130-131. Secretions of Salivary, Stomach, Exocrine Pancreas Flashcards

1
Q

What is the Enteric Nervous System? What are the functions of its two plexuses?

What are the functions of the parts of ANS?

What are the 3 modes of GI communication?

A

ENS: sensory n, interneurons, motor neurons in GI tract (modulated by brainstem), can do patterned motor activity
Myenteric (Auerbach’s) Plexus: b/w smooth muscle layers (longitudinal, circular), peristalsis/GI motility
Submucosal (Meissner’s) Plexus: submucosal, gland secretion, MM innervation

ANS: parasymp = Excitatory (absorption, secretion, motility); symp = inhibitory (acts on blood vessels - 3 ganglion - celiac g, SMG, IMG)

GI comms:

  1. Endocrine (hormone from cell to blood for effects at great distance)
  2. Paracrine/Autocrine (diffuses to immediate vicinity
  3. Neurocrine (nerve innervates specific tissue with synapse)
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2
Q

What are the 4 phases of GI activity

A
  1. Cephalic: head, sight/smell/sound/thought food
  2. Gastric: food in stomach
  3. Intestinal: food in intestine
  4. Interdigestive: in b/w meals, stomach/small intestine are empty
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3
Q

What are the 3 main salivary glands, what kind of fluid does each one secrete, and how are they innervated?

A
  1. Parotid Gland: serous fluid
  2. Submandibular: serous + mucous secreting
  3. Sublingual: serous + mucous secretine

Innervation: Exclusively ANS (cholinergic inputs)
Parasymp = high volume secretion of saliva, VD (CN7, CN9 synapse to CN5)
Symp = low volume secretion of saliva, independent VC (T1 spinal nerves - superior cervical ganglion - follow blood supply to glands)

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4
Q

What are the three key components of salivary glands?

A
  1. Acinus: produce ultrafiltrate like fluid
  2. Intercalated Duct: for saliva transport
  3. Striated Duct: modify secretion compositions
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5
Q

What is the molecular basis of salivary acini function?
What is composed of in saliva from acini secretions?
What is the effect of ANS stim?

A

mLc: Driver = Na/K ATPase basolateral (Na out)
Effect = basolateral H/Na exchanger and NKCC cotransport
H/Na exchange: high H efflux = bicarb buildup in cell = bicarb SECRETED apical channel
NKCC: high K and Cl secretions through apical channels

Saliva: high bicarb, Cl, K (not considered plasma ultrafiltrate because requires ATP)
alpha amylase: secreted from vesicles, digests starch - breaks interior alpha 1,4 bonds (not essential, inactivated by stomach acid)

Cells: contractile myoepithelial cells: ANS activation to squeeze fluid into duct

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6
Q

What is the molecular basis of salivary striated duct secretions and function?
How does salivary composition change?
What is the effect of ANS Stim?

A

Ducts: modify secretion composition, tight junctions limit water movement

Driver = Na/K ATPase basolateral (drives Na removal from saliva, K secretion to saliva)
Effect = H/Na exchanger basolateral
(more bicarb in cell = bicarb secretion via bicarb/Cl exchanger apical)

Composition: More bicarb, less Cl in saliva; less Na, more K

ANS stim via m3AChR: high intracell Ca activates Cl/bicarb exchanger = increased bicarb secretion to saliva

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7
Q

How does salivary composition vary with fluid flow?

How does salivary tonicity compare to plasma?

A

Low Flow: more time for striated duct modification: MORE hypotonic (LESS Na/Cl/H2O, more K, more bicarb)

High Flow: less time to reduce Na from secretion: LESS hypotonic (more Na, less K, more Cl)

All salivary gland secretions are hypotonic with respect to plasma

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8
Q

List the cells and their functions within the stomach oxyntic glands. Where are oxyntic glands located?

A

Superficial epithelial cell = produce plasma-like fluid
Mucous neck cell
Stem/Regenerative Cell
Parietal Cell: Acid secreting
Chief Cell: secretes pepsinogen
ECF cell: secretes histamine (paracrine signal)
D cell: somatostatin secreting

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9
Q

Describe the molecular mechanics of parietal cells. What is the function of the acid they secrete?

A

Proton pumps in tubulovesicles = when stimulated, fuse together to increase surface area of proton pumps = increase gastric acid secretion
Proton pump: H/K ATPase (K in, H out)
key: H2O hydrolyzed to H+/-OH in cell: H+ pumped out, OH- moved to interstitium as bicarb (via CA)
Cl- secretted via passive channel

Acid fx: anti-microbial (protection), activates pepsin from pepsinogen, good pH for pepsin function, denatures peptides (easier for pepsin to work)

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10
Q

How is acid secretion regulated?

  • direct path
  • indirect path
  • pathways in parietal cell
  • inhibitory control
A

Direct: ACh, Gastrin, Histamine stim parietal cell
Indirect: ACh, Gastrin stim ECF cell = histamine release = stim parietal cell

Parietal Cell: ACh/Gastrin act thru Adenylyl cyclase and increase cAMP; Histamine increases intracell Ca (both act synergistically to increase H+)

SST: from D Cells, inhibits ECL cells (lower histamine) and inhibits parietal cells (lower H secretion)

Stretch = drives acid/pepsinogen secretion via vagal-vagal loops or local loops

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11
Q

What stimulates pepsinogen release?
How is pepsinogen activated?

How does gastric acid composition vary by flow rate?

A

stim pepsinogen release by ACh, Gastrin, Histamine
Activated to pepsin by low pH and pepsin (positive feedback)

High flow: secretion mainly from parietal cells (high H/Cl, low Na, low K)
Low flow: secretion mainly from surface epithelial cells (high Na/Cl, low H, Low K)

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12
Q

What is the function of the gastric mucosal barrier? What cells are protective?

What happens with damage to the mucosal barrier?

A

Fx: prevent stomach from digesting itself
Mucus gel: layer of insoluble mucus - traps alkaline fluid underneath (neutralizes escaped acid to protect from damage)
Surface mucus cells produce isotonic fluid with bicarb, and secrete bicarb to interstitial space to protect bloodstream

Damage: irritate bloodstream = mast cell activation = histamine release = increase acid secretion (bad positive feedback)

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13
Q

What are the cells in the pyloric region?

A

Not acid secreting, but stimulate parietal cells for acid secretion
G Cells: secrete gastrin
D Cells: secrete STT

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14
Q

How does the tonicity of exocrine pancreas secretions compare to blood?

How does pancreas composition vary as a function of flow?

A

ALL secretions are ISOTONIC (pancreatic acinar cells - enzymes; duct cells - high bicarb)

High flow: more bicarb secretion, low bicarb net secretion due to high bicarb stimuli

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15
Q

What is the molecular mechanism for secretions in pancreatic acini and duct cells?

A

Acini: vesicle enzyme secretion of alpha-amylase (carbs), lipase (fats), proteolytic enzymes (proteins) - stored inactivated in zymogen granules (activated by enzymes on epithelial brush border of cells in intestinal lumen)

Ducts: Driver = Na/K ATPase basolateral
Effect: basolateral Na/H exchanger (H out of cell, high bicarb, bicarb secreted via Cl/bicarb exchanger)
higher flow = more active Na/K ATPase = more active Cl/bicarb exchange

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16
Q

How are acini and duct secretions regulated?

A

Acini: ACh, CCK = increase Ca = increase enzyme secretion
Secretin/VIP = increase cAMP = increase enzyme secretion

Duct: Secretin, ACh, CCK = increase bicarb secretion

17
Q

How is digestion regulated in the cephalic, gastric, and intestinal phases?

A

Cephalic: Vagus n. (ACh) to Parietal Cell (Acid secretion), G Cell (Gastrin - parietal cell - more acid), pancreatic acini (more enzymes), pancreatic duct (more bicarb)

Gastric: stretch = G cell stim = high gastrin = parietal cell (increased acid), pancreatic duct (increased bicarb)

Intestinal:
Acid in duodenum = S Cells = Secretin = pancreatic duct bicarb secretion (neutralize acid)
Fat in duodenum = S cells (Secretin) and I cells (CCK to pancreatic duct and acini - secrete enzymes/bicarb to digest protein/fat)
Acid/Fat in duodenum trigger vagal-vagal loop = more ACh to pancreatic duct/acini
Peptides in duodenum = I cells = more CCK (pancreatic duct/acini secretions)

18
Q

How are pancreatic enzymes modified by long term diet?
Describe the acid cycle of stim.
What are the 4 functions of CCK?

A

Eat more carbs = more amylase produced in vesicles (sudden diet change = risk of malabsorption syndrome)
Stomach secretes acid to duodenum = secretin release by S cells = bicarb secretion to neutralize acid from pancreatic duct

  1. Gallbladder contraction (bile secretion)
  2. Pancreas acini secretion (enzymes)
  3. Block stomach emptying
  4. Relax sphincter of Oddi (for bile/pancreatic secretions)
    All help increase digestion of carbs, lipids, proteins