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Gastrointestinal control

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Gastrointestinal control Powered By Docstoc
					OVERALL CONTROL OF
        GIT
GIT AND ACCESSORY GLANDS
               GI FUNCTIONS
                   Function
Esophagus          Transit
                   Storage, H+/peptic
Stomach
                   digestion,intrinsic factor
Small Intestine:
  Duodenum
                   Digestion & Absorption
  Jejunum
  Ileum
Large Intestine    Absorption
  Colon            Storage
  Rectum           Defecation
       DIGESTIVE PROCESSES
4 basic processes:

•   Motility         Controlled by:
•   Secretion
•   Digestion        • Neural
•   Absorption       • Chemical
                     • Myogenic
 REGULATION OF GI MOTILITY & SECRETION

• Receptors in the GI wall detect changes in
  GIT lumen.
• The stimuli are:
  – Distension of GIT (mechanoreceptor)
  – Acidic chyme (chemoreceptor)
  – Osmolality of chyme (osmoreceptor)
  – Products of digestion (e.g. peptides & fatty
    acids)
      Control of the GI tract depends on the
                  location of food
• The sight, smell, taste, and mental images of
food trigger the cephalic phase of digestion
via the vagus nerve (CN X) which includes:
    osalivation
    ogastric juice production
     gastric
    ogastric contractions

• Increased volume of food in the stomach
and subsequent stimulation of stomach
stretch receptors triggers the gastric phase
of digestion which includes:
   ogastric juice production
   oincreased gastric motility
Small volume            Large volume
→ weaker contractions   → stronger contractions



•Larger volumes of food in the stomach
produce stronger gastric contractions than
smaller volumes of food.
• Chemical composition of food influences the rate of
digestion: lipid rich meals take longer to digest than
carbohydrate rich meals




 Carbohydrate rich meal
                                     Lipid rich meal
 → shorter digestion time
                                     → Longer digestion time

                            Emotional stressors cause the
                            brain to override the intrinsic
                            controls of digestion and
                            subsequently cause problems such
                            as constipation, diarrhea, and
                            stomachaches.
• As food moves into the small intestine
(duodenum), the chemical composition and volume
of that food triggers specific reflexes during the
intestinal phase of digestion which may include:
   opancreatic secretion of bicarbonate into the
   duodenum
   opancreatic secretion of digestive enzymes
   into the duodenum
   ogall bladder release of bile into the duodenum
   osegmentation contractions of the small
   intestine
• The small intestine reflexively slows gastric
emptying to allow for neutralizing, enzymatic
digestion, and absorption of its contents
   Nerves and hormones control secretions entering
                 the small intestine

• Fat in the duodenum causes it to release of CCK,
  which triggers contraction of the gall bladder and
  release of bile into the duodenum.
• Acid in the duodenum causes it to release of secretin,
  which causes the release of bicarbonate into the
  duodenum from the pancreas and liver.
• Distention of the small intestine and/or
  acidic/hypertonic chyme trigger a neural reflex that
  increases intestinal juice secretion.
• Sympathetic stimulation decreases intestinal digestive
  activity while parasympathetic stimulation increases
  it.
Reflexes coordinate and modulate digestive
                  activity
• Reflexes (stimulus, integration, and
response) that are totally controlled by the
enteric nervous system are termed short
reflexes.

• Reflexes that involve the CNS as an
integration center are called long reflexes.

• Short and long reflexes can occur
simultaneously.
               GI REFLEXES

SHORT RFLX - sensory aff fibres send impulse
  within ENS
(e.g. control secretion, peristalsis, mixing
  contraction etc.)
LONG RFLX:
• Sensory aff from GIT to prevertebral symp.
  Ganglia.
(e.g. gastrocolic rflx, enterogastric reflx etc)
• Sensory aff from GIT to spinal cord / brain
  stem.
(e.g. defecation rflx, pain rflx)

[Pain rflx can cause general (-) of entire GIT]
• Gastro-enteric reflex - distension of stomach
  increase the excitability of small intestine
  (motor and secretory)
• Gastro-ileal reflex - distension of stomach
  intensifies the activity of the terminal ileum and
  opens the ileo-cecal sphincter
• Gastro- and duodeno-colic reflexes -
  distension of stomach or duodenum initiate
  'mass movements' of the colon.
• Ileo-gastric reflex - distension of an ileal
  segment inhibits gastric motility.
• Intestino-intestinal reflex - cessation of
  intestinal motility upon excessive distention.
              CONTROL OF GI Fx
                              CONTROL


        NEURAL                MYOGENIC                 CHEMICAL


EXTRINSIC     INTRINSIC       Visceral SM     ENDOCRINE       PARACRINE
   (ANS)        (ENS)         Phasic Cont.    GI Hormones      Histamine
 Parasymp.   Myenteric Plx    Tonic Cont.    (Gastrin, CCK,   Somatostatin
   Symp.     Submucosal Plx                   Secretin etc)
  CONTROL MECHANISMS




e.g. VIP   e.g. histamine,     e.g. gastrin, CCK,
     ACh        somatostatin         secretin
ENS
               Intrinsic (ENS)
• 2 layers:
  – Myenteric (Auerbach’s) plexus
  – Submucosal (Meissner’s) plexus

• Functions:
  – Myenteric - mainly control movements (ms
    contraction)
  – Submucosal - mainly control secretion,
    absorption & local blood flow
• The plexuses are interconnected.

• They contain:
  – motor neurons - supply smooth ms.
  – secretory neurons - control endocrine &
    exocrine secretion in mucosa.
  – sensory neurons - respond to pH, stretch,
    osmolarity, products of digestion.
  – Interneurons
  [Neurotransmitter released by ENS (Guyton)]
          EXTRINSIC (ANS)




PARASYMPATHETIC        SYMPATHETIC
  The Autonomic Nervous System




Parasympathetic NS      Sympathetic NS
            Parasympathetic
• Outflow: vagus (CN X), [except that supply
  mouth & pharyngeal region] & sacral
  segment (S 2-4)

• Postganglionic neurons located in the
  myenteric & submucosal plexuses.

• Stimulation: increase activity of ENS
              Sympathetic
• Outflow: spinal cord btw segment T5 - L2
  (intermedio-lateral horn).

• Most pregang fibres enter symp chains &
  synapse with postgang neurons in
  mesenteric ganglia & celiac ganglion, which
  then terminate in ENS.

• Stimulation: decrease activity of ENS.
Symp exert its effects in 2 ways:
• direct effects of NAdr on smooth ms to
  cause (-).
• effects of NAdr to (-) ENS activity.
On non-sphincter ms - activate β-adrenergic
 rec. - relaxation

On sphincter ms - stimulate α-adrenergic
 rec. - contraction
            Hormones modulate digestive activity
•    GI hormones are peptides (amino
    acid based).

•    GI hormones include gastrin,
    cholecystokinin (CCK), secretin,
    glucose-dependent insulinotropic
    peptide (GIP) and motilin.

•   Enteroendocrine cells of the GI
    mucosa secrete the peptide
    hormones.

•   GI hormones, like all hormones, enter
    the circulatory system, and then
    return to the target organ(s); in this
    case, back to the GI tract.

•   Potentiation of hormones involves the
    combined effect of two or more
    hormones being greater than the sum
    of their individual actions
• Pyloric antrum G cells
secrete gastrin, which
stimulates HCl production
and growth of the gastric
mucosa.
                   Gastrin
• Discovered by Edkins (1905).
• Secreted by G cells of stomach antrum.
• Stimulus: peptide/a.a, Ca2+ in gaster;
  distension of gastric wall; vagus nerve; Adr.
• Major actions: increase acid & pepsin
  secretion; promote mucosal growth;
  increase gastric motility.
• CCK is secreted by the “I” cells in
 the duodenum and jejunum.

• CCK cause gall bladder contraction
 and subsequent release of bile into
 the duodenum.

• CCK causes the pancreas to release
 digestive enzymes into the
 duodenum.

• CCK inhibits gastric emptying.

• CCK stimulates growth of the
 pancreas and gall bladder mucosa.
           Cholecystokinin (CCK)
• Discovered in 1928 by Ivy & Oldberg.
• Secreted by endocrine cells in small intestine.
• Stimulus: Peptide/a.a., fatty acid in small intestine.
• Major actions: increase pancreatic HCO3- & enz.;
  stimulate gallbladder contraction; promote
  pancreatic growth; (-) gastric emptying; enhance
  secretin action.
• Duodenal “S” cells
produce secretin.

• Secretin causes the
pancreas and to a lesser
extent the liver, to
release bicarbonate into
the duodenum.

•Secretin inhibits HCl
secretion by the
stomach
                  Secretin
• First hormone discovered in 1902 by Bayliss
  & Starling.
• Secreted by S cells in duodenum.
• Stimulus: acid in lumen of duodenum.
• Major actions: increase pancreatic & bile
  HCO3-; promote pancreatic growth; (-) HCl.
• Duodenal and jejunum
cells secrete GIP.

• When glucose is
present, GIP stimulates
the pancreas to secrete
insulin, thus enhancing
the secretion of insulin.
                        GIP
• Discovered by Brown et al. (1969).
• Formerly known as Gastric Inhibitory Peptide.
• Now - Glucose-dependent Insulinotropic Peptide.
• Produced by K cells in mucosa of duodenum &
  jejunum.
• Stimulus: prot, fat products & glucose in small
  intestine.
• Major actions: Increase insulin; (-) acid secretion.
• Duodenal and jejunum
cells secrete motilin during
the postabsorptive state.

• Motilin stimulates GI
motility thereby moving
intestinal contents toward
the end of the ileum.
                      Motilin
• Discovered in 1970 by Brown et al.
• Secreted by endocrine cells in small intestine.
• Stimulus: nerve
(During fasting - periodic release every 1.5 - 2 hrs)
• Action: increase gastric & intestinal motility.
                   PARACRINE
• Molecules secreted into ECF / lumen by epithelial
  cells in GIT wall.
• Somatostatin (-) gastrin release when antral
  mucosa is acidified (pH<1.5); & (-) gastric acid
  secretion from parietal cells.
• Histamine - released by gastrin & (+) acid
  secretion; potentiate the action of gastrin and Ach
  on acid secretion.
• H2-rec blocker (-) acid secretion (e.g. cimetidine,
  ranitidine)
• Enteroendocrine cells in
  the pylorus release gastrin
  into the bloodstream; it
  returns to the stomach to
  exert its effects.

• Paracrine cells in the
  fundus and body of the
  stomach release histamine     Gastrin

  into the lamina propria
  interstitium.
• Peptides in the stomach trigger the release of
  gastrin from G-cells into the bloodstream.

• Gastrin stimulates HCl secretion by parietal
  cells and histamine secretion by paracrine
  cells.

• Histamine acts synergistically with gastrin to
  stimulate HCl release from parietal cells.
      SMOOTH MUSCLE CONTRACTION
• Phasic contractions - contract & relax
  alternately (esophagus, small bowel, gastric
  antrum).
• Tonic contractions - sustained contraction
  (sphincter).
• The amplitude of phasic ms and tone of
  tonic ms can be modulated by neurocrines,
  endocrines and paracrines.
ELECTRICAL ACTIVITY OF SM
                  Reference
• Guyton & Hall. Textbook of medical physiology.

• Sherwood. Human physiology - from cells to
  systems.

• Ganong. Review of medical physiology.

• Johnson. Gastrointestinal physiology.
             Learning Issues
Motility of GIT:
• Propulsive movement
  – peristalsis
  – mass movement
• Non-propulsive movement - for mixing
  – segmentation
  – haustration
      AFFERENT SENSORY FIBRES
• Sensory nerve endings originate in the GI
  epithelium or wall.
• Stimulated by:
  1) irritation of GI mucosa
  2)xssive distension / stretch
  3) presence of specific chemical subs. (e.g.
  gluc, a.a.)
• Fn: to initiate many vagal reflx signals to
  GIT.
• Gastro-intestinal hormones are steroids.
• Secretin is secreted from the pancreas.
• Secretin stimulates flow of pancreatic secretion
  with a high concentration of bicarbonate ions.
• Cholecystokinin is the most important
  hormone concerned in the neutralization in the
  small intestine of acid from the stomach.
• Gastrin increases gastric acid secretion.
          HORMONAL CONTROL


• All are peptides.

• GI hormones released by mucosa of gaster
  & small intestine.

• Stimulus - nerves, distension, chemical.
                  Extrinsic Nerves


They regulate
GIT motility &
secretion in
response to
changes in the
environment
(e.g. emotions,
smell & taste)

				
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