Oral and Esophageal Pathology Flashcards
Oral Canker Sore (Aphthous Ulcers)
- -Common, shallow, superficial mucosal ulcerations
- -Painful and recurrent
- -Regress within several weeks
- -Can be associated with IBD, celiac disease
Mucosal fibroma (irritation fibroma)
- -Proliferation of squamous mucosa and underlying subepithelial fibrous tissue
- -Usually secondary to chronic irritation
Squamous papilloma
- -Exophytic papillary proliferation of squamous mucosa w/fibrovascular core
- -May be associated w/HPV infection, trauma/irritation
- -Can become invasive squamous cell carcinoma
Pyogenic granuloma
- -Polypoid, red lesion, lobular reactive proliferation of capillaries (eruptive hemangioma)
- -Usually on gingiva of children, young adults, pregnant women
Glossitis
- -Inflammation of tongue.
- -Beefy red appearance (Vit B12 deficiency)
- -Secondary to atrophy of papillae of tongue and thinning of mucosa.
Plummer-Vinson Syndrome
Iron deficiency anemia, glossitis, esophageal dysphagia (associated wi/esophageal webs)
Geographic tongue (benign migratory glossitis)
- -Migratory, “map-like” appearance
- -Patches will migrate over tongue.
- -From focal loss of papillae w/formation of smooth red patches.
- -Usually asymptomatic, may have mild burning sensation
- -Tends to run in families
Microscopic appearance of geographic tongue
Intraepithelial neutrophilic inflammation present
Bisphosphonate-related osteonecrosis of the jaw**
- -Bisphosphonate medications (Fosamax) used to treat osteoporosis
- -Side effect is focal mandibular and maxillary osteonecrosis, sometimes following minor trauma
Hairy leukoplakia
- -White, confluent patches of “fluffy” hyperkeratosis (thickening of keratin layer)
- -White plaques to raised white lesions of vertical corrugations
- -Lateral sides of tongue
- -Lesions can’t be scraped off
- -Occurs in immunocompromised ind. secondary to EBV
Clinical significance of hairy leukoplakia
May be first presenting sign of HIV
Leukoplakia
–White patch/plaque in oral cavity that can’t be scraped off or characterized by another disease
Histological features of leukoplakia
–Hyperkeratosis with or without parakeratosis, often irregular epithelial hyperplasia with or without dysplasia
Clinical significance of leukoplakia
5-25% demonstrate precancerous squamous dysplasia (along w/squamous hyperpasia and hyperkeratosis)
Erythroplakia
–Red, velvety patch in oral cavity that can be flat or slightly eroded
Clinical significance of erythroplakia
–Higher incidence of precancerous dysplasia higher than in leukoplakia
Erythroplakia histology
Evidence of dysplasia and/or carcinoma
Erythroplakia and leukoplakia risk factors
- -Adults
- -Tobacco use
Actinic Cheilitis
–Leukoplakic lesion of lower lip with loss of distinct demarcation between lower lip border and skin of lip
Histologic features of actinic cheilitis
–Disordered maturation of epithelium w/cytologic atypia, increased mitotic activity, hyperkeratosis, connective tissue solar changes, increased hyperchromatia
Risk factors for oral cavity squamous cell carcinoma
- -Tobacco and EtOH use (especially if both used)
- -Oncogenic HPV (better outcome if P16)
- -Exposure to sunlight and pipe smoking
- -Middle-aged adults and older
Typical first presenting symptom of oral cavity SCC
Enlarged cervical neck lymph node
Laryngeal SCC risk factors
- -Tobacco smoke and EtOH use
- -HPV
Typical presenting sign of laryngeal SCC
Hoarseness, and can metastasize to cervical lymph nodes
Nasopharyngeal SCC risk factors
- -EBV
- -Rare tumor in US, common in African children and Southern China (in adults)
Patterns of Nasopharyngeal SCC
Keratinizing, nonkeratinizing, undifferentiated carcinoma
Inverted sinonasal papillomas
Benign neoplasms arising from sinonasal mucosa and are composed of squamous or columnar epithelial proliferation
Why are inverted sinonasal papillomas more likely to recur than other papillomas?
Inverted growth pattern consisting of thickened epithelial nests arising from the surface and growing down into the stroma
–Malignant transformation can occur
Most common sites of metastases for oral cavity SCC
Cervical neck lymph nodes (local). Distant–mediastinal lymph nodes, lungs, liver, bone
Xerostomia
- -Dry mouth from decrease in saliva production
- -Causes: Sjogren’s syndrome, previous radiation therapy, side effect of prescribed medications
Sialadentis
- -Inflammation of salivary glands
- -Causes: trauma, bacterial or viral infection, autoimmune disease (Sjogren’s)
Sialolithiasis
–Stone in salivary duct that can cause obstruction and secondary bacterial infection (due to staph aureus or strep viridans)
LESA (Lymphoepithelial sialadenitis or Mikulicz disease)
- -Autoimmune disease involving salivary glands
- -50% of cases are salivary gland manifestations of Sjogren’s syndrome
Pathologic features of LESA
–Polyclonal lymphoid inflammation of salivary gland–> gland enlargement and lymphoepithelial lesion
What do you need to distinguish LESA from?
Primary lymphoma of salivary gland
Causes of mucocele
- -Retention mucocele: blockage of minor salivary gland
- -Extravasation mucocele: traumatic injury of minor salivary gland
Mucocele appearance
- -Fluid-filled mucosal nodule w/varying degrees of inflammation
- -Leakage of contents into surrounding connective tissue stroma
Ranula
Mucocele that occurs when sublingual duct damage. Can be quite large and dissect into neck
Pleomorphic adenoma
- -Most common salivary gland tumor
- -Usually in parotid gland (but can occur in both major and minor salivary glands)
- -Benign tumor
Microscopic appearance of pleomorphic adenoma
–Mix of proliferating epithelial (ductal and myoepithelial) cells assocaited with mesenchymal matrix of myxoid, hyaline, chondroid tissue
Key clinical features of pleomorphic adenoma
- -Painless, discrete masses
- -Seem well-circumscribed, but have extensions
- -Carcinoma can arise in pleomorphic adenoma (rare though)
Warthin tumor (papillary cystadenoma lyphomastosum)
- -2nd most common salivary gland tumor
- -Almost always in the parotid gland
- -Multifocal and bilateral
- -Smokers have 8x higher risk
Warthin tumor microscopic appearance
Well-encapsulated, papillary, cystic lesion() w/dual layer of bland, neoplastic, eosinophilic epithelium. Associated with reactive lymphoid stroma*
Mucoepidermoid carcinoma
- -Most common MALIGNANT salivary gland tumor
- -most common malignant salivary gland tumor in children
- -60-70% in parotid gland, can occur at any age
- -High grade tumors have survival rate of 50%
Mucoepidermoid carcinoma microscopic appearance
Mixture of squamous cell, mucus-secreting cells, intermediate cells, clear vacuolated cells containing mucin.
–OFten infiltrate margins, even though they grossly appear encapsulated
Adenoid cystic carcinoma
- -Slow growing, relentless, predilection for NEURAL INVASION
- -Can occur in major glands, 50% occur in minor salivary glands
- -Can reoccur decades after removal
- -Most common malignant tumor of minor salivary glands
Adenoid cystic carcinoma microscopic appearance
Cribiform pattern enclosing secretions
Most common benign salivary gland tumors
- -Pleomorphic adenoma 50%
- -Warthin tumor
- -Oncocytoma
- -Other (basal cell and canicular adenoma)
Most common malignant salivary gland tumors
- -Mucoepidermoid carcinoma (15%)
- -Adenocarcinoma (NOS) (10%)
- -Acinic cell carcinoma (5%)
- -Adenoid cystic carcinoma (5%)
- -Malignant mixed tumor (3-5%)
Esophageal stenosis
- -Can be congenital
- -Usually due to injury and inflammation from chronic gastroesophageal reflux, irradiation or caustic injury
Tracheoesophageal fistula
Type C most common (esophageal atresia w/distal tracheoesophageal fistula)
Esophageal mucosal webs
Protrusions of mucosa that can cause obstruction
- -Usually in upper esophagus
- -Plummer-Vinson Syndrome
Schatzki rings
- -Like esophageal webs, but thicker and circumferential, may contain muscularis propria
- -Located in lower esophagus
Mallory-Weiss Syndrome
- -Presence of longitudinal mucosal lacerations in the distal esophagus and proximal stomach
- -Usually associated w/severe retching or vomiting
- -Hx of heavy EtOH use in 40-80%
- -Can be cause of upper GI bleeding
Boehaave Syndrome
- -Transmural rupture of distal esophagus w/pneumomediastinum
- -Can be complication of Mallory-Weiss Syndrome
Zenker’s diverticulum
- -Located above upper esophageal sphincter (*) as outpouching of mucosa through weakened posterior cricopharyngeus muscle
- -Not true diverticulum
- -Can accumulate food producing mass and painful swallowing, regurgitation and diverticululitis
- -Seen on barium study
Achalasia
- -Incomplete lower esophageal sphincter relaxation, increased LES tone, aperistalsis of esophagus
- -Primary: caused from idiopathic degeneration of neurons in esophageal wall myenteric plexus
- -Secondary: Chaga’s disease, infiltrative malignancy of esophagus, amyloidosis, sarcoidosis
Hiatal hernia
- -From separation of diaphragmatic crura and protrusion of stomach into thorax through the defect
- -Congenital or acquired later in life
- -Similar symptoms to GERD w/inflammation, ulceration, stricture, hematemesis
Most common type of hiatal hernia
Sliding type (Type 1) (98% of hiatal hernias)
3 most common types of infectious esophagitis in immunocompromised patients
- -Candida
- -Herpes simplex
- -CMV
Pathogenic mechanism of eosinophilic esophagitis
- -Likely some allergic reaction to food allergens
- -Mild eosinophilia in 40-50% of patients
- -Many patients have other allergies
Microscopic appearance of eosinophilic esophagitis
Increased eosinophilic inflammation (>15 eosinophils/HPF), w/ basal epithelial hyperplasia, in absence of acute inflammation, squamous hyperplasia
Clinical presentation of eosinophilic esophagitis in adults
Food impaction, persistent dysphagia, and GERD symptoms that fail to resolve to medical therapy
Clinical presentation of eosinophilic esophagitis in children
Feeding disorders, vomiting, abdominal pain, dysphagia and food impaction
Barrett’s esophagus
- -Conversion of normal squamous mucosa of esophagus to METAPLASTIC COLUMNAR EPITHELIUM as result of chronic GERD
- -Endoscopically recognizable and confirmed pathologically to have intestinal metaplasia (Goblet Cells)
- -Occurs in 10% of patients with symptomatic GERD
Diagnosis of Barrett’s esophagus requires what?
Endoscopic and histologic evidence of metaplastic columnar epithelium (endoscopy and biopsy)
What does Barrett’s Esophagus have an increased risk for?
Esophageal glandular dysplasia and adenocarcinoma
Esophageal adenocarcinoma
- -Often arises from Barrett’s esophagus and long-standing GERD
- -Progression can occur through stepwise acquisition of genetic and epigenetic changes
- -Amplification of EGFR seen in some tumors
Esophageal adenocarcinoma location and symptoms
- -Usually in distal 1/3 of esophagus
- -Pain on swallowing, hematemesis, chest pain, progressive weight loss
Treatment for some types of esophageal adenocarcinoma
Neoadjuvant radiation and chemotherapy prior to resection (advanced)
Some endoscopic mucosal resection can be used to treat tumors with no or minimal invasion
Esophageal squamous cell carcinoma risk factors
–EtOH and tobacco use, caustic esophageal injury, achalasia, tylosis, Plummer-VInson syndrome, very hot beverages, and HPV
Esophageal squamous papilloma cause (most common)
HPV
Most common benign mesenchymal tumor of esophagus
Leiomyoma
