GI phys Lecture 2 Flashcards
Difference between segmentation and Peristalsis
Peristalsis: involves smooth muscle / longitudinal muscle interaction, moving contents forward. Propulsion.
Segmentation: purpose is to mix contents. Promotes digestion
Secretion:
Acinar Cells / Duct cells
Acinar cells connected to duct cells, both are polarized. (transporters are different from apical and basolateral).
Acinar cells: synthesize / secrete pdts.
Duct cells: transport fluid / electrolytes
Increase of flow rate, what happens?
Na increases, plateaus
HCO3- (bicarbonate) increases, plateaus
Cl- increases, linear
K+ decreases, plateus
Sjogren Syndrome
Difficulty in tasting/chewing/swallowing/speaking
Dry mucosa, parotid glands enlarged. Autoimmune disorder
LES and cardia, what is there
Mucus and Bicarbonate.
Bicarbonate there to maintain pH bc u don’t want acid in esophagus
Fundus and upper body secretions
H+, intrinsic factor, mucus, bicarbonate, pepsinogen and lipase
has parietal cells that secrete HCl
Antrum and lower body contain…
Mucus and bicarbonate
Tubulovesicles
Contain H+, K+ ATPase, morphological change occurs, making canaliculus have more surface area from resting to secreting. In parietal cells.
Apical (lumen) transporters of Parietal cells
H / K exchanger
K and Cl can leave through channels
Does not secrete HCl directly, secretes H+ ions and Cl-
Basolateral transporters of Parietal cells
HCO3- / Cl-
Na / K
CO2 can come from blood / plasma
Which receptors are stimulatory and inhibitory for parietal cells? Which are the secondary messengers associated with these?
Basolateral receptors of ACh, gastrin, histamine stimulate parietal cells, secreting HCl.
M3 = ACh
H2 = Histamine
CCK-B = Gastrin
ECL cell make histamine
Somatostatin (SST) from D cells is ALWAYS inhibitory.
Ca++ for ACh and Gastrin, cAMP for Histamine are the secondary messengers
Mechanism of G cells in Antrum
GRP (gastrin releasing peptide) stimulates G cells which makes Gastrin which stimulates parietal secretion of HCl.
D cells stimulate SST which inhibit G cell production of Gastrin.
Note that Gastrin is not a NT (it is a GI hormone) and must be transported via blood.
PPI (proton pump inhibitor) mechanism
Inhibits final step, H+ K+ ATPase in parietal cells.
Effects of H. Pylori and how it affects gastric mucosa:
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Increase NH3 production
Decrease number antral D cells
Increase prod. of gastrin
Increase acid secretion
Inflammatory responses release cytokines
Effects of NSAIDS and how it damages gastric mucosa
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Less mucous and bicarbonate production, increase gastrin secretion, decrease gastric blood flow, neutrophils release free radicals and proteases.
NSAIDS inhibit prostaglandins, u need prostaglandins for healthy gastric mucosa.