GI:Physiology Flashcards

1
Q

What is the source of gastrin?

A

G cells of the antrum

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2
Q

What is the source of CCK?

A

I cells of the duodenum and jejunum

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3
Q

What is the source of secretin?

A

S cells of the duodenum

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4
Q

What is the source of somatostatin?

A

D cells of the pancreatic islets and GI mucosa

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5
Q

What is the source of glucose-dependent insulinotropic peptide?

A

K cells of the duodenum and jejunum

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6
Q

What is the source of vasoactive intestinal peptide?

A

Parasympathetic ganglia in sphincters, gallbladder, small intestine

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7
Q

What is the source of motilin?

A

Small intestine

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8
Q

What are the three key actions of gastrin?

A

Increase gastric H+ secretion
Increase growth of gastric mucosa
Increase gastric motility

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9
Q

What causes an increase in gastrin release?

A

Stomach distension or alkalization
Amino acids and peptides
Vagal stimulation

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10
Q

What causes a decrease in gastric secretion?

A

Stomach pH <1.5

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11
Q

What syndrome shows a very high level of gastrin

A

Zollinger-Ellison syndrome

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12
Q

What is the effect of chronic PPI use on gastrin

A

Causes an increase in gastrin

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13
Q

What two amino acids are potent stimulators of gastrin release?

A

Phenylalanine

Tryptophan

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14
Q

What are the 4 main actions of CCK?

A

Increase pancreatic secretion
Increase gallbladder contraction
Decrease gastric emptying
Increase sphincter of Oddi relaxation

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15
Q

What causes an increase in CCK secretion?

A

Fatty acids and amino acids

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16
Q

How does CCK cause pancreatic secretion?

A

Acting on neural muscarinic pathways

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17
Q

What are the three main actions of secretin?

A

Increase pancreatic bicarbonate secretion
Decrease gastric acid secretion
Increase bile secretion

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18
Q

What causes an increase in secretin release?

A

Acid and fatty acids in the lumen of the duodenum

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19
Q

What are the 4 key actions of somatostatin?

A

Decrease gastric acid and pepsinogen secretion
Decrease pancreatic and SI fluid secretion
Decrease gallbladder contraction
Decrease insulin and glucagon release

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20
Q

What increases the release of somatostatin? Decreases

A

Increased by acid

Decreased by vagal stimulation

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21
Q

Why does somatostatin have “antigrowth hormone effects”?

A

Inhibits the digestion and absorption of hormones needed for growth

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22
Q

What are the exocrine and endocrine actions of glucose-dependent insulinotropic peptide?

A

Exocrine: Decrease gastric H+ secretion
Endocrine: Increase insulin release

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23
Q

What causes the release of glucose-dependent insulinotropic peptide?

A

Increased by fatty acids, amino acids, and oral glucose

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24
Q

What is another name for glucose-dependent insulinotropic peptide?

A

Gastric inhibitory peptide

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25
Q

What is the effect of glucose-dependent insulinotropic peptide on the rate at which an oral load of glucose is used compared to an IV load?

A

Oral glucose load is used more rapidly–> GIP secreted and increased insulin release

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26
Q

What are two key actions of vasoactive intestinal polypeptide?

A

Increase intestinal water and electrolyte secretion

Increase relaxation of intestinal smooth muscle and sphincters

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27
Q

What increases VIP release? Decreases?

A

Increased by distension and vagal stimulation

Decreased by adrenergic input

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28
Q

What is a VIPoma?

A

Non alpha, non beta islet cell pancreatic tumor that secretes VIP

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29
Q

What is the presentation of a VIPoma?

A

Copious watery diarrhea
Hypokalemia
Acholorhydia

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30
Q

What is the role of NO in the GI tract?

A

Increase in smooth muscle relaxation, including the lower esophageal sphincter

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31
Q

What disease results from loss of NO excretion at the lower esophageal sphincter?

A

Achalasia

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32
Q

What is the main role of motilin?

A

Products migrating motor complexes

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33
Q

What causes an increase in motilin?

A

Fasting state

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34
Q

What is an example of a motilin receptor agonist that can be used to stimulate intestinal peristalsis

A

Erythromycin

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35
Q

What releases intrinsic factor?

A

Parietal cells of the stomach

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36
Q

What releases gastric acid?

A

Parietal cells of the stomach

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37
Q

What releases pepsin?

A

Chief cells of the stomach

38
Q

What releases HCO3- in the GI?

A
Mucosal cells (stomach, duo, salivary galnds, pancreas)
Brunner's glands (duodenum)
39
Q

What is the main role of intrinsic factor?

A

Binds vitamin B12 for uptake at the terminal ileum

40
Q

What results from autoimmune destruction of parietal cells?

A

Chronic gastritis

Pernicious anemia

41
Q

What is the action of gastric acid?

A

Decreases the stomach pH

42
Q

What increases the release of gastric acid?

A

Histamine
ACh
Gastrin

43
Q

What decreases the release of gastric acid?

A

Somatostatin
GIP
Prostaglandin
Secretin

44
Q

What is a gastrinoma?

A

Gastrin secreting tumor that causes continuous high levels of acid secretion and ulcrers

45
Q

What causes an increase in pepsin secretion?

A

Vagal stimulation and local acid

46
Q

What is the role of pepsin?

A

Protein digestion

47
Q

What converts inactive pepsinogen to pepsin?

A

H+

48
Q

What increases bicarbonate secretion?

A

Secretin increases pancreatic and biliary secretion

49
Q

What stimulates secretion from the parotid, submandibular, and sublingual glands?

A

Sympathetic and parasympathetic activty

50
Q

What is the role of the following components of saliva:

  1. Amylase
  2. HCO3
  3. Mucins
A
  1. Digestion of starch
  2. Neutralization of bacterial acids
  3. Lubrication of food
51
Q

Though saliva is normally hypotonic, what can cause it to be more isotonic?

A

Higher flow rates–less time for the absorption of solutes

52
Q

What is the main way in which gastrin increases acid secretion?

A

Primarily through effects on ECL cells leading to histamine release
**rather than direct effects on parietal cells

53
Q

What is the effect of Atropine on parietal cells?

A

Blocks vagal stimulation of parietal cells

Vagal stimulation of G cells is unaffected because GRP is used rather than ACh

54
Q

What is the receptor for gastrin on gastric parietal cells?

A

CCK(B) receptor

55
Q

What is the receptor for ACh on gastric parietal cells? What inhibits the receptor?

A

M3 receptor

Atropine

56
Q

What G protein pathway does ACh/M3 receptor and gastrin/CCKB receptor act through?

A

Gq
IP3/DAG
Increase in H+/K+ exchanger

57
Q

How does histamine lead to an increase in H+/K+ ATPase activity in gastric parietal cells?

A

Binds H2 receptor
Increases cAMP
Increases ATPase activity

58
Q

What is the effect of prostaglanding/misoprostol on the gastric parietal cell proton pump?

A

Increase Gi
Inhibits cAMP
Less activation of the H+/K+ proton pump

59
Q

Where are Brunner’s glands located?

A

Duodenal submucosa

60
Q

What do Brunner’s glands secrete?

A

Alkaline mucus

61
Q

When will you see hypertrophy of Brunner’s glands?

A

Peptic ulcer disease

62
Q

What is high in pancreatic secretions when there is low flow? High flow?

A

Low flow: high Cl-

High flow: high HCO3-

63
Q

What is the role of pancreatic alpha amylase?

A

Starch digestion

64
Q

What is the role of pancreatic lipase, phsopholipase A, and colipase?

A

Fat digestion

65
Q

What are the proteases that the pancreas secretes?

A

Trypsin
Chymotrypsin
Elastase
Carboxypeptidase

66
Q

What form are pancreatic proteases secreted in?

A

Proenzymes called zymogens

67
Q

What converts trypsinogen to trypsin?

A

Enterokinase/enteropeptidase (enzyme secreted from the duodenal mucosa)

68
Q

What enzyme starts carbohydrate digestion and hydrolyzes alpha 1-4 linkages to yield disaccharides like maltose and alpha limit dextrins?

A

Salivary amylase

69
Q

What enzyme is at the highest concentration in the duodenal lumen and hydrolyzes starch to oligosaccharides and disaccharides?

A

Pancreatic amylase

70
Q

What enzymes are found at the brush border of the intestine and are the rate limiting step in carbohydrate digestion?

A

Oligosaccharide hydrolases: produce monosaccharides from oligo and disaccharides

71
Q

What is the only form of carbohydrates that can be absorbed by enterocytes?

A

Monosaccharides–glucose, galactose, fructose

72
Q

How are glucose and galactose taken up into the enterocytes?

A

SGLT1 (Na+ dependent)

73
Q

How is fructose taken up into enterocytes?

A

GLUT5 (facilitated diffusion)

74
Q

How are glucose, galactose, and fructose transported to the blood from enterocytes?

A

GLUT-2

75
Q

What is the role of the D-xylose absorption test?

A

Distinguishes GI mucosal damage from other causes of malabsorption

76
Q

Where in the GI tract is iron absorbed?

A

Absorbed as Fe2+ in the duodenum

77
Q

Where in the GI tract is vitamin B12 absorbed/

A

Terminal ileum

78
Q

Where in the GI tract is folate absorbed?

A

Jejunum

79
Q

What are peyer’s patches?

A

Unencapsulated lymphoid tissue that is found in the lamina propria and submucosa of the ileum

80
Q

Peyer’s patches contain specialized __ cells that take up antigen

A

M cells

81
Q

B cells stimulated in the germinal centers of Peyer’s patches differentiate into ___ secreting plasma cells

A

IgA

82
Q

What is bile composed of?

A
Bile salts
Phospholipids
Cholesterol
Bilirubin
Water
Ions
83
Q

What catalyzes the rate-limiting step of the synthesis of bile acids from cholesterol?

A

Cholesterol 7alpha hydroxylase

84
Q

What are bile salts?

A

Bile acids conjugated to glycine or taurine, making them water soluble

85
Q

What are the three key functions of bile?

A
  1. Digestion and absorption of lipids and fat-soluble vitamins
  2. Cholesterol excretion (only way chol is excreted)
  3. Antimicrobial activity (membrane disruption)
86
Q

Bilirubin is a product of ___ catabolism

A

Heme

87
Q

What is bilirubin conjugated to in the liver?

A

Glucuronate

88
Q

What is the difference between indirect and direct bilirubin?

A

Indirect: unconjugated, water insoluble
Direct: conjugated with glucuronic acid, water soluble

89
Q

What is conjugated bilirubin converted to in the gut by bacteria?

A

Urobiliogen

90
Q

What is urobiliogen converted to in the kidney?

A

urobilin

91
Q

What is bilirubin excreted as in the feces?

A

Stercobilin