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MSK, Rheum, Derm > Wright - Acne, Fungal, Viral Infections > Flashcards

Wright - Acne, Fungal, Viral Infections Flashcards

1
Q

What are the 4 key factors in acne pathogenesis?

A
  • Sebaceous gland hyperplasia
  • Abnormal follicular desquamation: dead skin cell buildup at opening
  • Propionibacterium acnes colonization
  • Inflammation
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2
Q

What is this?

A
  • Microcomedo:
    1. Non-inflammatory comedones: blackhead (open) and whitehead (closed)
    2. Inflammatory lesions: papules, pustules, nodules, cysts
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3
Q

How do you assess acne patient?

A

No consensus, but combine lesion counting with global assessment of severity

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4
Q

What are the topical and systemic acne treatments?

A
  • Topical:
    1. OTC: benzoyl peroxide, salicylic acid -> for very mild acne (sal acid less effective)
    2. Prescription: antimicrobials, retinoids, combos
  • Systemic:
    1. ABs, oral contraceptives, isotretinoin (acutane)
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5
Q

Benzoyl peroxide

A
  • MOA: kills P. acnes
    1. Mild comedolytic
    2. Mild anti-inflammatory
  • Limits development of P. acnes AB resistance
  • Combine with retinoid to increase efficacy
  • No resistance reported
  • Generally recognized as safe (GRASE) by FDA: AEs include irritation, bleaching, allergic contact dermatitis (1:500; variety of formulations)
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6
Q

What topical ABs are used to treat acne?

A
  • Clindamycin, erythromycin: antibac, anti-inflam
    1. AEs: irritation, colitis (colon inflammation) reported with clindamycin (not a high risk)
  • NOT recommended as monotherapy: slow onset, resistance, and NOT comedolytic
    1. Add topical benzoyl peroxide (BP), or use combo product: usually pretty easy to get, and covered by insurance
  • Really need to target comedone plug above all else
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7
Q

Topical retinoids

A
  • Adapalene, Tretinoin, Tazarotene (pregnancy X)
  • MOA: normalize follicular desquamation (comedolytic), anti-inflammatory, and enhance penetration of other compounds
  • Indications: FIRST-LINE tx for all types of acne
    1. Preferred for maintenance therapy
  • Side Effects: local irritation
  • Can also help with wrinkles
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8
Q

What are the pros and cons of retinoid combo products?

A
  • Some combo products w/AB or BP
  • Pros: once a day (compliance)
  • Cons: fixed retinoid (low concentration) and $$$$
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9
Q

When are systemic ABs given for acne?

A
  • Mod-severe inflammatory (most not FDA approved for acne -> only Minocycline)
    1. On these for several months
  • MOA: antibacterial, anti-inflammatory -> do NOT have comedolytic effects
  • Goal is maintenance w/topical
  • Preferred oral ABs (pts >=8): Tetracycline, Doxycycline, Minocycline
    1. Less commonly Erythromycin/Bactrim
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10
Q

What are the AE’s with the systemic ABs?

A
  • Generally well-tolerated: recommend taking with food (not dairy products bc can affect absorption)
  • Severe AEs (uncommon):
    1. Tetracycline: GI upset, teeth staining (<8 yr)
    2. Doxycycline: photosensitivity, esophagitis (drink water)
    3. Minocycline: dyspigmentation, lupus-like rxn, pseudomotor cerebri, SJS, DHS (drug hypersensitivity syndrome)
    4. Erythromycin: GI sensitivity
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11
Q

Oral contraceptives for acne

A
  • Females w/mod-severe inflam/mixed acne, esp. if flare with periods
  • Anti-androgen effects suppress sebum production
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12
Q

What are the indications for Isotretinoin?

A
  • Used to be called acutane (oral)
  • Severe
  • Scarring
  • Refractory
  • Very rarely start w/this -> most severe cases only
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13
Q

What is the MOA of the oral retinoids?

A
  • Target all 4 factors of acne pathogenesis:
    1. DEC size/activity of sebaceous glands -> reduces sebum production by >90%
    2. Normalize follicular keratinization, preventing new comedones
    3. Inhibit P. acnes
    4. Anti-inflammatory
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14
Q

What are the common AEs of the oral retinoids? Serious AEs?

A
  • Common: dry lips, skin, and eyes, nosebleeds, mild headaches, muscle aches, backaches
  • Serious: TERATOGENIC -> iPledge
    1. Depression, suicidal ideation (no causal relationship established)
    2. Skeletal changes: more concerning for younger pts (fractures, hyperostosis, epiphyseal closure)
    3. IBD: data conflicting (UC > CD)
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15
Q

What is the simple treatment algorithm for acne?

A
  • Mild comedonal: topical retinoid
  • Mild inflammatory/mixed: topical retinoid + topical antimicrobial
  • Moderate inflammatory/mixed: topical retinoid + topical antimicrobial + oral antimicrobial
  • Severe inflammatory:
    1. Minimal scarring: topical retinoid + topical antimicrobial + oral antimicrobial
    2. Scarring or multiple treatment failures: Isotretinoin
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16
Q

What is this? How would you treat it?

A
  • Mild-mod comedonal acne
  • Topical retinoid
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17
Q

What is this? How would you treat it?

A
  • Mild mixed acne
  • Topical retinoid + topical AB
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18
Q

What is this? How would you treat it?

A
  • Moderate mixed acne
  • Topical retinoid + topical AB + oral AB
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19
Q

What is this? How would you treat it?

A
  • Severe mixed acne
  • Minimal scarring: topical retinoid + topical AB + oral AB
  • More severe scarring: Isotretinoid (have to come in monthly for 6 to 9 months)
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20
Q

What basic skin care should people with acne do?

A
  • Gentle cleansing 1-2 times a day with mild, fragrance-free cleanser
  • Oil-free moisturizer with SPF 30+ bid and prn
  • Avoid OTC acne washes and topicals because too irritating/drying
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21
Q

What are some common acne myths? Are they true?

A
  • Acne is NOT caused by poor hygiene or dirt
  • Diet controversial:
    1. High glycemic index diet may lead to hyperinsulinemia and stimulate androgen synthesis (relationship to METABOLIC SYNDROME; particular subset of acne pts)
    2. Milk, particularly teenage boys who drink a lot of milk
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22
Q

What are some important aspects of acne pt education?

A
  • Discourage picking bc can lead to permanent scarring
  • Post-inflammatory hyperpigmentation
  • Explain how to use medicines (pee-sized amount)
  • Potential side effects
  • Consistent use for 6-8 weeks minimum
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23
Q

When should you refer pts with acne?

A
  • Severe Acne (cysts, nodules, scars)
  • No response or poor response to treatment after 12 weeks
  • If systemic antibiotics needed >1 year
  • Isotretinoin being considered: females will NEED OCP (oral contraceptives)
  • Acne associated with a systemic disease
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24
Q

What is rosacea? Causes?

A
  • Relapsing and remitting facial erythema in pts over 30 years old (4 types); usually women with fair skin
  • Causes:
    1. Inflammation
    2. Demodex folliculorum
    3. Vascular abnormalities: tend to be prone to flushing
    4. Genetics
    5. Triggers: sunlight, exercise, hot/cold, stress, foods, alcohol
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25
Q

What are the clinical manifestations of rosacea? Types?

A
  • Redness, flushing, pimples
  • Four types:
    1. Erythematotelangiectatic
    2. Papulopustular
    3. Phymatous: permanent swelling in the nose
    4. Ocular
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26
Q

What is the tx for rosacea?

A
  • Topical: usually a combo if severe
    1. Metronidazole (cream or gel)
    2. Azelaic acid
    3. Sodium sulfacetamide with sulfur
  • Systemic: if more moderate to severe disease
    1. Oral tetracyclines
  • Other: IPL (intense pulse light therapy), laser, sx
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27
Q

What is this? Suspected triggers?

A
  • Periorifical dermatitis: women 20-45 yrs and prepubertal children (aka, periorbital dermatitis)
  • Suspected triggers:
    1. Steroids, topical
    2. OCP (oral contraceptives)
    3. Menstruation, pregnancy
    4. Fluorinated toothpaste
    5. Stress
    6. Candida, demodex mites
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28
Q

What are the clinical manifestations of periorifical dermatitis?

A
  • Rash or “pimples” around mouth
    1. Nose, eyes, labia
    2. Papules, pustules, vesicles
  • May be kind of eczematous
  • Granulomatous variant: longstanding in youth (top image)
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29
Q

What is the treatment for periorifical dermatitis?

A
  • Discontinue all topical steroids
  • Mild: topical antibiotics
  • Severe: oral antibiotics
  • May need topical non-steroidal anti-inflam (like Tacrolimus)
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30
Q

What causes folliculitis? How do you tell which one it is?

A
  • Very common in hair-bearing areas
  • Can usually determine cause via where it is occurring and PMH
  • Most common causes are bacterial:
    1. Staph aureus
    2. Streptococcus
    3. Pseudomonas
  • Other Causes:
    1. Fungal: pityrosporum orbiculare (yeast, fungus hybrid)
    2. Mites: demodex folliculorum
    3. Mechanical (i.e., on buttocks)
    4. Eosinophilic folliculitis: HIV, transplant pts
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31
Q

What is this? How would you treat it?

A
  • Clinical manifestations of folliculitis -> follicular based papules/pustules on hair-bearing areas
  • Caused often based on where it is occurring and past medical history (PMH)
  • TREATMENT: AB soaps/washes
    1. Topical ABs: ok to use these by themselves in this context
    2. Topical antifungals
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32
Q

What is hydradenitis suppurativa?

A
  • Apocrine gland bearing areas: axillary, inguinal, inframammary folds
    1. Prevalence is 1-4%; mostly WOMEN
  • Risk factors: obesity, cigarette smoking, and family history
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33
Q

What are the clinical manifestations of hidradenitis suppurativa? Txs?

A
  • Clinical manifestations: recurrent, persistent painful abscesses
    1. Sinus tracts: chronic drainage
    2. Scars
    3. Also get comedones, a key to confirming the dx
  • Treatment:
    1. Mild: topical and/or oral antibiotics
    2. Moderate to severe: intra-lesional steroids, TNF-α inhibitors, surgery
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34
Q

What are the HSV types?

A
  • dsDNA
  • HSV-1: peri-oral, lips, oral cavity
    1. Abs in 85% of adults; can get initial outbreak when little, and not recurrences after that
  • HSV-2: genital -> Abs in 20-25% of adults (can also infect the mouth)
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35
Q

What are the 3 infection states of HSV? What will pt hx look like for each?

A
  • Primary: direct contact (vesicles) -> 3-7 days after exposure
    1. Pain, burning, tingling, fever, malaise, LAD
  • Latent: via sensory nerves to ganglion
    1. Tends to be milder
  • Recurrent: viral shedding
    1. Fever, sun exposure, stress
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36
Q

What are the clinical manifestations of HSV?

A
  • Clusters of monomorphous (all look the same) vesicles with an erythematous base
  • “Punched out” erosions and crusted papules
  • Usually start out with clear contents that become cloudy over time
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37
Q

What do you see here?

A
  • HSV
  • Clusters of monomorphous (all look the same) vesicles with an erythematous base
  • “Punched out” erosions and crusted papules
  • Usually start out with clear contents that become cloudy over time
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38
Q

How do you confirm HSV diagnosis?

A
  • Tzanck smear: look for multinucleated giant cells
    1. Viral culture (48 hrs), PCR (faster, more $), direct fluorescent Ab -> really just depends on the institution
  • Most of the time this is a clinical diagnosis
  • Can look like other conditions in children, however (like atopic dermatitis)
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39
Q

What is this?

A
  • Tzanck smear for HSV: note the multinucleated giant cells
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40
Q

What should be in your differential for HSV?

A
  • Impetigo: bacterial infection of skin with strep or staph (top image)
  • Aphthous stomatitis (canker sore): tend to be larger and fewer in number (abscesses) -> middle image
  • Syphilitic chancre: bottom image
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41
Q

What is the treatment for HSV?

A
  • Mild: topical antiviral -> not as effective as oral
  • Moderate to severe: systemic antiviral
  • Oral or IV for pts who may be immunosuppressed
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42
Q

What is shingles? What are the triggers?

A
  • Reactivation of latent VZV (in dorsal root ganglia; dsDNA)
    1. 20-30% lifetime risk (if you had chicken pox as a child)
  • Incidence/severity INC: after age 60, and in ppl who are immunosuppressed
  • Triggers: trauma, stress, fever, radiation, immuno-suppression
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43
Q

What are the clinical manifestations of shingles?

A
  • Prodrome: pain, pruritus, burning
  • Grouped vesicles over a dermatome: can get some additional lesions outside the dermatome too-
    1. Trunk most common
  • Trigeminal nerve (V1, ophthalmic): 10 to 15%
    1. Vesicles at tip/side of nose (Hutchinson’s sign) -> nasociliary branch
    1. Eye: blindness
  • V2 and/or V3: facial palsy
    1. Ear: tinnitus, vertigo, deafness
  • Rash resolves within 3-5 weeks
  • Postherpetic neuralgia (esp. common on the face, and in older patients) -> 5-20%
    1. Typically over 40 yrs old
  • Can get permanent scarring
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44
Q

What is this?

A
  • Shingles: VZV
  • Patients may think this is a bite at first
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45
Q

How can you confirm a VZV diagnosis?

A
  • Tzanck smear
  • Viral culture
  • PCR
  • Same as with HSV (which should also be in your differential -> would not be as painful, or along the dermatome)
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46
Q

Treatment and prevention of shingles?

A
  • Oral antiviral w/in 72 hrs and pain med, esp. with facial type
  • Vaccine (Zostavax) for people 60 yrs and older
    1. Decreases risk of shingles by 51% and neuralgia by 67%
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47
Q

What is molluscum contagiosum?

A
  • Cutaneous infection caused by Pox virus (dsDNA)
  • Transmission: skin to skin, autoinoculation, fomites
    1. Risk factors: atopic dermatitis, immuno-suppression, bathing/sleeping together
    2. Children should not be kept out of school; casual contact should not spread disease
  • Resolve spontaneously in months to years, but may leave depressed scar (that improves over time)
    1. Discoloration common
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48
Q

What are the clinical manifestations of molluscum contagiosum?

A
  • Small or lg pink to skin-colored 2-10 mm dome-shaped waxy papules
    1. +/- central umbilication (can’t rely on this for diagnosis)
  • May cause “molluscum dermatitis:” pruritis
  • Face, upper chest, extremities, other (common in creases: armpits, behind the knees, but really can be anywhere)
  • Parents worry about eyelids -> conjunctivitis and keratitis are possible, but not common
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49
Q

What is this?

A

Molluscum contagiosum

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50
Q

What do you see here?

A
  • Inflamed molluscum
  • True infection is rare -> usually signals immune response and imminent resolution
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51
Q

What should be on your differential for molluscum?

A
  • Acne (left): comedones, no umbilication
  • Folliculitis (right): papules or pustules, no umbilication
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52
Q

What are the tx options for molluscum?

A
  • Numerous methods, but NO CLEAR EVIDENCE to support any of them
  • Active Nonintervention: self-limited
  • Physical Destruction
    1. Curettage: more likely to leave scarring
    2. Cryotherapy
    3. Cantharidin: liquid that contains a vesicant (causes blister that dries up and falls off)
  • Local Irritation: topical retinoids, keratolytics
  • Immunomodulators:
    1. Topical: Imiquimod -> very expensive and irritating
    2. Systemic: intralesional antigens, cimetidine
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53
Q

What is Cantharidin?

A
  • Chemical vesicant extracted from the blister beetle that is used to treat molluscum and warts
  • Research: 90% cleared after avg of 2 applications; side effects -> erythema, blistering, pain
  • High rate of parental and physician satisfaction
  • Superficial blisters, so NO SCARRING -> some discoloration possible, but it will go away
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54
Q

What are warts? Causes?

A
  • Common viral infection: HPV -> certain types have predilection to infect certain locations
  • dsDNA
  • >100 types
  • Anywhere: hands, feet most common
  • Benign, involute -> painful, embarrassing
  • Some oncogenic: 16, 18, 31, 33
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55
Q

How are warts transmitted?

A
  • Contact:
    1. Direct: hetero or autoinoculation
    2. Indirect: fomites -> warm, moist surfaces, e.g., towels
  • Site of entry: traumatized skin (can be subclinical abrasion or fissure)
  • Incubation period: 1-6 months
  • Duration variable: 2/3 resolve within 2 years
  • Mechanism: cell-mediated immunity -> production of cytokines that elicit immune response against the virus
56
Q

What are 4 common types of warts?

A
  • Verrucae Vulgaris: common warts
  • Verrucae Plantaris: plantar warts
  • Verrucae Plana: flat warts
  • Condylomata Acuminata: anogenital warts
57
Q

Verrucae vulgaris

A
  • Hands most common: periungual, subungual
    1. Can occur anywhere, including oral mucosa
  • Single or multiple skin-colored hyperkeratotic papules and/or plaques
    1. Dome shaped
    2. Exophytic
    3. Filiform (on a stalk)
  • Clues to diagnosis: paring surface reveals “black dots” -> thrombosed capillaries
    1. Disruption of normal skin lines
58
Q

What are these?

A
  • Filiform warts: can be snipped off
59
Q

Flat warts

A
  • Face, neck, arms, legs most common
  • Smooth, skin-colored to slightly tan/pink flat-topped thin papules (3-5 mm) and/or plaques
  • Few or many
  • Shaving can facilitate spread
60
Q

What are these?

A

Flat warts

Note the Koebnerization in the bottom image (coalescing, linear lesion)

61
Q

Plantar warts

A
  • Plantar foot, toes
  • Tend to be most symptomatic
    1. Weight bearing surfaces
    2. Develop endophytic (grows inward) component, painful
  • Coalesce into clusters
    1. Mosaic wart: big one that causes a blister (top image)
  • Paring surface should reveal “black dots:” if you can’t tell what it is (bottom image -> micro-thromboses)
  • Note the thrombosed capillaries in the bottom image
62
Q

What are these?

A

Endophytic warts

63
Q

DDx for plantar warts?

A
  • Callus: left
  • Corn: top right
  • Black heel (bottom right): common in athletes, and may sometimes be confused with warts
64
Q

What is the clinical presentation of anogenital warts?

A
  • Skin-colored to pink/tan soft papules: 1-5 mm
    1. Usually multiple
    2. May form large masses (cauliflower-like)
  • Usually asymptomatic
    1. Irritation may cause pain, bleeding
65
Q

How are anogenital warts transmitted?

A
  • Transmission:
    1. Sexual contact
    2. Vertical (perinatal)
    3. Benign (nonsexual) heteroinoculation (like a grandparent whiping a baby’s bottom)
    4. Autoinoculation: hands to genitalia or perianal area
    4. Fomite (e.g., towels)
66
Q

What is the treatment for warts?

A
  • No specific antiviral therapy for HPV infections -> many txs, but lack of evidence-based medicine
  • Two broad categories:
    1. Destructive (physical or chemical): freezing, burning (may just grow back), cutting off, laser
    2. Immunomodulatory: topical, oral, injections
  • Best evidence for topical salicylic acid, in a review
67
Q

What are the 2 HPV vaccines?

A
  • Gardasil: 16, 18, 6, 11
  • Cervarix: 16 and 18
68
Q

What are the indications for tx of warts? What factors are important?

A
  • INDICATIONS: painful, extensive, enlarging, subject to trauma, cosmetically objectionable
  • Choice of tx depends on multiple factors:
    1. Age/personality of child
    2. Number
    3. Size
    4. Location
    5. Previous therapy
69
Q

What are the 6 types of superficial fungal infections?

A
  • Tinea capitis: head
  • Tinea corporis: body
  • Tinea manuum: hand
  • Tinea cruris: groin creases
  • Tinea pedis: feet
  • Tinea unguium: onychomycosis
70
Q

What is a dermatophyte? 3 primary genera? Yeast?

A
  • Tinea or “ringworm”
    1. Soil, on animals, on humans
    2. Digest keratin and invade hair, skin, nails
  • 3 primary genera:
    1. Trichophyton
    2. Microsporum
    3. Epidermophyton
  • Yeast:
    1. Tinea versicolor
    2. Candidiasis
71
Q

What is tinea capitis? Caused by?

A
  • “Ringworm:” fungal infection of skin, hair of scalp
  • Most common in kids: 3-7 yrs old (M>F), but freq in younger/older kids too (3-8% US prevalence)
  • Caused by:
    1. Trichophyton tonsurans (>90% in US; AA)
    2. Microsporum canis (Caucasian)
  • Tends to come from cats, and AA children more than Caucasian/Hispanic
72
Q

How is tinea capitis transmitted? What are the predisposing factors?

A
  • Transmission: humans (via asymptomatic carriage; most common), animals, soil
    1. Fomites: brushes, combs, hats, hair clippers, etc.
  • Predisposing factors: large family size, crowded living conditions, and low SES
73
Q

What do these two images show?

A
  • TINEA CAPITIS
  • “Seb derm”-like plaques (left): look more like dandruff -> diffuse
  • Localized plaques (right)
  • Clinically, largely characterized by scaling and patchy alopecia, BUT variety of patterns/range of features may be seen
    1. Doesn’t always look like rings, or what you see on the body
74
Q

What is this?

A
  • Patchy alopecia in tinea capitis: can be subtle or quite severe
  • A lot of hair breakage, particularly at the surface of the skin
75
Q

What do you see here?

A
  • Patchy alopecia in tinea capitis: can be subtle or quite severe
  • A lot of hair breakage, particularly at the surface of the skin
76
Q

What is going on here?

A
  • Broken hair shafts in tinea capitis
  • If the child has dark hair, you may see a “black dot” pattern (base of the hair is still in the follicle)
  • This is generally caused by T. tonsurans, which grows on the inside of the hair shafts, weakening them and causing them to break off at the scalp
77
Q

What’s up with these dudes?

A
  • Pustules in tinea capitis
  • Sometimes just a few and sometimes many
  • When you see pustules, even in the absence of other significant findings, you should have a high index of suspicion for a primary fungal infection and OBTAIN A FUNGAL CULTURE
  • Can also be superimposed bacterial infection
78
Q

What is going on here?

A
  • Kerions from tinea capitis: may cause permanent scarring alopecia -> esp likely if allowed to go on for a long time without proper treatment
  • May see severe inflam rxn on the scalp -> follicles will recover and most of the hair will re-grow most of the time
    1. Need to be taken seriously and treated to prevent permanent damage
79
Q

Do pts w/tinea capitis get LAD?

A
  • YES!
  • Studies show that presence of posterior cervical and sub-occipital LAD correlate well with a + fungal culture in the setting of scaling and alopecia
80
Q

How is a tinea capitis diagnosis confirmed?

A
  • Gold standard is FUNGAL CULTURE
    1. Standard bacterial culturette
    2. Moisten cotton tip of swab (tap water okay)
    3. Rub vigorously over affected area
  • She reiterated how important this was multiple times
  • M. Canis often takes even higher dose and longer course to clear, especially if more severe infection, making CULTURE IMPORTANT (even though many physicians will not do this)
  • KOH of scale (attached image) & broken hairs may also be helpful
81
Q

What should be on your DDx for tinea capitis?

A
  • Seborrheic dermatitis
  • Psoriasis
  • Alopecia areata
82
Q

What is this?

A
  • Seborrheic dermatitis: usually more CHRONIC than tinea capitis
  • Unusual after infancy and before puberty
    1. Infants with “cradle cap:” waxy yellow scale
    2. Teens and adults with “dandruff:” diffuse dry or oily white to yellow scale
  • Diffuse dry or oily white/yellow scale
  • Thought that Malasezia is involved
83
Q

What is this?

A
  • Psoriasis: frequently affects the scalp
  • Erythematous plaques with silvery scale
  • Favors postauricular and posterior hairline
84
Q

What do you see here?

A
  • Alopecia areata: well-circumscribed, smooth bald patches
  • Generally, you won’t see any scale or other skin changes
  • Smooth bald patches that are very NON-INFLAM (may have pinkish-orange hue, but no scale or inflammatory pustules)
  • No LAD or broken hairs
85
Q

What is the pharm treatment for tinea capitis?

A
  • Requires SYSTEMIC antifungal to penetrate hair follicle (can’t use a topical anti-fungal because can’t get inside the hair shaft)
  • Griseofulvin is gold standard
  • M.canis infections may require higher doses and longer course for clearance
  • Give with fatty food to enhance absorption; may divide bid if large volume of liquid
  • Side effects rare: headache, GI, photosensitivity, morbilliform eruption
    1. Heme and hepatic toxicity very uncommon
  • Routine lab monitoring NOT recommended
    1. CBC, LFT’s for course longer than 8 wks
86
Q

What are the non-pharm treatments for tinea capitis?

A
  • Antifungal shampoo 2-3 times per week (once per week if pt only washes hair once each week)
    1. Ketoconazole 2% or Selenium sulfide 2.5%
    a. Aid in removal of scale
    b. Eradicate spores, which helps DEC transmission
    c. Helpful adjunctive therapy
    2. Consider use by all household members
  • Fomite education: don’t share combs, brushes, hats, etc.
87
Q

Besides Griseofulvin, what are the other tx options for tinea capitis?

A
  • Terbinafine: approval for 4 and older (6-wk course)
    1. Oral; have to draw baseline LFTs and CBC (parents usually do NOT like this)
    2. M. Canis doesn’t respond well to this
    3. AEs: headache, GI, dizziness, drug rxns, hepatotoxicity, rare hematologic
  • Systemic azoles NOT routinely used -> may give Fluconazole to infants (<couple></couple>

<p>1. More $, liver toxicity, drug interactions </p>

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88
Q

How should kerions be treated in tinea capitis?

A
  • Marked inflam may cause scarring and permanent hair loss (e.g., the kid might wear a hat every day for awhile, making it harder to notice the damage)
  • Rapid aggressive therapy indicated
  • Severe: consider systemic steroids (for 2 weeks)
    1. Rapid resolution of inflammation
    2. Decreased pain
  • If the patient has a kerion, you should think about whether you need medications in addition to the systemic anti-fungal
89
Q

What is tinea corporis?

A
  • Superficial fungal infection of skin
  • Transmission via contact with infected person or animal
  • Young children (M. Canis > trichophyton)
  • Older child/adults (T. Rubrum and o/trichophyton)
    1. Young child with T. rubrum likely has parent with tinea pedis and/or onychomycosis
90
Q

What are the clinical manifestations of tinea corporis?

A
  • Classic: one or more well-defined annular scaly erythematous plaques with central clearing and a scaly, vesicular, papular, or pustular border
    1. Annular: emphasized border, and central area that looks more like regular skin
91
Q

What is this?

A

Tinea corporis

92
Q

What do you see here?

A
  • Tinea incognito (tinea corporis): use of topical steroids may alter appearance
  • Steroid can calm inflammation, but not clear it -> ruins the appearance of the infection, leading to difficult dx (incognito)
93
Q

What is this? Tx?

A
  • Majocchi’s granuloma: granulomatous folliculitis
    1. Form of tinea corporis (Trichophyton rubrum)
  • Erythematous plaques or patches studded with papules and/or nodules
  • Deeper infection of follicles
  • Usually requires systemic therapy to penetrate follicles
94
Q

How do you diagnose tinea corporis?

A
  • Clinical presentation: history and PE
  • KOH prep: scrape active border
  • Fungal culture
  • Most of the time, you’ll have to rely heavily on your presentation to make an educated guess -> often don’t have time to do a KOH in prep
95
Q

What things might be on your differential for tinea corporis?

A
  • Nummular atopic dermatitis
  • Psoriasis
  • Granuloma annulare
96
Q

What is this?

A
  • Nummular atopic dermatitis
  • NOT ANNULAR (everything round is not annular)
  • Very pruritic: much more itchy than typical fungal infection would be
97
Q

What do we have here?

A
  • Psoriasis: “dull pink” erythema
  • NOT tinea corporis because:
    1. Silvery or white micaceous scale
    2. Nummular lesions
    3. Distribution -> tends to favor scalp, behind ears, over elbows and knees
98
Q

What is this?

A
  • Granuloma annulare
  • NOT tinea corporis because:
    1. No scale
    2. Raised, “rubbery” rim
    3. Location: dorsal hands, wrists, feet, ankles
99
Q

What is the treatment for tinea corporis?

A
  • Topical for superficial/localized:
    1. BID for at least 2-4 weeks
    2. Treat affected area and rim of “normal” skin
  • If no improvement, reconsider diagnosis
    2. If culture +, proceed to oral therapy
  • Systemic therapy for: disseminated/severe, immunocompromised host, Majocchi’s, tinea faciei (on the face)
100
Q

What’s the deal with using combo products for tinea corporis?

A
  • Combo antifungal/steroid often result in persistent, worsening infection
  • Relatively strong topical steroids: atrophy, striae, telangiectasias
  • Fairly weak anti-fungal
  • Generally NOT RECOMMENDED
  • Pts use the product until they get atrophy of skin, and other effects of steroid use, but still have fungal infection -> much better off doing the culture, and doing one or the other
101
Q

What is tinea manuum? Clinical manifestations?

A
  • Skin of hands; most comm in MEN (Trichophyton)
  • Rare in children
  • Clinical manifestations:
    1. Chronic dryness of palms
    2. Redness/scaling
    3. Two patterns:
    a. Palmar: fine scale, may be unilateral
    b. Dorsal: annular, red, scaly
102
Q

What is this? Dx?

A
  • Tinea manuum
  • Diagnosis via KOH (branched septated hyphae) and fungal culture
103
Q

What is the differential for tinea manuus?

A
  • Other dermatitis: irritant, contact
  • Psoriasis
  • Really important to GET CULTURE and see what this is
104
Q

How do you treat tinea manuus?

A
  • Topical antifungal for dorsum, limited
  • Palms require oral antifungal
105
Q

What is tinea cruris?

A
  • Skin of groin, aka, “jock itch” -> rare in children
  • MEN > women
  • Risk factors: obesity, heat, humidity
  • Trichophyton
106
Q

What are the clinical manifestations of tinea cruris?

A
  • Pruritic
  • Red, annular, scaly plaques over groin and medial thighs
  • Penis, scrotum not affected
107
Q

What is this? How would you dx it?

A
  • Tinea cruris (jock itch)
  • KOH and fungal culture
108
Q

What should be in your DDx for tinea cruris?

A
  • Candidiasis: NOT tinea bc much more irregular border satellite pustules
  • Erythrasma: NOT tinea bc no scale and coral red fluorescence (see attached image)
  • Other: psoriasis, seb derm
109
Q

What is the treatment for tinea cruris?

A
  • Topical anti-fungal if it is pretty limited
    1. Powders helpful (dry up the area)
  • Oral AF if refractory, severe (or have deeper follicular involvement)
  • Treat tinea pedis also -> LOOK AT WHOLE BODY
  • Recurrences are common
110
Q

What is tinea pedis? Risk factors?

A
  • “Athlete’s foot” -> 10% world population
  • Males
  • Risk factors: occlusive shoes, communal pools, showers
111
Q

What are the clinical manifestations of tinea pedis?

A
  • Itching, scaling on soles, between toes
    1. Blistering
  • Moccasin: fine dry scale over soles (T. rubrum)
  • Vesiculobullous: vesicles/bullae on soles, esp. insteps (T. mentagrophytes)
112
Q

What is this?

A

Tinea pedis: usually more concentrated on medial edge of the foot

113
Q

How do you diagnose tinea pedis?

A

KOH and fungal culture

114
Q

What should be on your differential for tinea pedis?

A
  • Contact dermatitis: dorsal feet affected
  • Dyshidrotic eczema: “tapioca vesicles”
    1. Can be hard to differentiate between this and vesiculobullous type, but CULTURE is what helps here
115
Q

What is this?

A

Contact dermatitis: e.g., leather, etc.

NOT tinea pedis

116
Q

What is this?

A
  • Dyshidrotic eczema
  • Usually a lot itchier than tinea pedis, but this is a very subjective thing
  • CULTURE is the key
117
Q

What is tinea unguium? Risk factors?

A
  • Nail infection -> 60% over age 70
  • Males
  • Tricophyton
  • Non-dermatophyte molds, yeasts
  • Risk factors: immunosuppressed, diabetes, HIV, poor circulation, trauma, dystrophy (already abnormal and more susceptible)
118
Q

What are the clinical manifestations of tinea unguium? Patterns?

A
  • Discoloration, thickening, onycholysis
  • 4 patterns:
    1. Distal subungual: most common
    2. Proximal subungual
    3. White superficial
    4. Candida
  • Nails may separate from the nail bed
119
Q

What is this?

A
  • Distal subungual = most common of the 4 types of tinea unguium
  • Invasion of distal nail plate, onycholysis with thickening and discoloration
120
Q

What is this?

A
  • Proximal subungual variation of tinea unguium
  • Uncommon
  • HIV positive patient: considered pathognomonic for HIV
121
Q

What is this?

A
  • Proximal subungual variation of tinea unguium
  • Uncommon
  • HIV positive patient: considered pathognomonic for HIV
122
Q

What is this?

A
  • White superficial variation of tinea
  • White plaques on dorsal nail plate: from top downward
123
Q

What is this?

A
  • Candida
  • Distal fingertips red and swollen, and nails destroyed
  • Won’t see this in typical dermatophyte infections
124
Q

What is chronic paronychia?

A
  • Nail dystrophy
  • Candida albicans
    1. Confirm with stain and culture
    2. Treatment
    a. Topical ketoconazole if mild
    b. Oral fluconazole if severe (3 mos for fingernails) -> baseline CBC, LFT’s
  • Most of the time this has been going on for quite awhile, and you will give Fluconazole
125
Q

What do you see here?

A
  • Trachyonychia: 20 nail dystrophy (may not affect all nails)
    1. Ridging, grooves, pitting, discoloration, fragility
    2. Pretty rapidly progresses to involve all nails
  • Causes: idiopathic, lichen planus, psoriasis, other
    1. Don’t really know what causes this (idiopathic), but can see in setting of psoriasis
126
Q

What do you see here?

A
  • Beau’s lines: transverse grooves or furrows
  • Stress causes temporary arrest of nail matrix
    1. Usually after some type of viral or febrile illness in kids
    2. Plate stops growing, and re-starts, leaving a gap (totally common, and nails grow back normally) -> NOT fungus
  • Nail may shed completely (onychomadesis)
127
Q

What is going on here? Why?

A
  • Usually symmetrical: often both great toes, 2nd toes, or 5th toes, e.g., pressure from ill-fitting shoes
  • Jamming will show breakage, splitting, hemorrhage
    1. Smaller toes often times a little thicker (due to friction)
  • NOT fungus -> if symmetrical, less likely to be fungus
128
Q

What happened here?

A
  • Habit tic deformity
  • Habitual picking at the cuticle
129
Q

How would you diagnose a nail fungal infection?

A
  • KOH prep: preferably from subungual debris
  • Fungal culture of nail clipping (couple pieces of nail)
  • Fungal stain of nail clipping: PAS = periodic acid-Schiff (see attached image; kind of old-fashioned)
130
Q

What is the treatment for tinea unguium?

A
  • Topicals generally not very effective bc they:
    1. Do not penetrate nail plate well
    2. Do not reach nail matrix
    3. Penlac (Ciclopirox) for superficial infection not involving lunula (visible, crescent-shaped part of the root of the nail) -> w/softening agent (urea cream)
  • Systemic therapy: Griseofulvin in the past (but low cure rate and high recurrences)
    1. Terbinafine: 6 wks for fingernails, and 12 wks for toenails -> baseline CBC and LFTs (repeat in 2-4 weeks)
    2. Other: itraconazole, fluconazole -> tend to be more expensive and have more potential side effects
131
Q

How long does it take fingernails and toenails to grow out?

A
  • Fingernails: 4 to 6 months
  • Toenails: 12 to 18 months
132
Q

What is tinea versicolor?

A
  • Aka, pityriasis versicolor (not a true infection)
  • Common superficial fungal disorder of skin
  • Yeast forms of dimorphic fungus Malassezia furfur (same as seb derm); also pityrosporum orbiculare and pityrosporum ovale
    1. Normal skin flora
  • Usually presents in adolescence (when oil and sebaceous glands are more active), but may be seen in younger children too
133
Q

What are the clinical manifestations of tinea versicolor?

A
  • Multiple scaling, oval macules, patches and thin plaques over upper trunk, prox arms, & sometimes face and neck
  • Hyper- or hypopigmented: azelaic acid production (diffuses down and impairs melanocyte function)
    1. Depending on baseline complexion, level of sun exposure (may look lighter on dark skin and darker on light skin)
  • More prominent in summer when sun exposure intensifies pigmentation differences
134
Q

What is this?

A
  • Multiple scaling, oval macules, patches and thin plaques over upper trunk, prox arms, & sometimes face and neck
  • Hyper- or hypopigmented: azelaic acid production (diffuses down and impairs melanocyte function)
    1. Depending on baseline complexion, level of sun exposure (may look lighter on dark skin and darker on light skin)
  • More prominent in summer when sun exposure intensifies pigmentation differences
135
Q

What do you see here? Dx?

A
  • Pityriasis alba
  • Most common on face (mostly children, and more M than F)
  • Usually atopic background
  • Less extensive than pityriasis versicolor
  • Diagnosis: KOH prep w/spaghetti and meatball appearance (hyphae and spores)
    1. Usually don’t culture, but DIAGNOSE CLINICALLY
136
Q

How do you treat pityriasis?

A
  • Education: course tends to be chronic, and recurrences common, esp. when weather gets hot
  • Topical therapy: selenium sulfide lotion/shampoo 2.5% OR ketoconazole shampoo 2%
    1. Applied for 10 min. daily for 1-2 weeks, then 2-3 times per week for maintenance
    2. May need maintenance tx, esp. in warmer months
  • Severe, recurrent, fails topical therapy -> systemic therapy (adult dosing)
    1. Ketoconazole 400 mg po x 1: work up sweat, wait 10-12 hr to shower and repeat in 1 week
    2. Fluconazole 200-400 mg po x 1: may repeat in 1 week if severe
    3. Should still use topical for maintenance
137
Q

Candidiasis? Clinical manifestations? Tx?

A
  • Intertriginous
  • Paronychia
  • Angular Cheilitis: oral commissures (increased moisture) -> elderly, lip lickers, denture (see attached image)
    1. Clinical manifestations: painful, erythematous fissures and small pustules
    2. Treatment: topical anti-yeast cream -> DEC moisture

MSK, Rheum, Derm (21 decks)

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