FISIOLOGI PENCERNAAN

dr. Rhiza Mohammad Ishaq Sobari

Dept. Physiology
1. JELASKAN MEKANISME ABSORPSI MAKANAN
DI USUS HALUS DAN USUS BESAR
(KARBOHIDRAT,LEMAK,ASAM
AMINO,ION,DAN AIR)?
2. BAGAIMANAKAH PENGATURAN SALURAN
PENCERNAAN,JELASKAN?
3. APA ITU PERISTALTIK,JELASKAN ?
4. JELASKAN MEKANISME PERJALANAN
MAKANAN DI SALURAN CERNA?
 CopyrightThe McGraw-Hill Companies, Inc. Permission required for reproduction or display.

AREA ABDOMEN DIBAGI 9 region.

 FUNGSI TGI
 Fungsi umum: memindahkan zat nutrien, air dan
garam dari zat makanan ke lingkungan dalam untuk
didistribusikan ke sel-sel melalui sistem sirkulasi
(fx zat makanan: energi, pembangun, pengganti sel
rusak)
Fungsi eksresi hanya funsi kecil sistem pencernaan (fx
eksresi tu oleh paru dan ginjal)
 KEGIATAN DASAR TGI
Fungsi TGI merupakan rangkaian terintegrasi dari beberapa
kegiatan:
1. Gerakan (Motility): gerakan mencampur, mengaduk dan
mendorong isi lumen ok adanya kontraksi otot polos
dinding TGI.
• Gerakan mendorong (propulsif),merupakan gerakan
mendorong isi lumen ke depan dengan berbagai
kecepatan tidak sama sesuai fungsi tiap segmen
• Gerakan mencampur ada 2
–Mencampur dengan getah pencernaan untuk membantu pencernaan
–Mendekatkan seluruh isi lumen ke permukaan TGI untuk
mempermudah penyerapan)
2. Pencernaan (digestion) – proses pemecahan
secara mekanik maupun kimia molekul-molekul
besar yang masuk TGI menjadi molekul kecil shg
dapat diabsorbsi epitel sal cerna
– mechanical breakdown by chewing
– chemical breakdown by HCl and digestive enzymes

3. Sekresi (secretion) –sekresi air, elektrolit, enzim, liur

empedu, mukus ke saluran pencernaan
4. Absorbsi (absorption) – proses penyerapan/
pemindahan molekul hasil pencernaan (zat
nutrien organik/anorganik, air ) dari lumen TGI
menembus dinding usus untuk masuk ke
pembuluh darah atau limfe
• passive diffusion and active transport
5. Ekskresi- Eliminasi makanan yang tidak dapat
dicerna dan produk sisa dikeluarkan dari tubuh.
 BAGIAN UTAMA SISTEM
PENCERNAAN
 saluran gastrointestinal (GIT)
Mulut, faring, esofagus, lambung, usus halus, usus
besar, rektum, anus
Organ-organ kelenjar terkait
Kelenjar saliva, hati, kandung empedu dan pankreas
 Figure 15-3

Many functions in the

gut are found in specific
locations along its
length. Most of the
absorption of nutrients
occurs in the small
intestine, so most of
digestion is
accomplished there or
upstream.
 STRUKTUR UMUM TGI
 Panjang 4,5 m (dewasa)
 Permukaan biasanya tidak datar / licin tapi berkelok-
kelok, menambah luas permukaan absorbsi
 Struktur jaringan berbeda tetapi mirip
4 Lapisan GIT
Figure 15-6
nutrients

The gut wall has a layered organization, with the absorptive cells lining
the lumen and neural and muscular components below. Blood and
lymph vasculature is abundant to transport absorbed nutrients.
 1. Mukosa
• Mulai dari lambung
• Mukosa : sel epitel : sekresi mukus & hormon
• Invaginasi jaringan epitel kedalamnya membentuk
kelenjar eksokrin
• Kelenjar eksokrin : sekresi asam, enzim, ion-ion
kedalam lumen
• Di bawah lapisan epitel: Lamina Propia, Jaringan ikat
: dilalui pembuluh darah kecil, serat saraf & saluran
limfe
• Lamina propria dipisahkan jaringan ikat di bawahnya
oleh suatu lapisan tipis otot polos yaitu muskularis
mukosa
 2. Sub Mukosa
• Jaringan ikat kedua di bawahnya
• Lapisan ini dilalui pembuluh darah & limfe lebih
besar, cabangnya menembus lapisan mukosa di atas
& lapisan otot di bawahnya
• Terdapat jala saraf disebut pleksus sub mukosa (
meissner)
 3. Muskularis Eksterna
• Jaringan otot polos
• Kontraksinya menimbulkan gaya mendorong &
memindahkan isi saluran GI
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
• Diantara kedua otot polos terdapat pleksus saraf lain
yang lebih eksentif yaitu:
Pleksus mienterikus (AUERBACH)

• Kesemuanya (dengan Pleksus sub mukosa dan Neuron

lain di Saluran GI) membentuk sistem saraf enterik yang
mengendalikan keaktifan motorik dan sekretorik
(pemototngan simpatis dan parasimpatis tdk
menghilangakan aktivitas motorik dan sekretorik)
 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
 Pengaturan fungsi pencernaan
 Bersifat kompleks dan sinergis.
 Tersedia lingkungan yang optimal untuk perncernaan dan
absorbsi, sehingga perlu pengendalian sekresi kelnjar dan
kontrakasi otot
 Tidak banyak dipengaruhi keadaan nutrisi tubuh tapi sangat
dipengaruhi volume dan komposisi kandungan lumen TGI
 Banyak reseptor yang mendeteksi keadaan lingkuangan lumen
• Refleks yang ada di TGI umumnya dirangsang
oleh:
– Regangan dinding oleh isi lumen
– Osmolaritas kimus (konsentrasi zat terlarut)
– Keasaman kimus (konsentrasi ion H)
– Hasil pencernaan KH, L, P (monosakarida, asam
lemak, peptida, asam amino)
• Rangsang diterima reseptor → aferen →
pengolahan → eferen → efektor (lapisan otot
TGI dan kelj eksokrin)
Figure 15-13

The enteric nervous system coordinates digestion,

secretion, and motility to optimize nutrient absorption.
Its activity is modified by information from the CNS
and from local chemical and mechanical sensors.
1. Neural controls
 Saraf Extrinsic (3) : Berasal dari luar TGI, cabang
saraf otonom, Fungsi otonom otot polos:Irama listrik
dasar saluran pencernaan.
1) Sympathetic
2) Parasympathetic
3) Somatic
 Saraf Intrinsic (2): Kemampuan mengatur dirinya
sendiri, Langsung pengaruhi motilitas, sekresi getah
pencernaan, hormon pencernaan
1) Myenteric plexus
2) Submucosal plexus

 SNS and PNS modulate the enteric nervous system

as opposed to directly controlling smooth muscle of
bowel
mekanoreseptor, osmoreseptor yang akan memicu
refleks saraf atau sekresi hormon
Terdapat refleks pendek (sekresi hormon yg
dipengaruhi saraf intrinsik) dan Refleks panjang bila
yang terlibat jalur saraf otonom
1. Mekanisme neural (pengaturan saraf)
– Neuron sensoris & interneuron pada pleksus mienterikus
tanggap thd reflek lokal, ini disebut reflek pendek,
mengatur aktivitas satu daerah sal cerna: peristaltik lokal,
sekresi kel digestif
– Neuron motoris pada pleksus meinterikus mengatur
kontraksi otot polos dan sekresi kelenjar
– Informasi sensoris dari reseptor jg dilanjutkan ke SSP yg
menghasilkan refleks panjang: kontrol tingkat tinggi sal
cerna & kelj. Neuron motoris: saraf IX, X, saraf pelvikus
– Dapat dipengaruhi hormon digestif
2. Mekanisme hormonal:
– Paling sedikit 18 hormon
– Hormon ini mempengaruhi semua aspek fungsi
digestif dan sistem yg lain
– Peptid yg dihasilkan sel neuroendokrin yg
didistribusikan melalui sirkulasi
– Masing-masing hormon mempunyai organ
target
Terutama respon terhadap lokal spesifik isi
lumen yg bekerja langsung pada sel endokrin
atau tak langsung mll plesus intrinsik dan
ekstrinsik
CCK :
Cholecytokinin

GIP:
Gluc-dep. Insulino-
Tropic peptide

Each hormone:

Feedback
Multiple Targets
3. Mekanisme lokal:
– Prostaglandin, histamin, dan bahan kimia lain yg
dilepaskan ke cairan interstitial dapat
berpengaruh pada sel sekitar
– Mesenger lokal ini penting dalam kordinasi
tanggap terhadap perubahan pH lokal, rangsang
fisik atau kimia lain.
 FASE-FASE PENGENDALIAN TGI
Pengendalian neural, hormonal dan lokal pada
garis besarnya dibagi mjd 3 fase berdasar
rangsang yang memulai:
1.Fase sefalik: rangsang reseptor di kepala:
penglihatan, penghidu, pengecapan, mengunyah,
keadaan emosi
jalur eferen nya melibatkan saraf parasimpatis dan
simpatis, kmdn mengaktifkan saraf enterik dan
pengaruhi sekresi dan kontraksi
2. Fase gastrik:
Rangsang dari lambung: peregangan, asam,
peptide.
3. Fase intestinal
Rangsang dari dalam usus halus: peregangan, keasaman,
osmolaritas, berbagai hasil pencernaan

Fase ini tdk berlangsung berurutan kecuali pada

permulaan makan
 Gerakan TGI

• Otot polos saluran cerna menunjukkan siklus

ritmik yang disebabkan adanya pacesetter
cells dalam muskularis mukosa dan muskularis
eksterna
• Kontraksi terkoordinasi dari muskularis
eksterna penting dalam pergerakan makanan
dalam sal cerna mll peristaltik dan segmentasi
• Peristaltik/propulsif:
– Kontraksi otot bergelombang yang memindahkan
bolus sepanjang sal cerna
– Manifestasi 2 reflek utama dalam sistem saraf
enterik dirangsang oleh adanya bolus dalam
lumen usus
– Bolus  distensi mekanik & iritasi mukosa usus
rangsang neuron enterik aferen sinap:
• Interneuron yg mengandung asetilkolin dan substansi P
rangsang kontraksi otot polos di atas bolus
• Interneuron yg mengandung nitrik oksid, vasoaktif
intestinal peptid dan ATP rangsang relaksasi otot polos
di bawah bolus
 Peristalsis
• Bolus of food →Mechanical
distension and mucosal irritation
→ stimulates afferent enteric
neurons → 2 effects
1. Excitatory motor neurons above
the bolus activated →
contraction of smooth muscle
above the bolus
• Via Ach, substance P
2. Inhibitory motor neurons →
stimulate relaxation of smooth
muscle below the bolus
• Via nitric oxide, vasoactive
intestinal peptide and ATP
• Segmentasi :
– Usus halus dan usus besar
– Mengocok dan membuat fragmen dari bolus
untuk mencapur dengan sekresi usus
Perjalanan makanan

1. Digesi pregastrik
2. Lambung
3. Usus halus
4. Usus besar
 Digesi pregastrik:
Pengendalian makan, prehensi, mastikasi,
menelan

1. Pengendalian makan
 Tubuh dalam keadaan status lapar, kemudian
menghilang dengan adanya makanan dalam sal
cerna, aliran nutrisi ke dalam darah & faktor lain.
 Keseimbangan ini dipengaruhi:
a. Peranan susunan saraf pusat:
Pusat pengendalian makan terletak pada:
• Hipotalamus lateral : pusat lapar
(lesianoreksilost weight)
• Hipotalamus ventromedial : pusat kenyang
(lesiover eatobese)
b. Faktor pregastrik
 Penampilan makanan
 Rasa, bau makanan
 Pengalaman kesukaan dan penolakan
terhadap makanan
 Faktor psikologis: ketakutan, depresi dan
interaksi sosial
c. Faktor gastrointestinal dan pascaabsorptif
• Penuhnya lambung dan usus
– Derajat pengisian lambung dan usus halus melalui
saraf vagus ke hipotalamus kenyang
– keluarnya kolesistokininkenyang

• Kadar nutrien seperti glukosa dan asam amino

akan berpengaruh terhasap kadar
kolesistokinin, insulin, glukagon kenyang
 MAKAN = FEEDING

FISIOLOGIS
• Diatur oleh otak
• Stimuli adequat saluran
cerna
• Mekanisme mengontrol
keseimbangan energi
PSIKOLOGIS
• Motivasi makanan
• Kesenangan makanan
• Hambatan budaya terhadap
makanan

INGESTI – FOOD INTAKE

LAPAR (HUNGER) Makanan

SELERA (APPETIK) Kualitas

KENYANG (SATIETY)
 PUSAT PENGATUR FOOD INTAKE

1. Nc. Lateral Hipothalamus

a.Stimuli, makan terus >> menyebabkan obesitas
b.Dextruksi, inanisi (kurang nafsu makan)
Maka Nc. Lateralis yang merupakan pusat lapar
menjadi hunger center dan feeding center
2. Nc. Ventromedial Hypothalamus
a.Stimuli, merasa kenyang, inanisi
b.Dextruksi, makan terus >> menyebabkan obesitas
Maka sebagai pusat kenyang
 PUSAT LAIN YANG BERHUBUNGAN DENGAN
PROSES MAKAN
1. Medulla Oblongata
- Aktivitas makan : salivasi, mastikasi,
deglutisi
2. Nc. Amygdala
- Stimuli, aktivitas mekanik
- Dextruksi, meningkatnya produksi makan,
menurunnya makan dan buta dalam memilih
3. Kortex sistim limbik
- stimuli, meningkatnya produksi makanan
atau menurunnya produksi makan serta
dorongan mencari makanan bila lapar
 Fc. YANG MENGATUR FOOD INTAKE

1. REGULASI NUTRITIONAL (Regulasi Jangka Panjang)

- Mengatur setiap persediaan nutrient tersebut
- Persediaan menurun maka stimuli cepat lapar
- Persediaan meningkat maka lapar hilang dan
kenyang
- Fc. Nutritional yang berhubungan dengan pusat
lapar yaitu glucosa, asam amino dan lemak
- Fc. Nutritional yang berhubungan dengan suhu
yaitu jika dingin maka nafsu makan bertambahnya
sedangkan suhu panas maka makan berkurang

Maka ada hubungan pusat regulasi suhu dengan pusat food intake
2. REGULASI ALIMENTER
- Regulasi non-metabolit
- Regulasi jangka pendek
- Berhubungan dengan saluran pencernaan
- Lambung dan duodenum penuh sehingga inhibisi
pusat lapar yang mengakibatkan hasrat makan
menurun
- Stimuli melalui N X (cholecystokinin)

Ket. Fc. Penghambat yaitu Gastric Inhibitary Peptida

Mucosa usus halus
 PSIKOLOGIK KULTURAL SOSIAL

KORTEKS CEREBRAL

KELAPARAN
PUSAT KEPUASAAN
(SATIETY CENTER) PUSAT MAKAN
Nc. VENTROMEDIAL
(FEEDING CENTER)
Hypothalamus
Ventrolateral
1. Pengisian Lambung
2. Perbedaan besar glucosa
dalam sistem artesiovenous
3. Amphetamine
Kontrol pemasukan makanan
– Hipotalamus
• Terdapat pusat lapar (lateral) dan pusat kenyang
(ventromedial)
• Banyak faktor yang mempengaruhi kedua pusat
tersebut
– Kontrol pemasukan makanan jangka pendek
integrasi banyak masukan yang memberitahu
status energi
Faktor yang berpenaruh dalam kontrol masukan makanan

1. Ukuran simpanan lemak

• Teori lipostatik : pe ↑ simpanan lemak di jar
adiposa memberi sinyal rasa kenyang
• Kontrol jangka panjang→ BB konstan
• gliserol dalam darah (indikator jumlah total lemak
trigliserida dalam jar lemak) memberi sinyal
kenyang
• Persentasi pingisian tiap sel lemak (gemuk sel
lemak banyak)
2. Tingkat distensi saluran pencernaan
– Kontrol jangka pendek
– Kosong/penuh TGI memberi sinyal lapar/kenyang
– Stimulasi reseptor regang di lambung menekan pemasukan
makanan
– Lebih ke arah pengosongan lambung, (pengaruh kontrol ke
pemasukan makanan sedikit)
3. Tingkat pemakaian glukosa
– Teori glukostatik : kenyang krn sinyal yang
ditimbulkan oleh pe ↑ penggunaan glukosa oleh
sel
– Peningkatan sekresi insulin (menyertai kelebihan
nutrien dan mendorong penggunanan glukosa)
memberi sinyal kenyang
4. Intensistas produksi kekuatan sel
– Teori iskimetrik: sinyak untuk kontrol Jangka
pendek pemasukan makanan bukan defisit atau
surplus salah satu nutrien (ex glukosa) tapi
berkaiatan besarnya produksi tenaga sel (ATP)
– Perubahan ketersediaan nutrien dapat
menyebabkan perubahan kecepatan pertukaran
ATP/ADP: rendah → lapar, tinggi → kenyang
5. Tingkat sekresi kolesistokinin
– Hormon saluran pencernaan yang dikeluarkan oleh
mukosa duodenum Sinyal rasa kenyang
– Kolesistokinin dikeluarkan sebagai respon adanya
makanan pada usus halus
6. Pengaruh neurotransmiter
– Norepineprin dan neuro peptida Y:
me↑konsumsi karbohidrat
– Dopamin serotonin menekan konsumsi
karbohidrat
7. Pengaruh psikososial
– Sinyal involunter
– Makan bukan karena lapar atau berhenti karena
kenyang
– Makan harus 3 kali sehari
– Makan untuk hiburan, bisnis
– Makan karena kenikmatan
– Tidak makan karena stres, cemas, depresi, rasa
bosan
2. Proses prehensi:
Proses memasukan makanan ke dalam mulut
3. Proses mastikasi/mengunyah
 Mengunyah : pemecahan partikel besar menjadi
kecil yang dapat ditelan tanpa menimbulkan rasa
tercekik
 Tujuan mengunyah:
 menghancurkan makanan (mekanik)
 saliva melicinkan dan membasahi makanan yang
kering, mencapur makanan merata dengan zat yang
ada dalam saliva,
 Stimulasi aferen fase sefalik pencernaan
 Membentuk bolus
• Melibatkan neuromuskular dan kelenjar saliva
• Makanan hasil proses mengunyah disebut
bolus
• Mengunyah merupakan tindakan ritmis, kontrol
oleh saraf somatik yang dikendalikan secara
sadar (volunter), juga refleks karena tekanan
makanan pada gusi
 Kelenjar saliva
• Sekresi mukus ke dalam mulut
• Fungsi membasahi & melumas partikel
makanan sebelum di telan
• Disekresi 3 kelenjar eksokrin
a. Parotis:25 %
b. Submandibularis:70%
c. Sublingualis:5%
• Jumlah sekresi saliva / hari 1500 cc :99,5% air, 0,5%
protein & elektrolit:
a. enzim pencernaan
1. Lipase lingual : di sekresi kel. Ebner lidah,
Aktif di lambung dan dpt mencerna 30%
lemak makanan
2. Ptialin/amilase saliva ( di sekresi kel.
Saliva), Mencerna tepung, ph optimal 6,7,
Dihambat asam lambung
b. Bahan Anorganik saliva: Na, K, Cl, bikarbonat
c. Bahan organik lain (glikoprotein) dalam saliva:
musin, jika bercampur air membentuk larutan
kental (viskous) yaitu mukus
d. Antibodi (IgA)+lysozim: kontrolpopulasi bakteri
oral
– Fungsi saliva
• Membasahi dan melembutkan makanan,
memudahkan proses menelan
• Membasahi mulut, membantu proses bicara
• Melarutkan molekul yang merangsang reseptor
kecap
• Memulai pencernaan karbohidrat
• Anti bakteri
• Mempertahankan Ph mulut ( 7,0)
• Mengandung hormon: epidermal growth faktor,
nerve growth faktor, somastotatin, bradikinin
Also, dissolve molecules for Taste
(and woundhealing)
• Pengendalian sekresi saliva, kontinue melalui saraf
otonom. Pusat saliva di medula oblongata
– Refleks tidak bersyarat/sederhana: dari
lidah/mulut dan esofagus/lambung/usus halus
atas
– Refleks bersyarat/didapat: tanpa rangsang oral,
tp dari korteks serebri (melihat, mendengar,
memikirkan makanan)
Rangsang parasimpatis: encer volume besar
Rangsang simpatis: vol kecil, byk bahan organik
4. Proses menelan
 Proses komplek saraf volunter dan involunter
dan sistem otot
 menelan merupakan refleks yang ditimbulkan
oleh perangsangan reseptor dinding faring oleh
bolus, aferen: N. V, VII, XII, eferen N X, efektor
otot esofagus
– closely coordinated with breathing and
associated activities (i.e. talking)
• Fase menelan:
1. Fase oral: tindakan volunter, bolus didorong ke
orofaring oleh lidah, rangsang reseptor taktil sp
ke batang otak, yang memulai reflek menelan
2. Fase faringeal: kurang dari 1 detik, selama fase
faringeal pernafasan dihambat secara refleks
(lumen laring menutup, epiglotis berputar
kearah belakang untuk menutup laring, laring
terangkat kedepan shg lubang esofagus melebar
(involunter),
3. Fase esofageal: lidah menekan ke arah
belakang, kontraksi peristaltik faring, bolus
terdorong ke esofagus (involunter)
fase faringeal
• palatum molle keatas
• lipatan palatopharyngeal ke medial
(mencegah refluks makanan ke nasofaring)
• pita suara berdekatan
• seluruh larynx didorong ke atas depan ke
arah epiglotis, epiglotis berputar ke
belakang menutupi laring, mencegah bolus
masuk trachea & meregangkan pintu
oesophagus (spinter esophangeal atas
melemas)
5. saat larynx terangkat & spinter esophangeal
melemas), m.konstr. faring superior
kontraksi kuat mendororng bolus jauh ke
dalam faring
setelah bolus melewati SEA, SEA menutup
→ mulai gelombang peristaltik berjalan
sepanjang esofagus
 Main functions of swallowing

– to transport the food bolus from the pharynx into the

stomach
– to prevent esophagopharyngeal reflux and
gastroesophagal reflux
 Figure 15-14

The swallowing reflex is coordinated by the medulla oblongata,

which stimulates the appropriate sequence of contraction and
relaxation in the participating skeletal muscle, sphincters, and
smooth muscle groups. Add: Chewing reflex
FOREGUT: Conduction and Storage of Food in Humans
• Esofagus manusia:
– 1/3 atas: otot rangka, 2/3 bawag otot polos
– Panjang 25 cm
– Istirahat sfingter esofagus atas dan bawah
tertutup, kontraksi secara tonik untuk cegah
refluks dari lambung
• Muntah:
– rasa tidak enak yang disebabkan
pengosongan lambung secara berlawanan,
isi TGI keluar melewati mulut.
– Penyebab muntah karena di TGI:
• Iritasi kuat: toksin bakteri, alkohol,
• Peregangan berlebihan
• Perangsangan berlebihan ex, makanan sgt
berbumbu
Aferen: N vagus dan simpatikus ke pusat
muntah di medula oblongata
• Muntah karena perangsangan
chemoreceptor trigger zone oleh obat,
motion sickness
• Muntah karena perangsangan otak diluar
pusat muntah oleh rangsang listrik, obat
(morfin, derivat digitalis)
• Mekanisme?
 Obat-obat : Morphin, Digitalis
Motion Sickness

Chemoreceptor
Trigger Zone

Pusat Muntah
Vagal
off
Vagal afferent
Sympahic
off

* - Psikis, Gelisah, Bau Pusat Muntah

 MEKANISME MUNTAH

Bernafas dalam larynx mendorong sampai

Oesopaghus terbuka menutup glotis
palatum mole menutup nases post
Kontraksi kuat otot abdomen dan diafragma
memeras lambung kemudian tekanan intragastrik
meningkat sehingga isi lambung keluar melalui
oesophagus
 LAMBUNG / GASTER
• Kantung muskuler terletak antara esofagus & usus
• Lambung penuh: 1-1,5 L
• Bagian korpus & fundus (berdinding tipis), Kelj.nya
sekresi mukus, asam HCL, proenzim pepsinogen, faktor
instrinsik (castle)
• Bagian bawah lambung (antrum) mempunyai otot
lebih tebal, Kelj.nya sekresi hormon gastrin
Figure 15-16

Specialized cells
in the stomach
synthesize and
secrete mucous
fluid, enzyme
precursors,
hydrochloric acid,
and hormones.

The abundant smooth muscle in the

stomach is responsible for gastric motility.
• Sel epitel lambung tda sel mukus yg
mensekresi mukus yg kaya bikarbonat.
• Mukus (abar bikarbonat-mukosa) berfungsi
melapisi dan melicinkan permukaan
lambung, penting dalam melindungi epitel
dari asam, pepsin dan kimia lain
• Zat yang dapat merusak abar: etanol, cuka,
garam empedu, aspirin, OAINS
• Sekresi di lambung
a.pada fundus & korpus:
1. sel parietal : sekresi HCL, faktor intrinsik
(merangsang absorbsi vit B12)
2. sel chief : sekresi pepsinogen (proenzim
inaktif, oleh asam lambung diubah menjadi
pepsin suatu enzim proteolotik aktif),
Pada bayi mensekresi renin/khimosin
(menggumpalkan susu) & lipase gastrik (mulai
pencernaan lemak dlm susu)
b. Pada antrum & pylorus:
1. Sel G: sekresi hormon gastrin yg meransang
sekresi sel parietal dan sel chief, rangsang
sekresi dinding lambung (mencapur &
mengaduk isi lambung)
2. Sel D: sekresi hormon somatostatin yg
menghambat sekresi gastrin
Figure 15-17

Chief cells synthesize

and secrete the protease
precursor known as
pepsinogen.
Parietal cells synthesize and secrete the hydrochloric acid
responsible for the acidic pH in the gastric lumen.
lambung
• Fungsi lambung
– Menyimpan, melarutkan & mencerna parsial
makanan yang masuk lambung.
– Meneruskan makanan ke usus dalam jumlah
optimal untuk di absorbsi secara maksimal
– Sekresi HCl
– Sekresi enzim pepsinogen yang memulai
pencernaan protein
– Produksi faktor intrinsik yang dibutuhkan untuk
absorbsi vitamin B12
– Menghasilkan kimus (campuran kental)
• HCl lambung
– Memusnahkan bakteri yang masuk lambung ( tidak
efektif 100%)
– Memecah partikel makanan (membantu memecah
dinding sel tumbuhan dan jar ikat pada daging),
– Membentuk larutan molekul yang disebut KIMUS
– Aktivasi pepsin
– Sehari sekitar 2 L
Figure 15-18

Acid production by the parietal cells in the stomach

depends on the generation of carbonic acid;
subsequent movement of hydrogen ions into the
gastric lumen results from primary active transport.
1. Carbon dioxide (CO2) diffuses
into the cell.
2. CO2 is combined with water
(H2O) in an enzymatic reaction
Blood
that is catalyzed by carbon Parietal cell
vessel
anhydrase (CA) to form CI–
carbonic acid (H2CO3).
3. Carbonic acid dissociates 6
into a bicarbonate ion HCO– 3 HCO–
4
3
3 CI–
(HCO–3) and a hydrogen ion
(H+). 2 CA H2CO3 H+
4. HCO–3 is transported back CO2 + H2O ATP 5 H+
into the bloodstream. An ADP
1 Duct of
anion exchange molecule
CO2 gastric
in the plasma membrane
gland
exchanges HCO–3 for a K+ 7
K+
chloride ion (Cl–) (counter
transport).
To stomach
5. The hydrogen ion (H+) is
Serosal
actively transported into the
surface
duct of gastric gland. K+
6. Chloride ions (Cl–) diffuse
with the charged hydrogen
ions.
7. Some potassium (K+) are
counter transported into the cell
in exchange for the hydrogen
ions.
 Blood
vessel
Parietal cell

CO2

CO2

To stomach
Serosal
surface

Carbon dioxide (CO2) diffuses into the cell.

 Parietal cell

CA H2CO3
CO2 + H2O

To stomach

CO2 is combined with water (H2O) in an enzymatic reaction that is

catalyzed by carbon anhydrase (CA) to form carbonic acid (H2CO3).
 Parietal cell

HCO–3

H2CO3 H+

To stomach

Carbonic acid dissociates into a bicarbonate ion (HCO–3) and a

hydrogen ion (H+).
 Blood
vessel
Parietal cell
CI–

HCO–3 HCO–3 CI–

To stomach
Serosal
surface

HCO–3 is transported back into the bloodstream. An anion

exchange molecule in the plasma membrane exchanges HCO–3
for a chloride ion (Cl–) (counter transport).
 Parietal cell

H+
ATP H+
ADP Duct of
gastric
gland

To stomach

The hydrogen ion (H+) is actively transported into the duct of

gastric gland.
 Parietal cell
CI–

CI–
H+
ATP H+
ADP Duct of
gastric
gland

To stomach

Chloride ions (Cl–) diffuse with the charged hydrogen ions.

 Parietal cell
CI–

CI–
H+
ATP H+
ADP Duct of
gastric
K+ +
gland
K

To stomach
Serosal
K+ surface

Some potassium (K+) are counter transported into the cell in

exchange for the hydrogen ions.
• Setalah makan, sekresi HCL naik, kadar
bikarbonat darah yang berasal dari lambung
naik, pH darah dan pH urin naik (postprandial
alkaline tide)
• Sekresi asam HCL dirangsang oleh: histamin,
asetilkolin, gastrin
Figure 15-19

One inhibitory and

three stimulatory
signals that alter
acid secretion by
parietal cells
in the stomach.

FOOD
Figure 15-21
The acidity in the gastric lumen converts the protease
precursor pepsinogen to pepsin; subsequent conversions
occur quickly as a result of pepsin’s protease activity.

FOOD
 Pengendalian sekresi lambung

1. Mekanisme saraf: refleks pendek, refleks

panjang) melibatkan neuron kolinergik,
merangsang sekresi HCL, pepsin, mukus
2. Mekanisme hormonal: gastrin rangsang sekresi
HCL, pepsin, dan pertumbuhan mukosa
lambung
3. Mekanisme lokal: alkohol dan kafein langsung
merangsang mukosa, meningkatkan sekresi
lambung
• Pengaturan aktivitas (motilitas & sekresi) lambung diuraiakan
dalam 3 fase:
1. Fase sefalik: respon melalui parasimpatis & N vagus
yang diinduksi keaktifan di SSP.
rangsang: makanan dalam mulut, rangsang visual,
penghidu, pikiran
Status emosi dpt rangsang/hambat fase ini (marah
meningakt, stress, cemas menurun)
2. Fase gastrik: respon melalui refleks lokal. Rangsang:
makanan dalam lambung: regangan, kimia t.u. asam
amino dan hasil cerna protein lain,kafein,alkohol
3. Fase intestinal:rangsang di duodenum-produk
pencernaan protein
Figure 15-20

Local and distant

(CNS) information
modulates the
Enteric Nervous
System’s activity
regarding gastric
motility and secretion.
Cephalic Phase
1. The taste or smell of food, tactile
sensations of food in the mouth, or
Taste or smell of food
even thoughts of food stimulate the
Tactile sensation in mouth
medulla oblongata (green arrow).

2. Parasympathetic action potentials

are carried by the vagus nerves to
the stomach (pink arrow).
Medulla oblongata
3. Preganglionic parasympathetic 1
vagus nerve fibers stimulate
postganglionic neurons in the enteric 5
plexus of the stomach. Secretions
stimulated
Vagus nerves
4. Postganglionic neurons stimulate 2 3
secretion by parietal and chief cells
and stimulate gastrin secretion by 4
Gastrin
endocrine cells.
Circulation

5. Gastrin is carried through the

circulation back to the stomach
(purple arrow), where it stimulates Stomach
secretion by parietal and chief cells.
 Cephalic Phase

Taste or smell of food

Tactile sensation in mouth

Medulla oblongata

The taste or smell of food, tactile sensations of food in the mouth, or

even thoughts of food stimulate the medulla oblongata (green arrow).
 Cephalic Phase

Vagus nerves

Parasympathetic action potentials are carried by the vagus

nerves to the stomach (pink arrow).
 Cephalic Phase

Vagus nerves

Preganglionic parasympathetic vagus nerve fibers stimulate

postganglionic neurons in the enteric plexus of the stomach.
 Cephalic Phase

Gastrin

Stomach

Postganglionic neurons stimulate secretion by parietal and chief

cells and stimulate gastrin secretion by endocrine cells.
 Cephalic Phase

Secretions
stimulated

Gastrin
Circulation

Gastrin is carried through the circulation back to the stomach (purple

arrow), where it stimulates secretion by parietal and chief cells.
 Medulla Vagus nerves
oblongata

1
Gastric Phase Secretions
stimulated
1. Distention of the stomach activates a
parasympathetic reflex. Action potentials 2 Distention
are carried by the vagus nerves to the
medulla oblongata (green arrow).

2. The medulla oblongata stimulates stomach

secretions (pink arrow). 3 Local reflexes
stimulated by
3. Distention of the stomach also activates stomach
local reflexes that increase stomach distention
secretions (purple arrow).
Stomach
 Gastric Phase

Medulla Vagus nerves

oblongata

Distention

Local reflexes
stimulated by
Stomach
stomach distention

Distention of the stomach activates a parasympathetic reflex.

Action potentials are carried by the vagus nerves to the medulla
oblongata (green arrow).
 Gastric Phase

Vagus nerves

Secretions
stimulated
Decreased
gastric
secretions

Stomach

The medulla oblongata stimulates stomach secretions (pink arrow).

 Gastric Phase

Distention

Local reflexes
Stomach stimulated by
stomach distention

Distention of the stomach also activates local reflexes that

increase stomach secretions (purple arrow).
Figure 15-24

Delivery of acid and nutrients into the small intestine initiates

signaling that slows gastric motility and secretion, utilizing
neural communication and endocrine signals known as the
enterogastrones; this slowdown in delivery helps to allow
adequate time for digestion and absorption in the duodenum.
Intestinal Phase
1. Chyme in the duodenum with Vagus
a pH less than 2 or containing nerves
fat digestion products (lipids)
inhibits gastric secretions by
three mechanisms.

Medulla oblongata
2. Sensory vagal action potentials Decreased
to the medulla oblongata Vagus gastric
(green arrow) inhibit motor nerves secretions
action potentials from the
medulla oblongata (pink arrow). 2 Local
1 reflexes
pH<2 3
3. Local reflexes inhibit gastric or lipids
secretion (orange arrows).

4. Secretin, gastric inhibitory Secretin, gastric inhibitory

polypeptide, and cholecystokinin
4
peptide, cholecystokinin
produced by the duodenum Circulation
(brown arrows) inhibit gastric
secretions in the stomach.
 Intestinal Phase

pH<2
or lipids

Chyme in the duodenum with a pH less than 2 or containing

fat digestion products (lipids) inhibits gastric secretions by
three mechanisms.
 Intestinal Phase

Mechanism One
Vagus
nerves

Medulla
oblongata Decreased
gastric
Vagus secretions
nerves

pH<2
or lipids

Sensory vagal action potentials to the medulla oblongata (green

arrow) inhibit motor action potentials from the medulla oblongata
(pink arrow).
 Intestinal Phase

Mechanism Two

Decreased
gastric
secretions

Local
reflexes
pH<2
or lipids

Local reflexes inhibit gastric secretion (orange arrows).

 Intestinal Phase

Mechanism Three

Decreased
gastric
secretions

pH<2
or lipids
Circulation
Secretin, gastric inhibitory
peptide, cholecystokinin

Secretin, gastric inhibitory polypeptide, and cholecystokinin

produced by the duodenum (brown arrows) inhibit gastric
secretions in the stomach.
 Gastric Motility
• Electric activity
– peristaltic waves occur 3/min,
– action potentials are myogenic
– Ach, gastrin, CCK increase
– epinephrine and VIP decrease strength
• Gastroduodenal junction
– electrical rhythm : 10-12 SW/min
– functions
– sympathetic - constriction
– parasympathetic - both excitatory (constriction)
and inhibitory (relaxation)
– hormonal constrictors (slows gastric emptying)
Figure 15-22

Waves of smooth muscle contraction mix and propel the

ingested contents of the gastric lumen, but only a small
amount of the material enters the small intestine (duodenum)
as a result of each wave cycle.
Kecepatan pengosongan lambung tergantung pada:
1. Keadaan di lambung:
a. Jenis makanan: KH>Protein> lemak meninggalkan lambung
b. Volume: semakin besar vol semakin cepat meninggalkan
lambung
2. Keadaan duodenum:
a. Volume/peregangan dinding
b. Hiperosmolaritas
c. Keasaman (ph , 3,5)
d. Hasil pencernaan protein
e. Lemak dan asam lemak
Kesemuanya menginhibisi pengosongan lambung mll
a. Saraf (refleks enterogastrik)
b. Hormon
 Figure 15-23

Rhythmic waves of smooth muscle contraction in the

gut are the result of waves of action potentials moving
along via gap junctions.
• what slows gastric emptying:
– Hypertonic chyme
– duodenal pH <3.5
– presence of amino acids and peptides in
duodenum
– fatty acids and monoglycerides
• signals: what promotes emptying
– stomach distension and gastrin
 Hunger contractions
• when stomach empty for long time
• rhythmic
• cause tetanic contraction for 2-3 min,
siklusnya 90-120 menit
• most intense in young persons
– high degree of GI tonus
– low blood sugar level
• begins 12-24 hrs after last food intake
 Summary of gastric emptying control

• Stomach factors: degree of filling and

excitatory effect of gastrin on peristalsis
• duodenal factors: enteric nervous and hormonal
reflexes
• emptying slows when:
– too much chyme in duodenum
– chyme is excessively acidic, unprocessed
protein/fat, hypo- or hypertonic or irritating
 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
Absorbsi pada lambung hampir tidak ada:
– sel epitel dibungkus mukus alkali, tdk langsung
berhub dg khime
– Sel epitel tidak punya mekanisme transpor spt
usus halus
– Permukaan lambung relatif tidak dapt ditembus
air
– Pencernaan dalam lambung hanya sebagian
Usus Halus
• Diameter ± 4 cm, panjang 6 m
• Mulai dari lambung sampai usus besar
• 3 segmen : duodenum, jejenum, ileum
• Mempunyai banyak lipatan/ vili
• Penting untuk absorbsi makanan: 90%
DUODENUM
Jejenum

ileum
 Vilus
• Pusat vilus berisi pembuluh limfe yang buntu
• Lakteal, kapiler merupakan cabang arteriola
serta bermuara ke venula
• Setiap 5 hari diganti
Figure 15-7

nutrients

By projecting
into the lumen,
the villi increases
the surface area
for absorption of
nutrients.

the The absorptive cells

on villi are fringed
with microvilli, which
further increase the
absorptive surface.
Liur pencernaan yang dialirkan ke usus halus

• Liur Pankreas
• Empedu:
• Liur usus halus
 Liur usus halus
1,8 L /hari
1. Kelenjar Brunner: di mukosa duodenum,
merangsang sekresi:
– Mukus :melindungi mukosa duodenum dari iritasi HCl &
pepsin
– Buffer :me  pH (khime dlm duodenum pH: 1-2 sp 7-8)
– Hormon urogastron :mensekresi gastrin dan rangsang
pembelahan sel induk sepanjang sal cerna
2. Kripte Lieberkuhn
Produksi enzim, cairan isotonik dan alkalin
3. Enterosit vili
menghasilkan: amilase, enterokinase, lipase,
peptidase, disakaridase, yang tidak
dikleuarkan ke lumen namun akan memecah
lemak, protein, karbohidrat begitu absorbsi
dimulai
 Liur Pankreas
• 1500 cc / hari
• Mengandung: bikarbonat, elektrolit: Na,K,Cl,enzim
• Mempunyai 2 fungsi:
1. Endokrin: sel endokrin sekresi insulin & glukagon
2. Eksokrin: berasal dari sel asinus dan epitel: keduanya
menghasilkan cairan disebut cairan pankreas (pancreatic juice)
yg dikleuarka ke usus halus.
• enzim yang dikeluarkan sel asinus berguna untuk memecah khime
menjadi molekul kecil yang mudah diabsorbsi.
• Sel epitel mengeluarkan air & ion untuk mengencerkan khime &
sebagai buffer
• Pengaturan sekresi melalui pengendalian hormon.
Bila khime masuk duodenum, maka
duodenum mengeluarkan hormon :
1. sekretin: memacu pankreas sekresi buffer air
dengan pH 7,5-8,8 dan buffer bicarbonat
serta fosfat
2. kolesistokinin: rangsang produksi dan sekresi
enzim pankreas
Figure 15-27

Secretin secretion from

the duodenum is triggered
by the arrival of acidic
chyme from the stomach.

Secretin is a hormone:
its receptors are found in
the pancreas, which
responds with additional
bicarbonate delivery, and
its receptors are also
associated with the
stomach; this
enterogastrone inhibits
gastric motility and
secretion.
Figure 15-28
Cholecystokinin secretion
from the small intestine is
triggered by the arrival of
amino acids and fatty acids
in the chyme.
Cholecystokinin is a
hormone: its receptors are
in the pancreas, which
responds with additional
enzyme delivery, and
in the gall bladder, which
contracts to deliver more
bile, and in the sphincter
of Oddi, which relaxes to
facilitate delivery of the
enzymes and bile salts (it is
also an enterogastrone).
Figure 15-26
Were digestive enzymes synthesized in their active form, they
would digest the very cells that make them. Hence, inactive
precursors (e.g., trypsinogen) become activated (trypsin,
which activates many
other precursors) only after
they are transported to
the appropriate place.

FOOD
 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)
 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
 Fungsi Hati
• Organ vital:
1. hepatosit : melakukan fungsi sekresi (empedu)
2. Sel Kupffer:
• fagosit patogen, sel debris,sel darah rusak,
• penyimpanan besi, beberapa lemak, logam
beratSekresi empedu
Hati
HATI

HATI
SEL HATI
Kandung empedu

Kandung empedu
Kelenjar empedu
 Figure 15-29

Bile formation by cells in the liver includes 6 components:

bile salts, lecithin, bicarbonate ions, cholesterol, bile
pigments, and trace metals.
The bile is funneled into the gall bladder and then delivered
into the duodenum upon stimulation from CCK.
 Figure 15-4

Digestive secretions from the liver and the pancreas are

delivered into the duodenum of the small intestine
through the sphincter of Oddi.
 Empedu
• 0,5-1 L/hari, tda: Air 97%, garam empedu 0,7%,
pigmen empedu ( 0,2%), kolesterol, garam anorganik,
as. Lemak, lesitin, fosatase alkalis
• Komponen yang paling penting adalah garam
empedu
• pH 7.8-8.6
• Fungsi memudahkan pencernaan & absorbsi lemak
• Aktifkan lipase
• Empedu diproduksi terus menerus, dialirkan ke
duodenum secara intermiten bila khime
mengandung lipid dg rangsang kholesistokinin
• Pada fase interdigesi: empedu disimpan dalam
kandung empedu, sehingga konsentrasi meningkat,
asam dan pekat
• Pengaturan sekresi empedu:
– food entering the duodenum causes
galbladder to empty,
- Adanya lemak dalam duodenum rangsang sekresi
hormon CCK
- CCK menginduksi kontraksi ritmik kandung empedu
- CCK menginduksi relakasasi sphincter of Oddi
- Adanya asam dalam duodenum merangsang sekresi
HCO3 dari saluran empedu.
Figure 15-31

Cholecystokinin
(CCK) stimulates the
gall bladder, which
responds by
contracting and
delivering more
bile to the duodenum
through the sphincter
of Oddi, which relaxes
(opens) in response
to CCK.
 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
 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
 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
 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
 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)
Figure 15-30

Up to 95% of the
cholesterol-based bile
salts are “recycled” by
reabsorption along
the intestine.

Increasing dietary fiber

is thought to reduce
blood cholesterol
content by trapping a
greater percentage of
the bile in bulkier,
more fibrous feces.
 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

• 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 proces
- 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
Figure 15-32

Most of the contractions

of the small intestine are
of the mixing and churning
actions portrayed here as
segmentation contractions;
peristalsis and the
downstream movement
of materials is infrequent.
 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
 Absopsi usus halus
• Pengiriman bahan-bahan saluran cerna ke
sirkulasi, terutama tjd di usus halus, ok
daerah permukaan yg luas
• Absopsi efisien bila:
1. Bentuk hasil pencernaan baik
2. Permukaan absorpsi adekuat
3. Kecepatan bahan-bahan dalam usus halus
4. Kofaktor dan atau karier spesifik
MEKANISME PERCERNAAN & ABSORBSI

PROSES SENYAWA
PENCERNAAN KECIL
KH
LEMAH DIABSORPSI
PROTEIN
PROSES DASAR PENCERNAAN :
HYDROLISIS

R” - R’ + H2O R”OH + R’H

 PRINSIP DASAR ABSORPSI

• Cairan yang diabsorpsi 7,5 liter (hasil sekresi) dan 1,5 liter
(makanan) maka menghasilkan 8 s.d. 8,5 liter diabsorpsi di
usus halus.
• Lambung mengabsorpsi zat yang larut dalam lemak yaitu
Alkohol dan obat-obatan

• Permukaan Absorpsi Villi

• Lipatan-lipatan valvula conniventes

 MEKANISME DASAR ABSORPSI

• TRANSPORT AKTIF : memberi energi, yang bergerak

melawan potensial listrik

• DIFUSSI : Transport melalui membran akibat pergerakan

molekul
 ABSORPSI DALAM USUS HALUS
KH = RATUSAN GRAM
LEMAK = 100 GRAM
AA = 50 - 100 GRAM
ION = 50 - 100 GRAM
AIR = 8 - 9 LITER

ABSORPSI AIR :
Absorpsi Isoosmotik berupa Diffusi dan Osmosis
Figure 15-5
Digestive secretions
are mostly water,
with the average
amounts indicated
here. Note that only
100 ml are excreted
in feces, so the
mechanisms for water
absorption are efficient
(recall the kidneys’
primary role in water and
osmotic homeostasis).

2000 g in, 150 g out

 Mekanisme pencernaan dan absorpsi

1. Absorbsi air dan elektrolit

– 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
– 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
 ABSORPSI ION
25 - 35 Gram Na Transport Aktif
Na+ Transport Aktif
Ion Cl- Diffusi Pasif

H2O Na H2O

Na
Active
Transport
H2O
OSMOSIS DIFFUSI
Na

H2O
2. Pencernaan & absorpsi karbohidrat
300g ingested per day as
– complex polysaccharides: 64% starch, 0.5%
glycogen
– Disaccharides: 26% sucrose, 6.5% lactose, 3%
MALTOSA
– complete hydrolysis would yield 80%
glucose, 14% fructose, 5% galactose kapiler
 Carbohydrate digestion

• pancreatic juices cannot further hydrolyse

oligosaccharides
• brush border oligosaccharidases
• brush border lactase, sucrase-isomaltase and maltase
release 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
 PENCERNAAN KARBOHIDRAT

KH
Ptyalin = 40%
HCl = ?
Panc. Amylase = 50%
Intestinae Amylase = ?

MALTOSE LACTOSA SUCROSA

ISOMALTOSE
MALTOSE
ISOMALTOSE LACTASE SUCRASE
(INTESTINE) (INTESTINE) (INTESTINE)

GLUCOSA GALACTOSA FRUKTOSA

MULUT
• Saliva menjadi ptyalin ( Alpha - Amilase)
• Sebagian besar KH yang dimakan menjadi pelindung tipis
yaitu sellulosa dan tidak dapat dicernakan

LAMBUNG
• Ptyalin dari saliva : pH 4.0 tak aktif
• HCl : Menghidrolisis KH

- Amylase Pancreas - Sukrase

- Lactase - Maltase
- Isomaltase
In a normal diet, bulk is Carbs, 250-800 g (ex. Atkins)
+ 125 g protein, +25-160 g fat.
 LEMAK
• 60-100 g perhari,
• lipids- mainly triacylglycerols
• Dicerna muali dimulut oleh enzim lipase lingual dan pankreas
mjd asam lemak dan monogliserida
• Garam empedu, membentuk emulsi lemak lebih halus
disebut misel
• Misel difusi mll membran ke sitoplasma
• Sel usus halus sintesa Trigliserida baru, bergabung dengan
steroid dan fosfolipid membentuk KILOMIKRON
• Sel usus halus sekresi kilomikron ke interstitial melalui
eksositosis
• Kilomikron difusi ke lakteal akhirnya ke p. limfe
 USUS HALUS
• EMULSIFIKASI OLEH ASAM EMPEDU
• BAGIAN HIDROXIL GARAM EMPEDU SANGAT LARUT
DALAM AIR
• BAGIAN STESE LARUT DALAM LEMAK BERGUNA
UNTUK MENURUNKAN TEGANGAN PERMUKAAN
LEMAK
LIPASE PANCREAS

Pancreatic
LEMAK EMULSI LEMAK Lipase
EMPEDU

F.A. & GLISERAL= 40%

GLICERIDA = 60%
 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
4. inside cells resynthesis of triacylglycerols, cholesterol and
phospholipids to chylomicrons
5. 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)
Figure 15-9

A molecular model
of a bile salt, with the
cholesterol-derived
“core” in yellow.

A space-filling model
of a bile salt. The
non-polar surface
helps emulsify fats, and
the polar surface
promotes water solubility.
Figure 15-10

Bile salts and

phospholipids
convert large fat
globules into smaller
pieces with polar
surfaces that inhibit
reaggregation.
Figure 15-11

Emulsified fat globules are

small enough that lipase
enzymes gain access to
degrade triglycerides
to monoglycerides and
fatty acids, which enter
the absorptive cells by
simple diffusion or
aggregate to form loosely
held micelles, which readily
break down.
Figure 15-12

Big Blobs of Fat

Small Blobs of Fat

Micelles

Fatty Acids and

Monoglycerides

Chylomicron Assembly

Distribution and Processing

 PROTEIN

• > 100g ingested daily as oligopeptides

• Sangat kompleks
• digested by proteolytic enzymes, PEPSIN
• proteolytic enzymes secreted as zymogens (inactive
proenzeymes)
• endopeptidases - cleave internal peptide bonds
• exopeptidases - carboxy or amino terminal cleavage
• BENTUK ASAM AMINO kapiler
• 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
 PERCERNAAN PROTEIN
PROTEIN (HEWANI DAN NABATI) ASAM AMINO
RANTAI PANJANG DENGAN IKATAN PEPTIDA

Pepsin Proteosa
PROTEIN
pH 2 Lambung Pepton
Polypeptida
Tripsin
Chymotropsin
Coerboxypeptidase
POLIPEPTIDA +
ASAM AMINO
Peptidase

ASAM AMINO
 PROTEIN

Asam Amino berikatan Ikatan Peptida

Pencernaan protein dengan proses Hidrolisis

NH H
2
R CH C OH + H N CH COOH

O R

R CH C N CH COOH + H2O
O R
 Location Secretion product

Carbohydrates Mouth Salivary Amylase

Upper-stomach Salivary Amylase
Small intest. Pancreatic amylase

Carbs (fiber) Large intestine (Bacterial digestion)

Protein Stomach Pepsin

Small intest. Trypsin, Chymotrypsin

Fat Small intest. Pancreatic Lipase

Vitamins (fat) Small intest.

Vitamins (water) Small intest.

 Product Absorption pathway

Carbohydrates Fru Facilitated diffusion

Glu/Gal Active Transport / Sodium

Protein Amino Acids Active transport / Sodium

Proteins (except.) endo-exocytosis
(infants mainly)

Fat Free Fatty Acids Diffusion

Monoglyc. Diffusion

Vitamins (fat) A, D, E, K Diffusion (via micelles)

Vitamins (water) B-12 Binds to Intrin. Factor.

Endocytosis

Iron Active Transport

then into ferritin
USUS besar

USUS BESAR
• Terdiri atas:
– sekum
– Apendiks: jaringan limfoid
– Kolon: asenden, tranfersum, desenden, kolon
sigmoid (akhir kolon desenden:)
– rektum
• Fungsi usus besar / kolon
– Fungsi utama menyimpan feses sebelum defekasi
dan mengatur pengeluaran feses
– Absorbsi :
• air & elektrolit dengan proses perbedaan osmotik
• vitamin yg dihasilkan kerja bakteri:
– Vitamin K: larut lemak, untuk pembekuan darah
– Biotin: larut lemak, penting untuk metabolisne glukosa
– Vitamin B5: asam pantotenat: larut air, untuk membuat
hormon steroid & beberapa neurotransmiter
• Bakteri mengubah bilirubin menjadi urobilinogen
(diabsorpsi ke sirkulasi, dibuang melalui urin) dan
sterkobilin
– Sekresi:
• mukus yang diproduksi oleh sel goblet untuk
“pelumas” feses dan epitel
• HCO3 , untuk menyeimbangkan asam produksi
bakteri
– Bakteri kolon membantu pencernaan selulosa dan
karbohidrat
– Bakteri kolon memecah peptid menjadi:amonia,
indol, skatol
– methane and H2 dari diit – produksi gas
Figure 15-33

In the large intestine, active transport of sodium, coupled with

osmotic absorption of water, are the primary activities.
Microbes here are active in the production of vitamin K.
 Otot kolon

• Lapisan otot polos longitudinal di sebelah luar tidak

menutupi usus besar sepenuhnya, hanya 3 pita otot
yang terpisah yaitu taenia koli

• Taenia lebih pendek dari otot sirkuler di bawahnya

sehingga lapisan di bawahnya membentuk kantung,
haustra

• Gerakan lambat:
– maintaining an appropriate intraluminal bacterial mass
ANUS
 Sphincters
• Internal anal sphincter
– Voluntary or involuntary?
• Involuntary
– Type of muscle?
• Smooth muscle
– Tonically contracted
 Sphincters
• External anal sphincter
– Voluntary or involuntary?
• Voluntary
– Type of muscle?
• Striated muscle
– Nerve and segment?
• Pudendal nerve (S2-S4)
 Gerakan kolon
• Frekwensi rendah
• 3-4 times/day
• Gerakan masa / mass movements: kontraksi masif
mendorong isi kolon ke bagian distal UB dan
disimpan sp tjd defekasi
• Gerakan masa dirangsang oleh makanan dalam
lambung disebut refleks gastrokolon
• Umumnya diikuti defekasi
 Defecation
Pengeluaran feses melalui reflek defekasi
– Massa feses bergerak menuju rektum
– merangsang reseptor regang di rektum
– Memicu refleks defekasi dan keinginan BAB
– Sfingter anus internus (otot polos) melemah, rektum
serta kolon sigmoid berkontraksi kuat.
– Apabila sfingter anus eksternus (otot rangka/kontrol
sadar) melemas terjadi defekasi
– Defekasi dibantu gerakan mengejan volunter:
kontrakasi otot abdomen dan ekspirasi paksa ,
glotis menutup, sehingga tekanan intraabdomen
meningkat
 Normal Defecation
• Rectosigmoid distention stimulates rectorectal reflex
– Bowel proximal to bolus
• contracts
– Bowel distal to bolus
• relaxes
• Reflex relaxation of internal anal sphincter
– Rectoanal inhibitory reflex
– Correlates with the “urge to go”
• Volitional contraction of levator ani
 Normal Defecation
• Volitional control of levator ani
– Opens proximal anal canal
– Relaxes external sphincter and puborectalis
– Allows straighter anorectal passage
• May increase with
– Valsalva
– Increasing intraabdominal pressure (squat)
 Normal Defecation
• Defecation deferred by volitionally contracting
(2)…
– Puborectalis
– External anal sphincter
– Then, internal anal sphincter relaxation reflex will
fade (within approx 15 sec) and urge will resolve
until triggered again
 Normal Defecation
• Protective mechanisms
– EAS will tense in response to small colonic
contractions
• Via spinal cord reflex (conus) and modulated by higher
centers
 Presence of food Stomach
in the stomach
1. The presence of food in
the stomach and chyme
in the duodenum Presence of chyme
stimulate mass in the duodenum 1

movement in the colon. Colon

2. Mass movements are 2 2

integrated by the enteric
plexus. 2 2
Mass movements
Stimulates
3. They propel the contents mass 3
of the colon toward the movement 2 2
rectum.

4. The presence of feces in 4

the rectum stimulates Stimulation

parasympathetic and of local
Feces
defecation Stimulation of
local reflexes that result reflexes parasympathetic
in defecation. controlled
defecation
Rectum reflexes
 Presence of food
in the stomach

Presence of chyme
in the duodenum
Colon

The presence of food in

the stomach and chyme in
the duodenum stimulate
mass movement in the Stimulates Mass movements
colon. mass
movement

Rectum
 Colon

Mass movements are

integrated by the
enteric plexus. Mass movements

Rectum
 Colon

They propel the contents of the

Mass movements
colon toward the rectum.

Rectum
 Stomach

Colon

The presence of feces in the

rectum stimulates
parasympathetic and local
reflexes that result in defecation. Mass movements

Stimulation Stimulation of
of local parasympathetic
defecation Feces
controlled
reflexes defecation
Rectum reflexes