Physiology: Shelf Review #6 - Gi

Front 1

how's the nervous system of the GI tract divided?

Back 1

meisner's (submucosal) and myenteric plexuses.

Front 2

effects of parasympathetic and sympathetics on the GI tract? where do they synapse?

Back 2

parasympathetics are generally extitatory, sympathetics are generally inhibitory.

parasympathetics come from the vagus and pelvic nerves. preganglionics synapse on the myenteric/meisner's plexuses.

note that sympathetic postganglionics synapse on the plexuses too.

Front 3

so that's the extrinsic nerves - what's intrinsic?

Back 3

the enteric plexus is inherent. uses local reflexes. controlls most functions.

Front 4

what are our official gastric hormones?

Back 4

CCK, Gastrin, secretin, and GIP (gastric inhibitory peptide).

Front 5

what makes gastrin appear and what is its effect?

Back 5

secreted in response to a meal, ups H+ secretion by parietal cells.

Front 6

what cells make gastrin? in response to what?

Back 6

g cells of the stomach. responds to small peptides and distension. also, GRP (gastrin releasing protein)

H+ feeds back on it to shut it down.

Front 7

Where does CCK come from? What does it do?

Back 7

CCK comes from I cells in the duodenum. Responds to small peptides and fatty acids/monoglycerides.

makes the galbladder contract and stimulates pancreatic ENZYME secretion.

INHIBITS GASTRIC EMPTYING - this is good 'cause fatty meals take longer to digest.

Front 8

secretin?

Back 8

from S-cells in the duodenum. Fatty acids and H+ cause it to be released.

It's main effect is on the pancrease to release its HCO3- fluids

Also makes HCO3- secretion come from the galbladder. Also encourages blie aid production.

ALSO - stops acid secretion from parietal cells in the stomach.

Front 9

GIP? Oral vs. IV?

Back 9

GIP released in response to oral glucose and causes insulin secretion.

this is why oral glucose works better than IV to get insulin produced.

also stops H+ secretion from parietal cells.

unique because it's the only one that responds to PROTEINS, FAT, and CARBS (oral glucose specifically).

Front 10

what are our intestinal paracrines?

Back 10

somatosatin (STOP EVERYTHING)

histamine (increase H+ secretion).

Front 11

so acid secretion - what things turn it up, which turn it down

Back 11

up by distension, gastrin, gastrin releasing peptide, histamine.

down by somatostatin, secretin, and GIP (GIP's other function is to directly stimulate insulin release)
also off by VIP

Front 12

what are our neurocrines?

Back 12

VIP - causes relaxation of stuff including lower esophageal sphincter, also stimulates HCO3- secretion by the pancreas

GRP

Enkephalins - contract GI smooth muscle and stop fluid secretion. this is why opiates are great at stopping pooping.

Front 13

what's the pacemaker of GI smooth muscle?

Back 13

cells of cajal. make slow waves.

note that they don't produce action potentials, simply regulate them.

Front 14

talk about slow waves:

Back 14

waves of depolarization that aren't under anyone's control

note that the action potentials on top of these waves ARE under hormonal control.

slowest in stomach, highest in duodenum.

Front 15

how does the lower esophogeal sphincter open?

Back 15

by VIP. this is receptive relaxation.

Front 16

even during fasting, what happens in the stomach and when?

Back 16

migrating myoelectric complex comes by and gets rid of old food.

Front 17

what's the gastroilial reflex?

Back 17

food in the stomach causes the iliocolic sphincter to open.

Front 18

what's hirschprung's disease?

Back 18

megacolon

absence of the enteric nervous system. colon fills up pretty fast.

Front 19

what's in saliva that's interesting? how does it change?

Back 19

amylase and lingual lipase.

also, it's hypotonic.

also, lots of K+ and HCO3-.

flow rate changes it - when it flows slowly, it's MOST HYPOTONIC.

when it goes fast, don't have time to pump stuff out of it so it's more hypertonic.

the acinar cells make something identical to plasma.

then the ducts remove Na and Cl, and secrete K+ and HCO3-.

Front 20

what's unique about saliva's regulation?

Back 20

para and sympa both up it.

Front 21

in addition to H+, what's the other important thing released from parietal cells?

where does pepsinogen come from?

Back 21

intrinsic factor for binding b12

chief cells make pepsinogen.

Front 22

what's alkaline tide?

Back 22

H+ in parietal cells is made from Co2 and H20 with carbonic anhydrase. K+ pumped in, H+ and Cl- pumped out.

this leaves bicarb, which goes out the BL side in exchange for Cl- and moves up to the brush border.

Front 23

what will a vagotomy do to the stomach?

Back 23

stops Ach which makes H+ get released.

also stops the indirect method, which is GRP.

should still have h2 receptors to respond to histamine. also, gastrin should still work.

Front 24

what things inhibit H+ secretion from parietal cells?

Back 24

high H+ stops gastrin.

in the duodenum, high H+ turns on GIP and secretin. both of these stop it.

Front 25

what are some drugs that help stop acid secretion?

Back 25

omeprazol (proton pump inhibitors)

cimetadine (block H2 receptors)

Front 26

what's interesting about pancreatic secretions? flow rate?

Back 26

LOTS of hco3-

equal to plasma in sodium and potassium.

isotonic.

pancreatic lipases, amylases, and proteases.

higher flow rate = MORE BICARB.


works because HCO3- is secreted in exchange for Cl- : that's why their concentrations are opposite.

Front 27

difference between CCK and secretin on the pacnreas?

Back 27

secretin is more about HCO3- secretion.

CCK is more about enzymatic secretion. these are amylases, proteases, and lipases.

Front 28

what does CF do?

Back 28

stops enzymatic secretion from the pancreas.

Front 29

go through bile acid making

Back 29

primary acids (cholic and chenodeoxycholic) made from cholesterol.

in the intestine, bacteria make it secondary bile acids (deoxy/litho)

get attached to glycine or taurine to make BILE SALTS.

stored AND CONCENTRATED in galbladder (galbladder removes H20).

Front 30

how do bile salts get back?

Back 30

terminal ileum has an Na+/Bile salt COTRANSPORTER, which is secondarily active.
end up in the portal circulation, destined for the liver.

Front 31

what kinds of carbs are absorbed?

Back 31

only monosaccharides:

glucose, galactose, fructose.

alpha amylases break up the alpha 1,4 linkages. making maltose, maltotriose, and alpha limit desxtrins.

Front 32

how do glucose galactose and fructose get into hte cells?

Back 32

glucose and galactose use Na+ dependent SGLT1 transporter. Sugar uphill, Na+ downhil.

Fructose - uses facilitated difussion, so IT CAN'T BE TAKEN IN AGAINST A CONCENTRATION GRADIENT.

Front 33

what about proteins? how are they digested?

Back 33

pepsinogen helps.
pancreatic enzymes important: trypsin, chymotrypsin, elastase, carboxypeptidases.

note that trypsin is activated by enterokinase, and can then go on to activate the rest.

proteins can be as peptides, dipeptides, or tripeptides when absorbed.

Front 34

contrast peptides with di/tri peptides:

Back 34

Na+ dependent amino acid cotransport gets free AA's into cells.

dipeptides/tripeptides are ABSORBED FASTER. might require H+?

Front 35

fats?

Back 35

bile salts emulsify.

pancreatic lipases digest it. then formed into micelles.

FA's, monoglycerides, and cholesterol go across into cells. note that glycerols is hydrophillic and doesn't stay in micelles.

in the cells, everything's re-esterified, put into chilomicrons, put into the lymph, thoracic duct, into blood.

NOTE - need APOPROTEIN B to make CHILOMICRONS.