GI Flashcards

1
Q

what cells make gastrin?

A

G cells

antrum of stomach, duodenum

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2
Q

gastrin function?

A

increase gastric acid secretion
increase gastric mucosal growth
increase gastric motility

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3
Q

regulation of gastrin secretion?

A

stimulated by: distention, alkaline, AAs, peptide, VAGUS
inhibited by: pH < 1.5

** increased in chronic atrophic gastritis, ZES, chronic PPIs

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4
Q

what cells make somatostatin?

A

D cells

pancreatic islets, GI mucosa

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5
Q

somatostatin function?

A

decrease secretion of: gastric acid, pepsinogen, pancreatic fluid, insulin/glucagon
decrease GB contraction

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6
Q

regulation of somatostatin?

A

stimulated by acid

inhibited by VAGUS

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7
Q

what cells make CCK?

A

I cells

duodenum, jejunum

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8
Q

CCK function?

A

stimulate: pancreatic secretion, GB contraction, sphincter of Oddi relaxation
inhibit: gastric emptying

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9
Q

CCK regulation?

A

stimulated by FAs, AAs

** acts on neural muscarinic pathways –> pancreatic secretion

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10
Q

what cells make secretin?

A

S cells

duodenum

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11
Q

secretin functions?

A

stimulates pancreatic HCO3 secretion, bile secretion

inhibits gastric acid secretion

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12
Q

secretin regulation?

A

stimulated by acid, FAs in duodenal lumen

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13
Q

what cells make GIP?

A

K cells

duodenum, jejunum

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14
Q

GIP function?

A

exocrine: decrease gastric acid secretion
endocrine: stimulate insulin release

** oral glucose load more potent than IV glucose in terms of insulin release b/c of GIP response to oral glucose

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15
Q

regulation of GIP?

A

stimulated by FAs, AAs, oral glucose

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16
Q

what makes motilin?

A

SI

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17
Q

what does motilin do?

A

produces migrating motor complexes

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18
Q

motilin regulation?

A

increased in fasting state

** receptor agonists (e.g. erythromycin) used to stimulate intestinal peristalsis

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19
Q

what makes VIP?

A

parasympathetic ganglia: sphincters, GB, SI

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20
Q

VIP function?

A

increased intestinal water and electrolyte secretion

increased relaxation of intestinal smooth mm and sphincters

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21
Q

VIP regulation?

A

stimulated by distention, VAGUS
inhibited by ADRENERGIC input

** VIPoma: copious watery diarrhea, hypokalemia, achlorhydria

22
Q

what substance is implicated in LES tone of achalasia?

A

NO (loss of it)

23
Q

what makes intrinsic factor? what does it do?

A

parietal cells, stomach

B12 blah blah blah

24
Q

what makes gastric acid?

A

parietal cells, stomach

25
Q

regulation of gastric acid?

A

stimulated by gastrin, histamine, ACh (vagus)

inhibited by SST, GIP, PGs, secretin

26
Q

what makes pepsin?

A

chief cells, stomach

27
Q

regulation of pepsin?

A

stimulated by VAGUS, local acid

** pepsinogen –> pepsin in presence of H+

28
Q

what makes HCO3 in GI tract?

A

mucosal cells and Brunner glands (duodenum)

29
Q

regulation of HCO3 secretion?

A

stimulated by pancreatic and biliary secretion with secretin

30
Q

what are enterochromaffin-like cells?

A

stimulated by gastrin –> make histamine –> stimulates parietal cell HCl release

** primary mechanism of gastrin –> HCl stimulation (greater contribution than direct stimulation of parietal cells)

31
Q

intracellular pathway for vagal stimulation of parietal cells?

A

ACh –> M3 receptor –> Gq –> IP3/Ca –> HCl release via H/K ATPase

32
Q

intracellular pathway for (direct) gastrin stimulation of parietal cells?

A

binds CCKb receptor –> Gq –> IP3/Ca –> HCl release

33
Q

intracellular pathway for histamine stimulation of parietal cells?

A

binds H2 receptor –> Gs –> cAMP –> HCl release

34
Q

intracellular pathway for PG/SST inhibition of parietal cells?

A

bind receptor –> Gi –> decreased cAMP –> decreased HCl release

35
Q

what converts trypsinogen to trypsin?

A

enterokinase/enteropeptidase

enzyme on brush-border (duodenum and jejunum)

36
Q

carb absorption in gut?

A

only monosaccharides absorbed
glu and gal –> SGLT1 (Na dependent) –> GLUT2 –> blood
fru –> GLUT5 (facilitated diffusion) –> GLUT2 –> blood

37
Q

vit/minerals absorbed in SI?

A

iron (Fe 2+) - duodenum
folate
B12 - TI, absorbed with bile salts, needs IF

38
Q

what are M cells?

A

in Peyer patches, present antigen to immune cells

39
Q

where are Peyer patches?

A

ileum - lamina propria and submucosa

40
Q

where do plasma cells of Peyer patches live?

A

lamina propria

41
Q

what is in bile?

A
bile salt = bile acids + gly/taurine
phospholipids
cholesterol
bilirubin
water
ions
42
Q

what enzyme catalyzes rate limiting step of bile synthesis?

A

cholesterol 7 alpha hydroxylase

43
Q

functions of bile?

A

lipid/fat sol vitamin digestion/absorption
cholesterol excretion
antimicrobial activity

44
Q

first step of heme metabolism?

A

heme oxygenase converts to biliverdin

45
Q

what does biliverdin become?

A

unconjugated bili

46
Q

is unconjugated bili water soluble?

A

NO!

47
Q

what enzyme makes conjugated bili?

A

UDP glucuronosyl transferase - adds glucuronic acid

48
Q

what converts conjugated bili to urobilinogen?

A

gut bacteria

49
Q

what is stercobilin?

A

form in which bili is excreted in stool - gives brown color

50
Q

what is urobilin?

A

form in which bili is excreted in urine - gives yellow color