Pathology of Upper GIT I

Dr S. Ngwenya
Division of Anatomical Pathology
Oral cavity

Oesophagus Inflammatory
Infectious
Stomach and
Neoplastic
duodenum

Other

Small intestine

Colorectum
 Objectives
• Discuss a few oral cavity disorders that are specific to this site
and may explain other symptoms from other parts of the
gastrointestinal tract including leukoplakia, hairy leukoplakia,
sialadenitis and Sjogren syndrome.
• List the causes of acute oesophagitis.
• Describe the aetiology and pathogenesis of chronic / reflux
associated oesophagitis.
• Discuss the aetiology, pathogenesis, pathological findings and
complications of Barrett oesophagus.
• The normal histology of the small bowel and morphological
changes of injury.
• The aetiology of coeliac disease, the macroscopic and
microscopic features.
 Hairy leukoplakia
• Occurs in immunocompromised patients
– 80% have HIV
– 20% in transplant pts and cancer therapy
• Gross
– White
– Confluent patches of fluffy (hairy) hyperkeratotic
thickenings
– Lateral aspect of the tongue
 Hairy leukoplakia
• Microscopy
– Hyperparakeratosis
– Acanthosis with balloon cells
– Koilocytes, suggestive of HPV infection
 Candidiasis/thrush
• By far the most common fungal infection in the oral
cavity
• C. Albicans is a normal component of the oral flora in
+/- 50% of the population
 Risk factors
• Immune status
• Strain of Candida albicans
• Composition of individuals flora
 Clinical forms
• Three major clinical forms:
1. Pseudomembranous
– superficial curdy gray-white inflammatory
membrane (matted organisms &
fibrinosuppurative exudates)
– easily scraped off to reveal an erythematous
inflammatory base
2. Erythematous
3. Hyperplastic
Candidiasis / thrush
 Leukoplakia
- Any white patch or plaque that cannot be
scaped off and cannot be characterised as any
other disease
– Patches of keratosis
– Premalignant (5-25%)
– Risk factors:
– Heavy cigarette smoking
– Excessive alcohol consumption
– Poor dental hygiene
– Chewing betel quids
 Leukoplakia
• Pathology
– Occur anywhere in the oral cavity
– Solitary or multiple white patches or plaques with
sharply demarcated borders
– Hyperatosis, acanthosis and dysplastic changes
 Salivary glands
• Sialadenitis
– Inflammation of salivary glands
– Bacterial is rare
• An ascending infection from the mouth
 Xerostomia
• Abnormal dryness of the mouth
• Causes:
– Sjogren syndrome – autoimmune atrophy of
salivary glands
– Generalised dehydration
 Oesophagus
• Congenital and Mechanical disorders
• Inflammatory disorders
• Tumours
 Congenital and mechanical
disorders
• Heterotopic tissue
• Fundic type gastric tissue above the distal sphincter
• Atresia
• Failure of embryonical canalization of the oesophagus
• Diverticula
• Outpouching of the wall of hollow viscus
• Hiatus hernia
• The presence of part of the stomach above the
diaphragm
 Congenital and mechanical
disorders
• Achalasia
• Rare
• Contractility of lower oesophagus is lost
• Oesophageal varices
• Localised dilatation of veins
• Occurs in patients with portal hypertension
• Portosystemic shunting of blood when venous flow
through the liver is impaired
• Mallory-Weiss tears
 Inflammatory disorders of the
oesophagus
• Oesophagitis:
– Inflammation of the oesophageal mucosa

• Acute: - infectious:
• viral (HSV,CMV, other (HIV)
• Fungal
• Bacteria
• pill & corrosive substances
Candida oesophagitis
Herpes oesophagitis
 Chronic oesophagitis
• Aetiology:
– Specific causes are rare and include:
• Tuberculosis
• Crohn disease
– Nonspecific cause are very common
• Results from regurgitation of gastric contents
• Reflux oesophagitis
 Oesophagus:
1. Oesophagitis: Inflammation of the oesophageal mucosa

a. Acute: - infectious: viral (HSV,CMV, other (HIV))

fungal
bacteria
- pill & corrosive substances

b. Chronic - usually REFLUX associated with subsequent Barrett

oesophagus
- Eosinophilic oesophagitis

2. Carcinoma: a. squamous
b. adenocarcinoma ex-Barrett oesophagus
 Reflux oesophagitis
• GER is retrograde flow of gastric and/or duodenal contents
into the eosophagus.
• GERD is a symptomatic condition or histopathologic alteration
resulting from episodes of GER.
• Reflux oesophagitis is subset of GERD pts with histological
changes in the oesophageal mucosa.
 Reflux oesophagitis
• Contributing factors (loss of anti-reflux mechanisms):

•Defective or weak LES

•Presence of a sliding hiatal hernia
•Delayed gastric emptying
•Increased gastric acid production
•Bile reflux
•Impaired oesophageal peristalsis with transient LES relaxation
•Decreased salivary gland secretions
 Morphology
• Desquamation of the superficial squamous
cells
• Basal cell hyperplasia
• Elongation of papillae
• Chronic inflammation with eosinophils and
lymphocytes
 Complications
• Ulceration
• Haemorrhage
• Perforation
• Healing by fibrosis and scar formation
resulting in oesophageal stricture
• Barrett oesophagus
 Barrett oesophagus
• Results from longstanding reflux
• Lower oesophagus is lined by columnar
mucosa
• Premalignant condition
 Diagnosis
• Clinicopathological correlation
• Endoscopy:
– Columnar lined oesophagus
– Extension of pink columnar mucosa replacing the
pearl white stratified squamous epithelium
• Histology:
– Columnar intestinalised mucosa
– Columnar epithelium with goblet cells
Endoscopy
Pink columnar
mucosa
Microscopy
 Small intestine:
- Uncommon when compared to stomach/duodenum and large bowel

- Mostly infective (cholera, typhoid) and rare diseases such as Whipple’s (due to
Tropheryma whippelii) and coeliac disease, sprue, etc.

- NB – AIDS

- NB – lymphoma!
Normal histology:

Vast surface area

 Function
• Enzymatic digestion
• Absorption of nutrients
Response to injury - villous atrophy
 1. Enterocolitis

- Infectious – viral, bacterial, parasitic

- Malabsorption

- Idiopathic inflammatory bowel disease (IBD)

 Malabsorption
• Defective absorption of
• fats,
• fat-soluble
• other vitamins
• proteins,
• Carbohydrates
• Electrolytes and minerals
• Hallmark is steatorrhoea (excessive faecal fat
content)
 Malabsorption

a. Defective intraluminal digestion

b. Primary mucosal cell abnormalities
c. Reduced small bowel surface area (Coeliac)
d. Lymphatic obstruction
e. Infection
f. Iatrogenic
 Coeliac disease (Gluten-sensitive
enteropathy)
- chronic disease

- sensitivity to gluten

- autoimmune T-cell mediated chronic inflammatory reaction

 Incidence
• 1 in 2000
• Worldwide but rare amongst Asians and
Africans,
• Prevalence in European countries 0.05-
0.2%
 Clinical manifestations
• Anytime early childhood to late adulthood
• Abdominal discomfort, diarrhoea and
steatorrhea
• likely that the development and severity of
symptoms is related to the length of
intestine involved rather than the severity
of the mucosal pathology in a single
biopsy
 Aetiology
• IMMUNOLOGIC DISORDER
• Genetically susceptible individuals
• Two separate genes:
– HLA-DQ2 and
– HLA-DQ8
• Gene susceptibility loci are present on C5
and C19
 Pathogenesis
• In the proper genetic environment
exposure to gliadin, or the prolamin
fraction of gluten found in wheat, rye and
barley results in a local immune response;
the immune response involves both Ab
and cell-mediated injury
 Coeliac disease diagnosis
• Malabsorption - total
• Intestinal lesion by small bowel biopsy
• Unequivocal improvement in both symptoms
and mucosal histology on gluten withdrawal
from the diet
 Morphology
• Variable
• Depends on the stage of the disease
• Villous atrophy
• Increased intraepithelial T lymphocytes
Ischaemic necrosis / enteritis
Adhesion bands