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GI Physiology
Part 1: Metabolic Pathways
Part 2: GI Physiology
Part 3: GI Disorders
Part 1: Metabolic Pathways
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
 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.
Glucagon and Insulin
 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 convert 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!
 High blood glucose levels stimulate the release of insulin.
 Insulin allows glucose to be taken up and used by insulin-dependent tissues.
Thus, glucagon and insulin are part of a feedback system that keeps blood glucose levels at a
stable level
Summary Table of substances secreted in the GI system. This table will be on the first quiz.
Region of the Organ
Acinar cells
Acinar cells
Breaks down starch and carbohydrates into
Breaks down fat into fatty acids
Amylase (enzyme)
Lipase (enzyme)
Protease enzymes (trypsin,
Breaks down proteins into amino acids and
Acinar cells
also kills intestinal parasites and bacteria
Acinar cells
Bicarbonate (not an enzyme) Raises pH in duodenum
Causes glycogenolysis, the process which
breaks down glycogen into glucose to raise
Islet of Langerhans;
blood glucose. Also causes gluconeogenesis
Alpha cells
glucagon (hormone)
to make new glucose molecules
Islet of Langerhans; Beta
Removes glucose in bloodstream and brings
insulin (hormone)
it into cells. Lowers blood glucose levels.
Islet of Langerhans;
Inhibits gastrin, insulin, and glucagon
Delta cells
Somatostatin (hormone) (inhibits digestive system)
Bile (a detergent)
Salivary glands
Amylase (enzyme)
Mucous (not an enzyme)
Prostaglandins (not an
Parietal cells
HCl (not an enzyme)
Parietal cells
Intrinsic factor (not an
Emulsifies fat (makes fat droplets smaller)
Breaks down fat into fatty acids
Breaks down starch and carbohydrates into
Breaks down fat
Protect the stomach lining
Protect the stomach lining
Breaks down fat
Allows Pepsinogen to be converted to
pepsin, and it also kills bacteria
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
Gastrin (hormone)
Secretin (hormone)
CCK (hormone)
K cells
GIP (hormone)
Motilin (hormone)
Maltase, Lactase, Sucrase
Breaks proteins into amino acids
Tells parietal cells to secrete HCl
Tells pancreas to secrete bicarbonate
Tells pancreas to secrete proteases and
lipase, 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
Initiates perstalsis and tells Chief cells to
secrete pepsinogen
Break down complex carbohydrates into
 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.
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.
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.
Aerobic vs. Anaerobic Respiration
(in the
result in 6 ATP’s.
respiration (in
our cytoplasm)
will result in only
2 ATP’s.
More importantly, we get our NAD back, so glycolysis can continue.
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
Lactic Acid Build-up
 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.
 When you add oxygen to lactic acid, it either goes back to being pyruvate, which is
used to fuel the Krebs cycle (aerobic respiration), or it is converted to glucose in the
ATP and Creatinine Phosphate
 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
 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?
 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 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).
Part 2
GI Physiology
Digestion Problems
 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
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
 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
 It also contains mucus, a glycoprotein which helps soften the food and form it into a
 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.
 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
 The parietal cells of the stomach secrete hydrochloric acid (gastric acid) and intrinsic
 Hydrochloric acid (HCl), along with pepsin (from the chief cells), breaks down
proteins to their individual amino acids.
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© 2005 Elsevier
© 2005 Elsevier
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.
Stomach Acid Diseases
 Hypochlorhydria
 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
 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
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.
 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
 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
 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.
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.
Small Intestine
 Duodenum
 When there is no more chyme entering the duodenum, it secretes glucosedependent 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 into fatty acids.
Lipid digestion and absorption
 Lipid digestion utilizes lingual and pancreatic lipases, to release fatty acids and
 Bile salts improve chemical digestion by emulsifying lipid drops
 Lipid-bile salt complexes called micelles are formed
Fatty Acid Absorption
 Bile salts form micelles (small droplets of lipids)
 Lipase breaks down the lipids into fatty acids and monoglycerides.
 Fatty acids and monoglycerides enter intestinal cells via diffusion; bile salts are then
reused to ferry more lipids to the intestinal cell.
 Fatty acids are used to make triglycerides for storage.
 The rest of the fatty acids and monoglycerides are combined with proteins within the
intestinal cells to make chylomicrons.
 Chylomicrons enter lacteals and are transported to the blood circulation via lymph
Small Intestine
 Jejunum
 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.
 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.
Pancreas Enzymes
 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
 Lipases
 Digestion of fats, oils, and fat-soluble vitamins
 Amylases
 Break down starch molecules into smaller sugars.
 Break down carbohydrates into maltose
 Proteases
 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 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:
 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
The Pancreas
 Exocrine function (98%)
 Acinar cells make, store, and secrete pancreatic enzymes
 Endocrine function –
  cells (delta cells) release somatostatin (inhibitory to gastrin and insulin and
 β-cells –release insulin
 α-cells-Release glucagon
The Pancreas as an Endocrine Gland
 Insulin
 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
 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!
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 toxins, drugs and hormones.
Large Intestine
 The large intestine absorbs water, electrolytes and some of the final products of
 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
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
 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).
Phases of gastric secretion
 Cephalic phase
 Gastric phase
 Intestinal phase
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 D cells to secrete
somatostatin. That causes the G cells to stop secreting gastrin. That caused the parietal
cells to stop secreting HCl.
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 amino acids 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.
 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
D cells
 D cells can be found in the stomach, intestine and the Islets of Langerhans in the
 When gastrin is present, D cells increase somatostatin output.
 When D cells are stimulated by Ach, they decrease somatostatin output.
 Somatostatin is also known as growth hormone-inhibiting hormone.
 It suppresses the release of gastrointestinal hormones
 Gastrin
 Cholecystokinin (CCK)
 Secretin
 It suppresses the release of pancreatic hormones.
 It slows down the digestive process.
 It inhibits insulin release.
 It inhibits the release of glucagon.
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
 As protein enters the stomach, it binds to hydrogen ions, which raises the pH of the
 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.
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.
Part 3
GI Disorders
GI Disorders
 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)
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
 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).
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.
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.
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
Differential Diagnosis (DDx)
 A differential diagnosis is a list of possible things that may be causing a patient’s
 DDx for H. pylori infection
Peptic ulcer
Stomach cancer
Gastroesophageal reflux disease
Hepatic congestion
Biliary colic
Inferior myocardial infarction
Referred pain (pleurisy, pericarditis)
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)
 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).
 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.
Pancreas Disorders
 Gestational Diabetes
 Type I diabetes
 Type II diabetes
 Pancreatitis
 Cancer
 Chronic pancreatitis
 alcohol
 cystic fibrosis
 Acute pancreatitis
 Gallstones
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
 Hyperglycemia results in diabetic coma
 Type II diabetes and metabolic syndrome– adult onset
 Usually occurs after age 40
 Cells have lowered sensitivity to insulin
 Controlled by dietary changes and regular exercise
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
 Pancreatitis means inflammation of pancreas. Autodigestion theory can explain
 Chronic pancreatitis  alcohol
- most common cause in adults
 cystic fibrosis - most common cause in children
 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
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 intestine cancer).
 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 fat-soluble 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
 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
 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.
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).
 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-the-counter 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
 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.
Uses of animal gut by humans
 The stomachs of calves have commonly been used as a source of rennet for making
 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.
The oldest known condoms, from 1640 AD, were made from animal intestine.