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Benign epidermal neoplasms Flashcards

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Dermatology Board Prep flashcards
1
Q

What is the underlying pathogenesis of solar lentigines

A

Epidermal hyperplasia
Variable proliferation of melanocytes
Accumulation of melanin within keratinocytes in response to chronic exposure to UVR

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2
Q

What somatic mutations have been identified in solar lentigines

A

FGFR3

PIK3CA

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3
Q

What somatic mutations have been identified in PUVA lentigines

A

BRAF

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4
Q

What mutations have been identified in seb ks

A

FGFR3 and PIK3CA

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5
Q

Mutations in lichenoid keratosis

A

FGFR3, PI3KCA

HRA >KRAS

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6
Q

Mutation in dermatosis papulosa nigra

A

FGFR3

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7
Q

Mutation in stucco keratosis

A

PIK3CA

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8
Q

Mutation in epidermal naevi

A

FGFR3, PIK3CA

HRA > NRAS > KRAS

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9
Q

Mutation in acneiform naevus with hypopigmented background skin

A

FGFR2

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10
Q

Mutation in naevus comedonicus

A

NEK9

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11
Q

Dermoscopy of solar lentigo

A

Diffuse light brown structureless area
Sharply demarcated and/or moth eaten borders
fingerprting
reticular pattern with thin lines that are occasionally short and interrupted

Variant: ink spot lentigo - striking jet black colour and a stellate outline, black branching pattern

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12
Q

How are PUVA lentigines clinically, pathologically and genetically different

A

Darker brown
Stellate appearance
On histo: lentiginous hyperplasia of large melanocytes, mild cytologic atypia
Often contain BRAF mutations

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13
Q

Solar lentigines pathology

A

Rete ridges: club shaped or bud like extensions
Increased basal layer pigmentation
Melanocytes may be slightly increased in number
DOPA-stained: increased melanogenesis, these cells have more numerous as well as longer and thicker dendritic processes than the melanocytes of normal skin
Superficial dermis: melanophages, occasionally mild peri-vascular lymphocytic infiltrate
Solar elastosis

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14
Q

Pathogenesis of seb ks

A

Some genetic (Caucasians)
Sun exposure - link to solar lentigines
Genes: FGFR3 and PIK3CA

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15
Q

Pathogenesis of irritated seb ks

A

Apoptosis within areas of squamous differentation
HPV not really a culprit
Rarely from bacterial infection

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16
Q

What are some features that help differentiate seb ks from melanocytic neoplasms

A

Keratotic plugging (although you can see in some compound and intradermal melanocytic naevi)
Stuck on appearance
Overlying scale

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17
Q

Conditions associated with abrupt seb k eruption and regression

A

Pregnancy
Coexisting inflammatory dermatoses
Malignancy: Leser Trelat

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18
Q

What cancers can arise in seb ks, and which is most common

A

Most common: BCC

Others: SCC, bowens, cutaneous melanoma, KA

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19
Q

What is Leser Trelat associated with?

A

Malignancy: particularly gastric, colonic adenocarcinoma, breast carcinoma, lymphoma
Can occur before, during or after
40% have associated pruirtus
Majority on back, followed by extremities, face and abdomen
20% have malignancy acanthosis nigricans (may appear at the same time or shortly after the sign of Leser Trelat)

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20
Q

What is the pathogenesis of Leser Trelat?

A

Thought to be related to secretion of growth factor by the neplasm which leads to epithelial hyperplasia

It has been hotly contested given so many people > age have got seb ks

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21
Q

Histologic types of seb ks

A
  1. Acanthotic (most common)
  2. Hyperkeratotic
  3. Reticulated
  4. Irritated
  5. Clonal
  6. Melanoacanthoma

(CHAIRM)

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22
Q

Basic seb k histology

A

Varying degrees of hyperkeratosis, acanthosis and papillomatosis

Key features:

  1. Horn pseudocysts: cross-sectioned epidermal invaginations
  2. Acanthosis: result of an accumulation of benign squamous and basaloid keratinocytes - typically projecting outward and upward in an irregular fashion
  3. String sign: sharp demarcation at the base of most lesions
  4. Church spires: papillomatosis and hyperkeratosis
  5. No dermal involvement

Some contain basaloid cells over squamous - smaller, uniform appearance, large oval-shaped nuclei
No atypia

23
Q

Inflamed seb k histology

A

Mild keratinocyte atypia

Mitotic figures

24
Q

Acanthotic seb k histology

A

Smooth surfaced, dome shaped papule
Slight hyperkeratosis and papillomatosis
Thickened epidermis with ++ basaloid cells
Invaginated horn pseudocysts are most prevalent in this variant
Melanin increased - primarily concentrated in keratinocytes and is transferred from neighbouring melanocytes

25
Q

Hyperkeratotic seb k histology

A

Prominent hyperkeratosis and papillomatosis - ‘church spires’
Squamous cells&raquo_space; basaloid cells
Not much pigment
Less pseudocysts

26
Q

Reticulated or adenoid seb k histology

A

Delicate strands of epithelium that extend from the epidermis in an interlacing pattern
Double row or more of basaloid cells that may be hyperpigmented
Horn pseudocysts may be present
Solar lentigo often seen at lateral margins

27
Q

Irritated seb k histology

A

Lymphoid infiltrate - can be perivascular, diffuse or licehnoid
Spongiosis
Keratinocyte necrosis
Squamous eddies are common - whorls of eosinophilic keratinocytes
Often lack the sharply demarcated horizontal base seen with most seb ks

28
Q

Clonal seb k histology (aka nested)

A

Well defined nests of loosely packed cells within the epithelium
Nests are composed of variably sized kerastinocytes that are paler than adjacent cells and have a uniform appearance
May also contain melanocytes
Can have Borst-Jadassohn phenomenon: intraepidermal epithelioma - you see this with eccrine poroma and other intraepidermal sweat glands, Bowens

29
Q

Melanoacanthoma seb k histology

A

Seb k that mimics MIS

Negative for Melan-A/MART-1 and S100

30
Q

What conditions are thought to be variants of seb ks

A

DPN
Stucco keratosis
Inverted follicular keratoses

31
Q

Can solar lentigines become seb ks

A

Yes: over time the buds of pigmented basaloid cells become thicker and there is greater acanthosis

32
Q

What is a melanoacanthoma?

A

Heavily pigmented: keratincoytes contain the nulk of pigment (have long dendrites), and there are melanocytes distributed throughout the lesion
The heavy pigmentation is explained by the blockage of transfer of melanin to keratinocytes - resulting in an increase in the amount of melanin within melanocytes
Different to a seb k, is a ddx for melanoacanthoma seb k
Histo: minimal epidermal hyperplasia, look more like a heavily pigmented lentigo simplex with a proliferation of dendritic melanocytes within the basal layer of the epithelium

33
Q

Seb k ddx

A
  1. The variants: DPN, stucco keratosis, inverted follicular keratoses
  2. Other benign epidermal and melanocytic neoplasms:
    - solar lentigo
    - acrochordon
    - melanocytic naevus
    - tumour of the follicular infundibulum - superficial distinct plate-like epithelial proliferation - multiple slender epidermal connections composed of basaloid or pale cells
    - eccrine poroma (for acanthotic and iritated –> poromas are homogenous, small basophilic cells with delicate fibrovascular stroma and narrow ductal lumina with eosinophilic, PAS-positive, diastase resistant cuticles)
    - melanoacanthoma
    - AN
    - epidermal naevus
    - CARP
    - acrokeratosis verruciformis of Hopf
    - acanthoma fissuratum (epidermal hyperplasia due to friction)
  3. Malignancies:
    - Bowen disease (can have Borst Jadassohn phenomenon)
    - SCC
    - melanoma (particulary verrucous)
  4. Infectious:
    - verruca vulgaris
    - condyloma accuminatum
34
Q

Seb k rx

A 
LN2
C&C/shave
Electrodessication
Laser: Erb:Yag
AKT inhibitors - possible future topical therapy
35
Q

Pathogenesis of lichenoid keratosis

A

Inflammation of solar lentigo, ak or seb k

Lichenoid infiltrate of lymphocytes secondary to a stimulus from an unidentified epidermal antigen

36
Q

Common site for lichenoid keratosis

A

Forearm and upper chest, less frequent occurrence on shins and other chronically sun exposed sites

37
Q

Lichenoid keratosis dermoscopy

A

Light brown pseudonetworks due to residual solar lentigo
Overlapping pinkish areas due to lichenoid inflammation
Annular granular structures and gray pseudonetworks in the early regressing stage
White blue-gray fine dots can be seen in the late regressing stage
Blue-gray dots or globules - representing melanophages - are also considered typical of an LK

38
Q

Lichenoid keratosis pathology

A
  1. Lichenoid change: lymphocytes with scattered histiocytes, +/- eos and plasma cells, full interface dermatitis - basal vacuolar alteration, melanin incontinence, colloid bodies (if ++ melanin incontinence can be called pigmented LK)
  2. Epidermal changes: can have parakeratosis, can have frank separation of epidermis from the infiltrate in the dermis –> sub-epidermal cleft or blister cavity
  3. Changes of solar lentigo or macular seb k present at periphery of specimen
  4. Regression - can undergo, loosely fibrotic papillary dermis with scattered lymphocytes and melanophages. Can be confused for a melanoma, but a regressed melanoma will have a dense band of melanophages with lymphocytes and dilated blood vessels, with thin epidermis
  5. Mimicks MF (Pautrier like microabscesses, alignment of lymphocytes along the basal layer, epidermotropism) and lupus (atrophic variant)
39
Q

Naevus comedonicus epidemiology

A

Half present at birth
Others appear in childhood, usually before age 10
Adulthood is rare and associated with irritation or trauma

40
Q

What is the underlying pathogenesis of naevus comedonicus

A

Growth dysregulation affecting the mesodermal portion of the pilosebaceous unit
NEK9 (NIMA related kinase 9 gene) has been identified as mosaic activating mutation

41
Q

How is a Munro acne naevus different to naevus comedonicus

A

Has FGFR2 mutation - has pre-existing linear hypopigmentation, peripubertal onset of acne, and histo shows an atrophic comedonal wall with prominent associated sebaceous lobules

42
Q

Can you get a skin cancer in naevus comedonicus

A

Yes very rare reports of SCC or KA

43
Q

Where is naevus comedonicus distributed

A

Face most commonly, then trunk, neck, upper extremity
Can also occur on palms, soles, glans penis
Elbows and knees: can be verrucous in appearance

Worsens with hormones

44
Q

What is familial dyskeratotic comedones

A

Rare autosomal dominant disorder in which comedones arise during childhood or adolescece
Widely scattered to trunk and extremities
No linear configuration

45
Q

Ddx for naevus comedonicus

A 
Infantile acne
Chloracne
Familial dyskeratotic comedones
Dilated pore naevus
Porokeratotic eccrine ostial and dermal duct naevi
46
Q

CARP associations

A 
Obesity
Menstrual irregularities
DM
Pituitary disorders
Thyroid disorders
47
Q

CARP pathogenesis postulations

A
  1. ?Malassezia furfur response
  2. ?Insulin resistance
  3. Keratinization disorder
48
Q

CARP pathology

A

Hyperkeratosis
Acanthosis
Papillomatosis
Sparse, superficial perivascular infiltrates of lymphocytes
‘Dirty feet’: club-shaped, bulbous epidermal rete ridges that protrude slightly into the papillary dermis with pigment at their bases

49
Q

CARP ddx

A

AN
Tinea versicolor
Darier
Retention hyperkeratosis

Histo: seb k, epidermal naevus, AN, papillomatous epithelial proliferation

50
Q

Clear cell papulosis epidermiology

A

Chinese and other Asian children

51
Q

Where does clear cell papulosis appear

A

Milk lines (mammary ridge)

52
Q

Clear cell papulosis pathogenesis

A

? benign extra mammary Paget disease

Clear cells in lesional skin suggests histogenic relationship with Toker cells

53
Q

Clear cell papulosis clinical

A

Multiple white macules or papules 2-10 mm in diameter that favour the anterior chest, abdomen and lumbar region, and milk lines
Rarely the face

54
Q

Clear cell papulosis histology

A

Mild acanthosis
Slightly disorganized arrangement of epidermal keratinocytes
Numerous clear cells scattered primarily along the basal layer of the epidermis but also within its upper layers
Cells have ++ mucin in their cytoplasm
Stain with PAS, ALcian blue, mucicarmine, colloidal iron

Immunohistochemistry: clear cells express CEA, cytokeratins: CK7, AE1/3, CAM5.2, EMA, gross cystic disease fluid protein
Negative for CD1a, S100 and HMB45

Histologically looks like Paget disease

Derm (57 decks)

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