Location, Location, Location
Just a Phase
Main Players
Movin' Out
Speculation I Say!
100
Where in the gastric pits are G-cells located? How about D cells? ECL cells? Chief cells? Parietal cells? Where is mucous secreted? To get credit you must answer each part.
What is: G cells are nearer to the bottom. ECL cells are around the sides, as are D cells. Chief cells and Parietal cells are scattered throughout. Mucous is secreted in the mucous neck region, near the top.
100
What is a key difference between neural stimulation in the Cephalic and Gastric Phase? Think about cell types affected.
What is that the neural stimulation in the cephalic phase results from somatosensory input resulting in vagal stimulation through enteric nerves of parietal cells, ECL cells, Chief cells and G-cells directly. Vagal stimulation during the gastric phase exists but stimulates only parietal cells directly. A major source of stimulation of G cells during this phase comes from the reception of phenylalanine and alanine and peptides as well as a reduction in pH resulting in a decrease in somatostatin caused by buffering of the acidity of the stomach.
100
What are the main affects of secretin?
What is inhibition of gastric secretion, except for chief cell secretion, increase in pancreatic secretion of bicarbonate ions, increase rate of bile and intestinal secretion, increase mucous production. Decreases gastric motility.
100
The STRENGTH of smooth muscle contractions in the stomach depend on the frequency of this.
What is action potentials.
100
What affect would systemic mastocytosis have on digestion?
What is increased production of acid by parietal cells due to increased histamine production.
200
What region of the stomach has the most G-cells? What substances do mucous cells secrete?
What is the pyloric antrum and bicarbonate and mucous.
200
What phase stimulates the process of bidirectional movement of chyme in the small intestine? What is this called?
What is the cephalic phase and segmentation.
200
What are the main affects of Gastrin? What stimulates it? What second messenger does Gastrin act through in ECL cells? At what acidity is it producing gastrin at a lower rate? At what acidity will it stop producing gastrin?
What is increase gastric motility, increase gastric secretions ( Chief cells and ECL). ACh stimulates it as well as peptides, some amino acids, alcohol and caffeine. Gs protein, activates PLC, changes PIP3 to IP3 and DAG, increase cellular calcium, activate kinases, increase activity of ATPase that imports protons. At an acidity of 3 it will be inhibited and then at an acidity of 1.5 it will stop producing gastrin.
200
An excitatory input to stomach smooth muscle will do what to the frequency of peristaltic contractions?
What is not change them.
200
What do they now give with NSAIDs used long-term to prevent damage to the lining of the stomach? Think about an inhibitor of parietal cell secretion that mimics a natural inhibitor of parietal cell activity but is not somatostatin.
What is a prostaglandin. Prostaglandins inhibit the secretions of parietal cells.
300
The proximal stomach, including the cardia, the fundus and the body, produces what kind of contractions, weak or strong? What is its response to ingestion of food?
The proximal stomach produces weak contractions. It relaxes in response to food and is mostly responsible for storage.
300
How long does the cephalic phase last? The gastric? The intestinal?
What is 1/2 hour, 3-4 hours and 3-4 hours.
300
Where is CCK released? What does it do? What stimulates its release?
What is the duodenum. It stimulates ECL and Chief cell secretion but overwhelmingly stimulates D cell secretion of somatostatin and thus decreases gastric secretions. It increases gallbladder contraction and release of digestive enzymes from pancreas. It relaxes the hepatopancreatic ampullar sphincter Fatty acids and other lipids stimulate its release.
300
List 4 molecules that result in inhibitory stimulation of smooth muscle in the stomach as a result of sympathetic stimulation.
What is NO, NANC (non-adrenergic, non-cholinergic mechanisms), VIP (vasoactive intestinal peptide), PACAP (Pituitary adenylate cyclase activating peptide), or ATP
300
What affect will secretin have on Zollinger-Ellison syndrome?
What is no great affect. Zollinger-Ellison sydrome results in gastrin-secreting adenomas of the stomach and they do not obey regulatory mechanisms.
400
What affect will motilin have on the proximal stomach? Sympathetic ennervation? What about (CCK, Secretin, Glucagon, Gastrin, Somatostatin and VIP)?
Motilin will cause its contraction, sympathetics will cause it to relax. The last group will also cause relaxation.
400
List four changes in intestinal chyme that will trigger the intestinal phase.
What is: osmolarity, distension, fats and peptides and acidity. What will these prompt duodenal cells to release?
400
Describe the exact mechanism whereby ACh, gastrin, secretin and CCK increase release of pepsinogen.
What is What is: the intracellular messenger for acetylcholine, gastrin and cholecystokinin is Ca2+. Receptor stimulation by these secretagogues leads to the production of inositol trisphosphate to release Ca2+ from intracellular stores. Secretin stimulates adenylate cyclase to produce cAMP from ATP. Rises in intracellular Ca2+ and cAMP initiate cytoskeletal activity that leads to the movement of zymogen granules containing pepsinogen to the apical surface of the cell, where they fuse with the membrane and discharge their contents by exocytosis.
400
Name the cells in the gastric wall that are the pacemaker cells of the stomach.
What is Interstitial Cells of Cajal. Do these pacemaker cells cause contractions by themselves?
400
A 37-year-old male with AIDS presents with a fever, anorexia, weight loss, and GI bleeding. Physical examination reveals a palpable abdominal mass. Endoscopy and biopsy reveal a small-bowel malignancy, indicating surgical resection. Removal of proximal segments of the small intestine would most likely result in a decrease in which of the following? a. Basal acid output b. Maximal acid output c. Gastric emptying of liquids d. Gastric emptying of solids e. Pancreatic enzyme secretion
what is E, pancreatic enzyme secretion
500
What cell type will be most effected in chronic atrophic gastritis? Think about the location of the problem.
What is parietal cells.
500
You decide to turn to a diet of exclusively sugary sodas, drunk slowly over the course of the day. What phase are you bypassing and what molecule released in your duodenum is first signalling the increase in insulin in your body?
What is the Gastric phase (sugar does not stimulate gastrin production - and if you drink slowly you will not trigger your stretch receptors sufficiently) and GLP-I will cause the first surge of insulin in your body.
500
A 32-year-old woman presents to the Emergency Department with abdominal pain and diarrhea accompanied by steatorrhea. Gastric analysis reveals a basal acid output (12 mmol/h) greater than normal (<5 mmol/h). The steatorrhea is most likely due to which of the following? a. Inactivation of pancreatic lipase due to low duodenal pH b. Delayed gastric emptying c. Decreased gastric acid secretion d. Decreased secretion of intrinsic factor e. Decreased pyloric sphincter tone
What is A. Inactivation of pancreatic lipase due to low duodenal pH. Can you think of a similar mechanism that would cause B12 deficiency in the setting of Zollinger-Ellison syndrome?
500
What is the segment of peristaltic activity that travels down the stomach and small intestine in the interdigestive period?
What is migrating myoelectric complex.
500
A 49 yo man undergoes vagotomy for his peptic ulcer disease. As a result, which of the following GI motor activities will be affected most? A. secondary esophageal peristalsis B. distension induced intestinal segmentation C. orad stomach accommodation D. caudad stomach peristalsis E. migrating motor complexes
What is the orad stomach accomodation. All of the others do not result from stimulation of the vagal nerve.
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