Pathology of the Mouth and Oesophagus Flashcards
Describe leukoplakia
- White patches >5mm in diameter - cannot be removed by rubbing or classified as any other diagnosable disease
- Undergoes malignant transformation
What sites can leukoplakia be found and how are they distributed?
- Anywhere in oral cavity e.g buccal mucosa, floor of mouth, ventral surface of tongue, palate
- Found individually or collectively with other plaques
Describe the appearance of leukoplakia.
- White patches or plaques with sharply defined borders
- Surface may be smooth or wrinkled
Describe oral candidiasis
Describe microscopic findings for leukoplakia.
- Surface stratified squamous epithelium
- Hyperkeratosis and acanthosis
- May show lesions with variable degree of dysplastic changes (including carcinoma in situ).
Describe erythroplakia.
- Greater risk of malignant transformation than leukoplakia
- Atypical epithelium
- Speckled leukoerythroplakia has characteristics of leukoplakia and erythroplakia
Describe appearance of erythroplakia.
- Red, velvety area within oral cavity
- Remains level with or slightly depressed in relation to surrounding mucosa
Why would a biopsy be done during leukoplakia and erythroplakia?
- Rule out dysplasia or carcinoma
What would subepithelial regions show in leukoplakia and erythroplakia?
- LEUKOPLAKIA - Inflammatory infiltrate of lymphocytes and macrophages - intensity proportional to degree of dysplasia
- ERYTHROPLAKIA - Vascular dilation and intense inflammatory reaction
Describe spread of oral cancer.
- Soft tissues of cheek, mandible or maxilla and perineural spaces
- Rare - regional lymph node metastasis
- Unreported - distant metastasis
Describe gross appearance and microscopy of oral cancer.
- GROSS - Large, fungating, soft papillary growth
- MICROSCOPY - Evidence of hyperkeratosis, acanthosis and papillomatosis on surface epithelium. Swollen rete pegs extending into deeper tissue
Describe oral cancer pathogenesis.
- Inactivation of p16 gene - leading to hyperplasia/hyperkeratosis
- Mutation of p53 gene - progression to dysplasia
- Overexpression of cyclin D1 gene - activates cell cycle progression
What are some risk factors for squamous cell carcinoma?
- Radiation exposure
- Welding, metal refining, diesel exhaust, wood stove, and asbestos exposure
- Chronic irritation of the mucosa - due to ill-fitting dentures, jagged teeth, or chronic infections
- Vitamin A deficiency and immunosuppression
- Poor nutrition.
Describe squamous cell carcinoma.
- Most common malignancy of the oral cavity
- Strong association with alcohol and smoking
- 30 % have regional lymph node metastases at presentation
- Overall 5-year survival ~ 50 % .
Describe microscopic appearance of squamous cell carcinoma.
- Infiltrative nests composed of squamous epithelium and intercellular bridges
- Keratin formation visible
What is general presentation of oesophageal diseases?
- Dysphagia
- Chest pain
- Regurgitation and heartburn
- Pain lasting minutes to hours radiating to back
What do the oesophageal diverticula refer to?
- Pouches lined by one or more layers of oesophageal wall
- False (pulsion) diverticula result from herniation of mucosa through muscular defects
- True (traction) diverticular consist of mucosal, muscular and serosal layers - result from perioesophageal/mediastinal inflammation and scarring e.g TB of lymph nodes
What are the 3 characteristic locations where oesophageal diverticula occur?
- Immediately above the upper oesophageal sphincter (Zenker diverticulum)
- Near the midpoint of the oesophagus
- Immediately above the lower oesophageal sphincter (epiphrenic diverticulum).
Describe pulse pouching.
- Involves pharyngeal puch
- Sac distended during swallowing of food
- Pushes down behind oesophagus causing compression
- EXAMPLE OF A CAUSE is abnormal function of upper oesophageal sphincter
What is hiatal hernia characterised by?
- Separation of diaphragmatic crura and increased space between muscular crura and oesophageal wall
What are the 2 types of hiatal hernia?
- Sliding hernia (95%): Characterized by upward dislocation of cardio-oesophageal junction. Oesophagitis resulting from the reflux is commonly seen.
- Para-oesophageal/Rolling hernia (5%): A part of the stomach passes through diaphragm, enters the thorax without any displacement of the cardio-oesophageal junction.
What is the clinical presentation and treatment for hiatal hernia?
- PRESENTATION - Dysphagia, chest pain
- Treatment - surgical repair
Why is reflux unusual in rolling hernia?
Junction is preserved
Describe achalasia.
- Failure of LES to relax with swallowing
- Presents with progressive dysphagia
Describe cardiac achalasia.
- Oesophagus dilated proximal to LES
- Barium swallows shows ‘bird beak’ sign
- Loss of ganglion cells in myenterix plexus
- Treatment - LES balloon dilation or myotomy
- Increased risk for oesophageal carcinoma
How is cardiac achalasia screened for and diagnosed?
- SCREENING - CCK test causing fall in sphincterr pressure
- DIAGNOSIS - ‘Bird beak sign’ on barium swallow and manometry
Decsribe GORD
- Reflux of gastric contents into lower oesophagus
- Diagnosed by 24 hour pH study
- Reflux associated with obesity, overeating, alcohol intake, smoking and pregnancy
- Presents with heartburn and regurgitation
- COMPLICATIONS - Bleeding, stricture, bronchospasm, asthma and Barrett oesophagus
How can GORD progress to cancer?
- Delayed gastric emmptying, increased acidity and decreased LES tone lead to initial lesions
- Scarring progresses to recurrent injury
- This progresses to strictures, pain and obstruction etc.
- This progresses to pre-malignant Barrett’s oesophagus leading to cancer
Describe cellular changes induced by GORD.
- Epithelial changes - increased cell desquamation
- Thickening due to increased basal cell activity
Describe Barrett’s oesophagus.
- Metaplastic changes in oesophageal lining - normal squamous epithelium changed to columnar epithelium
- Due to GORD
- Classified based on long segments (if >3cm involved) or short segment (if <3 cm involved)
Describe microscopy behind Barrett’s oesophagus.
- Intestinal metaplasia - normal squamous lining replaced by columnar mucosa
- In this area, goblet cells with distinct mucous vacuoles visible
- Metaplasia - risk factor for adenocarcinoma development
- Dysplasia may be seen
What is the gross appearance of Barrett’s Oesophagus?
- Appears as one or several patches of red
- Velvety mucosa extending from gastro-oesophageal junction upwards into oesophagus
What are the complications of Barrett’s Oesophagus?
- Chronic peptic ulceration
- Risk of oesophageal adenocarcinoma
List some risk factors for squamous cell carcinoma.
- Smoking and drinking
- Prolonged oesophagitis/coeliac disease
- Achalasia
- Genetic alterations e.g amplification of EGFR and cyclin D1
Describe endoscopic appearance of oesophageal cancer.
- Fungating or exophytic: Tumor protrude into and obstruct the lumen.
- Ulcerative: Growth with elevated ulcer edges.
- Infiltrating, or stenotic: Least common, predominantly intramural
Where are oesophageal cancers most commonly found?
Middle third of oesophagus
Describe adenocarcinoma of the oesophagus.
- Usually in distal third of oesophagus
- Appears as early lesions - flat or raised patches that either infiltrate or ulcerate
- Appears as malignant tumour with intestinal-type morphology of cells forming glands
- Tumours commonly produce mucin
How can morphology of a tumour be described?
Site
Size
Shape
Surface
Consistency
Surrounding
What are some risk factors for adenocarcinoma?
- Barrett’s Oesophagus
- Smoking
- Obesity
- Genetic alterations e.g overexpression of p53, nuclear translocation of b-catenin
What criteria is used to stage oesophageal cancer?
TNM Staging