Transcript Digestive System

Digestive System
Keri Muma
Bio 6
Digestive Organs

Organs of the Alimentary Canal
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Mouth
Pharynx
Esophagus
Stomach
Small Intestines
Large Intestines
Digestive Organs
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Accessory organs
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Salivary glands
Teeth
Pancreas
Liver
Gallbladder
Histology of the Alimentary Canal
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Mucosa – innermost layer lining the lumen, mucus
membrane epithelium
Submucosa – areolar CT layer
Muscularis externa – inner circular and outer
longitudinal layer of smooth muscle
Serosa – outermost layer lining the external surface
Functions
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Ingestion – taking
food in
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Propulsion –
movement of food
along the digestive
tract
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Peristalsis
Segmentation
Peristalsis
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Involuntary waves of contraction and
relaxation of muscles in the organ walls
Propel digestive material forward through the
digestive tract
Segmentation
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Contractions that churn and break apart
digestive material
Functions
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Digestion – breaking
down food into smaller
molecules
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Mechanical – changing
physical structure
Chemical – changing
chemical structure
Functions
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Absorption
–
transport of nutrients
from the lumen of the
gastrointestinal tract to
the blood
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Defecation
–
elimination of
indigestible substances
from the body
Regulation of Digestive Tract Activity
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Regulation of digestion involves:
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Autonomous smooth muscle
Mechanical and chemical stimuli – stretch
receptors, osmolarity, and presence of substrate
in the lumen
Gastrointestinal hormones
Extrinsic nerves control by CNS centers
Intrinsic nerves control by local centers (Enteric
Nervous System)
Autonomous Smooth Muscle

Visceral smooth muscle is autonomous

Smooth muscle pacemaker cells display rhythmic,
spontaneous variations in membrane potentials (slow
wave potential)
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Hormones, mechanical stress, and nerve stimuli
determines the starting point of the slow wave
potentials
Autonomous Smooth Muscle
Receptors of the GI Tract
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Receptors respond to changes in the digestive
tract
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Mechanoreceptors – respond to stretch or pressure
Osmoreceptors – changes in osmolarity
Chemoreceptors – pH, presence of substrates, and
end products of digestion
Their activation produces short and/or long
reflexes that will:
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Activate or inhibit digestive glands
Activate or inhibit smooth muscle
Nervous Control of the GI Tract
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Long reflexes
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Stimulus may be within or outside the GI tract
Involves integration in CNS (usually in the
medulla) and output sent via autonomic nerves to
GI tract
Extrinsic control
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Can alter muscle and gland activity
Can alter levels of hormone secretions
Modify intrinsic activity
Coordinate different parts of the GI tract
 Example: chewing food causes increased gastric
secretions in stomach (feed forward mechanism)
Nervous Control of the GI Tract
Nervous Control of the GI Tract
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Short reflexes
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Involves the enteric nervous system - myenteric
and submucous plexus within the digestive tract
wall
Intrinsic control - entire reflex arc is carried out
within the GI tract (responds to local stimuli)
Coordinates local activity, can work independently
of the CNS or it can be influenced by extrinsic
nerves because it is linked to long autonomic
reflex arcs
Nervous Control of the GI Tract
Digestive Peptides
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Gastrointestinal peptides can act as digestive
hormones and paracrine signals
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Released into the blood or ECF by cells of the
digestive tract
Can act on digestive organs and accessory
organs to excite or inhibit motility or secretions
Can also act on the brain to trigger hunger or
satiety
See table 21-1 in your textbook for a summary of
these hormones and their effects
Mouth
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Chewing begins mechanical digestion by breaking
food into smaller pieces and mixing food with saliva
Compacts food into a bolus
The salivary enzyme amylase begins the chemical
digestion of carbohydrates
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Polysaccharides
Maltose
amylase
Mouth
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Saliva
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Secreted from serous and mucous cells in the salivary
glands
Composition
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97-99.5% water
Digestive enzyme – salivary amylase
Mucus – moistens food and holds bolus together
Lysozyme and IgA – antibacterial action
Control of Salivation
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Salivary secretion is enhanced by two reflexes:
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Simple reflex - ingested food stimulates
chemoreceptors and pressoreceptors that trigger the
salivary center in the medulla
Acquired reflex - the thought
of food, cortex triggers the
salivary center in the medulla
Control of Salivation
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Autonomic Nervous System (ANS)
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Parasympathetic – larger volume of saliva, watery
and rich with amylase
Sympathetic – smaller volume, more mucus,
results in dry mouth
Deglutition (Swallowing)
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Involves the coordinated activity of the tongue, soft palate,
pharynx, and esophagus
Buccal phase – bolus is forced into the oropharynx (voluntary)
Pharyngeal-esophageal phase – controlled by the medulla and
lower pons (involuntary)
Peristalsis moves food through the pharynx and the esophagus
Stomach
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Food enters stomach from the esophagus through the
gastroesophageal sphincter
Digestion in the Stomach
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Functions of the stomach:
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Mixes and stores food until it can be emptied into
the small intestines
Degrades the bolus both physically and
chemically
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Food is mixed with gastric juices to produce chyme
Enzymatically digests proteins with the enzyme pepsin
Secretes intrinsic factor required for absorption of
vitamin B12
Gastric Phase: Long and Short Reflexes
Digestion in the Stomach
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Four phases of gastric motility
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Gastric filing
Storage
Mixing
Emptying
Digestion in the Stomach
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Gastric filling
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Stomach relaxes as it fills, rugae flatten out
Stomach dilates in response to gastric filling (1L)
Gastric storage
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Peristaltic contractions are weak in the body of the
stomach, so little mixing occurs
Digestion in the Stomach
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Gastric mixing
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Takes place in the muscular antrum
Occurs as chyme is propelled forward against the
closed pyloric sphincter by peristaltic contractions
Gastric Secretions
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Exocrine
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Mucous cells – produce mucus
to protect stomach wall from
harsh acids
Parietal cells – produce HCL and
intrinsic factor
Chief cells – produce
pepsinogen, an inactive form of
the protein digesting enzyme
pepsin
Digestion in the Stomach
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Chemical digestion of
proteins begins in the
stomach
Pepsinogen is converted
into pepsin by HCl
Pepsin breaks down
proteins into peptide
fragments
Proteins
Peptides
Pepsin
Gastric Secretions
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Endocrine
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G cells – produce the hormone
gastrin which stimulates gastric acid
secretion
Paracrine
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ECL cells – secrete histamine,
stimulates secretion from parietal
cells
D cells – secrete somatostatin,
inhibits secretions from parietal, ECL
cells, and G cells
Regulation of Gastric Secretion
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Neural and hormonal mechanisms regulate
the release of gastric juices
Excitatory and inhibitory events occur in three
phases:
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Cephalic (reflex) phase: prior to food entry
Gastric phase: once food enters the stomach
Intestinal phase: as partially digested food enters
the duodenum
Regulation of Gastric Secretion
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Cephalic phase – prior to food entry
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Excitatory events include:
 Sight or thought of food
 Stimulation of taste, smell, pressure receptors;
chewing
 Vagal stimulation releases ACh – stimulates
parietal, G cells, and ECL cells
Inhibitory events include:
 Loss of appetite or depression
 Decrease in stimulation of the parasympathetic
division
Regulation of Gastric Secretion
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Gastric Phase
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Excitatory events include:
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Stomach distension - activation of stretch receptors
(neural activation)
Activation of chemoreceptors by peptides, caffeine,
and alkaline pH
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Triggers release of gastrin into the blood
Inhibitory events include:
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An acidic pH lower than 2 - triggers release of
somatostatin
Summary of Gastric Secretions
Regulation of Gastric Secretions
Regulation and Mechanism of HCl Secretion
Figure 23.17
Regulation of Gastric Secretion
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Intestinal Phase
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Mostly inhibitory
Inhibitory phase – distension of duodenum, presence
of fatty, acidic, or hypertonic chyme in the duodenum
 Initiates local reflexes and vagal nuclei
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Closes the pyloric sphincter
Release of hormones that inhibit gastric secretion
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Cholecystokinin and Secretin – decrease gastric
secretions and slows gastric motility
Gastric inhibitory peptides (GIP) – inhibits gastric acid
secretion, also promotes insulin release from
pancreas
Release of Gastric Juice
Figure 23.16
Digestion in the Stomach
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Gastric emptying
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A strong enough peristaltic wave can push a small
amount of chyme through the pyloric sphincter
before it closes tightly
The rate of gastric emptying is controlled by both
gastric and duodenal factors
Digestion in the Stomach
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Gastric factors that increase gastric
emptying
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Amount of chyme in the stomach – the
stomach empties at a rate that is proportional
to the volume of chyme
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Distention – triggers smooth muscle and
intrinsic plexuses
Fluidity of chyme
Signaling by the vagus nerve (extrinsic control)
The hormone gastrin
Rate of Gastric Emptying
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The duodenum controls gastric emptying by
reducing peristaltic activity in the stomach until it
is ready to accommodate more chyme
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Duodenal factors that decrease gastric emptying
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Fatty chyme – digested and absorbed slower than
other nutrients in the duodenum
Acidity – chyme must be completely neutralized
Hypertonicity – need time for absorption of
nutrients to catch up with digestion
Distention – needs to cope with volume before
receiving more
Regulation of Gastric Emptying
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Gastric emptying is regulated by:
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The neural enterogastric reflex -when the
duodenum fills stretch receptors are
stimulated and the pyloric sphincter closes
Hormonal mechanisms:
 Cholecystokinin and secretin – released by
duodenal endocrine cells into the blood; will
inhibit gastric motility
Regulation of Gastric Emptying
Figure 23.19
Small Intestines
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Extends from the pyloric sphincter to
the ileocecal valve
Main function is chemical digestion
and absorption of nutrients
Three regions:
 Duodenum – first part
 Chemical digestion, absorption
 Jejunum – middle
 Absorption
 Ileum – last part, joins the
large intestines
Small Intestines
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Surface area for absorption is increased by villi and
microvilli
Substances must pass through an epithelial cells and then
diffuse through the interstitial fluid in the underlying CT into
a capillary or lacteal
Duodenum
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Chyme enters the duodenum where it is mixed
with bile from the liver and digestive enzymes
from the pancreas
Functions of the Liver
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Produces bile to aid in the digestion of fats
Stores excess nutrients and releases them
when needed
Detoxifies drugs and metabolites
Produces plasma proteins
Production of Bile by the Liver
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Hepatocytes produce bile and secrete it into bile
ducts that empty into the common hepatic duct.
The sphincter of Oddi at the base of the common bile
duct prevents bile from entering the duodenum
between meals
Bile will back up into the gallbladder where it is
concentrated and stored
Function of Bile
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Bile is secreted into the duodenum to emulsify fats
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Bile increases the surface area for lipase to work on fats
Composition of Bile
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Bile is composed of:
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Aqueous alkaline solution
Bile salts
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Nonpolar portion – cholesterol based
steroid
Polar portion
Cholesterol
Lecithin – a phospholipid
Bilirubin – byproduct of
RBC destruction
Regulation of Bile Release
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Acidic, fatty chyme causes the duodenum
to release:
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Cholecystokinin (CCK) and secretin into the
bloodstream
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Secretin transported in blood stimulate the liver to
produce bile
Cholecystokinin causes the gallbladder to contract
and the sphincters to relax
Vagal stimulation causes weak contractions
of the gallbladder
Regulation of Bile Release
Figure 23.25
Recycling of Bile Salts
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Most bile salts are
reabsorbed back into
the blood in the ileum
are returned by the
hepatic portal system
About 5% of bile
escapes in feces
The Pancreas
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Secretes pancreatic juices into the duodenum that
break down all categories of food
Acini cells secrete digestive enzymes
Duct cells secrete NaHCO3– which neutralizes acidic
chyme
Regulation of Pancreatic Secretion
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When chyme enters the duodenum CCK and
secretin enter the bloodstream
Upon reaching the pancreas:
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CCK induces the secretion of enzyme-rich
pancreatic juice
Secretin causes secretion of bicarbonate-rich
pancreatic juice
Vagal stimulation also causes release of
pancreatic juice
Regulation of Pancreatic Secretion
Figure 23.28
Summary of Intestinal-Phase
See Table 21-1 on page 702
for summary of hormones
Pancreatic Enzymes
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Proteolytic enzymes are released in an inactive
form and are activated in the duodenum
Each breaks different peptide bonds resulting in
short peptides and amino acids
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Trypsinogen
Enterokinase
Chymotrypsinogen
Procarboxypeptidase
Trypsin
Trypsin
Trypsin
Chymotrypsin
Carboxypeptidase
Proteolytic Enzyme Activation
Pancreatic Enzymes
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Amylase – hydrolyzes polysaccharides into
disaccharides
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Nucleases – hydrolyzes nucleic acids into nucleotides
Lipase – hydrolyzes triglycerides into monoglycerides
and fatty acids
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Brush Border Enzymes
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Final chemical digestion is carried out by brush
border enzymes found in the plasma membrane of
the small intestine’s mucosal cells
 Disaccharides
Monosaccharides
Maltase
Sucrase
Lactase
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Peptides
Amino Acids
aminopeptidase
Absorption in the Small Intestines
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Most electrolytes, nutrients and vitamins are
completely absorbed
Vitamins
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Fat soluble vitamins such as A, D, E, and K are
absorbed along with lipids
Water soluble vitamins such as C and B are
passively absorbed with water
Vitamin B12 is combined with intrinsic factor and
absorbed by receptor mediated endocytosis in the
ileum
Absorption in the Small Intestines
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Minerals
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Ca2+ and iron are absorbed on an as needed
basis mostly by active transport
Ca2+ absorption:
 Depends on blood levels of ionic calcium
 Is regulated by vitamin D and parathyroid
hormone (PTH)
Absorption in the Small Intestines
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Iron
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Absorbed iron is
stored in the epithelial
cells as ferritin until
needed
If blood iron levels are
low it is released into
the blood
Carried in the blood by
transferrin to the bone
marrow to be used for
RBC production
Electrolyte Absorption
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Cl-, H20, glucose, and amino acids absorption
depends on active transport of Na+ into the interstitial
fluid
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Active transport of Na+ creates a concentration gradient
Water follows the osmotic gradient and anions passively follow
the electrical gradient established by
sodium
Na+ re-entry through a cotransporter
can drive solutes against the
concentration gradient
Absorption of Nutrients
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Absorption of sugars and amino acids
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Facilitated diffusion via cotransport with Na+,
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Driven by secondary active transport
Enter the capillary bed in the villi
Transported to the liver via the hepatic portal vein
Absorption of Sugars
Absorption of Amino Acids
Absorption of Lipids

When micelles get close to the
absorptive surface lipids are
released and diffuse into intestinal
cells where they are:
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Synthesized into triglycerides in the
SER
Combine with proteins to form
chylomicrons in the golgi apparatus
Released by exocytosis
Enter lacteals and are transported
to systemic circulation via lymph
Motility in the Small Intestine
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Segmentation is the most common motion of the
small intestine
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It is initiated by intrinsic pacemaker cells (Cajal cells)
Mixes chyme with digestive juices and exposes it to the
absorptive surface of the small intestines
Moves contents steadily toward the ileocecal valve
Factors enhancing the intensity of segmentation
contractions:
 Distention
 Gastrin
 Extrinsic nerves
Motility in the Small Intestine

After nutrients have been absorbed:
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A series of peristaltic waves called the migrating
motility complex begins with each wave starting
distal to the previous
Sweeps remnants of the previous meal, bacteria,
mucosal cells, and debris into the large intestine
Regulated by the hormone motilin which is
released during the postabsorptive state by
mucosa endocrine cells
Motility of the Small Intestines

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Ileum empties into the cecum through the
ileocecal valve
The gastroileal reflex – ileocecal sphincter
relaxes and allows chyme to pass into
the large intestine


Triggered by food
entering stomach
Gastrin and increased
motility of the
small intestines
Large Intestines

Frames the small intestines
Extends from the ileocecal valve to the anus

Functions
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Absorb remaining water, electrolytes, vitamin K
Eliminates indigestible food from the body
Motility of the Large Intestines
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Segmentation in the large intestines occurs less
frequently (3 to 4 times a day)
Gastrocolic reflex – contraction of the ascending
and transverse colon results in mass movement of
content forward into the rectum

Triggered by gastrin and extrinsic nerves when food
enters the stomach
Defecation Reflex


Distention of the
rectum triggers stretch
receptors causing the
internal sphincter to
relax (involuntary)
When the external
sphincter is voluntarily
relaxed defecation
occurs
Figure 23.32