HistoPath - Upper GI Flashcards
(45 cards)
What is the z-line in the oesophagus
the point at which epithelium transitions from being stratified squamous epithelium to columnar
What are the layers of the oeseophagus
Epithelium
Submucosa
Muscularis externa
What is the gross structure of the stomach
Inlet: cardia
Fundus → body → antrum → pylorus
What do the presence of goblet cells in the stomach suggest
goblet cells are NOT normally seen in the stomach
The presence of goblet cells in the stomach is a feature of intestinal metaplasia
What are the layers of the normal stomach body and antrum, and what is the difference between them
- Gastric mucosa columnar epithelium (foveolar, mucin secreting)
- Lamina propria
- Muscularis mucosa
Body: lamina propria has specialised glands
Antrum: non-specialised glands, lacks specialised cells
What is the villous:crypt ratio in the duodenum and what happens the villi and crypt during proliferation
2: 1 villous: crypt ratio
When the villi get damaged, the crypts will proliferate to replace the damage villi
The cells proliferate in the crypt and then migrate upwards to the tip of the villous and shed at the top
What type of epithelium is found in the duodenum
Glandular epithelium with goblet cells (intestinal type)
What are the histological features of acute oesophagitis
Neutrophils
gross: Redness and inflammation of the oesophagus
What are the complications of acute oesophagitis
Ulceration:
- Necrotic slough
- Inflammatory exudate
- Granulation tissue
Fibrosis
Haemorrhage
Perforation
Stricture
Barrett’s oesophagus
What is the difference between an ulcer and an erosion
Ulcer = depth of tissue loss goes past muscularis mucosa (into submucosa)
Erosion = depth of tissue loss stops before muscularis mucosa (not into submucosa)
What is Barrett’s oesophagus
columnar-lined oesophagus (CLO)
Metaplastic process where squamous epithelium of the lower oesophagus is replaced by columnar epithelium
Reversible process
What are the two main types of Barrett’s oesophagus
CLO (metaplasia WITHOUT goblet cells = gastric metaplasia (Columnar epithelium)
CLO with IM (metaplasia WITH goblet cells = intestinal metaplasia (IM) = higher cancer risk)
What are the pathways to cancer in the GI tract
Flat pathway
Upper GI
Metaplasia → dysplasia → cancer
Polyp pathway
Lower GI
Adenoma precursor common
Describe the flat pathway to cancer development
(0) Squamous epithelium
(1) Metaplasia = not pre-malignant because reversible (however, metaplasia can progress to dysplasia)
(2) Dysplasia = changes showing some of the cytological and histological features of malignancy but with no invasion through the basement membrane (this is the stage that screening identifies at)
1. Low grade
2. High grade
(3) Adenocarcinoma = abnormal cells invade through the basement membrane
Can spread underneath the columnar epithelium
Describe adenocarcinoma of the oesophagus (site, causes, histological features)
Most common oesophageal cancer in developed countries
Lower 1/3 of the oesophagus
Associated with GORD and Barrett’s
All adenocarcinomas make glands and secrete mucin
Histology: mucin | glandular epithelium
Describe squamous cell carcinoma of the oesophagus (site, causes, histological features)
Upper 2/3 most common mid-oesophagus)
Associated with smoking and alcohol
Histology: Invades submucosa | cells produce keratin | intercellular bridges
What is the prognosis for oesophageal carcinoma
Poor prognosis
Diagnosis at pre-invasive stage is important
What are the features of oesophageal varices
Portal HTN
Porto-systemic anastomoses
Haemorrhoids
High mortality from bleeding and rebleeding
What is gastritis
Inflammation of the gastric mucosa
What are the causes of acute gastritis and what type of cells are involved
Chemical = Aspirin/NSAIDs, Alcohol, Corrosives
Bacterial = H. pylori, other (CMV, strongyloides in immunocompromised people)
Neutrophils
What are the causes of chronic gastritis and what type of cells are involved
Autoimmune (atrophic) = autoantibodies (i.e. anti-parietal cell ABs) BODY
Bacterial (atrophic/ non-atrophic) = H. pylori, other (CMV, strongyloides) ANTRUM
Chemical (NSAIDs, bile reflux) ANTRUM
D = Inflammatory Bowel Disease (Crohn’s)
Lymphocytes (may have co-existent neutrophils due to co-existent acute inflammatory processes)
What is the link between H. pylori and gastric cancer
Whilst H. pylori can bind to epithelial cells and inject toxins into intercellular junctions, they do NOT directly invade the epithelium
Can lead to CLO-IM-dysplasia, adenocarcinoma or lymphoma (MALToma)
8x fold increase in risk of gastric cancer
Chronic infection → MALToma (Abx can reverse lymphoma before it transforms)
What cancers are associated with atrophic and non-atrophic disease of the stomach
Atrophic → adenocarcinoma
Antrum-predominant gastritis
duodenal ulcer
Non-atrophic → MALToma
Non-atrophic pan-gastritis
MALToma
How does the site of gastritis within the stomach affect the outcome
Antrum predominant (atrophic) → duodenal ulcer
Body-predominant (atrophic) → gastric ulcer, adenocarcinoma (flat pathway)
Pan-gastritis (non-atrophic) → MALToma
