GI 05 & 06 Flashcards
Gastric phase of integrated response to a meal
Food has entered the stomach
What are the major functions of the stomach (7)?
- temporary storage of meal
- Secrete H (kill microbes, convert pepsinogen ā> pepsin)
- secrete intrinsic factor
- secrete mucus and HCO3 (protect gastric mucosa)
- secrete water (lube bolus and suspend nutrients in solution)
- motor activity (mix H and pepsin with bolus)
- coordinate motor activity of SM and emptying of stomach contents into duodenum
Major paracrine hormone of the stomach
histamine
Major endocrine hormones of the stomach
Gastrin (also from duodenum), somatostatin (also from duodenum and pancreas)
Gastric pits
Formed by folding of columnar epithelium , the pits are the opening were gastric glands empty
Parietal / oxyntic cells secrete what?
Hcl, intrinsic factor
Purpose of Hcl
Kill microbes, activate pepsin from pepsinogen
purpose of intrinsic factor
this is a glycoprotein that binds to vitamin B12 that makes it absorbable by ileum (IF is an essential factor)
Purpose of mucus neck cells
Secrete mucus to protect gastric mucosa
Peptic / Chief cells secrete what?
Pepsinogen (this will eventually be pepsin) - this is active only in acidic environments and will cleave proteins
Enterochromaffin-like cells (ECL) secrete what
Histamine (paracrine); this is the most powerful stimulator of Hcl secretion
D cells secrete what
Somatostatin (endocrine) - powerful inhibitor of Hcl secretion
G cells secrete what
Gastrin (endocrine) rom pyloric region - this leads to HCl Secretion
What are the 6 secretory cells of the gastric fundus an antrum
Parietal (Hcl, IF), mucus, peptic/chief cells (pepsinogen), D cells (somatostatin) G cells (Gastrin), and ECL cells (histamine)
What are the āmajorā gastric secretions: (4/5)
Hcl, pepsinogen, bicarb + mucus, intrinsic factor
In humans, what are the only essential components of gastric juice in a healthy individual
intrinsic factor
How is H generated and secreted via parietal cells
Carbonic anhydrase takes CO2 from cellular respiration and makes HCO3 and H.
H exchanges with K to go into gastric lumen; Cl follows H via a Cl channel.
HCO3 exits into blood via a Cl/HCO3 exchanger. NKA on basolateral membrane as well.
Secretion of epithelial HCO3
Surface epithelial cells secrete a fluid with Na, Cl, K and HCO3. This is isotonic for the ions, hypertonic in HCO3 compared to plasma. The HCO3 is trapped in mucous and makes the alkaline part of the mucosal barrier-thus net result is a neutral pH zone
What drug inhibits the H-K ATPase, and what cells do this hit and what secretion does it target?
Omeprazole
Parietal cells
HCl
What cells secrete mucus
mucus neck cells
What is mucus composed of
Primaily carbs - they are glycoproteins though, which mkes them susceptible to digestion by pepsins
PSNS stimulation of the stomach
vagus nerve (strongest stimulant for H secretion; but also terminate on ENS fibers that innervate ECL and G cells, too). Vagal stimulation also secretes pepsinogen, mucus, IF, and HCO3 - and it is triggered by distention
What 3 substances stimulate H secretion by parietal cells?
Acetylcholine (neural), histamine (paracrine), gastrin (endocrine)
What are the second messengers of Ach stimulation in parietal cells
IP3/Ca
What drug blocks Ach effect on parietal cells?
Atropine
Histamine effect on gastric secretion
Released from ECL cells - has aracrine effect on pareital cells
What does histamine bind to
H2 receptors on pareital cells
What is the second mesenger for histamine
cAMP - stimulates H secretion
What drug blocks Histamine frm interacting with parietal cells
Cimetidine
Gastrin effect on gastric secretions
Secreted by G cells - endocrine effect on parietal cells
What does gastrin bind to
CCKB receptors on parietal cells
What are the second messengers associated with Gastrin
IP3/Ca
If Cimetidine is used, what is the overall effect on gastric juice?
Blocks histamine effects directly, blocks histamine potentiated effect of Ach on Gastrin
If atropine is used, what is the effect on gastric uices
blocks direct effect of Ach, blocks Ach potentiated effects of histamine and gastrin
What is the effect of somatostatin and prostaglandin on HCl secretions
Reduction of Hcl secreions
In the cephalic and oral phase how much of gastric HCl secretion occurs? In the gastric phase?
30; 60. Who knows where the other 10% comes from but iām not paid enough to care
Stimulation of gastric secretions in the cephalic/oral phase (3)
Direct stimulation of paretial phase by Ach (neural)
Indirect stimulation of G cells by vagus to produce gastrin-endocrine effect
Indirect stimulation of ECL cells by vagus (Ach) and gstrin (CCKB) to produce histamine (paracrine)
What mechanisms stimulate Hcl secretion in gastric phase
AA, distention, small peptides, also long loop (vagovgal) reflex from distention, and a DIRECT effect of AA and small peptides on G cells to stimulate gastrin release
If you ahve alcohol or caffeine this also does this
Feedback inhibition of parietal cells
Somatostatin from D cells is released when there is H detected, this inhibits gastrin release from G cells and histamine release from ECL cells
What are the two ways the stomach can be divided by motility
orad, caudad
Thickness of stomach wall in orad region?
Thin
Thickness of stomach wall in caudad region
Thick
What is receptive relaxation
The distention of the lower esophagus and opening of LES is accompanied by distention of orad stomach - happens via vagovagal reflex (VIP)
Goal of motility in caudad area
mix and digest
Retropulsion
Most chyme is going to be propelled back into stomach for further mixing and breakdown and is not allowed into duodenum
PSNS innervation is excitatory, or inhibitory inlower stomach
excitatory (ach, substance P) - leads to mixing and motility (Grinding fxn)
Gastric emptying - speed, what kind of food leaves (solid/liquid)
Slow, takes 3h, mostly liquid, solids must be reduced to particles less than 1mm^3
Gastroduodenal junction
Pylorus
Function of pylorus
Filter size of food particles, emptying gastric contents into duodenum at a rate duodenum can digest chyme, prevent reflux of chyme into bolus
What controls the pylorus
hormonal endocrine, paracrine, and nervous functions
If cck senses there is fat in duodenum what happens to the pylorus
it is shut
What are PSNS and SNS activity on pylorus
Closing - both of them
Gastric ulcers
Ulcers due to erosion of gastric barrier and getting to the wall of the stomach - less common
Duodenal ulcers
H secretory rates are high and H delivered to duodenum overpowers bufferng ability of HCO3 release in from pancreas into duodenum
Zollinger Ellison syndrome (gastrinoma)
A tumor (gastrinoma) is usually responsible, and you get high quantities of gastrin released - this leads to a ton of H release by parietal cells, and increased number of parietal cells. This leads to duoenal ulcers and stearrhea since low duodenal ph will inactivate pancreatic lipase and undigested fats show up in stool. treatments include inhibiting H secretion (like with cimetidine or omerazole) and removing the tumor (no shit)
