Physiology - GI - INTEGRATED CONTROL OF SECRETION

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  1. Describe and explain the time-dependent relationship between gastric H+ concentration and rate of gastric acid secretion after ingestion of food.
    • 1. rate stays low; [H] drops; soon after ingestion
    • 2. rate rises; [H] keeps dropping;
    • 3. rate peaks and declines; [H] rises
  2. Define the cephalic, gastric and intestinal phases of secretion. Discuss the origin of the activation, the primary organs stimulated and the cellular receptors activated for each phase.
    • cephalic
    • begins before food gets in stomach
    • head, food, smell, taste
    • salivary gland
    • mechanoreceptor, chemoreceptor
    • ACh -> nicotinic or M3

    • gastric
    • stomach; food enters stomach
    • mechnoreceptor, chemoreceptor

    • intestinal
    • food enters small intestine
    • small intestine, pancreas, liver and gallbladder
  3. Compare vagovagal (long) and intramural (short) reflexes. Explain the effects of vagotomy and atropine on release of gastric acid, gastrin, histamine and somatostatin and the receptors involved.
    • long: involving CNS, target area much wider
    • short: limited to the local area
    • vagotomy, high/low atropine all block gastric acid release. nicotinic ACh receptor, M3.
    • vagotomy and high atropine block gastrin release. nicotinic ACh receptor, GRP receptor.
    • vagotomy, high/low atropine all block histamine release. nicotinic ACh receptor, M3.
    • vagotomy and atropine stim somatostatin release.
  4. Explain the weak stimulation of the pancreas and gallbladder by circulating gastrin during the cephalic and gastric phase.
    • cephalic acidity high, somatostatin is released, inhibit gastrin release
    • gastric, somatostain releasing inhibited, gastrin released.
    • gastrin has very weak stim on pancreas and gallbladder in human. very few CCK-A receptor.
  5. Compare the direct and indirect regulation of gastric acid secretion by gastrin, histamine and somatostatin during the cephalic phase.
    • low gastrin, histamine, due to the inhibition from somatostatin
    • Somatorstatin inhibits gastric acid
  6. For the gastric phase, describe the role of gastric distention, lumenal acidity and digestive products on gastric acid regulation. Compare and describe the importance of long and short reflexes.
    • distention-> mechanoreceptor-> long and short flexes; long-> ...-> ACh -> parietal -> secrete
    • lumenal acidity low -> somatostatin secretion inhibited -> gastric acid secrete inhibition removed, inhibition on other stimulator on gastric acid release are also removed
    • low acidity, digestive product -> chemoreceptor -> vagovagal -> ACh -> stim all gastric releasing related components
  7. Compare the regulation of the stomach, pancreas and gall bladder during the intestinal phase.
    s
  8. Define enterogasterone, List examples of enterogasterones and the factors that stimulate their release.
    • CCK
    • direct: digestive product
    • indirect: CCKRF<-digestive products; monitor peptide

    • GIP
    • digestive products: glucose, AA, FA
    • inhibits parietal and G-cells, and motility

    • secretin
    • duodenal pH<4.5
    • stim neuro reflex
    • stim pancreatic and hepatic duct cells secretion, volume, HCO3
    • inhibit G-cells
  9. acid continually secreted
    • - low basal - at night
    • - brain begins preparing for food
    • - food ingestion - neurocrine, paracrine, endocrine signals
    • - integrated at all levels
    • - 3 phases - Cephalic, Gastric, Intestinal; names reflect location of stimulating receptors
    • - end of digestion complex mechanisms reverse all processes
  10. time course related to acid
    • Image Upload
    • 1) Interdigestive Period – basal secretory activity (10%) - time 0 to ingestion
    • - vagally mediated; diminished w/ vagotomy
    • - circadian rhythm: peaks midnight; troughs 7:00am
    • - low food buffers
    • - low acid secretion
    •   - low pH(1-3)
    •   - due to somatostatin (SST) release - powerful paracrine inhibitor
    • 2) Activation - neural, endocrine, paracrine signals
    • 3) Restoration of Basal Levels
  11. Interdgestive Phase – primary __cell regulators
    D-

    • 1) Gastric Acidity
    • - high acidity -+-> somatostatin release ---> secretion of all organs with SST receptors; protective

    • 2) ACh
    • – inhibits somatostatin secretion
    • - weak inhibitor - vagal pathways weakly activated during interdigestive phase
    • - remove somatostatin inhibition to allow gland activation
    •   - begins in Cephalic Phase
  12. CEPHALIC PHASE - General Properties
    - Receptors are located ____
    - begins when?
    - pathway
    • - in head
    • - before nutrients enter stomach
    •   - conditioned -- smell, sight, thought of food (Pavlov's dog)
    •   - unconditioned - taste of food (chemoreceptors)

    • Long vago-vagal pathways activated
    • - afferent and efferent fibers -> cephalic receptors and lower organs
    • - postganglionic fibers -> salivary glands, stomach, pancreas, gallbladder, smooth muscle
    • - ACh released
    •   - begins somatostatin inhibition, remove inhibition of GI organs w/ SST receptors
    •       - somatostatin inhibition is not yet complete because the stomach is still empty, and the acidity stimulates somatostatin release, only 30% of the acid gets stimulated during the phase
    •   - lower organs prepare to process food

    • total 2000 vagal fibers -> 10 million ganglia in the intrinsic plexus
    • inhibit the entire pathway by vagotomy
  13. Salivary Glands - Neural Regulation in cephalic phase
    - most important transmitter __
    - Salivary gland activated via ___
    • - ACh
    • - 2 receptors
    •   1) chemoreceptors – taste, smell; KEY
    •   2) mechanoreceptors – chewing, grinding
    • 3 Responses
    • - Conditioned response - Pavlov - sight, smell, thought
    • - Unconditioned response - food enters mouth
    • - Emotional states
    •   - anger and hostility - increase
    •   - fear and depression - decreases
  14. Neural regulation of stomach in cephalic phase
    - pathway
    - transmitter
    - target
    • – vagal pathways
    • - ACh – most important stimulus
    • - activates 5 gastric cell types (parietal cell, G-cell, ECL cell (in fundus), chief cells, mucous cells)
  15. Control on Parietal Cell -> _______
    - preganglionic receptor _____
    - postganglionic receptor _____
    - vagotomy:
    • HCl - Intrinsic Factor
    • - nicotinic receptor: high (dose; works on preganglionic) atropine blocks
    • - M3 = muscarinic receptor: low (dose; works on preganglionic) atropine blocks
    • - bilateral completely blocks
  16. Control on Antral G-Cells
    - preganglionic receptor _____
    - postganglionic transmitter _____
    - vagotomy:
    • - high atropine blocks; ACh is the transmitter
    • - low atropine no effect: ACh is not transmitter; it is GRP (gastrin releasing peptide) instead
    • - bilateral blocks

    inhibited by H+
  17. Pancreas - Regulation in cephalic phase
    vagal pathway involved

    • ACh
    • - vagovagal pathways
    • - primarily stimulate acinar cells
    • - secretion: low volume, high enzymes

    • Gastrin
    • - little stimulation
    • - have very little effect in human
    • - low circulating levels
    • - low affinity for CCK-Type-A receptor
    •   - little additive effect with ACh

    Secretion - 20% maximum; any release is weak
  18. Gallbladder and liver - neural regulation during cephalic phase
    • Vagal activity causes weak gallbladder contractions and relaxation of Sphincter of Oddi.
    • Low level activity - vagus
    • - ACh - weak contractions
    • - weak relaxation sphincter Oddi
    • - mechanism not understood
  19. Summary of Cephalic Phase – Comparative Stimulation of Organ Systems
    • Salivary gland
    • - stimulation - thought, smell, taste food
    • - pure neural regulation
    • - parasympathetic and sympathetic

    • Lower Organs
    • - weaker secretion
    • - neurocrines, endocrines, paracrines
    • - stimuli short lived - phase self destructs if food does not enter stomach
    • - gastric acidity increases
    •   - inhibits G-cell secretion
    •   - activates somatostatin release
    •   - potention and additive effects removed
    •   - "brakes" on G-, parietal and ECL cells restored
  20. Gastric Phase
    • - begins when food enters stomach
    • - more acid (60%) secreted than cephalic phase (30%)
    • - receptors activated by food
    • - low volume (neural stim is weak; major stimulator - pancreatic hormone - has not been released yet), high enzyme contents
  21. Gastric Secretion - Neural Regulation - Gastric phase
    • 1) Mechanoreceptors
    • - gastric body and antrum
    • - detect distention and stretch
    • - activate two neural pathways
    •   1) short reflexes
    •   - within gut wall
    •   - intrinsic plexus; works w/o vagus
    •   - cholinergic - atropine blocked
    •   2) long reflexes
    •   - vagovagal - sensory neurons -> CNS -> vagus -> effector
    •   - activate ECL, G-cells

    • 2) Chemoreceptors
    • - long vago-vagal reflexes - primary neural pathway
    • - Digestion Products: small peptides and amino acids from pepsin and HCl digestion
    •   - release hormones
    • - low Acidity (pH > 3)
    •   - inhibition on G-cell removed; gastrin released
    •   - inhibits somatostatin secretion
    • - removes inhibition from other organs
  22. Pancreas and gallbladder - Gastric Regulation in gastric phase
    • - Similar to cephalic phase
    •     - vago vagal pathways
    •     - weak stimulation, low volume
    •     - weak gallbladder contractions
    •     - sphincter Oddi relaxes

    - Major organ regulators not yet released

    • - Activation secondary to
    •    - activation - stomach distention
    •        - gastrin release - gastropancreatic vago-vagal pathway
    •        - in human - little effect on acinar cell
    •     - activation - protein digestion products
    •        - stimulate gastrin from antral and duodenal G-cells
    •        - humans - gastrin - little effect
    •        - rat - binds to CCK Type A pancreatic receptor
    •     - ACh – weak neural stimulus
  23. Intestinal Phase – third secretory phase - ___% acid secreted
    5-10
  24. INTESTINAL PHASE
    • - begins 2 hours after eating
    • - significant gastric content - emptied into duodenum
    •     - mechanorceptors and chemoreceptors stimulated
    •        - neural and hormonal pathways activated - long reflexes - brain and other organs
    •     - gradual depletion gastric food buffers
    •        - secretion still rising
    •        - gastric acidity increases
  25. Stomach - Intestinal Regulation (INTESTINAL PHASE) - Early stimulatory phase
    - maintains gastrin and acid secretion ([H]) till stomach empties

    • - distention - duodenal mechanoreceptors
    •     - vago-vagal reflexes - cholinergic

    • - protein digestion products - small peptides and AAs - stim hormones released from small intestine
    •     - gastrin – from G cells of proximal intestine; G34 (big gastrin)
    •     - entero-oxyntin: unknown cells; directly stimulates parietal cell
    • - rate peaks (~3hr) then slowly declines to 0
    • - food buffer declines
  26. Later inhibitory phase - Intestinal phase
    • - 4-5 hours
    • - strong inhibition of HCl and gastrin release
  27. 3 Gastric Mediators - Later inhibitory phase - Intestinal phase
    1) reduced contents - less distention

    • 2) increased acidity (pH < 3) <- loss food buffers
    • - less gastrin
    • - more somatostatin

    • 3) enterogasterones
    • - hormones released from duodenum
    •   - CCK - from I - cells - indirect
    •     - inhibits acid secretion and gastric emptying via D-cells
    • - regulate enterogastric reflex
    •     - integrate secretion and motility
  28. CCK regulation
    1) Cephalic - Gastric Phases
    2) intestinal phase
    • - limited release <- neural stimulation
    • - purpose: prepare food to digest when enter small intestine
    • - tightly match CCK release with availability of pancreatic enzymes

    • - predominant regulator - direct or indirect
    • - direct release <- fatty acids or amino acids
    • - indirect release <- 2 factors <- fatty acids and amino acids (and neural pathways)
    •     - CCK Releasing Peptide
    •        - paracrine; small intestine epithelium
    •     - Monitor Peptide <- pancreas acinar
    • - factors protelytically degraded (by trypsin) after digestion
  29. 3 Stimuli - trigger enterogasterone release
    • 1) luminal fatty acids – most potent releaser - two hormones
    • - CCK - I -cells – Type A receptors
    •   - bind to and activates D-cells -> somatostatin release -> inhibits parietal cells
    • - GIP
    •     - gastric Inhibitory peptide
    •     - from intestinal K-Cells
    •     - released by glucose, amino acids, fatty acids
    •     - directly inhibits parietal and G-cells
    •     - inhibits motility

    • 2) duodenal acidity (pH < 4.5) – releases secretin – S- cells
    • - activate neural reflex - duodenum and stomach
    • - inhibits G-cells - mechanism not known

    3) hyperosmotic solutions - unknown regulator and mechanism; inhibits gastric acid secretion
  30. Pancreas - Intestinal Regulation - intestinal phase
    • - 80% secretion occurs this phase
    • - acinar and duct cells regulated separately
    • - regulators
    • - digestion products and hormones
  31. Pancreas - Indirect Neural Regulation - intestinal phase
    • Acinar cell regulation
    • - species dependent
    • - CCK - Direct Stimulation (historical model)
    •     - rodents - direct binding to CCK Type A receptor
    •     - direct release of acinar enzymes
    •     - duct cell binding - potentiates secretin
    • - CCK - Indirect Model
    •     - humans - no or very few CCK receptors - indirect effect
    •     - CCK directly activates vago vagal pathways
    •     - ACh (M-3 receptor) - direct acinar cell regulator

    • Duct cell regulation
    • - Secretin – most important for volume and HCO3-
    • - direct and same in humans and rodents
    • - potentiates CCK and ACh
  32. Gallbladder - Indirect Neural Regulation - intestinal phase
    • Hormonal Regulation - primary
    • - CCK
    •   - strong contractions gall bladder
    •   - relaxes sphincter Oddi

    - Gastrin: weaker

    • - Secretin
    •   - stimulates hepatic duct cell - increases volume

    • Neural Regulation – lesser importance
    • - via long vago vagal reflexes
    • - ACh , gastrin - weak gall bladder contractions
    • - not well defined
Author:
akhan
ID:
315645
Card Set:
Physiology - GI - INTEGRATED CONTROL OF SECRETION
Updated:
2016-02-12 02:48:17
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Description:
Physiology - GI - INTEGRATED CONTROL OF SECRETION
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