Transcript Regulasi Sistem Percernaan

dr. Nuraiza Meutia,M.Biomed
Departemen Fisiologi FK USU
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Aktivitas saluran cerna untuk menjalankan
proses percernaan diatur oleh sistem saraf
dan endokrin.
Saluran cerna memiliki kemandirian untuk
kedua sistem tersebut.
Terjadi aktivitas terintegrasi antara kedua
sistem  mengatur aktivitas motorik dan
sekretorik
Pada akhir perkuliahan, anda harus dapat :
1.
Menjelaskan anatomi fungsional dinding GIT
2.
Menjelaskan aktivitas utama GIT
3.
Menjelaskan persarafan otonom yang mengatur GIT
4.
Menjelaskan letak dan fungsi pleksus saraf di GIT
5.
Menyebutkan nama dan efek neurotransmitter yang
bekerja di ENS
6.
Menjelaskan peran hormon dalam kontrol GIT (nama
hormon, sumber, target dan efek)
7.
Menjelaskan proses integrasi sistem saraf dan endokrin di
GIT
8.
Menjelaskan perbedaan refleks lokal dan refleks sentral
dalam regulasi kerja GIT
9.
Menjelaskan aktivitas listrik pada otot polos GIT
10.
Menjelaskan mekanisme kontraksi dan jenis motilitas GIT
11.
Menjelaskan contoh-contoh refleks GI
12.
Menjelaskan regulasi aktivitas lambung, usus halus, usus
besar, pankreas dan kandung empedu.
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Struktur Dinding GIT
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Aktivitas GIT :
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Motilitas
Sekresi
Digesti
Absorbsi
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Fungsi sistem regulasi di GIT :
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Mengatur aktivitas motilitas dan sekresi
Mengatur aliran darah ke GIT
Menerima dan menyampaikan informasi
melalui neuron sensori (aferen) , dari
reseptor-reseptor yang menerima
stimulus mekanikal, thermal, osmotik dan
kimiawi.
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GIT NEURAL
CONTROL
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Aktivitas GIT diatur oleh sistem Saraf
Otonom
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Terdiri dari :
- Divisi parasimpatetik
- Divisi simpatetik
- Enteric Nervous System (ENS)
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Parasimpatetik
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N. Vagus & N.pelvik
Neuron preganglionik panjang; postganglionik
pendek, bersinaps dengan neuron ENS
Stimulasi  eksitasi aktivitas ENS
Mengandung serat sensori aferen (80 %)
N.Vagus bersinaps ke neuron ENS di esophagus,
lambung,usus halus, sebagian kolon, kandung
empedu, & pankreas
N.Pelvik bersinaps dengan ENS di usus besar
Neurotransmitter : Ach
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Parasympathetic
Nervous System
Craniosacral
 Simpatetik
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Serat simpatetik ke GIT berasal dari
medula spinalis segmen T-5 sampai L-2.
Neurotransmitter : norepinefrin
Aktivitas simpatetik  inhibisi motilitas
dan sekresi GIT, konstriksi sfinkter dan
pembuluh darah.
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Sympathetic
Nervous
System
Thoracolumbar
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Enteric Nervous System
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Enteric Nervous System (ENS) terdapat di seluruh dinding GIT,
mulai esophagus sampai anus.
Terbentuk dari 100 juta neuron (mengimbangi spinal cord).
Memiliki 3 jenis neuron : sensori, motorik, & interneuron
ENS tersusun atas 2 pleksus utama :
(1) Myenteric plexus atau Auerbach's Plexus: berada di antara
lapisan otot sirkular dan longitudinal (outer plexus). Fungsi :
mengontrol motilitas GIT
(2) Submucosal Plexus atau Meissner's plexus : berada di
lapisan submukosa (inner plexus). Fungsi : mengatur sekresi
dan aliran darah lokal, sensing perubahan lumen, dan gerak
pelipatan mukosa.
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ENS dapat berfungsi secara mandiri, terlepas dari
pengaturan sistem simpatetik dan parasimpatetik.
Meskipun, persarafan ekstrinsik dapat sangat
mempengaruhi ENS, menyebabkan inhibisi atau
eksitasi fungsi GIT.
Ujung saraf sensori mengirimkan serat aferen ke
kedua pleksus ENS, dan juga ke : (1) ganglia
prevertebral sistem simpatetik, (2) spinal cord, dan
(3) nervus vagus menuju batang otak.
Informasi sensorik dapat menimbulkan refleks
lokal dan sentral
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Figure 62-4; Guyton & Hall
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Neurotransmitters and Neuromodulators in the ENS
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GIT HORMONAL
CONTROL
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GIT merupakan kelenjar endokrin terbesar
Hormon dihasilkan oleh sel enteroendokrin yang
tersebar di antara sel-sel epitel mukosa lambung
dan usus  Enteric Endocrine System.
Sekresi hormon terjadi akibat stimuli tertentu, dan
berhenti bila stimuli lenyap.
Sel-sel GIT menghasilkan regulator peptida, yang
berfungsi secara parakrin atau sebagai Nts, untuk
mempengaruhi motilitas, aliran darah, dan
pertumbuhan mukosa GIT.
GIT Hormones
HORMONE
ORIGIN
STIMULUS
ACTIONS
G cells of the stomach
Small peptides and
↑ Gastric H+ secretion
amino acids
Stimulates growth of gastric mucosa
Distention of the
stomach
Vagal stimulation (GRP)
I cells of the duodenum
and jejunum
Small peptides and
amino acids
Fatty acids
↑ Pancreatic enzyme secretion
↑ Pancreatic HCO3- secretion
Stimulates contraction of the gallbladder
and relaxation of the sphincter of Oddi
Stimulates growth of the exocrine
pancreas and gallbladder
Inhibits gastric emptying
S cells of the duodenum
H+ in the duodenum
Fatty acids in the
duodenum
↑ Pancreatic HCO3- secretion
↑ Biliary HCO3- secretion
↓ Gastric H+ secretion
Inhibits trophic effect of gastrin on
gastric mucosa
Fatty acids
Amino acids
Oral glucose
↑ Insulin secretion from pancreatic β
cells
↓ Gastric H+ secretion
Fat
Acid
Nerve
Stimulates:
Gastric motility
Intestinal motility
Gastrin
Cholecystokinin (CCK)
Secretin
Glucose-Dependent K cells of the Duodenum
Insulinotropic Peptide and jejunum
(GIP)
Motilin
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M cells of the duodenum
and jejunum
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GIT
NEURAL
HORMONAL CONTROL
INTEGRATION
Nervous and hormonal influences do not function
independently
- Neural activity  release of hormones
- Hormones  neural activity
- Simultaneous effects
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3 tipe refleks GI :
1. Refleks yang terintegrasi seluruhnya di dinding GIT (ENS):
mengatur sekresi dan motilitas secara lokal.
2. Refleks dari GIT  ke ganglia prevertebral simpatetik 
kembali ke GIT. Sehingga respon terjadi di bagian lain GIT.
Misal : r.gastrokolik, r.enterogastrik, & r.kolonoileal.
3. Refleks dari GIT  ke spinal cord atau batang otak 
kembali ke GIT.
Misalnya : (1) refleks dari lambung & duodenum ke Bt.otak,
kembali melalui N.Vagus untuk mengatur aktivitas sekresi
dan motorik lambung. (2)refleks nyeri yang mengakibatkan
inhibisi GIT.(3)refleks defekasi.
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Nerves
Reflex or
Hormone
secretion
Regulasi Aliran Darah ke GIT
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Vasodilator : CCK, Secretin, Gastrin, VIP; kinin(kallidin &
bradykinin)
Penurunan konsentrasi oksigen  peningkatan aliran
darah 50-100 %
Pengaruh persarafan otonom :
Stimulation of the Parasympathetic nerves going to the stomach and
lower colon increases local blood flow at the same time that it
increases glandular secretion.
Sympathetic stimulation, by contrast, has a direct effect on essentially
all the gastrointestinal tract to cause intense vasoconstriction of the
arterioles with greatly decreased blood flow. But the local metabolic
vasodilator mechanisms override the sympathetic vasoconstiction
effects, returning the normal blood flow to GI muscle and
glands...”autoregulatory escape”
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Stres atau cemas dapat menginduksi : inhibisi
aktivitas saluran cerna bagian atas - dan stimulasi
fungsi motorik saluran cerna bagian bawah
Disebabkan pengaruh corticotropin-releasing
factor (CRF) endogen terhadap reseptor CRF di
sistem saraf pusat.
Interaksi CRF pada reseptor CRF-2 menyebabkan
inhibisi pengosongan lambung .
Sedangkan reseptor CRF-1 berperan dalam
menghasilkan respon peningkatan motilitas kolon
saat stres.
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Aktivitas Listrik pada Otot polos GIT
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Di sepanjang otot polos GIT
terjadi fluktuasi potensial
membran sepanjang waktu.
Perubahan potensial ini
menyebabkan otot polos
dapat berkontraksi.
Aktivitas listrik ini 2 jenis :
(a) slow waves
(b) spikes.
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a. Slow Waves
 Bukan potensial aksi, fluktuasi depolarisasi dan repolarisasi .
 Amplitudo 5-15 mV
 Frekuensi berbeda di berbagai bagian GIT : lambung 3 x/mnt
; duodenum 12 x/mnt; ileum terminal 8-9 x/mnt.
 Berperan untuk mensinkronkan irama kontraksi di sepanjang
GIT.
Origin of slow waves. They may originate
in the interstitial cells of Cajal (the GI
pacemaker), which are abundant in the
myenteric plexues. These interstitial
cells form a network with each other and
are interposed between the smooth
muscle layers, with synaptic-like
contacts to smooth muscle cells.
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Source of Slow Waves in GIT Muscles
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b. Spike Potential
 Apabila pada suatu tempat, potensial membran istirahat
meningkat, maka slow wave dapat mencetuskan
potensial aksi (spike potential)  kontraksi otot.
 Faktor yang dapat mendepolarisasi membran :
 Peregangan otot
 Ach
 Stimulasi parasimpatetik
 Stimulasi hormonal
 Faktor yang meng-hiperpolarisasi membran :
 Norepinephrine
 Stimulasi simpatetik
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Figure 62-3; Guyton & Hall
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Peristalsis
Penjalaran gelombang
mendorong bolus
Segmentasi
Gerakan mencampur
dan mengaduk
bolus.
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Mass movements
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Peristaltik haustra
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Relaxation Reflexes
Gastric Reservoir
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2.
The main functions of the upper part of the
stomach (Reservoir part ):
To maintain a continuous compression
To accommodate the received food without significant
gastric wall distention or pressure (Storage of food)
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Gastric secretion is controlled by both neural
and hormonal mechanisms
Under normal conditions the gastric mucosa
creates as much as 3 liters of gastric juice
every day
Gastric juice is an acid solution that has the
potential to dissolve nails
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Nervous control is regulated by long (vagus
nerve mediated) and short (local enteric)
nerve reflexes
When the vagus nerves actively stimulate
the stomach, secretory activity of virtually all
of its glands increase
The sympathetic nerves depress secretory
activity
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Hormonal control of gastric secretion is
largely from the presence of gastrin
Gastrin stimulates the secretion of both
enzymes and HCL in the stomach
Hormones produced by the small intestine
are largely gastrin antagonists
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Stimuli acting at three distinct sites, the
head, stomach, and small intestine,
provoke or inhibit gastric secretory activity
Accordingly the three phases are called
cephalic, gastric, and intestinal phases
However, the effector site is the stomach
in all cases and once initiated, one or all
threephases may be occurring at the
same time
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The cephalic reflex phase of gastric
secretion occurs before food enters the
stomach
It is triggered by the aroma, taste, sight, or
though of food
During this phase the brain gets the
stomach ready for food
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Inputs from activated olfactory receptors and
taste buds are relayed to the hypothalamus
which in turn stimulates the vagal nuclei of
the medulla oblongata, causing motor
impulses to be transmitted via the vagus
nerves to the parasympathetic nerve ganglia
Eneteric ganglionic neurons in turn stimulate
the stomach glands
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The enhanced secretory activity that results
when we see or think of food is a
conditioned reflex and occurs only when we
like or want the food
If we are depressed or have no appetite, this
part of the cephalic reflex is suppressed
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Once food reaches the stomach, local
neural and hormonal mechanisms initiate
the gastric phase
This phase provides about two-thirds of the
gastric juice released
The most important stimuli are distension,
peptids, and low acidity
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Stomach distension activates stretch
receptors and initiates both local
(myentertic) reflexes and the long vagovagal
reflexes
In vagovagal reflex, impulses travel to the
medulla and then back to the stomach via
vagal fibers
Both types of reflexes lead to acetylcholine
(ACH) release, which in turn stimulates the
output of more gastric juice by cells
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Figure 24.15b
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Though neural influences initiated by
stomach distension are important, the
hormone gastrin probably plays a greater
role in stimulating stomach gland secretion
during the gastric phase
Chemical stimuli provided by partially
digested proteins (peptids)caffine (colas,
coffee) and rising pH directly active gastrin
secreting entoendocrine cells called G cells
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Although gastrin also stimulates the release
of enzymes, its main target is the HCL
secreting parietal cells, which it prods to
spew out even more HCL
Highly acidic (pH below 2) gastric contents
inhibit gastrin secretion
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When protein foods are in the stomach, the
pH of the gastric contents generally rises
because proteins act as buffers to tie up H+
The rise in pH stimulates gastrin and
subsequently HCL release, which in turn
provides the acidic conditions needed for
protein digestion
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The more protein in the meal, the greater the
amount of gastrin and HCL released
As proteins are digested, the gastric
contents gradually become more acidic,
which again inhibits the gastrin secreting
cells
This negative feedback mechanism helps
maintain optimal pH and working conditions
for the gastric enzymes
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G cells are also activated by the neural
reflexes already described
Emotional upsets, fear, anxiety, or anything
that triggers the fight-or-flight response
inhibits gastric secretion because (during
such times) the sympathetic division
overrides parasympathetic controls of
digestion
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The control of the HCL secreting parietal
cells is unique and multifaceted
Basically, HCL secretion is stimulated by
three chemicals, all of which work through
second-messenger systems Ach released by
parasympathetic nerve fibers and gastrin
secreted by G cells
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Ach released by parasympathetic nerve
fibers and gastrin
secreted by G cells
bring about their
effects by increasing
intercellular Ca++
levels
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Histamine
released by
mucosal cells
called
histaminocytes
acts through
cyclic AMP
(cAMP)
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As hydrogen ions are secreted, chloride ions
(Cl-) are also pumped into the lumen to
maintain an electrical balance in the
stomach
The Cl- is obtained from blood plasma, while
the H+ appears to come from a breakdown of
carbonic acid formed by the combination of
carbon dioxide and water and within the
parietal cells
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CO2 + H2O  H2CO3
 H+ + HCO3As H+ is pumped
from the cell and
HCO3- is ejected
through the basal
cell membrane into
the capillary blood
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The result of ejection of the bicarbonate ion
into the capillary blood is that blood draining
from the stomach is more alkaline than the
blood serving it
The phenomenon is called the alkaline tide
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The intestinal phase of gastric secretion has
two components
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One excitatory
One inhibitory
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The excitatory aspect is set into motion as
partially digested food begins to fill the initial
part (duodenum) of the small intestine
This stimulates intestinal mucosal cells to
release a hormone that encourages the
gastric glands to continue their secretory
activity
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The effects of this hormone imitate those
of gastrin, so it has been named intestinal
(enteric) gastrin
However, intestinal mechanisms stimulate
gastrin secretion only briefly
As the intestine distends with chyme
containing large amounts of H+, fats,
partially digested proteins, and irritating
substances, the inhibitatory component is
triggered in the form of the enterogastric
reflex
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The enterogastric reflex is actually a trio of
reflexes that
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Inhibit the vagal nuclei in the medulla
Inhibit local reflexes
Activate sympathetic fibers that cause the
pyloric sphincter to tighten and prevent further
food entry into the small intestine
As a result, gastric secretory activity declines
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These inhibitions on gastric activity product
the small intestine to harm due to excessive
acidity and match the small intestine’s
processing abilities to the amount of chyme
entering it at a given time
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In addition, the factors just named trigger the
release of several intestinal hormones collectively
called enterogastrones which include
 Secretin
 Cholecystokinin (CCK)
 Vasoactive intestinal peptide (VIP)
 Gastric inhibitory peptide (GIP)
All of these hormones inhibit gastric secretion
when the stomach is very active
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Figure 24.15c
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Secretion of pancreatic juice is regulated
both by local hormones and by the
parasympathetic nervous system
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Both hormones act on the pancreas, but secretin
targets the duct cells, prompting their release of
watery bicarbonate-rich pancreatic juice, Whereas
CCK stimulates the acini to release enzyme-rich
pancreatic juice
Vagal stimulation causes release of pancreatic
juice primarily during the cephalic and gastric
phases of gastric secretion
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Normally, the amount of HCL produced in the
stomach is exactly balanced by the amount of
bicarbonate (HCO3) actively secreted by the
pancreas
HCO3 is secreted into the pancreatic juice, and
H+ enters the blood
Consequently, the pH of venous blood returning
to the heart remains relatively unchanged
because alkaline blood draining from the
stomach is neutralized by the acidic blood
draining the pancreas
Regulation of Pancreatic Secretions
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Secretin
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CCK
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Acidity in intestines induces
Secretin release
Secretin releases pancreatic
Sodium Bicarbonate (HCO3-)
Fats and proteins induce CCK
release
CCK releases pancreatic
digestive enzymes
GIP
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Fatty acids and sugar causes
induce GIP release
GIP induces insulin release
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Although the liver makes bile continuously
bile does not usually enter the small
intestine until the gallbladder contract
The major stimulus for gallbladder
contraction is the intestinal hormone
cholecystokinin (CCK)
CCK is released to the blood when acidic,
fatty chyme enters the duodenum
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Besides causing the gallbladder to contract, CCk
has two other important effects
 It stimulates secreation of pancreatic juice
 It relaxes the hepatppancreatic sphincter so
that bile and pancreatic juice can enter the
duodenum
Parasympathetic impulses delivered by the
vagus nerves have a minor impact on
stimulating gallbladder contraction
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The rectum is
usually empty, but
when feces are
forced into it by
mass
movements,
stretching of the
rectal walls
initiates the
defecation reflex
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This is a spinal
cord mediated
reflex that causes
the walls of the
sigmoid colon and
the rectum to
contract and the
anal sphincters to
relax
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Distension or
stretch of the
rectal walls
triggers a
depolarization of
sensory
(afferent) fibers
which synapse
with the spinal
cord
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Parasympathetic
motor (efferent)
fibers, in turn,
stimulate
contraction of the
rectal walls and
relaxation of the
internal anal
sphincter
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If it is convenient to
defecate, voluntary
signals stimulate
the relaxation of
the external anal
sphincter
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As feces are forced into the anal canal, impulses
reach the brain allowing us to decide whether the
external(voluntary) anal sphincter should remain
open or closed
If defection is delayed, the reflex contractions end
within a few seconds and the walls relax
With the next mass movement, the reflex is initiated
again and again until one chooses to defecate