SGM Page 1 8/26/2014

GI Physiology Review
I. SPHINCTERS: Divides GI tract into functional segments; areas of ig intraluminal P to !revent reflu" of contents;
controlled #$ %&S' (one)*a$+ valves
Sphincter Muscle Type Function
,!!er
-so!ageal
Striated Se!arates mout/!ar$n" from eso!agus
.o*er
-so!ageal
Smoot Se!arates eso!agus from stomac
P$loric Smoot Se!arates stomac from duodenum
S!incter of
/ddi
Smoot Se!arates !ancreato#iliar$ ducts from
duodenum
Ileocecal Smoot Se!arates small instestine from large intestine
Internal 0nal Smoot %ontrol defecation
-"ternal 0nal Striated %ontrol defecation
II. NERES:
) S&S 1 P&S s$na!se on -&S !le"uses 2interneurons3 *ic integrate te commands 1 !uts tem into action
) &eural control of gut is 4I-505%4I%6 GI stimuli enteric &S !reverte#ral ganglia P&S 1 S&S iger
#rain centers
07 P&S 8 generall$ e"citator$ to secretion 1 motor function of te gut; e"trinsic innervation 2long refle"es3
!G"S nerve6 9 80: of vagal fi#ers are afferents 2transmit sensor$ info from gut3
PE#IC NERES
;7 S&S 8 celiac' su!erior' 1 inferior mesenteric; generall$ ave an ini#itor$ effect on secretor$ 1 motor function in
gut 2!aral$sis of motor function */ reduced s!lancnic #lood flo*3; u! to 9<0: of S&S fi#ers are afferents;
e"trinsic innervation 2long refle"es3
%7 -&=-5I% &-5>/,S S?S=-M6 (little #rain+ in gut to coordinate 1 !rogram GI function; em#edded in *all of
gut; long 1 sort refle"es 2loo!s3 tat res!ond to luminal stimuli
@@ -&S as #ot e"citator$ and ini#itor$ neurotransmitters tat can #e used to coordinate functions
M$ENTERIC %!"ER&!CH'S( P#E)"S6 control of M/=/5 activit$ in gut 2smoot muscle function3
S"&M"C*S!# %MEISSNER'S( P#E)"S6 M,%/S0. functions 2secretion 1 a#sor!tion; 1 regulates
local #lood flo*3
) >0G/>0G0. 5-A.-B6 moment to moment adCustments reDuired for o!timal digestive functions in u!!er GI tract
) Pain ini#its gastric em!t$ing
III. GI EN+*CRIN*#*G$
) 0P,D cells line GI' contain rece!tors tat are (sensitive+ to s!ecific luminal stimuli 2contents3
) Aamilies of !e!tides6 213 #ind to same rece!tor 1 223 same 2
nd
messenger
Hor,one *rigin Respon- to !ction
Gastrin
2gastrin famil$3
G cells in antrum Distension of stomac or !resence of
amino acids / !e!tides in antrum
E acid secretion
2effects similar to %%F3
Secretin
2Secretin famil$3
S cells in
duodenum
Dudodenal acidit$ E #icar#onate secretion
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%olec$stoGinin
2%%F8 Gastrin
famil$3
I cells in
duodenum
Aat 1 !rotein digestion !roducts in
duodenum
%ontracts gall #ladder
E enH$me secretion
2similar effects to gastrin3
Glucose de!endent
insulinotro!ic
!e!tide 2GIP3
Motilin M cells in lo*er
stomac 1
duodenum
E fasting contractions
>asoactive
intestinal
!ol$!e!tide 2>IP)
Secretin famil$3
E #icar# secretion
2similar to secretin3
&eurotensin 1
Pol$!e!tide ?
%ells in te
ileum
Presence of fat Slo* intestinal motilit$ 2I.-0.
;50F-3 I J gastric em!t$ing
I. G!STRIC !CI+ SECRETI*N
) Aundus 1 #od$6 !arietal cells 8 secrete acid
) 0ntrum6 G cells 2secrete gastrin3 1 D cells; #ut &/ acid secretion
!. Cell Types
.. P/riet/l Cells 2o"$ntic cells3 8 secrete acid; 4K 2im!ortant in Gilling micro#es' converts !e!sinogen to
!e!sin' etc3' %l)' IA 2a#sor!tion of vitamin ;123L
0. Peptic Cells 2cief cells3 8 !e!sinogen 2converted to !e!sin in te !resence of acid; !e!sin digests !rotein3
1. Mucous Cells 8 mucous' #icar#onateL2!rotects lining of stomac3
&. Mech/nis, o2 !ci- Secretion
) canges in ion concentration6 (meal)stimulated secretion+
) *en !arietal cells are stimulated' acid secretion increases' #ut non)!arietal secretion remains te same; causes te M&aKN
to decrease due to dilution
C. Mech/nis, o2 P/riet/l Cell Secretion
.. &aK / FK 0=Pase !um! on #asolateral mem#rane I J intracellular M&aKN 1 E MFKN
0. .uminal FK is e"canged for intracellular 4 using te energ$ de!endent 4 / F 0=Pase !um! at te luminal
mem#rane 2IMP/5=0&= =05G-= A/5 =4-50P?3
1. %ar#onic an$drase 4 is e"canged for F O luminal mem#rane
3. ;icar#onate moves out of cell O #asolateral mem#rane passively in e"cange for %l) 20.F0.I&- =ID-3
+. G/stric Mucos/l &/rrier
.. 0lGaline =ide I E #lood !4 locall$
0. Mucous coating on e!itelial cells I !rotective #arrier
1. =igt Cunctions
3. Mucosal #lood flo* Es during acid secretion
4. %ell turnover
5. -nteric nervous s$stem
E. Regul/tion o2 !ci- Secretion
) -ndogenous su#stances
) Stimulation of te !arietal cell6 2i3 central control mediated #$ te vagus troug te -&S release of &=s; 2ii3 !eri!eral
control includes te -&S 1 4 cell t$!es6
.. Parietal cells 2fundus36 contain rece!tors for 0%' gastrin' 1 istamine *ic all stimulate acid secretion
0. -nterocromaffin)liGe cells 2-%. cells in fundus 1 antrum36 interface #/* central and !eri!eral control of
acid secretion
1. D cells 2antrum 1 fundus36 secrete somatostatin 8 release stimulated #$ lo* intramural !4 2E acid3 and is
ini#ited #$ vagal stimulation 1 istamine; antral cell somatostatin acts in !aracrine fasion to I&4I;I=
gastrin release from G cells; fundic cell somatostatin acts to ini#it istamine release from -%. cells
F. Ph/ses in the Sti,ul/tion o2 !ci- Secretion %ph/ses overl/p(
.. Inter-igestive ph/se %2/sting(
0. Ceph/lic ph/se %prep/r/tory(6 mediated #$ vagus nerve; initiated #$ sigt' smell' taste' or tougt of food
1. G/stric ph/se6 initiated #$ arrival of food in stomac; mediated !rimaril$ #$ gastrin; >ago)vagal refle"es
2distension in stomac3 1 local refle"es
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3. Intestin/l ph/se6 initiated #$ arrival of food in duodenum; !rimaril$ ini#itor$ to acid secretion; secretin'
%%F' GIP' 1 enteroglucagon released in res!onse to stimuli 1 ini#it acid secretion
G. P/ncre/tic Secretion
) !ancreatic Cuice is isotonic to !lasma at all rates of secretion
) anions include Cl- & bicarb; concentration of anions var$ *it te rate of secretion 2E M#icar#N I J M%lN3
) cations include K + & Na+; cations &/= affected #$ te rate of secretion
) ;icar#onate e"its into lumen via %l / #icar#onate e"cange; c0MP activated %l cannel in te luminal mem#rane allo*s
recirculation of %l I CFTR ch/nnels 2not !resent in !atients *it c$stic fi#rosis3
) Pancreatic Cuice also contains !roteins; man$ are !roteol$tic enH$mes 1 are secreted as inactive !roenH$mes *ic are
activated in intestinal lumen
H. Regul/tion o2 P/ncre/tic Secretion
.. Hor,ones6
) Secretin 21 /or >IP3 is released #$ te entr$ of acid into te duodenum 1 stimulates #icar# 1 *ater secretion from te
duct cells; #ot secretin 1 >IP E intracellular levels of c0MP3
) %%F 2 1 /or gastrin3 is released #$ te !resence of 00s 1 fats in te duodenum 1 stimulates enH$me secretion from
acinar cells; gastrin 1 %%F E intracellular calcium
) Potentiation 8 occurs as a result of interaction #/* intracellular !at*a$s activated #$ %%F 1 secretin #inding to cell
rece!tors
0. Nerves6
) Pancreas under nervous control
) >ago)vagal refle"es initiated #$ entrance of cime into intestine
) Stimulation of vagus Es enH$me secretion from te acinar cells 2mediated #$ 0%3 1 to a lesser e"tent #icar# 1 *ater
secretion from duct cells 2mediated #$ >IP
) S&S ini#its vagal 1 secretin induced secretion 1 ma$ ini#it !ancreatic secretion indirectl$ #$ reducing #lood flo*
I. P/tterns o2 Secretion
6M/7or 2unction o2 p/ncre/tic en8y,es in the -igestion o2 nutrients is to /i- in their /9sorption: ,/7or
role o2 p/ncre/tic 9ic/r9on/te secretion is to provi-e / 2unction/l intr/lu,in/l pH 2or the /ction o2 en8y,es 9y
neutr/li8ing HCl e,ptie- 2ro, the sto,/ch
.. Ceph/lic ph/se: activated #$ sig' smell' taste' 1 act of eating food; mediated #$ >0G,S nerve *ic
stimulates enH$me secretion 21 to a lesser e"tent #icar# 1 fluid secretion troug vagal release of >IP3
0. G/stric ph/se: initiated #$ entr$ of food into stomac; stimulation of enH$me secretion induced #$ vagus
continues 1 augmented #$ action of gastrin
1. Intestin/l ph/se6 initiated #$ entr$ of food into duodenum; accounts for 70-80% of pancreatic secretory
response to a meal; first real increase of #icar# 1 fluid secretion; mediated #$ release of secretin from S cells in intestine
in res!onse to acid; %%F is release from intestinal I cells in res!onse to fatt$ acids 1 !e!tides
) entero!ancreatic refle" involves vagal release of 0% in res!onse to !resence of fatt$ acids or amino acids in
duodenum
III. Hep/to9ili/ry Secretion6 #ile is reDuired for digestion 1 a#sor!tion of fats 1 for e"cretion of *ater)insolu#le su#stances
;. Co,position o2 &ile6
com!osted of inorganic 1 organic su#stances
;ile acids 1 salts6 #ile salts M,S= #e conCugated in order to #e solu#le in *ater
maCor #ile !igments are #iliru#in 1 #iliverdin 2meta#olites of emoglo#in3
!ro!ortion of !os!oli!ids' #ile salts' 1 colesterol is im!ortant in solu#iliHing colesterol; a decrease in lecitin or #ile
salts /5 an increase in colesterol results in #ile tat is su!ersaturated *it colesterol colesterol *ill tend to
!reci!itate and form G0.. S=/&-S
;. &ile For,/tion < formed in liver #$ e!atoc$tes 1 ductal cells' secreted into #ile canaliculi' stored in gall #ladder
1 delivered to duodenum troug !a!illa of >ater
) the ,/7or source o2 9ile /ci-s in the 9ile is N*T 2ro, -e novo synthesis 9ut 2ro, upt/=e 2ro, 9loo-. Con7ug/te-
9ile /ci-s 9oun- to /l9u,in /re t/=en up 9y hep/tocytes 2ro, the 9/sol/ter/l si-e 9y so-iu, -epen-ent process
%e>tre,ely e22icient(
) #iliru#in u!taGe #$ te e!atoc$te is relativel$ I&-AAI%I-&=
?. Regul/tion o2 &ili/ry Secretion
) su#stances tat E #ile flo* I %4/.-5-=I%S
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.. ;ile acid de!endent #ile flo*6 Duantit$ of #ile salts secreted #$ te liver; #ile salts and #ile acids are
coleretics #/c te$ E #ile flo* #$ !roviding an osmotic force for *ater 1 solutes to follo*; s$ntesis 1
secretion of #ile acids is &/= under an$ direct neural or ormonal control 8 %%F Es #ile flo* #$ releasing
#ile from te gall #ladder
0. ;ile acid inde!endent flo*6 amount of fluid containing *ater and electrol$tes tat is secreted dail$ #$ te
liver; comes from 2 sources6
a7 canalicular cells contri#ute solutes 1 *ater follo*s !assivel$
#7 duct cells modif$ te #ile as it !asses; M/S= IMP/5=0&= is te secretion of #icar#onate is
controlled #$ secretin; %A=5 cannels are involved; somatostatin ini#its te secretor$ effect
of secretin
#. Enterohep/tic Circul/tion
) recirculation of #ile salts from liver to small intestine 1 #acG; !rinci!al source of #ile acids in #ile
) 9 Q0)Q<: of conCugated #ile salts are activel$ rea#sor#ed in terminal ileum #$ a &aK de!endent trans!ort !rocess; rest
are e"creted *it feces
) rate of de novo s$ntesis is determined #$ rate of return to te liver
M. G/ll9l/--er < stores @ concentr/tes 9ile -uring inter-igestive perio- @ e,pties contents into -uo-enu,
-uring -igestion
) #ile is concentrated 1 acidified #$ rea#sor!tion of *ater #$ te osmotic gradient !roduced #$ te active a#sor!tion of
&a' %l' 1 #icar#onate
) gall #ladder contraction 1 s!incter of /ddi rela"ation occur in res!onse to vagal stimulation during te ce!alic !ase
1 via vago)vagal refle"es during te gastric !ase
) fat 1 !rotein digestion !roducts in te duodenum in te intestinal !ase stimulates te release of %%F 2maCor stimulant
for gall #ladder contraction 1 s!incter of /ddi rela"ation3
I. G/strointestin/l S,ooth Muscle
!. Resting Me,9r/ne Potenti/l in S,ooth Muscle Cells
ARMP is due to se!aration of carges across te mem#rane
A %ircular smoot muscle as slo* r$tmic fluctuations of te mem#rane !otential 2slo* *aves or #asal
electrical r$tm3; slo* *aves are M?/G-&I% 2are an inerent !ro!ert$ of smoot muscle cell; !resent even *en
tere are &/ contractions3
A &/s/l Electric/l Rhyth, %&ER(6 slo* *ave freDuenc$; slo* *aves are res!onsi#le for timing' s!eed' and
direction of GI contractions; contractions are determined #$ te net neural 2e"citator$ 1 ini#itor$3 1 mecanical
2stretc3 in!ut to te muscle O te to! of te slo* *ave; s!read is de!endent u!on ga! Cunctions
) -"citation of tis net*orG is controlled #$ te interstiti/l cells o2 C/7/l %ICC( B p/ce,/=er cells
) slo* *aves 2;-53 +* N*T initi/te contr/ctions' #ut govern te rate at *ic contractions can occur
&. Neur/l /n- Intr/cellul/r Co,,unic/tions
.. #ongitu-in/l S,ooth Muscle6 tinner 1 fe* ne"uses; !rimar$ stimulus is e"citator$ via 0% *ic
diffuses to cells to !roduce contraction
0. Circul/r S,ooth Muscle6 ticG 1 a#undant ne"uses; functions as electrical s$nc$tium; -&S functions to
control te inerentl$ e"cita#le electrical s$nc$tium
) PRIM!R$ NE"R!# INP"T T* SM**TH M"SC#E CE##S IS INHIBITORY
%IPC NITRIC *)I+E(
C. Neur/l Control o2 Contr/ctions
A *itout neural control' eac slo* *ave *ould activate a muscle contraction; reason for overall in!ut to
circular smoot muscle #eing ini#itor$ 2>IP; nitric o"ide3
+. Types o2 GI contr/ctions
.. Tonic contr/ctions: !resent in te fundus of stomac' gall#ladder' 1 s!incters 2smoot muscle3;
!"S N!# ave a ;-5
0. Seg,ent/l contr/ctions: !ro!ert$ of circular smoot muscle 1 ma"7 R in an$ region is determined #$
te ;-5 freDuenc$; facilitate te mi"ing of c$me 1 !roduce a net movement of c$me a#orall$ due to
te gradient of ;-5 along te stomac 1 sm7 intestine
1. Perist/ltic Contr/ctions: !ro!ulsive movements tat reDuire coordination #/* longitudinal 1 circular
smoot muscle
3. Inhi9ite- or /9sent: te GI tract as !eriods of Duiescence
E. Re2le>es: !rimaril$ serve to communicate information #/* distal segments of gut
.. sort refle"es 8 reside entirel$ in te -&S
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0. long refle"es 8 2a3 travel from gut to !reverte#ral ganglia 2S&S3 1 #acG or 2#3 travel from gut to S% or
#rain 1 #acG 2S&S 1 P&S3
1. Im!ortant coordinating refle" is te v/gov/g/l re2le>
. G/stric Motility
!. Motor Functions o2 the Sto,/ch
.. Storage 8 reservoir
0. Mi"ing
1. -m!t$ing
&. G/stric Motor P/tterns
.. F/sting consists of P !ases:
i. p$ase % 8 !eriod of motor inactivit$
ii. p$ase %% 8 !eriod of intermittent motor activit$
iii. p$ase %%% 8 a !eriod of 5-G,.05' 5-P-=I=I>- contractions6 Migr/ting Motility
Co,ple> %MMC( is a c$clic motor !attern tat occurs in te interdigestive !eriod;
de!endent u!on an intact -&S 8 !revents #acterial overgro*t and clears te sm7 intestine
) !ase III activit$ is associated *it an E in !lasma motilin levels
666666666FEE+ING INTERR"PTS THE MMC666666666666
0. Fe- St/te:
i. Receptive rel/>/tion is a vagall$ mediated rela"ation of te !ro"imal stomac to allo* for E
in intragastric volume */ little E in intragastric P; vagovagal refle"; &= is >IP or nitric o"ide
ii. Aollo*ing entr$ of food into te !ro"imal stomac I slo* sustained contractions 21)6
minutes3; refle"ivel$ mediated #$ release of 0% in res!onse to distension; tonic contractions
tat are &/= controlled #$ ;-5
iii. Prop/g/te- perist/ltic contr/ctions occur in te distal stomac 1 teir ma"7 freDuenc$ is
controlled #$ slo* *aves 2P/min in tis area3; tritur/tion 8 re!etition of retro!ulsion #acG
into te antrum results in te mi"ing of gastric contents 1 grinding of large !articles to
smaller ones I !revents mala#sor!tion
iv. G/stric e,ptying:
) stomac acts !rimaril$ to !romote gastric em!t$ing #$ contractions *ic move te gastric contents distall$
) duodenum generall$ o!!oses gastric em!t$ing
@Aactors tat regulate gastric em!t$ing6
17 >olume
27 Particle SiHe
P7 %aloric content 1 meal com!osition
47 /smolalit$
<7 !4
67 4ormones 2gastrin' secretin' %%F' 1 GIP3 8 all slo* gastric em!t$ing
S7 &eural mecanisms6 enterogastric refle" I cemical or mecanical stimulation of te
duodenal mucosa ini#its gastric !eristalsis 1 slo*s gastric em!t$ing
A!G*T*M$6 E in gastric em!t$ing of liDuids #/c of im!aired rece!tive rela"ation of te !ro"imal stomac 1 a J in
gastric em!t$ing of solids #/c of reduced force of antral contractions 8 so grinding of !articles is prolon&ed
I. Intestin/l Motility
!. G/stric vs. S,/ll intestine ,otility
.. ;-5 is faster in intestine
0. Peristaltic *aves D/ &/= travel entire intestine
1. &/ storage of food in sm7 intestine
@@@@@@ S=-PTIS- decline of ;-5 along te sm7 intestine 212/min in duodenum 8)Q/min in ileum3 @@@@@@@ 2assures transit
of food is a#oral3
&. S,/ll intestine ,otor p/tterns
.. F/sting: 9 Q0 mins I MM% travels from stomac to terminal ileum
0. Fe-: most !rominent contractions after a meal are segmentation contractions follo*ed #$ !eristaltic
contractions; vagus is needed to maintain te fed !attern; !resence of fat in ileum induces I.-0.
;50F- I slo*s intestinal transit 2ormone involved is &P? 1 P??3 *ic allo*s more time for
a#sor!tion
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C. Types o2 contr/ctions
.. Seg,ent/tion 2mi"ing contractions I a#sor!tion36 c$me is dis!laced in ;/=4 directions; circular
smoot muscle; most common t$!es of contractions after a meal
0. Perist/lsis6 oral to a#oral seDuence of adCacent contractions resulting in net !ro!ulsion of c$me; occurs
in res!onse to distension of te lumen; reDuires coordination of #ot longitudinal and circular smoot
muscle 2!eristaltic refle"3 1 is mediated #$ -&S; &= for e"citator$ I 0%; &= for ini#itor$ I >IP or
nitric o"ide
+. Ileocec/l ;unction
) smoot muscle s!incter tat is tonicall$ contracted
) valve functions to !revent reflu" of colonic contents into te ileum
II. Motility o2 the #/rge Intestine
!. Small vs #/rge Intestine Motility:
.. =e colon does N!# $ave an ''C
0. (") is slo*er in te ascending colon tan in te transverse or descending segments of te colon; no
!ro"imal to distal gradient
1. transit is muc S./T-5 in te colon tan in te sm7 intestine
3. %olon as a stora&e function
4. 'ass peristalsis is o#served in .g7 intestine
5. %olon as bacteria
&. Slo* Tave AreDuenc$ 2&ER36
) slo*est near te ileocecal Cunction 1 Es until te mid transverse colon
) dela$ in transit of c$me to facilitate mi"ing reDuired for a#sor!tion !rovided #$ ;-5 freDuenc$ less in rigt colon
C. Types o2 Contr/ctions:
.. H/ustr/tions: 2a3 mi"ing movemtns are te most freDuent 1 occur !rimaril$ in te rigt colon; 2#3
austral migration results in te net movement of c$me a#orall$
0. M/ss Move,ent: mass !eristalsis 8 least freDuent !attern; moves contents large distances in an a#orad
direction
+. E22ect o2 Fee-ing on Colonic Motility:
.. N* interdigestive !attern %MMC( as te colon is rarel$ em!t$
0. Fee-ing Es te R of austrations' initiates mass movements 1 Js te R of mi"ing contractions in te
colon; tus defecation occurs after a meal freDuentl$ 2gastrocolic refle"3
E. +e2ec/tion: 9oth volunt/ry /n- re2le> /ctivity involve-
.. Re2le> %ano)rectal distension(6 initiated #$ mild distension *ic activates retros!incteric refle" *ic
rela"es internal anal s!incter 1 elicits urge to defecate; mild distension of te rectum also induces a
refle"ive contraction of te e"ternal anal s!incter
Aif te urge to defecate is dela$edLte rectum rela"es to accommodate te Ed volume' te internal s!incter
regains its tone 1 te e"ternal anal s!incter rela"es I Continence
0. olunt/ry !ctivity < in res!onse to mild distension' te urge to defecate can #e continued #$
voluntaril$ rela"ing te e"ternal anal s!incter
III. D/ter /n- Ion Tr/nsport
!. D/ter tr/nsport: in te small intestine and colon is P0SSI>-; net direction of *ater movement is de!endent
u!on6
.. .ocation along te #o*el6 igest >/.,M- of *ater is a#sor#ed in te !ro"imal 2duodenum to
CeCunum3 intestine; most efficient a#sor!tion of *ater is in te distal segments 2ileum 1 colorectal areas3
due to larger !ore siHe 1 lo*er resistance tigt Cunctions 8 creates a !ro"imal to distal gradient of
osmotic !ermea#ilit$
0. .uminal osmolalit$6 in te duodenum' te c$me is adCusted to !lasma isotonicit$ #$ net secretion or
net a#sor!tion of *ater across te mucosa
1. 5ate of solute trans!ort6 in segments distal to te duodenum' te c$me is isosmotic to !lasma 1 *ater
a#sor!tion is cou!led to solute trans!ort 2E solute trans!orted I E *ater a#sor#ed3
&. So-iu, Tr/nsport %N/ -rives /9sorption -ue to electroche,ic/l gr/-ient(
) occurs in villus cells; #ot active and !assive trans!ort of sodium
) de!endent u!on te #asolateral &a / F !um!; &a enters te cell along its electrical 1 cemical gradient
) in te small intestine' org/nic solutes /re couple- to N/ tr/nsport %secon-/ry /ctive tr/nsport(; im!ortant after a
meal
) electroneutr/l tr/nsport o2 so-iu, in te ileum involves &a/4 1 %l/#icar# e"cange; ini#ited #$ c0MP 1 Ed
intracellular calcium; stimulated #$ Js in intracellular calcium; im!ortant durin& fastin&
) !assive a#sor!tion secondar$ to *ater trans!ort I S*#ENT +R!G or convection; im!ortant after a meal
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C. Intestin/l Secretion %-riven 9y Cl( < /nion -epen-ent
) %loride e"its cell troug selective ion cannel 2%A=53; cannel regulated #$ canges in intracellular c0MP
) Induction of secretion #$6
.. 0ctive anion secretion
0. 4ig luminal osmolalit$ 8 !rimar$ mecanism for fluid secretion in !ro"imal duodenum
1. increased interstitial $drostatic P6 secondar$ filtration
3. Decreased solute a#sor!tion6 te ini#ition of neutral &a%l trans!ort is o#served in res!onse to some
ormones 1 colera to"in; effect is mediated #$ a rise in intracellular c0MP
) 0gonists increase net secretion by increasin& c+',- increasin& intracellular calcium or increasin& c.', I all act on
te e!itelial cell to increase openin& of C/#) c$loride c$annels
+. D/ter /n- Electrolyte Tr/nsport in the Colon
.. .arge intestine /9sor9s w/terC N/C ClC @ secretes ? @ 9ic/r9on/te
0. Pore si8e is gre/ter @ resist/nce is lower in te CeCunum and ileum tan in te large intestine 2&/
!assive a#sor!tion of &a #$ convection in colon3
1. !ctive tr/nsport o2 nutrients is N*T present in the colon
3. Miner/lcorticoi-s increase &a in te large intestine #ut not in te small intestine; glucocorticoids
increase &a a#sor!tion in #ot areas
) D/ter tr/nsport6 diarrea results *en te rate of fluid entr$ into te colon is more tan te ma"7 a#sor!tive ca!acit$ 29
47< ./da$3
) N/ /9sorption is electrogenic 2net transfer of carge moving do*n3
) !l-osterone incre/ses N/ /9sorption @ ? secretion
I). C/r9ohy-r/te /n- Protein !9sorption in the S,/ll Intestine
!. Intr/lu,in/l +igestion
.. Carbo$ydrases
) %ar#o$drate digestion #egins *it s/liv/ry EA/,yl/se in te mout
) Most intraluminal digestion taGes !lace in te small intestine #$ action of p/ncre/tic EA/,yl/se 2secreted as an active
enH$me in !ancreatic Cuice3
0. ,roteases
) Protein digestion #egins in te stomac *it te action of pepsin 2released from cief cells in res!onse to v/g/l
sti,ul/tion3
) Most im!ortant durin& intestinal p$ase
) Secretion of !roteol$tic enH$mes of !ancreas is stimulated #$ CC? 2released due to !resence of !rotein digestion
!roducts in duodenum3
) Proteases secreted as inactive !roenH$mes 1 are activated in te duodenum #$ entero=in/se 2#rus #order enH$me
released #$ action of #ile salts3; converts tr$!sinogen to tr$!sin 2ten activates more tr$!sinogen as *ell as oter !roteases3
) Products of digestion I small !e!tides 1 free amino acids
&. C/r9ohy-r/te !9sorption in the s,/ll intestine
.. (rus$ border di&estion0 2%ar#o$drases I maltase' sucrase' lactase' 1 isomaltase3
0. /&.? monosaccarides are a#sor#ed #$ te enteroc$te; final !roducts are glucose' galactose' 1
fructose
) Fructose6 carrier mediated facilitated diffusion using G#"T 4 tr/nsporter
) Glucose @ G/l/ctose6 sare common trans!ort 2SG#T.3 !rocess linGed to &a trans!ort 2secondar$ active trans!ort3
) Glucose 1 galactose e"it cell via facilitated diffusion using a &a inde!endent carrier 2G#"T 0( at te #asal mem#rane 1
secondaril$ #$ !assive diffusion into ca!illaries
) &ormall$ 8 all car#s are a#sor#ed #$ mid)CeCunum
C. Protein !9sorption in the s,/ll intestine
.. "nterocyte peptidases0 Digestion at te #rus #order !roduces free amino acids' di)' 1 tri!e!tides
0. /ree amino acids are a#sor#ed #$ 4 different mecanisms6 4 trans!orters; mostl$ &a de!endent 2P3;
s!ecific for s!ecific amino acids
1. Most !rotein is a#sor#ed in te form of di) 1 tri!e!tides; intracellular !e!tidases $drol$He tese small
!e!tides into amino acids
3. 0mino acids and remaining !e!tides leave te cell #$ facilitated or !assive diffusion
+. !9sorption o2 D/ter Solu9le it/,ins
SGM Page 8 8/26/2014
.. &. or &5 or &0 or ri9o2l/vinC nicotinic /ci-C @ vit/,in C are a#sor#ed #$ facilitated or !assive
diffusion 1 carrier)mediated trans!ort
0. &.0 /9sorption reDuires formation of a com!le" *it intrinsic factor 2IA3 !roduced #$ !arietal cells of
te stomac; com!le" remains in te lumen until te ileum *ere it #inds to s!ecific rece!tors on te
enteroc$tes; after #inding' ;12 is activel$ a#sor#ed 1 a!!ears in #lood #ound to transco#alamin
). #ipi- !9sorption in the S,/ll Intestine
!. Intr/lu,in/l +igestion
.. Digestion #egins *it lingu/l lip/se in te saliva
0. Aat is emulsified in te duodenum into small dro!lets #$ te action of #ile salts 1 lecitin *it te el!
of intestinal contractions
1. =e !resence of fat in te duodenum triggers te release of CC? *ic stimulates !ancreatic enH$me
secretion7
3. P/ncre/tic lip/se is secreted in its 0%=I>- form; it $drol$Hes =Gs 1 acts onl$ at te oil)*ater
interface
4. P/ncre/tic colip/se 2secreted as !rocoli!ase 1 is activated #$ tr$!sin3 #inds to =Gs 2in !resence of #ile
salts3 at te oil)*ater interface 1 to li!ase allo*ing li!ase to *orG *itout #eing inactivated #$ #ile salts
5. +iet/ry phospholipi-s are $drol$Hed #$ !os!oli!ase 02 2secreted as a !roenH$me3; in te !resence
of calcium 1 #ile salts 8 cleaves te fatt$ acid from te !os!oli!ids
F. Cholesterol is !resent in te diet !rimaril$ as colesterol ester; cholesterol ester/se is secreted in te
!ancreatic Cuice 1 cleaves te fatt$ acid from te ester to $ield free colesterol
&. !9sorption o2 F/t
.. Solu9ili8/tion o2 F/t
) te emulsified !roducts must form MI%-..-S *it #ile salts #efore te$ can #e a#sor#ed
) formation of mi"ed micelles 2micelles containing li!id digestion !roducts3 facilitates te movement of fat solu#le
su#stances troug te aDueous c$me
0. Cellul/r "pt/=e
) Mi"ed micelles must !ass troug 2 #arriers6
i. te unstirred *ater la$er 2contains mucous coat3
ii. li!id mem#rane #arrier
) micelles move along te microvilli allo*ing teir li!ids to !assivel$ diffuse across te microvillus mem#rane 1 into te
enteroc$te
) te rate of e1c$an&e of lipid products is de!endent u!on te concentr/tion gr/-ient 1 te solu9ility o2 the lipi-
pro-uct in te cell mem#rane 2generall$ ra!id3
) conCugated #ile salts are a#sor#ed in te terminal ileum #$ a &a de!endent active trans!ort !rocess
C. Intr/cellul/r Met/9olis,
.. ReAesteri2ic/tion. 0fter te li!id !roducts enter te enteroc$te' te$ enter te S-5 *ere te$ are
reconstituted
0. Chylo,icron 2or,/tion @ secretion. 5eformed li!ids coalesce into c$lomicrons 2core of =Gs 1
colesterol surrounded #$ !os!oli!ids coat3; trans!orted out of cell #$ e"oc$tosis
1. +lmost all lipid is absorbed by mid-2e2unum *it$ most in t$e duodenum
+. !9sorption o2 F/t Solu9le it/,ins
) >itamins 0' D' -' 1 F are a#sor#ed in te !ro"imal intestine troug te formation of micelles *it #ile salts
E. +igestion @ !9sorption o2 Nutrients in the Colon
.. &/cteri/ in the colon: aero#ic 1 anaero#ic; R of #acteria due to slo* motilit$
0. Nutrient /9sorption.
) car#s can #e converted into s$ort c$ain fatty acids #$ #acterial fermentation 2!rovide maCor source of gas3
) carbo$ydrate malabsorption increases osmotic load to colon 1 increases incidence of diarrea
) li!id digestion continues #$ #acterial li!ases; $dro"$ fatt$ acids stimulate fluid secretion; colesterol is ,&=/,%4-D
in te colon
) ;ile acids enter te colon 1 are meta#oliHed #$ te #acteria; stimulate fluid secretion; #ile salt mala#sor!tion can #e due
to resection or d$sfunction of te distal ileum
F. Colonic G/s Sources
.. S*allo*ed air7
0. %ar#on dio"ide
1. >olatile A0s
3. Diffusion of gas from #lood to lumen
4. ;acteria maGe $drogen from car#s delivered to lumen
5. Metane 1 car#on dio"ide are !roduced #$ colonic #acteria
F. &itrogen is te most %/MM/& gas in normal individuals