (itching)

• Edema (swelling)
X. Aging and the Integumentary System
• Scaling, vesicles, or plaques
Changes include:

• Thinner epidermis
II. ATOPIC AND ALLERGIC SKIN DISORDERS
• Decreased collagen

• Reduced sweat and oil production

1. Atopic Dermatitis (Eczema)
• Delayed wound healing
Definition
A chronic, relapsing, inflammatory skin disorder characterized by intense pruritus, dry skin, Diagnosis
and eczematous lesions, commonly associated with asthma and allergic rhinitis.
• Clinical diagnosis based on history and appearance

• Elevated IgE levels

Pathophysiology
• Positive family history of atopy
• Genetic defect in skin barrier proteins (filaggrin deficiency) → increased
transepidermal water loss
Management
• Increased penetration of allergens and microbes
• Emollients to restore skin barrier
• Type I hypersensitivity reaction mediated by Immunoglobulin E (IgE)
• Topical corticosteroids (reduce inflammation)
• Overactivation of T-helper 2 (Th2) cells → cytokine release → inflammation
• Antihistamines (relieve itching)

• Avoidance of triggers
Clinical Manifestations

• Severe pruritus (hallmark)

Nursing Rationale
• Dry, scaly skin (xerosis)
Maintaining skin hydration prevents allergen penetration and reduces immune activation.
• Erythematous patches and plaques

• Lichenification (thickened skin from chronic scratching)

2. Contact Dermatitis
• Distribution varies by age:
Types
o Infants: face, scalp, extensor surfaces
1. Irritant Contact Dermatitis
o Children/adults: flexural areas (elbows, knees, neck)
2. Allergic Contact Dermatitis

Triggers
Definition
• Allergens (dust mites, pollen, food)
Inflammation of the skin resulting from direct contact with an irritant or allergen.
• Stress

• Heat and sweating

Pathophysiology
• Harsh soaps and detergents
• Irritant type: direct chemical damage to skin cells
 • Allergic type: Type IV delayed hypersensitivity reaction • Topical corticosteroids

o T-cell mediated immune response • Cool compresses

o Sensitization phase followed by elicitation phase • Antihistamines for pruritus

Common Triggers Nursing Rationale

• Nickel Early identification and avoidance prevent chronic skin damage and infection.

• Latex

• Poison ivy (urushiol) III. PAPULOSQUAMOUS DISORDERS

• Cosmetics

• Detergents 3. Psoriasis

Definition

Clinical Manifestations A chronic, immune-mediated inflammatory skin disease characterized by rapid

keratinocyte proliferation, resulting in thick, scaly plaques.
• Erythema

• Edema
Pathophysiology
• Vesicles or bullae
• Immune dysregulation involving T lymphocytes
• Pruritus
• Excessive cytokines (Tumor Necrosis Factor-alpha [TNF-α], Interleukins)
• Lesions confined to area of exposure
• Accelerated epidermal turnover:

o Normal: 28 days
Diagnosis
o Psoriasis: 3–5 days
• History of exposure

• Patch testing (for allergic type)

Clinical Manifestations

• Well-demarcated erythematous plaques

Management
• Silvery-white scales
• Removal of offending agent
 • Common sites: Nursing Rationale

o Scalp Suppressing immune activity reduces keratinocyte overproduction and inflammation.

o Elbows

o Knees IV. AUTOIMMUNE BLISTERING DISORDERS

o Lower back

• Auspitz sign: pinpoint bleeding when scales removed 4. Pemphigus Vulgaris

• Nail pitting Definition

A life-threatening autoimmune blistering disease involving intraepidermal blister

formation.
Triggers

• Stress
Pathophysiology
• Infection (especially Streptococcus)
• Autoantibodies against desmoglein (cell adhesion proteins)
• Trauma (Koebner phenomenon)
• Loss of keratinocyte adhesion (acantholysis)
• Certain medications (beta-blockers, lithium)
• Fragile blisters that rupture easily

Diagnosis
Clinical Manifestations
• Clinical evaluation
• Flaccid bullae
• Skin biopsy if uncertain
• Painful erosions

• Oral mucosal involvement (early sign)

Management
• Positive Nikolsky sign (skin sloughs when rubbed)
• Topical corticosteroids

• Vitamin D analogs
Diagnosis
• Phototherapy
• Skin biopsy
• Systemic immunosuppressants (severe cases)
• Direct immunofluorescence
 • Corticosteroids

Management • Immunomodulators

• Systemic corticosteroids

• Immunosuppressive therapy V. HYPERSENSITIVITY AND URTICARIAL DISORDERS

Nursing Rationale 6. Urticaria (Hives)

High risk for infection and fluid loss due to loss of skin integrity. Definition

A vascular reaction of the skin characterized by transient wheals and pruritus.

5. Bullous Pemphigoid

Definition Pathophysiology

A chronic autoimmune blistering disorder affecting elderly patients, involving subepidermal • Mast cell degranulation
blisters.
• Histamine release

• Increased capillary permeability

Pathophysiology

• Autoantibodies against basement membrane

Triggers
• Separation between epidermis and dermis
• Food

• Drugs
Clinical Manifestations
• Infections
• Tense bullae
• Stress
• Severe pruritus

• Negative or mild Nikolsky sign

Clinical Manifestations
• Less mucosal involvement than pemphigus vulgaris
• Raised wheals

• Erythema
Management
• Intense itching
 • Lesions resolve within 24 hours • Immunosuppressants

Management PART III – NEOPLASTIC SKIN DISORDERS

• Antihistamines Neoplastic skin disorders involve abnormal, uncontrolled proliferation of skin cells, which
may be benign (non-cancerous) or malignant (cancerous). Malignant lesions carry risk for
• Avoid triggers
local destruction, metastasis (spread), and death.

Nursing Rationale
I. OVERVIEW OF SKIN NEOPLASMS
Prevent progression to angioedema or anaphylaxis.
Risk Factors (General)

• Chronic ultraviolet (UV) radiation exposure

VI. CONNECTIVE TISSUE AND IMMUNOLOGIC SKIN DISEASES
• Fair skin, light eyes, light hair

• History of sunburns (especially blistering burns)

7. Lupus Erythematosus (Cutaneous Lupus)
• Immunosuppression (organ transplant, HIV)
Definition
• Exposure to carcinogens (arsenic, radiation)
An autoimmune disease with cutaneous manifestations, either localized or systemic.
• Genetic predisposition

Rationale:
Clinical Manifestations Ultraviolet radiation damages deoxyribonucleic acid (DNA) in skin cells, leading to
mutations and uncontrolled cell growth.
• Butterfly (malar) rash

• Photosensitivity
II. BENIGN SKIN NEOPLASMS
• Discoid lesions
Benign tumors do not metastasize but may cause cosmetic or functional issues.
• Alopecia

1. Seborrheic Keratosis
Management
Definition
• Sun protection
A common, benign epidermal tumor composed of immature keratinocytes.
• Topical/systemic corticosteroids
Clinical Manifestations Management

• “Stuck-on” appearance • Surgical excision if painful or growing

• Waxy, brown, black, or tan plaques

• Well-demarcated borders 3. Nevus (Mole)

• Common on trunk, face, scalp Definition

Diagnosis A benign proliferation of melanocytes.

• Clinical examination Types

• Dermoscopy (if uncertain) • Congenital nevi

Management • Acquired nevi

• No treatment required unless symptomatic • Dysplastic nevi (atypical; premalignant)

• Cryotherapy or curettage if irritated ABCDE Rule (Assessment)

Rationale • A – Asymmetry

Seborrheic keratosis has no malignant potential, but may resemble melanoma. • B – Border irregularity

• C – Color variation

2. Lipoma • D – Diameter > 6 mm

Definition • E – Evolving

A benign tumor of adipose (fat) tissue in the dermis or subcutaneous layer. Rationale

Clinical Manifestations Changes in nevi may indicate malignant transformation.

• Soft, rubbery, movable mass

• Painless III. MALIGNANT SKIN NEOPLASMS (SKIN CANCERS)

• Slow-growing

Diagnosis A. BASAL CELL CARCINOMA (BCC)

• Clinical exam Definition

• Ultrasound or biopsy if atypical The most common skin cancer, arising from basal cells of the epidermis.
Risk Factors B. SQUAMOUS CELL CARCINOMA (SCC)

• Chronic sun exposure Definition

• Older age Malignant tumor of keratinizing epidermal cells.

• Fair skin Risk Factors

Clinical Manifestations • UV exposure

• Pearly or translucent papule • Actinic keratosis

• Telangiectasia (visible blood vessels) • Chronic wounds or scars

• Central ulceration (“rodent ulcer”) • Immunosuppression

• Usually on face, neck, ears Clinical Manifestations

Pathophysiology • Firm, red nodule

• UV-induced DNA damage • Scaly, crusted lesion

• Local invasion without metastasis • Non-healing ulcer

Diagnosis • Common on sun-exposed areas

• Skin biopsy (definitive) Pathophysiology

Management • Malignant transformation of keratinocytes

• Surgical excision (Mohs micrographic surgery) • Potential for metastasis (especially lips, ears)

• Curettage and electrodesiccation Diagnosis

• Radiation therapy (rare cases) • Skin biopsy

Prognosis Management

• Excellent • Surgical excision

• Rare metastasis • Mohs surgery

Rationale • Radiation therapy if inoperable

Early removal prevents local tissue destruction. Prognosis

• Good if treated early

 • Metastasis risk increases with depth Pathophysiology

Rationale • UV radiation → DNA mutations

Untreated SCC can invade deeper tissues and spread to lymph nodes. • Early lymphatic and hematogenous spread

• High metastatic potential

C. MALIGNANT MELANOMA

Definition Diagnosis

A highly aggressive cancer arising from melanocytes. • Excisional biopsy

Epidemiology • Breslow thickness (depth of invasion)

• Less common than BCC and SCC • Clark level (anatomic depth)

• Responsible for most skin cancer deaths

Risk Factors Management

• Severe blistering sunburns • Wide surgical excision

• Dysplastic nevi • Sentinel lymph node biopsy

• Family history • Immunotherapy (checkpoint inhibitors)

• Fair skin • Targeted therapy

Clinical Manifestations • Chemotherapy (advanced cases)

• Changes in existing mole

• Irregular borders Prognosis

• Multiple colors (brown, black, red, blue) Depends on depth:

• Rapid growth • Thin lesions → excellent survival

• Bleeding or ulceration • Advanced disease → poor prognosis

ABCDE Rule (Critical)

Same as nevi but mandatory for melanoma screening. Rationale

Early detection is critical; melanoma metastasizes rapidly.

 • Monthly self-skin exams

IV. PREMALIGNANT SKIN LESIONS • Annual dermatologic screening for high-risk individuals

1. Actinic Keratosis

Definition VI. COMPARATIVE SUMMARY TABLE

Premalignant lesion caused by chronic sun exposure. Disorder Malignancy Metastasis Prognosis
Clinical Manifestations Basal Cell Carcinoma Malignant Rare Excellent
• Rough, scaly patches
Squamous Cell Carcinoma Malignant Possible Good–Fair
• Pink or flesh-colored
Melanoma Malignant High Variable
• Common on face, scalp, hands
Actinic Keratosis Premalignant No Preventable
Significance

• Can progress to squamous cell carcinoma

GENETIC AND CONGENITAL SKIN DISORDERS
Management
These are skin conditions present at birth or caused by inherited genetic mutations. They
• Cryotherapy
often affect skin integrity, pigmentation, keratinization, connective tissue, or immune
• Topical 5-fluorouracil function, and many have systemic implications.

• Photodynamic therapy

I. OVERVIEW OF GENETIC & CONGENITAL SKIN DISORDERS

V. NURSING ASSESSMENT & EDUCATION Definition
Assessment • Congenital disorders: present at birth (may or may not be inherited)

• Full-body skin inspection • Genetic disorders: caused by inherited or spontaneous gene mutations

• Monitor for new or changing lesions Clinical Importance

• Palpate lymph nodes if cancer suspected • Often chronic and lifelong

Patient Education • Many impair skin barrier function, increasing risk for:

• Sun protection (SPF ≥ 30) o Infection

• Avoid peak UV hours (10 AM–4 PM) o Fluid loss

 o Temperature dysregulation • Regular skin cancer screening

• May be associated with neurologic, musculoskeletal, or systemic abnormalities • Visual support

Rationale

II. MAJOR GENETIC & CONGENITAL SKIN DISORDERS Melanin protects against ultraviolet (UV) radiation; absence increases cancer risk.

1. Albinism 2. Vitiligo (Genetic + Autoimmune overlap)

Definition Definition

A genetic disorder characterized by decreased or absent melanin production due to A disorder characterized by loss of melanocytes, resulting in depigmented patches.
defects in melanin synthesis.
Pathophysiology
Pathophysiology
• Autoimmune destruction of melanocytes
• Caused by mutations affecting tyrosinase, the enzyme needed to convert tyrosine
• Genetic predisposition (familial clustering)
into melanin
Clinical Manifestations
• Normal number of melanocytes, but impaired melanin production
• Well-demarcated white patches
Clinical Manifestations
• Symmetrical distribution
• Very light skin, hair, and eyes
• Common on hands, face, genital area
• Photophobia (light sensitivity)
• No scaling or inflammation
• Reduced visual acuity
Diagnosis
• Increased risk for sunburn and skin cancer
• Clinical examination
Diagnosis
• Wood’s lamp (enhances depigmented areas)
• Clinical appearance
Management
• Genetic testing (confirmation)
• Topical corticosteroids
• Ophthalmologic examination
• Calcineurin inhibitors
Management
• Phototherapy
• No cure
• Psychological support
• Strict sun protection
Rationale

Loss of pigment is cosmetic but significantly affects psychosocial well-being. 4. Epidermolysis Bullosa (EB)

Definition

3. Ichthyosis Vulgaris A group of inherited disorders characterized by extreme skin fragility, leading to blister
formation with minimal trauma.
Definition
Pathophysiology
A genetic disorder of keratinization causing dry, scaly skin resembling fish scales.
• Genetic mutations affecting proteins that anchor epidermis to dermis
Pathophysiology
• Separation occurs at different skin layers depending on type
• Mutation leads to abnormal keratinocyte differentiation
Major Types
• Impaired shedding of dead skin cells
Type Level of Skin Separation
• Reduced skin hydration

Clinical Manifestations EB Simplex Epidermis

• Fine, white or gray scales Junctional EB Dermal–epidermal junction

• Most prominent on extensor surfaces (legs, arms) Dystrophic EB Dermis

• Worsens in cold, dry climates Clinical Manifestations
• Often spares flexural areas
• Blistering from friction
Diagnosis • Open wounds
• Clinical
• Scarring and deformities
• Family history • Risk of infection
Management
• Nutritional deficiencies
• Daily emollients Diagnosis
• Urea or lactic acid–containing creams
• Skin biopsy
• Gentle exfoliation • Genetic testing
Rationale Management
Hydration improves desquamation and restores skin barrier function.
• No cure
 • Wound care Rationale

• Infection prevention Skin findings are often the first sign of systemic disease.

• Nutritional support

• Pain management 6. Tuberous Sclerosis Complex

Rationale Definition

Loss of skin integrity compromises the primary protective barrier. A genetic disorder causing benign tumors in multiple organs, including skin.

Pathophysiology

5. Neurofibromatosis Type 1 (NF1) • Mutations lead to uncontrolled cell growth

Definition • Hamartomas form in skin and organs

A genetic disorder affecting neural crest cells, with prominent skin findings. Skin Manifestations

Pathophysiology • Hypomelanotic macules (“ash leaf spots”)

• Mutation in NF1 gene → abnormal cell growth • Facial angiofibromas

• Tumors develop along nerves • Shagreen patches (thickened skin)

Clinical Manifestations Diagnosis

• Café-au-lait spots (light brown macules) • Clinical features

• Neurofibromas (soft nodules) • Imaging (brain, kidneys)

• Axillary or inguinal freckling • Genetic testing

• Possible skeletal abnormalities Management

Diagnosis • Multidisciplinary care

• Clinical criteria • Treatment of organ involvement

• Genetic testing

Management 7. Port-Wine Stain (Nevus Flammeus)

• Surveillance for complications Definition

• Surgical removal of tumors if needed A congenital vascular malformation causing permanent red or purple skin discoloration.
Pathophysiology

• Abnormal capillary dilation SUMMARY TABLE

• Does not regress spontaneously Disorder Primary Defect Key Feature

Clinical Manifestations Albinism Melanin synthesis Very light skin
• Flat, well-defined reddish patch
Vitiligo Melanocyte destruction Depigmented patches
• Common on face or neck
Ichthyosis Keratinization defect Scaly skin
• Darkens with age
Epidermolysis bullosa Skin anchoring proteins Blistering
Diagnosis

• Clinical Neurofibromatosis Tumor suppressor gene Café-au-lait spots

Management Tuberous sclerosis Cell growth regulation Hamartomas

• Laser therapy Port-wine stain Capillary malformation Red/purple patch

• Monitoring for associated syndromes (e.g., Sturge–Weber)

VI. Burns and Traumatic Skin Injuries

III. NURSING AND CLINICAL CONSIDERATIONS

Common Complications A. Overview of Burns and Skin Trauma

• Infection Burns and traumatic skin injuries involve damage to the integumentary system caused by
• Fluid loss thermal, chemical, electrical, radiation, or mechanical forces. Because the skin is the first
line of defense, damage can result in:
• Impaired thermoregulation
• Fluid and electrolyte imbalance
• Psychosocial distress
• Infection
Key Nursing Priorities
• Impaired thermoregulation
• Skin integrity maintenance
• Altered sensation
• Infection prevention
• Shock
• Education on chronic care
• Multisystem organ failure (severe cases)
• Emotional support
 • Industrial current

B. Burns • Lightning

Characteristics:

I. Etiology (Causes) of Burns • Small entry and exit wounds

1. Thermal Burns • Extensive internal tissue damage

Caused by exposure to: • Risk of cardiac arrhythmias

• Flame Rationale: Electricity follows the path of least resistance (nerves, blood vessels).

• Hot liquids (scalds)

• Steam 4. Radiation Burns

• Hot objects Caused by:

Rationale: Heat denatures cellular proteins, causing coagulative necrosis. • Sun exposure (ultraviolet radiation)

• Radiation therapy

2. Chemical Burns Rationale: Radiation damages DNA and skin cell replication.

Caused by:

• Acids (e.g., sulfuric acid) 5. Friction Burns

• Alkalis (e.g., lye, ammonia) Caused by:

Key difference: • Abrasion (e.g., road rash)

• Acids → coagulation necrosis (surface damage) Rationale: Combination of mechanical injury and thermal damage.

• Alkalis → liquefaction necrosis (penetrates deeper)

Rationale: Alkalis cause more severe tissue destruction due to deeper penetration. II. Classification of Burns by Depth

3. Electrical Burns 1. Superficial Burns (First-Degree Burns)

Caused by: Structures involved:

• Household electricity • Epidermis only

Clinical manifestations: • Slower healing

• Redness (erythema) Healing:

• Pain • Weeks to months

• No blisters • Risk for scarring and contractures

• Skin intact

Example: Sunburn 3. Full-Thickness Burns (Third-Degree Burns)

Healing: Structures involved:

• 3–7 days • Epidermis

• No scarring • Dermis

Rationale: Epidermal regeneration occurs rapidly due to intact basal layer. • Subcutaneous tissue

Clinical manifestations:

2. Partial-Thickness Burns (Second-Degree Burns) • White, brown, or charred skin

a. Superficial Partial-Thickness • Dry and leathery (eschar)

• Epidermis + upper dermis • No pain (nerve destruction)

Findings: Healing:

• Blisters • Requires skin grafting

• Moist appearance Rationale: Loss of regenerative skin layers prevents spontaneous healing.

• Severe pain

• Red or pink color 4. Fourth-Degree Burns

b. Deep Partial-Thickness Involves:

• Epidermis + deeper dermis • Muscle

Findings: • Bone

• Pale or mottled • Tendons

• Less pain (nerve damage) Rationale: Extensive tissue destruction with high mortality risk.
 → High infection risk

III. Classification of Burns by Extent (Total Body Surface Area – TBSA)

Rule of Nines (Adults) 4. Hypermetabolic State

• Head and neck: 9% • Increased energy expenditure

• Each upper extremity: 9% • Protein catabolism

• Anterior trunk: 18% Rationale: Body attempts to repair tissue damage.

• Posterior trunk: 18%

• Each lower extremity: 18% V. Clinical Manifestations of Severe Burns

• Perineum: 1% • Pain or numbness

Rationale: TBSA determines fluid resuscitation needs and prognosis. • Edema

• Hypotension

IV. Pathophysiology of Severe Burns • Tachycardia

1. Fluid Shifts • Decreased urine output

• Capillary permeability increases • Signs of infection

• Plasma leaks into interstitial space • Eschar formation

→ Hypovolemic shock

VI. Diagnostic Evaluation

2. Electrolyte Imbalance 1. Physical Assessment

• Hyperkalemia (cell destruction) • Burn depth

• Hyponatremia (fluid shifts) • TBSA

• Airway involvement

3. Immune Suppression • Circulatory status

• Loss of skin barrier

• Reduced white blood cell function 2. Laboratory Studies

 • Complete Blood Count (CBC)

• Electrolytes III. Contusions (Bruises)

• Arterial Blood Gases (ABGs) • Blunt trauma

• Serum lactate • Blood leakage into tissues

Rationale: Detects shock, hypoxia, infection, and metabolic disturbances.

IV. Avulsions

VII. Principles of Burn Management (Brief Overview) • Skin forcibly detached

• Airway management first • High risk of necrosis

• Breathing and oxygenation

• Circulation (IV fluids – Parkland formula) V. Pressure Injuries (Pressure Ulcers)

• Infection prevention Cause

• Pain management • Prolonged pressure

• Wound care and grafting • Reduced blood flow

Stages

C. Traumatic Skin Injuries • Stage I: Non-blanchable erythema

• Stage II: Partial-thickness skin loss

I. Abrasions • Stage III: Full-thickness skin loss

• Superficial scraping of skin • Stage IV: Muscle/bone exposure

• Minimal bleeding Rationale: Ischemia leads to tissue necrosis.

• High infection risk

D. Nursing and Clinical Significance

II. Lacerations • Burns compromise fluid balance, immunity, and thermoregulation

• Irregular tearing of tissue • Early intervention saves lives

• May involve deeper structures • Skin trauma can lead to chronic wounds and infection
 • Prevention and assessment are critical nursing roles Which finding is most characteristic of impetigo caused by Staphylococcus aureus?

A. Dry, scaly patches with lichenification

B. Honey-colored crusted lesions on an erythematous base
Got it C. Painful grouped vesicles along a dermatome
Here are 5 high-quality multiple-choice questions (MCQs) based on the Integumentary D. Deep ulcerations with necrotic tissue
System, specifically integrating inflammatory/immunologic, infectious, neoplastic,
genetic/congenital disorders, and burns/trauma. Correct Answer: B
Each question includes the correct answer and a clear rationale, written at a top-notch
Rationale:
nursing/medical level.
Impetigo is a highly contagious superficial bacterial infection, commonly seen in children.
Classic features include:
MCQ 1 — Inflammatory / Immunologic Disorder
• Honey-colored crusts
A patient with psoriasis vulgaris is most likely to exhibit which of the following skin findings?
• Erythematous base
A. Vesicular lesions with intense pruritus localized to flexural areas
• Caused by Staphylococcus aureus or Streptococcus pyogenes
B. Well-demarcated erythematous plaques with silvery scales on extensor surfaces
C. Painless nodules with central umbilication Option C describes herpes zoster.
D. Bullae formation caused by autoantibodies against desmoglein Option D suggests necrotizing soft tissue infection.
Option A is more consistent with eczema.
Correct Answer: B

Rationale:
MCQ 3 — Neoplastic Skin Disorder
Psoriasis vulgaris is a chronic inflammatory autoimmune skin disorder characterized by:
Which characteristic most strongly suggests malignant melanoma rather than a benign
• Hyperproliferation of keratinocytes
nevus?
• Well-demarcated erythematous plaques
A. Symmetry and uniform color
• Silvery-white scales B. Diameter less than 6 mm
C. Asymmetry, irregular borders, and color variation
• Commonly affects extensor surfaces (elbows, knees, scalp) D. Lesion present since childhood with no changes
Option A describes atopic dermatitis. Correct Answer: C
Option C describes molluscum contagiosum.
Option D describes pemphigus vulgaris, an autoimmune blistering disorder. Rationale:

Melanoma is identified using the ABCDE criteria:

MCQ 2 — Infectious Skin Disorder • A – Asymmetry

 • B – Border irregularity A. Superficial (first-degree) burn
B. Partial-thickness (second-degree) burn
• C – Color variation
C. Full-thickness (third-degree) burn
• D – Diameter > 6 mm D. Fourth-degree burn

• E – Evolution (change over time) Correct Answer: B

Option C includes classic malignant features. Rationale:

Options A, B, and D are typical of benign nevi.
Partial-thickness (second-degree) burns:

• Involve epidermis + dermis

MCQ 4 — Genetic / Congenital Disorder
• Present with:
A newborn presents with fragile skin that blisters easily in response to minimal trauma. This
o Blistering
finding is most consistent with:
o Moist appearance
A. Psoriasis
B. Bullous impetigo o Severe pain (nerve endings exposed)
C. Epidermolysis bullosa
First-degree burns affect only the epidermis.
D. Stevens–Johnson syndrome
Third-degree burns destroy all skin layers and are typically painless due to nerve
Correct Answer: C destruction.
Fourth-degree burns extend into muscle and bone.
Rationale:

Epidermolysis bullosa is a genetic connective tissue disorder characterized by:

• Defective proteins anchoring skin layers

• Extreme skin fragility

• Blistering with minimal friction or trauma

Bullous impetigo is infectious.

Stevens–Johnson syndrome is a severe drug reaction, not congenital.
Psoriasis does not cause blistering at birth.

MCQ 5 — Burns and Trauma

Which burn injury involves destruction of the epidermis and dermis, often appearing red,
blistered, and painful?