stomach physiology (demonaco) Flashcards
intrinsic factor and the stomach
IF binds to B12, which is required for B12 to be absorbed in the ileum
How does the stomach sterilize food?
Via gastric acids (HCl, pepsin)
What do the parietal cells of the proximal portion of the stomach secrete?
HCl, IF
stimuli: Ach, histamine, gastrin
What do the Chief cells of the proximal portion of the stomach secrete?
Pepsinogen
- inactive form of pepsin
- proteolytic enzyme of the gastric juice
stimuli: vagal cholinergic NTs (Ach)
What do the endocrine cells of the proximal & distal portions of the stomach secrete?
gastrin, histamine
stimuli: protein digestion, vagal stimuli
HCl and pepsinogen relationship
Food present in stomach –> parietal cells stimulated (via Ach, histamine, gastrin) –> HCl is secreted –> HCl breaks down pepsinogen –> pepsin breaks down peptide bonds via hydrolysis
= the start of gastric digestion in the stomach!
What hormones inhibit HCl secretion?
Secretin
peptide hormone released by duodenal S-cells
- inhibits gastric acid secretion (as contents move out of stomach and into dudoedenum)
- in response to acid
CCK (cholecystokinin)
- in response to fat
GIP (Gastrin Inhibitory peptide)
- in response to carbohydrates
What hormones stimulate HCl secretion?
- gastrin (produced by gastric endocrine cells)
- histamine (produced by gastric mast cells and binds to H2 receptor – non-gastric MCTs can cause GI ulceration due to histamine release)
- Ach (vagal – gastric distention)
All 3 bind to parietal cell receptors to promote gastirc acid release!
What drug works best at inhibiting gastric acid secretion?
Proton pump inhibitors (PPIs) – Omeprazole, pantoprazole
Gastrinoma
- tumor of G-cells (endocrine cells that release Gastrin)
- excessive amts. of gastrin secreted –> GI ulceration, gastric hypertrophy
- tx = PPIs
Gastrin = a “trophic factor” – causes small growth (hypertrophy) of the gastric mucosa
5 gastric protective mechanisms against its own acids
tight junctions = in mucus layer (gap junctions are in the muscular layer)
3 layers of the gastric mucosal barrier
submucosa -> gastric epithelial cells -> mucosa
What mediates gastric blood flow?
Prostaglandin
- NSAIDs and corticosteroids decrease gastric mucosal blood flow
The 3 phases of gastric activity
1. Cephalic Phase – promotes gastric activity/anticipation phase (conscious awareness or thought of food – vagal stimulation)
2. Gastric Phase - promotes gastric distension via vagal and local neural reflexes, mostly in response to gastrin. -> HCl (parietal cells) & Pepsinogen (chief cells) released
3. Intestinal Phase – inhibits gastric activity - reflexes & negative hormonal feedbacks from SI mucosa by CCK & GIP (in response to CHO, fat and acid present in the duodenum)
Interdigestive phase
“housekeeper” – phase in between meals
- moves fasting content (larger particles) into the duodenum (pylorus does not close)
What diets move fastest -> slowest through stomach (gastric emptying)
Carbs > proteins > fat
The presence of fat, such as oleate, in the meal results in stimulation of cholecystokinin (CCK) secretion in the duodenum; in turn, this inhibits antral motility, stimulates pyloric tone and delays gastric emptying
What part of stomach allows food to enter?
Cardia
the cardiac spincter (LES)
What part of the stomach allows for storage of food, has mild peristaltic waves and no mixing or mechanical digestion occurs?
Fundus
What part of the stomach is highly mobile where strong peristaltic and reverse peristaltic waves occur, mixing food with enzymes and HCl?
Body
What part of the stomach is the “real grinder” where strong contractions occur and mechanical digestion is completed?
Antrum – delivers tiny digesta to the pylorus – pyloris returns bits too large for the dudoenum back to gastric antrum or body
The pylorus only allows particles through to the duodenum of what sizes?
No larger than 1-2mm
During filling, the stomach ?. During empyting, the stomach ?.
relaxes; contracts
