Physiology

of
Digestion
Dr. Yudi Herlambang
Prof dr Abdul Majid
Dr Nur Aiza
Department of Physiology
School of Medicine
University of Sumatera Utara

Nutrient

Assimilated

Digestive
system

Food
Non Nutrient

Eliminated

Primary Functions of Digestive System

Activity necessary:
Motility

Secretio
n

Digestio
n

Absorptio
n

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)
Secretio
muscular contraction.
n
Endocrine (secretion of hormones that
regulate digestive process)
Exocrine (secretion of water, enzymes,
acid, bicarbonate, into GI tract enzyme &
other digestive juices.

Digestio
n

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

Absorptio
n 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

Mout
h:

Mouth:

Teeth

grind and tear food into smaller pieces

increases surface area upon which digestive
enzymes work

Salivary glands
(parotid, submaxillary,
sublingual)
secrete
saliva

parotid gland
parotid duct
lubricates and softens sublingual gland
submandibular gland

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.

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

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.
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
Parietal (oxyntic) cells,
secrete :
- HCl .
- Intrinsic factor binds
Pyloric gland Alkaline
vit. B12
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 inhibitory
hormones (enterogastrones)

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

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

Divisions (@ 12 feet long total
length)
3 segments (12 ft long, 22 ft in
cadaver)
duodenum = upper portion (@ 1
foot long) closest to stomach
jejunum = middle section

nutrients, fluids, and

electrolytes

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

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

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

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

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

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

Intestinal Contractions and Motility

2 major types of
contractions occur in
the small intestine:
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.

Insert fig. 18.14

Brush border
enzymes

reassembly

Large
Intestine

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

 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

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

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

PATOGENESIS & TERAPI

GASTRITIS DAN TUKAK
PEPTIK

PENDAHULUA
Penyebab gastritis
N dan tukak peptik
adalah multifaktor

Patofisiologi dasar adalah gangguan

keseimbangan antara faktor-faktor agresif
dan faktor-faktor defensif
Sebagian penderita yang telah diobati
dan sembuh ternyata kambuh lagi
Kualitas penyembuhan luka diduga
berperan penting dalam terjadinya
kekambuhan penyakit ini

Pathophysiology of Peptic Ulceration

I.

Gastric acid secretion homeostatatis and gastroduodenal

motility

II.

Epithelial defense mechanism

III.

HP

IV. NSAID
V.

Other ulcerogenic
Multiple causes of PUD
NSAIDs

Gastric acid
Defense

H. Pylori

Inflammation

Stress

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.

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

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

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

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

Thank You

Pencernaan di rongga mulut

Pengaturan salivasi

Struktur oesophagus

Proses menelan

Struktur & Fungsi

Lambung

Sekresi &
Gerakan
Lambung

Gerakan Lambung

Muntah
(Vomitus)

Pancreas

Pengaturan
sekresi pancreas

Fungsi Hati

Hepar & Fesica

Vellea

Pengaturan
sekresi empedu

Usus Halus

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.

Physiology of
Digestion
Dr. Yudi
Herlambang

Department of Physiology
School of Medicine
University of Sumatera Utara