Stomach Flashcards
Retropulsion
Occurs when peristaltic contractions originating from the pacemaker region in the midstomach reach the pyloric sphincter in cloe it
=>Chyme propelled back into stomach to be further digested
Receptive Relaxation
Mediated by a vagovagal reflex, this is the relaxation of the stomach to accommodate to a recently ingested meal
Migrating Myoelectric Complex
Contractions occurring in 90 minute intervals during fasting to clear the stomach of any residual food
*Mediated by motilin; hunger pangs will disappear after 3-4 day
Order of gastric emptying
Liquids>Carbs>Proteins>Fats
Gastric Emptying
Controlled by signals from the duodenum in response to:
Decreased pH
Distention of proximal stomach
Increased fat/protein digestion products
Gastroparesis
Impaired emptying of the stomach producing symptoms of fullness, nausea, vomiting
*Most commonly caused by diabetes or anticholinergics
Dumping Syndrome
Lower end of S.I. fills to quick w/ undigested food; nausea, vomiting, eventually sweating and dizziness
- Common after stomach surgery
- Symptoms due to hypoglycemia
Oxyntic Gland mucosa
Found in the proximal stomach; secrete primarily acid, pepsinogen, intrinsic factor, and mucus
*Mucus neck cells in isthmus serve as stem cell; chief cells and parietal cells also present
Pyloric gland mucosa
Found in the distal stomach; secretes primarily gastrin
HCl
- Begins digestion of protein
- Activates pepsinogen
- Kills bacteria
Pepsin
Released by vagal stimulation and splits interior peptide bonds of proteins
Mucus
Soluble: Secreted in active stomach; lubricates chyme
Insoluble: Secreted in inactive stomach to trap HCO3- in layer on mucosa to protect from acidic damage
Intrinsic Factor
Binds Vitamin B12 and allows for absorption in the ileum
*Lack of IF=>pernicious anemia
Tubulovesicles
Inserted into the luminal membrane of parietal cells when gastric acid is secreted
*Become H+ pumps/K+ antiporter
Mechanism of Acid Secretion
Carbonic anhydrase converts CO2 from cell metabolism to H+ and HCO3-
H+ => secreted out of H+/K+ ATPase
HCO3- => Antiported out w/ Cl-; Cl- travels thru membrane channels to the lumen
*K= enters via a Na/K+ ATPase and leaves via a K+ channel to power the H+/K+ ATPase on the luminal side
Ionic Composition of Gastric Juices
Low flow => NaCl
High Flow => HCl
*Vomiting may lead to hypokalemia due to high presence of K+ in the lumen
Stimulants of Acid Secretion
- Ach-binds to muscarinic receptors and activates PLC
- Gastrin- binds to gastrin receptors and activates PLC
- Histamine- binds to H2 receptors and activates AC
* All eventually raise intercellular Ca2+ and insert H+-pumps in the apical membrane
H2 receptor blockers
Blocks the potentiating effects of histamine on gastrin and Ach; effectively lowers the secretion of gastric acid
Inhibitors of acid secretion
- Decreased pH
- pH will drop after initial rise from ingested meal - Somatostatin
- released in response to acid in the antrum
3 Chyme in the duodenum
-Neural and hormonal mechanisms inhibit gastrin release
Basal secretion phase
Occurs in absence of gastric stimulation; pH is low causing the mucosa to be acidified
Cephalic phase of acid secretion
Initiated by the though, taste, smell of food; afferent pathways to vagus nerve stimulate efferent impulses to the stomach
=>Stimulates parietal cell and GRP release
Gastric phase of acid secretion
Rise in pH once food enters stomach causes gastrin to be released; stretched mechanoreceptors stimulate local and vagovagal reflexes to secrete acid
- AAs and peptides can also cause release of gastrin from G-cells
- Strongest phase of acid secretion
Intestinal phase of secretion
Initiated by presence of protein digestion products in the duodenum
=>Increased gastrin secretion
Gastric ulcers
Breakdown of the protective barrier of the stomach
Duodenal ulcers
Increased levels of acid/gastrin/pepsin damage the lining of the duodenum
- Pts also have lower HCO3- secretion and defective defensive mechanisms against acid
- Much more common than gastric ulcers and often have H. Pylori infxn
H.pylori
Produces urease to neutralize acid in the stomach and corkscrews in thru the mucosa; might even poison nearby cells w/ ammonia
*Inhibits secretion of somatostatins to further cause ulcerations
Retching
Involuntary motions of vomiting w/o production
*Includes esophageal dilation, flaccid fundus, abominal contration, closure of soft palate over nasopharynx
Vomiting Center
Found in the medulla and activated by: Tickling throat Distention of stomach Vestibular stimulation Pain Sights/smell
*Direct activation will cause vomiting w/o nauseas or retching
Chemoreceptor Trigger Zone
In area postrema and is activated by radiation, motion sickness, drugs
=>Sends signals to vomiting center and NTS
Hyperemesis of Pregnancy
Severe vomiting and nausea causing weight loss during pregnancy
-Baby will come out normal though
Effects of protracted vomiting
- Metabolic alkalosis
- Dehydration
- Hypokalemia
- Hyponatremia
Possible inhibitors of gastric emptying
Decreased pH
Increased fat/protein digestion products
Increased distention of the stomach
Increased duodenal pressure
*Inhibits the flow of excess chyme into the SI
Treating ulcers
Antibiotics and H+ pump inhibitors
