Introduction to dermatopathology.

Introduction

The following information is from an introductory course on dermatopathology intended for medical students and registrars / residents [1].

Hematoxylin and eosin (H&E) staining

Hematoxylin (H) is dark blue or purple. histology spot that has a positive charge and binds to the negative charge basophilic substances, such as DNA and RNA. It can be considered mainly nuclear stain. In contrast, eosin (E) is a negatively charged pink, red, or orange stain that highlights positively charged acidophilic (easily stained) substances, such as amino acids side chains (e.g. lysine and arginine) that are relatively abundant in the cytoplasm.

Normal skin

The normal skin illustrations in the figure below show relatively thin skin on the wrist (bottom) and thicker skin on the bottom of the foot (left, a acral site). Note that only acral sites have a lucid stratum (a transparent layer of dead skin cells). Fine, spiny intercellular desmosomes at thorny stratum They are also visible. Within epidermisnokeratinocytes have comparatively hyperchromatic nuclei.

Seborrheic keratosis

Seborrheic keratoses are fine.demarcated proliferations monotonous, sometimes cuboidal, epidermal keratinocytes are characterized by curb-fill 'horn'cysts within the epidermis.

Psoriasis

Psoriasis show acanthosis (epidermal hyperplasia), with flattened challenge and parakeratosis (retention of keratinocytes nuclei in the stratum corneum) Neutrophils in the stratum corneum (Munro microabscesses) orr upper epidermis (pustule by Kogoj) They are pathognomonic. The epidermis thins above elongated dermal papillae.

Lichen planus

Lichen planus exhibits a classic lichenoid inflammatory pattern (often described as a 'sawtooth' appearance) in which there are prominent mononuclear cells at the dermal-epidermal junction causing damage. Basal keratinocytes may show vascular degeneration due to immune-mediated apoptosis. Other features are hypergranulosis (thickening of granular stratum), acanthosis, epidermal thinning, pigment incontinence (pigment within melanophages on top dermis) and spongiosis (edema within the epidermis). (See Lichen planus pathology.)

Basal cell carcinoma

There are several subtypes of basal cell carcinoma (BCC) in which there is a peripheral palisade of basal keratinocytes with hyperchromatic nuclei. In the figure below, the left injury is a shallow BCC, and the correct one is a infiltrative BCC Following histological slide processing, shrink artifact results clefts. (See Pathology of basal cell carcinoma).

Dermatitis herpetiform

Dermatitis herpetiformis is a blistering disorder characterized by neutrophils at the tips of the dermal and subepidermal papillae vesicles full of neutrophils. Eosinophils, spongiosis and perivascular inflammation They are also typical. In this mess direct immunofluorescence reveals granulate immunoglobulin (Ig) A in the papillary dermis. (See DermNet NZ's page on dermatitis herpetiformis pathology.)

Drug eruption

Pathological findings in drugs rashes they are diverse and include many of the features seen in other types of lesions, such as spongiosis, interface activity, and variable lichenoid inflammation.

Mycosis fungoides

Mycosis fungoides is a type of T cell lymphoma characterized by epidermal Tlymphocytes with hyperchromatic nuclei that can form pathognomonic and Pautrier micro abscesses. Other features seen in mycosis fungoides are perivascular lymphocytes, spongiosis, and surface. serum Cortex. (See the DermNet NZ page on the pathology of mycosis fungoides.)

Actinic keratosis

An actinic keratosis classically shows atypical basal keratinocytes and the 'flag sign'(alternate parakeratosis and orthokeratosis) which generally saves attached prominent Epidermal structures hyperkeratosis, acanthosis and solar elastosis are often present hypertrophic The variant is notable for a thick stratum corneum.

Scaly cell carcinoma in the place

Squamous cell carcinoma (SCC) in situ results in full thickness atypia keratinocytes. Typically there is parakeratosis, mitotic figures, acanthosis and solar elastosis. Atypical squamous cells Do not spread to the dermis. (See the DermNet NZ page on squamous cell carcinoma in situ pathology.)

Cutaneous squamous cell carcinoma

Results of cutaneous SCC in dyskeratosis and invades beyond the basement membrane into the dermis. Cellular atypia can be described as glassy. Other features seen in cutaneous SCC include ulceration (serum cortex) and keratin beads. (See the DermNet NZ page on squamous cell carcinoma pathology.)

Melanocytic nevus

Melanocytic naevi can be intradermal, where there are proliferations (or 'nests') of melanocytes within the dermis, compound, where there are nests of melanocytes in the dermis and also nests of junctional melanocytes at the bottom of the rete papilla; or junctional, where there are nests of melanocytes at the junction of the epidermis and dermis, but there are no dermal melanocytes. A blue nevus is characterized by deeply pigmented spindle cell melanocytes and lies under a relatively acellular dermal skin stroma.

Nevi with varying levels of atypical characteristics can be called atypical or dysplastic due to architectural asymmetry, rete bridge, wider junction than dermal components, cellular atypia, fibroplasiaand lymphocytic infiltration. The images are from an acral site, showing a thick stratum corneum. (See the DermNet NZ pages on melanocytic nevus pathology and blue nevus pathology.)

Melanoma

Melanoma is a evil one proliferation of atypical melanocytes. Histologic features include a dark cytoplasm, pagetoid scattering (abnormal cells within the highest levels of the epidermis) and irregular cell nests. Melanoma in situ is confined to the epidermis, whereas invader Melanoma extends beyond the basement membrane into the dermis. Reagent, perilesional Lymphocytic inflammation is common. (See the DermNet NZ page on melanoma pathology.)

Molluscum contagiosum

The classic histology of molluscum contagiosum is epidermal hyperplasia, with a crater containing mollusk bodies (Henderson-Patterson bodies). These are large keratinocytes with eosinophilic intracytoplasmic inclusions that they put aside the core. (See the DermNet NZ page on molluscum contagiosum pathology.)

Viral warts

Two different subtypes of viral warts are shown in the following figure: common wart (the common wart, left) and flat wart (the flat wart, right). Wart vulgaris is characterized by hyperkeratosis, hypergranulosis, parakeratosis, blood in the stratum corneum, and prominent acanthosis. the ridge crests point inward. Large warts are highly vascularized with enlargement capillaries on the periphery and dermal papilla. Flat warts are flat warts that lack hypertrophic features. Usually there are koilocytes with a perinuclear halo in the upper epidermis. (See the DermNet NZ pages on Verruca vulgaris pathology and Verruca plana pathology).

Herpes Simplex

Herpes Simplex infection results in extended keratinocytes necrosis and balloon cells with the "3 M" - multinucleation, core molding (closely juxtaposed cores that conform to each other's shape) and margin of chromatin. (See the DermNet NZ page on the pathology of herpes virus infection.)

Bullous pemphigoid

Bullous pemphigoid is recognized by a subepidermal division, which generates tension bullas as seen in the figure below (the image on the left). The right side images in the figure showcleft formation with a rapid eosinophilic infiltrate. Direct immunofluorescence shows the statement IgG or C3 along the basement membrane. (See the DermNet NZ page on bullous pemphigoid pathology.)

Pemphigus vulgaris

Pemphigus vulgaris is a bullous disease in which there are acantholysis of keratinocytes above the basal layer of the epidermis (referred to as the 'tombstone' pattern). There is usually a superficial perivascular inflammatory infiltrate. Direct immunofluorescence shows IgG deposition between epidermal keratinocytes creating a network pattern. (See the DermNet NZ page on pemphigus vulgaris pathology.)