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YEAR 5: Histopathology > Histo: Skin Pathology > Flashcards

Histo: Skin Pathology Flashcards

1
Q

How thick is a normal epidermis, dermis and subcutaneous fat put together?

A

6 mm

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2
Q

What types of fibres are found in the layer underneath the epidermis?

A

Collagen

Elastic fibres

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3
Q

What structures are found within the dermis?

A
  • Blood vessels
  • Sweat glands
  • Hair follicles
  • Sebaceous glands
  • Nerve fibres

these are embedded in collagen matrix

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4
Q

How is palmar-plantar skin different from skin in other parts of the body?

A

There are no sebaceous glands

There is a very thick corneal layer

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5
Q

Describe the effects of ageing on the skin.

A

Skin becomes fragile with very little epidermis

Collagen and elastic fibres are of poor quality

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6
Q

List some different types of inflammatory reaction patterns in the skin.

A
  • Vesiculobullous - forms bullae
  • Spongiotic - becomes oedematous
  • Psoriasiform - becomes thickened
  • Lichenoid - forms a sheeny plaque
  • Vasculitic - associated with vasculitis
  • Granulomatous - associated with granulomas

first 4 occur in epidermis

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7
Q

What is bullous pemphigoid? Describe the macroscopic appearance.

A
  • Vesiculobullous condition
  • Occurs in elderly patients on their flexor surfaces
  • Characterised by the formation of large tense bullae

NOTE: it has a 10-20% mortality

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8
Q

Outline the pathophysiology of bullous pemphigoid.

A
  • Autoimmune disorder driven by IgG and C3 which attack the hemidesmosomes of the basement membrane (specifically BPAg1 and 2)

Hemidesmosomes = specialised structures in epithelial cells that anchor the cells to the underlying basement membrane

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9
Q

How can bullous pemphigoid be definitively diagnosed?

A

Skin biopsy

Immunofluoresence shows IgG and C3 deposition along the dermo-epidermal junction

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10
Q

Describe the macroscopic appearance of pemphigus vulgaris.

A

Blisters are smaller and flaccid meaning that they rupture easily exposing a red raw surface underneath

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11
Q

Outline the pathophysiology of pemphigus vulgaris.

A

IgG-mediated autoimmune disease against desmosomes within the epidermis
(specifically desmoglein 3 and sometimes desmoglein 1)

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12
Q

What is acantholysis?

A
  • Loss of intercellular connections leading to loss of cohesion between keratinocytes

NOTE: this can occur due to a lot of dermatological conditions so immunofluorescence is needed to identify where the immune-mediated attack is taking place

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13
Q

Describe the macroscopic appearance of pemphigus foliaceus.

A
  • You rarely see intact bullae because they are so thin and fragile
  • You are likely to see some flaky remnants of old bullae
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14
Q

Outline the pathophysiology of pemphigus foliaceus.

A

IgG-mediated attack against desmoglein 1 on the outer layer of keratinocytes
(where the stratum corneum is found)

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15
Q

Describe the appearance of discoid eczema.

A
  • Very itchy
  • flexural surfaces
  • discoid plaques
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16
Q

Describe the clinical presentation of contact dermatitis.

A
  • Itchy erythematous rash usually on the hands or feet (areas most commonly exposed to irritants)
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17
Q

What is hyperkeratosis? What is parakeratosis?

A
  • In hyperkeratosis, stratum corneum of the epidermis thickens
  • In parakeratosis, the superficial cells of the epidermis retain their nuclei
18
Q

What type of inflammatory skin reaction is eczema?

A

Spongiotic because there is oedema between the keratinocytes

19
Q

What are the main immune mediators in eczema?

A
  • T cell mediated
  • Eosinophils are also recruited

NOTE: this pattern is also seen in drug reactions

20
Q

Describe the typical presentation of plaque psoriasis.

A
  • This is a psoriasiform reaction pattern
  • Tends to present as silvery plaques on the extensor surfaces
21
Q

How is the keratinocyte turnover time different in psoriasis compared to normal skin?

A
  • Normal skin turnover = 50 days (time for keratinocyte to go from the bottom of the epidermis to the top)
  • Psoriasis = 7 days
  • This leads to thickening of the epidermis and you get a layer of parakeratosis at the top
22
Q

Which layer of the epidermis disappears in plaque psoriasis and why?

A

Statum granulosum - there is not enough time to form it

23
Q

What can neutrophil recruitment to the epidermis in plaque psoriasis cause?

A

Formation of Munro’s microabscesses - cardinal of sign of psorasis (seen within the stratum corneum)

24
Q

What is lichen planus and what are its main features?

A

Lichenoid reaction pattern

  • T-cell mediated
  • Presents with purple papules and plaques on the wrists and arms
  • In the mouth it presents as white lines (Wickham striae)
25
Q

Describe the histological appearance of lichen planus.

A
  • There is band-like lymphocytic infiltration just under the epidermis
  • Distinction between dermis and epidermis is difficult to see due to lymphocyte-mediated destruction of the bottom layer of keratinocytes

NOTE: this is also seen in mycosis fungoides

26
Q

What type of inflammatory skin reaction results in pyoderma gangrenosum?

A

Vasculitic

27
Q

Describe the classic macroscopic appearance of seborrhoeic keratosis.

A

‘Stuck on’ appearance

Waxy, raised, pigmented lesion

28
Q

Which histological feature is classic of seborrhoeic keratosis?

A

Horn cysts - entrapped keratin surrounded by proliferating epidermis

NOTE: the epidermis is proliferating in an ordlerly manner

29
Q

Describe the appearance of sebaceous/epidermal cyst.

A
  • Smooth surface
  • Non-mobile
  • Tend to have a punctum
  • Can get infected/rupture
  • Can smell really bad
30
Q

Describe the histological appearance of a sebaceous cyst.

A
  • Looks like the surface has become invaginated to form a cyst
  • Lined by squamous epithelium
31
Q

Describe the macroscopic appearance of a basal cell carcinoma.

A

Rolled, pearly edge with a central ulcer and telangiectasia

32
Q

Describe the histological appearnace of a basal cell carcinoma.

A
  • Cancer arises from the keratinocytes along the bottom of the epidermis (basal cells)
  • They can infiltrate through the basement membrane
  • They are locally infiltrative but don’t metastasise
  • Basaloid
  • Clefting
  • Peripheral palisading
33
Q

What is Bowen’s disease?

A

Squamous cell carcinoma in situ

SCCs can locally invade (more aggressive than BCCs) and can metastasise

34
Q

Describe the macroscopic and histological appearance of a benign junctional naevus (mole).

A
  • They are circumscribed and uniformly pigmented
  • Melanocytes expand in their normal position to form nests of melanocytes on the basal layer
35
Q

Describe the normal migration of melanocytes as they mature.

A

As they mature they become smaller and go deeper

36
Q

What are some clinical signs suggestive of a malignant melanoma?

A
  • Assymetry
  • Border irregularity
  • Colours
  • Diameter (>6 mm)
  • Evolution
37
Q

Describe the histological appearance of malignant melanoma.

A
  • Melanocytes start migrating upwards through the epidermis (pagetoid spread)
  • Proliferation of melanocytes with cytological atypia
  • They become active and lose the ability to differentiate
  • Melanoma thickness > 4 mm has a > 50% mortality
38
Q

Actinic keratosis histology?

A

Type of dysplastic condition

  • atypia of epidermis (basal)
  • abnormal stratum corneum parakeratosis
39
Q

Bowen’s disease histology?

A
  • full thickness atypia (dysplasia)
  • basement membrane intact
  • increased mitotic activity
40
Q

Squamous Cell Carcinoma histology?

A
  • Pleomorphic (irregular) squamous epithelial cells arising from epidermis + extending into dermis
  • Central keratinisation surrounded by concentric layers of abnormal squamous cells (KERATIN PEARL)
  • Tumour often pink
41
Q

Main prognostic factors for melanoma?

A
  • breslow thickness (histological)
  • ulceration (+/-)
42
Q

How is Breslow thickness measured?

A

from stratum granulosum to deepest melanoma cell

used for staging

YEAR 5: Histopathology (33 decks)

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