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Characteristics of esophageal secretions
Basically all mucous
Types of glands in the esophagus
Compound/branched mucous glands in the top and bottom of the esophagus
Simple mucous glands in the middle
Function of cardiac gastric glands (a type of deep tubular gland)
Secretes mucus
Function of fundic/oxyntic/gastric glands (a type of deep tubular gland)
Secretes HCl, pepsinogen, intrinsic factor, and mucus
Cells in oxyntic glands that secrete mucus
Mucous neck cells
Cells in oxyntic glands that secrete pepsinogen
Peptic/chief cells
Cells in oxyntic glands that secrete intrinsic factor and HCl
Parietal/oxyntic cells
Function of pyloric gastric glands (a type of deep tubular gland)
Secretes mucus and gastrin (and some pepsinogen) in the bottom 20% of the stomach
Surface mucous cell (foveolar cell) function
Secretes a THICK layer of viscous mucus over the entire stomach
Surface mucous cells (foveolar cells) vs goblet cells
Thicker mucus with bicarb added
What stimulates secretion from surface mucous cells (foveolar cells)
Contact with food or any irritation
Epithelium of the non-glandular region of the horse stomach
Stratified squamous epithelium
EGUS pathology
Ulcers in the nonglandular regions
EGUS risk factors
High grain diet
Intermittent/bolus feeding
Being a race horse (running)
Phases of gastric secretion
Cephalic phase
Gastric phase
Intestinal phase
Cephalic phase of gastric secretion
Stimulated by senses and though, nothing is in the stomach
What mediates the cephalic phase of gastric secretion
Neural signals from amygdala and hypothalamus that travel along the vagus nerve
Gastric phase of gastric secretion
Stimulated by food in the stomach
What mediates the gastric phase of gastric secretion
Vagal reflexes, ENS, and gastrin
Intestinal phase of gastric secretion
Stimulated by food in the upper small intestine
What mediates the intestinal phase of gastric secretion
Potentially duodenal mucosa, not entirely known yet
Which phase of gastric secretion results in most of the secretion volume
Gastric phase
Which phase of gastric secretion results in the least secretion volume
Intestinal phase
How does the PS-ANS increase gastric secretions
Ach upregulates activity of peptic cells (pepsinogen), parietal cells (HCl), and mucous cells (mucus)
How does gastrin increase gastric secretions
Gastrin acts on ECL cells that are deep to the parietal cells. The ECL cells produce histamine → parietal cells → HCl secretion
Characteristics of mucus from pyloric glands
Lots of thin mucus that lubricates food
What cells in pyloric glands secrete gastrin
G cells
Why is pepsin secreted as the proenzyme pepsinogen
Prevents autodigestion of cells if it is only active in the gastric lumen
Where does pepsin get deactivated again
In the duodenum
Function of intrinsic factor
From parietal cells, necessary for the absorption of cobalamin
Why is chronic gastritis bad (in relation to glands and cells)
Damages parietal cells → no intrinsic factor → no cobalamin absorption → pernicious anemia
Summary of the process of HCl production
H+ and Cl- are pumped into the canaliculi of parietal cells for secretion, and bicarb is secreted into the blood
Structures that prevent the stomach acid from making its way back into cells or the blood stream
Tight junctions on canaliculi and adjacent cells
How do NSAIDs and steroids cause ulcers
NSAID/Steroids block COX-1 → lowered prostaglandin, which normally helps decrease acid production and increase protective secretions
Types of meds for treating ulcers
H+/K+ ATPase inhibitor (omeprazole)
Histamine-2-receptor antagonist → inhibitory signal to parietal cells (opposite of gastrin)
Sucralfate → reacts with acid to form a barrier, absorbs pepsin