Chapter 24 Digestion

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Chapter 24
Digestion
Albert Grazia, M.S., N.D.
(516) 486-8332
www.naturedoc.info
Albert Grazia, M.S., N.D.
www.naturedoc.info
1
Chapter 24
The Digestive System
• Structure
– Gross Anatomy
– Histology
• Function
– Mechanical
– Chemical
• Development
• Disorders
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• The digestive system consists of a
tubular structure (Alimentary canal)
designed for the digestion and
absorption of food as well as the
expulsion of unusable ingested
materials.
• This system also has accessory
structures that play roles in other
systems of the body as well as the
digestive system.
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Functions of the digestive system:
• 1. Ingest the food
• 2. Break it down into small
molecules that can cross plasma
membranes
• 3. Absorb these nutrient molecules
• 4. Eliminate non-digestible wastes
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Our digestive system goes through 9
basic steps:
• 1. Teeth- Digestion starts here.
• The job of the teeth is to start tearing and
crushing the food down into small enough
pieces so that it can fit down our throats.
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2. Saliva- The salivary gland in located
underneath the back of our tongue. It
creates our saliva or spit.
This helps soften the food in the mouth so that
it is easier to swallow.
Saliva is also the first of several chemicals
that start to break down foods into simpler
forms.
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• 3. Tongue- The tongue is a muscle that works with the food
and saliva to form a "ball" that can be swallowed.
• Of course, the tongue also contains taste buds that helps us
tell the difference between salty, sour, sweet, and bitter
foods.
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• 4. Esophagus- The esophagus is simply a
transportation tube from the mouth to the
stomach.
• When we swallow, what we are really doing
is closing a trap door in our throat called the
epiglottis.
• This sends food down the esophagus and
prevents food from going down the trachea
(or windpipe) and into our lungs.
• Food moves down the esophagus using
muscles not gravity.
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• 5. Stomach- The first stop after the esophagus is
•
•
•
•
•
the stomach.
Once the food gets to the stomach the stomach uses
chemicals to try to make the food tinier.
These chemicals are called gastric juices and the
include hydrochloric acid and enzymes (chemicals
that break down food).
The food is moved around in the stomach and
mixed with the chemicals for about 3 or 4 hours.
When it is done in the stomach, the food is now a
cream-like liquid call chyme.
The food is still not small enough the get into our
blood stream and it has not provided the body with
anything useful yet.
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• 6. Liver/Gall Bladder- At this point, our
food is hit with more chemicals.
• The liver makes a chemical called bile but
bile is not stored in the liver. Instead it is
stored in the gall bladder.
• When the gall bladder mixes bile with our
food, it does an important job: breaking
down the fat (from milk, butter, cheeses)
into tiny droplets.
• This fat will supply us with much energy
later.
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7. Pancreas- The pancreas also adds a
digestive chemical as the food leaves the
stomach.
This digestive juice works on breaking down
the carbohydrates (from breads, potatoes,
etc.) and the proteins (from meats, cereals,
peanut butter)
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8. Small Intestine- The small intestine is the real
hero of the digestive system.
The small intestine is a tube that is about 22 feet
long! This is where the real digestion takes place.
As the food passes through, it is mixed with the
new chemicals and soon our "food" is now
digested small enough to be put to use by the
body.
Along the walls of the intestine are thousands of tiny
fingers called villi. Blood vessels (capillaries) in
the villi can absorb the tiny food molecules and
send them off to the rest of our body through the
blood.
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• 9. Large Intestine- Whatever the body cannot put
to use is sent to the large intestine.
• Many plants, for example, contain cellulose which
cannot be digested.
• The big job of the large intestine is to remove
water. Water has been necessary up until now but
it is no longer needed and in the large intestine
water is sent into the blood stream .
• Food spends about 12 hours in the large intestine
where it become feces and later leaves the body
through the anal opening when we go to the
bathroom.
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Overview of GI tract Functions
• Mouth---bite, chew, swallow
• Pharynx and esophagus---transport
• Stomach----mechanical
disruption; absorption of water
& alcohol
• Small intestine--chemical &
mechanical digestion &
absorption
• Large intestine----absorb
electrolytes & vitamins (B and K)
• Rectum and anus---defecation
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Layers of the GI Tract
1. Mucosal layer
2. Submucosal
layer
3. Muscularis layer
4. Serosa layer
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Mucosa
• Epithelium
– stratified squamous(in mouth,esophagus & anus) = tough
– simple columnar in the rest
• secretes enzymes and absorbs nutrients
• specialized cells (goblet) secrete mucous onto cell surfaces
• enteroendocrine cells---secrete hormones controlling organ function
• Lamina propria
– thin layer of loose connective tissue
– contains BV and lymphatic tissue
• Muscularis mucosae---thin layer of smooth muscle
– causes folds to form in mucosal layer
– increases local movements increasing absorption with exposure to “new” nutrients
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Submucosa
• Loose connective tissue
– containing BV, glands and lymphatic tissue
• Meissner’s plexus--– parasympathetic
– innervation
• vasoconstriction
• local movement by
muscularis mucosa
smooth muscle
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Muscularis
• Skeletal muscle = voluntary control
– in mouth, pharynx , upper esophagus and anus
– control over swallowing and defecation
• Smooth muscle = involuntary control
– inner circular fibers & outer longitudinal fibers
– mixes, crushes & propels food along by peristalsis
• Auerbach’s plexus (myenteric)-– both parasympathetic & sympathetic innervation of
circular and longitudinal smooth muscle layers
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Serosa
• An example of a serous membrane
• Covers all organs and walls of cavities not
open to the outside of the body
• Secretes slippery fluid
• Consists of connective tissue covered with
simple squamous epithelium
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Peritoneum
• Peritoneum
– visceral layer covers
organs
– parietal layer lines the
walls of body cavity
• Peritoneal cavity
– potential space
containing a bit of
serous fluid
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Parts of the Peritoneum
•
•
•
•
•
Mesentery
Mesocolon
Lesser omentum
Greater omentum
Peritonitis =
inflammation
–
–
–
–
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trauma
rupture of GI tract
appendicitis
perforated ulcer
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Peritonitis
• Acute inflammation of the peritoneum
• Cause
– contamination by infectious microbes during
surgery or from rupture of abdominal organs
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Greater Omentum, Mesentery &
Mesocolon
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Lesser Omentum
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Mouth
• Lips and cheeks-----contains buccinator muscle that keeps food
between upper & lower teeth
• Vestibule---area between cheeks and teeth
• Oral cavity proper---the roof = hard, soft palate and uvula
– floor = the tongue
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Pharyngeal Arches
• Two skeletal muscles
• Palatoglossal muscle
– extends from palate to
tongue
– forms the first arch
– posterior limit of the mouth
• Palatopharyngeal muscle
– extends from palate to
pharyngeal wall
– forms the second arch
– behind the palatine tonsil28
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Salivary Glands
•
•
•
•
Parotid below your ear and over the masseter
Submandibular is under lower edge of mandible
Sublingual is deep to the tongue in floor of mouth
All have ducts that empty
into the oral cavity
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Composition and Functions of Saliva
• Wet food for easier swallowing
• Dissolves food for tasting
• Bicarbonate ions buffer acidic foods
– bulemia---vomiting hurts the enamel on your teeth
• Chemical digestion of starch begins with enzyme
(salivary amylase)
• Enzyme (lysozyme) ---helps destroy bacteria
• Protects mouth from infection with its rinsing
action---1 to 1 and 1/2qts/day
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Salivary Gland Cellular Structure
• Cells in acini (clusters)
• Serous cells secrete a watery fluid
• Mucous cells (pale staining) secrete a slimy, mucus
secretion
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Salivation
• Increase salivation
– sight, smell, sounds, memory of food, tongue
stimulation---rock in mouth
– cerebral cortex signals the salivatory nuclei in
brainstem---(CN 7 & 9)
– parasympathetic nn. (CN 7 & 9)
• Stop salivation
– dry mouth when you are afraid
– sympathetic nerves
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Mumps
• Myxovirus that attacks the parotid gland
• Symptoms
– inflammation and enlargement of the parotid
– fever, malaise & sour throat (especially
swallowing sour foods)
– swelling on one or both sides
• Sterility rarely possible in males with
testicular involvement (only one side
involved)
• Vaccine available since 1967
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Structure and Function of the Tongue
• Muscle of tongue is
attached to hyoid,
mandible, hard
palate and styloid
process
• Papillae are the
bumps---taste buds
are protected by
being on the sides of
papillae
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Tooth Structure
•
•
•
•
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Crown
Neck
Roots
Pulp cavity
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Composition of Teeth
• Enamel
– hardest substance in
body
– calcium phosphate or
carbonate
• Dentin
– calcified connective
tissue
• Cementum
What is the gingiva?
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– bone-like
– periodontal ligament
penetrates it
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Dentition
• Primary or baby teeth
– 20 teeth that start erupting at 6 months
– 1 new pair of teeth per month
• Permanent teeth
– 32 teeth that erupt between 6 and 12 years of age
– differing structures indicate function
• incisors for biting
• canines or cuspids for tearing
• premolars & molars for crushing and grinding food
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Primary and Secondary Dentition
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Digestion in the Mouth
• Mechanical digestion (mastication or chewing)
• breaks into pieces
• mixes with saliva so it forms a bolus
• Chemical digestion
– amylase
• begins starch digestion at pH of 6.5 or 7.0 found in mouth
• when bolus & enzyme hit the pH 2.5 gastric juices hydrolysis ceases
– lingual lipase
• secreted by glands in tongue
• begins breakdown of triglycerides into fatty acids and glycerol
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Pharynx
• Funnel-shaped tube extending from internal
nares to the esophagus (posteriorly) and larynx
(anteriorly)
• Skeletal muscle lined by mucous membrane
• Deglutition or swallowing is facilitated by saliva
and mucus
– starts when bolus is pushed into the oropharynx
– sensory nerves send signals to deglutition center in
brainstem
– soft palate is lifted to close nasopharynx
– larynx is lifted as epiglottis is bent to cover glottis
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Esophagus
• Collapsed muscular
tube
• In front of vertebrae
• Posterior to trachea
• Posterior to the heart
• Pierces the
diaphragm at hiatus
– hiatal hernia or
diaphragmatic hernia
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Histology of the Esophagus
• Mucosa = stratified squamous
• Submucosa = large mucous glands
• Muscularis = upper 1/3 is skeletal, middle is mixed,
lower 1/3 is smooth
– upper & lower esophageal sphincters are prominent
circular muscle
• Adventitia = connective tissue blending with
surrounding connective tissue--no peritoneum
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Physiology of the Esophagus - Swallowing
• Voluntary phase---tongue pushes food to back of oral cavity
• Involuntary phase----pharyngeal stage
–
–
–
–
breathing stops & airways are closed
soft palate & uvula are lifted to close off nasopharynx
vocal cords close
epiglottis is bent over airway as larynx is lifted
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Swallowing
• Upper sphincter relaxes when
larynx is lifted
• Peristalsis pushes food down
– circular fibers behind bolus
– longitudinal fibers in front of bolus shorten the
distance of travel
• Travel time is 4-8 seconds for solids and 1 sec for
liquids
• Lower sphincter relaxes as food approaches
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Gastroesophageal Reflex Disease
• If lower sphincter fails to open
– distension of esophagus feels like chest pain or heart attack
• If lower esophageal sphincter fails to close
– stomach acids enter esophagus & cause heartburn (GERD)
– for a weak sphincter---don't eat a large meal and lay down
in front of TV
– smoking and alcohol make the sphincter relax worsening
the situation
• Control the symptoms by avoiding
– coffee, chocolate, tomatoes, fatty foods, onions & mint
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Anatomy of Stomach
• Which side is it on?
• Size when empty?
– large sausage
– stretches due to rugae
• Parts of stomach
–
–
–
–
cardia
fundus---air in x-ray
body
pylorus---starts to narrow as approaches pyloric
sphincter
• Empties as small squirts of chyme leave the
stomach through the pyloric valve
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The stomach has five
major functions;
•Temporary food
storage
•Control the rate at
which food enters the
duodenum
•Acid secretion and
antibacterial action
•Fluidisation of stomach
contents
•Preliminary digestion
with pepsin, lipases etc.
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Pylorospasm and Pyloric Stenosis
• Abnormalities of the pyloric sphincter in
infants
• Pylorospasm
– muscle fibers of sphincter fail to relax trapping
food in the stomach
– vomiting occurs to relieve pressure
• Pyloric stenosis
– narrowing of sphincter indicated by projectile
vomiting
– must be corrected
surgically
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Histology of the Stomach
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Mucosa & Gastric Glands
• Hydrochloric acid
converts pepsinogen from
chief cell to pepsin
• Intrinsic factor
– absorption of vitamin B12
for RBC production
• Gastrin hormone (g cell)
– “get it out of here”
•
•
•
•
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release more gastric juice
increase gastric motility
relax pyloric sphincter
constrict esophageal
sphincter preventing entry
53
Submucosa
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Muscularis
• Three layers of
smooth muscle-outer longitudinal,
circular & inner
oblique
• Permits greater
churning &
mixing of food
with gastric juice
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Serosa
• Simple squamous epithelium over a bit of
connective tissue
• Also known as visceral peritoneum
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Mucosal layer on the surface is made up simple columnar cells and a
mucosal muscularis on the deep side .
Submucosa contains fibrous connective tissue and blood vessels.
The muscularis externa is made up of a circular and a longitudinal
muscle layer with a myenteric plexus in between the layers. A very
thin layer of
Serosa is also present .
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Physiology--Mechanical Digestion
• Gentle mixing waves
– every 15 to 25 seconds
– mixes bolus with 2 quarts/day of gastric juice to
turn it into chyme (a thin liquid)
• More vigorous waves
– travel from body of stomach to pyloric region
• Intense waves near the pylorus
– open it and squirt out 1-2 teaspoons full with
each wave
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Physiology--Chemical Digestion
• Protein digestion begins
– HCl denatures (unfolds) protein molecules
– HCl transforms pepsinogen into pepsin that breaks
peptides bonds between certain amino acids
• Fat digestion continues
– gastric lipase splits the triglycerides in milk fat
• most effective at pH 5 to 6 (infant stomach)
• HCl kills microbes in food
• Mucous cells protect stomach walls from being
digested with 1-3mm thick layer of mucous
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Regulation of Gastric Secretion and Motility
• Cephalic phase
• Gastric phase
• Intestinal phase
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Cephalic Phase = “Stomach Getting Ready”
• Cerebral cortex =sight, smell, taste &
thought
– stimulate parasympathetic nervous system
• Vagus nerve
– increases stomach muscle and glandular
activity
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Gastric Phase = “Stomach Working”
• Nervous control keeps stomach active
– stretch receptors & chemoreceptors provide information
– vigorous peristalsis and glandular secretions continue
– chyme is released into the duodenum
• Endocrine influences over stomach activity
– distention and presence of caffeine or protein cause G
cells secretion of gastrin into bloodstream
– gastrin hormone increases stomach glandular secretion
– gastrin hormone increases stomach churning and
sphincter relaxation
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Intestinal Phase = “Stomach Emptying”
• Stretch receptors in duodenum slow stomach activity &
increase intestinal activity
• Distension, fatty acids or sugar signals medulla
– sympathetic nerves slow stomach activity
• Hormonal influences
– secretin hormone decreases stomach secretions
– cholecystokinin(CCK) decreases stomach emptying
– gastric inhibitory peptide(GIP) decreases stomach secretions,
motility & emptying
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Absorption of Nutrients by the Stomach
•
•
•
•
Water especially if it is cold
Electrolytes
Some drugs (especially aspirin) & alcohol
Fat content in the stomach slows the passage of alcohol to
the intestine where absorption is more rapid
• Gastric mucosal cells contain alcohol dehydrogenase that
converts some alcohol to acetaldehyde-----more of this
enzyme found in males than females
• Females have less total body fluid that same size male so
end up with higher blood alcohol levels with same intake
of alcohol
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Regulation of Gastric Emptying
• Release of chyme is regulated by neural
and hormonal reflexes
• Distention & stomach contents increase
secretion of gastrin hormone & vagal
nerve impulses
– stimulate contraction of esophageal sphincter
and stomach and relaxation of pyloric
sphincter
• Enterogastric reflex regulates amount
released into intestines
– distension of duodenum & contents of chyme
– sensory impulses sent to the medulla inhibit
parasympathetic stimulation of the stomach
but increase secretion of cholecystokinin and
stimulate sympathetic impulses
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– inhibition
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emptying
65
Vomiting (emesis)
• Forceful expulsion of contents of stomach &
duodenum through the mouth
• Cause
– irritation or distension of stomach
– unpleasant sights, general anesthesia, dizziness & certain drugs
• Sensory input from medulla cause stomach contraction &
complete sphincter relaxation
• Contents of stomach squeezed between abdominal muscles
and diaphragm and forced through open mouth
• Serious because loss of acidic gastric juice can lead to
alkalosis
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Anatomy of the Pancreas
• 5" long by 1" thick
• Head close to curve in
C-shaped duodenum
• Main duct joins
common bile duct from
liver
• Sphincter of Oddi on
major duodenal papilla
• Opens 4" below pyloric
sphincter
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Histology of the Pancreas
• Acini- dark clusters
– 99% of gland
– produce pancreatic
juice
• Islets of Langerhans
– 1% of gland
– pale staining cells
– produce hormones
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Composition and Functions of Pancreatic Juice
• 1 & 1/2 Quarts/day at pH of 7.1 to 8.2
• Contains water, enzymes & sodium bicarbonate
• Digestive enzymes
– pancreatic amylase, pancreatic lipase, proteases
–
–
–
–
–
trypsinogen---activated by enterokinase (a brush border enzyme)
chymotrypsinogen----activated by trypsin
procarboxypeptidase---activated by trypsin
proelastase---activated by trypsin
trypsin inhibitor---combines with any trypsin produced inside
pancreas
– ribonuclease----to digest nucleic acids
– deoxyribonuclease
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Pancreatitis
• Pancreatitis---inflammation of the pancreas
occurring with the mumps
• Acute pancreatitis---associated with heavy
alcohol intake or biliary tract obstruction
– result is patient secretes trypsin in the pancreas &
starts to digest himself
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Regulation of Pancreatic Secretions
• Secretin
– acidity in intestine
causes increased sodium
bicarbonate release
• GIP
– fatty acids & sugar
causes increased insulin
release
• CCK
– fats and proteins cause
increased digestive
enzyme release
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Anatomy of the Liver and Gallbladder
• Liver
–
–
–
–
weighs 3 lbs.
below diaphragm
right lobe larger
gallbladder on
right lobe
– size causes right
kidney to be
lower than left
• Gallbladder
– fundus, body &
neck
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Histology of the Gallbladder
•
•
•
•
Simple columnar epithelium
No submucosa
Three layers of smooth muscle
Serosa or visceral peritoneum
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• The gallbladder is a muscular sac located
under the liver. It stores and concentrates the
bile produced in the liver that is not
immediately needed for digestion. Bile is
released from the gallbladder into the small
intestine in response to food. The pancreatic
duct joins the common bile duct at the small
intestine adding enzymes to aid in digestion.
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Bile Production
• One quart of bile/day is secreted by the liver
– yellow-green in color & pH 7.6 to 8.6
• Components
– water & cholesterol
– bile salts = Na & K salts of bile acids
– bile pigments (bilirubin) from hemoglobin molecule
• globin = a reuseable protein
• heme = broken down into iron and bilirubin
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Pathway of Bile Secretion
• Bile capillaries
• Hepatic ducts connect to form common hepatic duct
• Cystic duct from gallbladder & common hepatic duct join to
form common bile duct
• Common bile duct & pancreatic duct empty into duodenum
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Regulation of Bile Secretion
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Histology of the Liver
• Hepatocytes arranged in lobules
• Sinusoids in between hepatocytes
are blood-filled spaces
• Kupffer cells phagocytize microbes
& Grazia,
foreign
matter
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Flow of Fluids Within the Liver
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Blood Supply to the Liver
• Hepatic portal vein
– nutrient rich blood
from stomach, spleen
& intestines
• Hepatic artery from
branch off the aorta
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Liver Functions--Carbohydrate Metabolism
• Turn proteins into glucose
• Turn triglycerides into glucose
• Turn excess glucose into glycogen
& store in the liver
• Turn glycogen back into glucose as
needed
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Liver Functions --Lipid Metabolism
• Synthesize cholesterol
• Synthesize lipoproteins----HDL and
LDL(used to transport fatty acids in
bloodstream)
• Stores some fat
• Breaks down some fatty acids
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Liver Functions--Protein Metabolism
• Deamination = removes NH2 (amine group)
from amino acids so can use what is left as
energy source
• Converts resulting toxic ammonia (NH3)
into urea for excretion by the kidney
• Synthesizes plasma proteins utilized in the
clotting mechanism and immune system
• Convert one amino acid into another
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Other Liver Functions
• Detoxifies the blood by removing or altering drugs &
hormones(thyroid & estrogen)
• Removes the waste product--bilirubin
• Releases bile salts help digestion by emulsification
• Stores fat soluble vitamins-----A, B12, D, E, K
• Stores iron and copper
• Phagocytizes worn out blood cells & bacteria
• Activates vitamin D (the skin can also do this with 1 hr
of sunlight a week)
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Liver Detoxification
• One of the liver's primary functions is filtering the
blood. Almost 2 quarts of blood pass through the
liver every minute for detoxification. Filtration of
toxins is absolutely critical as the blood from the
intestines contains high levels of bacteria, bacterial
endotoxins, antigen-antibody complexes, and
various other toxic substances.
• When working properly, the liver clears 99% of the
bacteria and other toxins during the first pass.
• However, when the liver is damaged, such as in
alcoholics, the passage of toxins increases by over
a factor of 10.
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• The liver's second detoxification process involves
the synthesis and secretion of bile. Each day the
liver manufactures approximately 1 quart of bile,
which serves as a carrier in which many toxic
substances are dumped into the intestines.
• In the intestines, the bile and its toxic load are
absorbed by fiber and excreted.
• However, a diet low in fiber results in inadequate
binding and reabsorption of the toxins.
• This problem is magnified when bacteria in the
intestine modify these toxins to more damaging
forms.
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• However, when the excretion of bile is
inhibited (i.e. cholestasis from gallstones in
bile duct), toxins stay in the liver longer.
• Another common cause of cholestasis and
impaired liver function is alcohol ingestion.
In some sensitive individuals, as little as 1
ounce of alcohol can produce damage to the
liver, which results in fat being deposited
within the liver.
• All active alcoholics demonstrate fatty
infiltration of the liver.
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• The liver utilizes a two-step enzymatic
detoxification process for the neutralization of
unwanted chemical compounds.
• These not only include drugs, pesticides, and
toxins from the gut, but also normal body
chemicals such as hormones and inflammatory
chemicals (e.g. histamine) which become
toxic if allowed to build up.
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Phase I Detox Pathway
• Phase I enzymes directly neutralize some
chemicals, but most are converted to intermediate
forms that are then processed by phase II enzymes.
• These intermediate forms are much more
chemically active and therefore more toxic.
• If the phase II detoxification systems are not
working adequately, these intermediates can
cause substantial damage, including the
initiation of carcinogenic processes.
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• Phase I detoxification of most chemical
toxins involves a group of enzymes which,
collectively, have been named cytochrome
P450. Some 50-100 enzymes make up the
cytochrome P450 system.
• Since the activity of cytochrome P450 varies
from person to person, so does an individual's
risk for various diseases, such as cancer.
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Phase II Detox pathway
• Phase II detoxification typically involves
conjugation in which various enzymes in the
liver attach small chemicals to the toxin.
• This conjugation reaction either neutralizes
the toxin or makes the toxin more easily
excreted through the urine or bile.
• Phase II enzymes act on some toxins
directly, while others must first be activated
by the phase I enzymes.
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• Another potential problem occurs because the toxins
transformed into activated intermediates by phase I are
substantially more reactive. Unless quickly removed
from the body by phase II detoxification mechanisms,
they can cause widespread problems, especially
carcinogenesis.
• Therefore, the rate at which phase I produces activated
intermediates must be balanced by the rate at which phase
II finishes their processing.
• People with a very active phase I detoxification system
coupled with slow or inactive phase II enzymes are termed
pathological detoxifiers.
• These people may suffer unusually severe toxic reactions
to environmental poisons.
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• An imbalance between phase I and phase
II can also occur when a person is
exposed to large amounts of toxins or
exposed to toxins for a long period of
time.
• In these situations, the critical nutrients
needed for phase II detoxification are
depleted, which allows the highly toxic
activated intermediates to build up.
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Summary of Digestive Hormones
• Gastrin
– stomach, gastric & ileocecal sphincters
• Gastric inhibitory peptide--GIP
– stomach & pancreas
• Secretin
– pancreas, liver & stomach
• Cholecystokinin--CCK
– pancreas, gallbladder, sphincter of Oddi, &
stomach
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Anatomy of the Small Intestine
• 20 feet long----1 inch in diameter
• Large surface area for majority of
absorption
• 3 parts
– duodenum---10 inches
– jejunum---8 feet
– ileum---12 feet
• ends at ileocecal valve
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Histology of Small Intestine
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Histology of the Small Intestine
• Structures that increase surface area
– plica circularis
• permanent ½ inch tall folds that contain part of
submucosal layer
• not found in lower ileum
• can not stretch out like rugae in stomach
– villi
• 1 Millimeter tall
• Core is lamina propria of mucosal layer
• Contains vascular capillaries and lacteals(lymphatic
capillaries)
– microvilli
• cell surface feature known as brush border
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Functions of Microvilli
• Absorption and digestion
• Digestive enzymes found at cell surface on
microvilli
• Digestion occurs at cell surfaces
• Significant cell division within intestinal
glands produces new cells that move up
• Once out of the way---rupturing and
releasing their digestive enzymes & proteins
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Cells of Intestinal Glands
• Absorptive cell
• Goblet cell
• Enteroendocrine
– secretin
– cholecystokinin
– gastric inhibitory
peptide
• Paneth cells
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– secretes lysozyme
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Hormone Regulators
The hormones that control digestion are gastrin, secretin, and
cholecystokinin (CCK):
• Gastrin causes the stomach to produce an acid for
dissolving and digesting some foods. It is also
necessary for the normal growth of the lining of
the stomach, small intestine, and colon.
• Secretin causes the pancreas to send out a
digestive juice that is rich in bicarbonate. It
stimulates the stomach to produce pepsin, an
enzyme that digests protein, and it also stimulates
the liver to produce bile.
• CCK causes the pancreas to grow and to produce
the enzymes of pancreatic juice, and it causes the
gallbladder to empty.
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Nerve Regulators
• Acetylcholine causes the muscle of the digestive organs to
squeeze with more force and increase the "push" of food and
juice through the digestive tract. Acetylcholine also causes the
stomach and pancreas to produce more digestive juice.
• Adrenaline relaxes the muscle of the stomach and intestine
and decreases the flow of blood to these organs.
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Goblet Cells of GI epithelium
Unicellular glands that
are part of simple
columnar epithelium
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Roles of Intestinal Juice & Brush-Border Enzymes
• Submucosal layer has duodenal glands
– secretes alkaline mucus
• Mucosal layer contains intestinal glands = Crypts of
Lieberkuhn(deep to surface)
– secretes intestinal juice
• 1-2 qt./day------ at pH 7.6
– brush border enzymes
– paneth cells secrete lysozyme kills bacteria
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Mechanical Digestion in the Small Intestine
• Weak peristalsis in
comparison to the
stomach---chyme
remains for 3 to 5 hours
• Segmentation---local
mixing of chyme with
intestinal juices--sloshing back & forth
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Chemical Digestion in Small Intestine
• Chart page 853--groups enzymes by region
where they are found
• Need to trace breakdown of nutrients
– carbohydrates
– proteins
– lipids
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Digestion of Carbohydrates
•
•
•
•
Mouth---salivary amylase
Esophagus & stomach---nothing happens
Duodenum----pancreatic amylase
Brush border enzymes (maltase, sucrase &
lactase) act on disaccharides
– produces monosaccharides--fructose, glucose &
galactose
– lactose intolerance (no enzyme; bacteria
ferment sugar)--gas & diarrhea
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Lactose Intolerance
• Mucosal cells of small intestine fail to
produce lactase
– essential for digestion of lactose sugar in milk
– undigested lactose retains fluid in the feces
– bacterial fermentation produces gases
• Symptoms
– diarrhea, gas, bloating & abdominal cramps
• Dietary supplements are helpful
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Digestion of Proteins
• Stomach
– HCl denatures or unfolds proteins
– pepsin turns proteins into peptides
• Pancreas
– digestive enzymes---split peptide bonds
between different amino acids
– brush border enzymes-----aminopeptidase or
dipeptidase------split off amino acid at amino
end of molecule or split dipeptide
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Digestion of Lipids
• Mouth----lingual lipase
• Small intestine
– emulsification by bile
– pancreatic lipase---splits into fatty acids &
monoglyceride
– no enzymes in brush border
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• The gut produces chylomicrons following the
absorption of fat.
• The TG component of chylomicrons is removed
by lipoprotein lipase located on the vascular
endothelium of muscle, myocardium, and adipose
tissue.
• The resulting chylomicron remnants are cleared
from the circulation by hepatic receptors that
recognize apolipoprotein (Apo) E.
• The liver exports TG into the circulation in the
core of VLDL particles.
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Digestion of Nucleic Acids
• Pancreatic juice contains 2 nucleases
– ribonuclease which digests RNA
– deoxyribonuclease which digests DNA
• Nucleotides produced are further digested
by brush border enzymes (nucleosidease
and phosphatase)
– pentose, phosphate & nitrogenous bases
• Absorbed by active transport
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Regulation of Secretion & Motility
• Enteric reflexes that respond to presence of
chyme
– increase intestinal motility
– VIP (vasoactive intestinal polypeptide)
stimulates the production of intestinal juice
– segmentation depends on distention which
sends impulses to the enteric plexus & CNS
• distention produces more vigorous peristalsis
• 10 cm per second
• Sympathetic impulses
decrease motility
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Absorption in Small Intestine
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Absorption of Monosaccharides
• Absorption into epithelial cell
– glucose & galactose----sodium symporter(active transport)
– fructose-----facilitated diffusion
• Movement out of epithelial cell into bloodstream
– by facilitated diffusion
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Absorption of Amino Acids & Dipeptides
• Absorption into epithelial cell
– active transport with Na+ or H+ ions (symporters)
• Movement out of epithelial cell into blood
– diffusion
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Absorption of Lipids
• Small fatty acids enter cells & then blood by simple diffusion
• Larger lipids exist only within micelles (bile salts coating)
• Lipids enter cells by simple diffusion leaving bile salts behind in
gut
• Bile salts reabsorbed into blood & reformed into bile in the liver
• Fat-soluble vitamins are enter cells since were within micelles
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Absorption of Lipids (2)
• Inside epithelial cells fats are rebuilt and coated with
protein to form chylomicrons
• Chylomicrons leave intestinal cells by exocytosis into a lacteal
– travel in lymphatic system to reach veins near the heart
– removed from the blood by the liver and fat tissue
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Absorption of Electrolytes
• Sources of electrolytes
– GI secretions & ingested foods and liquids
• Enter epithelial cells by diffusion & secondary active
transport
– sodium & potassium move = Na+/K+ pumps (active transport)
– chloride, iodide and nitrate = passively follow
– iron, magnesium & phosphate ions = active transport
• Intestinal Ca+ absorption requires vitamin D &
parathyroid hormone
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Absorption of Vitamins
• Fat-soluble vitamins
– travel in micelles & are absorbed by simple
diffusion
• Water-soluble vitamins
– absorbed by diffusion
• B12 combines with intrinsic factor before it is
transported into the cells
– receptor mediated endocytosis
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Absorption of Water
• 9 liters of fluid dumped
into GI tract each day
• Small intestine reabsorbs
8 liters
• Large intestine reabsorbs
90% of that last liter
• Absorption is by osmosis
through cell walls into
vascular capillaries inside
villi
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Anatomy of Large Intestine
•
•
•
•
•
5 feet long by 2½ inches in diameter
Ascending & descending colon are retroperitoneal
Cecum & appendix
Rectum = last 8 inches of GI tract anterior to the sacrum & coccyx
Anal canal = last 1 inch of GI tract
– internal sphincter----smooth muscle & involuntary
– external sphincter----skeletal muscle & voluntary control
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Appendicitis
• Inflammation of the appendix due to blockage
of the lumen by chyme, foreign body,
carcinoma, stenosis, or kinking
• Symptoms
– high fever, elevated WBC count, neutrophil count
above 75%
– referred pain, anorexia, nausea and vomiting
– pain localizes in right lower quadrant
• Infection may progress to gangrene and
perforation within 24 to 36 hours
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Histology of Large Intestine
• Mucosa
– smooth tube -----no villi or plica
– intestinal glands fill the the mucosa
– simple columnar cells absorb water & goblet cells secrete mucus
• Submucosal & mucosa contain lymphatic nodules
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Histology of Large Intestine
• Muscular layer
– internal circular layer is normal
– outer longitudinal muscle
• taeniae coli = shorter bands
• haustra (pouches) formed
• epiploic appendages
• Serosa = visceral peritoneum
• Appendix
– contains large amounts of
lymphatic tissue
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Mechanical Digestion in Large Intestine
• Smooth muscle = mechanical digestion
• Peristaltic waves (3 to 12 contractions/minute)
– haustral churning----relaxed pouches are filled from
below by muscular contractions (elevator)
– gastroilial reflex = when stomach is full, gastrin
hormone relaxes ileocecal sphincter so small intestine
will empty and make room
– gastrocolic reflex = when stomach fills, a strong
peristaltic wave moves contents of transverse colon
into rectum
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Chemical Digestion in Large Intestine
• No enzymes are secreted only mucous
• Bacteria ferment
– undigested carbohydrates into carbon dioxide
& methane gas
– undigested proteins into simpler substances
(indoles)----odor
– turn bilirubin into simpler substances that
produce color
• Bacteria produce vitamin K and B in colon
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Absorption & Feces Formation in
the Large Intestine
• Some electrolytes---Na+ and Cl• After 3 to 10 hours, 90% of H2O has been
removed from chyme
• Feces are semisolid by time reaches transverse
colon
• Feces = dead epithelial cells, undigested food
such as cellulose, bacteria (live & dead)
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Defecation
• Gastrocolic reflex moves
feces into rectum
• Stretch receptors signal
sacral spinal cord
• Parasympathetic nerves
contract muscles of rectum
& relax internal anal
sphincter
• External sphincter is
voluntarily controlled
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Defecation Problems
• Diarrhea = chyme passes too quickly through
intestine
– H20 not reabsorbed
• Constipation--decreased intestinal motility
– too much water is reabsorbed
– remedy = fiber, exercise and water
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Dietary Fiber
• Insoluble fiber
– woody parts of plants (wheat bran, vegie skins)
– speeds up transit time & reduces colon cancer
• Soluble fiber
– gel-like consistency = beans, oats, citrus white
parts, apples
– lowers blood cholesterol by preventing
reabsorption of bile salts so liver has to use
cholesterol to make more
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Development of the Digestive System
• Endoderm forms primitive gut with help from the splanchnic
mesoderm --- resulting tube is made up of epithelial, glandular,
muscle & connective tissue
• Differentiates into foregut, midgut & hindgut
• Endoderm grows into the mesoderm to form salivary glands, liver,
gallbladder & pancreas
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Development of the Digestive System
• Stomodeum
develops into oral
cavity
– oral membrane
ruptures
• Proctodeum
develops into anus
– cloacal membrane
ruptures
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Aging and the Digestive System
• Changes that occur
–
–
–
–
–
decreased secretory mechanisms
decreased motility
loss of strength & tone of muscular tissue
changes in neurosensory feedback
diminished response to pain & internal stimuli
• Symptoms
– sores, loss of taste, peridontal disease, difficulty swallowing,
hernia, gastritis, ulcers, malabsorption, jaundice, cirrhosis,
pancreatitis, hemorrhoids and constipation
• Cancer of the colon or rectum is common
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Diseases of the GI Tract
•
•
•
•
•
•
Dental caries and periodontal disease
Peptic Ulcers
Diverticulitis
Colorectal cancer
Hepatitis
Anorexia nervosa
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• Cancer of the Liver - The most
common primary malignant tumor of
the liver is an hepatocellular carcinoma.
Chronic carriers of hepatitis B virus,
particularly those with chronic hepatitis
or cirrhosis, are at substantially
increased risk of developing
hepatocellular carcinoma.
• Recent research also indicates that
patients who have long- standing
chronic hepatitis C virus infection are
also at increased risk for the
development of hepatocellular
carcinoma.
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• Chronic Hepatitis - an ongoing injury
to the cells of the liver with
inflammation which lasts for longer than
six months.
• Causes of chronic hepatitis are viruses,
metabolic or immunologic abnormalities
and medications.
• Signs and symptoms may include
fatigue, mild discomfort in the upper
abdomen, loss of appetite and aching
joints.
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• Cirrhosis - a group of chronic liver
diseases in which normal liver cells
are damaged and replaced by scar
tissue, decreasing the amount of
normal liver tissue.
• Cirrhosis and other liver diseases
take the lives of over 25,000
Americans each year and rank
eighth as a cause of death in the
United States.
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