GI endocrinology Flashcards

1
Q

What is the difference between acinar cells and duct cells?

A

•Acinar cells

–Serous cells = protein part including enzymes + ionic solutions

–Mucous cells = mucins

•Duct cells = modify ionic concentrations

General principle: Acinar cells secrete and duct cells modify

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2
Q

What enzyme cleaves pepsinogen to pepsin?

A

Trick question - there isn’t one - it’s the acidic environment that causes it to cleave.

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3
Q

What cells (3) are unique to the epithelium in the body/oxyntic region of the stomach and what do they secrete?

A

~parietal cells - HCl, intrinsic factor

~chief cells - pepsinogen

~ECL cells - histamine

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4
Q

What cells (2) are unique to the epithelium in the pyloric region of the stomach and what do they secrete?

A

~neuroendocrine G cells - gastrin (increase digestion)

~neuroendocrine D cells - somatostatin (slow down digestion)

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5
Q

What is the alkaline tide?

A

In acid-secreting parietal cells, for each H+ pumped into lumen, one HCO3- enters blood

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6
Q

How do we deal with the alkaline tide? (can’t have highly alkaline blood for long)

A

Pancreas releases bicarb from the blood into the small intestine tract to neutralize the H+ flood from the stomach

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7
Q

How is stomach acid secretion regulated?

A
  • Four chemical messengers regulate the insertion of H+/K+ -ATPase into plasma membrane: ACh, gastrin, histamine, and somatostatin
  • Parietal cells contain receptors for all four agents (go: ACh, gastrin, histamine; stop: somatostatin)
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8
Q

ACh: who releases? what receptors?

A

ACh released by vagus or enteric neurons acting on mAChR (M3)

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9
Q

Gastrin: who releases? what receptors?

A

Gastrin released by G cells in antrum and duodenum acting on CCKB receptor

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10
Q

Histamine: who releases? what receptors?

A

Histamine released by ECL cells acting on H2 receptor

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11
Q

Somatostatin: who releases? what receptors?

A

Somatostatin released by D cells in antrum and duodenum acting on SSTR2 receptor

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12
Q

What are the three phases of gastric acid secretion?

A

~cephalic (taste, smell, thought of food -> medulla oblongata -> vagus -> increase in gastric secretion)

~gastric (distention of stomach -> increase of gastric secretion)

~intestinal (chyme containing lipids, amino acids, lots of H+ signals medulla oblongata to decrease gastric secretion)

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13
Q

What hormones released by the duodenum inhibit gastric secretions in the stomach?

A

secretin

CCK (cholecystokinin)

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14
Q

Which hormone is dominant in the cephalic phase?

A

CCK

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15
Q

Which hormone is dominant in the intestinal phase?

A

secretin

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16
Q

CCK and secretin inhibit gastric secretions; what are their effects at the pancreas?

A

stimulate enzyme secretion

17
Q

What does cholera do that causes disease?

A

choleratoxin binds Gs protein -> increase cAMP -> insertion and opening of CFTR chloride channel -> increases cAMP -> chloride is going to be lost in huge quantities -> diarrhea

18
Q

What substance stimulates secretion of bile from gallbladder?

A

CCK (contracts gallbladder)

19
Q

What substance stimulates secretion of digestive enzymes from pancreas?

A

CCK (relaxes sphincter of Oddi)

20
Q

What are two devastating effects of diseases that disrupt the terminal ileum, such as Crohn’s?

A
  1. poor bile reuptake, which mostly occurs here
  2. poor B12-IF absorption, which occurs here
21
Q

What is the problem that occurs in the gut in cystic fibrosis?

A

decreased secretions of chloride = impaired flow and mucosa of intestine

Cystic fibrosis = abnormal function of CFTR chloride channel