UNIT 5

SKIN AND THE INTEGUMENTARY SYSTEM

DR Adefuye AO
 Learning outcomes
ANATOMY & PHYSIOLOGY:

• Describe the four major types of membranes.

• Describe the structure of the layers of skin.
• List the general functions of each layer of the skin.
• Describe the accessory organs associated with the skin.
• Explain the functions of each accessory organ.
• Explain how the skin helps regulate body temperature.
• Summarize the factors that determine skin colour.

PATHOPHYSIOLOGY:

• Explain the pathological features and effects of the following skin conditions:
o Dermatitis (eczema)
o Fungal infections
o Bacterial infections
o Viral infections
o Ulcers
o Burns
o Skin cancers
o Albinism
 Introduction

 Two or more kinds of tissues grouped together and performing specialized functions constitute an organ.

 For example, epithelial membranes, which are thin, sheet-like structures that are usually composed of
epithelial and underlying connective tissues and covering body surfaces and lining body cavities, are
organs.

 The cutaneous membrane (skin), with various accessory organs, makes up the integumentary organ system
 Types of Membranes
 The three major types of epithelial membranes are serous, mucous, and cutaneous.

 Serous membranes - line the body cavities that lack openings to the outside and reduce friction between
the organs and cavity walls.

 They form the inner linings of the thorax and abdomen, and they cover the organs within these cavities.

 A serous membrane consists of a layer of simple squamous epithelium (mesothelium) and a thin layer of
loose connective tissue.

 Cells of a serous membrane secrete watery serous fluid, which helps lubricate the surfaces of the
membrane.
 Mucous membranes - line the cavities and tubes that open to the outside of the body.

 These include the oral and nasal cavities and the tubes of the digestive, respiratory, urinary, and reproductive
systems.

 A mucous membrane consists of epithelium overlying a layer of loose connective tissue; however, the type of
epithelium varies with the location of the membrane.

 For example, stratified squamous epithelium lines the oral cavity, pseudostratified columnar epithelium lines
part of the nasal cavity, and simple columnar epithelium lines the small intestine.

 Goblet cells within a mucous membrane secrete mucus.

 The cutaneous membrane - is an organ of the integumentary organ system and is more commonly called skin.
 Skin and Its Tissues

 The skin is one of the larger and more versatile organs of the body, and it is vital in maintaining homeostasis.

 It is a protective covering that prevents many harmful substances, as well as microorganisms, from entering
the body.

 Skin also retards water loss by diffusion from deeper tissues and helps regulate body temperature.

 It houses sensory receptors, contains immune system cells, synthesizes various chemicals, and excretes small
quantities of waste.
 The skin includes two distinct tissue layers.

 The outer layer, called the epidermis is composed of stratified squamous epithelium.

 The inner layer, or dermis, is thicker than the epidermis, and it is made up of connective tissue containing
collagen and elastic fibers, epithelial tissue, smooth muscle tissue, nervous tissue, and blood.

 A basement membrane that is anchored to the dermis by short fibrils separates the two skin layers.

 Beneath the dermis, masses of loose connective and adipose tissues bind the skin to underlying organs.

 These tissues are not part of the skin. They form the subcutaneous layer or hypodermis.
 Epidermis
 Since the epidermis is composed of stratified squamous epithelium, it lacks blood vessels.

 However, the deepest layer of epidermal cells, called the stratum basale, is close to the dermis and is
nourished by dermal blood vessels.

 Cells of the stratum basale can divide and grow because they are well nourished. As new cells enlarge, they
push the older epidermal cells away from the dermis toward the surface of the skin.

 The farther the cells travel, the poorer their nutrient supply becomes, and, in time, they die.

 The cell membranes of older skin cells (keratinocytes) thicken and develop many desmosomes that
 fasten them to each other.
 At the same time, the cells begin to harden, a process called keratinization, when strands of tough, fibrous,
waterproof keratin proteins are synthesized and stored within the cell.

 As a result, many layers of tough, tightly packed dead cells accumulate in the epidermis, forming an
outermost layer called the stratum corneum.

 The dead cells that compose it are eventually shed.

 The structural organization of the epidermis varies from region to region. It is thickest on the palms of the
hands and the soles of the feet, where it may be 0.8–1.4 mm thick.
 In most areas, only four layers can be distinguished.
- They are the stratum basale (stratum germinativum, or basal cell layer), which is the deepest layer;
- The stratum spinosum, a thick layer;
- The stratum granulosum, a granular layer; and
- The stratum corneum, a fully keratinized layer (horny layer).

 An additional layer, the stratum lucidum (between the stratum granulosum and the stratum corneum) is in the
thickened skin of the palms and soles.

 The cells of these layers change shape as they are pushed toward the surface.

 In body regions other than the palms and soles, the epidermis is usually very thin, averaging 0.07– 0.12 mm.

 The stratum granulosum may be missing where the epidermis is thin.

 In healthy skin, production of epidermal cells is closely balanced with loss of dead cells from the stratum
corneum, so that skin does not wear away completely.

 In fact, the rate of cell division increases where the skin is rubbed or pressed regularly, causing the growth
of thickened areas called calluses on the palms and soles and keratinized conical masses on the toes called
corns.
(a) The layers of the epidermis are distinguished by changes in cells as they are pushed toward the surface of the
skin. (b) Micrograph from the palm of the hand (50×)
Layers of the Epidermis
 Specialized cells in the epidermis called melanocytes produce the dark pigment melanin that provides skin
colour.

 Melanin absorbs ultraviolet radiation in sunlight, preventing mutations in the DNA of skin cells and other
damaging effects.

 Melanocytes lie in the deepest portion of the epidermis and in the underlying connective tissue of the
dermis.
Melanocytes (arrows) that are mainly in the stratum basale at the deepest layer of the epidermis produce the pigment
melanin.
 Dermis
 The boundary between the epidermis and dermis is usually uneven. This is because the epidermis has
ridges projecting inward and the dermis has conical dermal papillae passing into the spaces between the
ridges.

 Fingerprints form from these undulations of the skin at the distal end of the palmar surface of a finger.

 Fingerprints are used for purposes of identification because they are individually unique.

 The pattern of a fingerprint is genetically determined, and the prints form during fetal existence.

 The dermis binds the epidermis to the underlying tissues.

 It is largely composed of irregular dense connective tissue that includes tough collagenous fibers and elastic
 On the average, the dermis is 1.0 –2.0 mm thick; however, it may be as thin as 0.5 mm or less on the eyelids
or as thick as 3.0 mm on the soles of the feet.

 The dermis also contains muscle fibers. Some regions, such as the skin that encloses the testes (scrotum),
contain many smooth muscle cells that can wrinkle the skin when they contract.

 Other smooth muscles in the dermis are associated with accessory organs such as hair follicles and glands.

 Many striated muscle fibers are anchored to the dermis in the skin of the face. They help produce the
voluntary movements associated with facial expressions.

 Nerve fibers are scattered throughout the dermis.

 Motor fibers carry impulses to dermal muscles and glands, and sensory fibers carry impulses away from
specialized sensory receptors, such as touch receptors.

 One type of dermal sensory receptor, Pacinian corpuscles, is stimulated by heavy pressure; whereas another
type, Meissner’s corpuscles, senses light touch.

 Still other receptors respond to temperature changes or to factors that can damage tissues.

 The dermis also contains blood vessels, hair follicles, sebaceous glands, and sweat glands.
 Subcutaneous Layer
 The subcutaneous layer (hypodermis) beneath the dermis consists of loose connective and adipose
tissues.

 The collagenous and elastic fibers of this layer are continuous with those of the dermis.

 Most of these fibers parallel the surface of the skin, extending in all directions.

 As a result, no sharp boundary separates the dermis and the subcutaneous layer.

 The adipose tissue of the subcutaneous layer insulates, helping to conserve body heat and impeding the
 entrance of heat from the outside.

 The amount of adipose tissue varies greatly with each individual’s nutritional condition.
 It also varies in thickness from one region to another. For example, adipose tissue is usually thick over the
abdomen, but absent in the eyelids.

 The subcutaneous layer contains the major blood vessels that supply the skin.

 Branches of these vessels form a network (rete cutaneum) between the dermis and the subcutaneous layer.

 They, in turn, give off smaller vessels that supply the dermis above and the underlying adipose tissue.
 Accessory Organs of the Skin
 Accessory organs of the skin extend downward from the epidermis and include hair follicles, nails, and skin
glands. As long as accessory organs remain intact, severely burned or injured dermis can regenerate.

 Hair Follicles
 Hair is present on all skin surfaces except the palms, soles, lips, nipples, and parts of the external
reproductive organs; however, it is not always well developed.

 Each hair develops from a group of epidermal cells at the base of a tube-like depression called a hair follicle.

 This follicle extends from the surface into the dermis and contains the hair root, the portion of hair
embedded in the skin.

 The epidermal cells at its base are nourished from dermal blood vessels in a projection of connective tissue
(hair papilla) at the deep end of the follicle.
 As these epidermal cells divide and grow, older cells are pushed toward the surface.

 The cells that move upward and away from the nutrient supply become keratinized and die.

 Their remains constitute the structure of a developing hair shaft that extends away from the skin surface.

 In other words, a hair is composed of dead epidermal cells.

 Both hair and epidermal cells develop from the same types of stem cells.

 Usually a hair grows for a time and then rests while it remains anchored in its follicle. Later a new hair
begins to grow from the base of the follicle, and the old hair is pushed outward and drops off.

 Sometimes, however, the hairs are not replaced. When this occurs in the scalp, the result is baldness
(Alopecia).
 Genes determine hair color by directing the type and amount of pigment that epidermal melanocytes
produce. For example, dark hair has much more melanin than blond hair.

 The white hair of a person with the inherited condition albinism lacks melanin altogether.

 Bright red hair contains an iron pigment (trichosiderin) that is not in hair of any other color.

 A mixture of pigmented and unpigmented hair usually appears gray.

 A bundle of smooth muscle cells, forming the arrector pili muscle, attaches to each hair follicle. This muscle is
positioned so that a shorthair within the follicle stands on end when the muscle contracts.

 If a person is upset or very cold, nerve impulses may stimulate the arrector pili muscles to contract, raising
gooseflesh, or goose bumps. Each hair follicle also has associated with it one or more sebaceous (oil-
(a) A hair grows from the base of a hair follicle when epidermal cells divide and older cells move outward and become
keratinized. (b) A light micrograph of a hair follicle (160×).
 Nails
 Nails are protective coverings on the ends of the fingers and toes.

 Each nail consists of a nail plate that overlies a surface of skin called the nail bed.

 Specialized epithelial cells that are continuous with the epithelium of the skin produce the nail bed.

 The whitish, thickened, half-moon–shaped region (lunula) at the base of a nail plate is the most active growing
region.

 The epithelial cells here divide, and the newly formed cells are keratinized. This gives rise to tiny, keratinized
scales that become part of the nail plate, pushing it forward over the nail bed.

 In time, the plate extends beyond the end of the nail bed and with normal use gradually wears away.
Nails grow from epithelial cells that divide and become keratinized in the lunula.
 Skin Glands
 Sebaceous glands – Contain groups of specialized epithelial cells and are usually associated with hair follicles.

 They are holocrine glands, and their cells produce globules of a fatty material that accumulate, swelling and
bursting the cells. The resulting mixture of fatty material and cellular debris is called sebum.

 Sebum is secreted into hair follicles through short ducts and helps keep the hairs and the skin soft, pliable, and
waterproof.

 Acne results from excess sebum secretion.

 Sebaceous glands are scattered throughout the skin but are not on the palms and soles.

 In some regions, such as the lips, the corners of the mouth, and parts of the external reproductive organs,
A sebaceous gland secretes sebum into a hair follicle
 Sweat glands (sudoriferous glands) - are widespread in the skin.

 Each gland consists of a tiny tube that originates as a ball-shaped coil in the deeper dermis or superficial
subcutaneous layer.

 The coiled portion of the gland is closed at its deep end and is lined with sweat-secreting epithelial cells.

 The most numerous sweat glands, called Eccrine glands, respond throughout life to body temperature
elevated by environmental heat or physical exercise.

 These glands are common on the forehead, neck, and back, where they produce profuse sweat on hot days
or during intense physical activity.

 They also cause the moisture that appears on the palms and soles when a person is emotionally stressed
 The fluid the eccrine sweat glands secrete is carried by a tube (duct) that opens at the surface as a pore

 Sweat is mostly water, but it also contains small quantities of salts and wastes, such as urea and uric acid.

 Thus, sweating is also an excretory function.

 The secretions of certain sweat glands, called apocrine glands, develop a scent as they are metabolized by
skin bacteria.

 Apocrine sweat glands become active at puberty and can wet certain areas of the skin when a person is
emotionally upset, frightened, or in pain.

 Other sweat glands are structurally and functionally modified to secrete specific fluids, such as the
ceruminous glands of the external ear canal that secrete ear wax and the female mammary glands that
Note the difference in location of the ducts of the eccrine and apocrine sweat glands
 Regulation of Body Temperature
 The regulation of body temperature is vitally important because even slight shifts can disrupt the rates of
metabolic reactions.

 Normally, the temperature of deeper body parts remains close to a set point of 37° C (98.6° F).

 The maintenance of a stable temperature requires that the amount of heat the body loses be balanced by
the amount it produces.

 The skin plays a key role in the homeostatic mechanism that regulates body temperature.
 Mechanism of heat production and loss
 Because cellular metabolism releases heat, the most active cells are the major heat producers. These include
skeletal and heart muscle cells and the cells of certain glands, such as the liver.

 In intense heat, nerve impulses stimulate structures in the skin and other organs to release heat. For
example, physical exercise, active muscles release heat, which the blood carries away.

 The warmed blood reaches the part of the brain (the hypothalamus) that controls the body’s temperature set
point, which signals muscles in the walls of specialized dermal blood vessels to relax.

 As the vessels dilate (vasodilation), more blood enters them and some of the heat the blood carries escapes
to the outside.

 At the same time, deeper blood vessels contract (vasoconstriction), diverting blood to the surface, and the
skin reddens.
 The heart is stimulated to beat faster, moving more blood out of the deeper regions.

 The primary means of body heat loss is radiation, by which infrared heat rays escape from warmer surfaces to
cooler surroundings. These rays radiate in all directions, much like those from the bulb of a heat lamp.

 Conduction and Convection release less heat.

 In Conduction, heat moves from the body directly into the molecules of cooler objects in contact with its
surface. For example, heat is lost by conduction into the seat of a chair when a person sits down. The heat loss
continues as long as the chair is cooler than the body surface touching it.

 Heat is also lost to the air molecules that contact the body. As air becomes heated, it moves away from the
body, carrying heat with it, and is replaced by cooler air moving toward the body. This type of continuous
circulation of air over a warm surface is Convection.
 Another means of body heat loss is Evaporation.

 When the body temperature rises above normal, the nervous system stimulates eccrine sweat glands to
release sweat onto the surface of the skin.

 As this fluid evaporates, it carries heat away from the surface, cooling the skin.

 With excessive heat loss, the brain triggers a different set of responses in skin structures. Muscles in the walls
of dermal blood vessels are stimulated to contract; this decreases the flow of heat-carrying blood through the
skin, which tends to lose colour, and helps reduce heat loss by radiation, conduction, and convection.

 At the same time, sweat glands remain inactive, decreasing heat loss by evaporation. If the body temperature
continues to drop, the nervous system may stimulate muscle fibers in the skeletal muscles throughout the
body to contract slightly.
Body temperature regulation is an example of homeostasis.
 Skin Colour

 Heredity and the environment determine skin colour.

 Genetic Factors
 Regardless of racial origin, all people have about the same number of melanocytes in their skin.

 Differences in skin color result from differences in the amount of melanin these cells produce, which is
controlled by several genes. The more melanin, the darker the skin.

 The distribution and the size of pigment granules within melanocytes also influence skin colour. The granules
in very dark skin are single and large; those in lighter skin occur in clusters of two to four granules and are
smaller.

 People who inherit mutant melanin genes have nonpigmented skin, part of albinism. It affects people of all
races and also many other species.
 Environmental Factors

 Environmental factors such as sunlight, ultraviolet light from sunlamps, and X rays affect skin colour.

 These factors rapidly darken existing melanin, and they stimulate melanocytes to produce more pigment and
transfer it to nearby epidermal cells within a few days.

 This is why sunbathing tans skin. Unless exposure to sunlight continues, however, the tan fades as pigmented
epidermal cells become keratinized and wear away

 Physiological Factors - Blood in the dermal vessels adds color to the skin. For example, when blood is well
oxygenated, the blood pigment hemoglobin is bright red, making the skins of light complexioned people
appear pinkish. On the other hand, when the blood oxygen concentration is low, hemoglobin is dark red, and
the skin appears bluish—a condition called cyanosis.
 Pathophysiology of skin disorders
 PRIMARY DISORDERS OF THE SKIN
 Primary skin disorders are those originating in the skin.

 They include infectious processes, acne and rosacea, papulosquamous dermatoses, allergic disorders and drug
reactions, and arthropod infestations.

 Although most of these disorders are not life threatening, they can affect the quality of life.

 The skin is subject to invasion by a number of microorganisms, including fungi, bacteria, and viruses.

 Normally, the skin flora, sebum, immune responses, and other protective mechanisms guard the skin against
infection. Depending on the virulence of the infecting agent and the competence of the host’s resistance,
infections may result.
 Fungal Infections

 Fungi are free-living, saprophytic, plantlike organisms, certain strains of which are considered part of the
normal skin flora.

 Fungal or mycotic infections of the skin are traditionally classified as superficial or deep.

 The superficial mycoses, more commonly known as tinea or ringworm, invade only the superficial
keratinized tissue (skin, hair, and nails).

 Deep fungal infections involve the epidermis, dermis, and subcutis.

 Infections that typically are superficial may exhibit deep involvement in immunosuppressed individuals.
 Superficial Fungal Infections.
 Superficial fungal infections affect various parts of the body, with the lesions varying according to site and
fungal species.

 Tinea can affect the body (tinea corporis), face and neck (tinea faciei), scalp (tinea capitis), hands (tinea
manus), feet (tinea pedis), or nails (tinea unguium).

 Tinea corporis (ringworm of the body) - can be caused by any of the fungi. Although tinea corporis affects all
ages, children seem most prone to infection.

 Transmission is most commonly from kittens, puppies, and other children who have infections.

 The lesions vary, depending on the fungal agent. The most common types of lesions are oval or circular
patches on exposed skin surfaces and the trunk, back, or buttocks. Less common are foot and groin infections.
 The lesion begins as a red papule and enlarges, often with a central clearing.

 Patches have raised red borders consisting of vesicles, papules, or pustules.

 The borders are sharply defined, but lesions may coalesce.

 Pruritus, a mild burning sensation, and erythema frequently accompany the skin lesion.

Tinea of the body caused by Microsporum canis.

 Tinea capitis (ringworm of the scalp) - occurs in two forms: primary (noninflammatory) and secondary
(inflammatory).

 Depending on the invading fungus, the lesions of the noninflammatory type can vary from grayish, round,
hairless patches to balding spots or black dots on the head. The lesions vary in size and are most commonly
seen on the back of the head.

 The individual usually is asymptomatic, although pruritus may exist.

 Children between 3 and 14 years of age are primarily affected, although an increasing number of adults are
receiving diagnoses of the infection.
 The inflammatory type of tinea capitis has a rapid onset, and lesions usually are localized to one area.

 The initial lesion consists of a pustular, scaly, round patch with broken hairs.

 A secondary bacterial infection is common and may lead to a painful, circumscribed, boggy, and indurated
lesion called a kerion.

 The highest incidence is among children and farmers who work with infected animals.

Tinea of the scalp caused by Microsporum audouini

 Tinea pedis (athlete’s foot, or ringworm of the feet) is a common dermatosis primarily affecting the spaces
between the toes, the soles of the feet, or the sides of the feet.

 The lesions vary from a mildly scaling lesion to a painful, exudative, erosive, inflamed lesion with fissuring.

 Lesions often are accompanied by pruritus, pain, and foul odor. Some persons are prone to chronic tinea
pedis, whereas others have a milder form that is exacerbated during hot weather or when the feet are
exposed to moisture or occlusive shoes

Chronic tinea of sole of the foot caused by Trichophyton rubrum.

 Tinea manus (ringworm of the hands) usually is a secondary infection with tinea pedis as the primary
infection.

 In contrast to other skin disorders such as contact dermatitis and psoriasis, which affect both hands, tinea
manus usually occurs only on one hand.

 The characteristic lesion is a blister on the palm or finger surrounded by erythema.

 Chronic lesions are scaly and dry. Cracking and fissuring may occur.

 The lesions may spread to the plantar surfaces of the hand. If chronic, tinea manus may lead to tinea of the
fingernails
 Tinea unguium is a dermatophyte infection (onychomycosis) of the nails. Toe nails are involved more
commonly than fingernails.

 The infection often begins at the tip of the nail, where the fungus digests the nail keratin. Initially, the nail
appears opaque, white, or silvery. The nail then turns yellow or brown.

 The condition often remains unchanged for years. During this time it may involve only one or two nails and
may produce little or no discomfort.

 Gradually, the nail thickens and cracks as the infection spreads.

 Permanent discoloration and distortion result as the nail separates from the underlying epidermis.
 Less common forms of tinea unguium are superficial white onychomycosis, in which areas of the nails
become powdery white and erode, and proximal subungual onychomycosis (PSO), in which there is rapid
invasion of the nail, leaving it white with no additional thickening of the nail.

 Although it is one of the less common forms of tinea unguium, PSO has increased among people with
acquired immunodeficiency syndrome (AIDS).

Tinea of the fingernail caused by Trichophyton rubrum

 Diagnosis and treatment
 Diagnosis of superficial fungal infections is primarily done by microscopic examination of skin scrapings for
fungal spores, the reproducing bodies of fungi.

 Potassium hydroxide (KOH) preparations are used to prepare slides of skin scrapings.

 KOH disintegrates human tissue and leaves behind the threadlike filaments, called hyphae, that grow from the
fungal spores.

 Cultures also may be done.

 Superficial fungal infections may be treated with topical or systemic antifungal agents.
 Candida Infections.
 Candidiasis (moniliasis) is a fungal infection caused by Candida albicans.

 This yeast like fungus is a normal inhabitant of the gastrointestinal tract, mouth, and vagina.

 The skin problems result from the release of irritating toxins on the skin surface.

 Some persons are predisposed to candidal infections with conditions such as diabetes mellitus, antibiotic
therapy, pregnancy, use of birth control pills, poor nutrition, and immunosuppressive diseases.

 Oral candidiasis may be the first sign of infection with human immunodeficiency virus (HIV).

 C. albicans thrives in warm, moist intertriginous areas of the body.

 The rash is red with well-defined borders.

 Patches erode the epidermis, and there is scaling.

 Mild to severe itching and burning often accompany the infection.

 Severe forms of infection may involve pustules or vesiculopustules.

 In addition to microscopic analysis, a candidal infection often can be differentiated from a tinea infection by
the presence of satellite lesions.

 These satellite lesions are maculopapular and are found outside the clearly demarcated borders of the
candidal infection.
 Satellite lesions often are diagnostic of diaper rash complicated by Candida.

 The appearance of candidal infections varies according to the site.

 Diagnosis usually is based on microscopic examination of skin or mucous membrane scrapings placed in
KOH solution.

 Depending on the site of infection and extent of involvement, topical and oral antifungal agents may be
used in treatment.
 Bacterial Infections
 Bacteria are considered normal flora of the skin. Most bacteria are not pathogenic, but when pathogenic
bacteria invade the skin, superficial or systemic infections may develop.

 Bacterial skin infections are commonly classified as primary or secondary infections.

 Primary infections are superficial skin infections such as impetigo or ecthyma.

 Secondary infections consist of deeper cutaneous infections, such as infected ulcers.

 Diagnosis usually is based on cultures taken from the infected site.

 Treatment measures include antibiotic therapy and measures to promote comfort and prevent the spread of
infection.
 Impetigo - Impetigo is a common superficial bacterial infection caused by staphylococci or group A β-
hemolytic streptococci (GABHS), or both.

 It is common among infants and young children, although older children and adults occasionally contract
the disease.

 Impetigo initially appears as a small vesicle or pustule or as a large bulla on the face or elsewhere on the
body. As the primary lesion ruptures, it leaves a denuded area that discharges a honey-colored serous
liquid that hardens on the skin surface and dries as a honey-colored crust with a “stuckon” appearance.
New vesicles erupt within hours.

 Topical mupirocin, which has few side effects, may be effective for limited disease. If the area is large or if
there is concern about complications, systemic antibiotics are used.
Impetigo of the face.
 Ecthyma is an ulcerative form of impetigo, usually secondary to minor trauma. It is caused by GABHS,
Staphylococcus aureus, or Pseudomonas.

 It frequently occurs on the buttocks and thighs of children.

 The lesions are similar to those of impetigo.

 With extensive ecthyma, there is a low-grade fever and extension of the infection to other organs.

 Treatment usually involves the use of systemic antibiotics.

Ecthyma on the buttocks of a 13-year-old boy
 Viral Infections
 Viruses are intracellular pathogens that rely on live cells of the host for reproduction.

 They have no organized cell structure but consist of a DNA or RNA core surrounded by a protein coat.

 The viruses seen in skin lesion disorders tend to be DNA containing viruses.

 Viruses invade the keratinocyte, begin to reproduce, and cause cellular proliferation or cellular death.

 The rapid increase in viral skin diseases has been attributed to the use of corticosteroid drugs, which have
immunosuppressive qualities, and the use of antibiotics, which alter the bacterial flora of the skin.
 Verrucae - Verrucae, or warts, are common, benign papillomas caused by DNA-containing human
papillomaviruses (HPV).

 The lesions are circumscribed, symmetrical epidermal neoplasms that are often elevated above the skin and
often appear papillary.

 Histologically, there is an irregular thickening of the stratum spinosum and greatly increased thickening of the
stratum corneum.

 Treatment usually is directed at inducing a “wart-free” period without producing scarring. Warts resolve
spontaneously when immunity to the virus develops.

 Removal is usually done by applying a keratolytic agent, such as salicylic acid, that breaks down the wart
tissue, or by freezing with liquid nitrogen. Various types of laser surgery, electrosurgery, and the use of
cytotoxic or antiviral therapy also have been successful in wart eradication.
Common and periungual warts.
 Herpes Simplex - Herpes simplex virus (HSV) infections of the skin and mucous membrane (i.e., cold sore or
fever blister) are common.

 Two types of herpesviruses infect humans: type 1 and type 2.

 HSV-1 usually is confined to the oropharynx, and the organism is spread by respiratory droplets or by direct
contact with infected saliva.

 Genital herpes usually is caused by HSV-2, although HSV-1 also can cause genital herpes.

 There is no cure for oropharyngeal herpes simplex; most treatment measures are palliative. Penciclovir cream,
a topical antiviral agent, applied at the first symptom may be used to reduce the duration of an attack.
Recurrent herpes simplex of the face.
 Herpes Zoster - Herpes zoster (shingles) is an acute, localized vesicular eruption distributed over a
dermatomal segment of the skin.

 It is caused by the same herpesvirus, varicella-zoster, that causes chickenpox.

 It is believed to be the result of reactivation of a latent varicella-zoster virus that was dormant in the sensory
dorsal root ganglia since a childhood infection.

 During an episode of herpes zoster, the reactivated virus travels from the ganglia to the skin of the
corresponding dermatome.

 Although herpes zoster is not as contagious as chickenpox, the reactivated virus can be transmitted to
nonimmune contacts.
 The incidence of herpes zoster increases with age; it occurs 8 to 10 times more frequently in persons older
than 60 years than in younger persons.

 The lesions of herpes zoster typically are preceded by a prodrome consisting of a burning pain, tingling
sensation, extreme sensitivity of the skin to touch, and pruritus along the affected dermatome.

 This may be present for 1 to 3 days or longer before the appearance of the rash. During this time, the pain
maybe mistaken for a number of other conditions, such as heart disease, pleurisy, various musculoskeletal
disorders, or gastrointestinal disorders.

 The treatment of choice for herpes zoster is the administration of an antiviral agent. The treatment is most
effective when started within 72 hours of rash development
 Eczema
 Atopic eczema (atopic dermatitis) is a common skin disorder that occurs in two clinical forms: infantile and
adult.

 It is associated with a type I hypersensitivity reaction

 The infantile form is characterized by vesicle formation, oozing, and crusting with excoriations. It usually
begins in the cheeks and may progress to involve the scalp, arms, trunk, and legs.

 The skin of the cheeks may be paler, with extra creases under the eyes, called Dennie-Morgan folds.

 There is marked follicle involvement in persons with black skin.

 Lesions may be hypopigmented or hyperpigmented or both on a black-skinned person.

 The infantile form usually becomes milder as the child ages, often disappearing by the age of 15 years.

 Adolescents and adults usually have dry, leathery, and hyperpigmented or hypopigmented lesions located in
the antecubital and popliteal areas.

 These may spread to the neck, hands, feet, eyelids, and behind the ears. Itching may be severe with both
forms. Secondary infections are common

Atopic eczema on an infant’s face and on a wrist.

 Treatment of atopic eczema is designed to target the underlying abnormalities such as dryness, pruritus,
superinfection, and inflammation.

 It involves allergen control, basic skin care, and medications.

 Because dry skin and pruritus often exacerbate the condition, hydration of the skin is essential to treating
atopic dermitis.

 Mild or healing lesions may be treated with lotions containing a mild antipruritic agent. Acute weeping
lesions are treated with soothing lotions, soaks, or wet dressings.

 Topical corticosteroids provide an effective form of treatment but can cause local and systemic side effects
 Nummular eczema (discoid eczema)
 The lesions of nummular eczema (discoid eczema) are coin shaped (nummular) papulovesicular patches
mainly involving the arms and legs.

 Lichenification and secondary bacterial infections are common.

 Most nummular eczema is chronic, with weeks to years between exacerbations. Exacerbations occur more
frequently in the cold winter months.

 The exact cause of nummular eczema is unknown. There usually is a history of asthma, hay fever, or atopic
dermatitis.

 Ingestion of iodides and bromides usually aggravates the condition. Treatment is palliative. Frequent Topical
corticosteroids, coal tar preparations, and ultraviolet light treatments are prescribed as necessary
Nummular eczema of the buttocks
 Burns
 Burns are classified as first degree, second-degree superficial, second-degree deep partial thickness, third-
degree full thickness, and fourth degree.

 A first-degree burn is limited to the epidermis. The most common example of a first-degree burn is
sunburn, which results from exposure to the sun.

 In a second-degree burn, the epidermis and part of the dermis are damaged.

 A third-degree burn damages the epidermis and dermis, and vessels and tissue are visible.

 In fourth-degree burns, the damage extends through deeply charred subcutaneous tissue to muscle and
bone.
CLASSIFICATIONS OF BURNS
Causes
 Thermal burns, the most common type, frequently result from: residential fires etc.

 Chemical burns result from contact, ingestion, inhalation, or injection of acids, alkalis, or vesicants.

 Electrical burns

 Friction or abrasion burns occur when the skin rubs harshly against a coarse surface.

 Sunburn results from excessive exposure to sunlight.

Pathophysiology
 The injuring agent denatures cellular proteins. Some cells die because of traumatic or ischemic necrosis.

 Loss of collagen cross-linking also occurs with denaturation, creating abnormal osmotic and hydrostatic
pressure gradients that cause the movement of intravascular fluid into interstitial spaces.

 Cellular injury triggers the release of mediators of inflammation, contributing to local and, in the case of major
burns, systemic increases in capillary permeability.

 Specific pathophysiologic events depend on the cause and classification of the burn.
 First-degree burns
 A first-degree burn causes localized injury or destruction to the skin (epidermis only) by direct (such as
chemical spill) or indirect (such as sunlight) contact.
 The barrier function of the skin remains intact, and these burns aren't life threatening.

 Second-degree superficial partial-thickness burns

 These burns involve destruction to the epidermis and some dermis.
 Thin-walled, fluid-filled blisters develop within a few minutes of the injury.
 As these blisters break, the nerve endings become exposed to the air.
 Because pain and tactile responses remain intact, subsequent treatments are very painful.
 The barrier function of the skin is lost.
 Second-degree deep partial-thickness burns
 These burns involve destruction of the epidermis and dermis, producing blisters and mild to moderate edema
and pain. The hair follicles are still intact, so hair will grow again.
 Compared with second-degree superficial partial-thickness burns, there's less pain sensation with this burn
because the sensory neurons have undergone extensive destruction.
 The areas around the burn injury remain very sensitive to pain.
 The barrier function of the skin is lost.

 Third- and fourth-degree burns

 A major burn affects every body system and organ.
 A third-degree burn extends through the epidermis and dermis and into the subcutaneous tissue layer.
 A fourth-degree burn involves muscle, bone and interstitial tissues.
 Within only hours, fluids and protein shift from capillary to interstitial spaces, causing edema.
 There's an immediate immunologic response to a burn injury, making burn wound sepsis a potential threat
 Signs and symptoms depend on the type of burn and may include:

- Localized pain and erythema, usually without blisters in the first 24 hours (first-degree burn)

- Chills, headache, localized edema, and nausea and vomiting (more severe first-degree burn)

- Thin-walled, fluid-filled blisters appearing within minutes of the injury, with mild to moderate edema and pain

(second-degree superficial partial-thickness burn)

- White, waxy appearance to damaged area (second-degree deep partial-thickness burn)

- White, brown, or black leathery tissue and visible thrombosed vessels due to destruction of skin elasticity,

without blisters (third-degree burn)

- Silver-colored, raised area, usually at the site of electrical contact (electrical burn)

- Voice changes, coughing, wheezing, soot in mouth or nose, and darkened sputum (with smoke inhalation and

pulmonary damage).
 Diagnosis
 Diagnosis involves determining the size and classifying the wound.
 The following methods are used to determine size:
- Percentage of BSA (body surface area) covered by the burn using the Rule of Nines chart
- Lund-Browder chart (more accurate because it allows BSA changes with age); correlation of the burn’s depth
and size to estimate its severity.

 Major burns are classified as:

- third-degree burns on more than 10% of BSA
- second-degree burns on more than 25% of adult BSA (over 20% in children)
- burns of hands, face, feet, or genitalia
- burns complicated by fractures or respiratory damage
- electrical burns
- all burns in poor-risk patients.
 Moderate burns are classified as:
- third-degree burns on 2% to 10% of BSA
- second-degree burns on 15% to 25% of adult BSA (10% to 20% in children).

 Minor burns are classified as:

- third-degree burns on less than 2% of BSA
- second-degree burns on less than 15% of adult BSA (10% in children).
 Ulcer (Pressure ulcer)
 Pressure ulcers, commonly called pressure sores or bedsores, are localized areas of cellular necrosis that
occur most often in the skin and subcutaneous tissue over bony prominences.

 These ulcers may be superficial, caused by local skin irritation with subsequent surface maceration, or deep,
originating in underlying tissue.

 Deep lesions often go undetected until they penetrate the skin, but by then, they've usually caused
subcutaneous damage.

 Most pressure ulcers develop over five body locations: sacral area, greater trochanter, ischial tuberosity, heel,
and lateral malleolus.

 Collectively, these areas account for 95% of all pressure ulcer sites.
 Patients who have contractures are at an increased risk for developing pressure ulcers due to the added
pressure on the tissue and the alignment of the bones.

 Age also has a role in the incidence of pressure ulcers. Muscle is lost with aging, and skin elasticity decreases.
Both these factors increase the risk for developing pressure ulcers.

 Partial-thickness ulcers usually involve the dermis and epidermis; these wounds heal within a few weeks.

 Full-thickness ulcers also involve the dermis and epidermis, but in these wounds, the damage is more severe
and complete.

 There may also be damage to the deeper tissue layers. Ulcers of the subcutaneous tissue and muscle may
require several months to heal. If the damage has affected the bone in addition to the skin layers,
osteomyelitis may occur, which will prolong healing times.
Pathophysiology
 A pressure ulcer is caused by an injury to the skin and its underlying tissues.

 The pressure exerted on the area causes ischemia and hypoxemia to the affected tissues because of
decreased blood flow to the site.

 As the capillaries collapse, thrombosis occurs, which subsequently leads to tissue edema and
progression to tissue necrosis.

 Ischemia also adds to an accumulation of waste products at the site, which in turn leads to the
production of toxins.

 The toxins further break down the tissue and eventually lead to the death of the cells.
Diagnosis is based on:
 Physical examination showing presence of the ulcer

 Wound culture with exudate or evidence of infection

 Elevated white blood cell count with infection

 Possibly elevated erythrocyte sedimentation rate

 Total serum protein and serum albumin levels showing severe hypoproteinemia.
 Staging pressure ulcers
• The staging system described below is based on the recommendations of the National Pressure Ulcer Advisory
Panel (NPUAP) (Consensus Conference, 1991) and the Agency for Health Care Policy and Research (Clinical
Practice Guidelines for Treatment of Pressure Ulcers, 1992).

 STAGE 1
• A stage 1 pressure ulcer is an observable pressure-related alteration of intact skin.

• The indicators, compared with the adjacent or opposite area on the body, may include changes in one or more
of the following factors: skin temperature (warmth or coolness), tissue consistency (firm or boggy feel), or
sensation (pain or itching).

• The ulcer appears as a defined area of persistent redness in lightly pigmented skin; in darker skin, the ulcer
may appear with persistent red, blue, or purple hues.
 STAGE 2
 A stage 2 pressure ulcer is characterized by partial-thickness skin loss involving the epidermis or dermis.

 The ulcer is superficial and appears as an abrasion, blister, or shallow crater.

 STAGE 3
 A stage 3 pressure ulcer is characterized by full-thickness skin loss involving damage or necrosis of
subcutaneous tissue, which may extend down to, but not through, the underlying fascia.

 The ulcer appears as a deep crater with or without undermining of adjacent tissue.

 STAGE 4
 Full-thickness skin loss with extensive destruction, tissue necrosis, or damage to muscle, bone, or support
structures (for example, tendon or joint capsule) characterize a stage 4 pressure ulcer. Tunneling and sinus
tracts also may be associated with stage 4 pressure ulcers.
 Skin Cancer
 There has been an alarming increase in skin cancers during the past several decades.

 Since the 1970s, the incidence rate of malignant melanoma, the most serious form of skin cancer, has
increased significantly.

 These increases are, on average, 4% per year, from 5.7 per 100,000 in 1973 to 13.8 per 100,000 in 1996, with
approximately 47,700 new cases and 9600 deaths each year from melanoma.

 There also are approximately 1.3 million cases each year of highly curable basal cell and squamous cell
cancers.

 The rising incidence of skin cancer may be attributed primarily to increased sun exposure associated with
societal and lifestyle shifts.
 The thinning of the ozone layer in the earth’s stratosphere is thought to be an important factor in this
incidence rate.

 Society’s emphasis on suntanning also is implicated.

 Although the factors linking sun exposure to skin cancer are incompletely understood, both total cumulative
exposure and altered patterns of exposure (in the case of melanoma) are strongly implicated.

 Basal cell and squamous cell carcinomas are associated with total cumulative exposure to ultraviolet radiation,
whereas melanomas are associated with intense intermittent exposure.

 Basal cell and squamous cell carcinomas occur more commonly on maximally sun-exposed parts of the body,
such as the face and back of the hands and forearms.

 In contrast, melanomas occur most commonly in areas of the body that are exposed to the sun intermittently.
 Malignant Melanoma
 Malignant melanoma is a malignant tumor of the melanocytes. It is a rapidly progressing, metastatic form of
cancer.

 The increased incidence of melanoma that has occurred during the past several decades has been attributed
to an increase in sun exposure.

 The risk is greatest in fair-skinned people, particularly those with blond or red hair who sunburn and freckle
easily.

 Fortunately, the increased risk of melanoma has been associated with a concomitant increase in the 5-year
survival rate, from approximately 40% in the 1940s to 90% at present.

 Public health screening measures, early diagnosis, increased knowledge of precursor lesions, and greater
public knowledge of the disease may account for earlier intervention
 Severe, blistering sunburns in early childhood and intermittent intense sun exposures (trips to sunny
climates) contribute to increased susceptibility to melanoma in young and middle age adults.

 Roughly 90% of malignant melanomas in whites occur on sun-exposed skin. However, in African Americans
and Asians, roughly 67% occur on non–sun-exposed areas, such as mucous membranes and subungual,
palmar, and plantar surface.

 Although sun exposure remains a significant risk factor for melanoma, other potential risk factors have been
identified, including atypical mole/dysplastic nevus syndrome, immunosuppression, prior PUVA therapy, and
exposure to ultraviolet light at tanning salons.

 PUVA (psoralen and ultraviolet A) is an ultraviolet light therapy treatment for eczema, psoriasis, graft-versus-host disease, vitiligo,
mycosis fungoides, large-plaque parapsoriasis and cutaneous T-cell lymphoma using the sensitizing effects of the drug psoralen.
 Using statistical analysis, it has been determined that six factors independently influence the risk for
development of malignant melanoma:

- Family history of malignant melanoma,

- Presence of blond or red hair,
- Presence of marked freckling on the upper back,
- History of three or more blistering sunburns before 20 years of age,
- History of 3 or more years of an outdoor job as a teenager, and
- Presence of actinic keratosis.

 Persons with two of these risk factors had a 3.5-fold increased risk of malignant melanoma, and those with
three or more risk factors had a 20-fold increased risk.
 Malignant melanomas differ in size and shape. Usually, they are slightly raised and black or brown.

 Borders are irregular, and surfaces are uneven. Most seem to arise from pre-existing nevi or new molelike
growths.

 There may be surrounding erythema, inflammation, and tenderness.

 Periodically, melanomas ulcerate and bleed. Dark melanomas are often mottled with shades of red, blue,
and white.

 These three colors represent three concurrent processes: melanoma growth (blue), inflammation and the
body’s attempt to localize and destroy the tumor (red), and scar tissue formation (white).

 Malignant melanomas can appear anywhere on the body

A) Normal mole with even, round contour and sharply defined borders. (B) Changes in appearance of a mole: asymmetry.
(C) Changes in appearance of a mole: border irregularity. (D) Changes in appearance of a mole: color and uneven
pigmentation. (E) Changes in the appearance of a mole: diameter greater than 6 mm. (F) Changes in the surface of a mole:
scaliness, oozing, and bleeding.
 Four types of melanomas have been identified: superficial spreading, nodular, lentigo maligna, and acral
lentiginous.

 Superficial spreading melanoma is characterized by a raised-edged nevus with lateral growth.

 It has a disorderly appearance in color and outline.
 This lesion tends to have biphasic growth, horizontally and vertically.
 It typically ulcerates and bleeds with growth.
 This type of lesion accounts for 70% of all melanomas and is most prevalent in persons who sunburn easily
and have intermittent sun exposure.

 Nodular melanomas, which account for 15% to 30% of melanomas, are raised dome shaped lesions that can
occur anywhere on the body.
 They are commonly a uniform blue-black color and tend to look like blood blisters.
 Nodular melanomas tend to rapidly invade the dermis from the start with no apparent horizontal growth
 Lentigo maligna melanomas, which account for 4% to 10% of all melanomas, are slow growing, flat nevi
that occur primarily on sun-exposed areas of elderly persons.
 Untreated lentigo maligna tends to exhibit horizontal and radial growth for many years before it invades
the dermis to become lentigo maligna melanoma.

 Acral lentiginous melanoma, which accounts for 2% to 8% of melanomas, occurs primarily on the palms of
 the hands, soles of the feet, nail beds, and mucous membranes.
 It has the appearance of lentigo maligna.
 Unlike other types of melanomas, it has a similar incidence in all ethnic groups

 Because virtually all the known risks of melanoma are related to susceptibility and magnitude of
ultraviolet light exposure, protection from the sun’s rays plays a critical role in the prevention of malignant
melanoma.
 Early detection is critical with malignant melanoma.

 Regular self-examination of the total skin surface in front of a mirror under good lighting provides a method
for early detection. It requires that a person undress completely and examine all areas of the body using a full
mirror.

 An ABCD rule has been developed to aid in early diagnosis and timely treatment of malignant melanoma.

 The acronym stands for Asymmetry, Border irregularity, Color variegation, and Diameter greater than 0.6 cm
(pencil eraser size).

 Diagnosis of melanoma is based on biopsy findings from a suspect lesion.

 Treatment is usually surgical excision, the extent of which is determined by the thickness of the lesion,
invasion of the deeper skin layers, and spread to regional lymph nodes.
 Basal Cell Carcinoma
 Basal cell carcinoma is the most common skin cancer in humans, accounting for 75% of all nonmelanoma skin
cancers.

 Like other skin cancers, basal cell carcinoma has increased in incidence during the past several decades. Basal
cell carcinoma usually occurs in persons who were exposed to great amounts of sunlight.

 The incidence is twice as high among men as women and greatest in the 55-75-year-old age group.

 Basal cell carcinoma usually is a nonmetastasizing tumor that extends wide and deep if left untreated.

 These tumors are seen most frequently on sun-exposed areas of the body, such as the head and neck, but do
occur on other skin surfaces that were not exposed to the sun.
 Histological types
 Although there are several histologic types of basal cell carcinoma, nodular ulcerative and superficial basal cell
carcinomas are the most frequently occurring types.

 Nodular ulcerative basal cell carcinoma is the most common type. It is a nodulocystic structure that begins as
a small, flesh-colored or pink, smooth, translucent nodule that enlarges with time.

 Telangiectatic vessels frequently are seen beneath the surface.

 Over the years, a central depression forms that progresses to an ulcer surrounded by the original shiny, waxy
border.

 Basal cell carcinoma in darker-skinned persons usually is darkly pigmented and frequently misdiagnosed as
other skin diseases, including melanoma.
 The second most common form is superficial basal cell carcinoma, which is seen most often on the chest or
back.

 It begins as a flat, nonpalpable, erythematous plaque. The red, scaly areas slowly enlarge, with nodular
borders and telangiectatic bases.

 This type of skin cancer is difficult to diagnose because it mimics other dermatologic problems.

 All suspected basal cell carcinomas should undergo biopsy for diagnosis.

 The treatment depends on the site and extent of the lesion.

 The most important treatment goal is complete elimination of the lesion. Also important is the maintenance
of function and optimal cosmetic effect. Curettage with electrodesiccation, surgical excision, irradiation, and
chemosurgery are effective in removing all cancerous cells.
Basal cell carcinoma and wrinkling of the hand
 Squamous Cell Carcinoma
 Squamous cell carcinomas are malignant tumors of the outer epidermis.

 They are commonly found on the sun-exposed area of the skin of people with fair complexions.

 Metastasis is more common with squamous cell carcinoma than with basal cell carcinoma.

 The mechanisms of squamous cell carcinoma development are unclear. Most squamous cell cancers occur in
sun-exposed areas of the skin, and persons who spend much time outdoors, have lighter skin, and live in
lower latitudes are more affected.

 The increase in the incidence of squamous cell carcinomas is consistent with increased ultraviolet radiation
exposure. Other suspected causes include exposure to arsenic (i.e., Bowen’s disease), gamma radiation, tars,
and oils
 There are two types of squamous cell carcinoma: intraepidermal and invasive.

 Intraepidermal squamous cell carcinoma remains confined to the epidermis for a long time.

 However, at some unpredictable time, it may penetrate the basement membrane to the dermis and
metastasize to the regional lymph nodes.

 It then converts to invasive squamous cell carcinoma.

 The invasive type can develop from intraepidermal carcinoma or from a premalignant lesion (e.g.,
actinic keratoses).

 It may be slow growing or fast growing with metastasis.

 Squamous cell carcinoma is a red-scaling, keratotic, slightly elevated lesion with an irregular border, usually
with a shallow chronic ulcer.

 Later lesions grow outward, show large ulcerations, and have persistent crusts and raised, erythematous
borders.

 The lesions characteristically occur on the nose, forehead, helixes of the ears, lower lip, and back of the
hands.

 In blacks, the lesions may appear as hyperpigmented nodules and occur more frequently on non–sunexposed
areas.

 Treatment measures are aimed at the removal of all cancerous tissue using methods such as electrosurgery,
excision surgery, chemosurgery, or radiation therapy.
Squamous cell carcinoma of the chin.
 Further reading
1. Contrast and compare the following lesions: macule, patch, papule, plaque, nodule, pustule, blister, callus, and corn.
2. Describe the three types of ultraviolet radiation and relate them to sunburn, aging skin changes, and the development of
skin cancer.
3. Relate the behavior of fungi to the production of superficial skin lesions associated with tinea or ringworm.
4. State the cause and describe the appearance of impetigo and ecthyma.
5. Compare the viral causes, manifestations, and treatments of verrucae, herpes simplex, and herpes zoster lesions.
6. Describe the pathogenesis of acne vulgaris and relate it to measures used in treating the disorder.
7. Describe the differences and similarities between erythema multiforme minor, Stevens-Johnson syndrome, and toxic
epidermal necrolysis.
8. Define the term papulosquamous and use the term to describe the lesions associated with psoriasis, pityriasis rosea, and
lichen planus.
9. Describe the origin of nevi and state their relationship to skin cancers.
10. Compare the appearance and outcome of basal cell carcinoma, squamous cell carcinoma, and malignant melanoma.