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

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

26
What is the exocrine regulatory effect of glucose-dependent insulinotropic peptide?

Decreased secretion of gastric acid

27
What is the endocrine regulatory effect of glucose-dependent insulinotropic peptide?

Increased release of insulin

28
A patient eats a meal with a large load of fatty acids, amino acids, and glucose. What happens to activity levels of K cells?

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

29
Why is an oral glucose load used more rapidly by the body than an equivalent load that is given intravenously?

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

30
Where is vasoactive intestinal polypeptide (VIP) secreted within the gastrointestinal tract?

Parasympathetic ganglia in sphincters, gallbladder, and small intestine

31
Vasoactive intestinal polypeptide (VIP) ____ (increases/decreases) intestinal water and electrolyte secretion.

Increases

32
What effect does vasoactive intestinal peptide (VIP) have on intestinal smooth muscle and sphincters?

Relaxation of these structures

33
What stimuli increase secretion of vasoactive intestinal peptide (VIP)?

Distention, vagal stimulation

34
What is a negative regulator of vasoactive intestinal peptide (VIP) release?

Adrenergic input

35
A patient presents with watery diarrhea, hypokalemia, and achlorhydria. What is the most likely tumor causing this syndrome?

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

36
A patient has profuse watery diarrhea. CT shows a pancreatic mass; labs show hypokalemia and achlorhydria. What nervous system is to blame?

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

37
Which small messenger molecule causes an increase in smooth muscle relaxation in the gut, particularly in the lower esophageal sphincter?

Nitric oxide

38
A man with dysphagia has uncoordinated esophageal peristalsis and increased lower esophageal sphincter tone. What is the pathophysiology?

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

39
What is the function of motilin?

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

40
Motilin secretion is ____ (increased/decreased) in a fasting state.

Increased

41
What hormone is produced by the small intestine and associated with intestinal peristalsis?

Motilin

42
What does CCK act on, resulting in pancreatic secretion?

Neuronal muscarinic pathway

43
A man takes erythromycin for a bacterial infection. He develops diarrhea not due to gut flora depletion. Are his MMCs to blame?

Yes, as erythromycin is a potent stimulator of motilin receptors, which increase intestinal peristalsis, likely causing the man's diarrhea
44
In pernicious anemia, destruction of gastric ____ cells leads to deficiency of ____ required for vitamin B12 uptake in the ____.

Parietal; intrinsic factor; terminal ileum

45
A patient has chronic abdominal pain and numerous peptic ulcers refractory to proton pump inhibitors. What tumor should be suspected?

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

46
Describe how pepsin is activated.

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

47
What is the primary role of pepsin? What cells secrete it, and where are these cells found?

Functions in protein digestion; secreted by the gastric chief cells

48
Bicarbonate is secreted by ____ cells and ____ glands; its function is to ____ acid.

Mucosal; Brunner; neutralize

49
A patient with a gastrinoma can be expected to also have excessive activation of which pro-enzyme?

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

50
Produced by these cells found in this organ, pepsinogen becomes pepsin when there is a high acid content in the stomach.

Chief cells of the stomach

51
Increased levels of what three molecules cause parietal cells to release gastric acid?

Acetylcholine, histamine, and gastrin

52
Decreased levels of which hormones will cause parietal cells to secrete gastric acid?

Somatostatin, GIP, prostaglandin, secretin

53
Increased secretin levels increase the secretion of this molecule, whose main purpose is to neutralize acid.

Bicarbonate

54
Where is bicarbonate typically trapped in the GI system?

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

55
A patient has vitamin B12 deficiency. What part of the GI system could be damaged, impacting vitamin B12 levels?

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

56
Where are bicarbonate-secreting mucous glands found? What about bicarbonate-secreting Brunner glands?

Stomach, duodenum, salivary glands, pancreas; duodenum
57
The proton pump of parietal cells can be found on which side of the cell?

The luminal side

58
The proton pump of the parietal cells pumps ____ into the cell and sends ____ out of the cell and into the lumen.

Potassium ions; protons

59
A patient in the United States with raw epigastric pain after eating might get relief with which class of medication?

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

60
How does acetylcholine stimulate acid production by parietal cells?

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

61
In what two ways does gastrin stimulate acid production by parietal cells?

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

62
Carbonic anhydrase is an enzyme that converts carbonic acid to what two molecules in the parietal cell?

Carbon dioxide and water

63
As a proton leaves the parietal cell on the luminal side, bicarbonate leaves the cell via the basolateral side and causes what effect?

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

64
What is the second messenger that is used in histamine-induced acid secretion?

cAMP, stimulated by the H2 receptor

65
What substances inhibit acid secretion by the parietal cells?

Prostaglandins, somatostatin

66
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)

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

67
A woman with too much gastric acid takes a drug that decreases parietal cell cAMP levels. By what pathway does this drug act?

Acts via the Gi pathway to decrease parietal cell cAMP levels and lower acid secretion (the drug is misoprostol, a prostaglandin analog)
68
What are the six components of bile?

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

69
What is the only means of cholesterol excretion from the body?

Via bile

70
Bile acid conjugation makes bile _____ (more/less) soluble by biding to which two amino acids?

More, glycine and taurine

71
In a patient who is unable to produce bile, what physiologic functions would be impaired?

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

72
A patient has defective cholesterol 7&945;-hydroxylase activity. Does this affect his ability to absorb vitamins in any way?

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

Bile has antimicrobial activity via bacterial membrane disruption
74
A patient with hemolytic anemia would be likely to have which abnormal result on liver function tests?

Unconjugated hyperbilirubinemia (bilirubin is a breakdown product of heme)

75
What is the essential structural difference between direct and indirect bilirubin?

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

76
How is bilirubin excreted from the body?

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

77
What type of bilirubin is water soluble: direct or indirect? What type is water insoluble?

Direct bilirubin is water soluble; indirect bilirubin is water insoluble

78
Unconjugated bilirubin travels through the circulation bound to ____. This complex can be measured as ____.

Albumin; indirect bilirubin

79
A patient with impaired bile acid conjugation would develop which abnormality on liver function tests?

Conjugated (direct) hyperbilirubinemia

80
____ is excreted renally, giving ____ its classic yellow color.

Urobilin; urine

81
If exposed to conjugated bilirubin, colonic bacteria will produce what?

Urobilinogen

82
A patient taking antibiotics wipes out his gut flora. His urine is noted to be paler than usual. Why is this the case?

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

83
About ____% of urobilinogen is excreted as stercobilin in feces and about ____% goes to the kidney and liver.

80; 20

84
Of the urobilinogen that goes to the kidneys and liver, about ____% is excreted renally and ____% enters the enterohepatic circulation.

10; 90

85
A patient with an obstruction in stercobilin deposition has feces of what characteristic color?

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

86
Urobilinogen cannot be excreted in urine. What form is it excreted in feces, and in a normal patient, what color is the stool?

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

87
In an experiment, tagged urobilinogen in the gut can be expected to be later found in which organ?

Liver, via enterohepatic circulation

88
Which enzyme catalyzes bilirubin conjugation?

UDP-glucuronosyltransferase