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GI Final Exam > Secretions of the GI tract and the pancreas > Flashcards

Secretions of the GI tract and the pancreas Flashcards

1
Q

What salivary gland is the largest and has only serous cells and makes 25% of the saliva and has AMYLASE?

A

Parotid glands

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2
Q

Which glands are the mixed glands that contain both serous and mucous cells, secrete glycoprotein, and secrete most of the saliva?

A

Submaxillary and sublingal glands

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3
Q

Where does blood supply come from in the salivary glands?

A

from the branches of the external carotid artery

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4
Q

What cells secrete the initial saliva?

A

the acinar cells

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5
Q

Which cells have motile extensions, contract to eject saliva, and contain an actinomycin?

A

myoepithelial cells

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6
Q

What contains myoepithelial cels and has saliva that is similar in ionic composition to plasma?

A

the intercalated duct

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7
Q

What is lined by columnar epithelial (ductal) cells that modify the inital saliva to produce the final hypotonic saliva?

A

Striated duct

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8
Q

Is saliva a simple ultra filtrate of plasma?

A

no

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9
Q

What are the electrolyte conentrations in saliva?

A

high K and HCO3

low Na and Cl

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10
Q

What are the two main steps int he formation of slaiva?

A
  • formation of isotonic, plasma-like solution by acinar cells
  • modification of the isotonic solution by the ductal cells
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11
Q

What is the combined action at the salivary gland?

A

absorption of Na and Cl and secretion of K and HCO3

*net absorption of solute** more NaCl absorbed than KHCO3 secreted

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12
Q

How does HCO3 leave the cell?

A

through CFTR channels or the cl HCO3 exchanger both at the apical membrane

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13
Q

What do CF patients lack?

A

the CFTR (cAMP gated)

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14
Q

How does saliva become hypotonic as it flows through the ducts?

A

the ductal cells are water impermeable

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15
Q

What is the concentration of saliva like at a high flow rate

A

like plasma or initial saliva

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16
Q

Saliva at a low flow rate concentrations?

A

low NaCl and high K

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17
Q

What does not apply to HCO3 in the saliva duct?

A

the contact time thing….. HCO3 is always pretty high in the saliva

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18
Q

Where does the sympathetic innervation for the saliva gland go?

A

the periarterial spaces

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19
Q

How does vasopressin and aldosteron modif the composition of saliva?

A

by decreasing its Na and increasing K concentrations

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20
Q

describe the parasympathetic pathway in saliva?

A

Ach binds mAchR which activates IP3 and Ca2+

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21
Q

describe the sypmathetic pathway of saliva things?

A

NE binds B adrengergics and makes cAMP

*both ps and symp stimulate the salivary cells

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22
Q

Which thing dominates, parasympathetic or sympathetic?

A

Parasympathetic always

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23
Q

What are 2 unusual feature in the regulation of salivary secretion?

A
  • it’s exculisvely under the control of the ANS

- it’s increased by BOTH parasymp and symp stimulation

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24
Q

What hydrolyzes all infested protein if HCl is absent?

A

pancreatic enzymes

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25
Q

What are the components of gastric juice?

A

HCl, pepsingoen, mucus, intrinsic factor, H2O

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26
Q

What is intrinsic factor needed for?

A

the absorption of vit. B12 in the ileum

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27
Q

Describe the oxyntic gland?

A

located in the prox 80% of stomach

secretes acid

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28
Q

Describethe pylroic gland?

A

in the antrum

synthesizes and releases GASTRIN

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29
Q

What does Gastrin do?

A

goes into the circulation and goes to parietal cells and inhibits them from making more IF and HCl

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30
Q

What do mucus cells do?

A

secrete mucus, HCO3 , and pepsinogen

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31
Q

What is th main function of low gastric pH?

A

to convert pepsinogen to pepsin

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32
Q

Where is Hcl formed?

A

at the villus-like membrane of the canaliculi which are continuous with the lumen

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33
Q

How is H+ secreted into the gastric lumen?

A

the K/H antiporter

  • remember that Cl will follow H into the lumen
  • result is net secretino of Hcl and net absorption of HCO3
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34
Q

What does histamine do?

A

stimulates Hcl secretion

  • released from ECL cells
  • binds to H2 receptors on parietal cells (cimetidine blocks this)
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35
Q

What stimulates histamine release?

A

Gastrin and Ach

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36
Q

Which regulatory thing of Hcl secretion is blocked by atropine?

A

Ach the neurotransmitter

37
Q

What does Ach even do?

A
  • stimulates HCl secretion
  • released from vagus n.
  • binds to M3 mAchR on parietal cells
  • atropine blocks it
  • IP3/ Ca cascade
  • indirectly stimulates ECL cells (they release histamine)
38
Q

What does gastrin do?

A
  • hormone
  • stimulates HCl secretion
  • secreted by G cells in the antrum and delivered back to stomach via circulation
  • stimulates ECL cells which release histamine
39
Q

What does gastrin bind?

A

CCKB receptors on parietal cells—>IP3/Ca2+

-CCKA is specific for CCK remember

40
Q

What stimulates gastrin release?

A

gastric distension and presence of small peptides and aa’s and stimulation of the vagus N.

41
Q

Does atorpine block the vagal stimulation of G cells?

A

NO!

42
Q

What does Somatostatin do?

A

inhibits HCL secretion

-released from D cells in the antrum

43
Q

What does somatostatin bind?

A

SSTR2 on parietal cells

-inhibits AC so no H+ secretion

44
Q

What is potentiation?

A

when the combined response of two stimulants exceeds the sum of their individual responses

45
Q

What were the examples of potentiation that we talked about?

A

histamine potentiates action sof Ach and gastrin

Ach potentiates the actions of histamine and gastrin

46
Q

What does omeprazole do?

A

blocks the H+/K+ ATPase

47
Q

What does Cimetidine do?

A

antagonist of H2 receptors, used to treat duodenal and gastric ulcers and GERD

48
Q

As pH falls, what happens to gastrin release?

A

it gets inhibited

-passive feedback mechanism

49
Q

What are the 2 different pathways that the vagus nerve can go in the stomach?

A
  • release Ach onto parietal cells
  • release GRP onto G-cells (atropine doesn’t block)
  • remember that distension will also cause Ach to be released onto G-cells in the antrum
50
Q

What is the cephalic phase of Gastric secretion?

A

30-% ofHcl secreted because of this

  • just a response to a meal
  • vagus n. to parietal cell
  • vagus n. to gastrin to parietal cell
51
Q

What would abolish the cephalic phase of gastric secretion?

A

A Vagotomy

52
Q

What is the gastric phase of secretion?

A

60% of HCl made

  • stim is distension of stomach and presence of aa’s and stuff
  • we get the same stuff happening as in cephalic, but with distention and aa’s being a local reflex (gastrin to parietal cell
53
Q

What is the intestine phase of secretion?

A

10% of HCl secreted

  • distention of SI- stimulates acid secretion
  • digested protein stimulates INTESTINAL G cell which to release gastrin to get tot he parietal cells
54
Q

What does gastric juice composition depend on?

A

the secretion rate

55
Q

What is the final juice like at low secretion rates?

A

a solution of NaCl

56
Q

What happens at higher secretion rates for gastric juice?

A

the concentration of Na decreases and that of H+ increases

-at peak rates, it’s mainly HCl

57
Q

What does the vagus nerve do to a SST cell?

A

inhibits it so that we can make some acid

58
Q

What in the gastric lumen will stimulate the release of SST?

A

H+

-feedback

59
Q

What secretes pepsinogen?

A

chief cells and mucus cells in the oxyntic glands

60
Q

What nerve stimulation is the most imporatn stimulus for pepsinogen secretion?

A

vagus n.

61
Q

What can pepsin do?

A

digest proteins and convert more pepsinogen to pepsin

62
Q

What is the optimal pH of pepsin?

A
  1. 8-3.5

- the pH of the lumen is normally like 6

63
Q

What is IF required for?

A

absorption of Vit. B12 in the ileum

*this is the only secretion by the stomach that is required

64
Q

What does failure to secrete IF lead to

A

pernicious anemia

-but it won’t show up for a while because the liver stores a shit ton of B12

65
Q

What protects the gastric mucosa?

A

HCO3, mucus, PG’s, mucosal blood flow, and growth factors

66
Q

What damages the gastric mucosa?

A

acid, pepsin, NSAIDs, Helicobacter pylori, aspirin, alcohol, bile, and stress

67
Q

Describe a gastric ulcer

A

forms primarily because of the mucosal barrier is defective

-the bacteria H pylori releases cytotoxins that breakdown the mucosal barrier and underlying cells

68
Q

What enzyme allows the bacteria to colonize the gastric mucosa?

A

urease

  • converts urea to NH3, which alkalinizes the local environment
  • this is used for a diagnostic test
69
Q

Describe a duodenal ulcer

A
  • more common than gastric
  • forms because H+ SECRETORY RATES ARE HIGHER THAN NORMAL
  • role of H. pylori is indirect
  • When the acid gets to the duodenum, it overwhelms the buffer capacity of HCO3 in pancreatic juice
70
Q

What is the role of H. Pylori in the duodenal ulcer?

A
  • inhibits SST secretion from D cells (inhibition of inhibition)
  • it also spreads to the duodenum and inhibits duodenal HCO3 secretion
71
Q

What is Zollinger ellison syndrome?

A

when acid secretory rates are the highest

  • tumor usually in the pancreas that secretes gastrin like crazy
  • low duodenal pH inactivates pancreatic lipases which results in Steatorrhea*
72
Q

What are the treatment options for Zollinger-Ellison syndrome?

A

Cimetidine, omeprazole, and surgical removal of the tumor

73
Q

What are the 2 main components of the exocrine pancreas’s secretion?

A
  • aqueous solution containing HCO3

- enzymatic secretion

74
Q

What cells of the pancreas secret the enzymatic portion?

A

Acinar cells

75
Q

What cells of the pancreas secrete the HCO3 aqueous solution?

A

Ductal and centroacinar cells

76
Q

Where do the sympathetic nerves to the pancreas come from?

A

the celiac and superior mesenteric plexuses

77
Q

Where do the parasympathetic nerves to the pancreas come from?

A

the vagus nerve

  • synapse in ENS
  • postganglionic synpases on exocrin pancreas
78
Q

What is the main difference between salivary glands and exocrine pancreas glands when it comes to innervation?

A
  • in salivary glands, everything stimulates saliva production
  • in pancreas, psymp stimulates it and sympathetic inhibits secretion
79
Q

Which enzymes are secreted as active forms?

A

pancreatic amylases and lipases

80
Q

Which enzymes are secreted as inactive forms?

A

pancreatic proteases

-convert to active forms in the lumen of the duodenum

81
Q

What kind of tonic is the secretion of the pancreatic duct?

A

isotonic

82
Q

How doe ductal cells modify the pancreatic secretion?

A

-net secretion of HCO3 and net absorption of H+

83
Q

How does flow rate affect the pancreatic juice?

A
  • high flow rate: HCO3 is highest and Cl is lowest
  • Low flow rate: other way around
  • Na is always high and K is always low
84
Q

What maintains the reciprocal relationship of HCO3 and Cl- ions?

A

the HCO3/Cl- exchanger in the apical membrane of ductal cells

85
Q

What mainly comes out of the cephalic and gastric phase of pancreatic secretion?

A

enzymatic stuff

86
Q

What comes out of the intestinal phase of pancreatic secretion?

A

both enzymatic and aqueous secretions

-80% of pancreatic secretion

87
Q

Where does CCK come from in the duodenum?

A

I cells

88
Q

Where does secretin come from in the duodenum?

A

S cells

89
Q

How does acute pancreatitis occur?

A

when pancreatic enzymes are activated in pancreatic tissue rather than in the lumen of the intestin
-results in autodigestion of pancreatic tissue

GI Final Exam (10 decks)

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