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DT 53
1. MUCOSA:
epithelium
lamina propria:
muscularis mucosae
exocrine cells
endocrine/paracrine cells
2.SUBMUCOSA
connective tissue,
blood vessels, glands
submucosal plexus
(Meissners plexus)
SUBMUCOSAL PLEXUS
(MEISSNERS PLEXUS)
MYENTERIC PLEXUS
(AUERBACHS PLEXUS)
CIRCULAR MUSCLE
LONGITUDINAL MUSCLE
3.MUSCULARIS EXTERNA
smooth muscle cell layer
inner circular layer
outer longitudinal layer
myenteric nerve plexus (Auerbachs plexus)
4.
SEROSA
(adventitia)
Movement of materials along the digestive tract is
controlled by:
Hormonal mechanisms
Enhance or inhibit smooth muscle contraction
Neural mechanisms
ANS- Parasympathetic nerves(Vagus nerve,
Pelvic n.) - Sympathetic nerves (T6-12)
Enteric nervous system
- Submucosal plexus
- Myenteric plexus, receptors
Local mechanisms
Coordinate response to changes in pH or
chemical stimuli
Control of the digestive system
Intrinsic Nervous System
(gut brain)
Nerves that interconnect within GI organs and
plexuses, independent of the autonomic system.
Auerbachs, Meissners plexus contribute!
Receptor neurons are sensory (detect stretch,
damage), effector neurons are motor (cause SM
contraction)
Excitatory NTs- Ach, Subs.P ( contraction )
Inhibitory NTs- VIP , NO (relaxation of smooth
muscle)
The rate of basal electric rhyth (BER) is about
4/min in the stomach.It is about 12/min in the
duodenum and falls to about 8/min in the distal
ileum.
After vagotomy of the stomach wall, peristalsis in
the stomach becomes irregular .
MMC (migrating motor complex or interdigestive
myoelectric motor complex ) : tnnn antrum n:
ileum, tn nluz ::::w: :u aaw:w: az ::anaw:ua::wu ntu a
Deglutition (swallowing) begins as voluntary
activity
Oral phase is voluntary & forms a food bolus
Pharyngeal & esophageal phases are involuntary &
cannot be stopped
To swallow, larynx is raised so that epiglottis covers
continued
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ileum, tn nluz ::::w: :u aaw:w: az ::anaw:ua::wu ntu a
:uu::nuaw:
Peristalsis tn nu uluz ::u auaw:
Mastication (chewing) mixes food with saliva
which contains salivary amylase
An enzyme that catalyzes partial digestion of starch
To swallow, larynx is raised so that epiglottis covers
entrance to respiratory tract
A swallowing center in medulla orchestrates
complex pattern of contractions required for
swallowing
Mechanisms of Swallowing Reflex
ORAL PHASE
PHARYNGEAL PHASE
ESOPHAGEAL PHASE
Voluntary pushing of the food by the tongue
Swallowing. Breathing stops.
Epiglottis blocks trachea. UES
relaxes and superior constrictor
muscles of pharynx contract
starting Peristaltic wave.
Bolus passes UES, UES constricts
(reflex). Primary peristalsis wave
starts 3 to 5 cm/sec. If esophagus is
not distended enough a second
wave initiates( secondary peristalsis
wave).
Afferents by V, IX, X
Efferents by XII, IX, V and X
Esophagus connects pharynx to stomach
Upper third contains skeletal muscle
Middle third contains mixture of skeletal & smooth
Terminal portion contains only smooth
Passes through diaphragm via esophageal hiatus
continued
18-22
1
o
Peristalsis:
Initiated by
n auv aaau(Salivary glands )
- 3 n lnq q: Parotid gland (ln nn avuan avnv a);
Glossopharyngeal nerve,
Submandibular gland ( ln sanvv1nva a4 )& Sublingual gland ( ln a v )tau4
nuFacial nerve
Medical events can alter composition of saliva
Congenital xerostomia (absence of saliva )
Sjogrens syndrome ;atrophy of the glands&
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Initiated by
swallowing (not after
vagotomy)
2
o
Peristalsis:
Caused by residual
food in esophagus
Vagal nuclei run the
show (ambiguus,
DMN)
Sjogrens syndrome ;atrophy of the glands&
decreased salivation
Digitalis increased concentration of calcium &
potassium in saliva
Addisons disease- increased salivary sodium
Cushings syndrome, aldosteronism, pregnancy -
decreased salivary sodium
Tumors of mouth or esophagus, Parkinsons disease
- excessive salivation
Peristalsis propels
food thru GI tract
= wave-like muscular
contractions
After food passes
into stomach, the
gastroesophageal
sphincter constricts,
preventing reflux
continued
Fig 18.4
18-23
ORAL CAVITY
NEUROLOGICAL CONTROL
Hormonal Control
- Gastrin nv:n vnavtnaav1na nv:tna:a a4tvasv
- Secretin, Cholecystokinin (CCK) uuu4navtnaav1na nv:tna:a a4s aa4
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++
++
E
pH<2 at antrum
GIP,Secretin,CCK
FUNCTION
tnaaunv:tna:
(HCO
3
-
)
+HCL
PEPSIN
-u auvnv
activity pH<3
tnua:un
navna4av
sa4enzyme
nnsuvt B12
naun u
navna4nvn
GASTRIN
Ca
K
H
PROTEIN
KINASES
HISTAMINE
GS
AC
ATP cAMP
ACETYLCHOLINE
Ca
PROSTAGLANDINS
GI
muscarinic H2
CCK2
E2
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&
ECL cells { EntercChromaffin- like },
- Parasympathetic activation
of gastric motility & gastric juice secretion
Gastric phase of gastric-acid secretion
Intestinal phase of gastric-acid secretion
Can be mediated by enteric NS & paracrines; &
regulated by ANS & hormones
Gastroileal reflex refers to increased motility of
ileum & movement of chyme thru ileocecal
sphincter in response to increased gastric
activity
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activity
Ileogastric reflex decreases gastric motility in
response to distension of ileum
Intestino-intestinal reflex causes relaxation of
rest of intestine when any part is overdistended
PANCREATIC AND BILLIARY SECRETIONS
Acinar cell na4 Enzyme
compartment ( Amylase, Lipase,
Trypsinogen, Chymotrypsinogen.)
- nnnv:n vnu CCK > Vagus
nerve > Gastrin
Pancreatic interlobular duct cell
na4v a ua: electrolyte ( bicarbonate )
- nnnv:n vnu Secretin > CCK
HCO3- + H+ = H20 + CO2
CCK
Secretin
HCO
3
Cl
Fluid secretio
gallbladder
bile
digestive
enzyme secre
Pancreas
emptying
bile volume
Fat in
duodenum
Low pH
in
duodenum
weak effect
Major digestive enzymes: acinar cells
- amylase
- lipase, colipase
- prophospholipase
- trypsinogen (autocatalytic)
- trypsin inhibitors
- chymotrypsinogen
- proelastase
- procarboxypeptidase
- RNAase, DNAase
Cleave peptide bonds
Hydrolyze DNA/RNA
Categories of Pancreatic Enzymes
Proteases
Nucleases
Bile production
Salts emulsify fats, contain pigments as
bilirubin
Storage
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Hydrolyze DNA/RNA
Collagen digestion
Phospholipids to fatty acids
Triglycerides to fatty acids+
glycerol
Starch to maltose + glucose
Nucleases
Elastases
Phospholipases
Lipases
Amylase
Storage
Glycogen, fat, vitamins, copper and iron
Nutrient interconversion
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
Bile acids are derivatives of cholesterol.
Primary bile acids made in liver, converted to
secondary bile acids by enteric bacteria
95% of bile acids are absorbed by ileum.
Principal bile acids are:
Cholic acid.
Chenodeoxycholic acid.
Combine with glycine or taurine to form bile salts.
Bile salts aggregate as micelles.
Bile pigment
Free bilirubin combines with glucuronic acid and
forms conjugated bilirubin.
Secreted into bile.
Converted by bacteria in intestine to urobilinogen.
Urobilinogen is absorbed by intestine and enters
the hepatic vein.
Recycled, or filtered by kidneys and excreted in
urine. ( forms urobilin by oxidation on exposure
to air )
Urobilinogen enter the faeces darkening them
( refered to as stercobilinogen, which is oxidized to
stercobilin on exposure to air).
Absorption mechanism of monosaccharides
Digestion by brush border enzymes occurs in close vicinity
to monosaccharide transporters.
Glucose and galactose: SGLT1
absorption via a secondary active (uphill), Na-dependent transport
Fructose: GLUT5
absorption by facilitated (carrier mediated), Na-independent mechanism
ATP
Na +
Galactose
Glucose
Fructose
Brush
border
K +
2 GLUT5
mucosal
capillaries
GI tract
lumen
SGLT1 sodium-glucose transport protein1 for glucose and galactose
(secondary active transport)
GLUT5 transport protein rather specific for fructose (facilitated transport)
GLUT2 transport protein for glucose, fructose and galactose across
basolateral membrane (facilitated transport)
Galactose
Glucose
Na +
Fructose
GLUT2
SGLT1
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Lactose intolerance
(hypolactasia)
Decline lactase with age
Lactose fermented in colon
Gas and volatile FA
Water retention
diarrhea
Not all populations
Northern European low
incidence
Asian/African Americans
High
b 1-4 linkage
Proteins
Digestion and Absorption
Digestion
Stomach
peptidases
denature in stomach.
Pancreas and small intestine
hydrolyze with brush border enzymes
cleave between different amino acids
Endopeptidases ( trypsin, chymotrypsin, elastase ) break bonds
in middle of protein
Exopeptidases ( carboxypeptidase, aminopeptidase ) cleave
peptide bonds from ends of polypeptides
Carboxypeptidase - breaks apart carboxyl end of protein
Brush border enzymes aminopeptidases,
carboxypeptidases, and dipeptidases
Proteins Absorption
- small intestine, into blood capillaries
- amino acids by Na+ linked cotransport, di- & tri-peptides by H+
linked cotransport at luminal border
- peptides hydrolyzed in intestinal cell
- amino acids by facilitated diffusion at basolateral membrane
* secreted as inactive precursor moving down concentration gradient
into capillaries then onto the liver
Fats
monoglycerides diffuse into
cells
leave micelles behind
micelles are recycled
until run out of fats
Cholymicrons
coated with protein to
prevent sticking together
combine with apoproteins
- proteins carriers to become
soluble
lipoproteins are made in the
liver = HDL's, LDL's,
VLDL's