Oesophagogastric and Bariatrics Flashcards
(47 cards)
What is the physiology of the gut-brain axis when food is consumed?
- Enteroendocrine cells sense luminal factors, such as nutrients.
- EEC’s secrete gut hormones such as oxyntomodulin (OXM), and glucagon-like peptide 1 (GLP-1), which alert the CNS that nutrients are in the gut.
- Paracrine mechanisms (vagal, spinal afferents) also alert the CNS.
- This signaling acts on the hindbrain and hypothalamus to reduce food intake, increased energy expenditure, slow GI motility, and increase nutrient utilisation.
- Adipose tissue acts as an endocrine and immune organ.
- Ghrelin - produced by the enteroendocrine cells in the stomach - stimulates hunger and increases gastric motility.
- Leptin - produced by adipocytes - inhibits hunger
- White adipose tissue produces cytokines such as IL-6 an TNFa - some of which are pro-inflammatory mediators and contribute to the obesity related complications.
What are the mechanisms of weight loss after bariatric surgery?
Hormonal signaling
- Patients have reduced food intake with decreased pre-meal hunger and increased satiety.
- Metabolic surgery increases the amount of post-prandial gut secretion of entero-endocrine hormones (GLP-1, GLP-2)
- Changes in nutrient concentrations, and higher nutrient loads to distal gut segments result in higher levels of peptides secreted by EEC’s which increase satiety.
- GLP-1 increases which slows gastric emptying, inhibits glucagon release, and promotes insulin secretion from the pancreas.
- Ghrelin production (hunger hormone) is reduced
Neural signaling
- Vagal nerve signaling increased which reduces food intake and hunger.
Gut microbiota
- After bariatric surgery, there is a change in gut microbiota which changes the energy utilisation of these microbes which may contribute to weight loss.
Bile acids
- Plasma bile acid levels a higher in patients after bariatric surgery.
- High bile acids correlate with lower post-prandial BSL.
- BA also promote other peptides including GLP-1 (which stimulates satiety)
- BA usually stay high for 3-4 years after surgery, and promote intestinal hypertrophy.
What are the NICE guidelines for suitability for metabolic surgery
BMI 40+
BMI 35-40 with a metabolic complications.
BMI 30+ with diabetes which cannot be controlled by medication.
How does Liraglutide work (Saxenda)
GLP-1 agonist
- stimulates glucose dependent insulin secretion
- delays gastric emptying
What is the normal “phi” angle for a gastric band
What is another sign of a slipped band
10-60 degrees
“O” sign
What are the different types of sleeve leaks
Type 1
Phlegmon only
Type2
Abscess with or without contrast extravasation.
Type 3
Generalised peritonitis - gas and fluid throughout abdomen.
Type 4
Chronic leak
What are the CT findings for an internal hernia after bypass?
Mesenteric swirl sign.
Retroperitoneal stranding.
Increased volume of bowel in LUQ.
Closed loop SBO
What is the aetiology and treatment of BP limb obstruction?
Ileus
Mechanical
Iatrogenic vagal injury which delays gastric emptying.
Need to
- consider revising JJ
- gastostomy to decompress stomach
What is early dumping and late dumping?
Early dumping
- Symptoms occur 10-30 minutes after a meal. Rapid transition of hyperosmolar chyme into the SI causes fluid shift from the vascular to the intestinal lumen, leading to increased volume in the small bowel.
- This can cause abdominal cramps, tachycardia, diarrhoea and nausea.
Late dumping
- Also known as post-prandial hyperinsulinemia hypoglycaemia.
Occurs 1-3 hours after a meal.
- Exact mechanism is unclear but is likely to due rapid absorption of carbohydrate which exaggerates the glucose mediated insulin response.
What are the different types of gastric ulcer
Type 1
- antral near incisura
- not associated with acid hypersecetion.
- more likely to be malignant.
Type 2
- two ulcers
- distal lesser curve and duodenal
- associated with acid hypersecretion.
Type 3
- pre-pyloric
- associated with acid hypersecretion.
Type 4
- proximal body
- not associated with acid hypersecretion
What is the pathophysiology of H pylori in causing ulcers and gastritis?
- Colonises the gastric mucosa causing inflammation and subsequent breakdown of the protective mucus layer.
- It also impairs the secretion of bicarbonate, resulting in the stomach juice becoming more acidic.
- D cells of the stomach, which produce somatostatin are damaged - this results in increased production of gastrin - further driving down the pH.
- Because of the low pH content entering D1, gastric metaplasia occurs, which results in mucosa which is more prone to ulceration.
over time, when patients develop pangastritis, there can be a reduction in gastric acid secretion - which drives intestinal metaplasia and the subsequent gastric carcinoma pathway
What are the virulence factors of H pylori
Urease
- Converts urea into ammonia - ammonia is alkaline - helps H pylori neutralize the stomach acid around the bacteria - allowing it to survive.
* Ammonia also has a toxic effect on gastric epithelium contributing to inflammation.
Flagella
* Allows it to move through mucus layer.
Adhesins
* BabA and SabA - allows H pylori to stick to gastric epithelial cells.
Cytotoxins
* CagA - cytotoxin gene A - is delivered into the cell and disrupts signaling resulting in inflammation.
* Also increases risk of gastric cancer.
LPS layer
- Has low immunogenicity, allowing immune escape for years.
How do NSAIDS result in ulcer formation?
- Prostaglandin has protective functions for the gastric mucosa - stimulates mucin and bicarbonate production, and enhances mucosal blood flow.
- NSAIDS inhibit prostaglandin synthesis - by inhibiting COX which transforms arachidonic acid to prostaglandin.
- This subsequently results in mucin breakdown, bicarbonate reduction, and ulcer disease.
What are the different tests which can be performed for H pylori
Non-invasive tests
* Breath urease test – labelled urea tablet is swallowed, H pylori converts labelled urea to ammonia and c02, labelled c02 is exhaled. Significant false negative rates but false positive results are very rare. PPI’s need to be stopped prior to testing to avoid false negative’s
* Faecal test – looks for H pylori antigens in the stool. This is the most cost effective test - again PPI’s need to be stopped for 2 weeks to avoid false negative’s.
* Serology – poor test as it can’t distinguish past from present infection.
Invasive
* Endoscopy + biopsy and visualization - is gold standard
* Antral and gastric biopsies should be obtained for H. pylori.
* Rapid Urease test (also known as CLO test). Tissue is placed on slide, if H pylori is present, then urea will be converted to ammonia and C02 and change the pH. Change is detected by a reagent similar to litmus paper.
What endoscopic features suggest and ulcer might be malignant?
- Ulcerated mass protruding into the lumen.
- Folds around the ulcer which are nodular, fused, or stop short of the ulcer margin.
- Overhanging, irregular, or thickened ulcer margins.
How should you biopsy of a gastric ulcer?
- All 4 quadrants of the ulcer should be biopsied.
- If you are really concerned about the ulcer being malignant then use jumbo forceps.
How do you manage a large duodenal ulcer perforation?
Damage control options
- Pyloric exclusion + Nissen procedure + gastrojejunostomy
* The front wall of the duodenum is sutured directly onto the pancreas - which allows the duodenum to be closed.
* Omentum is then placed around the duodenum along with drains.
* The duodenum should be decompressed with an NGT
Pyloric exclusion with a Melcot catheter placed into the duodenal bulb + gastrojejunostomy
- Again should decompress the duodenum with an NGT
What are the components of the Rockall score? What is it used for?
A - age
B - blood pressure/presence of shock.
C - co-morbidities
D - diagnosis
E - endoscopic stigmata of recent bleeding.
Used to estimate the risk of re-bleeding
What is the Forest classification?
What is the risk of re-bleed for the first 4
Ia
- spurting bleeding.
- 60%
Ib
- oozing bleeding.
- 50%
IIa
- visible vessel
- 40%
IIb
- adherent clot.
- 30%
IIc
- flat spot in ulcer crater.
III
- clean based ulcer.
What are the options to achieve haemostasis when endoscopically controlling a bleeding peptic ulcer?
- Adrenaline injection - results in vasospasm and local tamponade. Shouldn’t be used alone.
- Bipolar diathermy
- Endoscopic clips - are also useful as can be marker if the patient subsequently requires embolization.
- Topical haemostatic sprays - i.e. haemospray - this acts as a mechanical barrier - when in contact with the bleeding site, it forms a barrier over the vessel wall, which allows concentration of clotting factors
What are the steps for surgically controlling a bleeding duodenal ulcer?
- Generally the bleeding ulcer will be in D1.
- The duodenum should be opened longitudinally in D1
- Generally a U-stitch is placed at the superior and inferior aspect of the ulcer which will ligate the GDA.
- If bleeding is ongoing place further sutures at 9 and 12 o’clock.
- This ligate a transverse pancreatic artery which can be coming off the GDA
- You have to be careful to not pick up the bile duct - can probe ampulla and determine location
- Can even place ureteric catheter into the bile duct.
- The duodenum should then be closed transversely using 4/0 PDS.
How would you assess a patient with a refractory peptic ulcer?
- Check compliance PPI therapy and NSAID avoidance.
- Re-rest for H. pylori
- Evaluate other medications patient takes.
- Ensure not smoking.
- If unsure about compliance can check gastrin level (if normal are not compliant as PPI’s suppress gastrin)
- Fasting gastrin levels should be checked or provocative test - to diagnose a gastrinoma.
- Need to again consider malignancy i.e. repeat biopsies.
What genetic syndromes are associated with gastric cancer?
FAP
Li-Fraumeni
Hereditary diffuse gastric cancer
Lynch Syndrome
Peutz-Jeghers syndrome.
What is the WHO classification of gastric cancer?
Histopathological classification
- Tubular – similar to intestinal type gastric cancer
- Papillary – similar to intestinal type gastric cancer.
- Mucinous
- Poorly cohesive signet Ring – similar to diffuse gastric cancer
- Mixed
