Chapter 10: Epithelial pathology Flashcards
Squamous papilloma
-‐ Most common soft tissue mass of the soft palate
-‐ HPV 6 and 11
-‐ Papillomatosis: extensive coalescing papillary lesions. Seen in acanthosis nigricans, Goltz-‐Gorlin (focal dermal hypoplasia) and nevus unius lateris
-‐ Laryngeal papillomatosis: juvenile-‐onset (aggressive when HPV11, can obstruct airway, related to maternal history of genital warts) and adult-‐onset. Hoarseness common. May progress into SCC (smokers and previous RT)
-‐ Vaccine for HPV 6, 11, 16 and 18
Verruca vulgaris
-‐ HPV 2, 4,6, and 40
-‐ Cutaneous horn: extreme accumulation of compact keratin in verruca vulgaris, SK, AK, and SCC
-‐ Prominent granular cell layer, elongated rete rigdes converge to center of lesion (cupping effect)
Condyloma acuminatum
Multifocal epithelial hyperplasia (Heck’s disease)
-‐ HPV 13, 32
-‐ Association with HLA-‐DR4
-‐ Abrupt and considerable acanthosis of the epithelium (extends upwards, so lesional rete rigdes are at level of the normal epith).
-‐ Mitosoid cell: cell with altered nucleus resembling a mitotic figure
Sinonasal papillomas (Schneiderian papillomas)
Fungiform (exophytic, everted, septal)
-‐ HPV 6, 11
-‐ Almost exclusively found in nasal septum
-‐ No malignant potential
Sinonasal papillomas (Schneiderian papillomas)
Inverted
-‐ Most common; HPV 6, 11, 16, 18
-‐ Most lateral nasal wall and sinuses (usually MX)
-‐ Monoclonal; CD44+ (vs papillary SCC)
-‐ Most aggressive and up to 25% SCC transformation
Sinonasal papillomas (Schneiderian papillomas)
Cylindrical (oncocytic)
-‐ Least common; no association with HPV
-‐ Most lateral nasal wall and sinuses (usually MX)
-‐ Hybrid or mixed: inverted + cylindrical
-‐ Less aggressive and lower potential for malignant transformation
Sinonasal polyps
-‐ Non-‐neoplastic proliferations composed of epithelial and stromal elements
-‐ Inflammatory: adults; history of rhinitis, allergy, aspirin intolerance and diabetes. Multiple, often bilateral. If seen in children, investigate cystic fibrosis
-‐ Antrochoanal: arise in antrum and extend to nasal cavity. 90% single.
-‐ Histo: INF-‐> sessile, thick BM, myxoid or gelatinous stroma which is highly inflamed, may show Charcot-‐Leyden crystals. AA -‐> pedunculated, not as inflamed.
Respiratory epithelial adenomatoid hyperplasia
-‐ Adenomatoid proliferation of resp ciliated cells in the nasal cavity, sinuses and nasopharynx
-‐ Glands often directly communicate with overlying mucosa
-‐ Pink basement membrane material separating glands from edematous inflamed stroma
Molluscum contagiosum
-‐ Caused by Molluscum virus (DNA poxvirus). Risk factors: HIV, atopic dermatitis and Darier’s.
-‐ Multiple papule of skin, which remain small for years and then spontaneously resolve in 6-‐9m
-‐ Histo: Bloated keratinocytes contain large, intranuclear viral inclusions named moluscum bodies
-‐ Moluscum bodies aka Henderson-‐Paterson
Verruciform xanthoma
-‐ Seen with lichen planus, lupus, pemphigus, Warty diskeratoma, GVHD, dysplasia, SCC
-‐ May have a history of trauma
-‐ Xanthoma cells: granules PAS+, diastase resistant; cells CD68+ and cathepsin B+
Seborrheic keratosis
-‐ FGFR3, PIK3CA gene mutation. Related to sun-‐exposure and hereditary tendency
-‐ Dermatosis papulosa nigra: AD form of SK. Found in 30% of AA.
-‐ Types: acanthotic, hyperkeratotic and adenoid
-‐ Inverted follicular keratosis of Helwig: irritated SK. Shows squamous eddies (whorled epithelial pattern due to metaplasia of lesional cells)
-‐ Leser-‐Trelat sign: sudden onset of pruritic SK can signify internal malignancy
Sebaceous hyperplasia
-‐ Sebaceous glands are holocrine
-‐ Associated with cyclosporine, corticoids, hemodyalisis and Muir-‐Torre syndrome
-‐ Muir-‐Torre syndrome: visceral malignancies, sebaceous adenomas/ca, and keratoacanthomas
-‐ Expressed sebum on compression (ddx with BCC)
-‐ Rhinophyma: Hypertrophy of sebaceous glands of nasal dome. Seen in pts with long standing acne roseace. Enlarged, bumpy nasal dome (~ tuberous sclerosis). Hx of facial flushing with driking hot liquids, alcohol and spicy foods. Histo: hyperplasia of sebaceous glds
Ephelis
-‐ MC1R gene mutation
Actinic lentigo
-‐ Age spots on face, hands, and arms (old individuals) due to UV damage
-‐ More common in people with facial freckles
Lentigo simplex
-‐ Clinically equal to non elevated nevus (early nevus?) on skin not exposed to sunlight
-‐ If multiple, consider lentiginosis profuse, Peutz-‐Jeghers and LEOPARD
-‐ LEOPARD: lentigines (multiple), electrocardiographic abnormalities, ocular hypertelorism, pulmonary stenosis, abnormal genitalia, retarded growth and deafness
Melasma (mask of pregnancy)
-‐ Associated with pregnancy, oral contraceptives, and hormonal replacement therapy
Oral melanotic macule
-‐ Focal increase in melanin and possible # of melanocytes. Unrelated to sun exposure.
-‐ Laugier-‐Hunziker syndrome: pigmentation of lips and buccal mucosa and longitudinal melanochyia (linear pigmentation of nail)
Oral melanoacanthoma
-‐ Reactive process. Almost exclusive in blacks and female predilection
Acquired melanocytic nevus
-‐ Junctional (macule, pigmented), compound (papule, less pigment), intradermal/intramucosal (papillary, hair, no pigment). Many involute spontaneously.
-‐ Type A (superficial, epithelioid), type B (middle, lymphocyte-‐like), type C (deeper, spindle cells)
Variants of melanocytic nevus
-‐ Congenital nevus: small <20 cm; large> 20 cm.
-‐ Giant hairy nevus: congenital nevus with hypertrichosis
-‐ Bathing trunk nevus (garment nevus): very large congenital nevus
-‐ Congenital nevus: 3-‐15% transformation into melanoma. Also increased risk CNS melanotic neoplasms
-‐ Halo nevus: shows hypopigmented halo due to destruction of melanocytes by immune system.
Seen in pts with recent melanoma excision
-‐ Spitz nevus: Histo ~ to melanoma (epithelioid and spinde cells), but young age and small size.
S100+ and NSE+. Has Kamino body (eosinophilic globoid seen in Spitz nevus)
-‐ Blue nevus: Tyndal effect gives color. Common and cellular.
-‐ Combined nevus: blue nevus + overlying melanocytic nevus
-‐ LAMB = lentigines, atrial and mucocutaneous myxomas, blue nevi (subset of Carney complex)
-‐ Balloon cell nevus: large, pale, polyhedral balloon cells (clear cells)
-‐ Nevus of Ota: aka oculodermal melanocytosis. Diffuse distribution of prolif melanocytes.
Unilateral facial and/or ocular slate-‐blue pigmentation (follows TN V1/V2)
-‐ Dysplastic nevus: usually develops in light-‐exposed areas, premalignant, melanocytes show nuclear atypia and may be syndrome-‐associated
Leukoplakia
-‐ Dysplasia found in 5-‐25% of cases.
-‐ Sanguinaria-‐associated keratosis: on MX vestibule or alv mucosa
-‐ Microorganisms: syphilis (dorsal tongue leukoplakia), candida, HPV
-‐ Alveolar ridge keratosis: in retromolar pad or alveolar ridge
-‐ Thin (mild) -‐> thick (homogenous) -‐> nodular (granular) -‐> verrucous
-‐ PVL: multiple lesions starting in gingiva and then spreading to other areas in non-‐smoking females. Clinically can become similar to VC and transform into SCC (within 8y)
-‐ Erythroleukoplakia: red areas which are so atrophic that can no longer produce keratin
-‐ Overall SCC progression: 4% (mild), 10% (mod), 35% (sev), 47% (erythrleuko) (in 2-‐4y)
Erythroplakia
-‐ Most in FOM, tongue and soft palate
Smokeless tobacco keratosis (snuff dipper’s keratosis; tobacco pouco keratosis)
-‐ Smokeless tobacco (spit tobacco): chewing tobacco, dry snuff and moist snuff (most pop)
-‐ Causes painless gingival recession, possibly with bone destruction
-‐ Keratosis: thin, gray-‐white plaque with blending borders, on the area where tobacco is placed
-‐ Snuff pouch: pouch revealed by stretching the mucosa with snuff dipper’s
-‐ Chevrons: parakeratin pointed projections above epithelial layers.
-‐ May show amyloid-‐like areas around basement membranes and blood vessels
-‐ Dry snuff higher risk of developing SCC (VC may also develop)
-‐ Should resolve within 2 weeks of habit removal (if more than 6, it’s true leukoplakia)
Oral submucosal fibrosis
-‐ Pale and marble-‐like stiff mucosa in betel quid (areca nut) users (affects ECM equilibrium).
-‐ CC: trismus and pain when eating spicy foods. More in BM, SP and reromolar area
-‐ Betel chewer’s mucosa: brown-‐red mucosa (not pre-‐cancerous).
-‐ Betel quid lichenoid lesions: ~ lichen planus
-‐ Dysplasia n 10-‐15% of cases; SCC in 6%; near 8% progress into SCC