Skin pathology Flashcards
Normal skin structure: what are the layers of the epidermis?
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
What are some inflammatory reaction patterns?
Vesiculobullous Spongiotic Psoriasiform
Lichenoid Vasculitic Granulomatous
Bullous pemphigoid (vesiculobullous)
- 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
Pemphigus vulgaris (vesiculobullous)
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
What is acantholysis?
Acantholysis refers to the loss of attachments between keratinocytes, resulting in the formation of rounded, detached cells within the blister.
Pemphigus foliaceus (vesiculobullous)
Top layer is very thin so never blisters
IgG-mediated – outer layer of stratum corneum shears off
Diagnose with immunofluorescence
Discoid eczema
- Flexor surfaces
- Very itchy; plaques form
Contact dermatitis
- 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
- Pathophysiology:
Plaque psoriasis
- 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
Lichen planus (lichenoid)
- 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
Pyoderma gangrenosum
- Vasculitis (not actually gangrenous)
- Presents as non-healing ulcer
- Often, first manifestation of a systemic disease
- E.G. colitis, hepatitis, leukaemia
Seborrhoeic keratosis
“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
Sebaceous cyst
- Transluminates, central punctum, circumscribed, hot
- Squamous cell lining surrounding the cyst
Basal cell carcinoma
- 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
Bowen’s disease
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)
SCC
- 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.
SCC
- 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.
What are cafe-au-lait spots
- a form of melanocytic naevus
- flat, pigmented spots on the skin.
The most common symptom of NF1
What are cafe-au-lait spots
- a form of melanocytic naevus
- flat, pigmented spots on the skin.
The most common symptom of NF1
Benign lesions (4 LEVELS)
(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
Malignant Melanoma characteristics
Irregular border
Variable pigmentation
Bleeding
Itchy
Growing
Malignant Melanoma histopathology
- 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
ABCDE of Dermatology
Asymmetry
Border
Colour
Diameter
Evolution
