gastric secretory function Flashcards
7 functions of the stomach
- reservoir
- mixing
- tituration
- secretion
- digestion
- defence
- absorption
what are the 3 sections to the stomach
- fundus
- body
- antum
what landmark signifies the end of the stomach
pyloric sphincter
what does the antrum produce (3)
- mucus
- pepsinogen
- gastrin
what does the stomach body produce(3)
- mucus
- pepsinogen
- HCl
what role does the stomach play in RBC production
secretes intrinsic factor which allows B12 to be absorbed -> recquired for haemaglobin formation
what are the exocrine gastric secretions (3)
- HCl (aka gastric acid)
- pepsinogen
- intrinsic factor
what are the endocrine gastric secretions (3)
- gastrin
- leptin
- ghrelin
what are the paracrine gastric secretions (2)
- somatostatin
- histamine
what are the 4 types of gastric control
- exocrine
- endocrine
- paracrine
- neurocrine
how does the body prevent itself from getting gastric ulcers due to HCl
- tight control system - acid only produced when needed
- defence and repair mechanisms - HCO3- for buffering, rapid repair
why is there a high energy requirement for HCl secretion
H+ must be actively pumped against its gradient which requires lots of ATP
what are the defensive forces of the stomach (against HCl/peptic enzymes - 6)
- surface mucus secretion
- bicarbonate secretion into mucus (buffer)
- mucosal blood flow
- apical surface membrane transport
- epithelial regenerative capacity
- elaboration of prostaglandins
what are the 7 main cell types of the stomach and what do they secrete
- parietal cell - HCl and intrinsic factor
- chief cell - pepsinogen, leptin
- enterochromaffin-like cell (ECL) - histamine
- G-cell - gastrin
- D-cell - somatostatin
- epithelial cell
- progenitor cell
what are the layers of the stomach wall (inner -> outer, 8)
Stomach Lining Must Surely Overcome Crappy Lunch Sandwiches
1. mucosa
-> Surface epithelium
-> Lamina propria
-> Muscularis mucosae
2. Submucosa
3. muscularis
-> Oblique layer
-> Circular layer
-> Longitudinal layer
4. serosa
what are the layers of the gastric glad (inner -> outer, 6)
- gastric lumen
- gastric pit (secretes HCO3-)
- gland region
-> mucous neck cells
-> chief cells
-> parietal cells - muscularis mucosa
what cells are found in corpus (body) glands of the stomach and what part of the gland are they found in (8)
- surface cells (pit)
- progenitor cells (isthmus)
- parietal cells (neck)
- D - cells (neck + some in base)
- ECL cells (neck + some in base)
- EC cells (neck) - secrete seratonin
- X cells (neck) - secrete ghrelin
- chief cells (base)
what cells are found in antral glands of the stomach and what part of the gland are they found in (7)
- surface cells (pit)
- G cells (pit + some in base)
- D cells (pit + some in base)
- ECL cells (pit + some in base)
- EC cells (pit)
- progenitor cells (progenitor zone)
- deep mucous gland cells (base)
what are the 3 conventional phases of gastric secretion and what stimulates them
- cephalic - vagus nerve mediated stimulation due to thought or oral ingestion of food
- gastric - food in stomach resulting in HCl secretion
- intestinal - food in small intestines, initially HCl secretion stimulated but later inhibited
what mediates the cephalic phase of gastric secretion
vagus nerve -> Ach
what mediates the gastric phase of gastric secretion (2)
- neural mediation -> both long nerve (vagus) and short reflexes (intramucosal) responding to stomach distension
- gastrin -> pH dependent mainly
what 4 factors affect gastrin function
- pH
- vagus nerve
- nutrient stimulation
- stomach distension
what mediates the intestinal phase of gastric secretion
hormones -> gastrin and enteric inhibitors (e.g. PYY, GLPs, enterogastrones)
what are the different forms of gastrin (2)
- gastric antrum (G-17)
- duodenum (G17 and G-34)
what is the main physiological stimulant of gastric acid (HCl)
gastrin
how does pH level determine gastrin secretion
a rise in pH results in gastrin secretion, but a pH < 3 inhibits gastrin secretion -> works as -ve feedback loop
what factors can directly stimulate gastrin secretion
- Ca2+
- amines
what type of receptors does gastrin bind to?
CCK receptos - 7 transmembrane receptors
what hormone can control gastrin secretion
somatostatin
how do D cells aid in gastrin inhibition
D cells detect high levels of H+ (i.e. low pH) -> intracellular [Ca2+] levels raised -> somatostatin release (acts in paracrine manner) -> inhibits gastrin secretion
what is the parietal-ECL-D cell unit
functional cellular unit of acid secretion located in the gastric body
how does the parietal-ECL-D cell unit work
- gastrin + vagus nerve act on ECL cell
- ECL cell secretes histamine
- histamine activates parietal cell
- D cell inhibits gastrin secretion via SST release due to pH drop => inhibits parietal cell activation
what are the 3 main stimulants of gastric acid secretion
- ACh
- Gastrin
- Histamine
how does ACh cause gastric acid release (2)
- vagus nerve mediated stimulation of gastrin -> histamine stimulation -> parietal cell activation
- direct stimulation of parietal cell via M3 muscarinic receptor (elevates Ca2+)
how does gastrin cause gastric acid release
- stimulates histamine release
- directly stimulates parietal cell (CCK2R)
how does histamine cause gastric acid release
directly stimualtes parietal cell - histamine H2 receptor stimulates cAMP in parietal cell
what are the main inhibitors of gastric acid secretion and how (2)
- somatostatin - inhibits gastrin and histamine secretion and inhibits the parietal cell directly
- PGE2 - inhibits parietal cell directly
acute effect of gastrin on ECL cells
histamine release (raised Ca2+)
intermediate effect of gastrin on ECL cells
histamine synthesis
chronic effect of gastrin on ECL cells
growth response -> hyperplasia
what happens to the canaliculus of parietal cells when they are active
it increases in size and resting pumps are inserted into the canaliculus membrane
what pump is involved in HCl formation in the canaliculus of a parietal cell
- H+/K+ ATPase (H+ into canaliculus) -> lots of energy is required to move H+ in opposing its gradient
(2. Cl- moves in down its gradient)
what are the 3 most important molecules that bind to parietal cells in the mucosa
- Ach
- gastrin
- histamine
what is the ultimate goal of the ECL cell
to release histamine in order to bind to the basolateral membrane of parietal cells and cause the insertion of a K+/H+ pump into the apical membrane
what is the main role of gastrin in secretion
to act on ECL cells causing them to secrete histamine
what are the 3 main activators of gastric acid secretion and what triggers them
- vagus nerve (thought of food, food in mouth, food in stomach);
- gastrin secretion (pH dependent mostly, vagal control, direct control)
- histamine secretion (gastrin, vagal control)
what is the bicarbonate tide
efflux of bicarbonate into the blood after acid secretion can be detected and is known as the alkaline tide -> neutralises the blood
what cells amplify the pro-acid secretion signals
ECL cells
what are the 3 main inhibitors of gastric acid secretion
- emptying of the stomach (less vagal reflex, less gastrin release)
- low stomach pH (inhibits the release of gastrin, -ve feedback mechanism)
- endocrine -ve feedback (somatostatin secretions)
what diseases result in to too much gastric acid secretion (7)
excess gastrin:
1. gastrinoma (ZE syndrome - not a tumour, just hyperplasia)
2. short bowel syndrome
3. non-gastrin ZES
4. G cell hyperfunction
5. H. pylori
excess histamine:
6. systemic mastocytosis
- hypercalcaemia (calcium is important in gastric acid release)
what is mastocytosis
a rare disorder characterized by abnormal accumulation and activation of mast cells in the skin, bone marrow and internal organs
what diseases result in too little gastric acid secretion (6)
- autoimmune gastritis
- H.pylori gastritis
- drugs
- vagotomy
- infectious diarrhoea
- gastric adenocarcinoma (colonisation of stomach w bacteria + carcinogens)
what upper GI diseases occur with normal acid secretion (4)
- GORD
- NSAID-induced disease
- functional dyspepsia
- stress ulcerations (cushing’s, curler’s)
what is zollinger-ellison syndrome
a condition in which a gastrin-secreting tumour or hyperplasia of the islet cells in the pancreas causes overproduction of gastric acid, resulting in recurrent peptic ulcers
what is atrophic gastritis and what can be sen on imaging
a chronic inflammation and thinning of your stomach lining accompanied by a change in your stomach lining cells to mimic intestinal cells -> absence of rugae is seen
