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Karan - MBBS Year 1: Gastrointestinal Week 1 > Pathology of the Mouth and Oesophagus > Flashcards

Pathology of the Mouth and Oesophagus Flashcards

1
Q

Describe leukoplakia

A
  • White patches >5mm in diameter - cannot be removed by rubbing or classified as any other diagnosable disease
  • Undergoes malignant transformation
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2
Q

What sites can leukoplakia be found and how are they distributed?

A
  • Anywhere in oral cavity e.g buccal mucosa, floor of mouth, ventral surface of tongue, palate
  • Found individually or collectively with other plaques
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3
Q

Describe the appearance of leukoplakia.

A
  • White patches or plaques with sharply defined borders
  • Surface may be smooth or wrinkled
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4
Q

Describe oral candidiasis

A
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5
Q

Describe microscopic findings for leukoplakia.

A
  • Surface stratified squamous epithelium
  • Hyperkeratosis and acanthosis
  • May show lesions with variable degree of dysplastic changes (including carcinoma in situ).
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6
Q

Describe erythroplakia.

A
  • Greater risk of malignant transformation than leukoplakia
  • Atypical epithelium
  • Speckled leukoerythroplakia has characteristics of leukoplakia and erythroplakia
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7
Q

Describe appearance of erythroplakia.

A
  • Red, velvety area within oral cavity
  • Remains level with or slightly depressed in relation to surrounding mucosa
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8
Q

Why would a biopsy be done during leukoplakia and erythroplakia?

A
  • Rule out dysplasia or carcinoma
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9
Q

What would subepithelial regions show in leukoplakia and erythroplakia?

A
  • LEUKOPLAKIA - Inflammatory infiltrate of lymphocytes and macrophages - intensity proportional to degree of dysplasia
  • ERYTHROPLAKIA - Vascular dilation and intense inflammatory reaction
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10
Q

Describe spread of oral cancer.

A
  • Soft tissues of cheek, mandible or maxilla and perineural spaces
  • Rare - regional lymph node metastasis
  • Unreported - distant metastasis
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11
Q

Describe gross appearance and microscopy of oral cancer.

A
  • GROSS - Large, fungating, soft papillary growth
  • MICROSCOPY - Evidence of hyperkeratosis, acanthosis and papillomatosis on surface epithelium. Swollen rete pegs extending into deeper tissue
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12
Q

Describe oral cancer pathogenesis.

A
  • Inactivation of p16 gene - leading to hyperplasia/hyperkeratosis
  • Mutation of p53 gene - progression to dysplasia
  • Overexpression of cyclin D1 gene - activates cell cycle progression
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13
Q

What are some risk factors for squamous cell carcinoma?

A
  • 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.
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14
Q

Describe squamous cell carcinoma.

A
  • 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 % .
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15
Q

Describe microscopic appearance of squamous cell carcinoma.

A
  • Infiltrative nests composed of squamous epithelium and intercellular bridges
  • Keratin formation visible
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16
Q

What is general presentation of oesophageal diseases?

A
  • Dysphagia
  • Chest pain
  • Regurgitation and heartburn
  • Pain lasting minutes to hours radiating to back
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17
Q

What do the oesophageal diverticula refer to?

A
  • 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
18
Q

What are the 3 characteristic locations where oesophageal diverticula occur?

A
  • Immediately above the upper oesophageal sphincter (Zenker diverticulum)
  • Near the midpoint of the oesophagus
  • Immediately above the lower oesophageal sphincter (epiphrenic diverticulum).
19
Q

Describe pulse pouching.

A
  • 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
20
Q

What is hiatal hernia characterised by?

A
  • Separation of diaphragmatic crura and increased space between muscular crura and oesophageal wall
21
Q

What are the 2 types of hiatal hernia?

A
  • 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.
22
Q

What is the clinical presentation and treatment for hiatal hernia?

A
  • PRESENTATION - Dysphagia, chest pain
  • Treatment - surgical repair
23
Q

Why is reflux unusual in rolling hernia?

A

Junction is preserved

24
Q

Describe achalasia.

A
  • Failure of LES to relax with swallowing
  • Presents with progressive dysphagia
25
Q

Describe cardiac achalasia.

A
  • 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
26
Q

How is cardiac achalasia screened for and diagnosed?

A
  • SCREENING - CCK test causing fall in sphincterr pressure
  • DIAGNOSIS - ‘Bird beak sign’ on barium swallow and manometry
27
Q

Decsribe GORD

A
  • 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
28
Q

How can GORD progress to cancer?

A
  • 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
29
Q

Describe cellular changes induced by GORD.

A
  • Epithelial changes - increased cell desquamation
  • Thickening due to increased basal cell activity
30
Q

Describe Barrett’s oesophagus.

A
  • 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)
31
Q

Describe microscopy behind Barrett’s oesophagus.

A
  • 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
32
Q

What is the gross appearance of Barrett’s Oesophagus?

A
  • Appears as one or several patches of red
  • Velvety mucosa extending from gastro-oesophageal junction upwards into oesophagus
33
Q

What are the complications of Barrett’s Oesophagus?

A
  • Chronic peptic ulceration
  • Risk of oesophageal adenocarcinoma
34
Q

List some risk factors for squamous cell carcinoma.

A
  • Smoking and drinking
  • Prolonged oesophagitis/coeliac disease
  • Achalasia
  • Genetic alterations e.g amplification of EGFR and cyclin D1
35
Q

Describe endoscopic appearance of oesophageal cancer.

A
  • Fungating or exophytic: Tumor protrude into and obstruct the lumen.
  • Ulcerative: Growth with elevated ulcer edges.
  • Infiltrating, or stenotic: Least common, predominantly intramural
36
Q

Where are oesophageal cancers most commonly found?

A

Middle third of oesophagus

37
Q

Describe adenocarcinoma of the oesophagus.

A
  • 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
38
Q

How can morphology of a tumour be described?

A

Site
Size
Shape
Surface
Consistency
Surrounding

39
Q

What are some risk factors for adenocarcinoma?

A
  • Barrett’s Oesophagus
  • Smoking
  • Obesity
  • Genetic alterations e.g overexpression of p53, nuclear translocation of b-catenin
40
Q

What criteria is used to stage oesophageal cancer?

A

TNM Staging

Karan - MBBS Year 1: Gastrointestinal Week 1 (6 decks)

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