Physiology of

Digestion
Dr. Yudi
Herlambang

Department of Physiology
School of Medicine
University of Sumatera Utara

Nutrien
t

Food
Non
Nutrient

Assimilated

Digesti
ve
system
Eliminate
d

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
Organs of GI tract include:
System

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
layer.
(adventitia):
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 glandsparotid gland

produce
parotid duct
sublingual gland
watery
secretion. submandibular 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

salivary centre
in medulla

pressure receptors
and chemoreceptors
in the mouth

simple
reflex

other inputs
Conditioned
reflex

autonomic nerves
salivary glands
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 (intraabdominal).
Disorder o/t LES tone major cause
esophageal reflux heart burn.

Proses menelan

Struktur & Fungsi

Lambung

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 wall

 Stomach:
lower region of
stomach (antrum)
secretes the hormone
gastrin.
Additional secretions:
Histamine (ECL cell)
Somatostatin

HCl
Gastrin
Histamine
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
increase numbers of
enzyme in plasma
membrane.+ +
H K ATP-ase
Somatostatin inhibits
acid secretion.

Gastrin

Pepsinogen

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 secretion by G
cells.

Gastrin

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

 Microvilli

Anatomy

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 CO2, 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

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

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

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 fatsoluble 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

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

DIGESTIVE ACTIVITIES OF
LARGE INTESTINE
STRUCTURE

Mucosa

ACTIVITY

Secretes
mucus

RESULT

Lubricates colon &

protects mucosa

Absorbs water Maintains water

balance; solidifies
feces; absorbs
vitamins & some ions

DIGESTIVE ACTIVITIES OF
LARGE INTESTINE
STRUCTURE

Lumen

ACTIVITY

Bacterial
activity

RESULT

Breaks down
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

Muscularis

ACTIVITY

RESULT

Haustral
churning

Contractions move
contents from haustrum
to haustrum

Peristalsis

Contractions of circular
& longitudinal muscles
move contents along
length of colon

DIGESTIVE ACTIVITIES OF
LARGE INTESTINE
STRUCTURE

Muscularis

ACTIVITY

RESULT

Mass
peristalsis

Forces contents into

sigmoid colon

Defecation
reflex

Eliminates feces by
contractions in sigmoid
colon & rectum

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