Download doc 2012 Digestion Study Guide

Digestion Study Guide
Lecture I
The basis of the digestive system is to intake food, process it into manageable forms (FFAs,
amino acids, etc.), absorb useful nutrients and excrete waste.
Types of digestive systems:
I. Open – found in earthworms.
Act as extensions of the external environment.
Food enters one end (anterior) and exits another (posterior).
II. In higher organisms, the GI-tract both grows (4.5m long in an adult human male, with
several infoldings to maximize absorption) and differentiates into several
physiologically distinct structures.
 Mouth
 Stomach
 Small Intestine
 Large Intestine
 Anus
 Accessory Organs: Liver, pancreas, salivary glands
Anatomy of the GI-Tract – From outermost to innermost
Keep in mind that the muscle in the top third of the digestive system and the anal
sphincter is striated (under voluntary control). The remaining 2/3 is smooth.
Outermost Layer – Serosa – Tough connective tissue. Attached to the abdominal wall to
support the GI-tract.
Muscularis Externa – Layers of smooth muscle that cause contractions
necessary for moving food.
Longitudinal Muscle – outermost layer of muscle that causes longitudinal
contractions (shortening of the GI-tract).
Myenteric Plexus – neuronal network that lies between muscle layers.
“Talks” to the GI epithelium and submucosal plexus via enteric fibers.
Ennervated by the ANS.
Circular Muscle – innermost layer of muscle that causes constriction of
the tract. Thicker than longitudinal layer.
Submucosa Submucosal Plexus – ENS' second projection in the GI-tract. Possesses
function similar to the myenteric plexus.
Major blood and lymphatic vessels.
Mucosa – innermost layer of GI cells.
Muscularis Mucosa – Thin layer of smooth muscle involved in vili
movement.
Lamina Propria – Loose connective tissue through which minor blood
vessels and lymphatics pass.
Epithelium – innermost layer of the mucosa. Contains exocrine cells that
secrete mucus into the lumen and endocrine cells that release hormones
into the blood. Invaginations of the epithelium form exocrine glands that
can secrete digestive enzymes into the lumen.
Innermost Layer: Lumen – the inside of the GI-tract.
More on the Plexuses:
Both form part of the Enteric Nervous System (ENS), which is an independent,
integrative nervous system capable of initiating and regulating activities.
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Sensory Neurons have receptors in the mucosa or the muscle layers.
Effector neurons which carry out ('effect') the desired response.
Interneurons which “talk” to other neurons and get more innervation.
Effector Neurons can be excitatory, releasing Acetylcholine (Ach) onto muscarinic
receptors, or inhibitory, releasing NANC.
Atropine blocks the muscarinic receptors.
There are two types of reflexes governed out by the ENS – short and long.
SHORT reflexes do not talk to higher centers. In response to a stimulus, receptors relay
information to the nerve plexuses, which activate (or inhibit) a muscular or glandular
response.
By contrast, LONG reflexes involve autonomic activation of the ENS.
Parasympathetic Activation:
The impulse begins in the medulla, working its way via the vagus nerve
to the tract wall, where it synapses on enteric neurons (releases Ach onto
them).
This synapsing induces Ach release by the enteric neurons, which has an
overall excitatory effect.
Sympathetic Activation:
The impulse begins in the spinal chord, traveling to a ganglion where the
fiber synapses Ach before continuing to the enteric ganglia.
At the enteric ganglia, the fiber releases NA, which has an overall
inhibitory effect.
The sympathetic system innervates smooth muscle in blood vessels,
causing vasoconstriction.
The activity of the stomach is regulated by neural (described above) and hormonal
mechanisms. How do hormones help?
The hypothalamic 'feeding center' can cause release of ghrelin (appetite
stimulator) from the stomach or leptin (a signal of satiety) from adipocytes.
The mucosa, however, contains its own endocrine system called the DES
(Diffuse Endocrine System) which is the largest, most diverse endocrine system
in the body.
Lecture II
There are three different forms of hormonal regulation.
 Autocrine – hormones released by a cell act on it..
 Paracrine – hormones released by a cell act on others in the vicinity.
 Endocrine – hormones released by a cell travel through the bloodstream
to a target tissue.
Gut hormones (mostly peptides) are usually endocrine.
They are usually released in the mucosa of the stomach and the small intestine by
stimulation (nervous, chemical, mechanical).
Now we move on to initiation and regulation of the first activity of the GI-tract: Motility.
Propulsion of material to be digested results from pressure gradients and variations in
resistance.
Pressure gradients can occur in two ways: segmentation (two sections of the tract
clamp down, pushing food forward) or peristalsis (a rolling wave of pressure that
moves the bolus along).
Normally GI flow is slow, aboral, and meets little resistance.
Swallowing (Deglutition) has three phases: oral, pharyngeal, and esophageal.
1. Oral Phase – involves transport from the anterior mouth to the pharynx by
the tongue.
Under voluntary control (regulated in the cortex) which are not strictly necessary for this to occur –
they only initiate the reflex.
Involuntary aspects are regulated in the medulla. These are necessary.
2. Pharyngeal Phase – fully involuntary.
Since the pharynx is common to respiration and digestion, the bolus cannot be allowed to enter the
lungs.
Larynx moves under the tongue, the palate rises to protect the nose, the epiglottis covers the glotti
(which rub together as an additional protective measure) and there is momentary apnea.
To enter the esophagus, the Upper Esophageal Sphincter (UES) opens
as vagal impulses cease Ach release.
3. Esophageal Phase – under some control.
The pharynx contracts, pushing the bolus through.
The respiratory elements (glotti, palate, etc.) relax.
A primary peristaltic wave is generated by sequential vagal somatic
fibers (see below)..
The esophagus lies within the thoracic cavity, an area under negative pressure. To
prevent food from moving up from the stomach into the esophagus, we need an upper
and lower sphincter.
The upper third of the esophagus is activated by vagal somatic fibers. The remainder by
autonomic fibers.
Peristalsis in the upper third of the esophagus results from the sequential firing of vagal
motor neurons, activating progressively more distal regions of the musculature (striated
portion).
Peristalsis in the rest of the esophagus results from both sequential vagal autonomic
fibers (as in the upper third) but also by sequential enteric neurons. If the former are cut,
but a few enteric neurons can still be activated, peristalsis will still occur normally.
Lecture III
Primary peristalsis occurs every time we swallow, but if the bolus gets stuck, the enteric
reflexes will induce secondary peristalsis to dislodge it.
The Lower Esophageal Sphincter (LES) is the terminal 4cm of the esophagus, located
equally above and below the diaphragm.
Its failure leads to acid reflux and pyrosis (heartburn).
In the resting state, it is closed to maintain the pH of the oesophagus (since it's under
negative pressure stomach juices would prolapse into the oesophagus if it were open).
Relaxation is initiated by neuronal release of NANC, and is part of the deglutition
reflexes.
The placement of the LES is crucial – if pressure is applied to the abdomen, it will press
on the LES as well, preventing the pressure gradient from reversing. If the sphincter is
pulled upward (a condition called hiatus hernia), pressure applied to the abdomen results
in prolapse.
Hormonal Modulation
Gastrin – Can sometimes modulate pressure.
Progesterone – Lowers pressure to ensure there is no reflux during parturition.
The Stomach:
 Involved in storage
 Physical disruption of contents to chyme
 Propulsion to duodenum
The stomach is divided into two parts – the proximal (used for storage) and distal (used
for mixing and propulsion).
The proximal stomach is composed of the fundus and upper 1/3 of the corpus, the distal
stomach is the lower 2/3 of the corpus and the antrum.
The proximal stomach is the region of the stomach that undergoes Receptive Relaxation
– distension in response to a meal without significant changes in pressure.
This is initiated by vago-vagal reflexes – an impulse is sent through the vagus to
the deglutition center, and returns on the vagus to release NANC, relaxing the stomach. This is part of
the deglutition reflexes.
If the vagi to the proximal stomach are cut, distension of the stomach to
accomodate a meal causes great increase in pressure.
Lecture IV
The stomach contains intrinsic motor and electrical activity as part of its propulsive
function.
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Peristalsis – The main form of movement in the distal stomach, beginning
1/3 of the way down the corpus, sweeping over the distal stomach and
pyloric sphincter.
Peristaltic amplitude is related to the magnitude of the stimulus.
Smooth muscle gives the direction and velocity of peristalsis.
Local distension gives rise to enteric reflexes that initiate
peristalsis.
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BER (Basic Electrical Rhythm) – Rhythmic depolarizations of the distal
stomach that are constantly present. Influences maximum contraction
frequency since the ERA can only occur during the plateau of the BER.
ERA (“Spikes”) - Sharp depolarizations that occur during the plateau
period of the BER. These are coupled to contraction of the stomach.
Stimulated by local stretch or Ach.
Ca2+ dependent. Spreads from cell to cell myogenically.
Interstitial Cells of Cajal – non-neuronal, non-muscle cells located between the muscle
layers and enteric plexuses. May be implicated in the initiation of the BER.
The peristaltic waves in the stomach begin in the pacemaker cells in the upper corpus,
spreading towards the pyloric sphincter with increasing velocity. Because the ERA is
intermitent, it results in massive potentiation at the sphincter, slamming it shut
forcefully, along with the entire antrum.
This event is dubbed antral systole.
Basic characteristics of the pyloric sphincter:
 Default state is open, slammed shut by antral systole.
 When slammed shut by systole, its lumen shrinks, allowing it to behave
as a filter – particles too big to pass rebound to the back of the stomach.
The repeated propulsion of particles back against the stomach generates turbulent flow –
which is useful in breaking down food into chyme.
Solid and Liquid Emptying
Liquid emptying is quite basic – pressure difference between the antrum and
corpus is enough to push liquids through, since it can fit through the pyloric
sphincter with little difficulty.
The pressure difference isn't too big because of receptive relaxation. For
this reason, vagotomy to the proximal stomach raises the pressure
gradient. Vagotomy to the distal stomach has little effect on liquid
emptying.
Solid emptying is more complex. It requires a fundic (proximal) reservoir and an
antral (distal) pump.
The latter is dependent on the frequency of contraction, the fluidity of the
chyme, and the amplitude of the contraction.
Antral peristalsis is initiated by distension and a vago-vagal reflex.
Muscle stretching causes Ach release by local enteric neurons, and a
vago-vagal reflex induces more Ach release from enteric neurons For this
reason, vagotomy to the antrum causes sluggish solid emptying.
The Enterogastric Reflex – Modulation of the intensity of contractions by one or
more parameters. The duodenum mediates the rate of gastric emptying
Degree of Distension? (More distension induces emptying)
Acidity? (Low pH inhibits gastric emptying)
Osmolarity? (Hypo- or hypertonicity inhibits emptying)
Chemical Composition? (Fats induce more propulsion than proteins or
carbs)
If any of these parameters are not met (chyme is not ready to be emptied),
inhibitory enteric neurons and sympathetic stimulation will inhibit
peristalsis.
These paramaters also induce release of secretin, CCK, and GIP as part of
the enterogastrone hormonal complex, which inhibit peristalsis.
As a rule, gastric factors (distension) increase motility. Duodenal factors inhibit it.
Lecture V
VOMITING – in order to vomit, we need to reduce resistance to upward flow.
Distal stomach contracts to prevent aboral flow.
Proximal sotmach stops contracting.
The abdonmen squeezes, generating a pressure gradient that favors movement up
the throat and out the mouth.
Regulation
Vomiting is initiated in many different ways:
 Afferent pharyngeal impulses.
 Irritation of the GI-tract.
 Biochemical disequilibrium.
 Motion sickness.
 Pain.
 Psychogenic factors.
These various impulses are sent to the medullary 'vomiting center', where an
efferent response may be induced.
Part of this response is autonomic disequilibrium (fluctuating precedence of
sympathetic and parasympathetic systems), nausea, and retching.
Individuals go from tachy- to bradycardia.
Uncoordinated abdominal spasms move content upward, inducing
secondary peristalsis when too weak to push food out. This is what is
referred to as retching.
Retching ceases when the abdominal spasms are too strong, and food is
forced out.
The vomiting center cannot be regulated medically as part of anti-nausea
medication. Instead, medication and toxins work on the CTZ (Chemoreceptor
Trigger Zone), a region of the brain that 'talks' to the vomiting center.
The CTZ does not need to be present for vomiting to occur, but the vomiting
center does.
THE UPPER SMALL INTESTINE (DUODENUM)
Functions:
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Neutralization
Osmotic Equilibration
Digestion
Absorption
Effective mixing
Slow propulsion
The intestine has its own electrical activity, the frequency of which is governed
by the BER. Like the stomach, the spikes are phase-locked to the BER, and
contraction is initiated by stretch or Ach.
However, the intestinal BER is faster than the stomach's, and slows down from as
the bolus moves from the proximal to the distal region.
Intestinal muscles contract mostly via segmentation. This is induced by the ENS
and modulated by the ANS.
Segmentation propels food forward by relaxing circular muscle ahead and
longitudinal muscle behind the bolus and contraction of longitudinal muscle
ahead and circular muscle behind the bolus.
THE COLON
The colon's motility is far more sluggish than that of the small intestine.
It does not digest – absorbs water and ions.
The ileocecal sphincter is normally closed to prevent bacterial colonization. It
opens in response to local distension of the ileum and closes during local
distension of the colon.
Colonic segmentation and peristalsis are governed by an irregular BER, which
speeds up to evacuate waste to the rectum for defecation.
There are several local reflexes that facilitate waste evacuation during ingestion,
etc.
Gastroileal Reflex – Entrance of a bolus into the stomach causes ileocecal
sphincter to relax.
Gastrocolic Reflex – Distension of the stomach increases the activity of the distal
colon. This is the primary reflex we condition against during potty training.
Ileocolic Reflex – Activity in the ileum reinforces the gastrocolic reflex.
In the interdigestive period, the GI-tract undergoes intense, repetitive contractions that
move sequentially from the stomach to the distal ileum as part of the MMC (Migrating
Motor Complex).
This has 3 phases – no spikes, irregular spikes, and vigorous contractions.
Each segment of the GI-tract undergoes these phases sequentially, and the MMC
restarts when it reaches the bottom.
Lecture VI
Digestion is the process by which enzymes break down food into absorbable nutrients.
This process occurs mostly in the stomach, although some digestion does occur in the
SI.
Secretion – energy-dependent, blood-flow dependent process that causes release of ion
and/or enzyme-filled liquid.
 Protons
 Amylases
 Proteases
 Lipases
Glands higher up on the digestive tract (salivary glands) are activated neuronally. This
regulation shifts to a hormonal mechanism at the lower end of the digestive tract.
Thus, the stomach is under both neuronal and hormonal regulation.
The parasympathetic system promotes secretion, the sympathetic
represses it.
Glands – Secrete saliva.
0.5-1.5 L/day
Contains sodium, potassium, chloride, bicarbonate
Hypotonic to plasma
pH of 6.5 – 7
Contains ptyalin – salivary amylase – that breaks down polysaccharides
to maltose.
 Contains mucin – contributes to saliva's viscosity, and smooths rough
particles.
 Not much lipase activity.
The Salivary
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Lysozyme – bactericidal agent.
There are three salivary glands, each with its own secretion.
 Parotid – watery secretion.
 Sublingual – viscous secretion.
 Submandibular – both.
Saliva secretion is regulated by the ANS. Since this involves Ach release and
reception, atropine can block saliva secretion (used by dentists during surgery).
Parasympathetic activation is the main regulator. By dumping Ach on muscarinic
receptors, it promotes secretion and vasodilation. The neurotransmitter for the
sympathetic system is unknown, but sympathetic activation does not shut off
secretion. Rather, it causes release of very viscous saliva and vasoconstriction.
Secretion can be initiated by sensory receptors in the mouth, which talk to the
medullary salivary center, or by psychic factors, such as the smell of food, which
have the same effect.
To this end, secretion has three main phases:
 The psychic phase – the smell of food causes some secretion.
 The gustatory phase – entrance of food into the mouth causes secretion.
The gustatory and psychic phases constitute the cephalic phase.
 The gastrointestinal phase.
When food reaches the stomach, it encounters mixed gastric juice, the gastric secretion.
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1.5 -2 L/day
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Isotonic to plasma.
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Contains sodium, potassium, chloride, and LOTS of protons.
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Cumulative pH is 1-2.
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Contains pepsinogen – a protease.
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Contains Intrinsic Factor – necessary for Vitamin B12 absorption. This is the
only secretion necessary to life.
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Contain mucin.
The stomach secretes an alkaline fluid (pH 7.2 – 7.5) rich in muscin.
Glands in the fundus and corpus, however, secrete acid (from oxyntic cells), pepsinogen
(from Chief cells), and mucin (from mucus neck cells).
These cells make up tubular glands in the fundus and corpus.
PARIETAL (OXYNTIC) CELLS
Parietal cells contain lots of mitochondria to power the active transport of protons from
the circulation. The glands they are on also project several large invaginations
(canaliculi) into the cell to maximize transport.
Mechanism of secretion:
 Chloride ions are actively pumped across the canalicular membrane.
 Protons, generated from the autoionization of water, are actively pumped
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across the canalicular membrane by a potassium-hydrogen ATPase.
Carbon dioxide reacts with water in the presence of carbonic anhydrase to
form carbonic acid.
Carbonic acid reacts with remaining hydroxide to form bicarbonate and
water.
The bicarbonate leaves the cell passively, raising the basicity of the
circulation. This eventually causes basic urine.
Secreted HCl precipitates proteins and denatures them. It also activates pepsinogen,
facilitating digestion.
CHIEF CELLS
Chief cells secrete pepsinogen, which becomes activated at low pH (pushed to pepsin,
the active form).
Pepsin has a positive feedback effect – it can activate pepsinogen.
Parietal cells also secrete intrinsic factor, the absence of which causes pernicious anemia.
Mucin prevents destruction of the epithelia by acid.
The epithelia are protected by tight junctions (gastric-mucosal barrier, GMB), and a
muci-bicarb layer that slows down proton and neutralizes them with bicarbonate.
There is also a high turnover rate of epithelium cells, preventing their degradation.
Lecture VII
Digestion is hormonally regulated with three hormones:
 Gastrin
 Histamine
 Somatostatin
The cephalic phase of digestion is vagally-mediated (since it's at the top end of the GI-tract).
The Parasympathetic system induces release of HCl, pepsin, and mucin in addition to
vasodilation. The sympathetic system has an opposite effect.
In the gastric phase, distension of the stomach causes enteric reflexes. The result is similar to
neural stimulation – HCl, pepsin and mucin are released.
Additionally, certain vago-vagal responses occur that magnify the secretion.
Undigested amino acids or protein chunks (secretagogues) induce release of gastrin, which
hyperactivates parietal cells, producing lots of HCl.
Gastrin is also released during the cephalic phase (in anticipation of food), and by local
distension and vago-vagal reflexes).
Gastrin also possesses a unique regulation mechanism. While gastrin release is an
example of positive feedback (secretagogues induce release, which leads to more
secretagogues), if the pH of the stomach drops below 2, somatostatin inhibits gastrin
release completely.
Gastrin can also induce parietal cell proliferation, and induce an ulcer if there is too
much acid.
But what about histamine? Administration of histamine induces release of Hcl-rich gastric juice.
There have been two hypotheses about the activity of histamine in the stomach:
 The common-mediator hypothesis: gastrin and Ach induce release of
histamine, which interacts with parietal cells. This was proven wrong.
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The receptor interaction hypothesis: there are three receptors on a parietal
cell – one for gastrin, another for Ach, and a final one for histamine.
Failure of one to bind induces changes in the remaining two. Also proven
wrong.
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The permissive hypothesis: histamine forms a 'tonic background' to the
parietal cells as it is constantly produced, sensitizing them to other
stimuli. If this background is disrupted, HCl secretion will be impacted.
When secretagogues move to the duodenum, they begin to exert a negative effect on gastrin
release via the enterogastric reflex.
By the time food has moved to the intestine, it has been:
 Reduced to semi-liquid consistency – chyme.
 Acidified, but no change to osmotic pressure.
 Somewhat digested. (Polysaccharides -> disaccharides, polypeptides ->
oligopeptides, but not much lipolysis).
However, the bolus still needs:
 To neutralize the chyme.
 To osmotically equilibrate the chyme.
 To actually digest and absorb nutrients.
This is where the pancreas comes into play.
The pancreas is an accessory digestive organ with both endocrine and exocrine
components. It secretes pancreatic juice from Acinar Cells.
 0.5 – 1.5 L/day
 Rich in bicarbonate, contains sodium, potassium, and chloride.
 pH of 7.2-8.2.
This juice contains digestive enzymes such as trypsinogen, chymotripsin, elastase, etc.
Trypsinogen is by far the most important, as when it is activated (by
enterokinase, an intestinal enzyme) to produce trypsin, a protease, it can also
activate other pancreatic proteins.
So that trypsin and other digestive proteins don't chew up the pancreas, its
activation must occur outside the pancreas. For this reason, the pancreas secretes
trypsin inhibitor.
Lecture VIII
The liver produces a secretion discharged into the duodenum called bile.
Bile leaves the liver through the bile ducts, which coalesce into the common bile duct
and pass to the Sphincter of Oddi.
If the sphincter is open, bile moves to the duodenum.
If it's closed, bile moves through the cystic duct to the gallbladder.
Composition/function of bile:
 Isotonic – slightly more bicarbonate than plasma.
 PH 7.8-8.2.
 Neutralizes chyme.
 3% solids – does NOT contain digestive enzymes.
Bile Acids (bile salt)
Bile pigments (bilirubin)
Cholesterol
Phospholipids
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Secretion is continuous.
Very little enters the duodenum with the entrance of a meal.
The gallbladder dehydrates bile, saturating it. There is more solids in cholecystic bile
than in hepatic bile. This slightly lowers the pH, but increases the viscosity.
Cholecystectomy (removal of the gallbladder by surgery) does NOT lead to a failure to
process fats. While patients must be more careful about their fat intake, the body retains
its ability to metabolize fatty acids without a gall bladder.
Bile salts are synthesized from cholesterol in the liver.
They facilitate digestion of hydrophobic molecules by micelle formation.
Stabilize emulsions.
Digest vitamins A,D,E,K.
There is a total bile salt pool of 3.5g.
We synthesize 0.5g every day, but release 15-20g.
90% is reabsorbed at the ileum, reentering the digestive system at the liver via
the portal circulation.
10% to the colon.
Functions of bile salts:
 Intraportal – regulate volume of bile secreted and synthesis of bile salts.
The more bile salts returned, the larger the volume of bile secreted.
If the ileum is removed, we have less bile secreted.
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Intrahepatic – Keep cholesterol in solution.
Cholesterol is incredibly soluble in bile.
Cholesterol precipitation causes gallstones.
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Intraintestinal – emulsify and transport fats.
Bile salts act as a detergent to form stable emulsions in the
intestinal fluid.
Induce peristaltic contractions to break up fats.
Assist in the transport from the lumen to intestinal cells of fat and
hydrophobic molecules.
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Colonic – promote defecation.
Inhibit sodium, water reuptake.
The presence of too much bile salts in the colon causes diarrhea –
a situation common in Crohn's Disease.
How are these various juices regulated?
Pancreas – during the gustatory phase of secretion, a large volume of alkaline
juice (induced by secretin) and a small volume of enzyme-rich juice (regulated
by vagal impulses) are released.
Bile Salts Choleretics – act on the liver to produce more bile (stool softeners).
Cholagogues – induce emptying of the gall bladder and relaxation of the
sphincter of Oddi (more bile in the SI).
Lecture IX
The intestinal mucosa is composed of villi (outcroppings) and crypts (invaginations).
Villi complete digestion and absorb food particles, while crypts secrete an
alkaline fluid (Succus entericus).
Crypts contain proliferative zones – areas of quick cell division wherein the new
cells displace the old secretory cells.
Succus Entericus
 Isotonic
 pH 7.5 – 9
Villi do not secrete enzymes. Rather, they are held in the brush border (lumen/vilus
interface) in anticipation of food.
 Enterokinase (activates trypsinogen)
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Amylase (unimportant)
Lipase (unimportant)
Many aminopeptidases to complete protein digestion.
Dipeptidases
Disaccharases
1. Sucrase
2. Maltase
3. Isomaltase
4. Lactase
Digestion and absorption are completed in the SI.
Colonic Secretion
 Small
 Very alkaline
 Isotonic
 Viscous – contains mucin
 NO digestive enzymes
 Resident flora (bacteria)
Absorption is an important process, as we secrete 7L of fluid daily from various GI
glands (salivary, intestine, parietal cells, etc.).
If we ingest 2L of water every day, we must thus reabsorb 9L of water.
Additionally, we need to reabsorb many ions and digested lumen proteins.
For this reason, the intestine contains a huge surface area/volume ratio – it
contains circular folds, villi, and microvilli to maximize reabsorption.
Each villus is in contact with blood vessels to recycle fluid, ions, etc.
Iron and calcium are only reabsorbed in the duodenum.
Carbohydrates and proteins can be absorbed down the whole length of the GIT.
Vitamin B12 and bile acids can only be absorbed in the ileum.