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91 Cards in this Set

  • Front
  • Back
regulation gastrin
incr by stomach distention, aa, peptides, vagal stim
decr by H+ and stomache acid pH<1.5
regulation CCK
decr by secretin and stomach pH<1.5
incr by fa,aa
regulation SS
incr by acid
inhib by vagus
function of gastric inhib peptide
exocrine-decr gastric H secretion
endo-incr insulin rel
where secretin made
duo S cells
CCK made
duo, jej I cells
SS made
pancreas and GI mucosa, D cells
GIP made
duo and jej K cells
action gastrin
incr gastric H+ sxn, incr gastric mucosa
action CCK
incr pan enz and HCO3 sxn,
stim gb cxn/sphincter of Odi relax
inhib gastric emptying
(also growth exo pancreas)
potent stim of gastrin
phenylalanine and tryptophan
secretin action
incr pan, biliary HCO3 sxn
inhib gastric acid sxn
SS action
-inhib gastric acid and pepsinogen sxn
-inhib pan and SI fluid sxn
-gb cxn
-rel insulin AND glucagon
elements salivary sxns
-alpha amylase
-mucins (glycoproteins)
source and action gastric acid
parietal cells of stomach, decr pH
regulation gastric acid
incr by His, Ach
decr by S, SS, GIP, PG
source, optimal pH of pepsin
chief cells of stomach, optimal pH 1-3
regulation, source HCO3
mucosal cells of stomach and duo, stim by secretin
how pepsinogen activated
summary CCK:
trigger, cause
trigger-aa,fa enter duo
cause-cxn gb, relax sphincter of Odi, pan sxn, inhib gastric emptying
parasymp effect on GI
-increase sxns (saliva, gastric, pan, HCO3)
-relax sphincter
-enteric NS causing peristalsis
source, action VIP
source-sm m and n of intestines
action-relaxes intestinal sm m, pan HCO3 sxn, inhib gastric H+sxn
symp effect on GI
incr saliva
decr splanchnic BF
decr motility
constricts sphincters
modulation of gastric acid sxn (receptors)
H2, M3, gastrin R, PG R (PGI2 and E2)
carb digesting in mouth?yields?
alpha amylase hydro 1,4 links
maltose, maltotriose, alpha-limited dextrans
panc amylase digestion? yields?
hydrolyses starch in duo to oligosacc, maltose, maltotriose
rate limiting step carb digestion
oligosacc hydrolases at brush border
rxn at brush border
oligosacc hydrolases produce monosacc (glu, galactose, fructose) which can be absorbed
where does trypsin come from
secreted from pancreas as trypsinogen, activated by enterokinase (duo brush border enz)
name proteases? where from?
trypsin, chymotrypsin, elastase carboxypepidases sxn from pan as pro-enzymes.
trypsinogen cleaved by enterokinase, trypsin goes and cleaves everyone else
note: pepsinogen activated by H+ (pepsin principle enz gastric sxns)
name enz in fat digestion
lipase, phospholipase A, colipase
where heme catabolized
RE system
what do kidneys excrete of bili
urobilirubin (4mg/d)
what of bili is excreted in feces
where does urobilinogen come from
conversion of bile in colon
risk stomach cancer
nitrosamines, achlorhydia, chronic gastritis
erythema nodosum charact of?
Crohn's abd pain ER, besides GI what could it be?
cholesterol gallstones
how does His change gastrin's effect
potentiates, Ach, His and gastrin all potentiate ea other's effect on H+ sxn. Same with pancreatic stimulators
T/F: atropine completely blocks H+ sxn
F, H+ sxn still would occur 2/2 GRP NT of indirect path
name parasymp innerv of various parts GI
vagus thru upper LI, then pelvic n plexus for lower LI, rectum, anus
describe synapse of symp on intestine
starts at spinal cord T8-L2, these preganglionic synapse on prevertebral gangion that then synapse on ENS
ENS is composed of
myenteric and submuccosal ganglions
myenteric is AKA? fxn?
Auerbachs, fxn: motility
submucosal plexus AKA? fxn?
Meissner's, fxn: sxn, BF
where is myenteric plexus? where located compared to submucosal?
myenteric=bw circular and longit mscl
submucosal=closer to lumen, bw circular mucosa and muscularis mucosa
what hormone is rel in response to all three types energy (carb, fat, protein)
gastrin stim by parasymp is done by what? NT?
vagus, NT=GRP
what do tgs stimulate
no hormone, they don't cross intestinal cell mem so can't stim CCK
what hormone is like CCK in structure? how so?
gastrin and CCK both have the same 5 terminal C aa and the activity of the hormone lies in the C-terminal heptapeptide
GIP is like what hormone in structure? how so?
homologous to glucagon and secretin
aa are stim for?
gastrin, GIP, CCK
fa stim for?
CCK, Secretin, GIP
what does gastric distention stim
effect of atropine on gastrin sxn
does not block vagal mediated gastrin sxn bc that uses GRP as NT
what three hormones mainly work on pancreas/biliary
CCK, secretin, SS
acid stimulates which hormone
secretin and SS
fxn of enkephalins in GI? relation to diphenoxylate?
stimulate cxn GI, esp sphincters, inhibits intestinal sxn fluid and electrolytes. that's why you can use diphenoxylate (opoiod) for diarrhea
officially considered Paracrine in action
SS and His
officially considered GI neurocrine
VIP,GRP, enkephalins
what type cxns find where (phasic v tonic)?
phasic-esophagus, antrum, SI
tonic-LES, orad stomach, iliocecal and internal anal sphincter
how are slow waves created? how differ throughout GI? how GI cxns?
how do neurons and H act in this system?
slow waves by interstitial cells of Cajal, slow waves are characteristic for each part GI
cxns come from AP on top of slow waves which are modulated by neurons and hormones
LES relax by..
vagal stimulation with VIP as NT
what creates receptive relaxation
vagovagal reflex and CCK
describe motility of stomach, NT
every 90 min a cxn clears of food, mediator is motilin
how gastric emptying controlled
inhibited by fat via CCK and acid entering duo (direct neural reflex)
describe SI motility
consist of sergmentation and peristaltic cxns
describe motility LI
massive movements 1-3/d
describe saliva composition, enzyme contents, and how changes with flow
hi K, HCO3, hypotonic
contains: alpha amylase, lingual lipase, kallikrein
at low flow low osmo and hi K
describe saliva production process
acini produce initial saliva, similar to plasma (isotonic)
then ducts reabsorb Na and Cl and secrete K and HCO3
ducts are impermeable to water and so creates saliva that is hypotonic
effects aldosterone GI
saliva ductal cells (increase Na reabsorp, increase K sxn), controls colon absorption of Na (occurs passively)
describe specifics parasymp saliva neural stimulation--including receptor and 2nd mssgr
parasymp CN7,9 use M3 R-->Gq-->IP3-->increase Ca
alkaline tide
as gastric parietal cell secretes H+ it does so with Cl and the creation of H+ also creates HCO3, it must take in this Cl and secrete HCO3.
Cl is aborbed via HCO3/Cl-
where does HCO3 from parietal cells go
(ie alkaline tide) secreted in pancreatic sxns
describe composition of pan sxns and how vary w flow rate
hi HCO3 and low Cl, isotonic
low flow=Cl
hi flow=HCO3
describe process of producing pan sxns
acinar cells=small vol Na, Cl
ductal cells=sxn HCO3, absorb Cl (isotonic)
second mssgr for secretin
second mssgr for CCK
describe primary, secondary bile acids
primary (in hepatocytes)=cholic acid and chenodeoxycholic
2 (bac in intestine)=deoxycholic acid, lithocholic acid
how form bile salts
take secondary bile acid, conjugate with taurine or glycine
what transporter used to absorb bile
Na-bile acid co transporter in terminal ileum
what are the 3 oligosaccharidases
maltase, alpha dextrinase, sucrase
sucrase is broken down into
glucose and fructose
how is glu taken up by intestine? transporter?
Na dependent co transport (SGLT1) (while Na/K at basolateral mem keeps pumping Na out)
how is fructose absorbed
facilitated diffusion (can't go ag concentration gradient)
T/F Trypsinogen not converted by trypsin
F trypsin CAN convert trypsinogen to trypsin (also enterokinase)
what forms of aa can be absorbed
aa, dipeptides, tripeptides
how free aa absorbed
Na depend aa cotransport, there are 4 (neutral, acidic, basic, imino)
how dipeptides and tripeptides absorbed
H depend cotransport
describe K in GI absorption/sxn
absorbed in SI by passive diffusion, paracellularly, actively secreted in colon
describe Na balance in GI absorption/sxn
most important is SI
Na-glu cotransport
Na-aa cotransport
Na-H exchange
then colon passively absorbed (controlled by aldosterone)