Dermatopathology 1 - Non-Neoplastic Skin Diseases Flashcards
- What does the dermis consist of?
- What is the hypodermis also called?
- Erector pili muscle, sebaceous glands, sweat glands, hair follicles.
- Peniculus.
Perivascular dermatitis without epidermal involvement.
Inflammatory infiltrate around potentially dilates superficial blood vessels.
Can also be associated w/ superficial oedema.
- looks like dermal pallor on histopathology. (unusual lightness of skin colour compared to normal complexion.
Associated with acute lesions including urticaria and type I hypersensitivity reactions.
Typically in horse and dogs.
Condition oedematous and patient pruritic. - not commonly found on biopsies (transient so not commonly sampled).
Perivascular dermatitis with epidermal hyperplasia.
Inflammatory infiltrate around superficial blood vessels.
Also thickening of the epidermis.
May see formation of rete pegs - epidermis dips up and down into the dermis.
Excess accumulation of keratin on epidermal surface (hyperkeratosis).
Epidermal hyperplasia:
- Non-specific finding.
- Reflects chronic irritation or altered turnover of the keratinocytes
- Often accompanied by hyperkeratosis and follicular keratosis.
- can lead to plugging and subsequent dilation of the follicles.
May see loss of pigment from epidermis = pigmentary incontinence - pigment either free in superficial dermis or found inside macrophages following phagocytosis.
Seen w/ keratinisation defects, callus, allergic dermatitis (type I hypersensitivity).
- histopathologicval features identical so cannot be differentiated on histopathology.
– cannot diagnose skin allergy from skin biopsy and from histopathological findings.
Also seen w/ contact dermatitis (rare) and sarcoptic mange.
Histopathological features of type I hypersensitivity (allergic dermatitis).
Epidermal hyperplasia.
Spongiosis (oedema between the epidermal cells).
Hyperkeratosis and follicular keratosis.
Dermal oedema.
Superficial perivascular dermatitis involving mast cells and eosinophils.
Late stage mononuclear cell infiltrate.
Perivascular dermatitis w/ epidermal spongiosis/intercellular oedema.
Acute process.
- if progresses, oedema may lead to rupture of intercellular bridges and formation of a spongiotic vesicle.
Can be seen with UV damage, involving white sparsely haired extremities.
Direct form - sunburn/solar dermatitis/primary phototoxicity.
Indirect form - via photodynamic agent e.g. plant or drug.
Vasculitis.
Inflammatory cells attack blood vessel wall.
Leads to loss of blood supply to that area of skin = ischaemia > necrosis.
May see lots of inflammatory cells within the vessel wall.
BUT inflammatory cells migrate from blood vessels into dermis - can be difficult to distinguish from normal cell movement in mild cases.
Fibrin deposition within the blood vessel so thrombus formation, perivascular haemorrhage and oedema.
- can be associated with fibrinoid necrosis of the vessel wall – glassy pink appearance on histology.
Rare pattern, immune complex, affecting peripheral capillaries e.g. tail tip, ear tips, footpads.
Interface dermatitis.
Inflammatory cells and typically lymphocytes obscure the dermal-epidermal junction.
Associated with thickening or clefting of basement membrane, apoptotic keratinocytes which appear more eosinophilic and shrunken then their neighbouring keratinocytes.
Hydropic degeneration of basal keratinocytes (intracellular oedema) - vacuolated (bubblies).
Uncommon to rare.
Seen w/ autoimmune and immune-mediated skin diseases where cytotoxic T cells kill keratinocytes.
Immune complexes deposit at basement membrane zone.
Various forms of cutaneous lupus erythematous, systemic lupus erythematous, erythema multiforme, drug reactions.
Uncommon to rare diseases.
Nodular to diffuse granulomatous dermatitis.
Nodular accumulation of inflammatory cells at any level of the dermis.
Can either increase in size to diffuse the effect of the biopsy specimen.
OR multifocal nodules coalescing to form a diffuse pattern.
Mostly associated with granulomatous inflammation where macrophages predominate. Also see lymphocytes and plasma cells, multinucleate giant cells, eosinophils and neutrophils (pyogranulomatous inflammation).
Suggests infection - bacterial, fungal, protozoal, foreign material.
Nodular or have draining tracts.
Deep bacterial granulomatous dermatitis w/ staphylococcus = ‘botryomycosis’.
Can also see other deep infections w/ actinomyces/nocardia.
Darkly staining grains = typical feature.
Gram staining to help with identification but culture needed to confirm.
Intraepidermal vesicular-pustular dermatitis.
Within the epidermis.
Affecting the surface and follicular epidermis.
Can be very superficial and subcorneal to deep and termed suprabasal.
When inflammatory cells are sparse = vesicle.
When content is highly cellular = pustular.
Often associated with some degree of dermal inflammatory infiltrate.
Pustule forms by breakdown of intercellular bridges = acantholysis.
- seen w/ bacterial, and sometimes dermatophyte infection, autoimmune diseases e.g. pemphigus foliaceus.
- once broken down, fluid and sometimes free-floating rounded keratinocytes (acantholytic keratinocytes) can be found within the pustule w/ or w/o inflammatory cells (neutrophils and/or eosinophils in pemphigus foliaceus).
- superficial pyoderma most common cause of pustules – most typically seen in the dog.
- often find bacteria within the pustule itself w/ degenerate neutrophils. Acantholytic keratinocytes rare.
- pattern seen in Porcine exudative dermatitis (‘greasy pig disease’) – S. hyicus.
- Pemphigus foliaceus = sterile pustular disease.
- seen with other causes of cutaneous inflammation e.g. insect bite dermatitis.
Subepidermal vesicular-pustular dermatitis.
Rare and associated w/ autoimmune and immune mediated skin diseases e.g. Bullous pemphigoid:
- dog, cat, horse.
- autoantibody to BMZ component.
Also seen with very rare diseases such as mechanobullous disease in dogs, cats, sheep, cattle. - inherited defect, in young animals after trauma.
Skin disease centred on hair follicles.
More common.
3 stages:
- perifolliculitis – inflammatory infiltrate surrounds hair follicle.
- folliculitis – cells invade follicle wall and sometimes make their way into the follicle lumen.
- furunculosis – follicle wall rupture. May be free hair shaft in dermis after follicle wall destroyed. Hair shaft acts like a foreign body and draws in more inflammatory cells.
Most common causes:
- pyoderma, dermatophytosis, demodicosis.
Deep pyoderma can occur when folliculitis develops into furunculosis.
- leads to a pyogranulomatous dermal infiltrate.
Can be localised e.g. anal furunculosis.
Fibrosing dermatitis.
Occurs after inflammation.
Associated with replacement of normal dermal and adnexal structures with granulation tissue e.g. replacement of hair follicles and sebaceous glands.
Non-specific.
Associated with end stage of intense destructive inflammatory reaction or can signify a more ongoing, insidious process.
Not always clinically apparent as a scar.
Panniculitis.
Inflammation of the fat.
Often secondarily involves deep dermis or can be secondary to the deep dermis.
3 forms:
- lobular – multinodular appearance to inflammatory infiltrate.
- septal – inflammatory cells seen in connective tissue between lobules of fat.
- diffuse – mix of both.
Can see all 3 forms in 1 patient.
Cannot be used to identify underlying disease process.
Atrophic dermatopathy.
Reduction in normal cutaneous structures.
Most commonly associated with endocrinopathies e.g. hyperadrenocorticism, hypothyroidism, excess oestrogen and others.
Different stages of hair cycle can be found but telogen (resting phase) often predominates.
Clinical signs:
- alopecia (bilateral, symmetrical).
- increase or decrease pigmentation.
- coarse, dry, dull, brittle coat.
- secondary keratinisation / infection.
Thin, hyperkeratotic epidermis
- keratotic refers to scale made of non-nucleated keratinocytes.
- parakeratotic refers to scale made of nuclear keratinocytes.
Telogen hair follicles may show marked follicular keratosis.
Atrophy of adnexal structures.
Skin biopsy indications.
Neoplasia - suspected or obvious.
Unusual or serious generalised dermatosis.
Condition that is poorly responsive to therapy.
Other diagnostic tests not helpful.
Vesicles, bullae, erosions, ulcerations.
