L30 Flashcards
We are not producing gastric acid 24/therefore you have to switch it off.
what would happen if it wasn’t
If you did this you would over acidify the stomach causing gastric ulcers which could lead to internal beading and then death
there are 2 sites of feedback inhibition. what are they and what do they involve
body/corpus, which is site of acid secretion
antral region, which is site of gastrin secretion
both of these involve somatostatin
how does the corpus of the stomach body inhibit gastric secretions
Corpus of the body senses stretch therefore if there is less stretch then there is less stimulation of the ENS reducing gastric secretion
how does the antrum of the stomach inhibit gastric secretions
In the antrum there is a detected for acidity therefore if it gets too acidic it means that there is not enough food in the stomach to absorb it therefore it stops gastrin secretion so that there is less gastric secretion
what does the presence of H+
ions in lumen of the antrum cause
stimulates somatostatin secreting
cells (D cells) to produce
somatostatin
what is the function of somatostatin in the stomach/what does it act on
somatostatin acts as a paracrine hormone and inhibits gastrin production by G cells to decrease gastric secretions
it can also act as a endocrine hormone to inhibits parietal cell to decrease gastric secretions
what cells release somatostatin
D cells located in the antrum and body of the stomach
describe the ENS input to the D cells
The input from the ENS is negative
This is because when you are eating you get distention of the stomach which causes a positive signal to increase gastric acid and you need to switch off the off system.
The input from the ENS going to the D cells is always there as long as there is food in the stomach. When the signal becomes less (because of less stretch) the negative input from the ENS becomes less which causes the D cells to become more active.
There is no food in the stomach anymore therefore you release the break and increase somatostatin. This is also the vagovagal reflex
in the antrum somatostatin has an endocrine and paracrine effect?
im 99% sure
somatostatin cells in body/fundus produce somatostatin to limit acid secretion
somatostatin is released by D-cells
in the body/fundus of the stomach somatostatin acts as a paracrine hormone. it causes…
inhibits acid secretion by parietal cells
inhibits ECL cells so reduces histamine production
The feedback inhibition of gastric acid secretion
A. is mainly based on the enteric nerve system.
B. is mainly dependent on gastrin.
C. is entirely based on paracrine feedback.
D. is independent of the stomach body region.
E. is mainly facilitated by somatostatin.
A. ENS is the break for the D cells therefore less ENS input is what causes less gastric acid secretion
B.Somatostatin
C. Also endocrine (basted of the acidity of the antrum)
D. There are D cells in the body of the stomach (paracrine function)
E is correct
when do we switch gastric secretion on and off
cephalic phase = on
intestinal phase = off
when does the rate of gastric secretion increase and decreases
the increase will happen right after we eat food (gastric phase) and then about an hour after we have eaten it switches off (intestinal phase)
describe the Cephalic phase
prepares stomach for arrival of food
stimuli such as thought sight smell of food also the act of chewing and the presence of food in mouth
stimulates secretion via parasympathetic nervous system (PNS)
who does the PSN regulate acid secretion via the ENS
PNS stimulates ENS which in turn directly stimulates the parietal cells.
it also stimulates release of gastrin from antral region into blood
which stimulates parietal cells in body of stomach and stimulates ECL cells to secrete histamine which stimulates parietal cells
stimulates histamine release from ECL cells
paracrine stimulation of parietal cells
what does the ENS have input to in terms of the cephalic phase
we sense food through our special sensors which go to higher centers, from here the PNS is stimulated which then stimulate the ENS which stimulates……
ENS = ACh
ECL = histamine
G cells = gastrin
these all have positive input to the parietal cells which leads to an increase in acid secretion
describe the gastric phase
the stomach controls secretion through receptors which respond to…
stretch (distention)
products of digestion (antrum)
these receptors stimulate secretion via…
ENS - local reflex (products of digestion)
external reflex involving the CNS (due to distention) vagovagal reflex (from medulla)
As soon as the chyme leaves the stomach we need to switch off the secretion because otherwise we could over acidify
describe the intestinal phase
the intestine controls secretion by the stomach and its main effect (on the stomach) is to inhibit secretion
what causes the intestinal phase to switch off the gastric secretions
the presence of H+, monosaccharides, amino acids and fats in the duodenum
also the stretch of the duodenum
what happens when the presence of H+, monosaccharides, amino acids and fats in the duodenum (also the stretch of the duodenum) is detected in the duodenum
it releases CCK and secretin which are the negative regulators of G cells and parietal cells
CCK and secretion are also activated of the pancreas to cause bicarbonate and other pancreatic secretions
Therefore this steep is very coordinated (switches off the stomach and switches n the pancreas which is the next step for neutralisation)
Gastric acid secretion
A. is increased in the intestinal phase.
B. is regulated by acid and digestion products in the duodenum.
C. is mainly driven by sight, smell and thought.
D. is independent of the cephalic phase.
E. is down-regulated by the enteric nerve system.
A. switched off
C. mailly driven by gastric phase not cephalic
D, cephalic phase = on switch (preps the stomach)
E. upregulated
B is the correct answer