alimentary mechanisms Flashcards

gut hormones: explain the role of key gut hormones (gastrin, somatostatin, cholecystokinin, glucose-dependent insulinotropic peptide & secretin) in the regulation of gut function

1
Q

what cells secrete gut hormones (paracrine of neurocrine factors)

A

enteroendocrine cells of alimentary canal

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2
Q

specialisations of enteroendocrine cells for production and secretion of hormones

A

small apical membrane with lots of sensory apparatus (fingers of cytoplasm) and mitochondria (changes in gut contents or activation by neurotransmitters), broad basolateral surface which is close to blood vessels for rapid distribution of many secretory vesicles into blood by exocytosis

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3
Q

where are most gut hormones secreted from

A

endocrine cells in mucosa or submucosa of stomach, small intestine and pancreas

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4
Q

distance of effects of gut hormones

A

most regulate nearby organs as primary effect, but to get there must travel long way via liver, heart and lungs

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5
Q

2 examples of paracrine cells in GIT

A

D-cells (in stomach), enterochromaffin-like cells (in gastric mucosa)

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6
Q

what do D-cells secrete and what does it do

A

somatostatin, which inhibits secretion of acid from parietal cells in gastric pits

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7
Q

what do enterchromaffin-like cells secrete and what does it do

A

histamine, which binds to H2 receptors on parietal cells and stimulates acid secretion

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8
Q

hormones which affect gut hormone function

A

somatostatin, secretin, cholecystokinin, gastrin, glucose-dependent insulinotropic peptide

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9
Q

what cells produce gastrin and where are they

A

G-cells in distal end of stomach (gastric antrum), proximal duodenum, pancreas

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10
Q

lengths of gastrin produced (3)

A

34 amino-acid mostly, 17 and 14 also

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11
Q

3 stimuli of gastrin secretion

A

presence of single amino acids and small peptides in stomach; mechanoreceptors in stomach wall detect presence of meal (stretch); parasympathetic nervous system (vagus nerve causing release of gastrin-releasing peptide from vagal efferents)

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12
Q

3 effects of gastrin secretion

A

increased gastric acid secretion, gastric emptying, pepsinogen secretion

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13
Q

negative feedback loop of gastrin secretion

A

if pH of chyme <3, secretion reduced to protect duodenal mucosa

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14
Q

what cells produce secretin and where are they

A

S-cells in duodenum and jejunum

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15
Q

stimuli of secretin secretion

A

drop in pH (<4.5) in duodenal kumen following acid chyme leaving stomach through pyloric sphincter

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16
Q

3 effects of secretin secretion

A

stimulation of secretion of pancreatic HCO3- to neutralise acid; at high concentrations: reduced acid secretion by stomach, reduced gastric emptying to prevent further exacerbation of acidic environment in small intestine

17
Q

what cells secrete somatostatin and where are they

A

D-cells in stomach, gut mucosa, pancreas

18
Q

stimuli of somatostatin secretion

A

mixed meal and reduced pH

19
Q

inhibitory effects of somatostatin (hence universal inhibitor)

A

acid secretion, mobility, exocrine secretion, endocrine secretion, absorption

20
Q

how does somatostatin reduce acid secretion

A

via inhibiting G-cells from secreting gastrin and inhibiting enterochromaffin-like cells from secreting histamine

21
Q

what cells secrete cholecystokinin and where are they

A

I-cells in small intestine

22
Q

stimuli of CCK secretion

A

small peptides and fats after mixed meal

23
Q

effects of CCK secretion without input from ANS

A

increased secretion of pancreatic enzymes, reduced gastric emptying, increased gall bladder contraction, reduced appetite

24
Q

what cells secrete glucose-dependent insuliotropic peptide and where are they

A

K-cells in duodenum and jejunum

25
Q

stimuli of glucose-dependent insuliotropic peptide secretion

A

mixed meal nutrients (especially glucose)

26
Q

effects of glucose-dependent insuliotropic peptide secretion

A

increased insulin secretion; in high concentrations causes reduced acid secretion and reduced gastric emptying

27
Q

functions of GI endocrine system

A

regulate mechanical processes of digestion, chemical and enzymatic processes of digestion, control of post-absorptive processes, effect on growth and development

28
Q

somatostatin analogue use (e.g. octreotide)

A

treat neuroendocrine tumours

29
Q

why use somatostatin analogue not somatostatin (3)

A

somatostatin has short half life (be able to be turned off and broken down quickly), whereas analogue lasts longer in circulation; selectivity; peptide hormones must inject as otherwise broken down and not absorbed

30
Q

where is peptide YY (PYY) located

A

L cells throughout mucosa of terminal ileum, colon and rectum

31
Q

stimulus of peptide Y

A

post prandially (particularly protein)

32
Q

peptide YY functions

A

reduces intestinal motility, gallbladder contraction and pancreatic exocrine secretion; inhibitor of intestinal fluid and electrolyte secretion; inhibits food intake