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ANATOMI & FISIOLOGI

SISTEM PENCERNAAN

OLEH :
MICIKO UMEDA, SKp., MS.Biomed

Chapter 1: Introduction to
Anatomy and Physiology
BIOL 131
Mr. Ripper

Digestive System

Copyright The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

AREA ABDOMEN DIBAGI 9 region.

Organ GI

A. Mulut
Mengunyah : pemecahan
partikel besar menjadi kecil

Kelenjar saliva
Sekresi

mukus ke dalam mulut


Fungsi membasahi & melumas partikel
makanan sebelum di telan
Disekresi

3 kelenjar eksokrin

a. Parotis
b. Submandibularis
c. Sublingualis

Saliva
Mengandung

enzim pencernaan
a. Lipase lingual : di sekresi kel. Ebner lidah
- Aktif di lambung, mencerna 30%
lemak makanan
b. Ptialin/amilase saliva ( di sekresi kel. Saliva)
- Mencerna tepung, ph 6,7,
- Dihambat asam lambung

Kandungan saliva
Musin

: bahan organik jika bercampur


air membentuk larutan kental ( viskous)
Mukus
Anorganik : Na, K, Cl, bokarbonat
1500 cc saliva / hari
99,5% air, 0,5% protein & elektrolit

Fungsi saliva
Memudahkan

proses menelan
Membasahi mulut, membantu proses
bicara
Melarutkan molekul yang merangsang
reseptor kecap

Fungsi saliva
Anti

bakteri
Mempertahankan Ph mulut ( 7,0)
Mengandung hormon: epidermal
growth faktor, nerve growth faktor,
somastotatin, bradikinin

B. Faring & esofagus


Tidak

ikut serta dalam proses


pencernaan
Jalur masuk makanan & minuman
ke lambung

Esofagus

Esofagus

Sel mukosa esofagus

B. Faring & esofagus


Motilitas

segmen ini berkaitan


dengan proses menelan, karena
perangsangan reseptor dinding
faring oleh bolus.

ESOFAGUS

DIVERTIKULUM

C. Lambung

lambung

C. LAMBUNG / GASTER
Kantung

muskuler terletak antara


esofagus & usus
Bagian korpus & fundus ( berdinding
tipis)
Sekresi mukus, asam HCL, proenzim
pepsinogen, faktor instrinsik ( castle)

C. Lambung
Bagian

bawah lambung : antrum


mempunyai otot lebih tebal
Sekresi hormon gastrin

HCl lambung
Memecah

partikel makanan
Membentuk larutan molekul yang
disebut KIMUS
Tidak mampu memecah protein & lemak
Memusnahkan bakteri yang masuk
lambung ( tidak efektif 100%)

Fungsi lambung
Menyimpan

, melarutkan & mencerna


parsial makanan yang masuk lambung.
Meneruskan makanan ke usus untuk di
absorbsi secara maksimal
Produksi enzim pepsin : memecah
ikatan peptida

Sel mukosa lambung

D. Usus Halus

Internal Usus halus

Usus Halus
Diameter

4 cm
Mulai dari lambung sampai usus besar
Panjang 275 cm
3 segmen : duodenum, jejenum, ileum
Mempunyai banyak lipatan/ vili

Usus halus

Fungsi usus halus


Absorbsi

bahan makanan
Berlangsung terutama di duodenum &
jejenum
Absorbsi cairan elektrolit

vili

Vilus
Pusat

vilus berisi pembuluh limfe yang buntu


Lakteal, kapiler merupakan cabang arteriola
serta bermuara ke venula
Setiap 5 hari diganti

Absorbsi usus halus


Karbohidrat
Hasil

akhir pencernaan : monosakarida


( glukosa,galaktosa, fruktosa)

Transfort aktif
Tidak perlu insulin

Liur usus halus


Mukosa

usus halus terdapat kelenjar


Brunner ( duodenum)
Hasilkan mukus
Melindungi mukosa duadenum dari iritasi
HCl & pepsin
Kelenjar intestinal/ crypte Lieberkuh
Produksi enzim, cairan isotonik

DUODENUM

duodenum

Sel duodenum

Jejenum

ileum

Jejenum

SISTEM PENCERNAAN

Gastro intestinal track ( GIT)


Permukaan

biasanya tidak datar / licin


Berkelok-kelok, menambah luas permukaan
absorbsi
Struktur jaringan berbeda tetapi mirip
4 Lapisan GIT

1. Mukosa
Mulai

dari lambung
Mukosa : sel epitel : sekresi mukus &
hormon
Invaginasi jaringan epitel kedalamnya
membentuk kelenjar eksokrin
Kelenjar eksokrin : sekresi asam, enzim, ionion kedalam lumen

Sistem Pencernaan

Lamina Propia
Di

bawah lapisan epitel


Jaringan ikat : dilalui pembuluh darah kecil,
serat saraf & saluran limfe
Lamina

propria dipisahkan jaringan ikat di


bawahnya oleh suartu lapisan tipis otot polos
yaitu muskularis mukosa

2. Sub Mukosa
Jaringan

ikat kedua dibawahnya


Lapisan ini dilalui pembuluh darah & limfe
lebih besar, cabangnya menembus lapisan
mukosa diatas &lapisanotot di bawahnya
Terdapat

jala saraf disebut pleksus sub


mukosa ( meissner)

3. Muskularis Eksterna
Jaringan

otot polos
Kontraksinya menimbulkan gaya mendorong
& memindahnkan isi saluran GI

3. Muskularis Eksterna
Terdiri

2 lapisan
a. Otot sirkuler : sebelah dalam, tebal,
kelilingi lumen, jika kontraksi lumen
menyempit

b. Otot longitudinal : sebelah luar , lebih tipis,


bila kontraksi saluran GI memendek

3. Muskularis Eksterna
Diantara

kedua otot polos terdapat pleksus


saraf lain yang lebih eksentif yaitu:
a. Pleksus mienterikus (AUERBACH)
b. Pleksus sub mukosa
c. Pleksus mienterikus/ intramural
d. Neuron lain di Saluran GI membentuk
sistem saraf enterik

4. Serosa
Selapis

jaringan ikat , diliputi sel gepeng ,


mengelilingi permukaan luar saluran GI
Sekresi cairan serosa, untuk membasahi &
mencegah gesekan dengan organ lain
Lembar jaringan ikat tipis2 ( Mesenterium,),
hubungkan serosa ke dinding abdomen,
menopang segmen GI ke rongga abdomen

Hati

Fungsi Hati
Sekresi

empedu
Sekresi sel epitel saluran empedu

Kelenjar eksokrin GI
Kelenjar

Saliva

Hati
Pankreas

HATI

HATI

SEL HATI

Kandung empedu
Kandung empedu

Bentuk gangguan pada kelenjar


empedu

Liur pencernaan yang dialirkan ke


usus halus
Liur

Pankreas
Empedu:
Liur usus halus

Kelenjar empedu

Liur Pankreas
1500

cc / hari
bikarbonat, elektrolit: Na,K,Cl,enzim
Pengaturan sekresi melalui pengendalian
hormon

Empedu
Air

97%, garam empedu 0,7%, pigmen


empedu ( 0,2%), kolesterol, garam
anorganik, as. Lemak, lesitin, fosatase alkalis
Fungsi memudahkan pencernaan & absorbsi
lemak
Aktikan lipase

Protein
Hasil

akhir pencernaan protein : as. Amino


Transort aktif

Lemak
Hasil

akhir pemecahan lemak: asam lemak


bebas, gliserol, monogliserioda

Integration of Metabolism:
Review of Roles of Systems in Muscle Contraction

Figure 25-1: Energy metabolism in skeletal muscle

USUS besar

USUS BESAR

Fungsi Usus besar


Menyerap

air & elektrolit


Menyimpan bahan feses saat
deekasi

Gangguan usus
Konstipasi
Megakolon
Diare

Usus besar

FOTO RONGSEN

FOTO RONGSEN

USUS BESAR

USUS BESAR

ANUS

ANUS

SIROSIS HEPATIS

Organ organ GIT

Oesophagus : saluran makanan


Lambung : menyimpan makanan sementara dan memecah
makanan lebih halus
Usus kecil : mencerna dan absorbsi makanan
Usus besar : pembentukan dan penyimpanan feses
Kelenjar ludah, pankreas, hati : produksi enzim dan cairan
untuk membantu mencerna makanan

5 proses gut

Motility Gerakan usus untuk mendorong makanan dalam


usus
secretion Kelenjar eksokrin mengeluarkan sekresinya ke
saluran pencernaan
digestion Mengubah molekul besar menjadi molekul kecil
absorption hasil cerna makanan dan nutrisi bergerak menuju
dinding usus untuk masuk ke pembuluh darah
elimination makanan yang tidak dapat dicerna dan produk
sisa dikeluarkan dari tubuh.

Mencerna dan absorbsi

Aktivitas motorik Mengunyah, mencampur kneading,


grinding, mixing, propulsion
secretory activity - lubrication and epithelial protection
provision of digestive juices (transport of salts and water synthesis of proteins)
digestive activity - digestive enzymes - other factors, pH,
bile salts

absorption - transport of salts water and organic


compounds

integrative control - enteric nervous system, gut


endocrine system

Aktivitas sekresi dan mencerna

Kontrol sekresi dan komposisi cairan

Enzim pencernaan

Kontrol sekresi enzim

Faktor ang mempengaruhi aktivitas enzim

3 Komponen makanan carbohydrates, fats, proteins


Mencerna makanan hydrolysis dengan enzim khusus

Karbohidrat formed by condensation of H+ and OH- groups


hydrolysis restores the H+ and OH- groups

triglycerides are 3 fatty acid molecules condensed with a


glycerol molecule
hydrolysis by lipases separates these molecules

proteins amino acids joined together with peptide bonds


hydrolysis by proteases/peptidases

Carbohydrates

300g ingested per day as

complex polysaccharides
64% starch, 0.5% glycogen
disaccharides
26% sucrose, 6.5% lactose
monosaccharides
3% fructose

complete hydrolysis would yield 80% glucose, 14%


fructose, 5% galactose

Complex carbohydrates - polymeric glucose

1-4 and 1-6 bonds in starch (straight chain) and


amylopectin (branched) attacked by salivary and
pancreatic amylase

maltose and triose and dextrins - broken down to glucose


monomers by intestinal maltase and isomaltase

sucrase (sucrose to glucose-fructose) and lactase


(lactose to galactose-glucose)

cellulose - glucose in 1-4 - not broken down

Proteins

> 100g ingested daily as oligopeptides

digested by proteolytic enzymes

proteolytic enzymes secreted as zymogens (inactive


proenzeymes)

endopeptidases - cleave internal peptide bonds

exopeptidases - carboxy or amino terminal cleavage

Fats

60-100g perhari

fAsam lemak

Triasil gliserol

cholestrol (esterified)

Dicerna dengan enzim lipase

Functional movements in the gut 2

Mixing movements

these are quite variable in different parts of the gut

some involve peristaltic contractions against a sphincter


resulting in churning
in other cases local constrictive contractions occur every
few cms lasting only a few seconds and then starting
somewhere else resulting in chopping

Main functions of mastication

to disrupt food mechanically to facilitate the action of digestive


enzymes

to mix food with saliva to initiate carbohydrate digestion by


salivary -amylase

stimulate afferent receptors that trigger the cephalic phase of


digestion

to form the food into a bolus in preparation for the onset of


swallowing

Functions of saliva

1-1.5 l secreted per day

to provide a fluid medium to dissolve food and to provide


a lubricant to aid in chewing and swallowing
to irrigate the mouth - to keep it moist and to prevent
growth of infectious agents in the mouth - saliva contains
lysozyme,
peroxidase and IgA all of which have anti-bacterial/viral
effects
moist buccal cavity is essential for clear speech
secrete digestive enzymes and growth factors (NGF,EGF)
allow taste

Main salivary glands

parotid - (from greek parotis - near the ear) - serous


endpieces

submandibular - mainly serous with some mixed


mucosals

sublingual - mainly mucous

serous - water, electrolytes and amylase


mucous - secretes mucins, electrolytes and water

3 basic salivary cell types

acini (endpieces) - involved in secretion of primary fluid,


electrolytes across a water permeable epithelium and mucous
ducts - mainly involved in Na and Cl absorption and K and
HCO3 secretion as well as secretion of various growth factors
and enzymes - membrane is impermeable to water
myoepithelial cells - prevent overdistension structures due to
buildup of intraluminal pressures during secretion

Nervous control of salivary secretion

endpieces and ducts are innervated by parasympathetic and


sympathetic nerves
the main agonists are ACh (parasympathetic) and noradrenaline
(sympathetic)
main stimulus of secretion is from the parasympathetic pathway acting
via signals from the salivary nuclei
excited by both taste and tactile areas of the tongue
also excited via stimuli arriving at the salivary nuclei from higher centres
of CNS - such as smell or thinking of food
salivation also occurs in response to reflexes from stomach and upper
intestines following gastric irritability - saliva serving to dilute the digesta

Two stage hypothesis of salivary formation

first stage - primary juice with plasma like conc of Na, K, Cl


and HCO3 secreted by the water permeable endpieces
autonomic stimulation increases rate of juice secretion
without altering its composition
second stage - as juice passes along the water
impermeable duct it is modified by absorption of Na and
Cl and secretion of K and HCO3
since rate of absorption of Na and Cl is greater than rate of
K and HCO3 secretion - result is a final saliva rich in K and
HCO3 - but dependent on the rate of flow

Main exportable proteins from salivary glands

Mucins - glycoproteins which serve to mechnically protect


the epithelium and stop it drying out
lubricate food
protect the lining of the stomach and small intestine from
acids and digestive enzymes
trapping microorganisms
Digestive enzymes - mainly -amylase which digests
starch - main role is to promote oral hygeine by facilitating
dislodgement of food particles impacted around the teeth
(dietary starch digestion by pancreatic amylase in the
duodenum)

Main functions of swallowing

to transport the food bolus from the pharynx into the stomach
to prevent esophagopharyngeal reflux and gastroesophagal
reflux
swallowing involves
complex interactions between voluntary and involuntary nervous
and muscular systems
closely coordinated with breathing and associated activities (i.e.
talking)

Four phases of swallowing

preparatory
oral
pharyngeal
eosophagal
preparatory is voluntary and involves bolus formation and
lubrication during mastication

Four phases of swallowing 2

Oral phase - bolus propelled into the pharynx by


progressive contact of the tongue against the palate in a
posterior direction

Pharyngeal stage - a single contraction peak coinciding


with the beginning of the peristaltic wave
soft palate elevates and seals the nasopharynx to prevent
postnasal regurgitation
larynx ascends and epiglottis tilts downwards - facilitates
closure of the laryngeal vestibule and removes laryngeal
inlet from the oncoming bolus
Upper oesophageal relaxation commences with the onset
pharyngeal phase

Four phases of swallowing 3

Esophageal stage
as UES closes primary peristalsis occurs - a progressive circular
contraction that proceeds distally - induced by the swallow secondary
peristalsis then proceeds in the oesophageal body which is invoked purely
by intrinsic reflexes eg - by distension
the lower oesophageal sphincter relaxes shortly after a swallow due to
cessation of tonic neural excitation to the sphincter as well as inhibition by
NANC inhibitory neurons
this receptive relaxation of the LES ahead of the food bolus allows easy
propulsion of the food into the stomach
improper relaxation of the sphincter leads to achalasia
the tonic constriction of the LES helps to prevent significant reflux of the
contents of the stomach into the oesophagus

Stomach

distal to the LES lies a valvelike mechanism underneath the


diaphragm
increased intrabdominal pressure caves the oesophagus
inwards also serving to stop reflux
stomach is divided into 3 main parts the fundus, body
(corous) and the antrum

Stomach function 2

store food before emptying it into small intestine


begin digestive process
stomach secretes 2-3 l of gastric juice/day
homogenise the food to form chyme - a milky, murky semifuid
or paste-like mixture resulting from food mixing with gastric
secretions

Stomach musculature

proximal
maintains a steady tone
relaxes during swallowing (receptive relaxation)
and when the food enters the stomach
(accomodation)
distal
exhibits strong peristaltic waves driven by a
pacemaker region. These waves which homogenise
the food are essentially driven by intrinsic neurons

Stomach storage function

Storage function of the stomach is served by the smooth muscle of


the fundus and body
Initially following a swallow receptive relaxation occurs in the
stomach due to afferent neurones in the walls of the oesophagus

Subsequently distension sensing afferents in the stomach wall


reduces the tone of the muscle wall allowing it to bulge progressively
outward (accomodation) to a limit of approx 1.5l without any
significant increase in intragastric pressure

There are also tonic contractions that maintain a continuous


gastroduodenal pressure gradient (due to vagal efferents) that
ensures that the solids progress into the distal stomach

Basic Electrical Rhythm

Unlike muscle cells of the proximal stomach, cells of


the distal stomach exhibit spontaneous action
potentials.

In the distal and antral regions of the stomach


electrical activity ischaracterised by the presence of
slow waves ~3/min - also called basic electrical
rhythm set by the pacemaker cells

these slow waves travel as a ring around the stomach


towards the pylorus

Antral Peristalsis

as the stomach fills with food - powerful antral peristaltic


waves are initiated from the pacemaker region following
the same pattern as the slow waves

each time a peristaltic wave passes over the antrum it


digs into the contents of the antrum - yet the opening of
the pyloris is only small so that only a small amount can
pass
the pyloric muscle itself contracts such that most of the
contents are squirted back through the peristaltic ring
into the body of the stomach this is an important mixing
process called retropulsion

Hunger contractions

intense contractions which occur in the body of the stomach


when it has been empty for a long time
rhythmic contractions which can become extremely strong and
fuse together resulting in a continual tetanic contraction lasting
for as long as 2-3 min
most frequent in young healthy persons with a high degree of
gastrointestinal tonus

Stomach tubular glands

oxyntic gland (greek oxys = sour) - on the body and


fundus
consists of 3 cell types
Parietal cells - large acid secreting cells - also secrete
intrinsic factor
Chief cells - principle source of pepsinogen
Mucous neck cell - secrete a mucous glycoprotein
also surface mucous cells which secrete mucous and
HCO3

Stomach tubular glands 2

pyloric glands - in the antrum


secrete mainly mucous to protect pyloris
gastrin from G cells
some pepsinogen
NO parietal cells

Main components involved in digestion

HCl
acid denaturation of digested food
activate pepsinogens
convert ferric salts into absorbable forms
kill ingested bacteria that would destroy vitamin B12
Intrinsic factor - absorption of dietary vitamin B12
absence of intrinsic factor leads to anaemia due to the failure of red blood cells
to develop
Pepsinogen - principle enzyme (endoprotease) of the gastric juice
pepsinogens are inactive forms which convert to an active form upon exposure
to gastric juice
when gastric juice is neutralised in the duodenum the pepsin is inactivated

Gastric-mucosal protection barrier

the surface epithelia secrete a thick alkaline mucus that


adheres to the surface and forms a protective barrier
between the epithelium and the acid and pepsin in the
gastric lumen

mucus is heavily glycosylated to protect it from proteolysis


by pepsin but it is nevertheless degraded so maintenance
of this layer requires continued synthesis and secretion of
mucus

the mucus layer is also heavily buffered by NaHCO3


secreted by the surface epithelial cells thus there is a pH
gradient across this gel

Three phases of gastric secretion

the functional activity within the stomach is carefully


coordinated with alimentation and digestive function
throughout the entire GIT

this is separated into 3 phases

cephalic phase
gastric phase
intestinal phase

Cephalic phase

directly controlled by the brain


accounts for ~30% of the response to a meal
mediated through efferent fibres from the brain receptors associated with
smell taste sight and chewing
occurs within few minutes after appropriate afferent stimulus & can occur in
response to conditioned stimuli
vagal efferents stimulate ACh in the region of the secretory cells in the main
body of the stomach
-stimulate secretion of acid
-stimulate histamine release - histamine acts as a powerful paracrine
stimulant of HCl secretion by parietal cells
also in the antrum where vagal efferent impulses release gastrin releasing
peptide which in turn causes G cells in the antrumto release gastrin - which
in turn stimulastes receptors on parietal and chief cells

Gastric phase 1

regulated by events within the stomach


accounts for ~60% of the response to a meal
stimulus due to the presence of food & involves
neural & humoral responses
distension of the stomach activates intrinsic
neurones but supports little secretory response
unless potentiated by secretagogues
distension activates the vago-vagal reflex - using
vagus nerve to transmit afferent impulses to the
medulla which return via the vagal efferents to
stimulate secretion - similar to cephalic phase (ie
secretion of acid & gastrin & pepsinogen)

Gastric phase 2

nature of the food in the antrum has a profound effect the presence of polypeptides in the antrum stimulate G
cells to secrete gastrin
lowering of the pH of the surface of the antral mucosa
greatly inhibits the gastric phase of secretion - this is due
to the release of somoatostatin form endocrine cells in
the gastric mucosa - somatostatin acts in a paracrine
fashion to inhibit gastrin secretion
this paracrine mechanism is a important aspect of
negative feedback regulation of gastric HCl secretion

Intestinal phase

accounts for less than 10% of the response to a meal


principle feedback mechanism is via hormones released by the
duodenal mucosa
some G cells spread from pylorus into duodenum - minor effect
secretin - has inhibitory effect on gastric acid secretion by
causing release of somatostatin - also reduces gastric motility
acid in the duodenum feedsback via intrinsic nerves
fats cause the release of CCK and GIP - CCK stimulates chief
cells to secrete pepsinogen and may enhance pyloric
constriction
GIP (gastric inhibitory peptide) inhibits parietal sectretion and
output of gastrin via paracrine release of somtostatin

HCl secretion by parietal cells

ACh - acetylcholine released by postganglionic neurons of the


vagus

Gastrin - endocrine stimulant released by G-cells

Histamine - a paracrine stimulant released by enterochromaffin-like


cells in close proximity to the basal aspect of parietal cells

both ACh and gastrin act to increase cytosolic Ca


histamine acts via adenylate cyclase to stimulate acid secretion
(somatostin operates via the same system to inhibit!)
histamine in effect potentiates HCl secretion

Basis of HCl secretion

H+ extruded by a H+/K+-ATPase which uses one ATP to pump out one


H+ in exchange for one K+

the apical surface of the parietal cell is invaginated by canals (called


secretory canaliculi). The cells also contain a huge pool of
tubulovesicles which contain large numbers of H+/K+ ATPase
molecules

upon stimulation the tubulovesicles fuse with the canalicular membrane


resulting in a greatly enhanced surface area of elongated microvilli

following removal of stimulation the H+/K+ATPases are recycled back


into the tubulovesicle compartment

Stimulation of Chief Cells

pepsinogen synthesised by chief cells is stored in


granules near the apical pole of the cell
following stimulation the granules fuse with the membrane
and release their contents
the main regulator is ACh which acts by elevating Ca
CCk also acts through the same mechansim
secretin acts via adenylate cyclase
somatostatin can act to inhibit secretin induced stimulation

Ulcers

due to the breakdown of the gastric mucosal barrier


chemical agents (alcohol, aspirin)
stress
Helicobacter pylori
treat with antibiotics
antihistamines - cimetidine
H-K-ATPase antagonists (omeprazole)

Vomiting by numbers

1) diaphragm descends while the glottis remains closed leading


to negative intrathoracic & oesophageal pressure (retching)

2) 0.5s later stomach and LES relax andthe abdominal wall


muscles contract propelling the gastric contents through the LES

3) contraction of the oesophageal longitudinal muscle shortens


the oesophagus and the thoracic cage expands further lowering
pressure

4) gastric antrum contracts and the UES relaxes with expulsion of


vomit(us)

Gastric emptying

The pyloric sphincter remains partially open - enough to allow


water and other fluids to leave the stomach

intense antral peristaltic contractions forcing chyme through the


tonically contracted pylorus - the peristaltic waves provide a
pumping action - the so-called pyloric pump

in addition the tone of the pyloric sphincter itself can be


modulated by both humoral and neural signals

Gastric emptying 2

Rate of gastric emptying is determined by signals from the


stomach and the duodenum

stomach signals are either nervous signals cause by distension


or by gastrin

gastrin has stimulatory effects on motor functions of the


stomach as well as enhancing the pyloric pump

Enterogastric Reflexes

when food enters the duodenum multiple nervous reflexes are initiated from
the duodenal wall that pass back to the stomach to slow or stop stomach
emptying if the volume of chyme has become too great these go via either
enteric, extrinisic nerves or via the vagus and have 2 strong effects
1) inhibition of antral propulsive contractions
2) increase slightly the tone of the pyloric sphincter
factors that are continually monitored that can excite the enterogastric reflexes
are:
degree of distension of duodenum
irritation of the duodenum
degree of acidity of duodenum
osmolality of chyme
presence of breakdown products

Migrating Motor Complex

develops 4-5 hours after a meal and recurs every 90-120 min until food is
once more ingested
cycle consists of an inactive phase - followed by a brief phase ofintense
peristaltic activity which migrates along the intestine and may begin wither
in the proximal stomach or duodenum
a new complex starts whenever an earlier complex approaches the
terminal ileum
function of MMC is housekeeping - the means by which the residues (ie
indigestible and large particulate matter) are removed from the stomach
between meals
also helps to control bacterial growth in the small bowel- a common
consquence of bactrial overgrowth is steatorrhea which results from
maldigestion of dietary fat

Exocrine Pancreas

secretes about 2 l of fluid/day into duodenum via sphincter of Oddi


(secretion increases ~10x postprandially)

secretes digestive enzymes from the acini and an alkaline (HCO3


rich) juice from the ducts

alkaline juice serves to neutralise acid from stomach and to provide


the correct pH for enzyme activity

interestingly - pancreas contains no myoepithelial cells thus when


intraductal pressures rise acinar cells may rupture releasing digestive
enzymes into the interstitium leading to chronic pancreatitis (ie in CF
where ductal secretions are abnormally viscous)

Pancreatic enzymes

digestive enzymes secreted as inactive precursors (zymogens) to


prevent autodigestion

important proteolytic enzymes are trypsin, chymotrypsin and


carboxypeptidases
other enzymes are pancreatic lipase
pancreatic amylase

trypsinogen is activated by enteropeptidase which is secreted by


intestinal mucosa in response to chyme
trypsin then activates the other proenzymes
trypsin inhibitor secreted to delay activation of trypsinogen

Pancreatic fluid secretion

acini secrete a Cl- rich secretion similar to salivary glands


ducts secrete HCO3 (when insufficient alkalkine fluid is
produced for maximum enzyme activity is reduced leading
to malabsorption and malnutrition)
In CF there is chronic pancreatitis with reduced HCO3
because lipases and bile salts are sensitive to pH staetorrhea is a common problem in patients with CF
(insufficient alkali) or patients with gastrinomas who
secrete excess acid in the stomach

Pancreatic fluid secretion 2

HCO3 secretion is a secondary active transport process

CO2 diffuses in from the blood and is combined with water


by the enzme carbonic anhydrase (CA) to form HCO3 and
H+ - the H+ is exchanged for Na+ by the Na-H exchanger
using the Na+ gradient maintained by the Na+/K+ ATPase.
ie Na-H exchanger and ATPase keep on creating a
gradient for H+ to drive CA.

HCO3 leaves the cell via an apical Cl/HCO3 exchanger


with Cl recycling via a Cl channel

Stimuli of Pancreatic Secretion

ACh - parasympathic vagus nerves as well as myenteric


cholinergics
Gastrin - liberated during gastric phase of stomach
secretion
CCK (cholecystokinin) - secreted by duodenal and upper
jejunal mucosa when food enters small intestine

these 3 all stimulate production of digestive enzymes by


the acini and act via IP3 to release intracellular Ca

Secretin - same duodenal and upper jejunal mucosa but


secretin acts via cAMP on the ductal cells to increase
HCO3 secretion

Phases of pancreatic secretion

cephalic phase ~15% mainly causes secretion of enzymes into the


acini - vagus mediated

gastric phase ~15% gastric distension by means of vago-vagal


reflex evokes enzyme secretion
gastrin release by antral lumen causing more enzyme release

intestinal phase ~70% -pancreatic HCO3 secretion strongly


stimulated when duodenal pH is acid - S cells secrete secretin into
the blood and this stimluates pancreatic duct cells
chyme also causes I cells to release CCK which causes pancreatic
enzymes to be secreted (mainly due to peptones and fatty acids)

Liver and Bile

One main function of liver is to secrete bile (600-1200ml/day)

Bile has an important role in fat digestion and absorption


bile salts (which are cholesterol metabolites sythesised in
hepatocytes) emulsify large fat particles into minute particles
that can be attacked by lipases
also aid in the transport and absorption of the digested fat
products to and into the intestinal mucosa

bile serves as a means for excretion of several waste products


from the blood, especially bilirubin and the excess cholesterol
synthesised by the liver

Bile secretion

Bile is secreted in 2 stages by the liver

1) Bile is secreted initially by the hepatocytes and contains large


amounts of bile acids, cholesterol, lecithin etc and is secreted into
the bile canaliculi the lie between the hepatic cells in the hepatic
plates

2) The bile empties into the terminal bile ducts, the hepatic duct and
finally common bile duct - here the bile either empties directly into
the duodenum or is diverted through the cystic duct into the
gallbladder on its way through the duct a secondary secretion is added - a
watery solution of Na and HCO3

Enterohepatic circulation

Up to 94% of bile salts are reabsorbed by active transport in the


distal ilieum

they enter the portal blood and pass to the liver where they are
reabsorbed by the venous sinusoids

~20g of bile salts are required to digest & absorb 100g dietary fat
however the total amount of bile salts is ~5 g and only
0.5g /day is synthesised by the liver
the rest is due to recirculation (on average each bile salt
molecule recirculates 18 times before being lost in the faeces)

Bile salts

Bile salts are synthesised by hepatocytes from cholesterol (most


common are cholic, chenodeoxycholic and deoxycholic acids)
they are then conjugated to either glycine or taurine giving rise to
glycocholates and taurocholates this step makes a highly polar
molecule - the lipophilic steroid backbone and the hydrophilic amino
acid - these conjugates can then function as detergents.
cholesterol can be secreted into the bile at much higher
concentrations than it solubility in water would allow
since they are present at concentrations above the critical micellar
conc they spontaneously aggregate with fats to form micelles
the different bile salts have different pKas - to cope with the different
pHs encountered in the duodenum

Gallbladder

Bile is normally stored in the gallbladder until it is need in


the duodenum

The volume of the gallbladder is only 20-60 ml however it


can store up to 12 hours worth of bile secretion (~450 ml)

This is made possible because the gallbladder mucosa


absorb Na & Cl and osmotically removing the water
concentrating the other constituents - normally 5 fold but
can be as high as 20-fold

Emptying of gallbladder

food entering the duodenum causes galbladder to empty


three processes involved
- CCK induced rhythmic contractions of the gallbaldder
- CCK induced relaxation of the sphincter of Oddi
relaxation phase of peristaltic waves moving down the
duodenum also relax sphincter of Oddi
presence of fat is important in getting gallbladder to empty
secretin stimulates secretion of HCO3 rich juice from bile
ducts

Control of bile salt secretion by bile salts

in bile-salt dependent flow - (~40% of total flow) - bile salts are


extracted from the portal blood by a Na-bile salt cotransporter and
bound to a cytosolic protein which brings them to the apical
membrane where they are secreted by a Na-independent carrier thus it is a saturable process
bile-salt independent flow -(40%) - unknown mechanism depending
on the secretion of organic cations - this step is important for the
excretion of steroids
alkali secretion by bile duct epithelium - ~20%
as the concentration of bile salts in the plasma rises so does the
rate of bile salt secretion - the secretion rate being highest during
digestion when the levels of bile salts are highest

Haemoglobin breakdown

Haem is broken down to bilirubin by macrophages

bilirubin (yellow) is then absorbed by hepatocytes and conjugated with


glucoronic acid to form bilirubin glucorinide which is excreted into the
bile canaliculi

once in the intestine it is converted by bacteria to urobilinogen which is


highly water soluble - some is reabsorbed into the blood which is then
re-excreted into the gut by the liver

about 5% gets to the kidneys and is oxidesed to urobilin and gives


urine its yellow colour
in faeces it is oxidised to stercobilin

Jaundice

Jaundice (yellowish tint to the body) is due to large


quantities of bilirubin in extracellular fluids

1) haemolyitc jaundice - red blood cells are haemolysed


rapidly and hepatocytes cannot secrete faster than it is
formed leading to high plasma concentrations of bilirubin
(thalasseamia)

2) obstructive jaundice - the bile ducts are blocked by a


gallstone or a cancer or due to damage in hepatitis

Gallstones

when cholesterol precipitates in the gallbladder

amount of cholesterol in bile is in part determined by the amount of


dietary cholesterol - so people on a high fat diet are prone to
gallstones

inflammation of the gall bladder epithelium can lead to a chronic low


grade infection that alters the transport properties of the epithelium

treated by removal of gallbladder (cholecystectomy) or prolonged


treatment with chenodeoxycholic acid which is a natural bile acid

Small intestinal motility

postprandially the small intestine has several vital functions


- to mix food with digestive secretions
- to circulate chyme so that mucosal contact is maximal
- to propel contents in a net distal direction
- to clear residua left over from the digestive process
- to transport continuing secretions from the upper gut during fasting
regional motor specialisation of the small bowel
-jejunum (40% of small bowel) acts primarily as a mixing and conduit
segment
-ilieum (distal 60%) retains chyme until digestion and absorption are
complete
-terminal ileum and ileocolonic junction control emptying of contents into
the colon & minimise coloileal reflux

Small Intestine

major site of digestion and absorption of nutrients

divided into 3 segments

duodenum (20 cm)


jejunum (2.5 m)
illeum (3.6m)

Small intestinal motility 2

muscularis externa of the small intestine consists of 2


layers
thick inner layer of circular muscle and thin outer
longitudinal layer

there is a basal slow wave and when spikes are


superimposed rhythmic muscular contractions occur with
the same frequency as the slow waves

the slow waves have a higher frequency at the proximal


end (11/min) and only 8/min distally - this means that the
net movement of intestinal contents is in the direction of
the large intestine

Gastro-ileal reflex

the motor response of the terminal ilieum to feeding


chyme may remain in the terminal ilieum for several hours
until another meal is eaten when signals from the upper GIT intensify peristalsis in
the ilieum expels the remaining chyme.
as in the stomach - the presence of nutrients in the ilieum
exert a negative effect on jejunal motility and transit - the
ilieal brake
particularly in the case of fat and partially digested
carbohydrate
this prolongs the stay of chyme in the ilieum facilitating
absorption

Control of small intestine motility

poorly understood but both both extrinsic and intrinsic


nerves as well as humoral factors are involved

initiation and maintenance of postprandial motor patterns


requires an intact vagus

gastrin and CCK both enhance motility - gastrin relaxes


sphincter
secretin inhibits motility
NANC neurones may be important in relaxing sphincter

Fluid movement in intestine

intestinal membrane highly permeable to water

water therefore flows according to osmotic gradient

absorption movement of water and nutrients from gut to lymph


and blood

most nutrients absorbed by upper half of intestine

Fluid movement in intestine 2

brush border of small inestine greatly increases surface


area for absorption

main process is absorption of Na (and Cl)

Na can go via Na channels or Na-nutrient cotransporters

Na is then pumped into the blood by Na-K ATPase which


maintains a net gut>blood Na gradient

Cholera

crypt cells secrete Cl via cAMP Cl channels

CT modifies Gs so that it is always active

Gs then stimulates adenylate cyclase to produce cAMP

Cl is then secreted into the intestine

Na and osmotically obliged water then follow

Cholera 2

results in a huge flow of water into the intestines

secretory diarrhoea

initially fluid good to wash away bacteria

loss of 5-10l/day

treated by administration of NaCl

Carbohydrate digestion

pancreatic juices cannot further hydrolyse oligosaccharides

brush border oligosaccharidases


brush border lactase, sucrase-isomaltase and
maltaserelease monosaccharides (glucose, galactose and
fructose)

glucose and galactose taken up by SGLT1


fructose by GLUT5
all three transported via GLUT2 out into the portal vein and
to the liver

Lactose intolerance

lactose intolerance due to a defect in lactase enzyme

insufficient amounts of lactose are provided to the transporter


leading to poor absorption and subsequent build up of
osmotically active lactose
this in turn leads to a watery diarrhoea

Protein absorption

aminopeptidases in brush borders

peptides are broken down to individual amino acids (as well as


di & tripeptides) by oligopeptidases

reabsorption but gut cells similar to that of sugars


both Na-dependent and independent uptake pathways

Fat absorption

lipids- mainly triacylglycerols

1 - large oil droplets (shearing forces in gut)


2 - emulsified oil drops with bile salts

pancreatic lipase at oil-water interface

3 - formation of micelles

micellescome to the absorptive surface of gut monoglycerides and


free fatty acids are then absorbed

Fat absorption 2

inside cells resynthesis of triacylglycerols, cholesterol


and phospholipids to chylomicrons

secreted into lacteal and to systemic circulation

to adipose tissue where the chylomicron is stripped of its


triacylglycerols and chylomicron remnant goes to liver - dietary
cholesterol to liver

free fatty acids are also synthesised to prostaglandins


(can act as local gut hormones)

Coeliac disease

strong inflammatory reaction in intestinal mucosa

due to immune reaction to gluten products

results in atrophy of villi and disturbance of absorption

subsequent severe diahorrea

treat by elimination of gluten from diet

Motor functions of the colon

mixing the contents to promote absorption of water and


electrolytes
maintaining an appropriate intraluminal bacterial mass
transporting contents in a net distal direction
storing fecal material until defecation
rapid emptying of colonic contents during defecation

ceacum, ascending colon and rectum act as reservoirs for the


storage of feces

the rest (transverse, descending and sigmoid colon) acts to propel


the feces from the first to the second reservoir

Otot kolon

bundles of the outer longitudinal muscle are grouped into 3


thick bands- taeniae of the colon

Lapisan dalam berisi otot sirkulert

taniae are shorter than underlying circular muscle coat giving


rise to haustra

CFungsi usus besar / kolon

Absorbsi air & elektrolit ( sedikit villi)i

Sekresi HCO3 , untuk menyeimbangkan asam produksi bakeri

Mengasilkan mukus untuk pelumas feses

Bakteri kolon membantu pencernaan selulosa dan karbohidrat

Bacteria ~30%masa kering feses


methane and H2 dari diit produksi gas

Gerakan kolon

Frekwensi lrendah segmentasi pada kolon proksimal


Menempelnya feses pada mukosa usus
mass movements - a contraction wave passing over the
proximal colon driving contents into distal colon
3-4 times/day
usually followed by defecation
mass movement triggered by food in stomach - long
reflex gastrocolic reflex

Defecation

Massa feses bergerak meneuju rektum

defecation reflex mulai dengan regangan

Refleks panjang dan pendek

l sphincter anus dapat dikontrol secara sadar l

Gerakan otot terkordinasi