Physiology of

Digestion
Dr. Yudi
Herlambang

Department of Physiology
School of Medicine
University of Sumatera Utara
Nutrien Assimilated
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 Primary Functions of Digestive System
Activity necessary:
Motility;
Movement of food through tract ,includes
ingestion, mastication (chewing food and
mixing with saliva), deglutition (swallowing) and
peristalsis (rhythmic contractions along GI tract
that propel food)
muscular contraction.

Secretion;
Endocrine (secretion of hormones that regulate
digestive process)
Exocrine (secretion of water, enzymes, acid,
bicarbonate, into GI tract enzyme & other
Digestion;
Hydrolysis reactions that break ingested
polymers (large molecules) into their smaller
subunits (monomers) breakdown of
substances.
proteins into amino acids
fats into glycerol and free fatty acids
complex sugars into monosaccharides
Absorption;
Transfer of monomer subunits across wall of
small intestine into blood or lymph
transport modified nutrients.
Regulation;
Neural:
There are two nerve nets (plexuses)
in GI tract that contain neurons and
interneurons
sub mucosal (Meissner)
Myenteric (Auerbach)
Plexuses = brain of the gut
stimulated by stretch (bolus of food),
chemicals, and stomach content (local
stimuli)
Activity of plexuses can be modified
 Neural regulation via autonomic nervous
system
GI tract receives both sympathetic and
parasympathetic innervations
Parasympathetic via vagus nerve and
spinal nerves in sacral region (to lower
portion of large intestine)
stimulates motility and secretion; favors
digestion
Sympathetic
reduces motility and secretory activity
and stimulates sphincter contraction
Hormonal.
Paracrine regulation
production of hormone-like molecules
that are produced in one cell and
travel through interstitial fluid (not
bloodstream) to affect activity of
nearby cells
Hormone regulation
production of hormones that are
released into the bloodstream and
carried to target tissues within
digestive system where they affect
digestive activity
 Components of Digestive
System
Organs of GI tract include:
Organs of GI tract include:
oral (buccal) cavity (mouth) and
pharynx
esophagus
stomach
small and large intestine
rectum and anus.
Accessory digestive organs include:
teeth, tongue, and salivary glands
liver and gall bladder
 4 layers of the GIT wall
1. Tunica Mucosa:
Epithelial lining cells
Lamina propria:
loose connective tissue.
blood & lymph vessel.
immune system cells
(macrophage, lymphoid tissue,
lymphocytes, IgA, IgM)
Muscularis mucosae
inner circular fibers.
outer longitudinal fibers.

Villi.
Microvilli.
 2. Tunica Submucosa:

Blood & lymphatic vessels

Nerve plexus (enteric nervous
system)
submucosal nerve plexus
(Meissner)
control secretion in the
GIT
control motility o/t villi
 3. Tunica
Muscularis:
Innermost circular layer intestinal
lumen.
Myenteric nerve plexus (Auerbach)
control of motility.
Outer longitudinal layer shorten the
4. Tunica serosa
tube
Outermost
(adventitia):
layer.
Larger nerves & blood vessels travel in
a bed of connective & adipose tissue.
Mechanisms of Defense of the
GIT the external &
An interface between
internal environments
An external nutrients imported into
internal bloodstream

Must be defended from pathogens,

irritants, and corrosive products.
 Secretion/Digestion
Mouth:
Teeth
grind and tear food into smaller
pieces
increases surface area upon
which digestive enzymes work

Salivary glands
parotid gland
produce parotid duct
watery sublingual gland
.
secretionsubmandibular gland
 Salivary glands
(parotid, submaxillary, sublingual)

secrete saliva
lubricates and softens food; aids
in swallowing
contains amylase = enzyme that
begins breakdown of
carbohydrates
 SALIVARY GLANDS
Sympathetic and parasympathetic responses are not antagonistic

1. Parasympathetic system has the dominant role - continuous

2. Increased parasympathetic stimulation produces a watery saliva

rich in enzymes

3. Increased sympathetic stimulation produces a smaller volume of

thick saliva rich in mucus inhibits secretion (dry mouth when
nervous)

NB Salivary secretion is the only digestive secretion

completely under neural control
 CONTROL OF SALIVARY SECRETION

cerebral cortex other inputs

Conditioned
salivary centre reflex
in medulla

simple autonomic nerves

reflex
pressure receptors
and chemoreceptors salivary glands
in the mouth

salivary secretion
Oropharynx
To convey food into the
esophagus.
Important role in swallowing.
 Pharynx =
throat
Cavity at back of mouth
opening to
both esophagus (digestive
tract)
and trachea (windpipe)

Voluntary raising of larynx to

close
(epi)glottis and prevent food
entry
into windpipe
 Esophagus.
Hollow muscular tube connecting pharynx
and stomach.
Bounded by sphincters.
Lined w/ stratified squamous epithelium.
Lower esophageal (gastro esophageal)
sphincter ; transition from low pressure
( intrathoracic ) high pressure (intra-
abdominal).
Disorder o/t LES tone major cause
esophageal reflux heart burn.
stomach
Stomach wall
 Secretion/Digestion
Stomach:
Temporary stores ingested food. sphincters prevent
backward flow of materials into esophagus and
regulate release of stomach contents into small
intestine
Churn, mixes food with gastric juice.
Mechanical and chemical breakdown of ingested
material
Produces, mucus, HCl and pepsinogen.
HCl converts pepsinogen into pepsin.
Sterilization of stomach contents by acid
Pepsin digests proteins into peptide fragments.
Absorbs some water, alkohol, glucose.
Binds vit. B12 allows abs. in ileum
 Stomach:
lower region of
stomach (antrum)
secretes the hormone
gastrin.
HCl
Additional secretions:
Histamine (ECL cell) Gastrin

Histamine
Somatostatin
Pepsinogen
Mucous cell, secrete mucous
protects mucosa (epithel) from acid
& pepsin.
Chief cells, secrete :
- Gastric lipase.
- Pepsinogen HCl Pepsin

Prietal (oxyntic) cells, secrete :

- HCl .
- Intrinsic factor binds vit. B12
Pyloric gland Alkaline mucus.
 Control of Acid Secretion

Secretion is
dependent upon
activity of H, K-ATPase
pump.
Gastrin, histamine
and acetylcholine Gastrin

increase numbers of
enzyme in plasma
Pepsinogen
membrane.+ +
H K ATP-ase
Somatostatin inhibits
acid secretion.
 Control of Acid Secretion
May be considered as three separate phases.

1. Cephalic phase.
2. Gastric phase.
3. Intestinal phase.
 1. CEPHALIC PHASE

Vagus nerve

Sight, smell or
thought of food

Parasympathetic activation
of gastric motility & gastric juice secretion
 2. GASTRIC PHASE

Food arrival causes

muscular reflexes & Gastrin
gastrin secretion by G
cells.

FOOD
GO

Gastrin stimulates secretion from both

chief &
 3. INTESTINAL PHASE

Arrival of food in duodenum

triggers release of hormones
that inhibit gastric motility &
secretions.

Secretin &
Cholecystokinin (CCK)

Circulation
 Intestinal phase
signals come from intestine
and have inhibitory effect i.e.
slow the rate of gastric
secretion
stretch of duodenum, and
increase in osmolality
stimulate nerve reflex that
inhibits gastric motility and
secretion
presence of fat in duodenum
stimulates secretion of
Hormones Released During the Intestinal Phase
When acidic chyme arrives, hormones are released by
the duodenum.

1. Secretin
stimulates pancreas to secrete bicarbonate ions
that neutralise stomach acid
inhibits gastric secretion and motility of stomach

2. Cholecystokinin (CCK)
stimulates production / release of pancreatic enzymes
stimulates bile release from gallbladder
inhibits gastric secretion and motility of stomach
 Digestion in the stomach
CHO digestion is halted because acidic
pH of the stomach inactivates salivary
amylase
Little fat digestion occurs in the
stomach
Protein digestion begins in the stomach
Involves mechanical breakdown of proteins
by the churning actions of the stomach
Involves the chemical digestion of proteins
by acid and hormones
Gastric (stomach) acid = hydrochloric acid (HCl)
Pepsin
 Protein Digestion in the
Stomach
Parietal cells
secrete acid (hydrochloric acid = HCL) &
intrinsic factor
stimulated to produce acid by gastrin
Chief cells
secrete pepsinogen & gastric lipase
Pepsinogen = inactive hormone
Pepsinogen converted to pepsin (active
hormone) by acidic pH of the stomach
Pepsin breaks large proteins down into
smaller peptides
 Protein Digestion in the
Stomach
G cells
Secrete gastrin
Gastrin = hormone
target tissues = chief cells and parietal cells
in stomach
stimulates gastric juice production
HCL from parietal cells
Pepsinogen from chief cells
Decreases pH of stomach
Promotes conversion of pepsinogen to pepsin
 It also activates gastroileal reflex which moves
chyme from ileum to colon
Parasympathetic stimulation releases gastrin
releasing peptide (GRP), which stimulates G cell
release of gastrin

Mucus cells - secretes mucus to protect epithel

against acid and digestive enzymes
 Absorption in the Stomach
Almost all products of digestion are
absorbed in the intestine
Notable exceptions
alcohol and aspirin can be absorbed
directly through stomach wall
due to their lipid solubility
absorption of aspirin through stomach wall
associated with bleeding, may be related
to peptic ulcers in people taking large
dosages
 Chyme
Food in stomach is liquified
mixed with stomach juices to form
pasty liquid material = chyme
Chyme = material passed from
stomach to small intestine
 Small Intestine
Functions in digestion
CHO digestion resumes and is completed here
Protein digestion continues and completes here
Fat digestion is initiated and completed here
Also functions to absorb nutrients, fluids, and
electrolytes
Divisions (@ 12 feet long total length)
duodenum = upper portion (@ 1 foot long) closest
to stomach
jejunum = middle section
ileum = lower section closest to large intestine
 Anatomy
3 segments (12 ft long, 22 ft in cadaver)
Duodenum
Jejunum
Ileum
 Anatomy

Features that increase surface area

Circular folds (valvulae conniventes, kerckrings
folds, plicae circularis)
Project into lumen 3-10 mm
Prominent in duodenum and jejunum and disappear near
mid ileum
Responsible for feathery appearance on barium radiographs
Villi
4-5 million in entire length
0.5-1.5 mm long
Account for velvet-like appearance
 Anatomy
Microvilli
1.0 um long
Brush border
 Anatomy
Structure of the villus
Lacteal
Anatomy
Goblet cells and absorptive cells
Anatomy
Brush border enzymes
Anatomy
Crypts of Lieberkuhn
 Physiology
Two primary function
Digestion
Absorption of nutrients and water
Digestion
Mainly in duodenum small intestine and
pancreatic enzymes
Bicarbonate from pancreas neutralizes acids
Mucous protects from acids
Bile emulsifies fats
 Hormones Important in
Sm. Intestine Digestive
Activity
Secretin
Cholecyctokinin (CCK)
Enterokinase
Pancreatic enzymes
Lipase, Amylase, Peptidases,
Trypsinogen, Trypsin
 Physiology
Digestive enzymes
Salivary amylase
Pepsin
Pancreatic enzymes:
Trypsin
Chymotrypsin
Carboxypeptidase
Nucleases
Pancreatic lipase
Pancreatic amylase
Intestinal enzymes:
Peptidases
Disaccharidases
Lipase
Nucleotidases
 Physiology
Hormones
Cholecystokinin secretion stimulated by fat in
duodenum
Contraction of gall bladder
Pancreatic secretion of enzyme rich material
Secretin secretion stimulated by low pH in
duodenum
Secretion of bile from the liver
Pancreatic secretion of HCO3- rich juice
 Physiology

Absorption
Nutrients broken down into simple sugars, fatty acids
and amino acids
Principle sites of absorption
Duodenum: iron, calcium, vitamins, fats, sugars, amino
acids, vitamins
Jejunum: fat, sugar, amino acid (largely complete by mid
jejunum), vitamins
Ileum: vitamin B12 and bile salts
Most bile salts are absorbed and recirculated to the liver
important in maintaining bile pool
 Anatomy and Physiology
Anatomy
 Anatomy and Physiology
Functions (converts chyme to feces)
Absorption of water and electrolytes (mainly on right
side)
Absorbs 800 ml water/day
Capacity 1500-2000 ml/day (when exceeded results in
diarrhea)
Sigmoid colon reservoir for dehydrated fecal mass
~200 g feces/day
Water 80-90%
Food residue
Bacteria
Cells
Unabsorbed minerals
 Anatomy and Physiology
Secretes mucus (no enzymes)
Bacteria produce vitamin K and several Bs
Flatus (NH3, CO2, H2, H2S, CH4)
CO2 produced when fatty acids and HCl are neutralized by
bicarbonate
Bacterial fermentation of carbohydrates produces CO 2, H2,
CH4
~1000 ml expelled each day
Excess occurs with aerophagia and diets high in indigestible
carbohydrates
Rectum and anus sites of some of most common
disorders known to humans
Constipation
Hemorrhoids
Abscesses and fistulas
Colon and rectal cancer
 Digestion
Most occurs by hydrolysis reactions
- reactions that add water to break
chemical bonds
Enzymes involved:
amylase - breaks complex sugars to
disaccharides
lipases - breaks down lipids
proteases - breaks down proteins
 Hormonal Control of
Intestinal Secretion
S cells secrete secretin
secretin target tissue = pancreatic ducts and liver
induces release of water and HCO3- from
pancreatic duct cells and secretion of HCO 3- into
bile by liver
HCO3- neutralizes acidic chyme
Stimuli for secretin secretion
acid (pH less than 4.5 stimulates secretion)
secretin = natures antacid
 Hormonal Control of
Intestinal Secretion
(continued)
I cells secrete cholecystokinin (CCK)
CCK target tissues = pancreatic acinar
cells and gall bladder
induces secretion of digestive enzymes
from pancreatic acinar cells
induces contraction of gall bladder,
which releases bile into small intestine
Stimuli for CCK secretion
presence of protein and/or fat in chyme
CCK and Appetite Control

CCK also thought to act on satiety

center in brain and inhibit appetite
Butabindid = drug that interfers
with enzyme responsible for CCK
degradation (breakdown)
keeps CCK in system longer
boosts appetite inhibition
used to treat obesity
 Pancreatic Enzymes
Amylase - breaks CHO starch to maltose,
maltriose, and small branched structures
Lipase - breaks down triglycerides into
fatty acids and glycerol
Proteolytic enzymes break peptides down
to amino acids and dipeptide fragments
Trypsinogen
converted to trypsin by enzyme (enterokinase)
located along inner wall of small intestine
trypsin converts other pancreatic zymogens
(inactive forms) to their active forms within the
small intestine
 Pancreatic Enzymes
(continued)
Most pancreatic enzymes are produced
as inactive molecules = zymogens
Are transported to small intestine in
zymogen form
Protects the pancreas from self
digestion
 CHO Digestion in Sm.
Intestine
Pancreatic amylase secreted into
duodenum in response to secretin
Is active in the intestine because the
acidic chyme is neutralized by HCO3-
also secreted from pancreas in response
to secretin
Amylase converts complex CHOs to
maltriose, maltose, and short
branched sugars
 Small Intestine (continued)
Inner surface (epithelial layer)
extensively folded and covered with
smaller folds (villi) and even smaller
folds (microvilli) increase surface
area for absorption to occur
Site of absorption of carbohydrates,
lipids, amino acids, calcium and iron
in duodenum and jejunum
Bile salts, Vit B12, water, and
electrolytes mainly in ileum
 CHO Absorption in the Sm.
Intestine
Enzymes in the brush border complete
breakdown of maltotriose, maltose, and
branched sugars, lactose and sucrose
Lactase converts lactose to glucose and
galactose
Sucrase converts sucrose to glucose and
fructose
Isomaltase converts branched sugars
glucose, maltose and unbranched short
oligosaccharides
Maltase converts maltose to glucose
 CHO Absorption in the Sm.
Intestine (continued)
Epithelial cells that line the sm. Intestine absorb
monosaccharides by active or facilitated transport
Glucose and galactose are actively co-transported
with sodium using the same transporter and
Fructose is absorbed by passive facilitated
transport using a different transporter protein
than that used by glucose and galactose
Monosaccharides enter bloodstream and are
transported to liver and converted to glycogen or
sent to bloodstream for immediate, direct
ultilization or storage by cells
 Fat Digestion in Sm.
Intestine
Limited fat digestion occurs prior to sm.
Intestine
Some lipases in saliva and gastric secretions
Lipase = enzyme important in fat digestion
Secreted into sm. intestine from pancreas in
response to secretin
breaks down triglycerides to free fatty acids
and monoglycerides
Activity is dependent upon the amount of
surface area on which it can work
Phospholipase A2 digests phospholipids
Bile is essential for proper fat digestion
 Digestion and Absorption of
Lipids in Small Intestine
Fats stimulate I cell release of CCK
CCK triggers release of bile from
gall bladder
Bile emulsifies fats
breaks large fat globules into smaller
globules
does not actually break bonds between
glycerol and fatty acids
Increases surface area available for
pancreatic lipase to act
 Liver
Largest organ in body
Blood supply
hepatic artery delivers oxygenated blood
hepatic portal vein
products absorbed into capillaries in the
intestines do not directly enter general
circulation
this blood is delivered first to the liver by the
hepatic portal vein, and then passed on to
the general circulation
liver has first crack at absorbed nutrients,
except lipids
 Liver (continued)
Digestive functions
secretes bile - essential for digestion and
absorption of fats
Function - overall is to filter and process nutrient-rich blood,
not just a digestive function
regulates carbohydrate metabolism through glycogen storage and
release
regulates many aspects of lipid metabolism, eg., cholesterol
synthesis and release of ketones
detoxifies blood
urea and bile synthesis
 Liver (continued)

Non-digestive functions
circulatory functions; destroys aged or
abnormal blood cells and produces clotting
factors
converts protein metabolites to urea for
elimination by kidneys
immune function (Kupffer cells)
functions as blood reservoir in regulation of
blood volume
 Bile Synthesis
This is the main digestive function of the liver;
Approximately 1 liter per day is produced
bile salts are cholesterol derivatives and function to
emulsify fats
bile salts are recycled, not excreted
main bile pigment is bilirubin, derived from RBC heme
bile is synthesized in the liver and stored in the
gallbladder
release is stimulated by cholecystokinin and vagus nerve
 Bile
Product of the liver cells
bile contains bile pigment, bile salts,
phospholipids, cholesterol, and inorganic ions
bile pigment = bilirubin = breakdown product of
hemoglobin
bile salts = derivatives of cholesterol that are
combined with taurine or glycine, form micelles =
lipid aggregates with non-polar parts in central
region and polar regions toward water
Essential for absorption of fat from the
digestive tract
Emulsifies fat; breaks large fat globules into
smaller fat droplets, provides greater surface
area on which lipase can act
 Gall Bladder

Located on underside of liver

Bile produced in liver is carried to gall
bladder, concentrated, and stored until
secretion into the small intestine
Gall bladder contraction forces bile into
small intestine
Cholecystokinin = hormone released by I
cells of small intestine
stimulates release of digestive enzymes from
pancreas and bile from gall bladder
 Micelles
Aggregates of bile salts, free fatty acids,
monglycerides, lysolecithin, and fat-
soluble vitamins
Arranged with non-polar regions to
center, polar, water-soluble portions to
outside
makes lipids more water soluble in lumen of
intestine
Micelle is transported to epithelial cells
lining small intestine
 Importance of Micelle
Formation
Intestinal epithelial layer is covered by an
unstirred water layer
Fats are nonpolar, and therefore insoluble in
water
Micelles are structures whose outer borders are
polar, but whose inner segments are nonpolar
Outer polar portion can dissolve in the unstirred water
layer and be transported to epithelial cell surfaces
Nonpolar contents can then be removed from micelle
and absorbed individually, or in some cases the
micelle itself may be absorbed
 Chylomicrons
Inside epithelial cells, triglycerides and
phospholipids are re-synthesized
Resynthesized triglycerides and
phospholipids are combined with cholesterol
and protein inside the cell to form
chylomicrons
Chylomicrons are released into the
lymphatic system - NOT INTO HEPATIC
PORTAL VEIN
liver does not get first crack at lipids
 Protein Digestion in Sm.
Intestine
Proteolytic enzymes are released (in inactive,
zymogen forms) from the pancreas in
response to secretin
Trypsinogen = inactive precursor that is
converted (by enterokinase) to trypsin in the
brush border of the small intestine
Trypsin converts other zymogens to their
active forms
Collectively, the proteolytic enzymes break
proteins and peptides into single amino acids,
or di- and tripeptides
Absorption of Amino Acids
in Sm. Intestine
Amino acids are absorbed by the
epithelial cells of the small intestine by
active co-transport with sodium
Di- and tripeptides are also absorbed by
epithelial cells of the small intestine and
then broken down into amino acids
within the epithelial cells
Epithelial cells release amino acids into
portal blood, which is transported first to
the liver, then to rest of the body
 Absorption of Intact
Proteins
Does not occur to any considerable amount
in adult humans
Infants can absorb proteins through the
intestinal wall, therefore can obtain some
immune protection from antibodies found in
colostrum
Colostrum contains components that
promote closure of the GI tract, which then
makes the GI tract impermeable to proteins
 Aging Effects on Digestive
System
Neural coordination diminished
Biochemical changes
reductions in levels of digestive
enzymes and hormones
decreased sensitivity to stimuli
(hormones and other stimuli)
Vascular changes
vascular supply diminished
Collectively, changes may result in
compromised nutrition in the elderly
 Alcohol
Alcohol
in small amounts = stimulant and relaxant
in higher doses = CNS depressant and
toxicant for brain and stomach (causes
headache and nausea associated with
hangover)
Chronic long-term use increases anxiety
Tolerance develops
requires ingestion of more alcohol for same
effects
 Alcohol Metabolism
Ethanol + NAD+ Acetaldehyde + NADH +
H+
alcohol dehydrogenase

Acetaldehyde + NAD+ Acetate + NADH

acetaldehyde dehydrogenase

Alcohol metabolism in stomach (20%) and liver (80%)

Ethanol = preferred substrate of liver; will be
preferentially used by liver if available
 Alcohol Metabolism
(continued)
50% of Asian population has mutation of
mitochondrial aldehyde dehydrogenase
causes inability to properly metabolize
acetaldehyde
acetaldehyde levels increase 20X that in
normal individuals
acetaldehyde can be toxic to cells
produces flushing of skin, nausea, dizziness,
heart palpitations
 Cirrhosis

Liver accumulates fat, and

undergoes other structural changes
Liver is also deprived of needed
proteins
malnutrition associated with heavy
alcohol abuse
Liver fails to function normally
 Alcohol and the
Cardiovascular System
Alcohol abuse can harm heart muscle
and produce hypertension
hypertension can produce hemorrhagic
stroke
Moderate use of alcohol may have some
protective benefit
more death from coronary heart disease
and heart attack in people who complete
abstain from alcohol use versus those who
indulge mildly to moderately
 Alcoholism and Genetics
Genetic predisposition for alcoholism
Related to dopamine (D2) receptor gene
specific form of the gene results in fewer
dopamine receptors being produced
this form of the gene occurs more often in
alcoholics than non-alcoholics
substance abusers use alcohol or other
stimulants to try to stimulate dopamine-
dependent brain areas involved in
behavior reward/reinforcement
 Intestinal Contractions and Motility

2 major types of
contractions occur in the
small intestine: Insert fig. 18.14
Peristalsis:
Slow movement.
Pressure at the pyloric end
of small intestine is greater
than at the distal end.
Segmentation:
Major contractile activity of
the small intestine.
Contraction of circular
smooth muscle.
Mix chyme.
 Contractions of Intestinal Smooth
Muscles
Occur automatically in
response to endogenous
pacemaker activity.
Rhythm of contractions is
paced by graded
depolarizations called slow
waves.
Slow waves produced by
interstitial cells of Cajal.
Slow waves spread from 1
smooth muscle cell to another
through nexuses.
 Contractions of Intestinal Smooth Muscles

When slow waves above threshold, it triggers APs by opening of VG

Ca2+ channels.
Inward flow of Ca2+:
Produces the upward depolarization phase.
Stimulates contraction of smooth muscle.
Repolarization:
VG K+ channels open.
Slow waves decrease in amplitude as they are conducted.
May stimulate contraction in proportion to the magnitude of
depolarization.
Parasympathetic NS, stretch and gastrin increase the amplitude of
slow waves.
Stimulate APs.
SNS decrease APs.
+30

Vg K+ Channel

Vg Ca++ Channel

-55
Intestinal Smooth Muscle Action Potential
Cells and Electrical Events in the Muscularis
Brush border
enzymes

reassembly
 Colon
Anatomi & Histology
1,5 1,8 m.
Various segment.
Columnar epithelium at the surface (few, short),
no villi, few folds (except in the distal rectum).
Goblet cells.
Endocrine cells.
Absortive cells.
 Large Intestine
Larger diameter, shorter length (@ 4
feet) than small intestine
separated from small intestine by
ileocecal valve
Collects food residue (indigestible)
material
Site of final water reabsorption - causes
chyme to become solid (forms feces)
Stores feces until eliminated from body
 Bacteria live in the colon and stimulate the
production of vitamin K and some of the B
complex vitamins
Mucus is produced but no enzymes are
secreted in the large intestine
 Large Intestine
(continued)
Divisions
cecum = section nearest small
intestine (appendix attached in this
region)
colon = major portion
ascending
transverse
descending
sigmoid (leads to rectum)
 Water Absorption in the
Intestine
Majority ( 98%) of water that enters
gut is (re)absorbed
85% (re)absorbed in small intestine
13% in large intestine
Absorption of water is passive process
osmotic gradient created by active
transport of ions
water moves according to its gradient
LargeIntestine
 Large
Intestine
 Colon: Function

Absorb H2O and electrolytes

Secretion of mucus
Formation, propulsion & storage of
unabsorbed material (feces)
Some digestion by bacteria
Mass Peristaltic Movements (2-3x day)
Moves through in 12-24 hours
 DIGESTIVE ACTIVITIES OF
LARGE INTESTINE
STRUCTURE ACTIVITY RESULT

Mucosa Secretes Lubricates colon &

mucus protects mucosa

Absorbs Maintains water

water balance; solidifies
feces; absorbs
vitamins & some ions
DIGESTIVE ACTIVITIES OF
LARGE INTESTINE
STRUCTURE ACTIVITY RESULT

Lumen Bacterial Breaks down

activity undigested
carbohydrates,
protein, & amino acids
into products that can
be expelled in feces
or absorbed &
detoxified by liver

Synthesizes certain B
vitamins & vitamin K
 DIGESTIVE ACTIVITIES OF
LARGE INTESTINE
STRUCTURE ACTIVITY RESULT

Muscularis Haustral Contractions move

churning contents from
haustrum to haustrum
Peristalsis Contractions of circular
& longitudinal muscles
move contents along
length of colon
 DIGESTIVE ACTIVITIES OF
LARGE INTESTINE
STRUCTURE ACTIVITY RESULT

Muscularis Mass Forces contents into

peristalsis sigmoid colon

Defecation Eliminates feces by

reflex contractions in
sigmoid colon &
rectum
 Large Intestine
Digestion and Absorption
Fermentation breaks down undigested complex
CHO and proteins
Produce lactate and short chain fatty acids used by the
colonocytes for energy
Bacteria produce absorbable vitamins like K
Gases are produced in the large intestine
Colon is responsible for absorbing most of the
water that enters it in the form of chyme
Colonocytes absorb NaCl
 Secretion
&H2O
absorption

2000ml150ml=?
 Ion&
Vitamin
absorption
Rectum
 The
Defecation
Reflex
 Defecation process

Reflex relaxation of internal sphincter

Valsalva maneouvre raising intraabdominal
pressure
Relaxation of puborectalis (anorectal angle)
Voluntary relaxation of external sphincter
 Defecationreflex
>15mmHg
 Continence mechanism

Rectum normally empty

Colonic movements distend rectum -
150 mls, 25 cm H2O which activate
defecation reflex
Voluntary inhibition (external sphincter)
movement of faecal material back into
colon
 Disorders of the GI tract
Mouth and throat
gingivitis - infection of the gum, can lead to
periodonititis involving the supporting bone of the
teeth
Vincents disease - a kind of gingivitis caused by a
spirochete
Leukoplakia - characterized by thickened white
patches on the mucous membranes of the mouth -
common in smokers and may be a precursor to
cancer
 Symptoms of esophageal disorders
Dysphagia
Subjective awareness of an impairment of swallowing
Major symptom for diseases of the pharynx or esophagus
Occurs in some non-esophageal disorders resulting from
vascular or neurologic disease
May be of obstructive or motor origin
Obstructive causes
Stricture
Tumors
Motor causes
Impaired peristalsis
Dysfunction of UES or LES
Common motor disorders achalasia, scleroderma, diffuse esophageal
spasm
 Symptoms of esophageal disorders cont.

Pyrosis (heart burn)

Caused by reflux of gastric acid or bile secretions
Persistent reflux caused by incompetent LES
results from excess stretching of the lower esophagus; not
due to hyperacidity of the stomach
Odynophagia
Pain induced by swallowing
Regurgitation
Back flow into mouth
Effortless (as opposed to vomiting)
Common in infants
Reflects both LES incompetence and failure of UES to serve as
regurgitation barrier
 Disorders of esophageal motility
Achalasia
Definition = uncommon hypomotility disorder characterized by
weak and uncoordinated peristalsis or aperistalsis within the
body of the esophagus, elevated LES pressure and failure of
LES to relax completely
Foods and liquids accumulate in lower esophagus
Exact etiology unknown
May be degeneration of Aurbachs plexus
Most common symptom is dysphagia
Regurgitation during meals
Nocturnal regurgitation may result in aspirations and chronic pulmonary
infections or sudden death
Food in esophagus may lead to inflammatory changes, erosions, or
cancer
 Disorders of esophageal motility
Achalasia - cont.
Treatment
Palliative, measures to relieve obstruction of lower
esophagus
No way to restore peristalsis
Two forms of therapy
Dilation of LES with pneumatic bag or mercury filled bag
(bougie)
Surgery to open LES accompanied by pyloroplasty
 Disorders of esophageal motility cont.

Diffuse esophageal spasm

Definition = uncoordinated, nonpropulsive contractions in
response to swallowing
Cause unknown more common in patients > 50
Fairly common
Usually asymptomatic
Sometimes dysphagia and odynophagia that are aggravated by cold
foods, large boluses and nervous tension
Sometimes chest pain that may be confused with angina
Treatment
Avoid cold foods and large meals
Antacids, sedatives, nitroglycerine
Esophageal dilation is symptoms persistent and distressing
 Disorders of esophageal motility cont.

Scleroderma
Esophageal motor dysfunction occurs in > 2/3 of
patients with progressive systemic sclerosis
(scleroderma)
Atrophy of smooth muscle in lower portion of
esophagus
Incompetence of LES often leads to reflux
esophagitis and subsequent stricture formation in
lower esophagus
 Esophagitis
Definition = inflammation of the esophageal
mucosa
May be acute or chronic
Innocuous type follows ingestion of hot liquids
Most common significant form caused by acid
reflux
Are infectious forms Candida albicans (thrush),
herpes virus
Acute, severe follows ingestion of strong alkalis or
acids
This is Candida esophagitis. Tan-yellow plaques are seen
in the lower esophagus, along with mucosal hyperemia.
The same lesions are also seen at the upper right in the
The lower esophagus here shows sharply demarcated ulcerations that
have a brown-red base, contrasted with the normal pale white
esophageal mucosa at the far left. Such "punched out" ulcers are
suggestive of herpes simplex infection.
 Esophagitis
Chronic reflux esophagitis and Hiatus Hernia
Most common form
Cause incompetence of LES and reflux of gastric
or intestinal juice into esophagus
often associated with hiatus hernia
Mechanisms that prevent reflux
Tone of sphincter in LES
Angle of entry creates a flap valve
Intra-abdominal pressure closes segment of esophagus
below diaphragm
 Esophagitis cont.

Hiatus (hiatal) hernia

Herniation of portion of stomach into chest
2 types
Direct or sliding (most common)
Gastroesophageal junctions slides into thoracic cavity
LES opens causing reflux
Often asymptomatic
Paraesophageal or rolling
Part of fundus roles through hiatus
LES remains competent and no reflux
Major complication is strangulation
Important clinical consideration is if there is reflux
 Esophagitis cont.

Treatment of sliding hernia

Goal is to prevent reflux or neutralize reflux
Frequent small meals
H2 blockers (ranitidine)
Protective agents (sucraflate)
Loose weight
Avoid stooping forward
Elevate head during sleep
Surgery if evidence that persistent reflux is causing esophagitis
or stricture formation
 Disorders of the GI tract
Stomach
Hiatal hernia - a weakness in the diaphragm at the
point where the esophagus connects allowing the
stomach or other abdominal organs protrude
upwards
nausea and vomiting - caused by an interruption of
forward movement of nutrition; reverse peristalsis
 Disorders of the GI tract
Stomach, continued
gastritis - inflammation of the stomach mucosa;
causes include irritation by spicy food, drugs, alcohol,
or nicotine
stomach cancer - males are more susceptible than
females; symptoms usually long standing indigestion
peptic ulcer - most common ages 30-45; causative
factors include smoking, drinking; anti-inflammatory
drugs and bacterium, Helicobacter pylori
 Gastritis inflammation or hemorrhagic condition of
the mucosa
Acute superficial gastritis
Erodes surface of epithelium in diffuse or localized
patterns
Causes
Drugs NSAIDS
Chemicals alcohol, bile acids, pancreatic enzymes, caffeine,
strong spices
Helicobacter pylori
Clinical manifestations
Vague abdominal discomfort
Epigastric tenderness
Bleeding
Vomiting
Hematemesis
This is a typical acute gastritis with a diffusely hyperemic
gastric mucosa. There are many causes for acute gastritis:
alcoholism, drugs, infections, etc.
Gastritis inflammation or hemorrhagic condition of the mucosa - cont.

Usually resolves when offending agent removed

Antiemitic drugs to relieve nausea and vomiting
May need to correct fluids and electolytes
Acid blockers and antacids
Sulcrafate to coat stomach lining
 Gastritis - cont.

Chronic atrophic gastritis

Progressive atrophy of glandular epithelium with
loss of parietal and chief cells
Decreased HCl, pepsin and intrisic factor production
Caused mainly by H. pylori
More often in elderly
Alcohol, hot tea and smoking may predispose
May lead to gastric ulcers or carcinoma
Gastritis is often accompanied by infection with Helicobacter pylori.
This small curved to spiral rod-shaped bacterium is found in the
surface epithelial mucus of most patients with active gastritis. The rods
are seen here with a methylene blue stain.
This of gastric mucosa reveals the presence of many short, curved rod-like organisms
overlying the mucosa. These are Helicobacter pylori organisms, whose home is the
gastric mucus. The incidence of H. pylori infection increases with age, with half of
American adults infected by age 50. H. pylori organisms break down mucosal
glycoproteins and damage epithelial cells, leading to inflammation--a chronic gastritis
that is asymptomatic in most cases. Peptic ulcer disease, particularly duodenal
ulceration, is strongly associated with H. pylori infection, which may also play a role in
development of gastric carcinoma. Antibiotic treatment of H. pylori reduces these
complications
 Gastritis - cont.

Symptoms generally varied and vague

Feeling of fullness
Anorexia
Vague epigastric distress
Treatment varies depending on cause
Antibiotics
Avoid irritants
Correct iron deficiency if present
Vitamin B12 supplement
 Peptic ulcer disease
General consideration
Definition = circumscribed breaks in the continuity
of the mucosa, extending below the epithelium
Erosions do not extend below epithelium
Chronic ulcers have scar tissue at base, acute dont
Can be anywhere in GI tract exposed to acid-pepsin
gastric juice
Other factors also contribute
H. pylori
Mucosal bicarbonate secretion
Stress
Genetics
A 1 cm acute gastric ulcer is shown here in the upper
fundus. The ulcer is shallow and sharply demarcated, with
surrounding hyperemia. It is probably benign. However, all
gastric ulcers should be biopsied to rule out a malignancy.
The strongest association
with Helicobacter pylori is
with duodenal peptic
ulceration--over 85% of
duodenal ulcers. Seen
here is a penetrating acute
ulceration in the duodenum
just beyond the pylorus. An
acute duodenal ulcer is
seen in two views on upper
endoscopy in the lower
panels.
 Peptic ulcer disease - cont.

Pathogenesis
Two factors prevent stomach from digesting itself
Gastric mucosal barrier
First line of defense
NSAIDS cause changes in mucosa that my facilitate its digestion
by pepsin
Destruction of barrier believed to be important factor in
pathogenesis of gastric ulcers
Results of back diffusion of H+ injuring underlying tissues
Antrum more susceptible to back diffusion than fundus
Duodenum resistant to ulceration due to Brunners glands
which produce a highly alkaline secretion
Peptic ulcer disease - cont.

Epithelial barrier
Depends on abundant vascular supply and continual,
rapid regeneration of epithelial cells (~3 days)
Other factors
500,000 new cases/year (10-12 % of population affected)
Duodenal ulcers occur in much younger group than gastric
Lower incidence in women
Caffeine increases acid production
Emotional stress (how one deals with stress)
>90% of duodenal ulcers are on anterior or posterior wall
within 3 cm of pyloric ring
40-60% have family history
 Peptic ulcer disease - cont.

Clinical features
Principle feature is chronic, intermittent epigastric
pain typically relieved by food
~25% have bleeding (more common with
duodenal)
Other signs and symptoms
Vomiting
Red or coffee-ground emesis
Nausea
Anorexia
Weight loss
Pain-food-relief pattern may not be typical of
gastric ulcers food sometimes aggravates
 Peptic ulcer disease - cont.

Benign vs malignant ulcers

4% of gastric ulcers are malignant
Malignant (carcinoma) ulcers have shaggy, necrotic base while
benign have smooth, clean base
 Peptic ulcer disease - cont.

Medical treatment
Primary consideration is to inhibit or buffer acid to
relieve symptoms and promote healing
Antacids increase pH so pepsin isnt activated
Dietary management small frequent meals, avoid
alcohol and caffeine
Anticholinergics inhibit vagal stimulation
Antimicrobial therapy
Physical and emotional rest
Ulcers caused by H. pylori are successfully treated
with antimicrobial agents, bismuth salts, and H2
blockers
65-95% eradication rates
 Peptic ulcer disease - cont.

Complications
Hemorrhage
Most frequent complication 15-20%
Most common in ulcers of the posterior wall of duodenal bulb due to
proximity of arteries
Symptoms depend on severity
Anemia
Occult blood in stool
Black and tarry stool
Hematemesis
Shock
Mortality up to 10% - higher for patients over 50
 Peptic ulcer disease - cont.

Perforation
Approximately 5% of all ulcers perforate - accounts for
65% of deaths from peptic ulcers
Usually on anterior wall of duodenum or stomach
Thought to be due to excess acid and often a result of
NSAIDS
Characteristic presentation
Sudden onset of excruciating pain in upper abdomen
chemical peritonitis
Patient fears to move or breath
Abdomen becomes silent to auscultation and board
like rigidity to palpation
Treatment immediate surgery
 Peptic ulcer disease - cont.

Obstruction
Obstruction of gastric outlet in ~5% of patients
Due to inflammation and edema, pylorospasm or scarring
More often with duodenal ulcers
Symptoms
Anorexia
Nausea
Bloating after eating
Pain and vomiting when severe
Treatment
Restore fluids and electrolytes
Decompress stomach with nasogastric tube
Surgical correction - pyloroplasty
 Peptic ulcer disease - cont.

Intractability
Medical therapy fails to control symptoms adequately,
resulting in frequent, rapid recurrences
Typically surgery is recommended
 Peptic ulcer disease - cont.

Surgical treatment for patients who do not respond to

therapy
For duodenal ulcers aim is to permanently reduce stomachs
capacity to secrete acid and pepsin
Vagotomy
Cut vagal branches to stomach
Eliminates cephalic phase
Several techniques
Antrectomy
Removal of entire antrum
Eliminates gastric phase
Vagotomy plus antrectomy
Eliminates both cephalic and gastric phases
 Peptic ulcer disease - cont.

Partial gastrectomy
Removal of distal 50-75% of stomach
Gastric remnant anastamosed to duodenum (Billroth I)
or jejunum (Billroth II)
For gastric ulcers
Usually partial gastrectomy and a gastroduodenal
anastomosis
Normally do not do vagotomy as patients have
normal to low acid production
 Peptic ulcer disease - cont.

Postoperative Sequelae
Dumping syndrome ~20% of patients
Rapid emptying of hyperosmotic chyme into intestine
Rapid fluid shift from vascular compartment into intestinal lumen
Hypotension
Reflex tachycardia, diaphoresis and vasoconstriction
Feeling of fullness, nausea, vomiting and diarrhea common
Symptoms usually during or within minutes of meal
 Peptic ulcer disease - cont.

Hypoglycemia
May occur within 2-3 hrs after eating
Due to excess release of enteroglucagon from intestine which sensitizes
beta cells
Over corrects the hyperglycemia
Treatment
Eat frequent, small meals
Low carbohydrate and high protein diet
Restrict liquids at mealtime
 Malabsorption intestinal mucosal absorption of
single or multiple nutrients is impaired resulting in inadequate
movement of digested food into blood or lymphatic system

Causes (box page 346)

Prior gastric surgery
Pancreatic disorders
Chronic pancreatitis, cancer, cystic fibrosis
Hepatobiliary disease
Bile tract obstruction, cirrhosis, hepatitis
Disease of small intestine
Nontropical sprue, enteritis. giardiasis
Hereditary disorders
Lactase deficiency
Drug-induced malabsorption
Neomycin, calcium carbonate
 Disorders of the GI tract

Stomach, continued
pyloric stenosis - more common in males than
females, causes persistent vomiting because of
the stricture in the pyloric sphincter; requires
surgery to repair
 Disorders of the GI tract
Intestinal disorders
diarrhea - abnormal frequent watery stools;
danger is dehydration and electrolyte imbalance;
cause is excess activity of the colon, faulty
absorption or infection
constipation - acute due to obstruction or
diverticular inflammation (diverticulitis).
Chronic includes spastic constipation caused by
overuse of laxatives or enemas; flaccid
constipation usually caused by inactivity
 Intestinal obstruction

Definition = an interference with the normal

flow of intestinal contents through the intestinal
tract
May be acute or chronic, partial or complete
Chronic obstruction usually involves colon as a result of a
tumor
Most obstructions involve SI
Complete is serious and requires early diagnosis and
emergency surgery to save life
 Intestinal obstruction

2 types of obstructions
Non-mechanical peristalsis is inhibited by toxic or
traumatic alteration in motility
Mechanical caused by extrinsic pressure
Simple mechanical obstruction only one point of
obstruction
Closed-loop obstruction at least 2 points of obstruction
(can lead to infarction due to strangulation)
 Intestinal obstruction
Etiology
Non-mechanical
Common after abdominal surgery
Can be caused by peritonitis
Accompanies many traumatic conditions (rib fracture, concussion
of spinal cord or fracture of spine)
Mechanical
About 50% of all are in adults and result from adhesions following
previous surgeries
Malignant tumors, diverticulitis and vulvulus are the most
common causes in middle aged and older people
Inguinal or femoral hernia common causes of SI obstruction
Intussusception is the most common cause in infants and small
children
Foreign objects and congenital abnormalities also common causes
in infants and children
 Intestinal obstruction
Pathophysiology events similar regardless of
cause
Wall is distended by fluid and gas
Distension reduces movement of water and ions from
lumen to blood
~8 Liters secreted into GI tract each day
Vomiting and intestinal secretion result in fluid and electrolyte
loss
Shock due to reduced ECF volume
Continued distension results in viscous cycle of
decreased fluid absorption and increased secretion
Local effects include ischemia and increased
permeability due to necrosis resulting in absorption of
bacterial toxins into peritoneal cavity and systemic
circulation
 Intestinal obstruction

Signs and symptoms

Cardinal symptoms
Abdominal distension
Pain
Vomiting
Absolute constipation
Abdominal radiograph essential for diagnosis
 Intestinal obstruction

Treatment
Correct fluid and electrolyte imbalance
Relieve distention and vomiting by intubation and
decompression
Control peritonitis and shock
Remove obstruction
Small bowel obstruction more serious and rapid than
colonic
Mortality for non strangulation 5-8% if surgical intervention
is soon enough
Delay or development of strangulation or other
complications raises mortality to 35-45%
 Disorders of the GI tract

Intestinal Disorders, continued

Colon cancer - one of the most common types
in the US - usually adenocarcinomas that arise
from the mucosal lining. Occurrence is equal
in the sexes, however, rectal cancer is greater in
men than women. Early detection is afforded
with fecal occult blood testing and
sigmoidoscopy
 Disorders of the GI tract

Liver Disorders
Hepatitis - inflammation of the liver by drugs, alcohol or
infection
A - transmitted in fecal matter; rarely fatal; infection affords life-
long immunity; Vaccine available
B - transmitted by direct exchange of blood or body fluids; Vaccine
available
C - primarily transmitted by direct exchange of blood; sexual
transmission can occur, but limited
D - transmitted by direct exchange of blood, only in concert with
HepB infection
E - transmitted by fecal contamination of water
 Disorders of the GI tract

Liver Disorders, continued

Cirrhosis - chronic disease in which active liver
cells are replaced by inactive connective tissue;
most common cause is alcoholism compounded
with malnutrition. In later stages there is
hampering of portal circulation causing
congestion in the peritoneal cavity - ascites
Cancer - the liver is a common site for
metastases
 Disorders of the GI tract

Liver Disorders, continued

Jaundice - yellow coloring of the skin and eyes;
cause is damage to the liver making it unable to
conjugate bilirubin or a blockage in the bile
ducts with bile pigment accumulation in the
blood
 Disorders of the GI tract

Gallbladder
Gall stones (cholelithiasis) - formed from
cholesterol and block the ducts; pain occurs
when the stones prevent the flow of bile and
hamper the digestive process
Cholecystitis - Inflammation of the gall bladder
 Disorders of the GI tract

Pancreas
Pancreatitis - inflammation of the pancreas
caused by blockage of the bile ducts causing
the pancreatic enzymes to back up into the
gland which causes destruction of the tissue;
another cause is infection of the pancreas.
 Disorders of the GI tract

Digestive Disorders
Anorexia - chronic loss of appetite; causes can be
physical (heavy exercise) or mental (more likely to be
emotional and/or social rather than physiological
disruption in the brain). Anorexia nervosa affects
mostly young women
Bulimia (binge-purge syndrome) - prevention of the
absorption of food because of induce vomiting or
large doses of laxatives
 Overalllessons:
Thelargeintestinefunctionstostoresymbionts,absorbwater,
vitamins,wastes,andtoxins.
Thelargeintestinehasnovilli,butdoeshaveafoldedepithelium.
Thececumdoesmostofthewaterresorption.
Thecolonmovescontentsalongbyperistalsis.
Defecationismainlyautonomicexceptforthefinalstep.
Manynutrientsareabsorbedviacotransportwithions.
Na+mustbepumpedoutofcellsactively.
Thebrushborderhasenzymeswhichbreakdownpolysaccharides
&peptidesintomonomersbeforeabsorption.
Waterisabsorbedbypassiveosmosis.
Lipidsareabsorbedthroughmembrane&exocytosedtolacteal.
Thank You