Difference between revisions of "Non-malignant skin disease"

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=====Without koilocytes=====
=====Without koilocytes=====
The sections show skin with elongated rete ridges, acanthosis, hypergranulosis,
The sections show skin with elongated rete ridges that curve toward the centre of the lesion, acanthosis, hypergranulosis, hyperkeratosis in vertical columns, and dilated blood vessels at the dermal-epidermal
hyperkeratosis in vertical columns, and dilated blood vessels at the dermal-epidermal
junction. Minimal basilar nuclear enlargement is present.  No definite koilocytic change is
junction. Minimal basilar nuclear enlargement is present.  No definite koilocytic change is
apparent.
apparent.

Revision as of 12:36, 10 January 2013

Non-malignant skin disease is relatively common. The pathology may or may not be specific. Some diseases require clinical information to diagnose.

An introduction to dermatopathology is in the dermatopathology article. Nevi (moles) and other melanocytic lesions are dealt with in the article melanocytic lesions. Inflammatory skin conditions are dealt with in inflammatory skin disorders.

Other

Lichen simplex chronicus

  • Abbreviated LSC.
  • AKA squamous cell hyperplasia.[1]

General

Etiology:[4]

  • Pruritus (itchness) -> mechanical trauma -> lichenification (thickened/leathery[5].

Microscopic

Features:[6]

  • Acanthosis (epithelial thickening) - irregular.
  • Hyperkeratosis.

Other features:[7]

  • Spongiosis (epidermal intercellular edema -- cells appear to have a clear halo around 'em).
  • Parakeratosis = retention of nuclei in the stratum corneum.

DDx:

Images:

Sign-out

SKIN, PUNCH BIOPSY:
- LICHEN SIMPLEX CHRONICUS.
- NEGATIVE FOR MALIGNANCY.

Oral

RETROMOLAR PAD, RIGHT, PUNCH BIOPSY:
- ORAL LICHEN SIMPLEX CHRONICUS.
- NEGATIVE FOR MALIGNANCY.

Micro

The sections show a squamous mucosa with irregular psoriasiform change, parakeratosis, and focal hypergranulosis. There is no inflammation at the interface. Epidermal intercellular bridges are easily seen. There is no significant nuclear atypia. Mitoses are not evident.

Prurigo nodularis

  • Abbreviated PN.
  • AKA chronic prurigo and picker nodule.[3]

General

Gross

  • Dome-shaped/raised - papular (<1 cm) or nodular (>1 cm).[9]

Microscopic

DDx:

Sign out

SKIN LESION, LEFT CHIN, BIOPSY: 
- PRURIGO NODULARIS.

Micro

The sections show a raised lesion with compact hyperkeratosis and irregular acanthosis. Spongiosis is seen focally. There is minimal hypergranulosis.

There is no thinning of the suprapapillary plate and no dilated superficial blood vessels. There is no interface activity.

Very common

Dermatomycosis

General

Note:

  • Dermatophytosis (ring worm) is a type of dermatomycosis.

Microscopic

Features:

  • Microorganisms - key feature.
    • Often hyphae (candida) - like twigs of a tree... branching.
      • May be very fragmented in section ~ size of a neutrophil.
  • Perivascular inflammation, esp. neutrophils.
  • Exocytosis - blood cell infiltrate the epidermis.

Images:

Stains

Sign out

SKIN, BIOPSY:
- SKIN WITH SUPERFICIAL FUNGAL ORGANISMS CONSISTENT WITH CANDIDA.
- REACTIVE CHANGES OF THE EPITHELIUM.

Micro

The sections show skin with a neutrophilic infiltrate in the superficial epidermis. PAS-D staining demonstrates fungal organisms with a morphology suggestive of candida.

The epithelium has parakeratosis, acanthosis and spongiosis. No mitotic activity is appreciated. The keratinocytes are moderately enlarged and have evident nucleoli.

Cicatrix

  • AKA scar, dermal scar.

General

  • Previous surgery, biopsy, trauma.

Microscopic

Features:

  • Loss of dermal papilla.
  • Dense collagen - fibers run parallel to the dermal-epidermal (DE) junction[10] - key feature.
  • Loss of adnexal structures.

Other feature:

  • Thin-walled blood vessels.
    • Described as running perpendicular to the surface[10] - this may not be apparent.

Note:

  • There should not be any nuclear hyperchromasia or pleomorphism.[11]

DDx:

Image:

IHC

  • S100 focal/scattered +ve.
    • Desmoplastic melanoma strong +ve.
  • HMB-45 -ve.
    • Sclerosing blue nevus +ve.

Sign out

SKIN, LOWER MID BACK, RE-EXCISION:
- DERMAL SCAR.
- SOLAR ELASTOSIS.

Micro

The sections show skin with a dermis with dense collagen fibres that run parallel to the skin surface without adnexal structures. The overlying dermal-epidermis interface lacks the typical undulation.

Fibroepithelial polyp

  • AKA acrochordon.
  • AKA skin tag.

General

Gross

  • Raised skin-coloured lesion.

Image:

Microscopic

Features:

  • On a stalk / epithelium on three sides.
  • Benign epidermis.

DDx:

Images:

Sign out

SKIN ("SKIN TAG"), THIGH, EXCISION:
- FIBROEPITHELIAL POLYP.

Micro

The sections show a fragment of skin with epithelium on three sides. The epithelium matures and is not hypertrophic. Orthokeratosis is present. The core of the lesion has fibrous tissue. There is no inflammation.

Inflamed

The sections show a fragment of skin with epithelium on three sides. The epithelium matures and is acanthotic. Minimal parakeratosis is present. The core of the lesion consists of fibrous tissue with a mild lymphocyte-predominant dermal infiltrate. Rare siderophages are present.

There is mild basal nuclear enlargement. No significant nuclear atypia is apparent. The dermal-epidermal interface is well-demarcated. Rare basal mitotic activity is identified.

Actinic keratosis

Bowenoid actinic keratosis redirects to here.

General

Risk factors:[18]

  • Sun exposure.
  • Immune suppression (e.g. organ transplant recipients).

Gross

Features:

  • Yellow-brown scaly, patches.
  • Sandpaper sensation - on touching.
  • May be pigmented.[19]

Microscopic

Features:[20]

  • Epidermal nuclear atypia:
    • Variation is size, shape and staining - must involve basilar layer.
      • Nuclear enlargement - key feature.
      • Hyperchromasia.
  • Abnormal epidermal architecture:
  • +/-Parakeratosis - may alternate with orthokeratosis, esp. early lesions.[21]
  • +/-Irregular acanthosis.

Note:

  • May be full thickness - known as bowenoid actinic keratosis.[22]

DDx:

Images:

Histologic subtypes of actinic keratosis

Like most common things, there are several variants:[21]

  • Hypertrophic actinic keratosis.
    • Increased thickness of: (1) epidermis and, (2) stratum corneum.[24]
  • Acantholytic actinic keratosis.
  • Proliferative actinic keratosis - downward finger-like projections of the epidermis.
  • Pigmented actinic keratosis.
  • Lichenoid actinic keratosis.

Sign out

SKIN LESION, RIGHT THIGH, BIOPSY:
- HYPERTROPHIC ACTINIC KERATOSIS.
- SOLAR ELASTOSIS.
- NEGATIVE FOR MALIGNANCY.

Bowenoid

SKIN LESION, RIGHT DISTAL FOREARM, BIOPSY:
- BOWENOID ACTINIC KERATOSIS, COMPLETELY EXCISED IN PLANE OF SECTION.
- EXTENSIVE SOLAR ELASTOSIS.
- NEGATIVE FOR MALIGNANCY.

Micro

General

The sections show skin with basilar epidermal nuclear enlargement and hyperchromasia with irregular nuclear palisading. Hyperkeratosis and parakeratosis is present. A granular layer is present. The dermal-epidermal interface is sharply-demarcated. There is focal inflammation at the interface. Extensive solar elastosis is present.

There is no clefting of the lesion from the surrounding stroma. The surrounding stroma does not have a myxoid quality.

Bowenoid

The sections show skin with epidermal nuclear enlargement and hyperchromasia with irregular nuclear palisading. The lesion involves the full thickness of the epidermis; however, it spares adnexal and follicular epithelium. Proliferative activity is present. Hyperkeratosis and parakeratosis is present. A granular layer is present. The dermal-epidermal interface is sharply-demarcated. There is focal inflammation at the interface. Extensive solar elastosis is present.

There is no clefting of the lesion from the surrounding stroma. Intercellular bridges are identified.

Actinic cheilitis

General

Microscopic

See actinic keratosis.

Sign out

LESION, LOWER LIP, BIOPSY: 
- ACTINIC CHEILITIS.
- SOLAR ELASTOSIS.

Micro

The sections show skin with moderate basal nuclear hyperchromasia and atypia, and parakeratosis. The squamous epithelium has maturation to the surface. There is no inflammation at the dermal-epidermal interface. Solar elastosis is present.

Seborrheic keratosis

  • Abbreviated SK.

General

  • Benign.
  • Most common tumour in older people.[25]
  • "Large number" of SKs = paraneoplastic syndrome (Leser–Trélat sign).[26]

Epidemiology:

  • Old people.
  • Usually in sun exposed area.[27]

Gross

  • "Stuck-on" appearance - raised lesion.

Image(s):

Microscopic

Features:[26]

  • Raised above skin surface.
  • Border sharply demarcated.
  • Hyperkeratosis - stratum corneum extra thick.
    • May be minimal.
  • Horn cysts - intraepidermal collections of keratin - key feature.
    • Actually invaginations - not true cysts; thus, they may more accurately be called pseudohorn cysts.[28]
  • Clusters of cells with brown granular material in the superficial dermis/dermoepidermal junction - pigmented melanocytes.

DDx:[29]

Images:

Histologic subtypes

Like very common lesion, there are subtypes:[29]

  • Acanthotic seborrheic keratosis - thickened stratum spinosum; thick epidermis.
  • Reticulated seborrheic keratosis - vaguely resembles fibroepithelioma of Pinkus (BCC, fibroepitheliomatous pattern).
  • Irritated seborrheic keratosis - spongiosis (epidermal intercellular edema) and inflammation.
  • Digitated seborrheic keratosis - papillomatous projections.

Sign out

SKIN, MID BACK, SHAVE BIOPSY:
- SEBORRHEIC KERATOSIS.

Micro

The sections show skin with acanthosis, pseudohorn cysts, parakeratosis, hyperkeratosis and focal basal epidermal pigmentation. There is no basal nuclear atypia, no mitoses and there are no melanocytic nests. There is minimal dermal inflammation. There is no solar elastosis.

Without horn pseudocysts

The sections show skin with acanthosis, a thin layer of compact keratin and focal basal epidermal pigmentation. Dilated blood vessels surrounded by collagen are seen in the superficial dermis. No pseudohorn cysts are identified. A granular layer is present.

There is no basal nuclear atypia. There is no mitotic activity and no melanocytic nests. There is no solar elastosis. No koilocytes are apparent.

Minimal hyperkeratosis

The sections show skin with acanthosis, pseudohorn cysts, rare parakeratosis, minimal hyperkeratosis and focal basal epidermal pigmentation. There is no basal nuclear atypia, no appreciable mitotic activity and there are no melanocytic nests. There is minimal dermal inflammation. Solar elastosis is present.

Pilomatricoma

  • AKA calcifying epithelioma of Malherbe[31], AKA pilomatrixoma.

General

  • Benign skin tumour.
  • Most common solid skin tumour of children.[32]
  • CTNNB1 gene mutation important in pathogenesis.[33]

Clinical:

  • Hard nodule - calcification.
  • +/-Painful.

Treatment:

  • Surgical excision.[32]

Microscopic

Features:[34]

  • Nodular circumscribed lower dermis/subcutaneous adipose lesion; thus, usu. surrounded by connective tissue.
    • Sharpy demarcated island of cells.
    • Calcification in 75%.
  • Cells:[35]
    • Basaloid epithelial cells - have prominent nucleoli.
    • Anucleate squamous cells ("ghost cells").
    • Giant cell foreign body type granulomas (form in reaction to keratin).

Notes:

  • Keratin a prominent feature on cytology - lots of orange stuff.
  • May ossify.

Images:

DDx:

Sign out

SKIN LESION, RIGHT ARM, EXCISION:
- PILOMATRICOMA.

Dermatofibroma

  • Abbreviated DF.

General

  • AKA fibrous histiocytoma.
  • Reactive process -- it is not a neoplasm.
  • Usually associated with previous trauma.
    • In women... usually legs.

Microscopic

Features:[37]

  • Prominent fibrous bundles, especially at the edge of the lesion.
    • Surrounded by spindle cells (fibroblasts).
      • Usually thought of as fibroblasts surrounded by fibrous material ("collagen-trapping").
  • Lack of adnexal structures, i.e. no sweat glands, no hair.
  • +/-Epidermal changes - known as "dirty fingers":[38]
    • Acanthosis (thickened epithelial layer - specifically thickened stratum spinosum).
    • Basal keratinocyte hyperpigmentation.

DDx:

Images:

Subtypes

Like all common things... there are subtypes:[39]

  • Cellular.
  • Deep penetrating.
  • Lipidized - with foamy macrophages, hemorrhage and Touton-like giant cells.
  • Epithelioid cell histiocytoma.
  • Fibrotic.
  • Aneurysmal - large blood filled + features of lipidized.
  • Granular cell dermatofibroma.
  • Dermatofibroma with monster cells.
Cellular dermatofibroma

Features:

  • High cell density in the dermis - "blue" at low power.
  • Collagen bundles - key feature.

Images:

IHC

Features:[41][42]

  • Factor XIIIa +ve.
    • Usually negative in DFSP.
  • CD34 -ve.
    • Usually positive in DFSP.
  • D2-40 +ve.[43]
    • Usually negative in DFSP.

Ezcema

General

  • A nebulous thingy.
  • Very common.

DDx:

Microscopic

Features:[44]

  • Spongiosis (epidermal edema); keratinocytes spacing increased - key feature.
  • +/-Interdermal vesicles.
  • +/-Eosinophils (may suggest Rx reaction).
  • Perivascular lymphocytes.

Acne vulgaris

General

  • Extremely common - esp. among adolescents.
  • Very rarely seen by pathologists.

Treatments:

  • Antibiotic (minocycline).
  • Isotretinoin AKA all-trans retinoic acid (ATRA).

Gross

  • Papules, pustules, nodules or cysts.
    • White, black or erythematous.

Images:

Microscopic

Features:[45]

  • Folliculitis:[46]
    • Neutrophils around hair follicle and infiltrate into it - including the follicular canal.
  • Epidermal invagination or cyst at site of a hair follicle - contains:
    • Sebum.
    • +/-Bacteria (Propionibacterium acnes) and inflammatory cells - typically neurophils.

Subtyped into:

  1. Open comedones ("blackheads") - no extension to epidermal surface.
  2. Closed comedones ("whiteheads") - to epidermal surface have wide opening.

DDx - acneiform disorder:[46]

  • Rosacea.
  • Infective folliculitis.
  • Perioral dermatitis.
  • Acne vulgaris.

Image:

Solar elastosis

  • AKA actinic elastosis.

General

  • Very common.
  • Caused by sun exposure - specifically UV light.[47]
    • Severity correlated with cumulative exposure to UV light..[48]
  • Often co-localized with skin cancers - as UV light is risk factor for skin cancers.[48]
  • Benign.

Microscopic

Features:

  • Grey, spaghetti-like material in the superficial dermis.

DDx:

Note:

  • It doesn't really look like anything else.
    • The DDx above is things to think about that are associated with sun damaged skin.

Images:

Sign out

SKIN, RIGHT CHEEK, RE-EXCISION:
- DERMAL SCAR.
- EXTENSIVE SOLAR ELASTOSIS.

Very common - viral

Verruca vulgaris

  • AKA common wart.

General

  • Etiology - HPV.
  • Very common.

Notes:

Gross

Features:

  • Papule or plaque with granular surface.
  • Classic location: hand.

Images:

Microscopic

Features:[49]

  • Hyperkeratosis (more keratin - thick stratum corneum) - in "columns"; keratin in separate towers - not a flat thick sheet.
  • Hypergranulosis (thicker stratum granulosum).
  • Papillomatous hyperplasia:
    • Rete ridge lengthening (~7-10x normal) and thickening.
    • Rete ridge curvature toward the centre of the lesion (like the roads to the Palace of Versailles) - important.
  • Large blood vessels at the dermal-epidermal junction - between the rete ridges.
  • +/-Viral changes - perinuclear halo, nucleus small and hyperchromatic[50] - virtually diagnostic when present.
    • +/-Binucleation.

Memory device: there is more of everything - more s. corneum, s. granulosum, s. spinosum, longer rete ridges, more (larger) blood vessels.

DDx:

Images:

Sign out

SKIN LESION, RIGHT LOWER LEG, SHAVE BIOPSY:
- VERRUCA VULGARIS.

Micro

The sections show skin with elongated rete ridges, acanthosis, hypergranulosis, hyperkeratosis in vertical columns, focal parakeratosis, dilated blood vessels at the dermal-epidermal junction and koilocytic change. Mild basilar nuclear atypia is present.

Without koilocytes

The sections show skin with elongated rete ridges that curve toward the centre of the lesion, acanthosis, hypergranulosis, hyperkeratosis in vertical columns, and dilated blood vessels at the dermal-epidermal junction. Minimal basilar nuclear enlargement is present. No definite koilocytic change is apparent.

No parakeratosis is identified. Mild solar elastosis is identified. No melanocytic nests are apparent. Mitotic activity is not apparent.

Verruca plana

General

  • Common.
  • Usu. hands and face.[51]

Microscopic

Features:[51]

  • Orthokeratosis with basketweave pattern.
  • Hypergranulosis.
  • Viral keratohyaline.
  • Koilocytes.
  • Acanthosis - yet flat surface and base.

Notes:

  • It differs from verruca vulgaris... (1) orthokeratosis, (2) flat surface and base.

Less common

Chronic folliculitis

Folliculitis redirect here.

General

  • Common.
  • Infrequently biopsied.

Gross

DDx gross:

Microscopic

Features:

  • Inflammation around the hair follicle - key feature.
    • Lymphocytes - usu. predominant.
  • +/-Chronic changes:
    • Acanthosis.
    • Hyperkeratosis.
    • Hypergranulosis.

DDx:

Sign out

SKIN LESION, UPPER ARM, BIOPSY:
- CHRONIC FOLLICULITIS WITH SECONDARY SURFACE CHANGES.

Micro

The sections show hair-bearing skin with abundant lymphocytes around and within the hair follicle wall.

The non-hair follicle epidermis has acanthosis, hypergranulosis and compact hyperkeratosis. There is no inflammatory cell infiltrate in the non-hair follicle epidermis or at the non-hair follicle interface.

There are no granulomas.

Clear cell acanthoma

General

  • Benign.
  • Elderly.
  • Classically on the leg.[53]
  • Rare.
  • Clinically not distinct.
    • Suspected clinically in only ~3% of cases.[54]

Microscopic

Features:[55]

  • Psoriasiform pattern - epidermal thickening (acanthosis).
  • Keratinocytes:
    • Pale or light pink cytoplasm (when compared to surrounding non-lesional keratinocytes).
    • Separated from one another (spongiosis).
  • +/-Stratum corneum neutrophils.

DDx:

Images:

Chondrodermatitis nodularis chronica helicis

  • AKA chondrodermatitis nodularis helicis.
  • Abbreviated CNCH.

General

  • Tender/painful - key clinical feature.
  • Typically right ear - people more often sleep on this one.[56]
  • Usually >40 years old.

Etiology:

  • Trauma/mechanical.

Gross

  • Papule on ear.
  • +/-Erythematous.
  • +/-Crust.

Clinical DDx:[56]

Images:

Microscopic

Features:[56]

  • Dermal inflammation.
  • Epithelial hyperlasia.
  • Fibrosis.
  • Cartilaginous pathology:
    • Perichondrial inflammation - key feature.
    • Perichondrial disruption.
    • +/-Necrosis.
    • +/-Hemorrhage.

Images:

Sign out

Superficial biopsy

SKIN LESION, LEFT ANTIHELIX OF EAR, BIOPSY:
- SUPERFICIAL SKIN WITH ACANTHOSIS, HYPERKERATOSIS, MODERATE SOLAR ELASTOSIS, 
  HYPERGRANULOSIS AND A MILD LYMPHOCYTIC PERIVASCULAR INFILTRATE.
- NO CARTILAGE IS IDENTIFIED.
- NEGATIVE FOR DYSPLASIA AND MALIGNANCY.

COMMENT:
The findings are non-specific. Chondrodermatitis cannot be excluded.

Cutaneous calcinosis

  • AKA calcinosis cutis.

General

  • Benign in itself; underlying cause may not be benign.
  • May be a scrotal lesion - known as scrotal calcinosis.[57]

Subtypes:[58]

  1. Dystrophic - due to death of cells; may be related to a tumour.
  2. Metastatic - due to chronic renal failure; hyperkalemia; paraneoplastic phenomenon.
  3. Iatrogenic - post surgical.
  4. Idiopathic.

Microscopic

Features:

  • Dermal calcification:
    • Acellular purple blobs on H&E.
      • +/-Artefactual tearing of surrounding tissue due to processing (cutting).
      • +/-Small artefactual lines ~1-2 micrometers due to processing (cutting).
    • Usu. well-circumscribed.

Images:

Dilated pore of Winer

General

  • Benign.
  • Looks like zit.

Microscopic

Features:[59]

  • Dilated hair follicle with keratin.
  • Acanthosis.
  • Budding of epidermis (into dermis).

Lichenoid keratosis

  • AKA lichen planus-like keratosis.
  • AKA lichenoid keratosis.

General

Clinical DDx:[60]

Microscopic

Features:[61]

  • Hyperkeratosis.
  • Parakeratosis.
  • Band of inflammatory cells at DE junction (lichenoid inflammation).
  • Dead keratinocytes (Civatte bodies).
  • Dermal melanophages.

DDx:

Images:

Sign out

SKIN LESION, MID-MIDDLE BACK, PUNCH BIOPSY:
- LICHENOID KERATOSIS.

Granuloma annulare

General

  • Benign and self-limited condition.
  • Etiology unknown - may be assoc. with trauma.[62]

Gross

  • Typically extremities - usu. arms and hands.[62]

Microscopic

Features:[63]

  • Dermal palisading granuloma - typically superficial-to-mid dermis - surrounds:
    • Necrotic collagen - key feature.
      • Nuclei "missing" - have undergone karyolysis.
    • Mucin - important.
      • Loose/pale, paucicellular, eosinophilic.
  • Chronic inflammatory cells.

Notes:

  1. There may be multiple small foci with intervening normal dermis.[62]
  2. Granuloma annulare can be subclassified into subcutaneous and interstitial.
  3. Histomorphologically similar to Rheumatoid nodule.
  4. Neutrophils may be seen.[64]

DDx:

Images:

Stains

Image:

Necrobiosis lipoidica

General

Associated with:

Microscopic

Features:[62]

  • Dermal palisading granuloma around:
    • Necrotic collagen - key feature.
      • Nuclei "missing" - have undergone karyolysis.
  • Little mucin, no normal dermis between foci.
  • Plasma cells - common.[65]
  • May involve adipose tissue.

DDx:

Images:

Keloid

  • Hypertrophic scar redirects to this section.

General

  • Sites of previous trauma/surgery, esp. in dark skinned individuals.[37]

Microscopic

Features:[37]

  • Thick collagen bundles - surrounded by paler staining fibroblasts - key feature.
  • Lesion replaces adnexal structures, e.g. hair, sweat glands.

DDx:

  • Hypertrophic scar.[68]

NB:

  • Reported as "keloidal-type collagen"; the clinician decides between hypertrophic scar and keloid.

Images:

Sign out

SKIN LESION, LEFT SCAPULA, EXCISION:
- DERMAL SCAR WITH KELOIDAL-TYPE COLLAGEN, SEE COMMENT.

COMMENT:
The findings are consistent with a hypetrophic scar and keloid; clinical correlation is required.

Angiofibroma

See also: nasopharyngeal angiofibroma.
Should not be confused with angiokeratoma.
Fibrous papule redirects here.

General

  • May be seen in the context of tuberous sclerosis - especially "butterfly area of the face".[37]
  • Solitary lesions in adults are known as fibrous papules and classically arise on the nose.[69]

Clinical:

  • Firm, dome-shaped, flesh coloured.

Microscopic

Features:[37]

  • Dome-shaped.
  • Fibrotic dermis.
    • Enlarged fibroblasts.
  • Dilated small vessels.

Image:

Molluscum contagiosum

General

  • Etiology: caused by molluscum contagiosum virus.

Microscopic

Features:

  • A suprabasilar epidermal lesion consisting of "molluscum bodies", i.e. molluscum bodies are found above the stratum basale.[71]
  • Molluscum bodies - key feature:
    • Large cells with abundant granular eosinophilic cytoplasm.
    • Small peripheral nucleus.

Notes:

  • Molluscum bodies very vaguely resemble signet ring cells -- but:
    • Cytoplasm eosinophilic and granular.
    • Nucleus usually smaller than in signet ring cell.
    • Molluscum bodies are only the epidermis - an uncommon place to find SRCs without finding them elsewhere.
  • The granular eosinophilic cytoplasm represents accumulated virons.

DDx:

  • Nothing really - it is very distinctive.

Image(s):

Superficial dermal infiltrates

Discussed in detail by Alsaad and Ghazarian.[72]

Dermal perivascular lymphoeosinophilic infiltration

  • Abbreviated DPLI.

Microscopic appearance is just what it is called:

  • Lymphocytes and eosinophils around the vessels in the superficial dermis.

DDx:[72]

Notes:

  • May superficially resemble cutaneous lymphoma.[73]

Images:

Congenital dermal melanocytosis

  • AKA Mongolian spots.
  • Classically seen in asian children.

Gross:

  • Brown or blue-grey patch in the lumbosacral area.

Mastocytosis

General

Classification:[74]

  1. Cutaneous (only) - usually children.
    • Urticaria pigmentosa.
    • Others.
  2. Systemic - usually adults.
    • Indolent subvariant.
    • Aggressive subvariant.
    • Leukemic subvariant.

Microscopic

Features:[75]

  • Cells in the superficial/mid dermis that are:
    • Lymphocyte-like with more cytoplasm that is granular.
      • Cells may have spindled or stellate morphology.
      • Tend to be more abundant around vessels.
  • +/-Eosinophils (common).
  • +/-Edema - often prominent; gives cells a white halo.

Notes:

  • Lymphocyte vs. mast cell:
    • Lymphocytes = round; mast cells = ovoid.

Images:

Stains

IHC

  • CD117 +ve.
  • Tryptase +ve.[76]

Ichthyosis

General

  • Comes in different flavours.
  • Usu. inherited... thus a pediatric condition.

Gross

  • Fish scale-like appearance.

Image:

Microscopic

Features:[75]

  • Thick stratum corneum without basket-weave pattern.

Palmar fibromatosis

  • AKA Dupuytren's contracture.
  • AKA Dupuytren disease.

General

Clinical:[77]

  • Usually older - 60s or 70s (years old).
  • Male > female.
  • Associated with:
    • Alcohol abuse.
  • May be familial.

Gross

  • Ring finger - classic location.[citation needed]
  • Nodular.
  • Poorly demarcated.

Image:

Microscopic

Features:[78][79]

  • Poorly demarcated, usu. multiple lesions/multiple nodules.
  • Composed of bland spindle cells in dense collagen.
    • Pale grey cytoplasm (moderate quantity).
    • Pale ovoid nuclei with small round nucleoli.
  • Giant cells - rare.

Note:

  • No nuclear atypia.
  • Mitotic figures - rarely present, none atypical.
  • May see Pacinian corpuscle (AKA lamellar corpuscle) as an incidental finding.

DDx:[79]

Images:

IHC

  • Beta-catenin +ve (cytoplasmic & nuclear).[81]

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PALMAR FASCIA, LEFT, FASCIECTOMY:
- PALMAR FIBROMATOSIS.
Micro

The sections show multiple poorly-demarcated nodules composed of bland spindle cells with moderate pale grey cytoplasm and pale ellipsoid nuclei with small round nucleoli. The poorly-demarcated nodules are completely surrounded by dense collagen. Calcification is not present. There is no nuclear atypia or necrosis. Mitotic activity is not identified. Benign fibroadipose tissue is present.

Missed fibromatosis

PALMAR FASCIA, LEFT, FASCIECTOMY:
- PALMAR FASCIA WITHIN NORMAL LIMITS AND BENIGN FIBROADIPOSE TISSUE -- IN AN
  INDIVIDUAL WITH A CLINICAL HISTORY OF PALMAR FIBROMATOSIS.
- NEGATIVE FOR MALIGNANCY.
Micro

The sections show dense collagen (tendon) without an apparent pathology. Calcification is not present. There is no nuclear atypia or necrosis. Mitotic activity is not identified. Benign fibroadipose tissue is present. Lamellar corpuscles are present. The tissue was submitted in toto and levels were cut.

Straight
PALMAR FASCIA, RIGHT, FASCIECTOMY:
- PALMAR FASCIA WITHIN NORMAL LIMITS.
- NEGATIVE FOR FIBROMATOSIS.

COMMENT:
The tissue was submitted in toto and levels were cut.
Micro

The sections show dense collagen (tendon) without an apparent pathology. Calcification is not present. There is no nuclear atypia or necrosis. Mitotic activity is not identified. Benign fibroadipose tissue is present. Lamellar corpuscles are present.

Angiomyoma

General

  • Benign.
  • Female > male.[82]

Microscopic

Features:

  • Well-circumscribed lesion with fascicular architecture.
  • Spindle cells/epithelioid cell with moderate eosinophilic (pink) cytoplasm.
  • Thick-walled blood vessels. (???)

Images:

Angiokeratoma

General

Notes:

Microscopic

Features:[83]

  • Ectatic superficial dermal vessels.
  • Overlying hyperkeratosis (thick stratum corneum).

Others features:[citation needed]

  • Irregular acanthosis.
  • Longer rete ridges.

DDx:

Images:

Inverted follicular keratosis

  • Abbreviated IFK.[84]

General

  • Benign skin lesion.
  • Central face - middle age.[85]
  • Uncommon.
  • May be considered a variant of seborrheic keratosis that is predominantly endophytic.[30]

Clinical DDx:[85][86]

Microscopic

Features:[85]

  • Keratinocyte of cytologically benign proliferation.
  • "Squamous eddies" (whorls of keratin).
  • Coarse keratohyaline granules.

DDx:

Images:

Sign out

SKIN LESION, FACE, BIOPSY:
- INVERTED FOLLICULAR KERATOSIS.

Focal cutaneous mucinosis

General

  • Benign.
  • May be associated with systemic disease.[87]

Microscopic

Features:

  • Light blue whispy material in the dermis - key feature.

DDx:

Panniculitis

This is dealt with in the panniculitis article.

DDx for panniculitis:

Rare

Necrotizing fasciitis

Not to be confused with nodular fasciitis.
  • AKA flesh-eating disease.

General

  • High mortality.
  • May be diagnosed at frozen section.[88]
  • Classically associated with Group A streptococcus.

Treatment:

  • Operative debridement.

Microscopic

Features:

  • Necrosis of fascia - key feature.[89]
    • PMNs and necrotic debris (amorphous grey or pink material).

Note:

  • Fat lobules between septae may be normal.

DDx:

Images:

Porokeratosis

General

  • Genetic.
  • Several subtypes.

Notes:

  • Not the same as punctate porokeratotic keratoderma.[90]

Microscopic

Features:

  • Cornoid lamella (pathognomonic) - key feature:
    • Compact keratosis over a hair follicle.
  • +/-Rete ridge loss.

Images:

Nevus sebaceous

  • AKA nevus sebaceous of Jadassohn.

General

  • Congenital.
  • Face or scalp.

Microscopic

Features:

  • Abundant sebaceous glands.

Image:

Nevus lipomatosus superficialis

  • Abbreviated NLS.
  • AKA nevus lipomatosus cutaneous superficialis, abbreviated NLCS.
  • AKA nevus lipomatosus.[91]

General

Clinically separated into:[94]

  • Solitary - one lesion.
  • Multiple - more than one lesion.

Gross

Features:[92]

  • Pedunculated lesion.
  • Soft.
  • Usually lower trunk or gluteal region.[95]

Image:

Microscopic

Features:[96]

DDx:

Images:

Sign out

SKIN LESION ("SKIN TAG"), LEFT HIP, EXCISION:
- NEVUS LIPOMATOSUS SUPERFICIALIS.

Bullous disease

Cysts

See also

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