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AAOMP Guide > Chapter 10: Epithelial pathology > Flashcards

Chapter 10: Epithelial pathology Flashcards

1
Q

Squamous papilloma

A

-­‐ 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

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2
Q

Verruca vulgaris

A

-­‐ 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)

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3
Q

Condyloma acuminatum

A

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

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4
Q

Sinonasal papillomas (Schneiderian papillomas)
Fungiform (exophytic, everted, septal)

A

-­‐ HPV 6, 11
-­‐ Almost exclusively found in nasal septum
-­‐ No malignant potential

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5
Q

Sinonasal papillomas (Schneiderian papillomas)
Inverted

A

-­‐ 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

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6
Q

Sinonasal papillomas (Schneiderian papillomas)
Cylindrical (oncocytic)

A

-­‐ 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

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7
Q

Sinonasal polyps

A

-­‐ 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.

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8
Q

Respiratory epithelial adenomatoid hyperplasia

A

-­‐ 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

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9
Q

Molluscum contagiosum

A

-­‐ 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

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10
Q

Verruciform xanthoma

A

-­‐ 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+

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11
Q

Seborrheic keratosis

A

-­‐ 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

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12
Q

Sebaceous hyperplasia

A

-­‐ 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

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13
Q

Ephelis

A

-­‐ MC1R gene mutation

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14
Q

Actinic lentigo

A

-­‐ Age spots on face, hands, and arms (old individuals) due to UV damage
-­‐ More common in people with facial freckles

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15
Q

Lentigo simplex

A

-­‐ 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

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16
Q

Melasma (mask of pregnancy)

A

-­‐ Associated with pregnancy, oral contraceptives, and hormonal replacement therapy

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17
Q

Oral melanotic macule

A

-­‐ 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)

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18
Q

Oral melanoacanthoma

A

-­‐ Reactive process. Almost exclusive in blacks and female predilection

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19
Q

Acquired melanocytic nevus

A

-­‐ 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)

20
Q

Variants of melanocytic nevus

A

-­‐ 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

21
Q

Leukoplakia

A

-­‐ 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)

22
Q

Erythroplakia

A

-­‐ Most in FOM, tongue and soft palate

23
Q

Smokeless tobacco keratosis (snuff dipper’s keratosis; tobacco pouco keratosis)

A

-­‐ 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)

24
Q

Oral submucosal fibrosis

A

-­‐ 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

25
Q

Nicotine stomatitis

A

-­‐ Dry mud appearance
-­‐ Reverse smoker’s palate: significant potential for dysplasia and carcinoma
-­‐ Should resolve upon discontinuation of habit within 1 month

26
Q

Actinic keratosis

A

-­‐ Due to sun damage in fair-­‐skinned individuals
-­‐ Risk factors: immunosuprresion, albinism, xeroderma pigmentosum, Cockayne syndrome, Bloom syndrome and Rothmund-­‐Thompson syndrome
-­‐ Bowenoid actinic keratosis: when full thickness dysplasia is present
-­‐ 10% progress to SCC

27
Q

Actinic cheilitis

A

-­‐ Similar to actinic keratosis of the skin in behavior and pathophysiology
-­‐ Sun damage to lip of fair-­‐skinned people and outdoor occupation (farmer’s lip, sailor’s lip)
-­‐ Estimated 6-­‐10% SCC progression
-­‐ Vermiolionectomy may be employed

28
Q

Keratoacanthoma

A

-­‐ Causes: UV (95% on sun-­‐exposed skin), HPV (26 or 37), tar exposure, immunosupp and trauma
-­‐ Seen in Muir-­‐Torre syndrome
-­‐ Phases: growth (6 wks), stationary (6 wks) and involution (6-­‐12 mths)
-­‐ Fergunson Smith: multiple non-­‐involuting KAs, early life, hereditary (AD 9q22-­‐31)

-­‐ Eruptive Grzybowski: 100’s of small KAs in skin and upper digestive tract; sign of internal malignancy
-­‐ Histo: center of lesion is crater-­‐like and keratin-­‐filled. Surrounding epithelium constricts neck of lesion. Downward proliferation pushes adjacent tissues and its extent is regular (inverted cup)

29
Q

Squamous cell carcinoma

A

-­‐ US: 3% of all cancers; 35,000 new cases (2011), 5300 deaths per year; 8th M/15th F
-­‐ Plummer-­‐Vinson (Paterson-­‐Kelly):  risk of SCC of esophagus, oropharynx and posterior mouth
-­‐ Esophageal webs: intertwining fibrous bands of scar in esophagus, higher malignancy rate
-­‐ Tertiary syphilis: increased risk dorsal tongue SCC
-­‐ HPV: SCC of the oropharynx (16, 18, 31 and 33)
-­‐ Locations: tongue, FOM, soft palate, gingiva, cheek, labial mucosa and hard palate
-­‐ Gingiva: in post MD, similar to PG or IFH. Least associated with tobacco and most common in F
-­‐ Distant mets: lung, liver and bones
-­‐ Desmoplasia (scirrhous change): dense fibrosis in CT induced by SCC cells
-­‐ Pts with SCC at risk for develop add synchronous (33%) or metachronous (66%; w/in 3y) cancers of the upper aerodig tract, esophagus, stomach and lung

30
Q

Verrucous carcinoma (Ackerman’s tumor)

A

-­‐ Also seen in larynx, vagina, penis, anus, sinonasal, esophagus, breast, axilla, ear and soles of feet
-­‐ Associated with smokeless tobacco. May also arise from PVL
-­‐ Oral florid papillomatosis: old name for PLV and VC
-­‐ 20% may show concurrent SCC (if so, tx as SCC)
-­‐ 90% survival with sx w/ou neck dissection

31
Q

Papillary squamous cell carcinoma

A

-­‐ Seen posteriorly (oropharynx, hypopharynx, larynx and sinonasal tract-­‐worst prognosis)
-­‐ Exophytic and looks like papilloma with fibrovascular cores
-­‐ Cytologically looks like CIS and is not hyperkeratotic and not highly invasive
-­‐ HPV 6,11,16,18+

32
Q

Spindle cell carcinoma (pseudosarcoma, sarcomatoid SCC)

A

-­‐ SCC (in situ or invasive) + invasive spindle cell component. Oral cavity and larynx.
-­‐ Due to dysfunctional cadherin-­‐catenin complex
-­‐ 1/3 develop as recurrence after RT for WD-­‐SCC (dedifferentiation)
-­‐ IHC: + for CK (AE1/AE3, CAM 5.2)
-­‐ Depth of invasion related to prognosis; tumor size unrelated

33
Q

Adenosquamous carcinoma

A

-­‐ Combination of adenocarcinoma and SCC (maybe it’s a mucoep). Located posteriorly.

34
Q

Adenoid squamous cell carcinoma

A

-­‐ Due to acantholysis (not true glandular structures)
-­‐ Mostly on lip

35
Q

Basaloid squamous cell carcinoma

A

-­‐ Most in larynx, pyriform sinus and base of tongue
-­‐ Superficial SCC (WD or in situ) + basaloid epithelium. Comedonecrosis common.

36
Q

Carcinoma of the maxillary sinus

A

-­‐ Weak association with tobacco

37
Q

Sinonasal adenocarcinoma, intestinal-­‐type

A

-­‐ Strong assocation with wood dusts exposure (more in men); sporadic more in women
-­‐ Second most common glandular sinonasal malignancy, after adenoid cystic carcinoma
-­‐ Most on ethmoid sinus (men), followed by nasal cavity and MX sinus (women)
-­‐ Mimics colonic adenoca (glands lined with plemorphic columnar cells in back-­‐to-­‐back pattern)
-­‐ Types: papillary, colonic, solid, mucinous and mixed
-­‐ CK20+, CDX2+, CK variable

38
Q

Sinonasal adenocarcinoma, non intestinal-­‐type

A

-­‐ Divided into low-­‐grade and high-­‐grade
-­‐ HG: males, MX sinus, markedly atypical and pleomorphic. LG: no sex predilection, nasal cavity
-­‐ Histo: small glands lined with a single layer of uniform cells (seromucinous carcinoma), B2B

39
Q

Sinonasal undifferentiated carcinoma (SNUC)

A

-­‐ Origin: schneiderian membrane or olfactory epithelium
-­‐ Some cases assoc w/ smoking, EBV and RT (weak)
-­‐ Histo: nests, trabeculae, ribbons of medium-­‐sized polygonal cells with organoid apperance
-­‐ Comedonecrosis common
-­‐ IHC: CK (7,8,19); negative for chromogranin and synaptophysin

40
Q

Olfactory neuroblastoma (esthesioneuroblastoma)

A

-­‐ Arises from olfactory epithelium, high in the nasal cavity close to cribiform plate
-­‐ Rare <10y (unlike usual neuroblastoma). Bimodal peaks (15y and 50y). Most in adults
-­‐ Histo: nests of round cells separated by fibrovascular septa. May have neurofibrillary stroma
-­‐ True rosettes (Flexner-­‐Wintersteiner) and pseudorosettes (Homer Wright)
-­‐ Type: A (in nasal cavity), B (ext to paranasal sinus) and C (beyond nose and paranasal sinuses)
-­‐ IHC: CD56, NSE, synaptophysin and chromogranin

41
Q

Neuroendocrine carcinomas

A
  • Oat cell ca in lung; Carcinoid tumor in GI
  • Mills scheme: WDNEC (carcinoid tumor), MDNEC (atypical carcinoid tumor), PDNEC small cell (small cell undiff) and PDNEC large cell (large cell undiff)
  • MDNEC: most common non-­‐squamous tumor of the larynx, tobacco related
  • Histo: “Salt and pepper” nuclei, nuclear molding, crush artifact
  • NSE+, chromogranin+, synaptophysin+
42
Q

Nasopharyngeal carcinoma

A

-­‐ Group of malignancies that arise from lining epithelium of lymphoid-­‐rich nasopharynx
-­‐ High incidence in China; intermediate in SE Asia; low in US
-­‐ Assoc factors: EBV, vitamin C def, salt fish diet (nitrosamines)
-­‐ Rule out whenever recurrent persistent otitis media occurs in a middle aged person
-­‐ Most common site or origin: lateral wall at Rosenmuller’s fossa
-­‐ In 60% of pts, first sign is an enlarged metastatic lymph node

-­‐ Types: keratinizing (type 1, SCC); nonkeratizining, differentiated (type 2); nonkeratinizing, undifferentiated (type 3, lymphoepitelioma, lymphoepithelial carcinoma)
-­‐ Type 1 has worse prognosis, probably because due to response to radiation
-­‐ Lymphoepithelioma: Regaud type (clusters, nests or aggregates of neoplastic epithelial cells with lymphocytes) and Schminke type (dispersed tumor cells forming a syncitial net)

43
Q

Basal cell carcinoma

A

-­‐ Most common of all cancers
-­‐ Mainly due to UV. Also arsenic ingestion, immunosuppresion, PUVA (for psoriasis)
-­‐ Seen in Gorlin syndrome, xeroderma pigmentosum, albinism, Rasmussen, Rombo and Bazex-­‐ Christol-­‐Dupre syndromes
-­‐ PTCH (9q22) mutation +p53 mutation+ SMO
-­‐ Clinical patterns: noduloulcerative (most common-­‐telangiectatic vessels, aka rodent ulcer), pigmented (nodular with melanocytes), sclerosing (morpheaform-­‐ mimics scar), superficial (multifocal-­‐ mimics psoriasis), and syndromic (sun exposed and not exposed areas)
-­‐ Basosquamous carcinoma: “collision” tumor of BCC and SCC
-­‐ Mohs micrographic surgery: frozen sections to determine if BCC/SCC was entirely removed

44
Q

Merkell cell carcinoma

A

-­‐ Merkel cells of the epidermis are primarily associated with nerve endings
-­‐ Risk factors: UV light and immunosuppresion (transplant, HIV and lymphocytic leukemia).
-­‐ May be caused by the Merkell cell polyoma virus (MCPyV)
-­‐ 75% facial skin. Dome shaped nodule with smooth surface and telangiectasias (rarely ulcerates).
-­‐ AEIOU: Asymptomatic; Expands rapidly; Immunosuppressed; Older people; UV exposed areas
-­‐ IHC: CK20+ (perinuclear dot-­‐like); also synapt, chromogr A and NSE; TTF-­‐1 to exclude lung met
-­‐ Grimelius stain shows granules
-­‐ 25% of pts develop additional malignancies (SCC skin, hem malig or breast/ovary adenoca.)

45
Q

Microcystic adnexal carcinoma (sclerosing sweat duct carcinoma)

A

-­‐ Cytologically bland but locally aggressive
-­‐ Plaque-­‐like indurated lesion of the upper lip
-­‐ Histo: squamous/basaloid cells; horn cysts in superficial portion; ductal structures in deeper portions; neural/vascular invasion; and desmoplastic stroma

46
Q

Melanoma

A

-­‐ 50-­‐70% BRAF mutation (Ras-­‐Raf-­‐Erk pathyway).
-­‐ Types: superficial spreading (most common), nodular (sometimes amelanotic), lentigo maligna melanoma (melanoma in situ, arises from lentigo maligna-­‐Hutchinson’s freckle), and acral/mucosal lentiginous melanoma (most common in oral cavity and blacks)
-­‐ Superficial spreading: interscapular area in males, back of leg in female
-­‐ IHC: HMB-­‐45, Melan-­‐A, Mart-­‐1, Fontana-­‐Masson, S-­‐100
-­‐ Prognosis: Breslow classification (depth of invasion assoc w/ poor prognosis for skin lesions)
-­‐ Elevated serum lactic dehydrogenase (LDH) and ulceration: poor prognosis (skin)
-­‐ BNAS: worse prognosis (interscapular back, post and lat neck, posterior upper arm, and scalp)
-­‐ Better prognosis for women and pts < 50y
-­‐ Oral: 13-­‐22% survival (better for younger, worse for amelanotic)

AAOMP Guide (25 decks)

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