Physiology: Gi #4: Salivary Glands

Front 1

what are our major salivary glands and what do they produce?

Back 1

The parotid gland - largest, makes serous fluid.

The submandibular and sublingual glands both make a mixture of serous and mucous fluid.

Front 2

stimulation of saliva release - how is this different than the rest of the GI system?

Back 2

under only NEURAL control - no hormone effect on the salivary glands.

also, here both parasympathetics and sympathetics cause secretion. in the rest of the GI, para is generally stimulatory while sympa is generally inhibitory.

Front 3

speaking of para and sympa, how does each affect the release of saliva and to what effect? what secondary messagers

Back 3

sympathetic secretions are transient (less constant) and protein-rich (think of sticky mouth when scared).

parasympathetic response is more sustained and produces a higher amount of fluid.

sympathetics operate via norepinephrine and cAMP increase.

Parasympathetics operate via Ca++ increase.

Front 4

what's that other random substance that can make saliva secretion happen?

Back 4

substance p - works like parasympathetics (through Ca++)

Front 5

what are some major components of saliva, and what are they good for?

Back 5

water/mucous, amylase and lipase (for starch and fat digestion), HCO3- (acid balance),

lactoferrin and muramidase (antibacterial by binding iron and breaking cell walls, respectively)

EGF makes new cells grow.

Protein R binds B12 and is important for later binding to b12 receptor.

Front 6

osmolarity of plasma vs. saliva: how is it different?

how does increasing the rate of flow change this?

Back 6

saliva is HYPOOSMOTIC - though it containes MORE K+ and more HCO3-.

It contains less chlorine and less sodium (NaCl).

faster saliva flow (as in eating) prevents the saliva from having time to change and become hypoosmotic - meaning that it's LESS hypoosmotic (closer to regular plasma).

Front 7

which cells in the salivary glands produce primary and secondary saliva?

Back 7

primary saliva (similar to that found in plasma) is made by the acinar cells.

the duct cells (striated and excretory) modify it into secondary saliva

Front 8

acinar cells: what channels do they have? how does para/sympa change things?

Back 8

the BL side, as always, has the Na/K transporter. Also, it has the Na/K/2Cl co-transporter, bringing all 3 ions into the cell from the plasma.

also, it has a Na+/H+ antiporter (i assume this makes bicarb?)

on the apical side, there are channels: a K+ channel, and a dual anion (Cl- and HCO3-) transporter.

Na+ gets to the apical side paracellularly, driven by the electrical - made by the anions leaving into the lumnen.

Raising Ca++ concentration (parasympathetics) tends to dramatically up the bicarb leaving: this is because Ca++ turns on the K+ channels, more K+ leaves and creates a more electronegative environment in the lumen pulling HCo3- and Cl- through its shared channel.

I guess this also happens with upped cAMP (sympathetics), but not totally sure.

Front 9

duct cells: what are they called and what are they doing to make secondary saliva?

Back 9

striated/excretory ducts:

the BL side has our typical Na/K exchanger.

Also, it's still making bicarb, so it's got an H+ out, Na+ in antiporter.


Apical side:
It's got an eNaC channel letting Na+ in.

It needs to get bicarb out, so remember that it's got a Cl- in and HCo3- out antiporter

K+ has to be high in the lumen: does this with an H+ in the cell/K+ out of the cell antiporter.

this helps run the Na/H+ exchanger (Na in to the lumen, K+ out).

Front 10

neural salivary control - what brain regions control it and what CN's are efferents?

Back 10

the superior and inferior salivary nuclei.

7th nerve from the superior, goes to the submandibular and sublingual.

9th nerve goes from inferior to the otic to the parotid.

Front 11

b12: what's the story?

Back 11

originally, b12 is bound to food proteins: the low acidity and churning of the stomach releases it. it's now free to bind "binding proteins" (of which protein R is probably one).

at low pH, these binding proteins have a high affinity for b12 (higher than its affinity for INTRINSIC FACTOR, made by the parietal cells).

once you get into the duodenum, pancreatic juice degrade the binding protein (r), and allows intrinsic factor to bind.

Illial enterocytes have binding regions for B12/IF - these uptakethe b12.

Front 12

so, what diseases can lead to b12 deficiency?

Back 12

pernicious anemia can be caused by:

failure of your parietal cells to release intrinsic factor (as in atrophic gastritis)

failure to cleave the binding proteins off (not enough pancreatic juice, as in pancreatic exocrine insufficency)

failure to absorb the IF-B12 complex (ilial disease, resection)

Front 13

what's up with iron absorption? what % of what we eat gets absorbed?

Back 13

only 10% of what we eat ends up getting absorbed: the rest ends up in poop.

two transporters: transferrotin and ferritin.

Transferrotin binds and keeps iron and acts as an intracellular pool, making Fe available when we need it.

Ferritin binds up Fe and is then lost when the cells sough off: this prevents over-dosing on iron.