Acute Gastritis

Stomach inflammation
Triggered by damage to the gastric mucosa

Exists as acute/chronic

Acute Gastritis
Transient acute inflammatory response to damaged gastric mucosa
* superficial & self-limiting

Symptoms
Epigastric burning
Nausea
Vomiting
Severe:
Severe pain/Haematemesis/Melaena (partially digested blood)/Shock
a/w/ mucosal erosion/ulceration/haemorrhage/acute necrotising gastritis

Aetiology
Mainly chemicals
Alcohol
Smoking
NSAIDs
ChemoTx
Bile reflux

Stress
Hospital
Trauma
Burns

Infections
HSV
CMV

Pathology
Inflammation occurs from:

• Decreased gastric blood flow = compromised mucosal defences
• Decreased bicarbonate production = disrupted protective mucus layer
• Direct epithelium damage

Ix
Mucosa - normal/slightly erythematous
Micro
Oedema
Vascular congestion
Acute inflammatory cells in mucosa (neutrophil polymorphs)
Severe
Erosions
Ulceration
Haemorrhage

Erosions + Haemorrhage = acute erosive gastritis.

Oesophageal Tumours - Adenocarcinoma

Commonly Caucasian men in 50s

Risk Factors
Smoking
Alcohol
Barrett's Oesophagus

Aetiology
Commonly arises in areas of Barrett's Oesophagus
Associated with dysplastic epithelium
Progression from in-situ to invasive carcinoma less clear than SCC
Genetics: p53 gene mutation & chromosome 17p allele loss possibly involved tumour genesis

Ix
Distal oesophagus
Flat, ulcerating, infiltrative lesions
Classified as early/advanced tumours

Microscopy
Commonly intestinal-type differentiation
Less commonly gastric-type differentiation
* with mucus production

Clinical Course
* advanced at diagnosis, extending to surrounding structures, as tumours have to be large enough to produce dysphagia and local complications
Early Dx 5yr survivals = 75%
Overall 5yr survival = 5-10%

Oesophageal Tumours - Squamous Cell Carcinoma

Malignant oesophageal tumours = 5% of cancers.
Most common = squamous cell carcinomas & adenocarcinomas
SCC = 90% of oesophageal carcinomas
Higher incidence in China & Japan
Western world, however, AdCa = SCC

Both present with:
Dysphagia
Weight Loss
Anaemia

Squamous Cell Carcinoma

Commonly presents in 50s & males

Risk Factors
Environment:
Diet
Nitrates (smoked/pickled foods)
Smoking
Alcohol
Nutritional deficiencies

Host:
Long-standing oesophagitis
Achalasia
Plummer-Vinson Syndrome

Pathology
Ill-defined genetic associations
Epithelial dysplasia leads to carcinoma in-situ (intraepithelial neoplasia) leads to invasive carcinoma

Ix
80% in lower 2/3 of oesophagus
Endoscopy
protruding (60%)
flat (15%)
excavating (25%)

Microscopy
Early/advanced (invasion of submucosa) lesions
Poorly differentiated/Well differentiated (Squamous cells with keratinization and intercellular bridges)

Staging = TNM classification

Cx

Metastases occur early to:

LNs

Mediastinum

Liver

Bone

Barrett's Oesophagus

The word oesophagus reminds me of the muppet Snuffleupaguss.

Moving on.

Barrett's Oesophagus
aka Columnar-Lined Oseophagus aka CLO

Does exactly what it says on the tin. No, it doesn't sell shoes, silly, not that bit of the tin - the CLO bit.
Barrett's is the occurrence of metaplasia in the distal oesophagus, where its squamous epithelium is replaced by columnar epithelium, of the gastric/intestinal type.

Aetiology
It is a complication of chronic oesophagitis.and occurs in 10% of people with symptomatic GORD, and 40% of those with peptic oesophageal strictures.

Ix
Endoscopy!
 - abnormal red mucosa lies as islands or circumferential bands between the normal white squamous epithelium of the oesophagus and the normal gastric mucosa.
http://library.med.utah.edu/WebPath/GIHTML/GI416.html
.
Micro:
Sudden transition from squamous epithelium to columnar epithelium, proximal to GOJ.
Considered 'typical' Barrett's mucosa if it includes intestinal metaplasia i.e. goblet cells.
http://library.med.utah.edu/WebPath/GIHTML/GI171.html

Complications
x30/40 increased risk of adenocarcinoma of the oesophagus.
This can't be taken lightly, therefore CLO patients are required to undergo frequent endoscopy and biopsies.
The aim is to diagnose and treat and dysplastic changes when they occur, and treat any invasive disease ASAP.

Adenocarcinoma identified on biopsy
http://library.med.utah.edu/WebPath/GIHTML/GI406.html

Gastro-Oesophageal Reflux Disease, Ulcerations & Strictures, oh my!

GORD!!! Can you believe it?! GORD!!!
Enough of that.

Gastro-duodenal contents can enter the lower oesophagus, just for the hell of it, and a small amount of reflux, as it is known, can be perfectly normal. When abnormal reflux causes oesophagitis, however, this is known as Gastro-Oesophageal Reflux Disease.
Only a % of these actually have symptoms, though.

Symptoms:
Dysphagia

Regurgitation

Nocturnal asthma

Aetiology
Increased abdominal pressure

(pregnancy/obesity/trauma/vomiting)
Lower oesophageal sphincter incompetence
(smoking/alcohol/hiatus hernia/systemic sclerosis)
Decreased muscosal protection
(NSAIDs)

Ix
Endoscopy
 - normal/erythema
Biopsy +/- Barium Swallow

Histology
NB there is a poor correlation between symptom severity and the actual histological findings.
There are 3 diagnostic histological features in biopsies:

1. Epithelial Hyperplasia
2. Congestion of the lamina propria
3. Chronic inflammatory cells within muscosa

Neutrophils are suggestive of ulceration

Complications

• Mucosal erosions
• Ulceration
• Lower oesophageal stricture
• Bleeding
• Barrett's Oesophagus

Erosive & Ulcerative Oesophagitis
Well visualised at endoscopy.
Similar to those found in PUD.


Benign Strictures
Occur when recurrent/persistent ulceration leads to oesophageal fibrosis
These can be focal/circumferential = stenosis & dysphagia

Tx
Underlying causes/Sx

Oesophagitis

Oesophageal inflammation.
Affects 5% of the adult Western population.

Symptoms:
Retro-sternal burning (heartburn)
 - worse with leaning forward, or drinking hot liquids
Severe Presentation:
Dysphagia/Bleeding/Haematemesis/Melaena

Pathology:
Occurs due to damage to the oesophageal mucosa

Aetiology:
Risk factors include -
*GORD
Infection (candida/herpes/CMV/bacteria)
Chemicals (NSAIDS/toxins)
Radiotherapy
Crohn's

Acute Oesophagitis
http://library.med.utah.edu/WebPath/GIHTML/GI002.html
Neutrophils infiltrate the submucosa and squamous mucosa

Normal Oesophagus
http://library.med.utah.edu/WebPath/GIHTML/GI209.html

Hiatus Hernia

Definition:
"partial or total herniation of the stomach/gastro-oesophageal junction (GOJ) through the diaphragmatic hiatus, into the thoracic cavity"

Presentation:
Common, mostly > 50yrs
Can be asymptomatic/symptoms of reflux oesophagitis

Aetiology
Increased abdo pressure
Low residue diet
Laxity of diaphragmatic hiatus or peri-oesophageal attachments

Classification:
There are two main types of hiatus hernia:

• Sliding (most common)

In this, the GOJ is pulled up through the diaphragmatic hiatus (DH) +/- the stomach

• Para-oesophageal (5%)

In this, a part of stomach (*greater curve), slides up through the hiatus, between the oesophagus & the diaphragm. The GOJ remains secure.
It is x 4 more common in females.
Extreme cases - "upside down stomach" when the entire stomach herniates into the thoracic cavity.

Complications
Similar to reflux oesophagitis:

• mucosal erosions
• ulceration
• lower oesophageal stricture
• bleeding
• Barrett's Oesophagus