3. GI Tract
External environment for the digestive process
Regulation of digestion involves:
Mechanical and chemical stimuli – stretch receptors,
osmolarity, and presence of substrate in the lumen
Extrinsic control by CNS centers
Intrinsic control by local centers
4. Receptors of the GI Tract
Mechano- and chemoreceptors respond to:
Stretch, osmolarity, and pH
Presence of substrate, and end products of digestion
They initiate reflexes that:
Activate or inhibit digestive glands
Mix lumen contents and move them along
5. Nervous Control of the GI Tract
Intrinsic controls
Nerve plexuses near the GI tract initiate short reflexes
Short reflexes are mediated by local enteric plexuses
(gut brain)
Extrinsic controls
Long reflexes arising within or outside the GI tract
Involve CNS centers and extrinsic autonomic nerves
7. Secretions of the Stomach
Chyme: ingested food plus stomach secretions
Mucus: surface and neck mucous cells
Viscous and alkaline
Protects from acidic chyme and enzyme pepsin
Irritation of stomach mucosa causes greater mucus
Intrinsic factor: parietal cells. Binds with vitamin B12 and helps it to
be absorbed. B12 necessary for DNA synthesis
HCl: parietal cells
Kills bacteria
Stops carbohydrate digestion by inactivating salivary amylase
Denatures proteins
Helps convert pepsinogen to pepsin
Pepsinogen: chief cells. Packaged in zymogen granules released by
exocytosis. Pepsin catalyzes breaking of covalent bonds in proteins.
G-cells: secrete the hormone gastrin which stimulates HCl secretion
from parietal cells
8. Hydrochloric Acid Production
1. CO2 and Cl-
diffuse from the
blood into the stomach cell.
2. CO2 combines with H2O
to form H2CO3.
3. H2CO3 dissociates into
bicarbonate (HCO3-
) and H+
.
4. H+
combines with Cl-
in duct
of gastric gland to form HCl-
.
5. An ATP pump is necessary to
pump the HCl-
into the duct
since the concentration of
HCl-
is about a million times
more concentrated in the
duct than in the cytosol of the
cell.
9. Regulation of Gastric Secretion
Neural and hormonal mechanisms regulate the
release of gastric juice
Stimulatory and inhibitory events occur in three
phases
Cephalic (reflex) phase: prior to food entry
Gastric phase: once food enters the stomach
Intestinal phase: as partially digested food enters the
duodenum
11. Cephalic Phase
The taste or smell of food, tactile
sensations of food in the mouth, or
even thoughts of food stimulate the
medulla oblongata.
Parasympathetic action potentials
are carried by the vagus nerves to the
stomach.
Preganglionic parasympathetic vagus
nerve fibers stimulate postganglionic
neurons in the enteric plexus of the
stomach.
Postganglionic neurons stimulate
secretion by parietal and chief cells
(HCl and pepsin) and stimulate the
secretion of the hormone gastrin.
Gastrin is carried through the
circulation back to the stomach
where it stimulates further secretion
of HCl and pepsin.
12. Gastric Phase
Distention of the stomach
activates a parasympathetic
reflex. Action potentials are
carried by the vagus nerves to
the medulla oblongata.
Medulla oblongata stimulates
further secretions of the
stomach.
Distention also stimulates
local reflexes that amplify
stomach secretions.
13. Intestinal Phase
Chyme in the duodenum with a
pH less than 2 or containing lipids
inhibits gastric secretions by three
mechanisms
1. Sensory input to the medulla from
the duodenum inhibits the motor
input from the medulla to the
stomach. Stops secretion of pepsin
and HCl.
2. Local reflexes inhibit gastric
secretion
3. Secretin, gastric inhibitory
polypeptide, and cholecystokinin
produced by the duodenum
inhibit gastric secretions in the
stomach.
14. Regulation of Gastric Emptying
Gastric emptying is regulated by:
The neural enterogastric reflex
Hormonal (enterogastrone) mechanisms
These mechanisms inhibit gastric secretion and
duodenal filling
Carbohydrate-rich chyme quickly moves through
the duodenum
Fat-laden chyme is digested more slowly causing
food to remain in the stomach longer
17. Histology of
the Liver
Connective tissue septa branch from
the porta into the interior
Divides liver into lobules
Nerves, vessels and ducts follow the
septa
Lobules: portal triad at each corner
Three vessels: hepatic portal vein,
hepatic artery, bile duct (hepatic duct
in diagram)
Central vein in center of lobule
Central veins unite to form hepatic
veins that exit liver and empty into
inferior vena cava
Hepatic cords: radiate out from
central vein. Composed of
hepatocytes
Hepatic sinusoids: between
cords, lined with endothelial cells
and hepatic phagocytic
(Kupffer) cells
Bile canaliculus: between cells
within cords
18. Functions of the Liver
Bile production: 600-1000 mL/day. Bile salts (bilirubin), cholesterol,
fats, fat-soluble hormones, lecithin
Neutralizes and dilutes stomach acid
Bile salts emulsify fats. Most are reabsorbed in the ileum.
Secretin (from the duodenum) stimulates bile secretions,
increasing water and bicarbonate ion content of the bile
Storage
Glycogen, fat, vitamins, copper and iron. Hepatic portal blood
comes to liver from small intestine.
Nutrient interconversion
Amino acids to energy producing compounds
Hydroxylation of vitamin D. Vitamin D then travels to kidney
where it is hydroxylated again into its active form
Detoxification
Hepatocytes remove ammonia and convert to urea
Phagocytosis
Kupffer cells phagocytize worn-out and dying red and white blood
cells, some bacteria
Synthesis
Albumins, fibrinogen, globulins, heparin, clotting factors
19. Composition of Bile
A yellow-green, alkaline solution containing bile
salts, bile pigments, cholesterol, neutral fats,
phospholipids, and electrolytes
Bile salts are cholesterol derivatives that:
Emulsify fat
Facilitate fat and cholesterol absorption
Help solubilize cholesterol
Enterohepatic circulation recycles bile salts
The chief bile pigment is bilirubin, a waste
product of heme
22. Pancreas
Pancreas both endocrine and exocrine
Head, body and tail
Endocrine: pancreatic islets. Produce
insulin, glucose, and somatostatin
Exocrine: groups acini (grape-like
cluster) form lobules separated by
septa.
Intercalated ducts lead to
intralobular ducts lead to
interlobular ducts lead to the
pancreatic duct.
Pancreatic duct joins common bile duct
and enters duodenum at the
hepatopancreatic ampulla controlled
by the hepatopancreatic ampullar
sphincter
23. Pancreatic Secretions: Pancreatic Juice
Aqueous. Produced by columnar epithelium lining smaller ducts. Na+
, K+
,
HCO3
-
, water. Bicarbonate lowers pH inhibiting pepsin and providing
proper pH for enzymes
Enzymatic portion:
Trypsinogen
Chymotrypsinogen
Procarboxypeptidase
Pancreatic amylase
Pancreatic lipases
Deoxyribonucleases and ribonucleases
Interaction of duodenal and pancreatic enzymes.
Enterokinase from the duodenal mucosa and attached to the brush
border activates trypsinogen to trypsin.
Trypsin activates chymotrypsinogen to chymotrypsin
Trypsin activates procarboxypeptidase to carboxypeptidase.
Trypsin, chymotrypsin and carboxypeptidase digest proteins: proteolytic.
Pancreatic amylase continues digestion of starch
Pancreatic lipase digests lipids
Deoxyribonucleases and ribonucleases digest DNA and ribonucleic acid,
respectively
26. Secretions of Large Intestine
Mucus provides protection
Parasympathetic stimulation increases rate of goblet cell secretion
Pumps: bacteria produce acid and the following remove
acid from the epithelial cells that line the large intestine
Exchange of bicarbonate ions for chloride ions
Exchange of sodium ions for hydrogen ions
Bacterial actions produce gases (flatus) from particular
kinds of carbohydrates found in legumes and in artificial
sugars like sorbitol
Bacteria produce vitamin K which is then absorbed
Feces consists of water, undigested food (cellulose),
microorganisms, sloughed-off epithelial cells
27. Digestion, Absorption,
Transport
Digestion
Breakdown of food molecules for absorption into
circulation
Mechanical: breaks large food particles to small
Chemical: breaking of covalent bonds by digestive enzymes
Absorption and transport
Molecules are moved out of digestive tract and into
circulation for distribution throughout body
28.
29. Carbohydrates: Hydrolyzed into Monosaccharides
Glucose is transported to cells requiring energy; insulin influences
rate of transport
30. Lipids
Include triglycerides, phospholipids, steroids,
fat-soluble vitamins
Bile salts surround fatty acid and glycerol to
form micelles
Chylomicrons are 90% triglyceride, 5%
cholesterol, 4% phospholipid, 1% protein.
Chylomicrons enter blood stream and travel to
adipose tissue. In blood, triglycerides converted
back into fatty acids and glycerol where they are
transported into the adipose cells, then
converted back into triglycerides.
33. Lipoproteins
All lipids carried in the blood are done so
in combination with protein to make them
soluble in plasma.
Cholesterol: 15% ingested; 85%
manufactured in liver and intestinal
mucosa
Lipids are lower density than water;
proteins are higher density than water
Chylomicrons: 99% lipid and 1% protein
(extremely low density); enter lymph
VLDL: 92% lipid, 8% protein
Form in which lipids leave the liver
Triglycerides removed from VLDL and
stored in adipose cells. VLDL has been
converted to LDL.
LDL: 75% lipid, 25% protein
Transports cholesterol to cells
Cells have LDL receptors
# of LDL receptors become less once
cell’s lipid/cholesterol needs are met.
HDL: 55% lipid, 45% protein
Transports excess cholesterol from
cells to liver
35. Proteins
Pepsin breaks proteins into smaller polypeptide
chains
Proteolytic enzymes produce small peptide chains
Dipeptides, tripeptides, amino acids
After absorption, amino acids are are carried through
the hepatic portal vein to the liver.
37. Chemical Digestion: Nucleic Acids
Absorption: active transport via membrane carriers
Absorbed in villi and transported to liver via hepatic
portal vein
Enzymes used: pancreatic ribonucleases and
deoxyribonuclease in the small intestines
38. Electrolyte Absorption
Most ions are actively absorbed along the length of
small intestine
Na+
is coupled with absorption of glucose and amino acids
Ionic iron is transported into mucosal cells where it binds
to ferritin
Anions passively follow the electrical potential
established by Na+
K+
diffuses across the intestinal mucosa in response
to osmotic gradients
Ca2+
absorption:
Is related to blood levels of ionic calcium
Is regulated by vitamin D and parathyroid hormone (PTH)
39. Water Absorption
95% of water is absorbed in the small intestines
by osmosis
Water moves in both directions across
intestinal mucosa
Net osmosis occurs whenever a concentration
gradient is established by active transport of
solutes into the mucosal cells
Water uptake is coupled with solute uptake,
and as water moves into mucosal cells,
substances follow along their concentration
gradients
40. Water and Ions
Water: can move in
either direction
across wall of small
intestine depending
on osmotic gradients
Ions: sodium,
potassium, calcium,
magnesium,
phosphate are
actively transported
43. Gastrointestinal System(GIS)Gastrointestinal System(GIS)
The main function of the GIS is to process
ingested food into molecular forms that are
transferred, with salts and water to the body’s
internal environment where the circulatory
system can distribute them to cells.
This system includes the Gastrointestinal Tract
(GI) which is made up of; mouth, pharynx,
oesophagus, stomach, small intestine, large
intestine and accessory organs.
The accessory organs include; salivary glands,
liver, gall bladder and pancreas
44.
45. Organ Exocrine
secretions
Digestion Absorption Bulk transport/
Function
Mouth and
Pharynx
Salivary glands
Salt and
water
Mucus
Amylase
Chewing breaks
down food
particles
Amylase partially
digests
polysaccharides
No Moistens and lubricates
food particles
Oesophagus Mucus No No Moves food to stomach
by peristaltic waves
Provides lubrication
Stomach HCl
Pepsins
Mucus
Solubilises food
particles, kills
microbes,
activates
pepsinogens to
pepsin
Pepsins break
down protein
No Store food particles
Regulate rate at which
contents are emptied
into the small intestine
Pancreas Enzymes
Bicarbonate
Carbohydrates
Fats
Proteins and
Nucleic acids
No Neutralize HCl
entering the small
intestine
46. Organ Exocrine
secretions
Digestion Absorption Bulk transport/
Function
Liver Bile Salts
Bicarbonate
Organic
waste
products
and trace
metals
Solubilizes water
insoluble fats
No Neutralizes HCl entering
the small intestine
Elimination of feces
Gall Bladder No No No Stores and concentrates
bile between meals
Small
Intestine
Enzymes
Salt and
water
Mucus
Hydrolytic
enzymes break
down
carbohydrates,
fats and proteins
into
monosaccharides
, fatty acids,
amino acids
Monosaccharides,
fatty acids, amino
acids, vitamins,
minerals, water
Maintain fluidity of
luminal contents
Lubrication
Large Intestine Mucus No Salt, water Storage and concentration
of undigested matter
Mixing and propulsion of
contents
Defecation
47. Structure of the GI Tract WallStructure of the GI Tract Wall
The wall of the gastrointestinal tract has the same
general structure from mid-oesophagus to the
anus.
The wall comprises:
- mucosa,
-submucosa,
-muscularis externa
- serosa.
48.
49.
50.
51. Walls of the GI Tract
In the small intestine finger like projections called villi
which extend from the luminal surface. The centre of
each villus is occupied both by lacteal (single blind-
ended lymphatic vessel) and a capillary network.
The surface of each villus is covered with a layer of
epithelial cells whose surface membrane form
projections called microvilli
52.
53. Epithelial Function
The increased surface area of the wall in the small
intestine by villi and microvill allow for mass
absorption.
The invaginatons in the wall form exocrine glands
and allow passage of substances.
They also have a paracrine function which refers to
the ability of the endocrine cells within the epithelial
layer to release hormones and bind to the receptors of
nearby cells to affect their function.
54. Epithelia Lifetime
17 Billion epithelial cells are replaced each day.
The entire epithelium of the small intestine is
replaced approximately every five days.
The rapid cell turnover makes the lining of the
intestinal tract suseptible to damage by agents that
inhibit cell division (e.g. anticancer drugs)
55. Digestion & Absorption ObjectivesDigestion & Absorption Objectives
Describe the process involved in the breakdown and absorption of
ingested carbohydrates.
Describe fat absorption, resynthesis of triglycerides and
phospholipids, the formation of chylomicrons and the absorption
into the lacteals.
Describe the absorptive mechanisms involved in protein
absorption.
Describe the absorption mechanisms for the different water- and
fat soluble vitamins, noting the special role of intrinsic factor in the
absorption of vitamin B 12.
Describe the epithelial processes involved in the active absorption
56. Digestion and AbsorptionDigestion and Absorption
Overview of the four basic
digestive processes:
Digestion: dissolving and
breaking down process of food
into small molecules.
Absorption: the process
whereby molecules produced
from digestion moves from the GI
tract across a layer of epithelial
cells and enters the blood.
Secretion: The release of
substances that aid in digestion.
( HCL acid, bile and digestive
enzymes)
Motility: Contraction of the GI
tract .
59. Digestion and AbsorptionDigestion and Absorption
Glucose & Galactose
enter epithelial cells via
sodium-linked
secondary active
transport across the
epithelial membrane.
Fructose enters by
facilitated diffusion.
These monosaccharides
exit via the Basolateral
Membrane by facilitated
diffusion transporters
and then diffuse into the
capillaries.
60. Digestion and AbsorptionDigestion and Absorption
Proteins
Proteins need to be broken down into smaller molecules (amino
acids, dipeptides & tripeptides) before they can be absorbed
by the small intestine.
Proteases involved in this process are :
-Pepsin: secreted as pepsinogen into the stomach
-Trypsin: secreted as trypsinogen into small intestine.
-Chymotrypsin: secreted as chymotrypsinogen, into small
intestine.
-Carboxypeptidase: secreted as procarboxypeptidase into
small intestine.
-Aminopeptidase (brush border enzyme) is also used.
63. Digestion and AbsorptionDigestion and Absorption
Free Amino acids enter absorptive
epithelial cells via sodium-linked
secondary active transport across
the apical membrane.
Others are transported via
facilitated diffusion into cells.
Dipeptides and Tripeptides are
actively transported across the
apical membrane and then broken
down to amino acids within the cell.
Amino acids from the cell enter
the capillaries via facilitated
diffusion across the basolateral
64. Digestion and AbsorptionDigestion and Absorption
Fats
Fats are ingested in the form of Triglycerides.
Fat digestion occurs almost entirely in the small intestine
whereby lipase splits bonds linking fatty acids to the first and
third carbon atoms of glycerol. Two fatty acids and a
monoglyceride are produced.
Ingested fats aggregate into large lipid droplets in the upper
portion of the stomach. (insolubility in water).
Emulsification: breakdown of large lipid droplets into smaller
droplets resulting in an increased rate of digestion.
66. Digestion and AbsorptionDigestion and Absorption
‘Mechanical disruption of fat
globlets’ (contractions of stomach and
small intestine) & ‘ An emulsifying
agent’ (Phospholipids in food and
secreted bile salts) is needed for the
emulsification of fat.
Non polar regions on phospholipids
and bile salts associate with the non
polar interior of the lipid droplets.
Repulsion of other lipid droplets occurs
preventing reaggregation.
Although accessibility to lipase is
impaired, colipase (secreted from
pancreas) binds lipase onto the
surface of the lipid droplet.
67. Digestion and AbsorptionDigestion and Absorption
Micelles: similar in structure to
emulsion droplets & comprise clusters of
bile salts, fatty acids, monoglycerides &
phospholipids. (Polar ends oriented
toward micelle surface; nonpolar
portions form micelle’s core).
Micelles continuously breakdown &
reform which increases absorption.
Broken-down micelles release its
contents (fatty acids and
monoglycerides) which diffuse into
epithelial cells.
Fatty acids and monoglycerides enter the
intestinal lumen and triglycerides are
released into the interstitial fluid.
Re-synthesis of triglycerides occurs on
68. Digestion and AbsorptionDigestion and Absorption
Chylomicrons: extracellular fat
droplets
containing triglycerides and other
lipids (phospholipids, cholesterol &
fat-soluble vitamins)
which have been absorbed in the
absorption process.
Chylomicrons released from
epithelial cells enter lacteals and then
into the lymph.
A basement membrane(extracellular
glycoprotein layer) prevents entry of
chylomicrons into the capillaries.
70. Digestion and AbsorptionDigestion and Absorption
Water & Minerals:
Small amounts of water are absorbed in the stomach in spite of the
absence of solute absorbing mechanisms.
Significant absorption takes places in the epithelial membranes of the
small intestine.
A water concentration difference is required for net water diffusion and
this is established via active absorption of solutes.( active transport of
sodium across epithelium)
Water moves by osmosis across the epithelium.
Iron absorption
Increased iron deposition leads to hemochromatosis.
71. Mouth
Food enters the digestive
tract through the mouth.
As food enters the mouth,
breakdown begins:
Mechanical breakdown by
chewing (teeth) and actions
of the tongue.
Chemical breakdown of
starch by production of
salivary amylase from the
salivary glands.
72. SalivaSaliva
Salivary amylase
hydrolyzes internal α1-4
bonds within starch.
A second digestive
enzyme, lingual lipase,
is produced by lingual
serous glands on the
tongue and in the back
of the mouth.
This enzyme hydrolyzes
dietary triacylglycerols
(triglycerides) in the
stomach.
Mucus secretions found in
saliva contain
glycoproteins.
Mucus lubricates food and
coats and protects the oral
mucosa.
73. The secretion of saliva is controlled by
both sympathetic and parasympathetic
neurons.
There is no hormonal regulation of
salivary secretion.
In the absence of ingested material, a low
rate of salivary secretion keeps the mouth
moist.
In the presence of food, salivary secretion
increases markedly.
This reflex response is initiated by
chemoreceptors (acidic fruit juices are a
particularly strong stimulus) and pressure
receptors in the walls of the mouth and on
the tongue.
Increased secretion of saliva is
accomplished by a large increase in
blood flow to the salivary glands,
which is mediated by both neural
activity and paracrine/autocrine
agents released by the active cells in
the salivary gland.
The volume of saliva secreted per
gram of tissue is the largest
secretion of any of the body’s
exocrine glands.
74. SwallowingSwallowing
Swallowing is a complex reflex initiated when
pressure receptors in the walls of the pharynx are
stimulated by food or drink forced into the rear of
the mouth by the tongue.
These receptors send afferent impulses to the
swallowing center in the brainstem medulla
oblongata.
This center then elicits swallowing via efferent
fibers to the muscles in the pharynx and esophagus
as well as to the respiratory muscles.
75.
76. Swallowing is an example of a reflex in which multiple
responses occur in a temporal sequence determined by
the pattern of synaptic connections between neurons in a
brain coordinating center.
Since both skeletal and smooth muscles are involved, the
swallowing center must direct efferent activity in both
somatic nerves (to skeletal muscle) and autonomic nerves
(to smooth muscle).
Simultaneously, afferent fibers from receptors in the
esophageal wall send information to the swallowing
center that can alter the efferent activity.
77. PharynxPharynx
Swallowing moves ingested material (bolus) from the mouth into the pharynx.
The pharynx is 14-16cm long.
As the ingested material (bolus) moves into the pharynx, the soft palate elevates
and lodges against the back wall of the pharynx.
This prevents food from entering the nasal cavity.
Impulses from the swallowing center inhibit respiration, raise the larynx, and
close the glottis (the area around the vocal cords and the space between them).
This keeps food from moving into the trachea.
As the tongue forces the food farther back into the pharynx, the food tilts a flap
of tissue, the epiglottis, backward to cover the closed glottis, thereby preventing
food from entering the trachea.
78. PharynxPharynx
The pharynx is
divided into three
sections:
the nasopharynx
the oropharynx
the laryngopharynx
79. How the Esophagus Works….How the Esophagus Works….
As a person swallows, food moves
from the mouth to the throat,
also called the pharynx (1).
The upper esophageal sphincter
opens (2) so that food can enter
the esophagus,
where waves of muscular
contractions, called peristalsis,
propel the food downward (3).
The food then passes through the
lower esophageal sphincter (4)
and moves into the stomach (5).
80. “Food goin’ down d wrong
hole”
http://kidshealth.org/kid/watch/er/choking.html
81. Once in the esophagus, the
food is moved toward the
stomach by a progressive wave
of muscle contractions that
proceeds along the esophagus,
compressing the lumen and
forcing the food ahead of it.
Such waves of contraction in
the muscle layers surrounding
a tube are known as peristaltic
waves.
One esophageal peristaltic
wave takes about 9 s to reach
the stomach.
82. Upper Esophageal
Sphincter
Lower Esophageal
Sphincter
The esophageal phase of
swallowing begins with
relaxation of the upper
esophageal sphincter.
Immediately after the food
has passed, the sphincter
closes, the glottis opens, and
breathing resumes.
The lower esophageal
sphincter opens and remains
relaxed throughout the
period of swallowing,
allowing the arriving food to
enter the stomach.
After the food has passed,
the sphincter closes,
resealing the junction
between the esophagus and
the stomach.
83. The ability of the lower esophageal sphincter to
maintain a barrier between the stomach and the
esophagus when swallowing is not taking place is
aided by the fact that the last portion of the
esophagus lies below the diaphragm, and is subject
to the same abdominal pressures as is the stomach.
This prevents the formation of a pressure gradient
between the stomach and esophagus that could
force the stomach’s contents into the esophagus.
84. Heartburn
Some people have
less efficient lower
esophageal
sphincters, resulting
in repeated episodes
of refluxed
gastric contents into
the esophagus
(gastro-esophageal
reflux), heartburn,
and in extreme cases,
ulceration, scarring,
obstruction, or
perforation of the
lower esophagus.
The lower
esophageal sphincter
not only undergoes
brief periods of
relaxation during a
swallow but also in
the absence of a
swallow.
During these periods
of relaxation, small
amounts of the acid
contents from the
stomach are
normally refluxed
into the esophagus.
85. Multiple mechanisms,
including neural and
hormonal, regulate
gastroesophageal
sphincter pressure.
The musculature of the
gastroesophageal
sphincter has a tonic
pressure.
It is normally higher than
the intragastric pressure
(the pressure within the
stomach).
This high tonic pressure at
the gastroesophageal
sphincter keeps the
sphincter closed.
Keeping this sphincter
closed is important.
It prevents
gastroesophageal reflux:
the movement of
substances from the
stomach back into the
esophagus.
86. The StomachThe Stomach
The stomach is a typically J shaped enlargement
of the GI tract.
It connects the oesophagus to the duodenum
(the first part of the small intestine).
87. Anatomy of the StomachAnatomy of the Stomach
The stomach has four (4)
main regions:
The cardia
The fundus
The body
The pyloric region
The pyloric antrum
The pyloric canal
The phyloricsphinter
88. Histology of the StomachHistology of the Stomach
The stomach wall is composed of the same four(4) basic
layers as the rest of the GI tract, with certain
modifications.
The surface of the mucosa is a layer of simple columnar
epithelial cells called mucous surface cells.
The epithelial cells extend down into the lamina propia,
where they form columns of secretory cells called gastric
glands that line many narrow channels called gastric
pits.
Secretions from the gastric glands flow into each gastric
pit and into the lumen of the stomach.
89. Gastric pits contain four (4) major secretory cells:
Chief cells
Pepsinogen
Activation of pepsinogen by low pH to form pepsin
Once pepsin is formed, it can act on pepsinogen to produce more pepsin
Pepsin is a protease for protein digestion
Parietal cells
HCl
Kills microbes in food
Denatures protains
Converts pepsinogen to pepsin
Intrincis factors
Needed for absorption of vitamin B12
G-cells (enteroendocrine cell)
Secretes gastrin hormone
Gastrin activates gastric juice secretion and gastric smooth muscle “churning”
Gastrin activates gastroileal reflex which moves chyme from ileum to colon
Mucus cells
Protective role of mucus against acid and digestive enzymes
90. The submucosa layer of the stomach is composed of
areolar connective tissue.
The muscularis has three (3) (rather than two) layers of
smooth muscle:
An outer longitudinal layer
A middle circular layer
An inner oblique layer (limited to the body of the
stomach).
The serosa (simple squamous mesothelium and areolar
connective tissue) covering the stomach is part of the
viseral peritoneum.
91.
92. Functions of the StomachFunctions of the Stomach
Storage
Because of its accordionlike folds (called rugae), the wall of the
stomach can expand to store two to four liters of material.
Temporary storage is important because you eat considerably
faster than you can digest food and absorb its nutrients.
Mixing
The stomach mixes the food with water and gastric juice to
produce a creamy medium called chyme.
Controlled release
Movement of chyme into the small intestine is regulated by
a sphincter at the end of the stomach, the pyloric sphincter.
93. Physical breakdown
Three layers of smooth muscles (rather than the usual two) in
the muscularis externa churn the contents of the stomach,
physically breaking food down into smaller particles. In
addition, HCl denatures (or unfolds) proteins and loosens the
cementing substances between cells (of the food). The HCl also
kills most bacteria that may accompany the food.
Chemical breakdown
Proteins are chemically broken down by the enzyme pepsin.
Chief cells, as well as other stomach cells, are protected from
self-digestion because chief cells produce and secrete an inactive
form of pepsin, pepsinogen. Pepsinogen is converted to pepsin
by the HCl produced by the parietal cells. Only after pepsinogen
is secreted into the stomach cavity can protein digestion begin.
Once protein digestion begins, the stomach is protected by the
layer of mucus secreted by the mucous cells.
95. HCl is produced in the parietal cells through a complex
series of reactions.
Carbon dioxide diffuses into the parietal cell and the
enzyme carbonic anhydrase catalyzes a reaction between
the carbon dioxde and water to form carbonic acid.
Carbonic acid dissociates into bicarbonate ion and
hydrogen ion and the bicarbonate ion is transported back
into the bloodstream.
An ion exchange molecule in the plasma membrane
exchange bicarbonate going out for chloride coming in.
96. Proton pumps powered by H+/K+ ATPases is used to
transport the potassium and hydrogen ions.
The hydrogen ions are actively transported into the duct
of the gastric gland and the negatively charged chloride
ions diffuse with the positively charged hydrogen ions.
Potassium ions are counter transported into the parietal
cells in exchange for hydrogen ions. The potassiun ions
leak back into the lumen via potassium channels.
The net result is production of HCl in the parietal cells
and its secretion into the duct of the gastric gland.
97. Four (4) chemical messengers regulate acid secretion:
GastrinGastrin
released from G-cell
stimulates acid secretion
Acetylcholine (Ach)Acetylcholine (Ach)
released from the plexus neurons
stimulates acid secretion
HistamineHistamine
released from ECL cells
stimulates acid secretion
potentiates the response to gastrin and Ach.
SomatostatinSomatostatin –
released from endocrine cells in the gastric wall
Acts on parietal cells to inhibit acid secretion
Inhibits release of gastrin and histamine
Parietal cell membranes contain receptors for all 4 of these molecules. Not
only do these chemical messengers act directly on the parietal cells, they also
influence each other’s secretion.
Pepsinogen secretion parallels acid secretion, i.e. most of the factors stimulate
or inhibit acid secretion exert the same effect on pepsinogen secretion.
98. Three Phases of Gastric SecretionThree Phases of Gastric Secretion
Regulation of stomach secretion is divided into three (3)
phases:
• Cephalic
• Gastric
• Intestinal
99. Cephalic phase:Cephalic phase:
Taste, sight, tactile sensation of
or thought of food in the mouth
sends nervous impulse to the
medulla oblongata.
These impulses cause
parasympathetic neurons via the
vagus nerves to stimulate
secretion of HCl, pepsinogen and
mucus in the stomach.
The parasympathetic stimulation
also results in secretion of
gastrin from the lower part of
the stomach.
Gastrin travels through the
bloodstream and further
stimulated HCl and pepsinogen
secretion in the upper and
middle part of the stomach.
100. Gastric Phase:Gastric Phase:
Food has entered and
distended the stomach. The
pH of the stomach is also
altered because protein has
entered the stomach and
buffered some of the stomach
acid causing a low pH.
This distention activated a
parasympathetic reflex via the
medulla oblongate, and also
has a direct stimulatory effect
on the gastric glands. The
result is the continued
secretion of HCl and
pepsinogen.
Negative feedback control of
acid secretion is done by
somatostatin. As the contents
of the gastric lumen become
more acidic, the stimuli that
promote acid secretion
decrease.
101. Intestinal phaseIntestinal phase
Chyme has entered the duodenum so
gastric secretion is no longer needed.
When the chyme contains lipids from
the digestion of fats or contains enough
HCl to bring its pH to below 2, gastric
secretion is inhibited.
The lipid and hydrogen ions inhibit
gastric secretion by three simultaneous
actions.
They cause impulses to go to the
medulla oblongata to decrease
parasympathetic stimulation of
gastric glands
They set up local reflexes, via
neurons in the wall of the gut,
that decrease gastric secretion.
They cause the release of three
local hormones collectively called
enterogastrones (secretin, CCK
inhibitory peptides) which travel
via the circulation to the gastric
glands and inhibit their secretion.
103. After food enters the stomach, gentle, rippling, peristaltic
movements called mixing waves pass over the stomach
every 15-25 seconds.
These waves macerate food, mix it with gastric juice and
reduce it to a soupy liquid called chyme.
As digestion proceeds, more vigorous mixing waves begin
at the body of the stomach and intensify as they reach the
pylorus.
As food reaches the pylorus, each mixing wave forces
several milliliters of chyme into the duodenum through
the pyloric sphincter.
Most chyme is forced back into the body of the stomach
where mixing continues.
104. The next wave pushes the chyme forward again and forces a little
more into the duodenum.
These forward and backward movement of gastric contents are
responsible for most mixing in the stomach.
The rhythm of gastric waves are generated by pacemaker cells in
the longitudinal smooth muscle layer.
These smooth muscle cells undergo spontaneous depolarization-
repolarization cycles (slow waves) known as basic electrical
rhythm of the stomach.
These slow waves are conducted through gap junctions along the
stomach’s longitudinal muscle layer and also induce similar slow
waves in overlying circular muscle layer.
105.
106. Slow wave oscillations in the membrane potential of
gastric smooth muscle fibers trigger bursts of action
potentials when threshold potential is reached at the
wave peak.
Membrane depolariztion bring the slow wave closer
to threshold. Increasing the action potential
frequency and thus the force of smooth muscle
contraction.
107. Regulation of Gastric EmptyingRegulation of Gastric Emptying
Stimulation of gastric emptying:
Gastric emptying, the periodic release of chyme from the stomach into
the duodenum, is regulated by both neural and hormonal reflexes, as
follows:
1. Stimuli (distention of the stomach, presence of partially digested
proteins, alcohol and caffeine) initiate gastric emptying.
2. These stimuli increase the secretion of gastrin and generate
parasympathetic impulses in the vagus (X) nerves.
3. Gastrin and nerve impulses stimulate contraction of the lower
oesophagus sphincter, increase motility of the stomach and relax the
pyloric sphincter.
4. The net effect of these actions is gastric emptying.
108. Inhibition of Gastric emptying
Inhibition of Gastric emptying is controlled by the enterogastric
reflex and CCK.
1. Stimuli (distention of the duodenum and the presence of fatty
acids, partially digested proteins and glucose) in the duodenal
chyme initiate gastric emptying.
2. These stimuli the enterogastric reflex: Nerve impulses propagate
from the duodenum to the medulla oblongata, where they inhibit
parasympathetic stimulation and stimulate sympathetic activity in
the stomach. The same stimuli also increase secretion of CCK.
3. Increased sympathetic impulses and CCK both decrease gastric
motility.
4. The net effect if these actions is inhibition of gastric emptying.
111. The proteolytic enzymes are secreted in inactive
forms (zymogens) and then activated in the
duodenum by other enzymes.
Activation is acquired in steps and is catalyzed by
enterokinase. This is embedded in the luminal
plasma membrane of the intestinal epithelial cells.
Proteolytic enzymes splits off a peptide from
pancreatic trypsinogen thus forming the active
enzyme trypsin
112. When activated trypsin which is also a proteolytic
enzyem similarly splits off peptide fragments and in so
doing activates the other pancreatic zymogens (this is
in addition to its role in protein digestion).
Note bicarbonates function is to neutralize acid
entering the deodenum from the stomach.
Also CCK responsible for the secretion of enzymes,
(inclusive of those for fat, and protein digestion).
CCK’s release is dependent on the levels/presence of
fatty acids and amino acids in the duodenum
113. Glucagon, Insulin and Blood Glucose
Regulation
The islets of Langerhans (clusters of emdocrine cells)
secrets these two peptide hormones.
Insulin
Secreted by beta cells of islets of Langerhans within
the pancreas when blood glucose level.
Stimulates the uptake of glucose from the blood
stream and does this by increasing the transport of
glucose from the blood to muscle cells and
adipocytes. Also a net uptake of glucose by the liver.
114. Insulin secretion and subsequently signaling leads to
the movement of a glucose transport protein GLUT 4
from the intracellular vesicles to the cell membrane.
(*)
Once in the cell membrane the GLUT4 protein allows
more glucose to enter the cell thus lowering the blood
glucose level.
Note insulin secretion is not only dependent on blood
glucose levels. Secretion is also dependent on:
Elevated amino acid concentration
Hormonal controls
The autonomic neurons to the islets of Langerhans
115.
116.
117. Glucagon
Secreted by the alpha cells of Langerhans within the
pancreas at low blood glucose levels also by neural
and hormonal inputs to these islets.
Stimulates the release of glucose to the blood stream.
It binds to specific receptors to set off a chain of
events which makes glucose available i.e.
Increased glycogenolysis (glycogen break down
Increased gluconeogenesis
Increases in the synthesis of ketones
118. BILE SECRETION AND LIVER
FUCTION
Bile is secreted by liver cells into a number of small
ducts (the bile canaliculi which converge to form the
common hepatic duct.
Note bile salts and lecithin are synthesized in the liver
and helps to solubilize fat in the small intestine
Where as cholesterol, bile pigments and trace metals
are extracted from the blood by the liver and excreted
via the bile.
Bicarbonate ions neutralize acid in the duodenum
119.
120.
121. When fatty meals are being digested most of the bile salts
entering the intestinal tract via bile are absorbed by
specific sodium-coupled transporters in the ileum.
Absorbed bile salts are returned via the portal vein to the
liver where they are secreted once again.
Bile salts uptake from portal blood into hepatocytes is
driven by secondary active transport coupled to sodium
Cholesterol homeostasis in the blood and the process by
which cholesterol –lowering drugs work is maintained by
the secretion of bile followed by the excretion of
cholesterol in feces.
122. Bile pigments are substances formed from the heme
portion of hemoglobin when digestion of old or damaged
erythrocytes occurs in the spleen and liver.
Bile components are secreted by two different cells, they
are:
Hepatocytes which secrets bile salts and pigments, lecithin.
Epithelial cells which secrets most of the bicarbonate rich salt
solutions
Secretion of the salt solution by the bile ducts is
stimulated by secretin in response in response to acidity in
the duodenum.
Note the secretion of bile salts is controlled by the
concentration of bile salts within the blood
123. The liver is always secreting bile however, greater
secretion occurs at meal times (during and just after).
The sphincter of oddi is a ring of smooth muscles
surrounding the common bile duct at the point at
which it enters the duodenum. When closed the
diluted bile secreted by the liver is shunted into the
gallbladder. It is at this point the organic components
of bile (water and sodium chloride) are absorbed into
the blood
125. Secretion
Intestinal epithelium secretes mineral ions such as,
sodium, chloride and bicarbonate ions into the lumen
and water follows by osmosis.
Chloride is the primary ion that determines the
magnitude of fluid secretion.
Various hormonal ,paracine signals as well as toxins
and bacterial toxins can increase the frequency of these
channels and fluid secretion.
Water movement into the lumen occurs when the
stomach is hypertonic, this then causes osmotic
movement of water.
126. Absorption
All fluid secreted by the small intestine is absorbed
back into the blood.
Large volumes of fluid which includes, salivary, gastric,
hepatic, pancreatic secretions and ingested water is
simultaneously absorbed from lumen into the blood.
There is a large net absorption of water from small
intestine.
Absorption is achieved by transport of ions mostly
sodium from lumen into the blood with water followed
by osmosis.
127. Motility
Stationary concentration and relaxation of intestinal
segments occurs during the digestion of a meal.
Each contracting segment is a few cm long and the
digestion last for a few seconds.
Chyme in the lumen is forced up and down the
intestine.
Segmentation- the rhythmical contraction and
relaxation of the intestine.
Mixes the chyme in lumen and bringing it into
contact with intestinal wall.
128. Segmentation movement
-initiated by electrical activity by
pacemaker cells with circular smooth
muscle layer.
-intestinal basic electrical rhythm
produces oscillations in the smooth
muscle membrane potential. If
threshold is reached action potentials
are triggered that increase muscle
contraction.
-the frequency of segmentation is set
by the frequency of the intestinal basic
rhythm
-unlike the stomach that has a single
rhythm 3 mins/sec intestinal rhythm
varies along the length of the
intestine.
-each successive region have a
slightly lower frequency than the
129.
130.
131. Motility
Produces a slow migration of the intestinal contents
toward the large intestine.
Segmentation intensity can be altered by hormones:
Enteric nervous system and autonomic nerves.
Parasympathetic activity increases the force of
contraction.
Sympathetic stimulation decreases it.
132. Migrating myoelectric complex
Begins in the lower portion of stomach.
Repeated waves of peristaltic activity.
Moves any undigested material remaining in the small
intestine into the large intestine that is long enough to
grow and multiply excessively.
Rise in plasma concentration of intestinal hormone
MOTILIN initiates MMC.
Motilin stimulates MMCs via both the enteric and
autonomic nervous system.
133. Motility
Contractile activity in certain regions of the small
intestine can be altered by reflexes.
Eg, segmentation intensity in the ileum increases
during periods of gastric emptiness (gastroileal reflex)
Intestino intestinal reflex lead to complte cessastion of
motility.
134.
135. Large Intestine
6.5CM in diameter, 1.5m long
First portion Cecum
Cecum forms a blind ended pounch that extends to
appendix
COLON: 3 SEGMENTS
Ascending
Transverse
Descending (forms sigmoid colon)
Function –is to store and concentrate faecal material
before defecation.
136. Large intestine
Chyme enters the cecum through the ilocecal
sphincter.
Sphincter relaxes each time the terminal portion of
the ileum contracts.
Chyme enters the large intestine.
The primary absorptive process in the intestine is
active transport of Na+ from lumen to blood. Also
osmotic absorption of water.
There is a net movement of K+ from blood into the
large intestine lumen. Stimulated by cAMP
137. Motility &Defecation
Contraction of circular smooth muscle produce
segmentation motion.
Slower than small intestine
Following a meal a wave contraction known as mass
movement spreads over transverse segment of intestine
to rectum
Unlike a peristaltic wave in the small intestine, the
smooth muscle in the intestine remains contracted for
some time after mass mov’t
Parasympathetic input increases segmental
contractions whereas sympathetic input decreases
colonic contractions
139. DEFINITION
Peptic Ulcer Disease (PUD)= These are areas of tissue
degradation that can be caused by increased acid and
pepsin or impaired mucosal defenses such as
decreased bicarbonate secretions.
Ulcers are normally found in the stomach (gastric),
duodenum (duodenal) and oesophagus (oesophagal).
140.
141. Common Risk Factors for Gastric
Mucosal Disruption
Associated with Helicobacter pylori.
Alcohol
NSAID- Induced gastritis or ulcers are frequently
“silent”.
Corticosteroids
Tobacco
Coffee/ Caffeine
146. Vomiting
Vomiting is the forceful expulsion of the contents of
the stomach and upper intestinal tract through the
mouth.
It is a complex co-ordination by a region in the
brainstem, the medulla oblongata.
147.
148. Causes of Vomiting
Gastric contents get into the respiratory tract
Food poisoning
Overeating
Concussion
Vomiting can be induced by stimulation of the
chemoreceptor zone, vestibular apparatus and the GI tract
150. Diagnosis
Blood Tests- to check electrolytes and blood cell
count
Urinalysis- to check for dehydration and infection
CT Scan- to check for head injuries
X-ray
151. Treatment
Most of the time, vomiting go away on their own and
could be managed at home.
If vomiting occurs, fluids are given by the mouth or
through a vein into the bloodstream.
152. Gallstones
Gallstones are solid particles that form from the bile
in the gallbladder. There are two types of them: 1.
Cholesterol Stones and 2. Pigment Stones.
Gallstones can be any size, from as tiny as a grain of
sand to large as a golf ball.
153.
154. Problems of Gallstones
Gallstones within the gallbladder often cause no problems. If
they are too large or too many, they cause extreme pain. They
may also cause problems if they move out of the gallbladder.
If there movements lead to blockage of any of the ducts
connecting the gallbladder, liver or pancreas with the intestine,
serious complications may occur.
Blockage of a duct can cause bile or digestive enzymes to be
trapped in the duct.
If these conditions go untreated, they can even cause death.
155. Gallstone Causes
The stones form when the amount of cholesterol or
bilirubin in the bile is high.
Pigment stones form most often in people with liver
disease or blood disease, who have high levels of
bilirubin.
Poor muscle tone may keep the gallbladder from
emptying completely. The presence of residual bile
may promote the formation of gall stones.
156. Risk Factors for the Formation of
Gallstones
Female Gender
Being Overweight
Losing a lot of weight quickly on a starvation diet
Taking of certain medications such as birth control
pills or cholesterol lowering drugs.
157. Treatment
Intake of only clear liquids to give the gallbladder a
rest.
Avoid fatty or greasy meals.
Use of painkillers.
Use of drugs made with bile acids.
Gallstone surgery called Cholecystectomy.
160. Lactase
Enzyme
Embedded in luminal plasma membranes of intestinal
epithelial cells
Present at birth
Production decreases after 2 yrs
Lactose intolerance- inability to digest lactase.
161. Increases concentration in small intestine
Decreases osmotic gradient, therefore, water retained
in lumen.
Lactose-containing fluid moves to large intestine
bacteria digests lactose metabolizes
monosaccharides
produces gas & short chain fatty acids
162. Gas distends colon and produces pain
Short chain fatty acids draws water into intestinal
lumen which leads to diarrhea
Lactose intolerance causes mild discomfort to severe
dehydrating diarrhea
Solution: lactose free products/lactase tablets
165. Crohn’s Disease
Occurs anywhere along GI tract (mouth–anus)
Most common at the end of the ileum
Inflammation and thickening of bowel wall
causes narrowing or blockage of lumen and
hence, pain
1st
symptoms – pain in lower right abdomen &
diarrhea (sometimes fever)
Often mistaken for acute appendicitis
Relief: defecation (temporary)
166. Colitis
Confined to colon
Caused by disruption of normal mucosa with
bleeding, edema & ulcerations
In an extreme case bowel wall thins and tissue lost, so
holes break bowel wall
Symptoms: diarrhoea , rectal bleeding,
abdominal cramps
167. IBD con’t
Most common in caucasians (late teens to early 20’s
and > 60)
Caused by environmental and genetic factors
As a result of weak immune system and poor tissue
repair
Responses to normal microorganisms in intestinal
lumen
168. Treatment
Initially – 5-aminosalicylate drugs
e.g. sulfasalazine antibacterial &
anti-inflammatory
effect
In severe case – glucocorticoids or removal of
diseased bowel
New drug therapy – immunosuppressive medicines
Diet changes aid in healing
(NB: overuse of glucocorticoids may cause bone loss)
169. CONSTIPATION AND
DIARRHEA
Common Belief: Unless you have a bowel
movement everyday, ‘toxic’ substances from fecal
matter (in large colon) will poison you!
WHAT DO YOU THINK???
170. Toxic agents after a prolonged period of time – still to
be discovered
HOWEVER, fecal retention for days or weeks may
lead to:-
Headache
Loss of appitite
Nausea
Abdominal distention
These are all symptoms of CONSTIPATION
171. The longer the fecal matter remains in large intestine,
the more water absorbed, feces become drier and
defecation becomes difficult and painful
Common in the elderly, or anyone with damage to the
enteric nervous system (decreased motility of large
intestine) or emotional stress
Cure –distension from dietary fibre or laxatives
172. Dietary fibre – cellulose & other complex
polysaccharides
- not digested in small intestine, produces
distension in large intestine, leads to motility
- Bran, Fruits, Veggies
Laxatives – increase frequency/ease of defecation
- fiber is a laxative
- mineral oils (lubricate feces)
- Mg & Al salts (epsom salts) (water retention)
- Caster oil (stimulates intestinal tract)
- causes dependence
173. Diarrhea
Large, frequent, watery, stools
Causes:
fluid absorption, fluid secretion
Increased motility caused by distension (not
the other way around!)
Secretory diarrhoea – bacterial, protozoan &
viral diseases (E. coli)
- Cholera and Traveller's
diarrhoea
174. CHOLERA
- Caused by bacteria
Releases toxin that stimulates cyclic AMP
Opens chloride channels
Increase in chloride ions
Increase water content in lumen
Massive life threatening diarrhoea (dehydration,
decreased blood vol.)
175. TRAVELLER’S DIARRHEA
- Produced by several species of bacteria, parasites,
viruses
- Produces secretary diarrhoea (same process at
cholera)
Other consequences of severe diarrhoea are
potassium depletion, metabolic acidosis
176. Treatment
Dehydrating effect can be
balanced by drinking salt-
glucose solution to replace
fluids (by active transport).
Until diarrhoea subsides, a
change is diet can help.
Avoid caffeine, greasy
foods, high fibre foods
and lactose rich foods
Editor's Notes
Insert Process Fig. 24.12 with verbiage. Insert Animation: Hydrochloric Acid Production by Parietal Cells in the Gastric.exe
Insert Process Fig. 24.13 A. Insert Animation: Three Phases of Gastric Secretion.exe
Insert Process Fig. 24.13 B with verbiage. Insert Animation: Three Phases of Gastric Secretion.exe
Insert Process Fig. 24.13 C with verbiage. Insert Animation: Three Phases of Gastric Secretion.exe
The tongue is the only muscle in the body attached at one end
Tongue Held Down Tight
Have you ever wondered what keeps you from swallowing your tongue? Look in the mirror at what's under your tongue and you'll see your frenulum (say: fren-yuh-lum). This is a membrane (a thin layer of tissue) that connects your tongue to the bottom of your mouth. In fact, the whole base of your tongue is firmly anchored to the bottom of your mouth, so you could never swallow your tongue even if you tried!
Thou mayest preserve discretion and that thy lips may keep knowledge Proverbs 5:2
Why you need saliva to taste foods. In order for food to have taste, chemicals from the food must first dissolve in saliva. Once dissolved, the chemicals can be detected by receptors on taste buds.
Saliva also breaks down food caught in the teeth, protecting them from bacteria that cause decay. Furthermore, saliva lubricates and protects the teeth, the tongue, and the tender tissues inside the mouth.
Excessive saliva can be caused by either an increase in your body's production of saliva or a decrease in your ability to swallow or keep saliva in your mouth.
Causes of increased saliva production
Dentures that are new or don't fit well
GERD
Infection in your mouth
Medications, such as clozapine, isoproterenol, pilocarpine and reserpine
Pregnancy
Stomatitis (an inflammation of mucous membranes in your mouth)
Teething
Rarer causes of increased saliva production include the following conditions:
Arsenic poisoning
Bell's palsy (a condition that causes facial muscle weakness or paralysis)
Esophageal atresia (a disorder present at birth in which the esophagus doesn't develop properly)
Mercury poisoning
Rabies (a deadly virus spread to people from the saliva of infected animals)
Syphilis (a bacterial infection usually spread by sexual contact)
Tuberculosis (an infectious disease that affects your lungs)
Causes of a decreased ability to swallow or to retain saliva in your mouth
Acute sinusitis
Allergies
Enlarged adenoids
Tumors that affect your tongue or lip movement
Conditions that affect your muscle coordination or the function of your oral cavity also may decrease your ability to swallow or to retain saliva in your mouth. These conditions include:
Autism
Cerebral palsy (a disorder that affects your ability to coordinate body movements)
Down syndrome
Multiple sclerosis (a disease in which your body's immune system attacks the sheath that covers your nerves)
Parkinson's disease
Stroke
“Food going down the wrong hole” Trachea( respiratory syst.)
You have 2 tubes connected to your mouth. One is your oesophagus, the normal route for food, the other is your trachea which is involved in respiration.There are several safety mechanisms present to prevent food/drink going down the wrong way. The first is a skin flap at the back of your throat called the epiglottis. This covers your trachea when you swallow food. On top of your trachea is your larynx, which contains your vocal cords. These cords will close and go into spasm if food/water gets to them. Finally if the food/water gets into your trachea, you have a cough reflex which should expel it.
Sensory Nerves
Nerve signals originating in the mouth bring information to the brain about the food we are chewing. For instance they "tell" the brain about the size, temperature and texture of food. This information directs the efforts of the muscles of chewing which work together to generate a food bolus that is suitable for swallowing. As the swallowing reflex advances through its different phases, these nerves trigger the reflexive closing of the larynx and the epiglottis, which prevent food and liquid particles from entering the lungs.
swallowing is one of the most complicated tasks performed by the nervous system. It occurs in three sequential phases that require the carefully coordinated function of muscles in the mouth, pharynx, larynx and esophagus -- all of which are under the control of cranial nerves.
sensory nerves involved in swallowing:
Trigeminal (cranial nerve V)
Facial (cranial nerve VII)
Glossopharyngeal (cranial nerve IX)
Vagus (cranial nerve X)
Cranial Nerve Nuclei
The muscles of swallowing are controlled by several cranial nerve nuclei. These are:The nucleus ambiguous (of the vagus and glossopharyngeal nerves)
The dorsal motor nucleus (of the vagus nerve)
The hypoglossal nucleus (of the hypoglossal nerve)
The nasopharynx (epi)(nasal part of the pharynx) is the uppermost part of the pharynx. It extends from the base of the skull to the upper surface of the soft palate;[1] it differs from the oral and laryngeal parts of the pharynx in that its cavity always remains patent (open).
The Oropharynx(meso) (oral part of the pharynx) reaches from the Uvula to the level of the hyoid boneThe Laryngopharynx (hypo)the portion of the pharynx below the upper edge of the epiglottis, opening into the larynx and esophagus
The esophagus is 25cm long.
From the mouth, the bolus is passed through the pharynx into the esophagus.
The esophagus conducts food to the stomach by peristalsis.
Skeletal muscles surround the esophagus just below the pharynx and form the upper esophageal sphincter.
Smooth muscles in the last portion of the esophagus form the lower esophageal sphincter.
Achalasia-decreased mobility of the lower 2/3 of the esophagus along with constriction of the LES
2)Heartburn can occur after a large meal, which can raise the pressure in the stomach enough to force acid into the esophagus.
Gastro-esophageal reflux can also cause coughing and irritation of the larynx in the absence of any esophageal symptoms.
5) The acid in the esophagus triggers a secondary peristaltic wave and also stimulates increased salivary secretion.
This helps to neutralize the acid and clear it from the esophagus.
The enzymes secreted by the pancreas digest respectively:
Fat
Polysaccharides
Proteins
Nucleic acids to fatty acids
Sugars
Amino acids
Nucleotides
Zymogen secretion protects pancreatic cells from autodigestion
Note pancreatic secretion increases during a meal, mainly as result of stimulations by hormones secretin a primary stimulant of bicarbonate secretion. Secretin major stimulus is the acidity of the deodenum
The afferent nerve ending of the intestinal wall is acted upon by luminal and fatty acids which initiates reflexes that acts on the pancreas thus increasing both enzyme and bicarbonate secretion.
Note cephalic and gastric stimuli also play a role in the pancreatic exocrine secretion. This is possible by way of the parasypathetic nerves to the pancreas. Therefore the taste of foods or the distension of the stomach by food will lead to increased pancreatic seceretion.
(*)It is for this effect insulin is best known. Failure of glucose transport is the main characteristic of and the acute risk associated with diabetes
Where amino acid concentration increases in the blood after ingestion of a protein containing meal. Therefore increasing plasma glucose which stimulates the uptake of these amino acids by the muscle an other cells thereby lowering their concentration.
In the case of hormonal control an example would be GIP (glucose-dependent insulinotropic peptide) which is secreted by endocrine cells in the GI tract in response to eating stimulates insulin secretion. With this mechanism insulin is secreted earlier and therefore not dependent on blood glucose level only thus avoiding peaks in the blood glucose concentration (for example just after meal time)
Its major physiological effects are in the liver and opposes those of insulin
The end result of these chain of events would be increased plasma concentration of glucose and ketones which are important for the postabsorptive period and to prevent hypoglycemia.
Note bile contains six major ingredients these are:
Bile salts
Lecithin (a phospholipid)
Cholesterol (The liver also secrets cholesterol from the blood into bile)
Bile pigment and small amounts of other metabolic end products
Trace metals
Bicarbonate ions and other salts
A small cross section of the liver showing the location of the bile canaliculi and ducts with respect to blood and liver cells. The bile (green) is formed by uptake by liver cells (hepatocyte) of bile salts and secreted into bile canaliculi
The cyclic pathway of bile salts is known as enterohepatic circulation
Note a small amount of bile salts escapes during is cycle and is lost in feces. This however, does not hamper bile’s most important component as the liver synthesizes cholesterol to replace them.
The predominate bile pigment is bilirubin which is yellow in colour thus urine gains it colour from bilirubin. Note while passing through the intestinal tract some bile pigments are absorbed into the blood, others undergo bacterial enzyme modification gaining a brown colour characteristic to that of feces where as, the remainder is excreted via urine.
The sphincter of oddi relaxes shortly after the start of a fatty meal while, the gallbladder contracts discharging concentrated bile into the duodenum.
The hormone CCK (cholecystokinin) is responsible for signaling gallbladder contraction and sphincter relaxation
http://digestive.niddk.nih.gov/ddiseases/pubs/lactoseintolerance/index.aspx
Age group Amount of calcium to consume daily, Age group in milligrams (mg)
0–6 months 210 mg
7–12 months 270 mg
1–3 years 500 mg
4–8 years 800 mg
9–18 years 1,300 mg
19–50 years 1,000 mg
51–70+ years 1,200 mg
Gas - Flatus
Congenital/ secondary or developmental intolerance
Congenital – gene mutation that prevents production of lactase. Happens soon after birth.
Secondary – desiese that destroys the lining of the small intestine along with lactase. (Celiac sprue.)
Aisan’s 100% by age 5. Blacks 70% by age 10.
not the same as lactose deficiency.
Developmental – adult-type hypolactasia. Spoken about above.
DISTENSION – The state of being distended, enlarged, swollen from internal pressure.
IBD- derived form Crohn’s and Ulcerative Colitus
Crohn’s and ulcerative colitus – result form a genetic predisposition to having an inappropiate immune response to infection
Constipation – result of decreased colonic motility. Symptoms produced by over distension of rectum, and not by the absorption of toxic bacterial products
Definition - having a bowel movement fewer than three times per week. ( National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK))
It is a symptom not a disease
For more info: http://digestive.niddk.nih.gov/ddiseases/pubs/constipation/
Can be caused by decreased fluid absorption, increased fluid secretion or both.
Def’n - loose, watery stools. Having diarrhea means passing loose stools three or more times a day. Acute diarrhea is a common problem that usually lasts 1 or 2 days and goes away on its own.
For more info : http://digestive.niddk.nih.gov/ddiseases/pubs/diarrhea/index.aspx