MEDICAL SURGERY: The Integumentary System

Skin is the largest body organ, constituting 15% to 20 % of the body weight and consisting of
three primary layers

Figure 1-4 General structure of the skin and its relationship to the superficial fascia. SNELL,
R.S. Clinical anatomy by regions (8th ed.). Lippincott Williams & Wilkins
SIGNS AND SYMPTOMS OF SKIN DISEASE

• Pruritus (itching)
• Urticaria (hives): appearance of smooth, slightly elevated patches (wheals); redder or
paler than the surrounding skin often accompanied by severe itching.
• Rash: generalized term for an eruption on the skin
• Blisters (vesicle or bulla): fluid-containing elevated lesions of the skin with clear watery
or bloody contents
• Xeroderma: mild form of ichthyosis/excessive dryness of the skin; characterized by dry,
rough, discolored skin with the formation of scaly desquamation (shedding of the
epithelium in small sheets)
• Other symptoms
o unusual spots
o moles
o cysts
o fibromas
o nodules
o swelling
o changes in nail beds

ATOPIC DERMATITIS

Definition and Incidence.

• most common type of eczema
• present during the first year of life and affecting more than 10% o f children.
• word atopic (from atopy) refers to a group of three associated allergic disorders:
asthma, allergic rhinitis (hay fever), and AD.
Etiologic and Risk Factors and Pathogenesis
• exact cause of AD is unknown
Pathogenesis
• often associated with increased levels of serum IgE and with sensitization to food
allergens
• Some foods may be responsible for exacerbations of skin inflammation, but their
pathogenic role must be clinically assessed before an avoidance diet is recommended
• Xerosis (abnormal dryness) associated with AD is usually worse during periods of low
humidity and over the winter months in northern latitudes
• Compared with normal skin, the dry skin of AD has a reduced water-binding capacity, a
higher transepidermal water loss, and a decreased water content .
Clinical Manifestations
• AD begins in many people during infancy in the form of a red, oozing, crusting rash
classified as acute dermatitis
• As the child grows, the chronic form of dermatitis results in skin that is dry, thickened,
and brownish-grey in color (lichenified)
 • The rash tends to become localized to the large folds of the extremities as the person
become s older.
• found mainly on flexor surfaces (eg elbows and knees, neck, sides of the face, eyelids,
and the backs of hands and feet)
• Xerosis and pruritus are the major symptoms of AD
Medical Management
• goal of medical therapy
o Break the inflammatory cycle that causes excess drying, cracking, itching, and
scratching.
o Personal hygiene, moisturizing the skin, avoidance of irritants, topical
pharmacology, and systemic medications (e.g., antibiotics, antihistamines, and
rarely, systemic corticosteroids) are treatment techniques currently available.

infantile atopic dermatitis

CONTACT DERMATITIS
Etiologic Factors, Incidence, and Pathogenesis
• Can be an acute or chronic skin inflammation caused by exposure to a chemical,
mechanical, physical, or biologic agent.
• one of the most common environmental skin diseases occurring at any age
• As people age, they may develop delayed cell-mediated hypersensitivity to a variety of
substances that come in contact with the skin.
• Common sensitizers
o include nickel (found in jewelry and many common foods)
o chromates (used in tanning leathers)
o wool fats (particularly lanolin found in moisturizers and skin creams)
o rubber additives
o topical antibiotics (typically neomycin and bacitracin)
o topical anesthetics, such as benzocaine or lidocaine
Clinical Manifestations
• Intense pruritus (itching) , erythema (redness) , and edema of the skin occur 1 to 2 days
after exposure in previously sensitized persons
• begin at the site of exposure but then extend to more distant sites
• may progress to vesiculation, oozing (watery discharges), crusting, and scaling
 • If these symptoms persist, the skin become s thickened, with prominent skin markings
and pigmentation changes
Medical Management
• If contact dermatitis is suspected, the client should be referred to a physician.
• Diagnosis
o Detailed history, careful examination
o Patch testing to identify causative agent
• Treatment
o Primary treatment
 Removal of offending agent
o Treatment of the skin is secondary
 Avoid contact with strong soaps, detergents, solvents, bleaches, and other
strong chemicals.
 involved skin should be lubricated frequently with emollients
 Topical anesthetics or steroids (topical or sometimes systemic) or both
may be prescribed.

Primary contact dermatitis

ECZEMA AND DERMATITIS

• Eczema or dermatitis is a superficial inflammation of the skin caused by irritant
exposure, allergic sensitization (delayed hypersensitivity), or genetically determined
idiopathic factors.
• three primary stages
o Acute dermatitis
o Subacute dermatitis
o Chronic dermatitis
• Incidence and Etiologic Factors
o a commo n skin disorder in older people
 o May be caused by hypoproteinemia, venous insufficiency, allergens, irritants, or
underlying malignancy, such as leukemia or lymphoma.
• Medical Management
o Avoidance of irritants; cutaneous hydration; topical glucocorticoids; treatment of
infected lesions [often with Staphylococcus aureus (SA)—consider community-
acquired methicillin-resistant strains (CA-MRSA)]. Systemic glucocorticoids only
for severe exacerbations unresponsive to topical conservative therapy.
IMPETIGO
• Definition and Overview
o Superficial skin infection commonly caused by staphylococci or streptococci.
o most commonly found in infants, young children 2 to 5 years of age, and older
people.
o occurs as a secondary infection in conditions characterized by a cutaneous
barrier broken to microbes, such as eczema or herpes zoster excoriations
o Predisposing factors
 Close contact in schools,
 overcrowded living quarters,
 poor skin hygiene,
 anemia,
 malnutrition,
 minor skin trauma.
• Clinical Manifestations
o Small macules (flat spots) rapidly develop into vesicles (small blisters) that
become pustular (pus-filled). When the vesicle breaks, a thick yellow crust forms
from the exudate, causing pain, sur-rounding erythema, regional adenitis
(inflammation of gland), cellulitis (inflammation of tissue), and itching
• Medical Management
o Oral antibiotics
o Rarely, extensive lesions require systemic antibiotics to reduce the risk of
glomerulonephritis and to prevent this contagious condition from spreading
CELLULITIS
• Definition and Overview
o an acute inflammatory condition of the skin, is characterized by localized pain,
erythema, swelling, and heat.
• Etiology
o In adults - Streptococcus pyogenes or Staphylococcus
o In children - Haemophilus influenzae type B
o Other Causes
 Escherichia coli
 Pseudomonas, or fungi
• Predispoding Factors
o presence of edema or other cutaneous inflammation or wounds (e.g.,tinea,
eczema, burns, trauma)
 o Venous insufficiency or stasis
o Thrombophlebitis
o surgery,
o substance abuse
o immunocompromise (e.g., HIV infection, chemotherapy, auto-immune diseases,
chronic use of immunosuppressants)
o lymphedema
• Clinical manifestations
o erythematous,
o edematous,
o tender
o sometimes nodular
• Diagnosis
o Gram’s staining and culture - If there is a wound or portal of entry,
o aspiration or biopsy - If both a wound and a portal of entry are lacking
• Medical Management
o Primary Treatment:
 Nafcillin or oxacillin, 2 g IV q4–6h
o Alternative Treatment:
 Cefazolin, 1–2 g q8h
 Ampicillin/sulbactam, 1.5–3.0 g IV q6h
 Erythromycin, 0.5 – 1.0 g IV q6h
 Clindamycin, 600 – 900 mg IV q8h

HERPES ZOSTER
• Definition and Overview
o Eruption of grouped vesicles on an erythematous base usually limited to a single
dermatome (“shingles”); disseminated lesions can also occur, especially in
immunocompromised pts.
o represents a reactivation of Varicella-Zoster Virus (VZV) from dorsal root ganglia.
• Etiology
o peak incidence occurs between ages 50 and 70 years.
o Dermatomes T3 to L3 are most frequently involved.
o Dermatomal pain may precede lesions by 48–72 h
o usual duration of disease is 7–10 days but it may take as long as 2–4 weeks for
the skin to return to normal.
• Pathogenesis.
o results from reactivation of varicella virus that has been dormant in the cerebral
ganglia (extramedullary ganglia of the cranial nerves) or the ganglia of posterior
nerve roots from a previous episode of chickenpox.
o The immunologic mechanism that controls latency of VZV is not well understood.
One explanation is that the virus multiplies as it is reactivated and that it is
neutralized by antibodies remaining from the initial infection. If effective
 antibodies are not present, the virus continues to multiply in the ganglia,
destroying the host neuron and spreading down the sensory nerves to the skin.
o Factors associated with recurrent disease include aging, immunosuppression,
intrauterine exposure to VZV, and varicella at a young age (less than 18 months)
• Clinical manifestations
o Early symptoms of pain and tingling along the affected spinal or cranial nerve
dermatome are usually accompanied by fever, chills, malaise, and GI
disturbances. One to three days later red papules are seen along a dermatome
o lesions most commonly spread unilaterally around the thorax or vertically over
the arms or legs
• Diagnosis
o Isolation of VZV in tissue culture, detection of VZV DNA by PCR, or direct
immunofluorescent staining of cells from the lesion base
o Seroconversion or a fourfold or greater rise in antibody titer between
convalescent and acute-phase serum specimens.
o Frequently used techniques.
 fluorescent antibody to membrane antigen (FAMA) test
 adherence hemagglutination test
 enzyme-linked immunosorbent assay (ELISA)
• Medical Management
o Primary Treatment:
 Acyclovir, 800 mg PO 5 times daily for 7–10 days
o Alternative Treatment:
 Famciclovir, 500 mg PO tid for 7–10 days
 Valacyclovir, 1000 mg PO tid for 7 days

Herpes Zoster/shingles

WARTS (VERRUCAE)
• Definition and Overview
o Cutaneous neoplasms caused by human papilloma viruses (HPVs).
o Typically dome-shaped lesions with irregular filamentous surface.
 o Transmission is probably through direct contact , but autoinoculation is possible.
• Epidemiology
o incidence of warts is highest in children and young adults, but warts can occur at
any age.
• Clinical manifestations
o depend on the type of wart and its location.
• Classifications
o 50 different varieties of these viruses depending on their location on the skin
o most common wart (verruca vulgaris) is referred to as such and appears as a
rough, elevated, round surface most frequently on the extremities, especially the
hands and fingers.
• Pathogenesis
o verrucae are caused by HPV. Some members of the HPV family are associated
with preneoplastic and invasive cancers of the anogenital region. However, in
contrast to HPV-associated carcinomas, most warts are caused by distinct low-
risk HPV types that lack potential for causing malignant transformation.
Mechanistically, the virus subverts cell cycle control to allow increased
proliferation of epithelial cells and production of new virus. Normal immune
response usually limits the growth of these tumors, but immunodeficiency can be
associated with increased numbers and size of verrucae.

• Medical Management
o Cryotherapy with liquid nitrogen, keratinolytic agents (salicylic acid).
o For genital warts, application of podophyllin solution is effective but can be
associated with marked local reactions
o topical imiquimod has also been used.
Verruca vulgaris. A, Lesions are formed by symmetric zones of papillary epidermal
proliferation that often radiate symmetrically like the points of a crown (top). Nuclear pallor,
prominent keratohyalin granules, and related cytopathic changes of human papillomavirus are
confirmed at higher magnification (bottom). B, Multiple papules with rough, pebble-like
surfaces at infection sites.

BASAL CELL CARCINOMA

• Definition and Overview
o Most common form of skin cancer; most frequently on sun-exposed skin, esp.
face.
o Basal cell carcinoma is a slow-growing surface epithelial skin tumor originating
from undifferentiated basal cells contained in the epidermis.
o This type of carcinoma rarely metastasizes beyond the skin and does not invade
blood or lymph vessels but can cause significant local destruction.
• Epidemiology
o Until recently, this tumor rarely appeared before age 40 years and was more
prevalent in blond, fair-skinned males.
o In the age group under 30 years, more women than men develop skin cancer
associated with the use of indoor tanning booths with concentrated doses of UV
radiation
o most common malignant tumor affecting Caucasians, with a reported 100,000
new cases each year
o African Americans and Asians are rarely affected
• Etiology
o Predisposing Factors
 Fair complexion,
 chronic UV exposure,
 exposure to inorganic arsenic (i.e., Fowler’s solution or insecticides such
as Paris green),
 exposure to ionizing radiation.
o Prolonged sun exposure and intermittent sun exposure are the most common
causes of basal cell carcinoma; but immunosuppression genetic predisposition,
and rarely, the site of vaccinations are other possible causes
o Immunosuppressed organ transplant recipients are more likely to develop
squamous cell carcinoma, whereas HIV-infected adults are far more likely to
have basal cell carcinoma.
o Seen most frequently in geographic regions with intense sunlight in people with
outdoor occupations and on those areas most exposed, the face and neck.
o Dark-skinned people are rarely affected because their basal cells contain the
pigment melanin, a protective factor against sun exposure.
o Anyone who has had one basal cell carcinoma is at increased risk of developing
others. Recurrences of previously treated lesions are possible, usually within the
first 2 years after initial treatment.
• Types
 o Five General types
 noduloulcerative (most common),
 superficial (mimics eczema),
 pigmented (may be mistaken for melanoma),
 morpheaform (plaquelike lesion with telangiectasia—with keratotic is most
aggressive),
 keratotic (basosquamous carcinoma)
• Clinical Appearance
o Classically a pearly, translucent, smooth papule with rolled
• Pathogenesis.
o Basal cell carcinoma has been associated with dysregulation of the sonic
hedgehog, or PTCH, pathway. Inherited defects in the PTCH gene with
subsequent loss of heterozygosity in the numerous individual tumor foci cause
the familial basal cell carcinoma syndrome, Gorlin syndrome. Thus, PTCH
functions as a classic tumor suppressor. Since the PTCH pathway is also
important in embryonic development, subtle developmental anomalies are also
noted in these individuals. Some component of the PTCH pathway is also
mutated in the great majority of sporadic basal cell carcinomas; mutations in p53
are also common.
• Medical Management
o Local removal with electrodesiccation and curettage, excision, cryosurgery, or
radiation therapy
Basal cell carcinoma. A, The lesion is formed by multiple nodules of basaloid cells infiltrating a
fibrotic stroma. B, The cells have scant cytoplasm, small hyperchromatic nuclei, and a
peripheral palisade with clefting from the stroma. Note the similarity of these cells to the basal
cells of normal epithelium. C, This lesion is a prototypical pearly, smooth-surfaced papule with
associated telangiectatic vessels.

SQUAMOUS CELL CARCINOMA

• Definition and Overview

o Squamous cell carcinoma is the second most commo n skin cancer in whites,
usually arising in sun-damaged skin, such as the rim of the ear, the face, the lips
and mouth, and the dorsa of the hands
o a tumor of the epidermal keratinocytes and rarely occurs in dark-skinned people
• Types
o in situ (confined to the site of origin)
 usually confined to the epidermis but may extend into the dermis
 Common premalignant skin lesions associated with in situ carcinomas
• actinic keratosis
• Bowen's disease
o invasive (infiltrate surrounding tissue).
 can arise from premalignant lesions of the skin, including sun-damaged
skin, actinic dermatitis, scars, whitish discolored areas (leukoplakia),
radiation-induced keratosis, tar and oil keratosis, and chronic ulcers and
sinuses.
• Epidemiology
o peak incidence at 60 years of age and affects men more than women
• Etiology
o cumulative overexposure to UV radiation (e.g., outdoor employment or residence
in a warm, sunny climate),
o burns,
o presence of premalignant lesions such as actinic keratosis or Bowen's disease,
o radiation therapy,
o ingestion of herbicides containing arsenic,
o chronic skin irritation and inflammation,
o exposure to local carcinogens (tar, oil),
o hereditary disease such as xeroderma pigmentosum and albinism.
• Pathogenesis
o The most common exogenous cause of cutaneous squamous cell carcinoma is
UV light exposure, with subsequent unrepaired DNA.Individuals who are
immunosuppressed as a result of chemotherapy or organ transplantation, or who
have xeroderma pigmentosum, are at increased risk. In addition to inducing
mutations, UV light (UVB in particular) may have a transient immunosuppressive
effect on skin by impairing antigen presentation by Langerhans cells. This may
contribute to tumorigenesis by weakening immunosurveillance.
 Immunosuppressed patients, particularly organ transplant recipients, are likely to
be associated with high-risk HPV types. p53 mutations with associated UV
mutation signatures are common, as are activating mutations in RAS. As with
squamous cell carcinomas at other sites, those in the skin may be preceded by
in situ lesions.
• Medical Management
o Local excision and Moh’s micrographic surgery are most common; radiation
therapy in selected cases. Metastatic disease may be treated with radiation
therapy or with combination biologic therapy; 13-cis-retinoic acid 1 mg/d PO plus
IFN 3 million units/d SC.
Invasive squamous cell carcinoma. A, The carcinoma invades the dermis as irregular
projections of atypical squamous epithelium; this particular case is acantholytic (i.e., the
squamous cells are poorly cohesive). B, A nodular and hyperkeratotic lesion occurring on the
ear, unfortunately with early metastasis to a prominent postauricular lymph node (arrow).

LICHEN PLANUS
• Definition and Overview
o Disorder of unknown cause; can follow administration of certain drugs and in
chronic graft-versus-host disease; lesions are pruritic, polygonal, flat-topped, and
violaceous. Course is variable, but most pts have spontaneous remissions 6–24
months after onset of disease.
o Pruritic, purple, polygonal, planar papules, and plaques" are the tongue-twisting
traditional "p's" of this disorder of skin and mucosa. Lichen planus is self-limited
and usually resolves spontaneously 1 to 2 years after onset. Oral lesions may
persist for years.
• Pathogenesis
o The pathogenesis is not known. Expression of altered antigens at the level of the
basal cell layer and the dermoepidermal junction may elicit a CD8+ Tcell-
mediated cytotoxic immune response. The altered antigens could be due to viral
infection or perhaps drug treatment.
• Medical Management
o Topical glucocorticoids.
 Lichen planus. A, There is a band of lymphocytes along the dermoepidermal junction, and
the rete ridges have acquired a pointed, or "sawtooth," architecture. This is also an
interface dermatitis, but the infiltrate is more bandlike (lichenoid) than is seen in erythema
multiforme, and hyperkeratosis and hypergranulosis are definite signs of chronicity. B,
Multiple flat-topped papules with white, lacey or netlike markings (Wickham striae) are
characteristic.

PSORIASIS
• Definition and Overview
o Psoriasis is a common chronic inflammatory dermatosis affecting 1% to 2% of
people in the United States. In rare cases it is associated with arthritis, myopathy,
enteropathy, and spondylitic heart disease.
• Clinical Features
o Psoriasis most frequently affects the skin of the elbows, knees, scalp,
lumbosacral areas, intergluteal cleft, and glans penis. The most typical lesion is a
well-demarcated, pink to salmon-colored plaque covered by loosely adherent
 silver-white scale. Nail changes occur in 30% of cases of psoriasis and consist of
yellow-brown discoloration, with pitting, thickening, and crumbling and separation
of the nail plate from the underlying bed (onycholysis). In most cases, psoriasis is
limited in distribution, but it can be widespread and severe on occasion. There
are a variety of clinical subtypes of this disease, defined by the severity and
pattern of involvement.
• Pathogenesis
o Psoriasis is an immunologic disease with contributions from genetic susceptibility
and environmental factors. It is not known if the inciting antigens are self or
environmental. Sensitized populations of T cells enter the skin, including dermal
CD4+ TH1 cells and CD8+ T cells that accumulate in the epidermis. T cells
homing to the skin secrete cytokines and growth factors that induce keratinocyte
hyper-proliferation, resulting in the characteristic lesions. Psoriatic lesions can be
induced in susceptible individuals by local trauma, a process known as the
Koebner phenomenon. The trauma may induce a local inflammatory response
that promotes lesion development. While reserved for use in severe psoriatic
arthritis, recent therapeutics exploit advances in our understanding of T-cell
biology. Various clinically useful agents block (1) T-cell activation and
proliferation; (2) T cell trafficking and keratinocyte interaction with T cells; and (3)
binding of tumor necrosis factor to its receptor thus inhibiting T cell functions.
• Medical Management
o Maintain cutaneous hydration; topical glucocorticoids; topical vitamin D analogue
(calcipotriol) and retinoid (tazarotene); UV light (PUVA when UV used in
combination with psoralens); for severe disease methotrexate or cyclosporine;
acitretin can also be used but is teratogenic. Efalizumab (humanized monoclonal
antibody directed against CD11a) or alefacept (dimeric fusion protein: LFA-3/Fc
human IgG1) can be considered for chronic, moderate to severe plaque
psoriasis. Etanercept (dimeric fusion protein: TNF receptor/Fc human IgG1) is
approved for psoriatic arthritis and psoriasis.
Psoriasis. A, Established plaques show marked epidermal hyperplasia with uniform
downward extension of rete ridges (psoriasiform hyperplasia) as well as prominent
parakeratotic scale focally infiltrated by neutrophils. Superficial fungal infections can show
a strikingly similar epidermal pattern, and thus infection should be excluded using special
stains. B, Chronic plaques of psoriasis show silvery-white scale on the surface of
erythematous plaques.

ERYTHEMA MULTIFORME
• Definition and Overview
o A reaction pattern of skin consisting of a variety of lesions but most commonly
erythematous papules and bullae. “Target” or “iris” lesion is characteristic and
consists of concentric circles of erythema and normal flesh-colored skin, often
with a central vesicle or bulla.
• Clinical Features
o Erythema multiforme manifests with a broad range of severity. The forms
associated with infection, most often herpesvirus, are sometimes termed
erythema multiforme minor because of their less severe clinical presentation.
More severe forms of this disease are termed erythema multiforme major,
Stevens-Johnson syndrome, and toxic epidermal necrolysis. These latter
 clinical forms of this disease continuum can be life-threatening because they
can cause sloughing of large portions of the epidermis and loss of moisture
and infectious barriers. They are most often seen as idiopathic reactions to
drugs such as antibiotics or nonsteroidal anti-inflammatory agents.
• Pathogenesis
o The lesions of erythema multiforme result from the action of CLA positive, skin-homing
cytotoxic T cells that are concentrated in the central portion of the lesions, while CD4+
helper and Langerhan cells are more prominent in the raised, erythematous periphery.
The cytotoxic cells directed against an inciting drug or microbe presumably respond to
cross-reactive antigens of the basal cell layer of skin and mucosae and damage these
tissues.
• Medical Management
o Provocative agent should be sought and eliminated if drug-related. In mild cases
limited to skin, only symptomatic treatment is needed (antihistamines, NSAID).
For Stevens-Johnson, systemic glucocorticoids have been used, but are
controversial; prevention of secondary infection and maintenance of nutrition and
fluid/electrolyte balance are critical.
Erythema multiforme. A, Lesions show a central zone of dusky pink-gray discoloration that
correlates with epidermal necrosis or early blister formation, surrounded by a pink-red rim,
producing the characteristic target-like appearance of erythema multiforme minor. B,
Early lesions show alignment of lymphocytes along the dermoepidermal junction with
injury to basal epidermal cells as a result of the cytotoxic assault. This is an interface
dermatitis (there is destruction of cells at the epidermal-dermal interface), but it lacks the
chronic features seen in lichen planus, discussed below.

Sources:
Pathology implication for the Physical Therapist, 3rd edition
Harrison’s Manual of Medicine, 17th edition
Robbin’s Basic Pathology, 8th edition