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Gastrointestinal- First Aid > GI Physiology (345-349) > Flashcards

GI Physiology (345-349) Flashcards

1
Q

what cells produce cholecystokinin (located where)

A

I -cells (in the duodenum and jejunum)

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2
Q

what four actions does cholecystokinin produce

A

increased gastric emptying, increased pancreatic secretion, increased gall bladder contraction, increased sphincter of Oddi relaxation

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3
Q

what triggers release of cholecystokinin

A

increased fatty acids and amino acids

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4
Q

via what pathway does CCK act to increase pancreatic secretion

A

neural muscarinic pathways

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5
Q

what cells produce gastrin (located where)

A

G-cells in the antrum of the stomach

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6
Q

what does gastrin do

A

increases HCl secretion, increases growth of gastric mucosa, increases gastric motility

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7
Q

how is gastrin regulated

A

increased by stomach distension/ alkalinization, amino acids and peptides, vagal stimulation

decreased by pH < 1.5

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8
Q

which two amino acids are potent stimulators of gastrin secretion

A

phenylalamine and tryptophan

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9
Q

which cells produce glucose-dependent insulinotropic peptide (located where)

A

K cells (duodenum and jejunum)

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10
Q

what are the functions of glucose-dependent insulinotropic peptide

A

decreased gastric acid secretion

increased insulin release

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11
Q

what regulates glucose-dependent insulinotropic peptide secretion

A

GIP release is stimulated by fatty acids, amino acids and oral glucose

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12
Q

what’s the other name for glucose-dependent insulinotropic peptide

A

gastric inhibitory peptide (GIP)

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13
Q

how does GIP cause more rapid uptake of oral glucose than IV

A

oral glucose directly stimulates GIP, whereas IV glucose doesn’t –> rapid GIP spike in response to oral glucose load –> rapid insulin secretion

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14
Q

what produces motilin

A

small intestines

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15
Q

what does motilin do

A

produces migrating motor complexes (MMC’s)

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16
Q

when is motilin upregulated

A

during fasting state

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17
Q

what are motilin receptor agonists used for and name an example of a motilin receptor agonist

A

motilin receptor agonists are used to sitmulate intestinal peristalsis
(i.e. erythromycin)

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18
Q

what produces secretin (where are these cells located)

A

S- cells in the duodenum

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19
Q

what are the actions of secretin

A

promote pancreatic bicarb secretion
promote bile secretion
decrease gastrin secretion

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20
Q

what upregulates secretin

A

increased acid,

fatty acids in the lumen of the duodenum

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21
Q

what has to happen in the duodenum before pancreatic enzymes can function

A

bicarb must neutralize the gastric acid in the lumen

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22
Q

what cells produce somatostatin (located where)

A

D-cells in the pancreatic islets and GI mucosa

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23
Q

what are the actions of somatostatin

A

decreases secretion of: gastric acid, pepsinogen, pancreatic and small intestine fluid, insulin, and glucagon

decreases gallbladder contraction

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24
Q

what upregulates somatostatin?

what downregulates somatostatin?

A

upregulated by acid

downregulated by vagal stimulation

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25
Q

what does nitric oxide do

A

increase smooth muscle relaxation (including LES)

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26
Q

what GI regulatory molecule deficiency is thought to underlie achalasia

A

decreased NO secretion is implicated in increased LES tone of achalasia

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27
Q

what secretes vasoactive intestinal polypeptide (VIP)

A

parasympathetic ganglia in sphincters, gallblader and small intestines

28
Q

what are the actions of VIP

A

increase intestinal water and electrolyte secretion;

increase relaxation of intestinal smooth muscle and sphincters

29
Q

what upregulates and downregulates VIP

A

upregulated by distension and vagal stimulation;

decreased by adrenergic input

30
Q

what is a VIPoma

A

non-alpha, non-beta islet cell pancreatic tumor that secretes VIP

31
Q

what are the symptoms of a VIPoma

A

copious watery diarrhea, hypokalemia and achlorhydria

32
Q

what is the source and function of intrinsic factor

A

parietal cells;

binds vitamin B12 and promotes its absorption in the terminal ileum

33
Q

what is the source and function of gastric acid

A

produced by parietal cells;

decreases stomach pH

34
Q

how is gastric acid regulated

A

upregulated by histamine, ACh, and gastrin

downregulated by somatostatin, GIP, prostaglandin, and somatostatin

35
Q

where is pepsinogen secreted and what does it do

A

pepsinogen is secreted by chief cells in the stomach and is cleaved to pepsin by H+
pepsin promotes protein digestion

36
Q

what upregulates pepsin levels

A

vagal stimulation and local acid (to activate pepsinogen)

37
Q

where is bicarb secreted and what does it do

A

bicarb is secreted in the salivary glands, stomach, duodenum (Brunner’s glands) and pancreas;
bicarb neutralizes acid

38
Q

how is bicarb secretion regulated

A

secretin increases bicarb secretion by promoting pancreatic secretion and biliary secretion

39
Q

what kinds of secretory cells are found in the body of the stomach

A

parietal cells and chief cells

40
Q

what kinds of secretory cells are found in the antrum of the stomach

A

G cells, mucous cells, D cells (which are found throughout GI mucosa)

41
Q

what kinds of secretory cells are found in the duodenum

A

I cells, K cells, S cells, D cells, Brunner’s glands

42
Q

what’s the predominant way in which gastrin causes increased HCl secretion

A

by increasing histamine release from ECL cells

43
Q

what GPCR type pathway do M3 ACh and CCKb receptors act through

A

Gq

44
Q

what GPCR type pathway does histamine receptor act through

A

Gs

45
Q

what GPCR type pathway do prostaglandin and somatostatin receptors act through

A

Gi

46
Q

what do Brunner’s glands secrete and when do they become hypertrophied

A

alkaline mucus;

they become hypertrophied during peptic ulcer disease

47
Q

at what flow rate are pancreatic secretions high in bicarb

A

high flow

48
Q

at what flow rate are pancreatic secretions high in Cl-

A

low flow

49
Q

what is the tonicity of pancreatic secretions

A

isotonic

50
Q

what does alpha amylase do?

is it a zymogen?

A

starch digestion;

not a zymogen (it is secreted in its active form)

51
Q

name four pancreatic proteases

what form are they secreted in?

A

trypsin, chymotrypsin, elastase, carboxypeptidase

secreted as zymogens

52
Q

what enzymes does trypsin cleave/activate

A

trypsinogen –> trypsin (positive feedback)
chymotrypsinogen—>trypsin
proelastase –> elastase
procarboxypeptidase –> carboxypeptidase

53
Q

what enzyme cleaves and activates trypsinogen and where does this occur

A

enterokinase/ enteropeptidase;

found in the duodenal and jejunal mucosa

54
Q

what size of sugars are taken up by enterocytes (polysaccharides, disaccharides or monosaccharides)

A

monosaccharides only (glucose, fructose, galactose)

55
Q

which apical transporters take up glucose and galactose?

which take up fructose?

A

glucose and galactose are taken up by SGLT1 (Na+ dependent glucose cotransporter)
fructose is taken up by facilitated diffusion through GLUT5

56
Q

how are all sugards transported into the blood

A

GLUT-2

57
Q

what does a D-xylose absorption test tell you

A

D-xylose absorption test tells you if a malabsorption issue is due to damage to the GI mucosa;
D-xylose doesn’t require any enzymes, just intact mucosa, to be digested so if urine levels are normal there’s nothing wrong with the GI mucosa and the problem is some other etiology of malabsorption

58
Q

where are these absorbed:
iron
folate
B12

A

iron is absorbed in the duodenum
folate is absorbed in the jejunum and ileum
B12 is absorbed in the terminal ileum, along with bile acids

59
Q

describe Peyer’s patches and where they are found

A

unencapsulated lymphoid tissue containing B cells and M cells found in lamina propria and submucosa of ileum

60
Q

what do the M cells of Peyer’s patches do

A

constantly sample and present antigens to immune cells

61
Q

when stimulated what do the B cells of Peyer’s patches do

A

form germinal centers and differentiate into IgA-secreting plasma cells

62
Q

how is IgA transported into the lumen of the gut (what does it gain as it is released into lumen)

A

intraluminal transport via formation of receptor-IgA complex (exocytosed into lumen with a piece of the complex called secretory component)

63
Q

what are bile salts made of

A

bile acids conjugated to glycine or taurine

64
Q

what are the components of bile

A

bile salts, phospholipids, cholesterol, bilirubin, water and ions

65
Q

what catalyzes the rate limiting step of bile synthesis

A

7 alpha hydroxylase

66
Q

what are the functions of bile

A 
digestion and absorption of lipids and fat-soluble vitamins
cholesterol excretion (body's only means of doing so)
antimicrobial activity (via membrane disruption)

Gastrointestinal- First Aid (3 decks)

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