Derm
H&P, DX, Health Maintenance, Clinical TX, Scientific concepts
Dermatitis (Eczema)
Types: Contact, Atopic, Stasis, Lichen simplex chronicus, and Seborrheic Dermatitis
 A common probrom that causes the skiin to become inflamed.
Childhood stage is characterized by less exudation and often demonstrates lichenified
plaques in a flexural distribution, especially of the antecubital and popliteal fossae, volar
aspect of the wrists, ankles, and neck
Adult stage of atopic dermatitis is considerably more localized and lichenified and has a
similar distribution to the childhood stage, or may be primarily located on the hands and feet
Dermatitis (Seborrhea):
Superficial inflammation involving
hairy regions of the body
Diagnosis: In addition to itchy skin, three or more of the following are needed to make the
diagnosis:
 History of skin creases being involved. These include: antecubital fossae, popliteal
fossae, neck, areas around eyes, fronts of ankles.
 The presence of generally dry skin within the past year.
 Symptoms beginning in a child before the age of two years. This criterion is not used
to make the diagnosis in a child who is under four years old.
 Visible evidence of dermatitis involving flexural surfaces. For children under four
years old, this criterion is met by dermatitis affecting the cheeks or forehead and
outer aspects of the extremities.
 Laboratory testing, including IgE levels, is not used routinely in the evaluation of
patients with suspected atopic dermatitis and is not currently recommended
Treatment:
 The Goal is to reduce symptoms (pruritis and dermatitis), prevent exacerbations, and
minimize therapeutic risks
 Pt with MILD eczema: Low potency corticosteroid cream or ointment (Desonide
0.05% or hydrocortison 2.5%)
 Pt with MODERATE eczema: Medium to high potency
steroid: fluocinolone 0.025%, triamcinolone 0.1%, betamethasone dipropionate
0.05%)
 Pt with SEVERE disease: Phototherapy is usually administered three times per week.
Topical corticosteroids can be continued as needed during photoherapy.
Phototherapy is not suitable for infants and young children.
o In adults can use oral cyclosporine in short-term treatment: give 3-5mg/kg
perday in two divided doses for six weeks.
 Use Antihistamines for sedation and to control the itching
 If infection sets in ususally is S. aureus and treatment includes Mupirocin 2% cream
applied twice a day for 1-2 weeks
Health Maintenance:
 Elimination of exacerbating factors: Exacerbating factors in atopic dermatitis that
disrupt an abnormal epidermal barrier include excessive bathing without
subsequent moisturization, low humidity environments, emotional stress, xerosis
(dry skin), overheating of skin, and exposure to solvents and detergents
 If contact allergens cause the dermitis avoid those such as nickel and some
frqgrances)
 To maintain skin hydration, emollients should be applied at least two times per day
and immediately after bathing or hand-washing.
Seborrheic dermatitis: first appear soon after puberty or later in life. It is usually
characterized by well demarcated erythematous plaques with greasy-looking, yellowish
scales distributed on areas rich in sebaceous glands such as the scalp, the external ear, the
•
Reaction to Pityrosporum
ovale (yeast)
Nummular Eczema:
coin-shaped scaly lesions show
evidence of postinflammatory
hyperpigmentation.
center of the face, the upper part of the trunk, and the intertriginous areas
 In pt with HIV it tends to be more extensive and severe and difficult to control
 In infants it is called Cradle Cap
Clinical Course:
 It is chronic, and tends to worsen with stress and during the cold and dry winter
months.
Diagnosis: Usually made clinically based on the appearance and location of the lesions
 DDX: Psoriasis is the main condition that it can be confused with. Rosacea commonly
targets the face and can sometimes coexist with it.
Treatment/Management:
 Topical corticosteroids and topical antifungal agents were effective in treating the
acute phase of seborrheic dermatitis, and intermittent use of topical antifungals
prevented relapse
 On the scalp: Antifungal shampoos include selenium sulfide 2.5%, ketoconazole2%,
or ciclopirox 1% shampoo.
 On the Trunk and intertriginous areas: topical corticosteroid creams, topical
antifungal agents, or a combination of the two.
 For Severe or refractory seborrheic dermatitis: oral itraconazole (200 mg/day orally
for one week) was associated with improvement in erythema, scaling, and itching
Common but the cause remains unknown.
Clinical Manifestations: consists of intensely pruritic patches of eczematous dermatitis, each
showing evidence of papules, scaling, slight crusting, and some serous oozing on close
inspection. They can itch and burn and the symptoms may be worse at night
 Lesions are usually on the trunk and lower extremities, and the head is generally
spared. The onset is usually spontaneous, and inciting events often cannot be
identified, although some patients may have exposures to drying or irritating
substances (eg, excessive water exposure, chlorine, soaps)
Diagnosis: Clinical--> Each lesion tends to be circular, measuring 2 to 10 cm in diameter. Pt
may have 1-50 lesions
Treatment:
 A potent topical steroid in an emollient base is the treatment of choice. Systemic
steroids in short courses are occasionally required, and some clinicians add systemic
antibiotics in severe cases. It may be helpful to avoid irritants, if they can be
identified.

Dyshidrosis
N
Skin moisturization is an important part of the management of nummular dermatitis;
an emollient should be used generously and applied immediately after bathing
Clinical Manifestation: "Tapioca-looking" vesicles of 1-2mm on the palms, soles, and sides of
fingers associated with pruritis. Later the vesicles dry and area becomes scaly and fissured or
large bullae which result from coalescence of vesicles.
 Frequent relapses may result in chronic hand dermatitis, characterized by red,
lichenified, and scaling patches or plaques with fissures. Severe episodes can affect
the nail matrix and produce dystrophic nail changes such as horizontal ridging and
color changes
Diagnosis: Made from clinical findings and history:
 Tense, deep-seated vesicles or bullae localized on the palms and soles and often on
the lateral aspect of the fingers
 Intense pruritus
 Acute onset
 History of recurrence
 Many Dermatologist perform patch testing to determine if the diagnosis is
Dyshidrosis or contact dermatitis
Lichen simplex chronicus aka:
Neurodermatitis
Lichenified plaques within reach of
fingers
Lichen planus
Koebner phenomenon: Linear
scratch marks on anterior wrists,
penis or legs
Management:
 ID and avoid causative or exacerbating factors, treatment of skin inflammation
 First try general skin care which is aimed at reducing skin irritation and restoring the
skin: Use lukewarm water and soap-free cleansers to wash hands.
 Applying emollients (eg, petroleum jelly) immediately after hand drying and as
often as possible
 Wearing cotton gloves under vinyl or other nonlatex gloves when performing
wet work
 Removing rings and watches and bracelets before wet work
 Wearing protective gloves in cold weather
 Wearing task-specific gloves for frictional exposures (eg, gardening, carpentry)
 Avoiding exposure to irritants (eg, detergents, solvents, hair lotions or dyes,
acidic foods [eg, citrus fruit])
Treatment: For pt who dont respond to the above
 Topical coricosteroid ointment: apply twice daily for two to four weeks
 Severe disease: Systemic corticosteroids-->perdnisone 40-60mg QD for one week
 Refractory disease: phototherapy with oral or topical PUVA for patients with
confirmed diagnosis of dyshidrotic eczema who have frequent or severe episodes
that are not adequately controlled with topical or systemic corticosteroids or
topical tacrolimus
A skin condition caused by chronic itching and scratching. Common in children who cannot
stop scratching insect bites or other itchy skin conditions
Causes: May occur in those who have:
 Skin allergies, Eczema, psoriasis, Nervousness, anxiety, depression
Symptoms:
 Itching of the skin
 Skin lesions: plaque or patch, commonly found on the ankle, wrist, neck,
rectum/anal, forearms, thighs, lower leg, back of knee, inner elbow.
Diagnosis:
 Based on history and clinical DX of chronic itching and scratching.
Treatment:
 Counseling to help the patient stop scratching, stress management and behavioral
modification
 Antihistamines or sedatives to help with the prutitis
Complications: Scarring, hypo/hyper pigmentation or skin infection
Lichen planus is a mucocutaneous disorder that most commonly affects middle-aged adults.
Clinical Manifestations: The classic presentation of cutaneous lichen planus is a
papulosquamous eruption characterized by the development of flat-topped, violaceous
papules on the skin
 Described as the four P:
o Pruritic, Purple, Polygonal, Papules or Plaques
 May affect the skin, mucous membranes (especially the oral mucosa), scalp, nails,
and genitalia -->lacy or erosive lesions of the buccal and vaginal mucosa; nail
dystrophy
 Cutaneous lichen planus often spontaneously resolves after one to two years. Oral,
genital, scalp, and nail lichen planus tend to be more chronic.
Diagnosis: Based on the recognition of consistent clinical findings. A skin Biopsy can be used
to confirm a diagnosis (punch or shave which reaches the depth of mid-dermis)
Clinical Evaluation:
 Patients should be questioned about medications (drugs that may induce lichen
planus)
o ACEi (captopril, enalapril) B-Blockers (labetalol, propranolol, sotalol),
Thiazide diuretics, Gold salts, Penicillamine, methyldopa, quinidine,
Omeprazole, pravastatin, simvastatin
 Pruritus (a common symptom of cutaneous lichen planus),
 Oral or genital erosions or pain (findings suggestive of concomitant mucosal lichen
planus)
 Dysphagia or odynophagia (findings suggestive of esophageal disease). We also
typically inquire about risk factors for hepatitis C.
Treatment:
 First line: Topical corticosteroids for those with localized disease those with
generalized disease often systemic therapy or phototherapy or oral acitretin (oral
retinoids) is first line and topical corticosteroids are used as second line.
o 0.05% betamethasone dipropionate, 0.05%diflorasone diacetate
 Other treatments:
o Oral antihistamines (eg, hydroxyzinehydrochloride 10 to 50 mg four times a
day, as necessary) may be helpful in controlling pruritus
Variants of Cutaneous Lichen Planus:
Hypertrophic lichen planus – Hypertrophic lichen
planus is characterized by the development of
intensely pruritic, flat-topped plaques. The typical
site of involvement is the anterior lower legs. Of
note, the occasional development of cutaneous
squamous cell carcinoma has been reported in
patients with longstanding hypertrophic lichen
planus lesions
Annular lichen planus – Annular lichen planus is
characterized by the development of violaceous
plaques with central clearing Although the penis,
scrotum, and intertriginous areas are common
sites of involvement, annular lesions may occur in
other areas Central atrophy may be present.
Bullous lichen planus – Patients with bullous lichen planus develop vesicles or bullae
within the sites of existing cutaneous lichen planus lesions. The legs are a common site
of lesion development
Actinic lichen planus – Actinic lichen planus (also known as lichen planus tropicus)
presents with a photodistributed eruption of hyperpigmented macules, annular
papules, or plaques This variant is most commonly seen in the Middle East, India, and
east Africa
Lichen planus pigmentosus – Lichen planus pigmentosus presents with gray-brown or
dark brown macules or patches that are most commonly found in sun-exposed or
flexural areas [27]. Pruritus is minimal or absent. The term “lichen planus pigmentosusinversus” is used to describe patients with primarily flexural involvement
Inverse lichen planus – Inverse lichen planus is
characterized by erythematous to violaceous
papules and plaques in intertriginous sites, such
as the axillae, inguinal creases, inframammary
area, or limb flexures Associated
hyperpigmentation is common. Scale and
erosions may be present.
Atrophic lichen planus – Atrophic lichen planus presents with violaceous, round or oval,
atrophic plaques. The legs are a common site of involvement and lesions often clinically
resemble extragenital lichen sclerosus. A rare annular atrophic variant of lichen planus
characterized by violaceous papules that enlarge peripherally leaving an atrophic center
that demonstrates complete loss of elastic fibers on pathology has also been reported
Lichen planopilaris (follicular lichen planus) – The scalp is the classic site for lichen
planopilaris. However, follicular involvement manifesting as follicular papules may be
observed in other body sites, particularly in patients with the Graham-Little-PiccardiLasseur syndrome.
Pityriasis Roasea:
An acute, self-limited, exanthematous skin disease characterized by the appearance of
slightly inflammatory, oval, papulosquamous lesions on the trunk and proximal areas of the
extremities
Etiology: Viral Etiology-->sometimes preceded by a prodrome
Clinical Features; Disease of older children and young adults. More common in women
 Prodrome of headache, malaise, and pharyngitis may occur in a small number of
cases, but except for itching, the condition is usually asymptomatic.
 In 50 to 90 percent of cases, the eruption begins with a "herald" or "mother" patch, a
single round or oval, sharply delimited, pink or salmon-colored lesion on the chest,
neck, or back
 The eruption spreads centrifugally or from the top down over the course of a few
days. Erythema gradually subsides, desquamation is completed, and the eruption
fades, leaving little residual changes, except occasional mild post-inflammatory
changes in light-skinned individuals. Most cases are clear in four to six weeks;
occasionally the disease will persist for several months. PR generally has only mild
effects on quality of life, at least in children
Diagnosis:
 Presence of herald patch by history or on exam and the absence of pruritus
 Herald patches can resemble tinea corporis so KOH can distinguish the two.
Treatment: No treatment other than reassurance and pt education.
 For patient with mild itching and who want therapy use a medium potency topical
corticosteroid
 Severe itching and those who desire rapid resolution of the rash for cosmetic
reasons treat with oral acyclovir 400mg 5x a day for 1 week.
Psoriasis
Common benign, chronic inflammatory skin disease with both genetic basis and known
environmental triggers.
Can begin at any age the peak times are ages 20-30 and 50-69.
Clinical findings:
 Silvery scales on bright red, well-demaracted plaques, usually on the knees, elbows
and scalp-->Favored sites: scalp, elbows, knees, palms, soles, sacral, intergluteal fold
and nails.
 Koebner phenomenon-->injury or irritation of normal skin tends to induce lesions of
psoriasis at the site.
 Nail findings including pitting and oncycholysis (separation of the mail plate from the
bed)
 Mild Itching
 May be associated with psoriatic arthritis-->found in the DIP joints
Diagnosis:
 Most of the time DX can be made by H&P but a skin biopsy is performed to r/o other
DZ.
Treatment: Numerous topical and systemic therapies are available.

Erythema Multiforme
Psychosocial aspects: Frustrating disease so many patients may benefit from
counseling and or treatment psychoactive meds
 Pt with small plaques: phototherapy is the best.
 Scalp: start with tar shampoo and use daily unless thick scale then use 6% salicylic
acid gel
 Mild disease: Calcipotriene ointment 0.005% or calcitroil ointment 0.003%, both
vitamin D analogs, are used BID. (cant use calcipotriene on face or groin)
o For facial or intertriginous areas, topical tacrolimus or pimecrolimus may be
used as alternatives or as corticosteroid sparing agents, though
improvement may not be as rapid. Localized phototherapy is another option
for recalcitrant disease.
 Moderate disease: Affecting 10-30% BSA
o Use UV phototherapy and a systemic agent like Calcipotriene and
betamethasone dipropionate
 Severe disease: Requires phototherapy or systemic therapies such as
retinoids, methotrexate, cyclosporine, or biologic immune modifying agents. Biologic
agents used in the treatment of psoriasis include the anti-TNF
agents adalimumab,etanercept, and infliximab and the anti-IL12/23 antibodyustekinumab. Improvement usually occurs within weeks. (usually
needs referral to dermatologist)
Health maintenance:
 Increased risk for metabolic syndrome and lymphoma
 Comorbid disease in psoriasis:
o CKD, Atherosclerotic disease, COPD and nonalcoholic fatty liver disease, IBD
 Exacerbating factors:
o Drugs: BB, Lithium, and antimalarial drugs. Others which can worsen include
ACEi, NSAIDS and terbinafine.
o Even small doses of systemic corticosteroids may lead to severe rebound
flares
o Infections: bacterial and viral
Prognosis: Chronic and unpredictable. Be sure to monitor pt over 40yo from metabolic
syndrome which will correlate with the severity of their skin disease.
Acute, immune-mediated condition characterized by the appearance of distinctive target-like
lesions on the skin. These lesions are often accompanied by erosions or bullae involving the
oral, genital, and/or ocular mucosae.
Etiology: Infection, medications, malignancy, autoimmune disease, immunization, radiation,
sarcoidosis, and menstruation have been linked to the development of EM.
 HSV is the most common cause of EM minor
 Drugs are the most common cause of EM major in aduts
Clinical Manifestations:
 Apperance: Target lesions consist of three components: a dusky central area or
blister, a dark red inflammatory zone surrounded by a pale ring of edema and an
erythematous halo on the extreme periphery of the lesion
 Distribution: extensor surfaces of the acral extremities, and subsequently spread in a
centripetal manner. The face, neck, palms, soles, flexural surfaces of the
extremities, and/or trunk may also be involved
 Usually asymptomatic, some patients may experience itching and burning
 Systemic symptoms: Prodromal symptoms (eg, fever, malaise, myalgias) are
uncommon in mild cases of EM but can be seen in cases with significant mucosal
involvement. Cough and respiratory symptoms may be present in patients with EM
related to M. pneumoniae infection
 Course: Appear over 3-5 days and resolve w/in two weeks and the skin lesions do
Steven- Johnson syndrome:
Toxic epidermal necrolysis (TEN)
not scar
Diagnosis:
 The history of the eruption and clinical findings provide the most important
information for the diagnosis of erythema multiforme (EM). Patients should be asked
about signs or symptoms of HSV, M. pneumoniae, or other infections, as well as new
medications and systemic symptoms
 Lab studies: In severe cases, elevations of the erythrocyte sedimentation rate, white
blood cell count, and liver enzymes may be detected
 Biopsy: Pathologic findings in EM typically include basal cell vacuolar degeneration,
scattered necrotic keratinocytes, and lymphocyte exocytosis
Treatment: Varies according to disease severity
 Goals targeted toward reducing pain or pruitis in mild disease
 Approx. 90% are triggered by infection so need to treat the inciting infection
 Mild disease: Topical corticosteroids and oral antihistamines used in pt with itching
and burning. Painful oral erosion treat with a high potency topical corticosteroid gel
and mouthwashes that contain a mixture of lidocaine, diphenhydramine, and
antacids
 Severe oral mucosal involvement: Prednisone 40-60mg/day tapered over 2-4 wks
 Ocular involvement may lead to keratitis, conjunctival scaring or visual impairment
Skin detachment is <10 percent of the body surface (picture 1A-C). Mucous membranes are
affected in over 90 percent of patients, usually at two or more distinct sites (ocular, oral, and
genital)
Etiology: An immunologic mechanism or Maybe drugs may induce fixed drug eruptions:
 Antibacterial agents (trimethoprim-sulfamethoxazole, tetracyclines, penicillins,
quinolones, dapsone)
 NSAIDs (acetylsalicylic acid, ibuprofen, naproxen, mefenamic acid)
 Acetaminophen (paracetamol)
 Barbiturates
 Antimalarials
Clinical manifestation:
 Presents with well demarcated round to oval, dusky red tobrown/black macules that
may evolve into edematous plaques with or without vesiculation or blistering Lesions
are usually solitary, buy may occur in small groups.
Diagnosis:
 Clinical: History of drug intake in the hours or days preceding the eruption. Usually
straightforward, based upon lesion morphology and history.
o Single or a small number of round or oval, demarcated, erythematous or
hyperpigmented macules or plaques located most often on the lips,
genitalia, and extremities
 Biopsy: Should be done if the patient has fever or malaise and when the dx is
uncertain
 Patch testing can also be used to confirm the dx.
Treatment: Drug withdrawl and avoidance of the offending agent.
 Symptomatic treatment of the acute eruption may include medium to high potency
topical corticosteroids (pednisone 0.5-1mg/kg per day for 3-5 days) and systemic
antihistamines (diphendramine or hydroxyzine).
Toxic epidermal necrolysis (TEN) is a potentially life-threatening dermatologic disorder
characterized by widespread erythema, necrosis, and bullous detachment of the epidermis
and mucous membranes, resulting in exfoliation and possible sepsis and/or death (see the
image below). Mucous membrane involvement can result in gastrointestinal hemorrhage,
respiratory failure, ocular abnormalities, and genitourinary complications.

TEN involves detachment of >30 percent of the body surface area. Mucous
membranes are involved in the majority of cases.
Drugs associated with TEN:
 Antibacterial drugs: Sulfonamides (4.5 cases per million users per week),
Chloramphenicol, Macrolides (eg, erythromycin), Penicillins and Quinolones (eg,
ciprofloxacin, trovafloxacin )
 Anticonvulsants: Phenobarbital, Phenytoin Carbamazepine, Valproic acid and
Lamotrigine
 NSAIDs: Oxicams (eg, piroxicam, tenoxicam) - Implicated more often than other
NSAIDs, Ibuprofen, Indomethacin, Sulindac, and Tolmetin
Bullous pemphigoid
Erysipelas
Presentation: Flu like prodrome: Malaise, Rash, Fever, Cough, Arthralgia, Myalgia, rhinitis,
HA, anorexia and N/V w/ or w/o diarrhea
Diagnosis: Pathologic analysis of the skin lesion. Necrotic keratinocytes with full-thickness
epithelial necrosis and detachement is consistent with the diagnosis of TEN. Perivascular and
scattered lymphocytic infiltration of dermis.
 Order CBC-->leukopenia
 ESR-> elevated
Treatment: Must have prompt recognition of the disorder
 Supportive care with fluid and electrolyte balance, nutritional support, pain
management and protective dressing
 Since pt tend to lose their epidermis need to treat with ABX to protect S.aureus
 Antihistamines may be used when reepithelialization begins
 Heparin is indicated for prophylaxis of thromboembolic events
 Analgesic are needed because treatment is much like a second-degree burn-->use
morphine sulfate or fentnyl or demerol
A benign prutitic disease characterized by tense blisters in flexural areas, usually remitting in
5-6 years with a course characterized by exacerbation and remission.
 Most persons affected are over the age of 60 and men 2x more then women.
Clinical manifestations:
 The appearance of blisters may be preceded by urticarial or edematous lesions for
the month.
 Oral lesion are present in 1/3 of those affected.
Diagnosis: Made by biopsy and direct immunofluorescence exam. Light microscopy shows a
subepidermal blister.
Treatment: Goal: decrease blister formation and pruritis and promote healing of blisters and
erosions
 Mild disease: Prednisone 0.75mg/kg daily is often used to achieve rapid control.
Tetracycline or erythromycin 500mg TID alone or in combo with nicotinamide can be
used but just slower in onset of action.
 Dapsone is effective in mucous membranes.
 Severe disease or if the above doesnt work: Methotrexate 5-25mg weekly, or
axathioprine, 50mg QD-TIB may be used as steroid sparing agents.
 Refractory cases: Mycophenolate mofetial (1g BID)
Pathogensis:
 The mechanisms that lead to bullous pemphigoid and MMP are not fully understood,
but most likely involve autoantibody-mediated damage to epithelial basement
membrane zone, a complex structure that mediates adhesion, permeability, and
cellular organization and differentiation
It is a superficial form of cellulitis that occurs classically on the cheek, caused by B-Hemolytic
strep
Clinical Manifestations:


Cellulitis:
Urticaria
Symptoms: pain, malaise, chills, and moderate fever.
Signs: Edematous, spreading, circumscribed, hot, erythemaough area w/ or w/o
vesicles or bullae. Central face is frequently involved.
 Labs: leukocytosis is almost invariably present and blood cultures may be positive
Complications: Unless promptly treated, death may resulf from extension of the process and
systemic toxicity, esp in the elderly.
Treatment:
 Place pt on bed rest with head of the bed elevated.
 IV ABX with cover B-hemolytic strep and staph in the first 48hr.
 A first generation cephalosporin 250mg orally four times a day or if PCN allergic,
clindamycin 250mg BID for 7-14 days
A diffuse spreading infection of the dermis and subcutanceous tissue, usually in lowerleg
 MC d/t gram-positive cocci like B-hemolytic strep and S. aureus
Clinical Manifestation:
 Edematous, expanding, erythematous, warm plaque w/ or w/o vesicles or bullae.
 Pain, chills and fever are commonly present. and Septicemia may develop
 Lab findings: leukocytosis or at least neutrophilia. Blood cultures may be postive.
 Culture to find out what bacteria is causing the break down.
Treatment:
 NonABX therapy: Elevation facilitates gravity drainage of edema and inflammatory
substances. The skin should be sufficiently hydrated to avoid dryness and cracking
without interdigital maceration.
 ABX: The approach to antibiotic selection for treatment of cellulitis depends on
whether the clinical presentation consists of purulent or nonpurulent cellulitis.
o Purulent: Empiric oral options: Clindamycin, Timethoprim-sulfamethoxazole,
Tetracyclin or Linezolid
o Non-purulent- Clindamycine, Amoxicillin or Lenezolid
Can result from many different stimuli on an immunologic or nonimmunologic basis. Most
come is IgE mediated.
 Most incidents are acute and self-limited over a period of 1-2 weeks.
 Chronic urticaria (episodes lasting >6 wks) may have an autoimmune basis.
 Special forms of urticaria have special features (dermatographism, cholinergic
uticaria, solar urticaria or cold urticaria)
Etiology: Common causes of new onset urticaria include infections, allergic reactions to
medications, foods, or insect stings and bites, reactions to medications that cause nonallergic
mast cell activation (eg, narcotics), and ingestion of nonsteroidal antiinflammatory
medications (NSAIDs)
Clinical Hx and PE:
 Were there other signs and symptoms of a generalized allergic reaction or
anaphylaxis? Patients may fail to report more subtle symptoms unless specifically
asked. The clinician should ask about chest tightness or difficulty breathing, hoarse
voice or throat tightness, nausea, vomiting, crampy abdominal pain,
lightheadedness, and other symptoms of anaphylaxis
 Did they ingest something new? Or exposed to something new, like a bug sting? Any
new medications? Any recent travel?
 Lesion should be visualized. Individual urticarial lesions usually appear and resolve
completely within 24 hours. If the patient is unsure of the duration of the lesions, a
lesion can be circled with a pen, and time to resolution noted
DX: Test for allergic causes with IgE antibodies skin test
Treatment: Initial should be focused on short-term relief of pruritus and angioedema if
present
 H1 antihistamines: diphenhydramine or hydroxyzine(1st generation) or Second
Acne Vulgaris
Rosacea:
generations which are preferred in children: Cetirizine or fexofenadine
 Brief course of Glucocorticoid: prednisone 30-60mg BID for 5-7 days in adults and
0.5-1mg/kg/day for children
 Local treatment is rarely rewarding so always treat systemically
The most common of all skin conditions
 Occurs at puberty, though onset may be delayed into the third or fourth decade.
 Open and closed comedones are the hallmark of acne vulgaris. But papules, pustules
and cysts are found as well.
 More common and more severe in males.
Clinical findings:
 Mild soreness, pain, or itching. The lesions occur mainly over the face, neck, upper
chest, back and shoulders.
 Severe: include inflammatory papules, pustules, ectatic pores, acne cysts and
scarring.
Complications: cyst formation, pigmentary changes in pigmented pts, severe scarring and
psychological problems may result.
Treatment:
 Education: avoid topical exposures to oils, cocoa butter and greases
 Diet: A low glycemic diet that results in weight loss has been reported to improve.
Treatment for Comedonal Acne:
 Topical Retinoids: Tretinoin very effective, start with 0.025% cream not gel and use
two nights a wk and build upto nightly.
 Benzoyl peroxide: 2.5%, 4% 5% 8% and 10% use with a water base to decrease
irritation
 ABX: used to decrease pustular and comedonal lesions
Treatment for Papular or cystic inflammatory acne:
 ABX are the mainstay for treatment! Oral or topically.
o Oral: tetracycline and doxycycline
 Mild: first choice is topical antibiotics: Clindamycin (Cleocin T) lotion (least irritating),
gel, or solution.
 Moderate: Tetracycline 500mg BID, Doxycycline 100mg BIDand start it in the evening
for 4-7 days.
o Always discuss contraceptives with women in child bearing age groups.
 Severe: Isotretinoin: A vitamin A analog which is used for the severe cystic acne->0.5-1mg/kg/d for 20 wks.
o Depression and hypertriglyceridemia, and hypercholesterolemia has been
reported so monitor your patients. Fasting blood sugars may also be
elevated.
o Intralesional injections can be done with triamcinolone acetonide
(2.5mg/mL, 0.05mL per lesion) will often hasten the resoultion of deeper
papules and occasional cysts.
o Laser dermabrasion can be done to improve cosmetic outcome.
Prognosis: eventually remits spontaneously but can persist throughout adulthood.
The pathogenesis is unknown. Topical corticosteroids applied to the lower face can induce
rosacea-like conditions
 Chronic facial disorder.
 A neurvascular component (erythema and telangiectasis and a tendency to fulsh
easily)
 A acneiform component (papules and pustules) may also be present.
 A glandular component accompanied by hyperplasia of the soft tissue of the nose
(rhinophyma)
Clinical findings:

Folliculitis
Impetigo:
Flushing or exacerbation of their rosacea d/t heat or cold, hot drinks, spicy food,
sunlight, exercise, EtOH, emotion or menopausal flushing.
 Involves: cheeks, nose, and chin and at sometimes the entire face.
 No comedones are seen
 Pt may have associated ophthalmic disease, including blepharitis and keratitis which
can require ABX therapy.
Treatment:
 Education: avoid the factos known to produce exacerbations. Wear broad spectrum
UVA sun screen.
 Local therapy: Metronidaxole creams or gel 0.75% BID or 1% QD topically. or
Clindamycin 1% BID. Response is noted w/in 4-8 wks
 Systemic therapy: Tetracycline 250 or 500mg PO BID on an empty stomach when
topical is inadequate.
 Isotretinoin may succeed if other medications fail. Dosage: 0.5mg/ke/day PO for 1228wks.
Etiology: Frequently caused by Staph infection but may also be caused by pseudomonas
aeruginosa (hot tubs), Klebsiella, enterobacter, E.coli.
 Nonbacterial: may be caused by friction and oils. Occlusion, perspiration and rubbing
may cause it.
Clinical findings:
 Symptoms range from slight burning and tenderness to intense itching. Lesion
consist of pustules of hair follicles
Complications: Abscess formation= major complication from bacterial folliculitis
Prevention: Be sure that the water in the hot tubs and spas is treated properly.
 Control blood glucose in DM may reduce the number of these infection
Treatment:
 Local: Anhydrous ethyl alcohol containing 6.25% aluminum chloride, applied to
lesions. Topical ABX are generally ineffective if bacteria have invaded the hair follicle
 Pseudomonas-->treat with ciprofloxacin 500mg BID for 5 days
 Systemic ABX are recommended for bacterial folliculitis d/t other organisms. 4-8 wks
with antistphylococcal ABX.
 Eosinphilic may be treated initially by combo of potent topical corticosteroids and
oral antihistamines: topical permethrin, or itraonazole 200-400mg QD
Prognosis: occasionally stubborn and persistent, requiring prolonged or intermittent courses
of ABX
Contagious and autoinoculable infection of the skin caused by Staph or Strep
Clinical findings:
 Consists of macules, vesicles, bullae, pustules and honey-colored gummy crusts that
when removed leave denuded red areas.
 Superficial blisters filled with purulent material that rupter easily. Crusted superficial
erosions.
 Positive gram stain and bacterial culture.
 Lab findings; S. aureus infection
Treatment: Soaks and scrubbing can be beneficial espically in unroofing lakes of pus under
thick crusts.
 Topical agents like bacitracin, mupirocin, or retapamulin can be attempted for
infection limited to small aras.
 Systemic ABX are indicated in most cases: Cephalexin 250mg four times a day or
Doxycycline 100mg BID
Recurrent impetigo is associated with nasal carriage of S aureus and is treated with rifampin
600mg QD for 5 days.
PT Education: Pt should not share towles if there is a case of impetigo in the household.
Tinea versicolor:
Tinea infections:
Seborrheic Keratoses:
Mild, superficial Malassezia infection of the skin (usually the upper truck)
 Yeast is a colonizer of all humans
 The eruption is often called to patients' attention by the fact that the involved areas
will not tan, and the resulting hypopigmentation may be mistaken for vitiligo.
Clinical findings:
 Mostly asymptomatic but in a few pt they note itching.
 Lesions are velvety, tan or pink macules or white macules that do not tan.
 Size: 4-5mm in diameter to large onfluent areas.
 Lesions initially do not look scaly, but scales may be obtained by scraping the area.
 Appear on the Central trunk(MC), upper arms, neck and groin.
 Lab findings: Large blunt hyphae and thick-walled budding spores are seen on KOH
(spaghetti and meatballs)
Treatment:
 Topical: Selenium sulfide lotion which may be applied to the neck and waist daily and
left on for 5-15 minutes for 7 days.
o Ketoconazole shampoo 1-2% latered on the chest and back
 Oral: Ketoconazole 200mg daily orally for 1 wk or 400mg single dose, w/ exercise to
the point of sweating after ingestion= short term cure in 90% of cases.
Three types of dermatophytes account for the majority of
infections: Epidermophyton, Trichophyton, and Microsporum. Dermatophytoses have varied
presentations, are named by location, and have similar treatments.
Types of Tinea infections:
 Tinea corporis: Annular patches with elevated borders surmounted by scale. If found
on the head of a child you would have to ask if any pets and if so they got it from the
cat she/he sleeps w/
 Tinea Cruris: groin w/ elevated scaling, serpiginous borders
 Tinea Pedis: Feet: scaling erythematous patches and plaques.
 Vesicles & pustules
 Tinea Manuum: hand, diffuse dry scaling palm
 Tinea Capitis: Scalp, scaling w/ alopecia. Red boggy swollen w/ pustules
Clinical Findings:
 Itching may be present. In classic lesion, rings of erythema have an advancing scaly
border and central clearing.
 Lab tests: KOH and fungal culture
Complications: extension of the disease down the hair follicles (more difficult to cure) and
pyoderma.
Prevention: Treat infected household pets (microsporum infection)
Treatment:
 Local: Topical antifungal, avoid Lotrison and Mycolog ineffective.
o Use: miconazole, clotrimazole, butenafine, and terbinafine
 Systemic: Griseofulvin 250-500mg BID only 4-6 wks.
Benign plaques, beige to brown or even black, 3-20mm in diameter, with a velvety or warty
surface.
They are extremely common espically for the elderly and may be mistaken for melanomas or
types of cutaneous neoplasms.
 Several scaly, well-circumscribed lesions that have a "stuck on appearance" are
present.
Treatment: May be frozen with liquid nitrogen or curetted if they itch or are inflamed, no
treatment is need
Scabies
Lice: Pediculosis capitis
Spider bites:
Caused by the female mite Sarcoptes scabiei var. hominis. Secondary bacterial infections
with group A Streptococcus pyogenes and Staphylococcus aureus may occur
 Scabies mite lives its entire life cycle within the epidermis of the skin
Etiology: Direct close contact with an infested person is the primary means of transmission
Fomite transmission may occur and is more common in severe and/or crusted cases
Symptoms:
 Pruritus is the major complaint. Incubation period for 2-6 wks.
 Inflammatory papules and excoriations in characteristic distribution
 Burrow is diagnostic
Diagnosis: by skin scraping
Treatment:
– Permethrin 5% cream
– Lindane
– Precipitated sulfur in petrolatum
– Ivermectin
Infestation of the skin of the scalp, trunk or pubic area. Body lice usually occur among people
who live in overcrowded dwellings with in adequate hygiene facilities.
Three different varieties:
 Pediculosis pubis caused by Phthirus pusbic "crabs"
 Pediculosis corporis caused by Pediculus humanus var corporis "body louse"
 Pediculosis capitis caused by Pediculus humanus var capitis "head lice"
Symptoms:
 Pruritus with excoriation espically over the upper shoulders, posterior flanks, and
neck.
 Head lice can be found on the scalp by small nits resembling pussy willow buds on
the scalp hair.
 occasionally, sky-blue macules on the inner thighs or lower abdomen in pubic louse
infestation
Treatment: Dispose of the infested clothing and address the pt social situation
 Pubic lice: permethrin rince 1% for 10 minutes and permethrin cream 5%applied for
8hr. Sexual contacts should be treated.
 Head lice: Permethrin 1% cream rince (Nix) topical over-the-counter pediculicide and
ovicide. Apply to the scalp and hair and left on for 8 hours before rinsing off
 Body lice: Malathion lotion 1% very effective but highly volatile and flammable so
apply in a well ventilated room or out doors
Brown recluse spider bite:
 LOXOCELES reclusa
 Worldwide distribution, but endemic in South central U.S. from Texas to California
 Distinguished fiddle-shaped marking on their anterodorsal cephalothoraxes
Symptoms:
 Initial envenomation may or may not be painful
 Aching & pruritus will evolve to a red halo surrounding a blue-gray/white sinking
central patch (red, white, blue sign). A necrotic center may develop toward the top
of the lesion. Bullae may erupt and over a period of 2 – 5 weeks the eschar sloughs,
leaving a deep, poorly healing ulcer.
 *Systemic symptoms/findings: fever, nausea, vomiting, arthalgias, weakness,
Alopecia:
leukopenia or hemolytic anemia.
BROWN RECLUSE SPIDER BITE LOOKS LIKE CUTENOUS ANTRAX!!!
Treatment:
 May require plastic surgery
 ? Use of Dapsone 50mg P.O. q24 hour
o Dapsone can cause hemolysis, always check for G6PD deficiency first and
check baseline and weekly liver panels b/c you dont want to give them
hepatitis!
 Admit if systemic symptoms
 Start prophylactic antibiotics to Reduce chance of secondary infection
Black widow Spider bite:
 Often found in wood piles, garages and under landscaping rocks
 Prevalence during April to October
 Bites usually occur on hand or arm
 Distinctive features of a red hourglass marking on abdomen
Symptoms:
 Clinically presents with severe and sustained muscle spasm produced by a
neurotoxic protein, which causes the release of acetylcholine and norepinephrine @
the presynaptic junction.
 *Within one hour of the bite, local redness and muscle cramping begins followed by
generalized cramping involving the large muscle groups . Other symptoms include
weakness, fever, salivation, vomiting, diaphoresis.
 *May be confused with “acute abdomen”-->very ridged abd.
 *Can lead to seizures, hypertensive crisis and respiratory arrest.
Treatment:
 Local wound care
 Tetanus
 Benzodiazepine/narcotics IV for symptom control-->supportive care!!
Cicatricial Alopecia: Baldness due top scarring
 May occur following chemical or phyiscal trauma, lichen planopilaris, bacterial or
fungal infections, severe herpes zoster, chronic DLS, scleroderma and excessive
ionizing radiation.
 The specific cause is often suggested by the history and distribution of hair loss and
appearance of the skin
Scarring alopecia are irreversible and permanent. Must DX and TX the scarring process
Baldness not associated with scarring:
Androgenetic (pattern) baldness***Most Common form**
 The earliest changes occur at the anterior portioni of the calvarium on either side of
the widow's peak and on the crown (vertex).
 Treatment: Minoxidil 5% is OTC and recommeded for person with recent onset <5yrs
and small areas.
o Finasteride (Propecia) 1mg orally daily
 Workup for women: serum testosterone, DHEAS, iron, total iron binding capacity,
thyroid function tests, and CBC will ID most other causes of hair thinning in
premenopausal women.
Telogen effluvium: Is the transitory increase in the number of hairs in the telogen (resting)
phase of hair growth cycle.
 May occur spontaneously appear at the termination of pregnancy or "crash dieting",
high fever, stress from surgery or shocck, malnutrition or may be provoked by
hormonal contraceptives.
 Symptoms: counts of hairs lost by the patient on combing or shampooing often
Onychomycosis:
Paronychia:
exceed 150per day, compared to an average of 70-100.
Alopecia areate: unknown cause but believed to be an immunologic process.
 Patches that are perfectly smooth without scarring. Tiny hair "exclamation hairs"
may be seen.
 The beard, brows, and lashes may be involved. Scalp (alopecia totalis), Scalp+body
(alopecia universalis)
 Can be seen in pt with Hashimoto thyroiditis, pernicious anemia, Addison disease
and vitiligo.
 Treatment: Intralesional corticosteriods used to treat, as well as Triamcinolon
acetonide 2.5-10mg/mL is injected in aliquots of 0.1mL at 1-2cm intervals no
exceeding a total dose of 30mg per month for adult
Trichotillomania: Pull out of one's own hair
 Patches of hair loss are irregular and short growing hairs are always present, since
they cannot be pulled out until they are long enough.
 Pt may be unaware of habit
Tinea unguium is a trichophyton infection of one or more finger or toenail.
Etiology: T. rubrum
Symptoms/signs:
 Nails are lusterless, brittle and hypertrophic and substance of the nail is friable.
Lab Dx: Portions of the nail should be cleared with 10% KOH and examined under
microscope for hyphae. Periodic acid-Schiff stain of histologic section of the nail plate will
also demonstrate the fungus.
Treatment: Difficult to treat b/c of long duration of therapy
 Systemic therapy is required to effectively treat. Topical has limited value
 Fingersnails: Griseofulvin 250mg PO TID for 6 months can be effective or Terbinafine
250mg daily for 6 wks
 Toenails: Terbinafine 250mg daily for 12 wks
It is a nail disease that is an often-tender bacterial or fungal infection of the hand or foot
where the nail and skin meet at the side or the base of a finger or toenail.
 infection generally starts in the paronychiumat the side of the nail, with local
redness, swelling, and pain
Etiology:
 caused by direct or indirect trauma to thecuticle or nail fold, and may be from
relatively minor events, such as dishwashing, an injury from a splinter or thorn,
nail biting, biting or picking at a hangnail, finger sucking, an ingrown nail,
or manicure procedures.
Signs/Symptoms:
 The skin typically presents as red and hot. These infections can be painful. Pus is
usually present, along with gradual thickening and browning discoloration of the
nail plate.
Treatment:
 Acute without abscess formation: local care (warm compresses or soaks to the


Melasma (chloasma)
affected digit for 20 minutes, three times per day).
Acute with abscess formation: Incision and drainage is performed after appropriate
local anesthesia (digital block or ethyl chloride spray) by the insertion of a number 11
surgical blade under the affected cuticle margin. Drainage is sufficient for many cases
of paronychia with abscess formation. For more severe cases, oral antibiotic therapy
can be used after drainage.
o ABX: Diclozacillin 250mg Four times a day or Cephalexin 500mg TID
Chronic: advised to keep their hands as dry as possible and to use gloves for all wet
work. Possible association between chronic paronychia and eczema, patients with
known contact allergies should also be advised to avoid irritant or allergen exposure.
Occurs as patterned hyperpigmentation of the face, usually as a direct effect of
estrogens.
It occurs not only during pregnancy but also in 30-50% of women taking Oral
Contraceptive and rarely in men.
Diagnosis:
 Melasma is usually diagnosed visually or with assistance of a Wood's lamp (340 400 nm wavelength). Under Wood's lamp, excess melanin in the epidermis can
be distinguished from that of the dermis
Treatment: Usually is ineffective as it comes back with continued exposure to the sun.
 3–4% hydroquinone cream, gel, or solution and a sunscreen containing UVA
photoprotectants (Avobenzone, Mexoryl, zinc oxide, titanium dioxide). Tretinoin
cream, 0.025–0.05%, may be added.
Vitiligo
Actinic Keratosis:
Basal Cell Skin Cancers
Pigment cells (Melanocytes) are destroyed.
Present in about 1% of the population, may be associated with other autoimmune
disorders such as autoimmune thyroid disease, pernicious anemia, DM, and Addison
disease
Treatment: Therapy is long and tedious, and the patient must be strongly motivated.
 If < 20% of the skin is involved (most cases), topical tacrolimus 0.1% twice daily
is the first-line therapy.

A superpotent corticosteroid may also be used, but local skin atrophy from
prolonged use may ensue.
 With 20–25% involvement, narrowband UVB or oral PUVA is best. Severe
phototoxic response (sunburn) may occur with PUVA. The face and upper chest
respond best, and the fingertips and the genital areas do not respond as well to
treatment. Years of treatment may be required.
Small macules or papules- flesh color or hyperpigmented. They occur on sun-exposed parts
in a fair complexion person.
DX testing: Biopsy to r/o squamous cell
PT Education:
 Considered pre-malignant.
 Any lesion that persist should be evaluated for biopsy
Treatment:
 Apply liquid nitrogen (cryotherapy) for a rapid eradication. Lesion will crust and
disappear in 10-14 days
 Photodynamic therapy
 Laser resurfacing
 Meds: Flurouracil cream to rub on the lesion 2-3 wks. or Imiquimod cream
Most common cancer in humans. Related to UV-B radiation
 Named for site of origin-->Basal Keratinocytes
 Do not Metastasize
 #1 Risk factor is the inability to tan so Skin types I and II
Types:
 Nodular BCC:
o Most common form
o Firm but friable, Translucent “pearly” surface and Telangiectasias present.
o Irregular growth
o Frequently ulcerate
o Nose is most common site
 Superficial Multicentric BCC
o Least aggressive
o Trunk and extremities most common, but sometimes face
o Can resemble eczema or psoriasis
 Pigmented BCC
o Melanin pigment--> Brown, black, or blue-black
o Pearly character with Telangiectasias
 Sclerosing BCC (Morpheaform)
Squamous Cell Skin Cancer
o Innocuous looking
o Potential for deep, wide extension
o Borders indistinct
o May extend well beyond visible borders
o Waxy appearance
Treatment Options:
 Cryotherapy
 Efudex cream or solution
 Shave biopsy with electro-desiccation and curettage (shave EDC)
 Excision
 MOHS Surgery (location or morpheaform)
 Done in areas where thiss conservation is important. Thos that are in high
risk locations like eyelids, nasal alae, and circum-auricular areas
 Radiation Therapy (unable to tolerate surgery or near end of life)
 Imiquimod (Aldara) topically
Follow-up is require 3 months after treatment and must get an annual skin exam.
Once BCC is DX there is a 44% chance of second BCC within 3 years
May start as an acitinic keratosis. It ariases in the squamous epithelium and is related to UVB radiation.
 Increased incidence after age 55
 Can Metastasize
 Common locations for SCC: Dorsum of hands, Scalp, and upper pinna.
Risk factors:
 Celtic ancestry: fair skin, blue eyes, freckles, red hair, inability to tan.
 Cumulative sun exposure (UV-B)
 Sites of chronic inflammation or ulceration
 Immune suppression
 Coal tar products
 Cigarette smoking
Risk factors for metastasis: Dependant on size, depth and differentiation
Types:
 In-situ SCC (Bowen's disease)
o Completely contained in the epidermis
o Sun exposed areas and looks like: Red, scaly patch
o Slow growing
 Nodular SCC:
o Presentation: Firm nodule, central ulceration and tender to palpation
Treatment:
 Cryotherapy
 Efudex cream or solution
 Shave biopsy with electro-desiccation and curettage
 Excision
 MOHS Surgery
 Radiation Therapy
 Photodynamic Therapy
Follow-up: 3 month after treatment and annual exam thereafter
Prevention:
 Avoid sun 11am to 3pm
 Use sunscreen apply 30 min prior to exposure and reapply q 2 hours, or after
swimming
 Educate your patients: Teach children to use sunscreen and protective clothing
 UV exposure increases with altitude: 4 or 5% for every 1000 ft. above sea level
Melanoma:
Kaposi Sarcoma
Arises from melanocytes. Early detection is crucial because early growth is radial!
 When detected early, surgical removal of thin melanomas can cure the condition in
most cases. Early detection is essential; there is a direct correlation between the
thickness of the melanoma and survival rate.
KNOW THE ABCDE's
 Asymmetry - one half unlike the other half.
 Border Irregular - scalloped or margins not sharp.
 Color - varied from one area to another shades of tan and brown; black; or white,
red, or blue.
 Diameter - larger than 6 mm (diameter of a pencil eraser)
 Elevation – if changed
Melanoma evovling!
Types:
 Superficial spreading melanoma (about 70% of diagnosed cases)
 Nodular melanoma (about 15% of diagnosed cases)
 Lentigo maligna melanoma (about 10% of diagnosed cases) aka insitu
 The papular and nodular areas will be blue or black in color denoting
invasion into the dermis. In addition, there may be gray areas indication
regression of the tumor.
 Acral lentiginous melanoma (about 5% of diagnosed cases)
 More common in the black or asians or in people who have pigment in their
skin
Treatment: Excision is the Mainstay TX!
The initial excision would basically excise the visible lesion. Once the depth of the lesion is
known, there are guidelines for margins of re-excision. For lesions less than 1mm in depth,
excision is usually curative and patients are followed clinically with lab work and CXR. Their
greatest risk is probably the development of a second melanoma.
Tumor thickness (mm)
Margins(cm)
5 yr survival
In situ
.5
99
Less than 1.0
1.0
91-95
1.0-4.0
2.0
63-89
More than 4.0
At least 2.0
45-67
Therapies:
 Cytokines
 (interleukins, interferon
 Adaptive cellular therapy
 Monoclonal antibody therapy
 Vaccine therapy
For those with deeper tumors, it gets more complicated. The lesions are still excised, but
consideration is given to more extensive evaluations for metastasis. The sentinel node, is the
first node that drains from the tumor site. This node is identified by lymphoscintography or
by simple injection of a blue dye intra-operatively. When the sentinel node is negative for
the presence of tumor cells, it has a 98-99% negative predictive value that the entire nodal
basin is negative.
Endemically in an often agressive form in young blacks. Occur largerly in homosexual men
with HIV as an AIDS-defining illness.
 Can complicate immunosuppressive therapy and stopping the immunosuppression
may result in improvement.
Etiology: Herpes virus 8 (HHV-8)
Signs/Symptoms:
 Red or purple plaques or nodules on cutaneous or mucosal surfaces. Marked edema
Molluscum Contagiosum
Verrucae:
may occur with few or no skin lesions.
 Pulmonary Kaposi sarcome can present with SOB, cough, hemoptysis or chest pain,
but can also just show up on the CXR
 Usually develops in pts with high CD4 counts and low viral loads in HIV infected pt.
DX testing: Commonly involves the GI tract and can be screened for by fecal occult blood
testing.
Treatment:
 Elderly: palliative local therapy with intralesional chemo or radiation is usually all
thats required
 In AIDS associated Kaposi sarcoma pt needs to be given anti-HIV antiretroviral b/c in
most cases this will help alone
 Others include: cryotherapy or intralesional vinblastine (0.1-0.5 mg/mL), Radiation
thereapy for accessible and space-occupying lesions.
 Laser surgery for certain intraoral or pharyngeal lesions.
 Systemic therapy for pt with rapidly progressive skin disease=more then 10 new
lesions per month, with edema or pain and with symptomatic visceral disease.
o Liposomal doxorubincin is highly effective in controlling these cases.
o Paclitaxel or other taxanes can be effective even in pt who do not respond
to anthracycline treatment
Spread by wet skin-to-skin contact and can be spread sexually.
Very common in patients with AIDS usually with a help T cell count <100mcL.
Etiology: Poxvirus
Presents:
 As single or multiple dome-shaped, waxy papules 2-5mm in diameter that are all
umbilicated.
 Lesions at first are firm, solid and flesh-colored but when reaching maturity become
soft, whitish or pearly grayu and may suppurate.
 Involvement is usually the face, lower abdomen and genitals
Diagnosis: easily by clinical presentation with the distincitive central umbilication of the
dome-shaped lesion
Treatment:
 Curettage or application of liquid nitrogen
 Light electrosurgery with a fine needle is also effective.
Warts: Verrucous papules anywhere on the skin or mucous membra es, unually no larger
than 1cm in diameter.
Etiology: Caused by human papillomaviruses (HPVs)
Clinical findings:
 Usually no symptoms.
 plantar warts: tenderness on pressure and resemble corns or calluses.
 Itching with angogenital warts
 Periungual warts may be dry, fissured and hyperkeratotic and may resemble
hangnails or other nonspecific changes.
Prevention: Vaccines avaiable against genital HPV
Treatment: Removal
 Liquid nitrogen
 Keratolytic agents and occlusion: salicyclic acid
 Podophyllum resin for gential warts apply by pt BID for 3 consecutive days for a cycle
of 4-6 wks.
 Imiquimod: 5% cream
 Operative removal with blunt dissection for plantar warts or snip biopsy for genital
warts.
 Laser therapy effective for recurrent warts, periungual warts, plantar warts and
condylamata acuminata.

Condyloma acuminatum aka
Anogenital warts
Immunotherapy: squaric acid dibutylester with a concentration of 0.2-2% directly to
the wart
The most common viral sexually transmitted disease in the US.
Etiology: HPV infection. Incubation period after exposure ranges from 3 wks to 8 months
Risk factors: Sexual activity
 Women: primarly caused by vaginal intercourse. Anal condylmata occur by extension
from vulvar or perineal infection or by receptive anal intercourse.
 Men: In men, the preputial cavity or penile shaft can be affected through heterosexual
or homosexual activity.
Clinical manifestations:



Symptoms vary depending on the number of lesion and their locations.
Small number of warts are often asymptomatic.
Other patients may have pruritus, bleeding, burning, tenderness, vaginal discharge
(women), or pain
Diagnosis:
 Usually be made by visual inspection of the affected area. The lesions, which are
skin-colored or pink, range from smooth flattened papules to a verrucous, papilliform
appearance
Treatment: 3 major approaches to treatment are chemical or physical destruction, immunolgic
therapy, and surgical therapy
Lipomas/Epithelial inclusion cysts
Epidermal inclusion cyst are derived from the upper part of the hair follicle.
 Usually asymptotic unless ruptured then inflamed and painful
Physical exam: Flesh-colored firm, but malleable nodule
Prevention: To prevent recurrence the entire cyst with lining must be removed.
Treatment: You can do nothing or you can make an incision and drain it
Acanthosis Nigricans
Lipoma: is a flesh colored, rubber, subcutaneous nodule. Most are stable or slow growing
Treatment: Excision and drainage
Etiology: May be acquired or inherited. Most pt have one of the follow:

Obesity

Endocrine and metabolic disorders, particularly disorders associated with insulin
resistance (aka Diabetes type II or PCOS)

Genetic syndromes with acanthosis nigricans

Familial acanthosis nigricans

Malignancy

Drug reactions- glucocorticoids, injected insulin, oral contraceptives, niacin, protease
inhibitors, chemo, testosterone, and aripiprazole
Clinical manifestations:

Presents with thickened, velvety to verrucous, grey-brown hyperpigmented plaques
on the skin. The back of the neck, sides of the neck, and axillae are the most common
sites of involvement

Early or mild stages skin affected has a dirty appearance and a rough or dry texture
Diagnosis: clinical examination is usually sufficient to establish a diagnosis
Workup:

Pt history: Age of onset, history or symptoms suggestive of an underlying
endocrinopathy, Family history, possible exposure to drugs that may induce it

PE: Height/weight, growth rate in children, physical signs of underlyiing
endocrinopathy, BP assessment

Labs: Screen for type II DM
Treatment: benign and often asymptomatic disorder, cosmetic concerns are typically the
primary indications for treatment.

Treatment of the underlying cause, when feasible, is the preferred method of
management, and obesity-related, drug-induced, and malignancy-associated
acanthosis nigricans appear to frequently respond well to this intervention.

Hidradenitis Suppurativa
Topical agents, such as topical retinoids, vitamin D analogs, and keratolytics are the
primary agents used in the treatment of localized lesions.
Follicular occlusion appears to result from a hormonally-induced increase in ductal
keratinocyte proliferation (follicular epithelial hyperplasia), leading to a failure of keratinocytes
to shed properly from the follicular epithelium, causing follicular hyperkeratosis and plugging
 Associated factors: Genetic susceptibility, mechanical stresses on the skin, obesity,
smoking, diet, and hormonal factors
Clinical manifestations:

Predominantly occurs in intertriginous areas
o axillae (most common site), inguinal area, inner thighs, perianal and perineal
areas, mammary and inframammary regions, buttocks, pubic region, scrotum,
vulva, chest, and, occasionally, the scalp and retroauricular areas
Clinical Staging: The Hurley clinical stages:

Stage I – Abscess formation (single or multiple) without sinus tracts
and cicatrization/scarring

Stage II – Recurrent abscesses with sinus tracts and scarring, single or multiple
widely separated lesions

Stage III – Diffuse or almost diffuse involvement, or multiple interconnected sinus
tracts and abscesses across the entire area
Disorders associated with hidradenitis suppurativa:
Diagnosis: usually can be made through the patient history and recognition of the
characteristic clinical manifestations

Lab studies: a biopsy should be performed if diagnosis is uncertain or if it has
features of squamous cell carcinoma
Treatment: In the absence of successful treatment, HS/AIcan remain active for many years.
The treatments for HS/AI target one or more of three major goals:
●To reduce the extent and progression of disease by healing existing inflammatory
lesions and preventing the formation of new lesions
●To remove chronic sinuses
●To limit scar formation
Stage 1 treatment: Topical clindamycin, intralesional corticosteroids or systemic ABX
Stage 2 treatment: Oral Tetracycline aka erythromycin or a combo therapy with clindamycin
and rifampin for those that fail the erythromycin treatment. Can also try hormonal therapy:
androgens
Stage 3 treatment: Surgery can be used to treat severe and refractory disease
Pilonidal Disease
Intergluteal pilonidal disease is an infection of the skin and subcutaneous tissue at or near the
upper part of the natal cleft of the buttocks. Pilonidal cavities are not true cysts and lack a fully
epithelialized lining; however, the sinus tracts may be epithelialized
Risk factors:
 Overweight/obesity
 Local trauma or irritation
 Sedentary lifestyle or prolonged sitting
 Deep natal cleft
 Family History
Clinical Manifestation:
 Symptoms of acute exacerbation include sudden onset of mild to severe pain in the
intergluteal region while sitting or performing activities that stretch the skin overlying
the natal cleft
 Intermittent swelling as well as mucoid, purulent, and/or bloody drainage in the area.
 Fever and malaise are generally associated with an undrained abscess.
 PE: one or more primary pores (pits) in the midline of the natal cleft and/or a painless
sinus opening cephalad and slightly lateral to the cleft
Diagnosis: Based on Physical exam findings of a pore (pit) or sinus in the natal cleft region
Treatment:

Acute Abscess: managed with an incision and drainage (I&D) procedure at the time
of presentation, usually under local anesthesia. The incision is generally performed
lateral to the midline or over the area of maximal fluctuance, and all visible hair within
Pressure ulcers
the sinus is debrided. Wounds are packed with gauze, and healing occurs by
secondary intention in the acute setting
 Chronic or recurrent disease: surgical excision of all sinus tracts.The surgical
procedures range from simple excision with or without primary closure to complex
flap reconstruction.
 ABX treatment: First choice would be a first generation cephalosporin (cefazolin) plus
Metronidazole
Stages of pressure ulcers:






Stage 1 - The skin is intact with non-blanchable redness in a localized area, usually
over a bony prominence. Darkly pigmented skin may not have visible blanching; its
color may differ from the surrounding area.
Stage 2 - Partial thickness loss of dermis, which presents as a shallow open ulcer with
a red-pink wound bed, without sloughing. Stage 2 ulcers may also present as an
intact or ruptured serum-filled blister.
Stage 3 - Full thickness tissue loss. Subcutaneous fat may be visible, but bone,
tendon or muscles are not exposed. Sloughing may be present but does not obscure
the depth of tissue loss. There may be undermining and tunneling.
Stage 4 - Full thickness skin loss with exposed bone, tendon or muscle. Sloughing or
eschar may be present on some parts of the wound bed. These ulcers often include
undermining and tunneling.
Unstageable - In addition, pressure ulcers are considered unstageable when there is
full thickness tissue loss and the base of the ulcer is covered by slough (yellow, tan,
gray, green, or brown) and/or eschar (tan, brown, or black) in the wound bed. Until
enough slough and/or eschar is removed to expose the base of the wound, the true
depth, and therefore stage, cannot be determined.
Deep tissue injury - Deep tissue injury is suspected when there is purple or maroon
localized area of discolored intact skin or blood-filled blister due to damage of
underlying tissue from pressure and/or shear. The area may be recognized by tissue
that is painful, firm, mushy, boggy, warmer, or cooler as compared to adjacent
tissue.
Clinical Manifestations and Diagnosis:
 Pressure ulcers are usually easy to identify by their appearance and location overlying
a bony prominence
Braden scale for pressure ulcers: the external factors
Treatment/Wound care:




Remove nonviable tissue – eschar and shough.
Monitor for signs and symptoms of infection.
Keep proper amount of moisture – not too wet, not too dry.
Measure and monitor routinely.
 Look for tunnels and undermining.
 Prevent further injury – reduce pressure, avoid shear and friction.
 Provide nutritional needs.
 Manage other chronic medical problems.
 Revaluate, if no change in 2 week consider new treatment plan.
Most pressure ulcers can be prevented, and those Stage I pressure ulcers that do appear
need not worsen under most circumstances. However, even the most vigilant nursing care
may not prevent the development and worsening of ulcers in some very high-risk individuals.
In those cases, intensive therapy must be aimed at reducing risk factors (such as improving
nutritional status), at preventive measures (such as frequent turning, and the use of mattress
overlays), and at treatment
Monitoring-->all of the below daily and document it
 Evaluation of the ulcer
 Status of the dressing, if present
 Status of the area surrounding the ulcer
 Presence of pain, and adequacy of pain control
 Presence of possible complications, such as infection
Treatment by ulcer stages:
 Stage 1 treatment — The development of stage 1 ulcers is a warning that more


Drug eruptions:
serious lesions may follow if appropriate preventive measures are not instituted in a
timely fashion. Stage 1 ulcers may be dressed with transparent films for protection.
Most importantly, preventive measures should be reviewed and intensified.
Stage 2 treatment — Stage 2 pressure ulcers usually require an occlusive or
semipermeable dressing to maintain a moist wound environment [32]. Wet-to-dry
dressings are avoided since these wounds generally require little debridement.
(See 'Dressing choices'below.)
Stages 3 and 4 — Treatment of wound infections, debridement of necrotic tissue,
and appropriate dressings will accelerate healing of Stage 3 and 4 pressure ulcers.
Surgery is necessary for some full thickness pressure ulcers
Usually, abrupt onset of widespread, symmetric erythematous eruption. Can mimic any
inflammatory skin condition.
A true allergic drug reaction involves a prior exposure (incubation period), reactions to doses
far below the therapeutic range.
 Rashes are the most common adverse reaction to drugs. Amoxicillin, TMP-SMZ and
ampicllin are the most common causes of urticarial and maculopapular reaction.
Signs and Symptoms: Simple vs Complex
 Simple drug eruptions involve an exanthem, usually appear in the second week
of drug therapy, and have no associated constitutional or laboratory findings.
 Complex drug eruptions (also called drug-induced hypersensitivity syndromes)
occur during the third week of treatment on average and have constitutional and
laboratory findings.
o Including fevers, chills, hematologic abnormalities: “DRESS” (DRug
Eruption with Eosinophilia and Systemic Symptoms).
Lab findings:
 CBC, liver biochemical tests, and renal function tests should be monitored.
 Skin biopsies may be helpful in making the diagnosis.
Treatment:
 Systemic manifestions should be treated as they arise like anemia, icterus and
purpura.
 Epinephrine IV or SC used in emergency along with systemic corticosteroids
Exanthems
Classically 6 diseases
Disease
Measles
(Rubeloa)
1st disease
Scarlet Fever
2nd disease
A widespread rash usually occuring in children.
Etiology: toxins or durgs, microorganism or can result from autoimmune disease
1st disease: Measles (rubeola)
2nd disease: Scarlet Fever
3rd disease: Rubella
4th disease: Dukes Disease
5th disease: Erythema Infectiosum
6th disease: Roseola Infantum
Etiology
*RNA- paramyovirus;
humans are the only
natural host
*URTract and reginonal
lymphnodes.
*Secondary viremia occurs
within 5-7 days as virus
infected monocytes spread
to other others.
*Virus is stable at room
temp 1-2 days
*Group A hemolytic
Clinical findings
4 phases: Incubation(8-12d), prodromal
(Catarrhal-3d with cough, coryza,
conjunctivitis and Koplik spots, high fever),
exanthematous (rash-begins on head and
moves south)(around d 14), and recovery
(rash fades, brownish color and
desquamation)
* Cervical lymphadenitis, splenomegaly and
mesenteric lymphadenopathy with abd pain
Treatment
*Supportive care: adequate hydration
and antipyretics.
*High does Vit-A
Prodrome: Sudden onset fever, pharyngitis,
HA and chills
*Tongue: yellow-white coat with protruding
papillae . After 4 – 5 days “strawberry
tongue”: this is the scrapping off of the
tongue
*Tonsillopharyngeal erthema, eduates
DX: Based on clinical presentation
and throat culture is the goal
standard.
Complications: Otitis media,
interstitial pneumonia or pneumonia.
Giant cell (Hecht) pneumonia
Goal is to prevent rheumatic fever
and reduce the spread of the
infection.
Rubella
(German or 3day measles)
3rd disease
Roseola
Infantum
(Exanthem
subitum)
6th disease
Erythema
Infectiosum
Fifth Disease
Hand- footmouth
syndrome
(Coxsackievirus
infection)
*RNA in the togavirus
family, humans are the
only natural host.
*Invades resp epithelium
and disseminatees via
primary viremia.
*Infection in utero results
in significant morbidity
from congenital rubella
syndrome
*HHV-6 so a DNA virus in
the herpes fam.
*Can be detected in the
saliva of healthy adults
*Parvovirus B19-DNA virus.
Benign in healthy children
*Can cause aplastic crisis in
pt with hemolytic anemias.
*Highly infectous
*Peak incidence in late
summer and in fall.
*Coxsackie virus A16
*Palate: Petechial macules
*Exanthum starts on the face
*Eruptive: Descends down and skin feels like
sand paper and spares the palms and soles.
*Desquamation: Palms and soles became to
peal
*Incubation period for postnatal rubella is
14-23d
*Retroauricular, posterior cervical and
posterior occupital lymphadenopathy
accompanied by erythematous,
maculaopapular, discrete rash-starts in fast
spreads to body.
*Other: mild pharyngitis, conjunctivitis,
anorexia, HA, malaise and low grade fever.
*ABX therapy: Penicillin
*High fever with abrupt onset that lasts 35days.
*Maculopapular rose-colored rash with
defervescence and lasts 1-3 days
*UR symptoms, nasal congestion,
erythematous TM, and cough
* No specific therapy- just supportive
care: adequate hydration and
antipyretics
*Incubations 4-14d may last 21d
*Begins with fever, malaise, myalgias and
HA
3 stages of rash: Begins with slapped cheek
rash and circumoral pallor. then
maculopapular truchal rash and then fades
into a lacy reticulated rash.
*Children with shortened erythrocyte life
span may develop a transient aplastic crisis
*Prodrome of fever, anorexia, sore throat.
*Oval blisters in acral distribution, usually
few in number
*Shallow ovla oral lesions on erythematous
base
*No specific therapy- just supportive
care: adequate hydration and
antipyretics.
Complications: Congenital rubella
syndrome: IUGR, cataracts, deafness,
neurologic deficits and patent ductus
arteriosus.
Complications: few deaths and some
encephalitis or virus associated
hemophagocytosis syndrome
* No specific therapy- just supportive
care: adequate hydration and
antipyretics
* those with severe anemia give
intravenous immunoglobulin
Complications: Fataliteis associated
with transient aplastic crisis are rare.
Inutero infection may result in fetal
heart failure, hydrops fetalis and fetal
death
* No specific therapy- just supportive
care: adequate hydration and
antipyretics