Lecture 5: Gastric, Pancreatic, Bile Secretions Flashcards

1
Q

What are the direct paths of vagal stimulation?

A

Vagus nerve -> Parietal cells -> ACh -> HCl
Vagus nerve -> GRP -> G Cells

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2
Q

What are the indirect paths of vagal stimulation

A

Rest of G cell path
Gastrin from G cells -> Systemic circulation -> HCl from parietal cells

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3
Q

Which pathway will atropine block?

A

Vagus nerve -> Parietal cells -> ACh -> HCl

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4
Q

Why will atrophne not block HCl secretion completely?

A

Only affecting 1 of 3 pathways

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5
Q

Name the phases of gastric HCl secretion

A

Cephalic, gastric, intestinal

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6
Q

Which phase accounts for 30% of total HCl?

A

Cephalic

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7
Q

Which phase accounts for 60% of total HCl?

A

Gastric

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8
Q

Which phase accounts for 10% of total HCl?

A

Intestinal

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9
Q

What are stimuli for the cephalic phase?

A

Smelling, tasting, chewing, swallowing, conditioned reflexes

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10
Q

What are the mechanisms to promote HCl secretion in the cephalic phase?

A

Direct stimulation of parietal cells by vagus nerve
Indirect stimulation via gastrin

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11
Q

What are the stimuli for the gastric phase?

A

Distention of stomach and presence of AA and peptides

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12
Q

What are the mechanisms to promote HCl secretion in gastric phase?

A
  1. Distention -> Vagal nerve stimulation -> Parietal cells
  2. Indirect via gastrin
  3. Distention of antrum -> Local reflexes -> Gastrin release
  4. AA + Peptides -> G cells -> Gastrin
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13
Q

What is the intestinal phase stimulated by?

A

Products of protein digestion

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14
Q

What is the intestinal phase stimulated by?

A

Products of protein digestion

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15
Q

When is HCl secretion inhibited (why is it no longer needed)

A

No longer needed for conversion of pepsinogen to pepsin

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16
Q

Decreased what of gastric contents inhibits HCl secretion?

A

pH

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17
Q

How does somatostatin directly inhibit HCl secretion?

A

Binds parietal cells and antagonizes histamine pathway by decreasing cAMP

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18
Q

How does somatostatin indirectly inhibit HCl secretion?

A

Inhibits both histamine and gastrin release

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19
Q

How do prostaglandins antagonize histamine in the inhibition of HCl secretion?

A

Reducing cAMP

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20
Q

What are the barriers to acid and pepsin damage to gastric mucosa?

A

Bicarbonate and mucus

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21
Q

What is peptic ulcer disease?

A

Ulcerative lesion of gastric or duodenal mucosa

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22
Q

Name the causes of peptic ulcer disease

A

Could be 1 or both:
Loss of mucus
Excessive H+ and pepsin secretion

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23
Q

Why do gastric ulcers form?

A

Because mucosal barrier is defective, so H+ and pepsin digest mucosa

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24
Q

Why do duodenal ulcers form?

A

Occur when H+ secretory rate higher than normal, overwhelm buffering capacity of pancreas

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25
Q

What is the SNS innervation of the exocrine pancreas?

A

Celiac and superior mesenteric plexuses

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26
Q

What is the PNS innervation of the exocrine pancreas?

A

Vagal nerve

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27
Q

What effect does PSNS stimulation have on exocrine pancreas?

A

Stimulates secretion

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28
Q

What effect does SNS stimulation have on exocrine pancreas?

A

Inhibits secretions

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29
Q

Name the two components of pancreatic secretions

A

Enzymatic component
Aqueous component

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30
Q

What is the enzymatic component of pancreatic secretions responsible for digesting?

A

Carbs, proteins, lipids

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31
Q

Where are the enzymes of pancreatic secretion synthesized?

A

Rough ER of acinar cells

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32
Q

Where are the enzymes of pancreatic secretion stored?

A

On zymogens

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33
Q

What form are amylase and lipases secreted by pancreas?

A

Active

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34
Q

What form are proteases secreted by pancreas?

A

Inactive (known as zymogens)

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35
Q

Pancreatic juice is ______

A

Isotonic

36
Q

What does pancreatic juice contain

A

Na, Cl, K, HCO3

37
Q

What cell produces initial aqueous component of pancreas secretion?

A

Centroacinar and ductal cells

38
Q

What cell modifies the secretion of pancreatic juice?

A

Ductal cells

39
Q

For pancreatic secretions, where does HCO3 go, and where does H+ go?

A

HCO3 goes to lumen
H+ goes to blood

40
Q

What transports are on the luminal membrane?

A

HCO3/Cl exchanger

41
Q

What transports are on the basolateral membrane?

A

Na/K ATPase
Na/K Exchanger

42
Q

How do Na+ and K+ concentrations in pancreatic juice compare to plasma?

A

Similar

43
Q

The concentrations of Cl and HCO3 of pancreatic juice…

A

Vary with flow rate

44
Q

T/F: The concentrations of Na+ and K+ in plasma vary with flow rate

A

False

45
Q

At high flow rates HCO3 concentration

A

Increases

46
Q

At low flow rates HCO3 concentration

A

Decreases

47
Q

At high flow rates Cl concentration

A

Decreases

48
Q

At low flow rates Cl concentration

A

Increases

49
Q

At high flow rates, what does pancreatic juice mostly contain?

A

Na, HCO3, water

50
Q

At low flow rates, what does pancreatic juice mostly contain?

A

Na, Cl, water

51
Q

What is aqueous portion of pancreatic secretion stimulated by?

A

H+ in duodenum (will need bicarb)

52
Q

What is the enzymatic portion of pancreatic secretions stimulated by?

A

Products of digestion

53
Q

Gastric phase accounts for what % of secretions?

A

80%

54
Q

Acinar cells contain receptors for what

A

CCK and ACh (muscarinic)

55
Q

H+ stimulates which cells to release what?

A

S cells to release secretin

56
Q

AA and peptides stimulate secretion of what?

A

CCK

57
Q

What potentiates action of CCK?

A

ACh

58
Q

Describe the pathway for aqueous secretion in pancreatic juice

A

H+ > S cells > Secretin > cAMP on ductal cells (Ach and CCK potentiate) > Secretion

59
Q

Describe the pathway for enzymatic secretion in pancreatic juice

A

Small peptides + fatty acids > I cells > CCK > IP3, Ca2+ (Ach potentiates) > Enzymes

60
Q

Ductal cells have receptors for what

A

CCK, ACh, Secretin

61
Q

Stimulation of ductal cell receptors stimulates

A

Bicarb for aqueous portion of pancreatic juice

62
Q

Mixture of bile salts, bile pigments, cholesterol, phospholipids, ions, water

A

Bile

63
Q

Emulsify lipids to prepare for digestion, then solubilizes products into micelles for absorption

A

Bile salts

64
Q

What is contained in the biliary system?

A

Liver, gallbladder, bile duct, duodenum, ileum, portal circulation

65
Q

What synthesize components of liver bile?

A

Hepatocytes

66
Q

What does CCK do in biliary system?

A

Stimulates contraction of gallbladder
Relaxes sphincter of Oddi

67
Q

What happens to bile salts after lipid absorption?

A

Recirculated to liver via reabsorption in ileum

68
Q

What is the composition of bile?

A

Bile salts, bile pigments, cholesterol, phospholipids, ions, water

69
Q

What is 50% of the composition of bile?

A

Bile salts

70
Q

What is 40% of the composition of bile?

A

Phospholipids

71
Q

What does liver conjugate to form bile salts?

A

Bile acids and AA (glycine and taurine)

72
Q

What are the two primary bile acids made by hepatocytes?

A

Colic acid and chenodeoxycholic acid

73
Q

What is the responsibility of bile acids?

A

Emulsify lipids so digestion can occur

74
Q

T/F: Bile acids are amphipathic

A

True

75
Q

Bile salts bind to form

A

Micelles

76
Q

What does the core of a micelle contain?

A

Products of digestion

77
Q

What two things equal a micelle?

A

Finely emulsified fat + bile salts

78
Q

What is the product of hemoglobin degradation?

A

Bilirubin

79
Q

What are the functions of the gallbladder?

A

Stores, concentrates, ejects bile
Filling of gallbladder
Concentration of bile
Ejection of bile

80
Q

Is bile produced continuously or periodically?

A

Continuously

81
Q

Bile ejection occurs how long after meal ingested

A

30 minutes

82
Q

CCK contacts and relaxes what for bile ejection

A

Contracts gallbladder
Relaxes sphincter of Oddi

83
Q

Bile is ejected in

A

Spurts

84
Q

Enterohepatic circulation

A

How most bile salts return to the liver

85
Q

What are bile salts transported from ileum lumen to portal blood by?

A

Na+/bile salt co-transporters