Final - Derm Flashcards

1
Q

Oculocutaneous Albinism (OCA)

A

Inherited disorder - melanocytes present, melanin production inadequate. Most of 4 main genotypes are autosomal recessive.

50% “type II” has loss of function in P gene (pink-eyed), 40% “type I” decreased tyrosinase activity.

Ocular involvement -> nystagmus, strabismus, and loss of visual acuity.

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2
Q

Acne Vulgaris

A

Involves sebaceous glands & hair follicles.

Non-inflammatory type has comedones.

  • Open comedones are follicular papules with central keratin plug that has oxidized.
  • Closed comedones follicular papules w/keratin plug trapped beneath epithelial surface.

Inflammatory acne has erythematous papules, nodules, and pustules.

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3
Q

4 Pathogenic components of Acne Vulgaris

A

Keratin plugging - blocks outflow of sebum due to changes of the infundibulum of the follicle

Hypertrophy - of the sebaceous glands, often result of hormonal stimulation

Colonization - of follicle by lipase-synthesizing bacteria *Propionibacterium acnes

Inflammation - of the follicle due to breakdown of the sebum into pro-inflammatory fatty acids.

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4
Q

Acne Rosacea

A

Cutaneous inflammation of the nose and malar aspects of the face

  • flushing episodes
  • telangiectasia & persistent erythema
  • papule & pusture formation
  • rhinophyma (permanent thickening of the nasal skin.

*Different amount & type of cathelicidin -> inappropriate activation of immune response, alternative processing of serene proteases

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5
Q

Cathelicidin in Acne Rosacea

A
  • Initially expressed as a pro peptide that requires proteolytic processing to generate biologically active LL-37 peptide.
  • Stratum corneum tryptic enzyme mediates this in the skin.
  • LL-37 contributes to effective innate immunity -> bactericidal, chemotactic, antiogenic biological activities
  • Expression of cathelicidin and SCTE (its proteolytic processing enzyme) increased in Acne Rosacea
  • Increased expression of the biologically active LL-37 & several unusual isoforms in rosacea lesions.
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6
Q

Folliculitis

A
  • Bacterial infection of hair follicles, usually Staph aureus*. (hot-tub folliculitis from inadequate disinfection)
  • Infected hairs typically fall out
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7
Q

Cellulitis/Erysipelas/Abscess

A

Acute bacterial infxn of skin & subq tissue. *Usually S. aureus or GABHS.

  • Pain & rapidly spreading erythema & edema
  • Strep enzymes (streptokinase, hyaluronidase, DNAase) lead to faster spreading
  • Fever, regional lymph node enlargement & lymphangitis (lymphatic dissemination, “blood poisoning” are possible)
  • Erysipelas is a superficial cellulitis w/involvement of the dermal lymphatics.
  • Occurs most frequently on face and legs.
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8
Q

Furucles (boils)

A
  • Tender nodules from cutaneous infection with S. aureus.

- Nodules are more superficial and generally smaller than abscesses.

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9
Q

Carbuncles

A
  • Collections of furuncles connected by subcutaneous tracts.
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10
Q

Impetigo/Ecthyma

A
  • Superficial skin infection by Strep of Staph
  • Vessicle/ bullae formation characteristic. Fluid weeps or erupts, then crusts **Honey Crusted Lesions*
  • Exfoliative bullous lesions caused by staph toxin
  • Ecthyma is an ulcerative form of impetigo
  • Chronic nasal discharge, moist environment, poor hygiene are risk factors.
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11
Q

Erythema Marginatum

A
    • Cutaneous manifestation of acute rheumatic fever*
  • Post-infectious, immune-mediated complication of GABHS pharyngitis
  • Lesions sharply demarcated areas of eythema w/central inclusion of normal-appearing integument.
  • Lesions move rapidly across the skin in minutes to hours
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12
Q

Erythema Migrans

A
  • Cutaneous manifestation of Borrelia burgdorferi! Lyme dz!
  • Vector is Ixodes scapularis - deer tick
  • EM is best clinical indicator of infection & first sign of the dz, occurs in 75% of infected.
  • Red macule of papule occurs 3-32 days after initial bite. Area expands, maybe central clearing
  • ~ 1/2 of pts develop multiple smaller lesions w/indurated centers. Cultured biopsies show spirochete, representing dissemination of the dz.
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13
Q

Molluscum Contagiosum

A
  • Poxvirus skin infection. Largest pathogenic poxvirus in humans. Spread by direct contact
  • Multiple firm, pink/purple/skin-colored papules w/umbilicated centers & a waxy core
  • “Molluscum bodies” are ellipsoid cytoplasmic inclusions seen on Giemsa stain of the exudate.
  • Inclusions occur in the stratum granulosum & stratum corneum
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14
Q

Verrucae/Warts

A

Skin lesions caused by HPV

  • transmission by direct contact.
  • spontaneous regression in 6-24 mos.

4 types
-Verruca vulgaris: most common type, typically on hands, 1cm papules w/rough, pebble-like verucoid surface.
-Verruca plana: flat warts occur on palmar surfaces & face, slightly elevated & smaller than the vulgarism.
-Verruca plantaris & palmaris: occur on soles & palms, scaly, 1-2cm, rough callus-like texture.
Condyloma acuminatum - venereal warts, HPV 6 & 11, on genitals, perigenital areas, perineum & anus. Soft, cauliflower or cocks-comb excresences.

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15
Q

Histology of Warts

A

Epidermal hyperplasia
- Papillomatous epidermal hyperplasia, often with undulant character
Koilocytosis
-*cytoplasmic vacuolization of more superficial cell layers creating pale halos around the nuclei
- prominent kerato-hyaline granules

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16
Q

3 Organisms that cause Rash specifically on Palms & Soles

A

“You drive CARS with your palms & soles”

  • CA= Coxsackievirus A (hand, foot, & mouth dz)
  • R= Rickettsia Rickettsii (rocky mountain spotted fever)
  • S= Syphilis (secondary)

Note - staph aureus & strep progenies can also , and Kawasaki’s does too.