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FF GI > GI Secretory Substances > Flashcards

GI Secretory Substances Flashcards

1
Q

The G cells of the stomach produce which hormone? Where are these cells found?


A

Gastrin; in the antrum of the stomach


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2
Q

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


A

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


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3
Q

Name at least two stimuli for the release of gastrin.


A

Distention, amino acids, vagal stimulation, alkalinization


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4
Q

What serves as negative feedback for gastrin release?


A

Acid secretion (a pH

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5
Q

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


A

Zollinger-Ellison syndrome due to ectopic production of gastrin


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6
Q

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


A

Gastrin


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7
Q

What are the actions of cholecystokinin?


A

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


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8
Q

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


A

Increases


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9
Q

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


A

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


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10
Q

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


A

S cells of the duodenum; acids and fatty acids


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11
Q

What are the actions of secretin?


A

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


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12
Q

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


A

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


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13
Q

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


A

Gastric acid; duodenum


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14
Q

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


A

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


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15
Q

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


A

Somatostatin


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16
Q

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


A

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


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17
Q

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


A

Decreases them


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18
Q

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


A

Decreases them


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19
Q

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


A

Decreases them


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20
Q

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


A

Decreases them


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21
Q

What effect does somatostatin have on the gallbladder?


A

Somatostatin decreases gallbladder contraction


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22
Q

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


A

Acid


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23
Q

What inhibits somatostatin release?


A

Vagal stimulation


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24
Q

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


A

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


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25
Q

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


A

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


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26
Q

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


A

Decreased secretion of gastric acid


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27
Q

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


A

Increased release of insulin


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28
Q

A patient eats a meal with a large load of fatty acids, amino acids, and glucose. What happens to activity levels of K cells?


A

They increase (all of these nutrients stimulate glucose-dependent insulinotropic peptide release)


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29
Q

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


A

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


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30
Q

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


A

Parasympathetic ganglia in sphincters, gallbladder, and small intestine


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31
Q

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


A

Increases


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32
Q

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


A

Relaxation of these structures


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33
Q

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


A

Distention, vagal stimulation


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34
Q

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


A

Adrenergic input


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35
Q

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


A

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


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36
Q

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


A

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


37
Q

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


A

Nitric oxide


38
Q

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


A

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


39
Q

What is the function of motilin?


A

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


40
Q

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


A

Increased


41
Q

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


A

Motilin


42
Q

What does CCK act on, resulting in pancreatic secretion?


A

Neuronal muscarinic pathway


43
Q

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


A

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

44
Q

In pernicious anemia, destruction of gastric ____ cells leads to deficiency of ____ required for vitamin B12 uptake in the ____.


A

Parietal; intrinsic factor; terminal ileum


45
Q

A patient has chronic abdominal pain and numerous peptic ulcers refractory to proton pump inhibitors. What tumor should be suspected?


A

Gastrinoma, which is a gastrin-secreting tumor that results in high levels of acid secretion


46
Q

Describe how pepsin is activated.


A

It is activated by vagal stimulation of increased acid output, which cleaves inactive pepsinogen to active pepsin


47
Q

What is the primary role of pepsin? What cells secrete it, and where are these cells found?


A

Functions in protein digestion; secreted by the gastric chief cells


48
Q

Bicarbonate is secreted by ____ cells and ____ glands; its function is to ____ acid.


A

Mucosal; Brunner; neutralize


49
Q

A patient with a gastrinoma can be expected to also have excessive activation of which pro-enzyme?


A

Pepsinogen (activated by acid, the release of which is stimulated by gastrin)


50
Q

Produced by these cells found in this organ, pepsinogen becomes pepsin when there is a high acid content in the stomach.


A

Chief cells of the stomach


51
Q

Increased levels of what three molecules cause parietal cells to release gastric acid?


A

Acetylcholine, histamine, and gastrin


52
Q

Decreased levels of which hormones will cause parietal cells to secrete gastric acid?


A

Somatostatin, GIP, prostaglandin, secretin


53
Q

Increased secretin levels increase the secretion of this molecule, whose main purpose is to neutralize acid.


A

Bicarbonate


54
Q

Where is bicarbonate typically trapped in the GI system?


A

Bicarbonate is trapped in the mucus that covers the gastric epithelium.


55
Q

A patient has vitamin B12 deficiency. What part of the GI system could be damaged, impacting vitamin B12 levels?


A

Parietal cells of the stomach or the terminal ileum (the latter is where vitamin B12 is absorbed as a complex with intrinsic factor)


56
Q

Where are bicarbonate-secreting mucous glands found? What about bicarbonate-secreting Brunner glands?


A

Stomach, duodenum, salivary glands, pancreas; duodenum

57
Q

The proton pump of parietal cells can be found on which side of the cell?


A

The luminal side


58
Q

The proton pump of the parietal cells pumps ____ into the cell and sends ____ out of the cell and into the lumen.


A

Potassium ions; protons


59
Q

A patient in the United States with raw epigastric pain after eating might get relief with which class of medication?


A

Proton pump inhibitors (H2 receptor blockers are also useful, but most guidelines recommend starting with a PPI first)


60
Q

How does acetylcholine stimulate acid production by parietal cells?


A

It activates an M3 receptor on the cells that directly stimulates acid secretion through the proton pump via a G-protein cascade


61
Q

In what two ways does gastrin stimulate acid production by parietal cells?


A

Gastrin primarily stimulates histamine production by ECL cells, and binds directly to parietal cell cholecystokinin (CCKB) receptors


62
Q

Carbonic anhydrase is an enzyme that converts carbonic acid to what two molecules in the parietal cell?


A

Carbon dioxide and water


63
Q

As a proton leaves the parietal cell on the luminal side, bicarbonate leaves the cell via the basolateral side and causes what effect?


A

The alkaline tide, a transient increase in interstitial pH secondary to gastric acid production/bicarbonate secretion from the parietal cell


64
Q

What is the second messenger that is used in histamine-induced acid secretion?


A

cAMP, stimulated by the H2 receptor


65
Q

What substances inhibit acid secretion by the parietal cells?


A

Prostaglandins, somatostatin


66
Q

Each of these pathways has an inhibitory drug to decrease acid release, except for which one? (ACh to M3, gastrin to CCKB, histamine to H2)


A

Gastrin to CCKB receptor, as gastrin has no clinically useful pharmacologic inhibitor


67
Q

A woman with too much gastric acid takes a drug that decreases parietal cell cAMP levels. By what pathway does this drug act?


A

Acts via the Gi pathway to decrease parietal cell cAMP levels and lower acid secretion (the drug is misoprostol, a prostaglandin analog)

68
Q

What are the six components of bile?


A

Bile salts, phospholipids, cholesterol, bilirubin, water, and ions


69
Q

What is the only means of cholesterol excretion from the body?


A

Via bile


70
Q

Bile acid conjugation makes bile _____ (more/less) soluble by biding to which two amino acids?


A

More, glycine and taurine


71
Q

In a patient who is unable to produce bile, what physiologic functions would be impaired?


A

Excretion of cholesterol, digestion and uptake of lipids and fat-soluble vitamins, & antimicrobial activity


72
Q

A patient has defective cholesterol 7&945;-hydroxylase activity. Does this affect his ability to absorb vitamins in any way?


A

Yes, as this impairs the rate-limiting step of bile synthesis (one of bile’s functions is to assist with vitamin digestion and absorption)


73
Q

In an experiment, bacteria within a Petri dish exposed to gallbladder secretions are noted to perish quickly. What is going on?


A

Bile has antimicrobial activity via bacterial membrane disruption

74
Q

A patient with hemolytic anemia would be likely to have which abnormal result on liver function tests?


A

Unconjugated hyperbilirubinemia (bilirubin is a breakdown product of heme)


75
Q

What is the essential structural difference between direct and indirect bilirubin?


A

Direct bilirubin is conjugated with glucuronic acid and is thus water soluble, whereas indirect bilirubin is not and is thus water insoluble


76
Q

How is bilirubin excreted from the body?


A

Bilirubin is excreted in bile (it is excreted in urine as urobilin and stool as stercobilin)


77
Q

What type of bilirubin is water soluble: direct or indirect? What type is water insoluble?


A

Direct bilirubin is water soluble; indirect bilirubin is water insoluble


78
Q

Unconjugated bilirubin travels through the circulation bound to ____. This complex can be measured as ____.


A

Albumin; indirect bilirubin


79
Q

A patient with impaired bile acid conjugation would develop which abnormality on liver function tests?


A

Conjugated (direct) hyperbilirubinemia


80
Q

____ is excreted renally, giving ____ its classic yellow color.


A

Urobilin; urine


81
Q

If exposed to conjugated bilirubin, colonic bacteria will produce what?


A

Urobilinogen


82
Q

A patient taking antibiotics wipes out his gut flora. His urine is noted to be paler than usual. Why is this the case?


A

Bilirubin conversion into urobilinogen is impaired; reabsorbed urobilinogen is converted into urobilin, giving urine its yellow color


83
Q

About ____% of urobilinogen is excreted as stercobilin in feces and about ____% goes to the kidney and liver.


A

80; 20


84
Q

Of the urobilinogen that goes to the kidneys and liver, about ____% is excreted renally and ____% enters the enterohepatic circulation.


A

10; 90


85
Q

A patient with an obstruction in stercobilin deposition has feces of what characteristic color?


A

Pale stools (obstruction inhibits its ability to be deposited in the gastrointestinal lumen, leading to pale stools)


86
Q

Urobilinogen cannot be excreted in urine. What form is it excreted in feces, and in a normal patient, what color is the stool?


A

Excreted in feces as stercobilin, which causes the brown color of stool


87
Q

In an experiment, tagged urobilinogen in the gut can be expected to be later found in which organ?


A

Liver, via enterohepatic circulation


88
Q

Which enzyme catalyzes bilirubin conjugation?


A

UDP-glucuronosyltransferase

FF GI (10 decks)

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