GI physio
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- 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
-bicarbonate
-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
- H+
-
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
- stercobilin
- where does urobilinogen come from
- conversion of bile in colon
- risk stomach cancer
- nitrosamines, achlorhydia, chronic gastritis
- erythema nodosum charact of?
- Crohns
- 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)
- GIP
- 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
- gastrin
- 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
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acinar cells=small vol Na, Cl
ductal cells=sxn HCO3, absorb Cl (isotonic) - second mssgr for secretin
- cAMP
- second mssgr for CCK
- IP3
- 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)