Gastro 2 Flashcards
Gastric Secretions and Motility stimulation
Increased parasympathetic activity via Ach and gastrin release
Local distension
Gastric Secretions and Motility inhibition
Low pH of stomach contents inhibits the release of gastrin
Feedback from duodenal overload (neural and hormonal)
Gastric Secretions and Motility stomach emptying
Liquids , carbs, protein, and fats
In presence of HCl, pepsinogen
is converted to pepsin
intrinsic factor is necessary for
absorption of vitamin B12
Somatostatin is released when
the pH falls below 3 to inhibit acid secretion
what is the most important physiological antagonist of HCl secretion
somatostatin
omeprazole is a
protein pump inhibitor
intestinal phase stimuli
Chyme in the duodenum leads to 2 things that will act to reduce acid secretion
a neural reflex that inhibits ACH release and the Enterogastrones are released to inhibit histamine release
first step of gastric secretion
food will stretch the walls of the stomach (distension), neural reflex to stimulate acid secretion
second step of gastric secretion
peptides and amino acids in food stimulate g cells to release gastrin which promotes secretion
food as a buffer
food also acts as a buffer raising the PH pH and thus removing the stimulus for somatostatin secretion from D cells
acid secretion in the gastric phase
When acid secretion is sufficient to lower pH, somatostatin can then inhibit gastrin release and digestion and the gastric phase is completed.
gastric secretion primary event
The primary event is of this phase is HCl release, it accounts for 60-70% acid secretion in response to a meal
what is catalyzed bycarbonic anhydrase during gastric HCl secretion
In the cell, CO2 produced from aerobic metabolism and combines with H2O to form H2CO3, H2CO3 then dissociates into H+and HCO3
how is H+ secreted during gastric HCl secretion
via the H+-K+ATPase channel into the lumen of the stomach
what follows H+ into the lumen and how?
Cl−follows H+into the lumen by diffusing throughCl−channels
HCO3−is absorbed into the blood via a
Cl−-HCO3−exchanger
Cl- in the cell
follow the positive charged H+ out of the cel but then is transported back into the cell via Cl−-HCO3−exchanger
alkaline tide
this is a high pH in gastric venous blood after a meal, caused by the Cl−-HCO3−exchanger