Skin Flashcards
Vitiligo: Typically spared areas (2).
Scalp and eyelashes.
Dermatophytosis: The “sandwich sign”.
Fungal hyphae between the parakeratotic layer and the overlying orthokeratosis.
Urticarial vasculitis:
A. Clinical features (3).
B. Duration of urticaria.
A. Recurrent urticaria, arthralgia, abdominal pain.
B. More than 24 hours.
Urticarial vasculitis: Histology.
Leukocytoclastic vasculitis without significant fibrin in vascular walls.
Urticarial vasculitis: Useful adjunctive laboratory tests (2).
Complement studies (CH50, C1q-binding assays).
DFA: May show vascular deposits of complement, immunoglobulins, or fibrin.
Urticarial vasculitis: Clinical associations (3).
Infectious hepatitis.
Infectious mononucleosis.
Autoimmune diseases.
Telangiectasia macularis eruptiva perstans: Histologic differences from urticaria (2).
Mast cells rather than eosinophils.
No significant dermal edema.
Lichen planus: Microbiological association.
Hepatitis C.
Lichen planus: Anatomic predilection of lesions (3).
Flexor surfaces.
Lower back.
Glans penis.
Oral lichen planus: Histologic differences from lichen planus of skin (3).
Parakeratosis.
Less epidermal hyperplasia.
Frequent ulceration.
Lichenoid drug eruption: Histologic differences from lichen planus (2).
Parakeratosis.
Eosinophils (sometimes).
Lichen striatus:
A. Age group.
B. Clinical appearance.
A. Children.
B. Unilateral eruption on extremities, trunk, neck.
Lichen striatus: Histologic differences from lichen planus.
Inflammatory infiltrate deep in reticular dermis around hair follicles and sweat glands.
Lichen nitidus:
A. Age group.
B. Clinical appearance.
A. Children.
B. Small, flat-topped papules.
Lichen nitidus: Histologic differences from lichen planus (4).
“Ball-in-claw” infiltrate.
Focal parakeratosis.
Epidermal atrophy.
Many histiocytes.
Lichen planopilaris vs. alopecia areata: Histology (2).
Lichen planopilaris: Infiltrate at base of follicular bulb; scarring.
Alopecia areata: Infiltrate along infundibulum; usually no scarring.
Erythema multiforme:
A. Infectious cause.
B. Pharmacological cause.
A. HSV.
B. Sulfonamides.
Toxic epidermal necrolysis: Drugs that cause it (3).
Sulfonamides.
β-lactam antibiotics.
NSAIDs.
Erythema multiforme: Histological feature of late lesion.
Dermal melanophages.
Erythema multiforme: Immunofluorescence.
IgM and C3 in the walls of superficial dermal vessels.
Angioedema: Histology.
Extension of the edema into the subcutis.
Acute GVHD:
A. Timing.
B. Clinical triad.
A. Within 3 months after transplant.
B. Rash, diarrhea, liver dysfunction.
Acute GVHD: Grade I.
Vacuolar change in basement membrane.
Acute GVHD: Grade II.
Necrotic keratinocytes, satellite necrosis.
Acute GVHD: Grade III.
More widespread necrosis of keratinocytes; separation at dermoepidermal junction.
Acute GVHD: Grade IV.
Full-thickness necrosis and loss of epidermis.
Chronic GVHD: Early phase.
Lichenoid, resembling lichen planus; satellite necrosis may be seen.
Chronic GVHD: Late phase.
Sclerosis, resembling scleroderma, but with epidermal atrophy.
Discoid lupus: Histology (4).
Hyperkeratosis with follicular plugging.
Epidermal atrophy.
Basal vacuolar change.
Thickened basement membrane.
Verrucous lesions of lupus: Histology (2).
Epidermal hyperplasia, papillomatosis.
Tumid lupus: Histology.
Superficial and deep infiltrate that spares epidermis; increased dermal mucin.
Lupus panniculitis: Histology.
Lobular panniculitis with hyaline fat necrosis.
Subacute and neonatal lupus: Histologic differences from discoid lupus (3).
Subacute and neonatal lupus show
− Prominent changes at the D-E junction.
− Less hyperkeratosis.
− Less inflammation.
Cutaneous lupus: Immunofluorescence.
Continuous granular deposition of IgG, IgM, and C3 at the dermoepidermal junction.
Cutaneous lupus: How to distinguish from polymorphous light eruption.
PLE: More papillary dermal edema than tumid lupus; no dermal mucin.
Cutaneous lupus: Lymphoma that may be in the differential diagnosis.
Subcutaneous panniculitis-like T-cell lymphoma must be distinguished from lupus panniculitis.
Lupus band test.
Direct immunofluorescence . . .
Discoid lupus: Positive in lesional skin only.
Systemic lupus: Positive in “normal” skin as well.
Anatomic location:
A. Heliotrope rash.
B. Gottron’s papules.
A. Eyelids.
B. Knuckles, knees, elbows.
Dermatomyositis may resemble which type of cutaneous lupus histologically?
Subacute lupus.
Dermatomyositis: Age group.
Children.
Adults aged 45-65.
Dermatomyositis: Immunofluorescence.
C5b-C9 around blood vessels.
Dermatomyositis: Lupus-band test.
Negative.
Id reaction:
A. Synonym.
B. Leading cause.
A. Autoeczematization.
B. Remote dermatophytosis.
Spongiotic dermatitis: Changes that indicate chronicity (3).
Epidermal hyperplasia.
Hyperkeratosis.
Papillary dermal fibrosis.
Seborrheic dermatitis: Histology (2).
Mild spongiosis.
Parakeratosis at follicular ostia.
Pityriasis rosea: Histology (3).
Focal spongiosis.
Mounds of parakeratosis.
Extravasated erythrocytes.
Eosinophilic spongiosis: Differential diagnosis (4).
Allergic contact dermatitis.
Bullous pemphigoid, early.
Pemphigus, early.
Incontinentia pigmenti.
Incontinentia pigmenti:
A. Inheritance.
B. Epidemiology.
A. X-linked dominant.
B. Mostly females.
Histology of incontinentia pigmenti: Vesicular stage (3).
Eosinophilic spongiosis.
Single dyskeratotic keratinocytes.
Whorls of squamous cells.
Histology of incontinentia pigmenti: Verrucous stage (4).
Hyperkeratosis.
Papillomatosis.
Dyskeratosis.
Occasional eosinophils.
Incontinentia pigmenti: Gene and its location.
IKBKG (a.k.a. NEMO) on Xp28.
Histology of incontinentia pigmenti:
A. Hyperpigmented stage.
B. Hypopigmented stage (3).
A. Many melanophages in the upper dermis.
B. Epidermal atrophy, loss of melanin, loss of adnexa.
Psoriasis: Anatomic sites (3).
Scalp.
Lumbosacral skin.
Extensor surfaces.
Psoriasis: Eponymous collections of neutrophils.
Microabscesses of Munro (stratum corneum).
Spongiform pustules of Kogoj (stratum spinosum).
Psoriasis: Appearance of granular layer.
Hypogranulosis underlying areas of parakeratosis.
Guttate psoriasis: Histology.
Less epidermal hyperplasia than in classic psoriasis.
Psoriatic arthritis:
A. Incidence.
B. Affected joints.
A. 15% of patients with psoriasis.
B. The DIP joints.
Psoriasis: Risk factor for severe disease.
AIDS.
Pityriasis rubra pilaris: Clinical appearance of fully developed disease.
Orange-red scaly plaques containing islands of normal skin.
Pityriasis rubra pilaris:
A. Stratum corneum.
B. Follicles.
A. Horizontal and vertical alternation of orthokeratosis and parakeratosis.
B. Dilatation of infundibula; follicular plugging.
Pityriasis rubra pilaris: Histological differences from psoriasis (4).
Thick suprapapillary plates.
Short, thick rete pegs.
Hypergranulosis.
No neutrophils in the parakeratotic layer.
Polymorphous light eruption: Typical patient and season.
Young woman, summer.
Polymorphous light eruption: Anatomic distribution.
Upper chest, extensor surfaces of arms.
Polymorphous light eruption: Histology (3).
Normal or slightly spongiotic epidermis.
Marked papillary dermal edema.
Superficial and deep perivascular lymphocytes.
Pityriasis lichenoides: Histology (5).
Parakeratosis and scale-crust.
Spongiosis and necrotic keratinocytes.
Basal vacuolar change.
Papillary dermal edema with extravasated RBCs.
Lymphocytes obscure the DEJ and form superficial and deep perivascular infiltrates.
Pityriasis lichenoides et varioliformis acuta, ulceronecrotic variant: Histology.
There may be lymphocytic vasculitis.
Pityriasis lichenoides: Distinction from lymphomatoid papulosis.
The latter has atypical, CD30-positive lymphocytes.
Fixed drug eruption: Histology (4).
Basal vacuolar change that may progress into bullae.
Necrotic keratinocytes.
Superficial and deep perivascular lymphocytes, neutrophils, eosinophils; sometimes also lichenoid.
Melanophages in the upper dermis.
Fixed drug eruption: Distinction from erythema multiforme.
Not always possible, but fixed drug eruption is more likely when there is a deeper infiltrate that includes neutrophils and eosinophils.
Fixed drug eruption: Instigators (3).
Sulfa drugs.
Aspirin.
Phenolphthalein.
Lymphomatoid papulosis: Infiltrate.
Wedge-shaped and consists of neutrophils, eosinophils, plasma cells, and atypical lymphocytes.
Lymphomatoid papulosis: Morphology of atypical lymphocytes.
May resemble the cells of
Mycosis fungoides (cerebriform nuclei).
Hodgkin’s lymphoma (Reed-Sternberg cells)
Anaplastic large-cell lymphoma.
Lymphomatoid papulosis: Feared outcome.
Progression to anaplastic large-cell lymphoma.
Secondary syphilis: Histology (5).
Parakeratosis with neutrophils.
Psoriasiform epidermal hyperplasia.
Focal spongiosis.
Basal vacuolar change.
Lichenoid mononuclear inflammation.
Lues maligna: Histology.
Thrombotic endarteritis of deep dermal vessels, leading to ischemic necrosis and ulceration.
Sweet’s syndrome: Clinical triad.
Fever.
Rash.
Leukocytosis.
Sweet’s syndrome: Anatomic locations of rash.
Face.
Trunk.
Extremities.
Sweet’s syndrome: Association (3).
AML or other myeloproliferative neoplasm.
Inflammatory disease.
Solid tumor.
Sweet’s syndrome: Histology (3).
Dense infiltrate of neutrophils with nuclear dust but without leukocytoclastic vasculitis.
Papillary dermal edema.
Dilated blood vessels with plump endothelial cells and extravasated RBCs.
Pyoderma gangrenosum: Associations (4).
Connective-tissue disease.
Hematopoietic malignancy.
Inflammatory bowel disease.
Liver disease.
Pyoderma gangrenosum: Inflammation.
Center of lesion: Neutrophils.
Border: Mixed infiltrate.
Periphery: Mononuclear.
Pyoderma gangrenosum: Vasculitis.
Secondary vasculitis may arise in the necrotic, neutrophil-rich center.
Pyoderma gangrenosum in Crohn’s disease.
May contain granulomas.
Eosinophilic cellulitis: Clinical presentation.
Red patches evolve into painful plaques; recurrent.
Eosinophilic cellulitis: Association with peripheral eosinophilia.
Seen in at least half of cases.
Eosinophilic cellulitis: Histology (3).
Dense, diffuse dermal infiltrate of eosinophils, sometimes with
− Flame figures.
− Necrobiosis with palisades of histiocytes.
Eosinophilic cellulitis: Possible causes (5).
Insect bites.
Parasites.
Infections.
MPNs.
Drugs.
Scabies: Name of mite.
Sarcoptes scabei.
Scabies: Most common sites of burrows (3).
Webs between fingers.
Palms.
Male genitals.
Xanthogranuloma: How many are congenital?
About 20%.
Xanthogranuloma: Constituent cells.
Histiocytes.
Touton giant cells.
Neutrophils, eosinophils, lymphocytes.
Xanthogranuloma: Immunohistochemical distinction from Langerhans’ cell histiocytosis.
Langerhans’ cells express CD1a, S100, and langerin.
Reticulohistiocytosis: Clinical forms.
Localized: Limited to skin.
Systemic: Involves skin, heart, bone, joints, lymph nodes.
Systemic reticulohistiocytosis: Associations (3).
Hyperlipidemia.
Internal malignancies.
Autoimmune disease.
Reticulohistiocytoma: Morphology of defining cell.
Epithelioid histiocyte with abundant, pale-pink, glassy cytoplasm.
Granuloma annulare: Typical anatomic sites.
Dorsa of hands and feet, knees, ankles, elbows.
Granuloma annulare: Distribution of histiocytes.
Palisaded, interstitial, or a combination of both.
Granuloma annulare: Histological distinction from rheumatoid nodule.
Rheumatoid nodule:
- Necrobiosis is more eosinophilic and sometimes fibrinoid; no mucin.
- Subcutaneous location.
Granuloma annulare in children.
May be subcutaneous and hence difficult to distinguish from rheumatoid nodule.
Rheumatoid nodule: Anatomic sites (2).
PIP joints, MCP joints.
Necrobiosis lipoidica: Classic anatomic site.
Shins.
Necrobiosis lipoidica: Appearance of necrobiosis.
Basophilic degeneration of collagen.
Necrobiosis lipoidica: Relevance to diabetes (2).
Occurs in less than 1% of diabetics.
Occurs at a later age in diabetics than in non-diabetics.
Necrobiotic xanthogranuloma:
A. Clinical association.
B. Typical anatomic location.
A. Paraproteinemia.
B. Periorbital skin.
Necrobiotic xanthogranuloma: Histology (3).
Foam cells, Touton giant cells, lymphocytes.
Intervening zones of necrobiosis.
Lymphoid follicles sometimes.
Lupus pernio:
A. Site of lesions.
B. Clinical significance.
A. Central face.
B. Increased risk of pulmonary sarcoidosis.
Löfgren’s syndrome: Clinical triad.
Hilar adenopathy, acute polyarthritis, erythema nodosum.
A variant presentation of sarcoidosis.
Sarcoidosis: Appearance of granulomas.
Noncaseating; minimal peripheral lymphocytic infiltrate.
Sarcoidosis: Appearance of panniculitis.
Lobular pattern; noncaseating granulomas.
Foreign substances that can cause sarcoidal granulomas (3).
Silica.
Beryllium.
Zirconium.
Inflammatory infiltrate of leprosy:
A. Tuberculoid.
B. Lepromatous.
C. Borderline.
A. Granulomas.
B. Foam cells; few lymphocytes.
C. Foam cells and epithelioid histiocytes in poorly formed granulomas; many lymphocytes.
Leprosy: Where to find organisms.
Abundant in lepromatous leprosy; few in tuberculoid leprosy.
Found in histiocytes, nerves, arrectores pilorum.
Histoid leprosy.
Histologically resembles a histiocytoma but is full of acid-fast bacilli.
Lupus vulgaris: Etiologies (2).
Hematogenous spread to skin from reactivated pulmonary focus of TB.
Lymphatic spread to skin from cervical lymph nodes.
Lupus vulgaris:
A. Anatomic site.
B. Clinical course.
A. Central face.
B. Peripheral extension with atrophy and occasional ulceration.
Lupus vulgaris: Histology (3).
Tuberculoid granulomas with little or no caseation.
In older lesions, fibrosis replaces granulomas.
Epidermis may be atrophic, ulcerated, or hyperplastic.
Lupus vulgaris: Demonstration of bacilli.
Special stains rarely help.
PCR is better.
Lupus vulgaris: Complication.
Development of SCC or BCC.
Deep mycoses: Typical histology.
Pseudoepitheliomatous hyperplasia with extensive dermal suppurative and granulomatous inflammation.
Deep mycoses: Appearance of panniculitis.
Lobular; suppurative and granulomatous.
Blastomycosis: Histology of spores (3).
8-15 μm, thick-walled, broad-based budding.
Paracoccidiomycosis: Histology of spores (2).
6-20 μm, narrow-based budding.
Chromoblastomycosis: Histology of spores (3).
6-12 μm, thick-walled, dark-brown and in clusters (“copper pennies”).
Cryptococcus: Histology of spores.
2-4 μm (4-12 μm with capsule), narrow-based budding.
Histoplasmosis: Histology of spores.
2-4 μm, clear halo.
Sporotrichosis: Histology of spores.
4-6 μm, round or oval.
Pseudoepitheliomatous hyperplasia with suppurative and granulomatous inflammation: Differential diagnosis (3).
Deep mycoses.
Atypical mycobacterial infections.
Halogenodermas.
Cryptococcus: Alternative histology.
Xanthomatous infiltrate, especially in the immunocompromised.
Tuberculoid leprosy: Appearance of granulomas.
Elongated, surrounded by lymphocytes, arranged along neurovascular bundles.
Cutaneous leishmaniasis: Causes (3).
Old World: L. tropica.
New World: L. brasiliensis, L. mexicana.
Cutaneous leishmaniasis: Detection of parasites in a biopsy (2).
More likely to be seen in early lesions.
Giemsa stain can help.
Cutaneous leishmaniasis: Histology of late lesion.
Tuberculoid granulomas and lymphocytes.
Parasites may be undetectable.
Rhinoscleroma: Classic cell.
Mikulicz cell: Large histiocyte.
Granuloma inguinale:
A. Cause.
B. Inflammatory infiltrate.
C. Classic histologic finding.
A. Calymmatobacterium granulomatis.
B. Histiocytes and neutrophils.
C. Donovan body: Encapsulated, round to oval, 2-3 μm.
Leukocytoclastic vasculitis: Typically affected vessel in the skin.
Superficial dermal postcapillary venule.
Leukocytoclastic vasculitis: Bacterial cause.
Neisseria meningitidis.
Leukocytoclastic vasculitis: Immunofluorescence (2).
Most cases: IgM, C3, and fibrinogen around dermal vessels.
Henoch-Schönlein purpura: IgA.
Leukocytoclastic vasculitis: Chronic forms (2).
Erythema elevatum diutinum.
Granuloma faciale.
Livedo vasculitis: Anatomic location.
Lower legs.
Livedo vasculitis: Histology.
Fibrinoid matter in vessel walls leads to occlusion and ulceration.
Usually little inflammation.