EPOB 3430 1-30-03 This lecture contains the last slide from 1-28-03

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IPHY 3430 1-27-11
Control of saliva secretion
Pressure and chemoreceptors in mouth-->
and/or input from cerebral cortex (thoughts,
smell, sight, sound)--->
Salivary center in
Medulla
PNS
Salivary glands
SNS output from other
centers (a. diminish
blood supply, b)
change composition
Swallowing
1. Voluntary stage--tongue moves bolus back to
back of tongue
2. Involuntary stage-- pressure receptors on
tongue send signal to swallowing centers in
pons and medulla-->
Output of swallowing centers:
1. motor output--a) tongue moves up to hard
palate to prevent food return to mouth
b) uvula elevated to seal off nasal passages
c.Larnyx is elevated and laryngeal muscles
contract vocal folds to seal off trachea.
d. Epiglottis tilted over glottis helps seal off
trachea.
e. After all these motor outputs occur,
pharyngeal muscles contract to force bolus into
esophagus.
2. Swallowing center inhibits inhalation
stimulus from medulla respiratory centers
Accomplishments in the mouth
1.
2.
3.
4.
Increase surface area of food
Moisten and lubricate food
Some carbohydrate digestion
Some pathogens killed
Stomach
1. Store food
2. Continue carbohydrate digestion
3. Begin protein digestion
4. Moisten and mechanical breakdown
5. No absorption of food
6. Some absorption of lipid-soluble
things like alcohol, aspirin, etc.
In oxyntic mucosa
In pyloric gland area
Surface epithelial cells
Gastric
pit
Mucosa cells
Gastric
gland
G cells
Chief cells
D cells
Parietal cells
Enterochomaffinlike (ECL) cells
Table 16-3, p. 596
Stomach secretions
1. More mucus from mucus glands
2. Parietal cell
a. intrinsic factor
b. HCl
3. Chief cell
a. pepsinogen
4. More water
Secretions and stomach contractions caused by
A. Pre-meal and during eating: vagus nerve
B. During eating and post meal
a. Local distension,
b. intrinsic nerve plexi
c. Vagus (to some extent)
d. G-cell (enteroendocrine cell) secretes gastrin
Fig. 16-9, p. 607
Benefits of acidification of stomach
contents:
1. Mechanical breakdown of food
2. Activation of pepsinogen
3. Low pH necessary for pepsin
activity
4. Low pH kills many pathogens
MOVEMENT OF CHYME FROM STOMACH INTO
SMALL INTESTINE
Factors that stimulate stomach emptying:
1. Degree of stomach distension (volume of chyme)
2. Hypotonic chyme
3. High gastrin concentration
Factors in duodenum that inhibit stomach emptying
(signaled to stomach by intrinsic nerve plexus and
secretin and cholecystokinin)
1. High acidity of chyme
2. High fat content of chyme
3. Hypertonic chyme
4. High distension of small intestine
5. High concentration of amino acids and/or fatty acids
ACCOMPLISHMENTS IN THE STOMACH
1. Some carbohydrate breakdown
2. Some protein breakdown
3. Most if not all pathogens killed
4. Chyme highly liquified
SMALL INTESTINE
1. Complete enzymatic breakdown
2. Almost complete absorption of
nutrients
The presence of chyme on intestinal wall
causes secretion of the following hormones:
1. Secretin
2. Cholecystokinin
SECRETIN
Target glands:
1. Stomach--inhibits emptying and secretions
2. Pancreas-causes release of aqueous NaHCO3
In small intestine
NaHCO3 + HCl --> NaCl + H2CO3 -->
NaCl + CO2 + H20
CHOLESYSTOKININ
Target organs:
a. Gall bladder--causes it to contract and release bile
b. Pancreas--causes release of aqueous solution
containing:
1.  amylase (carbohydrate)
2. Trypsinogen (protein)
3. Chymotrypsinogen (protein)
4. Procarboxypolypeptidase (protein)
5. Lipase (fats)
c. Stomach-inhibits gastric motility and secretion
d. Brain--regulation of food intake
WHEN PANCREATIC SECRETIONS
REACH SMALL INTESTINE VIA BILE
DUCT:
1. Enterokinase secreted by small intestine
wall activates trypsin from trypsinogen
2. Trypsin activates chymotrypsin from
chymotrypsinogen
3. Trypsin activates carboxypolypeptidase
from procarboxypolypeptidase
BILE
Synthesized by liver, stored in gall bladder
1.
2.
3.
4.
5.
6.
Water
Bilirubin
Cholesterol
Ions (Na, K, Cl)
Bile salts
Lecithin
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