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Medicine > Pancreatic, Salivary and Gastric Secretions > Flashcards

Pancreatic, Salivary and Gastric Secretions Flashcards

1
Q

Functions of saliva

A

Lubricate food
Form protective buffer
Initiates starch digestion

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2
Q

Function of pancreatic juice

A

Neutralises stomach acids (as is alkaline)

Completes digestion

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3
Q

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

A

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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4
Q

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

A

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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5
Q

Functions of serous salivary component?

A

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

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6
Q

Functions of mucous salivary component?

A

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

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7
Q

How is saliva secreted?

A

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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8
Q

What regulates salivary secretions?

A

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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9
Q

Acinar cell secretion mechanism?

A

Same as salivary primary secretion, except chloride channel is CFTR

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10
Q

Ductal cell mechanism of secretion?

A

Same as secondary modification in salivary glands

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11
Q

What enzymes are present in pancreatic secretions?

A

Proteases, amylases, lipases, nucleases

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12
Q

How is autodigestion prevented?

A

Packaging as zymogens (inactive enzymes activated in SI)

Protease inhibitors in secretory vesicles

Nondigestive proteases to degrade prematurely activated enzymes

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13
Q

Which digestive phases regulate pancreatic secretion, by what mechanism?

A

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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14
Q

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

A

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

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15
Q

Mechanism by which ACh induces secretion?

A

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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16
Q

Mechanism of action of secretin?

A

Gs coupled, PKA activating channels

17
Q

How many litres of GI secretions per day?

A

7

18
Q

What are the components of gastric secretion, and functions?

A

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

19
Q

Which cells secrete gastric acid and intrinsic factor?

A

Oxyntic glands

20
Q

What endocrine factors released where in stomach by endocrine cells?

A 
Gastrin = stims
Somatostatin = inhibits
Histamine = paracrine, stims

Pyloric antrum

21
Q

Which cells secrete pepsinogen?

A

Chief cells

22
Q

Which cells secrete mucous?

A

Mucous cells

23
Q

What do superficial epithelial cells secrete in stomach?

A

Mucus and HCO3-

24
Q

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

A

Isotonic solution - from superficial epithelial cells

25
Q

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

A

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

26
Q

What happens between unstimulated to stimulated parietal, oxyntic cell?

A

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

27
Q

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

A

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

28
Q

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

A

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

29
Q

What happens to blood during and just after meal?

A

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

30
Q

Which drug can inhibit the H/K ATPase?

A

Omeprazole

31
Q

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?)

A

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)

32
Q

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

A

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

33
Q

Explain Helicobacter pylori association with peptic ulceration

A

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

34
Q

What stimulates neurocrine stimulation of gastric secretion?

A

Thought, sight, smell, taste of food

Distension of stomach

35
Q

What stimulates endocrine stimulation of gastric secretion?

A

Protein digestion products stimulate gastric and duodenal G cells

36
Q

What stimulates pepsin release from which cells?

A

Chief cells and fusion of pepsinogen containing secretory granules

ACh (M3 receptor), gastrin, CCK —> Gq
Secretin —> Gs

37
Q

What stimulates mucous secretion from mucous cells?

A

ACh via M3 Gq coupled receptor

Medicine (62 decks)

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