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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
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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
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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.
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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.
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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
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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
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Compare the regulation of the stomach, pancreas and gall bladder during the intestinal phase.
s
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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
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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
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time course related to acid
 - 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
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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
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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
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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
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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)
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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
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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+
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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
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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
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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
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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
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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
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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
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Intestinal Phase – third secretory phase - ___% acid secreted
5-10
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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
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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
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Later inhibitory phase - Intestinal phase
- - 4-5 hours
- - strong inhibition of HCl and gastrin release
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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
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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
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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
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Pancreas - Intestinal Regulation - intestinal phase
- - 80% secretion occurs this phase
- - acinar and duct cells regulated separately
- - regulators
- - digestion products and hormones
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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
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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
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