Transcript Human Physiology - Maryville University

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Chapter 18
The Digestive System
18-1
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Chapter 18 Outline
Functions of GI Tract
Structure of Digestive System
From Mouth to Stomach
Stomach
Small Intestine
Large Intestine
Liver
Gall Bladder & Pancreas
Control & Phases of Digestion
Digestion & Absorption of Food Types
18-2
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Overview
Inside
gastrointestinal (GI) tract, food is broken down
by hydrolysis into molecular monomers
Absorption of monomers occurs in small intestine
18-3
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Fig 18.1
18-4
Functions of GI Tract
18-5
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Motility
Is
movement of food through GI tract by means of:
Ingestion--taking food into mouth
Mastication--chewing food & mixing it with saliva
Deglutition--swallowing food
Peristalsis--rhythmic wave-like contractions that
move food through GI tract
18-6
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Secretion
Includes
release of exocrine & endocrine products into
GI tract
Exocrine secretions include: HCl, H20, HC03-, bile,
lipase, pepsin, amylase, trypsin, elastase, & histamine
Endocrine includes hormones secreted into stomach &
small intestine to help regulate GI system
E.g. gastrin, secretin, CCK, GIP, GLP-1, guanylin,
VIP, & somatostatin
18-7
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Absorption
Is
passage of digested end products into blood or
lymph
18-8
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Storage and Elimination
Includes
temporary storage & subsequent elimination
of indigestible components of food
18-9
Structure of Digestive System
18-10
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Digestive System
Is
composed of GI tract (alimentary canal) & accessory
digestive organs
GI tract is 30 ft long; extends from mouth to anus
18-11
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Digestive System continued
 Organs
include oral
cavity, pharynx,
esophagus,
stomach, & small &
large intestine
 Accessory organs
include teeth,
tongue, salivary
glands, liver,
gallbladder, &
pancreas
Fig 18.2
18-12
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Layers of GI Tract
Are
called tunics
The 4 tunics are mucosa, submucosa, muscularis, &
serosa
Fig 18.3
18-13
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Mucosa
 Is
the absorptive & secretory layer lining lumen of GI tract
 In places is highly folded with villi to increase absorptive area
 Contains lymph nodules, mucus-secreting goblet cells, & thin
layer of muscle
Fig 18.3
18-14
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Submucosa
 Is
a thick, highly vascular layer of connective tissue where
absorbed molecules enter blood & lymphatic vessels
 Contains glands & nerve plexuses (submucosal plexus) that
carry ANS activity to muscularis mucosae
Fig 18.3
18-15
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Muscularis
Is
responsible for segmental contractions & peristaltic
movement through GI tract
Has an inner circular & outer longitudinal layer of
smooth muscle
Activity of these layers moves food through tract
while pulverizing & mixing it
Myenteric plexus between these layers is major
nerve supply to GI tract
Includes fibers & ganglia from both Symp &
Parasymp systems
18-16
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Serosa
 Is
outermost layer; serves to bind & protect
 Consists of areolar connective tissue covered with layer of
simple squamous epithelium
Fig 18.3
18-17
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Regulation of GI Tract
Parasympathetic
effects, arising from vagus & spinal
nerves, stimulate motility & secretions of GI tract
Sympathetic activity reduces peristalsis & secretory
activity
GI tract contains an intrinsic system that controls its
movements--the enteric nervous system
GI motility is influenced by paracrine & hormonal
signals
18-18
From Mouth to Stomach
18-19
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From Mouth to Stomach
Mastication
(chewing) mixes food with saliva which
contains salivary amylase
An enzyme that catalyzes partial digestion of starch
18-20
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From Mouth to Stomach continued
Deglutition
(swallowing) begins as voluntary activity
Oral phase is voluntary & forms a food bolus
Pharyngeal & esophageal phases are involuntary &
cannot be stopped
To swallow, larynx is raised so that epiglottis covers
entrance to respiratory tract
A swallowing center in medulla orchestrates
complex pattern of contractions required for
swallowing
18-21
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From Mouth to Stomach continued
Esophagus
connects pharynx to stomach
Upper third contains skeletal muscle
Middle third contains mixture of skeletal & smooth
Terminal portion contains only smooth
Passes through diaphragm via esophageal hiatus
18-22
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From Mouth to Stomach continued
 Peristalsis
propels food
thru GI tract
 = wave-like muscular
contractions
 After food passes
into stomach, the
gastroesophageal
sphincter constricts,
preventing reflux
Fig 18.4
18-23
Stomach
18-24
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Stomach
Is
most distensible part of GI tract
Empties into the duodenum
Functions in: storage of food; initial digestion of
proteins; killing bacteria with high acidity; moving
soupy food mixture (chyme) into intestine
18-25
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Stomach continued
 Is
enclosed by
gastroesophageal
sphincter on top &
pyloric sphincter on
bottom
 Is divided into 3
regions:
 Fundus
 Body
 Antrum
Fig 18.5
18-26
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Stomach continued
 Inner
surface of
stomach is highly
folded into rugae
 Contractions of
stomach churn
chyme, mixing it
with gastric
secretions
 Eventually these
will propel food
into small
intestine
Fig 18.5
18-27
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Stomach continued
Fig 18.7
 Gastric
mucosa
has gastric pits in
its folds
 Cells that line
folds deeper in
the mucosa, are
exocrine gastric
glands
18-28
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Stomach continued
 Gastric
glands contain cells
that secrete different
products that form gastric
juice
 Goblet cells secrete
mucus
 Parietal cells secrete
HCl & intrinsic factor
(necessary for B12
absorption in intestine)
 Chief cells secrete
pepsinogen (precursor
for pepsin)
Fig 18.7
18-29
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Stomach continued
Enterochromaffin-
like cells secrete
histamine &
serotonin
G cells secrete
gastrin
D cells secrete
somatostatin
Fig 18.7
18-30
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HCl in Stomach
 Is
produced by
parietal cells which
AT H+ into lumen via
an H+/ K+ pump (pH
≈1)
 Cl- is secreted by
facilitated diffusion
 H+ comes from
dissociation of
H2CO3
 Cl- comes from
blood side of cell in
exchange for HC03-
Fig 18.8
18-31
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HCl in Stomach continued
Is
secreted in response to the hormone gastrin; & ACh
from vagus
These are indirect effects since both stimulate
release of histamine which causes parietal cells to
secrete HCl
18-32
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HCl in Stomach continued
 Makes
gastric juice
very acidic which
denatures proteins
to make them more
digestible
 Converts
pepsinogen into
pepsin
 Pepsin is more
active at low pHs
Fig 18.9
18-33
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Digestion & Absorption in Stomach
Proteins
partially digested by pepsin
Carbohydrate digestion by salivary amylase is soon
inactivated by acidity
Alcohol & aspirin are only commonly ingested
substances absorbed
18-34
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Gastric and Peptic Ulcers
 Peptic
ulcers are erosions of mucous membranes of stomach or
duodenum caused by action of HCl
 In Zollinger-Ellison syndrome, duodenal ulcers result from
excessive gastric acid in response to high levels of gastrin
 Helicobacter pylori infection is associated with ulcers
 Antibiotics are useful in treating ulcers
 Acute gastritis is an inflammation that results in acid damage
due to histamine released by inflammation
 Why histamine receptor blockers such as Tagamet & Zantac
can treat gastritis
18-35
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Protective Mechanisms of Stomach
Include:
Impermeability
of parietal & chief cells to HCl
A layer of alkaline mucus containing HC03Tight junctions between adjacent epithelial cells
Rapid rate of cell division (entire epithelium replaced
in 3 days)
Prostaglandins (PGs) inhibit gastric secretions
Which is why PG blockers such as NSAIDs can
cause ulcers
18-36
Small Intestine
18-37
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Small Intestine (SI)
 Is
longest part of GI tract; approximately 3m long
 Duodenum is 1st 25cm after pyloric sphincter
 Jejunum is next 2/5s
 Ileum is last 3/5s; empties into large intestine
Fig 18.10
18-38
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Small Intestine (SI) continued
Absorption
of digested food occurs in SI
Facilitated by long length & tremendous surface area
18-39
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Small Intestine (SI) continued
 Surface
area
increased by
foldings &
projections
 Large folds are
plicae circulares
 Microscopic fingerlike projections are
villi
 Apical hair-like
projections are
microvilli
Fig 18.10
18-40
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Small Intestine (SI) continued
 Each
villus is covered with
columnar epithelial cells
interspersed with goblet
cells
 Epithelial cells at tips of
villi are exfoliated &
replaced by mitosis in
crypts of Lieberkuhn
 Inside each villus are
lymphocytes, capillaries,
& central lacteal
Fig 18.12
18-41
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Small Intestine (SI) continued
 A carpet
of hair-like microvilli project from apical surface of each
epithelial cell
 Create a brush border
18-42
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Intestinal Enzymes
 Attached
to microvilli are brush border enzymes that are
not secreted into lumen
 Enzyme active sites are exposed to chyme
18-43
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Intestinal Contractions and Motility
Fig 18.14
2
major types of contractions
occur in SI:
 Peristalsis
is weak & slow
& occurs mostly because
pressure at pyloric end is
greater than at distal end
 Segmentation is major
contractile activity of SI
 Is contraction of circular
smooth muscle to mix
chyme
18-44
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Intestinal Contractions & Motility continued
 Occur
automatically
via endogenous
pacemaker activity
 Contractions are
driven by graded
depolarizations
called slow waves
Fig 18.15
18-45
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Intestinal Contractions & Motility continued
 Slow
waves are
produced by nonneuronal interstitial
cells of Cajal (ICC)
 Conducted to
smooth muscle via
gap junctions
 Slow waves spread
from 1 smooth
muscle cell to
another thru
nexuses
Fig 18.16
18-46
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Intestinal Contractions & Motility continued
When
slow waves exceed threshold, trigger APs in
smooth muscle by opening V-gated Ca2+ channels
Influx of Ca2+ produces depolarization phase of AP &
stimulates contraction
Repolarization via K+ efflux
Contractions are modified by ANS activity
ACh from Parasymp increases amplitude & duration
of slow waves
NE & Epi from Symp decrease activity of intestines
18-47
Large Intestine
18-48
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Large Intestine (LI) or Colon
Has
no digestive function but absorbs H20,
electrolytes, B & K vitamins, & folic acid
Internal surface has no villi or crypts & is not very
elaborate
Contains large population of microflora
LI bacteria produce folic acid & vitamin K & ferment
indigestible food to produce fatty acids
18-49
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Large Intestine (LI) or Colon continued
 Extends
from
ileocecal valve at
end of SI to anus
 Outer surface bulges
to form pouches
(haustra)
 Chyme from SI
enters cecum, then
passes to ascending
colon, transverse
colon, descending
colon, sigmoid colon,
rectum, & anal canal
Fig 18.17
18-50
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Fluid & Electrolyte Absorption in LI
SI
absorbs most water but LI absorbs 90% of water it
receives
Begins with osmotic gradient set up by Na+/K+
pumps
Water follows by osmosis
Salt & water reabsorption stimulated by aldosterone
LI can also secrete H20 via AT of NaCl into intestinal
lumen
18-51
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Defecation
After
electrolytes & water have been absorbed, waste
material passes to rectum, creating urge to defecate
Defecation reflex begins with relaxation of external
anal sphincter allowing feces to enter anal canal
Longitudinal rectal muscles contract to increase
rectal pressure; internal anal sphincter relaxes
Excretion is aided by contractions of abdominal &
pelvic muscles which push feces from rectum
18-52
Liver
18-53
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Structure of Liver
 Liver
largest internal organ
 Hepatocytes form hepatic plates that are 1–2 cells thick
 Plates separated by sinusoids which are fenestrated &
permeable even to proteins
 Contain phagocytic Kupffer cells
Fig 18.20
18-54
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Hepatic Portal System
Food
absorbed in SI is delivered 1st to liver
Capillaries in digestive tract drain into hepatic portal
vein which carries blood to liver
Hepatic vein drains liver
Liver also receives blood from hepatic artery
18-55
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Liver Lobules
 Are
functional units formed by hepatic plates
 In middle of each is central vein
 At edge of each lobule are branches of hepatic portal vein &
artery which open into sinusoids
Fig 18.20
18-56
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Liver Lobules
 Bile
is secreted by hepatocytes in bile canaliculi
 Empty into bile ducts which flow into hepatic ducts that carry
bile away from liver
Fig 18.21
18-57
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Enterohepatic Circulation
 Is
recirculation of
compounds between
liver & intestine
 Many compounds are
released in bile,
reabsorbed in SI, &
returned to liver to be
recycled
 Liver excretes drug
metabolites into bile to
pass out in feces
Fig 18.22
18-58
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18-59
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Bile Production and Secretion
 Amounts
to 250–1500 ml/day
 Bile pigment (bilirubin) is produced in spleen, bone marrow, &
liver
 Is a derivative of heme groups (minus iron) from Hb
 Carried in blood attached to albumin
 Free bilirubin combines with glucuronic acid to form conjugated
bilirubin that is secreted into bile
 Converted by intestinal bacteria to urobilinogen
 30-50% of urobilogen is absorbed by intestine & enters
hepatic vein
 Thus enters enterohepatic circulation to be recycled or
filtered by kidneys & excreted in urine
18-60
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Metabolism of Heme and Bilirubin
Fig 18.23
18-61
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Bile Acids
 Are
formed in major
breakdown pathway for
cholesterol
 Are mostly cholic &
chenodeoxycholic acids
 Form bile salts by
combining with glycine
or taurine
 Bile salts aggregate
as micelles
 95% of bile acids are
absorbed by ileum
Fig 18.25
18-62
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Detoxification of Blood
Liver
can remove hormones, drugs, & other
biologically active molecules from blood by:
Excretion into bile
Phagocytosis by Kupffer cells
Chemical alteration of molecules
E.g. ammonia is produced by deamination of
amino acids in liver
 Liver converts it to urea which is excreted in
urine
18-63
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Detoxification of Blood continued
Liver
conjugates steroid hormones & xenobiotics with
groups that make them anionic
Which can be transported into bile or urine by
multispecific organic anion transport carriers &
excreted
Cytochrome P450 enzymes are involved in hepatic
metabolism of steroids & drugs
18-64
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Secretion of Glucose, Triglycerides &
Ketones
Liver
helps regulate blood glucose by removing it from
blood or releasing it to blood
Removes it via glycogenesis & lipogenesis
Or produces it via glycogenolysis &
gluconeogenesis
Can convert free fatty acids into ketone bodies
(ketogenesis) that can be used for energy during
fasting
18-65
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Production of Plasma Proteins
Albumin
& most of plasma globulins are produced by
liver
Albumin makes up 70% of total plasma protein &
contributes most to colloid osmotic pressure of blood
Globulins transport cholesterol & hormones, inhibit
trypsin, & are involved in blood clotting
Constitute many of the clotting factors
18-66
Gall Bladder & Pancreas
18-67
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Gallbladder
 Is
a sac-like organ attached to inferior
surface of liver
 Stores & concentrates bile
continuously produced by liver
 When SI is empty, sphincter of
Oddi in common bile duct closes &
bile is forced into gallbladder
 Expands as it fills with bile
 When food is in SI, sphincter of
Oddi opens, gall bladder
contracts, & bile is ejected thru
cystic duct into common bile duct
then to duodenum
Fig 18.26
18-68
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Pancreas
Is
located behind stomach
Has both endocrine & exocrine functions
Endocrine function performed by islets of
Langerhans
Secretes insulin & glucagon
Exocrine secretions include bicarbonate solution &
digestive enzymes
These pass in pancreatic duct to SI
Exocrine secretory units are acini
18-69
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Fig 18.26
18-70
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Fig 18.28
18-71
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Pancreatic Juice
Contains
water, bicarbonate, & digestive enzymes
Digestive enzymes include amylase for starch, trypsin
for proteins, and lipase for fats
Brush border enzymes are also required for
complete digestion
18-72
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Pancreatic Juice
 Most
pancreatic
enzymes are
produced in inactive
form (zymogens)
 Trypsin is activated
by brush border
enzyme,
enterokinase
 Trypsin activates
other zymogens
Fig. 18.29
Fig 18.30
18-73
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18-74
Control & Phases of Digestion
18-75
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Neural and Endocrine Regulation
 Neural
& endocrine mechanisms modify activity of GI system
 Vagus nerve is heavily involved in regulating & coordinating
digestive activities
 GI tract is both an endocrine gland & target for action of
hormones
 Hormones include secretin, gastrin, CCK, & GIP
18-76
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Regulation of Gastric Function
Gastric
motility & secretion occur automatically
Waves of contraction are initiated spontaneously by
pacesetter cells & secretion occurs in absence of
hormonal & neural input
ANS & hormonal effects are superimposed on
automatic activity
Extrinsic control of gastric function is divided into
cephalic, gastric, & intestinal phases
18-77
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Cephalic Phase
Refers
to control by brain of vagus activity
Stimulated by sight, smell, & taste of food
Activation of vagus:
Stimulates chief cells to secrete pepsinogen
Directly stimulates G cells to secrete gastrin
Directly stimulates ECL cells to secrete histamine
Indirectly stimulates parietal cells to secrete HCl
Continues into 1st 30 min of a meal
18-78
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Gastric Phase
Arrival
of food in stomach stimulates gastric phase
Gastric secretion stimulated by distension of stomach
& chemical nature of chyme
18-79
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Gastric Phase continued
 Short
polypeptides & amino
acids stimulate G cells to
secrete gastrin & chief cells
to secrete pepsinogen
 Gastrin stimulates ECL
cells to secrete histamine
which stimulates parietal
cell secretin of HCl
 This is a positive
feedback mechanism: As
more HCl & pepsinogen
are secreted, more
polypeptides & amino
acids are released
Fig 18.31
18-80
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Gastric Phase continued
 Secretion
of HCl is also
regulated by a negative
feedback mechanism:
 HCl secretion
decreases if pH <
2.5; at pH 1 gastrin
secretion stops
 D cells stimulate
secretion of
somatostatin which
inhibits gastrin
secretion
Fig 18.31
18-81
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Intestinal Phase
Begins
with inhibition of gastric activity when chyme
enters SI
Arrival of chyme in SI is detected by sensory neurons
of vagus
This causes a neural reflex that inhibits gastric
motility & secretion
Fat in chyme stimulates SI to secrete
enterogasterones--hormones that inhibit gastric
motility & secretion
Enterogasterones include somatostatin, CCK, &
GLP-1
18-82
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Enteric Nervous System
Submucosal
& myenteric plexuses contain as many
neurons as spinal cord
Includes preganglionic Parasymp axons, ganglion cell
bodies, postganglionic Symp axons; & afferent intrinsic
& extrinsic sensory neurons; interneurons, & glia
Peristalsis is controlled by enteric NS
18-83
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Enteric Nervous System continued
Fig 18.32
 For
peristalsis:
 ACh & substance
P stimulate
smooth muscle
contraction above
bolus
 NO, VIP, & ATP
stimulate smooth
muscle relaxation
below bolus
Insert fig. 18.31
18-84
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Paracrine Regulators of Intestine
ECL
cells release serotonin & motilin in response to
pressure & chemical stimuli in SI
Serotonin stimulates intrinsic afferents which
activate motor neurons in intrinsic NS
Motilin stimulates contraction in duodenum &
stomach antrum
Guanylin, from ileum & colon, stimulates production of
cGMP which inhibits absorption of Na+& causes
secretion of Cl- & H20
18-85
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Intestinal Reflexes
Can
be mediated by enteric NS & paracrines; &
regulated by ANS & hormones
Gastroileal reflex refers to increased motility of ileum &
movement of chyme thru ileocecal sphincter in
response to increased gastric activity
Ileogastric reflex decreases gastric motility in response
to distension of ileum
Intestino-intestinal reflex causes relaxation of rest of
intestine when any part is overdistended
18-86
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Secretion of Pancreatic Juice
Secretion
of pancreatic juice & bile is stimulated by
secretin & bile
Secretin is secreted in response to duodenal pH < 4.5
Stimulates release of HC03- into SI by pancreas &
into bile by liver
CCK is secreted in response to fat & protein content of
chyme in duodenum
Stimulates production of pancreatic enzymes
Enhances secretin
Stimulates contraction of sphincter of Oddi
18-87
Digestion & Absorption of Food Types
18-88
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Digestion & Absorption of Carbohydrates
Fig 18.33
 Most
carbohydrates are
ingested as starch-a polymer of glucose
 Salivary amylase begins
starch digestion
 Pancreatic amylase
converts starch to
oligosaccharides
 Oligosaccharides
hydrolyzed by SI brush
border enzymes
18-89
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Digestion & Absorption of Protein
Begins
in stomach when pepsin digests proteins to
form polypeptides
In SI, endopeptidases (trypsin, chymotrypsin, elastase)
cleave peptide bonds in interior of polypeptides
SI exopeptidases (carboxypeptidase, aminopeptidase)
cleave peptide bonds from ends of polypeptides
18-90
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Digestion & Absorption of Protein continued
 Protein
digestion in
SI results in free
amino acids,
dipeptides, &
tripeptides
 Which are
transported into
SI cells where di& tripeptides are
broken down to
amino acids
 Which are
secreted into
blood
Fig 18.34
18-91
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Digestion & Absorption of Lipids
Occurs
in SI
Arrival of lipids in duodenum causes secretion of bile
Fat is emulsified by bile salt micelles
Forms tiny droplets of fat dissolved in bile salt
micelles
Greatly increases surface area for fat digestion
18-92
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Digestion & Absorption of Lipids continued
 Pancreatic
lipase
hydrolyzes
triglycerides to free
fatty acids &
monglycerides
 Phospholipase A
breaks down
phospholipids into
fatty acids &
lysolecithin
Fig 18.35
18-93
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Digestion & Absorption of Lipids continued
 Products
of fat digestion dissolve in micelles forming mixed
micelles which move to brush border
Fig 18.36
18-94
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Digestion & Absorption of Lipids continued
 Free
fatty acids, monoglycerides, & lysolecithin leave micelles &
enter epithelial cells
 Inside epithelial cells, they are resynthesized into
triglycerides & phospholipids
Fig 18.37
18-95
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Digestion & Absorption of Lipids continued
 Triglycerides
& phospholipids combine with a protein to form
small particles called chylomicrons
 Which are secreted into central lacteals of SI villi
Fig 18.37
18-96
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Transport of Lipids
In
blood, endothelial lipoprotein lipase hydrolyzes
triglycerides to free fatty acids & glycerol for use in
cells
Cholesterol-containing remnants are taken up by liver
18-97
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Transport of Lipids continued
Cholesterol
& triglycerides from liver form VLDLs
which are secreted & take triglycerides to cells
Once triglycerides are removed, VLDLs become
LDLs
LDLs transport cholesterol to organs & blood
vessels
HDLs transport excess cholesterol back to liver
High ratio of HDL-cholesterol to total cholesterol
is believed to confer protection against
atherosclerosis
18-98