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American Manual
of Examination
in Medicine
(2CK)
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2015
Dermatology
American Manual
of Examination
in Medicine
(2CK)
Authors
Dolores Mendoza
Index
01. Skin Layers ....................................................................................................... 1
De rm ato l ogy
Skin
Chapter 01
Layers
There are three skin layers: epidermis, dermis and subcutaneous cellular tissue (Figure 1).
Superficial arteriovenous
plexus
Reticular layer
Epidermis
Dermis
Subcutaneous
tissue
Dermal Papillae
Sweat
gland
Sebaceous
(Oil) gland
Hair
follicle
Deep
arteriovenous
plexus
Terminology.
Chapter 02
Elemental
Cutaneous Lesions
Macule
Vesicle
Wheal
Fissure
Papule
Ulcer
Nodule
Cyst
Allergic and
Chapter 03
Clinical Presentation
Clinical presentation is usually in the form of greasy, erythematous
and desquamative papules or plaques on the scalp (cradle cap in the
cases of newborns), central area of the face, sternal region, axilla and/
or groin. In newborns, this presentation can be generalized, causing
Leiners erythroderma desquamativum; in adults, it is likely to be related to blepharitis.
Dierential diagnosis includes atopic eczema in children, but dierential diagnosis in adults reveals subacute erythematous lupus or pink
pityriasis when the trunk is involved and inverted psoriasis when skin
folds are aected.
Remember
Letterer-Siwe disease can cause lesions similar to infantile seborrheic
dermatitis. However, unlike infantile seborrheic dermatitis, Letterer-Siwe
disease is associated with lymphadenopathies and hepatosplenomegaly.
Remember
Impetigo key words (yellowish scabs) should not be mistaken for seborrheic
dermatitis key words (yellowish scales).
Immune-mediated
Diagnosis
Diseases
Atopic dermatitis has a clinical diagnosis. Patients may present with eosinophilia and increase of IgE values.
Treatment
It is essential for the patient to follow certain rules in his lifestyle. This
means the patient must avoid wearing perfumed products (like cologne
and cream), being exposed to extreme temperatures, the use of fabric
softeners and carpets or fluy toys (because of possible sensitization of
dust mites). Besides, the patient needs to wear 100% cotton clothing.
De rm ato l ogy
Diagnosis
Diagnosis is established with clinical records and epicutaneous tests of
contact. These tests are performed once lesions have been resolved, by
applying patches with allergens on healthy skin, leaving them in contact
with the skin during 48 hours. They are read after 48 and 96 hours. The
intensity of reaction is measured qualitatively: negative, weak positive
(erythema), strong positive (papules-vesicles) or extreme positive (blisters).
b. Seborrheic dermatitis in adult: erythematous desquamating papules or plates in fat areas of the facial region and scalp.
Diagnosis
Diagnosis of this condition is clinical.
Treatment
Treatment involves antifungals associated with topic corticoids. Seborrheic dermatitis on the scalp is usually linked to a keratolytic agent, like
the salicylic acid.
3.5. Psoriasis
Psoriasis is a chronic inflammatory disease of the skin that presents
with outbreaks. Psoriasis aects 1-2% of the population, and can appear at any age, with a maximum of incidence between 20 and 30 years
of age. There is a family history in a third of the patients.
Plates are the characteristic erythematous desquamating lesions, well
delimited, with a superficial thick and white-pearl scale.
The most frequent clinical form is vulgar psoriasis or psoriasis in plates.
Lesions are localized at extensor surfaces (elbows and knees) and the
scalp. The umbilical and the lumbosacral areas are often aected.
Nail involvement is frequent, and is most common with a pitting appearance. This form is little specific. The forms that combine hyperkeratosis and distal onycholysis are more specific. Oil spot is the most characteristic sign (Figure 3).
Treatment
Avoid contact with the allergen.
Treatment of acute eczema implies application of topic poultice (zinc
sulphate, sodium borate) and corticoids if lesions are limited, and system poultice if lesions are generalized.
Clinical Presentation
According to patients age:
a. Seborrheic dermatitis in infants. Yellowish scales on scalp, known
as cradle cab.
3.6. Urticaria
Diagnosis
Diagnosis of this condition is generally clinical.
If there is no certainty, a biopsy must be done, which will reveal hyperkeratosis, acanthosis and parakeratosis.
There is an increase in polymorphonuclears (sterile abscesses) in the
stratum corneum, which are called Munro abscesses.
Treatment (Table 1)
For moderate severe forms of psoriasis that do not respond to classical systemic treatments (see table). They are monoclonal antibodies against proinflammatory substances that are high in patients with
psoriasis [alpha tumor necrosis factor (TNF), interleukin, IL, 12 and
23]. Some of them are infliximab, adalimumab, ustekinumab and
etanercept.
TREATMENT
Topic
Clinical Presentation
Clinical presentation is characterized by the appearance of pruritic wheals
that last less than 24 hours and can be accompanied with angioedema.
USES
Mild-moderate
Moisturizing
psoriasis
Reductants (dithranol)
Hyperkeratotic plaques
Corticoids
Stable psoriasis
in plates
The most used
Vitamin D analogues
(calcitriol, calcipotriol and
tacalcitol)
Retinoids (acitretin)
Severe psoriasis,
pustular
or erythrodermic
It is not usually used
in women in fertile age
(see side effects)
Cyclosporine A
Inflammatory severe
psoriasis, resistant to
other treatments
Rapid action
Rebound effect
Nephrotoxicity
High blood pressure (HBP)
Epitheliomas and lymphomas
Hypertrichosis
Gingival hyperplasia
Hyperuricemia
Methotrexate
Severe psoriasis
resistant to other
treatments
Psoriatic arthropathy
Hepatotoxicity
Myelosuppression
Teratogenicity until 3 months after ending treatment
Photosensitivity
Tachyphylaxis
Percutaneous absorption
Possible new outbreak after stopping medication
Avoid prolonged treatment
De rm ato l ogy
Vasculitis urticaria should be ruled out when lesions last more than 24 hours
and are accompanied with systemic clinical symptoms (i.e., arthralgias).
Treatment
Stevens-Johnson Syndrome
and Toxic Epidermal Necrolysis
Clinical Presentation
3.7. Toxicodermas
Toxicodermas are quite variable cutaneous reactions that appear after
drug administration. They are one of the most frequent side eects of
drugs. The causative agents for many toxicodermas still remains unknown, either immunological or not, and clinical presentation does not
facilitate agent distinction.
Morbilliform exanthem is the most frequent. A morbilliform exanthem
is a generalized eruption formed by symmetric and confluent macules
and papules that usually start by the trunk.
They can appear one or two weeks after taking the drug.
Three dierent groups have been described, although many a time their
clinical symptoms overlap.
Erythema multiforme minor is the most frequent, with around 80%
of the cases. It usually precedes a symptomatic infection by simple
herpes virus (60%) or subclinical infection, about 15 days before.
Erythema multiforme minor manifests itself on extensor surfaces
at hands, elbows and feet, as a symmetric eruption of erythematous edematous lesions with target-shape, (herpes iris of Bateman
or rosette-patterned lesion), with a violaceous, sometimes bullous
center (Figure 5).
Mucosal aectation is rare, with small erosions in oral mucosa. Erythema multiforme minor tends to recurrence, with subsequent outbreaks
of herpetic lesions.
Diagnosis
Diagnosis is according to clinical presentation.
Treatment
Treatment implies withdrawal of potentially responsible drug. Topic or
systemic antihistamines and corticoids are given according to the extent
of symptoms (Figure 4).
Etiology
Remember
Diseases that have the Nikolsky sign are TEN, staphylococcal scalded skin
syndrome (SSSS) and pemphigus. In TEN, the whole epidermis comes off
(bad prognosis), while in SSSS, epidermal detachment occurs at the granular
layer.
Histopathology
Diagnosis
Treatment
In ME minor, only symptomatic treatment is prescribed, with topic
corticoids and oral antihistamines. Treatment for herpes simplex virus
(HSV) infection is useful, to prevent ME lesions if patient is in the initial
stage of the viral infection.
ME major requires treatment of the underlying infection or withdrawal
of implied drug and support measures. The use of oral steroids according to the patients general state is under discussion.
A patient with TEN requires to be admitted at the burn treatment room,
with monitoring of hematocrit, hydroelectrolytic balance, and antibiotic
prophylaxis and support measures. It is controversial the use of systemic corticoids, immunoglobulins and/or cyclosporine.
Treatment
Treatment entails eliminating underlying cause if found, then rest and
anti-inflammatories.
De rm ato l ogy
GENERALLY
PEMPHIGUS VULGARIS
Clinical presentation
Elderly
Sometimes mucosae
With pruritus
Tense blister
No Nikolsky
DERMATITIS
HERPES GESTATIONIS
IDIOPATHIC
Pregnant women
No mucosae
With pruritus
Herpetiform
No Nikolsky
HERPETIFORMIS
IgG
IgG
IgA
Histology
INTRAepidermal blister
There is acantholysis
SUBepidermal blister
There are eosinophils
SUBepidermal blister
There are eosinophils
SUBepidermal blister
Neutrophils in dermis
Treatment
Corticoids
Corticoids at high doses,
immunosuppressants, rituximab
and immunoglobulins
Corticoids
Remember
Relapse if new
pregnancy
Associated to enteropathy
by gluten! 90%
Intercellular
substance ac.
Lucid
layer
Thick
layer
Lineal
storage
in lucid
layer
Basal
sublayer
Granular
storage
in papillary
dermis
Anti-Collagen Ac.
Pemphigus
Pemphigoid bullous
Herpes gestationis
Acquired blistering
epidermolysis
Dermatitis
herpetiformis
Infectious Diseases
Chapter 04
Diagnosis
Diagnosis of this condition is mainly clinical. Virological culture is the
most reliable method of confirmation. The extent of a smear of the lesions (Tzanck cytodiagnosis) allows visualization of multinucleated cells,
and intranuclear inclusions, which become evident through histological
study.
Treatment
Figure 12. Herpes simplex
Contagion is produced by direct contact, though the carrier may be asymptomatic. After primary infection, virus remains silent in the sensitive portion of cranial or spinal ganglia. Immunosuppressed patients
endure the greatest severity of this condition.
Clinical Presentation
Extragenital simple herpes: recurring orofacial herpes simplex is
the most frequent. Most primary infections are asymptomatic. Only
5% manifest themselves in the form of herpetic gingivostomatitis, a
profile characterized by oral ulcers with cervical adenopathy and affectation of the patients general state (Figure 13). During relapses,
clinical symptoms are milder, with cluster vesicles on an erythematous base. Some factors facilitate relapses: trauma, sunlight, cold,
stress, fever, and the menstrual cycle.
Genital simple herpes is the most common cause of genital ulcers
after trauma. Primary infection is usually symptomatic and occurs
between 3 to 14 days after sexual contact. It causes clustered ulcers
in the balanopreputial sulcus or in the prepuce with painful inguinal
adenopathy. Relapses are less severe than primary infection and occur more frequently when genital herpes is due to HSV type II.
Mild forms do not need treatment. Treatment is required in the following cases:
Primary infection.
Severe or frequent relapses if they aect life quality.
Complications, like erythema multiforme and eczema herpeticum.
Drug of choice is oral acyclovir and its derivatives (valacyclovir, famciclovir). Topic antivirals have not proven useful, favoring maceration of
lesions, and thus, over infection. It is not infrequent that topic antivirals
cause allergic contact dermatitis due to hypersensitivity.
Varicella-Zoster Virus
A primary infection gives way to varicella (see Pediatrics section). After
varicella, the virus remains latent in the sensitive portion of the neural
ganglia and when relapse occurs, it leads to zoster herpes.
Varicella: the following symptoms appear after 15 days of incubation:
fever, cephalea, pruritus and polymorphic lesions in dierent stages:
macules, papules, vesicles (Figure 14), ulcers and scabs (starry sky
appearance). Mucosal (ulcers) and scalp involvement is characteristic.
Manipulation can leave scars. Bacterial over infection of lesions is the
most usual complication. About 20% of adults suer from varicella
De rm ato l ogy
Ophthalmic involvement can result in severe keratitis and requires urgent referral to an ophthalmologist. Suspicion should exist on patients
that present herpetic lesions on the tip of the nose) (Hutchinsons sign).
Disseminated zoster herpes: several dermatomes are aected bilaterally. Ramsay-Hunt syndrome is characteristic in the immunosuppressed.
Remember
Affectation of the nose tip makes it necessary for ophthalmological
examination because the nose tip is innervated by the same nerve that
innervates the cornea (first branch of the trigeminal nerve).
Treatment
Varicella without complications is treated symptomatically. Antivirals
are reserved for severe or complicated forms. There is a commercialized vaccine of live virus, whose indications are still under discussion.
Figure 14. Typical vesicles in patients with varicella
Zoster herpes: thoracic zoster herpes is the most usual. It seldom occurs more than once throughout a persons lifetime.
It is characterized by vesicles on pre-existing erythema, with
metameric distribution and lateral extension. The most common complication is post herpetic neuralgia, more frequent in
advanced age. Carbamazepine or tricyclic antidepressants (Figure 15).
Zoster herpes must be treated with antivirals when detected during the
first 48-72 hours and aecting patients with:
Immunosuppression.
Age above 55.
Special clinical forms previously cited.
Drugs to be used are oral acyclovir and its derivatives (valacyclovir and
famciclovir). They accelerate the cure of lesions and decrease the intensity of post herpetic neuralgia. Patients with renal failure need a dose
adjustment, as acyclovir is nephrotoxic. These patients are administered brivudine in a single daily dose.
Molluscum Contagiosum
Dome shaped pink papules with central umbilication (Figure 16). Molluscum contagiosum is typical of children that go to swimming pools. It
is also present in the genital zone after sexual contact and in immunosuppressed patients. It is caused by Poxvirus.
Diagnosis
Diagnosis is clinical. Histology reveals characteristic inclusion bodies.
Treatment
Lesions can resolve spontaneously.
Curettage, cryotherapy or local trichloroacetic acid are eective methods to destroy lesions.
Warts
Diagnosis
Diagnosis of this condition is clinical.
Impetigo is a very contagious superficial infection, without systemic repercussion and normally mixed etiology, by Gram positive cocci (streptococci and staphylococci). Classically, the most frequent accepted
cause was Streptococcus pyogenes. However, at present Staphylococcus
aureus stands out as the predominant cause.
Treatment
Genital warts are treated with cryotherapy, podophyllotoxin, trichloroacetic acid, imiquimod and 5-fluorouracil.
The most typical form is impetigo contagiosa (Figure 19), characterized by honey-colored (meliceric) scabs, which normally appear on
the face and other exposed areas. It is typical of children. Although
infrequent, poststreptococcal glomerulonephritis is a dreadful complication.
10
There are other less habitual forms, called bullous impetigo, exclusively
of staphylococcal origin. Clinical presentation involves the presence of
blisters and erosions on the aected skin, as a consequence of the epidermolytic toxins that these bacteria contain. Impetigo is treated with
topical mupirocin, penicillin or oral fusidic acid.
De rm ato l ogy
Cellulitis
Treatment
Cellulitis is an infection that aects deep dermis and subcutaneous cellular tissues, normally caused by streptococci (Streptococcus pyogenes
or of group A).
Treatment entails precocious surgical debridement. It is a surgical emergency. In addition to surgery, broad-spectrum antibiotherapy will be
needed.
Folliculitis
Folliculitis is an infection and inflammation of one or several follicles
caused mainly by staphylococci.
Clinical Presentation
Clinical Presentation
Folliculitis shows pustules with follicular distribution.
Cellulitis presents with erythematous plaques that are ill-defined, painful and hot. It is usually accompanied with fever and chills.
Diagnosis
Diagnosis is clinical. If there is an open door, a culture of this area may
help see the source germ and resistance to antibiotics.
It is important to rule out abscesses, osteomyelitis and necrotizing fasciitis.
If bacteremia is suspected, blood cultures need to be performed.
Characteristics of Folliculitis
1. Hot tub or swimming pool folliculitis: caused by Pseudomonas aeruginosa.
2. HIV associated pruritic folliculitis or eosinophilic folliculitis.
Treatment
Treatment
Treatment implies oral antibiotics for 7-10 days to cover Gram positive
cocci. They are intravenously administered in case of lack of response
to oral treatment, involvement of hands or periorbital zone, diabetes or
extremes of age.
Necrotizing Fasciitis
Necrotizing fasciitis is a deep infection up to muscular fascia that produces very intense pain and subsequent anesthesia.
In 10% of the cases, cellulitis is due to an infection by S. pyogenes. In the
remaining cases, it occurs by a polymicrobial infection caused by aerobes
and anaerobes, including S. aureus, E. coli and Clostridium perfringens.
Acne Vulgaris
Acne is an inflammatory disease of the pilosebaceous follicle, as a consequence of an alteration in follicular keratinization. It aects adolescents and young adults.
Clinical Presentation
Clinical presentation involves pain of sudden onset and edema on the
aected zone. Pain may progress to anesthesia. There appears subsequent erythema that progresses rapidly into necrosis.
Characteristic clinical signs are tissue necrosis, blisters, intense pain
and gas production.
Diagnosis
Diagnosis is clinical and requires image testing, X-rays or a computed
tomography CT.
A biopsy of the border of the lesion helps achieve diagnosis.
Etiology is multifactorial: alteration of keratinization of follicular infundibulum, quantitative and qualitative alteration of sebum production in
the sebaceous gland, and alterations of bacterial microflora (increase in
quantity of P. acnes).
Aggravating factors are stress, androgenic oral contraceptives, and the
use of cosmetic products that are not oil-free.
Clinical Presentation
A comedo is the initial lesion, which can be closed (whitehead) or open
(blackhead) and it evolves into inflammatory lesions that listed in ascending order of severity are papules, pustules, nodules and cysts.
Lesions progress and leave scars. Scars can be increased if lesions are
manipulated.
11
Diagnosis is clinical.
Treatment
Diagnosis
Diagnosis
Treatment
Treatment is performed with topical azoles. Oral administration applies
for extensive cases or immunosuppressed patients. Dierential diagnosis includes pink pityriasis and eczemas (Figure 21).
Pilonidal Cysts
Pilonidal cysts are abscesses in the sacrococcygeal region.
This type of cysts has predominance in men between 20 and 40 years
of age. It is believed that repeated trauma on the aected area favors
their appearance.
Clinical Presentation
Pilonidal cysts present with an indurated lesion that is fluctuating, hot,
painful, but non-adherent to deep planes in the sacrococcygeal region.
Pilonidal cysts may or may not be associated to cellulitis and purulent drainage.
Diagnosis
Diagnosis is clinical and anal or perirectal abscesses should be dismissed.
Treatment
Treatment implies an incision and surgical drainage.
On some occasions, a general surgery is required.
12
De rm ato l ogy
Treatment
Oral Candidiasis: fluconazole or nystatin.
Candidiasis of the skin (intertrigo): apply topical antifungal medication
and keep zone clean and dry.
Dermatophytosis or Tineas
Candidiasis
The most common triggering agent is Candida albicans. It is normally saprophytic, although, under certain conditions, candidiasis may become pathogenic (immunosuppression, humidity, pregnancy and contraceptives).
Non inflammatory tineas do not produce irreversible scarring alopecia, while inflammatory forms do. Tineas are treated with azoles derivatives.
Candidiasis of nail fold is usually associated with periungual inflammation (perionixis) and initial proximal aectation, which dierentiates it from tinea unguium (Figure 22).
Clinical Forms
Intertrigo: erythematous plaque in cutaneous folds. Atrophy and
fissures are typically deep in the skin fold, as well as satellite and
peripheral lesions (papules and/or pustules).
Mucosa involvement may cause diverse symptomatology, like vulvovaginitis, glossitis, and white papules in the anterior region of the
oral mucosa. Candidal balanitis is characterized by the presence of
punctiform erosions and pustules on gland and balanopreputial
sulcus. Candidal balanitis often appears after sexual intercourse or
after oral antibiotic intake.
Remember
Almost a 100% of HIV patients suffer from muguet throughout their disease
course.
13
Diagnosis
Diagnosis is clinical and by direct visualization.
Treatment
Pediculosis is treated with malathion, lindane or topical permethrin.
Scabies
Scabies is originated by an acarus known as Sarcoptes scabiei. It has an
incubation period of 1 month.
Clinical Presentation
Figure 25. Ringworm of the groin (tinea cruris)
Tinea unguium: subungual
hyperkeratosis with onycholysis, but without perionixis
(Figure 26).
Diagnosis
Clinical diagnosis is reached after
performing a culture.
Treatment
Treatment involves topical antifungal medication in localized
areas.
Scabies produces generalized pruritus, more intense at night. The patient usually catches the infestation, which is passed to the patients
relatives. It is common to find that a recent trip to a tropical country has
been made. Lesions appear between the fingers (Figure 27), in wrists,
feet, genitalia, mammary areola and axilla, but back and face are usually spared. The most specific lesion is the acarine burrow, in whose less
scaly end, the advancing zone, the mite lies. Nodules are frequent in
axilla and genitals (nodular scabies).
Norwegian scabies is typical of the immunosuppressed. Patients
present with generalized hyperkeratosis and scabs. Norwegian scabies produce little pruritus, but it is very contagious because there
are many acari.
Nodular scabies involves the persistence of pruritic nodules despite
treatment. Lesions usually appear in axilla and genitalia. Pruritus is
due to a hypersensitivity phenomenon because of the acarus, already dead. Nodular scabies is treated with corticoids.
Clinical Presentation
Figure 27. Scabies. Acarine burrow
Pediculosis capitis: intense pruritus predominant in retroauricular and
occipital regions, occasionally with excoriations and impetiginization
secondary to excoriations.
Pediculosis corporis: intense pruritus in patients with poor hygiene or
who live in overcrowded conditions.
Pediculosis pubis: genital and pubic pruritus. Brownish-grey macules,
called maculae ceruleae, are typical on underwear and skin. These pig-
14
Treatment
Permethrin cream at 5% is the treatment of choice. It is little toxic,
so it can be used in children and pregnant women.
Topical lindane at 1% irritates and is neurotoxic; therefore, it is contraindicated in pregnant women and children.
Oral ivermectin is utilized in cases of resistance to prior treatments.
There is still little experience as to its use, but in a first instance, a
De rm ato l ogy
4.6. Miscellaneous
Acanthosis Nigricans
4.5. Ischemia
Decubitus Ulcers
Decubitus ulcers are the result of ischemic necrosis by continuous pressure on an area, which restricts microcirculation in that zone.
Clinical Presentation
Decubitus ulcers are present in patients in bed with scarce mobilization.
It is favored by bone prominences and lack of fat tissue. If sensitivity
decreases, there is more risk of formation of decubitus ulcers.
Diagnosis
Diagnosis is achieved based on medical records and clinical presentation.
Treatment
Prevention is of the utmost importance as well as frequent mobilization of the patient in bed.
Once ulcers have been established, hydrocolloid dressings are used for
healing, but sometimes, surgical debridement is necessary.
Gangrene
Lichen Planus
Lichen planus is an inflammatory, idiopathic disease that equally aects
both genders, with higher frequency in middle age.
Lichen planus has been related to diverse drugs, like gold salts,
anti-malarial medication and thiazides. It has been also linked to
hepatitis C virus infection; however, this association is currently
doubtful.
Clinical Presentation
Clinical Presentation
Dry gangrene is due to ischemia, generally secondary to atherosclerosis. Clinical presentation involves pain, cold, and paleness of extremities. Once tissue is established, it turns bluish-black in color and dry.
Wet gangrene is owing to bacterial flora. Tissue presents with an edematous appearance, either with blisters or pus.
Gas gangrene caused by C. perfringens. It is normally located on recent surgery. Bacteria precociously destroy tissue, producing gas. It is a
medical emergency.
Diagnosis
Clinical diagnosis is obtained by microbiological culture.
Treatment
Treatment requires surgical debridement, with amputation if necessary,
and association of broad spectrum antibiotherapy.
Figure 29. Lichen planus of oral mucosa with typical whitish
Gas gangrene is treated with hyperbaric oxygen.
reticulate
15
Clinical Presentation
Violaceous papules
with white stretch marks
Lichenoid lymphocyte
infiltrate (band formation)
Destruction
of basal layer
Treatment
Mild forms are treated with topical corticoids.
Severe cases require oral corticoids, psoralens plus ultraviolet light of
the A wavelength (PUVA) or cyclosporine.
Rosacea
Rosacea is a chronic disease of unknown pathogenesis, characterized
by erythema and acneiform lesions on the face. It aects middle aged
women (between 30 and 50 years of age) more.
Rosacea etiopathogenesis is unknown, although there is involvement of
vasomotor lability, infection by Demodex folliculorum, photo exposure
and genetic predisposition.
Clinical Presentation
Diagnosis and Treatment
Rosacea symptomatology comprises facial flushing episodes that end
up by provoking a persistent erythema, telangiectasias and papulopustular lesions without comedos. Over time, ocular lesions and hyperplasia of soft tissue may develop.
Treatment
Vitiligo
Clinical Presentation
Moderate cases need doxycycline or oral minocyclines.
Severe cases are treated with oral isotretinoin at low doses.
Pink Pityriasis
Gilberts pink pityriasis is an acute self-limiting dermatosis, which mainly aects young adults. It is of unknown origin; although a viral etiology
is suspected (there is some speculation as to links with human herpesvirus type 7).
16
De rm ato l ogy
Treatment
Diagnosis
Diagnosis is clinical.
Treatment
Epidermoid Carcinoma
Epidermoid carcinoma is the second most frequent cutaneous tumor.
Solar photo exposure is the main etiological factor, which is why epidermoid carcinoma appears in zones of prolonged solar exposure, like the
face. Most carcinomas appear over premalignant lesions (actinic keratosis and leukoplakia, among others).
Clinical Presentation
Clinical presentation reveals erythematous or erythematosquamous
plaques. Over time, these plaques form papules and tumors, which often become ulcerative and bleed.
Figure 32. Vitiligo
Diagnosis
Diagnosis is based on clinical suspicion and histopathological confirmation.
4.7. Neoplasias
Seborrheic Keratosis
Seborrheic keratosis is the most frequent benign tumor in human beings, since it is part of cutaneous aging.
Clinical Presentation
Seborrheic keratosis presents with hyperkeratosic papules with an oily
or velvet-like texture, crests, fissures and horny plugs on their surface.
These papules are normally pigmented, showing a brownish-black color.
Treatment
Surgery with safety margins is the treatment of choice. In carcinomas
in situ, cryotherapy can be used, as well as topical imiquimod, electrocoagulation or CO2 laser techniques in destruction of tumors. Radiotherapy may also be used in some cases.
Treatment
Gorlins syndrome should be considered if multiple basal cellular carcinomas are found in non photo exposed areas.
Clinical Presentation
Basal cell carcinoma shows a pearly pink papule and superficial telangiectasias.
Actinic keratosis
Clinical Presentation
Actinic keratosis is characterized by erythematous and desquamative
papules, which are hyperkeratosic and rough on touch, developing a
chronic course.
Treatment
Surgery is the treatment of choice. Mohs surgery is performed in zones
where surrounding healthy tissue needs to be preserved. Other alternatives are cryotherapy, imiquimod, electrocoagulation, radiotherapy,
photodynamic therapy and intralesional interferon. Prognosis is excellent, as growth is slow and metastasis, exceptional.
17
Melanoma
Melanoma is the most aggressive cutaneous tumor, given its ability to
metastasize.
Risk factors comprise solar photo exposure, clear phototype, the presence of dysplastic nevus or a high number of melanocytic nevi. Family history is quite important, as some genetic mutations determine a
higher risk of developing the disease.
In situ
Extirpation 0.5 cm
Follow-up
Breslow < 1 mm
Extirpation 1 cm
Follow-up
Breslow 1 mm
Extirpation 2 cm
Sentinel ganglion
+
Lymphadenectomy
Interferon
Breslow > 4 mm
Clinical Forms
Figure 34. Melanoma treatment
See Figure 33.
Diagnosis
Kaposis sarcoma
The ABCDE criteria can help patients to see if they need to seek medical
consultation (asymmetry of lesion, uneven borders, color, and diameter
greater than 6 mm or abnormal evolution).
Clinical presentation
Treatment
The base of treatment is precocious surgical extirpation. If the Breslow
index is less than 1 mm, margins of 1 cm will be performed. If Breslow
index is greater than 1 mm, margins will be of 2 cm.
For melanomas with a Breslow index greater than 1 mm, the sentinel
ganglion must be located. This is the first draining lymph node of the
territory where the tumor is localized. If the ganglion is positive, regional lymphadenectomy will be performed along with interferon administration (Figure 34).
The elderly
Unilateral plaques
(lower extremities)
Not so frequent
Not so precocious
10%
70%
Elderly women
Young women
90% on face/photoexposed
zones of aging skins
(chronic exposure)
Better prognosis
Worst histological prognosis
Nodular melanoma
More frequent
Acral lentinginous melanoma
15%
Middle-aged men
Elderly men
On healthy skin
Any zone
Sudden onset
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CLASSIC KAPOSIS
De rm ato l ogy
Diagnosis
Diagnosis relies on clinical suspicion and histopathological confirmation.
Treatment
In more advanced stages of the disease, there is aectation of extracutaneous organs, such as lymph nodes, liver, spleen, lungs and bone
marrow. Besides, there may be blastic transformation. Other possible
complication is sepsis by Staphylococcus aureus.
These three stages usually develop consecutively; nevertheless, there
may patients whose debut starts directly with the tumoral stage.
Treatment of localized forms can include surgical extirpation, radiotherapy or intralesional vinblastine.
If the sarcoma is disseminated, options involve interferon or chemotherapy.
Mycosis Fungoides
Mycosis fungoides is a T-cell lymphoma of low-grade malignancy. Its
clinical course may be very slow and surpass 50 years. Three stages are
clinically dierentiated.
1. Eczematous or macular phase: predominantly truncular erythematous macules with years of evolution. They resemble a chromic eczema. Histology is unspecific at this stage.
2. Infiltrative plaque phase: infiltrated erythematous plaques appear.
Histology is diagnostic at this stage. A dermal infiltrate of atypical
lymphocytes band forms can be observed, composed of CD+4 T
lymphocytes with cerebriform nuclei. There is a marked epidermotropism with the presence of clusters of intraepidermal lymphocytes, called Pautriers microabscesses (Figure 35).
Remember
Microabscesses of mycosis fungoides are due to lymphocytes and are called
Pautriers abscesses. Psoriasis microabscesses result from neutrophils and
are labeled as Munro-Sabouraud.
Szary Syndrome
Szary syndrome can be considered as the leukemic phase of T-cell cutaneous lymphoma. It is defined by the triad: erythroderma (Figure 36,
lymphadenopathies and the existence of more than 1,000 Szary cells
per milliliter in peripheral blood. Szary cells are atypical T- lymphocyte
with cerebriform nuclei.
Very intense pruritus is characteristic. For many authors, Szary syndrome is an aggressive clinical form and a bad prognosis of a mycosis
fungoides.
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