Dermatopathology Flashcards

1
Q

everf

Summarise how different layers of the skin pick up stains (H&E)

A

Epiderm stain darker - keratinocytes
Then collagen in basement membrane - also pink
Hypodermis - doesn’t really pick up stain

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2
Q

Describe the layers of the epidermis

A

Made of stratified squamous epithelium
○ Begin life in basal layer - blue - a lot of nuclear material
○ Mature - lose nuclear material - die takes 28-40days

Spinous layer - hook the cells together - stratum spinosum
Granulosum - has granules that are purple
Stratum corneum - water tight barrier - then they are lost at top
Get interspersed melanocytes along the base

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3
Q

Features in the dermis

A

collagen
hair follicles,
nerves,
sebaceous glands

  • everything need for function
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4
Q

What are the major tissue reaction patterns in skin disorders

A

Spongiotic - intraepidermal intracellular oedema

lichenoid - basal cell damage, interface dermatitis

Psoriasiform - regular epidermal hyperplasia

Vesiculobullous - Blistering within or beneath the epidermis

granulomatous - chronic granulomatous inflammation

vasculopathic - pathological changes in cutaneous blood vessels

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5
Q

Which patterns of skin inflammation happen in the epidermis

A

Spongiotic
lichenoid
Psoriasiform
vesiculobullous

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6
Q

What patterns of skin inflammation happen in the dermis

A

Vasculitic
granulomatous

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7
Q

what pattern of skin inflammation happens in the subcutis

A

panniculitis eg erythema nodosum

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8
Q

What is an example of a spongiotic skin reaction

A

Eczema

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9
Q

What is the mechanism of eczema -> spongiotic reaction pattern

A

Lymphyctes in epidermis -> cytokines -> bring fluid in (make look like sponge)
If so much fluid -> vesicles

**Pathological hallmark is oedema **

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10
Q

Example of a lichenoid pattern of inflammation

A

Lichen planus

Erythema multiforme
TEN
SJS

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11
Q

Pathology of lichen planus

A

Papules and plaques, purple hue,
Wickham striae - white on top

Keratinocytes become antigenic
Lymphcytes come between dermis and epidermis - attack epidermal keratinocytes
Keratinocytes lost nuclei - apototic keratinocytes

epidermis can slough off -> become ill

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12
Q

Example of a psoriaform reaction

A

Psoriasis

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13
Q

Pathology of psoriasis

A

Get thickened epidemis
Epidermis rapidly turning over -> thicker

Hallmark - thick epidermis (psoriasiform hyperplasia)
No time for it to lose its nucleus - see the scale.
Cytokine mileu bring in the neutrophils - see neutrophils in the scale

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14
Q

Appearance and ix for psoriasis

A

Looks silvery
Effect extensor surface - elbow and knee

Can treat clinically w/o biopsy

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15
Q

Pathology of vesicobullous reaction pattern

A

Autoimmune
ab attack the epidermis

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16
Q

eg of vesicobullous reaction pattern

A

Bullous pemphigoid

pemphigus

17
Q

Summarise bullous pemphigoid

A

Any age group - common in elderly

Large tense bullae
Itchy

18
Q

Summarise pathology of bullous pemphigoid

A

Epidemal basement membrane - destroyed by IgG ab
**Space form between epidermis and dermis - fill with fluid
Lots of eosinophils **

*Direct immunofluresence - *Link to Ig
Get the IgG Ab attacking the basement membrane zone - see linear deposit of IgG where the membrane should be

19
Q

Pathology of phemphigus

A

Intercellular juntcion between spinous cells are attacked - cant hold together in epidermis

Foliaceous = superfical
vulgaris = deep

Vulgaris (intraepidermal blistering) - ab attack skin and mucous membrane -attack desmoglein 3 found in the intracellular junctions
Can be lethal - because the skin can slough off

Immunofluresnce around the individual cells - chickenwire pattern

20
Q

Clinical features of pemiphigus vulgaris

A
21
Q

Effect of sun damage on skin pathology

A

In superficial dermis - now grey, and disintergrated - dont have smooth collagen fibres - this is SOLAR ELASTOSIS

22
Q

Pathology of sebaceous cyst

A

Squamous cyst
benign skin tumour

23
Q

Pathology of seborrhoeic keratosis

A

In the epidermis

24
Q

Summarise BCC

A

Commonest primary skin cancer
Pearly appearance
Rolled edges
Telangiectasia

Virtually never mets
Locally aggressive
Can recur - so need to excise with good margin

Mutation in PTCH gene
Can have Gorhlin’s syndrome - consider if BCC in young

25
Q

Pathology of BCC

A

Blue tumours
Cleft artefact
Mitotic activity
Peripheral palisading - all cells stand in line

26
Q

What are actinic keratosis

A

precancerous lesion on chronically sun exposed skin

dysplastic lesion can transform to SCC

27
Q

Pathology of actinic keratosis

A
28
Q

Summarise SCC

A

2nd most common skin cancer

Can metastasise - BV, lymph
More aggressive

Irregular keratinous nodule or a firm erythematous plaque
Freq ulcerate

29
Q

What is Bowen’s disease

A

Before SCC get dysplasia

When dysplasia involve full thickness of epidermis, but doesn’t cross basement membrane - bowen’s disease
A lot of mitotic activity- look atypical

30
Q

Pathology of SCC

A

Squamous nest break through basement membrane - and into dermis
Pink
Get aggregates of pink cells
○ Keratin pearls
Increased mitotic activity
Perineural invasion - wrap around nerves and travel far

31
Q

Layer of the skin of benign naevi

A
32
Q

Pathology of benign naevi

A

Small clusters of melanocytes
well spaced
maturation with depth - as you get deeper the melanocytes get smaller and more spindly

33
Q

A-E EFG for malignant melanoma

A
34
Q

Pathology of malignant melanoma

A

Cellular atypia
Asymmetry
Pagetoid spread - Melanocyte ascend to top of epidermis - should be lower.
a lot of mitosis
disorgansied

35
Q

Px indicators for melanoma

A

BRESLOW THICKNESS
○ Histological measurement
○ Main factor that comes into staging melanomas
○ Measured between granular layer to the deepest melanoma cell in the dermis
Ulceration - presence/absence
BRAF V6000E mutations - if patient has this mutation, then you can use it to treat them,