Head & Neck Pathology Lab

Key questions

1. Q1What lines the oral cavity?

   Stratified squamous epithelium — keratinized on the gingiva, hard palate and dorsal tongue (masticatory mucosa); non-keratinized on the cheek, floor of mouth, ventral tongue and soft palate (lining mucosa).
2. Q2What does a normal tongue section show?

   Squamous mucosa with papillae on the dorsum over interlacing bundles of skeletal muscle running in three planes, with scattered minor salivary glands.
3. Q3What does a normal mixed salivary gland look like?

   Lobules of pale, foamy mucous acini and darker, granular serous acini (serous demilunes) draining into intercalated, striated and excretory ducts.
4. Q4Which major gland is which?

   Parotid = purely serous (with fat); submandibular = mixed, mostly serous; sublingual = mixed, mostly mucous.
5. Q5Why does the normal histology matter for reading slides?

   Every lesion is read as a departure from normal: thickened keratin (leukoplakia), loss of maturation (dysplasia), invasion through the basement membrane (SCC), lost acini with lymphocytes (sialadenitis, Sjögren).

Key questions

1. Q6What does leukoplakia look like on the slide?

   Thick surface keratin (hyperkeratosis) with acanthosis; may show dysplasia — atypical cells rising above the basal layer. Severe dysplasia shows full-thickness atypia short of invasion.
2. Q7What does erythroplakia look like on the slide?

   Thin, atrophic epithelium with marked dysplasia or carcinoma in situ and prominent vessels underneath — no thick keratin, so the vessels show through as red.
3. Q8Why is one white and one red?

   Keratin makes a lesion white (leukoplakia); thin epithelium over congested vessels makes it red (erythroplakia).
4. Q9Which is more dangerous?

   Erythroplakia — almost always dysplastic or worse. Leukoplakia is premalignant in 5–25%.
5. Q10How does candidiasis look on the slide, and why include it?

   Pseudohyphae and yeast in the surface keratin (PAS/GMS). It is a white patch that scrapes off — the key mimic of leukoplakia.
6. Q11Where does dysplasia lead?

   Mild → moderate → severe dysplasia → carcinoma in situ → invasive SCC; the grade does not reliably predict invasion, so these lesions need biopsy.

Key questions

1. Q12What drives conventional (HPV-negative) head and neck SCC?

   Tobacco and alcohol (synergistic) → field cancerization with TP53 mutation, CDKN2A (p16) loss and other hits, stepping from dysplasia to invasive carcinoma.
2. Q13What drives HPV-positive SCC?

   High-risk HPV (mostly HPV-16) in the tonsils/base of tongue: E6 degrades p53 and E7 inactivates Rb, so p16 is overexpressed.
3. Q14What does keratinizing SCC look like?

   Invasive nests of eosinophilic squamous cells with keratin pearls and intercellular bridges, often with desmoplastic stroma. Grossly, an ulcerated, firm base-of-tongue mass.
4. Q15What does non-keratinizing (HPV) SCC look like?

   Nests and sheets of basaloid cells with little keratin, often with central necrosis, arising from tonsillar crypt epithelium; strong diffuse p16.
5. Q16What predicts prognosis?

   Stage (size, nodes, distant spread) is most important; HPV-positive tumors do much better; tobacco-related tumors have field cancerization and second primaries.
6. Q17Why do head and neck SCC patients get second cancers?

   Field cancerization: the whole mucosa exposed to carcinogens carries mutations, so new primaries arise (about 3–7% per year).

Key questions

1. Q18Who gets HPV-positive oropharyngeal SCC?

   Younger (often 40s–50s) patients, men more than women, often non-smokers, linked to number of oral sex partners.
2. Q19How does it present?

   Commonly a painless, enlarging (often cystic) neck node with a small or hidden primary in the tonsil or base of tongue.
3. Q20Who gets HPV-negative SCC?

   Older patients with heavy tobacco and alcohol use; oral cavity, larynx, hypopharynx.
4. Q21How do outcomes compare?

   HPV-positive: better response to therapy and better survival. HPV-negative: worse survival, more second primaries.
5. Q22What is the site difference?

   HPV-positive: oropharynx (tonsils, base of tongue). HPV-negative: oral cavity (floor of mouth, ventral/lateral tongue), larynx.

Key questions

1. Q23What does angiofibroma look like on the slide?

   Dense, collagen-rich fibrous stroma with stellate fibroblasts and many thin-walled, staghorn-like vessels lacking muscle — they cannot contract, so they bleed.
2. Q24Who gets angiofibroma and how does it behave?

   Adolescent males; recurrent epistaxis and obstruction; benign but locally aggressive; β-catenin/APC pathway; surgery can cause brisk bleeding.
3. Q25What does inverted sinonasal papilloma look like?

   Thick nests of squamous/transitional epithelium growing downward ("inverted") into the stroma, with intraepithelial neutrophils and microcysts; lateral nasal wall/sinus; HPV-related in some.
4. Q26How does inverted papilloma behave?

   Recurs often and can transform to SCC (~10%) — so resect completely.
5. Q27What does non-keratinizing nasopharyngeal carcinoma look like?

   Syncytial sheets of large cells with vesicular nuclei and big nucleoli mixed with many lymphocytes (lymphoepithelial pattern); EBV-positive (EBER).
6. Q28Who gets NPC and how does it present?

   Southern Chinese and North/East African populations; EBV; often an enlarged neck node, epistaxis, obstruction, unilateral serous otitis (eustachian tube); radiosensitive.
7. Q29What does a laryngeal papilloma look like?

   Finger-like fronds of benign squamous epithelium over fibrovascular cores; koilocytes; HPV 6/11.
8. Q30How do juvenile and adult papillomas differ?

   Juvenile: multiple (papillomatosis), from birth-canal exposure, frequently recur, often regress at puberty. Adult: usually single, may recur.
9. Q31What does laryngeal SCC look like grossly and microscopically?

   Ulcerated, fungating mass of the true cord (glottis) that invades into the larynx; microscopically, keratinizing SCC; smokers, persistent hoarseness.

Key questions

1. Q32Which lesions present mainly with epistaxis?

   Juvenile nasopharyngeal angiofibroma (plus obstruction), pyogenic granuloma (lobular capillary hemangioma — pregnant women, septum) and nasopharyngeal carcinoma.
2. Q33Which lesions present mainly with obstruction?

   Sinonasal (inverted) papilloma, nasal polyps, angiofibroma and nasopharyngeal carcinoma (with a unilateral serous otitis).
3. Q34Which lesions present with hoarseness?

   Singer's nodules (reactive), laryngeal polyps, laryngeal papillomas (juvenile or adult) and laryngeal SCC.
4. Q35Unilateral nasal obstruction + epistaxis in a teenage boy?

   Juvenile nasopharyngeal angiofibroma.
5. Q36Unilateral nasal obstruction in a 50-year-old man with a recurring mass after excision?

   Inverted sinonasal papilloma.
6. Q37Neck mass + ear fullness in a Chinese-born adult?

   Nasopharyngeal carcinoma (EBV).
7. Q38Hoarse child with noisy breathing?

   Juvenile laryngeal papillomatosis (HPV 6/11).
8. Q39Hoarse teacher or singer?

   Singer's nodule — bilateral, on the anterior–middle third of the true cords.
9. Q40Hoarse 65-year-old smoker for 3 months?

   Laryngeal SCC until proven otherwise.

Key questions

1. Q41What does pleomorphic adenoma look like on the slide?

   Low power: well-circumscribed tumor with an incomplete capsule. High power: ducts and myoepithelial cells in a blue myxoid/chondroid (cartilage-like) stroma — epithelial + mesenchymal-looking elements.
2. Q42What does Warthin tumor look like?

   Cystic spaces lined by a double layer of pink oncocytic cells (packed with mitochondria) sitting on dense lymphoid stroma with germinal centers.
3. Q43What does mucoepidermoid carcinoma look like?

   A mix of squamoid (epidermoid) cells, mucus-secreting cells (mucicarmine+) and intermediate cells, often with cysts.
4. Q44What does adenoid cystic carcinoma look like?

   Small, dark basaloid cells in a cribriform ("Swiss cheese") pattern with hyaline/basophilic material in the holes, and perineural invasion.
5. Q45Which is the most common salivary tumor, and how does it behave?

   Pleomorphic adenoma: painless, slow, mobile parotid mass; recurs if enucleated (projections through the capsule); may undergo malignant change.
6. Q46Who gets Warthin tumor?

   Older smokers (men > women); parotid only; ~10% bilateral or multifocal; benign.
7. Q47Which is the most common malignant salivary tumor?

   Mucoepidermoid carcinoma (parotid most common; MAML2 fusion). Grade depends on the mucous/cystic vs solid/squamoid mix.
8. Q48Why does adenoid cystic carcinoma cause pain or facial palsy?

   Perineural invasion; it is slow but relentless, recurs, and spreads late (often to lung). Most common in minor salivary glands.
9. Q49What is the "size rule" for salivary tumors?

   The smaller the gland, the more likely a tumor is malignant: most parotid tumors are benign; ~40% of submandibular, ~50% of minor and 70–90% of sublingual tumors are malignant.
10. Q50How do inflammatory lesions look on the slide?

    Acute sialadenitis: neutrophils in ducts/acini. Chronic sialadenitis: lymphocytes, acinar loss, fibrosis, dilated ducts. Sjögren: lymphocytic infiltrate with lymphoepithelial (myoepithelial) islands.

Key questions

1. Q51Where is a branchial cleft cyst?

   Lateral neck, along the anterior border of the sternocleidomastoid (usually a second-arch/cleft remnant).
2. Q52Where is a thyroglossal duct cyst?

   Midline neck, near or just below the hyoid bone.
3. Q53What is the key physical sign of a thyroglossal duct cyst?

   It moves up with swallowing and with tongue protrusion (attached to the foramen cecum tract).
4. Q54What does a branchial cleft cyst look like on the slide?

   Cyst lined by squamous (or respiratory) epithelium with a wall of dense lymphoid tissue, often with germinal centers.
5. Q55What does a thyroglossal duct cyst look like on the slide?

   Cyst lined by squamous or respiratory (ciliated columnar) epithelium, with thyroid follicles in the wall.
6. Q56Who gets them and how are they treated?

   Both usually present in children/young adults, may become infected. Branchial: excise the cyst/tract. Thyroglossal: Sistrunk procedure (remove the cyst with the middle of the hyoid) to prevent recurrence.
7. Q57Which malignancy can hide in each?

   Thyroglossal duct cyst: papillary thyroid carcinoma (rare). Lateral neck "cyst" in an adult: consider cystic metastatic HPV-positive SCC first.