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Tinea barbae. This involves the beard area of men; the hair shafts are infected. The lesions are inammatory papules or pustular folliculitis.
Tinea corporis—ringworm.
ate, slowly spreading with a raised scaling border and central clearing. Large
plaques may form.
Tinea cruris—Jock itch.
mal thighs, and pubis. The tan or reddish scaling lesion is well demarcated
and may be asymptomatic.
Tinea versicolor—pityriasis versicolor. Infection with Pityrosporum ovale
(Malassezia furfur) causes a very supercial mildly scaling rash, usually on
the trunk or arms. Some patients have hypopigmented scaling macules and
patches. Hyperpigmented scaling macules and patches occur in others. The
lesions are asymptomatic but cosmetically bothersome.
Candidiasis. Skin infection is common in moist areas, especially the mouth
(thrush), vagina and vulva, under pendulous breasts, and on the perineum
and groin of incontinent patients. Lesions are raised, intensely erythematous,
and coalesce into plaques with smaller satellite lesions. C. albicans is the most
commonly identied species.
Sporotrichosis. This is a slowly progressive infection with Sporothrix
schenckii, a soil fungus implanted under the skin by trauma or abrasion.
An inoculation site ulcer is followed by nodular cutaneous or subcutaneous
lesions that suppurate, ulcerate, and drain through multiple sinuses. Regional lymphadenopathy is expected and dissemination to viscera or bone can
occur.
Deep fungal infections.
sue infections can cause skin disease. The lesions may be papules, nodules,
ulcers, or conuent masses. Travel history and places of residence are critical to hypothesizing the most likely organism. Reactivation of latent infection shortly after initiating anti-TNF therapy for rheumatic diseases is not
uncommon. Biopsy and culture are required for diagnosis. Cryptococcosis,
histoplasmosis, blastomycosis, aspergillosis, coccidioidomycosis are most
commonly encountered.
The erythematous lesions are circular or arcu-
This is an often-chronic infection in the groin, proxi-
Fungi most commonly associated with deep tis-
Bullous Skin Diseases.
Hereditary epidermolysis bullosa. These are inherited disorders of epidermal cohesion resulting in blistering following minor trauma. Large supercial blisters develop and break leaving shallow erosions. Severity varies with
the specic genetic defect and depth of blistering.
Pemphigus vulgaris.
leads to loss of epidermal cell adhesion. The rst lesions are often in the oral
mucosa, cutaneous bullae appearing later. Vesicles and accid bullae rupture
easily leaking serous uid. Slight skin shear causes blistering and a subsequent erosion (Nikolsky sign). Paraneoplastic pemphigus has histologic ndings
of pemphigus and pemphigoid.
Acquired IgG antibodies to epidermal desmosomes
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Bullous pemphigoid. Antibodies against hemidesmosomes in the basal
layer of the epidermis activate complement leading to separation of the basal
layer from the dermis. The entire body can be affected but predilection for
lower legs, axillae, abdomen, legs, and groin exists. Mucous membranes can
be involved. Early lesions may be erythematous papules or appear urticarial.
Tense bullae develop that may be serous or hemorrhagic; they rupture or heal
by drying and crusting.
Dermatitis herpetiformis.
enteropathy). The pathophysiology is uncertain. Symmetrically distributed
vesicles, papules, excoriations, and/or urticaria appear on the extensor surfaces of the arms and trunk. Pruritus is severe. Symptoms may precede the
skin lesions by several hours.
topathologic appearance but is immunopathologically distinct.
Bullous diabetic dermopathy.
appearing without trauma on the lateral aspects of the ngers in patients with
poorly controlled diabetes. The blisters are tense and nontender.
Skin Manifestations of Systemic Diseases.
Paroxysmal ushing, blanching, and cyanosis—carcinoid syndrome. Circulating serotonin causes paroxysms of cutaneous erythema intermixed with
areas of pallor and cyanosis. A given area of skin may exhibit all three colors
in rapid succession. Though most pronounced on the face and neck, it may
extend to the chest and abdomen.
Red burning extremities—erythromelalgia.
or acquired syndrome associated with drugs (e.g., nifedipine, bromocriptine)
or myeloproliferative diseases; it may antedate polycythemia vera or essential thrombocytosis by years.
the extremities, especially the feet and hands, aggravated by dependency.
Ambient temperatures above 31°C (87.8°F) usually initiate the attacks; they
are relieved by cold exposure. During a paroxysm, the limbs are red, warm,
swollen, and painful. The arterial pulses are present and normal.
Similar lesions occur with atherosclerosis, hypertension, frostbite, immersion foot, trench foot, peripheral neuritis, disseminated sclerosis, hemiplegia,
chronic heavy metal poisoning and gout.
This is common in celiac disease (gluten-sensitive
DDX: Linear IgA dermatosis has a similar his-
The lesions are sterile noninamed bullae
This is an autosomal dominant
The patient complains of painful erythema on
DDX:
Erythema multiforme. Target lesions appear on the palms and soles, feet,
forearms, and face; mucous membranes may be involved. The lesions evolve
over days and may be painful or pruritic. They may progress to bullae
(erythema multiforme bullosa).
pneumonia drug reactions (sulfonamides, anticonvulsants, penicillin), idio-
DDX: Psoriasis, secondary syphilis, urticaria.
pathic.
Panniculitis. Sterile inammation of subcutaneous fat takes two forms:
lobular, in which the fat lobule is primarily involved, and septal, in which
the vascular and brous septa separating lobules is involved. Patients pres-
ent with tender erythematous skin and subcutaneous swellings, usually over
areas of abundant subcutaneous fat. The epidermis is intact, and the lesions
are not uctuant. DDX: Angioedema is similar, but lesions are transient and
Inciting causes: Herpes simplex, mycoplasma
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not restricted to adipose tissue. Pyomyositis looks similar but lesions are
within muscle rather than fat.
CLINICAL OCCURRENCE: Septal Panniculitis: Erythema nodosum, eosin-
ophilic fasciitis, eosinophilia myalgia syndrome, scleroderma (localized and
diffuse), polyarteritis nodosa; Lobular Panniculitis: Trauma, cold injury, steroid induced, idiopathic lobular panniculitis, acinar pancreatic carcinoma,
SLE, sarcoidosis, vasculitis.
Erythema nodosum.
ous nodules appear on the anterior shins. They are violaceous and slightly
warm.
CLINICAL OCCURRENCE: Infections: Mycobacteria (tuberculosis, leprosy),
bacteria (cat-scratch disease, leptospirosis, tularemia, salmonellosis, yersiniosis), deep fungal infections, viruses (Epstein–Barr virus, lymphogranuloma
venereum, hepatitis B); Noninfectious: Pregnancy, drug reactions, inammatory bowel disease, sarcoidosis, paraneoplastic, Sweet syndrome, Behçet
syndrome.
Adiposis dolorosa (Dercum disease). In this rare form of obesity, symmetrical
adipose tissue masses on the trunk and limbs are painful and tender. If inammation is present, consider panniculitis [Campen RB, Sang CN, Duncan
LM. Case 25–2006: a 41-year-old woman with painful subcutaneous nodules.
N Engl J Med. 2006;355:714–722].
Serum sickness. See Serum sickness, Chapter 8, page 363.
Scleroderma.
tracted limiting movement of ngers without joint swelling or ankylosis. The
distribution and the pattern of organ involvement identies each syndrome.
CLINICAL OCCURRENCE: Diffuse cutaneous scleroderma, limited cutane-
ous scleroderma (CREST syndrome), morphea, toxic oil syndrome, arthralgia–myalgia syndrome, graft-vs-host disease, polyvinyl chloride exposure.
Diffuse cutaneous scleroderma. Tight shiny skin on the distal extremities and
face progresses to involve the proximal extremities and, to a lesser extent,
the trunk. Raynaud phenomena is common. Cutaneous sclerosis leads to
joint immobility, limited mouth opening, and poorly healing ulcers following
trauma. Dysphagia, hypertension, acute renal failure, and, less commonly,
pulmonary brosis complicates the course.
EN is a localized panniculitis. Tender subcutane-
The skin and underlying tissues become brotic and con-
Limited cutaneous scleroderma. The skin lesions are less extensive and favor the trunk. Severe pulmonary involvement with refractory pulmonary
hypertension and respiratory failure are common, but kidney disease is less
common. (CREST syndrome. CREST stands for the rst letters of its cardinal
features: Calcinosis cutis, Raynaud phenomenon, Esophageal dysfunction,
Sclerodactyly, and Telangiectasia.)
Morphea. Localized erythema and induration that can occur anywhere on
the body and become sclerotic plaques. They may be linear on the extremities.
Women are more affected than men. Visceral sclerosis does not occur. This can
be confused with lipodermatosclerosis from chronic stasis dermatitis.
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Nephrogenic systemic brosis (nephrogenic brosing dermopathy). Exposure to
gadolinium contrast for MRI imaging in the setting of chronic kidney disease is
the cause. Patients on dialysis for end-stage renal disease develop diffuse cuta-
neous and subcutaneous brosis most prominent on the legs. Systemic involvement is common with brosis of muscles, including the myocardium, and lung.
The course is progressive with loss of joint mobility. The face is spared.
Scleromyxedema.
skin is thickened, indurated, tight, and thrown into prominent folds. There is
decreased mouth and joint mobility.
Dermatomyositis.
suppurative inammation of skin and striated muscle; the cause is unknown.
Malaise, weight loss, muscle stiffness, and dysphagia are presenting symptoms; pruritus is especially characteristic. Classic signs are heliotrope discoloration of upper lids and nasal bridge and at-topped violaceous papules
(Gottron papules) over the dorsal interphalangeal joints. Erythematous rashes
or exfoliative dermatitis may be seen. Proximal muscle weakness and stiffness indicate muscle involvement. Tendon friction rubs, lymphadenopathy,
and splenomegaly may be found. Dermatomyositis can be a paraneoplastic
syndrome. Amyopathic dermatomyositis presents with skin signs and symptoms without proximal muscle weakness.
Lupus erythematosus. This group of inammatory disorders share similar
autoimmune pathophysiology.
Acute cutaneous lupus.
rash, precipitated by sunlight exposure; erythematous scaling papules and
plaques on the extensor surface of the ngers sparing the interphalangeal
joints; urticaria with purpura; and, hypersensitivity vasculitis.
Subacute cutaneous lupus. The skin lesions are psoriasiform plaques or annular erythematous lesions on the trunk, shoulders, extensor surfaces of the
arms, or other sun-exposed areas. Systemic involvement is uncommon.
Chronic cutaneous lupus—discoid lupus. Sharply dened plaques with adherent scale gradually expand in circles or ovals with central atrophy. The
lesions may occur on the face, scalp, forearms, and phalanges. The trunk is
less commonly involved. Follicular plugging is characteristic. DDX: Psoriasis,
lichen planus, conuent actinic keratoses, and polymorphic light eruptions
may be confused.
Usually associated with a monoclonal gammopathy, the
There is atrophy, edema, or brosis of the skin and non-
Several lesions occur: an acute malar or generalized
Systemic lupus erythematosus. See Chapter 13, page 586. This systemic dis-
ease has prominent, life-threatening involvement of other organs, including
the brain and kidneys. The skin ndings are those of acute cutaneous lupus,
subacute cutaneous lupus, and chronic cutaneous lupus, among other nonspecic skin manfestations (urticaria, vasculitis)
Pyoderma gangrenosum. Painful skin nodules progressing to necrotic ulcers
with undermined, violaceous edges most commonly on the legs, buttocks,
and abdomen; the face may be involved. The wound base does not granulate,
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the ulcers healing with thin scars. DDX: Ecthyma gangrenosum, necrotic softtissue infections, granulomatous angiitis, stasis ulcers.
CLINICAL OCCURRENCE: Most often idiopathic; when an association is
identied, inammatory bowel disease (ulcerative colitis, Crohn
most common. Other associations are paraproteinemia (myeloma,
gammopathy of unknown signicance [MGUS]), leukemia, rheumatologic
diseases, and chronic active hepatitis.
disease) is
monoclonal
Sweet syndrome.
and nodules most commonly on the arms and face rapidly coalesce forming
large plaques inltrated with neutrophils. Lesions heal with minimal scarring. It may be chronic and recurrent.
CLINICAL OCCURRENCE: Hematologic malignancies, myelodyspla-
sia, MGUS, Granulocyte-macrophage colony-stimulating factor (GMCSF)
administration, Yersinia infections, idiopathic.
Porphyrias.
nolevulinic acid to heme result in tissue accumulation of specic porphyrins.
Photosensitivity is the hallmark of cutaneous porphyrias. Severe mutilating
photosensitivity and hypertrichosis occur in hereditary erythropoietic protopor-
phyria. Porphyria cutanea tarda is acquired or inherited. The acquired form is
associated with liver disease (cirrhosis, hepatitis-C, hemochromatosis) and
chemical exposures. It presents as burning erythematous vesicles or blisters
on sun-exposed areas, often the backs of the hands or wrists, which heal with
atrophic hypopigmented scars. Variegate porphyria is inherited. The skin signs
are like porphyria cutanea tarda, but systemic disease is resembles acute
intermittent porphyria. Acute intermittent porphyria presents with abdominal
pain, neuropathy, and altered mental status without skin lesions.
Paraneoplastic skin disease.
known or occult malignant neoplasms. Consider an underlying cancer in association with the following conditions: neutrophilic dermatosis (Sweet syndrome,
pyoderma gangrenosum); reactive erythemas (erythroderma, exfoliative dermatitis); vascular dermatoses (vasculitis, erythromelagia); papulosquamous
disorders (ichthyosis); and vesiculobulous diseases (pemphigus, pemphigoid).
Sarcoidosis. Granulomatous skin lesions present as purple or brown asymptomatic papules or plaques on the torso and extremities; nodules may be
more common on the face and eyelids. They do not completely blanch with
pressure. See Chapter 8, page 346.
This is a sterile neutrophilic dermatosis. Painful papules
Inherited or acquired enzyme defects in the metabolism of ami-
Several skin diseases are seen in association with
Diabetes.
lipoidica is most often seen in diabetics. It begins as a brownish-red papule on
the shin that enlarges to a plaque, which spreads with a raised rolled border
surrounding a depressed atrophic center commonly with a yellowish coloration. Lesions may be single or multiple and merge by expansion. Diabetic
hand syndrome (diabetic cheiropathy) is thickening of subcutaneous tissue in
the palm and ngers limiting nger extension, demonstrated by the prayer
sign. Diabetic dermopathy is a chronic condition with crops of erythematous
papules appearing on the shins and forearms that heal with atrophic scars.
Diabetic bullous dermopathy presents with painless bland bullae often on the
Diabetes is associated with a variety of skin lesions. Necrobiosis
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sides of the ngers; it is associated with poor diabetes control. Mucocutaneous
candidiasis is much more common in diabetics with poor blood sugar control.
Calciphylaxis.
It is believed to be an ischemic injury resulting from calcium
deposition in the small arterioles of patients with advanced renal insufci
ency and secondary hyperparathyroidism with abnormal calcium-phosphate
metabolism.
This uncommon disorder presents with painful indurated
plaques with vascular mottling or retiform purpura which progress to infarction and ulceration. The lesions gradually enlarge circumferentially. It has
high morbidity and mortality.
Pseudoxanthoma elasticum. This is an inherited disorder of elastic tissue. There
is poor elastic tissue in skin, eye, cardiovascular system, and GI tract. Small, soft,
yellow-orange cutaneous papules run parallel to the natural skin folds of the
neck, axillae, groin, and abdomen. Angioid streaks are seen in retina. The skin
bruises easily. Disintegration of arteries in the GI tract causes hemorrhage.
Tuberous sclerosis. This is an autosomal dominant disorder of ectodermal
and mesodermal tissues with hamartoma formation in the skin, brain, and
kidneys. The skin signs are hypopigmented spots that may be multiple and
small or larger elongated macules, ash-leaf spots. Pink, eshy nodules up to
5 mm in size appear on the central face. Similar lesions are common around
the nails. Plaques on the back or buttock, Shagreen patches, represent connective tissue nevi.
Neurobromatosis (NF). Two forms, NF-1 and NF-2, are inherited as auto-
somal dominant disorders affecting the skin, bones, nervous system, and
endocrine organs.
Café au lait (coffee with milk) spots occur in childhood as
uniform pigmented macules from a few millimeters to several centimeters in
size. Neurobromas are brown, rounded, raised, often pedunculated, masses
that can be reduced below the skin surface with nger pressure (button-hole
sign). Plexiform neuromas are larger, soft, sagging, subcutaneous protrusions
from the skin surface; they may become huge. The lesions are often innumerable and particularly common in the axilla.
-
Vascular Disorders.
Raynaud disease and phenomenon. See Chapter 8, page 375 for a complete
discussion.
Warfarin skin necrosis—deciency of proteins C and S.
protein-C or protein-S deciency exposure to warfarin leads to intravascular coagulation and skin necrosis. One or two days after starting warfarin,
painful indurated lesions appear which progress to necrosis. Areas of adipose
tissue are primarily involved, e.g., breast, abdomen, buttocks, and thighs.
Meningococcemia. Patients with meningococcal meningitis and meningococcemia develop petechial hemorrhages, bright-pink tender maculopapules 2–10 mm in diameter involving the trunk and extremities, some
developing hemorrhagic centers. Large ecchymoses and hemorrhagic
vesicles may form. Gangrene, especially ngers and toes, may occur.
Livedo reticularis may be present.
With congenital
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Disseminated intravascular coagulation (DIC, consumption coagulopathy).
platelets and clotting factors and activating brinolysis leading to hemorrhage. Usually complicating preexisting multisystem disease, onset is
characterized by shock, purpura with ecchymoses and petechiae, fever,
and bleeding from multiple sites.
CLINICAL OCCURRENCE: Septicemia, malignancy (especially acute pro-
myelocytic leukemia, some adenocarcinomas and sarcomas), surgery, trauma,
complications of pregnancy (dead fetus, amniotic uid embolism, abruptio
placenta, septic abortion, preeclampsia, and eclampsia), envenomation, and
liver failure.
Thrombotic Thrombocytopenic Purpura (TTP) and Hemolytic Uremic
Syndrome (HUS). In TTP inhibition of ADAMTS-13, a metalloproteinase
enzyme that cleaves von Willebrand factor (VWF), allows circulation of large
VWF multimers. Platelet-rich arteriolar thrombi fragment erythrocytes and
cause ischemic infarcts in vital organs. The mechanism of HUS is not understood.
Most patients with TTP are young adults, more often women, with a
history of recent viral infection. Other risk factors are pregnancy, bee sting,
AIDS, SLE, mitomycin C, and recent organ transplantation. Petechiae are a
key sign. The classic TTP pentad is: (1) thrombocytopenia, (2) microangiopathic hemolytic anemia, (3) renal insufciency, (4) nonfocal neurologic decits, and (5) fever. Headache, confusion, delirium, seizures, and other mental
status changes develop in 90% of fatal cases. Rapid diagnosis and treatment
are necessary. Finding schistocytes on a peripheral blood smear rapidly establishes the diagnosis. Mortality is >90% without treatment. Relapses of TTP
following successful treatment are common. HUS in children produces the
same arteriolar lesions and laboratory ndings without CNS involvement.
HUS occurs sporadically and in epidemics associated with Escherichia coli
0157:H7 gastroenteritis.
Platelet-brin thrombi form in multiple vessels consuming
Immune thrombocytopenic purpura (ITP).
Immune-mediated platelet
destruction leads to thrombocytopenia, large circulating platelets, and megakaryocyte hyperplasia.
Easy bruising, petechiae, menorrhagia, epistaxis, or
other mucocutaneous bleeding signals ITP onset. The spleen is not palpable.
Children with acute ITP frequently recover without treatment. Adults with
very low platelet counts are at risk for intracranial hemorrhage and are more
likely to develop chronic thrombocytopenia. DDX: The history, physical
exam, and selected tests should exclude SLE, HIV infection, cytomegalovirus,
Epstein–Barr virus, drug-induced thrombocytopenia, hypersplenism, malignant lymphoma, and other disorders.
Purpura, abdominal pain and arthralgia—Schönlein–Henoch purpura
(anaphylactoid purpura). See Chapter 8, page 364.
Scurvy.
Punctate cutaneous perifollicular hemorrhages occur most com-
monly on the legs. Petechiae surround hair follicles containing tightly coiled
corkscrew hairs. Mucous membrane bleeding and loose teeth are characteristic.
Rickettsial spotted fever syndromes. See Chapter 4, page 49.
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Schamberg disease—pigmented purpuric dermatosis. A benign chronic
disorder with repeated crops of petechiae and orange to fawn-colored macules on feet and legs.
Atheroembolism (cholesterol emboli). Rupture of an atherosclerotic plaque
embolizes its cholesterol-rich contents producing ischemic infarction with
hemorrhage in downstream skin and organs. Embolization frequently fol-
lows endovascular procedures that mechanically disrupt vessel wall plaque.
Hours to 1–2 days postprocedure, pain and erythema are followed by retiform ecchymoses and purpura, which can progress to frank infarction. The
lesions, which may be palpable, range from 1 mm to 2 cm in size; toes and
ngertips may become necrotic (Fig. 6-25). Livedo reticularis is common. This
most commonly follows passage of intravascular catheters during diagnostic
or therapeutic procedures, or initiation of warfarin.
Palpable purpura—vasculitis.
Hereditary hemorrhagic telangiectasia (HHT, Osler–Weber–Rendu disease).
HHT is a Mendelian dominant trait with extensive arteriovenous malformations (AVM) developing in all organs. AVMs vary from small to quite large.
The skin is spotted with dull red lesions (telangiectasias), most developing
after puberty. Epistaxis is frequent before appearance of diagnostic skin and
mucous membrane lesions. The usual lesion is punctate, 1–2 mm in diameter,
usually not elevated, some appearing slightly depressed. Diascopy pressure
causes fading and the spots may pulsate. One or two ne supercial vessels
may radiate from the punctum. The mucosa is practically always involved,
especially the tip and dorsal tongue. Anterior nasal septal lesions cause frequent epistaxis. The most frequent sites of skin involvement are palms and
ngers, nail beds, lips, ears, face, arms, and toes. The trunk is least involved.
Spontaneous epistaxis, hemoptysis, hematemesis, melena, or hematuria are
seen. Pulmonary AVMs are common leading to polycythemia and clubbing.
Hepatic AVMs manifest as a RUQ abdominal bruit. Anemia and iron deciency
See Chapter 8, page 360.
FIG. 6-25 Atheroemboli (Blue Toes Syndrome). Left: Multiple sharply demarcated hemorrhagic blisters with
surrounding erythema and edema. The foot is intensely painful. Right: The same foot six weeks later.
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are common due to constant gastrointestinal blood loss. DDX: Arterial spiders
have more numerous radicles, smaller centers, and are less widely distributed.
Skin Neoplasms: A high index of suspicion is required to diagnose early-
stage skin cancers. They are often noticed at a visit for another problem.
Periodic complete skin exam should be performed on all patients.
Lipomas.
They are multiple and appear to be hereditary. Lipomas are common mostly
on the trunk and proximal extremities. They can be tender on rst appearance
and if traumatized. They are smooth or lobular, soft, and not attached to the
epidermis so mobile within the subcutaneous tissue. Most are 1–3 cm in size
but can be very large causing functional and cosmetic problems. Larger size
increases risk of liposarcoma. Multiple lipomas are associated with several
rare diseases: Cowden disease, Proteus syndrome, MEN type-1, and NF-1.
DDX: Epidermal inclusion cysts are attached to the epidermis.
Cutaneous nevi—moles.
within the epidermis or at the dermal-epidermal junction; genetics determines the number and type of moles. Moles may be congenital, but more
commonly they begin appearing during puberty and adolescence. Congenital
hairy nevi are large pigmented plaques with prominent hairs. Junctional nevi
are brown to black macules a few millimeters in diameter. Dermal nevi are
skin colored to reddish domed papules or nodules <1 cm in size. Compound
nevi have
Benign tumors of mature adipose tissue arise in any adipose tissue.
Nevi are benign proliferations of melanocytes
features of both junctional and dermal nevi (Fig. 6-26). Halo nevi
FIG. 6-26Cutaneous Nevi (Moles). Several benign nevi on the chest with different patterns of pigmentation.
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are surrounded by a depigmented halo; they may undergo complete regression. Blue nevi are dark blue to deep purple to almost black macules and
papules; the blue color results from the Tindel effect in being deep in the
dermis. Atypical moles have unusual features (asymmetry, irregular border,
mixed colors, >6 mm in diameter) raising suspicion for melanoma. Abnormal
histologic features on biopsy makes them dysplastic nevi. Serial photos are the
best way to follow multiple moles; dermatology referral is advised.
Malignant melanoma.
within the epidermis, invades the reticular and papillary dermis. Prognosis
is inversely related to depth of invasion. Melanomas are usually pig-
mented but amelanotic melanoma can occur. The lesions are macules or
papules that can become nodules which may ulcerate in advanced disease.
Melanoma may arise from preexisting nevi or appear on otherwise normal
skin. Risk factors include a personal or family history of malignant melanoma, blond or red hair, marked freckling on the upper back, and three or
more blistering sunburns before the age of 20 years. The American Cancer
Society uses the mnemonic ABCDE to help distinguish between melanoma
and benign moles. Melanomas have Asymmetry, Border irregularity, Color
variegation, a Diameter >6 mm, and Evolution of the lesion. Ask about
changes in color, shape, elevation, texture, surrounding skin, sensation, and
consistency. Any suspicious lesion should be referred to a dermatologist.
Never do a partial shave biopsy for possible melanoma; a full thickness biopsy is
required for staging.
Basal cell carcinoma.
skin, usually on the face or upper back, without a precursor lesion. The
lesions are pearly papules, often with surface telangiectasias. They slowly
enlarge and may ulcerate. They can have considerable local extension and
tissue destruction, but do not metastasize. Supercial basal cell cancers are often
shiny pink patches or thin plaques with telangiectasias and a slightly rolled
border. Uncommonly basal cell cancer presents as areas of sclerosing skin
atrophy, termed morpheaform basal cell carcinomas. When advanced, they are
erosive with elevated borders.
Actinic keratosis.
transform into squamous cell carcinoma. Actinic keratoses start as erythema-
tous macules or patches typically with sharp adherent scale. They are asymptomatic or associated with tingling or burning.
Malignant melanocyte proliferation, initially
This most common skin cancer arises on sun-exposed
Abnormal keratinocytes arising in sun-damaged skin can
Squamous cell carcinoma. These cancers arise in sun-damaged skin from pre-
existing actinic keratoses or in the genital region from human papilloma virus
infection. When limited to the epidermis (squamous cell carcinoma in situ, Bowen
disease) they present as sharply demarcated plaques with slight scaling up to
several centimeters in diameter. Invasive squamous cell carcinoma presents
as ulcerated indurated skin (common on the lip) or as an eroded exophytic
growth. They invade the dermis metastasizing to regional lymph nodes.
Keratoacanthoma. Often considered subtype of squamous cell cancer, it is a
solitary lesion growing rapidly to become an exophytic nodule with a central
keratin plug. Some spontaneously regress over weeks to months.
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