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84 Cards in this Set

  • Front
  • Back
Melanocytic nevus, junctional type. A, In clinical appearance, lesions are small, relatively flat, symmetric, and uniform. B, On histologic examination, junctional nevi are characterized by rounded nests of nevus cells originating at the tips of rete ridges along the dermoepidermal junction.
Melanocytic nevus, compound type. In contrast to the junctional nevus, the compound nevus (A) is more raised and dome-shaped. The symmetry and uniform pigment distribution suggest a benign process. Histologically (B), compound nevi combine the features of junctional nevi (intraepidermal nevus cell nests) with nests and cords of nevus cells in the underlying dermis.
Dysplastic nevus. A, Numerous clinically atypical nevi on the back. B, One such lesion (inset A) has a compound nevus component (left side of scanning field) and an asymmetric junctional nevus component (right side of scanning field). The former correlates grossly with the more pigmented and raised central zone and the latter with the less pigmented, flat peripheral rim. C, An important feature is the presence of cytologic atypia (irregularly shaped, dark-staining nuclei). The dermis underlying the atypical cells characteristically shows linear, or lamellar, fibrosis.
Melanoma. A, Typically, lesions are irregular in contour and pigmentation. Macular areas correlate with the radial growth phase, while raised areas usually correspond to nodular aggregates of malignant cells in the vertical phase of growth. B, Radial growth phase, showing irregular nested and single-cell growth of melanoma cells within the epidermis and an underlying inflammatory response within the dermis. C, Vertical growth phase, demonstrating nodular aggregates of infiltrating cells. D, High-power view of melanoma cells. The inset shows a sentinel lymph node with a tiny cluster of melanoma cells (arrow) staining for the melanocytic marker HMB-45. Even small numbers of malignant cells in a draining lymph node may confer a worse prognosis.
Seborrheic keratosis. A well-demarcated coinlike pigmented lesion containing dark keratin-filled surface plugs (inset) is composed histologically of benign basaloid cells associated with prominent keratin-filled "horn" cysts, some of which communicate with the surface (pseudo-horn cysts).
Adnexal tumors. A, Multiple cylindromas (papules) on the forehead are composed of islands of (B) basaloid cells containing occasional ducts that fit together like pieces of a jigsaw puzzle. C, Perinasal papules and small nodules of trichoepithelioma are composed of (D) buds of basaloid cells that resemble primitive hair follicles.
Adnexal tumors. A, Sebaceous adenoma; inset demonstrates sebaceous differentiation. B, Pilomatrixoma; inset shows hair matrical differentiation with characteristic maturation to anucleate "ghost cells." C, Apocrine carcinoma (well-differentiated); inset shows apocrine differentiation with characteristic luminal decapitation secretion.
Actinic keratosis. A, Excessive scale formation in this lesion has produced a "cutaneous horn." B, Basal cell layer atypia (dysplasia) is associated with marked hyperkeratosis and parakeratosis. C, Progression to full-thickness nuclear atypia, with or without the presence of superficial epidermal maturation, heralds the development of squamous cell carcinoma in situ.
Invasive squamous cell carcinoma. A, Lesions are often nodular and ulcerated as seen in this scalp tumor. B, Tongues of atypical squamous epithelium have transgressed the basement membrane, invading deeply into the dermis. C, A magnified image reveals invasive tumor cells showing enlarged nuclei with angulated contours and prominent nucleoli.
Basal cell carcinoma. Pearly, telangiectatic nodules (A) are composed of nests of uniformly atypical basaloid cells within the dermis (B) that are often separated from the adjacent stroma by thin clefts (C), an artifact of sectioning.
Benign fibrous histiocytoma (dermatofibroma). This firm, tan papule on the leg (A) shows a localized proliferation of benign-appearing spindle cells within the dermis (B). C, Note the characteristic overlying epidermal hyperplasia and the tendency of fibroblasts to surround individual collagen bundles.
Dermatofibrosarcoma protuberans. A, The tumor usually presents as a flesh-colored to erythematous nodule, and has a fibrotic appearance on sectioning. B, C, Characteristic storiform cellularity is noted histologically, and the lesion often infiltrates the subcutis in a manner that resembles "Swiss cheese" to some afficianados.
Cutaneous T-cell lymphoma. A, Several ill-defined, erythematous, often scaling, and occasionally ulcerated plaques. B, Microscopically, there is an infiltrate of atypical lymphocytes that show a tendency to accumulate beneath the epidermal layer and to invade the epidermis.
Mastocytosis. A, Solitary mastocytoma in a 1-year-old child. B, By routine histology, numerous ovoid cells with uniform, centrally located nuclei are observed in the dermis. C, Giemsa staining reveals purple, "metachromatic" granules within the cytoplasm of the cells.
Ichthyosis. Note prominent fishlike scales (A) and compacted, thickened stratum corneum (B).
Urticaria. A, Erythematous, edematous, often circular plaques are characteristic. B, Histologically, there is superficial dermal edema, manifested by spaces between collagen bundles, and dilated lymphatic and blood-filled vascular spaces; the epithelium is normal.
Eczematous dermatitis. A, Acute allergic contact dermatitis, with numerous vesicles on erythematous skin due to antigen exposure (in this case, laundry detergent in clothing). B, Histologically, intercellular edema within the epidermis creates small, fluid-filled intraepidermal vesicles.
Erythema multiforme. A, The target-like clinical lesions consist of a central blister or zone of epidermal necrosis surrounded by macular erythema. B, Early lesions show lymphocytes collecting along the dermoepidermal junction where basal keratinocytes have begun to become vacuolated. With time, necrotic/apoptotic keratinocytes accumulate in the overlying epithelium.
Clinical evolution of psoriasis. A, Early and eruptive lesions may be dominated by signs of inflammation, including small pustules and erythema (left). Established, chronic lesions demonstrate erythema surmounted by characteristic silver-white scale (right). B, Histologically, established lesions demonstrate marked epidermal hyperplasia, parakeratotic scale, and neutrophils within the superficial epidermal layers.
Lichen planus. A, This flat-topped pink-purple, polygonal papule has a white lacelike pattern that is referred to as Wickham stria. B, Biopsy specimen demonstrating a bandlike infiltrate of lymphocytes at the dermoepidermal junction, hyperkeratosis, hypergranulosis and pointed rete ridges (sawtoothing) as a result of chronic basal cell layer injury.
Schematic representation of histologic levels of blister formation. A, In a subcorneal blister the stratum corneum forms the roof of the bulla (as in pemphigus foliaceus). B, In a suprabasal blister a portion of the epidermis, including the stratum corneum, forms the roof (as in pemphigus vulgaris). C, In a subepidermal blister the entire epidermis separates from the dermis (as in bullous pemphigoid).
Pemphigus vulgaris. A, Eroded plaques are formed on rupture of confluent, thin-roofed bullae, here affecting axillary skin. B, Suprabasal acantholysis results in an intraepidermal blister in which rounded (acantholytic) epidermal cells are identified (inset). C, Ulcerated blisters in the oral mucosa are also common as seen here on the mucosal portion of the lip.
Pemphigus foliaceus. A, The delicate, superficial (subcorneal) blisters are much less erosive than seen in pemphigus vulgaris. B, Subcorneal separation of the epithelium is seen.
Direct immunofluorescence of pemphigus. A, In pemphigus vulgaris there is deposition of immunoglobulin along the plasma membranes of epidermal keratinocytes in a reticular or fishnet-like pattern. Also note the early suprabasal separation due to loss of cell-to-cell adhesion (acantholysis). B, In pemphigus foliaceus the immunoglobulin deposits are more superficial.
Bullous pemphigoid. A, Clinical bullae result from basal cell layer vacuolization, producing tense, intact subepidermal blisters that are difficult to rupture given the roof formed by the full thickness of the epidermis. Ulceration results upon rupture as the blisters are subepidermal. B, Histopathology shows an intact blister with eosinophils, as well as lymphocytes and occasional neutrophils, that may be intimately associated with basal cell layer destruction and the creation of the subepidermal cleft.
A, Linear deposition of complement along the dermoepidermal junction in bullous pemphigoid; the pattern has been likened to ribbon candy. B, Bullous pemphigoid antigen is located in the lowermost portion of the basal cell cytoplasm in association with hemidesmosomes (HD), with blister formation affecting the lamina lucida (LL) of the basement membrane zone. AF, anchoring fibrils; LD, lamina densa
Dermatitis herpetiformis. A, The blisters are associated with basal cell layer injury initially caused by accumulation of neutrophils (microabscesses) at the tips of dermal papillae.
Dermatitis herpetiformis. B, Selective deposition of IgA autoantibody at the tips of dermal papillae is characteristic.
Dermatitis herpetiformis. C, Lesions consist of intact and eroded (usually scratched) erythematous blisters, often grouped (seen here on elbows and arms).
Epidermolysis bullosa. A, Junctional epidermolysis bullosa showing typical erosions in flexural creases. B, A noninflammatory subepidermal blister has formed at the level of the lamina lucida.
Porphyria. A noninflammatory blister is forming at the dermoepidermal junction; note the seemingly rigid dermal papillae at the base that contain the altered superficial vessels.
Acne. A, Inflammatory acne associated with erythematous papules and pustules. B, A hair shaft pierces the follicular epithelium, eliciting inflammation and fibrosis. C, Open comedone.
Verruca vulgaris. A, Multiple papules with rough pebble-like surfaces. B (low power) and C, (high power) histology of the lesions showing papillomatous epidermal hyperplasia and cytopathic alterations that include nuclear pallor and prominent keratohyaline granules. D, In situ hybridization demonstrating viral DNA within epidermal cells.
Molluscum contagiosum. A focus of verrucous epidermal hyperplasia contains numerous cells with ellipsoid cytoplasmic inclusions (molluscum bodies) within the stratum granulosum and stratum corneum.
Tinea. A, Characteristic plaque of tinea corporis. Routine histology (B) shows a mild eczematous (spongiotic) dermatitis and focal neutrophilic abscesses. A periodic acid-Schiff stain (inset) reveals deep red hyphae within the stratum corneum.
The extra-ocular muscles are greatly distended in this postmortem dissection of tissues from a patient with thyroid (Graves) ophthalmopathy. Note that the tendons of the muscles are spared involvement.
In idiopathic orbital inflammation (orbital inflammatory pseudotumor) the orbital fat is replaced by fibrosis. Note the chronic inflammation, accompanied in this case by eosinophils
Pagetoid spread of sebaceous carcinoma. Neoplastic cells with foamy cytoplasm are detected within the epidermis. Invasive sebaceous carcinoma was identified elsewhere in this biopsy sample.
A, B, Cystic compound nevus of the conjunctiva.
A, B, Cystic compound nevus of the conjunctiva.
C, D, Conjunctival malignant melanoma. In C, note the deflection of the beam of the slit lamp over the surface of the lesion, indicative of invasion.
C, D, Conjunctival malignant melanoma. In C, note the deflection of the beam of the slit lamp over the surface of the lesion, indicative of invasion.
C, D, Conjunctival malignant melanoma.
Normal corneal microarchitecture. The corneal tissue is stained by periodic acid-Schiff (PAS) to highlight basement membranes. The inset at the upper left is a high magnification of the anterior layers of the cornea: the epithelium (e), Bowman layer (b), and the stroma (s). A very thin PAS-positive basement membrane separates the epithelium from the Bowman layer. Note that the Bowman layer is acellular. The inset at the lower right is a high magnification of the PAS-positive Descemet membrane and the corneal endothelium. The "holes" in the stroma are artifactitious spaces between parallel collagenous stromal lamellae.
Chronic herpes simplex keratitis. The cornea is thin and scarred (note the increased number of fibroblast nuclei). Granulomatous reaction in the Descemet membrane, illustrated in this photomicrograph (arrows), is a histologic hallmark of chronic herpes simplex keratitis.
Keratoconus. The tissue section is stained by PAS to highlight the epithelial basement membrane (ebm), which is intact, the Bowman layer (bl), situated between the epithelial basement membrane, and the stroma (s). Following the Bowman layer from the right side of the photomicrograph toward the center, there is a discontinuity, diagnostic of keratoconus. The epithelial separation just to the left of the Bowman layer discontinuity resulted from an episode of corneal hydrops, caused by a break in the Descemet membrane (not shown).
Fuchs dystrophy. This tissue section is stained by PAS to highlight the Descemet membrane, which is thick. Numerous droplike excrescences-guttata-protrude downward from the Descemet membrane. Endothelial cell nuclei are not seen. Epithelial bullae, not shown in this micrograph, were present, reflecting corneal edema.
Sequelae of anterior segment inflammation. This eye was removed for complications of chronic corneal inflammation (not visible at this magnification). The exudate (e) present in the anterior chamber would have been visualized with a slit lamp as an optical "flare." The iris is adherent focally to the cornea, obstructing the trabecular meshwork (anterior synechia, arrow), and to the lens (posterior synechiae, arrowheads). An anterior subcapsular cataract (asc) has formed. The radial folds in the lens are artifacts.
Exogenous panophthalmitis. This eye was removed after a foreign body injury. Note the suppurative inflammation behind the lens that is drawn up to the right of the lens to the cornea, the site of the wound. The central portion of the vitreous humor was extracted surgically (by vitrectomy). Note the adhesions to the surface of the eye at the eight o'clock position, indicating that the intra-ocular inflammation has spread through the sclera into the orbit: panophthalmitis.
Sympathetic ophthalmia. The granulomatous inflammation depicted here was identified diffusely throughout the uvea. The uveal granulomas may contain melanin pigment and may be accompanied by eosinophils.
Uveal melanoma. A, Fundus photograph from an individual with a relatively flat pigmented lesion of the choroid near the optic disc.
Uveal melanoma. B, Fundus photograph of the same individual several years later; the tumor has grown and has ruptured through the Bruch membrane.
Uveal melanoma. C, Gross photograph of a choroidal melanoma that has ruptured the Bruch membrane. The overlying retina is detached.
Uveal melanoma D, Epithelioid melanoma cells associated with an adverse outcome.
Uveal melanoma. E, Patterns rich in laminin (PAS positive) surround aggregates of melanoma cells; these patterns form a "fluid-conducting meshwork" in uveal melanoma and are associated with an adverse outcome.
The retina in hypertension. A, The wall of the retinal arteriole (arrow) is thick. Note the exudate (e) in the retinal outer plexiform layer.
The retina in hypertension. B, The fundus in hypertension. The diameter of the arterioles is reduced, and the color of the blood column appears to be less saturated (copper wire-like). If the wall of the vessel were thicker still, the degree of red color would diminish such that the vessels might appear clinically to have a "silver-wire" appearance. In this fundus photograph, note that the vein is compressed where the sclerotic arteriole crosses over it.
Nerve fiber layer infarct. A "cotton-wool spot" is illustrated in the inset, adjacent to a flame-shaped (nerve fiber layer) hemorrhage. The histology of a cotton-wool spot-an infarct of the nerve fiber layer of the retina-is illustrated in the photomicrograph. A focal swelling of the nerve fiber layer is occupied by numerous red to pink cytoid bodies (arrowheads), bulbous ends of severed axons. Hemorrhage (arrows) surrounding the nerve fiber layer infarct as illustrated here is a variable and inconsistent finding.
The ciliary body in chronic diabetes mellitus, PAS stain. Note the massive thickening of the basement membrane of the ciliary body epithelia, reminiscent of changes in the mesangium of the renal glomerulus.
The retina in diabetes mellitus (see Fig. 29-16 for a schematic of retinal structure). A, A tangle of abnormal vessels lies just beneath the internal limiting membrane of the retina on the right half of the photomicrograph (between arrows). This is an example of intraretinal angiogenesis known as intraretinal microangiopathy (IRMA). Note the retinal hemorrhage in the outer plexiform layer in the left half. The ganglion cell layer and the nerve fiber layer-the axons of the ganglion cells-are absent. The rarefied space beneath internal limiting membrane to the left of the focus of IRMA consists largely of elements of retinal glial (Müller) cells. Absence of the ganglion cell and nerve fiber layers is a hallmark of glaucoma. The chronic diabetes mellitus in this individual was complicated by iris neovascularization and secondary angle-closure glaucoma (neovascular glaucoma).
The retina in diabetes mellitus B, In this section stained by PAS, the internal limiting membrane is indicated by the thick arrows and the posterior hyaloid of the vitreous by the thin arrow. In the potential space between these two landmarks, the vessels to the left of the thin arrow are invested with a fibrous-glial stroma and would appear ophthalmoscopically as a white neovascular membrane. The thin-walled vessel to the right of the thin arrow is not invested with connective tissue. A posterior vitreous detachment in an eye such as this might exert traction on these new vessels and precipitate a massive vitreous hemorrhage.
The retina in diabetes mellitus C, Ophthalmoscopic view of retinal neovascularization (known clinically as neovascularization "elsewhere" in contrast with neovascularization of the optic disc) creating a neovascular membrane.
The cherry-red spot in Tay-Sachs disease. A, Fundus photograph of the cherry-red spot in Tay-Sachs disease.
The cherry-red spot in Tay-Sachs disease. B, Photomicrograph of the macula in an individual with Tay-Sachs disease, stained with PAS to highlight the accumulation of ganglioside material in the retinal ganglion cells. The presence of ganglion cells filled with gangliosides outside the fovea blocks the transmission of the normal orange-red color of the choroid, but absence of ganglion cells within the fovea (to the right of the vertical bar) permits the normal orange-red color to be visualized, accounting for the so-called cherry-red spot.
Age-related macular degeneration. A neovascular membrane is positioned between the RPE and Bruch membrane (BM). Note the blue discoloration of Bruch membrane to the right of the label, indicating focal calcification.
Age-related macular degeneration. A neovascular membrane is positioned between the RPE and Bruch membrane (BM). Note the blue discoloration of Bruch membrane to the right of the label, indicating focal calcification.
Retinoblastoma. A, Gross photograph of retinoblastoma.
Retinoblastoma. B, Tumor cells appear viable when in proximity to blood vessels, but necrosis is seen as the distance from the vessel increases. Dystrophic calcification (dark arrow) is present in the zones of tumor necrosis. Flexner-Wintersteiner rosettes-arrangements of a single layer of tumor cells around an apparent "lumen"-are seen throughout the tumor, and one such rosette is indicated by the white arrow.
The optic nerve in anterior ischemic optic neuropathy (AION) and papilledema. A, In the acute phases of AION the optic nerve may be swollen, but it is relatively pale because of decreased perfusion. B, In papilledema secondary to increased intra-cranial pressure, the optic nerve is typically swollen and hyperemic.
The optic nerve in anterior ischemic optic neuropathy (AION) and papilledema. C, Normally, the termination of Bruch membrane (arrowhead) is aligned with the beginning of the neurosensory retina, as indicated by the presence of stratified nuclei (arrow), but in papilledema the optic nerve is swollen, and the retina is displaced laterally. This is the histologic explanation for the blurred margins of the optic nerve head seen clinically in this condition
The retina and optic nerve in glaucoma. A, Left panel, normal retina; right panel, the retina in long-standing glaucoma (same magnification). The full thickness of the glaucomatous retina is captured (right), a reflection of the thinning of the retina in glaucoma. In the glaucomatous retina, the areas corresponding to the nerve fiber layer (NFL) and ganglion cell layer (GC) are atrophic; the inner plexiform layer (IPL) is labeled for reference. Note also that the outer nuclear layer of the glaucomatous retina is aligned with the inner nuclear layer of the normal retina due to the thinning of the retina in glaucoma. See Figure 29-16 for orientation.
The retina and optic nerve in glaucoma. B, Glaucomatous optic nerve cupping results in part from loss of retinal ganglion cells, the axons of which populate the optic nerve.
The retina and optic nerve in glaucoma. C, The arrows point to the dura of the optic nerve. Notice the wide subdural space, a result of atrophy of the optic nerve. There is a striking degree of cupping on the surface of the nerve as a consequence of long-standing glaucoma.
Normal and abnormal motor units. Normal motor units: Two adjacent motor units are shown (red and green neurons, red and pale-pink myocytes). Segmental demyelination: Random internodes of myelin are injured and are remyelinated by multiple Schwann cells, while the axon and myocytes remain intact. Axonal degeneration: The axon and its myelin sheath undergo anterograde degeneration (shown for the green neuron), with resulting denervation atrophy of the myocytes within its motor unit (pale-pink myocytes). Reinnervation of muscle: Sprouting of adjacent (red) uninjured motor axons leads to fiber type grouping of myocytes, while the injured axon attempts axonal sprouting. Myopathy: Scattered myocytes of adjacent motor units are small (degenerated or regenerated), whereas the neurons and nerve fibers are normal.
Compared with the normal ultrastructure of nerve (A), an "onion bulb" (B) is composed of a thinly myelinated axon (arrow) surrounded by concentrically arranged Schwann cells. Inset, Light-microscopic appearance of an onion bulb neuropathy, characterized by "onion bulbs" surrounding axons.
Electron micrograph of a degenerating axon (arrow) adjacent to several intact unmyelinated fibers (arrowheads). The axon is markedly distended and contains numerous degenerating organelles and dense bodies.
A, ATPase histochemical staining, at pH 9.4, of normal muscle showing checkerboard distribution of intermingled type 1 (light) and type 2 (dark) fibers. B, In contrast, fibers of both histochemical types are grouped together after reinnervation of muscle. C, A cluster of atrophic fibers (group atrophy) in the center (arrow).
Diabetic neuropathy with marked loss of myelinated fibers, a thinly myelinated fiber (arrowheads), and thickening of endoneurial vessel wall (arrow).
Normal appearance of peripheral nerve (A), with all the axons aligned in a single plane with sheaths of connective tissue, as compared with traumatic neuroma (B) showing disordered orientation of axons (pale purple) intermixed with connective tissue (blue).
Spinal muscular atrophy with groups of round atrophic muscle fibers, or panfascicular atrophy, resulting from denervation atrophy.
A, Duchenne muscular dystrophy (DMD) showing variation in muscle fiber size, increased endomysial connective tissue, and regenerating fibers (blue hue). B, Western blot showing absence of dystrophin in DMD and altered dystrophin size in Becker muscular dystrophy (BMD) compared with control (arrow
A, Nemaline myopathy with numerous rod-shaped, intracytoplasmic inclusions (dark purple structures). B, Electron micrograph of subsarcolemmal nemaline bodies, showing material of Z-band density located adjacent to nucleus, with normal sarcomeres (Z-band to Z-band) creating the typical cross-striation pattern of skeletal muscle.
A, Mitochondrial myopathy showing an irregular fiber with subsarcolemmal collections of mitochondria that stain red with the modified Gomori trichrome stain (ragged red fiber). B, Electron micrograph of mitochondria from biopsy specimen in A showing "parking lot" inclusions.
A, Dermatomyositis. Note the heliotrope rash affecting the eyelids. B, Dermatomyositis. The histologic appearance of muscle shows perifascicular atrophy of muscle fibers and inflammation. C, Inclusion body myositis showing a vacuole within a myocyte