02-17 PATH: Mouth & Esophagus Flashcards
● Discuss the common infections of the oral cavity and of the esophagus ● Describe the premalignant and malignant lesions of the oral mucosa ● Memorize the pathologic features of the three most common tumors of the salivary glands ● Define the pathologic features of the most important lesions of the esophagus: congenital anomalies, esophagitis, Barrett's, carcinoma
HSV Infection
- What cell is infected?
- interpret this slide
- other H&E Findings?
- Path Dx?
—epithelial cells infected
—slide on other side shows the loss of cohesion and intercellular edema in the epidermis that leads to herpetic ulcers
—Other H&E findings: surrouding area will have squamous hyperplasia; smudgy/steel gray intranuclear “Cowdry A” bodies
—Path dx = scraping of an ulcer base to look for Tzanck cells (multinucleated giant cells); epithelial cells with “3 M changes” [see pic here]:
- Multinucleated
- molding of nuclei and
- margination of nuclei
CMV Infection
- What cell is infected?
- H&E Findings?
—CMV infects endothelial and mesenchymal cells
—H&E findings: Owl’s eye nuclei and cytoplasmic inclusion [pic here]
- Dx here?
- DDx?
- Histo appearance?
- Dx = candidiasis (most often C. albicans)
- DDx = leukoplakia
- can scrape candida off; can’t scrape leukopl.
- Histo budding yeast w/ pseudo-hyphae (i.e. not septate) + inflammatory infiltrate
- Dx?
- Describe organism?
- Pathogenesis?
- Common species that cause infection?
Dx = Aspergillus
- Septate hyphae with parallel walls45° branching
- Angioinvasive
- Common pathogenic species A. niger A. fumigatus A. flavus
What are pseudohyphae?
“distinguished from true hyphae by their method of growth, relative frailty and lack of cytoplasmic connection between the cells” [Wiki]
Mucormycosis
- Describe appearance under microscope
- Pathogenesis?
- Example spp?
- Broad, bulbous, non-septate hyphae w/ 90° branching
- Angioinvasion
- Technically caused by any fungus in the order Mucorales
- Mucor*, *Rhizopus* and *Absidia genera are most commonly implicated genera
Dx?
- Expected H&E findings?
Pyogenic granuloma
- -Lobular capillary hemangioma with surface ulceration -Inflammation is secondary
Dx?
- Describe the lesion
Dx = Aphthous ulcer
- painful, shallow ulcer w/ erythematous ring
Dx?
- DDx
- Where else can this be seen?
- Clinical course
Leukoplakia - a clinically descriptive term, not a specific diagnosis
- Candidiasis (this will not scrape off vs. candidiasis)
- Can be seen anywhere in the oral cavity
- CIinical course: 5-25% progress to cancer
Dx?
- DDx
- Where else can this be seen?
- Clinical course
- Findings on H&E
Hairy Leukoplakia ≠ Leukoplakia
- Candiasis (this will not scrape off)
- Seen usu. only on lateral tongue
- Clinical course: caused by EBV in immunocompromised (80% HIV)
- benign vs. leukoplakia
- H&E: Hyperkeratosis, acanthosis, and “balloon” cells (see image here)
Dx?
- Clinical course
- Findings on H&E
Dx = Erythroplakia
- more ominous/↑er risk of transformation > leukoplakia
- H&E: atypical epithelial cells
Dx?
- Where else can this be seen?
- Clinical course
- Findings on H&E
Squamous Cell Carcinoma
- Most commonly under tongue
- 50% caused by HPV
- series of additive mutations e.g. p16 → p53 (loss tumor supp) → cyclin D mutation (immortalized)
- hypercellular/malignant looking epithelia
- show here: mod dysplasia → CIS → SCC
What % of tumors in each of the 3 types of salivary glands are malignant?
- Parotid – 30%
- Submandibular – 40%
- Sublingual – 80%
Dx this sample from a salivary gland mass
- Benign or malignant?
- Cell types seen?
- Most commonly occurs where?
Pleomorphic adenoma, accounts for 50% of benign salivary gland tumors
- Benign but w/ low but definite risk of malignant transformation (“Carcinoma ex pleomorphic adenoma”)
- 2% at 5 yrs; 10% at 15 yrs.
- Cell types: Biphasic tumor w/ ductal (epithelial) and myoepithelial cells
- More common in parotid than in submandib/subling glands
- 60% of parotid tumors are mixed tumors
Dx this salivary gland mass
- Benign or malignant?
- Gross appearance?
- Cell types seen?
- Most commonly occurs where?
Warthin tumor, 5-10% of benign salivary gland tumors
- Gross: tumors w/ motor-oil cysts
- Two components
- Epithelial (oncoctyic) component – dense, eosinophilic, granular cytoplasm (mitochondria) [see photo here w/ arrow pointing to oncocytic cell
- Lymphoid component
- Almost always in the parotid – 10% bilateral
Other FYI benign tumor mentioned: Oncocytoma (1%)
Dx this sample from a salivary gland mass
- Benign or malignant?
- Cell types seen?
- Subtypes + there clinical course?
Mucoepidermoid carcinoma, causes 15% of malignant salivary gland tumors
- Two components
- Mucus-secreting cells
- Squamous cells
- Subtypes
- Low Grade - mucous cells predominate, 15% recurrence; 90% 5-year survival (shown here w/ Mucicarmine stain)
- High Grade - squamous cells predominate, greater atypia • 25% recurrence; 50% 5-year survival (shown on front w/ H&E stain)
**other malignant tumors that were mentioned as an FYI:
- Adenoid cystic carcinoma (5%)
- Acinic cell carcinoma (5%)
- Malignant mixed tumors (3-5%)
Name this esophageal deformity associated w/ dysmotility.
Zenker’s Diverticulum
Name this esophageal deformity associated w/ dysmotility.
Achalasia
Name this esophageal deformity associated w/ dysmotility.
Hiatal hernia (sliding)
Name this esophageal deformity associated w/ dysmotility.
Hiatal Paraesophageal Hernia (rolling)
Which tracheoesophageal malformation is most common? How would a baby present?
Next most common?
esophageal atresia w/ tracheoesophageal fistula [pic here]
- this accounts for ~85% of Congenital Anomalies of the esophagus
- babies have rapidly distending abdomens + choking and regurg when feeding
- next most common (4%) is tracheoesophageal fistula (just a small lateral fistula between both full length lumens
Esophageal Webs
- Occur where in esophagus?
- Which demographic most commonly?
- What is a syndromic cause?
- Upper Esophagus
- Women over 40 yrs of age
- Syndromic Cause = Plummer-Vinson Syndrome
- Web
- Iron deficiency anemia
- Glossitis
- Cheilosis
- Risk for carcinoma of upper esophagus
Esophageal Rings
- List the two types
- Clinical presentation?
- “A” ring: in lower esophagus above the GE junction
- “B” (Schatzki’s) ring: at the GEJ, usu above a HH
- Clinical presentation with episodic dysphagia, only when you eat too quickly/eat something too big that get stuck on the “shelf” made by ring
Mallory-Weiss Tear
A laceration at GEJ caused by forceful vomiting
Boerhaave Syndrome
A catastrophic esophageal rupture from vomitting
- “56% of oesophageal perforations are iatrogenic, usually due to medical instrumentation such as an endoscopy or paraoesophageal surgery.[1] In contrast, the term Boerhaave’s syndrome is reserved for the 10% of oesophageal perforations which occur due to vomiting” [Wiki]
Dx this specimen from pt w/ heartburn
Reflux esophagitis
- Giveaway = eosinophils, seen up close here:
What’s going on in this autopsy specimen from a deceased patient w/ alcoholism?
Esophageal Varices
- Causes
- Develop in 90% of cirrhotic patients
- Consequence of portal HTN
- Major cause for bleeding in these patients
Epidemiology of esophageal cancer
- What is most common type worldwide? Causes? Occurs in which part of esophagus?
- Most common in U.S.? Causes? Occurs in which part of esophagus?
Squamous cell carcinoma (90% Esophageal Ca worldwide)
- Alcohol, tobacco, fungus-derived carcinogens, nitrosamines
- More common in African-Americans
- More common in mid-esophagus
Adenocarcinoma (50% of esophageal carcinoma among non-African Americans in USA)
*Squamous Cell – More common in African-Americans
- Incidence of adenocarcinoma is rapidly increasing
- Vast majority of adenoCA arises in Barrett’s
- Most arise in lower third of esophagus
Official definition of Barrett’s Esophagus
• Endoscopic evidence of columnar epithelium in the distal esophagus
AND
• Intestinal metaplasia (i.e. goblet cells) on a mucosal biopsy from this segment [seen here]
Dx this esophageal specimen?
adenocarcinoma
associated w/ Barrett’s metaplasia
This slide shows low grade dysplasia in Barrett’s (metaplastic) esophagus. How would high grade dyplasia in BE look histologically?
- increase cytosol to nucleus ratio
- cytological atypia
- architecture is dysplastic
