Stratum Corneum/Keratin Layers Flashcards by Jennifer Becker

lipophilic organism (saprophyte)

Malassezia furfur

How well did you know this?

Not at all

Perfectly

spaghetti and meatball appearance w/ KOH prep

Malassezia furfur

How well did you know this?

Not at all

Perfectly

Pathogenic phase of Malassezia furfur

Hyphal phase

How well did you know this?

Not at all

Perfectly

Hypopigmentation associated with Pityriasis versicolor is due to

a substance produced by the organism that inhibits melanosome production

How well did you know this?

Not at all

Perfectly

Hyperpigmentation associated with Pityriasis versicolor is due to

production of larger, unpacked, and heavily melanized melanosomes

How well did you know this?

Not at all

Perfectly

Pityrosporum folliculitis results from

hyperkeratosis that plugs the follicle

How well did you know this?

Not at all

Perfectly

Atopic dermatitis caused by Malassezia furfur results from

induction of beta-defensins in the skin

How well did you know this?

Not at all

Perfectly

tinea versicolor is associated with what climate/season

tropics, warmer months

How well did you know this?

Not at all

Perfectly

risk factors for tinea versicolor

Warm temperature, high humidity, use of oily creams, greasy skin, hyperhidrosis
Steroid use, antibiotic use
Malnutrition, diabetes, immunosuppression, slow rate of epithelial cell turnover

How well did you know this?

Not at all

Perfectly

Describe the lesions of tinea versicolor

Reddish/pale-brown, non-pruritic, non-inflammatory hypopigmented/hyperpigmented

How well did you know this?

Not at all

Perfectly

Location of lesions of tinea versicolor

trunk, upper arms, scalp, face and flexural areas

How well did you know this?

Not at all

Perfectly

Septicemia of Malassezia furfur is

Rare, increasing in stem cell transplant pts

How well did you know this?

Not at all

Perfectly

Malassezia furfur appearance w/ Wood’s Lamp

pale fluorescence

How well did you know this?

Not at all

Perfectly

Malassezia furfur appearance w/ KOH stain

yeast and hyphae “spaghetti and meatballs”

How well did you know this?

Not at all

Perfectly

Treatment for tinea versicolor

1-2.5% Selenium sulfide ointment or Zinc Pyrithione, Ketoconazole, Ciclopirox

How well did you know this?

Not at all

Perfectly

Acute occurrence of tinea versicolor can be treated w/

Calcineurin Inhibitor – Primecrolimus, Tacrolimus

How well did you know this?

Not at all

Perfectly

Treatment for tinea versicolor hyperpigmentation

Cycloserine

How well did you know this?

Not at all

Perfectly

Treatment for Seborrheic dermatitis caused by Malassezia furfur

2% Ketoconazole gel

How well did you know this?

Not at all

Perfectly

Treatment to decrease relapse rate of Seborrheic dermatitis caused by Malassezia furfur

Toll-like receptor 2 modifiers (decrease the topical IL-8 expression)

How well did you know this?

Not at all

Perfectly

Tinea Nigrans is caused by what agent

Hortaea (Exophiala) werneckii

How well did you know this?

Not at all

Perfectly

Typical pt with Tinea Nigrans

< 18 y/o, female, living/travel to Central or South America

How well did you know this?

Not at all

Perfectly

Tinea Nigrans is transmitted by

contact w/ decaying vegetation, wood, or soil

How well did you know this?

Not at all

Perfectly

Describe the lesion of Tinea Nigrans

Discrete, 1-8cm dark, brown-to-black, mottled, macule on the palmar surface of the fingers (occasionally the soles)

How well did you know this?

Not at all

Perfectly

Treatment for Tinea Nigrans

Topical keratinolytic agents

How well did you know this?

Not at all

Perfectly

Defenses against Tineas

Alpha-2-macroglobulin keratinase inhibitor Unsaturated transferrin (fungus can’t use Fe) Epidermal desquamation Lymphocytes, macrophages, epidermal Langerhans cells, dermal dendritic cells, neutrophils, and mast cells

Tineas infect which layer

keratinized layers

Immune required for fighting Tineas

CMI predominantly, humoral also

Risk Factors for Tinea infections

Warmer months, males, post-pubescents, family member with infection, contact w/ contaminated instruments/textiles/animals Obesity, hydration, and humidity Steroid use, antibiotic use

Microsporum and superficial pityriasis both

fluoresce apple to blue green

Brilliant coral red fluorescence

Erythrasma, bacterial infection of Corynebacterium minutissimum

Culture Tineas on

Dermatophyte Test Medium or Sabouraud-glucose agar containing chloramphenicol and cycloheximide + Cellufluor white

dermatophytid or “id” reaction

sterile vesicle which appears at a site distant from the focus indicating a CMI response or Type IV HSN - DTH

Tinea Incognito

altered clinical appearance due to inappropriate treatment – usually topical steroids

Lesions of Tinea Incognito

Appears less raised, less scaly, more pustular, more extensive

Long-term use of topical steroids on Tinea infections results in

atrophy (thin skin + striae in skin folds), purpura, telangiectasia

Classic Ringworm lesion

annular lesion w/ an active border and central clearing

Does ringworm involve mucosal membranes?

single/multiple fissures at corner of mouth + red, scaly adjacent skin rash

Candida – Perleche

Treatment for Tinea infections

o Potassium permanganate 1:5000 o Salicylic acid o 20% Sodium hyposulfite o Gentian violet o Whitfield’s, Sulfur, Tolnaftate, Desenex, Haloprogin, Clotrimazole, Naftin, Imidazole, Griseofulvin o Oral Antifungals: Lamisil, Itraconazole, Griseofulvin, Ketoconazole

Tinea pedis etiologic agents

1. Trichophyton mentagrophytes 2. Trichophyton rubrum 3. Epidermophyton floccosum

Symptoms of Tinea pedis are due to

interaction of fungi and bacteria

Lesion of typical Tinea pedis

Pruritic, inflamed, Pruritic, inflamed, scaling -> vesicular -> ulcers -> crusted lesions on soles and b/w toes

Intertriginous form of Tinea pedis

peeling, maceration of skin b/w toes, foul odor

Chronic, papulosquamous, hyperkeratotic form (moccasin type) form of Tinea pedis

pink skin covered by fine silvery-white scales, very persistent and difficult to treat

Moccasin type of Tinea pedis is caused by which agent

T. rubrum

Vesiculobulbous form of Tinea pedis

vesicles, vesiculopustules, or bullae on the plantar surface

“id” reaction is most common with what form of Tinea pedis

Vesiculobulbous form

Tinea manuum etiologic agents

1. Trichophyton rubrum (predominately) 2. Trichophyton mentagrophytes 3. Epidermophyton floccosum

Risk Factors for Tinea manuum

occupation that compresses interdigital spaces, concomitant tines pedis

Tinea cruris etiologic agents

1. Epidermophyton floccosum (predominately) 2. Trichophyton rubrum 3. Trichophyton mentagrophytes

Describe lesion of Tinea cruris

Reddish-brown lesions, sharply demarcated, raised, erythematous margins, pruritic

Tinea unguium etiologic agents

T. rubrum and T. metagrophytes

Distal Subungual Onychomycosis

nail thickens and often discolors | distal-> proximal

Proximal Subungual Onychomycosis

begins in nail fold (proximal) -> spreads distally

White Superficial Onychomycosis (Leukonychia mycotica)

nails lose luster, become opaque, brittle, and have a crumbling consistency

What is the most common tinea unguium form?

Distal Subungual Onychomycosis

What is the most common tines unguium form in AIDS patients?

Proximal Subungual Onychomycosis

If you find Proximal Subungual Onychomycosis, what test should be ordered?

CD4 count, P24 antigen

Treatment for tinea unguium?

3-4 months/fingernail infection; 4-6 months/toenail infection of antifungals

What test is done to confirm tinea unguium?

Periodic Acid-Schiff stain

Tinea corporis etiologic agents

1. Trichophyton | 2. Microsporum

Tinea corporis lesions

Single or multiple, dry, scaly, annular lesions , red borders w/ central clearing (classic ringworm)

Iris form or vesicular form of Tinea corporis lesions

highly inflammatory lesion composed of pustules, vesicles, and marked erythema

Tinea faciei lesions

Non-bearded areas - Annular red patches or, more commonly, indistinct red areas w/ little or no scaling

Tinea faciei worsens with

sunlight exposure