Transcript Digestive System Part 3

Digestive System Part 3
Honors Anatomy & Physiology Chapter 23
Regulation of Gastric Secretion
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Neural and hormonal mechanisms
Gastric mucosa  up to 3 L gastric juice/day
Vagus nerve stimulation  secretion 
Sympathetic stimulation  secretion 
Hormonal control largely gastrin
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 Enzyme and HCl secretion
Most small intestine secretions - gastrin antagonists
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Regulation of Gastric Secretion
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Three phases of gastric secretion
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Cephalic (reflex) phase – conditioned reflex
triggered by aroma, taste, sight, thought
Gastric phase – lasts 3–4 hours; ⅔ gastric juice
released
 Stimulated by distension, peptides, low acidity,
gastrin (major stimulus)
 Enteroendocrine G cells stimulated by caffeine,
peptides, rising pH  gastrin
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Stimuli of Gastric Phase
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Gastrin  enzyme and HCl release
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Low pH inhibits gastrin secretion (as between
meals)
Buffering action of ingested proteins 
rising pH  gastrin secretion
Three chemicals - ACh, histamine, and
gastrin - stimulate parietal cells through
second-messenger systems
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All three are necessary for maximum HCl
secretion
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HCl Formation
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Parietal cells pump H+ (from carbonic acid
breakdown) into stomach lumen
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K+ goes into cells to balance charge
HCO3– from carbonic acid breakdown
  blood (via Cl– and HCO3– antiporter)
  blood leaving stomach more alkaline 
Alkaline tide
Cl– (from blood plasma via antiporter) follows H+
HCl
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Figure 23.18 Mechanism of HCl secretion by parietal cells.
Gastric gland
Blood
capillary
Chief cell
CO2
CO2 + H2O
H2CO3
Stomach lumen
Carbonic
anhydrase
H+
K+
HCO3−
Alkaline
tide
Parietal cell
H+-K+
ATPase
H+
K+
HCI
HCO3−
Cl−
HCO3−- Cl−
Interstitial antiporter
fluid
Cl−
Cl−
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Regulation of Gastric Secretion
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Intestinal phase
 Stimulatory component
 Partially digested food enters small intestine 
brief intestinal gastrin release
 Inhibitory effects (enterogastric reflex and
enterogastrones)
 Chyme with H+, fats, peptides, irritating
substances  inhibition
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Enterogastric Reflex
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Three reflexes act to
 Inhibit vagal nuclei in medulla
 Inhibit local reflexes
 Activate sympathetic fibers  tightening of pyloric
sphincter  no more food entry to small intestine
 Decreased gastric activity  protects small
intestine from excessive acidity
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Intestinal Phase
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Enterogastrones released
 Secretin, cholecystokinin (CCK), vasoactive
intestinal peptide (VIP)
 All inhibit gastric secretion
If small intestine pushed to accept more chyme 
dumping syndrome
 Nausea and vomiting
 Common in gastric reduction for weight loss
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Figure 23.17 Neural and hormonal mechanisms that regulate release of gastric juice.
Inhibitory events
Stimulatory events
Cephalic
phase
Gastric
phase
1 Sight and thought
of food
Cerebral cortex
Conditioned reflex
2 Stimulation of
taste and smell
receptors
Hypothalamus
and medulla
oblongata
1 Stomach
distension
activates
stretch
receptors
Vagovagal
reflexes
Intestinal
phase
Stimulate
Inhibit
Vagus
nerve
Local
reflexes
2 Food chemicals
G cells
(especially peptides and
caffeine) and rising pH
activate chemoreceptors
1 Presence of
partially digested
foods in duodenum
or distension of the
duodenum when
stomach begins to
empty
Medulla
Vagus
nerve
Lack of
stimulatory
impulses to
parasympathetic
center
Cerebral
cortex
Gastrin
secretion
declines
G cells
Overrides
parasympathetic
controls
Sympathetic
nervous
system
activation
1 Loss of
appetite,
depression
1 Excessive
acidity
(pH < 2)
in stomach
2 Emotional
stress
Gastrin
release
to blood
Intestinal
(enteric)
gastrin
release
to blood
Stomach
secretory
activity
Enterogastric
reflex
Brief
effect
Local
reflexes
Vagal
nuclei
in medulla
Pyloric
sphincter
Release of
enterogastrones
(secretin, cholecystokinin,
vasoactive intestinal
peptide)
1 Distension
of duodenum;
presence of
fatty, acidic, or
hypertonic
chyme; and/or
irritants in
the duodenum
2 Distension;
presence of
fatty, acidic,
partially
digested food
in the
duodenum
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Gastric Contractile Activity
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Peristaltic waves move toward pylorus at rate of 3
per minute
 Basic electrical rhythm (BER) set by enteric
pacemaker cells (formerly interstitial cells of
Cajal)
 Pacemaker cells linked by gap junctions  entire
muscularis contracts
Distension and gastrin increase force of contraction
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Gastric Contractile Activity
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Most vigorous near pylorus
Chyme is either
 Delivered in ~3 ml spurts to duodenum, or
 Forced backward into stomach
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Figure 23.19 Deglutition (swallowing).
Pyloric
valve
closed
1 Propulsion: Peristaltic
waves move from the fundus
toward the pylorus
Pyloric
valve
slightly
opened
2 Grinding: The most
vigorous peristalsis and
mixing action occur close
to the pylorus. The pyloric
end of the stomach acts as a
pump that delivers small
amounts of chyme into the
duodenum.
Slide 1
Pyloric
valve
closed
3 Retropulsion: The peristaltic
wave closes the pyloric valve,
forcing most of the contents of
the pylorus backward into the
stomach.
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Regulation of Gastric Emptying
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As chyme enters duodenum
 Receptors respond to stretch and chemical
signals
 Enterogastric reflex and enterogastrones inhibit
gastric secretion and duodenal filling
Carbohydrate-rich chyme moves quickly through
duodenum
Fatty chyme remains in duodenum 6 hours or more
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Figure 23.20 Neural and hormonal factors that inhibit gastric emptying.
Presence of fatty, hypertonic,
acidic chyme in duodenum
Duodenal enteroendocrine cells
Chemoreceptors and
stretch receptors
Secrete
Enterogastrones
(secretin,
cholecystokinin,
vasoactive intestinal
peptide)
Target
Via short
reflexes
Enteric
neurons
Duodenal
stimuli
decline
Via long
reflexes
CNS centers
sympathetic
activity;
parasympathetic
activity
Contractile force and
rate of stomach
emptying decline
Initial stimulus
Stimulate
Physiological response
Inhibit
Result
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Homeostatic Imbalance
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Vomiting (emesis)
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Extreme stretching
 Intestinal irritants, e.g., bacterial toxins,
excessive alcohol, spicy food, certain drugs
Chemicals/sensory impulses  emetic center of
medulla
Excessive vomiting  dehydration, electrolyte and
acid-base imbalances (alkalosis)
caused by
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Intestinal Juice
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1-2 L secreted daily in response to distension or
irritation of mucosa
Slightly alkaline; isotonic with blood plasma
Largely water; enzyme-poor (enzymes of small
intestine only in brush border); contains mucus
Facilitates transport and absorption of
nutrients
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Large Intestine
“colon”
 larger in diameter but shorter than small
intestine (which it “frames”)
 functions:
1. dry out indigestible food residue by absorbing
water
2. elimination
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Parts of the Large Intestine
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Cecum
Appendix
Colon
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Ascending
Transvere
Descending
Rectum
Anal Canal
Cecum
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sack-like
1st part of large intetine
site of ileoceal valve: empties chyme into large
intestine from small intestine
Appendix
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Vermiforme appendix
vestigial organ
easily twists  small amounts food & bacteria
get trapped  appendicitis
Signs of Appendicitis
Appendicitis
Appendectomy
Colon
Colonoscopy
Colon
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Descending colon enters pelvis in LLQ where it
becomes S-shaped = sigmoid colon
Rectum
Wall of the Colon
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muscularis externa’s longitudinal layer in 3
bands called teniae coli
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“ribbons of the colon”
are normally partially contracted  colon wall
puckers forming haustra
Histology of Colon
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no villi (absorption
mostly in small
intestine)
many Goblet cells
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mucus (aids
movement of feces)
Rectum
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storage area for feces
Anal Canal
2 sphincters:
1. external sphincter
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skeletal muscle (voluntary)
internal sphincter
2.
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smooth muscle (involuntary)