- distention of stool causes contraction behind it and relaxation in front of it - mediated by ENS - controls secretion, peristalsis, and mixing

GI Regulation Flashcards by Anya McDermott

Neurotransmitters in the ANS

Preganglionic ALWAYS use Ach and nicotinic receptors
Postganglionic PSNS use Ach and muscarinic receptors
Postganglionic SNS use norepi or epi, EXCEPT for sweat glands, which use Ach

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Acetylcholine as a neurotransmitter causes what in the GI tract?

PSNS gets GI tract moving

Contraction of smooth muscle, relaxation of internal sphincters, and increase in secretions from salivary, gastric, and pancreatic glands

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Norepi as a neurotransmitter causes what in the GI tract

SNS stops the GI tract

Relaxes smooth muscle, contracts internal sphincters, and reduces watery glandular secretions

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Gastrin (source, stimulus, action)

G-cells of stomach antrum; few in duodenum
increases H+ secretion from parietal cells, grows gastric mucosa, and increase gastric motility
stimulated by AA and vagus (which uses GRP)
direct and indirect pathways (indirect being more powerful)
binds to CCKb

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CCK

Source, stimulus, action

released from I cells of duodenum and jejunum
binds to CCKa (specific for CCK) and CCKb (for CCK and gastrin)
causes contraction of gallbladder, relaxation of sphincter of Oddi, stimulation of secretions from exopancreas, promotes growth of exopancreas, and inhibits gastric emptying….secretory trifecta
released after gastrin in response to protein and lipids

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Secretin

Source, stimulus, action

released from S-cells of duodenum and jejunum
released after gastrin and CCK
the “anti-gastrin”
released in response to H+ and fatty acids
causes release of bicarb from pancreas for protection of duodenum and appropriate pH for pancreatic lipases needed for lipid absorption

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Incretins

Types, source, stimulus, response

GIP released from K-cells of duodenum
GLP-1 released from L-cells of ileum and colon
released in response to glucose, protein, or fat load
only hormone to be released in response to glucose, protein, or fat
in response to glucose, causes increased insulin release.

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Local GI reflexes

distention of stool causes contraction behind it and relaxation in front of it
mediated by ENS
controls secretion, peristalsis, and mixing

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Extrinsic Reflexes of GI tract

GASTROCOLIC: Signal from stomach causes evacuation from colon
ENTEROGASTRIC: Signal from small intestine inhibits stomach secretion and motility
COLONOIEAL: Signal from colon inhibits emptying of ileum

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Motility in mouth, esophagus, stomach, small intestine, large intestine

Chewing

Swallowing

Digestive period: receptive relaxation, accommodation, and gastric emptying. Interdigestive: migrating myoelectric complexes

Digestive period: segmentation. Interdigestive: peristalsis (MMC)

Haustral shuttling

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Function of secondary peristalsis and mechanism of initiation

Distention of esophagus stimulates stretch receptors
Clear esophagus of retained food and refluxed gastric contents
Little/no sensation

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Anti-reflux mechanisms

Mechanisms for infant and pregnant mother

LES pressure greater than stomach
Diaphragm pinching esophagus (INFANTS)
Secondary peristalsis (PREGNANT)
Reflexes

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Neuroendocrine effect on ECAs

Excitatory: Ach, gastrin
Increase ERA:ECA

Inhibitory: norepi, VIP, and nitric oxide
Decrease ERA:ECA

Can modulate, but not initiate!

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Interstitial cells of Cajal

Pacemaker cells that generate ECAs

Determine max rate of contraction

Lie btwn circular and longitudinal muscle layers

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What are ERAs? How do they affect contractions?

Local events on plateau of ECA that cause muscle contraction

Frequency of ERAs determine frequency of contraction

Multiple allow more Ca2+ into SMCs for a stronger and mores sustained contraction

Number and strength of contractions increased with increased ERA:ECA

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Neuroendocrine control of peristalsis

Behind bolus (oral to):
Longitudinal: relaxed (inhibitory neuroendocrines)
Circular: contracted (excitatory neuroendocrines)

In front of bolus (aboral to):
Longitudinal: contracted (excitatory neuroendocrines)
Circular: relaxed (inhibitory neuroendocrines)

Interneurons coordinate muscle contraction and relaxation so bolus follows pressure gradient

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Three phases of swallowing

Only phase that is voluntary

Oral-voluntary
Pharyngeal
Esophageal

Antral systole

Simultaneous contraction of terminal antrum and pylorus causes mixing via retrograde movement of contents and shearing of food

Chyme and liquids leave before antral systole

Driving forces of gastric empyting

Lower stomach peristalsis

2. Upper stomach tone

Inhibitors of gastric emptying

Pyloric sphincter tone

2. Duodenal contraction

Characteristics and functions of MMCs

=migrating motor complexes
Strong and intermittent waves of contraction in small intestine
Housekeeping-cleans out residual material and prevents bacterial overgrowth
During interdigestive period
Pylorus is open
Mediated by motilin

Affects of somatostatin

What cells release it? What causes its release?

Endocrine function: inhibits growth hormone

Paracrine function: suppresses release of gastrointestinal hormones
Inhibit G-cells from secreting gastrin in a negative feedback paracrine loop!

Released from D cells; stimulated by stomach acid to act in negative feedback paracrine loop

VIP

Vasoactive Intestinal Polypeptide (VIP)-mixed response, causing relaxation of SM but increased secretions (–>watery diarrhea)

Neuropeptide Y

Neuropeptide Y-acts like norepi, relaxes smooth muscle and

GRP

Gastrin-releasing peptide (GRP, bombesin)-acts like Ach, causing increased gastrin secretion

Enkephalins

(opiates)-mixed response, causing contraction of smooth muscle and sphincters and reduction of glandular secretions. Constipation

Substance P

Substance P-acts like Ach and is secreted with it, causing contraction of smooth muscle and increase in secretions

Neurotransmitters in the ENS

PSNS acting: Ach, GRP, and Substance P SNS acting: Norepi, epi, Neuropeptide Y Mixed: opiates and VIP

Saliva characteristics

Hypotonic Higher K+ and bicarb than plasma

Gastric secretion characteristics What would happen with vomitting?

Higher Cl-, H+, and K+ than in plasma Two major secretions: Oxyntic: from parietal cells, includes HCl, IF, and K+, which is stimulated by feeding Non-oxyntic: from chief cells and mucous cells, includes pepsinogen,mucous, and Na+ Blood pH would increase because lose H+

Pancreatic Juice Caracteristics

High bicarb | Concentration of K+ and Na+ equal to what is in blood

Effect of CCK and Ach on Secretin

Increase effect by acting on K+ channel through Ca2+, causing more leakage of K+

Secretin effect on CFTR

Stimulates CFTR and the translocation of the H+ K+ ATPase so more bicarb is released into the lumen (as is Cl-) Secretin stimulates adenosine cyclase to convert cAMP to PKa, which opens CFTR

Hartnup disease

- defective amino acid transporter - especially affects tryptophan (which is needed to make serotonin, melatonin, and niacin) - similar symptoms to niacin deficiency (pellegra) - can partially compensate with PepT1 action

Difference between liver and gallbladder bile

Cl-, Na+, bicarb, and water are reabsorbed when bile is in gallbladder. Lower concentration of these ions in gallbladder bile as compared to liver bile

Hirschsprung Disease

failure of neural crest migration leads to megacolon (lack of enteric NS)

Patterns of digestion and absorption

1. Glucose is not digested and is absorbed unchanged 2. Luminal hydrolysis-of polymers to monomers (peptides broken down into amino acids in the lumen before absorption) 3. Brush border hydrolysis-of polymers to monomers (polysaccharides broken down by brush border enzymes into monomers before absorption) 4. Intracellular hydrolysis-of di and tri peptides, which can be absorbed as is and broken down into individual amino acids in the enterocyte 5. Luminal hydrolysis followed by re-synthesis of TAGS, broken down into 2 fatty acids and monoglyceride before absorption, but reassembled in the enterocyte

Interdigestive absorption of NaCl

Parallel Na-H and Cl-bicarb exchange, which is ELECTRONEUTRAL Occurs in villous epithelia cells of ileum and colon CA generates intracellular carbonic acid which dissociates to bicarb and H+; both leave the cell so Cl- and Na+ can come into the cell (Na+ uses NHE channel) Increase in second messengers inhibit this mechanism

Nutrient dependent Na+ absorption

Villous epithelial cells of small intestine absorb most Na+ using SGLT1 or Na+/amino acid co-transporters Cl-, K+ and water will follow Na+ absorption into the cell, passively

Electrogeneic Na+ absorption

Large intestine Increased by mineralocorticoids Uses Na+/k+ pump

Electrogenic Cl- Secretion Where? Why does it matter?

From crypts of large and small intestine CFTR is the chloride channel

Types of Diarrhea

1. Osmotic: non-absorbable substance pulls water and electrolytes with it (ie lactose) 2. Secretory: electrolytes and fluid actively secreted into the gut (ie cholera) The B subunit of the cholera toxin causes activation of G-alpha