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Physiology
II
What are
the main influences that will start motility (3)?
contact,
distension, irritation
cephalic
phase of secretion--thinking of food causes salivation
basal
rhythm--continuous movement of GI tract, clears mucous and acid, even while you
are sleeping
--sphincters
relax while you are sleeping
Movement
mouth--chew--voluntary
and involuntary, salivation
Sjorngien's Syndrome--autoimmune disorder,
salivary and lacrimal glands disrupted--can't taste
pharyngeal
receptors--up to this point, you still have voluntary control
peristalsis--2
types of muscles, longitudinal and circular
Receptive
relaxation--relaxation of the next section that is not ready to receive the
bolus
Megaesophagus
(Achalasia)--failure of receptive relaxation at the cardiac sphincter--food
backs up in the esophagus and stretches it
Stomach--storage
organ, initiates the first part of digestion, food accumulates in stomach
around the walls, begins motility, begins in fundal region, and moves downward
and builds strength, mixes w/ acid, h20, mucous producing chyme (an acid milk
shake) controls the fxn of the rest of the GI tract--gastric emptying--motility
and rate of absorption in small intestine--pyloric sphincter, strongest
sphincter in the body, almost acts as a barrier prevent acid from moving into
small intestine, and aides in churning the stomach (retro propulsion)
dumping syndrome--after
abdominal surgery, everything moves from the stomach into small intestine
-deliver
in small amounts to aide in digestion and absorption along w/ neutralizing the
acid
Small
Intestine--pockets of constriction, have control if too much is dumped into the
small intestine under enteric control--Enterogastric reflex--starts in small
intestine and goes to the stomach--too much distension or irritation, slows
down the stomach
(segmented
movement of peristalsis)
Large
Intestine--
constipation--reduced
colonic motility
colon
when becomes over filled, no reason to continue filling small intestine
colonoilio
reflex--colon is too full, reduces motility of small intestine, reduces
emptying into small intestine
lipid
slows down the motility
gatrocolic
reflex--cleans out colon shortly after eating to make room for what was just
eaten
other
nervous systems augment the GI system
iliocecal
valve--2 flap valve, when contents of large intestine backup, it closes
appendix--at
about the same point as iliocecal valve
Large
Intestine--walled off segments (Haustra), fluid--pull out water and some
minerals
-compartmentalized,
turned over for water absorption
-becomes
more solid as moves into transverse colon and so on
Native
Japanese--large amount of stomach cancer
little colon cancer
Immigrant
Japanese--a little less stomach cancer
more colon cancer
1st
generation Japanese--little stomach cancer
more colon cancer
Americans--little
stomach cancer
high colon cancer
motility
is important for reduction of neoplasms in colon--gets rid of yucky stuff
colon--mass
movements
defecation
reflex--rectum is full, musts be emptied soon
voiding
is augmented by parasympathetic nerves
SECRETION
-mucous,
enzymes (substrate, proper environment), hormones (communicating molecule)(4
hormones--gastrin from the stomach, CCK (Chole cysto kinin) from duodenum for
big junks of protein and lipid, Secretin from duodenum for acid, Gastric
inhibitory peptide (GIP) duodenum to slow down gastric activity
G
cells--in antrial portion of stomach, monitor protein segment
size--inappropriate digestion, limits emptying
Gastrin--stimulate
gastric pits to pepsid and HCl
CCK--produced
by I cell, below pylorus, a lot of lipid leaving stomach, slows down gastric
emptying, lipid is difficult to absorb so takes longer
-stimulates enzyme releasing areas of
pancreas, acniar
Secretin--S
cells in response to too much acid
2 things
1.
reduces gastric emptying
2.
release bicarbonate, Ductual cells of pancreas
3 Phases
of Secretion
1. Cephalic--mouth watering thought
stimulus--vagus response, chewing,
swallowing, smell, taste
stimulate
at parietal cell--Ach
peptic
cell (Chief cell)--produce pepsinogen, inactive protease (enzymes are released
as an inactive enzyme) goes up the pit to parietal cell (produces HCl and
intrinsic B12) HCl activates pepsinogen to produce active pepsin
neck cell
secrete mucous, dense and viscous protects against autodigestion
peptic
ulcer--digestion of gastric lining
-wound must be present before bacteria
invade and cause them to enlarge
HCl acts
in digestion by breaking into smaller pieces but necessarily individual amino
acids
Tributyrase--short
chain fatty acids
Collaginases--breaks
up collagen fibers, protein connective tissue
40%
carbohydrate broken down in stomach
Ach aides
in HCl release
2. Gastric
3. Intestinal