Histopathology from Pasha
Inverted papilloma`cristae-laden senescnt mitochdria, endophytic growth
of epithelium
Rhinoscleroma Mikuicz`s cell (foamy histocytes containing the
bacteria, "moth-eaten" cytoplasm), Russell bodies (bloated plasma cells with
bifringent inclusions), pseudoepitheliomatous hyperplasia
Rhinosporidosis pseudoepitheliomatous hyperplasia, submucosal cysts,
fungal sporangia with chitinous shells
Aspergillosis histologyseptated 45 degree, Y-shaped (sabouraud`s ager
stain)
Mucormycosis histologynonseptated, 90 degree broad branching hyphae
Kuettner’s Tumor (Chronic Sclerosing Sialadenitis of the Submandibular
Gland) chronic inflammation with destruction of acinar cells, sclerosis,
“cirrhotic” changes
Radiation sialadeniits interstitial fibrosis
Benign Lymphoepithelial Cysts lymphoreticular infiltrate, clusters of
lymphoid tissue (germinal centers), acinar atrophy, ductal metaplasia
Pleomorphic Adenoma
Cellular Components:
1. myoepithelial component: spindle shaped with hyperchromatic nuclei, may
be more than one cell layer thick
2. epithelial components: varied growth patterns (trabecular, solid, cystic,
papillary)
3. stromal components: product of myoepithelial cells: myxoid, chondroid,
fibroid, or osteoid components
o fibrous pseudocapsule (except minor glands)
o micro-pseudopod extensions
Warthin’s Tumor
Biphasic Layers
o epithelial component: lines papillary projections; double lining of
oncocytes; inner or luminal cells, nonciliated, tall columnar nuclei at
luminal aspect; outer or basal cells are round, cuboidal with vesicular
nuclei
o lymphoid component: mature lymphocytes with germinal centers
mucous secreting cells
o Oncocytic Cell: metaplasia (cytoplasmic alteration) of myo- or
epithelial cells
1
Mucoepidermoid Carcinoma
o Low-Grade (Well-Differentiated) more mucinous cystic elements,
aggregates of mucoid cells with strands of epithelial cells, positive
keratin staining
o High-Grade (Poorly-Differentiated) less mucinous elements, more
solid nests of cells, requires mucin staining to differentiate from
squamous cell carcinoma, positive keratin staining
Adenoid Cystic Carcinoma (Cylindroma)
o low-grade cribiform (nests of cells with round spaces, “Swiss
cheese” appearance) or cylindromatous (tubular pattern) pattern,
o high-grade more solid pattern (dense cellular pattern with few
spaces)
Acinic Cell Carcinoma serous acinar cells or clear cytoplasm cells, several
configurations (microcystic, papillary, solid, follicular), lymphoid infiltrate
TB Laryngitis cellular inflammation, granuloma in subepithelium,
perichondritis
Scleroma of the Larynx/Rhinoscleroma pseudoepitheliomatous
hyperplasia of the larynx (similar to blastomycosis)
Granular Cell Tumor pseudoepitheliomatous hyperplasia near epithelial
borders (often confused with SSC), polygonal uniform cells with vesicular
nucleus, coarsely cytoplasmic eosinophilic granules, PAS and S-100 positive
Graves’ Disease hyperplasia, increased colloid material, papillary
projections
Hashimoto’s Thyroiditis fibrosis, lymphocytic infiltration
Thyroid Papillary Carcinoma papillary and follicular structures,
psammoma bodies (calcific), intranuclear vacuoles (“Orphan Annie” eyes),
multicentric
Hürthle Cell Tumors Hürthle cells (large granular eosinophilic cells,
trabecular pattern)
Medullary Thyroid Carcinoma small round cells, amyloid stroma, may
have calcification and fibrotic strands
Anaplastic Carcinoma giant and spindle cells variation, undifferentiated
“bizarre cells”
2
Actinomycosis branching anaerobic gram negative bacteria, sulfur granules
Pemphigus Vulgaris intraepithelial cell splitting (suprabasilar), attached
rows of basal cells to lamina propria (row of tombstones), Tzank cells (free
squamous cells, more spherical from loss of intracellular attachment)
Lichen Planus vacuolar alteration of the basal cell layer resulting in
Civatte bodies (degenerative eosinophilic ovoid keratinocytes), “saw tooth”
pattern of epidermal hyperplasia, lymphocytic infiltration of lamina propria
Primary Leukoplakia hyperkeratosis, acanthosis, atypia
Ameloblastoma various histological patterns, most common is the
follicular pattern with islands of epithelium lined with columnar cells, central
mass of loosely arranged cells (stellate reticulum), collagenous stroma
Pindborg Tumor (Calcifying Epithelial Odontogenic Tumor) sheets or
islands of epithelial cells with eosinophilic cytoplasm, may contain amyloid
with concentric calcifications or psammoma-like bodies (Liesegang rings)
Ameloblastic Odontoma presence of dentin and enamel (similar to a
dental follicle), “ghost” cells
Thyroglossal Duct Cyst lined with respiratory and squamous epithelium
Cat-Scratch Disease intracellular, gram-negative bacillus, Warthin-Starry
stain
Histocytosis X (Reticuloendotheliosis) sheets of polygonal histiocytes,
Birbeck granules (“zipper” pattern)
Sarcoidosis noncaseating granulomas, accumulation of T-cells,
mononuclear phagocytes, derangement of normal tissue architecture
Syphilis mononuclear infiltrate, obliterative arteritis, hydrops, gummas and
osteolytic lesions in optic capsule
Blastomycosis pseudoepitheliomatous hyperplasia, intraepithelial
microabscess, single bifringent broad based bud (“figure 8” formation)
Wegener’s Granulomatosis necrotizing granulomas (with multinucleated
giant cells) with vasculitis of upper and lower respiratory tract
Verrucous Carcinoma (Akerman’s Tumor) benign-appearing
(nonmitotic, no infiltration), well-differentiated squamous epithelium with
papillary projections, extensive hyperkeratosis, basement membrane intact,
“pushing” margins
3
Cholesteatoma compact sac of keratinizing squamous epithelium with a
central core of keratin debris
Glomus Tumors nests of nonchromaffin staining cells clustered among
vascular channels lined by epithelioid cells
Acoustic Neuroma Histologic Types
o Antoni Type A: histologically parallel nuclei, uniform spindle cells,
compact cells
o Antoni Type B: histologically less uniform, may have fatty or hyaline
degeneration, less cellular
Otosclerosis (Otospongiosis) active lesions reveal spongy bone seen as
blue with staining (blue mantles of Manasse), hypercellularity, active
osteocytes and osteoblasts, increased resorption spaces, and increased vascular
channels; inactive lesions reveal resorption spaces filled with collagen and
osteoid, sclerotic bone, and narrowed vascular spaces
Done by
Dr.khalid Badr
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