Gastrointestinal tract

Pathology

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Oral cavity
Glossitis
- Inflammation of the tongue

- Is beefy red tongue found in certain deficiency

states such as
Vit B-12 , pyridoxin, and IDA

- It results from atrophy of the lingual papillae &

thinning of the mucosa exposing the underlying
vasculature
Infections
Herpes simplex virus infections
- Most orofacial infections are caused by HSV1
- Typically age is b/n 2-4 yrs & usually asymptomatic
- In 10-20% of cases, the primary infection presents as
acute herpetic gingivostomatitis
- Is severe and diffuse involvement of oral mucosa
• Clinical presentation ;
- multiple painful vesicular lesion

• usually resolve spontaneously within 3-4 wks

• After primary infection virus remains
in latent form
- Can be reactivated & produce cold sore
- Predisposing factors include
 exposure to UV light
 immunosuppresion
 pregnancy or menstruation
 exposure to excessive heat or cold
- They usually heal within 7 to 10 days
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Morphology
- Vesicles range from few mm to large bullae &
are filled with clear fluid.
Tzanck smear( fluid from vesicle) :
- Identification of the intracellular inclusion bodies is diagnostic
Oral candidiasis
- Most common fungal infection in the oral cavity
- C. albicans is the common etiologic agent

- Usually affects immunosuppresed individuals

such as pts with AIDS, DM, transplant recipients

- Broad spectrum antibiotics is another risk factors

- Clinical/Presentation:
- A superficial, whitish membrane
which can be easily scraped off
(and show underlying erythema)

Tx- Respond to topical antifungals

Hairy leukoplakia
- Uncommon oral lesion
- Almost excusively affects HIV pts.
- EBV is a major etiologic agent
- C/P ;
- Whitish confluent hyperkeratotic plaque
- Morphology
- Acanthotic and hyperkeratotic squames cells with
hairy projections

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 Precancerous lesions
• Leukoplakia and Erythroplakia
• Leukoplakia
• Is whitish patch or plaque that can not be scraped
off
• Until proved otherwise, all leukoplakias must be
considered precancerous
• Range from benign to markedly dysplastic lesions

• Erythroplakia
• Reddish, possibly eroded area that may be
depressed or flat
• has much higher risk (10x) of malignant
transformation
Leukoplakia erythroplakia

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Tumors of oral cavity
• Squamous cell carcinoma
• Most common tumor of Head and Neck region
• Accounts for 95% of cancers of the oral cavity
• Risk factors-
Tobacco, alcohol, sunlight
• Common sites –
lower lip, floor of the mouth, tongue, and
hard palate,
• Diagnosed late and thus poor prognosis
• Metastasis: to cervical LNs
 esophagus

Achalasia (means ‘failure to relax)

• Due to absence of myenteric ganglia
• Result in incomplete relaxation of the LES in response
to swallowing.
• This produces progressive dilation of the proximal esophagus.
• Classic/p- is progressive dysphagia
• Regurgitation and aspiration may occur

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• Pathogenesis is primarily idiopathic

• Secondary achalasia may arise in Chagas disease

- Trypanosoma cruzi causes destruction of the
myenteric ganglia
• 5% risk of malignant transformation ( SCC )
• Other complications include :
 Candida esophagitis, and Diverticula
 Aspiration pneumonia

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Lacerations (Mallory – weiss syndrome)
- Longitudinal tears in the esophagus at the GEJ
- It usually occurs secondary to severe retching or vomiting
- Commonly affects alcoholics.
- May involve only the mucosa or can be transmural
• Clinical presentation (UGIB)
• Account for 5-10% of upper GI bleeding
• Laceration is not usually fatal healing tend to be
prompt
Behave syndrome is rupture of the oesophagus and
- is a rare and catastrophic event

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Esophageal varices
• Tortuous dilated vessels in submucosa of distal esophagus
• Usually due to portal hypertension
• Develops in 90% of cirrhotic patients
• Schistosomiasis is the 2nd most common cause
Clinical features-

• no symptoms until they rupture

• If ruptured, produces massive haemorrhage

Reflux esophagitis (GERD)

- Is due to reflux of gastric content into
the lower esophagus
- mucosal injury is mainly due to action of the gastric juice

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 Causative factors include
Decreased tone of LES
- pregnancy, alcohol & tobacco

Other risk factors for reflux disease:

male white
middle age
overweight
family history
Morphologic Changes
- depend on the duration and severity of the exposure.

- Mild- appear as simple hyperemia, with no histologic

abnormality

- Severe case- mucosal erosions to total ulceration into the

submucosa.
C/f
- Usually affects adults over age 40
- Dysphagia, heartburn & regurgitation of sour brash
- Severe cases - hematemesis or melena
- Complications of severe GERD are
• Bleeding
• Stricture
• Barrett oesophagus
Barrett esophagus ;
- The distal esophageal mucosa is replaced by
metaplastic columnar epithelium
- Diagnosis is confirmed only by biopsy
- the columnar mucosa contains
intestinal goblet cells
- is the single most important risk factor for esophageal
adenocarcinoma
• Pts. has 30-40x risk of developing
adenocarcinoma than the general population

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 Squamous cell carcinoma
- It is the most common type of cancer in esophagus (90%)
- Usually affects adults over age 50 and has male
predominance
- Commonest area is mid 1/3 esophagus

Dietary & environmental risk factors

- Tobacco, alcohol
- high levels of nitrosamines contained in some foods

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• Adenocarcinoma
- Second common after SCC
- Majority arise from Barrett esophagus
- has 10% lifetime risk of developing adenocarcinoma
- usually affects the distal 1/3rd of the esophagus
- Other risk factors similar to SCC :
Tobacco exposure & obesity
• Clinical presentation :patient present later with
- Wt loss, anorexia, odynophagia, dysphagia
and obstruction later

Prognosis is generally poor

Stomach

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Gastritis
• Inflammation of the gastric mucosa
• Can be acute or chronic
Acute gastritis
• Acute mucosal inflammatory process, usually of transient
nature
• Is frequently associated with
-Heavy use of NSAIDs
-Excessive alcohol consumption
-Smoking & severe stress (e.g. trauma, burn, surgery)

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Mechanisms include
- Increased acid secretion
- Decreased production of bicarbonate buffer
- Reduced blood flow
- Disruption of the adherent mucus layer
- Direct damage to the epithelium

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 Morphologic changes

- Edema, vascular congestion, neutrophilic infiltrate

and
erosion
- Neutrophils in the epithelium above the BM signify
active inflammation

Clinical features:

may cause variable epigastric pain

nausea and vomiting or may cause

acute erosive haemorrhagic gastritis

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Chronic gastritis

• The presence of chronic mucosal inflammatory changes

leading to mucosal atrophy and epithelial metaplasia

- usually in the absence of erosion

• Dysplasia may be seen

• Two common causes of chronic gastritis are H. pylori and

autoimmune gastritis

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Helicobacter pylori
- gram negative rod
- The most common etiologic association with PUD (90%)
- Commonly affects the antrum
- Present in 90% of pts. with chronic gastritis
- Most infected individuals are asymptomatic
 Epidemiology of Helicobacter Infections

 Transmition is feco-oral (person-to-person)

EPIDEMOLOGICALLY
 ~ 20% UNDER the age of 40 years are infected
 50% above the age of 60 years are infected
 H. pylori is uncommon in young children

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Special features which make it survive the lethal environment
is

 Secretion of urease enzyme

- which produces ammonia to neutralize gastric acid
 Binding of H.pylori to gastric epithelial cells via a bacterial
adhesion molecule
 Expression of cytotoxin ( which cause destruction of mucus
producing cells)
Diagnostic tests for detection of H.pylori
- Serologic test for antibodies
- Fecal bacterial Ag detection
- urea breath test
- Identification of H.pylori in gastric biopsy

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 Treatment, Prevention & Control
Triple Chemotherapy (synergism):
Proton pump inhibitor (e.g., omeprazole =
Prilosec(R))
One or more antibiotics (e.g., clarithromycin;
amoxicillin; metronidazole)

Inadequate treatment results in recurrence of symptoms

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Autoimmune gastritis

- 10% of chronic gastritis and tend to be diffuse

- AB mediated destruction of parietal cells and IF

- leads to loss of acid production

- Is associated with other autoimmune ds such as Hashimotos

thyroiditis

- Increased Risk of developing gastric carcinoma and carcinoid

tumors
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Histologic changes
• Active inflammation
- neutrophils with in glandular & surface epithelial layer
• Regenerative changes :
– Diffuse gastric mucosal metaplasia
- gastric epithelium is replaced by intestinal epithelium
• Atrophy – marked loss in glandular structures
• Dysplasia- is a precursor lesion of gastric cancer
Clinical features
- Usually asymptomatic OR
- Nausea, vomiting & upper abdominal discomfort
- May lead to PUD & gastric carcinoma
Peptic ulcer disease
• Is chronic most often solitary lesions
• Can occur at any part of the GI tract exposed to the aggressive
action of acid-peptic juices
• Ulcer extends beyond the muscularis mucosae

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Peptic ulcer disease
• Occurs in the FF sites in order of decreasing frequency
• Duodenum, first portion
• Stomach, usually antrum ( lesser curvature)
• Gastroesophageal junction

Pathogenesis
• Imbalance b/n the gastroduodenal mucosal defence
mechanisms and the damaging forces
• Gastric acid and pepsin are prerequisite for all peptic
ulcerations

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• H. pylori can cause PUD by different
mechanisms
• By Production of urease , protease and
phospholipase which damages gastric mucus and
surface epithelial cells
• Recruitment of inflammatory cells

Z-E syndrome exhibit multiple ulcerations due to excess

gastrin secretion by a tumor ( gastrinoma)

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C/F
• Epigastric burning or aching pain
• Classically, the pain is relieved by alkalis or food,
• Nausea, vomiting, bloating, and belching, are other features

Few pts present with complications;

• Bleeding
• Perforation
• Obstruction from edema or scarring

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