Skin Pathology Flashcards
Describe the layers of normal skin
- 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
Layers of skin: “Come, let’s get some beers”
Melanocytes in the basemenet
From birth to stratum basale - 28 days
What is this?
Epidermis
How are the inflammatory skin reactions divided?
“divided into morhopolofical patterns that characterise a group of skin disorders”
- Epidermis
- Dermis
- Subcutis
What are the epidermal inflammatory patterns?
Decribe spongiotic reactions
- Most common
- Eczema
- Exocytosis of lymphocytes into the epidermis. Vesicles containing antigen presenting langerhan cells and T cells interact
Describe Lichenoid inflmmation
Lichen - tree bark fungus –> lesions look like this
- Autoimmune
Irregularly thickened epidermis
Degernarative skin cells
Liquefaction degenration of the basal layer of the epidermis (keratinocytes)
Band of inflammatory cells just beneath the epidermis
Melanin beneath the pidermis
What is this?
Lichen planus
What time of inflammatory pattern are eruthema multiforme, TEN ans SJS
Lichenoid inflammation
- Band of lymphocytes
- Keratinoycte degenration
- Basal membrane breaking
Describe psoriasifrom reactions.
- Clincially : red patches and plaques
silvery scale
Well demaracated
- Abnormally rapid turnover (can be 7 days) of the epidermis results in the accumulation of the thick scale over sites of frequent trauma and irritation
- Parakeratosis and acanthosis under microscope
- Can have neutrophils
Describe vesiculobullous reaction patterns
- Autoimmune vesiculobullous
- Bullous pemphigoid
- Large tense bullae and intensely pruritic
- Antibodies attach the epidermal basement membrane (eosinophils)
- Blister is subepidermal
- Direct immunofluoresence - Linear IgG
- Pemphigus
- Pemphigus foliaceous - superficial
- Pemphigus vulgaris - deep form –> quite serious if not treated
- Antibodies attack the desmosomes (intracelliular bridges)
- Blister is intra epidermal
- Intraepidermal formation of blister
- Acantholysis - top epidermis gets off
- Bullous pemphigoid
What does this show?
Pemphigus vulgaris - intraepidermal bullae formation
How do we classify skin tumours
- Benign vs malignant
- Primary vs Metastatic
Describe seborrhaeoic keratosis.
Acanthosis - thickening of dermis
Benign
Describe BCCs
Can travel along nerves - local destruction
PTCH mutation – somatic mutation caused by UV exposure
Young patients can get it (inherited)
Describe the cells
BCC
- Casaloid
- Peripheral palisading
- Clefting
- Mitotic activity
Describe benign naevis
- Clincially all look benign
- Naevia are well organised
- Symmetrical
- Small melanocytes
- Can travel along the dermis
- Maturation with depth –> get smaller as they keep going deeper
How do we classify malignant melanoma?
What is this
- Malignant melanoma
- Pagetoid spread
- Asymmetry
- All cells look similar
- Blue
- Mitotic activity in the dermis
Name the prognostic indicators of melanoma
