Derma Megatable

1. NAIL CHANGES LESION DERMATOPHYTE ONYCHOMYCOSIS

AGE OF PREDILECTION

AREA OF PREDILECTION

Yellow discoloration, nail becomes brittle and separates from the nail bed resulting in the piling up of subungal keratin; breaks off, leaving an undermined black-yellow remnant to dead nail; skin of the toe & soles may be involved – branny, scaling, erythematous, well-defined patches Superficial without paronychial inflammation; Chalky white spots on or in the nail plate that is easily shaved off.

CANDIDAL ONYCHOMYCOSIS

Pink, swollen & tender cuticle with neighboring portion of the nail becoming dark, ridged and separates from the bed.

PSORIASIS

Pits on the nails, furrows or transverse depressions ( Beau’s Line), crumbling nail plate or leukonychia with a smooth or rough surface; nail bed splinter hemorrhages; hyponychium yellowish green discoloration may occur in area of onycholysis.

fingernails more affected

HALLMARK

ETIOLOGY

Starts at the distal corner of the nail and involves the junction of the nail and its bed; entire maybe affected

T. rubrum

Scaling of the nail under the overhaningcuticle and remains localized to a portion of the nail, however, in time entire nail may be involved Paronychia – characteristic feature; Begins on the lateral or proximal nail fold with expression of small amount of pus.

PREDISPOSING FACTORS

TREATMENT Itraconazole Dose: 200mg/day, bid for 1 week/mo Fingernails: 2 mos Toenails: 3 mos Terbinafine Dose: 250mg/day Fingernails: 6 wks Toenails: 12 wks

OTHER INFO Types:

1. Distal subungal onychomycosis 2. White superficial onychomycosis 3. Proximal subungal onychomycosis

Fluconazole Dose: 150-300mg once/wk for 6-12 months

T. mentagrophytes

Griseofulvin therapy

Candida Albicans

Common in homemakers and canners & others who have their hands mostly in water.

86.5 % of patient with psoariatic arthritis Others: Reiter’s disease, Pityriasis rubra pilaris, Sezary syndrome & acrokeratosis paraneoplastica

Griseofulvin does not treat nail disease caused by candida.

Intralesional injection of triamcinolone acetonide suspension, 3-5 mg/ml Topical 1% 5-FU solution MTX, PUVA, cyclosporine or acitretin

Involves all the nail plate; nail does not become friable , yellow, white

E r y t h e m a t o s u s

L e s i o n s

LESION MILIARIA RUBRA (Prickly Heat, Heat Rash)

AGE OF PREDILECTION

Dicrete, extremely pruritic, erythematous papulovesicles; may become confluent Accompanied by prickling, burning or tingling.

SCABIES

2A.NON-SCALY PAPULES AREA OF PREDILECTION Antecubital and popliteal fossae, trunk, inframmary areas, abdomen (waistline), inguinal region

HALLMARK

ETIOLOGY Miliaria (in general) retention of sweat as a result of occlusion of eccrine sweat ducts and pores.

TREATMENT

OTHER INFO Prickle cell layer – site of injury and sweat escape; spongiosis

S. epidermidis

Pruritic popular lesions and burrows w/c house the female mite and her young

Circle of Hebra – axillae, elbow, flexures, wrists, hands and crotch

Active scabies: Dull Red nodules

Sarcoptes scabei

Fierce itching at night

Mite burrows in stratum corneum ACNE VULGARIS

PREDISPOSING FACTORS Impedance of evaporation of moisture

-comedo (basic lesion)

-adolescents (15-18)

-papules, pustules, cysts, nodules, scars

-involution of disease before 25 years old

-face, neck, upper trunk, upper arms -oily seborrheic areas

Propionibacterium acnes (metabolize sebum to free fatty acid) -heredity, keratinous plug in lower infundibulum of hair follicle (primary defect), androgenic stimulation of sebaceous gland

Immunocompromised & institutionalized (Crusted Scabies), malnourished patients, w/ neurologic dsorders

Premethrin 5% cream

TOPICAL -benzoyl peroxide -topical retionoids -clindamiycin -erythro +benzoyl peroxide -sulfur, resorcin, salicylic acid -azeleic acid SYSTEMIC (inh. formation of new lesion) -tetracycline -minocycline -doxycycline -erythromycin -clindamycin -sulfonamides -OCP -spironolactone -dexamethasone -prednisone -vitamin A -isotretinoin

Transmission: close personal contact

1) 2) 3) 4)

atrophic papular atrophic hypertrophic

SURGICAL -comedo extractor INTRALESIONAL CORTICOSTEROID LESION

AGE OF PREDILECTION

AREA OF PREDILECTION

Principally in children

Scalp

HALLMARK

ETIOLOGY

PREDISPOSING FACTORS

TREATMENT

OTHER INFO

PEDICULOSIS (PHTHIRIASIS) 1.

PEDICUL OSIS CAPITIS

Intense pruritus of scalp Affected hairs become lusterless and dry

Pediculus humanus var. capitis (head louse)

May also occur in adults

Permethrin Pyrethrins, combined w/ piperonyl butoxide Enzymatic egg remover (CLEAR)

2. PEDICULOSIS CORPORIS

3. PEDICULOSIS PUBIS (pediculosis vestimenti or vagabond’s disease)

Generalized itching, accompanied by erythematous macules or urticarial wheals; or by excoriated papules, parallel linear scratch marks, and a pigmented thickening of skin from continued rubbing Maculae cerulae - occasional, peculiar bluish or slatecolored macules, nonpruritic, does not disappear on diascopic pressure -sides of the trunk, inner aspects of the thigh

Upper back; no involvement of hands and feet

Adults

Genital region and hypogastrium Rarely, axillae or eyelashes (pediculosis palpebrarum)

Dx established by generalized itching, parallel stretch marks, hyperpigtmentation, and erythematous macules.

Pediculus humanus var. corporis (body louse)

Px bathe thoroughly w/ soap and water Destruction of lice laundering the bedding and clothing. Disinfection

Permethrin Pyrethrins combined w/ piperonyl butoxide. Enzymatic egg remover (CLEAR) *retreatment in 1 wk recommended

INSECT BITES

*Pls read in Andrews =)

Secondary complications w/ impetigo and furunculosis are common due to itching.

Lice live in the seams of clothing, esp. wherever there is pressure (i.e. warmth) or in bedding. Dx supported by finding lice in the seams of clothing or in bedding.

Transmission: sexual intercourse; not infrequently from bedding

E r y t h e m a t o s u s

L e s i o n s

LESION FURUNCLE (BOIL) / CARBUNCLE

Furuncle - Acute, round, tender, circumscribed perifollicular staphylococcal abscess; generally ends in central suppuration. Carbuncle- 2 or more confluent furuncles, w/ separate heads *lesions begin in hair follicles, and often continue by autoinoculation -most undergo central necrosis and rupture thru the skin, discharging purulent, necrotic debris

2B.NON-SCALY NODULES

AGE OF PREDILECTION

AREA OF PREDILECTION Nape, axillae, buttocks *but may occur anywhere

HALLMARK

ETIOLOGY S. aureus

PREDISPOSING FACTORS Impairment of skin surface integrity -irritation, pressure, friction, hyperhidrosis, dermatitis, dermatophytosis, shaving Systemic disorders - alcoholism, malnutrition, blood dyscrasias, disorders of neutrophil fxn, immunosuppresion (AIDS) Atopic dermatitis -predisposes to carrier state

TREATMENT Penicillinaseresistant penicillin or 1st-gen. cephalosporin Bactobran – applied to anterior nares to help prevent recurrence

OTHER INFO Proximate cause is either contagion or autoinoculation from a carrier focus, usually in the nose or groin.

Predisposing ystemic disorders, renal dialysis - often nasal carriers

E r y t h e m a t o s u s

L e s i o n s

LESION FIXED DRUG ERUPTION

2C.NON-SCALY PLAQUES

AGE OF PREDILECTION

Begins as a red patch that soon evolves to an iris or target lesion identical to erythema multiforme, and may eventually blister and erode

AREA OF PREDILECTION Oral and genital mucosa

HALLMARK

dorsal hands, dorsal feet, extensor limbs, elbows and knees, and palms and soles

“target” or “iris” lesions

ETIOLOGY

PREDISPOSING FACTORS

TREATMENT

OTHER INFO

Stop taking the offending drug.

Nonpigmenting fixed drug eruption: large, tender, often symmetrical eythematous plaques ERYTHEMA MULTIFORME

ERYSIPELAS

CELLULITIS

Begin as sharply marginated, erythematous macules, which become raised, edematous papules over 24 to 48 hours “target” or “iris” lesion with 3 zones – central dusky purpura; an elevated, edematous, pale ring; and surrounding macular erythema Fiery-red swelling with characteristic raised, indurated border; distinctive features is the advancing edge of the patch Suppurative inflammation

Young adults

Usually has nondrug causes, most commonly herpes simplex infection

Prevention is cornerstone of treatment if HSV can be demonstrated as the trigger. Sunblock creams Antiherpetic antibiotic

Newborn, postpartum women

Face and legs

Any inflammation of the skin, especially if fissured or ulcerative, may provide an entrance for the causative streptococcus Usually follows some discernible wound

Systemic penicillin Erythromycin Locally, ice bags and cold compresses

Intravenous penicillinaseresistant penicillins or a first-generation cephalosporin

Acute tuberculoid leprosy of the face may look exactly like erysipelas, but the absence of fever, pain, or leukocytosis is distinctive.

LESION URTICARIA

EXFOLIATIVE DERMATITIS

wheals, white or red evanescent plaques, generally surrounded by a red halo or flare

Erythematous plaques

2. TUBERCULOID LEPROSY (TT)

AREA OF PREDILECTION covered areas, such as the trunk, buttocks, or chest

HALLMARK

ETIOLOGY

Although it occurs at all ages, there are 2 peaks of presentation: in children aged 10 to 20 years, and in adults 30 to 60 years of age. (true for all types)

PREDISPOSING FACTORS

drugs, food, food additives, infections, emotional stress, menthol, neoplasms, inhalants, viruses, parasites, alcohol

Face and extremities

skin becomes scarlet and swollen and may ooze a straw-colored exudate

HANSEN’S DISEASE (LEPROSY)

1. EARLY AND INDETERMINATE LEPROSY

AGE OF PREDILECTION

OTHER INFO Acute - < 6 weeks

Antihistamines

Chronic - > 6 wks

Avoidance of the trigger should be stressed

Psoriasis; excema, neurodermatitis; drug allergy; pityriasis rubra pilaris; seborrheic dermatitis, other dermatoses, malignant lymphoma Mycobacterium leprae

TREATMENT

topical steroid, soaks, and compresses systemic corticosteroids

The course of the disease may be very protracted, lasting a period of years, or it may simply persist and resist therapy.

immunosuppressives Dapsone (cornerstone of therapy) Dapsone + Rifampin -combination therapy initially Clofazimine Ethionamide

Often, the first lesion is a solitary, ill-defined hypopigmented macule that merges into the surrounding normal skin

Cheeks, upper arms, thigh, and buttocks

Typical lesion is the large, erythematous plaque with a sharply defined and elevated border that slopes

Face, limbs

Peripheral nerves are not enlarged, plaques and nodules do not occur.

The presence of palpable induration and neurologic findings distinguishes indeterminated and

down to a flattened atrophic center

tuberculoid lesions clinically.

Lesions are solitary or few in number (usually 3 or less)

3. BORDERLINE TUBERCULOID LEPROSY (BT)

Typical lesion is the large, erythematous plaque with a sharply defined and elevated border that slopes down to a flattened atrophic center Smaller and more numerous (usually 310) than tuberculoid leprosy lesions.

Face, limbs

Lesion is anesthetic or hypesthetic and anhidrotic, and superficial peripheral nerves serving or proximal to the lesion are enlarged, tender, or both

Satellite lesions around large macules or plaques are characteristic

4. BORDERLINE LEPROSY (BB)

Numerous (but countable) red, irregularly shaped plaques

Nerves may be thicker or tender, but anesthesia is ony moderate in the lesions

Small satellite lesions may surround larger plaques Lesions are generalized but asymmetrical

5. BORDERLINE LEPROMATOUS LEPROSY (BL)

Symmetrical, numerous (too many to count), and may include macules, papules,

Nerve involvement appears later. The involvement is

plaques, and nodules

symmetrical. Sensation and sweating over individual lesions is normal.

6. LEPROMATOUS LEPROSY (LL)

*HISTOID LEPROSY

Mainly pale lepromatous macules or lepromatous infiltrations, with numerous bacilli in the lesions.

Yellow-red, shiny, large papules and nodules in the dermis or subcutaneous tissue

There is little or no loss of sensation over the lesions, there is no nerve thickening, and there are no changes in sweating.

buttocks, lower back, face, and bony prominences

may appear de novo or in patients with dapsone resistance

E r y t h e m a t o s u s

L e s i o n s

LESION TINEA CAPITIS

Two types: Noninfammatory -multiple scaly lesions (gray patch), broken hair stubs

2F.PAPULOSQUAMOUS DISEASE

AGE OF PREDILECTION School children, city children (less commonly in infants and adults)

AREA OF PREDILECTION Scalp Noninflam – involve glabarous skin, eyelids and lashes

Inflammatory - scaly, erythematous papupar eruptions w/ loose broken off hairs w/ inflammation

HALLMARK Black dots Wood’s lampinfected hairs fluoresce green KOH- long septated hyphae

ETIOLOGY -All dermatophytes, except E. floccosum and T. concentricum

PREDISPOSING FACTORS more of boys in children, more women in adults

TREATMENT Griseofulvin for children -10mg/kg/day for 2-4 mos steroids may be given for inflammation

-most caused by T. tonsurans and M.canis

selenium sulfide or ketoconazole shampoo may be left on the scalp for 5 mins, 3x/wk  adjuct to oral antifungals

-may be ectothrix or endothrix

OTHER INFO Kerion celsiii – boggy indurated areas exuding pus -delayed type hypersensitivity rxn Favus – scalp, glabarous skin and nails -sulfur-yellow crusts form around loose hairs atrophy  glossy thin, paper white patch Scutulae – on glabarous skin, cupshaped crust >> follows >>> acute glomerulonephritis serotypes 49, 55, 57, 60 strains and strain M-type 2 childhood under 6 y/o

TREATMENT Self-limited

Systemic antiobiotics w/ topical therapy semisynthetic penicillin or firstgeneration cephalospori n bacitracin & mupirocin oitment

OTHER INFO Appears in bedridden patients and bundled children Mistaken for Toxidendron dermatitis Common sources of infection: Children – pets, dirty fingernails and other children in school Adults – barber shops, beuty parlors, meatpacking plants, swimming pools, and infected children

LESION STEVENSJOHNSON SYNDROME

HERPES SIMPLEX

Appear on the face and trunk and rapidly xtent (4 days) to their maximum extent Macular >>> desquamation >>> atypical targets with purpuric centers >>> coalesce form bullae then slough Vesicles are intraepidermal Dermis & epidermis containing infiltrates of leukocytes & serous exudates Ballooning degeneration of the epidermal cells to produce acantholysis Minute eosinophilic intranuclear bodies Recurrent Erythema Multiforme Minor: papules >>> classic target lesion

AGE OF PREDILECTION

AREA OF PREDILECTION Oral mucosa and conjunctiva

Orolabial Herpes: lips near the vermilion Herpes Gladiatorum: face, sides of nec, inner arms Herpetic Whitlow: infection of pulp of fingerip Herpetic Keratoconjunctiviti s: eye Recurrent Erythema Multiforme Minor: palms, elbows, knees, and oral mucosa

HALLMARK

ETIOLOGY

Fever and influenza like symptoms precede eruption

Medications: Trimethoprim/sulfamet hoxazole, Fansidar-R, sulfadoxone plus pyrimethamine & carbamazepine

Skin biopsy: lymphocytic infiltrate at dermoepidermal junction w/ necrosis of keratinocytes Tzanck Smear: multinucleate epidermal giant cell Orolabial Herpes: Onset - high fever, regional lymphadenopath y, and malaise Presentation – “cold-sore” or “fever blister” Herpetic Whitlow: tenderness & erythema of lateral nail fold Herpetic Keratoconjunctivi tis: Punctate or marginal keratitis or as a dendritic ulcer cause disciform keratits and leave scars that impair vision

HSV-1: orolabial herpes simplex, more common HSV-2: genital herpes Herpetic Whitlow: children: HSV1 adults: HSV-2

PREDISPOSING FACTORS

TREATMENT Similar to patients with extensive burn Intravenous immunoglobulin

HIV patients Orolabial Herpes: UVB

Acyclovir

OTHER INFO Involves less than 10% body surface Most common sequelae: Ocular scarring, vision loss & siccalike syndrome Herpetic Sycosis – following attack of facial herpes simplex, patient who shaves; transient Herpes Gladiatorum – HSV-1, wrestlers, rugby players Recurrent Erythema Multiforme Minor: recurrent SV-1 orolabial disease

LESION HERPES ZOSTER

SCABIES

Eruption >>> ppapules and plaques of erythema in the dermatome

Pruritic popular lesions and burrows w/c house the female mite and her young

AGE OF PREDILECTION

AREA OF PREDILECTION Sensory dorsal root ganglion cells Ophthalmic Zoster: ophtlamic division of the 5th cranial nerve Ramsay Hunt Syndrome: facial & auditory nerves

Circle of Hebra – axillae, elbow, flexures, wrists, hands and crotch Mite burrows in stratum corneum

HALLMARK

ETIOLOGY

Tzanck Smear: multinucleate epidermal giant cell

Varicella zoster virus

Histopathology: intraepidermak vesicles, ballon cells, acidophilic inclusion bodies

Active scabies: Dull Red nodules Fierce itching at night

PREDISPOSING FACTORS Immunosupression and age (Herpes Zoster Generalisatus): old or debilitated, lyphoreticular malignancy, AIDS

TREATMENT

OTHER INFO

Bed rest, local application oh heat & gentle pressure, antiviral treatment (Acyclovir)

Disseminated Herpes Zoster (Herpes Zoster Generalisatus) – more than 20 lesions outside the dermatome Postherpetic Neuralgia: major complication; pain 1 month after onset Other complications: motor nerve neuropathy

Sarcoptes scabei

Immunocompromised & institutionalized (Crusted Scabies), malnourished patients, w/ neurologic dsorders

Premethrin 5% cream

Transmission: close personal contact

6. BULLOUS DERMATOSIS LESION BULLOUS IMPETIGO

-strikingly large, fragile bullae -ruptures & leaves circinate, weepy or crusted lesions (impetigo circinata)

FIXED DRUG ERUPTION

-begins as an erythematous patch that soon evolves to an iris or target lesion and may eventually blister & erode -6 or fewer lesions occur but frequently single -prolonged inflammation results to hyperpigmentation

AGE OF PREDILECTION -newborn infants (4th & 5th days of life) -may occur at any age

-any age

AREA OF PREDILECTION -newborn: face & hands

HALLMARK

ETIOLOGY -Staphylococcus aureus

PREDISPOSING FACTORS -insect bite

TREATMENT -systemic antibiotics

-adults: axilla, groin, hands

-anywhere but half occurs on oral & genital mucosa

-recur at the same site with each exposure to the medication

-medications usually taken intermittently (NSAIDS, pyrazolone derivatives, naproxen, mefenamic acid, etc.)

-persons with FDE to pyrazolone derivatives are usually HLA-B22 positive

-stop offending medication & replace with alternative drug

OTHER INFO -weakness, fever, diarrhea with green stools, bacteremia, pneumonia, or meningitis, fatal termination -early manifestation of HIV infection -Nonpigmented FDR: occurs occasionally; characterized by large, tender, often symmetrical erythematous lesions that resolves; normally caused by pseudoephedrine hydrochloride -Baboon Syndrome: buttocks, groin & axilla are preferentially involved

LESION IRRITANT CONTACT DERMATITIS

-non-allergic inflammatory reaction of the skin

AGE OF PREDILECTION -any age

AREA OF PREDILECTION -in areas that has come in contact with irritants

-erythema vesicles, erosions, crusts, scaling

HALLMARK

ETIOLOGY -alkalis: soaps, detergent, ammonia, lye, toilet bowl cleaners -acids: hydrofluoric acids, HCl, nitric, sulfuric acids

PREDISPOSING FACTORS -condition of skin upon contact -skin may be vulnerable by reason of maceration from excessive humidity or exposure to water, heat, cold, pressure or friction

-Ca, Cu, Hg, Ni, Ag, Br, Cl, Fl, I -chlorinated compounds: Chloracne

TREATMENT -alkalis: immediate application of a weak acid (vinegar, lemon juice, 0.5% HCl) -oxalic acids: lime water -phenol: 65% EtOH or isopropyl alcohol -fluorine: magnesium oxide -periungal burns: 10% calcium gluconate solution

-dog collars: Flea Collar Dermatitis -capsaicin: Hunan hand

-phosphorus burns: rinse with water & apply copper sulfate -titanium HCl: wipe away, do not rinse!

ALLERGIC CONTACT DERMATITIS

-erythema, vesicles , erosions, crusts, scaling

-any age

-in areas that has come in contact with allergen (but it has to be previously sensitized)

-previous exposure to allergen

OTHER INFO