dermpath

• Skin biopsies are taken in cases of inflammatory disease to make a diagnosis, establish optimal therapy, and to tule out other conditions. In dermal neoplasias, skin biopsies are taken to confirm whether a lesion is neoplasia or inflammation, to confirm that an excision has achieved clean margins, to establish prognosis, and to monitor the effect of therapy.
• History prior to biopsy should include:

  • Age, sex, breed
  • Lesion description
  • Lesion distribution
  • Animal’s response (itchy / painful?)
  • If there is seasonality
  • If there is systemic disease
  • Treatments previously given

   
• When taking a skin biopsy, patients should ideally be removed from treatment 2-3 weeks prior. Clip hair but do not surgically prepare the skin.

  Take a punch, incision or excision biopsy, ideally taking multiple. If there are multiple lesions, biopsy them all. Fix in 10-20x volume formalin.

  Biopsies should be set on cardboard showing the direction of hair growth to give a long section when cut.
• The epidermis is made up of several layers (working outwards):

  • Basement membrane
  • Stratum basale (high mitotic rate)
  • Stratum spinosum (polygonal cells)
  • Stratum granulosum
  • Stratum corneum (keratin)
• In the dermis there are hair follicles, arrector pili muscles, sweat glands, and sebaceous glands which produce sebum.  Sweat glands are formed of simple cuboidal cells, forming ducts in the dermis.

  Sebaceous glands appear as clusters of cells with a foamy cytoplasm.
• The hair follicle cycle has several stages:

  1.      Growth phase (anagen)

  2.      Regression phase (catagen)

  3.      Quiescent phase (telogen)

  4.      Hair shedding (exogen)

  Endocrine diseases may push follicles to the telogen phase, so they quiesce and shed out, leading to alopecia.
• Types of hyperkeratosis:

  • Orthokeratosis – excess normal keratin, appears as white dandruff flakes e.g. vitamin A deficiency or primary cornification disorders
  • Parakeratosis – a thick layer of abnormal keratin where the nuclei are retained. (not terminally differentiated)  e.g. zinc responsive dermatosis.

  Hyperkeratosis can also be non-specific and a response to trauma or inflammation
• Papules are lesions with inflammatory cell or fluid influx, or hypertrophy, forming solid elevations of skin

   

  Pustules are lesions dominated by neutrophils, elevations of the skin filled with pus

   

  Collarettes are pustule ruptures where the stratum corneum peels away.
• Pattern analysis  is the most common histopathological approach to evaluating skin biopsies (i.e. a morphological approach). This can help us understand common pathogenic mechanisms and different diseases. E.g. perivascular dermatitis, interface dermatitis, vasculitis, nodular or diffuse, atrophic etc.
• In perivascular dermatitis there is a non-specific inflammatory pattern surrounding blood vessels in the dermis. This is a common finding so isn’t particularly diagnostic but occurs in hypersensitivity reactions, as a response to ectoparasites, and in bacterial infection.
• Interface dermatitis describes lesions targeting the upper level of the dermis or the dermo-epidermal junction. There is hydropic degeneration and apoptosis of cells in the stratum basale – not necessarily cell rich. E.g. response to some drugs, erythema, discoid and systemic lupus (immune mediated, causes crusting and depigmentation)
• Depigmentation of the skin usually occurs due to direct melanocyte damage and damage to the basal cell layer, causing pigmentary incontinence. Melanocytes effectively ‘drop’ their melanin.
• Vasculitis is a reaction targeted against blood vessels themselves in the skin. There is evidence of vascular endothelial cell damage, with the potential for necrosis and infarction. Usually idiopathic, but may be associated with infections, toxins, and DIC.
• Nodular and diffuse dermatitis usually begins as nodular inflammation of the defmis, which then coalesces and efface the normal dermal architecture. Many different cell types may be involved:

  • Neutrophils: abscesses or cellulitis
  • Macrophages: mycobacterial infections, leishmaniosis, foreign body
  • Pyogranulomatous (N+M): fungal and bacterial infections
  • Eosinophils: eosinophilic granuloma complex
  • Lymphocytes: vaccine reactions
• Intraepidermal vesicular or pustular dermatitis describes changes WITHIN the epidermal compartment, and may be a consequence of spongiosis, hydropic change, acantholysis or friction. Generally if:

  • Neutrophil dominated, caused by a bacterial infection, or pemphigus foliaceous
  • Eosinophil dominated, caused by parasitic disease, or allergic reaction
  • Minimal inflammation, pemphigus vulgaris cause. Seen as tomb stones attached to stratum basale, lifting other layers
• Subepidermal vesicular or pustular dermatitis is rare, where the entire epidermis is separated off. Commonly caused by bullous pemphigoid.
• Hair follicles and sebaceous glands can be targeted by:

  • Folliculitis (inflammation) and furniculosis (rupture of hair follicle) e.g. staph infection, demodex or ring worm. If hair shafts enter the dermis there will be a foreign body reaction.
  • Sebaceous adenitis – sebaceous glands are targeted by immune reactions, in chronic cases, glands may be entirely absent.  Patients present with alopecia and excessive scale on the skin
• Panniculits is inflammation of the subcutis, where subcutaneous adipose tissue becomes involved in the inflammatory reaction. This is often associated with deep dermal inflammation or foreign bodies. Can also be in response to physical injury, vitamin E deficiency and pancreatic disease.
• Atrophic dermatosis is atrophy of hair follicles and adnexal structures (in the dermis). This is most commonly associated with endocrinopathies e.g. Cushing’s, hyperthyroidism, causing follicular atrophy, sebaceous gland atrophy and diffuse orthokeratosis. There is increased likelihood of secondary bacterial skin infections. There may also be a prolonged telogen phase and dysplasia of hair shaft formation.