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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2664_Библиотеки_им_академика_М_И_Перельмана
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Dermatology
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Chapter Title
Learning Objectives
❏ Describe the mechanism of bullous and blistering diseases and approaches to treatment
❏ List the common dermatologic parasitic diseases, treatments, and common side effects
❏ Outline the treatment of skin and ulcer infections, including decubitis (pressure)
ulcers and acne
❏ Describe the presentation and management of scalp, hair, and scaling disorders
(eczema), and papulosquamous dermatitis
❏ Provide an overview of toxin-mediated diseases, hypersensitivity, and toxin-mediated
diseases
❏ Describe benign lesions, precancerous lesions, and malignant diseases of the skin and
their treatment and prognosis
00
12
Meissner
corpuscle
Epidermis
Dermis
Hair shaft
Hair
Figure 12-1. Skin
Sweat gland pore
Stratum corneum
Stratum lucidum
Stratum granulosum
Stratum spinosum
Stratum basale
Sweat gland duct
Arrector pilius
Sebaceous gland
Sweat gland
Root sheath
Bulb
Papilla
411
USMLE Step 2 CK
l Internal Medicine
BULLOUS/BLISTERING DISEASES
Pemphigus Vulgaris
Pathogenesis. Pemphigus vulgaris is an autoimmune disease of unclear etiology in which the
body essentially becomes allergic to its own skin. Antibodies are produced against antigens in
the intercellular spaces of the epidermal cells. They attack the “glue” that holds the epidermal
cells together. “Pemphix” is from the Greek word for bubble, which is what a bulla looks like
before it is broken. Pemphigus vulgaris is most often idiopathic, but ACE inhibitors or penicillamine can occasionally cause it.
Clinical Presentation. Vulgaris occurs in patients age 30s and 40s, whereas bullous pemphigoid
occurs in those age 70s and 80s. Pemphigus vulgaris is a much more serious and potentially
life-threatening disease than pemphigoid. Vulgaris occurs prominently in the mouth and often
starts there. The oral lesions are erosions, not bullae. The bullae are very thin and flaccid and
break easily. This leads to the loss of large volumes of skin surface area, so it acts like a burn.
This is because the bullae occur from destruction within the epidermis, making them thinner
and more fragile. The presence of the Nikolsky sign (the easy removal of skin by just a little
pressure from the examiner’s finger, pulling the skin off like a sheet) is seen in pemphigus vulgaris, staphylococcal scalded skin syndrome, and toxic epidermal necrolysis.
The lesions of pemphigus vulgaris are painful, not pruritic.
Diagnosis. The most accurate diagnostic test is to biopsy the skin and to use immunofluorescent stains. These stains will detect intercellular deposits of IgG and C3 in the epidermis.
Treatment. Treatment is with systemic glucocorticoids, such as prednisone. Topical steroids will
not be sufficiently strong. Before the invention of steroids, pemphigus vulgaris was often fatal,
with patients dying of sepsis and dehydrationjust like a burn patient. For those in whom steroids are ineffective or not tolerated, you can use azathioprine, mycophenolate, or cyclophosphamide. Rituximab and IVIG are also effective.
Bullous Pemphigoid
Pathogenesis. Pemphigoid is 2× as common as pemphigus vulgaris and occurs in elderly per-
sons age 70s and 80s. It can also be drug induced with sulfa drugs, including furosemide, penicillamine, and others.
Clinical Presentation. The defect occurs at the dermo-epidermal junction, so the layer of skin
that separates off is much thicker. Because the fracture of the skin causing the blisters is deeper,
the bullae are thicker walled and much less likely to rupture. Oral lesions are rare. Because the
bullae are tense and intact, the skin is better protected. There is no dressing for skin as good
as skin itself. Hence, there is much less fluid loss, and infection is much less likely as compared
with pemphigus vulgaris. Mortality is much less likely in bullous pemphigoid.
Diagnosis. The most accurate diagnostic test is a biopsy with immunofluorescent antibodies
at the dermo-epidermal junction (basement membrane).
412
Treatment. Systemic steroids, such as prednisone, are the standard means of treatment.
Tetracycline or erythromycin combined with nicotinamide is the alternative to steroids. Use
topical steroids only if no oral lesions are present.
Porphyria Cutanea Tarda
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Pathogenesis. Porphyria cutanea tarda is a disorder of porphyrin metabolism. Deficiency
of the enzyme uroporphyrinogen decarboxylase results in an abnormally high accumula-
tion of porphyrins, which then leads to a photosensitivity reaction. The test question should
give a history of HIV, alcoholism, liver disease, chronic hepatitis C, or a woman taking oral
contraceptives. The liver disease may be from any cause but is most likely to involve chronic
infectious hepatitis or hemochromatosis because porphyria cutanea tarda is associated with
increased liver iron stores. Diabetes is found in 25% of patients.
Clinical Presentation. Fragile, nonhealing blisters are seen on the sun-exposed parts of the
body, such as the backs of the hands and the face. This leads to hyperpigmentation of the skin
in general and hypertrichosis of the face.
Diagnosis. The diagnostic test is a level of urinary uroporphyrins. Uroporphyrins are elevated 2–5× above the coproporphyrins in this disease.
Treatment. The best initial step in management is to stop drinking alcohol (although it is
unlikely to be effective) and to discontinue all estrogen use. Combine treatment with barrier
sun protection, such as clothing, because most sunscreens do not seem to block the wavelength of light causing the dermal reaction. The most effective therapy to use if this is insufficient is phlebotomy to remove iron. Deferoxamine is used to remove iron if phlebotomy is
not possible. Also, the antimalarial drug chloroquine increases the excretion of porphyrins.
Chapter 12
l Dermatology
DRUG ERUPTIONS/HYPERSENSITIVITY
Urticaria
Pathogenesis. Acute urticaria is a hypersensitivity reaction most often mediated by IgE and
mast cell activation, resulting in evanescent wheals and hives. It is a type of localized, cutane-
ous anaphylaxis, but without the hypotension and hemodynamic instability. The most common causes of acute urticaria are allergic reactions to medications, insect bites, and foods, and
occasionally, the result of emotions. The most common medications are aspirin, NSAIDs, morphine, codeine, penicillins, phenytoin, and quinolones. ACE inhibitors are also associated with
urticaria, as well as angioedema. The most common foods are peanuts, shellfish, tomatoes, and
strawberries. Contact with latex in any form can also cause urticaria.
Clinical Presentation. Acute urticaria lasts <6 weeks in duration and two-thirds of cases are
self-limited. Chronic urticaria lasts >6 weeks in duration and is associated with pressure on
the skin, cold, or vibration. Pressure on the skin resulting in localized urticaria is also known
as dermatographism. In acute cases, the onset of the wheals and hives is usually within 30
minutes and lasts for <24 hours. Itching is prominent. In patients with chronic urticaria lasting >6 weeks, you should investigate the etiology.
Treatment. Urticaria is treated with H1 antihistamines. Severe, acute urticaria is treated with
older medications, such as diphenhydramine (Benadryl), hydroxyzine (Atarax), or cyproheptadine. If it is life-threatening, use H2 antihistamines when H1 antihistamines fail and add
systemic steroids. Chronic therapy is with newer, nonsedating antihistamines, such loratadine,
desloratadine, fexofenadine, or cetirizine. Astemizole and terfenadine should never be used
and are no longer marketed; they cause potentially fatal rhythm disturbances particularly
when combined with other medications, such as macrolide antibiotics, because of their effect
on the hepatic P450 system.
413
USMLE Step 2 CK
Note
For urticaria:
Answer “terfenadine” or
“astemizole” only when the
test question asks what will
kill the patient or which is the
most dangerous medication.
Answer “desensitization”
when the trigger cannot be
avoided, e.g., a beesting
in a farmer. Beta-blocker
medications must be stopped
prior to desensitization
because they inhibit
epinephrine, which may be
used if there is an anaphylactic
reaction.
l Internal Medicine
Wikipedia, James Heilman, MD
Figure 12-2. Urticaria
Morbilliform Rashes
Pathogenesis. A morbilliform rash is a milder version of a hypersensitivity reaction compared
with urticaria. This is the “typical” type of drug reaction and is lymphocyte mediated.
Clinical Presentation. The rash resembles measles and is usually secondary to medications
that the patient is allergic to, such as penicillin, sulfa drugs, allopurinol, or phenytoin. It is a
generalized, maculopapular eruption that blanches with pressure. The reaction can appear a
few days after the exposure and may begin even after the medication has been stopped.
Treatment. Antihistamines are effective, and steroids are rarely necessary.
Erythema Multiforme
Although erythema multiforme (EM) may be caused by the same types of medications that
cause urticaria and morbilliform rashes (penicillins, phenytoin, NSAIDs, and sulfa drugs), the
most common cause of EM is a reaction to infection. The majority of cases follow infection
with herpes simplex or Mycoplasma.
Clinical Presentation. The most characteristic feature of EM is target-like lesions that occur
especially on the palms and soles. These lesions can also be described as “iris-like.” Bullae are
not uniformly found. EM of this type usually does not involve mucous membranes.
Treatment is with antihistamines and by treating the underlying infection.
414
Wikipedia, James Heilman, MD
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Figure 12-3. Erythema Multiforme
Chapter 12
l Dermatology
Stevens-Johnson Syndrome
Pathogenesis. Stevens-Johnson syndrome (SJS) is sometimes called erythema multiforme
major. It is sometimes difficult to distinguish SJS from toxic epidermal necrolysis (TEN) and,
in fact, the two diseases may be considered a spectrum of severity of the same disorder. All of
these disorders may arise as a hypersensitivity response to the same set of medications, such
as penicillins, sulfa drugs, NSAIDs, phenytoin, and phenobarbital.
Clinical Presentation. SJS usually involves <10 to 15% of the total body surface area, and
the overall mortality rate is <5 to 10%. There is mucous-membrane involvement in 90% of
cases, most often of the oral cavity and the conjunctivae, although there may be extensive
involvement of the respiratory tract.
Treatment. These patients should be treated with early admission to a burn unit, withdrawal
of the offending drug, and supportive care. Respiratory-tract involvement may be so severe
as to require mechanical ventilation. Death occurs from a combination of infection, dehydration, and malnutrition.
There is no proven benefit for steroids. The best initial therapy for severe disease is IV
immunoglobulins. Other therapies of unclear value are cyclophosphamide, cyclosporine,
and thalidomide.
Toxic Epidermal Necrolysis
Pathogenesis. Toxic epidermal necrolysis (TEN) is the most serious version of a cutaneous
hypersensitivity reaction. Mortality may be as high as 40 to 50%.
Clinical Presentation. Much more of the body surface area (BSA) is involved and may range
from 30 to 100%. The Nikolsky sign is present, and the skin easily sloughs off. TEN has certain features similar to staphylococcal scalded skin syndrome; however, TEN is drug induced
as opposed to being caused by a toxin coming from an organism.
415
USMLE Step 2 CK
Clinical Pearl
Always do a chest x-ray on a
patient with EN, to exclude
sarcoidosis.
A biopsy of EN lesions
will show nonspecific
inflammation.
l Internal Medicine
Diagnosis. The diagnosis is usually clinical. The most accurate diagnostic test is a skin biopsy,
which will reveal full thickness epidermal necrosis. A skin biopsy is usually not necessary.
Treatment. Sepsis is the most common cause of death, but prophylactic systemic antibiotics
are not indicated. Systemic steroids are not effective and may, in fact, decrease survival.
Fixed Drug Reaction
Pathogenesis. This is a localized allergic drug reaction that recurs at precisely the same anatomic
site on the skin with repeated drug exposure. It is not known why the reactions are anatomically
localized and do not become generalized morbilliform rashes. The most commonly implicated
drugs include aspirin, NSAIDs, tetracycline, and barbiturates.
Clinical Presentation. Fixed drug reactions are generally round, sharply demarcated lesions
that leave a hyperpigmented spot at the site after they resolve.
Treatment. In addition to discontinuation of the offending drug, the reactions can be treated
with topical steroids.
Erythema Nodosum
Pathogenesis. Erythema nodosum (EN) is a localized inflammatory condition of the skin or
panniculitis. It is secondary to recent infections or inflammatory conditions. It is also associated with pregnancy. The most common causes of EN are recent streptococcal infections,
coccidioidomycoses, histoplasmosis, sarcoidosis, inflammatory bowel disease, syphilis, TB, and
hepatitis. Enteric infections such as Yersinia also cause the disorder.
Clinical Presentation. Erythema nodosum consists of multiple painful, red, raised nodules on
the anterior surface of the lower extremities. They are extremely tender to palpation. They do
not ulcerate, and they generally last about 6 weeks.
Diagnosis. ASLO titers can help determine who has recently had a streptococcal infection if
there is no other etiology apparent from the history.
Treatment. Therapy consists of treating the underlying disease, as well as the use of analgesics
and NSAIDs. Potassium iodide solution can be used in those who do not respond to symptomatic therapy. Erythema nodosum is usually a self-limiting condition.
INFECTIONS
Fungal Infections
Tinea pedis, cruris, corporis, versicolor, capitis, and onychomycosis
All of the superficial fungal infections of the body share a number of common characteristics leading to the same answer on the test for similar questions for each of these diseases.
“Superficial fungal infections” refer to those infections limited to the skin, nails, and hair.
Remember, though, that these answers would not be valid for more deep-seated, life-threatening infections, such as fungal endocarditis, meningitis, or abscesses.
416
Clinical Presentation and Diagnosis. All superficial fungal infections of the skin, hair, and
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nails are primarily diagnosed by their visual appearance and confirmed by a potassium hydroxide (KOH) test of the skin. The leading edge of the lesion on the skin or nails is scraped with
a scalpel to remove some of the epithelial cells or some of the nail and hair. KOH has the ability to dissolve the epithelial cells and collagen of the nail, but does not have the ability to melt
away the fungus. Hence, a KOH preparation gives an immediate diagnostic answer by revealing
fungal hyphae. This is particularly characteristic in tinea versicolor, where the Malassezia furfur
(Pityrosporum orbiculare) organism appears in a “spaghetti and meatballs” pattern.
The most accurate test is to culture the fungus. This is usually not clinically practical because
molds that grow on the skin (dermatophytes) take up to 6 weeks to grow even on specialized
fungal media. A specific species usually does not need to be isolated in most cases, unless it is
an infection of the hair or nails. In the case of nail and hair infections, oral therapy is necessary, and it is important to be precise because there are fewer medications that can be used to
effectively treat onychomycosis. Tinea tonsurans is the cause of >90% of cases of tinea capitis.
Treatment. For onychomycosis (nail infection) or hair infection (tinea capitis), the medications with the greatest efficacy are oral terbinafine or itraconazole. These medications are used
for at least 6 weeks for fingernails and 12 weeks for toenails. Terbinafine is potentially hepatotoxic, and it is important to periodically check liver function tests. Griseofulvin must be used
for 6 to 12 months in the treatment of fingernails and has much less antifungal efficacy than
terbinafine. Griseofulvin is no longer recommended in the treatment of onychomycosis of the
toenails. In the treatment of tinea capitis, griseofulvin is recommended for 6 to 8 weeks.
The other fungal infections of the skin that don’t involve hair or nails may be treated with
any of the following topical medications: ketoconazole, clotrimazole, econazole, terbinafine,
miconazole, sertaconazole, sulconazole, tolnaftate, or naftifine. There is no clear difference in
efficacy or adverse effects between them when used topically. Ketoconazole has more adverse
effects when used systemically, such as hepatotoxicity and gynecomastia. This is why ketoconazole is not a good choice for onychomycosis. There is no topical form of fluconazole.
Fluconazole is also less efficacious for dermatophytes of the nails when used systemically.
Chapter 12
Note
Drug of choice for oral
antifungal treatment:
• Tinea capitis and
onchomycosis
– Terbinafine or
itraconazole
l Dermatology
Antifungal medications generally should not be used in combination with topical steroids,
unless a diagnosis has been confirmed. Steroids in a cream can relieve redness and itching and
give the appearance of improvement even in impetigo and contact dermatitis.
Tinea versicolor
Definition. Skin infection characterized by multiple macules (usually asymptomatic), varying
in color from white to brown.
Etiology. Pityrosporum orbiculare (Malassezia furfur).
Clinical Presentation. Tan, brown, or white scaling macular lesions that tend to coalesce;
found on chest, neck, abdomen, or face. Lesions do not tan.
Diagnosis. Skin scrapings examined with 10% KOH under a microscope. The classic description is of “spaghetti and meatballs,” which refers to the hyphae and spores that can be seen in
the KOH prep.
Treatment. Topical selenium sulfide, clotrimazole, ketoconazole, or oral itraconazole. The need
for local or systemic therapy is decided on the basis of the amount of surface area involved.
417
USMLE Step 2 CK
l Internal Medicine
Clinical Correlate
Tinea versicolor has some additional features that are important in its management. It presents with
lesions of different colors from tan to pink (hence the name versicolor). The lesions often do not tan, and
they present with pale areas in the middle of a normal tan. This can be distinguished from vitiligo by the
fact that vitiligo has no pigmentation, whereas tinea versicolor presents with altered pigmentation. The
organism may also be contagious. A KOH preparation and fungal culture are used in the same manner
as for the other dermatophytes. The main therapeutic difference is the use of topical selenium sulfide
every 2 to 3 weeks versus oral therapy with itraconazole or fluconazole. This is not because of antifungal
resistance; it is because tinea versicolor is much more likely to involve large amounts of body surface area
so it is difficult to cover this volume of skin with an ordinary topical cream or lotion.
Candidiasis
Definition. A yeast infection usually involving skin and mucous membranes, but it can also
be systemic.
Etiology. Candida albicans. Usually spreads in patients with decreased host defenses. Patients
with any of the following have an increased susceptibility: systemic antibacterial therapy, obesity, diabetes mellitus, corticosteroid or antimetabolite therapy, pregnancy, debilitating disease
and blood dyscrasias, or HIV.
Clinical Presentation
• Intertriginous infection: Well-demarcated, erythematous, itchy, exudative patches, usually rimmed with small red-based pustules that occur in the groin, gluteal folds (diaper rash), axilla, umbilicus, and inframammary areas.
• Vulvovaginitis: White or yellowish discharge with inflammation of the vaginal wall
and vulva. Common in pregnant women and patients with diabetes mellitus.
• Oral candidiasis (thrush): White patches of exudates on tongue or buccal mucosa
• Candidal paronychia: Painful red swelling around the nail
Diagnosis. Potassium hydroxide on slide to visualize fungal forms. Culture is definitive.
Treatment
• Topical nystatin, clotrimazole, miconazole, ciclopirox, econazole, or terconazole
• Systemic amphotericin in serious invasive infections. Fluconazole in less serious
infections. Candida paronychia requires systemic therapy.
Bacterial Infections
Antistaphylococcal antibiotics
The most common bacterial organisms to cause skin infections of any kind are Staphylococcus
and Streptococcus. Antibiotics used to treat Staphylococcus are dicloxacillin, cephalexin (Keflex),
or cefadroxil (Duricef). Cefadroxil, cefazolin, or cephalexin are the preferred agents. If a
patient is allergic to penicillin, but the reaction is only a rash, then cephalosporins can be safely
used. There is far less than 5% cross-reaction between penicillins and cephalosporins. The IV
418
equivalents of oral dicloxacillin include oxacillin and nafcillin. The IV equivalent of cefadroxil is
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cefazolin.
If the penicillin reaction is anaphylaxis then cephalosporins cannot be used. The alternative
antibiotics that will treat the skin are macrolides, such as erythromycin, azithromycin, clarithromycin, or the newer fluoroquinolones (levofloxacin or moxifloxacin). Ciprofloxacin will
not adequately cover the skin. Vancomycin is only for IV use for skin infections, and oral vancomycin is not absorbed. Oral therapy for MRSA is with clindamycin, TMP/SMX, or doxycycline. The ultimate form of oral MRSA therapy is linezolid.
Impetigo
Definition. A superficial, pustular skin infection, seen mainly in children (ecthyma is an
ulcerative form of impetigo), with oozing, crusting, and draining of the lesions. It is a superficial bacterial infection of the skin largely limited to the epidermis and not spreading below
the dermal-epidermal junction.
Etiology. Group A beta-hemolytic Streptococcus and S. aureus (bullous impetigo).
Chapter 12
l Dermatology
Clinical Presentation. Because it is limited to the epidermis, the purulent material is easily able
to express itself through the surface; therefore, the patient history will describe the infection
with words such as “weeping,” “oozing,” “honey colored,” or “draining.” Impetigo occurs more
often in warm, humid conditions, particularly when there is poverty and crowding of children.
This is because it is both contagious and autoinoculable. More common on arms, legs, and
face. May follow trauma to skin. Begins as maculopapules and rapidly progresses to vesicular
pustular lesions or bullae. The crusts are described as having a golden or yellow appearance
and if untreated can progress to lymphangitis, furunculosis, or cellulitis, and acute glomerulonephritis. Impetigo may cause glomerulonephritis, but it will not cause rheumatic fever.
Treatment
• Oral first-generation cephalosporin or semisynthetic penicillin, e.g., oxacillin, cloxacillin, dicloxacillin (for severe or widespread cases)
• Topical mupirocin, bacitracin, or retapamulin for mild cases of impetigo
• Penicillin-allergic patients can be treated with macrolides such as clarithromycin or
azithromycin.
• TMP/SMZ, clindamycin, or doxycycline for MRSA
Erysipelas
Pathogenesis. Erysipelas is a bacterial infection of a deeper layer of the skin than impetigo.
Erysipelas involves both the dermis and epidermis and is most commonly caused by group A
Streptococcus (pyogenes).
Note
Group A streptococci and
S. aureus are the most
common causes of impetigo.
Note
Retapamulin is a topical
antibacterial more active
against staph and strep than
mupirocin or bacitracin are.
Clinical Presentation. Because it involves lymphatic channels in the dermis, erysipelas is more
likely to result in fever, chills, and bacteremia. It often involves the face, giving a bright red,
angry, swollen appearance. Usually bilateral, shiny red, indurated edematous tender lesions on
the face, arms, and legs. These lesions are often sharply demarcated from the surrounding normal skin. Differentiate from herpes, contact dermatitis, and angioneurotic edema.
Treatment. Semisynthetic penicillin or first-generation cephalosporin if you cannot distinguish it from cellulitis; penicillin (if Streptococcus is certain).
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