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Anatomy and Physiology
Questions and Answers, The Digestive System
QTD Clinical Anatomy and Physiology, Colville, Bassert
1. What are the cardia, fundus, pyloric
antrum, and pylorus of the stomach? What are each of their functions?
The cardia is the area immediately
surrounding the opening from the esophagus into the stomach. The cardia
sphincter helps reduce reflux of stomach contents back up into the esphogus.
The orientation of the esophagus as it enters the stomach also provides
a natural closure for the cardia as the stomach fills and distends. The
fundus is the section of stomach that forms a distendible, blind pouch
that expands as more food is swallowed. The body of the stomach is also
a distensible section in the “middle” of the stomach. The
pyloric antrum is the distal part of the stomach that grinds up swallowed
food and regurgitates the hydrochloric acid that is produced by the fundic
and body parietal cells. The pylorus is the muscular sphincter (ring of
muscle in tubular organ) that regulates the movement of chyme or digested
stomach contents, from the stomach to the into the duodenum (first part
of the small intestine) and prevents backflow of duodenal contents into
the stomach.
2. Describe what each of these cells produces:
Parietal, Chief, Mucous, and G cells. What do each of their products do?
Parietal cells (also called oxyntic cells in older texts) produce hydrochloric
acid.
Chief cells produce an enzyme producer called pepsinogen.
Mucous cells produce protective mucus.
The glands of the pyloric antrum contain endocrine cells called G cells which secrete the hormone gastrin. The presence of food in the blood stimulates the G cells to dump gastrin into the blood. It travels, among other places, to the gastric glands in the proximal part of the stomach, where it stimulates the release of hydrochloric acid from the parietal cells. Like the gastric gland in the fundus and body, the gastric glands in the pyloric antrum also contain many mucous cells.
3. How does motility differ in the fundus
versus the body or pyloric antrium?
The pylorus is the muscular sphincter (ring of muscle in the tubular organ)
that regulates the movement of chime (or digested stomach contents) from
the stomach into the duodenum) (first part of the small intestine) and
prevents the backflow of duodenal contents into the stomach.
The plyloric antrum is the distal part of the stomach
that grinds up swallowed food and regulatesthe hydrochloric acid that’s
produced by the fundic and body parietal cells. The fundus is the section
of stomach that forms a distensible, blind pouch that expands as more
food is swallowed.
4.Explain the effect that each of the following has on gastric
motility:
Gastrin, increased acidity in the duodenum, Secretin, Chlolecystokinin
(CCK).
Gastrin, which is produced by the G cells in the antrum of the stomach,
increases the production of hydrochloric acid in the stomach, and also
inhibits the muscle activity of the fundus, resulting in relaxation and
greater filling of the stomach. When food is initially swallowed, and
begins to distend the body and antrum of the stomach, gastrin is released
and signals the fundus to relax so that food can be accommodated. Any
factors that bring about distension of the intestines or an increased
acidity in the duodenum will inhibit stomach contraction, resulting in
delayed gastric emptying of the contents. This enterogastric reflex prevents
the stomach from pushing its contents into the duodenum before the small
intestine is ready to handle additional chime. Secretin is a hormone released
from the duodenum in response to excess stomach acid being present in
the small intestine. Secretin, like gastrin, can cause the fundus to relax,
but it also can inhibit peristalsis of the body and antrum of the stomach
to slow gastric emptying. Large amounts of fat or protein in the duodenum
also slow gastic emptying by inhibiting gastric contractions. In this
case, these nutrients stimulate the release of a hormone called cholecystokinin
which, like secretin, decreases contraction of the antrum, body, and (like
gastrin) the fundus.
5. What is the relationship between peposinogen and pepsin? What
does the pepsin do?
Peposingen is secreted by the chief cells and is a precursor for the enzyme,
pepsin. Under the influence of hydrochloric acid, pepsinogen is converted
into the active, proteolytic (protein digesting) enzyme pepsin in the
lumen of the stomach. The proteins broken down by the pepsin form chains
of amino acids but are not broken down into the elemental acids themselves.
This takes place in the small intestine. The presence of peptides in the
pyloric antrum of the stomach stimulates the G cells to release more gastrin,
which in turn stimulates more hydrochloric acid and pepsinogen to release.
Once the pepsin moves from the acidic pH pf the stomach to the more alkaline
pH of the duodenum, it is inactivated by the change in pH and stops functioning.
6. What is the difference between the terms
mucus, mucous, and mucin? What roles does bicarbonate play in the mucous
layer?
The mucus produced by the gastric glands is a complex of many substances
that provides a gelatinous, protective coating for the stomach. Mucins
are complex molecules produced by thegoblet cells in the gastric glands,
and they are the main constituent of the mucous coating. In addition to
the mucin, bicarbonate ion is also secreted onto the surface, making the
mucouscoat more alkaline. By alkalinizing the mucus, the hydrochloric
acid contacting it is neutralized to some degree.
7.What are the three receptors on the parietal
cells that stimulate hydrochloric acid production?
The parietal cell has three receptors on the “blood” side
of the cell (as opposed to the stomach lumen side) of the cell) that regulate
acid production. These receptors are for gastrin, acetylcholine (the neurotransmitter
of the parasympathetic nervous system) and histamine. Stimulation of all
three of these receptors results in the optimum amount of hydrogen and
chloride secretion (hence hydrochloric acid production.)
8. How does the stomach know when to stop
producing acid?
When the pH of the stomach contents in the good ol antrum drops below
three, gastrin release is inhibited. With the inhibition of gastrin release,
one of the three stimulants for hydrogen and chloride production is terminated,
and hydrochloric acid declines.
9. What effect do prostaglandins have on
mucus production, gastric blood flow, and the ability of the stomach to
heal itself?
Prostaglandins (PGS) are small molecular structures released
in the body that have a wide variety of effects. Among these is their
involvement in inflammation. They are the end product of a cascade of
steps in inflammation that ultimately result in redness, swelling, heat,
and pain associated with injury and or trauma and disease. Many have beneficial
activities, including regulating blood supply to the kidney, regulating
the normal estrus cycle, and maintaining the normal health and stability
of the GI tract. PGs cals stimulate the cells in the gastric glands to
produce the bicarbonate ion, which helps to make the mucous layer capable
of neutralizing the stomach acid to some degree.
10. Explain how NSAIDS produce sid effects
in the GI tract.
Nonsteroidal Antinflammatory drugs (NSAIDS) such as aspirin, carprofen,
(Rimadyl) meloxicam, (Metacam) and others, produce their anti-inflammatory
effect by blocking the production of inflammatory PGs.
Extra Information:
1.What are the compartments of the ruminant
stomach?
Which are the forestomachs and which one is the true stomach? The compartments
are the reticulum, the rumen, and the omasum. The abomasum is the true
stomach.
2. What exactly is hardware disease? With
which forestomach is it usually associated?
When reticulorumen contractions occur, a wire or sharp object may penetrate
the cranial wall of the or the reticulum, causing hardware disease. Because
the reticulum is separated from the heart by the diaphragm and a relatively
short distance, an object piercing thereticulum can also penetrate the
diaphragm and pericardium (outer membranous sac surrounding the heart)
causing pericarditis (inflammation of the pericardium).
3. What is rumination versus eructation?
What purposes do they serve?
Cud is regurgitated up the esophagus, where it is chewed or reswallowed.
This is rumination. Built up carbon dioxide or methane gas is expelled
from the rumen. This is eructation.
4. What is fermentation digestion? How is
it difference from nonfermentative digestion?
The ruminant animal derives much of its necessary sources of energy and
basic cellular building blocks from the fermentation of rechewed (remasticated)
plant material by bacterial and protozoal enzymes. This process is often
called fermentative digestion. The enzymes that break down foodstuffs
in fermentative digestion come from bacteria and protozoa, in contrast
to the nonfermentative processes in monogastric animals, wherein the enzymes
are produced byglands in and along the digestive tract. Thus ruminants
depend on microbes for their nutritional needs.
5. What is the relationship among cellulose,
pectin, cellase, glucose, and VFAs?
The enzymes produced by the digestive glands in the monogastric animals
cannot digest the cellulose and pectin that make up the wall of plant
cells. However, rumen bacterial surfaces have cellulose enzymes that can
digest cellulose effectively and transform the complex carbohydrate structure
of enzymes into much simpler monosaccharides and less complex polysaccarides.
The glucose sugar produced by this process is not immediately available
to the host animal. Instead, the glucose liberated from the plant materials
(and other carbohydrate sources, like starch) is absorbed into the microbes
and converted biochemically to volatile fatty acids, or VFAs.
6. What is the relationship among proteases,
peptides, and amino acids?
Like carbohydrates, proteins in the ruminant diet are attacked by anerobic
microbial enzymes in the rumen. Proteases (enzymes that break down proteins)
reduce the long proteins to short peptides (short chains of amino acids)
and the amino acid building blocks of the peptides and proteins. Just
as the breakdown of complex carbohydrates yielded simple sugars that were
used by the rumen microorganisms, the amino acids and peptides from the
protein breakdown
are also used by the rumen’s microbes.
7. What role does urea play in the rumen
function? Which organ converts ammonia to urea?
Additional nitrogen for rumen microbes comes from the ruminant’s
production of urea by the liver, which makes its way to the rumen via
the bloodstream and saliva. Urea is the end product of the liver’s
activity to convert possibly poisonous amounts of ammonia into substances
that can be used by the ruminant body.
8. How is the young calf’s GI tract
different from an adult’s? What is the role of the reticular groove?
A newborn ruminant’s digestive tract functions primarily as a monogastric
digestive system. The rumen and reticulum at birth are small compared
to the omasum and the abomasum and are essentially nonfunctional. Little
or no fermentative digestion occurs while the animal is nursing.
The abomasum (the true stomach) is the largest of four stomach compartments
for the first few weeks of life. Milk in the rumen of a young animal can
disrupt normal development of the fermentative digestive process. Therefore,
the ability of the reticulum to convey suckled milk directly into the
omasum is advantageous. The reticular groove also called the esophageal
groove, is a trough in the wall of the reticulum that extends from the
esophageal opening to the
opening of the omasum. When the calf nurses the muscles associated with
the groove contract and form a tubular structure that conveys swallowed
liquid from the esophageal opening directly to the omasum, essentially
bypassing the rumen and the reticulum.
More information than you would ever want
1.What are the three segments of the small
intestine? Which is usually the longest?
They are the dudodenum, the jejunum, and the ileum. The jejunum is generally
the longest.
2.What does the ileocecal sphincter do?
The sphincter is an anatomical and functional muscle that regulates movement
of the materials from the small intestine into the colon or cecum.
3.What are the villi, microvilli, brush
border, and crypts? How do they aid digestion and absorption of food?
The mucosa in the small intestine is adapted to provide a tremendously
large surface area for absorbing nutrients, thanks to the folds in the
intestinal wall and the millions of tiny, cylindrical fingerlike projections
called villi. In addition to the folds and the villi, each villus contains
thousands of small villi of its own called microvilli. This is why we
say it takes a villi.
The microvilli are so plentiful that they microscopically resemble short bristles on a brush, hence the layer of microvilli are often called the brush border. The cells of this brush border have many digestive enzymes and carrier molecules embedded in their cell membranes for the digestion and absorption of nutrients, vitamins, and minerals. The cells of each villus are constantly replenished. Surrounding each villus are invaginations in the intestinal mucosa called Crypts. The competing cells are called the Bloods. Get it? Crypts and Bloods.
4. What is the role of segmental contractions
in the small intestine? Why do animals get diarrhea if segmental
contractions are decreased?
Segmental contractions mix the intestinal contents and slow their movement
through the length of the intestine. These contractions churn the material
in the intestine, ensuring that digestive enzymes secreted into the lumen
of the intestine are mixed well with the contents. The churning motion
of the segmental contractions also brings digested materials into contact
with the surface of the intestinal tract for absorption. The inactive
intestinal tract resembles a garden hose in which contents can slide.
The result is (ugh) a high volume, small bowel diarrhea.
5. What is ileus? What causes it? Why would
antiparasympathetic drugs like atropine cause it?
A decrease in peristaltic waves can result in the ingesta moving too slowly
through the intestinal tract. Disease and stress (sympathetic nervous
system) inhibit peristalis and can result in a condition of decreased
movement of ingesta called illeus. Antiparasympathetic drugs like atropine
cause it because peristalis is inhibited.
6. What do CCK and prostaglandins do to the small intestine?
Unlike its role in the stomach, where it serves to decrease gastric emptying,
cholecystokinin (CCK) is thought to stimulate intestinal motility, as
are prostaglandins.
7. What are polysaccarides, disaccharides, and monsaccharides? Give examples
of each. What enzymes break down each of these?
Starch, glycerin, and various sugars constitute the complex
carbohydrates, or polysaccharides, (meaning many sugars) normally present
in domestic animal foods. Disaccharides are smaller sugar segments. The
disaccharides, which include sucrose, maltose, isomaltose (also called
dextrin) and lactose, are further digested into monosaccharides (meaning
one sugar) by the enzymes sucrase, maltase, isomaltase, and lactase, which
are found in the cell membranes of the microvilli. The resulting monosaccharides
are transported across the brush border by plainclothes policemen who
are working incognito for a drug cartel but it is business as usual as
the brush border cell membranes are absorbed into the body.
8. What are the proteases? What protease
is produced by the stomach? What effect do the proteases have on polypeptides?
A protease is a protein spitting enzyme. It is also a strip
tease that has paid her union dues and gone professional. Gastric pepsin
is the protease produced by the stomach. The effect that proteases have
on polypeptides is this – because proteins have so many differing
types of amino acids, and because different amino acids have different
types of chemical bonds with other amino acids, many differing proteases
are required to complete the
chemical digestion of proteins.
9. Explain how each of the following plays
a role in digestion of fats: emulsification, bile acids, liver, pancreatic
lipase, triglycerides, glycerol, fatty acids, monoglycerides, and micelles.
For fats to be adequately digested, fat globules must be broken down into
smaller pieces. This process is called emulsification and micelle formation.
In the stomach, the agitation of the plyloric antrum breaks the fat globules
into small droplets. As this emulsified liquid of fat droplets passes
into the small intestine, bile acids combine with the droplets to keep
them from forming back into globules. Bile acids have a water loving and
a water fearing end. The bile acid sticks the hydrophobic end into the
fat droplet, leaving the hydrophilic end exposed to the environment of
the intestinal tract. In doing so this makes the resulting fat droplet
water soluble.
Pancreatic lipases (fat digesting enzymes) penetrate the bile acid coating
and digest the fat (triglycerides) molecules to produce glycerol, fatty
acids, and monoglycerides.
Why do some animals get diarrhea when their
diet is suddenly changed?
Incomplete indigestion is as good an answer as any. The presence of these
undigested molecules osmotically retains water within and may even draw
water into the lumen of the intestine, producing diarrhea.
The Digestive System