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GI Week 3 > Pancreas, Gallbladder, and Liver Physiology > Flashcards

Pancreas, Gallbladder, and Liver Physiology Flashcards

1
Q

True or False: Amino acids enter enterocytes along with Na+ ions, using 5 different co-transporters that are selective for neutral aromatic, imino, positively charged and negatively charged amino acids.

A

True

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2
Q

True or False: Monosaccharides leave the enterocyte by means of a Na+ coupled transporter protein on the basolateral surface of the cell.

A

False

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3
Q

How does H+ in the duodenum lead to bicarbonate secretion?

A
  1. H+ ions in duodenum
  2. Activates secretin release
  3. Goes over to pancreas and leads to bicarbonate secretion
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4
Q

How do amino acids/fats in the duodenum lead to decreased motility?

A
  1. Amino acids/fats in duodenum
  2. Triggers release of CCK
  3. Slows things in your stomach down
  4. Both inhibit gastric motility as well as gastric secretion
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5
Q

What contraction does CCK control?

A

Sphincter of Oddi contraction

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6
Q

What is the Pancreas exocrine secretion?

A

~90% of cells

-Digestive enzymes and bicarbonate into the duodenum

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7
Q

How much exocrine pancreas secretions do we release each day?

A

1.5 L/day

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8
Q

What do Acinar cells (exocrine pancreas) release?

A

Secrete digestive enzymes

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9
Q

What do Centroacinar and Duct cells do in the exocrine pancreas?

A

They dilute pancreatic enzymes and make rich in sodium and bicarbonate.

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10
Q

What proteases are pancreatic acinar cell secretory products?

A
  • Trypsinogen
  • Chymotrypsinogen
  • Proelastase
  • Procarboxypeptidase A
  • Procarboxypeptidase B
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11
Q

What amylolytic enzymes are pancreatic acinar cell secretary products?

A

-Amylase

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12
Q

What Lipases are pancreatic acinar cell secretory products?

A
  • Lipase
  • Nonspecific esterase
  • Prophospholipase A2
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13
Q

What Nucleases are pancreatic acinar cell secretory products?

A
  • Deoxyribonuclease

- Ribonuclease

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14
Q

What “others” are pancreatic acinar cell secretory products?

A
  • Procolipase
  • Trypsin inhibitors
  • Monitor peptide
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15
Q

What do Enteropeptidase and Enterokinase do?

A

Targe trypsinogen to become trypsin

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16
Q

What is the function of Trypsin?

A
  1. Activates procolipase to become co-lipase
  2. Activates co-lipase to become lipase
    It’s important for pancreatitis that you’re not getting premature activation of these enzymes.
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17
Q

How are pancreatic enzymes synthesized?

A

They are synthesized with an N-terminal signal peptide, which targets them for the secretory pathway where they are packaged into zymogen granules and prevents them from being exposed to the cytosol.

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18
Q

What indicates the inactive form of pancreatic enzymes?

A

-ogen

pro-

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19
Q

During the cephalic/gastric phase, what percent of pancreatic exocrine secretion is enzyme?

A

30% enzyme, low volume acinar cells activated by parasympathetic efferents (ACh) from vagal centers in the brain and secondary to gastrin release.

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20
Q

During the Intestinal phase, what percent of pancreatic exocrine secretion is enzyme?

A

70% enzyme, increased enzyme, high volume. Acinar cells are activated by vago-vagal reflex and by fat/amino acids in duodenum.

  • I cells release CCK
  • H+ ions cause S cells to release secretin activating ductal cell secretion of bicarbonate
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21
Q

What things promotes compound exocytosis in acinar cells?

A

Secretagogues!

  • CCK and vagal stimualtion (ACh, GRP)
  • Ca2+ signaling most important with cAMP signaling playing a modifying role
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22
Q

What does vagal stimulation cause during the cephalic and gastric phases?

A

Vagal stimulation causes release of pancreatic enzymes including Monitor Peptide.

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23
Q

What do amino and fatty acids cause the release of during intestinal phase?

A

CCK-RP

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24
Q

What do CCK-RP and Monitor Peptide do?

A

Cause the release of CCK from I cells into the blood.

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25
Q

What does CCK increase the release of?

A

Monitor peptides and pancreatic enzymes

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26
Q

What happens toward the end of intestinal phase?

A
  • Pancreatic enzymes digest luminal nutrients.

- CCK-RP and Monitor peptide turning off CCK secretion.

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27
Q

What is CCK??

A

Cholecystokinin - Master regulator of duodenal cluster unit

  • Released when fat and protein are in the duodenum
  • Satiety signal
  • Also alters brain decreasing food intake
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28
Q

What does CCK do to the Gallbladder?

A

Contraction

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29
Q

What does CCK do to the Pancreas?

A

Acinar secretion

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30
Q

What does CCK do to the stomach?

A

Reduced emptying

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31
Q

What does CCK do to the Sphincter of Oddi?

A

Relaxation

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32
Q

Overall what does CCK promote?

A
  • Protein, carbohydrate, lipid absorption and digestion

- Matching of nutrient to digestive and absorptive capacity

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33
Q

What is the function of Enteropeptidase?

A

It’s in the duodenal brush boarder membrane and it cleaves trypsinogen to its active form, trypsin.

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34
Q

What does Trypsin activate?

A

Lipases and Endopeptidases, chymotrysin and elastase.

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35
Q

What causes Hereditary Pancreatitis?

A

It occurs due to a mutation in the trypsinogen PRSS1 gene causing activation of digestive enzymes in the pancreas which can lead to inflammation.

36
Q

How is Hereditary Pancreatitis passed on?

A

Autosomal Dominant

37
Q

What do S cells do when duodenal pH

A

Release secretin, which raises the pH by increasing bicarbonate secretion from the pancreatic ducts, biliary ducts and duodenal mucosa.

38
Q

Do you predict a patient on a PPI will have increased or decreased duodenal bicarbonate secretion postprandially?

A

Decreased (no longer an acid signal being released)

39
Q

What is the function of Secretin?

A

It initiates secretion of bicarbonate solution by pancreatic duct cells.

40
Q

What transporter provides “power” for the duct cells of the pancreas?

A

Na+/K+ ATPase on basolateral membrane generates the “power” in the form of a steep sodium gradient.

41
Q

What does Carbonic Anhydrase do in the duct cells of the pancreas?

A

Carbonic anhydrase promotes formation of H+ and HCO3- and come bicarbonate from the alkaline tide is taken up from the blood stream by NBC response to depolarization

42
Q

What exchanger is regulated by Secretin?

A

CFTR supplies the Cl- for the HCO3-/Cl- exchanger . This exchanger is regulated by secretin activation of cAMP.

43
Q

What would Cystic Fibrosis do to the Pancreas?

A

It would cause decreased bicarbonate because you aren’t getting Cl- going into the duct (also not getting water into the ducts). This leads to Pancreatic insufficient (90% reduction in number of ducts being functional/used)

44
Q

What are Causes of Pancreatitis?

A
  • Cystic fibrosis
  • Occlusion of pancreatic duct: gallstones, malignancy
  • Alcohol can be metabolized into products that cause hyper stimulation of acinar cells resulting in intracellular trypsin activation and cell death
45
Q

What are the effects of Pancreatitis?

A
  • Upper abdominal pain from autodigestion of pancreatic tissue can lead to vomiting and sympathetic activation
  • Enzymes spill over into circulation - elevated serum amylase and lipase levels
  • Malabsorption of fat and fat-soluble vitamins (A, D, E, K) steatorrhea
  • Malignancy, Diabetes, and Infections
46
Q

What does the pancreas provide enzymes for?

A

To promote digestion and bicarbonate to neutralize gastric acid.

47
Q

When is pancreatic secretion induced?

A

During cephalic and gastric phases, but maximal secretion occurs during intestinal phase due to the release of cholecystokinin and secretin.

48
Q

What do Acini and ducts secrete? What is the function of these products?

A

Acini - secrete inactive enzymes

Ducts - secrete fluid and bicarbonate to neutralize acid from the stomach

49
Q

How are pancreatic enzymes activated?

A

At the brush border by enteropeptidase

50
Q

Does the GI system maintain a state of homeostasis?

A

GI does NOT maintain a state of homeostasis, instead it generally assimilates everything presented to it in the diet.

51
Q

Why is the Hypothalamus important?

A

It’s important in regulating energy homeostasis by maintaining a balance between food intake and energy expenditure.

52
Q

What is GLP-1 and what does it do?

A

GLP-1 is an incretin.

It increases insulin and decreases glucagon.

53
Q

Why does oral glucose tend to lead to higher insulin than IV glucose?

A

Since glucose causes a release of glucagon-like peptide-1 (GLP-1) from intestinal L cells and glucose-dependent insulinotropic peptide (GIP) from K cells.

54
Q

How do some diabetes drugs work?

A

By increasing GLP-1 stability (glistens) and other are GLP-1 agonists.

55
Q

What four molecules stimulate insulin secretion of pancreatic beta-cells in the islets of Langerhans?

A
  • GLP-1
  • Amino acids
  • Cholecystokinin
  • ACh
56
Q

What are negative regulators of insulin?

A
  • Somatostatin secreted from neighboring D cells

- Norepinephrine

57
Q

When are plasma insulin levels higher?

A

After consuming glucose/amino acids than IV glucose

58
Q

What four molecules act as satiety signals at the hypothalamus?

A
  • GLP1
  • CCK
  • Insulin
  • Leptin (adipose tissue)
59
Q

What do satiety signals do?

A

They travel to the hypothalamus, decreasing food intake and increasing energy expenditure

60
Q

What can lack of sleep lower?

A

Leptin levels. Individuals with dec. leptin often experience hyperphagia or overeating.

61
Q

What is Ghrelin?

A

A peptide hormone produced in fundus of stomach during fasting stimulates appetite (orexigenic) and decreases energy expenditure through neuropeptide Y and agouti-related peptide.

62
Q

What are Ghrelin levels like in individuals with gastric bypass?

A

Individuals with gastric bypass have relatively flat ghrelin levels.

63
Q

What would be the consequence of giving gherkin prior to eating a buffet?

A

You could eat a lot more!

64
Q

Where is Gastrin secreted?

A

Stomach, by G cells

65
Q

What hormones are secreted in the Intestine (five)?

A
  1. Cholecystokinin (CCK)
  2. Secretin
  3. Motilin
  4. Gastric inhibitory peptide (GIP)
  5. Glucagon-like peptide-1 (GLP-1)
66
Q

What stimulates Gastrin release?

A

Peptides and amino acids; neural reflexes

67
Q

What is the target for Gastrin?

A

ECL cells and parietal cells

68
Q

What are the effects of gastrin?

A

Stimulates gastric acid secretion and mucosal growth

69
Q

What inhibits gastrin release?

A

Somatostatin

70
Q

What stimulates the release of CCK?

A

Fatty acids and some amino acids.

71
Q

What is the primary target for CCK?

A

Gallbladder, pancreas, stomach

72
Q

What are the primary effects of gastrin?

A
  • Stimulates gallbladder contraction and pancreatic enzyme secretion
  • Inhibits gastric emptying and acid secretion
73
Q

What does CCK promotes?

A

Satiety. Some effects may be due to CCK as neurotransmitter.

74
Q

What stimulates the release of Secretin?

A

Acid in small intestine

75
Q

What is the target for Secretin?

A

Pancreas, stomach

76
Q

What is the effect of Secretin?

A
  • Stimulates HCO3- secretion

- Inhibits gastric emptying and acid secretion

77
Q

What stimulates the release of Motilin?

A

Fasting: periodic release every 1.5-2 hours

78
Q

What are the targets of Motilin?

A

Gastric and intestinal smooth muscle

79
Q

What are the effects of Motilin?

A

Stimulates migrating motor complex.

80
Q

What inhibits Motilin?

A

Eating a meal

81
Q

What stimulates the release of Gastric Inhibitory Peptide (GIP)?

A

Glucose, fatty acids, and amino acids in small intestine

82
Q

What is the target for Gastric inhibitory peptide (GIP)?

A

Beta cells of pancreas

83
Q

What are the effects of GIP (gastric inhibitory peptide)?

A
  • Stimulates insulin release (Feedforward mechanism)

- Inhibits gastric emptying and acid secretion

84
Q

What stimulates the release of Glucagon-like peptide-1 (GLP-1)?

A

Mixed meal that includes carbohydrates or fats in the lumen.

85
Q

What is the primary target for GLP-1 (Glucagon-like peptide-1)?

A

Endocrine pancreas

86
Q

What are the primary effects of GLP-1 (glucagon-like peptide-1)?

A
  • Stimulates insulin release

- Inhibits glucagon release and gastric function

87
Q

What does Glucagon-like peptide-1 (GLP-1) promote?

A

Satiety

GI Week 3 (10 decks)

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