Gastric, Pancreatic, & Bile Secretions Flashcards

1
Q

Trace the direct path of vagal stimulation for HCl secretion. (2 pathways)

A

vagus nerve —> Ach —> parietal cells —> HCl
vagus nerve —> GRP —> G cells (first part)

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2
Q

Trace the indirect path of vagal stimulation for HCl secretion.

A

gastrin from G cells —> systemic circulation —> HCl from parietal cells (rest of pathway)

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3
Q

Why won’t atropine block HCl secretion completely?

A

you have GRP in the G cell path

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4
Q

T/F: The cephalic phase is the primary phase of HCl secretion at 60%

A

FALSE - only 30%

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5
Q

What are the stimuli for the cephalic phase in HCl secretion?

A

smelling, tasting, chewing, swallowing, conditioned reflexes

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6
Q

What are 2 mechanisms in the cephalic phase that promote HCl secretion?

A
  1. direct stimulation by vagus n - Ach
  2. indirect via gastrin
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7
Q

What are the stimuli for the gastric phase in HCl secretion?

A

distention of stomach and presence of aa and peptides (PROTEIN)

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8
Q

What are the 4 mechanisms in the gastric phase that promote HCl secretion?

A
  1. distention - vagal stimulation
  2. indirect via gastrin
  3. distention of antrum - local reflexes of gastrin
  4. amino acids and peptides - gastrin
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9
Q

What are the phases in HCl secretion?

A

cephalic
gastric
intestinal

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10
Q

What is the stimuli for the intestinal phase?

A

products of protein digestion

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11
Q

What inhibits HCl secretion?

A

decreased pH of gastric contents
somatostatin - directly and indirectly
prostaglandins

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12
Q

How does somatostatin DIRECTLY inhibit HCl secretion?

A

binds parietal cells
antagonizes histamine pathway by decreasing cAMP

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13
Q

How does somatostatin INDIRECTLY inhibit HCl secretion?

A

inhibits both histamine and gastrin release

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14
Q

What helps prohibit acid and pepsin damage to gastric mucosa?

A

bicarbonate
mucus

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15
Q

How does HCO3 help inhibit gastric mucosa damage?

A

gastric epithelial cells and neck cells that secrete HCO3- get trapped in mucus
acid is then neutralized
pepsin deactivated

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16
Q

What is peptic ulcer disease caused by?

A

loss of mucus
excessive H+ and pepsin secretion
combination of both factors

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17
Q

Peptic ulcer disease is classified as either

A

gastric or duodenal ulcers

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18
Q

Why do gastric ulcers occur?

A

mucosal barrier is defective - H+ ions and pepsin digest mucosa

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19
Q

What is one cause of gastric ulcers? (Hint: colonizes)

A

H. pylori colonizes gastric mucus and attaches to epithelial cells
releases cytotoxins

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20
Q

Why does H. pylori survive in acidic environments?

A

converts urea to ammonia which increases pH of local environment
binds cells inside of being shed

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21
Q

Why do duodenal ulcers occur?

A

when H+ secretory rate is higher than normal
overwhelming buffering capacity

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22
Q

What is Zollinger-Ellison syndrome?

A

high rates of H+ secretion due to high gastrin
delivery of H+ to duodenum
causes steatorrhea

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23
Q

Why does steatorrhea occur in Zollinger-Ellison syndrome?

A

low pH in the small intestine inactivates lipases, so there is no fat digestion

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24
Q

T/F: The exocrine pancreas comprises 90% of the pancreas

A

TRUE

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25
Q

The exocrine pancreas has ______ and _______ components

A

aqueous
enzymatic

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26
Q

There is a high amount of _____ to neutralize acid in the pancreas

A

HCO3-

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27
Q

The enzymatic components of the exocrine pancreas digest what

A

digest carbohydrates, proteins, and fat

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28
Q

What is the structure of exocrine glands in the pancreas?

A

acinus lines with acinar cells
ducts lined with ductal cells
centroacinar cells

29
Q

What do centroacinar cells of the exocrine pancreas do?

A

secrete the aqueous portion

30
Q

The exocrine pancreas has ________ innervation

A

PSNS
SNS

31
Q

Pancreatic secretions are [hypertonic/hypotonic/isotonic] to the blood

A

isotonic

32
Q

Fill in the blanks.

A
  1. acinar cells
  2. ductal cells
  3. Cl-
  4. HCO3-
  5. Na+
  6. K+
  7. H+
  8. Na+
33
Q

The innervation of the exocrine pancreas involves the SNS which has _________ plexuses. It is [stimulatory/inhibitory].

A

celiac and superior mesenteric (celiacomesenteric?)
inhibitory

34
Q

The innervation of the exocrine pancreas involves the PSNS which has _________ nerve. It is [stimulatory/inhibitory].

A

vagus
stimulatory

35
Q

Where are the enzymes of the enzymatic component of the pancreas?

A

on the rough ER facing cells

36
Q

After synthesis (enzymatic component of pancreas), everything is transferred to the ______ and stored as ________

A

golgi
zymogens (inactive form of enzyme)

37
Q

_______ are secreted in inactive form

A

proteases

38
Q

The juice in the aqueous component of the pancreas is [hypertonic/hypotonic/isotonic] and contains which ions?

A

isotonic
Na+
Cl-
HCO3-
K+

39
Q

The centroacinar and ductal cells of the aqueous component make the ______ secretion, then modified by _________

A

initial
transport processes in ductal cells

40
Q

What is on the luminal membrane for the aqueous component of the pancreatic secretions?

A

HCO3-/Cl- exchanger

41
Q

What is on the basolateral (blood) membrane for the aqueous component of the pancreatic secretions?

A

Na+/K+ ATPase
Na+/H+ exchanger

42
Q

Regarding pancreatic secretions, ______ goes into the lumen, and ______ goes into the blood.

A

HCO3-
H+

43
Q

What ion concentrations are constant regarding pancreatic secretions?

A

Na+
K+

44
Q

At high juice flow rates, HCO3- is [high/low] and Cl- is [high/low]

A

HCO3-: high
Cl-: low

45
Q

At low flow rates, solution contains mostly _____, ______, and ______

A

Na+
Cl-
water

46
Q

At high flow rates, solution contains mostly _____, ______, and ______

A

Na+
HCO3-
water

47
Q

T/F: Aqueous and enzymatic portions are regulated separately

A

TRUE

48
Q

Regulation of aqueous portion in the pancreas is stimulated by ______

A

H+ in duodenum

49
Q

Regulation of enzymatic portion is stimulated by ______

A

products of digestion

50
Q

What are the three phases regulating pancreatic secretion?

A

cephalic
gastric
intestinal

51
Q

The cephalic phase regarding pancreatic secretions is initiated by _______. What nerve?

A

smell
taste
conditioning
vagus nerve

52
Q

The gastric phase regarding pancreatic secretions is initiated by _______. What nerve?

A

distention of stomach
vagus nerveE

53
Q

What is the most important phase regulating pancreatic secretions?

A

intestinal phase (80% secretions)

54
Q

Acinar cells in the pancreas is [enzymatic/aqueous] and has receptors for

A

enzymatic
CCKA receptors, muscarinic

55
Q

In regulating enzymatic section of pancreatic secretions, there is a _____ stimulus from amino acids, peptides, and fatty acids

A

CCK

56
Q

What potentiates an action of CCK for acinar cells in the pancreas?

A

Ach

57
Q

Ductal cells in the pancreas is [enzymatic/aqueous] and has receptors for

A

aqueous
CCK, Ach, secretin

58
Q

How is secretin important with ductal cells and regulating aqueous pancreatic secretions?

A

stimulate aqueous HCO3- from pancreas

59
Q

The actions of secretin is potentiated by _____ and _____

A

CCK
Ach

60
Q

Bile secretion is needed for

A

digestion and absorption of lipids

61
Q

______ synthesize components of bile, flow out of bile ducts into gallbladder

A

hepatocytes

62
Q

CCK in the gallbladder does what?

A

stimulates contraction of gallbladder
relaxes sphincter of Oddi

63
Q

The liver conjugates bile acids with aa to form bile salts. Which amino acids primarily?

A

glycine
taurine

64
Q

What is bilirubin?

A

product of hemoglobin degradation

65
Q

The epithelial cells of the gallbladder do what?

A

absorb ions and water

66
Q

Bile is ejected ______ after a meal is ingested. It is ejected [continuously/in spurts]

A

30 minutes
in spurts

67
Q

Most bile salts return to the liver via _______ circulation

A

enterohepatic

68
Q

Bile salts are transported from the small intestine lumen into portal blood by ________

A

Na+/bile salt co-transporters

69
Q

Do bile salts get absorbed?

A

not normally