9: Upper GI Disease Flashcards
The oesophagus: cell type, anatomy
25cm average
submucosal glands (evidence of oesophageal tissue)
stratified squamous epithelium (proximal ⅔)
one cell thick columnar epithelium (distal ⅓)
joined by squamo-columnar junction/Z-line
Name 5 conditions of the oesophagus
- Reflux oesophagitis = GORD
- Barrett’s oesophagus
- Oesophageal adenocarcinoma
- Squamous cell oesophageal carcinoma (MOST COMMON TYPE WW squamous cell)
- Varices
Reflux oeseophagitis = GORD
Commonest cause of oeseophagitis (other cause is corrosive), stomach acid rises up into oesophagus
Inflammation → metaplasia → metaplasia (+/- goblet cells) → dysplasia → cancer
complications:
- Barrett’s oesophagus, ulceration, haemorrhage → haematemesis/melaena, stricture, perforation
Los Angeles classification
Mx:
- lifestyle (stop smoking, weight loss)
- PPI/H2 receptor antagonist
Barrett’s oesophagus (or columnar-lined oesophagus/CLO)
things to remember
what stain
Intestinal metaplasia of squamous mucosa → columnar epithelium (have +/- goblet cells) following chronic GORD → upward migration of the SCJ
- with goblet cells has HIGH CANCER RISK
stain with METHYLENE BLUE
seen in 10% of those with symptomatic GORD
can lead to adenocarcinoma: metaplasia → dysplasia → cancer
2 pathways to cancer
- Polyp pathway (lower GI pathway)
- Flat pathway (upper GI pathway; metaplasia (i.e. CLO ± IM) → dysplasia → cancer)
Oesophageal Adenocarcinoma (most common oesophageal cancer)
can be from Barrett’s oesophagus → usually seen distal ⅓
RFs = smoking, alcohol, obesity, prior radiation therapy
most common in caucasians, M
Squamous cell oesophageal carcinoma (most common type WW)
Alcohol + smoking
Other RFs = achalasia of cardia, Plummer-Vinson syndrome, nutritional deficiencies, nitrosamines, HPV (high prevalence areas)
6x more common in A-C, M
usually middle ⅓
Features = progressive dysphagia, odynophagia,, anorexia, severe weight loss
Rapid growth and early spread → palliative care
Oesophageal varices triad
with management
Triad
- portal HTN (back pressure) → engorged dilated veins → cirrhosis, portal vein thrombosis, IVC obstruction
- porto-systemic anastomoses
- haemorrhoids
vomits units of blood → melaena
high mortality from bleeding and rebreeding
mx:
- resuscitation with blood + crystalloids
- terlipressin (vasoconstrictor)
- Glasgow-Blatchford scoring
- Upper GI endoscopy
- Infuse with PPI inhibitor
Stomach things to remember
Most sensitive to ischaemia
layers = mucosa (epithelium → lamina propria → muscularis mucosa) → submucosa → muscularis propria
MUCOID CELLS, lined by gastric mucosa, columnar epithelium (mucin-secreting) and glands
- parietal cells
- P cells (chief cells)
Goblet cells NAD → indicates intestinal-type metaplasia
3 types of gastritis
complications
Acute (neutrophils)
- alcohol consumption, NSAIDs, acute H. pylori, severe stress (burns), corrosives (bleach)
Chronic (lymphocytes and plasma cells)
- A = autoimmune (pernicious anaemia)
- B = bacteria (H. pylori)
- C = corrosives (bile reflux, NSAIDs)
- D = IBD
- CMV (patients on immunosuppression) and Crohn’s
- Can lead to gastric ulcer formation
Special types
- chemical (foveolar hyperplasia, chronic inflammation)
- infection (CMV, HSV, strongyloides)
- IBD
Complications
- ulcer
- perforation → peritonitis/bleeding
- haemorrhage
- cancer
Chronic gastritis associated with H. pylori → MALT
Caused by H. pylori (G-ve curved rod) → chronic antigen stimulation
- hydrogenase +/- CAG pathogenicity island → poorer outcome
Induces development of lymphoid follicles in germinal centres
increased risk of LYMPHOMA
Mx: remove cause (H. pylori via triple therapy = PPI, clarithromycin + amoxicillin or metro)
Gastric ulcer
breach through muscularis mucosa into submucosa
epigastric pain +/- weight loss
WORSE WITH FOOD (unlike duodenal ulcers), relieved by antacids
RFs: H. PYLORI, smoking, NSAIDs, stress, delayed gastric emptying, mainly in elderly
Ix: Biopsy for H. pylori histology status = punched out lesions with rolled margins. ALL ULCERS BIOPSIED TO EXCLUDE MALIGNANCY
Complications: anaemia (IDA) perforation (erect CXR), malignancy
Gastric cancer 2 main types (95%)
intestinal = well-differentiated, mucin-containing glands
diffuse = poorly differentiated, single cells, no glands, linitis plastics, SIGNET RING CARCINOMA
others = SCC, maltoma, GIST, neuroendocrine tumours (Z-E syndrome)
Duodenum: cell type, features
2:1 villous: crypt ratio
- depends on height of villi/depth of crypt
- if villi shorter, crypts take up bigger proportion of the total length
- when villi get damaged, crypts will proliferate to replace the damaged villi
Duodenal ulcers
4x more common than mastic ulcers
epigastric pain, worse at night
RELIEVED BY FOOD AND MILK
younger adults
RFs: H. PYLORI (most common cause), drugs, aspirin, NSAIDs, steroids, smoking, acid secretion
complications: anaemia (IDA), perforation (erect CXR)
- posterior ulcer → perforation → peritonitis
- anterior ulcer → gastroduodenal artery → major haemorrhage
