Epidermal & Dermal Response to Injury Flashcards

(48 cards)

1
Q

why should a gross description of a lesion be submitted with a biopsy

A

skin biopsies are small (usually 6 mm punch biopsies)

requires adequate description of the gross appearance to achieve a final diagnosis

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2
Q

what are the two main steps of describing dermatologic lesions

A
  1. patterns - cell arrangement
  2. subcategories
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3
Q

what are the subcategories to describe patterns

A
  • character of cell infiltrate
  • superficial vs deep
  • primary spongiosis
  • necrotizing
  • ulcerative
  • hyperplastic
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4
Q

perivascular dermatitis

A

inflammation surrounding the vessels of the dermis

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5
Q

how common and how diagnostic is perivascular dermatitis

A

very common - ALL dermatitis starts as perivascular because cells extravasate from vessels

LEAST diagnostic pattern

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6
Q

what epidermal changes are seen in perivascular dermatitis

A
  • pruritus
  • inflammation
  • scratching/licking
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7
Q

acute histologic lesions of perivascular dermatitis

A
  • spongiosis
  • parakeratosis
  • hypogranulosis
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8
Q

chronic histologic lesions of perivascular dermatitis

A
  • compact hyperkeratosis
  • hypergranulosis
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9
Q

what does the depth of perivascular dermatitis tell you

A

superficial only: indicates an outside –> in process

superficial + deep: indicates an inside –> out process

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10
Q

what does type of cell infiltrate tell you about perivascular dermatitis

A

chronicity

cell type changes over time

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11
Q

what are specific features associated with perivascular dermatitis

A
  • keratinocyte swelling (intracellular edema)
  • diffuse superficial epidermal lysis
  • diffuse parakeratosis
  • keratinocyte apoptosis
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12
Q

what disease process is most consistent with keratinocyte swelling

A

viral infection

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13
Q

what disease process is most consistent with parakeratosis

A

metabolic process

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14
Q

cytotoxic interface dermatitis

A

single cell necrosis or apoptosis of keratinocytes

causes keratinocytes to become VACUOLATED

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15
Q

what are etiologies for cytotoxic interface dermatitis

A
  • autoimmune
  • immune-mediated
  • viral
  • ischemic
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16
Q

cell-rich interface

A

lichenoid inflammation associated with single cell necrosis
- subepidermal band of inflammatory cells

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17
Q

cell-poor interface

A

minimal to mild perivascular inflammation

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18
Q

pigmentary incontinence

A

damage to keratinocytes leading to “drop out” of melanin that gets phagocytized by dermal macrophages

causes leukoderma and leukotrichia

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19
Q

subepidermal clefting

A

basal cell damage leading to BMZ failure and dermal-epidermal separation

causes ulceration

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20
Q

vasculitis

A

inflammation of the blood vessels (arteries, veins, small vessels)

21
Q

what causes vasculitis

A

infectious
immune mediated

22
Q

signs of acute vasculitis

A

erythema
ecchymosis
hemorrhagic macules
palpable purpura
superficial ulcers
necrosis
no blanching on diascopy

23
Q

diascopy

A

pressing a glass slide against redness to determine if true color change or vasodilation

24
Q

histology of vasculitis

A

inflammatory cells migrating through vessel wall with NECROSIS of the wall

target of cell attack is the vascular wall

25
cell rich vasculitis
intact and degenerate inflammatory cells within wall various degrees of degenerative change
26
cell poor vasculitis
degenerative changes of the vascular walls lack of inflammation
27
intraepidermal vesicular/pustular dermatitis
accumulation of fluid (vesicles) or fluid + inflammatory cells (pustules) within the epidermal layer
28
what do vesicles and pustules turn into
rupture to form erosions and crusting
29
erosions
loss of the epidermis with intact basal cell layer
30
crusts
degenerated cells + serum + WBCs, RBCs
31
what lesions would you want to sample the edge for biopsy
vesicles/pustules erosions/ulcers
32
subepidermal vesicular/pustular dermatitis
accumulation of fluid or fluid + inflammatory cells below the epidermis (in BMZ)
33
what lesion occurs from sub epidermal dermatitis
ulceration due to splitting at the BMZ
34
what can lead to subepidermal dermatitis as a secondary lesion
1. cytotoxic interface dermatitis 2. neutrophilic inflammation 3. hypoxia 4. steroid drugs
35
folliculitis
inflammation of the hair follicle
36
perifolliculitis
perifollicular perivascular/nodular dermatitis
37
furunculosis
ruptured hair follicle leading to free keratin and hair shaft in the dermis elicits an immune response to foreign body in dermis
38
perforating folliculitis
superficial rupture of hair follicles
39
luminal folliculitis
inflammatory cells that cross the follicular epithelium and accumulate in the lumen of the follicle
40
what causes luminal folliculitis
infectious (bacterial, fungi, demodex, pelodera)
41
mural folliculitis
inflammatory cells migrate into the follicular epithelium (NOT the lumen)
42
what causes mural folliculitis
infectious auto-immune immune-mediated
43
bulbitis
inflammation of the hair bulb and deep hair follicle leads to alopecia with no other superficial lesions due to no hair follicle
44
what causes bulbitis
autoimmune
45
nodular to diffuse dermatitis
inflammation of the dermis in nodular aggregates or generalized/diffuse distribution
46
what causes nodular/diffuse dermatitis
neoplasia vs inflammatory (infectious vs noninfectious)
47
panniculitis
inflammation of the subcutis that occurs as an extension of dermatitis (dermal inflammation)
48
what causes panniculitis
infectious metabolic immune mediated idiopathic