Acts as first line of defense when unbroken.
Prevents excessive fluid loss.
Controls body temperature through:
Cutaneous vasodilation
Secretion and evaporation of sweat
Active in sensory perception.
Important defense against environmental hazards.
Synthesizes vitamin D on exposure to small amounts of ultraviolet light.
Layers of the skin:
Epidermis—avascular (has 5 layers)
Dermis
Subcutaneous tissue (hypodermis)
Stratum basale
Mitotic activity
Stratum spinosum
Cells connected by desmosomes
Protein synthesis
Stratum granulosum
Keratin formation begins
Stratum lucidum
Clear layer, keratinocytes degenerate here
Has Eleidin which later transforms to Keratin
Stratum corneum
Waterproofing barrier
Keratin
Waterproofing of the skin
Melanin
Skin pigment—determines skin color
Production depends on multiple genes and environment
Albinism
Lack of melatonin production
Vitiligo
Small areas of hypopigmentation
Melasma
Patches of darker skin
Connective tissue
Contains elastic and collagen fibers
Flexibility and strength of the skin
Contains nerves and blood vessels
Includes sensory receptors for:
Pressure
Touch
Pain
Heat
Cold
Nails
Hair follicles
Stratum basale—hair-producing
Arrector pili muscle associated with hair follicle
Sebaceous glands
Produce sebum
Secretion increases at puberty—influence of sex hormones
Sweat glands
Eccrine—all over body
Apocrine
Axillae, scalp, face, external genitalia
Beneath dermis
Connective tissue
Fat cells
Macrophages
Fibroblasts
Larger blood vessels
Nerves
Mixed flora—components differ in various areas of the body.
Microbes also reside under the fingernails, in hair follicles, and in glands.
Opportunistic infections may occur because of injury or other inflammatory lesion.
Infection may spread systemically from skin lesions.
The physical appearance of the lesion is necessary to make a diagnosis.
Skin lesions may be caused by:
Systemic disorders, e.g. Liver disease
Systemic infections, e.g. Chickenpox
Allergies to ingested food or drugs
Localized factors, e.g. exposure to toxins
Types of lesions
Location
Length of time lesion has been present
Changes occurring over time
Physical appearance
Color
Elevation
Texture
Type of exudate
Presence of pain or pruritus (itching)
Review Table 8-1
Macule: flat, circumscribed
Papule: small, solid elevation
Nodule: firm, raised, deep
Pustule: raised, often with a "head," filled with exudate or "pus"
Vesicle or blister: thin wall, raised, fluid filled
Ulcer: cavity in tissue
Plaque: Slightly elevated, flat, "scale"-like lesion
Fissure: crack in tissue
Associated with:
Allergic responses
Chemical irritation caused by insect bites
Infestations by parasites (e.g., scabies)
Mechanism not totally understood
Release of histamine in a hypersensitivity response causes marked pruritus
Infection may result from breaking the skin barrier caused by scratching
Exposure to an allergen
Metals, cosmetics, soaps, chemicals, plants
Sensitization occurs on first exposure.
Pruritic rash develops at site a few hours after exposure.
Direct chemical or mechanical irritation
Does not involve immune response
Is inflammatory because of direct exposure
Removal of irritant
Reduction of inflammation with topical glucocorticoids
Sensitization occurs on first exposure
Subsequent exposure results in manifestations, i.e. pruritic rash
Location of lesions is clue to identity of the allergen, i.e. poison ivy
Signs and Symptoms:
Pruritic area
Erythematous area
Edematous area
Area often covered with small vesicles
Chemical Irritation Manifestation
Edematous area
Erythematous area
May be pruritic or painful
Pathophysiology:
Result of type I hypersensitivity
Ingestion of substances
Examples: shellfish, drugs, certain fruits
Signs and Symptoms:
Eruption of hard, raised, erythematous lesion
Lesions are highly pruritic
Found:
Skin
May be scattered all over body
Occasionally in pharyngeal mucosa
Airway obstruction
Atopic—inherited tendency (Type I)
Common problem in infancy
Rash is erythematous, with serous exudate.
Commonly occurs on face, chest, and shoulders
In adults, rash is dry, scaly, and pruritic, often on flexor surfaces.
Pathophysiology
Chronic inflammation results from response to allergens.
Eosinophilia and increased serum IgE levels
Affected areas become sensitive to irritants:
Soaps
Certain fabrics
Temperature changes
Potential complication
Secondary infections due to scratching
Chronic inflammatory skin disorder
Autoimmune disease
Affects 1 – 3% of the population
Believed to be genetic in origin
Pathophysiology:
Onset usually in the teenage years
Marked by remission and exacerbations
Cases vary in severity
Results from abnormal T cell activation.
Excessive proliferation of keratinocytes
Cellular proliferation is greatly increased leading to thickening of the dermis and epidermis
Shedding occurs in one day rather than two week intervals
Signs and Symptoms
Red patches of skin covered with silvery scales
Small scaling spots (commonly seen in children)
Dry, cracked skin that may bleed
Itching, burning or soreness
Thickened, pitted or ridged nails
Swollen and stiff joints
(Can affect multiple organs)
Autoimmune disorder
Mainly two forms
Pemphigus vulgaris (mucosal)
Pemphigus foliaceous (Skin)
Severity varies among individuals
Autoantibodies disrupt cohesion between epidermal cells.
Causes blisters (bullae) to form
Skin sheds, leaving area painful and open to secondary infection.
May be life-threatening if extensive (e.g., Stevens-Johnson syndrome)
Signs and Symptoms
Blisters in mouth
Blisters spreading to the skin
Blisters are painful but not pruritic
Breathing difficulty due to swollen mouth and throat
May occur as skin disorder
May be systemic and affect viscera
Primary cause unknown
Pathophysiology:
Increased collagen deposition
Inflammation and fibrosis with decreased capillary networks
May cause renal failure, intestinal obstruction, respiratory failure caused by distortion of tissues
Signs and Symptoms:
Hard, shiny, tight, immovable areas of skin
Fingertips narrowed and shortened
Raynaud's phenomenon may be present (lack of blood flow to toes and fingers)
Facial expression is lost
Skin tightens, movement of the mouth and eyes may be impaired
The cutaneous form may also affect the microcirculation of various organs, eventually causing renal failure, intestinal obstruction, or respiratory failure due to pulmonary hypertension.
Pathophysiology
Progressive hand deformity
Cause is unknown
Knots of tissue under skin of palms
Fingers eventually pulled into bent position
May be caused by bacteria, viruses, fungi, other types of microbes, parasites
Caused by opportunistic microbes
Minor abrasions or cuts
Serious infections may develop.
Causative organism needs to be identified for appropriate treatment
Bacterial Infections:
Primary
Often caused by resident flora
Secondary
Developing in wounds or pruritic lesions
Infection of the dermis and subcutaneous tissue
Usually secondary to an injury
Causative organism
Usually Staphylococcus aureus
Sometimes Streptococcus
Frequently in lower trunks and legs
Especially in individuals with restricted circulation in the extremities; also in immunocompromised individuals
Area becomes red, swollen, and painful
Red streaks may develop, running along lymph vessels proximal to infected area
Signs and Symptoms
Reddened area
Edematous (swollen)
Pain
Red streaks along the lymph vessels proximal to the infected area
Usually caused by S. aureus
Begins at hair follicles
Face, neck, back
Frequently drains large amounts of purulent exudate
Autoinoculation
Squeezing boils can result in spread of infection to other areas of the skin.
Common infection in infants and children
May also occur in adults
S. aureus—highly contagious in neonates
Lesions commonly on face
Transmission may occur through close physical contact or through fomites
Pruritus common
Leads to scratching and further spread of infection
Signs and Symptoms
Small red vesicles, which rapidly enlarge
Vesicles rupture forming yellowish-brown crusty masses
Additional vesicles develop around the primary site by autoinoculation with hands, towels, or clothes
Pruritus is common, leading to scratching and further spread of infection
Fascia is the connective tissue that surrounds the blood vessels/nerve and muscles
Mixture of aerobic and anaerobic bacteria usually at site of infection
Severe inflammation and tissue necrosis
Usually caused by virulent strain of gram-positive, group A beta-hemolytic Streptococcus
Bacteria secrete toxins that break down fascia and connective tissue, causing massive tissue destruction.
Often a history of minor trauma or infection in the skin and subcutaneous tissue of an extremity
Signs and Symptoms
Local S/S:
Infected area appears markedly inflamed
Very painful
Infected area rapidly increases in size
Dermal gangrene is apparent
Systemic S/S:
Fever
Tachycardia
Hypotension
Mental confusion and disorientation
Possible organ failure
Caused by Mycobacterium leprae
Chronic disease classified into three major types
Clinical signs and symptoms vary.
Generally affects skin, mucous membranes, and peripheral nerves
Damage can lead to loss of limbs.
Mechanism of pathogenicity largely unknown
Herpes simplex type 1 (HSV-1)
Most common cause of cold sores or fever blisters
Herpes simplex type 2 (HSV-2)—genital herpes
Both types of HSV cause similar effects.
Primary infection may be asymptomatic
Virus remains latent in sensory nerve ganglia.
Recurrence may be triggered by:
Common cold, sun exposure, stress
Spread by direct contact with fluid from lesion
Spread of infection to others possible prior to appearance of lesions
Potential complication:
Spread of virus to eye
Keratitis
Herpetic whitlow
Painful infection of the fingers
Human papillomavirus (HPV) types 1 to 4
Frequently develop in children and young adults
Plantar warts are common.
Spreads by viral shedding of the skin surface
May resolve spontaneously with time
Genital warts (HPV types 6 and 11)
Most are superficial
Candida infection is associated with diabetes.
May spread systemically in immunocompromised individuals
Tinea capitis
Infection of the scalp
Common in school-age children
Erythema may be apparent.
Tinea corporis
Infection of the body, particularly of nonhairy parts
Round lesion with clear center (ringworm)
Pruritus may be present.
Tinea pedis
Athlete’s foot—involves the feet, particularly the toes
Associated with swimming pools and gymnasiums
May be part of normal flora that becomes opportunistic
Secondary bacterial infection may occur
Tinea unguium
Infection of the nails, particularly the toenails
Nails turn white, then brown.
Nail thickens and cracks.
Infection tends to spread to other nails.
Scabies
Invasion by mite Sarcoptes scabiei
Female burrows into epidermis
Lays eggs over a period of several weeks
Male dies after fertilizing the female
Female dies after laying the eggs.
Larvae migrate to skin surface.
Burrow into skin in search of nutrients
Intensely pruritic!
Larvae mature and cycle is repeated
Burrows appear on skin as tiny, light brown lines.
Pediculosis (lice)
Pediculus humanus corporis—body louse
Pediculus humanus capitis—head louse
Pediculus humanus pubis—pubic louse
Female lice lay eggs on hair shafts.
After hatching, louse bites human host, sucking blood for production of ova
Excoriations result from scratching.
Benign lesions usually associated with aging or skin damage.
Seborrheic keratoses
Proliferation of basal cells
Lead to oval elevation
May be smooth or rough
Actinic keratoses
On skin exposed to ultraviolet radiation
Commonly in fair-skinned persons
Lesion appears as pigmented, scaly patch
A sore that does not heal
A change in shape, size, color, or texture of a lesion, especially an expanding, irregular circumference or surface
New moles or odd-shaped lesions that develop
A skin lesion that bleeds repeatedly, oozes fluid, or itches
Reducing sun exposure at midday and early afternoon
Covering up with clothing
Remaining in shade
Wearing broad-brimmed hats to protect face and neck
Applying sunscreen or sunblock
Protecting infants and children from exposure and sun damage to skin
Painless, malignant tumor of the epidermis
Lesions most commonly found on exposed areas of the skin but also in oral cavity
Face and neck
Base of tongue
Excellent prognosis when lesion is removed within reasonable time
Invasive type arises from premalignant condition.
Highly metastatic form of skin cancer
Develops in melanocytes
From a nevus (mole)
Often appear as multicolored lesion with irregular border
Grow quickly
Change in shape, color, size, texture
May bleed
Melanoma is suspected in any nevus that shows:
Change in appearance
Change in border
Change in color
Increase in diameter
Occurs in those with AIDS and other immunodeficiencies
May affect viscera as well as skin
Malignant cells arise from endothelium in small blood vessels
Purplish macules
Nonpruritic, nonpainful
In immunocompromised patients, lesions develop rapidly over upper body.
Acts as first line of defense when unbroken, preventing pathogen entry and physical damage.
Prevents excessive fluid loss, maintaining hydration and electrolyte balance.
Controls body temperature through:
Cutaneous vasodilation: Increases blood flow to the skin surface, dissipating heat.
Secretion and evaporation of sweat: Cools the body as sweat evaporates.
Active in sensory perception:
Contains receptors for touch, pressure, pain, and temperature.
Important defense against environmental hazards:
UV radiation, pollutants, and mechanical irritants.
Synthesizes vitamin D on exposure to small amounts of ultraviolet light:
Essential for calcium absorption and bone health.
Layers of the skin:
Epidermis—avascular (has 5 layers):
Outermost layer, provides a waterproof barrier and creates our skin tone.
Relies on the dermis for nutrient supply.
Dermis:
Contains blood vessels, nerves, hair follicles, and glands.
Provides structural support and elasticity.
Subcutaneous tissue (hypodermis):
Adipose tissue for insulation and cushioning.
Contains larger blood vessels and nerves.
Stratum basale:
Mitotic activity: Cell division to replenish skin cells.
Contains melanocytes that produce melanin.
Stratum spinosum:
Cells connected by desmosomes: Provides strength and flexibility.
Protein synthesis: Production of keratin and other proteins.
Stratum granulosum:
Keratin formation begins: Cells accumulate granules containing keratin.
Cells begin to die as they move away from nutrient source.
Stratum lucidum:
Clear layer, keratinocytes degenerate here
Has Eleidin which later transforms to Keratin
Stratum corneum:
Waterproofing barrier: Dead, flattened cells filled with keratin.
Protects against abrasion and penetration.
Keratin:
Waterproofing of the skin: Provides a protective barrier.
Produced by keratinocytes.
Melanin:
Skin pigment—determines skin color
Production depends on multiple genes and environment
Protects against UV radiation.
Albinism:
Lack of melatonin production
Genetic condition resulting in absence of pigment in skin, hair, and eyes.
Vitiligo:
Small areas of hypopigmentation
Autoimmune condition causing loss of melanocytes.
Melasma:
Patches of darker skin
Often associated with hormonal changes, such as pregnancy.
Connective tissue:
Contains elastic and collagen fibers
Flexibility and strength of the skin
Supports epidermis and provides structure.
Contains nerves and blood vessels:
Includes sensory receptors for:
Pressure
Touch
Pain
Heat
Cold
Nails:
Protective keratinized structures on fingers and toes.
Hair follicles:
Stratum basale—hair-producing
Arrector pili muscle associated with hair follicle
Hair provides insulation and protection.
Sebaceous glands:
Produce sebum
Secretion increases at puberty—influence of sex hormones
Lubricates skin and hair.
Sweat glands:
Eccrine—all over body
Regulates body temperature through perspiration.
Apocrine:
Axillae, scalp, face, external genitalia
Produce thicker sweat with pheromones.
Beneath dermis
Connective tissue:
Fat cells: Provide insulation and energy storage.
Macrophages: Immune cells that engulf pathogens and debris.
Fibroblasts: Produce collagen and elastin.
Larger blood vessels
Nerves
Mixed flora—components differ in various areas of the body.
Includes bacteria, fungi, and viruses.
Microbes also reside under the fingernails, in hair follicles, and in glands.
Serve as a reservoir for potential infections.
Opportunistic infections may occur because of injury or other inflammatory lesion.
Disruption of skin barrier allows entry of pathogens.
Infection may spread systemically from skin lesions.
Bacteria can enter the bloodstream and cause widespread infection.
The physical appearance of the lesion is necessary to make a diagnosis.
Distribution, size, shape, color, and texture are important.
Skin lesions may be caused by:
Systemic disorders, e.g. Liver disease
Manifestations of internal diseases on the skin.
Systemic infections, e.g. Chickenpox
Viral or bacterial infections causing skin eruptions.
Allergies to ingested food or drugs
Immune responses triggered by allergens.
Localized factors, e.g. exposure to toxins
Irritants or chemicals causing local skin reactions.
Types of lesions
Location
Length of time lesion has been present
Changes occurring over time
Physical appearance
Color
Elevation
Texture
Type of exudate
Presence of pain or pruritus (itching)
Review Table 8-1
Macule: flat, circumscribed
Papule: small, solid elevation
Nodule: firm, raised, deep
Pustule: raised, often with a "head," filled with exudate or "pus"
Vesicle or blister: thin wall, raised, fluid filled
Ulcer: cavity in tissue
Plaque: Slightly elevated, flat, "scale"-like lesion
Fissure: crack in tissue
Associated with:
Allergic responses
Histamine release causes itching.
Chemical irritation caused by insect bites
Irritants trigger inflammatory response.
Infestations by parasites (e.g., scabies)
Mites burrowing into skin cause intense itching.
Mechanism not totally understood
Release of histamine in a hypersensitivity response causes marked pruritus
Infection may result from breaking the skin barrier caused by scratching
Secondary bacterial infections common.
Exposure to an allergen
Metals, cosmetics, soaps, chemicals, plants
Sensitization occurs on first exposure.
Pruritic rash develops at site a few hours after exposure.
Direct chemical or mechanical irritation
Does not involve immune response
Is inflammatory because of direct exposure
Removal of irritant
Reduction of inflammation with topical glucocorticoids
Sensitization occurs on first exposure
Subsequent exposure results in manifestations, i.e. pruritic rash
Location of lesions is clue to identity of the allergen, i.e. poison ivy
Signs and Symptoms:
Pruritic area
Erythematous area
Edematous area
Area often covered with small vesicles
Chemical Irritation Manifestation
Edematous area
Erythematous area
May be pruritic or painful
Pathophysiology:
Result of type I hypersensitivity
Ingestion of substances
Examples: shellfish, drugs, certain fruits
Signs and Symptoms:
Eruption of hard, raised, erythematous lesion
Lesions are highly pruritic
Found:
Skin
May be scattered all over body
Occasionally in pharyngeal mucosa
Airway obstruction
Atopic—inherited tendency (Type I)
Common problem in infancy
Rash is erythematous, with serous exudate.
Commonly occurs on face, chest, and shoulders
In adults, rash is dry, scaly, and pruritic, often on flexor surfaces.
Pathophysiology
Chronic inflammation results from response to allergens.
Eosinophilia and increased serum IgE levels
Affected areas become sensitive to irritants:
Soaps
Certain fabrics
Temperature changes
Potential complication
Secondary infections due to scratching
Chronic inflammatory skin disorder
Autoimmune disease
Affects 1 – 3% of the population
Believed to be genetic in origin
Pathophysiology:
Onset usually in the teenage years
Marked by remission and exacerbations
Cases vary in severity
Results from abnormal T cell activation.
Excessive proliferation of keratinocytes
Cellular proliferation is greatly increased leading to thickening of the dermis and epidermis
Shedding occurs in one day rather than two week intervals
Signs and Symptoms
Red patches of skin covered with silvery scales
Small scaling spots (commonly seen in children)
Dry, cracked skin that may bleed
Itching, burning or soreness
Thickened, pitted or ridged nails
Swollen and stiff joints
(Can affect multiple organs)
Autoimmune disorder
Mainly two forms
Pemphigus vulgaris (mucosal)
Pemphigus foliaceous (Skin)
Severity varies among individuals
Autoantibodies disrupt cohesion between epidermal cells.
Causes blisters (bullae) to form
Skin sheds, leaving area painful and open to secondary infection.
May be life-threatening if extensive (e.g., Stevens-Johnson syndrome)
Signs and Symptoms
Blisters in mouth
Blisters spreading to the skin
Blisters are painful but not pruritic
Breathing difficulty due to swollen mouth and throat
May occur as skin disorder
May be systemic and affect viscera
Primary cause unknown
Pathophysiology:
Increased collagen deposition
Inflammation and fibrosis with decreased capillary networks
May cause renal failure, intestinal obstruction, respiratory failure caused by distortion of tissues
Signs and Symptoms:
Hard, shiny, tight, immovable areas of skin
Fingertips narrowed and shortened
Raynaud's phenomenon may be present (lack of blood flow to toes and fingers)
Facial expression is lost
Skin tightens, movement of the mouth and eyes may be impaired
The cutaneous form may also affect the microcirculation of various organs, eventually causing renal failure, intestinal obstruction, or respiratory failure due to pulmonary hypertension.
Pathophysiology
Progressive hand deformity
Cause is unknown
Knots of tissue under skin of palms
Fingers eventually pulled into bent position
May be caused by bacteria, viruses, fungi, other types of microbes, parasites
Caused by opportunistic microbes
Minor abrasions or cuts
Serious infections may develop.
Causative organism needs to be identified for appropriate treatment
Bacterial Infections:
Primary
Often caused by resident flora
Secondary
Developing in wounds or pruritic lesions
Infection of the dermis and subcutaneous tissue
Usually secondary to an injury
Causative organism
Usually Staphylococcus aureus
Sometimes Streptococcus
Frequently in lower trunks and legs
Especially in individuals with restricted circulation in the extremities; also in immunocompromised individuals
Area becomes red, swollen, and painful
Red streaks may develop, running along lymph vessels proximal to infected area
Signs and Symptoms
Reddened area
Edematous (swollen)
Pain
Red streaks along the lymph vessels proximal to the infected area
Usually caused by S. aureus
Begins at hair follicles
Face, neck, back
Frequently drains large amounts of purulent exudate
Autoinoculation
Squeezing boils can result in spread of infection to other areas of the skin.
Common infection in infants and children
May also occur in adults
S. aureus—highly contagious in neonates
Lesions commonly on face
Transmission may occur through close physical contact or through fomites
Pruritus common
Leads to scratching and further spread of infection
Signs and Symptoms
Small red vesicles, which rapidly enlarge
Vesicles rupture forming yellowish-brown crusty masses
Additional vesicles develop around the primary site by autoinoculation with hands, towels, or clothes
Pruritus is common, leading to scratching and further spread of infection
Fascia is the connective tissue that surrounds the blood vessels/nerve and muscles
Mixture of aerobic and anaerobic bacteria usually at site of infection
Severe inflammation and tissue necrosis
Usually caused by virulent strain of gram-positive, group A beta-hemolytic Streptococcus
Bacteria secrete toxins that break down fascia and connective tissue, causing massive tissue destruction.
Often a history of minor trauma or infection in the skin and subcutaneous tissue of an extremity
Signs and Symptoms
Local S/S:
Infected area appears markedly inflamed
Very painful
Infected area rapidly increases in size
Dermal gangrene is apparent
Systemic S/S:
Fever
Tachycardia
Hypotension
Mental confusion and disorientation
Possible organ failure
Caused by Mycobacterium leprae
Chronic disease classified into three major types
Clinical signs and symptoms vary.
Generally affects skin, mucous membranes, and peripheral nerves
Damage can lead to loss of limbs.
Mechanism of pathogenicity largely unknown
Herpes simplex type 1 (HSV-1)
Most common cause of cold sores or fever blisters
Herpes simplex type 2 (HSV-2)—genital herpes
Both types of HSV cause similar effects.
Primary infection may be asymptomatic
Virus remains latent in sensory nerve ganglia.
Recurrence may be triggered by:
Common cold, sun exposure, stress
Spread by direct contact with fluid from lesion
Spread of infection to others possible prior to appearance of lesions
Potential complication:
Spread of virus to eye
Keratitis
Herpetic whitlow
Painful infection of the fingers
Human papillomavirus (HPV) types 1 to 4
Frequently develop in children and young adults
Plantar warts are common.
Spreads by viral shedding of the skin surface
May resolve spontaneously with time
Genital warts (HPV types 6 and 11)
Most are superficial
Candida infection is associated with diabetes.
May spread systemically in immunocompromised individuals
Tinea capitis
Infection of the scalp
Common in school-age children
Erythema may be apparent.
Tinea corporis
Infection of the body, particularly of nonhairy parts
Round lesion with clear center (ringworm)
Pruritus may be present.
Tinea pedis
Athlete’s foot—involves the feet, particularly the toes
Associated with swimming pools and gymnasiums
May be part of normal flora that becomes opportunistic
Secondary bacterial infection may occur
Tinea unguium
Infection of the nails, particularly the toenails
Nails turn white, then brown.
Nail thickens and cracks.
Infection tends to spread to other nails.
Scabies
Invasion by mite Sarcoptes scabiei
Female burrows into epidermis
Lays eggs over a period of several weeks
Male dies after fertilizing the female
Female dies after laying the eggs.
Larvae migrate to skin surface.
Burrow into skin in search of nutrients
Intensely pruritic!
Larvae mature and cycle is repeated
Burrows appear on skin as tiny, light brown lines.
Pediculosis (lice)
Pediculus humanus corporis—body louse
Pediculus humanus capitis—head louse
Pediculus humanus pubis—pubic louse
Female lice lay eggs on hair shafts.
After hatching, louse bites human host, sucking blood for production of ova
Excoriations result from scratching.
Benign lesions usually associated with aging or skin damage.
Seborrheic keratoses
Proliferation of basal cells
Lead to oval elevation
May be smooth or rough
Actinic keratoses
On skin exposed to ultraviolet radiation
Commonly in fair-skinned persons
Lesion appears as pigmented, scaly patch
A sore that does not heal
A change in shape, size, color, or texture of a lesion, especially an expanding, irregular circumference or surface
New moles or odd-shaped lesions that develop
A skin lesion that bleeds repeatedly, oozes fluid, or itches
Reducing sun exposure at midday and early afternoon
Covering up with clothing
Remaining in shade
Wearing broad-brimmed hats to protect face and neck
Applying sunscreen or sunblock
Protecting infants and children from exposure and sun damage to skin
Painless, malignant tumor of the epidermis
Lesions most commonly found on exposed areas of the skin but also in oral cavity
Face and neck
Base of tongue
Excellent prognosis when lesion is removed within reasonable time
Invasive type arises from premalignant condition.
Highly metastatic form of skin cancer
Develops in melanocytes
From a nevus (mole)
Often appear as multicolored lesion with irregular border
Grow quickly
Change in shape, color, size, texture
May bleed
Melanoma is suspected in any nevus that shows:
Change in appearance
Change in border
Change in color
Increase in diameter
Occurs in those with AIDS and other immunodeficiencies
May affect viscera as well as skin
Malignant cells arise from endothelium in small blood vessels
Purplish macules
Nonpruritic, nonpainful
In immunocompromised patients, lesions develop rapidly over upper body.