Chapter 19 Flashcards

1
Q

what is the histology of psoriasis?

A

Histology (Fig. 19.2B) shows
1. Acanthosis (epidermal hyperplasia)
2. Parakeratosis (hyperkeratosis with retention of keratinocyte nuclei in the
stratum corneum)
3. Collections of neutrophils in the stratum corneum (Munro microabscesses)
4. Thinning of the epidermis above elongated dermal papillae; results in bleeding
when scale is picked off (Auspitz sign)

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2
Q

what is the histology of lichen planus?

A

Histology shows inflammation of the dermal-epidermal junction with a ‘saw-tooth’ appearance (Fig. 19.3B).

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3
Q

what is lichen planus associated with?

A

C. Etiology is unknown; associated with chronic hepatitis C virus infection

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4
Q

what exactly is the antibody against in pemphigus vulgaris?

A

Autoimmune destruction of desmosomes between keratinocytes

Due to IgG antibody against desmoglein (type II hypersensitivity)

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5
Q

what exactly is the antibody against bullous pemphigoid?

A

Due to IgG antibody against basement membrane collagen

C. Presents as blisters of the skin (Fig. l9.5A); oral mucosa is spared.

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6
Q

what is the basic definition of erythema multiforme?

A
  • a skin DO that is a hypersensitivity reaction to INFECTIONS
  • sometimes drugs can do it
  • HERPES is most common trigger
  • mycoplasma also associated
  • type IV rxn
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7
Q

what is the morphology of erythema multiforme?

A

Multiple lesion types (multiforme)
• Macules, papules, vesicles
• Lesions similar for one patient • May differ between patients
• Hallmark: “Target lesion” • Dark/dusky central area

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8
Q

2 things acanthosis nigricans is associated with

A

Associated with insulin resistance (e.g., non-insulin-dependent diabetes) or malignancy (especially gastric carcinoma)

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9
Q

histology of basal cell carcinoma

A

Classic location is the upper lip.
Histology shows nodules of basal cells with peripheral palisading (Fig. 19.10B).
Treatment is surgical excision; metastasis is rare.

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10
Q

what are the weird risk factors for squamous cell carcinoma?

A

Risk factors stem from UVB-induced DNA damage and include prolonged exposure to sunlight, albinism, and xeroderma pigmentosum.

l. Additional risk factors include immunosuppressive therapy, arsenic exposure, and chronic inflammation (e.g., scar from burn or draining sinus tract).

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11
Q

what is vitiligo due to?

A

Due to autoimmune destruction of melanocytes

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12
Q

what are freckles due to?

A

Due to increased number of melanosomes (melanocytes are not increased)

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13
Q

what are the types of acquired nevi?

A

Acquired nevus arises later in life.

  1. Begins as nests of melanocytes at the dermal-epidermal junction (junctional nevus); most common mole in children
  2. Grows by extension into the dermis (compound nevus)
  3. Junctional component is eventually lost resulting in an intradermal nevus, which is the most common mole in adults.
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14
Q

what are the variants of melanoma?

A

Variants include

  1. Superficial spreading-most common subtype; dominant early radial growth- results in good prognosis.
  2. Lentigo malignant melanoma-lentiginous proliferation (radial growth); good prognosis
  3. Nodular- early vertical growth; poor prognosis
  4. Acral lentiginous- arises on the palms or soles, often in dark-skinned individuals; not related to UV light exposure
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15
Q

what is impetigo??

A

Superficial bacterial skin infection, most often due to S aureus or S pyogenes
B. Commonly affects children
C. Presents as erythematous macules that progress to pustules, usually on the face;
rupture of pustules results in erosions and dry, crusted, honey-colored serum.

WHY some impetigo is bullus and some are not? desmoglein cleavage!!

this same strain that makes the exfoliative toxin can also in some cases result in SSS (SSS becomes diffuse)

THESE ARE NOT DIFFUSE AND OCCUR IN CHILDREN

THE OTHER BLISTERING DISEASES DONT DO THAT

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16
Q

how is staph scaled skin syndrome distinguished from TEN?

A

SSS- destruction at the granulosum level
Distinguished histologically from toxic epidermal necrolysis by level of skin separation; separation in TEN occurs at the dermal-epidermal junction.

17
Q

histology of molluscum contagiosum

A
affected keratinocytes show
cytoplasmic inclusions (molluscum bodies, Fig. 19.15)
18
Q

erysipelas is an infection of the

A

superficial dermis

19
Q

cellulitis is an infection of the

A

deep dermis