physiology 1- GI regulatory substances

Question 1

Gastrin;- source

Answer 1

g cells

antrum of stomach

Question 2

What gastrointestinal functions would be impaired in a model gastrointestinal tract without G cells?

Answer 2

Increased acid secretion, promotion of growth of the gastric mucosa, increased gastric motility

Question 3

Name at least two stimuli for the release of gastrin

Answer 3

Distention, amino acids, vagal stimulation, alkalinization

Question 4

What serves as negative feedback for gastrin release?

Answer 4

Acid secretion (a pH

Question 5

A patient with PUD refractory to medical treatment has multiple gastric ulcers. Gastrin level is markedly elevated. Diagnosis?

Answer 5

Zollinger-Ellison syndrome due to ectopic production of gastrin

Question 6

A patient chronically on proton pump inhibitors or chronic gastritis might have increased levels of this gastric hormone due to lack of negative feedback.

Answer 6

Gastrin

Question 7

A man does not produce a hormone that inhibits insulin and growth hormone secretion. He is status post-small bowel resection. What happened?

Answer 7

Due to resection of the duodenum and jejunum, he has no I cells, which are responsible for synthesizing cholecystokinin

Question 8

What are the actions of cholecystokinin?

Answer 8

Stimulation of gallbladder contraction & pancreatic enzyme secretion, slowing of gastric emptying, increase in sphincter of Oddi relaxation

Question 9

The presence of fatty acids and amino acids in the duodenum ____ (increases/decreases) cholecystokinin secretion.

Answer 9

increases

Question 10

In cholelithiasis, pain worsens after the ingestion of what type of foods?

Answer 10

Fatty foods (this is due to stimulation of cholecystokinin release, which causes gallbladder contraction)

Question 11

A patient has a genetic defect in her neural muscarinic pathways. Will her gallbladder activity be affected?

Answer 11

Yes, as cholecystokinin uses those pathways to stimulate gallbladder contractions

Question 12

Secretin is produced by which cells? Where are these cells found? What stimulates this hormone’s release?

Answer 12

S cells of the duodenum; acids and fatty acids

Question 13

What are the actions of secretin?

Answer 13

Increases pancreatic bicarbonate secretion, increases bile acid secretion, decreases gastric acid secretion

Question 14

A patient has S cell dysfunction. What kinds of substances can this patient not digest well in his duodenum? Why is this the case?

Answer 14

Fatty acids; without secretin from S cells, he cannot alkalinize duodenal gastric acid, thus pancreatic enzymes will not function properly

Question 15

Secretin-stimulated pancreatic bicarbonate functions to neutralize ____ within the ____.

Answer 15

Gastric acid; duodenum

Question 16

A patient who is unable to produce secretin would have difficulty with the activity of enzymes from which organ?

Answer 16

The pancreas (the enzymes would be denatured and nonfunctional in the acidic environment created by unopposed gastric acid)

Question 17

A male has excess gastric acid, increased gallbladder contractions, and lots of insulin and glucagon release. What hormone does he lack?

Answer 17

Somatostatin

Question 18

This overarching inhibitory hormone of the gastrointestinal system is made by which cells? Where are these cells found?

Answer 18

Somatostatin is made by D cells of pancreatic islets and gastrointestinal mucosa

Question 19

If a patient is given somatostatin, how does this impact pepsinogen secretions?

Answer 19

Decreases them

Question 20

If a patient is given somatostatin, how does this impact gastric acid secretions?

Answer 20

Decreases them

Question 21

If a patient is given somatostatin, how does this impact pancreatic secretions?

Answer 21

Decreases them

Question 22

If a patient is given somatostatin, how does this impact fluid secretions in the small intestine?

Answer 22

Decreases them

Question 23

What effect does somatostatin have on the gallbladder?

Answer 23

Somatostatin decreases gallbladder contraction

Question 24

The presence of what substance in the gut lumen causes increased somatostatin release?

Answer 24

Acid

Question 25

What inhibits somatostatin release?

Answer 25

Vagal stimulation

Question 26

Given the functions of somatostatin, why is it classified as an antigrowth hormone?

Answer 26

Somatostatin inhibits digestion and absorption of nutrients, preventing the body from receiving growth nutrients (encourages somatostasis)

Question 27

Glucose-dependent insulinotropic peptide is made by which cells? Where are these cells found? What is another name for this hormone?

Answer 27

K cells of the duodenum and jejunum; gastric inhibitory peptide (GIP)

Question 28

What is the exocrine regulatory effect of glucose-dependent insulinotropic peptide?

Answer 28

Decreased secretion of gastric acid

Question 29

What is the endocrine regulatory effect of glucose-dependent insulinotropic peptide?

Answer 29

Increased release of insulin

Question 30

Why is an oral glucose load used more rapidly by the body than an equivalent load that is given intravenously?

Answer 30

Oral (but not intravenous) glucose stimulates glucose-dependent insulinotropic peptide, which stimulates insulin release

Question 31

Where is vasoactive intestinal polypeptide (VIP) secreted within the gastrointestinal tract?

Answer 31

Parasympathetic ganglia in sphincters, gallbladder, and small intestine

Question 32

Vasoactive intestinal polypeptide (VIP) ____ (increases/decreases) intestinal water and electrolyte secretion.

Answer 32

Increases

Question 33

What effect does vasoactive intestinal peptide (VIP) have on intestinal smooth muscle and sphincters?

Answer 33

Relaxation of these structures

Question 34

What stimuli increase secretion of vasoactive intestinal peptide (VIP)?

Answer 34

Distention, vagal stimulation

Question 35

What is a negative regulator of vasoactive intestinal peptide (VIP) release?

Answer 35

Adrenergic input

Question 36

A patient presents with watery diarrhea, hypokalemia, and achlorhydria. What is the most likely tumor causing this syndrome?

Answer 36

VIPoma, a non-α, non-β islet cell pancreatic tumor that secretes vasoactive intestinal peptide (VIP)

Question 37

A patient has profuse watery diarrhea. CT shows a pancreatic mass; labs show hypokalemia and achlorhydria. What nervous system is to blame?

Answer 37

This is a VIPoma causing WDHA syndrome (Watery Diarrhea, Hypokalemia, and Achlorhydria) due to parasympathetic ganglia

Question 38

Which small messenger molecule causes an increase in smooth muscle relaxation in the gut, particularly in the lower esophageal sphincter?

Answer 38

Nitric oxide

Question 39

A man with dysphagia has uncoordinated esophageal peristalsis and increased lower esophageal sphincter tone. What is the pathophysiology?

Answer 39

Achalasia causing increased lower esophageal sphincter tone secondary to loss of nitric oxide secretion

Question 40

What is the function of motilin?

Answer 40

Production of migrating motor complexes (MMCs) in the small intestine, thereby promoting peristalsis

Question 41

Motilin secretion is ____ (increased/decreased) in a fasting state.

Answer 41

Increased

Question 42

What hormone is produced by the small intestine and associated with intestinal peristalsis?

Answer 42

Motilin

Question 43

What does CCK act on, resulting in pancreatic secretion?

Answer 43

Neuronal muscarinic pathway

Question 44

A man takes erythromycin for a bacterial infection. He develops diarrhea not due to gut flora depletion. Are his MMCs to blame?

Answer 44

Yes, as erythromycin is a potent stimulator of motilin receptors, which increase intestinal peristalsis, likely causing the man’s diarrhea