Intro to GI physio Flashcards by Andrew Pruett

somatostatin

in GI tract: released by D cells in response to low pH, inhibits H secretion and other GI hormones

outside GI tract: released by delta cells of pancreas and hypothalamus

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Histamine

in the stomach: stored and secreted by enterochromaffin cells (in glands). acts on Parietal cells to increase H production

stimulates acid production

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Gastrin

hormone family
site of secretion
stimuli of secretion

gastrin-cck
G cells of stomach

small peptides and a.a.
distention of stomach
vagal stimulation

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Cholecystokinin (CCK)

hormone family
site of secretion
stimuli of secretion

gastrin-CCK
I cells of the duodenum and jejunum

small peptides and AA
FAs

pancreatic enzyme secretion
pancreative HCO3 secretion through potentiation of CCK (not a direct effect, it potentiates effects of secretion)
stimulation/contraction of gallbladder and relaxation of the spnicter of Oddi

stimulates growth of the exocrine pancreas and gallbladder (trophic effects)
inhibits gastric emptying

can also act as a paracrine signal

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Secretin

hormone family
site of secretion
stimuli of secretion

secretin-glucagon
S cells of the duodenum
H in the duodenum, FAs in the duodenum

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Glucose-dependent insulintropic peptide

secretin-glucagon family
duodenum and jejunum

FAs, a.a’s, oral glucose

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Gastrin’s actions

stimulates acid secretion and mucosal growth

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Zollinger-Ellison syndrome

gastrin secreting tumors
hypertrophy of gastric mucosa
duodenal ulcers
steatorrhea (fatty stools), pancreatic release is reduced

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CCK actions

stimulates growth of the exocrine pancreas and gallbladder (trophic effects)
inhibits gastric emptying

can also act as a paracrine signal

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secretin actions

increases pancreatic HCO3 secretion
increases biliary HCO3 secretion
decreases H secretion
inhibits trophic effect of gastrin on gastric mucosa 
can also act as a paracrine signal

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GIP actions

increases insulin secretion from pancreatic beta cells and decreases H secretion

oral glucose consumption is much more efficient way of releasing insulin than intravenous injection

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ACh in the GI tract

source, action

cholinergic neurons

actions include salivary secretions, pancreatic secretions, gastric secretions

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norepinephrine (NE)

source, action

adrenergic neurons

relaxation of smooth muscle
contraction of sphincters

increases salivary secretion

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vasoactive intestinal peptide (VIP)

source, action

neurons of the mucosa and smooth muscle

actions include relaxation of smooth muscle
increase in intestinal secretion
increased in pancreatic secretion

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GRP

source, acrion

gastrin releasing peptide

neurons from gastric mucosa

increases gastrin secretion

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Enkephalins

neurons of the mucosa and smooth muscle

causes contraction of smooth muscle and decreases intestinal secretion

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Neuropeptides Y

Neurons of the mucosa and smooth muscle.

relaxation of smooth muscle. decrease intestinal secretion.

substance P

Co-release with ACh

contraction of smooth muscle, salivary secretion

neuronal centers that control feeding and satiety are located in the

hypothalamus

Lateral nuclei (LH)

feeding center in the hypothalamus

ventromedial nuclei (VM)

satiety center

PDA

paraventricular nuclei
dorsomedial nuclei
arcuate nuclei

all hypothalamic centers involved in food intake

what stimuli are needed for hormone release?

physiological (food, acid, paracrine stimulation, glucose etc)

what stimuli are needed for NT release?

action potentials

alpha-MSH pw

neurons in arcuate nucleus secrete alpha-melanocortin (a-MSH) by pro-opiomelanocortin neurons (POMC) alpha-MSH binds to MCR-4 present in second order neurons to INHIBIT food intake and increases metabolism

"big picture" a-MSH

inhibits food intake and increases metabolism

Neuropeptide Y pw

neurons in arcuate nucleus are stimulated by hunger signals to release NPY NPY binds to Y1R neurons that release NPY also release agouti-related peptide AGRP is an antagonist of MCR-4 increases feeding behavior and storage of calories

alpha-MSH and NYP/AGRP are

antagonists: peptides from one inhibit the other system. AGRP is an MCR-4 antagonist.

obesity

some cases have been related to mutation in the POMC and MCR4 genes

POMC

neuron in the arcuate hypothalamus: releases alpha-MSH to MCR-4 and inhibits food intake

the "vagal" circuit (basic components)

vagus--> NT---> hypothalamus

Ghrelin

secreted mainly by endocrine cells in the stomach binds to growth hormone, secretagogue receptors in the hypothalamus it stimulates neurons that release NPY stimulates neurons that release NPY (big one) other actions include increasing: ``` appetite gastric motility gastric acid secretion adipogenesis insulin secretion ``` appears to initiate the feeding response

insulin

transported across the blood brain barrier binds to receptors in satiety and hunger centers within the hypothalamus (POMC and NPY systems) actions: decreasing appetite increasing metabolism in patients with type I diabetes mellitus, there is an increase in food intake associated with the decrease in insulin

CCK and Peptide YY

CCK released by I cells in the duodenum elicits satiety CCK ---> vagal ---> NTS ---> hypothalamic circuit --> decrease in ghrelin, decrease in gastric emptying

PYY released by EECs

released by EECs (L cells) of the ileum and colon binds to Y2 receptors of the hypothalamus, which inhibits NPY neurons and released inhibition of POMC neurons potential as appetite suppressor

Leptin

secreted by cells in adipose tissue and by endocrine cells in the stomach binds to receptors in satiety and hunger centers within the hypothalamus (POMC and NPY systems) appetite suppressing hormone: decreases appetite increases metabolism decreases ghrelin appears to be part of negative feedback system for the regulation of food intake

Paracrines

peptides secreted by endocrine cells of the GI tract act locally somatostatin histamine

hormones

peptides released from endocrine cells of the GI tract through the portal circulation, through the liver, and enter systemic circulation gastrin CCK secretin GIP

Neurocrines

synthesized by neurons of the GI tract and released following an action potential ``` ACh NEP VIP GRP enkephalins NPY substance P ```

Criteria for a GI hormone

substance must be secreted in response to physiologic stimuli function must be independent of neural activity it must be isolated, purified, and chemically identified, and synthesized only four qualify: CCK, secretin, gastrin, GIP