Physiology Of Gastric Acid Secretion

Question 1

3 components of stomach

Answer 1

Fundus
Body
Antrum

Question 2

Where is the oxyntic mucosa located?
What cells are present here?

Answer 2

Body of stomach
- Mucous cells, parietal cells, chief cells, and ECL cells

Question 3

Where is the pyloric gland area located?
What cells are present here?

Answer 3

Antrum of stomach
- G and D cells

Question 4

Gastric secretions:
Exocrine components
Endocrine and paracrine components

Answer 4

Exocrine:
- mucus from mucous cells
- HCl and Intrinsic factor from parietal cells
- Pepsinogen from chief cells

Endocrine:
- Histmaine from ECL cells
- gastric from G cells
- Somatostatin from D cells

Question 5

Secretion pathway of HCl in stomach

Answer 5

Done by parietal cells:
- CO2 is picked up from blood and made within cell via respiration —> binds with H2O via Carbonic anhydrase —> creates H and HCO3 —> H is pumped into lumen of stomach via H/K pump while HCO3 is pumped into blood via HCO3/Cl antiporter and then Cl moves into stomach down concentration down

Question 6

4 functions of HCl in stomach

Answer 6

1) converts pepsinogen to pepsin
2) breaks down CT and muscle fibres of digested food
3) breaks the tertiary structure of proteins
4) kills some ingested microorganisms

Question 7

Pepsinogen

Answer 7

Is the inactive form of pepsin and is activated by HCl into pepsin
- cleaves peptide bonds between amino acids
- stored in chief cells as zymogen granules (protects against autocatalysis of stomach wall)

Question 8

3 main components of Gastric Mucosal Barrier that prevent against injury

Answer 8

1) acid cannot penetrate the hydrophobic epithelial membrane
2) tight junctions prevent paracellular pathway of acid diffusion out of lumen
3) mucous from mucous cells lining gastric pits is protective
- lubrication, inhibits pepsin to protect against auto-digestion of stomach wall, and neutralizes gastric acid at epithelial surface

Question 9

Gastric Ulcer Formation

Answer 9

H. Pylori causes 80% of gastric ulcers, and NSAIDs cause 2nd most
- H. Pylori and its toxins VacA and CagA weaken mucosal barrier allowing acid and pepsin to penetrate the mucosal barrier
— VacA is a proton channel
— CagA is an oncogene that impairs cell repair

Histamine release from damaged epithelium enhance gastric acid and pepsin production (positive feedback loop)

H. Pylori can also stick their flagella into and burrow the self into mucosal membrane

Question 10

Intrinsic Factor
- released by?
- function?

Answer 10

Released by parietal cells
- required for absorption of vitamin B12 in the terminal ileum

Question 11

Pernicious anaemia

Answer 11

Is low RBC production
- caused by B12 deficiency as B12 is needed for DNA replication in RBC formation

Question 12

4 Chemical messengers that regulate gastric secretions

Answer 12

1. Achetylcholine (from vagal parasympathetic)
2. Gastric (secreted from G cells into the blood)
3. Histamine (released paracrinely via ECL cells)
4. Somatostatin (released from D cells)

Question 13

Acetylcholine function in stomach

Answer 13

Stimulates the below:
1) parietal cells to release H+
2) chief cells to release pepsinogen
3) ECL to release histamine
4) G cells to release gastrin

Question 14

Gastrin Function in stomach
1) secreted by?
2) effects on cells in stomach?
3) other functions

Answer 14

Secreted by G cells of the antrum into the blood in the presence of protein products in the stomach lumen
- causes:
1) parietal cells to release H, Chief cells to release pepsinogen and ECL to release histamine

Other functions?
A) is the primary factor for increasing gastric secretions during ingestion of a meal
B) promotes growth of gastric and duodenal mucosa to maintain their functionality

Question 15

Histamine
- released by?
- function

Answer 15

Released by ECL cells paracrinely in response to gastrin and ACh

Causes parietal cells to increase H+ secretion

Question 16

Somatostatin
- released by?
- function?

Answer 16

Released by D cells as pH drops in stomach (occurs as food leaves the stomach because proteins buffer pH)

• inhibit gastrin release and therefore H+, pepsinogen and histamine release

Question 17

Cephalon Phase of gastric secretions

Answer 17

taste, smell, sight and thought activate the cerebral cortex which activates the hypothalamus that sends projections down to the dorsal vagal motor nucleus of medulla which then sends axons down to Parietal and G cells of the stomach causing release of gastrin (G cells) and H+ from Parietal cells

Question 18

Gastric Phase of Gastric Secretions

Answer 18

Begins when food enters the stomach and proteins and peptides are the most potent stimuli
- Receptors in ENS initiate short- loop reflexes resulting in gastrin release from G cells
- a long-loop reflex (via vagus from stomach to Nodose ganglion, and then to dorsal vagal motor nucleus, and then back to stomach via vagus) also occurs activating H+ and gastrin secretions via vagal and ENS activity
- Histamine release is stimulated as well, augmenting H+ secretion
- distension, caffeine and alcohol also stimulate gastric juice production

Question 19

Intestinal phase of gastric secretion

Answer 19

Is inhibitory
- begins as chyme empties into the duodenum
- as the meal leaves the stomach, protein is removed, buffer against H is lost, pH decreases
— consequently, D cells release somatostatin that then inhibits parietal cell H+ production, chief cell pepsinogen production and ECL histamine secretion

• presence of fat, acid, hypertonic chyme and distension in the duodenum cause negative feedback via enterogastric reflexes and enterogastrones CCK and secretin
• also decrease gastric motility