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Pierce College
Putman/Biol 242
Unit 06 notes: Digestive System
GENERAL FUNCTIONS
1.
2.
3.
4.
Ingestion. This is the physical process of putting food into the body. The oral cavity is the organ of ingestion.
Digestion
a. Mechanical Digestion. This involves the taking of food particles and separating them down into
macromolecules. Although chemical bonds are broken, these bonds are broken using mechanical means,
not chemical means! It is the mechanical breaking of bonds. This mostly occurs in the oral cavity, with
some mechanical digestion also occurring in the stomach.
b. Chemical Digestion. This involves the taking of macromolecules and enzymatically and chemically
breaking the bonds holding macromolecules together, turning them into their monomer components. It is
the chemical breaking of bonds, forming monomers. Most chemical digestion occurs in the small intestine,
particularly the duodenum.
Nutrient Absorption. This process occurs almost solely in the small intestine.
Waste Compaction & Elimination. This occurs in the colon, through the rectum and anus.
FUNCTIONAL ANATOMY: MOUTH
1.
2.
3.
4.
5.
Principal site of mechanical digestion. The teeth and tongue are the major organs of mechanical digestion.
Breaks food into small particles. This creates the primary surface for enzyme action; enzymes (chemical
digestion) can only work on food that they come in contact with; thus, in order to chemically digest your food,
you must create an optimal amount of surface area, achieved by chewing your food well!
Salivary Glands
a. Three pairs
1) Parotid gland
2) Sublingual gland
3) Submandibular gland
b. Function:
1) Secrete mucus/saliva that serves to lubricate food. It is slightly alkaline, which retards the growth of
some forms of bacteria, such as those that cause tooth decay.
2) Secrete salivary amylase, which digests alpha-glycosidic linkeages. Thus, carbohydrate digestion begins
here!
Lingual Glands
a. Located in the lamina propria of the tongue
b. Secrete lingual lipase; thus, lipid digestion begins in the mouth.
Histology of mouth
a. Food is abrasive! Thus you need stratified squamous epithelium in the mouth (also oro- and
laryngopharynx) to allow for abrasion. Stratified squamous epithelium is keratinized (tough & waterresistant), and sloughs off easily. In fact, 20% of your protein intake is from sloughed off stratified
squamous cells!!!
FUNCTIONAL ANATOMY: ESOPHAGUS
1.
2.
3.
Esophagus connects laryngopharynx and stomach.
Muscular tube, normally flat; peristalsis moves food along
Swallowing:
a. Tongue moves bolus to back of oropharynx
b. Uvula moves up, blocking entrance into nasopharynx
c. Tongue pushes food into esophagus as epiglottis closes
d. Rhythmic contraction/relaxation of longitudinal & smooth muscles moves bolus down into stomach
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4.
Histology of esophagus starts as stratified squamous epithelium then transitions into transitional columnar
epithelium as it connects with stomach.
a. Function of transitional columnar epithelium is to secrete mucus onto stratum mucosa lining lumen.
1) Adds mucus to food
2) Partially protects mucosa of esophagus from stomach acid.
b. Upper esophagus keratinized stratified squamous epithelium
c. Lower esophagus transitional columnar—non-keratinized.
1) Labile to acid reflux erosion.
2) GERD: GastroEsophageal Reflux Disease. When cardiac sphincter relaxes at inappropriate times, such
as when you’re prone, allowing stomach acid to enter esophagus. This burns the esophagus, causing
“heartburn.” Chronic reflux is defined as GERD.
FUNCTIONAL ANATOMY: GENERAL HISTOLOGY OF GUT
1.
Mesentary
a. Consists of
1) Connective tissue, including adipose, that supports/cushions the gut.
2) Lymphoid tissue, with strong immune function. Macrophages in the mesentary protect the abdominal
cavity against any pathogens that might enter here.
b. Two special mesentaries:
1) Lesser Omentum. Connects between and stabilizes liver & stomach.
2) Greater Omentum. An “apron” of connective tissue that hangs down from the stomach and
transverse colon.
2.
Tunica Serosa (= Visceral Peritoneum)
a. Contains the major nerves, blood vessels & lymphatics going into the gut.
3.
Tunica Muscularis (= Muscularis Externa)
a. Consists of smooth muscle.
1) Longitudinal smooth muscle is outermost.
2) Circular smooth muscle is innermost EXCEPT in stomach
3) Oblique layer. Found only in stomach; is innermost in stomach.
4.
Myenteric Plexus
a. Coordinates longitudinal & circular muscles action, allowing for peristalisis.
5.
Submucosal Plexus
a. Senses material in gut, especially glutamines. Glutamines stimulate the appetite.
6.
Tunica Submucosa
a. Blood vessels & some glands located here
7.
Tunica Mucosa
a. Lines lumen
b. Secretive & absorptive; thus, has very high surface area!
c. Has muscularis interna that causes secretion from glands
d. Lymphatics (Peyer’s patches) located here; reticular tissue lymph nodules with immunological function
(sort of like intestinal tonsils!)
FUNCTIONAL ANATOMY: STOMACH
1.
Function
a. Storage is primary function; normally holds about 1 to 1.5 L (can distend to much larger), thus allowing for
opportunistic feeding!
b. Osmotic homeostasis. Water from the blood enters the lumen of stomach if ingested foods are hypertonic,
quickly triggering hypothalmic thirst centers.
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c.
d.
e.
Acidification of chyme. HCl is secreted into lumen with a pH of 1.9 to 2.0; however, it is diluted by chyme
to about 3.0 (still very acidic).
1) Function of the HCl is
a) chemical digestion as it facilitates the hydrolysis of polymers of all types,
b) activates proteases (pepsin) and 3) deactivates salivary amylase & lingual lipase.
2) The acidification of chyme also kills microbes, but this varies with age. Children and the elderly are
most susceptible to bacterial diseases such as E. coli because they secrete less HCl than other people. Kids
have the additional problem of not chewing their food fully; bacteria can “hide out” in unchewed food,
being protected from the sterilizing effects of stomach acid by a layer of food.
3) Not all microbes are killed by stomach acid. Helicobacter pylori, which causes ulcers, thrives in stomach
acid!
Regulation of Flow of Chyme
Mechanical Digestion
2.
Structure
a. Is a muscular bag
b. Cardiac sphincter (= gastroesophageal sphincter, = lower esophageal sphincter) separates stomach from
esophagus.
c. Pyloric sphincter separates stomach from duodenum.
d. Fundus is superior region; pyloris is inferior region.
e. Rugae:
1) Cross-hatched in fundus; this facilitates chyme mixing
2) Parallel in pyloris; this facilitates the flow (squirting) of chyme into duodenum.
3.
Histology
a. Generally, same layers as intestine (except for oblique layer of Tunica Muscularis).
b. Tunica Serosa (= Visceral Peritoneum)
c. Tunica Muscularis. Longitudinal smooth muscle (outermost), circular smooth muscle (middle), oblique
smooth muscle (innermost). Functions to mix & move chyme.
d. Tunica Submucosa. Contains major vessels, nerves, lymphatics.
e. Tunica Mucosa.
1) Muscularis mucosa. Moves secretions from gastric pits into lumen.
2) Columnar epithelium. (Recall: columnar cells are secretory & absorptive!)
3) Gastric Pits. Have capillaries surrounding the neck of pits which supply materials (such as H+ & Cl-) to
parietal cells; capillaries also collect materials absorbed from absorptive cells & convey materials into
blood circulatory system. Cell types & functions include:
a) Mucous Cells. Secrete mucus, which protects the mucosa against HCl.
b) Parietal Cells. Secrete HCl.
c) Chief Cells. Secrete pepsinogen (inactive pepsin) and gastric lipase.
d) G Cells. Secrete gastrin, a hormone. (G for gastrin.)
FUNCTIONAL ANATOMY: SMALL INTESTINE
1.
Function of small intestine: chemical digestion & absorption of monomers.
2.
Anatomy:
a. Duodenum. First 25 cm. Connects stomach to jejunum.
b. Jejunum. 1 meter in length. Connects duodunum to ileum.
c. Ileum. 2 meters in length. Connects jejunum to caecum of colon.
d. Veins from small intestine (and from rest of gut, for that matter) empty into hepatic portal vein.
e. Plicae Circularis. Circular ridges lining lumen of small intestine.
1) Facilitate mixing of chyme.
2) Increase surface area of small intestine allowing for enhanced secretion of digestive chemicals and
enzymes and for enhanced absorption of monomers.
3) The surface of the plicae circularis is folded up into villi.
f. Villi (Intestinal Villi). Finger-like projections of the plica circularis. Increases surface area.
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3.
Histology
a. Absorptive Cells. These are the main types of cells in the duodenum; they have high surface area
(microvilli) which they use to absorb monomers from the chyme in the lumen of the small intestine and to
secrete digestive enzymes including enterokinase, peptidases, maltase, sucrase and lactase. The microvilli
of absorptive cells look fuzzy under the microscope, so they make up a structure called the “brush border.”
b. Lacteals are one-way projections of the lymphatic system into the intestinal villi. Lacteals absorb fat
particles (lipoproteins) produced by absorptive cells which, in turn, have absorbed them from the lumen of
the gut; lipoproteins are NOT carried by the blood capillaries because they’re simply too big to enter
through the tiny fenestrations of the capillaries!
c. Goblet Cells secrete mucus, helping to lubricate the chyme, moving it along.
d. Blood Capillaries absorb all monomers digested in lumen, except for lipoproteins.
e. Crypts of Lieberkuehn (= Intestinal Crypts, = Intestinal Glands). These secrete “intestinal juice” into the
lumen, a fluid composed of water and mucus.
f. Brunner’s Glands (= Duodenal Glands). Found in duodenum, secrete sodium bicarbonate.
g. Enteroendocrine Cells. Sense materials (food) in chyme; secrete the hormones secretin & cholecystokinin
into blood.
h. Paneth Cells are immunological; they secrete both lysozyme and defensins, and have some phygocytic
function.
FUNCTIONAL ANATOMY: HEPATOPANCREAS COMPLEX
1.
Structures of hepatopancreas complex:
a. From the R & L lobes of the liver, bile is collected by the R & L bile ducts into the common hepatic duct.
b. The gall bladder secretes and stores bile via the cystic duct.
c. The cystic duct and common hepatic ducts join to form the common bile duct (= ductus choledochus).
d. The pancreatic duct (= Wirsung’s duct) drains digestive enzymes from the pancreas.
e. The pancreatic duct joins the common bile duct at ampulla vater. The ampulla vater connects into the
duodenum at the major duodenal papillus via the sphincter of Oddi.
f. An auxillary pancreatic duct (duct of Santorini) also drains the pancreas into the duodenum.
FUNCTIONAL ANATOMY: LIVER
1.
Produces & secretes bile continuously into bile ducts
a. Bile is degradation product of hemoglobin & erythrocytes
1) Spleen also degrades old erythrocytes into bile components; sends degradation products to liver via
hepatic portal vein
b. Liver removes bile components from spleen from hepatic portal, adds it to bile components it produces.
c. With sphincter of Oddi closed, bile in bile ducts backs up into gall bladder, where it’s stored.
2.
Functional Histology
a. Hepatic portal vein branches into hepatic sinusoids; blood runs through hepatic sinusoids, into central vein
of lobules, then into hepatic veins (then into inferior VC).
b. Kupffer cells (= stellate reticuloendothelial cells) in sinusoids (recall: Kupffers are macrophages!)
1) Digest old RBCs, releasing bilirubin into bile canals, which then goes into bile ducts.
2) Digest pathogens
3) Filter out debris
c. Hepatocytes
1) Remove/detoxify from blood a) alcohol, b) toxins, c) drugs, d) fat-soluble vitamins [thus reason liver oil
is so full of vitamins A, D, E & K!)
2) Absorb/secretes from/into blood a) glucose (from hepatic glycogen) and b) cholesterol (the major
source; we produce our own & don’t need any cholesterol in diet!)
3) Digest amino acids into urea and put into blood; urea is then removed by kidneys from the blood.
FUNCTIONAL HISTOLOGY: PANCREAS
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1.
Acinar cells, which make up 99% of pancreas, are exocrine (with ducts).
a. Secrete into duodenum
1) Sodium bicarbonate. The sodium bicarbonate from the duct cells of the pancreas and from the Brunner’s
glands of the duodenum serves to neutralize the very acidic gastric juice squirted out from the stomach into
the duodenum.
2) Inactive digestive enzymes.
FUNCTIONAL ANATOMY: COLON
1.
Anatomy
a. Ileocecal Valve separates ileum from caecum, controls movement of chyme into caecum.
b. Caecum.
1) First part of colon
2) Widest part of colon because quite a bit of water is still present in the material in the lumen.
3) Connects with appendix.
c. Appendix (= vermiform appendix).
1) A blind pouch; no known function in humans. May become blocked, inflamed, ruptured, releasing
bacteria into peritoneal cavity (abdominal cavity) causing appendicitis, a type of peritonitis.
d. Ascending Colon connects with caecum.
e. Hepatic Flexure is where ascending colon turns into transverse colon.
f. Transverse Colon runs between hepatic flexure and splenic flexure just inferior to costal margin of ribs.
g. Descending Colon runs from splenic flexure to sigmoid colon.
h. Sigmoid Colon is the “S-shaped” connection between the descending colon and rectum.
i. The Rectum is the tube between the sigmoid colon and final part of the colon, the Anus.
j. Sphincters.
1) Internal Anal Sphincter. Smooth muscle and involuntary.
2) External Anal Sphincter. Skeletal muscle and voluntary.
k. Teniae Coli. Longitudinal bands of smooth muscle; moves feces and creates haustrae.
2.
Function
a. Waste storage & compaction
b. Waste elimination
c. Vitamin K production/absorption
d. Water absorption
1) Although 90% of water is absorbed in the small intestine, 10% is absorbed in the colon.
2) Pathogens often inhibit the water-absorbing ability of the colon, thus causing diarrhea, which is
potentially fatal, if lost water is not quickly replaced into the system.
CHEMICAL DIGESTION: ORAL CAVITY
1.
2.
Salivary glands. Salivary amylase, which works optimally in a slightly basic pH, begins carbohydrate digestion.
Lingual glands. Secrete lingual lipase, which begins triglyceride digestion.
CHEMICAL DIGESTION: STOMACH
1.
Parietal cells secrete HCl
a. The H+ secreted into the lumen of the stomach comes from blood carbonic acid (formed from carbon
dioxide); thus the removal of acid (hydrogen ion) from the blood, and the subsequent release of bicarbonate
from parietal cells into the blood, causes the blood to become more alkaline (basic), creating what is called
an “alkaline tide.” This happens before and during eating.
b. Mechanism of HCl secretion:
1) Carbon dioxide diffuses into parietal cells of the tunica mucosa of the stomach.
2) Carbon dioxide combines with water to form carbonic acid, which is catalyzed greatly by carbonic
anhydrase.
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3) Carbonic acid dissociates into bicarbonate and hydrogen ion. The bicarbonate ion enters the blood as a
chloride enters the parietal cell via an antiport. The hydrogen ion is secreted from the parietal cell into the
stomach as potassium enters from the stomach, via an ATP-powered antiport.
4) Cloride also enters the parietal cell, along with sodium, via a sodium-powered symport.
5) Chloride exits the parietal cell into the stomach lumen as potassium exits the parietal cell, via a symport
(powered by potassium concentrations).
6) Sodium is pumped out of the parietal cell as potassium is pumped in via an ATP-powered antiport.
7) Note that sodium and potassium concentration gradients, along with ATP (and the simple diffusion of
carbon dioxide, powered by kinetic energy) are what produce HCl from the blood and pump it into the
lumen of the stomach.
2.
Chief Cells
a. Secrete pepsinogen, the inactive form of pepsin. HCl converts pepsinogen into pepsin, a protease that
works optimally in a very acidic pH.
1) Thus, protein digestion begins in the stomach.
b. Secrete gastric lipase.
c. Thus, lipid digestion, begun with lingual lipase, which is deactivated by the acidic environment of the
stomach, continues in the stomach at a different pH!
REGULATION OF GASTRIC SECRETION
1.
CEPHALIC PHASE (produces 70% of HCl needed for digestion)
a. Aroma, taste, sight, thought of food stimulate the medulla to send a signal via the vagus nerve (all
parasympathetic action) to the enteric ganglion of the stomach.
b. The enteric ganglion stimulates the G cells of the gastric glands to secrete the hormone, gastrin.
c. Gastrin stimulates the parietal cells of the gastric glands to then secrete HCl.
2.
GASTRIC PHASE
a. Stomach distension, low acid levels, peptides, caffein stimulate the medulla to send a signal via the vagus
nerve (all parasympathetic action) to the enteric ganglion of the stomach.
b. The enteric ganglion then stimulates
1) Chief cells of the gastric glands to secrete
a) Gastric lipase, which continues lipid digestion
b) Pepsinogen
2) G cells of the gastric glands to secrete gastrin
a) Gastrin stimulates the parietal cells to secrete
1) intrinsic factor, which stimulates the small intestine to absorb vitamin B-12, necessary
for normal RBC development (thus, lack of gastrin may lead to pernicious anemia),
2) HCl, which converts inactive pepsinogen into pepsin, thus starting protein digestion.
c. Stomach distension, low acid levels, peptides and caffein also stimulate local receptors to produce
1) Somatostatin, which inhibits digestion by
a) Inhibiting stomach activity:
1) Inhibiting all gastric secretions,
2) inhibiting gastric motility,
3) inhibiting gastric emptying.
b) Inhibiting pancreatic activity by inhibiting pancreatic juice secretion
c) Inhibiting small intestine activity by shunting blood away from the gut
d) Inhibiting gall bladder activity by tightening the sphincter of Oddi and inhibiting contractions
of gall bladder wall.
2) Serotonin, which stimulates stomach contraction
3) Histamine, which activates parietal cells into secreting HCl.
3.
INTESTINAL PHASE
a. Food entering the duodenum, duodenal distension, increased levels of acid or fats or small polypeptides
entering duodenum all do three things:
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1) Cause medulla to inhibit vagus nerve stimulation of the enteric ganglia, thus shutting down G cell
secretion of gastrin, thus shutting down HCl production, thus shutting down protein digestion in stomach.
2) Activates sympathetic fibers to close pyloric sphincter, thus stopping flow of chyme into duodenum
(allowing the chyme already in there to be digested)
3) Stimulating duodenal mucosa to secrete
a) Secretin, which stimulates the pancreatic duct cells to secrete bicarbonate into the pancreatic ducts
then into the duodenum
b) Vasoactive Intestinal Peptide (VIP), which inhibits gastric gland secretions
c) Gastric Inhibitory Peptide (GIP), which also inhibits gastric gland secretions
d) Cholecystokinin, which
1) relaxes the sphincter of Oddi, so bile can enter the duodenum,
2) contracts gall bladder, so bile is forced into duodenum,
3) stimulates pancreatic juice secretions.
b.
Pancreatic Juice Secretions.
1) Stimulated by cholecystokinin.
2) Active and inactive enzymes secreted by pancreas include:
a) Pancreatic lipase. Continues lipid digesting in duodenum in a new pH environment from that of
stomach.
b) Cholesterol ester hydrolase. Digests cholesterol.
c) Deoxyribonuclease. Digests DNA.
d) Ribonuclease. Digests RNA.
e) Trypsinogen. This is activated into trypsin by enterokinase, an enzyme secreted by the brush border.
Trypsin is a protease.
f) Chymotrypsinogen. This is activated into chymotrypsin by trypsin. Chymotrypsin is a protease.
g) Procarboxypeptidases. These are activated into carboxypeptidases by trypsin. The
carboxypeptidases are proteases.
h) Proelastase. This is activated into elastase by trypsin. Elastase is a protease.
i) Procolipase. This is activated into colipase by trypsin. Colipase is a lipase.
j) Prophospholipase. This is activated into phospholipase by trypsin. Phospholipase is a lipase,
digesting phospholipids.
ABSORPTION OF MONOMERS
1.
Monosaccharides
a. Glucose and galactose
1) Enter absorptive cells of intestinal villi via transporters powered by sodium gradients (secondary active
transport)
2) Exit absorptive cells into interstitial space via transporters powered by their own concentration gradients
(facilitated diffusion); absorbed freely into the capillaries.
b. Fructose
1) Enters absorptive cells using transporters powered by fructose concentration gradients (facilitated
diffusion).
2) Exits absorptive cells into interstitial space via transporters powered by fructose’s own concentration
gradient (facilitated diffusion); absorbed freely into the capillaries.
2.
Peptides & Polypeptides
a. Amino Acids (= Peptides)
1) Enter absorptive cells using transporters powered by sodium gradients (secondary active transport)
mostly, some by ATP.
2) Exit absorptive cells into interstitial space via transporters powered by their own concentration gradients
(facilitated transport); absorbed freely into the capillaries.
b. Dipeptides & Tripeptides
1) Enter absorptive cells using transporters powered by sodium gradients (secondary active transport).
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2) While inside absorptive cells, dipeptides & tripeptides are enzymatically digested into individual amino
acids, which then exit the absorptive cells into interstitial space via transporters powered by their own
concentration gradients (facilitated transport); peptides then absorbed freely into the capillaries.
3.
Lipids
a. Short-chain fatty acids, soluble in the lipid bilayer of cell membranes, move by simple diffusion from the
lumen of the gut, through the absorptive cells, into the interstitial space, then into blood capillaries.
b. Long-chain fatty acids, monoglycerides and glycerol are surrounded by bile salts in the gut in a process
called emulsification. These structures are called micelles. Lipids are hydrophobic, water insoluble, so must
be carried through the gut in micelles. Micelles contact the absorptive cell membranes, releasing the lipids,
which diffuse across the cell membranes into the absorptive cells. Inside the absorptive cells, the
monoglucerides & glycerol are recombined into triglycerides; varying amounts of protein surround the
triglycerides, along with varying amounts of cholesterol. These structures, called lipoproteins, leave the
absorptive cells into the interstitial space. Since they are so big, lipoproteins cannot enter through the
fenestrations of blood capillaries; instead, they enter lacteals where they enter the blood via the thoracic
duct. From the blood, body cells engulf the varying types of lipoproteins via endocytosis OR lipoprotein
lipases, on the endothelial walls of the capillaries, digest triacylglycerols into glycerol and fatty acids,
which are then immediately taken up by adjacent cells. The density of lipoproteins depends on the
percentage of protein in them. Low density lipoproteins contribute to vascular and coronary disease; high
density lipoproteins are associated with keeping the circulatory system healthy. Chylomicrons are very low
density lipoproteins (very bad).
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