Skin pathology Flashcards

1
Q

Normal skin structure: what are the layers of the epidermis?

A

Come, Let’s Get Some Beers = Stratum corneum, stratum lucidum, stratum granulosum, stratum spinosum, stratum basale

Epidermis, dermis and subcutaneous fat = ~6 mm thickness

Epithelial cells allow body fluids to come out but protects you from the outside

  • As you age, this layer becomes thinner

Underneath this, there is a supportive matrix composed of collagen and elastic fibres

  • Pathological changes can occur here (e.g. Ehlers-Danlos syndrome)
  • As you age, the collagen and elastic fibres become weaker

Dermis = blood vessels, sweat glands, hair follicles, sebaceous glands and nerve fibres

The location of skin is important (i.e. more sebaceous glands on the face)

  • Palmar-plantar skin = no sebaceous glands, very thick corneal layer
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2
Q

What are some inflammatory reaction patterns?

A

Vesiculobullous Spongiotic Psoriasiform

Lichenoid Vasculitic Granulomatous

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3
Q

Bullous pemphigoid (vesiculobullous)

A
  • Elderly, autoimmune, high mortality rate (10-20%)
  • Flexor surfaces, tense bullae
    • Dermo-epidermal junction affected

Pathophysiology:

  • IgG and C3 attack the basement membrane
    • Detected by immunofluorescence
    • IgG anti-hemidesmosome
  • Eosinophils recruited to release elastase
  • Elastase damages the anchoring proteins
  • Fluid fills up gap between BM and epithelium
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4
Q

Pemphigus vulgaris (vesiculobullous)

A

Flaccid blisters, rupture easily

  • Epiderma-epidermal junction affected

Pathophysiology:

  • IgG attacks between the keratin layers (acantholysis)
    • I.E. Loss of intracellular connections
  • Common for many conditions;
  • Need immunofluorescence to confirm
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5
Q

What is acantholysis?

A

Acantholysis refers to the loss of attachments between keratinocytes, resulting in the formation of rounded, detached cells within the blister.

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6
Q

Pemphigus foliaceus (vesiculobullous)

A

Top layer is very thin so never blisters

IgG-mediated – outer layer of stratum corneum shears off

Diagnose with immunofluorescence

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7
Q

Discoid eczema

A
  • Flexor surfaces
  • Very itchy; plaques form
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8
Q

Contact dermatitis

A
  • Itchy (latex, nickel)→ hyperparakeratosis (thickening)
  • Epidermis gets thicker → lichenification
    • Pathophysiology:
      • Epidermis gets thicker
      • Eczema is spongiotic because there is oedema in between the keratinocytes
      • T cell mediated and eosinophils are recruited
      • A differential for an eczematous reaction pattern is a drug reaction
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9
Q

Plaque psoriasis

A
  • Psoriasiform reaction pattern; extensor surfaces
  • Silver plaques (similar to discoid eczema)

Pathophysiology:

  • Normal keratinocyte turnover time = 56 days
  • Psoriasis keratinocyte turnover time = 7 days
  • Rapid turnover → epidermis thicker
  • A layer of parakeratosis forms at the top
  • Stratum granulosum disappears as not enough time to form it; and dilated vessels form
  • Munro’s microabscesses form, made up from recruitment of neutrophils
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10
Q

Lichen planus (lichenoid)

A
  • T-cell mediated; itchy
  • Papules and plaques of purplish-red colour on the wrists and arms
    • In mouth it presents as white lines (Wickham striae)

Pathophysiology:

  • T-lymphocytes have destroyed bottom keratinocytes
  • Creates band-like inflammation

Cannot see where dermis finished, and epidermis starts

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11
Q

Pyoderma gangrenosum

A
  • Vasculitis (not actually gangrenous)
  • Presents as non-healing ulcer
  • Often, first manifestation of a systemic disease
    • E.G. colitis, hepatitis, leukaemia
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12
Q

Seborrhoeic keratosis

A

“Cauliflower”, pigmented, gets caught on clothing (and taken off)

Stuck-on appearance, harmless and benign

Histopathology:

  • Lots of growth and ordered proliferation
  • Ordered and benign growth
  • “Horn cysts” – epidermis entrapping keratin
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13
Q

Sebaceous cyst

A
  • Transluminates, central punctum, circumscribed, hot
  • Squamous cell lining surrounding the cyst
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14
Q

Basal cell carcinoma

A
  • Rolled, pearly-edge, central ulcer, telangiectasia
    • “Rodent ulcer” as it burrows away
    • Benign but can disfigure
    • Occurs in sun-exposed areas

Histopathology:

  • Dysplastic change
  • Cancer from keratinocytes at bottom of epidermis
  • Cannot break through the BM → cannot metastasise
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15
Q

Bowen’s disease

A

Squamous cell carcinoma in situ [i.e. pre-cancerous]

  • Keratinocytes become more pleiomorphic and larger with mitotic figures
  • Bowen’s disease name changes depending on location (i.e. anal vs. cervix)
  • Dysplasia can be 1, 2 or 3 (low, moderate or high grade)
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16
Q

SCC

A
  • Subdivided into level of differentiation:
    • Poorly to well differentiated
    • Poorly differentiated means you cannot determine origin cell lineage
    • Peri-neural invasion can occur (i.e. local invasion)

Squamous cell carcinoma initially appears as a skin-colored or light red nodule, usually with a rough surface. They often resemble warts and sometimes resemble open bruises with raised, crusty edges. The lesions tend to develop slowly and can grow into a large tumor, sometimes with central ulceration.

16
Q

SCC

A
  • Subdivided into level of differentiation:
    • Poorly to well differentiated
    • Poorly differentiated means you cannot determine origin cell lineage
    • Peri-neural invasion can occur (i.e. local invasion)

Squamous cell carcinoma initially appears as a skin-colored or light red nodule, usually with a rough surface. They often resemble warts and sometimes resemble open bruises with raised, crusty edges. The lesions tend to develop slowly and can grow into a large tumor, sometimes with central ulceration.

17
Q

What are cafe-au-lait spots

A
  • a form of melanocytic naevus
  • flat, pigmented spots on the skin.

The most common symptom of NF1

18
Q

What are cafe-au-lait spots

A
  • a form of melanocytic naevus
  • flat, pigmented spots on the skin.

The most common symptom of NF1

19
Q

Benign lesions (4 LEVELS)

A

(1) Cafe-au-lait spots

(2) Junctional** nevus = melanocytes nest in the **epidermis

  • Flat and coloured
  • Normally, melanocytes sit in the basal layer of the epidermis
  • Melanocytes can, however, physiologically exist in the dermis
  • As you age, melanocytes usually drop into the dermis

(3) Compound** nevus = nests in **epidermis** and **dermis

  • Raised area
  • Surround by flat pigmented area

(4) Intradermal** naevus = nests in the **dermis

  • Raised area
  • Skin-coloured or pigmented
20
Q

Malignant Melanoma characteristics

A

Irregular border

Variable pigmentation

Bleeding

Itchy

Growing

21
Q

Malignant Melanoma histopathology

A
  • Histopathology = Pagetoid spread
    • The junctional melanocytes are not normally maturing and dropping out of the dermis – they are moving up through the dermis instead = “Pagetoid spread” this is NOT normal
    • Melanocytes also display mitotic figures (abnormal unless in pregnancy)
    • A melanoma with a thickness > 4 mm, it has a very high mortality (> 50%)

Staged by “Breslow Thickness

22
Q

ABCDE of Dermatology

A

Asymmetry

Border

Colour

Diameter

Evolution