Stomach Flashcards
3 major functions of the stomach
- temporal storage
- absorption of water soluble and lipid soluble substances (like alcohol and some drugs)
- preparation of the chyme for digestion in the SI
most of the protein components of food are what? in the stomach
broken down into smaller constituents
uses pepsin (acidic environment needed)
surface mucus cells in stomach
located at opening of gastric glands
secrete mucus
mucus neck cells in stomach
neck of gastric gland and secrete less viscous mucus than those located at the opening
also secrete HCO3-, and water to protect the lining of the stomach against acid
parietal (Oxyntic) cells
secrete HCL and intrinsic factor for B12 absorption
chief (zymogen) cells
basal region of glands
secrete pepsinogen via exocytosis
D cells in stomach
found in the antrum
secrete somatostatin –> inhibits acid secretion therefore gastrin release
enterochromaffin-like cells (ECLs)
scattered throughout the mucus
secrete histamine –> which stimulates acid secretion by the parietal cells
also increases blood flow locally
G cells in stomach
enteroendocrine cells that secrete gastrin
found mostly in the pyloric region
secreted into blood (not lumen of stomach) and stimulates gastric juice secretion and gastric/intestinal motility
EtOH and aspirin
can break down mucus…which is the protective glycocalyx for the stomach
so excessive uses of these can cause ulcers
pepsin
secreted by chief as pepsinogen and activated by acid (HCl)
pepsin = endopeptidase
gastric lipase
lipid breakdown
78% homologous to lingual lipase
intrinsic factor
vitamin B12-binding protein and considered a ‘essential factor’
loss = achlorhydria –> pernicious anemia
relationships between the concentration of these ions as the rate of secretion increases..
HCl
Na
K
H+ = increases rapidly
Cl- = increases but not as much as H+ … but also has a higher absolute value
Na+ = decreases
K+ = low absolute amount, but still see slight increase
maximal acid secretion is when after a meal
one hour after
lowest pH = 3 hours after
during this process the food acts a buffer to raise pH
parietal cell
distinctive characteristics:
- intracellular canalculi
- abundance of mitochondria
- extensive SER (tubulovesicular membranes)
parietal cell in the resting state
the tubulovesicles (containing transporters responsible for H+ and Cl- secretion) –> located underneath the plasma membrane
tubulovesicular membranes
in apical portion of the parietal cell and contain the H/K-ATPase
stimulation of parietal cells
cyctoskeletal rearrangement occurs leading to the fusion of the tubulovesicles membrane into the canalicular membrane
this increases surface area of apical membrane and the appearance of microvilli
as a consequence –> greatly increases number of H/K-ATPase and K+ and Cl- channels into the plasma membrane and O2 consumption to support acid secretion
carbonic anhydrase in parietal cell
secreted protons by these cells mostly are derived from the dissociation of water and the CA reaction
water –> H + OH
OH + CO2 –> HCO3- via CA –> goes out blood side membrane
H –> goes out into lumen via K/H-ATPase
apical membrane transporters of parietal cells
- H/K-ATPase –> how H+ is secreted into lumen
- K+ channel –> how you secrete (recycle) the K+ back into lumen to continue to use #1
- Cl- channel –> Cl - enters cell from blood side –> goes into lumen via this channel down gradient
basolateral membrane transporters of parietal cells
- Na/K-ATPase –> pumps in K+ from blood so can secrete K+ out apical membrane to supply fuel for H/K ATPase
- K+ channel
- Cl-/HCO3- exchanger –> pumps HCO3- out into blood … and Cl- into cell which will eventually go into lumen
receptor for gastrin on parietal cell
gastrin-cholecystokinin, CCK-B
receptor for Ach on parietal cell
muscarinic receptor, M3
receptor for histamine on parietal cell
H2
stimulation of CCK-B and M3 receptors on parietal cell –>
increases intracellular Ca2+, which stimulates HCl secretion
gastrin –> CCK-B (secreted by D cells into the blood vessels)
Ach –> M3 (from vagus nerve)
stimulation of H2 receptors on parietal cell –>
increases intracellular cAMP –> HCl secretion
histamine from ECL cell
‘potentiation effect’
the effect of 2+ stimulants is greater than just 1
Ex: gastrin + Ach –> larger increase in intracellular Ca2+
major humoral effectors (secretagogues) for gastric secretion
Gastrin (G)
Histamine (H)
ACh
neural effectors for gastric secretion
a. distention of stomach –> (+) mechanoreceptors –> (+) parietal cells directly through a short local reflex and by long-vagal reflexes
direct and indirect mechanisms for stimulating gastric secretion
Direct:
- ACh, H, and G all bind to their respective receptor on the parietal cell
Indirect:
- ACh and gastrin indirectly induce acid gastric secretion as a result of their stimulation of histamine release from ECL cells and possibly from mast cells in the lamina propria
H2 receptor blockers
block the H2 receptors on parietal cells but also inhibit the acid secretion stimulated by ACh and gastrin
where else are CCK-B and M3 receptors found - besides the parietal cell
(most important for gastric secretion regulation)
ECL cells
activation of these receptors –> (+) Histamine release –> (+) HCl secretion
phases of gastric secretion of acid (general)
- basal
- cephalic
- gastric
- intestinal
basal phase of gastric acid secretion
inter-digestive period…
cephalic phase of gastric acid secretion
shortest period
takes place before food enters the stomach
initiated by though, sight, smell and taste (no mental shit…why called cephalic)
A. Neurogenic influence = parasympathetic vagus nerve causes release of ACh –> (+) parietal cells, G cells, and ECL cells
** also stimulates chief cells –> pepsinogen
B. Endocrine influence = vagal stimulation also causes gastrin release which acts like ACh mostly
gastric phase of gastric acid secretion
longest phase….triggered by the presence of food in the stomach due to distension and chemical nature
A. Neurogenic influence = stomach distension stimulates mechanoreceptors leading to secretion of ACh due to parasympathetic reflexes
B. Endocrine influence = amino acids and peptides activate G-cells in the antrum
…gastrin therefore released into blood to stimulate further acid secretion and Histamine release
…gastrin secretion falls as pH of stomach falls between 2-3 and somatotstatin is released from D cells
intestinal phase of gastric acid secretion
presence of chyme in duodenum –> enterogastric reflex in order to (-) gastric secretion
acid in duodenum –> secretin released –> (-) G cells and reduces parietal response to gastrin
also…FAs in the duodenum and jejunum cause release of gastric inhibitory peptide (GIP) and CCK –> inhibit acid secretion and gastrin release
