Transcript The Digestive System

GI Physiology
Part 1: Metabolic Pathways
Part 2: GI Physiology
Part 3: GI Disorders
1
Simple and Complex Carbohydrates

There are three main simple sugars (AKA
monosaccharides or simple carbohydrates)




Glucose
Fructose
Galactose
If you join a glucose to any of these, you
get a disaccharide



Glucose + Glucose = Maltose
Glucose + Galactose = Lactose
Glucose + Fructose = Sucrose
2
Simple and Complex Carbohydrates
If you join many monosaccharides and/or
disaccharides together, it is called a
polysaccharide (AKA complex
carbohydrate).
 These are stored in the liver as glycogen.
They can be broken down later into
glucose as needed.
 The storage form in plants is called starch.
 When we eat starch, we covert it to
glycogen and then store it.

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Glucagon and Insulin


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Glucagon, a hormone secreted by the pancreas, raises blood
glucose levels.
Its effect is opposite that of insulin, which lowers blood
glucose levels.
The pancreas releases glucagon when blood sugar (glucose)
levels fall too low.
Glucagon causes the liver to beak down the stored glycogen
into glucose, which is released into the bloodstream. Since
glycogen is being broken down, this process is called
glycogenolysis. Don’t confuse this with glycolysis (break
down of glucose to ATP)!
High blood glucose levels stimulate the release of insulin.
Insulin allows glucose to be taken up and used by insulindependent tissues.
Thus, glucagon and insulin are part of a feedback system that
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keeps blood glucose levels at a stable level.
Glycolysis





Glycolysis is the process where cells take in
glucose and break it down into pyruvate, and ATP
is released.
This is how we get ATP from glucose.
Fructose and galactose can also be broken down
into pyruvate and ATP.
During glycolysis, NAD (an energy molecule) is
reduced to NADH. If you run out of NAD,
glycolysis will stop. Therefore, we need to oxidize
NADH to convert it back into NAD.
This can be done by aerobic or anaerobic
respiration, or fermentation.
5
Glycolysis


Notice that 2 ATP
molecules are used
during glycolysis, but 4
are made (2 pyruvate
molecules are made,
each of which generates
2 ATP).
There is a net gain
of 2 ATP molecules.
6
After Glycolysis




Immediately upon finishing glycolysis, the cell must
continue respiration in either an aerobic or anaerobic
direction; this choice is made based on the circumstances
of the particular cell.
A cell that can perform aerobic respiration and which finds
itself in the presence of oxygen will continue on to the
aerobic citric acid cycle in the mitochondria.
If a cell able to perform aerobic respiration is in a situation
where there is no oxygen (such as muscles under extreme
exertion), it will move into anaerobic respiration.
Some cells such as yeast are unable to carry out aerobic
respiration and will automatically move into a type of
anaerobic respiration called alcoholic fermentation.
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Aerobic vs. Anaerobic Respiration


Aerobic
respiration
(in the
mitochondria)will
result in 6 ATP’s.
Anaerobic
respiration (in
our cytoplasm)
will result in only
2 ATP’s.
More importantly, we get our NAD back, so glycolysis can continue.
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Making ATP by Aerobic Respiration






Takes place in the mitochondria
Requires oxygen
Breaks down glucose to produce ATP
Waste products are CO2 and H2O (we exhale
them)
The good thing about making ATP from our
mitochondria is that we can make a LOT of it.
The bad things are that it takes longer to make
it, and it requires oxygen, and a muscle cell may
have used up all the oxygen during a sprinting
run.
Making ATP by Anaerobic
Respiration
Takes place in the cytoplasm
 Does not require oxygen
 Breaks down glucose to produce ATP
 Waste product is lactic acid
 The good thing about making ATP this way
is that we can make it FAST.
 The bad thing is that it does not make
much ATP, and we deplete the reserves
quickly.

Lactic Acid Build-up
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
During strenuous workouts where oxygen becomes deficient, the
pyruvate product of glycolysis does not have enough oxygen to
use for aerobic respiration, so it has to undergo anaerobic
respiration.
The enzyme lactate dehydrogenase (LDH) is used to transfer
hydrogen from the NADH molecule to the pyruvate molecule.
Pyruvate with the extra hydrogen is called lactate.
Lactic acid is formed from lactate. This causes muscle aches and
fatigue.
Lactic acid is deactivated by the addition of oxygen to it.
Therefore, breathing heavily adds the oxygen to our system to
deactivate lactic acid, and the muscle pains go away. Warm water
or ultrasound will also increase oxygenated blood to the muscles,
easing muscle cramps from lactic acid.
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ATP and Creatinine Phosphate
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What do we do when we run out of ATP?
Muscle fibers cannot stockpile ATP in preparation
for future periods of activity.
However, they can store another high energy
molecule called creatinine phosphate.
Creatine phosphate is made from the excess ATP
that we accumulate when we are resting.
During short periods of intense exercise, the
small reserves of ATP existing in a cell are
used first.
Then creatinine phosphate is broken down to
produce ATP.
Aerobic vs. Anaerobic Respiration

When do we use aerobic respiration?

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Resting (can breathe easily)
Running marathons (can breathe easily on long
runs)


Marathon runners want to make sure there will be
enough readily available energy for the muscles, so
they eat a lot of carbohydrates over a two-day
period before the marathon. That’s why they load up on
pasta before a marathon.
When do we use anaerobic respiration?

Sprint running (can’t talk while sprinting!)
Gluconeogenesis



Gluconeogenesis is a metabolic pathway that
results in the generation of new glucose from
non-carbohydrate carbon substrates such as
lactate, glycerol, and amino acids. Therefore, if
we do not have enough glucose in our body, we
will break down proteins (muscles) to make
glucose.
It is one of the two main mechanisms to keep
blood glucose levels from dropping too low
(hypoglycemia).
The other means of maintaining blood glucose
levels is through the degradation of glycogen
(glycogenolysis).
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Part 2
GI Physiology
Figure 62-1; Guyton & Hall
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Digestion Problems
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Incomplete digestion may be a contributing
factor in the development of many ailments
including flatulence, bloating, belching, food
allergies, nausea, bad breath, bowel problems
and stomach disorders.
Digestive enzymes are primarily responsible for
the chemical breakdown of food and constitute a
large portion of digestive secretions.
The human body makes approximately 22
different enzymes that are involved in digestion.
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Digestive Enzymes
Saliva is secreted in large amounts (1-1.5
liters/day)
 Salivary glands contain the enzyme
salivary amylase.
 This enzymes breaks starch into smaller
sugars and is stimulated by chewing.
 It is important to chew food thoroughly as
this is the first stage of the digestive
process.

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Saliva
The saliva serves to clean the oral cavity
and moisten the food.
 It also contains digestive enzymes such as
salivary amylase, which aids in the
chemical breakdown of polysaccharides
such as starch into disaccharides such as
maltose.
 It also contains mucus, a glycoprotein
which helps soften the food and form it
into a bolus.

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Swallowing
The mechanism for swallowing is
coordinated by the swallowing center in
the medulla oblongata and pons.
 The reflex is initiated by touch receptors in
the pharynx as the bolus of food is pushed
to the back of the mouth.

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Stomach
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The stomach is responsible for the digestion of
protein and ionization of minerals.
Mucous cells (in the stomach) secrete mucous.
The pancreas secretes bicarbonate. Mucous,
bicarbonate, and prostaglandins protect the
stomach lining from being digested.
The parietal cells of the stomach secrete
hydrochloric acid (gastric acid) and intrinsic
factor.
Hydrochloric acid (HCl), along with pepsin (from
the chief cells), breaks down proteins to their
individual amino acids.
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Stomach Protection and Damage
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Stimuli for Stomach Secretions
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Stomach Acid
The acid itself does not break down food
molecules.
 It provides an optimum pH for the
activation of pepsin, and kills many
microorganisms that are ingested with the
food.
 It can also denature proteins.
 The parietal cells of the stomach also
secrete a glycoprotein called intrinsic
factor, which enables the absorption of
vitamin B-12.

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Stomach Acid Diseases

Hypochlorhydria
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Diseases associated with low gastric acidity:
Asthma, coeliac disease, eczema, osteoporosis and
pernicious anemia.
Hyperchlorhydria


Diseases associated with high gastric acidity:
Heartburn, gas and ulcers
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Hypochlorhydria
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
Deficient hydrochloric acid secretion
Causes malabsorption and may result in a
number of signs and symptoms.
These include bloating, belching, flatulence,
nausea, a sense of fullness immediately after
meals, indigestion, diarrhea, constipation, food
allergies, anemia (Folic acid, vitamin B12 and
iron will not be absorbed if there is too little
acid), undigested food in stool, chronic intestinal
parasites, abnormal flora and weak, peeling and
cracked fingernails.
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•
Small Intestine
Duodenum
– Absorption of minerals
– Receives pancreatic digestive enzymes
– Secretes hormones when acidic chyme enters duodenum
• Secretin
– Tells pancreas to secrete bicarbonate
– Tells liver to make bile
• Cholecystokinin (CCK)
– Tells pancreas to release protein-digesting enzymes
– Tells the gallbladder to release stored bile.
– Therefore, it stimulates digestion of fat and protein.
• GIP
– stimulates insulin secretion
• Motilin
– Initiates peristalsis (increases GI motility)
– Tells the Chief cells to secrete pepsinogen
– Secretes enzymes to break down polysaccharides
• Maltase: breaks maltose down into glucose
• Lactase: breaks lactose down to galactose plus glucose
• Sucrase: breaks sucrose down into fructose plus glucose
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Maltose


Maltose (malt sugar) is made of two glucose molecules
joined together.
Maltose is the disaccharide produced when amylase breaks
down starch.
Amylase
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


Maltase
Starch  Maltose  Glucose
Maltose is found in germinating seeds such as barley as
they break down their starch stores to use for food.
It is also produced when glucose is caramelized (browning
of sugar during cooking).
Foods containing maltose include malted milk shakes, malt
liquor and beer. People who lack the maltase enzyme get
diarrhea and gas if they ingest malt sugars.
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Lactose

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
Lactose is needed for milk production.
It is made in the body by combining glucose with
galactose.
When milk products are consumed, lactose is
broken down by the enzyme lactase.
Many Asian and Hispanic people lack the enzyme
lactase, so they are called lactose intolerant.
If they consume milk products, they cannot break
down lactose, so the E. coli in the colon get the
sugar. E. coli metabolism then causes gas. The
person may have diarrhea as well.
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Sucrose and Fructose
Sucrose is table sugar
 Fructose is fruit sugar


All polysaccharide sugars and starches are
broken down into glucose, which is
needed by the body for metabolism.
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Small Intestine

Duodenum
 When there is no more chyme entering the
duodenum, it secretes glucose-dependent
insulinotropic peptide (GIP).
 GIP is synthesized by K cells, which are found
in the duodenum and jejunum.
 GIP stimulates insulin secretion.
 Insulin is in the blood stream. It takes the
absorbed sugars and pulls them into cells that
need it.
 GIP also stimulates lipoprotein lipase activity in
adipocytes. This causes fat to be broken down 33
into fatty acids.
Lipid digestion and absorption

Lipid digestion utilizes
lingual and pancreatic
lipases, to release fatty
acids and
monoglycerides.
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
Bile salts improve chemical
digestion by emulsifying
lipid drops
Lipid-bile salt complexes
called micelles are formed
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Fatty Acid
Absorption
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Fatty acids and
monoglycerides enter
intestinal cells via
diffusion; bile salts can be
reused to ferry more
monoglycerides
They are combined with
proteins within the cells
Resulting chylomicrons are
extruded
They enter lacteals and are
transported to the blood
circulation via lymph
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Small Intestine

Jejunum
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Absorbs water-soluble
vitamins, protein and
carbohydrates.
The proteins began to be
broken down into amino acids
in the stomach by pepsin and
acid.
Proteins are further broken
down into amino acids in the
duodenum by trypsin and
chymotrypsin (made by the
pancreas and secreted into the
duodenum).
The carbohydrates are broken
down in the duodenum by
enzymes from the pancreas
and duodenum into sugars.
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Small Intestine

Ileum
 Absorbs fat-soluble vitamins, fat, cholesterol,
and bile salts.
 Fats are broken down into fatty acids in the
duodenum.
 First, bile emulsifies the fat (breaks it down
into droplets).
 Then, lipase (made in the pancreas) breaks
the fat into fatty acids, which are small
enough to be absorbed.
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Pancreas Enzymes
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

The pancreas secretes about one and a half liters
of pancreatic juice a day!
Pancreatic juice secretion is regulated by the
hormones secretin and cholecystokinin, which is
produced by the walls of the duodenum upon
detection of acid food, proteins and fats.
The enzymes produced by the pancreas include
 Lipases
 Amylases
 Proteases
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Pancreas Enzymes

Lipases

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Amylases
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Digestion of fats, oils, and fat-soluble vitamins
Break down starch molecules into smaller sugars.
Break down carbohydrates into maltose
Proteases
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Break down protein into smaller amino acids
Proteases include trypsin, chromotrypsin and
carboxypeptidase.
Proteases are also responsible for keeping the small
intestine free from parasites (intestinal worms, yeast
overgrowth and bacteria).
A lack of proteases can cause incomplete digestion that 39
can lead to allergies and the formation of toxins.
Regulation of Pancreatic Secretion



Secretin and CCK are
released when fatty or
acidic chyme enters the
duodenum
CCK and secretin enter the
bloodstream
Upon reaching the
pancreas:

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
CCK induces the secretion
of enzyme-rich pancreatic
juice
Secretin causes secretion
of bicarbonate-rich
pancreatic juice
Vagal stimulation also
causes release of
pancreatic juice
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The Pancreas

Exocrine function
(98%)


Acinar cells make,
store, and secrete
pancreatic enzymes
Endocrine function –



( cells) release
somatostatin (inhibitory
to gastrin, insulin, and
glucagon)
β-cells –release insulin
α-cells-Release glucagon
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The Pancreas as an Endocrine Gland

Insulin

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
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

Beta cells
Skeletal muscle and
adipose tissue need it to
make glucose receptors
Promotes glucose uptake
Prevents fat and glycogen
breakdown and inhibits
gluconeogenesis
Increases protein
synthesis
Promotes fat storage
Epi/Norepi inhibit insulin!
Help maintain glucose levels
during times of stress and
increase lipase activity in
order to conserve glucose
levels
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Picture from:http://www.dkimages.com/discover/Home/Health-and-Beauty/Human-Body/Endocrine-System/Pancreas/Pancreas-1.html
The Pancreas as an Endocrine Gland

Glucagon
 Increases blood glucose levels
 Maintains blood glucose
between meals and during
periods of fasting by breaking
down glycogen (stored in
liver) into glucose.
 Initiates glycogenolysis in
liver (within minutes).
 Stimulates gluconeogenesis.
This process involves
breaking down amino acids
(proteins) into glucose.
 Stimulates amino acid
transport to liver to stimulate
gluconeogenesis
 Nervous tissue (brain) does
not need insulin; but is
heavily dependent on glucose
levels!
Image from: http://www.dkimages.com/discover/previews/768/74261.JPG
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Liver and Gallbladder



The liver produces bile that is either stored by
the gallbladder or secreted into the small
intestine.
 Bile emulsifies fats and fat-soluble vitamins.
 It also helps keep the small intestine free from
parasites.
The liver does not make the digestive enzymes
for carbohydrates, amino acids and proteins (the
pancreas and small intestine do that), but the
liver does metabolize proteins, carbohydrates and
cholesterol.
It also is responsible for the detoxification of
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toxins, drugs and hormones.
Large Intestine



The large intestine absorbs water, electrolytes and some of
the final products of digestion.
It allows fermentation due to the action of gut bacteria,
which break down the substances which remain after
processing in the small intestine; some of the breakdown
products are absorbed. In humans, these include most
complex saccharides (at most three disaccharides are
digestible in humans)
Food products that cannot go through the villi, such as
cellulose (dietary fiber), are mixed with other waste
products from the body and become hard and concentrated
feces.
45
Physiology of the large intestine
Reabsorption of water
and electrolytes
 Coliform bacteria make:
Vitamins – K, biotin, and
B5
 Organic wastes are left in
the lumen – urobilinogens
and sterobilinogens
 Bile salts
 Toxins
Mass movements of material
through colon and rectum
 Defecation reflex
triggered by distention of
rectal walls


46
Coliforms
Coliforms is the term used for the bacteria
that normally inhabit our colon (large
intestine). E. coli is just one species of
coliform.
 A ratio of 80-85% beneficial to 15-20%
potentially harmful bacteria generally is
considered normal within the intestines.
 Harmful microorganisms also are kept at a
minimum by an extensive immune system
comprising the gut-associated lymphoid
tissue (GALT).

47
Phases of gastric secretion
Cephalic phase
 Gastric phase
 Intestinal phase

48
Cephalic phase



This phase occurs before food enters the stomach and
involves preparation of the body for eating and digestion.
Sight and thought stimulate the cerebral cortex. Taste and
smell stimulus is sent to the hypothalamus and medulla
oblongata.
After this it is routed through the vagus nerve and release
of acetylcholine.
Gastric secretion at this phase rises
to 40% of maximum rate. Acidity in
the stomach is not buffered by food
at this point and thus acts to
stimulate Delta cells to secrete
somatostatin. That causes the G
cells to stop secreting gastrin. That
caused the parietal cells to stop
secreting HCl.
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G cell secretion of gastrin
D cell secretion of somatostatin
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G cells and Gastrin






G cells are found deep within the gastric glands of the
stomach.
When food arrives in the stomach, the parasympathetic
nervous system is activated. This causes the vagus nerve
to release a neurotransmitter called Gastrin-releasing
peptide onto the G cells in the stomach.
Gastrin-releasing peptide, as well as the presence of
proteins in the stomach, stimulates the release of gastrin
from the G cells.
Gastrin tells parietal cells to increase HCl secretion, and it
also stimulates other special cells to release histamine.
Gastrin also tells the chief cells to produce pepsinogen.
Gastrin is inhibited by low pH (acid) in the stomach. When
enough acid is present, it turns off.
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Gastrin


Gastrin is released in response to
 Stomach distension
 Vagus nerve stimulation
 The presence of proteins or amino acids
Gastrin release is inhibited by
 The presence of enough HCl in the stomach
(negative feedback)
 Somatostatin also inhibits the release of
gastrin
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D cells
D cells can be found in the stomach,
intestine and the Islets of Langerhans in
the pancreas.
 When gastrin is present, D cells increase
somatostatin output.
 When D cells are stimulated by Ach, they
decrease somatostatin output.

53
Somatostatin






Somatostatin is also known as growth hormone-inhibiting
hormone.
It suppresses the release of gastrointestinal hormones
 Gastrin
 Cholecystokinin (CCK)
 Secretin
 GIP
It suppresses the release of pancreatic hormones.
It slows down the digestive process.
It inhibits insulin release.
It inhibits the release of glucagon.
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Gastric phase








This phase takes 3 to 4 hours. It is stimulated by distension of the
stomach, presence of food in stomach and decrease in pH.
Distention activates long and myenteric reflexes.
This activates the release of acetylcholine which stimulates the
release of more gastric juices.
As protein enters the stomach, it binds to hydrogen ions, which
raises the pH of the stomach.
Inhibition of gastrin and gastric acid secretion is lifted.
This triggers G cells to release gastrin, which in turn stimulates
parietal cells to secrete gastric acid.
Gastric acid is about 0.5% hydrochloric acid (HCl), which lowers
the pH to the desired pH of 1-3.
Acid release is also triggered by acetylcholine and histamine.
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Intestinal phase
This phase has 2 opposing actions: the
excitatory and the inhibitory.
 Partially digested food fills the duodenum.
 This triggers gastrin to be released.
 It also triggers the enterogastric reflex,
which inhibits the Vagus nerve.
 This activates the sympathetic nervouse
system, which causes the pyloric sphincter
to tighten to prevent more food from
entering the duodenum.

56
Digestive Enzymes
(fats in yellow, proteins in green, and sugars in red)
Salivary glands
-amylase
Stomach
pepsin
Duodenum
sucrase
maltase
lactase
Pancreas
amylase
trypsin
chymotrypsin
carboxypeptidase
lipase
57
Digestive Hormones and Substances
Stomach
gastrin
Intrinsic factor
HCl
Prostaglandins
Mucous
Liver
Bile
Duodenum
Secretin
CCK
GIP
Motilin
Pancreas
Glucagon
Insulin
Somatostatin
Bicarbonate
58
The Activities of Major Digestive Tract Hormones
59
Figure 24.22
Organ
Pancreas
Region of the Organ
Acinar cells
Acinar cells
Substances
Amylase (enzyme)
Lipase (enzyme)
Acinar cells
Acinar cells
Protease enzymes (trypsin,
chymotrypsin, carboxypeptidase)
Bicarbonate (not an enzyme)
Islet of Langerhans; Alpha
cells
Islet of Langerhans; Beta
cells
Islet of Langerhans; Delta
cells
glucagon (hormone)
insulin (hormone)
Somatostatin (hormone)
Function
Breaks down starch and carbohydrates into glucose
Breaks down fat into fatty acids
Breaks down proteins into amino acids and also kills intestinal parasites
and bacteria
Raises pH in duodenum
Causes glycogenolysis, the process which breaks down glycogen into
glucose to raise blood glucose. Also causes gluconeogenesis to make new
glucose molecules
Removes glucose in bloodstream and brings it into cells. Lowers blood
glucose levels.
Inhibits gastrin, insulin, and glucagon (inhibits digestive system)
Liver
Bile (a detergent)
Salivary glands
Amylase (enzyme)
Stomach
Mucous (not an enzyme)
Protect the stomach lining
Prostaglandins (not an enzyme)
Protect the stomach lining
Breaks down starch and carbohydrates into glucose
Parietal cells
HCl (not an enzyme)
Parietal cells
Intrinsic factor (not an enzyme)
Allows Vit B12 to be absorbed, which is needed to make RBCs. Without it,
you get megaloblastic (pernicous) anemia.
Chief cells
G cells
Pepsinogen --> pepsin (enzyme)
Gastrin (hormone)
Breaks proteins into amino acids
Tells parietal cells to secrete HCl
Duodenum
Secretin (hormone)
CCK (hormone)
K cells
GIP (hormone)
Motilin (hormone)
Allows Pepsinogen to be converted to pepsin, and it also kills bacteria
Tells pancreas to secrete bicarbonate
Tells pancrease to secrete proteases, and tells gallbladder to release
stored bile (stimulates fat and protein digestion)
Tells pancreas to release insulin and also causes fat to be broken down
into fatty acids
Initiates perstalsis and tells Chief cells to secrete pepsinogen
Maltase, Lactase, Sucrase (enzymes) Break down complex carbohydrates into glucose
60
Part 3
GI Disorders
Figure 62-1; Guyton & Hall
61
GI Disorders

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



Peptic ulcers
Pancreatitis
Celiac Disease
Inflammatory bowel disease (Crohn's disease and ulcerative colitis)
Irritable bowel syndrome
Appendicitis
Diverticulitis
Cancer
Gastroenteritis ("stomach flu“); an inflammation of the stomach and
intestines
Cholera (bacteria in sewage-contaminated food or water)
Giardiasis (protozoa in contaminated drinking water)
Yellow Fever (virus transmitted by tropical mosquito)
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Peptic Ulcers


Classification By Region/Location
 Duodenum (called duodenal ulcer)
 Esophagus (called esophageal ulcer)
 Stomach (called gastric ulcer)
Classification by Type
 Type I: Ulcer along the body of the stomach, most often
along the lesser curve.
 Type II: Ulcer in the body in combination with duodenal
ulcers. Associated with acid oversecretion.
 Type III: In the pyloric region. Associated with acid
oversecretion.
 Type IV: Proximal gastroesophageal ulcer
 Type V: Can occur throughout the stomach. Associated
with chronic NSAID use (such as aspirin).
63
Gastric and Duodenal
ulcers
Weakens
H. pylori, aspirin, ethanol,
NSAIDs,
bile salts

Strengthens
mucus, HCO3- secretion,
gastrin, PGs, epidermal growth
factor
Peptic ulcers occur when damaging effects of
acid and pepsin overcome ability of mucosa
to protect itself

Gastric ulcers - main problem is decreased ability of
mucosa to protect itself

Duodenal ulcers - main problem is exposure to increased
amounts of acid and pepsin
64
Two major causes of Peptic Ulcers:
1) 60% of gastric and up to 90% of
duodenal ulcers are due to a bacterium
called Helicobacter pylori.

The body responds by increasing gastrin
secretion, which erodes the stomach lining.
2) NSAIDs (non-steroidal anti-inflammatory
drugs, such as aspirin) block
prostaglandin synthesis.

Prostaglandins promote the inflammatory
reaction. They also are found in the stomach,
protecting it from erosion.
65
Does stress cause ulcers?
There is debate as to whether
psychological stress can influence the
development of peptic ulcers.
 Helicobacter pylori thrives in an acidic
environment, and stress has been
demonstrated to cause the production of
excess stomach acid.

66
Diagnosis of Helicobacter pylori




Urea breath test (noninvasive)
 Patient drinks a tasteless liquid which contains a
radioactive carbon atom as part of the substance that
the bacteria breaks down. After an hour, the patient will
be asked to blow into a bag that is sealed. If the patient
is infected with H. pylori, the breath sample will contain
radioactive carbon dioxide.
Biopsy
 Direct culture from a biopsy
 Histological examination and staining
 Direct detection of urease activity in a biopsy specimen
by rapid urease test
Measurement of antibody levels in blood
Stool antigen test
67
Differential Diagnosis (DDx)


A differential diagnosis is a list of possible things
that may be causing a patient’s symptoms.
DDx for H. pylori infection











Peptic ulcer
Gastritis
Stomach cancer
Gastroesophageal reflux disease
Pancreatitis
Hepatic congestion
Cholecystitis
Biliary colic
Inferior myocardial infarction
Referred pain (pleurisy, pericarditis)
Superior mesenteric artery syndrome
68
Risk and Transmission




The lifetime risk for developing a peptic ulcer is
approximately 10%.
In Western countries the prevalence of
Helicobacter pylori infections roughly matches
age (i.e., 20% at age 20, 30% at age 30, 80% at
age 80 etc.).
Prevalence is higher in third world countries.
Transmission is by food, contaminated
groundwater, and through human saliva (such as
from kissing or sharing toothbrushes or food
utensils)
69
Treatment



Younger patients with ulcer-like symptoms are
often treated with antacids or H2 antagonists
(blocks the acid secretion of parietal cells).
Patients who are taking NSAIDs may also be
prescribed a prostaglandin analogue
(Misoprostol) to help prevent peptic ulcers.
When H. pylori infection is present, the most
effective treatments are combinations of 2
antibiotics (e.g. Clarithromycin, Amoxicillin,
Tetracycline, Metronidazole) and 1 proton pump
inhibitor (PPI), sometimes together with a
bismuth compound. An example of a PPI is
Omeparazole (Prilosec).
70
Treatment



Ranitidine (Zantac) and Cimetidine (Tagamet)
provide relief of peptic ulcers, heartburn,
indigestion and excess stomach acid and
prevention of these symptoms associated with
excessive consumption of food and drink.
They decrease the amount of acid the stomach
produces allowing healing of ulcers.
Sucralfate, (Carafate) and strawberries have also
been used in successful treatment of peptic
ulcers.
71
Pancreas Disorders
Gestational Diabetes
 Type I diabetes
 Type II diabetes
 Pancreatitis
 Cancer
 Chronic pancreatitis




alcohol
cystic fibrosis
Acute pancreatitis

Gallstones
72
Disorders of the Pancreas: Diabetes
Mellitus


Gestational Diabetes
Type I diabetes –
develops suddenly,
usually before age 15



Destruction of the beta cells
Skeletal tissue and adipose
cells must use alternative
fuel and this leads to
ketoacidosis
Hyperglycemia results in
diabetic coma
73
Disorders of the Pancreas: Diabetes
Mellitus

Type II diabetes–
adult onset



Usually occurs after age
40
Cells have lowered
sensitivity to insulin
Controlled by dietary
changes and regular
exercise
74
Pancreatic Failure
 Digestion
is abnormal when pancreas
fails to secrete normal amounts of
enzymes.


Pancreatitis
Removal of pancreatic head - malignancy
 Without


pancreatic enzymes -
60% fat not absorbed (steatorrhea)
30-40% protein and carbohydrates not absorbed
75
Pancreatitis

Pancreatitis means inflammation of pancreas.
Autodigestion theory can explain condition.
 Chronic


alcohol - most common cause in adults
cystic fibrosis - most common cause in children




pancreatitis -
CF patients lack chloride transporter at apical membrane.
Watery ductal secretion decreases which concentrates acinar secretions in
ducts.
Destroys pancreas gland by autodigestion.
Acute pancreatitis 
Gallstones - most common cause
76
Celiac disease
(Sprue; gluten intolerance)




Genetic autoimmune disorder of the small
intestine, causing chronic diarrhea. The person is
allergic to gluten. Causes destruction of microvilli
and villi.
It is characterized by having pale, loose and
greasy stools (steatorrhea) which are voluminous
and malodorous.
It often presents with abdominal pain and
cramping, abdominal distension, and sometimes
mouth ulcers.
Without adjusting the diet, coeliac disease leads
to an increased risk of adenocarcinoma (small
77
intestine cancer).
Celiac disease
(Sprue; gluten intolerance)






They may develop ulcerative jejunitis and stricturing (narrowing
as a result of scarring with obstruction of the bowel).
The changes in the bowel make it less able to absorb
carbohydrates, fats, minerals (calcium and iron), and the fatsoluble vitamins A, D, E, and K.
Anemia may develop in several ways: iron malabsorption may
cause iron deficiency anemia, and folic acid and vitamin B12
malabsorption may give rise to megaloblastic anemia.
Calcium and vitamin D malabsorption may cause osteopenia
(decreased mineral content of the bone) or osteoporosis (bone
weakening and risk of fragility fractures).
A small proportion have abnormal coagulation due to vitamin K
deficiency and are slightly at risk for abnormal bleeding.
Coeliac disease is also associated with bacterial overgrowth of the
small intestine, which can worsen malabsorption or cause
malabsorption despite adherence to treatment.
78
Celiac disease
(Sprue; gluten intolerance)




Celiac disease is caused by an allergy to gluten.
Gluten is present in Wheat subspecies (such as spelt,
semolina and durum) and related species such as barley,
rye, triticale and Kamut. A small minority of coeliac patients
also react to oats. It is most probable that oats produce
symptoms due to cross contamination with other grains in
the fields or in the distribution channels. Generally, oats are
therefore not recommended.
Other cereals such as maize (corn), millet, rice, and wild
rice are safe for patients to consume, as well as non cereals
such as amaranth, quinoa or buckwheat.
Non-cereal carbohydrate-rich foods such as potatoes and
bananas do not contain gluten and do not trigger
symptoms.
79
Gluten-free diet





Several grains and starch sources are considered
acceptable for a gluten-free diet. The most frequently used
are corn, potatoes, rice, and tapioca.
Various types of bean, soybean, and nut flours are
sometimes used in gluten-free products to add protein and
dietary fiber.
Almond flour is a low-carbohydrate alternative to flour, with
a low glycemic index.
In spite of its name, buckwheat is not related to wheat;
pure buckwheat is considered acceptable for a gluten-free
diet, although many commercial buckwheat products are
actually mixtures of wheat and buckwheat flours, and thus
not acceptable.
Gram flour, derived from chickpeas, is also gluten-free (this
is not the same as Graham flour made from wheat).
80
Gluten-free diet




Gluten is used in foods in some unexpected ways, for
example as a stabilizing agent or thickener in products like
ice-cream and ketchup.
People wishing to follow a completely gluten free diet must
also take into consideration the ingredients of any over-thecounter or prescription medications and vitamins. Also,
cosmetics such as lipstick, lip balms, and lip gloss may
contain gluten and need to be investigated before use.
Glues used on envelopes may also contain gluten.
Most products manufactured for Passover are gluten free.
Exceptions are foods that list matzah as an ingredient,
usually in the form of cake meal.
A blood test for IgA antiendomysial antibodies can detect
celiac disease.
81
Uses of animal gut by humans







The stomachs of calves have commonly been used as a source of rennet
for making cheese.
The use of animal gut strings by musicians can be traced back to the third
dynasty of Egypt. In the recent past, strings were made out of lamb gut.
With the advent of the modern era, musicians have tended to use strings
made of silk, or synthetic materials such as nylon or steel. Some
instrumentalists, however, still use gut strings in order to evoke the older
tone quality. Although such strings were commonly referred to as "catgut"
strings, cats were never used as a source for gut strings.
Sheep gut was the original source for natural gut string used in racquets,
such as for tennis. Today, synthetic strings are much more common, but
the best gut strings are now made out of cow gut.
Gut cord has also been used to produce strings for the snares which
provide the snare drum's characteristic buzzing timbre.
"Natural" sausage hulls (or casings) are made of animal gut, especially
hog, beef, and lamb. Similarly, Haggis is traditionally boiled in, and served
in, a sheep stomach.
Chitterlings, a kind of food, consist of thoroughly washed pig's gut.
82
The oldest known condoms, from 1640 AD, were made from animal
intestine.