Lecture 7 - The Stomach & Gastric Disease Flashcards
Locate the fundus, body, antrum, pyloric sphincter, cardia and lower oesophageal sphincter on the stomach.
How does the type of epithelium change at the LOS?
- From stratified squamous epithelium before the LOS to simple columnar epithelium after the LOS.
How are peristalsis and perceptive relaxation related to each other?
- Peristalsis causes reflex reaction of proximal stomach (receptive relaxation) where the fundus distends (swells) so the stomach fill without significant rise in pressure
What are the 3 muscular layers of the stomach which help to break down food?
Why is the stomach more muscular at the antrum?
- Circular, longitudinal & oblique muscle layers provide forceful contractions
- So food moves faster as it moves distally accelerating smaller particles to the pyloric sphincter so larger ones can stay behind for further breakdown
How are gastric pits & glands formed?
What cells are found within the gastric glands?
- Pits are evaginations of epithelia which lead onto gastric glands
- Contains parietal cells, chief cells & enteroendocrine cells
- Chief cells release pepsinogen, converted into pepsin by acidic conditions in stomach. G-cells secrete gastrin, parietal cells secrete HCl
What are the protective mechanisms in the stomach that protect the epithelia from the acidic conditions of the stomach?
1) Surface mucous cells produce mucus layer in which stomach epithelia secrete bicarbonate ions (pH neural layer)
2) Rich blood supply to gastric mucosa can remove any acid putting it in blood stream
3) Prostaglandins increase blood flow, support the mucus layer and are generally protective
4) High turn over of epithelial cells, every 2-4 days
How do parietal cells control the secretion of acid?
- Parietal cell secrete acid via a H+/K+ proton pump.
- Tubulovesicles within the within parietal cells contain these proton pumps
- During resting phase, tubulovesicles don’t associate with apical membrane and therefore lack K+ permeability so acid cannot be released
- When stimulated, they come together to exchange H+ & K+ ions
What 3 triggers stimulates acid production by parietal cells/the switch into the active phase?
1) Sensory triggers e.g.: sight/smell/taste - corresponds to the cephalic phase of digestion and is responsible for 30% of HCl release
2) Gastric triggers e.g.: stretch from food, presence of AA’s - corresponds to gastric phase of digestion and is responsible for 60% of HCl release
3) Intestinal triggers e.g.: chyme in duodenum - corresponds to intestinal phase of digestion and is responsible for 10% of HCl release
What 3 receptors are present on parietal cells that stimulates acid release?
1) Gastrin - from G-cells (gastric triggers) binds to CCK receptor on parietal cell
2) ACh - from vagus nerve binds to mAChR
3) Histamine - from entero-chromaffin like (ECL) cells stimulated by vagal stimulation bind to H2 receptors
How is acid secretion secreted in parietal cells?
D-cells recognise drop in pH due to build up in acid, stimulates production of somatostatin. Inhibits G-cells from producing gastrin, and therefore HCl from parietal cells.
What is gastro-oesophageal reflux disease (GORD)?
What are the symptoms?
What are the risk factors?
- When contents of stomach reflux into the oesophagus or sometimes pharynx
- Heart burn, acidic taste, cough or asymptomatic
- Raised IA pressure - e.g.: obesity, pregnancy, LOS dysfunction, hiatus hernia (where LOS has herniated through diaphragm into thorax)
What are the complications of GORD?
What are the treatment options for GORD?
Complications:
- Oesophagitis
- Ulceration
- Fibrous strictures
- Barett’s oesophagus - metaplastic change from stratified squamous to columnar epithelium, increasing the risk of dysplasia and production of adenocarcinoma.
- Lifestyle changes: weight loss, avoid trigger foods, eat smaller foods, cut out alcohol & caffeine
- Proton pump inhibitors (PPI’s) - good for symptom relief
- Surgery - fundoplication (fundus wrapped around LO to help with sphincter mechanism)
What is gastritis?
What are the differences in causes & pathological changes between acute and chronic gastritis?
- Inflammation of the stomach mucosa
- Acute caused by NSAIDS, alcohol, chemo & bile reflux
- Chronic caused by infection with H.pylori or autoimmune conditions
How does autoimmune chronic gastritis cause its symptoms?
- Antibodies attack parietal cells, parietal cells lost
- Atrophy of body of stomach causes gastritis, but intrinsic factor also lost
- Loss of B12 absorption, leading to megaloblastic anaemia, neurological symptoms & anorexia
How does H. pylori cause chronic gastritis?
- Infects 50% of population, enters via faecal-oral or oral-oral route, adheres to epithelial lining of stomach
- Has urease which converts urea and water into CO2 & ammonia which has higher pH than in stomach so it creates its own environment to live in
- Ammonia causes stomach epithelia damage, also has CAG A gene which inserts protein into stomach epithelia causing inflammatory response by stimulating IL-8
What is the difference between H.pylori colonisation in the antrum vs the body/fundus?
How is H.pylori infection diagnosed & treated?
- Antral colonisation causes overactivity of G-cells, causing a lot of gastrin release and acid release from parietal cells. This makes chyme leaving stomach more acidic causing damage to duodenum - e.g.: duodenal ulcers
- Body colonisation causes atrophy of parietal cells, which can be a precursor to dysplastic changes increases risk of stomach cancer
- Ingest urea enriched w/C13, causes breakdown of urease in H.pylori to CO2 & H2O. C13 detected in CO2 exhaled, indicating presence of H.pylori
- Treated with 2 x PPI’s + 2 x antibiotics for 7 days
What is peptic ulcer disease (PUD) and where are peptic ulcers most common?
What is the difference between gastric & duodenal ulcers?
- Defect in gastric or duodenal mucosa that extends through muscularis mucosa. Most common in duodenum, but also on lesser curve and antrum of stomach
