Derma EAMC Reviewer

EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY
DERMATOLOGIC HISTORY AND PHYSICAL EXAM • Vesicle- Vesicles are circumscribed, elevated,
superficial and fluid-filled cavity <1 cm
Duration
• Bulla- A large (> 1cm) blister which arises from
- When the condition was first noted and long
cleavage at intraepidermal or subepidermal
Periodicity
• Pustule- a circumscribed, superficial cavity of the skin
- constant, waxing and waning, worst at night, worst in
which contains purulent discharge made of leukocytes
winter
Evolution • Wheal- Round or flat topped that is evanescent in 24-
48 hours due to edema in the papillary body of dermis
- How the condition has spread or developed over time
Location
- Where lesions were first noted and if it spread
SECONDARY LESIONS
Symptoms • Scales- Build-up of dead skin cells that flakes off the
- pruritus, pain, bleeding, non-healing surface arising from the outer most layer of the
Severity stratum corneum
- Especially for painful or pruritic conditions • Crusts- A dried collection of blood, serum or pus. Also
Ameliorating and Exacerbating Factors called a scab
- Relation to sun exposure, heat, cold, wind, trauma, and • Erosion- A moist, circumscribed, depressed lesion
exposure to chemicals, topical products, plants, perfumes that results from a loss of a portion or all of the viable
or metals epidermal or mucosal trauma. There is detachment of
Past Medical History epidermal layers with maceration, rupture of vesicles
or bullae
- history of chronic illness and those that are associated with
skin disease (asthma, allergies) • Ulcer- Lesion that involves loss of the epidermis and
Medication History part of the dermis
- A detailed history with those medications started recently • Fissure- Linear loss of continuity of skin surface or
Allergies mucosa results from excessive tension and decreased
- to medications, foods, environmental antigens, and elasticity
contactants • Atrophy- Diminution of some or all layer of the skin
Social History • Scar- Fibrous tissue replacement of the tissue defect
- Occupation, hobbies and leisure activities, alcohol and due to previous wound or ulcer
tobacco use, illicit drug use, sexual history • Excoriation- Punctate or linear abrasion produced by
Family History mechanical means caused by scratching usually
- of skin disease, atopy (atopic dermatitis, asthma, hay fever) involving only the epidermis
or skin cancer. • Lichenification- Repeated rubbing of skin results in
thickening and hyperpigmentation of skin
PRIMARY LESIONS SECONDARY LESIONS
• Macule • Scales BACTERIAL INFECTIONS
• Patch • Crust FURUNCLE (BOIL)
• Papule • Erosion
• deep-seated inflammatory nodule
• Plaque • Ulcer
• Nodule • Fissure • usually from a preceding, more superficial folliculitis
• Vesicle • Atrophy • evolving into an abscess
• Bullae • Scar • Etiologic agent: Staphylococcus aureus
• Pustule • Excoriation • Lesion: hard, tender, red nodule that enlarges and
• Wheal • Lichenification becomes painful and fluctuant after several days.
Rupture then occurs with discharge of pus.
PRIMARY LESIONS
• Macule- A circumscribed area of change in color, flat, CARBUNCLE
non-palpable, on skin or mucous membrane, < 1 cm • more extensive, deeper, communicating, and infiltrated
• Patch- Flat but larger than macules with a lesion
circumscribed area of change in color, flat, non- • Closely set furuncles coalesce
palpable on skin or mucous membranes, • Etiologic agent: Staphylococcus aureus
measuring >1 cm
• Lesion: initially red and indurated → Multiple pustules on
• Papule- are solid, raised lesions <1 cm caused by a the surface, draining externally around multiple hair
proliferation of cells in epidermis or superficial dermis. follicles→ yellow-gray irregular crater → heals slowly by
Maybe sessile, pedunculated, flat topped, rough, granulating →dense and readily evident permanent scar
smooth and umbilicated
• Plaque- Solid, plateau-like elevation >1cm caused by Furuncle and Carbuncle
a proliferation of cells in epidermis or superficial • SOP: hair-bearing sites (regions subject to friction,
dermis occlusion and perspiration)
• Nodule- Palpable, solid, round or ellipsoidal lesion > • Predisposing factors: Pre-existing lesions (atopic
or equal to 1 cm. It is caused by a proliferation of cells dermatitis, scabies, pediculosis)
into the mid-deep dermis from inflammatory
infiltrates, neoplasm or metabolic deposits
EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY 1

• Systemic host factors (obesity, blood dyscrasias Deep folliculitis/Sycosis barbae

treatment with glucocorticoids and cytotoxic agents, • Deep folliculitis with perifollicular inflammation
immunoglobulin deficiency states, DM) occurring in the bearded areas of the face and upper lip
• Diagnosis: Gram’s Stain • Same treatment with Superficical Folliculitis
- clusters of Gram-positive cocci, or isolation of S.
aureus on culture IMPETIGO
• Management: • Predisposing factors: crowding, poor hygiene, neglected
- Simple furunculosis - local application of moist heat minor skin trauma
- With surrounding cellulitis - systemic antibiotic • Diagnosis: Clinical signs, Gram stain and culture
- Large, painful, and fluctuant lesions - incision and • Treatment
drainage - Topical: Mupirocin, Retapumulin, Fusidic acid
Systemic antibiotics For penicillin allergic ointment BID x 10 days
Cloxacillin or Cephalexin Erythromycin - Systemic: Dicloxacillin 250-500mg PO QID 5-7days;
Adults: 250-500 mg QID x 10 Adults: 250-500 mg QID x 10 Amoxicillin-clavulanic acid 250-500mg QID 5-7 days;
days days
- Penicillin allergy: Azithromycin, Clindamycin or
Children: 30-50 MKD QID x Children: 30-50 MKD QID x
Erythromycin
10days 10 days
- CA-MRSA suspected: TMP-SMX, Clindamycin,
Co-amoxiclav Clindamycin Tetracycline, Doxycyline or Minocycline
Adults: 375 mg TID/ 625 mg Adults: 150-300 mg QID x 10
BID x 10 days days
Children: 25-50 MKD TID x Children: 15 MKD QID x 10
10days days
*CA MRSA -> Vancomycin
FOLLICULITIS
• pyoderma that begins within the hair follicle
• Etiologic agents: Staphylococcus aureus, Pseudomonas
aeruginosa and Gram negative bacterias such as: Proteus,
Klebsiella, E. coli Bullous impetigo
• Predisposing factors: Shaving, plucking or waxing hairy • Newborns & young children
areas, occlusion with clothing, adhesive plasters & • caused by coagulase(+) S. aureus
prosthesis,natural occlusion in intertriginous sites and
• SOP: face, trunk, extremities, buttocks, perineum
warm climate
• Lesion: vesicles turn to flaccid bullae that rupture & form
• Diagnosis: Clinical signs, Gram stain and culture
light brown crusts
Superficial Folliculitis/ Follicular or Bockhart impetigo • Ritter disease/Pemphigus neonatorum – extensive
bullous impetigo
• Lesion: small, fragile, dome-shaped pustule occurs at the
infundibulum (ostium or opening) of a hair follicle
Nonbullous Impetigo
• Children: Scalp
• More common
• Adult: Beard area, axillae, extremities, and buttocks of
• In industrialized nations: most commonly caused by S.
adults
aureus, less often by group A Streptococcus
• Treatment:
• In developing countries: group A Streptococcus
- Topical Therapy: Warm saline compress, topical
• Impetigo in the newborn: Group B
Mupirocin or Clindamycin BID x 10 days
• SOP: nose, mouth, extremities after trauma
- Systemic antibiotics
• Nasal carriers: very localized type of impetigo (anterior
Hot tub folliculitis nares and adjacent lip areas
• Caused by Pseudomonas aureginosa • Lesion: transient vesicle or pustule → honey-colored
crusted plaque
• Usually follows bathing in a communal “hot tub”
• follicular papules and pustules on the trunk CELLULITIS
• May resolve spontaneously • extends deeper into the dermis and subcutaneous tissue
• Treatment if symptomatic: Ciprofloxacin 500 mg BID x 10 • Predisposing factors: Liposuction and “skin popping”
days
• Etiologic agent : S. aureus and GAS
• Prevention: pools cleaned regularly
• Group B streptococci in the newborn
• pneumococci, Gram-negative bacilli in
Gram negative folliculitis
immunocompromised individuals
• Acne patients treated with oral antibiotics
• Escherichia coli and other Enterobacteriaceae and
• Erythematous follicular papules & pustules anaerobes →extremes of age, prolonged hospitalization,
• Management: Discontinue current antibiotics, Ampicillin percutaneous intravascular lines, diabetes,
250 mg QID x 10 days, topical benzoyl peroxide immunocompromised states, and glucocorticoids
• For severe unresponsive cases: Oral Isotretinoin

• Lesion: erythema, tenderness, pain, lack of distinct • If the process is not limited to the fascia → Streptococcal
margins between affected and normal skin, deeper, gangrene
firmer form of tender induration, fluctuance; occasionally • SOP: extremity
(+) crepitus on palpation • Lesion: indistinguishable from type I, but necrosis of the
overlying skin can be rapid and dramatic, revealing
ERYSIPELAS deeper structures, including tendon sheaths and muscle
• Type of superficial cutaneous cellulitis with marked
dermal lymphatic vessel involvement Antimicrobial Treatment for Necrotizing Infection of Skin, Fascia and Muscle:
• Predisposing factors: Lymphedema, venous stasis, web
intertrigo, and obesity
• Etiologic agent: group A β-hemolytic streptococcus >

group C or G streptococcus) > S. aureus
• Newborn: group B streptococci
• Lesion: begins on the face or a lower extremities,
heralded by pain, superficial erythema, and plaque-like
edema, sharply defined margin to normal tissue, “peau
d’orange appearance”
Cellulitis and Erysipelas

• Diagnosis: elevated WBC & ESR, Gram stain of aspirates,
Bacterial Culture, Skin biopsy and X-ray and imaging
ECTHYMA
Antimicrobial Treatment of Non-Necrotizing Infections (Cellulitis, Erysipelas): A cutaneous pyoderma characterized by thickly crusted
erosions or ulcerations
• Causes
- Usually a consequence of neglected impetigo
classically occluded by footwear and clothing
- Staphylococcus aureus
- Group A Streptococcus
- Poor hygiene
- Neglect
• Clinical Manifestations
- Ulcer has a “punched out” appearance when the dirty
grayish-yellow crust and purulent material are
debrided
- Margin of the ulcer is indurated, raised and violaceous
- The granulating base extends deeply into the dermis
- Lesions typically occur in the homeless and soldiers in
NECROTIZING FASCIITIS combat in a hot and humid climate
• Diagnosis: Open Surgical Exploration – GOLD STANDARD - Most commonly occurs on lower extremities
• Others: Biopsy, Culture, MRI or CT scan • Diagnosis
- Clinical
Type I Necrotizing Fasciitis - Gram stain and culture of S. aureus or GAS
• Polymicrobial infection (mix of facultative and anaerobic • Treatment
organisms) - Lesions are slow to heal
• Predisposing factors: Surgery, bowel perforation - Requiring several weeks of antibiotic treatment for
secondary to neoplasm or diverticulitis, trauma, or resolution
parenteral drug abuse via skin-popping, diabetes or - Management is the same as what is used for
malnutrition staphylococcal impetigo
• SOP: extremity, abdominal wall, perineum, or about
operative wounds PARONYCHIA
• MOST COMMON FORM OF NECROTIZING FASCIITIS Inflammation of the proximal nail fold
• Lesion: (+) painful → swelling, erythema, warmth, and • Causes
tenderness→skin color becomes purple, bullae develop, - Acute Paronychia is usually caused by infection
and frank cutaneous gangrene→ anesthetic as a result of - Individuals exposed to hand trauma or chronic
occlusion of small blood vessels and destruction of moisture are predisposed to staphylococcal
superficial nerves in the subcutaneous tissues, (+) paronychia, as well as to other causes of paronychia
crepitus (e.g., Candida, Pseudomonas, Streptococccus,
dermatophytes).
Type II Necrotizing Fasciitis and Streptococcal Gangrene - S. aureus is the major infectious cause of acute
• Monomicrobial (GAS) paronychia
• Usually healthy individuals

• Clinical Manifestations • Causes

- Site is usually around the finger nails - Exfoliatin A and B (ETA and ETB) proteins produced by
- often originating from a break in the skin, such as a S. aureus
hangnail - the epidermolysis takes place usually between the
- skin and soft tissue of the proximal and lateral nail stratum spinosum and granulosum
fold are red, hot, and tender - This results in a very thin-walled, flaccid blister that is
- if not treated, can progress to abscess formation easily disrupted, exhibiting a positive Nikolsky sign
• Diagnosis • Clinical Manifestations
- Mainly Clinical - Faint, orange–red macular exanthem or uniform
o History erythema sparing mucosal surfaces
o Physical examination - in association with a purulent conjunctivitis, otitis
media, nasopharyngeal infection, or, occasionally,
• Treatment
pyogenic skin infection such as bullous impetigo
- oral and topical antibiotics
- These serve as the staphylococcal foci from which the
o Mupirocin BID, Fusidic Acid BID toxin is released
o Dicloxacillin 250–500 mg PO QID for 5–7 days - Periorificial and flexural accentuation of the
o Amoxicillin plus clavulanic acid 25 mg/kg TID; exanthema
250–500 mg qid - Severe tenderness
o Cephalexin 25 mg/kg TID; 250–500 mg QID - Within 1–2 days the rash progresses from an
- incision and drainage of abscesses exanthematous scarlatiniform to a blistering eruption
- Very superficial tissue paper-wrinkling of the
ERYTHRASMA epidermis, which is characteristic, progresses to large
Erythrasma is a common superficial bacterial infection of the flaccid bullae in flexural and periorificial surfaces
skin characterized by well-defined but irregular reddish-brown - A positive Nikolsky sign
patches, occurring in the intertriginous areas, or by fissuring
- Large sheets of the epidermal surface are typically
white maceration in the toe clefts
shed, revealing a moist underlying erythematous,
• Causes base resembling a generalized scalding burn.
- Etiologic agent: Corynebacterium mutissimum • Diagnosis
- more common in tropical climate - Cultures from blisters are usually sterile
- more common in men - Tzanck smear shows acantholytic cells
- may occur in asymptomatic form in the genitocrural - Histopathology
area
o Acantholysis in the granular layer and
• Clinical Manifestations subcorneal cleft formation in early lesions
- completely asymptomatic o Intact, viable epidermis with shedding of the
- genitocrural form with considerable pruritus stratum corneum in the desquamative stage
- generalized form with scaly lamellated plaques on the o Dermis with few inflammatory cells
trunk, inguinal area, and web spaces of the feet • Treatment
- When pruritic, irritation of lesions may cause - Intravenous anti-staphylococcal antibiotics
secondary changes of excoriations and lichenification
- Mupirocin ointment to clearly impetiginized areas
• Diagnosis
- Managing fluid and electrolyte abnormalities
- Wood’s lamp exam: coral-red fluorescence
- Non-adherent dressings
- Pigment may persist after eradication of the
o Use of petrolatum-impregnated gauze
Corynebacterium as the pigment is within the stratum
corneum
- Gram stain and culture of Corynebactrium in the VIRAL INFECTIONS
lesions VARICELLA
o Rod-like, gram positive organisms • Varicella Zoster Virus (VZV)
• Treatment - Herpesvirus family
- For localized disease especially between the web - Entry → MUCOSA of upper respiratory tract &
spaces of the feet oropharynx → tonsillar T cells → reticuloendothelial
o Benzoyl peroxide wash and 5% gel system (major site of virus replication) and skin
o Clindamycin or erythromycin 2% cream • Prodrome (2-3 days)
- For widespread involvement: - fever, chills, malaise, headache, anorexia, severe
o Oral erythromycin backache, sore throat, dry cough
o 1 gram single dose of clarithromycin • Rash
- For secondary prophylaxis - FACE → scalp → trunk (relative sparing of the
o Benzoyl peroxide bar when showering extremities)
- scattered rather than clustered
STAPHYLOCOCCAL SCALDED SKIN SYNDROME - rose-colored macules → papules → vesicles →
The syndrome is a generalized exanthematous disease pustules → crusts → depressed scars
consisting of cutaneous tenderness and widespread superficial - *lesions in all stages are usually present on the body
blistering and denudation at the same time

- “DEWDROPS ON ROSEPETALS” • new lesions continue to appear for 1–4 days (occasionally
→ Erythematous papules,vesicles, crusts, and for as long as 7 days)
erosions at sites of excoriations • Tzanck Smear: (+) multinucleated giant cells & epithelial
• Tzanck Smear: (+) multinucleated giant cells & epithelial cells w/ acidophilic intranuclear inclusion bodies
cells w/ acidophilic intranuclear inclusion bodies - Same findings in Varicella
- Same findings in Herpes Zoster Infection • Complications:
• Complications: - Postherpetic neuralgia
- Child → Staph/Strep skin infections - Bacterial superinfection
- Adult → Primary Varicella Pneumonia - Skin necrosis, scarring, cutaneous dissemination
- Pregnant → Congenital VZV infection (immunocompromised)
- Symptomatic alone
*Rye Syndrome - Acyclovir 800 mg 5x/d x 7d
- Aspirin use during infection → acute encephalopathy - Famciclovir 500 mg PO q8 x 7d
with fatty liver degeneration - Valacyclovir 1g PO q8 x 7d
- occurs 2–7 days after the appearance of the rash ▪ Immunocompromised
▪ same as for Varicella
• Treatment:
- Neonate HPV (WARTS)
▪ Acyclovir 10mg/kg or 500mg/m3 q8 x 10d • Human Papillomavirus (HPV)
- Child - DNA virus
▪ Symptomatic alone ▪ E1 and E2: replication and transcription
▪ Valacyclovir 20 mg/kg q8 x 5d ▪ E5-7: transforming genes
▪ Acyclovir 20 mg/kg QID x5d ▪ E4: encodes a protein (release of virus from
- Adolescent keratin framework)
▪ Valacyclovir 1g PO q8 x 7d ▪ L1 and L2: viral capsid
- Adult HPV Type Clinical Lesions
▪ Acyclovir 800 mg 5x/d x 7d 1 Deep plantar/palmar warts
2, 4, 27, 29 Common warts
- Pregnancy
3, 10, 28, 49 Flat warts
▪ Acyclovir 7 Butcher’s warts
- Immunocompromised 13, 32 Oral focal epithelial hyperplasia
▪ Mild 5, 8, 9, 12, 14, 15, 17, Epidermodysplasia verruciformis
19-26, 36, 47, 50 In immunocompromised
a. Valacyclovir 1g PO q8 x 7d
6, 11 Anogenital warts, cervical condylomata
b. Famciclovir 500mg PO q8 x 7-10d 16, 18, 31, 33-35, 39, Anogenital warts, cervical condylomata
c. Acyclovir 800 mg PO 5x/d x 7-10d 40, 51-60 Bowenoid papulosis
▪ Severe Common warts (verruca vulgaris)
d. Acyclovir 10mg/kg IV q8 x 7-10d • scaly, rough, spiny papules or nodules
▪ Acyclovir resistant (advanced AIDS) • single or grouped
e. Foscarnet 40 mg/kg IV q8 until healed • hands and fingers
Flat warts (verruca plana)
HERPES ZOSTER • 1–4 mm, slightly elevated, flat-topped papules with
• Varicella Zoster Virus (VZV) minimal scale
- Herpesvirus family • face, hands, and lower legs
- Entry → MUCOSA of upper respiratory tract & Treatment for warts
oropharynx → tonsillar T cells → reticuloendothelial - Electrodessication with curettage
system (major site of virus replication) and skin → - Salicylic acid, lactic acid, tricholoroacetic acid
sensory nerves → centripetal to sensory ganglia → - Cryotherapy (liquid nitrogen)
LATENT VZV
• Prodrome MOLLUSCUM CONTAGIOSUM
- PAIN (>60 yo) and paresthesia • MC Virus (MCV)
- Rash - poxvirus
- nearly always unilateral - replicates within the cytoplasm
- Dermatomal: limited to the area of skin innervated by - MCV-1: Children
a single sensory ganglion
- MCV-2: adults, immunocompromised
- Most common: trigeminal nerve (ophthalmic division),
• IP: 2-7 weeks
and the trunk from T3 to L2
• small pink, pearly, or flesh-colored dome-shaped
- most severe and lasts longest in older people
papules with central dell / umbilication
- least severe and of shortest duration in children
• Spontaneous clearance (months to years)
• closely grouped vesicles on an erythematous base
• In adults, usually indicative of a more advanced state of
• erythematous macules and papules → Vesicles (within HIV, with higher viral load and lower CD4+ T-cell count
12–24 hrs) → pustules (day 3) → crust (day 7-10, persist
for 2–3 weeks)

• Curettage, Canthardin, retinoid creams, imiquimod HAND-FOOT-MOUTH DISEASE

cream, salicylic acid, trichloroacetic acid, cidofovir, and 1.5 year old child came in with chief complaint of loss of
silver nitrate paste and tape stripping appetite. Mother also reported incessant crying of the child
upon feeding. PE showed few ulcerative oral lesions.
Patient presented with grouped vesicles and crusting over the Cutaneous exam revealed vesicles over the palms and soles.
outer 1/3 of the lower lip associated with pain, burning
sensation and occasional pruritus. • Clues in diagnosing HFMD:
- Painful oral ulcers→ difficulty feeding child
OROLABIAL HERPES
- linear papulovesicular lesions over the sides of fingers,
• caused by HSV1 toes, and (sometimes) on buttocks
• acquired in childhood - Etiologic agent: Coxsackie Virus
• mostly associated with orofacial disease
• most common site: Outer 1/3 of the lower lip associated GERMAN MEASLES
with pain, burning sensation, pruritus Few days prior to consult, mother of a 3yo patient noted
petechiae on the soft palate and palpable cervical lymph
Patient presented with painful grouped vesicles with early nodes. These were accompanied by low grade fever. 1 day PTC,
central crusting on a red base arising on the shaft of the penis. the patient was noted to have pink macules and papules over
the forehead spreading inferiorly to the neck, trunk and
GENITAL HERPES extremities.
• HSV- 2 What is your diagnosis?
• most prevalent sexually transmitted disease worldwide • “3-day measles”
• the most common cause of ulcerative genital disease • caused by Rubella Virus (RNA Togavirus)
• correlates with sexual behavior • Transmission: inhalation of aerosolized respiratory
droplets
A patient presented with painful, grouped, confluent vesicles on • Period of infectivity: end of incubation period until
an erythematous base on the distal finger. Tzanck smear was disappearance of rash
done which revealed multinucleated giant cells. • Clinical Manifestation
- exanthema & Lymphadenopathy
HERPETIC WHITLOW - Forchheimer Sign- petechiae on soft palate (also seen
• caused by: in Infectious Mononucleosis)
- HSV1 (<20yo)
- HSV2 (>20yo) SUPERFICIAL FUNGAL INFECTIONS
DERMATOPHYTOSIS
HERPES SIMPLEX Classified further according to their natural habitats
• HSV both can infect oral and genital areas and cause • Humans, Animals, Soil
acute and recurrent infections Attach to and invade keratinized tissue of animals and humans
• Most recurrences are not symptomatic (asymptomatic • Skin, Hair, Nails
shedding)
• Diagnosis: Predisposing Factors
- is made by polymerase chain reaction, viral culture, or • Host factors
serology, depending on the clinical presentation
- Atopy
- Tzanck Smear: Multinucleated giant cells
- Icthyosis
• Treatment: - Immunosuppression (Intake of glucocorticoids,
- Acyclovir: 200mg 5x/day or 400mg TID azathioprine)
- Valacyclovir 1g BID - Systemic diseases (Diabetes mellitus, Cushing
- Famacylovir 250mg TID Syndrome)
- Regimens and dosages vary with the clinical setting • Local Factors
- Sweating
MEASLES (RUBEOLA) - Occlusion
A 3 year old child presented with erythematous, non-pruritic,
- Hot, humid weather
macules and papules beginning on the forehead gradually
progressing to the neck, trunk, and extremities. History - Occupational exposure
revealed URTI (high grade fever, cough, coryza, & conjuctivitis) - Geographic location
4 days prior to the eruption of the lesions. PE revealed tiny
white lesions surrounded by erythematous halo described as Genera
“grains of sands” over the buccal mucosa. Patterns of Integumentary Infections by
Superficial Mycoses
• Clues in diagnosing Measles: Genera Skin Hair Nails
- spreads centrifugally Trichophyton X X
Microsporum X X
- high grade fever precedes rash (~4 days)
Epidermophyton X X
- (+) Koplik Spots
Tinea Nigra X
▪ small, whitish lesions over the buccal mucosa Black Piedra X
▪ Pathognomonic for Measles White Piedra X

Transmission • Inflammatory
• Anthropophilic: Person to person - With scarring
• Zoophilic: Animal to human - Kerion – swollen, boggy, pus exuding mass, (+) pain
• Geophilic: Soil or environment to human - Favus – scutula, fetid odor
• Treatment
Pathogenesis - Infections involving hair-bearing skin usually
Broad armamentarium of enzymes act as virulence factors to necessitate oral antifungal treatment since
allow adherence and invasion of skin, hair, and nails, and also dermatophytes penetrating the follicle are usually out
to utilize keratin as a source of nutrients for survival of reach for topicals
• Secretion of specific keratinolytic proteases, lipases and ▪ Griseofulvin
ceramidases, the digestive products of which also serve ▪ Terbinafine
as fungal nutrients ▪ Fluconazole
▪ Itraconazole
1. Adherence to keratin
2. Invasion and growth ▪ Adjuvant: Selenium sulfide (1% and 2.5%), zinc
3. Host inflammatory response pyrithione (1% and 2%), povidone iodine (2.5%),
and ketoconazole (2%) are shampoo preparations
• Inflammatory host response against a spreading
dermatophyte followed by a reduction or clearance of
fungal elements from within the plaque
TINEA BARBAE
• Rarest of dermatophyte infection
• Result: classic “ringworm,” or annular morphology of
tinea corporis • Adult males exposed to farm animals
• Lesions: discrete follicular papules and pustules to kerion
Diagnostic Procedures like lesions
Clinical diagnosis confirmed by • Hairs are easily plucked off
• Microscopic detection of fungal elements (10-20% KOH) • May be easily mistaken for Staphylococcus aureus
- Active border, scaly lesion, depilate hair, crumbling folliculitis
debris (onychomycosis) • Treatment
• Culture - Oral antifungal is usually necessary
• Histologic evidence of the presence of hyphae in the - Ultramicronized Griseofulvin 500 mg twice daily for 6
stratum corneum. weeks
Supportive - Terbinafine 250 mg daily for 2–4 weeks
• Wood’s lamp examination - Itraconazole 200 mg daily for 2–4 weeks
- Coral red – Erythrasma, C. minutissimum - Fluconazole 200 mg daily for 4–6 weeks
- Greenish – Pseudomonas - Systemic glucocorticoids used for the first week→
- Pale white yellow – Tinea versicolor helpful in cases with severe inflammation
- Bright Green – M. audouinii, M. canis
TINEA CORPORIS
Classification • Refers to any dermatophytosis of glabrous skin except
• Tinea corporis (body) palms, soles, and the groin
• Tinea facialis (face) • Classic “ring worm” lesion
• Tinea cruris (groin) • Starts as eythematous macule or papule spreading
outward to form ring shaped scaly plaques with sharply
• Tinea manuum (hands)
marginated raised red borders with central clearing
• Tinea pedis (feet)
• Most common: T. rubrum
• Tinea capitis (scalp)
• Other organisms:
• Tinea barbae (beard)
- Epidermophyton floccosum
• Tinea unguium (nails)
- T. interdigitale
- M. canis
TINEA CAPITIS
- T. tonsurans
• Trichophyton and Microsporum species, with exception
of Trichophyton concentricum • Treatment
- M. Canis (most common in Europe) - Topical allylamines, imidazoles, tolnaftate,
butenafine, or ciclopirox twice a day for 2-4 weeks
• Prepubertal children
- Oral antifungal agents are reserved for widespread or
• Spores in the air
more inflammatory eruptions
• Possible transmission through contact with - Terbinafine 250 mg daily for 2–4 weeks
contaminated inanimate objects
- Itraconazole 200 mg daily for 1 week
• Several round patches of scale or alopecia, with or
- Fluconazole 150–300 mg weekly for 4–6 weeks
without inflammation
• Non-inflammatory TINEA FACIALE
- No scarring
• With or without central clearing
- “Gray Patch” – short stubs of broken hair
• + Pruritus
- “Black Dot” – hairs broken off at surface

TINEA CRURIS Treatment

• “jock itch” or “hadhad” in Tagalog • Mild interdigital tinea pedis without bacterial
• Usually bilateral involvement
• Scaly reddish to brownish plaques with advancing border - Topical allylamine, imidazole, ciclopirox, benzylamine,
tolnaftate, or undecenoic acid based creams
• Lesion starts on the crural fold as a single inflamed scaly
lesion with active margin extending downward on to the • Terbinafine cream applied twice daily for 1 week
thighs, occasionally migrating to the pubic regions, to the • Oral terbinafine is 250 mg daily for 2 weeks.
buttocks, and gluteal cleft area • Itraconazole in adults is given 400 mg daily for 1 week,
• In contrast to candidal infection, it very rarely involves 200 mg daily for 2–4 weeks, or 100 mg daily for 4 weeks
the scrotal area • Itraconazole in children is administered at 5 mg/kg/day
• Pruritus is always present and severe for 2 weeks
• Most common cause: T. rubrum and E. floccosum • Fluconazole 150 mg weekly for 3–4 weeks
• Treatment • Topical or systemic corticosteroids may be helpful for
- Topical allylamines, imidazoles, tolnaftate, symptomatic relief during the initial period of antifungal
butenafine, or ciclopirox treatment of vesiculobullous tinea pedis
- 2x a day for 2-4 weeks • Patients suspected of having Gram-negative co-
infections
- Oral antifungal agents are reserved for widespread or
more inflammatory eruptions
TINEA UNGUIUM (ONYCHOMYCOSIS)
- Terbinafine 250 mg daily for 2–4 weeks
• Most prevalent nail disease
- Itraconazole 200 mg daily for 1 week
• Risk factors
- Fluconazole 150–300 mg weekly for 4–6 weeks
- Nail trauma
TINEA MANUUM AND TINEA PEDIS - Immunosuppression (HIV infection, diabetes mellitus)
• Organisms - Peripheral vascular insufficiency
- T. rubrum (most common) • Begins as tinea pedis before extending to the nail bed
- T. interdigitale • Infected nail then becomes a reservoir for local
- E. floccosum. recurrence
• Most common cause: T. rubrum and T. interdigitale
TINEA PEDIS
- Four types Types
• Interdigital • Distolateral subungual type
▪ Most common presentation of tinea pedis - Most common form
▪ Begins as scaling, erythema and maceration of the - Begins with invasion of the stratum corneum of the
interdigital and subdigital skin of the feet, and in hyponychium and distal nail bed, forming a whitish to
particular between the lateral third and fourth brownish– yellow opacification at the distal edge of
and fourth and fifth toes the nail
▪ Rarely involves the dorsum - The infection then spreads proximally up the nail bed
to the ventral nail plate
▪ Occlusion and bacterial coinfection → produce
erosions with pruritus → malodor → “athlete’s - Hyperproliferation or altered differentiation of the
foot.” nail bed in response to the infection results in
subungual hyperkeratosis
• Chronic Hyperkeratotic (Moccasin)Type
- Progressive invasion of the nail plate results in an
▪ Patchy or diffuse scaling on the soles and the
increasingly dystrophic nail
lateral and medial aspects of the feet, in a
distribution similar to a moccasin on a foot • Proximal Subungual Type
▪ Most common: T. rubrum followed by E. - Infection of the proximal nail fold primarily with T.
floccosum and anthropophilic strains of T. rubrum and T. megninii
interdigitale - White to beige opacity on the proximal nail plate
• Vesiculobullous - Opacity gradually enlarges to affect the entire nail and
eventuates in subungual hyperkeratosis, leukonychia,
▪ Typically caused by zoophilic strains of T.
interdigitale (former T. mentagrophytes var. proximal onycholysis, and/or destruction of the entire
mentagrophytes) nail
▪ Tense vesicles larger than 3 mm in diameter, - Patients should be screened for HIV, as PSO has been
vesiculopustules, or bullae on the soles and considered a marker for this disease
periplantar areas • White Superficial Type
• Acute Ulcerative Type - Results from direct invasion of the dorsal nail plate
▪ Tinea pedis with zoophilic T. interdigitale along - White to dull yellow sharply bordered patches
with rampant bacterial superinfection with Gram- anywhere on the surface of the toenail
negative organisms - Usually caused by T. interdigitale
▪ Vesicles, pustules and purulent ulcers on the Treatment
plantar surface • Topical
▪ Cellulitis, lymphangitis, lymphadenopathy and - Ciclopirox 8% lacquer applied daily for 48 weeks
fever are frequently associated - Amorolfine 5% applied twice weekly

• Systemic - Potassium hydroxide (KOH) preparation

- Required for onychomycosis involving the matrix area, ▪ Confirmatory
or when a shorter treatment regimen or higher ▪ Demonstrates the characteristic fungal spores and
chance for clearance or cure is desired short cigar-butt hyphae (“spaghetti and
- Terbinafine, Fluconazole meatballs”)
▪ Visualization is enhanced through PAS stain
CUTANEOUS CANDIDIASIS • Treatment
Candidal Intertrigo - Topical
• Intertriginous area (inframammary, webspaces, axillae, ▪ Selenium sulfide
groins, intergluteal) ▪ Zinc pyrithione
• Erythematous areas surrounded by satellite pustules ▪ Sodium sulfacetamide
• Dry and scaly to moist and oozing ▪ Ciclopiroxolamine
• (+/-) pruritus, burning pain ▪ Azole and allylamine antifungal preparations
• Treatment: - Systemic
- Topical antifungals (e.g., clotrimazole, econazole, ▪ Ketoconazole, Fluconazole, and Itraconazole are
ciclopirox, miconazole, ketoconazole, and nystatin) the preferred oral agents
- Powder preparations
- Systemic antifungals for extensive cutaneous ACNE VULGARIS
infections, follicular involvement, or infections in
immunocompromised patients ACNE VULGARIS
• a self-limited disorder if the pilosebaceous unit that is
Paronychia seen primarily in adolescents.
• Redness, swelling of nail folds • Epidemiology
• pain, tenderness - Acne is common that is often has been termed
physiologic.
• Treatment:
- Acne prevalence hits its peak during the middle to late
- Topical imidazole in solution form initially
teenage period with more than 85% of adolescents
- Four percent thymol in ethyl alcohol is drying to affected and then steadily decreases.
candida (alternative)
- In some cases, acne may persist through the third
- Oral azoles (refractory cases) decade or even later particularly in women.
• Etiology
TINEA (PITYRIASIS) VERSICOLOR
- Key elements for pathogenesis:
• The infection occurs more frequently in regions with
▪ Follicular epidermal hyperproliferation
higher temperatures and relative humidity
▪ Excess sebum production
• No sex predominance
▪ Inflammation
• Most common among adolescents and young adults
▪ Presence of Propionibacterium acnes
- lipid-producing sebaceous glands are more active
• History
• Organisms: M. furfur, M. globosa
- Onset of lesions usually around puberty however it
• Predisposing factors: can also be seen in the neonatal or infantile age.
- Warm, humid environment
- Hyperandrogenism should be considered in female
- Hyperhidrosis patient on the ff:
- Oral contraceptive and systemic corticosteroid use ▪ Severe acne
- Cushing’s disease ▪ Hirsutism
- Immunosuppression ▪ Irregular menses
- Malnourished state - Drug-induced acne may be caused by the ff:
• Azelaic acid inhibits the action of the tyrosinase in the ▪ anabolic steroids / corticosteroids
melanin production pathway, which results in persistent ▪ corticotropin, phenytoin, lithium, isoniazid,
hypopigmentation vitamin B complexes, halogenated compounds,
• Scaly oval to round macules scattered over characteristic and certain chemotherapy medications, like
areas of the body, including the upper trunk, neck, and epidermal growth factor receptor (EGFR)
upper arms inhibitors.
• The macules often coalesce forming irregular shaped • Cutaneous Lesions
patches of pigmentary alteration - The primary site of acne is the face and to a lesser
• The color of patches varies from almost white to pink to degree the back, chest, and shoulders. On
reddish brown or fawn colored and may have a wrinkled - The trunk, lesions tend to be concentrated near the
surface appearance midline.
• The scale is characteristically described as dust-like or - Several types of lesions
furfuraceous ▪ Noninflammatory lesions are comedos
• Diagnostics o Open comedones - appears as a flat or
- Wood’s Lamp examination: slightly raised lesion with a central dark-
▪ Yellow–orange fluorescence thought to be due to colored follicular impaction of keratin and
the presence of pteridine lipid

o Closed comedones - appear as pale, slightly - Antiandrogens
elevated, small papules, and do not have a ▪ Spironolactone
clinically visible orifice. • Isotretinoin (oral retinoid)
▪ Inflammatory lesions vary from - Teratogenic
o Papules ▪ Effect on organogenesis
o Pustules ▪ Until 1 month after stopping
o Nodules - Recommended daily dosage 0.5–1 mg/kg/day
• Laboratory Test - Baseline complete blood count and liver function
- In general, laboratory workup is not indicated for tests needed, but the greatest attention is on serum
patients with acne unless hyperandrogenism is triglyceride levels
suspected.
• Treatment Acne Surgery
- The mechanism of action of the most common • Mainstay of therapy in the past used for the removal of
treatments for acne can be categorized in the comedones and superficial pustules
following categories as they relate to the
pathophysiology: Intralesional Glucocorticoids
▪ Correct the altered pattern of follicular • Can dramatically decrease the size of deep nodular
keratinization lesions
▪ Decrease sebaceous gland activity • Injection of a triamcinolone acetate suspension is
▪ Decrease the follicular bacterial population, recommended as the anti-inflammatory agent
particularly P. acnes
▪ Exert an anti-inflammatory effect Phototherapy
• Although ultraviolet B (UVB) can also kill P. acnes in vitro,
Treatment Algorithm for Acne Vulgaris (see appendix) UVB penetrates poorly to the dermal follicle and only
high doses causing sunburn have shown to improve acne
Lasers
• work by causing thermal damage to the sebaceous glands
ECZEMA
ATOPIC DERMATITIS
• Chronic, relapsing skin disease occurring more frequently
during infancy and childhood; associated with intense
Local Therapy pruritus
• Cleansing • Frequently with elevated IgE levels
- Twice daily washing with a gentle cleanser followed • Personal or family history of Atopic Dermatitis, allergic
by the application of acne treatments may encourage rhinitis and/or bronchial asthma;
a routine and therefore better compliance • 35% of patients will develop asthma later in life
• Topical Medications • Typical distribution and morphology:
- Sulfur/Sodium Sulfacetamide/Resorcinol - Facial and extensor surfaces in infants and young
- Salicylic Acid children
- Azelaic Acid - Flexural lichenification in older children and adults
- Benzoyl Peroxide
DYSHIDROTIC ECZEMA
- Antibiotics
▪ Topical Clindamycin and Erythromycin most • A special vesicular type of hand and foot dermatitis
common • Dermatoses of the fingers, palms and soles, characterized
- Retinoids by deep-seated, pruritic, clear “tapioca-like” vesicles or
maybe described as “sago-grains”
▪ both comedolytic and anti- inflammatory
properties • Later, there can be scaling, fissuring or lichenification
Systemic Therapy SEBORRHEIC DERMATITIS

• Antibiotics • Chronic, pruritic, recurrent, characterized by redness and
scaling
- Tetracyclines: Doxycycline and Minocycline
• Can range from white flakes to yellow greasy thick scales
- Macrolides: Erythromycin and Azithromycin
• Predilection sites: scalp, eyebrows, nasolabial folds,
• Hormonal Therapy: goal is to counteract the effects of
retroauricular area, sternum, shoulder blades & V areas
androgens on the sebaceous gland.
of chest and back
- Oral Contraceptives
• Malassezia furfur plays a role in its pathogenesis
- Glucocorticoids
- Gonadotropin-Releasing Hormone Agonists
▪ Leuprolide

IRRITANT CONTACT DERMATITIS First Line Therapy

• Exposure to a chemical capable of irritating the skin; • Identify and eliminate/avoid exacerbating factors
reaction usually ensues with single exposure • Keep skin hydrated
• Treat pruritus and prevent flares
• Hands are the most frequently affected area • Treat exacerbations (flares)
• Severe cases may even lead to necrosis • Treat secondary skin infections early
• Reaction depends on concentration of offending agent,
penetrability and thickness of the stratum corneum 1) Identify and Eliminate/Avoid Exacerbating Factors
• Avoid:
ALLERGIC CONTACT DERMATITIS
- Extremes in temperature
• An eczematous pruritic dermatitis due to re-exposure to
a previously sensitized substance - Coarse wool or synthetic fibers in clothing
- Strong soaps and detergents
- A classic delayed-type cell-mediated hypersensitivity
reaction - Anything known to increase disease severity
- Exposure to a strong allergen may take a week or so,
while exposure to a weak allergen may take months 2) Keep Skin Hydrated
to years • Hydrate with warm soaking bath for at least 10 minutes
followed by application of moisturizers and emollients
NUMMULAR DERMATITIS • Soap Free Cleansers
• Chronic, pruritic, inflammatory dermatitis occurring in - To cleanse, reduce irritation (if sensitive to soaps),
the form of coin-shaped plaques on an erythematous and reduce dryness (thereby increase absorption of
base other topicals).
• Site of predilection: lower legs, upper extremities • Emollients / Moisturizers
• Often seen in atopic individuals - To soften and soothe rough, dry skin and increase
absorbability of topical medications
ASTEATOTIC ECZEMA
• “Eczema craquele” 3) Treat Pruritus and Flares
• Due to excessive bathing with harsh soaps; common • Antihistamines
among elderly 1st GENERATION H1-TYPE
• Dry, crackled superficially fissured skin with slight scaling Chlorpheniramine maleate
associated with pruritus Dimethindene maleate
Clemastine fumarate
• Sites: legs, arms and hands but more severe on the shins
Diphenhydramine hydrochloride
and extensor arms
Hydroxyzine hydrochloride
2nd and 3rd GENERATION H1-TYPE
STASIS DERMATITIS
Cetirizine
• In a setting of Chronic venous insufficiency/ Varicosities
Loratadine
• Starts -> medial malleolus - inflammatory papules, Fexofenadine
scaling, crusting and erosions Desloratadine
• Hyperpigmentation - stippled with recent and old Ebastine
hemorrhages COMBINATION (Steroid + Antihistamine)
• Edema and infection may complicate the situation Betamethasone + Loratadine
- Fibrosis of the skin and subcutaneous tissue Betamethasone + Dexchlorpheniramine maleate
(lipodermatosclerosis) Betamethasone + Chlorpheniramine maleate
Prednisolone + Chlorpheniraminie maleate
- Ulceration
• Low to high potency topical corticosteroids (see appendix
LICHEN SIMPLEX CHRONICUS for potency table)
• Chronic dermatitis characterized by circumscribed - One of the ten definitive moments of modern
plaques with lichenification medicine
• Results from repetitive scratching and rubbing - Potent anti-inflammatory and immunosuppressive
effects
• Occurs more frequently in older individuals (>20 years old)
• Immunomodulatory agents (eg topical tacrolimus or
• Legs, back and sides of the neck, wrists ankles
pimercrolimus used on the face, eyelids, and skin folds)
Stepped Approach to Treatment of Eczema

4) Treat Secondary Skin Infections Early
• Conservative Therapy
• Skin infections with Stapylococcus aureus can be a
- Education - prevention recurrent problem
- Use of emollients/moisturizers • Treat with a short course of oral or topical antibiotics
- Antihistamines
• Fungal infections may complicate eczema and contribute
• Low to mid potency steroid creams to exacerbations.
• High potency steroid creams • Diagnosis and appropriate antifungal
• Phototherapy • treatment is recommended
• Immunomodulators

5) Follow-up Therapy • Lesions vary in size from pinpoint papules to plaques that
• Education of patient and family members: about the cover large areas of the body
chronic nature of eczema, exacerbating factors, and • Usually symmetric
appropriate therapy to achieve effective control of their
condition CLINICAL PATTERNS OF SKIN PRESENTATION
• THIS IS IMPORTANT AS IT ENSURES COOPERATION AND A. Plaque Type Psoriasis
COMPLIANCE WHICH LEADS TO BETTER OUTCOMES - Most common form
- Symmetrical, well-defined erythematous plaques
6) Treatment of Refractory Eczema varying in size from one to several centimeters with a
• Wet dressings dry, thin, silvery-white or micaceous scale
• Phototherapy - AOP: scalp, trunk, buttocks, limbs (extensor surfaces
- It involves the use of light to treat a medical condition. such as elbows and knees)
- Ultraviolet light therapy improves eczema symptoms
in some people. B. Guttate-Type Psoriasis
- PUVA or UVB - Dewdrop like 1mm-10mm, salmon-pink papules,
- ADR: erythema, blistering, nausea, lethargy, pruritus usually with a fine scale
• Systemic immunomodulators (Methotrexate, - Common in younger individuals (<30yo)
mycophenolate mofetil, systemic corticosteroids) - AOP: trunk and proximal extremities
• Hospitalization
• Allergen immunotherapy C. Erythrodermic Psoriasis
- Can develop gradually from chronic plaque disease or
Reminder in the Treatment for Eczema acutely with little preceding psoriasis
• Patient Education - Generalized form of the disease that affects all body
sites (>90% of BSA)
• Treat the patient, not just the rash
- Erythema: most common feature
- Only superficial scaling
PSORIASIS
PSORIASIS D. Pustular Psoriasis
• No gender predilection - Sheets of small, monomorphic pustules developing
• Peak age of onset 15-30 years within erythrodermic skin or along the edges of
• 2 types expanding inflammatory plaques
- Type 1 - May develop from established plaque psoriasis or
▪ Early disease onset (onset before the age of 40) may present de novo
▪ (+) family history and an association with HLA Cw6 - 2 types
and HLA DR7 ▪ Pustulosis palmaris et plantaris
- Type 2 ▪ Acrodermatitis continua Hallopeau
▪ Later disease onset (onset after the age of 40)
▪ (-) family history RELATED PHYSICAL FINDINGS
▪ Lack of any prominent HLA association 1. Nail Changes In Psoriasis
- Can affect the nail bed and nail matrix
ETIOLOGY AND PATHOGENESIS - Leads to thickening, pitting, discoloration and
splintering of the nail plate, and separation of the nail
• Disease of dysregulated inflammation
plate from the nail bed
• Mechanism of inheritance has not been completely clear
• HLA-Cw6 allele (PSORS1) : major susceptibility gene 2. Psoriatic Arthritis
- Associated with an earlier age of onset - Seronegative inflammatory arthritis with various
- Associated with a positive family history clinical presentations
• Environmental factors - Develops at an average of 12 years after the onset of
- Drugs skin lesions
- Skin trauma (Koebner’s phenomenon) - Strong genetic component (HLA B27)
- Infection
- Stress DIAGNOSTIC WORK UP
• Result of complex cutaneous immune reaction with a 1. Histopathologic findings
major inflammatory component involving elements of - Early lesion of pustular psoriasis: slight acanthosis of
the innate and adaptive immune systems and abnormal the epidermis
keratinocyte proliferation and differentiation - Older lesion: psoriasiform hyperplasia
• Mediators that orchestrate changes in psoriasis ▪ Spongiform pustules of Kogoj
- IL12, IL 23, TNFa, IFNy ▪ Hyperkeratosis and parakeratosis
▪ Munro’s microabscesses
CLINICAL FINDINGS
• Well demarcated, raised, erythematous plaque with
white-silvery scales

MANAGEMENT - MOA: interferes with intercellular redox regulation,

A. TOPICAL THERAPY inhibiting NF aB translocation
1. CORTICOSTEROIDS - Dosing: initiate at low dose, escalate dose weekly
- DOSING: Can be used as monotherapy 1-2x/day - Monitoring: CBC, comprehensive metabolic panel,
- Can be combined with other topical agents, UV and urinalysis repeat test monthly for 6 months
systemic agents
- Duration of use: 4. CYCLOSPORIN A
▪ Class I: available data for 2-4 weeks of treatment - MOA: Binds cyclophilin → blocks calcineurin →
reduce the effect on NF-AT in T cells → inhibition of
▪ Less potent agents: optimal endpoint unknown
IL-2 and other cytokines
▪ Gradual reduction in usage recommended
following clinical response 5. HYDROXYUREA
- MOA: inhibits ribonucleotide diphosphate reductase
2. CALCINEURIN INHIBITORS
- Monitoring: CBC, CMP, LFTs
- Dosing: apply 2x/day on affected areas, no duration
of course is specified
6. MYCOPHENOLATE MOFETIL
- More effective for intertriginous and facial psoriasis
- MOA: noncompetitive inhibitor of inosine
monophosphate dehydrogenase, blocking de novo
3. TAZAROTENE
purine biosynthesis
- Dosing: apply once at night to affected areas
- Monitoring: CBC, CMP
- Best used in combination with topical corticosteroids
- Contraindication 7. 6-THIOGUANINE
▪ Most common: skin irritation in lesional and - MOA: purine analog that interferes with purine
perilesional skin biosynthesis→ cell cycle arrest and apoptosis
▪ Photosensitizing - Monitoring: CBC, CMP, LFTs
4. VITAMIN D ANALOGS PROGNOSIS

- Dosing: apply 2x/day on affected areas - Guttate psoriasis: self-limited
- Use in combination with topical corticosteroids gives ▪ 12-16 weeks without treatment
added benefit
▪ 1/3-2/3 of the patients develop chronic plaque
- Contraindication type psoriasis
▪ Transient irritation in lesional and perilesional skin - Chronic plaque type
▪ Lifelong disease
5. EMOLLIENTS
- Erythrodermic and generalized pustular psoriasis
- Dosing: apply 1-3x/day
▪ Poor prognosis
- Standard adjunctive therapeutic approach to the
▪ Can be severe and persistent
treatment of psoriasis
6. SALICYLIC ACID HANSEN’S DISEASE

- Dosing: apply 1x/day ETIOLOGY
- May reduce keratinocyte-to-keratinocyte binding as • Leprosy is caused by acid fast bacilli called
well as reduce the pH of the stratum conrneum→ Mycobacterium leprae (M. leprae), It is an obligate
reduced scaling and softening of psoriatic plaques intracellular bacterium.
• It mainly affects the skin, peripheral nerves, eyes, mucosa
B. SYSTEMIC THERAPY of the upper respiratory tract
1. METHOTREXATE • Bacterium invades either dermal (cutaneous) nerves or
- Blocks dihydrofolate reductase → inhibition of purine main peripheral nerve trunks situated superficially, in
and pyrimidine synthesis→ inhibition of nucleic acid regions that are relatively cooler.
synthesis in activated t-cells and in keratinocytes →
antiproliferative and immunomodulatory effects PATHOGENESIS OF HANSEN’S DISEASE
- Given once weekly, orally or parenterally • Bacilli enter the body usually through respiratory system
- Maximum dose should not exceed 30mg/week • Migrate towards the neural tissue and enter the Schwann
- Monitoring: CBC, LFTs weekly cells
• Bacilli start multiplying slowly (about 12-14 days for one
2. ACITRETIN bacterium to divide into two) within the cells, get
- MOA: binds retinoic acid receptors → normalizing liberated from the destroyed cells and enter other
keratinization and proliferation of the epidermis unaffected cells
- Dosing: 25-50mg/day • As the bacilli multiply, bacterial load increases in the body
- Monitoring: CBC, LFTs, lipid profile, pregnancy test and infection is recognized by the immunological system
• Lymphocytes and histiocytes (macrophages) invade the
3. FUMARIC ACID ESTERS infected tissue

• At this stage clinical manifestation may appear as ill-defined outer

involvement of nerves with impairment of sensation and/ border
or skin patch (characteristic
punched out
• If it is not diagnosed and treated in the early stages, appearance)
further progress of the diseases is determined by the
strength of the patient’s immune response. Borderline MANY
Lepromatous Roughly
CLINICAL PRESENTATION OF HANSEN’S DISEASE (BL) symmetrical
RIDLEY CLASSIFICATION OF CLINICAL PRESENTATION Shiny papules,
nodules, plaques
+++ -
• Based on high resistance to low resistance With sloping
1. Tuberculoid (TT) edges
2. Borderline Tuberculoid (BT)
Lepromatous NUMEROUS
3. Borderline Borderline (BB) Leprosy (LL) Symmetrical
4. Borderline Lepromatous (BL) Erythematous
5. Lepromatous Leprosy (LL) shiny macules,
++++ -
papules, nodules
PERIPHERAL NERVE CHANGES *Saddle nose
Peripheral Nerve involvement is much more serious and causes deformity
permanent and progressive disability and crippling deformities
because neurons if destroyed do not regenerate and are
replaced by fibrous tissue. The common nerves involved are: Reactional States
Feature Reversal Reaction Relapse
• Facial Nerve
Onset Sudden (within a few Slow and insidious
• Greater auricular nerve hours) (weeks or months)
• Ulnar nerve Time of onset Occurs during Occurs long after
• Radial nerve treatment or within treatment is
six months of discontinued, after an
• Lateral popliteal nerve (Common peroneal nerve)
stopping treatment interval of at least 6
• Posterior Tibial nerve months
Old lesions Some or all existing The margins of some
WHO CLASSIFICATION: lesions become lesions may become
PAUCIBACILLARY MULITBACILLARY erythematous, shiny erythematous
LATENCY 5 years Up to 20 years and swollen
AFB SMEAR - + New lesions Several new lesions Few
CELL MEDIATED Strong Weak may develop in some
IMMUNE RESPONSE cases
LESIONS <=5 >=5 Ulceration Sometimes Unusual
FORM Tuberculoid Lepromatous Scaling Lesions desquamate Absent
CYTOKINE PROFILE IFN-Gamma and IL2 IL-4 and Il-10 as they subside
Nerve Common; many A single nerve
involvement nerves may rapidly becomes involved;
PHYSICAL FINDINGS become painful and Disturbances develop
Cardinal signs tender; Disturbances slowly
• Hypopigmented or reddish skin lesion(s) with definite develop rapidly
loss of sensation General Fever and malaise Not affected
condition are usual
• Enlargement plus tenderness of peripheral nerves Response to Excellent Lesions subside but
• Slit skin smear positive for acid fast bacilli corticosteroids reappear,
corticosteroids are not
CLASSIFICATION indicated in relapse
AFB Lepromin
Skin lesions REVERSAL REACTION ERYTHEMA
Smear Test
(TYPE 1) NODOSUM
Indeterminate SINGLE, ill-
LEPROSUM
defined,
- (TYPE 2)
PAUCIBACILLARY
hypopigmented/
erythematous Type/ Paucibacillary and Multibacillary only
Classification multibacillary
Tuberculoid SINGLE or FEW
(TT) Asymmetrical Etiology Change in delayed type Immune complex
Well-defined - ++++ hypersensitivity to M. disease (when M.
Hypopigmented leprae Leprae are killed
or erythematous There is also an and are
Borderline FEW associated increase in the decomposed; the
Tuberculoid Asymmetrical specific cell-mediated proteins from
(BT) Well-demarcated immunity in those dead bacilli cause
MULTIBACILLARY
Dry + + patients undergoing a an allergic

Annular with shift in classification reaction
clearly defined whether slight or marked
outer border Manifestations Leprosy lesions gradually Crops of painful
Borderline Asymmetrical become swollen and papules, nodules
Borderline Well demarcated erythematous (+/- new developing in a
(BB) inner border with
++ +/- lesions, nerve few hours and
clear center and lasting a few days.
enlargement, acute Successive crops 3) Multi-Bacillary Regimen
neuritis) may occur over Adult Child Child Frequency
Lasts for weeks or months many months/ (50-70kg) 10-14 yo <10yo and
years Duration
+ Fever, general
malaise and pain Rifampicin Day 1: Day 1: Day 1: Once a
Complications Skin ulceration, paralysis, Neuritis, iritis, 600mg 450mg 300mg month for
anesthesia orchitis, 12-18
lymphadenopathy, months
arthritis,
Clofazimine Day 1: Day 1: Day 1: Once a
proteinuria,
ulcerating lesions
300mg 150mg 100mg month for
then then then 12-18
50mg OD 50mg 50mg months
Diagnostics
every 2x a
• Blood Examination other week
- CBC PC, FBS, SGOT SGPT, Alkaline phosphatase, BUN, day
Creatinine Dapsone 100mg 50mg 25mg Once a day
- G6PD (should be normal to avoid hemolytic anemia for 12-18
caused by Dapsone) months
• Slit Skin Smear
• Skin Punch Biopsy MEDICATION NOTABLE SIDE EFFECTS
Rifampicin Hepatotoxicity
- Stains: H&E (Hematoxylin and Eosin), Fite Faraco
Clofazimine Red orange skin discoloration
• Others Dapsone Hemolysis, anemia, agranulocytosis
- Urinalysis
- Chest Xray
Second-Line Drugs
• LEPROMIN TEST
• Ofloxacin
- The lepromin or Mitsuda test consists of an
• Minocycline
intradermal injection of 0.1 ml of a suspension of
heat-killed M. leprae
Points to Remember in Medical Management
- The response is positive when a nodule forms at the
site of injection 3 to 4 weeks later, indicating that the • Contact tracing of detected Hansen’s Disease patients is
patient is able to mount a specific cell-mediated essential
response to the bacilli • Most effective way of preventing disabilities in leprosy
- The test provides prognostic, but not diagnostic, and to prevent further transmission lies in early diagnosis
information. and treatment with MDT
- It is positive in TT and BT leprosy • A patient on PB regimen should take 6 blister packs within
9 months while a patient on MB regimen should take 12
blister packs within 18 months
MANAGEMENT
A. Medical Management of Leprosy • If PB is reclassified to MB after 6 blister packs, start
treatment with MB regimen to complete 12 blister packs
• Multi Drug Therapy (MDT)
within 18 months
- Accepted standard treatment for leprosy
• Monitoring progress includes noting changes in character
- Proven safe and effective of lesion, pain in eyes, changes in color of sclera and
- Started as soon as diagnosis is made conjunctivae, new disabilities or progression of previous
- Combination of >2 anti-leprosy drugs disabilities, nerve damage.
- Renders patient non-infectious within 1 month after
starting treatment B. Medical Management of Reactional States
1) Single Lesion Paucibacillary (ROM Regimen) Type of
Features Management
Reaction
Adult Child
Dose Mild Reversal - Mildly swollen - Give only analgesics
(50-70kg) (3-14y/o) or ENL lesion - Do Nerve Function
Rifampicin 600mg 300mg Single Reaction - Low-grade fever Assessment (NFA)
Ofloxacin 400mg 200mg Single every 2 weeks
Minocycline 100mg 50mg Single - Advise bed rest
*Ofloxacin and Minocycline – not recommended for pregnant - Continue MDT
women and children < 5y/o Severe - Nerve damage - Give prescribed WHO
Reversal of less than 12 Prednisone treatment
2) Pauci-bacillary Regimen Reaction months (muscle - Continue MDT
Frequency weakness, loss - Do NFA every two
Adult Child Child
and of sensation, weeks
(50-70kg) 10-14 yo <10yo and/or nerve
Duration - Refer patients with
Rifampicin 600mg 450mg 300mg Once a pain)
persistent, recurrent
month for - Nerve and non-responding
6-9 tenderness reactions
months - Swollen lesions
in the face
Dapsone 100mg 50mg 25mg Once a day
for 6-9
months
Severe ENL - High fever - Give prescribed WHO 2. Papulosquamous SCLE (syn. disseminated DLE, subacute
Reaction disseminated LE, superficial disseminated LE, psoriasiform LE, pityriasiform
- Reddish Prednisone treatment
LE, and maculopapular photosensitive LE)
nodules - Continue MDT C. Chronic cutaneous LE (CCLE)
- Painful neuritis - Do NFA every 2 weeks 1. Classic discoid LE (DLE)
a. Localized DLE
- Joint pain - Refer patient with
b. Generalized DLE
- Skin ulceration persistent, recurrent 2. Hypertrophic/verrucous DLE
- Orchitis, iritis, and non-responding 3. Lupus profundus/lupus panniculitis
ostitis, reactions 4. Mucosal DLE
nephritis, a. Oral DLE
b. Conjunctival DLE
swollen hands,
5. Lupus tumidus (urticarial plaque of LE)
feet and face 6. Chilblain LE (chilblain lupus)
If Prednisone is contraindicated or insufficient to control 7. Lichenoid DLE (LE/lichen planus overlap, lupus planus
recurrence, give: Clofazimine or Thalidomide LE-Nonspecific Skin Disease
A. Cutaneous vascular disease
1. Vasculitis
COMPLICATIONS
a. Leukocytoclastic
• Common complications arise from peripheral nerve (1) Palpable purpura
injury, venous insufficiency or scarring (2) Urticarial vasculitis
b. Periarteritis nodosa-like cutaneous lesions
• One-quarter to one-third of newly diagnosed patients 2. Vasculopathy
have or will eventually have chronic disability secondary a. Degos disease-like lesions
to irreversible nerve injury of the hands or feet or from b. Secondary atrophie blanche (syn. livedoid vasculitis, livedo
vasculitis)
eye involvement
3. Periungual telangiectasia
• Exposure keratitis from dry eye, corneal insensitivity, and 4. Livedo reticularis
lagaophthalmos. Internal eye disease may result to 5. Thrombophlebitis
6. Raynaud phenomenon
blindness
7. Erythromelalgia (erythermalgia)
• Venous insufficiency, secondary to endothelial B. Nonscarring alopecia
involvement of deep vein valves, leads to stasis 1. “Lupus hair”
2. Telogen effluvium
dermatitis and leg ulcers
3. Alopecia areata
• Destruction of joints (Charcot joints) may occur due to C. Sclerodactyly
loss of protective pain sensation D. Rheumatoid nodules
E. Calcinosis cutis
• Sympathetic nerve involvement results in decreased F. LE-nonspecific bullous lesions
hidrosis, leading to dry palms and soles G. Urticaria
H. Papulonodular mucinosis
• Collapse of the nose in lepromatous leprosy is from the I. Cutis laxa/anetoderma
contracture of the scar tissue J. Acanthosis nigricans (type B insulin resistance)
K. Erythema multiforme
PROGNOSIS AND CLINICAL COURSE L. Leg ulcers
M. Lichen planus
• Can be cured without therapy: TT or BT who upgrade to
TT Etiology and Pathogenesis
• Disease is progressive with morbidity due to nerve injury • The interplay between host factors (susceptibility genes,
and/or superimposed reactional states hormonal milieu, etc.) and environmental factors
• Treatment arrests much of disease activity [ultraviolet (UV) radiation, viruses, and drugs] leads to
• Stocking-glove pattern of sensory impairment may loss of self-tolerance, and induction of autoimmunity.
progress. Peripheral neuritis of recent onset may improve • This is followed by activation and expansion of the
with corticosteroid treatment immune system, and eventuates in immunologic injury to
end organs and clinical expression of the disease
CONNECTIVE TISSUE DISEASES
LUPUS ERYTHEMATOSUS
• A group of heterogeneous illnesses that have in common
the development of immunity to self-nucleic acids and
their associated proteins, with skin-only disease at one
end of the spectrum and severe visceral involvement at
the other.
• James N. Gilliam divides the cutaneous manifestations of
LE into:
- LE-specific skin disease: lesions that show
characteristic histologic changes of LE
- LE-nonspecific skin disease: lesions that are not
histopathologically distinct for LE and/or may be seen
as a feature of another disease
LE-Specific Skin Disease [Cutaneous LE (CLE)]
A. Acute cutaneous LE (ACLE)
1. Localized ACLE (malar rash; butterfly rash)
2. Generalized ACLE (lupus maculopapular lupus rash, SLE rash, rash,
photosensitive lupus dermatitis)
B. Subacute cutaneous LE (SCLE)
1. Annular SCLE (syn. lupus marginatus, symmetric erythema
centrifugum, autoimmune annular erythema, lupus erythematosus gyratus
repens)

Clinical Findings • Less transient and heal with more pigmentary change;
Acute CLE less edematous and more hyperkeratotic
• confluent, symmetric erythema and edema are centered Chronic
over the malar eminences and bridges over the nose • Discoid LE: red-purple macules, papules or small plaques
(classic butterfly rash or malar rash) that rapidly develop a hyperkeratotic surface; sharply
• Head, chin and V area of the neck can be involved; severe demarcated, coin-shaped erythematous plaques covered
facial swelling by prominent, adherent scale that extends into the
orifices of dilated hair follicles
• Generalized ACLE: widespread morbiliform or
exanthematous eruption often focused over the extensor - Expand with erythema and hyperpigmentation at the
aspects of the arms and hands, sparing the knuckles periphery, leaving hallmark atrophic central scarring,
Subacute telangiectasia and hypopigmentation → large,,
confluent, disfiguring plaques
• Erythematous macules and/or papules that evolve into
- Hair-bearing skin → irreversible scarring alopecia;
hyperkeratotic papulosquamous or annular/polycyclic
keratotic plugs in dilated follicles
plaques
- Carpet tack sign – when adherent scale is lifted from
• Photosensitive lesions, occur predominantly in sun-
more advanced lesions, keratotic spikes can be seen
exposed areas (upper back, shoulders, extensor aspects
to project from the undersurface of the scale
of the arms, V area of the neck, lateral face – less
common) - Seen on the face, scalp, ears, V area of the neck,
extensor aspect of the arms
• Active edge of lesions: undergoes a vesiculobullous
change that subsequently produce a crusted appearance • Hypertrophic DLE: exaggerated hyperkeratosis in classic
DLE lesions
- Extensor aspects of arms, upper back, face
- Lupus planus: overlap of hypertrophic DLE and lichen
planus
- Lupus erythematosus hypertrophicus et profundus:
hypertrophic DLE plus violacous/dull red, indurated,
rolled borders and striking central, crateriform
atrophy
• Mucosal DLE: painless, erythematous patches that evolve
into sharply marginated, with irregularly scalloped, white
borders with radiating white striae and telangiectasia;
honeycomb appearance
- More common: buccal mucosa; others: palate,
alveolar process, tongue, vermilion border of the lips,
nasal, conjunctival, anogenital mucosa
• LE Profundus/LE Panniculitis:
- LE panniculitis: firm nodules, 1-3 cm in diameter,
overlying skin is attached to subcutaneous nodules
and is drawn inward to produce deep, saucerized
depressions
- Located on the head, proximal upper arms, chest,
back, breast, buttocks, thighs
- LE profundus: LE panniculitis + Classic DLE
• Chilblain LE: purple-red patches, papules and plaques on
the toes, fingers, face → scarred atrophic plaques with
associated telangiectases
- Precipitated by cold, damp climates
• LE Tumidus: succulent, edematous, urticaria-like plaques
with little surface change
Diagnostics
ANA with profile ANA: positive in >95% of SLE
(anti-dsDNA, -Sm) patients, develop within 1 year of
Complement levels onset
(C3, C4) Anti-dsDNA: specific for SLE,
heralds a flare (nephritis or
vasculitis), especially when
associated with declining levels of
C3 or C4
dsDNA LE nephritis
rRNP CNS LE
ssDNA Risk of SLE in DLE
Histones Drug-induced SLE
U1RNP Mixed CTD
Ro/SS-A SCLE, neonatal LE
La/SS-B SCLE
Chest x-ray To check for pleural effusion ophthalmologic examination every 6-12
12-L ECG / 2D echo To check for pericardial effusion or months.
pericarditis Hydroxychloroquine sulfate, 6-6.5
Urinalysis / 24 hr To check for proteinuria mg/kg, daily. 2-3 month delayed onset
urine (>0.5g/day or 3+) and cellular casts of therapeutic benefit.
BUN, Creatinine To check for other renal disorders No response after 8-12 weeks:
Electrolytes, ESR To check for electrolyte imbalance Quinacrine hydrochloride, 100 mg/day.
Cranial CT Scan To check for derangements in the Can be added to HQ without the
background of neurological enhancing the risk of retinopathy.
symptoms Inadequate control after 4-6 weeks:
CBC, peripheral blood To check for hemolytic anemia, Replace hydrochloroquine with
smear leukopenia, lymphopenia, Chloroquine diphosphate, 3mg/kg.
thrombocytopenia Adjust dose for decreased renal or
Skin punch biopsy (see below) hepatic function.
Immunohistology IgG > IgM > IgA and Complement Side Effects: Quinacrine – headache, GI
components deposited in a intolerance, hematologic toxicity,
Lupus band test continuous granular or linear pruritus, lichenoid drug eruptions,
band-like array at the dermal- mucosal or cutaneous pigmentary
epidermal junction pigmentation; yellow discoloration of
SLE: (+) lesional and non lesional skin and sclera; significant hemolysis
skin with G6PD deficiency
DLE: (+) lesional skin only Antimalarials – bone marrow
suppression, aplastic anemia
MANAGEMENT Non- Methotrexate: 10-25 mg once a week,
immunosuppres with folic acid (adjust if CrCl <60
• Evaluation to rule out underlying SLE disease activity
sive options for mL/min)
• Protection from sunlight and artificial sources of UVR antimalarial- Diaminodiphenylsulfone (Dapsone):
• Avoid the use of potentially photosensitizing agents refractory initial dose 25mg 2 x a day, can increase
(hydrochlorothiazide, tetracycline, griseofulvin, disease to 200-400 mg/day
piroxicam) SE: hemolysis and/or
methemoglobinemia, especially in G6PD
Local Therapy deficient
Sun Protection Avoid direct sun exposure, wear tightly Isotretinoin, 0.5-2.0 mg/kg/day, and
woven clothing and broad-brimmed hats Acitretin, 10-50 mg/day.
Regularly use broad-spectrum, water- SE: teratogenicity, mucocutaneous
resistant sunscreens (SPF ≥ 30 with an dryness, hyperlipidemia
efficient UVA blocking agent). Thalidomide, 50-200 mg/day (or
Apply UV blocking films. Lenalidomide)
Local Intermediate strength preparations SE: severe teratogenicity, sensory
Glucocorticoids (Triamcinolone acetonide 0.1%) for neuropathy, peripheral neuropathy,
sensitive areas relapse, thromboembolism
Superpotent topical class I agents Systemic Every effort should be made to avoid the
(Clobetasol propionate 0.05% or Glucocorticoids use of systemic glucocorticoids.
Betamethasone dipropionate 0.05%) – Intravenous pulse methylprednisolone –
produce the greatest benefit in CLE severe and symptomatic skin disease
Class I or II topical solutions and gels – Oral glucocorticoids (Prednisone), 20-40
best for treating the scalp mg/day, as a single morning dose –
Topical Pimecrolimus 1% cream and Tacrolimus supplemental therapy during the loading
Calcineurin 0.1% ointment phase of therapy with an antimalarial
Inhibitors agent
Intralesional Triamcinolone acetonide suspension 2.5- Controlled disease activity: daily dosage
Glucocorticoids 5.0mg/ml for the face; higher should be reduced to 5mg to 10 mg
concentration for other areas, every 4-6 decrements until activity flares again or
weeks until a daily dosage of 20mg/day is
More useful for DLE; hyperkeratotic achieved
lesions unresponsive to topical 2.5 mg decrements at 10 mg/day
glucocorticoids Prednisolone – significant liver disease
Active borders should be thoroughly (prednisone requires hydroxylation in
infiltrated the liver)
Others Topical Retinoids: Tazarotene 0.05% gel, Dose should be reduced at the earliest
Tretinoin 0.025% gel possible time because of side effects:
5% Imiquimod cream avascular (aseptic) bone necrosis –
susceptible to LE patient
Systemic Therapy steroid-bone loss occurs most rapidly in
Antimalarials Pretreatment ophthalmologic the first 6 months of use
examination. Antimalarial retinopathy is agents to prevent osteoporosis with the
extremely rare especially in the first 10 initiation of steroid therapy
years of therapy. Follow-up

Prognosis and Course • Gottron sign

Acute Depends on underlying SLE activity - confluent macular violaceous erythema, most
CLE pronounced over the metacarpophalangeal/
Subacute Intermittent recurrence of disease activity over interphalangeal joints, extending in a linear array
CLE long periods of time without significant overlying the extensor tendons of the hand and
progression of systemic involvement fingers
Chronic Untreated: indolent progression to large areas • Early Gottron papules
CLE of cutaneous dystrophy and scarring alopecia - seen over the distal interphalangeal joints along with
Psychosocially devastating and occupationally periungual erythema and dystrophic cuticles.
disabling
Treatment: skin disease can be controlled Primary skin changes of DM
Spontaneous remission occurs occasionally
• Pruritic, symmetric, confluent, macular violaceous
Older, inactive lesions can be active again
erythema variably affecting the skin overlying the
Rebound after discontinuation of treatment
extensor aspect of the fingers, hands, and forearms; the
SCC in chronic smoldering DLE lesions
arms, deltoid areas, posterior shoulders, and neck (the
5% of DLE patients → SLE
shawl sign); the V area of the anterior neck and upper
Generalized DLE with abnormal laboratory
chest; and the central aspect of the face, periorbital areas,
findings → increased risk of SLE
forehead, and scalp
DERMATOMYOSITIS (DM) • Lateral aspects of the hips and thighs (holster sign) are
Thought to evolve through multiple sequential phases: also frequently involved
• a genetically determined susceptibility phase • Poikiloderma atrophicans vasculare and calcinosis cutis
are often present
• an induction phase triggered by an environmental
stimulus
Muscle Disease
• an autoimmune expansion phase
• Initial clinical finding include lower-extremity weakness
• injury phase involving multiple immunologic effector manifested as difficulty in performing routine activities of
mechanisms daily living, such as rising from a chair
• Followed by upper extremity weakness manifested by
Idiopathic inflammatory myopathies (IIDMs)
difficulty in raising the arms above the head to perform
• Predominately target the skeletal musculature and/or routine activities such as combing the hair
skin and typically result in symptomatic skeletal muscle
• (+) pain or tenderness in the affected muscle groups
weakness and/or cutaneous inflammatory disease
• Weakness involving the upper one-third of the
Dermatomyositis (DM) esophagus and/or the laryngopharyngeal muscles may
present as dysphagia or a hoarse voice (dysphonia)
• Only idiopathic inflammatory myopathy that expresses a
characteristic pattern of primary cutaneous inflammation • Some patients with severe diaphragmatic disease require
mechanical ventilation
Classic Dermatomyositis • Cardiac failure may be present in the terminal phase of
• Cutaneous involvement in 30% to 40% of adults and in 95% the disease
of children
Diagnostic Criteria
• Occur most frequently in the fifth and sixth decades
The following are commonly used to define DM/PM skin
• Environmental factors have been implicated as disease lesions
triggers
• Heliotrope rash (red–purple edematous erythema on the
upper palpebra)
Drug-induced Dermatomyositis
• Gottron’s papules or sign (red–purple flat-topped
• Caused or exacerbated by systemic medications
papules, atrophy, or erythema on the extensor surfaces
• Present with both myositis and pathognomonic and finger joints)
cutaneous findings and resolve with discontinuation of
• Proximal muscle weakness (upper or lower extremity and
the medication
trunk)
• Long-term hydroxyurea therapy
• Elevated serum creatine kinase or aldolase level
• Can produce a DM-like cutaneous eruption
• Muscle pain on grasping or spontaneous pain
• Unique in that muscle weakness and other systemic
• Myogenic changes on EMG (short-duration, polyphasic
symptoms are absent
motor unit potentials with spontaneous fibrillation
• Painful leg ulcers, xerosis and cutaneous atrophy are potentials)
often seen
Treatment
Cutaneous Lesions Goal is to arrest inflammation in the skin and muscles and
• Gottron sign and gottron papules are pathognomonic obtain a clinical remission.
• Periorbital, confluent, macular, violaceous (heliotrope)
erythema/edema and periungual telangiectasia with
dystrophic cuticles, are highly characteristic

• Local Treatment Etiology

- Avoid excessive sun exposure • Several studies suggest that a (+) family history for SSc is
- Use effective broadspectrum sunscreens the strongest risk factor
- Topical glucocorticoids (classes I and II) • Ethnicity also contributes: Blacks with SSc are frequently
- Daily use of a medicated shampoo younger than whites
- Effective moisturization regimens • Approximately 1.5% of SSc patients have one or more
- Topical antipruritic agents affected first-degree relatives: a 10- to 15-fold higher risk
in family members than in the general population
- Pulsed dye laser therapy
• Several studies suggest an association of scleroderma
• Systemic Treatment with the following genes:
- Nonsedating or sedating antihistamines - HLA-DRB1*1302
- Anti-malarials - DQB1*0604/0605 haplotypes (with anti brillarin
positive patients)
▪ Hydroxychloroquine sulfate (6 mg/kg given as two
divided doses per day) - HLA SRB1*0301 (with anti-Pm-Scl antibodies)
- Systemic glucocorticoids remain the traditional first-
Clinical Manifestations
line therapy
Depend to a large extent on the subset and stage of disease
▪ Prednisone is given in divided doses of 1.0–1.5
• SKIN
mg/kg/day, whereas in children the dosage is 1–2
mg/kg/da - involvement is a cardinal feature of SSc; usually
appears first in the fingers and hands
- Methotrexate (7.5–25.0 mg) given once weekly
- nonpitting edema of the fingers (puffy fingers) hands,
- Cyclosporine and cyclophosphamide
and extremities
- Mycophenolate mofetil
- Sclerodactyly: induration and skin thickening of the
- High-dose intravenous γ globulin therapy fingers
- anti-TNF-α therapy has been used anecdotally to treat - Restricted mobility of joints (dermatogenous
both the muscular and cutaneous manifestations of contractures), and/or restricted breath-excursion
DM may be present
- Typical facial features:
Prognosis and Complications
▪ telangiectasias, a beak-shaped nose as well as
Classic DM
reduced mouth-aperture (microstomia)
• Pulmonary and cardiac complications were the most
- Calcinosis cutis: abnormal deposition of cutaneous
frequent causes of death
and/or subcutaneous calcium; occurs over pressure
• Cancer-associated myositis had the worst prognosis points (acral, joints)
• Juvenile-onset and overlap myositis had the best - “Salt and pepper skin”
prognosis
▪ hypo and hyperpigmented skin
• Cutaneous ulceration, internal malignancy, opportunistic - loss of hair follicles and sweat glands
infections and lymphoma may occur
• VASCULOPATHY
SCLERODERMA (SYSTEMIC SCLEROSIS)
- Approximately 50% of patients with SSc are affected
• Rare multisystem disease based on:
by digital ulceration associated with vasculopathy at
• Autoimmunological processes some point in their disease
• Vascular endothelial injury - Tender and painful pitting scars → ulcers
• Extensive activation of fibroblasts ▪ Finger/toe-tips, extensor surfaces of joints
• Most frequently affected organs: Skin, esophagus, lung, - Other complications:
heart, kidneys ▪ Critical digital ischemia, paronychia, infections,
gangrene, osteomyelitis, finger pulp loss
Epidemiology
• Worldwide distribution, affects all races • SYSTEMIC
• Women are more frequently affected by systemic - Cardiopulmonary
sclerosis (SSc) ▪ Dyspnea, non-productive cough, disturbed
• Women > Men (3:1 to 14:1) diffusion-capacity and cyanosis
• Age of disease onset ranges between 30 and 50 years ▪ Palpitations, irregular hearbeat
males have earlier onset than females ▪ Pulmonary arterial hypertension: most common
• SSc has the highest case-specific mortality of any of the cause of disease-related death
autoimmune rheumatic diseases, but it varies individually - Gastrointestinal
depending on: ▪ Most common internal organ involvement
- racial or ethnic differences ▪ Problems with motility, digestion, absorption,
- presence and severity of organ involvement excretion
- SSc subsets ▪ Dysphagia, heart burn (reflux), nausea, vomiting,
- age at diagnosis early satiety
- gender differences ▪ Hypomotility, bacterial overgrowth,
malabsorption, fecal incontinence

▪ Constipation alternating with diarrhea - Sildenafil PO
- Nephrologic - Epoprostenol/Iloprost/Beraprost PO
▪ Systemic renal crisis: Acute renal failure with • Renal (scleroderma renal crisis, headache, hypertension)
abrupt onset of moderate to severe HPN - Blood pressure control
(150/85mmHg) - ACE-inhibitors (Use in a stable patient is not
▪ Elevated serum creatine twice normal upper limit recommended
▪ Proteinuria of >/= 0.5g/day on two or more
occasions Monitoring
▪ End-organ damage: encephalopathy with • It is recommended that the clinically stable patient have
generalized seizures or pulmonary edema the following diagnostics:
- Musculoskeletal • Pulmonary function test annually
▪ Arthralgia, myalgia, loss in joint range of motion • High-resolution CT Scan (HRCT) if pulmonary function is
and joint contracture, symptoms of carpal tunnel, declining or if patient has developed new onset dyspnea
muscle weakness • Modified Rodnan skin score (at baseline then q3 months)
▪ Ear, Nose, Throat
• Blood pressure count periodically
▪ Sicca syndrome, poor dentition, hoarseness
• Autoantibodies at baseline
- Neurologic
• CBC, Urinalysis, BUN, Creatinine, AST, ALT periodically
▪ Facial pain and decreased sensation, hand
• Echocardiography
paresthesias and weakness, headache and stroke
- Reproductive • Malignancy screening
▪ Erectile dysfunction, dyspareunia Course and Prognosis
- Constitutional
• Largely depends on involvement of internal organs (lungs,
▪ Fatigue, weight loss heart, kidneys)
• Associated with a significant mortality rate: < 70% overall
Management
10-year survivial
• Skin findings
• Worse prognosis:
- Physical therapy and regular exercise
- Male sex
- Topical steroids, calcineurin inhibitors, moisturizing
- African-American race
creams
- Older age at diagnosis
- Immunosuppressive drugs, systemic steroids (short-
time) - (+) interstitial lung disease/pulmonary hypertension
- Phototherapy - High levels of modified Rodnan skin score
- Surgery (calcinosis cutis) - Rapid progression of disease
- Laser therapies • Immunosuppressive therapy
- Bleaching agents, salicylic acids and chemical peels - might interrupt the immune-mediated portion of the
pathogenetic cycle, resulting in disease improvement
• Vascular findings (Raynaud’s phenomenon, digital
ulcerations)
- Consistent warm keeping, Paraffin-bath DERMATOLOGIC EMERGENCIES
- Calcium channel blockers PO STEVENS JOHNSON SYNDROME & TOXIC EPIDERMAL
- Iloprost IV NECROLYSIS
- Bosentan PO • Rare and life-threatening reaction, mainly drug induced
- Sildenafil PO • Widespread apoptosis of keratinocytes provoked by the
activation of a cell-mediated cytotoxic reaction and
- Wound dressing (hydrocolloid membrane, mepilex)
amplified by cytokines, mainly granulysin
• Lung findings (dyspnea, dry cough, bibasilar rales, • A dozen “high risk” drugs account for half the cases and
alveolitis/lung fibrosis) up to 20% remain idiopathic
- Oxygen
Clinical
- Cyclophosphamide PO or IV
• Clinically begins within 8 weeks after the onset of drug
- Azathioprine PO
exposure for the first time
- Glucocorticoid
• About one-third of cases begin with nonspecific
• Gastrointestinal findings (reflux, dysphagia, diarrhea, symptoms (fever, headache, rhinitis cough or malaise),
obstipation) one-third with symptoms of mucous membrane
- Proton Pump Inhibitor involvement, and one-third with an exanthema
- H2-receptor-antagonists • Characterized by erythematous, dusky red, purpuric
- Change habit of eating macules, irregularly shaped, which progressively coalesce,
- Antibiotics (Erythromycin) evolving to flaccid blisters and epidermal detachment
• Cardiac (pulmonary arterial hypertension, shortness of predominating on the trunk and upper limbs and
breath, palpitations, peripheral edema) associated with mucous membrane involvement
- Oxygen • Skin lesions appear on the face and trunk and rapidly
spread (usually within 4 days) to their maximum extent
- Diuretics
- Bosentan PO

• Nikolsky’s sign (dislodgement of the epidermis by lateral EXFOLIATIVE DERMATITIS

pressure) is positive on erythematous zones • Diffuse erythema and scaling of the skin involving more
- At this stage, the lesions evolve to flaccid blisters, than 90% of the total body skin surface area
which spread with pressure and break easily • With male predominant (a male-to-female ratio of
- The necrotic epidermis is easily detached at pressure approximately 2:1 to 4:1)
points or by frictional trauma, revealing large areas of • Any age group can be affected with most studies
exposed, red, sometimes oozing dermis excluding children
• average age of disease onset varies from 41 to 61.
SJS (involvement of <10% BSA)
• Occurs in all races.
TEN (involvement of > 30% BSA)
SJS-TEN Overlap (involvement of 10-30% BSA) Etiology and Pathogenesis
• both are considered by some as parts of a disease
• Pre-existing dermatosis is the most frequent cause in
spectrum based on the following:
adults
▪ most commonly induced by the same medications
• Followed by drug hypersensitivity reactions and
▪ patients initially presenting with SJS may progress cutaneous T-cell lymphoma (CTCL) or Sézary syndrome
to extensive skin loss resembling TEN
• No underlying etiology is identified in approximately 20%
▪ histologic findings are indistinguishable of ED cases and are classified as idiopathic
▪ both are increased by the same magnitude in HIV
• Psoriasis is the most common underlying skin disease to
infection
cause ED followed by spongiotic dermatitis
High-risk drugs: antibacterial sulfonamides, aromatic Possible triggers for psoriatic ED include the following:
anticonvulsants, allopurinol, oxicam non-steroidal anti-
• Medications, such as lithium, terbinafine, and
inflammatory drugs, lamotrigine, nevirapine
antimalarials
Complications • Topical irritants including tars
• Sepsis (S. aureus, Pseudomonas) • Systemic illness
• Ophthalmic complications • Discontinuation of potent topical or oral corticosteroids
methotrexate, or biologics (efalizumab)
• Nail changes
• Infection including human immunodeficiency virus (HIV)
• Mouth sequelae
• Pregnancy
• Vulvar and vaginal complications
• Emotional stress
• Chronic lung disease
• Phototherapy burns
Prognosis and Clinical Course
History
• The epidermal detachment progresses for 5 to 7 days.
• History of dermatoses (psoriasis, atopic dermatitis) or a
Then, patients enter a plateau phase, which corresponds
systemic medical condition
to progressive re-epithelialization. This can take a few
days to a few weeks, depending on the severity of the • Medication history including naturopathic and over the
disease and the prior general condition of the patient. counter therapies
• Hospital mortality rate • Patients with history of psoriasis and atopic dermatitis
should be queried specifically regarding use of topical
- Overall: 22-25%
and systemic corticosteroids, methotrexate, and other
- SJS: 5-12%
systemic medications; topical irritants; systemic illness;
- TEN: >30% infection
• Primary skin diseases have a slower course while drug
Treatment reactions usually have a rapid onset and resolution
• Early recognition
• Withdrawal of offending drug Cutaneous Lesions
• Supportive care • Classic presentation is erythematous patches that
- Fluid replacement and electrolyte correction increase in size and coalesce into generalized red
- Nutritional support erythema with a shiny appearance
• Corticosteroids • Involves more than 90% of the patient’s skin surface
• IV Immunoglobulin • Fine white or yellow scaling begins a few days after
erythema, classically arising in the flexures
• Cyclosporine A
• Plate-like scaling may occur acutely and on the palms and
• Plasmapharesis or Hemodialysis
soles.
• Antitumor Necrosis Factor Agents
Related Physical Findings
Related physical findings due to ED of any etiology may include
the following:
• Tachycardia due to increased blood flow to the skin and
fluid loss due to disrupted epidermal barrier
• High-output cardiac failure secondary to the high-flow
state in ED

• Thermoregulatory disturbances can result in BLISTERING DISEASES

hyperthermia or less commonly hypothermia • range of chronic diseases wherein autoantibodies are
• Generalized lymphadenopathy directed against autoantigens in the epidermis or the
• Hepatomegaly which is more commonly seen in drug- basement membrane
induced ED • disorders of epidermal-dermal adhesions due to the
• Splenomegaly which has been most commonly involvement of adhesion proteins at the epidermis and
associated with lymphoma the dermal-epidermal junction
• Peripheral pedal or pretibial edema
Pemphigus
Laboratory Tests • characterized by intraepidermal blisters due to the loss of
• Most often not diagnostic and not specific cell-cell adhesion of keratinocytes (acantholysis)
• Common laboratory abnormalities include anemia, - Pemphigus Vulgaris
leukocytosis, lymphocytosis, eosinophilia, increased IgE, - Pemphigus Foliaceus
decreased serum albumin, and an elevated erythrocyte • occurs as a result of circulating antibodies of the IgG class;
sedimentation rate these antibodies bind to desmogleins
• Fluid loss may lead to electrolyte abnormalities and - PV: desmoglein 3 (in some, also desmoglein 1)
abnormal renal function (elevated creatinine level) - PF: desmoglein 1
• PV: flaccid blisters on skin and erosions on mucous
Treatment membranes
• Patients presenting acutely with ED may require • PF: scaly and crusted skin lesions
inpatient management due to significant fluid and
electrolyte imbalance and hemodynamic or respiratory • In most cases, the disease inexorably progresses to death
compromise unless treated aggressively with immunosuppressive
agents.
• Children presenting with erythroderma and fever should
• Management
be hospitalized and managed aggressively and nursed in
a warm (preferably 30°C–32°C) and humid environment - Glucocorticoids 2 to 3 mg/kg body weight of
for comfort and skin moisture, as well as to prevent prednisone until cessation of new blister formation
hypothermia and disappearance of Nikolsky sign.
• Gentle local skin care, including oatmeal baths and wet - Concomitant Immunosuppressive Therapy
dressings to weeping or crusted lesions, bland emollients, ▪ Azathioprine , 2–3 mg/kg body weight
and low-potency topical steroids should be started ▪ Methotrexate , either orally (PO) or IM at doses of
• High-potency topical steroids and topical 25 to 35 mg/week
immunomodulators, such as tacrolimus, should be ▪ Cyclophosphamide , 100–200 mg daily
avoided as systemic absorption may occur due to the ▪ Plasmapheresis
increased skin permeability and large surface area ▪ Gold therapy
involved
▪ Mycophenolate mofetil (1 g twice daily)
• Antihistamines for sedation and antipruritic effects
▪ High-dose intravenous immunoglobulin (HIVIg)
• Systemic antibiotics are required for patients with (2g/kg body weight every 3–4 weeks)
evidence of localized and systemic secondary infection ▪ Rituximab (monoclonal antibody to CD20)
• Diuretics and adequate fluid intake for pedal and - Other Measures
periorbital edema
▪ Cleansing baths, wet dressings, topical and
• All nonessential and possible offending medications intralesional glucocorticoids, antimicrobial
should be discontinued therapy per documented bacterial infections
• Folate supplementation and a diet of 130% of normal ▪ Correction of fluid and electrolyte imbalance
dietary requirements for protein to replace nutrient
losses Bullous Pemphigoid
• Determining the underlying etiology early is essential for • Interaction of autoantibody with bullous pemphigoid
definitive treatment of ED antigen [BPAG1 and BPAG2 (collagen type XVII)] in
• When the underlying cause of ED is unknown, empiric hemidesmosomes of basal keratinocytes
therapy with systemic agents, including methotrexate, • A bullous autoimmune disease usually in elderly patients
cyclosporine, acitretin, mycophenolate mofetil, and
• Pruritic papular and/or urticarial lesions with large tense
systemic corticosteroids, has been used
bullae
Prevention • Management
• Controlling the underlying cause - Systemic prednisone with starting doses of 50–100
mg/d continued until clear
• Medications and irritants that have previously caused ED
should be avoided - Azathioprine, 150 mg daily
• Systemic steroids should be avoided in patients with - IVIG, plasmapheresis
psoriasis to prevent rebound flares - sulfones (dapsone)
• Educating patients with underlying diseases (e.g., - Low-dose MTX 2.5 to 10 mg weekly
psoriasis, atopic dermatitis) about possible triggers of ED - Patients often go into a permanent remission after
(irritants, abrupt discontinuation of certain therapies) therapy and do not require further therapy
may also be helpful to prevent ED

- Local recurrences can sometimes be controlled with • Mucosal involvement is important and ranges from large
topical glucocorticoids asymptomatic oral erosions and ulceration to severe oral
disease alone, or severe generalized cutaneous
Cicatricial Pemphigoid involvement and oral disease
• Blisters that rupture easily and also erosions resulting • It is identical with chronic bullous disease of childhood
from epithelial fragility in the mouth; oropharynx; and, (CBDC), which is a rare blistering disease that occurs
more rarely, the nasopharyngeal, esophageal, genital, predominantly in children <5 years
and rectal mucosae • LAD has been associated with drugs: vancomycin, lithium,
• Ocular involvement may initially manifest as unilateral or phenytoin, sulfamethoxazole/trimethoprim, furosemide,
bilateral conjunctivitis with burning, dryness, and captopril, diclofenac, and others
foreign-body sensation. • There is a small risk of lymphoid malignancies, and
• The skin is involved in roughly 30% of patients. associated ulcerative colitis has been reported
• Management • Management
- Most patients respond to dapsone in combination - Patients respond to dapsone or sulfapyridine but in
with low-dose prednisone addition, most may require low-dose prednisone
Pemphigoid Gestationis Epidermolysis Bullosa Acquisita

• A rare pruritic and polymorphic inflammatory bullous • A chronic subepidermal bullous disease associated with
dermatosis of pregnancy and the postpartum period. autoimmunity to the type VII collagen within the
• Extremely pruritic vesicular eruption mainly on the anchoring fibrils in the basement membrane zone.
abdomen but also on other areas, with sparing of the • Four types
mucous membranes - Classic mechano-bullous presentation
• begins from the fourth to the seventh month of - Bullous pemphigoid–like presentation
pregnancy but can also occur in the first trimester and in - Cicatricial pemphigoid–like presentation
the immediate postpartum period - IgA bullous dermatosis–like presentation
• can be exacerbated by the use of estrogen and • Management
progesterone-containing medications
- High doses of systemic glucocorticoids, azathioprine,
• Management methotrexate, and cyclophosphamide
- geared to suppressing blister formation and relieving - Dapsone and high doses of colchicine
the intense pruritus.
- Supportive therapy
- Prednisone, 20–40 mg/d
Dermatitis Herpetiformis
• relates to IgA deposits in the skin
• Patients have antibodies to transglutaminases (TGs) that
may be the major autoantigens in this disease
• A chronic, recurrent, intensely pruritic eruption occurring
symmetrically on the extremities and the trunk
• Consists of tiny vesicles, papules, and urticarial plaques
that are arranged in groups
• Associated with gluten-sensitive enteropathy (GSE)
• Management
- Systemic Therapy: Dapsone 100–150 mg daily
- Obtain a glucose- 6-phosphate dehydrogenase level
- Sulfapyridine 1–1.5 g/d, with plenty of fluids
- A gluten-free diet may suppress the disease or allow
reduction of the dosage of dapsone or sulfapyridine,
but response is very slow
Linear IgA Dermatosis / Chronic Bullous Disease of

Childhood
• A rare, immune-mediated, subepidermal blistering skin
disease defined by the presence of homogeneous linear
deposits of IgA at the cutaneous basement membrane
zone
• LAD most often occurs after puberty
• Patients present with combinations of annular or
grouped papules, vesicles, and bullae that are distributed
symmetrically on trunk and extremities including elbows,
knees, and buttocks
• The lesions are very pruritic

APPENDIX
Treatment Algorithm for Acne Vulgaris
Potency of Topical Steroids

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EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY

EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY 1

• Systemic host factors (obesity, blood dyscrasias Deep folliculitis/Sycosis barbae

EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY 2

• Etiologic agent: group A β-hemolytic streptococcus >

Cellulitis and Erysipelas

EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY 3

• Clinical Manifestations • Causes

EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY 4

EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY 5

• Curettage, Canthardin, retinoid creams, imiquimod HAND-FOOT-MOUTH DISEASE

EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY 6

EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY 7

TINEA CRURIS Treatment

EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY 8

• Systemic - Potassium hydroxide (KOH) preparation

EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY 9

Systemic Therapy SEBORRHEIC DERMATITIS

EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY 10

IRRITANT CONTACT DERMATITIS First Line Therapy

Stepped Approach to Treatment of Eczema

EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY 11

EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY 12

MANAGEMENT - MOA: interferes with intercellular redox regulation,

4. VITAMIN D ANALOGS PROGNOSIS

6. SALICYLIC ACID HANSEN’S DISEASE

EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY 13

• At this stage clinical manifestation may appear as ill-defined outer

Dry + + patients undergoing a an allergic

EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY 16

EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY 18

Prognosis and Course • Gottron sign

EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY 19

• Local Treatment Etiology

EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY 20

EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY 21

• Nikolsky’s sign (dislodgement of the epidermis by lateral EXFOLIATIVE DERMATITIS

EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY 22

• Thermoregulatory disturbances can result in BLISTERING DISEASES

EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY 23

Pemphigoid Gestationis Epidermolysis Bullosa Acquisita

Linear IgA Dermatosis / Chronic Bullous Disease of

EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY 24

Treatment Algorithm for Acne Vulgaris

Potency of Topical Steroids

EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY 25

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