regulation Flashcards
summarise the enteric nervous system
intrinsic
10-100million neurons
rich plexus of ganglia (nerve and glial cells) - interconnected by unmyelinated nerve fibres
how many neurones does the CNS have
100billion
why are the neurons not myelinated
Speed not as important
role of the enteric nervous system
integrate the motor and secretory functions of the GI tract
independent of CNS
secretion controlled by the GI tract
panc, enzymes juice
conditions where the ENS is degenerated/dysfunctional
inflammation - ulcerative colitis -degeneration off enteric ns – not regulated
post-op
IBS – some problems associated with enteric Ns
Aging – constipation - motility, degeneration of ens with age
what fucntions does the ENS regulate
Motility
Blood flow
Water and electrolyte - Absorb ions that power water absorption
transport
Secretion
Absorption
describe the neurons in the ENS
sensory - respond to mech, thermal, osmotic and chemical stimuli eg CCK respond to the FA in the duodenum -> stim panc juice release
motor - axons end on sm - circular/longitudinal, secretory cells or bv
interneurons - between neurons, integration, coordinate stimuli
describe the myenteric plexus
between longitudinal and circular muscle
contral activity of muscularis externa - gut motor func
describe the submucosal plexus
Under epi layer – sense what going on in the lumen, change blood flow, endo and epi func – help digestion
plexuses down the gut
Sub and myenteric are continuous down the gut
describe minor plexuses
include deep musclualr plexus - inside the circular muscle
and ganglia supplying the biliary system and pancreas
describe the role of the ANS
automatic
sm, cardic, glands
symp and parasymp
describe the organisation of the sympathetic nervous system
cell bodies of preganglionic in thoracic and lumbar spinal cord - short
cell bodies of post are in the pre and para-vertebral ganglia
long postganglionic neurons
thoracic splanchnic nerves carry innervation to the fore and midgut - first 2/3 transverse colon
lumbar splanchnic to hindgut
role of the sympathetic nervous system
when don’t need to think about digestion too much – move blood flow to different areas
Evacuate bowels when scared – evolutionary because of shut down of symp
contraction of sphincters and vasoconstriction
neurotransmitter of the sympathetic ns
norepinephrine or noradrenaline (same thing)
describe the organisation of the PNS
cell bodies of preganglionic in brainstem and sacral spinal cord
cell body of post - close to target organs
preganglionic neurons synapse on ganglia close to gut wall/directly with enteric plexi
long pre and short postganglionic
most from vagus - to the transverse colon
remainder - pelvic nerves
role of the PNS
Digestive regulation
Stuff in stomach and duodenum – digestion complex
can cause excitation – sometimes turn something on and switch something else off
NT of PNS
Ach
relkationship between sympathetic NS and bv
regulate bv via the ENS
also reserves right to also control gut function directly – SNS canstop flow to gut - vasoconstrictor sympathetic fibres from coeliac, superior and inferior mesenteric arteries
ANS relationship with ENS
ANS neurons synapse on the ENS myenteric and submucosal plexi
interact and regulate the ENS function
how are afferent signals interperated
ENS receives local afferents - chemo and mechanoreceptors – effects downstream – don’t need to go back to brain
Some can go back to CN S – integrate func – output to modulate enteric ns
describe the innervation of the GI tract
intrinsic - neurons of enteric
extrinsic - afferents: pain, nausea (toxins), full
efferents: coordination
where are hormones of the GI endocrine system produced
endocrine cells in mucosa/submucosa of stomach, intestine and panc
what ‘type’ of endocrine
paracrine, neurocrine - hormone released from neurone – eg hypothalamic releasing factors
in gut – neurons release hormones rather than nT
summarise the GI tract as an endocrine system
Diffuse endocrine system – most cells not endocrine but there are endocrine cells within it – 15 epi layer are endo
All the way down gut
why does the distribution of the endocrine cells change down the GI tract
you want differnet functions to occur
what does L cell produce
Peptide YY and glucagone peptide 1
describe a flask cell
finger of cytoplasm – detection mech- chemoreceptor signal down cell – hormone release – into circulatuon
what cell produces CCK
I cells
how are I cells stimulated
Different receptors at top
Cell can tell what is going in gut – hormone release appropriately – see hoe much glucose, what stage of digestion, contents
what is the function of the GI tract endocrine system
regulation of mechanical processes - sm of GI, sphincter and gall bladder
and chemical and enzymatic processes of digestion - secretory cells, panc and liver
control of post absorbative processes involved in assimilation of digested food and CNS feedback regulating intake absorpative-= blood glucose level, appetite regulation
effects of growth and development of the GI - GLP2 – growth of intestine – target for drug for people with short bowel – need for normal gut func
how is insulin controlled by GI endocrine system
GIP - stim insulin from B cells
Peptide YY3-36 acts on the cns to suppress appetite
example of paracrine action sin the gut
histamine - from stomach wall - stimulus for parietal cells -> HCl
somatostatin - inhibit acid secretion by paracrine mechanisms
describe gastrin
- where
- stimulated by
- stimulates
- inhibited
synthesised in gastric antrum and upper SI
stimulated by - aa and peptides in lumen of stomach, stretch, vagus - when think of food
stimulates - gastric acid secretion
inhibited when pH< 3 -be feedback
describe somatostatin
syntheisised in D cells of gastric and duodenal mucosa, pancreas
universal inhibitor - gastric secretion, motility, intestinal and panc secretions, release hormones, nutrient and electrolyte transport, growth and proliferation
stimulated by mixed meal
treatment of neuroendocrine tumour
somatostatin - Analogue – neuroendocrine tumour treatment, difficult to pick – non-specific symptoms – suppressed hormone and tumour growth
why is a somatostatin analogue used - why cant we just use normal somatostatin
Peptide hormones have real;ly sshort half life – want to turn off gastrin – want to break it down quickly
Make analougue that has a longer half life so you don’t have to keep injecting blood
Different receptors – tweak molecule so it targets certain ones more – selectively
Need to inject – cant eat it because would just digest, maybe can encapsulate so can have oral treatment
describe secretin
secreted by S cells
in upper duodenum and jejunum
stimulus - acid in duodenum pH<4.5
stimulates pancreatic bicarb secretion - potentiated by CCK
secretin effects at high concentrations
If pH so low and really bhigh secretin need to stop gastrin – inhibit gastric acid and gastric emptying
describe CCK
secreted by cells mainly in SI
stimulated by fat and peptides in upper SI
independent of the vagus
stimulates - pancreatic enzyme release, delays gastric acid emptying, stimulates gallbladder contraction, decrease food intake and meal size
what does GIP stand for
gastric inhibitory polypeptide or glucose-dependant insulinotropic peptide
action of GIP
secreted by mucoal K cells - duodenum and jejunum
follow mixed meal
stimulate insulin secretion
effect of GIP receptor antagonists
reduce insulin release after a meal
why does food injected into the blood trigger less insulin than that ingested
incretin effect - GIP regulate the level of insulin in the GI tract
describe peptide YY
mucosa of terminal ileum, colon and rectum
released from L cells after eating
reduce motility, gall bladder contraction, pancreatic exocrine secretion, inhibit intestinal fluid and electrolyte secretion - PYY3-36 inhibits the food intake