The Stomach and Peptic Ulcer

Question 1

Describe the composition of a gastric pit and relative functions

Answer 1

• Parietal cells secrete HCl for digestion and Intrinsic factor for vitamin B12 absorption
• Mucous neck cells secrete mucous as a protective lining, and bicarbonate as a buffer against acid
• G cells are found in the antrum and release gastrin under raised pH. Gastrin stimulates the secretion of HCl from parietal cells
• Chief cells secrete pepsinogen for protein digestion (activated by HCl) and gastric lipase
• Enterochromaffin-like cells secrete Histamine which binds to H2 receptors on parietal cells for acid secretion
• D cells and located in the antrum and release somatostatin upon lowered pH. This then inhibits gastrin production from G cells and HCl production from parietal cells (via G-protein)

Question 2

How can H.Pylori cause gastric cancer?

Answer 2

Infection leads o superficial gastritis which becomes atrophic gastritis hypochlorydria. The atrophy involved leads to dysplasia and therefore cancer

Question 3

How does an H.Pylori infection cause peptic ulcers?

Answer 3

H.Pylori is adapted to live in acidic environment of the stomach by its own personal supply of urease, which produces ammonia from urea, and a hydrocarbonate buffer in order to buffer acidic conditions. Due to this, G and D cells can be confused into thinking that conditions are less acidic than they are, and therefore somatostatin production ceased and gastrin production increased. This result in increased acid production from the parietal cells which causes damage to duodenal cells.
Also, due to the inflammation of the infection, there is reduced mucin in the stomach and cell junction interuption so reduced protection from gastric acid

Question 4

How can we test for H.Pylori infection?

Answer 4

Breath tests - give drink with C14 urea and H.Pylori will break down, allowing Carbon14 Dioxide to be breathed out - detected

• CLO-test using a biopsy and drowing culture in agar plate for sign or H.pylori
• Faecal antigen test of H.pylori
• Blood ests looking for antibodies against h.pylori. This is efficient but will also prove presence after infection due to remainding immunity

Question 5

What are the other causes of peptic ulcers?

Answer 5

NSAID abuse- these inhibit COX pathway (COX I in this case), resulting in decreased prostaglandin production. As these increase blood flow, a reduction will decrease blood flow and therefore decrease mucus secretion, resulting in reduced protection against acidic conditions.
NSAIDs also trap hydrogen ions, increasing the risk of gastric bleeding through anti-platelt action

Zollinger-Ellison syndrome is a condition in which a gastrin-secreting tumour causes overproduction of gastric acid, resulting in recurring peptic ulcers.

Question 6

Describe the treatment processes for a peptic ulcer

Answer 6

Treat H.Pylori with antibiotics, or reduce NSAID use. If this isnt possible then switch to COX-II NSAID which wont have this affect

Histamine H2 receptor antagonist - e.g. cimetidine

Proton-pump inhibitor - e.g. omeprazole

Antacids for symptoms of acid excess. These come in Mg and Al forms but as Mg causes diarrhoea and Al constipation, usually given in a combination form

Alginates - act as mucous layer to protect against acid

Question 7

Explain a possible metabolic consequence of Histamine receptor antagonist

Answer 7

Due to decreased acid production, there will be decreased pepsin for protein digestion and decreased protein degredation.

Question 8

List potential side effects of omeprazole

Answer 8

diarrhoea, headaches, muscle pains and confusion

Question 9

Describe the vasculature of the stomach

Answer 9

The lesser curvature is supplied by Left and right gastric arteries

The greater curvature is supplied by Left and Right gastro-epiploic arteries (these anastamose)

Fundus is supplied by sort gastric arteries

Question 10

Describe the physiology of gastric secretions

Answer 10

1. Cephalic Phase account for 40% of secretion where the sight, smell or taste or food activates the vagus nerve, causing acetylcholine stimulation of parietal cells, ECL cells and G cells.
2. Gastric phase accounts for 50% of secretion and is the longest phase (lasts ~2.5 hours) where distesion of the stomach stimulates mechanoreceptors, causing a vago-vagal cholinergic reflex, affecting G cells, parietal cells and ECL cells. G cells are further activated by partially digested proteins.
3. Intestinal phase accounts for remainder 10% of gastric secretions.Proteins in the duodenum activate duodenal G cells to produce gatsrin. However, duodenal distension causes an enterogasrtic reflex in order to suppress gastric secretions:
   - Secretin inhibits the release of gastrin
   - CCK and GIP are released due to fatty acids in duodenum, and inhibit parietal cells and suppress gastrin
   - Somatostatin is released from D cells to inhibit parietal cells

Question 11

draw diagram to show the secretion of acid (5 marks)

Answer 11

-