Pancreatic, Salivary and Gastric Secretions Flashcards by LJPN Unknown

Functions of saliva

Lubricate food
Form protective buffer
Initiates starch digestion

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Function of pancreatic juice

Neutralises stomach acids (as is alkaline)

Completes digestion

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Outline the structure or a salivary/pancreatic gland (passage of secretions)

Lobules are one secretory unit, comprised of an acinus (group of secretory cells) lining an intercalated duct
Intercalated ducts drain into intralobular duct
Intralobular ducts drain into interlobular/extralobular ducts
These drain into salivary/pancreatic duct

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Three types of salivary gland, their contents and contribution to total?

Parotid - serous secretion (amylase containing), 25%

Submandibular - serous (amylase containing) and mucous (mucin containing), 70%

Sublingual - mucous secretion (mucin containing), 5%

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Functions of serous salivary component?

Lubrication (speech) and moistening (enzymes)
Germicidal
Protects teeth

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Functions of mucous salivary component?

Lubrication
Diffusion barrier to nutrients, drugs, toxins
Traps microbes
Protects against proteases

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How is saliva secreted?

Primary secretion
— basolateral NKCC accumulates Cl- in acinar cell, so Cl- diffuses across apical
—basolateral Na/K pumps Na out to power above transporter, high interstitial Na and negative charge of Cl- in lumen sets up paracellular diffusion gradient for Na into lumen through tight junctions
— Water follows
— Primary secretion therefore isotonic saline (like plasma)

Secondary Modification
— Ductal cells modify primary secretion
— Na reabsorbed through eNaC and Na/H exchanger powered by basolateral Na/K
— Cl reabsorbed through Cl/HCO3 exchanger exiting through Cl channel
— HCO3 consequently secreted
— K lost through apical K/H exchanger powered by Na/K
— water content not modified as ductal cells have low permeability
— more ions exit than enter though, so final saliva is hypotonic

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What regulates salivary secretions?

ANS

Para = ACh (M3–> IP3–>Ca->protein kinases—> increase apical cl permeability and basolateral k permeability/cytoskeletal elements export protein containing vesicles increases primary secretion, decreases secondary secretion
— large volumes of watery saliva

Sym (less pronounced) = NA (A—>phospholipase C same mech as above) or (B—>raises cAMP and PKA—> amylase secretion producing viscous saliva

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Acinar cell secretion mechanism?

Same as salivary primary secretion, except chloride channel is CFTR

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Ductal cell mechanism of secretion?

Same as secondary modification in salivary glands

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What enzymes are present in pancreatic secretions?

Proteases, amylases, lipases, nucleases

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How is autodigestion prevented?

Packaging as zymogens (inactive enzymes activated in SI)

Protease inhibitors in secretory vesicles

Nondigestive proteases to degrade prematurely activated enzymes

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Which digestive phases regulate pancreatic secretion, by what mechanism?

Cephalic phase — ACh (vagal nerve)
Gastric phase — ACh and gastrin (G cells, stimulated by vagus)
Intestinal phase — ACh, secretin (S cells) and CCK (I cells)

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Which pancreatic cells do ACh, CCK, gastrin and secretin act on?

ACh - ductal and acinar
CCK - ductal and acinar
Gastrin - ductal
Secretin - ductal

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Mechanism by which ACh induces secretion?

M3 is Gq coupled, IP3 induces Ca2+ release
Ca2+ and DAG activate PKC, PKC activates apical chloride channels and basolateral potassium channels, increasing chloride secretion

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Mechanism of action of secretin?

Gs coupled, PKA activating channels

How many litres of GI secretions per day?

What are the components of gastric secretion, and functions?

H+ = acidify contents of stomach
Pepsinogen = precursor to pepsin, digests proteins
Mucus and HCO3- = protective layer to prevent digestion of stomach
Intrinsic factor = used in SI to promote VitB12 absorption

Which cells secrete gastric acid and intrinsic factor?

Oxyntic glands

What endocrine factors released where in stomach by endocrine cells?

Gastrin = stims
Somatostatin = inhibits
Histamine = paracrine, stims

Pyloric antrum

Which cells secrete pepsinogen?

Chief cells

Which cells secrete mucous?

Mucous cells

What do superficial epithelial cells secrete in stomach?

Mucus and HCO3-

When unstimulated, what kind of solution does the stomach secrete? From which cells?

Isotonic solution - from superficial epithelial cells

When stimulated, how does the ionic content of the gastric secretion change and why?

Parietal cells begin secreting gastric acid, Na+ content goes down and H+ and Cl- content goes up

What happens between unstimulated to stimulated parietal, oxyntic cell?

When unstimulated, lots of tubulovesicles in the subapical cytoplasm containing H/K ATPase - the apical cytoplasm is deeply invaginated When stimulated, these tubulovesicles fuse with the apical membrane, forming canaliculi to increase surface area for secretion

Mechanism of action for producing gastric acid when parietal cell is stimulated

Carbonic anhydrase catalyses hydration of CO2 —> HCO3- and H+ H+ moves out into lumen via H/K ATPase exchanger (K recycled through apical channels) HCO3- moves out of basolateral membrane into interstitial fluid through Cl-/HCO3- exchanger Cl- moves through apical into lumen to form HCl Water follows

What prevents H/K tubulovesicles from acidifying parietal cells?W

Tubulovesicles have low potassium permeability, so H/K exchanger doesn’t work until it fuses with the apical membrane

What happens to blood during and just after meal?

Alkalinisation due to HCO3- being moved into blood from parietal cells

Which drug can inhibit the H/K ATPase?

Omeprazole

What three mechanisms trigger the cytoskeletal arrangement induced by protein kinase activation that mediates the insertion of tubulovesicles in parietal cells? (Basically, what causes gastric acid secretion?)

Neurocrine — ACh from vagus (M3-Gq coupled-IP3-Ca-PKC) Endocrine — Gastrin from G cells (CCKb receptor-Gq coupled-IP3-Ca-PKC) Paracrine — Histamine from Enterochromaffin-like cells (H2-Gs coupled-PKA)

What does ranitidine do? Why is it SO effective if there are two other mechanisms stimulating gastric acid release?

Antagonises H2 receptors Because ACh and Gastrin also cause histamine release and it is thought that the common mediator of gastric secretion is actually histamine, even-though neurocrine and endocrine pathways have a part to play

Explain Helicobacter pylori association with peptic ulceration

H.pylori inhibits somatostatin release Somatostatin is released from D cells and acts on a Gi coupled receptor inhibiting PKA It therefore reduces gastric acid secretion, so inhibiting somatostatin would lead to uncontrolled gastric acid secretion

What stimulates neurocrine stimulation of gastric secretion?

Thought, sight, smell, taste of food | Distension of stomach

What stimulates endocrine stimulation of gastric secretion?

Protein digestion products stimulate gastric and duodenal G cells

What stimulates pepsin release from which cells?

Chief cells and fusion of pepsinogen containing secretory granules ACh (M3 receptor), gastrin, CCK —> Gq Secretin —> Gs

What stimulates mucous secretion from mucous cells?

ACh via M3 Gq coupled receptor