Pages From Pathology Week 5 p15-28

7/30/2019 Pages From Pathology Week 5 p15-28

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Chronic Lupus Erythematosus (aka discoid LE)

Discoid Lupus much more skin limitied. Very rarelyprogresses to systemic disease. See post-inflammatoryhypopigmentation.

Above: Mucin production collagenbundles here are separated by mucin

Test q: Histologic features of Lupus Erythematosus include: interface vacuoles and focal epidermal atrophy

Interface Dermatitis w/lichenoid (band-like) inflammation

Lichen Planus Chronic but self-limiting disease Multiple, symmetric lesions on extremities (especially

wrists)

Pruritic, purple, polygonal papules Oral mucosal involvement common (see right)

oral lesions have lacy, white pattern. Dense band-like lymphocytic infiltrate hugs epidermis Epidermal changes:

Hyperkeratosis Wedge-shaped hypergranulosis

Saw-toothed basal layer

Thickening of granular layer

Individual necrotickeratinocytes (circled)

Test q:A 40y/o woman goes to her dentist who notes that she has 0.2 to 1.5cm scattered,white, reticulated areas on the buccal mucosa. The woman says that these lesions havebeen present for one year. She also has some 0.3-cm purple, pruritic papules on each elbow.

A biopsy specimen of a skin lesion shows a bandlike infiltrate of lymphocytes at the dermal-epidermal junction as well as degeneration of basal keratinocytes. The most likely diagnosisis: Lichen planus.

Figure: Damage tobasal layer of epidermis can see vacuoleswithin basalkeratinocytes as a resultof damage.Can see dramaticallythickened basementmembrane here.

Perivascular lymphocytes

Above: Lichen Planus Interface dermatitis,

so damage to the basal layer of keratinocytes due to attack by lymphocytes. Circle necrotic keratinocytes. See band-like infiltrateof lymphocytes. Thickening of epidermis increase in granular layer.


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Bullous Dermatosis: Bullae and vesicles are primary clinical manifestations Bullae = large blisters; vesicles = tiny blisters Diagnostic categories based on level of split in epidermis

Subcorneal (beneath SC), intraepidermal or subepidermal Diseases caused by Ig deposition i.e. autoimmune diseases

Pemphigus Vulgaris: Presents in the 4th-6th decades, M=F Autoimmune blistering disease

IgG against desmoglein 3 in desmosomes Desmosomes hold epithelial cells together loss of cell

adhesion within the epidermis Test q: In pemphigus vulgaris, IgG autoantibodies are directed against:

Desmosomes REPEATED x2

Variants: pemphigus vegetans and foliaceus Flaccid, fragile bullae Oral mucosa involvement (typically ruptures before you see it

clinically)

Above: In the base of the blister is one layer of the Above: Pemphigus Vulgaris Immunofluoresenceepidermis. The rest makes up the roof of the blister.

Bullous Pemphigoid: Generally affects elderly patients Bullae on extremities, intertriginous areas, abdomen and oral mucosa (1/3pts) Autoimmune disease

IgG against hemidesmosome proteins Hemidesmosomes bind epidermis to basement membrane

Subepidermal blistering process blisters have more strength because ofmore material in the roof. Blisters are tense and stay intact longer (ascompared to fragile blisters of PV, described above). Tense bullae

Pemphigus vulgaris. Intraepidermal, suprabasilar blister

with tombstone basal layer Mixed dermal inflammatoryinfiltrate, often with eosinophils Intraepidermal: looks like thisblister is under the whole epidermis,but note the one layer of cells leftunderneath. The rest makes up theroof of the blister.


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Above: Bullous Pemphigoid. Subepidermal Above: Blister contains edema Bullous Pemphigoid: Immunofluorescence.blister without tombstones or acantholysis. fluid and eosinophils. IgG bound to hemidesmosome located inNo epidermis in the base of the blister. basement membrane.

Dermatitis Herpetiformis Vesicular dermatosis not bullous 3

rdand 4

thdecades, M>F

Pruritic, burning vesicles, especially on extensor surfaces of extremities Strongly associated with celiac disease everyone w/DH either has Celiac disease or sub-clinical Celiac disease. Responds to gluten free diet (like celiac) IgA deposited in dermal papillae of skin

Incredibly itchy patients will scratch blisters DH Histologic Features- Subepidermal vesicles Neutrophilic microabscessbefore you ever see them in clinic.

DH Immunofluorescence.IgA deposits recruit in neutrophils.

Infections and Infestations:

Dermatophytosis: AKA: Tinea (capitis scalp, corporis body, barbae beard area, cruris groin, pedis foot), ringworm Dermatophytes infect outer keratin layer of skin

Test q:A 35y/o female presents w/small vesicles on extremeties. The rash is

extremely pruritic. She also has been diagnosed w/celiac disease. Diagnosis:Dermatitis herpetiformis REPEATED x2

Test q:A person w/dermatitis herpetiformis should avoid what food substance: gluten.

Test q:A 35y/o man has had an outbreak of pruritic lesions over the extensor surface

of the elbows and knees during the past month/ He has a history of malabsorptionthat requires him to eat a special diet, but he has had no previous skin problems. Onphys exam, the lesions are 0.4-0.7cm vesicles. A 3mm punch biopsy of one of the

lesions over the elbow is performed. Microscopic exam of the biopsy specimen showsaccumulation of neutrophils at the tips of dermal papillae and formation of smallblisters due to separation at the dermo-epidermal junction. Immunofluorescence

studies performed on this specimen show granular deposits of IgA localized to tips ofdermal papillae. Lab studies show serum anti-gliadin antibodies. Which of the

following is the most likely diagnosis? Dermatitis herpetiformis.

Test q: Neutrophilic microabscesses and fluffy IgA deposits on basement membraneanchoring febrils are characteristic of: Dermatitis herpetiformis.


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Dermatophytosis

Above: Tinea corporis expanding, annular,erythematous plaque w/elevated, scaly border.Annular because dermatophytes start in asmall area and grow outwards = ring.

Dermatophyte Infection: Histologic Features: Hyperkeratosis Parakeratosis Neutrophils in keratin Hyphae in keratin

Difficult to see on H&E Organisms grow in the stratum corneum do notgo down into epidermis at all.

Test q: Neutrophils in the stratum corneum are a commonfeature in: Psoriasis and dermatophytosis.

Test q:A 25y/o male joins a gym and works out regularly. Hedevelops a pruritic rash on his feet which shows white centersw/a red, scaly border. A diagnostic stain would be: PAS stain.

Warts (verrucae): Benign neoplasms caused by human papillomavirus (HPV)

>60 subtypes Certain subsets associated w/squamous cell carcinoma

Common Common wart (verruca vulgaris) Plantar/palmar wart - caused by diff HPV subtypes Genital wart (condyloma acuminatum) Flat wart

Occur at any age Self-limited

Verruca Vulgaris: Histologic Features Histology similar across all

the different subtypes. Papillomatosis projections

of epidermis

Acanthosis thickening ofepidermis Tortuous vessels within

papillae

KEY FEATURE = Koilocytes.Have clear area withincytoplasm due to viralparticles present.

PAS staindemonstratinghyphae

Shows fungal hyphae/spores veryclearly but only in s. corneum.


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Molluscum Contagiosum: Common especially in children Dome-shaped papules with a central keratin-filled crater Easily spread through contact DNA poxvirus Histologic Features: large, bright pink viralinclusions. Molluscum body: eosinophilic cytoplasmicinclusion in upper layers of epidermis.

Test q: A 35y/o man has noted a bump on his upper trunk for the past 6wk. On phys exam, there is a solitary 0.4cm flesh-colored nodule on the uppertrunk. The dome-shaped lesion is umbilicated, and a curd-like material can be expressed from the center. This material is smeared on a slide, andGiemsa stain shows many pink, homogenous, cytoplasmic inclusions. The lesion regresses over the next 2mo. Which of the following infectious agents

most likely produced this lesion? Molluscum contagiosum

Impetigo: Common superficial infection Staphylococcus or streptococcus Exposed surfaces Characteristic honey-colored crust Histologic Feature: Subcorneal pustule A lot of neutrophils in the stratum corneum can see gram positive cocci here.

Infestations: Scabies (Sarcoptes scabiei)

Above: The scabies mite. Scabies feces. Linear burrows.

Scabies like to burrow underneath the stratum corneum. Find them on the penis and web spaces of the fingers.

Figure: Scabies organismunderneath the stratum corneum.

Scabies feces underneath?


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Herpesvirus infections: HSV-1

Cold sores, fever blisters Oral infection most common Cutaneous blistering eruption, usually linear

HSV-2 Genital herpes

VZV varicella zoster Chicken pox

Figure:Herpes infects keratinocytes seemultinucleated cells (circled onehas 10-15 nuclei)

Figure: Germline mutation: born w/one mutated allele and one wild-type allele. During life, youll have hits from viruses, chemicals, otherenvironmental factors and you will lose the wildtype allele. Called LOH(loss of heterozygosity) uncontrolled proliferation.

Pages From Pathology Week 5 p15-28

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