Derm: lect 3 Flashcards

1
Q

list the dermatophyte infections

A

dermatophyte: fungi that require keratin for growth

  • tinea capitis
  • tinea corporis
  • tinea cruris
  • tinea pedis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

etiology of tinea capitis

A
  • Trichophytan species
  • Microsporum species
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

pathogenesis of tinea capitis

A
  • direct contact with infected individual or animal
  • contact with contaminated object
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

clinical presentation:

  • scaly patches with alopecia
  • patches of alopecia with black dots
  • widespread scaling with subtle hair loss
  • kerion
  • flavus
  • associated findings: cervical adenopathy; dermatophytid reaction
A

tinea capitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

identify the multiple cup-shaped yellow crusts

A

favus (scutula)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

diagnostic evaulation for tinea infections

A

KOH prep

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

treatment of tinea capitis

A
  • if you suspect microsporum: Griseofulvin x 6-12 weeks
  • if you suspect tichophyton: Terbinafine x 2-4 weeks
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Etiology of Tinea Corporis

A
  • Trichophyton rubrum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

epidemiology of tinea corporis

A
  • caregivers for children with tinea capitis
  • athletes with skin to skin contact
  • immunocompromised
  • pets
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

clinical presentation:

  • pruritic, annular, erythematous plaque with central clearing and and advancing border
A

tinea corporis (ringworm)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

treamtent of tinea corporis

A

topical antifungals (“azole”)

  • at least 2 weeks duration
  • avoid nystatin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

etiology of tinea cruris

A

trichophyton rubrum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

epidemiology of tinea cruris

A
  • usually caused by autoinoculation from tinea pedis
  • men > women
  • sweaty
  • obesity/skin folds
  • exacerbating factors: occlusive clothing; humidity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

clinical presentation:

  • well-marginated, annular plaque with scaly raised border
  • extends from the inguinal fold on the inner thigh
  • pruritus and pain
  • scrotum typically spared
  • can be chronic and progressive
A

Tinea Cruris

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

treatment for tinea cruris

A
  • topical antifungals
  • daily talcum powder
  • avoid nystatin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

etiology of tinea pedis

A

trichophyton rubrum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

epidemiology of tinea pedis

A
  • most common dermatophytosis worldwide
  • risk factors: occlusive footwear, communal baths/showers/pools
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

clinical presentation

  • self-limited, intermittent, recurrent
  • itchy/painful vesicles or bulla following sweating
  • secondary staph infections common
A

tinea pedis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

clinical presentation

  • slowly progressive, persists indefinitely
  • erosions/scales between toes (esp 3rd and 4th)
  • interdigital fissures
  • sharp demarcation with accumulated scales in creases
A

chronic tinea pedis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

treatment for tinea pedis

A
  • topical antifungal x 2 weeks
  • oral meds for chronic/extensive disease (terbanfine, itraconazole, fluconazole)
  • foot powder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

etiology of onychomycosis

A
  • trichophyton rubrum
  • trichophyton mentagrophytes
  • candida albicans
  • nondermatophyte molds
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

epidemiology of onychomycosis? what organism usually affects toenails? fingernails?

A
  • dermatophyte: usually toenails
  • yeast: usually fingernails
  • non-dermatophyte molds: rare
  • risk factors: advanced age, tinea pedis, genetics, immunodeficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

clinical presentation

  • typically starts with great toe, but all can be affected
  • white, brown, yellow discoloration starts at distal corner and spreads towards cuticle
  • distal end of nail breaks, exposing nail bed
A

distal subungual onychomycosis

  • most common subtype
24
Q

clinical presentation

  • white, brown, yellow discoloration starts near cuticle
  • with what patient population is this condition usually seen?
A

proximal subungual oncychomycosis

  • AIDS
25
Q

clinical presentation

  • dull, white spots on surface of the nail plate
  • spread centrifugally until entire nail is involved
  • can scrape the soft white areas for lab sample
A

white superficial onychomycosis

26
Q

clinical presentation

  • thickening of nail with yellow, brown discoloration
  • may cause paronychia
  • what is the etiology of this condition
A
  • yeast onychomycosis
  • candida albicans
  • common cause of fingernail oncyhomycosis
27
Q

treatment of onychomycosis

A
  • not obligatory
  • topicals generally ineffective
  • high rates of failure/reoccurance
  • treatment of dermatophyte onychomycosis: oral terbinafine (fingernails: 6 weeks; toenails: 12 weeks)
  • treatment of nondermatophyte onychomycosis: oral itraconazole
  • with these medications: keep eye on liver enzymes
28
Q

what is intertrigo

A
  • any infectious or noninfectious inflammatory condition of two closely opposed (intertriginous) skin surfaces
  • often due to candida species
29
Q

risk factors for candidal intertrigo

A
  • moisture (humidity, incontinence)
  • skin friction (obesity)
  • immunocomprimised
30
Q

clinical presentation

  • erythematous, macerated plaques and erosions
  • pruritus
  • fine peripheral scaling
  • satellite papules/pustules
  • affects groin, mammary and abd folds, web spaces, axillae
A

candidal intertrigo

31
Q

treatment for candidal intertrigo

A
  • preventative: drying agent, weight loss
  • topicals: Nystatin, Azoles
  • Systemic: fluconazole, intraconazole
32
Q

etiology of tinea versicolor (aka pityriasis versicolor)

A
  • malassezia species: normal fungal skin flora that becomes pathologic when it transforms into the mycelial form
33
Q

epidemiology of tinea versicolor

A
  • 2-8% prevalence in US
  • tropical climate
  • adolescents/young adults
  • risk factors: hyperhidrosis, malnourishment
34
Q

clinical presentation

  • macules, patches, plaques on trunk/UE
  • hypopigmented, hyperpigmented, or erythematous
  • varies with skin tone and location
  • often have fine scale
  • can coalesce
  • typically asymptomatic
A

Tinea Versicolor

35
Q

treatment of tinea versicolor

A
  • topical: azole antifungals (ketoconazole) x 2 weeks
  • systemic: extensive disease or failed topical: oral azole antifungals
36
Q

Rosacea

  • who is commonly affected
A
  • 1-10% in whites
  • high prevalence in fair-skinned
  • females > males
  • usually emerges in 30s
37
Q

clinical presentation

  • chronic redness of central face
  • flushing (wet or dry)
  • telangiectasia
  • skin sensitivity
  • dry appearance
A

Erythematotelangiectatic rosacea

38
Q

Clinical presentation

  • papules and pustules of central face
  • inflammation can be confluent
  • no comedones (dilated hair follicle filled with debris: characteristic sign of acne)
A

papulopustular rosacea

39
Q

Clinical presentation

  • tissue hypertrophy causing irregular contours
  • mostly nose by can involve cheeks, forehead and chin
  • mostly affects men
A

phymatous rosacea

40
Q

clinical presentation

  • affects children and adults
  • affects >50% of those with rosacea
  • dry eyes, pain, itching, blurry vision, photosensitivity, conjunctivitis, stye
A

ocular rosacea

41
Q

treatment for erythematotelangiectatic rosacea

A
  • behavior modification: avoid triggers, sun protection, gentle skin care
  • laser and pulsed light therapies, topical brimonidine
42
Q

treatment for papulopustular rosacea

A
  • mild moderate: topical metronidazole
  • mod-severe: oral tetracyclines or macrolides
43
Q

treatment for phymatous rosacea

A
  • early disease: isotretinoin
  • advanced disease: surgical debulking
44
Q

etiology of scabies

A

host-specific mite: sarcoptes scabiei

45
Q

life cycle of scabies

A
  • female mite excavates a burrow in the stratum corneum in which she lays 2-3 eggs/day for her 30 day lifespan
  • eggs hatch in 10 days
  • can live for 3 days away from host
46
Q

clinical presentation:

  • initial lesion
  • burrow is pathognomonic
  • common locations: back and head ofted spared
  • severe pruritus, worse at night
A

scabies

47
Q

treatment of scabies

A

scabicide

  • permethrin 5% cream - initial tx + 2nd application 1 week later
  • oral ivermectin
  • fomite control
48
Q

a large local reaction of a bee sting involved exaggerated erythema and swelling that gradually enlarges over 1-2 days and resolves in 5-10 days. What is the treatment?

A
  • cold compress, prednisone, antihistamine, NSAID
49
Q

what is the clinical presentation of a Widow spider bite

A
  • local reaction: blanched circular patch, surrounding red perimeter and a central punctum
  • venous causes catacholamine release: severe abd pain and muscle spasm, local diaphoresis, HA, N/V
  • often cause few symptoms because no venom injected
50
Q

treatment after widow spider bite

A
  • antiemetics
  • narcotic analgesics
  • tetanus
51
Q

Common clinical presentation of recluse spider bite

A
  • often painless initially
  • progress to severe pain in 2-8 hours
  • resolves in a week
52
Q

what is rare complication of a recluse spider bite

A

severe ulcerative necrosis

  • dark, depressed center develops after 1-2 days
  • systemic symptoms
53
Q

acquired skin depigmentation thought to be from autoimmune process directed against melanocytes

clinical presentation:

  • milk-white macules with homogenous depigmentation and well defined borders
  • slowly progressive
A

vitiligo

54
Q

treatment of vitiligo

A

repigmentation therapy

  • topical and systemic corticosteroids
  • UV light
55
Q

pathogenesis of hidradenitis Suppurativa

A
  1. follicular occlusion
  2. follicular rupture
  3. associated immune response
56
Q

clinical presentation

  • inflammatory nodules, sinus tracts, comedomes, and scarring
  • commonly seen in axilla, inguinal, and anogenital regions
A

hidradenitis suppurativa

57
Q

treatment of hidradenitis suppurativa

A
  • topical clindamycin
  • intralesional corticosteroids
  • systemic abx: doxycycline
  • surgery