YEAR 5: Histopathology PM (COPY) > Histo: Skin Pathology > Flashcards

Histo: Skin Pathology Flashcards

(42 cards)

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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?

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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?

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A

Spongiotic because there is oedema between the keratinocytes

19
Q

What are the main immune mediators in eczema?

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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.

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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?

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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?

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A

Statum granulosum - there is not enough time to form it

23
Q

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

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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?

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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
Describe the histological appearance of lichen planus.
* 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
What type of inflammatory skin reaction results in pyoderma gangrenosum?
Vasculitic
27
Describe the classic macroscopic appearance of seborrhoeic keratosis.
'Stuck on' appearance *Waxy, raised, pigmented lesion*
28
Which histological feature is classic of seborrhoeic keratosis?
**Horn cysts** - entrapped keratin surrounded by proliferating epidermis NOTE: the epidermis is proliferating in an ordlerly manner
29
Describe the appearance of sebaceous/epidermal cyst.
* Smooth surface * Non-mobile * Tend to have a punctum * Can get infected/rupture * Can smell really bad
30
Describe the histological appearance of a sebaceous cyst.
* Looks like the surface has become **invaginated** to form a cyst * Lined by **squamous epithelium**
31
Describe the macroscopic appearance of a basal cell carcinoma.
Rolled, pearly edge with a central ulcer and telangiectasia
32
Describe the histological appearnace of a basal cell carcinoma.
* 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
What is Bowen's disease?
Squamous cell carcinoma *in situ* SCCs can locally invade (more aggressive than BCCs) and can metastasise
34
Describe the macroscopic and histological appearance of a benign junctional naevus (mole).
* They are circumscribed and uniformly pigmented * Melanocytes expand in their normal position to form nests of melanocytes on the basal layer
35
Describe the normal migration of melanocytes as they mature.
As they mature they become smaller and go deeper
36
What are some clinical signs suggestive of a malignant melanoma?
* Assymetry * Border irregularity * Colours * Diameter (\>6 mm) * Evolution
37
Describe the histological appearance of malignant melanoma.
* 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
Actinic keratosis histology?
Type of dysplastic condition - **atypia** of epidermis (basal) - abnormal stratum **corneum parakeratosis**
39
Bowen's disease histology?
- full thickness atypia (dysplasia) - basement membrane intact - increased mitotic activity
40
Squamous Cell Carcinoma histology?
- **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
Main prognostic factors for melanoma?
- breslow thickness (histological) - ulceration (+/-)
42
How is Breslow thickness measured?
from stratum granulosum to deepest melanoma cell used for staging
YEAR 5: Histopathology PM (COPY)
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