Skin Pathology Flashcards
Define hyperkeratosis
Increased thickness of keratin layer
Define parakeratosis
Persistence of nuclei in the keratin layer
Define Acanthosis
Increased thickness of epithelium/ epidermis
Define papillomatosis
Irregular epithelial thickening
Define spongiosis
Oedema fluid between squamous cells in epidermis
Increases prominence of intercellular prickles (desmosomes)
In severe cases - vesicles filled by oedema fluid develop.
What are the 4 classifications of inflammatory skin diseases
•Spongiotic-intraepidermal oedema e.g. eczema
•Psoriasiform-elongation of rete ridges e.g. psoriasis
•Lichenoid-basal layer damage e.g. lichen planus and lupus
•Vesiculobullous-blistering e.g. pemphigoid, pemphigus and dermatitis herpetiformis
What are the 3 main types of eczema
atopic, irritant contact and allergic contact
What are the 3 stages of eczema
•Acute – massive spongiosis and vesiculation
•Subacute-less spongiosis – more acanthosis and scale
•Chronic-minimal spongisosis – prominent acanthosis and scale
Allergic contact eczema Pathophysiology
• Langerhans cells present antigen to T-lymphocytes
• Sensitised Memory T-cells in nodes recognise antigen
• T-lymphocytes then sent to epidermis
• Infiltrate epidermis and cause spongiotic eczematous reaction
Eosinophils often present (also a feature of drug trigger)
Psoriasis pathophysiology
Psoriasis diagnostic clues on microscopy
What are lichenoid disorders? Name some examples
Conditions characterised by damage to basal epidermis. Common condition is lichen planus
Other conditions include - discoid lupus, certain drug rashes, erythema multiform, toxic epidermal necrolysis
Lichen planus appearance
Itchy flat topped violaceous papules on skin & sore in the mouth
Lichen planus histology
•Irregular sawtooth acanthosis
•Hypergranulosis and orthohyperkeratosis
•Band-like upper dermal infiltrate of lymphocytes
•Basal damage with formation of cytoid bodies
What immunobullous disorders
name 3 examples of immunobullous diseases
Pemphigus (Pemphigus vulgaris)
Bullous pemphigoid
Dermatitis herpetiforms
What is Pemphigus
Rare autoimmune bullous disease that causes acantholysis & loss of integrity of epidermal cell adhesions.
Pemphigus vulgaris pathophysiology
•IgG auto-antibodies made against desmoglein 3
•Desmoglein 3 maintains desmosomal attachments
•Immune complexes form on cell surface
•Complement activation and protease release
•Disruption of desmosomes
•End result is ACANTHOLYSIS
What is acantholysis
lysis of intercellular adhesion sites
Pemphigus vulgaris presentation
Fluid filled blisters that rupture to form shallow erosions
Involves skin - especially scalp, face, axillae, groin & trunk
Involves mucosa - especially mouth & respiratory tract
Pemphigus vulgaris vs Bullous pemphigoid
Pemphigus vulgaris
- antibodies against epidermal cell desmosomes adhesions
- causes ancatholysis
- presents with shallow erosions
Bullous pemphigoid
- antibodies against hemidesmosomes
- causes loss of anchoring between basal cells & basement membrane
- presents with subepidermal blisters/ bullae
Bullous pemphigoid pathophysiology
Circulating antibodies (IgG) react with a major and/or minor antigen of the hemidesmosomes anchoring basal cells to basement membrane. The result is local complement activation and tissue damage
Basal cells/ epidermis lifts off of basement membrane forming a bulla (filled with fluid & some inflammatory cells)
